Carranza's Clinical Periodontology (2nd Southeast Asian Edition)

C ZA'S
Perlodontology
Yasser Magrami
Carranza's
Clinical Periodontology
SECOND SOUTH ASIA EDITION
Page left intentionally blank
Carranza's
Clinical Periodontology SECOND
SOUTH ASIA
EDITION
MG NEWMAN, PR KLOKKEVOLD,
DDS, FACD DDS, MS, FACD
Professor Emeritus, Section of Periodontics Associate Professor, Section of Periodontics
School of Dentistry Director, Postgraduate Periodontics
University of California Residency, School of Dentistry
Los Angeles, California University of California
Los Angeles, California
HH TAKEI, DDS,
EDITOR EMERITUS
MS, FACD
Distinguished Clinical Professor FA CARRANZA,
Section of Periodontics ..•.
School of Dentistry
DR ODONT, FACD
University of California Professor Emeritus, Section of Periodontics
Los Angeles, California School of Dentistry
University of California
ADAPTATION EDITORS
CD DWARAKANATH, MOS DG NAIK, MOS

Professor and Head Dean and Professor
Department of Periodontics and Department of Periodontics
Implantology Mani pal College of Dental Sciences
and Director of Post Graduate Studies Mangalore, India
Vishnu Dental College
Bhimavaram, India A UPPOOR, MOS
Associate Dean and Professor
N AMBALAVANAN, MOS Department of Periodontics
Manipal College of Dental Sciences
Professor and Head
Mangalore, India
Department of Periodontology
Meenakshi Ammal Dental College
A JAIN, MOS
and Hospital
Chennai, India Principal-cum-Professor
Dr HS Judge Institute of Dental Sciences
Panjab University
Chandigarh, India
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CARRANZA'S CLINICAL PERIODONTOLOGY, 12rn EDITION, Michael G Newman, Henry

H Takei, Perry R Klokkevold, and Fermin A Carranza
ISBN 978-0-323-18824-l
Copyright© 2015, 2012, 2006 by Saunders, an imprint of Elsevier Inc. All rights reserved.
This adaptation of Carranza's Clinical Periodontology, 12e by Michael G Newman, Henry H Takei, Perry R
Klokkevold and Fermin A Carranza was undertaken by RELX India Private Limited and is published by arrange-
ment with Elsevier Inc.
Carranza's Clinical Periodontology, Second South Asia Edition

Adaptation Editors: CD Dwarakanath, N Ambalavanan, DG Naik, A Uppoor and A Jain
Copyright© 2016 RELX India Private Limited.

Adaptation ISBN 978-81-312-4450-0
eISBN 978-81-312-4669-6
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Editors
ASSOCIATE AND SECTION EDITORS

FA Carranza, Dr Odont, FACD MG Newman, DDS, FACD
Professor Emeritus, Section of Periodontics Professor Emeritus, Section of Periodontics
School of Dentistry School of Dentistry
University of California University of California
Los Angeles, California Los Angeles, California
JL Forrest, RDH, EdD P Preshaw, BDS, FDS RCSEd, FDS (Rest Dent)
Professor of Clinical Dentistry RCSEd, PhD
Section Chair, Behavioral Science and Practice Management Professor of Periodontology
Director, National Center for Dental Hygiene Research Institute of Cellular Medicine
and Practice School of Dental Sciences
Herman Ostrow School of Dentistry of USC Newcastle University
University of Southern California Newcastle upon Tyne, United Kingdom
HH Takei, DDS, MS, FACD
S Jepsen, DDS, MD, MS, PhD Distinguished Clinical Professor, Section of Periodontics
Professor and Chairman School of Dentistry
Department of Periodontology University of California
Operative and Preventive Dentistry Los Angeles, California
University of Bonn, Germany
W Teughels, DDS, PhD
PR Klokkevold, DDS, MS, FACD Associate Professor
Associate Professor, Section of Periodontics Periodontology Unit
Director, Postgraduate Periodontics Residency KU Leuven-Department of Oral Health Services
School of Dentistry University Hospitals Leuven-Dentistry Department
University of California Leuven, Belgium
V
Contributors
E Abt, DDS, MS, MSc MJ Bloom, DMD

Director Clinical Associate Professor
General Practice Residency Program Ashman Department of Periodontology & Implant Dentistry
Advocate Illinois Masonic Medical Center New York University College of Dentistry
Chicago, Illinois Private Practice
New York, New York
A Aguirre, DDS, MS
Director, Advanced Oral and Maxillofacial Pathology J Bulkacz, Dr Odont, PhD
Professor, Department of Oral Diagnostic Sciences Lecturer, Section of Periodontics
University at Buffalo, The State University of New York School of Dentistry
Buffalo, New York University of California
EP Allen, DDS, PhD
Director B Butler, DDS
Center for Advanced Dental Education Private Practice
Dallas, Texas St. Petersburg, Florida
Affiliate Faculty Member
WF Ammons Jr, DDS, MSDt University of Washington
Professor Emeritus Seattle, Washington
Department of Periodontics
University of Washington PM Camargo, DDS, MS, MBA, FACD
School of Dentistry Professor and Tarrson Family Endowed Chair of Periodontics
Seattle, Washington Division of Associated Clinical Specialties
Section of Periodontics
MH Anderson, DDS, MS, MEdt Associate Dean of Clinical Dental Sciences
President and CEO, C3 Jian, Inc. School of Dentistry
Inglewood, California University of California
A Aoki, DDS, PhD
Instructor and Research Associate FA Carranza, Dr Odont, FACD
Section of Periodontology Professor Emeritus, Section of Periodontics
Department of Hard Tissue Engineering School of Dentistry
Tokyo Medical and Dental University University of California
Tokyo, Japan Los Angeles, California
RRAzzi, DDS L Chambrone, DDS, MSc, PhD, Pos-Doc

Assistant Clinical Professor Specialist in Periodontology
Department of Periodontics Specialist in Orthodontics & Dentofacial Orthopedics
University of Paris VII-School of Dentistry Assistant Professor, Dental Research Division,
Paris, France Department of Periodontology
Guarulhos University (UnG)
JG Bauer, DDS, MSEd, MSPH, MBA Guarulhos, SP, Brazil
Professor
Restorative, Geriatric and Evidence-Based Dentistry T-L Chang, DDS
Center for Dental Research Clinical Professor
School of Dentistry Division of Advance Prosthodontics
Loma Linda University School of Dentistry
Loma Linda, California University of California
'Deceased
vii
viii Contributors
S-C Cho, DDS S De Geest

Assistant Clinical Professor Post graduate student Periodontology
Director, Implant Program for International Dentists Department of Periodontology
Ashman Department of Periodontology and Implant Dentistry Catholic University of Leuven
New York University College of Dentistry School of Dentistry
New York, New York Oral Pathology and Maxillofacial Surgery
Leuven, Belgium
C-H Chou, PhD
Center for Pharmacogenomics and Complex Disease Research RR Derycke, DScD
Department of Oral Biology, New Jersey Dental School Private Practice
Department of Health Informatics, School of Health Paris, France
Related Professions
University of Medicine and Dentistry of New Jersey SR Diehl, PhD
Newark, New Jersey Professor of Oral Biology
Rutgers School of Dental Medicine
E Chung, DDS Professor of Health Informatics
Clinical Professor, Department of Advanced Prosthodontics Rutgers School of Health Related Professions
School of Dentistry Rutgers-The State University of New Jersey
University of California New Brunswick, New Jersey
J Do, DDS
SC Ciancio, DDS Lecturer, Section of Periodontics
Distinguished Service Professor and Chair School of Dentistry
Department of Periodontics and Endodontics University of California
State University of New York-School of Dentistry Los Angeles, California
Buffalo, New York
H Dommisch, DDS, PhD
DL Cochran, DDS, PhD Associate Professor
Professor and Chair Periodontology, Operative and Preventative Dentistry
Department of Periodontics University of Bonn
The University of Texas Health Science Center Bonn, Germany NRW
San Antonio, Texas Associate Professor
Oral Health Sciences
JP Cooney, BDS, MS University of Washington
Clinical Professor Emeritus Seattle, Washington
Restorative Dentistry
School of Dentistry DF Duperon, DDS, MSc
University of California Professor Emeritus
Los Angeles, California Section of Pediatric Dentistry
School of Dentistry
JJ Crall, DDS, ScD University of California
Professor Los Angeles, California
Pediatric Dentistry
School of Dentistry DH Etienne, DDS, MS
University of California Department of Periodontology, Service of Odontology
Los Angeles, California Pine-Salpetriere Hospital
Denis Diderot University, UFR of Odontology
JD Cross, DDS Paris, France
Private Practice
Springfield, Illinois RC Fazio, DMD
Associate Clinical Professor in Surgery
J Dadamio, MSc Yale Medical School
Research Associate College of Medicine
Periodontology Unit New Haven, Connecticut
KU-Leuven Private Practice
Department of Oral Health Sciences Norwalk, Connecticut
Leuven, Belgium
Contributors ix
RD Finkelman, DDS, PhD SK Haake, DMD, MDentSc, PhD

Senior Medical Director Associate Professor
Oncology/New Opportunities Section of Periodontics
AstraZeneca LP University of California, Los Angeles-School of Dentistry
Wilmington, Delaware Los Angeles, California
JP Fiorellini, DMD, DMSc TJ Han, DDS, MS, FACD

Professor and Chair Clinical Professor
Department of Periodontics Section of Periodontics
University of Pennsylvania School of Dental Medicine University of Southern California
Philadelphia, Pennsylvania School of Dentistry
JL Forrest, RDH, EdD
Professor of Clinical Dentistry GW Harrington, DDS, MSD
Section Chair, Behavioral Science and Practice Management Professor Emeritus and Chair
Director, National Center for Dental Hygiene Research and Department of Endodontics
Practice University of Washington
Herman Ostrow School of Dentistry of USC School of Dentistry
University of Southern California Seattle, Washington
Los Angeles, California MC Haytac, PhD
Professor
SH Froum, DDS
Cukurova University
Clinical Assistant Professor
Faculty of Dentistry
Ashman Department of Periodontology
and Implant Dentistry
Adana, Turkey
New York University, College of Dentistry
Private Practice JE Hinrichs, DDS, MS
New York, New York Professor and Director of Advanced Education
Program in Periodontology
SJ Froum, DDS, PC University of Minnesota
Diplomate of the American Board of Periodontology School of Dentistry
Diplomate of the International Congress of Minneapolis, Minnesota
Oral Implantology
Periodontics and Implant Dentistry EL Hogan, MD, DDS, MS
Clinical Professor and Director of Clinical Research Lecturer, Section of Periodontics
Department of Periodontology and Implant Dentistry School of Dentistry
New York University College of Dentistry University of California
New York, New York Los Angeles, California
Private Practice
New York, New York C-Y Huang, PhD
Senior Computer Scientist
G Galindo Center for Pharmacogenomics and Complex
Russell Investments Disease Research
New York, NY Department of Oral Biology, New Jersey Dental School
United States University of Medicine and Dentistry of New Jersey
Newark, New Jersey
C Godts, MSc, PhD
Research Associate PP Hujoel, PhD, DDS, MSD, MS
Periodontology Unit Professor
KU-Leuven Department of Oral Health Sciences
Department of Oral Health Sciences University of Washington
Leuven, Belgium School of Dentistry
Seattle, Washington
Y Gu, DDS, PhD
I Ishikawa, DDS, PhD
Associate Professor
Professor
Department of General Dentistry
Section of Periodontology
Stony Brook University
Department of Hard Tissue Engineering
School of Dental Medicine
Tokyo Medical and Dental University
Stony Brook, New York
Tokyo, Japan
x Contributors
CA Jahn, RDH, MS M Kebschull, Dr Med Dent

Senior Professional Relations Manager Consultant
Water Pik, Inc. Department of Periodontology,
Warrenville, Illinois Operative and Preventive Dentistry
University of Bonn
N Jakubovics, BSc, PhD Bonn, NRW, Germany
Lecturer in Oral Biology
Newcastle University DM Kim, DDS, DMSc
School of Dental Sciences Assistant Professor, Oral Medicine, Infection,
Newcastle upon Tyne, United Kingdom and Immunity
Director, Predoctoral Program in Periodontology
S Jepsen, DDS, MD, MS, PhD Harvard School of Dental Medicine
Professor and Chairman Boston, Massachusetts
Operative and Preventive Dentistry GU Kim, DDS, MS
University of Bonn Postgraduate Student in Implant Dentistry
Bonn, NRW, Germany Department of Periodontology and Implant Dentistry
New York University College of Dentistry
DL Jolkovsky, DMD, MS New York, New York
Private Practice Research and Lecture Coordinator
Davis, California Vizstara and Vizstara Professional
Lecturer, Section of Periodontics Englewood Cliffs, New Jersey
School of Dentistry
Los Angeles, California KL Kirkwood, DDS, PhD
Professor and Chair, Department of Oral Health Sciences
BP Kamel, Esq Associate Dean for Research
Managing Partner Director, Center for Oral Health Research
Kamel and Maxwell, Attorneys at Law James B. Edwards College of Dental Medicine
Los Angeles, California Professor of Microbiology and Immunology
Medical University of South Carolina College of Medicine
MK Kang, DDS, PhD Charleston, South Carolina
Professor and Chairman
Jack A. Weichman Endowed Chair PR Klokkevold, DDS, MS, FACD
Section of Endodontics Associate Professor, Section of Periodontics
School of Dentistry Director, Postgraduate Periodontics Residency
University of California School of Dentistry
Los Angeles, California University of California
DWK Kao, DDS, MS, DMD
Instructor VG Kokich, DDS, MSDt
Department of Periodontics Professor
University of Pennsylvania School of Dental Department of Orthodontics
Medicine University of Washington
Director, Predoctoral Periodontics School of Dentistry
Philadelphia, Pennsylvania Seattle, Washington
RT Kao, DDS, Phd OA Korczeniewska

Private Practice Research Associate II
Cupertino, California Rutgers School of Dental Medicine
Clinical Professor Rutgers-The State University of New Jersey
Division of Periodontology Newark, New Jersey
University of California, San Francisco
Adjunct Clinical Professor G Kotsakis
Department of Periodontology Resident in Periodontology
University of Pacific University of Minnesota
San Francisco, California Minneapolis, Minnesota
1Deceased
Contributors xi
F Kuo, MS BL Mealey, DDS, MS

Senior Bioinformatics Scientist Professor and Graduate Program Director
Rutgers School of Dental Medicine Department of Periodontics
Rutgers-The State University of New Jersey The University of Texas Health Sciences Center at San Antonio
Newark, New Jersey San Antonio, Texas
PR Melnick, DMD
I Laleman
Lecturer, Section of Periodontics
Post Graduate Student, Periodontology
School of Dentistry
Catholic University of Leuven
School of Dentistry
Oral Pathology and Maxillofacial Surgery RL Merin, DDS, MS
Leuven, Belgium Private Practice
Woodland Hills, California
CS Law, DMD MS
Associate Clinical Professor CW Miller, DDS
Sections of Pediatric Dentistry and Orthodontics Private Practice in General Dentistry
School of Dentistry Deer Park, Washington
University of California SA Miller, BA
Los Angeles, California Director
ebdLibrary
MB Lieberman, DDS Deer Park, Washington
Clinical Lecturer, Section of Periodontics
School of Dentistry KT Miyasaki, DDS, MS, PhD
University of California Associate Professor
Los Angeles, California Section of Oral Biology
University of California, Los Angeles-School of Dentistry
SM Mallya, BDS, MDS, PhD Los Angeles, California
Assistant Professor
I Needleman, BDS, MSc, PhD, MRDRCS(Eng),
Director, Oral and Maxillofacial Radiology Program
FDSRCS(Eng), FFPH, FHEA
Section of Oral and Maxiofacial Radiology
Professor of Restorative Dentistry and Evidence-Based
School of Dentistry
Healthcare
Honorary Consultant and Specialist in Periodontology
Director, International Centre for Evidence-Based Oral
Health (ICEBOH)
A Mariotti, BS, DDS, PhD
Unit of Periodontology
Professor and Chair
Division of Restorative Dental Sciences
Division of Periodontology
UCL Eastman Dental Institute
The Ohio State University
London, England
College of Dentistry
Columbus, Ohio MG Newman, DDS, FACD
Professor Emeritus, Section of Periodontics
MJ McDevitt, DDS School of Dentistry
Visiting Faculty University of California
Advanced Education in Periodontics Los Angeles, California
College of Dental Medicine
Georgia Regents University ML Nevins, DMD, MMSc
Augusta, Georgia Assistant Clinical Professor
Visiting Faculty Division of Periodontology
LD Pankey Institute Harvard School of Dental Medicine
Private Practice Boston, Massachusetts
Atlanta, Georgia RJ Nisengard, DDS, PhDt
Distinguished Teaching Professor
A McGregor, DDS Associate Dean for Advanced Education and Research
Private Practice State University of New York
Westlake Village, California School of Dentistry
Buffalo, New York
"Deceased
xii Contributors
KF Novak, DDS, MS, PhD B Pelsmaekers, DDS

Professor Private Practice
Department of Periodontics Leuven, Belgium
Center for Oral Health Research
University of Kentucky DA Perry, RDH, PhD
Lexington, Kentucky Professor and Associate Dean for Education and Student
Affairs
MJ Novak, BDS, LDS, PhD Department of Preventive and Restorative Dental Sciences
Professor of Periodontics and Associate Director School of Dentistry
Department of Periodontics University of California
Center for Oral Health Research San Francisco, California
University of Kentucky
Lexington, Kentucky FQ Pirih, DDS, PhD
Diplomate, American Board of Periodontology
J Otomo-Corgel, DDS, MPH Assistant Professor, Section of Periodontics
Greater Los Angeles Veteran's Administration School of Dentistry
Healthcare System University of California
Associate Clinical Professor, Section of Periodontics Los Angeles, California
School of Dentistry
University of California AM Polson, DMD, MS
Los Angeles, California Professor of Periodontics and D. Walter Cohen Chair
0 Ozcelik, PhD School of Dental Medicine at the University of Pennsylvania
Associate Professor Philadelphia, Pennsylvania
Cukurova University
Faculty of Dentistry PM Preshaw, BDS, FDS RCSEd, FDS (Rest Dent)
Department of Periodontology RCSEd, PhD
Adana, Turkey Professor of Periodontology
Institute of Cellular Medicine and School of Dental Sciences
K-B Park, DDS, MS, PhD Newcastle University
Former Assistant Researcher in Periodontics Newcastle upon Tyne, United Kingdom
School of Dentistry
University of California M Quirynen, DDS, PhD
Los Angeles, California Professor
Director, MINEC Institute of Clinical Periodontics and Department of Periodontology
Implantology Catholic University of Leuven
Lecturer in Oral Anatomy and Histology School of Dentistry
Kyung-Pook National University Oral Pathology and Maxillofacial Surgery
Taegu, Korea Leuven, Belgium
AM Pattison, RDH, MS TD Rees, DDS, MSD

Associate Professor Emeritus Professor
Division of Periodontics, Diagnostic Sciences Department of Periodontics
and Dental Hygiene Baylor College of Dentistry
Ostrow School of Dentistry Texas A&:M University
University of Southern California Dallas, Texas
MA Reynolds, DDS, PhD
CL Pattison, DDS Professor and Chair
Private Practice Director, Postdoctoral Periodontics
Los Angeles, California Department of Periodontics
Formerly, Instructor University of Maryland
Section of Periodontics School of Dentistry
School of Dentistry Baltimore, Maryland
Contributors xiii
C Rossa, Jr, DDS, MS, PhD G Shklar, DDS, MS

Associate Professor Professor Emeritus
Department of Diagnosis and Surgery Charles A. Brackett Professor of Oral Pathology
Faculdade de Odontologia de Araraquara Harvard University
Universidade Estadual Paulista School of Dental Medicine
UNESP Boston, Massachusetts
Araraquara, SP, Brazil
DR Silva, DDS, MS
ME Ryan, DDS, PhD Chair and Dr. Thomas K. Barber Endowed Chair
Professor and Chair Director, Pediatric Dentistry Residency Program
Department of Oral Biology and Pathology Associate Clinical Professor
School of Dental Medicine Section of Pediatric Dentistry
Medical Staff University Hospital School of Dentistry
Stony Brook Medicine University of California
Stony Brook University Los Angeles, California
Stony Brook, New York
TN Sims, DDS
M Sanz, MD, DDS
Lecturer, Section of Periodontics
Dean and Professor
School of Dentistry
Universidad Complutense de Madrid-Faculty of Dentistry
Madrid, Spain
Private Practice
Torrance and Santa Monica, California
ET Scheyer, DDS, MS
Private Practice
Peria Health Professionals PLLC SS Spackman, DDS, FASGD
Houston, Texas Associate Clinical Professor
Department of Oral Diagnosis, Radiology and Pathology
T Schleyer, DMD, PhD, MBA Department of Restorative Dentistry
Clem McDonald Professor of Biomedical Informatics School of Dentistry
Director, Center for Biomedical Informatics Loma Linda University
Regenstrief Institute, Inc. Loma Linda, California
Professor of Medicine
Department of Medicine FM Spear, DDS, MSD
Indiana University School of Medicine Founder and Director
Indianapolis, Indiana Spear Education
Seattle, Washington
CB Serhal, DDS, MSD, PhD
Consultant VW Spolsky, DMD, MPH
Department of Periodontology Associate Professor
Catholic University of Leuven UCLA School of Dentistry, Clinical Research Center
Private Practice Los Angeles, California
Periodontology and Implantology
Leuven, Belgium
PG Stathopoulou, DDS, MS, PhD
Assistant Professor-Director, Predoctoral Periodontics
DA Shanelec, DDS
Director
School of Dental Medicine
Microsurgery Training Institute
University of Pennsylvania
Santa Barbara, California
Philadelphia, Pennsylvania
K Shin, DDS, PhD

Professor C Stein, MS
Division of Periodontology Dental Medicine Student
Department of Oral Biology and Tissue Engineering Western University of Health Sciences
Meikai University College of Dental Medicine
School of Dentistry Pomona, California
Sakado-shi, Saitama, Japan
xiv Contributors
HH Takei, DDS, MS, FACD IA Urban, DMD, MD, PhD

Distinguished Clinical Professor, Section of Periodontics Assistant Professor
School of Dentistry Graduate Implant Dentistry
University of California Loma Linda University
Los Angeles, California Loma Linda, California
Private Practice
DP Tarnow, DDS Budapest, Hungary
Clinical Professor and Director of Implant Education
Columbia University College of Dental Medicine NB Uzel
New York, New York Former Instructor
Private Practice Department of Periodontics
New York, New York University of Pennsylvania
JJ Taylor, PhD
Senior Lecturer in Molecular Immunology S Van den Velde, MSc, PhD
Periodontal Immunobiology Research Group Research Associate
Institute of Cellular Medicine and School of Dental Sciences Catholic University of Leuven
Newcastle University School of Dentistry
Newcastle upon Tyne, United Kingdom Oral Pathology and Maxillofacial Surgery
Leuven, Belgium
S Tetradis, DDS, PhD
B Vandekerckhove, DDS, PhD
Professor and Chair
Instructor
Section of Oral and Maxillofacial Radiology
School of Dentistry
Catholic University of Leuven
School of Dentistry
Oral Pathology and Maxillofacial Surgery
Leuven, Belgium
W Teughels, DDS, PhD
Associate Professor JLT Vasquez, DDS, MS
Periodontology Unit Assistant Professor
KU Leuven-Department of Oral Health Services Department of Oral Diagnostic Sciences
University Hospitals Leuven-Dentistry Department School of Dental Medicine
Leuven, Belgium University at Buffalo, The State University of New York
Buffalo, New York
VT Math, BDS, PhD
Research Fellow T Vercellotti, DDS, MS
National Institute of Health Honorary Professor and Faculty
Bethesda, Maryland University College of London
London, England
T Thyvalikakath, DMD, MDS, PhD Private Practice
Associate Professor and Director Genova, Italy
Dental Informatics Core
Department of Restorative Dentistry K Wada, DDS, PhD, DMSc, DMD
Indiana University School of Dentistry Associate Professor
Indianapolis, Indiana Director of Implant Dentistry
Assistant Director of Postdoctoral Periodontics
LS Tibbetts, DDS, MSD Department of Periodontics
Private Practice University of Pennsylvania
Arlington, Texas School of Dental Medicine
KC Trabert, DDS, MEd
Clinical Professor, Section of Endodontics A Zacher, MBA
School of Dentistry Founder and Director of Snorer.com
University of California Co-founder, British Society of Dental Sleep Medicine
SJ Zackin, DMD
Sarasota, Florida
Contributors xv
CONTRIBUTORS TO THE ADAPTATION EDITION

N Ambalavanan, MOS DG Naik, MOS
Professor and Head Dean and Professor
Department of Periodontology Department of Periodontics
Meenakshi Ammal Dental College and Hospital Manipal College of Dental Sciences
Chennai, India Mangalore, India
CD Dwarakanath, MOS A Uppoor, MOS

Professor and Head Associate Dean and Professor
Department of Periodontics and Implantology Department of Periodontics
and Director of Post Graduate Studies Manipal College of Dental Sciences
Vishnu Dental College Mangalore, India
Bhimavaram, India
A Jain, MOS
Principal-cum-Professor
Dr HS Judge Institute of Dental Sciences
Panjab University
Chandigarh, India
About the Authors
MICHAEL G. NEWMAN, DDS, FACD

Dr. Michael G. Newman graduated from the University of California, Los Angeles (UCLA)
College of Letters and Sciences with a degree in psychology. He completed his dental training at
the UCLA School of Dentistry in 1972. Dr. Newman received a Certificate in Periodontics and
Oral Medicine at the Harvard School of Dental Medicine and a Certificate in Oral Microbiology
from the Forsyth Dental Institute under the mentorship of Dr. Sigmund Socransky. He is a
diplomate of the American Board of Periodontology and is Professor Emeritus of Periodontics
at the UCLA School of Dentistry. Dr. Newman is a fellow and past President of the American
Academy of Periodontology. In 1975, he won the Balint Orban Memorial Prize from the
American Academy of Periodontology. He had been in private practice of periodontics for
more than 25 years. In 2007, Dr. Newman received the Gold Medal, the highest honor
bestowed by The American Academy of Periodontology.
Dr. Newman has published more than 260 abstracts, journal articles, and book chapters
and has co-edited nine textbooks. He has served as an ad-hoc reviewer for the National
Institute of Dental and Craniofacial Research, was a consultant to the Council on Scientific
Affairs of the American Dental Association, and is a reviewer for numerous scientific and
professional journals and governmental research organizations.
Professor Newman has lectured throughout the world on microbiology, antimicrobials, evidencebased methodology, risk
factors, and diagnostic strategies for periodontal disease. He has a strong interest in applied science and transfer of new technology
for practical use. Dr. Newman is a consultant to major dental and pharmaceutical companies throughout the world. He is the
founding editor in chief of the Journal of Evidence-Based Dental Practice (JEBDP), The JEBDP Annual Report Series, and was the
associate editor of the International Journal of Oral and Maxillofacial Implants.
HENRY H. TAKEI, DDS, MS, FACD

Dr. Henry H. Takei graduated in 1965 from the Marquette University School of Dentistry
in Milwaukee, Wisconsin. He completed his Periodontics Certificate and Master of
Science degree in 1967 at the Marquette University and the Veterans Administration
Hospital in Wood, Wisconsin.
Dr. Takei is a Distinguished Clinical Professor of Periodontics at the UCLA School of
Dentistry and a Consultant in Periodontics at the Veterans Administration Hospital in
Los Angeles. He maintains a private practice limited to periodontics and implant surgery.
Dr. Takei has published numerous articles on periodontal surgery and has contrib-
uted chapters to five textbooks. He has been actively involved in continuing education
and has lectured throughout the world on clinical periodontology and implant surgery.
Dr. Takei has been honored nationally and internationally with awards from numerous
periodontal organizations, universities, and study clubs for his contributions to education.
He received the Distinguished Alumnus Award by Marquette University in 2001
and the Honorary Distinguished Alumnus Award by the University of California, Los
Angeles in 1998. The American Academy of Periodontology has honored Dr. Takei with
the prestigious Master Clinician Award in 2006.
xvii
xviii About the Authors
PERRY R. KLOKKEVOLD, DDS, MS, FACD

Dr. Perry R. Klokkevold graduated from the University of California, San Francisco
School of Dentistry in 1986. His postdoctoral clinical training includes a General
Practice Residency in Hospital Dentistry completed in 1987, a Postgraduate Periodontal
Residency completed in 1994, and a Surgical Implant Fellowship completed in 1995.
All of his postgraduate training was completed at the UCLA School of Dentistry. He
earned a Master of Science degree in Oral Biology at UCLA in 1995.
Dr. Klokkevold is a Diplomate of the American Board of Periodontology and a Fellow of
the American College of Dentists. He is an Associate Professor in the Division of Associated
Specialties, Section of Periodontics, at the UCLA School of Dentistry and Director of the
UCLA Postgraduate Periodontics Residency program. Dr. Klokkevold served as Clinical
Director and Director of the General Practice Residency program in Hospital Dentistry at
UCLA School of Dentistry from 1987 to 1992. He has maintained a faculty practice limited
to the specialty of periodontics and dental implant surgery at UCLA since 1995.
Dr. Klokkevold has published numerous articles for international journals and
has written several book chapters on topics that include juvenile periodontitis,
periodontal medicine, influence of systemic disease and risk factors on periodontitis,
bone regeneration, and dental implants. He has served as a reviewer for several
journals, including the Journal of Periodontology and the International Journal of Oral and
Maxillofacial Implants. Dr. Klokkevold has lectured nationally and internationally on
many periodontal and implant-related topics.
FERMIN A. CARRANZA, DR ODONT, FACD

Dr. Fermin A. Carranza graduated from the University of Buenos Aires School of
Dentistry in Argentina in 1948 and completed his postdoctoral training in periodon-
tics at Tufts University School of Dental Medicine in 1952 under the mentorship of
Dr. Irving Glickman.
Dr. Carranza is Professor Emeritus of Periodontology at the UCLA School of
Dentistry. He was head of the Department of Periodontics at the University of Buenos
Aires from 1966 to 1974, and at UCLA from 1974 until his retirement in 1994.
Dr. Carranza has published more than 218 scientific papers and abstracts on basic
and applied aspects of periodontics and 18 books, including the past five editions of
Clinical Periodontology. He has received numerous awards and recognition for his
work, including the IADR Science Award in Periodontal Disease and the Gies Award of
the American Academy of Periodontology.
Dr. Carranza has lectured throughout the world on clinical periodontology, pathology,
and therapy.
About the Adaptation Editors
Dr CD Dwarakanath ob- Dr Dilip G Naik obtained

tained his BDS degree from his BDS in 1983 and MDS
Government Dental College in Periodontology in 1986
Bangalore in 1975 and his from Manipal College of
Masters degree in Periodon- Dental Sciences, Manipal. He
tics from Madras Dental Col- is a founder staff of Manipal
lege, Madras in 1980. He has College of Dental Sciences,
been totally into academics Mangalore, having joined
having taught in India and in 1987. At present, he is
abroad for the last 36 years the Dean and Professor of
and has trained scores of Periodontology of Manipal
BDS and MDS students. College of Dental Sciences,
He has lectured extensively Mangalore. He had a stint of
throughout the country and 8 years at the Al-Arab Medi-
is one of the most sought after speakers in Periodontology in cal University, Benghazi,
India today Until now he has delivered more than 130 ora- Libya. He obtained a cer-
tions. At present he is working as Professor and Head of the tificate in Oral Implantology from Manipal University in the
Department of Periodontology and Director of Postgraduate year 2000. He has undergone training in Oral Implantology at
Studies, Vishnu Dental College, Bhimavaram. He has served Germany. He has been a keynote speaker at several national
as a member of the Board of Studies, PhD board and Research and international conferences. He has over 40 national and
grants, and Curriculum and syllabus committee of many international publications to his credit. He has conducted
universities. He has conducted many teachers' training pro- 12 national and international multicentric clinical trials. He
grams. He is also the former President of the Indian Society of was the Vice President of Indian Society of Periodontology for
Periodontology. 2 consecutive years.
Dr N Ambalavanan ob- Dr Ashita Uppoor graduated

tained his BDS degree from from Nair Dental College,
Madras University in 1981 Bombay in 1988 and went
and his MDS degree from on to do her MDS in Peri-
Madras University in 1985. odontology in 1994 from
He has been into academ- Manipal College of Dental
ics and taught for more Sciences, Manipal. Later, she
than 27 years to UG and
PG students. He is a Life
member of Indian Society of
r
,
', ·\~' · ·'
' ' '
,
J
.A
joined Manipal College of
Dental Sciences, Mangalore
as an assistant professor. At
Periodontology He was for- present she is the Associ-
mer Honorary Secretary and ate Dean and Professor of
former President of Madras Periodontology in the same institution. She has been teach-
branch of Indian Dental As- ing both UG and PG students for past 20 years. She has to
sociation. He has contrib- her credit publications in both national and international
uted chapters in Textbook of journals. She is currently the editor-in-chief of Journal of Inter-
Periodontology and Oral Implantology published by Elsevier. He disciplinary Dentistry.
has more than 30 scientific publications to his credit.
xix
xx About the Adaptation Editors
Dr Ashish Jain is presently from Harvard School of Dental Medicine, Harvard Univer-
working as Principal-cum- sity, USA. Dr Jain is recipient of Global Scholarship from ITI,
Professor at Dr Harvansh Switzerland. He is also an Adjunct Associate Research Investi-
Singh Judge Institute gator at Forsyth Institute, Harvard University and has been an
of Dental Sciences and Adjunct Associate Professor at Tufts University and an Adjunct
Hospital, Panjab University, Associate Professor at Boston University. Dr Jain has held the
Chandigarh. post of President, Indian Society of Periodontology. He was
He did his Masters in Assistant Editor of Journal of ISP and Founder Vice-President
Periodontology from Nair of Academy of Oral Implantologists. Dr Jain has been Editor
Dental College, Bombay. of Dentistry India, Official Publication of Dental Council of In-
Post MDS, he did a Post dia. He has been awarded Dr ML Soni Memorial Award in
Doctoral Fellowship at 2004 by International College of Dentists. He has more than
Goldman School of Dental 55 publications and lectures exclusively at various national
Medicine, Boston Univer- and international platforms and has delivered more than 70
sity. He did another Fellow- lectures so far.
ship in Implants Dentistry
Preface to the South Asia Edition
It was more than six decades ago, the first edition of this clas- You can refer the front inner cover of the book to ex-
sic textbook on Periodontology was published. Edition after plore online additional reading material. Besides these, you
edition has kept abreast with the advances in understanding will get access to the complimentary e-book also.
the mechanisms and causes of the diseases at the cellular It is our endeavor to present the entire revised edition in a
and molecular biology level. Newer modes of therapy and compact print edition. The entire exercise has been done with
clinical techniques have always found a mention in each edi- the goal of achieving clarity and for the reader to comprehend
tion. The contemporary philosophy of reconstruction and easily. We are confident that this new adapted version of the
regeneration of periodontal tissues, dental implants, and textbook will not only meet the requirements of the under-
perioesthetics have been exhaustively covered in the newer graduate but also the postgraduate, teacher, periodontist con-
editions. sultant, and general dental practitioner. We hope it will be the
We have made a humble effort in the Second South Asian number one choice among the dental fraternity as the classic
edition of this numero uno textbook to customize it according textbooks of Glickman's and Carranza's which are considered
to this expanse of the globe. This book is a culmination of as the Periodontology Encyclopedia.
the desire of educators, students, clinicians, researchers, and
policy makers, to have a textbook suited to the syllabus of CD Dwarakanath
the South Asian academia. Every attempt has been made to N Ambalavanan
preserve the same tradition of comprehensiveness and organi- DG Naik
zation of the original textbook. A Uppoor
A]ain
xxi
Preface to the 12th Edition
This twelfth edition is the most comprehensive textbook and This book is written for all individuals, from students
information resource about periodontology available any- to educators, clinicians to researchers, and from specialists
where. Using Elseviers advanced technology and high stan- to generalists. It is our belief that identifying periodontal
dards of quality, the international team of editors and con- needs of the public is primarily the role of general dentists
tributors have developed the most comprehensive periodontal and dental hygienists. The responsibility to examine, diag-
resource available. nose, and either treat or refer all periodontal problems is
Since publication of the first edition of this book 62 years unquestionable.
ago, periodontology has made tremendous progress. Analy- The multifaceted, complex task of producing the twelfth
sis of periodontal tissues and elucidation of the mechanisms edition required the collaboration of numerous experts from
and causes of disease have extended far beyond histology and various fields, and their contributions are invaluable. We know
physiology and into the realm of cellular and molecular bio- that this new edition will continue to be as useful to dentists,
logical understanding. hygienists, periodontists, students, educators, and researchers
New therapeutic goals and clinical techniques, based on as the previous editions have been and we know that it will
an improved understanding of disease, have facilitated bet- contribute to continuous progress of our profession.
ter outcomes and brought us closer to achieving the ultimate
goal of optimal periodontal health and function. Today, recon- MG Newman
struction and regeneration of lost periodontal structures, re- HH Tahei
placement of compromised teeth with implants, and creation PR Klokkevold
of esthetic results are integral parts of clinical practice. FA Carranza
xxiii
Acknowledgments
to the South Asia Edition
No words of appreciation are enough for my dear wife We wish to express our sincere thanks to Dr Neetha J Shetty
Rajashree, who has been my life partner and best friend for and Dr Sangeeta Nayak for helping us with the preparation of
the last 30 years, for her undiminished love, care, and under- this manuscript.
standing, and my sons Rahul and Rohit who have been my
strength and support as I stepped into my sixties. DG Naik
I thank the management of Vishnu Dental College for their A Uppoor
support and encouragement in all my academic activities.
I am extremely grateful to my colleague Dr Sruthima, for her This and any other piece of work or activities that I have
invaluable assistance in preparing the text and proofreading. ever been able to reach is solely the blessings of my parents,
My thanks to Dr Gautami, for her constant encouragement Shri NP Jain and Mrs Vijay Jain. Any further time taken out
and help and Dr Vinod, Intern, for his assistance during the for this work has been at the cost of my family. My wife, Dr
editing of the chapters. Rajni Jain deserves all the credit for putting up with me for
Finally I would like to thank my students from all over the last so many years and also letting me fulfill my commit-
India for their love, respect, and admiration which have been ments elsewhere. My kids, Vanshika and Ekansh, though
the source of my strength and motivation. would not understand the absence of their father most of
the times but I am sure would be happy to see their names
CD Dwarakanath mentioned here. I wish to acknowledge the support I have
received from my brother, Mr Vivek Jain and his family
I would like to thank my wife Ponni and my son Dr Vikram Meenu, Vidhika, and Kashvi for always being there. Fur-
and my parents Mrs and Mr Namasivayam and I also express ther, a special mention has to be made of Dr Shipra and
my gratitude to the teaching faculty of the Department of Dr Nymphea who have made tremendous contribution in
Periodontics ofMeenakshi Ammal Dental College for their en- the chapters that we have been able to put in for this work.
couragement and support during the preparation of this book. Finally God Almighty always.
N Ambalavanan A]ain
XXV
Acknowledgments
to the 12th Edition
The originator of this book and author of its first four editions, Marcelo Freire, Sasan Ghaffarigarakani, Mindy Gil, Tae Kwon,
published in 1953, 1958, 1964, and 1972, was Dr. Irving Lorenzo Mordini, Zuhair S. Natto, Justin Raanan, Teresa Sun,
Glickman, Professor and Chairman of the Department of Peri- Jeff Wang, Wichaya Wisitrasameewong, and Yau-hua Yu.
odontology at Tufts University School of Dental Medicine, in We express gratitude to our parents, colleagues, friends,
Boston, Massachusetts. and mentors who have always been so tolerant, encouraging,
After Dr. Glickman's death in 1972 at age 58, responsibility and understanding, and who guided our first steps in our pro-
for continuing this book moved to Dr. Fermin A. Carranza, fession and helped us develop our ideas in the field.
once a student and collaborator of Dr. Glickman. At the time, Dr. Newman: my family Susan, Andrea, Kara, Callahan
Dr. Carranza was Professor and Chairman of periodontics at and Natalie, Scott and Zoey; my parents Paul, Rose, John,
the School of Dentistry, University of California, Los Angeles and Inez. Sigmund S. Socransky, Fermin A. Carranza, Jr., and
(UCLA) The following four editions were published in 1979, Henry H. Takei: My gratitude to my co-editors and contrib-
1984, 1990, and 1996 under the guidance of Dr. Carranza, utors whose expertise and willingness to participate in this
who is now Professor Emeritus at UCLA. work have made this book an excellent educational standard.
In 2002, the task of maintaining the book's tradition of al- Dr. Takei: My wife, June; my children Scott and Akerni;
most half a century changed hands once again. Dr. Michael their spouses, Kozue and David; my grandchildren, Hana,
G. Newman and Dr. Henry H. Takei joined Dr. Carranza to Markus, Carter, and Arden. My graditude to my mentors Dr.
take major responsibility for the ninth edition. Subsequently, Fermin A. Carranza, Jr., Dr. Donald Van Scotter, Dr. Delbert
in 2006, Dr. Perry R. Klokkevold from UCLA joined them as Nachazel, and Dr. John Pfeiffer, Thank you to my three co-
a co-editor of the tenth edition. editors and friends Michael G. Newman, Fermin A. Carranza,
Advances in basic science and clinical techniques have in- Jr., and Perry R. Klokkevold. Special gratitude to Laura Miya be
creased the knowledge base so dramatically that it is virtually for her professional support. I would like to acknowledge and
impossible for a single individual to memorize and retain all thank all of my periodontal postdoctoral students at UCLA
of the information needed to practice excellently. It is also a for their help and support throughout the preparation of this
certainty that the enormity of providing the information of classic textbook.
a discipline must be borne by many experts willing to share Dr. Klokkevold: my wife, Angie; my daughters Ashley and
their experience and knowledge. Brianna; my parents Carl and Loretta; my gratitude and appre-
The editors are indebted to everyone who has worked tire- ciation for mentors Dr. Henry H. Takei, Dr. John Beumer III,
lessly to produce this milestone print and electronic edition of Dr. Bradley G. Seto, Dr. Charles N. Bertolami, and Dr. Thomas
Carranza's Clinical Periodontology. Han. I thank all of the UCLA Postgraduate Periodontal Residents
Many scientists and clinicians have shared their knowledge for the passion and inspiration they bring to me as an educator
and expertise from previous editions of Carranza's Clinical and clinician. Special thanks to my co-editors, Dr. Michael G.
Periodontology, but their names no longer appear as contribu- Newman, Dr. Henry H. Takei, and Dr. Fermin A. Carranza, Jr.,
tors to the present one. We express our deep gratitude to all of for their friendship, support, and encouragement.
them for their many valuable concepts and ideas. Dr. Carranza: my wife, Rita; my children Fermin, Patricia,
Our appreciation is given to Elsevier and particularly to and Laura; and my grandchildren, Irving Glickman, Fermin
Kathy Falk and Brian Loehr. Their expertise and detailed at- Carranza, Sr., and Romulo L. Cabrini. My gratitude also to my
tention to every word and every concept contributed greatly co-editors, who will continue the tradition of this book.
to producing a quality book and a truly useful website.
We also would like to thank the following residents for their
work on the website: Salem Alaqel, Mohammed N. Alasqah, MG Newman
Najla Al-Dabbagh, Shatha Alharthi, Sarah Almotlag, Raneem HH Takei
Alofi, Federico Ausenda, Seyed Hossein Bassir, Carlos Parra PR Klokkevold
Carrasquer, Daniel Coleman, Irina F Dragan, Waeil Elmisalati, FA Carranza
xxvii
Yasser Magrami
Contents
Editors v 8 Biofilm and Periodontal Microbiology 95

W Teughels • C Godts • M Quirynen • N Jakubovics
Contributors vii • N Ambalavanan
About the Authors xvii 9 Microbial Interactions with the Host

in Periodontal Diseases 109
About the Adaptation Editors xix RJ Nisengard • SK Haake • MG Newman
• KT Miyasaki • W Teughels • C Godts • M Quirynen
Preface to the South Asia Edition xxi • N Jakubovics • N Ambalavanan
Preface to the 12th Edition xxiii 10 The Role of Dental Calculus and Other
Predisposing Factors 113
Acknowledgments to the South Asia Edition xxv JE Hinrichs • VT Math • SR Diehl • C-H Chou
• F Kuo • C-Y Huang • OA Korczeniewska
Acknowledgments to the 12th Edition xxvii • N Ambalavanan
11 Smoking and Periodontal Disease 12 7

PART 1 PM Preshaw • L Chambrone • KF Novak
• N Ambalavanan
BIOLOGIC BASIS OF
PERIODONTOLOGY 12 Influence of Systemic Conditions 133
PR Klokkevold • BL Mealey • N Ambalavanan
SECTION I
Normal Periodontium 2 SECTION IV
1 Gingiva 3 Periodontal Pathology 149
JP Fiorellini • PG Stathopoulou • DG Naik • A Uppoor
13 Gingival Inflammation 151
2 Tooth Supporting Structures 19 JP Fiorellini • DM Kim • PG Stathopoulou
JP Fiorellini • PG Stathopoulou • DG Naik • A Uppoor • DG Naik • A Uppoor
3 Defense Mechanisms of the Gingiva 39 14 Clinical Features of Gingivitis 155

J Bulkacz • FA Carranza • DG Naik • A Uppoor JP Fiorellini • PG Stathopoulou • DG Naik • A Uppoor
4 Aging and the Periodontium 45 15 Gingival Enlargement 163

I Needleman • DG Naik • A Uppoor FA Carranza • EL Hogan • DG Naik • A Uppoor
16 Acute Gingival Infections 177

SECTION II PR Klokkevold • FA Carranza • DG Naik • A Uppoor
Classification and Epidemiology
17 Desquamative Gingivitis 187
of Periodontal Disease 49 CD Dwarakanath
5 Classification of Diseases and Conditions

18 The Periodontal Pocket 193
Affecting the Periodontium 51 FA Carranza • PM Camargo • DG Naik • A Uppoor
JE Hinrichs • G Kotsakis • DG Naik • A Uppoor
19 Abscesses of the Periodontium 205
6 Epidemiology of Gingival and Periodontal
DG Naik • A Uppoor
Disease 73
VW Spolsky • DG Naik • A Uppoor
20 Bone Loss and Patterns of Bone
Destruction 209
SECTION Ill FA Carranza • PM Camargo • HH Takei
• DG Naik • A Uppoor
Etiology of Periodontal Disease 83
7 Periodontal Pathogenesis 85 21 Periodontal Response to External Forces 221
PM Preshaw • N Ambalavanan FA Carranza • DG Naik • A Uppoor
xxix
xxx Contents
22 Chronic Periodontitis and Necrotizing 33 Treatment of Periodontal Abscess 371

Ulcerative Periodontitis 231 PR Melnick • HH Takei • A Uppoor • DG Naik
H Dommisch • M Kebschull • PR Klokkevold
• FA Carranza • DG Naik • A Uppoor SECTION IV
23 Aggressive Periodontitis 241 Nonsurgical Treatment 375
• FA Carranza • DG Naik • A Uppoor 34 Phase I Periodontal Therapy 3 77
DA Perry • HH Takei • A Jain
24 Pathology and Management of Periodontal
Problems in Patients With Human
35 Plaque Biofilm Control
DA Perry • A Jain
C, 383
Immunodeficiency Virus Infection 251
TD Rees • N Ambalavanan
36 Periodontal Instruments
and Instrumentation 403
25 Impact of Periodontal Infection on Systemic
AM Pattison • GL Pattison • PR Klokkevold • HH Takei
Health 261 • FA Carranza • A Jain
BL Mealey • PR Klokkevold • N Ambalavanan
37 Scaling and Root Planing 435
AM Pattison • GL Pattison • A Jain
PART 2 38 Antiinfective Therapy 449

CLINICAL PERIODONTICS SG Ciancio • A Mariotti • A Jain
SECTION I 39 Host Modulation C, 461

ME Ryan • Y Gu • A Jain
Diagnosis, Prognosis and Treatment
Plan 270 40 Breath Malodor C, 467
M Quirynen • I Laleman • J Dadamio • S De Geest
26 Clinical Diagnosis 271 • B Vandekerckhove • W Teughels • A Jain
HH Takei • FA Carranza • J Do • S Tetradis
• SM Mallya • M Sanz • MG Newman • M Quirynen
SECTION V
• CD Dwarakanath
Surgical Treatment 4 75
27 Clinical Risk Assessment 309
KF Novak • MJ Novak • CD Dwarakanath 41 Phase II Periodontal Therapy 4 77
FA Carranza • HH Takei • CD Dwarakanath
28 Determination of Prognosis 315
KF Novak • HH Takei • J Do • CD Dwarakanath 42 Periodontal and Periimplant Surgical
Anatomy 483
29 Rationale for Periodontal Treatment FA Carranza • PR Klokkevold • CD Dwarakanath
and Treatment Plan 327
FA Carranza • HH Takei • CD Dwarakanath 43 General Principles of Periodontal
Surgery 493
PR Klokkevold • HH Takei • FA Carranza
SECTION II
• CD Dwarakanath
Management of Patients with
Periodontal Diseases 335 44 Gingival Surgical Techniques 501
HH Takei • FA Carranza • K Shin
• CD Dwarakanath
30 Periodontal Treatment of Medically
Compromised Patients 337 45 The Periodontal Flap 507
PR Klokkevold • BL Mealey • J Otomo-Corgel
HH Takei • FA Carranza • J Do • K Shin
• CD Dwarakanath
• CD Dwarakanath
31 Treatment of Aggressive and Atypical Forms

46 Treatment of Gingival Enlargement 529
of Periodontitis 353 PM Camargo • FA Carranza • FQ Pirih • HH Takei
PR Klokkevold • A Uppoor • CD Dwarakanath
SECTION Ill 47 Resective Osseous Surgery 535

TN Sims • CD Dwarakanath
Diagnosis and Treatment of Periodontal
Emergencies 363 48 Periodontal Regeneration and Reconstructive
Surgery 547
32 Treatment of Acute Gingival Disease 365 RT Kao • HH Takei • DL Cochran • ML Nevins
PR Klokkevold • FA Carranza • DG Naik • A Uppoor • CD Dwarakanath
Contents xxxi
49 Furcation Involvement and Treatment 561 SECTION VII

TN Sims • HH Takei • CD Dwarakanath
Supportive Care 641
50 Periodontal Plastic and Esthetic 55 Supportive Periodontal Treatment 643
Surgery 573 RL Merin • DG Naik • A Uppoor
HH Takei • ET Scheyer • RR Azzi • EP Allen
• TJ Han • CD Dwarakanath
51 Advances in Periodontal Surgical Procedures

PART 3
(Microsurgery and Laser) 599 ORALIMPLANTOLOGY
DA Shanelec • LS Tibbetts • A McGregor • JD Cross
• RT Kao • B Butler • CD Dwarakanath 56 Biological Aspects of Dental Implants O 655
JP Fiorellini • K Wada • PG Stathopoulou
• PR Klokkevold • A Jain
SECTION VI
57 Diagnosis and Treatment Planning
Multidisciplinary Approach for in Implantology O 671
the Management of Periodontal PR Klokkevold • DL Cochran • S Tetradis
• SM Mallya • E Chung • T-L Chang • A Jain
Diseases 613
52 Diagnosis and Management of
58 Surgical Concepts of Implant Therapy O 697
PR Klokkevold • IA Urban • DL Cochran
Endodontic-Periodontic Lesions 615 • TJ Han • K-B Park • DA Shanelec • LS Tibbetts
KC Trabert • MK Kang • N Ambalavanan • T Vercellotti • DH Etienne • RR Derycke • A Jain
53 Periodontal-Restorative 59 Periimplant Disease and Management O 725

Interrelationships C,
623
FM Spear • JP Cooney • PR Melnick
SJ Froum • PR Klokkevold • S-C Cho • SH Froum • A Jain
• N Ambalavanan 60 Supportive Implant Treatment 733

J Do • PR Klokkevold • A Jain
54 Adjunctive Role of Orthodontic
Therapy 631
VG Kokich • N Ambalavanan Index 741
C, For additional online content, please visit the companion website www.medenact.com.
Online Resources
• The Historical Background of Periodontology
• Molecular Biology of Host-Microbe Interactions
• Gingival Disease in Childhood
• Necrotizing Ulcerative Periodontitis
• Masticatory System Disorders that Influence the Periodontium
• Sleep-Disordered Breathing
• Significance of Clinical and Biologic Information
• Conscious Sedation
• Periodontal Therapy in the Female Patient
• Periodontal Treatment for Older Adults
• Occlusal Evaluation and Therapy
• Multidisciplinary Approach to Dental and Periodontal Problems
• Results of Periodontal Treatment
• Atlas of Periodontal Diseases
• Electronic Dental Records and Decision Support Systems
• Locally Delivered, Controlled-Release Antimicrobials: Drug Development and Clinical Research
Part Outline
SECTION I Normal Periodontium SECTION IV Periodontal Pathology

1 Gingiva 13 Gingival Inflammation
2 Tooth Supporting Structures 14 Clinical Features of Gingivitis
3 Defense Mechanisms of the Gingiva 15 Gingival Enlargement
4 Aging and the Periodontium 16 Acute Gingival Infections
SECTION II Classification and Epidemiology 17 Desquamative Gingivitis
of Periodontal Disease 18 The Periodontal Pocket
5 Classification of Diseases and 19 Abscesses of the Periodontium
Conditions Affecting the
Periodontium
Destruction
6 Epidemiology of Gingival and
21 Periodontal Response to External
Periodontal Disease
Forces
SECTION Ill Etiology of Periodontal Disease
22 Chronic Periodontitis and Necrotizing
7 Periodontal Pathogenesis Ulcerative Periodontitis
8 Biofilm and Periodontal Microbiology 23 Aggressive Periodontitis
9 Microbial Interactions with the Host 24 Pathology and Management of
in Periodontal Diseases Periodontal Problems in Patients
10 The Role of Dental Calculus and Other With Human Immunodeficiency
Predisposing Factors Virus Infection
11 Smoking and Periodontal Disease 25 Impact of Periodontal Infection on
12 Influence of Systemic Conditions Systemic Health
SECTION I
Section Outline
1 Gingiva 3 Defense Mechanisms of the Gingiva
2 Tooth Supporting Structures 4 Aging and the Periodontium
Yasser Magrami
1
Gingiva
Chapter Outline
Definition and Scope of Periodontology Gingiva
Oral Mucosa
Definition and Scope of Oral Mucosa

Periodontology The oral mucosa consists of the following three zones:
Definition: Periodontology is the scientific study of periodon- 1. The gingiva and the covering of the hard palate, termed the
tium in health and disease. masticatory mucosa
Scope: Periodontology has experienced many exciting sci- 2. The dorsum of the tongue, covered by specialized mucosa
entific developments related to inflammation and systemic 3. The oral mucous membrane lining the remainder of the
health demonstrating that inflammation may link periodontal oral cavity
diseases to other chronic conditions (eg, heart disease, diabe-
tes). In addition, periodontology continues to bring clinical
advancements in reconstruction of oral hard and soft tissue Gingiva
as well as continued development of dental implants to the The gingiva is the part of the oral mucosa that covers the alveo-
profession. lar processes of the jaws and surrounds the necks of the teeth.
The periodontium (in Greek "peri" means "around" and
"odontos" means "tooth") is a dynamic structure composed
Clinical Features
of the tissues supporting and investing the teeth. It comprises
of four principal components which have been divided into In an adult, normal gingiva covers the alveolar bone and tooth
two parts: root to a level JUSt coronal to the cementoenamel junction. The
gingiva is divided anatomically into marginal, attached, and inter-
• gingiva whose main function is protection of the underlying
dental areas. Although each type of gingiva exhibits considerable
tissues
variation in differentiation, histology, and thickness according
• periodontal ligament, cementum and alveolar bone which
to its functional demands, all types are specifically structured to
comprises the attachment apparatus
function appropriately against mechanical and microbial dam-
Each of these periodontal components is distinct in its age. In other words, the specific structure of different types of
location, tissue architecture, biochemical composition, and gingiva reflects each one's effectiveness as a barrier to the pen-
chemical composition, but all of these components function etration by microbes and noxious agents into the deeper tissue.
together as a single unit. Recent research has revealed that
the extracellular matrix components of one periodontal com- Marginal Gingiva
partment can influence the cellular activities of adjacent struc- The marginal or unattached gingiva is the terminal edge or bor-
tures. Therefore, the pathologic changes that occur in one der of the gingiva that surrounds the teeth in collarlike fashion
periodontal component may have significant ramifications for (Figs. 1.1 and 1.2). In about 50% of cases, it is demarcated
the maintenance, repair, or regeneration of other components from the adjacent attached gingiva by a shallow linear depres-
of the periodontium. sion called the free gingival groove. The marginal gingiva is usu-
This section first discusses the structural components of ally about 1 mm wide, and it forms the soft-tissue wall of the
the normal periodontium; it then describes their develop- gingival sulcus. It may be separated from the tooth surface with
ment, vascularization, innervation, and functions. a periodontal probe. The most apical point of the marginal
3
4 PART 1 Biologic Basis of Periodontology
the probe depends on several factors, such as probe diameter,

probing force, and the level of inflammation. Consequently,
the probing depth is not necessarily exactly equal to the his-
tologic depth of the sulcus. The so-called probing depth of a
clinically normal gingival sulcus in humans is 2-3 mm.
Attached Gingiva
The attached gingiva is continuous with the marginal gingiva.
It is firm, resilient, and tightly bound to the underlying perios-
teum of alveolar bone. The facial aspect of the attached gingiva
extends to the relatively loose and movable alveolar mucosa; it
is demarcated by the mucogingival junction (Fig. 1.2).
The width of the attached gingiva is another important clinical
parameter. It is the distance between the mucogingival junc-
tion and the projection on the external surface of the bottom
FIGURE 1.1 Normal gingiva in a young adult. Note the demarca- of the gingival sulcus or the periodontal pocket. It should not
tion (mucogingival line) (arrows) between the attached gingiva and the
darker alveolar mucosa.
be confused with the width of the keratinized gingiva although
this also includes the marginal gingiva (Fig. 1.2)
The width of the attached gingiva on the facial aspect dif-
fers in different areas of the mouth. It is generally greatest in
the incisor region (ie, 3.5-4.5 mm in the maxilla, 3.3-3.9 mm
in the mandible) and narrower in the posterior segments
(ie, 1.9 mm in the maxillary first premolars and 1.8 mm in
the mandibular first premolars) (Fig. 1.3)
Because the mucogingival junction remains stationary
throughout adult life, changes in the width of the attached gin-
giva are caused by modifications in the position of its coronal
portion. The width of the attached gingiva increases by the age
Attached gingiva of 4 years and in supraerupted teeth. On the lingual aspect of
the mandible, the attached gingiva terminates at the Junction
of the lingual alveolar mucosa, which is continuous with the
mucous membrane that lines the floor of the mouth. The pala-
tal surface of the attached gingiva in the maxilla blends imper-
ceptibly with the equally firm and resilient palatal mucosa.
lnterdental Gingiva
The interdental gingiva occupies the gingival embrasure,
FIGURE 1.2 Diagram showing the anatomic landmarks of the gingiva. which is the interproximal space beneath the area of tooth
contact. The interdental gingiva can be pyramidal, or it can
gingival scallop is called the gingival zenith. Its apicocoronal and have a "col" shape. In the former, the tip of one papilla is
mesiodistal dimensions vary between 0.06 and 0.96 mm. located immediately beneath the contact point; the latter pres-
ents a valleylike depression that connects a facial and lingual
Gingival Sulcus papilla and that conforms to the shape of the interproximal
The gingival sulcus is the shallow crevice or space around the contact (Figs. 1.4 and 1.5) The shape of the gingiva in a
tooth bounded by the surface of the tooth on one side and the given interdental space depends on the presence or absence
epithelium lining the free margin of the gingiva on the other
side. It is V-shaped, and it barely permits the entrance of a peri-
odontal probe. The clinical determination of the depth of the
gingival sulcus is an important diagnostic parameter. Under
absolutely normal or ideal conditions, the depth of the gingival
sulcus is O mm or close to O mm. These strict conditions of
normalcy can be produced experimentally only in germ-free
animals or after intense and prolonged plaque control.
In clinically healthy human gingiva, a sulcus of some depth
can be found. The depth of this sulcus, as determined in his-
tologic sections, has been reported as 1.8 mm, with variations
from O to 6 mm; other studies have reported 1.5 mm and
0.69 mm. The clinical evaluation used to determine the depth
of the sulcus involves the introduction of a metallic instrument
(ie, the periodontal probe) and the estimation of the distance
it penetrates (ie, the probing depth). The histologic depth
(biologic depth) of a sulcus does not need to be exactly equal FIGURE 1.3 Mean width of the attached gingiva in the human per-
to the depth of penetration of the probe. The penetration of manent dentition.
1 Gingiva 5
FIGURE 1.7 lnterdental papillae (arrow) with a central portion formed

FIGURE 1.4 Site of extraction showing the facial and palatal inter- by the attached gingiva. The shape of the papillae varies according to the
dental papillae and the intervening col (arrow). dimension of the gingival embrasure. (Courtesy Dr Osvaldo Costa.)
FIGURE 1.8 An absence of interdental papillae and col where the

proximal tooth contact is missing. (Courtesy Dr Osvaldo Costa.)
interdental papillae are formed by the marginal gingiva of the

adjoining teeth. The intervening portion consists of attached
gingiva (Fig. 1. 7). If a diastema is present, the gingiva is firmly
bound over the interdental bone to form a smooth, rounded
FIGURE 1.5 Faciolingual section of a monkey showing the col surface without interdental papillae (Fig. 1.8).
between the facial and lingual interdental papillae. The col is covered
with nonkeratinized stratified squamous epithelium.
Microscopic Features
of a contact point between the adjacent teeth, the distance Microscopic examination reveals that gingiva is composed
between the contact point and the osseous crest, and the pres- of the overlying stratified squamous epithelium and the
ence or absence of some degree of recession. Fig. 1.6 depicts underlying central core of connective tissue. Although the
the variations in normal interdental gingiva. epithelium is predominantly cellular in nature, the connec-
The facial and lingual surfaces are tapered toward the tive tissue is less cellular and composed primarily of collagen
interproximal contact area, whereas the mesial and distal sur- fibers and ground substance. These two tissues are consid-
faces are slightly concave. The lateral borders and tips of the ered separately.
(A) (B)
(C) (D)
FIGURE 1.6 A diagram that compares anatomic variations of the interdental col in the normal gingiva (left side) and after gingival recession (right
side). A and B, Mandibular anterior segment, facial and buccolingual views, respectively. C and D, Mandibular posterior region, facial and buccolin-
gual views, respectively. Tooth contact points are shown with black marks in the lower individual teeth.
Gingival Epithelium cell with an increasing prevalence of tonofilaments; (2) the

General Aspects of Gingival Epithelium Biology. Histori- couple of intercellular junctions with the production of
cally, the epithelial compartment was thought to provide only keratohyalin granules; and (3) the disappearance of the
a physical barrier to infection and the underlying gingival nucleus.
attachment. However, we now believe that epithelial cells Three types of surface keratinization can occur in the gin-
play an active role in innate host defense by responding to gival epithelium.
bacteria in an interactive manner, which means that the epi- 1. Keratinization. A complete keratinization process leads
thelium participates actively in responding to infection, in sig- to the production of an orthokeratinized superficial horny
naling further host reactions, and in integrating innate and layer similar to that of the skin, with no nuclei in the stra-
acquired immune responses. For example, epithelial cells may tum corneum and a well-defined stratum granulosum
respond to bacteria by increased proliferation, the alteration of (Fig. 1. 10). Only some areas of the outer gingival epithe-
cell-signaling events, changes in differentiation and cell death, lium are orthokeratinized.
and, ultimately, the alteration of tissue homeostasis. To under- 2. Parakeratinization. It is considered to be an intermediate
stand this new perspective of the epithelial innate defense stage of keratinization and is the most prevalent surface
responses and the role of epithelium in gingival health and area of the gingival epithelium. These areas can progress to
disease, it is important to understand its basic structure and maturity or dedifferentiate under different physiologic or
function (Box 1. 1) pathologic conditions.
The gingival epithelium consists of a continuous lining In parakeratinized epithelia, the stratum corneum retains
of stratified squamous epithelium. There are three different pyknotic nuclei, and the keratohyalin granules are dis-
areas that can be defined from the morphologic and functional persed rather than giving rise to a stratum granulosum.
points of view: the oral or outer epithelium, the sulcular epi- 3. Nonkeratinization. The nonkeratinized epithelium (although
thelium, and the junctional epithelium. cytokeratins are the maJor component as in all epithelia)
The principal cell type of the gingival epithelium-as well has neither granulosum nor corneum strata, whereas su-
as of other stratified squamous epithelia-is the keratinocyte. perficial cells have viable nuclei.
Other cells found in the epithelium are the clear cells or non-
keratinocytes, which include the Langerhans cells, the Merkel Immunohistochemistry, gel electrophoresis, and immu-
cells, and the melanocytes. noblot techniques have made the identification of the charac-
The keratinocyte receives its name because it can synthe- teristic pattern of cytokeratins possible in each epithelial type.
size keratin. It constitutes about more than 90% of the cell The keratin proteins are composed of different polypeptide
population. subunits characterized by their isoelectric points and molecu-
The main function of the gingival epithelium is to protect lar weights. They are numbered in a sequence that is contrary
the deep structures while allowing for a selective interchange to their molecular weight. In general, basal cells begin synthe-
with the oral environment. This is achieved via the prolifera- sizing lower-molecular-weight keratins [eg, Kl9 ( 40 kD)], and
tion and differentiation of the keratinocytes. The proliferation they express other higher-molecular-weight keratins as they
of keratinocytes takes place by mitosis in the basal layer and migrate to the surface. Kl keratin polypeptide (68 kD) is the
less frequently in the suprabasal layers, in which a small pro- main component of the stratum corneum.
portion of cells remain as a proliferative compartment while a Other proteins unrelated to keratins are synthesized dur-
larger number begin to migrate to the surface. ing the maturation process. The most extensively studied are
Differentiation involves the process of keratinization, keratolinin and involucrin, which are precursors of a chemically
which consists of progressions of biochemical and mor- resistant structure (the envelope) located below the cell mem-
phologic events that occur in the cell as they migrate from brane, and filaggrin, which has precursors that are packed
the basal layer (Fig. 1.9) The main morphologic changes into the keratohyalin granules. At the sudden transition to the
include the following: (1) the progressive flattening of the horny layer, the keratohyalin granules disappear and give rise
FUNCTIONS CONSTANT RENEWAL

Mechanical, chemical, water, and microbial barrier Replacement of damaged cells
Signaling functions
CELL-CELL ATTACHMENTS
ARCHITECTURAL INTEGRITY Desmosomes
Cell-cell attachments Adherens junctions
Basal lamina Tight junctions
Keratin cytoskeleton Gap junctions
MAJOR CELL TYPE CELL-BASAL LAMINA
Keratinocyte Synthesis of basal lamina components
Hemidesmosome
OTHER CELL TYPES
Langerhans eel Is
Melanocytes
Merkel cells
Modified from Dale BA: Periodontal 2000 30:71, 2002.

1 Gingiva 7
Stratum
corneum
Stratum Lamellated
granulosum granules
Stratum
spinosum
Stratum
basale Granular endoplasmic
reticulum
Basement membrane
FIGURE 1.9 Diagram showing representative cells from the various layers of stratified squamous epithelium as seen by electron microscopy.
(Modified from Weinstock A: In Ham AW, editor: Histology, ed 7, Philadelphia, 1974, Lippincott.)
FIGURE 1.10 A, Scanning electron micrograph of keratinized gingiva showing the flattened keratinocytes and their boundaries on the surface of the
gingiva (X 1000). B, Scanning electron micrograph of the gingival margin at the edge of the gingival sulcus showing several keratinocytes about to be
exfoliated (X3000). (From Kaplan CB, Pameijer CH, Ruben MP: J Periodontal 48:446, 1977.)
to filaggrin, which forms the matrix of the most differentiated These desmosomes have a typical structure that consists of
epithelial cell, the corneocyte. two dense attachment plaques into which tonofibrils insert
Thus in the fully differentiated state, the corneocytes are and an intermediate, electron-dense line in the extracellular
mainly formed by bundles of keratin tonofilaments embed- compartment. Tonofilaments, which are the morphologic
ded in an amorphous matrix of filaggrin and surrounded by expression of the cytoskeleton of keratin proteins, radiate in
a resistant envelope under the cell membrane. The immuno- brushlike fashion from the attachment plaques into the cyto-
histochemical patterns of the different keratin types, envelope plasm of the cells. The space between the cells shows cyto-
proteins, and filaggrin change under normal or pathologic plasmic projections that resemble microvilli and that extend
stimuli, thereby modifying the keratinization process. into the intercellular space and often interdigitate.
Electron microscopy reveals that keratinocytes are intercon- Less frequently observed forms of epithelial cell con-
nected by structures on the cell periphery called desmosomes. nections are tight junctions (zonae occludens), in which the
membranes of the adjoining cells are thought to be fused.

Evidence suggests that these structures allow ions and small
molecules to pass from one cell to another.
Cytoplasmic organelle concentration varies among dif-
ferent epithelial strata. Mitochondria are more numerous in
deeper strata and decrease toward the surface of the cell.
Accordingly, the histochemical demonstration of succinic
dehydrogenase, nicotinamide adenine dinucleotide, cyto-
chrome oxidase, and other mitochondrial enzymes reveals a
more active tricarboxylic cycle in basal and parabasal cells,
in which the proximity of the blood supply facilitates energy
production through aerobic glycolysis.
Conversely, enzymes of the pentose shunt (an alterna-
tive pathway of glycolysis), such as glucose-6-phosphatase,
increase their activity toward the surface. This pathway pro-
duces a larger amount of intermediate products for the pro-
duction of ribonucleic acid (RNA), which in turn can be used
for the synthesis of keratinization proteins. This histochemical FIGURE 1.12 Human gingival epithelium, oral aspect. lmmunoper-
pattern is in accordance with the increased volume and the oxidase technique showing Langerhans cells.
amount of tonofilaments observed in cells reaching the sur-
face; the intensity of the activity is proportional to the degree
of differentiation. as modified monocytes derived from the bone marrow. They
The uppermost cells of the stratum spinosum contain contain elongated granules, and they are considered macro-
numerous dense granules called heratinosomes or Odland phages with possible antigenic properties. Langerhans cells
bodies, which are modified lysosomes. They contain a large have an important role in the immune reaction as antigen-
amount of acid phosphatase, an enzyme involved in the presenting cells for lymphocytes. They contain g-specific
destruction of organelle membranes, which occurs suddenly granules (Birbeck granules), and they have marked adenosine
between the granulosum and corneum strata and during triphosphatase activity They are found in the oral epithelium
the intercellular cementation of cornified cells. Thus acid of normal gingiva and in smaller amounts in the sulcular epi-
phosphatase is another enzyme that is closely related to thelium; they are probably absent from the junctional epithe-
the degree of keratinization. N onkeratinocyte cells are pres- lium of normal gingiva.
ent in gingival epithelium as in other malpighian epithe- Merkel cells are located in the deeper layers of the epithe-
lia. Melanocytes are dendritic cells located in the basal and lium; they harbor nerve endings, and they are connected to
spinous layers of the gingival epithelium. They synthesize adjacent cells by desmosomes. They have been identified as
melanin in organelles called premelanosomes or melanosomes tactile perceptors.
(Fig. 1.11). These contain tyrosinase, which hydroxylates The epithelium is joined to the underlying connective
tyrosine to dihydroxyphenylalanine (dopa), which in turn tissue by a basal lamina 300-400 A thick and lying approxi-
is progressively converted to melanin. Melanin granules mately 400 A beneath the epithelial basal layer. The basal
are phagocytosed and contained within other cells of the lamina consists of lamina lucida and lamina densa. Hemides-
epithelium and connective tissue called melanophages or mosomes of the basal epithelial cells abut the lamina lucida,
melanophores. which is mainly composed of the glycoprotein laminin. The
Langerhans cells are dendritic cells located among kerati- lamina densa is composed of type IV collagen.
nocytes at all suprabasal levels (Fig. 1.12). They belong to the The basal lamina, which is clearly distinguishable at the
mononuclear phagocyte system (reticuloendothelial system) ultrastructural level, is connected to a reticular condensa-
tion of the underlying connective tissue fibrils (mainly collagen
type IV) by the anchoring fibrils. Anchoring fibrils have been
measured at 750 nm in length from their epithelial end to their
connective tissue end, where they appear to form loops around
collagen fibers. The complex of basal lamina and fibrils is the
periodic acid-Schiff-positive and argyrophilic line observed at
the optical level (Fig. 1.13). The basal lamina is permeable to
fluids, but it acts as a barrier to particulate matter.
Structural and Metabolic Characteristics of Different Areas

of Gingival Epithelium. The epithelial component of the gin-
giva shows regional morphologic variations that reflect tissue
adaptation to the tooth and alveolar bone. These variations
include the oral epithelium, the sulcular epithelium, and the
junctional epithelium. Whereas the oral epithelium and the
sulcular epithelium are largely protective in function, the junc-
FIGURE 1.11 Pigmented gingiva of dog showing melanocytes (M) tional epithelium serves many more roles and is of consider-
in the basal epithelial layer and melanophores (C) in the connective able importance in the regulation of tissue health. It is now
tissue (Glucksman technique). recognized that epithelial cells are not "passive bystanders"
1 Gingiva 9
KS and Kl 4, which are stratification-specific cytokeratins, are

also present. Parakeratinized areas express Kl 9, which is usu-
ally absent from orthokeratinized normal epithelia.
In keeping with the complete or almost-complete matura-
tion, histoenzyme reactions for acid phosphatase and pentose-
shunt enzymes are very strong.
Glycogen can accumulate intracellularly when it is not
completely degraded by any of the glycolytic pathways. Thus
its concentration in normal gingiva is inversely related to the
degree of keratinization and inflammation.
Oral (Outer) Epithelium. The oral or outer epithelium cov-

ers the crest and outer surface of the marginal gingiva and
the surface of the attached gingiva. On average, the oral epi-
FIGURE 1.13 Normal human gingiva stained with the periodic acid- thelium is 0.2-0.3 mm in thickness. It is keratinized or para-
Schiff histochemical method. The basement membrane (8) is seen keratinized, or it may present various combinations of these
between the epithelium (EJ and the underlying connective tissue (CJ. conditions (Fig. 1.14). The prevalent surface, however, is
In the epithelium, glycoprotein material occurs in cells and cell mem-
parakeratinized. The oral epithelium is composed of four lay-
branes of the superficial hornified (HJ and underlying granular layers
(G). The connective tissue presents a diffuse, amorphous ground sub- ers: stratum basale (basal layer), stratum spinosum (prickle
stance and collagen fibers. The blood vessel walls stand out clearly in cell layer), stratum granulosum (granular layer), and stratum
the papillary projections of the connective tissue (P). corneum (cornified layer).
Sulcular Epithelium. The sulcular epithelium lines the gin-

in the gingival tissues; rather, they are metabolically active gival sulcus (Fig. 1. 15). It is a thin, nonkeratinized stratified
and capable of reacting to external stimuli by synthesizing a squamous epithelium without rete pegs, and it extends from
number of cytokines, adhesion molecules, growth factors, and the coronal limit of the junctional epithelium to the crest of
enzymes. the gingival margin (Fig. 1.16) It usually shows many cells
The degree of gingival keratinization diminishes with age with hydropic degeneration.
and the onset of menopause, but it is not necessarily related As with other nonkeratinized epithelia, the sulcular epithe-
to the different phases of the menstrual cycle. Keratinization lium lacks granulosum and corneum strata and Kl, K2, and
of the oral mucosa varies in different areas in the following KlO through Kl2 cytokeratins, but it contains K4 and Kl3,
order: palate (most keratinized), gingiva, ventral aspect of the the so-called "esophageal-type cytokeratins." It also expresses
tongue, and cheek (least keratinized). Kl 9, and it normally does not contain Merkel cells.
Keratins Kl, K2, and KlO through Kl2, which are specific Histochemical studies of enzymes have consistently
to epidermal-type differentiation, are immunohistochemi- revealed a lower degree of activity in the sulcular than in
cally expressed with high intensity in orthokeratinized areas the outer epithelium, particularly in the case of enzymes
and with less intensity in parakeratinized areas. K6 and Kl 6, related to keratinization. Glucose-6-phosphate dehydroge-
which are characteristic of highly proliferative epithelia, and nase expresses a faint and homogeneous reaction in all strata,
1 ,\
-~ I 0~ <1
U.,:!. ::,.a,--:.-...,!l . t ~9 , '
FIGURE 1.14 Variations in the gingival epithelium. A, Keratinized. B, Nonkeratinized. C, Parakeratinized. Horny layer (HJ, granular layer (G),
prickle cell layer (P), basal cell layer (Ba), flattened surface cells (5), and parakeratotic layer (Pk).
The sulcular epithelium is extremely important; it may

act as a semipermeable membrane through which injurious
bacterial products pass into the gingiva and through which
tissue fluid from the gingiva seeps into the sulcus. Unlike the
junctional epithelium, however, the sulcular epithelium is not
heavily infiltrated by polymorphonuclear neutrophil leuko-
cytes, and it appears to be less permeable.
Junctional Epithelium. The junctional epithelium consists of

a collarlike band of stratified squamous nonkeratinizing epi-
thelium. It is 3-4 layers thick in early life, but the number of
layers increases with age to 10 or even 20 layers. In addition,
the junctional epithelium tapers from its coronal end, which
may be 10-29 cells wide to 1-2 cells wide at its apical ter-
FIGURE 1.15 Scanning electron microscopic view of the epithelial
surface facing the tooth in a normal human gingival sulcus. The epithe- mination, which is located at the cementoenamel junction in
lium (Ep) shows desquamating cells, some scattered erythrocytes (E), healthy tissue. These cells can be grouped in two strata: the
and a few emerging leukocytes (L) (Xl 000). basal layer that faces the connective tissue and the suprabasal
layer that extends to the tooth surface. The length of the JUnc-
tional epithelium ranges from 0.25 to 1.35 mm (Fig. 1.17).
unlike the increasing gradient toward the surface observed The junctional epithelium is formed by the confluence of
in cornified epithelia. Acid phosphatase staining is negative the oral epithelium and the reduced enamel epithelium dur-
although lysosomes have been described in exfoliated cells. ing tooth eruption. However, the reduced enamel epithelium
Despite these morphologic and chemical characteristics, is not essential for its formation; in fact, the junctional epithe-
the sulcular epithelium has the potential to keratinize if it is lium is completely restored after pocket instrumentation or
reflected and exposed to the oral cavity or if the bacterial flora surgery, and it forms around an implant.
of the sulcus is totally eliminated. Conversely, the outer epi- Cell layers that are not juxtaposed to the tooth exhibit
thelium loses its keratinization when it is placed in contact numerous free ribosomes, prominent membrane-bound
with the tooth. These findings suggest that the local irritation structures (eg, Golgi complexes), and cytoplasmic vacuoles
of the sulcus prevents sulcular keratinization. that are presumably phagocytic. Lysosomelike bodies also are
present, but the absence of keratinosomes (Odland bodies)
and histochemically demonstrable acid phosphatase, which
are correlated with the low degree of differentiation, may
reflect a low-defense power against microbial plaque accu-
mulation in the gingival sulcus. Similar morphologic findings
have been described in the gingiva of germ-free rats. Polymor-
phonuclear neutrophil leukocytes are found routinely in the
junctional epithelium of both conventional rats and germ-free
rats. Research has shown that, although numerous migrating
polymorphonuclear neutrophil leukocytes are evident and
present around healthy junctional epithelium, a considerable
increase in polymorphonuclear neutrophil leukocyte numbers
can be expected with the accumulation of dental plaque and
gingival inflammation.
The different keratin polypeptides of the junctional epi-
thelium have a particular histochemical pattern. Junctional
epithelium expresses Kl9, which is absent from keratinized
epithelia, and the stratification-specific cytokeratins KS and
Kl 4. Morgan et al reported that reactions to demonstrate
K4 or Kl3 reveal a sudden change between sulcular and
junctional epithelia; the junctional area is the only stratified
nonkeratinized epithelium in the oral cavity that does not syn-
thesize these specific polypeptides. Another particular behav-
ior of junctional epithelium is the lack of expression of K6 and
FIGURE 1.16 Epon-embedded human biopsy specimen showing a Kl6, which is usually linked to highly proliferative epithelia,
relatively normal gingival sulcus. The soft-tissue wall of the gingival sul- although the turnover of the cells is very high.
cus is made up of the oral sulcular epithelium (ose) and its underlying
connective tissue (ct), whereas the base of the gingival sulcus is formed
Similar to sulcular epithelium, junctional epithelium exhib-
by the sloughing surface of the junctional epithelium (je). The enamel its lower glycolytic enzyme activity than outer epithelium, and
space is delineated by a dense cuticular structure (de). A relatively sharp it also lacks acid phosphatase activity.
line of demarcation exists between the junctional epithelium and the The junctional epithelium is attached to the tooth surface
oral sulcular epithelium (arrow), and several polymorphonuclear leuko-
cytes (pmn) can be seen traversing the junctional epithelium. The sulcus
(epithelial attachment) by means of an internal basal lamina.
contains red blood cells that resulted from the hemorrhage that occurred It is attached to the gingival connective tissue by an external
at the time of biopsy (X391; inset xSS). (From Schluger S, Youdelis R, basal lamina that has the same structure as other epithelial-
Page RC: Periodontal disease, ed 2, Philadelphia, 1990, Lea & Febiger.) connective tissue attachments elsewhere in the body.
1 Gingiva 11
FIGURE 1.17 Eruption process in cat's tooth. A, Unerupted tooth. Dentin (0), remnants of enamel matrix (E), reduced enamel epithelium (REE),
oral epithelium (OE), and artifact (a). B, Erupting tooth forming junctional epithelium (IE). C, Completely erupted tooth. Sulcus with epithelial
debris (5), cementum (C), and epithelial rests (ER).
The internal basal lamina consists of a lamina densa (adja- from colonizing the subgingival tooth surface. First, junc-
cent to the enamel) and a lamina lucida to which hemidesmo- tional epithelium is firmly attached to the tooth surface,
somes are attached. Hemidesmosomes have a decisive role in thereby forming an epithelial barrier against plaque bacteria.
the firm attachment of the cells to the internal basal lamina on Second, it allows access of gingival fluid, inflammatory cells,
the tooth surface. and components of the immunologic host defense to the gin-
Recent data suggest that the hemidesmosomes may also act gival margin. Third, junctional epithelial cells exhibit rapid
as specific sites of signal transduction and thus may participate turnover, which contributes to the host-parasite equilibrium
in the regulation of gene expression, cell proliferation, and and the rapid repair of damaged tissue. Some investigators
cell differentiation. Organic strands from the enamel appear have also indicated that the cells of the junctional epithelium
to extend into the lamina densa. The junctional epithelium have an endocytic capacity equal to that of macrophages and
attaches to afibrillar cementum that is present on the crown neutrophils and that this activity may be protective in nature.
(usually restricted to an area within 1 mm of the cementoe-
namel junction) and root cementum in a similar manner. Development of Gingival Sulcus. After enamel formation is
Three zones have been described in the junctional epi- complete, the enamel is covered with reduced enamel epithe-
thelium: apical, middle, and coronal. The apical zone shows lium (REE), which is attached to the tooth by a basal lamina
cells with germinative characteristics, the middle zone is of and hemidesmosomes. When the tooth penetrates the oral
maJor adhesiveness, and the coronal zone is one of greater mucosa, the REE unites with the oral epithelium and trans-
permeability. forms into the junctional epithelium. As the tooth erupts, this
Histochemical evidence for the presence of neutral poly- united epithelium condenses along the crown, and the ame-
saccharides in the zone of the epithelial attachment has been loblasts, which form the inner layer of the REE (Fig. 1.17),
reported. Data also have shown that the basal lamina of the gradually become squamous epithelial cells. The transforma-
junctional epithelium resembles that of endothelial and epi- tion of the REE into a junctional epithelium proceeds in an
thelial cells in its laminin content but differs in its internal apical direction without interrupting the attachment to the
basal lamina, which has no type IV collagen. These findings tooth. According to Schroeder and Listgarten, this process
indicate that the cells of the junctional epithelium are involved takes between 1 and 2 years.
in the production of laminin and play a key role in the adhe- The junctional epithelium is a continually self-renewing
sion mechanism. structure, with mitotic activity occurring in all cell layers.
The attachment of the junctional epithelium to the tooth is The regenerating epithelial cells move toward the tooth sur-
reinforced by the gingival fibers, which brace the marginal gin- face and along it in a coronal direction to the gingival sulcus,
giva against the tooth surface. For this reason, the junctional where they are shed (Fig. 1.18) The migrating daughter cells
epithelium and the gingival fibers are considered together as a provide a continuous attachment to the tooth surface. The
functional unit referred to as the dentogingival unit. strength of the epithelial attachment to the tooth has not been
In conclusion, it is usually accepted that the junctional epi- measured.
thelium exhibits several unique structural and functional fea- The gingival sulcus is formed when the tooth erupts into the
tures that contribute to preventing pathogenic bacterial flora oral cavity. At that time, the junctional epithelium and the REE
connective tissue) are capable of synthesizing deoxyribonu-

cleic acid (DNA), thereby demonstrating their mitotic activity.
The rapid shedding of cells effectively removes bacteria that
adheres to the epithelial cells and therefore is an important
part of the antimicrobial defense mechanisms at the dentogin-
gival junction.
Cuticular Structures on the Tooth. The term cuticle describes

a thin acellular structure with a homogeneous matrix that is
sometimes enclosed within clearly demarcated linear borders.
Listgarten has classified cuticular structures into coatings
of developmental origin and acquired coatings. Acquired
coatings include those of exogenous origin such as saliva,
bacteria, calculus, and surface stains. Coatings of developmen-
tal origin are those that are normally formed as a part of tooth
development. They include the REE, the coronal cementum,
and the dental cuticle.
After enamel formation is completed, the ameloblastic epi-
thelium is reduced to one or two layers of cells that remain
C attached to the enamel surface by hemidesmosomes and a
basal lamina. This REE consists of postsecretory ameloblasts
FIGURE 1.18 Junctional epithelium on an erupting tooth. The junc- and cells from the stratum intermedium of the enamel organ.
tional epithelium (IE) is formed by the joining of the oral epithelium In some animal species, the REE disappears entirely and very
(OE) and the reduced enamel epithelium (REE). Afibrillar cementum rapidly, thereby placing the enamel surface in contact with the
(AC) is sometimes formed on enamel after the degeneration of the REE.
The arrows indicate the coronal movement of the regenerating epithelial
connective tissue. Connective tissue cells then deposit a thin
cells, which multiply more rapidly in the JE than in the OE. E, Enamel; C, layer of cementum known as coronal cementum on the enamel.
root cementum. A similar cell turnover pattern exists in the fully erupted In humans, thin patches of afibrillar cementum sometimes
tooth. (Modified from Listgarten MA: J Can Dent Assoc 36:70, 1970.) may be seen in the cervical half of the crown.
Electron microscopy has demonstrated a dental cuticle that
consists of a layer of homogeneous organic material of vari-
form a broad band that is attached to the tooth surface from able thickness (approximately 0.25 µm) overlying the enamel
near the tip of the crown to the cementoenamel junction. The surface. It is nonmineralized, and it is not always present. In
gingival sulcus is the shallow, V-shaped space or groove between some cases, near the cementoenamel junction, it is deposited
the tooth and the gingiva that encircles the newly erupted tip over a layer of afibrillar cementum, which in turn overlies
of the crown. In the fully erupted tooth, only the junctional enamel. The cuticle may be present between the junctional
epithelium persists. The sulcus consists of the shallow space that is epithelium and the tooth. Ultrastructural histochemical stud-
coronal to the attachment of the junctional epithelium and bounded ies have shown that the dental cuticle is proteinaceous, and it
by the tooth on one side and the sulcular epithelium on the other. The may be an accumulation of tissue fluid components.
coronal extent of the gingival sulcus is the gingival margin.
Gingival Fluid (Sulcular Fluid). The value of the gingival
Renewal of Gingival Epithelium. The oral epithelium fluid is that it can be represented as either a transudate or an
undergoes continuous renewal. Its thickness is maintained by exudate. The gingival fluid contains a vast array of biochemi-
a balance between new cell formation in the basal and spinous cal factors, thereby offering its potential use as a diagnostic or
layers and the shedding of old cells at the surface. The mitotic prognostic biomarker of the biologic state of the periodon-
activity exhibits a 24-h periodicity, with the highest and lowest tium in health and disease. It also contains components of
rates occurring in the morning and evening, respectively. The connective tissue, epithelium, inflammatory cells, serum, and
mitotic rate is higher in nonkeratinized areas and increased microbial flora that inhabit the gingival margin or the sulcus
in gingivitis, without significant gender differences. Opinions (pocket).
differ with regard to whether the mitotic rate gets increased or In the healthy sulcus, the amount of gingival fluid is very
decreased with age. small. During inflammation, however, the gingival fluid flow
The mitotic rate in experimental animals varies among dif- increases, and its composition starts to resemble that of an
ferent areas of the oral epithelium in descending order: buccal inflammatory exudate. The main route of the gingival fluid
mucosa, hard palate, sulcular epithelium, junctional epithe- diffusion is through the basement membrane, through the rel-
lium, outer surface of the marginal gingiva, and attached gin- atively wide intercellular spaces of the junctional epithelium,
giva. The following have been reported as turnover times for and then into the sulcus. The gingival fluid is believed to do
different areas of the oral epithelium in experimental animals: the following: (1) cleanse material from the sulcus; (2) contain
palate, tongue, and cheek, 5-6 days; gingiva, 10-12 days, plasma proteins that may improve adhesion of the epithelium
with the same or more time required with age; and junctional to the tooth; (3) possess antimicrobial properties; and ( 4) exert
epithelium, 1-6 days. antibody activity to defend the gingiva.
With regard to junctional epithelium, it was previously
thought that only epithelial cells facing the external basal lam- Gingival Connective Tissue
ina were rapidly dividing. However, evidence indicates that The major components of the gingival connective tissue are
a significant number of the cells (eg, the basal cells along the collagen fibers (about 60% by volume), fibroblasts (5%),
1 Gingiva 13
vessels, nerves, and matrix (about 35%). The connective

tissue of the gingiva is known as the lamina propria, and it
consists of two layers: (1) a papillary layer subjacent to the
epithelium that consists of papillary projections between the
epithelial rete pegs; and (2) a reticular layer that is contiguous
with the periosteum of the alveolar bone.
Connective tissue has a cellular compartment and an
extracellular compartment composed of fibers and ground
substance. Thus, the gingival connective tissue is largely a
fibrous connective tissue that has elements that originate
directly from the oral mucosal connective tissue as well as
some fibers (dentogingival) that originate from the develop-
ing dental follicle.
The ground substance fills the space between fibers and cells;
it is amorphous, and it has a high water content. It is composed
of proteoglycans (mainly hyaluronic acid and chondroitin
sulfate) and glycoproteins (mainly fibronectin). Glycopro-
teins account for the faint periodic acid-Schiff-positive reac-
tion of the ground substance. Fibronectin binds fibroblasts
to the fibers and many other components of the intercellular
matrix, thereby helping to mediate cell adhesion and migra-
tion. Laminin, which is another glycoprotein found in the
basal lamina, serves to attach it to epithelial cells.
The three types of connective tissue fibers are collagen, retic-
ular, and elastic. Collagen type I forms the bulk of the lamina
propria and provides the tensile strength to the gingival tis-
sue. Type IV collagen (argyrophilic reticulum fiber) branches
between the collagen type I bundles, and it is continuous with
fibers of the basement membrane and the blood vessel walls. FIGURE 1.19 Faciolingual section of marginal gingiva showing gin-
gival fibers (F) that extend from the cementum (C) to the crest of the
The elastic fiber system is composed of oxytalan, elaunin, gingiva, to the outer gingival surface, and external to the periosteum of
and elastin fibers distributed among collagen fibers. There- the bone (BJ. Circular fibers (CF) are shown in cross-section between
fore, densely packed collagen bundles that are anchored into the other groups. (Courtesy Sol Bernick.)
the acellular extrinsic fiber cementum just below the terminal
point of the junctional epithelium form the connective tissue
attachment. The stability of this attachment is a key factor in
the limitation of the migration of junctional epithelium.
Gingival Fibers. The connective tissue of the marginal gin-

giva is densely collagenous, and it contains a prominent sys-
tem of collagen fiber bundles called the gingival fibers. These
fibers consist of type I collagen. The gingival fibers have the
following functions:
1. To brace the marginal gingiva firmly against the tooth
2. To provide the rigidity necessary to withstand the forces of
mastication without being deflected away from the tooth
surface
3. To unite the free marginal gingiva with the cementum of
the root and the adjacent attached gingiva
The gingival fibers are arranged in three groups: gingivo-
dental, circular, and transseptal.
The gingivodental fibers are those on the facial, lingual, and
interproximal surfaces. They are embedded in the cementum
just beneath the epithelium at the base of the gingival sul-
cus. On the facial and lingual surfaces, they project from
the cementum in a fanlike conformation toward the crest
and outer surface of the marginal gingiva where they ter-
minate short of the epithelium (Figs. 1.19 and l. 20). They
also extend externally to the periosteum of the facial and
lingual alveolar bones, terminating in the attached gingiva or
FIGURE 1.20 Diagram of the gingivodental fibers that extend from the
blending with the periosteum of the bone. Interproximally, cementum (1) to the crest of the gingiva, (2) to the outer surface, and
the gingivodental fibers extend toward the crest of the inter- (3) external to the periosteum of the labial plate. Circular fibers (4) are
dental gingiva. shown in cross-section.
The circular fibers course through the connective tissue of

the marginal and interdental gingivae and encircle the tooth
in ringlike fashion.
The transseptal fibers, which are located interproximally,
form horizontal bundles that extend between the cementum
of the approximating teeth into which they are embedded.
They lie in the area between the epithelium at the base of the
gingival sulcus and the crest of the interdental bone, and they
are sometimes classified with the principal fibers of the peri-
odontal ligament.
Page et al described a group of semicircular fibers that attach
at the proximal surface of a tooth immediately below the
cementoenamel junction, go around the facial or lingual mar-
ginal gingiva of the tooth, and attach on the other proximal FIGURE 1.21 Section of clinically normal gingiva showing some
degree of inflammation, which is almost always present near the base
surface of the same tooth; they also discussed a group of trans- of the sulcus.
gingival fibers that attach in the proximal surface of one tooth,
traverse the interdental space diagonally, go around the facial
or lingual surface of the adjacent tooth, again traverse the Blood Supply, Lymphatics, and Nerves. Microcirculatory
interdental space diagonally, and then attach in the proximal tracts, blood vessels, and lymphatic vessels play an important
surface of the next tooth. role in the drainage of tissue fluid and in the spread of inflam-
Tractional forces in the extracellular matrix produced by mation. In individuals with gingivitis and periodontitis, the
fibroblasts are believed to be the forces responsible for gen- microcirculation and vascular formation change greatly in the
erating tension in the collagen. This keeps the teeth tightly vascular network directly under the gingival sulcular epithe-
bound to each other and to the alveolar bone. lium and the junctional epithelium.
Three sources of blood supply to the gingiva are as follows
Cellular Elements. The preponderant cellular element in the (Figs. 1.22 and 1.23)
gingival connective tissue is the fibroblast. Numerous fibro-
blasts are found between the fiber bundles. Fibroblasts are of 1. Supraperiosteal arterioles along the facial and lingual sur-
mesenchymal origin and play a major role in the development, faces of the alveolar bone from which capillaries extend
maintenance, and repair of gingival connective tissue. As with along the sulcular epithelium and between the rete pegs of
connective tissue elsewhere in the body, fibroblasts synthe- the external gingival surface. Occasional branches of the
size collagen and elastic fibers as well as the glycoproteins and arterioles pass through the alveolar bone to the periodontal
glycosaminoglycans of the amorphous intercellular substance. ligament or run over the crest of the alveolar bone.
Fibroblasts also regulate collagen degradation through phago- 2. Vessels of the periodontal ligament, which extend into the
cytosis and the secretion of collagenases. gingiva and anastomose with capillaries in the sulcus area.
Fibroblast heterogeneity is now a well-established feature 3. Arterioles, which emerge from the crest of the interdental
of fibroblasts in the periodontium. Although the biologic and septa and extend parallel to the crest of the bone to anasto-
clinical significance of such heterogeneity is not yet clear, it mose with vessels of the periodontal ligament, with capil-
seems that this is necessary for the normal functioning of tis- laries in the gingival crevicular areas and vessels that run
sues in health, disease, and repair. over the alveolar crest.
Mast cells, which are distributed throughout the body, Beneath the epithelium on the outer gingival surface, capil-
are numerous in the connective tissue of the oral mucosa and laries extend into the papillary connective tissue between the
the gingiva. Fixed macrophages and histiocytes are present in epithelial rete pegs in the form of terminal hairpin loops with
the gingival connective tissue as components of the mono-
nuclear phagocyte system (reticuloendothelial system) and are
derived from blood monocytes. Adipose cells and eosinophils,
although scarce, are also present in the lamina propria.
In clinically normal gingiva, small foci of plasma cells and
lymphocytes are found in the connective tissue near the base
of the sulcus (Fig. 1.21). Neutrophils can be seen in relatively
high numbers in both the gingival connective tissue and the
sulcus. These inflammatory cells are usually present in small
amounts in clinically normal gingiva.
Repair of Gingival Connective Tissue. Because of the high

turnover rate, the connective tissue of the gingiva has remark-
ably good healing and regenerative capacity. Indeed, it may
be one of the best healing tissues in the body, and it gener-
ally shows little evidence of scarring after surgical procedures.
This is likely caused by the rapid reconstruction of the fibrous
FIGURE 1.22 Diagram of an arteriole penetrating the interdental alve-
architecture of the tissues. However, the reparative capacity olar bone to supply the interdental tissues (left) and a supraperiosteal
of gingival connective tissue is not as great as that of the peri- arteriole overlying the facial alveolar bone, sending branches to the sur-
odontal ligament or the epithelial tissue. rounding tissue (right).
1 Gingiva 15
_.,,,.
.".V.
r/?' I)
.
- -
".· <~i..V/,-r
/ .•. '
v.' ,{
\
FIGURE 1.23 Blood supply and peripheral circulation of the gingiva.
Tissues perfused with India ink. Note the capillary plexus parallel to the
sulcus (5) and the capillary loops in the outer papillary layer. Note also
the supraperiosteal vessels external to the bone (B), which supply the
gingiva, and a periodontal ligament vessel anastomosing with the sulcus
plexus. (Courtesy Sol Bernick.)
efferent and afferent branches, spirals, and varices (Figs. 1.23

and 1.24). The loops are sometimes linked by crosscommuni-
cations, and flattened capillaries serve as reserve vessels when FIGURE 1.24 Scanning electron microscopic view of the gingival tis-
the circulation is increased in response to irritation. sues of rat molar palatal gingiva after the vascular perfusion of plastic
Along the sulcular epithelium, capillaries are arranged in a and the corrosion of soft tissue. A, Oral view of gingival capillaries:
flat, anastomosing plexus that extends parallel to the enamel t, tooth; interdental papilla (arrowhead) (Xl 80). B, View from the tooth
side. Note the vessels of the plexus next to the sulcular and junctional
from the base of the sulcus to the gingival margin. In the col area, epithelium. The arrowheads point to vessels in the sulcus area with mild
a mixed pattern of anastomosing capillaries and loops occurs. inflammatory changes. g, Crest of the marginal gingiva; s, bottom of the
As mentioned previously, anatomic and histologic changes gingival sulcus; pl, periodontal ligament vessels (Xl 50). (Courtesy NJ
have been shown to occur in the gingival microcirculation of Sel/iseth and K Selvig, University of Bergen, Norway.)
individuals with gingivitis. Prospective studies of the gingival
vasculature in animals have demonstrated that, in the absence
labial, buccal, and palatal nerves. The following nerve struc-
of inflammation, the vascular network is arranged in a regu-
tures are present in the connective tissue: a meshwork of
lar, repetitive, and layered pattern. By contrast, the inflamed
terminal argyrophilic fibers, some of which extend into the
gingival vasculature exhibits an irregular vascular plexus pat-
epithelium; Meissner-type tactile corpuscles; Krause-type end
tern, with the microvessels exhibiting a looped, dilated, and
bulbs, which are temperature receptors; and encapsulated
convoluted appearance.
spindles.
The role of the lymphatic system in removing excess fluids,
cellular and protein debris, microorganisms, and other ele-
ments is important for controlling diffusion and the resolution Correlation of Clinical and Microscopic
of inflammatory processes. The lymphatic drainage of the gingiva Features
brings in the lymphatics of the connective tissue papillae. It
progresses into the collecting network external to the perios- An understanding of the normal clinical features of the gingiva
teum of the alveolar process and then moves to the regional requires the ability to interpret them in terms of the micro-
lymph nodes, particularly the submaxillary group. In addition, scopic structures that they represent.
lymphatics just beneath the junctional epithelium extend into
the periodontal ligament and accompany the blood vessels. Color
Neural elements are extensively distributed throughout the The color of the attached and marginal gingiva is generally
gingival tissues. Within the gingival connective tissues, most described as "coral pink"; it is produced by the vascular sup-
nerve fibers are myelinated and closely associated with the ply, the thickness and degree of keratinization of the epithe-
blood vessels. Gingival innervation is derived from fibers that lium, and the presence of pigment-containing cells. The color
arise from nerves in the periodontal ligament and from the varies among different persons and appears to be correlated
FIGURE 1.25 A, Clinically normal gingiva in

a young adult. B, Heavily pigmented (melanotic)
gingiva in a middle-aged adult. (From Glickman
I, Smulow /8: Periodontal disease: clinical, radio-
graphic, and histopathologic features, Philadelphia,
1974, Saunders.)
with the cutaneous pigmentation. It is lighter in blond indi- • Melanin pigmentation in the oral cavity is prominent in
viduals with fair complexions than in swarthy, dark-haired black individuals (Fig. 1.25)
individuals (Fig. 1.25). • Ascorbic acid directly downregulates melanin pigmentation
The attached gingiva is demarcated from the adjacent in gingival tissues.
alveolar mucosa on the buccal aspect by a clearly defined
According to Dummett, the distribution of oral pigmen-
mucogingival line. The alveolar mucosa is red, smooth, and
tation in black individuals is as follows: gingiva, 60%; hard
shiny rather than pink and stippled. A comparison of the
palate, 61 %; mucous membrane, 22%; and tongue, 15%.
microscopic structure of the attached gingiva with that of
Gingival pigmentation occurs as a diffuse, deep-purplish dis-
the alveolar mucosa provides an explanation for the differ-
coloration or as irregularly shaped brown and light-brown
ence in appearance. The epithelium of the alveolar mucosa
patches. It may appear in the gingiva as early as 3 h after birth,
is thinner and nonkeratinized, and it contains no rete pegs
and it is often the only evidence of pigmentation.
(Fig. 1.26). The connective tissue of the alveolar mucosa is
Oral repigmentation refers to the clinical reappearance of
loosely arranged, and the blood vessels are more numerous.
melanin pigment after a period of clinical depigmentation of
the oral mucosa as a result of chemical, thermal, surgical, phar-
Physiologic Pigmentation (Melanin). Melanin is a nonhe-
macologic, or idiopathic factors. Information about the repig-
moglobin-derived brown pigment with the following charac-
mentation of oral tissues after surgical procedures is extremely
teristics:
limited, and no definitive treatment is offered at this time.
• Melanin is responsible for the normal pigmentation of the
skin, the gingiva, and the remainder of the oral mucous Size
membrane. The size of the gingiva corresponds with the sum total of the
• Melanin is present in all normal individuals (often not in bulk of cellular and intercellular elements and their vascular
sufficient quantities to be detected clinically), but it is ab- supply. Alteration in size is a common feature of gingival
sent or severely diminished in albinos. disease.
Contour
The contour or shape of the gingiva varies considerably and
depends on the shape of the teeth and their alignment in the
arch, the location and size of the area of proximal contact, and
the dimensions of the facial and lingual gingival embrasures.
The marginal gingiva envelops the teeth in collarlike fash-
ion and follows a scalloped outline on the facial and lingual
surfaces. It forms a straight line along teeth with relatively flat
surfaces. On teeth with pronounced mesiodistal convexity (eg,
maxillary canines) or teeth in labial version, the normal arcuate
contour is accentuated, and the gingiva is located farther api-
cally. On teeth in lingual version, the gingiva is horizontal and
thickened (Fig. 1.27) In addition, the gingival tissue biotype
varies significantly. A thin and clear gingiva is found in one-
third of the population and primarily in females with slender
teeth with a narrow zone of keratinized tissue, whereas a clear,
thick gingiva with a broad zone of keratinized tissue is present
in two-thirds of the population and primarily in males.
Shape
The shape of the interdental gingiva is governed by the con-
FIGURE 1.26 Oral mucosa, facial, and palatal surfaces. The facial sur- tour of the proximal tooth surfaces and the location and shape
face (F) shows the marginal gingiva (MC), the attached gingiva (AC), of the gingival embrasures.
and the alveolar mucosa (AM). The double line marks the mucogingival
junction. Note the differences in the epithelium and the connective tis-
When the proximal surfaces of the crowns are relatively
sue in the attached gingiva and the alveolar mucosa. The palatal surface flat faciolingually, the roots are close together, the interdental
(P) shows the marginal gingiva (MC) and the thick, keratinized palatal bone is thin mesiodistally, and the gingival embrasures and
mucosa (PM). interdental gingiva are narrow mesiodistally. Conversely, with
1 Gingiva 17
FIGURE 1.27 A thickened, shel-flike contour of gingiva on a tooth

in lingual version aggravated by local irritation caused by plaque
accumulation.
FIGURE 1.28 Shape of the interdental gingival papillae correlated FIGURE 1.29 Gingival biopsy of the patient shown in Fig. 2.7 dem-
with the shape of the teeth and the embrasures. A, Broad interdental onstrating alternate elevations and depressions (arrows) in the attached
papillae. B, Narrow interdental papillae. gingiva that are responsible for the stippled appearance.
proximal surfaces that flare away from the area of contact, and the elevated and depressed areas are covered by stratified
the mesiodistal diameter of the interdental gingiva is broad squamous epithelium (Fig. 1.29). The degree of keratinization
(Fig. 1.28). The height of the interdental gingiva varies with and the prominence of stippling appear to be related.
the location of the proximal contact. Thus in the anterior Scanning electron microscopy has shown considerable
region of the dentition, the interdental papilla is pyramidal in variation in shape but a relatively constant depth of stippling.
form, whereas the papilla is more flattened in a buccolingual At low magnification, a rippled surface is seen, and this is
direction in the molar region. interrupted by irregular depressions that are 50 µm in diam-
eter. At higher magnification, cell micropits are seen.
Consistency Stippling is a form of adaptive specialization or reinforce-
The gingiva is firm and resilient and, with the exception of the ment for function. It is a feature of healthy gingiva, and the
movable free margin, tightly bound to the underlying bone. reduction or loss of stippling is a common sign of gingival
The collagenous nature of the lamina propria and its contigu- disease. When the gingiva is restored to health after treatment,
ity with the mucoperiosteum of the alveolar bone determine the stippled appearance returns.
the firmness of the attached gingiva. The gingival fibers con- The surface texture of the gingiva is also related to the pres-
tribute to the firmness of the gingival margin. ence and degree of epithelial keratinization. Keratinization is
considered a protective adaptation to function. It increases
Surface Texture when the gingiva is stimulated by toothbrushing. However,
The gingiva presents a textured surface similar to that of an research on free gingival grafts has shown that, when connec-
orange peel and is referred to as stippled (Fig. 1.25). Stip- tive tissue is transplanted from a keratinized area to a nonke-
pling is best viewed by drying the gingiva. The attached gingiva ratinized area, it becomes covered by a keratinized epithelium.
is stippled; the marginal gingiva is not. The central portion of This finding suggests a connective tissue-based genetic deter-
the interdental papillae is usually stippled, but the marginal mination of the type of epithelial surface.
borders are smooth. The pattern and extent of stippling vary
among individuals and among different areas of the same Position
mouth. Stippling is less prominent on lingual than facial sur- The position of the gingiva is the level at which the gingival
faces and may be absent in some persons. margin is attached to the tooth. When the tooth erupts into
Stippling varies with age. It is absent during infancy, it appears the oral cavity, the margin and sulcus are at the tip of the
in some children at about 5 years of age, it increases until adult- crown; as eruption progresses, they are seen closer to the root.
hood, and it frequently begins to disappear during old age. During this eruption process, as described previously, the
Microscopically, stippling is produced by alternate rounded junctional epithelium, the oral epithelium, and the reduced
protuberances and depressions in the gingival surface. The pap- enamel epithelium undergo extensive alterations and remod-
illary layer of the connective tissue projects into the elevations, eling while maintaining the shallow physiologic depth of the
sulcus. Without this remodeling of the epithelia, an abnor- Stage 2. The junctional epithelium proliferates so that part is
mal anatomic relationship between the gingiva and the tooth on the cementum and part is on the enamel. The base of the
would result. sulcus is still on the enamel.
Stage 3. The entire junctional epithelium is on the cementum,
Continuous Tooth Eruption. According to the concept and the base of the sulcus is at the cementoenamel junction.
of continuous eruption, eruption does not cease when the As the junctional epithelium proliferates from the crown
teeth meet their functional antagonists; rather, it continues onto the root, it does not remain at the cementoenamel
throughout life. Eruption consists of an active phase and a junction any longer than at any other area of the tooth.
passive phase. Active eruption is the movement of the teeth in Stage 4. The junctional epithelium has proliferated farther
the direction of the occlusal plane, whereas passive eruption is on the cementum. The base of the sulcus is on the cemen-
the exposure of the teeth via apical migration of the gingiva. tum, a portion of which is exposed. Proliferation of the
This concept distinguishes between the anatomic crown junctional epithelium onto the root is accompanied by de-
(ie, the portion of the tooth covered by enamel) and the ana- generation of the gingival and periodontal ligament fibers
tomic root (ie, the portion of the tooth covered by cementum) and their detachment from the tooth. The cause of this
and between the clinical crown (ie, the part of the tooth that degeneration is not understood. At present, it is believed
has been denuded of its gingiva and projects into the oral cav- to be the result of chronic inflammation and therefore a
ity) and the clinical root (ie, the portion of the tooth covered pathologic process.
by periodontal tissues). When the teeth reach their functional
As noted, apposition of bone accompanies active eruption.
antagonists, the gingival sulcus and the junctional epithelium
The distance between the apical end of the junctional epithe-
are still on the enamel, and the clinical crown is approximately
lium and the crest of the alveolus remains constant through-
two-third of the anatomic crown.
out continuous tooth eruption (ie, 1.07 mm).
Gottlieb and Orban believed that active and passive erup-
Exposure of the tooth via the apical migration of the gingiva
tion proceed together. Active eruption is coordinated with
is called gingival recession or atrophy. According to the concept
attrition; the teeth erupt to compensate for tooth substance
of continuous eruption, the gingival sulcus may be located on
that has been worn away by attrition. Attrition reduces the
the crown, the cementoenamel junction, or the root, depend-
clinical crown and prevents it from becoming disproportion-
ing on the age of the patient and the stage of eruption. There-
ately long in relation to the clinical root, thus avoiding exces-
fore, some root exposure with age would be considered normal
sive leverage on the periodontal tissues. Ideally, the rate of
and referred to as physiologic recession. Again, this concept is
active eruption keeps pace with tooth wear, thereby preserv-
not accepted at present. Excessive exposure is termed patho-
ing the vertical dimension of the dentition.
logic recession.
As teeth erupt, cementum is deposited at the apices and
furcations of the roots, and bone is formed along the fundus
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Although originally thought to be a normal physiologic
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2
Tooth Supporting Structures
Chapter Outline
Development of the Attachment Alveolar Process
Apparatus Clinical Considerations
Periodontal Ligament Vascularization of the Supporting
Cementum Structures
Development of the Attachment of a complex vascular and highly cellular connective tissue
that surrounds the tooth root and connects it to the inner wall
Apparatus of the alveolar bone. It is continuous with the connective tissue
After the crown has formed, the stratum intermedium and the of the gingiva, and it communicates with the marrow spaces
stellate reticulum of the enamel organ disappear. The outer through vascular channels in the bone. Although the average
and inner epithelia of the enamel organ remain and form REE. width of the periodontal ligament space is documented to be
The apical portion of this constitutes the Hertwig epithelial about 0.2 mm, considerable variation exists. The periodontal
root sheath, which will continue to grow apically and which space is diminished around teeth that are not in function and
determines the shape of the root. Before the beginning of root in unerupted teeth, but it is increased in teeth that have been
formation, the root sheath bends horizontally at the future ce- subjected to hyperfunction.
mentoenamel junction, thereby narrowing the cervical open-
ing and forming the epithelial diaphragm. The epithelial dia-
phragm separates the dental follicle from the dental papilla. Development of the
After root dentin formation begins, the Hertwig root sheath
Periodontal Ligament
breaks up and partially disappears; the remaining cells form
the epithelial clusters or strands known as the epithelial rests Once the root formation begins and outer dentinal layer
of Malassez (Fig. 27A). In multirooted teeth, the epithelial of root is formed, the periodontal ligament develops. The
diaphragm grows in such a way that tonguelike extensions external and internal enamel epithelia proliferate from the
develop horizontally, thereby leaving spaces for each of the cervical loop of the dental organ to form a Hertwig epithelial
future roots to form. root sheath. This sheath is double layered. Due to growth
The role of the Hertwig epithelial root sheath in root devel- changes, the root sheath is stretched and then it fragments to
opment, especially as it relates to the initiation of cementogen- form discrete clusters of the epithelial cells called "epithelial
esis, has become a focus of research. On the basis of various rests of Malassez." The enamel organ and Hertwig epithelial
studies, it is now generally accepted that there is a transient root sheath are surrounded by a dental sac that is formed
period of the secretion of proteins (eg, bone sialoprotein, os- by condensed cells. A thin layer of these cells lies adjacent
teopontin, amelin) by the cells of the Hertwig epithelial root to the dental (enamel) organ. This is known as dental fol-
sheath. In addition, research shows that growth and differen- licle. The cells of the dental follicle divide and differentiate
tiation factors may play roles in the development of the at- into the cementoblasts, fibroblasts, and osteoblasts. The fi-
tachment apparatus of periodontal tissues. Pluripotent dental broblasts synthesize the fibers and ground substance of the
follicle cells have been shown to differentiate into osteoblasts, periodontal ligament. These fibers of the periodontal liga-
cementoblasts, and periodontal fibroblasts. ment then get embedded at one end into the newly formed
cementum laid down by cementocytes and at the other end
Periodontal Ligament into the bone laid down by osteoblasts. When tooth erupts
in the oral cavity, these fibers get oriented in a characteris-
It is a specialized fibrous connective tissue that surrounds and tic manner. The fiber bundles of the periodontal ligament
attaches roots of teeth to the alveolar bone. It is also known as gradually thicken after the teeth have been in function for
Periodontal Membrane. The periodontal ligament is composed sometime.
19
The structural components of periodontal ligament:
Cellular elements:
1. synthesizing cells: fibroblasts, cementoblasts, osteblasts
2. resorptive cells: fibroblasts, cementoclasts, osteoclasts
3. epithelial cell rests of Malassez, pregenitor cells, defense
cells, such as mast cells and macrophages
Periodontal fibers
1. Principal fibers
Alveolar crest fibers, horizontal fibers, oblique fibers, apical
fibers, interradicular fibers
2. Other fibers
Oxytalan fibers, elaunin fibers
Ground substance
1. Glucosaminoglycans
a. hyaluronic acid
b. proteoglycans
2. Glycoproteins
a. water
b. fibronectin
c. laminin FIGURE 2.2 Collagen fibers embedded in the cementum (left) and
the bone (right) (silver stain). Note the Sharpey fibers within the bundle
bone (BB) overlying the lamellar bone.
Periodontal Fibers
The most important elements of the periodontal ligament are have also recently been identified in tooth cementum. Notable
the principal fibers, which are collagenous and arranged in among these proteins are osteopontin and bone sialoprotein.
bundles and which follow a wavy course when viewed in lon- These proteins are thought to contribute to the regulation of
gitudinal section (Fig. 2.1). The terminal portions of the prin- mineralization and to tissue cohesion at sites of increased bio-
cipal fibers that are inserted into the cementum and bone are mechanical strain.
termed Sharpey fibers (Fig. 2.2). The principal fiber bundles Collagen is a protein that is composed of different amino
consist of individual fibers that form a continuous anastomos- acids, the most important of which are glycine, proline, hy-
ing network between tooth and bone. Once embedded in the droxylysine, and hydroxyproline. The amount of collagen in
wall of the alveolus or in the tooth, Sharpey fibers calcify to a a tissue can be determined by its hydroxyproline content.
significant degree. They are associated with abundant noncol- Collagen is responsible for the maintenance of the frame-
lagenous proteins that are typically found in bone, and they work and the tone of tissue, and it exhibits a wide range
of diversity. There are at least 19 recognized collagen spe-
cies encoded by at least 25 separate genes dispersed among
12 chromosomes.
Collagen biosynthesis occurs inside the fibroblasts to
form tropocollagen molecules. These aggregate into microfi-
brils that are packed together to form fibrils. Collagen fibrils
have a transverse striation with a characteristic periodicity of
64 µm; this striation is caused by the overlapping arrange-
ment of the tropocollagen molecules. In collagen types I and
III, these fibrils associate to form fibers; in collagen type I, the
fibers associate to form bundles (Fig. 2.3).
Collagen is synthesized by fibroblasts, chondroblasts, os-
teoblasts, odontoblasts, and other cells. The several types of
collagen are all distinguishable by their chemical composition,
distribution, function, and morphology. The principal fibers
are composed mainly of collagen type I, whereas reticular fi-
bers are composed of collagen type Ill. Collagen type IV is
found in the basal lamina. The expression of type XII collagen
during the tooth development is timed with the alignment
and organization of periodontal fibers and is limited in tooth
FIGURE 2.1 Principal fibers of the periodontal ligament follow a development to cells within the periodontal ligament. Type
wavy course when sectioned longitudinally. The formative function of VI collagen has also been immunolocalized in the periodontal
the periodontal ligament is illustrated by the newly formed osteoid and
osteoblasts along a previously resorbed bone surface (left) and the ce-
ligament and the gingiva.
mentoid and cementoblasts (right). Note the fibers embedded in the The molecular configuration of collagen fibers provides
forming calcified tissues (arrows). V, Vascular channels. them with a tensile strength that is greater than that of steel.
2 Tooth Supporting Structures 21
Fiber
FIGURE 2.3 Collagen microfibrils, fibrils, fibers, and bundles.
FIGURE 2.5 Transseptal fibers (F) at the crest of the interdental bone.
FIGURE 2.4 Diagram of the principal fiber groups.
Consequently, collagen imparts a unique combination of flex-

ibility and strength to the tissues.
The principal fibers of the periodontal ligament are ar-
ranged in six groups that develop sequentially in the develop- FIGURE 2.6 Rat molar section showing alveolar crest fibers radiating
coronally.
ing root: the transseptal, alveolar crest, horizontal, oblique,
apical, and interradicular fibers (Fig. 2.4).
Transseptal fibers extend interproximally over the alveolar the largest group in the periodontal ligament, extend from the
bone crest and are embedded in the cementum of adjacent cementum in a coronal direction obliquely to the bone (see
teeth (Fig. 2.5). They are reconstructed even after destruc- Fig. 2.4). They bear the brunt of vertical masticatory stresses
tion of the alveolar bone that results from periodontal disease. and transform such stresses into tension on the alveolar bone.
These fibers may be considered as belonging to the gingiva The apical fibers radiate in a rather irregular manner from
because they do not have osseous attachment. the cementum to the bone at the apical region of the socket.
Alveolar crest fibers extend obliquely from the cementum They do not occur on incompletely formed roots. They pre-
just beneath the junctional epithelium to the alveolar crest vent tooth tipping, resist forces of luxation, and protect blood,
(Fig. 2.6). Fibers also run from the cementum over the alveolar lymph, and nerve supply
crest and to the fibrous layer of the periosteum that covers the The interradicular fibers fan out from the cementum to the
alveolar bone. The alveolar crest fibers prevent the extrusion tooth in the furcation areas of multirooted teeth. They resist
of the tooth and resist lateral tooth movements. The incision of tipping of tooth, forces of luxation and rotation.
these fibers during periodontal surgery does not increase tooth Other well-formed fiber bundles interdigitate at right angles
mobility unless significant attachment loss has occurred. or splay around and between regularly arranged fiber bundles.
Horizontal fibers extend at right angles to the long axis of Less regularly arranged collagen fibers are found in the inter-
the tooth from the cementum to the alveolar bone. They pre- stitial connective tissue between the principal fiber groups; this
vent lateral tooth movement. Oblique fibers, which comprise tissue contains the blood vessels, lymphatics, and nerves.
FIGURE 2.7 Epithelial rests of Malassez. A, Erupting tooth in a cat. Note the fragmentation of the Hertwig epithelial root sheath giving rise to epi-
thelial rests located along and close to the root surface. B, Human periodontal ligament with rosette-shaped epithelial rests (arrows) lying close to
the cementum (C).
Although the periodontal ligament does not contain ma- as the secretion of different collagen types and the production
ture elastin, two immature forms are found: oxytalan and of collagenase.
elaunin. The so-called oxytalan fibers run parallel to the root Osteoblasts, cementoblasts, osteoclasts, and odontoclasts
surface in a vertical direction and bend to attach to the cemen- are also seen in the cementa! and osseous surfaces of the peri-
tum in the cervical third of the root. They are thought to regu- odontal ligament.
late vascular flow. An elastic meshwork has been described in The epithelial rests of Malassez form a latticework in the
the periodontal ligament as being composed of many elastin periodontal ligament and appear as either isolated clusters of
lamellae with peripheral oxytalan fibers and elaunin fibers. cells or interlacing strands (Fig. 2.7), depending on the plane
Oxytalan fibers have been shown to develop de novo in the in which the microscopic section is cut. Continuity with the
regenerated periodontal ligament. junctional epithelium has been suggested in experimental
The principal fibers are remodeled by the periodontal liga- animals. The epithelial rests are considered remnants of the
ment cells to adapt to physiologic needs and in response to Hertwig root sheath, which disintegrates during root develop-
different stimuli. In addition to these fiber types, small col- ment (Fig. 27A)
lagen fibers associated with the larger principal collagen fibers Epithelial rests are distributed close to the cementum
have been described. These fibers run in all directions and throughout the periodontal ligament of most teeth; they are
form a plexus called the indifferent fiber plexus. most numerous in the apical area and the cervical area. They
diminish in number with age by degenerating and disappearing
or by undergoing calcification to become cementicles. The cells
Cellular Elements
are surrounded by a distinct basal lamina, they are intercon-
Four types of cells have been identified in the periodontal liga- nected by hemidesmosomes, and they contain tonofilaments.
ment: connective tissue cells, epithelial rest cells, immune sys- Although their functional properties are still considered to
tem cells, and cells associated with neurovascular elements. be unclear, the epithelial rests are reported to contain keratino-
Connective tissue cells include fibroblasts, cementoblasts, cyte growth factors, and they have been shown to be positive
and osteoblasts. Fibroblasts are the most common cells in for tyrosine kinase A neurotrophin receptor. In addition, epi-
the periodontal ligament; they appear as ovoid or elongated thelial rests proliferate when stimulated, and they participate
cells oriented along the principal fibers, and they exhibit in the formation of periapical cysts and lateral root cysts.
pseudopodia-like processes. These cells synthesize collagen The defense cells in the periodontal ligament include neutro-
and possess the capacity to phagocytose "old" collagen fibers phils, lymphocytes, macrophages, mast cells, and eosinophils.
and degrade them via enzyme hydrolysis. Thus, collagen turn- These cells, as well as those associated with neurovascular ele-
over appears to be regulated by fibroblasts in a process of in- ments, are similar to the cells found in other connective tissues.
tracellular degradation of collagen that does not involve the
action of collagenase. Ground Substance
Phenotypically distinct and functionally different subpop-
ulations of fibroblasts exist in the adult periodontal ligament. The periodontal ligament also contains a large proportion
They appear to be identical at both the light and electron mi- of ground substance that fills the spaces between fibers and
croscopic levels, but they may have different functions, such cells. This substance consists of two main components:
FIGURE 2.9 Foramina perforating the lamina dura of a dog jaw.
The tensional theory of tooth support states that the prin-

cipal fibers of the periodontal ligament are the major factors
in supporting the tooth and transmitting forces to the bone.
FIGURE 2.8 Cementicles in the periodontal ligament. One is lying
free and the other is adherent to the tooth surface.
When a force is applied to the crown, the principal fibers first
unfold and straighten, and they then transmit forces to the
alveolar bone, thereby causing an elastic deformation of the
bony socket. Finally, when the alveolar bone has reached its
limit, the load is transmitted to the basal bone. Many inves-
glycosaminoglycans, such as hyaluronic acid and proteogly-
tigators find this theory insufficient to explain the available
cans, and glycoproteins, such as fibronectin and laminin. It also
experimental evidence.
has a high water content (ie, 70%).
The viscoelastic system theory states that the displacement
The cell surface proteoglycans participate in several biologic
of the tooth is largely controlled by fluid movements, with fi-
functions, including cell adhesion, cell-cell and cell-matrix in-
bers having only a secondary role. When forces are transmitted
teractions, binding to various growth factors as coreceptors,
to the tooth, the extracellular fluid passes from the periodontal
and cell repair. The periodontal ligament may also contain
ligament into the marrow spaces of the bone through the fo-
calcified masses called cementicles, which are adherent to or
ramina in the cribriform plate. These perforations of the crib-
detached from the root surfaces (Fig. 2.8).
riform plate link the periodontal ligament with the cancellous
Cementicles may develop from calcified epithelial rests
portion of the alveolar bone; they are more abundant in the
around small spicules of cementum or alveolar bone traumati-
cervical third than in the middle and apical thirds (Fig. 2 9).
cally displaced into the periodontal ligament; from calcified
After the depletion of tissue fluids, the fiber bundles ab-
Sharpey fibers; and from calcified, thrombosed vessels within
sorb the slack and tighten. This leads to a blood vessel ste-
the periodontal ligament.
nosis. Arterial back pressure causes ballooning of the vessels
and passage of the blood ultrafiltrates into the tissues, thereby
Functions of Periodontal Ligament replenishing the tissue fluids.
The functions of the periodontal ligament are categorized as
Transmission of Occlusal Forces to Bone. The arrangement
physical, formative and remodeling, nutritional, and sensory.
of the principal fibers is similar to that of a suspension bridge
Physical Functions or a hammock. When an axial force is applied to a tooth, a
tendency toward displacement of the root into the alveolus
The physical functions of the periodontal ligament entail the
occurs. The oblique fibers alter their wavy, untensed pattern,
following:
assume their full length, and sustain the major part of the ax-
1. Provision of a soft-tissue "casing" to protect the vessels and ial force. When a horizontal or tipping force is applied, two
nerves from injury by mechanical forces phases of tooth movement occur. The first is within the con-
2. Transmission of occlusal forces to the bone fines of the periodontal ligament, and the second produces a
3. Attachment of the teeth to the bone displacement of the facial and lingual bony plates. The tooth
4. Maintenance of the gingival tissues in their proper relation- rotates about an axis that may change as the force is increased.
ship to the teeth The apical portion of the root moves in a direction that is
5. Resistance to the impact of occlusal forces (ie, shock ab- opposite to the coronal portion. In areas of tension, the prin-
sorption) cipal fiber bundles are taut rather than wavy. In areas of pres-
sure, the fibers are compressed, the tooth is displaced, and a
Resistance to Impact of Occlusal Forces (Shock Absorp- corresponding distortion of bone exists in the direction of root
tion). Two theories pertaining to the mechanism of tooth movement.
support have been considered: the tensional theory and the In single-rooted teeth, the axis of rotation is located in the
viscoelastic system theory. area between the apical third and the middle third of the root
(A) (B)
FIGURE 2.10 A, Diagram of a mandibular premolar in a resting state.
B, When a force is exerted on the tooth-in this case, in faciolingual di-
rection (arrow)-the tooth rotates around the fulcrum or axis of rotation
(black circle on root). The periodontal ligament is compressed in areas
of pressure and distended in areas of tension.
(Fig. 2. lOA) The root apex and the coronal half of the clinical
root have been suggested as other locations of the axis of rota-
tion. The periodontal ligament, which has an hourglass shape,
is narrowest in the region of the axis of rotation (Table 2.1).
In multirooted teeth, the axis of rotation is located in the bone
between the roots (Fig. 2.11). In compliance with the physi- FIGURE 2.11 Microscopic view of a rat molar subjected to occluso-
horizontal forces. Note the alternating widened and narrowed areas of
ologic mesial migration of the teeth, the periodontal ligament
the periodontal ligament as the tooth rotates around its axis of rotation.
is thinner on the mesial root surface than on the distal surface. The axis of rotation is in the interradicular space.
Formative and Remodeling Function
Periodontal ligament and alveolar bone cells are exposed Cartilage formation in the periodontal ligament, although
to physical forces in response to mastication, parafunction, unusual, may represent a metaplastic phenomenon in the re-
speech, and orthodontic tooth movement. Cells of the peri- pair of this ligament after injury.
odontal ligament participate in the formation and resorption The periodontal ligament is constantly undergoing remod-
of cementum and bone, which occur during physiologic tooth eling. Old cells and fibers are broken down and replaced by
movement, during the accommodation of the periodontium new ones, and mitotic activity can be observed in the fibro-
to occlusal forces, and during the repair of injuries. blasts and the endothelial cells. Fibroblasts form the collagen
Variations in cellular enzyme activity are correlated with fibers, and the residual mesenchymal cells develop into osteo-
the remodeling process. Although applied loads may induce blasts and cementoblasts. Therefore, the rate of formation and
vascular and inflammatory reactive changes in periodontal the differentiation of osteoblasts, cementoblasts, and fibroblasts
ligament cells, current evidence suggests that these cells have affect the rate of formation of collagen, cementum, and bone.
a mechanism to respond directly to mechanical forces via the Radioautographic studies with radioactive thymidine, pro-
activation of various mechanosensory signaling systems, in- line, and glycine indicate a high turnover rate of collagen in
cluding adenylate cyclase, stretch-activated ion channels, and the periodontal ligament. The rate of collagen synthesis is
via changes in cytoskeletal organization. twice as fast as that in the gingiva and four times as fast as that
TABLE 2.1
THICKNESS OF THE PERIODONTAL LIGAMENTS OF 172 TEETH FROM 15 HUMAN SUBJECTS

Average of Alveolar
Crest (mm) Average of Midroot (mm) Average of Apex (mm) Average ofTooth (mm)
Ages 11 through 16 years 0.23 0.17 0.24 021

(83 teeth from 4 jaws)
Ages 32 through 50 years 0.20 0.14 0.19 0.18
Ages 51 through 6 7 years 0.17 0.12 0.16 0.15
Age 24 years (1 case; 18 0.16 0.09 0.15 013
teeth from 1 jaw)
(Modified from Coolidge ED: J Am Dent Assoc 24:1260, 1937.)
in the skin, as established in the rat molar. A rapid turnover by uncalcified cementoid, sometimes become enclosed within
of sulfated glycosaminoglycans in the cells and amorphous the matrix and are trapped. After they are enclosed, they are
ground substance of the periodontal ligament also occurs. It referred to as cementocytes, and they will remain viable in a
should be noted that most of these studies have been per- manner similar to that of osteocytes.
formed in rodents and that information about primates and On the basis of immunochemical and ultrastructural stud-
humans is scarce. ies, Thomas and others have speculated that cementoblasts
can be of epithelial origin (ie, the Hertwig root sheath), having
Nutritional and Sensory Functions undergone an epithelial mesenchymal transformation.
The periodontal ligament supplies nutrients to the cementum, The two main types of cementum are acellular (primary)
bone, and gingiva by way of the blood vessels, and it also and cellular (secondary) cementum. Both consist of a calcified
provides lymphatic drainage as discussed later in this chapter. interfibrillar matrix and collagen fibrils.
In relation to other ligaments and tendons, the periodontal The two main sources of collagen fibers in cementum are
ligament is a highly vascularized tissue; almost 10% of its vol- Sharpey fibers (extrinsic), which are the embedded portion
ume in the rodent molar is blood vessels. This relatively high of the principal fibers of the periodontal ligament and which
blood vessel content may provide hydrodynamic damping to are formed by the fibroblasts, and fibers that belong to the
applied forces as well as high perfusion rates to the periodon- cementum matrix (intrinsic), which are produced by the ce-
tal ligament. mentoblasts. Cementoblasts also form the noncollagenous
The periodontal ligament is abundantly supplied with sen- components of the interfibrillar ground substance, such as
sory nerve fibers that are capable of transmitting tactile, pres- proteoglycans, glycoproteins, and phosphoproteins. Proteo-
sure, and pain sensations via the trigeminal pathways. Nerve glycans are most likely to play a role in regulating cell-cell and
bundles pass into the periodontal ligament from the periapical cell-matrix interactions, both during normal development
area and through channels from the alveolar bone that follow and during the regeneration of the cementum. In addition,
the course of the blood vessels. The bundles divide into single immunohistochemical studies have shown that the distribu-
myelinated fibers, which ultimately lose their myelin sheaths tion of proteoglycans is closely associated with the cemento-
and end in one of four types of neural termination: (1) free blasts and the cementocytes.
endings, which have a treelike configuration and carry pain The major proportion of the organic matrix of cementum is
sensation; (2) Ruffini-like mechanoreceptors, which are locat- composed of type I (90%) and type Ill (about 5%) collagens.
ed primarily in the apical area; (3) coiled Meissner corpuscles Sharpey fibers, which constitute a considerable proportion of
and mechanoreceptors, which are found mainly in the mid- the bulk of cementum, are composed of mainly type I col-
root region; and ( 4) spindlelike pressure and vibration end- lagen. Type Ill collagen appears to coat the type I collagen of
ings, which are surrounded by a fibrous capsule and located the Sharpey fibers.
mainly in the apex. Acellular cementum is the first cementum formed; it cov-
ers approximately the cervical third or half of the root, and it
Regulation of Periodontal Ligament Width does not contain cells (Fig. 2.12). This cementum is formed
Some of the most interesting features of the periodontal liga-
ment in animals are its adaptability to rapidly changing ap-
plied force and its capacity to maintain its width at constant
dimensions throughout its lifetime. These are important mea-
sures of periodontal ligament homeostasis that provide insight
into the function of the biologic mechanisms that tightly regu-
late the metabolism and spatial locations of the cell popula-
tions involved in the formation of bone, cementum, and peri-
odontal ligament fibers. In addition, the ability of periodontal
ligament cells to synthesize and secrete a wide range of regula-
tory molecules is an essential component of tissue remodeling
and periodontal ligament homeostasis.
Cementum
Cementum is the calcified, avascular mesenchymal tissue that
forms the outer covering of the anatomic root.
Development of Cementum D
The rupture of the Hertwig root sheath allows the mesenchy-
mal cells of the dental follicle to contact the dentin where they
start forming a continuous layer of cementoblasts.
Cementum formation begins with the deposition of a
meshwork of irregularly arranged collagen fibrils sparsely dis-
tributed in a ground substance or matrix called precementum FIGURE 2.12 Acellular cementum (AC) showing incremental lines
running parallel to the long axis of the tooth. These lines represent the
or cementoid. This is followed by a phase of matrix matura- appositional growth of cementum. Note the thin, light lines running into
tion, which subsequently mineralizes to form cementum. Ce- the cementum perpendicular to the surface; these represent the Sharpey
mentoblasts, which are initially separated from the cementum fibers of the periodontal ligament (PL). D, Dentin (X300).
the time of tooth eruption may place portions of mature enamel

in contact with the connective tissue, which then will deposit
an acellular and afibrillar type of cementum over the enamel.
On the basis of these findings, Schroeder has classified ce-
mentum as follows:
• Acellular afibrillar cementum (MC) contains neither cells
nor extrinsic or intrinsic collagen fibers, except for a miner-
alized ground substance. Acellular afibrillar cementum is a
product of cementoblasts and found as coronal cementum
in humans, with a thickness of 1-15 µm.
• Acellular extrinsic fiber cementum (AEFC) is composed al-
most entirely of densely packed bundles of Sharpey fibers
and lacks cells. Acellular extrinsic fiber cementum is a
product of fibroblasts and cementoblasts. It is found in the
cervical third of roots in humans, but it may extend farther
apically Its thickness is between 30 and 230 µm.
D • Cellular mixed stratified cementum (CMSC) is composed of
extrinsic (Sharpey) and intrinsic fibers, and it may contain
cells. Cellular mixed stratified cementum is a coproduct of
fibroblasts and cementoblasts. In humans, it appears pri-
marily in the apical third of the roots and apices and in
furcation areas. Its thickness ranges from 100 to 1000 µm.
FIGURE 2.13 Cellular cementum (CC) showing cementocytes lying • Cellular intrinsic fiber cementum (CIFC) contains cells but no
within the lacunae. Cellular cementum is thicker than acellular cemen- extrinsic collagen fibers. Cellular intrinsic fiber cementum
tum (see Fig. 2.15). The evidence of incremental lines also exists, but is formed by cementoblasts, and, in humans, it fills the re-
they are less distinct than in the acellular cementum. The cells adjacent sorption lacunae.
to the surface of the cementum in the periodontal ligament (PL) space
are cementoblasts. 0, Dentin (X300). Intermediate cementum is a poorly defined zone near the ce-
mentodentinal Junction of certain teeth that appear to contain
cellular remnants of the Hertwig sheath embedded in calcified
before the tooth reaches the occlusal plane, and its thickness ground substance.
ranges from 30 to 230 µm. Sharpey fibers make up most of Inorganic content of cementum (hydroxyapatite; Ca10[Po4]6
the structure of acellular cementum, which has a principal [OH}i) is 45-50%, which is less than that of bone (65%),
role in supporting the tooth. Most fibers are inserted at ap- enamel (97%), or dentin (70%). Opinions differ with regard
proximately right angles into the root surface and penetrate to whether the microhardness increases or decreases with age,
deep into the cementum, but others enter from several differ- and no relationship has been established between aging and
ent directions. Their size, number, and distribution increase the mineral content of cementum.
with function. Sharpey fibers are completely calcified, with Some of the molecules unique to the cementum have been
the mineral crystals oriented parallel to the fibrils as in dentin described. Recent work has investigated the role of cementum
and bone, except in a 10-50-µm-wide zone near the cemen- attachment protein, which is a collagenous cementum-derived
todentinal junction where they are only partially calcified. protein. Cementum attachment protein has been shown to
The peripheral portions of Sharpey fibers in actively mineral- promote the adhesion and spreading of mesenchymal cell
izing cementum tend to be more calcified than the interior types, with osteoblasts and periodontal ligament fibroblasts
regions, according to evidence obtained by scanning electron showing better adhesion than gingival fibroblasts and kera-
microscopy Acellular cementum also contains intrinsic colla- tinocytes. In addition, Ikezawa and coworkers described the
gen fibrils that are calcified and irregularly arranged or paral- characterization of cementum-derived growth factor, which is
lel to the surface. an insulin-like, growth factor-I-like molecule. Cementum-
Cellular cementum, which is formed after the tooth reaches derived growth factor has been shown to enhance the prolif-
the occlusal plane, is more irregular and contains cells (ce- eration of gingival fibroblasts and periodontal ligament cells.
mentocytes) in individual spaces (lacunae) that communicate
with each other through a system of anastomosing canaliculi
Permeability of Cementum
(Fig. 2.13). Cellular cementum is less calcified than the acellu-
lar type. Sharpey fibers occupy a smaller portion of the cellular In very young animals, acellular cementum and cellular cemen-
cementum and are separated by other fibers that are arranged tum are very permeable and permit the diffusion of dyes from
either parallel to the root surface or at random. Sharpey fibers the pulp and the external root surface. In cellular cementum,
may be completely or partially calcified, or they may have a the canaliculi in some areas are contiguous with the dentinal
central, uncalcified core surrounded by a calcified border. tubuli. The permeability of cementum diminishes with age.
Both acellular cementum and cellular cementum are ar-
ranged in lamellae separated by incremental lines parallel to
Cementoenamel Junction
the long axis of the root (see Figs. 2 .12 and 2 .13). These lines
represent "rest periods" in cementum formation, and they are The cementum at and immediately subjacent to the cemen-
more mineralized than the adjacent cementum. In addition, the toenamel junction is of particular clinical importance in root-
loss of the cervical part of the reduced enamel epithelium at scaling procedures. Three types of relationships involving the
I As a result of considerable physiologic variation in the thick-
\
ness of cementum among different teeth in the same person
and also among different persons, distinguishing between hy-
percementosis and the physiologic thickening of cementum is
D D D sometimes difficult. Nevertheless, the excessive proliferation
of cementum may occur with a broad spectrum of neoplastic
and nonneoplastic conditions, including benign cementoblas-
toma, cementifying fibroma, periapical cementa! dysplasia,
florid cemento-osseous dysplasia, and other benign fibro-
osseous lesions.
(A) s-10% (B) 30% (C) 60---B5%
Hypercementosis occurs as a generalized thickening of the
FIGURE 2.14 Normal variations in tooth morphology at the cemen- cementum, with nodular enlargement of the apical third of the
toenamel junction. A, Space between the enamel and the cementum
with the dentin (D) exposed. B, End-to-end relationship of enamel and
root. It also appears in the form of spikelike excrescences (ie,
cementum. C, Cementum overlapping the enamel. cementa! spikes) created by either the coalescence of cement-
ides that adhere to the root or the calcification of periodontal
fibers at the sites of insertion into the cementum.
cementum may exist at the cementoenamel junction. In about Radiographically, the radiolucent shadow of the periodon-
60-65% of cases, cementum overlaps the enamel (Fig. 2.14). tal ligament and the radiopaque lamina dura are always seen
This occurs when the enamel epithelium degenerates at its on the outer border of an area of hypercementosis, enveloping
cervical terminaton permitting the connective tissue to come it as it would in normal cementum. On the other hand, from
in direct contact with the enamel surface; in about 30%, an a diagnostic standpoint, periapical cementa! dysplasia, con-
edge-to-edge butt joint exists; and in 5-10%, the cementum densing osteitis, and focal periapical osteopetrosis may be dif-
and enamel fail to meet. This occurs when enamel epithelium ferentiated from hypercementosis, because all of these entities
in the cervical portion of the root is delayed in its seperation are located outside of the shadow of the periodontal ligament
from dentin. In this case, gingival recession may result in ac- and the lamina dura.
centuated sensitivity as a result of exposed dentin. The cause of hypercementosis varies and is not completely
understood. The spikelike type of hypercementosis gener-
Cementodentinal Junction ally results from excessive tension caused by orthodontic ap-
pliances or occlusal forces. The generalized type occurs in a
The terminal apical area of the cementum where it joins the in- variety of circumstances. In teeth without antagonists, hy-
ternal root canal dentin is known as the cementodentinal junction. percementosis is interpreted as an effort to keep pace with
When root canal treatment is performed, the obturating mate- excessive tooth eruption. In teeth that are subject to low-grade
rial should be at the cementodentinal junction. There appears to periapical irritation that arises from pulp disease, it is consid-
be no increase or decrease in the width of the cementodentinal ered compensation for the destroyed fibrous attachment to the
junction with age; its width appears to remain relatively stable. tooth. The cementum is deposited adjacent to the inflamed
Scanning electron microscopy of the human teeth reveals that periapical tissue. Hypercementosis of the entire dentition may
the cementodentinal junction is 2-3-µm wide. The fibril-poor occur in patients with Paget disease. Other systemic distur-
layer contains a significant amount of proteoglycans, and fibrils bances that may lead to or may be associated with hyperce-
intermingle between the cementum and the dentin. mentosis include acromegaly, arthritis, calcinosis, rheumatic
fever, and thyroid goiter.
Thickness of Cementum Hypercementosis itself does not require treatment. It could
pose a problem if an affected tooth requires extraction. In a
Cementum deposition is a continuous process that occurs at multirooted tooth, sectioning of the tooth may be required
varying rates throughout life. Cementum formation is most before extraction.
rapid in the apical regions where it compensates for tooth
eruption, which itself compensates for attrition.
Cementum Resorption and Repair
The thickness of cementum on the coronal half of the root
varies from 16 to 60 µm, which is about the thickness of a Permanent teeth do not undergo physiologic resorption as pri-
hair. It attains its greatest thickness (::; 150-200 µm) in the mary teeth do. However, the cementum of erupted (as well as
apical third and in the furcation areas. It is thicker in distal unerupted) teeth is subject to resorptive changes that may be
surfaces than in mesial surfaces, probably because of function- of microscopic proportion or sufficiently extensive to present
al stimulation from mesial drift over time. Between the ages a radiographically detectable alteration in the root contour.
of 11 and 70 years, the average thickness of the cementum Microscopic cementum resorption is extremely common;
increases threefold, with the greatest increase seen in the api- in one study, it occurred in 236 of 261 teeth (90.5%). The
cal region. Average thicknesses of 95 µmat the age of 20 years average number of resorption areas per tooth was 3.5. Of the
and of 215 um at the age of 60 years have been reported. 922 areas of resorption, 708 (76.8%) were located in the api-
Abnormalities in the thickness of cementum may range cal third of the root, 177 (19.2%) in the middle third, and 37
from an absence or paucity of cellular cementum (ie, cementa! (4 0%) in the gingival third. Approximately 70% of all resorp-
aplasia or hypoplasia) to an excessive deposition of cementum tion areas were confined to the cementum without involving
(ie , cementa! hyperplasia or hypercementosis). the dentin.
The term hypercementosis refers to a prominent thickening Cementum resorption may be caused by local or systemic
of the cementum. It is largely an age-related phenomenon, and factors, or it may occur without apparent etiology (ie, idio-
it may be localized to one tooth or affect the entire dentition. pathic). Local conditions that cause cementum resorption
FIGURE 2.16 Scanning electron micrograph of a root exposed by

periodontal disease showing a large resorption bay (R). Remnants of
the periodontal ligament (P) and calculus (C) are visible. Cracking of
the tooth surface occurs as a result of the preparation technique (X 160).
(Courtesy Dr John Sottosanti, La Jolla, CA.)
FIGURE 2.17 Resorption of cementum and dentin. A multinuclear

osteoclast in seen (X). The direction of resorption is indicated by the
arrow. Note the scalloped resorption front in the dentin (0). The ce-
mentum is the darkly stained band at the upper and lower right. P, Peri-
odontal ligament.
FIGURE 2.15 Cementa! resorption associated with excessive occlu-

sal forces. A, Low-power histologic section of the mandibular anterior giant cells and large mononuclear macrophages are generally
teeth. B, High-power micrograph of the apex of the left central incisor found adjacent to the cementum that is undergoing active re-
shortened by the resorption of cementum and dentin. Note the partial
sorption (Fig. 2 .17). Several sites of resorption may coalesce
repair of the eroded areas (arrows) and the cementicle at the upper right.
to form a large area of destruction. The resorptive process may
extend into the underlying dentin and even into the pulp, but
include trauma from occlusion (Fig. 2.15); orthodontic move- it is usually painless. Cementum resorption is not necessarily
ment; pressure from malaligned erupting teeth, cysts, and tu- continuous and may alternate with periods of repair and the
mors; teeth without functional antagonists; embedded teeth; deposition of new cementum. The newly formed cementum
replanted and transplanted teeth; periapical disease; and peri- is demarcated from the root by a deeply staining irregular line
odontal disease. Systemic conditions that are cited as predis- termed a reversal line, which delineates the border of the previ-
posing an individual to or inducing cementa! resorption in- ous resorption. A recent study showed that the reversal lines
clude calcium deficiency, hypothyroidism, hereditary fibrous of human teeth contain a few collagen fibrils and highly accu-
osteodystrophy, and Paget disease. mulated proteoglycans with mucopolysaccharides (glycosami-
Cementum resorption appears microscopically as baylike noglycans) and that fibril intermingling occurs only in some
concavities in the root surface. (Fig. 2.16) Multinucleated places between reparative cementum and resorbed dentin or
be exfoliated. Clinically, ankylosed teeth lack the physiologic

mobility of normal teeth, which is one diagnostic sign for anky-
lotic resorption. In addition, these teeth usually have a special
metallic percussion sound; if the ankylotic process continues,
they will be in infraocclusion. However, the clinical diagnosis of
ankylosis by mobility and percussion tests alone is only reliable
when at least 20% of the root surface is affected.
As the periodontal ligament is replaced with bone during an-
kylosis, proprioception is lost, because pressure receptors in the
periodontal ligament are deleted or do not function correctly
Furthermore, the physiologic drifting and eruption of teeth
can no longer occur, and thus the ability of the teeth and peri-
odontium to adapt to altered force levels or directions of force is
greatly reduced. Radiographically, resorption lacunae are filled
with bone, and the periodontal ligament space is missing.
FIGURE 2.18 A clinical human histology shows that new cementum and Since no definitive causes can be found in ankylotic root
new periodontal ligament fiber formed at a previous periodontal defect resorption, no predictable treatment can be suggested. Treat-
treated with recombinant human platelet-derived growth factor-BB with ment modalities range from a conservative approach, such as
~-tricalcium phosphate. (Courtesy Dr Daniel WK Kao, Philadelphia, PA.)
restorative intervention, to the surgical extraction of the af-
fected tooth.
When titanium implants are placed in the jaw, healing re-
cementum. Embedded fibers of the periodontal ligament rees- sults in bone that is formed in direct apposition to the implant
tablish a functional relationship in the new cementum. without an intervening connective tissue. This may be inter-
Cementum repair requires the presence of a viable connec- preted as a form of ankylosis. Since resorption of the metallic
tive tissue. If epithelium proliferates into an area of resorption, implant cannot occur, the implant remains indefinitely "anky-
repair will not take place. Cementum repair can occur in devi- losed" to the bone. In addition, a true periodontal pocket will
talized as well as vital teeth. not form; the apical proliferation of the epithelium along the
Histologic evidence demonstrates that cementum forma- root, which is a key element of pocket formation, is not pos-
tion is critical for the appropriate maturation of the periodon- sible because of the ankylosis.
tium, both during development and during the regeneration
of lost periodontal tissues. In other words, a variety of macro-
molecules present in the extracellular matrix of the periodon- Exposure of Cementum to the Oral
tium are likely to play a regulatory role in cementogenesis. Environment
The regeneration of cementum requires cementoblasts,
but the origin of the cementoblasts and the molecular factors Cementum becomes exposed to the oral environment in cases
that regulate their recruitment and differentiation are not fully of gingival recession and as a result of the loss of attachment
understood. However, recent research provides a better unin pocket formation. The cementum is sufficiently permeable
derstanding; for example, the epithelial cell rests of Malassez to be penetrated in these cases by organic substances, inor-
are the only odontogenic epithelial cells that remain in the ganic ions, and bacteria. Bacterial invasion of the cementum
periodontium after the eruption of teeth, and they may have occurs frequently in individuals with periodontal disease, and
some function in cementum repair and regeneration under cementum caries can develop.
specific conditions. The rests of Malassez may be related to
cementum repair by activating their potential to secrete ma- Alveolar Process
trix proteins that have been expressed in tooth development,
such as amelogenins, enamelins, and sheath proteins. Several The alveolar process is the portion of the maxilla and man-
growth factors have been shown to be effective in cementum dible that forms and supports the tooth sockets (alveoli). It
regeneration, including members of the transforming growth forms when the tooth erupts to provide the osseous attach-
factor superfamily (ie, bone morphogenetic proteins), platelet- ment to the forming periodontal ligament; it disappears grad-
derived growth factor, insulin-like growth factor, and enamel ually after the tooth is lost.
matrix derivatives (Fig. 2 .18). The alveolar bone develops around each tooth follicle dur-
ing odontogenesis. When a deciduous tooth is shed, its al-
Ankylosis veolar bone is resorbed. The succedaneous permanent tooth
Fusion of the cementum and the alveolar bone with oblitera- moves into place and develops its own alveolar bone from its
tion of the periodontal ligament is termed ankylosis. Ankylosis own dental follicle. As the tooth root forms and the surround-
occurs in teeth with cemental resorption, which suggests that ing tissues develop and mature, alveolar bone merges with
it may represent a form of abnormal repair. Ankylosis may the separately developing basal bone, and the two become
also develop after chronic periapical inflammation, tooth re- one continuous structure. Although alveolar bone and basal
plantation, and occlusal trauma and around embedded teeth. bone have different intermediate origins, both are ultimately
This condition is relatively uncommon, and it occurs most derived from neural crest ectomesenchyme.
frequently in the primary dentition. Mandibular basal bone begins mineralization at the exit of
Ankylosis results in the resorption of the root and its grad- the mental nerve from the mental foramen, whereas the max-
ual replacement by bone tissue. For this reason, reimplanted illary basal bone begins at the exit of the infraorbital nerve
teeth that ankylose will lose their roots after 4-5 years and will from the infraorbital foramen.
Just before mineralization, osteoblasts start producing bony structures. Therefore, the size, shape, location, and function
matrix vesicles. These vesicles contain enzymes (eg, alkaline of the teeth determine their morphology Interestingly, although
phosphatase) that help to jump start the nucleation of hy- the growth and development of the bones of the jaw determine
droxyapatite crystals. As these crystals grow and develop, they the position of the teeth, a certain degree of repositioning of the
form coalescing bone nodules, which, with fast-growing non- teeth can be accomplished through occlusal forces and in re-
oriented collagen fibers, are the substructure of woven bone sponse to orthodontic procedures that rely on the adaptability of
and the first bone formed in the alveolus. Later, through bone the alveolar bone and the associated periodontal tissues.
deposition, remodeling, and the secretion of oriented collagen The alveolar process consists of the following:
fibers in sheets, mature lamellar bone is formed.
1. An external plate of cortical bone is formed by haversian
The hydroxyapatite crystals are generally aligned with their
bone and compacted bone lamellae.
long axes parallel to the collagen fibers, and they appear to be
2. The inner socket wall of thin, compact bone called the
deposited on and within the collagen fibers in mature lamellar
alveolar bone proper is seen as the lamina dura in radio-
bone. In this way, bone matrix is able to withstand the heavy
graphs. Histologically, it contains a series of openings (ie,
mechanical stresses applied to it during function.
the cribriform plate) through which neurovascular bundles
Since the alveolar processes develop and undergo remodel-
link the periodontal ligament with the central component
ing with tooth formation and eruption, they are tooth-dependent
of the alveolar bone: the cancellous bone.
3. Cancellous trabeculae between these two compact layers
act as supporting alveolar bone. The interdental septum
consists of cancellous supporting bone enclosed within a
compact border (Fig. 2.19).
In addition, the bones of the Jaw include the basal bone,
which is the portion of the jaw located apically but unrelated
to the teeth (Fig. 2 20)
The alveolar process is divisible into separate areas on an
anatomic basis, but it functions as a unit, with all parts interre-
lated in the support of the teeth. Figures 2.21 and 2.22 show
the relative proportions of cancellous bone and compact bone
that form the alveolar process. Most of the facial and lingual
portions of the sockets are formed by compact bone alone;
cancellous bone surrounds the lamina dura in apical, apico-
lingual, and interradicular areas.
FIGURE 2.19 Mesiodistal section through the mandibular molars of
a 17-year-old girl obtained at autopsy. Note the interdental bony septa
between the first and second molars. The dense cortical bony plates rep-
resent the alveolar bone proper (ie, the cribriform plates) and are sup-
ported by cancellous bony trabeculae. The third molar is still in the early
stages of root formation and eruption.
Cortical plate ----t- II I/ /.\ \ Alveolar (A)~ (8) - (C) (D)
----
Spongy bone
Basal bone
Mandibular
canal
(E) (G) (H)

FIGURE 2.20 Section through a human jaw with a tooth in situ. The FIGURE 2.21 Relative proportions of cancellous bone and compact
dotted line indicates the separation between the basal bone and the al- bone in a longitudinal faciolingual section of, A, mandibular molars;
veolar bone. (Redrawn from Ten Cate AR: Oral histology: development, B, lateral incisors; C, canines; D, first premolars; E, second premolars;
structure, and function, ed 4, St Louis, 1994, Mosby.) F, first molars; G, second molars; and H, third molars.
FIGURE 2.22 The shape of the roots and the surrounding bone dis-
tribution in a transverse section of maxilla and mandible at the mid-
root level.
Composition of Alveolar Bone

Bone consists of two-third inorganic matter and one-third FIGURE 2.23 Rat alveolar bone. This histologic view shows two mul-
organic matrix. The inorganic matter is composed principally ti nucleated osteoclasts in the Howship lacuna.
of the minerals calcium and phosphate along with hydroxyl,
carbonate, citrate, and trace amounts of other ions such as
sodium, magnesium, and fluorine. The mineral salts are in is mediated by receptors on the chief cells of the parathyroid
the form of hydroxyapatite crystals of ultramicroscopic size glands, which then release parathyroid hormone. Parathy-
and constitute approximately two-third of the bone structure. roid hormone stimulates osteoblasts to release interleukin-1
The organic matrix consists mainly of collagen type I and interleukin-6, which stimulate monocytes to migrate
(90%), with small amounts of noncollagenous proteins such into the bone area. Leukemia-inhibiting factor, which is se-
as osteocalcin, osteonectin, bone morphogenetic protein, creted by osteoblasts, coalesces monocytes into multinucle-
phosphoproteins, and proteoglycans. Osteopontin and bone ated osteoclasts, which then resorb bone, thereby releasing
sialoprotein are cell-adhesion proteins that appear to be im- calcium ions from hydroxyapatite into the blood. This release
portant for the adhesion of both osteoclasts and osteoblasts. normalizes the blood level of calcium. A feedback mechanism
In addition, paracrine factors, including cytokines, chemo- for normal blood levels of calcium turns off the secretion of
kines, and growth factors, have been implicated in the local parathyroid hormone. Meanwhile, osteoclasts have resorbed
control of mesenchymal condensations that occur at the on- organic matrix along with hydroxyapatite. The breakdown of
set of organogenesis. These factors probably play a prominent collagen from the organic matrix releases various osteogenic
role in the development of the alveolar processes. substrates, which are covalently bound to collagen. This in
Although the alveolar bone tissue is constantly changing its turn stimulates the differentiation of osteoblasts, which ulti-
internal organization, it retains approximately the same form mately deposit bone. This interdependency of osteoblasts and
from childhood through adult life. Bone deposition by osteo- osteoclasts in remodeling is called coupling.
blasts is balanced by resorption by osteoclasts during tissue The bone matrix that is laid down by osteoblasts is non-
remodeling and renewal. It is well known that the number mineralized osteoid. While new osteoid is being deposited,
of osteoblasts decreases with aging; however, no remarkable the older osteoid located below the surface becomes mineral-
change in the number of osteoclasts has ever been reported. ized as the mineralization front advances.
Remodeling is the major pathway of bony changes in shape, Bone resorption is a complex process that is morphologi-
resistance to forces, repair of wounds, and calcium and phos- cally related to the appearance of eroded bone surfaces (ie,
phate homeostasis in the body Indeed, the coupling of bone Howship lacunae) and large, multinucleated cells (osteoclasts)
resorption with bone formation constitutes one of the fun- (Fig. 2.23). Osteoclasts originate from hematopoietic tissue
damental principles by which bone is necessarily remodeled and are formed by the fusion of mononuclear cells of asyn-
throughout its life. Bone remodeling involves the coordination chronous populations. When osteoclasts are active rather than
of activities of cells from two distinct lineages, the osteoblasts resting, they possess an elaborately developed ruffled border
and the osteoclasts, which form and resorb the mineralized from which hydrolytic enzymes are thought to be secreted.
connective tissues of bone. These enzymes digest the organic portion of the bone. The ac-
The regulation of bone remodeling is a complex process tivity of osteoclasts and the morphology of the ruffled border
that involves hormones and local factors acting in an auto- can be modified and regulated by hormones such as parathy-
crine and a paracrine manner on the generation and activity roid hormone (indirectly) and calcitonin, which has receptors
of differentiated bone cells. Bone contains 99% of the body's on the osteoclast membrane.
calcium ions and therefore is the major source for calcium Another mechanism of bone resorption involves the cre-
release when the calcium blood levels decrease; this is moni- ation of an acidic environment on the bone surface, thereby
tored by the parathyroid gland. A decrease in blood calcium leading to the dissolution of the mineral component of bone.
This event can be produced by different conditions, including

a proton pump through the cell membrane of the osteoclast,
bone tumors, and local pressure translated through the secre-
tory activity of the osteoclast.
Ten Cate described the sequence of events in the resorptive
process as follows:
1. Attachment of osteoclasts to the mineralized surface of
bone
2. Creation of a sealed acidic environment through the ac-
tion of the proton pump, which demineralizes bone and
exposes the organic matrix
3. Degradation of the exposed organic matrix to its constitu-
ent amino acids via the action of released enzymes (eg, acid
phosphatase, cathepsin)
4. Sequestering of mineral ions and amino acids within the
FIGURE 2.24 Deep penetration of Sharpey fibers into bundle bone
osteoclast
of a rat molar.
Notably, the cellular and molecular events involved in bone
remodeling have a strong similarity to many aspects of inflam-
mation and repair. The relationships among matrix molecules
[eg, osteopontin, bone sialoprotein, SPARC (secreted protein,
acidic, rich in cysteine), osteocalcin], blood clotting, and
wound healing are clearly evident.
Cells and lntercellular Matrix

Osteoblasts, which are the cells that produce the organic ma-
trix of bone, are differentiated from pluripotent follicle cells.
Alveolar bone is formed during fetal growth by intramembra-
nous ossification, and it consists of a calcified matrix with os-
teocytes enclosed within spaces called lacunae. The osteocytes
extend processes into canaliculi that radiate from the lacunae.
The canaliculi form an anastomosing system through the in-
tercellular matrix of the bone, which brings oxygen and nutri-
ents to the osteocytes through the blood and removes meta-
bolic waste products. Blood vessels branch extensively and
travel through the periosteum. The endosteum lies adjacent
to the marrow vasculature. Bone growth occurs via the ap-
position of an organic matrix that is deposited by osteoblasts.
Haversian systems (ie, osteons) are the internal mechanisms
that bring a vascular supply to bones that are too thick to be
supplied only by surface vessels. These are found primarily in
the outer cortical plates and the alveolar bone proper.
Socket Wall
The socket wall consists of dense, lamellated bone, some of
which is arranged in haversian systems and bundle bone. Bundle
bone is the term given to the bone adjacent to the periodontal lig-
ament that contains a great number of Sharpey fibers (Fig. 2.24).
It is characterized by thin lamellae arranged in layers parallel to
the root, with intervening appositional lines (Fig. 2.25). Bundle
bone is localized within the alveolar bone proper. Some Sharpey
fibers are completely calcified, but most contain an uncalcified
central core within a calcified outer layer. Bundle bone is not
unique to the jaws; it occurs throughout the skeletal system
wherever ligaments and muscles are attached.
The cancellous portion of the alveolar bone consists of tra-
beculae that enclose irregularly shaped marrow spaces lined FIGURE 2.25 Bundle bone associated with the physiologic mesial
with a layer of thin, flattened endosteal cells. Wide variation migration of the teeth. A, Horizontal section through the molar roots
during the process of mesial migration (left, mesial; right, distal). B, Me-
occurs in the trabecular pattern of cancellous bone, which is sial root surface showing osteoclasis of bone (arrows). C, Distal root sur-
affected by occlusal forces. The matrix of the cancellous tra- face showing bundle bone that has been partially replaced with dense
beculae consists of irregularly arranged lamellae separated by bone on the marrow side. PL, Periodontal ligament.
deeply staining incremental and resorption lines indicative of The periosteum consists of an inner layer composed of os-
previous bone activity, with an occasional haversian system. teoblasts surrounded by osteoprogenitor cells, which have the
Cancellous bone is found predominantly in the interra- potential to differentiate into osteoblasts, and an outer layer rich
dicular and interdental spaces and in limited amounts facially in blood vessels and nerves and composed of collagen fibers
or lingually, except in the palate. In the adult human, more and fibroblasts. Bundles of periosteal collagen fibers penetrate
cancellous bone exists in the maxilla than in the mandible. the bone, thereby binding the periosteum to the bone. The end-
osteum is composed of a single layer of osteoblasts and some-
Bone Marrow times a small amount of connective tissue. The inner layer is the
osteogenic layer, and the outer layer is the fibrous layer.
In the embryo and the newborn, the cavities of all bones are Cellular events at the periosteum modulate bone size
occupied by red hematopoietic marrow. The red marrow grad- throughout an individual's life span, and a change in bone size
ually undergoes a physiologic change to the fatty or yellow is probably the result of the balance between periosteal os-
inactive type of marrow. In the adult, the marrow of the jaw teoblastic and osteoclastic activities. Little is currently known
is normally of the latter type, and red marrow is found only about the control of periosteal osteoblastic activity or the
in the ribs, sternum, vertebrae, skull, and humerus. Howev- clinical importance of variations in periosteal bone formation.
er, foci of the red bone marrow are occasionally seen in the Moreover, the nature and impact of periosteal bone resorption
Jaws, often accompanied by the resorption of bony trabeculae. are virtually unexplored.
Common locations are the maxillary tuberosity, the maxillary
and mandibular molar and premolar areas, and the mandibu-
lar symphysis and ramus angle, which may be visible radio- lnterdental Septum
graphically as zones of radiolucency.
The interdental septum consists of cancellous bone that is
Periosteum and Endosteum bordered by the socket wall cribriform plates (ie, lamina dura
or alveolar bone proper) of approximating teeth and the facial
Layers of differentiated osteogenic connective tissue cover all and lingual cortical plates (Fig. 2 .26). If the interdental space
of the bone surfaces. The tissue that covers the outer surface is narrow, the septum may consist of only the cribriform plate.
of bone is termed periosteum, whereas the tissue that lines the In one study, for example, the space between the mandibu-
internal bone cavities is called endosteum. lar second premolars and first molars consisted of cribriform
FIGURE 2.26 lnterdental septa. A, Radiograph of the mandibular incisor area. Note the prominent lamina dura. B, lnterdental septa between the
mandibular anterior teeth shown in A. There is a slight reduction in bone height with widening of the periodontal ligament in the coronal areas. The
central cancellous portion is bordered by the dense bony cribriform plates of the socket, which form the lamina dura around the teeth in the radio-
graph. Attachments for the mental is muscle are seen between the canine and lateral incisors. (From Glickman I, Smulow /: Periodontal disease: clini-
cal, radiographic, and histopathologic features, Philadelphia, 7974, Saunders.)
FIGURE 2.27 Boneless "window" between adjoining close roots of

FIGURE 2.28 Normal bone contour conforms to the prominence of
molars.
the roots.
plate and cancellous bone in 85% of the cases and of only

cribriform plate in the remaining 15%. If the roots are too alignment. The bone margin is thinned to a knife edge, and
close together, an irregular "window" can appear in the bone it presents an accentuated arc in the direction of the apex.
between adjacent roots (Fig. 2.27). Between maxillary molars, On teeth in lingual version, the facial bony plate is thicker
the septum consisted of cribriform plate and cancellous bone than normal. The margin is blunt, rounded, and horizontal
in 66.6% of the cases; it was composed of only cribriform rather than arcuate. The effect of the root-to-bone angula-
plate in 20.8%, and it had a fenestration in 12.5%. tion on the height of alveolar bone is most noticeable on the
Determining root proximity radiographically is important. palatal roots of the maxillary molars. The bone margin is
The mesiodistal angulation of the crest of the interdental sep- located farther apically on the roots, and it forms relatively
tum usually parallels a line drawn between the cementoenamel acute angles with the palatal bone. The cervical portion of
junctions of the approximating teeth. The distance between the alveolar plate is sometimes considerably thickened on
the crest of the alveolar bone and the cementoenamel junction the facial surface, apparently as reinforcement against occlu-
in young adults varies between 0. 75 and 1.49 mm (average, sal forces (Fig. 2.29)
1.08 mm). This distance increases with age to an average of
2.81 mm. However, this phenomenon may not be as much a
function of age as of periodontal disease. Fenestration and Dehiscence
The mesiodistal and faciolingual dimensions and shape of
the interdental septum are governed by the size and convexity Isolated areas in which the root is denuded of bone and the
of the crowns of the two approximating teeth as well as by the root surface is covered only by periosteum and overlying gin-
position of the teeth in the jaw and their degree of eruption. giva are termed fenestrations. In these areas, the marginal bone
is intact. When the denuded areas extend through the mar-
ginal bone, the defect is called a dehiscence (Fig. 2.30).
Osseous Topography Such defects occur on approximately 20% of the teeth; they
The bone contour normally conforms to the prominence of occur more often on the facial bone than on the lingual bone,
the roots, with intervening vertical depressions that taper to- they are more common on anterior teeth than on posterior
ward the margin (Fig. 2.28). Alveolar bone anatomy varies teeth, and they are frequently bilateral. Microscopic evidence
among patients and has important clinical implications. The of lacunar resorption may be present at the margins. The
height and thickness of the facial and lingual bony plates are cause of these defects is not clear. Prominent root contours,
affected by the alignment of the teeth, the angulation of the malposition, and labial protrusion of the root in combination
root to the bone, and occlusal forces. with a thin bony plate are predisposing factors. Fenestration
On teeth in labial version, the margin of the labial bone is and dehiscence are important because they may complicate
located farther apically than it is on teeth that are in proper the outcome of periodontal surgery.
FIGURE 2.29 Variations in the cervical portion of the buccal alveolar plate. A, Shelflike conformation. B, Comparatively thin buccal plate.
FIGURE 2.31 Bony trabeculae realigned perpendicular to the mesial

root of a tilted molar.
FIGURE 2.30 Dehiscence on the canine and fenestration of the first
premolar.
Alveolar bone undergoes constant physiologic remodel-

ing in response to external forces, particularly occlusal forces.
Remodeling of Alveolar Bone Bone is removed from areas where it is no longer needed and
added to areas where it is presently needed.
In contrast with its apparent rigidity, alveolar bone is the least The socket wall reflects the responsiveness of alveolar bone
stable of the periodontal tissues, because its structure is in a to external forces. Osteoblasts and newly formed osteoid line
constant state of flux. A considerable amount of internal re- the socket in areas of tension; osteoclasts and bone resorp-
modeling takes place by means of resorption and formation, tion occur in areas of pressure. Forces exerted on the tooth
and this is regulated by local and systemic influences. Local also influence the number, density, and alignment of cancel-
influences include functional requirements on the tooth and lous trabeculae. The bony trabeculae are aligned in the path of
age-related changes in bone cells. Systemic influences are the tensile and compressive stresses to provide maximal resis-
probably hormonal (eg, parathyroid hormone, calcitonin, vi- tance to the occlusal force with a minimum of bone substance
tamin D3). (Fig. 2.31). When forces are increased, the cancellous bony
The remodeling of the alveolar bone affects its height, con- trabeculae increase in number and thickness, and bone may
tour, and density and is manifested in the following three ar- be added to the external surface of the labial and lingual plates.
eas: adjacent to the periodontal ligament, in relation to the A study has shown that the presence of antagonists of oc-
periosteum of the facial and lingual plates, and along the end- clusal force and the severity of periodontal disease increase
osteal surface of the marrow spaces. the extension of periodontal tissue resorption.
The periodontal ligament also depends on the stimulation
Clinical Considerations provided by function to preserve its structure. Within phys-
iologic limits, the periodontal ligament can accommodate
Physiologic Migration of the Teeth increased function with an increase in width (Table 2.2), a
thickening of its fiber bundles, and an increase in the diam-
Tooth movement does not end when active eruption is com- eter and number of Sharpey fibers. Forces that exceed the
pleted and the tooth is in functional occlusion. With time and adaptive capacity of the periodontium produce injury called
wear, the proximal contact areas of the teeth are flattened, and trauma from occlusion. Since trauma from occlusion can only
the teeth tend to move mesially. This is referred to as physi- be confirmed histologically, the clinician is challenged to
ologic mesial migration. By the age of 40 years, this process re- use clinical and radiographic surrogate indicators in an at-
sults in a reduction of about 0.5 cm in the length of the dental tempt to facilitate and assist with its diagnosis.
arch from the midline to the third molars. Alveolar bone is When occlusal forces are reduced, the number and thick-
reconstructed in compliance with the physiologic mesial mi- ness of the trabeculae are reduced. The periodontal ligament
gration of the teeth. Bone resorption is increased in areas of also atrophies and appears thinned; the fibers are reduced
pressure along the mesial surfaces of the teeth, and new layers in number and density, disoriented, and ultimately arranged
of bundle bone are formed in areas of tension on the distal parallel to the root surface (Fig. 2.32). This phenomenon is
surfaces (see Fig. 2 25) termed disuse atrophy or afunctional atrophy. With this con-
dition, the cementum is either unaffected or thickened, and
the distance from the cementoenamel junction to the alveolar
External Forces and the Periodontium
crest is increased.
The periodontium exists for the purpose of supporting teeth Decreased occlusal function causes changes in the peri-
during function, and it depends on the stimulation that it odontal microvasculature, such as the occlusion of blood ves-
receives from function for the preservation of its structure. sels and a decrease in the number of blood vessels. For exam-
Therefore, a constant and sensitive balance is present between ple, Murrell and coworkers reported that the application and
external forces and the periodontal structures. removal of orthodontic force produced significant changes
TABLE 2.2
COMPARISON OF PERIODONTAL WIDTH OF FUNCTIONING AND FUNCTIONLESS TEETH

IN A 38-YEAR-OLD MAN
Average Width of Periodontal Space
Entrance of Alveolus (mm) Middle of Alveolus (mm) Fundus of Alveolus (mm)
Heavy function 0.35 0.28 0.30

Left upper second bicuspid
Light function 0.14 0.10 0.12
Left lower first bicuspid
Functionless 0.10 0.06 0.06
Left upper third molar
(Modifiedfmm Kmnfeld R: J Am Dent Assoc 18:1242, 1931)
·: ~ '!~ - •
•- ,. I ),I
. ;:·J1'°'_·I,,.
~i~~I
i'
.
<<ft ;~fl
~ ) \<; ':
~j fl I
.:i : iii
' \ (
I) }
~ f'l I
• ~ I
FIGURE 2.32 Atrophic periodontal ligament (P) of a tooth devoid
of function. Note the scalloped edge of the alveolar bone (8), which
indicates that resorption has occurred. C, Cementum.
1·
in blood vessel number and density; however, no evidence- FIGURE 2.33 Vascular supply of a monkey periodontium perfused
based explanation exists for why the force stimulated such with India ink. Note the longitudinal vessels in the periodontal ligament
and the alveolar arteries passing through channels between the bone
changes in the number of blood vessels. marrow (M) and the periodontal ligament. 0, Dentin. (Courtesy Dr Sol
Orthodontic tooth movement is thought to result from Bernick, Los Angeles.)
site-specific bone remodeling in the absence of inflammation.
It is well recognized that tensional forces will stimulate the
formation and activity of osteoblastic cells, whereas compres- these gingival vessels in turn anastomose with the periodontal
sive forces promote osteoclastic activity. ligament vessels of the cervical region.
The vessels within the periodontal ligament are contained
Vascularization of the Supporting in the interstitial spaces of loose connective tissue between
the principal fibers, and they are connected in a netlike plexus
Structures that runs longitudinally and closer to the bone than the ce-
The blood supply to the supporting structures of the tooth is mentum (Figs. 2.33 and 2.34) The blood supply increases
derived from the inferior and superior alveolar arteries to the from the incisors to the molars; it is greatest in the gingival
mandible and maxilla, and it reaches the periodontal ligament third of single-rooted teeth, less in the apical third, and least
from three sources: apical vessels, penetrating vessels from the in the middle; it is equal in the apical and middle thirds of
alveolar bone, and anastomosing vessels from the gingiva. multirooted teeth; it is slightly greater on the mesial and dis-
The branches of the apical vessels supply the apical region tal surfaces than on the facial and lingual surfaces; and it is
of the periodontal ligament before the vessels enter the dental greater on the mesial surfaces of the mandibular molars than
pulp. The transalveolar vessels are branches of the intraseptal on the distal surfaces.
vessels that perforate the lamina dura and enter the ligament. The vascular supply to the bone enters the interdental
The intraseptal vessels continue to vascularize the gingiva; septa through nutrient canals together with veins, nerves,
Lymphatics supplement the venous drainage system. Lym-

phatic channels that drain the region just beneath the junc-
tional epithelium pass into the periodontal ligament and ac-
company the blood vessels into the periapical region. From
there, they pass through the alveolar bone to the inferior den-
tal canal in the mandible or the infraorbital canal in the max-
illa and then go on to the submaxillary lymph nodes.
REFERENCES
References for this chapter are found on the companion
website www.medenact.com.
SUGGESTED READINGS
Ainamo J, Loe H: Anatomical characteristics of gingiva: a clinical and mi-
croscopic study of the free and attached gingiva,J Peliodontol 37:5, 1966.
Bernick S: Innervation of the teeth and periodontium, Dent Clin North Am
FIGURE 2.34 Vascular supply to the periodontal ligament in a rat
July 503, 1959.
molar as viewed by scanning electron microscopy after perfusion with
Carranza FA, Carranza FA Jr: The management of the alveolar bone in the
plastic and tissue corrosion. Middle and apical areas of the periodontal
treatment of the periodontal pocket,] Periodontol 27:29, 1956.
ligament are shown with longitudinal blood vessels from the apex (be-
Gottlieb B: Biology of the cementum,] Periodontol 13:13, 1942.
low) to the gingiva (above), perforating vessels entering the bone (b),
Grant D, Bernick S: Formation of the periodontal ligament, J Pe,iodontol
and many transverse connections (arrowheads). Apical vessels (a) form
43:17, 1972.
a cap that connects with the pulpal vessels. (Courtesy NJ Selliseth and K
listgarten MA: The ultrastructure of human gingival epithelium, Am J Anat
Selvig, University of Bergen, Norway.)
114:49, 1964.
Orban B: Tissue changes in traumatic occlusion, J Am Dent Assoc 15:2090,
1928.
Schroeder HE, listgarten MA: The gingival tissues: the architecture of peri-
and lymphatics. Dental arterioles, which also branch off of odontal protection, Periodontal 2000 13:91, 1997.
the alveolar arteries, send tributaries through the periodontal Selvig KA: The fine structure of human cementum, Acta Odontol Scand
ligament, and some small branches enter the marrow spaces 23:423, 1965.
of the bone through the perforations in the cribriform plate. Tarnow DP, Magner AW, Fletcher P: The effect of the distance from the contact
Small vessels that emanate from the facial and lingual compact point to the crest of bone on the presence or absence of the interproximal
dental papilla,] Pe,iodontol 63:995, 1992.
bone also enter the marrow and spongy bone. Ten Cate AR: The development of the periodontium. In Melcher AH, Bowen
The venous drainage of the periodontal ligament accom- WH, editors: Biology of the periodontium, New York, 1969, Academic Press.
panies the arterial supply. Venules receive blood through Turesky S, Glickman I, Litwin T: A histochemical evaluation of normal and
the abundant capillary network. In addition, arteriovenous inflamed human gingivae, J Dent Res 30: 792, 1951.
Weinmann JP, Sicher H: Bone and bones: fundamentals of bone biology, ed 2, St
anastomoses bypass the capillaries and are seen more fre- Louis, 1955, Mosby.
quently in apical and interradicular regions; their signifi- Zander HA, Hurzeler B: Continuous cementum apposition, J Dent Res
cance is unknown. 37:1035, 1958.
Yasser Magrami
3
Defense Mechanisms
of the Gingiva
J Bulkacz • FA Carranza • DG Naik • A Uppoor
Chapter Outline
Sulcular Fluid Saliva
Leukocytes in the Dentogingival Area
The gingival tissue is constantly subjected to mechanical and threads around and into the sulcus, and techniques involving mi-
bacterial aggressions. The saliva, the epithelial surface, and the cropipettes and intracrevicular washings.
initial stages of the inflammatory response provide resistance The absorbing paper strips are placed within the sulcus (in-
to these actions. Section 1 reviews the role of the epithelium, trasulcular method) or at its entrance (extrasulcular method)
including its degree of keratinization and its turnover rate. (Fig. 3.1). The placement of the filter paper strip in relation
This chapter describes the permeability of the junctional and to the sulcus or pocket is important. The Brill technique
sulcular epithelia and the role of the sulcular fluid, leukocytes, involves inserting it into the pocket until resistance is en-
and saliva. countered (Fig. 3. lA). This method produces some degree of
irritation of the sulcular epithelium that by itself can trigger
the flow of fluid
Sulcular Fluid To minimize this irritation, Loe and Holm-Pedersen placed
The presence of sulcular fluid, or gingival crevicular fluid the filter paper strip just at the entrance of the pocket or over
(GCF), has been known since the 19th century, but its com- the pocket entrance (Fig. 3.lB and C). In this way, fluid that
position and its possible role in oral defense mechanisms were seeps out is picked up by the strip, but the sulcular epithelium
elucidated by the pioneering work of Waerhaug and Brill and is not in contact with the paper.
Krasse during the 1950s. The latter investigators introduced Preweighed twisted threads were used by Weinstein and
filter paper into the gingival sulci of dogs that had previously colleagues. The threads were placed in the gingival crevice
been injected intramuscularly with fluorescein; within 3 min, around the tooth, and the amount of fluid collected was esti-
the fluorescent material was recovered on the paper strips. mated by weighing the sample thread.
This indicated the passage of fluid from the bloodstream Capillary tubes of known internal diameter are inserted
through the tissues and the exiting of fluid via the gingival into the entrance of the gingival crevice. Isolation and dry-
sulcus. ing of a site is done first. GCF gets collected by capillary
In subsequent studies, Brill confirmed the presence of GCF action. Since the internal diameter is known, the volume of
in humans and considered it as a "transudate." However, oth- fluid collected can be accurately determined by measuring
ers demonstrated that GCF is an inflammatory exudate rather the distance which the GCF has migrated. This technique
than a continuous transudate. In strictly normal gingiva, little appears to be ideal as it provides an undiluted sample of "na-
or no fluid can be collected. tive" GCF whose volume can be accurately assessed. How-
More recently, interest in the development of tests for the ever, it is difficult to collect an adequate volume of GCF in
detection or prediction of periodontal disease has resulted in a short period atraumatically. A further complication of this
numerous research papers about the components, origin, and technique is the difficulty of removing the complete sample
function of GCF from the tubing.
Crevicular washings can be used to study GCF from clini-
cally normal gingiva. One method involves the use of an ap-
Methods of Collection pliance that consists of a hard acrylic plate that covers the
The most difficult hurdle to overcome when collecting GCF is maxilla, with soft borders and a groove that follows the gin-
the scarcity of material that can be obtained from the sulcus. gival margins; it is connected to four collection tubes. The
Many collection methods have been tried. These methods in- washings are obtained by rinsing the crevicular areas from one
clude the use of absorbing paper strips, the placement of twisted side to the other with the use of a peristaltic pump.
39
FIGURE 3.1 Placement of a filter strip in the gingival sulcus for the
collection of fluid. A, lntrasulcular method. B and C, Extrasulcular
methods.
A modification of the previous method involves the use

of two injection needles that have been fitted one within the
other so that, during sampling, the inside (ejection) needle is
at the bottom of the pocket and the outside (collecting) needle
is at the gingival margin. The collection needle is drained into
a sample tube via continuous suction.
Permeability of Junctional and Sulcular FIGURE 3.2 Electronic device for measuring the amount of fluid col-
Epithelia lected on filter paper.
The initial studies by Brill and Krasse involving the use of

fluorescein were later confirmed with substances such as India min. Challacombe used an isotope dilution method to mea-
ink and saccharated iron oxide. Substances that have been sure the amount of GCF present in a particular space at any
shown to penetrate the sulcular epithelium include albumin, given time. His calculations for human volunteers with mean
endotoxin, thymidine, histamine, phenytoin, and horseradish gingival indices of less than 1 showed that the mean GCF vol-
peroxidase. These findings indicate permeability to substanc- ume in the proximal spaces from the molar teeth ranged from
es with a molecular weight of up to 1000 kD. 0.4 3 to 1.56 µL
Squier and Johnson reviewed the mechanisms of penetra- Problems with GCF collection and data interpretation are
tion through an intact epithelium. The intercellular movement as follows:
of molecules and ions along with intercellular spaces appears Contamination: The major sources of contamination of GCF
to be a possible mechanism. Substances that take this route do samples would be blood, saliva, or plaque.
not traverse the cell membranes. Sample time: The problem with prolonged collection times
is that the nature of the GCF sample collected is likely to
change with the composition concentration (protein, IGM).
Amount
Volume determination: Evaporation is considered to be a sig-
The amount of GCF collected on a paper strip can be evalu- nificant problem in accurate volume determination of GCF
ated in a variety of ways. The wetted area can be made more samples.
visible by staining with ninhydrin; it is then measured plani- Recovery from the strips: Conflicting results have been de-
metrically on an enlarged photograph or with a magnifying scribed between different research groups, possibly because
glass or a microscope. of entrapment within, or binding of GCF proteins to the filter
An electronic method has been devised for measuring the papers. Complete recovery of the content is difficult.
fluid collected on a "blotter" (Periopaper) with the use of an
electronic transducer (Periotron, Harco Electronics, Winni- Composition
peg, Manitoba, Canada) (Fig. 3.2). The wetness of the paper
strip affects the flow of an electronic current and provides The components of GCF can be characterized according to
a digital readout. Three models of Periotron have been pro- individual proteins, specific antibodies, antigens, and en-
duced (the 600,6000 and now the 8000) and each one has zymes of several specificities. The GCF also contains cellular
been shown to be an efficient means of measuring the volume elements.
of fluid collected on filter paper strips. One of the limitations Many research efforts have attempted to use GCF com-
of the Periotron has its inability to measure volumes of GCF ponents to detect or diagnose active disease or to predict
greater than 1.0 µL patients who are at risk for periodontal disease. So far, more
A comparison of the ninhydrin-staining method and the than 40 compounds found in GCF have been analyzed, but
electronic method performed in vitro revealed no significant their origin is not known with certainty. These compounds can
differences between the two techniques. be derived from the host or produced by the bacteria in the
The amount of GCF collected is extremely small. Measure- gingival crevice, but their source can be difficult to elucidate;
ments performed by Cimasoni showed that a strip of paper examples include ~-glucuronidase, which is a lysosomal en-
1.5-mm wide and inserted 1 mm within the gingival sulcus of zyme, and lactic acid dehydrogenase, which is a cytoplasmic
a slightly inflamed gingiva absorbs about O .1 mg of GCF in 3 enzyme. The sources of collagenases may be fibroblasts or
3 Defense Mechanisms of the Gingiva 41
Host cells
Microbial plaque • Lcucocync enzymes Damaged host tissues

• Lactoferrin
• Lysoeyme
• Endotoxlns (LPS) • MyclopcroAidasc • Collagen
• Enzymes (acid • Proteoitlycan
phosphatase, alkaline • Matrix proteins
phosphatase) (Ostooncclln)
• Metabolic end products
(Prostaglandin like
product. Trypsin like
enzyme)
Rosi factors
(lmmunc response)
• lmmunoglobulins
(lgG, lgA, lgM)
• Complement factor
• Eicosanoids
• Cytokines (IL-I)
FIGURE 3.3 Composition of GCF.
polymorphonuclear leukocytes [PMNs (neutrophils)], or col- The methodology used for the analysis of GCF components
lagenases may be secreted by bacteria. Phospholipases are lyso- is as varied as the diversity of those components. Examples
somal and cytoplasmic enzymes, but they are also produced by include fluorometry for the detection of metalloproteinases;
microorganisms. The majority of GCF elements detected thus enzyme-linked immunosorbent assays to detect enzyme lev-
far have been enzymes, but there are nonenzymatic substances els and interleukin-Lb (IL-1~); radioimmunoassays for the
as well. detection of cyclooxygenase derivatives and procollagen Ill;
high-pressure liquid chromatography to detect timidazole;
Cellular Elements and direct and indirect immunodot tests for the detection of
Cellular elements found in GCF include bacteria, desquamat- acute-phase proteins.
ed epithelial cells, and leukocytes (ie, PMNs, lymphocytes,
and monocytes/macrophages), which migrate through the Cellular and Humoral Activity in Gingival
sulcular epithelium. Crevicular Fluid
Electrolytes Monitoring periodontal disease is a complicated task, because
very few noninvasive procedures can follow the initiation and
Potassium, sodium, and calcium have been studied in the
progress of the disease. The analysis of GCF constituents in
GCF Most studies have demonstrated a positive correlation
health and disease may be extremely useful as a result of GCF's
of calcium and sodium concentrations with the sodium/
simplicity and because GCF can be obtained with noninvasive
potassium ratio seen with inflammation. methods.
The analysis of GCF has identified cell and humoral re-
Organic Compounds sponses in both healthy individuals and in those with peri-
Both carbohydrates and proteins have been investigated. odontal disease. The cellular immune response includes the
Glucose hexosamine and hexuronic acid are two of the com- appearance of cytokines in GCF, but there is no clear evidence
pounds that are found in GCF Blood glucose levels do not of a relationship between cytokines and disease. However, Il-
correlate with GCF glucose levels; glucose concentration in la and ll-1~ are known to increase the binding of PMNs
GCF is 3-4 times greater than that in serum. This is inter- and monocytes/macrophages to endothelial cells, to stimulate
preted not only as a result of the metabolic activity of adjacent the production of prostaglandin E2 and the release of lyso-
tissues but also as a function of the local microbial flora. somal enzymes, and to stimulate bone resorption. Preliminary
The total protein content of GCF is much less than that of evidence also indicates the presence of interferon-a in GCF,
serum. No significant correlations have been found between which may have a protective role in periodontal disease be-
the concentration of proteins in GCF and the severity of gin- cause of its ability to inhibit the bone resorption activity of
givitis, pocket depth, or extent of bone loss. ll-1~
Metabolic and bacterial products identified in GCF include Because the amount of fluid recoverable from gingival
lactic acid, urea, hydroxyproline, endotoxins, cytotoxic sub- crevices is small, only the use of very sensitive immunoassays
stances, hydrogen sulfide, and antibacterial factors. permits the analysis of the specificity of antibodies. A study
Many enzymes have also been identified (Fig. 3.3). that compared antibodies in different crevices with serum
antibodies directed at specific microorganisms did not pro-

vide any conclusive evidence regarding the significance of the
presence of antibodies in GCF among individuals with peri-
odontal disease.
Although the role of antibodies in the gingival defense
mechanisms is difficult to ascertain, the consensus is that, in
a patient with periodontal disease, a reduction in antibody
response is detrimental and an antibody response plays a pro-
tective role.
Clinical Significance
As mentioned previously, GCF is an inflammatory exudate. Its
presence in clinically normal sulci can be explained, because
gingiva that appears clinically normal invariably exhibits in-
flammation when it is examined microscopically.
The amount of GCF is greater when inflammation is
present, and it is sometimes proportional to the severity of
inflammation. GCF production is not increased by trauma
from occlusion, but it is increased by the mastication of coarse
foods, toothbrushing and gingival massage, ovulation, hor- FIGURE 3.4 Scanning electron microscope view of the periodontal
monal contraceptives, prosthetic appliances, and smoking. pocket wall. Several leukocytes are emerging (straight arrows), some
Other factors that influence the amount of GCF are circadian of which are partially covered by bacteria (curved arrow). Empty holes
correspond to tunnels through which leukocytes have emerged.
periodicity and periodontal therapy.
Circadian Periodicity
There is a gradual increase in the amount of GCF from 6:00
am to 10:00 pm and a decrease thereafter.
Sex Hormones
Female sex hormones increase GCF flow, probably because
they enhance vascular permeability. Pregnancy, ovulation, and
hormonal contraceptives, all increase GCF production.
Mechanical Stimulation
Chewing and vigorous gingival brushing stimulate the flow of
GCF Even the minor stimuli represented by the intrasulcular
placement of paper strips increases the production of fluid.
Smoking
Smoking produces an immediate transient but marked in-
crease in GCF flow.
Periodontal Therapy
There is an increase in GCF production during the healing
period after periodontal surgery. FIGURE 3.5 Scanning electron microscope view at higher magnifica-
tion than shown in Fig. 3.4. A leukocyte emerging from the pocket wall
is covered with bacteria (small arrows). The large, curved arrow points
Drugs in Gingival Crevicular Fluid to a phagosomal vacuole through which bacteria are being engulfed.
Drugs that are excreted through the GCF may be used advan-
tageously in periodontal therapy. Bader and Goldhaber dem-
onstrated in dogs that tetracyclines are excreted through the of the sulcus; from there, they travel across the epithelium to
GCF; this finding triggered extensive research that showed a the gingival sulcus where they are expelled (Figs. 3.4 and 3 5).
concentration of tetracyclines in GCF as compared with the Leukocytes are present in sulci even when histologic sec-
serum. Metronidazole is another antibiotic that has been de- tions of adjacent tissue are free of inflammatory infiltrate. Dif-
tected in human GCF ferential counts of leukocytes from clinically healthy human
gingival sulci have shown 91.2-91.5% PMNs and 8.5-8.8%
mononuclear cells.
Leukocytes in the Dentogingival Area Mononuclear cells were identified as 58% B lymphocytes,
Leukocytes have been found in clinically healthy gingival sulci 24% T lymphocytes, and 18% mononuclear phagocytes. The
in humans and experimental animals. The leukocytes found ratio of T lymphocytes to B lymphocytes was found to be re-
are predominantly PMNs. They appear in small numbers ex- versed from the normal ratio of about 3:1 found in peripheral
travascularly in the connective tissue adjacent to the bottom blood to about 1 :3 in GCF
3 Defense Mechanisms of the Gingiva 43
TABLE 3.1
ROLE OF SALIVA IN ORAL HEALTH

Function Salivary Components Probable Mechanism
Lubrication Glycoproteins, mucoids Coating similar to gastric mucin
Physical protection Glycoproteins, mucoids Coating similar to gastric mucin
Cleansing Physical flow Clearance of debris and bacteria
Buffering Bicarbonate and phosphate Antacids
Tooth integrity maintenance Minerals Maturation, rernineralization
Glycoprotein pellicle Mechanical protection
Antibacterial action lmmunoglobulin A Control of bacterial colonization
Lysozyme Breaks bacterial cell walls
Lactoperoxidase Oxidation of susceptible bacteria
Leukocytes are attracted by different plaque bacteria, but inhibiting the attachment of Actinomyces strains to hy-
they can also be found in the dentogingival region of germ- droxyapatite.
free adult animals. Leukocytes were reported in the gin-
gival sulcus in nonmechanically irritated (resting) healthy
gingiva, thereby indicating that their migration may be Salivary Antibodies
independent of an increase in vascular permeability. The
As with GCF, saliva contains antibodies that are reactive with
majority of these cells are viable and have phagocytic and
indigenous oral bacterial species. Although immunoglobulins
killing capacity. Therefore, leukocytes constitute a major
G (IgG) and M (IgM) are present, the preponderant immuno-
protective mechanism against the extension of plaque into
globulin found in saliva is immunoglobulin A (IgA). However,
the gingival sulcus.
IgG is more prevalent in GCF Major and minor salivary glands
Leukocytes are also found in saliva; this is discussed later
contribute all of the secretory IgA and lesser amounts of IgG
in this chapter. The main port of entry of leukocytes into the
and IgM. GCF contributes most of the IgG, complement, and
oral cavity is the gingival sulcus.
PMNs that, in conjunction with IgG or IgM, inactivate or op-
sonize bacteria.
Saliva Salivary antibodies appear to be synthesized locally, be-
cause they react with strains of bacteria that are indigenous
Salivary secretions are protective in nature because they main-
to the mouth but not with organisms that are characteristic
tain the oral tissues in a physiologic state (Table 3.1). Saliva
of the intestinal tract. Many bacteria found in saliva have
exerts a major influence on plaque by mechanically cleansing
been shown to be coated with IgA, and the bacterial deposits
the exposed oral surfaces, by buffering acids produced by bac-
on teeth contain both IgA and IgG in quantities that are great-
teria, and by controlling bacterial activity.
er than 1 % of their dry weight. It has been shown that IgA
antibodies present in parotid saliva can inhibit the attachment
Antibacterial Factors of oral Streptococcus species to epithelial cells. Gibbons and
colleagues suggested that antibodies in secretions may impair
Saliva contains numerous inorganic and organic factors that
the ability of bacteria to attach to mucosa! or dental surfaces.
influence bacteria and their products in the oral environment.
Inorganic factors include ions and gases, bicarbonate, sodium,
potassium, phosphates, calcium, fluorides, ammonium, and Enzymes
carbon dioxide. Organic factors include lysozyme, lactoferrin,
myeloperoxidase, lactoperoxidase, and agglutinins such as The enzymes that are normally found in the saliva are derived
glycoproteins, mucins, ~2-macroglobulins, fibronectins, and from the salivary glands, bacteria, leukocytes, oral tissues, and
antibodies. ingested substances; the major enzyme is parotid amylase.
Lysozyme is a hydrolytic enzyme that cleaves the linkage Certain salivary enzymes have been reported in increased con-
between structural components of the glycopeptide muramic centrations in periodontal disease: hyaluronidase and lipase,
acid-containing region of the cell wall of certain bacteria in ~-glucuronidase and chondroitin sulfatase, aspartate amino-
vitro. Lysozyme works on both Gram-negative and Gram- transferase and alkaline phosphatase, amino acid decarboxyl-
positive organisms; its targets include Veillonella species and ases, catalase, peroxidase, and collagenase.
Actinobacillus actinomycetemcomitans. It probably repels certain Proteolytic enzymes in the saliva are generated by both the
transient bacterial invaders of the mouth. host and oral bacteria. These enzymes have been recognized
The lactoperoxidase-thiocyanate system in saliva has been as contributors to the initiation and progression of periodon-
shown to be bactericidal to some strains of Lactobacillus and tal disease. To combat these enzymes, saliva contains antipro-
Streptococcus by preventing the accumulation of lysine and teases that inhibit cysteine proteases such as cathepsins and
glutamic acid, both of which are essential for bacterial growth. antileukoproteases that inhibit elastase. Another antiprote-
Another antibacterial finding is lactoferrin, which is effective ase, which has been identified as a tissue inhibitor of matrix
against Actinobacillus species. metalloproteinase, has been shown to inhibit the activity of
Myeloperoxidase, which is an enzyme that is similar to collagen-degrading enzymes.
salivary peroxidase, is released by leukocytes; it is bac- High-molecular-weight mucinous glycoproteins in sa-
tericidal for Actinobacillus, but it has the added effect of liva bind specifically to many plaque-forming bacteria. The
glycoprotein-bacteria interactions facilitate bacterial accumu- sometimes referred to as orogranulocytes, and their rate of mi-
lation on the exposed tooth surface. The specificity of these gration into the oral cavity is termed the orogranulocytic migra-
interactions has been demonstrated. The interbacterial matrix tory rate. Some investigators think that the rate of migration
of human plaque appears to contain polymers that are similar correlates with the severity of gingival inflammation and that
to salivary glycoproteins and that may aid in the maintenance it is therefore a reliable index for the assessment of gingivitis.
of the integrity of plaque. In addition, these glycoproteins
selectively adsorb to the hydroxyapatite to make up part of
the acquired pellicle. Other salivary glycoproteins inhibit the Role in Periodontal Pathology
sorption of some bacteria to the tooth surface and to epithelial Saliva exerts a major influence on plaque initiation, matu-
cells of the oral mucosa. This activity appears to be associated ration, and metabolism. Salivary flow and composition also
with the glycoproteins that possess blood group reactivity An- influence calculus formation, periodontal disease, and caries.
other effect of mucin is the deletion of bacterial cells from the The removal of the salivary glands in experimental animals
oral cavity via aggregation with mucin-rich films. significantly increases the incidence of dental caries and peri-
Glycoproteins and a glycolipid that is present on mamma- odontal disease in addition to delaying wound healing.
lian cell surfaces appear to serve as receptors for the attach- In humans, an increase in inflammatory gingival diseases,
ment of some viruses and bacteria. Thus, the close similarity dental caries, and rapid tooth destruction that is associated
between the glycoproteins of salivary secretions and the com- with cervical or cemental caries is partially a consequence of
ponents of the epithelial cell surface suggests that the secre- decreased salivary gland secretion (xerostomia). Xerostomia
tions can competitively inhibit antigen sorption and that they may result from sialolithiasis, sarcoidosis, Sjogren syndrome,
therefore may limit pathologic alterations. Mikulicz disease, irradiation, the surgical removal of the sali-
vary glands, and other factors.
Salivary Buffers and Coagulation Factors
The maintenance of the physiologic hydrogen ion concentra- REFERENCES
tion (pH) at the mucosal epithelial cell surface and the tooth References for this chapter are found on the companion
surface is an important function of salivary buffers. The pri- website www.medenact.com.
mary effect of these buffers has been studied in relationship to
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the bicarbonate-carbonic acid system. SUGGESTED READINGS
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The number of PMNs varies from person to person at dif- Lamster IB, Novak Mj: Host mediators in gingival crevicular fluid: implica-
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4
Aging and the Periodontium
I Needleman • DG Naik • A Uppoor
Chapter Outline
Classification of Elderly Population Aging and the Response to Treatment
Effects of Aging on the Periodontium of the Periodontium
Effects of Aging on the Progression of
Periodontal Diseases
Classification of Elderly Population bacterial antigens, a decreased resistance to functional trau-

ma, or both. If so, such changes may influence long-term
Aging is a natural process. Old age should be regarded as periodontal outcomes. However, other studies have found
a normal, inevitable biological phenomenon. The gradual no age-related differences in the gingival epithelium of hu-
changes taking place in the dental tissues after the teeth are mans or dogs. Other reported changes with aging include
fully formed and are referred to as age changes. the flattening of rete pegs and altered cell density. Conflicting
data regarding the surgical regeneration times for gingival
The "Elderly" Segment of the Population epithelium have been ascribed to problems with research
methodology.
1. People aged 65-74 years are the new or young elderly who The effect of aging on the location of the junctional epithe-
tend to be relatively healthy and active. lium has been the subject of much speculation. Some reports
2. People aged 75-84 years are the old or mid-old, who vary show migration of the junctional epithelium from its position
from those being healthy and active to those managing an in healthy individuals (ie, on the enamel) to a more apical
array of chronic diseases. position on the root surface with accompanying gingival re-
3. People of 85 years and older are the oldest-old, who tend to cession. However, in other animal studies, no apical migration
be physically frailer. This last group is the fastest-growing has been noted. With continuing gingival recession, the width
segment of the older adult population. of the attached gingiva would be expected to decrease with
age, but the opposite appears to be true. This is attributed to
Increased health awareness and improvements in preventive the eruptive movement of the teeth rather than to the intrinsic
dentistry have led to decreasing tooth loss for all age groups. aging phenomenon. The migration of the junctional epithe-
The effects of this shift in tooth retention need to be considered lium to the root surface could be caused by the tooth erupting
carefully. In particular, increased life expectancy and greater through the gingiva in an attempt to maintain occlusal contact
health expectations may lead to changes in demand from older with its opposing tooth (passive eruption) as a result of tooth
individuals for periodontal treatment and potentially a subsurface loss from attrition (Fig. 4.1).
stantial increase in supportive periodontal therapy. Therefore, The consensus is that gingival recession is not an inevitable
an understanding of the impact of aging on the periodontium physiologic process of aging but rather it can be explained
is critical. This chapter will first review the literature concern- by the cumulative effects of inflammation or trauma on the
ing the fundamental aspects of aging on the periodontal tis- periodontium (Fig. 4.2); this is discussed in more detail later
sues; broader aspects of aging will then be examined and their in this chapter. Changes in the apoptotic gene expression of
possible effects on treatment outcomes discussed. gingival tissue with age have recently been reported in non-
human primates. This finding requires further research to un-
derstand its potential impact on gingival homeostasis and the
Effects of Aging on the Periodontium pathogenesis of periodontal diseases.
Gingival Epithelium
Gingival Connective Tissue
Thinning and decreased keratinization of the gingival epithe-
lium have been reported with age. The significance of these Increasing age results in coarser and denser gingival connec-
findings could mean an increase in epithelial permeability to tive tissues. Qualitative and quantitative changes to collagen
45
Continued eruption resulting from

attrition and tooth surface loss
• • Occlusal plane
\ (D; T ;~; T\ ;~; (C) • •
Gingival
margin
......... ~.r!~!~.~1. ~i-~~!~'.1.1. ~~~~i-~ _l~~t!?.~.
....... · , · ()rig·i~-~j ~~~~~i~-~~~;,;~I 'i~~~ii~~
1
1
••••t•••••••of•••••t••••••••l•••••4••••••••1•••••••1•••••••<1'••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••
Mucogingival junction
The distance from the mucogingival junction
to the gingival margin approximates to the width of
attached gingiva.
FIGURE 4.1 Diagram showing the relationship of the gingival margin with the crown and root surface. A, Normal relationship with the gingival mar-
gin 1-2 mm above the cementoenamel junction. B, Wear of the incisal edge and continued tooth eruption. The gingival margin remains in the same
position as shown in A. Therefore, the root surface is exposed, and clinical recession is evident. The width of the attached gingiva has not changed.
C, Wear of the incisal edge and continued tooth eruption. The gingival margin has moved with the tooth; therefore, the entire dentogingival complex
has moved coronally, with a resulting increase in the width of the attached gingiva. D, No wear of incisal edge is evident. The gingiva has moved
apically, and clinical recession is evident. The width of attached gingiva is reduced.
FIGURE 4.2 Three scenarios illustrating the variation of the position of the gingival margin with age. A, Overeruption with recession in an older
individual (ie, a 68-year-old woman) with generalized recession and a history of previously treated periodontitis. Note some overeruption of the lower
anterior teeth and wear of teeth related to oral hygiene measures. B, Radiographs of the patient shown in A. C, Overeruption without recession in an
older individual (ie, a 72-year-old woman) with no periodontitis but marked lower incisor tooth wear and overeruption. Note how the gingival margin
has migrated coronally with the erupting teeth. D, Extensive recession in a younger individual (ie, a 32-year-old man) with marked recession and no
history of periodontitis. The recession has resulted from a combination of anatomically thin tissues and toothbrush-related trauma.
have been reported. These include an increased rate of con- Periodontal Ligament
version of soluble to insoluble collagen, increased mechanical
strength, and increased denaturing temperature. These results Changes in the periodontal ligament that have been report-
indicate increased collagen stabilization caused by changes in ed with aging include decreased number of fibroblasts and
the macromolecular conformation. Not surprisingly, an in- a more irregular structure, thus paralleling the changes seen
creased collagen content has been found in the gingivae of in the gingival connective tissues. Other findings include de-
older animals, despite a lower rate of collagen synthesis decreased organic matrix production, epithelial cell rests, and
creasing with age. increased amounts of elastic fiber. Conflicting results have
4 Aging and the Periodontium 47
been reported for changes in the width of the periodontal liga- Bacterial Plaque
ment in human and animal models. Although true variation
may exist, this finding probably reflects the functional status Dentogingival plaque accumulation has been suggested to
of the teeth in the studies: the width of the space will decrease increase with age. This might be explained by the increase
if the tooth is unopposed (ie, hypofunction) or increase with in hard-tissue surface area as a result of gingival recession
excessive occlusal loading. Both scenarios can be anticipated and the surface characteristics of the exposed root surface
as a result of tooth loss in this population. These effects may as a substrate for plaque formation as compared to enamel.
also explain the variability in studies that have reported quali- Other studies have shown no difference in plaque quantity
tative changes within the periodontal ligament. with age. This contradiction might reflect the different age
ranges of experimental groups as variable degrees of gingi-
val recession and root surface exposure. For supragingival
Cementum plaque, no real qualitative differences have been shown for
plaque composition. With regard to subgingival plaque, one
Some consensus regarding the effect of aging on cementum study has shown subgingival flora to be similar to normal
exists. An increase in cementa! width is a common finding;
flora, whereas another study reported increased numbers
this increase may be 5-10 times with increasing age. This of enteric rods and pseudomonads in older adults. Mom-
finding is not surprising, because deposition continues after belli suggests caution when interpreting this finding be-
tooth eruption. The increase in width is greater apically and cause of the increased oral carriage of these species among
lingually Although cementum has limited capacity for remod- older adults. It has been speculated that a shift occurs in
eling, an accumulation of resorption bays explains the finding the importance of certain periodontal pathogens with age,
of increasing surface irregularity
specifically including an increased role for Porphyromonas
gingivalis and a decreased role for Aggregatibacter actinomy-
Alveolar Bone cetemcomitans. However, differentiating true age effects from
the changes in ecologic determinants for periodontal bacte-
Reports of morphologic changes in alveolar bone mirror ria will be difficult.
age-related changes in other bony sites. Specific to the peri-
odontium are findings of a more irregular periodontal sur-
face of bone and the less-regular insertion of collagen fibers. Immune and Inflammatory Responses
Although age is a risk factor for the bone mass reductions in Recent advances in the study of the effects of aging on the im-
individuals with osteoporosis, it is not causative and there- mune response (ie, immunosenescence) have altered the un-
fore should be distinguished from physiologic aging pro- derstanding of this phenomenon. In particular, more recent
cesses. Overriding the diverse observations of bony changes studies have set tighter controls on excluding individuals with
with age is the important finding that the healing rate of bone systemic conditions known to affect the immune response.
in extraction sockets appears to be unaffected by increasing As a result, age has been recognized as having much less ef-
age. Indeed, the success of osseointegrated dental implants, fect on the alteration of the host response than previously
which relies on intact bone healing responses, does not ap- thought. Differences between younger and older individuals
pear to be age-related. However, balancing this view is the re- can be demonstrated for T and B cells, cytokines, and natural
cent observation that bone graft preparations (ie, decalcified killer cells but not for polymorphonuclear cells and macro-
freeze-dried bone) from donors who were more than 50 years phage activity McArthur concluded the following: "Measure-
old possessed significantly less osteogenic potential than graft ment of indicators of immune and inflammatory competency
material from younger donors. The possible significance of suggested that, within the parameters tested, there was no
this phenomenon for normal healing responses needs to be evidence for age-related changes in host defenses correlating
investigated. with periodontitis in an elderly (65 to 75 years) group of indi-
viduals, with and without disease." Recent laboratory studies
have shown age-related changes in the expression of proin-
Tooth-Periodontium Relationship
flammatory mediators and innate immunity with the potential
There is loss of tooth substance due to attrition leading to re- to alter the pathology of periodontal diseases or antimicrobial
duction in cuspal height and inclination due to wear. function. However, the relevance of these findings to the clini-
The degree of attrition is influenced by the musculature, cal situation has not been demonstrated. Age-related differ-
consistency of food, tooth hardness, occupational factors, ences in the inflammatory response among individuals with
and habits such as grinding and clenching. The rate of attri- gingivitis have been clearly demonstrated and are discussed
tion may be coordinated with other age-related changes such later in this textbook.
as continuous tooth eruption and gingival recession. As the In relation to systematic inflammatory responses, (-reactive
tooth erupts, cementum is usually deposited in the apical re- protein (CRP) is an acute phase protein that is widely regarded
gion of the root. as a marker of inflammatory burden and response to bacterial
The reduction in bone height that occurs with aging is not infection. When investigating serum CRP levels among indi-
necessarily related to occlusal wear. Bone loss results in an viduals who are 60-75 years old and comparing individuals
increase in crown to root ratio. Wear of teeth also occurs on with progressive periodontitis with those with stable disease,
the proximal surfaces accompanied by mesial migration of CRP levels were increased in those with progressive periodon-
teeth. Proximal wear reduces the anteroposterior length of the titis and no other systemic conditions. This may indicate that
dental arch by approximately 0.5 cm by age 40. Progressive inflammatory burden can be investigated with the use of CRP
attrition and proximal wear result in a maxillary-mandibular although there is growing evidence that CRP alone may not be
overjet in the molar area and an edge to edge bite anteriorly as reliable a marker in older people.
Although many contradictions exist, a survey of the litera- studies that have done so clearly demonstrate that, despite the
ture demonstrates that some age-related changes are evident histologic changes in the periodontium with aging, no differ-
in the periodontium and the host response. Whether these ences in response to nonsurgical or surgical treatment have
changes are significant in the alteration of the progression of been shown for periodontitis. However, if plaque control is
periodontal diseases or the response of an older adult to peri- not ideal, the continued loss of attachment is inevitable. Fur-
odontal treatment will be examined next. thermore, without effective periodontal therapy, the progres-
sion of disease may be faster with increasing age. Attempts
to increase plaque control by chemical means have also been
Effects of Aging on the Progression
reported.
of Periodontal Diseases A purely biologic or physiologic review indicates that aging
In a classic experimental gingivitis study, subjects were ren- has some impact on the structure and function of the peri-
dered free of plaque and inflammation through frequent pro- odontium as well as on the immune response and the nature
fessional cleaning. After this was achieved, the subjects ab- of either supragingival or subgingival plaque. However, these
stained from oral hygiene measures for a period of 3 weeks changes have a negligible impact on an individual's respon-
to allow gingivitis to develop. In this experimental model, a siveness to treatment. Aging may affect other aspects of the
comparison of developing gingivitis between younger and old- management of periodontal health like root caries, and the
er individuals demonstrated a greater inflammatory response resulting difficulties should not be underestimated. Interest-
in older subjects, both in humans and in dogs. In the older ingly, a recent study has identified greater compliance with
age group (ie, 65-80 years), the findings included a greater supportive maintenance among older individuals as com-
amount of infiltrated connective tissue, increased gingival pared to younger patients.
crevicular fluid flow, and an increased gingival index. Other
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Blackwell.
SECTION II
Classification and Epidemiology

of Periodontal Disease
Section Outline
5 Classification of Diseases and 6 Epidemiology of Gingival and
Conditions Affecting the Periodontium Periodontal Disease
5
Classification of Diseases
and Conditions Affecting
the Periodontium
JE Hinrichs • G Kotsakis • DG Naik • A Uppoor
Chapter Outline
Gingival Diseases Periodontitis Associated With
Periodontitis Endodontic Lesions
Necrotizing Periodontal Diseases Developmental or Acquired Deformities
Abscesses of the Periodontium and Conditions
Our understanding of the causes and pathogenesis of oral inflammation may recur but without any evidence of further
diseases and conditions is continually changing with an in- attachment loss.
crease in scientific knowledge. In light of this, a classifica- From this evidence, it has been concluded that plaque-
tion can be most consistently defined by the differences in induced gingivitis may occur on a periodontium with no at-
the clinical manifestations of diseases and conditions; they tachment loss or on a periodontium with previous attach-
are clinically consistent and require little (if any) clarification ment loss that is stable and not progressing. This implies that
by scientific laboratory testing. The classification presented gingivitis may be the diagnosis for inflamed gingival tissues
in this chapter is based on the most recent internationally associated with a tooth with no previous attachment loss or
accepted consensus opinions of the diseases and conditions with a tooth that has previously undergone attachment and
that affect the tissues of the periodontium; it was presented bone loss (ie, with reduced periodontal support) but that is
and discussed at the 1999 International Workshop for the not currently losing attachment or bone even though gingival
Classification of the Periodontal Diseases organized by the inflammation is present (Fig. 5.2). For this diagnosis to be
American Academy of Periodontology (AAP). Box 5 .1 pres- made, longitudinal records of periodontal status, including
ents the overall classification system, and each disease or clinical attachment levels, should be available.
condition is discussed where clarification is needed. In each
case, the reader is referred to pertinent reviews on the subject Gingivitis Associated with Dental Plaque Only
and specific chapters within this book that discuss the topics Plaque-induced gingival disease is the result of an interaction be-
in more detail. tween the microorganisms found in the dental-plaque biofilm,
the tissues, and inflammatory cells of the host. The plaque-host
interaction can be altered by the effects of local factors, systemic
Gingival Diseases factors, medications, and malnutrition, all of which can influ-
ence the severity and duration of the response. Local factors may
Dental Plaque-Induced Gingival Diseases
contribute to gingivitis formation in addition to plaque-retentive
Gingivitis that is associated with dental-plaque formation is calculus formation on the crown and root surfaces. These fac-
the most common form of gingival disease (Fig. 5.1). Box 5.2 tors are contributory because of their ability to retain plaque
outlines the classifications of gingival diseases. Gingivitis microorganisms and to inhibit the removal of those microorgan-
has been previously characterized by the presence of clinical isms via patient-initiated plaque-control techniques.
signs of inflammation that are confined to the gingiva and
associated with teeth showing no attachment loss. Gingivitis Gingival Diseases Modified by Systemic Factors
has also been observed to affect the gingiva of periodontitis- Systemic factors that contribute to gingivitis-such as the endo-
affected teeth that have previously lost attachment but that crine changes associated with puberty (Fig. 5.3), the menstrual
have received periodontal therapy to stabilize any further at- cycle, pregnancy (Fig. 5.4), and diabetes-may be exacerbated
tachment loss. In these treated cases, plaque-induced gingival as a result of alterations in the gingival inflammatory response
51
GINGIVAL DISEASES ABSCESSES OF THE PERIODONTIUM

Plaque-induced gingival diseases' Gingival abscess
Nonplaque-induced gingival lesions Periodontal abscess
Pericoronal abscess
CHRONIC PERIODONTITISb
Localized PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS
Generalized Endodontic-periodontal lesion
Periodontal-endodontic lesion
AGGRESSIVE PERIODONTITIS
Combined lesion
Localized
Generalized DEVELOPMENTAL OR ACQUIRED DEFORMITIES AND
CONDITIONS
PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC
Localized tooth-related factors that predispose an individual to
DISEASE
plaque-induced gingival diseases or periodontitis
Necrotizing Periodontal Diseases Mucogingival deformities and conditions around the teeth
Necrotizing ulcerative gingivitis Mucogingival deformities and conditions on edentulous ridges
Necrotizing ulcerative periodontitis Occlusal trauma
-These diseases may occur on a periodontium with no attachment loss or on a periodontium with attachment loss that is stable and not progressing.
"Chronic periodontitis can be further classified on the basis of its extent and severity. As a general guide, extent can be characterized as localized
( <30% of sites involved) or generalized (> 30% of sites involved). Severity can be characterized on the basis of the amount of clinical attachment
loss (CAL) as follows: slight, 1 or 2 mm CAL; moderate, 3 or 4 mm CAL; and severe, 25 mm CAL.
Data from Armitage GC: Ann Periodontol 4:1, 1999.
contraceptives by premenopausal women has been associated

with a higher incidence of gingival inflammation and the de-
velopment of gingival enlargement, which may be reversed by
discontinuation of the oral contraceptive.
Gingival Diseases Modified by Malnutrition

Gingival diseases modified by malnutrition have received at-
tention because of clinical descriptions of bright red, swollen,
and bleeding gingiva associated with severe ascorbic acid (vita-
min C) deficiency or scurvy Nutritional deficiencies are known
to affect immune function, and they may alter the host's ability
to protect himself or herself against some of the detrimental
FIGURE 5.1 Plaque-related gingivitis and marginal and papillary inflam-
mation, with 1-4-mm probing depths and generalized zero clinical attach- effects of cellular products, such as oxygen radicals. Unfor-
ment loss, except for the recession seen with mandibular right first premolar. tunately, little scientific evidence is available to support the
role for specific nutritional deficiencies in the development or
to plaque. This altered response appears to result from the severity of gingival inflammation or periodontitis in humans.
effects of systemic conditions on the host's cellular and im-
munologic functions. These changes are most apparent dur- Nonplaque-lnduced Gingival Lesions
ing pregnancy, when the prevalence and severity of gingival
inflammation may increase, even in the presence of low levels Oral manifestations of systemic conditions that produce le-
of plaque. Blood dyscrasias (eg, leukemia) may alter immune sions in the tissues of the periodontium are rare. These effects
function by disturbing the normal balance of the immunologi- are observed more frequently among lower socioeconomic
cally competent white blood cells that supply the periodon- groups, in developing countries, and in immunocompromised
tium. Gingival enlargement and bleeding are common findings individuals. Benign mucous membrane pemphigoid is an ex-
that may be associated with the swollen, spongy gingival tissues ample of a nonplaque-induced lesion without socioeconomic
caused by the excessive infiltration of blood cells (Fig. 5 5). implications. Sloughing gingival tissues leaves painful ulcer-
ations of the gingiva (Fig. 5.SA-B). Autoimmune antibodies
Gingival Diseases Modified by Medications are targeted at the basement membrane & cleave it from the
Gingival diseases that are modified by medications are increas- underlying connective tissue(Fig. 5.8 C and D).
ingly prevalent as a result of the increased use of drugs known
to induce gingival enlargement. These include anticonvulsant Gingival Diseases of Specific Bacterial Origin
drugs, such as phenytoin, immunosuppressive drugs, such as Gingival diseases of specific bacterial origin are increasing in
cyclosporine (Fig. 5.6), and calcium-channel blockers, such prevalence, especially as a result of sexually transmitted diseas-
as nifedipine (Fig. 5. 7), verapamil, diltiazem, and sodium es, such as gonorrhea (N. gonorrhoeae), and to a lesser degree,
valproate. The development and severity of gingival enlarge- syphilis (I pallidum). Oral lesions may be a result of systemic
ment in response to medications are patient-specific and may infection or direct infection. Streptococcal gingivitis or gingivo-
be influenced by uncontrolled plaque accumulation, as well stomatitis is a rare entity that may present as an acute condition
as by elevated hormonal levels. The increased use of oral with fever, malaise, and pain associated with acutely inflamed,
5 Classification of Diseases and Conditions Affecting the Periodontium 53
BOX 5.2
DENTAL-PLAQUE-INDUCED GINGIVAL DISEASES 3. Varicella zoster

These diseases may occur on a periodontium with no attachment B. Other
loss or on a periodontium with attachment loss that is stable and Ill. Gingival diseases of fungal origin
not progressing. A. Candida species infections: generalized gingival
candidiasis
I. Gingivitis associated with dental plaque only B. Linear gingival erythema
A. Without local contributing factors C. Histoplasmosis
B. With local contributing factors (see Box 5.4) D. Other
II. Gingival diseases modified by systemic factors IV. Gingival lesions of genetic origin
A. Associated with the endocrine system A. Hereditary gingival fibromatosis
1. Puberty-associated gingivitis B. Other
2. Menstrual cycle-associated gingivitis V. Gingival manifestations of systemic conditions
3. Pregnancy-associated conditions A. Mucocutaneous lesions
a. Gingivitis 1. Lichen planus
b. Pyogenic granuloma 2. Pemphigoid
4. Diabetes mellitus-associated gingivitis 3. Pemphigus vulgaris
B. Associated with blood dyscrasias 4. Erythema multiforme
1. Leukemia-associated gingivitis 5. Lupus erythematosus
2. Other 6. Drug-induced conditions
Ill. Gingival diseases modified by medications 7. Other
A. Drug-influenced gingival diseases B. Allergic reactions
1. Drug-influenced gingival enlargements 1. Dental restorative materials
2. Drug-influenced gingivitis a. Mercury
a. Oral contraceptive-associated gingivitis b. Nickel
b. Other c. Acrylic
IV. Gingival diseases modified by malnutrition d. Other
A. Ascorbic acid-deficiency gingivitis 2. Reactions attributable to the following:
B. Other a. Toothpastes or dentifrices
NONPLAQUE-INDUCED GINGIVAL LESIONS b. Mouth rinses or mouthwashes
I. Gingival diseases of specific bacterial origin c. Chewing-gum additives
A. Neisseria gonorrhoeae d. Foods and additives
B. Treponema pallidum 3. Other
C. Streptococcus species VI. Traumatic lesions (factitious, iatrogenic, or accidental)
D. Other A. Chemical injury
II. Gingival diseases of viral origin B. Physical injury
A. Herpes virus infections C. Thermal injury
1. Primary herpetic gingivostomatitis VII. Foreign-body reactions
VIII. Not otherwise specified
2. Recurrent oral herpes
Data from Holmstrup P: Ann Periodontol 4:20, 1999; and Mariotti A: Ann Periodontol 4:7, 1999.
diffuse, red, and swollen gingiva with increased bleeding and

occasional gingival abscess formation. The gingival infections
are usually preceded by tonsillitis and they have been associ-
ated with group A ~-hemolytic Streptococcal infections.
Gingival Diseases of Viral Origin

Gingival diseases of viral origin may be caused by a variety of
deoxyribonucleic acid- and ribonucleic-acid viruses, with the
most common being the herpes viruses (Fig. 5.9A-B). Lesions
are frequently related to the reactivation of latent viruses,
especially as a result of reduced immune function. The oral
manifestations of viral infection have been comprehensively
reviewed. Viral gingival diseases are treated with topical or
systemic antiviral drugs (Fig. 5 9C-D).
FIGURE 5.2 The maxillary second molar exhibits mild inflammation Gingival Diseases of Fungal Origin
at the mesial-palatal surface. However, the clinical attachment loss has
been stable for 15 years after the placement of an apically positioned Gingival diseases of fungal origin are relatively uncommon
flap and periodontal maintenance. The diagnosis is a history of moderate in immunocompetent individuals, but they occur more fre-
periodontitis, but the case is in remission. quently in immunocompromised individuals and in those
FIGURE 5.4 Clinical image of pyogenic granuloma in a 27-year-old

pregnant woman.
FIGURE 5.3 A 13-year-old girl with hormone-exaggerated marginal

and papillary inflammation, with 1-4-mm probing depths yet minimal
clinical attachment loss. A, Facial view; B, lingual view.
with normal oral flora that has been disturbed by the long-
term use of broad-spectrum antibiotics. The most common
oral fungal infection is candidiasis, which is caused by infec-
tion with Candida albicans; it can also be seen under prosthetic
devices, in individuals using topical steroids, and in individu-
FIGURE 5.5 A 12-year-old girl with a primary medical diagnosis of
als with decreased salivary flow, increased salivary glucose,
leukemia who exhibits swollen and spongy gingiva.
or decreased salivary pH. A generalized candidal infection
may manifest as white patches on the gingiva, tongue, or oral
FIGURE 5.6 Clinical images of a 9-year-old boy with severe gingival overgrowth as a result of a heart transplant and cyclosporine therapy.
. ' ·. A!'''rB'~
,r- .e~·-
t~·
~ 11 ·. ,,,
.
l.~,~,,--
. ,.· i, •••
-, . . \
.. . .. '· ii.
.
'./' ,
.• :\
- -~..
'\.
(A) (B) -
~
FIGURE 5.7 Clinical images of gingival overgrowth after the use a of calcium-channel blocker to control hypertension.
FIGURE 5.8 A 62-year-old woman with benign mucous membrane pemphigoid. A and B, Clinical images with sloughing of the epithelial surface.
C, Hematoxylin-eosin stain depicting the separation of the epithelium from the connective tissue. D, lmmunofluorescent-labeled antibodies in the
basement membrane.
FIGURE 5.9 A and B, A 29-year-old man with primary herpetic infection and severe gingival inflammation. C and D, Six weeks after treatment with
systemic acyclovir.
FIGURE 5.10 A, Localized pronounced gingival inflammation in response to a nickel allergy. Band C, Biopsy of a dense infiltrate of plasma cells.
mucous membrane that can be removed with gauze and that and present as an isolated finding; alternatively, it may be as-
leave a red, bleeding surface. In individuals with human im- sociated with several more generalized syndromes.
munodeficiency virus (HIV), candidal infection may present
as erythema of the attached gingiva; this has been referred Gingival Manifestations of Systemic Conditions
to as linear gingival erythema or HIV-associated gingivitis. Gingival manifestations of systemic conditions may appear
The diagnosis of candidal infection can be made by cul- as desquamative lesions, ulcerations of the gingiva, or both.
ture, smear, or biopsy. Less common fungal infections have Allergic reactions that manifest with gingival changes are un-
also been described. common but have been observed in association with several
restorative materials (Fig. 5.lOA), toothpastes, mouthwashes,
Gingival Diseases of Genetic Origin chewing gums (Fig. 5.11), and foods (Box 5.2) The diagno-
Gingival diseases of genetic origin may involve the tissues of sis of these conditions may prove difficult and may require
the periodontium and have been described in detail. One of an extensive history and the selective elimination of poten-
the most clinically evident conditions is hereditary gingival tial causes. Histologic traits of biopsies from gingival aller-
fibromatosis, which exhibits autosomal-dominant or (rarely) gic reactions include a dense infiltrate of eosinophilic cells
autosomal recessive modes of inheritance. The gingival en- (Fig. 5 lOB-C).
largement may completely cover the teeth, delay eruption,
Traumatic Lesions
Traumatic lesions may be self-inflicted and factitious in ori-
gin, which means that they are produced by intentional or
unintentional artificial means (Fig. 5.12). Other examples of
traumatic lesions include toothbrush trauma that results in
gingival ulceration, recession, or both. Iatrogenic trauma (ie,
induced by the dentist or health professional) to the gingiva
can be caused by the induction of orthodontic cement or pre-
ventive or restorative materials (Fig. 5. 13A). Peripheral ossify-
ing fibroma may develop in response to the embedment of a
foreign body, Fig. 5.13B-C and the complete resolution after
4 weeks after excisional biopsy (Fig 5.13D) Alternatively, ac-
cidental damage to the gingiva may occur as a result of minor
burns from hot foods and drinks.
Foreign-Body Reactions
Foreign-body reactions lead to localized inflammatory con-
FIGURE 5.11 A generalized severe allergic response of the gingiva in
response to an additive in chewing gum. ditions of the gingiva and are caused by the introduction of
Periodontitis
Periodontitis is defined as "an inflammatory disease of the
supporting tissues of the teeth caused by specific microorgan-
isms or groups of specific microorganisms, resulting in pro-
gressive destruction of the periodontal ligament and alveolar
bone with increased probing depth formation, recession, or
both." The clinical feature that distinguishes periodontitis
from gingivitis is the presence of clinically detectable attach-
ment loss. This loss is often accompanied by periodontal
pocket formation and changes in the density and height of
the subjacent alveolar bone. In some cases, recession of the
marginal gingiva may accompany attachment loss, thereby
masking ongoing disease progression if only probing depth
FIGURE 5.12 Self-inflicted gingival dehiscence induced via the measurements are taken without measurements of clinical
patient's fingernail.
attachment levels. Clinical signs of inflammation-such as
changes in color, contour, and consistency, as well as bleed-
ing with probing-may not always be positive indicators of
foreign material into the gingival connective tissues through ongoing attachment loss. However, the presence of continued
breaks in the epithelium. Common examples include the intro- bleeding with probing during sequential visits has proved to
duction of amalgam into the gingiva during the placement of a be a reliable indicator of the presence of inflammation and the
restoration, the extraction of a tooth, or an endodontic apicoec- potential for subsequent attachment loss at the bleeding site.
tomy with retrofill leaving an amalgam tattoo (Fig. 5. l 4A), with The attachment loss associated with periodontitis has been
resultant metal fragment observed during biopsies (Fig. 5.14B); shown to progress either continuously or in episodic bursts
abrasives may also be introduced during polishing procedures. of disease activity.
FIGURE 5.13 A, Proliferative gingival overgrowth as a result of the impaction of foreign body. B, Histology of peripheral ossifying fibroma. C, Higher
magnification of the image shown in B. D, Four weeks after excisional biopsy.
FIGURE 5.14 A, Gingival pigmentation associated with previous apicoectomy and amalgam retrofill. B, Biopsy depicting metal fragments.
TABLE 5.1
CLASSIFICATION OF THE VARIOUS FORMS OF PERIODONTITIS

Classification Forms of Periodontitis Disease Characteristics
American Academy of Periodontology Adult periodontitis Age of onset > 35 years, slow rate of disease progression,
World Workshop in Clinical no defects in host defenses
Periodontics, 1989
Early-onset periodontitis (may be Age of onset <35 years, rapid rate of disease progression,
prepubertal, juvenile, or rapidly defects in host defenses, associated with speci fie
progressive) rnicroflora
Periodontitis associated with systemic Systemic diseases that predispose to rapid rates of
disease periodontitis: diseases: diabetes, Down syndrome,
HIV infection, PLS
Necrotizing ulcerative periodontitis Similar to acute necrotizing ulcerative gingivitis but with
associated clinical attachment loss
Refractory periodontitis Recurrent periodontitis that does not respond to treatment
European Workshop in Periodontology, Adult periodontitis Age of onset: fourth decade of life, slow rate of disease
1993 progression, no defects in host response
Early-onset periodontitis Age of onset <40 years, rapid rate of disease progression,
defects in host defense
Necrotizing periodontitis Tissue necrosis with attachment and bone loss
American Academy of Periodontology Chronic periodontitis, aggressive See Box 5.3
International Workshop for periodontitis, periodontitis as a
Classification of Periodontal manifestation of systemic disease,
Diseases, 1999 necrotizing periodontitis
Although many classifications of the different clinical mani- periodontal therapy are currently poorly defined and apply
festations of periodontitis have been presented over the past to many disease entities. In addition, the clinical and caus-
20 years, consensus workshops in North America in 1989 and ative manifestations of the different diseases outlined in North
in Europe in 1993 identified that periodontitis may present in America in 1989 and in Europe in 1993 were not consistently
early-onset, adult-onset, and necrotizing forms (Table 5.1). In observed in different countries around the world and did not
addition, the AAP consensus concluded that periodontitis may always fit the models presented. As a result, the AAP held an
be associated with systemic conditions (eg, diabetes, HIV) and International Workshop for the Classification of Periodontal
that some forms of periodontitis may be refractory to conven- Diseases in 1999 to further refine the classification system
tional therapy Early-onset disease was distinguished from adult- with the use of current clinical and scientific data. The result-
onset disease by the age of onset (35 years of age was set as an ing classification of the different forms of periodontitis was
arbitrary separation of diseases), the rate of disease progression, simplified to describe three general clinical manifestations of
and the presence of alterations in host defenses. The early-onset periodontitis; chronic periodontitis, aggressive periodonti-
diseases were more aggressive, occurred in individuals younger tis, and periodontitis as a manifestation of systemic disease
than 35 years old, and were associated with defects in host de- (Table 5.1 and Box 5.3).
fenses; alternatively, adult forms of disease were slowly progres-
sive, became clinically more evident during the fourth decade
Chronic Periodontitis
of life, and were not associated with defects in host defenses. In
addition, early-onset periodontitis was subclassified into prepu- Chronic periodontitis is the most common form of periodon-
bertal, juvenile, and rapidly progressive forms with localized or titis; Box 5.3 includes the characteristics of this form of peri-
generalized disease distributions. odontitis. Chronic periodontitis is most prevalent in adults,
Extensive clinical and basic scientific research involving but it can also be observed in children; therefore, the age range
these disease entities has been performed in many countries, of more than 35 years that had been previously designated for
and some disease characteristics that were outlined 10 years the classification of this disease has been discarded. Chronic
ago no longer stand up to rigid scientific scrutiny In particu- periodontitis is associated with the accumulation of plaque
lar, supporting evidence was lacking for the distinct classifica- and calculus; it generally has a slow to moderate rate of dis-
tions of adult periodontitis, refractory periodontitis, and the ease progression, but periods of more rapid destruction may
various different forms of early-onset periodontitis as outlined also be observed. Increases in the rate of disease progression
by the AAP Workshop for the International Classification of may be caused by the impact of local, systemic, or environ-
Periodontal Diseases in 1999 (Table 5 .1). mental factors that may influence the normal host-bacteria
It has been observed that chronic periodontal destruction interaction. Local factors may influence plaque accumulation
caused by the accumulation of local factors (eg, plaque, cal- (Box 5.4); systemic diseases (eg, diabetes mellitus, HIV) may
culus) can occur before the age of 35 years and that the ag- influence the host's defenses; and environmental factors (eg,
gressive disease seen in young patients may be independent of cigarette smoking, stress) may also influence the response of
age and instead have a familial (genetic) association. With re- the host to plaque accumulation. Chronic periodontitis may
spect to refractory periodontitis, little evidence supports that occur as a localized disease in which less than 30% of evalu-
this condition is indeed a distinct clinical entity; the causes of ated sites demonstrate attachment and bone loss, or it may oc-
continued loss of clinical attachment and alveolar bone after cur as a more generalized disease in which more than 30% of
The disease periodontitis can be subclassified into the following • Hyperresponsive macrophages that produce increased levels
three major types on the basis of clinical, radiographic, of prostaglandin E2 and interleukin-1 ~
historical, and laboratory characteristics. • In some cases, self-arresting disease progression
Aggressive periodontitis may be further classified into
CHRONIC PERIODONTITIS localized and generalized forms on the basis of the common
The following characteristics are common to patients with features described here and the following specific features:
chronic periodontitis:
LOCALIZED FORM
• Prevalent in adults but can occur in children • Circumpubertal onset of disease
• Amount of destruction consistent with local factors • Localized first molar or incisor disease with proximal attachment
• Associated with a variable microbial pattern loss on at least two permanent teeth, one of which is a first molar
• Subgingival calculus frequently found • Robust serum-antibody response to infecting agents
• Slow to moderate rate of progression with possible periods of
rapid progression GENERALIZED FORM
• Possibly modified by or associated with the following: • Usually (but not always) affects people who are <30 years old
• Systemic diseases (eg, diabetes mellitus, HIV) • Generalized proximal attachment loss that affects at least three
• Local factors that predispose an individual to periodontitis teeth other than the first molars and incisors
• Environmental factors (eg, cigarette smoking, emotional stress) • Pronounced episodic nature of periodontal destruction
• Poor serum-antibody response to infecting agents
Chronic periodontitis may be further subclassified into
localized and generalized forms and characterized as slight, PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC DISEASES
moderate, or severe on the basis of the common features Periodontitis may be observed as a manifestation of the
described previously and the following specific features: following systemic diseases:
• Localized form: <30% of sites involved 1. Hematologic disorders
• Generalized form: >30% of sites involved a. Acquired neutropenia
• Slight: 1-2 mm of clinical attachment loss b. Leukemia
• Moderate: 3-4 mm of clinical attachment loss c. Other
• Severe: ~5 mm of clinical attachment loss 2. Genetic disorders
a. Familial and cyclic neutropenia
AGGRESSIVE PERIODONTITIS b. Down syndrome
c. Leukocyte adhesion deficiency syndromes
The following characteristics are common to patients with
d. PLS
aggressive periodontitis:
e. Chediak-Higashi syndrome
• Otherwise clinically healthy patient f. Histiocytosis syndromes
• Rapid attachment loss and bone destruction g. Glycogen storage disease
• Amount of microbial deposits inconsistent with disease severity h. Infantile genetic agranulocytosis
• Familial aggregation of diseased individuals i. Cohen syndrome
j. Ehlers-Danlos syndrome (types IV and VIII, autosomal
The following characteristics are common but not universal:
dominant)
• Diseased sites infected with Aggregatibacter k. Hypophosphatasia
actinomycetemcomitans I. Other
• Abnormalities in phagocyte function 3. Not otherwise specified
Data from Flemmig TF: Ann Periodontol 4:32, 1999; Kinane DF: Ann Periodontol 4:54, 1999; and Tonetti MS, Mombelli A: Ann Periodontol 4:39, 1999.
i:f•iiii Developmental or Acquired Deformities and Conditions

LOCALIZED TOOTH-RELATED FACTORS THAT MODIFY a. Pseudopocket
OR PREDISPOSE INDIVIDUALS TO PLAQUE-INDUCED b. Inconsistent gingival margin
GINGIVAL DISEASES OR PERIODONTITIS c. Excessive gingival display
1. Tooth anatomic factors d. Gingival enlargement (see Box 5.2)
2. Dental restorations and appliances e. Abnormal color
3. Root fractures MUCOGINGIVAL DEFORMITIES AND CONDITIONS
4. Cervical root resorption and cementa! tears OF THE EDENTULOUS EDGES
1. Vertical or horizontal ridge deficiency
MUCOGINGIVAL DEFORMITIES AND CONDITIONS
2. Lack of gingiva or keratinized tissue
AROUND THE TEETH
3. Gingival or soft-tissue enlargements
1. Gingival or soft-tissue recession 4. Aberrant frenum or muscle position
a. Facial or lingual surfaces 5. Decreased vestibular depth
b. lnterproximal (papillary) 6. Abnormal color
2. Lack of keratinized gingiva
3. Decreased vestibular depth OCCLUSAL TRAUMA
4. Aberrant frenum or muscle position 1. Primary occlusal trauma
5. Gingival excess 2. Secondary occlusal trauma
Data from Blieden TM: Ann Periodontol 4:91, 1999; Halman WW: Ann Periodontol 4:102, 1999; and Pini Prato GP: Ann Periodontol 4:98, 1999.
FIGURE 5.15 A, Clinical image of plaque-related slight early chronic periodontitis with 1-2 mm of clinical attachment loss in a 40-year-old woman.
B, Radiographic images of the patient.
FIGURE 5.16 A, Clinical image of plaque-related moderate chronic periodontitis with 3-4 mm of clinical attachment loss in a 53-year-old man who
smokes. B, Radiographic images of the patient.
sites are affected. The disease may also be described by the family history of aggressive disease that is suggestive of a ge-
severity of disease as slight (1-2 mm of loss; Fig. 5.15), mod- netic trait (Box 5.3). This form of periodontitis was previously
erate (3-4 mm of loss; Fig. 5.16), or severe (;:::5 mm of loss; classified as early-onset periodontitis (Table 5.1) and there-
Fig. 5 .17) on the basis of the amount of clinical attachment fore still includes many of the characteristics previously iden-
loss (Box 53). tified with the localized and generalized forms of early-onset
periodontitis. Although the clinical presentation of aggressive
Aggressive Periodontitis disease appears to be universal, the causative factors involved
are not always consistent. Box 5.3 outlines additional clinical,
Aggressive periodontitis differs from the chronic form primar- microbiologic, and immunologic characteristics of aggressive
ily by the rapid rate of disease progression seen in an otherwise disease that may be present. As was previously described for
healthy individual (Figs. 5.18 and 5 19); the absence of large early-onset disease, aggressive forms of periodontitis usually
accumulations of plaque and calculus; and the presence of a affect young individuals during or shortly after puberty and
FIGURE 5.17 A, Clinical image of plaque-related severe advanced chronic periodontitis with >5 mm of clinical attachment loss in a 47-year-old
woman. B, Radiographic images of the patient.
FIGURE 5.18 A, Clinical image of plaque-related aggressive moderate periodontitis with 1-7 mm of PD and 3-4 mm of clinical attachment loss in
a 31-year-old man. B, Radiographic images of the patient.
may be observed during the second and third decades of life Periodontitis as a Manifestation
(ie , 10-30 years of age). The disease may be localized as pre- of Systemic Disease
viously described for localized juvenile periodontitis or gen-
eralized as previously described for generalized Juvenile peri- Several hematologic and genetic disorders have been as-
odontitis and rapidly progressive periodontitis (Table 5.1). sociated with the development of periodontitis in affected
Box 5.3 provides the common features of the localized and individuals (Box 5.3). The majority of these observations of
generalized forms of aggressive periodontitis. effects on the periodontium are the result of case reports,
FIGURE 5.19 A, Clinical image of plaque-related aggressive severe periodontitis with 3-13 mm of PD and 7-15 mm of clinical attachment loss in a
32-year-old man. B, Radiographic images of the patient.
and few research studies have been performed to investigate Impaired neutrophil function is considered to be the prima-
the exact nature of the effect of the specific condition on the ry cause of PLS that eventually results in the deregulation of the
tissues of the periodontium. It is speculated that the major polymorphonuclear leukocyte response to microbial infection.
effect of these disorders is through alterations in host-defense Although the subgingival microflora associated with PLS is di-
mechanisms that have been clearly described for disorders verse, opportunistic periodontal pathogens such as A actinomy-
(eg, neutropenia, leukocyte adhesion deficiencies) but that cetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Fu-
are less well understood for multifaceted syndromes. The sobacterium nucleatum, and Prevotella intermedia are frequently
clinical manifestation of many of these disorders appears identified among plaque samples from PLS patients.
at an early age and may be confused with aggressive forms Sarcoidosis is a chronic disease that is expressed as a cell-
of periodontitis with rapid attachment loss and the poten- mediated, delayed-type hypersensitivity that primarily affects
tial for early tooth loss. With the introduction of this form the lungs, lymph nodes, skin, eyes, liver, spleen, and small
of periodontitis in this and previous classification systems bones of the hands and feet. Sarcoidosis rarely affects the
(Table 5.1), the potential exists for overlap and confusion be- oral cavity, with incidence of occurrence in descending order
tween periodontitis as a manifestation of systemic disease and noted in the lymph nodes, lips, soft palate, buccal mucosa,
both, the aggressive and the chronic form of disease, when gingiva, tongue, and bone. Fig. 5.25 depicts the pretreatment
a systemic component is suspected. At present, periodonti- pattern of bone loss and recession associated with sarcoidosis,
tis as a manifestation of systemic disease is the diagnosis to be with pulmonary parenchymal fibrous infiltrate being noted in
used when the systemic condition is the maJor predisposing the lungs as depicted by a white lacy pattern on a chest radio-
factor and when local factors (eg, large quantities of plaque graph (Fig. 5.25C). Histologic features of sarcoidosis include
and calculus) are not clearly evident. In the case in which the presence of an intense chronic inflammatory infiltrate with
periodontal destruction is clearly the result of local factors focal areas of noncaseating granulomas and a positive Kveim
but has been exacerbated by the onset of conditions, such test (Fig. 5.26C). The remineralization of alveolar bone is not-
as diabetes mellitus (Figs. 5.20 and 5 21) or HIV infection, ed on radiographs obtained 1 year after the systemic adminis-
the diagnosis should be chronic periodontitis modified by the tration of steroids (eg, prednisone) (Fig. 5 26A)
systemic condition.
Papillon-Lefevre syndrome (PLS) is an autosornal-reces- Bisphosphonate-Related Osteonecrosis
sive disorder caused by mutations in the cathepsin C gene
of the Jaw
located on chromosome llql4. The clinical manifestations
of the syndrome include severe aggressive periodontitis Bisphosphonates (BPs) are pyrophosphate analogs with a high
and diffuse keratoderma on the palms and on the soles, the affinity for hydroxyapatite crystals. They inhibit osteoclast-
knees, or both (Figs. 5.22 and 5.23). The consanguinity of mediated bone resorption and play a key role in the manage-
the parents is a common finding in approximately one-third ment of osteolytic bone disorders, including osteoporosis, Paget
of the cases. (Fig. 5.24) disease, bone metastasis, and multiple myeloma. However,
FIGURE 5.20 A, Clinical image of plaque-related showing severe aggressive periodontitis in a 53-year-old man who smokes and who has diabetes
and a hemoglobin A,, level of 10.7. B, Radiographic images of the patient.
FIGURE 5.21 Selective probing depths of the same 53-year-old diabetic patient shown in Fig. 5.20 with severe aggressive periodontitis.
their prolonged use is associated with bisphosphonate-related mobility, and paresthesia, thereby culminating in a reduced
osteonecrosis of the jaw (BRON]). ability to eat and speak. BRON] occurs most frequently in
The American Association of Oral and Maxillofacial Sur- the mandible (65%), followed by the maxilla (26%), and
geons defines BRONJ as "exposed bone in the maxillofacial both jaws (95%) The frequency of BRON] is higher in the
area occurring in the absence of head and neck irradiation posterior region of the jaw. Among patients who develop
and showing no evidence of healing for at least 8 weeks after BRO NJ, approximately 60% of cases occur after an inva-
identification in patients treated with BP therapy" (Figs. 5.27 sive dental procedure (eg, tooth extraction), whereas 40%
and 5.28). The incidence ofBRONJ among patients with cancer develop spontaneously. Radiographic evaluation is usually
who are receiving intravenous BP ranges from 0.72% to 7.4%. inconclusive for early lesions; in advanced cases, a poorly
BRON] lesions may be asymptomatic, or they may be defined moth-eaten radiolucency is noted with radiopaque
present with pain, purulent discharge, swelling, tooth sequestra.
FIGURE 5.22 Panoramic radiograph and clinical photographs of a 13-year-old girl with PLS. (Courtesy Dr Georgios Kotsakis, Minneapolis, MN.)
FIGURE 5.23 Patient with PLS exhibiting hyperkeratosis on the palms of the hands and the soles of the feet. (Courtesy Dr Georgios Kotsekis,
Minneapolis, MN.)
Necrotizing Periodontal Diseases accompanied by fever, malaise, and lymphadenopathy al-

though these characteristics are not consistent. Two forms of
The clinical characteristics of necrotizing periodontal diseases necrotizing periodontal disease have been described; necrotiz-
may include (but are not limited to) ulcerated and necrotic ing ulcerative gingivitis (NUG) (Fig. 5 29) and necrotizing ulcer-
papillary and marginal gingiva covered by a yellowish-white ative periodontitis (NUP) (Fig. 5.30) NUG has been previously
or grayish slough or pseudomembrane, blunting and crater- classified as "gingival disease" or "gingivitis," because clinical
ing of the papillae, bleeding on provocation or spontane- attachment loss is not a consistent feature; NUP has been clas-
ous bleeding, pain, and fetid breath. These diseases may be sified as a form of "periodontitis," because attachment loss is
Pedigree chart Periodontitis Associated With
DO DO Endodontic Lesions
The classification of lesions that affect the periodontium and
the pulp is based on the sequence of the disease process.
-~
Endodontic-Periodontal Lesions
II OTD In endodontic-periodontal lesions, pulpal necrosis precedes
periodontal changes. A periapical lesion that originates with
pulpal infection and necrosis may drain to the oral cavity
through the periodontal ligament, thereby resulting in the
Ill
13yo izvc lOyo •o

9yo 7yo
FIGURE 5.24 No history of consanguinity was reported in this case. How-
ever, approximately one-third of diagnosed PLS cases descend from same
4yo
destruction of the periodontal ligament and the adjacent al-
veolar bone. This may be present clinically as a localized,
deep, periodontal probing depth that extends to the apex of
the tooth (Fig. 5.31A). A resultant extensive alveolar ridge de-
fect (Fig. 5.31B and C) may necessitate reconstructive surgery
(Fig. 5.31D) before the placement of implants and prostheses
ancestor. Offsprings 1111, 11I3, and 1II4 display a PLS phenotype. All siblings (Fig. 5.32) to reestablish a functional and aesthetic outcome.
should be thoroughly examined by a periodontist after a case of PLS has
Pulpal infection may also drain through accessory canals, es-
been diagnosed. (Courtesy Dr Ceorgios Kotsakis, Minneapolis, MN.)
pecially in the area of the furcation, and this may lead to furcal
involvement through the loss of clinical attachment and alveo-
lar bone.
present. Recent reviews of the causative and clinical character-
istics of NUG and NUP have suggested that the two diseases
represent clinical manifestations of the same disease, except Periodontal-Endodontic Lesions
that distinct features of NUP are clinical attachment and bone In periodontal-endodontic lesions, bacterial infection from a
loss. As a result, both NUG and NUP have been determined to periodontal pocket associated with a loss of attachment and
comprise a separate group of diseases that have tissue necrosis root exposure may spread through the accessory canals to the
as a primary clinical feature (Box 5.1). pulp, thereby resulting in pulpal necrosis. In the case of ad-
vanced periodontal disease, the infection may reach the pulp
Abscesses of the Periodontium through the apical foramen. Scaling and root planing remove
cementum and underlying dentin, which may lead to chronic
A periodontal abscess is a localized purulent infection of peri- pulpitis through the bacterial penetration of dentinal tubules.
odontal tissues, and it is classified by its tissue of origin. The However, many teeth that have been affected by periodontitis
clinical, microbiologic, immunologic, and predisposing char- that have been scaled and root planed show no evidence of
acteristics are discussed in Chapter 19. pulpal involvement.
FIGURE 5.25 Sarcoidosis pretreatment. A, The intraoral radiographs depict more extensive bone loss than clinical attachment loss for the anterior
teeth. B, Extensive recession plus clinical attachment loss. C, Pulmonary parenchymal fibrous infiltrate.
FIGURE 5.26 Sarcoidosis after treatment with prednisone. A, lntraoral radiographs depict the remineralization of bone. B, Reduction in gingival
inflammation while extensive recession and clinical attachment loss persist. C, Pretreatment biopsy.
FIGURE 5.27 Exposed bone on the buccal lower premolar and molar
·t; . ~ ~-
in a patient with BP-associated osteonecrosis of the jaw after extrac-
tion of the first molar. (Courtesy Dr Vivek Thumbigere Math, Minne-
.... .~-;
· ;~ ~-,--:.
apolis, MN.)
r.
FIGURE 5.29 A, Ulcerative gingivitis illustrating the sloughing of the

marginal gingiva. B, Phase-contrast microscopy reveals Spirochetes in
the subgingival plaque sample.
Combined Lesions
Combined lesions occur when pulpal necrosis and a periapical
lesion occur on a tooth that is also periodontally involved. An
angular intrabony defect that communicates with a periapi-
cal lesion of pulpal origin results in a combined periodontal-
endodontic lesion.
In all cases of periodontitis associated with endodontic le-
sions, the endodontic infection should be controlled before
FIGURE 5.28 Patient with BP-associated osteonecrosis of the jaw
with exposed bone on the lingual aspect of the lower premolar and
the definitive management of the periodontal lesion is begun,
molar after root canal treatment. (Courtesy Dr Vivek Thumbigere Math, especially when regenerative or bone-grafting techniques are
Minneapolis, MN.) planned.
Tooth Anatomic Factors

Tooth anatomic factors are associated with malformations of
tooth development or tooth location. Anatomic factors (eg,
cervical enamel projections, enamel pearls) have been associ-
ated with clinical attachment loss, especially in furcation areas.
Cervical enamel projections are found on 15-24% of man-
dibular molars and on 9-25% of maxillary molars, and strong
associations have been observed with furcation involvement.
Palatogingival grooves, which are found primarily on maxillary
incisors, are observed in 8.5% of individuals, and they are asso-
ciated with increased plaque accumulation, clinical attachment,
and bone loss. Proximal root grooves on incisors and maxillary
premolars also predispose individuals to plaque accumulation,
inflammation, and the loss of clinical attachment and bone.
Tooth location is considered important for the initiation
and development of disease. Malaligned teeth predispose
individuals to plaque accumulation with resultant inflamma-
tion in children, and they may predispose adults to clinical
attachment loss, especially when they are associated with poor
oral-hygiene habits. In addition, open contacts have been as-
sociated with an increased loss of alveolar bone, most likely
through food impaction.
FIGURE 5.30 A, Necrotizing ulcerative periodontitis with severe Dental Restorations and Appliances
clinical attachment loss in a 28-year-old man with human immuno- Dental restorations or appliances are frequently associated with
deficiency virus. B, Spirochetes are noted on the surface of sloughed
epithelial cells.
the development of gingival inflammation, especially when they
are located subgingivally This may apply to subgingivally placed
onlays, crowns, fillings, and orthodontic bands. Restorations
Developmental or Acquired may impinge on the biologic width by being placed deep in the
Deformities and Conditions sulcus or within the junctional epithelium. This may promote
inflammation and the loss of clinical attachment and bone, with
Localized Tooth-Related Factors apical migration of the junctional epithelium, and the reestab-
That Modify or Predispose Individuals lishment of the attachment apparatus at a more apical level.
to Plaque-Induced Gingival Diseases
Root Fractures
or Periodontitis
Root fractures that are caused by traumatic forces or by re-
In general, these localized tooth-related factors contribute to storative or endodontic procedures (5 .33A-C) may lead to
the initiation and progression of periodontal disease through periodontal involvement through the apical migration of
the enhancement of plaque accumulation or the prevention plaque along the fracture when the fracture originates coronal
of effective plaque removal via normal oral-hygiene measures. to the clinical attachment and is exposed to the oral environ-
These factors fall into the four subgroups outlined in Box 5.4. ment, with a resulting alveolar ridge defect (Fig. 5.33D).
FIGURE 5.31 A and C, Clinical images of extensive loss of the

alveolar ridge as a result of a periapical endodontic lesion. B,
A computed tomography image that depicts alveolar bone loss.
D, A computed tomography image of a ridge that was regener-
ated with the use of allogenic bone graft and a tenting screw
and membrane.
FIGURE 5.32 The same patient who was depicted in Fig. 5.31. A and B, A computed tomography image of a regenerated ridge, with implants placed
in areas #7, #9, and #10. C and D, Clinical image of the implant-supported bridge.
FIGURE 5.33 A and B, Clinical images of a fistula

tract. C, Root fracture. D, Resultant alveolar ridge
defect.
Cervical Root Resorption and Cementa! Tears gingiva (Fig. 5.36), the alveolar mucosa, and frenula muscle
Cervical root resorption (as noted on the computed tomog- attachments. A mucogingival deformity is a significant depar-
raphy scans shown in Fig. 5.34A and B) and cementa! tears ture from the normal shape of the gingiva and the alveolar
may lead to periodontal destruction when the lesion com- mucosa, and it may involve the underlying alveolar bone.
municates with the oral cavity and allows bacteria to migrate
subgingivally. Avulsed teeth that are reimplants frequently de- Mucogingival Deformities and Conditions
velop ankylosis and cervical resorption many years after re-
of the Edentulous Ridges
implantation. The atraumatic removal of such ankylosed teeth
& the reconstruction of resultant ridge defects with bone Mucogingival deformities, such as a lack of stable keratin-
grafts,dental implants& prosthesisi are viable solutions for ized gingiva between the vestibular fornices and the floor of
such defects (Fig. 5 35) the mouth (Fig. 5 3 7 A), may require soft-tissue grafting and
vestibular deepening before prosthodontic reconstruction
Mucogingival Deformities and Conditions (Fig. 5.37B-D). Alveolar bone defects in edentulous
Around the Teeth ridges (Fig. 5.38A and B) usually require corrective surgery
(Fig. 5.38C and D) to restore form and function before the
Mucogingival deformity is a generic term used to describe placement of implants and prostheses to replace missing teeth
the mucogingival junction and its relationship to the (Fig. 5 37-5 39)
FIGURE 5.34 A and B, Computed tomography scanning reveals severe cervical root resorption of the maxillary central incisors and periapical ab-
scess. C, Crowns fractured as a result of resorption. D, Biopsy of soft tissue from the resorption .
•..•.
•.., ,, '.' •.
:-.
..... ~...• :• .
,.-
(A)":--~ / ~-
r.:. ~ t··-~- ,..

:..y.,__i:e,,
..,,.·-,-.;·
-~ .
• _. • -.· I •..:.
.••. >
(B)
FIGURE 5.36 A, Mucogingival defect depicted by recession. B, De-

FIGURE 5.35 A, Posttreatment clinical image of the same patient defects extend into the alveolar mucosa which lack keratinized gingiva.
picted in Fig. 5.34 with implant-supported crowns and veneers on the
lateral surfaces. B and C, Computed tomography images of bone grafts
and implants replacing central incisors that were lost as a result of severe
cervical root resorption.
FIGURE 5.37 A, Mucogingival ridge defect from the floor of the mouth to the vestibular fornix. B, A partial-thickness flap with vestibular deepening.
C, The placement of free gingival graft. D, The reestablishment of vestibular depth and keratinized attached gingiva.
FIGURE 5.38 A, Clinical image of an edentulous ridge defect. B, Pretreatment computed tomography image of the defect. C, Ridge that was recon-
structed with the use of a ramus block graft. D, Computed tomography scan of the grafted site.
FIGURE 5.39 A, Clinical image of the ridge 6 months after grafting. B, Placement of implants in the areas of teeth #23 and #25. C, Porcelain-fused-
to-metal crowns for the maxillary incisors and an implant-supported bridge from teeth #23 through #25.
Occlusal Trauma Attstrom R, Vander Velden U: Summary of session 1. In Lang N, Karring T,

editors: In Proceedings of the 1st European workshop in periodontology, Berlin,
The causes of trauma from occlusion and the effect of this 1993, Quintessence.
Caton J: Periodontal diagnosis and diagnostic aids: consensus report. Proceed-
trauma on the periodontium are discussed in detail in ings of the World Workshop in Clinical Peliodontics, Chicago, 1989, American
Chapter 21. Academy of Periodontology.
Hellstein JW, Adler RA, Edwards B, et al: Managing the care of patients receiv-
ing antiresorptive therapy for prevention and treatment of osteoporosis:
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48. Thumbigere-Math V, Sabino MC, Gopalakrishnan R, et al: Bisphospho-
rosis: executive summary of recommendations from the American Dental
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Association Council on Scientific Affairs, J Am Dent Assoc 142: 124 3-
agement, and treatment outcomes of 26 patients, J Oral Maxillofac Surg
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67 1904-1913, 2009.
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49. Tonetti MS, Mombelli A: Early-onset periodontitis, Ann Peliodontol 4:39,
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21. Jernberg GR, Bakdash MB, Keenan KM: Relationship between proximal
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4:54, 1999.
6
Epidemiology of Gingival and
Periodontal Disease
VW Spolsky • DG Naik • A Uppoor
Chapter Outline
Indices Used to Study Periodontal
Problems
Epidemiologic surveys conducted throughout the world point to demiologic research has clarified the prevalence of periodontal
the almost universal distribution of caries and periodontal dis- disease, provided new insights on its pathogenesis through con-
ease. Progress in the study of the epidemiology of periodontal trolled clinical trials, and focused attention on assessing treat-
diseases has been slower than that in the study of dental caries ment needs for improving the periodontal health of the public.
because of several important factors that do not exist in the study One of the most valuable techniques employed in dental
of dental caries. The pathologic changes of dental caries involve epidemiology is the epidemiologic index. Epidemiologic indices
hard, calcified tissues, whereas periodontal disease involves soft are attempts to quantitate clinical conditions on a graduated scale,
and hard tissues. Unlike dental caries, periodontal disease does thereby facilitating comparison among populations examined by the
not lend itself easily to objective measurement, because the signs same criteria and methods. Unlike the absolute or definitive di-
of periodontal pathologic alteration involve color changes in the agnosis that can be made of disease in a solitary patient, an epi-
soft tissues, swelling, bleeding, and bone changes that are reflect- demiologic index (which is a numerical value) estimates only
ed in crevice depth changes or pathologic pockets, as well as loss the relative prevalence or occurrence of the clinical condition.
of tooth function because of tooth mobility. Therefore, examining Prevalence is the proportion of persons affected by a disease at
the teeth for the signs of dental caries is far easier than evaluating a specific point in time, as determined by a cross-sectional survey.
the pathologic variables used to define periodontal diseases. Incidence is defined as the rate of occurrence of a new dis-
Dental epidemiology is the study of the pattern (distribution) ease in a population during a given interval of time.
and dynamics of dental diseases in a human population. "Pattern" In general, indices are actually underestimates of the true
implies that certain people are affected by a disease and that clinical condition.
the association between the disease and the affected popu- A good epidemiologic index must be easy to use, permit
lation can be described by variables such as age, sex, racial the examination of many people in a short period of time,
or ethnic group, occupation, social characteristics, place of define clinical conditions objectively, be highly reproducible
residence, susceptibility, and exposure to specific agents. The in assessing a clinical condition when used by one or more
term dynamics refers to a temporal pattern (distribution) and examiners, be amenable to statistical analysis, and be strongly
is concerned with trends, cyclic patterns, and the time that related numerically to the clinical stages of the specific disease
elapses between the exposure in citing factors and the onset under investigation. Calibration or standardization in refer-
of the specific disease. Russell defined dental epidemiology as ence to the use of an index's criteria by an examiner or exam-
"not so much the study of disease as a process as it is a study iners is imperative to ensure the reliability of the data.
of the condition of the people in whom the disease occurs." In general, there are two types of dental indices.
The purpose or objective of epidemiology is to increase the The first type of index measures the number or proportion
understanding of the disease process (ie, to identify the risk of people in a population with or without a specific condition
factors or determinants of disease), thereby leading to the de- at a specific point in time or interval of time.
velopment of methods of control and prevention. In addition, The second type of dental index measures the number of
epidemiology attempts to discover populations at high and people affected and the severity of the specific condition at a
low risk, to define the specific problem under investigation, specific time or interval of time.
and to determine trends in disease patterns. More explicitly, the second type of index not only helps to
The design, conduct, and interpretation of clinical trials of identify the person in the population affected with a specific
preventive and curative measures are also within its purview. condition but also assesses the condition under study on a
Ainamo has astutely described the significance of epidemio- graduated scale. Most of the indices described in this chapter
logic research to the understanding of periodontal disease. Epi- are of the second type.
73
Indices Used to Study Periodontal of gingival inflammation. The facial surface of the gingiva
around a tooth was divided into three gingival scoring units:
Problems the mesial dental papilla (P), the gingival margin (M), and the
Although there are many indices for recording and quantitat- attached gingiva (A). The presence or absence of inflammation
ing the entities that make up periodontal disease, space limita- on each gingival unit was recorded as 1 or 0, respectively The
tions only permit the inclusion of indices that have historically P, M, and A numerical values for all teeth were totaled sepa-
contributed to the understanding of periodontal diseases or rately and then added together to express the PMA Index score
are currently in frequent use. A scholarly overview of epide- per person. Although all of the facial tissues surrounding all
miologic research in periodontal disease is provided by Ai- of the teeth could be assessed in this manner, usually only the
namo. The indices that are discussed in this chapter can, for maxillary and mandibular incisors, the canines, and the pre-
the purpose of convenience and reason, be divided according molars are examined. The developers of this index eventually
to the following measured variables: added a severity component for assessing gingivitis; the papil-
lary units (P) were scored on a scale of 0-5 and the marginal
1. The degree of inflammation of gingival tissues (M) and attached (A) gingivae were scored on a scale of 0-3.
2. The degree of periodontal destruction The value of this index lies in its broad application to epi-
3. The amount of plaque accumulated demiologic surveys and clinical trials and in its capacity for
4. The amount of calculus present use in individual patients. The criteria for and approach to
In addition, indices developed to assess treatment needs assessing gingival inflammation developed by Schour and
will be discussed. Massler served as the basis for many other indices. Examples
of indices that are based on modifications of the PMA Index
are those developed by Muhlernann and Mazor, Lobene, and
Indices Used to Assess Gingival Suomi and Barbano.
Inflammation
Periodontal Index
Papillary-Marginal-Attachment Index The Periodontal Index (PI) was intended to estimate the ex-
Originally, the Papillary-Marginal-Attachment (PMA) Index tent of deeper periodontal disease that the PMA Index could
was used to count the number of gingival units affected with measure by determining the presence or absence of gingival
gingivitis. This approach was predicated on the belief that the inflammation and its severity, pocket formation, and mastica-
number of units affected correlated with the degree or severity tory function. The criteria given in Table 6.1 are used to assess
TABLE 6.1
THE PERIODONTAL INDEX

Score Criteria and Scoring for Field Studies Additional Criteria Followed in the Clinical Test
0 Negative. There is neither overt inflammation in the investing Radiographic appearance is essentially normal.
tissues nor loss of function owing to destruction of
supporting tissues.
Mid Gingivitis There is an overt area of inflammation in the
free gingivae, but this area does not circumscribe the tooth.
2 Gingivitis Inflammation completely circumscribes the tooth,
but there is no apparent break in the epithelial attachment.
4 (Used when radiographs are available.) There is early, notch-like resorption of the alveolar crest.
6 Gingivitis with pocket formation. The epithelial attachment has There is horizontal bone loss involving the entire
been broken, and there is a pocket (not merely a deepened alveolar crest, up to half of the length of the tooth
gingival crevice as a result of swelling in free gingivae). root.
There is no interference with normal masticatory function;
the tooth is firm and has not drifted.
8 Advanced destruction with loss of masticatory function. The There is advanced bone loss involving more than
tooth may be loose, may have drifted, may sound dull one-half of the length of the tooth root or a
on percussion with a metallic instrument, or may be definite infrabony pocket with widening of
depressible in its socket. the periodontal ligament. There may be root
resorption or rarefraction at the apex.
Rule: When in Doubt, Assign the Lesser Scores
Periodontal index score per person = Sum of individual scores
Number of teeth present
Clinical Condition Group Pl Scores Stage of Disease
Clinically normal 0-0.2
supportive tissues
Simple gingivitis 0.3-0.9 Reversible
Beginning destructive 0.7-1.9
periodontal disease
Established destructive 1.6-5.0 Irreversible
periodontal disease
Terminal disease 3.8-8.0
(Modified from Russell AL The periodontal index. J Periodontal 38:585, 1967)
6 Epidem iology of G ingival and Periodontal Disease 75
TABLE 6.2
CRITERIA FOR SEVERAL COMPONENTS OF THE PERIODONTAL DISEASE INDEX

Gingival Status (Gingivitis Index)
0 = Absence of signs of inflammation
1 = Mid to moderate inflammatory gingival changes, not extending around the tooth
2 = Mild to moderately severe gingivitis extending all around the tooth
3 = Severe gingivitis characterized by marked redness, swelling, tendency to bleed, and ulceration
Cr-evicular Measurements
A. If the gingival margin is on the enamel, measure from the gum margin to the cementoenamel junction and record the measurement. If the
epithelial attachment is on the crown and the cementoenamel junction cannot be felt by the probe, record the depth of the gingival sulcus on
the crown. Then record the distance from the gingival margin to the bottom of the pocket if the probe can be moved apically to the cementoe-
namel junction without resistance or pain. The distance from the cementoenamel junction to the bottom of the pocket can then be found by
subtracting the first from the second measurement.
B. If the gingival margin is on the cementum, record the distance from the cementoenamel junction to the gingival margin as a minus value.
Then record the distance from the cementoenamel junction to the bottom of the gingival sulcus as plus value. Both loss of attachment and
actual sulcus depth can easily be assessed from the scores.
Periodontal Disease Index (PDI) Criteria for Surveys
If the gingival sulcus in none of the measured areas extended apically to the cementoenamel junction, the recorded score for gingivitis is the PD!
score for the tooth. If the gingival sulcus in any of the two measured areas extended apically to the cementoenamel junction but not more than
3 mm (including 3 mm in any area), the tooth is assigned a PD! score of 4. The score for gingivitis is then disregarded in the PD! score for that
tooth. If the gingival sulcus in either of the two recorded areas of the tooth extends apically to from 3 to 6 mm (including 6 mm) in relation
to the cemntoenamel junction, the tooth is assigned a PD! score of 5 (again, the gingivitis score is disregarded). Whenever the gingival sulcus
extends more than 6 mm apically to the cementoenamel junction in any of the measured areas of the tooth, the score of 6 is assigned as the
PD! score for that tooth (again disregarding the gingivitis score).
Shick-Ash Modification of Plaque Criteria
0 = Absence of dental plaque
1 = Dental plaque in the interproximal area or at the gingival margin covering less than one-third of the gingival half of the facial or lingual
surface of the tooth
2 = Dental plaque covering more than one-third but less than two-thirds of the gingival half of the facial or lingual surface of the tooth
3 = Dental plaque covering two-thirds or more of the gingival half of the facial or gingival surface of the tooth
Calculus Criteria
0 = Absence of calculus
1 = Supragingival calculus extending only slightly below the free gingival margin (not more than 1 mm)
2 = Moderate amount of supragingival and subgingival calculus or subgingival calculus alone
3 = An abudance of supragingival and subgingival calculus
all of the gingival tissues circumscribing each tooth (ie, all of The criteria used to assess the tissue circumscribing the
the tissue circumscribing a tooth is considered a scoring or Ramfjord teeth combine elements of the PMA Index and the
gingival unit). Since the PI measures both reversible and ir- PI and appear in Table 6.2. A numerical score for the gingival
reversible aspects of periodontal disease, it is an epidemio- status component of the PDI (ie, the Gingivitis Index score per
logic index with a true biologic gradient. A PI score for an person) [see Section "Gingival Index (Loe and Silness)"] is ob-
individual is determined by adding all of the tooth scores tained by adding the value for all of the gingival units and divid-
and dividing by the number of teeth examined. Since only ing by the number of teeth present. The PDI has been used in
a mouth mirror and no calibrated probes or radiographs are epidemiologic surveys, longitudinal studies of periodontal dis-
used when performing a PI examination, the results tend to ease, and clinical trials of therapeutic or preventive procedures.
underestimate the true level of periodontal disease, especially
early bone loss, in a population. The number of periodontal Gingival Index (Loe and Silness)
pockets without obvious supragingival calculus is also under- The Gingival Index (GI) was developed solely for the purpose
estimated in the Pl. of assessing the severity of gingivitis and its location in four
possible areas. The tissues surrounding each tooth are divided
Gingivitis Component of the Periodontal into four gingival scoring units: the distofacial papilla, the fa-
Disease Index cial margin, the mesiofacial papilla, and the entire lingual gin-
The Periodontal Disease Index (PDI) is similar to the Pl in gival margin. To minimize examiner variability in scoring, the
that both are used to measure the presence and severity of lingual surface is not subdivided because it will most likely
periodontal disease. The PDI does so by combining the assess- be viewed indirectly with a mouth mirror. A blunt instru-
ments of gingivitis and gingival sulcus depth on six selected ment, such as a periodontal pocket probe, is used to assess
teeth (teeth# 16, 21, 24, 36, 41 and 46) This group of teeth, the bleeding potential of the tissues. Each of the four gingival
frequently referred to as the Ramfjord teeth, have been tested units is assessed according to the criteria shown in Table 6.3.
as reliable indicators for the various regions of the mouth. Cal- Totaling the scores around each tooth yields the GI score
culus and plaque are also examined to assist in formulating a for the area. If the scores around each tooth are totaled and
comprehensive assessment of periodontal status and are de- divided by four, the GI score for the tooth is obtained. Totaling
scribed in the following discussions. all of the scores per tooth and dividing by the number of teeth
TABLE 6.3
CRITERIA FOR THE GINGIVAL INDEX, THE PLAQUE INDEX, AND THE MODIFIED GINGIVAL INDEX
Gingival Index (GI)
0 = Normal gingiva
1 = Mild inflammation. slight change in color, slight edema, no bleeding on palpation
2 = Moderate inflammation, redness, edema, and glazing; bleeding on probing'
3 = Severe inflammation, market redness and edema, ulcerations; tendency to spontaneous bleeding
Plaque Index (PI)
0 = No plaque in the gingival area
1 = A film of plaque adhering to the free gingival margin and adjacent area of the tooth. The plaque may be recognized only by running a probe
across the tooth surface
2 = Moderate accumulation of soft deposits within the gingival pocket and on the gingival margin and/or adjacent tooth surface that can be seen
by the naked eye
3 = Abundance of soft matter within the gingival pocket and/or on the gingival margin and adjacent tooth surface
Modified Gingival Index (MGI)
0 = Absence of inflammation
1 = Mild inflammation; slight change in color, little change in texture of portion of the marginal or papillary gingival unit
2 = Mild inflammation; criteria as mentioned earlier but involving the entire marginal or papillary gingival unit
3 = Moderate inflammation; glazing, redness, edema, and/or hypertrophy of the marginal or papillary gingival unit
4 = Severe inflammation; marked redness, edema, and/or hypertrophy of the marginal or papillary gingival unit, spontaneous bleeding,
congestion, or ulceration
'A periodontal probe is drawn horizontally along the soft tissue wall of the entrance to the gingival sulcus.
examined provides the GI score per person. The GI may also All of Muhlemann indices are predicated on an under-
be used to evaluate a segment of the mouth a group of teeth. standing of sulcular bleeding as a precursor of gingival in-
The numerical scores of the GI are associated with varying flammation and as the first sign of inflammation. The GI of
degrees of clinical gingivitis as follows: Loe and Silness, however, uses the presence of a slight color
change and the absence of bleeding when a blunt instrument
is used to palpate the soft tissue wall at the gingival margin to
Gingival Scores Degree of Gingivitis indicate initial gingival inflammation. Although the correla-
0.1-10 Mild tion between the two variables (inflammation and bleeding) is
1.1-2.0 Moderate not perfect, the histologic evidence for associating inflamma-
2.1-3.0 Severe tion with the GI criteria is stronger than that for associating
gingival fluid flow and the SBI. From the epidemiologic view-
point, it is better to measure single elements than to measure
The index can be used to determine the prevalence and a combination of several. The MGI illustrated how the signs of
severity of gingivitis in both epidemiologic surveys and in an inflammation and bleeding in the GI were separated.
individual. This latter attribute has contributed to making the Several other indices are worthy of mention. The Bleeding
GI the index of choice in controlled clinical trials of preventive Points Index was developed to assess a patient's oral hygiene
or therapeutic agents. performance. It determines the presence or absence of gingi-
Lobene and coworkers created the modified GI (MGI) by val bleeding interproximally and on the facial and lingual sur-
eliminating the bleeding criterion, making the MGI a nonin- face of each tooth. A periodontal probe is drawn horizontally
vasive index. By redefining the criteria for mild and moderate through the gingival crevice of a quadrant, and the gingiva is
inflammation, the MGI increases sensitivity in the lower por- examined for bleeding after 30 s.
tion of the scoring scale. The criteria for the MGI are given in The Gingival Bleeding Index also assesses the presence or
Table 6.3. absence of gingival bleeding, but only at the interproximal
spaces and using unwaxed dental floss. The floss is thought
Indices of Gingival Bleeding to assess a larger area more quickly than a periodontal probe,
Two indices that combine the clinical estimates of inflamma- and it can be used by both the professional and the patient
tion and bleeding have been described. The Sulcus Bleeding when the latter is instructed to perform self-evaluation in con-
Index (SBI) of Muhlernann and Mazor uses bleeding on gentle trol program.
probing as the first criterion for indicating gingival inflam- The Interdental Bleeding Index, also referred to as the
mation. In 1971, Muhlernann and Son added an additional Eastman Interdental Bleeding Index, utilizes a triangle-shaped
category to the original criteria, resulting in a 0-5 scale for toothpick made of soft, pliable wood to stimulate the inter-
assessing inflammation or sulcular bleeding. proximal gingival tissue. The presence or absence of bleed-
Several years later Muhlernann assessed sulcus bleeding on ing with a specific stimulus permits the dentist and, perhaps
probing at the interdental papilla. This Papillary Bleeding In- more important, the patient to monitor interproximal gingi-
dex (PBI) used a scale of 0-4. A timing component was added val health. The interproximal cleaner is inserted horizontally
to the PBI by Barnett and coworkeres in an effort to make the between the teeth from the facial surface, depressing the in-
PBI more sensitive than the GI in assessing gingival changes. terproximal papilla by up to 2 mm. The wooden cleaner is
6 Epidem iology of Gingival and Periodontal Disease 77
TABLE 6.4 Indices Used to Measure Periodontal

CRITERIA USED BY THE NIDR TO ASSESS
Destruction
GINGIVAL INFLAMMATION AND CALCULUS The destruction of bone is still the most important criterion
Gingival Inflammation (Bleeding Index)
for assessing the severity of periodontal disease. Some of the
approaches to measuring bone loss that are discussed are gin-
0 = No bleeding present gival crevice measurements, radiographic evaluations of bone
1 = Bleeding results after probe is placed in gingival sulcus up to loss, and assessments of gingival recession and tooth mobility
2 mm and drawn along the inner surface of the gingival sulcus
Calculus Assessment (Calculus Index) Gingival Sulcus Measurement Component of the POI
0 = Calculus is absent The technique developed by Ramfjord for determining gingi-
1 = Supragingival calculus,' but no subgingival calculus is present val sulcus depth with a calibrated periodontal probe involves
2 = Supragingival and subgingival calculus, or subgingival calculus
measuring the distance from the cement-enamel junction to
only is present
the free gingival margin and the distance from the free gingival
'Supragingival calculus includes calculus located on the exposed crown and margin to the bottom of the gingival sulcus or pocket. The
root of the tooth and extending to 1-mm below the free gingival margin. difference between the two measurements yields the clinical
attachment level. This is considered the most important clini-
inserted and removed 4 times, and the presence or absence of cal measurement (ie, the "gold standard") in determining the
bleeding within 15 sis noted. The lnterdental Bleeding Index status of the perodontium. Ramfjord technique is considered
score is determined by dividing the number of bleeding sites useful in epidemiologic surveys, longitudinal studies of peri-
by the number of sites evaluated. odontal disease, and clinical trials of preventive and therapeu-
The Gingival Bleeding Index (GBI) of Ainamo and Bay was tic agents.
developed as an easy and suitable way for the practitioner to The first measurement in this two-step process may be
assess a patient's progress in plaque control. The presence or used in assessing gingival loss (recession) or gain. It is con-
absence of gingival bleeding is determined by gentle probing sidered more accurate and reliable in clinical trials than the
of the gingival crevice with a periodontal probe. The appear- Gingival Recession Index used in epidemiologic surveys.
ance of bleeding within 10 s indicates a positive score, which The criteria developed by Ramfjord for making sulcus
is expressed as a percentage of the total number of gingival depth determinations are shown in Table 6.2. The Rarnfjord
margins examined. criteria are most applicable to longitudinal studies of peri-
odontal disease and clinical trials of preventive or therapeutic
Gingival Index Used by the National Institute agents. Either the six teeth used by Ramfjord (teeth) (teeth
of Dental Research 16, 21, 24, 36, 41, and 44) or other teeth appropriate to the
The dichotomous criteria used by the National Institute of objective of the study may be assessed. Quadrants of teeth or
Dental Research (NIDR) to assess gingival inflammation all teeth should be considered in longitudinal studies.
(Table 6. 4) are the presence or absence of bleeding. Two sites In an epidemiologic survey (eg, a cross-sectional survey)
per tooth (mesial-buccal interproximal and mid-buccal on all in which the purpose is to determine the prevalence of total
teeth excluding the molars; and mesial-buccal interproximal periodontal disease, only the six index teeth should be used.
and mid-buccal of the mesial root of molars) on one-half of The set of criteria for a cross-sectional survey is the PDI (see
the maxillary arch and the contralateral half of the mandibular Table 6.2) The PDI score for the individual is obtained by
arch are assessed after excess moisture is dried with air. The totaling the scores of the teeth and dividing by the number of
decision of starting at either the right or left half of the maxil- teeth examined (a maximum of six).
lary arch is decided randomly The NIDR probe (a periodontal
probe that is graduated in 2-mm increments, with alternating Extent and Severity Index
increments colored in yellow) is gently inserted up to 2 mm The Extent and Severity Index (ESI) was developed because
into the gingival sulcus at the midpoint of the buccal and then of a lack of satisfaction with pervious indices of periodontal
drawn gently into the mesial-buccal interproximal area. After disease and because of the emergence of a newer conceptual
all the sites in both halves of the arches are probed (ie, the model of periodontal disease pathogenesis developed by So-
gingival sulcus is palpated), the bleeding sites are counted. cransky and coworkers. The older model, the Pl, was based
This number is divided by the total number of sites assessed on the concept of periodontal disease as a slowly progressing,
and then multiplied by 100 to yield the percentage of sites continuous disease process; it dealt with gingivitis as part of
with gingival bleeding. the biological gradient that extended from health to advanced
In conclusion, the use of gingival bleeding indices is de- periodontal disease. In the newer model, periodontal disease
sirable, because bleeding is a more objective indicator than is viewed as a chronic process with intermittent periods of
early gingival color changes and provides evidence of recent activity and remission that affects individual teeth and sites
plaque exposure. In general, the indices that utilize apical around teeth at different rates within the same mouth. Un-
probing (ie, probing to the bottom of the gingival sulcus or like the PI, which uses a mouth mirror only, the ESI uses a
pocket) (Palpation refers to the gentle touching of the sur- periodontal probe (the NIDR periodontal probe) to determine
face gingival tissue with the blunt end of a periodontal probe attachment levels.
and/or the gentle sweeping of the probe in a horizontal di- The ESI score is a bivariate statistic. It expresses the per-
rection along the inner surface of the gingival sulcus without centage of sites that exhibit disease (E for Extent) and mea-
apical pressure), however, are more suitable for diagnosing sures mean attachment loss in millimeters (S for Severity).
periodontitis and for assessing the effects of subgingival Hence the ESI = (E, S). Disease is defined arbitrarily as any
pocket therapy. site with more than 1 mm of attachment loss. Unlike the PI,
which examines the tissues surrounding all teeth present, the the presence and extent of plaque on a scale of 0-3, looking
ESI is based on probe measurements (at the mesiobuccal in- specifically at all interproximal facial and lingual surfaces of
terproximal and mid-buccal locations on all teeth excluding the index teeth. The criteria are suitable for longitudinal stud-
molars and at the mesiobuccal interproximal and mid-buccal ies of periodontal disease. Even though the plaque component
of the mesial root of molars) at 14 sites in half of the maxillary is not a part of the PDI score, it is helpful in a total assessment
arch and at 14 sites in the contralateral mandibular arch. The of periodontal status.
decision to start at either the right or left half of the maxillary Shick and Ash modified the original criteria of Ramfjord by
arch is made randomly. Attachment level measurements are excluding consideration of the interproximal areas of the teeth
made using the criteria ofRamfjord (see Table 6.2). Carlos and and "restricting the scoring of plaque to the gingival half' of
coworkers found that interexaminer agreement on site scores the facial and lingual surfaces of the index teeth. The criteria
was within 1 mm more than 95% of the time. Unlike the PI for the Shick-Ash modification of the Ramfjord plaque criteria
or PDI, the ESI describes the distribution (extent) of disease. are shown in Table 6.2.
Currently, the NIDR diagnostic criterion includes the method- The plaque score per person is obtained by totaling all of
ology of the ESI but has modified the definition of disease to the individual tooth scores and dividing by the number of
be more than 3 mm of attachment loss. teeth examined. These modified plaque criteria are suitable
for clinical trials of preventive or therapeutic agents.
Radiographic Approaches to Measuring Bone Loss
In general, the use of radiographs in the study of the epidemi- Simplified Oral Hygiene Index
ology of periodontal disease would appear to overcome some Greene and Vermillion developed the Oral Hygiene Index
of the criticisms of the more subjective clinical measurements. (OHI) in 1960 and later simplified it to include only six tooth
Radiographs present a permanent objective record of inter- surfaces that were representative of all anterior and poste-
dental bone levels; in longitudinal studies they may ensure rior segments of the mouth. This modification was called the
less variability than poorly standardized evaluations by dental Simplified OHI (OHI-S). The OHI-S measures the surface
examiners, and they offer the only method available for mak- area of the tooth that is covered by debris and calculus. The
ing crown and root measurements. Their disadvantages are imprecise term debris was used because it was not practical to
that they are not useful in the buccal or lingual assessment of distinguish among plaque, debris, and materia alba. In addi-
bone level, they do not provide adequate information on soft tion, the practicality of determining the weight and thickness
tissue attachment, and their value may be lost if improper an- of the soft deposits prompted the assumption that the dirtier
gulation is used. Furthermore, obtaining radiographs of sur- the mouth is, the greater is the tooth surface area covered by
vey participants, without the intent of providing treatment if debris. This assumption also implied a time factor, because
needed, is unethical. the longer oral hygiene practices are neglected, the greater
Only a few indices have been specifically designed to eval- the likelihood that the surface area of the tooth will be cov-
uate the radiographic assessment of periodontal disease, but ered by debris.
other more precise techniques for making reasonably accurate The OHI-S consists of two components: a Simplified Debris
measurements from radiographs have been developed. Index (DI-S) and a Simplified Calculus Index (CI-S) Each com-
Of historical interest are indices developed by Dunning ponent is assessed on a scale of 0-3. Only a mouth mirror and
and Leach (the Gingival-Bone Count Index), which records a shepherd crook or sickle type dental explorer and no disclos-
the gingival condition on a scale of 0-3 and the level of the ing agent are used for the examination. The six teeth surfaces
crest of the alveolar bone, and a similar index by Sheiham and examined in the OHI-S are the facial surfaces of teeth# 16, 11,
Striffer. The strength of each of these radiographic indices is 26, and 31 and the lingual surfaces of teeth# 36 and 46.
in epidemiologic surveys in which evaluation time is limited Each tooth surface is divided horizontally into gingival,
because of large study populations. middle, and incisal thirds. For the DI-S, a dental explorer is
The Periodontitis Severity Index (PSI) assesses the presence placed on the incisal third of the tooth and moved toward
or absence of periodontitis as the product of clinical inflam- the gingival third according to the criteria in Table 6.5. The
mation (CIS) and interproximal bone loss (BLS) determined DI-S score per person is obtained by totaling the debris score
radiographically using a modified Schei ruler. Due to the need per tooth surface and dividing by the number of surfaces
for periapical radiographs, the PSI is limited to longitudinal examined.
studies and lacks validation. The CI-S assessment is performed by gently placing a den-
tal explorer into the distal gingival crevice and drawing the
Indices Used to Measure Plaque Accumulation
explorer into the distal gingival crevice and drawing it subgin-
In general, most of the indices used to measure plaque accu- givally from the distal contact area to the mesial contact area
mulation utilize a numerical scale to measure the extent of the (one-half of a tooth's circumference is considered a scoring
surface area of a tooth covered by plaque. For these purpos- unit). The criteria for scoring the calculus component of the
es, plaque is defined as a soft, nonmineralized tooth deposit, OHI-S are given in Table 6.5. The CI-S score per person is ob-
which includes debris and materia alba. tained by totaling the calculus scores per tooth surface and di-
viding by the number of surfaces examined. The OHI-S score
Plaque Component of the PDI
per person is the total of the DI-Sand CI-S scores per person.
The first index that attempted to use a numerical scale to as- The clinical levels of oral cleanliness for debris that can be
sess the extent of plaque covering the surface area of a tooth associated with group DI-S scores are as follows:
was developed by Ramfjord. The plaque component of the
PDI is used on the six teeth selected by Ramfjord (teeth #3, Good 0.0-0.6
9, 12, 19, 25, and 28) (teeth 16, 21, 24, 36, 41, and 46) after Fair 0.7-1.8
staining with Bismarck brown solution. The criteria measure Poor 1.9-3.0
6 Epidemiology of Gingival and Periodontal Disease 79
TABLE 6.5 TABLE 6.6
CRITERIA FOR SCORING THE ORAL DEBRIS (DI-S) TURESKY-GILMORE-GLICKMAN MODIFICATION

AND CALCULUS (CI-S) COMPONENTS OF THE OF THE QUIGLEY-HEIN PLAQUE INDEX
SIMPLIFIED ORAL HYGIENE INDEX (OHI-S)
0 = No plaque
Oral Debris Index (D1-S) 1 = Separate necks of plaque at the cervical margin of the tooth
2 = A thin continuous band of plaque (up to 1 mm) at the cervical
0 = No debris or stain present margin
1 = Soft debris covering not more than one-third of the tooth 3 = A band of plaque wider than 1 mm but covering less than one-
surface or the presence of extrinsic stains without other debris, third of the crown
regardless of surface area covered 4 = Plaque covering at least one-third but less than two-third of the
2 = Soft debris covering more than one-third but not more than crown
two-third of the exposed tooth surface 5 = Plaque covering two-third or more of the crown
3 = Soft debris covering more than two-third of the exposed tooth
surface
Calculus Index (CI-S)
0 = No calculus present because of the objective definitions of each numerical score.
1 = Supragingival calculus covering not more than one-third of the The strength of this plaque index is its application to longitu-
exposed tooth surface dinal studies and clinical trials of preventive and therapeutic
2 = Supragingival calculus covering more than one-third but agents. The Turesky-Gilmore-Glickman modification of the
not more than two-third of the exposed tooth surface or the Quigley-Hein criteria is considered one of the two indices of
presence of individual necks of subgingival calculus around choice when assessing plaque in clinical trials.
the cervical portion of the tooth, or both
3 = Supragingival calculus covering more than two-third of the Plaque Index
exposed tooth surface or a continuous heavy band of subgingivai
The Plaque Index (PII) is unique among the indices described
calculus around the cervical portion of the tooth, or both
so far because it ignores the coronal extent of plaque on the
tooth surface area and assesses only the thickness of plaque at
The clinical levels of oral hygiene that can be associated the gingival area of the tooth. Since it was developed as a com-
with group OHI-S scores are as follows: ponent to parallel the GI of Loe and Silness, it examines the
same scoring units of the teeth: distofacial, facial, mesiofacial,
Good 0.0-1.2 and lingual surfaces. A mouth mirror and a dental explorer
Fair 1.3-3.0 are used after air drying of the teeth to assess plaque. Unlike
Poor 3.1-6.0 most indices, the PII does not exclude or substitute for teeth
The importance of the OHI-S is that, like the PI of Rus- with gingival restorations or crowns. Either all or only selected
sell, it has been used extensively throughout the world and teeth may be used in the PII. The criteria for the PII of Silness
has contributed greatly to the understanding of periodontal and Loe are given in Table 6.3.
disease. It was also used in the Ten-State Nutrition Survey 1 The PII score for the area is obtained by totaling the four
NHS, NHANES I, and HHANES. The high degree of correla- plaque scores per tooth. If the sum of the PII scores per tooth
tion (r = 0.82) between the OHI-S and tin PI makes it pos- is divided by four, the PII score for the tooth is obtained. The
sible, if one of the two scores is known, to calculate the other PII score per person is obtained by adding the PII scores per
score with regression analysis. The maJor strength of the OHI- tooth and dividing by the number of teeth examined. The PII
S is its use in epidemiologic surveys and in evaluation of den- may be obtained for a segment of the mouth or a group of
tal health education programs (longitudinal studies). It can teeth in a similar manner.
also evaluate an individual's level of oral cleanliness and can, The strength of the PII is in its application to longitudinal
to a more limited extent, be used in clinical trials. The index is studies and clinical trials. In spite of the studies that have been
easy to use because the criteria are objective, the examination conducted to ensure the reliability of PII data, the assessment
may be performed quickly, and a high level of reproducibility of plaque thickness is so subjective that obtaining valid data
is possible with a minimum of training sessions. requires highly trained and experienced examiners.
Turesky-Cilmore-Clickman Modification of the Other Plaque Indices
Quigley-Hein Plaque Index The Modified Navy Plaque Index records the presence or ab-
In 1962, Quigley and Hein reported a plaque measurement sence of plaque with a score of 1 or 0, respectively, on nine
that focused on the gingival third of the tooth surface. They areas of each tooth surface of the six index teeth used by Ram-
examined only the facial surfaces of the anterior teeth, using a fjord Like the Patient Hygiene Performance (PHP) Index of
basic fuchsin mouthwash as a disclosing agent and a numeri- Podshadley and Haley, the Modified Navy Plaque Index is of
cal scoring system of 0-5. Turesky and coworkers strength- value in assessing health education programs and the ability of
ened the objectivity of the Quigley-Hein criteria by redefining individuals to perform oral hygiene practices.
the scores of the gingival third area. The Turesky-Gilmore- A variation of the Modified Navy Plaque Index is the Distal
Glickman modification of the Quigley-Hein criteria appears Mesia! Plaque Index (DMPI), which places more emphasis on
in Table 6.6. Plaque was assessed on the facial and lingual the gingival and interproximal areas of a tooth. Plaque is one of
surfaces of all of the teeth after using a disclosing agent. A the two factors measured in the Irritants Index, which is a com-
plaque score per person was obtained by totaling all of the ponent of the Gingival Periodontal Index ( GPI) of O'Leary and
plaque scores and dividing by the number of surfaces exam- coworkers. The presence and coronal extent of plaque are scored
ined. This system of scoring plaque is relatively easy to use on a scale of 0-3. Other factors that contribute to the Irritants
Index are supragingival and subgingival calculus and subgingival is used to measure the deposits of calculus on the lingual surfaces
irritants, such as overhanging or deficient restorations. of the six mandibular anterior teeth. The Probe Method of Cal-
culus Assessment has been shown to possess a high degree of
PHP Index inter- and intraexaminer reproducibility. However, extensive
Patient Hygiene Performance index (PHP) by Podshadley and training under an experienced investigator is required to master it.
Haley was the first index developed for the sole purpose of
assessing an individual's performance in removing debris after Calculus Surface Index
toothbrushing instruction. It records the presence or absence The Calculus Surface Index (CSI) is one of two indices that
of debris as 1 or 0, respectively, using the six surface of the are used in short-term (eg, less than 6 weeks) clinical trials of
six OHI-S teeth. The PHP Index is more sensitive than the calculus-inhibiting agents. The objective of this type of study
OHI-S because it divides each tooth surface into five areas: is to determine rapidly whether a specific agent has any effect
three longitudinal thirds, with the middle third subdivided on reducing or preventing supragingival or subgingival calcu-
horizontally into thirds. Scoring is preceded by the use of a lus. The CSI assesses the presence or absence of supragingival
disclosing agent. The index is easy to use because its criteria and/or subgingival calculus on the four mandibular incisors.
are dichotomous and it can be performed quickly. Its value The index has also been applied to the six mandibular anterior
hes chiefly in its application to individual patient education. teeth. The presence or absence of calculus is determined by
Two other indices with a similar purpose that also use di- visual examination or by tactile examination using a mouth
chotomous criteria are the Plaque Control Record and the mirror and a sickle-type dental explorer.
plaque portion of the Bleeding Points Index. A companion index to the CSI is the Calculus Surface Se-
Bjorby and Loe developed a Retention Index that not only verity Index (CSSI). The CSSI measures the quantity of calcu-
examined supragingival and subgingival calculus but also lus present on the surfaces examined for the CSI.
grossly assessed dental caries and the quality of the margins of
restorations. Collectively, all of these variables were scored on Marginal Line Calculus Index
a numerical scale of 0-3. A second index that is frequently used in short-term clini-
cal trials of anticalculus agents is the Marginal Line Calculus
Index (MLCI). This index was developed to assess the accu-
Indices Used to Measure Calculus
mulation of supragingival calculus on the gingival third of the
In general, the indices used to assess calculus may be conve- tooth or, more specifically, supragingival calculus along the
niently divided into those that are most appropriate to epiderni- margin of the gingiva.
ologic surveys; those that are appropriate to longitudinal studies,
with an examination every 3-6 months; and those that are used Calculus Index Used by NIDR
in short-term clinical studies, usually no longer than 6 weeks. The NIDR uses a three-point ordinal scale for the assessment
of calculus (see Table 64) Unlike the NIDR gingival assess-
Calculus Component of the Simplified Oral Hygiene ment, the Calculus Index assigns only one score per tooth,
Index after examining both the mid-buccal and mesial-bussal inter-
The Simplified Calculus Index (CI-S) component of the OHI-S proximal sites, on one-half of the maxillary and one-half of
was previously discussed with indices used to measure plaque the contralateral mandibular arch. As in the gingival assess-
accumulation because it is less separable from the combined ment, the decision to start at either the right or left half of the
scoring system than are any of the other indices that include maxillary is made randomly. Both sites are examined for the
several component measures. The value of the CI-S compo- presence and extent of calculus (with either the NIDR peri-
nent is its application to epidemiologic surveys and longitu- odontal probe or a no. 17 dental explorer) after all of the teeth
dinal studies of periodontal disease. Table 6.5 presents the in one-half of an arch are air dried. The Calculus index score
specific criteria of the OHI-S used to assess calculus. is obtained by dividing the score for each tooth by the number
of teeth examined.
Calculus Component of the Periodontal Disease Index
The calculus component of the PDI assesses the presence and Indices Used to Assess Treatment Needs
extent of calculus on the facial and lingual surfaces of Ram-
fjord's six index teeth (ie, teeth #16, 21, 36, 41, 44, and 46) Interpretations of the indices described in this section are to
on a numerical scale of 0-3. A mouth mirror and a dental be viewed with caution because of the difficulty that exists
explorer and/or a periodontal probe are used in the examina- concerning the estimation of treatment need. Without know-
tion. The criteria for assigning a score to each tooth surface ing the response of the periodontal tissues to phase 1 or initial
for the calculus component of the PDI are given in Table 6.2. therapy, any estimate of treatment needs may be subject to
The calculus scores per tooth are totaled and then divided over- or underestimation of what is clinically prudent.
by the number of teeth examined to yield the calculus score
per person. Like the CI-S of the OHI-S, the calculus compo- CPI
nent of the PDI has a high degree of examiner reproducibility, The GPI is a modification of the PDI of Ramfjord for the
can be performed quickly, and has its best application in epi- purpose of screening persons to determine who needs peri-
demiologic surveys and longitudinal studies. odontal treatment. The GPI assesses three components of
periodontal disease: gingival status, periodontal status (crev-
Probe Method of Calculus Assessment ice depth); and, collectively materia alba, calculus, and over-
The Probe Method of Calculus Assessment was developed for hanging restorations. The latter triad is independently called
longitudinal studies of the quantity of supragingival calculus the Irritation Index. Only the criteria for the gingival status
formed. A periodontal probe graduated in millimeter divisions component are described.
6 Epidemiology of Gingival and Periodontal Disease 81
TABLE 6.7
CRITERIA FOR THE PERIODONTAL TREATMENT NEED SYSTEM (PTNS) CLASSIFICATION

PTNS Classification Unit Plaque Calculus and/or Overhangs Inflammation Pocket Depth
Class 0 Mouth No No No Not considered
Class A Mouth Yes No Yes ~5mm
Class B Quadrant Yes Yes Yes <5mm
Class C Quadrant Yes Yes Yes >5mm
(Adapted [rom Johansen JR, Gjermo P, Bellini HT: A system to classify the need for periodontal treatment. Acta Odontol Scand 31: 297, 1973, by permission of Scandina-
vian Univasity Press.)
The maxillary and mandibular arches are each divided into Periodontal Treatment Need System
three segments: the six anterior teeth, the left posterior teeth, The next index to evolve with the purpose of assessing treat-
and the right posterior teeth. The primary objective in using ment needs was the Periodontal Treatment Need System
the index is to determine the tooth or surrounding tissues (PINS), which has been used with interesting results. It at-
with the severest condition within each of the six segments. tempts to place individuals into one of four classes based on
Each segment is assessed for each of the three components of treatment procedures relative to time requirements. It consid-
periodontal disease described previously The specific criteria ers the presence or absence of gingivitis and plaque and the
for the gingival status component of the GPI are as follows: presence of pockets 5 mm or deeper in each quadrant of the
0 = tissue tightly adapted to the teeth; firm consistency with mouth, as shown in Table 6.7.
physiologic architecture. Community Periodontal Index ofTreatment Needs
1 = slight to moderate inflammation, as indicated by changes
in color and consistency, involving one or more teeth in In 1977, the WHO appointed an expert committee to re-
the same segment but not completely surrounding any one view the methods available to review periodontal status and
tooth. treatment needs. The index that resulted after extensive field
2 = the aforementioned changes either singly or combined testing by investigators from the WHO and the International
completely encircling one or more teeth in a segment. Dental Federation (FDI) was called the Community Periodon-
3 = marked inflammation, as indicated by loss of surface tal Index of Treatment Needs (CPITN). The CPITN was "pri-
continuity (ulceration), spontaneous hemorrhage, loss of marily designed: assess periodontal treatment needs rather
faciolingual continuity or any interdental papilla, marked than pet status." Combining elements of the GPI and PINS
deviation from normal contour (such as gross thickening or CPITN assesses the presence or absence of gingival bleeding
enlargement covering more than one-third of the anatomic on gentle probing; the presence or absence of supragingival
crown), recession, and clefts. or subgingival calculus; and the presence or absence of peri-
odontal pockets, subdivided into shallow and deep. A spe-
The area with the highest score determines the gingival cially designed periodontal probe with a 0.5-mm ball tip and
score for the entire segment, and the gingival status for the gradations corresponding to shallow and deep pocket was de-
mouth is obtained by dividing the sum of the gingival scores veloped to probe for bleeding and calculus and to determine
by the number of segments. pocket depth. In epidemiologic surveys, 10 index teeth are
The GPI has been used extensively in military populations. examined, but only the worst finding from the index teeth
Unlike the traditional indices used in epidemiology (which is recorded of individual patients, only the worst finding
attempt primarily to assess the status of a specific disease con- from all of the teeth in a sextant is recorded, resulting in six
dition, with only the crudest suggestion of determining treat- scores. The CPITN criteria for determining periodontal status
ment needs), the GPI was developed for the specific purpose and the corresponding treatment needs to appear in Table 6.8.
of detecting periodontal disease early so that treatment may be Each subject or sextant of teeth is classified according to one
instituted promptly of the treatment needs.
TABLE 6.8
CRITERIA FOR THE COMMUNITY PERIODONTAL INDEX OF TREATMENT NEEDS

Periodontal Status Treatment Needs
0 = Healthy periodontium 0 = No treatment needed
1 = Bleeding observed, directly or by using mouth mirror, after sensing I = Oral hygiene needs improvement
2 = Calculus felt during probing, but the entire black area" of the probe is visible II = I + professional scaling
3 = Pocket 4 or 5 mm (giving margin is situated on black area" of probe) II = I + profession scaling
4 = Pocket > 6 mm (black area' of probe not visible) Ill = I + II + complex treatment"
'Portion of probe between 3.5 and 5.5 mm.

"Complex treatment may require scaling and root planning under local anesthesia, with or without surgical exposure for access.
TABLE 6.9
CODES AND CRITERIA FOR COMMUNITY PERIODONTAL INDEX

Code Criteria for Periodontal Status Code Criteria for Loss of Attachment
0 Healthy 0 Loss of attachment 0-3 mm (CEJ not visible and CPI

score 0-3)
Bleeding observed, directly or by using a mouth mirror, Loss of attachment 4-5 mm (CEJ within the black band)
after probing
2 Calculus detected during probing, but all of the black 2 Loss of attachment 6-8 mm (CEJ between the upper limit
band on the probe visible of the black band and the 8.5-mm ring)
3 Pocket 4-5 mm (gingival margin within the black band 3 Loss of attachment 9-11 mm (CEJ between the 8.5 and
on the probe) 11.5-mm rings).
4 Pocket 6 mm or more (black band on the probe not 4 Loss of attachment 12 mm or more
visible)
X Excluded sextant (less than two teeth present) X Excluded sextant ( <2 teeth)
9 Not recorded 9 Not recorded (CEJ neither visible nor detectable
The value of the CPITN is that it permits rapid examination When the CEJ is not visible and the highest CPI score for
of a population to determine periodontal treatment needs. How- a sextant is less than 4 (probing depth less than 6 mm), any
ever, a lot of effort is expended and a great deal of useful infor- loss of attachment for that sextant is estimated to be less than
mation is lost when only the worst score per sextant is recorded. 4 mm (loss of attachment score= 0). The extent of loss of at-
tachment is recorded using the following codes (Table 6.9).
To ensure the reliability of periodontal indices, all studies
Community Periodontal Index should incorporate measures of reliability into the study de-
This index is a modification of the CPITN. The modification is sign. Since there is no agreement as to the best statistical meth-
done by the inclusion of measurement of "loss of attachment" od for describing reliability, several methods should be used.
and elimination of the "treatment needs" category A mouth
mirror along with Community Periodontal Index (CPI) probe REFERENCES
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Selection of Teeth
SUGGESTED READINGS
Teeth are selected as
Burt BA, Eklund SA: Dentistry, dental practice and the community, ed 6,
• Index teeth (upto 19 years)-16, 11, 26, 36, 31, 46 Philadelphia, 2005, Elsevier.
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Loe H, Silness P: Periodontal disease in pregnancy, Acta Odontol Scand 21 :533,
37, 36,31,46,47 1963.
Loe H: The gingival index the plaque index and the retention index systems,
J Periodontal 38:610-616, 1967.
Loss of Attachment Massler M: The P-M-A index for assessment of ginigivitis, J Periodontal
38:592, 1967.
Information on loss of attachment may be collected from in- Muhlemann HR, Son S: Gingival sulcus bleeding-a leading symptom in ini-
dex teeth. The most reliable way of examining loss of attach- tial gingivitis, Helvetia Odontologica Acta 15: 107, 1971.
ment in each sextant is to record this immediately after re- Rarnfjord SP: The periodontal disease index,] Periodontol 38:602, 1967.
cording the CPI score for that particular sextant. The highest Turesky S, Gilmore ND, Glickman l: Reduced plaque formation by the chlo-
romethyl analogue of Vitamin C,J Periodontol 41:41-43, 1970.
scores for CPI and loss of attachment may not necessarily be Volpe AR: Indices for measurement of hard deposits in clinical studies of oral
found on the same tooth in a sextant. hygiene and periodontal disease,] Periodontal Res 9(Suppl 14):31, 1974.
Loss of attachment should not be recorded for children un- World Health Organization: Orn/ health surveys; Basic methods, ed 4, Gemeva,
der the age of 15. 1997, WHO.
6 Epidemiology of Gingival and Periodontal Disease 82.e1
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dex. Comparison with Gingival Index during the resolution of gingivitis,
1. Abdellatif HM, Burt BA: An epidemiological investigation into the rela-
tive importance of age and oral hygiene status as determinants of peri-
J P,·ev Dent 6:135, 1980.
17. Beagrie GS, James GA: The association of posterior tooth irregularity and
odontitis, J Dent Res 66:13, 1987.
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2. Adams RA, Nystrom GP: A periodontitis severity index, J Pe,iodontol
18. Beck JD, Loe H: Epidermiological principles in studying periodontal dis-
57:176, 1986.
eases, Periodontology 2000(2):34, 1993.
3. Addy M, Griffiths D, Dummer P, et al: The distribution of plaque and
19. Bellini HT: A system to determine the periodontal therapeutic needs of a
gingivitis and the influence of toothbrushing hand in a group of South
population. Oslo, 1973, Universitetsforlagets trykningssentral.
Wales 11-12 year old children,] Clin Periodontol 14:564, 1987.
20. Bellini HT, Gjermo P: Application of the Periodontal Treatment Need Sys-
4. Agerholm OM, Sidi AD: Reasons given for extraction of permanent teeth by
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Dent Oral Epidemiol 1:22, 1973.
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SECTION Ill
Section Outline
7 Periodontal Pathogenesis 10 The Role of Dental Calculus and
8 Biofilm and Periodontal Microbiology Other Predisposing Factors
9 Microbial Interactions with the Host 11 Smoking and Periodontal Disease
in Periodontal Diseases 12 Influence of Systemic Conditions
7
Periodontal Pathogenesis
PM Preshaw • N Ambalavanan
Chapter Outline
Inflammatory Responses in the Immune Responses in Periodontal
Periodontium Pathogenesis
Linking Pathogenesis to Clinical Signs Cells of Immunity and Inflammation
of Disease Concept of Host Susceptibility
Resolution of Inflammation
Periodontal disease is complex in nature. It is a multifactorial is partly embedded within the body (within connective tis-
disease, which is largely influenced by genetic, environmental, sue), crosses an epithelial surface, and is partly exposed to
and microbial factors. Pathogenesis is defined as "the origina- the outside world (within the confines of the mouth). The
tion and development of a disease." Knowledge of pathogen- bacteria that colonize this surface are effectively outside of the
esis helps us to understand about the processes that lead to body (although they are in the subgingival crevice), yet the in-
the development of this disease and consequently the changes flammatory response that develops is located within the body.
it produces in the structure and function of the periodontium. These factors add complexity to our understanding of the role
In broad terms, the pathogenesis of a disease is the mecha- of the biofilm and the immune-inflammatory responses that
nism by which a causative factor or factors cause the disease. are part of periodontal tissue breakdown.
Periodontal disease results from a complex interplay
between the subgingival biofilm and the host immune- Inflammatory Responses in the
inflammatory events that develop in the gingival and peri-
odontal tissues in response to the challenge presented by the Periodontium
bacteria. It is generally accepted that gingivitis precedes peri- It is now clear that the great majority of the tissue breakdown
odontitis, but it is clear that not all cases of gingivitis progress in periodontal disease results from the host's inflammatory pro-
to periodontitis. With gingivitis, the inflammatory lesion is cesses. The bacteria are important because they initiate and per-
confined to the gingiva; however, with periodontitis, the in- petuate the inflammation, but they are only directly responsible
flammatory processes extend to additionally affect the peri- for a relatively small proportion of the tissue damage that occurs.
odontal ligament and the alveolar bone. The net result of these
inflammatory changes is the breakdown of the fibers of the Microbial Virulence Factors
periodontal ligament, resulting in clinical loss of attachment
together with resorption of the alveolar bone. The subgingival biofilm initiates and perpetuates inflamma-
Periodontal disease is a unique clinical entity. With most tory responses in the gingival and periodontal tissues. The
infections, a single infective organism causes the disease (eg, subgingival bacteria also contribute directly to tissue dam-
human immunodeficiency virus/acquired immunodeficiency age by the release of noxious substances, but their primary
syndrome, syphilis, tuberculosis), and the identification of importance in periodontal pathogenesis is that of activating
that organism provides the basis for the diagnosis. With peri- immune-inflammatory responses that in turn result in tissue
odontal disease, a large number of species are identifiable in damage, which may well be beneficial to the bacteria located
the periodontal pocket, and many more are as yet unknown within the periodontal pocket by providing nutrient sources.
because they have not been cultured. It is impossible to con- Microbial virulence factors that are important in these pro-
clude that a single species or even a group of species causes cesses are as follows:
periodontal disease. Many of the species that are considered
important in periodontal pathogenesis may simply reside in Lipopolysaccharide
deep pockets because the pocket is a favorable environment in Lipopolysaccharides (LPSs) are large molecules composed of
which they can survive (ie, it is warm, moist, and anaerobic, a lipid component (lipid A) and a polysaccharide component.
with a ready supply of nutrients). Many of the unique features They are found in the outer membrane of Gram-negative
of periodontitis are derived from the anatomy of the peri- bacteria, they act as endotoxins (LPSs are frequently referred
odontium, in which a hard, nonshedding surface (the tooth) to as endotoxins), and they elicit strong immune responses.
85
LPSs triggers a series of intracellular events, the net result of cocci, filaments, and rods) have been identified in the inter-
which is the increased production of inflammatory mediators cellular spaces of the epithelium. Periodontal pathogens such
(most notably cytokines) and the differentiation of immune as P gingivalis and Aggregatibacter actinomycetemcomitans have
cells (eg, dendritic cells) for the development of effective im- been reported to invade the gingival tissues, including the
mune responses against the pathogens. connective tissues. Fusobacterium nucleatum can invade oral
It is important to remember that a component of Gram- epithelial cells, and bacteria that routinely invade host cells
positive cell walls, lipoteichoic acid, also stimulates immune may facilitate the entry of noninvasive bacteria by coaggregat-
responses although less potently than LPSs. Both LPSs and ing with them (Fig. 7 .1)
lipoteichoic acid are released from the bacteria present in the The reports of bacteria present in the tissues have some-
biofilm and stimulate inflammatory responses in the tissues, times been used to justify the use of antibiotics for the treat-
thereby resulting in increased vasodilation and vascular per- ment of periodontitis as a means of attempting to eliminate
meability, the recruitment of inflammatory cells by chemo- those organisms that are located in the tissues and that are
taxis, and the release of proinflammatory mediators by the therefore "protected" from mechanical disruption by root sur-
leukocytes that are recruited to the area. LPSs in particular are face debridement. It has also been reported that bacteria in the
of key importance for initiating and sustaining inflammatory tissues may represent a "reservoir for reinfection" after non-
responses in the gingival and periodontal tissues. surgical management.
Bacterial Enzymes and Noxious Products Fimbriae

Plaque bacteria produce a number of metabolic waste prod- The fimbriae of certain bacterial species, particularly
ucts that contribute directly to the tissue damage. These in- P gingivalis, may also play a role in periodontal pathogenesis.
clude noxious agents such as ammonia (NH3) and hydrogen P gingivalis fimbriae stimulate immune responses, such as IL-6
sulfide (H2S) as well as short-chain carboxylic acids such as secretion leading to sustained inflammation. Bacterial fimbri-
butyric acid and propionic acid. These substances have pro- ae are therefore important for modifying and stimulating im-
found and harmful effects on host. mune responses in the periodontium.
Plaque bacteria produce proteases, which are capable of
breaking down structural proteins of the periodontium such Bacterial Deoxyribonucleic Acid and Extracellular
as collagen, elastin, and fibronectin. Bacteria produce these Deoxyribonucleic Acid
proteases to digest proteins and thereby provide peptides for Bacterial DNA stimulates immune cells. Extracellular DNA
bacterial nutrition. Bacterial proteases disrupt host responses, (eDNA) is likely to play a role in the development and struc-
compromise tissue integrity, and facilitate the microbial inva- ture of the biofilms formed by oral bacteria, and it has been
sion of the tissues. For example, Porphyromonas gingivalis pro- identified as an important component of the matrix in a num-
duces two classes of cysteine proteases known as gingipains that ber of bacterial biofilms. It has been demonstrated that DNA
have been implicated in periodontal pathogenesis. isolated from P gingivalis, A. actinomycetemcomitans, and Pep-
tostreptococcus micros stimulates macrophages and gingival
Microbial Invasion fibroblasts to produce proinflammatory cytokines such as
Microbial invasion of the periodontal tissues has long been a TNF-a and IL-6 in a dose-dependent manner which could
contentious topic. In histologic specimens, bacteria (including contribute to periodontal pathogenesis.
FIGURE 7.1 Invasion of epithelial cells by Fusobacterium nuc/eatum. In both images, a single epithelial cell is shown being penetrated by invading
F. nuc/eatum bacteria; three or four bacteria are evident in A, and one bacterium is evident in B. A, The ruffled surface of the epithelial cells (multiple
small fingerlike projections that are much smaller than the F. nuc/eatum bacteria) is likely to be an artifact. B, F. nuc/eatum may facilitate the coloniza-
tion of epithelial cells by bacteria that are unable to adhere or invade directly as evidenced by the single coccoid bacterium (Streptococcus cristatus)
that has coaggregated with the F. nuc/eatum bacterium as it penetrates the epithelial cell. (Courtesy A and B, Dr Edwards AE, Imperial College, London,
Ors Rudney JD, Crossman TJ, Bath University, UK and the University of Minnesota, US.)
7 Periodontal Pathogenesis 87
Host-Derived Inflammatory Mediators Antiinflammatory Cytokines

The balance between proinflammatory and antiinflammatory
The inflammatory and immune processes that develop in the
periodontal tissues in response to the long-term presence of the events is crucial for determining disease progression. Some of
subgingival biofilm are protective by intent but result in con- the antiinflammatory cytokines include ll-10, TGF-~, ll-lRa
(IL-1 Receptor antagonist).
siderable tissue damage. This has sometimes been referred to as
bystander damage, which denotes that the host response is main- Prostaglandins
ly responsible for the tissue damage that occurs, thereby leading
The prostaglandins (PGs) are a group of lipid compounds
to the clinical signs and symptoms of periodontal disease.
Having understood that the majority of the tissue dam- derived from arachidonic acid, a polyunsaturated fatty acid
age in periodontitis is derived from the excessive and dys- found in the plasma membrane of most cells. Arachidonic
regulated production of a variety of inflammatory mediators acid is metabolized by cyclooxygenase-1 and -2 (COX-1 and
COX-2) to generate a series of related compounds called the
and destructive enzymes in response to the presence of the
prostanoids, which includes the PGs, the thromboxanes and
subgingival plaque bacteria, it is important to review the key
the prostacyclins. PGs are important mediators of inflamma-
types of mediators that orchestrate the host responses. These
can be broadly divided into the cytokines, the prostanoids, tion, particularly prostaglandin E2 (PGE2), which results in
and the matrix metalloproteinases (MMPs). vasodilation and induces cytokine production by a variety of
cell types. COX-2 is upregulated by ll-1~, INF-a, and bacte-
Cytokines rial LPS, resulting in increased production of PGE2 in inflamed
tissues. PGE2 is produced by various types of cells and most
Cytokines play a fundamental role in inflammation, and they significantly in the periodontium by macrophages and fibro-
are key inflammatory mediators in periodontal disease. They blasts. PGE2 results in the induction of MMPs and osteoclastic
are soluble proteins, and they act as messengers to transmit bone resorption, and it has a maJor role in contributing to the
signals from one cell to another. Cytokines are effective in very tissue damage that characterizes periodontitis.
low concentrations, they are produced transiently in the tis-
sues, and they primarily act locally in the tissues in which Matrix Metalloproteinases
they are produced. Cytokines are able to induce their own ex- MMPs are a family of proteolytic enzymes that degrade extra-
pression in either an autocrine or paracrine fashion, and they cellular matrix molecules such as collagen, gelatin, and elastin
have pleiotropic effects (ie, multiple biologic activities) on a (Table 7 1) They are produced by a variety of cell types, in-
large number of cell types. (Autocrine signaling means that cluding neutrophils, macrophages, fibroblasts, epithelial cells,
the autocrine agent [in this case cytokines] binds to receptors osteoblasts, and osteoclasts. MMPs can be divided into colla-
on the cell that secreted the agent, whereas paracrine signaling genases, gelatinases/type IV collagenases, stromelysins, matri-
affects other nearby cells.) Simply put, cytokines bind to cell lysins, membrane-type metalloproteinases, and others.
surface receptors and trigger a sequence of intracellular events Key inhibitors of MMPs found in the serum include the
that lead ultimately to the production of protein by the target glycoprotein a1-antitrypsin and a2-macroglobulin, a large
cell, which alters that cell's behavior and could result in, for plasma protein produced by the liver that is capable of in-
example, the increased secretion of more cytokines in a posi- activating a wide variety of proteinases. Inhibitors of MMPs
tive feedback cycle that leads to inflammation. that are found in the tissues include the tissue inhibitors of
Cytokines are produced by a large number of cell types, metalloproteinases (TIMPs), which are produced by many cell
including infiltrating inflammatory cells (eg, neutrophils, mac- types; the most important in periodontal disease is TIMP-1.
rophages, lymphocytes) as well as resident cells in the peri- MMPs are also inhibited by the tetracycline class of antibiot-
odontium (eg, fibroblasts, epithelial cells). Cytokines signal, ics, which has led to the development of a subantimicrobial
broadcast, and amplify immune responses, and they are fun- formulation of doxycycline as a licensed systemic adjunctive
damentally important for regulating immune-inflammatory drug treatment for periodontitis that exploits the anti-MMP
responses and for combating infections. However, they also properties of this molecule.
have profound biologic effects that lead to tissue damage with
chronic inflammation; the prolonged and excessive produc-
tion of cytokines and other inflammatory mediators in the Linking Pathogenesis to Clinical Signs
periodontium leads to the tissue damage that characterizes of Disease
the clinical signs of the disease. For example, cytokines medi-
ate connective tissue and alveolar bone destruction through Advanced forms of periodontal disease are characterized by
the induction of fibroblasts and osteoclasts to produce proteo- the distressing symptoms of tooth mobility and tooth migra-
lytic enzymes (ie, MMPs) that break down structural compo- tion. These result from the loss of attachment between the
nents of these connective tissues. tooth and its supporting tissues after the breakdown of the
Cytokines play a key role at all stages of the immune re- inserting fibers of the periodontal ligament and the resorption
sponse in periodontal disease. Some of the important proof alveolar bone.
inflammatory cytokines are IL-la, IL-1~, IL-6, and INF-a. When the bacterial challenge persists, the cellular and flu-
These cytokines play a key role in the initiation, regulation, id infiltrate continues to develop, and neutrophils and other
and perpetuation of innate immune responses in the peri- inflammatory cells soon occupy a significant volume of the
odontium, thereby resulting in vascular changes and the mi- inflamed gingival tissues. Neutrophils are key components
gration of effector cells such as neutrophils into the periodon- of the innate immune system, and they play a fundamental
tium as part of a normal immune response to the presence of role in maintaining periodontal health, despite the constant
subgingival bacteria. challenge presented by the plaque biofilm. Neutrophils are
TABLE 7.1
BIOLOGIC ACTIVITIES OF SELECTED MATRIX METALLOPROTEINASES RELEVANT TO PERIODONTAL DISEASE

MMPType Enzyme Biologic Activity
Collagenases MMP-1,8,13 Degrade interstitial collagens (types I, 11, and lll)
Digest ECM and non-ECM molecules
MMP-1 Keratinocyte migration and reepithelialization
Platelet aggregation
MMP-13 Osteoclast activation
Gelatinases MMP-2,9 Degrade denatured collagens and gelatin
MMP-2 Differentiation of mesenchymal cells with inflammatory phenotype
Epithelial cell migration
Increased bioavailability of MMP-9
Stromelysins MMP-3,10,11 Digest ECM molecules
MMP-3 Activates pro-MMPs
Disrupted cell aggregation
Increased cell invasion
Matrilysins MMP-7 Disrupted cell aggregation
Increased cell invasion
Membrane-type MMPs MMP-14,15,16,17,24,25 Digest ECM molecules
Activate pro-MMP-2 (except MT4-MMP)
MTl-MMP Epithelial cell migration
Degrade collagen types I, 11, and lll
ECM, Extracellular matrix; MMPs, matrix metalloproteinases; MT, membrane type.
(Adapted from Hannas AR, Paeirn]C, Granjeirn JM, et al.· Acta Odontol Scand 65:1-13, 2007.)
protective leukocytes that phagocytose and kill bacteria, and Attempts at effective oral hygiene are rendered more difficult
deficiencies in neutrophil functioning result in increased by the deepening of the pocket, and the cycle continues.
susceptibility to infections in general, as well as periodontal
disease. Neutrophils also release large quantities of destruc-
Alveolar Bone Resorption
tive enzymes (eg, MMPs) as they migrate through the tissues
(particularly MMP-8 and MMP-9), which results in the break- As the advancing inflammatory front approaches the alveolar
down of structural components of the periodontium and the bone, osteoclastic bone resorption commences. This is a protec-
development of collagen-depleted areas. Neutrophils also re- tive mechanism to prevent bacterial invasion of the bone, but it
lease their potent lysosomal enzymes, cytokines, and reactive ultimately leads to tooth mobility and even tooth loss. The resorp-
oxygen species (ROS) extracellularly, thereby causing further tion of alveolar bone occurs simultaneously with the breakdown
tissue damage. Neutrophil hyperactivity in periodontitis has of the periodontal ligament in the inflamed periodontal tissues.
also been suggested, which leads to the overproduction of Histologic studies have confirmed that the bone resorbs
damaging ROS and other mediators. so that there is always a width of noninfiltrated connective
The very first step in the development of the pocket re- tissue of about 0.5-1.0 mm overlying the bone. It has also
sult from a combination of factors, including the detachment been demonstrated that bone resorption ceases when there
of cells at the coronal aspect of the junctional epithelium, is at least a 2.5-mm distance between the site of bacteria in
whereas those at the apical aspect migrate apically into the the pocket and the bone. Osteoclasts are stimulated by pro-
collagen-depleted areas; intraepithelial cleavage occurs within inflammatory cytokines and other mediators of inflammation
the junctional epithelium. Epithelial tissues do not have their to resorb the bone, and the alveolar bone "retreats" from the
own blood supply and must rely on the diffusion of nutri- advancing inflammatory front. Osteoclasts are multinucleated
ents from the underlying connective tissues. Thus, as the epi- cells that are formed from osteoclast progenitor cells and mac-
thelium proliferates and thickens, necrosis of epithelial cells rophages, and osteoclastic bone resorption is activated by a
that are more distant from the connective tissues can lead to variety of mediators (eg, IL-lP, INF-a, IL-6, PGE2).
intraepithelial clefts and splits, which also contribute to the
early stages of pocket formation. Resolution of Inflammation
A cycle of chronic inflammation is therefore established in
which the presence of subgingival bacteria drives inflamma- Inflammation is an important defense mechanism to combat
tory responses in the periodontal tissues; this is characterized the threat of bacterial infection, but inflammation also results
by the infiltration by leukocytes, the release of inflammatory in tissue damage associated with the development and progres-
mediators and destructive enzymes, connective tissue break- sion of most chronic diseases associated with aging, including
down, and the breakdown and proliferation of the epithelium periodontal disease. It is becoming evident that the resolution
in an apical direction. The junctional and pocket epithelium of inflammation (ie, turning off inflammation) is regulated by
becomes thin and ulcerated and bleeds more readily, which specific mechanisms that restore homeostasis. It is possible
results in more bleeding with probing. The bacteria in the that controlling or augmenting these mechanisms may lead
pocket are never fully eliminated because they are effectively to the development of new treatment strategies for managing
outside of the body, but their continued presence drives the chronic diseases such as periodontitis, and the mechanisms
destructive inflammatory response in the periodontal tissues. that regulate resolution of inflammation have begun to be
identified. The resolution of inflammation results in a return to fundamental form of specific adaptive immunity referred to as
homeostasis, and it is mediated by specific molecules, includ- the specific immune response. The ability of T cells and B cells
ing a class of endogenous, proresolving lipid mediators that in- to recognize specific oligomeric structures on a pathogen and
cludes the lipoxins, resolvins, and protectins. These molecules generate progeny that also recognize the structure enables the
are actively synthesized during the resolution phases of acute immune system to respond more rapidly and effectively when
inflammation; they are antiinflammatory, and they inhibit neu- reexposed to that same pathogen.
trophil infiltration.
Cells of Immunity and Inflammation
Immune Responses in Periodontal
Cells of the immune system that are important in inflamma-
Pathogenesis tion and host defenses include mast cells, dermal dendro-
Immune responses are categorized as either innate or adap- cytes (histiocytes), peripheral dendritic cells, neutrophils,
tive. Innate immune responses may adapt with exposure to monocytes/macrophages, T cells, B cells, and natural killer
the same pathogen but subside once the threat has been elimi- (NK) cells (Fig. 7 2) Other hematopoietic leukocytes, in-
nated. An example of innate immunity is phagocytic cells (ie, cluding basophils, eosinophils, erythrocytes, and platelets,
monocytes, macrophages, neutrophils), which possess a num- also participate in certain forms of inflammation or immune
ber of inherently antimicrobial peptides and proteins that kill function.
many different pathogens rather than one specific pathogen. Cells possess receptors, which are molecules on the cell
In contrast, the specific immune responses will increase after surfaces that enable the cell to interact with other molecules
exposure to a pathogen and usually maintain higher levels for or cells. Receptors reflect and dictate the function of cells.
years. Lymphocytes (eg, T cells, B cells) are important in the Historically, the names given to receptors are often related to
Tissues
Blood
@
@:Kcm1,
·y1
Bone marrow
Pre-Tcell
Lymphoid
Multi potent
stem cell
I ·
Basophil
~ stem cell (;::\ Myeloid
~ w--\Q)-.."'m""....+@
T cell /~
./ ,
@ Eoslnophil
@
. M~
~
Activated
Tcell
©
Erythrocyte ~
egakaryocyte
@ l>,
(Q) Lymph
Node
~
Plasmacyte ~ Afferent lymphatics Peripheral Macrophage
dendritic cell
FIGURE 7.2 The main cells of the immune system are derived from the lymphoid and myeloid arms of the hematopoietic system. In the bone
marrow, the myeloid arm gives rise to peripheral dendritic cells (DCs), phagocytes (neutrophils and monocytes), mast cell precursors, basophils,
eosinophils, platelets, and erythrocytes. In the tissues, peripheral DCs, monocytes, and mast cell precursors further differentiate. The monocyte can
become a macrophage. In the bone marrow, the lymphoid arm gives rise to natural killer (NK) cells, B cells, and pre-T cells. The pre-T cells differenti-
ate to T cells in the thymus. Secondary lymphoid organs, including lymph nodes and the spleen, are areas where antigen-presenting cells, B cells, and
DCs present antigen to T cells. Terminal differentiation of B and T cells also occurs in these organs.
function. In addition to these common names, a systematic fail to eliminate infection (eg, in the susceptible host), then
nomenclature known as the CD (cluster of differentiation) has the effector cells of adaptive immune response (lympho-
been developed. cytes) are activated.
The immune system is essential for the maintenance of
periodontal health, and it is central to the host response to Saliva
periodontal pathogens. However, if the immune response is Saliva that is secreted from the three major salivary glands
dysregulated, inappropriate, persistent, or excessive in some (ie, parotid, submandibular, and sublingual) as well as from
way, then damaging chronic inflammatory responses such the numerous minor salivary glands has an important role in
as those observed with periodontal disease can ensue. It is the maintenance of oral and dental health. The action of shear
now widely appreciated that immune responses are complex forces associated with saliva flow is important for preventing
biologic networks in which pathogen recognition, innate im- the attachment of bacteria to the dentition and the oral muco-
munity, and adaptive immunity are integrated and mutually sa! surfaces. Human saliva also contains numerous molecular
dependent. components that contribute to host defenses against bacterial
We need to understand how the polymicrobial plaque colonization and periodontal disease (Table 7.2). These com-
biofilm (as opposed to individual species of periodontal ponents include molecules that nonspecifically inhibit the for-
pathogens) interacts with host immune defenses. We also mation of the plaque biofilm by inhibiting adherence to oral
need to appreciate specific immunologic properties that surfaces and promoting agglutination (eg, mucins), those that
relate to the unique anatomy of the periodontium; to under- inhibit specific virulence factors (eg, histatins that neutralize
stand how immune responses contribute to the dynamic as- LPS), and those that inhibit bacterial cell growth (eg, lacto-
pects of periodontal disease and its various clinical courses; ferrin) and that may induce cell death. Saliva also contains
and to gain a comprehension of how elements of host im- specific immunoglobulin A (IgA) antibodies to periodontal
munity contribute to tissue destruction, resolution, repair, pathogens that target specific antigens and that inhibit bacte-
and regeneration. rial adherence.
Epithelial Tissues
Innate Immunity
The epithelial tissues play a key role in host defense, because
Defenses against infection include a wide range of mechani- they are the main site of the initial interactions between
cal, chemical, and microbiologic barriers that prevent patho- plaque bacteria and the host, and they are also the site of the
gens from invading the cells and tissues of the body. Saliva, invasion of microbial pathogens. The epithelium of the sul-
GCF, and the epithelial keratinocytes of the oral mucosa, all cular and gingival epithelial tissues provides protection for
protect the underlying tissues of the oral cavity and in par- the underlying periodontal tissue in addition to acting as a
ticular the periodontium. The commensal microbiota (eg, in barrier against bacteria and their products. By contrast, the
dental plaque) may also be important for providing protection unique microanatomic structure of the junctional epithelium
against infection by pathogenic microorganisms through ef- has significant intercellular spaces; it is not keratinized, and it
fective competition for resources and ecologic niches and also exhibits a higher cellular turnover rate. These properties ren-
by stimulating protective immune responses. der the junctional epithelium permeable, thereby allowing for
The term innate immunity refers to the elements of the the inward movement of microbes and their products and the
immune response that are determined by inherited factors outward movement of GCF and the cells and molecules of
(and therefore innate), that have limited specificity, and that innate immunity. Furthermore, the spaces between the cells
are "fixed" in that they do not change or improve during of the junctional epithelium widen with inflammation, which
an immune response or as a result of previous exposure to results in increased GCF flow.
a pathogen. The recognition of pathogenic microorganisms Epithelial cells also constitutively express antimicrobial
and the recruitment of effector cells (eg, neutrophils) and peptides, and the synthesis and secretion of these molecules is
molecules (eg, the complement system) are central to effec- upregulated in response to periodontal bacteria. Neutrophils
tive innate immunity. Innate immune responses are orches- are also a source of antimicrobial peptides (ie, o-defensms).
trated by a broad range of cytokines, chemokines, and cell Antimicrobial peptides are small, polycationic peptides that
surface receptors, and the stimulation of innate immunity disrupt bacterial cell membranes and thereby directly kill bac-
leads to a state of inflammation. If innate immune responses teria with broad specificity.
TABLE 7.2
CONSTITUENTS OF SALIVA THAT CONTRIBUTE TO INNATE IMMUNITY

Saliva Constituent Host Defense Function
Antibodies (eg, immunoglobulin A) Inhibit bacterial adherence, promote agglutination

His ta tins Neutralize lipopolysaccharides, inhibit destructive enzymes
Cystatins Inhibit bacterial growth
Lactoferrin Inhibits bacterial growth
Lysozyme Lyses bacterial cell walls
Mucins Inhibits bacterial adherence, promotes agglutination
Peroxidase Neutralizes bacterial hydrogen peroxide
Epithelial cells that are directly stimulated with bacterial molecules (eg, ICAM-1) on endothelial and epithelial cells
components and cytokines produce MMPs, which contrib- with ~2 integrins on neutrophils facilitates neutrophil mi-
ute to a loss of connective tissue. Epithelial cells also secrete gration. The migration of neutrophils contributes to the dis-
a range of cytokines in response to periodontal bacteria ruption of the junctional epithelium via the degradation of
(eg, P gingivalis, A. actinomycetemcomitans, F. nucleatum, P in- the basement membrane through protease release and the
termedia), which signal immune responses. These include the action of Reactive Oxygen Species (ROS).
proinflammatory cytokines IL-1~, TNF-a, and IL-6 as well as The neutrophils that infiltrate the periodontium express
the chemokine IL-8 (CXCL8) and the monocyte chemoattrac- Fe receptors and complement receptors commensurate with
tant protein-1 (MCP-1), which serve to signal neutrophil and their function during the phagocytosis of opsonized bacteria
monocyte migration from the vasculature into the periodontal and bacterial antigens. Within the sulcus itself, 95% of the
tissue. cells are neutrophils. Because neutrophils are present in both
health and disease, the transmigration is thought to be a pro-
Gingival Crevicular Fluid cess distinct from that of GCF flow.
GCF originates from the postcapillary venules of the gingival
plexus. It has a flushing action in the gingival crevice, but
Adaptive Immunity
it also likely functions to bring the blood components (eg,
neutrophils, antibodies, complement components) of the host Adaptive immunity has evolved to provide a focused and in-
defenses into the sulcus. The flow of GCF increases in inflam- tense defense against infections that overwhelm innate im-
mation, and neutrophils are an especially important compo- mune responses. Adaptive immunity contrasts with innate
nent of GCF in periodontal health and disease. immunity with regard to the dynamic of the underlying cellu-
lar and molecular responses: adaptive immunity is slower and
Pathogen Recognition and Activation of Cellular reliant on complex interactions between APCs and T and B
Innate Responses lymphocytes. A key element is the antigen specificity of the re-
If plaque bacteria and their products penetrate the periodontal sponses that facilitates the specific targeting of a diverse range
tissues, specialized "sentinel cells" of the immune system rec- of effector elements, including cytotoxic T cells and antibod-
ognize their presence and signal protective immune respons- ies. Another facet is the ability of adaptive immune responses
es. These cells include macrophages and dendritic cells, which to improve during exposure to antigen and on subsequent in-
express a range of pattern recognition receptors (PRRs) that fection events.
interact with specific molecular structures on microorganisms The importance of adaptive immune responses in peri-
called Microbe Associated Molecular Patterns (MAMPs). The odontal pathogenesis is endorsed by histologic studies of
activation of PRRs activates innate immune responses to pro- established lesions in periodontal disease. The population
vide immediate protection, and adaptive immunity is also acti- of leukocytes in the periodontium in gingivitis (ie, the ear-
vated with the aim of establishing a sustained antigen-specific ly stages of responses to the plaque biofilm) and in stable
defense. Excessive and inappropriate or dysregulated immune periodontal lesions (ie, those in which tissue destruction is
responses lead to chronic inflammation and the concomitant apparently not progressing) is dominated by T cells, and
tissue destruction associated with periodontal disease. these cells are clustered mainly around blood vessels. Cell
surface marker studies suggest that these cells are activated
Neutrophil Function but not proliferating. In addition, there is a predominance
Although macrophages have phagocytic capabilities, neutro- of the helper T-cell subset (ie, CD4-expressing T cells) over
phils are the "professional" phagocytes that are critical to the the cytotoxic T-cell subset (ie, CDS-expressing T cells).
clearance of bacteria that invade host tissues. Neutrophils are These T cells are considered to be proactively maintaining
present in clinically healthy gingival tissues, and they migrate tissue homeostasis in the face of the microbial challenge
through the intercellular spaces of the junctional epithelium of the plaque biofilm. By contrast, in active (progressing)
into the sulcus. This is part of a "low-grade defense" against periodontitis, B cells and plasma cells predominate and are
plaque bacteria, and it is necessary to prevent inflammation associated with pocket formation and the progression of
and periodontal tissue damage. The importance of neutro- disease.
phils to the maintenance of periodontal health is demon-
strated clinically by the observations of severe periodontitis Antigen-Presenting Cells
in patients with neutrophil defects and the association of peri- APCs are sentinel cells in mucosa! tissues such as the peri-
odontitis with experimental immunosuppression in animal odontium. These cells detect and take up microorganisms and
models. their antigens, after which they may migrate to lymph nodes
Small foci of other leukocytes (eg, lymphocytes, plasma and interact with T cells to present antigen. The periodontium
cells, macrophages) are also found in the healthy gingiva. is often compared to other mucosa! tissues and the skin in
A small proportion (1-2 % ) of the intercellular spaces in terms of its repertoire of immune cells, and it contains a num-
healthy junctional epithelium are occupied by neutrophils ber of "professional" APCs, including B cells, macrophages,
(and other leukocytes at various stages of differentiation), and at least two types of dendritic cells (ie, dermal dendritic
but this can increase to 30% with even modest inflamma- cells and Langerhans cells). These cells naturally express the
tion. Neutrophils migrate from the gingival plexus to the major histocompatibility complex class II molecules necessary
extravascular connective tissue and then into the junctional for antigen presentation to T-cell receptors, and they may take
epithelium via the basement membrane. The presence of a up specific antigens and transport them to local lymph nodes,
layer of neutrophils in the junctional epithelium forms a host thereby facilitating the activation of specific effector T cells
defense barrier between subgingival plaque and the gingival and the generation of an antigen-specific immune response to
tissue. At the molecular level, the interaction of adhesion periodontal pathogens.
T Cells The significance of antibodies in periodontitis is not clear.

There are a number of different subsets of thymic lymphocytes It is not known if these antibodies have a protective function
(ie, T cells) that develop in the bone marrow and thymus and or whether they participate in disease pathogenesis. Although
migrate to the peripheral tissues to participate in adaptive im- there is some evidence for a correlation between clinical pa-
mune responses. The expression of the cell surface molecules rameters of disease and titers of specific antibodies to peri-
(CD4 or CDS) or particular T-cell antigen receptors (a~ or yo) odontal pathogens, other studies report an inverse correlation
broadly defines functional T-cell subsets that emerge from the of antibody levels and avidity with periodontal destruction.
thymus. The role of T cells in periodontal disease has been In addition, specific antibodies to periodontal pathogens are
established through immunohistologic studies of diseased tis- found in healthy individuals as well as in those with periodon-
sues. CD4+ helper T cells are the predominant phenotype in tal disease.
the stable periodontal lesion, and it is thought that alterations
Complement Systems
in the balance of effector T-cell subsets within the CD4+ popu-
lation may lead to progression toward a destructive, B-cell- In cases of periodontal disease, the host defense also is depen-
dominated lesion. dent on a functional complement system, which coordinates
the recruitment and activation of inflammatory cells, bacte-
B Cells rial opsonization, phagocytosis, and lysis. The complement
system is critical to the linking of innate and adaptive immu-
B cells help control extracellular antigens such as bacteria, nity by regulating the activation of both B cells and T cells,
fungal, yeast, and virions. B cells recognize diverse antigens either directly or through effects on antigen-presenting cells
using the B-cell antigen receptor (BCR). The high affinity in- (APCs).
teraction between the BCR and antigen enables the B cell to The activation of the complement cascade involves the
bind and ingest the antigen. Ingested antigen is degraded and sequential activation and proteolytic cleavage of a series of
presented to T cells. After antigen presentation some B cells serum proteins via three distinct mechanisms, namely the
differentiate to produce plasma cells dedicated to the produc- classical, lectin, and alternative. Classical pathway activation
tion and secretion of antibodies. occurs in response to antigen-antibody complexes that are
recognized by the Clq subunit of Cl. However, the lectin
Antibodies pathway is triggered through the interaction of a secreted
Specific antibodies are produced in response to an increas- pattern-recognition receptor (mannose-binding lectin) with
ing bacterial challenge in periodontal disease and are the end- specific carbohydrate groups on the surface of a variety of
point of B-cell activation. Circulating antibodies may be more microorganisms. Both the classical and the lectin pathways
important than locally produced antibodies. Even so, these then proceed through C4 and C2 cleavage for the genera-
generally appear in a high titer but have low biologic activity, tion of the classical/lectin C3 convertase (C4bC2b). The
so there is some doubt as to their effectiveness. Commensu- alternative pathway is initiated by the hydrolysis of C3 to
rate with the appearance of antibodies against plaque bacte- C3(H20), which is a C3b analog that forms the initial alter-
rial antigens is the appearance of differentiated plasma cells native pathway for C3 convertase, or through bacterial lipo-
that characterize the established lesion in periodontal disease. polysaccharide and lipooligosaccharide molecules in concert
High levels of antibodies appear in GCF (in addition to those with microbial-derived properdin. The alternative pathway
in the circulation), and these are produced locally by plasma also serves as a positive feedback loop for the classical and
cells in periodontal tissues. Antibodies to periodontal patho- lectin pathways. All three pathways converge at the third
gens are primarily IgG, with few IgM or IgA types produced. component of complement (C3), which upon activation
Many species of oral bacteria elicit a polyclonal B-cell by pathway-specific C3 convertases leads to the generation
response (with the consequent production of specific an- of key effector molecules. These include the C3a and CSa
tibodies against those bacteria). However, these responses anaphylatoxins, which activate specific G-protein-coupled
augment responses against nonoral bacteria and may lead to receptors and which mediate the mobilization and activa-
the production of autoantibodies (eg, antibodies against col- tion of leukocytes. Also important are the C3b opsonins,
lagen and connective tissue proteins), which may contribute which promote phagocytosis through complement receptors,
to tissue destruction in periodontal disease. The incidence and the CSb-9 membrane attack complex, which can lyse
and levels of specific serum and GCF IgG antibodies are targeted pathogens.
raised with chronic periodontitis, which suggests that local The complement systems have also been shown to provide
and peripheral generation of antibodies may be important in a barrier against the spread of bacterial infections; to facilitate
the immune response to periodontal pathogens. Antibodies clotting mechanisms; to mobilize hematopoietic stem cells
(ie, IgA) to periodontal pathogens are also found in saliva. and progenitor cells from the bone marrow; to help replenish
Variations in the levels of specific antibodies to different new leukocytes; and to activate the differentiation of specific
species in different clinical presentations suggest differences T-cell subsets. The dysregulation of complement activities
in pathogenesis. For example, antibodies to A. actinomy- may lead to a failure to protect the host against pathogens
cetemcomitans of the IgG2 subclass predominate in aggressive and amplify inflammatory tissue damage. In the context of
periodontitis. periodontal inflammation, complement subversion appears to
Other P gingivalis molecules (ie, fimbriae and hemaggluti- play a major role in periodontal pathogenesis.
nin) also act as antigens. Specific antibodies are also generated Activated complement components are found in the gin-
by serotype-specific carbohydrate antigens (eg, capsular poly- gival crevicular fluid of patients with chronic periodontitis
saccharide of P gingivalis, carbohydrate of A. actinomycetem- as compared with healthy sites. Virtually all of the comple-
comitans LPS). ment components have been detected in chronically inflamed
gingiva or in the gingival crevicular fluid of patients as com-

pared with healthy control samples. Finally, local complement _____ Hyperresponsive
activation may promote periodontal inflammation predomi-
Cl)
nantly via (Sa-induced vasodilation, increased vascular per- (J)
C
meability and flow of inflammatory exudate, and chemotactic 0
a.
(J)
recruitment of inflammatory cells, especially neutrophils. ~
~ .- ---- Normal
0 Disease
Concept of Host Susceptibility <ii
E
ihreshoTd
E ----- Hyporesponsive
The immune and inflammatory processes that result from .!!!
c
the challenge presented by the subgingival biofilm are com-
plex and mediated by a large number of proinflammatory
and antiinflammatory cytokines and enzymes that function
as a network of mediators with overlapping roles and activ- Bacterial challenge
ity Immune responses to the bacterial challenge do not oc-
cur in isolation but rather take place in the context of other FIGURE 7.3 Inflammatory response characteristics in relation to
host and environmental factors that influence these responses bacterial challenge. A given bacterial challenge results in differing lev-
and thereby determine the progression of disease. A number els of inflammatory response according to the response profile of an
of risk factors increase susceptibility to periodontal disease, individual. Most people are close to normal and produce a certain level
of inflammatory mediators for a given challenge. Those who are hyper-
including smoking, diabetes, nutritional factors, and stress; responders generate an excessive inflammatory response for the same
these are considered in detail elsewhere in this book. bacterial challenge and cross the threshold into active disease at an ear-
A feature of human development and evolution has been lier stage. Those who are hyporesponsive produce lower levels of in-
that quantitative and qualitative differences exist in immune flammatory mediators and, despite a significant bacterial challenge, may
never develop periodontitis. (Modified from Champagne CM, Buchanan
responses between individuals. Indeed, infectious agents (eg,
W, Reddy MS, et al: Periodontal 2000 31: 167-180, 2003.)
bacteria) exert evolutionary selection pressures on the species
that they infect. This may be relevant in periodontal disease,
and a large number of studies have confirmed that immune
cells from patients with periodontal disease secrete higher Our improved understanding of the diseases processes in
quantities of proinflammatory cytokines than those who are periodontitis has led to the development of a biologic sys-
periodontally healthy. Cytokine profiles are also different in tems model for representing periodontal pathogenesis. This
those individuals with immune-mediated diseases as com- involves bacterial components, environmental factors, specific
pared with healthy controls. inflammatory mechanisms, and host-genetic variations that
These observations have led to the development of the con- are associated with disease. A biologic systems approach pro-
cept of the "hyperinflammatory trait" in which certain indi- vides a framework for viewing the contributions and relative
viduals possess a hyperinflammatory phenotype and that this importance of all of the components that contribute to the
accounts for their increased susceptibility to chronic inflam- clinical presentation of disease. Thus, in the context of peri-
matory conditions such as periodontitis. Such a trait may also odontal disease, such a system would include a person level,
underpin shared susceptibility between conditions such as a genetic/epigenetic level, the biologic phenotype, and, ulti-
periodontitis and cardiovascular disease or diabetes. However, mately, the clinical phenotype (Fig. 7.4). Such systems pro-
at present, it is not possible to identify with certainty those vide a more comprehensive view of the disease as a complex
patients who may possess some form of hyperinflammatory regulatory network in which aspects of the specific genetic
trait. factors, environmental exposures, and other modifying factors
Figure 7.3 is a schematic illustration of how increasing that an individual is exposed to determine the development of
bacterial (ie, LPS) challenge can result in differing levels of the disease state.
inflammatory response according to the response profile of To summarize, it is clear that the subgingival bacteria ini-
an individual patient. Most individuals would be considered tiate and perpetuate the immune-inflammatory responses in
normal, and, for a given bacterial challenge, they would pro- the periodontal tissues. These responses are characterized by
duce a certain level of inflammatory mediators in the peri- classic signs of inflammation that are modified as a result of
odontal tissues. For those who are hyperresponders, the same the unique anatomy of the periodontium and the dentogin-
bacterial challenge results in a greater inflammatory response, gival apparatus. The inflammatory events that develop in re-
which over time would result in increased tissue breakdown, sponse to the bacterial challenge are protective by intent, but
earlier presentation of the clinical signs of disease, and a clini- they result in the majority of tissue damage and breakdown
cal interpretation of having increased susceptibility to peri- that lead to the clinical signs of periodontitis. Individuals vary
odontitis. Those individuals who are hyporesponsive pro- with regard to their susceptibility to periodontal disease and
duce low levels of inflammatory mediators and are therefore also in the threshold level at which a stable periodontal site
somewhat resistant to the development of periodontitis even progresses to an active site. Such variations are genetically de-
though plaque may be present and they may have widespread termined, and they are influenced by environmental risk fac-
gingivitis. The nature of the inflammatory response will be tors, some of which are modifiable and some of which are not.
governed by genetic factors and environmental factors, and The challenge for the future is to identify at-risk individuals
it may vary over time within the same individual (eg, if envi- who possess the hyperinflammatory trait so that disease can
ronmental factors such as smoking status, stress, or systemic be prevented by careful management strategies before tissue
disease should change). loss has occurred.
Person level
Biofilm characteristics
Environmental factors
•Smoking
•Diabetes
•Obesity
Genetic/epigenetic level
Gene polymorphisms
Epigenetic modifications
Age
Gender
Biological phenotype
Host immune-inflammatory response
Cellular and molecular changes
Inflammatory biomarkers
FIGURE 7.4 A biologic systems model of periodontitis. The outermost level of this model is the Person Level, which represents an individual's
unique characteristics as they are related to periodontitis. These include the compositional characteristics of the subgingival biofilm as well as known
risk factors and environmental exposures such as smoking and diabetes. The Person Level characteristics interact with the Genetic/Epigenetic Level
characteristics, which include nonmodifiable factors such as age, gender, and genetic composition. Gene polymorphisms are known to be associated
with periodontal disease, and epigenetics refers to changes in phenotype (ie, clinical disease expression) caused by mechanisms other than changes in
the underlying DNA sequence. Epigenetics can be defined as all of the meiotically and mitotically inherited changes in gene expression that are not
encoded in the DNA sequence itself. Epigenetic modifications are important permissive and suppressive factors for controlling the expressed genome
via gene transcription. Two major epigenetic mechanisms are the posttranslational modification of histone proteins in chromatin and the methylation
of DNA. The Genetic/Epigenetic Level characteristics influence the Biological Phenotype, which is characterized by the specific immune-inflamma-
tory responses (ie, cellular and molecular events and the production of inflammatory mediators) that are associated with the Clinical Phenotype (ie,
the clinical presentation of the disease). This model reflects how different individuals with the same presentation (eg, periodontitis) may have very
different predisposing and risk factors. The model depicts the different biologic factors that underpin the development of periodontal disease in differ-
ent individuals and that ultimately may be used to classify disease via the contribution provided to the clinical phenotype at each level. (Data from
Offenbacher S, Barros SP, Beck JD: J Periodontal 79: 1577-7 584, 2008.)
SUGGESTED READINGS of the Seventh European Workshop on Periodontology, J Clin Periodontal

38(Suppl 11) 44-48, 2011.
Champagne CM, Buchanan W, Reddy MS, et al: Potential for gingival crevice
Kornman KS: Mapping the pathogenesis of periodontitis: a new look, J Peri-
fluid measures as predictors of risk for periodontal diseases, Periodontal
odontal 79:1560-1568, 2008.
2000 31167-180, 2003.
Offenbacher S, Barros SP, Beck JD: Rethinking periodontal inflammation,
Gemmell E, Seymour Gj: Immunoregulatory control of Thl/Ih2 cytokine
profiles in periodontal disease, Periodontal 2000 35:21-41, 2005.
J Periodontal 79:1577-1584, 2008.
Preshaw PM, Taylor JJ: How has research into cytokine interactions and their
Gemmell E, Yamazaki K, Seymour Gj: The role of T cells in periodontal
role in driving immune responses impacted our understanding of peri-
disease: homeostasis and autoimmunity, Periodontal 2000 43:14-40,
odontitis? J Clin Periodontal 38(Suppl 11):60-84, 2011.
2007.
Kinane OF, Preshaw PM, Loos BG: Host-response: understanding the cellu-
lar and molecular mechanisms of host-microbial interactions-consensus
8
Biofilm and Periodontal
Microbiology
W Teughels • C Godts • M Quirynen • N Jakubovics • N Ambalavanan
Chapter Outline
Ecosystems of the Oral cavity Virulence Factors of
Bacteria and Their Biofilm Mode of Living Periodontopathogens
Dental Plaque Biofilm Future Advances in Periodontal
Bacterial Transmission and Translocation Microbiology
Microbiologic Specificity of Periodontal
Diseases
The human fetus inside the uterus is sterile, but, as soon as diversity and numbers in the oral cavity increase as more teeth
it passes through the birth canal, it acquires vaginal and fecal erupt and provide more areas for the adherence and retention
microorganisms. Within 2 weeks, a nearly mature microbiota of bacteria.
is established in the gut of the newborn baby. After wean- It is obvious that the periodontal microbiota is extremely
ing (> 2 years), the entire human microbiota is formed and complex. More than 500 different species are capable of coloniz-
comprises a very complex collection of hundreds of different ing the adult mouth and that an individual typically harbors
types of bacteria that totals to approximately 1014 microbial around 50-150 different species. Most oral bacteria are harm-
cells. From this moment onward, our body contains 10 times less commensals under normal circumstances. This means
more bacteria than human cells. It has been estimated that, that this microbiota live in harmony with their host but that,
for a normal, healthy human being, the bacterial population under specific conditions (ie, increased mass and/or pathoge-
comprises 2 kg of the total body weight. nicity, suppression of commensal or beneficial bacteria, and/or
The colonization of the oral cavity also starts close to the reduced host response), diseases can occur. The importance of
time of birth. Within hours after birth, the sterile oral cavity the commensal microbiota is clearly illustrated by the devel-
will be colonized by low numbers of mainly facultative and opment of yeast infections when the normal oral microbiota
aerobic bacteria. At that time, the oral microbiota of newborns is reduced, such as after a longer period of systemic antibiotic
closely resembles the mother's vaginal microbiota or, for new- usage.
borns delivered by cesarean section, the mother's skin micro-
biota. From the second day, anaerobic bacteria can be detected
in the infant's edentulous mouth. The number of oral bacteria Ecosystems of the Oral cavity
increases gradually as a result of exposure to the external en-
On the basis of physical and morphologic criteria, the oral cav-
vironment. Streptococcus salivarius and Streptococcus mitis have
ity can be divided into six major ecosystems (also called niches),
been identified as the first and most dominant oral microbes
each with the following distinct ecologic determinants:
to colonize the oral cavity of newborn infants. Veillonella spp.,
Neisseria spp., Actinomyces spp., and Staphylococcus spp. are 1. the intraoral and supragingival hard surfaces (teeth, im-
also among the first colonizers of the oral cavity. After tooth plants, restorations, and prostheses)
eruption, a more complex oral microbiota is established. The 2. subgingival regions adjacent to a hard surface, including
species that colonize the teeth after eruption include Strep- the periodontal/periimplant pocket (characterized by the
tococcus sanguinis, Lactobacillus spp., and Streptococcus oralis. presence of crevicular fluid, the root cementum or implant
Oral streptococci, including S. oralis, Streptococcus anginosus, surface, and the pocket epithelium)
mutans Streptococci (Streptococcus mutans and Streptococcus 3. the buccal palatal epithelium and the epithelium of the
sobrinus), and Streptococcus gordonii are commonly reported to floor of the mouth
be present after the first year of life. In addition, anaerobes, 4. the dorsum of the tongue
including Fusobacterium spp. and Prevotella spp., can also be 5. the tonsils
detected in young children. In later childhood, the bacterial 6. the saliva
95
In health, there is a core set of microorganisms that are produced by bacteria within the biofilm are retained and con-
almost universally present in these ecosystems. This core centrated, which fosters metabolic interactions among the dif-
microbiome includes members of the phyla Firmicutes ferent bacteria.
(Streptococcus spp., Veillonella spp., and Granulicatella spp.),
Proteobacteria (Neisseria spp., Campylobacter spp., and Hae-
mophilus spp.), Actinobacteria (Corynebacterium spp., Rothia Dental Plaque Biofilm
spp., and Actinomyces spp.), Bacteroidetes (Prevotella spp., Dental plaque is composed primarily of microorganisms en-
Capnocytophaga spp., and Porphyromonas spp.), and Fusobac- cased within an extracellular matrix. One gram of plaque (wet
teria (Fusobacterium spp.). weight) contains approximately 1011 bacteria. The number of
In the periodontal pocket, different strategies contribute to bacteria in supragingival plaque on a single tooth surface can
bacterial survival, such as adhesion to the pocket epithelium, exceed 109 cells. In a periodontal pocket, counts can range
when dentine is encountered, and the colonization of the from 103 bacteria in a healthy crevice to more than 108 bac-
dentine tubules. The crevicular fluid with its constant outflow teria in a deep pocket. It has been estimated that more than
does not favor the maintenance of unattached bacteria in the 500 distinct microbial phylotypes can be present as natural
periodontal pocket. inhabitants of dental plaque.
It has been suggested that teeth are the primary habitat Any individual may harbor 150 or more different species.
for periodontopathogens, because soon after a full-mouth Nonbacterial microorganisms that are found in plaque include
tooth extraction in patients with severe periodontitis, key archaea, yeasts, protozoa, and viruses.
pathogens, such as Aggregatibacter actinomycetemcomitans and The intercellular matrix consists of organic and inorganic
Porphyromonas gingivalis disappeared from the oral cavity as materials derived from saliva, gingival crevicular fluid, and
determined by bacterial culturing techniques. Prevotella interbacterial products.
media and other black-pigmented Prevotella spp. did remain, Organic constituents of the matrix include polysaccharides,
but at lower detection frequencies and numbers. proteins, glycoproteins, lipid material, and DNA. Albumin,
The same applies to edentulous infants and wearers of which probably originates from crevicular fluid, has been
full dentures in whom significant proportions of periodonto- identified as a component of the plaque matrix. The lipid
pathogens have been recorded, with the exception of A acti- material consists of debris from the membranes of disrupted
nomycetemcomitans and P gingivalis. Therefore, teeth are con- bacterial and host cells, bacterial vesicles, and possibly food
sidered as a port of entry for periodontopathogens. debris. Glycoproteins from the saliva are an important compo-
nent of the pellicle that initially coats a clean tooth surface,
Bacteria and Their Biofilm Mode but they also become incorporated into the developing plaque
biofilm. Polysaccharides produced by bacteria also contribute
of Living to the organic portion of the matrix. They play a major role in
Biofilms are composed of microbial cells encased within a ma- maintaining the integrity of the biofilm.
trix of extracellular polymeric substances, such as polysaccha- The inorganic components of plaque are predominantly cal-
rides, proteins, and nucleic acids. cium and phosphorus, with trace amounts of other minerals,
Biofilm bacteria are often up to 1000 times more resistant such as sodium, potassium, and fluorine. The source of inor-
to antimicrobial agents than their planktonic counterparts. ganic constituents of supragingival plaque is primarily saliva.
Bacteria that grow in multispecies biofilms interact closely As the mineral content increases, the plaque mass becomes
with neighboring cells. Sometimes these interactions are mu- calcified to form calculus. Calculus is frequently found in ar-
tually beneficial as is the case when one organism removes eas of the dentition adjacent to salivary ducts (eg, the lingual
another's waste products and uses them as an energy source. surface of the mandibular incisors and canines and the buc-
In other instances, bacteria compete with their neighbors by cal surface of the maxillary first molars), which reflects the
secreting antibacterial molecules, such as inhibitory peptides high concentration of minerals available from saliva in those
(bacteriocins) or hydrogen peroxide (H202). In addition, the regions. The inorganic components of subgingival plaque are
biofilm mode of growth facilitates cell-cell signaling and derived from crevicular fluid. The calcification of subgingival
DNA exchange between bacteria. It is clear that microbial plaque also results in calculus formation. Subgingival calculus
ecology within biofilm communities is highly complex. Bio- is typically dark green or dark brown, which probably reflects
films are heterogeneous; variations in biofilm structure ex- the presence of blood products that are associated with sub-
ist within individual biofilms and between different types of gingival hemorrhage.
biofilms. However, a number of structural features that are
common to many biofilms have been noted. For example, Structure of a Mature Dental Plaque
biofilms frequently contain microcolonies of bacterial cells.
Biofilm
Water channels are commonly found in biofilms, and these
can form a primitive circulatory system that removes waste Dental plaque (Fig. 8.1) is defined clinically as a structured,
products and brings fresh nutrients to the deeper layers of resilient, yellow-grayish substance that adheres tenaciously to
the film. the intraoral hard surfaces, including removable and fixed res-
The bacteria exist and proliferate within the intercellular torations. The tough extracellular matrix makes it impossible
matrix through which the channels run. The matrix confers to remove plaque by rinsing or with the use of sprays. Plaque
a specialized environment that distinguishes the bacteria can thus be differentiated from other deposits that may be
that exist within the biofilm from those that are free-floating; found on the tooth surface, such as materia alba and calculus.
("planktonic state") in solutions, such as saliva or crevicular Materia alba refers to soft accumulations of bacteria, food mat-
fluid. The biofilm matrix functions as a barrier. Substances ter, and tissue cells that lack the organized structure of dental
8 Biofilm and Periodontal Microbiology 97
the subgingival region. Both morphologic and microbiologic

studies of subgingival plaque reveal distinctions between the
tooth-associated regions and the soft-tissue-associated regions
of subgingival plaque (Fig. 8 2A-D)
The tooth-associated cervical plaque that adheres to the
root cementum does not markedly differ from that observed
in gingivitis. At this location, filamentous microorganisms
dominate, but cocci and rods also occur. This plaque is domi-
nated by Gram-positive rods and cocci, including S. mitis,
S. sanguinis, Actinomyces oris, Actinomyces naeslundii, and Eu-
bacterium spp. However, in the deeper parts of the pocket, the
filamentous organisms become fewer in number; in the apical
FIGURE 8.1 Clinical picture of 10-day-old supragingival plaque. The portion, they seem to be virtually absent. Instead, the micro-
first signs of gingival inflammation (arrows) are becoming visible. biota is dominated by smaller organisms without a particular
orientation. The apical border of the plaque mass is separated
from the junctional epithelium by a layer of host leukocytes,
plaque and that are easily displaced with a water spray. Calcu- and the bacterial population of this apical tooth-associated re-
lus is a hard deposit that forms via the mineralization of dental gion shows an increased concentration of Gram-negative rods
plaque and that is generally covered by a layer of unmineral- (Fig. 8.2D).
ized plaque (Table 8 1). The layers of microorganisms that face the soft tissue lack
Dental plaque is broadly classified as supragingival or sub- a definite intermicrobial matrix and contain primarily Gram-
gingival on the basis of its position on the tooth surface to- negative rods and cocci, as well as large numbers of filaments,
ward the gingival margin. flagellated rods, and Spirochetes. Studies of plaque associated
with crevicular epithelial cells indicate a predominance of
• Supragingival plaque is found at or above the gingival mar-
species, such as S. oralis, Streptococcus intermedius, Parvimo-
gin; when in direct contact with the gingival margin, is re-
nas micra (formerly Micromonas micra and Peptostreptococcus
ferred to as marginal plaque.
micros), P gingivalis, P intermedia, Tannerellaforsythia, and Fu-
• Subgingival plaque is found below the gingival margin be-
sobacterium nucleatum. Host-tissue cells (eg, white blood cells
tween the tooth and the gingival pocket epithelium.
and epithelial cells) may also be found in this region. Bacte-
Supragingival plaque typically demonstrates the stratified ria are also found within the host tissues, such as in the soft
organization of a multilayered accumulation of bacterial mor- tissues and within epithelial cells, as well as in the dentinal
photypes. Gram-positive cocci and short rods predominate at tubules.
the tooth surface, whereas Gram-negative rods and filaments, The composition of the subgingival plaque depends on the
as well as Spirochetes predominate at the outer surface of the pocket depth. The apical part is more dominated by Spiro-
mature plaque mass. chetes, cocci, and rods, whereas in the coronal part more fila-
In general, the subgingival microbiota differs in composi- ments are observed.
tion from the supragingival plaque, primarily because of the The site specificity of plaque is significantly associated with
local availability of blood products and a low reduction-oxi- diseases of the periodontium. Marginal plaque, for example,
dation (redox) potential, which characterizes the anaerobic is of prime importance during the initiation and develop-
environment. ment of gingivitis. Supragingival plaque and tooth-associated
The environmental parameters of the subgingival region dif- subgingival plaque are critical in calculus formation and root
fer from those of the supragingival region. The gingival crevice caries, whereas tissue-associated subgingival plaque is im-
or pocket is bathed by the flow of crevicular fluid, which con- portant in the tissue destruction that characterizes different
tains many substances that bacteria may use as nutrients. Host forms of periodontitis. Biofilms also establish on artificial sur-
inflammatory cells and mediators are likely to have consider- faces exposed to the oral environment, such as prostheses and
able influence on the establishment and growth of bacteria in implants.
TABLE 8.1
DIFFERENCES BETWEEN TOOTH DEPOSITS

Materia Alba Dental Plaque Calculus
White cheeselike accumulation Resilient clear to yellow-grayish substance Hard deposit that forms via the
mineralization of dental plaque
Soft accumulation of salivary proteins, some Primarily composed of bacteria in a matrix Generally covered by a layer of
bacteria, many desquamated epithelial cells, of salivary glycoproteins and extracellular unmineralized dental plaque
and occasional disintegrating food debris polysaccharides
Lacks an organized structure and is therefore Considered to be a biofilm
not as complex as dental plaque
Easily displaced with a water spray Impossible to remove by rinsing or with the
use of sprays
Plaque/bacteria
Epithelial-
associated
plaque --:., I
Bacteria within
connective tissue ,\ ~ 1"' " €tQ
0
Bacteria on 0
bone surface _;__ -fl'
(A)
FIGURE 8.2 A, Diagram depicting the plaque-bacteria association between the tooth surface and the periodontal tissues. B, Scanning electron pho-
tomicrograph of a cross-section of cementum (C) with attached subgingival plaque (AP). The area shown is within a periodontal pocket. C, Scanning
electron micrograph of cocci and filaments associated with the surface of pocket epithelium in a case of marginal gingivitis. (X3000.) D, Left, Dia-
grammatic representation of the histologic structure of subgingival plaque. Right, Histologic section of subgingival plaque. Arrow with box, Sulcular
epithelium. White arrow, Predominantly Gram-negative unattached zone. Black arrow, Tooth surface. Asterisk, Predominantly Gram-positive attached
zone. (8, Courtesy Dr J. Sottosanti, La Jolla, CA.)
Formation of Dental Plaque Biofilm phosphoproteins (eg, statherin), histidine-rich proteins,

and other molecules that can function as adhesion sites (re-
The process of plaque formation can be divided into three ceptors) for bacteria. The salivary pellicle can be detected
main phases: (1) formation of the pellicle on the tooth surface; on clean enamel surfaces within 1 min after their introduc-
(2) initial adhesion/attachment of bacteria; and (3) secondary tion into the mouths of volunteers. By 2 h, the pellicle is
colonization/plaque maturation. essentially in equilibrium between adsorption and detach-
ment although further pellicle maturation can be observed
Formation of the Pellicle for several hours.
All surfaces in the oral cavity, including the hard and soft Consequently, bacteria that adhere to tooth surfaces do
tissues, are coated with a layer of organic material known not contact the enamel directly but interact with the acquired
as the acquired pellicle. The pellicle on tooth surfaces con- enamel pellicle. However, the pellicle is not merely a passive
sists of more than 180 peptides, proteins, and glycopro- adhesion matrix. Many proteins retain enzymatic activity when
teins, including keratins, mucins, proline-rich proteins, they are incorporated into the pellicle, and some of these, such
as peroxidases, lysozyme, and a-amylase, may affect the phys- TABLE 8.2
iology and metabolism of the adhering bacterial cells.
OVERVIEW OF PRIMARY AND SECONDARY
Initial Adhesion/ Attachment of Bacteria COLONIZERS IN DENTAL PLAQUE
The initial steps of transport and interaction with the surface
Primary colonizers S gordonii
are essentially nonspecific (ie, they are the same for all bacte- S. intermedius
ria). The specific interactions between microbial cell surface S. mitis
"adhesin" molecules and receptors in the salivary pellicle de- S. oralis
termine whether a bacterial cell will remain associated with S. sanguinis
the surface. Only a relatively small proportion of oral bacteria Actinomyces gerencseriae
possess adhesins that interact with receptors in the host pelli- Actinomyces israelii
cle, and these organisms are generally the most abundant bac- A. naeslundii
teria in biofilms on tooth enamel shortly after cleaning. Over A. oris
the first 4-8 h, 60-80% of bacteria present are members of the A. actinomycetemcomitans serotype a
Capnocytophaga gingivalis
genus Streptococcus. Other bacteria that are commonly present
Capnocytophaga ochracea
at this time include species that cannot survive without oxy- Capnocytophaga sputigena
gen (obligate aero bes), such as Haemophilus spp. and Neisseria Eihenella corrodens
spp., as well as organisms that can grow in the presence or ab- Actinomyces odontolyticus
sence of oxygen (facultative anaerobes), including Actinomy- Veillonella parvula
ces spp. and Veillonella spp. These species are considered the Secondary colonizers Campylobacter gracilis
"primary colonizers" of tooth surfaces. The primary colonizers Campylobacter ,·ectus
provide new binding sites for adhesion by other oral bacteria. Campylobacter showae
The metabolic activity of the primary colonizers modifies the Eubacterium nodatum
local microenvironment in ways that can influence the ability A. actinomycetemcomitans serotype b
F nucleatum spp nucleatum
of other bacteria to survive in the dental plaque biofilm. For
F nucleatum spp vincentii
example, by removing oxygen, the primary colonizers provide F nucleatum spp polymorphum
conditions of low-oxygen tension that permits the survival Fusobacterium periodonticum
and growth of obligate anaerobes. P micra
P intermedia
Prevotella loescheii
Secondary Colonization and Plaque Maturation Prevotella nigrescens
The primary colonizing bacteria (Table 8 2) adhered to the Streptococcus constellatus
tooth surface provide new receptors for attachment by other I forsythia
bacteria as part of a process known as "coadhesion." Together P gingivalis
Treponema denticola
with the growth of adherent microorganisms, coadhesion leads
to the development of microcolonies and eventually to a ma-
ture biofilm. When many genetically distinct bacteria adhere
to each other and form clumps it is referred to as coaggregation. use of probiotics. Special examples of coaggregations are the
Different species-or even different strains of a single corncob formation (Fig. 8.3), in which Streptococci adhere to
species-have distinct sets of coaggregation partners. Fu- filaments of Corynebacterium matruchotii or Actinomyces spp.,
sobacteria coaggregate with all other human oral bacteria, and the test-tube brush formation, composed of filamentous
whereas Veillonella spp., Capnocytophaga spp., and Prevotella bacteria to which Gram-negative rods adhere.
spp. bind with Streptococci and/or Actinomyces. Each newly An analysis of more than 13,000plaquesamples that assessed
accreted cell becomes itself a new surface and therefore may 40 subgingival microorganisms using a DNA-hybridization
act as a coaggregation bridge to the next potentially accreting
cell type that passes by.
Well-characterized interactions of secondary colonizers
(Table 8.2) with early colonizers include the coaggregation of
F nucleatum with S. sanguinis, P loescheii with A oris, and C.
ochracea with A oris. Secondary colonizers (Table 8.2), such
as P intermedia, P loescheii, Capnocytophaga spp., F nucleatum,
and P gingivalis, do not initially colonize clean tooth surfaces
but rather adhere to bacteria that are already in the plaque
mass. The transition from early supragingival dental plaque to
mature plaque growing below the gingival margin involves a
shift in the microbial population from primarily Gram-positive
organisms to high numbers of Gram-negative bacteria. There-
fore, during the later stages of plaque formation, coaggregation
between different Gram-negative species is likely to predomi-
nate. Examples of these types of interactions are the coaggrega- FIGURE 8.3 Long-standing supragingival plaque near the gingival
tion of F nucleatum with P gingivalis or I denticola. margin demonstrates a "corn-cob" arrangement. A central Gram-
The idea that coaggregation is important during the forma- negative filamentous core supports the outer caecal cells, which are
tion of oral biofilms opens new perspectives, especially for the firmly attached by interbacterial adherence or coaggregation.
FIGURE 8.4 A diagram of the association among subgingival species. The data were derived from 13,261 subgingival plaque samples taken from
the mesial aspect of each tooth in 185 adult subjects. Each sample was individually analyzed for the presence of 40 subgingival species with the use
of checkerboard DNA-DNA hybridization. Associations were sought among species via cluster analysis and community ordination techniques. The
complexes to the left are comprised of species that are thought to colonize the tooth surface and to proliferate at an early stage. The orange complex
becomes numerically dominant later; it is thought to bridge the early colonizers and the red complex species, which become numerically more domi-
nant during the later stages of plaque development. (Adapted from 5ocransky 55, Haffajee AD, Cugini MA, et al:) Clin Periodontal 25: 7 34, 7998.)
methodology defined color-coded "complexes" of periodontal tooth surface, which is an amount nearly undetectable clini-
microorganisms that tend to be found together in health or cally). This "lag time" is a result of the microbial population
disease. The composition of the different complexes was based that must reach a certain size before it can easily be detected
on the frequency with which different clusters of microorgan- by a clinician. During the following 3 days, coverage pro-
isms were recovered, and the complexes were color-coded gresses rapidly to the point at which, after 4 days, an average
for easy conceptualization (Fig. 8.4). Interestingly, the early of 30% of the total coronal tooth area will be covered with
colonizers are either independent of defined complexes (A. plaque.
naeslundii and A oris) or members of the yellow (Streptococcus The microbial composition of the dental plaque will shift
spp.) or purple complexes (A odontolyticus). The microorgan- towards a more anaerobic and a more Gram-negative flora,
isms primarily considered secondary colonizers fell into the including an influx of Fusobacteria, filaments, spiral forms,
green-, orange-, and red complexes. The green complex in- and Spirochetes (Fig. 8.5) This was clearly illustrated in ex-
cludes E. corrodens, A. actinomycetemcomitans serotype a, and perimental gingivitis studies. With this ecologic shift within
Capnocytophaga spp. The orange complex includes Fusobacte- the biofilm, there is a transition from the early aerobic envi-
rium, Prevotella, and Campylobacter spp. The green and orange ronment, which is characterized by Gram-positive facultative
complexes include species recognized as pathogens in peri- species, to a highly oxygen-deprived environment, in which
odontal and nonperiodontal infections. The red complex con- Gram-negative anaerobic microorganisms predominate. Bac-
sists of P gingivalis, T forsythia, and T denticola. This complex terial growth in older plaque is much slower than in newly
is of particular interest because it is associated with bleeding formed dental plaque, presumably because nutrients become
on probing. The existence of complexes of species in plaque is limiting for much of the plaque biomass.
another reflection of bacterial interdependency in the biofilm
environment. Topography of Supragingival Plaque
Early plaque formation on teeth follows a typical topographic
Factors That Affect Supragingival Dental pattern, with initial growth along the gingival margin and
Plaque Formation from the interdental spaces (ie , the areas protected from shear
forces). Later, a further extension in the coronal direction can
Clinically, early undisturbed plaque formation on teeth fol- be observed. This pattern may change severely when the tooth
lows an exponential growth. During the first 24 h when start- surface contains irregularities that favor growth
ing with a clean tooth surface, plaque growth is negligible By multiplication, the bacteria subsequently spread out
from a clinical viewpoint (ie, <3% coverage of the vestibular from these starting up areas as a relatively even monolayer.
Oral hygiene
GI Gingivitis
1.0
0.5
0 5 10 15 20 25 30 Days
FIGURE 8.5 Artistic impression of the 1965 published classic experimental proof of the bacterial etiology of gingivitis using the experimental
gingivitis model. In plaque-free subjects with clinically noninflamed gingiva, plaque will slowly develop on the teeth when all mechanical plaque
control is stopped. With time, the plaque composition changes. During the first few days, the plaque is mainly composed of Gram-positive (+) cocci
and rods. Later on, the composition is shifted toward more Gram-negative species and more rods and filaments; finally, Gram-negative(-) Spirochetes
appear (see morphotypes in black). Within a few days, a mild gingivitis ensues (black line; gingival index of 1 according to Loe and Silness). From the
moment that proper plaque control is reestablished (vertical line), the plaque composition returns to the initial situation, and the symptoms of gingivitis
disappear. (From Loe H, Theilade E, Jensen 58: Experimental gingivitis in man, J Periodontal 36: 177, 1965.)
Surface irregularities are also responsible for the so-called gingival margins than on those adjacent to healthy gingivae.
"individualized" plaque-growth pattern, which is repro- These studies suggest that the increase in crevicular fluid
duced in the absence of optimal oral hygiene. This phe- production enhances plaque formation. Probably some sub-
nomenon illustrates the importance of surface roughness in stances from this exudate (eg, minerals, proteins, and carbo-
plaque growth, which should lead to proper clinical treat- hydrates) favor both the initial adhesion and/or the growth
ment options. of the early colonizing bacteria. In addition, it is known that,
during the night, the plaque growth rate is reduced by about
Surface Microroughness 50%. This seems surprising, because one would expect that
Rough intraoral surfaces (eg. crown margins, implant abut- reduced plaque removal and the decreased salivary flow at
ments, and denture bases) accumulate and retain more plaque night would enhance plaque growth. The fact that the supra-
and calculus in terms of thickness, area, and colony-form- gingival plaque obtains its nutrients mainly from the saliva
ing units. Ample plaque also reveals an increased maturity/ appears to be of greater significance than the antibacterial
pathogenicity of its bacterial components, which is charac- activity of saliva.
terized by an increased proportion of motile organisms and
Spirochetes and/or a denser packing of them. Smoothing an
Metabolism of Dental Plaque Bacteria
intraoral surface decreases the rate of plaque formation.
The majority of nutrients for dental plaque bacteria origi-
Individual Variables That Influence Plaque Formation nate from saliva or gingival crevicular fluid although the host
The rate of plaque formation differs significantly between sub- diet provides an occasional but nevertheless important food
jects and these differences may overrule surface characteris- supply. The transition from Gram-positive to Gram-negative
tics. A distinction is often made between "heavy" (fast)- and microorganisms observed in the structural development of
"light" (slow)-plaque formers. dental plaque is paralleled by a physiologic transition in the
A multiple regression analysis showed that the clinical wet- developing plaque.
tability of the tooth surfaces, the saliva-induced aggregation of The early colonizers (eg, Streptococcus and Actinomyces
oral bacteria, and the relative salivary flow conditions around spp.) use oxygen and lower the redox potential of the envi-
the sampled teeth explained 90% of the variation. ronment, which then favors the growth of anaerobic species.
Many of the Gram-positive early colonizers use sugars as an
Variation Within the Dentition
energy source. The bacteria that predominate mature plaque
are anaerobic and asaccharolytic (ie, they do not break down
Within a dental arch, large differences in plaque growth rate sugars), and they use amino acids and small peptides as en-
can be detected. In general, early plaque formation occurs ergy sources.
faster: in the lower pw (as compared with the upper jaw), Laboratory studies have demonstrated many metabolic
in molar areas, on the buccal tooth surfaces (as compared interactions among the different bacteria found in dental
with palatal sites, especially in the upper jaw), and in the plaque (Fig. 8.6). For example, lactate and formate are by-
interdental regions (as compared with the buccal or lingual products of the metabolism of Streptococci and Actinomyces
surfaces). spp.; they may be used in the metabolism of other plaque
microorganisms, including Veillonella spp. and A. actinomy-
Impact of Gingival Inflammation and Saliva cetemcomitans.
Several studies clearly indicate that early in vivo-plaque The growth of P gingivalis is enhanced by metabolic
formation is more rapid on tooth surfaces facing inflamed by-products produced by other microorganisms, such as
Streptococcus____. p-Amino Biofilms and Antimicrobial Resistance

Acil:~ f' ~
Lactate
A
?
benzoate' S. mutans
//
Bacteria growing in microbial communities adherent to a
surface do not "behave" the same way as bacteria growing
/ NH4 CO2 suspended in a liquid environment (ie, in a planktonic or
unattached state). For example, the resistance of bacteria to
Veil/one/la antimicrobial agents is dramatically increased in the biofilm.
Almost without exception, organisms in a biofilm are 1000-
Menadione 1500 times more resistant to antibiotics as compared to their
planktonic state. The mechanisms of this increased resistance
l
Campylobacter differ from species to species, from antibiotic to antibiotic, and
'\
Protoheme
P. gingivalis
P. intermedia
for biofilms growing in different habitats.
An important mechanism of resistance appears to be the
slower rate of growth of bacterial species in a biofilm, which
makes them less susceptible to many but not all antibiotics.
The biofilm matrix, although not a significant physical bar-
rier to the diffusion of antibiotics, does have certain properties
that can retard antibiotic penetration. For example, strongly
Hemin charged or chemically highly reactive agents can fail to reach
a-Globulin
the deeper zones of the biofilm, because the biofilm acts as
Host an ion-exchange resin that removes such molecules from
FIGURE 8.6 Schematic illustration of metabolic interactions among solution.
different bacterial species found in plaque and between the host and In addition, extracellular enzymes, such as ~-lactamases,
the plaque bacteria. These interactions are likely to be important to the
survival of bacteria in the periodontal environment. (Based on Carls-
formaldehyde lyase, and formaldehyde dehydrogenase may
son J: Microbiology of plaque associated periodontal disease. In: Lindhe become trapped and concentrated in the extracellular matrix,
/, ed: Textbook of clinical periodontology, Munksgaard, 1983, Munks- and as such inactivate some antibiotics (especially positively
gaard International Publishers; Grenier D: Infect lmmun 60:5298, 1992; charged hydrophilic antibiotics).
Loesche WJ: Periodontics 6:245, 1968; and Walden WC, Hentges DJ: Some antibiotics, such as the macrolides, which are posi-
Appl Microbial 30:781, 1975.)
tively charged but hydrophobic, are unaffected by this pro-
cess.
succinate from C. ochracea and protoheme from C. rectus. Recently, "super-resistant" bacteria were identified within
Overall, the total plaque population is more efficient than any a biofilm. These cells have multidrug-resistance pumps that
one constituent organism at releasing energy from the avail- can extrude antimicrobial agents from the cell. Since these
able substrates. pumps place the antibiotics outside of the outer membrane,
Metabolic interactions also occur between the host and the the process offers protection against antibiotics that target, for
plaque microorganisms. example, cell-wall synthesis. The penetration and efficacy of
The bacterial enzymes that degrade host proteins mediate antimicrobials against biofilm bacteria are critical issues for
the release of ammonia, which may be used by bacteria as a the treatment of periodontal infections.
nitrogen source. Hemin iron from the breakdown of host he- Antibiotic resistance may be spread through a biofilm via
moglobin may be important in the metabolism of P gingivalis. the intercellular exchange of DNA. The high density of bacte-
Increases in steroid hormones are associated with signifi- rial cells in a biofilm facilitates the exchange of genetic infor-
cant increases in the proportions of P intermedia found in mation among cells of the same species and across species and
subgingival plaque. These nutritional interdependencies are even across genera. Conjugation (ie, the exchange of genes
probably critical to the growth and survival of microorganisms through a direct interbacteria connection formed by a sex pi-
in dental plaque, and they may partly explain the evolution lus), transformation (ie, the movement of small pieces of DNA
of the highly specific structural interactions observed among from the environment into the bacterial chromosome), plas-
bacteria in plaque. mid transfer, and transposon transfer have all been shown to
occur in biofilms.
Communication Between Biofilm Bacteria
Bacterial cells do not exist in isolation. In a biofilm, bacteria Bacterial Transmission
have the capacity to communicate with each other. One ex- and Translocation
ample of this is quorum sensing, in which bacteria secrete a
signaling molecule that accumulates in the local environment The transmission of pathogens from one locus to another is an
and triggers a response, such as a change in the expression of important aspect of infectious diseases. In theory, such trans-
specific genes, once they reach a critical threshold concentra- mission may jeopardize the outcome of periodontal therapy;
tion. The threshold concentration is reached only at a high in addition, the transmission of pathogens from one person to
cell density, which helps the bacteria to sense that the popula- another may be important in terms of disease transmission.
tion has reached a critical mass or quorum. The significance of such an intraoral transmission or of a verti-
Quorum sensing appears to play diverse roles in, for ex- cal or horizontal transmission is, however, difficult to prove or
ample, modulating the expression of genes for antibiotic re- to quantify. Molecular fingerprinting techniques have clearly
sistance, encouraging the growth of beneficial species in the illustrated that periodontal pathogens are transmissible within
biofilm, and discouraging the growth of competitors. members of a family.
The existence of an "intraoral" translocation of bacteria (ie, plaque hypothesis and the ecologic plaque hypothesis, most
from one niche to another) has been observed. Microorgan- of the therapeutic interventions are still based on the basic
isms are often transmitted to the neighboring teeth (probably principles of the nonspecific plaque hypothesis.
via saliva) and could even reach the contralateral quadrant
after transmission with a dental explorer.
Specific Plaque Hypothesis
Previously noninfected pockets may get colonized with
A. actinomycetemcomitans via a single course of probing with a The specific plaque hypothesis underlines the importance of
probe that had been previously inserted in an infected pocket the qualitative composition of the resident microbiota. The
of the same patient. pathogenicity of dental plaque depends on the presence of or
Quirynen and coworkers used a treatment strategy called an increase in specific microorganisms. This concept encap-
"one-stage, full-mouth disinfection" to investigate the im- sulates that plaque that harbors specific bacterial pathogens
pact of intraoral translocation on the outcome of nonsurgical may provoke periodontal disease because key organisms pro-
periodontal therapy This strategy attempted to suppress the duce substances that mediate the destruction of host tissues.
translocation of periodontopathogens from all of their intraoral The association of specific bacterial species with disease came
habitats (ie, mucous membranes, tongue, and saliva) to root- about during the early 1960s, when the microscopic exami-
planed periodontal pockets. Comparative studies between the nation of plaque revealed that different bacterial morphot-
one-stage, full-mouth approach and the standard therapy (ie, ypes were found in healthy versus periodontally diseased
root planing per quadrant with 2-week intervals that allow for sites. At about the same time, major advances were made in
translocation) has shown that one-stage full-mouth disinfec- the techniques used to isolate and identify periodontal mi-
tion leads to gain in attachment, pocket-depth reduction, and croorganisms. These included improvements in procedures
significantly lower pathogenic microorganisms. to sample subgingival plaque, in the handling of samples to
prevent killing the bacteria, and in the media used to grow
the bacteria in the laboratory. The result was a tremendous
Microbiologic Specificity increase in the ability to isolate periodontal microorganisms
and considerable refinement in the bacterial taxonomy Ac-
of Periodontal Diseases ceptance of the specific plaque hypothesis was spurred by
Nonspecific Plaque Hypothesis the recognition of A actinomycetemcomitans as a pathogen
in localized aggressive periodontitis. These advances led to
During the mid- l 900s, periodontal diseases were thought to a series of association studies focused on identifying specific
result from an accumulation of plaque over time, eventually periodontal pathogens by examining the microbiota associ-
in conjunction with a diminished host response and increased ated with states of health and disease in cross-sectional and
host susceptibility with age. This theory, which is called the longitudinal studies.
nonspecific plaque hypothesis, was supported by epidemiologic
studies that correlated, both age and the amount of plaque,
Criteria for the Identification
with evidence of periodontitis.
According to the nonspecific plaque hypothesis, periodon- of Periodontopathogens
tal disease results from the "elaboration of noxious products During the 1870s, Robert Koch developed the classic crite-
by the entire plaque flora." When only small amounts of ria by which a microorganism can be judged to be a caus-
plaque are present, the noxious products are neutralized by ative agent in human infections. These criteria, known as
the host. Similarly, large amounts of plaque would cause a Koch postulates, stipulate that the causative agent must do the
higher production of noxious products, which would essen- following:
tially overwhelm the host's defenses.
Several observations contradicted these conclusions. First, 1. Be routinely isolated from diseased individuals.
some individuals with considerable amounts of plaque and 2. Be grown in pure culture in the laboratory.
calculus, as well as gingivitis never developed destructive 3. Produce a similar disease when inoculated into susceptible
periodontitis. Furthermore, individuals who did present with laboratory animals.
periodontitis demonstrated considerable site specificity with 4. Be recovered from lesions in a diseased laboratory animal.
regard to the pattern of disease. Some sites were unaffected, Difficulties exist with regard to the application of these cri-
whereas advanced disease was found in adjacent sites. In the teria to polymicrobial diseases, and the applicability of Koch
presence of a uniform host response, these findings were in- postulates has been increasingly challenged in recent years.
consistent with the concept that all plaque was equally patho- In the case of periodontitis, there are three primary problems:
genic. Recognition of the differences in plaque at sites of dif- (1) the inability to culture all of the organisms that have been
ferent clinical status (ie, disease vs health) led to a renewed associated with disease (eg, many of the oral Spirochetes), (2)
search for specific pathogens in periodontal diseases and a the difficulties inherent in defining and culturing sites of ac-
conceptual transition from the nonspecific- to the specific tive disease, and (3) the lack of a good animal model system
plaque hypothesis. for the study of periodontitis. In fact, if the ecologic plaque
Inherent to the nonspecific plaque hypothesis, is the con- hypothesis proves to be correct, it must be inherently impos-
cept that the control of periodontal disease depends on the sible to fulfill Koch postulates, because no single organism or
reduction of the total amount of plaque. The current stan- group of organisms is responsible for all cases of disease.
dard treatment of periodontitis by debridement (nonsurgical Sigmund Socransky, a researcher at the Forsyth Dental Cen-
or surgical) and oral hygiene measures still focuses on the re- ter in Boston, proposed a set of criteria by which periodontal
moval of plaque and its products. Although the nonspecific microorganisms may be judged to be potential pathogens.
plaque hypothesis has been discarded in favor of the specific
Predominantly
Gram-positive micobiota,
Plaque Reduced LowGCF flow many facultative anaerobes,
reduction
X
inflammation
Inflammatory
response
X higher Eh
Environmentalx
change
gingival health
Ecological shift
Plaque Increased High GCF flow Predominantly

accumulation inflammation lower Eh Gram-negative micobiota,
many obligate anaerobes,
peridontal disease
FIGURE 8.7 Ecologic plaque hypothesis in relation to periodontal diseases: gingivitis and periodontitis. The accumulation of plaque causes the
inflammation of adjacent tissues (gingivitis) and other environmental changes that favor the growth of Gram-negative anaerobes and proteolytic spe-
cies, including periodontopathogens. The increased proportions of such species results in the destruction of periodontal tissues (ie, periodontitis). Eh,
Redox potential; CCF, gingival crevicular fluid. (Adapted from Marsh PD: Adv Dent Res 8:263, 1994.)
According to these criteria, a potential pathogen must do the homeostasis. Disease is associated with the overgrowth of
following specific members of the dental plaque biofilm when the lo-
cal microenvironment changes, but it is not necessarily the
1. Be associated with disease; as evidenced by increases in the
same species in each case. An important consideration of the
number of organisms at diseased sites.
ecological plaque hypothesis is that therapeutic intervention
2. Be eliminated or decreased in sites that demonstrate the
can be useful at a number of different levels. Eliminating the
clinical resolution of disease with treatment.
etiological stimulus-whether it is microbial, host, or envi-
3. Induce a host response in the form of an alteration in the
ronmental-will help to restore microbial homeostasis. Tar-
host cellular or humoral immune response.
geting specific microorganisms may be less effective, because
4. Be capable of causing disease in experimental animal
the conditions for disease will remain.
models.
5. Produce demonstrable virulence factors that are respon-
sible for enabling the microorganism to cause the destruc- Microorganisms associated with
tion of the periodontal tissues. Periodontal Health and Disease
These criteria, support the role of A actinomycetemcomitans Periodontitis is currently considered to be a mixed infection.
as a periodontal pathogen in the pathogenesis of Localized This has significant implications for both the diagnosis and
Aggressive Periodontitis treatment of periodontitis. For the diagnosis, some evaluate
the presence of up to 40 species, but it still is unclear wheth-
Ecological Plaque Hypothesis er some combinations of species are more pathogenic than
others. The treatment is directed toward the eradication or
During the 1990s, Marsh and coworkers developed the "eco- reduction of the number of key periodontopathogens. Be-
logical plaque hypothesis" as an attempt to unify the existing cause several species may be involved, the appropriate use
theories regarding the role of dental plaque in oral disease of antimicrobials (especially antibiotics) is extremely difficult
(Fig. 87). According to the ecological plaque hypothesis, to define, because not all expected periodontopathogens are
both the total amount of dental plaque, as well as the spe- equally susceptible to the same antibiotic.
cific microbial composition of plaque may contribute to the
transition from health to disease. The health-associated den-
Periodontal Health
tal plaque microbiota is considered to be relatively stable
over time and in a state of dynamic equilibrium or "micro- The recovery of microorganisms from periodontally healthy
bial homeostasis." Perturbations in the host response may be sites is lower as compared with diseased sites (Table 8.3).
brought about by an excessive accumulation of nonspecific The bacteria associated with periodontal health are primarily
dental plaque, by plaque-independent host factors [eg, the Gram-positive facultative species (Fig. 8.8) and members of
onset of an immune disorder, changes in hormonal balance the genera Streptococcus and Actinomyces (eg, S. sanguinis, S.
(eg, during pregnancy), or by environmental factors (eg, mitis, A. oris, A. israelii, A. gerencseriae, A. viscosus, and A naes-
smoking, diet)]. Changes in the host status, such as inflam- lundii). Small proportions of Gram-negative species that are
mation, tissue degradation, and/or high gingival crevicular also found, most frequently include P intermedia, F nucleatum,
fluid flow, may lead to a shift in the microbial population in Capnocytophaga, Neisseria, and Veillonella spp. Microscopic
plaque. As a result of microenvironmental changes, the num- analyses indicate that a few Spirochetes and motile rods may
ber of beneficial species may decrease, whereas the number also be present.
of potentially pathogenic species increases. This gradual shift Certain bacterial species have been proposed to be protec-
in the entire microbial community, known as dysbiosis, may tive or beneficial to the host, including S. sanguinis, V parvula,
result in a chronic disease, state such as periodontitis. The and C. ochracea. They are typically found in high numbers
ecologic plaque hypothesis is entirely consistent with obser- at periodontal sites that do not demonstrate attachment loss
vations that disease-associated organisms are minor compo- (inactive sites) but in low numbers at sites where active peri-
nents of the oral microbiota in health; these organisms are odontal destruction occurs. These species probably function
kept in check by interspecies competition during microbial to prevent the colonization or proliferation of pathogenic
TABLE 8.3
SUMMARY OF BACTERIAL SPECIES SIGNIFICANTLY ASSOCIATED WITH DIFFERENT CLINICAL CONDITIONS BASED ON CULTURE, POLYMERASE
CHAIN REACTION, AND CHECKERBOARD DATA
Necrotizing Abscesses
Chronic Localized Aggressive Aggressive Periodontal of the
Health Gingivitis Periodontitis Periodontitis Periodontitis Diseases Periodontium Periimplantitis
A. guencseriae A. naeslundii A. actinomycetem- Capnocytophaga spp. A. actinomycetemcomitans F nucleatum F nucleatum Capnocytophaga spp
comitans serotype b (serotype b)
A. israelii Actinomyces C. ,·ectus A. actinomycetemcomitans E. nodatum P. intermedia P. micra A.actinomycetemcomitans
viscosus (high leukotoxin clone)
A. naeslundii Capnocytophaga E. corrodens C. rectus P.intermedia Spirochetes P. intermedia C. rectus
spp.
A oris 5. anginosus E. nodatum E. corrodens Spirochetes Treponema spp. Spirochetes F nucleatum
A. viscosus 5. mitis F nucleatum E. nodatum Treponema spp. P. gingi val is P. micra
C. gingi val is 5. oralis P. micra F nucleatum P. gingi valis P. intermedia
C. ochracea 5. sanguinis P. intermedia P. intermedia I forsythia Spirochetes
Capnocytopliaga spp. V parvula Spirochetes Spirochetes T denticola Treponema spp.
C. sputigena A. actinomy- Treponema spp. Treponema spp. C. gracilis Enterobacter spp.
cetemcomitans
serotype a
Eubacterium Campylobacter Enterobacter spp. Leptotrichia buccalis Campylobacter sl10wae P. gingivalis
saburreum concisus
F periodonticum C. rectus L. buccalis P. gingivalis Prevotella nigrescens T. Jorsythia
F polymorphum E. corrodens P. gingivalis I forsythia T. denticola
Neissetia spp. E. nodatum Selenomonas noxia T denticola Pseudomonas aeruginosa
Propionibactetium F nucleatum I forsythia Staphylococcus aureus 3
acnes Ol
:::,
5. anginosus Haemophilus spp. T denticola Staphylococcus epidermidis 0..
5. gordonii P. micra P. nigrescens ~

S mitis P. intermedia and 0
0..
0
Spirochetes :::,
Streptococcus oralis 5. intermedius or
5. sanguinis Treponema spp.
V parvula
..•
0
VI
D Facultative organisms
D Anaerobic organisms
+ Cocci
- Cocci
Health Gingivitis Periodontitis
FIGURE 8.8 Pie charts based on culturing studies that represent the relative proportion of different morphotypes in subgingival samples in
cases of periodontal health, gingivitis, and periodontitis. A clear distinction is made between facultative species and obligate anaerobic species.
Spirochetes are not included.
microorganisms. Clinical studies have shown that sites with Chronic Periodontitis
high levels of C. ochracea and S. sanguinis are associated with a
greater gain in attachment after therapy, thereby further sup- The microscopic examination of plaque from sites with chron-
porting this concept. A better understanding of plaque ecol- ic periodontitis has consistently revealed elevated proportions
ogy and the interactions between bacteria and their products of Spirochetes. The cultivation of plaque microorganisms
in plaque will undoubtedly reveal many other examples. from sites of chronic periodontitis reveals high percentages
of anaerobic (90%), Gram-negative (75%) bacterial species.
In patients with chronic periodontitis, the bacte-
Gingivitis ria that are most often detected at high levels include P.
The development of gingivitis has been extensively studied gingivalis, T forsythia, P. intermedia, P. nigrescens, C. rectus, E.
in a model system referred to as experimental gingivitis and corrodens, F nucleatum, A. actinomycetemcomitans (often sero-
initially described by Loe et al. Periodontal health is first es- type b), Treponema (T denticola), Selenomonas spp. (S. noxia),
tablished in human subjects via cleaning and rigorous oral and Enterobacter spp. When periodontally active sites (ie, with
hygiene measures that are followed by abstinence from oral recent attachment loss) were examined in comparison with
hygiene for 21 days. After 8 h without oral hygiene, bacteria inactive sites (ie, with no recent attachment loss), concentra-
may be found at concentrations of 103-104 mtrr? of tooth sur- tions of C. rectus, P. gingivalis, P. intermedia, F nucleatum, and
face, and they will increase in number by a factor of 100-1000 T forsythia were found to be elevated in the active sites. Fur-
during the next 24-h period. After 36 h, the plaque becomes thermore, detectable levels of P. gingivalis, P. intermedia, T for-
clinically visible. The initial micro biota of experimental gingi- sythia, C. rectus, and A. actinomycetemcomitans are associated
vitis (Fig. 8.5) consists of Gram-positive rods, Gram-positive with disease progression, and their elimination via therapy is
cocci, and Gram-negative cocci. The transition to gingivitis is associated with an improved clinical response. Both P. gingi-
evidenced by inflammatory changes; it is accompanied first by valis and A. actinomycetemcomitans are known to invade host
the appearance of Gram-negative rods and filaments and then tissue cells, which may be significant in aggressive forms of
by spirochetal and motile microorganisms. periodontitis.
The subgingival microbiota of dental plaque-induced Studies have documented an association between chronic
gingivitis (chronic gingivitis) differs from that of both health periodontitis and viral microorganisms of the herpesviruses
and chronic periodontitis (Table 8.3). It consists of roughly group, most notably EBV-1 and hCMV Furthermore, the pres-
equal proportions of Gram-positive (56%) and Gram-neg- ence of subgingival EBV-1 and hCMV are associated with high
ative (44%) species, as well as facultative (59%) and an- levels of putative bacterial pathogens, including P. gingivalis,
aerobic ( 41 %) microorganisms. It should be noted that the T forsythia, P. intermedia, and T denticola. These data support
majority of predominant species in chronic periodontitis are the hypothesis that viral infection may contribute to peri-
already present in the gingivitis state, but mostly in small odontal pathogenesis, but the potential role of viral agents
numbers. remains to be determined.
Predominant Gram-positive species include Streptococcus
spp. (S. sanguinis, S. mitis, S. intermedius, S. oralis, S. angino- Localized Aggressive Periodontitis
sus), Actinomyces spp. (A. oris and A. naeslundii), E. nodatum,
and P. micra. The Gram-negative microorganisms are predom- The microbiota associated with localized aggressive peri-
inantly Capnocytophaga spp., Fusobacterium spp., Prevotella odontitis is predominantly composed of Gram-negative,
spp., C. gracilis, C. concisus, V parvula, Haemophilus spp., and capnophilic (ie, CO2-requiring), anaerobic rods (Table 8 3)
E. corrodens. Microbiological studies indicate that almost all localized ju-
Pregnancy-associated gingivitis is an acute inflammation venile periodontitis sites harbor A. actinomycetemcomitans,
of the gingival tissues that is associated with pregnancy. This which may comprise as much as 90% of the total cultivable
condition is accompanied by increases in steroid hormones microbiota. Other organisms found in significant levels in-
in the crevicular fluid and dramatic increases in the levels of clude P. gingivalis, E. corrodens, C. rectus, F nucleatum, B. ca-
P. intermedia and C. rectus, which use the steroids as growth pillus, Eubacterium brachy, Capnocytophaga spp., and Spiro-
factors. chetes. Recent studies have also shown high proportions of
E. nodatum, P intermedia, Treponema spp. (I denticola), L. buc- F nucleatum, P intermedia, P gingivalis, P micra, and I forsythia.
calis, and I forsythia. In addition, herpesviruses, including Periradicular lesions, which arise as a consequence of end-
EBV-1 and hCMV, have also been associated with localized odontic infections, appear to have a similar microbial compo-
aggressive periodontitis. sition, with a microbiota that is dominated by anaerobes. In
A. actinomycetemcomitans is generally accepted as the pri- addition, Streptococcus spp. can also be detected.
mary etiologic agent in most but not all cases of localized ag-
gressive periodontitis. A high leukotoxic clone is uniquely
Periimplantitis
associated with aggressive forms of periodontitis. Mechanical
debridement in combination with systemic antibiotic treat- The term periimplantitis refers to an "inflammatory process"
ment is necessary to control the levels of A actinomycetem- that affects the tissues around an already osseointegrated
comitans associated with this disease due to the ability of this implant and that results in the loss of supporting bone.
organism to invade host tissues. Healthy periimplant pockets are characterized by high pro-
portions of coccoid cells, a low ratio of anaerobic-to-aerobic
Generalized Aggressive Periodontitis species, a low number of Gram-negative anaerobic species,
and low detection frequencies for periodontopathogens.
It is a severe form of periodontitis that occurs at a relatively Implants with periimplantitis reveal a microbiota that en-
young age (ie, between 20 to 40 years). It is characterized by se- compasses conventional periodontal pathogens (Table 8.3),
vere gingivitis, a large number of deepened pockets, and a high as well as the cariogenic bacterium S. mutans. Species such
tendency for bleeding on probing. In relation to the patient's as A actinomycetemcomitans, P gingivalis, T forsythia, P mi-
age, there is a lot of bone destruction. It is sometimes consid- cra, C. rectus, F nucleatum, P intermedia, T denticola, and
ered as a generalized form of localized aggressive periodontitis. Capnocytophaga spp. are often isolated from failing sites,
From a microbiological point of view, it has a lot of similarities but they can also be detected around healthy periimplant
with localized aggressive periodontitis (Table 8.3). However, sites. Other species, such as P aeruginosa, Enterobacter spp.,
aggressive periodontitis is clearly more dominated by P gingi- Candida albicans, and Staphylococci, are also frequently de-
valis, P intermedia, T forsythia, and Treponema spp. (I denticola) tected around implants.
and less by A actinomycetemcomitans. Recent checkerboard
DNA-DNA hybridization studies also indicate high propor-
tions of E. nodatum, C. gracilis, C. showae, and P nigrescens. Virulence Factors
of Periodontopathogens
Necrotizing Periodontal Diseases Virulence factors of periodontal microorganisms can be subdi-
Necrotizing periodontal diseases (Fig. 8. 9) are present as an vided as follows: (1) factors that promote colonization (adhes-
acute inflammation of the gingival and periodontal tissues ins), (2) toxins and enzymes that degrade host tissues, and (3)
that is characterized by the necrosis of the marginal gingival mechanisms that protect pathogenic bacteria from the host.
tissue and the interdental papillae. Clinically, these conditions Refer to Chapter 9.
are often associated with stress or HIV infection. They may
be accompanied by malodor and pain and possibly systemic Future Advances in Periodontal
symptoms, including lymphadenopathy, fever, and malaise.
Microbiological studies indicate that high levels of P interme- Microbiology
dia and especially of Spirochetes and F nucleatum are pres- Scientific progress at the end of the 20th century, particu-
ent in necrotizing ulcerative gingivitis lesions. Spirochetes are larly in the field of molecular biology, has led to significant
found to penetrate necrotic tissue and apparently unaffected advances in our understanding of periodontal microbiology.
connective tissue. DNA-based methodologies for the identification and detec-
tion of specific bacteria and viruses offer remarkable time
Abscesses of the Periodontium and cost advantages as compared with culturing techniques.
A dramatic increase in the number of samples that can be
Investigations reveal that bacteria that are recognized as peri- examined and the number of microorganisms enumerated is
odontal pathogens are commonly found in significant num- now possible. Perhaps even more relevant is the present abil-
bers in periodontal abscesses. These microorganisms include ity to detect microorganisms that cannot be cultivated so far,
which has underscored the limitations of our knowledge of
this complex ecologic niche. Greater awareness of the role of
the host response in periodontal disease will further improve
the understanding of the severity and therapy of periodontal
infections. Finally, the recognition of the beneficial activity
of several groups of commensal species may open new strat-
egies for the treatment of periodontal disease, such as the use
of probiotics or microbial replacement therapy.
REFERENCES
FIGURE 8.9 Clinical picture of lower front teeth with necrotizing References for this chapter are found on the companion
gingivitis . website www.medenact.com.
SUGGESTED READINGS Jakubovics NS, Palmer RJ: Oral microbial ecology: current research and new per-
spectives, Caister Academic Press, 2013, p. 1.
Berezow AB, Darveau RP: Microbial shift and periodontitis, Periodontal 2000
Samaranayake LP, Keung LW, Jin L: Oral mucosa! fungal infections, Periodon-
55:36-47, 2011.
tal 2000 49:39-59, 2009.
Bergquist R: Parasitic infections affecting the oral cavity, Periodontal 2000
Slots]: Oral viral infections of adults, Peliodontol 2000 49:60-86, 2009.
49 96-105, 2009.
Teles RP, Haffajee AD, Socransky SS: Microbiological goals of periodontal
Griffen AL, Beall CJ, Campbell JH, et al: Distinct and complex bacterial pro-
therapy, Peliodontol 2000 42 180, 2006.
files in human periodontitis and health revealed by 165 pyrosequencing,
Zijnge V, van Leeuwen MB, Degener JE, et al: Oral biofilm architecture on
ISMEJ 61176-1185, 2012.
natural teeth, PLoS ONE 5(2):e9321, 2010.
Hajishengallis G, Darveau RP, Curtis MA: The keystone-pathogen hypothesis,
Nat Rev Microbial 10:717-725, 2012.
9
Microbial Interactions with the
Host in Periodontal Diseases
RJ Nisengard • SK Haake • MG Newman • KT Miyasaki
W Teughels • C Godts • M Quirynen • N Jakubovics • N Ambalavanan
Chapter Outline
Bacterial Colonization and Survival in the Microbial Mechanisms of Host Tissue
Periodontal Region Damage
Host Tissue Invasion
Bacterial Evasion of Host Defense
Mechanisms
The interaction of the microorganism with the host deter- tissues. Thus, virulence properties can be broadly categorized
mines the course and extent of Periodontal diseases. Micro- into two groups: (1) factors that enable a bacterial species to
organisms may exert pathogenic effects directly by causing colonize and invade host tissues and (2) factors that enable
tissue destruction or indirectly by stimulating and modulating a bacterial species to cause host tissue damage directly or
host responses. The host response is mediated by the microbi- indirectly.
al interaction and inherent characteristics of the host, includ-
ing genetic factors that vary among individuals. In general, the Bacterial Colonization and Survival
host response functions in a protective capacity by preventing
in the Periodontal Region
the local infection from progressing to a systemic, life-threat-
ening infection. However, local alteration and destruction of The gingival sulcus and periodontal pocket are bathed in gin-
host tissues as a result of the microbial-host interactions may gival crevicular fluid, which flows outward from the base of
manifest as periodontal disease. the pocket. Bacterial species that colonize this region must
In general, Gram-negative facultative or anaerobic bacteria attach to available surfaces to avoid displacement by the fluid
appear to be associated with periodontal disease. Predomi- flow. Therefore, adherence represents a virulence factor for
nant bacterial species that have been implicated in the disease periodontal pathogens.
processes include Porphyromonas gingivalis, Aggrigatibacter The surfaces available for attachment include the tooth
actinomycetemcomitans, Tannerella forsythia, Fusobacterium or root, tissues, and preexisting plaque mass. Numerous in-
nucleatum, Prevotella intermedia, Campylobacter rectus, Pepto- teractions between periodontal bacteria and these surfaces
streptococcus micros, and Eikenella corrodens. The properties have been characterized, and in some cases the molecules
of these microorganisms that enable it to cause disease are responsible for mediating these highly specific interactions
referred to as virulence factors. have been determined (Table 9.1). Bacteria that initially col-
From a simplistic viewpoint, to function as a pathogen, a onize the periodontal environment most likely attach to the
bacterium must colonize the appropriate host tissue site and pellicle- or saliva-coated tooth surface. A relevant example
then cause destruction of the host tissues. In periodontitis, the is the adherence of Actinomyces viscosus and Porphyromo-
initial step in the disease process is the colonization of the peri- nas gingivalis through fimbriae on the bacterial surface to
odontal tissues by pathogenic species. Entry of the bacterium proline-rich proteins found on saliva-coated tooth surfaces.
itself (invasion) or of bacterial products into the periodontal Through its fimbriae, P gingivalis also binds to epithelial cells
tissues may be important in the disease process. Furthermore, and fibroblasts.
inherent in successful colonization of host tissues is the ability Bacterial attachment to preexisting plaque is studied by
of the bacterium to evade host defense mechanisms aimed at examining the adherence between different bacterial strains
eliminating the bacterium from the periodontal environment. (coaggregation). One of the best-characterized interactions
The process of tissue destruction results from the interac- is the adherence of A. viscosus through surface fimbriae to a
tion of bacteria or bacterial substances with host cells, which polysaccharide receptor on cells of Streptococcus sanguis. These
directly or indirectly lead to degradation of the periodontal types of interactions are thought to be of primary importance
109
TABLE 9.1
SELECT BACTERIAL ADHESINS AND TARGET SUBSTRATES

Probable
Attachment Surface Substrate Bacterial Species Bacterial Adhesion Substrate Receptor
Tooth Saliva-coated mineralized A. viscosus Fimbriae Saliva-treated hydroxyapatite
surfaces
A. viscosus Fimbriae Proline-rich proteins
Saliva-coated surfaces 5. mitis 70- to 90-kD protein Sialic acid residues
F nucleatum 300- to 330-kD outer Galactosyl residues
membrane protein
Tissue Epithelial cells P gingi val is Fimbriae Galactosyl residues
A. viscosus Fimbriae Galactosyl residues
Fibroblasts A. naeslundii Surface protein Galactosyl or mannose residues
T. denticola
Polymorphonuclear A. viscosus Fimbriae Galactosyl residues
leukocytes
A. naeslundii Protein Galactosyl residues
F nucleatum
Connective tissue P gingivalis Membrane protein Fibrinogen, fibronectin
components P intermedia Membrane protein Fibrinogen
Preexisting plaque S sanguis A. viscosus Fimbriae Repeating on polysaccharide
heptasaccharide mass S sanguis C. ochraceus Heat-sensitive protein Rhamnose, fucose,
acetylneuraminic acid
A. naeslundii N-residue
A. israelii
5. sanguis P loescheii 75-45 kD fimbrial Galactosyl residues
A. israelii proteins
P gingivalis F nucleatum Heat- and protease- Galactosyl residues
sensitive protein
T. denticola
P micros
(Data from 5ocransky 55, Haffajee AD: J Periodontal Res 26:195, 1991; Lantz MS, Allen RD, Baune/is P, et al: J Bacteriol 172:716, 1990; Lantz MS, Allen RD, Duck
LW, et al: J Bacteriol 173:4263, 1991; Bas HA, van Steenbergen M: FEMS Microbial Lett 182:57, 2000; and Kolenbrander PE, Panish KD, Andersen RN, et al: Infect
lmmun 63:4584, 1995)
in the colonization of the periodontal environment. In addi- The clinical significance of bacterial invasion is not clear.
tion, the adherence of bacteria to host tissues likely plays a Bacterial species that have been identified as capable of tissue
role in colonization and may be a critical step in the process invasion are strongly associated with disease, and the ability
of bacterial invasion. Thus, the ability of P gingivalis to attach to invade has been proposed as a key factor that distinguishes
to other bacteria, epithelial cells, and the connective tissue
components fibrinogen and fibronectin are all likely to be
important in the virulence of this microorganism.
Host Tissue Invasion

The presence of bacteria in host tissues in patients with nec-
rotizing ulcerative gingivitis (NUG) has been recognized for
years, based on histologic studies. Investigations carried out
largely in the 1980s demonstrated the presence of bacteria in
periodontal tissues in gingivitis, advanced chronic adult peri-
odontitis, and juvenile periodontitis. Both Gram-positive and
Gram-negative bacteria, including cocci, rods, filaments, and
spirochetes, have been observed in gingival connective tissue
and in proximity to alveolar bone. Bacteria may enter host tis-
sues through ulcerations in the epithelium of the gingival sul-
cus or pocket and have been observed in intercellular spaces
of the gingival tissues (Fig. 9.1). Another means of tissue inva-
sion may involve the direct penetration of bacteria into host
epithelial or connective tissue cells. Laboratory investigations FIGURE 9.1 Interface between pocket epithelium and connective tis-
sue separated by the basement lamina (BL). Abundant bacteria can be
have demonstrated the ability of A actinomycetemcomitans, seen in the intercellular spaces. Numerous infiltrating polymorphonu-
P gingivalis (Fig. 13.5), F nucleatum, and Treponema denticola clear leukocytes (L) are seen between epithelial cells (EC). Some leuko-
to invade host tissue cells directly. cytes show engulfed bacteria. (X3908.)
9 Microbial Interactions with the Host in Periodontal Diseases 111
pathogenic from nonpathogenic Gram-negative species or protects cells from the host immune system. Several periodon-
strains. Certainly, localization of bacteria to the tissues pro- topathogens are resistant to complement-mediated phagocy-
vides an ideal position from which the organism can effec- tosis, and it is thought that the proteolysis of complement
tively deliver toxic molecules and enzymes to the host tissue components contributes to resistance to some extent. P gin-
cells, and this may be the significance of invasion as a viru- givalis gingipains have been shown to degrade complement
lence factor. Indeed, some investigators have speculated that components C3, C4, CS, and factor B. More recently, a cys-
the "bursts of disease activity" observed in periodontitis may teine protease of P intermedia called interpain A has also been
be related to phases of bacterial invasion of the tissues. An shown to degrade C3.
additional possibility is that bacteria in the tissues may en- Periodontal bacteria neutralize or evade host defenses
able persistence of that species in the periodontal pocket by through numerous other mechanisms (Table 9.2). For ex-
providing a reservoir for recolonization. Consistent with this ample, immunoglobulins might function to facilitate phago-
hypothesis is the observation that mechanical debridement cytosis of bacteria by opsonization or may block adherence
alone is insufficient, and that systemic antibiotics in combi- by binding to the bacterial cell surface and restricting access
nation with surgical therapy is required, to eliminate A. ac- to bacterial adhesins. The production of immunoglobulin-
tinomycetemcomitans from lesions in patients with localized degrading proteases by specific microorganisms may counter-
aggressive periodontitis (LAP). act these host defenses. Similarly, bacteria produce substances
that suppress the activity of or kill polymorphonuclear leu-
Bacterial Evasion of Host Defense kocytes (PMNs) and lymphocytes normally involved in host
defenses. An example of this is the production by A. actino-
Mechanisms
mycetemcomitans of two toxins (a leukotoxin and cytolethal
To survive in the periodontal environment, bacteria must distending toxin) that may be important in the virulence of
neutralize or evade the host mechanisms involved in bacte- this microorganism in aggressive periodontitis and possibly in
rial clearance and killing. Pathogenic bacteria have many and chronic periodontitis. Similarly, I forsythia and F nucleatum
varied strategies for evading or subverting the host immune have been shown to induce apoptosis, a form of cellular "sui-
system, including the following: (1) the production of an cide," in lymphocytes. Many periodontal pathogens stimulate
extracellular capsule; (2) the proteolytic degradation of host the production of interleukin-8 (IL-8), a proinflammatory
innate or acquired immunity components; (3) the modulation chemokine that provides a signal for the recruitment of neu-
of host responses by binding serum components on the bacte- trophils (PMNs) to a local site. P gingivalis is able to inhibit the
rial cell surface; and (4) the invasion of gingival epithelial cells. production of IL-8 by epithelial cells, which may provide the
The majority of P gingivalis isolates from periodontitis pa- microorganism with an advantage in evading PMN-mediated
tients are encapsulated. It is hypothesized that the capsule killing.
TABLE 9.2
SELECT BACTERIAL PROPERTIES INVOLVED IN EVASION OF HOST DEFENSE MECHANISMS

Host Defense Mechanism Bacterial Species Bacterial Property Biologic Effect
Specific antibody P gingivalis lgA- and lgG-degrading proteases Degradation of specific antibody
P intermedia
P melaninogenica
Capnocytophaga spp.
Polymorphonuclear function A actinomycetem-comitans Leukotoxin Inhibition of PMN leukocytes (PMNs)
F nucleatum Heat-sensitive surface protein Apoptosis (programmed cell death) of PMN
P gingivalis Capsule Inhibition of phagocytosis
T denticola Inhibition of superoxide Decreased bacterial killing
production
Lymphocytes A. actinomycetem-comitans Leukotoxin Killing of mature B and T cells; nonlethal
suppression of activity
Cytolethal distending toxin Impairment of function by arresting of
lymphocyte cell cycle
F nucleatum Heat-sensitive surface protein Apoptosis of mononuclear cells
I forsythia Cytotoxin Apoptosis of lymphocytes
P intermedia Suppression Decreased response to antigens and
mitogens
T denticola
A actinomycetem-comitans
Release of interleukin-8 PMN P gingivalis Inhibition of IL-8 production by Impairment of to bacteria
response (IL-8) epithelial cells
(Data from Socransky SS, Haffajee AD: J Periodontal Res 26:195, 1991; Jewett A, Hume WR, Le H, et al: Infect Im mun 68:1893, 2000; Shenker BJ, McKay T, Datar S,
et al: J Immunol 162:4773, 1999; Arakawa S, Nakajima T, Ishikura H, et al: Infect Immun 68:4611, 2000; Darveau RP, Belton CM, Reife RA, et al: Infect Immun
66:1660, 1998; and Huang GT, Haake SK, KimJW, et al: Oral Microbial Immunol 131301, 1998)
Microbial Mechanisms of Host Tissue TABLE 9.3

Damage BACTERIAL ENZYMES CAPABLE OF DEGRADING
HOST TISSUES
Tissue Destruction-Promoting Factors
Bacterial Enzyme Species
Many bacterial proteins that interact with host cells are recog-
nized by the immune system, and they may trigger immune Collagenase P gingivalis
responses. Fimbriae of P gingivalis and A actinomycetemcomi- A actinomycetemcomitans
tans are highly antigenic. Inflammation is a major contributor Trypsinlike enzyme P gingivalis
A. actinomycetemcomitans
to tissue destruction in periodontal disease. However, a num-
T denticola
ber of bacterial products directly promote tissue destruction Arysulfatase C. rectus
in addition to modulating host immunity, with extracellular Neuraminidase P ginivalis
proteolytic enzymes being the most notable (Table 9.3). T forsythia
Bacterial proteolytic activity in dental plaque-and, in P melaninogenica
particular, trypsin like protease activity-is closely correlated Fibronectin-degrading enzyme P gingivalis
with clinical markers of periodontal disease. P intermedia
Trypsin like proteases are produced by P gingivalis, Phospholipase A P intermedia
T denticola, and I forsythia. Proteases supply nutrition in the P melaninogenica
form of peptides or amino acids to the bacteria that produce
them. During this process, they may cause the extensive deg-
radation of host extracellular proteins.
However, the bulk of the host tissue-degrading activity is bacteria into host tissues. The host immune system involves
restricted to a small number of these enzymes. In the case of a complex network of interactions among cells and regula-
P gingivalis, three enzymes known as gingipains are responsible tory molecules. Bacterial products may perturb the system,
for at least 85% of the total host protein-degradation activity. resulting in tissue destruction. Well-characterized inter-
The gingipains belong to the cysteine protease fam- actions involve the release of interleukin-1 (IL-1), tumor
ily, and they use an active-site cysteine residue for catalysis. necrosis factor (TNF), and prostaglandins from monocytes,
Gingipains are classed as "Arg-gingipains" (RgpA and RgpB) macrophages, and PMNs exposed to bacterial endotoxin
or "Lys-gingipains" (Kgp) on the basis of their ability to cleave (lipopolysaccharide).These host-derived mediators have the
Arg-Xaa or Lys-Xaa peptide bonds (Xaa represents any ami- potential to stimulate bone resorption and activate or inhibit
no acid). Gingipains are multifunctional proteins that play other host immune cells.
important roles in adhesion, tissue degradation, and the eva- Thus, it is obvious that periodontal destruction involves a
sion of host responses. complex interplay between bacterial pathogens and the host
However, the exact role of bacterially derived proteases in tissues. For some time it has been recognized that "not all
the disease process has not been determined because similar dental plaque is equal" and that specific bacterial pathogens
enzymes (eg, collagenases) in the periodontal environment appear to be responsible for the changes resulting in disease.
originate from host tissue cells. Indeed, one mechanism by It also has been recognized that in the process of effectively
which bacteria may indirectly cause tissue damage is by in- limiting the bacterial assault of the periodontal tissues, host
duction of host tissue proteinases such as elastase and matrix defense mechanisms contribute to the destruction of tissues
metalloproteinases (MMPs). locally The challenge for the future is to be able to bet-
Some bacterial products inhibit the growth or alter the ter identify the more virulent bacterial strains and the more
metabolism of host tissue cells; these include a number of susceptible hosts. In this manner it may be possible to pre-
metabolic byproducts such as ammonia; volatile sulfur com- dict accurately the individuals at risk for future disease and
pounds; and fatty acids, peptides, and indoles. Bacterial to develop more effective strategies to prevent the onset and
enzymes may facilitate tissue destruction and invasion of progression of periodontitis.
10
The Role of Dental Calculus
and Other Predisposing Factors
JE Hinrichs • VT Math • SR Diehl • C-H Chou • F Kuo
• C-Y Huang • OA Korczeniewska • N Ambalavanan
Chapter Outline
Calculus Inherited Variation and Risk
Other Predisposing Factors of Periodontitis
Genetic Susceptibility to Periodontal
Disease
The primary cause of gingival inflammation is bacterial may be evaluated by careful tactile perception with a delicate
plaque. Other predisposing factors include calculus, faulty dental instrument such as an explorer. Subgingival calculus
restorations, complications associated with orthodontic ther- is typically hard and dense; it frequently appears to be dark
apy, self-inflicted injuries, and the use of tobacco, in addition brown or greenish black in color (Fig. 10.3), and it is firmly
to several others. These will be discussed in turn. attached to the tooth surface. Supragingival calculus and sub-
gingival calculus generally occur together, but one may be
present without the other. Microscopic studies demonstrate
Calculus that deposits of subgingival calculus usually extend nearly to
Calculus consists of mineralized bacterial plaque that forms the base of periodontal pockets in individuals with chronic
on the surfaces of natural teeth and dental prostheses. periodontitis but do not reach the junctional epithelium.
When the gingival tissues recede, subgingival calculus be-
comes exposed and is therefore reclassified as supragingival
Supragingival and Subgingival Calculus
(Fig. 10.4A). Thus, supragingival calculus can be composed of
Supragingival calculus is located coronal to the gingival margin both supragingival calculus and previous subgingival calculus.
and therefore is visible in the oral cavity It is usually white or A reduction in gingival inflammation and probing depths with
whitish yellow in color; hard, with a claylike consistency; and a gain in clinical attachment can be observed after the removal
easily detached from the tooth surface. After removal, it may rap- of subgingival plaque and calculus (Fig. 10.4B)
idly recur, especially in the lingual area of the mandibular inci-
sors. The color is influenced by contact with such substances as
Prevalence
tobacco and food pigments. It may localize on a single tooth or
group of teeth, or it may be generalized throughout the mouth. The formation of supragingival calculus was observed early in
The two most common locations for the development of life in individuals who do not have access to preventive dental
supragingival calculus are the buccal surfaces of the maxillary care, probably shortly after the teeth erupted. The first areas
molars (Fig. 10.1) and the lingual surfaces of the mandibular to exhibit calculus deposits were the facial aspects of maxillary
anterior teeth (Fig. 10.2). Saliva from the parotid gland flows molars and the lingual surfaces of mandibular incisors. The
over the facial surfaces of the upper molars via the parotid deposition of supragingival calculus continued as individuals
duct, whereas the submandibular duct and the lingual duct aged, and it reached a maximal calculus score when the af-
empty onto the lingual surfaces of the lower incisors from the fected individuals were around 25-30 years old. At this time,
submaxillary and sublingual glands, respectively. In extreme most of the teeth were covered by calculus although the facial
cases, calculus may form a bridgelike structure over the inter- surfaces had less calculus than the lingual or palatal surfaces.
dental papilla of adjacent teeth or cover the occlusal surface of Calculus accumulation appeared to be symmetric, and, by the
teeth that are lacking functional antagonists. age of 45 years, these individuals had only a few teeth (typi-
Subgingival calculus is located below the crest of the mar- cally the premolars) without calculus. Subgingival calculus
ginal gingiva and therefore is not visible on routine clinical appeared first either independently or on the interproximal
examination. The location and extent of subgingival calculus aspects of areas where supragingival calculus already existed.
113
FIGURE 10.1 Supragingival calculus is depicted on the buccal surfaces

of maxillary molars adjacent to the orifice for the parotid duct.
FIGURE 10.2 Extensive supragingival calculus is present on the lingual FIGURE 10.4 A, A 31-year-old white man with extensive supragingival
surfaces of the lower anterior teeth. and subgingival calculus deposits throughout his dentition is shown. B,
One year after receiving thorough scaling and root planing to remove
supragingival and subgingival calculus deposits, followed by restorative
care. Note the substantial reduction in gingival inflammation.
FIGURE 10.3 Dark pigmented deposits of subgingival calculus are

shown on the distal root of an extracted lower molar.
By the age of 30 years, all surfaces of all teeth had subgingival

calculus without any pattern of predilection.
Both supragingival calculus and subgingival calculus may
be seen on radiographs. Highly calcified interproximal calcu-
lus deposits are readily detectable as radiopaque projections
that protrude into the interdental spaces (Fig. 10.5). However,
the sensitivity level of detecting calculus by radiographs is in-
consistent. The location of calculus does not indicate the bot-
tom of the periodontal pocket, because the most apical plaque
is not sufficiently calcified to be visible on radiographs.
Composition
Inorganic Content
Supragingival calculus consists of inorganic (70-90%) and
organic components. The major inorganic proportions of FIGURE 10.5 A bitewing radiograph illustrating subgingival calculus
calculus have been reported as approximately 76% calcium deposits that are depicted as interproximal spurs (arrows).
10 The Role of Dental Calculus and Other Predisposing Factors 115
phosphate, (Ca3[PO4]i); 3% calcium carbonate (CaCOJ; and

traces of magnesium phosphate (Mg3[PO4]2) and other metals.
The percentage of inorganic constituents in calculus is similar
to that of other calcified tissues of the body. The principal
inorganic components have been reported as approximately
39% calcium, 19% phosphorus, 2 % carbon dioxide, and 1 %
magnesium as well as trace amounts of sodium, zinc, stron-
tium, bromine, copper, manganese, tungsten, gold, alumi-
num, silicon, iron, and fluorine.
At least two-third of the inorganic component is crystal-
line in structure. The four main crystal forms and their ap-
proximate percentages are as follows: hydroxyapatite, 58%;
magnesium whitlockite, 21 %; octacalcium phosphate, 12%;
and brushite, 9%.
Two or more crystal forms are typically found in a sample
of calculus. Hydroxyapatite and octacalcium phosphate are
detected most frequently (ie, in 97-100% of all supragingival FIGURE 10.6 Calculus attached to the pellicle on the enamel surface
calculus) and constitute the bulk of the specimen. Brushite is and the cementum. An enamel void (E) has been created during the
more common in the mandibular anterior region, and magne- preparation of the specimen. C, Cementum; CA, calculus; P, pellicle.
sium whitlockite is found in the posterior areas. The incidence
of the four crystal forms varies with the age of the deposit.
Organic Content
The organic component of calculus consists of a mixture of
protein-polysaccharide complexes, desquamated epithelial
cells, leukocytes, and various types of microorganisms.
Between 1.9% and 9.1 % of the organic component is car-
bohydrate, which consists of galactose, glucose, rhamnose,
mannose, glucuronic acid, galactosamine, and sometimes
arabinose, galacturonic acid, and glucosamine. All of these
organic components are present in salivary glycoprotein, with
the exception of arabinose and rhamnose. Salivary proteins
account for 5.9-8.2% of the organic component of calculus
and include most amino acids. Lipids account for 0.2% of the
organic content in the form of neutral fats, free fatty acids,
cholesterol, cholesterol esters, and phospholipids.
The composition of subgingival calculus is similar to that of
supragingival calculus, with some differences. It has the same
hydroxyapatite content, more magnesium whitlockite, and
less brushite and octacalcium phosphate. The ratio of calcium
to phosphate is higher subgingivally, and the sodium content
increases with the depth of periodontal pockets. These altered
compositions may be attributed to the origin of subgingival
calculus being plasma, whereas supragingival calculus is par-
tially composed of saliva constituents. Salivary proteins pres-
ent in supragingival calculus are not found subgingivally. Den-
FIGURE 10.7 Nondecalcified specimen with calculus (CA) attached to
tal calculus, salivary duct calculus, and calcified dental tissues enamel (E) surface just coronal to the cementoenamel junction (CEJ).
are similar in inorganic composition. Note plaque (P) on the surface of the calculus; dentin (0) and cementum
(C) are also identified. (Courtesy Dr Michael Rohrer, Minneapolis, MN.)
Attachment to the Tooth Surface

Formation
Differences in the manner in which calculus is attached to the
tooth surface affect the relative ease or difficulty encountered Calculus is mineralized dental plaque. The soft plaque is hard-
during its removal. Four modes of attachment have been de- ened by the precipitation of mineral salts, which usually starts
scribed. Attachment by means of an organic pellicle on ce- between the first and fourteenth days of plaque formation.
mentum is depicted in Fig. 10.6, and attachment on enamel is Calcification has been reported to occur within as little as
shown in Fig. 10. 7. Mechanical locking to surface irregulari- 4-8 h. Calcifying plaques may become 50% mineralized in
ties such as caries lesions or resorption lacunae also occurs. 2 days and 60-90% mineralized in 12 days. All plaque does
The fourth mode of attachment consists of the close adapta- not necessarily undergo calcification. Early plaque contains
tion of the undersurface of calculus to depressions or gently a small amount of inorganic material, which increases as the
sloping mounds of the unaltered cementum surface, as shown plaque develops into calculus. Plaque that does not develop
in Fig. 10.8, and the penetration of bacterial calculus into ce- into calculus reaches a plateau of maximal mineral content
mentum. within 2 days. Microorganisms are not always essential in
Theories Regarding the Mineralization of Calculus

The theoretical mechanisms by which plaque becomes miner-
alized can be stratified into two categories.
1. Mineral precipitation results from a local rise in the degree
of saturation of calcium and phosphate ions, which may be
brought about in the following several ways:
a. A rise in the pH of the saliva causes the precipitation of cal-
cium phosphate salts by lowering the precipitation constant.
The pH may be elevated by the loss of carbon dioxide
and the formation of ammonia by dental plaque bacte-
ria or by protein degradation during stagnation.
b. Colloidal proteins in saliva bind calcium and phosphate
ions and maintain a supersaturated solution with respect
to calcium phosphate salts. With the stagnation of saliva,
colloids settle out, and the supersaturated state is no
FIGURE 10.8 Undersurface of subgingival calculus (C) previously at- longer maintained, thereby leading to the precipitation
tached to the cementum surface (5). Note the impression of cemen-
tum mounds in the calculus (arrows). (Courtesy Dr John Sottosanti,
of calcium phosphate salts.
La Jolla, CA.) c. Phosphatase liberated from dental plaque, desquamated
epithelial cells, or bacteria precipitates calcium phosphate
by hydrolyzing organic phosphates in saliva, thereby in-
calculus formation, because calculus occurs readily in germ- creasing the concentration of free phosphate ions. Esterase
free rodents. is another enzyme that is present in the cocci and fila-
Saliva is the source of mineralization for supragingival mentous organisms, leukocytes, macrophages, and des-
calculus, whereas the serum transudate called gingival cre- quamated epithelial cells of dental plaque. Esterase may
vicular fluid furnishes the minerals for subgingival calculus. initiate calcification by hydrolyzing fatty esters into free
The calcium concentration/content in plaque is 2-20 times fatty acids. The fatty acids form soaps with calcium
that found in saliva. Early plaque of heavy calculus formers and magnesium that are later converted into the less-
contains more calcium, three times more phosphorus, and soluble calcium phosphate salts.
less potassium than that of noncalculus formers, thereby sug- 2. Seeding agents induce small foci of calcification that en-
gesting that phosphorus may be more critical than calcium large and coalesce to form a calcified mass. This concept
for plaque mineralization. Calcification entails the binding of has been referred to as the epitactic concept or, more ap-
calcium ions to the carbohydrate-protein complexes of the propriately, as heterogeneous nucleation. The seeding agents
organic matrix and the precipitation of crystalline calcium in calculus formation are not known, but it is suspected
phosphate salts. Crystals form initially in the intercellular that the intercellular matrix of plaque plays an active role.
matrix and on the bacterial surfaces and finally within the The carbohydrate-protein complexes may initiate calcifi-
bacteria. cation by removing calcium from the saliva (chelation) and
The calcification of supragingival plaque and in the at- binding with it to form nuclei that induce the subsequent
tached component of subgingival plaque begins along the in- deposition of minerals.
ner surface adjacent to the tooth. Separate foci of calcification
increase in size and coalesce to form solid masses of calculus. Role of Microorganisms in the Mineralization
Calcification may be accompanied by alterations in the bacte- of Calculus
rial content and staining qualities of the plaque. As calcifica- Mineralization of plaque generally starts extracellularly
tion progresses, the number of filamentous bacteria increases around both Gram-positive and Gram-negative organisms,
and the foci of calcification change from basophilic to eosino- but it may also start intracellularly Filamentous organisms,
philic. Calculus is formed in layers, which are often separated diphtheroids, and Bacterionema and Veillonella species have
by a thin cuticle that becomes embedded in the calculus as the ability to form intracellular apatite crystals. Mineralization
calcification progresses. spreads until the matrix and the bacteria are calcified.
The initiation of calcification and the rate of calculus ac- Bacterial plaque may actively participate in the mineraliza-
cumulation vary among individuals, among tooth variety in tion of calculus by forming phosphatases, which changes the
the same dentition, and at different times in the same person pH of the plaque and induces mineralization, but the prevalent
On the basis of these differences, persons may be classified as opinion is that these bacteria are only passively involved and are
heavy, moderate, or slight calculus formers or as noncalculus simply calcified with other plaque components. The occurrence
formers. The average daily increment in calculus formers is of calculus-like deposits in germ-free animals supports this
from 0.10% to 0.15% of dry weight calculus. Calculus for- opinion. However, other experiments suggest that transmissible
mation continues until it reaches a maximum, after which it factors are involved in calculus formation and that penicillin in
may be reduced in amount. The time required to reach the the diets of some of these animals reduces calculus formation.
maximal level has been reported to be between 10 weeks and
6 months. Etiologic Significance
The decline from maximal calculus accumulation, which
is referred to as the reversal phenomenon, may be explained by Distinguishing between the effects of calculus and plaque on
the vulnerability of bulky calculus to mechanical wear from the gingiva is difficult, because calculus is always covered
food and from the cheeks, lips, and tongue. with a nonmineralized layer of plaque. A positive correlation
between the presence of calculus and the prevalence of gingi-

vitis exists, but this correlation is not as great as that between
plaque and gingivitis. The initiation of periodontal disease
in young people is closely related to plaque accumulation,
whereas calculus accumulation is more prevalent in chronic
periodontitis found in older adults.
The incidence of calculus, gingivitis, and periodontal dis-
ease increases with age. It is extremely rare to find periodontal
pockets in adults without at least some subgingival calculus
being present although the subgingival calculus may be of
microscopic proportions.
Calculus does not contribute directly to gingival inflam-
mation, but it provides a fixed nidus for the continued accu- FIGURE 10.9 Tobacco stains on the apical third of the clinical crown
mulation of plaque and its retention in close proximity to the caused by cigarette smoking.
gingiva. Subgingival calculus is likely to be the product rather
than the cause of periodontal pockets. Plaque initiates gingi-
val inflammation, which leads to pocket formation, and the periodontal destruction. Inadequate dental procedures that
pocket in turn provides a sheltered area for plaque and bacte- contribute to the deterioration of the periodontal tissues are
rial accumulation. The increased flow of gingival fluid asso- referred to as iatrogenic factors. Iatrogenic endodontic com-
ciated with gingival inflammation provides the minerals that plications that can adversely affect the periodontium include
mineralize the continually accumulating plaque that results in root perforations, vertical root fractures, and endodontic fail-
the formation of subgingival calculus. Aggressive periodontitis ures that may necessitate tooth extraction.
areas with detectable subgingival calculus were much more Characteristics of dental restorations and removable partial
likely to experience a loss of periodontal attachment than sites dentures that are important to the maintenance of periodon-
that did not initially exhibit subgingival calculus. tal health include the location of the gingival margin for the
Although the bacterial plaque that coats the teeth is the restoration, the space between the margin of the restoration
main etiologic factor in the development of periodontal dis- and the unprepared tooth, the contour of the restorations, the
ease, the removal of subgingival plaque and calculus constitute occlusion, the materials used in the restoration, the restorative
the cornerstone of periodontal therapy. Calculus plays an im- procedure itself, and the design of the removable partial den-
portant role in maintaining and accentuating periodontal dis- ture. These characteristics are described in this chapter as they
ease by keeping plaque in close contact with the gingival tissue relate to the etiology of periodontal disease. A more compre-
and by creating areas where plaque removal is impossible. hensive review with special emphasis on the interrelationship
between restorative procedures and the periodontal status is
presented in Chapter 53.
Materia Alba, Food Debris, and Dental
Stains Margins of Restorations
Materia alba is an accumulation of microorganisms, desqua- Overhanging margins of dental restorations contribute to the de-
mated epithelial cells, leukocytes, and a mixture of salivary velopment of periodontal disease by (1) changing the ecologic
proteins and lipids, with few or no food particles; it lacks the balance of the gingival sulcus to an area that favors the growth
regular internal pattern observed in plaque. It is a yellow or of disease-associated organisms (predominantly Gram-negative
grayish-white, soft, sticky deposit, and it is somewhat less ad- anaerobic species) at the expense of the health-associated or-
herent than dental plaque. The irritating effect of materia alba ganisms (predominantly Gram-positive facultative species) and
on the gingiva is caused by bacteria and their products. (2) inhibiting the patients access to remove accumulated plaque.
Most food debris is rapidly liquefied by bacterial enzymes The frequency of overhanging margins on proximal resto-
and cleared from the oral cavity by salivary flow and the me- rations has varied in different studies from 16.5% to 75%. A
chanical action of the tongue, cheeks, and lips. The rate of highly significant statistical relationship has been reported be-
clearance from the oral cavity varies with the type of food and tween marginal defects and reduced bone height. The removal
the individual. Aqueous solutions are typically cleared within of overhangs allows for the more effective control of plaque,
15 min, whereas sticky foods may adhere for more than 1 h. thereby resulting in a reduction of gingival inflammation and
Dental plaque is not a derivative of food debris, and food de- a small increase in radiographic alveolar bone support.
bris is not an important cause of gingivitis. The location of the gingival margin of a restoration is di-
Pigmented deposits on the tooth surface are called dental rectly related to the health status of the adjacent periodontal
stains. Stains are primarily an aesthetic problem and do not tissues. Numerous studies have shown a positive correlation
cause inflammation of the gingiva. The use of tobacco prod- between margins located apical to the marginal gingiva and
ucts (Fig. 10. 9), coffee, tea, certain mouthrinses, and pig- the presence of gingival inflammation. Subgingival margins
ments in foods can contribute to stain formation. are associated with large amounts of plaque, more severe gin-
givitis, and deeper pockets. Even high-quality restorations, if
placed subgingivally, will increase plaque accumulation, gin-
Other Predisposing Factors gival inflammation, and the rate of gingival fluid flow. Mar-
Iatrogenic Factors gins placed at the level of the gingival crest induce less severe
inflammation, whereas supragingival margins are associated
Deficiencies in the quality of dental restorations or prosthe- with a degree of periodontal health similar to that seen with
ses are contributing factors to gingival inflammation and nonrestored interproximal surfaces.
FIGURE 10.10 A, Inflamed marginal and papillary gingiva adjacent to an overcontoured porcelain-fused-to-metal crown on the maxillary left cen-
tral. B, Radiograph of an ill-fitting porcelain-fused-to-metal crown.
Roughness in the subgingival area is considered to be a Contours/Open Contacts

maJor contributing factor to plaque buildup and subsequent Overcontoured crowns and restorations tend to accumulate
gingival inflammation. The subgingival zone is composed plaque and handicap oral hygiene measures in addition to
of the margin of the restoration, the luting material, and the possibly preventing the self-cleaning mechanisms of the
prepared and unprepared tooth surfaces. Sources of margin- adjacent cheek, lips, and tongue (Fig. 10.10). Restorations
al roughness include grooves and scratches in the surface of that fail to reestablish adequate interproximal embrasure
acrylic resin, porcelain, or gold restorations; the separation of spaces are associated with papillary inflammation. Under-
the restoration margin and the luting material from the cervi- contoured crowns that lack a protective height of contour
cal finish line, thereby exposing the rough surface of the pre- do not retain as much plaque as overcontoured crowns and
pared tooth ; the dissolution and disintegration of the luting therefore may not be as detrimental during mastication as
material between the preparation and the restoration, thereby once thought.
leaving a space; and inadequate marginal fit of the restora- The contour of the occlusal surface as established by the
tion. Subgingival margins typically have a gap of 20-40 µm marginal ridges and related developmental grooves normally
between the margin of the restoration and the unprepared serves to deflect food away from the interproximal spaces.
tooth. Colonization of this gap by bacterial plaque undoubt- The optimal cervico-occlusal location for a posterior contact
edly contributes to the detrimental effect of margins placed in is at the longest mesiodistal diameter of the tooth, which is
a subgingival environment. generally just apical to the crest of the marginal ridge. The
integrity and location of the proximal contacts along with the
Retained Cement/Periimplantitis contour of the marginal ridges and developmental grooves
Periimplantitis is an inflammatory disease that affects the tis- typically prevent interproximal food impaction. Food impac-
sues around dental implants and that results in progressive tion is the forceful wedging of food into the periodontium
bone loss. The prevalence of periimplantitis among implant by occlusal forces. As the teeth wear down, their originally
supported prosthesis/restoration ranges from 28% to 56%. convex proximal surfaces become flattened and the wedging
The early diagnosis of this condition and its proper manage- effect of the opposing cusp is exaggerated. Cusps that tend to
ment are critical to the longevity of the implant and supported forcibly wedge food into interproximal embrasures are known
prosthesis. as plunger cusps. The interproximal plunger cusp effect may
Local factors such as retained residual cement or the inad- also be observed when missing teeth are not replaced and the
equate seating of the implant abutment or prosthesis can lead relationship between the proximal contacts of adjacent teeth
to bone loss around an implant. In a retrospective study, it was is altered. An intact proximal contact precludes the force-
found that 81 % of the implants diagnosed with periimplanti- ful wedging of food into the interproximal embrasure space,
tis had residual cement associated with their cement-retained whereas a light or open contact is conducive to impaction.
restorations. The surgical removal of the residual cement The classic analysis of the factors that lead to food impac-
resolved the infection and halted the periimplantitis in 74% tion was made by Hirschfeld, who recognized the following
of the implants. factors: uneven occlusal wear, the opening of the contact point
The possible adverse effect of traumatic occlusion on as a result of a loss of proximal support or from extrusion,
implants has been correlated with early implant failures. congenital morphologic abnormalities, and improperly con-
However, the relationship between traumatic occlusion and structed restorations.
periimplantitis is to date a controversial issue. In vivo ex- The presence of the previously mentioned abnormalities
periments have shown that, in the absence of periimplant in- does not necessarily lead to food impaction and periodontal
flammation, the application of excessive occlusal stress leads disease. A study of interproximal contacts and marginal ridge
to only minor alterations in the marginal bone level. Alter- relationships in three groups of periodontally healthy males
natively, the application of excessive occlusal forces in the revealed that 0.7-76% of the proximal contacts were defec-
presence of plaque-induced inflammation can significantly tive and that 33.5% of adjacent marginal ridges were uneven.
increase the rate of bone loss around implant-supported res- However, greater probing depth and a loss of clinical attach-
torations. ment have been reported for sites that exhibited both an open
FIGURE 10.11 A, Lower incisor showing a prominent root with gingival recession and a lack of attached gingiva. B, Three months after the placement
of a free gingival graft, which resulted in a gain in attached gingiva and a reduction in gingival recession.
contact and food impaction as compared with contralateral subgingival margins of a tooth or for the purpose of obtaining
control sites without open contacts or food impaction. Exces- an impression may mechanically injure the periodontium and
sive anterior overbite is a common cause of food impaction leave behind impacted debris that are capable of causing a
on the lingual surfaces of the maxillary anterior teeth and the foreign body reaction.
facial surfaces of the opposing mandibular teeth. These areas
may be exemplified by attachment loss with gingival recession.
Malocclusion
Materials The irregular alignment of teeth as found in cases of malocclu-
In general, restorative materials are not in themselves injuri- sion may make plaque control more difficult. Several authors
ous to the periodontal tissues. One exception to this may be have found a positive correlation between crowding and peri-
self-curing acrylics. odontal disease, whereas other investigators did not find such
Plaque that forms at the margins of restorations is simi- a correlation. Uneven marginal ridges of contiguous posterior
lar to that found on adjacent nonrestored tooth surfaces. The teeth have been found to have a low correlation with pock-
composition of plaque formed on all types of restorative ma- et depth, loss of attachment, plaque, calculus, and gingival
terials is similar, with the exception of that formed on silicate. inflammation. Roots of teeth that are prominent in the arch
Although surface textures of restorative materials differ with (Fig. 10 .11)-such as in a buccal or lingual version or that are
regard to their capacity to retain plaque, all can be adequately associated with a high frenal attachment and small quantities
cleaned if they are polished and accessible to methods of oral of attached gingiva-frequently exhibit recession.
hygiene. The undersurface of pontics in fixed bridges should The failure to replace missing posterior teeth may have
barely touch the mucosa. Access for oral hygiene is inhibited adverse consequences on the periodontal support for the re-
with excessive pontic-to-tissue contact, thereby contributing maining teeth. The following hypothetical scenario illustrates
to plaque accumulation that will cause gingival inflammation the possible ramifications of not replacing a missing poste-
and possibly the formation of pseudopockets. rior tooth. When the mandibular first molar is extracted, the
initial change is a mesial drifting and tilting of the mandibu-
Design of Removable Partial Dentures lar second and third molars with extrusion of the maxillary
Several investigations have shown that, after the insertion of first molar. As the mandibular second molar tips mesially, its
partial dentures, mobility of the abutment teeth, gingival in- distal cusps extrude and act as plungers. The distal cusps of
flammation, and periodontal pocket formation all increase. the mandibular second molar wedge between the maxillary
This is because partial dentures favor the accumulation of first and second molars and open the contact by deflecting the
plaque, particularly if they cover the gingival tissue. Partial maxillary second molar distally Subsequently, food impaction
dentures that are worn during both night and day induce may occur and be accompanied by gingival inflammation with
more plaque formation than those worn only during the the eventual loss of the interproximal bone between the max-
daytime. These observations emphasize the need for careful illary first and second molars. This example does not occur in
and personalized oral hygiene instruction to avoid the harm- all cases in which mandibular first molars are not replaced.
ful effects of partial dentures on the remaining teeth and the However, the drifting and tilting of the remaining teeth with
periodontium. The presence of removable partial dentures an accompanying alteration of the proximal contacts is gener-
induces not only quantitative changes in dental plaque but ally a consequence of not replacing posterior teeth that have
also qualitative changes, thereby promoting the emergence of been extracted.
spirochetal microorganisms. Tongue thrusting exerts excessive lateral pressure on the
anterior teeth, which may result in the spreading and tilt-
Restorative Dentistry Procedures ing of the anterior teeth (Fig. 10.12). Tongue thrusting is
The use of rubber dam clamps, matrix bands, and burs in an important contributing factor to tooth migration and the
such a manner as to lacerate the gingiva results in varying de- development of an anterior open bite. Mouth breathing may
grees of mechanical trauma and inflammation. Although such be observed in association with a habit of tongue thrusting
transient injuries generally undergo repair, they are need- and an anterior open bite. Marginal and papillary gingivitis
less sources of discomfort to the patient. The forceful pack- is frequently encountered in the maxillary anterior sextant in
ing of a gingival retraction cord into the sulcus to prepare the cases that involve an anterior open bite with mouth breathing.
FIGURE 10.12 A, Anterior open bite with flared incisors as observed in association with a habit of tongue thrusting. B, Radiographs show severe
periodontal destruction (arrows) in the molar regions.
However, the role of mouth breathing as a local causative fac-

tor is unclear, because conflicting evidence has been reported.
Restorations that do not conform to the occlusal pattern of
the mouth result in occlusal disharmonies that may cause in-
jury to the supporting periodontal tissues. More issues involv-
ing deeper initial probing depths, worse prognoses, and greater
mobility have been observed for teeth with occlusal discrepan-
cies as compared with teeth without initial occlusal discrepan-
cies. Histologic features of the periodontium for a tooth that
has been subjected to traumatic occlusion include a widened
subcrestal periodontal ligament space, a reduction in the col-
lagen content of the oblique and horizontal fibers, an increase FIGURE 10.13 Gingival inflammation and enlargement associated
in vascularity and leukocyte infiltration, and an increase in the with an orthodontic appliance and poor oral hygiene.
number of osteoclasts on bordering alveolar bone. However,
these observations are generally apical and separate from the
bacteria-induced inflammation that occurs at the base of the
sulcus. On the basis of current human trials, it is still impos- Plaque Retention and Composition
sible to definitively answer the question, "Does occlusal trauma Orthodontic appliances tend to retain bacterial plaque and
modify the progression of periodontal attachment loss that is food debris, thereby resulting in gingivitis (Fig. 10 13), and
associated with periodontal inflammation?" (See Chapter 21 for they are also capable of modifying the gingival ecosystem. An
a more detailed explanation of periodontal trauma from occlu- increase in Prevotella melaninogenica, Prevotella intermedia, and
sion and the periodontal response to external forces.) Actinomyces odontolyticus and a decrease in the proportion of
facultative microorganisms was detected in the gingival sulcus
after the placement of orthodontic bands. More recently, A
Periodontal Complications Associated actinomycetemcomitans was found in at least one site in 85% of
children who were wearing orthodontic appliances. By con-
with Orthodontic Therapy trast, only 15% of unbanded control subjects were positive for
Orthodontic therapy may affect the periodontium by favor- A. actinomycetemcomitans.
ing plaque retention, by directly injuring the gingiva as a re-
sult of overextended bands, and by creating excessive forces, Gingival Trauma and Alveolar Bone Height
unfavorable forces, or both on the tooth and its supporting Orthodontic treatment is often started soon after the eruption
structures. of the permanent teeth when the junctional epithelium is still
adherent to the enamel surface. Orthodontic bands should

not be forcefully placed beyond the level of attachment, be-
cause this will detach the gingiva from the tooth and result in
the apical proliferation of the junctional epithelium with an
increased incidence of gingival recession.
The mean alveolar bone loss per patient for adolescents
who underwent 2 years of orthodontic care during a 5-year
observation period ranged between 0.1 and 0.5 mm. This
small magnitude of alveolar bone loss was also noted in the
control group and therefore considered to be of little clinical
significance. However, the degree of bone loss during adult
orthodontic care may be higher than that observed in adoles-
cents, especially if the periodontal condition is not treated be-
fore the initiation of orthodontic therapy. Therefore, orthodontic FIGURE 10.14 Gingival recession on a maxillary canine caused by
treatment should not be commenced in the presence of uncontrolled self-inflicted trauma from the patient's fingernail.
periodontal disease.
a role in the development of lesions on the distal surface of
Tissue Response to Orthodontic Forces second molars-particularly in those who are more than
Orthodontic tooth movement is possible because the peri- 25-years old-include the presence of visible plaque, bleed-
odontal tissues are responsive to externally applied forces. ing on probing, root resorption in the contact area between
Alveolar bone is remodeled by osteoclasts that induce bone the second and third molars, the presence of a pathologically
resorption in areas of pressure and by osteoblasts that form widened follicle, the inclination of the third molar, and the
bone in areas of tension. Although moderate orthodontic forc- close proximity of the third molar to the second molar. Other
es ordinarily result in bone remodeling and repair, excessive potential but rare iatrogenic adverse consequences of the re-
force may produce necrosis of the periodontal ligament and moval of the third molars include permanent paresthesia (ie,
the adjacent alveolar bone. Excessive orthodontic forces also numbness of the lip, tongue, and cheek).
increase the risk of apical root resorption. The prevalence of
severe root resorption (ie, resorption of more than one-third Habits and Self-Inflicted Injuries
of the root length) during orthodontic therapy in adolescents
has been reported at 3%. The incidence of moderate to severe Patients may not be aware of their self-inflicted injurious hab-
root resorption for incisors among adults who range in age its that may be important to the initiation and progression
from 20 to 45 years has been reported as 2 % before treatment of their periodontal disease. Mechanical forms of trauma can
and 24.5% after treatment. Risk factors associated with root stem from the improper use of a toothbrush, the wedging of
resorption during orthodontic treatment include the duration toothpicks between the teeth, the application of fingernail
of treatment, the magnitude of the force applied, the direction pressure against the gingiva, pizza burns, and other causes
of the tooth movement, and the continuous versus intermit- (Fig. 10 .14). Sources of chemical irritation include the topical
tent application of forces. It is important to avoid excessive force application of caustic medications such as aspirin or cocaine,
and too-rapid tooth movement during orthodontic treatment. allergic reactions to toothpaste and chewing gum, the use of
The use of elastics to close a diastema may result in se- chewing tobacco, and concentrated mouthrinses. Accidental
vere attachment loss with possible tooth loss as the elastics and iatrogenic gingival injuries may be caused by a variety of
migrate apically along the root. The surgical exposure of im- chemical, physical, and thermal sources, yet they are generally
pacted teeth and orthodontic-assisted eruption has the poten- self-limiting. Iatrogenic injuries are often acute, whereas facti-
tial to compromise periodontal attachment on adjacent teeth. tious injuries tend to be more chronic in nature.
However, the majority of impacted teeth that are surgically
exposed and aided in their eruption by orthodontic treatment Trauma Associated with Oral Jewelry
subsequently exhibited more than 90% of their attachment as The use of piercing jewelry in the lip or tongue has become
being intact. more common recently among teenagers and young adults.
It has been reported that the dentoalveolar gingival fibers The incidence of lingual recession with pocket formation and
that are located within the marginal and attached gingiva are radiographic evidence of bone loss was 50% among subjects
stretched when teeth are rotated during orthodontic therapy. with a mean age of 22 years who wore lingual "barbells" for
The surgical severing or removal of these gingival fibers in 2 or more years. Chipped lower anterior teeth were noted in
combination with a brief period of retention may reduce the 4 7% of the patients who wore tongue-piercing jewelry for
incidence of relapse after orthodontic treatment that is intend- 4 years or more. Patients need to be informed of the risks of
ed to realign rotated teeth. wearing oral jewelry and cautioned against such practices.
Toothbrush Trauma
Extraction of Impacted Third Molars
Abrasions of the gingiva as well as alterations in tooth struc-
Numerous clinical studies have reported that the extraction ture may result from aggressive brushing in a horizontal or
of impacted third molars often results in the creation of ver- rotary fashion. The deleterious effect of excessively forceful
tical defects distal to the second molars. This iatrogenic ef- brushing is accentuated when highly abrasive dentifrices are
fect is unrelated to flap design, and it appears to occur more used. The gingival changes that are attributable to toothbrush
often when third molars are extracted from individuals who trauma may be acute or chronic. The acute changes vary with
are more than 25-years old. Other factors that appear to play regard to their appearance and duration, from scuffing of
FIGURE 10.15 The overzealous use of a toothbrush resulted in denu- FIGURE 10.16 Chemical burn caused by aspirin; note the sloughing
dation of the gingival epithelial surface and exposure of the underlying gingival tissue and the resultant recession.
connective tissue as a painful ulcer.
the epithelial surface to denudation of the underlying con- smokeless tobacco is similar to that of smoking cigarettes in
nective tissue with the formation of a painful gingival ulcer that the consumption of a 34-g container of smokeless tobacco
(Fig. 10.15). Diffuse erythema and denudation of the attached is approximately equal to 1.5 packs of cigarettes. Histologic
gingiva throughout the mouth may be a striking result of features of oral leukoplakia associated with smokeless tobacco
overzealous brushing. Signs of acute gingival abrasion are fre- include (1) a chevronlike pattern of hyperkeratosis with focal
quently noted when the patient first uses a new brush. Punc- areas of inflammation; and (2) hyperplasia in the basal cell layer
ture lesions may be produced when heavy pressure is applied (Fig. 10.17). Increased incidences of gingival recession, cervical
to firm bristles that are aligned perpendicular to the surface root abrasion, and root caries have been reported with smoke-
of the gingiva. A forcibly embedded toothbrush bristle may less tobacco (Fig. 10.18). The incidence of gingival recession
be retained in the gingiva and cause an acute gingival abscess. among adolescents who use smokeless tobacco has been re-
Chronic toothbrush trauma results in gingival recession ported at 42% as compared with 17% among nonusers.
with denudation of the root surface. lnterproximal attachment
loss is generally a consequence of bacteria-induced periodon-
Radiation Therapy
titis, whereas buccal and lingual attachment loss is frequently
the result of toothbrush abrasion. The improper use of dental Radiation therapy has cytotoxic effects on both normal cells
floss may result in lacerations of the interdental papilla. and malignant cells. A typical total dose of radiation for
head and neck tumors is in the range of 5000-8000 cGy
Chemical Irritation (cGy = 1 rad) and equivalent to 50-80 Sieverts (Sv). The total
Acute gingival inflammation may be caused by chemical irri- dose of radiation is generally given in partial incremental doses
tation that results from either sensitivity or nonspecific tissue referred to as Jractionation. Fractionation helps to minimize the
injury. In allergic inflammatory states, the gingival changes adverse effects of radiation while maximizing the death rate for
range from simple erythema to painful vesicle formation and the tumor cells. Fractionated doses are typically administered
ulceration. Severe reactions to ordinarily innocuous mouth- in the range of 100-1000 cGy or 1-10 Sv per week.
washes, dentifrices, and denture materials are often explain- Radiation treatment induces an obliterative endarteritis that
able on this basis. results in soft-tissue ischemia and fibrosis while irradiated bone
Acute inflammation with ulceration may be produced by becomes hypovascular and hypoxic. Adverse effects of head
the nonspecific injurious effect of chemicals on the gingival tis- and neck radiation therapy include dermatitis and mucositis
sues. The indiscriminate use of strong mouthwashes, the topi- of the irradiated area as well as muscle fibrosis and trismus,
cal application of corrosive drugs, such as aspirin (Fig. 10 .16) which may restrict access to the oral cavity. The mucositis typi-
or cocaine, and accidental contact with drugs such as phe- cally develops 5-7 days after radiation therapy is initiated. Sa-
nol or silver nitrate are common examples of chemicals that liva production is permanently impaired when salivary glands
cause irritation of the gingiva. A histologic view of an aspirin- that are located within the portal of radiation receive 6000 cGy
induced chemical burn shows vacuoles with serous exudates (60 Sv) or more. Xerostomia results in greater plaque accumu-
and an inflammatory infiltrate in the connective tissue. lation and a reduced buffering capacity of saliva. Effective oral
hygiene, professional dental prophylaxis cleanings, fluoride
Smokeless Tobacco applications, and frequent dental examinations are essential to
control caries and periodontal disease. The use of customized
Snuff and chewing tobacco constitute the two main forms of trays appears to be a more effective method of fluoride applica-
smokeless tobacco. Snuff is a fine-cut form of tobacco that is tion as compared with the toothbrush.
available loosely packed or in small sachets. Chewing tobacco Periodontal attachment loss and tooth loss have been re-
is a more coarse-cut tobacco that is available in the form of ported to be greater among patients with cancer who were
loose leaves, a solid block, a plug, or as a twist of dried leaves. treated with high-dose unilateral radiation as compared with
Chewing tobacco is typically placed in the mandibular buccal the nonradiated control side of the dentition. Patients who are
vestibule for several hours, during which time saliva and dilute diagnosed with oral cancer and who require radiation thera-
tobacco are periodically expectorated. The nicotine uptake of py should ideally be assessed for dental needs (ie, mucositis,
FIGURE 10.17 A, Histologic features of oral leukoplakia associated with smokeless tobacco. Note the chevronlike pattern of hyperkeratosis with
focal areas of inflammation. B, Hyperplasia in the basal cell layer.
caused by mutations of single genes, evidence indicates that

inherited variation in DNA has a role roughly equal to that of
the environment in determining who remains periodontally
healthy versus who is affected by this disease.
In genetic studies, more than 23,000 genes need to be
considered as potential hypotheses or "candidates" for being
disease risk factors. Depending on the gene's size and the fre-
quency of genetic recombination in the gene's chromosomal
region, scientists need to evaluate between a handful or up to
several hundred inherited DNA variants in each gene as po-
tential "biornarkers" of disease risk. Each one of these variants
essentially amounts to a test of the hypothesis as to whether
the variant is associated with disease risk. Furthermore, many
complex diseases have been found to be very strongly associ-
ated with DNA variation in parts of the human genome where
FIGURE 10.18 Oral leukoplakia, recession, and clinical attachment
no genes are known to exist but where the genetic material
loss associated with the use of smokeless tobacco. may have important functional effects nonetheless.
Only by carefully studying the genetics of a disease in pop-
ulations and pedigrees, can we hope to begin to unearth the
xerostomia, faulty restorations, periapical lesion, coronal and
complex interactions between genes and the environment that
cervical decay, and periodontal status) before the initiation of
underlie individual differences in disease susceptibility. This
radiation treatment. The treatment and prevention of trismus,
field of research is known as genetic epidemiology.
oral fungal infections, odontogenic infections, osteoradione-
crosis, decay, and periodontal disease are critical to minimize
oral morbidity for these patients. Dental and periodontal in- Genetic Study Designs
fections have the potential to be severe risks for patients who
have been treated with head and neck radiation. The risk of 1. Familial aggregation and relative risk
osteoradionecrosis for oncology patients can be minimized by Many diseases run in families, and the degree of cluster-
evaluating their oral status, providing dental care, and allowing within the family can be estimated by comparing the
ing time for tissue repair before the commencement of radio- number of disease cases in relatives of patients to the risk
therapy. of disease in the general population. Difficulties with this
The risk of osteoradionecrosis must be evaluated before the approach relate to the fact that, in addition to having many
performance of atraumatic extractions or limited periodontal genes in common, family members also share many as-
surgical procedures in previously irradiated sites. Therefore, pects of a common environment (eg, diet, nutrition, smok-
the dentist may choose to consult with the patient's oncologist ing, infectious organisms, shared socioeconomic factors).
before the initiation of therapy.
2. Twin studies
Genetic Susceptibility to Periodontal The comparison of disease occurrence or severity in identi-
Disease cal (monozygotic) versus nonidentical (dizygotic) twins is
a very powerful method for distinguishing between effects
Periodontal diseases occur due to complex interplay between caused by variation in genes versus factors in the environ-
the genes and the environment, both playing very important ment. This requires us to make what is usually a reason-
roles. With the exception of a handful of very rare syndromes able assumption that the environments of pairs of identical
twins are no more or less similar than the environments fected by the disease to be recruited and clinically and mo-
shared by pairs of nonidentical twins. If variation among lecularly evaluated for a relatively small number of genetic
individuals in disease susceptibility or severity is caused en- markers. Investigators usually try to recruit families with
tirely by factors in the environment, then we expect pairs two or more close relatives, such as sibling pairs, who are
of identical twins to be no more similar to each other than affected by the disease as well as parents and other siblings
pairs of nonidentical twins. All twins (whether identical or who may be unaffected.
nonidentical) are expected to be more similar to their co-
5. Association Analysis
twins, on average, than to unrelated members of their lo-
cal population because they were raised in the same family Another approach is called association analysis although
environment, with similar diets, microbial exposures, and this had been relegated to studies of HLA and a few other
so on. However, if genetic variation plays an important role markers of special interest during the prime of linkage ap-
in determining a certain trait, then genetically identical twin proaches. Association analyses are sometimes referred to as
pairs will be more similar to each other than nonidentical case-control studies although this is only one of several sam-
twin pairs. This is because identical twins share 100% of the pling methods that can be used (including studies of fami-
same genes, whereas nonidentical twin pairs share only 50% lies). Genotype frequencies of an inherited DNA variant
of their parents' genes on average. Genetic epidemiologists for a group of periodontitis cases are statistically compared
calculate a measure called heritability that is based on these with the frequencies of the variant in a matched group of
correlations and that estimates the portion of all variation in periodontally healthy control subjects. If the genotype fre-
the trait that is attributable to inherited genetic variation. quencies differ so greatly that the results are very unlikely
to occur by chance, then we conclude that the genotype
3. Segregation Analysis
that is more common in the cases as compared with the
Another method used by genetic epidemiologists to under- controls is "associated with" increased disease risk. The
stand and distinguish different mechanisms of transmis- good news is now clearly in: association studies have been
sion of diseases through families is called segregation anal- a boon for the discovery of inherited genetic variation im-
ysis. This is relatively straightforward for traits in which portant for a wide range of complex diseases, including
mutation in a single gene causes the disease to develop diabetes, cardiovascular disease, metabolic disorders, obe-
with nearly 100% certainty in carriers, whereas persons sity, and mental illnesses.
who do not inherit the mutation are at little or no risk. For
example, carriers of a single copy of the Huntington disease 6. Candidate gene approach
gene mutation or carriers of two copies of a cystic fibrosis A gene-mapping approach that tests whether one allele of
gene mutation always develop these diseases if they reach a gene occurs more often in patients with the disease than
the ages at which symptoms of these conditions normally in subjects without the disease. These methods are also
emerge. By tracking the transmission of these diseases in referred to as association analyses, and they aim to iden-
families, it is obvious, for example, that Huntington dis- tify which genes are associated with the disease. Candidate
ease is a dominant single-gene disorder: it is transmitted genes are chosen on the basis of their known or presumed
with 50% probability to offspring of affected individuals function (ie, they have some plausible role in the disease
and thus it is often found occurring across many genera- process, such as producing a protein that is important in
tions of large pedigrees. By contrast, parents of children the disease pathogenesis).
with cystic fibrosis are very rarely affected themselves, and
25% of siblings are affected by cystic fibrosis when the dis-
ease is present in a nuclear family. This pattern of trans- Inherited Variation and Risk
mission is expected if a disease is recessive (ie, it requires of Periodontitis
the inheritance of a mutated gene copy from both parents,
who themselves have one normal and one mutated copy As a result of the appropriate focus on the role of bacterial in-
and so are not affected). For most common "complex" dis- fections in the disease pathogenesis of periodontitis, inherited
eases, however, having a high-risk gene does not automati- human genetic variation is often referred to as host defense or,
cally lead to development of the disease; this phenomenon somewhat more broadly, host response. However, these terms
is called reduced penetrance. Furthermore, several genes cover only a small portion of the range of gene functions that
or even dozens of different genes may influence disease may be important for periodontitis risk. Many additional bio-
susceptibility; this is known as oligogenic inheritance and logic processes that are not directly related to defenses against
genetic heterogeneity. Environmental exposures are also or responses to infection by microbial pathogens are also
important modifiers of disease risk. Such highly complex likely to play important roles in determining an individual's
combinations of multiple genetic and environmental risk susceptibility to this disease.
factors make the challenge of deciphering genetic mecha-
nisms by merely observing transmission patterns in fami-
Periodontitis in Genetic Syndromes
lies using the segregation analysis approach unfeasible.
A number of extremely rare conditions consistently include
4. Linkage Analysis
periodontitis among the array of clinical manifestations that
One method that has been highly successful for finding define a syndrome. Many genetic syndromes involve muta-
molecular defects related to simple genetic diseases caused tions of single genes or larger chromosomal regions. Some of
by the mutation of a single gene, such as cystic fibrosis and the syndromes that include periodontitis are caused by muta-
Huntington disease, is linkage analysis. This gene-mapping tions in specific genes. For example, mutations in the cathep-
strategy requires families with one or more members af- sin C gene have been shown to cause both Papillon-Ufevre
syndrome and Haim-Munk syndrome as well as some forms carcinogens. HLA complex genes play a central role in the
of nonsyndromic prepubertal periodontitis, and they may also immune system by presenting extracellular peptides that are
be associated with a risk of aggressive periodontitis. Periodon- important for either self-recognition or initiating immune re-
titis frequently occurs with some subtypes of Ehlers-Danlos sponses to foreign pathogens. The Fey receptor genes (FcyRS)
syndrome, Kindler syndrome, Down syndrome (trisomy 21), encode receptors for the Fe portion of immunoglobulin G, and
leukocyte adhesion deficiencies, hypophosphatasia, two types they are involved in the removal of antigen-antibody complex-
of neutropenia, and aplasia of the lacrimal and salivary glands. es from the circulation as well as other antibody-dependent re-
sponses. Formyl peptide receptor (FPRl) is a G-protein-cou-
pled receptor of phagocytic cells that interacts with bacterial
Nonsyndromic Aggressive and Chronic
peptides and that mediates chemotaxis, degranulation, and
Periodontitis superoxide production involved in inflammation. Cytokines
Finding evidence for the association of inherited genetic varia- such as the interleukins (IL-1, IL-2, IL-4, IL-6, IL-10), tumor
tion with aggressive and chronic periodontitis for cases that necrosis factor (TNF), and lymphotoxin-alpha (LTA) play a
present without the cooccurrence of anomalies or disorders number of important roles in the immunopathology of peri-
of other parts of the body is classified as nonsyndromic periodontal disease. Various studies have shown mild to moderate
odontitis. The elevated risk of periodontitis that is associated genetic association for the above mechanisms involved in the
with metabolic conditions (eg, diabetes, which is addressed pathogenesis of periodontal diseases.
elsewhere in this book) is more appropriately considered a In dentistry, a test based on genetic variations of the IL-la
comorbidity rather than being a cause for the designation of and IL-1 ~ cytokine and receptor antagonist genes to predict
a syndrome. the progression and severity of periodontitis has been com-
Twin studies have shown that chronic periodontitis has mercialized and is offered today although it does not appear
very substantial heritability, and we know that aggressive to be widely used. A number of reviews of the large number of
periodontitis aggregates strongly in families. Neither segrega- studies of the IL-1 gene polymorphisms indicate that genetic
tion analyses nor gene-mapping linkage studies are capable variation at these loci may be associated with a modest effect
of providing reliable information about the genetic etiology on disease risk.
of a highly complex disease such as periodontitis. However,
during the past decade, several hundred papers have reported SUGGESTED READINGS
associations of nonsyndromic aggressive and chronic peri- Albandar J, Kingman A, Brown L, et al: Gingival inflammation and subgingi-
odontitis with polymorphisms in a number of candidate genes. val calculus as determinants of disease progression in early-onset periodon-
titis, J Clin Periodontol 25:231, 1998.
Association tests involve the evaluation of candidate genes
Anerud A, Loe H, Boysen H: The natural history and clinical course of calcu-
that were selected on the basis of known or postulated mecha- lus formation in man,] Clin Periodontol 18:160, 1991.
nisms of disease pathogenesis. Frazer KA, Murray SS, Schork NJ, et al: Human genetic variation and its con-
For example, when bacteria challenge gingival tissue, CD 14 tribution to complex traits, Nat Rev Genet 10(4):241-251, 2009.
binds lipopolysaccharide, and TLR4 plays a key role in patho- Jeffcoat M, Howell T: Alveolar bone destruction due to overhanging amalgam
in periodontal disease,] Periodontol 51:599, 1980.
gen recognition and the activation of innate immunity. Lacto- Kinane DF, Shiba H, Hart TC: The genetic basis of periodontitis, Periodontal
transferrin (LTF) plays an antimicrobial role as the first line of 2000 39 91-117, 2005.
host defense, and it can also neutralize endotoxin and inhibit Kugelberg C: Third molar surgery, Curr Opin Dent 2:9, 1992.
the induction of nuclear factor-xf (NF-K~) in monocytes in Lupi J, Handelman C, Sadowsky C: Prevalence and severity of apical root
response to lipopolysaccharides. Myeloperoxidase (MPO) is resorption and alveolar bone loss in orthodontically treated adults, Am J
O,·thod Dentofacial Orthop 109:28, 1996.
an oxidative enzyme expressed in polymorphonuclear leuko- Sorensen J, Larsen I, Jorgensen K: Gingival and alveolar bone response to
cytes. It is involved in the defense against periodontal bacteria marginal fit of subgingival crown margins, Scand] Dent Res 94:109, 1986.
and is also able to mediate inflammatory tissue destruction in Wilson TG Jr: The positive relationship between excess cement and peri-
periodontal disease. Glutathione S-transferase mu 1 (GSTMl) implant disease: a prospective clinical endoscopic study, J Pehodontol
80 1388-1392, 2009.
and N-acetyltransferase 2 (NAT2) genes are responsible for the Zander H: The attachment of calculus to root surfaces, J Periodontol 24:16,
detoxification of a wide range of chemicals, including tobacco 1953.
11
Smoking and Periodontal
Disease
PM Preshaw • L Chambrone • KF Novak • N Ambalavanan
Chapter Outline
The Smoking Epidemic Effects of Smoking on Response
Effects of Smoking on the Prevalence and to Periodontal Therapy
Severity of Periodontal Diseases Effects of Smoking Cessation on
Effects of Smoking on the Etiology and Periodontal Treatment Outcomes
Pathogenesis of Periodontal Disease
The Smoking Epidemic formaldehyde, hydrogen cyanide, and many other toxic and
irritant compounds, including more than 60 known carcino-
Smoking is highly prevalent and can be considered as an epi- gens, such as benzo(a)pyrene and dimethylnitrosamine. The
demic in both developed and developing nations. In India particulate phase includes nicotine, "tar" (itself made up of
30% of the population, 15 years or older (195 million peo- many toxic chemicals), benzene, and benzo(a)pyrene. Tar is
ple), have either smoked or chewed tobacco; of which 4 7% inhaled with the smoke. In its condensate form, it is a sticky
are men and 14% are women; this translates to almost-154 brown substance that stains fingers and teeth, yellow and
million men and 4 lmillion women. However, the prevalence brown. Nicotine, which is an alkaloid, is found within the
may be underestimated by 5% and 0.5% for smoking among tobacco leaf and evaporates when the cigarette is lighted. It is
men and women, respectively Tobacco consumption was sig- quickly absorbed in the lungs, and it reaches the brain within
nificantly higher in the poor, less educated class and those of 10-19 s. Nicotine is highly addictive. It causes a rise in blood
lower socioeconomic status. The prevalence of tobacco con- pressure, increased heart and respiratory rates, and peripheral
sumption has increased up to the age of 50 years and has then vasoconstriction.
leveled or declined. Smoking is the major risk factor for periodontitis, and it
Worldwide, it is estimated that approximately 13% of the affects the prevalence, extent, and severity of disease. Since
population, 15 years old or older, are smokers [ie, there are smoking has an adverse impact on the clinical outcome of
> 1.3 billion smokers (around 1 billion men and 300 million nonsurgical and surgical therapy, as well as, the long-term
women)]; and that tobacco kills up to half of its users; which in- success of implant placement, smoking status of patients
cludes more than 80% of smokers who live in low- and middle- should be assessed (Box 11.1)
income countries. Globally, smoking accounts for 1 in 5
deaths among men 30 years old and older; and 1 in 20 deaths
among women 30 years old and older. Effects of Smoking on the Prevalence
Smoking is harmful to almost every organ in the body and
it is associated with multiple diseases that reduce life expec- and Severity of Periodontal Diseases
tancy and quality of life. Diseases associated with smoking
Gingivitis
include, lung cancer, heart disease, stroke, emphysema, bron-
chitis, and cancers of the oral cavity, bladder, kidney, stomach, Controlled clinical studies have demonstrated that, in hu-
liver, and cervix. Approximately half of the long-term smokers man models of experimental gingivitis, the development of
will die early as a result of smoking, and those who die before inflammation in response to plaque accumulation is reduced
the age of 70 years will lose an average of 20 years of life. Most in smokers as compared to nonsmokers (Table 11.1). In ad-
deaths from smoking are due to lung cancer, chronic obstruc- dition, cross-sectional studies have consistently demonstrated
tive pulmonary disease, and coronary heart disease. that smokers present with less gingival inflammation than
Tobacco smoke contains thousands of noxious chemicals, nonsmokers. These data suggest that smokers have a de-
and it comprises a gaseous phase and a solid (particulate) creased expression of clinical inflammation in the presence of
phase. The gas phase contains carbon monoxide, ammonia, plaque accumulation as compared with nonsmokers.
127
BOX 11.1 ~ge of Assessing Smoking Status

CURRENT SMOKERS
Ask about current smoking and past smoking. Many smokers are trying to quit and therefore by simply asking how many cigarettes
they are smoking today may not give an accurate assessment of their lifetime exposure [eg, a patient who is currently smoking
5 cigarettes/day may have been smoking 40 cigarettes/day until yesterday when (s)he decided to cut down]. Try to get an indication
of their approximate level of smoking (eg, the average number of cigarettes/day for a certain number of years). It can also be useful to
calculate the number of pack-years:
Pack - years= Number of packs smoked per day x Number of years of smoking
In other words, 1 pack-year is the cumulative exposure that corresponds with the smoking of 1 pack of 20 cigarettes/day for 1 year. For
example, a smoker who has smoked 20 cigarettes/day for 15 years has 15 pack-years of smoking.
FORMER SMOKERS
Ask the patient about his or her past smoking. A patient with periodontitis may have a significant smoking history that has had an
impact on his periodontal status even if (s)he no longer smokes. Former smokers should always be congratulated for their achievement
in quitting, but it is also very important to document the following:
• how much they used to smoke
• how many years they smoked
• when they quit
IS THE PATIENT'S RESPONSE ACCURATE?
The inaccurate or false reporting of smoking status is common; patients will tell you what they think you want to hear, or they may
be embarrassed because they have not managed to cut down yet. Many patients report smoking 20 cigarettes/day, because this is
the number of cigarettes in a pack in most countries, so 20 may be a convenient response rather than an accurate response. Cultural
factors may also influence responses.
WHEN IS A SMOKER NOT A SMOKER?
• Smokers have smoked 2: 100 cigarettes in their lifetime and currently smoke.
• Former smokers have smoked 2: 100 cigarettes in their lifetime and do not currently smoke.
• Nonsmokers have not smoked 2: 100 cigarettes in their lifetime and do not currently smoke.
It must be noted that many periodontal research studies have not used these definitions, and this can sometimes make it difficult
to interpret the studies, particularly in the context of what constitutes a former smoker. For example, from an exposure point of
view, there is a big difference between someone who smoked 5 cigarettes/day for 10 years and who quit 30 years ago as compared
with someone who smoked 40 cigarettes/day for 20 years and quit 6 months ago. It is always best in clinical practice to gather full
information about each patient's smoking history.
TABLE 11.1 longitudinal studies have demonstrated that pocket depth, at-
tachment loss, and alveolar bone loss are more prevalent and
EFFECTS OF SMOKING ON THE PREVALENCE severe in patients who smoke as compared to nonsmokers. On
AND SEVERITY OF PERIODONTAL DISEASE average, smokers were 4 times as likely to have periodontitis
Periodontal Disease Impact of Smoking
as compared with persons who had never smoked after ad-
justing for age, gender, race/ethnicity, education, and income/
Gingivitis J, Gingival inflammation and bleeding poverty ratio. Former smokers were 1. 7 times more likely
on probing to have periodontitis than persons who had never smoked.
Periodontitis i Prevalence and severity of periodontal This study also demonstrated a dose-response relationship
destruction
between cigarettes smoked per day and the odds of having
i Pocket depth, attachment loss, and
bone loss
periodontitis. In subjects smoking 9 or fewer cigarettes per
i Rate of periodontal destruction day, the odds for having periodontitis were 2.8, whereas sub-
i Prevalence of severe periodontitis jects who smoked 31 or more cigarettes per day were almost
i Tooth loss 6 times more likely to have periodontitis. In former smokers,
i Prevalence with increased number the odds of having periodontitis declined with the number of
of cigarettes smoked per day years since quitting.
J, Prevalence and severity with smoking Older adult smokers are approximately 3 times more likely
cessation to have severe periodontal disease, and the number of years
1, Decreased; i, increased. of tobacco use is a significant factor in tooth loss, coronal root
caries, and periodontal disease.
Periodontitis Smoking has also been shown to affect periodontal disease
severity in younger individuals. Cigarette smoking is associ-
Although gingival inflammation in smokers appears to be ated with increased severity of generalized aggressive peri-
reduced in response to plaque accumulation as compared to odontitis in young adults, and those who smoke are 3.8 times
nonsmokers, an overwhelming body of data points to smok- more likely to have periodontitis as compared to nonsmokers.
ing as a major risk factor for increasing the prevalence and se- In addition, smokers are more than 6 times as likely as non-
verity of periodontal destruction. Multiple cross-sectional and smokers to demonstrate continued attachment loss.
11 Smoking and Periodontal Disease 129
Effects of Smoking on the Etiology Immune-Inflammatory Responses

and Pathogenesis of Periodontal The immune response of the host to plaque accumulation is
Disease essentially protective. In periodontal health, a balance exists
between the bacterial challenge of plaque and the immune-
The increased prevalence and severity of periodontal destruc- inflammatory responses in the gingival tissues, with no result-
tion associated with smoking suggests that the host-bacterial ing loss of periodontal support. By contrast, periodontitis is
interactions normally seen with chronic periodontitis are al- associated with an alteration in the host-bacterial balance that
tered, thereby resulting in a more extensive periodontal break- may be initiated by changes in the bacterial composition of
down (Table 11.2). This imbalance between bacterial challenge the subgingival plaque, changes in the host responses, or a
and host response may be caused by changes in the composi- combination of both.
tion of the subgingival plaque (eg, increases in the numbers Smoking exerts a major effect on the immune-inflamma-
and virulence of pathogenic organisms), changes in the host tory response that results in an increase in the extent and
response to the bacterial challenge, or a combination of both. severity of periodontal destruction. The deleterious effects
of smoking appear to result in part from the downregulation
Microbiology of the immune response to bacterial challenge. The neu-
trophil is an important component of the host response to
Using checkerboard DNA-DNA hybridization technology the bacterial challenge, and alterations in neutrophil num-
to screen for 29 different subgingival species, it was found ber or function may result in localized and systemic infec-
that members of the orange and red complexes-including tions. Critical functions of neutrophils include chemotaxis
Eihenella nodatum, Fusobacterium nucleatum ss vincentii, Pre- (directed locomotion from the bloodstream to the site of
votella intermedia, Peptostreptococcus micros, Prevotella nigres- infection), phagocytosis (internalization of foreign particles
cens, Tannerella forsythia, Porphyromonas gingivalis, and Trepo- such as bacteria), and hilling ( via oxidative and nonoxidative
nema denticola-were significantly more prevalent in current mechanisms).
smokers than in nonsmokers and former smokers. The in- Neutrophils obtained from the peripheral blood, oral cavity,
creased prevalence of these periodontal pathogens was caused saliva of smokers, or those exposed in vitro to whole tobacco
by an increased colonization of shallow sites (pocket depth smoke or nicotine, have been shown to demonstrate function-
::;4 mm), with no differences among smokers, former smok- al alterations in chemotaxis, phagocytosis, and the oxidative
ers, and nonsmokers in pockets 4 mm or greater. In addition, burst. In vitro studies of the effects of tobacco products on
these pathogenic bacteria were more prevalent in the maxilla neutrophils have shown detrimental effects on cell movement
than the mandible. These data suggest that smokers have a as well as on the oxidative burst. In addition, levels of anti-
greater extent of colonization by periodontal pathogens than body to the periodontal pathogens essential for phagocytosis
nonsmokers or former smokers; and that this colonization may and killing of bacteria, specifically immunoglobulin G2, have
lead to an increased prevalence of periodontal breakdown. been reported to be reduced in smokers as compared to non-
smokers with periodontitis, thereby suggesting that smokers
TABLE 11.2 may have reduced protection against periodontal bacteria.
By contrast, elevated levels of tumor necrosis factor-a have
EFFECTS OF SMOKING ON THE ETIOLOGY been demonstrated in the gingival crevicular fluid of smok-
AND PATHOGENESIS OF PERIODONTAL DISEASE ers, and elevated levels of prostaglandin E2, neutrophil elas-
tase, and matrix metalloproteinase-8 have also been found.
Etiologic Factor Impact of Smoking
These data suggest that smoking may impair the response of
Microbiology No effect on rate of plaque accumulation neutrophils to plaque-bacteria but that it may also increase the
i Colonization of shallow periodontal release of tissue-destructive enzymes.
pockets by periodontal pathogens
i Levels of periodontal pathogens in
deep periodontal pockets Physiology
Immune-inflammatory Altered neutrophil chemotaxis,
response phagocytosis, and oxidative burst Previous studies have shown that the clinical signs of inflam-
i Tumor necrosis factor-a and mation are less pronounced in smokers than in nonsmokers.
prostaglandin E2 in gingival crevicular The response of the microcirculation to plaque accumulation
fluid appears to be altered in smokers as compared with nonsmok-
i Neutrophil collagenase and elastase in ers. With developing inflammation, increases in gingival ere-
gingival crevicular fluid vicular fluid flow, bleeding on probing, and gingival blood
i Production of prostaglandin E, vessels are lower in smokers than in nonsmokers. Subgingival
by monocytes in response to
lipopolysaccharide
temperatures are lower in smokers than nonsmokers and re-
Physiology j, Gingival blood vessels with i covery from the vasoconstriction caused by local anesthetic
inflammation administration takes longer in smokers. These cumulative
J, Gingival crevicular fluid flow data suggest that significant alterations are present in the gin-
and bleeding on probing with i gival microvasculature of smokers as compared to nonsmok-
inflammation ers and that these changes lead to decreased blood flow and
J, Subgingival temperature decreased clinical signs of inflammation. This explains the
i Time needed to recover from local long-observed phenomenon of a transient increase in gingival
anesthesia bleeding when a smoker quits; patients need to be warned
,J,, Decreased; i, increased. about this phenomenon.
Effects of Smoking on Response observed after surgical therapy. In a longitudinal-comparative

study of the effects of four different treatment modalities (cor-
to Periodontal Therapy onal scaling, root planing, modified Widman flap surgery, and
osseous resection surgery), smokers (with "heavy" defined as
Nonsurgical Therapy
?.20 cigarettes/day and "light" defined as .:,; 19 cigarettes/day)
Numerous studies have indicated that current smokers do not consistently showed less pocket reduction and less gain in
respond as well to periodontal therapy as nonsmokers or for- clinical attachment as compared with nonsmokers or former
mer smokers do (Table 11.3). The majority of clinical research smokers. These differences were evident immediately after the
supports the observation that pocket-depth reduction is more completion of therapy and continued throughout 7 years of
effective in nonsmokers than in smokers after nonsurgical supportive periodontal therapy. During the 7 years, deteriora-
periodontal therapy, including oral hygiene instruction, scal- tion at furcation areas was greater in heavy and light smok-
ing, and root-surface debridement. In addition, gains in clini- ers than in former smokers and nonsmokers. Smoking has
cal attachment as a result of nonsurgical treatment are less pro- also been shown to have a negative impact on the outcomes
nounced in smokers than in nonsmokers. When a higher level of guided-tissue regeneration and the treatment of infrabony
of plaque control can be achieved as part of nonsurgical care, defects by bone grafts. By 12 months after guided tissue re-
the differences in the resolution of 4-6-mm pockets between generation therapy at deep-infrabony defects, smokers dem-
nonsmokers and smokers became clinically less significant. onstrated less than half the attachment gain that was observed
It can be concluded that smokers do not respond as well in nonsmokers. Similarly, after the use of bone grafts for the
to nonsurgical therapy as nonsmokers. With excellent plaque treatment of infrabony defects, smokers showed less reduc-
control, these differences may be minimized, but the empha- tion in pocket depths as compared with nonsmokers.
sis is on truly excellent plaque control. When comparing cur- Open flap-access surgery without regenerative or grafting
rent smokers with former smokers and nonsmokers, the for- procedures is the most common surgical procedure used for
mer and nonsmoking subjects appear to respond equally well accessing the root and bone surfaces. By 6 months after this
to nonsurgical care, thereby reinforcing the need for patients procedure, smokers showed significantly less reduction of
to be informed of the benefits of smoking cessation. deep pockets (?. 7 mm) than nonsmokers (3 mm for smokers
vs 4 mm for nonsmokers) and significantly less gain in clinical
attachment (1.8 mm for smokers vs 2.8 mm for nonsmok-
Surgical Therapy and Implants
ers) even though all of the patients received supportive peri-
The less favorable response of the periodontal tissues to non- odontal therapy every month for 6 months. Tobacco smoking
surgical therapy that is observed in current smokers is also also affects the outcomes of periodontal plastic surgery. Sig-
nificantly greater root coverage and greater gains in clinical
attachment levels were recorded for nonsmokers as compared
TABLE 11.3 with smokers after the treatment of gingival recession defects
by subepithelial connective-tissue grafts. Furthermore, smok-
EFFECTS OF SMOKING ON RESPONSE TO ers showed significantly less sites with complete root coverage
PERIODONTAL THERAPY than were seen in the nonsmokers.
In patients who had undergone implant therapy, smoking
Therapy Effects of Smoking
increased the risk of implant failure. The risk for implant fail-
Nonsurgical ,J, Clinical response to root-surface ure in smokers appears to be approximately double the risk
debridement for failure in nonsmokers; and the risks appear to be higher
,J, Reduction in pocket depth in the maxillary implants and when implants are placed in
,J, Gain in clinical attachment levels poor-quality bone. Smoking has also been shown to be a risk
,J, Negative impact of smoking with i
factor for periimplantitis, with a majority of studies showing
level of plaque control
Surgery and implants ,J, Pocket-depth reduction and ,J, gain
a significant increase in periimplant-bone loss as compared
in clinical attachment levels after to nonsmokers. Collectively, these data indicate that implant
access-flap surgery failure is more common among smokers than nonsmokers.
t Deterioration of furcations after surgery All patients who are considering implant therapy should be
,J, Gain in clinical attachment levels, informed about the benefits of smoking cessation and the
,J, bone fill, i recession, and i risks of smoking for the development of periimplantitis and
membrane exposure after guided implant failure.
tissue regeneration
,J, Root coverage after grafting procedures
for localized gingival recession Maintenance Therapy
,J, Pocket depth reduction after
bone-graft procedures
The detrimental effect of smoking on treatment outcomes
i Risk for implant failure and appears to be long lasting and independent of the frequen-
periimplantitis cy of maintenance therapy. After four different modalities of
Maintenance care t Pocket depth and attachment loss therapy, (scaling, scaling and root planing, modified Widman
during maintenance therapy flap surgery, and osseous surgery), maintenance therapy was
i Disease recurrence in smokers performed by a hygienist every 3 months for 7 years. Smok-
t Need for retreatment in smokers ers consistently had deeper pockets than nonsmokers and less
i Tooth loss in smokers after surgical gain in attachment when evaluated each year for the 7 -year
therapy period. Even with more intensive maintenance therapy given
,J,, Decreased; i, increased. every month for 6 months after flap surgery, smokers had
11 Smoking and Periodontal Disease 131
deeper and more residual pockets than nonsmokers although cessation counseling for a period of 12 months, those
no significant differences in plaque or bleeding on probing individuals who successfully quit smoking for the entire
scores were found. These data suggest that the effects of smok- 12 months of the study had the best response to the peri-
ing on the host response and the healing characteristics of the odontal treatment.
periodontal tissues may have a long-term effect on pocket The benefit of smoking cessation on the periodontium
resolution in smokers, possibly requiring more intensive man- is likely to be mediated through various pathways, such as
agement during the maintenance phase. Smokers also tend a shift toward a less pathogenic microbiota, the recovery of
to experience more periodontal breakdown than nonsmokers the gingival microcirculation, and improvements in certain as-
after therapy pects of the immune-inflammatory responses. In conclusion,
Tobacco smoking was positively associated with tooth smoking is the major risk factor for periodontitis, and smok-
loss even when regular recall maintenance care was per- ing cessation should be an integral part of periodontal therapy
formed (overall, smokers had a risk of losing their teeth that among patients who smoke.
was up to 380% higher than that of nonsmokers). Similarly,
smoking has a detrimental effect on periimplant-tissue sta- SUGGESTED READINGS
tus even when patients are under strict periimplant preven- Chambrone L, Chambrone D, Lima LA, et al: Predictors of tooth loss during
tive maintenance care. It is clear from these studies that: long-term periodontal maintenance: a systematic review of observational
(1) smokers may present with periodontal disease at an studies,] Clin Periodontal 37:675-684, 2010.
early age; (2) that they may be difficult to treat effectively Chambrone L, Preshaw PM, Rosa EF, et al: Effects of smoking cessation on
the outcomes of non-surgical periodontal therapy: a systematic review and
with conventional therapeutic strategies; (3) that they may individual patient data meta-analysis,) Clin Periodontol 40:607-615, 2013.
continue to have progressive or recurrent periodontitis; and Heasman L, Stacey F, Preshaw PM, et al: The effect of smoking on periodon-
( 4) that they may have an increased risk of tooth loss or pe- tal treatment response: a review of clinical evidence, J Clin Periodontal 33:
riimplant bone loss even when an adequate maintenance 241-253, 2006.
control is established. Preshaw PM, Heasman L, Stacey F, et al: The effect of quitting smoking on
chronic periodontitis,J Clin Periodontal 32:869-879, 2005.
Rosa EF, Corraini P, de Carvalho VF, et al: A prospective 12-month study of
Effects of Smoking Cessation the effect of smoking cessation on periodontal clinical parameters, J Clin
Periodontol 38:562-571, 2011.
on Periodontal Treatment Outcomes Tomar SL, Asma S: Smoking-attributable periodontitis in the United States:
findings from NHANES Ill. National Health and Nutrition Examination
Smoking cessation positively influenced periodontal treat- Survey,] Periodontal 71:743-751, 2000.
ment outcomes. When patients received nonsurgical therapy Warnakulasuriya S, Dietrich T, Bornstein MM, et al: Oral health risks of to-
as treatment for their periodontitis, in addition to smoking bacco use and effects of cessation, Int Dent] 60:7-30, 2010.
12
Influence of Systemic
Conditions
PR Klokkevold • BL Mealey • N Ambalavanan
Chapter Outline
Endocrine Disorders and Hormonal Genetic Disorders
Changes Stress and Psychosomatic Disorders
Hematologic Disorders and Immune Nutritional Influences
Deficiencies Medications
Many systemic diseases, disorders, and conditions have been characterized by chronic hyperglycemia. Diminished insulin
implicated as risk indicators or risk factors in periodontal production, impaired insulin action, or a combination of both
disease. Individual host immune response to periodontal result in the inability of glucose to be transported from the
pathogens is very important and likely explains many of the bloodstream into the tissues, which in turn results in high
differences in disease severity observed from one individual blood glucose levels and the excretion of sugar in the urine.
to the next. Furthermore, systemic diseases, disorders, and Lipid and protein metabolism are altered in diabetes as well.
conditions alter host tissues and physiology, which may im- Uncontrolled diabetes (chronic hyperglycemia) is associated
pair the host's barrier function and immune defense against with several long-term complications, including microvas-
periodontal pathogens, thereby creating the opportunity for cular diseases (retinopathy, nephropathy, or neuropathy),
destructive periodontal disease to progress. macrovascular diseases (cardiovascular and cerebrovascular
The interrelationships between periodontal infections and conditions), an increased susceptibility to infections, and poor
host defense are complex. A number of environmental, physical, wound healing.
and psychosocial factors have the potential to alter periodontal There are two major types of diabetes, type 1 and type 2,
tissues and the host immune response, thereby resulting in more with several less common secondary types. Type 1 diabetes mel-
severe periodontal disease expression. It is important to recog- litus, which was formerly known as insulin-dependent diabetes
nize that the systemic diseases, disorders, or conditions them- mellitus, is caused by a cell-mediated autoimmune destruction
selves do not cause penodontitis; rather, they may predispose, of the insulin-producing beta cells of the islets of Langerhans
accelerate, or otherwise increase the disease's progression. in the pancreas, which results in insulin deficiency. Type 1
diabetes accounts for 5-10% of all cases of diabetes and most
Endocrine Disorders and Hormonal often occurs in children and young adults. This type of dia-
betes results from a lack of insulin production, and it is very
Changes unstable and difficult to control. It has a marked tendency
Endocrine diseases such as diabetes and hormonal fluctua- toward ketosis and coma, it is not preceded by obesity, and it
tions that are associated with puberty and pregnancy are well- requires the injection of insulin to be controlled. Patients with
known examples of systemic conditions that adversely affect type 1 diabetes mellitus present with the symptoms that are
the condition of the periodontium. Endocrine disturbances traditionally associated with diabetes, including polyphagia,
and hormone fluctuations affect the periodontal tissues di- polydipsia, polyuria, and predisposition to infections.
rectly, modify the tissue response to local factors, and produce Type 2 diabetes mellitus, which was formerly known as
anatomic changes in the gingiva that may favor plaque accu- noninsulin-dependent diabetes mellitus, is caused by periph-
mulation and disease progression. eral resistance to insulin action, impaired insulin secretion,
and increased glucose production in the liver. The insulin-
producing beta cells in the pancreas are not destroyed by cell-
Diabetes Mellitus mediated autoimmune reaction. It typically begins as insulin
Diabetes mellitus is an extremely important disease from a resistance, which leads to the reduced pancreas production of
periodontal standpoint. It is a complex metabolic disorder insulin as the demand increases. Type 2 diabetes is the most
133
common form of diabetes, and it accounts for 90-95% of all those without diabetes up to the age of 30 years. After 30,
diagnosed cases in adults. Individuals are often not aware patients with diabetes have a greater degree of periodontal de-
they have the disease until severe symptoms or complications struction, possibly related to more disease destruction over
occur. Type 2 diabetes generally occurs in obese individuals, time. Patients who have had overt diabetes for more than
and it can often be controlled by diet and oral hypoglycemic 10 years have a greater loss of periodontal support than those
agents. Ketosis and coma are uncommon. Type 2 diabetes can with a diabetic history of less than 10 years. This destruction
present with the same symptoms as type 1 diabetes but typi- may also be related to the diminished tissue integrity that con-
cally in a less severe form. tinues to deteriorate over time. There is a higher prevalence
An additional category of diabetes is hyperglycemia second- and severity of periodontal disease in individuals with dia-
ary to other diseases or conditions. A prime example of this betes as compared to nondiabetic persons with similar local
type of hyperglycemia is gestational diabetes associated with factors. Also there is a greater loss of attachment, increased
pregnancy. Gestational diabetes develops in 2-10% of all preg- bleeding on probing, and increased tooth mobility. As with
nancies but disappears after delivery. Women who have had other systemic conditions associated with periodontitis, dia-
gestational diabetes are at increased risk of developing type betes mellitus does not cause gingivitis or periodontitis, but
2 diabetes. Other secondary types of diabetes are those as- evidence indicates that it alters the response of the periodon-
sociated with diseases that involve the pancreas and the de- tal tissues to local factors, thereby hastening bone loss and
struction of the insulin-producing cells. Endocrine diseases delaying postsurgical healing. Frequent periodontal abscesses
(eg, acromegaly, Cushing syndrome), tumors, pancreatecto- appear to be an important feature of periodontal disease in
my, and drugs or chemicals that cause altered insulin levels patients with diabetes.
are included in this group. Experimentally induced types of
diabetes generally belong in this category rather than in the Bacterial Pathogens
categories of type 1 or 2 diabetes mellitus. The glucose content of gingival fluid and blood is higher in
individuals with diabetes than in those without diabetes with
Oral Manifestations similar plaque and gingival index scores. The increased glu-
Numerous oral changes have been described in patients with cose in the gingival fluid and blood of patients with diabe-
diabetes, including cheilosis, mucosa! drying and cracking, tes could change the environment of the microflora, thereby
burning mouth and tongue, diminished salivary flow, and inducing qualitative changes in bacteria that may contribute
alterations in the flora of the oral cavity, with greater pre- to the severity of periodontal disease observed in those with
dominance of Candida albicans, hemolytic streptococci, and poorly controlled diabetes. Patients with type 1 diabetes melli-
staphylococci. An increased rate of dental caries has also been tus and periodontitis have been reported to have a subgingival
observed in patients with poorly controlled diabetes. It is im- flora that is composed mainly of Capnocytophaga, anaerobic
portant to note that these changes are not always present, that vibrios, and Actinomyces species. Porphyromonas gingivalis, Pre-
they are not specific, and that they are not pathognomonic votella intermedia, and Aggregatibacter actinomycetemcomitans,
for diabetes. Furthermore, these changes are less likely to be Black-pigmented species-especially P gingivalis, P intermedia,
observed in patients with well-controlled diabetes. Individu- and C. rectus-are prominent in severe periodontal lesions on
als with controlled diabetes have a normal tissue response, a those with type 2 diabetes.
normally developed dentition, a normal defense against infec-
tions, and no increase in the incidence of caries. Polymorphonuclear Leukocyte Function
The influence of diabetes on the periodontium has been The increased susceptibility of patients with diabetes to infec-
thoroughly investigated. Although it is difficult to make de- tion has been hypothesized as being caused by polymorpho-
finitive conclusions about the specific effects of diabetes on nuclear leukocyte (PMN) deficiencies that result in impaired
the periodontium, a variety of changes have been described, chemotaxis, defective phagocytosis, or impaired adherence.
including a tendency toward an enlarged gingiva, sessile or In patients with poorly controlled diabetes, the function of
pedunculated gingival polyps, polypoid gingival prolifera- PMNs, monocytes, and macrophages is impaired. As a result,
tions, abscess formation, periodontitis, and loosened teeth the primary defense mounted by PMNs against periodontal
(Fig. 12.1). Perhaps the most striking changes in patients with pathogens is diminished and bacterial proliferation is more
uncontrolled diabetes are the reductions in the defense mech- likely.
anisms and the increased susceptibility to infections, which
lead to destructive periodontal disease. In fact, periodontal Altered Collagen Metabolism
disease is considered to be the sixth complication of diabe- Chronic hyperglycemia impairs collagen structure and func-
tes. Periodontitis in patients with type 1 diabetes appears to tion, which may directly impact the integrity of the peri-
start after the age of 12 years, and it has a fivefold increased odontium. Decreased collagen synthesis, osteoporosis, and
prevalence in teenagers. Severe gingival inflammation, deep a reduction in alveolar bone height have been demonstrated
periodontal pockets, rapid bone loss, and frequent periodon- in diabetic animals. Chronic hyperglycemia adversely af-
tal abscesses often occur in patients with poorly controlled fects the synthesis, maturation, and maintenance of collagen
diabetes and poor oral hygiene. Children with type 1 diabetes and extracellular matrix. In the hyperglycemic state, numer-
tend to have more destruction around the first molars and in- ous proteins and matrix molecules undergo a nonenzymatic
cisors, but this destruction becomes more generalized at older glycosylation, thereby resulting in accumulated glycation end-
ages. In patients with juvenile diabetes, extensive periodontal products (AGEs). The formation of AGEs occurs at normal glu-
destruction often occurs as a consequence of having a more cose levels as well; however, in hyperglycemic environments,
severe disease at a younger age. AGE formation is excessive. Many types of molecules are af-
Investigators have reported that the rate of periodontal de- fected, including proteins, lipids, and carbohydrates. Collagen
struction appears to be similar for those with diabetes and is cross-linked by AGE formation, which makes the collagen
12 Influence of Systemic Conditions 135
FIGURE 12.1 Periodontal condition in patients with diabetes. A, Adult with diabetes (blood glucose level >400 mg/dl). Note the gingival inflam-
mation, spontaneous bleeding, and edema. B, The same patient as shown in A. Improved control of diabetes was noted after 4 days of insulin therapy
(blood glucose level <100 mg/dl). The clinical periodontal condition has improved without local therapy. C, Adult patient with uncontrolled diabetes.
Note the enlarged, smooth, erythematous gingival margins and papilla in the anterior area. D, The same patient as shown in C. This is a lingual view
of the right mandibular area. Note the inflamed and swollen tissues in the anterior and premolar areas. E, Adult patient with uncontrolled diabetes.
There is a suppurating abscess on the buccal surface of the maxillary premolars.
less soluble and less likely to be normally repaired or replaced. female patient. During puberty and pregnancy, these changes
Cellular migration through cross-linked collagen is impeded, are characterized by nonspecific inflammatory reactions with
and, perhaps more importantly, tissue integrity is impaired as a predominant vascular component, which leads clinically to
a result of damaged collagen that remains in the tissues for a marked hemorrhagic tendency. Oral changes during meno-
longer periods (ie, collagen is not renewed at a normal rate). pause may include thinning of the oral mucosa, gingival reces-
As a result, collagen in the tissues of patients with poorly con- sion, xerostomia, altered taste, and burning mouth.
trolled diabetes is older and more susceptible to pathogenic
breakdown (ie, less resistant to destruction by periodontal in- Puberty
fections). AGEs and receptors for AGEs (RAGEs) play a central Puberty is often accompanied by an exaggerated response
role in the classic complications of diabetes, and they may of the gingiva to plaque. Pronounced inflammation, edema,
play a significant role in the progression of periodontal disease and gingival enlargement result from local factors that might
as well. Poor glycemic control, with the associated increase ordinarily elicit a comparatively mild gingival response. As
in AGEs, renders the periodontal tissues more susceptible to adulthood approaches, the severity of the gingival reaction di-
destruction. minishes even when local factors persist. However, the com-
plete return to normal health requires the removal of these
factors. Although the prevalence and severity of gingival dis-
Female Sex Hormones ease are increased during puberty, gingivitis is not a universal
Gingival alterations during puberty, pregnancy, and meno- occurrence for all adolescents. With good oral hygiene, it can
pause are associated with physiologic hormonal changes in the be prevented.
FIGURE 12.2 Periodontal condition during pregnancy. A, Marginal erythema and easily bleeding gingiva in a woman who is 5 months pregnant.
B, Localized incipient gingival enlargement between the maxillary central and lateral incisors in a woman who is 4 months pregnant. C, Generalized
gingival enlargement of the interdental papilla and gingival margins on the facial surface of the maxillary incisors in a pregnant woman. D, Extensive
gingival enlargement localized on the buccal surface of the mandibular premolars in a pregnant woman. These lesions are often referred to as "preg-
nancy tumors."
Menstruation discrete "tumorlike" masses, which are referred to as preg-

During the menstrual period, the prevalence of gingivitis in- nancy tumors (Fig. 12.2D). Microscopically, gingival disease
creases. Some patients may complain of bleeding gums or a during pregnancy appears as nonspecific, vascularizing, and
bloated, tense feeling in the gums during the days preced- proliferative inflammation. Marked inflammatory cellular in-
ing menstrual flow. The exudate from inflamed gingiva is infiltration occurs, with edema and degeneration of the gingival
creased during menstruation, which suggests that preexisting epithelium and connective tissue. The epithelium is hyper-
gingivitis is aggravated by menstruation; however, the ere- plastic, with accentuated rete pegs, reduced surface keratini-
vicular fluid of normal, healthy gingiva is unaffected. Tooth zation, and various degrees of intracellular and extracellular
mobility does not change significantly during the menstrual edema and infiltration by leukocytes. Newly formed engorged
cycle. The salivary bacterial count is increased during men- capillaries are present in abundance.
struation and at ovulation, which occurs up to 14 days earlier. Bacterial-hormonal interactions may change the composi-
tion of plaque and lead to gingival inflammation .Subgingival
flora changes to a more anaerobic flora as pregnancy progress-
Pregnancy es. P intermedia appears to be the only microorganism that in-
As with other systemic conditions, pregnancy itself does not creases significantly during pregnancy. This increase appears
cause gingivitis. Gingivitis during pregnancy is caused by to be associated with elevations in systemic levels of estradiol
bacterial plaque, just as it is in nonpregnant women. The and progesterone and to coincide with the peak in gingival
hormonal changes of pregnancy accentuate the gingival re- bleeding. It has also been suggested that, during pregnancy, a
sponse to plaque and modify the resultant clinical picture. depression of the maternal I-lymphocyte response may be a
No notable changes occur in the gingiva during pregnancy in the factor in the altered tissue response to plaque. Gingivitis be-
absence of local Jactors. Tooth mobility, pocket depth, and comes more severe by the eighth month and decreases during
gingival fluid are increased during pregnancy. The severity the ninth month of pregnancy. Plaque accumulation follows a
of gingivitis is increased during pregnancy beginning in the similar pattern.
second or third month. Patients with mild chronic gingivitis Partial reduction in the severity of gingivitis occurs by
that attracted no particular attention before the pregnancy be- 2 months postpartum, and, after 1 year, the condition of the
come aware of the gingiva because previously inflamed areas gingiva is comparable to that of patients who have not been
become enlarged, edematous, and more notably discolored pregnant. Tooth mobility, pocket depth, and gingival fluid are
(Fig. 12.2A-C). also reduced after pregnancy.
Pronounced ease of bleeding is the most striking clinical The aggravation of gingivitis during pregnancy has been
feature. The gingiva is inflamed and varies in color from bright attributed principally to the increased levels of progesterone,
red to bluish red. The marginal and interdental gingivae are which produce dilation and tortuosity of the gingival micro-
edematous; they pit on pressure, appear smooth and shiny, vasculature, circulatory stasis, and increased susceptibility to
are soft and pliable, and sometimes have a raspberry-like ap- mechanical irritation, all of which favor the leakage of fluid
pearance. The extreme redness results from marked vascular- into the perivascular tissues. A marked increase in estrogen
ity, and there is an increased tendency to bleed. The gingival and progesterone occurs during pregnancy, with a reduction
changes are usually painless unless that are complicated by after parturition. It has also been suggested that the accen-
acute infection. In some cases, the inflamed gingiva forms tuation of gingivitis, which occurs during pregnancy has two
peaks: during the first trimester, when there is an overproduc-

tion of gonadotropins, and during the third trimester, when
estrogen and progesterone levels are highest. The destruction
of gingival mast cells by the increased sex hormones and the
resultant release of histamine and proteolytic enzymes may
also contribute to the exaggerated inflammatory response to
local factors.
Hormonal Contraceptives
Hormonal contraceptives aggravate the gingival response to
local factors in a manner similar to that seen during preg-
nancy; when these drugs are taken for more than 1.5 years,
there is an increase in periodontal destruction. Although some
brands of oral contraceptives produce more dramatic changes
than others, no correlation has been found to exist on the ba-
sis of differences in the progesterone or estrogen content of
various brands. Cumulative exposure to oral contraceptives
apparently has no effect on gingival inflammation or oral de- (A)
bris index scores.
Menopause
During menopause, the usual rhythmic hormonal fluctuations
of the female cycle are ended as estradiol ceases to be the ma-
jor circulating estrogen. As a result, females can develop a gin-
givostomatitis. This condition occurs during menopause or
during the postmenopausal period. Mild signs and symptoms
sometimes appear, and these are associated with the earliest
menopausal changes. Menopausal gingivostomatitis is not a
common condition.
The gingiva and the remaining oral mucosa are dry and
shiny, they vary in color from abnormal paleness to redness,
and they bleed easily. Fissuring occurs in the mucobuccal fold
in some women, and comparable changes may occur in the
vaginal mucosa. Microscopically, the gingiva exhibits atrophy
of the germinal and prickle cell layers of the epithelium and,
in some patients, areas of ulceration. The patient complains
of a dry, burning sensation throughout the oral cavity that is
associated with extreme sensitivity to thermal changes; abnor- FIGURE 12.3 A, Periapical radiograph of a brown tumor in a patient
mal taste sensations described as "salty," "peppery," or "sour"; with hyperparathyroidism. B, Occlusal radiographic view of the brown
tumor. Note the expansion of the lingual cortical plate and the move-
and difficulty with removable partial prostheses. The signs
ment of the premolar. (Courtesy Dr L. Roy Eversole, San Francisco, CA.)
and symptoms of menopausal gingivostomatitis are somewhat
comparable with those of chronic desquamative gingivitis (see
Chapter 17). Signs and symptoms similar to those of meno- widening of the periodontal ligament space, absence of the
pausal gingivostomatitis occasionally occur after ovariectomy lamina dura, and radiolucent cystlike spaces (Fig. 12.3).
or sterilization by radiation in the treatment of malignant Bone cysts become filled with fibrous tissue with abundant
neoplasms. hemosiderin-laden macrophages and giant cells. These cysts
have been called brown tumors, but they are not tumors. More
Hyperparathyroidism accurately, these cysts are reparative giant cell granulomas.
In some cases, these lesions appear in the periapical region
Parathyroid hypersecretion produces generalized demineral- of teeth, and they can lead to a misdiagnosis of a lesion of
ization of the skeleton, increased osteoclasis with prolifera- endodontic origin.
tion of the connective tissue in the enlarged marrow spaces,
and the formation of bone cysts and giant cell tumors. The
disease is called osteitis fibrosa cystica or van Rechlinghausen Hematologic Disorders and Immune
bone disease. Loss of the lamina dura and giant cell tumors
in the jaws are late signs of hyperparathyroid bone disease,
Deficiencies
which in itself is uncommon. The complete loss of the lamina All blood cells play an essential role in the maintenance of a
dura does not occur often. The loss of lamina dura may also healthy periodontium. White blood cells (WBCs) are involved
occur with Paget disease, fibrous dysplasia, and osteomalacia. in inflammatory reactions, and they are responsible for cellular
Reports have suggested that 25-50% of patients with hyper- defense against microorganisms as well as for proinflammatory
parathyroidism have associated oral changes. These changes cytokine release. Red blood cells (RBCs) are responsible for
include malocclusion and tooth mobility, radiographic evi- gas exchange and nutrient supply to the periodontal tissues
dence of alveolar osteoporosis with closely meshed trabeculae, and platelets, and they are necessary for normal hemostasis as
is considered moderate neutropenia, and an ANC of less than

500 cells/µL indicates a severe neutropenia. Infections are
sometimes difficult to manage and may be life threatening,
particularly with severe neutropenia.
Agranulocytosis
Agranulocytosis is a more severe neutropenia that involves not
only neutrophils but also basophils and eosinophils. It is de-
fined as an ANC of less than 100 cells/µL. It is characterized
by a reduction in the number of circulating granulocytes, and
it results in severe infections, including ulcerative necrotizing
lesions of the oral mucosa, the skin, and the gastrointestinal
and genitourinary tracts. Less severe forms of the disease are
FIGURE 12.4 Ecchymosis that is evident on the lateral aspects of
called neutropenia or granulocytopenia.
the soft palate and tonsillar pillars of a patient with chemotherapy- Drug idiosyncrasy is the most common cause of agranu-
induced thrombocytopenia. locytosis, but, in some cases, its cause cannot be explained.
Agranulocytosis has been reported after the administration
of drugs such as aminopyrine, barbiturates and their deriva-
well as for the recruitment of cells during inflammation and tives, benzene ring derivatives, sulfonamides, gold salts, and
wound healing. Consequently, disorders of any blood cells arsenical agents. It generally occurs as an acute disease. It may
or blood-forming organs can have a profound effect on the be chronic or periodic, with recurring neutropenic cycles (eg,
periodontium. cyclic neutropenia).
Certain oral changes (eg, hemorrhage) may suggest the The onset of disease is accompanied by fever, malaise, gen-
existence of a blood dyscrasia. However, a specific diagnosis eral weakness, and sore throat. Ulceration in the oral cavity,
requires a complete physical examination and a thorough he- the oropharynx, and the throat is characteristic. The mucosa
matologic study. Comparable oral changes occur in more than exhibits isolated necrotic patches that are black and gray and
one form of blood dyscrasia, and secondary inflammatory that are sharply demarcated from the adjacent uninvolved ar-
changes produce a wide range of variation in the oral signs. eas. The absence of a notable inflammatory reaction caused by
Hemorrhagic tendencies occur when the normal hemo- a lack of granulocytes is a striking feature. The gingival margin
static mechanisms are disturbed. Abnormal bleeding from the may or may not be involved. Gingival hemorrhage, necrosis,
gingiva or other areas of the oral mucosa that is difficult to increased salivation, and fetid odor are accompanying clinical
control is an important clinical sign that suggests a hemato- features. With cyclic neutropenia, the gingival changes recur
logic disorder. Petechiae and ecchymosis (Fig. 12.4) observed with recurrent exacerbation of the disease. The occurrence of
most often in the soft palate area are signs of an underlying generalized aggressive periodontitis has been described in pa-
bleeding disorder. It is essential to diagnose the specific eti- tients with cyclic neutropenia.
ology to appropriately address any bleeding or immunologi- Since infection is a common feature of agranulocytosis, the
cal disorder. Deficiencies in the host immune response may differential diagnosis involves consideration of such condi-
lead to severely destructive periodontal lesions. These defi- tions as necrotizing ulcerative gingivitis, noma, acute necro-
ciencies may be primary (inherited) or secondary (acquired) tizing inflammation of the tonsils, and diphtheria. Definitive
and caused by either immunosuppressive drug therapy or the diagnosis depends on the hematologic findings of pronounced
pathologic destruction of the lymphoid system. Leukemia, leukopenia and the almost complete absence of neutrophils.
Hodgkin disease, lymphomas, and multiple myeloma may re-
sult in secondary immunodeficiency disorders.
Leukemia
Leukocyte (Neutrophil) Disorders Leukemia is an important disease to understand and appreci-
ate because of its seriousness and its periodontal manifesta-
Disorders that affect the production or function of leukocytes tions. The leukemias are malignant neoplasias of WBC pre-
may result in severe periodontal destruction. PMNs (neutro- cursors that are characterized by the following: (1) the diffuse
phils) in particular play a critical role in bacterial infections, replacement of the bone marrow with proliferating leukemic
because PMNs are the first line of defense. A quantitative cells; (2) abnormal numbers and forms of immature WBCs
deficiency of leukocytes (eg, neutropenia, agranulocytosis) in the circulating blood; and (3) widespread infiltrates in the
is typically associated with a more generalized periodontal liver, spleen, lymph nodes, and other body sites.
destruction that affects all teeth. According to the cell type involved, leukemias are classified
as lymphocytic or myelogenous. A subgroup of the myelogenous
Neutropenia leukemias are the monocytic leukemias. The term lymphocytic
Neutropenia is a blood disorder that results in low levels of indicates that the malignant change occurs in cells that nor-
circulating neutrophils. It is a serious condition that may be mally form lymphocytes. The term myelogenous indicates that
caused by diseases, medications, chemicals, infections, idio- the malignant change occurs in cells that normally form RBCs,
pathic conditions, or hereditary disorders. It may be chronic some types of WBCs, and platelets. According to their evolu-
or cyclic and severe or benign. It affects as many as one in tion, leukemias can be acute (which is rapidly fatal), subacute,
three patients who are receiving chemotherapy for cancer. An or chronic. In acute leukemia, the primitive "blast" cells re-
absolute neutrophil count (ANC) of 1000-1500 cells/µL is di- leased into the peripheral circulation are immature and non-
agnostic for mild neutropenia. An ANC of 500-1000 cells/µL functional; in chronic leukemia, the abnormal cells tend to
be more mature and have normal morphologic characteristics

and functions when released into the circulation. All leuke-
mias tend to displace normal components of the bone marrow
elements with leukemic cells, thereby resulting in the reduced
production of normal RBCs, WBCs, and platelets, which leads
to anemia, leukopenia (a reduction in the number of nonmalig-
nant WBCs), and thrombocytopenia. Anemia results in poor
tissue oxygenation, thereby making tissues more friable and
susceptible to breakdown. A reduction of normal WBCs in the
circulation leads to a poor cellular defense and an increased
susceptibility to infections. Thrombocytopenia leads to bleed-
ing tendency, which can occur in any tissue but which in par-
ticular affects the oral cavity, especially the gingival sulcus.
Some patients may have normal blood counts while leukemic
cells reside primarily in the bone marrow. This type of disease
is called aleukemic leukemia.
The Periodontium in Leukemic Patients
Oral and periodontal manifestations of leukemia may include
leukemic infiltration, bleeding, oral ulcerations, and infec-
tions. The expression of these signs is more common with
acute and subacute forms of leukemia than with chronic
forms.
FIGURE 12.6 Adult male with acute myelocytic leukemia. A, An in-
Leukemic Infiltration. Leukemic cells can infiltrate the traoral view showing pronounced gingival enlargements of the entire
gingival margin and interdental papilla areas of both arches. B, Occlusal
gingiva and, less frequently, the alveolar bone. Gingival in- view of the maxillary anterior teeth. Note the marked enlargement in
filtration often results in leukemic gingival enlargement (see both the facial and the palatal aspects. (Courtesy Dr Spencer Woolfe,
Chapter 15). A study of 1076 adult patients with leukemia Dublin, Ireland.)
showed that 3.6% of the patients with teeth had leukemic
gingival proliferative lesions, with the highest incidence seen and cyanotic, with a rounding and tenseness of the gingival
in patients with acute monocytic leukemia (66. 7%), followed margin. The abnormal accumulation of leukemic cells in the
by those with acute myelocytic-monocytic leukemia (18. 7%) dermal and subcutaneous connective tissue is called leukemia
and acute myelocytic leukemia (3. 7%). It should be noted, cutis, and it forms elevated and flat macules and papules.
however, that monocytic leukemia is an extremely rare form Microscopically, the gingiva exhibits a dense, diffuse infil-
of the disease. Leukemic gingival enlargement is not found tration of predominantly immature leukocytes in the attached
in edentulous patients or in patients with chronic leukemia, and marginal gingiva. Occasionally, mitotic figures indicative
thereby suggesting that it is the accumulation of immature of ectopic hematopoiesis may be seen. The normal connective
leukemic blast cells in the gingiva adjacent to tooth surfaces tissue components of the gingiva are displaced by the leuke-
with bacterial plaque. Leukemic gingival enlargement consists mic cells (Fig. 12.7). The nature of the cells depends on the
of a basic infiltration of the gingival corium by leukemic cells
that increases the gingival thickness and that creates gingi-
val pockets in which bacterial plaque accumulates, thereby
initiating a secondary inflammatory lesion that contributes to
the enlargement of the gingiva. It may be localized to the in-
terdental papilla area (Fig. 12 5), or it may expand to include
the marginal gingiva and partially cover the crowns of the
teeth (Fig. 12.6A-B). Clinically, the gingiva appears bluish red
FIGURE 12.7 Human histologic appearance of leukemic infiltrate

with dense diffuse infiltration of predominantly immature leukocytes.
The normal connective tissue components of the gingiva are displaced
FIGURE 12.5 Leukemic infiltration that causes localized gingival by the leukemic cells. The cellular accumulation is denser in the en-
swelling of the interdental papillae between the maxillary lateral and tire reticular connective tissue layer. (Courtesy Dr Russell Christensen,
central incisors. Note the tense induration of the area. University of California, Los Angeles, CA.)
type of leukemia. The cellular accumulation is denser in the Acute gingivitis and lesions that resemble necrotizing ul-
entire reticular connective tissue layer. In almost all cases, cerative gingivitis are more frequent and severe in patients
the papillary layer contains comparatively few leukocytes. The with terminal cases of acute leukemia. The inflamed gingiva
blood vessels are distended and contain predominantly leuke- in patients with leukemia differs clinically from that found
mic cells, and the RBCs are reduced in number. The epithe- in nonleukemic individuals. The gingiva is a peculiar bluish
lium presents a variety of changes, and it may be thinned or red, it is spongelike and friable, and it bleeds persistently on
hyperplastic. Common findings include degeneration associ- the slightest provocation or even spontaneously in leukemic
ated with intercellular and intracellular edema and leukocytic patients. This greatly altered and degenerated tissue is ex-
infiltration with diminished surface keratinization. tremely susceptible to bacterial infection, which can be so
The microscopic picture of the marginal gingiva differs severe as to cause acute gingival necrosis with pseudomem-
from that of other gingival locations in that it usually exhib- brane formation or bone exposure. These are secondary oral
its a notable inflammatory component in addition to the leu- changes that are superimposed on the oral tissues altered by
kemic cells. Scattered foci of plasma cells and lymphocytes the blood dyscrasia. They produce associated disturbances
with edema and degeneration are common findings. The in- that may be a source of considerable difficulty to the patient,
ner aspect of the marginal gingiva is usually ulcerated, and such as systemic toxic effects, loss of appetite, nausea, blood
marginal necrosis with pseudomembrane formation may also loss from persistent gingival bleeding, and constant gnaw-
be seen. The periodontal ligament and alveolar bone may also ing pain. Eliminating or reducing local factors (eg, bacte-
be involved in acute and subacute leukemia. The periodontal rial plaque) can minimize the severe oral changes associated
ligament may be infiltrated with mature and immature leuko- with leukemia. In some patients with severe acute leukemia,
cytes. The marrow of the alveolar bone exhibits a variety of symptoms may only be relieved by treatment that leads to the
changes, such as localized areas of necrosis, thrombosis of the remission of the disease.
blood vessels, infiltration with mature and immature leuko- In those with chronic leukemia, oral changes that suggest
cytes, occasional RBCs, and the replacement of the fatty mar- a hematologic disturbance are rare. The microscopic changes
row with fibrous tissue. of chronic leukemia may consist of replacing the normal fatty
marrow of the jaws with islands of mature lymphocytes or
Bleeding. Gingival hemorrhage is a common finding in leu- lymphocytic infiltration of the marginal gingiva without dra-
kemic patients even in the absence of clinically detectable gin- matic clinical manifestations. The existence of leukemia is
givitis. Bleeding gingiva can be an early sign of leukemia. It is sometimes revealed by a gingival biopsy performed to clarify
caused by the thrombocytopenia that results from the replace- the nature of a troublesome gingival condition. In such cases,
ment of the bone marrow cells with leukemic cells and from the gingival findings must be corroborated by medical ex-
the inhibition of normal stem cell function by leukemic cells amination and hematologic study. In patients with diagnosed
or their products. This bleeding tendency can also manifest leukemia, gingival biopsy may indicate the extent to which
in the skin and throughout the oral mucosa, where petechiae leukemic infiltration is responsible for the altered clinical ap-
are often found, with or without leukemic infiltrates. A more pearance of the gingiva. Although such findings are of interest,
diffuse submucosal bleeding manifests as ecchymosis (see their benefit to the patient is insufficient to warrant routine gin-
Fig. 12.4). Oral bleeding has been reported as a presenting gival biopsy studies in patients with leukemia. Furthermore, it is
sign in 17. 7% of patients with acute leukemia and in 4. 4% of important to note that the absence of leukemic involvement
patients with chronic leukemia. Bleeding may also be a side in a gingival biopsy specimen does not rule out the possibility
effect of the chemotherapeutic agents used to treat leukemia. of leukemia. A gingival biopsy in a patient with chronic leu-
kemia may reveal typical gingival inflammation without any
Oral Ulceration and Infection. In patients with leukemia, suggestion of a hematologic disturbance.
the response to bacterial plaque or other local irritation is al-
tered. The cellular component of the inflammatory exudate
Anemia
differs both quantitatively and qualitatively from that found
in nonleukemic individuals in that there is a pronounced in- Anemia is a deficiency in the quantity or quality of the blood
filtration of immature leukemic cells in addition to the usual as manifested by a reduction in the number of erythrocytes
inflammatory cells. As a result, the normal inflammatory re- and in the amount of hemoglobin. Anemia may be the result
sponse may be diminished. of blood loss, defective blood formation, or increased RBC
Granulocytopenia (diminished WBC count) results from the destruction. Anemias are classified according to cellular mor-
displacement of normal bone marrow cells by leukemic cells, phology and hemoglobin content as follows: (1) macrocytic
which increases the host susceptibility to opportunistic micro- hyperchromic anemia (pernicious anemia); (2) microcytic
organisms and leads to ulcerations and infections. Discrete, hypochromic anemia (iron deficiency anemia); (3) sickle cell
punched-out ulcers that penetrate deeply into the submucosa anemia; and ( 4) normocytic-normochromic anemia (hemo-
and that are covered by a firmly attached white slough can lytic or aplastic anemia).
be found on the oral mucosa. These lesions occur in sites of Pernicious anemia results in tongue changes in 75% of pa-
trauma (eg, the buccal mucosa) in relation to the line of oc- tients. The tongue appears red, smooth, and shiny as a result
clusion or on the palate. Patients with a history of herpesvirus of atrophy of the papillae (Fig. 12 8) There is also marked
infection may develop recurrent herpetic oral ulcers (often in pallor of the gingiva (Fig. 12 9) Iron deficiency anemia in-
multiple sites) and large atypical forms, especially after che- duces similar tongue and gingival changes. A syndrome that
motherapy is instituted. consists of glossitis and ulceration of the oral mucosa and
A gingival (bacterial) infection in leukemic patients can oropharynx and that induces dysphagia (Plummer-Vinson
be the result of an exogenous bacterial infection or an exist- syndrome) has been described in patients with iron deficien-
ing bacterial infection (eg, gingival or periodontal disease). cy anemia. Sickle cell anemia is a hereditary form of chronic
unknown etiology, as with Werlhof disease), or it may occur

secondary to some known etiologic factor that is responsible
for a reduced amount of functioning marrow and a resultant
reduction in the number of circulating platelets. Such etiolog-
ic factors include aplasia of the marrow; displacement of the
megakaryocytes in the marrow as with leukemia; replacement
of the marrow by tumor; and destruction of the marrow by
irradiation or radium or by drugs such as benzene, aminopy-
rine, and arsenical agents.
Thrombocytopenic purpura is characterized by a low plate-
let count, a prolonged clot retraction and bleeding time, and a
normal or slightly prolonged clotting time. There is spontane-
ous bleeding into the skin or from the mucous membranes.
Petechiae and hemorrhagic vesicles occur in the oral cavity,
particularly in the palate, the tonsillar pillars, and the buccal
mucosa. The gingivae are swollen, soft, and friable. Bleeding
occurs spontaneously or with the slightest provocation, and
it is difficult to control. Gingival changes represent an abnormal
FIGURE 12.8 A smooth tongue in a patient with pernicious anemia.
response to local irritation. The severity of the gingival condi-
tion is dramatically alleviated by removal of the local factors.
Genetic Disorders
Many systemic conditions associated with or that predispose
an individual to periodontal destruction include genetic disor-
ders that result in an inadequate number or reduced function
of circulating neutrophils. This underscores the importance of
the neutrophil in the protection of the periodontium against
infection. Severe periodontitis has been observed in individu-
als with primary neutrophil disorders such as neutropenia,
agranulocytosis, Chediak-Higashi syndrome, and lazy leuko-
cyte syndrome. In addition, severe periodontitis has also been
observed in individuals who exhibit secondary neutrophil im-
pairment, which is seen in those with Down syndrome, Papil-
Ion-Lefevre syndrome, and inflammatory bowel disease.
FIGURE 12.9 The diffuse pallor of the gingiva in a patient with ane- Chedlak-Higashl Syndrome
mia. The discolored and inflamed gingival margin stands out in sharp
contrast to the adjacent pale and attached gingiva. Chediak-Higashi syndrome is a rare disease that affects the
production of organelles found in almost every cell. It affects
mostly the melanocytes, platelets, and phagocytes. It causes
hemolytic anemia that occurs almost exclusively in blacks. It partial albinism, mild bleeding disorders, and recurrent bacte-
is characterized by pallor, jaundice, weakness, rheumatoid rial infections. Neutrophils contain abnormal, giant lysosomes
manifestations, and leg ulcers. Oral changes include gener- that can fuse with the phagosome, but their ability to release
alized osteoporosis of the jaws, with a peculiar stepladder their contents is impaired. As a result, the killing of ingested
alignment of the trabeculae of the interdental septa, along microorganisms is delayed. Patients with Chediak-Higashi
with pallor and yellowish discoloration of the oral mucosa. syndrome are susceptible to repeated infections that can be
Periodontal infections may precipitate sickle cell crisis. Aplas- serious and life threatening. Aggressive periodontitis has been
tic anemia results from a failure of the bone marrow to pro- described in these patients.
duce erythrocytes. The etiology is usually the effect of toxic
drugs on the marrow or the displacement of RBCs by leuke-
Lazy Leukocyte Syndrome
mic cells. Oral changes include pale discoloration of the oral
mucosa and increased susceptibility to infection because of Lazy leukocyte syndrome is characterized by an individual's
the concomitant neutropenia. susceptibility to severe microbial infections, neutropenia, de-
fective chemotactic response by neutrophils, and an abnormal
inflammatory response. Those who are diagnosed with lazy
Thrombocytopenia
leukocyte syndrome are susceptible to aggressive periodonti-
Thrombocytopenia is a term that is used to describe the condi- tis, with the destruction of bone and early tooth loss.
tion of a reduced platelet count that results from either a lack
of platelet production or an increased loss of platelets. Purpura
Leukocyte Adhesion Deficiency
refers to the purplish appearance of the skin or mucous mem-
branes where bleeding has occurred as a result of decreased Leukocyte adhesion deficiency (LAD) is a very rare genetic
platelets. Thrombocytopenic purpura may be idiopathic (ie, of disorder; only a few hundred cases have been diagnosed.
Since LAD is an inherited disease, it is categorized as a pri-

mary immunodeficiency that is most often diagnosed at birth.
Many children with LAD do not survive.
LAD results from an inability to produce or a failure to
normally express an important cell surface integrin ( CD 18),
which is necessary for leukocytes to adhere to the vessel wall
at the site of infection. When leukocytes cannot effectively
adhere to the vessel wall near the site of infection, they can-
not migrate to the infection. As a result, bacterial infections
are able to continue to destroy host tissues unimpeded by
the normal host immune response. Infections act similarly to
those observed in neutropenic patients, because phagocytes
are unable to reach the site of infection. Cases of periodontal FIGURE 12.11 Severe periodontal destruction in a 14-year-old
disease that are attributed to LAD are rare. They begin during patient with Down syndrome. Note the extensive loss of periodontal
or immediately after the eruption of the primary teeth. Ex- support around the mandibular incisors as evidenced by severe gingival
tremely acute inflammation and proliferation of the gingival recession. Moderate to heavy bacterial plaque is associated with moder-
tissues with the rapid destruction of bone are found. Profound ate gingival inflammation in the area.
defects in peripheral blood neutrophils and monocytes and

an absence of neutrophils in the gingival tissues have been
noted in patients with LAD. These patients also have frequent eruption. The microscopic changes reported include marked
respiratory tract infections and sometimes otitis media. Both chronic inflammation of the lateral wall of the pocket with a
the primary and permanent teeth are affected, often resulting predominantly plasma cell infiltrate, considerable osteoclas-
in early tooth loss. tic activity with an apparent lack of osteoblastic activity, and
an extremely thin cementum. Bacterial flora studies of plaque
in a patient with Papillon-Lefevre syndrome revealed a simi-
Papillon-Lefevre Syndrome larity to bacterial flora in patients with chronic periodontitis.
Papillon-Lefevre syndrome is a very rare inherited condition Spirochete-rich zones in the apical portion of the pockets as
that appears to follow an autosomal-recessive pattern. Parents well as spirochete adherence to the cementum and microcol-
are not affected, and both must carry the autosomal genes for ony formation of Mycoplasma species have been reported with
the syndrome to appear in their offspring. It may occur in Papillon-Lefevre syndrome. Gram-negative cocci and rods ap-
siblings, and it has no gender predilection. The syndrome is pear at the apical border of the plaque. This syndrome may
characterized by hyperkeratotic skin lesions, severe destruc- be associated with neutrophil defects as a contributing factor.
tion of the periodontium, and, in some cases, calcification of
the dura. The cutaneous and periodontal changes usually ap- Down Syndrome
pear together when the patient is between the ages of 2 and
4 years. The skin lesions consist of hyperkeratosis and ichthy- Down syndrome (mongolism, trisomy 21) is a congenital dis-
osis of localized areas on the palms, soles, knees, and elbows. ease caused by a chromosomal abnormality and characterized
Periodontal involvement consists of early inflammatory by mental deficiency and growth retardation. The prevalence
changes that lead to bone loss and exfoliation of teeth. The of periodontal disease in patients with Down syndrome is
primary teeth are lost by 5 or 6 years of age. The perma- high, occurring in almost 100% of patients who are less than
nent dentition then erupts normally, but, within a few years, 30 years old. Although plaque, calculus, and local irritants
the permanent teeth are also lost as a result of destructive (eg, diastemata, crowding of teeth, high frenum attachments,
periodontal disease (Fig. 12.10). At a very early age (usu- malocclusion) are present and oral hygiene is poor, the se-
ally 15-20 years), patients are often edentulous except for verity of periodontal destruction exceeds that explainable by
the third molars. These may be lost as well a few years after local factors alone. Periodontal disease in those with Down
syndrome is characterized by the formation of deep periodon-
tal pockets associated with substantial plaque accumulation
and moderate gingivitis (Fig. 12.11). These findings are usu-
ally generalized although they tend to be more severe in the
lower anterior region. Moderate recession is sometimes seen
in this region as well. The disease progresses rapidly. The high
prevalence and increased severity of periodontal destruction
associated with Down syndrome is most likely explained by
poor PMN chemotaxis, phagocytosis, and intracellular killing.
Stress and Psychosomatic Disorders

Psychologic conditions, particularly psychosocial stress, have
been implicated as risk indicators for periodontal disease. The
FIGURE 12.10 This intraoral clinical view of a 17-year-old boy with
most notable example is the documented relationship be-
Papillon-Lefevre syndrome shows early tooth loss and severe bone tween stress (eg, experienced by soldiers at war or by students
loss around the remaining teeth as evidenced by gingival recession. during examinations) and acute necrotizing ulcerative gingi-
The missing teeth were exfoliated. vitis (see Chapter 16). The presence of necrotizing ulcerative
gingivitis among soldiers stressed by wartime conditions in immune response directly through an increased release of
the trenches led to one of the early diagnostic terms used to neurotransmitters, including epinephrine, norepinephrine,
describe this condition: "trench mouth." neurokinin, and substance P, which interact directly with
lymphocytes, neutrophils, monocytes, and macrophages via
receptors that cause an increase in their tissue-destructive
Psychosocial Stress, Depression, function. Thus, in a manner similar to cortisol production,
the "stress-induced" release of these neurotransmitters re-
and Coping
sults in an upregulated immune response that increases the
Recently, several clinical studies and a systematic review of potential for destruction by the cellular response to peri-
the subject have documented a positive relationship between odontal pathogens.
psychosocial stress and chronic forms of periodontal disease. It is important to remember that, although stress may
All individuals experience stress, but these events do not predispose an individual to more destruction from periodon-
invariably result in destructive periodontitis. The types of titis, the presence of periodontal pathogens remains as the
stress that lead to periodontal destruction appear to be more essential etiologic factor. In other words, stress alone does not
chronic or long term and less likely to be controlled by the cause or lead to periodontitis in the absence of periodontal
individual. Life events such as the loss of a loved one (eg, pathogens.
spouse, family member), a failed relationship, loss of employ-
ment, and financial difficulties are examples of stressful life
Influence of Stress on Periodontal
events that are typically not controllable by the individual or
not perceived by the individual as being under his or her con- Therapy Outcomes
trol, thereby rendering the person with a feeling of "helpless- Psychologic conditions such as stress and depression may
ness." The duration of the stressful life event will also have also influence the outcome of periodontal therapy. Depres-
an influence on the total impact of the stress-induced dis- sion might have a negative effect on periodontal treatment
ease destruction. One of the most important aspects related outcomes.
to the influence of stress on periodontal disease destruction Stress impairs the inflammatory response and matrix
is the manner in which the individual copes with the stress. degradation. Greater psychologic stress was significantly
Emotional coping methods appear to render the host more associated with lower levels of interleukin-1 and matrix
susceptible to the destructive effects of periodontal disease metalloproteinase-9 as well as with a significantly more pain-
than do practical coping methods. Furthermore, emotional ful, poorer, and slower recovery.
coping is more common in situations that must be accepted Both stressful life events and the individual's personality
and among individuals who feel helpless in the situation. and coping skills are factors to consider when assessing the
risk of periodontal disease destruction and the potential for
Stress-Induced lmmunosuppression successful periodontal therapy. If patients with emotional or
defensive coping skills are identified, care should be taken to
Stress and psychosomatic disorders most likely impact peri- ensure that they receive information in a manner that does not
odontal health via changes in the individual's behavior and elicit a "defensive" reaction.
through complex interactions among the nervous, endocrine,
and immune systems. Individuals under stress may have
poorer oral hygiene, they may start or increase the clench- Psychiatric Influence of Self-Inflicted
ing and grinding of their teeth, and they may smoke more
frequently. All of these behavioral changes increase their Injury
susceptibility to periodontal disease destruction. Likewise, Psychosomatic disorders may result in harmful effects to the
individuals who are under stress may be less likely to seek health of tissues in the oral cavity through the development
professional care. of habits that are injurious to the periodontium. Neurotic
In addition to the many behavioral changes that may in- habits such as grinding or clenching the teeth, nibbling on
fluence periodontal disease destruction, psychosocial stress foreign objects (eg, pencils, pipes), nail biting, and excessive
may also impact the disease through alterations in the im- use of tobacco are all potentially injurious to the teeth and the
mune system. The influence of stress on the immune system periodontium. Self-inflicted gingival injuries, such as gingival
and systemic health conditions (eg, cardiovascular disease) recession, have been described in both children and adults.
is well known. Stress-related immune system changes clearly However, these types of self-inflicted, factitious injuries do not
have the potential to affect the pathogenesis of periodon- appear to be common among psychiatric patients.
tal disease as well. One possible mechanism involves the
production of cortisol. Stress increases cortisol production
from the adrenal cortex by stimulating an increase in the
release of adrenocorticotropic hormone from the pituitary
Nutritional Influences
gland. Increased cortisol suppresses the immune response Some clinicians enthusiastically adhere to the theory in peri-
directly through the suppression of neutrophil activity, im- odontal disease that assigns a key role to nutritional deficien-
munoglobulin G production, and salivary immunoglobulin cies and imbalances. Previous research did not support this
A secretion. All of these immune responses are critical for view, but numerous problems in experimental design and data
the normal immunoinflammatory response to periodontal interpretation could be responsible for making these research
pathogens (see Chapter 7). The resulting "stress-induced" findings inadequate. The majority of opinions and research
immunosuppression increases the potential for destruction findings regarding the effects of nutrition on oral and peri-
by periodontal pathogens. Stress may also affect the cellular odontal tissues point to the following:
1. There are no nutritional deficiencies that by themselves can Vitamin E Deficiency

cause gingivitis or periodontitis. However, nutritional de- Vitamin E serves as an antioxidant to limit free-radical re-
ficiencies can affect the condition of the periodontium actions and to protect cells from lipid peroxidation. Cell
and thereby may accentuate the deleterious effects of membranes, which are high in polyunsaturated lipids, are the
plaque-induced inflammation in susceptible individuals. major site of damage in patients with vitamin E deficiency. No
Theoretically, one may presume that an individual with a relationship has been demonstrated between deficiencies in
nutritional deficiency is less able to defend against a bacte- vitamin E and oral disease, but systemic vitamin E appears to
rial challenge as compared with a nutritionally competent accelerate gingival wound healing in the rat.
individual.
2. There are nutritional deficiencies that produce changes in the
oral cavity. These changes include alterations of the tissues Water-Soluble Vitamin Deficiency
of the lips, oral mucosa, gingiva, and bone. These altera-
tions are considered to be the periodontal and oral mani- Vitamins B and C are water-soluble vitamins that are required
festations of nutritional disease. in the human diet.
The role of nutrition in periodontal disease may be related B-Complex Deficiency
to the effect of nutrition on inflammation. A recent review of The vitamin B complex includes thiamin, riboflavin, niacin,
the literature evaluating the effect of nutritional factors on in- pyridoxine (B6), biotin, folic acid, and cobalamin (B12). Oral
flammation demonstrated that subtle shifts in nutritional sta- disease is rarely caused by a deficiency in just one component of
tus are associated with the prevalence of periodontitis. More the B-complex group; the deficiency is generally multiple. Oral
specifically, they reported that the results of contemporary changes that are common to B-complex deficiencies are gingi-
animal and human studies have demonstrated the role of spe- vitis, glossitis, glossodynia, angular cheilitis, and inflammation
cific micronutrients in the modulation of the host's inflamma-
of the entire oral mucosa. The gingivitis in individuals with
tory response by reducing inflammatory biomarkers, which
vitamin B deficiencies is nonspecific because it is caused by
may in turn be responsible for periodontal destruction. The bacterial plaque rather than by the deficiency; however, gingi-
evidence for the effect of nutrition on inflammation is sig- vitis is subject to the deficiency's modifying effect.
nificant. Data suggest that diets that contain foods rich in The human manifestations of thiamin deficiency, called beri-
antioxidants are beneficial, whereas foods that contain high beri, are characterized by paralysis; cardiovascular symptoms,
levels of refined carbohydrates are detrimental to the inflam- including edema; and loss of appetite. Frank beriberi is rare in
matory process. the United States. Oral disturbances that have been attributed to
thiamin deficiency include hypersensitivity of the oral mucosa;
Fat-Soluble Vitamin Deficiency minute vesicles (simulating herpes) on the buccal mucosa, under
the tongue, or on the palate; and erosion of the oral mucosa.
Vitamins A, D, and E are fat-soluble vitamins that are required The symptoms of riboflavin deficiency (ariboflavinosis) in-
in the human diet. clude glossitis, angular cheilitis, seborrheic dermatitis, and a
superficial vascularizing keratitis. The glossitis is character-
Vitamin A Deficiency ized by a magenta discoloration and atrophy of the papillae.
A maJor function of vitamin A is to maintain the health of In mild to moderate cases, the dorsum exhibits a patchy atro-
the epithelial cells of the skin and mucous membranes. A de- phy of the lingual papillae and engorged fungiform papillae,
ficiency of vitamin A results in dermatologic, mucosal, and which project as pebblelike elevations. With severe deficiency,
ocular manifestations. In the absence of vitamin A, degen- the entire dorsum is flat, with a dry and often fissured surface.
erative changes occur in epithelial tissues, thereby resulting Changes observed in riboflavin-deficient monkeys include se-
in a keratinizing metaplasia. Since epithelial tissues provide vere lesions of the gingiva, the periodontal tissues, and the
a primary barrier function to protect against invading mi- oral mucosa, including noma. Angular cheilitis begins as an in-
croorganisms, vitamin A may play an important role in pro- flammation of the commissure of the lips, and this is followed
tecting against microbial invasion by maintaining epithelial by erosion, ulceration, and fissuring. Riboflavin deficiency is
integrity. not the only cause of angular cheilitis. A loss of vertical di-
Little information is available regarding the effects of vi- mension, together with the drooling of saliva into the angles of
tamin A deficiency on the oral structures in humans. Sev- the lips, may produce a condition similar to angular cheilitis.
eral epidemiologic studies have failed to demonstrate any Candidiasis may develop in the commissures of debilitated
relationship between this vitamin and periodontal disease in persons; this lesion has been termed perleche. Supplemental
humans. riboflavin is ineffective to resolve cases of glossitis and angular
cheilitis that are not caused by vitamin deficiency.
Vitamin D Deficiency Niacin deficiency results in pellagra, which is characterized
Vitamin D or calciferol is essential for the absorption of calci- by symptoms of dermatitis, gastrointestinal disturbances,
um from the gastrointestinal tract and the maintenance of the neurologic and mental disturbances (dermatitis, diarrhea,
calcium-phosphorus balance. A deficiency of vitamin D and or dementia), glossitis, gingivitis, and generalized stornati-
an imbalance in calcium-phosphorus intake result in rickets tis. This condition is rare, but it may occasionally result from
in young children and osteomalacia in adults. No studies have malabsorption or alcoholism. Glossitis and stomatitis may be
demonstrated a relationship between vitamin D deficiency the earliest clinical signs of niacin deficiency. The gingiva may
and periodontal disease. be involved in aniacinosis with or without tongue changes.
The most common finding is necrotizing ulcerative gingivitis, 4. Decreasing levels of ascorbic acid may affect both the che-
usually in areas of local irritation. motactic and migratory actions of leukocytes without in-
Oral manifestations of vitamin B-complex and niacin de- fluencing their phagocytic activity.
ficiency in experimental animals include black tongue and 5. An optimal level of ascorbic acid is apparently required to
gingival inflammation, with destruction of the gingiva, the maintain the integrity of the periodontal microvasculature
periodontal ligament, and the alveolar bone. Necrosis of the as well as the vascular response to bacterial plaque and
gingiva and other oral tissues as well as leukopenia are termi- wound healing.
nal features of niacin deficiency in experimental animals. 6. The depletion of vitamin C may interfere with the eco-
Folic acid deficiency results in macrocytic anemia with meg- logic equilibrium of bacteria in plaque and thus increase
aloblastic erythropoiesis accompanied by oral changes, gas- its pathogenicity. However, no evidence demonstrates this
trointestinal lesions, diarrhea, and intestinal malabsorption. effect.
In humans with sprue and other folic acid deficiency states,
However patients with acute or chronic vitamin (-deficient
generalized stomatitis occurs, which may be accompanied
states and no plaque accumulation demonstrate minimal (if
by ulcerated glossitis and cheilitis. Ulcerative stomatitis is an
any) changes in their gingival health status.
early indication of the toxic effect of the folic acid antagonists
(eg, methotrexate) used for the treatment of leukemia. A sig-
nificant reduction of gingival inflammation occurs after the Protein Deficiency
systemic or local use of folic acid as compared with placebo.
Protein depletion results in hypoproteinemia with many
This reduction occurred with no change in plaque accumu-
pathologic changes, including muscular atrophy, weakness,
lation. Gingival changes associated with pregnancy and oral
weight loss, anemia, leukopenia, edema, impaired lactation,
contraceptives may be partly related to suboptimal levels of
decreased resistance to infection, slow wound healing, lym-
folic acid in the gingiva.
phoid depletion, and reduced ability to form certain hor-
mones and enzyme systems. Protein deprivation has been
Vitamin C (Ascorbic Acid) Deficiency shown to cause changes in the periodontium of experimen-
Severe vitamin C deficiency in humans results in scurvy, a tal animals. The following observations have been made in
disease that is characterized by hemorrhagic diathesis and protein-deprived animals: degeneration of the connective
delayed wound healing. Vitamin C is required in the human tissue of the gingiva and the periodontal ligament, osteo-
diet as well as in other primates, guinea pigs, and some rare porosis of the alveolar bone, impaired deposition of the ce-
flying mammals. Since vitamin C is abundant in fruits and mentum, delayed wound healing, and atrophy of the tongue
vegetables, scurvy is uncommon in developed countries. It epithelium.
may occur in infants during their first year of life if formulas In other words, protein deprivation results in periodontal
are not fortified with vitamins and in older persons, espe- tissues that lack integrity and that, as a result, are more vul-
cially those living alone and with restricted diets. Malnutri- nerable to breakdown when challenged by bacteria.
tion associated with alcoholism may predispose an individual
to scurvy.
Scurvy results in the defective formation and maintenance Medications
of collagen, the impairment or cessation of osteoid formation,
and impaired osteoblastic function. Vitamin C deficiency is Bisphosphonates
also characterized by increased capillary permeability, sus-
Bisphosphonates are a class of medications widely prescribed
ceptibility to traumatic hemorrhages, hyporeactivity of the
for the treatment of osteoporosis and various types of cancer.
contractile elements of the peripheral blood vessels, and
They have recently been implicated in osteonecrosis of the jaw
sluggishness of blood flow. Clinical manifestations of scurvy
(ONJ), a serious condition that is characterized by nonheal-
include hemorrhagic lesions into the muscles of the extremi-
ing, often painful exposure of nonvital and often sequestrating
ties, the joints, and sometimes the nailbeds; petechial hemor-
bone in the jaws. Corticosteroids have long been prescribed
rhages, often around the hair follicles; increased susceptibility
to suppress the immune system for the control and manage-
to infections; and impaired wound healing. Bleeding, swollen
ment of autoimmune disease, during cancer treatment, and as
gingiva, and loosened teeth are common features of scurvy.
an antirejection medication for transplant patients. The use
of bisphosphonates in cancer treatment is aimed at prevent-
Possible Etiologic Factors. Ascorbic acid may play a role in
ing the often lethal imbalance of osteoclastic activity. During
periodontal disease through one or more of the following sug-
the treatment of osteoporosis, the goal is simply to harness
gested mechanisms:
osteoclastic activity to minimize or prevent bone loss and, in
1. Low levels of ascorbic acid influence the metabolism of many cases, to increase bone mass by creating an advantage
collagen within the periodontium, thereby affecting the for osteoblastic activity.
ability of the tissue to regenerate and repair.
2. Ascorbic acid deficiency interferes with bone formation Bisphosphonates and Periodontal Bone Loss
and leads to the loss of periodontal bone. Changes that do The bone-preserving action of bisphosphonates has been
occur in alveolar bone and other bones as a result of failure studied and advocated for use in the prevention of bone
of the osteoblasts to form osteoid take place very late in the loss from periodontal disease. Interestingly, alendronate was
deficiency state. found to significantly reduce bone loss in cases with less bone
3. Suboptimal levels of vitamin C would lead to failure to mass or less bone density. Alendronate was shown to have a
maintain the epithelium's barrier function to bacterial significant positive (bone-preserving) effect on bone density
products. in jaws.
Corticosteroids for osteoporosis, with some of these factors putting them at

risk for the progression of periodontitis as well.
In humans, the systemic administration of cortisone and ad- Estrogen deficiency and osteopenia or osteoporosis togeth-
renocorticotropic hormone appears to have no effect on the er are risk factors for alveolar bone loss in postmenopausal
incidence or severity of gingival and periodontal disease. women with a history of periodontitis. Estrogen deficiency
However, renal transplant patients receiving immunosup- may play a significant role in the progression of periodontitis
pressive therapy (prednisone or methylprednisolone, azathio- in osteopenic or osteoporotic women. In patients with peri-
prine, or cyclophosphamide) have significantly less gingival odontal disease and concomitant postmenopausal osteoporo-
inflammation than control subjects with similar amounts of sis, the possibility exists that the lack of estrogen influences
plaque. the activities of bone cells and immune cells in such a way that
Medications which cause gingival overgrowth are discussed the progression of alveolar bone loss will be enhanced. It was
in Chapter 15. found that there is less risk for tooth loss and improved oral
health among postmenopausal women receiving hormone re-
placement therapy.
Other Systemic Conditions
Osteoporosis Congenital Heart Disease
Congenital heart disease occurs in about 1 % of live births.
Osteoporosis is a disease that is characterized by low bone
Approximately 40% of individuals born with heart defects
mass and structural deterioration that leads to an increased
would die without treatment. However, the prognosis has
risk of bone fracture. The condition has a higher predilection
been dramatically improved with advances in cardiac surgery.
for females (80%) as compared to males (20%). The loss of
Cardiac defects can involve the heart, the adjacent vessels, or
bone mass and the incidence of osteoporosis increases with
a combination of both. The most striking feature of congenital
age for both men and women, with women being affected ear-
heart disease is cyanosis caused by the shunting of deoxygen-
lier than men. The rate of bone loss is greatest for women
ated blood from the right to the left, thereby resulting in the
during the perimenopausal years, when estrogen levels de-
return of poorly oxygenated blood to the systemic circulation.
crease. A bone mineral density (BMD) test is used to measure
In severe cases, cyanosis is obvious at birth, particularly in the
an individual's bone mass. BMD is measured with the use of
presence of tetralogy of Fallot. Chronic hypoxia causes im-
a dual-energy X-ray absorptiometry scan. The dual-energy X-
paired development, compensatory polycythemia (ie , an in-
ray absorptiometry value or I-score is a comparison of the
crease in RBCs and hemoglobin), and clubbing edema of toes
patient's BMD to that of a healthy 30-year-old adult with peak
and fingers. Polycythemia is significant because it can result in
bone mass. The World Health Organization defines osteopo-
hemorrhagic or thrombotic tendencies. Patients with congeni-
rosis and osteopenia by measures of "standard deviations" as
tal heart defects are often at risk for infective endocarditis as a
compared with that of a normal, healthy, young adult. Thus,
result of turbulent blood flow in the heart and the associated
a I-score between +l and -1 is considered normal, whereas
cardiovascular defects. The need for prophylactic antibiotics
a I-score between -1 and -2.5 indicates low bone density or
should be evaluated before dental therapy.
osteopenia and a I-score of less than -2.5 (ie, more than 2.5
In addition to the obvious cyanosis of the lips and the oral
standard deviations below normal) is diagnostic for osteopo-
mucosa, oral abnormalities associated with cyanotic con-
rosis (Table 12 1)
genital heart disease include the delayed eruption of both
One of the most significant consequences of osteoporosis
the primary and permanent dentitions, increased positional
is the increased risk of bone fracture. All bones affected by
abnormalities, and enamel hypoplasia. The teeth often have
osteoporosis are susceptible to fracture. Although it is logical
a bluish-white appearance with an increased pulp vascular
to surmise a relationship between osteoporosis and periodon-
volume. Gingival disease and other oral symptoms have been
titis, it has been a challenging hypothesis to prove. One of the
reported in children with congenital heart disease. Reports
difficulties is the fact that both osteoporosis and periodontitis
seem to indicate more severe caries and periodontal disease in
are chronic, multifactorial diseases that result in bone loss,
patients with cyanotic congenital heart defects. However, the
and bone loss in each condition is exacerbated by local and
apparent increase in dental disease may be attributed to poor
systemic factors. Gender, genetic predisposition, inactivity,
oral hygiene and a general lack of dental care rather than a
deficient diets (eg, deficient in calcium or vitamin D), alcohol,
disease-related etiology.
smoking, hormones, and medications put individuals at risk
Tetralogy of Fallot
As its name implies, tetralogy of Fallot is characterized by four
TABLE 12.1 cardiac defects: (1) ventricular septa! defect; (2) pulmonary
DEFINITIONS OF OSTEOPOROSIS AND stenosis; (3) malposition of the aorta to the right; and (4)
OSTEOPENIA INDICATED BY T-SCORES compensatory right ventricular enlargement. Clinical features
include severe cyanosis, audible heart murmurs, and breath-
T-Score Bone Mineral Density Category lessness. Cyanosis and breathlessness cause cerebral anoxia
;c,:-1 Normal and syncope. Oral changes include a purplish-red discolor-
-lto-2.5 Low (osteopenia) ation of the lips and the gingiva. Severe marginal gingivitis
:s;-2.5 Osteoporosis and periodontal destruction have been reported. The discol-
oration of the lips and the gingiva corresponds to the general
Ranges of T-scores are based on standard deviations outside of normal, which
is based on the bone mineral density of a healthy 30-year-old adult. degree of cyanosis and returns to normal after corrective heart
(Adapted from World Health Organization Definitions) surgery. The tongue appears coated, fissured, and edematous,
and there is extreme reddening of the fungiform and filiform

papillae. The number of subepithelial capillaries is increased,
but this also returns to normal after heart surgery.
Eisenmenger Syndrome
Among patients with ventricular septa! defects, about half
of those with large defects (ie, those > 1.5 cm in diameter)
develop Eisenmenger syndrome. This syndrome is distin-
guished by a greater blood flow from the stronger left ventri-
cle to the right ventricle (backward flow) through the septa! FIGURE 12.12 Bismuth gingivitis. Note the linear black discoloration
defect. This causes increased pulmonary blood flow, which of the gingiva in a patient who is receiving bismuth therapy.
in turn leads to progressive pulmonary fibrosis, small-vessel
occlusion, and high pulmonary vascular resistance. With in-
creasing pulmonary resistance, the right ventricle hypertro-
eruptions, bullous and purpuric lesions, herpes-zoster-like
phies, the shunt becomes bidirectional, and ultimately, blood
eruptions, and pigmentation of the skin and mucous mem-
flow is reversed (ie, it flows from right to left). The increased
branes are among the dermatologic lesions attributed to bis-
vascular resistance builds pressure in the right ventricle,
muth intoxication. Acute bismuth intoxication, which is seen
thereby causing right ventricular hypertrophy, and a reverse
less frequently, is accompanied by methemoglobin formation,
in the direction of the blood flow, which results in a right-to-
cyanosis, and dyspnea.
left shunt.
Bismuth pigmentation in the oral cavity usually appears
The natural history of a patient with untreated Eisen-
as a narrow, bluish-black discoloration of the gingival margin
menger syndrome is a gradual increase in cyanosis over many
in areas of preexisting gingival inflammation (Fig. 12.12).
years that eventually leads to cardiac failure. Cyanosis of the
Such pigmentation results from the precipitation of par-
lips, cheeks, and buccal mucous membranes is observed in
ticles of bismuth sulfide associated with vascular changes
these patients, but it is much less severe than in those with
in inflammation; it is not evidence of intoxication but sim-
tetralogy of Fallot. Severe, generalized periodontitis has been
ply indicates the presence of bismuth in the bloodstream.
reported in patients with Eisenmenger syndrome. However,
Bismuth pigmentation in the oral cavity also occurs in cases
similar to patients with other types of congenital heart dis-
of intoxication; it assumes a linear form if the marginal gin-
ease, the incidence of periodontal disease reported in those
giva is inflamed.
with Eisenmenger syndrome may be related more to poor oral
hygiene and a general lack of dental care than to any specific, Lead Intoxication
syndrome-related etiology.
Lead is slowly absorbed, and toxic symptoms are not par-
ticularly definitive when they do occur. There is a pallor of
Hypophosphatasia the face and lips and gastrointestinal symptoms that consists
of nausea, vomiting, loss of appetite, and abdominal colic.
Hypophosphatasia is a rare familial skeletal disease that is Peripheral neuritis, psychologic disorders, and encephali-
characterized by rickets, poor cranial bone formation, cranio- tis have been reported. Oral signs include salivation, coated
stenosis, and the premature loss of the primary teeth, particu- tongue, a peculiar sweetish taste, gingival pigmentation, and
larly the incisors. Patients have a low level of serum alkaline ulceration. Gingival pigmentation is linear (Burtonian line),
phosphatase, and phosphoethanolamine is present in serum steel gray, and associated with local inflammation. Oral signs
and urine. may occur without toxic symptoms.
Teeth are lost with no clinical evidence of gingival inflam-
mation, and they show reduced cementum formation. In pa- Mercury Intoxication
tients with minimal bone abnormalities, the premature loss Mercury intoxication is characterized by headache, insomnia,
of the deciduous teeth may be the only symptom of hypo- cardiovascular symptoms, pronounced salivation (ptyalism),
phosphatasia. In adolescents, this disease resembles localized and a metallic taste. Gingival pigmentation in linear form re-
"juvenile" (aggressive) periodontitis. sults from the deposition of mercuric sulfide. The chemical
also acts as an irritant, which accentuates the preexisting in-
flammation and often leads to notable ulceration of the gin-
Metal Intoxication giva and the adjacent mucosa as well as the destruction of the
The ingestion of metals such as mercury, lead, and bismuth underlying bone. Mercurial pigmentation of the gingiva also
in medicinal compounds and through industrial contact may occurs in areas of local irritation in patients without symp-
result in oral manifestations caused by either intoxication or toms of intoxication.
absorption without evidence of toxicity.
Other Chemicals
Bismuth Intoxication Other chemicals (eg, phosphorus, arsenic, chromium)
Chronic bismuth intoxication is characterized by gastrointes- may cause necrosis of the alveolar bone, with loosening and
tinal disturbances, nausea, vomiting, and jaundice as well exfoliation of the teeth. Inflammation and ulceration of the
as by an ulcerative gingivostomatitis, generally with pig- gingiva are usually associated with the destruction of the
mentation and accompanied by a metallic taste and burn- underlying tissues. Benzene intoxication is accompanied by
ing sensation of the oral mucosa. The tongue may be sore gingival bleeding and ulceration with the destruction of the
and inflamed. Urticaria, different types of exanthematous underlying bone.
SUGGESTED READINGS Ruggiero SL, Dodson TB, Assael LA, et al: American Association of Oral and
Maxillofacial Surgeons position paper on bisphosphonate-related osteone-
Genco RJ, Ho AW, Grossi SG, et al: Relationship of stress, distress and inad-
crosis of the jaws-2009 update, J Oral Maxillojac Surg 67(Suppl 5):2-12,
equate coping behaviors to periodontal disease, J Pe,iodontol 70:711-723,
2009.
1999.
Schmidt AM, Weidman E, Lalla E, et al: Advanced glycation endproducts
Geurs NC, Lewis CE, Jeffcoat MK: Osteoporosis and periodontal disease pro-
(AGEs) induce oxidant stress in the gingiva: a potential mechanism under-
gression, Periodontal 2000 32:105-110, 2003.
lying accelerated periodontal disease associated with diabetes, J Pel'iodontal
Iacopino AM: Periodontitis and diabetes interrelationships: role of inflamma-
Res 31:508-515, 1996.
tion, Ann Periodontol 6:125-137, 2001.
Solomon DH, Mercer E, Woo SB, et al: Defining the epidemiology of
Loe H: Periodontal disease. The sixth complication of diabetes mellitus, Dia-
bisphosphonate-associated osteonecrosis of the jaw: prior work and cur-
betes Care 16:329-334, 1993.
rent challenges, Osteopoms Int 24(1):237-244, 2013.
Mealey BL, Moritz Aj: Hormonal influences: effects of diabetes mellitus and
Wimmer G, Janda M, Wieselmann-Penkner K, et al: Coping with stress: its
endogenous female sex steroid hormones on the periodontium, Pe1iodontol
influence on periodontal disease,] Pel'iodontol 73:1343-1351, 2002.
2000 32 59-81, 2003.
SECTION IV
Section Outline
13 Gingival Inflammation 21 Periodontal Response to External Forces
14 Clinical Features of Gingivitis 22 Chronic Periodontitis and N ecrotizing
15 Gingival Enlargement Ulcerative Periodontitis
16 Acute Gingival Infections 23 Aggressive Periodontitis
17 Desquamative Gingivitis 24 Pathology and Management
18 The Periodontal Pocket of Periodontal Problems in Patients
With Human Immunodeficiency
19 Abscesses of the Periodontium
Virus Infection
25 Impact of Periodontal Infection on
Destruction
Systemic Health
13
Gingival Inflammation
JP Fiorellini • DM Kim • PG Stathopoulou • DG Naik • A Uppoor
Chapter Outline
Stage I Gingival Inflammation: Stage Ill Gingival Inflammation:
The Initial Lesion The Established Lesion
Stage II Gingival Inflammation: Stage IV Gingival Inflammation:
The Early Lesion The Advanced Lesion
Pathogenesis can be defined as the unfolding of a disease pro- Microscopically, some classic features of acute inflamma-
cess, or the sequence of events in the development of a disease tion can be seen in the connective tissue beneath the JUnc-
from its earliest beginnings. The natural history of inflam- tional epithelium. Changes in blood vessel morphologic fea-
matory gingival and periodontal disease is not understood tures (eg, the widening of small capillaries or venules) and the
completely, and important aspects of its pathogenesis remain adherence of neutrophils to vessel walls (margination) occur
obscure. The sequence of events culminating in clinically ap- within 1 week and sometimes as early as 2 days after plaque
parent gingivitis has been separated into the initial, early, and has been allowed to accumulate. Leukocytes-mainly poly-
established stages, and periodontitis has been designated as morphonuclear neutrophils (PMNs)-leave the capillaries by
the advanced stage. In spite of extensive research, we still can- migrating through the walls via diapedesis and emigration.
not distinguish definitively between the normal gingival tissue They can be seen in increased quantities in the connective
and the initial stage of gingivitis. The factors comprising this tissue, the junctional epithelium, and the gingival sulcus. The
transition are not well understood. exudation of fluid from the gingival sulcus and extravascular
Pristine gingiva: normal gingiva that is free from "signifi- proteins are present.
cant" accumulation of inflammatory cells histologically may However, these findings are not accompanied by manifes-
be described as prestine gingiva or a state of superhealth tations of tissue damage that are perceptible at the light micro-
(Fig. 13.1). scopic or ultrastructural level; they do not form an infiltrate,
Clinically healthy gingiva: it looks clinically similar to and their presence is not considered to indicate pathologic
prestine gingiva but histologically features an inflammatory change.
infiltrate with predominantly neutrophils associated with Subtle changes can also be detected in the junctional epi-
junctional epithelium and lymphocytes in the subjacent con- thelium and the perivascular connective tissue at this early
nective tissue. stage. For example, the perivascular connective tissue matrix
Page and Schroeder in 1976 classified progression of gingi- becomes altered, and there is exudation and deposition of fi-
val and periodontal inflammation on the basis of clinical and brin in the affected area. In addition, lymphocytes soon begin
histopathological evidence. The descriptions of the initial and to accumulate. The increase in the migration of leukocytes
early lesion were intended to characterize the histopathol- and their accumulation within the gingival sulcus may be cor-
ogy of clinically healthy gingiva and early stages of gingivi- related with an increase in the flow of gingival fluid into the
tis while the established lesion featured "chronic" gingivitis sulcus.
(Table 13.1) The character and intensity of the host response determine
whether this initial lesion resolves rapidly, with the restoration
Stage I Gingival Inflammation: of the tissue to a normal state; alternatively, it may evolve into
a chronic inflammatory lesion. If the latter occurs, an infiltrate
The Initial Lesion (Fig. 13.2) of macrophages and lymphoid cells appears within a few days.
The first manifestations of gingival inflammation are vascular
changes that consist of dilated capillaries and increased blood Stage II Gingival Inflammation:
flow. These initial inflammatory changes occur in response to The Early Lesion (Fig. 13.3)
the microbial activation of resident leukocytes and the sub-
sequent stimulation of endothelial cells. Clinically, this initial The early lesion evolves from the initial lesion within about
response of the gingiva to bacterial plaque (ie, subclinical gin- 1 week after the beginning of plaque accumulation. Clinically,
givitis) is not apparent. the early lesion may appear as early gingivitis, and it overlaps
151
Microbial colonization
Few neutrophils migrate into

coronal part of junctional
epithelium and gingival
sulcus
(!)
(!)
Oo
Monocytes,
lymphocytes,
and O
neutrophils
in connective
tissue
FIGURE 13.1 Pristine gingiva.

FIGURE 13.2 Healthy gingiva.
with and evolves from the initial lesion with no clear-cut di-
viding line. As time goes on, clinical signs of erythema may
Increased neutrophil
appear, mainly because of the proliferation of capillaries and migration
the increased formation of capillary loops between rete pegs
or ridges. Bleeding on probing may also be evident. Gingival
fluid flow and the numbers of transmigrating leukocytes reach Increased infiltrate
their maximum between 6 and 12 days after the onset of clini-
cal gingivitis.
Microscopic examination of the gingiva reveals leukocyte
infiltration in the connective tissue beneath the junctional i 1· Kl Dilated vessels, vascular
epithelium, which consists mainly of lymphocytes (75%, with proliferation, increased
the majority being T cells) but that also includes some mi- collagen loss, very few
plasma cells
grating neutrophils as well as macrophages, plasma cells, and
mast cells. All of the changes seen in the initial lesion continue
to intensify with the early lesion. The junctional epithelium
becomes densely infiltrated with neutrophils, as does the gin-
gival sulcus, and the junctional epithelium may begin to show
the development of rete pegs or ridges.
The amount of collagen destruction also increases; 70% of
the collagen is destroyed around the cellular infiltrate. The
FIGURE 13.3 Early gingivitis.
main fiber groups that are affected appear to be the circular
and dentogingival fiber assemblies. Alterations in blood ves-
sel morphologic features and vascular bed patterns have also epithelium and cross the basement lamina; they are found in
been described. the epithelium, emerging in the pocket area PMNs are attract-
PMNs that have left the blood vessels in response to ed to bacteria and engulf them during the process of phago-
chemotactic stimuli from plaque components travel to the cytosis. PMNs release their lysosomes in association with the
TABLE 13-1
STAGES OF GINGIVITIS
Junctional
and Sulcular Predominant
Stage Time (Days) Blood Vessels Epithelia Immune Cells Collagen Clinical Findings
I. Initial lesion 2-4 Vascular dilation Infiltration by PMNs Perivascular loss Gingival fluid flow
Vasculitis PMNs
II. Early lesion 4-7 Vascular proliferation Same as stage I Lymphocytes Increased loss Erythema
Rete pegs around infiltrate Bleeding on probing
Atrophic areas
Ill. Established 14-21 Same as stage II, plus Same as stage Plasma cells Continued loss Changes in color, size,
lesion blood stasis II but more texture, and so on
advanced
PMNs, Polymorphonuclear leukocytes (neutrophils).
13 Gingival Inflammation 153
lesion can be described as moderately to severely inflamed

gingiva.
Greatly increased
neutrophil emigration In histologic sections, an intense and chronic inflammatory
reaction is observed. Several detailed cytologic studies have
been performed on chronically inflamed gingiva. A key fea-
ture that differentiates the established lesion is the increased
number of plasma cells, which become the preponderant in-
Marked proliferation of
flammatory cell type. Plasma cells invade the connective tis-
junctional epithelium sue not only immediately below the junctional epithelium but
also deep into the connective tissue, around the blood vessels,
and between the bundles of collagen fibers. The junctional
epithelium reveals widened intercellular spaces that are filled
with granular cellular debris, including lysosomes derived
from disrupted neutrophils, lymphocytes, and monocytes.
Increased plasma The lysosomes contain acid hydrolases that can destroy tissue
cells 10-30% components. The junctional epithelium develops rete pegs or
ridges that protrude into the connective tissue, and the basal
lamina is destroyed in some areas. In the connective tissue,
collagen fibers are destroyed around the infiltrate of intact and
disrupted plasma cells, neutrophils, lymphocytes, monocytes,
and mast cells.
FIGURE 13.4 Established gingivitis. The predominance of plasma cells is thought to be a pri-
mary characteristic of the established lesion. However, several
ingestion of bacteria. Fibroblasts show cytotoxic alterations, studies of human experimental gingivitis have failed to dem-
with a decreased capacity for collagen. onstrate plasma cell predominance in the affected connective
Meanwhile, on the opposite side of molecular events, tissues, including a study of 6 months' duration. Increases in
collagen degradation is related to matrix metalloproteinases the proportions of plasma cells were evident with longstand-
(MMPs). Different MMPs are responsible for extracellular ing gingivitis, but the time for the development of the classic
matrix remodeling within 7 days of inflammation, which "established lesion" may exceed 6 months.
is directly related to MMP-2 and MMP-9 production and An inverse relationship appears to exist between the num-
activation. ber of intact collagen bundles and the number of inflammato-
ry cells. Collagenolytic activity is increased in inflamed gingi-
val tissue by the enzyme collagenase. Collagenase is normally
Stage Ill Gingival Inflammation: present in gingival tissues; it is produced by some oral bacteria
The Established Lesion (Fig. 13.4) and by PMNs.
Over time, the established lesion evolves. It is characterized by Enzyme histochemistry studies have shown that chronical-
a predominance of plasma cells and B lymphocytes, and it is ly inflamed gingivae have elevated levels of acid and alkaline
probably in conjunction with the creation of a small gingival phosphatase, P-glucuronidase, P-glucosidase, P-galactosidase,
pocket lined with a pocket epithelium. The B cells that are esterases, aminopeptidase, and cytochrome oxidase. Neutral
found in the established lesion are predominantly of the im- mucopolysaccharide levels are decreased, presumably as a re-
munoglobulin Gl and G3 subclasses. sult of degradation of the ground substance.
With chronic gingivitis, which occurs 2-3 weeks after Established lesions of two types appear to exist; some re-
the beginning of plaque accumulation, the blood vessels be- main stable and do not progress for months or years, and
come engorged and congested, venous return is impaired, others seem to become more active and to convert to pro-
and the blood flow becomes sluggish (Fig. 13 5) The result gressively destructive lesions. In addition, the established le-
is localized gingival anoxemia, which superimposes a some- sions appear to be reversible in that the sequence of events
what bluish hue on the reddened gingiva. The extravasation that occurs in the tissues as a result of successful periodontal
of erythrocytes into the connective tissue and the breakdown therapy seems to be essentially the reverse of the sequence
of hemoglobin into its component pigments can also deepen of events observed as gingivitis develops. As the flora reverts
the color of the chronically inflamed gingiva. The established from that characteristically associated with destructive lesions
to that associated with periodontal health, the percentage of
plasma cells decreases greatly, and the lymphocyte population
increases proportionately.
Stage IV Gingival Inflammation:

The Advanced Lesion
The extension of the lesion into alveolar bone characterizes
the fourth stage, which is known as the advanced lesion or
phase of periodontal breakdown. Microscopically, there will be
continuous loss of collagen subjacent to the pocket epithe-
lium with fibrosis at more distant sites. The junctional epi-
FIGURE 13.5 Marginal supragingival plaque and gingivitis. thelium migrates apically from the cementoenamel junction.
The pocket epithelium is more permeable to the passage of gingivitis represents a risk factor for periodontal attachment
substances into and out of the underlying connective tissues loss and for tooth loss. However, whether periodontitis can
and temporarily ulcerated in many places. Alveolar bone loss occur without a precursor of gingivitis is not known at this
occurs. There are widespread manifestations of inflammatory time.
and immunopathologic tissue damage. At the advanced stage,
the presence of plasma cells dominates the connective tissue, REFERENCES
and neutrophils continue dominating the junctional epithe-
lium.
Patients with experimental gingivitis had significantly more
plaque accumulation, higher interleukin-If levels, and lower
interleukin-8 concentrations at 28 days. SUGGESTED READINGS
Gingivitis will progress to periodontitis only in individuals who Deinzer R, Weik U, Kolb-Bachofen V, et al: Comparison of experimental gin-
givitis with persistent gingivitis: differences in clinical parameters and cyto-
are susceptible. Patients who had sites with consistent bleeding kine concentrations,] Periodontal Res 2(4):318-324, 2007.
(gingival index = 2) had 70% more attachment loss as com- Lang NP, Schatzle MA, Loe H: Gingivitis as a risk factor in periodontal disease,
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13 Gingival Inflammation 154.el
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14
Clinical Features of Gingivitis
Chapter Outline
Course and Duration Clinical Findings
Description
Experimental gingivitis studies provided the first empiric ev- Recurrent gingivitis reappears after having been eliminated
idence that the accumulation of microbial biofilm on clean by treatment or disappearing spontaneously.
tooth surfaces results in the development of an inflammatory
process around gingival tissue. Research has also shown that
the local inflammation will persist as long as the microbial Description
biofilm is present adjacent to the gingival tissues and that the Localized gingivitis is confined to the gingiva of a single tooth
inflammation may resolve subsequently to a meticulous re- or group of teeth, whereas generalized gingivitis involves the
moval of the biofilm. entire mouth.
A similar or higher prevalence of gingivitis is reported for Marginal gingivitis involves the gingival margin and may in-
children and adolescents in other parts of the world. Whereas clude a portion of the contiguous-attached gingiva. Papillary
plaque remains the primary etiological factor that causes gin- gingivitis involves the interdental papillae and it often extends
givitis, other factors may affect the development of periodon- into the adjacent portion of the gingival margin. Papillae are
tal diseases. Recent experimental gingivitis studies suggest an involved more frequently than the gingival margin, and the
important role of the host response in the development and earliest signs of gingivitis often occur in the papillae. Diffuse
degree of gingival inflammation. gingivitis affects the gingival margin, the attached gingiva, and
In general, the clinical signs of inflammation in the gin- the interdental papillae. Gingival disease in individual cases is
gival tissue reflect the classic signs of inflammation-rubor described by combining the preceding terms as follows:
(redness), tumor (swelling), calor (warmth), and dolor (pain).
This is characterized by the presence of any of the following • Localized marginal gingivitis is confined to one or more areas
clinical signs-redness and sponginess of the gingival tissue, of the marginal gingiva (Fig. 14 2).
bleeding on provocation, changes in contour, and the pres- • Localized diffuse gingivitis extends from the margin to the
ence of calculus or plaque with no radiographic evidence mucobuccal fold in a limited area (Fig. 14 3).
of crestal bone loss. The histologic examination of inflamed • Localized papillary gingivitis is confined to one or more inter-
gingival tissue reveals ulcerated epithelium. The presence of dental spaces in a limited area.
inflammatory mediators negatively affects its epithelial func- • Generalized marginal gingivitis involves the gingival margins
tion as a protective barrier. Repair of this ulcerated epithelium in relation to all the teeth. The interdental papillae are usu-
depends on the proliferative or regenerative activity of the epi- ally affected (Fig. 144).
thelial cells. Removal of the etiologic agents that trigger the • Generalized diffuse gingivitis involves the entire gingiva.
gingival breakdown is essential. The alveolar mucosa and the attached gingiva are affect-
ed, so the mucogingival junction is sometimes obliterated.
(Fig. 14.5). Systemic conditions can be involved in the
Course and Duration cause of generalized-diffuse gingivitis and should be evalu-
Gingivitis can occur with a sudden onset for a short duration ated if they are suspected as an etiologic cofactor.
and can be painful. A less severe phase of this condition can
also occur. Clinical Findings
Chronic gingivitis is slow in onset and of long duration. It
is painless, unless it is complicated by acute or subacute ex- A systematic approach is required for the evaluation of the
acerbations, and it is the type that is most often encountered clinical features of gingivitis. The clinician should focus on
(Fig. 14.1). Chronic gingivitis is a fluctuating disease in which subtle tissue alterations because these may be of diagnostic
inflammation persists or resolves and normal areas become significance. A systematic clinical approach requires an order-
inflamed. ly examination of the gingiva for color, contour, consistency,
155
FIGURE 14.4 Generalized marginal gingivitis in the upper jaw with

areas of diffuse gingivitis.
FIGURE 14.1 Chronic gingivitis. The marginal and interdental gin-
givae are smooth, edematous, and discolored. Isolated areas of acute
response are seen.
FIGURE 14.5 Generalized diffuse gingivitis involves the marginal,

papillary, and attached gingivae.
FIGURE 14.2 Localized marginal gingivitis in the mandibular ante-

been shown that bleeding on probing appears earlier than
rior region. a change in color or other visual signs of inflammation. In
addition, the use of bleeding, rather than color changes to
diagnose early gingival inflammation, is advantageous as
bleeding is a more objective sign that requires less subjective
estimation by the examiner. Probing pocket-depth measure-
ments by themselves are of limited value for the assessment
of the extent and severity of gingivitis. For example, gingival
recession may result in a reduction of the probing depth and
thus cause an inaccurate assessment of the periodontal sta-
tus. Therefore, bleeding on probing is widely used by clini-
cians and epidemiologists to measure disease prevalence and
progression, outcomes of treatment, and to motivate patients
to perform necessary home care. Several gingival indices that
are based on bleeding have been developed. In general, gin-
FIGURE 14.3 Localized, diffuse, intensely red area on the facial sur- gival bleeding on probing indicates an inflammatory lesion
face of maxillary right lateral incisor and dark-pink marginal changes both in the epithelium and in the connective tissue that ex-
in the remaining anterior teeth.
hibits specific histologic differences as compared to healthy
gingiva. Even though gingival bleeding on probing may not
be a good diagnostic indicator for clinical attachment loss,
position, and ease and severity of bleeding and pain. This sec- its absence is an excellent negative predictor of future at-
tion discusses these clinical characteristics and the microscop- tachment loss. Therefore, the absence of gingival bleeding
ic changes that are responsible for each. on probing is desirable and implies a low risk of future clini-
cal attachment loss. Longitudinal findings revealed that sites
Gingival Bleeding on Probing with consistent bleeding (gingival index = 2) had 70% more
attachment loss than sites that were noninflamed over a 26-
The two earliest signs of gingival inflammation that precede year period in 565 males. Thus, persistent gingivitis can be
established gingivitis are as follows: considered as a risk factor for periodontal attachment loss
that may lead to tooth loss.
1. increased gingival crevicular fluid production rate.
Interestingly, numerous studies have shown that current
2. bleeding from the gingival sulcus on gentle probing
(Fig. 14.6) cigarette smoking suppressed the gingival inflammatory re-
sponse and smoking was found to exert a strong, chronic,
Gingival bleeding varies with regard to severity, duration, dose-dependent suppressive effect on gingival bleeding with
and ease of provocation. Bleeding on probing is easily de- probing in the Third National Health and Nutrition Examina-
tected clinically and therefore is of value for the early dition Survey. In addition, recent research reveals an increase in
agnosis and prevention of more advanced gingivitis. It has gingival bleeding with probing in patients who quit smoking.
14 Clinical Features of Gingivitis 157
FIGURE 14.6 Bleeding on probing. A, Mild edematous gingivitis; a probe has been introduced to the bottom of the gingival sulcus. B, Bleeding
appears after a few seconds.
Thus, people who are committed to a smoking-cessation pro-

gram should be informed about the possibility of an increase
in gingival bleeding associated with smoking cessation.
Gingival Bleeding Caused by Local Factors

Factors that contribute to plaque retention and that may lead
to gingivitis include anatomic and developmental tooth varia-
tions, caries, frenum pull, iatrogenic factors, malpositioned
teeth, mouth breathing, overhangs, partial dentures, lack
of attached gingiva, and recession. In addition, orthodontic
treatment and fixed retainers were associated with increased
plaque retention and increased bleeding on probing.
Chronic and Recurrent Bleeding
The most common cause of abnormal gingival bleeding on
probing is chronic inflammation. The bleeding is chronic or
recurrent, and it is provoked by mechanical trauma (eg, from
toothbrushing, toothpicks, or food impaction) or by biting
into solid foods (eg, apples).
In gingival inflammation, histopathologic alterations that
result in abnormal gingival bleeding include dilation and
engorgement of the capillaries and thinning or ulceration of
the sulcular epithelium (Fig. 14 7). Since the capillaries are
engorged and closer to the surface and because the thinned,
degenerated epithelium is less protective; and stimuli that are FIGURE 14.7 Microscopic view of the interdental space in a human
normally innocuous cause rupture of the capillaries and gin- autopsy specimen. Note the inflammatory infiltrate and the thinned
epithelium in the area adjacent to the tooth, as well as, the collagenous
gival bleeding. tissue in the outer half of the section.
Sites that bleed on probing have a greater area of inflamed
connective tissue (ie, cell-rich, collagen-poor tissue) than sites
that do not bleed. In most cases, the cellular infiltrate of sites can cause gingival bleeding even in the absence of gingival
that bleed on probing is predominantly lymphocytic, which is disease. Gingival burns from hot foods or chemicals increase
a characteristic of stage II (early) gingivitis. the ease of gingival bleeding.
The severity of bleeding and the ease of its provocation depend Spontaneous bleeding or bleeding on slight provocation
on the intensity of the inflammation. After the vessels are dam- can occur with acute necrotizing ulcerative gingivitis. With
aged and ruptured, interrelated mechanisms induce hemosta- this condition, engorged blood vessels in the inflamed con-
sis. The vessel walls contract, blood flow diminishes, blood nective tissue are exposed via the ulceration of the necrotic
platelets adhere to the edges of the tissue, and a fibrous clot surface epithelium.
is formed that contracts and results in approximation of the
edges of the injured area. Bleeding recurs when the area is Gingival Bleeding Associated with
irritated. Systemic Changes
In cases of moderate or advanced periodontitis, the pres-
ence of bleeding on probing is considered as a sign of active With some systemic disorders, gingival hemorrhage occurs
tissue destruction. spontaneously or after irritation and it is excessive and dif-
ficult to control. These hemorrhagic diseases represent a wide
Acute Bleeding variety of conditions that vary with regard to etiologic factors
Acute episodes of gingival bleeding are caused by injury, and and clinical manifestations. Such conditions have the com-
they can occur spontaneously in patients with acute gingival mon feature of a hemostatic mechanism failure and result in
disease. Laceration of the gingiva by toothbrush bristles dur- abnormal bleeding in the skin, the internal organs, and other
ing aggressive toothbrushing or by sharp pieces of hard food tissues, including the oral mucosa.
TABLE 14.1 Color Changes with Gingivitis

Change in color is an important clinical sign of gingival disease.
CAUSES OF GINGIVAL BLEEDING The normal gingival color is "coral pink," and it is produced
• Gingivitis by the tissue's vascularity and modified by the overlying epi-
• Poor oral hygiene thelial layers. For this reason, the gingiva becomes red when
• Inadequate plaque removal vascularization increases or when the degree of epithelial ke-
• Calculus accumulation ratinization is reduces or disappears. The color becomes pale
• Periodonttis when vascularization is reduced (in association with fibrosis
• Anticoagulants such as coumarin and heparin of the corium) or when epithelial keratinization increases.
• Self inflicated trauma such as improper flossing and toothbrushing
Thus, chronic inflammation intensifies the red or bluish-red
• Bleeding and coagulation disorders
• Vitamin C deficiency
color as a result of vascular proliferation and reduced kerati-
• Vitamin K deficiency nization. In addition, venous stasis will contribute a bluish
• Hormonal changes during pregnancy hue. The gingival color changes with increasing chronicity of
• Chemical irritants, such as aspirin the inflammatory process. The changes start in the interdental
• Leukemia papillae and the gingival margin and then spread to the at-
• Placement of new denture leading to denture sores/irritation tached gingiva.
Proper diagnosis and treatment require an understanding
of the tissue changes that alter the color of the gingiva at the
clinical level.
The hemorrhagic tendency may be due to failure of one Color changes in acute gingival inflammation differ with
or more of the hemostatic mechanism. Hemorrhagic disregard to both nature and distribution from those in patients
orders in which abnormal gingival bleeding is encountered with chronic gingivitis. The color changes may be marginal,
include vascular abnormalities [vitamin C deficiency, allergy diffuse, or patchlike, depending on the underlying acute con-
(eg, Henoch-Schonlein purpura)], platelet disorders (throm- dition. With acute necrotizing ulcerative gingivitis, the in-
bocytopenic purpura), hypoprothrombinemia (vitamin K de- volvement is marginal; with herpetic gingivostomatitis, it is
ficiency), other coagulation defects (hemophilia, leukemia, diffuse; and with acute reactions to chemical irritation, it is
and Christmas disease), deficient platelet thromboplastic fac- patchlike or diffuse.
tor as a result of uremia, multiple myeloma, and postrubella Color changes vary with the intensity of the inflammation.
purpura. The effects of hormonal replacement therapy, oral Initially, there is an increase in erythema. If the condition does
contraceptives, pregnancy, and the menstrual cycle are also not worsen, this is the only color change until the gingiva re-
reported to affect gingival bleeding. verts to normal. With severe acute inflammation, the red color
In addition, changes in androgenic hormones have long gradually becomes a dull, whitish-gray The gray discoloration
been established as significant modifying factors in gingivi- produced by tissue necrosis is demarcated from the adjacent
tis, especially among adolescents. Several reports have shown gingiva by a thin, sharply defined erythematous zone.
notable effects of fluctuating estrogen and progesterone lev-
els on the periodontium, starting as early as puberty Among
pathologic endocrine changes, diabetes is an endocrine condi- Metallic Pigmentation
tion with a well-characterized effect on gingivitis. In diabetes, Heavy metals (ie, bismuth, arsenic, mercury, lead, and silver)
marked inflammation affects both the epithelial and connec- that are absorbed systemically as a result of therapeutic use
tive tissues, which leads to the degeneration of the dermal or occupational or household environments may discolor the
papilla, an increase in the number of inflammatory cells, the gingiva and other areas of the oral mucosa. These changes are
destruction of reticulin fibers, and an accumulation of dense rare, but they should still be ruled out in suspected cases.
collagen fibers that causes fibrosis. Metals typically produce a black or bluish line in the gin-
Several medications have also been found to have adverse giva that follows the contour of the margin (Fig. 14.8). The
effects on the gingiva. For example, anticonvulsants, antihy- pigmentation may also appear as isolated black blotches in-
pertensive calcium-channel blockers, and immunosuppres- volving the interdental marginal and attached gingiva. This
sant drugs are known to cause gingival enlargement which differs from the tattooing produced by the accidental embed-
secondarily can cause gingival bleeding. The American Heart ding of amalgam or other metal fragments (Fig. 14. 9).
Association has recommended over-the-counter aspirin as a Gingival pigmentation from systemically absorbed metals
therapeutic agent for cardiovascular disease. Aspirin is of- results from the perivascular precipitation of metallic sulfides
ten prescribed for rheumatoid arthritis, osteoarthritis, rheu-
matic fever, and other inflammatory joint diseases. Thus, it
is important to consider aspirin's effect on bleeding during
a routine dental examination to avoid false-positive read-
ings, which could result in an inaccurate patient diagnosis
(Table 14 1)
Color Changes in the Gingiva

The color of the gingiva is determined by several factors, in-
cluding the number and size of blood vessels, the epithelial
thickness, the quantity of keratinization, and the pigments FIGURE 14.8 Bismuth gingivitis. Note the linear black discoloration of
within the epithelium. the gingiva in a patient who is receiving bismuth therapy.
oral mucosa. Localized bluish-black areas of pigment are often

caused by amalgam implanted in the mucosa (Fig. 14.9).
During recent years, the need for aesthetics in den-
tistry has increased, with a growing demand for a pleas-
ing smile. This has made many individuals more aware of
their gingival pigmentation, which may be apparent dur-
ing smiling and speech. Traditionally, gingival depigmen-
tation has been carried out with the use of nonsurgical
and surgical procedures, including chemical, cryosurgical,
and electrosurgical techniques (electrocautery, laser, and
scalpel). However, those techniques were met with skep-
FIGURE 14.9 Discoloration of the gingiva caused by embedded
ticism because of their varying degrees of success. More
metal particles (amalgam). recently, lasers have been used to ablate cells that produce
the melanin pigment; a nonspecific laser beam destroys
the epithelial cells, including those at the basal layer. In
in the subepithelial connective tissue. Gingival pigmentation
addition, selective ablation with the use of a laser beam
is not a result of systemic toxicity. It occurs only in areas of
with a wavelength that is specifically absorbed in melanin
inflammation in which the increased permeability of irritated
effectively destroys the pigmented cells without damaging
blood vessels permits the see page of the metal into the sur-
the nonpigmented cells. In both cases, radiation energy is
rounding tissue. In addition to inflamed gingiva, mucosa! areas
transformed into ablation energy, thereby resulting in cel-
that are irritated by biting or abnormal chewing habits (eg, in-
lular rupture and vaporization with minimal heating of the
ner surface of lips, cheek at level of occlusal line, and lateral
surrounding tissue.
border of tongue) are common sites of pigmentation. Pigmen-
tation can be eliminated by treating the inflammatory changes
without necessarily discontinuing the metal-containing medi- Changes in the Consistency of the Gingiva
cation.
Both chronic and acute inflammations produce changes in the
normal firm and resilient consistency of the gingiva. As previ-
Color Changes Associated with Systemic ously noted, in patients with chronic gingivitis, both destruc-
tive (edematous) and reparative (fibrotic) changes coexist; and
Factors
the consistency of the gingiva is determined by their relative
Many systemic diseases may cause color changes in the oral predominance (Figs. 14.10 and 1411) Table 14.2 summa-
mucosa, including the gingiva. In general, these abnormal rizes the clinical alterations in the consistency of the gingiva
pigmentations are nonspecific, and they should stimulate and the microscopic changes that produce them.
further diagnostic efforts or referral to the appropriate spe-
cialist.
Endogenous oral pigmentations can be caused by melanin,
bilirubin, or iron. Melanin oral pigmentations can be normal
physiologic pigmentations and they are often found in highly
pigmented ethnic groups. Diseases that increase melanin pig-
mentation include the following:
• Addison disease is caused by adrenal dysfunction, and it
produces isolated patches of discoloration that vary from
bluish-black to brown.
• Peutz-Jeghers syndrome produces intestinal polyposis and FIGURE 14.10 Chronic gingivitis. Swelling, loss of stippling, and
melanin pigmentation in the oral mucosa and the lips. discoloration occur when inflammatory exudate and edema are the
• Albright syndrome (polyostotic fibrous dysplasia) and van Reck- predominant microscopic changes. The gingiva is soft and friable and
bleeds easily.
linghausen disease (neurofibromatosis) produce areas of oral
melanin pigmentation.
The skin and the mucous membranes can also be stained
by bile pigments. Jaundice is best detected via the examina-
tion of the sclera, but the oral mucosa may also acquire a yel-
lowish color. The deposition of iron in hemochromatosis may
produce a blue-gray pigmentation of the oral mucosa. Sev-
eral endocrine and metabolic disturbances, including diabetes
and pregnancy, may result in color changes. Blood dyscrasias,
such as anemia, polycythemia, and leukemia, may also induce
color changes.
Exogenous factors that are capable of producing color
changes in the gingiva include atmospheric irritants, such as
coal and metal dust, and coloring agents in food or lozenges.
Tobacco causes hyperkeratosis of the gingiva, and it may also FIGURE 14.11 Chronic gingivitis. Firm gingiva is produced when fi-
induce a significant increase in melanin pigmentation of the brosis predominates in the inflammatory process.
TABLE 14.2
CLINICAL AND HISTOPATHOLOGIC CHANGES IN GINGIVAL CONSISTENCY

Clinical Changes Underlying Microscopic Features
Chronic gingivitis
1. Soggy puffiness that pits on pressure 1. Infiltration by fluid and cells of inflammatory exudate
2. Marked softness and friability, with ready 2. Degeneration of connective tissue and epithelium associated with injurious substances that
fragmentation on exploration with probe provoke the inflammation and the inflammatory exudate; change in the connective tissue-epi-
and pinpoint surface areas of redness and thelium relationship, with inflamed, engorged connective tissue expanding to within a few epi-
desquamation thelial cells of the surface; thinning of epithelium and degeneration associated with edema and
3. Firm, leathery consistency leukocyte invasion, separated by areas in which rete pegs are elongated to connective tissue
3. Fibrosis and epithelial proliferation associated with long-standing chronic inflammation
Acute forms of gingivitis
1. Diffuse puffiness and softening 1. Diffuse edema of acute inflammatory origin; fatty infiltration in xanthomatosis
2. Sloughing with grayish, flake like par- 2. Necrosis with formation of pseudomembrane composed of bacteria, polymorphonuclear leu-
ticles of debris adhering to eroded surface kocytes, and degenerated epithelial cells in fibrinous meshwork
3. Vesicle formation 3. lntercellular and intracellular edema with degeneration of nucleus and cytoplasm and rupture
of cell wall
Calcified Masses in the Gingiva

Calcified microscopic masses may be found in the gingiva.
These can occur alone or in groups, and they vary with re-
gard to size, location, shape, and structure. Such masses may
be calcified material that has been removed from the tooth
and traumatically displaced into the gingiva during scaling,
root remnants, cementum fragments, or cementicles. Chronic
inflammation and fibrosis, an occasional foreign body, and gi-
ant cell activity occur in relation to these masses. They are
sometimes enclosed in an osteoidlike matrix. Crystalline for-
eign bodies have also been described in the gingiva, but their
origin has not been determined.
Toothbrushing
Toothbrushing has various effects on the consistency of the FIGURE 14.12 Stippling seen on attached gingiva.
gingiva, such as promoting keratinization of the oral epithe-
lium, enhancing capillary gingival circulation, and thickening on whether the dominant changes are exudative or fibrotic.
alveolar bone. In animal studies, mechanical stimulation by Smooth surface texture is also produced by epithelial atrophy
tooth brushing was found to increase the proliferative activ- in atrophic gingivitis, and peeling of the surface occurs with
ity of the junctional basal cells in dog gingiva by 2.5 times as chronic desquamative gingivitis. Hyperkeratosis results in a
compared with the use of a scaler. These findings may indi- leathery texture and drug-induced gingival overgrowth pro-
cate that tooth brushing causes an increased turnover rate and duces a nodular surface.
desquamation of the junctional epithelial surfaces. This pro-
cess may repair small breaks in the junctional epithelium and
Changes in the Position of the Gingiva
prevent direct access to the underlying tissue by periodontal
pathogens. Traumatic Lesions
One of the unique features of the most recent gingival disease
Changes in the Surface Texture of the classification is the recognition of nonplaque-induced trau-
Gingiva matic gingival lesions as distinct gingival conditions. Traumat-
ic lesions-whether they are chemical, physical, or thermal-
The surface of normal gingiva usually exhibits numerous small are among the most common lesions in the mouth. Sources of
depressions and elevations that give the tissue an orange-peel chemical injuries include aspirin, hydrogen peroxide, silver
appearance referred as stippling. Stippling is restricted to the nitrate, phenol, and endodontic materials. Physical injuries
attached gingiva and predominantly localized to the subpapil- can include lip, oral, and tongue piercings, which can result in
lary area; but it extends to a variable degree into the interden- gingival recession. Thermal injuries can result from hot drinks
tal papilla (Fig. 14 12) Although the biologic significance of and foods. In acute cases, the appearance of slough (necrotiz-
gingival stippling is not known, some investigators conclude ing epithelium), erosion, ulceration, and the accompanying
that the loss of stippling is an early sign of gingivitis. How- erythema are common features. In chronic cases, permanent
ever, clinicians must take into consideration that its pattern gingival defects are usually present in the form of gingival re-
and extent vary in different mouth areas, among patients, and cession. Typically, the localized nature of the lesions and the
with age. lack of symptoms readily eliminate them from the differential
In patients with chronic inflammation, the gingival surface diagnosis of systemic conditions that may be present with ero-
is either smooth and shiny or firm and nodular, depending sive or ulcerative oral lesions.
Recession Position of gingiva
- - - - - Apparent
FIGURE 14.14 Different degrees of recession. Recession is slight

in mandibular right lateral incisor and second premolar and marked
in mandibular right canine and first premolar. The change in gingival
contour and the recession as seen in mandibular right first premolar is
referred to as Stillman's cleft.
FIGURE 14.13 Diagram of apparent and actual positions of the gin-

giva and visible and hidden recession. has been associated with gingival inflammation and recession.
Excessive incisal overlap may result in a traumatic injury to the
gingiva. Orthodontic movement in a labial direction in mon-
Gingival Recession keys has been shown to result in the loss of marginal bone and
Gingival recession is a common finding. The prevalence, ex- connective tissue attachment, as well as in gingival recession.
tent, and severity of gingival recession increase with age, and Standard oral hygiene procedures, whether they involve
this condition is more prevalent among males. toothbrushing or flossing, may lead to frequent transient and
minimal gingival injury Although toothbrushing is important
Positions of the Gingiva. By clinical definition, recession is for gingival health, faulty toothbrushing technique or brush-
the exposure of the root surface by an apical shift in the posi- ing with hard bristles may cause significant injury This type
tion of the gingiva. To understand recession, it is important to of injury may present as lacerations, abrasions, keratosis, and
distinguish between the actual and apparent positions of the recession, with the facial marginal gingiva being the most af-
gingiva. The actual position is the level of the coronal end of the fected. Thus, in these cases, recession tends to be more fre-
epithelial attachment on the tooth, whereas the apparent posi- quent and severe in patients with clinically healthy gingiva,
tion is the level of the crest of the gingival margin (Fig. 14.13). little bacterial plaque, and good oral hygiene.
The severity of recession is determined by the actual position of the Susceptibility to recession is also influenced by the posi-
gingiva and not by its apparent position. For example, in peri- tion of teeth in the arch, the root-bone angle, and the me-
odontal disease, the inflamed pocket wall covers part of the siodistal curvature of the tooth surface. On rotated, tilted, or
denuded root; thus some of the recession is hidden, and some facially displaced teeth, the bony plate is thinned or reduced
may be visible. The total amount of recession is the sum of in height. Pressure from mastication or moderate toothbrush-
the two. ing damages the unsupported gingiva and produces recession.
Recession refers to the location of the gingiva rather than to The effect of the angle of the root in the bone with recession
its condition. Receded gingiva can be inflamed, but it may be is often observed in the maxillary molar area. If the lingual
normal except for its position (Fig. 14.14). Recession may be inclination of the palatal root is prominent or if the buccal
localized to one tooth or to a group of teeth or it may be gen- roots flare outward, the bone in the cervical area is thinned or
eralized throughout the mouth. shortened, then recession results from repeated trauma of the
Gingival recession increases with age; the incidence var- thin marginal gingiva.
ies from 8% in children to 100% after the age of 50 years. The health of the gingival tissue also depends on properly
This has led some investigators to assume that recession may designed and placed restorative materials. Pressure from a
be a physiologic process related to aging. However, no con- poorly designed partial denture, such as an ill-fitting denture
vincing evidence has been presented for a physiologic shift clasp, can cause gingival trauma and recession. Overhanging
of the gingival attachment. The gradual apical shift is most dental restorations have long been viewed as a contributing
likely the result of the cumulative effect of minor pathologic factor to gingivitis because of plaque retention. In addition,
involvement and repeated minor direct trauma to the gingiva. there is general agreement that placing restorative margins
In some populations without access to dental care, recession within the biologic width frequently leads to gingival inflam-
however, may be the result of increasing periodontal disease. mation, clinical attachment loss, and, eventually, bone loss.
The following etiologic factors have been implicated in Clinically, the violation of biologic width typically manifests
gingival recession: faulty toothbrushing technique (gingival as gingival inflammation, deepened periodontal pockets, and
abrasion), tooth malposition, friction from the soft tissues gingival recession.
(gingival ablation), gingival inflammation, abnormal frenum A relationship may exist between smoking and gingival re-
attachment, and iatrogenic dentistry Trauma from occlusion cession. The multifactorial mechanisms may include reduced
has been suggested in the past, but its mechanism of action gingival blood flow and altered immune response but they are
has never been demonstrated. For example, a deep overbite not as yet conclusive.
Clinical Significance. Several aspects of gingival recession was occlusal adjustment. However, this association was never
make it clinically significant. Exposed root surfaces are sus- proved, and these indentations merely represent peculiar in-
ceptible to caries. Abrasion or erosion of the cementum ex- flammatory changes of the marginal gingiva.
posed by recession leaves an underlying dentinal surface that
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15
Gingival Enlargement
FA Carranza • EL Hogan • DG Naik • A Uppoor
Chapter Outline
Inflammatory Enlargement Enlargements Associated with Systemic
Drug-Induced Gingival Enlargement Diseases or Conditions
Idiopathic Gingival Enlargement Neoplastic Enlargement (Gingival Tumors)
False Enlargement
An increase in size of the gingiva is a common feature of gingi- • Marginal: Confined to the marginal gingiva
val disease. The accepted current terms for this condition are • Papillary: Confined to the interdental papilla
gingival enlargement and gingival overgrowth. These are strictly • Diffuse: Involving the marginal and attached gingivae and
clinical descriptive terms and they avoid the erroneous patho- papillae
logic connotations of terms used in the past, such as hypertro- • Discrete: An isolated sessile or a pedunculated, tumorlike
phic gingivitis and gingival hyperplasia. enlargement
The many types of gingival enlargement can be classified ac-
The degree of gingival enlargement can be scored as follows:
cording to etiologic factors and pathologic changes as follows:
1. Inflammatory enlargement • Grade 0: No signs of gingival enlargement
• Grade I: Enlargement confined to interdental papilla
a. chronic
• Grade II: Enlargement involves papilla and marginal gingiva
b. acute
• Grade III: Enlargement covers three quarters or more of the
2. Drug-induced enlargement
crown
a. general information
b. anticonvulsants
c. immunosuppressants Inflammatory Enlargement
d. calcium-channel blockers
Gingival enlargement may result from chronic or acute in-
3. Enlargements associated with systemic diseases or condi-
flammatory changes although chronic changes are much more
tions
common. In addition, inflammatory enlargements are usually
a. Conditioned enlargement
a secondary complication of any of the other types of enlarge-
1) pregnancy
ment, thereby creating a combined gingival enlargement. In
2) puberty
these cases, it is important to understand the double etiology
3) vitamin C deficiency
and to treat both causes adequately
4) plasma cell gingivitis
5) nonspecific conditioned enlargement (pyogenic
granuloma) Chronic Inflammatory Enlargement
b. Systemic diseases that cause gingival enlargement
Clinical Features
1) leukemia
2) granulomatous diseases (eg, Wegener granulomato- Chronic inflammatory gingival enlargement originates as a
sis and sarcoidosis) slight ballooning of the interdental papilla and marginal gin-
4. Neoplastic enlargement (gingival tumors) giva. In the early stages, it produces a life preserver-shaped
a. benign tumors bulge around the involved teeth. This bulge can increase in
b. malignant tumors size until it covers part of the crowns. The enlargement may
5. False enlargement be localized or generalized; it progresses slowly and pain-
lessly unless it is complicated by acute infection or trauma
With the use of the criteria of location and distribution, (Figs. 15.1 and 15 2)
gingival enlargement is designated as follows: Occasionally, chronic inflammatory gingival enlargement
• Localized: Limited to the gingiva adjacent to a single tooth occurs as a discrete sessile or pedunculated mass that resem-
or group of teeth bles a tumor. It may be interproximal or on the marginal or
• Generalized: Involving the gingiva throughout the mouth attached gingiva. The lesions are slow-growing masses and
163
.,
FIGURE 15.1 Chronic inflammatory gingival enlargement localized

to the anterior region.
FIGURE 15.3 Survey section of chronic inflammatory gingival

enlargement showing the inflamed connective tissue core and strands
of proliferating epithelium.
FIGURE 15.2 Chronic inflammatory gingival enlargement.
are usually painless. They may undergo a spontaneous reduc-

tion in size that is followed by exacerbation and continued
enlargement. Painful ulceration sometimes occurs in the fold FIGURE 15.4 Gingival enlargement in a mouth breather. Note the
between the mass and the adjacent gingiva. lesion that is sharply circumscribed to the anterior marginal and papil-
lary areas.
Histopathology
Chronic inflammatory gingival enlargements show the exu-
dative and proliferative features of chronic inflammation Acute Inflammatory Enlargement
(Fig. 15.3) Lesions that are clinically deep red or bluish-red Gingival Abscess
are soft and friable with a smooth, shiny surface, and they Periodontal Abscess
bleed easily. They also have a preponderance of inflammatory
cells and fluid, with vascular engorgement, new capillary for- Please find detailed description in Chapter 19.
mation, and associated degenerative changes. Lesions that are
relatively firm, resilient, and pink have a greater fibrotic com- Drug-Induced Gingival Enlargement
ponent with an abundance of fibroblasts and collagen fibers.
Gingival enlargement is a well-known consequence of the ad-
Etiology ministration of some anticonvulsants, immunosuppressants,
Chronic inflammatory gingival enlargement is caused by pro- and calcium-channel blockers. The condition may create
longed exposure to dental plaque. Factors that favor plaque speech, mastication, tooth eruption, and aesthetic problems.
accumulation and retention include poor oral hygiene, irrita- Clinical and microscopic features of the enlargements
tion by anatomic abnormalities, and improper restorative and caused by the different drugs are similar. These are presented
orthodontic appliances. first, followed by a description of the particular features of
each drug.
Gingival Changes Associated with Mouth Breathing
Gingivitis and gingival enlargement are often seen in patients General Information
who are mouth breathers. The gingiva appears red and edem-
atous, with a diffuse surface shininess of the exposed area. The Clinical Features
maxillary anterior region is the common site of such involve- The growth starts as a painless, beadlike enlargement of the
ment. In many cases, the altered gingiva is clearly demarcat- interdental papilla that then extends to the facial and lingual
ed from the adjacent unexposed normal gingiva (Fig. 15.4). gingival margins (Fig. 15.5). As the condition progresses, the
The exact manner in which mouth breathing affects gingival marginal and papillary enlargements unite, and they may devel-
changes has not been demonstrated. Its harmful effect is gen- op into a massive tissue fold that covers a considerable portion
erally attributed to irritation from surface dehydration. How- of the crowns; this may interfere with occlusion (Fig. 15.6).
ever, comparable changes could not be produced by air drying When uncomplicated by inflammation, the lesion is mul-
the gingiva of experimental animals. berry-shaped, firm, pale-pink, and resilient, with a minutely
15 Gingival Enlargement 165
FIGURE 15.5 Gingival enlargement associated with phenytoin therapy. A, Facial view. Note the prominent papillary lesions and the firm, nodular
surface. B, Occlusal view of the upper jaw.
in areas from which teeth have been extracted. Hyperplasia

of the mucosa in edentulous mouths has been reported but
is rare.
Drug-induced enlargement may occur in mouths with little or
no plaque and it may be absent in mouths with abundant depos-
its. However, some investigators believe that inflammation is a
prerequisite for development of the enlargement, which there-
fore could be prevented by plaque removal and fastidious oral
hygiene. Oral hygiene by means of toothbrushing or the use
of a chlorhexidine toothpaste reduces the inflammation but
does not lessen or prevent the overgrowth. Hassell et al have
hypothesized that, in noninflamed gingiva, fibroblasts are less
active or even quiescent and do not respond to circulating
FIGURE 15.6 Phenytoin gingival enlargement in a 5-year-old child
phenytoin, whereas fibroblasts within inflamed tissue are in
covering most of the clinical crowns of the teeth.
an active state as a result of the inflammatory mediators and
the endogenous growth factors that are present.
A genetic predisposition is a suspected factor for determin-
ing whether a person treated with phenytoin will develop gin-
gival enlargement.
The enlargement is chronic and it slowly increases in size.
Even if it is surgically removed, it recurs. Spontaneous disap-
pearance occurs within a few months after the discontinuation
of the drug. See Chapter 46 for more information about the
treatment of gingival enlargements, including the substitution
of drugs that do not induce gingival overgrowth.
Histopathology
Drug-induced gingival enlargement consists of a pronounced
FIGURE 15.7 Combined gingival enlargement resulting from the hyperplasia of the connective tissue and epithelium (Fig. 15 8).
inflammatory involvement of a phenytoin-induced overgrowth.
There is acanthosis of the epithelium and elongated rete pegs
extend deep into the connective tissue, which exhibits densely
lobulated surface and no tendency to bleed. The enlargement arranged collagen bundles with an increase in the number of
characteristically appears to project from beneath the gingival fibroblasts and new blood vessels. An abundance of amor-
margin from which it is separated by a linear groove. How- phous ground substance has also been reported. Structural
ever, the presence of the enlargement makes plaque control changes in the outer epithelial cell surface have been reported
difficult, often resulting in a secondary inflammatory process with cyclosporine-induced enlargements.
that complicates the gingival overgrowth caused by the drug. The enlargement begins as a hyperplasia of the connective
The resultant enlargement then becomes a combination of tissue core of the marginal gingiva and increases by its prolif-
the increase in size caused by the drug and the complicat- eration and expansion beyond the crest of the gingival margin.
ing inflammation caused by bacteria. Secondary inflammatory An inflammatory infiltrate may be found at the bottom of the
changes, not only add to the size of the lesion caused by the sulcus or pocket. Cyclosporine enlargements usually involve
drug but also produce a red or bluish-red discoloration, oblit- more highly vascularized connective tissue with foci of chron-
erate the lobulated surface demarcations, and increase bleed- ic inflammatory cells (particularly plasma cells).
ing tendency (Fig. 15. 7). The "mature"-phenytoin enlargement has a fibroblast-to-
The enlargement is usually generalized throughout the collagen ratio that is equal to that of normal gingiva from
mouth but it is more severe in the maxillary and mandibular normal individuals, which suggests that, at some point in the
anterior regions. It occurs in areas in which teeth are present development of the lesion, fibroblastic proliferation must have
(not in edentulous spaces), and the enlargement disappears been abnormally high. Recurring phenytoin enlargements
FIGURE 15.8 Microscopic view of gingival enlarge-

ment associated with phenytoin therapy. A, Hyper-
plasia and acanthosis of the epithelium and densely
collagenous connective tissue, with evidence of in-
flammation in the area adjacent to the gingival sulcus
(pocket). B, High-power view showing the extension of
deep rete pegs into the connective tissue.
appear as granulation tissue composed of numerous young cats also induces gingival enlargement in some cases. This led
capillaries and fibroblasts and irregularly arranged collagen Hassell et al to hypothesize that gingival enlargement may re-
fibrils with occasional lymphocytes. sult from the genetically determined ability or inability of the
host to deal effectively with the prolonged administration of
Anticonvulsants phenytoin.
The systemic administration of phenytoin accelerates the
The first drug-induced gingival enlargements reported were healing of gingival wounds in nonepileptic humans and in-
those produced by phenytoin (Dilantin) Dilantin is a hydan- creases the tensile strength of healing abdominal wounds in
toin that was introduced by Merritt and Putnam in 1938 for rats. The administration of phenytoin may precipitate mega-
the treatment of all forms of epilepsy except petit mal seizures. loblastic anemia and folic-acid deficiency.
Shortly thereafter, its relationship with gingival enlargement In conclusion, the pathogenesis of gingival enlargement in-
was reported. duced by phenytoin is not known, but some evidence links it
Other hydantoins that are known to induce gingival en- to a direct effect on specific, genetically predetermined sub-
largement are ethotoin (Peganone) and mephenytoin (Mesan- populations of fibroblasts, the inactivation of collagenase, and
toin). Other anticonvulsants that have the same side effect are plaque-induced inflammation.
the succinimides [ethosuximide (Zarontin), methsuximide
(Celontin)] and valproic acid (Depakene).
lmmunosuppressants
Gingival enlargement occurs in about 50% of patients receiv-
ing the drug although different authors have reported incidences Cyclosporine is a potent immunosuppressive agent that is
from 3% to 84.5%. It occurs more often in younger patients. Its used to prevent organ-transplant rejection and to treat several
occurrence and severity are not necessarily related to the dosage diseases of autoimmune origin. Its exact mechanism of action
after a threshold level has been exceeded. Phenytoin appears in is not well-known, but it appears to selectively and reversibly
the saliva. There is no consensus, however, regarding whether inhibit helper T cells, which play a role in cellular and hu-
the severity of the overgrowth is related to the levels of phe- moral immune responses. Cyclosporine A (Sandimmune and
nytoin in plasma or saliva. Some reports indicate a relationship Neoral) is administered intravenously or by mouth and dos-
between the drug dosage and the degree of gingival overgrowth. ages of more than 500 mg/day have been reported to induce
Tissue-culture experiments indicate that phenytoin stimu- gingival overgrowth.
lates the proliferation of fibroblastlike cells and epithelium. Cyclosporine-induced gingival enlargement is more vascu-
Two analogs of phenytoin (1-allyl-5-phenylhydantoinate and larized than phenytoin enlargement. Figures 15.9 and 15.10
5-methyl-5-phenylhydantoinate) have a similar effect on fi- Its occurrence varies according to different studies from 25%
broblast like cells. Fibroblasts from a phenytoin-induced gin- to 70%. It affects children more frequently, and its magnitude
gival overgrowth show increased synthesis of sulfated glycos- appears to be related more to the plasma concentration than
aminoglycans in vitro. Phenytoin may induce a decrease in to the patient's periodontal status. Gingival enlargement is
collagen degradation as a result of the production of an inac- greater in patients who are medicated with both cyclosporine
tive fibroblastic collagenase. and calcium-channel blockers, such as nifedipine.
In experimental animals, phenytoin causes gingival enlarge- The microscopic finding of many plasma cells plus the
ment that is independent of local inflammation. In cats, one of presence of an abundant amorphous extracellular substance
the metabolic products of phenytoin is 5-(parahydroxyphenyl)- has suggested that the enlargement is a hypersensitivity re-
5-phenylhydantoin; the administration of this metabolite to sponse to the cyclosporine.
FIGURE 15.9 Cyclosporine-associated gingival enlargement. A, Mild involvement located particularly on the papillae between upper central and
lateral incisors. B, Advanced generalized enlargement.
These drugs are the dihydropyridine derivatives [amlodip-

ine (Lotrel and Norvasc), felodipine (Plendil), nicardipine
(Cardene), nifedipine (Adalat and Procardia)]; the benzothi-
azine derivatives [diltiazem (Cardizem, Dilacor XR, and Ti-
azac)]; and the phenylalkylamine derivatives [verapamil (Calan,
Isoptin, Verelan, and Covera HS)].
Some of these drugs can induce gingival enlargement. Nife-
dipine, which is one of the most often used, induces gingival
enlargement in 20% of patients. Diltiazem, felodipine, nitren-
dipine, and verapamil also induce gingival enlargement. The
dihydropyridine derivative isradipine can replace nifedipine
in some cases; it does not induce gingival overgrowth.
Nifedipine gingival enlargement has been induced experi-
mentally in rats where it appears to be dose dependent in hu-
mans; however, this dose dependency is not clear. One report
indicates that nifedipine increases the risk of periodontal de-
struction in patients with type 2 diabetes mellitus.
Idiopathic Gingival Enlargement

Idiopathic gingival enlargement is a rare condition of un-
determined cause. It has been designated by terms, such as
gingivostomatosis, elephantiasis, idiopathic fibromatosis, he-
FIGURE 15.10 Microscopic view of cyclosporine-associated gingival
enlargement. Note the epithelial hyperplasia and fibrous stroma with
reditary gingival hyperplasia, and congenital familial fibro-
abundant vascularization. matosis.
In experimental animals (rats), the oral administration of General Information

cyclosporine was also reported to induce the abundant forma-
tion of new cementum. Clinical Features
In addition to gingival enlargement, cyclosporine induces The enlargement affects the attached gingiva, as well as the
other major side effects, such as, nephrotoxicity, hyperten- gingival margin and the interdental papillae. This is in con-
sion, and hypertrichosis. Another immunosuppressive drug, trast with phenytoin-induced overgrowth, which is often
tacrolimus, has been used effectively; it is also nephrotoxic, limited to the gingival margin and the interdental papillae
but it results in much less severe hypertension, hypertrichosis, (Fig. 15.5) The facial and lingual surfaces of the mandible
and gingival overgrowth. and maxilla are generally affected but the involvement may be
limited to either jaw. The enlarged gingiva is pink, firm, and
almost leathery in consistency, and it has a characteristic mi-
Calcium-Channel Blockers nutely pebbled surface (Fig. 15.11). In severe cases, the teeth
Calcium-channel blockers are drugs that were developed for are almost completely covered and the enlargement projects
the treatment of cardiovascular conditions, such as, hyper- into the oral vestibule. The jaws appear distorted as a result of
tension, angina pectoris, coronary artery spasms, and cardiac the bulbous enlargement of the gingiva. Secondary inflamma-
arrhythmias. They inhibit calcium-ion influx across the cell tory changes are common at the gingival margin.
membrane of heart and smooth muscle cells, thereby block-
ing the intracellular mobilization of calcium. This induces Histopathology
the direct dilation of the coronary arteries and arterioles and Idiopathic gingival enlargement shows a bulbous increase in
improves oxygen supply to the heart muscle; it also reduces the amount of connective tissue that is relatively avascular
hypertension by dilating the peripheral vasculature. and that consists of densely arranged collagen bundles and
FIGURE 15.11 Idiopathic gingival enlargement in a 14-year-old white male patient. A, Facial view. The gingiva is firm, with a nodular, pebbled
surface and partially covering the crowns of the teeth. B, Occlusal view of the lower jaw.
numerous fibroblasts. The surface epithelium is thickened modifying systemic influence. Bacterial plaque is necessary for
and acanthotic with elongated rete pegs. the initiation of this type of enlargement. However, plaque is not
the sole determinant of the nature of the clinical features.
Etiology The three types of conditioned gingival enlargement are
The cause is unknown and thus the condition is designated hormonal (pregnancy and puberty), nutritional (associated
as "idiopathic." Some cases have a hereditary basis but the ge- with vitamin C deficiency), and allergic. Nonspecific condi-
netic mechanisms involved are not well understood. A study tioned enlargement is also seen.
of several families found the mode of inheritance to be auto-
somal recessive in some cases and autosomal dominant in oth- Enlargement in Pregnancy
ers. In some families, the gingival enlargement may be linked Pregnancy gingival enlargement may be marginal and general-
to the impairment of physical development. The enlargement ized; or it may occur as a single mass or multiple tumorlike
usually begins with the eruption of the primary or secondary masses.
dentition and it may regress after extraction, which suggests During pregnancy, there is an increase in levels of both pro-
that the teeth (or the plaque attached to them) may be initiat- gesterone and estrogen, which by the end of the third trimes-
ing factors. The presence of bacterial plaque is a complicating ter reach levels 10- and 30 times the levels present during the
factor. menstrual cycle, respectively. These hormonal changes induce
Gingival enlargement has been described in tuberous scle- changes in vascular permeability, which leads to gingival ede-
rosis, which is an inherited condition characterized by a triad ma and an increased inflammatory response to dental plaque.
of epilepsy, mental deficiency, and cutaneous angiofibromas. The subgingival microbiota may also undergo changes, in-
cluding an increase in Prevotella intermedia.
Enlargements Associated with Marginal Enlargement. Marginal gingival enlargement dur-
Systemic Diseases or Conditions ing pregnancy results from the aggravation of previous in-
flammation and its incidence has been reported between 10%
Many systemic diseases can develop oral manifestations that
and 70%.
may include gingival enlargement. These diseases and con-
The clinical picture varies considerably. The enlargement
ditions can affect the periodontium via two different mecha-
is usually generalized, and it tends to be more prominent in-
nisms:
terproximally than on the facial and lingual surfaces. The en-
1. The magnification of an existing inflammation initiated by den- larged gingiva is bright red or magenta, soft, and friable; and
tal plaque. This group of diseases, which are discussed in has a smooth, shiny surface. Bleeding occurs spontaneously or
the "Conditioned Enlargements" section, includes some on slight provocation.
hormonal conditions (eg, pregnancy and puberty), some
nutritional diseases (eg, vitamin C deficiency), and some Tumor like Gingival Enlargement. The so-called pregnancy
cases in which the systemic influence is not identified (ie , tumor is not a neoplasm; it is an inflammatory response to
nonspecific conditioned enlargement). bacterial plaque and it is modified by the patient's condition.
2. The manifestation of the systemic disease independently of the It usually appears after the third month of pregnancy but it
inflammatory status of the gingiva. These mechanisms are may occur earlier. The reported incidence is 1.8-5%.
described in the "Systemic Diseases that Cause Gingival The lesion appears as a discrete, mushroomlike, flattened
Enlargement" section and the "Neoplastic Enlargement spherical mass that protrudes from the gingival margin or
(Gingival Tumors)" section. more often from the interproximal space and it is attached
by a sessile or pedunculated base (Fig. 15.12). It tends to ex-
pand laterally and pressure from the tongue and the cheek
Conditioned Enlargements
perpetuates its flattened appearance. It is generally dusky-red
Conditioned enlargements occur when the systemic condi- or magenta in color; it has a smooth, glistening surface that
tion of the patient exaggerates or distorts the usual gingival often exhibits numerous deep-red, pinpoint markings. It is a
response to dental plaque. The specific manner in which the superficial lesion that usually does not invade the underlying
clinical picture of conditioned gingival enlargement differs bone. The consistency varies; the mass is usually semifirrn;
from that of chronic gingivitis depends on the nature of the but it may have varying degrees of softness and friability. It is
FIGURE 15.14 Conditioned gingival enlargement during puberty in

a 13-year-old boy.
FIGURE 15.12 Localized gingival enlargement in a 27-year-old preg-
nant patient.
Enlargement in Puberty
Enlargement of the gingiva is sometimes seen during puberty.
It occurs in both male and female adolescents and appears in
areas of plaque accumulation.
The size of the gingival enlargement greatly exceeds that,
which is usually seen in association with comparable local
factors. It is marginal and interdental and is characterized by
prominent bulbous interproximal papillae (Fig. 15 .14). Often,
only the facial gingivae are enlarged and the lingual surfaces
are relatively unaltered; the mechanical action of the tongue
and the excursion of food prevent a heavy accumulation of
local irritants on the lingual surface.
Gingival enlargement during puberty has all of the clinical
features that are generally associated with chronic inflamma-
tory gingival disease. It is the degree of enlargement and its
FIGURE 15.13 Microscopic view of gingival enlargement in pregnant
patient showing an abundance of blood vessels and interspersed in-
tendency to recur in the presence of relatively scant plaque
flammatory cells. deposits that distinguish pubertal gingival enlargement from
uncomplicated chronic inflammatory gingival enlargement.
After puberty, the enlargement undergoes spontaneous reduc-
usually painless unless its size and shape foster the accumulation, but does not disappear completely until the plaque and
tion of debris under its margin or interfere with occlusion, in calculus are removed.
which case painful ulceration may occur. A longitudinal study of the subgingival micro biota of chil-
Although the microscopic findings are characteristic of gin- dren between the ages of 11 and 14 years and their association
gival enlargement during pregnancy, they are not pathogno- with clinical parameters implicated the Capnocytophaga spe-
monic because they cannot be used to differentiate pregnant cies in the initiation of pubertal gingivitis. Other studies have
and nonpregnant patients. reported that hormonal changes coincide with an increase in
the proportion of P intermedia and Prevotella nigrescens.
H istopathology
Gingival enlargement in pregnancy is called angiogranuloma. Histopathology
Both marginal and tumorlike enlargements consist of a central The microscopic appearance of gingival enlargement during
mass of connective tissue, with numerous diffusely arranged, puberty is chronic inflammation with prominent edema and
newly formed, and engorged capillaries lined by cuboid endo- associated degenerative changes.
thelial cells (Fig. 15 13), as well as a moderately fibrous stro-
ma with varying degrees of edema and chronic inflammatory Enlargement in Vitamin C Deficiency
infiltrate. The stratified squamous epithelium is thickened The enlargement of the gingiva is generally included in classic
with prominent rete pegs and some degree of intracellular and descriptions of scurvy. Acute vitamin C deficiency itself does
extracellular edema, prominent intercellular bridges, and leu- not cause gingival inflammation but it does cause hemorrhage,
kocytic infiltration. collagen degeneration, and edema of the gingival connective
Most gingival disease during pregnancy can be prevented tissue. These changes modify the response of the gingiva to
by the removal of plaque and calculus, as well as by the in- plaque to the extent that the normal defensive delimiting reac-
stitution of fastidious oral hygiene at the outset. During preg- tion is inhibited and the extent of the inflammation is exag-
nancy, treatment of the gingiva that is limited to the removal gerated, thereby resulting in the massive gingival enlargement
of tissue without the complete elimination of local irritants is seen in patients with scurvy (Fig. 15.15).
followed by the recurrence of gingival enlargement. Although Gingival enlargement with vitamin C deficiency is margin-
spontaneous reduction in the size of gingival enlargement typ- al; the gingiva is bluish-red, soft, and friable and has a smooth,
ically follows the termination of pregnancy, complete elimina- shiny surface. Hemorrhage that occurs either spontaneously
tion of the residual inflammatory lesion requires the removal or on slight provocation as well as surface necrosis with pseu-
of all plaque deposits and factors that favor its accumulation. domembrane formation are common features.
In rare instances, marked inflammatory gingival enlarge-

ments with a predominance of plasma cells can appear; these
are associated with rapidly progressive periodontitis.
A solitary plasma cell tumor or plasmocytoma has been de-
scribed in the nasopharynx and rarely in the oral mucosa. It is
a slow-growing pedunculated tumor with a pink and smooth
surface and is composed of normal plasma cells. It is usually
benign; however, in rare cases, it can be an oral manifestation
of multiple myeloma, which is a malignant tumor of the bone
marrow.
Nonspecific Conditioned Enlargement

(Pyogenic Granuloma)
FIGURE 15.15 Gingival enlargement in a patient with vitamin C de- Pyogenic granuloma is a tumorlike gingival enlargement that
ficiency. Note the prominent hemorrhagic areas. (Courtesy Dr Gerald
Shklar, Boston, MA.) is considered an exaggerated conditioned response to minor
trauma (Fig. 15.17). The exact nature of the systemic condi-
tioning factor has not been identified. Pyogenic granuloma is
Histopathology
similar in clinical and microscopic appearance to the condi-
tioned gingival enlargement seen during pregnancy. The dif-
In patients with vitamin C deficiency, the gingiva has a ferential diagnosis is based on the patient's history.
chronic inflammatory cellular infiltration with a superfi- Treatment consists of the removal of the lesions plus the
cial acute response. There are scattered areas of hemorrhage elimination of irritating local factors. The recurrence rate is
with engorged capillaries. Marked diffuse edema, collagen about 15%.
degeneration, and a scarcity of collagen fibrils and fibroblasts
are striking findings.
Systemic Diseases that Cause Gingival
Plasma Cell Gingivitis
Enlargement
Plasma cell gingivitis consists of a mild marginal gingival
enlargement that extends to the attached gingiva. The gingiva Several systemic diseases may result in gingival enlargement
appears red, friable, and sometimes granular; and it bleeds eas- by different mechanisms. These are uncommon cases and are
ily; usually does not induce a loss of attachment (Fig. 15 .16). only briefly discussed.
This lesion is located in the oral aspect of the attached gingiva
and therefore differs from plaque-induced gingivitis. Leukemia
Leukemic gingival enlargement may be diffuse or marginal
Histopathology and localized or generalized. It may appear as a diffuse en-
In patients with plasma cell gingivitis, the oral epithelium largement of the gingival mucosa, an oversized extension of
shows spongiosis and infiltration with inflammatory cells; ul- the marginal gingiva (Fig. 15.18), or a discrete tumorlike in-
trastructurally, there are signs of damage in the lower spinous terproximal mass.
layers and the basal layers. The underlying connective tissue
contains a dense infiltrate of plasma cells that also extends Clinical Features
to the oral epithelium, thereby inducing a dissecting type of In patients with leukemic enlargement, the gingiva is gener-
injury. ally bluish-red and has a shiny surface. The consistency is
An associated cheilitis and glossitis have been reported. moderately firm but there is a tendency toward Inability and
Plasma cell gingivitis is thought to be allergic in origin and hemorrhage that occur either spontaneously or with slight ir-
possibly related to components of chewing gum, dentifrices, ritation. Acute painful necrotizing ulcerative inflammatory in-
or various diet components. The cessation of exposure to the volvement may occur in the crevice formed at the junction of
allergen brings resolution of the lesion. the enlarged gingiva and the contiguous tooth surfaces.
FIGURE 15.16 Plasma cell gingivitis. A, Diffuse lesions on the facial surface of the anterior maxilla. B, Mandibular lesions. (Courtesy Dr Kim D.
Zussman, Thousand Oaks, CA.)
FIGURE 15.19 Wegener granulomatosis affecting the gingival tis-

FIGURE 15.17 Pyogenic granuloma. (Courtesy Dr Silvia Oreamuno, sues. The classic "strawberry gums" appearance of the mandibular
San Jose, Costa Rica.) gingiva is seen in this patient. A slight resemblance with desquamative
gingivitis is also evident.
The granulomatous papillary enlargement is reddish-

purple and bleeds easily on stimulation (Fig. 15 19)
Histopathology
Chronic inflammation involves scattered giant cells, foci of
acute inflammation, and microabscesses covered by a thin,
acanthotic epithelium. Vascular changes have not been de-
scribed with gingival enlargement in patients with Wegener
granulomatosis (Fig. 15.19), probably because of the small
size of the gingival blood vessels.
The cause of Wegener granulomatosis is unknown but
the condition is considered to be an immunologically medi-
ated tissue injury At one time, the usual outcome for patients
FIGURE 15.18 Leukemic gingival enlargement (acute myelocytic
leukemia). (Courtesy Dr Spencer Wolfe, Dublin, Ireland.) with this condition was death from kidney failure within a
few months; but more recently, the use of immunosuppressive
drugs has produced prolonged remissions in more than 90%
Patients with leukemia may also have a simple chronic in- of patients.
flammation without the involvement of leukemic cells, and
they may be present with the same clinical and microscopic Sarcoidosis. Sarcoidosis is a granulomatous disease of un-
features seen in patients without the systemic disease. Most known etiology. It starts in individuals during their twenties
cases, however, reveal features of both simple chronic inflam- or thirties, it predominantly affects blacks, and it can involve
mation and leukemic infiltrate. almost any organ, including the gingiva, in which a red,
True leukemic enlargement often occurs with acute leuke- smooth, painless enlargement may appear.
mia but may also be seen with subacute leukemia. It seldom
Histopathology
occurs with chronic leukemia.
Sarcoid granulomas consist of discrete, noncaseating whorls
Histopathology of epithelioid cells and multinucleated, and foreign body-type
Gingival enlargements in leukemic patients show various de- giant cells with peripheral mononuclear cells.
grees of chronic inflammation. Mature leukocytes and areas of
connective tissue are infiltrated with a dense mass of imma- Neoplastic Enlargement (Gingival
ture and proliferating leukocytes; the specific nature of which
varies with the type of leukemia. Engorged capillaries, edema-
Tumors)
tous and degenerated connective tissue, epithelium with vari- This section provides only a brief description of some of the
ous degrees of leukocytic infiltration, and edema are found. more common neoplastic and pseudoneoplastic lesions of the
Isolated surface areas of acute necrotizing inflammation with gingiva. The reader is referred to oral pathology texts for more
a pseudomembranous meshwork of fibrin, necrotic epithelial comprehensive coverage.
cells, polymorphonuclear leukocytes, and bacteria are often
seen.
Benign Tumors of the Gingiva
Granulomatous Diseases Epulis is a generic term that is used clinically to designate all
Wegener Granulomatosis. Wegener granulomatosis is a rare discrete tumors and tumorlike masses of the gingiva. It serves
disease that is characterized by acute granulomatous necrotiz- to locate the tumor but not to describe it. Most lesions referred
ing lesions of the respiratory tract, including nasal and oral to by this term are inflammatory rather than neoplastic.
defects. Renal lesions develop and acute necrotizing vasculitis Neoplasms account for a comparatively small proportion
affects the blood vessels. The initial manifestations of Wegener of gingival enlargements and they make up a small percent-
granulomatosis may involve the orofacial region and include age of the total number of oral neoplasms. In a survey of
oral mucosal ulceration, gingival enlargement, abnormal tooth 257 oral tumors, approximately 8% occurred on the gingiva.
mobility, exfoliation of teeth, and delayed healing response. In another study of 868 growths of the gingiva and palate
FIGURE 15.20 Papilloma of the gingiva in a 26-year-old man. FIGURE 15.21 Gingival giant-cell granuloma.
(of which 57% were neoplastic and the remainder inflamma- H istopathology
tory), the following incidences of tumors were noted: carcino- The papilloma lesion consists of fingerlike projections of strat-
ma, 11.0%; fibroma, 9.3%; giant-cell tumor, 8.4%; papilloma, ified squamous epithelium that are often hyperkeratotic with
7.3%; leukoplakia, 4.9%; mixed tumor (salivary-gland type), central cores of fibrovascular connective tissue.
2.5%; angioma, 1.5%; osteofibroma, 1.3%; sarcoma, 0.5%;
melanoma, 0.5%; myxoma, 0.45%; fibropapilloma, 0.4%; ad- Peripheral Giant-Cell Granuloma
enoma, 0.4%; and lipoma, 0.3%. Giant-cell lesions of the gingiva arise interdentally or from
the gingival margin; they occur most frequently on the labial
Fibroma
surface and they may be sessile or pedunculated. They vary
Fibromas of the gingiva arise from the gingival connective tis- in appearance from smooth, regularly outlined masses to ir-
sue or from the periodontal ligament. They are slow-growing regularly shaped, multilobulated protuberances with surface
spherical tumors that tend to be firm and nodular but that may indentations (Fig. 15.21). The ulceration of the margin is oc-
be soft and vascular. Fibromas are usually pedunculated. Hard casionally seen. The lesions are painless, vary in size, and
fibromas of the gingiva are rare; most of the lesions that are di- cover several teeth. They may be firm or spongy and their
agnosed clinically as "fibromas" are inflammatory enlargements. color varies from pink to deep red or purplish-blue. There
are no pathognomonic clinical features whereby these lesions
Histopathology
can be differentiated from other forms of gingival enlarge-
Fibromas are composed of bundles of well-formed collagen ment. Microscopic examination is required for definitive di-
fibers with scattered fibrocytes and variable vascularity. agnosis.
The so-called giant-cell fibroma contains multinucleated The prefix peripheral is needed to differentiate them from
fibroblasts. In another variant, mineralized tissue (bone, ce- comparable lesions that originate within the jawbone (ie, central
mentumlike material, and dystrophic calcifications) may be giant-cell granulomas).
found; this type of fibroma is called peripheral ossifyingfibroma. In some cases, the giant-cell granuloma of the gingiva is
locally invasive and causes destruction of the underlying bone
Papilloma
(Fig. 15.22). Complete removal leads to uneventful recovery.
Papillomas are benign proliferations of surface epithelium that
are, in many (but not all) cases, associated with the human Histopathology
papillomavirus (HPV). Gingival papillomas appear as solitary The giant-cell granuloma has numerous foci of multinuclear
wartlike or cauliflowerlike protuberances (Fig. 15.20). They giant cells and hemosiderin particles in a connective tissue
may be small and discrete, or they may be broad, hard eleva- stroma (Fig. 15.22). Areas of chronic inflammation are scat-
tions with minutely irregular surfaces. tered throughout the lesion with acute involvement occurring
FIGURE 15.22 A, Microscopic survey of a peripheral giant-cell granuloma. B, High-power study of the lesion demonstrating the giant cells and the
intervening stroma that make up the major portion of the mass.
invasive carcinomas. The biopsy of all leukoplakias is neces-

sary, with the most suspicious area being selected, to arrive at
a correct diagnosis and to then institute a proper therapy.
Histopathology
Leukoplakia exhibits hyperkeratosis and acanthosis. Prema-
lignant and malignant cases have a variable degree of atypical
epithelial changes that may be mild, moderate, or severe, de-
pending on the extent of involvement of the epithelial layers.
When dysplastic changes involve all layers, it is diagnosed as
a carcinoma in situ, and this may become invasive carcinoma
when the basement membrane is breached. Inflammatory in-
volvement of the underlying connective tissue is a common
associated finding.
Gingival Cyst
Gingival cysts of microscopic proportions are common but
they seldom reach a clinically significant size. When they do,
they appear as localized enlargements that may involve the
FIGURE 15.23 Bone destruction in the interproximal space between
the canine and lateral incisor caused by the extension of a peripheral marginal and attached gingiva. The cysts occur in the mandib-
giant-cell reparative granuloma of the gingiva. (Courtesy Dr Sam Toll.) ular canine and premolar areas; most often on the lingual sur-
face. They are painless but, with expansion, they may cause
erosion of the surface of the alveolar bone. The gingival cyst
should be differentiated from the lateral periodontal cyst (see
at the surface. The overlying epithelium is usually hyperplastic Chapter 20), which arises within the alveolar bone adjacent to
with ulceration at the base. Bone formation occasionally oc- the root and which is developmental in origin. Gingival cysts
curs within the lesion (Fig. 15 23) develop from odontogenic epithelium or from surface or sul-
cular epithelium traumatically implanted in the area. Removal
Central Giant-Cell Granuloma
is followed by uneventful recovery.
Giant-cell lesions arise within the jaws and produce central
cavitation. They occasionally create a deformity of the jaw that Histopathology
makes the gingiva appear enlarged. A gingival cyst cavity is lined by a thin, flattened epithelium
Mixed tumors, salivary gland types of tumors, and plasma- with or without localized areas of thickening. Less frequently,
cytomas of the gingiva have also been described but are not the following types of epithelium can be found: unkeratinized
often seen. stratified squamous epithelium, keratinized stratified squa-
Leukoplakia
mous epithelium, and parakeratinized epithelium with pali-
sading basal cells.
Leuhoplahia is a strictly clinical term defined by the World
Health Organization as a white patch or plaque that does not Other Benign Masses
rub off and that cannot be diagnosed as any other disease. The Other benign tumors have also been described as rare or
cause of leukoplakia remains obscure although it is associated infrequent findings in the gingiva. They include nevus, myo-
with the use of tobacco (smoke or smokeless). Other probable blastoma, hemangioma, neurilemoma, neurofibroma, mucus-
factors are Candida albicans, HPV-16 and HPV-18, and trauma. secreting cysts (mucoceles), and ameloblastoma.
Leukoplakia of the gingiva varies in appearance from a grayish
white, flattened, scaly lesion (Fig. 15 24) to a thick, irregularly
shaped, keratinous plaque. Malignant Tumors of the Gingiva
Most leukoplakias (80%) are benign; the remaining 20%
are malignant or premalignant, and only 3% of these are Carcinoma
Oral cancer accounts for less than 3% of all malignant tumors
in the body but it is the 6th most common cancer in males
and the 12th most common in females. The gingiva is not a
frequent site of oral malignancy, accounting for only 6% of
oral cancers.
Squamous cell carcinoma is the most common malignant
tumor of the gingiva. It may be exophytic, presenting as an
irregular outgrowth, or ulcerative, appearing as flat, erosive
lesions. It is often symptom-free, going unnoticed until com-
plicated by inflammatory changes that may mask the neo-
plasm but cause pain; sometimes it becomes evident after
tooth extraction. These masses are locally invasive and they
involve the underlying bone and periodontal ligament of
adjoining teeth and the adjacent mucosa (Fig. 15 25) Me-
FIGURE 15.24 Leukoplakia of the gingiva. tastasis is usually confined to the region above the clavicle;
FIGURE 15.25 Squamous cell carcinoma of the gingiva. A, Facial view. Note the extensive verrucous involvement. B, Palatal view. Note the mulber-
rylike tissue emerging between the second premolar and the first molar.
however, more extensive involvement may include the lung, False Enlargement
liver, or bone.
False enlargements are not true enlargements of the gingival
Malignant Melanoma tissues, but may appear as such, as a result of increases in the
size of the underlying osseous or dental tissues. The gingiva
Malignant melanoma is a rare oral tumor that tends to occur usually presents with no abnormal clinical features except the
in the hard palate and maxillary gingiva of older persons. It is massive increase in the size of the area.
usually darkly pigmented and is often preceded by localized
pigmentation. It may be flat or nodular, and it is character-
ized by rapid growth and early metastasis. It arises from me- Underlying Osseous Lesions
lanoblasts in the gingiva, cheek, or palate. Infiltration into the Enlargement of the bone subjacent to the gingival area oc-
underlying bone and metastasis to cervical and axillary lymph curs most often with tori and exostoses; but it can also oc-
nodes are common. cur with Paget disease, fibrous dysplasia, cherubism, central
giant-cell granuloma, ameloblastoma, osteoma, and osteosar-
Sarcoma. Fibrosarcoma, lymphosarcoma, and reticulum-cell coma. Figure 15.26 shows fibrous dysplasia (florid-type) in
sarcoma of the gingiva are rare; only isolated cases have been a 38-year-old black woman that induced an osseous enlarge-
described in the literature. Kaposi's sarcoma often occurs in ment in the mandibular molar area that appeared to be a gin-
the oral cavity of patients with acquired immunodeficiency gival enlargement. The gingival tissue can appear normal or it
syndrome, particularly in the palate and the gingiva. may have unrelated inflammatory changes.
Metastasis. Tumor metastasis to the gingiva occurs infre- Underlying Dental Tissues
quently. Such metastasis has been reported with various
tumors, including adenocarcinoma of the colon, lung car- During the various stages of eruption, particularly of the pri-
cinoma, melanoma, renal-cell carcinoma, hypernephroma, mary dentition, the labial gingiva may show a bulbous mar-
chondrosarcoma, and testicular tumor. ginal distortion caused by the superimposition of the bulk of
The low incidence of oral malignancy should not mislead the gingiva on the normal prominence of the enamel in the
the clinician. Ulcerations that do not respond to therapy in gingival half of the crown. This enlargement has been called
the usual manner, as well as all gingival tumors and tumor- developmental enlargement and often persists until the junc-
like lesions, must be biopsied and submitted for microscopic tional epithelium has migrated from the enamel to the cemen-
diagnosis. toenamel junction.
FIGURE 15.26 A, Apparent gingival enlargement associated with bone augmentation in a patient with fibrous dysplasia. B, Radiograph of the case
shown in A, depicting a ground-glass, mottled pattern.
NOTE: Refer online resource Atlas of Periodontal Diseases

available for numerous examples of gingival enlargements.
REFERENCES
SUGGESTED READINGS
Aas E: Hypaplasia gingivae diphenylhydantoinea, Oslo, 1963, Universitetsfor-
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Fowler CB: Benign and malignant neoplasms of the periodontium, Paiodontol
2000 21 33, 1999.
FIGURE 15.27 Developmental gingival enlargement. The normal bul-
Hallmon WW, RossmannJA: The role of drugs in the pathogenesis of gingival
bous contour of the gingiva around the incompletely erupted anterior
overgrowth, Periodontal 2000 21:176, 1999.
teeth is accentuated by chronic inflammation.
Kuffer R, Lombardi T: Premalignant lesions of the oral mucosa. A discussion
about the place of oral intraepithelial neoplasia (OJN), Oral Oneal 38:125,
2002.
In a strict sense, developmental gingival enlargements are Nuki K, Cooper SH: The role of inflammation in the pathogenesis of gingival
physiologic and they usually present no problems. However, enlargement during the administration of diphenylhydantoin sodium in
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tion, the composite picture gives the impression of extensive Rees TD: Drugs and oral disorders, Periodontal 2000 18:21, 1998.
Sapp JP, Eversole LR, Wysocki GP: Contempora1y oral and maxillofacial pathol-
gingival enlargement (Fig. 15.27). Treatment to alleviate the ogy, ed 2, Mosby, 2004, Elsevier.
marginal inflammation-rather than resection of the enlarge- Seymour RA, Thomason JM, Ellis JS: The pathogenesis of drug-induced gin-
ment-is sufficient for these patients. gival overgrowth,] Clin Paiodontol 23:165, 1996.
15 Gingival Enlargement 175.el
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16
Acute Gingival Infections
PR Klokkevold • FA Carranza • DG Naik • A Uppoor
Chapter Outline
Necrotizing Ulcerative Gingivitis Pericoronitis
Primary Herpetic Gingivostornatitis
Necrotizing Ulcerative Gingivitis bone loss occurs, the condition is called necrotizing ulcerative
periodontitis (NUP)
Necrotizing ulcerative gingivitis (NUG) is a microbial disease
of the gingiva in the context of an impaired host response. It is History
characterized by the necrosis and sloughing of gingival tissue, NUG is characterized by its sudden onset, sometimes after an
and it presents with characteristic signs and symptoms. episode of debilitating disease or acute respiratory tract in-
In the past it was also referred as Vincents infection, acute fection. A change in living habits, protracted work without
ulceromembranous gingivitis, Trench mouth, ulcerative gingi- adequate rest, poor nutrition, tobacco use, and psychological
vitis, Vincent stomatitis, Plaut-Vincent stomatitis, stomatitis stress are frequent features of the patient's history.
ulcerosa, fedid stomatitis, fusospirillary gingivitis and putrid
stomatitis. Oral Signs
Characteristic lesions are punched-out, craterlike depressions at
Historical Background the crest of the interdental papillae that subsequently extend to
NUG was recognized as far back as the 4th century B.C. by the marginal gingiva and rarely to the attached gingiva and
Xenophon, who mentioned that Greek soldiers were affected oral mucosa. The surface of the gingival craters is covered by
with "sore mouth" and foul smelling breath. John Hunter in a gray, pseudomembranous slough that is demarcated from the
1778 described the clinical findings and differentiated it from remainder of the gingival mucosa by a pronounced linear ery-
scury and chronic destructive periodontal disease. NUG oc- thema (Fig. 16.lA). In some cases, the lesions are denuded of
curred in epidemic form in the French army in 19th century, the surface pseudomembrane, thereby exposing the gingival
and in 1886 Hersch discussed some features associated with margin, which is red, shiny, and hemorrhagic. The charac-
the disease, such as lymph node enlargement, fever, malaise, teristic lesions may progressively destroy the gingiva and the
and increased salivation. In the 1890s, Plaut and Vincent de- underlying periodontal tissues (Fig. 16 lB).
scribed the disease and attributed its origin to fusiform bacilli Spontaneous gingival hemorrhage or pronounced bleed-
and spirochetes. ing after the slightest stimulation are additional characteristic
clinical signs (Fig. 16.1 Band C). Other signs that are often
found include a fetid odor and increased salivation.
Clinical Features NUG can occur otherwise in disease-free mouths, or it
NUG is usually identified as an acute disease. However, the can be superimposed on chronic gingivitis or periodontal
term acute in this case is a clinical descriptor and should not pockets. However, NUG or NUP does not usually lead to
be used as a diagnosis because there is no chronic form of the periodontal pocket formation because the necrotic changes
disease. Although the acronym ANUG is frequently used, it is involve the junctional epithelium; a viable junctional epithe-
a misnomer. NUG often undergoes a diminution in severity lium is needed for pocket deepening. It is rare in edentulous
without treatment, thereby leading to a subacute stage with mouths, but isolated spherical lesions occasionally occur in
milder clinical symptoms. Thus, patients may have a history the soft palate.
of repeated remissions and exacerbations, and the condition
can also recur in previously treated patients. Involvement may Oral Symptoms
be limited to a single tooth or group of teeth, or it may be The lesions are extremely sensitive to touch, and the patient of-
widespread throughout the mouth (Fig. 16.1) ten complains of a constant radiating, gnawing pain that is
NUG can cause tissue destruction that involves the peri- intensified by eating spicy or hot foods and chewing. There is
odontal attachment apparatus, especially in patients with a "metallic" foul taste, and the patient is conscious of an exces-
long-standing disease or severe immunosuppression. When sive amount of "pasty" saliva.
177
FIGURE 16.1 Necrotizing ulcerative gingivitis.

A, Typical punched-out papilla between the man-
dibular canine and the lateral incisor, covered
by a grayish-white pseudomembrane. B, More
advanced case showing the destruction of the
papillae, which results in an irregular marginal
contour. C, Typical lesions with spontaneous
hemorrhage. D, Generalized involvement of the
papillae and the marginal gingiva, with whitish
necrotic lesions.
Extraoral and Systemic Signs and Symptoms

Patients are usually ambulatory and have a minimum of sys-
temic symptoms. Local lymphadenopathy and a slight elevation
in temperature are common features of the mild and moderate
stages of the disease. In severe cases, there may be high fever,
increased pulse rate, leukocytosis, loss of appetite, and general
lassitude. Systemic reactions are more severe in children. In-
somnia, constipation, gastrointestinal disorders, headache, and
mental depression sometimes accompany the condition.
In very rare cases, severe sequelae such as gangrenous sto-
matitis and noma have been described.
Clinical Course
The clinical course can vary. If untreated, NUG may lead to
NUP where in there is a progressive destruction of the peri- FIGURE 16.2 Survey section of interdental papilla in a patient with
necrotizing ulcerative gingivitis. The top portion of the section shows
odontium as well as gingival recession accompanied by an in- the necrotic tissue that forms the gray marginal pseudomembrane. In the
crease in the severity of systemic complications. lower portion, note the ulceration and the accumulation of leukocytes
Stages in progression of NUG are described by Pindborg and fibrin.
and coworkers.
The lesion starts as:
1. erosion of the tip of the interdental papilla Histopathology
2. the lesion involving all of the papilla and also involving the
Microscopically, the NUG lesion is a nonspecific acute nee-
marginal gingiva
rotizing inflammation of the gingival margin that involves
3. the attached gingiva also get involved
both the stratified squamous epithelium and the underlying
4. exposure of the bone with complete loss of interdental pa-
connective tissue. The surface epithelium is destroyed and re-
pilla, marginal gingiva and the attached gingiva
placed by a meshwork of fibrin, necrotic epithelial cells, poly-
Horning and Cohen extended the staging as follows: morphonuclear leukocytes (neutrophils) (PMNs), and various
types of microorganisms (Fig. 16.2). This is the zone that ap-
• Stage 1: necrosis of the tip of the interdental papilla (93%)
pears clinically as the surface pseudomembrane. At the imme-
• Stage 2: necrosis of the entire papilla (19%)
diate border of the necrotic pseudomembrane, the epithelium
• Stage 3: necrosis extending to the marginal gingiva (21 %)
is edematous, and the individual cells exhibit varying degrees
• Stage 4: necrosis of the attached gingiva (1 %)
of hydropic degeneration. In addition, there is an infiltration
• Stage 5: necrosis involving the buccal and labial mucosa (6%)
of PMNs in the intercellular spaces.
• Stage 6: necrosis exposing alveolar bone (1 %)
The underlying connective tissue is markedly hyperemic,
• Stage 7: necrosis perforating skin of the cheek (0%)
with numerous engorged capillaries and a dense infiltration
According to Horning and Cohen Stage 1 is NUG, Stage 2 of PMNs. This acutely inflamed zone appears clinically as
may be either NUG or NUP because attachment loss may have the linear erythema beneath the surface pseudomembrane.
occurred, Stages 3 and 4 would correspond to NUP, Stages 5 Numerous plasma cells may appear in the periphery of the
and 6 would correspond to necrotizing stomatitis, and Stage 7 infiltrate; this is interpreted as an area of established chronic
would be noma. gingivitis on which the acute lesion became superimposed.
The epithelium and connective tissue alterations decrease

as the distance from the necrotic gingival margin increases,
blending gradually with the uninvolved gingiva.
It is noteworthy that the microscopic appearance ofNUG is
nonspecific. Comparable changes result from trauma, chemi-
cal irritation, or the application of caustic medications.
Relation of Bacteria to the Necrotizing

Ulcerative Gingivitis Lesion
Light and electron microscopy have been used to study the
relationship of bacteria to the characteristic lesion of NUG.
Lisgarten described the following four zones, which blend
with each other and may not all be present in every case:
Zone I: bacterial zone, the most superficial, consists of varied
bacteria, including a few spirochetes of small, medium, and
large type.
Zone 2: neutrophil rich zone contains numerous leukocytes,
preponderant neutrophils with bacteria, including many
spirochetes of various types between the leukocytes.
Zone 3: necrotic zone consists of disintegrated tissue cells, fi-
brillar material, remnants of collagen fibers, and numerous
intermediate and large spirochetes with few other organisms. FIGURE 16.3 Bacterial smear from a lesion in a patient with necro-
Zone 4: zone of spirocheteal infiltration consists of well- tizing ulcerative gingivitis. A, Spirochete. B, Bacillus fusiformis. C, Fila-
mentous organism (Actinomyces or Leptotrichia). D, Streptococcus. E,
preserved tissue infiltrated with intermediate and large Vibrio. F, Treponema microdentium.
spirochetes without other organisms.
Spirochetes have been found as deep as 300 µm from the
surface. The majority of spirochetes in the deeper zones are different from that of patients with marginal gingivitis, peri-
morphologically different from cultivated strains of Treponema odontal pockets, pericoronitis, or primary herpetic gingivo-
microdentium. They occur in nonnecrotic tissue before other stomatitis. However, bacterial studies are useful for the dif-
types of bacteria, and they may be present in high concentra- ferential diagnosis of NUG and specific infections of the oral
tions intercellularly in the epithelium adjacent to the ulcerated cavity (eg, diphtheria, thrush, actinomycosis, streptococcal
lesion and in the connective tissue. stornatitis).
Smears from the lesions (Fig. 16.3) show scattered bacte- The microscopic examination of a biopsy specimen is not
ria (predominantly spirochetes and fusiform bacilli), desqua- sufficiently specific to be diagnostic. It can be used to differ-
mated epithelial cells, and occasional PMNs. Spirochetes and entiate NUG from specific infections (eg, tuberculosis) or from
fusiform bacteria are usually seen with other oral spirochetes, neoplastic disease, but it does not differentiate between NUG
vibrios, and filaments. and other necrotizing conditions of nonspecific origin, such as
those produced by trauma or caustic medications.
Diagnosis Differential Diagnosis
Diagnosis is based on clinical findings of gingival pain, ul- NUG should be differentiated from other conditions that re-
ceration, and bleeding. A bacterial smear is not necessary semble it in some respects, such as herpetic gingivostomatitis
or definitive because the bacterial picture is not appreciably (Table 16.1); chronic pericdontitis; desquamative gingivitis
TABLE 16.1
DIFFERENTIATION BETWEEN NECROTIZING ULCERATIVE GINGIVITIS AND PRIMARY HERPETIC

GINGIVOSTOMATITIS
Necrotizing Ulcerative Gingivitis Primary Herpetic Gingivostomatitis
Etiology: interaction between host and bacteria, most probably Specific viral etiology
fusospirochetes
Necrotizing condition Diffuse erythema and vesicular eruption
Punched-out gingival margin; pseudomembrane that peels off and leaves Vesicles rupture and leave slightly depressed oval or spherical ulcer
raw areas
Marginal gingiva affected; other oral tissues rarely affected Diffuse involvement of gingiva; may include buccal mucosa and lips
Uncommon in children Occurs more frequently in children
No definite duration Duration of 7-10 days
No demonstrated immunity Acute episode results in some degree of immunity
Contagion not demonstrated Contagion
TABLE 16.2
DIFFERENTIATION AMONG NECROTIZING ULCERATIVE GINGIVITIS, CHRONIC DESQUAMATIVE

GINGIVITIS, AND CHRONIC PERIODONTAL DISEASE
Necrotizing Ulcerative Gingivitis Desquamative Gingivitis Chronic Destructive Periodontal Disease
Bacterial smears show fusospirochetal Bacterial smears reveal numerous epithelial cells Bacterial smears variable
complex and few bacterial forms
Marginal gingiva affected Diffuse involvement of marginal and attached Marginal gingiva affected
gingivae and other areas of oral mucosa
Acute history Chronic history Chronic history
Painful May or may not be painful Painless if uncomplicated
Pseudomembrane Patchy desquamation of gingival epithelium Generally no desquamation, but purulent
material may appear from pockets
Papillary and marginal necrotic lesions Papillae do not undergo necrosis Papillae do not undergo noticeable necrosis
Affects adults of both genders and Affects adults, most often women Generally found in adults, occasionally found
occasionally affects children in children
Characteristic fetid odor No odor Some odor present but not strikingly fetid
(Table 16.2); streptococcal gingivostomatitis; aphthous stoma- most commonly after chemotherapy in cancer patients or in
titis; gonococcal gingivostomatitis; diphtheritic and syphilitic patients with leukemia. The oral condition of patients with
lesions (Table 16.3); tuberculous gingival lesions; candidia- agranulocytosis is primarily necrotizing, but it lacks the severe
sis, agranulocytosis, and dermatoses (pemphigus, erythema inflammatory reaction seen with NUG. Blood studies serve to
multiforme, and lichen planus); and stomatitis venenata. differentiate between NUG and the gingival necrosis associ-
Treatment options for these diseases vary dramatically, and ated with agranulocytosis.
improper treatment may exacerbate the condition. In the case Vincents angina is a fusospirochetal infection of the oro-
of primary herpetic gingivostomatitis, early diagnosis may re- pharynx and throat as distinguished from NUG, which af-
sult in treatment with antiviral drugs that would be ineffective fects the marginal gingiva. Patients with Vincents angina have
for NUG, whereas the treatment of a case of herpes with the a painful membranous ulceration of the throat, with edema
debridement required for NUG could exacerbate the herpes. and hyperemic patches breaking down to form ulcers that are
Streptococcal gingivostomatitis is a rare condition that is covered with pseudomembranous material. The process may
characterized by a diffuse erythema of the gingiva and other extend to the larynx and the middle ear.
areas of the oral mucosa. In some cases, it is confined as a NUG in the patient with leukemia is not produced by leu-
marginal erythema with marginal hemorrhage. Necrosis of kemia itself, but it may result from the reduced host defense
the gingival margin is not a feature of this disease, and there mechanisms seen with leukemia. In addition, NUG may be
is no notable fetid odor. Bacterial smears show a preponder- superimposed on the gingival tissue alterations caused by leu-
ance of streptococcal forms, which were identified as Strepto- kemia. The differential diagnosis consists not of distinguish-
coccus viridans, but other studies report findings of group A ing between NUG and leukemic gingival changes but rather
~-hemolytic streptococcus. of determining whether leukemia is a predisposing factor in
Agranulocytosis is characterized by a marked decrease in the mouth of a patient with NUG. For example, if a patient
the number of circulating PMNs, lesions of the throat and with necrotizing involvement of the gingival margin also has
other mucous membranes, and ulceration and necrosis of generalized diffuse discoloration and edema of the attached
the gingiva that may resemble that of NUG and that occurs gingiva, the possibility of an underlying systemically induced
TABLE 16.3
DIFFERENTIATION AMONG NECROTIZING ULCERATIVE GINGIVITIS, DIPHTHERIA, AND SECONDARY

STAGE OF SYPHILIS
Necrotizing Ulcerative Gingivitis Diphtheria Secondary Stage of Syphilis (Mucous Patch)
Etiology: interaction between host and Specific bacterial etiology: Corynebacterium Specific bacterial etiology: T,·eponema pallidum
bacteria, most probably fusospirochetes diphtheriae
Affects marginal gingiva Rarely affects marginal gingiva Rarely affects marginal gingiva
Membrane removal easy Membrane removal difficult Membrane not detachable
Painful condition Less painful Minimal pain
Marginal gingivae affected Throat, fauces, and tonsils affected Any part of mouth affected
Serologic findings normal Serologic findings normal Serologic findings abnormal"
Immunity not conferred Immunity conferred by an attack Immunity not conferred
Doubtful contagiousness Contagion Only direct contact will communicate disease
Antibiotic therapy relieves symptoms Antibiotic treatment has minimal effect Antibiotic therapy has excellent results
'Wassermann, Kahn, Venereal Disease Research Laboratories.
gingival change should be considered. Leukemia is one of the NUG to address the continued susceptibility of the patient
conditions that would need to be ruled out. and to determine whether an underlying systemic disease is
NUG in the patient with human immunodeficiency virus present. Immunodeficiency may be related to varying levels
infection has the same clinical features, although it often of nutritional deficiency, fatigue caused by chronic sleep de-
follows an extremely destructive course that leads to NUP, privation, other health habits (eg, alcohol or drug abuse), psy-
with a loss of soft tissue and bone and the formation of bony chosocial factors, or systemic disease. Importantly, NUG may
sequestra. be the presenting symptom for patients with immunosuppres-
sion related to human immunodeficiency virus infection.
Etiology Local Predisposing Factors
Role of Bacteria Preexisting gingivitis, injury to the gingiva, and smoking are
Plaut in 1894 and Vincent in 1896 postulated that NUG was important predisposing factors. Although NUG may appear
caused by specific bacteria: fusiform bacillus and a spirochetal in an otherwise disease-free mouth, it most often occurs su-
organism. perimposed on preexisting chronic gingival disease and peri-
Opinions still differ with regard to whether bacteria are the odontal pockets. Deep periodontal pockets and pericoronal
primary causative factors of NUG. Several observations sup- flaps are particularly vulnerable areas because they offer a
port this concept, including that spirochetal organisms and favorable environment for the proliferation of anaerobic fu-
fusiform bacilli are always found in patients with the disease, siform bacilli and spirochetes. Areas of the gingiva that are
with other organisms also involved. Rosebury et al described traumatized by opposing teeth in malocclusion (eg, the palatal
a fusospirochetal complex that consists of T microdentium, in- surface behind the maxillary incisors, the labial gingival sur-
termediate spirochetes, vibrios, fusiform bacilli, and filamen- face of the mandibular incisors) may predispose an individual
tous organisms in addition to several Borrelia species. to the development of NUG.
Loesche et al described a predominant constant flora and The relationship between NUG and smoking has often been
a variable flora associated with NUG. The constant flora is mentioned in the literature. Pindborg reported that 98% of
composed of Prevotella intermedia in addition to Fusobacte- his patients with NUG were smokers and that the frequency
rium, Treponema, and Selenomonas species. The variable flora of this disease increases with increasing exposure to tobacco
consists of a heterogeneous array of bacterial types. smoke. The effect of smoking on periodontal disease in gen-
Treatment with metronidazole results in a significant re- eral has been the subject of numerous studies during the past
duction of Treponema species, Prevotella intermedia, and Fu- two decades, and smoking has been established as a high risk
sobacterium, with resolution of the clinical symptoms. The factor for disease Chapter 11.
antibacterial spectrum of this drug provides evidence for the
anaerobic members of the flora as etiologic agents. Systemic Predisposing Factors
These bacteriologic findings have been supported by im- NUG is not found in a well-nourished individual with a fully
munologic data that demonstrated increased immunoglobulin functional immune system. Therefore, it is important for the
G and M antibody titers for medium-sized spirochetes and clinician to determine the predisposing factors that lead to
P intermedia in patients with NUG as compared with titers immunodeficiency. Again, immunodeficiency may be related
in those patients with chronic gingivitis and healthy controls. to varying levels of nutritional deficiency; fatigue caused by
chronic sleep deficiency; other health habits (eg, alcohol or
Role of the Host Response drug abuse); and systemic disease (eg, diabetes, debilitating
Regardless of whether specific bacteria are implicated in the infection).
etiology of NUG, the presence of these organisms appears to
be insufficient to cause the disease. Nutritional Deficiency. Necrotizing gingivitis has been pro-
In the first place, the fusiform-spirochete flora is frequent- duced in animals by giving them nutritionally deficient diets.
ly found in patients who do not have NUG. In addition, exu- Several researchers found an increase in the fusospirochetal
dates from NUG lesions produce fusospirochetal abscesses flora in the mouths of the experimental animals, but the bac-
rather than typical NUG when such exudates are inoculated teria were regarded as opportunists that proliferate only when
subcutaneously into experimental animals. the tissues were altered by the deficiency. A poor diet has been
The role of an impaired host response in NUG has long cited as a predisposing factor for NUG and its sequelae in de-
been recognized. Even in the early descriptions of the dis- veloping African countries although the effects appear primar-
ease, NUG was associated with physical and emotional stress ily to diminish the effectiveness of the immune response.
as well as decreased resistance to infection. NUG has not been Nutritional deficiencies (eg, vitamin C, vitamin B2) accen-
produced experimentally in humans or animals by only the tuate the severity of the pathologic changes induced when the
inoculation of bacterial exudates from the lesions. In the ani- fusospirochetal bacterial complex is injected into animals.
mal model, local or systemic immunosuppression with glu-
cocorticoids (eg, ketoconazole) results in more characteristic Debilitating Disease. Debilitating systemic disease may pre-
lesions of NUG in infected animals. Furthermore, NUG is not dispose patients to the development of NUG. Such systemic
found in well-nourished individuals with a fully functional disturbances include chronic diseases (eg, syphilis, cancer),
immune system. All of the predisposing factors for NUG are severe gastrointestinal disorders (eg, ulcerative colitis), blood
associated with immunosuppression. Cogen et al described a dyscrasias (eg, leukemia, anemia), and acquired immunode-
depression in host defense mechanisms, particularly in PMN ficiency syndrome. Nutritional deficiency that results from
chemotaxis and phagocytosis, in patients with NUG.) debilitating disease may be an additional predisposing fac-
It is essential for the clinician to determine the predispos- tor. Experimentally induced leukopenia in animals may pro-
ing factors that lead to immunodeficiency in patients with duce ulcerative gangrenous stomatitis. Ulceronecrotic lesions
appear in the gingival margins of hamsters that are exposed transmissible denotes a capacity for the maintenance of an
to total body irradiation; these lesions can be prevented with infectious agent in successive passages through a susceptible
systemic antibiotics. animal host. The term communicable signifies a capacity for the
maintenance of infection by natural modes of spread, such as
Psychosomatic Factors direct contact through drinking water, food, and eating uten-
Psychologic factors appear to be important in the etiology of sils; via the airborne route; or by means of arthropod vectors.
NUG. The disease often occurs in association with stressful A disease that is communicable is described as contagious. It
situations (eg, induction into the armed forces, school exami- has been demonstrated that disease associated with the fuso-
nations). Psychologic disturbances as well as increased ad- spirochetal bacterial complex is transmissible; however, it has
renocortical secretion are also common in patients with the not been shown to be communicable or contagious.
disease. Attempts have been made to spread NUG from human
A significant correlation between disease incidence and to human without success. King traumatized an area in his
two personality traits-dominance and abasement-suggests gingiva and introduced debris from a patient with a severe
the presence of a NUG-prone personality. case of NUG. There was no response until he happened to fall
The mechanisms whereby psychologic factors create or ill shortly thereafter; subsequent to his illness, he observed
predispose an individual to gingival damage have not been the characteristic lesion in the experimental area. It may be
established, but alterations in digital and gingival capillary inferred with reservation from this experiment that systemic
responses that suggest increased autonomic nervous activity debility is a prerequisite for the contagion of NUG.
have been demonstrated in patients with NUG. It is a common impression that, because NUG often oc-
It can be concluded that opportunistic bacteria are the pri- curs among groups that use the same kitchen facilities, the
mary etiologic agents of NUG in patients who demonstrate disease is spread by bacteria on eating utensils. However, the
immunosuppression. Stress, smoking, and preexisting gingi- growth of fusospirochetal organisms requires carefully con-
vitis are common predisposing factors. trolled conditions and an anaerobic environment; they do not
ordinarily survive on eating utensils.
The occurrence of NUG in epidemic-like outbreaks does
Epidemiology and Prevalence
not necessarily mean that it is contagious. The affected groups
The prevalence of NUG appears to have been rather low in may be afflicted by the disease as a result of common predis-
the United States and Europe before 1914. During World posing factors rather than because of its spread from person
Wars I and II, numerous "epidemics" broke out among the to person. In all likelihood, both a predisposed immunocom-
Allied troops, but German soldiers did not seem to have been promised host and the presence of appropriate bacteria are
similarly affected. Epidemic-like outbreaks have also oc- necessary for the production of this disease.
curred among civilian populations. A study at a dental clinic
in Prague, Czech Republic, reported the incidence of NUG as
0.08% among patients between the ages of 15 and 19 years
Primary Herpetic Gingivostomatitis
old, 0.05% among those 20-24 years old, and 0.02% among Primary herpetic gingivostomatitis is an infection of the oral
those 25-29 years old. cavity caused by herpes simplex virus (HSY) type 1. It oc-
NUG occurs in individuals of all ages, with the highest curs most often among infants and children who are less than
incidence reported in patients between the ages of 15 and 6 years old, but it is also seen in adolescents and adults. It
30 years. It is not common among children in the United occurs with equal frequency in male and female patients. In
States, Canada, and Europe, but it has been reported in chil- most individuals, however, the primary infection is asymp-
dren from low socioeconomic groups in underdeveloped tomatic.
countries. In India, 54% and 58% of patients in two studies As part of the primary infection, the virus ascends through
were less than 10 years old. the sensory and autonomic nerves where it persists as la-
In a random school population in Nigeria, NUG occurred tent HSY in neuronal ganglia that innervate the site. In ap-
in 11.3% of children between the ages of 2 and 6 years old. proximately one third of the world's population, secondary
In a Nigerian hospital population, it was present in 23% of manifestations result from various stimuli, such as sunlight,
children who were less than 10 years old. It has been reported trauma, fever, and stress. These secondary manifestations in-
in several members of the same family in low socioeconomic clude herpes labialis (Fig. 16.4), herpetic stomatitis, herpes
groups. NUG is more common among children with Down genitalis, ocular herpes, and herpetic encephalitis. Secondary
syndrome than among other children with mental deficien- herpetic stomatitis can occur on the palate, on the gingiva
cies. (Fig. 16.5), or on the mucosa as a result of dental treatment
Opinions differ with regard to whether NUG is more com- that traumatizes or stimulates the latent virus in the ganglia
mon during the winter, summer, or fall and whether there is a that innervate the area; it may be present as pain away from
peak seasonal incidence. the site of treatment 2-4 days later. Careful inspection for
characteristic vesicles may be diagnostic (Fig. 16.4).
Communicability
Clinical Features
NUG often occurs in groups in an epidemic pattern. At one
time, NUG was considered contagious and involved required Oral Signs
reporting to the community health department, but it was Primary herpetic gingivostomatitis appears as a diffuse, ery-
later concluded not to be communicable. A distinction must thematous, shiny involvement of the gingiva and the adja-
be made between "communicability" and "transmissibility" cent oral mucosa, with varying degrees of edema and gin-
when referring to the characteristics of disease. The term gival bleeding. During its initial stage, it is characterized by
FIGURE 16.4 Recurrent herpetic vesicles in the lip. A, early stage and B, late stage showing brownish crusted lesions. (From Sapp JP, Eversole, LR,
Wysocki GP: Contemporary oral and maxillofacial pathology, ed 2, St Louis, 2002, Mosby.)
FIGURE 16.5 Recurrent intraoral herpetic vesicles, A, in the palate and B, in the gingiva. The latter location is rare. (From Sapp JP, Eversole, LR,
Wysocki GP: Contemporary oral and maxillofacial pathology, ed 2, St Louis, 2002, Mosby.)
course of the disease persist for several days after the ulcer-
ative lesions have healed. Scarring does not occur in the areas
of healed ulcerations.
Oral Symptoms
The disease is accompanied by generalized "soreness" of the oral
cavity, which interferes with eating, drinking, and oral hygiene.
The ruptured vesicles are the focal sites of pain; they are particu-
larly sensitive to touch, thermal changes, foods such as condi-
ments and fruit juices, and the action of coarse foods. In infants,
the disease is marked by irritability and refusal to take food.
FIGURE 16.6 Primary herpetic gingivostomatitis in a 12-year-old
boy, with diffuse erythematous involvement of the gingiva and a
spherical gray vesicle in the lip. (Courtesy Dr Heddie Sedano, Univer-
Extraoral and Systemic Signs and Symptoms
sity of California, Los Angeles, and University of Minnesota.) Cervical adenitis, fever as high as 101-105°F (38-40.6°(),
and generalized malaise are common.
the presence of discrete, spherical gray vesicles, which may
occur on the gingiva, the labial and buccal mucosae, the soft History
palate, the pharynx, the sublingual mucosa, and the tongue Primary herpetic gingivostomatitis is the result of an acute in-
(Fig. 16.6). After approximately 24 h, the vesicles rupture and fection by HSV, and it has an acute onset.
form painful small ulcers with red, elevated, halo-like margins
and depressed yellowish or grayish-white central portions. H istopathology
These occur either in widely separated areas or in clusters The virus targets the epithelial cells, which show "ballooning
where confluence occurs (Fig. 16. 7). degeneration" that consists of acantholysis, nuclear clearing,
Occasionally, primary herpetic gingivitis may occur with- and nuclear enlargement. These cells are called Tzancu cells.
out overt vesiculation. The clinical picture consists of diffuse, Infected cells fuse to form multinucleated cells, and intercellu-
erythematous, shiny discoloration and edematous enlarge- lar edema leads to the formation of intraepithelial vesicles that
ment of the gingivae with a tendency toward bleeding. rupture and develop a secondary inflammatory response with
The course of the disease is limited to 7-10 days. The dif- a fibropurulent exudate (Fig. 16.8). Discrete ulcerations that
fuse gingival erythema and edema that appear early during the result from the rupture of the vesicles have a central portion of
FIGURE 16.7 Involvement of the lip, gingiva, and tongue in primary herpetic gingivostomatitis. (From Sapp JP, Eversole, LR, Wysocki GP: Contem-
porary oral and maxillofacial pathology, ed 2, St Louis, 2002, Mosby.)
FIGURE 16.8 Biopsy showing intraepithelial viral vesicles that con- FIGURE 16.9 Aphthous lesion in the lip. The depressed gray center
tain fluid and debris, with a large number of viruses and virally altered is surrounded by an elevated red border. (From Sapp JP, Eversole, LR,
epithelial cells (ie, Tzanck cells). (Courtesy Dr Heddie Sedano, Univer- Wysocki GP: Contemporary oral and maxillofacial pathology, ed 2, St
sity of California, Los Angeles, and University of Minnesota.) Louis, 2002, Mosby.)
acute inflammation, with varying degrees of purulent exudate different clinical entity from primary herpetic gingivostomati-
surrounded by engorged blood vessels. tis. The ulcerations may look the same for the two conditions,
but diffuse erythematous involvement of the gingiva and acute
Diagnosis toxic systemic symptoms do not occur with RAS. A history of
previous episodes of painful mucosa! ulcerations suggests RAS
It is critical to arrive at a diagnosis as early as possible in a pa- rather than primary HSV
tient with a primary herpetic infection. Treatment with antivi- Information about erythema multiforme, bullous lichen pla-
ral medications can dramatically alter the course of the disease nus, and desquamative gingivitis can be found in Chapter 17.
by reducing symptoms and potentially reducing recurrences.
The diagnosis is usually established from the patient's history
Communicability
and the clinical findings. Material may be obtained from the
lesions and submitted to the laboratory for confirmatory tests, Primary herpetic gingivostomatitis is contagious. Most adults
including virus culture and immunologic tests that involve have developed immunity to HSV as a result of infection dur-
the use of monoclonal antibodies or deoxyribonucleic acid ing childhood, which, in most cases, is subclinical. For this
hybridization techniques. This should not delay treatment if reason, acute herpetic gingivostomatitis usually occurs in in-
strong clinical evidence exists for primary gingivostomatitis. fants and children. Recurrent herpetic gingivostomatitis has
been reported although it is not often clinically significant un-
less immunity is destroyed by debilitating systemic disease.
Differential Diagnosis
Studies that have demonstrated HSV in periodontal pockets
Primary herpetic gingivostomatitis should be differentiated suggest more recurrence of viral replication than has previ-
from several conditions. ously been recognized. Secondary herpetic infection of the
Lesions of recurrent aphthous stomatitis (RAS) range from skin, such as herpes labialis, does recur.
occasionally small (0.5-1 cm in diameter), well-defined,
round or ovoid shallow ulcers with a yellowish-gray central Pericoronitis
area surrounded by an erythematous halo, which heal in
7-10 days without scarring, to larger (1-3 cm in diameter) The term pericoronitis refers to inflammation of the gingiva
oval or irregular ulcers, which persist for weeks and heal in relation to the crown of an incompletely erupted tooth
with scarring (Fig. 16.9). The cause is unknown although (Fig. 16.10). It occurs most often in the mandibular third mo-
immunopathologic mechanisms appear to play a role. RAS is a lar area. Pericoronitis may be acute, subacute, or chronic.
of the flap, which then may interfere with complete closure

of the jaws and which can be traumatized by contact with
the opposing jaw, thereby aggravating the inflammatory
involvement.
The resultant clinical picture is a red, swollen, suppurating
lesion that is exquisitely tender, with radiating pains to the
ear, the throat, and the floor of the mouth. The patient is ex-
tremely uncomfortable as a result of pain, a foul taste, and an
inability to close the jaws. Swelling of the cheek in the region
of the angle of the jaw and lymphadenitis are common find-
ings. Trismus may also be a presenting complaint. In addition,
the patient may have systemic complications such as fever,
leukocytosis, and malaise.
Complications
Involvement may be localized in the form of a pericoronal
abscess. It may spread posteriorly into the oropharyngeal area
and medially to the base of the tongue, thereby making it dif-
ficult for the patient to swallow. Depending on the severity
and extent of the infection, there may be involvement of the
submaxillary, posterior cervical, deep cervical, and retropha-
FIGURE 16.10 Pericoronitis. An inflamed coronal flap is covering the ryngeal lymph nodes. Peritonsillar abscess formation, celluli-
distoocclusal surface of the impacted mandibular third molar. Note the tis, and Ludwigs angina are infrequent but potential sequelae
swelling and redness. (From Glickman I, Smulow J: Periodontal disease:
of acute pericoronitis.
clinical, radiographic and histopathologic features, Philadelphia, 1974,
Saunders.)
REFERENCES
Clinical Features website www.medenact.com
The partially erupted or impacted mandibular third molar
is the most common site of pericoronitis. The space between SUGGESTED READING
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culum) is an ideal area for the accumulation of food debris 1995.
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husk, nut fragment). McCarthy PL, Shklar G: Diseases of the oral mucosa, ed 2, Philadelphia, 1980,
Acute pericoronitis is identified by varying degrees of Lea & Febiger.
Sapp JP, Eversole LR, Wysocki GP: Contempormy oral and maxillofacial pathol-
inflammatory involvement of the pericoronal flap and ad- ogy, ed 2, St. Louis, 2004, Mosby.
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16 Acute Gingival Infections 185.el
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17
Desquamative Gingivitis
CD Dwarakanath
Chapter Outline
Desquamative Gingivitis Chronic Infections
Definition Idiopathic
Classification Clinical Features of Desquamative
Dermatoses Gingivitis
Endocrinal Imbalance Management
Desquamative Gingivitis 5. Psoriasis

6. Linear immunoglobulin A disease
Desquamative gingival lesions are unusual disorders which have 7. Dermatitis herptiformis
been recognized for over a century. They were called by vari- 8. Lupus erythematosus
ous names, and different etiological factors were proposed like 9. Erythema multiformae
nutritional deficiency, degeneration, hormonal derangement,
and so on. Tomes and Tomes reported this in 1894, Goodby
mentioned in his book in 1923, and the term chronic diffuse
Endocrinal Imbalance
desquamative gingivitis was given by Prinz in 1932. Merrit and
1. Estrogen deficiency in females (menopause, following hys-
Sorin published articles in 1933, whereas Schour and Massler
terectomy and oopherectomy)
gave the term "gingivosis" in anemic hospitalized children of
2. Testosterone deficiency in males
postwar Italy in 194 7. But the classic description and classifica-
tion were provided by McCarthy and others in 1960 followed
by inputs from Glickman and Smulow and Ziskin and Zegareli. Chronic Infections
1. Tuberculosis
Definition 2. Chronic candidiasis
Desquamative gingivitis is defined as an unusual, unique, 3. Histoplasmosis
nonplaque associated gingivitis characterized by intense dif-
fuse erythema and desquamation (peeling) of the surface epi- Idiopathic
thelium. It is often associated with ulceration of the marginal
and attached gingiva. It is not a specific disease entity but a Drug Reactions (Lichenoid Reactions)
clinical manifestation of a variety of conditions.
1. Toxic-antimetabolites
2. Allergic-barbiturates, antibiotics, and certain dental
Classification materials (Fig. 17.3)
Based on the etiological considerations, desquamative gingival
lesions are classified as under. Others (Conditions Which Mimic
This is a modification of the original classification formu-
lated by McCarthy and others. Desquamative Gingivitis)
1. Crohn disease
Dermatoses 2. Chronic ulcerative stomatitis
3. Plasma cell gingivitis (Fig. 174)
1. Lichen planus (Fig. 17 1) 4. Graft versus host disease
2. Benign mucous membrane phemphigoid (cicatricial 5. Factitious lesions
phemphigoid) 6. Kindler syndrome
3. Bullous phemphigoid 7. Wegener granulomatosis
4. Pemphigus vulgaris (Fig. 17.2) 8. Foreign body gingivitis
187
Upon perusal of the aforementioned list, it becomes clear

that the exact diagnosis of the condition resulting in desqua-
mative gingivitis is very vital to establish a correct therapeutic
approach for effective management. Despite the use of clinical
and laboratory parameters, including histopathologic and im-
munofluorescence studies, the cause of desquamative gingivitis
cannot be elucidated in up to one-third of the cases. However,
a majority of the cases seen in the clinical practice belong to
lichen planus, mucous membrane pemphigoid and pemphigus.
Clinical Features of Desquamative

Gingivitis
FIGURE 17.1 Desquamative gingivitis with Lichen planus. It is important that the clinician is familiar with the various
terms used to describe mucosal and skin lesions. A few of
them have been defined in the following:
• A Macule is a circumscribed flat area less than 1 cm of discol-
oration without elevation or depression of relative surface. eg,
erythema multiforme, hemangiomas, Koplik spots.
• A Papule is a circumscribed, elevated solid lesion less than
1 cm in diameter. eg, Papilloma.
• A Patch is a circumscribed flat area more than 1 cm. eg,
secondary syphilitic mucosal patch.
• A Vesicle is a small superficial circumscribed elevated lesion
less than 0.5 cm that contains serous fluid. eg, herpetic gin-
givitis, erythema multiforme.
• A Bulla is a bigger vesicle ( > 0. 5 cm).
• A Nodule is a palpable, solid lesion greater than 1 cm in
diameter found in the skin. eg, xanthoma.
FIGURE 17.2 Desquamative gingivitis with Pemphigus vulgaris. • A Pustule is an elevated, circumscribed lesion that contains
pus. eg, anthrax.
• An Ulcer is a break in the continuity of the epithelium due
to molecular disintegration.
• A Purpura is a reddish to purple flat lesion caused by blood
from vesicles leaking into submucosal tissue. Does not
blanch when pressed. Classified as petechiae or ecchymosis
depending on the size.
• Niholshy's sign refers to the ability to induce peeling of a
bulla as a consequence of applying lateral pressure to the
border of an intact bulla. It is used to identify suprabasal or
intraepithelial splits in the lesion. It is found in pemphigus.
• Auspitz's sign is the appearance of punctate bleeding spots
when a psoriasis lesion is scrapped off.
FIGURE 17.3 Lichenoid reaction due to allergy to acrylic crowns. • Tzanch cells are degenerated cells from the epithelium dis-
connected from adjacent cells caused by acantholysis usu-
ally seen in Herpes and Pemphigus.
• Acantholysis is the loss of intercellular connection such as
desmosomes resulting in loss of cohesion between kerti-
nocytes. It is present in pemphigus vulgaris but absent in
bullous pemphigoid.
Desquamative gingival lesions are seen in about 1.5-2.5%
of population with females being more affected than males. It
is most common in the third or fourth decade of life but can
be seen in younger individuals. Patients may be asymptomatic;
when symptomatic their complaints range from burning sensa-
tion to severe pain. Approximately 50% of the cases are confined
to gingiva but other intra oral and dermatological involvement
may be found. Lesions such as pemphigus vulgaris have sys-
temic impact, which transcends the boundaries of the oral cav-
ity and results in significant morbidity and even mortality
Glickman and Smulow have described three forms of des-
FIGURE 17.4 Plasma cell gingivitis. quamative gingivitis viz mild, moderate, and severe.
FIGURE 17.5 Mild form of desquamative gingivitis.

FIGURE 17.7 Severe form of desquamative gingivitis.
4. Biopsy and other investigations.

5. Local and systemic therapy.
Clinical History
A thorough clinical history is mandatory to begin the assess-
ment of desquamative gingivitis. Data regarding the symp-
toms associated with this condition as well as its historical
aspects (ie, when the lesion started, whether it has worsened,
if there is a habit that exacerbates the condition) provide the
FIGURE 17.6 Moderate form of desquamative gingivitis.
foundation for a thorough examination. Information regard-
ing previous therapy to alleviate the condition should also be
documented.
Mild Form (Fig. 17.5)
1. Diffuse erythema. Clinical Examination

2. Condition is usually painless. Recognition of the pattern of distribution of the lesions (ie, fo-
3. Some blanching may be seen. cal or multifocal, with or without confinement to the gingival
4. Patients may complain of intolerance to hot and spicy foods. tissues) provides leading information to begin the formula-
tion of a differential diagnosis. In addition, a simple clinical
Moderate Form (Fig. 17.6) maneuver such as Nikolsky's sign offers insight into the plau-
sibility of the presence of a vesiculobullous disorder. With a
1. Patchy distribution of bright red and gray areas. pledger of wet cotton roll, the lesions may be gently scrapped
2. Smooth, shiny, soft gingiva. to see any peeling of the surface epithelium. The handle of a
3. Burning sensation, sensitivity to temperature. mouth mirror or periodontal probe may gently be pressed on
4. Inhalation of air may be painful. the lesion to observe any tissue blanching. Examination of the
5. Massaging the gingiva results in peeling of the epithelium skin and eyes may reveal features leading to diagnosis.
with bleeding on brushing.
6. Intolerance to spicy foods, citrus fruits and drinks. Biopsy
7. Brushing is highly discomforting.
Given the extent and number of lesions that may be present in
an individual, an incisional biopsy is the best option to begin
Severe Form (Fig. 17.7)
the microscopic and immunologic evaluation. An important
consideration is the selection of the biopsy site. A perilesional
1. Wide areas of the oral cavity involved.
incisional biopsy should avoid areas of ulceration, because ne-
2. Surface epithelium appears shredded.
crosis and epithelial denudation severely hamper the diagnos-
3. Blowing of air causes a bubble in gingival epithelium.
tic process. Also biopsy is done best after initial scaling and
4. Very painful.
debridement so that plaque-associated marginal gingivitis does
5. Constant dry, burning sensation.
not confuse the picture. After the tissue is excised from the
oral cavity, the specimen can be bisected and then submitted
Management for microscopic examination. Buffered formalin (10%) should
be used to fix the tissue for conventional hematoxylin-eosin
Management of desquamative gingivitis involves five impor-
(H&E) evaluation. Michel's buffer (ammonium sulfate buffer,
tant steps:
pH 7.0) is used as transport solution for immunofluorescence
1. A meticulous history. assessment. In general, an incisional biopsy of uninvolved
2. Careful clinical examination. (normal) mucosa will show the same immunofluorescent find-
3. Opinion from a dermatologist if necessary. ings as the biopsy of the perilesional tissue. However, there are
notable exceptions, such as lichen planus and chronic cutane- 4. Dietary changes recommended with avoidance of spicy
ous lupus erythematosus, in which only the lesional tissue will foods.
exhibit the corresponding immunologic markers. 5. Good nutritional diet is vital.
6. Lifestyle changes should be enforced.
Microscopic Examination 7. Smoking and alcohol consumption should be avoided.
Sections of approximately 5 µm of formalin-fixed, paraffin-
embedded tissue stained with conventional H&-E are obtained
for light microscopy examination. Medications Used in Desquamative
Gingivitis
lmmunofluorescence
Topical steroids like triamcenalone acetonide, beclometha-
For direct immunofluorescence, unfixed frozen sections are sone, and so on are as follows
incubated with a variety of fluorescein-labeled, antihuman se-
rum (ie, anti-IgG, anti-IgA, anti-IgM, antifibrin, and anti-CJ). 1. Systemic corticosteroids like prednisolone, beclomthasone
With indirect immunofluorescence, unfixed frozen sections of 2. Systemic tetracycline
oral or esophageal mucosa from an animal such as a monkey 3. Topical cyclosporine
are first incubated with the patient's serum to allow for the at- 4. Dapsone
tachment of any serum antibodies to the mucosa! tissue. The 5. Azothioprine
tissue is then incubated with fluorescein-labeled antihuman 6. Cyclosporine
serum. Immunofluorescence tests are positive if a fluorescent 7. Cyclophosphamide
signal is observed in the epithelium, its associated basement 8. Methotrexate
membrane, or the underlying connective tissue. 9. Topical tacrolimus
Supportive Measures in the Management Alternative Treatment

of Desquamative Gingivitis
1. Photopheresis
1. Maximal emphasis provided for optimal oral hygiene. 2. Plasmapheresis
2. A super soft toothbrush with gentle brushing is ideal. 3. Free gingival graft
3. Caustic mouthwashes should be avoided. 4. Laser application
FIGURE 17.8 Desquamative gingivitis treated with topical triamcinalone acetonide. (A) Pretreatment, (B) Posttreatment.
FIGURE 17.9 Pemphigus vulgaris treated with systemic prednisolone and dapsone. (A) Pretreatment, (B) Posttreatment.
However, notwithstanding the above list depicting an array in custom trays, Oral Surg Oral Med Oral Pathol Oral Radio/ Endod 95:688,
of drugs some cases do not respond and the patient continues to 2003.
Gordon SC, Daley TD: Foreign body gingivitis: clinical and microscopic fea-
have problem leading to frustration of both the clinician and the tures of 61 cases, Oral Surg Oral Med Oral Pathol Oral Radial Endod 83:562,
former. Often it is the observation of the clinicians that lesions 1997.
respond as long as the patient is on steroid therapy and return Ismail SB, Kumar SK, Zain RB: Oral lichen planus and lichenoid reactions:
once the medication is stopped. Clinicians have to be very care- etiopathogenesis, diagnosis, management and malignant transformation,
ful particularly while prescribing steroids on a long-term basis. J Oral Sci 49:89, 2007.
Lodi G, Scully C, Carrozzo M, et al: Current controversies in oral lichen pla-
Frequently, many combinations of drugs have to be tried before nus: report of an international consensus meeting. Part 2. Clinical manage-
a satisfactory regimen is established (Figs. 17.8 and 17 9) The ment and malignant transformation, Oral Surg Oral Med Oral Pathol Oral
dental surgeon should work in collaboration with dermatolo- Radial Endod 100:164, 2005.
gist, ophthalmologist, and a general physician. The reader is ad- Nisengard RJ, Neiders M: Desquamative lesions of the gingiva, J Periodontal
52:500, 1981.
vised to refer standard textbooks of Oral Medicine for detailed Robinson JC, Lozada-Nur F, Frieden I: Oral pemphigus vulgaris: a review of
description of all the lesions and their management. the literature and a report on the management of 12 cases, Oral Surg Oral
Med Oral Pathol Oral Radial Endod 84:349, 1997.
Scully C, Mignogna M: Oral mucosa! disease: pemphigus, Br J Oral Maxillofac
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D'Cruz DP: Systemic lupus erythematosus, Br Med] 332:890, 2006. Scully C, Muzio LL: Oral mucosa! diseases: mucous membrane pemphigoid,
Gonzalez-Moles MA, Ruiz-Avila I, Rodriguez-Archilla A, et al: Treatment of Br J Oral Maxillofac Sw·g 46 358, 2008.
severe erosive gingival lesions by topical application of clobetasol propionate Solomon LW: Chronic ulcerative stomatitis, Oral Dis 14:383, 2008.
18
The Periodontal Pocket
FA Carranza • PM Camargo • DG Naik • A Uppoor
Chapter Outline
Classification Relationship of Attachment Loss and
Clinical Features Bone Loss to Pocket Depth
Pathogenesis Area Between Base of Pocket and
H istopathology Alveolar Bone
Periodontal Disease Activity Relationship of Pocket to Bone
Site Specificity Lateral Periodontal Cyst
Pulp Changes Associated With
Periodontal Pockets
The periodontal pocket, which is defined as a pathologi- Pockets can also be classified according to the involved
cally deepened gingival sulcus, is one of the most important tooth surface as (Fig. 18 3):
clinical features of periodontal disease. All different types of
• Simple, when only one tooth surface is involved.
periodontitis, share histopathologic features, such as tissue
• Compound, when two or more surfaces are involved.
changes in the periodontal pocket, mechanisms of tissue de-
• Complex or spiral, originating on one tooth surface and
struction, and healing mechanisms. However, they differ with
twisting around the tooth to involve one or more additional
regard to their etiology, natural history, progression, and re-
surfaces. These types of pockets are most common in furca-
sponse to therapy
tion areas.
Classification
Clinical Features
Deepening of the gingival sulcus may occur as a result of coro-
nal movement of the gingival margin, apical displacement of Signs
the gingival attachment, or a combination of the two process-
• Enlarged bluish-red marginal gingiva with rolled-out edge
es (Fig. 18.1). Pockets can be classified as follows:
separated from the tooth surface
• Gingival pocket is formed by gingival enlargement without • Reddish-blue vertical zone from the gingival margin to at-
destruction of the underlying periodontal tissues. The sul- tached gingiva/alveolar mucosa
cus is deepened because of the increased bulk of the gingiva • Break in faciolingual continuity of interdental gingiva
(Fig. 18.2A) • Shiny discolored puffy gingiva
• Periodontal pocket produces destruction of the supporting • Gingival bleeding
periodontal tissues, thereby leading to the loosening and • Purulent exudate from the gingival margin in response to
exfoliation of the teeth. The remainder of this chapter refers digital pressure
to this type of pocket. • Looseness, extrusion, and migration of teeth
• Development of diastema where none had previously existed
Two types of periodontal pockets exist, as follows:
• The only reliable method of locating periodontal pockets
• Suprabony (supracrestal or supraalveolar) occurs when the and determining their extent is careful probing of the gingi-
bottom of the pocket is coronal to the underlying alveolar val margin along each surface (Fig. 18.4)
bone (Fig. 18 2B)
• Intrabony (infrabony, subcrestal, or intraalveolar) occurs
Symptoms
when the bottom of the pocket is apical to the level of the
adjacent alveolar bone. With this second type, the lateral • Localized pain or sensation of pressure after eating, which
pocket wall lies between the tooth surface and the alveolar gradually diminishes
bone (Fig. 18 2C). • Foul taste in localized areas
193
FIGURE 18.4 Probing of a deep periodontal pocket. The entire length

of the periodontal probe has been inserted to the base of the pocket in
the palatal surface of the first premolar.
FIGURE 18.1 Illustration of pocket formation that indicates expansion

in two directions (arrows) from the normal gingival sulcus (left) to the • Tendency to suck material in the interdental areas
periodontal pocket (right). • Radiating pain deep in the bone
• Gnawing feeling or itching in the gingiva and urge to dig a
pointed instrument into the gums and relief obtained from
resultant bleeding
• Food sticks in between the teeth or teeth feel loose
• Sensitivity to heat and cold
• Toothache in absence of caries
Pathogenesis
The initial lesion in the development of periodontitis is the in-
flammation of the gingiva in response to a bacterial challenge.
Changes involved in the transition from the normal gingival
sulcus to the pathologic periodontal pocket are associated
with different proportions of bacterial cells in dental plaque.
Healthy gingiva is associated with few microorganisms, most-
ly coccoid cells and straight rods. Diseased gingiva is associ-
ated with increased numbers of Spirochetes and motile rods.
However, the microbiota of diseased sites cannot be used as
a predictor of future attachment or bone loss, because their
(A) (8) (C)
presence alone is not sufficient for disease to start or progress.
FIGURE 18.2 Different types of periodontal pockets. A, Gingival Pocket formation starts as an inflammatory change in the con-
pocket. There is no destruction of the supporting periodontal tissues. B,
Suprabony pocket. The base of the pocket is coronal to the level of the
nective tissue wall of the gingival sulcus. The cellular and fluid
underlying bone. Bone loss is horizontal. C, lntrabony pocket. The base inflammatory exudate causes degeneration of the surrounding
of the pocket is apical to the level of the adjacent bone. Bone loss is connective tissue, including the gingival fibers. Just apical to
vertical. the junctional epithelium, collagen fibers are destroyed, and the
area is occupied by inflammatory cells and edema (Fig. 18.5).
Early concepts assumed that, after the initial bacterial at-
tack, periodontal tissue destruction continued to be linked to
bacterial action. More recently, it was established that the host's
immunoinflammatory response to the initial and persistent
bacterial attack unleashes mechanisms that lead to collagen
and bone destruction. These mechanisms are related to vari-
ous cytokines, some of which are produced normally by cells
in noninflamed tissue and others by cells that are involved in
the inflammatory process, such as polymorphonuclear leuko-
cytes (PMNs), monocytes, and other cells, thereby leading to
collagen and bone destruction. This chapter describes the his-
tologic aspects of gingival inflammation and tissue destruction.
The two mechanisms associated with collagen loss are as
follows: (1) collagenases and other enzymes secreted by vari-
ous cells in healthy and inflamed tissue, such as fibroblasts,
FIGURE 18.3 Classification of pockets according to involved tooth PMNs, and macrophages, become extracellular and destroy
surfaces. A, Simple pocket. B, Compound pocket. C, Complex pocket. collagen (these enzymes that degrade collagen and other
FIGURE 18.5 lnterdental papilla with suprabony pockets on proxi- FIGURE 18.6 Low-power view of the base of the periodontal
mal tooth surfaces. Note the densely inflamed connective tissue with pocket and apical area. Note the dense inflammatory infiltrate on
the infiltrate extending between the collagen fibers and the proliferating the area of destroyed collagen fibers and the thin, fingerlike exten-
and ulcerated pocket epithelium. sion of epithelium covering the cementum, which has been denuded
of fibers.
matrix macromolecules into small peptides are called matrix

metalloproteinases); and (2) fibroblasts phagocytize collagen
fibers by extending cytoplasmic processes to the ligament-
cementum interface and degrade the inserted collagen fibrils
and the fibrils of the cementum matrix.
As a consequence of the loss of collagen, the apical cells of
the junctional epithelium proliferate along the root and extend
fingerlike projections that are two or three cells in thickness
(Fig. 18.6).
As a result of inflammation, PMNs invade the coro-
nal end of the junctional epithelium in increasing numbers
(Fig. 18. 7). The PMNs are not joined to one another or to the
epithelial cells by desmosomes. When the relative volume of
PMNs reaches approximately 60% or more of the junctional
epithelium, the tissue loses cohesiveness and detaches from
the tooth surface. Thus, the coronal portion of the junctional
epithelium detaches from the root as the apical portion mi-
grates, thereby resulting in its apical shift; the oral sulcular
epithelium gradually occupies an increasing portion of the
sulcus (then a pocket) lining.
Extension of the junctional epithelium along the root re-
quires the presence of healthy epithelial cells. Marked degen-
eration or necrosis of the junctional epithelium impairs rather
than accelerates pocket formation. (This occurs in necrotiz-
ing ulcerative gingivitis, which results in an ulcer rather than
pocket formation.)
Degenerative changes seen in the junctional epithelium at
the base of periodontal pockets are usually less severe than
those in the epithelium of the lateral pocket wall (Fig. 18 7).
Because the migration of the junctional epithelium requires FIGURE 18.7 View of the ulcerated lateral pocket wall of a peri-
healthy, viable cells, it is reasonable to assume that the de- odontal pocket. Note the extension of epithelial cells and the dense
generative changes seen in this area occur after the junctional accumulation of leukocytes within the epithelium and in the connective
epithelium reaches its position on the cementum. tissue.
FIGURE 18.8 A, Lateral wall of a periodontal pocket showing epithelial proliferative and atrophic changes, as well as, marked inflammatory infiltrate
and the destruction of collagen fibers. B, Slightly apical view of the same patient showing the shortened junctional epithelium.
The degree of leukocyte infiltration of the junctional epi- The junctional epithelium at the base of the pocket is usual-
thelium is independent of the volume of inflamed connective ly much shorter than that of a normal sulcus. Although marked
tissue; thus, this process may occur in gingiva with only slight variations are found with regard to the length, width, and con-
signs of clinical inflammation. dition of the epithelial cells, usually the coronoapical length of
With continued inflammation, the gingiva increases in bulk, the junctional epithelium is reduced to only 50-100 µm. The
and the crest of the gingival margin extends coronally. The api- cells may be well formed and in good condition, or they may
cal cells of the junctional epithelium continue to migrate along exhibit slight to marked degeneration (Figs. 18.6 and 18 8).
the root; and its coronal cells continue to separate from it. The The most severe degenerative changes in the periodontal
epithelium of the lateral wall of the pocket proliferates to form pocket occur along the lateral wall (Fig. 18. 7) The epithelium
bulbous, cordlike extensions into the inflamed connective
tissue. Leukocytes and edema from the inflamed connective
tissue infiltrate the epithelium that lines the pocket, thereby
resulting in various degrees of degeneration and necrosis.
The transformation of a gingival sulcus into a periodon-
tal pocket creates an area in which plaque removal becomes
impossible and a feedback mechanism is established. The ra-
tionale for pocket reduction is based on the need to eliminate
areas of plaque accumulation.
Histopathology
Changes that occur during the initial stages of gingival in-
flammation are presented in Chapter 10. After the pocket is
formed, several microscopic features are present, which will
be discussed in this section.
Soft-Tissue Wall
The connective tissue is edematous and densely infiltrated
with plasma cells (approximately 80%), lymphocytes, and a
scattering of PMNs. The blood vessels are increased in num-
ber, dilated, and engorged, particularly in the subepithelial
connective tissue layer. The connective tissue exhibits varying
degrees of degeneration. Single or multiple necrotic foci are
occasionally present. In addition to exudative and degenera-
FIGURE 18.9 Base of periodontal pocket showing extensive prolifera-
tive changes, the connective tissue shows proliferation of the tion of lateral epithelium next to atrophic areas, dense inflammatory infil-
endothelial cells, with newly formed capillaries, fibroblasts, trate, remnants of destroyed collagen fibers, and the junctional epithelium,
and collagen fibers (Fig. 18.5). which is apparently in a less altered state than the lateral pocket epithelium.
FIGURE 18.11 Transmission electron micrograph of the epithelium

in the periodontal pocket wall showing bacteria in the intercellular
FIGURE 18.10 Scanning electron micrograph of a section of pocket
spaces. 8, Bacteria; EC, epithelial cell; /5, intercellular space; L, leuko-
wall in advanced periodontitis in a human specimen showing bacte-
cyte about to engulf bacteria (X8000).
rial penetration into the epithelium and connective tissue. Scanning
electron microscope view of the surface of the pocket wall (A), sec-
tioned epithelium (8), and sectioned connective tissue (C). Curved ar-
rows point to areas of bacterial penetration into the epithelium. Thick
white arrows point to bacterial penetration into the connective tissue Filaments, rods, and coccoid organisms with predominant
through a break in the continuity of the basal lamina. CF, Connective Gram-negative cell walls have been found in intercellular
tissue fibers; (D), accumulation of bacteria (rods, cocci, and filaments) spaces of the epithelium. Hillmann et al have reported the
on the basal lamina; (F), filamentous organism on the surface of the presence of Porphyromonas gingivalis and Prevotella interme-
epithelium. The asterisk points to coccobacillus in the connective tissue.
dia in the gingiva of aggressive periodontitis cases. Actino-
bacillus actinomycetemcomitans has also been found in the
tissues.
of the lateral wall of the pocket presents striking prolifera- Bacteria may invade the intercellular space under ex-
tive and degenerative changes. Epithelial buds or interlac- foliating epithelial cells, but they are also found between
ing cords of epithelial cells project from the lateral wall into deeper epithelial cells, as well as accumulated on the base-
the adjacent inflamed connective tissue and may extend ment lamina. Some bacteria traverse the basement lamina
farther apically than the junctional epithelium (Figs. 18.8 and invade the subepithelial connective tissue (Figs. 18.10
and 18.9A-B). These epithelial projections, as well as the re- and 18.11).
mainder of the lateral epithelium, are densely infiltrated by The presence of bacteria in the gingival tissues has been in-
leukocytes and edema from the inflamed connective tissue. terpreted by different investigators as bacterial invasion or as
The cells undergo vacuolar degeneration and rupture to form the "passive translocation" of plaque bacteria. This important
vesicles. Progressive degeneration and necrosis of the epithe- point has significant clinicopathologic implications and has
lium lead to ulceration of the lateral wall, exposure of the not yet been clarified.
underlying inflamed connective tissue, and suppuration. In
some cases, acute inflammation is superimposed on the un-
derlying chronic changes. Mechanisms of Tissue Destruction
A comparative study of gingival changes in aggressive and The inflammatory response triggered by bacterial plaque
chronic periodontitis revealed more pronounced degenerative unleashes a complex cascade of events aimed at destroying
changes in the epithelium of aggressive cases with more open and removing bacteria, necrotic cells, and deleterious agents.
intercellular spaces, including microclefts and necrotic areas. However, this process is nonspecific; in an attempt to restore
The severity of the degenerative changes is not necessar- health, the host's cells (eg, neutrophils, macrophages, fibro-
ily related to pocket depth. Ulceration of the lateral wall may blasts, and epithelial cells) produce proteinases, cytokines,
occur in shallow pockets, and deep pockets are occasionally and prostaglandins that can damage or destroy the tissues.
observed in which the lateral epithelium is relatively intact or Chapter 23 describes in detail these aspects of inflammation
shows only slight degeneration. and the mechanisms of tissue destruction at the molecular level.
The epithelium at the gingival crest of a periodontal pocket
is generally intact and thickened, with prominent rete pegs.
Microtopography of the Gingival Wall
Bacterial Invasion Scanning electron microscopy has permitted the description
of several areas in the soft-tissue (gingival) wall of the peri-
Bacterial invasion of the apical and lateral areas of the pock- odontal pocket in which different types of activity take place.
et wall has been described in human chronic periodontitis. These areas are irregularly oval or elongated and adjacent to
FIGURE 18.13 Scanning electron micrograph of the periodontal

pocket wall, frontal view, in a patient with advanced periodontitis.
FIGURE 18.12 Scanning electron frontal micrograph of the peri- Note the desquamating epithelial cells and leukocytes (white arrows)
odontal pocket wall. Different areas can be seen in the pocket wall emerging onto the pocket space. Scattered bacteria can also be seen
surface. (A), Area of quiescence; (BJ, bacterial accumulation; (CJ, bac- (black arrow) (Xl 500).
terial-leukocyte interaction; (D), intense cellular desquamation. Arrows
point to emerging leukocytes and holes left by leukocytes in the pocket
wall (X800). 3. Areas of emergence of leukocytes, in which leukocytes appear
in the pocket wall through holes located in the intercellular
spaces (Fig. 18 13)
one another, and they measure about 50-200 µm. These find-
4. Areas of leukocyte-bacteria interaction, in which numer-
ings suggest that the pocket wall is constantly changing as a
ous leukocytes are present and covered with bacteria in
result of the interaction between the host and the bacteria.
an apparent process of phagocytosis. Bacterial plaque as-
The following areas have been noted:
sociated with the epithelium is seen either as an organized
1. Areas of relative quiescence, showing a relatively flat surface matrix covered by a fibrinlike material in contact with the
with minor depressions and mounds and occasional shed- surface of cells or as bacteria penetrating into the intercel-
ding of cells (Fig. 18 .12, area A). lular spaces (Fig. 18.12, area C)
2. Areas of bacterial accumulation, which appear as depres- 5. Areas of intense epithelial desquamation, which consist of semi-
sions on the epithelial surface, with abundant debris and attached and folded epithelial squames, which are sometimes
bacterial clumps penetrating into the enlarged intercellu- partially covered with bacteria (Fig. 18.12, area D).
lar spaces. These bacteria are mainly cocci, rods, and fila- 6. Areas of ulceration, with exposed connective tissue (Fig. 18.14).
ments, with a few Spirochetes (Fig. 18.12, area B). 7. Areas of hemorrhage, with numerous erythrocytes.
FIGURE 18.14 Left, Area of ulcer-

ation in the lateral wall of a deep
periodontal pocket in a human
specimen (X800). (A), Surface of
pocket epithelium in a quiescent
state; ( B), area of hemorrhage.
Right, Scanning electron micros-
copy (X3000) of the square on the
left. Connective tissue fibers and
cells can be seen at the bottom of
the ulcer.
TABLE 18.1
CORRELATION OF CLINICAL AND HISTOPATHOLOGIC FEATURES OF THE PERIODONTAL POCKET

Clinical Features Histopathologic Features
The gingival wall of the pocket presents various The discoloration is caused by circulatory stagnation; the flaccidity by the destruction of
degrees of bluish-red discoloration; flaccidity; gingival fibers and surrounding tissues; the smooth, shiny surface by atrophy of the
a smooth, shiny surface; and pitting on epithelium and edema; and the pitting on pressure by edema and degeneration.
pressure.
Less frequently, the gingival wall may be pink In such cases, fibrotic changes predominate over exudation and degeneration, particularly in
and firm. relation to the outer surface of the pocket wall. However, despite the external appearance
of health, the inner wall of the pocket invariably presents some degeneration and is often
ulcerated (see Fig. 18 15).
Bleeding is elicited by gently probing the soft- Ease of bleeding results from increased vascularity, the thinning and degeneration of the
tissue wall of pocket. epithelium, and the proximity of engorged vessels to the inner surface.
When explored with a probe, the inner aspect of Pain on tactile stimulation is caused by the ulceration of the inner aspect of the pocket wall.
the pocket is generally painful.
In many cases, pus may be expressed with the Pus occurs in pockets with suppurative inflammation of the inner wall.
application of digital pressure.
The transition from one area to another could result from bac-
teria accumulating in previously quiescent areas and triggering
the emergence of leukocytes and the leukocyte-bacteria inter-
action. This would lead to intense epithelial desquamation and
finally to ulceration and hemorrhage.
Periodontal Pockets as Healing Lesions

Periodontal pockets are chronic inflammatory lesions and thus
are constantly undergoing repair. Complete healing does not
occur because of the persistence of the bacterial attack, which
continues to stimulate an inflammatory response, thereby
causing degeneration of the new tissue elements formed dur-
ing the continuous effort at repair.
The condition of the soft-tissue wall of the periodontal
pocket results from the interplay of the destructive and con-
structive tissue changes. Their balance determines clinical fea-
tures, such as color, consistency, and surface texture of the
pocket wall. If the inflammatory fluid and cellular exudate
predominate, the pocket wall is bluish-red, soft, spongy, and
friable, with a smooth, shiny surface; at the clinical level, this
is generally referred to as an edematous pocket wall. If there is a
relative predominance of newly formed connective tissue cells
and fibers, the pocket wall is more firm and pink and clini-
cally referred to as a fibrotic pocket wall (Table 18.1 Edematous FIGURE 18.15 Periodontal pocket wall. The inner half is inflamed and
ulcerated; the outer half is densely collagenous.
and fibrotic pockets represent opposite extremes of the same
pathologic process rather than different disease entities. They
are subject to constant modification, depending on the rela-
tive predominance of exudative and constructive changes. salivary mucin, desquamated epithelial cells, and leukocytes.
Fibrotic pocket walls may be misleading, because they do not Plaque-covered calculus usually projects from the tooth sur-
necessarily reflect what is taking place throughout the pocket wall. face (Fig. 18.16). Purulent exudate, if present in the patient,
The most severe degenerative changes in periodontal tissues consists of living, degenerated, and necrotic leukocytes; living
occur adjacent to the tooth surface and the subgingival plaque. and dead bacteria; serum; and a scant amount of fibrin. The
In some cases, inflammation and ulceration on the inside of contents of periodontal pockets, when filtered free of organ-
the pocket are walled off by fibrous tissue on the outer aspect isms and debris, have been demonstrated to be toxic when
(Fig. 18 15) Externally the pocket appears pink and fibrotic, injected subcutaneously into experimental animals.
despite the inflammatory changes occurring internally
Significance of Pus Formation
Pocket Contents Pus is a common feature of periodontal disease but it is only a

secondary sign. The presence of pus or the ease with which it
Periodontal pockets contain debris that consists principally can be expressed from the pocket merely reflects the nature
of microorganisms and their products (enzymes, endotoxins, of the inflammatory changes in the pocket wall. It is not an
and other metabolic products), gingival fluid, food remnants, indication of the depth of the pocket or the severity of the
Pathologic exposure of the pulp occurs in severe cases. Root

caries may be the cause of toothache in patients with peri-
odontal disease and no evidence of coronal decay. Inactive le-
sions are well-defined darker lesions with a smooth surface
and a harder consistency on probing.
The dominant microorganism in root surface caries is Acti-
nomyces viscosus although its specific role in the development
of the lesion has not been established. Other bacteria, such as
Actinomyces naeslundii, Streptococcus mutans, Streptococcus sali-
varius, Streptococcus sanguinis, and Bacillus cereus, have been
found to produce root caries in animal models. Quirynen et al
reported that, when plaque levels and pocket depths decrease
after periodontal therapy (both nonsurgical and surgical), a
shift in oral bacteria occurs, thereby leading to a reduction
in periodontal pathogens, an increase in S. mutans, and the
development of root caries.
Involvement of the cementum is followed by bacterial pen-
etration of the dentinal tubules resulting in the destruction of
dentin.
Chemical Changes
The mineral content of the exposed cementum is increased,
for example, calcium, magnesium, phosphorus, and fluoride.
Microhardness, however, remains unchanged.
FIGURE 18.16 lnterdental papilla with ulcerated suprabony peri-
Cytotoxic Changes
odontal pockets on its mesial and distal aspects. Calculus is present on
the approximal tooth surfaces and within the gingiva. Bacterial endotoxins have been demonstrated in the cemen-
tum of untreated periodontally involved teeth.
Thus cementum may act to perpetuate the destructive ef-
destruction of the supporting tissues. Extensive pus forma- fects of periodontal disease by acting as a reservoir for poten-
tion may occur in shallow pockets, whereas deep pockets may tially destructive products.
exhibit little or no pus. The localized accumulation of pus Areas of cellular resorption of cementum and dentin are com-
constitutes an abscess, which is discussed later in this chapter. mon in roots that are unexposed by periodontal disease.
These areas are of no particular significance because they are
Root Surface Walls symptom-free, and, as long as the root is covered by the peri-
odontal ligament, they are likely to undergo repair. However,
The root surface wall of periodontal pockets often undergoes
if the root is exposed by progressive pocket formation before
changes that are significant because they may perpetuate the
repair occurs, these areas appear as isolated cavitations that
periodontal infection, cause pain, and complicate periodontal
penetrate into the dentin. These areas can be differentiated
treatment.
from caries of the cementum by their clear-cut outline and
Changes in the cementum can be classified as structural,
hard surface. They may be sources of considerable pain that
chemical, and cytotoxic features.
require the placement of a restoration.
Structural Changes
Surface Morphology ofTooth Wall
1. Presence of pathologic granules: They represent areas of col-
The following zones can be found in the bottom of a peri-
lagen degeneration or areas where collagen fibrils have not
odontal pocket (Fig. 18.17)
been fully mineralized.
2. Areas of Increased mineralization: It is a result of an ex- 1. Cementum covered by calculus, in which all of the changes
change, on exposure to the oral cavity, of minerals, and described in the preceding paragraphs can be found.
organic components at the cementum-saliva interface. 2. Attached plaque, which covers calculus and which ex-
3. Areas of demineralization: It is commonly related to root tends apically from it to a variable degree (typically 100-
caries. 500 µm).
3. The zone of unattached plaque that surrounds attached
Exposure of oral fluid and bacterial plaque results in pro-
plaque and extends apically to it.
teolysis of the embedded remnants of the Sharpey fibers; the
4. The zone of attachment of the junctional epithelium to the
cementum may be softened and may undergo fragmentation
tooth. The extension of this zone, which in normal sulci
and cavitation.
is more than 500 µm, is usually reduced in periodontal
Active root caries appear as well-defined, yellowish or light
pockets to less than 100 µm.
brown area, are frequently covered by plaque, and have a soft-
5. A zone of semidestroyed connective tissue fibers may be apical
ened or leathery consistency on probing. The tooth may not
to the junctional epithelium (see the "Pathogenesis" sec-
be painful, but exploration of the root surface reveals the pres-
tion earlier in this chapter).
ence of a defect, and penetration of the involved area with
a probe causes pain. Caries of the root may lead to pulpi- Zones 3, 4, and 5 make up the "plaque-free zone" seen in
tis, sensitivity to sweets and thermal changes, or severe pain. extracted teeth. The total width of the plaque-free zone varies
infiltrate composed predominantly of plasma cells, PMNs, or

both is seen. Bacterial samples from the pocket lumen that are
analyzed with dark-field microscopy show high proportions
Calculus
of motile organisms and Spirochetes.
Site Specificity
Attached Periodontal destruction does not occur in all parts of the
plaque
mouth at the same time; rather, it occurs on a few teeth at a
time or even only on some aspects of some teeth at any given
Unattached
time. This is referred to as the site specificity of periodontal
plaque disease. Sites of periodontal destruction are often found next
to sites with little or no destruction. Therefore, the severity of
periodontitis increases with the development of new disease
Junctional sites and with the increased breakdown of existing sites.
epithelium
Pulp Changes Associated With

Partiallly lysed
-
c.t. fibers 1 / -_/
•........ - 250 µ
1------l
Periodontal Pockets
The spread of infection from periodontal pockets may cause
pathologic changes in the pulp. Such changes may give rise to
painful symptoms or they may adversely affect the response
Intact ~
of the pulp to restorative procedures. Involvement of the pulp
c.t.fibersE:::::=
in periodontal disease occurs through either the apical fora-
men or the lateral pulp canals after pocket infection reaches
them. Atrophic and inflammatory pulpal changes occur in
FIGURE 18.17 Diagram of the area at the bottom of a pocket. c.t.,
Connective tissue.
such cases.
Relationship of Attachment Loss

according to the type of tooth (ie, it is wider in the molars and Bone Loss to Pocket Depth
than in the incisors) and the depth of the pocket (ie, it is nar-
rower in deeper pockets). It is important to remember that the The severity of the attachment loss in pocket formation is gen-
term plaque-free zone refers only to attached plaque, because erally but not always correlated with the depth of the pocket.
unattached plaque contains a variety of Gram-positive and This is because the degree of attachment loss depends on the
Gram-negative morphotypes, including cocci, rods, filaments, location of the base of the pocket on the root surface, whereas
fusiforms, and Spirochetes. The most apical zone contains pocket depth is the distance between the base of the pocket
predominantly Gram-negative rods and cocci. and the crest of the gingival margin. Pockets of the same depth
may be associated with different degrees of attachment loss
(Fig. 18.18) and pockets of different depths may be associated
Periodontal Disease Activity with the same amount of attachment loss (Fig. 18.19).
For many years the loss of attachment produced by periodon- The severity of bone loss is generally but not always corre-
tal disease was thought to be a slow but continuously pro- lated with pocket depth. Extensive attachment and bone loss
gressive phenomenon. More recently, as a result of studies of may be associated with shallow pockets if the attachment loss
the specificity of plaque bacteria, the concept of periodontal
disease activity has evolved.
According to this concept, periodontal pockets go through
periods of exacerbation and quiescence as a result of episodic
bursts of activity followed by periods of remission. Periods
of quiescence are characterized by a reduced inflammatory
response and little or no loss of bone and connective tissue
attachment. A buildup of unattached plaque, with its Gram-
negative, motile, and anaerobic bacteria, starts a period of exac-
j\ ) )
erbation during which bone and connective tissue attachment
are lost and the pocket deepens. This period may last for days,
weeks, or months, and it is eventually followed by a period
of remission or quiescence during which Gram-positive bac-
teria proliferate and a more stable condition is established.
-
These periods of quiescence and exacerbation are also known
as periods of inactivity and periods of activity. Clinically, active
FIGURE 18.18 Different pocket depths with the same amount of at-
periods show bleeding, either spontaneously or with prob- tachment loss. Arrows point to the bottom of the pocket. The distance
ing, and greater amounts of gingival exudate. Histologically, between the arrow and the cementoenamel junction remains the same
the pocket epithelium appears thin and ulcerated, and an despite different pocket depths.
is accompanied by recession of the gingival margin and slight

bone loss can occur with deep pockets.
Area Between Base of Pocket

and Alveolar Bone
Normally, the distance between the apical end of the junction-
al epithelium and the alveolar bone is relatively constant. The
distance between the apical extent of calculus and the alveolar
crest in human periodontal pockets is most constant, having a
mean length of 1.97 mm (±33 16%)
The distance from attached plaque to bone is never less
than 0.5 mm and never more than 2.7 mm. These findings
suggest that the bone-resorbing activity induced by the bacte-
FIGURE 18.19 Same pocket depth with different amounts of reces-
sion. A, Gingival pocket with no recession. B, Periodontal pocket of sim-
ria is exerted within these distances. However, the finding of
ilar depth as shown in A, but with some degree of recession. C, Pocket isolated bacteria or clumps of bacteria in the connective tissue
depth the same as shown in A and B, but with still more recession. and on the bone surface may modify these considerations.
FIGURE 18.20 Radiographic and microscopic features of intrabony pockets. A, Radiograph of a mandibular canine and premolar area showing
angular bone loss mesial to the second premolar. The type of bone loss between the first premolar and the canine is not radiographically apparent.
B, Mesiodistal histologic section of the teeth seen in A, showing an intrabony pocket mesial to the second premolar, as well as suprabony pockets
distal to the second premolar and mesial and distal to the first premolar. The mesial suprabony pocket of the first premolar appears to be coronal to a
vertical bone loss. C, Higher-power view of the area between the premolars. Note the angular bone loss and the transseptal fibers that cover the bone.
D, Higher-power view of the area between the premolars stained with Mallory connective tissue stain; clearly showing the direction of transseptal
fibers. E, Higher-power view of the area between the first premolar and the canine. Note the abundant calculus, the dense leukocytic infiltration of
the gingiva, and the angulation of the transseptal fibers and bone. The pocket is still suprabony. F, Mallory stain of a similar area to the one shown in
E. Note the destruction of the gingival fibers caused by inflammation and the angular fibers formed over angular bone loss, which are less affected by
the inflammation. Transseptal fibers extend from the distal surface of the premolar over the crest of the alveolar bone into the intrabony pocket. Note
the leukocytic infiltration of the transseptal fibers. (From Glickman I, Smulow /: Periodontal disease: clinical, radiographic and histopathologic features,
Philadelphia, 1974, Saunders.)
Relationship of Pocket to Bone

In infrabony pockets, the base of the pocket is apical to the
crest of the alveolar bone and the pocket wall lies between the
tooth and the bone. The bone loss is in most cases is vertical.
Alternatively, in suprabony pockets, the base is coronal to the
crest of the alveolar bone and the pocket wall lies coronal to
the bone. This type of bone loss is always horizontal.
This creates some microscopic differences that have some
therapeutic importance. They are the relationship of the soft-
tissue wall of the pocket to the alveolar bone, the pattern of
bone destruction, and the direction of the transseptal fibers of
the periodontal ligament (Figs. 18 20-18 22) FIGURE 18.21 After raising a flap for the treatment of the infrabony
In suprabony pockets, the alveolar crest gradually attains a pockets, the vertical bone loss around the mesial roots of the man-
dibular first and second molars can be seen.
more apical position in relation to the tooth but it retains its
general morphology and architecture. The interdental fibers
that run over the bone from one tooth to the other maintain
their usual horizontal direction. In infrabony pockets, the
morphology of the alveolar crest changes completely with the
formation of an angular bony defect. The interdental fibers,
in this case, run over the bone in an oblique direction be-
tween the two teeth of the interdental space. This may affect
the function of the area and also necessitate a modification in
treatment techniques. Table 18.2 summarizes the distinguish-
ing features of suprabony and infrabony pockets.
A periodontal abscess is a localized purulent inflammation
in the periodontal tissues (Fig. 18.23). It is also known as a
lateral abscess or a parietal abscess.
Lateral Periodontal Cyst

The periodontal cyst, which is also called lateral periodontal
cyst, is an uncommon lesion that produces localized destruc-
tion of the periodontal tissues along a lateral root surface,
most often in the mandibular canine-premolar area. It is con-
sidered to be derived from the rests of Malassez or other pro-
liferating odontogenic rests.
A periodontal cyst is usually asymptomatic without grossly
detectable changes; but it may present as a localized, tender
swelling. Radiographically, an interproximal periodontal cyst
appears on the side of the root as a radiolucent area bordered
by a radiopaque line. Its radiographic appearance cannot be FIGURE 18.22 Two suprabony pockets in an interdental space. Note
differentiated from that of a periodontal abscess. the normal horizontal arrangement of the transseptal fibers.
TABLE 18.2
DISTINGUISHING FEATURES OF SUPRABONY AND INTRABONY PERIODONTAL POCKETS

Suprabony Pocket lntrabony Pocket
The base of the pocket is coronal to the level of the alveolar bone. The base of the pocket is apical to the crest of the alveolar bone so that
the bone is adjacent to the soft-tissue wall (see Fig. 18.2).
The pattern of destruction of the underlying bone is horizontal. The pattern of bone destruction is vertical (angular) (see Figs. 18.20
and 18 21)
lnterproximally, transseptal fibers that are restored during progressive Interproximally, transseptal fibers are oblique rather than horizontal.
periodontal disease are arranged horizontally in the space between They extend from the cementum beneath the base of the pocket
the base of the pocket and the alveolar bone (see Fig. 18 22) along the alveolar bone and over the crest to the cementum of the
adjacent tooth (see Fig. 18.20).
On the facial and lingual surfaces, periodontal ligament fibers beneath On the facial and lingual surfaces, periodontal ligament fibers follow
the pocket follow their normal horizontal-oblique course between the angular pattern of the adjacent bone. They extend from the
the tooth and the bone. cementum beneath the base of the pocket along the alveolar bone
and over the crest to join with the outer periosteum.
SUGGESTED READINGS
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Lind he J, Liljenberg B, listgarten MA: Some microbiological and his-
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52:264, 1980.
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FIGURE 18.23 Periodontal abscess on an upper right central incisor.
1986.
Newman MG, Sims TN: The predominant cultivable microbiota of the peri-
odontal abscess,] Peliodontol 50:350, 1979.
Microscopically, the cystic lining may be (1) a loosely ar-
Page RC, Schroeder HH: Structure and pathogenesis. In Schluger S,
ranged, thin, nonkeratinized epithelium, sometimes with Youdelis R, Page R, editors: Periodontal disease, Philadelphia, 1977, Lea
thicker proliferating areas; or (2) an odontogenic keratocyst. & Febiger.
Quirynen M, Gizani S, Mongardini C, et al: The effect of periodontal therapy
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18 The Periodontal Pocket 204.el
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19
Abscesses of the Periodontium
DG Naik • A Uppoor
Chapter Outline
Gingival Abscess Pathogenesis and Histopathology
Pericoronal Abscess Diagnosis
Classification Differential Diagnosis
Etiology
The 1999 international workshop for the classification of peri- Pericoronal Abscess
odontal diseases organized by AAP has classified abscesses of
the periodontium as gingival abscess, periodontal abscess and Pericoronal abscess is one of the complications of pericoroni-
pericoronal abscess. (Consensus report. Abscesses of the peri- tis. It may spread posteriorly into the oropharyngeal areas and
odontium. Ann Periodontal 1999:4:83) medially to the base of the tongue, making it difficult for the
patient to swallow.
Gingival Abscess
Periodontal (Lateral) Abscess
A gingival abscess is defined as a localized purulent infec-
tion that involves the marginal gingiva or interdental papilla A periodontal abscess is a localized purulent inflammation in
(Fig. 19 1). The diagnosis of gingival abscess is uncomplicated the periodontal tissues (Fig. 19.2). It is also known as a lateral
as it is confined to only the gingival marginal tissues which are abscess or a parietal abscess.
previously a nondiseased site. It is often an acute inflamma-
tory response to the impaction of food material or a foreign Classification
body into the gingiva. The retrieval of the foreign body is thus
often diagnostic. According to Location
In its early stages, it appears as a red swelling with a smooth,
shiny surface. Within 24-48 h, the lesion usually becomes 1. Abscess in the supporting periodontal tissues along the lat-
fluctuant and pointed, with a surface orifice from which a pu- eral aspect of the root.
rulent exudate may be expressed. The adjacent teeth are often 2. Abscess in the soft tissue wall of the deep periodontal pocket.
sensitive to percussion. If permitted to progress, the lesion
generally ruptures spontaneously According to Onset or Course of Lesion
1. Acute periodontal abscess: It appears as a bright red ovoid ele-
Histopathology vation of the gingiva, which may be relatively firm or pointed
and soft. In most instances, pus may be expressed from the
The gingival abscess consists of a purulent focus in the con-
gingival margin by gentle digital pressure. It is accompanied
nective tissue surrounded by a diffuse infiltration of poly-
by symptoms such as throbbing, radiating pain, sensitivity
morphonuclear leukocytes, edematous tissue, and vascular
to percussion, tooth mobility, and, in some cases, lymphade-
engorgement. The surface epithelium has varying degrees of
nopathy and systemic effects such as fever and malaise.
intracellular and extracellular edema, invasion by leukocytes,
2. Chronic periodontal abscess: It usually presents a sinus that
and sometimes ulceration.
opens onto the gingival mucosa somewhere along the root
Etiology length. It is usually asymptomatic. However, the patient
may complain of intermittent exudation, dull gnawing
Acute inflammatory gingival enlargement results from bacte-
pain, slight elevation of the tooth, and a desire to bite
ria carried deep into the tissues when a foreign substance (eg,
down on and grind the tooth.
toothbrush bristle, piece of apple core, lobster shell fragment)
is forcefully embedded into the gingiva. The lesion is confined Acute lesions often subside but persist in the chronic
to the gingiva and should not be confused with periodontal or state, whereas chronic lesions may exist without being acute.
lateral abscesses. Chronic lesions frequently undergo acute exacerbation.
205
FIGURE 19.1 Gingival abscess on the facial gingival surface in the

space between the cuspid and the lateral incisor, unrelated to the gin- FIGURE 19.3 Pericoronitis. Inflamed coronal flap covering disto-
gival sulcus area. occlusal surface of impacted mandibular third molar. Note swelling and
redness. (From Glickman I, Smulow J: Periodontal disease: clinical, ra-
diographic and histopathologic features, Philadelphia, 1974, Saunders.)
f. Abscess can form due to inadequate scaling, which will

allow calculus to remain in the deepest pocket area,
while the resolution of the inflammation at the coro-
nal pocket area will occlude the normal drainage and
entrapment of the subgingival flora in the deepest part
of the pocket. Also calculus might get dislodged and
pushed into the soft tissue after procedures like scaling
(Fig. 19.3).
2. Nonperiodontitis Related Abscess
a. Impaction of foreign bodies, such as a toothbrush bristle,
FIGURE 19.2 Periodontal abscess on an upper right central incisor.
a piece of dental floss, orthodontic elastic, a dislodged ce-
mental tear, food (such as fish bone) into the gingival tis-
sue, and so on can result in abscess formation. Periodontal
Depending on Number abscesses caused by foreign bodies, related with oral hy-
1. Single periodontal abscess: They are usually related to local fac- giene aids, have been named "oral hygiene abscesses."
tors that contribute to the closure of the periodontal pocket. b. Lateral perforation of the root during endodontic ther-
2. Multiple periodontal abscess: They have been reported in apy and trauma to the tooth.
diabetes mellitus and medically compromised patients. c. Local factors affecting morphology of roots such as
cemental tears, external root resorption, invaginated
tooth, and cracked tooth may predispose to periodontal
Etiology abscess formation.
Periodontal abscesses have been associated either directly to
periodontitis (periodontitis related abscess) or to sites without Pathogenesis and Histopathology
the prior existence of a periodontal pocket (nonperiodontitis
related abscess). The entry of bacteria into the soft tissue pocket wall could be
the first event to initiate the periodontal abscess. Inflamma-
1. Periodontitis Related Abscess tory cells are then attracted by chemotactic factors released by
a. The existence of tortuous pockets, with cul-de-sac that the bacteria, and the concomitant inflammatory reaction leads
eventually becomes isolated, may favor the formation to destruction of the connective tissues, the encapsulation of
of abscess. the bacterial infection, and the production of pus.
b. The marginal closure of the periodontal pocket may Histologically intact neutrophils are found surrounding a
lead to an extension of infection into the surrounding central area of soft tissue debris and destroyed leukocytes. At
periodontal tissues due to the pressure of suppuration a later stage, a pyogenic membrane composed of macrophages
inside the closed pocket. and neutrophils is organized. An acute inflammatory reaction
c. The development of periodontal abscess in periodontitis surrounds the purulent area, and the overlying epithelium ex-
may occur at different stages during the course of the inhibits intracellular and extracellular edema and invasion of
fection as an exacerbation of an untreated periodontitis, leukocytes. Gram-negative bacteria may be seen invading the
during periodontal therapy, in refractory periodontitis, pocket epithelium and the altered connective tissue.
or during periodontal maintenance. Also, fibrin secre-
tions, leading to the local accumulation of pus, may fa-
vor the closure of gingival margin to the tooth surface.
Diagnosis
d. Changes in composition of the microflora, bacterial vir- The diagnosis of the periodontal abscess requires correlation
ulence, or in host defenses could also make the pocket of the history, and clinical and radiographic findings. The den-
lumen inefficient to drain the increased suppuration. tal history can provide information about previous periodon-
e. Treatment with systemic antibiotics without sub-gingi- tal treatments, endodontic therapy, and previous abscesses.
val debridement in patients with advanced periodonti- The suspected area should be carefully probed (Fig. 19 .4).
tis may also cause abscess formation. Continuity of the lesion with the gingival margin serves as the
19 Abscesses of the Periodontium 207
TABLE 19.2
DIFFERENTIATION BETWEEN PERIAPICAL

AND PERIODONTAL ABSCESS
Periapical Abscess Periodontal Abscess
Pain may be sharp, The pain is usually dull, steady,

intermittent, throbbing, and continuous
severe, and diffuse
Pain is not always localized, The pain is localized, and the
and the patient may not patient usually can locate the
be able to locate the offending tooth
offending tooth
Vitality test does not show Vitality test shows vital pulp
vital pulp
The tooth is painful to The tooth is usually not as painful
FIGURE 19.4 Clinical view showing deep periodontal pocket in rela- percussion or with to percussion or with movement
tion to upper right lateral incisor. movement
The abscess may be The abscess is associated with a
associated with deep preexisting periodontal pocket,
restoration caries, or both
TABLE 19.1
Swelling usually present in Swelling usually includes gingival
DIFFERENTIATION BETWEEN GINGIVAL apical area and sinus tract tissue and fistula tract is
formation is common uncommon
AND PERIODONTAL ABSCESS
Clinically may have no Clinically there is presence
Gingival Abscess Periodontal Abscess periodontal pocket, or if of periodontal pocket;
present, probes as narrow and radiographically there
It is confined to the marginal It involves the supporting defect is presence of vertical or
gingiva periodontal structures argular bone loss or fuscation
It often occurs in former It occurs in the course of chronic radiolucency
disease-free areas destructive periodontitis
It is an acute inflammatory The occlusion of the orifice of
response that results when a preexisting periodontal
a foreign object (apple pocket prevents drainage of the Differential Diagnosis
core, lobster fragment) is purulent material leading to
forcefully embedded into
The differential diagnosis of periodontal abscesses should
abscess formation
the gingiva be made using different signs and symptoms, such as pulp
Treatment involves only Treatment involves drainage, vitality, the presence of dental caries versus periodontal
drainage and irrigation irrigation, and pocket pockets, the location of abscess, and a careful radiograph-
elimination procedure ic examination. It is differentiated from gingival abscess
(Table 19 1) and periapical abscess (Table 19.2), which are
the other abscesses found in the oral cavity that have similar
clinical evidence that the abscess is periodontal. Other find- appearance and symptomatology although their etiologies
ings are ovoid swelling of the gingiva, pain, tooth mobility, are different.
tooth elevation, suppuration, either spontaneous or on digital
pressure, and the presence of deep periodontal pockets. Ra-
diographically, it appears as a discrete area of radiolucency SUGGESTED READINGS
along the lateral aspect of the root. However, lesions in the soft Corbet EF: Diagnosis of acute periodontal abscess, Pe,iodontol 2000 34:204,
tissue wall of a periodontal pocket are less likely to produce 2004.
Dahlen G: Microbiology and treatment of dental abscess and periodontic-
radiographic changes than those deep in the supporting tis- endodontic lesions, Periodontal 2000 28:206, 2002.
sues. Similarly, abscesses on the facial or lingual surfaces are Gilette WB, van house RL: 111 effects of improper oral hygiene procedures,
obscured by the radiopaucity of the root. J Am Dent Assoc 101:476-481, 1980.
20
Bone Loss and Patterns
of Bone Destruction
FA Carranza • PM Camargo • HH Takei • DG Naik • A Uppoor
Chapter Outline
Bone Destruction Caused by the Factors Determining Bone Morphology
Extension of Gingival Inflammation in Periodontal Disease
Bone Destruction Caused by Trauma Bone Destruction Patterns in Periodontal
from Occlusion Disease
Bone Destruction Caused by Systemic
Disorders
Although periodontitis is an infectious disease of the gingi- The transition from gingivitis to periodontitis is associ-
val tissue, changes that occur in bone are crucial because the ated with changes in the composition of bacterial plaque. In
destruction of bone is responsible for tooth loss. advanced stages of disease, the number of motile organisms
The height and density of the alveolar bone are normally and spirochetes increases, whereas the number of coccoid
maintained by an equilibrium, regulated by local and sys- rods and straight rods decreases. The cellular composition of
temic influences, between bone formation and bone resorp- the infiltrated connective tissue also changes with increasing
tion. When resorption exceeds formation, both bone height severity of the lesion. Fibroblasts and lymphocytes predomi-
and bone density may be reduced. The level of bone is the nate in stage 1 gingivitis, whereas the number of plasma cells
consequence of past pathologic experiences, whereas changes and blast cells increases gradually as the disease progresses.
in the soft tissue of the pocket wall reflect the present inflam- Seymour et al have postulated a stage of "contained" gingivitis
matory condition. Therefore, the degree of bone loss is not in which T lymphocytes are preponderant; they think that,
necessarily correlated with the depth of periodontal pockets, as the lesion becomes a B-lymphocyte lesion, it becomes pro-
the severity of ulceration of the pocket wall, or the presence gressively destructive.
or absence of pus. Heijl et al were able to convert, in experimental animals,
a confined, naturally occurring chronic gingivitis into a pro-
gressive periodontitis by placing a silk ligature into the sul-
Bone Destruction Caused by the cus and tying it around the neck of the tooth. This induced
ulceration of the sulcular epithelium, a shift in the inflam-
Extension of Gingival Inflammation
matory infiltrate from predominantly plasma cells to pre-
The most common cause of bone destruction in periodontal dominantly polymorphonuclear leukocytes, and osteoclastic
disease is the extension of inflammation from the marginal resorption of the alveolar crest. The recurrence of episodes
gingiva into the supporting periodontal tissues. The inflamma- of acute destruction over time may be one mechanism that
tory invasion of the bone surface and the initial bone loss that leads to progressive bone loss in individuals with marginal
follows mark the transition from gingivitis to periodontitis. periodontitis.
Periodontitis is always preceded by gingivitis, but not all gingi- The extension of inflammation to the supporting struc-
vitis progresses to periodontitis. Some cases of gingivitis appar- tures of a tooth may be modified by the pathogenic potential
ently never become periodontitis, and other cases go through of plaque and the resistance of the host. The latter includes
a brief gingivitis phase and rapidly develop into periodontitis. immunologic activity and other tissue-related mechanisms,
The factors that are responsible for the extension of inflam- such as the degree of fibrosis of the gingiva, probably the
mation to the supporting structures, thereby initiating the width of the attached gingiva, and the reactive fibrogenesis
conversion of gingivitis to periodontitis, are not clearly under- and osteogenesis that occur peripheral to the inflammatory
stood at this time. lesion.
209
FIGURE 20.1 A, An area of inflammation extending from the gingiva into the suprabony area. B, Extension of inflammation along the blood vessels
and between collagen bundles.
H istopathology
Gingival inflammation extends along the collagen fiber bun-
dles and follows the course of the blood vessels through the
loosely arranged tissues around them into the alveolar bone
(Fig. 20.1 A and B). Although the inflammatory infiltrate is
concentrated in the marginal periodontium, the reaction is a
much more diffuse one, often reaching the bone and elicit-
ing a response before evidence of crestal resorption or loss of
attachment exists. In the upper molar region, inflammation
can extend to the maxillary sinus, thereby resulting in thick-
ening of the sinus mucosa.
Interproximally, inflammation spreads to the loose connec-
tive tissue around the blood vessels through the fibers and
then into the bone through vessel channels that perforate
the crest of the interdental septum at the center of the crest
(Fig. 20.2), toward the side of the crest (Fig. 20 3), or at the
angle of the septum. In addition, inflammation may enter the
bone through more than one channel. Less frequently, the
inflammation spreads from the gingiva directly into the peri-
odontal ligament and from there into the interdental septum
(Fig. 20.4).
Facially and lingually, inflammation from the gingiva spreads
along the outer periosteal surface of the bone (Fig. 20.4) and
FIGURE 20.2 Inflammation that extends from the pocket area (top)
penetrates into the marrow spaces through vessel channels in between the collagen fibers, which are partially destroyed.
the outer cortex.
Along its course from the gingiva to the bone, the inflamma-
tion destroys the gingival and transseptal fibers, reducing them After inflammation reaches the bone via extension from
to disorganized granular fragments interspersed among the the gingiva (Fig. 20.6), it spreads into the marrow spaces and
inflammatory cells and edema. However, there is a continuous replaces the marrow with a leukocytic and fluid exudate, new
tendency to recreate transseptal fibers across the crest of the blood vessels, and proliferating fibroblasts (Fig. 20 7). Multi-
interdental septum farther along the root as the bone destruc- nuclear osteoclasts and mononuclear phagocytes increase in
tion progresses (Fig. 20.5). As a result, transseptal fibers are number, and the bone surfaces appear to be lined with How-
present even in cases of extreme periodontal bone loss. ship lacunae (Fig. 20 8)
The dense transseptal fibers form a firm covering over the In the marrow spaces, resorption proceeds from within
bone that is encountered during periodontal flap surgery after and causes a thinning of the surrounding bony trabeculae and
the superficial granulation tissue is removed. an enlargement of the marrow spaces; this is followed by the
20 Bone Loss and Patterns of Bone Destruction 211
FIGURE 20.3 A, Extension of inflammation into the center of the interdental septum. Inflammation from the gingiva penetrates the transseptal fibers
and enters the bone around the blood vessel in the center of the septum. B, The cortical layer at the top of the septum has been destroyed, and the
inflammation penetrates into the marrow spaces.
(A) (B)
FIGURE 20.4 Pathways of inflammation from the gingiva into the
supporting periodontal tissues in a patient with periodontitis. A, ln-
terproximally, from the gingiva into the bone (1), from the bone into
the periodontal ligament (2), and from the gingiva into the periodontal
ligament (3). B, Facially and lingually, from the gingiva along the outer
periosteum ( 1 ), from the periosteum into the bone (2), and from the FIGURE 20.5 Reformation of transseptal fibers. A mesiodistal section
gingiva into the periodontal ligament (3). through the interdental septum shows gingival inflammation and bone
loss. Recreated transseptal fibers can be seen above the bone margin,
where they have been partially infiltrated by the inflammatory process.
destruction of the bone and a reduction in bone height. Nor-
mally, fatty bone marrow is partially or totally replaced by a
fibrous type of marrow in the vicinity of the resorption. The amount of inflammatory infiltrate correlates with the
Bone destruction in periodontal disease is not a process degree of bone loss but not with the number of osteoclasts.
of bone necrosis. It involves the activity of living cells along However, the distance from the apical border of the inflam-
viable bone. When tissue necrosis and pus are present in peri- matory infiltrate to the alveolar bone crest correlates with both
odontal disease, they occur in the soft-tissue walls of peri- the number of osteoclasts on the alveolar crest and the total
odontal pockets rather than along the resorbing margin of the number of osteoclasts. Similar findings have been reported in
underlying bone. experimentally induced periodontitis in animals.
FIGURE 20.6 Extension of inflammation has reached the crestal

bone surface. FIGURE 20.8 Osteoclasts and Howship lacunae in the resorption of
crestal bone.
Beyond 2.5 mm, there is no effect; interproximal angular

defects can appear only in spaces that are wider than 2.5 mm
because narrower spaces would be destroyed entirely Tal cor-
roborated this with measurements in human patients.
Large defects that greatly exceed a distance of 2.5 mm from
the tooth surface (as described in aggressive types of peri-
odontitis) may be caused by the presence of bacteria in the
tissues.
Rate of Bone Loss

In a study of Sri Lankan tea laborers with no oral hygiene and
no dental care, Loe et al found the rate of bone loss to average
about 0.2 mm/year for facial surfaces and about 0.3 mm/year
for proximal surfaces when periodontal disease was allowed to
progress untreated. However, the rate of bone loss may vary,
depending on the type of disease present. Loe et al also identi-
fied the following three subgroups of patients with periodon-
tal disease on the basis of the interproximal loss of attachment
and tooth mortality (loss of attachment can be equated with
loss of bone although attachment loss precedes bone loss by
about 6-8 months):
1. Approximately 8% of persons had a rapid progression of
FIGURE 20.7 lnterdental septum in a human autopsy section. Exten- periodontal disease that was characterized by a yearly loss
sive inflammatory infiltrate has invaded the marrow spaces, entering of attachment of 0.1-1.0 mm.
from both the mesial and distal aspects. Fatty bone marrow has been
replaced by inflammatory cells and fibrous marrow.
2. Approximately 81 % of individuals had moderately pro-
gressive periodontal disease with a yearly loss of attach-
ment of 0.05-0.5 mm.
3. The remaining 11 % of persons had minimal or no progres-
Radius of Action
sion of destructive disease with a yearly loss of attachment
Garant and Cho suggested that locally produced bone resorp- of 0.05-0 09 mm.
tion factors may need to be present in the proximity of the
bone surface to exert their action. Page and Schroeder, on the Periods of Destruction
basis of Waerhaugs measurements made on human autopsy
specimens, postulated a range of effectiveness of about 1.5- Periodontal destruction occurs in an episodic, intermittent
2.5 mm in which bacterial plaque can induce loss of bone. manner, with periods of inactivity or quiescence that alternate
with destructive periods that result in the loss of collagen and bone resorption in periodontal disease, and it is consistent
alveolar bone and the deepening of the periodontal pocket. with the varied rates of progression observed clinically in indi-
Periods of destructive activity are associated with sub- viduals with untreated periodontal disease.
gingival ulceration and an acute inflammatory reaction that The periods of remission and exacerbation (or inactivity
results in the rapid loss of alveolar bone; it has been hypoth- and activity, respectively) appear to coincide with the quies-
esized that this coincides with the conversion of a predomi- cence or exacerbation of gingival inflammation as manifested
nantly I-lymphocyte lesion to one with a predominantly by changes in the extent of bleeding, the amount of exudate,
B-lymphocyte-plasma cell infiltrate. Microbiologically, and the composition of bacterial plaque. The presence of
these lesions are associated with an increase in the loose, bone formation in response to inflammation, even in those
unattached, motile, gram-negative, anaerobic pocket flora, with active periodontal disease, has an effect on the outcome
whereas periods of remission coincide with the formation of of treatment. The basic aim of periodontal therapy is the
a dense, unattached, nonmotile, gram-positive flora with a elimination of inflammation to remove the stimulus for bone
tendency to mineralize. resorption and therefore to allow the inherent constructive
It has also been suggested that the onset of periods of tendencies to predominate.
destruction coincide with tissue invasion by one or several
bacterial species and that this is followed by an advanced local
host defense that controls the attack. Bone Destruction Caused by Trauma
from Occlusion
Mechanisms of Bone Destruction Another cause of bone destruction in periodontal disease is
trauma from occlusion, which can occur in the absence or
The factors involved in bone destruction in periodontal dis-
presence of inflammation
ease are bacterial and host mediated. Bacterial plaque prod-
In the absence of inflammation, the changes caused by
ucts induce the differentiation of bone progenitor cells into
trauma from occlusion vary from increased compression and
osteoclasts and stimulate gingival cells to release mediators
tension of the periodontal ligament and increased osteocla-
that have the same effect. Plaque products and inflammatory
sis of alveolar bone to necrosis of the periodontal ligament
mediators can also act directly on osteoblasts or their pro-
and bone and the resorption of bone and tooth structure.
genitors, thereby inhibiting their action and reducing their
These changes are reversible in that they can be repaired if
numbers.
the offending forces are removed. However, persistent trauma
In addition, in patients with rapidly progressing diseases
from occlusion results in funnel-shaped widening of the
(eg, aggressive periodontitis), bacterial microcolonies or single
crestal portion of the periodontal ligament with resorption of
bacterial cells have been found between collagen fibers and
the adjacent bone. These changes, which may cause the bony
over the bone surface, which suggests a direct effect.
crest to have an angular shape, represent adaptation of the
Several host factors released by inflammatory cells are capa-
periodontal tissues aimed at "cushioning" increased occlusal
ble of inducing bone resorption in vitro, and they play a role
forces; however, the modified bone shape may weaken tooth
in periodontal disease. These include host-produced prosta-
glandins and their precursors, interleukin-la, interleukin-p, support and cause tooth mobility
When it is combined with inflammation, trauma from
and tumor necrosis factor-a.
occlusion aggravates the bone destruction caused by the
When injected intradermally, prostaglandin E2 induces
inflammation and results in bizarre bone patterns.
the vascular changes that are seen with inflammation; when
injected over a bone surface, prostaglandin E2 induces bone
resorption in the absence of inflammatory cells, with few Bone Destruction Caused
multinucleated osteoclasts, In addition, nonsteroidal antiin-
flammatory drugs (eg, flurbiprofen, ibuprofen) inhibit prosta-
by Systemic Disorders
glandin E2 production, thereby slowing bone loss in naturally Local and systemic factors regulate the physiologic equilib-
occurring periodontal disease in beagle dogs and humans. rium of bone. When a generalized tendency toward bone
This effect occurs without changes in gingival inflammation, resorption exists, bone loss initiated by local inflammatory
and it rebounds 6 months after the cessation of drug admin- processes may be magnified.
istration. This systemic influence on the response of alveolar bone,
as envisioned by Glickman during the early 1950s, consid-
ers a systemic regulatory influence in all cases of periodontal
Bone Formation in Periodontal Disease
disease. In addition to the virulence of plaque bacteria, the
Areas of bone formation are also found immediately adjacent nature of the systemic component rather than its presence or
to sites of active bone resorption and along trabecular surfaces absence influences the severity of the periodontal destruction.
at a distance from the inflammation in an apparent effort to This was called the bone factor concept. This concept of a role
reinforce the remaining bone (ie, buttressing bone formation). played by systemic defense mechanisms has been validated
This osteogenic response is clearly found in experimentally by the studies of immune deficiencies and host modulation in
produced periodontal bone loss in animals. In humans, it is severely destructive types of periodontitis
less obvious, but it has been confirmed by histometric and In recent years, interest has increased in the possible rela-
histologic studies. tionship between periodontal bone loss and osteoporosis.
Autopsy specimens from individuals with untreated dis- Osteoporosis is a physiologic condition of postmenopausal
ease occasionally show areas in which bone resorption has women that results in the loss of bone mineral content as well
ceased and new bone is being formed on previously eroded as structural bone changes. Periodontitis and osteoporosis
bone margins. This confirms the intermittent character of share a number of risk factors (eg, aging, smoking, certain
diseases, medications that interfere with healing). Some stud- Exostoses

ies show a relationship between skeletal density and oral bone
density; between crestal height and residual ridge resorption; Exostoses are outgrowths of bone of varied size and shape.
and between osteopenia and periodontitis, tooth mobility, and Palatal exostoses have been found in 40% of human skulls.
tooth loss. They can occur as small nodules, large nodules, sharp ridges,
Periodontal bone loss may also occur with generalized spikelike projections, or any combination of these (Fig. 20.10 A
skeletal disturbances (eg, hyperparathyroidism, leukemia, and B). Exostoses have been described in rare cases as develop-
histiocytosis X) via mechanisms that may be totally unrelated ing after the placement of free gingival grafts.
to the usual periodontal problem.
Trauma From Occlusion
Factors Determining Bone Trauma from occlusion may be a factor in determining the
dimension and shape of bone deformities. It may cause a
Morphology in Periodontal Disease thickening of the cervical margin of alveolar bone or a change
in bone morphology (eg, angular defects, buttressing bone)
Normal Variation in Alveolar Bone
on which inflammatory changes will later be superimposed.
Considerable normal variation exists within the morphologic
features of alveolar bone, and this affects the osseous contours Buttressing Bone Formation
produced by periodontal disease. The anatomic features that
substantially affect the bone-destructive pattern of periodon- Bone formation sometimes occurs in an attempt to buttress
tal disease include the following: bony trabeculae that are weakened by resorption. When it
occurs within the jaw, it is termed central buttressing bone forma-
• thickness, width, and crestal angulation of the interdental
tion. When it occurs on the external surface, it is referred to as
septa
peripheral buttressing bone formation. The latter may cause bulg-
• thickness of the facial and lingual alveolar plate
ing of the bone contour, which sometimes accompanies the
• presence of fenestrations and dehiscences
production of osseous craters and angular defects (Fig. 20.11).
• alignment of the teeth
• root and root trunk anatomy
• root position within the alveolar process Food Impaction
• proximity with another tooth surface.
Interdental bone defects often occur where proximal contact is
For example, angular osseous defects cannot form in thin abnormal or absent. Pressure and irritation from food impac-
facial or lingual alveolar plates, which have little or no cancel- tion contribute to the inverted bone architecture. In some
lous bone between the outer and inner cortical layers. In such cases, the poor proximal relationship may result from a shift
cases, the entire crest of the plate is destroyed and the height in tooth position as a result of extensive bone destruction that
of the bone is reduced (Fig. 20.9). precedes food impaction. In such patients, food impaction is
.&. I
,,,. (I
I I
I
I ,,
I '
'
I I
D.
I
(B) (C)
FIGURE 20.9 A, Lower incisor with thin labial bone. Bone loss can become vertical only when it reaches thicker bone in apical areas. B, Upper
molars with thin facial bone where only horizontal bone loss can occur. C, Upper molar with a thick facial bone that allows for vertical bone loss.
FIGURE 20.10 A, Exostosis in the facial aspect of the upper second premolar and molars. B, Exostosis in the palatal aspect of the first and second
molars. Note also the circumferential defect in the second molar (left).
Horizontal Bone Loss

Horizontal bone loss is the most common pattern of bone
loss in periodontal disease. The bone is reduced in height,
but the bone margin remains approximately perpendicular to
the tooth surface. The interdental septa and the facial and lin-
gual plates are affected but not necessarily to an equal degree
around the same tooth (Fig. 20 12A).
Bone Deformities (Osseous Defects)

Different types of bone deformities can result from periodon-
tal disease. These usually occur in adults, but they have also
been reported in human skulls with deciduous dentitions.
Their presence may be suggested on radiographs, but care-
ful probing and surgical exposure of the areas are required to
determine their exact conformation and dimensions.
Vertical or Angular Defects

Vertical or angular defects are those that occur in an oblique
direction, leaving a hollowed-out trough in the bone along-
side the root; the base of the defect is located apical to the
FIGURE 20.11 Lipping of facial bone. There is a peripheral buttressing surrounding bone (Figs. 20.12B, 20.13, and 20 14). In most
bone formation along the external surface of the facial bony plate and
at the crest. Note the deformity in the bone produced by the buttressing
instances, angular defects have accompanying infrabony peri-
bone formation and the bulging of the mucosa. odontal pockets; infrabony pockets, on the other hand, must
always have an underlying angular defect.
Goldman and Cohen classified angular defects on the basis
a complicating factor rather than the cause of the bone defect. of the number of osseous walls. Angular defects may have
Food impaction can be vertical-due to occlusal forces or one, two, or three walls (Figs. 20.15-20.18). The number of
lateral-due to pressure from the lips, cheeks, and tongue. walls in the apical portion of the defect is often greater than
that in its occlusal portion, in which case the term combined
Aggressive Periodontitis osseous defect is used (Fig. 20.19).
Vertical defects that occur interdentally can generally be
A vertical or angular pattern of alveolar bone destruction is seen on the radiograph although thick, bony plates may
found around the first molars in aggressive periodontitis. The sometimes obscure them. Angular defects can also appear on
cause of the localized bone destruction with this type of peri- facial and lingual or palatal surfaces, but these defects are not
odontal disease is unknown. seen on radiographs. Surgical exposure is the only sure way to
determine the presence and configuration of vertical osseous
Bone Destruction Patterns defects.
Vertical defects increase with age. Approximately 60% of
in Periodontal Disease persons with interdental angular defects have only a single
Periodontal disease alters the morphologic features of the defect. Vertical defects detected radiographically have been
bone in addition to reducing bone height. An understanding reported to appear most often on the distal and mesial sur-
of the nature and pathogenesis of these alterations is essential faces. However, three-wall defects are more frequently found
for effective diagnosis and treatment. on the mesial surfaces of the upper and lower molars.
FIGURE 20.12 A, Horizontal bone loss. Note the reduction in height of the marginal bone that exposes cancellous bone and reaches the furcation
of the second molar. B, Vertical (angular) bone loss on the distal root of the first molar.
FIGURE 20.16 Horizontal section of the lower molars at the midroot

level showing a two-wall osseous defect distal to second molar.
FIGURE 20.13 Angular (vertical) defects of different depths.
FIGURE 20.17 One-wall vertical defect on the mesial surface of the

lower first molar.
FIGURE 20.14 Angular defect on the mesial surface of the first molar.
Note also the furcation involvement. one-third (35.2%) of all defects and about two-third (62%) of
all mandibular defects and to occur twice as often in posterior
segments as in anterior segments.
Osseous Craters The heights of the facial and lingual crests of a crater have
Osseous craters are concavities in the crest of the interden- been found to be identical in 85% of cases, with the remaining
tal bone that is confined within the facial and lingual walls 15% being almost equally divided between higher facial crests
(Fig. 20.20). Craters have been found to make up about and higher lingual crests.
(A) (B) (C)

2 2
FIGURE 20.15 One-, two-, and three-walled vertical defects on the right lateral incisor. A, Three bony walls: distal ( 1 ), lingual (2), and facial (3).
B, Two-wall defect: distal (1) and lingual (2). C, One-wall defect: distal wall only (1).
FIGURE 20.18 Circumferential vertical defect in relation to the up-

per premolar. FIGURE 20.21 Reversed architecture. The elevated flap shows the
irregular bone margin.
I
I/ I
,£---
FIGURE 20.19 Combined type of osseous defect. Since the facial

wall is half the height of the distal (1) and lingual (2) walls, this is an
osseous defect with three walls in its apical half and two walls in its
FIGURE 20.22 Ledge produced by interproximal resorption.
occlusal half.
Reversed Architecture
Reversed architecture defects are produced by a loss of inter-
dental bone, including the facial plates and the lingual plates,
without a concomitant loss of radicular bone, thereby revers-
ing the normal architecture (Fig. 20.21). This mostly occurs
in necrotizing ulcerative periodontitis and are more common
in the maxilla.
Ledges
Ledges are plateau like bone margins that are caused by the
resorption of thickened bony plates (Fig. 20.22).
FIGURE 20.20 Diagrammatic representation of an osseous crater in
a faciolingual section between two lower molars. Left, Normal bone Furcation Involvement
contour. Right, Osseous crater.
The term furcation involvement refers to the invasion of the
bifurcation and trifurcation of multirooted teeth by periodon-
The following reasons for the high frequency of interdental
tal disease. The prevalence of furcation-involved molars is not
craters have been suggested:
clear. Although some reports indicate that the mandibular first
• The interdental area collects plaque and is difficult to clean. molars are the most common sites and that the maxillary pre-
• The normal flat or even slightly concave faciolingual shape molars are the least common, other studies have found higher
of the interdental septum in the lower molars may favor prevalence in the upper molars. The number of furcation
crater formation. involvements increases with age.
• Vascular patterns from the gingiva to the center of the crest The denuded furcation may be visible clinically or covered
may provide a pathway for inflammation. by the wall of the pocket. The extent of involvement is deter-
mined by exploration with a blunt probe, along with a simulta-
neous blast of warm air to facilitate visualization (Fig. 20.23).
Bulbous Bone Contours
Furcation involvements have been classified as grades I
Bulbous bone contours are bony enlargements that are caused through IV according to the amount of tissue destruction.
by exostoses (Fig. 20 .10), adaptation to function, or buttress- Grade I involves incipient bone loss; grade II involves par-
ing bone formation. They are found more frequently in the tial bone loss (cul-de-sac); and grade III involves total bone
maxilla than in the mandible. loss with a through-and-through opening of the furcation.
FIGURE 20.24 Different degrees of furcation involvement in a human

autopsy specimen. Furcation involvement is found in all three molars,
with an advanced lesion in the second molar and an extremely severe
lesion in the first molar that is exposing almost the entire mesial root.
loss around each individual root may be horizontal or angu-

lar, and frequently a crater develops in the interradicular
area (Fig. 20.25). Probing to determine the presence of these
destructive patterns must be done horizontally and vertically
around each involved root and in the crater area to establish
the depth of the vertical component.
Furcation involvement is a stage of progressive periodontal
FIGURE 20.23 A, A molar with slightly inflamed gingiva that is seen disease, and it has its same etiology. The difficulty and some-
clinically; however, it has a deep distal pocket. B, Flap elevation reveals
extensive bone loss and furcation involvement. (Courtesy Dr Terry Fiori,
times the impossibility of controlling plaque in furcations are
Palo Alto, CA.) responsible for the presence of extensive lesions in this area.
The role of trauma from occlusion in the etiology of furca-
tion lesions is controversial. Some assign a key role to trauma,
Grade IV is similar to grade Ill but includes gingival recession thinking that furcation areas are most sensitive to injury from
that exposes the furcation to view. excessive occlusal forces. Others deny the initiating effect of
Microscopically, furcation involvement presents no unique trauma and consider that inflammation and edema caused by
pathologic features. It is simply a phase in the rootward extension plaque in the furcation area tend to extrude the tooth, which
of the periodontal pocket. During its early stages, a widening of then becomes traumatized and sensitive.
the periodontal space occurs with cellular and fluid inflamma- Other factors that may play a role are the presence of
tory exudation, and this is followed by epithelial proliferation enamel projections into the furcation, which occurs in about
into the furcation area from an adjoining periodontal pocket. 13% of multirooted teeth, and the proximity of the furcation
Extension of the inflammation into the bone leads to resorption to the cementoenamel junction, which occurs in about 75% of
and a reduction in bone height. The bone-destructive pattern cases of furcation involvement.
may produce horizontal loss, or angular osseous defects associ- The presence of accessory pulpal canals in the furcation
ated with intrabony pockets may exist (Fig. 20.24). Plaque, cal- area may extend pulpal inflammation to the furcation. This
culus, and bacterial debris occupy the denuded furcation space. possibility should be carefully explored, particularly when
The destructive pattern of a furcation involvement varies mesial and distal bone retains its normal height. Accessory
in different cases and with the degree of involvement. Bone canals that connect the pulp chamber floor to the furcation
FIGURE 20.25 A, Photograph and, B, radiograph of different degrees of bone loss in a skull. There are furcation involvements in the first and second
molars; deep angular bone loss in the distal root of the first molar; and interradicular and interdental craters in the second molar and between the
second and third molars, respectively.
have been found in 36% of maxillary first molars, 12% of Glickman I: Inflammation and trauma from occlusion, co-destructive factors
maxillary second molars, 32 % of mandibular first molars, and in chronic periodontal disease,] Periodontal 34:5, 1963.
Goldman HM, Cohen OW: The intrabony pocket: classification and treat-
24% of mandibular second molars. ment,] Peliodontol 29:272, 1958.
The diagnosis of furcation involvement is made by clini- Goodson JM, Haffajee AD, Socransky SS: The relationship between attach-
cal examination and careful probing with a specially designed ment level loss and alveolar bone loss,] Clin Peliodontol 11:348, 1984.
probe. Radiographic examination of the area is helpful, but Heijl L, Rifkin BR, Zander HA: Conversion of chronic gingivitis to periodon-
titis in squirrel monkeys,] Periodontol 47:710, 1976.
lesions can be obscured by the angulation of the beam and the Kronfeld R: Condition of alveolar bone underlying periodontal pockets,
radiopacity of neighboring structures. J Periodontal 6:22, 1935.
Lindhe J, Liljenberg B, Listgarten MA: Some microbiological and histo-
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20 Bone Loss and Patterns of Bone Destruction 219.el
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21
Periodontal Response to
External Forces
FA Carranza • DG Naik • A Uppoor
Chapter Outline
Adaptive Capacity of the Periodontium Reversibility of Traumatic Lesions
to Occlusal Forces Effects of Excessive Occlusal Forces on
Trauma From Occlusion Dental Pulp
Stages of Tissue Response to Increased Influence of Trauma From Occlusion on the
Occlusal Forces Progression of Marginal Periodontitis
Effects of Insufficient Occlusal Force Pathologic Tooth Migration
Adaptive Capacity of the Periodontium injury is called a traumatic occlusion. Excessive occlusal forces
may also disrupt the function of the masticatory musculature
to Occlusal Forces and cause painful spasms, injure the temporomandibular
The periodontium attempts to accommodate the forces ex- joints, or produce excessive tooth wear. However, the term
erted on the crown. This adaptive capacity varies in different trauma from occlusion is generally used in connection with in-
persons and in the same person at different times. The effect jury in the periodontium.
of occlusal forces on the periodontium is influenced by the The criterion that determines if an occlusion is traumatic
magnitude, direction, duration, and frequency of the forces. is whether it produces periodontal injury; this criterion is not
When the magnitude of occlusal forces is increased, the peri- how the teeth occlude. Any occlusion that produces peri-
odontium responds with a widening of the periodontal liga- odontal injury is traumatic. Malocclusion is not necessary
ment space, an increase in the number and width of periodontal to produce trauma; periodontal injury may occur when the
ligament fibers and an increase in the density of alveolar bone. occlusion appears normal. The dentition may be anatomi-
Changing the direction of occlusal forces causes a reori- cally and aesthetically acceptable but functionally injurious.
entation of the stresses and strains within the periodontium Similarly, not all malocclusions are necessarily injurious to the
(Fig. 21.1) The principal fibers of the periodontal ligament periodontium. Traumatic occlusal relationships are referred to
are arranged so that they best accommodate occlusal forces by terms such as occlusal disharmony,functional imbalance, and
along the long axis of the tooth. Lateral (horizontal) and torque occlusal dystrophy. These terms refer to the effect of the occlu-
(rotational) forces are more likely to injure the periodontium. sion on the periodontium rather than to the position of the
The response of alveolar bone is also affected by the du- teeth. Since trauma from occlusion refers to the tissue injury
ration and frequency of occlusal forces. Constant pressure on rather than the occlusion, an increased occlusal force is not
the bone is more injurious than intermittent forces. The more traumatic if the periodontium can accommodate it.
frequent the application of an intermittent force, the more in-
jurious the force is to the periodontium.
Acute and Chronic Trauma
Trauma From Occlusion Trauma from occlusion may be acute or chronic. Acute trauma
from occlusion results from an abrupt occlusal impact such as
An inherent "margin of safety" that is common to all tissues that produced by biting on a hard object (eg, olive pit). Res-
permits some variation in occlusion without adversely affect- torations or prosthetic appliances that interfere with or alter
ing the periodontium. However, when occlusal forces exceed the direction of occlusal forces on the teeth may also induce
the adaptive capacity of the tissues, tissue injury results. The acute trauma.
resultant injury is termed trauma from occlusion, which is also Acute trauma results in tooth pain, sensitivity to percussion,
known as traumatism or occlusal trauma. and increased tooth mobility If the force is dissipated by a shift
Thus, trauma from occlusion refers to the tissue injury rath- in the position of the tooth or by the wearing away or correc-
er than the occlusal force. An occlusion that produces such an tion of the restoration, then the injury heals, and the symptoms
221
of the tissues to resist the occlusal forces, it is known as sec-

ondary trauma from occlusion.
Primary trauma from occlusion occurs if trauma from occlu-
sion is considered the primary etiologic factor in periodontal
destruction and if the only local alteration to which a tooth is
subjected is a result of occlusion. Examples include periodon-
tal injury produced around teeth with a previously healthy
periodontium after the following: (1) the insertion of a "high
filling"; (2) the insertion of a prosthetic replacement that cre-
ates excessive forces on abutment and antagonistic teeth; (3)
the drifting movement or extrusion of the teeth into spaces
created by unreplaced missing teeth; or ( 4) the orthodontic
movement of teeth into functionally unacceptable positions.
Most studies of the effect of trauma from occlusion involv-
ing experimental animals have examined the primary type of
FIGURE 21.1 Stress patterns around the roots changed by shifting trauma. Changes produced by primary trauma do not alter
the direction of occlusal forces (experimental model using photoelas- the level of connective tissue attachment and do not initiate
tic analysis). A, Buccal view of an ivorine molar subjected to an axial pocket formation. This is probably because the supracrestal
force. The shaded fringes indicate that the internal stresses are at the root
apices. B, Buccal view of an ivorine molar subjected to a mesial tilting
gingival fibers are not affected and therefore prevent the apical
force. The shaded fringes indicate that the internal stresses are along the migration of the junctional epithelium.
mesial surface and at the apex of the mesial root. Secondary trauma from occlusion occurs when the adaptive
capacity of the tissues to withstand occlusal forces is impaired
subside. Otherwise, periodontal injury may worsen and de- by bone loss that results from marginal inflammation. This re-
velop into necrosis accompanied by periodontal abscess for- duces the periodontal attachment area and alters the leverage
mation, or it may persist as a symptom-free chronic condition. on the remaining tissues. The periodontium becomes more
Acute trauma can also produce cementum tears (Fig. 21.2) vulnerable to injury, and previously well-tolerated occlusal
Chronic trauma from occlusion is more common than the forces become traumatic.
acute form, and it is of greater clinical significance. It most of- Figure 21.3 depicts three different situations on which ex-
ten develops from gradual changes in occlusion produced by cessive occlusal forces can be superimposed:
tooth wear, drifting movement, and extrusion of the teeth in 1. Normal periodontium with normal height of bone
combination with parafunctional habits (eg, bruxism, clench- 2. Normal periodontium with reduced height of bone
ing) rather than as a sequela of acute periodontal trauma. 3. Marginal periodontitis with reduced height of bone
Chronic TFO is further classified as primary and secondary
The first case is an example of primary trauma from occlu-
sion, whereas the last two represent secondary trauma from
Primary and Secondary Trauma occlusion. The effects of trauma from occlusion in these differ-
From Occlusion ent situations are analyzed in the following discussion.
It has been found in experimental animals that systemic
Trauma from occlusion may be caused by alterations in oc-
disorders can reduce tissue resistance and that previously tol-
clusal forces, a reduced capacity of the periodontium to with-
erable forces may become excessive. This could theoretically
stand occlusal forces, or both. When trauma from occlusion is
represent another mechanism by which tissue resistance to
the result of alterations in occlusal forces, it is called primary
increased forces is lowered, thereby resulting in secondary
trauma from occlusion. When it results from the reduced ability
trauma from occlusion.
Stages of Tissue Response to

Increased Occlusal Forces
Tissue response occurs in three stages: injury, repair, and
adaptive remodeling of the periodontium.
(A) (B) (C)

FIGURE 21.2 Cementa! tear, presumably caused by acute trauma
from occlusion in a human autopsy specimen. Note the repair process FIGURE 21.3 Traumatic forces can occur on, A, normal periodonti-
depositing bone on the displaced, torn cementum and recreating a peri- um with normal height of bone; B, normal periodontium with reduced
odontal ligament. height of bone; or C, marginal periodontitis with reduced height of bone.
21 Periodontal Response to External Forces 223
Stage I: Injury disintegration of the blood vessel walls and release of the con-
tents into the surrounding tissue occur. In addition, increased
Tissue injury is produced by excessive occlusal forces. The resorption of alveolar bone and resorption of the tooth surface
body then attempts to repair the injury and restore the peri- occur.
odontium. This can occur if the forces are diminished or if the Severe tension causes widening of the periodontal ligament,
tooth drifts away from them. If the offending force is chronic, thrombosis, hemorrhage, tearing of the periodontal ligament,
however, the periodontium is remodeled to cushion its im- and resorption of alveolar bone.
pact. The ligament is widened at the expense of the bone, Pressure severe enough to force the root against bone causes
which results in angular bone defects without periodontal necrosis of the periodontal ligament and bone. The bone is re-
pockets, and the tooth becomes loose. sorbed from viable periodontal ligament adjacent to necrotic
Under the forces of occlusion, a tooth rotates around a areas and from marrow spaces; this process is called undermin-
fulcrum or axis of rotation, which in single-rooted teeth is ing resorption.
located in the junction between the middle third and the api- The areas of the periodontium that are most susceptible to
cal third of the clinical root and in multirooted teeth in the injury from excessive occlusal forces are the furcations.
middle of the interradicular bone. This creates areas of pres- Injury to the periodontium produces a temporary depres-
sure and tension on opposite sides of the fulcrum (Fig. 21.4). sion in mitotic activity, in the rate of proliferation and dif-
Different lesions are produced by different degrees of pressure ferentiation of fibroblasts, in collagen formation, and in bone
and tension. If jiggling forces are exerted, these different le- formation. These return to normal levels after the dissipation
sions may coexist in the same area. of the forces.
Slightly excessive pressure stimulates resorption of the al-
veolar bone, with a resultant widening of the periodontal
ligament space. Slightly excessive tension causes elongation of Stage II: Repair
the periodontal ligament fibers and the apposition of alveo- Repair occurs constantly in the normal periodontium,
lar bone. In areas of increased pressure, the blood vessels are and trauma from occlusion stimulates increased repara-
numerous and reduced in size; in areas of increased tension, tive activity.
they are enlarged. The damaged tissues are removed, and new connective tis-
Greater pressure produces a gradation of changes in the sue cells and fibers, bone, and cementum are formed in an at-
periodontal ligament, starting with compression of the fibers, tempt to restore the injured periodontium (Fig. 21. 5). Forces
which produces areas of hyalinization. Subsequent injury to remain traumatic only as long as the damage produced ex-
the fibroblasts and other connective tissue cells leads to ne- ceeds the reparative capacity of the tissues.
crosis of areas of the ligament. Vascular changes are also pro- When bone is resorbed by excessive occlusal forces, the
duced: within 30 min, impairment and stasis of blood flow body attempts to reinforce the thinned bony trabeculae with
occur; at 2-3 h, blood vessels appear to be packed with eryth- new bone (Fig. 21.6). This attempt to compensate for lost
rocytes, which start to fragment; and between 1 and 7 days, bone is called buttressing bone formation, and it is an important
feature of the reparative process associated with trauma from
FIGURE 21.4 Areas of tension and pressure in opposite sites of the FIGURE 21.5 Experimental occlusal trauma in rats. Note the area of
periodontal ligament caused by experimentally induced orthodontic necrosis of the marginal periodontal ligament and resorption and re-
movement in a rat molar. modeling in the more apical periodontal sites.
Cartilage-like material sometimes develops in the peri-

odontal ligament space as an aftermath of the trauma. The
formation of crystals from erythrocytes has also been dem-
onstrated.
Stage Ill: Adaptive Remodeling of the

Periodontium
If the repair process cannot keep pace with the destruction
caused by the occlusion, the periodontium is remodeled in an
effort to create a structural relationship in which the forces are
no longer injurious to the tissues. This results in a widened peri-
odontal ligament, which is funnel shaped at the crest, and angular
defects in the bone, with no pocket formation. The involved teeth
become loose. Increased vascularization has also been reported.
FIGURE 21.6 Apical area of a premolar subjected to experimental
The three stages in the evolution of traumatic lesions have
occlusal trauma in a dog causing intrusion of the tooth and areas of
necrosis in the periodontal ligament. Note the active bone formation been differentiated histometrically by the relative amounts of
on the outer aspect of the bone and the resorptive activity in the periph- periodontal bone surface undergoing resorption or formation
ery of the necrotic site. (Fig. 21.8). The injury phase shows an increase in areas of re-
sorption and a decrease in bone formation, whereas the repair
phase demonstrates decreased resorption and increased bone
occlusion. It also occurs when bone is destroyed by inflamma- formation. After adaptive remodeling of the periodontium, re-
tion or osteolytic tumors. sorption and formation return to normal.
Buttressing bone formation occurs within the jaw (central
buttressing) and on the bone surface (peripheral buttress-
ing). During central buttressing, the endosteal cells deposit
Effects of Insufficient Occlusal Force
new bone, which restores the bony trabeculae and reduces Insufficient occlusal force may also be injurious to the sup-
the size of the marrow spaces. Peripheral buttressing occurs on porting periodontal tissues. Insufficient stimulation causes
the facial and lingual surfaces of the alveolar plate. Depending thinning of the periodontal ligament, atrophy of the fibers,
on its severity, peripheral buttressing may produce a shelf-like osteoporosis of the alveolar bone, and a reduction in bone
thickening of the alveolar margin, which is referred to as lip- height. Hypofunction can result from an open-bite relation-
ping (Fig. 21. 7), or a pronounced bulge in the contour of the ship, an absence of functional antagonists, or unilateral chew-
facial and lingual bone. ing habits that neglect one side of the mouth.
FIGURE 21.7 A, Widening of the periodontal ligament space in the cervical area and a change in the shape of the marginal alveolar bone as a result
of chronic prolonged trauma from occlusion in rats. B, Comparable changes in the shape of the marginal bone found in a human autopsy case.
Normal Injury Repair Adaptation the mechanisms by which trauma from occlusion may affect
- - -1- - - - , - - - - -1- - - periodontal disease.
~i~iWi~
Initial studies involved the placement of high crowns or
restorations on the teeth of dogs or monkeys, thereby result-
ing in a continuous or intermittent force in one direction.
These investigations provided an orthodontic type of force
and gave clear descriptions of changes that were occurring in
pressure zones and tension zones. These procedures usually
resulted in tooth displacement and consolidation in a new,
nontraumatized position.
Trauma from occlusion in humans, however, is the result of
forces that act alternatively in opposing directions. These were
analyzed in experimental animals with 'Jiggling forces," which
were usually produced by a high crown in combination with
an orthodontic appliance that would bring the traumatized
tooth back to its original position when the force was dissi-
1 7 14 28 60 120 pated by separating the teeth. With another method, the teeth
Days were separated by wooden or elastic material wedged inter-
proximally to displace a tooth toward the opposite proximal
FIGURE 21.8 Evolution of traumatic lesions as depicted experimen-
tally in rats by variations in relative amounts of areas of bone forma- side. After 48 h, the wedge was removed, and the procedure
tion and bone resorption in periodontal bone surfaces. The horizontal was repeated on the opposite side.
axis shows the number of days after the initiation of traumatic interfer- These studies resulted in a combination of changes pro-
ence. The vertical axis shows the percentage of bone surface undergoing duced by pressure and tension on both sides of the tooth,
resorption or formation. The stages in the evolution of the lesions are
represented in the top drawings, which show the average amount of
with an increase in the width of the ligament and increased
bone activity for each group. tooth mobility. None of these methods caused gingival inflam-
mation or pocket formation, and the results essentially repre-
sented different degrees of functional adaptation to increased
Reversibility of Traumatic Lesions forces.
To mimic the problem in humans more closely, studies
Trauma from occlusion is reversible. When trauma is artifi- were then conducted on the effect produced by jiggling trau-
cially induced in experimental animals, the teeth move away ma and simultaneous plaque-induced gingival inflammation.
or intrude into the jaw. When the impact of the artificially The accumulation of bacterial plaque that initiates gingivi-
created force is relieved, the tissues undergo repair. Although tis and results in periodontal pocket formation affects the mar-
trauma from occlusion is reversible under such conditions, it ginal gingiva, but trauma from occlusion occurs in the sup-
does not always correct itself, and therefore it is not always porting tissues and does not affect the gingiva (Fig. 21. 9). The
temporary or of limited clinical significance. The injurious marginal gingiva is unaffected by trauma from occlusion be-
force must be relieved for repair to occur. If conditions in hu- cause its blood supply is not affected even when the vessels of
mans do not permit the teeth to escape from or adapt to exces- the periodontal ligament are obliterated by excessive occlusal
sive occlusal force, periodontal damage persists and worsens. forces. It has been repeatedly proved that trauma from occlu-
The presence of inflammation in the periodontium as a re- sion does not cause pockets or gingivitis and that it also does
sult of plaque accumulation may impair the reversibility of not increase gingival fluid flow. Furthermore, experimental
traumatic lesions. trauma in dogs does not influence the bacterial repopulation
of pockets after scaling and root planing. However, mobile
Effects of Excessive Occlusal Forces teeth in humans harbor significantly higher proportions of
on Dental Pulp Force
The effects of excessive occlusal forces on the dental pulp
have not been established. Some clinicians report the disap-
pearance of pulpal symptoms after the correction of excessive
occlusal forces. Pulpal reactions have been noted in animals
subjected to increased occlusal forces, but these did not oc-
cur when the forces were minimal and occurred over short
0 Host-parasite-
reaction
periods.
~ Trauma from
occlusion
Influence of Trauma From Occlusion
on the Progression of Marginal
Periodon ti tis
The clinical impressions of early investigators and clinicians
assigned an important role to trauma from occlusion in the FIGURE 21.9 The reaction between dental plaque and the host
etiology of periodontal lesions. Since then, numerous stud- takes place in the gingival sulcus region. Trauma from occlusion ap-
ies have been performed that have attempted to determine pears in the tissues that are supporting the tooth.
Campylobacter rectus and Peptostreptococcus micros than non- area, which results in the transformation of a suprabony
mobile teeth. pocket into an intrabony pocket.
As long as inflammation is confined to the gingiva, the in- • Increased mobility of traumatically loosened teeth may
flammatory process is not affected by occlusal forces. When have a pumping effect on plaque metabolites, thereby in-
inflammation extends from the gingiva into the supporting creasing their diffusion.
periodontal tissues (ie, when gingivitis becomes periodonti-
tis), plaque-induced inflammation enters the zone that is in-
fluenced by occlusion, which Glickman has called the zone of Clinical and Radiographic Signs of Trauma
codestruction. From Occlusion Alone
Two groups have studied this topic experimentally, with
conflicting results, probably because of the different methods The most common clinical sign of trauma to the periodon-
tium is progressive tooth mobility. During the injury stage of
used. The Eastman Dental Center group in Rochester, NY, used
trauma from occlusion, the destruction of periodontal fibers
squirrel monkeys, produced trauma by repetitive interdental
occurs, which increases tooth mobility. During the final stage,
wedging, and added mild to moderate gingival inflammation;
the accommodation of the periodontium to increased forces
experimental times were up to 10 weeks. They reported that
entails a widening of the periodontal ligament, which also
the presence of trauma did not increase the loss of attach-
ment induced by periodontitis. The University of Gothenburg leads to increased tooth mobility. Although this tooth mobil-
ity is greater than the so-called normal mobility, it cannot be
group in Sweden used beagle dogs, produced trauma by plac-
considered pathologic, because it is an adaptation and not a
ing cap splints and orthodontic appliances, and induced se-
disease process. If it does become progressively worse, it can
vere gingival inflammation; experimental times were up to
then be considered pathologic.
1 year. This group found that occlusal stresses increase the
Other causes of increased tooth mobility include advanced
periodontal destruction induced by periodontitis.
When trauma from occlusion is eliminated, a substantial bone loss, inflammation of the periodontal ligament of peri-
odontal or periapical origin, and some systemic causes (eg,
reversal of bone loss occurs, except in the presence of peri-
pregnancy). The destruction of surrounding alveolar bone,
odontitis. This indicates that inflammation inhibits the po-
such as occurs with osteomyelitis or jaw tumors, may also
tential for bone regeneration. Thus, it is important to eliminate
increase tooth mobility.
the marginal inflammatory component in cases of trauma from
Radiographic signs of trauma from occlusion may include
occlusion, because the presence of inflammation affects bone regen-
eration after the removal of the traumatizing contacts. It has also the following:
been shown in experimental animals that trauma from occlu- 1. Increased width of the periodontal space, often with thick-
sion does not induce progressive destruction of the periodon- ening of the lamina dura along the lateral aspect of the
tal tissues in regions that are kept healthy after the elimination root, in the apical region, and in bifurcation areas. These
of preexisting periodontitis. changes do not necessarily indicate destructive changes,
Trauma from occlusion also tends to change the shape of because they may result from thickening and strengthen-
the alveolar crest. The change in shape consists of a widening ing of the periodontal ligament and alveolar bone, thereby
of the marginal periodontal ligament space, a narrowing of constituting a favorable response to increased occlusal
the interproximal alveolar bone, and a shelf-like thickening of forces.
the alveolar margin. Therefore, although trauma from occlu- 2. A "vertical" rather than "horizontal" destruction of the in-
sion does not alter the inflammatory process, it changes the terdental septum.
architecture of the area around the inflamed site. Thus, in the 3. Radiolucency and condensation of the alveolar bone.
absence of inflammation, the response to trauma from occlusion is 4. Root resorption.
limited to adaptation to the increased forces. In the presence of in-
In summary, trauma from occlusion does not initiate gingi-
flammation, however, the changes in the shape of the alveolar crest
vitis or periodontal pockets, but it may constitute an addition-
may be conducive to angular bone loss, and existing pockets may
al risk factor for the progression and severity of the disease.
become intrabony.
An understanding of the effect of trauma from occlusion on
Other theories that have been proposed to explain the in-
teraction of trauma and inflammation include the following: the periodontium is useful during the clinical management of
periodontal problems.
• Trauma from occlusion may alter the pathway of the ex-
tension of gingival inflammation to the underlying tissues.
This may be favored by the reduced collagen density and
Pathologic Tooth Migration
the increased number of leukocytes, osteoclasts, and blood Pathologic migration refers to tooth displacement that results
vessels in the coronal portion of increasingly mobile teeth. when the balance among the factors that maintain physiologic
Inflammation may then proceed to the periodontal liga- tooth position is disturbed by periodontal disease. Pathologic
ment rather than to the bone. Resulting bone loss would be migration is relatively common. It may be an early sign of dis-
angular, and pockets could become intrabony. ease, or it may occur in association with gingival inflammation
• Trauma-induced areas of root resorption uncovered by api- and pocket formation as the disease progresses.
cal migration of the inflamed gingival attachment may offer Pathologic migration occurs most frequently in the anterior
a favorable environment for the formation and attachment region, but posterior teeth may also be affected. The teeth may
of plaque and calculus and therefore may be responsible for move in any direction, and the migration is usually accom-
the development of deeper lesions. panied by mobility and rotation. Pathologic migration in the
• Supragingival plaque can become subgingival if the tooth occlusal or incisal direction is termed extrusion. All degrees
is tilted orthodontically or if it migrates into an edentulous of pathologic migration are encountered, and one or more
FIGURE 21.10 Labial migration of the maxillary central incisors, especially the right incisor. A, Frontal view; B, lateral view.
teeth may be affected (Fig. 21 10). It is important to detect during mastication, and the proliferating granulation tissue
migration during its early stages and to prevent more serious provide the force.
involvement by eliminating the causative factors. Even during Pathologic migration is also an early sign of localized ag-
the early stage, some degree of bone loss occurs. gressive periodontitis. Weakened by the loss of periodontal
support, the maxillary and mandibular anterior incisors drift
labially and extrude, thereby creating diastemata between the
Pathogenesis
teeth.
Two major factors play a role in maintaining the normal posi-
tion of the teeth: the health and normal height of the periodon- Changes in the Forces Exerted on the Teeth
tal attachment apparatus and the forces exerted on the teeth. Changes in the magnitude, direction, or frequency of the forc-
The latter includes the forces of occlusion and pressure from es exerted on the teeth can induce the pathologic migration of
the lips, cheeks, and tongue. Factors that are important in rela- a tooth or group of teeth. These forces do not have to be ab-
tion to the forces of occlusion include the following: (1) tooth normal to cause migration if the periodontium is sufficiently
morphologic features and cuspal inclination; (2) the presence weakened. Changes in the forces may result from unreplaced
of a full complement of teeth; (3) a physiologic tendency to- missing teeth or other causes.
ward mesial migration; (4) the nature and location of contact
point relationships; (5) proximal, incisal, and occlusal attri- Unreplaced Missing Teeth. The drifting of teeth into the
tion; and (6) the axial inclination of the teeth. Alterations in spaces created by unreplaced missing teeth often occurs.
any of these factors start an interrelated sequence of changes Drifting differs from pathologic migration in that it does not
in the environment of a single tooth or group of teeth that may result from the destruction of the periodontal tissues. How-
result in pathologic migration. Thus, pathologic migration oc- ever, it usually creates conditions that lead to periodontal dis-
curs under conditions that weaken the periodontal support, ease, and thus the initial tooth movement is aggravated by a
that increase or modify the forces exerted on the teeth, or both. loss of periodontal support (Fig. 21 11)
Drifting generally occurs in a mesial direction in combi-
Weakened Periodontal Support nation with tilting or extrusion beyond the occlusal plane.
The inflammatory destruction of the periodontium in patients The premolars frequently drift distally (Fig. 21.12). Although
with periodontitis creates an imbalance between the forces
that maintain the tooth in position and the occlusal and mus-
cular forces the tooth ordinarily needs to bear. The tooth with
weakened support is unable to maintain its normal position
in the arch and moves away from the opposing force unless
it is restrained by proximal contact. The force that moves the
weakly supported tooth may be created by factors such as oc-
clusal contacts or pressure from the tongue.
It is important to understand that the abnormality of
pathologic migration rests with the weakened periodontium;
the force itself is not necessarily abnormal. Forces that are ac-
ceptable to an intact periodontium become injurious when
periodontal support is reduced as in the tooth with abnor-
mal proximal contacts. Abnormally located proximal contacts
convert the normal anterior component of force to a wedging
force that moves the tooth occlusally or incisally. The wedging
force, which can be withstood by the intact periodontium,
causes the tooth to extrude when the periodontal support is
weakened by disease. As its position changes, the tooth is sub-
jected to abnormal occlusal forces, which aggravate the periodontal
destruction and the tooth migration.
Pathologic migration may continue after a tooth no longer con- FIGURE 21.11 Calculus and bone loss on the mesial surface of a ca-
tacts its antagonist. Pressures from the tongue, the food bolus nine that has drifted distally.
FIGURE 21.12 Maxillary first molar that has tilted and extruded into
the space created by a missing mandibular tooth.
FIGURE 21.13 No drifting or extrusion is present here, despite 4

years' absence of the mandibular teeth.
drifting is a common sequela when missing teeth are not re- FIGURE 21.14 Examples of the mutilation of occlusion associated
placed, it does not always occur (Fig. 21.13). with unreplaced missing teeth. Note, A, pronounced pathologic migra-
tion; B, disturbed proximal contacts; and C, functional relationships with
closing of the bite.
Failure to Replace First Molars. The pattern of changes that
may follow the failure to replace missing first molars is charac-
teristic. In extreme cases, it consists of the following:
1. The second and third molars tilt mesially, which results in
a decrease in vertical dimension (Fig. 21.14).
2. The premolars move distally, and the mandibular incisors
tilt or drift lingually. While drifting distally, the mandibular
premolars lose their intercuspating relationship with the
maxillary teeth, and they may tilt distally.
3. Anterior overbite is increased. The mandibular incisors
strike the maxillary incisors near the gingiva or traumatize
the gingiva.
4. The maxillary incisors are pushed labially and laterally
(Fig. 21.15)
5. The anterior teeth extrude because the incisal apposition
has largely disappeared.
6. Diastemata are created by the separation of the anterior
teeth (Fig. 2114)
The disturbed proximal contact relationships lead to food
impaction, plaque accumulation that result in gingival inflam- FIGURE 21.15 Maxillary incisors pushed labially in a patient with bi-
mation and pocket formation, which are followed by bone lateral unreplaced mandibular molars. Note the extrusion of the maxi 1-
loss and tooth mobility. Occlusal disharmonies created by the lary molars.
FIGURE 21.16 Pathologic migration associated with tongue pressure. A, Facial view; B, palatal view.
altered tooth positions traumatize the supporting tissues of REFERENCES

the periodontium and aggravate the destruction caused by the References for this chapter are found on the companion
inflammation. The reduction in periodontal support leads to website www.medenact.com.
the further migration of the teeth and the mutilation of the
occlusion.
SUGGESTED READINGS
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22
Chronic Periodontitis and
N ecrotizing Ulcerative
Periodontitis
• FA Carranza • DG Naik • A Uppoor
Chapter Outline
Chronic Periodontitis Microscopic Findings
Clinical Features Etiology of Necrotizing Ulcerative
Risk Factors for Disease Periodontitis
Necrotizing Ulcerative Periodontitis Malnutrition
Clinical Features Conclusions
Chronic periodontitis is the most prevalent form of periodon- known factors (ie, microbiologic, immunologic, and genetic)
titis, and it generally demonstrates the characteristics of a involved in the pathology of chronic periodontitis.
slowly progressing inflammatory disease. However, systemic
and environmental factors (eg, diabetes mellitus, smoking)
may modify the host's immune response to the dental biofilm Clinical Features
so that periodontal destruction becomes more progressive.
General Characteristics
Although chronic periodontitis is most frequently observed in
adults, it can occur in children and adolescents in response to Characteristic clinical findings in patients with untreated
chronic plaque and calculus accumulation. chronic periodontitis include the following (Figs. 22.1-22.3):
Chronic periodontitis has been defined as "an infectious dis-
• Supragingival and subgingival plaque and calculus
ease resulting in inflammation within the supporting tissues of
• Gingival swelling, redness, and loss of gingival stippling
the teeth, progressive attachment loss, and bone loss." This def-
• Altered gingival margins (eg, rolled, flattened, cratered
inition outlines the major clinical and etiologic characteristics
papillae, recessions)
of the disease: (1) microbial biofilm formation (dental plaque);
• Pocket formation
(2) periodontal inflammation (eg, gingival swelling, bleeding
• Bleeding on probing
on probing); and (3) attachment as well as alveolar bone loss.
• Attachment loss (angular or horizontally)
In addition to the local immune response caused by the
• Bone loss
dental biofilm, periodontitis may also be associated with a
• Root furcation involvement (exposure)
number of systemic disorders and defined syndromes. In most
• Increased tooth mobility
cases, patients with systemic diseases that lead to impaired
• Change in tooth position
host immunity may also show periodontal destruction. There-
• Tooth loss
fore, periodontitis is a disease that is not only limited to the
area of the oral cavity; it is also associated with severe systemic Chronic periodontitis can be clinically revealed with peri-
diseases (eg, cardiovascular disorders, diabetes mellitus). odontal screening and recording, which results in a periodon-
This chapter discusses clinical features that have been de- tal screening index rating. The condition is diagnosed via the
scribed for chronic periodontitis. In addition, the disease's eti- assessment of the clinical attachment level and the detection
ology is summarized with the use of categories that explain the of inflammatory changes in the marginal gingiva (Fig. 22.1).
231
FIGURE 22.1 Clinical features of generalized chronic periodontitis in a 49-year-old, medically healthy, male patient. The patient reported a smok-
ing habit of 15 cigarettes per day. At the first visit, the periodontal photostatus displays untreated chronic periodontitis with abundant dental plaque
and calculus deposits, gingival redness and swelling, and an alteration of the gingival texture (ie, loss of gingival stippling). The patient noticed multiple
recessions. In this case, recessions were the result of a loss of clinical attachment and alveolar bone. A, Right lateral view. B, Frontal view. C, Left lateral
view. D, Maxillary view. E, Mandibular view. (Reprinted from Kebschu/1 and Dommisch, Thieme, 2012.)
Measurements of periodontal pocket depth in combination During chronic periodontitis, the local inflammatory re-
with the location of the marginal gingiva allow for conclusions sponse may lead to different patterns of bone loss, including
to be drawn regarding the loss of clinical attachment (Figs. 22.2 vertical (angular) and horizontal bone destruction. Although
and 22.3). Dental radiographs display the extent of bone loss, vertical bone loss is associated with intrabony pocket forma-
which is indicated by the distance between the cementoenamel tion, horizontal bone loss is usually associated with suprabony
junction and the alveolar bone crest (Fig. 22.3). The distinc- (supra-alveolar) pockets.
tion between aggressive and chronic periodontitis is sometimes
difficult, because the clinical features may be similar at the time
Disease Severity
of the first examination. At later time points during treatment,
aggressive and chronic periodontitis may be differentiated by The severity of periodontal destruction that occurs as a result
the rate of disease progression over time, the familial nature of of chronic periodontitis is generally considered a function of
aggressive disease, the disease's resistance to periodontal anti- time in combination with systemic disorders that impair or
infective therapy, and the presence of local factors. enhance host immune responses. With increasing age, attach-
ment loss and bone loss become more prevalent and more
severe as a result of an accumulation of destruction. Disease
Disease Distribution severity may be described as mild, moderate, or severe based
Chronic periodontitis is considered a site-specific disease. on the amount of clinical attachment loss:
Local inflammation, pocket formation, attachment loss, and
• Mild chronic periodontitis: when no more than 1-2 mm of
bone loss are the consequences of direct exposure to the sub-
clinical attachment loss has occurred.
gingival plaque (biofilm) As a result of this local effect, pocket
• Moderate chronic periodontitis: when 3-4 mm of clinical
formation and attachment as well as bone loss may occur on
attachment loss has occurred.
one surface of a tooth, whereas other surfaces maintain nor-
• Severe periodontitis: when 5 mm or more of clinical attach-
mal attachment levels. As a result of the site-specific nature,
ment loss has occurred.
the number of teeth with clinical attachment loss classifies
chronic periodontitis into the following types:
• Localized chronic periodontitis: less than 30% of the sites
Symptoms
show attachment and bone loss. Chronic periodontitis is commonly a slowly progressive dis-
• Generalized chronic periodontitis: 30% or more of the sites ease that does not cause the affected individual to feel pain.
show attachment and bone loss. Therefore, most patients are unaware that they have developed
22 Chronic Periodontitis and Necrotizing Ulcerative Periodontitis 233
ST ST
I - t:,11 - t t '-,, ••• .
FIGURE 22.2 Documentation of the periodontal attachment level in the same patient as shown in Fig. 22.1 at the time of the first visit. The red
line displays the gingival margin as it reflects the recessions. Clinical attachment loss is illustrated by the filled (blue) area on the root surfaces. The
deepest periodontal pocket was measured at 9 mm. Class I (green) and Class II (yellow) furcation involvements were documented. Bleeding with
periodontal probing (ie, gingival inflammation) is reflected by red dots. As a result of the patient's history of smoking, the bleeding on probing score
was relatively low, although the patient presented advanced attachment loss. Tooth mobility is indicated by the green line (tooth #19). (Reprinted from
Kebschu/1 and Dommisch, Thieme, 2012.)
a chronic disease that is also associated with other systemic advanced attachment and bone loss, tooth mobility, tooth
diseases (eg, cardiovascular disease). For the majority of the movement, and, in rare occasions, tooth loss may be reported.
patients, gingival bleeding during oral hygiene procedures or In those individuals with advanced disease progression, ar-
eating may be the first self-reported sign of disease occurrence. eas of localized dull pain or pain sensations that radiate to
As a result of the gingival recession, patients may notice black other areas of the mouth or head may occur. The presence of
triangles between the teeth or tooth sensitivity in response areas of food impaction may add to the patient's discomfort.
to temperature changes (ie, cold and heat). In patients with Gingival tenderness or "itchiness" may also be found.
FIGURE 22.3 Collage of a total of 11 radiographs showing the radiographic periodontal status at the time of diagnosis. Compare this with
Figs. 22.1 and 22.2. Note the generalized horizontal and localized angular and vertical bone loss on the mesial and distal sites of the molars. The
radiographs show deep subgingival restorations (teeth #2 and #19), overhanging margins of restorations (teeth #14 and #15), a carious lesion (tooth
#14), and insufficient root canal treatment (tooth #18). (Reprinted from Kebschu/1 and Dommisch, Thieme, 2012.)
Disease Progression • The random or episodic-burst model proposes that periodon-

tal disease progresses by short bursts of destruction fol-
Patients appear to have the same susceptibility to plaque- lowed by periods of no destruction. This pattern of disease
induced chronic periodontitis throughout their lives. The rate is random with respect to the tooth sites affected and the
of disease progression is usually slow, but it may be modified chronology of the disease process.
by systemic, environmental, and behavioral factors. The onset • The asynchronous, multiple-burst model of disease progres-
of chronic periodontitis can occur at any time, and the first sion suggests that periodontal destruction occurs around
signs may be detected during adolescence in the presence of affected teeth during defined periods of life and that these
chronic plaque and calculus accumulation. Due to its slow bursts of activity are interspersed with periods of inactivity
rate of progression, however, chronic periodontitis usually be- or remission. The chronology of these bursts of disease is
comes clinically significant when a patient reaches his or her asynchronous for individual teeth or groups of teeth.
mid-30s or later.
Chronic periodontitis does not progress at an equal rate
in all affected sites throughout the mouth. Some involved ar- Prevalence
eas may remain static for long periods, whereas others may Chronic periodontitis increases in prevalence and severity with
progress more rapidly More rapidly progressive lesions occur age, and it generally affects both genders equally Periodonti-
most frequently in interproximal areas, and they may also be tis is an age-associated (not an age-related) disease. Nonethe-
associated with areas of greater plaque accumulation and in- less, the prevalence of periodontitis increases with age so that
accessibility to plaque-control measures (eg, furcation areas, 40% of patients who are 50 years old or older and almost
overhanging margins of restorations, sites of malposed teeth, 50% of patients who are 65 years old or older show moder-
areas of food impaction). ate periodontal destruction. The prevalence of severe forms of
Further factors that influence disease progression may be periodontitis also increases with age. Up to 30% of patients
of systemic origin. Patients with poorly adjusted diabetes mel- develop severe periodontitis by the time they are 40 years old
litus show a significantly higher risk of developing a severe or older. Generally, 50% of the human population experiences
progression of chronic periodontitis. at least one form of periodontal disease (Figs. 22.4 and 22.5).
Several models have been proposed to describe the rate of
disease progression. In these models, progression is measured
by determining the amount of attachment loss during a given Risk Factors for Disease
period as follows:
A number of different factors influence the etiopathology of
• The continuous model suggests that disease progression is chronic periodontitis. The composition of the oral microflora
slow and continuous, with affected sites showing a con- is a major etiologic factor that leads to periodontal destruc-
stantly progressive rate of destruction throughout the duration. In this context, the extent of the periodontal destruction
tion of the disease. depends on the host's immune competence as well as genetic
100%
D None or mild periodontitis
D Moderate periodontitis
• Severe periodontitis
80%
60%
18-29 30-39 40-54 55-64 65-81 Age
808 1200 1856 600 908 n (summarized)
FIGURE 22.4 Prevalence of periodontitis in the United States and Germany, 2007-09. (Eke Pl, Dye BA, Wei L, et al: Prevalence of periodontitis in
adults in the United States: 2009 and 20 70. J Dent Res 9 7 :9 74-920, 207 2.)
100%
D Mild periodontitis
D Moderate periodontitis
• Severe periodontitis
80%
60%
40%
20%
30-34 35-49 50-64 65+ Age
435 1352 1128 828 n
FIGURE 22.5 Prevalence of periodontitis in the United States, 2009-10. (Eke Pl, Dye BA, Wei L, et al: Prevalence of periodontitis in adults in the
United States: 2009 and 20 70. J Dent Res 9 7 :9 7 4-920, 20 7 2.)
predispositions that influence individual susceptibility to dis- extend subgingivally, and furcations exposed by loss of bone
ease. In addition, both systemic diseases and environmental promote plaque retention.
factors interfere with the development and progression of
chronic periodontitis.
Systemic Factors
Chronic periodontitis is a complex disease that may not
Microbiological Aspects
only be limited to the infection of local sites. In several in-
Plaque accumulation on the tooth and gingival surfaces at stances, periodontitis is also associated with other systemic
the dentogingival junction is considered the primary ini- disorders, such as Haim-Munk syndrome, Papillon-Lefevre
tiating agent in the etiology of gingivitis and chronic peri- syndrome, Ehlers-Danlos syndrome, Kindlers syndrome,
odontitis. Attachment and bone loss are associated with an and Cohen syndrome. Patients with diseases that impair the
increase in the proportion of Gram-negative organisms in host immune response (eg, human immunodeficiency virus,
the subgingival biofilm, with specific increases in organisms acquired immunodeficiency syndrome) may also show peri-
that are known to be exceptionally pathogenic and virulent. odontal destruction. It is also known that osteoporosis, a se-
Porphyromonas gingivalis, Tannerella forsythia, and Treponema verely unbalanced diet, and stress as well as dermatologic,
dentico!a-otherwise known as the "red complex"-are fre- hematologic, and neoplastic factors interfere with periodontal
quently associated with ongoing attachment and bone loss inflammatory responses.
in patients with chronic periodontitis. The development In addition to being associated with defined syndromes,
and progression of chronic periodontitis may not depend on periodontitis also occurs with severe systemic diseases, such
the presence of one specific bacterium or bacterial complex as diabetes mellitus, cardiovascular disorders, stroke, and
alone. It is assumed that chronic periodontitis is the result lung disorders.
of a multispecies infection with a number of different bacte-
ria that influence the proinflammatory immune response of Immunologic Factors
the host. Periodontal pathogens may invade the periodontal
tissue and thus induce an immune response with increas- Chronic periodontitis is a disease that is induced by bac-
ing concentrations of proinflammatory mediators that may teria organized in the dental biofilm. However, the onset,
enhance periodontal breakdown. In addition, a number of progression, and severity of the disease depend on the in-
periodontal pathogens are capable of producing proteases dividual host's immune response. Patients may show altera-
that directly influence tissue stability and host immune tions in their peripheral monocytes, which are related to
responses. the reduced reactivity of lymphocytes or an enhanced B-cell
As the dental biofilm develops, early signs of an inflam- response. B-cells, macrophages, periodontal ligament cells,
matory reaction occur in the gingival margin (ie, gingivitis), gingival fibroblasts, and epithelial cells synthesize proin-
without actual attachment loss. Generally, optimal plaque flammatory mediators (eg, interleukin-1 ~, interleukin-6,
control leads to the complete resolution of this early gingival interleukin-8, prostaglandin E2, tumor necrosis factor-a)
inflammation. Alternatively, with neglected oral hygiene, in- that modify innate and adaptive immune responses at peri-
flammation will progress and eventually result in the loss of odontal sites.
attachment around teeth. Although not all patients with gin-
givitis develop periodontitis, it is known that all patients with
Genetic Factors
periodontitis experienced prior gingivitis. The occurrence of
periodontitis depends on the individual immune response Periodontitis is considered to be a multifactorial disease that
that modifies the onset and progression of the disease. is influenced by local, systemic, and immunologic factors, as
described previously. Each factor is in turn directly related
to individual genetic conditions. Genetic variations such as
Local Factors
single nucleotide polymorphisms (SNPs) and genetic copy
Plaque accumulation and biofilm development are the prima- number variations may directly influence innate and adaptive
ry causes of periodontal inflammation and destruction. There- immune responses as well as the structure of periodontal tis-
fore, factors that facilitate plaque accumulation or that prevent sues. Periodontal destruction has been found among family
plaque removal by oral hygiene procedures can be detrimen- members and across different generations within a family,
tal to the patient. Plaque-retentive factors are important for thereby suggesting a genetic basis for the susceptibility to
the development and progression of chronic periodontitis, periodontal disease. In a number of studies, the prevalence of
because they retain microorganisms in proximity to the peri- aggressive and chronic periodontitis has been investigated in
odontal tissues, thereby providing an ecologic niche for bio- families with a history of one or more family members with
film maturation. Calculus is considered the most important periodontitis. The data from those studies have demonstrated
plaque-retentive factor as a result of its ability to retain and variable results, with a likelihood of heritability of up to 50%.
harbor plaque bacteria on its rough surface as well as inside. Variations are mainly the result of different study designs as
As a consequence, calculus removal is essential for the mainte- well as the number of evaluated individuals.
nance of a healthy periodontium. In addition, tooth morphol- Studies of SNPs in the interleukin-1 gene led to early con-
ogy may influence plaque retention. Roots may show grooves clusions that alterations in sequences of immunologically
or concavities, and, in some instances, enamel projections on relevant genes may explain the heritability of periodontitis.
the surface or the furcation entrances. These morphologic Genome-wide association studies have revealed a signifi-
variations may facilitate plaque retention, subgingival calculus cant association between periodontitis and coronary heart
formation, and disease progression. In addition, subgingival disease. Although four different genetic variations have been
and overhanging margins of restorations, carious lesions that identified and validated, it is most likely that a higher number
of genes require variations to result in the development of • Fewer signs of gingivitis (eg, less bleeding with probing)
periodontitis. • Greater incidence of furcation involvement
As a result of the consumption of tobacco, reactive oxygen
Environmental and Behavioral Factors (ie, radicals) is released that chemically irritates periodontal
tissues via DNA damage, the lipid peroxidation of cell mem-
In addition to microbial, immunologic, and genetic factors,
branes, the damage of endothelial cells, and the induction of
the development and progression of chronic periodontitis is
smooth muscle cell growth.
further influenced by environmental and behavioral factors,
Psychological factors (eg, stress, depression) also negatively
such as smoking and psychological stress. Smoking is a major
influence the progression of chronic periodontitis. Patients
risk factor for the development and progression of generalized
with periodontitis often report the experience of family- or
chronic periodontitis. Periodontitis is influenced by smoking
work-related stress. Positive correlations between cortisol lev-
in a dose-dependent manner. The intake of more than 10 ciga-
els and periodontal indices (eg, plaque index, gingival index),
rettes per day tremendously increases the risk of disease pro-
bone loss, and missing teeth have been recorded. In addition,
gression as compared with nonsmokers and former smokers.
stress as an etiologic factor was even more strongly associated
As compared with nonsmokers, the following features are
with periodontitis when patients were smokers as compared
found in smokers:
with nonsmokers.
• Increased periodontal pocket depth of more than 3 mm
• Increased attachment loss REFERENCES
• More recessions
• Increased loss of alveolar bone
• Increased tooth loss
Necrotizing Ulcerative
Periodontitis
Necrotizing ulcerative periodontitis (NUP) may be an extension Clinical Features

of necrotizing ulcerative gingivitis (NUG) into the periodontal
structures that leads to periodontal attachment and bone Similar to NUG, clinical cases of NUP are defined by necrosis
loss. Alternatively, NUP and NUG may be different diseases. and ulceration of the coronal portion of the interdental papil-
To date, there is little evidence to support the progression of lae and gingival margin, with a painful, bright-red marginal
NUG to NUP or to establish a relationship between the two gingiva that bleeds easily.
conditions as a single disease entity. However, numerous The distinguishing feature of NUP is the destructive progres-
clinical descriptions and case reports of NUP clearly dem- sion of the disease, which includes periodontal attachment
onstrate many clinical similarities between the two condi- and bone loss. Deep interdental osseous craters typify peri-
tions. Until a distinction between NUG and NUP can be odontal lesions of NUP (Fig. 22.6). However, "conventional"
proved or disproved, it has been suggested that NUG and periodontal pockets with deep probing depth are not found,
NUP be classified together under the broader category of because the ulcerative and necrotizing nature of the gingi-
necrotizing periodontal diseases, although with differing levels val lesion destroys the marginal epithelium and connective
of severity. tissue, thereby resulting in gingival recession. Periodontal
NUG has been recognized and described in the literature for pockets are formed because the junctional epithelial cells
centuries. The features of NUG are presented in Chapter 16. remain viable and can, therefore, migrate apically to cover
The term necrotizing ulcerative periodontitis was first ad- areas of lost connective-tissue attachment. The necrosis of the
opted at the 1989 World Workshop in Clinical Periodon- junctional epithelium in patients with NUG and NUP creates
tics. It was changed from the 1986 term necrotizing ulcer- an ulcer that prevents this epithelial migration, and a pocket
ative gingivoperiodontitis, which represented the condition cannot form. Advanced lesions of NUP lead to severe bone
of recurrent NUG that progresses to a chronic form of loss, tooth mobility, and ultimately tooth loss. In addition
periodontitis that includes attachment and bone loss. The to these manifestations, as previously mentioned, patients
adoption of NUP as a disease entity occurred in 1989 when with NUP may present with oral malodor, fever, malaise, or
there was a heightened awareness and an increase in the lymphadenopathy.
number of necrotizing periodontitis cases being diagnosed
and described in the literature. Specifically, more cases of Microscopic Findings
NUP were being described among immunocompromised
patients, especially those who were human immunodefi- In a study involving the use of transmission electron mi-
ciency virus (HIV) positive or who had acquired immu- croscopy and scanning electron microscopy of the microbial
nodeficiency syndrome (AIDS). In 1999, the subclassifica- plaque overlying the necrotic gingival papillae, Cobb and
tions of NUG and NUP were included as separate diagnoses coworkers demonstrated striking histologic similarities
under the broader classification of "necrotizing ulcerative between NUP in HIV-positive patients and previous de-
periodontal diseases." scriptions of NUG in HIV-negative patients. Microscopic
22 Chronic Periodontitis and Necrotizing Ulcerative Periodontitis 237.el
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FIGURE 22.6 Necrotizing ulcerative periodontitis in a 45-year-old, HIV-negative, white, male patient. A, Buccal view of the maxillary cuspid-
bicuspid area. B, Palatal view of the same area shown in A. C, Buccal view of the mandibular anteriors. Note the deep craters associated with
bone loss.
examination revealed a surface biofilm composed of a mixed Etiology of Necrotizing Ulcerative

microbial flora with different morphotypes and a subsurface
flora with dense aggregations of spirochetes (ie, the bacterial Periodontitis
zone). Below the bacterial layers were dense aggregations of The etiology of NUP has not been determined, although a
polymorphonuclear leukocytes (PMNs) (ie, the neutrophil- mixed fusiform-spirochete bacterial flora appears to play a
rich zone) and necrotic cells (necrotic zone). The biopsy key role. Since bacterial pathogens are not solely respon-
technique used in this study did not allow for the observa- sible for causing the disease, some predisposing "host"
tion of the deepest layer and thus was not able to identify the factors may be necessary. Numerous predisposing factors
spirochetal infiltration zone, which is classically described have been attributed to NUG, including poor oral hygiene,
in NUG lesions. In addition to the NUG-like microscopic preexisting periodontal disease, smoking, viral infections,
features of NUP described in this study, high levels of yeasts immunocompromised status, psychosocial stress, and
and herpes-like viruses were observed. This latter finding malnutrition.
is most likely indicative of the conditions afforded to op- NUG and NUP are more prevalent and more severe among
portunistic microbes in the immunocompromised host (ie, patients with HIV These patients require urgent treatment,
HIV-positive patients). because untreated lesions can progress rapidly; within a few
Necrotizing forms of periodontitis appear to be more days, severe bone loss around affected teeth can be seen.
prevalent among patients with more severe immunosup- Smoking, malnutrition, and high plaque levels all increase
pression. Case reports have depicted NUP as a progressive the risk of NUG and need to be changed so that treatment
extension of HIV periodontitis (ie, chronic to necrotic pro- success is obtained.
gression). Glick and coworkers found a high correlation Clinicians should check all patients who present with NUP
between the diagnosis of NUP and immunosuppression in to ascertain their HIV status. NUP can progress rapidly and
HIV-positive patients. Those patients who presented with lead to tooth exfoliation, so treatment should include local de-
NUP were 20.8 times more likely to have CD4+ counts of bridement, local antiplaque agents, and systemic antibiotics.
less than 200 cells/mm3 as compared with HIV-positive The early diagnosis and treatment of NUP are crucial, because
patients without NUP The authors consider a diagnosis of the osseous defects that occur during the late stages of the
NUP to be a marker of immune deterioration and a predic- disease are extremely difficult to resolve.
tor of the diagnosis of AIDS. Others have suggested that
NUP may be used as an indicator of HIV infection in undi-
agnosed patients. Shangase and coworkers reported that a Microbial Flora
diagnosis of NUG or NUP in systemically healthy, asymp- Assessment of the microbial flora of NUP lesions is almost
tomatic South-African patients was strongly correlated with exclusively limited to studies involving patients with HIV
HIV infection. Of patients presenting with NUG or NUP, or AIDS, with some conflicting evidence. Murray and co-
39 of 56 (69.6%) were subsequently found to be infected workers reported that cases of NUP in HIV-positive pa-
with HIV tients demonstrated significantly greater numbers of the
opportunistic fungus Candida albicans and a higher prevalence Patients with NUG have been found to have had significantly
of Aggregatibacter actinomycetemcomitans, Prevotella intermedia, more anxiety, higher depression scores, a greater magnitude of
Porphyromonas gingivalis, Fusobacterium nucleatum, and Cam- recent stressful events, more overall distress and adjustments
pylobacter species as compared with HIV-negative controls. In related to these events, and more negative life events. Although
addition, they reported a low or variable level of spirochetes, the role of stress in the development of NUP has not been
which is inconsistent with the flora associated with NUG. reported specifically, the many similarities between NUG and
Citing differences in microbial flora, they refuted the no- NUP would suggest that similar relationships to stress may exist.
tion that the destructive lesions seen in HIV-positive patients The mechanisms that predispose an individual with stress
were related to NUG lesions; they suggested that the flora of to necrotizing ulcerative periodontal diseases have not been
NUP lesions in HIV-positive patients is comparable to that of established. However, it is well known that stress increases the
chronic periodontitis lesions, thus supporting their concept systemic cortisol levels, and sustained increases in cortisone
that necrotizing periodontitis in the HIV-positive patient is an have a suppressive effect on the immune response.
aggressive manifestation of chronic periodontitis in the im-
munocompromised host.
In contrast with these findings, Cobb and coworkers
Malnutrition
reported that the microbial composition of NUP lesions Direct evidence of the relationship between malnutrition and
in HIV-positive patients was very similar to that of NUG necrotizing periodontal disease is limited to descriptions of nee-
lesions, as discussed previously. With the use of electron rotizing infections in severely malnourished children. Lesions
microscopy, the researchers described a mixed microbial resembling NUG but that progress to become gangrenous sto-
flora with various morphotypes in 81.3% of specimens. matitis or noma have been described in children with severe
The subsurface microbial flora featured dense aggregations malnutrition in underdeveloped countries. In the advanced
of spirochetes in 87.5% of specimens. The authors also re- stages, NUG lesions extended from the gingiva to other areas
ported opportunistic yeasts and herpes-like viruses in 65.6 of the oral cavity, becoming gangrenous stomatitis (noma) and
and 56.5% of NUP lesions, respectively. The differences be- causing exposure, necrosis, and sequestration of the alveolar
tween these reports may be explained by the limitations of bone.
obtaining viable cultures of spirochetes as compared with A possible explanation is that malnutrition, particularly
the more definitive electron microscopic observation of spi- when extreme, contributes to a diminished host resistance
rochetes. to infection and necrotizing disease. It is well documented
In a recent review article, Feller and Lemmer suggested that that many of the host defenses-including phagocytosis; cell-
spirochetes, herpesviruses, candida, and HIV all have poten- mediated immunity; and complement, antibody, and cytokine
tially pathogenic roles in NUP lesions in the HIV-seropositive production and function-are impaired in malnourished indi-
individual. Spirochetes have the ability to modulate the host's viduals. The depletion of nutrients to cells and tissues results
innate and adaptive immune responses and to stimulate host in immunosuppression and increases disease susceptibility.
inflammatory reactions, which may reduce the local immune Thus, it is reasonable to conclude that malnutrition can pre-
competence and facilitate the development of necrotizing dis- dispose an individual to opportunistic infections or intensify
ease. Activated herpesviruses have the capacity to deregulate the severity of existing oral infections.
the host's immune system, which may lead to an increase in
the colonization and activity of other pathogenic microorgan-
isms. Candida albicans has been reported to produce eico- Conclusions
sanoids, thereby leading to the release of proinflammatory NUP and NUG share many clinical and micro biologic features,
mediators, which may facilitate spirochete colonization and but NUP is distinguished by a more severe condition with
invasion and promote the development of necrotizing peri- periodontal attachment and bone loss. Indeed, some patients
odontal diseases. with NUP, particularly those with compromised immunity, can
have a severe and rapidly progressive disease. It appears that an
lmmunocompromised Status impaired immune response and a lowered host resistance to
infection are significant factors in the onset and progression
Clearly, both NUG and NUP lesions are more prevalent of NUP The best example of an immunocompromised host
among patients with compromised or suppressed immune with a predisposition for NUP is the patient with HIV or AIDS.
systems. Numerous studies-particularly those evaluating As with the other infection-related complications of HIV and
patients with HIV or AIDS-support the concept that a di- AIDS, the immunocompromised status of affected patients
minished host response is present in those individuals who renders them vulnerable to opportunistic periodontal infec-
have been diagnosed with necrotizing ulcerative periodontal tions, including NUP Several other factors have been identified
diseases. Whereas a compromised immune system (ie, "im- in cases of NUG that may also play a role in NUP, including
mune compromise") in the HIV-infected patient is driven by smoking, viral infections, psychosocial stress, and malnutri-
impaired I-cell function and altered I-cell ratios, evidence tion. Although none of these factors alone is sufficient to cause
indicates that other forms of compromised immunity predis- necrotizing disease, in combination with other immunocom-
pose individuals to NUG and NUP as well. promising conditions, they undoubtedly have the potential to
adversely influence the host response or resistance to infection.
Psychologic Stress
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23
Aggressive Periodontitis
H Dommisch • M Kebschull • PR Klokkevold • FA Carranza
• DG Naik • A Uppoor
Chapter Outline
Historical Background Pathobiology and Risk Factors
Classification and Clinical Characteristics Diagnosis
Periodontitis is the pathological manifestation of the host re- from adult periodontitis may occur among adolescents and
sponse against bacterial challenge that stems from a polymi- young adults.
crobial biofilm at the biofilm-gingival interface. The term juvenile periodontitis was introduced by Chaput et al
There are several sub forms of the disease, which are mainly in 196 7 and by Butler in 1969. In 1971, Baer defined it as "a dis-
characterized by their clinical phenotype (ie, the rate of disease of the periodontium occurring in an otherwise healthy ad-
ease progression and other features) rather than their (still olescent which is characterized by a rapid loss of alveolar bone
partially unknown) etiology. This chapter addresses aggres- about more than one tooth of the permanent dentition. The
sive periodontitis, which features the rapid loss of periodontal amount of destruction manifested is not commensurate with
attachment and tooth-supporting bone in otherwise healthy the amount of local irritants." In 1989, the World Workshop in
patients. Clinical Periodontics categorized this disease as localized juve-
nile periodontitis and as a subset of the broad classification of
early-onset periodontitis. Under this classification system, age
Historical Background of onset and distribution of lesions were of primary importance
In 1923, Gottlieb described a patient with a fatal case of epi- when making a diagnosis of this condition.
demic influenza and a disease that he called "diffuse atrophy In 1999, the World Workshop in Periodontics introduced a
of the alveolar bone." This disease was characterized by a loss novel classification that was meant to eliminate the shortcom-
of collagen fibers in the periodontal ligament and their re- ings of earlier endeavors to classify periodontal disease. Most
placement by loose connective tissue and extensive bone re- importantly, the new 1999 classification sought "to discard
sorption, which resulted in a widened periodontal space. The classification terminologies that were age-dependent or re-
gingiva apparently was not involved. In 1928, Gottlieb attrib- quired knowledge of rates of progression." In the new classifi-
uted this condition to the inhibition of continuous cementum cation scheme, several rapidly progressing periodontitis forms
formation, which he considered essential for the maintenance were united under the term aggressive periodontitis.
of the periodontal fibers. At that time, he called the disease
"deep cementopathia," and he hypothesized that this was a
"disease of eruption" and that the cementum initiated a for-
eign-body response. As a result, it was postulated that the host
Classification and Clinical
attempted to exfoliate the tooth, thereby resulting in the ob- Characteristics
served bone resorption and pocket formation.
In 1938, Wannenmacher described incisor and first molar Features
involvement and called the disease "parodontitis marginalis The 1999 International Workshop for the Classification of
progressiva." Several explanations have evolved for the etiol- Periodontal Diseases and Conditions defined the entity of ag-
ogy and pathogenesis of this type of disease. Many authors gressive periodontitis as being characterized by three primary
considered this to be a degenerative, noninflammatory disease features (Table 23.1):
process and therefore gave it the name periodontosis. Other
investigators denied the existence of a degenerative type of 1. The rapid loss of attachment and tooth-supporting bone.
periodontal disease and attributed the changes observed to With aggressive periodontitis, as compared to the more
trauma from occlusion. Finally, in 1966, the World Workshop common variant chronic periodontitis, the loss of at-
in Periodontics concluded that the concept of periodontosis tachment progresses significantly faster. To evaluate this
as a degenerative entity was unsubstantiated and that the term rapid course of destruction, the evaluation of clinical or
should be eliminated from periodontal nomenclature. Howev- radiographic data from earlier points in time is neces-
er, the committee did recognize that a clinical entity different sary, which helps in making an estimate of the start of the
241
TABLE 23.1
DIAGNOSTIC CRITERIA TO DISTINGUISH CHRONIC AND AGGRESSIVE PERIODONTITIS

Criterion Aggressive Periodontitis Chronic Periodontitis
Rate of progression Rapid Slow but rapid episodes are possible

Familiar aggregation Typical Can be present when families share imperfect
oral hygiene habits
Presence of etiological factors (eg, plaque, Often minimal Often commensurate with observed
calculus, and overhanging restorations) periodontal destruction
Age Often in young patients (ie, <35 years old) Often in older patients (ie, > 55 years old)
but can be found in all age groups but can be found in all age groups
Clinical inflammation signs Sometimes lacking (especially in patients with Commensurate with amount of etiological
localized aggressive periodontitis) factors present
disease. Note that the age of the patient per se is not a pri- history questionnaires and by interviewing the patient.
mary criterion for the diagnosis of aggressive periodontitis. However, it is advisable to verify similar cases in the fam-
Since earlier clinical records are often not available, many ily, if possible, because many individuals may not be fully
clinicians argue that a severe loss of attachment in young aware of their diagnoses. Many cases of "bad teeth that run
patients may conceivably be the result of a rapid course of in the family" turn up to be caries related or likely due to
disease progression. However, this is not generally true; chronic periodontitis.
the neglect of all oral hygiene in a periodontitis-susceptible
In addition, the Workshop defined several secondary features
individual over a decade will lead to severe attachment loss
that are generally found in aggressive periodontitis cases but that
even with a slow rate of progression. On the other hand,
are not universally necessary to diagnose the disease entity:
severe attachment loss in an older individual is not neces-
sarily the result of long-lasting, slowly progressing disease. 1. Inconsistency of the low amounts of present etiological
It is therefore inappropriate to use the age of an affected factors (ie, plaque) and the observed pronounced tissue
individual as a primary diagnostic criterion for the distinc- destruction.
tion of aggressive and chronic periodontitis. Note that, 2. Strong colonization by Aggregatibacter actinomycetem-
with chronic periodontitis, there are reportedly periods of comitans (Aa) and, in some populations, Porphyromonas
rapid disease progression that can by themselves be misin- gingivalis.
terpreted as aggressive periodontitis. 3. Immunological differences that do not entail the diagnosis
2. The subject is otherwise healthy (ie, not suffering from any sys- of periodontitis as a manifestation of systemic disease.
temic disease or condition that could be responsible for the pres- a. Hyperresponsive macrophages
ent periodontitis). b. Abnormalities of neutrophil function
There are systemic diseases that lead to severely altered 4. Self-limiting disease.
host defenses against periodontal pathogens, often result-
ing in the rapid loss of attachment and tooth loss at early
age. This disease is designated "periodontitis as a manifes- Subgroups
tation of systemic disease". Note that the specific properties
or abnormalities of some types of immune cells, listed later Aggressive periodontitis can be subclassified into localized and
in this chapter and reported to be often associated with the generalized forms. The diagnosis of the subcategory is based
diagnosis of aggressive periodontitis, do not themselves on clinical, radiographic, and historic data. These include the
qualify for the aforementioned diagnosis. age of onset, the involvement of teeth other than first molars
3. The presence offamiliar aggregation. and incisors (ie, the first permanent teeth to erupt), and the
The familiar aggregation of aggressive periodontitis cases presence of a systemic antibody response against periodontal
is a feature that can be evaluated via medical and dental pathogens (Table 23 2).
TABLE 23.2
DIAGNOSTIC CRITERIA FOR LOCALIZED AND GENERALIZED AGGRESSIVE PERIODONTITIS

Criterion localized Aggressive Periodontitis Generalized Aggressive Periodontitis
Age of onset Circumpubertal Most often <30 years of age, but can also
occur in older individuals
Serum-antibody response Robust Poor
against infecting agents
Destruction pattern Localized attachment loss at incisors and first molars; Generalized interproximal attachment loss
interproximal attachment loss at two or more permanent teeth, at three or more permanent teeth other
one of which is a first molar, and involvement of two or fewer than the first molars and incisors
teeth other than the first molars and incisors
Additional Episodic nature of attachment loss
23 Aggressive Periodontitis 243
(B)
FIGURE 23.1 Generalized aggressive periodontitis. Generalized aggressive periodontitis in a 28-year-old Caucasian, female, nonsmoking patient.
A, Clinical views with minimal amounts of calculus and plaque. B, Radiographically, bone loss of 50% or more was present at all teeth.
Generalized Aggressive Periodontitis tissue that is often proliferating, ulcerated, and fiery red.
Generalized aggressive periodontitis (GAP) is the subgroup of Bleeding may occur spontaneously or with slight stimulation,
periodontal disease that is characterized by the highest sever- and suppuration may be an important feature. This tissue
ity and extent of disease and also by its large heterogeneity. response is thought to occur during the destructive stage in
Clinically, GAP is characterized by "generalized interproxi- which attachment and bone are actively lost.
mal attachment loss affecting at least three permanent teeth In other cases, the gingival tissues may appear pink, free of
other than first molars and incisors." inflammation, and occasionally with some degree of stippling,
The diagnosis of GAP encompasses the diseases that were although stippling may be absent. However, despite the ap-
previously classified as generalized juvenile periodontitis and parently mild clinical appearance, deep pockets can be dem-
rapidly progressive periodontitis. onstrated by probing. Page and Schroeder thought that this
Two gingival tissue responses can be found in cases of GAP tissue response coincides with periods of quiescence in which
(Figs. 23.1 and 23.2). One involves severe, acutely inflamed the bone level remains stationary.
FIGURE 23.2 Generalized aggressive periodontitis. Severe generalized aggressive periodontitis in a 22-year-old black, male patient with a family
history of early tooth loss through periodontal disease. A, Clinical view showing minimal plaque and inflammation. A provisional wire-and-resin splint
had been placed by the general practice dentist to stabilize the teeth. B, Radiographs showing the severe and generalized nature of the disease, with
all erupted teeth affected.
Prevalence and Distribution by Age and Gender. Among The localized distribution of lesions in LAP is unexplained,
the young Israeli army recruits, it was found that 1.8% suf- but the following reasons have been suggested:
fered from GAP When using extrapolation, as proposed by
1. After initial colonization of first permanent teeth to erupt
Demmer and Papapanou, a prevalence of about 1 % to a maxi-
(first molars and incisors), Aa evades the host defenses by
mum of 15% in individuals aged 25-35 years was found, de-
various mechanisms initiating the destruction of periodon-
pending on the study
tal tissues. After this initial attack, adequate immune de-
Specifically, data from the German Study of Health in
fenses are stimulated to produce opsonic antibodies that
Pomerania indicated an extrapolated prevalence within dif-
enhance the clearance of invading bacteria. This way, colo-
ferent age groups of 13% (::::;29 years) and 7% (30-39 years),
nization of other site may be prevented.
whereas the highest extrapolated prevalence was found in the
2. Bacteria antagonistic to Aa may colonize the periodontal
Erie County Study, with up to 15% of individuals aged 25-
tissues and inhibit it from further colonization.
35 years being affected.
3. For unknown reasons, Aa may lose its leucotoxin produc-
Radiographic findings:. Radiographic picture in GAP can
ing ability
range from severe bone loss associated with a minimal num-
4. A defect in the cementum formation may be responsible
ber of teeth to advanced bone loss affecting the majority of
for the localization of the lesions.
teeth in the dentition.
It is characterized by more pronounced systemic antibody
titers against periodontal pathogens than are found in patients
Localized Aggressive Periodontitis with GAP This could indicate that, in individuals who are sus-
Localized aggressive periodontitis (LAP) is usually found in ceptible to disease but who also have the ability to enact a ro-
younger individuals than GAP (Figs. 23.3 and 23.4). Clini- bust response against pathogens, the disease might be limited
cally, "it is characterized as having localized first molar/incisor in extent (ie, LAP). Alternatively, in individuals with a lesser
presentation with interproximal attachment loss on at least humoral response, the disease would not be limited to the first
two permanent teeth, one of which is a first molar, and in- permanent teeth, and the patient would develop GAP This
volving no more than two teeth other than first molars and would mean that LAP and GAP would merely be phenotypic
incisors variations of the same underlying disease. This assumption is
FIGURE 23.3 Localized aggressive periodontitis. Localized aggressive periodontitis in a 15-year-old black, female patient who had a twin with
similar disease. A, Clinical view showing minimal plaque and inflammation, except for localized inflammation on the distal side of the maxillary left
central incisor and the mandibular right central incisor. B, Radiographs showing localized, vertical, angular bone loss associated with the maxillary
and mandibular first molars and the mandibular central incisors. The maxillary incisors show no apparent involvement. C, Surgical appearance of the
localized, vertical, angular bony defects affecting the mandibular incisors. Note the wide circumferential nature of the defects and the lack of calculus
on the root surfaces.
backed by several reports that show a sequence of LAP and a prevalence rate of 0 .1 % . In the United States, a national
GAP in the same individuals over time. survey of adolescents between the ages of 14 and 17 years
At the same time, there exist several lines of evidence reported that 0.53% had LJP Blacks were at a much higher
that support the claim that LAP constitutes a disease on its risk for LJP, and black male teenagers were 2.9 times more
own, with dissimilar underlying molecular and cellular likely to have the disease than black female adolescents. By
mechanisms. contrast, white female teenagers were more likely to have LJP
than white male adolescents. Several other studies have found
Prevalence and Distribution by Age and Gender. The prev- the highest prevalence of LJP among black males, who are
alence of LAP in an Israeli army population between the ages followed in descending order by black females, white females,
of 18 and 30 years old was 4.3%. In this cohort, presence of and white males.
LAP was highly correlated with North African origin and cur- LJP was reported to affect both males and females and it
rent smoking. is seen most frequently in the period between puberty and
In addition to these recent data, there exist several stud- 20 years of age. Some studies have suggested a predilection
ies on the prevalence of localized juvenile periodontitis (LJP) for female patients, particularly in the youngest age groups,
among diverse populations. LJP is the predecessor of LAP al- whereas others reported no male or female differences in inci-
though the two conditions are not exactly interchangeable. dence when studies are designed to correct for ascertainment
The prevalence of this disease in geographically diverse ado- bias.
lescent populations was estimated to be less than 1 %. Most Radiographic findings. Vertical loss of alveolar bone noted
reports suggested a low prevalence of about 0.2%. Two inde- around the first molars and incisors begin around puberty in
pendent radiographic studies of 16-year-old adolescents, (one otherwise healthy teenagers. Classical arc-shaped loss of alve-
in Finland and the other in Switzerland) followed the strict olar bone extending from the distal surface of second premo-
diagnostic criteria, delineated by Baer, and reported a preva- lar to the mesial surface of second molar is appreciated in LAP
lence rate of 0.1 %. A clinical and radiographic study of 7266 Bone defects are usually wider than those that are usually
English adolescents who were 15-19 years old also showed seen with chronic periodontitis.
FIGURE 23.4 Localized aggressive periodontitis. Localized aggressive periodontitis in an 18-year-old Caucasian, female, nonsmoking patient.
Familiar aggregation was reported. A, Clinical view showing recessions at the incisors and first molars.
Current Understanding epidemiological studies. The prevalence of aggressive peri-

odontitis of approximately 1 %-15% among subjects, who are
Taken together, these data primarily inicate that the dis- 35 years old or younger, in combination with the severity and
crimination of aggressive periodontitis from other forms of tendency for the rapid progression of this disease, strongly
periodontitis is not always easy, especially when seeing the suggest that all patients in this age group should be screened
patient only for a single examination as it is the case in most regularly for the presence of periodontal disease.
FIGURE 23.4 (cont.) B, lntraoperative view showing advanced, localized, angular bony defect associated with a first molar. C, Radiographs showing
pronounced localized, angular bone loss. (Courtesy Dr Hendrik Schulze, Bonn, Germany.)
Pathobiology and Risk Factors reported familiar aggregation of aggressive periodontitis

cases could be also, to a certain point, explained by an in-
All forms of periodontitis share certain common pathobiologi- fection or the within-family transmission of specific micro-
cal principles as polymicrobial, biofilm-mediated, and chronic organisms.
inflammatory diseases at the biofilm-gingival interface. For Therefore, several studies have sought to identify the spe-
now, we will focus on the biological reasons for the rapid cific microbial properties of aggressive periodontitis cases.
course of destruction in patients with aggressive periodontitis, However, when evaluating GAP and LAP as a single entity and
including looking at research that has investigated the specific solely focusing on a small number of "classic" pathogens, it
properties of aggressive periodontitis in periodontal microbi- has been concluded that microbiological infection patterns
ology, immunology, and genetics. could not reliably distinguish between this entity and chronic
periodontitis cases.
However, data from a limited number of studies, involving
Microbiology both classic microbiological tools and more recent molecular
Periodontitis is caused by specific microorganisms in a sus- techniques, suggest that differences exist in microbiological
ceptible host. In the subgingival biofilm, up to 700 bacterial composition between both (1) LAP and both GAP and chronic
species have been identified, some of which have been identi- periodontitis and (2) CAP and chronic periodontitis.
fied as being causative.
The observed higher rate of disease progression in ag- Specific Bacteria in Localized Aggressive
gressive versus chronic periodontitis could possibly be Periodontitis
explained by the presence of specific microorganisms that In patients with LAP, the situation seems to be different. In
cause and perpetuate tissue destruction. In addition, the these cases, several lines of evidence point to a strong role of
specific microorganisms, most notably A. actinomycetemcomi- Abnormalities in Localized Aggressive Periodontitis

tans. For decades, this bacterial species has been associated Earlier work suggested that individuals with LAP were char-
with LAP, and its presence predicted the development of LAP acterized by an inherited defect of neutrophil function that
in two longitudinal studies. Longitudinal studies are of criti- led to a dampened immune response against the microflora
cal importance for the demonstration of a causal relationship, inhabiting the periodontal pocket. Specifically, when chal-
whereas cross-sectional studies can by definition only show lenged with periodontal pathogens, the LAP neutrophils
correlations that cannot be used to infer causality. were reported to show impaired chemotaxis, phagocytosis,
In the first longitudinal study, age-, gender- and race- and killing of bacteria. Alternatively, it was also hypothesized
matched juvenile carriers and noncarriers of A. actinomycetem- that these impaired defense properties were in fact acquired
comitans (serotypes a, b, and c were equally distributed, with defects caused by prolonged exposure to an inflammatory
no presence of A. actinomycetemcomitans strain JP2) were fol- microenvironment.
lowed longitudinally. After 1 year of follow-up, 80% of the Today, the understanding of neutrophil biology is that
carriers and only 10% of the noncarriers had developed peri- neutrophils arriving at a site with uncontrolled periodontal
odontitis. inflammation are primed to attack the invading pathogens
In the second and larger longitudinal study, the highly by releasing lytic enzymes. These enzymes may, on the other
leukotoxic A. actinomycetemcomitans (serotype b) strain JP2, hand, accelerate tissue destruction. It is hypothesized that
which has a 530-bp deletion in its leukotoxin gene operon the observed dampened neutrophil function in deep aggres-
that leads to a 10- to 20-fold higher production of leukotoxin, sive periodontitis lesions is due to the heavy commitment of
was found to be directly related to the occurrence of LAP in primed neutrophils to debridement and decreased potency for
children in Northern Africa. Specifically, the odds ratio for fu- chemotaxis and defense.
ture attachment loss among carriers of the JP2 strain was 18.0
as compared to 3.0 for carriers of other, non-JP2 strains of A.
Genetics: Family Studies
actinomycetemcomitans. Similar findings can also be found in
West African countries, such as Ghana. This is in contrast with A familial aggregation of aggressive periodontitis cases is a sec-
the eastern parts of Africa where no studies have reported the ondary feature of the disease entity; it is often (but not always)
presence of JP2 clone strains in patients with periodontitis. found with aggressive periodontitis. To assess the familial
A recent study of the occurrence of JP2 clone strains in component of the disease, twin studies were performed, and
patients with aggressive periodontitis demonstrated a high in- these demonstrated a strong genetic component with a likely
cidence of both LAP and GAP, which suggests that both sub- autosomal-dorninant inheritance pattern and a 70% (African-
classes could be more related than initially thought. Americans) to 73% (Caucasians) penetrance.
In addition, it needs to be noted that LAP is clearly not
a monoinfection with A. actinomycetemcomitans; as with all Genetics: Polymorphisms
entities involving periodontitis, LAP features a polymicrobial Accordingly, extensive work has been carried out to determine
biofilm. In support of this notion is the fact that there are also the inherent genetic traits that underlie this familiar aggrega-
reports of confirmed cases of LAP that did not involve A. acti- tion.
nomycetemcomitans. First, it was suspected that an inherent susceptibility to
periodontitis would be likely the result of mutations in the
DNA encoding for proteins of inflammatory mediators; this
Host Response to Bacterial Challenge
is the candidate gene approach. DNA regions that were se-
The inflammatory host response toward pathogens is gener- lected on the basis of a priori knowledge of the disease patho-
ally attributed to be responsible for a larger proportion of the biology were assessed for sequence variations, and these were
tissue destruction in periodontitis than the invading periodon- most often single nucleotide polymorphisms. On the basis of
tal pathogens themselves. The rapid progression of aggressive small sample sizes and often suboptimal study designs that
periodontitis implies that-in addition to the aforementioned conceivably led to false-positive results, single nucleotide
composition of the subgingival microbiological flora-specific polymorphisms within genes that encoded for cytokines,
properties of this inflammatory response render the individu- such as, interleukins-la, -1~, -6, and so on were reported
als with aggressive periodontitis, both more susceptible to dis- to be associated with aggressive periodontitis. However, with
ease and to the loss of more attachment in a shorter amount current knowledge, it has to be realized that these findings
of time. were possibly spurious or the result of confounding: all of the
"classical" candidate gene associations could not be replicated
Host Response Specific to Aggressive Periodontitis in today's larger and better-controlled cohorts. Note that, in
With regard to GAP, a recent review concluded that "there the case of genetic association studies, metaanalyses are not
appears to be no difference between aggressive and chronic generally suitable tools to overcome the problems of small,
periodontitis in terms of their histopathology and immunopa- heterogeneous cohorts.
thology." Still, it has to be acknowledged that this could mean During recent years, a consortium investigating a large
that there exist no differences or, rather, that "the differences number of aggressive periodontitis cases and controls, identi-
between both disease entities only reflect variations in the de- fied a common susceptibility locus for aggressive periodontitis
gree of severity of susceptibility rather than actual different and myocardial infarction, and these findings were replicated
immunopathologies." in independent cohorts.
Most recently, the stronger activation of natural killer cells Taken together, these data indicate that there is evidence
and natural killer T cells in patients with aggressive pericdon- for a strong genetic component in aggressive periodontitis. It
titis was suggested to be causative for the enhanced tissue de- is very likely that the low number of identified and replicated
struction that has been observed in these patients. susceptibility loci for aggressive periodontitis are the result
of extremely low sample numbers and issues in study design The diagnosis of systemic health is made by assessing
than the lack of biological association the medical history of the patient, usually with the use of a
questionnaire and a short interview; this process is repeat-
Environmental Factors That Affect Susceptibility ed every other year. In subjects with suspected aggressive
The amount and duration of smoking are important variables periodontitis, the primary-care physician can be consulted
that can influence the extent of destruction seen in young to rule out any underlying systemic illnesses or conditions.
adults. Patients with GAP who smoke have more affected teeth Radiographs will help in confirming the diagnosis based on
and a greater loss of clinical attachment than nonsmoking pa- clinical findings.
tients with GAP However, smoking may not have the same For futher information for the treatment of aggressive peri-
impact on the attachment levels in younger patients with LAP odontitis, please refer to Chapter 31.
Diagnosis SUGGESTED READINGS

Armitage GC: Comparison of the microbiological features of chronic and ag-
Assessment of Clinical Presentation gressive periodontitis, Periodontol 2000(53):70-88, 2010.
Armitage GC, Cullinan MP: Comparison of the clinical features of chronic
The most reliable diagnostic marker for periodontitis is periodon- and aggressive periodontitis, Periodontol 2000(53):12-27, 2010.
tal probing. However, this technique merely assesses a loss of at- Demmer RT, Papapanou PN: Epidemiologic patterns of chronic and aggres-
sive periodontitis, Periodontol 2000(53):28-44, 2010.
tachment; it does not classify subcategories of periodontal disease. Fine DH, Markowitz K, Furgang D, et al: Aggregatibacter actinomycetemcomi-
The diagnosis of aggressive periodontitis in the clinic is tans and its relationship to initiation of localized aggressive periodontitis:
therefore made by jointly assessing the primary and secondary longitudinal cohort study of initially healthy adolescents, J Clin Microbial
features of aggressive periodontitis, as described previously. 45(12) 3859-3869, 2007.
As a result of the small but significant prevalence of this se- Haubek D, Ennibi OK, Poulsen K, et al: Risk of aggressive periodontitis in
adolescent carriers of the JP2 clone of Agg,·egatibacter (Actinobacillus) ac-
vere category of periodontal disease, it is also recommended to tinomycetemcomitans in Morocco: a prospective longitudinal cohort study,
routinely screen for the presence of attachment loss in younger Lancet 371(9608):237-242, 2008.
patients with the use of Periodontal Screening and Recording Kebschull M, Guarnieri P, Demmer RT, et al: Molecular differences between
or the Periodontal Screening Index every year. In patients with chronic and aggressive periodontitis,J Dent Res 92(12):1081-1088, 2013.
Laine ML, Crielaard W, Loos BG: Genetic susceptibility to periodontitis, Peri-
significant findings, a more thorough clinical assessment that odontal 58(1):37-68, 2012, 2000.
includes the evaluation of periodontal probing depth and at- Nowak M, Kramer B, Haupt M, et al: Activation of invariant NK T cells in
tachment loss at six sites per tooth should be performed. periodontitis lesions, J Immunol l 90(5):2282-2291, 2013.
In addition, patients who are at risk for developing aggres- Schaefer AS, Richter GM, Dommisch H, et al: CDKN2BAS is associated with
periodontitis in different European populations and is activated by bacte-
sive periodontitis should be more closely monitored. These rial infection,] Med Genet 48(1) 38-47, 2011.
are primarily subjects with a known familiar aggregation of Smith M, Seymour GJ, Cullinan MP: Histopathological features of chronic
aggressive periodontitis (eg, the child of a patient with aggres- and aggressive periodontitis, Periodontal 2000(53):45-54, 2010.
sive periodontitis who is already being treated in the practice).
23 Aggressive Periodontitis 249.el
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24
Pathology and Management of
Periodontal Problems in Patients
With Human Immunodeficiency
Virus Infection
TD Rees • N Ambalavanan
Chapter Outline
Pathogenesis Dental Treatment Complications
Classification and Staging Gingival and Periodontal Diseases
Oral and Periodontal Manifestations Periodontal Treatment Protocol
of Human Immunodeficiency Virus
Infection
Acquired immunodeficiency syndrome (AIDS) is characterized by other immune cell functions. Recent evidence indicates that
profound impairment of the immune system. The condition was innate immune response may play a role in controlling HIV
first reported in 1981, and a viral pathogen, the human immuno- replication. Chemokine receptor type 5 (CCRS) is found on
deficiency virus (HIV), was identified in 1984. The condition was the surface of CD4 cells, and it often serves as a point of entry
originally thought to be restricted to male homosexuals. Subse- for HIV into the cell.
quently, it was also identified in male and female heterosexuals B lymphocytes are not infected, but the altered function
and bisexuals who participated in unprotected sexual activities of infected T4 lymphocytes secondarily results in B-cell dys-
or who abused injected drugs. Currently, sexual activity and regulation and altered neutrophil function. This may place the
drug abuse remain the primary means of transmission. HIV-positive individual at increased risk for malignancy and
HIV has a strong affinity for cells of the immune system, disseminated infections with microorganisms such as viruses,
most specifically those that carry the CD4 cell surface recep- mycobacterioses, and mycoses. HIV-positive individuals are
tor molecule. Thus, helper T lymphocytes (T4 cells) are most also at increased risk for adverse drug reactions as a result of
profoundly affected, but monocytes, macrophages, Langer- altered antigenic regulation. Epithelial cells of the mucosa may
hans cells, and some neuronal and glial brain cells may also become infected, and they may allow for the access of the virus
be involved. Viral replication occurs continuously in the lym- into the bloodstream. Some evidence suggests that oral epi-
phoreticular tissues of the lymph nodes, the spleen, the gut- thelial cells may harbor HIV virions and infect CD4+ cells by
associated lymphoid cells, and the macrophages. direct cell-to-cell transfer or by transporting and releasing low
In 1986, a second type of HIV was isolated in Western levels of infectious virions. Most evidence, however, indicates
Africa, and subsequently the two were named HIV-1 and HIV- that oral transmucosal viral transmission occurs after mild or
2. HIV-2 is very similar to HIV-1, but it appears to be less viru- severe traumatic injury or punctures of the mucous mem-
lent, and it causes AIDS much more slowly Infection with HIV- branes. This allows for the infection of circulating host defense
2 is rarely identified outside of Africa and countries that have cells such as lymphocytes, macrophages, and dendritic cells.
been intimately associated with that area. Viral mutations may HIV has been detected in most body fluids, although it
play a role in the increasing resistance to antiretroviral therapy is found in high quantities only in blood, semen, and cere-
brospinal fluid. Transmission occurs almost exclusively by
sexual contact, the illicit use of injection drugs, or exposure
Pathogenesis to blood or blood products. Transmission after human bites
In patients with untreated or inadequately treated HIV infec- has been reported, although the risk is extremely low. The
tion, the overall effect is the gradual impairment of the im- high-risk population includes homosexual and bisexual men;
mune system via interference with T4 (CD4) lymphocytes and users of illegal injection drugs; persons with hemophilia or
251
other coagulation disorders; recipients of blood transfusions as being definitive for AIDS. This change was based on the rec-
before Apr. 1985; infants of HIV-infected mothers (in whom ognition that severe immunodeficiency results in an increased
transmission occurs by fetal transmission, at delivery, or by risk for opportunistic, life-threatening conditions. Many HIV-
breastfeeding); promiscuous heterosexuals; and individuals positive individuals have been designated as patients with
who engage in unprotected sex with HIV-positive cohorts AIDS solely because of a low CD4 cell count or percentage,
even in the absence of life-threatening conditions. More re-
cently, HIV plasma bioload has been identified as a significant
Classification and Staging factor related to the transmissibility and severity of the disease.
The World Health Organization (WHO) and the CDC each
have published guidelines regarding the definition of HIV in- Testing for Human Immunodeficiency
fection and HIV disease staging. In both sets of guidelines,
Virus Infection
HIV infection is confirmed, if possible, with the use of labora-
tory criteria. However, in many parts of the world, laboratory The enzyme-linked immunosorbent assay (ELISA) and
testing is not available. Consequently, in the WHO concept, Western blot (WB) tests were the original methods for deter-
clinical findings may be used to establish the diagnosis and to mining the presence of HIV-1 and HIV-2 antibodies in serum
determine a patient's eligibility for antiretroviral therapy. or plasma, and they are still considered the gold standard of
The WHO staging and case definition system was devel- confirmatory testing. The ELISA test is performed first, and it
oped in 1990 and revised in 2007. Staging is primarily based is repeated if the first test is positive. If it is positive a second
on the clinical appearance of the disease, and it includes the time, WB is performed, and a positive finding is considered
following diagnostic for the infection. Both ELISA and WB require the
presence of circulating HIV antibodies, which may take sev-
Clinical stage 1: Asymptomatic infection or persistent gener-
eral weeks or even months to become detectible. Thus, false-
alized lymphadenopathy
negative tests are possible and repeat testing may be required,
Clinical stage 2: Mild symptoms such as mild unexplained
although modern testing methods are highly accurate. Today,
weight loss, angular cheilitis, herpes zoster, recurrent oral
several other test methods are based on the presence of an
ulcerations, papular pruritic eruptions, seborrheic derma-
HIV antigen. Although these tests are expensive, they may be
titis, fungal infections, and recurrent respiratory infections
of benefit, especially for early diagnosis after exposure.
Clinical stage 3: Advanced symptoms such as severe weight
The window of time between exposure and the develop-
loss, chronic diarrhea, persistent intermittent or constant
ment of antibodies can lead to an increased risk for disease
fever, pulmonary tuberculosis, severe bacterial infections,
transmission, and some evidence suggests that early treatment
unexplained anemia, neutropenia, chronic thrombocytope-
during that window can significantly minimize the intensity
nia persistent oral candidiasis, oral hairy leukoplakia, acute
of the infection and positively influence treatment outcomes.
necrotizing stomatitis, gingivitis, and periodontitis
Consequently, during recent years, several test methods have
Clinical stage 4: Severe symptoms such as HIV wasting syn-
been developed that detect the presence of HIV genes, RNA,
drome, Pneumocystis pneumonia, chronic herpes simplex
or deoxyribonucleic acid (DNA). These tests may offer the
infection of more than 1 month duration, esophageal can-
advantage of the earlier confirmation of recent exposure and
didiasis, extrapulmonary tuberculosis, Kaposi's sarcoma,
infection. Several rapid HIV tests are currently available that
cytomegalovirus (CMV) infection, lymphoma, candidiasis
can provide results in minutes as opposed to days. In some
(of the trachea, bronchi, or lungs), invasive cervical carci-
instances, collection kits are available for personal use, includ-
noma, and others
ing one that collects oral fluids. At this time, the US Food
AIDS may be present with either clinical stage 3 or stage and Drug Administration has approved approximately seven
4 disease. A CD4 count of less than 350/mm3 is considered of these rapid tests as well as three that test for HIV and for
diagnostic for AIDS in adults and in children who are 5 years coinfection with the hepatitis C virus; one of these also tests
old or older. Advanced HIV infection in infants is based on for hepatitis B virus. Rapid tests may require the collection
a CD4+ cell value of less than 30% if the patient is less than of oral fluids, plasma, serum, or whole blood, and the CDC
12 months old; of less than 25% among those between 12 encourages their use in most health care settings. It must be
and 35 months old; and of less than 20% among those be- recognized that rapid tests may have a relatively high number
tween the ages of 36 and 59 months. (These are the WHO of false-negative results as well as some false-positive results,
case definitions of HIV for surveillance and the revised clinical so repeat testing and follow-up testing with ELISA and WB
staging and immunologic classifications of HIV-related disease are often indicated. Rapid tests may be of special benefit in
in adults and children.) undeveloped countries, where medical laboratory testing may
In 1982, the CDC developed a surveillance case definition not be readily available.
for AIDS based on the presence of opportunistic illnesses or A few weeks to a few months after initial exposure, some
malignancies secondary to defective cell-mediated immunity HIV-infected individuals may experience acute symptoms,
in HIV-positive individuals. The 1993 revision added invasive such as the sudden onset of an acute mononucleosis-like ill-
cervical cancer in women, bacillary tuberculosis, and recurrent ness that is characterized by malaise, fatigue, fever, myalgia,
pneumonia to the AIDS designation. Currently 25 specific clin- erythematous cutaneous eruption, oral candidiasis, oral ulcer-
ical conditions found in HIV-positive individuals can establish ations, and thrombocytopenia. This acute phase may last for
the diagnosis of AIDS. The most significant change in the most up to 2 weeks, with seroconversion occurring 3-8 weeks later.
recent CDC case definition was the inclusion of severe im- However, antigenic viremia may sometimes be present for an
munodeficiency (CD4+ T lymphocyte count of <200/mm3 or extended time before seroconversion occurs. Some individuals
CD+ T lymphocyte percentage of < 14% of total lymphocytes) experience asymptomatic HIV infection, whereas others may
24 Pathology and Management of Periodontal Problems in Patients With Human Immunodeficiency Virus Infection 253
become asymptomatic after the initial acute infection. In either Protease inhibitors are potent antiretrovirals that also are
case, infected individuals eventually become seropositive for metabolized by the CYP3A4 isoenzyme of the hepatic p450
HIV antibody, but the mean time from infection until the devel- system, which means that adverse drug interactions are com-
opment of AIDS is now estimated to be up to 15 years or more. mon to other antiretroviral agents and non-HIV agents. Gas-
trointestinal intolerance, hyperlipidemia, insulin resistance,
and lipodystrophy are common.
Centers for Disease Control The only fusion inhibitor that has currently been approved
and Prevention Surveillance Case is enfuvirtide. Because it is administered subcutaneously, in-
jection site reactions are common. Enfuvirtide is rarely used
Classification alone for the management of HIV infection.
Patients with AIDS have been grouped as follows, according Combined antiretroviral drug therapy has been extremely
to the 1993 CDC Surveillance Case Classification: successful for changing HIV infection from a rapidly progres-
sive fatal disease to a chronic condition that often can be man-
• Category A includes patients with acute symptoms or as- aged successfully. This type of therapy has improved survival
ymptomatic diseases as well as individuals with persistent rates to nearly normal while suppressing or eliminating sus-
generalized lymphadenopathy with or without malaise, fa- ceptibility to some opportunistic diseases and disorders.
tigue, or low-grade fever (Fig. 26 1)
• Category B patients have symptomatic conditions such as
oropharyngeal or vulvovaginal candidiasis, herpes zoster, Highly Active Antiretroviral Therapy
oral hairy leukoplakia, and idiopathic thrombocytopenia or
constitutional symptoms of fever, diarrhea, and weight loss. With HAART therapy, combinations of three or more antiret-
• Category C patients are those with outright AIDS as mani- roviral drugs are administered simultaneously for long peri-
fested by life-threatening conditions or as identified by ods of time in an effort to block HIV replication and plasma
CD4+ T lymphocyte levels of less than 200 cells/mm3. viral load and to restore immune function while minimiz-
ing antiretroviral drug resistance and adverse drug effects.
The CDC staging categories reflect progressive immuno- The goals are the improvement of the patient's quality of
logic dysfunction, but patients do not necessarily progress life and the reduction of HIV-related morbidity and mortal-
serially through the three stages, and the predictive value ity. Three commonly used combinations are one NNRTI plus
of these categories is not known. However, because HAART two NRTls; one or two protease inhibitors plus two NRTls; or
drugs may cause severe adverse side effects, many AIDS treat- three NRTls. One NRTI three-drug combination is available in
ment centers continue to follow these guidelines to determine a single tablet, but this antiretroviral therapy does not neces-
when to initiate or discontinue multidrug therapy. sarily qualify as HAART.
HAART has to be proven very successful for achiev-
ing a significant increase in the survival and quality of life
Antiretroviral Therapy of HIV-infected individuals, and life expectancy is markedly
To date, 36 drugs or drug combinations from 6 separate drug increased for many individuals using this therapy. However,
classes have been approved by the US Food and Drug Admin- not everyone benefits equally from HAART. Survival time is
istration for the treatment of HIV and AIDS infection. shorter despite HAART among individuals who are injected
Nucleoside reverse transcriptase inhibitors (NRTls) were drug abusers, in those with AIDS before the initiation of ther-
the first class of antiretrovirals to be developed. They act by apy, in those with a very high viral load before the initiation
competing for incorporation into the proviral chain, thereby of therapy (ie, > 100,000 copies/ml), in those who are incon-
eliminating chain elongation. They are effective against both sistent in their adherence to the drug regimen, and in those
HIV-1 and HIV-2. NRTls are the principal drugs in use today who discontinue the drugs. Other factors that affect life expec-
in drug combinations. tancy in the era of HAART include smoking; excessive alcohol
Nonnucleoside reverse transcriptase inhibitors (NNRTls) consumption; older age at initiation of therapy; comorbidities
bind to the active site in the developing HIV-1 viral chain and such as hepatitis C or other viral, bacterial, or fungal infec-
arrest its development. These drugs are quite effective, but tions; chronic liver, kidney, or cardiovascular conditions; and
they rapidly develop resistance via a single-step mutation. diabetes mellitus
Protease inhibitors are active against both HIV-1 and HIV-2.
They bind to the HIV protease enzyme and result in the for-
mation of noninfectious HIV virions. Fusion inhibitors bind Oral and Periodontal Manifestations
to the gp4 l glycoprotein membrane on HIV and prevent virus of Human Immunodeficiency Virus
fusion into susceptible CD4 cells. The drugs are administered Infection
by subcutaneous injection. Some entry inhibitors block the
access of HIV to CCRS receptors on macrophages and to T Oral lesions are common in HIV-infected patients, although geo-
cells that are helping to preserve immune function and reduce graphic and environmental variables may exist. Previous reports
viral load. Integrase inhibitors block the incorporation of viral have indicated that most patients with AIDS have head and
DNA into CD4 cell DNA after viral RNA has been converted neck lesions, whereas oral lesions are quite common among
into DNA by the reverse transcription enzyme. Combination HIV-positive individuals who do not yet have AIDS. Several
antiviral agents are composed of multiple drugs with various reports have identified a strong correlation between HIV in-
sites of viral disruption of incorporation into CD4 cells. These fection and oral candidiasis, oral hairy leukoplakia, atypical
combinations represent the transformation of antiretroviral periodontal diseases, oral Kaposi's sarcoma, and oral non-
therapy into HAART. Hodgkin's lymphoma.
Oral lesions less strongly associated with HIV infection

include melanotic hyperpigmentation, mycobacterial infec-
tions, necrotizing ulcerative stomatitis (NUS), miscellaneous
oral ulcerations, and viral infections (eg, herpes simplex virus
[HSY], herpes zoster, and condyloma acuminatum). Lesions
that are seen in HIV-infected individuals with undetermined
frequency include less common viral infections (eg, CMV,
molluscum contagiosum), recurrent aphthous stomatitis, and
bacillary angiomatosis (epithelioid angiomatosis).
The advent of HMRT has resulted in the greatly dimin-
ished frequency of oral lesions associated with HIV infection
and AIDS. FIGURE 24.2 Gingival erythematous candidiasis that is suggestive of
desquamative gingivitis.
Oral Candidiasis
Candidiasis is the most common oral lesion associated with In Candida-related angular cheilitis, the commissures of the
HIV disease, and it has been found in approximately 90% of lips appear erythematous, with surface crusting and fissuring.
patients with AIDS. It usually has one of four clinical presen- The diagnosis of candidiasis is made by the clinical eval-
tations: pseudomembranous, erythematous, or hyperplastic uation, culture analysis, or microscopic examination of a
candidiasis or angular cheilitis. tissue sample or smear of material scraped from the lesion
Pseudomembranous candidiasis (thrush) presents as painless (oral cytology), which shows hyphae and yeast forms of the
or slightly sensitive, yellow-white, curd-like lesions that can organisms. When oral candidiasis appears in patients with
be readily scraped and separated from the surface of the oral no apparent predisposing causes, the clinician should be
mucosa. This type is most common on the hard and soft pal- alerted to the possibility of HIV infection. Many patients
ate and the buccal or labial mucosa, but it can occur anywhere who are at risk for HIV infection who present with oral can-
in the oral cavity didiasis also have esophageal candidiasis, which is a diag-
Erythematous candidiasis may be present as a component of nostic sign of AIDS.
the pseudomembranous type, appearing as red patches on the
buccal or palatal mucosa, or it may be associated with depa-
Oral Hairy Leukoplakia
pillation of the tongue. If the gingiva is affected, it may be mis-
diagnosed as desquamative gingivitis (Figs. 24.1 and 24 2). Oral hairy leukoplakia (OHL) primarily occurs in persons
Some evidence suggests that erythematous candidiasis in more with HIV infection. It is found on the lateral borders of the
common among HIV-positive individuals with CD4+ counts tongue, it frequently has a bilateral distribution, and it may
between 200 and 500 cells/µL, whereas the pseudomembra- extend to the ventrum. OHL is caused by the Epstein-Barr vi-
nous form occurs in patient with less than 200 CD4+ cells/µL. rus (EBY), and it is the only EBY lesion with which viral shed-
Viral load is most often elevated to more than 100,000 copies/ ding in saliva is common. The lesion is characterized by an as-
ml. However, it should be emphasized that any form of can- ymptomatic, poorly demarcated, keratotic area that ranges in
didiasis can be found in individuals who are only minimally size from a few millimeters to several centimeters (Fig. 24.3A).
immunocompromised. Often, characteristic vertical striations are present, and these
Hyperplastic candidiasis is the least common form, and it impart a corrugated appearance; the surface may also be shag-
may be seen in the buccal mucosa and the tongue. It is more gy and appear "hairy" when dried. The lesion does not rub off,
resistant to removal than the other types. and it may resemble other keratotic oral lesions.
Microscopically, the OHL lesion shows a hyperparakeratot-
ic surface with projections that often resemble hairs. Beneath
the parakeratotic surface, acanthosis and some characteristic
"balloon cells" that resemble koilocytes are seen (Fig. 24.3B).
It has been demonstrated that these cells contain viral par-
ticles of the human herpesvirus group; these particles have
been interpreted as EBV
Epithelial dysplasia is not a feature, and, in most OHL le-
sions, little or no inflammatory infiltrate in the underlying
connective tissue is present.
OHL is found almost exclusively on the lateral borders of
the tongue, although it has been reported on the dorsum of
the tongue, the buccal mucosa, the floor of the mouth, the ret-
romolar area, and the soft palate. In addition, most of these le-
sions reveal surface colonization by Candida organisms, which
are secondary invaders and not the cause of the lesion.
OHL was originally thought to be caused by the human
papillomavirus, but subsequent evidence has indicated an as-
sociation with EBV Regardless of the cause, biopsy identifica-
tion of a lesion that is suggestive of OHL should dictate that
FIGURE 24.1 Palatal erythematous candidiasis. HIV testing be performed. It should be emphasized that the
KS is the most common oral malignancy associated with

AIDS. This angioproliferative tumor is a rare, multifocal,
vascular neoplasm; it was originally described in 1872 as oc-
curring in the skin of the lower extremities of older men of
Mediterranean origin. The causative agent has been identified
as human herpesvirus-8 (HHV-8).
Lymphedema of the neck and face has been reported in as-
sociation with oral lesions. The cause of the lymphedema has
not been determined, but it may result from the compression
of lymphatics by expanding lesions. The presence of facial
lymphedema is considered to be an ominous sign that is as-
sociated with a fatal outcome. During the early stages, the oral
lesions are painless, reddish-purple macules of the mucosa.
As they progress, the lesions frequently become nodular, and
they can easily be confused with other oral vascular entities,
such as hemangioma, hematoma, varicosity, and pyogenic
granuloma (when occurring in the gingiva).
Lesions may manifest as nodules, pa pules, or nonelevated
macules that are usually brown, blue, or purple, although
occasionally the lesions may display normal pigmentation.
The lesions may become painful if they become ulcerated or
traumatized by opposing teeth as they enlarge. Diagnosis is
based on histologic findings. Gingival KS lesions may be ex-
acerbated by existing periodontal lesions, or necrotizing peri-
odontal diseases may be superimposed on existing gingival
KS. On occasion, the expansion of gingival lesions may result
FIGURE 24.3 Oral hairy leukoplakia on the left lateral border of the
tongue. A, Clinical view. B, Biopsy confirmation of oral hairy leukopla-
in bone resorption, and increased tooth mobility and loss has
kia. Note the ballooned epithelial cells near the surface of the epithelium. been reported. The treatment of oral KS includes antiretrovi-
ral agents, laser excision, cryotherapy, radiation therapy, and
intralesional injection with vinblastine, interferon-y, scleros-
ing agents, or other chemotherapeutic drugs. Nichols and
severity of the lesion is not correlated with the likelihood of
colleagues described the successful use of intralesional injec-
developing AIDS; thus, small lesions are as diagnostically sig-
tions of vinblastine at a dose of 0.1 mg/cm2 with the use of a
nificant as extensive lesions.
0.2 mg/ml solution of vinblastine sulfate in saline. However,
comparable results may be obtained with the use of injections
Kaposi's Sarcoma and Other Malignancies of 3% sodium tetradecyl sulfate, a sclerosing agent that was
previously used for the treatment of varicose veins. The scle-
Oral malignancies occur more frequently in severely immu-
rosing agent offers the advantage of being relatively inexpen-
nocompromised individuals than in the general population.
sive and easy to use. Destructive periodontitis has also been
An HIV-positive individual with non-Hodgkin's lymphoma
reported in conjunction with gingival KS. In such patients,
(NHL) or Kaposi's sarcoma (KS) is categorized as having AIDS
scaling and root planing as well as other periodontal therapy
(Fig. 24.4). Oral lesions are reported in approximately 4% of
may be indicated in addition to intralesional or systemic che-
individuals with NHL, and the gingiva and palate are common
motherapy.
sites. The incidence of oral squamous cell carcinoma may also
Today, some authorities recommend the treatment of oral
increase among HIV-infected individuals. An epidemic form
KS with the use of a combination of HAART and systemic
of KS has been described in HIV-positive individuals, and it is
cytotoxic therapy.
an AIDS-defining condition.
Non-Hodgkin's Lymphoma
Lymphoma represents a heterogeneous malignancy that
is characterized by the proliferation of lymphoid cells. It is
broadly classified as Hodgkin's disease (14%) or NHL NHL in
individuals with HIV infection is an AIDS-defining condition,
and elevated cumulative viremia may be a strong predictor of
AIDS-related lymphoma.
The risk of NHL is associated with a number of infec-
tions; EBY-associated lesions may include Burkitts lym-
phoma and HIV-associated lymphoma. NHL is treated
by chemotherapy, and HAART does not appear to sig-
nificantly reduce the incidence or prognosis of the ma-
lignancies, although HIV-associated NHL may be less
FIGURE 24.4 Non-Hodgkin's lymphoma of the anterior mandibular common. Oral lesions usually appear as erythematous,
gingiva. painless enlargements that may become ulcerated as a
result of traumatic injury. In some cases, bone involve- Oral Hyperpigmentation

ment occurs. Lesions commonly affect the gingival, pal-
atal, and alveolar mucosa, and they may mimic dental An increased incidence of oral hyperpigmentation has been
infections. Diagnosis is based on physical examination, described in HIV-infected individuals. Oral pigmented areas
complete blood count with differential, imaging studies, often appear as spots or striations on the buccal mucosa, the
and lymph node and tissue biopsy. Patients with AIDS palate, the gingiva, or the tongue (Fig. 24.6 A,B). At present,
and NHL may require the management of HIV-related most reports describing the oral features of HIV/AIDS or post-
opportunistic infections, chemotherapy-induced muco- HAART HIV/AIDS come from areas of the world in which racial
sitis and thrombocytopenia, and possibly graft-versus- pigmentation may be common. In these areas, oral evaluation
host disease, if hematopoietic cell transplantation is may often be accomplished by nondental health care workers.
performed. Consequently, it is not possible to accurately assess the degree
of HIV-related oral hyperpigmentation before or after ART.
In some cases, the pigmentation may relate to the pro-
Bacillary (Epithelioid) Angiomatosis longed use of drugs such as zidovudine, ketoconazole, or
Bacillary (epithelioid) angiomatosis (BA) is an infectious clofazimine. Zidovudine is also associated with the excessive
vascular proliferative disease with clinical and histologic fea- pigmentation of the skin and nails, although similar hyperpig-
tures similar to those of KS. BA is caused by facultative intra- mentation has been reported in some individuals who have
cellular Gram-negative mobile bacilli of the genus Bartonella never taken zidovudine. On occasion, oral pigmentation may
and the order Rickettsia (eg, Bartonella henselae, Bartonella be the result of adrenocorticoid insufficiency that has been
quintana). Cats are the primary host of B. henselae, and the induced in an HIV-positive individual via the prolonged use
infection is usually transmitted to humans by bites, scratches, of ketoconazole or by Pneumocystis jiroveci, CMV, or other viral
or fleas (ie, cat-scratch fever). Man is the primary reservoir infections (Fig. 24.6)
for B. quintana, and it is usually transmitted by human lice.
BA can occur in immunocompetent persons, but it is most Atypical Ulcers
commonly associated with AIDS. Skin lesions are similar to
those associated with KS or cat-scratch disease. Gingival BA Atypical ulcers (nonspecific oral ulcerations) in HIV-infected
manifests as red, purple, or blue edematous soft-tissue lesions individuals may have multiple etiologies that include neo-
that may cause the destruction of periodontal ligament and plasms such as lymphoma, KS, and squamous cell carcinoma.
bone (Fig. 24 5) HIV-associated neutropenia may also feature oral ulcerations.
The condition is more prevalent in HIV-positive individu- Neutropenia has been successfully treated with the use of
als with low CD4 levels. recombinant human granulocyte colony-stimulating factor,
The diagnosis of BA is based on biopsy, which reveals an with the resultant resolution of oral ulcers. Severe and pro-
"epithelioid" proliferation of angiogenic cells accompanied longed oral ulcers have been successfully managed with the
by an acute inflammatory cell infiltrate. The causative organ-
ism in the biopsy specimen may be identified with the use
of Warthin-Starry silver staining or electron microscopy.
The differential diagnosis of BA includes KS, angiosarcoma,
hemangioma, pyogenic granuloma, and nonspecific vascular
proliferation. BA is usually treated with the use of broad-
spectrum antibiotics such as erythromycin or doxycycline.
Gingival lesions may be managed by using the antibiotic in
conjunction with conservative periodontal therapy and pos-
sibly the excision of the lesion. To date, no reports have been
found regarding the effect of HAART on BA incidence among
HIV-positive individuals. However, one case report described
a fatal outcome of B. quintana-derived BA during HAART-
induced immunity restoration.
FIGURE 24.6 Drug-induced hyperpigmentation as a result of zid-

ovudine use. A, Palatal hyperpigmentation. B, Tongue hyperpigmenta-
FIGURE 24.5 Bacillary angiomatosis mimicking Kaposi's sarcoma. tion in the same patient.
FIGURE 24.7 Abnormal herpetic lesions in individuals with human immunodeficiency virus. A, The lip crusting of primary herpetic gingivostoma-
titis. B, Ulcerations of the gingiva, the alveolar mucosa, and the vestibule in the same patient.
use of prednisone or thalidomide, a drug that inhibits tissue Salivary function does not appear to be affected by HAART,
necrosis factor-a. Recurrence is likely, however, if either drug despite the fact that some individual antiretroviral medications
is discontinued. are reported to induce xerostomia. However, it is clear that
HIV-infected patients have a higher incidence of recurrent xerostomia is a relatively common condition among HIV-in-
herpetic lesions and aphthous stomatitis (Figs. 2 4. 7 A and B). fected individuals and that up to 10% of these patients may
Approximately 10% of HIV-infected patients have herpes in- be affected. Xerostomia appears to become more severe as im-
fection, and multiple episodes are common. The CDC HIV munosuppression worsens, and increased candidal carriage is
classification system indicates that mucocutaneous herpes associated with reduced salivary flow rate.
that lasts more than 1 month is diagnostic of AIDS in HIV-
infected individuals. Aphthae and aphthae-like lesions are
common when patients are followed throughout the course of Dental Treatment Complications
their immunosuppression.
Concerns have been expressed regarding the potential for
In healthy patients, herpetic and aphthous lesions are self-
postoperative complications (eg, hemorrhage, infection, de-
limiting and relatively easy to diagnose as a result of their
layed wound healing) in individuals with HIV or AIDS. Medi-
characteristic clinical features (ie, herpes on the keratinizing
cally compromised patients must be carefully managed in the
mucosa and aphthae on the nonkeratinizing surfaces). In HIV-
dental office to avoid undue treatment complications. How-
infected patients, the clinical presentation and course of these
ever, systematic reviews of the literature indicate that special pre-
lesions may be altered. Herpes may involve all mucosal sur-
cautions are usually not necessary based simply on the HIV status
faces and extend to the skin, and it may persist for months
of patients when performing periodontal treatment procedures such
(Fig. 26 21). Atypical large, persistent, nonspecific, and pain-
as dental prophylaxis, scaling and root planing, periodontal sur-
ful ulcers are common in immunocompromised individuals.
gery, extractions, and the placement of implants. On occasion, the
If healing is delayed, these lesions are secondarily infected, poor overall health status of an individual with AIDS may limit
and they may become indistinguishable from persistent her-
periodontal therapy to conservative, minimally invasive proce-
petic or aphthous lesions.
dures, and antibiotic therapy may be required. When possible,
Recurrent aphthous stomatitis has been described in
antibiotics should be avoided in significantly immunocompro-
HIV-infected individuals, but the overall incidence may be
mised individuals to minimize the risk of opportunistic infec-
no greater than that found in the general population. Recur- tions (ie, candidiasis), superinfection, and drug resistance.
rent aphthous stomatitis may occur, however, as a compo-
nent of the initial acute illness of HIV seroconversion. The
incidence of major aphthae may be increased, and the oro- Gingival and Periodontal Diseases
pharynx, esophagus, or other areas of the gastrointestinal
tract may be involved. Considerable research has focused on the nature and inci-
Proven methods for the treatment of recurrent aphthous dence of periodontal diseases in HIV-infected individuals.
stomatitis include topical or intralesional corticosteroids, Some studies suggest that chronic periodontitis is more com-
chlorhexidine or other antimicrobial mouthrinses, oral tetra- mon in this patient population, but others do not. Periodontal
cycline rinses, and topical amlexanox. Systemic corticosteroid diseases are more common among HIV-infected users of injec-
therapy may be necessary in some cases. Consequently, in pa- tion drugs, but this may relate to poor oral hygiene and a lack
tients with HIV infection and recurrent aphthae, closely coor- of dental care rather than decreased CD4 cell counts. How-
dinated medical and dental therapy may be necessary ever, some unusual types of periodontal diseases do seem to
occur with greater frequency among HIV-positive individuals.
Salivary Gland Disorders and Xerostomia
Linear Gingival Erythema
Salivary gland hypofunction and xerostomia may be most
common among HIV-infected men during both the early and A persistent, linear, easily bleeding, erythematous gingivi-
advanced stages of HIV infection and immunosuppression. tis has been described in some HIV-positive patients. The
administration of a systemic antifungal agent, such as flucon-

azole, for 7-10 days.
It is important to remember that LGE is often refractory
to treatment. If so, the patient should be carefully monitored
for developing signs of more severe periodontal conditions
(eg, NUG, NUP, NUS). The patient should be placed on a
2- to 3-month recall maintenance interval and retreated as
necessary. As mentioned previously, despite the occasional
resistance of LGE to conventional periodontal therapy, spon-
taneous remission may occur for reasons that are not yet
FIGURE 24.8 Linear gingival erythema and necrotizing ulcerative known.
gingivitis in a patient with acquired immunodeficiency syndrome.
Necrotizing Ulcerative Gingivitis

intensity of the erythema is disproportionate to the amount of Some reports have described an increased incidence of NUG
plaque present. There is no ulceration, pocketing, or attach- among HIV-infected individuals, although this has not been
ment loss, and the condition does not respond predictably to substantiated by other studies.
conventional periodontal therapy Lesions that are clinically There is no consensus regarding whether the incidence
identical to linear gingival erythema were observed before the of NUG increases in HIV-positive patients. However, a re-
advent of HIV in association with severely immunocompro- cent study evaluated the HIV status of individuals who
mised individuals or in those with NUG. presented with necrotizing periodontal diseases, and 69%
Linear gingival erythema (LGE) may or may not serve were found to be HIV seropositive. The treatment of NUG
as a precursor to rapidly progressive NUP (Figs. 24.8). The in these patients does not differ from that used for HIV-
microflora of LGE may closely mimic that of periodontitis negative individuals.
rather than gingivitis. However, Candida infection has been im- The affected gingiva may be exquisitely painful, and cau-
plicated as a major etiologic factor, and human herpesviruses tion must be taken to avoid undue patient discomfort. Ba-
have been proposed as possible triggers or cofactors. Linear sic treatment may consist of the cleaning and debridement
gingivitis lesions may be localized or generalized in nature. of affected areas with a cotton pellet soaked in peroxide after
The erythematous gingivitis may be limited to marginal tis- the application of a topical anesthetic. Escharotic oral rinses
sue, extend into attached gingiva in a punctate or diffuse ery- such as hydrogen peroxide should only rarely be used for any
thema, or extend into the alveolar mucosa. patient, and they are especially contraindicated in immuno-
Although LGE may sometimes be unresponsive to correc- compromised individuals. The patient should be seen daily
tive therapy, such lesions may undergo spontaneous remis- or every other day for the first week, and the debridement of
sion. Concomitant oral candidiasis and LGE lesions have been affected areas is repeated at each visit. Plaque-control methods
identified, which suggests a possible etiologic role for candi- are gradually introduced. A meticulous plaque-control pro-
dal species in LGE. In one study, direct microscopic cultures gram should be taught and started as soon as the sensitivity
from LGE lesions implicated Candida dubliniensis in four pa- of the area allows it. After initial healing has occurred, the
tients, all of whom experienced complete or partial remission patient should be able to tolerate scaling and root planing, if
after systemic antifungal therapy. It is not yet known whether needed.
candidal infections are etiologic in all LGE cases. A recent The patient should avoid tobacco, alcohol, and condi-
systematic review indicates that LGE is more common among ments. An antimicrobial oral rinse such as chlorhexidine glu-
HIV-infected populations but that most individuals who are conate 0.12% should be prescribed.
HIV-positive do not experience LGE. Systemic antibiotics such as metronidazole or amoxicillin
Others have reported that LGE is most often found in HIV- may be prescribed for patients with moderate to severe tissue
positive individuals whose CD4+ counts are depressed (ie, destruction, localized lymphadenopathy, or systemic symp-
200 to 500 cells/mm3 or <200 cells/mm3) or whose viral loads toms. Metronidazole may be the antibiotic of choice because
are elevated, thereby suggesting that it may represent an early it has been demonstrated to be effective for the treatment of
marker of progressive immunodeficiency or even the transi- NUG, and its narrow bactericidal spectrum may minimize the
tion to outright AIDS. risk of secondary opportunistic infections such as candidiasis.
LGE-like lesions can sometimes be adequately managed The use of prophylactic antifungal medication should be con-
by following the therapeutic principles associated with mar- sidered if antibiotics are prescribed.
ginal gingivitis. However, it has been suggested that gingivitis The periodontium should be reevaluated 1 month after the
lesions that respond to conventional therapy do not repre- resolution of acute symptoms to assess the results of treatment
sent LGE. The affected sites should be scaled and polished. and to determine whether further therapy will be necessary.
Subgingival irrigation with chlorhexidine or 10% povidone-
iodine may be beneficial. The patient should be carefully in-
structed regarding the performance of meticulous oral hygiene
Necrotizing Ulcerative Periodontitis
procedures. The condition should be reevaluated 2-3 weeks A necrotizing, ulcerative, rapidly progressive form of peri-
after initial therapy If the patient is compliant with home care odontitis occurs more frequently among HIV-positive indi-
procedures and the lesions persist, the possibility of a candi- viduals, although such lesions were described long before
dal infection should be considered. It is doubtful that topical the onset of the AIDS epidemic. NUP appears to represent an
antifungal rinses will reach the base of the gingival crevices. extension of NUG in which bone loss and periodontal attach-
Consequently, the treatment of choice may be the empiric ment loss occur.
gangrenosa, cancrum oris, or noma but that was originally

reported in nutritionally deprived individuals, especially in
Africa. However, today noma is very common in sub-Saharan
African children with HIV NUS may be associated with severe
immunodeficiency, regardless of the cause of onset.
Treatment for NUS may include an antibiotic such as met-
ronidazole and the use of an antimicrobial mouth rinse such
as chlorhexidine gluconate. If osseous necrosis is present, it
is often necessary to remove the affected bone to promote
wound healing.
FIGURE 24.9 Necrotizing ulcerative periodontitis. Note the adjacent
A number of longitudinal studies and prevalence studies have
linear gingival erythema. suggested that HIV-positive individuals are more likely to ex-
perience chronic periodontitis than the general population.
Most studies, however, do not take into account the level of
NUP is characterized by soft-tissue necrosis, rapid perioral hygiene, the presence of preexisting gingivitis, poor diet,
odontal destruction, and interproximal bone loss (Fig. 24.9). the age of the patient, smoking, other periodontal disease risk
Lesions may occur anywhere in the dental arches; they are factors, the degree of immunodeficiency in the population
usually localized to a few teeth, although generalized NUP is studied, or whether the individuals in the study are injection
sometimes present after marked CD4+ cell depletion. Bone is drug users (IDUs); these confounding factors cloud the issue.
often exposed, which results in necrosis and subsequent se- With proper home care and appropriate periodontal treat-
questration. NUP is severely painful at onset, and immediate ment and maintenance, HIV-positive individuals can an-
treatment is necessary. Occasionally, however, patients under- ticipate reasonably good periodontal health throughout the
go spontaneous resolution of the necrotizing lesions, which course of their disease. The median period between initial
leave painless, deep interproximal craters that are difficult to HIV infection and outright AIDS is approximately 15 years,
clean and that may lead to conventional periodontitis. Some and the life expectancy of persons living with AIDS has been
evidence suggests slight differences between the microbial flo- significantly prolonged with current anti-HIV drug therapy.
ra found in NUP lesions and that found in chronic periodon- This indicates that HIV-infected patients are potential can-
titis, but most data implicate a similar microbial component didates for conventional periodontal treatment procedures,
in both diseases. An increasing number of studies, however, including periodontal surgery and implant placement. Treat-
have identified the presence of candidal organisms and hu- ment decisions should be based on the overall health status
man herpesviruses of various types in individuals with necro- of the patient, the degree of periodontal involvement, and the
tizing ulcerative periodontal diseases. The exact role of these motivation and ability of the patient to perform effective oral
organisms is not yet fully understood. As discussed previously, hygiene (Fig. 24.10).
the reported periodontal health of HIV-infected individuals is
subject to wide variations.
Therapy for NUP includes local debridernent; scaling and Periodontal Treatment Protocol
root planing; in-office irrigation with an effective antimicrobi- It is imperative that medically compromised patients, includ-
al agent such as chlorhexidine gluconate or povidone-iodine ing those with HIV or AIDS, be safely and effectively managed
(Betadine); and the establishment of meticulous oral hygiene, in dental practice. Several universal treatment considerations
including the home use of antimicrobial rinses or irrigation. are important to ensure that this is achieved.
In patients with severe NUP, antibiotic therapy may be nec-
essary, but it should be used with caution in HIV-infected
patients to avoid an opportunistic and potentially serious Health Status
localized candidiasis or even candidal septicemia. If an anti- The patient's health status should be determined from the
biotic is necessary, metronidazole (250 mg, with two tablets health history, the physical evaluation, and consultation with
taken immediately and then two tablets taken 4 times daily
for 5-7 days) is the drug of choice. The prophylactic prescrip-
tion of a topical or systemic antifungal agent is prudent if an
antibiotic is used.
Necrotizing Ulcerative Stomatitis

NUS has occasionally been reported in HIV-positive patients.
NUS may be severely destructive and acutely painful, and it
may affect significant areas of oral soft tissue and underlying
bone. It may occur separately or as an extension ofNUP, and it
is often associated with the severe suppression of CD4 immune
cells and an elevated viral load. The condition appears to be
identical to cancrum oris (noma), a rare necrotizing destruc- FIGURE 24.10 Periodontal health in an individual with advanced ac-
tive process that has been variously described as stomatitis quired immunodeficiency syndrome.
the patient's physician. Treatment decisions will vary, depend- regarding elective periodontal procedures should be made
ing on the patient's state of health. For example, delayed wound with the informed consent of the patient and after medical
healing and an increased risk of postoperative infection are consultation, when possible.
possible complicating factors in patients with AIDS, but nei-
ther concern should significantly alter treatment planning for
Maintenance Therapy
an otherwise healthy, asymptomatic, HIV-infected patient with
a normal or near-normal CD4 count and a low viral bioload. It is imperative that the patient maintains meticulous per-
sonal oral hygiene. In addition, periodontal maintenance re-
calls visits should be conducted at short intervals (ie, every
Infection Control Measures 2-3 months), and any progressive periodontal disease should
The clinical management of HIV-infected periodontal patients be treated vigorously.
requires strict adherence to established methods of infection As mentioned previously, systemic antibiotic therapy
control. Compliance, especially with universal precautions, should be administered with caution. Blood and other medi-
will eliminate or minimize risks to both patients and the den- cal laboratory tests may be required to monitor the patient's
tal staff. Immunocompromised patients are potentially at risk overall health status, and close consultation and coordination
for acquiring as well as transmitting infections in the dental with the patient's physician are necessary.
office and other health care facilities.
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25
Impact of Periodontal Infection
on Systemic Health
BL Mealey • PR Klokkevold • N Ambalavanan
Chapter Outline
Focal Infection Theory Revisited Periodontal Disease and Coronary Heart
Evidence-Based Clinical Practice Disease/ Atherosclerosis
Subgingival Environment as a Reservoir Periodontal Disease and Stroke
for Bacteria Periodontal Disease and Diabetes Mellitus
Periodontal Disease and Mortality Periodontal Medicine in Clinical Practice
Periodontal disease is an inflammatory disease initiated by The focal infection theory fell into disrepute during the
bacterial pathogens. Environmental, physical, social, and host 1940s and 1950s when widespread extraction-often of the
stresses may affect and modify disease expression through a entire dentition-failed to reduce or eliminate the systemic
multitude of pathways. Evidence has also shed light on the conditions to which the supposedly infected dentition had
converse side of the relationship between systemic health and been linked. The theory, while offering a possible explanation
oral health: the potential effects of inflammatory periodontal for perplexing systemic disorders, had been based on very
diseases on a wide range of organ systems. little (if any) scientific evidence. However, Hunter ideas did
Periodontal infection may significantly enhance the risk encourage extensive research in the areas of microbiology and
for certain systemic diseases or alter the natural course of immunology.
systemic conditions. Conditions in which the influences of
periodontal infection are documented include coronary heart Evidence-Based Clinical Practice
disease (CHD) and (HD-related events such as angina, infarc-
tion, atherosclerosis, and other vascular conditions; stroke; Many of the precepts of the focal infection theory are being re-
diabetes mellitus; preterm labor, low-birth-weight delivery, vived today in light of recent research demonstrating links be-
and preeclampsia; and respiratory conditions such as chronic tween oral and systemic health. However, for the "hypothesis
obstructive pulmonary disease (Box 25.1). not to fall into disrepute for a second time, there must be no
unsubstantiated attributions, no theories without evidence."
Today's era of evidence-based medicine and dentistry provides
Focal Infection Theory Revisited an excellent environment in which to examine the possible
relationships between oral infection and systemic disorders.
In 1900, British physician William Hunter first developed
To establish a relationship between conditions A and B, dif-
the idea that oral microorganisms were responsible for a wide
ferent levels of evidence must be examined. All scientific evi-
range of systemic conditions that were not easily recognized
dence is not given the same weight. The stronger the evidence,
as being infectious in nature. He claimed that the restoration
the more likely it is that a true relationship exists between
of carious teeth instead of extraction resulted in the trapping
the conditions. Table 25.1 describes these various levels of
of infectious agents under restorations. In addition to caries,
evidence.
pulpal necrosis, and periapical abscesses, Hunter also identi-
fied gingivitis and periodontitis as foci of infection. He advo-
cated the extraction of teeth with these conditions to eliminate Subgingival Environment as a
the source of sepsis. He also thought that oral organisms had Reservoir for Bacteria
specific actions on different tissues and that these organisms
acted by producing toxins, thereby resulting in low-grade The subgingival microbiota in patients with periodontitis
"subinfection" that produced systemic effects over prolonged provides a significant and persistent Gram-negative bacterial
periods. Hunter theory became widely accepted in Britain and challenge to the host that is met by a potent immunoinflam-
eventually in the United States, thereby leading to the whole- matory response. These organisms and their products, such as
sale extraction of teeth. lipopolysaccharide (LPSs), have ready access to the periodontal
261
Periodontal Disease and Mortality

Periodontal status was found to be a significant predictor of
CARDIOVASCULAR/CEREBROVASCULAR SYSTEM mortality independent of other factors, such as smoking, al-
Atherosclerosis cohol use, cholesterol levels, blood pressure, family history of
Coronary heart disease heart disease, education level, and body mass. Patients with
Angina the most alveolar bone loss, who averaged more than 21 % al-
Myocardial infarction veolar bone loss, the risk of dying was found to be 70% higher
Cerebrovascular accident (stroke) than those without bone loss. Interestingly, alveolar bone loss
ENDOCRINE SYSTEM increased the risk of mortality more than smoking (52% in-
Diabetes mellitus creased risk), which is a well-known risk factor for mortality.
There is a higher incidence of (HD-related events such as MI
REPRODUCTIVE SYSTEM and unstable angina among men less than 60 years old with
Preterm low-birth-weight infants alveolar bone loss as compared with those without bone loss.
Preeclampsia Those with the highest level of periodontal attachment loss
RESPIRATORY SYSTEM has a significantly higher risk of death as compared with those
Chronic obstructive pulmonary disease with the least attachment loss. The mortality rate over a 9-year
Acute bacterial pneumonia period was 15. 7% in those with the greatest attachment loss
as compared with 7.9% in subjects with the lowest level of
periodontal attachment loss.
Studies support the association between poor oral health
tissues and to the circulation via the sulcular epithelium, and an increased risk for mortality. In a prospective longitu-
which is frequently ulcerated and discontinuous. Even with dinal study of subjects with type 2 diabetes, those with severe
treatment, the complete eradication of these organisms is dif- periodontitis had 3.2 times the risk of death from ischemic
ficult, and their reemergence is often rapid. The total surface heart disease or kidney disease as compared with subjects
area of pocket epithelium in contact with subgingival bacte- without periodontitis or with only slight periodontitis after
ria and their products in a patient with generalized moder- adjusting for other risk factors, including age, sex, duration
ate periodontitis has been estimated to be approximately the of diabetes, glycemic control, macroalbuminuria, body mass
size of the palm of an adult hand, with even larger areas of index, serum cholesterol concentration, hypertension, and
exposure in cases of more advanced periodontal destruc- current smoking.
tion. Bacteremias are common after mechanical periodontal
therapy, and they also occur frequently during normal daily
function and oral hygiene procedures. Just as the periodontal Periodontal Disease and Coronary
tissues mount an immunoinflammatory response to bacteria
and their products, systemic challenge with these agents also
Heart Disease/Atherosclerosis
induces a major vascular response. This host response may (HD-related events are a major cause of death. MI has been
offer explanatory mechanisms for the interactions between associated with acute systemic bacterial and viral infections,
periodontal infection and a variety of systemic disorders. and MI is sometimes preceded by influenza-like symptoms.
TABLE 25.1
EVALUATION OF EVIDENCE
Type of Evidence Strength of Evidence Description
Case report +/- • Provides relatively weak retrospective anecdotal evidence

• May suggest that further study is needed
Cross-sectional study + • Compares groups of subjects at a single point in time
• Stronger than a case report
• Fairly easy to conduct
• Relatively inexpensive to conduct
Longitudinal study ++ • Follows groups of subjects over time
• Stronger than a cross-sectional study
• Studies with a control group much stronger than studies without controls
• More difficult and expensive to conduct
Intervention trial +++ • Examines the effects of some intervention
• Studies with a control group (ie, placebo) much stronger than studies without controls
• Strongest form of evidence is the randomized controlled intervention trial
• Difficult and expensive to conduct
Systematic review ++++ • Systematically evaluates evidence from multiple studies, especially randomized controlled
trials
• Uses clearly defined guidelines for the selection of evidence to be included or excluded
from the review
• Examines for heterogeneity in the overall data to indicate variations in study design,
sample populations, and assessment methodologies
25 Impact of Periodontal Infection on Systemic Health 263
Traditional risk factors such as smoking, dyslipidemia, hyper-

tension, and diabetes mellitus do not explain the presence of Systemic or periodontal
infection
coronary atherosclerosis in a large number of patients. Local-
ized infection that results in a chronic inflammatory reaction
has been suggested as a mechanism underlying CHD in these
individuals.
In cross-sectional studies of patients with acute MI or t Fibrinogen
confirmed CHD who are compared with age- and gender-
matched control patients, patients with MI had significantly
t White blood cell count
worse dental health (eg, periodontitis, periapical lesions, car- t von Willebrand factor
ies, pericoronitis) as compared with controls. This associa-
tion between poor dental health and MI was independent of
known risk factors for heart disease, such as age, cholesterol
levels, hypertension, diabetes, and smoking. Because athero- t Blood viscosity
sclerosis is a major determinant of (HD-related events, dental
health has also been related to coronary atheromatosis. There
is evidence that the extent of periodontal disease may be as-
sociated with CHD. For example, there may be a greater risk lschemic heart
for (HD-related events, such as MI, when periodontitis affects disease
a greater number of teeth in the mouth as compared with sub-
jects who have periodontitis that involves fewer teeth. FIGURE 25.1 The effect of infection on blood viscosity. Increased
plasma fibrinogen and von Willebrand factor cause hypercoagulability.
Among younger males between the ages of 25 and
When these are combined with an increased white blood cell count,
49 years, period on ti tis increased the risk of CHD by 70%. the blood viscosity increases, thereby increasing the risk of coronary
The level of oral hygiene was also associated with heart dis- ischemia.
ease. Patients with poor oral hygiene, as indicated by higher
debris and calculus scores, had a two-fold increased risk for
CHD. Not all studies, however, support this concept; some Routine daily activities such as mastication and oral hy-
show little independent effect of periodontal status on the giene procedures result in frequent bacteremia with oral or-
risk for CHD after adjusting for commonly accepted cardio- ganisms. Periodontal disease may predispose the patient to an
vascular risk factors. It can be stated that only a moderate increased incidence of bacteremia, including the presence of
degree of evidence exists to support an association between virulent Gram-negative organisms associated with periodon-
periodontal disease and atherosclerosis, MI, and cardiovas- titis. There is a greater risk of bacteremia after tooth brush-
cular disease; however, causality is unclear. A comprehen- ing in patients with higher levels of plaque, calculus, and
sive review of the evidence was recently performed by an gingivitis as compared with those with minimal plaque and
American Heart Association working group. That group con- gingival inflammation. The periodontium, when affected by
cluded that "periodontal disease is associated with athero- periodontitis, also acts as a reservoir of endotoxins (LPSs) from
sclerotic vascular disease independent of known confound- Gram-negative organisms. Endotoxins can pass readily into
ers." However, the working group cautioned that evidence the systemic circulation during normal daily function, thereby
of a causal link between periodontitis and vascular diseases inducing damage to the vascular endothelium and precipitat-
did not yet exist. Importantly, insufficient evidence exists ing many negative cardiovascular effects.
to show that the treatment of periodontal disease has any
impact on the risk of heart disease. Intervention trials are Thrombogenesis
needed to make this determination. Platelet aggregation plays a major role in thrombogenesis, and
most cases of acute Ml are precipitated by thromboembolism.
Oral organisms may be involved in coronary thrombogenesis.
Effect of Periodontal Infection Platelets selectively bind some strains of Streptococcus sangui-
Although a direct causal link between periodontal diseases nis, which is a common component of supragingival plaque,
and vascular diseases has not been shown to date, there are and Porphyromonas gingivalis, which is a pathogen closely as-
numerous mechanisms-both direct and indirect-through sociated with periodontitis. The aggregation of platelets is
which periodontal infection may affect the onset or progres- induced by the platelet-aggregation-associated protein (PAAP)
sion of atherosclerosis and CHD. expressed on some strains of these bacteria. In animal models,
the intravenous infusion of PAAP-positive bacterial strains re-
Systemic Infections sulted in alterations of heart rate, blood pressure, cardiac con-
Systemic infections are known to induce a hypercoagulable tractility, and electrocardiogram readings consistent with Ml.
state and to increase blood viscosity (Fig. 25.1). Fibrinogen Platelet accumulation also occurred in the lungs, which lead
levels and white blood cell counts are often increased in pa- to tachypnea. No such changes were seen with the infusion
tients with periodontal disease. Individuals with poor oral of PAAP-negative strains. PAAP-positive bacteria caused ag-
health may also have significant elevations in coagulation fac- gregation of circulating platelets, which resulted in the forma-
tor Vlll/von Willebrand factor antigen, thereby increasing the tion of thromboemboli and the resultant cardiac and pulmo-
risk of thrombus formation. Thus, periodontal infection may nary changes. Thus, periodontitis-associated bacteremia with
also promote increased blood viscosity and thrombogenesis, certain strains of S. sanguinis and P. gingivalis may promote
which leads to an increased risk for central and peripheral acute thromboembolic events via interaction with circulating
vascular disease. platelets.
Periodontal infection
Gram-negative bacteremia/LPS
(C)
(B)
Endothelial damage
Platelet adhesion/aggregation
7
Monocyte infiltration/proliferation
Cytokine/growth factor producti:J

n
Thrombus formation
Atheromatous
plaque; thick
vessel wall
FIGURE 25.2 Pathogenesis of atherosclerosis. A, Monocytes and mac-

rophages adhere to the vascular endothelium. B, Monocytes and macro-
phages penetrate into the arterial media and produce proinflammatory
Atheroma formation
Vessel wall thickening
Thromboembolic events 7
FIGURE 25.3 The influence of periodontal infection on atheroscle-
cytokines and growth factors. C, The ingestion of oxidized low-density rosis. Periodontal pathogens and their products result in damage to the
lipoprotein enlarges monocytes to form foam cells. D, Smooth muscle vascular endothelium. Monocytes and macrophages enter the vessel wall
proliferation and plaque formation thicken vessel walls and narrow the and produce cytokines that further increase the inflammatory response
lumen. M0+, Hyperinflammatory monocyte/macrophage phenotype. and propagate the atheromatous lesion. Growth factor production leads
to smooth muscle proliferation in the vessel wall. Damaged endothe-
lium also activates platelets, thereby resulting in platelet aggregation and
Atherosclerosis potentiating thromboembolic events. LPS, Lipopolysaccharide.
Atherosclerosis is a focal thickening of the arterial intima, the
innermost layer lining the vessel lumen, and the media, the
thick layer under the intima that consists of smooth muscle, obtained from humans during endarterectomy, more than half
collagen, and elastic fibers (Fig. 25.2). Early during the for- of the lesions contained periodontal pathogens, and many
mation of atherosclerotic plaques, circulating monocytes ad- atheromas contained multiple different periodontal species.
here to the vascular endothelium. This adherence is mediated Periodontal diseases result in chronic systemic exposure to
through several adhesion molecules on the endothelial cell products of these organisms. Low-level bacteremia may ini-
surface. These adhesion molecules are upregulated by a num- tiate host responses that alter coagulability, endothelial and
ber of factors, including bacterial LPSs, prostaglandins, and vessel wall integrity, and platelet function, thereby resulting
proinflammatory cytokines. After binding to the endothelial in atherogenic changes and possible thromboembolic events
cell lining, monocytes penetrate the endothelium and migrate (Fig. 25.3).
under the arterial intima. The monocytes ingest circulating Acute-phase proteins such as C-reactive protein (CRP) and
low-density lipoprotein in its oxidized state and become en- fibrinogen are produced in the liver in response to inflamma-
gorged, thereby forming the foam cells that are characteristic tory or infectious stimuli and act as inflammatory markers.
of atheromatous plaques. Atheromatous plaque formation and CRP induces monocytes and macrophages to produce tissue
thickening of the vessel wall narrow the lumen and dramati- factor, which stimulates the coagulation pathway and increas-
cally decrease blood flow through the vessel. Arterial throm- es blood coagulability. Increased fibrinogen levels may con-
bosis often occurs after an atheromatous plaque ruptures. tribute to this process. CRP also stimulates the complement
Plaque rupture exposes circulating blood to arterial collagen cascade, thereby further exacerbating inflammation.
and tissue factor from monocytes and macrophages that ac- Elevations in serum CRP and fibrinogen levels are well-
tivate platelets and the coagulation pathway. Platelet and fi- accepted risk factors for cardiovascular disease. Recent
brin accumulation forms a thrombus that may occlude the efforts have focused on periodontitis as a potential trig-
vessel and result in ischemic events such as angina or Ml. The ger for systemic inflammation. Serum CRP and fibrinogen
thrombus may separate from the vessel wall and form an em- levels are often elevated in subjects with periodontitis as
bolus, which may also occlude vessels, again leading to acute compared with subjects without periodontitis. These acute-
events such as Ml or cerebral infarction (stroke). phase proteins may act as intermediary steps in the pathway
from periodontal infection to cardiovascular disease (see
Role of Periodontal Disease in Myocardial Figs. 25.3 and 254). Thus, periodontal diseases may have
or Cerebral Infarction both direct effects on the major blood vessels (eg, atheroma
formation) and indirect effects that stimulate changes in the
Patients with periodontitis are at increased risk for the thick- cardiovascular system (eg, the elevation of systemic inflam-
ening of the walls of the major coronary arteries. In Atheromas matory responses).
neurologic defect than did stroke not preceded by infection.

M0+ phenotype Periodontal Stroke patients with a preceding infection had slightly higher
pathogens
levels of plasma fibrinogen and significantly higher levels of
CRP as compared with those without infection.
Stroke is classified as either hemorrhagic or nonhernor-
rhagic stroke. Nonhemorrhagic stroke or ischemic stroke is
Periodontitis usually caused by thromboembolic events and cerebrovascu-
J
lar atherosclerosis, whereas hemorrhagic stroke often results
from a vascular bleed such as an aneurysm. Periodontal dis-
ease has been associated primarily with an increased risk of
Chronic bacterial challenge nonhemorrhagic stroke.
Proinflammatory cytokines Periodontal infection may contribute directly to the patho-
Acute-phase reactants genesis of atherosclerosis by providing a persistent bacterial
challenge to the arterial endothelium, thereby contributing to
the monocyte and macrophage-driven inflammatory process
that results in atheromatosis and the narrowing of the vessel
Risk factors for Vascular effects lumen. Furthermore, periodontal infection may stimulate a
atherosclerosis series of indirect systemic effects, such as the elevated produc-
tion of fibrinogen and CRP, which serve to increase the risk
of stroke (see Figs. 25.3 and 25.4). Finally, bacteremia with
PAAP-positive bacterial strains from the supragingival and
Hypercoagulability subgingival plaque can increase platelet aggregation, thereby
Atheroma formation contributing to thrombus formation and subsequent throrn-
Thromboembolism boembolism, which is the leading cause of stroke.
FIGURE 25.4 The cardiovascular and periodontal consequences of
the hyperresponsive monocyte/macrophage phenotype. In combina-
Periodontal Disease
tion with other risk factors, the M0+ phenotype predisposes individuals
to both atherosclerosis and periodontitis. Bacterial products and inflam-
and Diabetes Mellitus
matory mediators associated with periodontitis affect vascular endothe- It is clear from epidemiologic research that diabetes increas-
lium, monocytes and macrophages, platelets, and smooth muscle, and es the risk for and severity of periodontal diseases. The in-
they may increase blood coagulability. This may further increase athero-
sclerosis and result in thromboembolism and ischemic events.
creased prevalence and severity of periodontitis typically seen
in patients with diabetes-especially those with poor meta-
bolic control-led to the designation of periodontal disease
as the "sixth complication of diabetes." In addition to the five
In subjects with chronic periodontitis, serum levels of "classic" complications of diabetes (Box 25.2), the American
IL-6 and CRP are reduced after scaling and root planing. Diabetes Association has officially recognized that periodon-
Inflammatory periodontal disease is also associated with al- tal disease is common among patients with diabetes, and
tered vascular endothelial function as compared with peri- the Association's Standards of Care include taking a history
odontally healthy individuals. Altered vascular endothelial of current or past dental infections as part of the physician's
function is a major risk factor for acute thrombotic events. examination. In fact, since 2009, the American Diabetes Asso-
After scaling and root planing with a resultant decrease in ciation's Standards of Medical Care in Diabetes have included
periodontal inflammation, markers of vascular health also the assessment of a patient's history of "dental disease" as part
improve significantly over time. The functional assessment of the recommended medical history during the diabetic pa-
of vascular endothelial function also returns to normal af- tient evaluation. In addition, these standards specifically rec-
ter scaling and root planing. These results suggest that peri- ommend that the physician refer patients with diabetes to a
odontal inflammation adversely affects the health of the dentist for a comprehensive periodontal examination.
vascular endothelium, whereas a reduction in inflammation Periodontitis has also been associated with the classic
improves endothelial health. Whether these changes directly complications of diabetes. Diabetic adults with severe peri-
impact the risk of acute cardiovascular events remains to be odontitis at baseline had a significantly greater incidence of
determined. kidney and macrovascular complications over the subsequent
1-11 years than did diabetic adults with only gingivitis or
Periodontal Disease and Stroke
Ischemic cerebral infarction or stroke is often preceded by sys-
temic bacterial or viral infection. In one study, patients with
cerebral ischemia were 5 times more likely to have had a sys- 1. Retinopathy
temic infection within 1 week before the ischemic event than 2. Nephropathy
were nonischemic control subjects. Recent infection was a sig- 3. Neuropathy
nificant risk factor for cerebral ischemia; it was independent 4. Macrovascular disease
5. Altered wound healing
of other known risk factors such as hypertension, history of
6. Periodontal disease
a previous stroke, diabetes, smoking, and CHD. Interestingly,
the presence of systemic infection before the stroke resulted in From Loe H: Periodontal disease: the sixth complication of diabetes mellitus
significantly greater ischemia and a more severe postischemic Diabetes Care 16(Suppl 1 ):329, 1993.
mild periodontitis. This was true despite both groups having

similar glycemic control. One or more cardiovascular compli-
cations occurred in 82 % of patients with severe periodontitis
versus 21 % of patients without severe periodontitis. Again,
Gram-negative
periodontal
infection
Periodontal
treatment l
severe periodontitis preceded the onset of clinical diabetic Decreased
complications in these subjects. inflammation
Among diabetic patients with periodontitis, periodontal
]
therapy may have beneficial effects on glycemic control. This Increased Improved
J
may be especially true for patients with relatively poor glyce- insulin insulin
mic control and more advanced periodontal destruction before resistance sensitivity
treatment. Fifty years ago, the potential benefits of periodontal
therapy were first described in young adults with type 1 diabe-
tes and severe periodontitis. Treatment with scaling and root
l
planing, surgery, selected tooth extraction, and systemic anti-
Worsened Improved
biotics resulted in decreased insulin demand. Combination of glycemic glycemic
subgingival mechanical debridement and systemic doxycycline control control
may result in short-term improvement in glycemia in diabetic
patients with severe periodontitis and poor metabolic control.
FIGURE 25.5 Potential effects of periodontal infection and peri-
Periodontal therapy was associated with a significant im- odontal therapy on glycemia in patients with diabetes.
provement in glycemic control overall in those with type 2
diabetes but not in those with type 1 disease, despite improve-
ment in the periodontal condition of both groups. However, it and reduce inflammation may restore insulin sensitivity over
was found that a greater glycemic response to periodontal ther- time, thereby resulting in improved metabolic control.
apy occurred among those patients with type 1 diabetes whose
glycemic control is relatively poor than among those whose Periodontal Disease and Pregnancy
glycemic control is already good before periodontal treatment.
Use of systemic antibiotics for treatment of chronic peri-
Outcome
odontitis for patients with poorly controlled diabetes and Low-birth-weight (LBW) infants (ie, those weighing <2500 g
severe periodontitis was found to be beneficial. Antibiotics at birth) are 40 times more likely to die during the neonatal
remain an adjunct to the necessary mechanical removal of period than normal-birth-weight (NBW) infants. LBW infants
plaque and calculus. Tetracyclines are also known to suppress who survive the neonatal period are at increased risk for con-
the glycation of proteins and to decrease the activity of tissue- genital anomalies, respiratory disorders, and neurodevelop-
degrading enzymes such as matrix metalloproteinases. These mental disabilities.
changes may contribute to improvements in the metabolic The primary cause of LBW deliveries is preterm labor or
control of diabetes. A low-dose form of doxycycline (20 mg) premature rupture of membranes (PROM). Factors such as
has been introduced with the specific purpose of reducing the smoking, alcohol, or drug use during pregnancy; inadequate
production of collagen-degrading matrix metalloproteinases prenatal care; race; low socioeconomic status; hypertension;
(see Chapter 39). This dose has no antibiotic effects, and it high or low maternal age; diabetes; and genitourinary tract
does not induce antimicrobial resistance with long-term use. infections increase the risk of preterm LBW delivery. Research
Because diabetes is associated with the greatly elevated pro- has examined the relationship between maternal infection and
duction of collagenase, low-dose doxycycline has been used preterm labor, PROM, and LBW delivery The true extent of
for the treatment of periodontitis in diabetic subjects. this relationship is difficult to determine, because the majority
of maternal infections may be subclinical. Genitourinary tract
infections have been associated with adverse pregnancy out-
Periodontal Infection Associated with comes. Women with bacteriuria have increased rates of pre-
Glycemic Control in Diabetes term delivery, and the antibiotic treatment of bacteriuria has
resulted in a significant decrease in preterm delivery rates as
An understanding of the effects of other infections is useful compared with placebo treatment. Vaginal colonization with
to delineate the mechanisms by which periodontal infection group B streptococci or Bacteroides species increases the risk of
influences glycemia. It is well known that systemic inflam- PROM, preterm delivery, and LBW infants.
mation plays a major role in insulin sensitivity and glucose Although the direct effects of microorganisms may play
dynamics. As discussed previously, periodontal diseases can an important role in many cases of preterm labor, PROM,
induce or perpetuate an elevated systemic chronic inflamma- and LBW delivery, indirect mechanisms may also be opera-
tory state, which is reflected in increased serum CRP, IL-6, tive. Bacterial infection of the chorioamnion or extra placental
and fibrinogen levels seen in many people with periodontitis. membrane may lead to chorioamnionitis, a condition that is
It is possible that chronic Gram-negative periodontal infec- strongly associated with PROM and preterm delivery. How-
tions may also result in increased insulin resistance and poor ever, many cases of histologic chorioamnionitis demonstrate
glycemic control. In patients with periodontitis, persistent negative bacterial cultures, which indicate that infection is not
systemic challenge with periodontopathic bacteria and their the sole cause of this condition. It is likely that an indirect
products may act similar to well-recognized systemic infec- mechanism may be active in which the cascade of host prod-
tions (Fig. 25.5). This mechanism would explain the worsen- ucts produced in response to infection is often responsible for
ing of glycemic control associated with severe periodontitis. preterm labor. Maternal infection may lead to the presence of
Periodontal treatment designed to decrease the bacterial insult amniotic bacterial products, such as LPSs from Gram-negative
potential mechanism by which periodontal disease could af-

Bacterial fect pregnancy outcome is via the systemic dissemination of
infection
periodontal pathogens. Women who had LBW infants had
significantly higher levels of Aggregatibacter (formerly Actino-
bacillus) actinomycetemcomitans, Tannerella forsythia, P gingiva-
lis, and Treponema denticola in their subgingival plaque than
Bacteria and products in amnion did the control women who had NBW infants. Women who
had LBW infants also had higher levels of gingival crevicular
fluid (GCF), PGE2, and IL-1. Thus, women who had LBW in-
fants often had a higher prevalence and severity of periodon-
Inflammatory response with
cytokine production in amnion
7J titis, more gingival inflammation, higher levels of putative
periodontal pathogens, and an elevated subgingival inflam-
matory response as compared with women who had NBW
infants; furthermore, the increased bacterial challenge may
have broader systemic effects, thereby resulting in an elevated
Increased amniotic challenge to the fetal immune system.
prostaglandin production Periodontal disease may increase the risk for preeclampsia.
This hypertensive disorder affects about 5-10% of pregnan-
cies, and it is a major cause of perinatal and maternal mor-
bidity and mortality. Preeclampsia has multiple potential
Preterm labor etiologies, several of which involve vascular changes in the
placenta that are similar to those seen with atherosclerosis.
FIGURE 25.6 Mechanisms by which infection may induce preterm The presence of periodontitis during pregnancy or a worsen-
labor.
ing of periodontal disease during pregnancy is associated with
a two-fold to 2.5-fold increased risk for preeclampsia.
organisms, which stimulate the production of host-derived cy- Although periodontal therapy during gestation was not as-
tokines in the amnion and the decidua (Fig. 25.6). These cy- sociated with decreased preterm birth rates, it was found that
tokines, including IL-1, INF-a, and IL-6, stimulate increased periodontal treatment during gestation may be most appro-
prostaglandin production from the amnion and the decidua, priate for women with a greater risk for adverse pregnancy
which leads to the onset of preterm labor. A premature rise in outcomes. It is clear that scaling and root planing provided
PGE2 and PGF2a is characteristic of preterm labor, regardless during the second and third trimester of gestation are safe pro-
of whether clinical or subclinical maternal genitourinary tract cedures. Scaling and root planing during pregnancy are associ-
infection is detected. ated with either a decrease or no change in adverse pregnancy
outcome rates. Children of women who received scaling and
Role of Periodontitis root planing during gestation have similar cognitive, motor,
and language development during the first 2 years of life as
Periodontitis is a remote Gram-negative infection that may compared with the children of women who did not receive
play a role in LBW infants. As discussed previously, periodon- periodontal therapy until the postpartum period. Thus, the
topathic organisms and their products may have wide-ranging clinician should feel comfortable providing scaling and root
effects that are most likely mediated through the stimulation planing during the second and third trimester of pregnancy.
of host cytokine production in target tissues. A remote non-
disseminated infection with P gingivalis originating from peri-
odontal infection may result in abnormal pregnancy outcomes Periodontal Disease and Chronic
in this model. P gingivalis-induced experimental periodonti-
tis in animal models resulted in decreased fetal birth weight
Obstructive Pulmonary Disease
and increased amniotic fluid levels of INF-a and PGE2. This Chronic obstructive pulmonary disease (COPD) is character-
provides direct evidence that periodontal infection can affect ized by airflow obstruction that results from chronic bronchi-
the fetal environment and pregnancy outcomes. These animal tis or emphysema. COPD shares similar pathogenic mecha-
studies have led to the examination of the potential effects of nisms with periodontal disease. With both diseases, a host
periodontitis on pregnancy outcome in humans. It was found inflammatory response is mounted in response to chronic
that women who had LBW infants also had significantly great- challenge by bacteria in periodontal disease and by factors
er clinical attachment loss than women who had NBW infants. such as cigarette smoke associated with COPD. The resulting
After adjusting for known risk factors for LBW delivery, wom- neutrophil influx leads to the release of oxidative and hydro-
en with periodontitis that resulted in more than 3 mm of at- lytic enzymes that cause tissue destruction directly. The re-
tachment loss in at least 60% of sites had a 7.5-fold increased cruitment of monocytes and macrophages leads to the further
risk of having an LBW infant. In fact, periodontitis contributed release of proinflammatory mediators.
to more preterm LBW cases than did smoking or alcohol use Less is known about the clinical relationship between peri-
during pregnancy gestation as compared with women without odontal disease and COPD as compared with CHD and other
periodontitis. This indicates a strong association between peri- systemic conditions. A recent systematic review of 14 studies
odontal infection and adverse pregnancy outcomes. and almost 4000 subjects showed a significant two-fold in-
It is estimated that the risk of having preterm or LBW increased risk of COPD in those with periodontal disease as com-
fants in mothers with periodontal disease was 2.83 times as pared with those without. However, more evidence is needed
compared with mothers without periodontal disease. One to establish a strong relationship between the two diseases.
Periodontal Disease and Acute Periodontal Medicine in Clinical

Respiratory Infections Practice
Pneumonia is an infection of the lungs that is caused by bac- The concept of periodontal diseases as localized entities that
teria, viruses, fungi, or mycoplasma and that is broadly cat- affect only the teeth and the supporting apparatus is over-
egorized as either community-acquired or hospital-acquired simplified. Rather than being confined to the periodontium,
pneumonia. A wide variety of bacteria may cause pneumonia, inflammatory periodontal diseases may have wide-ranging
and the spectrum of offending organisms differs greatly be- systemic effects. In most persons, these effects may be rela-
tween community-acquired and hospital-acquired infections. tively inconsequential or at least not clinically evident. In sus-
Community-acquired bacterial pneumonia is caused primarily by ceptible individuals, however, periodontal infection may act
the inhalation of infectious aerosols or by the aspiration of as an independent risk factor for systemic disease, and it may
oropharyngeal organisms. To date, no associations have been be involved in the basic pathogenic mechanisms of these con-
found between oral hygiene or periodontal disease and the ditions. Furthermore, periodontal infection may exacerbate
risk for acute respiratory conditions such as pneumonia in existing systemic disorders.
community-dwelling individuals.
The same cannot be said for individuals in the hospital Patient education regarding Periodontal
setting. Hospital-acquired (nosocomial) bacterial pneumonia
has a very high morbidity and mortality rate. The incidence
Disease and Systemic Health
of nosocomial pneumonia is highest among severely ill pa- Periodontitis is a Gram-negative infection that often results
tients, such as those in intensive care units or on ventila- in severe inflammation, and it potentially involves the intra-
tory support. Although nosocomial pneumonia is most often vascular dissemination of microorganisms and their products
caused by Gram-negative aerobic organisms, many cases are throughout the body. However, periodontitis tends to be a
the result of infection by anaerobic bacteria, including those "silent" disease until destruction results in acute oral symp-
that are typically found in the subgingival environment. toms. Most patients-and many medical professionals-do
Hospital-acquired pneumonia is usually caused by the aspi- not recognize the potential infection that may exist within the
ration of oropharyngeal contents. Oropharyngeal coloniza- oral cavity. Patient education is a priority. Patient education ef-
tion with potential respiratory pathogens (PRPs) is generally forts in the realm of periodontal medicine must emphasize the
a transient phenomenon; however, such colonization in- inflammatory nature of periodontal infections, the increased
creases during hospitalization. The longer the hospital stay, risk for systemic disease associated with the infection, and
the greater the prevalence of PRPs. PRPs are found predomi- the biologically plausible role that periodontal infection may
nantly in the gastrointestinal tract, and they may be passed play in systemic disease. Few individuals had their choles-
via esophageal reflux into the oropharynx, where they colo- terol levels evaluated until the knowledge of the link between
nize. Subsequent aspiration may lead to pneumonia. Dental cholesterol and heart disease became widespread. Likewise,
plaque has been shown to serve as a reservoir of PRPs; such an increased appreciation of the potential effects of periodon-
colonization in plaque results in a persistent source of po- tal infection on systemic health may result in increased patient
tential aspiration. demand for periodontal evaluation.
Poor oral hygiene is common in the hospital and nursing
home settings, especially among severely ill patients. PRPs are
more often isolated from the supragingival plaque and buc- SUGGESTED READING
cal mucosa of patients in intensive care units than in outpa- Beck JD, Offenbacher S: The association between periodontal diseases and
tient settings. Thus, organisms that are not routinely found cardiovascular diseases: a state-of-the-art review, Ann Periodontal 6:9-15,
2001.
in dental plaque become plaque colonizers after prolonged D'Aiuto F, Parkar M, Andreou G: Periodontitis and systemic inflammation:
hospitalization. Subgingival plaque may also harbor PRPs, control of the local infection is associated with a reduction in serum inflam-
and putative periodontal pathogens have been associated with matory markers,] Dent Res 83:156-160, 2004.
nosocomial pneumonia. Furthermore, anaerobic organisms Kebschull M, Demmer RT, Papapanou PN: Gum bug, leave my heart alone"-
epidemiologic and mechanistic evidence linking periodontal infections and
from periodontal pockets may serve as the primary inoculum atherosclerosis,] Dent Res 89:879-902, 2010.
for suppurative respiratory diseases (eg, pulmonary abscesses) Lockhart PB, Bolger AF, Papapanou PN, American Heart Association Rheu-
that involve significant morbidity and mortality. matic Fever, Endocarditis, and Kawasaki Disease Committee of the Council
Thus, interventions that are used to improve oral hygiene, on Cardiovascular Disease in the Young, Council on Epidemiology and
such as mechanical toothbrushing and chemical antimicrobial Prevention, Council on Peripheral Vascular Disease, and Council on Clinical
Cardiology: et al: Periodontal disease and atherosclerotic vascular disease:
rinses, have the potential to decrease the risk of nosocomial does the evidence support an independent association?: a scientific statement
pneumonia in high-risk patients, such as those in intensive from the American Heart Association, Circulation 125:2520-2544, 2012.
care units or those on ventilators. It was found that "one in Mealey BL, Oates TW: Diabetes mellitus and periodontal diseases, J Periodon-
10 cases of death from pneumonia in elderly nursing home tal 77:1289-1303, 2006.
Ross RL: Atherosclerosis-an inflammatory disease, N Engl J Med 342:
residents may be prevented by improving oral hygiene."
115-126, 1999.
Scannapieco FA, Bush RB, Paju S: Associations between periodontal disease
and risk for nosocomial bacterial pneumonia and chronic obstructive pul-
Role of Periodontal Disease in Erectile monary disease: a systematic review, Ann Periodontal 8:54-69, 2003.
Tonetti MS, D'Aiuto F, Nibali L: Treatment of periodontitis and endothelial
Dysfunction function, New Engl J Med 356:911-920, 2007.
Williams RC: Understanding and managing periodontal diseases: a notable
Although some preliminary studies suggest a relationship be- past, a promising future,] Periodontal 79:1552-1559, 2008.
tween periodontitis and erectile dysfunction, more research is Xiong X, Beukens P, Fraser WO, et al: Periodontal disease and adverse preg-
needed to understand the mechanisms of interaction. nancy outcomes: a systematic review, BJOG 113:135-143, 2006.
Part Outline
SECTION I Diagnosis, Prognosis SECTION V Surgical Treatment

and Treatment Plan 41 Phase II Periodontal Therapy
26 Clinical Diagnosis 42 Periodontal and Periimplant Surgical
27 Clinical Risk Assessment Anatomy
28 Determination of Prognosis 43 General Principles of Periodontal
29 Rationale for Periodontal Treatment Surgery
and Treatment Plan 44 Gingival Surgical Techniques
SECTION II Management of Patients with 45 The Periodontal Flap
Periodontal Diseases 46 Treatment of Gingival Enlargement
30 Periodontal Treatment for Medically 47 Resective Osseous Surgery
Compromised Patients
48 Periodontal Regeneration
31 Treatment of Aggressive and Reconstructive Surgery
and Atypical Forms
49 Furcation Involvement and Treatment
of Periodontitis
50 Periodontal Plastic and Esthetic Surgery
SECTION Ill Diagnosis and Treatment
of Periodontal Emergencies 51 Advances in Periodontal Surgical
Procedures (Microsurgery and Laser)
32 Treatment of Acute Gingival Diseases
SECTION VI Multidisciplinary Approach
33 Treatment of Periodontal Abscess
for the Management of Periodontal
SECTION IV Nonsurgical Treatment Diseases
34 Phase 1 Periodontal Therapy 52 Diagnosis and Management
35 Plaque Biofilm Control of Endodontic-Periodontic Lesions
36 Periodontal Instruments 53 Periodontal-Restorative
and Instrumentation Interrelationships
37 Scaling and Root Planing 54 Adjunctive Role of Orthodontic
38 Antiinfective Therapy Therapy
39 Host Modulation SECTION VII Supportive Care
40 Breath Malodor 55 Supportive Periodontal Treatment
SECTION I
26 Clinical Diagnosis 28 Determination of Prognosis

27 Clinical Risk Assessment 29 Rationale for Periodontal Treatment
and Treatment Plan
26
Clinical Diagnosis
HH Takei • FA Carranza • J Do • S Tetradis • SM Mallya
M Sanz • MG Newman • M Quirynen • CD Dwarakanath
Chapter Outline
Overall Appraisal of the Patient Advanced Diagnostic Techniques
Radiographic Aids in the Diagnosis of Conventional Routine Diagnostic Methods
Periodontal Disease Status of Current Conventional Diagnostic
Normal lnterdental Bone Methods
Radiographic Techniques Requirements of Newer Diagnostic
Bone Destruction in Periodontal Methods
Disease Advances in Radiographic Assessment
Radiographic Appearance of Periodontal Advances in Microbiologic Analysis
Disease Advances in Characterizing the Host
Digital lntraoral Radiography Response
Conclusion Conclusion
Diagnosis can be defined as the art of identifying a condition Overall Appraisal of the Patient
or disease and differentiating it from other entities. Proper
diagnosis is essential for intelligent treatment. Periodontal In the first meeting, the clinician should attempt an overall
diagnosis should first determine whether a disease is pres- appraisal of the patient. This includes the consideration of the
ent; it should then identify the disease's type, extent, patient's mental and emotional status, temperament, attitude,
distribution, and severity; and it should finally provide an and physiologic age. It also helps to build up rapport with the
understanding of the underlying pathologic processes and patient, which is extremely vital for obtaining cooperation and
their causes. In general, periodontal diseases fall into the fol- confidence for all of the subsequent treatment procedures.
lowing categories:
1. The gingival diseases (Box 26 1) Chief Complaint
2. The various types of periodontitis (Table 26.1)
The chief complaint of the patient and the dental history is re-
3. The periodontal manifestations of systemic diseases
corded in his/her own words. Many patients may not present
(Chapter 12)
with any specific periodontal problem but might have been
The periodontal diagnosis is determined after the careful merely referred for a routine periodontal assessment or often
analysis of the case history and the evaluation of the clinical just for an oral prophylaxis.
signs and symptoms, as well as the results of various tests (eg, But many may report bleeding gums; loose teeth; spread-
probing, mobility assessment, radiographs, blood tests, and ing of the teeth with the appearance of spaces where none
biopsies). existed before; foul taste in the mouth; and an itchy feeling in
The interest should be in the patient who has the disease the gums that is relieved by digging with a toothpick. There
and not simply in the disease itself. Diagnosis must therefore may also be pain of varied types and duration including con-
include a general evaluation of the patient and a consideration stant, dull, gnawing pain, dull pain after eating, deep radiat-
of the oral cavity. ing pains in the jaws, acute throbbing pain, sensitivity when
Diagnostic procedures must be systematic and organized chewing, sensitivity to hot and cold, burning sensation in the
for specific purposes. It is not enough to assemble facts; the gums, and extreme sensitivity to inhaled air.
findings must be pieced together so that they provide a mean- The past dental history should include visits to the dentist
ingful explanation of the patient's periodontal problem. The and the type of dental or periodontal treatment undertaken
following is the recommended sequence of procedures for the previously. It is important, particularly in acute and severe
diagnosis of periodontal diseases. conditions, to establish the chronologic sequence of events,
271
272 PART 2 Clinical Periodontics
BOX 26.1 brushing or eating, at night, or with regular periodicity;

whether it is associated with the menstrual period or oth-
• Chronic marginal gingivitis er specific factors; the duration of the bleeding; and the
• Acute necrotizing ulcerative gingivitis manner in which it is stopped, should be noted.
• Acute herpetic gingivostomatitis 6. A bad taste in the mouth and areas of food impaction
• Allergic gingivitis
should be mentioned.
• Gingivitis associated with skin diseases
• Gingivitis associated with endocrine-metabolic
7. Whether the patient's teeth feel "loose" or insecure; if he
disturbances or she has any difficulty chewing; and whether there is
• Gingivitis associated with hematologic-immunologic any tooth mobility; should be assessed.
disturbances 8. The patient's general dental habits, such as grinding or
• Gingival enlargement associated with medications clenching of the teeth during the day or at night; soreness
• Gingival tumors of teeth or jaw muscles in the morning; tobacco smok-
ing or chewing, nail biting, or biting on foreign objects,
should be noted.
9. The patient's history of previous periodontal problems, in-
which have led to the present condition. Further history cluding the nature of the condition and if it was previously
should include reference to the following: treated; the type of treatment received (surgical or nonsur-
1. Visits to the dentist should be listed, including their fre- gical); and the approximate period of termination of the
quency, the date of the most recent visit, the nature of previous treatment need to discussed. If in the opinion
the treatment and oral prophylaxis, cleaning by a dentist of the patient, the present problem is a recurrence of the
or hygienist, and the frequency and date of most recent previous disease, what does he or she think caused it?
cleaning. 10. Whether the patient wears any removable prosthesis and
2. The patient's oral-hygiene regimen should be described, if the prosthesis enhances or deters the existing dentition
including toothbrushing frequency, time of day, method, or the surrounding soft tissues needs to be noted.
type of toothbrush and dentifrice, and interval at which 11. Whether the patient has implants needs to be noted.
brushes are replaced. Other methods for mouth care,
such as mouthwashes, interdental brushes, other devices,
water irrigation, and dental floss, should also be listed.
Medical History
3. Any orthodontic treatment, including its duration and Most of the medical history is obtained at the first visit and
the approximate date of termination, should be noted. it can be supplemented by pertinent questioning during the
4. If the patient is experiencing pain in the teeth or in the subsequent visits. The health history can be obtained verbally
gingiva, the manner in which the pain is provoked, its na- by questioning the patient and recording his or her responses
ture and duration, and the manner in which it is relieved on a blank piece of paper or by means of a printed question-
should be described. naire that the patient can complete. Figure 26.1 is the medi-
5. The presence of any gingival bleeding, including when cal questionnaire form recommended by the American Dental
it first occurred; whether it occurs spontaneously, on Association.
TABLE 26.1
FEATURES OF TYPES OF PERIODONTITIS

Generalized Prepubertal (now Localized Necrotizing
Aggressive included under Aggressive Ulcerative
Parameter Chronic Periodontitis aggressive category) Periodontitis Periodontitis
Age (years) 35+ 20-35 <11 11-19 15-35
Calculus Moderate to abundant Scanty to moderate Scanty Moderate Scanty
Disease progression Slow Rapid Rapid Rapid Rapid
Distribution Generalized; associ- Generalized; no con- Primary molars and First molars and ?
ated with etiologic sistent pattern incisors incisors, and no
factors more than two
other teeth
Prevalence United States, > 50%; United States, 4-5%; 7 <0.50%
Sri Lanka, 81 % Sri Lanka, 11 %
Racial predilection No No No More common No
among blacks
Familial tendency No 7 Yes Yes
Gender distribution More severe among
men
Polymorphonuclear leuko- No Yes Yes Yes Yes
cyte/macrophage defects
Association with systemic No Some cases Yes Yes Yes
problems
Response to therapy Very good Variable Poor Good Variable
26 Clinical Diagnosis 273
Health History Form American Dental A,;..sociation

[ E-mail: Today·s Date: www.ada.org
As required by law, our office adheres to wrrtten polioes and procedures to protect the privacy of information about you that we create, rece1ve or maintain. Your
answers are for our records only and wdl be kept conf1dent1al subject to applicable laws. Please note that you will be asked some quesuons about your responses to
this questionnaire and there may be add,uonal questions concerning your health This Information Is vital to allow us to provide appropnate care for you. This office
does not use this information to d1scnminate
Nam Home Phone. JncJude .,•• codo Bus,ness/Cen Phone. ,- .,.,.

l.lsl Mrckle ( ) (
Address: Coty State: Zip.
fl-'.-:. Ing •ddtffl
Occupabon: Height. Weight Date of birth. Sex. M
SSII or Patient ID Emergency Contact. RelabOnshlp: Home Phone. Cell Phone.

( ) (
lricWt1~codts
If you are compleMg this form for another person, what 1s your retanonslup to that person?
Vo.1rt"'1~
Do you have any of the following diseases or problems:
AcllVc IUlwrculosis ..•.•. -· •... •. .• •.
Ref.xioruhlp
(Chock DK if you Don't Know th• onnwr 10 th• qu•stlon/ v..C No DK
D D
Pc1s,s1e111 cough greater than a 3 week durauor, •................................................................................................................................................ (• 0 0
Cough that produces blood , ~ C D D
Been exposed to anyone with tuberculosis .. . .- .• .. .. . •...... •. .. •. . .. •.••...•.....• O D D
If rou answer yes to any of the 4 items above, please stop and return this form to the receptionist.
De nta I Inf Orm ati On For the follo'Mfl9 quesaons, pledse_ mark co your responses to rhe followrng quesaons.
v•• No DK Yes No OK
Do your gums bleed when you brush or lloss? , 0 Do you have earaches or neck pains? 0 0 D
Are your teeth sensuree to cold, hot, S'llee!S or pressure? I Do you have any cllck1ng, popping or doscomfort In the Jaw? I., 0 U
Does food or floss catch between your teeth? .. .. ........•.............. D Do you brux or gnnd your teeth? . . . .. . .. . . . .. .. D D D
Is your mouth dry 1 .. . .. .. .. . . .. .. . ...••••••••.. .. . 0 Do you have sores or ukers 1n your mouth? ..........................•.... 0 0 0
H,ive you had any periodontal (gum) treatments? J r 11 Do you wear dentures or pamals? 0 [1 0
Have you ever had orthodonuc (braces) treatment? 0 0 Do you participate' in active recreauonal activmes? C O D
Have you had any problems assoceted with pre<Jious dental Have you rNer had a serious injury to your head or mouth?. . •.. O O O
t,e.hncnt? .. .. . . . II [ Date of your last dental exam:
Is your home water supply fluoridated? D D D Whdt w•> done at that bme?
Do you dnnk bottled or filtered water' D D D
If yes, how olten 7 Circle one. DAILY/ WEEKLY / OCCASIONAi.LY Date of last dental x-r~ys:
Ale you cuirently e~penenc,ng dental pain or discomfort? D
What ,s the reason for your dental v1s1t today?
How do you feel about your smile?
Med i Ca I I n f Orm at i On
Ale you now under the care of a phys:cian?.
Physician Name:
Please marl: O<J your response to indicate rf yoo have or have nor had any of the followrng diseases or problems.
~~~
............. D D D
Phone. 1no\Jde .,._, ,_
Have you had a senous Illness, operauon or been
hospitalized In the past 5 years?
-~~
0 0 0
If yes, what was the illness or problem?
Address/City/State/ZJp
Are you taking or have you recently taken any prescnption
Ale you 1n good health 7 .. .. . D D D or aver the counter med,clne(s)? .. .. D D D
Has there been any change In your general health 1V1thon If so, please hst all, Including vitamins, natural or herbal preparations
the past yea,7 . ....• .. . ...........•.................... D D D and/or diet supplements:
II yes. what condluon 1s being treated?
Date of last phys,cal exam:
0 2007 Aim>rican OertJI Assod.lt,o,,

f'.ormSSOO
FIGURE 26.1 Medical history form from the American Dental Association. (Form© American Dental Association. Reprinted with permission.)
Medi Ca I I n f Orm at i On Please mark (X) your response to indicate if you have or have not had any of the fol/owing diseases or problems,
if you Don't Know the answer to the que.stlon)
(Che de DK Yes No OK Ye$ No OK
Do you wear contact lenses? •...•.....•..•..•.•.........•.....•.•.•...•.....•..•...... D D 0 Do you use controlled substances (drugs)? ..•.•.. •.•...•... ...•.•.•... .•... D D 0
Joint Replacement. Have you had an orthopedic total jornt (hip. Do you use tobacco (smoking, snuff, chew, bid,s)? ..............•.... D D D
knee. elbow, finger) replacement 7 D D 0 II so, how interested are you in stopping?
Date If yes, have you had any complications? _ (Cirde one) VERY / SOMEWHAT / NOT IITTERESTEO
Are you taking or scheduled to begin taking either of lhe Do you dnnk alcoholic beverages? , . ...........•.. , ...•..•. .. •....•.. D D D
medications, a'endronate (FosamaX-) or nsedronate (AC!onet•) If yes, how much alcohol did you drink in the last 24 hours? _
for osteoporosis or Paget's disease 7 D D D If yes, how much do you typically dnnk In a week? _
Since 2001, were you treated or are you presently scheduled WOMEN ONLY Are you:
to begm treatment with the intravenous brsphosphonetes Pregnant? ........................................•.....................................•. D D D
(Aredia• or Zometa•) for bone pain, hypercalcemia or skeletal Number of weeks: _
compl,cations resulling from Pagers disease. multiple myeloma Taking birth control pills or hormonal replacement? ......•...•......•... D D D
or metastatic cancer?.. ....•..•..•.......•...•..•....•...•..•....•.•.•...•....... DD D Nursing? ....................•............................................•.....•................ D D D
Date Treatment began _
Allergies • Are you allergic to or have you had a reaction to Yes No DK Yes No OK
To all yes responses, specify type of reaction. Metals D D D
Local anesthetics. 0 D 0 Latex ~ubber) D D 0
Asp,rm D D D lodme 0 D 0
Peruollin or other enubioucs "- D D D Hay fever/seasonal D D D
Barbiturates, sedatives, or sleeping pllls ' ' D D D Animals D D 0
Sulfa drugs 1 ' 0 D D Food 0 D 0
Codeine or other narcotics __ .____,, D D D Other D D D
Please mark (X) your response to indicate i( you beve or have not had any of the following diseases or prablem».
Y~ No OK YH No DK Ye, No OK
Arllficlal (piosthe!Jc) heart va•,e •.•...........•...•..•.....••..•..•. :'.: .L.:...... ... .J 0 Autoimmune disease 0 0 0 Hepa1i1,s. jaundice or
Pre•,,ous lnfecwe endoca,olt,s ....•.................•. ~ ..•.. ::: .. ~ .• .! D O Rheumatoid arth11Us •.........•.• 0 0 0 IM!rdl"'1S<> D D D
Damaged ealves in transplanted heart - D D Systemic lupus e,ythematosus D D D Epilepsy... •.. •. D D D
Congenital hea't doease (CHO) Asthma..... •. ..•.....•.. 0 D D Fainting sp<>lls 01 seizures...... J lJ [l
Unfl'pa red, cyanot,c C HD .. D D Bronch~1s ...•.••• 0 D D I
Neuro ogical disorders D D D
RepaIfl'd (completely) in Ll<I 6 monIhs o' q. Emphy,em.1 •. ... ••. ••. 0 0 D If yes, speclly . _
Repaired CHO ,_,th residual defects.. .. .. .. . 0 C SlnU'i trouble .. .. •............... D DD Sleep diso1der ...................... D D D
Exccpr for the condmons ltstcd abovt', antJb10nc propnyl.ms ,s no i'or;gcr rccomm«xkd
TubcrculostS ....•.•......•...•......• D on Mental heahh disorders ....... D D D
frx tin)' OrllPr lt,tm ol CHD Cancer/Chemotherapy/ Specify:
Rad1auon Trcauncnt ........•. D [J 0 Recurrent infections -- DD D
Yes No DK Yts No DK Chest pain upon exertion •...•. D DD TypP of lnfect10n·
Card10'1ascular disease. .. ... D D D fvlltral valve prolap DD D Chronic pain 0 0 D Kidnll'f problems ......••......•... D D 0
Angina .. C D O Pacemaker . DD D Diabetes 'fype I or II ...•....• 0 DD N1ghI sweats .... .... ... .. .... IJ rJ 0
4rterioscleros,s .. .. .. . .. .•. D D D Rheumatic fever . DD Eaung disorder ,. D DD Ostcopo1os,s •.•.•....•......•.•..•... D D D
Congestive heart fa,lure .••••.. D D O Rheumatic heart drsea,e • D DD MJlnutnt1on DD Pecs1:!i-Umt swollen gldn~
Damaged heart vaves .....••.... ...i D D Abnormal bleeding .........•.•. D on Gastr<>ntest,nal disease. 0 DD in neck.. .......................•.... 0 D D
Heart attack .............•....... ::J n r Anem•a ......•.....................• rr G.E. Rrflu"'pe"is1cnt Severe headaches/
Heart murmur •.•.•....•.•..•.•.... , ~1 D D Blood uansfu,ion , ..••.•.....•.... D :JD heartburn D D 0 migraines ....... .......... DD 0
Low blood p=Ie ....•.......... ~ r I L If yes. dat•~-------- Ulcers .........................•.... , [I fl [l ,re or rap.d weight toss •. DD D
Hlgh blood piessure .•............ D D D Hemoph,ha ......•...•.•........•.... D 0 0 Thyroid problems ~ .•. '.:>: D 0 D SP><ual~ cransmntPd cir;(',111' DD D
Other congenital heart AIDS or HIV lnfect10n .....•...•. D DD Stroke ..•....•.•.•....•.•.•...•...•..~..• D [J . E.xcessfi.~ unnat'on DD D
defects .. •. .. . •. • .. ....• D D O Arthnns • . .. . ..•. •. .. .. .. . , ..•. DD Glaucoma •...•.•..•...•.........•....•. O D
Has a physician or previous dentist recommended that you take antibiotics pnor to your dental treatment? •........•...... :'.':. :".-: •....•...•.••...•...•.•...•.•.•.•.•..•.•. D D 0
Name of physician or denust making recommendation: Phone
Do you have any disease, condition, or problem not l,sted above that you think I should know about? ..............•...................................................•... D D O
Please explain:
NOTE: Both doctor and patient are encouraged to discuss any and all relevant patient health Issues prior to treatment.
I certify that I have read and understand the above and that the 1nformatt00 given on this form rs accurate I understand the imporlance of a truthful health
history and that my denust and his/her staff will rely on this Information for treating me. I ad(nowledge that my questions, If any, about Inquiries set fonh
above have been answered to my sanstaction. I will not hold my dentist, or any other member of his/her staff, responsible for any action they take or do not
take because of errors 01 ormssrons that I may have made in the completion of th,s form.
Signature of Patienl/legal Guardian; Date.
FOR COMPLETION BY DENTIST

Comments: _
FIGURE 26.1 (cont.)

FIGURE 26.2 A full-mouth intraoral radiographic series (17 periapical films and 4 bite-wing films) used as an adjunct for periodontal diagnosis.
The importance of the medical history should be clearly

carefully analyzed to determine their effect (if any) on the
explained because patients often omit information that they
oral tissues to avoid administering medications that would
cannot relate to their dental problems. The patient should be
interact adversely with them. Special inquiry should be
made aware of the following: (1) the possible role that some
made regarding the dosage and duration of therapy with
systemic diseases, conditions, or behavioral factors may play
anticoagulants and corticosteroids. Patients who are tak-
in the cause of periodontal disease; (2) the presence of condi-
ing the family of drugs called bisphosphonates, which are
tions that may require special precautions or modifications of
often prescribed for patients with osteoporosis, should be
the treatment procedure (Chapter 30); and (3) the possibil-
cautioned about possible problems related to osteonecrosis
ity that oral infections may have a powerful influence on the
of the jaw after undergoing any form of surgical procedure
occurrence and severity of a variety of systemic diseases and involving the bone.
conditions (Chapter 25) (Fig. 26.2).
4. All medical problems (eg, cardiovascular, hematologic, and
The medical history should include reference to the
endocrine) including infectious diseases, sexually trans-
following:
mitted diseases, and high-risk behavior for human immu-
1. If the patient is under the care of a physician, the nature nodeficiency virus infection should be listed. Chapter 24
and duration of the problem and its therapy should be dis- discusses the subject of human immunodeficiency virus
cussed. The name, address, and telephone number of the infection.
physician should be recorded because direct communica- 5. Any possibility of occupational disease should be noted.
tion with him or her may be necessary. 6. Abnormal bleeding tendencies, such as nosebleeds, pro-
2. Details regarding hospitalizations and operations includ- longed bleeding from minor cuts, spontaneous ecchymo-
ing the diagnosis, the type of operation, and any untoward ses, a tendency toward excessive bruising, and excessive
events (eg, anesthetic, hemorrhagic, or infectious compli- menstrual bleeding, should be cited. These symptoms
cations) should be provided. should be correlated with the medications that the patient
3. A list of all medications being taken and whether they were is taking.
prescribed or obtained over the counter should be includ- 7. The patient's allergy history should be taken including that
ed. All of the possible effects of these medications should be related to hay fever, asthma, sensitivity to foods, sensitivity
FIGURE 26.3 A panoramic radiograph showing temporomandibular joints and "cystic" spaces in the jaw. Areas of periodontal bone loss are not
seen in detail.
to drugs (antibiotics, lignocaine), and sensitivity to dental

materials (eg, eugenol and acrylic resins).
8. Information is needed regarding the onset of puberty and,
for females, menopause, menstrual disorders, hysterecto-
my, pregnancies, and miscarriages.
9. A family medical history should be taken, including that of
bleeding disorders and diabetes.
Casts
Casts from dental impressions are useful adjuncts during
the oral examination. They indicate the position of the gin-
FIGURE 26.4 Poor oral hygiene. The gingival inflammation is associ-
gival margins (recession) and the position and inclination of ated with plaque and calculus.
the teeth, the proximal contact relationships, and the food
impaction areas. In addition, they provide a view of the lin-
gual-cuspal relationships. Casts are important records of the Inflammatory nodes become enlarged, palpable, tender,
dentition before it is altered by treatment. Finally, casts also and fairly immobile. The overlying skin may be red and warm.
serve as visual aids during discussions with the patient and Patients are often aware of the presence of "swollen glands."
they are useful for pretreatment and post treatment compari- Primary herpetic gingivostomatitis, necrotizing ulcerative gin-
sons, as well as for reference at recall visits. They are also help- givitis, and acute periodontal abscesses may produce lymph-
ful to determine the position of implant placement if the case node enlargement. After successful therapy, lymph nodes
requires it (Fig. 26 3). return to normal in a matter of days to weeks.
Clinical Photographs lntraoral examination

Color photographs are useful for recording the appearance of Oral Hygiene
the tissue before and after treatment. Photographs cannot al- The cleanliness of the oral cavity is appraised in terms of the
ways be relied on for the comparison of subtle color changes in extent of accumulated food debris, plaque, and tooth surface
the gingiva but they do depict gingival morphologic changes. stains (Fig. 26.4). Disclosing solution may be used to detect
With the advent of digital clinical photography, record keep- plaque that would otherwise be unnoticed. The amount of
ing for mucogingival problems (eg, areas of gingival recession, plaque detected, however, is not necessarily related to the
frenum involvement, and papilla loss) has become important. severity of the disease present. For example, aggressive peri-
odontitis is a destructive type of periodontitis in which plaque
is minimal.
Extraoral Examination
Any facial asymmetry, temporomandibular disorders, region- Oral Malodor
al lymph nodes, and competency of the lip seal should be Oral malodor, which is also termed fetor ex ore, fetor oris, or
checked. halitosis, is a foul or offensive odor that emanates from the oral
cavity. Mouth odors may be of diagnostic significance and their
origin may be either oral or extraoral (remote). Chapter 40
Examination of the Lymph Nodes
discusses in detail the problems related to oral malodor.
As acute periodontal, periapical, and other oral diseases may The entire oral cavity should be carefully examined. The
result in lymph node changes, the clinician should routinely examination should include the lips, the floor of the mouth,
examine and evaluate the lymph nodes of the head and neck. the tongue, the palate, and the oropharyngeal region, as well
Lymph nodes can become enlarged or indurated as a result as the quality and quantity of saliva. Although findings may
of an infectious episode, malignant metastases, or residual fi- not be related to the periodontal problem, the dentist should
brotic changes. detect all pathologic changes that are present in the mouth.
Standard textbooks that address oral medicine and oral diag-

nosis cover these topics in detail.
Examination of the Teeth and Implants

The teeth are examined for caries, poor restorations, devel-
opmental defects, anomalies of tooth form, wasting, hyper-
sensitivity, and proximal-contact relationships. The stability,
position, number of implants, and their relationship to the
adjacent natural dentition are also examined.
Wasting Diseases of the Teeth
Wasting is defined as any gradual loss of tooth substance,
which is characterized by the formation of smooth, polished
surfaces without regard to the possible mechanism of this loss.
The forms of wasting are erosion, abrasion, and attrition.
Erosion, which is also called corrosion, is a sharply defined
wedge-shaped depression in the cervical area of the facial- FIGURE 26.6 Flat, shiny, discolored surfaces produced by occlusal
wear.
tooth surface. The long axis of the eroded area is perpendicu-
lar to the vertical axis of the tooth. The surfaces are smooth,
hard, and polished. Erosion generally affects a group of teeth. toothbrushing is the most common cause. Tooth position
During the early stages, it may be confined to the enamel but (facial) is also a major factor in the abrasive loss of the root
it generally extends to involve the underlying dentin, as well surface. The degree of tooth wear from toothbrushing de-
as the cementum. pends on the abrasive effect of the dentifrice and the angle of
The etiology of erosion is not known. Decalcification by brushing. Horizontal brushing at right angles to the vertical
acidic beverages or citrus fruits in combination with the ef- axis of the teeth results in the severest loss of tooth substance.
fect of acidic salivary secretion are suggested causes. Sognnaes Occasionally, abrasion of the incisal edges occurs as a result
refers to these lesions as dentoalveolar ablations and attributes of habits, such as holding objects (eg, bobby pins and tacks)
them to forceful frictional actions between the oral soft tis- between the teeth.
sues and the adjacent hard tissues. In patients with erosion, Attrition is occlusal wear that results from functional con-
the salivary pH, the buffering capacity, and the calcium and tacts with opposing teeth. Such physical wear patterns may
phosphorus content have been reported as normal, and the occur on incisal, occlusal, and interproximal tooth surfaces.
mucin level is elevated. A certain amount of tooth wear is physiologic but accelerated
Abrasion refers to the loss of tooth substance that is induced wear may occur when abnormal anatomic or unusual func-
by mechanical wear other than that of mastication. Abrasion tional factors are present.
results in saucer-shaped or wedge-shaped indentations with a Occlusal or incisal surfaces worn by attrition are called fac-
smooth, shiny surface. Abrasion starts on the exposed cemen- e ts. When active tooth grinding occurs, the enamel rods are
tum surfaces rather than on the enamel and it extends to involve fractured and become highly reflective to light. Thus, shiny,
the dentin of the root. A sharp "ditching" around the cementoe- smooth, and curviplanar facets are usually the best indicator
namel junction (CEJ) appears to be the result of the softer ce- of ongoing frictional activity. If dentin is exposed, a yellowish-
menta! surface as compared to the much harder enamel surface. brown discoloration is frequently present (Fig. 26.6). Facets
Continued exposure to the abrasive agent in combination vary with regard to size and location, depending on whether
with decalcification of the enamel by locally formed acids may they are produced by physiologic or abnormal wear. At least
result in a loss of enamel followed by a loss of the dentin of one significant wear facet has been reported in 92 % of adults
the crown. and facet prevalence approaches universality. Facets are usu-
Toothbrushing with an abrasive dentifrice (Fig. 26.5) and ally not sensitive to thermal or tactile stimulation.
the action of clasps are frequently mentioned, but aggressive Facets generally represent functional or parafunctional
wear, as well as iatrogenic dental treatment through corono-
plasty (occlusal adjustment). However, coronoplasty does not
appear to contribute to higher ratings of wear. Excessive wear
may result in the obliteration of the cusps and the formation
of either a flat or a cuneiform (cupped-out) occlusal surface.
Contrary to earlier thought, attrition in young adults from
modern societies is not age related. This suggests that a sig-
nificant amount of attrition, when present in young adults is
unlikely to occur, as a result of functional wear and it is prob-
ably the result ofbruxing activity. Attrition has been correlated
with age when older adults are considered.
The angle of the facet on the tooth surface is potentially sig-
nificant to the periodontium. Horizontal facets tend to direct
FIGURE 26.5 An abrasion attributed to aggressive toothbrushing
forces on the vertical axis of the tooth to which the periodon-
(arrow). The involvement of the roots is followed by the undermining tium can adapt most effectively. Angular facets direct occlusal
of the enamel. forces laterally and increase the risk of periodontal damage.
However, gradual attrition may be compensated for by con-

tinuous tooth eruption without alveolar bone growth and it is
characterized by a lack of inflammatory changes on the alveo-
lar bone surfaces.
Another mechanism of tooth wear that has been studied
recently is called abfraction, and it results from occlusal load-
ing surfaces causing tooth flexure, mechanical microfractures,
and tooth substance loss in the cervical area.
These four mechanisms of tooth wear (erosion, abrasion,
attrition, and abfraction) can combine with each other to re-
sult in an increased degree of tooth wear.
Dental Stains
Dental stains are pigmented deposits on the teeth. They
should be carefully examined to determine their origin.
Hypersensitivity
Root surfaces exposed by gingival recession may be hypersen-
sitive to thermal changes or tactile stimulation. Patients often FIGURE 26.7 Tooth mobility is checked with a metal instrument and
direct the clinician to the sensitive areas. These may be located one finger.
by gentle exploration with a probe or cold air.
Proximal Contact Relations
When a force such as that applied to teeth in occlusion is
Open contacts allow for food impaction. The tightness of con- discontinued, the teeth return to their original position in two
tacts should be checked by means of clinical observation and stages: (1) the first is an immediate, spring like elastic recoil;
with dental floss. Abnormal contact relationships may also and (2) the second is a slow, asymptomatic recovery move-
initiate occlusal changes, such as a shift in the midline be- ment. The recovery movement is pulsating and it is appar-
tween the central incisors with labial flaring of the maxillary ently associated with the normal pulsation of the periodontal
canine, buccal, or lingual displacement of the posterior teeth, vessels, which occurs in synchrony with the cardiac cycle.
and an uneven relationship of the marginal ridges. Teeth op- Many attempts have been made to develop mechanical or
posite an edentulous site may supraerupt, thereby opening electronic devices for the precise measurement of tooth mo-
the proximal contacts. bility. Although standardization of grading mobility would be
helpful for the diagnosis of periodontal disease and for evalu-
Tooth Mobility ating treatment outcomes, these devices are not widely used.
All teeth have a slight degree of physiologic mobility, which As a general rule, mobility is graded clinically by holding the
varies for different teeth and at different times of the day. It tooth firmly between the handles of two metallic instruments
is greatest when arising in the morning and it progressively or with one metallic instrument and one finger (Fig. 26. 7). An
decreases. The increased mobility in the morning is attributed effort is then made to move it in all directions. Abnormal mo-
to slight extrusion of the tooth as a result of limited occlusal bility most often occurs faciolingually. Mobility is graded ac-
contact during sleep. During the waking hours mobility is recording to the ease and extent of tooth movement as follows:
duced by chewing and swallowing forces, which intrude the
• Grade 0: Normal mobility;
teeth in the sockets. These 24-hour variations are less marked
• Grade I: Slightly more than normal;
in persons with a healthy periodontium than in those with oc-
• Grade II: Moderately more than normal; and
clusal habits, such as bruxism and clenching.
• Grade III: Severe mobility faciolingually, mesiodistally, or
Single-rooted teeth have more mobility than multirooted
both in combination with vertical displacement.
teeth, with incisors having the most mobility. Mobility occurs
primarily in a horizontal direction although some axial mobil- Mobility beyond the physiologic range is termed abnormal
ity occurs to a lesser degree or pathologic. It is pathologic in that it exceeds the limits of
Tooth mobility occurs in the following two stages: normal mobility values. However, the periodontium is not
necessarily diseased at the time of examination.
1. The initial or intrasocket stage occurs when the tooth
Increased mobility is caused by one or more of the follow-
moves within the confines of the periodontal ligament
ing factors.
(PDL). This is associated with viscoelastic distortion of the
ligament and the redistribution of the periodontal fluids, 1. Loss of tooth support (bone loss) can result in mobility. The
interbundle content, and fibers. This initial movement oc- amount of mobility depends on the severity and distribu-
curs with forces of about 100 lb, and it is on the order of tion of bone loss at individual root surfaces, the length,
0.05-0.10 mm (50-100 µm). shape of the roots, and the root size as compared to that
2. The secondary stage occurs gradually and entails the elastic of the crown. A tooth with short, tapered roots is more
deformation of the alveolar bone in response to increased likely to loosen than one with normal-size or bulbous roots
horizontal forces. When a force of 500 g is applied to the with the same amount of bone loss. One should carefully
crown, the resulting displacement is about 100-200 µm evaluate postorthodontic cases for possible apical shorten-
for incisors, 50-90 µm for canines, 8-10 µm for premo- ing of the root, which may lead to excessive mobility. Since
lars, and 40-80 µm for molars. bone loss usually results from a combination of factors and
FIGURE 26.8 Periodontal disease with pathologic migration of the anterior teeth. A, Clinical photograph. B, Radiographic view.
does not occur as an isolated finding, the severity of tooth Peptostreptococcus micros, and possibly Porphyromonas gingiva-
mobility does not necessarily correspond to the amount of lis as compared to nonmobile teeth.
bone loss.
2. Trauma from occlusion (ie, injury produced by excessive oc- Trauma from Occlusion
clusal forces or incurred as a result of abnormal occlusal Trauma from occlusion refers to tissue injury produced by oc-
habits, such as bruxism and clenching) is a common cause clusal forces rather than to the occlusal forces themselves
of tooth mobility. Mobility is also increased by hypofunc- (Chapter 21). The criterion that determines that an occlusion
tion. Mobility produced by trauma from occlusion occurs is traumatic is whether it causes damage in the periodontal
initially as a result of resorption of the cortical layer of tissues; therefore, the diagnosis of trauma from occlusion is
bone, which leads to reduced fiber support and later as made from the condition of the periodontal tissues. The peri-
an adaptation phenomenon that results in a widened periodontal findings are then used as a guide for locating the re-
odontal space. sponsible occlusal relationships.
3. Extension of inflammation from the gingiva or from the peri- Periodontal findings that suggest the presence of trauma
apical region into the PDL results in changes that increase from occlusion include excessive tooth mobility, particularly in
mobility. The spread of inflammation from an acute peri- teeth that show radiographic evidence of a widened periodon-
apical abscess may increase tooth mobility in the absence tal space; vertical or angular bone destruction; infrabony pock-
of periodontal disease. ets; and pathologic migration, especially of the anterior teeth.
4. Periodontal surgery temporarily increases tooth mobility These are discussed in more detail in the following sections.
immediately after the intervention and for a short period.
5. Tooth mobility is increased during pregnancy and it is Pathologic Migration of the Teeth
sometimes associated with the menstrual cycle or the use
Alterations in tooth position should be carefully noted, par-
of hormonal contraceptives. This is unrelated to periodontal
ticularly with a view toward identifying abnormal forces, a
disease and it occurs presumably because of physicochem-
tongue-thrusting habit, or other habits that may be contribut-
ical changes in the periodontal tissues.
ing factors (Chapter 21). Premature tooth contacts in the pos-
6. Pathologic processes of the jaws that destroy the alveolar bone
terior region that deflect the mandible anteriorly contribute
or the roots of the teeth can also result in mobility. Osteo-
to the destruction of the periodontium of the maxillary ante-
myelitis and tumors of the jaws belong to this category.
rior teeth and to pathologic migration (Fig. 26.8) The loss of
One study has suggested that pockets around mobile posterior teeth can lead to the facial "flaring" of the maxillary
teeth harbor higher proportions of Campylobacter rectus, anterior dentition. This is due to the increased trauma that
the mandibular anterior dentition places against the palatal graphics and voice-activated technology allow for the easy re-
surface of the maxillary anterior dentition. Pathologic migra- trieval and comparison of data.
tion of the anterior teeth in young persons may be a sign of
localized aggressive (juvenile) periodontitis. Plaque and Calculus
There are many methods available for assessing plaque and
Sensitivity to Percussion calculus accumulation. The presence of supragingival plaque
Sensitivity to percussion is a feature of acute inflammation of and calculus can be directly observed and the amount can be
the PDL. Gentle percussion of a tooth at different angles to measured with a calibrated probe. For the detection of sub-
the long axis often helps with the localization of the site of an gingival calculus, each tooth surface is carefully checked to
inflammatory involvement. the level of the gingival attachment with a no. 17 or no. 3A
explorer (Fig. 26 10). Warm air may be used to deflect the
Dentition with the Jaws Closed gingiva and to aid in the visualization of the calculus.
Examination of the dentition with the jaws closed can detect Although radiographs may sometimes reveal heavy cal-
conditions, such as irregularly aligned teeth, extruded teeth, culus deposits interproximally and, even on the facial and
improper proximal contacts, and areas of food impaction, all lingual surfaces, they cannot be relied on for the thorough
of which may favor plaque accumulation. detection of calculus.
Excessive overbite, which is seen most often in the anterior
region, may cause the impingement of the teeth on the gingiva Gingiva
and food impaction, followed by gingival inflammation, gingi- The gingiva must be dried before accurate observations can
val enlargement, and pocket formation. The real significance be made (Fig. 26.11). Light reflection from moist gingiva ob-
of the detrimental effect of an excessive anterior overbite on scures detail. In addition to visual examination and explora-
gingival health is still controversial. tion with instruments, firm but gentle palpation should be
In open-bite relationships, abnormal vertical spaces exist used to detect pathologic alterations in normal resilience, as
between the maxillary and mandibular teeth. The condition well as to locate areas of exudate.
occurs most often in the anterior region although posterior Features of the gingiva to consider include color, size, con-
open bite is occasionally seen. Reduced mechanical cleans- tour, consistency, surface texture, position, ease of bleeding,
ing by the passage of food may lead to the accumulation of and pain (Chapter 14). Any deviation from the norm should
plaque, debris, calculus formation, and the extrusion of teeth. be evaluated and not overlooked. The distribution of gingival
With crossbite, the normal relationship of the mandibular disease and its acute or chronic nature should also be noted.
teeth to the maxillary teeth is reversed, with the maxillary Clinically, gingival inflammation can produce two basic
teeth being lingual to the mandibular teeth. Crossbite may types of tissue response: edematous and fibrotic. Edematous
be bilateral, unilateral, or may affect only a pair of antago- tissue response is characterized by a smooth, glossy, soft, red
nists. Trauma from occlusion, food impaction, spreading of gingiva. With the fibrotic tissue response, some of the char-
the mandibular teeth, and associated gingival and periodontal acteristics of normalcy persist; the gingiva is more firm, stip-
disturbances may be caused by crossbite. pled, and opaque; it is usually thicker; and the margin appears
rounded.
Functional Occlusal Relationships
The examination of functional occlusal relationships is an Use of Clinical Indices in Dental Practice
important part of the diagnostic procedure. Dentitions that There has been a tendency to extend the use of indices that
appear to be normal when the jaws are closed may present were originally designed for epidemiologic studies into dental
marked functional abnormalities. practice. Of all of the indices proposed, the gingival index and
the sulcus-bleeding index appear to be the most useful and are
most easily transferred to clinical practice.
Examination of the Periodontium
The gingival index provides an assessment of the gingival
The periodontal examination should be systematic, starting inflammatory status that can be used in practice to compare
in the molar region in either the maxilla or the mandible and gingival health before and after phase 1 therapy or before and
proceeding around the arch. This prevents the overemphasis after surgical therapy It can also be used to compare the gin-
of unusual findings at the expense of other conditions that, al- gival status at recall visits. Attaining good intraexaminer- and
though less striking, may be equally important. It is important interexaminer calibration is imperative in the dental office.
to detect the earliest signs of gingival and periodontal disease. The sulcus-bleeding index provides an objective and easily re-
Charts to record the periodontal and associated findings producible assessment of the gingival status. It is extremely use-
provide a guide for a thorough examination and record of the ful for detecting early inflammatory changes and the presence
patient's condition (Fig. 26.9A and B). They are also used to of inflammatory lesions located at the base of the periodontal
evaluate the response to treatment and for comparison at re- pocket, which is an area inaccessible to visual examination. Pa-
call visits. However, excessively complicated mouth charting tients can easily understand this index; therefore, it can be used
may lead to a frustrating maze of minutiae rather than clarifi- to enhance the patient's motivation for plaque control.
cation of the patient's problem.
During the last decade, electronic clinical records have
Periodontal Pockets
been developed and are increasingly being used by general
dentists and periodontists. Most systems provide rapid and Examination for periodontal pockets must include their pres-
easy access to information, and allow for the incorporation ence and distribution on each tooth surface, the pocket depth,
of digital, clinical, and radiographic images. Computerized the level of attachment on the root, and the type of pocket (ie,
dental-examination systems that make use of high-resolution suprabony or infrabony).
UCLA Dental Center DENTAL EXAMINATION

2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
Date
!111!§ ;===
Imp-Impacted
_= I 11111111 11111111
Un-Unerupted
X-Extracted or missing
/-To be extracted
Blue-Existing Restorations
Red-Caries or
Defective Restorations
Marginal Bleeding
Probe Bleeding-(circled),
~~~~!m==
_I I I I I I I I I I I I I I I I I
~~~~!m== l l l l l l l I I I l l l J J l l
Food Impacted
Open Contact
Furcation
(I-IV)
Gingival Margin
Mucogingival
Problem
Restoration
Overhang
Date
(A)
tll!I!~==
==I 32
11
31 30
11
29 28
11
27 26
11
25 24
11
23 22
11
21 20
11
19 18
I I
17
FIGURE 26,9 A, University of California, Los Angeles, periodontal chart. B, Computerized diagram showing various periodontal parameters.
(Courtesy University of California, Los Angeles, School of Dentistry.)
PROBING DEPTH (mm) 321 246 324 363 444 252 363 555 555 146 467 664 444 343 132
14 14
10 10
6 6
BUCCAL 2 2
RECESSION (mm) 565 353 222 111 351 153 153 555 112 321 123 321 123 143 234
PROBING DEPTH (mm) 321 246 324 363 444 252 363 555 555 146 467 664 444 343 132
14 14
10 10
6 6
LINGUAL 2 2
RECESSION (mm) 565 353 222 111 351 153 153 555 112 321 123 321 123 143 234
MOBILITY 1+ + 1+ 2 2+ 3 4 1 3+ 3 2+ 2 1+
(8)
FIGURE 26.9 (cont.)
FIGURE 26.11 Normal gingiva with incipient gingivitis in teeth #11

and #22. Normal surface features are better revealed by drying gingiva.
FIGURE 26.10 Top left, Detection of the smoothness of various ir- FIGURE 26.12 Periodontal pockets around the mandibular anterior
regularities on the root surface with the outward motion of a probe or teeth showing rolled margins, edematous inflammatory changes, and
explorer. Top center, Calculus. Top right, Caries. Bottom left and right, abundant calculus and plaque. Note the suppuration from tooth #6.
Irregular margins of restorations.
The presence of bleeding, suppuration, and loose extruded

Signs and Symptoms teeth may also denote the presence of a pocket (Fig. 26.12).
Although probing is the only reliable method of detecting Periodontal pockets are generally painless, but they may
pockets, clinical signs, such as color changes (ie, a bluish-red give rise to symptoms, such as localized or sometimes radiat-
marginal gingiva or a bluish-red vertical zone that extends ing pain or the sensation of pressure after eating that gradu-
from the gingival margin to the attached gingiva), a "rolled" ally diminishes. A foul taste in localized areas, sensitivity to
edge separating the gingival margin from the tooth surface, or hot and cold, and toothache in the absence of caries is also
an enlarged, edematous gingiva may suggest their presence. sometimes present.
FIGURE 26.13 Blunted silver points assist with locating the base of
the pocket.
FIGURE 26.15 A, In a normal sulcus with a long junctional epithelium

(between arrows), the probe penetrates about one third to half the length
of the junctional epithelium. B, In a periodontal pocket with a short
junctional epithelium (between arrows), the probe penetrates beyond
the apical end of the junctional epithelium.
The probing depth is the distance to which a probe penetrates

into the pocket. Probes that are presently used are described
in Chapter 36.
The following landmarks have to be borne in mind while
probing.
1. The crest of the gingival margin.
2. The base of the sulcus.
(A) 3. The cementoenamel junction.
FIGURE 26.14 A, The biologic or histologic pocket depth is the actual
4. The crest of the alveolar bone.
distance between the gingival margin and the attached tissues (ie, the 5. The mucogingival line.
bottom of the pocket). B, The probing or clinical pocket depth is the
depth of penetration of the probe.
Probe penetration can vary depending on the force of in-
troduction, the shape and size of the probe tip, the direction
of penetration, the resistance of the tissues, the convexity of
Detection of Pockets the crown, and the degree of tissue inflammation. Several
The only accurate method of detecting and measuring peri- studies have determined the depth of penetration of a probe in
odontal pockets is by careful exploration with a periodontal a sulcus or pocket. Armitage et al used beagle dogs to evaluate
probe. Pockets are not detected by radiographic examination. the penetration of a probe with the use of a standardized force
The periodontal pocket is a soft-tissue change. Radiographs of 25 g. They reported that in patients with healthy gingiva,
indicate areas of bone loss in which pockets may be sus- the probe penetrated the epithelium to about two thirds of its
pected, but they do not show pocket presence or depth and length; in patients with gingivitis, it stopped 0 .1 mm short of
consequently they show no difference before and after pocket its apical end; and in patients with periodontitis, the probe tip
elimination unless bone has been modified. consistently went past most of the apical cells of the junctional
Gutta-percha points or calibrated silver points can be used epithelium (Fig. 26 15).
with the radiograph to determine the level of attachment of In human-periodontal pockets, the probe tip penetrates to
the periodontal pockets (Fig. 26.13) They may be used effec- the most coronal intact fibers of the connective tissue attach-
tively for individual pockets or in clinical research, but their ment. The depth of penetration of the probe in the connec-
routine use throughout the mouth would be difficult to man- tive tissue apical to the junctional epithelium in a periodontal
age. Clinical examination and probing are more direct and pocket is about 0.3 mm. This is important when evaluat-
efficient. ing differences in probing depth before and after treatment,
because the reduction in probe penetration may be a result
Pocket Probing of reduced inflammatory response rather than of a gain in
There are two different pocket depths: (1) the biologic or histo- attachment.
logic depth, and (2) the clinical or probing depth (Fig. 26.14). The probing forces have been explored by several investi-
The biologic depth is the distance between the gingival gators. Forces of 0.75 N have been found to be well tolerated
margin and the base of the pocket (ie, the coronal end of the and accurate. Interexaminer error (ie, depth discrepancies
junctional epithelium). This can be measured only in care- between examiners) was reported to be as much as 2.1 mm
fully prepared and adequately oriented histologic sections. (with an average of 1.5 mm) in the same areas.
q
rt L- -·
I
I I\)\ I
--~,, r-'i )
,-,-,_
I '' ,, _ \.. - ,-
1 ""'I' f- - I I
I .., "f -,, I /
,... I-.., I I \ I /
- \
\. ~,
', \
'J'
' /
, , FIGURE 26.18 Exploring with a periodontal probe (left) may not de-
I I
, I I
tect furcation involvement; specially designed instruments (ie, Nabers
I I
\ I
I I
I ,, I ,
probes) (right) can enter the furcation area.
FIGURE 26.16 "Walking" the probe to explore the entire pocket. changes in the position of the gingival margin. Therefore, it
may be unrelated to the existing attachment of the tooth.
Alternatively, the level of attachment is the distance be-
tween the base of the pocket and a fixed point on the crown,
such as the CE]. Changes in the level of attachment can be
the result of a gain- or loss of attachment, and they can af-
ford a better indication of the degree of periodontal destruc-
tion or gain. Shallow pockets attached at the level of the apical
third of the root connote more severe destruction than deep pockets
attached at the coronal third of the roots (see Chapter 18 and
Figs. 18 17-1819)
Determining the Level of Attachment
When the gingival margin is located on the anatomic crown, the
level of attachment is determined by subtracting from the
,
I
depth of the pocket the distance from the gingival margin to
the CE]. If both are the same, the loss of attachment is zero.
\ ,, \
\
When the gingival margin coincides with the CEJ, the loss
I
\
,_,
of attachment equals the pocket depth.
\
,_,
When the gingival margin is located apical to the CEJ, the
FIGURE 26.17 Vertical insertion of the probe (left) may not detect loss of attachment is greater than the pocket depth. Therefore,
interdental craters; oblique positioning of the probe (right) reaches
the depth of the crater.
the distance between the CEJ and the gingival margin should
be added to the pocket depth. Drawing the gingival margin
on the chart where pocket depths are entered helps to clarify
Probing Technique this important point.
The probe should be inserted parallel to the vertical axis of
the tooth and "walked" circumferentially around each sur- Bleeding on Probing
face of each tooth to detect the areas of deepest penetration The insertion of a probe to the bottom of the pocket elicits
(Fig. 26.16). bleeding if the gingiva is inflamed and if the pocket epitheli-
In addition, special attention should be directed to detect- um is atrophic or ulcerated. Noninflamed sites rarely bleed. In
ing the presence of interdental craters and furcation involve- most cases, bleeding on probing is an earlier sign of inflamma-
ments. To detect an interdental crater, the probe should be tion than gingival color changes (Chapter 14). However, color
placed obliquely from both the facial and lingual surfaces to changes may present without bleeding on probing. Depending
explore the deepest point of the pocket located beneath the on the severity of inflammation, bleeding can vary from a tenu-
contact point (Fig. 26.17) In multirooted teeth, the possibil- ous red line along the gingival sulcus to profuse bleeding. If peri-
ity of furcation involvement should be carefully explored. The odontal treatment is successful, bleeding on probing will cease.
use of specially designed probes (eg, Nabers probes) allows To test for bleeding after probing, the probe is carefully
for an easier and more accurate exploration of the horizontal introduced to the bottom of the pocket and gently moved lat-
component of furcation lesions (Fig. 26.18). erally along the pocket wall. Sometimes bleeding appears im-
mediately after the removal of the probe; other times, it may
Level of Attachment and Pocket Depth be delayed for a few seconds. Therefore, the clinician should
Pocket depth is the distance between the base of the pocket and recheck for bleeding 30-60 s after probing.
the gingival margin. It may change from time to time, even As a single test, bleeding on probing is not a good pre-
in patients with untreated periodontal disease, as a result of dictor of progressive attachment loss; however, its absence is
FIGURE 26.19 A, The limitations of periodontal probing. B, Probing pressure caused by probe angulation, the presence of subgingival calculus, and
the presence of overhanging restorations. (A, Courtesy Dr J. Frontan.)
an excellent predictor of periodontal stability. When bleeding some problems in terms of reproducibility of the measure-
is present in multiple sites of advanced disease, bleeding on ments. Accuracy and reproducibility depend not only on root
probing is a good indicator of progressive attachment loss. Ar- morphology and tissue changes but also, very importantly,
mitage analyzed the literature on this subject up to 1996. He on the probing technique, the probing force, the size of the
performed a metaanalysis of the various papers and conclud- probe, the angle of insertion of the probe, and the precision of
ed that the presence of bleeding on probing in a "treated and the probes calibration (Fig. 26.19).
maintained patient population" is an important risk predictor
for increased loss of attachment. Probing Force
The insertion of a soft wooden interdental stimulator in the One of the main problems of reproducibility has been the vari-
interdental space produces a similar bleeding response. This ation of probing force. The development of pressure-sensitive
tool can be used by the patient to self-examine the gingiva for probes has helped to overcome this. It has been shown that,
the presence of inflammation. with forces of up to 30 g, the tip of the probe remains within
the junctional epithelium, whereas forces of up to 50 g are
When to Probe necessary to reach the bone level.
The probing of pockets is performed at various times for di-
agnosis and monitoring the course of treatment and mainte- Probe Angulation
nance. The initial probing of moderate or advanced cases is Standardization of the probe tip (ie, < 1 mm) and the ad-
usually hampered by the presence of heavy inflammation and dition of registration stents to maintain reproducible probe
abundant calculus and it cannot be done very accurately. Prob- angulation have been used to overcome this error. New
ing at this stage is also difficult as a result of the discomfort commercially available, computer-assisted technology has
and pain that occurs when the gingival tissues are inflamed. been used to improve probing accuracy and reproducibil-
The purpose of this initial probing, together with the clini- ity. In addition to more accurate measurements, the data
cal and radiographic examination, is to determine whether derived from automatic probing can become a part of the
the tooth should be saved or extracted. After the patient has electronic record. Once incorporated, clinical changes and
performed adequate plaque control for some time and the cal- patterns of disease activity can be easily determined. These
culus has been removed, the major inflammatory changes dis- records also provide feedback to the patient. The Florida
appear, an accurate probing of the pockets can be performed. Probe System (Fig. 26.20) consists of a probe handpiece,
The purpose of this second probing is to accurately establish a digital readout, a foot switch, a computer interface, and
the level of attachment and the degree of involvement of roots a computer. The end of the probe is 0.4 mm and it recip-
and furcations. Data obtained from this probing provides rocates through a sleeve that provides a reference by which
valuable information for treatment decisions. measurements are made.
Later during periodontal treatment, probings are done to These measurements are made electronically and trans-
determine changes in pocket depth and to ascertain healing ferred automatically when the foot switch is pressed or when
progress after different procedures. a voice command is given. Constant probing force is provided
by coil springs inside the probe handpiece and a digital read-
Probing Around Implants out (Fig. 26.21). This method combines the advantages of a
Since implants are susceptible to bone loss, probing around constant probing force with precise electronic measurement
them becomes part of examination and diagnosis. A tradi- and computer storage of data; thereby eliminating the poten-
tional periodontal probe may be used under light force (eg, tial errors associated with visual reading and the need for an
0.25 N) without damaging the periimplant-mucosal seal. assistant to record the measurements.
Several studies have been made comparing the Florida
Automatic and Electronic Periodontal Probing Probe with conventional probing. The automatic probe ap-
The use of the periodontal probe is the classic method to de- pears to underestimate deep probing depths but to show less
tect pocket depth and loss of attachment. However, it presents variability than conventional probing. The automatic probe
or inactive state, measurements taken at different times have to

be compared. The precise assessment and comparison of the
clinical attachment level (CAL) at different intervals of time
can determine whether the attachment is being lost, which
indicates that the lesion is active. The exact measurement of
this important clinical parameter is done from the CEJ to the
bottom of the pocket and therefore requires that the location
of this landmark be determined exactly and reproducibly
The Florida Probe provides a means of recording relative
CAL changes over time. A later model of the probe has a mod-
ified sleeve with a prominent 0.125-mm edge to facilitate a
"catch" of the CE]. The width of this edge is considered small
enough not to interfere with probing-depth measurements,
thus providing concurrent measurements of CAL and pocket
depth. Of course, this measurement does not predict the fu-
FIGURE 26.20 Automated periodontal probes: Florida Probe Sys- ture but only shows what happened during the period of time
tem. Integration of direct electronic measurements with constant prob- between the two measurements. The precise determination of
ing force, with computer storage and online data readout.
disease activity will have a direct effect on diagnosis, progno-
sis, and therapy. The goals of therapy may change, depending
also has the problem of providing little tactile sensitivity, on the state of the periodontal lesion.
thereby making it more difficult to "walk" the probe.
Electronic systems, such as the Interprobe and the Peri-
probe, provide constant probing force and computer storage
Amount of Attached Gingiva
of data; but their reproducibility is only slightly better than It is important to establish the relationship between the bot-
that of conventional methods. tom of the pocket and the mucogingival line. The width of
The lack of standardization between probings by different in- the attached gingiva is the distance between the mucogingival
dividuals and at different times by the same individual depend junction and the projection on the external surface of the bot-
not only on root morphology and tissue changes but also on the tom of the gingival sulcus or the periodontal pocket. It should
probing technique, the probing force, the size of the probe, the not be confused with the width of the keratinized gingiva, be-
angle of insertion of the probe, and the precision of the probes cause the latter also includes the marginal gingiva (Fig. 26.22).
calibration. For measurements of clinical attachment loss, it is The width of the attached gingiva is determined by sub-
necessary to identify the location of the CEJ and this offers an- tracting the sulcus or pocket depth from the total width of the
other hurdle for the standardization of measurements. gingiva (ie , the gingival margin to the mucogingival line) This
is done by stretching the lip or cheek to demarcate the mu-
Determination of Disease Activity cogingival line while the pocket is being probed (Fig. 26.23).
The amount of attached gingiva is generally considered to be
Currently, there are no accurate methods to determine the ac- insufficient when the stretching of the lip or cheek induces the
tivity or inactivity of a lesion. Inactive lesions may show little movement of the free gingival margin.
or no bleeding with probing and minimal amounts of gingival Other methods that are used to determine the amount of
fluid. Active lesions bleed more readily with probing and have attached gingiva include pushing the adjacent mucosa cor-
large amounts of fluid and exudates, although active and non- onally with a dull instrument or painting the mucosa with
active sites may show no differences with regard to bleeding Schiller potassium iodide solution, which stains keratin.
with probing, even in patients with aggressive periodontitis.
The bacterial flora in a healthy gingival sulcus, as revealed by
dark-field microscopy, consists mostly of coccoid cells. The
Degree of Gingival Recession
bacterial flora of a periodontal pocket shows a greater number During periodontal examination, it is necessary to record the
of Spirochetes and motile bacteria. data regarding the amount of gingival recession. This mea-
For the determination of pocket depth or attachment levels surement is taken with a periodontal probe from the CEJ to
to provide information about whether the lesion is in an active the gingival crest and it is drawn on the patient's chart.
FIGURE 26.21 Florida Probe System. A, Handpiece for assessing probing pocket depths. B, Handpiece for assessing relative CALs.
Alveolar Bone Loss

C
Alveolar bone levels are evaluated via both clinical and radio-
graphic examination. Probing is helpful for determining the
following: (1) the height and contour of the facial and lingual
bones, which are obscured on the radiograph by the roots;
and (2) the architecture of the interdental bone. Transgingival
probing, which is performed after the area is anesthetized, is a
more accurate method of evaluation and it provides additional
information about bone architecture.
Palpation
Palpating the oral mucosa in the lateral and apical areas of the
tooth may help to locate the origin of radiating pain that the
patient cannot localize. Infection deep in the periodontal tis-
sues and the early stages of a periodontal abscess may also be
detected by palpation.
FIGURE 26.22 The shaded area shows the attached gingiva, which
extends between the projection on the external surface of the bottom
of the pocket (A) and the mucogingival junction (8). The keratinized
Suppuration
gingiva may extend from the mucogingival junction (8) to the gingival
The presence of an abundant number of neutrophils in the
margin (C).
gingival fluid transforms it into a purulent exudate. Several
studies have evaluated the association between suppuration
and the progression of periodontitis and they have reported
that this sign is present in a very low percentage of diseased
sites (ie , 3-5%). Therefore it is not, by itself, a good indicator.
Clinically, the presence of exudate in a periodontal pocket
is determined by placing the ball of the index finger along the
lateral aspect of the marginal gingiva and applying pressure in
a rolling motion toward the crown (Fig. 26.24). Visual exami-
nation without digital pressure is not enough. The purulent
exudate is formed in the inner pocket wall, and therefore the
external appearance may give no indication of its presence.
Exudate formation does not occur in all periodontal pockets
but digital pressure often reveals it in pockets where its pres-
ence is not suspected.
Periodontal Abscess
A periodontal abscess is a localized accumulation of exudate
within the gingival wall of a periodontal pocket. Periodontal
abscesses may be acute or chronic.
FIGURE 26.23 To determine the width of the attached gingiva, A, the

pocket is probed, and then B, the probe is placed on the outer surface
while the lip or cheek is extended to demarcate the mucogingival line.
C, Another method that can be used to demarcate the mucogingival line FIGURE 26.24 Purulent exudate expressed from a periodontal
is pushing the lip or cheek coronally. pocket by digital pressure.
FIGURE 26.26 Nodular mass at the orifice of a draining sinus.
Continuity of the lesion with the gingival margin indicates

that the abscess is periodontal.
The abscess is not necessarily located on the same surface
of the root as the pocket from which it is formed. A pocket
at the facial surface may give rise to a periodontal abscess in-
terproximally It is common for a periodontal abscess to be
located at a root surface other than that along which the pock-
et originated, because drainage is more likely to be impaired
FIGURE 26.25 Acute periodontal abscesses on A, the buccal aspect
of tooth #19 and B, the lingual aspect of tooth #20 in the same patient.
when a pocket follows a tortuous course.
In children, a sinus orifice along the lateral aspect of a
root is usually the result of periapical infection of a decidu-
ous tooth. In the permanent dentition, such an orifice may be
The acute periodontal abscess appears as an ovoid elevation caused by a periodontal abscess or by apical involvement. The
of the gingiva along the lateral aspect of the root (Fig. 26.25). orifice may be patent and draining, or it may be closed and
The gingiva is edematous and red, with a smooth, shiny sur- appear as a red, nodular mass (Fig. 26.26). The exploration
face. The shape and consistency of the elevated area vary; the of such masses with a probe usually reveals a pinpoint orifice
area may be domelike and relatively firm or it may be pointed that communicates with an underlying sinus.
and soft. In most cases, exudate may be expressed from the
gingival margin with gentle digital pressure. Periodontal Abscess and Gingival Abscess
The acute periodontal abscess is accompanied by symp-
toms, such as throbbing, radiating pain, and tenderness of the The principal differences between the periodontal abscess
gingiva to palpation. Other symptoms may include sensitivity and the gingival abscess are location and history ( Chapter 19).
of the tooth to palpation; tooth mobility, lymphadenitis, and The gingival abscess is confined to the marginal gingiva and
less frequently, systemic effects, such as fever, leukocytosis, it often occurs in previously disease-free areas. It is usually an
and malaise. Occasionally, the patient may have symptoms of acute inflammatory response to the forced entry of the foreign
an acute periodontal abscess without any notable clinical le- material into the gingiva. The periodontal abscess involves the
sion or radiographic changes. supporting periodontal structures and it generally occurs dur-
The chronic periodontal abscess usually presents a sinus that ing the course of chronic destructive periodontitis.
opens onto the gingival mucosa along the length of the root.
There may be a history of intermittent exudation. The orifice Periodontal Abscess and Periapical
of the sinus may appear as a difficult-to-detect pinpoint open-
Abscess
ing, which when probed, reveals a sinus tract that leads deep
into the periodontium. The sinus may be covered by a small, Several characteristics can be used as guidelines when dif-
pink, beadlike mass of granulation tissue. The chronic peri- ferentiating a periodontal abscess from a periapical abscess.
odontal abscess is usually asymptomatic. However, the patient If the tooth is nonvital, the lesion is most likely periapical.
may report episodes of dull, gnawing pain, a slight elevation However, a previously nonvital tooth can have a deep peri-
of the tooth, and a desire to bite down and grind the tooth. odontal pocket that can abscess. Moreover, a deep periodontal
The chronic periodontal abscess often undergoes acute exac- pocket can extend to the apex and cause pulpal involvement
erbations with all of the associated symptoms. and necrosis.
Diagnosis of the periodontal abscess requires the correla- An apical abscess may spread along the lateral aspect of
tion of the history with the clinical and radiographic findings. the root to the gingival margin. However, when the apex and
The suspected area should be probed carefully along the gin- lateral surface of a root are involved with a single lesion that
gival margin in relation to each tooth surface to detect a chan- can be probed directly from the gingival margin, the lesion is
nel from the marginal area to the deeper periodontal tissues. more likely to have originated as a periodontal abscess.
Radiographic findings are helpful for differentiating be- a complete intraoral series is required for periodontal diagnosis and
tween a periodontal lesion and a periapical lesion. Early acute treatment planning.
periodontal- and periapical abscesses present no radiographic
changes. Ordinarily, a radiolucent area along the lateral sur-
Laboratory Aids to Clinical Diagnosis
face of the root suggests the presence of a periodontal abscess,
whereas apical rarefaction suggests a periapical abscess. How- When unusual gingival or periodontal problems are detected
ever, acute periodontal abscesses that show no radiographic that cannot be explained by local causes, the possibility of
changes often cause symptoms in teeth with long-standing, contributing systemic factors must be explored. The signs and
radiographically detectable periapical lesions that do not con- symptoms of oral manifestations of systemic disease have to
tribute to the patient's complaint. Clinical findings, such as be clearly understood and analyzed and their presence dis-
the presence of extensive caries, pocket formation, lack of cussed with the patient's physician.
tooth vitality, and the existence of continuity between the gin- Numerous laboratory tests aid in the diagnosis of systemic
gival margin and the abscess area, often prove to be of greater diseases that may contribute to periodontal and oral diseases;
diagnostic value than the radiographic appearance. these tests will also be needed for the making treatment de-
A draining sinus on the lateral aspect of the root suggests cisions when dealing with medically compromised patients
periodontal rather than apical involvement; a sinus from (Chapter 30). Analyses of blood smears, blood cell counts,
a periapical lesion is more likely to be located further api- white blood cell differential counts, and erythrocyte sedimen-
cally. However, sinus location is not conclusive. In many in- tation rates are used to evaluate the presence of blood dyscra-
stances, particularly in children, the sinus from a periapical sias and generalized infections. Determinations of coagulation
lesion drains on the side of the root rather than at the apex time, bleeding time, clot retraction time, prothrombin time,
(Chapter 52) partial thromboplastin time, and capillary fragility, as well as
bone marrow studies, may be required at times. Estimation
lntraoral Radiographic Survey of blood sugar levels and corresponding urine analysis are re-
quired to rule out undiagnosed diabetes.
The radiographic survey should consist of a minimum of
14 intraoral films and 4 posterior bite-wing films (Fig. 26 2).
Histopathologic examination
Panoramic radiographs are a simple and convenient
method of obtaining a survey view of the dental arch and Chronic gingivitis, acute gingival lesions, different types of
the surrounding structures (Fig. 26.3). They are helpful for periodontitis are diagnosed based on the history, clinical fea-
the detection of developmental anomalies, pathologic lesions tures, and radiographs and do not require any microscopic
of the teeth and jaws and fractures, as well as for the dental investigation. However, certain types of gingival enlarge-
screening examinations of large groups. They provide an over- ments particularly neoplasms and desquamative gingival
all informative radiographic picture of the distribution and se- conditions need biopsy and subsequent histopathologic
verity of bone destruction with periodontal disease; however, examination.
Radiographic Aids in the Diagnosis

of Periodontal Disease
Radiographs are valuable for diagnosis of periodontal disease, The width and shape of the interdental bone and the angle
estimation of severity, determination of prognosis, and evalua- of the crest normally vary according to the convexity of the
tion of treatment outcome. However; radiographs are an adjunct proximal tooth surfaces and the level of the CEJ of the ap-
to the clinical examination, not a substitute for it. proximating teeth. The faciolingual diameter of the bone is re-
Radiographs demonstrate changes in calcified tissue; they lated to the width of the proximal root surface. The angulation
do not reveal current cellular activity but rather reflect the ef- of the crest of the interdental septum is generally parallel to a
fects of past cellular experience on the bone and roots. line between the CEJs of the approximating teeth (Fig. 26.27).
When there is a difference in the level of the CEJs, the crest of
Normal lnterdental Bone the interdental bone appears angulated rather than horizontal.
Evaluation of bone changes in periodontal disease is based

mainly on the appearance of the interdental bone because the
Radiographic Techniques
relatively dense root structure obscures the facial and lingual In conventional radiographs, periapical- and bite-wing pro-
bony plates. The interdental bone normally is outlined by a jections offer the most diagnostic information and are most
thin, radiopaque line adjacent to the PDL and at the alveo- commonly used in the evaluation of periodontal disease.
lar crest, referred to as the lamina dura (Fig. 26.27). Since the To properly and accurately depict periodontal bone status,
lamina dura represents the cortical bone lining the tooth socket, proper techniques of exposure and processing are required.
the shape and position of the root, and changes in the angulation of The bone level, pattern of bone destruction, PDL space width,
the X-ray beam produce considerable variations in its appearance. as well as, the radiodensity, trabecular pattern, and marginal
the projected image, making the bone margin appear closer to

the crown. The level of the facial bone is distorted more than
that of the lingual. Inappropriate horizontal angulation results
in tooth overlap, changes the shape of the interdental bone
image, alters the radiographic width of the PDL space and the
appearance of the lamina dura, and may distort the extent of
furcation involvement (Fig. 26.28).
Periapical radiographs frequently do not reveal the correct
relationship between the alveolar bone and the CE]. This is
particularly true in cases in which a shallow palate or the floor
of the mouth does not allow ideal placement of the periapi-
cal film. Bite-wing projections offer an alternative that images
periodontal bone levels better. For bite-wing radiographs, the
film is placed behind the crowns of the upper and lower teeth
FIGURE 26.27 Crest of interdental bone normally parallel to a line parallel to the long axis of the teeth. The X-ray beam is direct-
drawn between the CEJ of adjacent teeth (arrow). Note also the radi-
opaque lamina dura around the roots and interdental bone.
ed through the contact areas of the teeth and perpendicular
to the film. Thus, the projection geometry of the bite-wing
films allows the evaluation of the relationship between the
interproximal alveolar crest and the CEJ without distortion
contour of the interdental bone, vary by modifying exposure (Figs. 26.29 and 26.30). If the periodontal bone loss is severe
and development time, type of film, and X-ray angulation. and the bone level cannot be visualized on regular bite-wing
Standardized reproducible techniques are required to ob- radiographs, films can be placed vertically to cover a larger
tain reliable radiographs for pretreatment and posttreatment area of the jaws (Fig. 26.31). More than two vertical bite-wing
comparisons. films might be necessary to cover all the interproximal spaces
Prichard established the following four criteria to deter- of the area of interest.
mine adequate angulation of periapical radiographs.
1. The radiograph should show the tips of molar cusps with
little or none of the occlusal surface showing. Bone Destruction in Periodontal
2. Enamel caps and pulp chambers should be distinct. Disease
3. lnterproximal spaces should be open.
Early destructive changes of bone that do not remove suffi-
4. Proximal contacts should not overlap unless teeth are out
cient mineralized tissue cannot be captured on radiographs.
of line anatomically.
Therefore slight radiographic changes of the periodontal tis-
For periapical radiographs, the long-cone paralleling sues suggest that the disease has progressed beyond its earliest
technique most accurately projects the alveolar bone level stages. The earliest signs of periodontal disease must be detected
(Fig. 26 28) The bisection-of-the-angle technique elongates clinically.
FIGURE 26.28 Comparison of long-cone paralleling and bisection-of-the-angle techniques. A, Long-cone paralleling technique, radiograph of
dried specimen. B, Long-cone paralleling technique, same specimen as A. Smooth wire is on margin of the facial plate and knotted wire is on the lin-
gual plate to show their relative positions. C, Bisection-of-the-angle technique, same specimen as A and B. D, Bisection-of-the-angle technique, same
specimen. Both bone margins are shifted toward the crown, the facial margin (smooth wire) more than the lingual margin (knotted wire), creating the
illusion that the lingual bone margin has shifted apically. (Courtesy Dr Benjamin Patur, Hartford, CT.)
(A) Periapical radiograph
• X-ray beam
Film
FIGURE 26.30 A, Periapical and B, bite-wing radiographs from full-

mouth series of a patient with periodontitis. The periapical film clearly
underestimates the amount of bone loss (white arrows). Due to the ap-
(B) Bite-wing radiograph propriate projection geometry, the alveolar crest height is accurately de-
picted on the bite-wing radiograph (white arrows).
FIGURE 26.29 Schematic diagram of A, periapical and B, bite-wing
radiographs. Angulation of the X-ray beam and the film on the periapi-
cal radiograph distort the distance between the alveolar crest and the
CEJ (compare a-b versus a1-b1). In contrast, the projection geometry of
the bite-wing radiograph allows a more accurate depiction (a2-b2) of the
distance between the alveolar crest and the CEJ (a-b).
Amount
Bone Loss Radiographs are an indirect method for determining the

amount of bone loss in periodontal disease. They image
The radiographic image tends to underestimate the severity the amount of remaining bone rather than the amount lost.
of bone loss. The difference between the alveolar crest height The amount of bone lost is estimated to be the difference
and the radiographic appearance ranges from O to 1.6 mm, between the physiologic bone level and the height of the
mostly accounted for by X-ray angulation. remaining bone.
FIGURE 26.31 Vertical bite-wing films can be used to cover a larger area of the alveolar bone.
FIGURE 26.32 Generalized horizontal bone loss.
The distance from the CEJ to the alveolar crest has been
analyzed by several investigators. Most studies, conducted in
adolescents, suggest a distance of 2 mm to reflect normal peri-
odontium. This distance may be greater in older patients.
Distribution
The distribution of bone loss is an important diagnostic sign.
It points to the location of destructive local factors in different
areas of the mouth and in relation to different surfaces of the
same tooth.
Pattern of Bone Destruction

In periodontal disease the interdental bone undergoes chang-
es that affect the lamina dura, crestal radiodensity, size and
shape of the medullary spaces, and height and contour of the
bone. Height of interdental bone may be reduced, with the
crest perpendicular to the long axis of the adjacent teeth (hori-
zontal bone loss Fig. 26.32) or angular or arc-shaped defects FIGURE 26.33 Angular bone loss on first molar with involvement of
( vertical bone loss; Fig. 26.33) could form. the furcation.
FIGURE 26.34 Angular bone loss on mandibular molar partially ob-

scured by a dense mylohyoid ridge.
Radiographs do not indicate the internal morphology or

depth of craterlike defects. Also, radiographs do not reveal the
extent of involvement on the facial and lingual surfaces. Bone
destruction of facial and lingual surfaces is masked by the
dense root structure and bone destruction on the mesial- and
distal root surfaces may be partially hidden by superimposed
anatomy, such as a dense mylohyoid ridge (Fig. 26.34). In
most cases, it can be assumed that bone losses seen interden-
tally continue in either the facial or the lingual aspect, creating
a troughlike lesion. FIGURE 26.35 lnterdental lesion that extends to the facial or lingual
Dense cortical facial and lingual plates of interdental bone surfaces in a troughlike manner.
obscure destruction of the intervening cancellous bone. Thus

a deep craterlike defect between the facial and lingual plates
might not be depicted on conventional radiographs. To record Radiographic Appearance
destruction of the interproximal cancellous bone radiographi- of Periodontal Disease
cally, the cortical bone must be involved. A reduction of only
0.5-1.0 mm in the thickness of the cortical plate is sufficient Periodontitis
to permit radiographic visualization of the destruction of the
Radiographic changes in periodontitis follow the pathophysiol-
inner cancellous trabeculae.
ogy of periodontal tissue destruction and include the following.
lnterdental bone loss may continue facially and/or lingually
to form a troughlike defect that could be difficult to appreciate 1. Fuzziness and disruption of lamina dura crestal cortication
radiographically. These lesions may terminate on the radicu- continuity is the earliest radiographic change in periodon-
lar surface or may communicate with the adjacent interdental titis (Fig. 26.38A and B) and results from bone resorption
area to form one continuous lesion (Fig. 26.35). activated by extension of gingival inflammation into the
Fig. 26.36 shows two adjacent interdental lesions connect- periodontal bone. Depicting these early changes depends
ing on the radicular surface to form one interconnecting os- greatly on the radiographic technique, as well as on ana-
seous lesion. Along with clinical probing of these lesions, the tomic variations (thickness and density of interdental bone
use of a radiopaque pointer placed in these radicular defects and position of adjoining teeth). No correlation has been
will demonstrate the extent of the bone loss. found between crestal lamina dura in radiographs and
Periodontal bone loss should be differentiated from nor- the presence or absence of clinical inflammation, bleed-
mal anatomy or anatomic variants that can resemble dis- ing on probing, periodontal pockets, or loss of attachment.
ease. For example, nutrient canals in the alveolar bone can Therefore it can be concluded that the presence of an in-
appear as linear and circular radiolucent areas (Fig. 26.37). tact crestal lamina dura may be an indicator of periodontal
These canals can be seen more frequently in the anterior health, whereas its absence lacks diagnostic relevance.
mandible although they can be present throughout the al- 2. Continued periodontal bone loss and widening of the
veolar ridge. periodontal space results in a wedge-shaped radiolucency
Finally, it should be emphasized that radiographs can only at the mesial or distal aspect of the crest (Fig. 26.38B).
assess the amount of periodontal bone that is present and de- The apex of the area is pointed in the direction of the root.
duce the extent of bone loss. However, it is sometimes neces- 3. Subsequently, the destructive process extends across the
sary to determine whether the reduced bone level is the result alveolar crest, thus reducing the height of the interdental
of periodontal disease that is no longer destructive (usually af- bone. As increased osteoclastic activity results in increased
ter treatment and proper maintenance) or whether destructive bone resorption along the endosteal margins of the med-
periodontal disease is present. Differentiation between treated ullary spaces, the remaining interdental bone can appear
versus active periodontal disease can only be achieved clini- partially eroded (Fig. 26 38C)
cally. Radiographically, detectable changes in the normal corti- 4. The height of the interdental septum is progressively re-
cal outline of the interdental bone are corroborating evidence duced by the extension of inflammation and the resorption
of destructive periodontal disease. of bone (Fig. 26 38D).
(A} (B)
(C)
(D)
FIGURE 26.36 A, lnterdental mesial and distal lesions. B, Facial or lingual outlines of actual lesion. C, Occlusal view of lesion. D, Radiograph of
mesial and facial lesions.
5. Frequently, a radiopaque horizontal line can be observed Furcation Involvement

across the roots of a tooth. This opaque line demarcates
the portion of the root where the labial or lingual bony Definitive diagnosis of furcation involvement is made by clini-
plate has been partially or completely destroyed from the cal examination, which includes careful probing with a spe-
remaining bone-supported portion (Fig. 26.39). cially designed probe (eg, Nabers). Radiographs are helpful,
but root superimposition, caused by anatomic variations and/
or improper technique, can obscure radiographic representa-
lnterdental Craters tion of furcation involvement. As a general rule, bone loss is
lnterdental craters are seen as irregular areas of reduced den- greater than it appears in the radiograph. A tooth may pres-
sity on the alveolar bone crests. Craters are generally not ent marked bifurcation involvement in one film (Fig. 26.40A)
sharply demarcated but gradually blend with the rest of the but appear to be uninvolved in another (Fig. 26.40B). Radio-
bone. Conventional radiographs do not accurately depict the graphs should be taken at different angles to reduce the risk of
morphology or depth of interdental craters, which sometimes missing furcation involvement.
appear as vertical defects. The recognition of a large, clearly defined radiolucency in
the furcation area is easy to identify (see Fig. 26.40A), but less
clearly defined radiographic changes are often overlooked. To
assist in the radiographic detection of furcation involvement,
the following diagnostic criteria are suggested.
1. The slightest radiographic change in the furcation area
should be investigated clinically, especially if there is bone
loss on adjacent roots (Fig. 26.41).
2. Diminished radiodensity in the furcation area, in which
outlines of bony trabeculae are visible, suggests furcation
involvement (Fig. 26.42).
3. Whenever there is marked bone loss in relation to a single
molar root, it may be assumed that the furcation is also
involved (Fig. 26.4 3)
Periodontal Abscess
The typical radiographic appearance of the periodontal ab-
scess is a discrete area of radiolucency along the lateral aspect
FIGURE 26.37 Prominent nutrient canals in the mandible. of the root (Figs. 26.44 and 26.45). However, the radiographic
FIGURE 26.39 Horizontal lines across the roots of the central inci-
sors (arrows). The area of the roots below the horizontal lines is partially
or completely denuded of the facial and lingual bony plates.
(C) (D)
FIGURE 26.38 Radiographic changes in periodontitis. A, Normal ap-
pearance of interdental bone. B, Fuzziness and a break in the continuity
of the lamina dura at the crest of the bone distal to the central incisor
(left). There are wedge-shaped radiolucent areas at the crest of the other
interdental bone. C, Radiolucent projections from the crest into the in-
terdental bone indicate extension of destructive processes. D, Severe
bone loss.
picture is often not characteristic (Fig. 26.46). This can be due

to the following.
1. The stage of the lesion. In the early stages, the acute peri-
odontal abscess is extremely painful but presents no radio-
graphic changes.
2. The extent of bone destruction and the morphologic changes of
the bone.
3. The location of the abscess. Lesions in the soft tissue wall
of a periodontal pocket are less likely to produce radio- FIGURE 26.40 A, Furcation involvement indicated by triangular radio-
graphic changes than those deep in the supporting tissues. lucency in bifurcation area of mandibular first molar. The second molar
presents only a slight thickening of the periodontal space in the bifurca-
Abscesses on the facial or lingual surface are obscured by tion area. B, Same area as A, different angulation. The triangular radiolu-
the radiopacity of the root. Interproximal lesions are more cency in the bifurcation of the first molar is obliterated, and involvement
likely to be visualized radiographically. of the second molar bifurcation is apparent.
FIGURE 26.41 Early furcation involvement suggested by fuzziness in

the bifurcation of the mandibular first molar, particularly when associ-
ated with bone loss on the roots.
FIGURE 26.44 Radiolucent area on lateral aspect of root with chron-

ic periodontal abscess.
FIGURE 26.42 Furcation involvement of mandibular first and second

molars indicated by thickening of periodontal space in furcation area.
The furcation of the third molar is also involved, but the thickening of
the periodontal space is partially obscured by the external oblique line.
FIGURE 26.45 Typical radiographic appearance of periodontal

abscess on right central incisor.
Therefore radiographs alone cannot provide final diagnosis

of a periodontal abscess but need to be accompanied by care-
ful clinical examination.
Clinical Probing
Regenerative and resective flap designs and incisions re-
quire prior knowledge of the underlying osseous topog-
FIGURE 26.43 Furcation involvement of the first molar partially ob- raphy. Careful probing of these pocket areas after scaling
scured by the radiopaque lingual root. The horizontal line across the
distobuccal root demarcates the apical portion (arrow), which is cov- and root planing often require local anesthesia and defini-
ered by bone, from the remainder of the root, where the bone has been tive radiographic evaluation of the osseous lesions. Radio-
destroyed. graphs taken with periodontal probes, gutta-percha points,
FIGURE 26.46 Chronic periodontal abscess. A, Periodontal abscess in the left maxillary first premolar area. B, Extensive bone destruction on the
mesial surface of the first premolar. gutta-percha point traces to the root apex.
FIGURE 26.47 A, Radiograph of maxillary cuspid. This view does not show facial bone loss. B, Radiograph of same maxillary cuspid as A, with
gutta-percha points placed in the facial pocket to indicate bone loss.
or other indicators (eg, Hirschfeld pointers) placed into the Trauma from Occlusion
anesthetized pocket show the true extent of the bone lesion.
As indicated previously, the attachment level on the radicu- Trauma from occlusion can produce radiographically detect-
lar surface or interdental lesions with thick facial or lingual able changes in the thickness of the lamina dura, morphology
bone cannot be visualized in the radio graph. The use of ra- of the alveolar crest, width of the PDL space, and density of
diopaque indicators is an efficient and necessary diagnostic the surrounding cancellous bone.
aid (Fig. 26 4 7) Traumatic lesions manifest more clearly in faciolingual
aspects because mesiodistally, the tooth has the added sta-
bility provided by the contact areas with adjacent teeth.
Localized Aggressive Periodontitis Therefore slight variations in the proximal surfaces may
indicate greater changes in the facial and lingual aspects.
Localized aggressive (formerly "localized juvenile") periodon-
The radiographic changes listed next are not pathognomonic of
titis is characterized by the following:
trauma from occlusion and must be interpreted in combination
1. Initially, bone loss in the maxillary and mandibular inci- with clinical findings, particularly tooth mobility, presence of
sor and/or first molar areas, usually bilaterally, resulting in wear facets, pocket depth, and analysis of occlusal contacts
vertical, arclike destructive patterns (Fig. 26.48). and habits.
2. As the disease progresses, loss of alveolar bone may become The injury phase of trauma from occlusion produces a loss
generalized but remains less pronounced in the premolar of the lamina dura that may be noted in apices, furcations, and
areas. marginal areas. This loss of lamina dura results in widening of
FIGURE 26.48 Localized aggressive periodontitis. The accentuated bone destruction in the anterior and first molar areas is considered to be char-
acteristic of this disease.
suggest that the tooth is being subjected to increased forces.

Successful attempts to reinforce the periodontal structures by
widening the PDL space is accompanied by increased width of
the lamina dura and sometimes by condensation of the perial-
veolar cancellous bone.
More advanced traumatic lesions may result in deep angu-
lar bone loss, which, when combined with marginal inflam-
mation, may lead to intrabony pocket formation. In terminal
stages, these lesions extend around the root apex, producing a
wide, radiolucent periapical image (cavernous lesions).
Root resorption may also result from excessive forces on
the periodontium, particularly those caused by orthodontic
appliances. Although trauma from occlusion produces many
areas of root resorption, these areas are usually of a magnitude
insufficient to be detected radiographically
Digital lntraoral Radiography

Over the last two decades, advances in digital imaging
technology have driven a rapid growth of digital intraoral
radiography as a convenient alternative to conventional film-
based radiography These technologies have been integrated
into patient management systems, enabling dental offices to
maintain a fully electronic patient record (Fig. 26.S0A). The
FIGURE 26.49 Widened periodontal space caused by trauma from digital records can be easily shared among dentists and other
occlusion. Note the increased density of the surrounding bone caused healthcare providers enabling telediagnosis, and also facilitat-
by new bone formation in response to increased occlusal forces.
ing transmission to third parties for reimbursement.
Digital intraoral radiographic systems use either solid-state
the PDL space (Fig. 26.49). The repair phase of trauma from detectors or photostimulable phosphor (PSP) plates. Systems
occlusion leads to an attempt to strengthen the periodontal with solid-state detectors use either charge-coupled devices
structures to better support the increased loads. Radiographi- (CCDs) or complementary metal-oxide semiconductor (CMOS)
cally, this is manifested by a widening of the PDL space, which chips as image receptors. These receptors are typically wired
may be generalized or localized. and connected to a computer using a universal serial bus (USB)
Although microscopic measurements have determined connection. Wireless sensors are also available and require the
normal variations in the PDL space width along the root sur- use of disposable batteries. With CCD/CMOS-based receptors,
face, these are generally not detected radiographically Thus, images are recorded and displayed on a computer monitor vir-
when seen on the radiographs, PDL space variations in width tually in real time. These sensors are bulkier than film and the
(A)
FIGURE 26.50 A, Image display of a full-mouth radiographic series acquired using complementary metal-oxide semiconductor (CMOS) receptors.
Specific features of the software program allow for image manipulation, measurements, and annotations. B, The "perio" image enhancement filtration
applied to highlight the contrast of alveolar bone. Note the presence of calculus and the better depiction of the alveolar crestal bone.
active image-recording area is slightly smaller than that of film. and contrast of the image can be altered to highlight specific
A second technology for intraoral radiography is PSP plates. anatomic regions, depending on the diagnostic task. The im-
These receptors are the same size as intraoral radiographic film. ages can be magnified to allow closer examination of a specific
Unlike CCD/CMOS receptors, PSP plates do not provide a real- area of interest. Importantly, a variety of image-enhancement
time display of the radiographic image. On interaction with filters can be applied, for example to sharpen (enhance edg-
X-ray photons, PSP crystals in the plate store energy, creating a es) images. Some software programs have preprogrammed al-
latent radiographic image. The stored energy is then released by gorithms that can be applied for specific diagnostic tasks, for
stimulating the plate with an appropriate wavelength of light. example, to enhance interproximal caries, periodontal bone,
With PSP systems, the workflow is somewhat similar to that of pulp canals, and so forth (Fig. 26.S0B). However, it is impor-
silver halide emulsion film. Following radiographic exposure, tant to recognize that such image manipulations can produce
the PSP plate is scanned by a laser beam, converting the latent artifacts that may be misinterpreted as disease. Clinicians
radiographic image into a digital image. should be aware of such artifacts produced by digital-image
Following capture, digital radiographic images can be en- manipulation. In addition to the image-manipulation fea-
hanced to augment radiographic diagnosis. The brightness tures, digital radiographic images facilitate patient education,
allow for easy storage and sharing with other healthcare pro- underestimate the amount of periodontal bone loss and early
viders, and can be easily integrated into electronic patient changes are usually not detected. Significant interdental bone
records. loss can occur and may not be detectable on periapical radio-
graphs because the density of the intact buccal and lingual or
Conclusion palatal bone plates obscure changes that occur as the result
of periodontitis. Comparison of periapical radiographs of the
Periapical radiographic examination should be part of each same area taken at different times will only be reliable in docu-
patient's periodontal evaluation and should be coupled with menting dramatic changes in bone levels, since variations in
a detailed recording of pocket depths, gingival margin lo- angulation of the beam, placement of the film, and develop-
cation, and bleeding on probing. Radiographic evaluation ment of the image make accurate measurements taken over
should be updated every 2 years. Periapical radiographs often time very difficult and unreliable.
Advanced Diagnostic Techniques

Periodontal diseases are polymicrobial infections that disrupt 2. Epidemiologic surveys can be carried out easily and the
host homeostasis. It is an established fact that microorganisms results are usually a true representation of the periodontal
are necessary but not sufficient to produce disease. The rate of status of the population.
occurrence, progression, and severity of the disease is highly 3. In a clinical setting, most but not, all of the patients can be
variable. There are bursts of activity and inactivity with no treated adequately.
uniform model of disease progression.
Periodontal diseases are conventionally classified as gin-
givitis, which is inflammation of gingiva without destruction The Negatives
of the supporting tissues and periodontitis, which is char- 1. The measurements are not accurate and are often mis-
acterized by loss of connective tissue attachment. Whereas leading.
gingivitis is a predictable response to the buildup of dental 2. Full-mouth recording is required as the disease is site-
biofilm, it need not necessarily progress to periodontitis. The specific.
time, mode, and events of transition from gingivitis to peri- 3. Exact etiology cannot be determined. Many hidden con-
odontitis are unclear. Whereas the disease susceptibility is ditions cannot be identified.
related to the whole person, the disease itself is considered 4. Small changes occurring over a specific time cannot be
site-specific. There is an interplay of multitude of factors, appreciated.
such as microbiologic immunologic, systemic, genetic, and 5. There are no reliable markers of current disease activity.
behavioral. 6. There are no reliable markers available to identify indi-
viduals/sites at risk.
Conventional Routine Diagnostic 7. It is difficult to determine the prognosis accurately and
hence to form an appropriate treatment plan.
Methods 8. They are prone for inter- and intraexaminer errors.
The basic methods of periodontal diagnosis have more or less 9. A great variability exists in the interpretation of the findings.
remained the same for the last half of the century. These in- 10. A universally accepted classification system does not exist.
clude the following methods.
1. Thorough dental and medical case history.
2. Recording clinical signs of periodontal inflammation. Requirements of Newer Diagnostic
3. Measurement of probing depth, CAL, and gingival reces- Methods
sion with manual probes.
4. Routine radiographs including orthopantamogram, bite- 1. Accurate measurement of disease.
wing, and intraoral periapical films. 2. Identify individuals/sites at risk for future breakdown.
5. Routine hematologic tests. 3. Identify the etiologic factor precisely.
6. Histopathologic examination incase of uncommon gingi- 4. Identify the exact nature of transition from gingivitis to
val and mucosa! disorders. periodontitis.
5. Able to aid in the determination of the prognosis.
6. Simple to use (preferably chair side) and provide quick
Status of Current Conventional results.
Diagnostic Methods 7. Demonstrate high specificity and sensitivity.
8. Minimally invasive.
The Positives 9. User-friendly with a low learning curve.
10. Should not be expensive.
1. They can be performed swiftly with minimum equipment In order to meet the above requirements, research has
and effort and are inexpensive. been going on worldwide and over the last two decades and a
number of advanced diagnostic techniques in different arenas of tissue, as shown by the reduced inflammation in smokers
have been proposed but none has emerged as the ideal and compared to nonsmokers.
best suited to overcome all the limitations of the traditional The disparity between measurements also depends on the
methods. probing technique, probing force, size of the probe, angle of
Whereas vast improvement has been seen in the measure- insertion of the probe, and precision of the probe calibration.
ment of the disease process by advances in the various equip- Further the presence of subgingival calculus and the convex-
ment, little has been gained about the disease process itself, ity of the crown compound the problem. All these variables
which would ultimately translate into patient care. contribute to the large standard deviations (0.5-1.3 mm) in
This section focuses on some of the advanced diagnostic clinical probing results, which make detection of small chang-
aids. This is by no means complete and exhaustive. Many es difficult.
limitations have remained at the research level, in laboratories Since the mid-1980s, different probe prototypes have been
without any clinical application, whereas a few are available developed and tested to overcome these limitations. One of
commercially. the main problems in reproducibility has been the variation in
probing force which may range anywhere from 15 to 100 N.
Different studies have shown that the penetration of the probe
Periodontal Probing
positively correlated with the probing force. This has been
The most widely used diagnostic tool, for the clinical assess- solved with the development of pressure-sensitive probes,
ment of connective tissue destruction in periodontitis, is the which have a standardized, controlled insertion pressure. Ex-
periodontal probe. In fact, increased probing depth and loss amples include the True Pressure Sensitive Probe (TPS) and
of clinical attachment are pathognomonic for periodontitis Yeaple Probe (useful in assessment of dentinal hypersensitiv-
and therefore, pocket probing is a crucial and mandatory pro- ity). Still the problem of data readout and storage remain.
cedure in diagnosing periodontitis and evaluating periodontal New technology and hightech computers are becoming
therapy. Currently, the "gold standard" for recording changes the rule rather than the exception during patient treatment.
in periodontal status is longitudinal measurement of CALs Computer applications and new devices are being developed
from the CEJ or a relative attachment level from a fixed refer- and marketed to improve diagnosis, enhance therapy, and
ence point. Reduction of pocket depth and gain of clinical at- monitor treatment outcomes. Additionally, computerization
tachment are the major clinical outcome measurements used offers the entire dental team the ideal potential to achieve ex-
to determine success of treatment. aminer standardization so that future comparison of health
Periodontal probes have been classified as follows: and disease becomes simpler and more precise and remains
cost-effective. This has resulted in the development of new
First generation-manual probes, for example, William, UNC
periodontal probing systems. After a National Institute of
15, WHO, Michigan O probe, etc.
Craniofacial Research (NIDCR) workshop on the quantitative
Second generation-pressure sensitive probes, for example,
evaluation of periodontal diseases by physical measurement
TPS probe, Yeaple probe, etc.
techniques, there was a proposal to develop and clinically
Third generation-computer linked probes, for example, Flor-
evaluate an improved periodontal pocket depth-attachment
ida probe, Inter probe, Foster miller probe, etc.
level measurement system that would meet the nine NIDCR
Fourth generation-three-dimensional probes.
criteria shown in Table 26.2.
Fifth generation-ultrasonography.
Following these criteria, the Florida Probe System was
The reader should not get confused with the names of developed. This automated probe system consists of a probe
other probes, such as DNA probe and Diamond probe, which handpiece, digital readout, foot switch, computer interface,
are used in microbiologic assays. and computer. The end of the probe tip is O. 4 mm in diameter.
The use of a manual periodontal probe presents many This probe tip reciprocates through a sleeve and the edge of
problems in terms of sensitivity and reproducibility of the the sleeve provides a reference by which measurements are
measurements. Readings of clinical pocket depth obtained made. These measurements are made electronically and trans-
with the periodontal probe do not normally coincide with ferred automatically to the computer when the foot switch is
the histologic pocket depth because the probe normally pressed. Constant probing force is provided by coil springs
penetrates the coronal level of the junctional epithelium inside the probe handpiece and digital readout. This probing
and the precise location of the probe tip depends on the de- method combines the advantages of constant probing force
gree of inflammation of the underlying connective tissues. with precise electronic measurement and computer storage
If the tissue is inflamed, it offers less resistance to probe of data, thus eliminating the potential errors associated with
penetration and the probe tip either coincides with or is visual reading and the need for an assistant to record the mea-
apical to the coronal level of connective tissue attachment. surements.
Conversely, after subgingival instrumentation, healed gin- These automated probes offer many solutions to the prob-
giva demonstrates an increased resistance to periodontal lems of conventional probing but also introduce problems.
probing. Again, these facts may not be true when making The probing elements lack tactile sensitivity, mainly because
the clinical diagnosis in smokers. The reduced inflamma- of their independent movement, which forces the operator to
tion and bleeding and increased fibrosis reported in smok- predetermine an insertion point and angle. In addition, the
ers might affect clinical probing measurements because of use of a fixed-force setting throughout the mouth, regardless
decreased probe tip penetration. A probing validity study of the site or inflammatory status, may generate inaccurate
showed that, with a constant-force probe, clinical probing measurements or patient discomfort. One common problem
depth at molar sites in smokers was lower than in nonsmok- reported in studies comparing the Florida Probe System with
ers; which may reflect more closely the true pocket depth conventional probing is the underestimation of deep prob-
and attachment levels with decreased probe tip penetration ing depths by the automated probe. Several studies even
TABLE 26.2
CRITERIA DEFINED BY NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH (NIDCR)

FOR OVERCOMING LIMITATIONS OF CONVENTIONAL PERIODONTAL PROBING
Limitation Conventional Probing NIDCR criteria
Precision 1 mm 0.1 mm
Range 12 mm 10mm
Probing force N onstandardized Constant and standardized
Applicability Noninvasive and easy to use Noninvasive, lightweight, and easy to use
Reach Easy to access any location around all teeth Easy to access any location around all teeth
Angulation Subjective A guidance system to ensure proper angulation
Security Easily sterilized Complete sterilization of all portions entering the mouth
Simple stainless steel instrument No biohazard from material or electric shock
Readout Depending on voice dictation and recording Direct electronic reading and digital output in writing
suggested that the use of this automated probing system does and shows promise in measuring CALs in humans. However,
not offer any advantage over conventional probing, rendering longitudinal clinical studies and long-term evaluation of peri-
a similar level of reproducibility However, other studies have odontal patients with this new instrument are lacking.
clearly shown that with the use of trained operators and per-
forming the "double-pass" method, the measurements taken
Ultrasonography in Periodontics
with the Florida Probe System have significantly fewer vari-
ables (lower standard deviation) than those obtained with a This method was first used by Spranger as early as in 1971.
conventional probe. The Florida Probe System obtained mean It provides noninvasive painless probing with predetermined
standard deviations (reproducibility) for CAL measurements guidance path. Since it needs extensive training to use and is
of about 0.3 mm, which is clearly superior to an average of expensive, it had not found favor in the general clinical setup.
0.82 mm (range, 0.52-1.30 mm) reported by Haffajee et al Commercial equipment, such as Perioimager, Perioalert, and
using manual probing. US probe, are available.
Few more commercially available electronic probing sys-
tems, such as the Interprobe and Periprobe, have also been
Gingival Temperature
evaluated. They provide constant probing force, computer
storage of data, and precise electronic management of the re- Researchers have attempted to develop other measures of
sulting inflammation. However, clinical evaluations have re- periodontal inflammation that may be useful when the usual
ported only slightly improved reproducibility compared with clinical signs are unreliable. One such measurement is sub-
conventional probing. gingival temperature. Kung et al claim that thermal probes
Other electronic-probing systems reported in the literature are sensitive diagnostic devices for measuring early inflam-
have never been released for general use. One of these sys- matory changes in the gingival tissues. One commercially
tems is an electronic probe (Foster-Miller) capable of cou- available system, the PerioTemp probe (Abiodent), enables
pling pocket-depth measurement with detection of the CEJ, the calculation of the temperature differential (DT, with a
from which the CAL is automatically detected. Researchers sensitivity of 0.1 'C) between the probed pocket and the sub-
at the University of Toronto have described a probe (Toronto gingival temperature. This temperature differential is useful
Automated) that, as with the Florida probe, uses the occlusal- because it allows consideration of differences in core tem-
incisal surface to measure relative CALs. The sulcus is probed perature between individuals. Individual temperature differ-
with a 0.5-mm nickel-titanium wire that is extended under ences are compared with those expected for each tooth, and
air pressure. It controls angular discrepancies by means of a higher-temperature pockets are signaled with a red-emitting
mercury-tilt sensor that limits angulation within ±30 degree, diode. Studies have demonstrated that the subgingival tem-
but it requires reproducible positioning of the patient's head perature at diseased sites is increased compared to healthy
and cannot easily measure second or third molars. sites and that a natural anteroposterior temperature gradient
The assessment of CAL provides information relating to the exists within the dental arches (posterior sites warmer than
gain or loss of connective-tissue attachment to the root surface anterior sites). In addition, mandibular sites were reported to
and it is the most practical method of determining that the be warmer than maxillary sites. The reason why temperature
disease is progressing (active) when a significant loss of at- increases with probing depth remains unknown. A possible
tachment has occurred over time. explanation is an increase in cellular and molecular activity
The Florida Probe System provides a means of recording caused by increased periodontal inflammation with increas-
relative CAL changes over time. Modification of the Florida ing probing depth.
Probe has recently been developed and tested to increase ac- In subsequent reports, Haffajee et al also found that ele-
curacy in detecting the CE]. This new electronic probe has a vated subgingival site temperature was particularly related to
modified sleeve, which includes a prominent 0.125-mm edge attachment loss in shallow pockets and that Prevotella inter-
to facilitate a "catch" of the CE]. The width of this edge is media, P micros, P gingivalis, Tannerella forsythia, and Aggrega-
considered small enough not to interfere with probing-depth tibacter actinomycetemcomitans had elevated proportions in the
measurements, offering clinicians measurement of CAL, and total microbiota in sites with elevated temperatures. Whether
probing depth concurrently This Florida PASHA Probe can the pathogens are responsible for the higher temperature by
reproducibly and reliably identify the CEJ in human skulls initiating the inflammatory process or whether the increased
temperature provides an environment susceptible for the areas (bone loss). Quantitative changes in comparison with
pathogens, remains unclear. the baseline images can be detected using an algorithm for
gray-scale levels. This is accomplished by means of computer-
assisted subtraction radiography. This technique requires a
Advances in Radiographic paralleling technique to obtain a standardized geometry and
Assessment accurate super imposable radiographs.
Studies have shown a high degree of correlation between
Dental radiography is the traditional method used to assess changes in alveolar bone determined by subtraction radiog-
the destruction of alveolar bone associated with periodonti- raphy and CAL changes in periodontal patients after therapy
tis. Although radiographs cannot accurately reflect the bone and increased detectability of small osseous lesions compared
morphology buccally and lingually, they provide useful infor- to the conventional radiographs from which the subtraction
mation on interproximal bone levels. Moreover, they provide images are produced. Subtraction radiography has also been
information on the periodontium that cannot be obtained applied to longitudinal clinical studies. Subtraction radiogra-
by other noninvasive methods (eg, root length, root proxim- phy is a technique that facilitates both qualitative and quan-
ity, presence of periapical lesions, and estimates of remain- titative visualization of even minor density changes in bone
ing alveolar bone). However, it is well-known that substantial by removing the unchanged anatomic structures from the im-
volumes of alveolar bone must be destroyed before the loss age. This enhances the detection of bone structures with true
is detectable in radiographs, specifically, more than 30% of density change and significantly improves the sensitivity and
the bone mass at the alveolar crest must be lost for a change accuracy of the evaluation. The main disadvantage of digital
in bone height to be recognizable on radiographs. Therefore, subtraction radiography techniques is the need of an almost
conventional radiographs are very specific but lack sensitivity. identical projection alignment during the exposure of the se-
Numerous cross-sectional and longitudinal epidemiologic quential radiographs, which makes this method impractical in
studies have used radiographs as the principal method of a clinical setting.
determining the presence or absence of periodontal destruc- Recently, a new image subtraction method, called diagnos-
tion. The primary criterion for bone loss in these studies was tic subtraction radiography (DSR), has been introduced com-
the distance from the CEJ to the alveolar crest, as measured bining the use of a positioning device during film exposure
from bite-wing radiographs. The threshold distance of bone with specialized software designed for digital-image subtrac-
loss has varied from 1 to 3 mm, although most of the studies tion using conventional personal computers in dental offices.
have used greater than 2 mm as the criterion for bone loss.
This low degree of sensitivity primarily results from the sub-
jectivity of radiographic assessment and the inherent sources Computer-Assisted Densitometric Image
of variability affecting conventional radiographic technique, Analysis System
such as (1) variations in projection geometry; (2) variations
in contrast and density caused by differences in film process- In the computer-assisted densitometric image analysis sys-
ing, voltage, and exposure time; and (3) masking of osseous tem ( CADIA), a video camera measures the light transmitted
changes by other anatomic structures. The variations in pro- through a radiograph and the signals from the camera are con-
jection geometry can be reduced by the use of standardized verted into gray-scale images. The camera is interfaced with
long-cone paralleling radiographic techniques .To standardize an image processor and a computer that allow the storage and
the radiographic assessment, radiographs should be obtained mathematic manipulation of the images.
in a constant and reproducible plane, using film holders with CADIA appears to offer an objective method for following
a template containing some type of impression material, alveolar bone density changes quantitatively over time. Also,
which is placed in a constant position on a group of teeth; compared to digital subtraction analysis, CADIA has shown
and an extension arm that can be precisely attached to both a higher sensitivity and a high degree of reproducibility and
the film holder and the X-ray tube. The use of a paralleling accuracy. This technique has also been applied to longitudinal
radiographic technique should be standard to all radiographic clinical studies.
assessments for periodontal diagnosis. The use of individual- Other advanced radiographic equipment include Comput-
ized film holders has been shown to be valid in evaluating ed Tomography (CT), Tune Aperture Computed Tomography
bone changes in longitudinal studies and clinical trials. (TACT), Cone-beam CT (CBCT), Local CT, and Optical Co-
herence Tomography (OCT). They are, however, used only
for research purposes and have no place in day-to-day dental
Digital Radiography practice.
Please refer to the section "Digital Intraoral Radiography" in
this chapter.
Advances in Microbiologic Analysis
Subtraction Radiography It is well known that certain microorganisms from the sub-
gingival microbiota, particularly Gram-negative anaerobes,
Subtraction radiography, a well-established technique in are the major etiologic factors of chronic and aggressive peri-
medicine, has been introduced as a technique in periodontal odontitis. Although the subgingival microenvironment in the
diagnosis. This technique relies on the conversion of serial ra- periodontal pocket is characterized by a wide diversity of or-
diographs into digital images. The serially obtained digital im- ganisms, with more than 700 species isolated from different
ages can then be superimposed and the resultant composite individuals and as many as 40 from a single site, only a few
viewed on a video screen. Changes in the density and volume species have been associated with disease. Despite the diffi-
of bone can be detected as lighter areas (bone gain) or dark culty in identifying all the members of the oral microbiota and
understanding how they interact with each other and with the pathogens in a pocket may be undetected particularly if they
host, a limited number of microorganisms have demonstrated are in low numbers. The most important drawback, how-
a clear etiologic role and have been identified as periodontal ever, is that culturing requires sophisticated equipment and
pathogens. Evidence for etiology is based on the fulfillment experienced personnel and is relatively time-consuming and
of several criteria, as described by Socransky. Using these expensive. When using this method, clinicians must be con-
criteria, strong evidence has been demonstrated for A. acti- fident that the laboratory has the appropriate technology and
nomycetemcomitans (Aa), P gingivalis (Pg), and Tforsythia (If). expertise in periodontal microbiology to communicate useful
Moderately strong evidence has been demonstrated for other diagnostic and therapeutic information to them.
bacteria isolated from the subgingival microbiota, including
Campylobacter rectus (Cr), Eubacterium nodatum, Fusobacteri-
Direct Microscopy
um nucleatum (Fn), P micros (Pm), P intermedia (Pi), Prevotella
nigrescens (Pn), and Spirochetes, such as Ireponema denticola Dark-field or phase-contrast microscopy has been suggested as
(Id).Viruses belonging to the herpes group have also been im- an alternative to culture methods on the basis of its ability
plicated. to assess directly and rapidly the morphology and motility of
Microbiologic tests to identify the putative pathogens have bacteria in a plaque sample. However, most of the main puta-
the potential to support the diagnosis of the various forms of tive periodontal pathogens, including Aa, Pg, If, E. corrodens
periodontal disease, to serve as indicators of disease initiation (Ee), and Eubacterium species are nonmotile and therefore this
and progression (ie, disease activity) and to determine which technique cannot identify these species. Microscopy is also
periodontal sites are at higher risk for active destruction. Mi- unable to differentiate among the various species of Irepone-
crobiologic tests can also be used to monitor periodontal ther- ma. Therefore, dark-field microscopy is not ideal for the diag-
apy directed at the suppression or eradication of periodontal nosis of periodontal diseases but could be used to educate and
pathogenic microorganisms. motivate the patients.
The utility of microbial identification as an aid in the treat-
ment planning of patients with periodontitis has been tested
lmmunodiagnostic Methods
in a limited number of studies, mostly case reports involv-
ing patients with aggressive or nonresponding periodontitis. Immunologic assays employ antibodies that recognize specific
The aim of most of these studies was to guide the selection bacterial antigens to detect target microorganisms. This reac-
of adjunctive antimicrobial therapy based on the microbial tion can be revealed using a variety of procedures, including
information. Although no conclusions could be drawn from direct- and indirect immunofluorescent (microscopy) assays
these studies, many of them reported better results following (IFAs), flow cytometry, enzyme-linked immunosorbent assays
antimicrobial therapy. (ELISA), membrane assays, and latex agglutination.
The utility of microbiologic testing as an indicator of heal- Direct IFA employs both monoclonal and polyclonal anti-
ing or disease progression has been suggested by several pro- bodies conjugated to a fluorescein marker that binds with the
spective studies where the detection or lack of detection of bacterial antigen to form a fluorescent immune complex de-
putative periodontal pathogens was significantly associated tectable under a microscope. Indirect IFA employs a secondary
with a different clinical response. In most of these studies fluorescein-conjugated antibody that reacts with the primary
the absence of these pathogens was a better indicator of peri- antigen-antibody complex. Both direct and indirect IFAs are
odontal health than their presence being a predictor of future able to identify the pathogen and quantify the percentage of
periodontal disease. Some studies showed that the presence of the pathogen directly using a plaque smear. IFA has been used
these pathogens above certain critical levels increased the risk mainly to detect Aa and Pg. In fact, IFA microscopy has the
for periodontitis recurrence. added advantage of not requiring viable bacterial cells. Com-
parative studies indicate that the sensitivity of these assays is
Bacterial Culturing very high.
Cytojluorography or flow cytometry for the rapid identifica-
Historically, culture methods have been widely used in stud- tion of oral bacteria involves labeling bacterial cells from a
ies aimed at characterizing the composition of the subgingi- patient plaque sample with both species-specific antibody
val microflora and are still considered the reference method and a second fluorescein-conjugated antibody. The suspen-
("gold standard") when determining the performance of new sion is then introduced into the flow cytometer, which sepa-
microbial diagnostic methods. Generally, plaque samples are rates the bacterial cells into an almost single-cell suspension
cultivated under anaerobic conditions and the use of selec- by means of a laminar flow through a narrow tube. The so-
tive and nonselective media, with several biochemical and phistication and cost involved in this procedure precludes
physical tests, allows the identification of different putative its wide use.
pathogens. The main advantage of this method is that the cli- ELISA is similar in principle to other radioimmunoassays
nician can obtain relative and absolute counts of the cultured but instead of the radioisotope, an enzymatically derived color
species. Moreover, it is the only in vitro method able to assess reaction is substituted as the label. The intensity of the color
antibiotic susceptibility of the microbes. depends on the concentration of the antigen and is usually
However, culture techniques have important shortcom- read photometrically for optimal quantification. ELISA has
ings. Culture methods can only grow live bacteria; there- been used primarily to detect serum antibodies to periodontal
fore, strict sampling and transport conditions are essential. pathogens although it has also been used in research studies
Moreover, some of the putative pathogens, such as Ireponema to quantify specific pathogens in subgingival samples using
species and If, are fastidious and difficult to culture. The sen- specific monoclonal antibodies.
sitivity of culture methods is rather low. The detection limits A membrane immunoassay has been adapted for chairside
for selective and non selective media vary and hence specific clinical diagnostic use (Evalusite). It involves linkage between
the antigen and a membrane-bound antibody to form an im- Chromosomal DNA is dispersed in the bacterial cell without a
munocomplex that is later revealed through a colorimetric membrane envelope. Diagnostic assays employing molecular
reaction. Evalusite has been designed to detect Aa, Pg, and Pi biology techniques require specific DNA fragments that rec-
albeit with a detection limit. ognize complementary-specific bacterial DNA sequences from
Latex agglutination is a simple immunologic assay based on target microorganisms. Development of a microbiologic diag-
the binding of protein to latex. Latex beads are coated with nostic test using this technology therefore requires the abil-
the species-specific antibody and when these beads come in ity to extract the bacterial DNA from the plaque sample and
contact with the microbial cell surface antigens or antigen amplify the specific DNA sequence of the target periodontal
extracts, crosslinking occurs; its agglutination or clumping is pathogens.
then visible, usually in 2-5 min. Due to their simplicity and
rapidity, these assays have great potential for chairside detec- Nucleic Acid Probes
tion of periodontal pathogens. However, these assays have A probe is a known nucleic-acid molecule (DNA or RNA)
only been tested for research purposes and are not clinically from a specific microorganism artificially synthesized and
available. labeled for its detection when placed with a plaque sample.
In summary, immunologic assays for oral bacteria provide DNA probes use segments of a single-stranded nucleic acid,
a quantitative or semiquantitative estimate of target microor- labeled with an enzyme or radioisotope that is able to hybrid-
ganisms. These methods have shown a higher sensitivity and ize to the complementary nucleic acid sequence and thus de-
specificity than bacterial culturing for the detection of target tect the presence of target microorganism.
microorganisms (Aa, Pg, and If). However, they require the Whole genomic probes for the detection of Aa, Pg, Pi, and
use of monoclonal antibodies to ensure high specificity and Id have been developed and tested and are the basis of com-
the detection limits are not significantly lower than with bac- mercially available diagnostic methods (eg, DMDx and Om-
terial culturing. These tests also have the advantage of not nigene). When compared to culture, van Steenberghe et al
requiring stringent sampling and transport methodology to reported a sensitivity of 96% and specificity of 86% for Aa
ensure bacterial viability However, immunologic assays are and 60% and 82 % for Pg, respectively, in pure laboratory iso-
limited to the number of antibodies tested, are not amenable lates. However, when tested in clinical specimens, both sen-
for studying antibiotic susceptibility, and lack the validity of sitivity and specificity were reduced significantly, suggesting
well-controlled clinical studies. crossreactivity with unknown bacteria in subgingival plaque
samples. To overcome this drawback, oligonucleotide probes
complementary to variable regions of the 16S rRNA bacterial
Enzymatic Methods genes have been developed for the detection of various peri-
If, Pg, Id, and Capnocytophaga species share a common en- odontal pathogens. These bacterial 16S rRNA genes contain
zymatic profile. All have a trypsinlike enzyme. The activity both regions shared by different bacteria and short stretches of
of this enzyme can be measured with the hydrolysis of the variable regions shared only by specific organisms of the same
colorless substrate N-benzoyl-DL-arginine-2-na phthylamide species or genus.
(BANA). When the hydrolysis takes place, it releases the Checkerboard DNA-DNA Hybridization Technology
chromophore naphthylamide, which turns orange-red when
a drop of fast garnet is added to the solution. Diagnostic kits Socransky et al developed this technique by for the detection
have been developed using this reaction for the identification and levels of 40 bacterial species often found in the oral cav-
of this bacterial profile in plaque isolates (Perioscan). Beck ity. The assay uses whole genomic, digoxigenin-labeled DNA
used the BANA test as a risk indicator for periodontal attach- probes, and facilitates rapid processing of large numbers of
ment loss. Collectively, results using this diagnostic method plaque samples with multiple hybridization for up to 40 oral
suggest that positive BANA findings are a good indication that species in a single test. The DNA probes used in this tech-
Id, Pg, or both are present at sampled sites. One of the poten- nology are usually adjusted to permit detection of cells of
tial difficulties of this test is that it may be positive at clinically each species. It is from this study that the classical microbial
healthy sites and whether this test can detect sites undergoing complexes were named depending on the order of their ap-
periodontal destruction has yet to be proved. Further, because pearance (purple, blue, green, yellow, orange, and red). The
it only detects a very limited number of pathogens, its nega- method requires sophisticated laboratory equipment and ex-
tive result does not rule out the presence of other important pertise, is highly specific, and thus this assay has not been
periodontal pathogens. generalized for diagnostic purposes.
It is particularly applicable, however, for epidemiologic
research and ecologic studies because it does not require vi-
Diagnostic Assays Based on Molecular able bacteria and allows for the assessment of large number of
plaque samples and multiple species.
Biology Techniques
The development of techniques in molecular biology aimed Polymerase Chain Reaction
at the detection of bacterial pathogens not only has allowed Polymerase chain reaction (PCR) has emerged as the most
the acquisition of knowledge in microbial genetics, but also powerful tool for the amplification of genes and their RNA
has set the bases for the development of improved diagnostic transcripts. This technique, developed in 1985, is the single
techniques. The principles of molecular biology techniques technique used almost universally to study DNA and RNA
reside in the analysis of DNA, RNA, and the structure or func- obtained from a variety of tissue sources. PCR allows large
tion of protein. The genetic material of a bacterium is com- quantities of DNA to be obtained in a simplified and auto-
posed of a chromosomal DNA and transferring RNA (tRNA), mated manner. It typically begins with the isolation of DNA
ribosomal RNA (rRNA), and messenger RNA (mRNA). from a fresh tissue specimen.
Since the advent of PCR technology, different microbio- disease. Most efforts to date have been based on the use of
logic tests have been developed for the detection of bacteria components of GCF and, to a lesser extent, saliva and blood.
and viruses using a variety of DNA extraction methods and Different studies have demonstrated a high correlation be-
primers. The PCR test was able to detect periodontal organ- tween clinical and histologic signs of gingivitis and increased
isms more often than cultivation. Although these microbial amounts of GCF flow. In addition, more than 60 components
tests using standard PCR are extremely specific and sensitive, of GCF have been studied and can be divided into three main
they have a major limitation of being only qualitative thereby groups: host-derived enzymes, tissue-breakdown products, and in-
reducing their application in clinical situations. flammatory mediators.
The importance of a quantitative assessment of the target For the collection of GCF, a number of approaches have
bacteria has led to the recent development of quantitative PCR been used, ranging from paper strips, microcapillary tubes
methods. The first assays used endpoint PCR. However, this and micropipettes, to microsyringes and plastic strips. The
technique obtains PCR product in the saturated phase, dis- most common method is the use of paper strips. These
regarding the early exponential phase; therefore the amount strips are placed in the gingival sulcus for a standard time
of PCR product obtained shows a weak correlation with the until the filter paper is saturated. The fluid volume collected
initial DNA quantity. To overcome this limitation, real-time on the strips can be then quantified in a number of ways.
PCR assays (RT-PCR) have been developed. With this tech- At present, the most common way is using the Periotron.
nology, using a single copy of these genes per cell, produces This electronic device measures the change in capacitance
a good correlation between the fluorescent signal measured across the wetted strip and this change is converted to a
and the number of cells that have been obtained. Although digital readout, which can be correlated to the volume of
demonstrating a high degree of sensitivity, specificity, and re- GCF Researchers have established that the Periotron 8000
producible quantification, RT-PCR requires expensive labora- achieves the easiest and quickest measurement and shows
tory equipment, which makes this method very expensive for a high correlation with other clinical gingival indices. Re-
routine diagnostic clinical microbiology. search on GCF has focused on the search for biochemical
markers involved in the progression of periodontitis, as dis-
cussed later.
Advances in Characterizing the Host Saliva is another fluid that can be easily collected and
Response may contain both locally and systemically derived markers
of periodontal disease, which can be evaluated for diagnostic
Our understanding of the initiation and progression of peri- purposes. Saliva can be collected from the parotid, subman-
odontal disease and the pathogenic processes involved has ex- dibular, and sublingual glands, or as "whole saliva" consisting
panded enormously in light of advances in clinical and basic of a mixture of oral fluids, including secretions from the ma-
science research. Diagnostic tests have been developed that jor and minor salivary glands, in addition to constituents of
add quantitative data of the inflammatory process to conven- nonsalivary origin (eg, GCF, bacteria and bacterial products,
tional clinical measures. These tests may provide information desquamated cells, and expectorated bronchial secretions).
on the destructive process itself, current activity of the disease, In addition, saliva samples can be collected with or without
rate of disease progression, patterns of destruction, extent and stimulation. The use of saliva for periodontal diagnosis has
severity of future breakdown, and likely response to therapy. been the subject of considerable research activity although no
With this information, clinicians would be able to better in- saliva-based diagnostic tests are available to be used in clinical
dividualize their therapeutic approach, thus customizing the practice. Proposed diagnostic markers in saliva include pro-
recommended treatment. teins and enzymes of host origin, phenotypic markers, host
Assessment of the host response involves the study of me- cells, hormones (cortisol), bacteria and bacterial products,
diators, by immunologic or biochemical methods, that are and volatile compounds and ions.
recognized as part of the individual's response to the peri-
odontal infection. These mediators are either specifically
identified with the infection, such as antibody to a putative Inflammatory Mediators and Products
pathogen, or represent a less specific reaction, such as the Cytokines are potent local mediators of inflammation that
local release of inflammatory mediators, host-derived en- are produced by a variety of cells. Cytokines that are pres-
zymes, or tissue breakdown products. The host response in ent in GCF that have been investigated as potential diag-
periodontal disease involves aspects of acute and chronic nostic markers include tumor necrosis factor alpha (TNFa),
inflammation, as well as humoral and cellular immune re- interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-8
sponses. Mediators representing each of these systems have (IL-8) IL-1, IL-6, and TNFa are cytokines produced by a
been evaluated using diagnostic tests in clinical periodontics variety of cells at inflamed sites. They are potent immuno-
from samples that usually involve noninvasive or minimally regulatory molecules with a variety of biologic effects, in-
invasive techniques. cluding metalloproteinase stimulation and bone resorption.
Therefore, they seem good candidates for markers of dis-
Source of Samples ease progression. Cross-sectional studies have shown good
correlation with disease status and severity but not disease
Potential sample sources include saliva, gingival crevicular progression. Prostaglandin E2 (PGE2) is a product of the
fluid (GCF), gingival crevicular cells, blood serum, blood cyclooxygenase pathway of the metabolism of arachidonic
cells, and urine. However, analysis of urine shows little prom- acid. It is a potent mediator of inflammation and induces
ise except for its use in the differential diagnosis of tooth loss bone resorption. In cases of untreated periodontitis, the con-
related to hypophosphatasia in young children, in whom the centration of PGE2 in GCF increases during active phases of
presence of phosphoethanolamine in urine is diagnostic of the periodontal destruction.
Host-Derived Enzymes GCF from diseased sites are significantly higher than from
healthy sites. Only one longitudinal study has associated
Various enzymes are released from host cells during the initia- whole-mouth ALP levels with the progression of periodontitis
tion and progression of periodontal disease. and this study has not been reproduced.
Matrix components may be dissolved either by extracellular ~G is a lysosomal enzyme found in the primary (azu-
matrix metalloproteinase-dependent or plasmin-dependent rophilic) granules of neutrophils. Cross-sectional data clearly
cleavage reactions and the subsequent larger fragments may show elevated ~G activity in sites with more severe periodon-
be disposed off through a phagocytic pathway through cleav- tal disease. Two longitudinal studies from the same research
age by lysosomal proteinases. The proteases and enzymes in- group have shown that the concentration of ~G may have a
volved in these processes may have use as diagnostic aids and predictive value in identifying patients at higher risk for losing
thus their role should be considered further. attachment. Elastase is a serine protease also stored in the pri-
The breakdown of collagen occurs during inflammation, mary granules of neutrophils. Cross-sectional studies clearly
tissue breakdown, remodeling and tissue repair, or wound indicate that GCF samples taken from sites with periodonti-
healing. This process can occur by two different pathways, an tis have significantly higher elastase activity than GCF from
intracellular or an extracellular route. Under nonpathologic healthy or gingivitis sites. A rapid chairside test kit (Perio-
conditions, phagocytosis and intracellular digestion of colla- check) has been developed to detect neutral proteases in GCF
gen fibrils is a process observed at a high level in dynamic, soft A limited number of longitudinal studies have evaluated their
connective tissues, such as gingiva and PDL. In the pathologic value as markers of periodontal disease progression. They
conditions of periodontal disease, the balance between syn- have shown some predictive value for disease progression in
thesis and degradation is disrupted and the collagen fibrils of a short-term evaluation of an untreated population, but it re-
the PDL are broken down, together with the supporting alveo- mains unclear if its validity can be applied to a treated popu-
lar bone. Different enzymes involved in both the intracellular lation in a maintenance program. Similar results have been
and the extracellular pathway of tissue destruction have been obtained studying cathepsins. These enzymes are a group of
investigated as potential diagnostic markers of periodontitis. acidic lysosomal enzymes that play an important role in in-
Among the intracellular destruction enzymes that have re- tracellular protein degradation. Although they have shown
ceived the most attention as possible markers of active peri- correlation with disease severity and significant decrease after
odontal destruction are aspartate aminotransferase (AST), periodontal therapy, they have not been evaluated longitudi-
akaline phosphatase (ALP), ~-glucuronidase (~G), and elas- nally as markers of disease progression.
tase. These enzymes are released from dead and dying cells MMPs are members of a large subfamily of zinc-dependent
of the periodontium, mostly from polymorphonuclear leu- and calcium-dependent proteolytic enzymes (proteinases)
kocytes (PMNs-neutrophils). Extracellular digestion has responsible for remodeling and degradation of extracellular
been associated with the activity of matrix metalloproteinases matrix components. The homeostasis of extracellular matrices
(MMPs). This family of enzymes is produced by inflammatory, is regulated by the release of MMPs by different cells, such as
epithelial, and connective tissue cells at affected sites. fibroblasts and macrophages, and the presence of tissue in-
AST is an enzyme released from dead cells from a vari- hibitors of MMPs (TIMPs) that are widely distributed in tis-
ety of tissues throughout the body, including the heart (after sues and fluids. Different cross-sectional studies have shown
myocardial infarction) and the liver (during hepatitis). Several that high MMP levels and low TIMP levels are associated with
studies evaluating the association between elevated AST levels periodontitis.
in GCF and periodontal disease have demonstrated a marked In chronic periodontitis, the collagen fibrils of the PDL are
elevation in AST levels in GCF samples from sites with severe degraded, together with the supporting alveolar bone. In this
gingival inflammation and sites with a recent history of pro- pathologic condition, collagen degradation is likely to occur
gressive attachment loss. A rapid chairside test kit for AST has through an MMP-mediated pathway. The concerted action
been developed (Periogard and Pocket watch). The test in- of MMP-2 (gelatinase A), MMP-9 (gelatinase B), MMP-8
volves collection of GCF with a filter paper strip, which is then (collagenase-2), MMP-13 (collagenase-3), and MMP-3
placed in tromethamine-hydrochloride buffer. A substrate re- (stromelysin-1) eventually has a significant role in the initial
action mixture containing L-aspartic and ketoglutaric acids are destruction of periodontal extracellular-matrix macromol-
added and allowed to react for 10 min. In the presence of AST, ecules. Evidently, MMP activity is associated with inflamma-
the aspartate and glutarate are catalyzed to oxalacetate and tion related to gingivitis and especially to periodontitis. The
glutamate. The addition of a dye, such as fast red, results in a impact on the ability of MMPs to differentiate gingivitis and
colored product, the intensity of which is proportional to the periodontitis diagnostically will depend on identifying the en-
AST activity in the GCF sample. A potential problem with the zyme that clearly differentiates between gingivitis and peri-
AST test is its inability to discriminate between sites with se- dontitis, as well as between stable and progressive periodontal
vere inflammation but with no attachment loss from sites that tissue-destructive conditions.
are losing attachment. It remains to be demonstrated whether A substantial body of evidence now indicates that MMPs
this test offers some advantage over existing clinical measures and TIMPs are produced locally in the periodontium and that
of disease. Using this chairside test, Kamma et al showed a MMP-8 plays an important role in periodontal tissue destruc-
high degree of correlation between the presence of putative tion. GCF from periodontitis patients contains pathologically
periodontal pathogens and positive AST scores at periodontal elevated levels of MMP-8 in catalytically active form. Associa-
sites that clinically were considered to be potentially disease- tion between increased GCF-collagenase-MMP-8 activity and
active in patients with aggressive periodontitis. progressive loss of connective tissue attachment has been dem-
ALP is an enzyme found in many cells of the periodonti- onstrated, and longitudinal studies have shown a significant
um, including osteoblasts, fibroblasts, and neutrophils. Cross- decrease in GCF-MMP-8 activity after successful treatment.
sectional studies show that concentrations of this enzyme in The reduction in GCF-MMP-8 levels after therapy indicates
TABLE 26.3 fibronectin, laminin, osteocalcin, osteopontin, bone sialopro-

tein, osteonectin, and tenascin). All these matrix components
COMMON COMMERCIAL DIAGNOSTIC AIDS are theoretically detectable and potentially informative in
AND THEIR USES terms of their clinical diagnostic utility.
Commercial Name Purpose
Analysis of GCF obtained from sites with periodontitis
clearly shows elevated levels of hydroxyproline from collagen
Peria Temp Gingival temperature breakdown and glycosaminoglycans from matrix degradation.
Periotest Tooth and implant mobility Other bone and connective tissue proteins, including osteo-
Osstell apparatus Implant mobility calcin and type I collagen peptides, have been correlated with
Perioscopy, DetecTar, and Detection of calculus
the progression of alveolar bone loss induced in beagle dogs.
Diagnodent,
Keylaser3 Combined detection and removal of
Both markers gave high positive predictive values and now
calculus need to be extended to longitudinal studies in humans.
Perioscan Detection of BANA organisms and List of some of the common advanced diagnostic aids are
calculus summarized in Table 26.3.
Halimeter, OralChroma, Halitosis
and Diamond Probe/
Peria 2000 Conclusion
Digora Digital radiography
Newtom QR-DVT CBCT Although there are many potential markers for periodontal
Evalusite Detection of Aa, Pg, and Pi disease activity and progression, numerous factors still ham-
Ultradent Ultrasonic imaging per their use as diagnostic tests of proven utility. There is still
Periocheck Neutral proteinase a lack of a proven "gold standard" of disease progression, and
PST Genetic susceptibility thus the correlation of these potential markers with proven
Prognostik and Biolise Elastase clinical attachment loss may be a potential confounder in any
Perioguard and Pocket AST proposed test. After all these years of intensive research, we
Watch
still lack a proven diagnostic test that demonstrates a high
TOPAS Detection of toxins from GCF
TOPAS Bacterial toxins and proteases
predictive value for disease progression, has a proven impact
MMP-dipstick test MMP-8 on disease incidence and prevalence, and is simple, safe, and
Evalusite ELISA for Aa, Pg, and Pi cost-effective.
MicroDent Test PCR for Pg, Aa, If, Id, and Pi.
MyPerioPath RT-PCR SUGGESTED READINGS
PST and MyPerio!D Genetic susceptibility test
Abrams K, Caton], Polson AM: Histologic comparisons of interproximal gin-
ParoCheck and Phylochip Oligonucleotide-microarray
gival tissues related to the presence or absence of bleeding, J Periodontal
technology 55:629, 1984.
Omnigene Nucleic-acid probe Armitage GC: Periodontal diseases: diagnosis, Ann Periodontal 1:37, 1996.
Badersten A, Nilveus R, Egelberg J: Reproducibility of probing attachment
levels measurements,] Clin Periodontol 11:475, 1984.
that MMP-8 is one molecule with potential diagnostic use as Badersten A, Nilveus R, EgelbergJ: Effect of nonsurgical therapy Vil. Bleed-
an indicator of current disease status and possibly as a predic- ing, suppuration and probing depth in sites with probing attachment loss,
tor of future disease. To test this hypothesis, a chairside-test J Clin Peliodontol 12:432, 1985.
Baderstcn A, Nilveus R, Egelberg J: Scores of plaque, bleeding, suppuration
stick for detection of MMP-8 in GCF has recently been devel- and probing depth to predict probing attachment loss. Five years of obser-
oped. Studies of periodontitis patients have shown that this vation following nonsurgical periodontal therapy, J Clin Periodontal 7: 102,
diagnostic test is able to differentiate between gingivitis and 1990.
periodontitis and significant reductions of this indicator have Egermark-Erikson I, Carlsson GE, Ingerva\1 B: Prevalence of mandibular dys-
function and orofacial parafunction in 7-, 11-, and 15-year old Swedish
been demonstrated in response to treatment (scaling and root children, Eur J Orthod 13:163, 1981.
planing) of periodontitis. Greenberg J, Laster L, Listgarten MA: Transgingival probing as a potential
estimator of alveolar bone level, J Periodontal 4 7:514, 1976.
Greenstein G: The role of bleeding upon probing in the diagnosis of peri-
Tissue-Breakdown Products odontal disease. A literature review,] Periodontal 55:684, 1984.
Misch KA, Yi ES, Sarment DP: Accuracy of conebeam computed tomography
One of the maJor features of periodontitis is the destruction for periodontal defect measurements,] Periodontol 77:1261-1266, 2006.
of collagen and extracellular matrices. The connective tissues Tetradis S, Anstey P, Graff-Radford S: Cone beam computed tomography in
of the periodontium are composed of fibrous elements, in- the diagnosis of dental disease, J Calif Dent Assoc 38:27-32, 2010.
cluding proteins, such as collagen, elastin, and nonfibrous Tyndall A, Rathore S: Cone-beam CT diagnostic applications: caries, peri-
odontal bone assessment, and endodontic applications, Dent Clin North Am
components, including a variety of glycoproteins (laminin, 52:825, 2008.
fibronectin, and proteoglycans), as well as minerals, lipids, Vandenberghe B, Jacobs R, Bosmans H: Modern dental imaging: a review of
and water- and tissue-bound growth factors. The extracellular the current technology and clinical applications in dental practice, Eur
matrix of the periodontium is composed of a diverse number Radio/ 20:2637-2655, 2010.
van der Stele PF: Filmless imaging: the uses of digital radiography in dental
of macromolecules; the predominant one is collagen, and the practice,] Am Dent Assoc 136:1379-1387, 2005.
other components include proteoglycan (versican, decorin, White SC, Pharoah MJ: Oral radiology: principles and interpretation, ed 6,
biglycan, and syndecan) and noncollagen proteins (elastin, St. Louis, 2009, Mosby, Elsevier.
27
Clinical Risk Assessment
KF Novak • MJ Novak • CD Dwarakanath
Chapter Outline
Definitions Risk Markers/Predictors for Periodontal
Risk Factors for Periodontal Disease Disease
Risk Determinants/Background Clinical Risk Assessment for Periodontal
Characteristics for Periodontal Disease Disease
Risk Indicators for Periodontal Disease Conclusions
Definitions smokers, previous smokers, and nonsmokers have shown that

Risk assessment is defined by numerous components. Risk is smoking has a negative impact on the response to therapy.
the probability that an individual will develop a specific dis- However, former smokers respond similarly to nonsmokers.
ease in a given period. The risk of developing the disease will These studies demonstrate the therapeutic impact of interven-
vary from individual to individual. tion strategies on patients who smoke.
Rish Jactors may be environmental, behavioral, or biologic
factors that, when present, increase the likelihood that an in- Diabetes
dividual will develop the disease. Risk factors are identified
through longitudinal studies of patients with the disease of Diabetes is a clear risk factor for periodontitis. Epidemiologic
interest. Exposure to a risk factor or factors may occur at a data demonstrate that the prevalence and severity of peri-
single point in time; over multiple, separate points in time; odontitis are significantly higher in patients with type 1 or
or continuously. However, to be identified as a risk factor, the type 2 diabetes mellitus than in those without diabetes, and
exposure must occur before disease onset. Interventions often that the level of diabetic control is an important variable in
can be identified and when implemented, can help modify this relationship.
risk factors.
The term risk determinant/background characteristic, which Pathogenic Bacteria and Microbial
is sometimes substituted for the term risk factor, should be Tooth Deposits
reserved for those risk factors that cannot be modified.
Rish indicators are probable or putative risk factors that have It is well documented that accumulation of bacterial plaque
been identified in cross-sectional studies but not confirmed at the gingival margin results in the development of gingivitis
through longitudinal studies. and that the gingivitis can be reversed with the implementa-
Rish predictors/markers, although associated with increased tion of oral hygiene measures. These studies demonstrate a
risk for disease, do not cause the disease. causal relationship between accumulation of bacterial plaque
These factors are also identified in cross-sectional and lon- and gingival inflammation. However, a causal relationship
gitudinal studies. between plaque accumulation and periodontitis has been more
Box 27.1 lists elements of these categories of risk for peri- difficult to establish. Often, patients with severe loss of attach-
odontal disease. ment have minimal levels of bacterial plaque on the affected
teeth, indicating that the quantity of plaque is not of major im-
portance in the disease process. However, although quantity
Risk Factors for Periodontal Disease may not indicate risk, there is evidence that the composition,
or quality, of the complex plaque biofilm is of importance.
Tobacco Smoking
In terms of quality of plaque, three specific bacteria have
Tobacco smoking is a well-established risk factor for peri- been identified as etiologic agents for periodontitis: Aggrega-
odontitis (Box 27.1). A direct relationship exists between tibacter actinomycetemcomitans (formerly Actinobacillus acti-
smoking and the prevalence of periodontal disease. This asso- nomycetemcomitans), Porphyromonas gingivalis, and Tannerella
ciation is independent of other factors such as oral hygiene or forsythia (formerly Bacteroides Jorsythus). Porphyromonas gingi-
age. Studies comparing the response to periodontal therapy in valis and I forsythia are often found in chronic periodontitis,
309
individuals receiving routine dental care does not result in sig-

nificant loss of attachment, the presence of calculus in other
groups of patients, such as those not receiving regular care
RISK FACTORS and patients with poorly controlled diabetes, can have a nega-
Tobacco smoking tive impact on periodontal health.
Diabetes
Pathogenic bacteria
Microbial tooth deposits Risk Determinants/Background
RISK DETERMINANTS/BACKGROUND Characteristics for Periodontal
CHARACTERISTICS
Genetic factors
Disease
Age
Genetic Factors
Gender
Socioeconomic status Evidence indicates that genetic differences between indi-
Stress viduals may explain why some patients develop periodontal
RISK INDICATORS disease and others do not. Studies conducted in twins have
HIV/AIDS shown that genetic factors influence clinical measures of gin-
Osteoporosis givitis, probing pocket depth, attachment loss, and interproxi-
Infrequent dental visits mal bone height. The familial aggregation seen in localized
RISK MARKERS/PREDICTORS
and generalized aggressive periodontitis also is indicative of
genetic involvement in these diseases.
Previous history of periodontal disease
Bleeding on probing
Kornman et al demonstrated that alterations in specific
HIV, human immunodeficiency virus; AIDS, acquired genes encoding the inflammatory cytokines interleukin-la
immunodeficiency syndrome. (IL-la) and interleukin-Iji (IL-1~) were associated with
severe chronic periodontitis in nonsmoking subjects. How-
ever, results of other studies have shown limited association
between these altered genes and the presence of periodon-
whereas A actinomycetemcomitans is often associated with titis. Overall, it appears that changes in the IL-1 genes may
aggressive periodontitis. Cross-sectional and longitudinal be only one of several genetic changes involved in the risk
studies support the delineation of these three bacteria as risk for chronic periodontitis. Therefore, although the alteration
factors for periodontal disease. Additional evidence that these in the IL-1 genes may be a valid marker for periodontitis in
organisms are causal agents includes the following: defined populations, its usefulness as a genetic marker in the
1. Their elimination or suppression impacts the success of general population may be limited.
therapy. Immunologic alterations, such as neutrophil abnormalities,
2. There is a host response to these pathogens. monocytic hyperresponsiveness to lipopolysaccharide stimu-
3. Virulence factors are associated with these pathogens. lation in patients with localized aggressive periodontitis, and
4. Inoculation of these bacteria into animal models induces alterations in the monocyte/macrophage receptors for the
periodontal disease. Fe portion of antibody, also appear to be under genetic con-
trol. In addition, genetics play a role in regulating the titer
Although not completely supported by these criteria for of the protective immunoglobulin G2 (IgG2) antibody re-
causation, moderate evidence also suggests that Campylo- sponse to A actinomycetemcomitans in patients with aggressive
bacter rectus, Eubacterium nodatum, Fusobacterium nucleatum, periodontitis.
Prevotella intermedia, Prevotella nigrescens, Peptostreptococcus
micros, Streptococcus intermedius, and Treponema denticola are
etiologic factors in periodontitis.
Age
Therefore the quantity of plaque present may not be as im- Both the prevalence and severity of periodontal disease in-
portant as the quality of the plaque in determining risk for crease with age. It is possible that degenerative changes related
periodontitis. to aging may increase susceptibility to periodontitis. However,
Anatomic factors, such as furcations, root concavities, de- it also is possible that the attachment loss and bone loss seen
velopmental grooves, cervical enamel projections, enamel in older individuals are the results of prolonged exposure to
pearls, and bifurcation ridges, may predispose the periodon- other risk factors over a person's life, creating a cumulative
tium to disease as a result of their potential to harbor bacte- effect over time. In support of this, studies have shown mini-
rial plaque and present a challenge to the clinician during mal loss of attachment in aging subjects enrolled in preventive
instrumentation. Similarly, the presence of subgingival and programs throughout their lives. Therefore it is suggested that
overhanging margins can result in increased plaque accu- periodontal disease is not an inevitable consequence of the
mulation, increased inflammation, and increased bone loss. aging process and that aging alone does not increase disease
Although not clearly defined as risk factors for periodontitis, susceptibility. However, it remains to be determined whether
anatomic factors and restorative factors that influence plaque changes related to the aging process, such as intake of medi-
accumulation may play a role in disease susceptibility for spe- cations, decreased immune function, and altered nutritional
cific teeth. status, interact with other well-defined risk factors to increase
The presence of calculus, which serves as a reservoir for susceptibility to periodontitis.
bacterial plaque, has been suggested as a risk factor for peri- Evidence of loss of attachment may have more conse-
odontitis. Although the presence of some calculus in healthy quences in younger patients. The younger the patient, the
longer the patient has for exposure to causative factors. In ad- inclusion of patients with AIDS (vs patients who were exclu-
dition, aggressive periodontitis in young individuals often is sively HIV seropositive) in some studies.
associated with an unmodifiable risk factor such as a genetic Conflicting results also exist in studies examining the level
predisposition to disease. Therefore, young individuals with of immunosuppression and severity of periodontal destruc-
periodontal disease may be at greater risk for continued dis- tion. Some studies support that as the degree of immunosup-
ease as they age. pression increases in adults with AIDS, periodontal pocket
formation and loss of clinical attachment also increase. Re-
sults of other studies have found no relationship between
Gender periodontal diseases and HIV/AIDS status. Evidence also sug-
Gender plays a role in periodontal disease. Surveys con- gests that AIDS-affected individuals who practice good pre-
ducted in the United States since 1960 demonstrate that ventive oral health measures, including effective home care
men have more loss of attachment than women. In addition, and seeking appropriate professional therapy, can maintain
men have poorer oral hygiene than women, as evidenced by periodontal health. Therefore, although it seems reasonable
higher levels of plaque and calculus. Therefore, gender dif- to hypothesize that HIV infection and immunosuppression
ferences in prevalence and severity of periodontitis appear are risk factors for periodontal disease, the evidence is not
to be related to preventive practices rather than any genetic conclusive.
factor.
Osteoporosis
Socioeconomic Status Osteoporosis has been suggested as another risk factor for
Gingivitis and poor oral hygiene can be related to lower socio- periodontitis. Although studies in animal models indicate that
economic status (SES). This can most likely be attributed to osteoporosis does not initiate periodontitis, evidence indicates
decreased dental awareness and decreased frequency of dental that the reduced bone mass seen in osteoporosis may aggra-
visits compared with more educated individuals with higher vate periodontal disease progression. However, reports in
SES. After adjusting for other risk factors, such as smoking humans are conflicting. In a study of 12 women with osteopo-
and poor oral hygiene, lower SES alone does not result in in- rosis and 14 healthy women, von Wowern et al reported that
creased risk for periodontitis. the women with osteoporosis had greater loss of attachment
than the control subjects. In contrast, Kribbs examined pocket
depth, bleeding on probing, and gingival recession in women
Stress with and without osteoporosis. Although the two groups had
The incidence of necrotizing ulcerative gingivitis increases significant differences in bone mass, no differences in peri-
during periods of emotional and physiologic stress, suggesting odontal status were noted. However, it appears that a link may
a link between the two. Emotional stress may interfere with exist between osteoporosis and periodontitis, and additional
normal immune function and may result in increased levels studies may need to be conducted to determine whether os-
of circulating hormones, which can affect the periodontium. teoporosis is a true risk factor for periodontal disease.
Stressful life events, such as bereavement and divorce, appear
to lead to a greater prevalence of periodontal disease, and an Infrequent Dental Visits
apparent association exists between psychosocial factors and
risk behaviors such as smoking, poor oral hygiene, and chron- Identifying failure to visit the dentist regularly as a risk factor
ic periodontitis. Adult patients with periodontitis who are refor periodontitis is controversial. One study demonstrated an
sistant to therapy are more stressed than those who respond to increased risk for severe periodontitis in patients who had not
therapy. Individuals with financial strain, distress, depression, visited the dentist for 3 or more years, whereas another dem-
or inadequate coping mechanisms have more severe loss of onstrated that there was no more loss of attachment or bone
attachment. Although epidemiologic data on the relationship loss in individuals who did not seek dental care compared
between stress and periodontal disease are limited, stress may with those who did over a 6-year period. However, differences
be a putative risk factor for periodontitis. in the ages of the subjects in these two studies may explain
the different results. Additional longitudinal and intervention
studies are necessary to determine whether infrequency of
Risk Indicators for Periodontal dental visits is a risk factor for periodontal disease.
Disease
HIV/AIDS Risk Markers/Predictors for
It has been hypothesized that the immune dysfunction associ- Periodontal Disease
ated with HIV infection and AIDS increases susceptibility to
Previous History of Periodontal Disease
periodontal disease. Early reports on the periodontal status
of patients with AIDS or individuals who are HIV seroposi- A history of the previous periodontal disease is a good
tive revealed that these patients often had severe periodontal clinical predictor of risk for future disease. Patients with
destruction characteristic of necrotizing ulcerative periodonti- the most severe existing loss of attachment are at the great-
tis. More recent reports, however, have failed to demonstrate est risk for future loss of attachment. Conversely, patients
significant differences in the periodontal status of individu- currently free of periodontitis have a decreased risk for de-
als with HIV infection and healthy controls. The apparent veloping loss of attachment compared with those who cur-
discrepancy in these reports may have been caused by the rently have periodontitis.
Bleeding on Probing predisposition for aggressive periodontitis), a previous his-

tory of periodontal disease, and information concerning the
Bleeding on probing is the best clinical indicator of gingival frequency of oral health care in the past. Important elements
inflammation. Although this indicator alone does not serve identified during the clinical examination can include the
as a predictor for loss of attachment, bleeding on probing location and extent of bacterial plaque accumulation, pres-
coupled with increasing pocket depth may serve as an excel- ence of plaque-retentive factors (eg, overhanging restorations,
lent predictor for future loss of attachment. Lack of bleeding subgingival margins), presence of anatomic plaque-retentive
on probing does appear to serve as an excellent indicator of areas (eg, grooves, furcation involvements), presence of cal-
periodontal health. culus, extent of attachment loss, and presence or absence of
bleeding on probing.
Clinical Risk Assessment for Once the social, demographic, medical history, dental his-
tory, and clinical presentation data are collected, they must
Periodontal Disease be analyzed to identify patients at risk for developing peri-
Information concerning individual risk for developing the odontal disease. This analysis can be accomplished by the
periodontal disease is obtained through careful evaluation of healthcare provider and/or through the use of a computer-
the patient's demographic data, medical history, dental history, based risk assessment tool. One example of this type of tool
and clinical examination (Box 27.2). The elements that con- is the Periodontal Assessment Tool (PAT), which is one com-
tribute to increased risk can be identified through the collec- ponent of the Pre Viser Oral Health Information Suite (OHIS).
tion of demographic data, including the patient's age, gender, The PAT utilizes input from 23 items that are part of a routine
and SES. The medical history may reveal elements such as a periodontal examination to generate both a quantification of
history of diabetes, smoking, HIV/AIDS, or osteoporosis, as current disease and a risk score for future disease. The score,
well as the perceived level of stress. The dental history can re- which is based on an individual patient's set of risk factors
veal a family history of early tooth loss (suggestive of a genetic and history, ranges from 1 (lowest risk) to 5 (highest risk). It
has been proposed that utilizing this tool will provide a more
objective, quantitative way to assess risk for periodontitis
than clinical opinion. Ultimately, a thorough risk assessment
should improve clinical decision making, as well as patient
outcomes.
DEMOGRAPHIC DATA Once an at-risk patient is identified and a diagnosis is
Age made, the treatment plan may be modified accordingly. For
Duration of exposure to risk elements example, patients with a history of cigarette smoking should
Postmenopausal women be informed of the relationship between smoking and peri-
Evidence of aggressive disease odontitis. They also should be informed of the impact of
Male gender smoking on their prognosis and the likelihood of success of
Preventive practices their periodontal therapy if they continue to smoke. Part of
Frequency of care
their recommended treatment plan for initial therapy may
Socioeconomic status
Dental awareness include referral to a smoking cessation program or imple-
Frequency of care mentation of self-administered smoking cessation aids. As
another example, a patient diagnosed with severe, chronic
MEDICAL HISTORY
periodontitis may be encouraged to be tested for the IL-1-
Diabetes positive genotype. If positive, the patient's treatment may in-
Tobacco smoking volve the administration of systemic antimicrobial agents and
HIV/AIDS
host modifiers that would not be used in a patient without
Osteoporosis
Stress this genetic marker. If alterations in the host response are
Dental History identified, the prognosis and treatment plan may be modi-
Family history of early tooth loss fied. Previously identified risk elements also may need to be
Genetic predisposition to aggressive disease reassessed at the reevaluation stage of treatment. This is espe-
Previous history of periodontal disease cially important in patients who do not respond favorably to
Frequency of dental care periodontal therapy.
Clinical examination
Plaque accumulation
Microbial sampling for putative periodontal pathogens Conclusions
Calculus
Bleeding on probing Risk assessment involves identifying elements that either
Extent of loss of attachment may predispose a patient to developing periodontal disease
Aggressive forms of disease or may influence the progression of disease that already
Tooth examination exists. In either case, these patients may require modifica-
Plaque retentive areas tion of their prognosis and treatment plan. In addition to
Anatomic factors an evaluation of the factors contributing to their risk, these
Restorative factors patients should be educated concerning their risk, and
HIV, human immunodeficiency virus; AIDS, acquired
when appropriate, suitable intervention strategies should
immunodeficiency syndrome.
be implemented.
SUGGESTED READINGS Michalowicz BS, Diehl SR, Gunsolley JC, et al: Evidence of a substantial ge-
netic basis for risk of adult periodontitis, J Periodontal 71(11): 1699-1707,
Genco RJ, Ho AW, Grossi SG, et al: Relationship of stress, distress and inad-
2000.
equate coping behaviors to periodontal disease, J Periodontal 70(7):711-
Papapanou PN, lindhe J, Sterrett JD, et al: Considerations on the contri-
723, 1999.
bution of ageing to loss of periodontal tissue support, J Clin Periodontal
Haber J, Wattles J, Crowley M, et al: Evidence for cigarette smoking as a major
18(8) 611-615, 1991.
risk factor for periodontitis,J Periodontol 64(1):16-23, 1993.
Stanford TW, Rees TD: Acquired immune suppression and other risk factors/
Ismail Al, Burt BA, Eklund SA: Epidemiologic patterns of smoking and peri-
indicators for periodontal disease progression, Periodontal 2000 32: 118-
odontal disease in the United States, J Am Dent Assoc 106(5):617-621,
135, 2003.
1983.
Loe H, Thcilade E, Jensen SB: Experimental gingivitis in man, J Periodontal
36:177-187, 1965.
28
Determination of Prognosis
KF Novak • HH Takei • J Do • CD Dwarakanath
Chapter Outline
Definitions Reevaluation of Prognosis After Phase I
Types of Prognosis Therapy
Factors in Determination of Overall
Prognosis
Definitions 2. Individual tooth prognosis: The individual tooth prognosis is

determined after the overall prognosis and is affected by
Prognosis is a forecast. It is a prediction of the probable course, it. For example, in a patient with a poor overall prognosis,
duration, and outcome of a disease and the likelihood of its the dentist in all likelihood would not attempt to retain a
response to treatment, based on a general knowledge of the tooth that has a questionable prognosis because of local
pathogenesis of the disease and the presence of risk factors. It is conditions (see Box 28.1). Many of the factors listed un-
established after the diagnosis is made and before the treatment der local, prosthetic, and restorative factors have a direct
plan is established. The prognosis is based on specific infor- effect on the prognosis of individual teeth, in addition to
mation about the disease and the manner in which it can be any overall systemic or environmental factors that may be
treated, but it can also be influenced by the clinician's previous present.
experience with treatment outcomes (successes and failures) as
they relate to the particular case. It is important to note that Prognosis is also classified as
determination of prognosis is a dynamic process. As such, the 1. Therapeutic prognosis: It deals with the response of the
prognosis initially assigned should be reevaluated after comple- tissues to treatment and successful arrest of disease pro-
tion of all phases of therapy, including periodontal maintenance. cess.
Prognosis is often confused with the term risk. Risk gener- 2. Prosthetic prognosis: It indicates the ability of the remaining
ally deals with the likelihood that an individual will develop teeth to support a prosthesis.
a disease in a specified period (see Chapter 6). Rish ]actors are
those characteristics of an individual that put the person at Further, prognosis can be divided as
increased risk for developing a disease. In contrast, prognosis is 1. Short-term prognosis: where estimation is made for the next
the prediction of the course or outcome of a disease. Prognostic 3-5 years.
factors are characteristics that predict the outcome of disease 2. Long-term prognosis: where the teeth are expected to remain
once the disease is present. In some cases, risk factors and in health and function beyond 5 years.
prognostic factors are the same. For example, patients with
diabetes or patients who smoke are more at risk for acquiring
periodontal disease, and once they have it, they generally have Types of Prognosis
a worse prognosis. Although some factors may be more important than others
Determination of prognosis is mostly based upon the past when assigning a prognosis, consideration of each factor may
events and may not depict accurately what is going to happen be beneficial to the clinician.
in the future as the actual outcome may vary. The reader can Historically, prognosis classification schemes have been
refer to excellent reports of McGuire and Nunn in their study designed based on studies evaluating tooth mortality. One
"Prognosis versus Actual outcome." scheme follows the following classification:
For descriptive purposes and better understanding, prog-
nosis is classified as follows: Good prognosis: Control of etiologic factors and adequate peri-
odontal support ensure the tooth will be easy to maintain
1. Overall prognosis: which is concerned with the patient and by the patient and clinician.
dentition as a whole and determined by several factors in- Fair prognosis: Approximately 25% attachment loss and/or
cluding the type of disease, age of the patient, systemic Class I furcation involvement (location and depth allow
background, etc. proper maintenance with good patient compliance).
315
Consiaer Wlien Determining a Prognosis

OVERALL CLINICAL FACTORS ANATOMIC FACTORS
Patient age Short, tapered roots
Disease severity Cervical enamel projections
Plaque control Enamel pearls
Patient compliance Bifurcation ridges
Root concavities
Developmental grooves
SYSTEMIC AND ENVIRONMENTAL FACTORS
Root proximity
Smoking Furcation involvement
Systemic disease or condition Tooth mobility
Genetic factors
Stress PROSTHETIC AND RESTORATIVE FACTORS
Abutment selection
LOCAL FACTORS Caries
Plaque and calculus Nonvital teeth
Subgingival restorations Root resorption
Poor prognosis: 50% attachment loss, Class II furcation in- evaluated. The provisional prognosis allows the clinician to initi-
volvement (location and depth make maintenance possible ate treatment of teeth that have a doubtful outlook in the hope
but difficult) that a favorable response may tip the balance and allow the teeth
Questionable prognosis: > 50% attachment loss, poor crown- to be retained. The reevaluation phase in the treatment sequence
to-root ratio, poor root form, Class II furcations (location allows the clinician to examine the tissue response to scaling,
and depth make access difficult) or Class llI furcation in- oral hygiene, and root planing, as well as to the possible use of
volvements; > 2+ mobility; root proximity. chemotherapeutic agents and to decide whether the patient re-
Hopeless prognosis: Inadequate attachment to maintain health, quires further surgical treatment. The patient's compliance with
comfort, and function. the proposed treatment plan also can be determined.
It should be recognized that good, fair, and hopeless prog-
noses in this classification system could be established with a
reasonable degree of accuracy. However, poor and question- Overall Versus Individual Tooth Prognosis
able prognoses are likely to change to other categories because As described earlier the overall prognosis is concerned with the
they depend on a large number of factors that can interact in dentition as a whole. Factors that may influence the overall
unpredictable number of ways. prognosis include patient age; current severity of disease; sys-
In contrast to schemes based on tooth mortality, Kwok and temic factors; smoking; the presence of plaque, calculus, and
Caton have proposed a scheme based on "the probability of other local factors; patient compliance; and prosthetic possi-
obtaining stability of the periodontal supporting apparatus." bilities. It should answer the following questions:
This scheme is based on the probability of disease progres-
sion as related to local and systemic factors (see Box 28.1). • Should treatment be undertaken?
Although some of these factors may affect disease progression • Is treatment likely to succeed?
more than others, consideration of each factor is important in • When prosthetic replacements are needed, are the remain-
assigning a prognosis. It is as follows: ing teeth able to support the added burden of the prosthesis?
Favorable prognosis: Comprehensive periodontal treatment
and maintenance will stabilize the status of the tooth. Fu-
ture loss of periodontal support is unlikely.
Factors in Determination of Overall
Questionable prognosis: Local and/or systemic factors influenc- Prognosis
ing the periodontal status of the tooth may or may not be
controllable. If controlled, the periodontal status can be sta- Type of Disease
bilized with comprehensive periodontal treatment. If not, Prognosis for Patients With Gingival Disease
future periodontal breakdown may occur.
Dental Plaque-Induced Gingival Diseases
Unfavorable prognosis: Local and/or systemic factors influenc-
Gingivitis Associated With Dental Plaque Only. Plaque-
ing the periodontal status cannot be controlled. Compre-
induced gingivitis is a reversible disease that occurs when
hensive periodontal treatment and maintenance are unlike-
bacterial plaque accumulates at the gingival margin. This dis-
ly to prevent future periodontal breakdown.
ease can occur on a periodontium that has experienced no
Hopeless prognosis: The tooth must be extracted.
attachment loss or on a periodontium with nonprogressing
Since periodontal stability is assessed on a regular basis us- attachment loss. In either case, the prognosis for patients with
ing clinical measures, it may be more useful in making treat- gingivitis associated with dental plaque only is good, provided
ment decisions and prognosis predictions than trying to deter- all local irritants are eliminated.
mine the likelihood of the tooth being lost. Plaque-Induced Gingival Diseases Modified by Systemic
In many of these cases, it may be advisable to establish a Factors. The inflammatory response to bacterial plaque at the
provisional prognosis until phase I therapy is completed and gingival margin can be influenced by systemic factors, such
as endocrine-related changes associated with puberty, men- generally good, provided the inflammation can be controlled
struation, pregnancy, and diabetes, and the presence of blood through good oral hygiene and the removal of local plaque-
dyscrasias. In many cases, the frank signs of gingival inflam- retentive factors (Fig. 28.1). In patients with more severe dis-
mation that occur in these patients are seen in the presence ease, as evidenced by furcation involvement and increasing
of relatively small amounts of bacterial plaque. Therefore the clinical mobility, or in patients who are noncompliant with
long-term prognosis for these patients depends not only on oral hygiene practices, the prognosis may be downgraded to
the control of bacterial plaque but also on control or correc- fair to poor.
tion of the systemic factor(s).
Plaque-Induced Gingival Diseases Modified by Medica- Aggressive Periodontitis
tions. Gingival diseases associated with medications include Aggressive periodontitis can be present in a localized or a
drug-influenced gingival enlargement, often seen with phenyto- generalized form. Two common features of both forms are
in, cyclosporine, and nifedipine and in oral contraceptive-as- (1) rapid attachment loss and bone destruction in an other-
sociated gingivitis. In drug-influenced gingival enlargement, wise clinically healthy patient and (2) a familial aggregation.
reductions in dental plaque can limit the severity of the lesions. These patients often present with limited microbial deposits
However, plaque control alone does not prevent development that seem inconsistent with the severity of tissue destruction.
of the lesions, and surgical intervention is usually necessary However, the deposits that are present often have elevated
to correct the alterations in gingival contour. Continued use levels of Aggregatibacter actinomycetemcomitans or Porphyromo-
of the drug usually results in recurrence of the enlargement, nas gingivalis. These patients may also present with phagocyte
even after surgical intervention (see Chapter 16). Therefore the abnormalities and a hyperresponsive monocyte/macrophage
long-term prognosis depends on whether the patient's systemic phenotype. These clinical, microbiologic, and immunologic
problem can be treated with an alternative medication that features would suggest that patients diagnosed with aggressive
does not have gingival enlargement as a side effect. periodontitis would have a poor prognosis.
In oral contraceptive-associated gingivitis, frank signs of However, the clinician should consider additional specific
gingival inflammation can be seen in the presence of relatively features of the localized form of disease when determining the
little plaque. Therefore, as seen in plaque-induced gingival prognosis (Fig. 28.2). Localized aggressive periodontitis usu-
diseases modified by systemic factors, the long-term progno- ally occurs around the age of puberty and is localized to first
sis in these patients depends on not only the control of bacte- molars and incisors. The patient often exhibits a strong serum
rial plaque but also on the likelihood of continued use of the antibody response to the infecting agents, which may contrib-
oral contraceptive. ute to localization of the lesions. When diagnosed early, these
Gingival Diseases Modified by Malnutrition. Although cases can be treated conservatively with oral hygiene instruc-
malnutrition has been suspected to play a role in the devel- tion and systemic antibiotic therapy, resulting in an excellent
opment of gingival diseases, most clinical studies have not prognosis. When more advanced disease occurs, the progno-
shown a relationship between the two. One possible exception sis can still be good if the lesions are treated with debride-
is severe vitamin C deficiency In early experimental vitamin ment, local and systemic antibiotics, and regenerative therapy
C deficiency, gingival inflammation and bleeding on probing In contrast, although patients with generalized aggressive
were independent of plaque levels present. The prognosis in periodontitis also are young patients (usually under age 30),
these patients may depend on the severity and duration of the they present with generalized interproximal attachment loss
deficiency and on the likelihood of reversing the deficiency and a poor antibody response to infecting agents. Secondary
through dietary supplementation. contributing factors, such as cigarette smoking, are often pres-
Nonplaque-Induced Gingival Lesions. Nonplaque- ent. These factors, coupled with the alterations in host defense
induced gingivitis can be seen in patients with a variety of seen in many of these patients, may result in a case that does
bacterial, fungal, and viral infections. Since the gingivitis in not respond well to conventional periodontal therapy (scal-
these patients is not usually attributed to plaque accumula- ing with root planing, oral hygiene instruction, and surgical
tion, prognosis depends on elimination of the source of the in- intervention). Therefore these patients often have a fair, poor,
fectious agent. Dermatologic disorders, such as lichen planus, or questionable prognosis, and the use of systemic antibiotics
pemphigoid, pemphigus vulgaris, erythema multiforrne, and should be considered to help control the disease (see Chap-
lupus erythematosus, can also manifest in the oral cavity as ter 40)
desquamative gingivitis (see Chapter 18). Prognosis for these
patients is linked to management of the associated derrnato- Periodontitis as Manifestation of Systemic Diseases
logic disorder. Finally, allergic, toxic, and foreign body reac- Periodontitis as a manifestation of systemic diseases can be
tions, as well as mechanical and thermal trauma, can result divided into the following two categories:
in gingival lesions. Prognosis for these patients depends on
1. Periodontitis associated with hematologic disorders such
elimination of the causative agent.
as leukemia and acquired neutropenias.
2. Periodontitis associated with genetic disorders such as fa-
milial and cyclic neutropenia, Down syndrome, Papillon-
Prognosis for Patients With Periodontitis Lefevre syndrome, and hypophosphatasia.
Chronic Periodontitis Although the primary etiologic factor in periodontal
Chronic periodontitis is a slowly progressive disease associ- diseases is bacterial plaque, systemic diseases that alter the
ated with well-known local environmental factors. It can be ability of the host to respond to the microbial challenge
present in a localized or generalized form. In cases in which presented may affect the progression of disease and therefore
the clinical attachment loss and bone loss are not very ad- the prognosis for the case. For example, decreased numbers
vanced (slight-to-moderate periodontitis), the prognosis is of circulating neutrophils (as in acquired neutropenias) may
FIGURE 28.1 Chronic periodontitis in systemically healthy, nonsmoking 60-year-old male; overall prognosis is good. A, Gingival inflammation
and fair oral hygiene. B, Although local factors are present, the patient presents with adequate remaining bone support and a good prognosis, provided
local factors can be control led.
contribute to widespread destruction of the periodontium. predisposing factor is bacterial plaque. However, this disease
Unless the neutropenia can be corrected, these patients pres- is usually complicated by the presence of secondary factors
ent with a fair-to-poor prognosis. Similarly, genetic disorders such as acute psychologic stress, tobacco smoking, and poor
that alter the way the host responds to bacterial plaque [as nutrition, all of which can contribute to immunosuppres-
in leukocyte adhesion deficiency (LAD) syndrome] can also sion. Therefore superimposition of these secondary factors on
contribute to the development of periodontitis. Since these a preexisting gingivitis can result in the painful, necrotic le-
disorders generally manifest early in life, the impact on the sions characteristic of NUG. With control of both the bacterial
periodontium may be clinically similar to generalized aggres- plaque and the secondary factors, the prognosis for a patient
sive periodontitis. The prognosis in these cases will be fair with NUG is good. However, the tissue destruction in these
to poor. cases is not reversible, and poor control of the secondary fac-
Other genetic disorders do not affect the host's ability to tors may make these patients susceptible to recurrence of the
combat infections but still affect the development of periodon- disease. With repeated episodes of NUG, the prognosis may
titis. Examples include hypophosphatasia, in which patients be downgraded to fair.
have decreased levels of circulating alkaline phosphatase, The clinical presentation of NUP is similar to that of NUG,
severe alveolar bone loss, and premature loss of deciduous except the necrosis extends from the gingiva into the peri-
and permanent teeth, and the connective tissue disorder, odontal ligament and alveolar bone. In systemically healthy
Ehlers-Danlos syndrome, in which patients may present with patients, this progression may have resulted from multiple
the clinical characteristics of aggressive periodontitis. In both episodes of NUG, or the necrotizing disease may occur at a
examples the prognosis is fair to poor. site previously affected with periodontitis. In these patients,
the prognosis depends on alleviating the plaque and second-
Necrotizing Periodontal Diseases ary factors associated with NUG. However, many patients
Necrotizing periodontal disease can be divided into necrotic presenting with NUP are immunocompromised through sys-
diseases that affect the gingival tissues exclusively [necrotiz- temic conditions, such as HIV infection. In these patients the
ing ulcerative gingivitis (NUG)] and necrotic diseases that prognosis depends on not only reducing local and secondary
affect deeper tissues of the periodontium, resulting in loss factors but also on dealing with the systemic problem.
of connective tissue attachment and alveolar bone [necro- In advanced cases, prognosis may be better established af-
tizing ulcerative periodontitis (NUP)]. In NUG, the primary ter reviewing the effectiveness of phase I therapy.
FIGURE 28.2 Generalized severe chronic periodontitis; overall prognosis is poor. A, Gingival inflammation, periodontal pockets, and pathologic
migration. B, Severe bone destruction. Note several hopeless teeth.
Determination of the prognosis of a tooth or teeth can be younger patient may have an aggressive type of periodontitis,
difficult, particularly for teeth with previous disease. Many or disease progression may have increased because of systemic
factors can influence disease progression and the response to disease or smoking. In addition, although the younger patient
therapy, and the specific influence of any one factor is un- would ordinarily be expected to have a greater reparative ca-
known and likely different from one patient to another. In ad- pacity, the occurrence of so much destruction in a relatively
dition, each patient can respond differently at different times. short period would exceed any naturally occurring periodon-
All these issues make determination of a prognosis difficult. tal repair.
Therefore the prognosis is often determined after initial
treatment is provided, assuming a favorable outcome. The Rate of Disease Progression
prognosis is delayed until after initial therapy because the eti- Studies have demonstrated that a patient's history of previous
ology depends on the host response. During initial therapy, periodontal disease may be indicative of their susceptibility
the patient's motivation and commitment, acknowledged as for future periodontal breakdown. A rapid loss of bone in a
critical in all periodontal therapy, also can be determined, as short time is indicative of factors beyond local irritants and
well as the host response and healing capacity of the patient. often difficult to control. Prognosis is poor in such cases.
Clearly, enhancing the host response to plaque's microbial
challenge will significantly and positively influence the peri- Height of the Remaining Bone
odontal prognosis. Likewise, an inability to enhance the host The prognosis can also be related to the height of the remain-
response will negatively influence the prognosis. Either out- ing bone. Assuming bone destruction can be arrested, is there
come, however, will allow the clinician to determine a more enough bone remaining to support the teeth? The answer is
accurate prognosis. readily apparent in extreme cases, that is, when there is so lit-
tle bone loss that tooth support is not in jeopardy (Fig. 28.1),
Age of the Patient or when bone loss is so severe that the remaining bone is ob-
For two patients with comparable levels of remaining con- viously insufficient for proper tooth support(Fig. 28.2). Most
nective tissue attachment and alveolar bone, the prognosis is patients, however, do not fit into these extreme categories.
generally better for the older of the two. For the younger pa- The height of the remaining bone is usually somewhere in
tient, the prognosis is not as good because of the shorter time between, making bone level assessment alone insufficient for
frame in which the periodontal destruction has occurred; the determining the overall prognosis.
Systemic Background treatment can influence treatment recommendations, such as

The patient's systemic background affects overall prognosis the use of adjunctive antibiotic therapy or increased frequency
in several ways. For example, evidence from epidemiologic of maintenance visits. Third, identification of young individu-
studies clearly demonstrates that the prevalence and severity als who have not been evaluated for periodontitis, but who are
of periodontitis are significantly higher in patients with type recognized as being at risk because of the familial aggregation
1 and type 2 diabetes than in those without diabetes and that seen in aggressive periodontitis, can lead to the development
the level of control of diabetes is an important variable in this of early intervention strategies. In each of these cases, early di-
relationship (see Chapter 13). Therefore patients at risk for agnosis, intervention, and alterations in the treatment regimen
diabetes should be identified as early as possible and informed may lead to an improved prognosis for the patient.
of the relationship between periodontitis and diabetes. Simi-
Smoking
larly, patients diagnosed with diabetes must be informed of
the impact of diabetic control on the development and pro- Epidemiologic evidence suggests that smoking may be the
gression of periodontitis. It follows that the prognosis in these most important environmental risk factor impacting the de-
cases depends on patient compliance relative to both medi- velopment and progression of periodontal disease. Therefore
cal and dental status. Well-controlled diabetic patients with it should be made clear to the patient that a direct relationship
slight-to-moderate periodontitis who comply with their rec- exists between smoking and the prevalence and incidence of
ommended periodontal treatment should have a good prog- periodontitis. In addition, patients should be informed that
nosis. Similarly, in patients with other systemic disorders that smoking affects not only the severity of periodontal destruc-
could affect disease progression, prognosis improves with cor- tion but also the healing potential of the periodontal tissues.
rection of the systemic problem. As a result, patients who smoke do not respond as well to
The prognosis is questionable when surgical periodontal conventional periodontal therapy as patients who have never
treatment is required but cannot be provided because of the smoked. Therefore the prognosis in patients who smoke and
patient's health. Incapacitating conditions that limit the pa- have slight to moderate periodontitis is generally fair to poor.
tient's performance of oral procedures (eg, Parkinson disease) In patients with severe periodontitis, the prognosis may be
also adversely affect the prognosis. Newer "automated" oral poor to hopeless.
hygiene devices, such as electric toothbrushes, may be helpful However, it should be emphasized that smoking cessation
for these patients and may improve their prognosis. can affect the treatment outcome and therefore the progno-
sis. Patients with slight-to-moderate periodontitis who stop
smoking can often be upgraded to a good prognosis, whereas
Genetic Factors those with severe periodontitis who stop smoking may be up-
Periodontal diseases represent a complex interaction between graded to a fair prognosis.
a microbial challenge and the host's response to that chal-
lenge, both of which may be influenced by environmental fac- Stress
tors such as smoking. In addition to these external factors, Physical and emotional stress, as well as substance abuse,
evidence also indicates that genetic factors may play an im- may alter the patient's ability to respond to the periodontal
portant role in determining the nature of the host response. treatment performed. These factors must be realistically faced
Evidence for this type of genetic influence exists for patients when attempting to establish a prognosis.
with both chronic and aggressive periodontitis. Genetic poly-
morphisms in the interleukin-1 (IL-1) genes, resulting in Number of Remaining Teeth and Their Distribution
increased production of IL-1~, have been associated with a As a rule more the number of teeth remaining better is the
significant increase in risk for severe, generalized, and chronic overall prognosis because the prosthetic solution becomes
periodontitis. It has been demonstrated that knowledge of the easier. More teeth to be replaced increases the load on the
patient's IL-1 genotype and smoking status can aid the clini- remaining teeth. Similarly, the distribution of remaining teeth
cian in assigning a prognosis. Genetic factors also appear to is vital. It is better to have stronger teeth such as canines, first
influence serum immunoglobulin G2 (IgG2) antibody titers and second molars of either jaw rather than incisors and third
and the expression of FcyRII receptors on the neutrophil, both molars.
of which may be significant in aggressive periodontitis. Other
genetic disorders, such as leukocyte adhesion deficiency type Patient Compliance and Cooperation
1, can influence neutrophil function, creating an additional The prognosis for patients with gingival and periodontal dis-
risk factor for aggressive periodontitis. Finally, the familial ag- ease is critically dependent on the patient's attitude, desire to
gregation that is characteristic of aggressive periodontitis indi- retain the natural teeth, and willingness and ability to main-
cates that additional as yet unidentified genetic factors may be tain good oral hygiene. Without these, treatment cannot suc-
important in susceptibility to this form of disease. ceed. Patients should be clearly informed of the important
The influence of genetic factors on prognosis is not simple. role they must play for the treatment to succeed. If patients
Although microbial and environmental factors can be altered are unwilling or unable to perform adequate plaque control
through conventional periodontal therapy and patient edu- and to receive the timely periodic maintenance checkups and
cation, genetic factors currently cannot be altered. However, treatments that the dentist deems necessary, the dentist can
detection of genetic variations linked to periodontal disease (1) refuse to accept the patient for treatment or (2) extract
can potentially influence the prognosis in several ways. First, teeth that have a hopeless or poor prognosis and perform
early detection of patients at risk because of genetic factors scaling and root planing on the remaining teeth. The dentist
can lead to early implementation of preventive and treat- should make it clear to the patient and in the patient record
ment measures for these patients. Second, identification of that further treatment is needed but will not be performed
genetic risk factors later in the disease or during the course of because of the lack of patient cooperation.
Factors in Determination of Prognosis of Individual splinting may have a beneficial impact on the overall and in-
Teeth dividual tooth prognosis.
The following factors are important in the consideration of
prognosis of individual teeth. It is once again stressed here Anatomical Factors
that the survival of individual tooth is dependent upon the Anatomic factors that may predispose the periodontium to
overall prognosis of the entire dentition and affected by it. disease and therefore affect the prognosis include short, ta-
When the overall prognosis is hopeless, it is difficult to antici- pered roots with large crowns; cervical enamel projections
pate better prognosis of individual teeth. and enamel pearls; intermediate bifurcation ridges; root con-
cavities; and developmental grooves. The clinician must also
Tooth Mobility consider root proximity and the location and anatomy of fur-
The principal causes of tooth mobility are loss of alveolar cations when developing a prognosis.
bone, inflammatory changes in the periodontal ligament, and Prognosis is poor for teeth with short, tapered roots and
trauma from occlusion. Tooth mobility caused by inflamma- relatively large crowns (Fig. 28.3). Due to the disproportion-
tion and trauma from occlusion may be correctable. However, ate crown-to-root ratio and the reduced root surface available
tooth mobility resulting from loss of alveolar bone is not likely for periodontal support, the periodontium may be more sus-
to be corrected. The likelihood of restoring tooth stability ceptible to injury by occlusal forces.
is inversely proportional to the extent to which mobility is Cervical enamel projections (CEPs) are flat, ectopic exten-
caused by loss of the supporting alveolar bone. A longitudi- sions of enamel that extend beyond the normal contours of
nal study of the response to treatment of teeth with different the cementoenamel junction. CEPs extend into the furcation
degrees of mobility revealed that pockets on clinically mobile of 28.6% of mandibular molars and 17% of maxillary molars.
teeth do not respond as well to periodontal therapy as pockets CEPs are most likely to be found on buccal surfaces of maxil-
on nonmobile teeth exhibiting the same initial disease sever- lary second molars. Enamel pearls are larger, round depos-
ity. Another study, however, in which ideal plaque control was its of enamel that can be located in furcations or other areas
attained, found similar healing in both hypermobile and firm on the root surface. Enamel pearls are seen less frequently
teeth. The stabilization of tooth mobility through the use of (1.1-5. 7% of permanent molars; 75% appearing in maxillary
FIGURE 28.3 Generalized aggressive periodontitis and poor crown-to-root ratio in 28-year-old patient; overall prognosis is poor. A, generalized
periodontal attachment loss and pocket formation. B, Moderate to advanced bone destruction. The contrast between the well-formed crowns and the
relatively short, tapered roots worsens the prognosis.
32 2 PA R T 2 Clinical Periodontics
third molars) than CEPs. An intermediate bifurcation ridge appear more marked on maxillary first premolars, the mesio-
has been described in 73% of mandibular first molars, cross- buccal root of the maxillary first molar, both roots of man-
ing from the mesial to the distal root at the midpoint of the dibular first molars, and the mandibular incisors. Any tooth,
furcation. The presence of these enamel projections on the however, can have a proximal concavity Although these con-
root surface interferes with the attachment apparatus and may cavities increase the attachment area and produce a root shape
prevent regenerative procedures from achieving their maxi- that may be more resistant to torquing forces, they also create
mum potential. Therefore their presence may have a negative areas that can be difficult for both the dentist and the patient
effect on the prognosis for an individual tooth. to clean.
Scaling with root planing is a fundamental procedure in Other anatomic considerations that present accessibility
periodontal therapy Anatomic factors that decrease the effi- problems are developmental grooves, root proximity, and fur-
ciency of this procedure can have a negative impact on the cation involvements. The presence of any of these can worsen
prognosis. Therefore the morphology of the tooth root is an the prognosis. Developmental grooves, which sometimes appear
important consideration when discussing prognosis. Root con- in the maxillary lateral incisors [palatogingival groove; or in
cavities exposed through loss of attachment can vary from shal- the lower incisors, create an accessibility problem (Fig. 28.6)].
low flutings to deep depressions (Figs. 28.4 and 28 5) They They initiate on enamel and can extend a significant distance
on the root surface, providing a plaque-retentive area that is
difficult to instrument. These palatogingival grooves are found
on 5.6% of maxillary lateral incisors and 3.4% of maxillary
central incisors. Similarly, root proximity can result in inter-
proximal areas that are difficult for the clinician and patient
P 17%
to access. Finally, access to the furcation area is usually difficult
to obtain (Fig. 28. 7). In 58% of maxillary and mandibular
first molars, the furcation entrance diameter is narrower than
the width of conventional periodontal curettes. Maxillary first
premolars present the greatest difficulties, and therefore their
) prognosis is usually unfavorable when the lesion reaches the
mesiodistal furcation. Maxillary molars also present some dif-
ficulty; sometimes their prognosis can be improved by resect-
ing one of the buccal roots, thereby improving access to the
area. When mandibular first molars or buccal furcations of
MB94% DB31o/o.
maxillary molars offer good access to the furcation area, their
prognosis is usually better.
I I
,-.\ ~ 0.3 mm
Level of Clinical Attachment
The determination of the level of clinical attachment reveals
FIGURE 28.4 Root concavities in maxillary first molars sectioned
2-mm apical to the furca. The furcal aspect of the root is concave in
the approximate extent of root surface that is devoid of peri-
94% of the mesiobuccal (MB) roots, 31 % of the distobuccal (DB) roots, odontal ligament; the radiographic examination shows the
and 17% of the palatal (P) roots. The deepest concavity is found in the amount of root surface still invested in bone. Pocket depth is
furcal aspects of the mesiobuccal root (mean concavity, 0.3 mm). The less important than the level of attachment because it is not
furcal aspect of the buccal roots diverges toward the palate in 97% of necessarily related to bone loss. In general, a tooth with deep
teeth (mean divergence, 22 degree). (Redrawn from Bower RC: J Peri-
odontal 50:366, 1979.)
pockets and little attachment and bone loss has a better prog-
nosis than one with shallow pockets and severe attachment
and bone loss. However, deep pockets are a source of infec-
tion and may contribute to progressive disease.
Prognosis is adversely affected if the base of the pocket
(level of attachment) is close to the root apex. The presence
of apical disease as a result of endodontic involvement also
worsens the prognosis. However, surprisingly good apical and
lateral bone repair can sometimes be obtained by combining
,. I endodontic and periodontal therapy
I I
\ I
\ I Type of Bone Defect
I I I I
M 100% 11 I l I I I/ D99% The type of defect also must be determined. The prognosis
\ I I I
I I
\ I
I I I I for horizontal bone loss depends on the height of the exist-
l I
I I
I I
I I
ing bone because it is unlikely that clinically significant bone
I I I height regeneration will be induced by therapy In the case
I I
of angular, intrabony defects, if the contour of the existing
\ 1 >1 '~0.5mm bone and the number of osseous walls are favorable, there is
0.7mm ~ ',~ I I
an excellent chance that therapy could regenerate bone to ap-
FIGURE 28.5 Root concavities in mandibular first molars sectioned proximately the level of the alveolar crest.
2-mm apical to the furca. Concavity of the furcal aspect was found in
100% of mesial (M) roots and 99% of distal (D) roots. Deeper concavity
When greater bone loss has occurred on one surface of a
was found in the mesial roots (mean concavity, 0.7 mm). (Redrawn from tooth, the bone height on the less involved surfaces should
Bower RC: J Periodontal 50:366, 1979.) be taken into consideration when determining the prognosis.
FIGURE 28.6 Palatogingival groove. A, Probe in place to indicate a deep pocket along the palatogingival groove. B, Radiograph with a gutta-percha
point placed in the pocket. C, The area is surgically opened. Note the palatogingival groove along the entire palatal portion of the root. (Courtesy
Dr Nadia Chugal, University of California, Los Angeles.)
0 ! / ~
0
....,.----.._
0
, I '
• /l\.
FIGURE 28.7 The furcation entrance is narrower than a standard cu-

(A)
/j (B) I
\ I
FIGURE 28.8 Prognosis for tooth A is better than for tooth B, despite
less bone on one of the surfaces of A. Because the center of rotation of
rette in 58% of first molars. (Redrawn from Bower RC: J Periodontal tooth A is closer to the crown, the distribution of occlusal forces to the
50:366, 7979.) periodontium is more favorable than in B.
Due to the greater height of bone in relation to other surfaces, Caries, Nonvital Teeth, and Root Resorption
the center of rotation of the tooth will be nearer the crown For teeth mutilated by extensive caries, the feasibility of ad-
(Fig. 28.8). This results in a more favorable distribution of equate restoration and endodontic therapy should be con-
forces to the periodontium and less tooth mobility sidered before undertaking periodontal treatment. Extensive
idiopathic root resorption or root resorption resulting from
Subgingival Restorations
orthodontic therapy jeopardizes the stability of teeth and
Subgingival margins may contribute to increased plaque ac- adversely affects the response to periodontal treatment. The
cumulation, increased inflammation, and increased bone loss periodontal prognosis of treated nonvital teeth does not dif-
when compared with supragingival margins. Furthermore, fer from that of vital teeth. New attachment can occur to the
discrepancies in these margins (eg, overhangs) can negatively cementum of both nonvital and vital teeth.
impact the periodontium. The size of these discrepancies and
duration of their presence are important factors in the amount Teeth Adjacent to Edentulous Areas
of destruction that occurs. In general, however, a tooth with a Teeth that serve as abutments are subjected to increased
discrepancy in its subgingival margins has a poorer prognosis functional demands. More rigid standards are required when
than a tooth with well-contoured supragingival margins. evaluating the prognosis of teeth adjacent to edentulous areas.
FIGURE 28.9 Extraction of severely involved tooth to preserve bone on adjacent teeth. A, Extensive bone destruction around the mandibular first
molar. B, Radiograph made years after extraction of the first molar and replacement by a prosthesis. Note the excellent bone support. C, Extraction
of periodontally involved bicuspid and molar. D, Implant replacement of both teeth. (Courtesy Dr 5. Angha, University of California, Los Angeles.)
A tooth with a post that has undergone endodontic treatment The overall prognosis requires a general consideration of
is more likely to fracture when serving as a distal abutment bone levels (evaluated radiographically) and attachment levels
supporting a distal removable partial denture. Additionally, (determined clinically) to establish whether enough teeth can
special oral hygiene measures must be instituted in these be saved either to provide a functional and aesthetic dentition
areas. or to serve as abutments for a useful prosthetic replacement of
the missing teeth.
Strategic Importance of the Tooth At this point, the overall prognosis and the individual tooth
In dealing with a tooth with a questionable prognosis, the prognosis overlap because the prognosis for key individual
chances of successful treatment should be weighed against teeth may affect the overall prognosis for prosthetic rehabilita-
any benefits that would accrue to the adjacent teeth if the tion. For example, saving or losing a key tooth may determine
tooth under consideration were extracted. Strategic extraction whether other teeth are saved or extracted or whether the
of teeth was first proposed as a means of improving the overall prosthesis used is fixed or removable. When few teeth remain,
prognosis of adjacent teeth and/or enhancing the prosthetic the prosthodontic needs become more important, and some-
treatment plan. It has now been expanded to include the ex- times periodontally treatable teeth may have to be extracted
traction of teeth with a questionable prognosis to enhance the if they are not compatible with the design of the prosthesis.
likelihood of partial restoration of the bone supporting the ad-
jacent teeth (Fig. 28.9A-D) or successful implant placement.
With the growing evidence of the long-term success of den- Reevaluation of Prognosis After Phase
tal implants, it is proposed that a "watch and wait" approach
may allow an area to deteriorate to the point that placing an
I Therapy
implant is no longer a viable option. This means that the prac- A frank reduction in pocket depth and inflammation after
titioner should weigh the potential success of one treatment phase I therapy indicates a favorable response to treatment
option (extraction and implant placement) versus the other and may suggest a better prognosis than previously assumed.
(periodontal therapy and maintenance) carefully when assign- If the inflammatory changes present cannot be controlled or
ing a prognosis to questionable teeth. reduced by phase I therapy, the overall prognosis may be un-
favorable. In these patients, the prognosis can be directly re-
Plaque Control lated to the severity of inflammation. Given two patients with
Bacterial plaque is the primary etiologic factor associated with comparable bone destruction, the prognosis may be better for
periodontal disease (see Chapter 9). Therefore effective re- the patient with the greater degree of inflammation because a
moval of plaque on a daily basis by the patient is critical to the larger component of that patient's bone destruction may be at-
success of periodontal therapy and to the prognosis. tributable to local irritants. In addition, phase I therapy allows
the clinician an opportunity to work with the patient and the Kwok V, Caton JG: Commentary: prognosis revisited: a system for assigning
patient's physician to control systemic and environmental fac- periodontal prognosis,] Periodontol 78(11):2063-2071, 2007.
McGuire MK: Prognosis versus actual outcome: a long-term survey of
tors such as diabetes and smoking, which may have a positive 100 treated periodontal patients under maintenance care, J Pe,iodontol
effect on prognosis if adequately controlled. 62(1) 51-58, 1991.
The progression of periodontitis generally occurs in an McGuire MK, Nunn ME: Prognosis versus actual outcome. 11. The effective-
episodic manner, with alternating periods of quiescence and ness of clinical parameters in developing an accurate prognosis,] Periodon-
tal 67(7):658-665, 1996a.
shorter destructive stages. No methods are available at present McGuire MK, Nunn ME: Prognosis versus actual outcome. III. The effective-
to determine accurately whether a given lesion is in a stage of ness of clinical parameters in accurately predicting tooth survival, J Peri-
remission or exacerbation. Advanced lesions, if active, may odontal 67(7):666-674, 19966.
progress rapidly to a hopeless stage, whereas similar lesions in McGuire MK, Nunn ME: Prognosis versus actual outcome. IV The effective-
a quiescent stage may be maintainable for long periods. Phase ness of clinical parameters and IL-1 genotype in accurately predicting prog-
noses and tooth survival,] Periodontol 70(1):49-56, 1999.
I therapy will, at least temporarily, transform the prognosis Miyamoto T, Kumagai T,JonesJA, et al: Compliance as a prognostic indicator:
of the patient with an active advanced lesion, and the lesion retrospective study of 505 patients treated and maintained for 15 years,
should be reanalyzed after completion of phase I therapy. J Periodontal 77(2):223-232, 2006.
Miyamoto T, Kumagai T, Lang MS, et al: Compliance as a prognostic indi-
cator. II. Impact of patient's compliance to the individual tooth survival,
SUGGESTED READINGS J Periodontol 81(9):1280-1288, 2010.
Bower RC: Furcation morphology relative to periodontal treatment. Furcation Nunn ME, Fan J, Su X, et al: Development of prognostic indicators using
entrance architecture,] Periodontal 50(1):23-27, 1979a. classification and regression trees for survival, Periodontal 2000 58(1):
Bower RC: Furcation morphology relative to periodontal treatment. Furcation 134-142, 2012.
root surface anatomy,] Periodontal 50(7):366-374, 19796.
29
Rationale for Periodontal
Treatment and Treatment Plan
Chapter Outline
What Does Periodontal Therapy The Treatment Plan
Accomplish? Master Plan for Total Treatment
Factors That Affect Healing Sequence of Therapeutic Procedures
Healing After Periodontal Therapy Explaining Treatment Plan to
Periodontal Reconstruction the Patient
What Does Periodontal Therapy of safety of the periodontium to the buildup of plaque, in ad-
dition to reducing tooth mobility It should be remembered
Accomplish? that total plaque elimination as obtained in experimental
The effectiveness of periodontal therapy is made possible by studies may not be possible in human subjects.
the remarkable healing capacity of the periodontal tissues.
Periodontal therapy can restore chronically inflamed gingiva
so that, from a clinical and structural point of view, it is almost Systemic Therapy
identical with gingiva that has never been exposed to exces- Systemic therapy may be employed as an adjunct to local
sive plaque accumulation. measures for specific purposes such as controlling systemic
Properly performed, periodontal treatment can eliminate complications from acute infections or chemotherapy and
pain, exudate, gingival inflammation, and bleeding. It can also preventing harmful effects of post treatment bacteremia. The
reduce periodontal pockets, eliminate infection, arrest the de- control of systemic diseases that aggravate the patient's peri-
struction of soft tissue and bone, and reduce abnormal tooth odontal condition is always a consideration, so proper precau-
mobility Other benefits are to establish optimal occlusal functions can be instituted during therapy
tion, restore tissue destroyed by disease, reestablish physiologic Systemic therapy for treatment of the periodontal condi-
gingival contour, and prevent the recurrence of disease, which tion in conjunction with local therapy is indicated in patients
will all help to maintain the natural dentition (Fig. 29.1). with aggressive periodontitis. In these diseases, systemic anti-
biotics are used to eliminate the bacteria that invade the gin-
gival tissues and can repopulate the pocket after scaling and
Local Therapy
root planing.
The cause of periodontitis and gingivitis is bacterial plaque In addition, periodontal manifestations of systemic diseas-
accumulation on the tooth surface close to the gingival tissue. es are treated primarily by other local measures.
The accumulation of plaque can be favored by a variety of In the late 20th century, the concept of host modulation was
local factors, such as calculus, overhanging margins of resto- introduced as a medical approach to periodontal treatment.
rations, and food impaction. The removal of plaque and all of The classic 1979 paper by Nyman, Schroeder, and Lindhe
the factors that favor its accumulation is the primary goal in local reported that it was possible to block periodontal bone loss
therapy. in animals with the aspirin-like drug indomethacin. Evidence
Abnormal forces on the tooth can increase tooth mobility was then presented that some nonsteroidal antiinflammatory
The thorough elimination of plaque and the prevention of its drugs (NSAIDs), such as flurbiprofen and ibuprofen, can re-
formation can help maintain periodontal health even if trau- duce the development of experimental gingivitis, as well as
matic forces are allowed to persist. However, the elimination the loss of alveolar bone in periodontitis. These drugs are pro-
of trauma may increase the chances for bone regeneration and pionic acid derivatives and act by inhibiting the cyclooxygen-
the gain of attachment. Although this point is not widely ac- ase pathway of arachidonic acid metabolism, thereby reducing
cepted, it appears that creating occlusal relationships that are prostaglandin formation. These NSAIDs can be administered
more tolerable to the periodontal tissues increases the margin by mouth or applied topically
327
Treatment procedures Clinical results
Epithelium:
Restore surface
continuity
...J
Elimination
of
gingival
inflammation
l Reduction
of abnormal
tooth
mobility
T
I .
i
Connective tissue:
s Cessation Establishment
Attach bone to
s of of optimal
= cementum and
p===;, u gingival occlusal
Local establish bone
e
height
bleeding I relationships
L__
r
e
,-------
Systemic
as required
J s
Bone:
I
Elimination of Restoration
p periodontal of destroyed
0 Restore balance
pockets and periodontal
n
s
between formation
and resorption
I infection tissues
e
I
I
- -,
I
I
Restoration of
Cementum: Cessation
physiologic
Attach periodontal of pus
fibers formation I gingival
contour
Cessation Prevention
of of
bone loss recurrence
FIGURE 29.1 Tissue response and clinical results after periodontal treatment.
Another drug that has a strong inhibitory effect on bone re- corrected before or during local procedures. However, local
sorption is alendronate, a bisphosphonate, which is currently used factors, particularly plaque microorganisms, are the most
to treat metabolic diseases in humans, such as Paget disease or common deterrents to healing after periodontal treatment.
hypercalcemia of malignancy, which result in bone resorption. Healing is also delayed by (1) excessive tissue manipula-
Experimental studies in monkeys have shown that alendronate tion during treatment, (2) trauma to the tissues, (3) the pres-
reduced the bone loss associated with periodontitis. ence of foreign bodies, and ( 4) repetitive treatment procedures
Host modulation is still in its experimental stages, and pro- that disrupt the orderly cellular activity in the healing process.
tocols for its clinical use have not been established. However, An adequate blood supply is needed for the increased cellular
current studies indicate that future treatment modalities may activity during healing. If the blood supply is impaired or in-
attempt not only to control the bacterial cause of the disease sufficient, areas of necrosis will develop and delay the healing
but also to suppress the self-destructive components of the process.
host inflammatory response. Healing is improved by debridement (removal of degener-
ated and necrotic tissue), immobilization of the healing area,
and pressure on the wound. The cellular activity in healing
Factors That Affect Healing entails an increase in oxygen consumption, but healing of the
gingiva is not accelerated by artificially increasing the oxygen
In the periodontium, as elsewhere in the body, healing is af-
supply beyond the normal requirements.
fected by local and systemic factors.
Local Factors Systemic Factors

Systemic conditions that impair healing may reduce the ef- The effects of systemic conditions on healing have been exten-
fectiveness of local periodontal treatment and should be sively documented in animal experiments but are less clearly
29 Rationale for Periodontal Treatment and Treatment Plan 329
defined in humans. Healing capacity diminishes with age,

probably because of the atherosclerotic vascular changes com-
mon in aging and the resulting reduction in blood circulation.
Healing is delayed in patients with generalized infections and
in those with diabetes and other debilitating diseases. ~
Healing is impaired by insufficient food intake; bodily con-
ditions that interfere with the use of nutrients; and deficien-
cies in vitamin C, proteins, and other nutrients. However, the
nutrient requirements of the healing tissues in minor wounds,
such as those created by periodontal surgical procedures, are
usually satisfied by a well-balanced diet.
Healing is also affected by hormones. Systemically ad-
ministered glucocorticoids such as cortisone hinder repair
by depressing the inflammatory reaction or by inhibiting the
growth of fibroblasts, the production of collagen, and the for-
mation of endothelial cells. Systemic stress, thyroidectomy,
testosterone, adrenocorticotropic hormone (ACTH), and large (A) (B)
doses of estrogen suppress the formation of granulation tissue
FIGURE 29.2 Two possible outcomes of pocket elimination. A, Peri-
and impair healing. Progesterone increases and accelerates the
odontal pocket before treatment. B, Normal sulcus reestablished at the
vascularization of immature granulation tissue and appears to level of the base of the pocket. C, Periodontium restored on the root
increase the susceptibility of the gingiva to mechanical injury surface previously denuded by disease; this is called new attachment.
by causing dilation of the marginal vessels. Shaded areas show denudation caused by periodontal disease.
Healing After Periodontal Therapy from the inherent regenerative capacity of the tissues. A brief
"spurt" in regenerative activity occurs immediately after peri-
The basic healing processes are the same after all forms of odontal treatment, but no local treatment procedures promote
periodontal therapy These processes consist of the removal of or accelerate regeneration.
degenerated tissue debris and the replacement of tissues de-
stroyed by disease. This implies regeneration and repair of the
periodontal structures but not necessarily a gain in attachment. Repair
Techniques to gain attachment and bone level are discussed in Repair simply restores the continuity of the diseased marginal
the sections on new attachment and periodontal reconstruction. gingiva and reestablishes a normal gingival sulcus at the same
level on the root as the base of the preexisting periodontal
Regeneration pocket (Fig. 29 2B) This process, called healing by scar, arrests
bone destruction but does not result in gain of gingival at-
Regeneration is the natural renewal of a structure, produced tachment or bone height. This return of the destroyed peri-
by growth and differentiation of new cells and intercellular odontium to health involves regeneration and mobilization of
substances to form new tissues or parts. Regeneration occurs epithelial and connective tissue cells into the damaged area
through growth from the same type of tissue that has been and increased local mitotic divisions to provide sufficient
destroyed or from its precursor. In the periodontium, gingi- numbers of cells (Fig. 29 3).
val epithelium is replaced by epithelium, and the underlying
connective tissue and periodontal ligament are derived from
connective tissue. Bone and cementum are replaced by con-
nective tissue, which is the precursor of both. Undifferenti-
ated connective tissue cells develop into osteoblasts and ce-
mentoblasts, which form bone and cementum.
Regeneration of the periodontium is a continuous physi-
ologic process. Under normal conditions, new cells and tis-
sues are constantly being formed to replace those that mature
and die; this is termed wear and tear repair. It is manifested by
(1) mitotic activity in the epithelium of the gingiva and the con-
nective tissue of the periodontal ligament, (2) the formation of
new bone, and (3) the continuous deposition of cementum.
Regeneration is occurring even during destructive periodon-
tal disease. Most gingival and periodontal diseases are chronic
inflammatory processes and as such are healing lesions. Regen-
eration is a part of healing. However, bacteria and bacterial prod-
ucts that perpetuate the disease process, along with the resulting
inflammatory exudate, are injurious to the regenerating cells and
tissues, thus preventing completion of the healing process.
FIGURE 29.3 Sources of regenerating cells in the healing stages of a
By removing bacterial plaque and creating the conditions periodontal pocket. Left, lntrabony pocket. Right, After therapy the clot
to prevent its new formation, periodontal treatment removes formed is invaded by cells from, A, the marginal epithelium; 8, the gingival
the obstacles to regeneration and enables the patient to benefit connective tissue; C the bone marrow; and, 0, the periodontal ligament.
For the diseased gingiva and attachment apparatus to

regain (totally or partially) their level on the root (Fig. 29 2C),
therapy must include special materials and techniques. If these
are not used or are not successful, tissues undergo repair only,
which involves regeneration of tissue to remodel the attach-
ment apparatus but does not include regaining attachment
level or new bone height. For this reason, we prefer to use the
term reconstruction of the periodontium to refer to the crucial
therapeutic techniques that seek to rebuild the periodontium
and result in a significant gain of attachment and bone height.
New Attachment
New attachment is the embedding of new periodontal liga-
ment fibers into new cementum and the attachment of the
gingival epithelium to a tooth surface previously denuded by
disease. (A) (B)
The critical phrase in this definition is "tooth surface pre-
viously denuded by disease" (Fig. 29.4, area B) The attach- FIGURE 29.5 Epithelial adaptation after periodontal treatment. A,
Periodontal pocket. B, After treatment. The pocket epithelium is closely
ment of the gingiva or the periodontal ligament to areas of the adapted to but not attached to the root.
tooth from which they have been removed in the course of
treatment (or during preparation of teeth for restorations) rep-
resents simple healing or reattachment of the periodontium, that the "deep sulcus" persists in an inactive state, causing no
not new attachment. The term reattachment refers to repair in further loss of attachment. A post therapy depth of 4 mm or
areas of the root not previously exposed to the pocket such as even 5 mm may therefore be acceptable in these cases.
after surgical detachment of the tissues or following traumatic
tears in the cementum, tooth fractures, or the treatment of
periapical lesions (Fig. 29.4, area D)
Periodontal Reconstruction
Epithelial adaptation differs from new attachment in that it As previously discussed, the term periodontal reconstruction
is the close apposition of the gingival epithelium to the tooth refers to the process of regeneration of cells and fibers and
surface, with no gain in height of gingival fiber attachment. remodeling of the lost periodontal structures that results in
The pocket is not completely obliterated although it may not (1) gain of attachment level, (2) formation of new periodontal
permit passage of a probe (Fig. 29 5) ligament fibers, and (3) a level of alveolar bone significantly
However, studies have shown that these deep sulci lined coronal to that present before treatment.
by long, thin epithelium may be as resistant to disease as true A technique to attain these ideal results has been a constant
connective tissue attachments. The absence of bleeding or se- but elusive goal of periodontal therapy for centuries. Since the
cretion on probing, the absence of clinically visible inflamma- 1970s, renewed laboratory and clinical research efforts have
tion, and the absence of stainable plaque on the root surface resulted in new concepts and techniques that have moved us
when the pocket wall is deflected from the tooth may indicate much closer to attaining this ideal result of therapy Melcher
pointed out that the regeneration of the periodontal ligament is
the key to periodontal reconstruction because it "provides conti-
nuity between the alveolar bone and the cementum and also be-
cause it contains cells that can synthesize and remodel the three
connective tissues of the alveolar part of the periodontium."
During the healing stages of a periodontal pocket, the area
is invaded by cells from four different sources (Fig. 29.3): oral
epithelium, gingival connective tissue, bone, and periodontal
ligament.
The final outcome of periodontal pocket healing depends
on the sequence of events during the healing stages. If the epi-
thelium proliferates along the tooth surface before the other
tissues reach the area, the result will be a long junctional epi-
thelium. If the cells from the gingival connective tissue are the
first to populate the area, the result will be fibers parallel to
the tooth surface and remodeling of the alveolar bone with
no attachment to the cementum. If bone cells arrive first, root
resorption and ankylosis may occur. Finally, only when cells
from the periodontal ligament proliferate coronally, there is
FIGURE 29.4 Enamel surface (A). Area of cementum denuded by new formation of cementum and periodontal ligament.
pocket formation (8). Area of cementum covered by junctional epithe-
lium (C). Area of cementum apical to junctional epithelium (0). The term
Several methods, based on different concepts and resulting
new attachment refers to a new junctional epithelium and attached con- in various techniques, have been recommended to improve the
nective tissue fibers formed on area 8. likelihood of gaining new attachment and increased bone levels.
The Treatment Plan

After the diagnosis and prognosis have been established, the periodontal environment. The master plan of periodontal
treatment is planned. The plan should encompass short- and treatment encompasses different areas of therapeutic objec-
long-term goals. tives for each patient according to his or her needs. It is based
The short-term goals are the elimination of all infectious on the diagnosis, disease severity, risk factors, and other fac-
and inflammc state of health. This may require periodontal tors outlined in previous chapters.
procedures, as well as other dental therapy, such as endodon-
tics and correcting oral mucous membrane pathology. Refer- Extracting or Preserving a Tooth
ral to other dental and medical specialties will be necessary.
Periodontal treatment requires long-range planning. Its value
From a periodontal viewpoint, the short-term goals are im-
to the patient is measured in years of healthy functioning of
portant, since they consist of the elimination of gingival inflam-
the entire dentition and not by the number of teeth retained
mation and correction of the conditions that cause and perpetu-
at the time of treatment. Treatment is directed to establishing and
ate it. These include not only elimination of root accretions but
maintaining the health of the periodontium throughout the mouth
also pocket eradication or reduction and establishment of good
rather than attempting spectacular effarts to "tighten loose teeth."
gingival contours and mucogingival relationships conducive to
In the past two decades, implant replacement of missing
good periodontal health. Restoration of carious areas and the
teeth has become a predictable course of therapy. Therefore
correction of poor existing restorations may also be necessary.
The long-term goals are the reconstruction of a healthy attempts to save questionable teeth may jeopardize adjacent
teeth and may lead to the loss of bone needed for implant
dentition that fulfills all functional and esthetic requirements.
therapy. Teeth on the borderline of a hopeless prognosis do
Long-term planning involves consideration of prosthetic re-
not contribute to the overall usefulness of the dentition. Such
construction of the dentition, which may require implant
teeth become sources of recurrent problem to the patient and
therapy, including surgical preparation of the implant site.
detract from the value of the greater service rendered by the
Also, the need for orthodontic treatment should be evaluated.
establishment of periodontal health in the remainder of the
The financial impact of long-term treatment requires careful
oral cavity.
consideration and understanding by the patient. The age and
Removal, retention, or temporary (interim) retention of
medical health status of the patient must also be considered.
one or more teeth is a very important part of the overall treat-
The treatment plan is the blueprint for case manage-
ment. It includes all procedures required for the establishment plan. A tooth should be extracted under the following
conditions:
ment and maintenance of oral health. It should be orderly
but at the same time flexible as it is difficult to determine at • It is so mobile that function becomes painful.
times how the teeth respond to therapy. The whole success • It can cause acute abscesses during therapy.
of the treatment should not depend upon the response of • There is no use for it in the overall treatment plan.
one or two teeth. Planning treatment involves the following
In some cases, a tooth can be retained temporarily, post-
decisions:
poning the decision to extract until after treatment is com-
• Need for emergency treatment (pain, acute infections) pleted. A tooth in this category can be retained under the
• Teeth that will require removal following conditions:
• Periodontal pocket therapy techniques (surgical or nonsur-
• It maintains posterior stops; the tooth can be removed after
gical)
treatment when it can be replaced by an implant or another
• Endodontic therapy
• The need for occlusal correction, including orthodontic type of prosthesis.
• It maintains posterior stops and may be functional after
therapy
implant placement in adjacent areas. When the implant is
• The use of implant therapy
restored, these teeth can be extracted.
• The need for caries removal and the placement of tempo-
• In the anterior esthetic zone, a tooth can be retained dur-
rary and final restorations
ing periodontal therapy and removed when treatment is
• Prosthetic replacements that may be needed and which
teeth will be abutments if a fixed prosthesis is used completed and a permanent restorative procedure can be
performed. The retention of this tooth should not jeopar-
• Decisions regarding esthetic considerations in periodontal
dize the adjacent teeth. This approach avoids the need for
therapy
temporary appliances during therapy.
• Sequence of therapy
• Extraction of hopeless teeth can also be performed during
Unforeseen developments during treatment may necessi- periodontal surgery of the adjacent teeth. This approach re-
tate modification of the initial treatment plan. However, except duces the number of appointments needed for surgery in
for emergencies, no therapy should be initiated until a treatment the same area.
plan has been established.
In the formulation of the treatment plan, in addition to the
proper function of the dentition, esthetic considerations play
an important role. Different patients value esthetics differently
Master Plan for Total Treatment according to their age, gender, profession, and social status.
The aim of the treatment plan is total treatment, that is, the The clinician should carefully evaluate and consider a final es-
coordination of all the short- and long-term goals for the thetic outcome of treatment that will be acceptable to the pa-
purpose of creating a well-functioning dentition in a healthy tient without jeopardizing the basic need of attaining health.
With the predictable use of implants, questionable teeth

should be carefully evaluated as to whether their removal and
replacement with an implant may be a better and more satis- PRELIMINARY PHASE
factory course of therapy. Treatment of emergencies:
In complex cases, interdisciplinary consultation with other • Dental or periapical
specialty areas is necessary before a final plan can be made. • Periodontal
The opinion of orthodontists and prosthodontists is especially • Other
important for the final decision in these patients.
Extraction of hopeless teeth and provisional replacement if
Occlusal evaluation and therapy may be necessary during
needed (may be postponed to a more convenient time)
treatment, which may necessitate planning for occlusal ad-
justment, orthodontics, and splinting. The correction of brux- NONSURGICAL PHASE (PHASE I THERAPY)
ism and other occlusal habits may also be necessary. Plaque control and patient education:
Systemic conditions should be carefully evaluated because • Diet control (in patients with rampant caries)
they may require special precautions during the course of • Removal of calculus and root planing
periodontal treatment. The tissue response to treatment pro- • Correction of restorative and prosthetic irritational factors
cedures may be affected, or the preservation of periodontal • Excavation of caries and restoration (temporary or final,
health may be threatened after treatment is completed. The depending on whether a definitive prognosis for the tooth
patient's physician should always be consulted when the pa- has been determined and the location of caries)
tient presents with medical and systemic problems that may • Antimicrobial therapy (local or systemic)
• Occ/usal therapy
affect the periodontal therapy.
• Minor orthodontic movement
Supportive periodontal care is also of paramount importance • Provisional splinting and prosthesis
for case maintenance. Such care entails all procedures for
maintaining periodontal health after it has been attained. It EVALUATION OF RESPONSE TO NONSURGICAL PHASE
consists of instruction in oral hygiene and recall therapy at Rechecking:
regular intervals according to the patient's needs. • Pocket depth and gingival inflammation
• Plaque and calculus, caries
Sequence of Therapeutic Procedures SURGICAL PHASE (PHASE II THERAPY)
• Periodontal therapy, including placement of implants
Periodontal therapy is an inseparable part of dental therapy. The • Endodontic therapy
list of procedures presented in Box 29.1 includes periodontal
RESTORATIVE PHASE (PHASE Ill THERAPY)
procedures (in italics) and other procedures not considered to
be within the province of the periodontist. These procedures • Final restorations
are listed together in to emphasize the close relationship of • Fixed and removable prosthodontic appliances
• Eva I uation of response to restorative procedures
periodontal therapy with other phases of therapy performed
• Periodontal examination
by general dentists or other specialists.
The sequence in which these phases of therapy are per- MAINTENANCE PHASE (PHASE IV THERAPY)
formed may vary to some extent in response to the require- Periodic rechecking:
ments of the case. However, the preferred sequence, which • Plaque and calculus
covers the vast majority of cases, is shown in Fig. 29.6. • Gingival condition (pockets, inflammation)
Although the phases of treatment have been numbered, • Occlusion, tooth mobility
the recommended sequence does not follow the numbers. • Other pathologic changes
Phase I, or the nonsurgical phase, is directed to the elimination Periodontal procedures are in italics.
of the etiologic factors of gingival and periodontal diseases.
When successfully performed, this phase stops the progres-
sion of dental and periodontal disease.
Immediately after completion of phase I therapy, the pa-
tient should be placed on the maintenance phase (phase IV) to
Emergency phase
preserve the results obtained and prevent any further deterio-
ration and recurrence of disease. While on the maintenance
phase, with its periodic evaluation, the patient enters into the
surgical phase (phase II) and the restorative phase (phase Ill) of
t
Nonsurgical phase
treatment. These phases include periodontal surgery to treat
and improve the condition of the periodontal and surround-
ing tissues. This may include regeneration of the gingiva and
bone for function and esthetics, placement of implants, and
Maintenance phase
restorative therapy.
Explaining Treatment Plan

Surgical phase Restorative phase
to the Patient
The following discussion includes suggestions for explaining
the treatment plan to the patient: FIGURE 29.6 Preferred sequence of periodontal therapy.
Be specific. Tell your patient, "You have gingivitis" or "You have serious potential risk of systemic disease, which in some
periodontitis," then explain exactly what these conditions are. cases ranks as high on the danger list as smoking.
Avoid vague statements. Do not use statements such as "You 2. It is not feasible to place restorations or fixed bridges on
have trouble with your gums" or "Something should be done teeth with untreated periodontal disease because the use-
about your gums." Patients may not understand the signifi- fulness of the restoration would be limited by the uncer-
cance of such statements and may disregard them. tain condition of the supporting structures.
Begin your discussion on a positive note. Talk about the teeth 3. Failure to eliminate periodontal disease not only results in
that can be retained and the long-term service they can be the loss of teeth already severely involved but also shortens
expected to render. Do not begin your discussion with the the life span of other teeth. With proper treatment, these
statement, "The following teeth have to be extracted." This teeth can serve as the foundation for a healthy, functioning
creates a negative impression, which adds to the erroneous at- dentition.
titude of hopelessness the patient already may have regarding
Therefore the dentist should make it clear to the patient
his or her mouth. Make it clear that every effort will be made
that if the periodontal condition is treatable, the best results
to retain as many teeth as possible, but do not dwell on the
are obtained by prompt treatment. If the condition is not
patient's loose teeth. Emphasize that the important purpose of
treatable, the teeth should be extracted.
the treatment is to prevent the other teeth from becoming as
It is the dentist's responsibility to advise the patient of the
severely diseased as the loose teeth.
importance of periodontal treatment. However, if treatment is
Present the entire treatment plan as a unit. Avoid creating the
to be successful, the patient must be sufficiently interested in
impression that treatment consists of separate procedures,
retaining his or her natural teeth and to maintain the neces-
some or all of which may be selected by the patient. Make
sary oral hygiene. Individuals who are not particularly per-
it clear that dental restorations and prostheses contribute as
turbed by the thought of losing their teeth are generally not
much to the health of the gingiva as the elimination of inflam-
good candidates for periodontal treatment.
mation and periodontal pockets. Do not speak in terms of
"having the gums treated and then taking care of the necessary
restorations later" as if these were unrelated treatments. SUGGESTED READINGS
Patients often seek guidance from the dentist with ques- Beaumont RH, O'Leary TJ, Kafrawy AH: Relative resistance oflongjunctional
tions such as the following: epithelial adhesions and connective tissue attachments to plaque-induced
inflammatton.] Periodontol 55:213, 1984.
• "Are my teeth worth treating?" Caffesse RG, Ramljord SP, Nasjleti CE: Reverse bevel periodontal [laps in
• "Would you have them treated if you had my problem?" monkeys,) Peliodontol 39:219, 1968.
Kantor M, Polson AM, Zander HA: Alveolar bone regeneration after removal
• "Why don't I just go along the way I am until the teeth re- of inflammatory and traumatic factors, J Periodontal 4 7:687, 1976.
ally bother me and then have them all extracted?" Lind he J, Ericsson I: The influence of trauma from occlusion on reduced but
healthy periodontal tissues in dogs,) Clin Periodontol 3:110, 1976.
Explain that "doing nothing" or holding onto hopelessly Lind he J, Nyman S: The effect of plaque control and surgical pocket elimina-
diseased teeth as long as possible is inadvisable for the follow- tion on the establishment and maintenance of periodontal health: a lon-
ing reasons: gitudinal study of periodontal therapy in cases of advanced periodontal
disease,) Clin Pe,iodontol 2:67, 1975.
1. Periodontal disease is a microbial infection, and research Magnusson I, Runstad L, Nyman S, et al: A long junctional epithelium: a
has clearly shown it to be an important risk factor for se- locus minoris resistentiae in plaque infection? J Clin Periodontal 10:33,
vere life-threatening diseases such as stroke, cardiovascular 1983.
Melcher AH: On the repair potential of periodontal tissues, J Pe,iodontol
disease, pulmonary disease, and diabetes, as well as for 47:256, 1976.
premature low-birth-weight babies in women of childbear- Polson AM: Interrelationship of inflammation and tooth mobility (trauma) in
ing age. Correcting the periodontal condition eliminates a pathogenesis of periodontal disease, J Clin Periodontal 7 :351, 1980.
SECTION II
Management of Patients with

Periodontal Diseases
Section Outline
30 Periodontal Treatment for Medically 31 Treatment of Aggressive and Atypical
Compromised Patients Forms of Periodontitis
30
Periodontal Treatment of
Medically Compromised Patients
PR Klokkevold • BL Mealey • J Otomo-Corgel • CD Dwarakanath
Chapter Outline
Cardiovascular Diseases Pulmonary Diseases
Endocrine Disorders Medications and Cancer Therapies
Hemorrhagic Disorders Pregnancy
Renal Diseases Infectious Diseases
Liver Diseases
The average life span of human beings has increased world- the age of 30 years be checked for increased blood pressure in
wide and consequently, the number of elderly patients requir- dental office. If there is any discrepancy, the patient should be
ing dental and periodontal management has also increased. referred to a physician. For a patient with a previously diag-
Many of these patients are likely to have one or more systemic nosed hypertension, the clinician should assess whether it is
problems. The changing life style today has resulted in even controlled or not and the type of medication that the patient
younger patients suffering from chronic diseases, such as dia- is taking. It is well established that calcium-channel blockers,
betes mellitus, hypertension, and other cardiovascular diseas- such as nifidepine, amlodipine, diltiazem, etc, cause gingival
es. Therefore it is the responsibility of the clinician to identify overgrowth. Nausea, sedation, oral dryness, and lichenoid-
the patient's medical problem and formulate a proper manage- drug reactions are the other adverse effects with certain classes
ment plan. Failure to do this results in serious complications. of antihypertensive agents.
It is reiterated here that the dental practitioners should me- Hypertension is divided into primary and secondary types.
ticulously obtain the medical history of the patient. Further Primary (essential) hypertension occurs when no underlying
it is also the responsibility of the clinician to be familiar with pathologic abnormality can be found to explain the disease.
the current understanding of the various medical disorders, Approximately 95% of all hypertensive patients have primary
their management, and the recommendations provided by the hypertension (Table 30.1). The remaining 5% have secondary
concerned authorities from time to time. hypertension in which an underlying etiology can be found
This chapter provides a broad outline of the periodon- and often treated. Examples of the conditions responsible
tal management of the patient with some common systemic for secondary hypertension are renal disease, endocrinologic
problems. Coordination with the patient's physician or refer- changes, and neurogenic disorders.
ral to an appropriate medical consultant is mandatory, which Regardless of the type of hypertension, the following guide-
greatly helps in avoiding potential medicolegal problems. lines should govern the periodontal management:
1. Consult the physician clearly explaining the nature of peri-
Cardiovascular Diseases odontal therapy.
The incidence and prevalence of cardiovascular diseases are 2. Schedule the appointments preferably in the afternoons.
increasing rapidly even in younger patients, and next to ma- 3. Check the blood pressure before starting the treatment.
lignancy, are the most common cause of death in many coun- 4. No treatment should be provided if the systolic BP is great-
tries around the world. These disorders include hypertension, er than 180 mmHg and/or the diastolic BP is higher than
ischemic heart disease, previous cardiac bypass surgery, con- 110 mmHg.
gestive cardiac failure (CCF), infective endocarditis, and pres- 5. Use local anesthetics with an adrenaline (epinephrine)
ence of cardiac pacemakers, defibrillators, and so on. concentration of 1: 100000 or less. Use of anesthetic solu-
tions without adrenaline, as was done in the past, is not
recommended since the management of pain and bleed-
Hypertension
ing is far more vital to prevent endogenous secretion of
Hypertension is a silent killer and is undiagnosed in many adrenaline. Aspirate before injection to prevent depositing
patients. Hence it is recommended that every patient above into a blood vessel.
337
TABLE 30.1
CLASSIFICATION OF ADULT BLOOD PRESSURE (BP)

Classification Systolic BP (mmHg) Diastolic BP (mmHg) Dental-Treatment Modifications
Normal <120 <80 No changes in dental treatment
Prehypertension 120-139 80-89 No changes in dental treatment
Monitor BP at each appointment
Stage 1 hypertension 140-159 90-99 Inform patient of findings
Routine medical consultation/referral
No changes in dental treatment; minimize stress
Stage 2 hypertension ~160 ~100 Inform patient
Medical consultation/referral
If systolic BP is < 180 mm Hg and diastolic is < 110 mmHg,
perform selective dental care (routine exam, prophylaxis,
restorative nonsurgical endodontics, and periodontics);
minimize stress
If systolic BP ~ 180 mmHg or diastolic ~ 100 mmHg, give
immediate medical consultation/referral, and perform
emergency dental care only (to alleviate pain, bleeding,
and infection)"; minimize stress
Consider stress-reduction protocol
BP, Blood pressure.
'Risk of providing emergency dental care must outweigh risk of possible hypertensive complications.
6. Keep the procedures as short as possible. 4. Discontinue the procedure if the patient becomes fatigued,
7. Avoid intraligamentary injections. uncomfortable, or has a sudden change in heart rhythm
8. Use conscious sedation in very anxious patients. or rate during a periodontal procedure, as soon as pos-
9. Make sure the bleeding has stopped completely before sible. A patient who has an anginal episode in the den-
dismissing the patient. tal chair should receive the following emergency medical
10. Beware of postural hypotension while adjusting the den- treatment:
tal chair. a. Discontinue the periodontal procedure.
b. Administer one tablet (0.3-0.6 mg) of nitroglycerin
lschemic Heart Diseases and Other sub lingually
c. Reassure the patient and loosen restrictive garments.
Cardiovascular Disorders d. Administer oxygen to the patient in a reclined position.
Ischemic heart disease includes disorders, such as angina pec- e. If the signs and symptoms cease within 3 min, complete
toris and myocardial infarction (MI). Angina pectoris occurs the periodontal procedure if possible, making sure that
when myocardial oxygen demand exceeds supply, resulting the patient is comfortable. Terminate the procedure at
in temporary myocardial ischemia. Patients with a history of the earliest convenient time.
unstable angina pectoris (angina that occurs irregularly or on f. If the anginal signs and symptoms do not resolve with
multiple occasions without predisposing factors) should be this treatment within 2-3 min, administer another dose
treated only for emergencies and then in consultation with of nitroglycerin, monitor the patient's vital signs, call
their physician. Patients with stable angina (angina that oc- the patient's physician, and be ready to accompany the
curs infrequently, is associated with exertion or stress, and is patient to the emergency department.
easily controlled with medication and rest) can undergo elec- g. A third nitroglycerin tablet may be given 3 min after
tive dental procedures. Since stress often induces an acute the second. Chest pain that is not relieved by three tab-
anginal attack, stress reduction is important. Profound local lets of nitroglycerin indicates a possible Ml. The patient
anesthesia is vital and conscious sedation may be indicated should be transported to the nearest emergency medi-
for anxious patients. Supplemental oxygen delivered by nasal cal facility immediately
cannula may also help prevent intraoperative anginal attacks. Restrictions on use of local anesthetics containing epineph-
rine are similar to those for the patient with hypertension. In
Principles of Periodontal Management addition, intraosseous injection with epinephrine-containing
local anesthetics using special systems (eg, Stabident and Fair-
1. Consult the patient's physician and obtain the farmer's fax Dental) should be done cautiously in patients with isch-
fitness to undergo periodontal therapy emic heart disease, because it results in transient increases in
2. Instruct the patient to bring their medications, particularly, heart rate and myocardial oxygen demand.
if they are on nitroglycerin. In recent years, nitroglycerin lingual spray formulations
3. Keep the procedures short. Include smaller areas in the have been popular in hospital pharmacies because of the in-
mouth for each visit. creased shelf life as compared to nitroglycerin tablets. The
30 Periodontal Treatment of Medically Compromised Patients 339
lingual spray has been reported to provide a greater and more dental treatment because such activation often causes sudden
rapid vasodilation with a longer duration of action. patient movement. Stabilization of the operating field dur-
MI is the other category of ischemic heart disease encoun- ing periodontal treatment with bite blocks or other devices
tered in dental practice. Dental treatment is generally deferred can prevent unexpected trauma.
for at least 6 months after MI because peak mortality occurs
during this time. After 6 months, MI patients can usually be
Infective Endocarditis
treated using techniques similar to those for a stable angina
patient. IE is a disease in which microorganisms colonize the damaged
Cardiac (aortocoronary) bypass, femoral artery bypass, an- endocardium or heart valves. Although the incidence of IE is
gioplasty, and endarterectomy have become common surgi- low, it is a serious disease with a poor prognosis, despite mod-
cal procedures in patients with ischemic heart disease. If one ern therapy. The term infective endocarditis is preferred to the
of these procedures was performed on a patient recently, the previous term bacterial endocarditis because fungi and viruses
physician should be consulted before elective dental therapy can also cause the disease. The organisms most often encoun-
to determine the degree of heart damage or arterial occlusive tered in IE are a-hemolytic Streptococci (eg, Streptococcus
disease, the stability of the patient's condition, and the poten- viridans). However, nonstreptococcal organisms often found
tial for infective endocarditis (IE) or graft rejection. Prophy- in the periodontal pocket have been increasingly implicated,
lactic antibiotics are usually not necessary for cardiac bypass including Eikenella corrodens, Aggregatibacter actinomycetem-
patients unless recommended by the cardiologist. comitans, Capnocytophaga, and Lactobacillus species.
IE has been divided into acute and subacute forms. The
Congestive Cardiac Failure acute form involves virulent organisms, generally nonhemo-
lytic Streptococci and strains of Staphylococci, which invade
CCF is a condition in which the pump function of the heart normal cardiac tissue, produce septic emboli, and cause in-
is unable to supply sufficient amounts of oxygenated blood to fections that run a rapid, generally fatal course. The subacute
meet the body's needs. form, conversely, results from colony formation on damaged
Patients with poorly controlled or untreated CCF are not endocardium or heart valves by low-grade pathogenic organ-
candidates for elective dental procedures. These individuals are isms; the classic example is rheumatic carditis consequent to
at risk for sudden death, usually from ventricular arrhythmias. rheumatic fever.
For patients with treated CCF, the clinician should consult Since the last American Heart Association (AHA) publica-
with the physician regarding the severity of CCF, underlying tion on prevention of IE in 1997, many have questioned the
etiology, and current medical management. Medical manage- efficacy of antimicrobial prophylaxis to prevent IE in patients
ment of CCF may include use of calcium-channel blockers, who undergo dental or other procedures and have suggested
direct vasodilators, diuretics, angiotensin-converting enzyme that the AHA guidelines should be revised. Members of the
(ACE) inhibitors, a-receptor blockers, and cardiotonic agents, Rheumatic Fever, Endocarditis, and Kawasaki Disease Com-
such as digoxin. Each of these medications has potential side mittee of the AHA Council on Cardiovascular Disease in the
effects that may have an impact on periodontal therapy. Due Young, and a national and international group of experts
to the presence of orthopnea (inability to breathe unless in on IE extensively reviewed data published on the preven-
an upright position) in some CHF patients, the dental chair tion of IE. The committee concluded that only an extremely
should be adjusted to a comfortable level for the patient rather small number of IE cases might be prevented by antibiotic
than being placed in a supine position. Short appointments, prophylaxis for dental procedures (even if such therapy was
stress reduction with profound local anesthesia and possibly 100% effective). Consequently, the guidelines were changed
conscious sedation, and use of supplemental oxygen should and published in a 2008 report. The new guidelines advise
be considered. that IE prophylaxis should only be recommended for cardiac
conditions with the highest risk of adverse outcome from IE
Cardiac Pacemakers and Implantable (Box 30.1). For these patients, antibiotic prophylaxis is rec-
Cardioverter-Defibrillators ommended for all dental procedures that involve manipula-
tion of the gingival tissues, periapical tissues, or perforation
Cardiac arrhythmias are most often treated with medica- of the oral mucosa. Antibiotic prophylaxis is not indicated for
tions; however, some are also treated with implantable pace- individuals on the basis of an increased lifetime risk of con-
makers or automatic cardioverter-defibrillators. Pacemakers tracting IE.
are usually implanted in the chest wall and enter the heart The practice of periodontics is intimately concerned with
transvenously. Automatic cardioverter-defibrillators are more the prevention of IE. However, bacteremia may occur even
often implanted subcutaneously near the umbilicus and have in the absence of dental procedures, especially in individuals
electrodes passing into the heart transvenously or are directly with poor oral hygiene and significant periodontal inflamma-
attached to the epicardium. Consultation with the patient's tion. In fact, IE is much more likely to result from frequent
physician allows the determination of the underlying cardiac exposure to random bacteria associated with daily activities
status, the type of pacemaker or automatic cardioverter- rather than a dental procedure. Thus, the prevention of peri-
defibrillator, and any precautionary measures to be taken. odontal inflammation is paramount. The AHA states that pa-
Older pacemakers were unipolar and could be disrupted by tients who are at risk for IE should "establish and maintain
dental equipment that generated electromagnetic fields, such the best possible oral health to reduce potential sources of
as ultrasonic and electrocautery units. Newer units are bipolar bacterial seeding." To provide adequate preventive measures
and are generally not affected by dental equipment. Automatic for IE, the clinician's major concern should be to reduce the
cardioverter-defibrillators activate without warning when cer- microbial population in the oral cavity so as to minimize soft-
tain arrhythmias occur. This may endanger the patient during tissue inflammation and bacteremia.
bacteremia. Susceptible patients should be encouraged to

maintain the highest level of oral hygiene once soft-tissue
inflammation is controlled.
3. During periodontal treatment, currently recommended antibi-
otic prophylactic regimens should be practiced with all high-risk
Previous history of infective endocarditis patients (Table 30.2). If any doubt regarding susceptibility
Prosthetic cardiac valves or prosthetic material used for exists, the patient's physician should be consulted. In pa-
cardiac valve repair tients who have been receiving continuous oral penicillin
Congenital heart disease (CHO), with the following
for secondary prevention of rheumatic fever, penicillin-
conditions:
resistant a-hemolytic Streptococci are occasionally found
• Unrepaired cyanotic CHO, including palliative shunts and in the oral cavity It is therefore recommended that an al-
conduits ternate regimen be followed instead. Likewise, if the peri-
• Completely repaired congenital heart defect with prosthetic odontal patient is taking a systemic antibiotic as part of
material or device, whether placed by surgery or by catheter
periodontal therapy, changes in the IE prophylaxis regimen
intervention, during the first 6 months after the procedure
• Repaired CHO with residual defects at the site or adjacent
may be indicated. For example, a patient currently taking
to the site of a prosthetic patch or prosthetic device (which a penicillin agent after regenerative therapy may be placed
inhibit endothelialization) on azithromycin before the next periodontal procedure.
Patients with early-onset forms of periodontitis often have
Cardiac transplantation recipients who develop cardiac
high levels of A actinomycetemcomitans in the subgingival
val vu Iopa thy
plaque. This organism has been associated with IE and is
'Recommendations by the American Heart Association. often resistant to penicillin. Therefore, in patients with ag-
From Takahashi M, et al: Prevention of infective endocarditis: guidelines gressive periodontitis who should be given prophylaxis,
from the American Heart Association, 116:1736, 2007. Slots et al suggested the use of tetracycline, 250 mg, 4
times daily for 14 days to eliminate or reduce A actinomy-
cetemcomitans, followed by the conventional prophylaxis
Preventive measures to reduce the risk of IE should consist
protocol, at the time of dental treatment.
of the following:
4. Periodontal treatment should be designed for susceptible pa-
1. Define the susceptible patient. A careful medical history will tients to accommodate their particular degree of periodontal
disclose the previously mentioned susceptible patients. involvement. The nature of periodontal therapy enhances
Health questioning should cover history of all potential the problems related to the prophylaxis of subacute IE.
categories of risk. If any doubt exists, the patient's physi- Patients are faced with long-term therapy, healing periods
cian should be consulted. that extend beyond a 1-day antibiotic regimen, multiple
2. Provide oral-hygiene instruction. Oral hygiene should be visits, and procedures that easily elicit gingival bleeding.
practiced with methods that improve gingival health. In
The following guidelines should aid in the development
patients with significant gingival inflammation, oral hy-
of periodontal treatment plans for patients susceptible to IE:
giene should initially be limited to gentle procedures (ie,
oral rinses and gentle toothbrushing with a soft brush) to • Periodontal disease is an infection with potentially wide-
minimize bleeding. As gingival health improves, more ag- ranging systemic effects. In patients at risk for IE, every effort
gressive oral hygiene may be initiated. Oral irrigators are should be made to eliminate this infection. Teeth with severe
generally not recommended because their use may induce periodontitis and a poor prognosis may require extraction.
TABLE 30.2
RECOMMENDED ANTIBIOTIC PROPHYLAXIS REGIMENS FOR PERIODONTAL PROCEDURES IN ADULTS

AT RISK FOR INFECTIVE ENDOCARDITIS
Regimen Antibiotic Dosage'
Standard oral regimen Amoxicillin 2g
30-60 min before procedure
Alternate regimen for patients allergic to Clindamycin 600 mg; 30-60 min before procedure
amoxicillin/penicillin
or
Azithromycin or clarithromycin 500 mg; 30-60 min before procedure
or
Cephalexin or cefadroxil' 2 g; 30-60 min before procedure
Patients unable to take oral medications Ampicillin 2 g Intramuscularly or intravenously within 30 min
before procedure
Patients unable to take oral medications and Clindamycin 600 mg Intravenously within 30 min before
allergic to penicillin procedure (must be diluted and injected slowly)
or
Cefazolin" 1 g Intramuscularly or intravenously within 30 min
before procedure
"Cephalosporins should not be used in patients with immediate-type hypersensitivity reactions to penicillins (eg, urticaria, angioedema, and anaphylaxis).
"Adult dosages listed. Children's dosages are lower.
Teeth with less severe involvement in a motivated patient 2. After 6 months, periodontal therapy may be performed
should be retained, treated, and maintained closely using short appointments with an emphasis on minimiz-
• All periodontal treatment procedures (including probing) ing stress. Profound local anesthesia should be obtained
require antibiotic prophylaxis; gentle oral-hygiene meth- using the minimal effective dose of local anesthetic agents.
ods are excluded. Pretreatment chlorhexidine rinses are Concentrations of epinephrine greater than 1:100,000 are
recommended before all procedures, including periodontal contraindicated.
probing, because these oral rinses significantly reduce the 3. Light conscious sedation (inhalation, oral, or parenteral)
presence of bacteria on mucosa! surfaces. may be used for anxious patients. Supplemental oxygen
• To reduce the number of visits required and thereby mini- should be maintained thorough cerebral oxygenation.
mize the risk of developing resistant bacteria, numerous 4. Stroke patients are frequently placed on oral anticoagu-
procedures may be accomplished at each appointment, de- lants. Previously, it was thought that for procedures en-
pending on the patient's needs and ability to tolerate dental tailing significant bleeding, such as periodontal surgery
treatment. or tooth extraction, the anticoagulant regimen might
• When possible, allow at least 7 days between appointments need adjustment, depending on the level of anticoag-
(preferably 10-14 days). If this is not possible, select an ulation at which the patient is maintained. However,
alternative antibiotic regimen for appointments within a recent evidence regarding the risks of altering antico-
7 -day period. agulation therapy suggests that it may be more prudent
• Evidence does not support or refute a need to place pa- to provide treatment without changing it (see refer to
tients at a risk for IE on extended antibiotic regimens after section on "Anticoagulant/Antiplatelet Therapy" under
treatment. Therefore, patients who have had periodontal "Medications and Cancer Therapies"). Any changes
surgery are not generally placed on antibiotics for the first in anticoagulant therapy regimens for a stroke patient
week of healing (unless there are specific indications to do should always be done in consultation with the patient's
so). If patients are placed on such regimens, the dosages physician.
are inadequate to prevent endocarditis during ensuing ap- 5. BP should be monitored carefully Recurrence rates
pointments. Therefore the standard prophylactic antibiotic for CVAs are high, as are rates of associated functional
dose is still needed. For example, if a patient was placed on deficits.
250 mg of amoxicillin, 3 times a day for 10 days, after peri-
odontal surgery and was returning to the office for more
treatment on the 7th day, the patient would still require a Endocrine Disorders
full 2-g dose of amoxicillin before that treatment. Alterna-
tively, clindamycin or azithromycin could be used at the Diabetes
second appointment.
The diabetic patient requires special precautions before peri-
• Regular recall appointments, with an emphasis on oral-
odontal therapy The two major types of diabetes are type 1
hygiene reinforcement and maintenance of periodontal (formerly known as "insulin-dependent diabetes") and type 2
health, are extremely important for patients susceptible to IE.
(formerly called "noninsulin-dependent diabetes"). Over the
past decade, the medical management of diabetes has changed
significantly in an effort to minimize the debilitating compli-
Cerebrovascular Accident
cations associated with this disease. Patients are more tightly
A cerebrovascular accident (CVA), or stroke, results from isch- managing their blood-glucose levels (glycemia) through diet,
emic changes (eg, cerebral thrombosis caused by an embolus) oral agents, and insulin therapy
or hemorrhagic phenomena. Hypertension and atherosclerosis If the clinician detects intraoral signs of undiagnosed or
are predisposing factors for CVA and should alert the clinician poorly controlled diabetes, a thorough history is indicated.
to evaluate the patient's medical history carefully for the pos- The classic signs of diabetes include polydipsia (excessive
sibility of early cerebrovascular insufficiency and to be aware thirst), polyuna (excessive urination), and polyphagia (exces-
of symptoms of the disease. A physician's referral should pre- sive hunger, often with unexplained concurrent weight loss).
cede periodontal therapy if the signs and symptoms of early If the patient has any of these signs or symptoms, or if the cli-
cerebrovascular insufficiency are evident. nician's index of suspicion is high, further investigation with
To prevent a repeat stroke, active infections should be treat- laboratory studies and physician consultation is indicated.
ed aggressively because even minor infection may alter blood Periodontal therapy has limited success in the presence of
coagulation, trigger thrombus formation, and subsequent cere- undiagnosed or poorly controlled diabetes.
bral infarction. The clinician should counsel the patient about If a patient is suspected of having undiagnosed diabetes,
the importance of thorough oral hygiene. Poststroke weakness the following procedures should be performed:
of the facial area or paralysis of extremities may make oral- 1. Consult the patient's physician.
hygiene procedures extremely difficult. The clinician may need
2. Analyze laboratory tests: fasting blood glucose and casual
to modify oral-hygiene instruments for ease of use, perhaps
glucose (Box 30.2)
in consultation with an occupational therapist. Long-term
3. Rule out acute orofacial infection or severe dental infec-
chlorhexidine rinses may greatly aid in plaque control.
tion; if present, provide emergency care immediately
Dental clinicians should treat post-CVA patients with the 4. Establish best possible oral health through nonsurgi-
following guidelines in mind: cal debridement of plaque and calculus; institute oral-
1. No periodontal therapy (unless for an emergency) should hygiene instruction. Limit more advanced care until
be performed for 6 months because of the high risk of diagnosis has been established and a good glycemic con-
recurrence during this period. trol is obtained.
Guidelines for Managing a Diabetic

Diabetes mellitus may be diagnosed by any one of three
Patient in the Dental Office
different laboratory methods. Whichever method is used, it Almost all diabetic patients use glucometers for immediate
must be confirmed on a subsequent day by using any one of blood glucose self-monitoring. These devices use capillary
the following three methods. blood from a simple finger stick to provide blood-glucose
1. Symptoms of diabetes plus casual (nonfasting) plasma readings in seconds. Diabetic patients should be asked wheth-
glucose 2:200 mg/dl. Casual glucose may be drawn at er they have glucometers and how often they use them. Since
any time of day without regard to time since the last meal. these devices provide instantaneous assessment of blood glu-
Classic symptoms of diabetes include polyuria, polydipsia, cose, they are highly beneficial in the dental-office environ-
and unexplained weight loss. ment. The following guidelines should be observed:
2. Fasting plasma glucose 2:126 mg/dl. "Fasting" is defined as
no caloric intake for at least 8 h. (Normal fasting glucose is 1. For a controlled diabetic for a nonsurgical therapy, no anti-
70-100 mg/dl.) biotic premedication is required. However, before surgical
3. Two-hour postprandial glucose 2:200 mg/dl during an procedures prophylactic antibiotics are recommended.
oral glucose tolerance test.' The test should be performed 2. Patients should be asked to bring their glucometer to the
using a glucose load containing the equivalent of 75 g
dental office at each appointment.
of anhydrous glucose dissolved in water. (Normal 2-h
3. Patients should check their blood glucose before any long
postprandial glucose is <140 mg/dl.)
procedure to obtain a baseline level. Patients with blood-
'The third method is not recommended for routine clinical use. glucose levels at or below the lower end of normal before
Data from American Diabetes Association: Diabetes Care 26(Suppl 1 ):5, 2003. the procedure may become hypoglycemic intraoperatively.
It is advisable to have such a patient consume some car-
bohydrates before starting the treatment. For example, if
Tests for Diabetes and Metabolic Control a 2-h procedure is planned and the pretreatment glucose
For an undiagnosed or suspected diabetic patient, with or level is 70 mgldL (lower end of normal range), providing
without symptoms, a glucose tolerance test should be done. 4 oz of juice preoperatively may help prevent hypoglycemia
For an already diagnosed patient, the metabolic control during treatment. If pretreatment-glucose levels are exces-
is assessed by the glycosylated hemoglobin assay (HbAlC) sively high, the clinician should determine whether or not
(Box 30.3, Table 30 3). the patient's glycemic control has been poor recently. This
can be done by thorough patient questioning and by deter-
mining the most recent HbAlc values. If glycemic control
has been poor over the preceding few months, the pro-
cedure may need to be postponed until a better glycemic
control is established. If glycemic control has been good
and the current high-glucometer reading is a fairly isolated
4%-6% Normal event, the surgical procedure may proceed.
<7% Good diabetes control 4. If the procedure lasts several hours, it is often beneficial to
7%-8% Moderate diabetes control check the glucose level during the procedure to ensure that
>8% Action suggested to improve diabetes control the patient does not become hypoglycemic.
5. After the procedure, the blood glucose can be checked
'American Diabetes Association guidelines.
again to assess fluctuations over time.
6. If the patient feels symptoms of hypoglycemia during the
procedure, blood-glucose levels should be checked imme-
TABLE 30.3 diately. This may prevent onset of severe hypoglycemia,
which is a medical emergency (Box 30. 4).
COMPARISON OF HBA 1 C VALUES TO ESTIMATED
AVERAGE GLUCOSE MEASUREMENTS The most common dental-office complication, seen in
diabetic patients taking insulin, is symptomatic low-blood
HbAlc (%) Estimated Average Glucose (mg/dl)
glucose, or hypoglycemia. Hypoglycemia is also associated
5.0 97 with the use of numerous oral agents. In patients receiv-
5.5 111 ing conscious sedation, the warning signs of an impending
6.0 126
6.5 140
7.0 154
7.5 169
8.0 183
Shakiness or tremors
8.5 197
212
Confusion
9.0
226
Agitation and anxiety
9.5
Sweating
10.0 240
Tachycardia
10.5 255
ll.0 269
Dizziness
Feeling of "impending doom"
11.5 283
Unconsciousness
12.0 298
Seizures
HbAlc, Glycosylated hemoglobin Ale.
hypoglycemic episode may be masked, making the patient's going to be particularly long, the insulin dose before treat-
glucometer one of the best diagnostic aids. Hypoglycemia ment may need to be reduced. Likewise, if the patient will
does not usually occur until blood-glucose levels fall below have dietary restrictions after treatment, insulin or sulfonyl-
60 mg/dl. However, in patients with poor glycemic con- urea dosages may need to be reduced.
trol who have prolonged hyperglycemia (high-blood glucose Consultation with the patient's physician is prudent and al-
levels), a rapid drop in glucose can precipitate signs and lows both practitioners to review the proposed treatment plan
symptoms of hypoglycemia at levels well above 60 mgldl. and determine any modifications needed. When a periodontal
As medical management of diabetes has intensified over surgery is indicated, it is usually best to limit the size of the
the last decade, the incidence of severe hypoglycemia has ris- surgical fields so that the patient will be comfortable enough
en. The clinician should question diabetic patients about past to resume a normal diet immediately.
episodes of hypoglycemia. Hypoglycemia is more common
in patients with a better glycemic control. When planning a
Thyroid and Parathyroid Disorders
dental treatment, it is best to schedule appointments before
or after periods of peak-insulin activity. This requires knowl- Periodontal therapy requires minimal alterations in the pa-
edge of the pharmacodynamics of the drugs being taken by tient with adequately managed thyroid disease. Patients with
the diabetic patient. Patients taking insulin are at the greatest thyrotoxicosis and those with inadequate medical management
risk, followed by those taking sulfonylurea agents. Metformin should not receive periodontal therapy until their conditions
and thiazolidinediones generally do not cause hypoglycemia. are stabilized. Patients with a history of hyperthyroidism should
Insulins are classified as rapid-acting, short-acting, inter- be carefully evaluated to determine the level of medical man-
mediate-acting, or long-acting agents. The categories vary in agement and they should be treated in a way that limits stress
their onset, peak, and duration of activity. It is important that and infection. Hyperthyroidism may cause tachycardia and
the clinician establish exactly which type of insulin the dia- other arrhythmias, increased cardiac output, and myocardial
betic patient takes, the amount, the number of times per day, ischemia. Medications, such as epinephrine and other vaso-
and the time of the last dose. Periodontal treatment often can pressor amines, should be given with caution in patients with
be timed to avoid peak-insulin activity. Many diabetic patients treated hyperthyroidism although the small amounts used in
take multiple injections each day, in which case it is difficult, dental anesthetics rarely cause problems. These drugs should
if not impossible, to avoid peak-insulin activity. Determining not be given to patients with thyrotoxicosis or poorly con-
glucose levels with the patient's glucometer, before the treat- trolled thyroid disorders. Patients with hypothyroidism require
ment, during long procedures, and at the end of the proce- careful administration of sedatives and narcotics because of
dure provides a better understanding of the patient's insulin the potential for excessive sedation.
pharmacodynamics and helps prevent hypoglycemia. Routine periodontal therapy may be provided to patients
If hypoglycemia occurs during a dental treatment, therapy with parathyroid disease once that disorder has been iden-
should be immediately terminated. If a glucometer is avail- tified and the proper medical treatment is given. However,
able, the blood glucose level should be checked. Treatment patients who have not received medical care may have signifi-
guidelines include the following: cant renal disease, uremia, and hypertension. Also, if hyper-
calcemia or hypocalcemia is present, the patient may be more
1. Provide approximately 15 g of oral carbohydrate to the
prone to cardiac arrhythmias.
patient:
a. 4-6 oz of juice or soda
b. 3-4 tsp of table sugar Adrenal Insufficiency
c. Hard candy with 15 g of sugar
Acute adrenal insufficiency is associated with significant mor-
2. If the patient is unable to take food or drink by mouth, or
bidity and mortality as a result of peripheral vascular col-
if the patient is sedated:
lapse and cardiac arrest. Therefore, the periodontist should
a. Give 25-30 ml of 50% dextrose intravenous (IV),
be aware of the clinical manifestations and ways of prevent-
which provides 12.5-15.0 g of dextrose, or
ing acute adrenal insufficiency in patients with histories of
b. Give 1 mg of glucagon IV (glucagon results in rapid
primary adrenal insufficiency (Addison disease) or secondary
release of stored glucose from the liver), or
adrenal insufficiency (most often caused by use of exogenous
c. Give 1 mg of glucagon intramuscularly or subcutane-
glucocorticosteroids) (Box 30.5).
ously (if no IV access is present).
The use of systemic corticosteroids is common in pa-
Emergencies resulting from hyperglycemia are rare in the den- tients with allergic, endocrine, respiratory, joint, intestinal,
tal office. They generally take days to weeks to develop. However, neurologic, renal, liver, skin, and connective-tissue disorders.
the glucometer may be used to rule out hyperglycemic emergen-
cies, such as diabetic ketoacidosis, a life-threatening event.
Since periodontal therapy may render the patient unable to
eat for some time, adjustment in insulin or oral agent dosages
may be required. It is absolutely critical that patients eat their
normal meal before dental treatment. Taking insulin without Mental confusion, fatigue, and weakness
eating is the primary cause of hypoglycemia. If the patient Nausea and vomiting
Hypertension
is restricted from eating before treatment (eg, for conscious
Syncope
sedation), normal insulin doses will need to be reduced. As a Intense abdominal pain, lower back pain, and leg pain
general guideline, well-controlled diabetic patients, having rou- Loss of consciousness
tine periodontal treatment, may tahe their normal insulin doses Coma
as long as they also eat their normal meal. If the procedures are
Significant complications associated with corticosteroid use situation, when testing is not possible, increasing the steroid
include alterations in glucose metabolism (steroid-induced dia- dose before the procedure can decrease the chances of an
betes), increased risk of infection, altered wound healing, osteo- acute adrenal crisis.
porosis, skin disorders, cataracts, glaucoma, and suppression of Management of the patient in an acute adrenal insufficien-
the hypothalamic-pituitary-adrenal (HPA) axis. In the normal cy crisis is as follows:
healthy patient, stress activates the HPA axis, stimulating in-
1. Terminate periodontal treatment.
creased endogenous cortisol production by the adrenal glands.
2. Summon medical assistance.
Exogenous steroids may suppress the HPA axis and impair the
3. Administer oxygen.
patient's ability to respond to stress with increased endogenous
4. Monitor vital signs.
cortisol production, leading to the potential for an acute adrenal
5. Place the patient in a supine position.
crisis. The degree of adrenal suppression depends on the drugs
6. Administer 100 mg of hydrocortisone sodium succinate
used, dose, duration of administration, time elapsed since ste-
intramuscularly or IV over 30 s.
roid therapy was terminated, and route of administration.
It has been a common practice in the past to administer
prophylactic systemic steroids before dental treatment for pa- Hemorrhagic Disorders
tients who are taking or who have recently taken exogenous
steroids. Such steroid supplementation may not be required Patients with a history of bleeding problems caused by disease
for many periodontal procedures. In fact, adrenal crisis is rare or drugs should be managed to minimize risks of hemorrhage.
in dentistry, especially when associated with secondary adre- Identification of these patients through the health history, clin-
nal suppression caused by steroid use. Shapiro et al found ical examination, and clinical laboratory tests is paramount.
that patients taking 5-20 mg/day of prednisone maintained at Health questioning should cover (1) history of bleeding after
least some adrenal reserve after immediate termination of ste- previous surgery or trauma, (2) past and present drug history,
roid therapy. Higher doses may suppress the adrenal glands to (3) history of bleeding problems among relatives, and (4) ill-
a greater degree. Although exogenous steroids may suppress nesses associated with potential bleeding problems.
normal adrenal cortisol secretion for an extended period, the Clinical examination should detect the presence of jaun-
ability of the adrenal gland to respond to stress may return dice, ecchymosis, spider telangiectasia, hemarthrosis, pete-
quickly after termination of steroid therapy. chiae, hemorrhagic vesicles, spontaneous gingival bleeding,
Despite its rarity, the severe consequences of adrenal cri- and gingival hyperplasia. Laboratory tests should include
sis suggest caution in patient management. Before providing methods to measure the hemostatic, coagulation, or lytic
extensive dental treatment to a patient with a history of re- phases of the clotting mechanism, depending on clues regard-
cent or current steroid use, physician consultation is indicated ing which phase is involved (Table 304). These tests include
to determine whether the patient's treatment needs warrant bleeding time, tourniquet test, complete blood cell count,
supplemental steroids. Use of a stress-reduction protocol and prothrombin time (PT), partial thromboplastin time (PTT),
profound local anesthesia will help minimize the physical and and coagulation time.
psychologic stress associated with therapy and reduce the risk Bleeding disorders may be classified as coagulation disor-
of an acute adrenal crisis. ders, thrombocytopenic purpuras, or nonthrombocytopenic
Current evidence indicates that a vast majority of individu- purpuras.
als with adrenal insufficiency can receive routine dental treat-
ment without the need for supplemental glucocorticosteroids. Coagulation Disorders
Patients currently taking corticosteroids generally have enough
exogenous and endogenous cortisol to handle routine den- The main inherited coagulation disorders include hemophilia
tal procedures if their usual dose is taken within 2 h of the A, hemophilia B, and von-Willebrand disease (Table 30 5).
planned procedure. Thus, for most patients, supplemental cor- Hemophilia A results in a deficiency of coagulation factor Vlll
ticosteroid administration is not required when uncomplicated and the clinical severity of the disorder depends on the level
minor surgical procedures, including periodontal surgery, are of factor Vlll remaining. Patients with severe hemophilia who
performed with local anesthesia, with or without sedation. have less than 1 % of normal factor Vlll levels may have severe
Individuals, who may be at a risk for adrenal crisis requiring bleeding on the slightest provocation, whereas those with more
supplementation, include those who are undergoing lengthy, moderate hemophilia (1-5% factor VIII) have less frequent
major surgical procedures, those expected to have significant spontaneous hemorrhage but still bleed with minimal trauma.
blood loss, and those who have extremely low adrenal func- Patients with mild hemophilia (6-30% factor Vlll) rarely bleed
tion. For these individuals, consultation with their physician spontaneously but may still have hemorrhage after severe trau-
and steroid supplementation is indicated. Low adrenal func- ma or during surgical procedures. The clinician should consult
tion can be identified with an adrenocorticotropic hormone the patient's physician before a dental treatment to determine
(ACTH)-stimulation test. A rapid assay is also available to the risk for bleeding and treatment modifications required.
determine the degree of adrenal reserve by measurement of To prevent surgical hemorrhage, factor Vlll levels of at least
serum cortisol levels after 30- and 60-min IV administration 30% are needed. Parenteral l-deamino-8-D-arginine vasopres-
of synthetic corticotropin. sin (DDAVP; desmopressin) can be used to raise factor Vlll
For a patient who is identified as being at risk, the need for levels twofold to threefold in patients with mild or moderate
corticosteroid prophylaxis depends on the drug used because hemophilia. DDAVP has the significant advantage of avoiding
of the variance in equivalent therapeutic doses. the risk of viral disease transmission from factor Vlll infusion
Glucocorticosteroid coverage regimens vary, but most pro- and is considered the drug of choice in responsive patients.
vide a twofold to fourfold increase in coverage, depending Most patients with moderate and severe hemophilia require
on the stress produced by the procedure. In an emergency infusion of factor Vlll concentrate before surgical procedures.
TABLE 30.4
LABORATORY TESTS FOR BLEEDING DISORDERS

Hemostatic Tests
Vascular Platelet Coagulation Lytic
1. Tourniquet test 1. Platelet count 1. PT measures extrinsic and common 1. Euglobin-clot lysis time
N: 10 petechiae N: 150,000-300,000 mm" pathways: factors I, 11, V, Vil, and X. N: <90 min
Abn: > 10 petechiae Abn: Thrombocytopenia N: 11-14 s (depending on laboratory) Abn: >90 min
occurs at <100,000 mrrr '; measured against control
clinical bleeding occurs at PT reported as international
<80,000 mrrr ': spontaneous normalized ratio (INR):
bleeding occurs at N.· INR= 1.0
<20,000 mrrr' Abn: INR > 1.5
2. Bleeding time
3. Clot retraction
4. Complete blood-cell count
2. Bleeding time 2. PTT measures intrinsic and
N: 1-6 min common pathways: factors Ill, IX,
Abn. >6 min XI, and low levels of factors I, 11, V,
X, and Xll
N: 25-40 s (depending on laboratory)
measured against control
Abn: > 1.5 times normal
3. Clotting (coagulation) time
N: 30-40 min
Abn: >l h
Clinical Disease Association
Vascular (capillary) wall defect Thrombocytopenia Increase in fibrinolytic
activity
Rule out: Rule out: All th,·ee tests:
Thrombocytopenia Vascular-wall defect Liver disease
Purpuras Acute/chronic leukemia Warfarin therapy
Telangiectasia Aplastic anemia Aspirin or NSAID therapy
Aspirin or NSAID therapy Liver disease Malabsorption syndrome or long-term
Leukemia Renal dialysis antibiotic therapy (lack of vitamin K
Renal dialysis utilization)
PT: Factor Vil deficiency
PTT: Hemophilia and renal dialysis
N, Normal; Abn, abnormal; PT, prothrombin time; PTT, partial thromboplastin time; NSAID, nonsteroidal antiinflammatory drug.
TABLE 30.5
INHERITED COAGULATION DISORDERS

Type Prolonged Normal Treatment
Hemophilia A PTT PT DDAVP (desmopressin) factor Vlll concentrate or cryoprecipitate

Bleeding time Fresh-frozen plasma
Fresh whole blood
£-Aminocaproic acid (Amicar)
Tranexamic acid
Hemophilia B PTT PT Purified prothrombin complex concentrates
Bleeding time Factor IX concentrates
Fresh-frozen plasma
von-Willebrand disease Bleeding time PT DDAVP (desmopressin) factor Vlll concentrate or cryoprecipitate
PTT Platelet count
Variable factor VIII deficiency
PT, Prothrombin time; PTT, partial thromboplastin time; DDAVP, l-deamino-8-D-arginine vasopressin.
Before 1985, the risk of viral disease transmission from these amount of existing factor IX. Surgical therapy requires a factor
infusions was high. In recent years, virally safe, highly purified IX level of 30-50% and is usually achieved by administra-
monoclonal antibody or recombinant DNA factor VIII prod- tion of purified prothrombin complex concentrates or factor
ucts have come into widespread use. IX concentrates.
Hemophilia B, or Christmas disease, is a deficiency of fac- von-Willebrand disease results from a deficiency of von-
tor IX. The severity of the disorder depends on the relative Willebrand factor, which mediates adhesion of platelets to the
injured vessel wall and is required for primary hemostasis. Traditional recommendations for periodontal treatment are as
von-Willebrand factor also carries the coagulant portion of follows:
factor Vlll in the plasma. The disorder has three major sub-
1. Consult the patient's physician to determine the nature
types with a wide range of clinical severity. In fact, many cases
of the underlying medical problem and the degree of re-
of von-Willebrand disease go undiagnosed, and bleeding dur-
quired anticoagulation.
ing dental treatment may be the first sign of the underlying
2. The procedure to be done determines the acceptable INR.
disease. More severe forms require preoperative factor Vlll
Infiltration anesthesia, scaling, and root planing may be
concentrate or cryoprecipitate infusion. Patients with milder
done safely in patients with an INR <3.0. Block anes-
forms respond favorably to administration of DDAVP before
thesia, minor periodontal surgery, and simple extractions
periodontal surgery or tooth extraction.
usually require an INR <2.0-2.5. Complex surgery, mul-
Periodontal treatment may be performed in patients with
tiple extractions or implant placement may require an INR
these coagulation disorders, provided that sufficient precau-
<1.5-2.0.
tions are taken. Probing, scaling, and prophylaxis can usually
3. The physician must be consulted about any changes (dis-
be done without medical modification. More invasive treat-
continuing or reducing) in anticoagulant dosage until the
ments, such as local-block anesthesia, root planing, or surgery
desired INR is achieved. The dentist must inform the phy-
dictate prior physician consultation.
sician the extent of intraoperative and postoperative bleed-
During treatment, local measures to ensure clot forma-
ing that is usually expected with the procedures planned.
tion and stability are of major importance. Complete wound
If the INR is higher than the level at which significant
closure and application of pressure will reduce hemorrhage.
bleeding is likely to accompany a particular procedure,
Antihemostatic agents, such as oxidized cellulose or purified
the physician may change the anticoagulant therapy. Of-
bovine collagen, may be placed over surgical sites or into ex-
ten, the anticoagulant is discontinued for 2-3 days before
traction sockets. The antifibrinolytic agent £-aminocaproic acid
periodontal treatment (clearance half-life of warfarin is 36-
(Amicar), given orally or via IV, is a potent inhibitor of initial
42 h), and the INR is checked on the day of therapy. If the
clot dissolution. Tranexamic acid is a more potent antifibnno-
INR is within the acceptable target range, the procedure is
lytic agent than Amicar and has been shown to prevent ex-
performed and the anticoagulant is resumed immediately
cessive oral hemorrhage after periodontal surgery and tooth
after treatment.
extraction. It is available as an oral rinse and may be used
4. Careful technique and complete wound closure are para-
either alone or in combination with systemic tranexamic acid
mount. For all procedures, application of pressure can
for several days after surgery.
minimize hemorrhage. Use of oxidized cellulose, micro-
Not all coagulation disorders are hereditary. Liver dis-
fibrillar collagen, topical thrombin, and tranexamic acid
ease may affect all phases of blood clotting because most co-
should be considered for persistent bleeding.
agulation factors are synthesized and removed by the liver.
Long-term alcohol abusers or chronic hepatitis patients often NOTE: Discontinuing anticoagulant therapy before dental
demonstrate inadequate coagulation. Coagulation may be im- surgery (as previously stated) was common in the past. How-
paired by vitamin K deficiency, often caused by malabsorp- ever, many clinicians no longer recommend discontinuing
tion syndromes, or by prolonged antibiotic administration, anticoagulation medications for many procedures because it
which alters the intestinal microflora that produces vitamin K. has a significant potential risk to the patient's health. Recent
Dental-treatment planning for patients with liver disease evidence related to the risks of altering anticoagulant therapy
should include the following: along with the lack of evidence for bleeding complications
suggest that treating patients without reducing or discontinu-
1. Physician consultation.
ing medications may be more prudent.
2. Laboratory evaluations: PT, bleeding time, platelet count,
Heparin is generally used for short-term anticoagulation
and PTT (in patients in later stages of liver disease).
and is given IV (usually in a hospital environment). It is a
3. Conservative, nonsurgical periodontal therapy, whenever
powerful anticoagulant with duration of action of 4-8 h. Peri-
possible.
odontal treatment is rarely required while a patient is taking
4. If surgery is required (may require hospitalization):
heparin.
a. International normalized ratio (INR; PT) should gener-
ally be less than 2.0. For simple surgical procedures, Antiplatelet Medications
INR less than 2.5 is generally safe.
Aspirin interferes with normal platelet aggregation and can
b. Platelet count should be more than 80,000 mm>'.
result in prolonged bleeding. Since it binds irreversibly to
platelets, the effects of aspirin last at least 4-7 days. Aspirin is
Anticoagulant Medications generally used in small doses of 325 mg or less per day, which
The most common cause of abnormal coagulation may be usually does not alter bleeding time. In general, patients tak-
drug therapy Patients with prosthetic heart valves or histo- ing low doses of aspirin daily do not need to discontinue as-
ries of MI, CVA, deep vein thrombosis (DVT), or thromboern- pirin therapy before periodontal procedures. However, higher
bolism are frequently placed on anticoagulant therapy using doses may increase bleeding time and predispose the patient to
coumarin derivatives, such as dicumarol and warfarin. These postoperative bleeding. For patients taking more than 325 mg
drugs are vitamin K antagonists that decrease production of of aspirin per day, aspirin may need to be discontinued for
vitamin K-dependent coagulation factors II, VII, IX, and X. 7-10 days before surgical therapy that might result in signifi-
The effectiveness of anticoagulation therapy is monitored by cant bleeding, in consultation with the physician. Nonsteroidal
PT-laboratory test. The recommended level of therapeutic antiinflammatory drugs (NSAIDs), such as ibuprofen, also in-
anticoagulation for most patients is an INR of 2.0-3.0, with hibit platelet function. Since NSAIDs bind reversibly, the effect
prosthetic heart valve patients generally in the 2.5-3.5 range. is transitory, lasting only a short time after the last drug dose.
The bleeding time is used when questions arise about the po- 2. Before chemotherapy, a complete periodontal treatment
tential effect of aspirin or NSAIDs. Aspirin should not be pre- plan should be developed with a physician
scribed for patients who are receiving anticoagulation therapy a. Monitor hematologic laboratory values daily: bleeding
or who have illnesses related to bleeding tendencies. time, coagulation time, PT, and platelet count.
b. Administer antibiotic coverage before any periodontal
treatment because infection is a major concern.
Thrombocytopenic Purpuras c. Extract all hopeless, nonmaintainable, or potentially
Thrombocytopenia is defined as a platelet count of less than infectious teeth at least 10 days before the initiation of
100,000 mrrr'. Bleeding caused by thrombocytopenia may be chemotherapy, if systemic conditions allow.
seen with idiopathic thrombocytopenic purpuras, radiation d. Periodontal debridement (scaling and root planing)
therapy, myelosuppressive drug therapy (eg, chemotherapy), should be performed and thorough oral-hygiene in-
leukemia, or infections. Purpuras are hemorrhagic diseases structions given if the patient's condition allows. Twice-
characterized by extravasation of blood into the tissues under daily rinsing with 0.12 % chlorhexidine gluconate is
the skin or mucosa, producing spontaneous petechiae (small- recommended after oral-hygiene procedures. Recog-
red patches) or ecchymoses (bruises). nize the potential for bleeding caused by thrombocy-
Periodontal therapy for patients with thrombocytope- topenia. Use pressure and topical hemostatic agents as
nia should be directed toward reducing inflammation by indicated.
removing local irritants to avoid the need for a more aggres- 3. During the acute phases of leukemia, patients should re-
sive therapy. Oral-hygiene instructions and frequent mainte- ceive only emergency periodontal care. Any source of po-
nance visits are paramount. Physician referral is indicated for tential infection must be eliminated to prevent systemic
a definitive diagnosis and to determine any alterations in the dissemination. Antibiotic therapy is frequently the treat-
planned therapy. Scaling and root planing are generally safe ment of choice, combined with nonsurgical or surgical de-
unless platelet counts are less than 60,000 mm". No surgi- bridement as indicated.
cal procedures should be performed unless the platelet count 4. Oral ulcerations and mucositis are treated palliatively with
is greater than 80,000 mrrr'. Platelet transfusion may be re- agents, such as viscous lidocaine. Systemic antibiotics may
quired before surgery. Surgical technique should be as atrau- be indicated to prevent secondary infection.
matic as possible and local hemostatic measures should be 5. Oral candidiasis is common in leukemic patients and can
applied. be treated with nystatin suspensions (100,000 U/ml,
4 times daily) or clotrimazole vaginal suppositories (10 mg,
4-5 times daily).
Nonthrombocytopenic Purpuras 6. For patients with chronic leukemia and those in remis-
Nonthrombocytopenic purpuras result from either vascular sions, scaling and root planing can be performed without
wall fragility or thrombasthenia (impaired platelet aggrega- complication, but periodontal surgery should be avoided if
tion). Vascular wall fragility may result from hypersensitiv- possible.
ity reactions, scurvy, infections, chemicals (phenacetin and a. Platelet count and bleeding time should be measured
aspirin), dysproteinemia, and other causes. Thrombasthenia on the day of the procedure. If either is low, postpone
occurs in uremia, Glanzmann disease, aspirin ingestion, and the appointment and refer the patient to a physician.
von-Willebrand disease. Both types of nonthrombocytopenic
purpura may result in immediate bleeding after gingival inju- Agranulocytosis
ry. Treatment consists primarily of direct pressure applied for
at least 15 min. This initial pressure should control the bleed- Patients with agranulocytosis (cyclic neutropenia and granu-
ing unless coagulation times are abnormal or reinjury occurs. locytopenia) have an increased susceptibility to infection.
Surgical therapy should be avoided until the qualitative and The total white-blood cell count is reduced and granular
quantitative platelet problems are resolved. leukocytes (neutrophils, eosinophils, and basophils) are
reduced or nil. These disorders are often marked by early,
severe periodontal destruction. When possible, periodontal
Blood Dyscrasias treatment should be done during periods of disease remis-
sion. At such times, treatment should be as conservative as
Numerous disorders of red and white blood cells may affect
possible while reducing potential sources of systemic infec-
the course of periodontal therapy. Alterations in wound heal-
tion. After physician consultation, severely affected teeth
ing, bleeding, tissue appearance, and susceptibility to infec-
should be extracted. Oral-hygiene instruction should in-
tion may occur. Clinicians should be aware of the clinical
signs and symptoms of blood dyscrasias, availability of screen- clude the use of chlorhexidine rinses twice daily. Scaling and
ing laboratory tests, and need for physician referral. root planing should be performed carefully under antibiotic
protection.
Leukemia
Renal Diseases
Altered periodontal treatment for patients with leukemia is
based on their enhanced susceptibility to infections, bleeding The most common causes of renal failure are glomerulone-
phritis, pyelonephritis, kidney cystic disease, renovascular
tendency, and the effects of chemotherapy. The treatment plan
for leukemia patients is as follows: disease, drug nephropathy, obstructive uropathy, and hyper-
tension. Renal failure may result in severe electrolyte imbal-
1. Refer the patient for medical evaluation and treatment. ances, cardiac arrhythmias, pulmonary congestion, CHF, and
Close cooperation with the physician is required. prolonged bleeding. Since the dental management of patients
with renal disease may need to be drastically altered, physi- 1 h. If appointments last longer, allow the patient to walk
cian consultation is necessary to determine the stage of renal about for a few minutes, then resume therapy.
disease, regimen for medical management, and alterations in 5. Refer the patient to the physician if uremic problems de-
periodontal therapy. The patient in chronic renal failure has a velop, such as uremic stomatitis. To prevent systemic dis-
progressive disease that ultimately may require kidney trans- semination, refer to the physician if oral infections do not
plantation or dialysis. It is preferable to treat the patient be- promptly resolve.
fore, rather than after, transplant or dialysis.
The renal transplant patient's greatest foe is infection.
The following treatment modifications should be used:
Transplant patients take immunosuppressive drugs that
1. Consult the patient's physician. greatly reduce resistance to infection. Excessive bleeding
2. Monitor BP (patients in end-stage renal failures are usually may occur during or after periodontal treatment because of
hypertensive). drug-induced thrombocytopenia, anticoagulation, or both.
3. Check laboratory values: PTT, PT, bleeding time, and A periodontal abscess is a potentially life-threatening situa-
platelet count; hematocrit; blood-urea nitrogen (do not tion; therefore a dental-team approach should be used before
treat if <60 mg/dl.); and serum creatinine (do not treat if transplantation to determine which teeth can be easily main-
<1.5 mg/dL). tained. Many organ transplant centers now include dental
4. Eliminate areas of oral infection to prevent systemic infec- examination in their standard pretransplant protocol. Teeth
tion. with severe bone and attachment loss, furcation invasion,
a. Good oral hygiene should be established. periodontal abscesses, or extensive surgical requirements
b. Periodontal treatment should aim at eliminating inflam- should be extracted, leaving an easily maintainable dentition.
mation or infection and providing easy maintenance. In addition to the recommendations for patients with chronic
Questionable teeth should be extracted if medical pa- renal failure, the following should be considered for the renal
rameters permit. transplant patient:
c. Frequent recall appointments should be scheduled. 1. Hepatitis B and C screening.
5. Drugs that are nephrotoxic or metabolized by the kidney 2. Determination of the level of immune-system compromise
should not be given (eg, phenacetin, tetracycline, and ami- resulting from antirejection drug therapy.
noglycoside antibiotics). Acetaminophen may be used for 3. Prophylactic antibiotics (using AHA recommendations or
analgesia and diazepam for sedation. Local anesthetics, specific regimens based on physician consultation). Not all
such as lidocaine, are generally safe. transplant patients require antibiotic coverage, and physi-
The patient who is receiving dialysis requires modifications cian consultation is warranted before prescribing.
in treatment planning. The three modes of dialysis are inter-
mittent peritoneal dialysis (IPD), chronic ambulatory perito- Liver Diseases
neal dialysis (CAPD), and hemodialysis. Only hemodialysis
patients require special precautions. These patients have a Liver diseases may range from mild conditions to complete
high incidence of viral hepatitis, anemia, and prolonged hem- liver failure. Major causes of liver disease include drug tox-
orrhage. The risk for hemorrhage is related to anticoagulation icity, cirrhosis, viral infections (eg, hepatitis B and C), neo-
during dialysis, platelet trauma from dialysis, and the uremia plasms, and biliary-tract disorders. Since the liver is the site of
that develops with renal failure. Hemodialysis patients have production for most of the clotting factors, excessive bleeding
either an internal arteriovenous fistula or an external arterio- during or after periodontal treatment may occur in patients
venous shunt. This shunt is often located in the arm and must with severe liver disease. Many drugs are metabolized in the
be protected from trauma. Thus, in addition to guidelines for liver; thus liver disease alters normal drug metabolism. Treat-
patients with chronic renal disease, the following recommen- ment recommendations for patients with liver disease include
dations are made for those receiving hemodialysis: the following:
1. Consultation with the physician concerning current stage
1. Screen for hepatitis B and hepatitis C antigens and anti-
of disease, risk for bleeding, potential drugs to be pre-
bodies before any treatment.
2. Provide antibiotic prophylaxis to prevent endarteritis of scribed during treatment, and required alterations to peri-
the arteriovenous fistula or shunt. (IPD and CAPD patients odontal therapy.
2. Screening for hepatitis Band C.
do not generally require prophylactic antibiotics.)
3. Check laboratory values for PT and PTT.
3. Patients receive heparin anticoagulation on the day of
4. Check laboratory values for INR.
hemodialysis. Therefore periodontal treatment should
be provided on the day after dialysis, when the effects of For the liver transplant patient, as with kidney and other
heparinization have subsided. Hemodialysis treatments are organ transplantation, infection is a major concern. Transplant
generally performed 3-4 times a week. (IPD and CAPD pa- patients take immunosuppressive drugs that greatly reduce
tients are not systemically heparinized; therefore they usu- resistance to infection. Excessive bleeding may occur dur-
ally do not have the potential bleeding problems associated ing or after periodontal treatment because of drug-induced
with hemodialysis.) thrombocytopenia, anticoagulation, or both. Dental or peri-
4. Be careful to protect the hemodialysis shunt or fistula odontal infections are potentially life threatening. A pretrans-
when the patient is in the dental chair. If the shunt or fis- plantation evaluation is recommended to determine which
tula is placed in the arm, do not cramp the limb; BP read- teeth can be maintained without risk of infection. Teeth with
ings should be taken from the other arm. Do not use the limb severe bone and attachment loss, furcation invasion, peri-
for the injection of medication. Patients with leg shunts odontal abscesses, or extensive surgical requirements should
should avoid sitting with the leg dependent for longer than be extracted.
Hepatitis instrumentation, air syringe, or high-speed handpieces;

remember that saliva contains a distillate of the virus.
To date, six distinct viruses causing viral hepatitis have been Prerinsing with chlorhexidine gluconate for 30 s is
identified: hepatitis A, B, C, D, E, and G viruses. In addition, highly recommended.
a single-stranded DNA virus known as transfusion-transmitted g. When the procedure is completed, all equipment
virus has recently been identified in cases of acute and chronic should be scrubbed and sterilized. If an item cannot be
hepatitis; its role as an etiologic agent is still undetermined. sterilized or disposed of, it should not be used.
These forms of viral hepatitis differ in their virology, epi-
demiology, and prophylaxis. Since the majority of hepatitis If a percutaneous or permucosal injury occurs during den-
infections are undiagnosed, the clinician must be aware of tal treatment of a HBV carrier, the current Centers for Disease
high-risk groups, such as renal dialysis patients, healthcare Control and Prevention (CDC) guidelines recommend admin-
workers, immunosuppressed patients, patients who have re- istration of hepatitis B immune globulin (HBIG). The HBV vac-
ceived multiple blood transfusions, homosexuals, drug users, cine should also be administered if the injured individual has
and institutionalized patients. not previously received it. Unfortunately, postexposure pro-
The following guidelines are offered for treating hepatitis phylaxis with immune globulin or antiviral agents is generally
patients: ineffective if a percutaneous injury occurs during treatment of
a hepatitis C carrier.
1. If the disease, regardless of type, is active, do not provide
periodontal therapy unless the situation is an emergency. Pulmonary Diseases
In an emergency case, follow the protocol for patients posi-
The periodontal treatment of a patient with pulmonary dis-
tive for hepatitis B surface antigen (HBsAg).
ease may require alteration, depending on the nature and the
2. For patients with a past history of hepatitis, consult the
severity of the respiratory problem. Pulmonary diseases range
physician to determine the type of hepatitis, course and
from obstructive lung diseases (eg, asthma, emphysema, bron-
length of the disease, mode of transmission, and any
chitis, or acute obstruction) to restrictive ventilatory disorders
chronic liver disease or viral carrier state.
caused by muscle weakness, scarring, obesity, or any condi-
3. For recovered HAV or HEV patients, perform routine peri-
tion that could interfere with effective lung ventilation. Com-
odontal care.
bined restrictive-obstructive lung disease may also develop.
4. For recovered HBV and HDV patients, consult with the
The clinician should be aware of the signs and symptoms
physician and order HBsAg and anti-HBs (antibody to
of pulmonary disease, such as increased respiratory rate, cy-
HBV surface antigen) laboratory tests.
anosis, clubbing of the fingers, chronic cough, chest pain,
a. If HBsAg and anti-HBs tests are negative but HBV is
hemoptysis, dyspnea or orthopnea, and wheezing. Patients
suspected, order another HBs determination.
with these problems should be referred for medical evalua-
b. Patients who are HBsAg positive are probably infective
tion and treatment. Most patients with chronic lung disease
(chronic carriers); the degree of infectivity is measured
may undergo routine periodontal therapy if they are receiv-
by an HBsAg determination.
ing adequate medical management. Caution should be prac-
c. Patients who are anti-HBs positive may be treated rou-
ticed in relation to any treatment that may depress respiratory
tinely (they have antibody to HBsAg).
function.
d. Patients who are HBsAg negative may be treated rou-
Acute respiratory distress may be caused by a slight airway
tinely.
obstruction or depression of respiratory Junction. Due to their
5. For HCV patients, consult with the physician to determine
limited vital lung capacity, these patients also have decreased
the patient's risk for transmissibility and current status of
cough effectiveness. They must continually deal with the
the chronic liver disease.
mental anxiety caused by air hunger and alter their position
6. If a patient with active hepatitis, positive-HBsAg (HBV car-
in attempts to improve their ventilatory efficiency.
rier) status, or positive-HCV carrier status requires emer-
The following guidelines should be used during periodon-
gency treatment, use the following precautions:
tal therapy:
a. Consult the patient's physician regarding the status.
b. If bleeding is likely during or after treatment, measure 1. Identify and refer patients with signs and symptoms of
PT and bleeding time. Hepatitis may alter coagulation; pulmonary disease to their physician.
change treatment accordingly. 2. In patients with known pulmonary disease, consult with
c. All personnel in clinical contact with the patient should their physician regarding medications (antibiotics, ste-
use full-barrier technique, including masks, gloves, roids, and chemotherapeutic agents) and the degree and
glasses or eye shields, and disposable gowns. severity of pulmonary disease.
d. Use as many disposable covers as possible, covering 3. Avoid elicitation of respiratory depression or distress:
light handles, drawer handles, and bracket trays. Head- a. Minimize the stress of a periodontal appointment. The
rest covers should also be used. patient with emphysema should be treated in the af-
e. All disposable items (eg, gauze, floss, saliva ejectors, ternoon, several hours after sleep, to allow for airway
masks, gowns, or gloves) should be placed in a one- clearance.
lined wastebasket. After treatment, these items and all b. Avoid medications that could cause respiratory depres-
disposable covers should be bagged, labeled, and dis- sion (eg, narcotics, sedatives, or general anesthetics).
posed of, following proper guidelines for biohazardous c. Avoid bilateral mandibular-block anesthesia, which
waste. could cause increased airway obstruction.
f. Aseptic technique should be followed at all times. d. Position the patient to allow maximal ventilato-
Minimize aerosol production by not using ultrasonic ry efficiency, be careful to prevent physical airway
obstruction, keep the patient's throat clear, and avoid therapeutic levels. In contrast, 5 of 526 (0.95%) patients who
excess periodontal packing. experienced 575 interruptions of continuous anticoagulant
4. In a patient with a history of asthma, especially if asthma therapy, suffered serious embolic complications; 4 of these
attacks are frequent, make sure the patient's medication patients died. In a prospective study of 131 patients undergo-
(inhaler) is available. The inhaler should be readily acces- ing 511 extractions, patients whose oral anticoagulant therapy
sible on the countertop in the dental-treatment room. was reduced 72 h before surgery to achieve an INR of 1.5-2.0
5. Patients with active fungal or bacterial respiratory diseases (target 1.8) were found to have postoperative bleeding war-
should not be treated unless the periodontal procedure is ranting subsequent local intervention in 10 cases (15.1 %).
an emergency. There were only six cases (9.2%) in the group that continued
their oral anticoagulant therapy (mean INR = 2. 9).
Medications and Cancer Therapies These studies suggest that the risks of serious morbidity
associated with discontinuing anticoagulant or antiplatelet
Some medications prescribed to cure, manage, or prevent therapy should be avoided and that the risk of bleeding while
diseases have effects on periodontal tissues, wound healing, maintaining this therapy is minimal.
or the host immune response that require an understanding,
appreciation, and in some cases, modification of treatment. Corticosteroids
Bisphosphonates, anticoagulation medications, antiplatelet
medications, steroids, chemotherapy, and radiation therapy Patients who habitually use corticosteroids have an increased
are briefly addressed here. likelihood of developing hypertension, osteoporosis, and pep-
tic-ulcer disease. Care should be taken to minimize the risk of
adverse outcomes in these patients. BP should be monitored,
Bisphosphonates
and medications that may exacerbate peptic ulceration [eg,
Bisphosphonate medications are primarily used to treat cancer acetylsalicylic acid (ASA), NSAIDs] should be avoided.
(IV administration) and osteoporosis (oral administration). Stressful events, such as trauma, illness, surgery, emotional
They have also been tried as host-modulatory agents in the stress, or an athletic event, normally increase circulating en-
treatment of periodontitis. dogenous cortisol levels through the stimulation of the HPA
The major complication is development of bisphospho- axis. Pain appears to increase the requirement for cortisol re-
nate-related osteonecrosis of the jaw. This happens in patients lease. There is a concern that the normal release of cortisol in
who have been given large doses for a period of over 3 years. response to stressful events, such as a dental procedure, may
Hence, such patients are to be evaluated very carefully before be impaired in patients exposed to habitual corticosteroid use.
surgery or when implant placement is considered. Particularly Hence, the concern of whether patients who are habitually tak-
in patients on IV therapy of bisphosphonates, surgical proce- ing corticosteroids require perioperative supplementation for
dures are avoided. dental procedures. Historically, recommendations were based
on the medication type, amount, and duration of corticosteroid
use. However, the current thinking about the need for periop-
Anticoagulant/ Anti platelet Therapy
erative corticosteroid supplementation has been adjusted.
As stated earlier the current evidence indicates that these Studies investigating the stress response to minor general
medications should not be discontinued during periodontal and oral surgical procedures conclude that significant increas-
therapy. The risk of serious situations, such as embolism, is es in cortisol are generally not seen until 1- 5 h after surgery
much more important than that of bleeding. It is important to and appear to be associated more with postoperative pain and
study hematological values like bleeding time, clotting time, the loss of local anesthesia than with the preoperative- and
PT, INR ( <2), and PTT intraoperative stress of the procedure. In fact, the administra-
Controlled clinical studies have demonstrated that intra- tion of adequate analgesics in the postoperative period can
operative bleeding is not likely to be a problem with simple diminish the release (requirement) of cortisol.
extractions or periodontal surgery if antiplatelet therapy (eg, Evidence indicates that a vast majority of individuals with
aspirin) is continued. In these studies, there were no episodes adrenal insufficiency can receive routine dental treatment
of uncontrolled bleeding, all bleeding was controlled with lo- without the need for supplemental glucocorticosteroids. Pa-
cal measures, and there were no cases of postoperative bleed- tients taking corticosteroids usually have enough exogenous
ing problems. Conversely, the risk of stopping antiplatelet and endogenous cortisol to handle routine dental procedures
therapy may be serious. In a retrospective evaluation of 52 if their usual dose is taken within 2 h of the planned pro-
patients undergoing cataract surgery, 1 in 10 whose antiplate- cedure. Thus, for most patients, supplemental corticosteroid
let therapy was stopped or reduced, suffered a stroke. administration is not required when uncomplicated mi-
Similarly, clinical studies of patients on anticoagulant nor surgical procedures, including periodontal surgery, are
therapy undergoing extractions and other oral surgical pro- performed with local anesthesia with or without sedation.
cedures have demonstrated minimal bleeding problems when Topical corticosteroids generally have minimal HPA effect and
therapy is continued. In a review of the literature, Wahl et al steroid supplementation is not required for these patients.
reported that only 12 patients ( < 1.3%, 950 total) receiving Individuals who may be at risk for an adrenal crisis re-
continuous anticoagulant therapy required more than local quiring supplementation include those who are undergoing
measures to control hemorrhage after minor oral surgical pro- lengthy, major surgical procedures, those expected to have
cedures (2400 total). Most of the 950 patients had anticoagu- significant blood loss, and those who have an extremely low
lation levels that were well-above the currently recommended adrenal function. Low adrenal function can be identified with
therapeutic levels. Only three patients ( <0.31 %) had antico- an ACTH-stimulation test. For these individuals, consultation
agulation levels within or below the currently recommended with the physician and steroid supplementation is indicated.
lmmunosuppression and Chemotherapy Pregnancy

Immunosuppressed patients have impaired host defenses as The aim of periodontal therapy for the pregnant patient is to
a result of an underlying immunodeficiency or drug admin- minimize the potential exaggerated inflammatory response
istration (primarily related to organ transplantation or cancer related to pregnancy-associated hormonal alterations. Me-
chemotherapy). Since chemotherapy is often cytotoxic to the ticulous plaque control, scaling, root planing, and polishing
bone marrow, destruction of platelets and red and white blood should be the only nonemergency periodontal procedures
cells results in thrombocytopenia, anemia, and leukopenia. performed.
Immunosuppressed individuals are at an increased risk for The second trimester is the safest time to perform treat-
infection, and even minor periodontal infections can become ment. However, long, stressful appointments, as well as
life threatening if immunosuppression is severe. Bacterial, vi- periodontal surgical procedures, should be delayed until the
ral, and fungal infections may manifest intraorally. Patients re- postpartum period. As the uterus increases in size during the
ceiving bone-marrow transplantation require special attention second- and third trimesters, obstruction of the vena cava and
because these patients receive an extremely high dose of che- aorta may occur if the patient is placed in a supine position.
motherapy and are particularly susceptible to dissemination The reduction in return cardiac blood supply may cause su-
of oral infections. pine hypotensive syndrome, with decreased placental perfusion.
Treatment in these patients should be directed toward the Decreasing BP, syncope, and loss of consciousness may occur.
prevention of oral complications that could be life threatening. This can be prevented by placing the patient on her left side
The greatest potential for infection occurs during periods of or simply by elevating the right hip 5-6 in. during treatment.
extreme immunosuppression; therefore treatment should be Appointments should be short and the patient should be al-
conservative and palliative. It is always preferable to evaluate lowed to change positions frequently. A fully reclined position
the patient before the initiation of chemotherapy. Teeth with should be avoided if possible.
a poor prognosis should be extracted, with thorough debride- Other precautions during pregnancy relate to the potential
ment of remaining teeth to minimize the microbial load. The toxic or teratogenic effects of therapy on the fetus. Ideally, no
clinician must teach and emphasize the importance of good medications should be prescribed. However, analgesics, an-
oral hygiene. Antimicrobial rinses, such as chlorhexidine, are tibiotics, local anesthetics, and other drugs may be required
recommended, especially for patients with chemotherapy-in- during pregnancy, depending on the patient's needs. Before
duced mucositis, to prevent secondary infection. being prescribed, all drugs should be reviewed for potential
Chemotherapy is usually performed in cycles, with each adverse effects on the fetus.
cycle lasting several days, followed by intervening periods As for all patients, use of dental radiographs during preg-
of myelosuppression and recovery. If periodontal therapy is nancy should be kept to a minimum. The small amount of
needed during chemotherapy, it is best done the day before radiation exposure during diagnostic dental radiography
chemotherapy is given, when white-blood cell counts are poses little, if any, risk to the fetus as long as the mother is
relatively high. Coordination with the oncologist is critical. properly shielded. The ADA has stated that "normal radio-
Dental treatment should be done when white cell counts are graphic guidelines do not need to be altered because of preg-
above 2000 mm:", with an absolute granulocyte count of nancy." Use of a properly positioned lead apron is an absolute
1000-1500 mrrr '. requirement.
Radiation Therapy Infectious Diseases

The use of radiotherapy, alone or in conjunction with surgi- Since many infectious diseases are occult in nature and be-
cal resection, is common in the treatment of head- and neck cause medical histories are often inaccurate or incomplete, all
tumors. The side effects of ionizing radiation include dra- periodontal patients should be treated as though they have an
matic perioral changes of significant concern to dental-health infectious disease. Protection of patients, clinicians, and office
personnel. The extent and severity of mucositis, dermatitis, staff requires the use of universal (standard) precautions for
xerostomia, dysphagia, gustatory alteration, radiation caries, all patients, maximizing prevention of infection and crosscon-
vascular changes, trismus, temporomandibular Joint degener- tamination. This section provides a brief discussion of hepati-
ation, and periodontal change depend on the type of radiation tis and tuberculosis in relation to the precautions required in
used, fields of irradiation, number of ports, types of tissues in periodontal therapy.
the fields, and dosage.
Periodontal care is important before and after radiation
Tuberculosis
therapy. Complete periodontal examination including radio-
graphs must be carried out and basic periodontal therapy The patient with tuberculosis should receive only emergency
including extraction of teeth with questionable prognosis care, following the guidelines listed in the section on hepatitis
should be completed before the start of radiation therapy. under "Liver Diseases." If the patient has completed chemo-
Post radiation therapy, there is always a risk of osteoradio- therapy, the patient's physician should be consulted regarding
necrosis, which does not decrease with time. Development of infectivity and the results of sputum cultures for Mycobacte-
xerostomia is a serious concern. Hence palliative therapy is rium tuberculosis. When medical clearance has been given and
recommended at this stage as any surgery, extractions, etc., the sputum culture results are negative, these patients may
may cause osteoradionecrosis. Fluoride treatments, regular be treated normally. Any patient who gives a history of poor
noninvasive oral prophylaxis, and salivary substitution are re- medical follow-up (eg, lack of yearly chest radiographs) or
quired. Use of ultrasonic scalers should be avoided because of shows signs or symptoms indicative of tuberculosis should
the brittleness of the teeth. be referred for evaluation. Adequate treatment of tuberculosis
requires a minimum of 18 months and thorough posttreat- Detection, Evaluation, and Treatment of High Blood Pressure QNC 7):
ment follow-up should include chest radiographs, sputum resetting the hypertension sails, Hypertension 41: 1178-1179, 2003.
Marx RE: Oral and intravenous bisphosphonate-induced osteonecrosis of the jaws,
cultures, and a review of the patient's symptoms by the physi- Hanover Park, 2007, Quintessence.
cian at least every 12 months. Mealey BL: Periodontal implications: medically compromised patients, Ann
Periodontol 1:256-321, 1996.
Mealey BL: Impact of advances in diabetes care on dental treatment of the
Hepatitis diabetic patient, Compend Cantin Educ Dent 19:41-44, 1998.
Pallasch TJ, Slots J: Antibiotic prophylaxis and the medically comprised
Please refer to the section under "Liver Diseases." patient, Pelidontol 2000 10:107, 1996.
Wade ML, Suzuki JB: Issues related to diagnosis and treatment of bisphos-
phonate-induced osteonecrosis of the jaws, Grnnd Rounds Ornl-Sys Med
SUGGESTED READINGS 2:46-53, 2007.
American Academy of Orthopaedic Surgeons and the American Dental As- Wilson W, Taubert KA, Gewitz M, et al: Prevention of infective endocardi-
sociation: Evidence-based guideline and evidence report. Prevention of tis: guidelines from the American Heart Association: a guideline from the
orthopaedic implant infection in patients undergoing dental procedures. American Heart Association Rheumatic Fever, Endocarditis and Kawasaki
2012. http://www.aaos.org/research/guidelines/PUD P/PUD P _guideline. pdf. Disease Committee Council on Cardiovascular Disease in the Young, and
The sixth report of the Joint National Committee on prevention, detection, the Council on Clinical Cardiology Council on Cardiovascular Surgery and
evaluation, and treatment of high blood pressure QNC VI) Arch Intern Med Anesthesia, and the Quality of Care and Outcomes Research Interdisciplin-
157:2413-2446, 1997. ary Working Group,] Am Dent Assoc 138(6):739-760, 2007.
Lenfant C, Chobanian AV, Jones OW, et al: Joint National Committee on the Yagiela JA: Adverse drug interactions in dental practice: interactions associ-
Prevention, Detection, Evaluation, and Treatment of High Blood Pres- ated with vasoconstrictors. Part Vof a series,] Am Dent Assoc 130:701-709,
sure: Seventh report of the Joint National Committee on the Prevention, 1999.
31
Treatment of Aggressive and
Atypical Forms of Periodontitis
PR Klokkevold • A Uppoor
Chapter Outline
Aggressive Periodontitis Necrotizing Ulcerative Periodontitis
Periodontitis Refractory to Treatment
The majority of patients with common forms of periodontal some patients with aggressive periodontitis. Also, in a small
disease respond predictably well to conventional therapy, in- number of cases, a systemic disease, such as neutropenia,
cluding oral hygiene instruction, nonsurgical debridement, can be identified that clearly explains the unusual severity of
surgery, and supportive periodontal maintenance. However, the periodontal disease for that individual. In most patients
patients diagnosed with aggressive and some atypical forms with aggressive periodontitis, however, systemic diseases or
of periodontal disease often do not respond as predictably or disorders cannot be identified. In fact, the irony is that these
as favorably to conventional therapy. Fortunately, only a small patients are typically quite healthy. Numerous attempts to
percentage of patients with periodontal disease are diagnosed examine immunologic profiles in patients with aggressive
with aggressive periodontitis. Patients who are diagnosed periodontitis have failed to identify any specific etiologic
with periodontal disease (any type) that is refractory to treat- factors common to all patients.
ment present in small numbers as well. Even fewer patients The prognosis for patients with aggressive periodontitis de-
are diagnosed with necrotizing ulcerative periodontitis. Each pends on (1) whether the disease is generalized or localized,
of these atypical disease entities poses significant challenges (2) the degree of destruction present at the time of diagnosis,
for the clinician not only because they are infrequently en- and (3) the ability to control future progression. Generalized
countered but also because they may not respond favorably aggressive periodontitis rarely undergoes spontaneous remis-
to conventional periodontal therapy. Furthermore, the severe sion, whereas localized forms of the disease have been known
loss of periodontal support associated with these cases leaves to arrest spontaneously. This unexplained curtailment of dis-
the clinician faced with uncertainty about treatment outcomes ease progression has sometimes been referred to as a "burn-
and difficulty in making decisions about whether to save com- out" of the disease. It appears that cases of localized aggressive
promised teeth or to extract them. periodontitis often have a limited period of rapid periodontal
attachment and alveolar bone loss, followed by a slower, more
chronic phase of disease progression. Overall, patients with
Aggressive Periodontitis generalized aggressive periodontitis tend to have a poorer
Aggressive periodontitis, by definition, causes rapid de- prognosis because they typically have more teeth affected by
struction of the periodontal attachment apparatus and the the disease and because the disease is less likely to go sponta-
supporting alveolar bone. The responsiveness of aggressive neously into remission compared with patients with localized
periodontitis to conventional periodontal treatment is unpre- forms of aggressive periodontitis.
dictable, and the overall prognosis for these patients is poorer
than for patients with chronic periodontitis. Because these
Therapeutic Modalities
patients do not respond "normally" to conventional meth-
ods and their disease progresses unusually fast, the logical Early detection is critically important in the treatment of aggres-
question is whether there are problems associated with an sive periodontitis (generalized or localized) because preventing
impaired host immune response that may contribute to such further destruction is often more predictable than attempting to
a different disease and result in a limited response to the usual regenerate lost supporting tissues. Therefore, at the initial diag-
therapeutic measures. Indeed, defects in polymorphonuclear nosis, it is helpful to obtain any previously taken radiographs to
leukocyte (PMN, neutrophil) function have been identified in assess the rate of progression of the disease. Together with future
353
radiographs, this documentation will also facilitate the clinician's It is important to realize the limitations of surgical therapy
assessment of treatment success and control of the disease. and to appreciate the possible risk that surgical therapy may
Treatment of aggressive periodontitis must be pursued with further compromise teeth that are mobile because of extensive
a logical and regimented approach. Several aspects of treat- loss of periodontal support. For example, in a patient with
ment must be particularly considered when managing a pa- severe horizontal bone loss, surgical resective therapy may re-
tient with aggressive periodontitis. One of the most important sult in increased tooth mobility that is difficult to manage, and
aspects of treatment success is to educate the patient about the a nonsurgical approach may be indicated. Therefore careful
disease, including the causes and the risk factors for disease, evaluation of the risks versus the benefits of surgery must be
and to stress the importance of the patient's role in the success considered on a case-by-case basis.
of treatment. Essential therapeutic onsiderations for the clini-
cian are to control the infection, arrest disease progression, Regenerative Therapy. The concept and application of peri-
correct anatomic defects, replace missing teeth, and ultimately odontal regeneration has been established in patients with
help the patient maintain periodontal health with frequent chronic forms of periodontal disease. The use of regenera-
periodontal maintenance care. Educating family members is tive materials, including bone grafts, barrier membranes, and
another important factor because aggressive periodontitis is wound-healing agents, are well documented and often used.
known to have familial aggregation. Thus family members, Intrabony defects, particularly vertical defects with multiple
especially younger siblings, of the patient diagnosed with ag- osseous walls, are often amenable to regeneration with these
gressive periodontitis should be examined for signs of disease, techniques. Most of the success and predictability of peri-
educated about preventive measures, and monitored closely. It odontal regeneration have been achieved in patients with
cannot be stressed enough that early diagnosis, intervention, chronic periodontitis; much less evidence is available about
and if possible, prevention of disease is more desirable than the use of periodontal regeneration for patients with aggres-
attempting to reverse the destruction that results from aggressive periodontitis.
sive periodontitis. Periodontal regenerative procedures have been successfully
demonstrated in patients with localized aggressive periodon-
Conventional Periodontal Therapy titis in some clinical case reports. Dodson et al demonstrated
Conventional periodontal therapy for aggressive periodonti- the regenerative potential of a severe, localized osseous defect
tis consists of patient education, oral hygiene improvement, around a mandibular incisor in a healthy, 19-year-old black
scaling and root planing, and regular (frequent) recall main- man diagnosed with localized aggressive periodontitis. The
tenance. It may or may not include periodontal flap surgery. patient presented with severe bone loss localized around one
Unfortunately, the response of aggressive periodontitis to con- of the mandibular incisors. Using open-flap surgical debride-
ventional therapy alone has been limited and unpredictable. ment, root surface conditioning (tetracycline solution), and
Patients who are diagnosed with aggressive periodontitis at an allogenic bone graft reconstituted with sterile saline and
an early stage and who are able to enter therapy may have a tetracycline powder, the surgeons reduced the probing pocket
better outcome than those who are diagnosed at an advanced depth from 9 to 12 mm down to 1 to 3 mm (3 mm of reces-
stage of destruction. In general, the earlier the disease is diag- sion was noted), and significant bone fill of the defect (about
nosed, the more conservative the therapy and the more pre- 80%) was reported (Fig. 31.1). This case illustrates the poten-
dictable the outcome. tial for healing severe defects in patients with localized aggres-
Teeth with moderate to advanced periodontal attachment sive periodontitis, especially when local factors are controlled
loss and bone loss often have a poor prognosis and pose the and sound surgical principles are followed. The authors cited
most difficult challenge. Depending on the condition of the several factors that likely contributed to the success of this
remaining dentition, treatment of these teeth may have a lim- case, including a probable transition of disease activity from
ited prospect for improvement and may even diminish the aggressive to chronic, tooth stabilization before surgery, sound
overall treatment success for the patient. Clearly, some of surgical management of hard and soft tissues, and good post-
these teeth should be extracted; however, other teeth may be operative care.
pivotal to the stability of that individual's dentition, and thus It is important to note that although the potential for re-
it may be desirable to attempt treatment to maintain them. generation in patients with aggressive periodontitis appears to
Treatment options for teeth with deep periodontal pockets be good, expectations are limited for patients with severe bone
and bone loss may be nonsurgical or surgical. Surgery may loss. This is especially true if the bone loss is horizontal and if
be purely resective, regenerative, or a combination of these it has progressed to involve furcations.
approaches.
Antimicrobial Therapy
Surgical Resective Therapy. Resective periodontal surgery The presence of periodontal pathogens, specifically Aggre-
can be effective to reduce or eliminate pocket depth in pa- gatibacter actinomycetemcomitans, has been implicated as
tients with aggressive periodontitis. However, it may be dif- the reason that aggressive periodontitis does not respond to
ficult to accomplish if adjacent teeth are unaffected, as often conventional therapy alone. These pathogens are known to
seen in cases of localized aggressive periodontitis. If a signifi- remain in the tissues after therapy to reinfect the pocket. In
cant height discrepancy exists between the periodontal sup- the late 1970s and early 1980s, the identification of A. acti-
port of the affected tooth and the adjacent unaffected tooth, nomycetemcomitans as a major culprit and the discovery that
the gingival transition (following the bone) will often result in this organism penetrates the tissues offered another perspec-
deep probing pocket depth around the affected tooth despite tive to the pathogenesis of aggressive periodontitis and offered
surgical efforts. A less-than-ideal outcome must be taken into new hope for therapeutic success, namely, antibiotics. The use
consideration before deciding to treat increased pocket depth of systemic antibiotics was thought to be necessary to elimi-
surgically. nate pathogenic bacteria (especially A actinomycetemcomitans)
31 Treatment of Aggressive and Atypical Forms of Periodontitis 355
(D)
FIGURE 31.1 Clinical photographs and periapical radiographs demonstrating regenerative success in patient with localized aggressive peri-
odontitis. A, Periapical radiograph of the right lateral incisor at the initial diagnosis. Notice the severe, vertical bone loss associated with the right
lateral incisor. Tooth has been splinted to adjacent teeth for stability. B, Facial view of the circumferential osseous defect around the lower right lateral
incisor during open flap surgery. There is complete loss of buccal, lingual, mesial, and distal bone around the lateral incisor, with minimal bone sup-
port limited to the apical few millimeters. C, Facial view of reentered surgical site 1 year after treatment. Bone fill around all surfaces demonstrates
remarkable potential for regeneration of a large osseous defect in a young patient with localized aggressive periodontitis. D, Periapical radiograph
taken 1 year after regenerative therapy. Note the increased radiopacity and bone fill. (From Dodson SA, Takei HH, Carranza FA Jr: Int J Periodont Restor
Dent 7 6:455, 7 996.)
from the tissues. Indeed, several authors have reported suc- under local anesthesia over two treatment appointments, and
cess in the treatment of aggressive periodontitis using antibi- the patient was treated with systemic amoxicillin (500 mg,
otics as adjuncts to standard therapy. 3 times a day for 2 weeks) during the period of treatment.
There is compelling evidence that adjunctive antibiotic All areas responded favorably with probing pocket depths
treatment frequently results in a more favorable clinical re- decreasing from 3 to 13 mm down to 2 to 5 mm. Bleeding
sponse than mechanical therapy alone. Systemic antimicrobi- on probing diminished from generalized to very few isolated
als in conjunction with scaling and root planing offer benefits areas. He has been on periodontal maintenance with good re-
over scaling and planing alone in terms of clinical attachment sults for more than 5 years.
level, probing pocket depth, and reduced risk of additional at- Clearly, numerous studies support the use of adjunc-
tachment loss. Patients with deeper, progressive pockets seem tive tetracycline along with mechanical debridement for the
to benefit the most from systemic administration of adjunctive treatment of A. actinomycetemcomitans-associated aggressive
antibiotics. Many different antibiotic types and regimens were periodontitis (Box 31.1). Given the possible emergence of
reviewed. tetracycline-resistant A. actinomycetemcomitans, there is con-
Figure 31.2 shows the before and after results of an aggres- cern that tetracycline may not be effective. In these cases the
sive periodontitis case treated nonsurgically with scaling and combination of metronidazole and amoxicillin may be ad-
root planing and adjunctive antibiotic therapy. The patient, a vantageous. The combination of these two antibiotics with
34-year-old Asian male, presented with a complaint of loose conventional periodontal therapy provides better disease con-
teeth and bleeding gums. He requested treatment to save his trol and better clinical improvement in attachment levels in
teeth. Treatment consisted of patient education including oral difficult-to-manage periodontitis cases than similar periodon-
hygiene instructions and nonsurgical therapy with adjunctive tal therapy without antibiotics. Similar effects were seen for a
antibiotics. All teeth were thoroughly scaled and root planed variety of antibiotic types. However, a lack of sufficient sample
sizes among studies makes it difficult to offer specific recom- particular infection probably depends on the case. Choices must
mendations about which antibiotics were most effective. be made based on patient-related and disease-related factors.
The criteria for selection of antibiotics are not clear. Good
clinical and microbiologic responses have been reported with Microbial Testing. Some investigators and clinicians ad-
several individual antibiotics and antibiotic combinations vocate microbial testing to identify the specific periodontal
(Table 31.1). The optimal antibiotic or combination for any pathogens responsible for disease and to select an appropriate
FIGURE 31.2 lntraoral clinical photographs and full-mouth radiographs (before and after treatment) of a 34-year-old Asian male with aggressive
periodontitis. A and B, lntraoral clinical photographs of pretreatment periodontal condition. Note the gingival edema, inflammation, and bleeding.
Probing pocket depths ranged from 3 to 13 mm with generalized bleeding on probing and purulent exudate. C, Pretreatment full-mouth radiographs
demonstrating generalized severe horizontal bone loss. Note the periapical radiolucency at the apex of the upper left premolar indicating pulpal
disease. D and E, lntraoral clinical photographs of posttreatment (5 years) results. Treatment included nonsurgical scaling and root planing along with
adjunctive systemic antibiotics (amoxicillin). Patient improved oral hygiene and continued to be seen for professional maintenance every 3 months.
Probing pocket depths have been maintained in the range of 2-5 mm with only a few localized areas of bleeding on probing. F, Posttreatment (5 years)
full-mouth radiographs demonstrating no additional bone loss. Endodontically involved maxillary premolar was extracted and replaced with a remov-
able partial denture.
(Continued)
FIGURE 31.2 (cont.)
antibiotic based on sensitivity and resistance. There may be In practice, antibiotics are often used empirically without
specific cases in which bacterial identification and antibiotic- microbial testing. Nonetheless, the use of microbial testing
sensitivity testing is invaluable. For example, in localized should be considered whenever a case of aggressive periodon-
aggressive periodontitis cases, tetracycline-resistant Actinoba- titis is not responding or if the destruction continues despite
cillus species have been suspected. If antibiotic susceptibility good therapeutic efforts.
tests determine that tetracycline-resistant species exist in the
lesion, the clinician may be advised to consider another anti- local Delivery. The use of local delivery to administer an-
biotic or an antibiotic combination, such as amoxicillin and tibiotics offers a novel approach to the management of peri-
metronidazole. odontal "localized" infections. The primary advantage of local
BOX 31.1 Systemic Tetracycline in Treatment of Aggressive Periodontitis

Systemic tetracycline (250 mg of tetracycline hydrochloride four begin taking the antibiotic approximately 1 h before surgery.
times daily for at least 1 week) should be given in conjunction Doxycycline, 100 mg/day, may be used instead of tetracycline.
with local mechanical therapy. If surgery is indicated, systemic Chlorhexidine rinses should be prescribed and continued for
tetracycline should be prescribed and the patient instructed to several weeks to enhance plaque control and facilitate healing.
TABLE 31.1
ANTIBIOTIC THERAPY FOR AGGRESSIVE PERIODONTITIS

Associated Microflora Antibiotic of Choice
Gram-positive organisms Amoxicillin-clavulanate potassium (Augmentin)

Gram-negative organisms Clindamycin
Nonoral Gram-negative, facultative rods Ciprofloxacin
Pseudomonads, Staphylococci
Black-pigmented bacteria and Spirochetes Metronidazole
Prevotella intermedia, Porpliyromonas gingivalis Tetracycline
Aggregatibacter actinomycetemcomitans Metronidazole-amoxicillin
Metronidazole-ciprofloxacin
Tetracycline
P gingivalis Azithromycin
therapy is that smaller total dosages of topical agents can be Treatment Planning and Restorative
delivered inside the pocket, avoiding the side effects of sys-
Considerations
temic antibacterial agents while increasing the exposure of the
target microorganisms to higher concentrations, and therefore Successful management of patients with aggressive periodon-
more therapeutic levels, of the medication. Local delivery titis must include tooth replacement as part of the treatment
agents have been formulated in many different forms, includ- plan. In some advanced cases of aggressive periodontitis, the
ing solutions, gels, fibers, and chips. overall treatment success for the patient may be enhanced if
severely compromised teeth are extracted. The outcome of
Full-Mouth Disinfection treatment for these teeth is limited, and more importantly, the
Another approach to antimicrobial therapy in the control of retention of severely diseased teeth over time may result in
infection associated with periodontitis is the concept of full- additional bone loss and teeth that are further compromised.
mouth disinfection. The concept, described by Quirynen The risk of further bone loss is even a greater concern now
et al, consists of full-mouth debridement (removal of all with the current success and predictability of dental implants
plaque and calculus) completed in two appointments within and the desire to preserve bone for implant placement. Any
a 24-hour period. In addition to scaling and root planing, the additional alveolar bone loss in an area that has already un-
tongue is brushed with a chlorhexidine gel (1 %) for 1 min- dergone severe bone loss may further compromise residual
ute, the mouth is rinsed with a chlorhexidine solution (0.2 %) anatomy and impair the opportunity for tooth replacement
for 2 minutes, and periodontal pockets are irrigated with a with a dental implant. This is especially true for certain ar-
chlorhexidine solution (1 %). eas with poor bone quality or limited bone volume, such as
A few reports have included patients with aggressive the posterior maxilla. Fortunately, healing of extraction sites is
(early-onset) periodontitis in their evaluation of the one- typically uneventful in patients with aggressive periodontitis,
stage, full-mouth disinfection protocol. As with the ad- and bone augmentation of defect sites is predictable.
vanced chronic periodontitis group, De Soete et al found a When hopeless teeth are extracted, they need to be re-
significant reduction in probing pocket depth and gain in placed. The desire to replace missing teeth in a permanent
clinical attachment in patients with aggressive periodonti- manner without preparation of adjacent teeth for a fixed par-
tis up to 8 months after treatment compared with controls tial denture motivated clinicians to attempt transplantation of
(scaling and root planing by quadrant at 2-week inter- teeth from one site to another. Transplantation of developing
vals). They also found significant reductions in periodontal third molars to the sockets of hopeless first molars has been
pathogens up to 8 months after therapy. Porphyromonas gin- attempted with limited success. Clearly, the success and pre-
givalis and Tannerella forsythia were reduced to levels below dictability of dental implants have obviated the need for at-
detection. tempting to transplant teeth to edentulous sites.
Host Modulation Use of Dental Implants

A novel approach in the treatment of aggressive periodontitis Initially, the use of dental implants was suggested and imple-
and difficult-to-control forms of periodontal disease is the ad- mented with much caution in patients with aggressive peri-
ministration of agents that modulate the host response. Sev- odontitis because of an unfounded fear of bone and implant
eral agents have been used or evaluated to modify the host loss. However, evidence to the contrary appears to support
response to disease. the use of dental implants in patients treated for aggressive
periodontal disease. Thus it is possible to consider the use of concluding that a case truly is refractory. A patient with peri-
dental implants in the overall treatment plan for patients with odontitis that is refractory to treatment often does not have any
aggressive periodontitis. distinguishing clinical characteristics on initial examination
compared with cases of periodontitis that respond normally.
Clinical Consideration. It is important to recognize that Therefore the initial treatment would follow conventional
special consideration must be given to the risk of occlusal therapeutic modalities for periodontitis. After treatment, if the
overload of implants placed in a periodontally compromised patient has not responded as expected, the clinician should
dentition. This is especially true when only one or a few im- rule out the following conditions:
plants are used to replace a limited number of teeth with an
1. Inadequately treated periodontitis. Most forms of periodon-
implant-supported fixed crown or bridge in a patient with a
titis can be treated effectively with currently available
majority of the remaining dentition being mobile. The immo-
modalities if they are performed properly. After treat-
bility of implants in a dentition that does not have a stable
ment, if it is determined that the patient has not respond-
vertical occlusal stop may lead to implant overloaded.
ed, the clinician must evaluate whether the therapy was
adequately performed. Undetected or inaccessible sub-
gingival calculus may be present in one or more areas.
Periodontal Maintenance Retreatment may be the best way to ensure that therapy
was adequately performed. All root surfaces must be me-
When patients with aggressive periodontitis are transferred
ticulously inspected.
to maintenance care, their periodontal condition must be
2. Poor plaque control. Plaque control is essential to the suc-
stable (i.e., no clinical signs of disease and no periodontal
cess of periodontal therapy. Patients must understand the
pathogens). Each maintenance visit should consist of a med-
role of bacterial plaque in their disease process, and they
ical history review, an inquiry about any recent periodontal
must comply with daily oral hygiene instructions. Thus
problems, assessment risk of factors, a comprehensive peri-
patient compliance and the adequacy of their daily plaque
odontal and oral examination, thorough root debridement,
control should be assessed before concluding that a case of
and prophylaxis, followed by a review of oral hygiene in-
periodontitis is refractory to treatment.
structions. If oral hygiene is not good, patients may benefit
3. Endodontic infection. The presence of nonperiodontal infec-
most from a review of oral hygiene instructions and visual-
tions in the area can perpetuate periodontal disease activ-
ization of plaque in their own mouth before debridement
ity and prevent a normal healing response to conventional
and prophylaxis.
periodontal therapy. Endodontic infection of teeth in the
Frequent maintenance visits appear to be one of the most
area should be suspected and ruled out before concluding
important factors in the control of disease and the success of
that a case is refractory to treatment. The clinician should
treatment in patients with aggressive periodontitis. A support-
suspect an endodontic etiology especially in those patients
ive periodontal maintenance program aimed at early detection
with localized recurrent disease.
and treatment of sites that begin to lose attachment should be
established. The duration between these recall visits is usu- A case may be considered refractory to treatment only when
ally short during the first period after the patient's comple- loss of periodontal attachment and bone continues after well-
tion of therapy, generally no longer than 3-month intervals. executed treatment in a patient with good oral hygiene and no
Acute episodes of gingival inflammation can be detected and other infections or etiologic factors.
managed earlier when the patient is on a frequent monitoring Clinicians are in a quandary when presented with a patient
cycle. Monitoring as frequently as every 3 to 4 weeks may be who is not responding to periodontal therapy. Therapeutic
necessary when the disease is thought to be active. If signs of means must be broad in scope and thorough to ensure that
disease activity and progression persist despite therapeutic ef- all aspects of the host response are addressed. At a minimum,
forts, frequent visits and good patient compliance, microbial a frequent and intensive recall maintenance and home care
testing may be indicated. The rate of disease progression may program is necessary. Mechanical debridement with scaling
be faster in younger individuals, and therefore the clinician and root planing can reduce total supragingival and subgin-
should monitor such patients more frequently. Over time the gival bacterial masses, but major periodontal pathogens may
recall maintenance interval can be adjusted (more or less of- persist. Surgical treatment may aid in providing access for
ten) to suit the patient's level of oral hygiene and control of debridement and in elimination of bacterial pathogens. In ad-
disease, as determined by each examination. dition, the morphology of the gingival tissues should be modi-
fied to facilitate daily plaque removal by the patient.
Periodontitis Refractory to Treatment Systemic antibiotic therapy is administered to reinforce
mechanical periodontal treatment and support the host de-
Although refractory periodontitis is not currently considered fense system in overcoming the infection by killing subgin-
a separate disease entity, patients who fail to respond to con- gival pathogens that remain after conventional mechanical
ventional therapy are considered to have periodontitis that is periodontal therapy. Many antibiotics have been used accord-
"refractory" to treatment. It is possible to characterize any form ing to the target microflora with various degrees of success
of periodontal disease (e.g., chronic periodontitis, aggressive (Table 31.1). For patients with refractory disease who fail to
periodontitis) as refractory to treatment. respond to initial antibiotic therapy, subsequent treatment
These cases are difficult to manage because the etiology should include microbial testing with bacterial identification
behind their lack of response to therapy is unknown. Initially, and antimicrobial susceptibility.
because contributing factors may have been overlooked, it Antibiotic resistance is a potential problem. Patients with
is important to evaluate the adequacy of treatment attempts periodontitis that is refractory to treatment often present with
thoroughly and to consider other possible etiologies before a history of previous tetracycline therapy, and thus they may
have a microflora that is resistant to this drug. Tetracycline- occurs, the clinician should consider a different antimicro-
resistant bacteria have been isolated from patients with peri- bial therapy based on microbial susceptibility analysis. At this
odontitis refractory to treatment. However, some patients with point in the therapy, strong consideration should be given to
refractory disease may still benefit from the use of tetracycline consulting with the patient's physician for an evaluation of a
or one of its derivatives. possible host immune system deficiency or a metabolic prob-
Cases of periodontitis (refractory) in which the associated lem such as diabetes.
microflora consists primarily of Gram-positive microorganisms
have been successfully treated with amoxicillin-clavulanate po-
tassium. Many efforts have been made to establish the most Necrotizing Ulcerative Periodontitis
appropriate regimen of antibiotic therapy for these patients.
Similar antimicrobial regimens, consisting of 250 mg of amox- Necrotizing ulcerative periodontitis (NUP) is a rare disease,
icillin and 125 mg of clavulanate potassium, have been ad- especially in developed countries. These patients often have
ministered 3 times daily for 14 days, with scaling and root an underlying predisposing systemic factor that renders them
planing, and produced a reduction in attachment loss for at susceptible to necrotizing ulcerative periodontal disease. For
least 12 months. A regimen of one capsule containing the this reason, patients presenting with NUP should be treated in
same amount of drug every 6 h for 2 weeks, with intrasulcular consultation with their physician.
full-mouth lavage using a 10% povidone-iodine solution and A comprehensive medical evaluation and diagnosis of any
chlorhexidine oral rinses twice daily, resulted in a reduction in condition that may be contributing to an altered host immune
attachment loss that persisted at approximately 34 months. A response should be completed. It is also important to rule out
regimen of 500 mg of metronidazole 3 times daily for 7 days any hematologic disease (eg, leukemia) before initiating treat-
was shown to be effective in treating periodontitis (refractory) ment of a case that has a similar presentation to NUP
in patients who were culture positive for T forsythia in the Treatment can be initiated only after a thorough medi-
absence of A actinomycetemcomitans. cal history and examination to identify the existence of any
Clindamycin is a potent antibiotic that penetrates well into systemic diseases. Treatment for NUP includes local debride-
gingival fluid, although it is not usually effective against A ment of lesions with scaling and root planing, lavage, and
actinomycetemcomitans and Eikenella corrodens. However, instructions for good oral hygiene. It may be necessary to
clindamycin has been effective in controlling the extent and use local anesthesia during the debridement because lesions
rate of disease progression in refractory cases in patients who are frequently painful. The use of ultrasonic instrumentation
have a microflora susceptible to this antibiotic. A regimen of with profuse irrigation may enhance debridement and flush-
clindamycin hydrochloride, 150 mg, 4 times daily for 7 days, ing of the deep lesions. Achieving good oral hygiene may
combined with scaling and root planing produced a decrease be challenging as well until the lesions and associated pain
in the incidence of disease activity from an annual rate of 8% resolve.
to an annual rate of 0.5% of sites per patient. Clindamycin Antimicrobial adjuncts, such as chlorhexidine, added to
should be prescribed with caution because of the potential the oral hygiene regimen may be effective in contributing to
for pseudomembranous colitis from superinfections with the daily reduction of bacterial loads. Patients frequently com-
Clostridium difficile. Patients should be warned and advised to plain of pain. The use of locally applied topical antimicrobials
discontinue the antibiotic if symptoms of diarrhea develop. and systemic antibiotics, as well as systemic analgesics, should
Azithromycin may be effective in periodontitis that is re- be used as indicated by signs and symptoms.
fractory to treatment, especially in patients infected with Patients with NUP often harbor bacteria, fungi, viruses,
P gingivalis. and other nonoral microorganisms, complicating the selec-
Combinations of antibiotic therapy may offer greater prom- tion of antimicrobial therapy Superinfection or overgrowth of
ise as adjunctive treatment for the management of refractory fungi and viruses may be propagated by antibiotic therapy
periodontitis. The rationale is based on the diversity of puta- Antifungal and/or antiviral agents can be considered prophy-
tive pathogens and no single antibiotic being bactericidal for all lactically against these infections or after they are diagnosed.
known pathogens. Combination antibiotic therapy may help Since oral hygiene for these patients is complicated by the
broaden the antimicrobial range of the therapeutic regimen be- painful lesions, alternative methods should be encouraged. In
yond that attained by any single antibiotic. Other advantages such patients, irrigation with diluted cleansing and antibacte-
include lowering the dose of individual antibiotics by exploit- rial agents can be of some benefit.
ing possible synergy between two drugs against targeted organ- Ultimately, the successful treatment of NUP may depend
isms. In addition, combination therapy may prevent or fore- on the resolution or treatment of the systemic condition (eg,
stall the emergence of bacterial resistance. Many combinations immune compromise) that predisposed the individual to the
of antibiotics have demonstrated significant improvement in disease. Evaluation and treatment of patients with known sys-
the clinical aspects of the disease. Examples of combinations temic conditions, such as HIV infection, should be coordi-
include amoxicillin-clavulanate or metronidazole-amoxicil- nated with the patient's physician.
lin for the treatment of A actinomycetemcomitans-associated
periodontitis; metronidazole-doxycycline for the prevention
of recurrent periodontitis; metronidazole-ciprofloxacin for the SUGGESTED READINGS
treatment of recurrent cases containing a microflora associ- Al-Zahrani MS: Implant therapy in aggressive periodontitis patients: a system-
ated with enteric rods and pseudomonads; and amoxicillin- atic review and clinical implications, Quintessence Int 39:211-215, 2008.
doxycycline in the treatment of periodontitis associated with Bollen CM, Mongardini C, Papaioannou W, et al: The effect of a one-stage
full-mouth disinfection on different intra-oral niches. Clinical and micro-
A. actinomycetemcomitans and P gingivalis. biological observations,) Clin Periodontal 25:56-66, 1998.
Some cases of periodontitis that are refractory to treatment Buchmann R, Nunn ME, Van Dyke TE, et al: Aggressive periodontitis: 5-year
may not respond to a given antibiotic regimen. When this follow-up of treatment,) Peliodontol 73:675-683, 2002.
Haffajee AD, Uzel NG, Arguello EI, et al: Clinical and microbiological changes Nevins M, Langer B: The successful use of osseointegrated implants for the
associated with the use of combined antimicrobial therapies to treat "refrac- treatment of the recalcitrant periodontal patient,] Periodontol 66:150-157,
tory" periodontitis, J Clin Periodontal 31 :869-877, 2004. 1995.
Herrera D, Sanz M,Jepsen S, et al: A systematic review on the effect of system- Quirynen M, Mongardini C, de Soete M, et al: The role of chlorhexidine in
ic antimicrobials as an adjunct to scaling and root planing in periodontiris the one-stage full-mouth disinfection treatment of patients with advanced
patients,] Clin Periodontol 29(Suppl 3) 136-159, 2002. adult periodontitis. Long-term clinical and microbiological observations,
Lang N, Bartold PM, Cullinan M, et al: Consensus report: aggressive peri- J Clin Periodontal 27:578-589, 2000.
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31 Treatment of Aggressive and Atypical Forms of Periodontitis 361.el
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Dent Res 12:32-39, 1998. 2:8-21, 1982.
SECTION Ill
I
Diagnosis and Treatment of Periodontal
Emergencies
Section Outline
32 Treatment of Acute Gingival Disease 33 Treatment of Periodontal Abscess
32
Treatment of Acute Gingival
Disease
PR Klokkevold • FA Carranza • DG Naik • A Uppoor
Chapter Outline
Necrotizing Ulcerative Gingivitis Acute Herpetic Gingivostomatitis
Acute Pericoronitis
The treatment of acute gingival disease entails the alleviation the history of the acute disease and its onset and duration, as
of the acute symptoms and elimination of all other periodontal follows:
diseases, both chronic and acute, throughout the oral cavity.
• Is the disease recurrent?
Treatment is not complete if periodontal pathologic changes
• Are the recurrences associated with specific factors such
or factors capable of causing them are still present.
as menstruation, particular foods, exhaustion, or mental
stress?
Necrotizing Ulcerative Gingivitis • Has there been any previous treatment? When and for how
long?
Necrotizing ulcerative gingivitis (NUG) results from an im-
paired host response to a potentially pathogenic microflora. The clinician should also inquire as to the type of treatment
Depending on the degree of immunosuppression, NUG may received and the patient's impression regarding its effect.
occur in a mouth essentially free of other gingival involve- The examination of the patient should include general ap-
ment or may be superimposed on underlying chronic gingival pearance, presence of halitosis, presence of skin lesions, vital
disease. Treatment should include the alleviation of the acute signs including temperature, and palpation for the presence of
symptoms and the correction of the underlying chronic gin- enlarged lymph nodes, especially submaxillary and submental
gival disease. The former is the simpler part of the treatment, nodes.
whereas the latter requires more comprehensive procedures. The oral cavity is examined for the characteristic lesion of
The treatment of NUG consists of (1) alleviation of the NUG (see Chapters 16 and 22, its distribution, and the pos-
acute inflammation by reducing the microbial load and re- sible involvement of the oropharyngeal region. Oral hygiene
moval of necrotic tissue, (2) treatment of chronic disease ei- is evaluated, with special attention to the presence of peri-
ther underlying the acute involvement or elsewhere in the oral coronal flaps, periodontal pockets, and local factors (eg, poor
cavity, (3) alleviation of generalized symptoms such as fever restorations, distribution of calculus). Periodontal probing of
and malaise, and (4) correction of systemic conditions or fac- NUG lesions is likely to be very painful and may need to be
tors that contribute to the initiation or progression of the gin- deferred until after the acute lesions are resolved.
gival changes. Chapter 24 provides further information on the The goals of initial therapy are to reduce the microbial load and
management and treatment of NUG in patients with acquired remove necrotic tissue to the degree that repair and regeneration of
immunodeficiency syndrome (AIDS). normal tissue barriers are reestablished. Treatment during this
Treatment of NUG should follow an orderly sequence ac- initial visit is confined to the acutely involved areas, which are
cording to specific steps at three clinical visits. isolated with cotton rolls and dried. A topical anesthetic is ap-
plied, and after 2 or 3 min the areas are gently swabbed with a
First Visit moistened cotton pellet to remove the pseudomembrane and
nonattached surface debris. Bleeding may be profuse. Each
At the first visit, the clinician should do a complete evalua- cotton pellet is used in a small area, then discarded; sweeping
tion of the patient, including a comprehensive medical his- motions over large areas with a single pellet are not recom-
tory with special attention to recent illness, living conditions, mended. After the area is cleansed with warm water, the su-
dietary background, cigarette smoking, type of employment, perficial calculus is removed. Ultrasonic scalers are very useful
hours of rest, risk factors for HIV, and psychosocial parameters for this purpose because they do not elicit pain, and the water
(eg, stress, depression). The patient is questioned regarding jet and cavitation aid in lavage of the area.
365
FIGURE 32.1 A, Initial view of the anterior gingival tissues in a 22-year-old white female smoker with acute NUG. B, Palatal view of the same patient.
C, Facial view of the same patient, 2 days after initial scaling and cessation of smoking. D, Palatal view of the same patient, 2 days after initial scaling
and cessation of smoking. (From Rose LF, Mealey BL, Genco Rf, Cohen OW: Periodontics: medicine, surgery, and implants, Mosby, St. Louis, 2005.)
Subgingival scaling and curettage are contraindicated at Patients are asked to report back to the clinician in
this time because these procedures may extend the infection 1-2 days. The patient should be advised of the extent of total
into the deeper tissues and may also cause bacteremia. Unless treatment that the condition requires and warned that treat-
an emergency exists, procedures, such as extractions or periodon- ment is not complete when pain stops. The patient should be
tal surgery, are postponed until the patient has been symptom free informed of the presence of chronic gingival or periodontal
for 4 weeks, to minimize the likelihood of exacerbating the acute disease, which must be eliminated to reduce the likelihood of
symptoms. recurrence of the acute symptoms.
Patients with moderate or severe NUG and local lymph- A large variety of drugs have been used in the treatment
adenopathy or other systemic signs or symptoms are placed of NUG. Topical drug therapy, however, is only an adjunc-
on an antibiotic regimen of amoxicillin, 500 mg orally every tive measure; no drug, when used alone, can be considered
6 h for 10 days. For amoxicillin-sensitive patients, other an- complete therapy Systemic antibiotics, when used, also re-
tibiotics are prescribed, such as erythromycin (500 mg every duce the oral bacterial flora and alleviate the oral symptoms,
6 h) or metronidazole (500 mg twice daily for 7 days). Sys- but they are only an adjunct to the complete local treatment
temic complications should subside in 1-3 days. Antibiotics that the disease requires. In patients treated by drugs alone
are not recommended in NUG patients who do not have systemic or by systemic antibiotics alone, the acute painful symptoms
complications. often recur after treatment is discontinued.
Instructions to the Patient Second Visit

The patient is discharged with the following instructions:
At the second visit, 1 or 2 days after the first visit, the patient
1. Avoid tobacco, alcohol, and condiments. is evaluated for amelioration of signs and symptoms. The pa-
2. Rinse with a glassful of an equal mixture of 3% hydrogen tient's condition is usually improved; the pain is diminished or
peroxide and warm water every 2 hand/or twice daily with no longer present. The gingival margins of the involved areas
0.12 % chlorhexidine solution. are erythematous but without a superficial pseudomembrane.
3. Get adequate rest. Pursue usual activities, but avoid exces- Scaling is performed if necessary and sensitivity permits.
sive physical exertion or prolonged exposure to the sun, as Shrinkage of the gingiva may expose previously covered cal-
in golf, tennis, swimming, or sunbathing. culus, which is gently removed. The instructions to the pa-
4. Confine toothbrushing to the removal of surface debris tient are the same as those given previously
with a bland dentifrice and an ultrasoft brush; overzealous
brushing and the use of dental floss or interdental cleaners
Third Visit
will be painful. Chlorhexidine mouth rinses are also help-
ful in controlling plaque throughout the mouth. At the next visit, approximately 5 days after the second visit,
5. An analgesic, such as a nonsteroidal antiinflammatory the patient is evaluated for resolution of symptoms, and a
drug (NSAID; eg, ibuprofen), is appropriate for pain relief. comprehensive plan for the management of the patient's peri-
6. Patients who have systemic complications, such as high odontal conditions is formulated. The patient should be es-
fever, malaise, anorexia, and general debility and who have sentially symptom free. Some erythema may still be present
been put on an antibiotic treatment are told that bed rest in the involved areas, and the gingiva may be slightly painful
is necessary, as well as copious fluid consumption and ad- on tactile stimulation (Fig. 32. lA-B). The patient is instruct-
ministration of analgesics for relief of pain. ed in plaque control procedures which are essential for the
32 Treatment of Acute Gingival Disease 367
FIGURE 32.2 Treatment of acute NUG. A, Before treatment. Note the characteristic interdental lesions. B, After treatment, showing restoration of
healthy gingival contour.
success of the treatment and the maintenance of periodontal 2. In the next stage, the bulk and redness of the crater mar-
health. The patient is further counseled on nutrition, smok- gins are reduced, indicating a reduction in inflammation
ing cessation, and other conditions or habits associated with and reepithelialization, but the surface remains shiny
a potential recurrence. The hydrogen peroxide rinses are dis- (Fig. 32.lC-D)
continued, but chlorhexidine rinses can be maintained for 2 3. This is followed by the early signs of restoration of normal
or 3 weeks. Scaling and root planing are repeated if necessary. gingival contour and color, indicating reestablishment of
Unfortunately, the patient often discontinues treatment be- the normal barrier function of the epithelium, including
cause the acute condition has subsided; however, this is when keratinization, and further reduction of inflammation.
comprehensive treatment of the patient's chronic periodontal 4. In the final stage, the normal gingival color, consistency,
problem should start. surface texture, and contour may be restored. Portions of
Appointments should be scheduled for the treatment of the root exposed by the acute disease may be covered by
chronic gingivitis, periodontal pockets, and pericoronal flaps, healthy gingiva (Fig. 32 2).
as well as for the elimination of all forms of local irritation.
The patient should be reevaluated at 1 month to determine Additional Treatment Considerations
compliance with oral hygiene, health habits, psychosocial fac-
tors, the potential need for reconstructive or esthetic surgery, Contouring of Gingiva as Adjunctive Procedure
and the interval of subsequent recall visits. Even in cases of severe gingival necrosis, healing often leads
to restoration of the normal gingival contour although normal
architecture of the gingiva may be achieved only after several
Gingival Changes With Healing weeks or months. However, if there has been loss of interden-
tal bone, if the teeth are irregularly aligned, or if the entire
The characteristic lesion of NUG undergoes the following
papilla is lost, healing sometimes results in the formation of
changes in the course of healing in response to treatment:
a shelf-like gingival margin, which favors retention of plaque
1. Removal of the surface pseudomembrane exposes the un- and recurrence of gingival inflammation as well as being an
derlying red, hemorrhagic, craterlike depressions in the esthetic problem. This can be corrected by an attempt to re-
gingiva, indicating inflammation caused by necrosis and store lost tissue through periodontal plastic procedures or by
microbial infiltration of tissue that has lost the normal bar- reshaping the gingiva surgically (Fig. 32 3). Effective plaque
rier function of the epithelium. control by the patient is particularly important to establish
FIGURE 32.3 Reshaping the gingiva in the treatment of acute NUG. A, Before treatment, showing bulbous gingiva and interdental necrosis in
the mandibular anterior area. B, After treatment. Gingival contours still undesirable. C, Final result. Physiologic contours obtained by reshaping the
gingiva.
and maintain the normal gingival contour in areas of tooth Acute Pericoronitis
irregularity.
The treatment of pericoronitis depends on the severity of the
Role of Drugs inflammation, the systemic complications, and the advisabil-
A large variety of drugs have been used for topical treat- ity of retaining the involved tooth. All pericoronal flaps should
ment of NUG. Topical drug therapy is only an adjunctive be viewed with suspicion. Persistent symptom-free pericoro-
measure. No drug, when used alone, can be considered complete nal flaps should be removed as a preventive measure against
treatment. subsequent acute involvement.
Escharotic drugs, such as phenol, silver nitrate, chromic The treatment of acute pericoronitis consists of (1) gently
acid, or potassium bichromate, should not be used. They are flushing the area with warm water to remove debris and exu-
necrotizing agents that alleviate pain by destroying the nerve date and (2) swabbing with antiseptic after elevating the flap
endings of the ulcerated gingiva. However, they also destroy gently from the tooth with a scaler. The underlying debris is
young cells needed for repair and delay healing. Repeated use removed, and the area is flushed with warm water (Fig. 32.4).
of these agents results in loss of gingival tissue that is not re- The occlusion is evaluated to determine if an opposing tooth
stored when the disease subsides. is occluding with the pericoronal flap. It may be necessary
to reduce soft tissue surgically and/or to adjust the opposing
tooth to alleviate pain. Antibiotics can be prescribed in severe
Persistent or Recurrent Cases cases and for patients who may have clinical evidence of dif-
Adequate local therapy with optimal home care will resolve fuse microbial infiltration of the tissue. If the gingival flap is
most cases of NUG. If a case of NUG persists despite therapy swollen and fluctuant, an incision may be necessary to estab-
or if it recurs, the patient should be reevaluated, with a focus lish drainage and relieve pressure.
on the following factors: Once the acute symptoms have subsided, the prognosis
of the tooth can be evaluated. The decision will be governed
1. Reassessment of differential diagnosis to rule out diseases that by the likelihood of whether the tooth will continue eruption
resemble NUG. Several diseases and conditions may ini- into a functional position or if impaction and the factors pre-
tially present with a similar appearance as NUG, such as disposing to pericoronitis will persist. Bone loss on the distal
desquamative gingivitis. A renewed search for skin lesions surface of the second molar is a concern when third molars
and other signs or symptoms should be undertaken, with are impacted along the distal surface. The problem is signifi-
a biopsy if warranted. cantly greater if the third molars are extracted after the roots
2. Underlying systemic disease causing immunosuppression. are formed or when patients are older (ie , mid-twenties or
In particular, HIV infection may frequently present with later). To reduce the risk of bone loss around second molars,
symptoms of NUG or necrotizing ulcerative periodontitis partially or completely impacted third molars should be ex-
(NUP). The patient should be reassessed for risk factors tracted early in their development.
and may need counseling about testing for HIV or other If the decision is made to retain the tooth, the pericoronal
suspected underlying systemic diseases (eg, lymphoprolif- flap is surgically reduced (see Fig. 32.4). It is necessary to
erative disease). The patient will likely need referral to his remove the tissue distal to the tooth, as well as the flap on the
or her physician for further evaluation. occlusal surface. Incising only the occlusal portion of the flap
3. Inadequate local therapy. Too often, treatment is discontin- leaves a deep distal pocket, which invites recurrence of acute
ued when the symptoms have subsided, without eliminat- pericoronal involvement. It is critical to leave the patient with
ing the chronic gingival disease and periodontal pockets a cleansable site. On healing, the patient needs appropriate
that remain after the superficial acute condition is relieved. instruction in long-term maintenance.
Remaining calculus and other local factors that predispose
to gingival inflammation may permit recurrence. Recur-
rent acute involvement in the mandibular anterior area Acute Herpetic Gingivostomatitis
can be associated with persistent pericoronal inflammation
Primary infection with herpes simplex virus in the oral cavity
arising from partial eruption and pericoronal inflammation
results in a condition known as acute herpetic gingivostoma-
of third molars. The anterior involvement is less likely to
titis, which is an oral infection often accompanied by systemic
recur after the third molar situation is corrected.
signs and symptoms. This infection typically occurs in chil-
4. Inadequate compliance. Poor plaque control, heavy use of
dren, but it can occur in adults as well. It runs a 7-10-day
tobacco, ineffective stress management, and continued
course and usually heals without scarring. A recurrent her-
malnutrition can also contribute to persistence or recur-
petic episode may be precipitated in individuals with a history
rence of NUG.
of herpesvirus infections by dental treatment, respiratory in-
The clinician should evaluate the quality and consistency of fections, sunlight exposure, fever, trauma, exposure to chemi-
plaque control. Further assessment and counseling on tobac- cals, and emotional stress.
co use will also determine the role of tobacco in this patient. Treatment consists of early diagnosis and immediate initia-
If the clinician perceives that psychosocial factors are unre- tion of antiviral therapy. Until recently, therapy for primary
solved and are complicating health behaviors and contribut- herpetic gingivostomatitis consisted of palliative care. With
ing to immunosuppression, the patient should be referred to the development of antiviral therapy, however, the stan-
the appropriate professional. A reassessment of the patient's dard of care has changed. In a randomized double-blind
nutritional state, with potential dietary analysis or nutritional placebo-controlled study, Amir et al demonstrated that an-
testing, may be required. tiviral therapy with 15 mg/kg of an acyclovir suspension
32 Treatment of Acute Gingival Disease 369
(D)
(C)
FIGURE 32.4 Treatment of acute pericoronitis. Osseous surgery may be necessary in some cases. A, Inflamed pericoronal flap (arrow) in relation
to the mandibular third molar. B, Anterior view of third molar and flap. C, Lateral view with scaler in position to gently remove debris under flap.
D, Anterior view of scaler in position. E, Incorrect removal of the tip of the flap, permitting the deep pocket to remain distal to the molar. F, Removal of
section of the gingiva distal to the third molar after the acute symptoms subsided. The line of incision is indicated by the broken line. G, Appearance
of the healed area.
given 5 times daily for 7 days substantially changes the plaque and food debris. An NSAID (eg, ibuprofen) can be
course of the disease without significant side effects. Acy- given systemically to reduce fever and pain. Patients may
clovir reduced symptoms, including fever, from 3 days to use either nutritional supplements or topical anesthetics
1 day; decreased new extraoral lesions from 5.5 to O days; (eg, viscous lidocaine) before eating to aid in proper nutri-
and reduced difficulty with eating from 7 to 4 days. Fur- tion during the early phases in acute herpetic gingivosto-
thermore, viral shedding stopped at 1 day for the acyclovir matitis. Periodontal therapy should be postponed until the
group compared with 5 days for the control group. Overall, acute symptoms subside to avoid the possibility of exacer-
oral lesions were present for only 4 days in the acyclovir bation (Fig. 32 5)
group but for 10 days in the control group. Although no Local or systemic application of antibiotics is sometimes
clear clinical evidence indicates that this regimen will re- advised to prevent opportunistic infection of ulcerations, es-
duce recurrences, research data suggest that a greater num- pecially in the immunocompromised patient. If the condi-
ber of latent virus copies incorporated into ganglia will in- tion does not resolve within 2 weeks, the patient should be
crease the severity of recurrences. referred to a physician for medical consultation. The patient
In summary, if primary herpetic gingivostomatitis is should be informed that herpetic gingivostomatitis is con-
diagnosed within 3 days of onset, acyclovir suspension tagious at certain stages such as when vesicles are present
should be prescribed: 15 mg/kg 5 times daily for 7 days. If (highest viral titer). All individuals exposed to an infected
diagnosis occurs after 3 days in an immunocompetent pa- patient should take precautions. Herpetic infection of a cli-
tient, acyclovir therapy may have limited value. All patients, nician's finger, referred to as herpetic whitlow, can occur if a
including those presenting more than 3 days after disease seronegative clinician becomes infected with a patient's her-
onset, may receive palliative care, including removal of petic lesions.
FIGURE 32.5 Treatment of acute herpetic gingivostomatitis. A, Before treatment. Note diffuse erythema and surface vesicles. B, Before treatment,
palatal view, showing gingival edema and ruptured vesicle on palate. C, One month after treatment, showing restoration of normal gingival contour
and stippling. D, One month after treatment, palatal view.
SUGGESTED READINGS Langlais RP, Miller CS: Color atlas of common oral diseases, ed 2, New York,
1998, Williams & Wilkins.
Amir J, Harel L, Smetana Z, et al: Treatment of herpes simplex gingivosto-
Matusow RJ: Acute primary herpetic gingivostomatitis in non-immuno-
matitis with acyclovir in children: a randomised double-blind placebo-
compromised adults and an HSV-1 isolation technique, Compendium
controlled study, BM] 314:1800, 1997.
13(8) 662-666, 1992.
Ash MM Jr, Costich ER, Hayward JR: A study of periodontal hazards of third
Regezi JA, Sciubba JJ: Oral pathology: clinical-pathologic correlations, Philadel-
molars,] Periodontol 33:209, 1962.
phia, 1989, Saunders.
Corbet EF: Diagnosis of acute periodontal lesions, Peliodontol 2000 34:
Wade DN, Kerns DG: Acute necrotizing ulcerative gingivitis-periodontitis: a
204-216, 2004.
literature review, Mil Med 163(5):337-342, 1998.
Johnson BD, Engel D: Acute necrotizing ulcerative gingivitis: a review of diag-
Williamson RT: Diagnosis and management of recurrent herpes simplex in-
nosis, etiology and treatment,] Periodontol 57(3):141-150, 1986.
duced by fixed prosthodontic tissue management: a clinical report, J Pros-
Kureishi A, Chow AW: The tender tooth. Dentoalveolar, pericoronal, and
thet Dent 82:1, 1999.
periodontal infections, Inject Dis Clin North Am 2(1):163-182, 1988.
370.el PART 2 Clinical Periodontics
REFERENCES 7. Linghorne WJ, McIntosh WG, Tice JW, et al: The relation of ascorbic acid
intake to gingivitis,] Can Dent Assoc 12:49, 1946.
1. Amir J, Hare! L, Smetana Z, et al: Treatment of herpes simplex gingivosto-
8. Mitchell OF, Baker BR: Topical antibiotic control of necrotizing gingivitis,
matitis with acyclovir in children: a randomised double-blind placebo-
] Periodontol 39:81, 1968.
controlled study, BM] 314:1997, 1800.
9. RegeziJA, SciubbaJJ: Oral pathology.· clinical-pathologic correlations, Phila-
2. Ash MM Jr, Costich ER, Hayward JR: A study of periodontal hazards of
delphia, 1989, Saunders.
third molars,] Periodontal 33:209, 1962.
10. Snyder Ml, Church DH, Rickles NH: Primary herpes infection of right
3. Burket LW: Oral medicine, ed 3, Philadelphia, 1946, Lippincott.
second finger, Oral Surg 27:598, 1969.
4. Glickman I, Johannessen LB: The effect of a six percent solution of chro-
11. Wade AB, Blake G, Mirza K: Effectiveness of metronidazole in treating the
mic acid on the gingiva of the albino rat: a correlated gross, biomicro-
acute phase of ulcerative gingivitis, Dent Pract 16:440, 1966.
scopic, and histologic study,] Am Dent Assoc 41:674, 1950.
12. Wade AB, Blake GC, Manson JD, et al: Treatment of the acute phase of
5. King JD: Nutritional and other factors in "trench mouth" with special
ulcerative gingivitis (Vincent's type), Br Dent] 115:372, 1963.
reference to the nicotinic acid component of the vitamin B2 complex, Br
13. Williamson RT: Diagnosis and management of recurrent herpes simplex
Dent] 74:113, 1943.
induced by fixed prosthodontic tissue management: a clinical report,
6. Langlais RP, Miller CS: Color atlas of common oral diseases, ed 2, New York,
] Prnsthet Dent 82:1, 1999.
1998, Williams & Wilkins.
33
Treatment of Periodontal
Abscess
PR Melnick • HH Takei • A Uppoor • DG Naik
Chapter Outline
Specific Treatment Approaches
Specific Treatment Approaches blade. The tissue lateral to the incision can be separated with
a curette or periosteal elevator. Fluctuant matter is expressed,
Treatment of the periodontal abscess includes two phases: re- and the wound edges approximated under light digital pres-
solving the acute lesion, followed by the management of the sure with a moist gauze pad.
resulting chronic condition (Box 33.1). In abscesses presenting with severe swelling and inflam-
mation, aggressive mechanical instrumentation should be de-
layed in favor of antibiotic therapy so as to avoid damage to
Acute Abscess healthy contiguous periodontal tissues.
The acute abscess is treated to alleviate symptoms, control the Once bleeding and suppuration have ceased, the patient
spread of infection, and establish drainage. Before treatment, may be dismissed. For those who do not need systemic antibi-
the patient's medical history, dental history, and systemic con- otics, posttreatment instructions include frequent rinsing with
dition are reviewed and evaluated to assist in the diagnosis warm salt water (1 tbsp/8-oz glass) and periodic application
and to determine the need for systemic antibiotics (Boxes 33.2 of chlorhexidine gluconate either by rinsing or locally with
and 33.3). a cotton-tipped applicator. Reduced exertion and increased
fluid intake are often recommended for patients showing sys-
Drainage Through Periodontal Pocket temic involvement. Analgesics may be prescribed for comfort.
The peripheral area around the abscess is anesthetized with By the following day, the signs and symptoms have usually
sufficient topical and local anesthetic to ensure comfort. The subsided. If not, the patient is instructed to continue the pre-
pocket wall is gently retracted with a periodontal probe or viously recommended regimen for an additional 24 h. This of-
curette in an attempt to initiate drainage through the pocket ten results in satisfactory healing and the lesion can be treated
entrance (see Fig. 33.1). Gentle digital pressure and irriga- as a chronic abscess.
tion may be used to express exudates and clear the pocket
(Fig. 33.2) If the lesion is small and access uncomplicated, Chronic Abscess
debridement in the form of scaling and root planing may be
undertaken. As with a periodontal pocket, the chronic abscess is usu-
If the lesion is large and drainage cannot be established, ally treated with scaling and root planing or surgical therapy.
root debridement by scaling and root planing or surgical access Surgical treatment is suggested when deep vertical or furca-
should be delayed until the major clinical signs have abated. tion defects are encountered that are beyond the therapeutic
In these patients, use of adjunctive systemic antibiotics with capabilities of nonsurgical instrumentation (Fig. 33.3). The
short-term high-dose regimens is recommended (Box 33.3). patient should be advised of the possible postoperative
Antibiotic therapy alone without subsequent drainage and sequelae usually associated with periodontal nonsurgical
subgingival scaling is contraindicated. and surgical procedures. As with the acute abscess, antibi-
otic therapy may be indicated.
Drainage Through External Incision
The abscess is dried and isolated with gauze sponges. Topi-
Gingival Abscess
cal anesthetic is applied, followed by local anesthetic injected
peripheral to the lesion. A vertical incision through the most Treatment of the gingival abscess is aimed at reversal of
fluctuant center of the abscess is made with a No. 15 surgical the acute phase and when applicable, immediate removal
371
1. Drainage through pocket retraction or incision

2. Scaling and root planing
3. Periodontal surgery
4. Systemic antibiotics
5. Tooth removal
Modified from Sanz M, Herrera D, van Winkelhoff AJ: The periodontal

abscess. In Lindhe, J: Clinical periodontology, Copenhagen, 2000,
Munksgaard.
1. Cellulitis (nonlocalized, spreading infection)

2. Deep, inaccessible pocket FIGURE 33.2 Gentle digital pressure may be sufficient to express
3. Fever purulent discharge.
4. Regional lymphadenopathy
5. lmmunocompromised patient
of the cause. To ensure procedural comfort, topical, or local

anesthesia by infiltration is administered. When possible,
scaling and root planing are completed to establish drainage
and remove microbial deposits. In more acute situations, the
ANTIBIOTIC OF CHOICE fluctuant area is incised with a No. 15 scalpel blade, and exu-
Amoxicillin, 500 mg date may be expressed by gentle digital pressure. Any foreign
• 1.0-g loading dose, then 500 mg 3 times a day for 3 days. material (eg, dental floss, impression material) is removed.
• Reevaluation after 3 days to determine the need for The area is irrigated with warm water and covered with moist
continued or adjusted antibiotic therapy. gauze under light pressure.
Once bleeding has stopped, the patient is dismissed with
PENICILLIN ALLERGY
instructions to rinse with warm salt water every 2 h for the
Clindamycin
remainder of the day After 24 h the area is reassessed, and
• 600-mg loading dose, then 300 mg 4 times a day for 3 days. if resolution is sufficient, scaling not previously completed is
Azithromycin (or Clarithromycin) (To be used with caution undertaken. If the residual lesion is large or poorly accessible,
in patients with high baseline cardiovascular risk.) surgical access may be required.
• 1.0-g loading dose, then 500 mg 4 times a day for 3 days.
Data from American Academy of Periodontology: / Periodontal 67:1553,

2004. Pericoronal Abscess
As with the other abscesses of the periodontium, the treat-
ment of the pericoronal abscess is aimed at management of
the acute phase, followed by resolution of the chronic condi-
tion. The acute pericoronal abscess is properly anesthetized
for comfort, and drainage is established by gently lifting the
soft tissue operculum with a periodontal probe or curette. If
the underlying debris is easily accessible, it may be removed,
followed by gentle irrigation with sterile saline. If there is re-
gional swelling, lymphadenopathy, or systemic signs, systemic
antibiotics may be prescribed.
The patient is dismissed with instructions to rinse with
warm salt water every 2 h, and the area is reassessed after
24 h. If discomfort was one of the original complaints, appro-
priate analgesics should be employed. Once the acute phase
has been controlled, the partially erupted tooth may be de-
finitively treated with either surgical excision of the overlying
tissue or removal of the offending tooth.
FIGURE 33.1 Diagnosis of periodontal abscess.

33 Treatment of Periodontal Abscess 373
FIGURE 33.3 A, Chronic periodontal abscess of maxillary right canine. B, Using local anesthesia, periodontal probe is inserted to determine severity
of the lesion. C, Using mesial and distal vertical incisions, a full-thickness flap is elevated, exposing severe bone dehiscence, a subgingival restora-
tion, and root calculus. D, Root surface has been planed free of calculus and the restoration smoothed. E, Full-thickness flap has been replaced to
its original position and sutured with absorbable sutures. F, At 3 months, gingival tissues are pink, firm, and well adapted to the tooth, with minimal
periodontal probing depth.
REFERENCES Herrera D, Roldan S, Gonzalez I, et al: The periodontal abscess. I. Clinical and
microbiology findings,] Clin Periodontol 27:287, 2000a.
References for this chapter are found on the companion Herrera D, Roldan S, Sanz M: The periodontal abscess: a review, J Clin Peri-
website www.medenact.com. odontol 27 377, 2000b.
Lang N, Soskolne WA, Greenstein G, et al: Consensus report: abscesses of the
periodontium, Ann Peliodontol 4(1):83, 1999.
SUGGESTED READINGS Meng HX: Periodontal abscess, Ann Periodontol 4:79, 1999.
American Academy of Periodontology: parameter on acute periodontal dis- Minsk L: Diagnosis and treatment of acute periodontal conditions, Compend
eases,] Periodontal 71(5 Suppl):863-866, 2000. Cantin Educ Dent 27(1):8-11, 2006.
Corbet EF: Diagnosis of acute periodontal lesions, Periodontal 2000 34:204, Sanz M, Herrera D, van Winkelhoff Aj: The periodontal abscess. In Lindhe J,
2004. editor: Clinical periodontology, Copenhagen, 2000, Munksgaard.
Dahlen G: Microbiology and treatment of dental abscesses and periodontal-
endodontic lesions, Periodontal 2000 28:206, 2002.
33 Treatment of Periodontal Abscess 373.el
REFERENCES 13. Genco RJ: Using antimicrobials agents to manage periodontal diseases,
1. Abrams H, Kopczyk R: Gingival sequela from a retained piece of dental
J Am Dent Assoc 122:31, 1991.
14. Hafstrom CA, Wikstrom MB, Renvert SN, et al: Effect of treatment on
Iloss.] Am Dent Assoc 106:57, 1983.
some periodontopathogens and their antibody levels in periodontal
2. Abrams H, Cunningham C, lee S: Periodontal changes following coronal/
abscesses, J Periodontal 65: 1022, 1994.
root perforation and formocresol pulpotomy,J Endod 18:399, 1992.
15. Herrera D, Roldan S, Sanz M: The periodontal abscess: a review,] Clin
3. American Academy of Periodontology: position paper: systemic antibiot-
Periodontol 27:377, 2000.
ics in periodontics,) Periodontol 67:1553, 2004.
16. Herrera D, Roldan S, Gonzalez 1, et al: The periodontal abscess. 1. Clinical
4. Ammons WF Jr, Harrington GW: The periodontic-endodontic continu-
and microbiology findings,] Clin Periodontal 27:287, 2000.
um. In Newman MG, Takei HH, Carranza FA, editors: Carranza's clinical
17. Kaldahl WB, Kalwarf Kl, Patil KO, et al: long-term evaluation of peri-
periodontology, ed 9, Philadelphia, 2002, Saunders.
odontal therapy. I. Response to 4 therapeutic modalities, J Periodontal
5. Becker W, Berg L, Becker B: The long-term evaluation of periodontal
67 93, 1996.
treatment and maintenance in 95 patients, Int J Periodont Restor Dent
18. lewis MA, Macfarlane TW: Short-course high-dosage amoxicillin in the
2:55, 1984.
treatment of acute <lento-alveolar abscess, Br Dent] 161:299, 1986.
6. Carranza FA, Camargo PM: The periodontal pocket. In Newman MG,
19. Manson JD: Periodontics, ed 3, Philadelphia, 1975, lea & Febiger
Takei HH, Carranza FA, editors: Carranza's clinical periodontology, ed 9,
20. Martin MV, Longman LP, Hill JB, et al: Acute dentoalveolar infections:
an investigation of the duration of antibiotic therapy, Br Dent] 183:135,
7. Chace R, low SB: Survival characteristics of periodontally involved teeth:
1997.
a 40-year study,] Periodontol 64:701, 1993.
21. Mcleod DE, Lainson PA, Spivey JD: Tooth loss due to periodontal
8. Corbet EF: Diagnosis of acute periodontal lesions, Periodontal 2000
abscess: a retrospective study,] Periodontol 68:963, 1997.
34:204, 2004.
22. Meng HX: Periodontal abscess, Ann Periodontal 4: 79, 1999.
9. Dahlen G: Microbiology and treatment of dental abscesses and periodon-
23. O'Leary TJ, Standish SM, Bloomer RS: Severe periodontal destruction
tal-endodontic lesions, Periodontal 2000 28:206, 2002.
following impression procedures,] Periodontol 44:43, 1973.
10. Delio Russo NM: The post-prophylaxis periodontal abscess: etiology and
24. Sanz M, Herrera D, van Winkelhoff AJ: The periodontal abscess. ln Lind he
treatment, Int] Periodont Restor Dent 5:29, 1985.
J, editor: Clinical periodontology, Copenhagen, 2000, Munksgaard.
11. Epstein S, Scopp IW: Antibiotics and the intraoral abscess, J Pe,iodontol
25. Takei HH: Treatment of the periodontal abscess. In Newman MG,
48:236, 1977.
Takei HH, Carranza FA, editors: Cairnnza's clinical periodontology, ed 9,
12. Garrett S, Polson A, Stoller N, et al: Comparison of a bioabsorbable GTR
barrier to a non-absorbable barrier in treating human class II furcation
26. Topoll H, Lange D, Muller R: Multiple periodontal abscesses after sys-
defects: a multi-center parallel design randomized single-blind study,
temic antibiotic therapy,] Clin Peliodontol 17:268, 1990.
SECTION IV
Section Outline
34 Phase I Periodontal Therapy 37 Scaling and Root Planing
35 Plaque Biofilm Control 38 Antiinfective Therapy
36 Periodontal Instruments and 39 Host Modulation
Instrumentation 40 Breath Malodor
34
Phase I Periodontal Therapy
DA Perry • HH Takei • A Jain
Chapter Outline
Rationale Healing
Treatment Sessions Decision to Refer for Specialist Treatment
Sequence of Procedures Conclusion
Results
Phase I therapy or cause-related therapy is the first in the plaque-biofilm control will continue to lose attachment re-
chronologic sequence of procedures that constitute periodon- gardless of the surgical procedures performed. In addition,
tal treatment. The objective of phase I therapy is to alter or phase I therapy provides an opportunity for the dentist to
eliminate the microbial etiology and factors that contribute to evaluate tissue response and provide reinforcement about
gingival and periodontal diseases to the greatest extent possi- homecare, both of which are crucial elements to the overall
ble, therefore halting the progression of disease and returning success of treatment.
the dentition to a state of health and comfort. Phase I therapy Based on the knowledge that microbial plaque biofilm is
is referred to by a number of names, including initial therapy, the major etiologic agent in gingival inflammation, one spe-
nonsurgical periodontal therapy, and cause-related therapy. All cific aim of phase I therapy for every patient is effective daily
terms refer to the procedures performed to treat gingival and plaque-biofilm removal at home. These homecare procedures
periodontal infections, up to and including tissue reevalua- can be complex, time-consuming, and often require changing
tion, which is the point at which the course of ongoing care long-standing habits. Good oral hygiene is more easily accom-
is determined. plished if the tooth surfaces are free of calculus deposits and
other irregularities so that surfaces are easily accessible. Man-
Rationale agement of contributing all local factors is required in phase
I therapy. The following list of elements makes up phase I
Phase I therapy is defined by the evidence-based American therapy:
Association of Periodontology practice guidelines as the initia-
1. complete removal of calculus (see Chapters 3 7);
tion of a comprehensive daily plaque-control regimen, man-
2. correction or replacement of poorly fitting restorations and
agement of periodontal-systemic interrelationships as needed,
prosthetic devices (see Chapter 52);
thorough removal of supra- and subgingival bacterial plaque
3. restoration or temporization of carious lesions;
biofilm and calculus, chemotherapeutic agents as necessary,
4. orthodontic tooth movement (see Chapter 21);
and elimination of local factors, such as defective restorations
5. treatment of food impaction areas;
and treatment of carious lesions. These procedures are a re-
6. treatment of occlusal trauma;
quired part of periodontal therapy, regardless of the extent of
7. extraction of hopeless teeth; and
disease present. In many cases, only phase I therapy will be
8. possible use of antimicrobial agents including necessary
required to restore periodontal health, or it will constitute the
plaque sampling and sensitivity testing (see Chapters 8
preparatory phase for surgical therapy. Figs. 34.1 and 34.2
and 38)
show the results of phase I therapy in two patients with chron-
ic periodontitis. The goal of cause-related phase I periodontal
therapy has been succinctly stated as the approach aimed at
removal of pathogenic biofilms, toxins and calculus, and the rees-
Treatment Sessions
tablishment of a biologically acceptable root surface. After careful analysis and diagnosis of the specific periodontal
Phase I therapy is a critical aspect of periodontal treat- condition present, the dentist must develop a treatment plan
ment. Data from clinical research indicate that the long-term that includes all required procedures and estimates the num-
success of periodontal surgical treatment is dependent upon ber of appointments necessary to complete phase I therapy. In
maintaining the plaque-biofilm control results achieved with most cases, patients require several treatment sessions for the
phase I therapy. In fact, patients who do not have an adequate complete debridement of tooth surfaces. All of the following
377
FIGURE 34.1 Results of phase I therapy, severe chronic periodontitis. A, 45-year-old patient with deep-probe depths, bone loss, severe swelling,
and redness of the gingival tissues. B, Results 3 weeks after the completion of phase I therapy. Note that the gingival tissue has returned to a normal
contour, with redness and swelling dramatically reduced.
FIGURE 34.2 Results of phase I therapy, moderate chronic periodontitis. A, 52-year-old patient with moderate attachment loss and probe depths
in the 4-6-mm range. Note that the gingiva appears pink because it is fibrotic. Inflammation is present in the periodontal pockets but disguised by
the fibrotic tissue. Bleeding occurs on probing. B, Lingual view of the patient with more visible inflammation and heavy calculus deposits. C and D,
18 months after phase I therapy, the same areas show significant improvement in gingival health. The patient returned for regular maintenance visits
at 4-month intervals.
conditions must be considered when determining the phase I Sequence of Procedures

treatment plan:
• general health and tolerance of treatment; Step 1: Plaque-Biofilm Control Instruction
• number of teeth present; Plaque-biofilm control is an essential component to the suc-
• amount of subgingival calculus; cessful periodontal therapy and instruction should begin at
• probing pocket depths; the first treatment appointment. The patient must learn to
• attachment loss; correctly brush the teeth, focusing on applying the bristles
• furcation involvements; at the gingival third of the clinical crowns of the teeth, and
• alignment of teeth; begin using floss or other aids for interdental cleaning. This is
• margins of restorations; sometimes referred to as targeted oral hygiene and emphasizes
• developmental anomalies; thorough biofilm removal around the periodontal tissues.
• physical barriers to access (ie, limited opening or tendency The multiple appointment approach to phase I therapy per-
to gag); and mits the dentist to evaluate, reinforce, and improve the pa-
• patient cooperation and sensitivity (requiring use of anes- tient's oral-hygiene skills (Chapter 35 details plaque-control
thesia or analgesia). options).
34 Phase I Periodontal Therapy 379
Step 2. Removal of Supragingival and therapy because of the infectious nature of the caries process.
Subgingival Plaque Biofilm and Calculus Healing of the periodontal tissues will be maximized by re-
moving the reservoir of bacteria in these lesions so that they
Removal of calculus is accomplished using scalers, curettes, ultra- cannot repopulate the microbial plaque.
sonic instrumentation, or combinations of these devices during
one or more appointments. Evidence suggests that the treatment
Step 5. Tissue Reevaluation
results for chronic periodontitis are similar for all instruments. In
addition to calculus removal, bacterial plaque biofilm and some After scaling, root planing, and other phase I procedures, the
cementum are removed by instrumentation procedures as a mat- periodontal tissues require approximately 4 weeks to heal so
ter of course. At one time it was thought that all cementum had that the connective tissues have time to heal and accurate probe
to be systematically planed off of root surfaces in order to leave depths can be measured. Patients also need the opportunity to
a glassy hard surface free of accumulated bacterial toxins. The improve their homecare skills required to reduce inflammation
rationale was that cementum became necrotic from penetration and adopt new habits that ensure the success of treatment. At
of lipopolysaccharide endotoxins from the microbial biofilm and the reevaluation appointment, periodontal tissues are probed,
would interfere with healing. Lipopolysaccharides are loosely at- and all related anatomic conditions are carefully evaluated to
tached and easily removed from cementum so that instrumenta- determine if further treatment, including periodontal surgery,
tion beyond the thorough removal of calculus and plaque bio- is indicated. Additional improvement from periodontal surgi-
film will not improve treatment outcomes. As a consequence, the cal procedures can be expected only if phase I therapy resulted
term debridement is now used as commonly than root planing. in the gingiva being free of overt inflammation and the patient
Laser treatment has also been advocated for periodontal has adopted effective daily plaque-biofilm control procedures.
therapy by and some dentists. However, recent reviews suggest
that further well-designed studies are needed to confirm im-
proved outcomes. In addition, gingival curettage, the systemat- Results
ic removal of the soft-tissue lining of the pockets has not been
Scaling and root planing therapy has been studied extensive-
shown to improve results of treatment and there is, little if any,
ly to evaluate its effects on periodontal disease. Many stud-
change in outcomes from performing irrigation or lavage of
ies indicated that this treatment is both effective and reliable.
periodontal pockets during phase I-treatment appointments.
Studies ranging from 1 month to 2 years in length demon-
Photodynamic therapy has also been posited as an adjunct
strated up to 80% reduction in bleeding on probing and mean
to scaling and root planing. This therapy uses lasers at spe-
probing-depth reductions of 2-3 mm. Others demonstrated
cific wavelengths to "target microorganisms treated with a
that the percentage of periodontal pockets of 4-mm or greater
photosensitizer." Studies have not found this intervention to
depth was reduced more than 50% and up to 80%. Figs. 34.1
be useful as an alternative to scaling and root planing, or to
and 34.2 show examples of the effectiveness of phase I therapy
improve treatment outcomes, and further research needs to be
It is also important to recognize that deeper probing depths
conducted to ascertain the efficacy of this treatment.
present the dentist with greatly increased instrumentation
One other interesting approach to calculus removal and
challenges due to the complexity of root anatomy and diffi-
debridement is full-mouth disinfection. The technique is to
culty of access. Badersten et al showed in the 1980s that more
perform the full-mouth treatment at one session, or multiple
residual calculus remained in deeper pockets on up to 44%
sessions within a day or so, and using disinfectants with the
of the surfaces. Other studies have confirmed these findings,
intention preventing reinfection of treated sites from untreat-
including those comparing the use of hand instruments to
ed sites. This treatment approach may also be used for phase I
powered scaling instruments.
therapy, but it has not been shown to be superior to any other
Additional individual treatments, such as caries control and
phase I-therapy treatment plan.
correction of poorly fitting restorations, clearly augment the
There are multiple approaches to planning and performing
healing gained through good plaque-biofilm control and de-
nonsurgical phase I therapy Decisions as to how to proceed
bridement by making tooth surfaces accessible to cleaning pro-
should be discussed and agreed upon by the patient and the
cedures. Fig. 34.3 demonstrates the effects of an overhanging
dentist based on the amount of disease present and patient
amalgam restoration on gingival inflammation in an otherwise
comfort. Staged therapy permits the advantage of evaluating
healthy periodontium. Maximal healing from phase I treatment
and reinforcing oral-hygiene care and the one or two appoint-
is not possible when local conditions retain biofilm and pro-
ment therapies can be more efficient in reducing the number
vide reservoirs for repopulation of periodontal pathogens.
of office visits the patient is required to attend.
Step 3. Recontouring Defective Healing

Restorations and Crowns Healing of the gingival epithelium consists of the formation of
Corrections for restorative defects, which are plaque traps, may a longjunctional epithelium rather than new connective tissue
be made by smoothing surfaces and overhangs with burs or attachment to the root surfaces. The attachment epithelium
hand instruments or by replacing restorations. These procedures reappears about 1 week after therapy Gradual reductions in
can be completed concurrently with other phase I procedures. inflammatory cell population, crevicular-fluid flow, and repair
of connective tissue result in decreased clinical signs of inflam-
Step 4. Management of Carious Lesions mation, including less redness and swelling. One or two mil-
limeters of recession are often apparent as the result of tissue
Removal of the carious tissue and placement with either shrinkage. Connective-tissue fibers are disrupted and lysed by
temporary or permanent restorations is indicated in phase I the disease process and also by the inflammatory reaction to
FIGURE 34.3 Effects of overhanging amalgam margin on interproximal gingiva of maxillary first molar in otherwise healthy mouth. A, Clinical
appearance of rough, irregular, and overcontoured amalgam. B, Gentle probing of interproximal pocket. C, Extensive bleeding elicited by gentle prob-
ing indicating severe inflammation in the area.
treatment. These tissues require 4 or more weeks to reorganize surgical intervention. This is the measurement above which
and heal, and complete healing can take months. therapy will result in clinical attachment gain, and below it
Transient root sensitivity frequently accompanies the heal- will result in clinical attachment loss. This determination was
ing process. Although evidence suggests that relatively few made based on statistical analysis of surgical outcomes data. A
teeth in a few patients become highly sensitive, this develop- similar 5-mm standard has been commonly used as a guideline
ment is common and can be disconcerting to patients. The for identifying candidates for surgical referral based on the
extent of the sensitivity can be diminished through good understanding that the typical root length is about 13 mm and
plaque-biofilm removal. Warning patients about the potential the crest of the alveolar bone is at a level approximately 2 mm
outcomes of the teeth appearing longer because of shrinkage apical to the bottom of the pocket. When there is 5 mm of
of periodontal tissues and tooth root sensitivity at the begin- clinical attachment loss, the crest of bone is about 7 mm apical
ning of the treatment sequence will avoid surprise if these to the cementoenamel junction, therefore only about half the
changes occur. Unexpected and possibly uncomfortable con- bony support for the tooth remains. Periodontal surgery can
sequences to treatment may result in distrust and loss of mo- help improve support for teeth in these cases through pocket
tivation to continue therapy reduction, bone augmentation, and regeneration procedures.
Fig. 34.4 depicts the relationship of clinical attachment loss to
tooth support.
Decision to Refer for Specialist In addition to consideration of 5-mm probing depths, other
Treatment factors must also be factored into the decision to refer are listed.
Often, periodontal conditions heal sufficiently well after phase 1. Extent of disease and generalized or localized deep involve-
I therapy that no further treatment is required beyond routine ment. Extensive bone loss, even in localized areas, suggests
maintenance, making the treatment of most periodontal patients the need for specialized surgical techniques.
the responsibility of the general dentist. However, advanced or 2. Root length. Short roots are more seriously jeopardized by
complicated cases benefit from specialist care. It has been dem- 5 mm of clinical attachment loss than long roots.
onstrated by Heitz-Mayfield and Lang that surgical treatment 3. Hypermobility. Excessive tooth mobility suggests contribut-
in deep pockets, those >6 mm, gained 0.6 mm more probing ing factors and a more guarded prognosis.
depth reduction and 0.2 mm more clinical attachment gain than 4. Difficulty of scaling and root planing. The presence of deep
did deep pockets treated with scaling and root planing alone. pockets and furcations makes instrumentation much more
That group also confirmed that in pockets of 4-6 mm probing difficult and results can often be improved with surgical
depth, scaling and root planing resulted in 0.4 mm more at- access.
tachment gain than surgical procedures, and shallow pockets of 5. Restorability and importance of particular teeth for reconstruc-
1-3 mm had 0.5 mm less attachment loss compared to surgical tion. Long-term prognosis of each tooth is important when
results. It is critical to be skilled in determining which patients considering extensive restorative work.
would benefit from specialist care and should be referred. 6. Age of the patient. Younger patients with extensive attach-
The concept of the critical probing depth of 5.4 mm has been ment loss are more likely to have aggressive forms of dis-
advanced to assist in making the determination to proceed to ease that require extensive therapy
34 Phase I Periodontal Therapy 381
control of plaque biofilm levels by patients are particularly

significant. Phase I therapy should be comprehensive and
include scaling, root planing, and oral-hygiene instructions,
and other therapies, such as caries control, replacement of
defective restorations, occlusal therapy, orthodontic tooth
movement, and cessation of confounding habits, such as
tobacco use. Comprehensive reevaluation after phase I ther-
apy is essential to determine treatment options and to esti-
mate prognosis. Many patients can have their periodontal
disease controlled with phase I therapy alone and may not
require further surgical intervention. For patients who do
need surgical intervention, phase I therapy is an advanta-
geous element of treatment in that it permits tissue heal-
ing, thus improving the surgical management and healing
response of the tissues.
Periodontal surgical intervention should be considered
for patients with critically deep pocket depths and those
with 5 mm or more of attachment loss still present after
phase I therapy. Periodontal specialists can best provide
treatment to preserve the teeth for these patients with ad-
FIGURE 34.4 The 5-mm standard for referral to a periodontist is
vanced disease. It is also important to note that patients
based on root length, probing depth, and clinical attachment loss. The who do not demonstrate the ability to successfully control
standard serves as a reasonable guideline to analyze the case for re- plaque biofilm at home, on a daily basis, are poor candi-
ferral for specialist care. CEJ, Cementoenamel junction. (Redrawn with dates for successful surgical outcomes and should be closely
permission from Armitage C, editor: Periodontal maintenance therapy,
monitored on a recall-maintenance program unless condi-
Berkeley, California, 197 4, Praxis.)
tions change.
7. Lack of resolution of inflammation after scaling and planing. If REFERENCES

inflammation persists, further therapy is often necessary to
gain the most positive results. References for this chapter are found on the companion
Every patient is unique, and the decision process for each
patient is complex. The considerations presented in this chap- SUGGESTED READINGS
ter should provide guidance understanding the significance of American Academy of Periodontology, Ad Hoc Committee on the Parameters
phase I therapy and in making referral decisions. of Care: Phase I therapy, J Periodontal 7l(Suppl 5):856, 2000.
American Academy of Periodontology, Task Force to Update the Guidelines
for Periodontal Therapy: Comprehensive periodontal therapy: a statement
Conclusion by the American Academy of Periodontology, J Paiodontol 82:94 3, 2011.
Dentino A, Lee S, Mailhot J, et al: Principles of periodontology, Periodontal
The major goal of phase I therapy is to control the factors 2000 6116, 2013.
responsible for the periodontal inflammation; the remov- Heitz-Mayfield LJA, Lang NP: Surgical and nonsurgical periodontal therapy
al of subgingival bacterial biofilms, and the subsequent Learned and unlearned concepts, Periodontal 2000 62:218, 2013.
34 Phase I Periodontal Therapy 381.el
REFERENCES 12. Heitz-Mayfield LJA, Lang NP: Surgical and nonsurgical periodontal ther-
apy Learned and unlearned concepts, Periodontal 2000 62:218, 2013.
1. American Academy of Periodontology, Ad Hoc Committee on the Pa-
13. loannou I, Dimitriadis N, Papadimitriou K, et al: Hand instrumentation ver-
rameters of Care: Chronic periodontitis with slight to moderate loss of
sus ultrasonic debridement in the treatment of chronic periodontitis: a ran-
periodontal support,] Periodontol 71(Suppl 5):853, 2000.
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2. American Academy of Periodontology, Ad Hoc Committee on the Param-
14. Lang N, Tan WC, Krahenmann MA, et al: A systematic review of the ef-
eters of Care: Chronic periodontitis with advanced loss of periodontal
fects of full-mouth debridement with and without antiseptics in patients
support, J Periodontal 71(Suppl 5):856, 2000.
with chronic periodontitis,J Clin Periodontal 35:8, 2008.
15. Lightner LM, O'Leary TJ, Drake RB, et al: Preventive periodontics treat-
eters of Care: Periodontal maintenance, J Pe,iodontol 71(Suppl 5):849,
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2000.
16. lindhe J, Kock G: The effect of supervised oral hygiene on the gingiva of chil-
4. American Academy of Periodontology, Ad Hoc Committee on the Pa-
dren: progression and inhibition of gingivitis,] Pe1iodontal Res 1:260, 1966.
rameters of Care: Refractory periodontitis,J Periodontal 7l(Suppl 5):859,
17. Mongardini C, van Steenberghe D, Dekeyser C, et al: One stage full-
2000.
versus partial-mouth disinfection in the treatment of chronic adult or
generalized early-onset periodontitis. I. long-term clinical observations,
eters of Care: Phase 1 therapy,] Periodontal 7l(Suppl 5):856, 2000.
6. American Academy of Periodontology, Task Force to Update the Guide-
18. Perry DA, Beemsterboer PB: Periodontology [ov the dental hygienist, ed 4,
lines for Periodontal Therapy: Comprehensive periodontal therapy:
Philadelphia, 2013, Elsevier, Chapter 13.
a statement by the American Academy of Periodontology, J Periodontal
19. Quirynen M, Mongardini C, Pauwels M, et al: One stage full- versus
82:943, 2011.
partial-mouth disinfection in the treatment of chronic adult or general-
7. Badersten A, Nilveus R, Egelberg J: Effect of non-surgical periodontal
ized early-onset periodontitis. 11. long-term impact on microbial load, J
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20. Suomi JD, Greene JC, Vermillion JR, et al: The effect of controlled oral
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9. Cobb CM: Non-surgical pocket therapy: mechanical, Ann Pe,iodontol
21. Swierkot K, Nonnenmacher Cl, Mutters R, et al: One-stage full-mouth
1:443, 1996.
disinfection versus quadrant and full-mouth root planing,] Clin Periodon-
10. Dentino A, Lee S, Mailhot], et al: Principles of periodontology, Periodon-
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22. Tammaro S, Wennstrom Jl, Bergenholtz G: Root-dentin sensitivity fol-
11. Eberhard J, Jepsen S, jervoe-Storm PM, et al: Full-mouth disinfection for
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the treatment of adult chronic periodontitis. Cochrane Database Syst Rev
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Jan 23 (1) CD004622, 2008.
35
Plaque Biofilm Control
DA Perry • A Jain
Chapter Outline
The Tooth Brush Clinical Outcomes of Irrigation
Powered Toothbrushes Individuals with Special Considerations
Dentifrices Chemical Plaque Biofilm Control With
Toothbrushing Methods Oral Rinses
lnterdental Cleaning Aids Disclosing Agents
Gingival Massage Patient Motivation and Education
Oral Irrigation Conclusions
Mechanism of Action of Irrigation
Microbial plaque biofilm control is an effective way of treat- experimental setting with periodontally healthy subjects to
ing and preventing gingivitis and is an essential part of all prevent inflammation. The American Dental Association
the procedures involved in the treatment and prevention of (ADA) recommends that individuals brush twice per day
periodontal diseases. It is critical to the long-term success and use floss or other interdental cleaners once per day to
of all periodontal and dental treatment. In 1965, Loe et al effectively remove microbial plaque biofilms and prevent gin-
conducted the classic study demonstrating the relationship givitis. They recommend twice daily brushing because most
between microbial plaque biofilm accumulation and the individuals do not adequately remove microbial biofilms at
development of experimental gingivitis in humans. Subjects one brushing and doing it a second time improves the results.
in the study stopped brushing and other plaque biofilm con- Periodontal lesions are predominantly found in inter-
trol procedures, resulting in the development of gingivitis in dental locations, so toothbrushing alone is not sufficient to
every person within 7-21 days. The composition of the bio- control gingival and periodontal diseases. It has been dem-
film bacteria also shifted so that more virulent Gram-negative onstrated in healthy subjects that plaque biofilm formation
organisms predominated, and these changes were shown to begins on the interproximal surfaces where the toothbrush
be reversible within 7 days. Good supragingival biofilm con- does not reach. Masses of biofilm first develop in the molar
trol has also been shown to affect the growth and composition and premolar areas, followed by the proximal surfaces of
of subgingival plaque so that it favors a healthier microflora the anterior teeth and the facial surfaces of the molars and
and reduces calculus formation. Carefully performed daily premolars. Lingual surfaces accumulate the least amount of
home plaque biofilm control, combined with frequent pro- biofilm. Patients consistently leave more plaque biofilm on
fessionally delivered plaque biofilm and calculus removal, the posterior teeth than the anterior teeth, with interproxi-
reduces the amount of supragingival biofilm; decreases the mal surfaces retaining the highest amounts of biofilm, exactly
total number of microorganisms in moderately deep pockets, the places in which periodontal infections begin. In addition,
including furcation areas; and greatly reduces the quantity of periodontal patients have increased susceptibility to disease,
periodontal pathogens. Reviews of home care procedures in complex defects in gingival architecture, and long exposed
2011 and 2013 confirm the positive effects of daily plaque root surfaces to clean, compounding the difficulty of doing a
biofilm removal but cautions that these gains appear to be thorough job of cleaning.
small and best results also require professional maintenance Chemical inhibitors of plaque biofilm and calculus that
care. are incorporated in mouthwashes or dentifrices also play
Microbial biofilm growth occurs within hours, and it important roles in controlling microbial biofilms. Fluorides
must be completely removed at least once every 48 h in the delivered through toothpastes and mouthrinses are essential
383
for caries control. Many products are available as adjunctive are the important considerations. The effectiveness of and
agents to mechanical techniques. These medicaments, as with potential injury from different types of brushes depend to a
any drug, should be recommended and prescribed according great degree on how the brushes are used. Data from in vitro
to the needs of individual patients. studies of abrasion by different manual toothbrushes suggest
Daily plaque biofilm control permits each patient to assume that brush designs permitting the bristles to carry more tooth-
responsibility for oral health every day. Without it, optimal paste while brushing contribute to abrasion more than brush
oral health through periodontal treatment cannot be attained bristles themselves. However, it has been shown that use of
or preserved. Elements of biofilm control include mechanical hard toothbrushes, vigorous horizontal brushing, and use of
cleaning and chemical adjuncts. extremely abrasive dentifrices may lead to cervical abrasions
of teeth and recession of gingiva.
The Tooth Brush
Toothbrush Design
Toothbrushes vary in size and design as well as in length, hard-
ness, and arrangement of the bristles (Fig. 35.1). The ADA has Toothbrush bristles are grouped in tufts that are usually
described the range of dimensions of acceptable brushes: as arranged in three or four rows (Fig. 35.1). Two types of bristle
having a brushing surface 1-1.25 in. long and 5/16-3/8 in. material are used in toothbrushes: natural bristles from hogs
wide, 2-4 rows of bristles, and 5-12 tufts per row. A study and artificial filaments made of nylon. Both remove microbial
compared four commercially available toothbrushes for total plaque biofilms, but nylon bristle brushes vastly predominate
plaque biofilm removal at a single brushing; all four tooth- the market.
brushes removed biofilms equally, and the authors concluded The amount of force used to brush is not critical for effective
that no one design was superior to others. plaque biofilm removal. Vigorous brushing is not necessary and
When recommending a particular toothbrush, ease of use can lead to gingival recession, wedge-shaped defects in the cer-
by the patient and the perception that the brush works well vical area of root surfaces, and painful ulceration of the gingiva.
FIGURE 35.1 Manual toothbrushes. A, Toothbrushes from the nineteenth and twentieth centuries, one with an ivory handle from about 1890
(left), one with a composition handle from the 1950s (center), and one with a sterling silver handle from the early twentieth century (right). The
ivory-handled brush belonged to a dental student who used the handle to practice cutting preparations and filling the "preps" with amalgam or gold
foil. B, Various types of toothbrushes are available; note the variation in brush head and handle design. C, Brush heads, showing various bristle con-
figurations. (Antique brushes courtesy Dean John 0.8. Featherstone, University of California, San Francisco School of Dentistry Historical Collection,
San Francisco.)
35 Plaque Biofilm Control 385
Toothbrushes must also be replaced periodically although

the amount of visible bristle wear does not appear to affect
plaque biofilm removal for up to 9 weeks. Most clinicians rec-
ommend that toothbrushes be replaced every 3-4 months.
Introduction of modern bristle designs provided for safer
and more effective brushing and laid the foundation for the
further development of brush heads, bristle designs, and ergo-
nomic handles. Successive innovations addressing clinical/
patient needs have included the introduction of end-rounded
filaments, indicator filaments, multilevel filaments, polishing
cup filaments, toe tufts, bristles of varying density, and tapered
filaments. Some of the advantages of such innovations are
End rounding: End-rounded bristles are less likely to result in
gingival trauma and are gentler and safer than stiff, sharp-
edged filament.
The indicator bristles: They are created by infusing a blue food-
grade dye into the outer layer of the bristles. As the brush
is used, the color gradually dissipates. Since worn filaments
are more likely to damage the gingivae and are less effective
at removing plaque, they inform the users when to replace
their toothbrush.
Trim: Research has consistently shown that multilevel-
trimmed brushes are more effective for plaque removal
than flat trimmed, especially at interproximal sites. Brushes
incorporating rows of tall, thin, elliptically-shaped tufts, to-
gether with rows consisting of shorter tufts in a row along FIGURE 35.2 Multilevel bristles for effective plaque disruption and
both sides of the brush head, enhance cleaning efficacy by removal. A, Tall thin bristle tufts that crisscross that optimize interproxi-
improving reach into interproximal areas and gingival mar- mal cleaning. B, Short, dense bristle tufts that criscross effectively clean
smooth surfaces.
gins. As a result, major manufactures such as Oral-B, Col-
gate, GSK, and so on introduced brushes with multilevel
trim to improve brushing efficacy in hard-to-reach areas. The angled, multilevel bristles and tufts of just the right
Polishing cup filaments: Another innovation was introduction stiffness together ensure the most effective brushing under
of polishing cup bristles. These consist of tightly-packed normal home care conditions.
center bristles that help to keep the dentifrice against the
tooth surface, thereby aiding extrinsic stain removal. The Powered Toothbrushes
bristles feel stiff because they are densely packed and short.
They are surrounded by taller, angled bristle tufts that hug By 193 7, the first powered toothbrush had been created in
the tooth and help the dentifrice polish extrinsic stain off Switzerland. In the same year, Motodent Inc. of Los Angeles
the tooth surfaces. launched a powered toothbrush that had individual arms des-
Soft, medium and hard bristles: Brushes are available with soft, ignated for each family member. The movement of the early
medium, and hard bristles. While it is generally believed brushheads used side-to-side or elliptical motions aimed to
that use of a hard-bristled brush will result in more tooth mimic the motion of a person using a manual brush. In 1964,
abrasion than a soft-bristled brush, it is the use of a tooth- the ADA Council on Dental Therapeutics reorganized the GE
brush and toothpaste together that may result in dental power toothbrush as an effective cleansing device. At this time,
abrasion and sensitivity. Soft bristles flex more than hard powered toothbrushes were only recommended for people
bristles, letting the brush head accommodate more tooth- with limited physical and mental capacities. However, by the
paste between the bristles, and therefore more of the abra- 1980s-90s, a new generation of power brushes had arrived.
sive. Additionally, although hard bristles may be effective This period witnessed innovative brush designs and modes of
for plaque removal, they have the propensity to result in action that improved the effectiveness of this toothbrush cat-
trauma to the gingival tissues. Using an effectively designed egory and allowed people to remove plaque more effectively.
soft-bristled toothbrush and low abrasive toothpaste re- Numerous clinical studies confirmed that power toothbrushes
duces the risk of both gingival and tooth abrasion while were more effective than manual. Improved tooth surface
effectively removing plaque and stain. Bristle hardness is cleaning, as well as a reducing and controlling gingivitis, were
proportional to the square of the diameter and inversely shown to be the greatest benefits of power toothbrushes. In
proportional to the square of bristle length. Diameters of long-term studies, power toothbrushes provided better plaque
common bristles range from 0.007 in. (0.2 mm) for soft reduction and protection against gingivitis than manual tooth-
brushes to 0.012 in. (0.3 mm) for medium brushes and brushes. Nevertheless, within the power toothbrush category,
0.014 in. (04 mm) for hard brushes. there are significant differences in efficacy between tooth-
Angled bristles: Brushes with cross-action bristles have been brushes with different modes of action [eg, oscillating/rotating,
demonstrated to be superior to numerous manual tooth- side-to-side (sonic), and counter-oscillation].
brush designs in short- and long-term clinical trials, for ex- Currently, powered toothbrushes have oscillating and rotat-
ample, Oral- B Cross Action Power Toothbrush (Fig. 35 2). ing motions (Fig. 35.3), and some brushes use low-frequency
contribute to the cosmetic benefits or physical properties of

the dentifrice. This section describes the most common denti-
frice ingredients used to provide anticaries, antibacterial, anti-
calculus, whitening, and antihypersensitivity benefits.
Caries prevention
Caries is simply the result of a series of demineralization/
remineralization cycles where, over time, demineralization
conditions prevail. One of the most effective methods to
prevent caries is by promoting remineralization and slow-
ing down demineralization. This can be accomplished with
fluoride therapy. Fluoride's presence in low concentration and
high frequency is more effective at preventing caries than high
levels of fluoride used in low frequency Fluoridated dentifrice
is the best method for delivering fluoride to the tooth surface.
Fluoride can be delivered in several different chemical
forms:
FIGURE 35.3 Powered toothbrush designs offer options in head
shape and size. • stannous fluoride (SnF2)
• sodium fluoride (NaF)
• sodium monofluorophosphate
acoustic energy to enhance cleaning ability The frequency • amine fluoride
at which the brush head oscillates should be in the range of • aluminum fluoride (A1F3)
8500-9000 oscillations per minute. In addition, the brush a. Stannous fluoride. Stannous fluoride (SnF2; also called tin
head should be angled 3-5 degrees from the handle to help fluoride) was first formulated successfully into a denti-
users reach posterior regions and allow effortless progression frice to deliver an anticaries benefit by Proctor & Gamble.
from tooth to tooth. Its CREST formulation included 0.454% stannous fluo-
Typically, comparison studies of powered toothbrushes, ride and the abrasive calcium pyrophosphate.
manual toothbrushes, or other powered devices demon- b. Sodium fluoride. Sodium fluoride (NaF) has greater sta-
strate slightly improved plaque biofilm removal by powered bility than stannous fluoride and thus is easier to formu-
toothbrushes in short-term clinical trials. A recent Cochrane late. Sodium fluoride delivers a highly reactive fluoride
review reported that mechanical brushes with oscillating and ion (Crest with Fluoristat).
rotating motions reduced microbial plaque biofilm 11 % and c. Sodium monofluorophosphate. Sodium monofluorophos-
demonstrated 6% greater reduction in gingival bleeding than phate (MFP) was introduced into Colgate's first fluoridated
manual brushing. These improvements were maintained over dentifrice. MFP is a fluoridated compound that requires
3 months. Although long-term benefits have not been estab- enzymatic activation by a salivary enzyme (alkaline phos-
lished, this particular style of mechanical brush resulted in phatase) to release bioavailable fluoride.
better microbial plaque biofilm and gingivitis reduction in a
number of well-controlled studies.
Patient acceptance of powered toothbrushes is good. One Anticalculus
study reported that 88.9% of patients introduced to a pow-
By 1980s, agents were discovered that could provide better
ered toothbrush would continue to use it. However, patients
calculus and stain control. The chemical agents used for cal-
have also been reported to quit using powered toothbrushes
culus control in dentifrice are
after 5 or 6 months, presumably when the novelty is gone.
Powered toothbrushes have been shown to improve oral health a. Pyrophosphate. Pyrophosphate occurs naturally in saliva
for (1) children and adolescents, (2) children with physical or and plays a role in inhibiting calculus formation. These
mental disabilities, (3) hospitalized patients, including older molecules chelate calcium, slowing the rate of nucleation
adults who need to have their teeth cleaned by caregivers, and (crystal formation) and calcification of plaque. The pyro-
( 4) patients with fixed orthodontic appliances. phosphate binds to calcium in a growing crystal, essentially
blunting further crystal growth at that site and effectively
decreasing calculus buildup. Crest Tartar Control contains
Dentifrices 3.3% pyrophosphate. It was the first tartar control denti-
People have used various compounds (eg, pumice, oyster frice introduced to the market and the first dentifrice to
shells, and chalk) to clean their teeth since around 5000 BC. receive the ADA seal for tartar control.
However, only since the 1950s have dentifrices been used to b. Sodium hexametaphosphate (HMP). Sodium HMP is a large
prevent and treat specific diseases and conditions. The most polyphosphate molecule and has multiple calcium binding
recent advances in dentifrices have been in the area of deliver- sites in one molecule. It is a very effective calculus inhibi-
ing multiple benefits in one dentifrice and in the introduction tor. Sodium HMP is too large of a molecule to enter into
of new products to treat dentinal hypersensitivity Dentifrice tooth enamel, so there is no danger of it entering between
ingredients help reduce caries, plaque, gingivitis, calculus, enamel rods and sequestering calcium from sound enamel.
stain, halitosis, and hypersensitivity Some ingredients pro- Since it works only on the surface, it is sometimes called a
vide a therapeutic benefit while other ingredients or additives calcium surface-active builder.
c. Zinc. Zinc salts (eg, zinc citrate, zinc chloride, zinc lactate) a. Stannous. Stannous ion (Sn2+) is an effective antibacterial
are used in some tartar control dentifrices and oral rinses agent. In early formulations of stannous fluoride denti-
and have been shown to be moderately effective at con- frices, stannous was not stable or bioavailable. Current
trolling calculus. Positively charged zinc ion (Zn2+) inhibits stannous-containing dentifrices have been formulated to
crystal growth by substituting for calcium in the crystal lat- circumvent stannous instability and bioavailability chal-
tice of calcium phosphate. This corrupts the crystal forma- lenges. Crest Gum Care, introduced in 1995, contained
tion and slows crystal growth. However, zinc-containing stabilized stannous and delivered antibacterial benefits.
dentifrices have some limitations such as poor bioavailabil- Stannous exerts antibacterial effects by two actions. One
ity and an astringent taste. is by being bactericidal and its nonspecific interaction with
d. Gantrez. Gantrez is a copolymer of methylvinyl ether (PVM) the bacterial membrane that causes membrane disruption.
and maleic acid (MA) and acts as a chelating agent. It is an The second mode of antibacterial activity is through stan-
ingredient in Colgate Total. It acts by binding (chelating) nous ion's inhibition of metabolic enzymes, which further
calcium ions, thus inhibiting plaque mineralization. lead to reduction of bacterial growth, prevention of bacte-
rial adhesion to oral surfaces (eg, enamel) and reduction in
bacterial byproducts. Stannous can also have an astringent
Whitening Agents
taste and cause extrinsic staining of teeth and fillings.
Stain control and whitening are key benefits of modern b. Triclosan. Triclosan is a broad-spectrum antibacterial agent
dentifrices. These are accomplished via ingredients that tar- that inserts into and disrupts the bacterial membrane.
get specific types of tooth stain. Dentifrices primarily work Being a nonpolar molecule, it has an affinity for the hy-
against extrinsic stains. Bleaching products that contain drophobic environment of the lipid bilayer. This causes
hydrogen peroxide or carbamide peroxide (ie, dental office leakage of cellular components, ultimately leading to cell
bleaching trays) address intrinsic stains as well as extrinsic death.
stains. c. Zinc. Zinc ion (Zn2+), in addition to having anticalculus
benefits, also has mild antibacterial properties. It has been
a. Extrinsic stain. Extrinsic (surface) stains can be relatively
suggested that zinc binds to the membranes of microor-
easily removed on a daily basis by proper tooth brushing
ganisms, inhibiting cell division and slowing the growth
with a dentifrice.
cycle. Adding zinc to a dentifrice formulation also pres-
Physical action. Most dentifrices contain mild abrasives
ents some challenges such as poor bioavailability and an
that help clean precipitated stain particles from the tooth
unpleasant taste.
surface; controlling surface stains with home care. The
d. Chlorhexidine. Chlorhexidine is a chemical agent with a
abrasivity of dentifrice is measured in terms of Relative
bactericidal action. Similar to triclosan, chlorhexidine
Dentin Abrasivity, or RDA. The lower the RDA, the less
acts to disrupt bacterial membranes, resulting in bacterial
abrasive the dentifrice. This means less potential to wear
death. Chlorhexidine is primarily used as a therapeutic
tooth structure through tooth brushing. Since dentifrices
ingredient in mouthwash and some dentifrices, however,
with lower RDA values are less abrasive, they also tend
it has some side effects such as poor taste and staining.
to have less potential to remove surface stain. The Inter-
national Standards Organization (ISO) specification states
that a dentifrice should not exceed an RDA of 250, which Anti hypersensitivity
is considered safe for hard tissues.
It has been reported that up to 57% of the adult population
Chemical action. Polyphosphates, which are dentifrice
suffers from Dentinal hypersensitivity. Dentinal hypersensitiv-
ingredients used to control calculus, also target extrin-
ity is generally treated in one of the two ways.
sic stain. One of the most effective ingredients with this
dual action is sodium HMP, which is used in several den- • chemical desensitization of the tooth nerve endings
tifrices. Stain molecules, or chromogens, are usually nega- • tubule occluding agents or barriers to reduce dentin perme-
tively charged molecules and have an affinity for positively ability.
charged ions like calcium (Ca2+) in the tooth enamel and a. Nerve Depolarization Agents. Potassium ion (K+), sodium
cross-link pellicle proteins. HMP is also negatively charged ion (Na"), and chloride ion (Cl) are important ions in-
with a strong affinity for calcium. HMP can displace stain volved in the electrical activity of nerve cells. When the
molecules from calcium binding sites. It binds to the tooth nerve cell is at rest, the potassium ion concentration is
surface and integrates into the pellicle to prevent addition- higher on the inside of the cell than on the outside, while
al stain molecules from binding. the sodium ion concentration is higher on the outside of
b. Intrinsic stain. Intrinsic stains are stains and discolorations the cell than on the inside. When the nerve cell is stimu-
that are located below the enamel surface. Due to their lated, these ions cross the nerve cell membrane through
diverse etiology, intrinsic stain treatment varies with the channels and move from an area of high concentration
cause. Bleaching is usually used to remove or minimize to an area of lower concentration (referred to as the con-
intrinsic discolorations. centration gradient). Thus, potassium ions flow from
the inside to the outside of the cell and the sensation of
pain is transmitted. Potassium ion is a desensitization
Antibacterial Action
agent because it diffuses through dentin tubules and in-
Adding antibacterial action to dentifrice was another major creases the extracellular potassium concentration at the
therapeutic breakthrough. Several modern dentifrice ingredi- nerve ending, eliminating the potassium ion concentra-
ents have the potential to kill or inhibit bacteria that cause tion gradient across the nerve cell membrane. Without
plaque, gingivitis, and oral malodor. this concentration gradient, the nerve cell becomes
depolarized and will not respond to stimuli, thus the Flavors/Sweeteners

sensation of pain will not be transmitted. Potassium ion Flavoring agents and sweeteners are added to improve the
can be delivered in a variety of salt forms (eg, potassium dentifrice taste. Common flavoring agents and sweeteners
nitrate, potassium citrate). The most common potassi- include peppermint, saccharin, and xylitol.
um salt used in sensitivity dentifrice is potassium nitrate
(KN03) (Sensodyne). Surfactants
b. Tubule Bloching or Occluding Agents. Another strategy Surfactants (detergents) create the foaming and aid in the
to treat/prevent dentinal hypersensitivity is to reduce cleaning process by helping to loosen plaque and debris.
the permeability of the dentin by occluding or block- Sodium lauryl sulfate (SLS) is the surfactant most commonly
ing the exposed dentin tubules. This prevents stimuli used.
from causing fluid flow in the tubules, thereby pre-
venting the nerve endings inside the tooth from being Colors/Visuals
stimulated. Strontium chloride was one such desensi- Finally, coloring agents are added to provide dentifrice with
tizing ingredient which worked via formation of stron- pleasing colors. The opacity of a paste dentifrice comes from
tium salt precipitates. the addition of titanium dioxide. Mica is used to provide a
c. Newer tubule-occluding agents. Other tubule-occluding sparkly appearance in some dentifrices, such as those mar-
agents new to the market include arginine with calcium keted to children.
carbonate (Pro-Argin), strontium acetate, and calcium
sodium phosphosilicate (Novamin).
Toothbrushing Methods
Arginine, found naturally in saliva, may have a natural
function of ushering calcium to open tubules for incorpora- Many methods for brushing the teeth have been described
tion of calcium phosphate into dentin. Calcium carbonate and promoted as being efficient and effective. These meth-
creates a basic environment. Calcium phosphate salts are less ods can be categorized primarily according to the pattern of
soluble at higher pH (more basic), therefore the combination motion when brushing and are primarily of historic interest,
of high local calcium concentration at the dentin tubule at as follows:
basic pH promotes rapid precipitation of calcium phosphate Roll: Roll or modified Stillman technique
salts. Vibratory: Stillman, Charters, and Bass techniques
Strontium (Sr2+) is a metal ion, and in the oral cavity it can Circular: Fones technique
form insoluble metal salts that can plug dentin tubules. Vertical: Leonard technique
Stannous ion is also a tubule-occluding agent that treats Horizontal: Scrub technique
dentinal hypersensitivity through hydrolysis and oxidation
reactions, which form many insoluble metal salts that can pre- Patients with periodontal disease are most frequently
cipitate in dentinal tubules and on the dentin surface. taught a sulcular brushing technique using a vibratory
motion to improve access to the gingival margin areas. It is
important for patients to understand that the plaque biofilm
Other Dentifrice Ingredients removal at the dento-gingival junction is necessary to pre-
vent caries as well as periodontal disease. This is referred to
Nontherapeutic dentifrice components include binders, sur-
as "target hygiene." The method most often recommended
factants, buffering agents, humectants, preservatives, sweet-
is the Bass technique because it emphasizes the placement of
eners, flavorings, and dyes. These components are essential to
the bristles at this most important area. This sulcular place-
keep the dentifrice properly mixed with a smooth consistency,
ment of the bristle and adapting the bristle tips to the gin-
and they make the product palatable to the consumer. Three
gival margin to reach the supragingival plaque biofilm and
dentifrice ingredients (abrasive, humectants, and solvent) typ-
accessing some of the subgingival biofilm may be the most
ically represent about 95% of the dentifrice ingredients.
important aspect of "target hygiene." A controlled vibrat-
Humectants ing motion is used to dislodge microbial plaque biofilm and
avoid trauma. The brush is systematically placed on all the
Humectants retain moisture so that the dentifrice does not dry
teeth in both arches. Figures 35.4 and 35.5 illustrate this
out. Humectants, such as glycerin and sorbitol, also inhibit
brushing technique.
bacterial growth and provide flowability to the dentifrice.
Binders Bass Technique
Binders, also referred to as thickeners, provide texture and
determine how "thick" or "runny" the dentifrice is. Binders are 1. Place the head of a soft brush parallel with the occlusal
used for cohesiveness, to provide body, and to prevent ingre- plane, with the brush head covering three to four teeth,
dients from separating. Xanthan gum, carboxymethyl cellu- beginning at the most distal tooth in the arch.
lose (CMC) carbomers, carrageenan, and synthetic cellulose 2. Place the bristles at the gingival margin, pointing at a
are all commonly used dentifrice binders. 45-degree angle to the long axis of the teeth.
3. Exert gentle vibratory pressure, using short, back-and-
Buffers forth motions without dislodging the tips of the bristles.
Manufacturers use buffers as part of their dentifrice formula- This motion forces the bristle ends into the gingival sulcus
tion to keep the pH constant. Trisodium phosphate, pyro- area (Fig. 35. 4), as well as partly into the interproximal
phosphates, and sodium citrate are examples of dentifrice embrasures. The pressure should be firm enough to blanch
buffers. the gingiva.
(B)
FIGURE 35.4 Bass method. A, Place the toothbrush so that the bristles are angled approximately 45 degree from the tooth surfaces. B, Start at the
most distal tooth in the arch, and use a vibrating, back-and-forth motion to brush.
I
I
I
I
I
I
I
I
,,, I f
I
_, "' I
(B) 45-----.J
FIGURE 35.5 Bass method. A, Proper position of the brush in the mouth aims the bristle tips toward the gingival margin. B, Diagram shows the ideal
placement, which permits slight subgingival penetration of the bristle tips.
Brushing With Powered Toothbrushes • Brushing with either a manual or a powered toothbrush re-
quires a systematic routine to clean all the accessible areas.
The various mechanical motions built into powered tooth- • Patients will modify any technique to their needs but must
brushes do not require special techniques. The patient needs achieve the goal of brushing effectively until the teeth are
to only place the brush head next to the teeth at the gingival free of plaque biofilm on all accessible surfaces.
margin, using a targeted hygiene approach, and proceed sys-
tematically around the dentition. A routine method of brush-
ing all the teeth, similar to the method described for manual
brushing, should also be used with powered toothbrushes
lnterdental Cleaning Aids
(Fig. 35.6). Any toothbrush, regardless of the brushing method used,
does not completely remove interdental plaque biofilms. This
Recommendations is true for all brushers, even periodontal patients with wide-
open embrasures. Daily interdental plaque biofilm removal is
• Targeted hygiene focuses brushing efforts on the cervical crucial to augment the effects of toothbrushing because most
and interproximal portions of the teeth where microbial dental and periodontal diseases originate in interproximal
plaque biofilm accumulates first. areas.
FIGURE 35.6 Positioning the powered toothbrush head and bristle tips so that they reach the gingival margin is critical to achieving the most
effective cleaning results. A, Straight-head placement. B, Round-head placement.
Tissue destruction associated with periodontal disease

often leaves large, open spaces between teeth and long,
exposed root surfaces with anatomic concavities and furca-
tions. These areas shelter plaque biofilms and are both difficult
for patients to clean and poorly accessible to the toothbrush.
Patients need to understand that the purpose of interdental
cleaning is to remove microbial plaque biofilms, not just dis-
lodge food wedged between teeth. Many tools are available
for interproximal cleaning and they should be recommended
based on the size of interdental spaces, presence of furcations,
tooth alignment, and presence of orthodontic appliances or
fixed prostheses. Also, ease of use and patient cooperation are
important considerations. Common aids are dental floss and
interdental cleaners such as wooden or plastic tips and inter-
dental brushes. FIGURE 35.7 Dental floss should be held securely in the fingers or
tied in a loop.
Dental Floss
2. Stretch the floss tightly between the thumb and forefinger
Dental floss is the most widely recommended tool for remov- (Fig. 35.7), or between both forefingers, and pass it gen-
ing biofilm from proximal tooth surfaces. Floss is made tly through each contact area with a firm back-and-forth
from nylon filaments or plastic monofilaments and comes in motion. Do not snap the floss past the contact area because
waxed, unwaxed, thick, thin, and flavored varieties. Some this may injure the interdental gingiva. In fact, zealous
prefer monofilament flosses made of a nonstick material snapping of floss through contact areas creates proximal
because they are slick and do not fray. Clinical research has grooves in the gingiva.
demonstrated no significant differences in the ability of the 3. Once the floss is apical to the contact area between the
various types of floss to remove dental plaque biofilm; they all teeth, wrap the floss around the proximal surface of one
work equally well. Waxed dental floss was thought to leave a tooth, and slip it under the marginal gingiva. Move the
waxy film on proximal surfaces, thus contributing to biofilm floss firmly along the tooth up to the contact area and
accumulation and gingivitis. It has been shown, however, that gently down into the sulcus again, repeating this up-and-
wax is not deposited on tooth surfaces and that improvement down stroke 2 or 3 times (Fig. 35.8). Then, move the floss
in gingival health is unrelated to the type of floss used. Fac- across the interdental gingiva, and repeat the procedure on
tors influencing the choice of dental floss include the tightness the proximal surface of the adjacent tooth.
of tooth contacts, roughness of proximal surfaces, and the 4. Continue through the whole dentition, including the distal
patient's manual dexterity, not the superiority of any one prod- surface of the last tooth in each quadrant. When the work-
uct. Therefore recommendations about type of floss should be ing portion of the floss shreds or becomes dirty, move to a
based on ease of use and personal preference. fresh portion of floss.
Technique Flossing can be facilitated by using a floss holder (Fig. 35. 9A).
Floss holders are helpful for patients lacking manual dexter-
The floss must contact the proximal surface from line angle
ity and for caregivers assisting patients in cleaning their teeth.
to line angle to clean effectively. It must also clean the entire
A floss holder should be rigid enough to keep the floss taut
proximal surface, including accessible subgingival areas, not
when penetrating into tight contact areas, and it should be
just be slipped apical into the contact area. Flossing technique
simple to string with floss. The disadvantage is that floss tools
requires the following:
are time-consuming because they must be rethreaded fre-
1. Start with a piece of floss long enough to grasp securely; quently when the floss shreds.
12-18 in. is usually sufficient. It may be wrapped around Disposable, single-use floss holders with prethreaded floss
the fingers, or the ends may be tied together in a loop. are also available. Short-term clinical studies suggest that plaque
FIGURE 35.8 Dental floss technique. The floss is slipped between the
contact area of the teeth (in this case, teeth #7 and #8), is wrapped
around the proximal surface, and removes plaque by using several
up-and-down strokes. The process must be repeated for the distal sur-
face of tooth #8.
biofilm reduction and improvement in gingivitis scores are sim-

ilar for patients using disposable floss devices as for patients
who hold the floss with their fingers (Fig. 35 9B).
Powered flossing devices are also available (Fig. 35 .10). The
devices have been shown to be safe and effective, but no better
at plaque biofilm removal than holding the floss in the fingers.
Establishing a lifelong habit of flossing the teeth is difficult
to achieve for both patients and dentists, regardless of whether FIGURE 35.10 Powered flossing devices can be easier for some patients
one uses a tool or flosses with the fingers. In fact, the daily use to use than handheld floss. The tip is inserted into the proximal space, and
of floss is universally low. It has been reported that only about a bristle or wand comes out of the tip and moves in a circular motion when
8% of young teenagers in Great Britain flossed daily, with simi- the device is turned on (left). Alternately, the device moves the prestrung
floss in short motions to provide interproximal cleaning (right).
lar percentages reported for other countries. No information is
available about the establishment of long-term flossing habits
comparing the various tools to finger flossing. However, the • Flossing tools work as well as flossing with the traditional
tools may be useful to help some individuals begin flossing method.
or to make flossing possible if patients have limited dexterity. • The flossing habit is difficult to establish.
Recommendations lnterdental Cleaning Devices

• The benefits of interproximal cleaning using dental floss are Concave root surfaces such as the mesial aspect of the maxillary
undisputed. first bicuspid and furcations are often present in periodontal
FIGURE 35.9 Floss holders can simplify the manipulation of dental floss. A, Reusable floss tools require stringing the floss around a series of knobs
and grooves to secure it. B, Disposable floss tools have prestrung floss and are easy to use, but the floss may shred and break, requiring several tools
to complete flossing the teeth.
(A) (B) (C) interdental devices have handles for convenient manipulation
around the teeth and in posterior areas. Clinical research has
shown that the devices are effective on lingual and facial tooth
surfaces as well as on proximal surfaces.
Technique. Interdental brushes of any style are inserted

through interproximal spaces and moved back and forth be-
tween the teeth with short strokes. The diameter of brush
should be slightly larger than the gingival embrasures to be
cleaned. This size permits bristles to exert pressure on both
proximal tooth surfaces, working their way into concavities
on the roots.
Single-tufted brushes provide access to furcation areas, or
isolated areas of deep recession, and work well on the lingual
FIGURE 35.11 lnterproximal embrasure spaces vary greatly in
surfaces of mandibular molars and premolars. These areas are
patients with periodontal disease. In general, A, embrasures with no often missed when using a toothbrush and floss.
gingival recession are adequately cleaned using dental floss; B, larger
spaces with exposed root surfaces require the use of an interproximal Wooden or Rubber Tips
brush; and C, single-tufted brushes clean efficiently in interproximal
Wooden toothpicks are used either with or without a han-
spaces with no papillae.
dle (Fig. 35.12A and B). Access is easier from the buccal
surfaces for tips without handles but is limited primarily to
patients who have experienced significant attachment loss the anterior and bicuspid areas. Wooden toothpicks used on
and recession, and they are not cleaned well with dental floss. handles improve access to all areas and have been shown
A comparison study of dental floss and interdental brushes to be as effective as dental floss in reducing plaque biofilm
used by patients with moderate to severe periodontal disease and bleeding scores in subjects with gingivitis. Triangular
showed that the interproximal brushes removed slightly more wooden tips are also available; this design is most useful in
interproximal plaque biofilm and that subjects found them the anterior areas when used from the buccal surfaces of the
easier to use than dental floss. However, no differences were teeth. Rubber tips are conical and are mounted on handles
seen in probe depth reductions or bleeding indices. There- or the ends of toothbrushes; they are reusable and can be
fore interproximal cleaning aids, such as interdental brushes, easily adapted to all proximal surfaces in the mouth. Plastic
are adequate for proximal cleaning of teeth when interdental tips that resemble wooden or rubber tips are also available
spaces permit access. and are used in the same way.
Embrasure spaces vary greatly in size and shape.
Figure 35.11 provides a representation of the size and anat- Technique. Toothpicks are common devices and readily avail-
omy of three types of embrasures and the type of interdental able in most homes. They can be used around all surfaces
cleaner often recommended for each. As a general rule, the of the teeth when attached to commercially available handles
larger the space, the larger the device needed to clean it. (Fig. 35 12B) Once mounted on the handle, the toothpick is
broken off so that it is only 5- or 6-mm long. The tip of the
lnterdental Brushes
toothpick is used to trace along the gingival margin and into
A wide variety of interdental cleaning devices are available for the proximal areas from both the facial and the lingual surface
removing microbial plaque biofilm from between the teeth of each tooth (Fig. 35.13). Toothpicks mounted on handles
(Fig. 35.12). The most common types are conical or cylin- are efficient for cleaning along the gingival margin, can pen-
drical brushes, tapered wooden toothpicks that are round or etrate into periodontal pockets and furcations, and permit
triangular in cross section, and single-tufted brushes. Many patients to target their hygiene efforts at the gingival margin.
Soft, triangular wooden picks or plastic picks are placed in
the interdental space with the base of the triangle resting on
the gingiva and the sides in contact with the proximal tooth
surfaces (Fig. 35.14). The pick is then repeatedly moved in
and out of the embrasure several times to remove the biofilm.
The disadvantage of triangular wooden or plastic tips is that
they do not reach well into the posterior areas or on the lin-
gual surfaces.
Rubber tips should be placed into the embrasure space,
resting on the gingiva, and used in a circular motion. They can
be applied to interproximal spaces and other defects through-
out the mouth and are easily adaptable to lingual surfaces.
Recommendations
• Often a toothbrush and dental floss are not sufficient to
clean interdental spaces adequately, so it is extremely im-
FIGURE 35.12 lnterproximal cleaning devices include wooden tips (A portant to find an interdental device that the patient likes
and B), interproximal brushes (C-F), and rubber tip stimulators (G). and will use.
FIGURE 35.13 Wooden toothpick. A, The tip is a common wooden toothpick held in a handle and broken off. It is used to clean subgingivally and
reach into periodontal pockets. B, The tip can also be used to clean along the gingival margins of the teeth and reach under the gingiva.
and connective tissue. The increased keratinization occurs

only on the gingiva facing the oral cavity and not on the areas
more vulnerable to microbial attack, which are the sulcular
epithelium and the interdental areas where the gingival col is
present. Epithelial thickening, increased keratinization, and
increased blood circulation have not been shown to be ben-
eficial for restoring gingival health. Improved gingival health
associated with interdental stimulation is much more likely
the result of microbial plaque biofilm removal than gingival
massage.
Oral Irrigation
FIGURE 35.14 Triangular wooden tips are also popular with pa-
tients. The tip is inserted between the teeth, with the triangular portion Home/Self-Applied Irrigation
resting on the gingival papilla. The tip is moved in and out to remove
plaque; however, it is very difficult to use on posterior teeth and from the The body of evidence on the Oral Irrigators (also called water
lingual aspect of all teeth. flosser and dental water jet) consistently has been shown to
significantly reduce gingivitis, bleeding on probing, and peri-
odontal pathogens. These oral health improvements have
been demonstrated with the use of either water or an anti-
microbial agent. The evidence indicates the Oral Irrigators
effectively remove biofilm and are more effective than dental
floss when added to toothbrushing. Table 35.1 compares the
understanding of periodontal disease to significant develop-
ments in water flosser technology.
Mechanism of Action of Irrigation

The mechanism of action of irrigation occurs through the
direct application of a pulsed stream of water or other solu-
tion. Studies have found pulsation and pressure to be critical
(A) components of an irrigation device. Pulsating devices have
FIGURE 35.15 Cleaning of concave or irregular proximal tooth sur- been shown to be 3 times as effective as a continuous-stream
faces. Dental floss (A) may be less effective than an interdental brush (B) irrigating syringe. Pulsation provides for a compression and
on long root surfaces with concavities.
decompression phase that may account for expedient clear-
ing of bacteria from the pocket. A pulsating device allows for
• Many interdental cleaning aids are available for patients. control of the pressure rate. The majority of studies on home
The patient might need to try several devices before finding irrigation that have demonstrated clinical efficacy have been
one that is acceptable and cleans adequately. done using a water flosser with 1200-1400 pulsations per
• In general, the largest brush or device that fits into a space minute set on a medium to a high pressure setting (50-90 psi)
will clean most efficiently (Fig. 35 15) (Figs. 35.16 and 35.17). Oral irrigators with varying pulsation
and pressure are available, but like other self-care products,
research from one product brand should not be extrapolated
Gingival Massage to other brands since they may have used a different pressure
Massaging the gingiva with a toothbrush or an interdental setting and pulsation rate.
cleaning devices produces epithelial thickening, increased A pulsation rate of 1200-1400/min has been shown to
keratinization, and increased mitotic activity in the epithelium create two zones of hydrokinetic activity: the impact zone,
TABLE 35.1
INCREASED UNDERSTANDING OF THE BENEFITS OF A WATER FLOSSER

Understanding of Periodontal Diseases Significant Developments and Research in Dental Water Jet (DWJ)
(Approximate Years) Technology
Nonspecific Plaque Era (1965)

Plaque was considered to be a homogenous, toxic substance DWJ initially introduced to dental community in early 1960s.
that caused gingivitis. Gingivitis could progress slowly Clinical and laboratory studies showed the following:
to periodontitis. Amount of plaque and length of time • DWJ is a significant aid to oral hygiene procedures.
plaque attached to tooth were paramount factors in • DWJ can decrease plaque formation.
disease. All plaque was considered essentially the same, • Use of DWJ significantly reduces gingivitis and calculus formation as adjunct
and all plaque was considered bad. to tooth brushing.
• These devices do not produce bacteremia.
Specific Plaque Hypothesis Era (1975)

Supragingival and subgingival plaque shown to be different. Clinical studies in the 1970s through 1990s continued to show significant
Supragingival plaque begins first, then with time can clinical reductions in bleeding, inflammation, and plaque formation using
grow apically and evolve into subgingival plaque, which DWJ and marginal irrigation with water, chlorhexidine gluconate, and
can cause bone destruction around a tooth. essential oils."
Elevation of specific bacterial species associated with specific Studies show that DWJ irrigation with a jet tip can reach subgingival areas
periodontal diseases. Periodontal pathogens are located inhabited by periodontal pathogens.
subgingivally.
Host Bacteria Interrelationship Era (1985) and Era of Periodontal Medicine (Present)
Diabetes and other systemic diseases shown to make patient There is an improvement in clinical parameters in diabetic patients using DWJ
more susceptible to periodontal diseases. and reduced inflammatory mediators over traditional routine oral hygiene
regimens.
Moderate-to-severe periodontitis increases systemic inflammation, which
is associated with cardiovascular disease and Gram-negative bacteria in
periodontal pockets (biofilms) have been associated with arthromas.
In 2009, at a consensus meeting, the American journal of Cai·diology and journal of
Periodontology issued guidelines for patients with atherosclerotic cardiovascular
disease who have untreated or uncontrolled periodontitis that stated these
patients should be treated with a focus on reducing and controlling the bacte1ial
accumulations and eliminating inflammation.
Clinical benefits of oral irrigation found to be related to reduction of
proinflammatory mediators in serum (ie, reduces systemic inflammation).
Efficiency of DWJ irrigation at removing biofilm ex vivo and in vivo shown in
scanning electron microscopy studies.
DWJ irrigation (along with tooth brushing) is an effective alternative to dental
floss for the reduction of bleeding, gingivitis, and plaque and in some cases,
may provide superior results for reducing bleeding and gingivitis.
FIGURE 35.16 A Water flosser with 1400 ppm and a pressure setting FIGURE 35.17 A cordless dental water jet, which also has 1400 ppm.
that ranges from 20 to 90 psi. (Courtesy Water Pik, Inc., Fort Collins, CO.) (Courtesy Water Pik, Inc., Fort Collins, CO.)
FIGURE 35.18 Pulsation creates two zones of hydrokinetic activity:

the impact zone and the flushing zone. (Courtesy Water Pik, tnc., Fort
Collins, CO.)
FIGURE 35.20 Site-specific tip. (Courtesy Water Pik, lnc., Fort Collins,
CO)
FIGURE 35.19 Jet tip. (Courtesy Water Pik, lnt:., Fort Collins, CO.)
in which the solution initially contacts, and the flushing zone,

in which the solution reaches into the subgingival sulcus FIGURE 35.21 Tip with soft tapered bristles. (Courtesy Water Pik,
(Fig. 35 18) The outcome of hydro kinetic activity is subgin- lnc., Fort Collins, CO.)
gival penetration.
Home irrigation has been demonstrated to penetrate sub-
gingivally with both a jet tip (Fig. 35.19) and a soft, site-spe-
cific, subgingival tip (Pik Pocket subgingival irrigation tip,
Water Pik, Inc., Fort Collins, CO) (Fig. 35 20). Supragingival
irrigation is irrigation with a jet tip placed above the gingival
margin resulting in penetration of a solution into the subgin-
gival sulcus to approximately 50%.
The jet tip is generally used for full-mouth irrigation.
Recently, other types of supragingival tips enhanced with soft,
tapered bristles (Fig. 35.21) have been introduced and shown
to be effective in increasing the removal of plaque. Irrigation
with the soft, site-specific tip is called subgingival irrigation. This
refers to the placement of the tip, which is placed slightly below
the gingival margin (Fig. 35 22). The subgingival tip is used for
the localized irrigation of a specific site such as a deep pocket,
furcation, implant, or crown and bridge. Studies with this site-
specific, subgingival tip show that it can deliver a solution into a
pocket of 6 mm or less up to 90% of its depth. In pockets deeper FIGURE 35.22 The Pik Pocket tip is gently placed slightly subgingi-
than 6 mm, the depth of penetration has been shown to be 64%. vally. (Courtesy Water Pik, ltu:., Fort Collins, CO.)
Safety depth, periodontal pathogens, and inflammatory mediators.

Home irrigation has been studied and found safe and effective
Concerns regarding the safety of oral irrigation with regard to for those with gingivitis, implants, crown and bridge, orthodon-
soft tissue damage and penetration of bacteria into the pocket tics, intermaxillary fixation, and diabetes; patients who are non-
have been voiced although no scientific evidence exists to compliant with dental floss; and in periodontal maintenance.
support these assumptions. The published research shows a Early studies found that irrigation with water leads to a
different profile starting with early studies that showed a histo- reduction in calculus: up to as much as 50% over brushing
logical reduction of inflammation. Subsequent studies showed alone. A study conducted with the scanning electron micro-
the reduction of subgingival pathogens even in pockets up to scope found that a 3-s pulsating lavage at a 60 psi with either
6 mm and an ultra structural study found no differences in a jet tip or small brush tip removed 99% of plaque biofilm
the epithelial lining of the pocket compared to the nonirrigated (Figs. 35.23 and 35 24) A single-use study that compared
sites. Studies that have measured the clinical attachment level irrigation to string floss in addition each in addition to manual
and probing pocket depth have reported either no change or a brushing found irrigation to be 29% more effective at whole
significant improvement supporting no detrimental effects on mouth plaque removal.
the attachment or junctional epithelium. Manipulation of tissue As early as the 1960s, it was shown that oral irrigation with
in any level of periodontal disease will cause a bacteremia. The water added to toothbrushing reduced gingivitis by 52% com-
incidence of bacteremia using a pulsating oral irrigator ranges pared to a 30% reduction for toothbrushing alone. Through-
from 7% in people with gingivitis to 50% in people with peri- out the years, other researchers have found concurring results
odontitis. These findings are in line with other self-care tech- with the use of plain water. The use of an antimicrobial agent,
niques such as tooth brushing and flossing (20-68%), wooden such as diluted chlorhexidine (Table 35.3), or an essential oil,
toothpicks or sticks (20-40%) and mastication (7-51 %). generally enhances reductions in gingivitis and bleeding.
Emerging evidence indicates that home irrigation may play
Clinical Outcomes of Irrigation a role in modulating the host response, particularly the inflam-
matory mediators associated with clinical attachment loss and
Table 35.2 highlights the body of evidence on the dental water alveolar bone loss. This evidence lends support to the safety
jet. Evaluated outcomes include removal of plaque biofilm and of irrigation, as well as its potential for helping periodontal
reductions in calculus, gingivitis, bleeding on probing, probing maintenance patients maintain stability
TABLE 35.2
REDUCTION OF INFLAMMATION AND PLAQUE BIOFILM

--
% Bleeding % Gingivitis % Plaque Biofilm
Study Duration N Agent Used Reduction Reduction Reduction
Al-Mubarak et al 3 months 50 Water 43.8 66.9 64.9

Barnes et al 4 weeks 105 Water 36.2-59.2 10.8-15.1 8.8-17.3
Brownstein et al 8 weeks 44 CHX (0 06%) 52-59 25.4-31.1' 14.3-19'
Water NR NR
Burch et al 2 months 47 Water 57.1-76.6 NR 52-55. 7
Chaves et al 6 months 105 CHX (004%) 54 26 35
Water 50 26 16
Ciancio et al 6 weeks 61 Essential oils" 27.6 54-55.7 23-24
Water and alcohol 5% 13.6-31.2 59.8-61.9 9/6-13.3
Cutler et al 2 weeks 52 Water 56 50 40
Flemmig et al 6 months 175 CHX (0 06%) 35.4 42.5 53.2
Water 24 23.1 0.1
Flemmig et al 6 months 60 Acetylsalicylic acid 3% 8.9 55.6
Water 50 29.2 0
Felo et al 3 months 24 CHX (006%) 62 45 29
Fine et al 6 weeks 50 Essential oils" 14.8-21.7 NR 36.8-37. 7
Water 7.5-10.6 NR 15.5-18.4
Jolkovsky et al 3 months 58 CHX (0.4%) NR 33.1 51.6
Water NR 18.6 25.6
Lobene et al 5 months 155 Water NR 52.9 7.9
Newman et al 6 months 155 Water 22.8 17.8 6.1
Water and zinc sulfate (0.57%) 8.8 6.5 9.2
Rosema et al 30 days 104 Water 17% NR
Sharma et al 4 weeks 128 Water 84.5 NR 38.9
Walsh et al 8 weeks 8 CHX (0 2%) NR 45 77
Quinine salt NR 14 0
Magnuson 4 weeks 40 implants Water 81.8 NR NR
CHX, Chlorhexidine; NR, not reported.
'Percentages were reported for differences between CHX and water irrigation groups.
"Reported the range for prophy and nonprophy groups.
Data from Cianco SG: Compendium Contin Educ Dent 30:7-14, 2009.
bleeding which was 2.45 times better than using string floss.
For those with special medical considerations, home irriga-
tion has been studied and shown safe and effective in a group
of individuals with either type 1 or type 2 diabetes.
Conclusions
Home irrigation is safe and effective for a wide variety of
patients, including those in periodontal maintenance; those
with calculus buildup, gingivitis, orthodontic appliances,
maxillary fixation, crown and bridge, implants, and diabetes;
and those who are noncom pliant with floss. Clinical outcomes
include the reduction of plaque, calculus, gingivitis, bleed-
ing on probing, probing depth, periodontal pathogens, and
inflammatory mediators.
FIGURE 35.23 The use of the Pik Pocket tip around an implant.
(Courtesy Water Pik, Inc., Fort Collins, CO.)
Chemical Plaque Biofilm Control

With Oral Rinses
Plaque control is the key to prevention of periodontal dis-
eases. It can be achieved mechanically (as discussed earlier)
or chemically. Chemical plaque control, however, should be
regarded as an adjunct to and not a substitute for mechanical
plaque control.
Mouthwash, mouthrinse, oral rinse, or mouth bath is a liq-
uid which is held in the mouth passively or swirled around
the mouth by contraction of the perioral muscles and /or
movement of the head, and gargled.
An ideal chemical plaque control agent should possess the
properties of Substantivity (ability of agent to bind to tissue
surfaces and be released over time); Penetrability (ability to
penetrate deeply into the biofilm); and Selectivity (ability to
affect specific bacteria in a mixed population).
The extent of stability of the active agent in the presence of
FIGURE 35.24 Control tooth with no irrigation. (Courtesy Water Pik, salivary and/or bacterial enzymes, it's solubility into the oral
Inc., Fort Collins, CO.) environment, its adequate bioavailability; its accessibility to
the site of action and the ionic interactions between agent and
receptor sites are other important factors which affect delivery
TABLE 35.3 to, and clearance of the plaque control agents from the oral
cavity.
CHLORHEXIDINE DILUTIONS (BASED ON Chemical plaque control agents may be grouped into first-,
0.12% CONCENTRATION) SHOWN EFFECTIVE second- and third-generation antimicrobial agents (Table 35.4).
IN CLINICAL TRIALS Some of the antimicrobial agents are discussed in the fallowing:
Amount of Chlorhexidine Rinse: The agent that has shown the most
Concentrations Amount of Water Chlorhexidine positive antibacterial results to date is chlorhexidine, a digua-
nidohexane with pronounced antiseptic properties. Several
0.02% 5 parts 1 part other clinical investigations confirmed the initial finding that
0.04% 3 parts 1 part
two daily rinses with 10 ml of a 0.2% aqueous solution of
0.06% 1 part 1 part
chlorhexidine digluconate almost completely inhibited the
development of dental plaque, calculus, and gingivitis in the
human model for experimental gingivitis. Clinical studies of
Individuals with Special several months' duration have reported plaque reductions
Considerations of 45-61 % and, more importantly, gingivitis reductions of
27-67%. The 0.12% chlorhexidine digluconate preparation
Some clinical trials have focused on groups with special oral available in the United States for reducing plaque and gin-
or medical health needs. Both children and adults undergo- givitis has been shown to be equally effective as the higher-
ing orthodontic therapy have shown significant benefits from concentration product. It has a broad antimicrobial spectrum.
using a water flosser. A new, small brush tip that cleans and At low concentrations it causes leakage of intracellular potas-
irrigates simultaneously has been shown to remove 3. 7 6 times sium and reduction in bacterial acid production. At higher
more plaque than brushing and flossing with a floss threader. concentrations it is able to induce bacterial cell wall disruption
For individuals with implants, manual brushing and irrigat- and coagulation of the cytoplasmic constituents. It also inhib-
ing with water over 4 weeks showed an 81.8% reduction in its enzymes involved in bacterial adhesion, bacterial growth
35 Plaque Biofilm Control 397.el
Caries Control by low concentration topical fluoride delivered by toothpastes

or other topical applications. It also has been demonstrated
Dental caries, particularly root caries, is a problem for peri- that the use of fluoride dentifrice containing 5000 ppm of flu-
odontal patients because of attachment loss and exposed root oride was more effective in reversing active root caries lesions
surfaces associated with the disease process and periodontal than the fluoride level of ll00 ppm found in conventional
therapeutic procedures. Root caries develops through a pro- toothpastes.
cess similar to coronal caries, involving the alternating cycle
of demineralization and remineralization of the surfaces and Recommendations
other risk factors associated with diet and salivary flow. The
demineralization process requires the fermentation of car- • All periodontal patients should be encouraged to use a
bohydrates in the plaque biofilm by oral bacteria, resulting fluoride-containing toothpaste daily, 1000-ll00 ppm, to
in loss of mineral from the root surface. Lactobacillus and reduce demineralization and enhance remineralization of
Streptococcus species are involved in the root caries process, as tooth surfaces.
with coronal caries. The major difference is that the amount of • Patients at high risk for caries, including those with a his-
organic material in the root surfaces is greater than in enamel, tory of root lesions or who have active lesions, should
so once the demineralization has occurred, the organic use higher-concentration fluoride toothpaste or gels,
matrix-mostly collagen-is exposed. Organic material is 5000 ppm, daily until the risk for caries is controlled, then
then further broken down by bacterial enzymes, resulting in maintain with the lower concentration toothpastes and
rapid destruction of the root surface. mouthrinses.
Fluoride works primarily by topical effects to prevent and • Periodic chlorhexidine rinsing to control cariogenic bacte-
reverse the caries process, whether in enamel, cementum, or ria in the oral cavity should also be used as part of a caries
dentin. Low concentrations of topical fluoride inhibit demin- risk management program.
eralization, enhance remineralization, and inhibit the enzyme • Other considerations in caries control, such as diet and
activity in bacteria by acidifying the cells. Adult patients ben- reduced salivary flow, should be evaluated as with all dental
efit from the prevention and reversal of root caries provided patients.
TABLE 35.4
CLASSIFICATION OF CHEMICAL PLAQUE CONTROL AGENTS

Second Generation Chemical Plaque Third Generation Chemical Plaque
First Generation Chemical Plaque Control Agents Control Agents Control Agents
Phenolic compounds Bisbiguanides Delmopinol

Phenol Chlorhexidine
Thymol Alexidine
Triclosan
Listerine (menthol, thymol, eucalyptol)
Hexylresorcinol
Quaternary ammonium compounds Bispyridines
Cetylpyridinium chloride Octenidine Hydrochloride
Benzethonium chloride
Antibiotics
Vancomycin, Niddamycin, Kanamycin
Halogens
Iodine, Fluorides
Metallic ions
Zinc, copper, tin, silver, mercury ions
Herbal extracts
Sanguanaria extract
Antiplaque Enzymes
Mucinase, Mutanase, Dextranase, Amyloglucosidase
Oxygenating/Oxidizing agents
Peroxides
and metabolism. Approximately 30% of the chlorhexidine Hexitidine: A synthetic hexahydropyridine with mechanism
applied is retained in the oral soft tissues, which serve as a of action similar to chlorhexidine. However, it has little anti-
reservoir for slow release of the agent over extended periods plaque effect at clinically acceptable concentrations. Higher
of time. Localized, reversible side effects to chlorhexidine use concentrations are associated with corresponding increase in
may occur, primarily brown staining of the teeth, tongue, and frequency of desquamative lesions.
silicate and resin restorations and transient impairment of Enzymes: Peroxidases have been added to mouthrinses and
taste perception. Chlorhexidine has very low systemic toxic dentifrices to ensure presence of sufficient hydrogen peroxide
activity in humans, has not produced any appreciable resis- to control proliferation of plaque bacteria.
tance of oral microorganisms, and has not been associated Triclosan: This is a nonionic, broad spectrum antimicro-
with teratogenic alterations. bial agent, currently being incorporated into dentifrices and
Nonprescription Essential Oil rinse: One of the most exten- mouthrinses because of its high retentivity in the oral cavity
sively used and researched mouthrinse, Listerine (named and hence a positive, linear dose-response antiplaque and
after Lister), is a combination of phenol-related essential antigingivitis effect. Its antiinflammatory effect can be attrib-
ions, thymol and eucalyptol, mixed with menthol and methyl uted to its ability to inhibit both cyclo-oxygenase and lipo-
salicylate in a hydroalcoholic base. It is antiinflammatory and oxygenase, thereby retarding prostaglandin and leukotriene
has the ability to suppress odorigenic bacteria. The nonion- production. Total (Colgate Oral Pharmaceuticals Inc. Canton,
ized molecules cause inactivation of essential enzymes at Mass.) contains triclosan and Gantrez (a copolymer of polyvi-
low concentrations and disruption of cell proteins at high nyl methyl and maleic acid) and is the first dentifrice sold in
concentrations. the USA to receive the ADA's Seal of Acceptance for the reduc-
Heavy metal ions: Divalent metal ions possess antiplaque tion of plaque and gingivitis.
potential as a result of their ability to bind plaque components Delmopinol: This is a substituted amino-alcohol, which dis-
via electrostatic forces, thereby altering the surface charge rupts the bacterial matrix formation, thereby interfering with
and adherence potential of bacteria. They are able to displace bacterial attachment. This surface-modifying agent is less
calcium ions from the pellicle and bacterial surfaces, have effective than chlorhexidine on established gingivitis patients.
antiglycolytic effect, and reduce pathogenecity of established Transient anesthesia of the dorsum of the tongue, mucosa!
plaque by suppressing plaque acidogenecity soreness, taste disturbances and erosions are the various side
Quaternary ammonium compounds: These cationic anti- effects attributed to this compound.
septics interact with plaque in a manner similar to that of
Chlorhexidine, but are less effective because of their rapid
clearance from the oral cavity
Disclosing Agents
Sanguinarine: A mixture of bezophenanthridine alkaloids, Removal of plaque at regular intervals is critical for oral
this extract of the bloodroot plant Sanguinaria Canadensis health maintenance. However, plaque is relatively invisible to
is effective against both Gram-positive and Gram-negative the naked eye. Therein comes the role of Plaque Disclosing
bacteria. Its ability to interfere with the steps in bacterial Agents, which are agents capable of staining bacterial biofilms
cell wall synthesis may be responsible for its antimicrobial on the surfaces of teeth, tongue, and gingiva, making it visible
activities. for easy detection and removal (Fig. 35 .25). They play a vital
FIGURE 35.25 Effect of a disclosing agent. A, Unstained, the teeth look clean, but close inspection shows subtle signs of gingivitis. B, Plaque shows
as dark-red particulate matter when stained with a disclosing dye. It is useful to demonstrate toothbrushing in the patient's mouth with the teeth dis-
closed and plaque visible.
role in patient motivation and education; help the clinicians in patient and education and instruction from the dentist, fol-
determining the plaque indices; and also help the researcher lowed by encouragement and reinforcement. Keeping records
in evaluating the effectiveness of plaque control devices. of patient performance facilitates this process. Figure 35.26
Various dyes that have been utilized to detect plaque are provides an example of a plaque biofilm control record that
Erythrosine (most widely used, stains the plaque area red, permits repeated measures and comparison over time.
but may also stain the soft tissues), Skinners Iodine solution
(formerly widely used, unacceptable taste, high incidence of Motivation for Effective Plaque
allergic reactions), Fast green, Mercurochrome preparations, Biofilm Control
Bismark Brown, Merbromin, Basic Fushcin, Phloxine B plus
Patent Blue (Two-tone dye, stains older/mature plaque blue Motivating patients to perform effective plaque biofilm control
and newer/immature plaque pink/red, does not stain the soft is one of the most critical and difficult elements of long-term
tissues), and Fluorescein (fluoresces yellow-green under UV success in periodontal therapy. It requires both commitment
light, expensive, does not stain the soft tissues, but a special by the patient to change daily habits and regular return visits
light is required to visualize the stained plaque). for maintenance and reinforcement. The scope of this compli-
Disclosing agents are available as solutions or wafers com- ance problem is immense. It has been shown that patients
mercially. Solutions are applied to the teeth as concentrates on stop using interproximal cleaning aids after a very short time.
cotton swabs or diluted as rinses. Wafers are crushed between Heasman et al followed 100 patients treated for moderate to
the teeth and swished around the mouth for a few seconds severe periodontal disease and taught to use one or more inter-
and then spit out. Either form can be used for plaque biofilm dental cleaning aids. It was found that only 20% used the aids
control instruction in the office and dispensed for home use to after 6 months. Of those who had started using three devices,
aid periodontal patients in evaluating the effectiveness of their one-third had stopped all interdental cleaning at 6 months;
oral hygiene routines. the others used one or two of the aids. The situation is no
better when looking at patient willingness to return for office
visits. In one study of 1280 patients, most of whom had peri-
Patient Motivation and Education
odontal surgery in multiple sites after intensive scaling, root
In periodontal therapy, plaque biofilm control has two impor- planing, and home care instruction, 25% never returned for
tant purposes: to minimize gingival inflammation and to pre- a follow-up visit; only 40% returned regularly. Wilson et al
vent the recurrence or progression of periodontal diseases reported that 67% of periodontal patients were noncompli-
and caries. Daily mechanical removal of plaque biofilm by the ant with return visits in a 20-year retrospective of a private
patient, including the use of appropriate antimicrobial agents, periodontal practice.
is the only practical means for improving oral health on a long- Adopting new habits and returning for office visits is not
term basis. The process requires interest on the part of the an impossible task. To be successful, the patient (1) must be
Plaque Control Record . 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Plaque Score:
32 31 30 29 28 27 26 25 24 23 22 21 20 19 18 17
Date:
Plaque Score:
2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
32 31 30 29 28 27 26 25 24 23 22 21 20 19 18 17
Date:
Plaque Score:
2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
32 31 30 29 28 27 26 25 24 23 22 21 20 19 18 17
Date:
FIGURE 35.26 The plaque control record can be an effective motivator for patients. This form permits easy comparison of scores over time.
(Courtesy Dean John D. 8. Featherstone, University of California, San Francisco School of Dentistry, San Francisco)
receptive and understand the concepts of pathogenesis, treat- lips may retain it for up to several hours. Use petroleum jelly
ment, and prevention of periodontal disease; (2) must be will- to keep the dye off the patient's lips.
ing to change the habits of a lifetime; and (3) must be able to Toothbrushing should be demonstrated in the patient's
adjust personal beliefs, practices, and values to accommodate mouth while the patient observes using a hand mirror. The
new regimens. Manual skills must be developed to establish patient then repeats the procedures with the dentist giving
an effective plaque biofilm control regimen. In addition, the assistance, correction, and positive reinforcement. Repeat the
patient must understand the dentist's critical role in treating demonstration and instruction process with dental floss and
and maintaining periodontal health. If not, long-term success interdental cleaning aids according to the patient's needs.
of treatment is much less likely. Encourage patients to clean the teeth thoroughly at least
once a day. Be sure to inform them that home care proce-
Education and Scoring Systems dures on a full dentition take 5-10 min, and for complex peri-
odontal cases, home care procedures may take 30 min. The
Many patients prefer to believe that treatment is a passive pro- patient should set aside a convenient time and place in the
cess, so it is incumbent on the dentist to educate and rein- daily schedule to perform the procedures reliably every day.
force to each patient their personal role in long-term success Subsequent instruction visits should be used to reinforce or
of therapy. Our health-conscious society is an advantage with modify previous instructions, periodically recording the state
regard to patient education. Most patients know what gingi- of gingival health and amount of plaque biofilm.
vitis is because they have heard about it on television or read Some strategies simply do not work. Waiting until the end
about it in magazines or on the web. They are willing to spend of the appointment, for example, when the patient is sore,
time and money to try new products such as toothbrushes and exhausted, and possibly anesthetized is not conducive to
mouthrinses. learning. Failing to provide positive reinforcement, handing
Patients must also be informed that periodic assessment the patient too many tools, and relying only on pamphlets and
and debridement of the teeth in the dental office are required printed material to provide education are likely to result in an
to prevent recurrence of periodontal diseases and identify insufficient or ineffective instruction process.
problems that may arise. These procedures work best when
combined with an individualized oral hygiene regimen prac-
ticed daily at home. Therefore time spent in the dental office Recommendations
teaching the patient how to perform microbial plaque biofilm The following list provides some strategies that will assist you
control procedures is central to care. Patients sometimes have in educating and motivating your patients:
the concept that "cleanings" every few months are sufficient
for calculus and biofilm removal and disease control. Only the • Provide encouragement.
combination of regular office visits with conscientious home • Demonstrate how devices work, and allow the patient to
care has been shown to significantly reduce gingivitis and loss practice with them.
of supporting periodontal tissues over the long term. • Provide samples so that the patient does not have to stop
Periodontal patients should be shown how periodontal and buy products on the way home; the patient may not
disease has manifested in their own mouth. Stained plaque follow through with the purchase.
biofilm, the bleeding of inflamed gingiva, and demonstrations • Show improvements at subsequent appointments, even if
of the periodontal probe inserted into pockets are impressive they are modest.
demonstrations of the presence of pathogens and symptoms • Use positive reinforcement; threats are not effective.
of disease. It also is of educational value to patients to have
their oral cleanliness and periodontal condition recorded peri-
odically so that improvements in performance can be used for
Conclusions
positive reinforcement. The plaque biofilm control record and • All patients require the regular use of a toothbrush, either
the bleeding points index are simple indices and useful for manual or electric, at least once per day. The brushing
patient education and motivation. method should emphasize access to the gingival margins
(dento-gingival junction) of all accessible tooth surfaces,
Instruction and Demonstration referred to as targeted hygiene, and extension as far onto the
proximal surfaces as possible.
Patients can reduce the incidence of plaque biofilm and gingi- • Dental floss should be used in all interdental spaces that are
vitis with repeated instruction and encouragement much more filled with gingiva.
effectively than with self-acquired oral hygiene habits. How- • Interdental aids such as interproximal brushes, wooden tips,
ever, instruction in how to clean teeth must be more than a rubber tips, or toothpicks should be used in all areas where
cursory chairside demonstration on the use of a toothbrush. It the toothbrush and floss techniques cannot adequately
is a painstaking procedure that requires patient participation, remove the plaque biofilm. This includes large embrasure
careful supervision with correction of mistakes, and reinforce- spaces and furcation areas as well as the mesial surface of
ment during return visits, until the patient achieves the neces- the maxillary first bicuspid, which presents a concavity on
sary proficiency. Any strategy for introducing plaque biofilm the root surface near the cemento enamel junction.
control to the periodontal patient includes several elements. • Daily at-home subgingival irrigation is useful for reduction
At the first instruction visit, the patient should be given a new of inflammation and maintenance for patients with resid-
toothbrush, an interdental cleaner, and a disclosing agent. The ual deep pockets and those who struggle with mechanical
patient's plaque biofilm should be disclosed otherwise it is dif- interproximal cleaning devices. The effectiveness of irri-
ficult for the patient to see (Fig. 35 25). Polished dental resto- gation is enhanced by the addition of a chlorhexidine or
rations do not take up the stain, but the oral mucosa and the essential oil rinse as an irrigant.
Plaque Biofilm Control Record (O'Leary Index) on the chart. Repeat on the lingual-palatal aspect, recording
Have the patient use a disclosing solution or tablet and bleeding only for the direct lingual surface, not for the mesial
examine each tooth surface (except occlusal surfaces) for the or distal surfaces. This results in four separate scores for
presence or absence of stained biofilm at the dento-gingival each tooth and does not score the mesial and distal surfaces
junction. Plaque biofilm is recorded on the appropriate box twice. Repeat the steps for each quadrant. The percentage
in a diagram for four surfaces on each tooth. After all teeth of the number of bleeding surfaces is calculated by divid-
have been scored, the index number is calculated for the per- ing the number of surfaces that bled by the total number of
centage of surfaces with biofilm by dividing the number of tooth surfaces (four per tooth) and by multiplying by 100 to
surfaces with microbial plaque biofilm by the total number convert the score to a percentage. This index is designed to
of surfaces scored and then multiplying by 100. A reasonable demonstrate gingival inflammation characterized by bleeding
goal for patients is 10% or fewer surfaces with plaque bio- rather than presence of microbial plaque biofilm. Again, a
film. If biofilm is always present in the same areas, provide goal of 10% or fewer bleeding points is good, but 0 is ideal.
instructions to improve cleaning procedures in those areas. It If a few bleeding points repeatedly occur in the same areas,
is extremely difficult to achieve a perfect score of 0, so patients cleaning procedures for those areas should be reinforced or
should be rewarded for approaching it. modified.
Some frequently used plaque biofilm indices do not require
staining the teeth including the Plaque Index of Silness and Significance of Plaque Biofilm Scores
Loe. These are more convenient to use and often more accept- and Bleeding Scores
able to patients, but they are not as dramatic for patient Plaque biofilm scores are helpful as indicators of patient
education. compliance and success with daily home care procedures.
However, biofilm levels themselves do not necessarily reflect
Bleeding Points Index gingival health or risk of disease progression, even though the
The bleeding points index provides an evaluation of gingi- location of the plaque biofilm is highly correlated with the
val inflammation around each tooth in the patient's mouth. presence of gingivitis. Bleeding is a much better indicator of
Retract the cheek, and place the periodontal probe 1 mm into predicting success in controlling inflammation and reducing
the sulcus or pocket at the distal aspect of the most posterior the chance of disease progression. Although bleeding on prob-
tooth in the quadrant on the buccal surface. Carry the probe ing is not the most specific or sensitive measures of health,
lightly across the length of the sulcus to the mesial interprox- it has a strong negative correlation to disease progression. If
imal area on the facial aspect. Continue along all the teeth in bleeding is absent at any given site in the mouth, reflecting
the quadrant from the facial aspect. Wait 30 s, and record the good plaque biofilm control and disease management, it is
presence of bleeding on the distal, facial, and mesial surfaces unlikely that periodontal disease will progress.
• Caries control requires the daily use of a dentifrice with Genovesi AM, Lorenzi C, Lyle DM, et al: Periodontal maintenance follow-
low-concentration fluoride. Topical oral rinses and gels ing scaling and root planing. A randomized single-center study compar-
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36
Periodontal Instruments
and Instrumentation
AM Pattison • GL Pattison • PR Klokkevold • HH Takei
• FA Carranza • A Jain
Chapter Outline
Classification of Periodontal Instruments General Principles of Instrumentation
Surgical Instruments Instrument Sharpening
Periodontal instruments are designed for specific purposes 5. Cleansing and polishing instruments, such as rubber cups,
such as removing calculus, planing root surfaces, curetting brushes, and dental tape, are used to clean and polish
the gingiva, and removing diseased tissue. On first investiga- tooth surfaces. Also available are air-powder abrasive sys-
tion, the variety of instruments available for similar purposes tems for tooth polishing.
appear confusing. With experience, however, clinicians select
The wearing and cutting qualities of some types of steel
a relatively small set that fulfills all requirements.
used in periodontal instruments have been tested, but specifi-
cations vary among manufacturers. Stainless steel is used most
Classification of Periodontal often in instrument manufacture. High-carbon-content steel
Instruments instruments are also available and are considered by some cli-
nicians to be superior.
Periodontal instruments are classified according to the pur- Each group of instruments has characteristic features;
poses they serve, as follows: individual therapists often develop variations with which
1. Periodontal probes are used to locate, measure, and mark they operate most effectively. Small instruments are recom-
pockets, as well as determine their course on individual mended to fit into periodontal pockets without injuring the
tooth surfaces. soft tissues.
2. Explorers are used to locate calculus deposits and caries. The parts of each instrument are referred to as the working
3. Scaling, root-planing, and curettage instruments are used for end, shank, and handle (Fig. 36.1)
removal of biofilm and calcified deposits from the crown
and root of a tooth, removal of altered cementum from the
Periodontal Probes
subgingival root surface, and debridement of the soft tissue
lining the pocket. Scaling and curettage instruments are Periodontal probes are used to measure the depth of pockets
classified as follows: and to determine their configuration. The typical probe is a
• Sickle scalers are heavy instruments used to remove tapered, rodlike instrument calibrated in millimeters, with a
supragingival calculus. blunt, rounded tip (Fig. 36.2). There are several other designs
• Curettes are fine instruments used for subgingival scal- with various millimeter calibrations (Fig. 36.3). The WHO
ing, root planing, and removal of the soft tissue lining probe has millimeter markings and a small, round ball at the
the pocket. tip (Fig. 36 3E). Ideally, these probes are thin, and the shank
• Hoe, chisel, and file scalers are used to remove tenacious is angled to allow easy insertion into the pocket. Furcation
subgingival calculus and altered cementum. Their use is areas can best be evaluated with the curved, blunt Nabers
limited compared with that of curettes. probe (Fig. 364)
• Ultrasonic and sonic instruments are used for scaling and When measuring a pocket, the probe is inserted with a
cleansing tooth surfaces and curetting the soft tissue firm, gentle pressure to the bottom of the pocket. The shank
wall of the periodontal pocket. should be aligned with the long axis of the tooth surface to
4. Periodontal endoscopes are used to visualize deeply into sub- be probed. Several measurements are made to determine the
gingival pockets and furcations, allowing the detection of level of attachment along the surface of the tooth.
deposits.
403
ra1e I Handle Blif e
~~~~~
Shan~ L Shank j
FIGURE 36.1 Parts of a typical periodontal instrument.
FIGURE 36.2 Periodontal probe is composed of the handle, shank,

and calibrated working end.
FIGURE 36.5 Five typical explorers. A, II17; B, II23; C, EXD 11-12; D,
II3; E, ll3CH Pigtail.
(A1 (BJ (C) (Dl
(A) (B) (C) (D)

FIGURE 36.3 Types of periodontal probes. A, Marquis color-cod-
FIGURE 36.6 Insertion of two types of explorers and a periodontal
ed probe. Calibrations are in 3-mm sections. B, University of North
probe in a pocket for calculus detection. A, The limitations of the pig-
Carolina-15 probe, a 15-mm long probe with millimeter markings at
tail explorer in a deep pocket. B, Insertion of the II3 explorer. C, Limita-
each millimeter and color coding at the 5, 10, and 15 mm. C, University
tions of the II3 explorer. D, Insertion of the periodontal probe.
of Michigan "O" probe, with Williams markings (at 1, 2, 3, 5, 7, 8, 9,
and 10 mm). D, Michigan "O" probe with markings at 3, 6, and 8 mm.
E, WHO probe, which has a 0.5-mm ball at the tip and millimeter mark-
ings at 3.5, 8.5, and 11.5 mm and color coding from 3.5 to 5.5 mm.
Explorers
Explorers are used to locate subgingival deposits and carious
areas and to check the smoothness of the root surfaces after
root planing. Explorers are designed with different shapes and
angles, with various uses (Fig. 36.5), as well as limitations
(Fig. 36.6). The periodontal probe can also be useful in the
detection of subgingival deposits (Fig. 36 6D).
Scaling and Curettage Instruments

Scaling and curettage instruments are illustrated in Fig. 36.7.
Sickle Scalers
Sickle scalers have a flat surface and two cutting edges that
converge in a sharply pointed tip. The shape of the instru-
ment makes the tip strong so that it will not break off during
use (Fig. 36.8). The sickle scaler is used primarily to remove
supragingival calculus (Fig. 36.9). Due to the design of this
instrument, it is difficult to insert a large sickle blade under
the gingiva without damaging the surrounding gingival tis-
sues (Fig. 36.10). Small, curved sickle scaler blades such as
the 204SD can be inserted under the ledges of calculus several
FIGURE 36.4 Curved #2 Nabers probe for detection of furcation ar- millimeters below the gingiva. Sickle scalers are used with a
eas, with color-coded markings at 3, 6, 9, and 12 mm. pull stroke.
36 Periodontal Instruments and Instrumentation 405
FIGURE 36.10 Subgingival adaptation around the root is better with

the curette than with the sickle; f, facial; /, lingual.
(C) (D)
FIGURE 36.7 The five basic scaling instruments. A, Curette; B, sickle;
C, file; D, chisel; E, hoe.
FIGURE 36.11 Both ends of a U15/30 scaler.
FIGURE 36.8 Basic characteristics of a sickle scaler: triangular shape, It is important to note that sickle scalers with the same basic
double-cutting edge, and pointed tip.
design can be obtained with different blade sizes and shank
types to adapt to specific uses. The UlS/30 (Fig. 36.11), Ball,
and Indiana University sickle scalers are large. The Jaquette
J
sickle scalers #l, 2, and 3 have medium-size blades. The curved
204 posterior sickle scalers are available with large, medium, or
small blades (Fig. 36.12). The Montana Jack sickle scaler and
the Nevi 2, Nevi 3, and Nevi 4 curved posterior sickle scalers
are all thin enough to be inserted several millimeters subgin-
givally for removal of light to moderate ledges of calculus. The
selection of these instruments should be based on the area to
be scaled. Sickle scalers with straight shanks are designed for
use on anterior teeth and premolars. Sickle scalers with contra-
angled shanks adapt to posterior teeth.
Curettes
The curette is the instrument of choice for removing deep sub-
gingival calculus, root planing altered cementum, and remov-
ing the soft tissue lining the periodontal pocket (Fig. 36 13)
Each working end has a cutting edge on both sides of the blade
and a rounded toe. The curette is finer than the sickle scalers
FIGURE 36.9 Use of a sickle scaler for removal of supragingival and does not have any sharp points or corners other than the
calculus. cutting edges of the blade (Fig. 36.14 ). Therefore, curettes can
FIGURE 36.14 Basic characteristics of a curette: spoon-shaped blade

and rounded tip.
FIGURE 36.12 Three different sizes of 204 sickle scalers.
J J (A) (B)
FIGURE 36.15 Principal types of curettes as seen from the toe of
the instrument. A, Universal curette. B, Gracey curette. Note the offset
blade angulation of the Gracey curette.
shank may vary, but the face of the blade of every universal
curette is at a 90-degree angle (perpendicular) to the lower
shank when seen in cross-section from the tip (Fig. 36.15A).
The blade of the universal curette is curved in one direction
from the head of the blade to the toe. The Barnhart curettes
#1-2 and 5-6 and the Columbia curettes #13-14, 2R-2L, and
4R-4L (Figs. 36.16 and 36 17 A) are examples of universal cu-
rettes. Other popular universal curettes are the Younger-Good
#7-8, McCall's #17-18, and the Indiana University #17-18
FIGURE 36.13 The curette is the instrument of choice for subgingival (Fig. 36 17B).
scaling and root planing.
Area-Specific Curettes
be adapted and provide good access to deep pockets, with Gracey Curettes. Gracey curettes are representative of the
minimal soft tissue trauma (Fig. 36.10). In cross-section, the area-specific curettes, a set of several instruments designed
blade appears semicircular with a convex base. The lateral and angled to adapt to specific anatomic areas of the denti-
border of the convex base forms a cutting edge with the face of tion (Fig. 36.18). These curettes and their modifications are
the semicircular blade. There are cutting edges on both sides probably the best instruments for subgingival scaling and root
of the blade. Both single- and double-end curettes may be ob- planing because they provide the best adaptation to complex
tained, depending on the preference of the operator. root anatomy.
As shown in Fig. 36.10, the curved blade and rounded toe Double-ended Gracey curettes are paired in the following
of the curette allow the blade to adapt better to the root sur- manner:
face, unlike the straight design and pointed end of a sickle
scaler, which can cause tissue laceration and trauma. There Gracey #1-2 and 3-4: Anterior teeth
are two basic types of curettes: universal and area specific. Gracey #5-6: Anterior teeth and premolars
Gracey #7-8 and 9-10: Posterior teeth: facial and lingual
Gracey #11-12: Posterior teeth: mesial (Fig. 36.19)
Universal Curettes. Universal curettes have cutting edges
Gracey #13-14: Posterior teeth: distal (Fig. 36.20)
that may be inserted in most areas of the dentition by altering
and adapting the finger rest, fulcrum, and hand position of Single-ended Gracey curettes can also be obtained; a set
the operator. The blade size and the angle and length of the of these curettes comprises 14 instruments. Although these
(A)
(C)
FIGURE 36.16 A, Double-ended curette for the removal of subgingival calculus. B, Cross-section of the curette blade (arrow) against the cementa!
wall of a deep periodontal pocket. C, Curette in position at the base of a periodontal pocket on the facial surface of a mandibular molar. D, Curette
inserted in a pocket with the tip directed apically. E, Curette in position at the base of a pocket on the distal surface of the mandibular molar.
FIGURE 36.18 Reduced set of Gracey curettes. A, #5-6; B, #7-8; C,

#11-12; and D, #13-14.
because they are angled approximately 60-70 degrees from

the lower shank (Fig. 36.lSB). This unique angulation allows
FIGURE 36.17 A, Columbia #4R-4L universal curette. B, Younger-
Good #7-8, McCall's #17-18, and Indiana University #17-18 universal
the blade to be inserted in the precise position necessary for
curettes. subgingival scaling and root planing, provided that the lower
shank is parallel with the long axis of the tooth surface being
scaled.
curettes are designed to be used in specific areas, an experi- Area-specific curettes also have a curved blade. Whereas
enced operator can adapt each instrument for use in several the blade of the universal curette is curved in one direction
different areas by altering the position of his or her hand and (Fig. 36.21A), the Gracey blade is curved from head to toe
the position of the patient. and also along the side of the cutting edge (Fig. 36.2 lB)
The Gracey curettes also differ from the universal curettes Thus, only a pull stroke can be used. Table 36.1 lists some of
in that the blade is not at a 90-degree angle to the lower the major differences between Gracey (area-specific) curettes
shank. The term offset blade is used to describe Gracey curettes and universal curettes.
FIGURE 36.19 Gracey #11-12 curette. Note the double turn of the FIGURE 36.20 Gracey #13-14 curette. Note the acute turn of the
shank. blade.
Gracey curettes are available with either a "rigid" or a "fin-

ishing" type of shank. The rigid Gracey has a larger, stronger,
and less flexible shank and blade than the standard finishing
Gracey. The rigid shank allows the removal of moderate to
heavy calculus without using a separate set of heavy scalers,
such as sickles and hoes. Although some clinicians prefer the
enhanced tactile sensitivity that the flexible shank of the fin-
ishing Gracey provides, both types of Gracey curettes are suit-
able for root planing.
Recent additions to the Gracey curette set have been the
Gracey #15-16 and 17-18. The Gracey #15-16 is a modifi-
cation of the standard #11-12 and is designed for the mesial (A) (8)
surfaces of posterior teeth (Fig. 36.22). It consists of a Gracey FIGURE 36.21 A, Universal curette as seen from the blade. Note that
#11-12 blade combined with the more acutely angled #13-14 the blade is straight. B, Gracey curette as seen from the blade. The blade
is curved; only the convex cutting edge is used.
shank. When the clinician is using an intraoral finger rest, it is
often difficult to position the lower shank of the Gracey # 11-12
so that it is parallel with the mesial surfaces of the posterior clearance and better access to all posterior distal surfaces. The
teeth, especially on the mandibular molars. The new shank an- horizontal handle position minimizes interference from oppos-
gulation of the Gracey #15-16 allows better adaptation to posing arches and allows a more relaxed hand position when scal-
terior mesial surfaces from a front position with intraoral rests. ing distal surfaces. In addition, the blade is I-mm shorter to
If alternative fulcrums, such as extraoral or opposite-arch rests, allow better adaptation of the blade to distal tooth surfaces.
are used, the Gracey #11-12 works well and the new #15-16 is Extended-Shank Curettes. Extended-shank curettes, such
not essential. The Gracey #17-18 is a modification of the #13- as the After Five curettes (Hu-Friedy, Chicago), are modifica-
14. It has a terminal shank elongated by 3 mm and a more actions of the standard Gracey curette design. The terminal shank
centuated angulation of the shank to provide complete occlusal is 3-mm longer, allowing extension into deeper periodontal
TABLE 36.1
COMPARISON OF AREA-SPECIFIC (GRACEY) AND UNIVERSAL CURETTES

Gracey Curette Universal Curette
Area of use Set of many curettes designed for speci fie areas and surfaces. One curette designed for all areas and surfaces.
Cutting Edge
Use One cutting edge used; work with outer edge only Both cutting edges used; work with either outer or inner
edge.
Curvature Curved in two planes; blade curves up and to the side. Curved in one plane; blade curves up, not to the side.
Blade angle Offset blade; face of blade beveled at 60 degree to shank. Blade not offset; face of blade beveled at 90 degree to
shank.
(Modified from Pattison G, Pattison A: Periodontal instrumentation, ed 2, Norwalk, CT, 1992, Appleton & Lange.)
FIGURE 36.24 Comparison of After Five curette with standard Gracey

curette. Rigid Gracey #13-14 adapted to the distal surface of the first mo-
lar and rigid After Five #13-14 adapted to the distal surface of the second
molar. Notice the extra-long shank of the After Five curette, which allows
deeper insertion and better access. (Pattison A, Pattison C, Matsuda S.
Periodontal Instrumentation, ed 3, Pearson Education, (in press)).
FIGURE 36.22 Gracey #15-16. New Gracey curette, designed for

mesioposterior surfaces, combines a Gracey 1111-12 blade with a
Gracey 1113-14 shank. (Pattison A, Pattison C, Matsuda S. Periodontal
Instrumentation, ed 3, Pearson Education, (in press)).
(A) (8) (C) (D)
FIGURE 36.25 Comparison of After Five curette and Mini Five cu-
rette. The shorter Mini Five blade (half the length) allows increased ac-
cess and reduced tissue trauma.
FIGURE 36.23 After Five curette. Note the extra 3 mm in the terminal
shank of the After Five curette compared with the standard Gracey curette. prevents full insertion of the standard Gracey or After Five
A, 115-6; B, 117-8; C, #11-12; D, #13-14. (Pattison A, Pattison C, Matsuda 5. blade, the Mini Five curettes can be used with vertical strokes,
Periodontal Instrumentation, ed 3, Pearson Education, (in press)). with reduced tissue distention, and without tissue trauma
(Fig. 36.26).
pockets of 5 mm or more (Figs. 36.23 and 36.24). Other In the past the only solution in most of these areas of dif-
features of the After Five curette include a thinned blade for ficult access was to use the Gracey curettes with a toe-down
smoother subgingival insertion and reduced tissue disten- horizontal stroke. The Mini Five curettes, along with other
tion and a large-diameter, tapered shank. All standard Gracey short-bladed instruments relatively recently introduced, open
numbers except for the #9-10 (ie, #l-2, #3-4, #5-6, #7-8, a new chapter in the history of root instrumentation by allow-
#ll-12, or #13-14) are available in the After Five series. The ing access to areas that previously were extremely difficult or
After Five curettes are available in finishing or rigid designs. impossible to reach with standard instruments. The Mini Five
For heavy or tenacious calculus removal, rigid After Five cu- curettes are available in both finishing and rigid designs. Rigid
rettes should be used. For light scaling or deplaquing in a Mini Five curettes are recommended for calculus removal.
periodontal maintenance patient, the thinner, finishing After The more flexible, shanked, finishing Mini Five curettes are
Five curettes will insert subgingivally more easily. appropriate for light scaling and deplaquing in periodontal
Mini-Bladed Curettes. Mini-bladed curettes, such as the maintenance patients with tight pockets. As with the After
Hu-Friedy Mini Five curettes, are modifications of the After Five series, the Mini Five curettes are available in all standard
Five curettes. The Mini Five curettes feature blades that are Gracey numbers, except the #9-10.
half the length of the After Five or standard Gracey curettes The recently introduced Micro Mini Five Gracey curettes
(Fig. 36.25). The shorter blade allows easier insertion and ad- (Hu-Friedy, Chicago) have blades that are 20% thinner and
aptation in deep, narrow pockets; furcations; developmental smaller than the Mini Five curettes (Figs. 36.27 and 36.28)
grooves; line angles; and deep, tight, facial, lingual, or palatal These are the smallest of all curettes, and they provide excep-
pockets. In any area in which root morphology or tight tissue tional access and adaptation to tight, deep, or narrow pockets;
FIGURE 36.26 Comparison of standard rigid Gracey #5-6 with rigid

Mini Five #5-6 on the palatal surfaces of the maxillary central inci-
sors. Mini Five curette can be inserted to the base of these tight anterior
pockets and used with a straight vertical stroke. Standard Gracey or After
Five curette usually cannot be inserted vertically in this area because the
blade is too long. (Pattison A, Pattison C, Matsuda 5. Periodontal Instru-
mentation, ed 3, Pearson Education, (in press)).
FIGURE 36.27 Micro Mini Five Gracey curettes. A, #1-2; B, #7-8; C,
narrow furcations; developmental depressions; line angles; #11-12; D, #13-14.
and deep pockets on facial, lingual, or palatal surfaces. In ar-
eas in which root morphology or tight, thin tissue prevents
easy insertion of other mini-bladed curettes, the Micro Mini Langer and Mini-Langer Curettes. The Langer and Mini
Five curettes can be used with vertical strokes without causing Langer curettes are a set of three curettes combining the shank
tissue distension or tissue trauma. design of the standard Gracey #5-6, 11-12, and 13-14 cu-
The Gracey Curvettes are another set of four mini-bladed rettes with a universal blade honed at 90 degree rather than
curettes; the Sub-0 and the #l-2 are used for anterior teeth the offset blade of the Gracey curette. This marriage of the
and premolars, the #11-12 is used for posterior mesial sur- Gracey and universal curette designs allows the advantages
faces, and the # 13-14 for posterior distal surfaces. The blade of the area-specific shank to be combined with the versatility
length of these instruments is 50% shorter than that of the of the universal curette blade. The Langer #5-6 curette adapts
conventional Gracey curette, and the blade has been curved to the mesial and distal surfaces of anterior teeth; the Langer
slightly upward (Fig. 36 29) This curvature allows the Gracey #l-2 curette (Gracey #11-12 shank) adapts to the mesial and
Curvettes to adapt more closely to the tooth surface than distal surfaces of mandibular posterior teeth; and the Langer
any other curettes, especially on the anterior teeth and on #3-4 curette ( Gracey # 13-14 shank) adapts to the mesial and
line angles (Fig. 36.30). However, this curvature also carries distal surfaces of maxillary posterior teeth (Fig. 36.32). These
the risk of gouging or "grooving" into the root surfaces on instruments can be adapted to both mesial and distal tooth
the proximal surfaces of the posterior teeth when the Gracey surfaces without changing instruments. The standard Langer
Curvette #11-12 or 13-14 is used. Additional features that curette shanks are heavier than a finishing Gracey but less
represent improvements on the standard Gracey curettes are rigid than the rigid Gracey. Langer curettes are also available
a precision-balanced blade tip in direct alignment with the with either rigid or finishing shanks and can be obtained in
handle, a blade tip perpendicular to the handle, and a shank the extended-shank (After Five) and mini-bladed (Mini Five)
closer to parallel with the handle. versions.
For many years, the Morse scaler, a miniature sickle, was
the only mini-bladed instrument available. However, the Schwartz Periotrievers
mini-bladed curettes have largely replaced this instrument The Schwartz Periotrievers are a set of two double-ended, high-
(Fig. 36 31) ly magnetized instruments designed for the retrieval of broken
FIGURE 36.28 Comparison of Gracey curette blades. A, Micro Mini Five #7-8; B, Mini Five #7-8; C, Standard #7-8.
II I' I
I
I
I
I (C)
I
11
I
I
I
.,. -- ""'7-----::;;
,,
----
FIGURE 36.29 Gracey Curvette blade. This diagram shows the 50%
shorter blade of the Gracey Curvette superimposed on the standard
Gracey curette blade (dotted lines). Notice the upward curvature of
the Curvette blade and blade tip. (Redrawn from Pattison C, Pattison
A: Periodontal instrumentation, ed 2, Norwalk, Conn, 7992, Appleton
& Lange.)
FIGURE 36.32 Langer curettes combine Gracey-type shanks with

universal curette blades. A, #5-6; B, #1-2; and C, #3-4. (Pattison A,
Pattison C, Matsuda S. Periodontal Instrumentation, ed 3, Pearson
Education, (in press)).
FIGURE 36.30 Gracey Curvette Sub-0 on the palatal surface of a

maxillary central incisor. The long shank and short, curved, and blunted
tip make this a superior instrument for deep anterior pockets. This curette
provides excellent blade adaptation to the narrow root curvatures of
the maxillary and mandibular anterior teeth. (Pattison A, Pattison C,
Matsuda S. Periodontal Instrumentation, ed 3, Pearson Education, (in
press)).
~~~
~.,::A~,."f.
FIGURE 36.33 Schwartz Periotriever tip designs. The long blade is
for general use in pockets, and the contra-angled tip is for use in furca-
(A) (B).,. (C) tions. (From Pattison C, Pattison A: Periodontal instrumentation, ed 2,
Norwalk, CT, 7992, Appleton & Lange.)
instrument tips from the periodontal pocket (Figs. 36.33

and 36.34). They are indispensable when the clinician has
broken a curette tip in a furcation or deep pocket.
Plastic and Titanium Instruments for Implants
Several different companies are manufacturing plastic and
titanium instruments for use on titanium and other implant
abutment materials. It is important that plastic or titanium
instruments be used to avoid scarring and permanent damage
to the implants (Figs. 36 35-36.37)
Hoe Scalers
Hoe scalers are used for scaling of ledges or rings of calculus
(Fig. 36.38) The blade is bent at a 99-degree angle; the cut-
ting edge is formed by the junction of the flattened terminal
surface with the inner aspect of the blade. The cutting edge
is beveled at 45 degree. The blade is slightly bowed so that it
FIGURE 36.31 Comparison of three different mini-bladed instru- can maintain contact at two points on a convex surface. The
ments designed for use on the maxillary and mandibular anterior
teeth. A, Hu-Friedy Mini Five 115-6; B, Hu-Friedy Curvette Sub-0; C,
back of the blade is rounded, and the blade has been reduced
Hartzell Sub-0. (Pattison A, Pattison C, Matsuda S. Periodontal Instru- to minimal thickness to permit access to the roots without
mentation, ed 3, Pearson Education, (in press)). interference from the adjacent tissues.
(A) (B)
FIGURE 36.34 Broken instrument tip attached to the magnetic tip FIGURE 36.36 New lmplacare II implant instruments (Hu-Friedy,
of the Schwartz Periotriever. (From Pattison C, Pattison A: Periodontal Chicago). These implant instruments have autoclavable stainless steel
instrumentation, ed 2, Norwalk, CT, 1992, Appleton & Lange.) handles and five different cone-socket plastic tip designs. A, New Barn-
hart 5-6 curette tips and B, New Langer 1-2 curette tips.
' (C)
FIGURE 36.37 Titanium Implant Curettes (Paradise Dental Tech-

nologies, Missoula, MT). A, Barnhart #5-6; B, Langer #1-2; and C, NEB
128B-L5 Mini.
where files were once used. Files are sometimes used for re-
FIGURE 36.35 Plastic probe: Colorvue(Hu-Friedy, Chicago).
moving overhanging margins of dental restorations.
Hoe scalers are used in the following manner: Chisel Scalers

The chisel scaler, designed for the proximal surfaces of teeth
1. The blade is inserted to the base of the periodontal
too closely spaced to permit the use of other scalers, is usually
pocket so that it makes two-point contact with the tooth
used in the anterior part of the mouth. It is a double-ended in-
(Fig. 36.38). This stabilizes the instrument and prevents
strument with a curved shank at one end and a straight shank
nicking of the root.
at the other (Fig. 36 39); the blades are slightly curved and
2. The instrument is activated with a firm pull stroke toward
have a straight cutting edge beveled at 45 degree.
the crown, with every effort being made to preserve the
The chisel is inserted from the facial surface. The slight
two-point contact with the tooth.
curve of the blade makes it possible to stabilize it against the
McCall's #3, 4, 5, 6, 7, and 8 are a set of six hoe scalers de- proximal surface, whereas the cutting edge engages the cal-
signed to provide access to all tooth surfaces. Each instrument culus without nicking the tooth. The instrument is activated
has a different angle between the shank and handle. with a push motion while the side of the blade is held firmly
against the root.
Files
Files have a series of blades on a base (Fig. 36.39). Their pri- Quetin Furcation Curettes
mary function is to fracture or crush large deposits of tenacious The Quetin furcation curettes are actually hoes with a shal-
calculus or burnished sheets of calculus. Files can easily gouge low, half-moon radius that fits into the roof or floor of the
and roughen root surfaces when used improperly. Therefore, furcation. The curvature of the tip also fits into developmental
they are not suitable for fine scaling and root planing. Mini- depressions on the inner aspects of the roots. The shanks are
bladed curettes are currently preferred for fine scaling in areas slightly curved for better access, and the tips are available in
'
''> 2-point
/
/ contact
/
/
(A)
(B) FIGURE 36.40 Quetin furcation curettes: BL2 (larger) and BL 1

FIGURE 36.38 A, Hoe scalers designed for different tooth surfaces, (smaller). (Pattison A, Pattison C, Matsuda 5. Periodontal Instrumenta-
showing "two-point" contact. B, Hoe scaler in a periodontal pocket. The tion, ed 3, Pearson Education, (in press)).
back of the blade is rounded for easier access. The instrument contacts
the tooth at two points for stability.
New diamond files are sharply abrasive and should be
used with light, even pressure against the root surface to
avoid gouging or grooving. When viewing the root surface
with the dental endoscope after all tactilely detectable depos-
(A) its are gone, small embedded remnants of calculus in the root
surface can be observed. Diamond files are used similar to
an emery board to remove these minute remnants of calculus
from the root, creating a surface that is free of all visible accre-
tions. Diamond files can produce a smooth, even, clean, and
highly polished root surface.
Diamond files must be used carefully because they can
cause overinstrumentation of the root surface. They will re-
move too much root structure if they are used with excessive
force, are poorly adapted to root morphology, or used too long
in one place.
Diamond files are particularly effective when used with the
dental endoscope, which reveals residual deposits and directs
the clinician to the exact area for instrumentation.
Ultrasonic and Sonic Instruments
Ultrasonic instruments may be used for removing plaque,
scaling, curetting, and removing stain (see Chapter 3 7).
FIGURE 36.39 A, Chisel scaler and B, file scaler. Dental Endoscope
A dental endoscope has been introduced for use subgingi-
two widths (Fig. 36.40) The BU (buccal-lingual) and MDl vally in the diagnosis and treatment of periodontal disease
(mesial-distal) instruments are small and fine, with a 0.9-mm (Fig. 36.42). The Perioscopy system (Perioscopy, Inc., Oak-
blade width. The BL2 and MD2 instruments are larger and land, CA) consists of a 0.99-mm diameter, reusable fiberoptic
wider, with a 1.3-mm blade width. endoscope over which is fitted a disposable, sterile sheath.
These instruments remove burnished calculus from re- The fiberoptic endoscope fits onto periodontal probes and
cessed areas of the furcation where curettes, even the mini- ultrasonic instruments that have been designed to accept it
bladed curettes, are often too large to gain access. Using (Fig. 36. 4 3). The sheath delivers water irrigation that flushes
mini-bladed Gracey curettes and Gracey Curvettes in the roof the pocket while the endoscope is being used, keeping the
or floor of the furcation may unintentionally create gouges and field clear. The fiberoptic endoscope attaches to a medical-
grooves. The Quetin instruments, however, are well suited for grade charged-coupled device (CCD) video camera and light
this area and lessen the likelihood of root damage. source that produces an image on a flat-panel monitor for
viewing during subgingival exploration and instrumentation.
Diamond-Coated Files This device allows clear visualization deeply into subgingival
Diamond-coated files are unique instruments used for final pockets and furcations (Fig. 36.44). It permits operators to
finishing of root surfaces. These files do not have cutting detect the presence and location of subgingival deposits and
edges; instead, they are coated with very-fine-grit diamond guides them in the thorough removal of these deposits. Mag-
(Fig. 36.41) The most useful diamond files are the buccal- nification ranges from 24 to 48 times, enabling visualization
lingual instruments, which are used in furcations and also of even minute deposits of plaque and calculus. Using this
adapt well to many other root surfaces. device, operators can achieve levels of root debridement and
(
(A) (8)
FIGURE 36.41 Diamond files. A, #1,2 (Brasseler, Savannah, GA); B, #3,4 (Brasseler); C, SDCN 7, SDCM/D 7. (Pattison A, Pattison C, Matsuda 5.
Periodontal Instrumentation, ed 3, Pearson Education, (in press)).
FIGURE 36.43 Viewing periodontal explorers (left/right/full view-

ing) for the Perioscopy system. (Courtesy Perioscopy Incorporated,
Oakland, CA.)
FIGURE 36.42 Perioscopy system, dental endoscope. (Courtesy

Perioscopy Incorporated, Oakland, CA.)
cleanliness that are much more difficult or impossible to pro-

duce without it. The Perioscopy system can also be used to FIGURE 36.44 Perioscopic instrumentation permits deep subgingi-
evaluate subgingival areas for caries, defective restorations, val visualization in pockets and furcations. (Courtesy Perioscopy Incor-
root fractures, and resorption. porated, Oakland, CA.)
EVA System coated and the other side is smooth. The files can be mount-
Probably the most efficient and least traumatic instruments for ed on a special dental handpiece attachment that generates
correcting overhanging or overcontoured proximal alloy and reciprocating strokes of variable frequency When the unit is
resin restorations are the motor-driven diamond files of the activated interproximally with the diamond-coated side of the
EVA prophylaxis instrument. These files, which come in sym- file touching the restoration and the smooth side adjacent to
metric pairs, are made of aluminum in the shape of a wedge the papilla, the oscillating file swiftly planes the contour of the
protruding from a shaft; one side of the wedge is diamond restoration and reduces it to the desired shape.
FIGURE 36.45 Metal prophylaxis angle with rubber cup and brush.
FIGURE 36.47 Cavitron ProphyJet air-powder polishing device.

(Courtesy Dentsply International, York, PA.)
Air-Powder Polishing
The first specially designed handpiece to deliver an air-
powered slurry of warm water and sodium bicarbonate for
polishing was introduced in the early 1980s. This device,
called the Prophy-Jet (Dentsply International, York, PA), is very
effective for the removal of extrinsic stains and soft deposits
(Fig. 36.4 7). The slurry removes stains rapidly and efficiently
by mechanical abrasion and provides warm water for rinsing
and lavage. The flow rate of abrasive cleansing power can be
FIGURE 36.46 Disposable plastic prophylaxis angle with rubber cup
adjusted to increase the amount of powder for heavier stain
and with brush. removal. Currently, many manufacturers produce air-powder
polishing systems that use various powder formulas.
The results of studies on the abrasive effect of the air-
Cleansing and Polishing Instruments powder polishing devices using sodium bicarbonate and
Rubber Cups aluminum trihydroxide on cementum and dentin show that
significant tooth substance can be lost. Damage to gingival
Rubber cups consist of a rubber shell with or without webbed
tissue is transient and insignificant clinically, but amalgam
configurations in the hollow interior (Fig. 36.45). They are
restorations, composite resins, cements, and other nonmetal-
used in the handpiece with a special prophylaxis angle. The
lic materials can be roughened. Polishing powders containing
handpiece, prophylaxis angle, and rubber cup must be steril-
glycine rather than sodium bicarbonate recently have been in-
ized after each patient use, or a disposable plastic prophy-
troduced for subgingival biofilm removal from root surfaces.
laxis angle and rubber cup may be used and then discarded
Air-powder polishing can be used safely on titanium implant
(Fig. 36. 46). A good cleansing and polishing paste that con-
surfaces.
tains fluoride should be used and kept moist to minimize fric-
Patients with medical histories of respiratory illnesses and
tional heat as the cup revolves. Polishing pastes are available
hemodialysis are not candidates for the use of the air-powder
in fine, medium, or coarse grits and are packaged in small,
polishing device. Powders containing sodium bicarbonate
convenient, single-use containers. Aggressive use of the rub-
should not be used on patients with histories of hypertension,
ber cup with any abrasive may remove the layer of cementum,
sodium-restricted diets, or medications affecting the electro-
which is thin in the cervical area.
lyte balance. Patients with infectious diseases should not be
Bristle Brushes treated with this device because of the large quantity of aero-
sol created. A preprocedural rinse with 0.12% chlorhexidine
Bristle brushes are available in wheel and cup shapes
gluconate should be used to minimize the microbial content
(Fig. 36.45). The brush is used in the prophylaxis angle with
of the aerosol. High-speed evacuation should also be used to
a polishing paste. Since the bristles are stiff, use of the brush
eliminate as much of the aerosol as possible.
should be confined to the crown to avoid injuring the cemen-
tum and the gingiva.
Surgical Instruments
Dental Tape
Periodontal surgery is accomplished with numerous instru-
Dental tape with polishing paste is used for polishing proxi-
ments; Figure 36.48 shows a typical surgical cassette. Peri-
mal surfaces that are inaccessible to other polishing instru-
odontal surgical instruments are classified as follows:
ments. The tape is passed interproximally while being kept at
a right angle to the long axis of the tooth and is activated with 1. Excisional and incisional instruments
a firm labiolingual motion. Particular care is taken to avoid 2. Surgical curettes and sickles
injury to the gingiva. The area should be cleansed with warm 3. Periosteal elevators
water to remove all remnants of paste. 4. Surgical chisels
B
FIGURE 36.48 A typical series of periodontal surgical instruments divided into two cassettes. A, From left, Mirrors, explorer, probe, series of
curettes, needleholder, rongeurs, and scissors. B, From left, Series of chisels, Kirkland knife, Orban knife, scalpel handles with surgical blades (nos.
15C, 15, and 12D), periosteal elevators, spatula, tissue forceps, cheek retractors, mallet, and sharpening stone. (Courtesy A, Hu-Friedy, Chicago, IL;
Courtesy 8, C. Hartzell & Son, Concord, CA.)
(A)
(B)
FIGURE 36.49 Gingivectomy knives. A, Kirkland knife; B, Orban in- FIGURE 36.50 Surgical blades. A-C, Nos. 15, 12D, and 15C. These
terdental knife. blades are disposable.
5. Surgical files flaps and general purposes. The no. 15C blade, which is a
6. Scissors narrower version of the no. 15 blade, is useful for making the
7. Hemostats and tissue forceps initial, scalloping-type incision. The slim design of this blade
allows for incising into the narrow interdental portion of the
Excisional and lncisional Instruments flap. All of these blades are discarded after one use.
Periodontal Knives (Gingivectomy Knives) Electrosurgery (Radiosurgery) Techniques and
The Kirkland knife is representative of the knives that are typi- Instrumentation
cally used for gingivectomy. These knives can be obtained as The terms electrosurgery and radiosurgery are currently used
either double-ended or single-ended instruments. The entire to identify surgical techniques performed on soft tissue with
periphery of these kidney-shaped knives is the cutting edge the use of controlled, high-frequency electrical (radio) cur-
(Fig. 36.49A) rents in the range of 1.5-7.5 million cycles per second (mega-
hertz). There are three classes of active electrodes: single-wire
lnterdental Knives electrodes for incising or excising; loop electrodes for plan-
The Orban knife (nos. 1 and 2; Fig. 36.49B) and the Merri- ing tissue; and heavier, bulkier electrodes for coagulation
field knife (nos. 1 through 4) are examples of knives that can procedures.
be used for interdental areas. These spear-shaped knives have The four basic types of electrosurgical techniques are elec-
cutting edges on both sides of the blade, and they are designed trosection, electrocoagulation, electrofulguration, and electro-
with either double-ended or single-ended blades. desiccation.
Electrosection, which is also referred to as electrotomy or
Surgical Blades acusection, is used for incisions, excisions, and tissue planing.
Scalpel blades of different shapes and sizes are used in peri- Incisions and excisions are performed with single-wire active
odontal surgery. The most common blades are nos. 12D, 15, electrodes that can be bent or adapted to accomplish any type
and 15C (Fig. 36 50). The no. 12D blade is a beak-shaped of cutting procedure.
blade with cutting edges on both sides, which allow the oper- Electrocoagulation provides a wide range of coagulation and
ator to engage narrow, restricted areas with both pushing and hemorrhage control by using the electrocoagulation current.
pulling cutting motions. The no. 15 blade is used for thinning Electrocoagulation can prevent bleeding or hemorrhage at the
FIGURE 36.51 A Prichard surgical curette. The curettes that are used FIGURE 36.52 Woodson periosteal elevator.
in surgery have wider blades than those that are used for conventional
scaling and root planing.
initial entry into soft tissue, but it cannot stop bleeding after
blood is present. All forms of hemorrhage must be stopped
first by some form of direct pressure (eg, air, compress, hemo-
stat). After bleeding has momentarily stopped, the final seal-
ing of the capillaries or large vessels can be accomplished with
a short application of the electrocoagulation current. The ac-
tive electrodes that are used for coagulation are much bulkier
than the fine tungsten wire used for electrosection. Electrosec-
tion and electrocoagulation are the procedures that are most
often used in all areas of dentistry. The two monoterminal
techniques, electrofulguration and electrodesiccation, are not FIGURE 36.53 Back-action chisel.
in general use in dentistry.
The most important basic rule of electrosurgery is this:
always keep the tip moving. The prolonged or repeated applica-
tion of current to tissue induces heat accumulation and un-
desired tissue destruction, whereas interrupted application at
intervals adequate for tissue cooling (5-10 s) reduces or elimi-
nates heat buildup. Electrosurgery is not intended to destroy
tissue; it is a controllable means of sculpturing or modifying
oral soft tissue with little discomfort and hemorrhage for the
patient.
The indications for electrosurgery in periodontal therapy
and a description of wound healing after electrosurgery are
presented in Chapter 44. Electrosurgery is contraindicated for
patients who have incompatible or poorly shielded cardiac
pacemakers. FIGURE 36.54 Ochsenbein chisels are paired, with their cutting edg-
es in opposite directions.
Surgical Curettes and Sickles

Ochsenbein chisel is a useful chisel with a semicircular inden-
Larger and heavier curettes and sickles are often needed dur- tation on both sides of the shank that allows the instrument
ing surgery for the removal of granulation tissue, fibrous inter- to engage around the tooth and into the interdental area. The
dental tissues, and tenacious subgingival deposits. The Prich- Rhodes chisel is another popular back-action chisel.
ard curette (Fig. 36.51) and the Kirkland surgical instruments
are heavy curettes, whereas the Ball scaler (nos. B2 and B3)
Tissue Forceps
is a popular heavy sickle. The wider, heavier blades of these
instruments make them suitable for surgical procedures. The tissue forceps is used to hold the flap during suturing. It
is also used to position and displace the flap after the flap has
Periosteal Elevators been reflected. The DeBakey forceps is an extremely efficient
instrument (Fig. 36 55).
The periosteal elevators are needed to reflect and move the
flap after the incision has been made for flap surgery. The
Scissors and Nippers
Woodson and Prichard elevators are well-designed periosteal
instruments (Fig. 36 52) Scissors and nippers are used in periodontal surgery to re-
move tabs of tissue during gingivectomy, to trim the margins
Surgical Chisels of flaps, to enlarge incisions in periodontal abscesses, and to
remove muscle attachments in mucogingival surgery. Many
The back-action chisel is used with a pull motion (Fig. 36.53), types are available, and individual preference determines the
whereas the straight chisel [eg, Wedelstaedt, Ochsenbein choice. The Goldman-Fox no. 16 scissors has a curved, bev-
(nos 1 and 2)] is used with a push motion (Fig. 36 54) The eled blade with serrations (Fig. 36 56)
and retraction for optimal visibility, and sharp instruments are

fundamental prerequisites. A constant awareness of tooth and
root morphologic features and of the condition of the peri-
odontal tissues is also essential. Knowledge of instrument
design enables the clinician to select the proper instrument
for the procedure and the correct area in which it will be per-
formed. In addition to these principles, the basic concepts of
grasp, finger rest, adaptation, angulation, and stroke must be
understood before clinical instrument-handling skills can be
mastered.
FIGURE 36.55 DeBakey tissue forceps. Accessibility: Positioning of Patient and

Operator
Accessibility facilitates thoroughness of instrumentation. The
position of the patient and operator should provide maximal
accessibility to the area of operation. Inadequate accessibility
impedes thorough instrumentation, prematurely tires the op-
erator, and diminishes his or her effectiveness.
The clinician should be seated on a comfortable operat-
ing stool that has been positioned so that the clinician's feet
are flat on the floor with the thighs parallel to the floor. The
clinician should be able to observe the field of operation while
keeping the back straight and the head erect.
The patient should be in a supine position and placed so
that the mouth is close to the resting elbow of the clinician.
For instrumentation of the maxillary arch, the patient should
be asked to raise the chin slightly to provide optimal visibility
and accessibility. For instrumentation on the mandibular arch,
it may be necessary to raise the back of the chair slightly and
FIGURE 36.56 Goldman-Fox scissors. request that the patient lower the chin until the mandible is
parallel to the floor. This will especially facilitate work on the
Needleholders lingual surfaces of the mandibular anterior teeth.
Needleholders are used to suture the flap at the desired posi-

Visibility, Illumination, and Retraction
tion after the surgical procedure has been completed. In ad-
dition to the regular types of needleholders (Fig. 36.57A), the Whenever possible, direct vision with direct illumination from
Castroviejo needleholder is used for delicate, precise tech- the dental light is most desirable (Fig. 36 58). If this is not
niques that require the quick and easy grasp and release of the possible, indirect vision may be obtained by using the mouth
suture (Fig. 36.57B) mirror (Fig. 36.59) and indirect illumination may be obtained
by using the mirror to reflect light to where it is needed
(Fig. 36.60). Indirect vision and indirect illumination are of-
General Principles of Instrumentation ten used simultaneously (Fig. 36.61).
Effective instrumentation is governed by a number of general Retraction provides visibility, accessibility, and illumination.
principles that are common to all periodontal instruments. Depending on the location of the area of operation, the fingers
Proper position of the patient and the operator, illumination and/or the mirror are used for retraction. The mirror may be
(B)
FIGURE 36.57 A, Conventional needleholder; B, Castroviejo needleholder
FIGURE 36.58 Direct vision and direct illumination in the mandibu- FIGURE 36.61 Combination of indirect illumination and indirect vi-
lar left premolar area. sion for the lingual surfaces of the maxillary anterior teeth.
FIGURE 36.59 Indirect vision using the mirror for the lingual sur-
faces of the mandibular anterior teeth. FIGURE 36.62 Retracting the cheek with the mirror.
2. Use of the mirror alone to retract the lips and cheek

(Fig. 36.62)
3. Use of the fingers of the nonoperating hand to retract the
lips (Fig. 36.63)
4. Use of the mirror to retract the tongue (Fig. 36.64)
5. Combinations of the preceding methods
When retracting, care should be taken to avoid irritation
to the angles of the mouth. If the lips and skin are dry, soft-
ening the lips with petroleum jelly before instrumentation is
a helpful precaution against cracking and bleeding. Careful
retraction is especially important for patients with a history
of recurrent herpes labialis because these patients may easily
develop herpetic lesions after instrumentation.
Condition and Sharpness of Instruments

FIGURE 36.60 Indirect illumination using the mirror to reflect light
onto the maxillary left posterior lingual region. Before any instrumentation, all instruments should be inspect-
ed to make sure that they are clean, sterile, and in good con-
dition. The working ends of pointed or bladed instruments
used for retraction of the cheeks or the tongue; the index fin-
must be sharp to be effective. Sharp instruments enhance tac-
ger is used for retraction of the lips or cheeks. The following
tile sensitivity and allow the clinician to work more precisely
methods are effective for retraction:
and efficiently (see later discussion). Dull instruments may
1. Use of the mirror to deflect the cheek while the fingers lead to incomplete calculus removal and unnecessary trauma
of the nonoperating hand retract the lips and protect the because of the excess force usually applied to compensate for
angle of the mouth from irritation by the mirror handle their ineffectiveness.
FIGURE 36.63 Retracting the lip with the index finger of the nonop- FIGURE 36.65 Modified pen grasp. The pad of the middle finger rests
erating hand. on the shank. (Pattison A, Pattison C, Matsuda 5. Periodontal Instrumen-
tation, ed 3, Pearson Education, (in press)).
FIGURE 36.64 Retracting the tongue with the mirror. FIGURE 36.66 Standard pen grasp. The side of the middle finger rests
on the shank. (Pattison A, Pattison C, Matsuda 5. Periodontal Instrumen-
tation, ed 3, Pearson Education, (in press)).
Maintaining a Clean Field
Despite good visibility, illumination, and retraction, instru- subgingival area should be clean, dry, and clearly visible for a
mentation can be hampered if the operative field is obscured brief interval.
by saliva, blood, and debris. The pooling of saliva interferes
with visibility during instrumentation and impedes control Instrument Stabilization
because a firm finger rest cannot be established on wet, slip-
pery tooth surfaces. Adequate suction is essential and can be Stability of the instrument and the hand is the primary req-
achieved with a saliva ejector or, if working with an assistant, uisite for controlled instrumentation. Stability and control are
an aspirator. essential for effective instrumentation and avoidance of injury
Gingival bleeding is an unavoidable consequence of sub- to the patient or clinician. The two factors of major impor-
gingival instrumentation. In areas of inflammation, bleed- tance in providing stability are the instrument grasp and the
ing is not necessarily an indication of trauma from incorrect finger rest.
technique but rather may indicate ulceration of the pocket
epithelium. Blood and debris can be removed from the opera- Instrument Grasp
tive field with suction and by wiping or blotting with gauze A proper grasp is essential for precise control of movements
squares. The operative field should also be flushed occasion- made during periodontal instrumentation. The most effective
ally with water. and stable grasp for all periodontal instruments is the modified
Compressed air and gauze squares can be used to facili- pen grasp (Fig. 36 65) Although other grasps are possible, this
tate visual inspection of tooth surfaces just below the gingi- modification of the standard pen grasp (Fig. 36.66) ensures the
val margin during instrumentation. A jet of air directed into greatest control in performing intraoral procedures.
the pocket deflects a retractable gingival margin. Retractable The thumb, index finger, and middle finger are used to
tissue can also be deflected away from the tooth by gently hold the instrument as a pen is held, but the middle finger
packing the edge of a gauze square into the pocket with the is positioned so that the side of the pad next to the fingernail
back of a curette. Immediately after the gauze is removed, the is resting on the instrument shank. The index finger is bent
FIGURE 36.68 lntraoral conventional finger rest. The fourth finger

rests on the occlusal surfaces of adjacent teeth.
FIGURE 36.67 Palm and thumb grasp, used for stabilizing instru-
ments during sharpening. (Pattison A, Pattison C, Matsuda 5. Periodon-
tal Instrumentation, ed 3, Pearson Education, (in press)).
at the second joint from the fingertip and is positioned well

above the middle finger on the same side of the handle.
The pad of the thumb is placed midway between the mid-
dle and index fingers on the opposite side of the handle. This
creates a triangle of forces, or tripod effect, that enhances con-
trol because it counteracts the tendency of the instrument to
turn uncontrollably between the fingers when scaling force is
applied to the tooth. This stable modified pen grasp enhances
control because it enables the clinician to roll the instrument
in precise degrees with the thumb against the index and mid-
dle fingers to adapt the blade to the slightest changes in tooth
contour. The modified pen grasp also enhances tactile sensi- FIGURE 36.69 lntraoral cross-arch finger rest. The fourth finger rests
on the incisal surfaces of teeth on the opposite side of the same arch.
tivity because slight irregularities on the tooth surface are best
perceived when the tactile-sensitive pad of the middle finger
is placed on the shank of the instrument. of the middle and fourth fingers during scaling strokes results
The palm and thumb grasp (Fig. 36 67) is useful for stabiliz- in a loss of power and control because it forces the clinician
ing instruments during sharpening and for manipulating air to rely solely on finger flexing for activation of the instrument.
and water syringes, but it is not recommended for periodontal Finger rests may be generally classified as intraoral finger
instrumentation. Maneuverability and tactile sensitivity are so rests or extraoral fulcrums. lntraoral finger rests on tooth sur-
inhibited by this grasp that it is unsuitable for the precise, con- faces ideally are established close to the working area. Varia-
trolled movements necessary during periodontal procedures. tions of intraoral finger rests and extraoral fulcrums are used
whenever good angulation and a sufficient arc of movement
Finger Rest cannot be achieved by a finger rest close to the working area.
The finger rest serves to stabilize the hand and the instru- The following examples illustrate the different variations of
ment by providing a firm fulcrum as movements are made to the intraoral finger rest:
activate the instrument. A good finger rest prevents injury and 1. Conventional: The finger rest is established on tooth surfaces
laceration of the gingiva and surrounding tissues by poorly immediately adjacent to the working area (Fig. 36 68).
controlled instruments. The fourth (ring) finger is preferred 2. Cross-arch: The finger rest is established on tooth surfaces
by most clinicians for the finger rest. Although it is possible to on the other side of the same arch (Fig. 36.69).
use the third (middle) finger for the finger rest, this is not rec-
3. Opposite arch: The finger rest is established on tooth sur-
ommended because it restricts the arc of movement during the faces on the opposite arch (eg, mandibular arch finger rest
activation of strokes and severely curtails the use of the middle for instrumentation on the maxillary arch) (Fig. 36. 70).
finger for both control and tactile sensitivity. Maximal control 4. Finger on finger: The finger rest is established on the index
is achieved when the middle finger is kept between the instru- finger or thumb of the nonoperating hand (Fig. 36 71).
ment shank and the fourth finger. This "built-up" fulcrum is
an integral part of the wrist-forearm action that activates the Extraoral fulcrums are essential for effective instrumenta-
powerful working stroke for calculus removal. Whenever pos- tion of some aspects of the maxillary posterior teeth. When
sible, these two fingers should be kept together to work as a properly established, they allow optimal access and angulation
one-unit fulcrum during scaling and root planing. Separation while providing adequate stabilization. Extraoral fulcrums are
FIGURE 36.70 lntraoral opposite-arch finger rest. The fourth finger FIGURE 36.72 Extraoral palm-up fulcrum. The backs of the fingers
rests on the mandibular teeth while the maxillary posterior teeth are rest on the right lateral aspect of the mandible while the maxillary right
instrumented. posterior teeth are instrumented.
FIGURE 36.73 Extraoral palm-down fulcrum. The front surfaces of the

FIGURE 36.71 lntraoral finger-on-finger rest. The fourth finger rests fingers rest on the left lateral aspect of the mandible while the maxillary
on the index finger of the nonoperating hand. left posterior teeth are instrumented.
not "finger rests" in the literal sense because the tips or pads finger-reinforced rest, and Fig. 36. 75 shows the thumb-
of the fingers are not used for extraoral fulcrums as they are reinforced rest.
for intraoral finger rests. Instead, as much of the front or back
surface of the fingers as possible is placed on the patient's face Instrument Activation
to provide the greatest degree of stability. The two most com-
mon extraoral fulcrums are used as follows: Adaptation
Adaptation refers to the manner in which the working end of a
1. Palm up: The palm-up fulcrum is established by resting the
periodontal instrument is placed against the surface of a tooth.
backs of the middle and fourth fingers on the skin overly-
The objective of adaptation is to make the working end of
ing the lateral aspect of the mandible on the right side of
the instrument conform to the contour of the tooth surface.
the face (Fig. 36.72).
Precise adaptation must be maintained with all instruments
2. Palm down: The palm-down fulcrum is established by rest-
to avoid trauma to the soft tissues and root surfaces and to
ing the front surfaces of the middle and fourth fingers on
ensure maximum effectiveness of instrumentation.
the skin overlying the lateral aspect of the mandible on the
Correct adaptation of the probe is quite simple. The tip and
left side of the face (Fig. 36. 73).
side of the probe should be flush against the tooth surface as ver-
Both intraoral finger rests and extraoral fulcrums may be tical strokes are activated within the crevice. Bladed instruments
reinforced by applying the index finger or thumb of the non- (eg, curettes) and sharp-pointed instruments (eg, explorers)
operating hand to the handle or shank of the instrument for are more difficult to adapt. The ends of these instruments are
added control and pressure against the tooth. The reinforc- sharp and can lacerate tissue, so adaptation in subgingival areas
ing finger is usually employed for opposite-arch or extraoral becomes especially important. The lower third of the working
fulcrums when precise control and pressure are compro- end, which is the last few millimeters adjacent to the toe or tip,
mised by the longer distance between the fulcrum and the must be kept in constant contact with the tooth while it is mov-
working end of the instrument. Fig. 36.74 shows the index ing over varying tooth contours (Fig. 36.76). Precise adaptation
FIGURE 36.74 Index finger-reinforced rest. The index finger is placed

on the shank for pressure and control in the maxillary left posterior lin-
gual region. FIGURE 36.76 Gracey curette blade divided into three segments. A,
The lower one-third of the blade, consisting of the terminal few mil-
limeters adjacent to the toe; B, the middle one-third; and, C, the upper
one-third, which is adjacent to the shank.
FIGURE 36.75 Thumb-reinforced rest. The thumb is placed on the

handle for control in the maxillary right posterior lingual region.
FIGURE 36.77 Blade adaptation. The curette on the left is properly
adapted to the root surface. The curette on the right is incorrectly adapt-
ed; the toe juts out, lacerating the soft tissues.
is maintained by carefully rolling the handle of the instrument
against the index and middle fingers with the thumb. This ro-
tates the instrument in slight degrees so that the toe or tip leads Correct angulation is essential for effective calculus remov-
into concavities and around convexities. On convex surfaces al. For subgingival insertion of a bladed instrument such as a
such as line angles, it is not possible to adapt more than 1 or 2 curette, angulation should be as close to O degree as possible
mm of the working end against the tooth. Even on what appear (Fig. 36. 78A). The end of the instrument can be inserted to
to be broader, flatter surfaces, no more than 1 or 2 mm of the the base of the pocket more easily with the face of the blade
working end can be adapted because the tooth surface, although flush against the tooth. During scaling and root planing, op-
it may seem flat, is actually slightly curved. timal angulation is between 45 and 90 degrees (Fig. 36.78B).
If only the middle third of the working end is adapted on The exact blade angulation depends on the amount and na-
a convex surface so that the blade contacts the tooth at a tan- ture of the calculus, the procedure being performed, and the
gent, the toe or sharp tip will jut out into soft tissue, causing condition of the tissue. Blade angulation is diminished or
trauma and discomfort (Fig. 36.77). closed by tilting the lower shank of the instrument toward
If the instrument is adapted so that only the toe or tip is in the tooth. It is increased or opened by tilting the lower shank
contact, the soft tissue can be distended or compressed by the away from the tooth. During scaling strokes on heavy, tena-
back of the working end, also causing trauma and discomfort. cious calculus, angulation should be just less than 90 degree
A curette that is improperly adapted in this manner can be so that the cutting edge "bites" into the calculus. With angu-
particularly damaging because the toe can gouge or groove lation of less than 45 degree, the cutting edge will not bite
the root surface. into or engage the calculus properly (Fig. 3678C). Instead,
it will slide over the calculus, smoothing or "burnishing" it. If
Angulation angulation is more than 90 degree, the lateral surface of the
Angulation refers to the angle between the face of a bladed blade, rather than the cutting edge, will be against the tooth,
instrument and the tooth surface. It may also be called the and the calculus will not be removed and may become bur-
tooth-blade relationship. nished (Fig. 36 78D). After the calculus has been removed,
--
.I '
I
I
I
I
I
11
I I
I I
I
I
I
I
I
l I I I J
\ I I I I l
l ( I I
I I I
I I I
I I
(
I
I
(B) ~
I /
1_, I I
I
(A)' I (C) I
(A) (B) (C) (D) FIGURE 36.79 Three basic stroke directions. A, Vertical; B, oblique;
C, horizontal.
FIGURE 36.78 Blade angulation. A, 0 degree: correct angulation for
blade insertion. B, 45-90 degrees: correct angulation for scaling and
root planing. C, Less than 45 degree: incorrect angulation for scaling and
root planing. D, More than 90 degree: incorrect angulation for scaling
and root planing, correct angulation for gingival curettage.
or oblique strokes. The direction, length, pressure, and num-
ber of strokes necessary for either scaling or root planing are
determined by four major factors: (1) gingival position and
angulation of just less than 90 degree may be maintained, or tone, (2) pocket depth and shape, (3) tooth contour, and ( 4)
the angle may be slightly closed as the root surface is smoothed the amount and nature of the calculus or roughness.
with light, root-planing strokes. The exploratory strohe is a light, "feeling" stroke that is used
When gingival curettage is indicated, angulation greater with probes and explorers to evaluate the dimensions of the
than 90 degree is deliberately established so that the cutting pocket and to detect calculus and irregularities of the tooth
edge will engage and remove the pocket lining (Fig. 36. 78D) surface. With bladed instruments such as the curette, the ex-
ploratory stroke is alternated with scaling and root-planing
Lateral Pressure strokes for these same purposes of evaluation and detection.
Lateral pressure refers to the pressure created when force is The instrument is grasped lightly and adapted with light pres-
applied against the surface of a tooth with the cutting edge of sure against the tooth to achieve maximal tactile sensitivity.
a bladed instrument. The exact amount of pressure applied The scaling strohe is a short, powerful pull stroke that is
must be varied according to the nature of the calculus and used with bladed instruments for the removal of both supra-
according to whether the stroke is intended for initial scal- gingival and subgingival calculus. The muscles of the fingers
ing to remove calculus or for root planing to smooth the root and hands are tensed to establish a secure grasp, and lateral
surface. pressure is firmly applied against the tooth surface. The cut-
Lateral pressure may be firm, moderate, or light. When ting edge engages the apical border of the calculus and dis-
removing calculus, lateral pressure is initially applied firm- lodges it with a firm movement in a coronal direction. The
ly or moderately and is progressively diminished until light scaling motion should be initiated in the forearm and trans-
lateral pressure is applied for the final root-planing strokes. mitted from the wrist to the hand with a slight flexing of the
When insufficient lateral pressure is applied for the removal fingers. Rotation of the wrist is synchronized with movement
of heavy calculus, rough ledges or lumps may be shaved to of the forearm. The scaling stroke is neither initiated in the
thin, smooth sheets of burnished calculus that are difficult wrist or fingers nor is it carried out independently without the
to detect and remove. This burnishing effect often occurs in use of the forearm.
areas of developmental depressions and along the cementoe- It is possible to initiate the scaling motion by rotating the
namel junction. wrist and forearm or by flexing the fingers. The use of wrist
Although firm lateral pressure is necessary for the thor- and forearm action versus finger motion has long been de-
ough removal of calculus, indiscriminate, unwarranted, or bated among clinicians. Perhaps the strong opinions on both
uncontrolled application of heavy forces during instrumenta- sides should be the most valid indication that there is a time
tion should be avoided. Repeated application of excessively and a place for each. Neither method can be advocated exclu-
heavy strokes often nicks or gouges the root surface. sively because a careful analysis of effective scaling and root-
The careful application of varied and controlled amounts planing technique reveals that both types of stroke activation
of lateral pressure during instrumentation is an integral part are necessary for complete instrumentation. The wrist and
of effective scaling and root-planing techniques and is critical forearm motion, pivoting in an arc on the finger rest, produces
to the success of both these procedures. a more powerful stroke and is therefore preferred for scaling.
Finger flexing is indicated for precise control over stroke length
Strokes in areas such as line angles and when horizontal strokes are
Three basic types of strokes are used during instrumenta- used on the lingual or facial aspects of narrow-rooted teeth.
tion: the exploratory stroke, the scaling stroke, and the root- The push scaling motion has been advocated by some clini-
planing stroke. Any of these basic strokes may be activated by cians. In the push stroke, the instrument engages the lateral or
a pull or a push motion in a vertical, oblique, or horizontal coronal border of the calculus, and the fingers provide a thrust
direction (Fig. 36.79). Vertical and oblique strokes are used motion that dislodges the deposit. Since the push stroke may
most frequently. Horizontal strokes are used selectively on line force calculus into the supporting tissues, its use, especially in
angles or deep pockets that cannot be negotiated with vertical an apical direction, is not recommended.
The root-planing strohe is a moderate to light pull stroke that

is used for final smoothing and planing of the root surface.
Although hoes, files, and ultrasonic instruments have been
used for root planing, curettes are widely acknowledged to
be the most effective and versatile instruments for this pro-
cedure. The design of the curette, which allows it to be more
easily adapted to subgingival tooth contours, makes curettes
particularly suitable for root planing in periodontal patients. a
With a moderately firm grasp, the curette is kept adapted to
the tooth with even, lateral pressure. A continuous series of
long, overlapping shaving strokes is activated. As the surface
t>b
becomes smoother and resistance diminishes, lateral pressure
is progressively reduced.
Instruments for Scaling and Root Planing

Universal Curettes
The working ends of the universal curette are designed in FIGURE 36.80 Adaptation of the universal curette on a posterior
pairs so that all surfaces of the teeth can be treated with one tooth. Cross-sectional representations of the same universal curette
double-ended instrument or a matched pair of single-ended blade as its cutting edges (a and b) are adapted to the mesial and distal
instruments (Fig. 36 16) surfaces of a posterior tooth.
In any given quadrant, when approaching the tooth from
the facial aspect, one end of the universal curette adapts to
the mesial surfaces and the other end adapts to the distal sur- specially designed for subgingival scaling and root planing in
faces. When approaching from the lingual aspect in the same periodontal patients.
quadrant, the double-ended universal curette must be turned
end for end because the blades are mirror images. This means Gracey Curettes
that the end that adapts to the mesial surfaces on the facial As discussed earlier, Gracey curettes are a set of area-specific
aspect also adapts to the distal surfaces on the lingual aspect, instruments that were designed by Dr Clayton H. Gracey of
and vice versa. Both ends of the universal curette are used Michigan in the mid-1930s (Fig. 36 18) Four design features
for instrumentation of the anterior teeth. On posterior teeth, make the Gracey curettes unique: (1) they are area specific, (2)
however, because of the limited access to distal surfaces, a only one cutting edge on each blade is used, (3) the blade is
single working end can be used to treat both mesial and distal curved in two planes, and ( 4) the blade is "offset" (Table 46 1.)
surfaces by using both its cutting edges. To do this, the instru- Each of these features directly influences the manner in which
ment is first adapted to the mesial surface with the handle the Gracey curettes are used, as discussed next.
nearly parallel to the mesial surface. Since the face of the uni-
versal curette blade is honed at 90 degree to the lower shank, Area Specificity. There are seven pairs of curettes in the set.
if the lower shank is positioned so that it is absolutely parallel The Gracey curettes #l-2 and 3-4 are used on anterior teeth.
to the surface being instrumented, the tooth-blade angulation The Gracey #5-6 may be used on both anterior and premolar
is 90 degree. To close this angle and thus obtain proper work- teeth. The facial and lingual surfaces of posterior teeth are in-
ing angulation, the lower shank must be tilted slightly toward strumented with Gracey curettes #7-8 and 9-10. The Gracey
the tooth. The distal surface of the same posterior tooth can #l l-12 is designed for mesial surfaces of posterior teeth, and
be instrumented with the opposite cutting edge of the same the #13-14 adapts to the distal surfaces of posterior teeth. Al-
blade. This cutting edge can be adapted at proper working though these guidelines for areas of use were originally es-
angulation by positioning the handle so that it is perpendicular tablished by Dr Gracey, it is possible to use a Gracey curette
to the distal surface (Fig. 36 80) in an area of the mouth other than the one for which it was
When adapting the universal curette blade, as much of the specifically designed if the general principles regarding these
cutting edge as possible, should be in contact with the tooth curettes are understood and applied. Gracey curettes need not
surface, except on narrow convex surfaces such as line angles. be reserved exclusively for periodontal patients. In fact, many
Although the entire cutting edge should contact the tooth, clinicians prefer Gracey curettes for general scaling because of
pressure should be concentrated on the lower third of the their excellent adaptability.
blade during scaling strokes. During root-planing strokes,
however, lateral pressure should be distributed evenly along Single Cutting Edge Used. As with a universal curette, the
the cutting edge. Gracey curette has a blade with two cutting edges. Unlike the
The primary advantage of these curettes is that they are universal curette, however, the Gracey instrument is designed
designed to be used universally on all tooth surfaces in all so that only one cutting edge is used. To determine which
regions of the mouth. However, universal curettes have lim- of the two is the correct cutting edge to adapt to the tooth,
ited adaptability for the treatment of deep pockets in which the blade should be held face up and parallel to the floor.
apical migration of the attachment has exposed furcations, When viewed from this angle, the blade can be seen to curve
root convexities, and developmental depressions. For this rea- to the side. One cutting edge forms a larger outer curve, and
son, many clinicians prefer the Gracey curettes and the new the other forms a shorter, small inner curve. The larger outer
modifications of Gracey curettes, which are area specific and curve, which has also been described as the "inferior cutting
FIGURE 36.81 Determining the correct cutting edge of a Gracey cu-

rette. When viewed from directly above the face of the blade, the cor-
rect cutting edge is the one forming the larger, outer curve on the right.
FIGURE 36.82 Correct cutting edge of a Gracey curette adapted to

edge" or as the cutting edge farther away from the handle, is the tooth.
the correct cutting edge (Fig. 36.81).
Blade Curves in Two Planes. As with the toe of the uni-

versal curette, the toe of the Gracey curette curves upward.
However, the toe of the Gracey curette also curves to the side,
as previously mentioned. This unique curvature enhances the
blade's adaptation to convexities and concavities as the work-
ing end is advanced around the tooth. Only the lower third
or half of the Gracey blade is in contact with the tooth during
instrumentation. The cutting edge of a universal curette blade,
however, is straight and does not curve to the side, making it
less adaptable to root concavities.
Offset Blade. Gracey curette blades are honed at an offset an-

gle, which means that the face of the blade is not perpendicu-
lar to the lower shank as it is on a universal curette. Instead,
Gracey curettes are designed so that the tooth-blade working FIGURE 36.83 Incorrect cutting edge of a Gracey curette adapted
angulation is 60-70 degrees when the lower shank is held to the tooth.
parallel to the tooth surface. Gracey curettes were originally
designed to be used with push strokes and were beveled to
to the tooth with the lower shank parallel to the surface
provide a tooth-blade angulation of 40 degree when the lower
of the tooth. With the toe pointed in the direction to be
shank was parallel to the tooth surface; for many years, Gracey
scaled (eg, mesially with a #7-8 curette), only the back of
curettes were available only in this form. Currently, Gracey
the blade can be seen if the correct cutting edge has been
curettes are available not only in the original push design but
selected (Fig. 36.82). If the wrong cutting edge has been
also in a modified version to be used with pull strokes. It is im-
adopted, the flat, shiny face of the blade will be seen in-
portant to understand this when purchasing Gracey curettes
stead (Fig. 36 83)
to avoid obtaining instruments that are not properly designed
2. Make sure the lower shank is parallel to the surface to be
for pull strokes. If Gracey curettes that are designed to be used
instrumented. The lower shank of a Gracey curette is that
with push strokes are used with pull strokes instead, they are
portion of the shank between the blade and the first bend
likely to burnish calculus rather than completely remove it.
in the shank. Parallelism of the handle or upper shank is
The design of the Gracey curette was modified in response
not an acceptable guide with Gracey curettes because the
to requests from clinicians who liked the shank design and
angulations of the shanks vary. On anterior teeth the lower
adaptability of the original Gracey instruments but were op-
shank of the Gracey #1-2, 3-4, or 5-6 should be paral-
posed to the use of push strokes for scaling and root planing.
lel to the mesial, distal, facial, or lingual surfaces of the
The push stroke is not recommended, especially for the nov-
teeth (Fig. 36.84). On posterior teeth the lower shank of
ice clinician, because it is likely to cause undue trauma to the
the #7 -8 or 9-10 should be parallel to the facial or lingual
junctional epithelium and to embed fragments of dislodged
surfaces of the teeth (Fig. 36.85); the lower shank of the
calculus in the soft tissues.
# 11-12 should be parallel to the mesial surfaces of the teeth
(Fig. 36 86); and the lower shank of the #13-14 should be
Principles of Use. The following general principles of use of
parallel to the distal surfaces of the teeth (Fig. 36 87).
the Gracey curettes are essentially the same as those for the
3. When using intraoral finger rests, keep the fourth and
universal curette; italicized principles apply only to Gracey
middle fingers together in a built-up fulcrum for maxi-
curettes:
mum control and wrist-arm action.
1. Determine the correct cutting edge. The correct cutting edge 4. Use extraoral fulcrums or mandibular finger rests for op-
should be determined by visually inspecting the blade and timal angulation when working on the maxillary posterior
confirmed by lightly adapting the chosen cutting edge teeth.
5. Concentrate on using the lower third of the cutting edge

for calculus removal, especially on line angles or when at-
tempting to remove a calculus ledge by breaking it away in
sections, beginning at the lateral edge.
6. Allow the wrist and forearm to carry the burden of the
stroke rather than flexing the fingers.
7. Roll the handle slightly between the thumb and fingers to
keep the blade adapted as the working end is advanced
around line angles and into concavities.
8. Modulate lateral pressure from firm to moderate to light
depending on the nature of the calculus and reduce pres-
sure as the transition is made from scaling to root-planing
strokes.
FIGURE 36.84 Gracey #5-6 curette adapted to an anterior tooth.
(Pattison A, Pattison C, Matsuda 5. Periodontal Instrumentation, ed 3,
Pearson Education, (in press)). Extended-Shank Gracey Curettes. Extended-shank Gracey
curettes, such as the After Five curettes, are 3-mm longer in
the terminal shank than the standard Gracey curettes but
are used with the same technique (Fig. 36.23). They are
most useful for deep pockets on maxillary and mandibu-
lar posterior teeth, where the longer terminal shank allows
better access, especially to deep mesial and distal pock-
ets (Fig. 36 24). Although the longer lower shank makes
access easier while using a conventional intraoral finger
rest, the use of an extraoral fulcrum allows better access
and adaptation to all the maxillary posterior teeth. Extended
shank Gracey curettes with rigid shanks should be used
for scaling of heavy calculus; those with regular, finishing
shanks should be used for periodontal maintenance patients
FIGURE 36.85 Gracey #7-8 curette adapted to the facial surface of a
with deep residual pockets.
posterior tooth. (Pattison A, Pattison C, Matsuda 5. Periodontal Instru-
mentation, ed 3, Pearson Education, (in press)). Mini-Bladed Gracey Curettes. Mini-bladed Gracey curettes,
such as the Mini Five curettes and the Gracey Curvettes, have
a terminal shank that is 3-mm longer than the standard Grac-
ey curettes and a blade that is 50% shorter. Micro Mini Five
curette blades are 20% smaller than Mini Five curette blades
(Figs. 36.28 and 36 29) These mini-bladed instruments are
generally used in the same manner as the Gracey curettes, ex-
cept for the following specific differences:
1. Mini-bladed curettes should not be used routinely in place
of standard Gracey or extended shank Gracey curettes.
Instead, they should be used to supplement conventional
curettes and ultrasonic instruments in areas difficult to ac-
cess, such as furcations, line angles, and deep, tight, or
narrow pockets (Fig. 36 30)
FIGURE 36.86 Gracey #11-12 curette adapted to the mesial surface 2. Large #4 handles are recommended for any mini-bladed
of a posterior tooth. (Pattison A, Pattison C, Matsuda 5. Periodontal
Instrumentation, ed 3, Pearson Education, (in press)).
instruments because the larger diameter of the handles al-
lows better control of the small blades.
3. Mini-bladed curettes can be used to scale with the toe di-
rected either mesially or distally In fact, these curettes of-
ten adapt more effectively to the root curvatures of many
posterior teeth when the blade is inserted with the toe
pointed distally and when strokes are activated from the
mesial toward the distal line angle (Fig. 36 88)
4. Use rigid-shank mini-bladed curettes for calculus removal.
Use the thinner, standard-shank mini-bladed curettes for
deplaquing during maintenance.
5. When using mini-bladed curettes for calculus removal,
use intraoral finger rests close to the working area. When
performing light root planing or deplaquing, either intra-
oral rests or extraoral fulcrums may be used. Extraoral ful-
FIGURE 36.87 Gracey #13-14 curette adapted to the distal surface
of a posterior tooth. (Pattison A, Pattison C, Matsuda 5. Periodontal
crums are usually necessary to gain access to deep pockets
Instrumentation, ed 3, Pearson Education, (in press)). on maxillary second and third molars.
0
FIGURE 36.89 The cutting edge of a curette is formed by the angular
junction of the face and the lateral surfaces of the instrument. When
FIGURE 36.88 Mini Five #13-14 curette adapted to the palatal sur- the instrument is sharp, the cutting edge is a fine line.
face of a maxillary molar with the toe directed distally. (Pattison A,
Pattison C, Matsuda 5. Periodontal Instrumentation, ed 3, Pearson
Education, (in press)).
6. Mini-bladed curettes are generally used with straight, ver-

tical strokes. They may also be used with oblique or hori-
FIGURE 36.90 The cutting edge of a dull curette is rounded.
zontal strokes, but because of the shortness of the blade,
these strokes might not extend far enough subgingivally
unless the tissue is very retractable. Horizontal strokes
with mini-bladed curettes are most effective when used in
the cementoenamel junction or in developmental depres-
sions JUSt below it.
When properly used, mini-bladed Gracey curettes allow
unprecedented access and effectiveness for both nonsurgical
and surgical root debridement. One study showed that Gracey
Curvettes performed better than standard Gracey curettes in
deep anterior pockets. In areas such as line angles, furcations,
and narrow, curved, facial, or palatal root surfaces, these min-
iature curettes provide excellent adaptation with better tac-
tile sensitivity than modified, slim ultrasonic tips. Studies FIGURE 36.91 Light reflected from the rounded cutting edge of a
also demonstrated that Gracey Curvette curettes performed dull instrument appears as a bright line.
better than ultrasonic slim tips on deep mandibular anterior

pockets, furcations, and furcation entrances. No comparison When the instrument is sharp, this junction is a fine line
of hand instruments and modified, slim ultrasonic tips can be running the length of the cutting edge. As the instrument is
made unless mini-bladed curettes have been fully employed. used, metal is worn away at the cutting edge, and the junc-
To date, some research has been done to compare the effec- tion of the face and lateral surface becomes rounded or dulled
tiveness of mini-bladed instruments with the modified, slim (Fig. 36.90). Thus, the cutting edge becomes a rounded sur-
ultrasonic tips. More of these studies need to be performed face rather than an acute angle, which is why a dull instru-
in vivo to guide clinicians in the optimal utilization of these ment cuts less efficiently and requires more pressure to do
newer types of instruments. its job.
Sharpness can be evaluated by sight and touch in one of
Instrument Sharpening the following ways:
It is impossible to carry out periodontal procedures efficiently 1. When a dull instrument is held under a light, the rounded
with dull instruments. A sharp instrument cuts more precisely surface of its cutting edge reflects light back to the observ-
and quickly than a dull instrument. To do its job at all, a dull er. It appears as a bright line running the length of the cut-
instrument must be held more firmly and pressed harder than a ting edge (Fig. 36 91). The acutely angled cutting edge of a
sharp instrument. This reduces tactile sensitivity and increases sharp instrument, conversely, has no surface area to reflect
the possibility that the instrument will inadvertently slip. There- light. When a sharp instrument is held under a light, no
fore, to avoid wasting time and operating haphazardly, clinicians bright line can be observed (Fig. 36.89).
must be thoroughly familiar with the principles of sharpening and 2. Tactile evaluation of sharpness is performed by draw-
able to apply them to produce a heen cutting edge on the instruments ing the instrument lightly across an acrylic rod known
they are using. Development of this skill requires patience and as a "sharpening test stick." A dull instrument will slide
practice, but clinical excellence cannot be attained without it. smoothly without "biting" into the surface and raising a
light shaving as a sharp instrument would.
Evaluation of Sharpness
Objective of Sharpening
The cutting edge of an instrument is formed by the angular
junction of two surfaces of its blade. The cutting edges of a The objective of sharpening is to restore the fine, thin, linear
curette, for example, are formed where the face of the blade cutting edge of the instrument. This is done by grinding the
meets the lateral surfaces (Fig. 36.89). surfaces of the blade until their junction is once again sharply
others are cylindrical or cone shaped. Unmounted stones may

be used in two ways: the instrument may be stabilized and
held stationary while the stone is drawn across it, or the stone
may be stabilized and held stationary while the instrument is
drawn across it.
Principles of Sharpening
1. Choose a stone suitable for the instrument to be sharp-

ened-one that is of an appropriate shape and abrasive-
ness.
2. Use a sterilized sharpening stone if the instrument to be
sharpened will not be resterilized before it is used on a
patient.
3. Establish the proper angle between the sharpening stone
and the surface of the instrument on the basis of an under-
standing of its design.
4. Maintain a stable, firm grasp of both the instrument and
FIGURE 36.92 Sharpening stones. Top to bottom, A flat India stone, a the sharpening stone. This ensures that the proper angula-
flat Arkansas stone, a cone-shaped Arkansas stone, and a ceramic stone. tion is maintained throughout the controlled sharpening
stroke. In this manner, the entire surface of the instrument
angular rather than rounded. For any given instrument, sev- can be reduced evenly, and the cutting edge is not improp-
eral sharpening techniques may produce this result. A tech- erly beveled.
nique is acceptable if it produces a sharp cutting edge without 5. Avoid excessive pressure. Heavy pressure causes the stone
unduly wearing the instrument or altering its original design. to grind the surface of the instrument more quickly and
To maintain the original design, the operator must understand may shorten the instrument's life unnecessarily.
the location and course of the cutting edges and the angles 6. Avoid the formation of a "wire edge," characterized by
between the surfaces that form them. It is important to restore minute filamentous projections of metal extending as a
the cutting edge without distorting the original angles of the roughened ledge from the sharpened cutting edge. When
instrument. When these angles have been altered, the instru- the instrument is used on root surfaces, these projections
ment does not function as it was designed to function, which produce a grooved surface rather than a smooth surface. A
limits its effectiveness. wire edge is produced when the direction of the sharpening
stroke is away from, rather than into or toward, the cut-
ting edge. When back-and-forth or up-and-down sharpen-
Sharpening Stones ing strokes are used, formation of a wire edge can be avoided
Sharpening stones may be quarried from natural mineral de- by finishing with a down stroke toward the cutting edge.
posits or produced artificially. In either case, the surface of the 7. Lubricate the stone during sharpening. This minimizes
stone is made up of abrasive crystals that are harder than the clogging of the abrasive surface of the sharpening stone
metal of the instrument to be sharpened. Coarse stones have with metal particles removed from the instrument. It also
larger particles and cut more rapidly; they are used on in- reduces heat produced by friction. Oil should be used for
struments that are dull. Finer stones with smaller crystals cut natural stones and water for synthetic stones.
more slowly and are reserved for final sharpening to produce a 8. Sharpen instruments at the first sign of dullness. A grossly
finer edge and for sharpening instruments that are only slight- dull instrument is inefficient and requires more pressure
ly dull. India and Arkansas oilstones are examples of natural when used, which hinders control. Furthermore, sharpen-
abrasive stones. Carborundum, ruby, and ceramic stones are ing such an instrument requires the removal of a great deal
synthetically produced (Fig. 36 92). of metal to produce a sharp cutting edge. This shortens the
Sharpening stones can also be categorized by their method effective life of the instrument.
of use.
Sharpening Individual Instruments
Mounted Rotary Stones
These stones are mounted on a metal mandrel and used in Universal Curettes
a motor-driven handpiece. They may be cylindrical, conical, Several techniques will produce a properly sharpened curette.
or disc shaped. These stones are generally not recommended Regardless of the technique used, the clinician must keep in
for routine use because they (1) are difficult to control pre- mind that the angle between the face of the blade and the
cisely and can ruin the shape of the instrument, (2) tend to lateral surface of any curette is 70-80 degrees (Fig. 36.93).
wear down the instrument quickly, and (3) can generate con- This is the most effective design for removing calculus and
siderable frictional heat, which may affect the temper of the root planing (Fig. 36 94A). Changing this angle distorts the
instrument. design of the instrument and makes it less effective. A cut-
ting edge of less than 70 degree is quite sharp but also thin
Unmounted Stones (Fig. 36 94B) It wears down quickly and becomes dull. A cut-
Unmounted stones come in a variety of sizes and shapes. ting edge of 90 degree or more requires heavy lateral pressure
Some are rectangular with flat or grooved surfaces, whereas to remove deposits (Fig. 36.94C). Calculus removal with such
(A) (B) (C)

FIGURE 36.96 A, New, unsharpened curette viewed from directly
above the face of the blade. B, curette has been correctly sharpened to
maintain the rounded toe. C, curette has been incorrectly sharpened,
producing a pointed toe.
FIGURE 36.93 When the sharpening stone forms a 100-110-degree

angle with the face of the blade, the 70-80-degree angle between the
---------
' I
face and the lateral surface is automatically preserved.
(A) (B)
FIGURE 36.97 A, Angulation is difficult to control when sharpening
the face of the blade and often results in unwanted beveling. B, Sharpen-
ing the face also weakens the blade by narrowing it from face to back.
(A) (B) (C)
FIGURE 36.94 A, Properly sharpened curette maintains a 70-80-degree 1. Apply the sharpening stone to the lateral surface of the cu-
angle between its face and lateral surface. B, Curette has been sharp- rette so that the angle between the face of the blade and the
ened so that one of its cutting edges is less than 70 degree. This fine edge stone is 100-110 degrees (Fig. 36.95; see also Fig. 36.93).
is quite sharp but dulls easily. C, One of the cutting edges of the curette
has been sharpened to 90 degree. Heavy lateral pressure must be ap-
2. Beginning at the shank end of the cutting edge and work-
plied to the tooth to remove deposits with such an instrument. ing toward the toe, activate the stone with short, up-and-
down strokes. Use consistent, light pressure and keep the
stone continuously in contact with the blade. Make sure
that the 100-110-degree angle is constantly maintained
(Fig. 36. 95)
3. Check for sharpness as previously described and con-
tinue sharpening as necessary. To prevent the toe of the
curette from becoming pointed, sharpen the entire blade
from shank end to toe. When approaching the toe, be
sure to sharpen around it to preserve its rounded form
(Fig. 36. 96)
4. As the stone is moved along the cutting edge, finish each
section with a down stroke into or toward the cutting edge;
this will minimize the formation of a wire edge. Check the
cutting edge under a light.
5. Sharpening the curette in this manner tends to flatten
the lateral surface. This can be corrected by lightly grind-
ing the lateral surface and the back of the instrument,
FIGURE 36.95 Using a palm grasp, operator holds the universal cu-
rette so that the face of the blade is parallel to the floor. The stone away from the cutting edge, each time the instrument is
makes a 100-110-degree angle with the face of the blade. sharpened.
6. When one edge has been properly sharpened, the opposite
cutting edge can be sharpened in the same manner.
an instrument is often incomplete, and root planing cannot be
done effectively.
The following technique is recommended because it en- Sharpening the Face of the Blade. This may be done by
ables the clinician to visualize the critical 70-80-degree angle moving a handheld cylindrical or cone-shaped stone back and
forth across the face of the blade. A similar stone mounted
easily and thereby consistently restores an effective cutting
in a handpiece may also be used by applying it to the face of
edge:
the blade with the stone rotating toward the toe. These meth-
Sharpening the Lateral Surface. When a flat, handheld ods are not recommended for routine use for the following
stone is correctly applied to the lateral surface of a curette to reasons:
maintain the 70-80-degree angle, the angle between the face 1. The angulation between the instrument and the stone is
of the blade and the surface of the stone will be 100-110 de- difficult to maintain, and therefore the blade may be im-
grees (Fig. 36 93). This can best be visualized by holding the properly beveled (Fig. 36 97A).
curette so that the face of the blade is parallel with the floor. A 2. Sharpening the face of the blade narrows the working end
palm grasp should be used and the upper arm braced against from face to back. This weakens the blade and makes it
the body for support. likely to bend or break while in use (Fig. 36 97B).
(A) (8)
FIGURE 36.98 A, Face of a universal curette is at 90 degree to its
shank. B, Face of a Gracey curette is offset, forming a 70-degree angle
with its shank.
FIGURE 36.100 Note that when a Gracey curette is held in proper

sharpening position, its shank is not perpendicular to the floor be-
cause of its offset blade angle. The stone meets the blade at an angle of
100-110 degrees. Compare this position with the sharpening position of
a universal curette, as shown in Fig. 36.95.
FIGURE 36.99 Cutting edges of a universal curette extend straight

from shank to toe. The cutting edges of a Gracey curette gently curve
from shank to toe. Only the larger, outer cutting edge at the right is used
for scaling and needs to be sharpened.
3. Sharpening the face of the blade with a handheld stone

using a back-and-forth motion produces a wire edge that
interferes with the sharpness of the blade.
FIGURE 36.101 Gracey curette on the left has been properly sharp-
Area-Specific (Gracey) Curettes ened to maintain a symmetric curve on its outer cutting edge. For the
curette on the right, the sharpening stone was activated too long in one
As with a universal curette, a Gracey curette has an angle place, thereby flattening the blade.
of 70-80 degrees between the face and lateral surface of its
blade. Therefore, the technique described for sharpening a
that the angle between the face of the blade and the stone
universal curette can be used to sharpen a Gracey curette.
is 100-110 degrees.
However, several unique design features that distinguish a
3. Activate short, up-and-down strokes, working from the
Gracey from a universal curette must be understood to avoid
shank end of the blade to the curved toe. Finish with a
distorting the design of the instrument while sharpening (see
down stroke.
earlier discussion).
4. Remember that the cutting edge is curved. Preserve the
As previously noted, Gracey curettes have an offset blade;
curve by turning the stone while sharpening from shank to
that is, the face of the blade is not perpendicular to the shank
toe. If the stone is kept in one place for too many strokes,
of the instrument as it is on a universal curette but is offset at
the blade will be flattened (Fig. 36.101, right).
a 70-degree angle (Fig. 36.98). A Gracey curette is further dis-
5. Evaluate sharpness as previously described. Continue
tinguished by the curvature of its cutting edges. When viewed
sharpening as necessary.
from directly above the face of the blade, the cutting edges of
a universal curette extend in straight lines from shank to toe; Extended-Shank and Mini-Bladed Gracey Curettes
both cutting edges can be used for scaling and root planing.
Extended-shank Gracey curettes, such as the After Five cu-
The cutting edges of a Gracey curette, conversely, curve gently
rettes, are sharpened in exactly the same manner as the stan-
from shank to toe, and only the larger, outer cutting edge is
dard Gracey curettes. Although the terminal shank is 3-mm
used for scaling and root planing (Fig. 36 99)
longer, the blade size and shape are very similar, and thus
With these points in mind, a Gracey curette is sharpened in
there is no difference in the sharpening technique.
the following manner:
Mini-bladed Gracey curettes, such as the Mini Five curettes,
1. Hold the curette so that the face of the blade is parallel Micro Mini curettes, or Gracey Curvettes, are also sharpened
with the floor. Since the blade is offset, the shank of the with the same technique. These blades are only half the length
instrument will not be perpendicular to the floor as it is of a standard Gracey blade, but the angle between the face and
with universal curettes (Fig. 36 100). the lateral surface of the blade is still 70-80 degrees. How-
2. Identify the edge to be sharpened. Remember that only one ever, sharpening too heavily or too often around the toe of a
cutting edge is used, so only that edge must be sharpened mini-bladed curette should be avoided to prevent excessive
(Fig. 36.101, left). Apply the stone to the lateral surface so shortening of the blade.
(A) (B)
FIGURE 36.102 Face of the blade on a straight sickle is flat from shank
to tip, A, whereas on the curved sickle the blade face forms a gentle
arc, B.
FIGURE 36.104 Large, flat stone may also be used to sharpen the
sickle. The stone is stabilized on a flat surface. The fourth finger of the
right hand guides the sharpening stroke as the instrument is pulled
across the face of the stone toward the operator.
FIGURE 36.103 As with the curette, the sickle has an angle of 70-80
degrees between the face of the blade and the lateral surface.
FIGURE 36.105 When the entire bevel on a chisel contacts the
sharpening stone, the angle between the instrument and the stone is
Sickle Scalers 45 degree. The cutting edge will be properly sharpened if this angle is
The two types of sickle scalers are the straight sickle and maintained as the instrument is pushed across the stone.
curved sickle. On a straight sickle the face of the blade is flat
from shank to tip, whereas on a curved sickle the face of the
blade forms a gentle curve (Fig. 36.102). However, the straight
and curved sickles have similar cross-sectional designs. As in
the curette, the angle between the face of the blade and the lat-
eral surface of a sickle is 70-80 degrees (Fig. 36.103) When
a sharpening stone is correctly applied to the lateral surface
to preserve this angle, the angle between the face of the blade
and the surface of the stone is 100-110 degrees. With this in
mind, the sickle scaler can be sharpened in a manner similar
to that described for the curette, except that the sickle has a
sharp, pointed toe that must not be rounded.
A large, flat stone may also be used to sharpen sickles
(Fig. 36.104). The stone is stabilized on a table or cabinet
with the left hand. The sickle is held in the right hand with a
modified pen grasp and applied to the stone so that the angle
between the face of the blade and the stone is 100-110 de- FIGURE 36.106 Chisel can also be sharpened on a stationary, flat
grees. The fourth finger is placed on the right-hand edge of sharpening stone.
the stone to stabilize and guide the sharpening movement.

The right hand then pushes and pulls the sickle across the To sharpen a chisel, stabilize a flat sharpening stone on a
surface of the stone. flat surface. Grasp the instrument with a modified pen grasp.
To avoid a wire edge, the operator finishes with a pull Establish a finger rest with the pads of the third and fourth
stroke, being sure that the proper angulation is always main- fingers against the straight edge of the sharpening stone. Ap-
tained. ply the flat beveled surface of the chisel to the surface of the
stone. If the entire surface of the bevel is contacting the stone,
Chisels and Hoes the 45-degree angle between the beveled surface and the face
Chisels have a single, straight cutting edge that is perpendicu- of the blade will be maintained, and the design of the instru-
lar to the shank. The face of the blade is continuous with the ment will not be altered (Figs. 36.105 and 36 106).
shank of the instrument, which may be directly in line with Using moderate, steady pressure, with the hand and arm
the handle or slightly curved. The end of the blade is beveled acting as a unit and the finger resting on the edge of the
at 45 degree to form the cutting edge. stone as a guide, push the instrument across the surface of
36 Periodontal Instrum ents and Instrum entation 433
FIGURE 36.107
45 degree l
-
Back-action chisels and hoes are sharpened with a
FIGURE 36.109 The two cutting edges of an interproximal knife are
formed by bevels on the front and back surfaces of the blade.
pull stroke.
FIGURE 36.108 Flat-bladed gingivectomy knives, such as this Kirk-

land knife, have a cutting edge that extends around the entire blade.
The entire cutting edge must be sharpened.
the sharpening stone. Release pressure slightly and draw the

instrument back to its starting point. Repeat the sharpening
stroke until a sharp edge has been obtained. Remember to FIGURE 36.110 Gingivectomy knife may be sharpened on a station-
finish with a push stroke to prevent the formation of a wire ary flat stone. The instrument is held with a modified pen grasp. The
edge. Check for sharpness as previously described. Examine fourth finger guides the sharpening stroke as the instrument is rolled
between the fingers so that all sections of the blade are sharpened.
the instrument carefully to be sure that its design has not been
inadvertently altered.
Back-action surgical chisels and hoe scalers are sharp- Interproximal Knives. The blades of interproximal knives
ened with exactly the same technique described for chisels have two long, straight cutting edges that come together at the
except that a pull stroke is used rather than a push stroke sharply pointed tip of the instrument. The cutting edges are
(Fig. 36.107) formed by bevels on the front and back surfaces of the blade.
The entire blade is roughly perpendicular to the lower shank
Periodontal Knives of the instrument (Fig. 36 109)
There are two general types of periodontal knives. The first As with the flat-bladed gingivectomy knives, only the bev-
type includes the disposable scalpel blades that come pre- els on the back surface of the interproximal knives need to be
packaged and are presharpened and sterilized by the manu- sharpened. Again, this can be accomplished by drawing the
facturer. These knives are not resharpened when they become instrument across a stationary stone or by holding the instru-
dull but are discarded and replaced. ment stationary and moving the stone across it.
The second type of periodontal knife is reusable and must
be sharpened when it becomes dull. The most common Stationary Stone Technique. Stabilize a flat sharpening stone
knives in this group are the flat-bladed gingivectomy knives on a flat surface. Grasp the handle of the instrument with a
(eg, Kirkland knives #lSK and 16K) and the narrow, pointed modified pen grasp, and apply the bevel on the back sur-
interproximal knives. face of the blade to the flat surface of the sharpening stone.
With moderate pressure, pull the instrument toward you
Flat-Bladed Gingivectomy Knives. These knives have broad, (Figs. 36.110 and 36111) Release pressure slightly, and re-
flat blades that are nearly perpendicular to the lower shank of turn to the starting point. Begin at one end of the cutting edge,
the instrument. The curved cutting edge extends around the and continue around the blade by rolling the handle of the
entire outer edge of the blade and is formed by bevels on both instrument slightly between the thumb and the first and sec-
the front and the back surface of the blade (Fig. 36 108). ond fingers. Finish each section of the blade with a pull stroke
When sharpening these instruments, only the bevel on the to prevent formation of a wire edge. Check for sharpness as
back surface of the instrument needs to be ground. This can described previously.
be done by drawing the blade across a stationary, flat sharpen-
ing stone or by holding the instrument stationary and drawing Stationary Instrument Technique. Grasp the instrument
the stone across its blade. with the palm. Apply the flat surface of a handheld sharpening
FIGURE 36.111 lnterproximal knife may be sharpened on a flat sta- FIGURE 36.112 lnterproximal knife may also be sharpened with a
tionary stone. The blade is drawn toward the operator. handheld stone. The instrument is held with a palm grasp, and the stone
is applied to the entire cutting edge.
stone to the bevel on the back surface of the blade (Fig. 36.112).
Begin at one end of the cutting edge, and with moderate pres-
Drisko CL, Cochran DL, Blieden T, et al: Position paper: sonic and ultra-
sure, draw the stone back and forth across the instrument. sonic scalers in periodontics. Research, Science and Therapy Commit-
To prevent the formation of a wire edge, finish each section tee of the American Academy of Period ontology, J Periodontal 71: 1792,
with a stroke into or toward the cutting edge. Proceed around 2000.
the entire length of the cutting edge by gradually rotating the Greenstein G: Nonsurgical periodontal therapy in 2000: a literature review,
J Am Dent Assoc 131:1580, 2000.
instrument and the stone in relation to one another. Kaldahl WB, Kalkwarf KL, Patil KO, et al: Long-term evaluation of periodon-
tal therapy l. Response to 4 therapeutic modalities, J Periodontal 67:93,
1996.
Acknowledgments Lindhe J, Nyman S: Long-term maintenance of patients treated for advanced
Dr Ashish Jain wants to acknowledge the contributions of Dr Shipra periodontal disease,] Clin Periodontol 11:504, 1984.
Lindhe J, Nyman S, Karring T: Scaling and root planing in shallow pockets,
Gupta, Associate Professor, Dr Harvansh Singh Judge Institute of Dental J Clin Periodontal 9:415, 1982.
Sciences and Hospital and Dr Nymphea Pandit, Professor & Head, DAV Magnusson!, Lindhe J, Yoneyama T, et al: Recolonization of a subgingival
(C) Dental College, Yamunagar in the preparation of this chapter. microbiota following scaling in deep pockets, J Clin Periodontal 11:193,
1984.
Pattison AM: The use of hand instruments in supportive periodontal treat-
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Claffey N: Decision making in periodontal therapy: the reevaluation, J Clin onset periodontitis. II. Long-term impact on microbial load, J Periodontal
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58. Wilson TG, Carnio J, Schenk R, et al: Absence of histologic signs of
conventional blade periodontal curer: an in vitro study, J Clin Pe,iodontol
chronic inflammation following closed subgingival scaling and root plan-
26:548, 1999.
ing using the dental endoscope: human biopsies-a pilot study, J Peri-
28. Lind he j: Evaluation of periodontal scalers. IL Wear following standard-
odontal 79(11):2036-204 l, 2008.
ized or diagonal cutting tests, Odontol Rev 17:121, 1966.
59. Wilson TG, Harrel SK, Nunn ME, et al: The relationship between the
29. Lindhe J, Jacobson L: Evaluation of periodontal scalers. L Wear following
presence of tooth-borne subgingival deposits and inflammation found
clinical use, Odontol Rev 17:1, 1966.
with a dental endoscope,] Paiodontol 79(11) 2029-2035, 2008.
37
Scaling and Root Planing
AM Pattison • GL Pattison • A Jain
Chapter Outline
Principles of Scaling and Root Planing Special Considerations
Mechanism of Action of Power Scalers Principles of Instrumentation
Type and Benefit of Power Instruments Evaluation
Clinical Outcomes of Power-Driven
Instruments
Principles of Scaling and Root Planing calculus form on enamel, the deposits are usually superficially
attached to the surface and are not locked into irregularities.
Definitions and Rationale Scaling alone is sufficient to remove biofilm and calculus com-
pletely from enamel, leaving a smooth, clean surface.
Scaling is the process by which biofilm and calculus are Root surfaces exposed to biofilm and calculus pose a differ-
removed from both supragingival and subgingival tooth ent problem. Deposits of calculus on root surfaces are frequently
surfaces. No deliberate attempt is made to remove tooth embedded in cementa! irregularities. Subgingival calculus is
substance along with the calculus. Root planing is the pro- porous and harbors bacteria and endotoxin and therefore
cess by which residual embedded calculus and portions of should be removed completely When dentin is exposed, bio-
cementum are removed from the roots to produce a smooth, film bacteria may invade dentinal tubules. Therefore, scaling
hard, clean surface. alone is insufficient to remove them, and a portion of the root
The primary objective of scaling and root planing is to surface must be removed to eliminate these deposits. Fur-
restore gingival health by completely removing elements thermore, when the root surface is exposed to biofilm and
that provoke gingival inflammation (ie, biofilm, calculus, the pocket environment, its surface is contaminated by toxic
and endotoxin) from the tooth surface (Fig. 37.1). Instru- substances, notably endotoxins. Evidence suggests that these
mentation has been shown to reduce dramatically the num- toxic substances are only superficially attached to the root
bers of subgingival microorganisms and produce a shift in and do not permeate it deeply Removal of extensive amounts
the composition of subgingival biofilm from one with high of dentin and cementum is not necessary to render the roots
numbers of Gram-negative anaerobes to one dominated by free of toxins and should be avoided. In areas where cemen-
Gram-positive facultative bacteria compatible with health. tum is thin, however, instrumentation may expose dentin.
After thorough scaling and root planing, a profound reduc- Although this is not the aim of treatment, such exposure may
tion in spirochetes, motile rods, and putative pathogens, such be unavoidable.
as Actinobacillus actinomycetemcomitans, Porphyromonas gin- Scaling and root planing should not be viewed as separate
givalis, and Prevotella intermedia, and an increase in coccoid procedures unrelated to the rest of the treatment plan. These
cells occur. These changes in the microbiota are accompanied procedures belong to the initial phase of an orderly sequence
by a reduction or elimination of inflammation clinically This of treatment. After careful analysis of a case, the number of
positive microbial change must be sustained by the periodic appointments needed to complete this phase of treatment is
scaling and root planing performed during supportive peri- estimated. Patients with small amounts of calculus and rela-
odontal therapy tively healthy tissues can be treated in one appointment. Most
Scaling and root planing are not separate procedures; all other patients require several treatment sessions. The dentist
the principles of scaling apply equally to root planing. The should estimate the number of appointments needed on the
difference between scaling and root planing is only a matter of basis of the number of teeth in the mouth, severity of inflam-
degree. The nature of the tooth surface determines the degree mation, amount and location of calculus, depth and activity of
to which the surface must be scaled or planed. pockets, presence of furcation invasions, patient's comprehen-
Biofilm and calculus on enamel surfaces provoke gingival sion of and compliance with oral hygiene instructions, and
inflammation. Unless they are grooved or pitted, enamel sur- need for local anesthesia.
faces are relatively smooth and uniform. When biofilm and
435
(E) (F)
FIGURE 37.1 Results of Phase I therapy. A to F, Moderate chronic periodontitis. A, Patient presenting with moderate attachment loss and probe depths
in the 4-6-mm range. Note the gingiva appears pink because it is fibrotic and the inflammation is deep in the periodontal pockets. B, Lingual view before
treatment, with more visible inflammation and heavy deposits of calculus. C and D, The same areas with significant improvement in gingival health
18 months after scaling, root planing, and plaque control therapy were provided; the patient returned for regular maintenance visits. E and F, Presenting
radiographs of the lower anterior teeth. Radiograph taken 18 months after Phase I therapy and maintenance shows no increase in bone loss.
When the rationale for scaling and root planing is thor- Detection Skills
oughly understood, it becomes apparent that mastery of these
skills is essential to the ultimate success of any course of peri- Good visual and tactile detection skills are required for the
odontal therapy. Of all clinical dental procedures, subgingival accurate initial assessment of the extent and nature of deposits
scaling and root planing in deep pockets are the most difficult and root irregularities before scaling and root planing. Valid
and exacting skills to master. It has been argued that such evaluation of results of instrumentation depends on these
proficiency in instrumentation cannot be attained, and there- detection skills.
fore periodontal surgery is necessary to gain access to root Visual examination of supragingival and subgingival calcu-
surfaces. Others have argued that although proficiency is pos- lus just below the gingival margin is not difficult with good
sible, it need not be developed because access to the roots can lighting and a clean field. Light deposits of supragingival cal-
be gained more easily with surgery. However, without mas- culus are often difficult to see when they are wet with saliva.
tering subgingival scaling and root-planing skills, the clini- Compressed air may be used to dry supragingival calculus
cian will be severely hampered and unable to treat adequately until it is chalky white and readily visible. Air also may be
those patients for whom surgery is contraindicated. directed into the pocket in a steady stream to deflect the
marginal gingiva away from the tooth so that subgingival angulation of slightly less than 90 degrees to the surface being
deposits near the surface can be seen. scaled. The cutting edge should engage the apical margin of
Tactile exploration of the tooth surfaces in subgingival areas the supragingival calculus while short, powerful, overlap-
of pocket depth, furcations, and developmental depressions is ping scaling strokes are activated coronally in a vertical or an
much more difficult than visual examination of supragingival oblique direction. The sharply pointed tip of the sickle can
areas and requires the skilled use of a fine-pointed explorer easily lacerate marginal tissue or gouge exposed root surfaces,
or probe. The explorer or probe is held with a light but stable so careful adaptation is especially important when this instru-
modified pen grasp. This provides maximal tactile sensitivity ment is being used. The tooth surface is instrumented until
for detection of subgingival calculus and other irregularities. it is visually and tactilely free of all supragingival deposits. If
The pads of the thumb and fingers, especially the middle fin- the tissue is retractable enough to allow easy insertion of the
ger, should perceive the slight vibrations conducted through bulky blade, the sickle may be used slightly below the free
the instrument shank and handle as irregularities in the tooth gingival margin. If the sickle is used in this manner, final scal-
surface are encountered. ing and root planing with the curette should always follow.
After a stable finger rest is established, the tip of the instru-
ment is carefully inserted subgingivally to the base of the Subgingival Scaling and Root-Planing
pocket. Light exploratory strokes are activated vertically on
Technique
the root surface. When calculus is encountered, the tip of the
instrument should be advanced apically over the deposit until Subgingival scaling and root planing are much more complex
the termination of the calculus on the root is felt. The distance and difficult to perform than supragingival scaling. Subgingi-
between the apical edge of the calculus and the bottom of the val calculus is usually harder than supragingival calculus and
pocket usually ranges from 0.2 to 1.0 mm. The tip is adapted is often locked into root irregularities, making it more tena-
closely to the tooth to ensure the greatest degree of tactile cious and therefore more difficult to remove. The overlying
sensitivity and avoid tissue trauma. When a proximal surface tissue creates significant problems in subgingival instrumenta-
is being explored, strokes must be extended at least halfway tion. Vision is obscured by the bleeding that inevitably occurs
across that surface past the contact area to ensure complete during instrumentation and by the tissue itself. The clinician
detection of interproximal deposits. When an explorer is used must rely heavily on tactile sensitivity to detect calculus and
at line angles, convexities, and concavities, the handle of the irregularities, guide the instrument blade during scaling and
instrument must be rolled slightly between the thumb and root planing, and evaluate the results of instrumentation.
fingers to keep the tip constantly adapted to the changes in In addition, the adjacent pocket wall limits the direc-
tooth contour. tion and length of the strokes. The confines of the soft tissue
Although exploration technique and good tactile sensitiv- make careful adaptation to tooth contours imperative to avoid
ity are important, interpreting various degrees of roughness and trauma. Such precise adaptation cannot be accomplished
making clinical judgments based on these interpretations also without a thorough knowledge of tooth morphologic features.
require much expertise. The beginning student usually has The clinician must form a mental image of the tooth surface
difficulty detecting fine calculus and altered cementum. Such to anticipate variations in contour, continually confirming
detection must begin with the recognition of ledges, lumps, or or modifying the image in response to tactile sensations and
spurs of calculus, then smaller spicules, then slight roughness, visual cues, such as the position of the instrument handle and
and finally a slight graininess that feels like a sticky coating shank. The clinician then must instantaneously adjust the
or film covering the tooth surface. Overhanging or deficient adaptation and angulation of the working end to the tooth. It
margins of dental restorations, caries, decalcification, and root is this complex and precise coordination of visual, mental, and
roughness caused by previous instrumentation are all typi- manual skills that makes subgingival instrumentation one of
cally found during exploration. These and other irregularities the most difficult of all dental skills. The curette is preferred by
must be recognized and differentiated from subgingival cal- most clinicians for subgingival scaling and root planing because of
culus. Because this requires a great deal of experience and a the advantages afforded by its design. Its curved blade, rounded
high degree of tactile sensitivity, many clinicians agree that the toe, and curved back allow the curette to be inserted to the
development of detection skills is as important as the mastery base of the pocket and adapted to variations in tooth contour
of scaling and root-planing technique. with minimal tissue displacement and trauma.
Sickles, hoes, files, and ultrasonic instruments also are
used for subgingival scaling of heavy calculus. Some small
Supragingival Scaling Technique
files (eg, Hirschfeld file) may be inserted to the base of the
Supragingival calculus is generally less tenacious and less cal- pocket to crush or initially fracture tenacious deposits. Larger
cified than subgingival calculus. Because instrumentation is files, hoes, sickles, and standard ultrasonic tips for suprag-
performed coronal to the gingival margin, scaling strokes are ingival use are too bulky and cannot be inserted easily into
not confined by the surrounding tissues. This makes adapta- deep pockets or areas where tissue is firm and fibrotic. Hoes
tion and angulation easier. It also allows direct visibility, as and files cannot be used to produce as smooth a surface as
well as a freedom of movement not possible during subgin- curettes. Hoes, files, and standard large ultrasonic tips are all
gival scaling. more hazardous than the curette in terms of trauma to the root
Sickles, curettes, and ultrasonic and sonic instruments are surface and surrounding tissues. Although thin ultrasonic tips
most often used for the removal of supragingival calculus; designed for scaling of deep pockets and furcations can be
hoes and chisels are less frequently used. To perform supra- inserted more easily subgingivally, they must be used on low
gingival scaling, the sickle or curette is held with a modified power. When low-power scaling is performed on heavy cal-
pen grasp, and a firm finger rest is established on the teeth culus or tenacious sheets of calculus, thin ultrasonic tips are
adjacent to the working area. The blade is adapted with an likely to burnish the calculus rather than thoroughly remove
tooth contour are followed. Scaling and root-planing strokes

should be confined to the portion of the tooth where calcu-
lus or altered cementum is found; this area is known as the
instrumentation zone. Sweeping the instrument over the crown
where it is not needed wastes operating time, dulls the instru-
ment, and causes loss of control.
The amount of lateral pressure applied to the tooth sur-
face depends on the nature of the calculus and whether the
strokes are for initial calculus removal or final root planing. If
heavy lateral pressure is continued after the bulk of calculus
has been removed and the blade is repeatedly readapted with
short, choppy strokes, the result will be a root surface rough-
ened by numerous nicks and gouges, resembling the rippled
(A) (B) (C) surface of a washboard. If heavy lateral pressure is continued
FIGURE 37.2 Subgingival scaling procedure. A, Curette inserted with with long, even strokes, the result will be excessive removal of
the face of the blade flush against the tooth. B, Working angulation (45- root structure, producing a smooth but "ditched" or "riffled"
90 degrees) is established at the base of the pocket. C, Lateral pressure
is applied, and the scaling stroke is activated in the coronal direction.
root surface. To avoid these hazards of overinstrumentation,
a deliberate transition from short, powerful scaling strokes to
longer, lighter root-planing strokes must be made as soon as
it. Therefore, ultrasonic scaling should be followed by careful the calculus and initial roughness have been eliminated.
assessment with an explorer and further instrumentation with When scaling strokes are used to remove calculus, force
curettes when necessary. can be maximized by concentrating lateral pressure onto the
Subgingival scaling and root planing are accomplished lower third of the blade (Fig. 36 76) This small section, the
with either universal or area-specific (Gracey) curettes using terminal few millimeters of the blade, is positioned slightly
the following basic procedure. The curette is held with a apical to the lateral edge of the deposit, and a short vertical or
modified pen grasp, and a stable finger rest is established. oblique stroke is used to split the calculus from the tooth sur-
The correct cutting edge is slightly adapted to the tooth, with face. Without withdrawing the instrument from the pocket,
the lower shank kept parallel to the tooth surface. The lower the lower third of the blade is advanced laterally and reposi-
shank is moved toward the tooth so that the face of the blade is tioned to engage the next portion of the remaining deposit.
nearly flush with the tooth surface. The blade is then inserted Another vertical or oblique stroke is made slightly overlap-
under the gingiva and advanced to the base of the pocket by ping the previous stroke. This process is repeated in a series
a light exploratory stroke. When the cutting edge reaches of powerful scaling strokes until the entire deposit has been
the base of the pocket, a working angulation of between 45 removed. The overlapping of these pathways or "channels" of
and 90 degrees is established, and pressure is applied later- instrumentation ensures that the entire instrumentation zone
ally against the tooth surface. Calculus is removed by a series is covered (Fig. 3 7 3)
of controlled, overlapping, short, powerful strokes primarily Engaging a large, tenacious ledge or piece of calculus with
using wrist-arm motion (Fig. 37.2). As calculus is removed, the entire length of the cutting edge is not recommended
resistance to the passage of the cutting edge diminishes until because the force is distributed through a longer section of
only a slight roughness remains. Longer, lighter root-planing the cutting edge rather than concentrated. Much more lat-
strokes are then activated with less lateral pressure until the eral pressure is required to dislodge the entire deposit in one
root surface is completely smooth and hard. The instrument stroke. Although some clinicians may possess the strength to
handle must be rolled carefully between the thumb and fin- remove calculus completely in this manner, the heavier forces
gers to keep the blade adapted closely to the tooth surface as required diminish tactile sensitivity and contribute to a loss
line angles, developmental depressions, and other changes in of control that results in tissue trauma. A single heavy stroke
t
~,,.
I
I
• I
(A) I
(B) (C) I
FIGURE 37.3 Instrumentation for calculus removal. A, Calculus is removed by engaging the apical or lateral edge of the deposit with the cutting
edge of a scaler; vertical movement of the instrument will remove the fragment of calculus engaged by the instrument, as seen in the shaded drawing.
B, The instrument is moved laterally and again engages the edge of the calculus, overlapping the previous stroke to some extent; the shaded drawing
shows further removal. C, The final portion of the deposit is engaged and removed. Note how the procedure is performed in an interdental space by
entering facially and lingually.
I
I
(A) (B) (C)
FIGURE 37.4 Shank position for scaling proximal surfaces. A, Cor-
rect shank position, parallel with the long axis of the tooth. B, Incorrect
shank position, tilted away from the tooth. C, Incorrect shank position,
tilted too far toward the tooth. Sextant: lingual aspect.
FIGURE 37.5 Maxillary right posterior sextant: facial aspect.
usually is not sufficient to remove calculus entirely. Instead,

the blade skips over or skims the surface of the deposit. when these two fingers are kept together in a built-up fulcrum.
Subsequent strokes made with the entire cutting edge tend Separation of the fingers commits the clinician to the exclusive
to shave the deposit down layer by layer. When a series of use of finger flexing for the activation of strokes.
these repeated whittling strokes is applied, the calculus may As instrumentation proceeds from one tooth to the next,
be reduced to a thin, smooth, burnished sheet that is difficult the body position of the operator and the location of the finger
to distinguish from the surrounding root surface. rest must be frequently adjusted or changed to allow paral-
A common error in instrumenting proximal surfaces is fail- lelism and wrist-arm motion. Various approaches to instru-
ing to reach the mid proximal region apical to the contact. This mentation in different areas of the mouth are illustrated here.
area is relatively inaccessible, and the technique requires more The examples shown provide maximal efficiency for the clini-
skill than instrumentation of buccal or lingual surfaces. It is cian and comfort for the patient. For most areas, more than
extremely important to extend strokes at least halfway across one approach is presented. Other approaches are possible and
the proximal surface so that no calculus or roughness remains are acceptable if they provide equal efficiency and comfort.
in the interproximal area. With properly designed curettes, The following approaches may be used:
this can be accomplished by keeping the lower shank of the
Maxillary right posterior sextant: Facial aspect (Fig. 37.5).
curette parallel with the long axis of the tooth (Fig. 37.4A).
Operator position: Side position.
With the lower shank parallel to the long axis, the blade of
Illumination: Direct.
the curette will reach the base of the pocket and the toe will
Visibility: Direct (indirect for distal surfaces of molars).
extend beyond the midline as strokes are advanced across
Retraction: Mirror or index finger of the nonoperating hand.
the proximal surface. This extension of strokes beyond the
Finger rest: Extraoral, palm up. Backs of the middle and
midline ensures thorough exploration and instrumentation of
fourth fingers on the lateral aspect of the mandible on
these surfaces. If the lower shank is angled or tilted away from
the right side of the face.
the tooth, the toe will move toward the contact area. Because
Maxillary right posterior sextant, premolar region only: Facial
this prevents the blade from reaching the base of the pocket,
aspect (Fig. 3 7 6).
calculus apical to the contact will not be detected or removed.
Operator position: Side or back position.
Strokes will be hampered because the toe tends to become
lodged in the contact. If the instrument is angled or tilted too
far toward the tooth, the lower shank will hit the tooth or the
contact area, preventing extension of strokes to the midproxi-
mal region (Fig. 37.4B-C).
The relationship between the location of the finger rest and
the working area is important for two reasons. First, the finger
rest or fulcrum must be positioned to allow the lower shank of
the instrument to be parallel or nearly parallel to the tooth sur-
face being treated. This parallelism is a fundamental require-
ment for optimal working angulation. Second, the finger rest
must be positioned to enable the operator to use wrist-arm
motion to activate strokes. On some aspects of the maxillary
posterior teeth, these requirements can be met only with the
use of extraoral or opposite-arch fulcrums. When intraoral fin-
ger rests are used in other regions of the mouth, the finger rest
must be close enough to the working area to fulfill these two
requirements. A finger rest that is established too far from the
working area forces the clinician to separate the middle finger
from the fourth finger in an effort to obtain parallelism and FIGURE 37.6 Maxillary right posterior sextant, premolar region only:
proper angulation. Effective wrist-arm motion is possible only facial aspect.
FIGURE 37.7 Maxillary right posterior sextant: lingual aspect. FIGURE 37.9 Maxillary anterior sextant: facial aspect, surfaces away
from the operator.
Visibility: Direct.
Retraction: Mirror or index finger of the nonoperating hand.
Finger rest: Intraoral, palm up. Fourth finger on the occlusal
surfaces of the adjacent maxillary posterior teeth.
Maxillary right posterior sextant: Lingual aspect (Fig. 3 7. 7).
Operator position: Side or front position.
Illumination: Direct and indirect.
Visibility: Direct or indirect.
Retraction: None.
Finger rest: Extraoral, palm up. Backs of the middle and
fourth fingers on the lateral aspect of the mandible on
the right side of the face.
Maxillary right posterior sextant: Lingual aspect (Fig. 37.8).
Operator position: Front position.
Visibility: Direct.
Retraction: None. FIGURE 37.10 Maxillary anterior sextant: facial aspect, surfaces
Finger rest: Intraoral, palm up, finger on finger. Index finger toward the operator.
of the nonoperating hand on the occlusal surfaces of the
maxillary right posterior teeth; fourth finger of the oper-
ating hand or the index finger of the nonoperating hand.
Retraction: Index finger of the nonoperating hand.
Maxillary anterior sextant: Facial aspect, surfaces away from Finger rest: Intraoral, palm up. Fourth finger on the incisal
edges or occlusal surfaces of adjacent maxillary teeth.
the operator (Fig. 37.9).
Operator position: Back position. Maxillary anterior sextant: Facial aspect, surfaces toward the
operator (Fig. 3 7 10)
Visibility: Direct. Operator position: Front position.
Visibility: Direct.
Retraction: Index finger of the nonoperating hand.
Finger rest: Intraoral, palm down. Fourth finger on the
incisal edges or the occlusal or facial surfaces of adjacent
maxillary teeth.
Maxillary anterior sextant: Lingual aspect, surfaces away from
the operator (surfaces toward the operator are scaled from a
front position) (Fig. 37.11).
Operator position: Back position.
Illumination: Indirect.
Visibility: Indirect.
Retraction: None.
Finger rest: Intraoral, palm up. Fourth finger on the incisal
edges or the occlusal surfaces of adjacent maxillary teeth.
Maxillary left posterior sextant: Facial aspect (Fig. 37.12)
Illumination: Direct or indirect.
FIGURE 37.8 Maxillary right posterior sextant: lingual aspect. Visibility: Direct or indirect.
FIGURE 37.11 Maxillary anterior sextant: lingual aspect, surfaces FIGURE 37.14 Maxillary left posterior sextant: lingual aspect.
away from the operator (surfaces toward the operator are scaled from
a front position).
Retraction: Mirror.
Finger rest: Intraoral, palm up. Fourth finger on the incisal
edges or the occlusal surfaces of adjacent maxillary teeth.
Maxillary left posterior sextant.· Lingual aspect (Fig. 3 7 14)
Visibility: Direct.
Retraction: None.
Finger rest: Intraoral, palm down, opposite arch, reinforced.
Fourth finger on the incisal edges of the mandibular an-
terior teeth or the facial surfaces of the mandibular pre-
molars, reinforced with the index finger of the nonoper-
ating hand.
Maxillary left posterior sextant. Lingual aspect (Fig. 37.15).
Visibility: Direct and indirect.
FIGURE 37.12 Maxillary left posterior sextant: facial aspect.
Retraction: None.
Finger rest: Extraoral, palm down. Front surfaces of the
Retraction: Mirror. middle and fourth fingers on the lateral aspect of the
Finger rest: Extraoral, palm down. Front surfaces of the mandible on the left side of the face. The nonoperating
middle and fourth fingers on the lateral aspect of the hand holds the mirror for indirect illumination.
mandible on the left side of the face. Maxillary left posterior sextant: Lingual aspect (Fig. 37 16)
Maxillary left posterior sextant: Facial aspect (Fig. 37.13). Operator position: Side or front position.
Operator position: Back or side position. Illumination: Direct.
Illumination: Direct or indirect. Visibility: Direct.
FIGURE 37.13 Maxillary left posterior sextant: facial aspect. FIGURE 37.15 Maxillary left posterior sextant: lingual aspect.
FIGURE 37.16 Maxillary left posterior sextant: lingual aspect. FIGURE 37.18 Mandibular left posterior sextant: lingual aspect.
FIGURE 37.17 Mandibular left posterior sextant: facial aspect. FIGURE 37.19 Mandibular anterior sextant: facial aspect, surfaces
toward the operator.
Retraction: None.
Finger rest: Intraoral, palm up. Fourth finger on the occlusal
surfaces of adjacent maxillary teeth.
Mandibular left posterior sextant.· Facial aspect (Fig. 37.17).
Retraction: Index finger or mirror of the nonoperating hand.
Finger rest: Intraoral, palm down. Fourth finger on the
incisal edges or the occlusal or facial surfaces of adjacent
mandibular teeth.
Mandibular left posterior sextant: Lingual aspect (Fig. 37.18).
Operator position: Front or side position.
Visibility: Direct.
Retraction: Mirror retracts tongue.
Finger rest: Intraoral, palm down. Fourth finger on the incisal FIGURE 37.20 Mandibular anterior sextant: facial aspect, surfaces
edges or the occlusal surfaces of adjacent mandibular teeth. away from the operator.
Mandibular anterior sextant: Facial aspect, surfaces toward the
operator (Fig. 3 7 19)
Operator position: Front position. Mandibular anterior sextant: Facial aspect, surfaces away from
Illumination: Direct. the operator (Fig. 37 20).
Visibility: Direct. Operator position: Back position.
Retraction: Index finger of the nonoperating hand. Illumination: Direct.
Finger rest: Intraoral, palm down. Fourth finger on the incisal Visibility: Direct.
edges or the occlusal surfaces of adjacent mandibular teeth. Retraction: Index finger or thumb of the nonoperating hand.
FIGURE 37.21 Mandibular anterior sextant: lingual aspect, surfaces FIGURE 37.23 Mandibular right posterior sextant: facial aspect.
away from the operator.
Finger rest: lntraoral, palm down. Fourth finger on the inci-

sal edges or the occlusal surfaces of adjacent mandibular
teeth.
Mandibular anterior sextant: Lingual aspect, surfaces away
from the operator (Fig. 37 21)
Operator position: Back position.
teeth.
Mandibular anterior sextant: Lingual aspect, surfaces toward
the operator (Fig. 37 22).
Illumination: Direct and indirect. FIGURE 37.24 Mandibular right posterior sextant: lingual aspect.
Visibility: Direct.
Finger rest: Intraoral, palm down. Fourth finger on the inci-
Retraction: Mirror or index finger of the nonoperating
hand.
teeth.
Finger rest: Intraoral, palm down. Fourth finger on the inci-
Mandibular right posterior sextant: Facial aspect (Fig. 37.23).
Operator position: Side or front position.
teeth.
Mandibular right posterior sextant: Lingual aspect (Fig. 3 7.24 ).
teeth.
Sonic and Ultrasonic Scaling

For many years, practitioners have sought ways to enhance
and prolong the outcomes from scaling and root planing.
In the office setting, technologic advances and new designs
of ultrasonic and sonic power scalers have transformed the
role of power-driven oscillating instruments in periodontal
therapy At home, the pulsating dental water has been clini-
cally proven to help patients maintain periodontal health
FIGURE 37.22 Mandibular anterior sextant: lingual aspect, surfaces by removing biofilm supragingivally and subgingivally and
toward the operator. reducing inflammation.
Mechanism of Action of Power Water contributes to three physiologic effects that enhance
the efficacy of power scalers: acoustic streaming, acoustic
Scalers turbulence, and cavitation. Acoustic streaming is the uni-
Various physical factors play a role in the mechanism of action directional fluid flow caused by ultrasound waves. Acoustic
of power scalers. These factors include frequency, stroke, and turbulence is created when the movement of the tip causes
water flow. In addition to rate of flow, the physiologic effects the coolant to accelerate, producing an intensified swirling
of water may play a role in the efficacy of power instrument. effect. This turbulence continues until cavitation occurs.
Frequency: Frequency is defined as the number of times Cavitation is the formation of bubbles in water caused by the
per second an insert tip moves back and forth during one high turbulence. The bubbles implode and produce shock
cycle in an orbital, elliptic, or linear stroke path. For example, waves in the liquid, creating further shock waves throughout
a frequency of 25,000 (25K) equates to the tip moving 25,000 the water. In vitro, the combination of acoustic streaming,
times per second, and a 30,000 (30K) frequency equates to acoustic turbulence, and cavitation has been shown to dis-
the tip moving 30,000 times per second. Frequency is impor- rupt microflora.
tant because it determines the area of the insert tip that is
considered active. Only the active portion of the insert can Type and Benefit of Power
remove hard and soft debris. A higher frequency results in a
smaller active area of an insert tip. An insert working in the Instruments
frequency of 30K would have an active tip area of 4.2 mm, Sonic units work at a frequency of 2000-6500 cycles per sec-
and a 25K tip has a working area of 4.3 mm. The working area ond and use a high- or low-speed air source from the dental
of a sonic scaler tip has not been determined. unit. Water is delivered via same tubing used to deliver water
Stroke: Stroke is the maximum distance the insert tip to a dental handpiece. Sonic scaler tips are large in diam-
travels during one cycle or stoke path. Amplitude is equal to eter and universal in design. A sonic scaler tip travels in an
one-half the distance of the stroke. The power knob on an elliptical or orbital stroke pattern. This stroke pattern allows
ultrasonic unit controls the stroke length of the insert during the instrument to be adapted to all tooth surfaces. Box 37.1
one cycle. Increasing the power knob increases the distance outlines the advantages and disadvantages of mechanized
the tip travels while the frequency remains constant. High instruments as compared to manual instruments.
power settings produce a longer stroke pattern, and lower Magnetostrictive ultrasonic devices work in a frequency
power settings provide a shorter stroke pattern. range of 18,000-50,000 cycles per second. Metal stacks that
Water Flow: Ultrasonic scalers may be designed as manu- change dimension when electrical energy is applied to power
ally or automatically tuned devices (Fig. 37.25). Both types magnetostrictive technology. Vibrations travel from the metal
of technology contain a water knob; this controls the volume stack to a connecting body that causes the vibration of the
of water being delivered to the insert tip. Manual-tuned units working tip. Tips move in an elliptical or orbital stroke pat-
have three control knobs on the front panel labeled water, tern. This allows the tip four active working surfaces.
tuning, and power. Manual technology allows the clinician Piezoelectric ultrasonic units work in a frequency range
to control the frequency of the unit by adjusting the tuning of 18,000-50,000 cycles per second (Fig. 37 26). They
knob. Auto-tuned units have two control knobs, water and have ceramic discs that are located in the handpiece power
power, and maintain a stable frequency. These units work
through feedback that constantly adjusts the insert to ensure
it is vibrating at the predetermined frequency level.
ADVANTAGES
Increased efficiency
Multiple surfaces of tip are capable of removing deposits
No need to sharpen
Less chance for repetitive stress injuries
Handpiece size large
Reduced lateral pressure
Less tissue distention
Water
Lavage
Irrigation
Acoustic microstreaming
DISADVANTAGES
More precautions and limitations
Client comfort (water spraying)
Aerosol production
Temporary hearing shifts
Noise
Less tactile sensation
Reduced visibility
FIGURE 37.25 Magnetostrictive ultrasonic device with turning knob
for power and water. From Darby ML, Walsh MM: Dental hygiene, ed 3, Saunders, St Louis, 2010.
specific in design. The straight tip design is ideal for use in

treating patients with gingivitis and deplaquing maintenance
patients. The right and left contra-angled instruments allow
for greater access and adaptation to root morphology. These
inserts are designed to work in a low power setting. They
can be used for exploration. The amount of water delivered
for lavage can be controlled through the selection of either
traditional flow or a focused tip delivery flow. Contra-angled
designs and larger, ergonomic grips enhance comfort and
ergonomics.
J
4
Clinical Outcomes of Power-Driven
Instruments
Numerous clinical outcomes have been evaluated from the
use of power-driven instruments. A systematic review of the
literature on the treatment of chronic periodontitis found no
difference in the efficacy of subgingival debridement using
ultrasonic/sonic scalers versus hand instruments in the treat-
ment of single-rooted teeth. A benefit for multirooted teeth
FIGURE 37.26 A piezoelectric ultrasonic device. (Courtesy Hu-Ftiedv,
could not be determined because of a lack of clinical data.
Chicago.) Likewise, a review by the American Academy of Periodontol-
ogy found no differences in outcomes between sonic, magne-
tostrictive, and piezoelectric scalers.
It is well established that power-driven instruments remove
biofilms, bacteria, and calculus through mechanical action.
With the advent of new designs and thinner tips, deplaquing of
root surfaces may be effectively accomplished by power-scalers.
Both sonic and ultrasonic instruments have been shown to be
effective in removing calculus similar to hand instrumentation.
Ultrasonic instruments through high-speed action produce a
cavitational activity and acoustic microstreaming that some
believe may help enhance the disruption of the bacteria in
subgingival biofilms.
The primary expected clinical outcomes from scaling and
root planing are a reduction in bleeding and probing depth
and a gain in clinical attachment. In comparing power scal-
FIGURE 37.27 Working sides of a piezoelectric tip. (Courtesy Hu-Friedy, ers to hand instruments, both types demonstrate similar out-
Chicago.) comes for reductions in bleeding on probing and probing
depth and gains in clinical attachment.
piezoelectric technology. They change in dimension as electri-
cal energy is applied to the tip. Piezoelectric tips move in a Special Considerations
linear pattern, giving the tip two active surfaces (Fig. 37.27).
A variety of insert tip designs and shapes are available for use. Furcations present one of the greatest scaling challenges. In
many instances, the opening of the furcation is narrower than
the conventional hand instrument. For this reason, power
Efficiency scalers may be recommended as a means to improve access
Power instrumentation has the potential to make scaling less when scaling furcations.
demanding, more time efficient, and more ergonomically
friendly. Modified tip designs allow for improved access in Aerosol Production
many areas, including furcations. Newer, slimmer designs
operate effectively at lower power settings, thus improving Universal infection control procedures can help minimize the
patient comfort. Sonic and ultrasonic tips can reduce the time amount of aerosol produced. Harrel and Molinari recommend
needed for scaling. three levels of defense in the reduction of dental aerosols. The
first recommended layer of defense is personal protective bar-
riers such as masks, gloves, and safety glasses. The second
Tip Designs layer is routine use of an antiseptic preprocedural rinse. The
There are tips designed to remove heavy supragingival calcu- final layer is the use of a high-speed evacuation device either
lus or to definitively debride periodontal pockets. Large diam- by a dental assistant or attached to the instrument being used.
eter tips are created in a universal design and are indicated for In all cases and with all patients, the Centers for Disease Con-
the removal of large, tenacious deposits. A high power setting trol and Prevention (CDC) guidelines for infection control
is generally recommended. Thinner diameter tips may be site should be adhered to.
Light pressure is needed with a power instrument. The

tip is traveling at a set frequency in a set stroke pattern.
1moaahn411a Increased clinician pressure on the tip causes decreased clin-
ical efficacy.
INDICATIONS Sonic/ultrasonic instrumentation requires removal from
• Supragingival debridement of dental calculus and extrinsic the coronal to the apical portion of the deposit. This stroke
stain pattern allows the insert to work at its optimal stroke pat-
• Subgingival debridement of calculus, oral biofilm, root tern and frequency for quick effective deposit removal.
surface constituents, and periodontal pathogens A deplaquing stroke should be used when the focus is
• Removal of orthodontic cement
removal of biofilm and soft debris for the resolution of
• Gingival and periodontal conditions and diseases
• Surgical interventions
gingival inflammation. This stroke entails accessing every
• Margination (reduces amalgam overhangs) square millimeter of the tooth surface during ultrasonic
deplaquing as a result of the limited lateral dispersion of
PRECAUTIONS the lavage subgingivally.
• Unshielded pacemakers
• Infectious diseases: human immunodeficiency virus,
hepatitis, tuberculosis (active stages) Evaluation
• Demineralized tooth surface
• Exposed dentin (especially associated with sensitivity)
The adequacy of scaling and root planing is evaluated when
• Restorative materials (porcelain, amalgam, gold, composite) the procedure is performed and again later, after a period of
• Titanium implant abutments unless using special insert, for soft tissue healing.
example, Quixonic SofTip Prophy Tips Immediately after instrumentation, the tooth surfaces
• Children (primary teeth) should be carefully inspected visually with optimal lighting
• lmmunosuppression from disease or chemotherapy and the aid of a mouth mirror and compressed air; surfaces
• Uncontrolled diabetes mellitus also should be examined with a fine explorer or probe. Sub-
CONTRAINDICATIONS gingival surfaces should be hard and smooth. Although com-
• Chronic pulmonary disease: asthma, emphysema, cystic plete removal of calculus is definitely necessary for the health
fibrosis, pneumonia of the adjacent soft tissue, little documented evidence of the
• Cardiovascular disease with secondary pulmonary disease necessity for root smoothness is available. Nevertheless, rela-
• Swallowing difficulty (dysphagia) tive smoothness is still the best immediate clinical indication
that calculus has been completely removed.
From Darby ML, Walsh MM: Dental hygiene, ed 3, Saunders, St Louis, 2010. Although smoothness is the criterion by which scaling and
root planing are immediately evaluated, the ultimate evalua-
tion is based on tissue response. Clinical evaluation of the soft
tissue response to scaling and root planing, including probing,
Cardiac Pacemakers should not be conducted earlier than 2 weeks postoperatively.
Reepithelialization of the wounds created during instrumenta-
Newer models of cardiac pacemakers often have bipolar tita- tion takes 1-2 weeks. Until then, gingival bleeding on prob-
nium insulation that shields the units from the effects of sonic- ing can be expected even when calculus has been completely
type devices making magnetostrictive, piezoelectric, and sonic removed because the soft tissue wound is not epithelialized.
instruments generally safe for use on people with pacemakers. Any gingival bleeding on probing noted after this interval is
However, a 1998 study by Miller et al found atrial and ventricu- more likely the result of persistent inflammation produced by
lar pacing was inhibited by electromagnetic interference pro- residual deposits not removed during the initial procedure
duced by a magnetostrictive ultrasonic scaler. A sonic scaler was or inadequate plaque control. Positive clinical changes after
also tested but did not produce the same effect. In light of this, instrumentation often continue for weeks or months. There-
as a precaution, some practitioners have advocated using only fore, a longer period of evaluation may be indicated before
hand instruments on individuals with pacemakers. There are no deciding whether to intervene with further instrumentation
Food and Drug Administration (FDA) warnings or precautions or surgery.
on the devices that prevent them from being used on patients Occasionally, the clinician may find that some slight root
with pacemakers. If in doubt, consult with the physician regard- roughness remains after scaling and root planing. If sound
ing any precautions or warnings from the manufacturer of the principles of instrumentation have been followed, the rough-
product. Box 37.2 outlines the indications, precautions, and ness may not be calculus. Because calculus removal, not root
contraindications of using mechanized instrumentation. smoothness, has been shown to be necessary for tissue health,
it might be more prudent in such a case to stop short of perfect
smoothness and reevaluate the patient's tissue response after
Principles of Instrumentation 2-4 weeks or longer. This avoids overinstrumentation and
Ultrasonic technique is different from instrumentation with removal of excessive root structure in the pursuit of smooth-
hand scalers. A modified pen grasp is used with an ultrasonic ness for its own sake. If the tissue is healthy after an interval
scaler along with an extraoral fulcrum. The purpose of the of 2-4 weeks or longer, no further root planing is necessary.
extraoral fulcrum is that it allows the operator to maintain If the tissue is inflamed, the clinician must determine to what
a light grasp and easier access physically and visually to the extent this is caused by biofilm accumulation or the presence
oral cavity. Alternate fulcrums of cross arch or opposite arch of residual calculus and to what degree further root planing
fulcrums are acceptable alternatives. is necessary.
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38
Antiinfective Therapy
SG Ciancio • A Mariotti • A Jain
Chapter Outline
Systemic Administration of Antibiotics Local Delivery Agents
Local Delivery Agents Overview of Local Delivery of
Definitions Antimicrobial Agents and Periimplant
Systemic Administration of Antibiotics Mucositis/1 mplantitis
Serial and Combination Antibiotic Conclusions
Therapy
Systemic Administration It is, therefore, logical to treat periodontal pockets via the
mechanical removal of local factors (including the calculus that
of Antibiotics harbors bacteria) and also by the disruption of the subgingi-
• Tetracyclines val plaque biofilm itself. Mechanical removal includes manual
• Metronidazole instrumentation (eg, scaling and root planing) and machine-
• Penicillins driven instrumentation (eg, ultrasonic scalers), and these
• Cephalosporins procedures can be considered "antiinlective therapy." Many
• Clindamycin chemotherapeutic agents are now available to clinicians who
• Ciprofloxacin treat periodontal diseases. Systemic antiinfective therapy (oral
• Macrolides antibiotics) and local antiinfective therapy (placing antiinfec-
tive agents directly into the periodontal pocket) can reduce
the bacterial challenge to the periodontium. It is also possible
Local Delivery Agents that systemically administered nonsteroidal antiinflammatory
agents may play a role in future adjunctive therapy.
• Subgingival chlorhexidine
Bacteria and their toxic products cause a loss of attach-
• Tetracycline-containing fibers
ment and a loss of bone. Ultimately, however, the host's own
• Subgingival doxycycline
immunologic response to this bacterial infection can cause
• Subgingival minocycline
even more bone destruction (ie, indirect bone loss) than that
• Subgingival metronidazole
caused by pathogenic bacteria and their by-products. This
It is well established that the various periodontal diseases immunologic response can be influenced by environmental
are caused by bacterial infection. Bacteria begin reattaching to (eg, tobacco use), acquired (eg, systemic disease), and ge-
the crowns of teeth soon after the teeth have been cleaned and netic risk factors. Chemotherapeutic agents can modulate
begin to form a bio.film. Over time, this supragingival plaque the host's immune response to bacteria and reduce the host's
biofilm becomes more complex, which leads to a succession self-destructive immunologic response to bacterial pathogens,
of bacteria that are more pathogenic. Bacteria grow in an api- thereby reducing bone loss. It is also incumbent on health
cal direction and become subgingival. Eventually, as bone is care providers to counsel patients about the detrimental ef-
destroyed, a periodontal pocket is formed. In a periodontal fects of systemic factors, including medications, stress, and
pocket, the bacteria form a highly structured and complex tobacco use.
biofilm. As this process continues, the bacterial biofilm ex- This chapter reviews the indications and protocols for opti-
tends so far subgingivally that the patient cannot reach it dur- mizing the use of antiinfective agents during the treatment of
ing oral hygiene efforts. In addition, this complex biofilm may periodontal diseases.
now offer some protection from the host's immunologic mech- It is important to note that significant work has been per-
anisms in the periodontal pocket as well as from antibiotics formed with the use of a systematic evidence-based approach to
used for treatment. It has been suggested that an antibiotic evaluate the various antiinfective and host modulation thera-
strength that is 500 times greater than the usual therapeutic pies (see Chapter 58). The metaanalysis of similar research
dose may be needed to be effective against bacteria that have studies has given power to statistical analysis to evaluate
become arranged in biofilms. antiinfective chemotherapeutic agents for the treatment of
449
TABLE 38.1
ANTIBIOTICS USED TO TREAT PERIODONTAL DISEASES

Category Agent Major Features
Penicillin' Amoxicillin Extended spectrum of antimicrobial activity; excellent oral absorption; used systemically
Augrnentin'' Effective against penicillinase-producing microorganisms; used systemically
Tetracyclines Minocycline Effective against a broad spectrum of microorganisms; used systemically and applied locally (subgingivally)
Doxycycline
Tetracycline Effective against a broad spectrum of microorganisms; used systemically and applied locally
(subgingivally)
Chemotherapeutically used in subantimicrobial doses for host modulation (Periostat)
Effective against a broad spectrum of microorganisms
Quinolone Ciprofloxacin Effective against Gram-negative rods; promotes health-associated microflora
Macrolide Azithromycin Concentrates at sites of inflammation; used systemically
Lincomycin derivative Clindamycin Used in penicillin-allergic patients; effective against anaerobic bacteria; used systemically
Nitroimidazole' Metronidazole Effective against anaerobic bacteria; used systemically and applied locally (subgingivally) as gel
'Indications: localized aggressive periodontitis, generalized aggressive periodontitis, medically related periodontitis, and refractory periodontitis.
"Amoxicillin and clavulanate potassium.
'Indications: localized aggressive periodontitis, generalized aggressive periodontitis, medically related periodontitis, refractory periodontitis, and necrotizing
ulcerative periodontitis.
periodontal diseases. Unfortunately, a standardized research Systemic Administration

protocol has not yet been implemented. As a result, some
studies-although relevant-have not been used in the evi- of Antibiotics
dence-based approach because of their study design. Further
Background and Rationale
evidence-based and similar research is needed to define pro-
tocols more precisely for the use of antiinfective agents to treat The treatment of periodontal diseases is based on the infec-
periodontal diseases. tious nature of these diseases (Table 38.1). Ideally, the caus-
ative microorganisms should be identified, and the most
effective agent should be selected with the use of antibiotic-
Definitions sensitivity testing. Although this appears simple, the difficulty
An antiinfective agent is a chemotherapeutic agent that acts lies primarily in identifying the specific etiologic microorgan-
by reducing the number of bacteria present. An antibiotic isms rather than the microorganisms that are simply associ-
is a naturally occurring, semisynthetic, or synthetic type of ated with various periodontal disorders.
antiinfective agent that destroys or inhibits the growth of An ideal antibiotic for use in the prevention and treatment
selective microorganisms, generally at low concentrations. of periodontal diseases should be specific for periodontal
An antiseptic is a chemical antimicrobial agent that can be pathogens, allogenic, nontoxic, substantive, not in general use
applied topically or subgingivally to mucous membranes, for the treatment of other diseases, and inexpensive. Current-
wounds, or intact dermal surfaces to destroy microorganisms ly, however, an ideal antibiotic for the treatment of periodontal
and to inhibit their reproduction or metabolism. In dentistry, diseases does not exist. Although oral bacteria are susceptible
antiseptics are widely used as the active ingredient in anti- to many antibiotics, no single antibiotic at the concentra-
plaque and antigingivitis oral rinses and dentifrices. Disinfec- tions achieved in body fluids inhibits all putative periodontal
tants (a subcategory of antiseptics) are antimicrobial agents pathogens. Indeed, a combination of antibiotics may be neces-
that are generally applied to inanimate surfaces to destroy sary to eliminate all putative pathogens from some periodon-
microorganisms. tal pockets (Table 38 2)
Antiinfective agents can be administered locally or orally. As always, the clinician-in concert with the patient-
When administered orally, many of these agents can be found must make the final decision regarding any treatment. Thus,
in gingival crevicular fluid (GCF). With either approach, their the treatment of the individual patient must be based on the
purpose is to reduce the number of bacteria present in the patient's clinical status, the nature of the colonizing bacteria,
diseased periodontal pocket. The systemic administration of the ability of the agent to reach the site of infection, and the
antibiotics may be a necessary adjunct for the controlling of risks and benefits associated with the proposed treatment
bacterial infection because bacteria can invade periodontal plan. The clinician is responsible for choosing the correct an-
tissues, thereby making mechanical therapy alone sometimes timicrobial agent. Some adverse reactions include allergic or
ineffective. The local administration of antiinfective agents, anaphylactic reactions, superinfections of opportunistic bac-
generally directly to the pocket, has the potential to provide teria, the development of resistant bacteria, interactions with
greater concentrations directly to the infected area and thus other medications, upset stomach, nausea, and vomiting.
reduce possible systemic side effects. Most adverse reactions take the form of gastrointestinal upset.
A single chemotherapeutic agent can also have a dual Other concerns include the cost of the medication and the
mechanism of action. For example, tetracyclines (especially patient's willingness and ability to comply with the proposed
doxycycline) are chemotherapeutic agents that can reduce therapy.
collagen and bone destruction via their ability to inhibit the No consensus exists regarding the magnitude of the risk
enzyme collagenase. As antibiotic agents, they can also reduce for the development of bacterial resistance. The common and
periodontal pathogens in periodontal tissues. indiscriminate use of antibiotics worldwide has contributed
38 Anti infective Therapy 451
TABLE 38.2
COMMON ANTIBIOTIC REGIMENS USED TO TREAT PERIODONTAL DISEASESa

Regimen Dosage/Duration
Single Agent
Amoxicillin 500 mg Three times daily for 8 days
Azithromycin 500 mg Once daily for 4-7 days
Ciprofloxacin 500 mg Twice daily for 8 days
Clindamycin 300 mg Three times daily for 10 days
Doxycycline or minocycline 100-200 mg Once daily for 21 days
Metronidazole 500 mg Three times daily for 8 days
Combination Therapy
Metronidazole + amoxicillin 250 mg of each Three times daily for 8 days
Metronidazole + ciprofloxacin 500 mg of each Twice daily for 8 days
'These regimens are prescribed after a review of the patient's medical history, periodontal diagnosis, and antimicrobial testing. Clinicians must consult pharmacol-
ogy references such as Mosby's GenRx or the manufacturer's guidelines for warnings, contraindications, and precautions.
Data from Jorgensen MG, Slots]: Compend Contin Educ Dent 21:111, 2000.
to increasing numbers of resistant bacterial strains over the from root surfaces may not eliminate this bacterium from the
last 15-20 years, and this trend is likely to continue given periodontal tissues. Systemic tetracycline can eliminate tissue
the widespread use of antibiotics. The overuse, misuse, and bacteria, and it has been shown to arrest bone loss and to
widespread prophylactic application of antiinfective drugs are suppress A actinomycetemcomitans levels in conjunction with
some of the factors that have led to the emergence of resistant scaling and root planing. This combination therapy allows for
microorganisms. Increasing levels of resistance of subgingi- the mechanical removal of root surface deposits and for the
val microflora to antibiotics has been correlated with the in- elimination of pathogenic bacteria from within the tissues.
creased use of antibiotics in individual countries. However, Increased posttreatment bone levels have been noted with
researchers have noted that the subgingival microflora tends the use of this method. As a result of increased resistance to
to revert to similar proportions of antibiotic-resistant isolates tetracyclines, metronidazole, or amoxicillin with metronida-
3 months after therapy. zole has been found to be more effective for the treatment of
aggressive periodontitis in children. Some investigators think
that metronidazole in combination with amoxicillin-clavu-
Tetracyclines
lanic acid is the preferable antibiotic.
Tetracyclines have been widely used for the treatment of peri- The long-term use of low antibacterial doses of tetracy-
odontal diseases. They have been frequently used to treat clines has been advocated in the past. One long-term study
refractory periodontitis, including localized aggressive peri- of patients taking low doses of tetracycline (ie, 250 mg/day
odontitis (LAP) (Table 38 1) Tetracyclines have the ability for 2-7 years) demonstrated the persistence of deep pockets
to concentrate in the periodontal tissues and to inhibit the that did not bleed after probing. These sites contained high
growth of Aggregatibacter actinomycetemcomitans. In addition, proportions of tetracycline-resistant, Gram-negative rods
tetracyclines exert an anticollagenase effect that can inhibit tis- (Fusobacterium nucleatum). After the antibiotic was discontin-
sue destruction and that may help with bone regeneration. ued, the flora was characteristic of sites with disease. There-
fore, it is not advisable to prescribe long-term regimens of
Pharmacology tetracyclines because of the possible development of resistant
The tetracyclines are a group of antibiotics that are produced bacterial strains. Although tetracyclines were often used in the
naturally from certain species of Streptomyces or that are de- past as antiinfective agents, especially for LAP and other types
rived semisynthetically. These antibiotics are bacteriostatic, of aggressive periodontitis, they are now frequently replaced
and they are effective against rapidly multiplying bacteria. by more effective combination antibiotics.
They generally are more effective against Gram-positive bac-
teria than Gram-negative bacteria. Tetracyclines are effective Specific Agents
for the treatment of periodontal diseases in part because their Tetracycline, minocycline, and doxycycline are semisynthetic
concentration in the gingival crevice is 2-10 times that found members of the tetracycline group that have been used in
in serum. This allows a high drug concentration to be deliv- periodontal therapy.
ered into the periodontal pockets. In addition, several studies
have demonstrated that tetracyclines at a low GCF concentra- Tetracycline. Treatment with tetracycline hydrochloride re-
tion (ie, 2-4 µglmL) are very effective against many periodon- quires the administration of 250 mg 4 times daily. It is in-
tal pathogens. expensive, but compliance may be reduced by the need to
take the medication so frequently. Side effects include gas-
Clinical Use trointestinal disturbances, photosensitivity, hypersensitivity,
Tetracyclines have been investigated as adjuncts for the treat- increased blood urea nitrogen levels, blood dyscrasias, diz-
ment of LAP A actinomycetemcomitans is a frequent micro- ziness, and headache. In addition, tooth discoloration occurs
organism that is associated with LAP, and it invades tissue. when this drug is administered to children who are 12 years
Therefore, the mechanical removal of calculus and plaque old or younger.
Minocycline. Minocycline is effective against a broad spec- systemically (ie, 750-1000 mg/day for 2 weeks), metronida-
trum of microorganisms. In patients with adult periodonti- zole reduces the growth of anaerobic flora, including spiro-
tis, it suppresses spirochetes and motile rods as effectively chetes, and it decreases the clinical and histopathologic signs
as scaling and root planing, with suppression evident up to of periodontitis. The most common regimen is 250 mg 3 times
3 months after therapy Minocycline can be given twice daily, daily for 7 days. Currently, the critical level of spirochetes that
thereby facilitating compliance as compared with tetracycline. is needed to diagnose an anaerobic infection, the appropriate
Although it is associated with less phototoxicity and renal time to give metronidazole, and the ideal dosage or duration
toxicity than tetracycline, minocycline may cause reversible of therapy are unknown. As monotherapy (ie, with no concur-
vertigo. Minocycline administered at a dose of 200 mg/day rent root planing), metronidazole is inferior and at best only
for 1 week results in a reduction in total bacterial counts, the equivalent to root planing. Therefore, if it is used, metronida-
complete elimination of spirochetes for up to 2 months, and zole should not be administered as monotherapy
the improvement of all clinical parameters. Soder and colleagues demonstrated that metronidazole
Side effects are similar to those of tetracycline; however, was more effective than placebo for the management of sites
there is an increased incidence of vertigo. It is the only tetracy- that were unresponsive to root planing. Nevertheless, many
cline that can discolor permanently erupted teeth and gingival patients still had sites that bled with probing, despite met-
tissue when administered orally ronidazole therapy The existence of refractory periodontitis
as a diagnostic consideration indicates that some patients do
Doxycycline. Doxycycline has the same spectrum of activity not respond to conventional therapy, which may include root
as minocycline, and it may be equally effective. Since doxy- planing, surgery, or both.
cycline can be given only once daily, patients may be more Studies have suggested that, when it is combined with
compliant. Compliance is also favored because its absorption amoxicillin or amoxicillin-clavulanate potassium (Augmen-
from the gastrointestinal tract is only slightly altered by cal- tin), metronidazole may be of value for the management of
cium, metal ions, or antacids, as is the absorption of other patients with LAP or refractory periodontitis. This is discussed
tetracyclines. Side effects are similar to those of tetracycline in more detail later in this chapter.
hydrochloride; however, it is the most photosensitizing agent
in the tetracycline category Side Effects
The recommended dosage when doxycycline is used as an Metronidazole has an Antabuse effect when alcohol is ingested.
antiinfective agent is 100 mg twice daily the first day, which The response is generally proportional to the amount ingested,
is then reduced to 100 mg daily To reduce gastrointestinal and it can result in severe cramps, nausea, and vomiting. Prod-
upset, 50 mg can be taken twice daily after the initial dose. ucts that contain alcohol should be avoided during therapy and
When given as a subantimicrobial dose (to inhibit collage- for at least 1 day after therapy is discontinued. Metronidazole
nase), 20 mg of doxycycline twice daily is recommended. also inhibits warfarin metabolism. Patients who are undergo-
Periostat (CollaGenex Pharmaceuticals Inc, Newtown, PA) ing anticoagulant therapy should avoid metronidazole because
and generic forms are currently available in a dose of 20 mg it prolongs prothrombin time. It also should be avoided in
of doxycycline. patients who are taking lithium. This drug produces a metallic
taste in the mouth, which may affect compliance.
Metronidazole
Penicillins
Pharmacology
Metronidazole is a nitroimidazole compound that was devel- Pharmacology
oped in France to treat protozoa! infections. It is bactericidal Penicillins are the drugs of choice for the treatment of many
to anaerobic organisms, and it is thought to disrupt bacte- serious infections in humans, and they are the most widely
rial DNA synthesis in conditions with a low reduction poten- used antibiotics. Penicillins are natural and semisynthetic de-
tial. Metronidazole is not the drug of choice for treating A rivatives of broth cultures of the Penicillium mold. They inhibit
actinomycetemcomitans infections. However, metronidazole is bacterial cell wall production and therefore are bactericidal.
effective against A actinomycetemcomitans when it is used in
combination with other antibiotics. Metronidazole is also ef- Clinical Use
fective against anaerobes such as Porphyromonas gingivalis and Penicillins other than amoxicillin and amoxicillin-clavulanate
Prevotella intermedia. potassium (Augmentin) have not been shown to increase peri-
odontal attachment levels, and their use in periodontal thera-
Clinical Use py does not appear to be justified.
Metronidazole has been used clinically to treat gingivitis,
acute necrotizing ulcerative gingivitis, chronic periodontitis, Side Effects
and aggressive periodontitis. It has been used as monotherapy Penicillins may induce allergic reactions and bacterial resis-
and also in combination with both root planing and surgery or tance; up to 10% of patients may be allergic to penicillin.
with other antibiotics. Metronidazole has been used success-
fully to treat necrotizing ulcerative gingivitis. Amoxicillin
Studies in humans have demonstrated the efficacy of met- Amoxicillin is a semisynthetic penicillin with an extended an-
ronidazole for the treatment of gingivitis and periodontitis. A tiinfective spectrum that includes Gram-positive and Gram-
single dose of metronidazole (250 mg orally) appears in both negative bacteria. It demonstrates excellent absorption after
serum and GCF in sufficient quantities to inhibit a wide range oral administration. Amoxicillin is susceptible to penicillin-
of suspected periodontal pathogens. When it is administered ase, which is a ~-lactamase produced by certain bacteria that
breaks the penicillin ring structure and thus renders penicil- Ciprofloxacin
lins ineffective.
Amoxicillin may be useful for the management of patients Pharmacology
with aggressive periodontitis in both localized and generalized Ciprofloxacin is a quinolone that is active against Gram-
forms. The recommended dosage is 500 mg 3 times daily for negative rods, including all facultative and some anaerobic
8 days. putative periodontal pathogens.
Amoxicillin-Clavulanate Potassium Clinical Use
The combination of amoxicillin with clavulanate potassium Since it demonstrates a minimal effect on Streptococcus spe-
makes this antiinfective agent resistant to penicillinase en- cies, which are associated with periodontal health, ciprofloxa-
zymes produced by some bacteria. Amoxicillin with clavu- cin therapy may facilitate the establishment of a microflora
lanate (Augmentin) may be useful for the management of that is associated with periodontal health. At present, cipro-
patients with LAP or refractory periodontitis. Bueno and col- floxacin is the only antibiotic in periodontal therapy to which
leagues reported that Augmentin arrested alveolar bone loss in all strains of A actinomycetemcomitans are susceptible. It has
patients with periodontal disease that was refractory to treat- also been used in combination with metronidazole.
ment with other antibiotics, including tetracycline, metroni-
dazole, and clindamycin. Side Effects
Nausea, headache, metallic taste in the mouth, and abdominal
discomfort have been associated with ciprofloxacin. Quino-
Cephalosporins lones inhibit the metabolism of theophylline, and caffeine and
Pharmacology concurrent administration can produce toxicity. Quinolones
have also been reported to enhance the effect of warfarin and
The family of ~-lactams known as cephalosporins is similar other anticoagulants.
in action and structure to the penicillins. These drugs are fre-
quently used in medicine, and they are resistant to a number
of ~-lactamases that are normally active against penicillin. Macro I ides
Clinical Use Pharmacology
Cephalosporins are generally not used to treat dental-related Macrolide antibiotics contain a many-membered lactone ring
infections. The penicillins are superior to cephalosporins with to which one or more deoxy sugars are attached. They inhibit
regard to their range of action against periodontal pathogenic protein synthesis by binding to the SOS ribosomal subunits of
bacteria. sensitive microorganisms. Macrolides can be bacteriostatic or
bactericidal, depending on the concentration of the drug and
Side Effects
the nature of the microorganism. The macrolide antibiotics
Patients who are allergic to penicillins must be considered to used for periodontal treatment include erythromycin, spira-
be allergic to all ~-lactam products. Rashes, urticaria, fever, mycin, and azithromycin.
and gastrointestinal upset have all been associated with cepha-
losporins. Clinical Use
Erythromycin does not concentrate in GCF, and it is not ef-
Clindamycin fective against most putative periodontal pathogens. For these
reasons, erythromycin is not recommended as an adjunct to
Pharmacology periodontal therapy.
Clindamycin is effective against anaerobic bacteria, and it has Spiramycin is active against Gram-positive organisms; it is
a strong affinity for osseous tissue. It is effective for situations excreted in high concentrations in saliva. It is used as an ad-
in which the patient is allergic to penicillin. junct to periodontal treatment in Canada and Europe, but it is
not available in the United States. Spiramycin has a minimal
Clinical Use effect on increasing attachment levels.
Clindamycin has demonstrated efficacy in patients with peri- Azithromycin is a member of the azalide class of macro-
odontitis that is refractory to tetracycline therapy. Walker and lides. It is effective against anaerobes and Gram-negative ba-
colleagues showed that clindamycin assisted with the stabi- cilli. After an oral dosage of 500 mg 4 times daily for 3 days,
lization of refractory patients; the dosage used was 150 mg significant levels of azithromycin can be detected in most tis-
4 times daily for 10 days. Jorgensen and Slots recommend a sues for 7-10 days. The concentration of azithromycin in tis-
regimen of 300 mg twice daily for 8 days. sue specimens from periodontal lesions is significantly higher
than that of normal gingiva. It has been proposed that azithro-
Side Effects mycin penetrates fibroblasts and phagocytes in concentrations
Clindamycin has been associated with pseudomembranous that are 100-200 times greater than that of the extracellular
colitis, but the incidence is higher with cephalosporins and compartment. The azithromycin is actively transported to sites
ampicillin. When needed, however, clindamycin can be of inflammation by phagocytes, where it is then released di-
used with caution, but it is not indicated for patients with rectly into the sites of inflammation as the phagocytes rupture
a history of colitis. Diarrhea or cramping that develops dur- during phagocytosis. Therapeutic use requires a single dose of
ing clindamycin therapy may be indicative of colitis, and 250 mg/day for 5 days after an initial loading dose of 500 mg.
clindamycin should be discontinued. If symptoms persist, the Data have suggested that azithromycin may be an effective
patient should be referred to an internist. adjunctive therapy for increasing attachment levels in patients
with aggressive periodontitis as well as for reducing the de- regimen harbored A actinomycetemcomitans 1 year later. The
gree of gingival enlargement. At this time, these data must metronidazole-ciprofloxacin combination is effective against
be carefully considered because the data were derived from A. actinomycetemcomitans; metronidazole targets obligate an-
small subject populations. Currently, the literature presents aerobes, and ciprofloxacin targets facultative anaerobes. This
conflicting reports regarding the efficacy of this antibiotic as is a powerful combination against mixed infections. Studies
an adjunct to periodontal therapy. A recent study concluded of this drug combination for the treatment of refractory pen-
that adjunctive azithromycin provides no additional benefit odontitis have documented marked clinical improvement. This
over nonsurgical periodontal treatment for the parameters combination may provide a therapeutic benefit by reducing or
investigated in patients with severe generalized chronic peri- eliminating pathogenic organisms and a prophylactic benefit
odontitis. Furthermore, a study in the New England Journal by giving rise to a predominantly streptococcal microflora.
of Medicine in 2012 reported that there was an increase in Systemic antibiotic therapy in combination with mechani-
cardiovascular deaths among patients who were receiving cal therapy appears to be valuable for the treatment of recal-
azithromycin; this increase was most pronounced among pa- citrant periodontal infections and LAP infections that involve
tients with a high baseline risk of cardiovascular disease. As A. actinomycetemcomitans. Antibiotic treatment should be
a result of this study, the US Food and Drug Administration reserved for specific subsets of periodontal patients who do
issued a warning that the drug can alter the electrical activity not respond to conventional therapy The selection of specific
of the heart, which may lead to a potentially fatal heart rhythm agents should be guided by the results of cultures and sensi-
known as prolonged QT interval. This rhythm causes the timing tivity tests for subgingival plaque microorganisms.
of the heart's contractions to become irregular. The warning
stated that physicians should use caution when giving the an-
tibiotic to patients who are known to have this condition or Pharmacologic Implications
who are at risk for cardiovascular problems.
Principles of antibiotic therapy for the proper selection of an
To ascertain the efficacy of azithromycin for the manage-
antibiotic minimally require the identification of the causative
ment of periodontal diseases, future studies will need to in-
organism, the determination of the antibiotic sensitivity, and
crease the number of subjects, improve diagnostic methods
an effective method of administration. The use of antibiotics to
and tools, and determine the appropriate dose, duration, and
treat gingival diseases is contraindicated because this is a local
frequency of azithromycin therapy.
infection that can be easily treated with scaling and appropriate
home care by the patient. With regard to destructive periodontal
Serial and Combination Antibiotic diseases, there are limited data to support the use of systemic
Therapy antibiotic treatment. Although bacterial infections of the peri-
odontium are considered to be important for the initiation of the
Rationale disease, currently there is no one microbe or group of microbes
that has been demonstrated to be the cause of these diseases. It is
Since periodontal infections may contain a wide diversity of therefore not surprising that systemic antibiotics have had only
bacteria, no single antibiotic is effective against all putative a modest effect on the management of periodontal diseases. At
pathogens. Indeed, differences exist in the microbial flora this time, systemic antibiotics for the treatment of periodontal
associated with the various periodontal disease syndromes. diseases have been indicated primarily for adjunctive use in the
These "mixed" infections can include a variety of aerobic, treatment of aggressive periodontal diseases (Table 38.3).
microaerophilic, and anaerobic bacteria, which may be both Guidelines for the use of antibiotics in periodontal therapy
Gram-negative and Gram-positive. In these cases, it may be include the following:
necessary to use more than one antibiotic, either serially or
in combination. Before combinations of antibiotics are used, 1. The clinical diagnosis and situation dictate the need for
however, the periodontal pathogens being treated must be possible antibiotic therapy as an adjunct for controlling ac-
identified and antibiotic-susceptibility testing performed. tive periodontal disease (Fig. 38.1). The patient's diagnosis
can change over time. For example, a patient who presents
Clinical Use with generalized, mild chronic periodontitis can return to
a diagnosis of periodontal health after initial therapy. How-
Antibiotics that are bacteriostatic (eg, tetracycline) generally ever, if this patient has been treated and continues to have
require rapidly dividing microorganisms to be effective. They active disease, the diagnosis may change to generalized se-
do not function well if a bactericidal antibiotic (eg, amoxicil- vere chronic periodontitis.
lin) is given concurrently When both types of drugs are required, 2. Disease activity as measured by continuing attachment
they are best given serially rather than in combination. loss, purulent exudate, and bleeding on probing may be
Rams and Slots reviewed combination therapy involving an indication for periodontal intervention and possible mi-
the use of systemic metronidazole along with amoxicillin, crobial analysis through plaque sampling.
amoxicillin-clavulanate (Augmentin), or ciprofloxacin. The 3. When they are used to treat periodontal disease, antibiot-
metronidazole-amoxicillin and metronidazole-Augmentin ics are selected on the basis of the patient's medical and
combinations provided excellent elimination of many organ- dental status, his or her current medications, and the re-
isms in adults with LAP who had been treated unsuccessfully sults of microbial analysis, if it is performed.
with tetracyclines and mechanical debridement. These drugs 4. Microbiologic plaque sampling may be performed accord-
have an additive effect that involves the suppression of A ac- ing to the instructions of the reference laboratory. The sam-
tinomycetemcomitans. Tinoco and colleagues found metronida- ples are usually taken at the beginning of an appointment
zole and amoxicillin to be clinically effective for the treatment before instrumentation of the pocket. Supragingival plaque
of LAP, although 50% of patients who were treated with this is removed, and an endodontic paper point is inserted
TABLE 38.3
THERAPEUTIC USES OF SYSTEMIC ANTIMICROBIAL AGENTS FOR VARIOUS PERIODONTAL DISEASES

Disease Systemic Antimicrobial Agents Adjunct or Stand-Alone Therapy
Gingival diseases Antibiotic use not recommended Not applicable

Necrotizing ulcerative gingivitis Antibiotics use not recommended unless accompanied by sys- As an adjunct when necessary
temic complications (eg, fever, swollen lymph nodes)
Chronic periodontitis Limited benefit; antibiotic use not recommended Not applicable
Aggressive periodontitis Antibiotic use recommended; for greatest benefit, therapeutic As an adjunct
levels of antibiotics should be achieved by the time scaling
and root planing are completed (all debridement should be
completed within a week); the optimal antibiotic type, dose,
frequency, and duration have not been identified
Necrotizing ulcerative periodontitis Antibiotic use dependent on the systemic condition of the patient As an adjunct when necessary
Periodontitis as a manifestation of Antibiotic use dependent on the systemic condition of the patient As an adjunct when necessary
systemic diseases
Periodontal abscess Antibiotic use not recommended Not applicable
Clinical diagnosis
Aggressive periodontitis
Refractory cases
Periimplant disease
Periodontal abscess
Debridement - SRP
Host modulation plus

Resolution Nonresolution
local delivery
Surgery
Antibiotics
Local and
Local delivery Systemic antibiotic
systemic antibiotic
Resolution Resolution Nonresolution
Resolution Non resolution Nonresolution Surgery
Surgery Systemic antibiotic Local delivery
Resolution Resolution Nonresolution
Nonresolution Surgery
Surgery
FIGURE 38.1 A decision tree for the selection of antibiotic therapy.

subgingivally into the deepest pockets present to absorb final decision with the patient. Risks and benefits concerning
bacteria in the loosely associated plaque. This endodontic antibiotics as adjuncts to periodontal therapy should be dis-
point is placed in reduced transfer fluid or a sterile transfer cussed with the patient before antibiotics are used.
tube and sent overnight to the laboratory The laboratory
will then send the referring dentist a report that includes the Local Delivery Agents
pathogens that are present and any appropriate antibiotic
Locally delivered antimicrobial agents are available as ad-
regimen. At this time, there are scant data to suggest that
juncts to scaling and root planing and as aids for the control of
microbial identification from a plaque sample can be used to
growth of bacteria on barrier membranes. Although they are
clinically improve the periodontal condition of the patient.
not discussed in this chapter, locally delivered nonsteroidal
5. Metaanalyses of randomized clinical trials and quasi-
experimental studies have shown that systemic antibiot- antiinflammatory agents are also being evaluated as adjunctive
ics can improve attachment levels when they are used as agents for the treatment of periodontal disease. When they are
placed into periodontal pockets, they reduce the subgingival
adjuncts to scaling and root planing. The same benefits
microflora, the probing depths, and the clinical signs of inflam-
could not be demonstrated when antibiotics were used as
mation. A recent systematic review concluded that "adjunctive
a stand-alone therapy.
local therapy generally reduced probing depth levels. Differ-
6. When systemic antibiotics were used as adjuncts to scal-
ing and root planing, improvements were observed in the ences between treatment and SRP-only groups in the baseline
attachment levels of patients with chronic and aggressive to follow-up period typically favored treatment groups but
usually only modestly (eg, from about 0.1 to nearly 0.5 mm).
periodontitis, although patients with aggressive periodon-
Effects for clinical attachment level gains were smaller and
titis experienced greater benefits. The mean attachment
statistical significance less common." A report about locally
level change depended on the antibiotic used; it ranged
delivered agents that was prepared by the American Academy
from 0.09 to 1.10 mm.
of Periodontology stated that "the clinician's decision to use
7. The identification of which antibiotics were most effective
for the treatment of destructive periodontal diseases was locally delivered agents should be based upon a consideration
of clinical findings, the patient's dental and medical history,
limited by the insufficient sizes of the samples found in
scientific evidence, patient preferences and advantages and
the randomized clinical trials used as part of a systematic
disadvantages of alternative therapies." The report also stat-
review. With the use of a metaanalysis to evaluate eight
ed that use of locally delivered agents may be of value when
different antibiotics or antibiotic combinations, only tetra-
cycline and metronidazole were shown to significantly im- probing depths of more than 5 mm with inflammation are still
prove attachment levels when they were used as adjuncts present after conventional therapy. However, if multiple sites
are present in the same quadrant, therapy other than locally
to scaling and root planing for patients with destructive
delivered agents should be considered.
periodontal diseases.
8. Debridement of root surfaces, optimal oral hygiene, and
frequent periodontal maintenance therapy are important Subgingival Chlorhexidine
parts of comprehensive periodontal therapy. As mentioned
previously, an antibiotic strength that is 500 times greater A resorbable delivery system has been tested for the subgingi-
val placement of chlorhexidine gluconate with positive clini-
than the systemic therapeutic dose may be required to
cal results (Fig. 38.2). This product is available in the United
be effective against bacteria that has been arranged into
States as well as in a number of other countries. The PerioChip
biofilms. It is therefore important to disrupt this biofilm
is a small chip (4 0 X 5.0 X 0.35 mm) that is composed of
physically so that the antibiotic agents can have access to
a biodegradable hydrolyzed gelatin matrix. It is cross-linked
the periodontal pathogens.
with glutaraldehyde, and it also contains glycerin and water
9. Although there are adequate data to suggest that systemic
into which 2.5 mg of chlorhexidine gluconate has been in-
antibiotics can be of benefit for the treatment of destructive
corporated per chip. This delivery system releases chlorhexi-
periodontal diseases, there are limited data available to iden-
dine and maintains drug concentrations in the GCF of more
tify which antibiotics are suitable for which infection; the op-
than 100 µg/mL for at least 7 days; these concentrations are
timum dosage, frequency, and duration of antibiotic therapy;
when the regimen with antibiotics should be introduced dur- well above the tolerance of most oral bacteria. Since the chip
ing the treatment schedule; the long-term outcomes of anti-
biotic use; the potential hazards of these agents (eg, antibi-
otic resistance, changes in oral microflora); and the economic
ramifications of this type of pharmacologic intervention.
The selection of an antibiotic must be made on the basis of

factors other than the empirical decisions made by the clini-
cian. Unfortunately, there is no one best choice of antibiotic at
present (ie, there is no "silver bullet"). Therefore, the clinician
must integrate the history of the patient's disease, the clinical
signs and symptoms, and the results of radiographic examina-
tions and possibly of microbiologic sampling to determine the
course of periodontal therapy. The clinician must obtain a thor-
ough medical history, including current medications and the
possible adverse effects of combining these medicines, before FIGURE 38.2 Placement of a chlorhexidine gluconate chip
prescribing any antibiotic therapy. The clinician must make the (PerioChip).
38 AntiinfectiveTherapy 457
biodegrades within 7-10 days, a second appointment for re-

moval is not needed.
Two multicenter, randomized, double-blind, parallel-
group, controlled clinical trials of this chip were conducted
in the United States and included a total of 44 7 patients from
10 centers. In these studies, patients received supragingival
prophylaxis for up to 1 h, which was followed by scaling
and root planing for 1 h. Chips were placed in target sites
with probing depths of 5-8 mm at baseline that bled with
probing and again at 3 and 6 months if the probing depth
remained at 5 mm or more. Sites in control subjects received
either a placebo chip (inactive) with scaling and root plan-
ing or scaling and root planing alone. Sites in test subjects
received either a chlorhexidine chip (active) with scaling and
root planing or scaling and root planing alone. Examinations
FIGURE 38.3 Placement of 10% doxycycline (Atridox) gel.
were performed at baseline and again at 3, 6, and 9 months.
At 9 months, significant decreases in probing depth from
baseline that favored the active chip as compared with con-
trols were observed: chlorhexidine chip with scaling and root when the Association had an acceptance program for profes-
planing, -0.95 ± 0.05 mm; placebo chip with scaling and sional products, although that program was terminated in
root planing, -0.69 ± 0.05 mm (P = .001); and scaling and 2008. This product is available in the United States and in a
root planing alone, -0.65 ± 0.05 mm (P = .00001). Although number of other countries.
statistically significant, the net clinical changes were limited. During a 9-month multicenter study of 180 patients, treat-
The proportion of pocket sites with a probing depth reduc- ment with 10% doxycycline gel alone was more effective than
tion of 2 mm or more was increased in the chlorhexidine chip the other treatments at all time periods, with the exception of
group (30%) as compared with scaling and root planing alone the 3-month clinical attachment level value. For the 10% dox-
(16%); this was a statistically significant difference on a per- ycycline gel group, the reduction in clinical attachment level at
patient basis (P < .0001) 9 months showed a gain of 0.4 mm as compared with vehicle
No signs of staining were noted in any of the previous three control; the reduction in probing depth was 0.6 mm greater
studies as a result of the chlorhexidine chip treatment as mea- than with vehicle control; and the reduction of bleeding with
sured by a stain index. Adverse effects were minimal, although probing was 0.2 units greater than with vehicle control. The
a few patients complained of slight pain and swelling during differences were clinically small but statistically significant.
the first 24 h after chip placement. Although resistance was not evaluated in this study, the lo-
cal application of doxycycline has previously been reported to
show transient increases in resistance in oral microbes and no
Tetracycline-Containing Fibers overgrowth of foreign pathogens.
The first local delivery product available in the United Two multicenter clinical trials each studied 411 patients
States-an ethylene/vinyl acetate copolymer fiber (diameter, with moderate to severe periodontitis. At baseline, patients
0.5 mm) that contained tetracycline (12.7 mg per 9 in.)-was were randomized to one of four treatment groups: 10%
extensively studied. When packed into a periodontal pocket, doxycycline gel, vehicle control, oral hygiene only, and scal-
it was well tolerated by the oral tissues. For 10 days, it sus- ing and root planing. Sites with probing depths of 5 mm or
tained tetracycline concentrations that exceeded 1300 µg/ml, more that bled with probing were treated at baseline and
which was well beyond the 32-64 µg/ml required to inhib- then again with the same treatment at 4 months. Clinical
it the growth of the pathogens that had been isolated from assessments were made for 9 months, and clinical attach-
periodontal pockets. By contrast, GCF concentrations of only ment level, probing depth, and bleeding on probing were
4-8 µg/ml were reported after systemic tetracycline adminis- measured. All treatment groups in both studies showed
tration (250 mg 4 times daily for 10 days for a total oral dose clinical improvements as compared with baseline over the
of 10 g). 9-month period. The results for all parameters measured
Studies demonstrated that tetracycline fibers applied with were significantly better in the 10% doxycycline gel group
or without scaling and root planing reduced probing depth, as compared with vehicle control and oral hygiene only.
bleeding with probing, and periodontal pathogens and pro- As compared with scaling and root planing, the effects of
vided gains in clinical attachment level. Such effects were 10% doxycycline gel as monotherapy on clinical attach-
significantly better than those attained with scaling and root ment level gain and probing depth reduction were equiva-
planing alone or with placebo fibers. No change in antibiotic lent. Most recently, a 6-month, randomized, multicenter,
resistance to tetracycline was found after tetracycline fiber placebo-controlled, examiner-masked study of 171 subjects
therapy among the tested putative periodontal pathogens. evaluated the combined use of systemically delivered doxy-
However, these fibers are no longer commercially available. cycline hyclate (20 mg twice daily) plus locally delivered
doxycycline hyclate gel (10%) in combination with scal-
ing and root planing versus scaling and root planing plus
Subgingival Doxycycline placebo. The results of the study showed that the combina-
A gel system involving the use of a syringe with 10% doxy- tion therapy provided statistically significantly greater clini-
cycline (Atridox) (Fig. 38.3) is available. It was the only local cal benefits than control therapy for all clinical measures
delivery system accepted by the American Dental Association at both 3 and 6 months. The clinical parameters measured
both reassessments. The number of sites that bled after deep

probing at 12 weeks also favored the minocycline group
(P < 0.05).
Subgingival Metronidazole
A topical medication that contains an oil-based metronidazole
25% dental gel (glyceryl monooleate and sesame oil) has been
tested in a number of studies. This product is not available
in the United States. It is applied in a viscous consistency to
the pocket, where it is liquidized by the body heat and then
hardens again, forming crystals when it comes in contact with
water. As a precursor, the preparation contains metronida-
zole-benzoate, which is converted into the active substance
FIGURE 38.4 Placement of minocycline microspheres (Arestin). by esterases in GCF Two 25% gel applications at a 1-week
interval have been used.
Studies have shown that metronidazole gel is equivalent to
were probing depth, clinical attachment level, bleeding with scaling and root planing, but they have not shown adjunctive
probing, and gingival health. benefits with scaling and root planing. In a 6-month study of
30 patients, treatment consisted of 2 applications of the dental
gel in two randomly selected quadrants at 1-week intervals
Subgingival Minocycline as well as simultaneous subgingival scaling of the remaining
A locally delivered, sustained-release form of minocycline quadrants. Oral hygiene instructions were given on day 21.
microspheres (Arestin) is available for subgingival placement Statistical analyses showed that both treatments effectively
as an adjunct to scaling and root planing (Fig. 38.4). The 2% reduced probing depth and bleeding with probing over the
minocycline is encapsulated into bioresorbable microspheres 6-month period. At the end of the follow-up period, the mean
in a gel carrier. This product is available in the United States reduction in probing depth was 1.3 mm after gel treatment
and in a number of other countries. As compared with con- and 1.5 mm after subgingival scaling. Bleeding with prob-
trols (ie, scaling and root planing with nonactive vehicle as ing was reduced by 35 and 42%, respectively. No significant
subgingival irrigant), there was a statistically significant in- differences between the two treatments were detected. Dark-
crease in the clinical attachment levels among patients who field microscopy showed a shift toward a seemingly healthier
presented with pockets with probing depths of 6 mm or microflora for both treatment modalities; this effect persisted
more. throughout the 6-month period.
In a four-center, double-blind, randomized trial, patients A large, multicenter study of 206 subjects investigated
with periodontal pockets at least 5 mm deep were selected, 2 applications of metronidazole gel in 2 randomly selected
and either 2 % minocycline gel or vehicle was applied once quadrants versus 2 quadrants of scaling. Probing depths were
every 2 weeks for four applications after initial scaling and reduced by 1.2 mm in the gel and by 1.5 mm in the scaling
root planing. A total of 34 3 teeth (976 sites) were included group. At 6 months, the differences between treatments were
in the minocycline group, with 299 teeth (810 sites) being statistically but not clinically significant. In addition, bleeding
included in the control group. Reductions in P gingivalis and on probing was reduced by 88% for both treatment groups.
P intermedia at weeks 2, 4, 6, and 12 and at weeks 6 and
12 for A. actinomycetemcomitans were statistically significant. Comparative Studies
These results demonstrated the advantages of supplement-
ing standard subgingival debridement with the application Few researchers have attempted to compare these devices side
of minocycline gel. The three primary clinical efficacy vari- by side. However, in one study, doxycycline polymer, metro-
ables in this study were probing depth, clinical attachment nidazole gel, and PerioChip were compared in 4 7 periodontal
level, and bleeding index. There was a trend toward clinical patients. The study found that all controlled-release polymer
improvement in both treatment groups for all three mea- devices increased gingival attachment levels but that there
sures, and the reduction in probing depth was significantly was a slightly greater improvement among patients who were
greater with minocycline gel. When sites with probing depth treated with the doxycycline polymer.
of at least 7 mm and significant bleeding at baseline were
considered, the improvements were greater than those seen Subgingival Moxifloxacin
with 5-mm pockets. The improvements with minocycline
were statistically significantly better than those seen in the Moxifloxacin is a fourth-generation synthetic fluoroquinolone
control group. with broad-spectrum antibacterial activity. This antibiotic in-
Applications of 2 % minocycline were also evaluated in hibits cell replication by modifying the actions of DNA gyrase
a 3-month study in 30 patients. Active or placebo gel was and topoisomerase IV Since moxifloxacin has been shown
placed subgingivally at planed sites in each subject, accord- to have antimicrobial activity against aerobic and anaerobic
ing to a double-blind protocol, immediately after scaling and bacteria, including a number of periodontal pathogens, it has
root planing and again 2 and 4 weeks later. Differences be- been introduced as a local delivery agent for the treatment
tween groups with regard to mean probing depth did not of destructive periodontal diseases. A recent study in Europe
reach statistical significance at any visit, but mean clinical suggested that the local delivery of 0.4% moxifloxacin may
attachment levels favored the minocycline group (P < .05) at be of benefit as an adjunct to scaling and root planning for
38 AntiinfectiveTherapy 459
the treatment of periodontitis. It should be noted that the by a statistically significant reduction of the bleeding with
mean incremental reduction in probing depth as compared probing value (P < 001).
with placebo was 0.4 mm, which is similar to the reduction Although studies evaluating the use of the PerioChip
found with other commercially available local delivery agents. (chlorhexidine) for periimplant mucositis were not identified,
As of this writing, this drug is not available in the United one 12-month study compared the clinical and microbiologic
States, but it is available in other parts of the world. results after the application of minocycline microspheres as an
adjunct to the mechanical treatment of incipient periimplant
infections as compared with an adjunctive treatment involv-
Overview of Local Delivery ing the application of 1 ml of a 1 % chlorhexidine gel. Sixteen
of Antimicrobial Agents and patients in the minocycline group and fourteen patients in
Periimplant Mucositis/lmplantitis the chlorhexidine group completed the study. The findings
of the study were that the adjunctive use of minocycline mi-
Since there are a number of similarities between the patho- crospheres resulted in improvements of probing depths and
gens involved in periodontitis periimplant mucositis and bleeding scores, whereas the adjunctive use of chlorhexidine
periimplantitis, it is logical that similar clinical approach- only resulted in the limited reduction of bleeding scores. For
es should be implemented for these two conditions. An the deepest sites of the treated implants in the minocycline
early study by Mombelli and colleagues that made use of group, the mean probing depth was reduced from 5.0 to
tetracycline-containing fibers that are no longer available 4.4 mm at 12 months. This study did not demonstrate any sig-
demonstrated in 25 patients with periimplant mucositis nificant difference in the levels of bacterial species or groups at
that there was a significant reduction of 4 periopathogenic any time point between the two antimicrobial agents tested.
species; however, other species (eg, P gingivalis, A. actino-
mycetemcomitans) had very low baseline levels and were not
significantly affected. There was a slight but not significant Conclusions
improvement in the probing depth at 12 months. The study
Scaling and root planing alone are effective for reducing pock-
showed that the local delivery of tetracycline from polymeric
et depths, gaining increases in periodontal attachment levels,
fibers may be used to improve the clinical and micro biologic
and decreasing inflammation levels (ie, bleeding with prob-
parameters around infected implants as compared with scal-
ing). When scaling and root planing are combined with the
ing and root planing alone.
subgingival placement of sustained-release vehicles, however,
In another study, investigators applied controlled-release
additional clinical benefits are possible, including the further
doxycycline (Atridox) into periimplant pockets and noted
reduction of pocket depths, additional gains in clinical attach-
differences as compared with scaling and root planing alone.
ment levels (eg, 0.39 mm with minocycline gel), and further
This study also showed the efficacy of such devices for the
decreases in inflammation. Improvements in clinical attach-
treatment of periimplant mucositis. Patients who received the
ment levels also occur with the chlorhexidine chip (0.16 mm)
doxycycline treatment showed significantly greater probing
and doxycycline gel (0.34 mm). When systemic antibiotics
attachment levels and lesser pocket probing depths and bleed-
are used as adjuncts to scaling and root planing, the evidence
ing indexes (P < .05) as compared with those who received
indicates that some systemic antibiotics (eg, metronidazole,
scaling and root planing alone.
tetracycline) provide additional improvements in attachment
A study by Persson and colleagues evaluated 31 implants
levels (0.35 mm for metronidazole; 0.40 mm for tetracycline)
with periimplantitis in 25 patients and monitored clinical
when used as adjuncts to scaling and root planing. The use
and radiographic changes over 12 months after the adjunc-
of antiinfective chemotherapeutic treatment adjuncts does not
tive placement of minocycline microspheres (Arestin). Mino-
result in significant patient-centered adverse effects.
cycline microspheres (Arestin) were locally delivered to each
The decision regarding when to use local or systemic anti-
implant site with bone loss and with a probing pocket depth
microbials should be made on the basis of the clinician's con-
(PPD) of 5 mm or more. Rescue therapy with Arestin was al-
sideration of the clinical findings, the patient's medical and
lowed at days 180 and 270 at any site exhibiting an increase
dental history, the patient's preferences, and the potential ben-
in PPD of 2 mm or more as compared with the previous visit.
efits of adjunctive therapy with these agents.
Six implants in six subjects were either rescued or exited as a
There are extensive reviews of the local delivery agents that
result of persisting active periimplantitis. Successful implants
are available for the treatment of periodontitis.
showed a statistically significant reduction in both PPD and
the percentage of sites with bleeding with probing between
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38 Anti infective Therapy 459.el
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39
Host Modulation
ME Ryan • Y Gu • A Jain
Chapter Outline
Systemically Administered Agents Subantimicrobial-Dose Doxycycline
Locally Administered Agents Emerging Host Modulatory Therapies
Host Modulation and Comprehensive Conclusions
Periodontal Management
HMT is a means of treating the host side of the host-bacteria inter- and bone morphogenetic proteins. This section discusses che-
action. The host response is responsible for most of the tissue motherapeutics developed as HMTs researched as adjuncts to
breakdown that occurs, leading to the clinical signs of peri- treat periodontitis to date, use of HMTs in clinical practice,
odontitis (ie, loss of connective tissue attachment and bone). and what the future might hold for HMTs.
HMTs offer the opportunity for modulating or reducing this
destruction by treating aspects of the chronic inflammatory
response. HMTs do not "switch off' normal defense mecha- Systemically Administered Agents
nisms or inflammation; instead, they ameliorate excessive or
Nonsteroidal Antiinflammatory Drugs
pathologically elevated inflammatory processes to enhance
the opportunities for wound healing and periodontal stability. NSAIDs inhibit the formation of prostaglandins, including
HMT can be used to reduce excessive levels of enzymes, PGE2, which is produced by neutrophils, macrophages, fibro-
cytokines, and prostanoids and should not reduce levels be- blasts, and gingival epithelial cells in response to the presence
low constitutive levels. HMTs can also modulate osteoclast of LPS, a component of the cell wall of gram-negative bacte-
and osteoblast function (Fig. 39 .3) but should not impact ria. PGE2 has been extensively studied in periodontal disease
normal tissue turnover. HMT is key to addressing many because it upregulates bone resorption by osteoclasts. Levels
of the risk factors that have adverse effects on the host re- of PGE2 have been shown to be elevated in patients with peri-
sponse, which are either not easily managed (eg, smoking, odontal disease compared with healthy patients. PGE2 also in-
diabetes) or cannot be changed (eg, genetic susceptibility). hibits fibroblast function and has inhibitory and modulatory
In addition, host modulatory agents might be used to in- effects on the immune response.
crease the levels of a person's own protective or antiinflam- NSAIDs inhibit prostaglandins and therefore reduce tissue
matory mediators. Use of systemic HMTs for treatment of a inflammation. They are used to treat pain, acute inflammation,
patient's periodontal condition may also provide benefits for and a variety of chronic inflammatory conditions. NSAIDs
other inflammatory disorders such as arthritis, cardiovascu- include the salicylates (eg, aspirin), indomethacin, and the
lar disease, dermatologic conditions, diabetes, rheumatoid propionic acid derivatives (eg, ibuprofen, flurbiprofen, and
arthritis, and osteoporosis. Also, patients who are currently naproxen). The ability of NSAIDs to block PGE2 production,
taking host modulatory agents, such as nonsteroidal anti- thereby reducing inflammation and inhibiting osteoclast ac-
inflammatory drugs (NSAIDs), bisphosphonates, or tetracy- tivity in the periodontal tissues, has been investigated in pa-
clines, as well as newer agents targeting specific cytokines tients with periodontitis. Studies have shown that systemic
for the management of medical conditions, may be experi- NSAIDs, such as indomethacin, flurbiprofen, and naproxen
encing periodontal benefits from these systemic medications administered daily for up to 3 years, significantly slowed the
prescribed for the management of other chronic inflamma- rate of alveolar bone loss compared with placebo. However,
tory conditions. NSAIDs have some serious disadvantages when considered
A variety of different drug classes have been evaluated as for use as a HMT for periodontitis. Daily administration for
host modulation agents, including the NSAIDs, bisphospho- extended periods is necessary for periodontal benefits to be-
nates, tetracyclines, enamel matrix proteins, growth factors, come apparent, and NSAIDs are associated with significant
461
39 Host Modulation 461.el
Host modulation is a relatively new term that has been in- understanding of the host response and the impact of a variety
corporated into our dental jargon, but it has not been well of risk factors.
defined. Host can be defined as "the organism from which a Anecdotally, many dentists have identified patients with
parasite obtains its nourishment," or in the transplantation abundant plaque and calculus deposits which may manifest
of tissue, "the individual who receives the graft." Modulation itself as gingivitis with shallow pocketing. By contrast, other
is defined as "the alteration of function or status of some- patients, despite maintaining a high standard of plaque con-
thing in response to a stimulus or an altered chemical or trol, succumb to aggressive forms of periodontitis, with deep
physical environment" (Taber's Medical Dictionary, 2004). In pocketing, tooth mobility, and early tooth loss. The former
diseases of the periodontium that are initiated by bacteria, group of patients is periodontal disease resistant, whereas the
the "host" clearly is the individual who harbors these patho- latter group is periodontal disease susceptible. Clearly, the re-
gens; however, it was not clear for many years whether it was sponse of the periodontal tissues to plaque is different in these
possible to modulate the host response to these pathogens two types of patients, and certain patients undergo advanced
and other stimuli leading to the breakdown of the attach- periodontal breakdown even though they achieve a high stan-
ment apparatus. Host modulation with chemotherapeutic dard of oral hygiene. The previous observations led research-
agents or drugs is the latest adjunctive therapeutic option ers to realize that the host response to the bacterial challenge
for the management of periodontal diseases. The concept of presented by subgingival plaque is perhaps the most impor-
host modulation is fairly new to the field of dentistry but tant determinant of disease severity, progression, and even
is universally understood by most physicians who routinely response to therapy. Although plaque bacteria are capable of
apply the principles of host modulation to the management causing direct damage to the periodontal tissues (eg, by re-
of a number of chronic progressive disorders such as arthri- lease of H2S, butyric acid, and other enzymes and mediators),
tis and osteoporosis. The concept of host modulation was it is now recognized that the great majority of the destructive
first introduced to dentistry by Williams and Golub et al events occurring in the periodontal tissues result from activa-
and then expanded on by many other scholars in the dental tion of destructive processes that occur as part of the host
profession. In 1990, Williams concluded "there are compel- immune-inflammatory response to plaque bacteria. The host
ling data from studies in animals and human trials indicating response is essentially protective by intent but paradoxically
that pharmacologic agents, that modulate the host responses can also result in significant tissue damage, including break-
believed to be involved in the pathogenesis of periodontal down of connective tissue fibers in the periodontal ligament
destruction, may be efficacious in slowing the progression and resorption of alveolar bone.
of periodontitis." In 1992, Golub and colleagues discussed In 1985, research began to focus on bacterial-host interac-
"host modulation with tetracyclines and their chemically tions. It had been recognized that although bacterial patho-
modified analogs." The future that these authors described gens initiate the periodontal inflammation, the host response
has arrived, and to better understand this new era in disease to these pathogens is equally, if not more, important in me-
management, we must first look to the pathogenesis of peri- diating connective tissue breakdown, including bone loss. It
odontitis. has become clear that the host-derived enzymes known as the
Many clinicians previously believed that periodontal dis- matrix metalloproteinases (MMPs), as well as changes in osteo-
ease was an inevitable consequence of aging and was uni- clast activity driven by cytokines and prostanoids, cause most
formly distributed in the population. They thought that dis- of the tissue destruction in the periodontium. This shift in
ease severity was directly correlated with plaque levels (ie, the paradigms, with a focus on the host response, led to the de-
worse the oral hygiene, the worse the periodontal disease) and velopment of host modulatory therapies to improve therapeutic
that disease progression occurred in a continuous, linear man- outcomes, slow the progression of disease, and allow for more
ner throughout life. Now, as a result of better epidemiologic predictable management of patients with periodontitis. This
data, there has been a paradigm shift in how clinicians and therapeutic strategy not only may be relevant to individuals at
scientists view the prevalence and progression of this common greater risk for periodontal disease but also may be important
disease. It has been well established that periodontal disease in the management of those at risk for a number of related
is not a natural consequence of aging and disease severity is systemic conditions. To better understand the host factors
not necessarily correlated with plaque levels. Theories about that clinicians are attempting to modulate, we need a more
the pathogenesis of periodontitis have evolved from a purely detailed assessment of the role of the host response in peri-
plaque-associated disease to the more recent hypotheses that odontal pathogenesis (Fig. 39.1). After the accumulation of
place considerable emphasis on the host's response to the subgingival plaque bacteria, a variety of microbial substances,
bacteria. The first Surgeon General's report on "Oral Health including chemotactic factors such as lipopolysaccharide (LPS),
in America," published in 2000, recognized the importance of microbial peptides, and other bacterial antigens, diffuse across
dental health in the overall general health and well-being of a the junctional epithelium into the gingival connective tissues.
patient. Recent research findings indicate possible associations The periodontium is anatomically unique in that the junc-
between chronic oral infections, such as periodontitis, and tional epithelium ends on the tooth surface, which is nonliv-
systemic disorders, such as diabetes, cardiovascular and lung ing tissue; there is no other such discontinuous lining over
diseases, stroke, osteoporosis, and rheumatoid arthritis. The the entire surface of the body. The dentogingival junction in-
Surgeon General's report assesses these emerging associations dicates a priori vulnerability to bacterial attack. Epithelial and
and explores factors that may underlie oral-systemic disease connective tissue cells are thus stimulated to produce inflam-
connections. Along with these findings and the emergence of matory mediators that result in an inflammatory response in
the discipline of periodontal medicine, there have been many the tissues. The gingival vasculature dilates (vasodilation) and
developments in therapeutic approaches to the management becomes increasingly permeable to fluid and cells. Fluid accu-
of periodontitis. The development of the chemotherapeutic mulates in the tissues, and defense cells migrate from the circu-
approach known as "host modulation" required a thorough lation toward the source of the chemotactic stimulus (bacteria
Genetic risk factors
i i
Antibody Cytokines ;
- ~
,
PMNs
--
Antigens - Host Prostanoida, Connective
, Clinical
Microbial immune- -J tissue and
signs of
challenge LPS
-
,
inflammatory
response
MMPs _
bone
metabolism
~, disease
,
Other ~
virulence
factors
-
,
t t
l Environmental and acquired
risk factors
Tissue breakdown products and ecological changes

l
FIGURE 39.1 Schematic illustration of the pathogenesis of periodontitis. The microbial challenge presented by subgingival plaque bacteria results
in an upregulated host immune-inflammatory response in the periodontal tissues that is characterized by the excessive production of inflammatory
cytokines (eg, interleukins, tumor necrosis factor), prostanoids (eg, prostaglandin E2) and enzymes, including the matrix metalloproteinases (MMPs).
These proinflammatory mediators are responsible for the majority of periodontal breakdown that occurs, leading to the clinical signs and symptoms of
periodontitis. The process is modified by environmental (eg, tobacco use) and acquired risk factors (eg, systemic diseases) and genetic susceptibility.
PMNs, Polymorphonuclear leukocytes; LPS, lipopolysaccharide. (Modified from Page RC, Kornman KS: The pathogenesis of human periodontitis: an
introduction, Periodontology 20: 7 2 7, 2009.)
and their products) in the gingival crevice. Neutrophils, or enzymes and inflammatory mediators indiscriminately into
polymorphonuclear leukocytes (PMNs), predominate in the the tissues. These enzymes include the MMPs, such as collage-
early stages of gingival inflammation to phagocytose and kill nase and gelatinase, which break down collagen fibers in the
plaque bacteria. Bacterial killing by PMNs involves both in- gingival and periodontal tissues. The infiltrating inflamma-
tracellular mechanisms (after phagocytosis of bacteria within tory and immune cells are accommodated by the breakdown
membrane-bound structures inside the cell) and extracellular of structural components of the periodontium. MMPs are a
mechanisms (by release of PMN enzymes and oxygen radicals primary target for host modulation. Pharmacologic agents or
outside the cell). As bacterial products enter the circulation, chemotherapeutics can be administered to suppress excessive
committed lymphocytes return to the site of infection and B levels of MMPs.
lymphocytes are transformed to plasma cells, which produce Macrophages are recruited to the area and are activated (by
antibodies against specific bacterial antigens. Antibodies are binding to LPS) to produce prostaglandins (eg, prostaglandin
released in the gingival tissues and, in the presence of comple- E2 [PGE2]), interleukins (eg, IL-la, IL-1~, IL-6), tumor ne-
ment, facilitate and enhance PMN phagocytosis and bacterial crosis factor alpha (INF-a), and MMPs. The cytokines (inter-
killing. leukins and INF-a) and prostanoids are additional targets for
Thus, a host immune-inflammatory response is established host modulatory therapeutics. Interleukins and INF-a bind
in the gingival tissues, and the clinical signs of gingivitis de- to fibroblasts, which are stimulated to produce additional
velop as the tissues become more edematous and erytherna- quantities of PGE2, interleukins, INF-a, and MMPs in posi-
tous. This response is essentially protective in intent to com- tive-feedback cycles. The concentration of these enzymes and
bat the bacterial infection and prevent ingress of bacteria into inflammatory mediators becomes pathologically high in the
the tissues. In persons who are not susceptible to periodontitis periodontal tissues. Host modulatory therapy (HMT) can be
(disease resistant), these primary defense mechanisms control used to interrupt these positive-feedback loops and ultimately
the infection, and chronic inflammation (ie, chronic gingivi- reduce the excessive levels of cytokines, prostanoids, and en-
tis) may persist indefinitely. In disease-susceptible individuals, zymes resulting in tissue destruction. MMPs break down col-
however, inflammatory events extend apically and laterally to lagen fibers, disrupting the normal anatomy of the gingival
involve deeper connective tissues and alveolar bone. There tissues ultimately resulting in destruction of the periodontal
is proliferation of the junctional epithelium, which becomes ligament. The inflammation extends apically, and osteoclasts
increasingly permeable and ulcerated, thus accelerating the are stimulated to resorb alveolar bone by the high levels of
ingress of bacterial products, and the inflammation worsens. prostaglandins, interleukins, and INF-a in the tissues. The
Further, defense cells are recruited to the area, including mac- osteoclasts themselves are targets for host modulation. Drugs
rophages and lymphocytes. Large numbers of PMNs migrate can be administered to downregulate osteoclastic activity and
into the tissues, secreting excessive quantities of destructive ultimately to inhibit bone resorption by these cells.
39 Host Modulation 461.e3
Risk factors (eg, genetics Reduction of

smoking, diabetes) risk factors
Overproduction of proinflammatory or Expression of host-derived antiinflammatory

destructive mediators and enzymes (eg, or protective mediators
IL-1, IL-6, PGE2, TNF-a, MMPs) (eg, IL-4, IL-10, IL-1 ra, TIMPs)
Underactivity or overactivity Host modulatory Resolution of

of aspects of host response therapy inflammation
Poor compliance Subgingival OHi, SAP, surgery, antiseptics, antibiotics

Poor plaque control bioburden to reduce bacterial challenge
( DISEASE
FIGURE 39.2 The periodontal balance. The balance between periodontal breakdown (disease) and periodontal stability (health) is tipped toward
disease by risk factors, excessive production of inflammatory cytokines and enzymes (eg, IL-I and IL-6, interleukin-1 and -6; PCE2, prostaglandin E2;
TNF-a, tumor necrosis factor alpha; MMPs, matrix metalloproteinases), underactivity or overactivity of aspects of the immune-inflammatory host
response, poor compliance, and a pathogenic microflora. The balance can be tipped toward health by risk factor modification, upregulation, and
restoration of balance between naturally occurring inhibitors of inflammation (eg, IL-4 and IL- I 0, interleukins-4 and -1 O; IL- Ira, interleukin-1 receptor
antagonist; TIMPs, tissue inhibitors of metalloproteinases); HMT, host modulatory therapy, and antibacterial treatments such as OHi (oral hygiene
instructions); SRP, scaling and root planing, surgery, antiseptics, and antibiotics.
The elevations in the proinflammatory or destructive me- down and restored at a more apical location. Plaque bacteria
diators in response to bacterial challenge are counterbalanced then migrate apically along the root surface deeper into the
by elevations in antiinflammatory or protective mediators pocket where the physical conditions favor the proliferation of
such as the cytokines IL-4 and IL-10, as well as other media- Gram-negative anaerobic species. Bacterial products continue
tors, such as IL-lra (receptor antagonist), and tissue inhibitors to challenge the host, and the host continues its frustrated
of metalloproteinases (TIMPs) (Fig. 39.2). Under conditions response against these bacteria and their products. Inflam-
of health, the antiinflammatory or protective mediators serve mation extends further and further apically, more bone is re-
to control tissue destruction. If there are adequate levels of sorbed, and periodontal ligament (PDL) is broken down. The
these antiinflammatory or protective mediators to keep the pocket deepens, and the associated attachment and bone loss
host response to the bacterial challenge in check, the individ- result in clinical and radiographic signs of periodontitis. In-
ual will be disease resistant. If an imbalance occurs, with ex- tervention is required to prevent eventual tooth loss and other
cessive levels of the proinflammatory or destructive mediators sequelae of the disease.
present in the host tissues, tissue destruction will ensue in the The nature of the host response to the presence of plaque
susceptible host. Another potential target for host modulation is modified by genetic factors (helping to explain why aggres-
could entail the use of pharmacologic agents, which either sive periodontitis tends to have a familial aggregation) and
mimic or result in elevations of endogenous antiinflammatory systemic and environmental factors (eg, smoking, diabetes,
or protective mediators. stress). These risk factors may lead to the imbalance between
Thus, plaque bacteria initiate the disease, and bacterial an- the proinflammatory and antiinflammatory mediators seen in
tigens that cross the junctional epithelium drive the inflamma- susceptible individuals (Fig. 39.2). Risk factors can affect on-
tory process. Therefore, bacteria are essential for periodontitis set, rate of progression, and severity of periodontal disease,
to occur, but they are insufficient by themselves to cause dis- as well as response to therapy (Box 39.1). Risk assessment is
ease. For periodontitis to develop, a susceptible host is also extremely important as we now recognize that some of these
required. The majority of periodontal breakdown (bone loss, risk factors can be modified to reduce a patient's susceptibility
attachment loss) is caused by host-derived destructive en- to periodontitis. Risk reduction strategies may include smok-
zymes (MMPs) and inflammatory mediators (prostaglandins, ing cessation, improved control of diabetes, nutritional sup-
interleukins) that are released during the cascade of destruc- plementation, improved oral hygiene, changes in medication,
tive events that occur as part of the inflammatory response stress management, weight loss, and more frequent dental vis-
(Fig. 39.1) Paradoxically, the inflammatory response, which its (Box 39.2). The use of chemotherapeutic agents or drugs
is essentially protective in design, is responsible for much specifically designed to treat periodontal diseases is emerging
of the breakdown of the soft and hard periodontal tissues. to aid as a risk reduction strategy Intervention in periodontal
Periodontal disease is characterized by high concentrations of disease can now include HMT as one of the available adjunc-
MMPs, cytokines, and prostanoids in the periodontal tissues, tive treatment options. The term adjunctive is meant to imply
whereas periodontal health is characterized by the opposite. "in addition to conventional therapies" or "in addition to other
The purpose of HMT is to restore the balance of proinflam- established therapies." For the management of periodontal
matory or destructive mediators and antiinflammatory or pro- diseases, conventional approaches were initially mechanical
tective mediators to that seen in healthy individuals. Pocket in nature, that is, surgery, as well as scaling and root planing
formation occurs as coronal junctional epithelium is broken (SRP). Initially, adjunctive therapies were solely antimicrobial
BOX 39.2
• Heredity: family history, PST test • Heredity: HMT chemotherapeutics

• Smoking: frequency, current history, past history • Smoking: cessation, HMT chemotherapeutics
• Diabetes: duration, control • Diabetes: improved control, work with physician; HMT
• Obesity chemotherapeutics
• Stress: reported by patient • Obesity: weight loss
• Medications: calcium channel blockers, phenytoin • Stress: management, HMT chemotherapeutics
(Dilantin), cyclosporin, drugs known to cause dry mouth • Medications: change medications, work with physician;
• Nutrition HMT chemotherapeutics
• Poor oral hygiene: plaque and calculus • Nutrition: supplements
• Faulty dentistry: overhangs, subgingival margins • Poor oral hygiene: improved oral hygiene, HMT
• Hormonal variations: pregnancy (increased estradiol chemotherapeutics
and progesterone), menopause (decreased estrogen, • Faulty dentistry: corrective dentistry
osteoporosis) • Hormonal variations: consult with physician, HMT
• lmmunocompromise: HIV, neutropenia chemotherapeutics
• Connective tissue diseases • lmmunocompromise: consult with physician, HMT
• Previous history of periodontitis chemotherapeutics
• Connective tissue diseases: consult with physician, HMT
PST, Periodontal screening test; HIV, human
chemotherapeutics
immunodeficiency virus
HMT, Host modulatory therapy
such as the use of antiseptics and antibiotics (local and/or tissues. However, the bacterial challenge is never completely
systemic). New adjunctive approaches involve modulation of eliminated after SRP, and recolonization by bacterial species
the host response. Researchers are also investigating HMTs, occurs. HMTs offer the potential for downregulating destruc-
which aim to modify or reduce destructive aspects of the tive aspects and upregulating protective aspects of the host re-
host response so that the immune-inflammatory response to sponse so that, in combination with conventional treatments
plaque is less damaging to the periodontal tissues. Removal to reduce the bacterial burden, the balance between health
of plaque by SRP targets one aspect of the pathogenic process (resolution of inflammation and wound healing) and disease
by reducing the bacterial burden and therefore the antigenic progression (continued proinflammatory events) is tipped in
challenge that drives the inflammatory response in the host the direction of a healing response.
Bisphosphonates
NSAIDs Periostat
Periostat .J
Antimicrobials ..J. Osteoclasts
½
Pockets
!
Bacterial
products _____. I cells
Host
___.. Prostagland
- Cytokines / I resorption
and
CAL
{IL-1, IL-6, TNF)
Connective
MMPs Tooth
tissue
mobility
t
Periostat
breakdown
and
loss
Bacterial + Host response component Clinical

component sequelae
FIGURE 39.3 Potential adjunctive therapeutic approaches. Possible adjunctive therapies and points of intervention in the treatment of periodontitis
are presented related to the pathologic cascade of events. CAL, Clinical attachment loss.
side effects, including gastrointestinal problems, hemorrhage has suggested that bisphosphonates also possess anticollage-
(from decreased platelet aggregation), and renal and hepatic nase properties. The ability of bisphosphonates to modulate
impairment. Furthermore, research shows that the periodon- osteoclast activity clearly may be useful in the treatment of
tal benefits of taking long-term NSAIDs are lost when patients periodontitis. Research has demonstrated that in naturally
stop taking the drugs, with a return to or even an accelera- occurring periodontitis in beagle dogs, treatment with the
tion of the rate of bone loss seen before NSAID therapy, often bisphosphonate, alendronate, significantly increased bone
referred to as a "rebound effect." For these reasons, the long- density compared with placebo. In animal models of experi-
term use of NSAIDs as an adjunctive treatment for periodonti- mentally induced periodontitis, bisphosphonates reduced
tis has never really developed beyond research studies. alveolar bone resorption. In human studies, these agents re-
It was previously anticipated that the selective cyclooxy- sulted in enhanced alveolar bone status and density.
genase-2 (COX-2) inhibitors may offer promise as adjunctive Some bisphosphonates have the unwanted effects of inhib-
treatments in the management of periodontitis. The enzyme iting bone calcification and inducing changes in white blood
cyclooxygenase, which converts arachidonic acid to prosta- cell counts. Also, there have been recent reports of avascular
glandins, exists in two functionally distinct isoforms, COX-1 necrosis of the jaws following bisphosphonate therapy, with
and COX-2. COX-1 is constitutively expressed and has anti- the resultant risk of bone necrosis following dental extrac-
thrombogenic and cytoprotective functions. Therefore, inhi- tions. The recent reports of bisphosphonate-related osteo-
bition of COX-1 by nonselective NSAIDs causes side effects necrosis of the jaw (BRONJ), although primarily associated
such as gastrointestinal ulceration and impaired hemostasis. with intravenous administration of bisphosphonates rather
COX-2 is induced after stimulation by various cytokines, than oral administration, has impeded the development of
growth factors, and LPS and results in the production of ele- bisphosphonates as an HMT to manage periodontitis. As with
vated quantities of prostaglandins. Inhibition of COX-2 by se- NSAIDs, at present there are no bisphosphonate drugs that are
lective COX-2 inhibitors results in reduction of inflammation. approved and indicated for treatment of periodontal diseases.
Researchers considered that the use of selective COX-2 inhibi-
tors offered the prospect for reducing periodontal inflamma-
Subantimicrobial-Dose Doxycycline
tion without the side effects typically observed after long-term
(nonselective) NSAID therapy, and preliminary studies identi- Subantimicrobial-dose doxycycline (SDD) is a 20-mg dose of
fied that selective COX-2 inhibitors slowed alveolar bone loss doxycycline (Periostat) that is approved and indicated as an
in animal models and modified prostaglandin production in adjunct to SRP in the treatment of chronic periodontitis. It is
human periodontal tissues. However, the selective COX-2 in- taken twice daily for 3 months, up to a maximum of 9 months
hibitors were later identified to be associated with significant of continuous dosing. The 20-mg dose exerts its therapeutic
and life-threatening adverse effects (ie, myocardial infarction), effect by enzyme, cytokine, and osteoclast inhibition rather
resulting in some drugs being withdrawn from the market. than by any antibiotic effect. Research studies have found no
In summary, NSAIDs (including the selective COX-2 specific detectable antimicrobial effect on the oral flora or the bac-
inhibitors) are presently not indicated as adjunctive HMTs in terial flora in other regions of the body and have identified
the treatment of periodontal disease. clinical benefit when used as an adjunct to SRP At present,
SDD (Periostat) is the only systemically administered HMT
specifically indicated for the treatment of chronic periodon-
Bisphosphonates
titis that is approved by the US Food and Drug Administra-
The bisphosphonates are bone-seeking agents that inhibit tion (FDA) and accepted by the American Dental Association
bone resorption by disrupting osteoclast activity. Their pre- (ADA). In addition, a modified-release SDD was recently ap-
cise mechanism of action is unclear, but research has shown proved by the FDA (Oracea) for the treatment of the com-
that bisphosphonates interfere with osteoblast metabolism mon skin disorder rosacea and is routinely prescribed within
and secretion of lysosomal enzymes. More recent evidence the dermatology community. Studies conducted by Preshaw
39 Host Modulation 463
et al, using this same modified-release SDD versus placebo in

266 subjects with periodontitis as an adjunct to SRP resulted
in significantly greater clinical benefits than SRP alone in the
treatment of periodontitis. It will be interesting to see what
the long-term benefits to oral health will be in rosacea patients
Risk factor
being prescribed this new drug. There has also been consid-
modification:
erable off-label use of this new modified-release SDD for the burden: smoking cessation
treatment of periodontal diseases based on the understanding SAP, topical therapy, diabetes
that once-a-day administration can increase the level of com- antimicrobials, control
pliance as compared to twice-a-day oral administration. surgical pocket
reduction
Locally Administered Agents

Nonsteroidal Antiinflammatory Drugs
Topical NSAIDs have shown benefit in the treatment of peri- Host response modulation:
odontitis. One study of 55 patients with chronic periodonti- subantimicrobial-dose doxycycline
tis who received topical ketorolac mouth rinse reported that for inhibition of MMPs
gingival crevicular fluid (GCF) levels of PGE2 were reduced
by approximately half over 6 months and that bone loss was
halted. In addition, locally administered ketoprofen has been
investigated. To date, topically administered NSAIDs have not
been approved as local HMTs for the management of peri- FIGURE 39.4 Complementary treatment strategies in periodontitis.
odontitis. The best chance for clinical improvement may come from implement-
ing complementary treatment strategies that target different aspects of
the periodontal balance. Reduction of the bacterial burden by scaling
Enamel Matrix Proteins, Growth Factors, and root planing (SRP) is the cornerstone of treatment and can be aug-
mented by the use of topical antimicrobials and surgical pocket therapy.
and Bone Morphogenetic Proteins In addition to this antibacterial treatment approach, the host response
can be treated by the use of host modulatory therapy, such as subanti-
A number of local HMTs have been investigated for potential microbial-dose doxycycline, for the inhibition of matrix metalloprotein-
use as adjuncts to surgical procedures, not only to improve ases (MMPs). Risk factor assessment and modification must form a key
wound healing but also to stimulate regeneration of lost bone, part of any periodontal treatment strategy, including smoking cessation
counseling. These different but complementary treatment strategies can
periodontal ligament, and cementum, restoring the com-
be used together as part of a comprehensive management approach.
plete periodontal attachment apparatus. These have included
enamel matrix proteins, bone morphogenetic proteins (BMP-2,
BMP- 7), growth factors (platelet-derived growth factor, insulin- chronic nature of the disease. Management includes thorough
like growth factor), and tetracyclines. The locally applied HMTs medical and dental history and examination (clinical chart-
currently approved by the FDA for adjunctive use during sur- ing and radiographs), assessment of risk factors, diagnosis,
gery are enamel matrix proteins (Emdogain), recombinant hu- development of a treatment strategy, initial and definitive
man platelet-derived growth factor-BB (GEM 21S), and BMP-2 treatment planning, review of treatment outcomes and reeval-
(INFUSE), which are covered in much greater detail in other uation, long-term supportive periodontal therapy (mainte-
chapters. The initial local host modulatory agent approved by nance care), and assessment of prognosis. In addition, as new
the FDA for adjunctive use during surgery to assist with clini- data continue to emerge regarding biochemical assessments of
cal attachment gain and wound healing was Emdogain; this disease activity (measuring levels of proinflammatory media-
has been followed by platelet-derived growth factor combined tors, bone and connective tissue breakdown products in the
with a resorbable synthetic bone matrix (GEM 21S) to assist GCF, saliva, and tissues of the oral cavity), new diagnostic and
in regenerative procedures approved recently by the FDA, as prognostic tests may become part of our established protocols
well as rhBMP-2 (INFUSE) soaked onto an absorbable collagen for comprehensive periodontal disease management in the fu-
sponge to assist with ridge and sinus augmentation. The tech- ture. However, controlling the bacteria that cause periodon-
nology behind GEM 21 has also been approved and marketed tal infections remains a central focus of effective periodontal
for use in wound healing, particularly in patients with diabe- treatment. Understanding the importance of the host response
tes, and INFUSE has been used for quite some time for the and the impact of risk factors now allows clinicians to provide
healing of fractures by the orthopedic community. complementary treatment strategies simultaneously for their
The remainder of this chapter focuses on the clinical util- patients (Fig. 39. 4)
ity of host modulation for nonsurgical procedures in clinical Those patients most likely requiring the use of HMT in-
practice and the use of SDD (Periostat) in clinical practice. clude those with risk factors that are either nonmodifiable or
not easily modified. If the decision is made to use HMT, this
Host Modulation and Comprehensive must be discussed with the patient and the rationale for treat-
ment thoroughly explained. This takes time at the chair side,
Periodontal Management but it is time well spent; patients become increasingly interest-
The term periodontal management suggests a much broader ed in their periodontal status and are more likely to develop
concept of periodontal care than the term periodontal treat- ownership of their management, thereby enhancing compli-
ment. This concept is extremely important considering the ance with all aspects of care, including plaque control, risk
reduction, and treatment protocols. Compliance with HMT The best chance for clinical improvement may come from a
is greatly facilitated if the rationale for prescribing is clearly combination of targeted treatment approaches for each pa-
explained. The need for compliance with the prescribed drug tient (Fig. 39.4) In fact, Novak et al published very strik-
regimen is important because with SDD, for example, a tablet ing improvements in probing depth reductions and clinical
must be taken twice daily (once in the morning and once in attachment level gains in a 6-month, randomized, multi-
the evening) and should not be taken with calcium supple- center, examiner-blinded, placebo-controlled study, which
ments. Compliance may be improved by administration of a showed that combination therapy of HMT (SDD) plus a
modified-release SDD capsule taken only once a day. It should locally delivered antimicrobial (doxycycline hyclate gel) and
be emphasized to the patient that the use of HMT is not a sub- SRP provided optimal improvements in clinical parameters
stitute for excellent plaque control (just as it is not a substitute when compared to SRP alone in the treatment of moderate-
for excellent debridement and root surface instrumentation to-severe periodontitis.
by the treating clinician). To achieve the best results, patients
must be interested and well informed about their condition
Subantimicrobial-Dose Doxycycline
so that compliance is maximized. Furthermore, patients must
also be convinced that comprehensive and frequent recall ap- As previously discussed, SDD is currently the only FDA-
pointments are absolutely necessary in the maintenance phase approved, systemically administered HMT indicated spe-
of this chronic and often progressive disease, which can be cifically in the treatment of periodontitis. SDD is used as an
very well controlled with adequate follow-up. adjunct to SRP and must not be used as a stand-alone therapy
In addition to patient motivation, oral hygiene instruction, (monotherapy). Because SDD, previously called "low-dose
and SRP to reduce the bacterial challenge, a key treatment doxycycline" (LDD) and currently marketed as Periostat, is
strategy when managing periodontitis patients is rish factor based on SDD, a member of the tetracycline family of com-
modification. The harmful effects of smoking on the periodon- pounds, the use of tetracyclines for the management of peri-
tal tissues are well documented, and successful smoking ces- odontal diseases must be put in perspective.
sation therapy will likely be a major benefit to patients with In regard to incorporation of a medical pharmacologic ap-
periodontitis. Smoking cessation counseling can be under- proach into the management of a disease in the dental practice
taken in the dental office (if staff are appropriately trained) or setting, no class of drugs has made more of an impact on peri-
through collaboration with the patient's physician or special- odontal therapy than the tetracyclines. They have been used
ized clinics. Given the evidence that smokers have worse peri- in conjunction with SRP, the "gold standard" of nonsurgical
odontal disease than nonsmokers and that the magnitude and therapy, as well as with both resective and regenerative surgi-
predictability of clinical improvements after treatment are sig- cal procedures. The tetracyclines have been used locally and
nificantly reduced in smokers, smoking cessation counseling systemically as antimicrobial agents and more recently, sys-
should form a major part of treatment for smokers with peri- temically as a host modulation agent (SDD). The tetracyclines
odontitis. Patients with poorly controlled diabetes are also at have been prescribed not only to address chronic periodon-
increased risk for periodontitis, and periodontal therapy may titis but also to manage specific and often more aggressive
have an impact on diabetic control. Collaboration with medi- types of periodontitis. Most recently, the tetracyclines have
cal colleagues when treating diabetic patients with periodon- been advocated for the management of patients with systemic
titis is warranted to ascertain the degree of diabetic control. diseases such as diabetes, rheumatoid arthritis, and rosacea
Other possible risks for periodontitis include nonmodifiable [doxycycline (Oracea)]; doxycycline has led to improvements
factors such as genetics, gender, and race. As the relevance in both the periodontal health of compromised diabetic pa-
of different risk factors is established through epidemiologic tients and long-term markers of glycemic control (eg, glycated
research, clinicians must remain aware of their responsibilities hemoglobin). As an adjunct to mechanical therapies, the goal
for informing and attempting to change patients' behaviors in of tetracycline therapy has been to enhance reattachment or
relation to modifiable risks. even to stimulate new attachment of the supporting apparatus
The management of patients with periodontitis can and osseous formation.
therefore involve the following complementary treatment This section concentrates on the use of these pleiotropic
strategies: compounds for modulation of the host response in the treat-
ment of periodontitis.
• Patient education and motivation, including oral hygiene
instruction; use of powered toothbrushes, antiseptics in
rinses, toothpastes, and irrigation; and explanation of the Mechanisms of Action
rationale for any adjunctive treatments.
In addition to its antibiotic properties, doxycycline (as well as
• Reduction of the bacterial burden by high-quality SRP
the other members of the tetracycline family) has the ability
• Site-specific antibacterial treatment with local delivery sys-
to downregulate MMPs, a family of zinc-dependent enzymes
tems or systemic antimicrobial therapy in select cases.
that are capable of degrading extracellular matrix molecules,
• Host response modulation by HMT.
including collagen. MMPs are secreted by the major cell types
• Risk factor modification and risk reduction strategies.
in the periodontal tissues (fibroblasts, keratinocytes, mac-
• Periodontal surgery with or without HMT.
rophages, PMNs, endothelial cells) and play a key role in
It is the responsibility of the dentist to customize the periodontitis. Excessive quantities of MMPs are released in
treatment plan for each individual patient by selecting and inflamed periodontal tissues, resulting in breakdown of the
providing appropriate treatments, following discussion and connective tissue matrix. The predominant MMPs in peri-
informed decision making by the patient. Good communi- odontitis, particularly MMP-8 and MMP-9, derive from PMNs
cation and showing an interest in the patient's condition are and are extremely effective in degrading type I collagen, the
essential to maximize compliance and modify risk factors. most abundant collagen type in gingiva and periodontal
39 Host Modulation 465
• Inhibition of production of epithelial-derived MMPs by

inhibiting cellular expression and synthesis
• Direct Inhibition of active MMPs by cation chelation

(dependent on Ca2+ and Zn2+ binding properties}
• Inhibition of oxidative activation of latent MMPs
(independent of cation-binding properties}
• Downregulates expression of key inflammatory
cytokines including IL· 1, IL-6, and TNF-a as well as
PGE2
J
• Scavenges and inhibits production of reactive oxygen
species (ROS} produced by PMNs (eg, HOCI, which
activates latent MMPs}
• Inhibition of MMPs and ROS protects a1 proteinase
inhibitor (a1-PI}, thereby indirectly reducing tissue
proteinase activity
• Stimulates fibroblast collagen production
• Reduces osteoclast activity and bone resorption

• Blocks osteoclast MMPs
• Stimulates osteoblast activity and bone formation
FIGURE 39.5 Schematic of periodontal pocket indicating the pleiotropic mechanisms by which doxycycline inhibits connective tissue break-
down. Downregulation of destructive events occurring in the periodontal tissues by doxycycline results from modulation of a variety of different
proinflammatory pathways. (From Golub LM, Lee HM, Ryan ME, et al: Adv Dent Res 12: 12, 1998.)
ligament. Levels of PMN-type MMPs have been shown to in- will likely emerge as drugs that have beneficial effects in a
crease with severity of periodontal disease and decrease after variety of disease states because of their host modulation ca-
therapy The release of large quantities of MMPs in the peri- pabilities.
odontium leads to significant anatomic disruption and break- Other potential HMTs include the novel anticytokine drugs
down of the connective tissues, contributing to the clinical developed for the management of rheumatoid arthritis, a
signs of periodontitis. disease with a pathobiology similar to that of periodontitis.
The rationale for using SDD as a HMT in the treatment Cytokines such as TNF-a have been targeted by TNF-a an-
of periodontitis is that doxycycline downregulates the activity tagonists (eg, infliximab, etanercept), which have been shown
of MMPs by a variety of synergistic mechanisms, including to be effective in treating rheumatoid arthritis. As yet, such
reductions in cytokine levels, and stimulates osteoblastic ac- drugs have not been evaluated in the treatment of periodontal
tivity and new bone formation by upregulating collagen pro- disease, but they could offer potential benefits given the im-
duction (Fig. 39 5) portance of inflammatory cytokines, such as TNF-a, in peri-
odontal pathogenesis. In addition, drugs designed to increase
the levels of antiinflammatory or protective mediators, such as
Emerging Host Modulatory Therapies IL-lra, can perform similar functions. In addition, evidence is
In the future, a variety of HMTs will likely be developed as emerging to support the benefits of combining HMTs that tar-
adjunctive treatments for periodontitis. One of the most get different aspects of the disease processes. For example, the
promising groups of potential HMTs is the chemically modified combination of SDD with bisphosphonates has also showed
tetracyclines ( CMTs). These nonantibiotic tetracycline analogs synergy in animal models of bone loss.
are tetracycline molecules that have been modified to remove Recent research has indicated that there is an active bio-
all antibiotic properties, but which retain host modulatory, chemical resolution phase involved in inflammation. Failure
anticollagenolytic effects. The CMTs are also designed to be of this resolution pathway may play a role in the pathogenesis
more potent inhibitors of proinflammatory mediators and can of periodontal diseases. Restoration of the resolution pathway
increase levels of antiinflammatory mediators such as IL-10. by the introduction of resolving molecules may provide new
Because they have no antimicrobial properties, the clinician potential therapeutic methods for the management of inflam-
would be able to increase the dose for more susceptible pa- matory periodontitis. In rabbit animal models of periodontitis,
tients with more risk factors and who might be more difficult topical application of Resolvin El has been shown to protect
to manage without getting side effects seen with antibiotics. bone loss mediated by osteoclasts. In the future, a combina-
CMTs, such as CMT-3 and CMT-8 (both of which lack antibi- tion of antiinflammatory drugs with resolving agents tested
otic activity but retain anti-MMP activity), have been shown in human clinical trials may provide evidence to support a
to inhibit osteoclastic bone resorption and promote bone for- brand new host modulation therapy for the management of
mation, enhance wound healing, and inhibit proteinases pro- periodontal diseases.
duced by periodontal pathogens. CMTs also are being studied As the concept of host modulation has become more wide-
for other effects, such as inhibition of tumor cell invasion and ly accepted, we have seen much research looking toward the
attenuation of intimal thickening after arterial injury CMTs development of new HMTs. Some have focused in the efficacy
Clinical Research Data on Distinct Patient clinical attachment as well as biochemical efficacy, based on
Populations the inhibition of collagenase activity and protection of se-
rum a1-antitrypsin (a naturally occurring protective media-
Tetracyclines work well as host modulation agents because of tor) from collagenase attack in the periodontal pocket. Golub
their pleiotropic effects on multiple components of the host et al showed that a 2-month regimen of SDD significantly de-
response (Fig. 39 3). The only enzyme (MMP) inhibitors that creased both the level of bone-type collagen breakdown prod-
have been approved for clinical use and tested for the treat- ucts (carboxy terminal telopeptide of type 1 collagen [ICTP];
ment of periodontitis are members of the tetracycline family carboxy terminal peptide, a pyridinoline-containing cross-
of compounds. In early studies investigating the use of differ- linked peptide of type 1 collagen) and MMP-8 and MMP-
ent commercially available tetracyclines, Golub et al reported 13 enzyme levels (neutrophil and bone-type collagenase) in
that the semisynthetic compound (eg, doxycycline) was more chronic periodontitis subjects (Fig. 39.6)
effective than the parent compound tetracycline in reducing The Phase Ill, 9-month, randomized, double-blind,
excessive collagenase activity in the GCF of chronic periodon- placebo-controlled trial conducted at five dental centers dem-
titis patients. Because doxycycline was found to be a more onstrated clinical efficacy and safety of SDD versus placebo as
effective inhibitor of collagenase than either minocycline or an adjunct to SRP The benefits of HMT as an adjunct to me-
tetracycline and because of its safety profile, pharmacokinetic chanical therapy were again seen, with statistically significant
properties, and ready systemic absorption, recent clinical tri- reductions in probing depths and gains in clinical attachment
als have focused on this compound. In an effort to eliminate levels, as well as the prevention of disease progression. When
the side effects of long-term tetracycline therapy, especially SDD administration was discontinued after 9 months of con-
the emergence of tetracycline-resistant organisms, SDD cap- tinuous therapy, the incremental improvements demonstrated
sules were prepared and tested. Each capsule contained 20 mg in the SDD group were maintained for at least 3 months. There
of doxycycline versus the commercially available 50 mg and was no rebound effect in either the pocket depth reductions
100 mg, antimicrobially effective, capsules or tablets. Multiple or the clinical attachment level gains; in fact, there appeared
clinical studies using SDD have shown no difference in the to be slight continued improvement in both these clinical pa-
composition or resistance level of the oral flora. More recent rameters, presumably because of the enhanced clinical status
studies also demonstrate no appreciable differences in either of the patients who had benefited from adjunctive SDD, and
fecal or vaginal microflora samples. In addition, these studies possibly also because of the known persistence or substan-
have shown no overgrowth of opportunistic pathogens, such tivity of doxycycline in the bone and soft tissue of the peri-
as Candida, in the oral cavity, gastrointestinal system, or geni- odontium. The clinical relevance of such findings confirms
tourinary system. the utility of an MMP inhibitor in the management of chronic
With regard to MMP inhibition, Golub et al reported that pericdontitis.
a 2-week regimen of SDD reduced collagenase in GCF and in
the adjacent gingival tissues surgically excised for therapeu- High-Risk Patients: Smokers. The harmful effects of cigarette
tic purposes. Subsequent studies using SDD therapy adjunc- smoking and the reduced response to periodontal treatment
tive to routine scaling and prophylaxis indicated continued in smokers compared with nonsmokers are well established.
reductions in the excessive levels of collagenase in the GCF A recent meta-analysis of randomized clinical trials of SDD
after 1 month of treatment. After cessation of SDD adminis- used as an adjunct to SRP revealed a benefit when using SDD
tration, however, there was a rapid rebound of collagenase in smokers with periodontitis (Table 39.1). A hierarchic treat-
activity to placebo levels, suggesting that a 1-month treatment response was observed such that nonsmokers who re-
ment regimen with this host modulation agent was insuffi- ceived SDD demonstrated the best clinical improvements and
cient to produce a long-term benefit. In contrast, during the smokers who received placebo had the poorest treatment re-
same study, a 3-month regimen produced a prolonged drug sponse. The responses of the smokers who received SDD and
effect without a rebound in collagenase levels to baseline the nonsmokers who received placebo were intermediate to
during the no-treatment phase of the study The mean levels the two extremes and were broadly identical. This suggests
of GCF collagenase were significantly reduced ( 4 7. 3 % from that even patients traditionally considered resistant to peri-
baseline levels) in the SDD group versus the placebo group, odontal treatment (ie, smokers) can benefit from SDD, with
who received scaling and prophylaxis alone (29 .1 % reduc- a treatment response similar to that expected when treating a
tion from baseline levels). Accompanying these reductions nonsmoker by scaling and root planing alone.
in collagenase levels were gains in the relative attachment
levels in the SDD group. Continuous drug therapy over sev- Special Patient Populations
eral months appears to be necessary for maintaining colla- More recent Phase IV (ie, postlicensing) clinical studies have
genase levels near normal over prolonged periods. However, revealed success using SDD in particular populations of sus-
it is reasonable to speculate that levels of these MMPs will ceptible individuals. Much interest has focused on genetic
eventually increase again in the more susceptible patients, susceptibility to periodontal disease, particularly whether a
and those individuals having the most risk factors and the specific variation in the genes that regulate the cytokine IL-1
greatest microbial challenge will require more frequent HMT confers increased susceptibility to disease. This polymorphism
than other patients. is known as the periodontitis-associated genotype (PAG), the
presence of which can be characterized using a commercially
General Patient Populations available screening test, the PST genetic susceptibility test. In-
Data from clinical trials of SDD are summarized in Table 39 .1. vestigation of patients who possess this gene polymorphism
In addition, a series of double-blind, placebo-controlled has been driven by the assumption that local phenotypic dif-
studies of 3, 6, and 9 months' duration all showed clinical ferences exist in chronic periodontitis associated with this
efficacy based on reductions in probing depth and gains in genotype (eg, that FAG-positive patients produce more IL-1
TABLE 39.1
SUMMARY OF DATA REPORTED IN CLINICAL TRIALS OF SUBANTIMICROBIAL-DOSE DOXYCYCLINE (SOD)

Mean PD Reduction % Sites with Cal % Sites with PD
reduction 6
Mean Cal Change (mm) (mm) Gain"
?o·
4-6mm 7+mm 4-6mm 7+mm Q.
0
Study (Year) Duration Study Groups (NJ Pockets Pockets Pockets Pockets :?.2 mm :?.3 mm :?.2mm :?.3mm ~-
n
Caton et al (2000) Study: 9 months (drug: 9 SRP + SDD (90) 1.03' 1.55" 0.956 1.686 46 22 47" 22" "'
months) SRP + placebo (93) 0.86 1.17 0.69 1.20 38 16 35 13
Novak et al (2002) Study: 9 months (drug: 6 SRP + SDD (10) 1.00 178 1.20 3.02 29 15 48 26
months) SRP + placebo (10) 0.56 1.24 0.97 1.42 21 11 21 6
Emingil et al (2004) Study: 12 months (drug: 3 SRP + SDD (10) 0.21 (all sites) 1.59' (all sites)
months) SRP + placebo (10) 0.05 (all sites) 1.32 (all sites)
Preshaw et al (2004) Study: 9 months (drug: 9 SRP + SDD (107) 1.276 2.09" 1.296 2.316 58" 336 626 376
months) SRP + placebo (102) 0.94 1.60 0.96 177 44 20 45 21
Lee et al (2004) Study: 9 months (drug: 9 SRP + SDD (240) l.56'(all sites) 1.63' (all sites)
months) SRP + placebo (17) 0.80 (all sites) 119 (all sites)
Choi et al (2004) Study: 4 months (drug: 4 SRP + SDD (15) 2.2' (test sites) 1.6" (test sites)
months) SRP + placebo (17) 0.6 (test sites) 1. 1 (test sites)
Gurkan et al (2005) Study: 6 months (drug: 3 SRP + SDD (13) 112 2.15 1.80 3.38
months) SRP + placebo (13) 0.78 176 1.46 2.57
Preshaw et al (2005)' Study: 9 months (drug:9 SRP + SDD' (116) 1.23' 1.896 1.226 2.16" 596 336 63d 37
months)
SRP + placebo" (135) 0.96 1.43 0.88 1.53 43 19 44 18
SRP + SDD., (81) 1.03 171 1.01 1.80 44 21 456 20
SRP + placebo" (60) 0.85 1.58 0.80 1.62 37 15 31 13
Mohammad et al Study: 9 months (drug: 9 SRP + SDD (12) 2.14d 3.18' 1.57d 3.22d
(2005) months) SRP + placebo (12) 0.02 0.25 0.63 0.98
G6rska and Nedzi- Study: 3 months (drug: 3 SRP + SDD (33) 0.33' (all sites) 0.29' (all sites)
Gora (2006) months) SRP + placebo (33) 0.04 (all sites) 0.08 (all sites)
Needleman et al Study: 6 months (drug: 3 SRP + SDD., (18) 0.65 (all sites) 1.40 (all sites)
(2007) months)
SRP + placebo •• (16) 0.40 (all sites) 0.98 (all sites)
N, Number of subjects; SRP, scaling and root planing; CAL, clinical attachment level, CAL change can be positive (CAL gain) or negative (CAL loss); PD, probing depth.
'p < 0.05 compared with placebo.
bp < 0.01 compared with placebo.
'Percentage of sites with CAL gain and PD reduction :?.2 mm and :?.3 mm calculated for all sites that had 6+ mm probing depths at baseline.
ap < 0.001 compared with placebo.
'Same study population as Preshaw et al (2004), stratified by smoking status:#, nonsmokers,##, smokers.
MMP-8 Collagenase 2 ICTP Carboxyterminal peptide,

MMP-13 Collagenase 3 a fragment of type 1 collagen
1200-.----------~---_
-_-_
-_-~ 350
DMMP-8
'g 1000 I ;± ; l•MMP-13
300
~ 250
~ 800
't:
iii 600
£ 200
0
~
E
400
t 150
C:
Q)
g 100
o 200 50
0 0
Baseline 1 month 2 months Baseline 1 month 2 months
MMP levels determined by Western blot GCF ICTP measured by RIA

Mean "' SEM for 7 subjects Mean "' SEM 5/6 subjects 4 sites/subject
• P < .05 vs. baseline
FIGURE 39.6 Effect of subantimicrobial-dose doxycycline (SOD) on gingival crevicular fluid (GCF) collagenase (MMP-8, MMP-13) and ICTP.
A 2-month regimen of SOD significantly decreased levels of matrix metalloproteinases (MMP-8 and MMP-13, neutrophil, and bone-type collagenases,
respectively) and ICTP compared with placebo in GCF samples of adult periodontitis patients. Decreased levels of GCF bone-type collagen breakdown
products (ICTP, pyridinoline-containing cross-linked peptide of type 1 collagen) in the SOD group versus the placebo group provides biochemical
evidence of a reduction in bone resorption. RIA, Radioimmunoassay. (From Golub LM, Lee HM, Greenwald RA, et al: lnflamm Res 46:310, 1997.)
cytokines for a given bacterial challenge, resulting in increased alone resulted in significantly greater mean probing depth re-
tissue damage and more extensive periodontal disease). How- ductions in pockets of 7 mm or greater at baseline as early as
ever, few studies exist of the impact of cytokine gene polymor- 1 month after therapy (2.52 vs 1.25 mm, respectively). These
phism on tissue IL-1 cytokine levels in periodontal disease improvements in the SDD group compared with the group re-
to support this, although IL-1~ levels in shallow periodontal ceiving mechanical therapy only were maintained during the
pockets have been reported to be higher in patients with the 5.25 months of therapy (2.85 vs 1.48 mm, respectively) and
genotype than those without. The studies that have investi- even at 3 months after stopping drug therapy (3.02 vs 1.41
gated associations between PAG and periodontal disease sta- mm), demonstrating that no rebound effect occurred. Because
tus have thus far generated conflicting data (as reviewed by of the beneficial effects of HMT in susceptible patients, multi-
Taylor et al). A reasonable assumption currently is that there center studies are using SDD in other susceptible populations,
are genetic associations between polymorphisms in the IL-1 including diabetic, osteoporotic, and institutionalized geriat-
gene cluster and periodontal disease but that unambiguous ric patients, as well as smokers.
results are not yet apparent because of the heterogeneity of the Since periodontitis is associated with many systemic dis-
disease and/or the variable design of the reported studies. Cul- eases (eg, osteoporosis, diabetes, and cardiovascular disease
linan et al concluded that IL-1 genotype is a contributory but [CVD]), researchers have investigated the effect of SDD on
nonessential risk factor for periodontal disease progression. these systemic conditions. Payne et al conducted a 2-year ran-
A 5-month preliminary investigation by Ryan et al was de- domized, double-blind, placebo-controlled trial in osteope-
signed to evaluate the impact of treatment on IL-1~ and MMP nic women at two dental centers demonstrating that SDD
levels in PST-positive (PAG) patients who presented with el- can effectively reduce the levels of localized and systemic in-
evated levels of these biochemical markers in their GCF These flammatory mediators in osteopenic patients in addition to
patients were initially treated with SRP, resulting in no change improving on the clinical measurements of periodontitis; SDD
in the levels of these biochemical markers after 1 month. Al- significantly reduced the progression of periodontal attach-
Shammari et al. reported similar findings, with no changes in ment loss and the severity of gingival inflammation and alveo-
GCF levels of IL-1 ~ and ICTP before and after SRP in patients lar bone loss in postmenopausal osteopenic women. Golub
who had not been genotyped. When the genotype-positive et al reported that collagenase activity in the GCF of these os-
patients received SDD and these biochemical markers were teopenic women was significantly reduced by SDD treatment.
monitored at 2 and 4 months, a significant decrease (50- ICTP showed a similar pattern of change during SDD treat-
61 %) in the IL-1~ and MMP-9 levels was noted after treatment with GCF collagenase activity and ICTP levels positively
ment with SDD. Correspondingly, gains in clinical attachment correlated at all time periods (P < 0.001). MMP-8 accounted
and reduced probing depths were also observed. The study for approximately 80% of total collagenase in the GCF, with
concluded that SDD may provide PST-positive patients with much lower levels of MMP-1 and -13. SDD dramatically re-
a therapeutic strategy that specifically addresses their exagger- duced the elevated MMP-8 levels by 60%. This 2-year study
ated host response. also demonstrated that long-term continuous use of SDD
Another recent study was conducted in susceptible patients did not produce antibiotic side effects, confirming what had
with severe generalized periodontitis using host modulation been reported previously in studies of continuous use of up
(SDD) as an adjunct to repeated subgingival debridement. to 12 months. Previously reported studies had demonstrated
Seventy percent of the patients who completed this 9-month a relationship between serum high-sensitivity (-reactive pro-
double-blind, placebo-controlled study were smokers. SDD as tein (hsCRP) concentration and biochemical bone turnover
an adjunct to mechanical therapy versus mechanical therapy markers in healthy pre- and postmenopausal women. These
findings suggested that low-grade systemic inflammation may who show little enthusiasm for complying with the treatment
be a common linking factor between the development of ath- plan or with oral hygiene practices are less likely to be good
erosclerosis and an increased bone turnover rate. A recently candidates for systemic drug therapy.
published study by Payne et al demonstrated that the 2-year
SDD regimen described above in postmenopausal women sig- Treatable Periodontal Conditions
nificantly reduced serum inflammatory biomarkers (hs-CRP SDD is indicated in the management of chronic periodontitis,
and MMP-9) and, among women more than 5 years post- and studies to date have focused on chronic and aggressive
menopausal, increased the high-density lipoprotein (HDL) forms of periodontitis. SDD should not be used in conditions
cholesterol level. These preliminary findings suggest that SDD such as gingivitis and periodontal abscess or when an antibi-
may play a role in managing the care of patients at risk for otic is indicated. SDD can be used in patients with aggressive
developing coronary artery disease. Other studies have shown periodontitis who are being treated nonsurgically. Further-
that SDD reduces systemic inflammatory biomarkers in CVD more, emerging studies have supported efficacy of SDD as an
patients and SDD decreases glycosylated hemoglobin (HbA1J adjunct to periodontal surgery. SDD may also be of benefit
assay in patients who are taking normally prescribed hypo- in cases that are refractory to treatment, as well as in patients
glycemic agents. The impact of SDD therapy on periodontitis with risk factors such as smoking, diabetes, osteoporosis/
may be amplified by the concurrent use of other HMTS used osteopenia, genetic susceptibility, and in whom the treatment
to manage other inflammatory diseases. Additional studies are response might be limited.
being conducted to investigate the impact of combined HMT
use not only on periodontal disease but on other chronic in- Side Effects
flammatory conditions. Doxycycline at antibiotic doses (~ 100 mg) is associated with
adverse effects, including photosensitivity, hypersensitivity re-
actions, nausea, vomiting, and esophageal irritation. However,
Suggested Uses and Other Considerations in the clinical trials of SDD (20-mg dose), it was reported that
Until relatively recently, treatment options for periodontal the drug was well tolerated, and the profile of unwanted ef-
disease have focused solely on reducing the bacterial chal- fects was virtually identical in the SDD and placebo groups.
lenge by nonsurgical therapy, surgery, and systemic or local The types of adverse events did not differ significantly be-
antimicrobial therapy. The development of SDD as an HMT, tween treatment groups, and the typical side effects of the
driven by research into the pathogenesis of periodontal dis- tetracycline class were not observed indicating that the ap-
ease, is a great example of how translational research can lead pearance of adverse events is dose related. Furthermore, there
to new treatments. By better understanding the biochemical was no evidence of adverse events that could be attributed to
processes that are important in periodontal disease, a pharma- antimicrobial effects of treatment and no evidence of develop-
cologic principle (doxycycline downregulates MMP activity) ing antibiotic resistance of the microflora after 2 years of con-
has been used in the development of a new drug treatment. tinuous use. Therefore, the drug appears to be well tolerated,
Data presented from research studies show the clinical ben- with a very low incidence of adverse effects.
efits of adjunctive SDD, and the science behind SDD has been
transferred into clinical practice. In other words, dentists now Sequencing Prescription with Periodontal Treatment
have the opportunity to use SDD for patient care, with the SDD is indicated as an adjunct to mechanical periodontal
aim being to enhance the treatment response to conventional therapy and should not be used as a stand-alone or mono-
therapy. therapy SDD should be prescribed to coincide with the first
round of SRP and is prescribed for 3 months, up to a maxi-
Candidate Patients mum of 9-2 4 months of continuous dosing depending on the
When deciding whether to use SDD as an adjunct to SRP, first patient risk. Modification of any risk factors, such as smoking,
consider the patient's motivation toward periodontal care, the nutrition, stress, contributing medications, faulty restorations,
medical history, and the patient's willingness to take a sys- poor oral hygiene, and poor diabetic control, should also be
temic drug treatment. SDD is contraindicated in any patient addressed at this time. A patient's refusal or inability to mod-
with a history of allergy or hypersensitivity to tetracyclines. It ify contributing risk factors is an important consideration for
should not be given to pregnant or lactating women or chil- treatment planning and evaluation of therapeutic responses.
dren younger than 12 years old (because of the potential for After initial periodontal treatment, the patient is enrolled
discoloration of the developing dentition). Doxycycline may into an intensive periodontal maintenance program. This in-
reduce the efficacy of oral contraceptives; therefore alternative volves regular monitoring of probing depths, reinforcement of
forms of birth control should be discussed, if necessary. There oral hygiene, and remotivation of the patient, with further SRP
is a risk of increased sensitivity to sunlight (manifested by an to disrupt the plaque biofilm and remove re-forming calculus
exaggerated sunburn) seen with higher doses of doxycycline, deposits. The 3-month prescription of SDD fits in well with
although this has not been reported in the clinical trials using the typical maintenance recall interval of 3 months, which in
the subantimicrobial dose. turn is based on the duration reported for recolonization of
The rationale for using SDD must be clearly explained to treated periodontal pockets.
the patient. By discussing the etiology of periodontal disease, Thus SDD therapy is commenced at the start of initial peri-
the available treatment options, and the anticipated outcomes, odontal therapy and continues for 3 months until the first
patients become more interested in their periodontal manage- reevaluation or maintenance appointment. At maintenance
ment, are more likely to comply with treatment, and take appointments, the need for further prescription of SDD can
more responsibility for managing their disease. Therefore, the be assessed. For patients demonstrating a good treatment
anticipated compliance and likely commitment to treatment response with significant reductions in probing depths, fur-
must also be gauged when considering SDD therapy. Patients ther SDD may not be necessary. Periodontal maintenance
39 Host Modulation 465.eS
care must continue, with an emphasis on plaque control, target different aspects of the pathogenic process: Local de-
monitoring, and prophylaxis. In other patients, the treatment livery systems deliver antimicrobial concentrations of an an-
response after completion of initial therapy may be less fa- tibacterial agent directly into the site of the pocket, whereas
vorable. Sites with persisting or progressing pockets may re- SDD is a systemic host response modulator. Thus combining
quire additional instrumentation, and the prescription of SDD these two complementary treatment strategies is another ex-
may be extended for an additional 3 months. SDD may be ample of how antibacterial therapy (SRP + local antibiotics)
combined with the use of locally applied antimicrobials and can be combined with HMT (SDD) to maximize the clini-
surgical procedures. Remember that periodontitis is a chronic cal benefit for patients. Preliminary results from a 6-month,
disease, and the treatment (whether SDD is used or not) is 180-patient clinical trial designed to evaluate the safety and
long term. The patient must be regularly reevaluated to de- efficacy of SDD combined with a locally applied antimicro-
termine disease stability or progression and the need for ad- bial [doxycycline hyclate (Atridox)] and SRP versus SRP alone
ditional active therapy. demonstrated that patients receiving the combination of treat-
Therefore, patients may cycle between phases of "active" ments experienced more than a 2-mm improvement in mean
treatment (SRP + SDD) and long-term periodontal mainte- attachment gains and probing depth reductions (P < 0 0001)
nance. The success of the maintenance phase of treatment will compared with SRP alone.
be affected by many factors, including the following:
Monitoring Benefits of Therapy
• Compliance with the maintenance regimen
To improve the ability of dentists to make appropriate treat-
• Compliance with oral hygiene instruction
ment decisions for patients undergoing periodontal therapy, it
• Presence of risk factors, such as smoking, poorly controlled
would be extremely useful if they had access to the types of di-
diabetes, or stress
agnostic tests available to their medical colleagues. Such tests
• Extent (ie, number) and severity (ie, depth) of residual deep
might be used, for example, to distinguish between active and
pockets
inactive lesions. Studies have shown that SRP alone, although
Maintenance therapy is more likely to be successful in pa- effective for improving clinical parameters such as probing
tients with good compliance, good oral hygiene, minimal or depths, may not be sufficient to reduce excessive levels of
no systemic risk factors, and minimal residual deep pocket- many underlying destructive mediators, particularly in more
ing. The patient who enters the maintenance program may susceptible patients. It would be valuable therefore if it were
have periodontal stability for months or years. However, possible to monitor the levels of such inflammatory media-
plaque control may deteriorate, the patient may develop or tors as treatment progresses. SDD results in downregulation
acquire new risk factors, and disease progression (ie, further of MMP activity in inflamed periodontal tissues. Therefore,
loss of attachment) may become apparent, indicating that a in theory, MMP levels could be monitored before, during,
further course of treatment is required. A further course of and after SRP plus SDD treatment. Published data support a
SRP will then be undertaken together with adjunctive SDD to concomitant reduction in MMP levels in GCF and improve-
restore periodontal stability. ments in clinical parameters when combining SDD and SRP
Although chair-side tests for MMPs have been developed, they
Combining with Periodontal Surgery or Local are not in widespread use because of concerns about their
Delivery Systems specificity or sensitivity.
Most clinical research to date has focused on using SDD as In the absence of new chair-side tests or a centralized di-
an adjunct to nonsurgical periodontal treatment. However, agnostic facility for monitoring the inflammatory status of the
emerging data in which SDD was used as an adjunct to ac- tissues, dentists must rely on clinical periodontal monitoring
cess flap surgery in 24 patients revealed better probing depth to assess the outcomes of treatment. In addition to the reduc-
reductions in surgically treated sites greater than 6 mm com- tions in probing depths and gains in attachment that may be
pared with surgically treated sites in patients given placebo. observed after SRP plus SDD, the quality of the periodontal
Furthermore, the SDD group demonstrated greater reductions tissues also tends to improve after treatment with SDD. More
in ICTP (carboxy-terminal peptide, a breakdown product of sensitive radiographic techniques, assessments of bone den-
collagen) than the placebo group, indicating that collageno- sity, and bone height changes used solely in clinical trials in
lytic activity was reduced in the patients taking SDD. the past may be possible in clinical practice in the future. Until
SDD treatment can also be combined with the local de- such diagnostic techniques are made widely available, how-
livery of antibiotics into the periodontal pocket through ever, clinicians must rely on clinical judgment to determine
sustained-delivery systems. The two treatment approaches the most appropriate course of therapy.
of available nutritional supplements such as fish oils. Studies management of periodontal risk factors. In the future, a range
have indicated that n-3 polyunsaturated fatty acid (n-3 PUFA; of HMTs targeting different aspects of the destructive cascade
fish oil), as an adjunct to oral hygiene instructions, can sig- of breakdown events in the periodontal tissues are likely to
nificantly lower GCF, IL-8, IL-6, and PGE2 levels compared to be developed as adjunctive treatments for periodontitis. The
placebo controls. Other studies have found that a combina- further development of these agents will permit dentists to
tion therapy with n-3 PUFA and low-dose aspirin as an ad- treat specific aspects of the underlying biochemical basis for
junct to regenerative procedures using decalcified freeze-dried periodontal disease. The goal is to maximize and make more
bone allografts result in greater mean probing depth reduc- predictable the treatment response by reducing inflammation
tions (P < 0 001) and gains in clinical attachment (P < 0.05) and inhibiting destructive processes in the tissues, which will
accompanied by a trend for modulation of the cytokine profile result in enhanced periodontal stability after conventional
of IL-1 ~ and IL-10 in GCF compared to placebo controlled re- periodontal treatments such as SRP and surgery. The dentist is
generative therapy. New collagenase (MMP) inhibitors known now in the exciting position to be able to combine established
as polyenolic zinc-binding compounds (PEZBINs; methoxy- treatment strategies with new systemic and local drug treat-
carbonyl curcumin) for periodontitis have also been investi- ments for this common, chronic disease.
gated. In vitro and in vivo findings demonstrate that these The findings discussed with regard to the use of HMT to
potential new host modulatory agents can decrease pathologi- better manage chronic periodontal disease may have appli-
cally elevated MMP levels in the plasma and gingiva of animal cations to other chronic systemic diseases such as arthritis,
models of periodontitis. Other approaches recently reported diabetes, osteoporosis, and cardiovascular disease. In addi-
indicate the therapeutic potential of a novel semisynthetic sul- tion, studies using locally applied antimicrobials as part of an
fated polysaccharide to suppress inflammatory mediators in intensive periodontal therapy (IPT) regimen have shown very
high-risk individuals, such as those with diabetes and smok- promising results. Future studies may demonstrate that in ad-
ers, based on their ability to reduce the impact of advanced dition to our current standard therapies, IPT with adjunctive
glycation end products (AGEs) thereby resulting in reductions antibiotics and/or host modulation for the management of
of proinflammatory mediators of disease. periodontal disease may have profound positive effects on the
overall health status of high-risk patients. The proper manage-
ment of local infection and inflammation (periodontitis) will
Conclusions have a significant impact on the general overall health of the
Periodontal pathogens and destructive host responses are population.
involved in the initiation and progression of periodontitis.
Therefore, the successful long-term management of this dis-
SUGGESTED READINGS
ease may require a treatment strategy that integrates therapies
Caton JG, Ciancio SG, Blieden TM, et al: Treatment with subantimicrobial
that address both etiologic components. Evidence for the role dose doxycycline improves the efficacy of scaling and root planing in pa-
of MMPs, cytokines, and other mediators in the pathogen- tients with adult periodontitis,J Periodontol 71:521, 2000.
esis of periodontal disease distinguishes them as viable targets Genco Rj: Current view of risk factors for periodontal diseases, J Periodontal
for a chemotherapeutic approach. The introduction of novel, 67:1041, 1996.
adjunctive therapies such as host modulation to enhance the Golub LM, Ciancio S, Ramamunhy NS, et al: Low-dose doxycycline therapy:
effect on gingival and crevicular fluid collagenase activity in humans, J Peri-
efficacy of existing mechanical procedures can contribute fa- odontal Res 25:321, 1990.
vorably to an integrated approach for the long-term, clinical Mariotti A: The extracellular matrix of the periodontium: dynamic and inter-
management of periodontitis. active tissues, Periodontal 2000 3:39, 1993.
HMTs are an emerging treatment concept in the manage- Novak MJ, Dawson DR III, Magnusson I, et al: Combining host modulation
and topical antimicrobial therapy in the management of moderate to se-
ment of periodontitis. The use of HMT as an adjunct may be vere periodontitis: a randomized multicenter trial, J Periodontal 79(1):33,
particularly useful in susceptible, high-risk patients in whom 2008.
a prolonged and excessive host response to the presence of Payne JB, Golub LM, Stoner JA, et al: The effect of subantimicrobial-dose-
bacteria promotes the activity of MMPs and osteoclasts. doxycycline periodontal therapy on serum biomarkers of systemic inflam-
SDD is the only systemically administered HMT currently mation: a randomized, double-masked, placebo-controlled clinical trial,
J Am Dent Assoc 142(3) 262, 2011.
approved and indicated as an adjunct to SRP for treating Preshaw PM: Host response modulation in periodontics, Peliodontol 2000
periodontitis. Clinical trials have demonstrated a clear treat- 48:92, 2008.
ment benefit when using SDD versus SRP alone. SDD should Ryan ME, Ramamurthy NS, Golub LM: Matrix metalloproteinases and their
be used as part of a comprehensive treatment strategy that inhibition in periodontal treatment, Curr Opin Periodontal 3:85, 1996.
Walker C, Preshaw PM, Novak J, et al: Long-term treatment with subantimi-
includes antibacterial treatments (SRP, plaque control, oral crobial dose doxycycline has no antibacterial effect on intestinal flora,] Clin
hygiene instruction, local antimicrobials, and periodontal sur- Periodontal 32 1163, 2005.
gery), host response modulation (SDD), and assessment and Williams RC: Periodontal disease, N Engl] Med 322(6):373, 1990.
Host Modulation Factors in Systemic linked to periodontal disease, such as CVD and diabetes. In
CVD, preliminary studies have indicated that individuals
Disorders with periodontal disease are almost twice as likely to have a
In susceptible patients demonstrating an excessive local fatal heart attack and three times as likely to have a stroke.
inflammatory response to the bacterial stimuli leading to MMPs and cytokines have been found to play a major role
periodontal disease, another consideration involves the loss in weakening the plaques formed with CVD, leading to rup-
of epithelial integrity in the periodontal pocket. This tissue ture and eventual thrombosis and infarction. In fact, Golub
response allows for bacterial penetration into the inflamed tis- et al suggested that tetracyclines could reduce the incidence
sues and eventual entry of the bacteria into the systemic circu- of acute myocardial infarction by blocking collagenase and
lation. Patients with untreated periodontitis have an increased stabilizing the collagen cap on the atheroscleromatous ar-
risk for transient bacteremias. Bacteremia and associated terial plaques. In diabetes, the same MMPs and cytokines
endotoxemia may incite the overproduction of destructive involved in the development of periodontitis as the sixth
proinflammatory mediators at distant sites in the periodon- long-term complication of diabetes also play a role in the
titis patient. Therefore, patients with periodontitis may be at development of other well-known complications of diabetes
greater risk for developing a number of systemic conditions such as nephropathy, angiopathy, retinopathy, and wound-
associated with a similar overactive host response to external healing problems. Modulation of these proinflammatory me-
stimuli such as cardiovascular disease and diabetic complica- diators in patients with diabetes may impede the develop-
tions. Elevated levels of cytokines, prostanoids, and enzymes ment of multiple long-term complications. An inhibitor of
are evident in all these conditions. MMPs, cytokines, and prostanoids used in the treatment of
In the era of periodontal medicine, systemic host modula- periodontitis may have an indirect effect on these disease
tory approaches need to be considered. As mentioned, host processes if a patient's risk for developing these disorders is
modulators used to manage periodontal disease, such as an increased by the presence of untreated periodontitis. HMT
MMP, cytokine, and prostanoid inhibitors, may have addi- may also directly aid in the treatment and prevention of CVD
tional beneficial effects on systemic diseases that have been and diabetic complications.
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40
Breath Malodor
M Quirynen • I Laleman • J Dadamio • S De Geest •
B Vandekerckhove • W Teughels • A Jain
Chapter Outline
Semantics and Classification Diagnosis of Malodor
Epidemiology Treatment of Oral Malodor
Etiology Conclusions
Fundamentals of Malodor Detection
Semantics and Classification and clinicians, and is still hardly covered in the medical
curricula. Halitosis can lead to personal discomfort and so-
Breath odor can be defined as the subjective perception after cial embarrassment and is still one of the biggest taboos of
smelling someone's breath. It can be pleasant, unpleasant, society. Almost $1 billion a year is spent in the United States
or even disturbing, if not repulsive. If unpleasant, the terms on deodorant-type mouth (oral) rinses, mints, and related
breath malodor, halitosis, bad breath, or fetor ex ore can be ap- over-the-counter products to manage bad breath. It would be
plied. These terms, however, are not synonymous with oral preferable to spend this money on a proper diagnosis and eti-
malodor. This term is restricted to halitosis with an origin in ologic care instead of short-term and even inefficient masking
the oral cavity. attempts.
There are three main categories of halitosis: genuine hali-
tosis, pseudo-halitosis, and halitophobia. Genuine halitosis is
the term that is used when the breath malodor really exists Etiology
and can be diagnosed organoleptically or by measurement of In the vast majority, breath malodor originates from the oral
the responsible compounds. A distinction should be made be- cavity. Gingivitis, periodontitis, and especially tongue coating
tween physiologic and a pathologic halitosis (Fig. 40 1) The are the predominant causative factors.
transient disturbing odor caused by food intake (eg, garlic, In general, one can identify two pathways for bad breath.
onions, and certain spices), smoking, or medication (eg, met- The first one involves an increase of certain metabolites in
ronidazole) do not reveal a health problem and are common the blood circulation (eg, due to a systemic disease), which
examples of physiologic halitosis. The same is true for "morn- will escape via the alveoli of the lungs during breathing
ing" bad breath as habitually experienced on awakening. This (blood-breath exchange) and it is commonly referred as
malodor is caused by a decreased salivary flow and increased "extraoral halitosis." The second pathway (intraoral halito-
putrefaction during the night and spontaneously disappears sis) involves an increase of either the bacterial load or the
after breakfast or after oral hygiene measures. A persistent amount of substrate for these bacteria at one of the lining
breath malodor, by definition, does reflect some pathology surfaces of the oropharyngeal cavity, the respiratory tract, or
(pathologic halitosis). The causes of this will be discussed lat- the esophagus. All types of infections, ulcerations, or tumors
er in the chapter. When an obvious breath malodor cannot be at one of the previously mentioned areas can thus lead to bad
perceived, but the patient is convinced that he or she suffers breath. Studies also suggest that oral malodor is associated
from it, this is called pseudo-halitosis. If the patient still believes with the total bacterial load of anaerobic bacteria in both
that there is bad breath after treatment of genuine halitosis saliva and tongue coating. The most commonly involved
or diagnosis of pseudo-halitosis, one considers halitophobia, bacteria are Porphyromonas gingivalis, Prevotella intermedia/
which is a recognized psychiatric condition. nigrescens, Aggregatibacter actinomycetemcomitans (previously
Actinobacillus actinomycetemcomitans), Campylobacter rec-
tus, Fusobacterium nucleatum, Peptostreptococcus micros, Tan-
Epidemiology nerella forsythia, Eubacterium spp, and spirochetes. A study
Breath malodor is a common complaint among the general conducted by Niles and Gaffar made clear that these Gram-
population. It has a significant socioeconomic impact, but negative species in particular cause an unpleasant smell by
unfortunately has been neglected until recently by scientists the production of sulfur compounds. However, because of
467
40 Breath Malodor 467.el
There are few studies that document the prevalence of oral Israeli groups, respectively, can be calculated when an organo-
malodor. Moreover, the studies that exist used different meth- leptic score of at least 2 is considered as being representative
odologies ranging from self-reported breath malodor to more for halitosis. With the same criterion, the calculated preva-
objective assessments such as the measurement of the volatile lence varied between 11.0 and 29.7% for the different age
sulfur compounds (VSCs). Since self-reported halitosis corre- groups in the Polish population. In conclusion, independent
lates weakly with objective measurements and tends to over- of the method used to assess oral malodor and independent of
estimate the problem, data should be interpreted carefully. the study population, the results point out that about one in
The incidence of halitosis remains poorly documented in four subjects suffer from persistent bad breath.
most countries. Large-scale studies have been performed for From large-scale inventories in multidisciplinary outpa-
the Japanese, Swedish, and Chinese populations. Smaller in- tient clinics for breath odor, no gender predominance seems
vestigations in Brazilian, Polish, and Israeli habitants have also to exist for bad breath although other studies indicate a higher
been reported. prevalence in women. It has also been observed that wom-
Despite the different approach of each study, if a VSC level en seek treatment more often than men. Age can range from
of 75 ppb (limit for social acceptance) is used as a threshold 5 years to more than 80 years. No association was found be-
for halitosis, the prevalence reported in the different popula- tween increased age and oral malodor. Most of the patients
tions can be calculated as 23% (late-morning group) and 20% had been complaining about breath malodor for several years
for the Japanese and Chinese studies, respectively. In line with before seeking proper advice (recent report of the department
this, prevalences of 27.5 and 29.8% for the Chinese and the involving 2000 patients).
A recent large-scale study including 2000 patients with that an intraoral condition is too easily considered as the cause
halitosis complaints showed that for those where bad breath while more important pathologies are overlooked. Indeed, for
could be objectively detected, the cause of it was mostly found a minority of patients ( 4% in the same recent study), extraoral
within the oral cavity (90%) Tongue coating (51 %), gingivi- causes could be identified, including ear-nose-throat (ENT)
tis/periodontitis (13%), or a combination (22%) accounted for pathologies, systemic diseases (eg, diabetes), metabolic or
the majority of the cases. Since a large part of the population hormonal changes, hepatic or renal insufficiency, bronchial
has a tongue coating or gingivitis/periodontitis, there is a risk and pulmonary diseases, or gastroenterologic pathologies.
Genuine halitosis L-cysteine

SH CH3
I I
~H, cystelne desullhydrase
Physiological halitosis Pathological halitosis
co + NH3 + H2S
CH-NH2 I
I COOH
COOH
Pyruvate
L-methionine
lntraoral halitosis Extraoral halitosis CH3
I CH3
s I
FIGURE 40.1 Genuine halitosis: classification.
I fH2
CH2 methionine y-lyase
I co + NH3 + CH3SH
CH, I
the large species diversity found in patients with halitosis, it I COOH
can be suggested that breath malodor is the result of com- fH-NH2
c,-ketobutyrate
plex interactions between several bacterial species. A recent COOH
study indicates that some Gram-positive microorganisms,

such as Streptococcus salivarius, also contribute to oral mal- Tryptophan to indole
odor production by deglycosylating salivary glycoproteins,
thus exposing their protein core to further degradation by
Gram-negative microorganisms.
Recently, the presence of Solobacterium moorei, a Gram-
O :JCH2-CHNH2-COOH
H
Tryptophanase
O:J H
• NH 3
• pyruvate
positive bacterium, has also been linked to oral malodor.
For oral malodor, the unpleasant smell of the breath main- L-lysine to cadaverine
ly originates from volatile sulphur compounds (VSCs), es-
pecially hydrogen sulfide (H2S), methylmercaptan (CH3SH), ~H2 Lysine dccarboxylasc ~H2
and (less significantly) dimethyl sulfide [(CH3)2S], as first fH2 ~Ho
discovered by Tonzetich. However, in certain conditions lfHoh lfH2l3 +CO,
(eg, when the saliva dries out on the mucosa! surfaces), fH·NH2 fH2
other compounds in mouth air may also play a role such as COOH NH,
diamines (eg, putrescine, cadaverine), indole, skatole, and
volatile organic acids like butyric or propionic acid. Most FIGURE 40.2 Proteolytic degradation by oral microorganisms of
four amino acids (two containing sulfur and two not containing sulfur)
of these compounds result from the proteolytic degradation
to malodorous compounds.
by oral microorganisms of peptides present in saliva (sulfur-
containing or nonsulfur-containing amino acids) (Fig. 40.2),
shed epithelium, food debris, gingival crevicular fluid (GCF),
interdental plaque, postnasal drip, and blood. In particular, consultation is thus preferably multidisciplinary, combining
Gram-negative, anaerobic bacteria possess such proteolytic the knowledge of a periodontologist or dentist, an ENT spe-
activity. cialist, an internist (if necessary), and a psychologist or psy-
For the extraoral causes of halitosis, other compounds chiatrist. In a recent study of 2000 patients, 16% were diag-
besides the VSCs may be involved. Bad-smelling metabo- nosed with pseudohalitosis or halitophobia.
lites can be formed/absorbed at any place in the body (eg,
the liver, the gut) and transported by the bloodstream to the lntraoral Causes
lungs. Exhalation of these volatiles in the alveolar air then
causes halitosis, at least when the concentrations of the bad- Tongue and Tongue Coating
smelling metabolites are sufficiently high. The crevicular fluid The dorsal tongue mucosa, with an area of 25 cm2, shows a
reflects the circulating molecules in the blood and can thus very irregular surface topography. The posterior part exhibits
also play a relevant role but due to the small amount probably a number of oval cryptolymphatic units, which roughen the
not a very dominant one. The extraoral causes are much more surface of this area. The anterior part is even rougher because
difficult to detect although they can sometimes be recognized of the high number of papillae: the filiform papillae with a
by a typical odor. Uncontrolled diabetes mellitus can be as- core of 0.5 mm in length, a central crater and uplifted bor-
sociated with a sweet odor of ketones, liver disease can be ders; the fungiform papillae, 0.5-0.8 mm in length; the foliate
revealed by a sulfur odor, and kidney failure can be character- papillae, located at the edge of the tongue, separated by deep
ized by a fishy odor because of the presence of dimethylamine folds; and the vallate papillae, 1 mm in height and 2-3 mm in
and trimethylamine. diameter. These innumerable depressions in the tongue sur-
In a special patient category, subjects imagine they have face are ideal niches for bacterial adhesion and growth, shel-
breath malodor; this is called imaginary breath odor or halito- tered from cleaning actions. Moreover, desquamated cells and
phobia. The latter has been associated with obsessive-compul- food remnants also remain trapped in these retention sites and
sive disorders and hypochondria. Well-established personality consequently can be putrefied by the bacteria. A fissurated
disorder questionnaires (eg, Symptom Checklist 90) allow the tongue (deep fissures on dorsum, also called scrotal tongue or
clinician to assess the patient's tendency for illusional breath lingua plicata) and a hairy tongue (lingua villosa) have an even
malodor. The presence of a psychologist or psychiatrist at rougher surface (Fig. 40 3)
the malodor consultation can be especially helpful for such The accumulation of food remnants intermingled with
patients. Due to the complexity of this pathology, a malodor exfoliated cells and bacteria forms a coating on the tongue
40 Breath Malodor 469
FIGURE 40.3 Different clinical pictures of heavily coated tongues.
dorsum. The latter cannot be easily removed because of the (IL-1) production by mononuclear cells, and cathepsin B pro-
retention offered by the irregular surface of the tongue dor- duction, thus further mediating connective tissue breakdown.
sum (Fig. 40.3). As such, the two factors essential for putre- It was also shown that human gingival fibroblasts developed
faction are united. Several investigators have identified the an affected cytoskeleton when exposed to methylmercaptan.
dorsal posterior surface of the tongue as the primary source of The same gas alters cell proliferation and migration. VSCs are
breath malodor. Indeed, high correlations have been reported also known to impede wound healing. Thus, when periodon-
between tongue coating and odor formation. tal surgery is planned, especially the insertion of implants, cli-
Both in healthy individuals and periodontitis patients with nicians should recognize this pathologic role of VSCs.
or without complaints of oral halitosis, a significant positive Some studies, however, have shown that when the pres-
correlation was found between the presence or amount of ence of tongue coating is taken into account, the correlation
tongue coating and levels of VSCs and/or organoleptic scores between periodontitis and oral malodor is much lower, indi-
of the mouth odor. In a group of 2000 patients visiting a mul- cating that tongue coating remains a key factor for halitosis.
tidisciplinary halitosis clinic, significant correlations were The prevalence of tongue coating is 6 times higher in patients
found between the organoleptic scores and tongue coating with periodontitis, and the same bacterial species associated
(R = 0.52; p < 0.001). In another study, it was also observed with periodontal disease can also be found in large numbers
that the amount of tongue coating was significantly greater in on the dorsum of the tongue, particularly when tongue coat-
the halitosis-positive group compared to the halitosis-negative ing is present. The reported association between periodontitis
group. and oral malodor may thus primarily be due to the effects of
Morita and Wang found that the volume of tongue coating periodontal disease on tongue coating and may explain why
and the percentile of sites with bleeding on probing were sig- other articles did not find a correlation.
nificantly associated with oral malodor. In 1992, Yaegaki and Other relevant malodorous pathologic manifestations of
Sanada demonstrated that, even in patients with periodontal the periodontium are pericoronitis (the soft tissue "cap" be-
disease, 60% of the VSCs were produced from the tongue ing retentive for microorganisms and debris), major recurrent
surface. oral ulcerations, herpetic gingivitis, and necrotizing gingivitis/
Recent research showed that the strongest determinant for periodontitis. Microbiologic observations indicate that ulcers
the presence of tongue coating is suboptimal oral hygiene. infected with Gram-negative anaerobes (ie, Prevotella and Por-
Other influencing factors were periodontal status, presence of phyromonas species) are significantly more malodorous than
a denture, smoking, and dietary habits. noninfected ulcers.
Periodontal Infections Dental Pathologies

A relationship between periodontitis and oral malodor has Possible causes within the dentition are deep carious lesions
been shown. However, not all patients with gingivitis and/or with food impaction and putrefaction, extraction wounds
periodontitis complain about bad breath, and there is some filled with a blood clot, and purulent discharge leading to
disagreement in the literature as to what extent oral malodor important putrefaction. The same applies to interdental food
and periodontal disease are related. Bacteria associated with impaction in large interdental areas and crowding of teeth
gingivitis and periodontitis are indeed able to produce VSCs. favor food entrapment and accumulation of debris. Acrylic
Several studies have shown that the VSC levels in the mouth dentures, especially when kept continuously in the mouth
correlate positively with the depth of periodontal pockets (the at night or not regularly cleaned, can also produce a typical
deeper the pocket, the more the bacteria, particularly anaero- smell. The denture surface facing the gingiva is porous and re-
bic species) and that the amount of VSCs in breath increases tentive for bacteria, yeasts, and debris, which are compounds
with the number, depth, and bleeding tendency of the peri- needed for putrefaction.
odontal pockets. It is important to realize that VSCs aggravate
the periodontitis process by, for example, increasing the per- Dry Mouth
meability of the pocket and mucosal epithelium and therefore Saliva has an important cleaning function in the oral cavity.
exposing the underlying connective tissues of the periodon- Patients with xerostomia often present with large amounts
tium to bacterial metabolites. Moreover, methylmercaptan of plaque on teeth and an extensive tongue coating. The in-
enhances interstitial collagenase production, interleukin-1 creased microbial load and the escape of VSCs when saliva is
drying up explain the strong breath malodor. Several studies dental history. This can be done with a questionnaire that the
link stress with VSC levels, but it is not clear whether this can patient fills out in the waiting room and/or orally at the be-
simply be explained by a reduction of salivary flow. Other ginning of the consultation, depending on the preferences of
causes of xerostomia are medication, alcohol abuse, Sjogren the examiner and the practical possibilities. To start with, the
syndrome (a common autoimmune rheumatic disease), and patient should be asked about the frequency of the halitosis
diabetes. (eg constantly, every day), the time of appearance during the
day (eg after meals can indicate a stomach hernia), when the
problem first appeared and whether others have identified the
Fundamentals of Ma/odor Detection
problem (to exclude imaginary breath odor). Also the medical
The breath of a person contains up to 150 different mole- history has to be recorded, with an emphasis on medication,
cules. The characteristics of the expired molecules determine and systemic diseases of the lungs, liver, kidneys, stomach,
whether we can smell them or not. Some gases can cause a and pancreas. Concerning the ENT history, attention should
striking odor at very low concentrations, whereas others need be paid to the presence of nasal obstruction, mouth breath-
to be present in much higher quantities. The perception of the ing, postnasal drip, allergy, tonsillitis, dysphagia, and previ-
molecules depends on the following factors: ous ENT encounters. The dental history includes questions
assessing the frequency of dental visits, the use of mouth
1. The odor itself (olfactory response) can be pleasant, unpleasant,
rinses, the presence and maintenance of a dental prosthesis,
or even repulsive.
and the frequency and the instruments used for tooth brush-
2. Each particular molecule has its specific concentration
ing, interdental cleaning, and tongue brushing and scraping.
before it can be detected (threshold concentration).
Finally, the patient is asked about his smoking, drinking, and
3. The odor power is the extent of concentration that is neces-
dietary habits.
sary to increase the odor score with one unit.
4. The volatility of the compound: Malodorous molecules
only express themselves when they become volatile. Clinical and Laboratory Examination
5. The substantivity: The capacity of the molecule to stay pres-
ent and thus to remain the cause of smell. Self-Examination
Smelling one's own breath by expiring in the hands kept in
Table 40.1 provides an overview of these essential char-
front of the mouth is not relevant because the nose gets used
acteristics for the key malodorous compounds, clearly high-
to the odor and the smell of the skin and soaps used for hand
lighting large interproduct variations. The odor power is the
washing may interfere. Moreover, studies have shown that
strongest for hydrogen sulfide and methylmercaptan; if the
self-assessment of oral malodor is notoriously unreliable and
concentration of these products increases 5 to 10-fold, the
one should be careful with the information obtained from the
odor will receive a higher organoleptic rating. For some other
patient. Conversely, it can be worthwhile to involve the pa-
compounds, increases of 25-100 times are needed to reach
tient in monitoring the results of therapy when an intraoral
a similar effect. Skatole and methylmercaptan are detected at
cause has been identified. For example, this can motivate the
the lowest concentrations (low threshold). The three sulfur
patient to continue the oral hygiene instructions. The follow-
molecules have the lowest volatility (ie, will escape the liquid
ing self-testing can be used:
phase first)
• Smelling a metallic or nonodorous plastic spoon after scrap-
ing the back of the tongue
Diagnosis of Ma/odor • Smelling a toothpick after introducing it in an interdental
area
Anamnesis
• Smelling saliva spit in a small cup or spoon (especially
Each consultation should start with a thorough questioning when allowed to dry for a few seconds so that putrefaction
about the breath malodor, eating habits, and medical and odors can escape from the liquid)
TABLE 40.1
ODOR THRESHOLD AND ODOR POWER OF KEY MALODOROUS

Odor Thresholds Odor Power Volatility (Henrys constants)
Greenman (X increase Volatility (Kee) in H20 at
Compounds Greenman (rnol/drrr') Devos (mol/drrr') to "up" score 1 unit) 20°c
Butyrate 2.3 X 10-10 2.4 X 10-10 10-fold 3.9 X 104

lsovalerate 1.8 X 10-11 2.5 X 10-11 42-fold 2.5 X 104
Skatole 7.2 X 10-13 1.0 X 10-12 8-fold 4.1 X 105
Trimethylamine 1.8 X 10-11 1.5 X 10-11 96-fold (low affinity) 2.0 X 102
Putrescine 9.1 X 10-10 1.0 X 10-9 27-fold 4.1 X 101
CH3SCH3 5.9 X 10-8 5.0 X 10-8 10-fold 1.7 X 101
H2S 6.4 X 10-10 5.0 X 10-10 4.8-fold zl.7 X 101
CH3SH 1.0 X 10-11 1.0 X 10-11 7.2-fold zl.7 X 101
CH3SH, Methylmercaptan; CH3SCH3, dimethylsulfide; H2S, hydrogen sulfide; K"' unit for Henrys Law constant.
'Devos M, Patte F, Roualt ], et al: Standardized human olfactory thresholds, Oxford, 1990, !RL Press at Oxford University Press.
Greenman], Duffield], Spencer P, et al: J Dent Res 83:81, 2004.
Extraoral Causes hepaticus, which has been mainly attributed to the accumula-
tion of dimethyl sulfide. Moreover, if the metabolizing func-
Ear-Nose-Throat tion of the liver fails, the concentration of certain metabolites,
During chronic or purulent tonsillitis, the deep crypts of the ton- normally processed in the liver, will increase and they will
sils accumulate debris and bacteria, especially periopathogens, enter the systemic circulation again and will be exhaled.
resulting in putrefaction. In the crypts, even calculus (eg, sub-
gingivally) can be formed (tonsilloliths or tonsil stones). Other Kidney
examples include acute pharyngitis (viral or bacterial) and post- Kidney insufficiency, primarily caused by chronic glomeru-
nasal drip. The latter is a rather common condition, which is lonephritis, will lead to an increase of the amines dimethyl-
perceived by patients as a liquid flow in the throat, originating amine and trimethylamine, which causes a typical fishy odor
from the nasal cavity. It is often associated with chronic sinusitis of the breath.
or regurgitation esophagitis in which the acidic content of the
stomach reaches the nasopharynx and causes mucositis. Ozena Systemic Metabolic Disorders
(caused by Klebsiella ozaenae) is a rare atrophic condition of the Uncontrolled diabetes mellitus results in the accumulation
nasal mucosa, with the appearance of crusts that causes a very of ketones, which have a sweet smell, like the odor of rotten
strong breath malodor. Finally, a foreign body in a nasal or sinus apples. Insulin resistance leads to an increase of triglycerides
cavity can cause local irritation, ulceration, and subsequent pu- and free fatty acids and ketones (such as acetone, acetoacetate,
trefaction (eg, children and mentally handicapped persons tend and hydroxybutyrate) are formed during lipolysis.
to put objects such as peas or wet paper in the nose).
Trimethylaminuria
Bronchi and Lungs Trimethylaminuria is a hereditary metabolic disorder that
Pulmonary causes include chronic bronchitis, bronchiecta- leads to a typical fishy odor of the breath, urine, sweat, and
sis (infection of standing mucus secretion in cystic dilations other bodily secretions. Trimethylaminuria is an enzymatic
through walls of bronchioles), pneumonia, pulmonary ab- defect that prevents the transformation of trimethylamine to
scesses, bronchial carcinoma, and carcinoma of the lung. The trimethylaminoxide, resulting in abnormal amounts of this
relevance of an early diagnosis is evident. molecule. The prevalence is unknown but approaches 1 % in
the United Kingdom.
Gastrointestinal Tract
In contrast to the common public opinion, even among Hormonal Causes
medical physicians, gastrointestinal pathologies are rarely At certain moments during the menstrual cycle, a typical
responsible for bad breath. The following pathologies might breath odor can develop; partners are often well aware of this
be responsible for less than 1 % of malodor cases: odor. Evidence also indicates that VSC levels in the expired air
are increased two- to fourfold around the day of ovulation and
• A Zenker diverticulum (a hernia in the esophageal wall, al-
in the perimenstrual period. Increases in VSCs are smaller in
lowing accumulation of food and debris and thus putrefac-
midfollicular phases.
tion) can cause a significant breath odor because it is not
In a study by Kleinberg and Codipilly, aqueous solutions of
separated from the oral cavity by any sphincter.
oral odoriferous volatiles were placed on the skin of the back
• A gastric diaphragmatic hernia (the fundus of the stomach
of the hand. Afterward, odor scores were given (organoleptic
protrudes through the diaphragm with relative sphincter
score, cfr. supra). The results are shown in Table 40.2. All me-
insufficiency, allowing gases to escape or contents to flow
tabolites caused an explicit odor, which decreased in intensity
back in the esophagus) can cause reflux of the gastric
over time. Some molecules disappeared very fast (eg, hydro-
contents up to the oropharynx. This is sometimes com-
gen sulfide and methylmercaptan), whereas others produced
bined with ructus in which air from the stomach suddenly
a bad smell for a longer period of time (eg, indole and skatole,
regurgitates.
for 10 min and longer).
• Regurgitation esophagitis (ulceration of the mucosa! lining
The olfactory response, rated by an organoleptic scale,
of the esophagus by acidic stomach contents flowing back
follows an exponential curve when correlated with the con-
because of an improper function of the sphincter).
centration of different gases. In other words, when the
• Intestinal gas production: Some gases (eg, dimethyl sulfide)
are absorbed but not metabolized by the intestinal endo-
thelium and thus transported by the blood. These gases can TABLE 40.2
then be exhaled through the lungs.
ODOR SCORES AT THE BACK OF THE HAND
There is some disagreement in the literature whether
Helicobacter pylori infection is associated with halitosis. In Start 1 min 3 min 10 min
a recent paper, H. pylori was shown to produce hydrogen Hydrogen sulfide 3 1 0 0
sulfide and methylmercaptan, which suggests that this mi- Methylmercaptan 3 1 0 0
croorganism can contribute to the development of halitosis. Acetic acid 3 4 0 0
Tangerman et al found no association between halitosis and Propionic acid 3 4 0 0
H. pylori infection. Butyric acid 4 4 2 2
Valerie acid 4 4 3 2
Liver Indole 4 4 4 2
Patients with various degrees of hepatocellular failure and/ Skatole 4 4 4 2
Putrescine 4 4 3 1
or portosystemic shunting of blood may acquire a sweet,
Cadaverine 4 4 2 1
musty, or even slightly fecal aroma of the breath, termed fetor
concentrations of the molecules were compared to their or- lotion, tooth paste, or mouthrinse; smoking; and the consump-
ganoleptic outcome, an optimal fit was only obtained when tion of alcohol or coffee are prohibited 12 h before the organo-
the concentrations of the gases were transformed to log val- leptic assessment is made. The patient should also not eat or
ues. The latter implies that all types of breath "measurements" drink on the morning of the organoleptic evaluation. The judge
[gas chromatography (GC), portable breath analyzers (eg, should not wear rubber gloves. Assessments should be repeated
Halimeter)] require log transformation to be comparable with because breath odor can fluctuate from day to day. The patient
organoleptic scores. should be encouraged to bring a confidant to the consultations
To obtain a reliable result, both the judge and patient need who can identify whether the perceived odor is the one previ-
to take a number of restrictions into account. Two days before ously noticed. Some of these guidelines are not only crucial for
the measurements they have to avoid the intake of spicy food, the organoleptic evaluation but also for a correct interpretation
garlic, and onions. The use of any fragrance, shampoo, body of the results obtained with certain breath analyzers (see later).
for barely noticeable odor, 2 for slight malodor, 3 for moder-

ate malodor, 4 for strong malodor, and 5 for severe malodor.
In this six-point system, 0 indicates a concentration of odor-
ant below a threshold, 1-4 are increasing occupancy of recep-
tor binding sites, and 5 is assumed to be close to saturation.
Before acting as a Judge, clinicians must ensure they do not
have anosmia (lost or impaired smelling capacity). A significant
fraction of the adult population has partial loss of smelling acuity
After age 60, a decline of smelling acuity is common. Candidate
odor judges should test their capacity to smell and recognize
different odors (qualitative assessment), as well as their capacity
to detect odors at low concentrations (quantitative assessment).
The first aspect can be checked by using, for example, a com-
mercially available test (Smell Identification Test, Sensonic) that
establishes a response curve based on the capacity to recognize
FIGURE 40.4 A, Miyazaki tongue coating index. Score O = none and discriminate among smells. After scratching an odorous sur-
visible, score 1 = less than one-third of the tongue dorsum covered, face in a booklet, several options of smells are proposed. If a sub-
score 2 = less than two-thirds, and score 3 = more than two-thirds; here ject lacks the capacity to recognize certain odors, it will reveal a
score 2 applies since less than two-thirds of the tongue dorsum is cov-
ered. B, Winkel tongue coating index. Divide the dorsum of the tongue
partial anosmia. The second aspect is tested by sniffing a series
is into six areas, that is, three in the posterior and three in the anterior of dilutions of substances such as isovaleric acid, phenethyl al-
part of the tongue. The tongue coating in each sextant is scored as O = no cohol, thiophene, and pyridine, which are inexpensive organic
coating, 1 = light coating, and 2 = severe coating. components. These are presented to the candidate judge as dilu-
tions, in one-log dilution steps, from 1 to 10-19_ Concentrations
• Licking the wrist and allowing it to dry (reflects the saliva of the odorous substances are presented in ascending order until
contribution to malodor) the subject detects the substance, then in descending order un-
til the person no longer detects it. This is the "psychophysical
Oropharyngeal Examination staircase method" for determination of the threshold level. The
threshold corresponds to the average between ascending and
The oropharyngeal examination includes inspection of deep descending levels. Clinicians can thus find out if their smelling
carious lesions, interdental food impaction, wounds, bleeding threshold level is acceptable. Abnormalities in the capacity to
of the gums, periodontal pockets, tongue coating, dry mouth, judge or perceive odors can be caused by a viral infection of the
and the tonsils and pharynx (for tonsillitis and pharyngitis). nasal cavities, a concussion, and smoking. Whereas an infection
The tongue coating can be scored with regard to the thick- can have a transient effect on olfactory performance, a concus-
ness and surface. Several methods have been proposed for the sion and smoking have permanent effects.
thickness, Gross and coworkers (1975) proposed an index,
ranging from 0 (=no coating) to 3 (=severe coating). Miyazaki Gas Chromatography
(Fig. 40.4A) assessed the tongue-coating status according to
the area: score 0 = none visible, score 1 = less than one-third A gas chromatograph can analyze air, saliva, or crevicular fluid
of the tongue dorsum covered, score 2 = less than two-third, (Fig. 40.8). About 100 compounds have been isolated from
and score 3 = more than two-third. the headspace of saliva and tongue coating, from ketones to
Winkel and coworkers considered both the extension alkanes, and sulfur-containing compounds to phenyl com-
and the thickness of the tongue coating. The dorsum of the pounds. In the expired air of a person, approximately 150
tongue is divided into six areas, that is, three in the posterior compounds can be found. The most important advantage of
and three in the anterior part of the tongue (Fig. 40.4B). The the technique is that when coupled with mass spectrometry, it
tongue coating in each sextant is scored as 0 = no coating,
1 = light coating, and 2 = severe coating. Score 1 is given when
the pink color underneath the coating is still visible; when this
is not the case a score 2 is given.
Attention should be paid to the morphology of the tongue.
For example, it should be noted if the tongue looks normal or
rough or has a deep sulcus or large papillae vallatae.
Organoleptic Rating
Even though devices are available, the organoleptic assess-
ment by a judge is still the gold standard in the examina-
tion of breath malodor. It is the easiest and most often used
method because it gives a reflection of the everyday situation
when halitosis is noticed. Moreover, the human nose can
smell 10,000 different odors. In an organoleptic evaluation, a
trained and preferably calibrated 'Judge" sniffs the expired air
FIGURE 40.8 Gas chromatography machinery, including thermal de-
and assesses whether it is unpleasant by using an intensity rat- sorber (TD) to release molecules trapped in special collectors); gas chro-
ing. Scoring is normally done according to the intensity scale matograph (CC) for separation of molecules; and mass spectrometer
of Rosenberg, where 0 represents absence of odor, 1 is given (MS) for identification of molecules.
The judge smells a series of different air samples (Fig. 40.5), Portable Volatile Sulfur Monitor
as follows:
The portable volatile sulfur monitor (Halimeter, lnterscan,
1. Breath odor: The subject expires through the mouth while Chatsworth, CA) is an electronic device that detects the pres-
the judge smells both at the beginning (rather oral) and ence of volatile sulfur compounds such as hydrogen sulfide and
at the end (rather extraoral) of the expiration. The first part methylmercaptan in breath. The instrument cannot discriminate
of the breath is derived from the mouth and dead-space among the different sulfur compounds. The sensitivity for meth-
aiwf the upper airways and nasopharynx, whereas the last ylmercaptan is 5 times lower than for hydrogen sulfide, and the
part is alveolar air from the lungs. device is almost insensitive to dimethyl sulfide. Moreover, etha-
2. Nasal breath odor: The subject expires through the nose, nol and other compounds can disturb the measurements.
keeping the mouth closed. When the nasal expiration is The mouth air is aspirated by inserting a drinking straw
malodorous, yet the air expired through the mouth is not, fixed on the flexible tube of the instrument (Fig. 40.6) The
a nasal/paranasal cause can be suspected. straw is kept inside the mouth, preferably above the poste-
3. Oral cavity odor: The subject opens the mouth and refrains rior part of the tongue dorsum, not touching the oral mucosa
from breathing while the judge places his or her nose close nor the tongue, while the subject keeps the mouth slightly
to the mouth opening (smelling the air while the patient open and breathes through the nose. The sulfur meter uses
counts from 1 to 20 reveals the same but favors oral mal- a voltametric sensor that generates a signal when exposed to
odor because drying of the palatal and tongue mucosa will sulfur-containing gases. Using a recorder or specific software,
occur, which promotes the expression of VSCs thus far a graphic presentation can be obtained, called a haligram
soluble in the salivary coating). (Fig. 40.7) that gives the response in function of the time.
4. Saliva: The patient is asked to lick his or her wrist. After The monitor needs regular calibration and replacement of the
drying, the judge gives a score. sensor biannually
5. Tongue coating: The judge smells a tongue scraping. This is The Halimeter is easy to use as a chairside test and is rela-
also presented to the patient or the confidant to evaluate tively inexpensive. Patients are usually less embarrassed, and
whether this smell is similar to the experienced malodor. the absence of odor in case of halitophobia can be more con-
Although the organoleptic assessment is still the gold vincingly proven than by an organoleptic assessment. Several
standard for diagnosis of halitosis, the method also has some studies have shown good correlations between the organolep-
important drawbacks. The assessment can, for example, be tic measurement and the Halimeter. An important drawback
influenced by several aspects such as the position of the head, of the device is that it detects only sulfur compounds and thus
hunger, and the experience of the judge. Odor judges are also is only useful for intraoral causes of halitosis. The absence of
supposed to rest their noses for several minutes between the VSCs does not prove that no breath odor is present.
tests to avoid habituation. The most important disadvantage A wide range of threshold limits for halitosis has been pro-
of the method, however, is that it clearly has a degree of sub- posed. Yaegaki and Sanade recommended a value of 75 ppb as
jectivity Researchers are trying to improve the reliability and the limit for social acceptance, whereas the Halimeters manu-
reproducibility of the organoleptic method. When using a facturer proposes 150 ppb. Following this recommendation,
panel of odor judges instead of one judge, the reliability is the sensitivity and specificity of the device toward the organo-
already considered to increase. Furthermore, the agreement leptic score has been calculated to be 63 and 98%, respective-
among judges may be improved by standardization of the ly Previous studies from our group showed that a reduction
sense of smell using an odor solution kit for measuring the in this threshold to 120 ppb improves the sensitivity of the
olfactory response. Training is also considered to reduce the device without detriment of their specificity. In patients with
odor judges' errors. oral malodor, VSCs concentrations easily reach 300-400 ppb.
FIGURE 40.5 A, Organoleptic assessment of the expired air. B, preferably, two calibrated experts will compare their scores at testing. C, Patient is
asked to lick her wrist. D, After allowing the wrist to dry, the clinicians organoleptically assess it to evaluate the volatiles originating from the saliva and
anterior part of the tongue. E, Inspection of the posterior part of the tongue and pharynx can reveal coating, ulcerations, or inflammation. F, A sample
of the coating is taken from the back of the tongue, which is pulled with a gauze pad. G, Clinician smells the air expired by the nose.
40 Breath Malodor 471.e3
FIGURE 40-6 The Halimeter, a portable sulfide monitor.
Halitosis - Record Printout Recorded: 07/14/2012 at 10:55
Patient Clinic
Name: Operator:
First name: Absolute max peak value: 498 ppbVSC
Date of birth: Average value of peaks: 0 ppbVSC
11 UUU_QPD l ,-
900 ppb -
800 QQb
1700 ppb
60_Q._£@_
498
500~ I
400 cob ,.
\ I
300 oob \ I
200 DPb l \ ~
100 ppb \ I\
0min
'- 2.5min
I '
5min 7.5min 10 min
FIGURE 40.7 Haligram.
to close their mouth for 30 s before sample collection and

afterward the sample is injected into the gas chromatograph.
The analysis starts automatically. There is a software packet
available, OralChroma Data Manager, which collects the data
from the OralChroma and graphically displays the sensor
responses on a computer screen. After 8 min, the process is
completed, and the concentration of the three gases will be
displayed in either ng/10 ml or ppb (nmol/mol) (Fig. 40 .10).
The accompanying software packet gives a clear overview
of the VSC measurement, but sometimes these graphics are
not correct because of a wrong assignment of the place of the
VSCs in the chromatogram. The latter can be corrected by
analyzing the chromatograph.
The OralChroma has the capacity to measure the concen-
tration of the three key sulfur compounds (hydrogen sulfide,
FIGURE 40.9 Portable gas chromatograph (GC). A small amount of methylmercaptan, and dimethyl sulfide) separately. This can
the breath sample, aspirated with a plastic syringe, is injected into the be helpful for a differential diagnosis. A high concentration of
input port of the GC. The computer displays the detection and amount
of the three importantVSCs (in ppb) within 8 min.
methylmercaptan compared to hydrogen sulfide indicates for
example periodontitis. If only hydrogen sulfide is increased,
there might be a problem with oral hygiene. Dimethyl sulfide
Elaborate gas chromatography is only available in special- can be present in case of some extraoral causes. Just like the
ized centers but is especially useful for identifying nonoral Halimeter, the OralChroma cannot detect other than sulfur
causes. It is expensive and needs trained personnel. compounds and some intraoral and extraoral causes can thus
A small, portable "gas chromatograph" (OralChroma, FIS be overlooked. The apparatus needs calibration and the sen-
Inc, Japan) has been introduced, which makes this technique sor and column need to be replaced every 2 years. Due to
available for periodontal clinics (Fig. 40.9). Sample collection software limitations, the use of the device as standalone unit is
occurs by use of a disposable syringe, which has to be inserted not recommended. Visual inspection of the chromatogram is
for two-thirds in the oral cavity of the patient. Patients have necessary to avoid erroneous results.
H~S
250
200
> 150
.s
:5 100
0.
:5
0
50
-50
0 30 60 90 120 150 180 210 240 270 300 330 360 390 420 450 480
FIGURE 40.10 Graphic from the OralChroma. The first peak indicates the level of hydrogen sulphide, the second of methylmercaptan, and the third
of dimethyl sulphide.
can detect virtually any compound when using adequate ma- Recently, a new colorimetric test offered the possibility of
terials and conditions. Moreover, it has a very high sensitivity assessing amines in saliva by means of a simple color scale. In
and specificity. a first clinical study, the test appeared to be able to distinguish
between volunteers with and without malodor. Besides the
Dark-Field or Phase-Contrast Microscopy correlation of the test results with the organoleptic rating, the
Oral malodor is typically associated with a higher incidence independent contribution to the odor of the amines in saliva
of motile organisms and spirochetes, so shifts in these pro- has been demonstrated.
portions allow monitoring of therapeutic progress. Another
advantage of direct microscopy is that the patient becomes
aware of bacteria being present in plaque, tongue coating, and Treatment of Oral Ma/odor
saliva. Too often, patients confuse plaque with food remnants. The treatment of oral malodor (thus with an intraoral ori-
gin) should preferably be cause-related. Since oral malodor is
Saliva Incubation Test
caused by the metabolic degradation of available proteins to
The analysis of the headspace earlier incubated saliva by gas malodorous gases by certain oral microorganisms, the follow-
chromatography reveals VSCs and other compounds such as ing general treatment strategies can be applied:
indole, skatole, lactic acid, methylamine, diphenylamine, cadaver-
ine, putrescine, urea, ammonia, dodecanol, and tetradecanol. By • masking the malodor
adding some proteins, such as lysine or cysteine, the produc- • mechanical reduction of intraoral nutrients (substrates) and
tion of respectively cadaverine or hydrogen sulfide is dramati- microorganisms
cally increased. Organoleptic evaluation (or assessment of the • chemical reduction of oral microbial load
VSCs) of the saliva headspace offers promising perspectives • rendering malodorous gases nonvolatile.
for monitoring treatment results. It is a less invasive test, es- Treatment should be centered on reducing the bacterial
pecially for the patient, than smelling breath in front of the load and micronutrients by effective mechanical oral hy-
oral cavity. giene procedures, including tongue scraping. Periodontal
Electronic Nose
disease should be treated and controlled, and as an auxiliary
aid, oral rinses containing chlorhexidine (CHX) and other
Electronic noses identify the specific components of an odor ingredients may further reduce the oral malodor. If breath
and analyze its chemical makeup. They consist of a mecha- malodor persists after these approaches, other sources of the
nism for chemical detection, such as an array of electronic malodor, such as the tonsils, lung disease, gastrointestinal
sensors, and a mechanism for pattern recognition. They are disease, and metabolic abnormalities (eg, diabetes), should
smaller, less expensive, and easier to use than, for example, be investigated.
gas chromatography, but can only be developed for specific
applications if the important metabolites are already known.
An artificial nose that has the same capacities as the human Masking the Malodor
nose would be ideal. Currently, although significant improve-
Treatments with rinses, mouth sprays, and lozenges contain-
ments still need to be made, the first trials thus far have been
ing volatiles with a pleasant odor have only a short-term ef-
promising.
fect. Typical examples are the mint-containing lozenges and
Chair-Side Test the aroma present in rinses without antibacterial components.
Another pathway is to increase the solubility of malodor-
A salivary chair-side test may be an alternative tool for the gen-
ous compounds in the saliva by increasing the secretion of
eral practitioner for diagnosing halitosis. Currently, several tests
saliva; a larger volume allows the retention of larger volumes
based on the detection of bacteria or metabolites involved in the
of soluble VSCs. The latter can also be achieved by ensuring
process of oral malodor are commercially available. All these
a proper liquid intake or by using a chewing gum; chewing
tests have reported acceptable correlation with the organo-
triggers the periodontal-parotid reflex, at least when the lower
leptic ratings and some of them even with the VSC level. The (pre)molars are still present.
BANA test is based on the ability of some bacterial species to
hydrolyze a synthetic trypsin substrate (N-benzoyl-DL-arginine-
2-naphthylamine). In this way, the test can detect three spe- Mechanical Reduction of lntraoral
cific bacteria: P gingivalis, Bacteroides forsythus, and Treponema Nutrients and Microorganisms
denticola related to periodontal disease. As already mentioned,
periodontitis is not the most common cause of oral malodor as Due to the extensive accumulation of bacteria on the dorsum
not all patients with periodontitis suffer from bad breath. of the tongue, tongue cleaning should be emphasized. Previ-
The P-galactosidase tests quantify, by means of chromo- ous investigations demonstrated that tongue cleaning reduces
genic substrates, bacterial enzymes involved in the initial both the amount of coating (and thus bacterial nutrients), as
degradation of oral mucin. P-galactosidase is one of the main well as the number of bacteria, and thereby improves oral
responsible enzymes for the removal of carbohydrate side malodor effectively. Other reports indicated that the reduction
chains, a limiting step of the proteolysis of glycoproteins. of the microbial load on the tongue after cleaning is negli-
It has been demonstrated that the presence of the enzyme gible and that the malodor reduction probably results from
accounts for the presence of oral malodor independently of the reduction of the bacterial nutrients.
the VSC level. The ninhydrin method is a colorimetric test Cleaning of the tongue can be carried out with a normal
to determine amino acids and low-molecular weight amines. toothbrush, but preferably with a tongue scraper if a coating
These compounds are, as VSC, final products of bacterial is established. Tongue cleaning using a tongue scraper reduces
proteolysis. the halitosis levels 75% after 1 week. This should be gentle
cleaning to prevent soft tissue damage. It is best to clean as far disadvantages, such as the increased tooth and tongue
backward as possible; the posterior portion of the tongue has staining, bad taste, and some temporary reduction in taste
the most coating. Tongue cleaning should be repeated until al- sensation.
most no coating material can be removed. Gagging reflexes of-
ten are elicited, especially when using brushes; practice helps Essential Oils
to prevent this. It can also be helpful to pull the tongue out Previous studies evaluated the short-term effect (3 h) of a Lis-
with a gauze pad. Tongue cleaning has the additional benefit terine rinse (which contains essential oils) compared with a
of improving taste sensation. placebo rinse. Listerine was found to be only moderately ef-
Interdental cleaning and toothbrushing are essential fective against oral malodor (±25% reduction vs 10% for pla-
mechanical means of dental plaque control. Both remove cebo of VSCs after 30 min) and caused a sustained reduction
residual food particles and organisms that cause putrefac- in the levels of odorigenic bacteria. Similar VSC reductions
tion. Clinical studies have shown that the mechanical ac- were found after rinsing for 4 days.
tion of toothbrushing alone has no appreciable influence on
the concentration of VSCs. In a short-term study, Tonzetich Chlorine Dioxide
showed a short-term effect in bad breath after brushing with Chlorine dioxide (ClO2) is a powerful oxidizing agent that can
a sodium monofluorophosphate (MFP) toothpaste. Howev- eliminate bad breath by oxidation of hydrogen sulfide, meth-
er, the effect was half of what was observed when combined ylmercaptan, and the amino acids, methionine, and cysteine.
with tongue brushing (73 and 30% reduction in VSCs, re- Studies demonstrated that a single use of a ClO2-containing
spectively). oral rinse slightly reduces mouth odor.
When chronic oral malodor arises as a consequence
of the presence of periodontitis, professional periodontal Two-Phase Oil-Water Rinse
therapy is needed. A one-stage, full-mouth disinfection, Rosenberg et al designed a two-phase oil-water rinse con-
combining scaling and root planing with the application taining CPC. The efficacy of oil-water-CPC formulations is
of chlorhexidine, reduced the organoleptic malodor levels thought to result from the adhesion of a high proportion of
up to 90%. In a recent study of the same authors, initial oral microorganisms to the oil droplets, which is further en-
periodontal therapy had only a weak impact on the VSC hanced by the CPC. A twice-daily rinse with this product (be-
levels, except when combined with a mouthrinse containing fore bedtime and in the morning) showed reductions in both
chlorhexidine. VSC levels and organoleptic ratings. These reductions were
Chewing gum may control bad breath temporarily be- superior to Listerine and significantly superior to a placebo.
cause it can stimulate salivary flow. The salivary flow itself
also has a mechanical cleaning capability. Not surprisingly, Triclosan
therefore, subjects with extremely low salivary flow rate
Triclosan, a broad-spectrum antibacterial agent, has been
have higher VSC ratings and tongue coating scores than
found to be effective against most oral bacteria and has a good
those with normal saliva production. Waler showed that
chewing a gum without any active ingredient can reduce compatibility with other compounds used for oral home care.
A pilot study demonstrated that an experimental mouth rinse
halitosis modestly.
containing 0.15% triclosan and 0.84% zinc produced a stron-
ger and more prolonged reduction in mouth odor than a Lis-
Chemical Reduction of Oral terine rinse. The anti-VSC effect of triclosan, however, seems
strongly dependent on the solubilizing agents. Flavoring oils
Microbial Load or anionic detergents and copolymers are added to increase
Together with toothbrushing, mouth rinsing has become a the oral retention and decrease the rate of release in tooth-
common oral hygiene practice. Formulations have been modi- pastes formulations containing triclosan. The effect of these
fied to carry antimicrobial and oxidizing agents with impact in formulations in oral malodor has been illustrated in several
the process of oral malodor formation. The active ingredients studies. Significant reduction of the breath scores was ob-
usually include antimicrobial agents such as chlorhexidine, served after a single use as well as after a week (28 and > 50%,
cetylpyridinium chloride (CPC), essential oils, chlorine diox- respectively), with a similar effect on the VSC levels (57% re-
ide, triclosan (TCN), amine fluoride and stannous fluoride, duction after 1 week use of the paste).
hydrogen peroxide, and baking soda. Some of these agents
have only a temporary effect on the total number of microor- Aminefluoride/Stannous Fluoride
ganisms in the oral cavity. The association of aminefluoride with stannous fluoride
(AmF/SnF2) resulted in encouraging reductions of morning
Chlorhexidine breath odor even when oral hygiene was insufficient. Recently,
Chlorhexidine is considered the most effective antiplaque and new evidence supporting the use of this AmF/SnF2 rinse be-
antigingivitis agent. Its antibacterial action can be explained came available. The formulation showed not only short-term
by disruption of the bacterial cell membrane by the chlorhexi- but also long-term effect on malodor indicators in patients
dine molecules, increasing its permeability and resulting in with obvious malodor.
cell lysis and death. Due to its strong antibacterial effects and Stannous fluoride also has shown to be effective in the
superior substantivity in the oral cavity, chlorhexidine rinsing management of oral malodor as component of a dentifrice
provides significant reduction in VSC levels and organoleptic reducing both organoleptic scores (OLS) and VSC levels. A
ratings. superior short-term and overnight benefit of a stannous-con-
Unfortunately, as mentioned in some trials, chlorhexi- taining dentifrice versus a control dentifrice on morning bad
dine at a concentration of 0.2% or greater also has some breath has been recently demonstrated in a metaanalysis.
Rosenberg et al showed that a 0.2% chlorhexidine regimen has been even more efficient than chlorhexidine alone, sug-
produced a 4 3% reduction in VSC values and > 50% reduc- gesting that the other compounds are also important. This is
tion in organoleptic mouth odor ratings. De Boever and Loe- explained by a synergistic effect between chlorhexidine and
sche reported that a 1-week rinsing with 0 .12 % chlorhexidine CPC on one hand and by the Zrr" on the other hand (see
gluconate, in combination with tooth and tongue brushing, following discussion). The latter was confirmed in a recent
significantly reduced VSC levels, mouth odor, and tongue randomized controlled trial (RCT) where amine fluoride/stan-
odor by 73, 69, and 78%, respectively. Morning halitosis was nous fluoride solution showed improved outcomes when zinc
reduced up to 90%. Halita (Dentaid, Spain), a solution (0 05% was added.
chlorhexidine, 0.05% CPC, 0.14% zinc lactate, no alcohol),
Hydrogen Peroxide reduction in VSC levels after 7 days use of a dentifrice contain-
Suarez et al reported that rinsing with 3% hydrogen perox- ing triclosan and a copolymer, but the benefit compared with
ide (H202) produced impressive reductions (±90%) in sulfur a placebo was relatively small (17% reduction). Similar reduc-
gases that persisted for 8 h. tions were also found in two other more recent studies.
Chewing gum can be formulated with antibacterial agents,
Oxidizing Lozenges such as fluoride or chlorhexidine, thus helping reduce oral
Greenstein et al reported that sucking a lozenge with oxidiz- malodor through both mechanical and chemical approaches.
ing properties reduces tongue dorsum malodor for 3 h. This Tsunoda et al investigated the beneficial effect of chewing
antimalodor effect may be caused by the activity of dehydro- gum containing tea extracts for its deodorizing mechanism.
ascorbic acid, which is generated by peroxide-mediated oxi- Epigallocatechin (EGCg) is the main deodorizing agent among
dation of ascorbate present in the lozenges. the tea catechins. The chemical reaction between EGCg and
CH3SH results in a nonvolatile product. Waler compared dif-
Baking Soda ferent concentrations of zinc in a chewing gum and found that
Baking soda dentifrices have been shown to confer a signifi- a 2-mg Zrr" acetate-containing chewing gum that remained
cant odor-reducing benefit for time periods up to 3 h. The in the mouth for 5 min resulted in an immediate reduction in
mechanisms by which baking soda produces its inhibition of the VSC levels of up to 45%, but the long-term effect was not
oral malodor is related to its bactericidal effects. mentioned.
Conversion of Volatile Sulfur Compounds Conclusions

Metal Salt Solutions Breath malodor has important socioeconomic consequences
Metal ions with affinity for sulfur are efficient in capturing and can reveal important diseases. A proper diagnosis and
the sulfur-containing gases. Zinc is an ion with two positive determination of the etiology allow initiation of the proper
charges (Zn'"), which will bind to the twice-negatively load- etiologic treatment. Although tongue coating and (less fre-
ed sulfur radicals, and thus can reduce the expression of the quently) periodontitis and gingivitis are by far the most com-
VSCs. The same applies for other metal ions such as stannous, mon causes of malodor, a clinician cannot take the risk of
mercury, and copper. Clinically, the VSC inhibitory effect was overlooking other, more challenging diseases. This can be
CuCl2 > SnF2 > ZnCl2. In vitro, the inhibitory effect was HgC done by a multidisciplinary consultation or, if this is not fea-
12 = CuCl2 = CdCl2 > ZnCl2 > SnF2 > SnCl2 > PbCl2. sible, a trial therapy to deal quickly with intraoral causes (eg,
Compared with other metal ions, Zn++ is relatively nontoxic the full-mouth one-stage disinfection, including the use of the
and noncumulative and gives no visible discoloration. Thus, proper mouthrinses, tongue scrapers, and toothpastes). For
Zrr" has been one of the most-studied ingredients for the con- more detailed information, the reader is encouraged to con-
trol of oral malodor. Schmidt and Tarbet already reported that sult van Steenberghe and recent review papers.
a rinse containing zinc chloride was remarkably more effective
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SECTION V
Section Outline
41 Phase II Periodontal Therapy 47 Resective Osseous Surgery
42 Periodontal and Periimplant Surgical 48 Periodontal Regeneration and
Anatomy Reconstructive Surgery
43 General Principles of Periodontal 49 Furcation Involvement and Treatment
Surgery 50 Periodontal Plastic and Esthetic
44 Gingival Surgical Techniques Surgery
45 The Periodontal Flap 51 Advances in Periodontal Surgical
46 Treatment of Gingival Enlargement Procedures (Microsurgery and Laser)
41
Phase II Periodontal Therapy
Chapter Outline
Objectives of the Surgical Phase Critical Zones in Pocket Surgery
Pocket Elimination Versus Pocket Indications for Periodontal Surgery
Maintenance Methods of Pocket Therapy
Reevaluation after Phase I Therapy
The World Workshop in Periodontics in 1989 outlined the Considering the above objectives periodontal surgical pro-
goals of periodontal therapy as summarized under cedures may broadly be grouped as follows (Box 41.1):
Immediate goal: To prevent arrest, control, or eliminate the 1. surgical pocket therapy for pocket reduction/eradication,
periodontal disease. including periodontal regeneration/new attachment;
Ideal goal: To promote healing through regeneration of the lost 2. plastic and esthetic surgical techniques;
form, function, and esthetics. 3. preprosthetic surgical procedures; and
Pragmatic goal: When the ideal goal is not achieved, the prag- 4. placement of implants and implant-related surgical
matic goal of the therapy would be to repair the damage procedures.
resulting from the disease.
Ultimate goal: Finally, the ultimate goal of the therapy is to Surgical Pocket Therapy
sustain the masticatory apparatus especially teeth or their
analogs in a state of health. Surgical pocket therapy can be directed toward (1) access sur-
gery to ensure the removal of irritants from the tooth surface
A majority of the patients are effectively managed by a or (2) elimination or reduction of the depth of the periodontal
comprehensive phase 1 therapy, which essentially consists pocket.
of nonsurgical procedures, such as scaling and root planing, The effectiveness of periodontal therapy is predicated on
optimal plaque control, occasional use of systemic and local success in the complete elimination of calculus, plaque, and
antimicrobials, and elimination of all plaque retention areas, diseased cementum from the tooth surface. Numerous inves-
including correction of faulty dentistry. However, some of the tigations have shown that the difficulty of this task increases
patients need surgical intervention for the following purposes: as the pocket becomes deeper. The presence of irregulari-
1. controlling or eliminating periodontal disease; ties on the root surface also increases the difficulty of the
2. regenerating lost tissues; procedure. As the pocket becomes deeper, the surface to be
3. correcting anatomic conditions that may favor periodontal scaled increases, more irregularities appears on the root sur-
disease, impair esthetics, or impede placement of the cor- face, and accessibility is impaired. The presence of furcations
rect prosthetic appliances; and will also create insurmountable problems for scaling the root
4. placing implants to replace lost teeth and improving the surface.
environment for their placement and function. These problems can be reduced by resecting or displacing
the soft-tissue wall of the pocket, thereby increasing the vis-
ibility and accessibility of the root surface. The flap approach
Objectives of the Surgical Phase and the gingivectomy technique attain this result.
The need to eliminate or reduce the depth of the pocket
The main objectives of surgical phase are:
is another important consideration. Pocket elimination con-
1. improvement of the prognosis of teeth and their replace- sists of reducing the depth of periodontal pockets to that of a
ments; physiologic sulcus to enable cleansing by the patient. By prop-
2. improvement of esthetics; er case selection, both resective techniques and regenerative
3. correction of anatomic and morphologic defects that may techniques can be used to accomplish this goal. The presence
favor plaque accumulation; of a pocket produces areas that are impossible for the patient
4. preparation the tissues to receive the dental implants; and to keep clean, which establishes the vicious cycle depicted in
5. placement of dental implants. Fig. 41.1.
477
Inactive Healed
P.erioi::lontal Surgery
POCKET REDUCTION SURGERY
Resective (gingivectomy, apically displaced flap, and
undisplaced flap, with or without osseous resection)
Regenerative (flaps with grafts and membranes)
CORRECTION OF ANATOMIC/MORPHOLOGIC DEFECTS
Plastic-surgery techniques to widen attached gingiva (free
gingival grafts and other techniques)
Esthetic surgery (root coverage and recreation of gingival
- -
papillae)
Preprosthetic techniques (crown lengthening, ridge
augmentation, and vestibular deepening)
Placement of dental implants, including techniques for
site development for implants (guided bone regeneration and
sinus grafts)
I !
Plaqu~
accumulation Gingival
~ innammation
Pocket
deepening
FIGURE 41.1 Accumulation of plaque leads to gingival inflammation

and pocket deepening, which in turn increases the area of plaque ac-
cumulation.
Restored
periodontium
FIGURE 41.2 Possible results of pocket therapy. An active pocket
Results of Pocket Therapy can become inactive and heal by means of a long junctional epithelium.
A periodontal pocket can be in an active state or a period Surgical pocket therapy can result in a healthy sulcus, with or without
gain of attachment. Improved gingival attachment promotes restoration
of inactivity or quiescence. In an active pocket, underlying of bone height, with reformation of periodontal ligament fibers and lay-
bone is being lost. It often can be diagnosed clinically by ers of cementum.
bleeding, either spontaneously or on probing. After Phase I
therapy, the inflammatory changes in the pocket wall sub-
sides, rendering the pocket inactive, and reducing its depth was localized or coronal to it. In the first case, there is no gain
(Fig. 41.2). The extent of this reduction depends on the of attachment and the area of the root that was previously
depth before treatment and the degree to which the depth the tooth wall of the pocket becomes exposed. This does not
is the result of the edematous and inflammatory component mean that the periodontal treatment has caused recession but
of the pocket wall. rather that it has uncovered the recession previously induced
Whether the pocket remains inactive depends on the depth, by the disease.
the individual characteristics of the plaque components, and The healthy sulcus can also be located coronal to the bot-
the host response. Recurrence of the initial activity is likely. tom of the preexisting pocket. This is conducive to a restored
Inactive pockets can sometimes heal with a longjunctional marginal periodontium; the result is a sulcus of normal depth
epithelium. However, this condition also may be unstable and with the gain of attachment. The creation of a healthy sulcus
the chance of recurrence and reformation of the original pock- and a restored periodontium entails a total restoration of the
et is always present because the epithelial union to the tooth status that existed before periodontal disease began, which is
is weak. However, one study in monkeys has shown that the the ideal result of treatment.
long junctional epithelial union may be as resistant to plaque
infection as a normal connective-tissue attachment. Pocket Elimination Versus Pocket
Studies have shown that inactive pockets can be main- Maintenance
tained for long periods with little loss of attachment by means
of frequent scaling and root-planing procedures. A more reli- Pocket elimination (depth reduction to gingival sulcus levels)
able and stable result is obtained, however, by transforming has traditionally been considered to be one of the main goals
the pocket into a healthy sulcus. The bottom of the healthy of periodontal therapy. It was considered vital because of the
sulcus can be located either where the bottom of the pocket need to improve accessibility to root surfaces for the therapist
41 Phase II Periodontal Therapy 479
during treatment and for the patient after healing. The prev- Reevaluation after Phase I Therapy
alent opinion is the presence of deep pockets after therapy
represents a greater risk of disease progression than shallow Longitudinal studies have noted that all patients should be
sites. Individual probing depths are not good predictors of treated initially with scaling and root planing and that a final
future clinical attachment loss. The absence of deep pockets decision on the need for periodontal surgery should be made
in treated patients, conversely, is an excellent predictor of a only after a thorough evaluation of the effects of Phase I thera-
stable periodontium. py. The assessment is generally made no less than 1-3 months
Longitudinal studies of different therapeutic modalities and sometimes, as much as 9 months after the completion of
over the last 30 years have given conflicting results. Some Phase I therapy. This reevaluation of the periodontal condition
studies have reported that meticulous scaling and root plan- should include reprobing the entire mouth. The presence of
ning at regular intervals, as part of maintenance visits, do ar- calculus, root caries, defective restorations, and signs of per-
rest the progression of the disease and the pockets become sistent inflammation should also be evaluated.
inactive as no bleeding on probing of the residual pockets oc-
curs in patients examined with a thin periodontal probe with-
out electing pain and exudation. Critical Zones in Pocket Surgery
However, the long-term sustainability of such a state is un- Criteria for the selection of one of the different surgical tech-
certain although one study in monkeys has shown that the niques for pocket therapy are based on clinical findings in the
long junctional epithelial union may be resistant to plaque soft-tissue pocket wall, tooth surface, underlying bone, and
infection as a normal connective attachment. attached gingiva.
These findings do not alter the indications for periodon-
tal surgery because the results are based on surgical expo-
sure of the root surfaces for thorough elimination of irritants. Zone 1: Soft-Tissue Pocket Wall
However, these findings emphasize the importance of the The clinician should determine the morphologic features,
maintenance phase and the close monitoring of both level of thickness, and topography of the soft-tissue pocket wall and
attachment and pocket depth, together with the other clini- persistence of inflammatory changes in the wall.
cal variables (bleeding, exudation, or tooth mobility). The
transformation of the initial deep, active pocket into a shallower,
inactive, and maintainable pocket requires some form of definitive Zone 2: Tooth Surface
pocket therapy and constant supervision thereafter. The clinician should identify the presence of deposits and al-
Pocket depth is an extremely useful and widely employed terations on the cementum surface and determine the acces-
clinical determinant, but it must be evaluated together with sibility of the root surface to instrumentation. Phase I therapy
the level of attachment and the presence of bleeding, exuda- should have solved many, if not all, of the problems on the
tion, and pain. The most important variable for evaluating tooth surface. Evaluation of the results of Phase I therapy
whether a pocket (or deep sulcus) is progressive is the level should determine the need for further therapy and the method
of attachment, which is measured in millimeters from the ce- to be used.
mentoenamel junction. The apical displacement of the level
of attachment places the tooth in jeopardy, not the increase in
pocket depth, which may be caused by coronal displacement Zone 3: Underlying Bone
of the gingival margin. The clinician should establish the shape and height of the al-
Pocket depth remains an important clinical variable that veolar bone next to the pocket wall through careful probing
contributes to decisions about treatment selection. Lindhe and clinical and radiographic examinations. Bony craters, hori-
et al compared the effect of root planing alone and with a zontal or angular bone losses, and other bone deformities are
modified-Widman flap on the resultant level of attachment important criteria in the selection of the treatment technique.
and in relation to the initial pocket depth. They reported that
scaling and root planing procedures induce loss of attachment
if performed in pockets shallower than 2.9 mm, whereas Zone 4: Attached Gingiva
gain of attachment occurs in deeper pockets. The modified- The clinician should consider the presence or absence of an
Widman flap induces loss of attachment if done in pockets adequate band of attached gingiva when selecting the pocket
shallower than 4.2 mm but results in a greater gain of attach- treatment method. Diagnostic techniques for mucogingival
ment than root planing in pockets deeper than 4.2 mm. The problems are described in Chapter 50. An inadequate at-
loss is a true loss of connective-tissue attachment, whereas tached gingiva may be caused by a high-frenum attachment,
the gain can be considered a false gain because of reduced marked gingival recession, or a deep pocket that reaches the
penetrability of connective tissues apical to the bottom of the level of the mucogingival junction. All these possible condi-
pocket after treatment. tions should be explored and their influence on pocket ther-
Furthermore, probing depths established after active thera- apy, determined.
py and healing (approximately 6 months after treatment) can
be maintained unchanged or reduced even further during a
maintenance period involving careful prophylaxis once every Indications for Periodontal Surgery
3 months.
The following findings may indicate the need for a surgical
Ramfjord et al showed that, regardless of the surgical tech-
phase of therapy.
nique used for pocket therapy, a certain pocket depth recurs.
The refore, maintenance of this depth without any further loss of 1. Persistent inflammation in areas with moderate to deep
attachment becomes the goal. pockets may require a surgical approach. In areas with
shallow pockets or normal sulci, persistent inflammation successfully solve the problems with the fewest undesirable
may point to the presence of a mucogingival problem that effects should be chosen. Clinicians who adhere to one technique
needs a surgical solution. to solve all problems do not use to the advantage of the patient,
2. Pockets on teeth in which a complete removal of root ir- the wide repertoire of techniques at their disposal.
ritants is not considered clinically possible may call for sur-
gery. This occurs frequently in molar and premolar areas. Approaches to Specific Pocket Problems
3. Areas with irregular bony contours, deep craters, and other
defects usually require surgical intervention. Therapy for Gingival Pockets
4. In cases of furcation involvement of grade II or Ill, a sur- Two factors are taken into consideration: (1) the character of
gical approach ensures the removal of irritants. Any nec- the pocket wall and (2) the accessibility of the pocket. The
essary root resection or hemisection also requires surgical pocket wall can be either edematous or fibrotic. Edematous
intervention. tissue shrinks after the elimination of local factors, there-
5. Intrabony pockets particularly on distal areas of molars, by reducing or totally eliminating pocket depth. Therefore
and pockets frequently complicated by mucogingival prob- scaling and root planing are the techniques of choice in
lems are usually unresponsive to nonsurgical methods. these cases.
6. Gingival overgrowths particularly caused by drugs, such Pockets with a fibrotic wall are not appreciably reduced in
as, phenytoin, cyclosporine, calcium-channel blockers depth after scaling and root planing; therefore they are elimi-
etc., are fibrotic and require surgical recontouring. nated surgically. Until recently, gingivectomy was the only
technique available; it solves the problem successfully, but in
cases of marked gingival enlargement (eg, severe phenytoin
Methods of Pocket Therapy enlargement), it may leave a large wound that goes through
The methods for pocket therapy can be classified under the a painful and prolonged healing process. In these patients,
following three main headings. a modified-flap technique can adequately solve the problem
with fewer postoperative problems.
1. New attachment/regenerative techniques with periodontal-
flap surgery. Therapy for Slight Periodontitis
2. Resective techniques, such as gingivectomy and respective In slight or incipient periodontitis, a small amount of bone
osseous surgery, were popular one time but are usually not loss occurs and pockets are shallow to moderate. In these pa-
preferred due to the shift in paradigm from resection to tients, the conservative approach with good oral hygiene will
conservation. generally suffice to control the disease. Incipient periodontitis
3. Removal of the tooth of the pocket by root resection or that recurs in previously treated sites may require a thorough
hemisection is again less often performed at present due to analysis of the causes for the recurrence. Occasionally, a surgi-
the superior success of dental implants. cal approach may be required to correct the problem.
Therapy for Moderate to Severe Periodontitis
Criteria for Method Selection in the Anterior Region
Scientific criteria to establish the indications for each tech- The anterior teeth are important esthetically; therefore the
nique are difficult to determine. Longitudinal studies follow- technique that causes the least amount of visual root exposure
ing a significant number of cases over a number of years, and should be considered. However, the importance of esthetics
standardizing multiple factors and many variables would be may be different for different patients and nonelimination of
needed. Clinical experience, however, has suggested the crite- the pocket may place the tooth in jeopardy. The final decision
ria for selecting the method to treat the pocket. The selection may have to be a compromise between health and esthetics,
of a technique for treatment of a particular periodontal lesion not attaining ideal results in either respect.
is based on the following considerations: Anterior teeth offer two main advantages to a conservative
approach: (1) they are all single rooted and easily accessible
1. characteristics of the pocket depth, relation to bone and
and (2) patient compliance and thoroughness in plaque con-
configuration;
trol are easier to attain. The refore, scaling and root planing are
2. accessibility to instrumentation, including presence of fur-
cation involvements; the techniques of choice for the anterior teeth.
Sometimes, however a surgical technique may be necessary
3. existence of mucogingival problems;
because of the need for improved accessibility for root plan-
4. response to phase I therapy;
ing or regenerative surgery of osseous defects. The papilla-
5. patient cooperation, including ability to perform effective
preservation flap can be used for both purposes and also offers
oral hygiene, smokers must be willing to stop their habit;
a better postoperative result, with less recession and reduced
6. age and general health of the patient;
soft-tissue crater formation interproximally.
7. overall diagnosis of the case: various types of gingival en-
When the teeth are too close interproximally, the papilla-
largement and types of periodontitis (eg, chronic marginal
preservation technique may not be feasible and a technique
periodontitis, localized aggressive periodontitis, and gen-
that splits the papilla must be used. The sulcular-incision flap
eralized aggressive periodontitis);
offers good esthetic results and is the next choice.
8. esthetic considerations; and
When esthetics is not the primary consideration, the
9. previous periodontal treatments.
modified-Widman flap can be chosen. This technique uses an
Each of these variables is analyzed in relation to the pocket internal bevel incision of about 1-2 mm from the gingival
therapy techniques available and a specific technique is se- margin without thinning the flap and may result in some mi-
lected. Of the many techniques, the one that would most nor recession.
41 Phase II Periodontal Therapy 481
Infrequently, bone contouring may be needed despite the interproximal areas better, where defects are frequently pres-
resultant root exposure. The technique of choice is the apically ent. Second and third choices are the sulcular flap and the modified-
displaced flap with bone contouring. Widman flap, maintaining as much of the papilla as possible.
When osseous defects with no possibility of reconstruc-
Therapy for Moderate to Severe Periodontitis tion are present, such as interdental craters, the technique of
in the Posterior Region choice is the flap with osseous contouring.
Treatment for premolars and molars usually poses no esthetic
problem but frequently involves difficult accessibility. Bone Surgical Techniques for Correction
defects occur more often in the posterior than the anterior of Morphologic Defects
sector and root morphologic features, particularly in relation The objectives and rationale for the techniques performed to
to furcations, may offer insurmountable problems for instru- correct morphologic defects (mucogingival, esthetic, and pre-
mentation in a close field. Therefore surgery is frequently in- prosthetic) are given in Chapter 50.
dicated in the posterior region.
The purpose of surgery in the posterior area is either en- Surgical Techniques for Implant Placement
hanced accessibility or the need for definitive pocket reduc- and Related Problems
tion requiring osseous surgery. Accessibility can be obtained The objectives and rationale for these techniques are described
by either the undisplaced or the apically displaced flap. in Chapter 58.
Most patients with moderate to severe periodontitis have However, it must be understood that the above guidelines
developed osseous defects that require some degree of osse- are broad in nature and differ from patient to patient. A good
ous remodeling or reconstructive procedures. When osseous clinician makes an astute judgment taking into consideration
defects amenable to reconstruction are present, the papilla- all the prevailing factors. Needless to emphasize that experi-
preservation flap is the technique of choice because it protects the ence is the key to success.
42
Periodontal and Periimplant
Surgical Anatomy
FA Carranza • PR Klokkevold • CD Dwarakanath
Chapter Outline
Mandible Muscles
Maxilla Anatomic Spaces
Exostoses
A sound knowledge of the anatomy of the periodontium and is often but not always visible on conventional radiographs.
the surrounding hard and soft structures is essential to deter- The opening of the mental foramen, which may be oval or
mine the scope and possibilities of periodontal and implant round in shape, typically faces upward and distally, with its
surgical procedures and to minimize their risks. The spatial posterosuperior border slanting gradually to the bone surface.
relationship of bones, muscles, blood vessels, and nerves as An "anterior loop" of the mental foramen has been described,
well as the anatomic spaces located in the vicinity of the peri- with the use of cadaver dissection, as a reverse turn and loop-
odontal or implant surgical field are particularly important. ing back of the mental nerve before its exit out of the mental
Only those features of periodontal and implant surgery rel- foramen; its length ranges from 0.5 to 5.0 mm. More recent
evance are mentioned in this chapter; the reader is referred to evaluation of the anterior loop of the mental nerve involving
books about oral anatomy for a more comprehensive descrip- the use of cone beam scans and cadaveric dissection reported
tion of these structures. this loop extension to range from 0.0 to 9.0 mm. The anterior
loop of the mental nerve has a high prevalence (88%), sym-
metric occurrence, and a mean length of 4.13 ± 1.08 mm. As
Mandible it emerges, the mental nerve divides into three branches. One
The mandible is a horseshoe-shaped bone connected to the branch of the nerve turns forward and downward to supply
skull by the temporomandibular Joints. It presents several the skin of the chin. The other two branches course anteriorly
landmarks of great surgical importance for both periodontal and upward to supply the skin and mucous membrane of the
and implant surgical procedures. lower lip and the mucosa of the labial alveolar surface.
The mandibular canal, which is occupied by the inferior al- Surgical trauma (eg, pressure, manipulation, postsurgi-
veolar nerve and vessels, begins at the mandibular foramen cal swelling) to the mental nerve can produce paresthesia of
on the medial surface of the mandibular ramus and curves the lip, which recovers slowly. Partial or complete cutting of
downward and forward until it becomes horizontal below the the nerve can result in permanent paresthesia, dysesthesia,
apices of the molars (Fig. 42.1). The distance from the canal to or both. Familiarity with the location and appearance of the
the apices of the molars is shorter in the third molar area and mental nerve reduces the likelihood of injury (Fig. 4 2.3).
increases as it goes forward. A small percentage (1 %) of man- In partially or totally edentulous jaws, the disappearance
dibular canals bifurcate in the body of the mandible, thereby of the alveolar portion of the mandible brings the mandibu-
resulting in two canals and two mental foramen. In the pre- lar canal and mental foramen closer to the superior border
molar area, the mandibular canal divides into two branches, (Figs. 42.4 and 42.5). When these patients reevaluated for the
with one exiting the mandible and the other continuing ante- placement of implants, the distance between the canal and
riorly: the incisive canal, which continues horizontally to the the superior surface of the bone as well as the location of the
midline, and the mental canal, which turns upward and opens mental foramen must be carefully determined to avoid surgi-
in the mental foramen. cal injury to the nerve (see Chapter 57).
The mental foramen, from which the mental nerve and ves- The anterior extension of the inferior alveolar nerve or in-
sels emerge, is located on the buccal surface of the mandible cisive nerve has been measured with the use of conventional
below the apices of the premolars, sometimes closer to the radiographs, computed tomography (CT) scans, cadaver
second premolar and usually halfway between the lower bor- dissections, and cone beam scans. This nerve, which is less
der of the mandible and the alveolar margin (Fig. 42 2). It evident on conventional radiographs and often unnoticed,
483
FIGURE 42.3 Mental nerve emerging from the foramen in the pre-
molar area.
FIGURE 42.1 Mandible, lingual surface view. Note the lingual or
mandibular foramen (blue arrow), where the inferior alveolar nerve en-
ters the mandibular canal, and the mylohyoid ridge (red arrows).
extends beyond the anterior loop of the mental foramen in
a horizontal direction toward the midline. The length of the
incisive canal has been reported to be up to 21.45 mm from
the mesial aspect of the mental foramen and to terminate just
4 mm from the midline.
The lingual nerve, along with the inferior alveolar nerve, is
a branch of the posterior division of the mandibular nerve. It
descends along the mandibular ramus medial to and in front
of the inferior alveolar nerve. The lingual nerve lies close to
the surface of the oral mucosa in the third molar area and goes
deeper as it travels forward (Fig. 42.6). It can be damaged dur-
ing anesthetic injections and during oral surgery procedures
(eg, third molar extractions). Less often, the lingual nerve may
be injured when a periodontal partial-thickness flap is raised
in the third molar region or when releasing incisions are made
in the area.
The alveolar process, which provides the supporting bone
to the teeth, has a narrower distal curvature than the body of
the mandible (Fig. 4 2. 7), thus creating a flat surface in the
FIGURE 42.2 Mandible, facial surface view. Note the location of the posterior area between the teeth and the anterior border of
mental foramen (blue arrow), which is slightly distal and apical to the the ramus. This results in the formation of the external oblique
apex of the second premolar, and the shelf-like area in the region of
ridge, which runs downward and forward to the region of the
the molars (red arrows) that is created by the external oblique ridge.
Note also the fenestration that is present in the second premolar (black second or first molar (Fig. 42.8) to create a shelf-like bony area.
arrow). Resective osseous therapy may be difficult or impossible in
FIGURE 42.4 Loss of the alveolar ridge in an edentulous patient brings the mental foramen and the inferior alveolar nerve canal closer to the
surface, which may lead to discomfort for the patient. A, Anterior view demonstrating a severe loss of vertical alveolar ridge height. B, Occlusal view
of the same patient demonstrating a loss of vestibular depth with alveolar bone loss.
42 Periodontal and Peri implant Surgical Anatomy 485
FIGURE 42.5 Panoramic radiograph of an edentulous patient with a

loss of alveolar bone height. This results in the mental foramen exiting FIGURE 42.8 Mandible; occlusal view of the ram us and molars. Note
the jaw at the superior aspect of the remaining bone (ridge crest), which the retromolar triangle area distal to the third molar (arrows).
is the denture-bearing surface. Pressure from the complete removable
denture over this area causes pain.
this area because of the amount of bone that must be removed
distally toward the ramus to achieve resection of a periodontal
osseous defect on the distal aspect of the mandibular second
or third molar.
Distal to the third molar, the external oblique ridge circum-
scribes the retromolar triangle (Fig. 42.8). This region is oc-
cupied by glandular and adipose tissue and covered by unat-
tached, nonkeratinized mucosa. If sufficient space exists distal
to the last molar, a band of attached gingiva may be present;
only in such a case can a distal flap procedure be performed
effectively.
The medial side of the body of the mandible is traversed
obliquely by the mylohyoid ridge, which starts close to the al-
veolar margin in the third molar area and continues anteriorly
in an apical direction, thereby increasing its distance from the
osseous margin as it travels forward (Fig. 42.9). The mylohy-
oid muscle inserts along this ridge and separates the sublingual
space, which is located above or more anteriorly and superi-
orly, from the submandibular space, which is located below or
FIGURE 42.6 Lingual view of the mandible showing the pathway of more posteriorly and inferiorly.
the lingual nerve (red), which goes near the gingiva in the third molar
area and then continues forward, going deeper and medially.
FIGURE 42.9 Lingual view of the mandible showing, A, the inferior

FIGURE 42.7 Occlusal view of the mandible. Note the shelf that is alveolar nerve entering the mandibular canal, B, the lingual nerve tra-
created in the facial molar areas by the external oblique ridge. Arrows versing near the lingual surface of the third molar, and, C, the attachment
show the attachment of the buccinator muscle. of the mylohyoid muscle inferiorly.
FIGURE 42.10 Occlusal view of the maxilla and the palatine bone. FIGURE 42.11 Occlusolateral view of the palate showing nerves
Note the opening of the incisive canal or the anterior palatine foramen (red) and vessels (blue) emerging from the greater palatine foramen
(red arrow) and the greater palatine foramen (blue arrows). and continuing anteriorly on the palate.
The area distal to the last molar, called the maxillary tuber-
Maxilla osity, consists of the posteroinferior angle of the infratemporal
The maxilla is a paired bone that is hollowed out by the maxil- surface of the maxilla. Medially it articulates with the pyra-
lary sinus and the nasal cavity. The maxilla has the following midal process of the palatine bone. It is covered by dense, fi-
four processes: brous connective tissue, and it contains the terminal branches
of the middle and posterior palatine nerves. Excision of the
• The alveolar process contains the sockets for and supports area for distal flap surgery may reach medially to the tensor
the maxillary teeth. palati muscle. The tensor palati muscle comes from the greater
• The palatine process extends horizontally from the alveolar wing of the sphenoid bone and ends in a tendon that forms
process to meet its counterpart from the opposite maxilla at the palatine aponeurosis, which expands, fanlike, to attach to
the midline intermaxillary suture, and it extends posteriorly the posterior border of the hard palate.
with the horizontal plate of the palatine bone to form the
hard palate.
• The zygomatic process extends laterally from the area above
the first molar and determines the depth of the vestibular
fornix on the lateral aspect of the maxilla.
• The frontal process extends in an ascending direction and ar-
ticulates with the frontal bone at the frontomaxillary suture.
The terminal branches of the nasopalatine nerve and ves-
sels pass through the incisive canal, which opens in the mid-
line anterior area of the palate (Fig. 42.10). The mucosa over-
lying the incisive canal presents a slight protuberance called
the incisive papilla. Vessels that emerge through the incisive
canal are of small caliber, and their surgical interference is of
little consequence.
The greater palatine foramen opens 3-4 mm anterior to the
posterior border of the hard palate (Fig. 42.11). The greater pal-
atine nerve and vessels emerge through this foramen and run
anteriorly in the submucosa of the palate, between the palatal
and alveolar processes (Fig. 42.12). Palatal flaps and donor sites
for gingival grafts should be carefully performed and selected to
avoid invading these areas, because profuse hemorrhage may
ensue, particularly if vessels are damaged at the palatine fora-
men. Vertical incisions in the molar region should be avoided.
The mucous membrane that covers the hard palate is
firmly attached to the underlying bone. The submucous
layer of the palate posterior to the first molars contains the
palatal glands, which are more compact in the soft palate
and which extend anteriorly, thereby filling the gap between FIGURE 42.12 Histologic frontal section of a human palate at the
the mucosa! connective tissue and the periosteum and pro- level of the first molar showing the location of the vessels and the
tecting the underlying vessels and nerve (Fig. 42.22). nerve surrounded by adipose and glandular tissue.
(A)
FIGURE 42.13 Location and anatomy of the maxillary sinus. A, Fron- FIGURE 42.14 Blood supply and innervation of the maxillary sinus.
tal view. B, Lateral view. A, Arterial blood supply. B, Innervation of the maxillary sinus.
The body of the maxilla is occupied by the maxillary sinus, The roots of the maxillary first and second molars are often
which is the largest of the paranasal sinuses. It is an air-filled close to the floor of the sinus. Less frequently, the roots of the
cavity located in the posterior maxilla superior to the teeth. premolars and third molars may protrude into the floor of
The lateral wall of the nasal cavity borders the sinus medially; the sinus. With increasing age, the maxillary sinus expands. It
it is bordered superiorly by the floor of the orbit and laterally becomes more and more pneumatized down around the roots
by the lateral wall of the maxilla, the alveolar process, and the of the maxillary teeth, sometimes resulting in exposure of the
zygomatic arch (Fig. 42.13). It is pyramidal in shape, with its roots through the bony floor into the sinus, with only the thin
apex in the zygomatic arch and its base at the lateral wall of mucosa! membrane covering the root surface. The ability to
the nasal cavity The size of the maxillary sinus varies from perform periodontal osseous surgery in the posterior maxilla
one individual to another (depending on the individual and may be limited when the sinuses are severely pneumatized.
his or her age) and from very small and narrow to quite large Blood supply to the maxillary sinus arises from the supe-
and expansive. rior alveolar (anterior, middle, and posterior) branches of the
The maxillary sinus is frequently subdivided (incompletely) maxillary artery (Fig. 4 2 .14, A) The maxillary artery, which
into recesses by one or more septa. Maxillary sinus septa vary is a large terminal branch of the external carotid artery, gives
in size and location. Clinical and radiographic examinations off many branches to supply the maxillary sinus, including
suggest that septa are frequently present (.:S:39% of sinuses). the infraorbital artery, which travels superiorly and anteriorly
CT scans are the preferred method for detecting septa, be- and gives off the anterior superior alveolar artery Branches
cause panoramic radiographs are not reliable (ie, 26.5% false of the greater palatine artery contribute to a lesser extent.
diagnosis of the presence or absence of septa). Septa are found Venous blood drains via the pterygoid plexus. Much of the
in the anterior (24%), middle (41 %), and posterior (35%) as- vasculature travels through channels in the bony walls of the
pects of the maxillary sinus, with the most common location maxillary sinus, with many branches anastomosing with the
being between the second premolar and the first molar. The highly vascularized Schneiderian membrane. Innervation of
height of septa vary as well, ranging from Oto 20.6 mm. Only the maxillary sinus is supplied by the superior alveolar (an-
0.5% of septa form a complete separation of the sinus spaces terior, middle, and posterior) nerves and the branches of the
into separate chambers. maxillary nerve (Fig. 42.14, B).
The entire maxillary sinus is lined with a thin mucosa! Knowledge of the arterial blood supply is particularly im-
membrane called the Schneiderian membrane. This special- portant when considering a lateral window approach to sinus
ized structure of the respiratory mucous membrane, with its floor elevation and bone augmentation. Solar and coworkers
motile cilia and rich blood supply, is well adapted to purify- found an intraosseous branch of the posterior superior alveo-
ing, moistening, and warming air to protect the lungs. The lar artery anastomosing with the infraorbital artery in 100%
entrance to the maxillary sinus, through the orifice or maxil- of their human cadaver specimens (134 sinuses, all males).
lary duct, is located at the superior medial aspect of the cav- On average, the vessel was located 18.9 mm from the alveolar
ity The orifice is relatively small, measuring only 3-6 mm crest. By studying 50 CT scans from 625 patients (both males
in length and diameter. An accessory opening is occasionally and females) who were undergoing sinus bone augmentation,
found inferior and posterior to the main opening. The maxil- Elian and colleagues found that the vessel was radiographi-
lary sinus drains into the middle meatus of the nasal cavity cally evident in 52.9% of sinuses. The vessel was located on
through the maxillary duct, which passes secretions median average of 16.4 mm from the alveolar crest, which is con-
ally to the semilunar hiatus. Normal amounts of secretion sistent with the previous study Human cadaver dissection and
are moved from the sinus by the spiral pattern of the beating CT scan evaluations of the vessels running through the lateral
cilia that surround the orifice. If the maxillary sinus becomes wall of the maxillary sinus have revealed that intraosseous
infected or chronically inflamed, swelling of the mucosa vessels are present in the lower two-third of the anterolateral
around the orifice impairs drainage. The floor of the maxil- wall in approximately 10.5% of cases (Fig. 42.15). In 57.1 %
lary sinus extends down below the level of the nasal cavity of cases (about 6% of all sinuses), the vessel diameter ranged
into the alveolar process. in size from 1 to 2.5 mm. The location of the artery in relation
FIGURE 42.15 A, Cross-sectional image from a cone beam computed tomography scan of the maxillary sinus demonstrating the presence of an
intraosseous vessel in the lateral wall approximately 20 mm from the alveolar crest. B, Sagittal section through the maxillary sinus in the same patient
demonstrating an intraosseous vessel extending along the maxillary sinus. The diameter of the intraosseous canal is 2 mm.
(Fig. 4 2 .17). Adequate determination of the extension of the

maxillary sinus into the surgical site is important to avoid
creating an oroantral communication, particularly in relation
to osseous reduction in periodontal surgery or the placement
of implants in edentulous areas. Determining the amount
of available bone in the anterior area, below the floor of the
nasal cavity, is also critical for the placement of implants (see
Chapter 57)
Exostoses
FIGURE 42.16 Radiograph of the maxillary molars and premolars,
Both the maxilla and the mandible may have exostoses or tori,
with the maxillary sinus apparently near the apices. which are considered to be within the normal range of ana-
tomic variation. Sometimes these structures may hinder the
removal of plaque by the patient and may have to be removed
to the position of the lateral window for sinus augmentation to improve the prognosis of neighboring teeth. Additional in-
presents a risk for bleeding complications in 10-20% of cases. dications for the removal of exostoses include the inability to
The inferior wall of the maxillary sinus is frequently comfortably wear removable prostheses over these areas. The
separated from the apices and roots of the maxillary poste- most common location of a mandibular torus is in the lingual
rior teeth by a thin, bony plate (Fig. 42.16) In edentulous area of the canines and the premolars, above the mylohyoid
posterior areas, the maxillary sinus bony wall may be only a muscle (Fig. 4 2 .18). Mandibular tori can also be found on
thin plate that is in intimate contact with the alveolar mucosa the buccal and labial surfaces of the mandibular teeth. Maxil-
lary tori are usually located in the midline of the hard palate
(Fig. 4 2 .19). Smaller tori may be seen over the palatal roots
of the maxillary molars, in the area above the greater palatine
foramen (Fig. 42.19), or on the buccal and labial surfaces of
the maxillary teeth (Fig. 42.20).
Muscles
Several muscles may be encountered when performing peri-
odontal and implant flap surgery, particularly during muco-
gingival surgery and bone augmentation procedures. These
are the mentalis, the incisivus labii inferioris, the depressor la-
bii inferioris, the depressor anguli oris (triangularis), the inci-
FIGURE 42.17 Radiograph of an edentulous molar maxillary area
sivus labii superioris, and the buccinator muscles. Their bony
demonstrating severe pneumatization of the maxillary sinus. There is attachments are shown in Fig. 42.21. These muscles provide
only a thin layer of cortical bone separating the sinus from the oral cavity. mobility to the lips and cheeks.
FIGURE 42.18 A, Clinical photograph of large mandibular tori on the lingual aspect of both the right and left mandible. B, Cross-sectional image of
a mandibular torus in the premolar area in the same patient.
FIGURE 42.20 Clinical photograph of large buccal exostosis in the

maxillary arch. There is also a large midline palatal torus.
FIGURE 42.19 A, Clinical photograph of large palatal torus located

in the midline of the palate. Notice the large tori on the palatal aspects
of the maxillary alveolar ridge as well. B, Cross-sectional image of the
maxillary midline torus in the same patient. Notice the torus located on
the palatal aspect of the alveolar ridge as well.
Anatomic Spaces
Several anatomic spaces or compartments are found close to the
operative field of periodontal and implant surgery sites. These
spaces contain loose connective tissue, but they can be easily
distended by hemorrhage, inflammatory fluid, and infection. FIGURE 42.21 Muscle attachments that may be encountered in mu-
Surgical invasion of these areas may result in dangerous cogingival surgery. I, Nasalis; 2, levator anguli oris; 3, buccinator; 4,
hemorrhage (intraoperative) or infections (postoperative) and depressor anguli oris; 5, depressor labii inferioris; 6, mental is.
-~~~--- Greater palatine vessels

and nerve
•• .,,,,. , .•• , Palatal glands
F· ~ 1~ jf /
, _ \ \ , ,:, l /
Lingual nerve
Mandibul~r canal
~ .>--'51 ,,•~):.•• / / Subrnandibular gland
'.)-.../f
~~ •.../_,.__ ( \ ·i/,i" J/ Hypoglossal nerve
. .,,,, ,, _ .._ '- 1r . . .__,,,
,_ 1 Mylohyoid muscle
,- , ~/' Digastric muscle

_. ~ Platysma muscle
Sublingual space
_ Submandibular space
FIGURE 42.22 Diagram of a frontal section of the human head at the level of the first molars depicting the most important structures in relation
to periodontal surgery. Note the location of the sublingual space, the submandibular space, and the greater palatine nerve and vessels.
should be carefully avoided. Some of these spaces are briefly and by the hypoglossal nerve (Fig. 42.22). Its boundaries are
described in the following paragraphs. For more information, the geniohyoid and genioglossus muscles medially, the lingual
the reader is referred to other sources. surface of the mandible below, and the mylohyoid muscle lat-
The canine fossa contains varying amounts of connective erally and anteriorly (Fig. 42.23). Infection of this area raises
tissue and fat. It is bounded superiorly by the quadratus la- the floor of the mouth and displaces the tongue, which results
bii superioris muscle, anteriorly by the orbicularis oris, and in pain and difficulty swallowing but little facial swelling.
posteriorly by the buccinator. Infection of this area results in The submental space is found between the mylohyoid
swelling of the upper lip, which obliterates the nasolabial fold, muscle superiorly and the platysma inferiorly. It is bounded
and of the upper and lower eyelids, which closes the eye. laterally by the mandible and posteriorly by the hyoid bone.
The buccal space is located between the buccinator and
the masseter muscles. Infection of this area results in swell-
ing of the cheek that may extend to the temporal space or
the submandibular space, with which the buccal space com-
municates.
The mental or mentalis space is located in the region of the
mental symphysis, where the mental muscle, the depressor
muscle of the lower lip, and the depressor muscle of the cor-
ner of the mouth are attached. Infection of this area results in
large swelling of the chin that extends downward.
The masticator space contains the masseter muscle, the
pterygoid muscles, the tendon of insertion of the temporalis
muscle, the mandibular ramus, and the posterior part of the
body of the mandible. Infection of this area results in swelling
of the face and severe trismus and pain. If the abscess occupies
the deepest part of this compartment, facial swelling may not
be obvious, but the patient may complain of pain and trismus.
Patients may also have difficulty and discomfort when moving
the tongue and swallowing.
The sublingual space is located below the oral mucosa in the FIGURE 42.23 Posterior view of the mandible showing, A, the at-
tachment of the mylohyoid muscles; 8, the geniohyoid muscles; C, the
anterior part of the floor of the mouth. It contains the sub- sublingual gland; 0, the submandibular gland, which extends below
lingual gland and its excretory duct, the submandibular or and also to some extent above the mylohyoid muscle; E, the sublingual
Wharton's duct; it is traversed by the lingual nerves and vessels nerve; and F, the inferior alveolar nerve.
It is traversed by the anterior belly of the digastric muscle. that may extend to the sublingual and submental spaces. It re-
Infections of this area arise from the region of the mandib- sults in the hardening of the floor of the mouth, and it may lead
ular anterior teeth and result in swelling of the submental to asphyxiation from edema of the neck and glottis. Although
region; infections become more dangerous as they proceed the bacteriology of these infections has not been completely
posteriorly. determined, they are presumed to be mixed infections with an
The submandibular space is found external to the sublin- important anaerobic component.
gual space, below the mylohyoid and hyoglossus muscles
(Figs. 42.22 and 42 23) This space contains the subman-
dibular gland, which extends partially above the mylohyoid SUGGESTED READINGS
muscle, thereby communicating with the sublingual space and Clarke MA, Bueltmann KW: Anatomical considerations in periodontal sur-
numerous lymph nodes. Infections of this area originate in the gery,] Peliodontol 42:610, 1971.
Dixon AD: Anatomy for students of dentistry, ed 5, New York, 1986, Churchill
molar or premolar area and result in swelling that obliterates Livingstone.
the submandibular line and in pain with swallowing. Ludwigs Dubrul El: Sicher and Dubrul's oral anatomy, cd 8, St Louis, 1988, Ishiyaku
angina is a severe form of infection of the submandibular space Euroarnerica.
43
General Principles
of Periodontal Surgery
PR Klokkevold • H H Takei • FA Carranza • CD Dwarakanath
Chapter Outline
Outpatient Surgery Indications
Hospital Periodontal Surgery Conclusions
Successful outcome of any surgical procedure depends on Informed Consent

careful planning. The surgeon must have a clear under- The patient should be informed at the initial visit about the di-
standing of the procedure that is going to be performed, agnosis, prognosis, and different possible treatments for his or
the equipment and instruments required, management of her condition, with the expected results and all pros and cons
any complications that may arise during or after the surgery. of each approach discussed as well. At the time of surgery, the
A checklist inclusive of all the factors should be followed patient should again be informed, verbally and in writing, of
strictly. the procedure to be performed, and he or she should indicate
The patient should be adequately prepared medically, psy- his or her agreement to undergo the procedure by signing the
chologically, and practically for all aspects of the intervention. consent form.
This chapter covers the preparation of the patient and the gen-
eral considerations that are common to all periodontal surgi- Premedication
cal techniques. Complications that may occur during or after For patients who are not medically compromised, the value
surgery are also discussed. of administering antibiotics routinely for periodontal surgery
Periodontal surgical procedures are usually performed in a has not been clearly demonstrated. Evidence of prophylactic
dental clinic and the patient is discharged immediately after. antibiotics before bone grafting, guided tissue regeneration, or
However, some patients and procedures may require hospital implant placement is incomplete. Some studies have reported
surgery. This will be described later in this chapter. reduced postoperative complications, including reduced pain
and swelling, when antibiotics are given before periodontal
Outpatient Surgery surgery and continued for 4-7 days after surgery. It is left to
the discretion of the clinician whether to administer antibi-
Patient Preparation otics for a particular patient or not. For those patients who
are medically compromised the prescribed protocol should be
Reevaluation After Phase I Therapy followed (see Chapter 30).
Initial therapy which basically consists of plaque control, scal- Similarly the benefits of administration of nonsteroidal an-
ing and root planing, and elimination of other local factors tiinflammatory drug ibuprofen 600-800 mg 1 h before sur-
including faulty dentistry is mandatory before any surgical gical procedure has not been fully established. However, the
procedure unless it is an emergency situation like drainage of use of preprocedural mouth rinse with 0.12 chlorhexidine has
periodontal or pericoronal abscess. been found to be very useful.
These procedures do the following: (1) eliminate some le-
sions entirely; (2) render the tissues more firm in consistency, Medical Evaluation
thereby allowing for a more accurate and delicate surgery; The patient's medical history should once again be reviewed
and (3) acquaint the patient with the office, the operator, and and any precautions required should be taken. Further, the
his or her assistants, create better rapport thus reducing the surgeon should ensure that on the day of the surgery the
patient's apprehension and fear. patient is not suffering from problems such as severe cold,
The reevaluation is normally done 4-8 weeks after the ini- cough, fever, etc., as these will not allow the surgeon to per-
tial therapy and consists of reprobing and reexamining all the form procedures freely. The patient should have had a relaxed
pertinent findings that previously indicated the need for the night's sleep on the previous day and eaten breakfast/lunch as
surgical procedure. applicable.
493
For the patient who is a smoker it is recommended that Thorough Debridement

smoking should be stopped for at least 3-4 weeks after sur-
gery if not completely. Although scaling and root planing have been performed pre-
viously as a part of Phase I therapy, all exposed root surfaces
should be carefully explored and planed as needed during
Emergency Equipment and Drugs surgery. In particular, areas of difficult access (eg, furcations,
The operator, all assistants, and office personnel should be deep pockets) often have rough areas or even calculus that
trained to handle all possible emergencies that may arise. was undetected during the preparatory sessions. The assistant
Drugs and equipment for emergency use should be readily who is retracting the tissues and using the aspirator should
available at all times. The nursing assistant should constantly also check for the presence of calculus and the smoothness
check the expiry date of these medicines. of each surface from a different angle. Similarly all unhealthy
Clinicians and assistants should have also undergone train- granulation tissue should be removed. It is better if the clini-
ing to deal with emergencies like syncope, shock, anaphylaxis, cian has separate sets of Gracey curettes for root planing and
and should be well versed with basic life support (BLS) and soft tissue manipulation.
cardiopulmonary resuscitation ( CPR) procedures.
Management of Bleeding During Surgery
Measures to Prevent Transmission Hemostasis is an important aspect of periodontal surgery, be-
of Infection cause good intraoperative control of bleeding permits an accu-
rate visualization of the extent of disease, the pattern of bone
The most optimal surgical protocol regarding asepsis and in- destruction, and the anatomy and condition of the root sur-
fection control should be strictly followed. faces. It provides the operator with a clear view of the surgical
site, which is essential for wound debridement and scaling
Anesthesia and Sedation and root planing. In addition, good hemostasis also prevents
the excessive loss of blood into the mouth, oropharynx, and
Periodontal surgery should be painless for the patient. He or stomach.
she should be assured of this at the outset and throughout
Periodontal surgery can produce profuse bleeding, espe-
the procedure. The most reliable means of providing painless cially during the initial incisions and flap reflection. After
surgery is the effective administration of local anesthesia. The flap reflection and the removal of granulation tissue, bleeding
area to be treated should be thoroughly anesthetized by means disappears or is considerably reduced. Typically, the control
of regional block and local infiltration. Injections directly into of intraoperative bleeding can be managed with aspiration.
the interdental papillae may also be helpful. Occasionally, for Continuous suctioning of the surgical site with an aspirator
prolonged surgeries a long-acting local anesthetic like bupiva-
is indispensable when performing periodontal surgery. Ex-
caine may be useful. cessive bleeding during surgery occurs because of soft and
The use of conscious sedation for periodontal surgery is
edematous gingiva due to improper Phase 1 therapy. Ragged
still not popular in most of the Asian countries including incisions, partial thickness flaps, or retention of periosteum
India. may also contribute to excessive bleeding. Damage to greater
palatine vessels during soft tissue graft harvesting could result
Surgical Plan in bleeding. Hence, correct incision and flap reflection and
well-prepared tissues are very important to ensure bloodless
After the anesthesia the surgical plan is reconfirmed with
surgery.
sounding or transgingival probing. The type of surgical tech- The application of pressure to the surgical wound with a
nique may be changed even at this stage if some osseous moist gauze can be a helpful adjunct to control site-specific
defects are detected during probing. bleeding. It is also important that the patient is not encour-
aged to rinse the mouth during the surgery as this will further
Tissue Management promote bleeding.
Occasionally despite good initial preparation and sound
1. Operate gently and carefully. In addition to being most con- surgical technique, excessive bleeding occurs during surgery.
siderate to the patient, this is also the most effective way to Hemostatic agents, such as absorbable gelatin sponge, oxi-
operate. Tissue manipulation should be precise, deliberate, dized cellulose, etc., are of limited use when there is continu-
and gentle. Thoroughness is essential, but roughness must ous bleeding. The best way to overcome this problem is to
be avoided, because it produces excessive tissue injury, pack the sites with cotton pledges and take one site at a time
causes postoperative discomfort, and delays healing. for instrumentation. If bleeding does not stop then it is pru-
2. Be certain that the instruments are sharp. Instruments must dent to close the flap and reexamine the patient later for any
be sharp to be effective; successful treatment is not pos- undiagnosed hemorrhagic disorders.
sible without sharp instruments. Dull instruments inflict
unnecessary trauma as a result of poor cutting and exces- Periodontal Dressings (Periodontal Packs)
sive force applied to compensate for their ineffectiveness. A
sterile sharpening stone should be available on the operat- In most cases, after the surgical periodontal procedures are
ing table at all times. completed, the area is covered with a surgical pack. In gener-
3. Proper instruments, such as right-sized BP blades, periosteal al, dressings have no curative properties; they assist healing by
elevator, suture needles etc., should be used for optimal tissue protecting the tissue rather than providing "healing factors."
management. The pack minimizes the likelihood of postoperative infection
43 General Principles of Periodontal Surgery 495
,. :,,
(A)
' (B)
FIGURE 43.1 Preparing the surgical pack (Coe-Pak). A,

Equal lengths of the two pastes are placed on a paper pad. B,
The pastes are mixed with a wooden tongue depressor for 2
or 3 min until. C, the paste loses its tackiness. D, The mixed
paste is placed in a paper cup of water at room temperature.
With lubricated fingers, it is then rolled into cylinders and (C) D)
placed on the surgical wound.
and hemorrhage, facilitates healing by preventing surface Antibacterial Properties of Packs

trauma during mastication, and protects the patient from pain Improved healing and patient comfort with less odor and
induced by contact of the wound with food or with the tongue taste have been obtained by incorporating antibiotics into the
during mastication. pack. Bacitracin, oxytetracycline (Terramycin), neomycin, and
nitrofurazone have been tried, but all of these may produce
Zinc Oxide-Eugenol Packs hypersensitivity reactions. The emergence of resistant organ-
Packs that are based on the reaction of zinc oxide and euge- isms and opportunistic infections has been reported. The
nol include the Wondr Pak, which was developed by Ward incorporation of tetracycline powder into the Coe-Pak is gen-
in 1923, and several other packs that use modified forms of erally recommended, particularly when long and traumatic
Ward's original formula. The addition of accelerators such as surgeries are performed.
zinc acetate gives the dressing a better working time.
Zinc oxide-eugenol dressings are supplied as a liquid and Allergy
a powder that are mixed before use. Eugenol in this type of Contact allergies to eugenol and rosin have been reported.
pack may induce an allergic reaction that produces reddening
of the area and burning pain in some patients. Preparation and Application of Dressing
Zinc oxide packs are mixed with eugenol or noneugenol liq-
Noneugenol Packs
uids on a wax paper pad with a wooden tongue depressor.
The reaction between a metallic oxide and fatty acids is the The powder is gradually incorporated with the liquid until a
basis for the Coe-Pak, which is the most widely used dressing. thick paste is formed.
This is supplied in two tubes, the contents of which are mixed The Coe-Pak is prepared by mixing equal lengths of paste
immediately before use until a uniform color is obtained. One from tubes that contain the accelerator and the base until
tube contains zinc oxide, an oil (for plasticity), a gum (for the resulting paste is a uniform color (Fig. 4 3. lA-C). A cap-
cohesiveness), and Lorothidol (a fungicide); the other tube sule of tetracycline powder can be added at this time. The
contains liquid coconut fatty acids that have been thickened pack is then placed in a cup of water at room temperature
with colophony resin (or rosin) and chlorothymol (a bacte- (Fig. 43.lD). After 2-3 min, the paste loses its tackiness, and
riostatic agent). This dressing does not contain asbestos or it can be handled and molded; it remains workable for 15-
eugenol, thereby avoiding the problems associated with these 20 min. The working time can be shortened by adding a small
substances. amount of zinc oxide to the accelerator (pink paste) before
Other noneugenol packs include cyanoacrylates and tissue spatula ting.
conditioners (methacrylate gels). However, these are not in The pack is then rolled into two strips that are approxi-
common use. mately the length of the treated area. The end of one strip is
bent into a hook shape and fitted around the distal surface of
Retention of Packs the last tooth to approach that tooth from the distal surface
Periodontal dressings are usually kept in place mechanically (Fig. 4 3.2A). The remainder of the strip is brought forward
by interlocking in interdental spaces and joining the lingual along the facial surface to the midline and gently pressed into
and facial portions of the pack. In isolated teeth or when sev- place along the gingival margin and interproximally. The sec-
eral teeth in an arch are missing, retention of the pack may be ond strip is applied from the lingual surface. It is joined to the
difficult. Numerous reinforcements and splints and stents for pack at the distal surface of the last tooth and then brought
this purpose have been described. The placement of dental forward along the gingival margin to the midline (Fig. 43.2B).
floss tied loosely around the teeth enhances retention of the The strips are joined interproximally by applying gentle pres-
pack. sure on the facial and lingual surfaces of the pack (Fig. 44.2C).
(A)
FIGURE 43.4 Periodontal pack should not interfere with the occlu-
sion.
experience. It is not a rigid requirement; the period may be ex-

tended, or the area may be repacked for an additional week.
Fragments of the surface of the pack may come off during
the week, but this presents no problem. If a portion of the
pack is lost from the operated area and the patient is un-
comfortable, it is usually best to repack the area. The clini-
cian should remove the remaining pack, wash the area with
warm water, and apply a topical anesthetic before replacing
the pack, which is then retained for 1 week. Again, the pa-
tient may develop pain from an overextended margin that
(8) irritates the vestibule, the floor of the mouth, or the tongue.
FIGURE 43.2 Inserting the periodontal pack. A, A strip of pack is
The excess pack should be trimmed away, with care taken to
hooked around the last molar and pressed into place anteriorly. B, The ensure that the new margin is not rough, before the patient
lingual pack is joined to the facial strip at the distal surface of the last is dismissed.
molar and fitted into place anteriorly. C, Gentle pressure on the facial
and lingual surfaces joins the pack interproximally.
Postoperative Instructions
After the pack is placed, printed instructions are given to the
patient to be read before he or she leaves the chair (Box 4 3 .1).
First Postoperative Week

When it is properly performed, periodontal surgery pres-
FIGURE 43.3 Continuous pack covers the edentulous space. ents no serious postoperative problems. Patients should be
told to rinse with 0.12 or 0.2% chlorhexidine gluconate
twice daily starting from the day after the surgical proce-
For isolated teeth separated by edentulous spaces, the pack
dure until normal plaque control techniques can be re-
should be made continuous from tooth to tooth to cover the
sumed. The following complications may arise during the
edentulous areas (Fig. 43.3).
first postoperative week, although they are the exception
When split flaps have been performed, the area should be
rather than the rule:
covered with tinfoil to protect the sutures before the pack is
placed. 1. Persistent bleeding after surgery. The pack is removed, the
The pack should cover the gingiva, but overextension onto bleeding points are located, the cause of bleeding is identi-
uninvolved mucosa should be avoided. Excess pack irritates fied and eliminated. The bleeding is stopped with pres-
the mucobuccal fold and the floor of the mouth, and it interjeres sure, electrosurgery, and the use of hemostatic agents.
with the tongue. Overextension also jeopardizes the remainder Sometimes a loose suture might have resulted in bleeding,
of the pack, because the excess tends to break off and to take which requires resuturing. After the bleeding is stopped,
pack from the operated area with it. Pack that interjeres with the the area is repacked.
occlusion should be trimmed away before the patient is dismissed 2. Sensitivity to percussion. Extension of inflammation into the
(Fig. 43.4). Failure to do this causes discomfort and Jeopar- periodontal ligament may cause sensitivity to percussion.
dizes retention of the pack. The patient should be questioned regarding the progress of
The operator should ask the patient to move the tongue the symptoms. Gradually diminishing severity is a favor-
forcibly out and to each side, and the cheek and lips should able sign. The pack should be removed and the gingiva
be displaced in all directions to mold the pack while it is still checked for localized areas of infection or irritation, which
soft. After the pack has set, it should be trimmed to eliminate should be cleaned or incised to provide drainage. Particles
all excess. of calculus that may have been overlooked should be re-
As a general rule, the pack is kept on for 1 week after surgery. This moved. Relieving the occlusion is usually helpful. Sensi-
guideline is based on the usual timetable of healing and clinical tivity to percussion may also be caused by excess pack,
Instructions After Periodontal Surgery Instructions for (Patient's Name)

The following information about your gum operation has been Do not brush over the pack. Brush and floss the areas of the
prepared to answer questions that you may have about how to mouth that are not covered by the pack as you normally would
take care of your mouth. Please read the instructions carefully; do. Use chlorhexidine oral rinses half an hour after brushing; a
our other patients have found them to be very helpful. prescription for this rinse has been given to you.
Although there will be little or no discomfort when the During the first day, apply ice intermittently to your face
anesthesia wears off, you should take the prescribed painkiller at over the operated area. It is also beneficial to suck on ice chips
the given dosage. intermittently during the first 24 hours. These methods will keep
We have placed a periodontal pack over your gums to tissues cool and reduce inflammation and swelling.
protect them from irritation. The pack prevents pain, helps You may experience a slight feeling of weakness or chills
with healing, and enables you to carry on most of your usual during the first 24 hours. This should not be a cause for alarm,
activities in comfort. The pack will harden in a few hours, but it should be reported at your next visit. Follow your regular
after which it can withstand most of the forces of chewing daily activities, but avoid excessive exertion of any type. Golf,
without breaking off. It may take a little while to become tennis, skiing, bowling, swimming, and sunbathing should be
accustomed to it. postponed for a few days after the operation.
The pack should remain in place until it is removed in the Swelling is not unusual, particularly in areas that required
office at your next appointment. If particles of the pack chip off extensive surgical procedures. The swelling generally begins
during the week, do not be concerned as long as you do not 1 to 2 days after the operation and subsides gradually after 3 or
have pain. If a piece of the pack breaks off and you are in pain 4 days. If this occurs, apply moist heat over the operated area. If
or if a rough edge irritates your tongue or cheek, please call the the swelling is painful or appears to become worse, please call
office. The problem can be easily remedied by replacing the the office.
pack. Occasionally, blood may be seen in the saliva for the first
For the first 24 hours after the operation, avoid hot and hard 4 or 5 hours after the operation. This is not unusual, and it will
foods. Later you can eat anything you can manage, but try to correct itself. If there is considerable bleeding beyond this, take
chew on the nonoperated side of your mouth. Semisolid or a piece of gauze, form it into the shape of the letter U, hold it
finely minced foods are suggested in case you find difficulty with your thumb and index finger, apply it to both sides of the
in chewing. Avoid citrus fruits and fruit juices, highly spiced pack, and hold it there under pressure for 20 minutes. Do not
foods, and alcoholic beverages; these will cause pain. Food remove it during this period to examine it. If the bleeding does
supplements or vitamins are generally not necessary. not stop at the end of 20 minutes, please contact the office. Do
Do not smoke. The heat and smoke will irritate your gums, not try to stop bleeding by rinsing the area with water.
and the immunologic effects of nicotine will delay healing and After the pack is removed, the gums most likely will bleed
prevent a completely successful outcome of the procedure more than they did before the operation. This is perfectly normal
that was performed. If possible, use this opportunity to give during the early stage of healing, and it will gradually subside.
up smoking. In addition to all other well-known health risks, Do not stop cleaning because of it. If any other problems arise,
smokers have more gum disease than nonsmokers. please cal I the office.
which interferes with the occlusion. Removal of the excess Removal of Pack and Return Visit
usually corrects the condition.
3. Swelling. During the first 2 postoperative days, some pa- When the patient returns after 1 week, the periodontal pack
tients may report a soft, painless swelling of the cheek in is taken off by inserting a surgical hoe along the margin and
the surgical area. Lymph node enlargement may occur, exerting gentle lateral pressure. Pieces of pack retained inter-
and the temperature may be slightly elevated. The area proximally and particles adhering to the tooth surfaces are
of operation itself is usually symptom free. This type of removed with scalers. Particles may be enmeshed in the cut
involvement results from a localized inflammatory reac- surface and should be carefully picked off with fine cotton
tion to the procedure. It generally subsides by the fourth pliers. The entire area is rinsed with peroxide to remove su-
postoperative day, without necessitating the removal perficial debris.
of the pack. If swelling persists, becomes worse, or is Findings at Pack Removal
associated with increased pain, amoxicillin (500 mg)
The following are usual findings when the pack is removed:
should be taken every 8 h for 1 week, and the patient
should also be instructed to rinse frequently with warm • If a gingivectomy has been performed, the cut surface is
saline. The antibiotic should also be used as a prophy- covered with a friable meshwork of new epithelium, which
lactic measure after the next procedure, starting before should not be disturbed. If calculus has not been completely
the surgical appointment. It is also stressed here that removed, red, bead-like protuberances of granulation tissue
enzymatic preparations such as trypsin, chymotrypsin, will persist. The granulation tissue must be removed with a
serratiopeptidase, and chlorzoxazone are ineffective in curette to expose the calculus so that it can be removed and
such situations. so the root can be planed. Removal of the granulation tissue
4. Feeling of weakness. Occasionally, patients report having without the removal of calculus is followed by recurrence.
experienced a "washed-out," weakened feeling for about • After a flap operation, the areas that correspond to the inci-
24 h after surgery. This represents a systemic reaction to sions are epithelialized, but they may bleed readily when
a transient bacteremia induced by the procedure. This touched; they should not be disturbed. Pockets should not
reaction is prevented by premedication with amoxicillin be probed.
(500 mg) every 8 h, beginning 24 h before the next proce- • The facial and lingual mucosa may be covered with a gray-
dure and continuing for 5 days postoperatively. ish-yellow or white granular layer of food debris that has
seeped under the pack. This is easily removed with a moist infection. Overextension of periodontal dressing and failure
cotton pellet. The root surfaces may be sensitive to a probe by the patient to follow postoperative instructions. A combi-
or to thermal changes, and the teeth may be stained. nation of ibuprofen and paracetamol taken 8 hourly usually
• Fragments of calculus delay healing. Each root surface should suffices. Presence of infection if any should be managed with
be rechecked visually to be certain that no calculus is pres- systemic antibiotics.
ent. Sometimes the color of the calculus is similar to that of
the root. The grooves on proximal root surfaces and the fur-
Treatment of Sensitive Roots
cations are areas where calculus is likely to be overlooked.
Root hypersensitivity is a relatively common problem in peri-
Repacking odontal practice. It may occur spontaneously when the root
After the pack is removed, it is usually not necessary to re- becomes exposed as a result of gingival recession or pocket
place it. However, repacking for an additional week is advised formation, or it may appear after scaling and root planing and
for the following types of patients: (1) those with a low pain surgical procedures. This type of sensitivity is manifested as
threshold who are particularly uncomfortable when the pack pain that is induced by cold or hot temperature (more often
is removed; (2) those with unusually extensive periodontal cold), by citrus fruits or sweets, or by contact with a tooth-
involvement; or (3) those who heal slowly Clinical judgment brush or a dental instrument.
helps when deciding whether to repack the area or leave the Root sensitivity occurs more frequently in the cervical area
initial pack on for more than 1 week. of the root, where the cementum is extremely thin. Scaling
and root planing procedures remove this thin cementum,
Tooth Mobility thereby inducing the hypersensitivity.
Tooth mobility is increased immediately after surgery, but it The transmission of stimuli from the surface of the dentin
diminishes below the pretreatment level by the fourth week. to the nerve endings located in the dental pulp or in the pulp-
al region of the dentin could result from the odontoblastic
process or from a hydrodynamic mechanism (ie, the displace-
Mouth Care Between Procedures
ment of dentinal fluid). The latter process seems more likely
Care of the mouth by the patient between the treatment of the and would explain the importance of burnishing desensitizing
first and the final areas as well as after surgery is completed is agents to obturate the dentinal tubule. An important factor for
extremely important. These measures should begin after the reducing or eliminating hypersensitivity is adequate plaque
pack is removed from the first surgery. The patient has been control. However, hypersensitivity may prevent plaque con-
through a presurgical period of instructed plaque control and trol, and therefore a vicious cycle of escalating hypersensitivity
should be reinstructed at this time. and plaque accumulation may be created.
Vigorous brushing is not feasible during the first week af- The patient should be informed about the possibility of
ter the pack is removed. However, the patient is informed root hypersensitivity before treatment is undertaken. The
that plaque and food accumulation impair healing, and he or following information about how to cope with the problem
she is advised to try to keep the area as clean as possible with should also be given to the patient:
the gentle use of soft toothbrushes and light water irrigation.
1. Hypersensitivity appears as a result of the exposure of den-
Rinsing with a chlorhexidine mouthwash or applying such a
tin, which is inevitable if calculus, plaque, and their prod-
rinse topically with cotton-tipped applicators is indicated for
ucts, which are buried in the root, are to be removed.
the first few postoperative weeks, particularly in advanced
2. Hypersensitivity slowly disappears over a few weeks.
cases. Brushing is introduced when the healing of the tis-
3. An important factor in reducing hypersensitivity is plaque
sues permits it; the vigor of the overall hygiene regimen is
control.
increased as healing progresses. Patients should be told that
4. Desensitizing agents must be used for several days or even
(1) more gingival bleeding will most likely occur than was
weeks until sensitivity disappears.
present before the procedure; (2) that this bleeding is per-
fectly normal and that is will subside as healing progresses; The reader is advised to refer standard textbooks and ar-
and (3) that it should not deter them from following their ticles for the detailed pathology and management of dentinal
oral hygiene regimen. hypersensitivity.
Management of Postoperative Pain Hospital Periodontal Surgery

Periodontal surgery that follows the basic principles outlined Ordinarily, periodontal surgery is an office procedure that is
here should produce only minor pain and discomfort. A study performed in quadrants or sextants, usually at biweekly or
of 304 consecutive periodontal surgical interventions revealed longer intervals. Under certain circumstances, however, it is
that 51.3% of the patients reported minimal or no postopera- in the best interest of the patient to treat the mouth with only
tive pain, and only 4.6% reported severe pain. Of these, only one surgery, with the patient in a hospital operating room and
20.1 % took five or more doses of analgesic. The same study under general anesthesia.
showed that mucogingival procedures result in 6 times more
discomfort and that osseous surgery is 3.5 times more uncom- Indications
fortable than plastic gingival surgery For the few patients who
may have severe pain, its control then becomes an important Indications for hospital periodontal surgery include the opti-
part of patient management. mal control and management of apprehension, convenience
Excessive postoperative pain may be caused due to long for individuals who cannot endure multiple visits to complete
duration of surgery, overzealous osseous tampering, and surgical treatment and patient protection.
Patient Apprehension Patients with systemic problems (eg, history of rheumatic

fever, cardiovascular problems) are premedicated as needed.
Gentleness, understanding, and preoperative sedation usually
suffice to calm the fears of most patients. For some patients, Anesthesia
however, the prospect of a series of surgical procedures is suf- Local or general anesthesia may be used. Local anesthesia is
ficiently stressful to trigger disturbances that jeopardize their the method of choice, except for especially apprehensive pa-
well-being and hamper treatment. Explaining that the treat- tients. It permits unhampered movement of the head, which
ment at the hospital will be performed painlessly and that it is necessary for optimal visibility and accessibility to the vari-
will be accomplished by a level of anesthesia that is neither ous root surfaces. Local anesthesia is used in the same manner
practical nor safe for patients in a dental office is an important as for routine periodontal surgery.
step in allaying patient fears. The thought of completing the When general anesthesia is indicated, it is administered
necessary surgical procedures in one session rather than in by an anesthesiologist. It is important that the patient also
repeated visits is an added comfort to many patients, because receives local anesthesia, administered as for routine peri-
it eliminates the prospect of repeated anxiety in anticipation odontal surgery, to ensure comfort for the patient and reduced
of each treatment. bleeding during the procedure. The judicious use of local an-
Patient Convenience
esthetics to block regional nerves allows the level of sedation
or general anesthesia to be lighter. Hence, the entire operation
With complete mouth surgery, there is less stress for the pa- is performed with a wider margin of safety.
tient and less time involved in postoperative care. For patients
whose occupation entails considerable contact with the pub- Positioning and Periodontal Dressing
lic, surgery performed at biweekly intervals sometimes pres- Surgery in the operating room is typically performed on the
ents a significant problem. It means that, for several weeks, operating table with the patient lying down and the table ei-
some area of the mouth will have undergone surgery and may ther positioned flat or with the head inclined up to 30 degrees.
be covered by a periodontal pack. With the complete mouth Some operating rooms are equipped with dental chairs that
technique, the surgery is completed in one visit. Although the can be used either flat or at up to 30 degrees of inclination.
pack may cover the entire treated area, it is usually only re- When general anesthesia is used, it is advisable to delay
tained for 1 week. Patients find this an acceptable alternative placing the periodontal dressing until the patient has recov-
to several weeks of discomfort in different areas of the mouth ered sufficiently to have a demonstrable cough reflex. Peri-
and multiple dressing applications. For a variety of other rea- odontal dressings placed before the end of general anesthesia
sons, patients may prefer to address their surgical needs in can be displaced during the recovery period and pose serious
one session under optimal "operating room" conditions. risks of blocking the airway.
Patient Protection
Some patients have systemic conditions that are not severe Postoperative Instructions
enough to contraindicate elective surgery but that may require After a full recovery from general anesthesia, most patients
special precautions that are best provided in a hospital setting. can be discharged home with a responsible adult. The effects
This group includes (but is not limited to) patients with severe of general anesthesia and sedative agents make the patient
cardiovascular disease, abnormal bleeding tendencies, hyper- drowsy for hours, and adult supervision at home is recom-
thyroidism, or uncontrolled hypertension. Treating such a pa- mended for up to 24 h after surgery. The typical postoperative
tient in a hospital operating room or an equivalent procedure instructions should be given to the responsible adult, and the
room with an anesthesiologist present to monitor and manage patient should be scheduled for a postoperative visit in 1 week.
the vitals signs and comfort level throughout the surgical pro-
cedure is the safest way to manage him or her.
The purpose of hospitalization is to protect patients by Conclusions
anticipating their special needs, not to perform periodontal The majority of periodontal surgeries can be carried out
surgery when it is contraindicated by the patient's general con- solely with the thorough application of local anesthesia, but
dition. For some patients, elective surgery is contraindicated, clinicians have the obligation to ensure a patient-centered
regardless of whether it is performed in the dental office or the approach that includes oral, intravenous, and inhalational se-
hospital. When consultation with the patient's physician leads dation in their spectrum of available services to be used as
to this decision, palliative periodontal therapy in the form of needed.
scaling and root planing, if permissible, is the necessary com- The efficient, precise, and minimally traumatic management
promise. of tissues is the way to obtain the best clinical outcomes. All
patients need oral analgesic support, and they should be given
Patient Preparation the necessary pain-relieving medications so that an effective
level of analgesic is present during the immediate postsurgical
Premedication period and thereafter as needed. The use of longer-acting local
Patients should be given a sedative the night before surgery. anesthesia agents (eg, bupivacaine) and protective periodontal
Benzodiazepines work well for most patients because they al- dressings also helps to reduce postsurgical pain.
low the patient to sleep well the night before surgery. If the pa- During the immediate postsurgical weeks, plaque control
tient is extremely nervous about the procedure, it is also help- and healing are enhanced by the use of antimicrobial mouth-
ful to advise him or her to take a benzodiazepine the morning rinses such as chlorhexidine. Postsurgical root sensitivity is
of surgery. This ensures that the patient will be as rested and well controlled by ensuring that plaque control is optimal,
relaxed as possible before surgery. and desensitizing agents will be needed only occasionally.
SUGGESTED READINGS Pack PO, Haber J: The incidence of clinical infection after periodontal sur-
gery: a retrospective study,] Periodontal 54:441, 1983.
Curtis JW Jr, Mclain JB, Hutchinson RA: The incidence and severity of com-
Freber H, Bergstrom J: Effect of cigarette smoking on periodontal healing fol-
plications and pain following periodontal surgery, J Periodontal 56:597,
lowing surgical therapy,] Clin Periodontol 17:324, 1990.
1985.
Sachs HA, Farnoush A, Checchi L, et al: Current status of periodontal dress-
Douglas de Oliveira OW, Oliveira-Ferreira F, Flecha OD, et al: Is surgical root
ings,} Periodontal 55:689, 1984.
coverage effective for the treatment of cervical dentin hypersensitivity? A
Sykes LM: Dentine hypersensitivity: a review of its aetiology, pathogenesis
systematic review,] Periodontol 84:295, 2013.
and management, SAD] 62:66, 2007.
Gangarosa LP Sr: Current strategies for dentist-applied treatment in the man-
Trowbridge HO, Silver DR: A review of current approaches to in-office man-
agement of hypersensitive dentine, Arch Oral Biol 39 Suppl:l0lS, 1994.
agement of tooth hypersensitivity, Dent Clin North Am 34:583, 1990.
Jones JK, Triplett RG: The relationship of cigarette smoking to impaired intra-
Westfelt E, Nyman S, Socransky SS: Significance of frequency of profession-
oral wound healing: a review of evidence and implications for patient care,
al cleaning for healing following periodontal surgery, J Clin Periodontol
J Oral Maxillofac Surg 50:237, 1992.
10:148, 1983.
44
Gingival Surgical Techniques
HH Takei • FA Carranza • K Shin • CD Dwarakanath
Chapter Outline
Gingival Curettage Gingivectomy by Chemosurgery
Gingivectomy Conclusions
Gingivectomy by Electrosurgery
Periodontal pocket reduction surgery limited to the gingival However, this rationale has been questioned because of the
tissues only and not involving the underlying osseous struc- following reasons.
tures, without the use of flap surgery, can be classified as gin- When the root is thoroughly planed, the major source
gival curettage, gingivectomy, and gingivoplasty. Both gingival cu- of bacteria disappears, and the pathologic changes in the
rettage and gingivectomy have limited use currently because tissues adjacent to the pocket resolve with no need to
of the change in the understanding of etiology of periodontal eliminate the inflamed granulation tissue by curettage. The
disease. existing granulation tissue is slowly resorbed, and the bac-
teria present in the tissue without replenishment of their
numbers from the plaque in the pocket are destroyed by
Gingival Curettage the defense mechanisms of the host. It has been shown that
scaling and root planing with additional curettage do not
The word curettage is used in periodontics to mean the scraping
of the gingival wall of a periodontal pocket to remove diseased improve the condition of the periodontal tissues beyond
soft tissue. Scaling refers to the removal of deposits from the root the improvement that results from scaling and root planing
alone.
surface, whereas planing means smoothing the root to remove
The second reason is the fact that curettage may not re-
infected and necrotic tooth substance. Scaling and root planing
move pocket lining and junctional epithelium consistently
may inadvertently include curettage to a certain degree. This
Third, it has also been shown that curettage done in an
is often called inadvertent curettage. However, they are differ-
ent procedures with different rationales and indications. Both anterior esthetic zone may result in more shrinkage compared
should be considered as separate parts of periodontal treatment. to root planing alone.
Notwithstanding the above reservations curettage might be
This chapter refers to the intentional curettage performed
still indicated in the following situations.
during the same visit as scaling and root planing or as a sepa-
rate procedure to reduce pocket depth by enhancing gingival 1. Curettage can be attempted as a nondefinitive proce-
shrinkage, new connective tissue attachment, or both. dure to reduce inflammation when aggressive surgical
techniques (eg, flaps) are contraindicated in patients
Rationale as a result of their age, systemic problems, psychologic
problems, or other factors. It should be understood that,
Curettage accomplishes the removal of the chronically in- in these patients, the goal of pocket elimination is com-
flamed granulation tissue that forms in the lateral wall of the promised, and their prognosis is impaired. The clinician
periodontal pocket. This tissue, in addition to the usual com- should attempt this approach only when the indicated
ponents of granulation tissues (ie, fibroblastic and angioblas- surgical techniques cannot be performed and both the
tic proliferation), contains areas of chronic inflammation, and clinician and the patient have a clear understanding of its
it may also contain pieces of dislodged calculus and bacterial limitations.
colonies. The latter may perpetuate the pathologic features of 2. Curettage is also frequently performed on recall visits as
the tissue and hinder healing. a method of maintenance treatment for areas of recurrent
This inflamed granulation tissue is lined by epithelium, inflammation and pocket depth, especially where pocket
and deep strands of epithelium penetrate into the tissue. The reduction surgery has previously been performed. Careful
presence of this epithelium is construed as a barrier to the at- probing should establish the extent of the required root
tachment of new fibers in the area. planing and curettage.
501
(A) (8)
FIGURE 44.1 Gingival curettage performed with a horizontal stroke
FIGURE 44.3 Excisional new attachment procedure. A, Internal bevel
of the curette.
incision to a point below the bottom of the pocket. B, After the excision
of tissue, scaling and root planing are performed.
Procedure
Other Techniques
Basic Technique
Other techniques for gingival curettage include the excisional
Curettage does not eliminate the causes of inflammation (ie,
new attachment procedure, ultrasonic curettage, and the use
bacterial plaque and deposits). Therefore, curettage should al-
of caustic drugs.
ways be preceded by scaling and root planing, which is the basic
periodontal therapy procedure. The use of local infiltrative
Excisional New Attachment Procedure. The excisional new
anesthesia for scaling and root planing is optional. However,
attachment procedure which was developed and used by the
gingival curettage will always require some type of local an-
US Naval Dental Corps is a definitive subgingival curettage
esthesia.
procedure that is performed with a knife. Its usefulness is very
The curette is selected so that the cutting edge is against
limited today as it has been found that most of the time heal-
the tissue. Curettage can be performed either by area-specific
ing occurs by formation of long junctional epithelium rather
Gracey curettes or Columbia Universal curettes. The instru-
than any true new attachment (Fig. 44.3).
ment is inserted to engage the inner lining of the pocket wall,
and it is then carried along the soft tissue, usually in a hori-
Ultrasonic Curettage. The use of ultrasonic devices has been
zontal stroke (Fig. 44.1) The pocket wall may be supported
recommended for gingival curettage. When applied to the gin-
by gentle finger pressure on the external surface. The curette
giva of experimental animals, ultrasonic vibrations disrupt tissue
is then placed under the most apical edge of the junctional
continuity, lift off the epithelium, dismember collagen bundles,
epithelium to undermine it.
and alter the morphologic features of fibroblast nuclei. Ultrason-
During subgingival curettage, the tissues attached between
ics are effective for debriding the epithelial lining of periodontal
the bottom of the pocket and the alveolar crest are removed
pockets. This results in a narrow band of necrotic tissue (micro-
with a scooping motion of the curette to the tooth surface
cauterization), which strips off the inner lining of the pocket.
(Fig. 44.2). The area is flushed to remove debris, and the tis-
The Morse scaler-shaped and rod-shaped ultrasonic instru-
sue is partly adapted to the tooth by gentle finger pressure. In
ments are used for this purpose. Some investigators found ul-
some cases, the suturing of separated papillae and the applica-
trasonic instruments to be as effective as manual instruments
tion of a periodontal pack may be indicated.
for curettage and that such tools resulted in less inflammation
(A) (8) (C)

FIGURE 44.2 Subgingival curettage. A, Elimination of pocket lining. B, Elimination of junctional epithelium and granulation tissue. C, Procedure
completed.
44 Gingival Surgical Techniques 503
and less removal of underlying connective tissue. The gingiva 2. Elimination of gingival enlargements.
can be made more firm for ultrasonic curettage by injecting 3. Elimination of suprabony periodontal abscesses.
the anesthetic solution directly into it.
Contraindications to gingivectomy include the following:
Caustic Drugs. These were used in the past and were by and 1. The need for osseous surgery or examination of the shape
large ineffective besides causing untoward damage to the tis- and morphology of bone.
sues. They are outdated and have no place in current peri- 2. Situations in which the bottom of the pocket is apical to
odontal practice. the mucogingival junction.
3. Aesthetic considerations, particularly in the anterior maxilla.
Healing After Scaling and Curettage The gingivectomy technique may be performed by means
of scalpels, electrodes, lasers, or chemicals. All of these tech-
Immediately after curettage, a blood clot fills the pocket area,
niques are reviewed in this chapter, although the surgical
which is totally or partially devoid of epithelial lining. Hem-
method is the only technique that is recommended.
orrhage is also present in the tissues with dilated capillaries
and abundant polymorphonuclear leukocytes, which appear
on the wound surface. This is followed by a rapid proliferation Surgical Gingivectomy
of granulation tissue with a decrease in the number of small
Step 1
blood vessels as the tissue matures.
The restoration and epithelialization of the sulcus generally The pockets on each surface are explored with a periodon-
require 2-7 days, and restoration of the junctional epithelium tal probe and marked with a pocket marker. Each pocket is
occurs in animals as early as 5 days after treatment. Immature marked in several areas to outline its course on each surface
collagen fibers appear within 21 days. Healthy gingival fibers (Figs. 44.4C-D, 44.5, and 44.6)
that are inadvertently severed from the tooth and tears in the
Step 2
epithelium are repaired during the healing process. Several in-
vestigators have reported that, in monkeys and humans treat- Periodontal knives (eg, Kirkland knives) are used for incisions
ed by scaling and curettage, healing results in the formation on the facial and lingual surfaces and on those distal to the ter-
of a long, thin junctional epithelium with no new connective- minal tooth in the arch. Orban periodontal knives are used for
tissue attachment. In some cases, this long epithelium is inter- interdental incisions (Fig. 44.4E-G) Bard-Parker blades (nos.
rupted by "windows" of connective-tissue attachment. 12 and 15) as well as scissors are used as auxiliary instruments.
The incision is started apical to the points marking the course
of the pockets, and it is directed coronally to a point between
Clinical Appearance After Scaling and the base of the pocket and the crest of the bone. It should be as
Curettage close as possible to the bone without exposing it to remove the
soft tissue coronal to the bone. Exposure of bone is undesirable.
Immediately after scaling and curettage, the gingiva appears
If this occurs, healing usually presents minimal complications if
hemorrhagic and bright red. After 1 week, the gingiva appears
the area is adequately covered by the periodontal pack.
reduced in height as a result of an apical shift in the position of
Either interrupted or continuous incisions may be used.
the gingival margin. The gingiva is also darker red than normal,
The incision should be beveled at approximately 45 degrees to
but it is much less red than it will have been on previous days.
the tooth surface, and it should recreate the normal festooned
After 2 weeks and with proper oral hygiene, the normal color,
pattern of the gingiva. Failure to bevel the incision will leave a
consistency, surface texture, and contour of the gingiva are at-
broad, fibrous plateau that will take a longer time to develop a
tained, and the gingival margin is well adapted to the tooth.
physiologic contour. During the interim, plaque and calculus
may lead to the recurrence of pockets.
Gingivectomy
Step 3
The word gingivectomy means "excision of the gingiva." By re-
Remove the excised pocket wall, clean the area, and closely
moving the pocket wall, gingivectomy provides visibility and
examine the root surface. The most apical zone consists of a
accessibility for complete calculus removal and the thorough
light, band-like zone where the tissues were attached. Coronal-
smoothing of the roots. This creates a favorable environment for
ly, calculus remnants, root caries, or resorption may be found.
gingival healing and restoration of a physiologic gingival contour.
Granulation tissue may be seen on the excised soft tissue.
The gingivectomy technique was widely performed in the
past. Improved understanding of healing mechanisms and the Step 4
development of more sophisticated flap methods have relegat-
Carefully curette the granulation tissue and remove any re-
ed the gingivectomy to a lesser role in the current repertoire of
maining calculus and necrotic cementum to leave a smooth
available techniques. However, it remains an effective form of
and clean surface.
treatment when indicated (Fig. 44.4).
Step 5
Indications and Contraindications Cover the area with a surgical pack (Fig. 44.41).
The gingivectomy technique may be performed for the follow-
ing indications: Gingivoplasty
1. Elimination of suprabony pockets, regardless of their Gingivoplasty is similar to gingivectomy, but its objective is
depth, if the pocket wall is fibrous and firm. different. Gingivectomy is performed to eliminate periodontal
FIGURE 44.4 Results obtained by treating a suprabony pocket with gingivectomy. A and B, Preoperative facial and palatal views. C, Marking of the
depth of the suprabony pocket. D, The bottoms of the pockets are indicated by pinpoint markings. E, A beveled palatal incision with an Orban knife.
F, A facial beveled incision with a Bard-Parker no. 15 blade extends apical to the perforations made by the pocket marker. Note that the beveled incision
can also be made with a Kirkland knife. G, The interdental incision and excision of the pocket wall with a Bard-Parker no. 12 blade. H, A completed
gingivectomy. I, The surgical site covered with periodontal dressing. J, One week after healing. Kand L, Results 22 months after the operation.
(A) (B)
FIGURE 44.6 Marking the depth of a suprabony pocket. A, A pocket
FIGURE 44.5 The pocket marker makes pinpoint perforations that marker in position. B, The beveled incision extends apical to the perfora-
indicate pocket depth. tion made by the pocket marker.
44 Gingival Surgical Techniques 505
pockets, and it includes reshaping as part of the technique. Gingivectomy by Electrosurgery

Gingivoplasty is a reshaping of the gingiva to create physi-
ologic gingival contours with the sole purpose of recontouring Advantages and Disadvantages
the gingiva in the absence of pockets.
Gingival and periodontal disease often produces defor- Electrosurgery permits an adequate contouring of the tissue
mities in the gingiva that are conducive to the accumulation and controls hemorrhage.
of plaque and food debris, which prolong and aggravate the It cannot be used in patients who have incompatible or
disease process. Such deformities include the following: (1) poorly shielded cardiac pacemakers. The treatment causes an
gingival clefts and craters; (2) crater-like interdental papillae unpleasant odor. If the electrosurgery point touches the bone,
caused by acute necrotizing ulcerative gingivitis; and (3) gin- irreparable damage can be inflicted. Furthermore, the heat gen-
gival enlargements. erated by injudicious use can cause tissue damage and a loss of
Gingivoplasty may be accomplished with a periodontal periodontal support when the electrode is used close to bone.
knife, a scalpel, rotary coarse diamond stones, or electrodes. When the electrode touches the root, areas of cementum can
The technique resembles that of the festooning of an artifi- be burned. Therefore, the use of electrosurgery should be limited to
cial denture, which consists of tapering the gingival margin, superficial procedures such as the removal of gingival enlargements,
creating a scalloped marginal outline, thinning the attached gingivoplasty, the relocation of the frenum and muscle attachments,
gingiva, creating vertical interdental grooves, and shaping the and the incision of periodontal abscesses and pericoronal flaps. Ex-
interdental papillae. treme care should be used to avoid contacting the tooth surface.
Electrosurgery should not be used for procedures that involve prox-
imity to the bone (eg, flap operations) or for mucogingival surgery.
Healing After Surgical Gingivectomy
The initial response after gingivectomy is the formation of Technique
a protective surface blood clot. The underlying tissue be-
comes acutely inflamed with necrosis. The clot is then re- The removal of gingival enlargements and gingivoplasty is
placed by granulation tissue. In 24 h, there is an increase performed with a needle electrode supplemented by a small
in new connective tissue cells, which are mainly angio- ovoid loop or diamond-shaped electrodes for festooning. A
blasts beneath the surface layer of inflammation and ne- blended cutting and coagulating (fully rectified) current is
crotic tissue. By the third day, numerous young fibroblasts used. During all reshaping procedures, the electrode is acti-
are located in the area. The highly vascular granulation vated and moved in a concise "shaving" motion.
tissue grows coronally and creates a new free gingival mar- For the treatment of acute periodontal abscesses, the inci-
gin and sulcus. Capillaries derived from the blood vessels sion to establish drainage can be made with the needle elec-
of the periodontal ligament migrate into the granulation trode without exerting pressure. The incision remains open
tissue, and, within 2 weeks, they connect with the gingival because the edges are sealed by the current. After the acute
vessels. symptoms subside, the regular procedure for the treatment of
After 12-24 h, epithelial cells at the margins of the wound the periodontal abscess is followed.
begin to migrate over the granulation tissue, thereby separat- For hemostasis, a ball electrode is used. Hemorrhage must
ing it from the contaminated surface layer of the clot. Epithe- first be controlled by direct pressure using air, a compress, or
lial activity at the margins reaches a peak after 24-36 h. a hemostat; the surface is then lightly touched with a coagu-
The new epithelial cells arise from the basal and deeper lating current. Electrosurgery is helpful for the control of iso-
spinous layers of the epithelial wound edge and migrate over lated bleeding points. Bleeding areas located interproximally
the wound over a fibrin layer that is later resorbed and re- are reached with a thin, bar-shaped electrode.
placed by a connective tissue bed. The epithelial cells ad- Frenum and muscle attachments can be relocated to facili-
vance by a tumbling action, with the cells becoming fixed tate pocket elimination with the use of a loop electrode. For
to the substrate by hemidesmosomes and a new basement this purpose, the frenum or muscle is stretched and sectioned
lamina. with the loop electrode and a coagulating current. For cases of
After 5-14 days, surface epithelialization is generally com- acute pericoronitis, drainage may be obtained by incising the
plete. During the first 4 weeks after gingivectomy, keratiniza- flap with a bent-needle electrode. A loop electrode is used to
tion is less than it was before surgery. Complete epithelial re- remove the flap after the acute symptoms subside.
pair takes about 1 month. Vasodilation and vascularity begin
to decrease after the day 4 of healing, and they appear to be Healing After Electrosurgery
almost normal by the day 16. Complete repair of the connec-
tive tissue takes about 7 weeks. Some investigators report no significant differences in gin-
The flow of gingival fluid in humans is initially increased gival healing after resection by electrosurgery as compared
after gingivectomy, and it diminishes as healing progresses. with resection with periodontal knives. Other researchers
Maximal flow is reached after 1 week, which coincides with find delayed healing, a greater reduction in gingival height,
the time of maximal inflammation. and more bone injury after electrosurgery. There appears to
Although the tissue changes that occur during postgin- be negligible difference in the results obtained after gingival
givectomy healing are the same in all individuals, the time resection with electrosurgery and those obtained with peri-
required for complete healing varies considerably, depending odontal knives. However, when used for deep resections close to
on the area of the incised surface and interference from local bone, electrosurgery can produce gingival recession, bone necrosis,
irritation and infection. In patients with physiologic gingi- and sequestration, a loss of bone height, furcation exposure, and
val melanosis, the pigmentation is diminished in the healed tooth mobility. These problems do not occur with the use of
gingiva. periodontal knives.
Laser Gingivectomy cautery. Although this technique may have some use for the
minimal reduction of redundant gingival tissue, many limiting
The lasers that are most often used in dentistry are the di- factors must be considered. Current periodontal surgery must
ode laser and the neodymium: yttrium-aluminum-garnet consider the following: (1) the conservation of keratinized
(N d:YAG) laser, which have wavelengths of 910 and 1064 nm, gingiva; (2) minimal gingival tissue loss to maintain aesthet-
respectively They are both in the infrared range, so they must ics; (3) adequate access to the osseous defects for definitive
be combined with other types of visible lasers for the beam to defect correction; and ( 4) minimal postsurgical discomfort
be seen and aimed. and bleeding by attempting surgical procedures that will al-
The diode laser has been used for the excision of gingival low for primary closure. The gingivectomy surgical technique
growths, although healing is delayed as compared to healing has limited use in current surgical therapy, because it does not
after conventional scalpel gingivectomy. The use of a laser for satisfy these considerations for periodontal therapy. The clini-
oral surgery requires precautionary measures to avoid reflect- cian must carefully evaluate each patient to address the proper
ing the beam on instrument surfaces, which could result in application of this surgical procedure.
injury to neighboring tissues and to the eyes of the opera-
tor. ( Chapter 51 includes additional information about laser
SUGGESTED READINGS
therapy.)
Engler WO, Ramfjord S, Hiniker Jj: Healing following simple gingivectomy: a
tritiated thymidine radioautographic study I. Epithelialization.,J Periodon-
Gingivectomy by Chemosurgery tol 37:289, 1966.
Glickman I: The results obtained with the unembellished gingivectomy tech-
Techniques to remove the gingiva with the use of chemicals nique in a clinical study in humans,] Paiodontol 27:247, 1956.
such as 5% paraformaldehyde or potassium hydroxide have Lindhe J, Westfelt E, Nyman S, et al: Healing following surgical and non-
surgical treatment of periodontal disease,] Clin Paiodontol 9:115, 1982.
been described in the past, but they are not currently used. Moskow BS: The response of the gingival sulcus to instrumentation: a histo-
logic investigation. II. Gingival curettage,] Periodontol 35:112, 1964.
Ramfjord SP, Costich ER: Healing after exposure of the periosteum on the
Conclusions alveolar process,] Periodontol 38:199, 1968.
Ram fjord SP, EnglerWD, Hiniker Jj: A radiographic study of healing following
The gingivectomy surgical technique has a long history of use simple gingivectomy. II. The connective tissue,] Periodontol 37:179, 1966.
in periodontal surgery. This technique has been attempted Stahl S, Witkin G, Cantor M, et al: Gingival healing. II. Clinical and histologic
with the use of scalpels, electrosurgery, laser, and chemical repair sequences following gingivectomy,J Peliodontol 39:109, 1968.
45
The Periodontal Flap
HH Takei • FA Carranza • J Do • K Shin • CD Dwarakanath
Chapter Outline
Indications Healing After Flap Surgery
Contraindications Different Flap Techniques
Classification of Flaps The Flap Technique for Pocket Therapy
Flap Design Undisplaced Flap
Incisions Apically Displaced Flap
Elevation of the Flap Flaps for Reconstructive Surgery
Debridement Distal Molar Surgery
Osseous Management Conclusion
Sutures and Suturing Techniques
Periodontal flap surgery is the most common type of surgery Contraindications

done in the oral cavity and is the basic requirement of several
periodontal procedures. It has been in existence for over a 1. When optimal results can be obtained by nonsurgical peri-
century and many techniques and modifications have evolved odontal therapy (Fig. 45.8)
and have been practiced. This chapter covers the basic prin- 2. Presence of unprepared, soft, and edematous gingival tis-
ciples of flap surgery followed by different techniques for vari- sues (Fig. 45 9).
ous situations, such as pocket therapy, regeneration, gingival 3. Medically compromised patients, in whom surgery is a
enlargements, etc. risky proposition.
Definition: A periodontal flap is a section of gingiva and/ 4. Patients presenting consistent poor oral hygiene and who
or mucosa that is surgically separated from the underlying are noncompliant.
tissues to provide visibility and access to the bone and root 5. Teeth with hopeless prognosis (Fig. 45 10).
surface. The flap also allows the gingiva to be displaced to a 6. When surgery is likely to result in an extreme esthetic dis-
different location in patients with mucogingival involvement. figurement.
Rationale: Removal of root-surface noxious agents and in-
flamed tissue to have an ideal gingival and bone morphology Classification of Flaps
without sacrificing investing and supporting tissues and com-
promising esthetics. Periodontal flaps are classified on the basis of the following
criteria:
Indications • bone exposure after flap reflection;
• placement of the flap after surgery; and
1. Presence of persistent moderate to deep pockets (> 5 mm)
• management of the interdental papilla.
even after a conscientious phase 1 therapy (Fig. 45.1).
2. Presence of osseous defects (Fig. 45.2). For bone exposure after reflection, the flaps are classified as
3. Presence of inflammation and disease activity at the base of either full-thickness (mucoperiosteal) or partial-thickness
sulcus as seen by bleeding on probing (Fig. 45.3). (mucosal) flaps (Fig. 45. llA and B).
4. Furcation involvement (Fig. 45.4). In a full-thickness flap, all of the soft tissue, including the
5. Regeneration of periodontal tissues by the use of bone periosteum, is reflected to expose the underlying bone. This
grafts, membranes etc. complete exposure of and access to the underlying bone is
6. Gingival overgrowth and asymmetry (Fig. 45.5). indicated when osseous surgery is contemplated.
7. Periodontal pockets adjacent to distal molars (Fig. 45.6). The partial-thickness flap includes only the epithelium
8. Other dental procedures, such as crown lengthening, api- and a layer of the underlying connective tissue. The bone re-
cectomy, etc (Fig. 45. 7) mains covered by a layer of connective tissue that includes the
507
FIGURE 45.1 Presence of persistent deep pocket. FIGURE 45.5 Drug-induced gingival enlargement.
FIGURE 45.2 Osseous defects showing inconsistent bone margin

FIGURE 45.6 Deep periodontal pocket on the distal surface of man-
and reverse architecture.
dibular second molar.
FIGURE 45.3 Bleeding on probing the base of the pocket. FIGURE 45.7 Root canal treated molar requiring crown lengthening.
periosteum. This type of flap is also called the split-thickness

flap. The partial-thickness flap is indicated when the flap is to
be positioned apically or when the operator does not want to
expose the bone in the presence of fenestrations, dehiscences,
and in plastic surgical procedures.
For flap placement after surgery, flaps are classified as either
(1) nondisplaced flaps, when the flap is returned and sutured in
its original position, or (2) displaced flaps, which are placed api-
cally, coronally, or laterally to their original position. These are
commonly performed in mucogingival procedures. Both full-
thickness and partial-thickness flaps can be displaced. How-
ever, to do so, the attached gingiva must be totally separated
from the underlying bone, thereby enabling the unattached
portion of the gingiva to be movable. Palatal flaps cannot be
FIGURE 45.4 Grade II furcation in maxillary molar. displaced because of the absence of unattached gingiva.
45 The Periodontal Flap 509
FIGURE 45.8 A, Severe periodontitis with poor oral hygiene. B, Result after nonsurgical therapy.
This includes the modified-Widman flap, the undisplaced flap,

Kirkland flap (nowadays called the access flap), the apically
displaced flap, and the flap for reconstructive procedures.
The papilla-preservation flap incorporates the entire papilla
in one of the flaps by means of crevicular interdental incisions
to sever the connective tissue attachment, as well as, a hori-
zontal incision at the base of the papilla to leave it connected
to one of the flaps. This technique is indicated in esthetic
zones and for bone-graft placement.
Flap Design
The design of the flap is dictated by the surgical judgment
of the operator and it may depend on the objectives of the
FIGURE 45.9 Unprepared tissues showing soft and edematous
gingiva.
procedure. The necessary degree of access to the underlying
bone and root surfaces and the final position of the flap must
be considered when designing the flap. The flap design may
Apically displaced flaps have the important advantage of also be dictated by the esthetic concerns of the area of surgery.
preserving the outer portion of the pocket wall and transform- Preservation of good blood supply to the flap is another im-
ing it into attached gingiva. Therefore, these flaps accomplish portant consideration (Figs. 45.12 and 45.13).
the double objective of eliminating the pocket and increasing The entire surgical procedure should be planned in ev-
the width of the attached gingiva. ery detail before the procedure is initiated. The surgical plan
For the management of the papilla, flaps can be conventional should include the type of flap, the exact location, type of
and papilla-preservation flaps. With the conventional flap, the incisions, the management of the underlying bone, the final
interdental papilla is split beneath the contact point of the two closure of the flap, and sutures. Although, some details may
approximating teeth to allow for the reflection of the buccal be modified during the actual performance of the procedure,
and lingual flaps. The incision is usually scalloped to main- detailed planning allows for a better clinical result.
tain gingival morphology and to retain as much papilla as pos-
sible. The conventional flap is used (1) when the interdental
spaces are too narrow, thereby precluding the possibility of
Incisions
preserving the papilla; (2) when the flap is to be displaced; and Periodontal flaps involve the use of horizontal (mesial-distal)
(3) when there is a break in continuity of the interdental papilla. and vertical (occlusal-apical) incisions.
FIGURE 45.10 A, Dentition with hopeless overall prognosis. B, OPG of the same case.
(A) (B)
Periosleum Periosleum
FIGURE 45.11 A, Diagram of the internal bevel incision (first incision) to reflect a full-thickness (mucoperiosteal) flap. Note that the incision ends on
the bone to allow for the reflection of the entire flap. B, Diagram of the internal bevel incision to reflect a partial-thickness flap. Note that the incision
ends on the root surface to preserve the periosteum on the bone.
, ' ,.. ••• I
I 1
'
t-1
0 ' ,
I I
,-1
0,
I I I\ I
I',_,' '.,.1\
(A) (B)
(C) (D)
FIGURE 45.12 Flap design for a conventional or traditional flap technique. A, Design of incisions: internal bevel incision, splitting the papilla,
and vertical incisions are drawn in interrupted lines. B, The flap has been elevated, and the wedge of tissue next to the tooth is still in place. C, All
marginal tissue has been removed to expose the underlying bone (see the defect in one space). D, The tissue has been returned to its original position.
The proximal areas are not totally covered.
incision has also been termed the first incision, because it is the
Horizontal Incisions
initial incision for the reflection of a periodontal flap; it has
Horizontal incisions are directed along the margin of the gin- also been called the inverse or reverse bevel incision, because
giva in a mesial or distal direction. Two types of horizontal its bevel is in the reverse direction from that of the gingivec-
incisions have been recommended: (1) the internal bevel inci- tomy incision. The no. 11 or 15 BP-surgical blades are used
sion, which starts at a distance from the gingival margin and to make this incision in most areas of the mouth except in the
which is aimed at the bone crest; and (2) the crevicular incision, mandibular posterior region where a no. 12 blade might be
which starts at the bottom of the pocket and which is directed preferred due to better access. That portion of the gingiva left
to the bone margin. In addition, the interdental incision is around the tooth contains the epithelium of the pocket lining
performed after the flap is elevated to remove the interdental and the adjacent granulomatous tissue. It is discarded after
tissue. the crevicular (second) and interdental (third) incisions are
The internal bevel incision is basic to most periodontal flap performed (Fig. 45 14)
procedures. It is the incision from which the flap is reflected to The internal bevel incision starts from a designated area on
expose the underlying bone and root. The internal bevel inci- the gingiva and it is then directed to an area at or near the crest
sion accomplishes three important objectives: (1) it removes of the bone (Fig. 45.15). The starting point on the gingiva is
the pocket lining; (2) it conserves the relatively uninvolved determined by whether the flap is apically displaced or not
outer surface of the gingiva, which, if apically positioned, be- (Fig. 45 16) Ideally the incision should begin one tooth be-
comes attached gingiva; and (3) it produces a sharp, thin-flap yond the designated surgical area and from the most posterior
margin for the adaptation to the bone-tooth junction. This tooth moving anteriorly.
I
\ ,-\ ,,-'f
I -: 0 L -1 0 /
r '\ ' ' ', I' '
~,'
-
\
' .••. -
"- I
......._,
(A) (B)
-0
(C)
FIGURE 45.13 Flap design for a sulcular incision flap. A, Design of incisions: sulcular incisions and vertical incisions are depicted by interrupted
lines. B, The flap has been elevated to expose the underlying bone (see the defect in one space). C, The tissue has been returned to its original position
to cover the i nterdental spaces.
(A) (B)
FIGURE 45.14 The three incisions necessary for flap surgery. A, First (internal bevel) incision; B, second (crevicular) incision; and C, third (inter-
dental) incision.
contains most of the inflamed and granulomatous areas that

constitute the lateral wall of the pocket, as well as, the JUnc-
tional epithelium and the connective tissue fibers that still
persist between the bottom of the pocket and the crest of the
bone. The incision is carried around the entire tooth. The
beak-shaped no. 12D blade is usually used for this incision.
A periosteal elevator is inserted into the initial internal bev-
el incision and the flap is separated from the bone. The most
apical end of the internal bevel incision is exposed and visible.
With this access, the surgeon is able to make the third incision,
which is also known as the interdental incision, to separate the
collar of gingiva that is left around the tooth. The Orban or
the Buck knife is usually used for this incision. The incision
is made not only around the facial and lingual radicular area,
FIGURE 45.15 Position of the knife to perform the internal bevel but also interdentally, where it connects the facial and lingual
incision. segments to free the gingiva completely around the tooth
(Figs. 45.14 and 4518)
These three incisions allow for the removal of the gingiva
The crevicular incision, which is also called the second inci- around the tooth (ie , the pocket epithelium and the adjacent
sion, is made from the base of the pocket to the crest of the granulomatous tissue). A surgical curette or a large scaler
bone (Fig. 45.17). This incision, together with the initial re- (Cumine) can be used for this purpose. After the removal of
verse bevel incision, forms a V-shaped wedge that ends at the large pieces of tissue, the remaining connective tissue in
or near the crest of bone (Fig. 45.18). This wedge of tissue the osseous lesion should be carefully curetted and removed
FIGURE 45.18 After the flap has been elevated, a wedge of tissue
remains on the teeth and is attached by the base of the papillae. An
interdental (third) incision along the horizontal lines seen in the inter-
dental spaces will sever these connections.
QJ I
I
(B) Incorrect Correct
FIGURE 45.16 A, The internal bevel (first) incision can be made at
varying locations and angles according to the different anatomic and
pocket situations. B, Occlusal view of the different locations in which
the internal bevel incision can be made. Note the scalloped shape of
the incisions.
(A) (B)
FIGURE 45.19 A, Incorrect and, B, correct locations of a vertical inci-
sion. This incision should be made at the line angles to prevent the split-
ting of a papilla or incising directly over a radicular surface.
to a few teeth to prevent needless exposure of bone of unin-

volved areas. These incisions must extend beyond the muco-
gingival line to reach the alveolar mucosa; this allows for the
release of the flap to be displaced.
In general, vertical incisions in the lingual and palatal areas
are avoided. Facial vertical incisions should not be made in
the center of an interdental papilla or over the radicular sur-
face of a tooth. Incisions should be made at the line angles of
a tooth either to include the papilla in the flap or to avoid it
completely (Fig. 45.19). The vertical incision should also be
designed to avoid short flaps (mesiodistal) with long, apically
FIGURE 45.17 Position of the knife to perform the crevicular (sec- directed incisions, because this could jeopardize the blood
ond) incision. supply to the flap. In other words, the base of the flap should
be broader than its margin.
so that the entire root and the bone surface adjacent to the
teeth can be observed.
Elevation of the Flap
Flaps can be reflected with the use of the horizontal inci-
sion only, if sufficient access can be obtained in this way and When a full-thickness flap is desired, reflection of the flap is
if apical, lateral, or coronal displacement of the flap is not accomplished with a blunt dissection. A periosteal elevator is
anticipated. If vertical incisions are not made, the flap is called used to separate the mucoperiosteum from the bone by mov-
an envelope flap. ing it mesially, distally, and apically until the desired reflection
is accomplished. No more than 1-2 mm of bone needs to be
exposed most of the times (Fig. 45 20)
Vertical Incisions
Sharp dissection is necessary to reflect a partial-thickness
Vertical or oblique-releasing incisions can be used on one or flap (Fig. 45.21). A combination of full-thickness and partial-
both ends of the horizontal incision, depending on the design thickness flaps may be indicated to obtain the advantages of
and purpose of the flap. Vertical incisions at both ends are both. The flap is started as a full-thickness procedure and then
necessary if the flap is to be apically or coronally displaced. a partial-thickness flap is made at the apical portion. In this
They are also preferred when the area of the surgery is limited way, the coronal portion of the bone-which may be subject
either resective or additive osseous surgery (see Chapters 4 7

and 48)
The entire surgical area is thoroughly irrigated and reexam-
ined for the presence of any debris, such as specks of calculus
prior to the flap replaced and sutured.
Sutures and Suturing Techniques

After all of the necessary procedures are completed, the flap is
placed in the desired position. The flap should remain in this
position without tension. It is convenient to keep the flap in
place with light pressure via the use of a piece of gauze to al-
low the blood clot to form.
The purpose of suturing is to maintain the flap in the de-
FIGURE 45.20 Elevation of the flap with a periosteal elevator to ob- sired position until healing has progressed to the point at
tain a full-thickness flap. Note the bone that is exposed with the full-
thickness flap. which sutures are no longer needed.
There are many types of sutures, suture needles, and ma-
terials. Suture materials may be either nonresorbable or re-
sorbable, and they may be further categorized as braided or
mono.filament. The resorbable sutures have gained popularity
because they enhance patient comfort and eliminate suture-
removal appointments (Box 45.1).
The monofilament type of suture alleviates the "wicking
effect" of braided sutures that may allow bacteria from the oral
cavity to be drawn through the suture into the deeper areas of
the wound.
The braided silk suture was the most common nonresorbable
suture used in the past because of its ease of use and low cost. It
is still used in many countries around the world. However the ex-
panded polytetrafluoroethylene, synthetic, monofilament suture
is an excellent nonresorbable suture that is preferred currently.
The most common resorbable sutures used today are the
FIGURE 45.21 Elevation of the flap with a Bard-Parker knife to ob- plain and chromic gut sutures. Both are monofilaments that
tain a split-thickness flap. Note that the bone is not exposed and that it are processed from purified collagen of either sheep or cattle
is covered by periosteal tissue.
intestines. The chromic suture is a plain-gut suture that has
been processed with chromic salts to make it resistant to enzy-
to osseous remodeling-is exposed, whereas the remaining matic resorption, thereby increasing the resorption time. The
bone is protected by the periosteum. synthetic resorbable sutures are also often used (Box 45.1).
Debridement Technique
After the flap is reflected, the process of debridement begins. The needle is held with the needle holder, and it should
First the granulation tissue is removed by sharp Gracey cu- enter the tissues at right angles and be no less than 2-3 mm
rettes. Once this is done, the bleeding stops considerably al- from the incision. The needle is then carried through the
lowing the operator to visualize the surgical field better. The
root surface is carefully planed with ultrasonic scalers and cu-
rettes. It is important that the flap is not allowed to dry during
the surgery. Frequent irrigation with normal saline not only
Nonabsorbable (Nonresorbable)
keeps the flap moist but also aids in debridement. Needless to Silk: braided
mention here is the importance of good aspiration. Nylon: monofilament
Recently, the need to completely degranulate the surgi- ePTFE: monofilament
cal field has been questioned by some researchers who claim Polyester: braided
that the granulation tissue may contain some growth factors, Absorbable (Resorbable)
which could be beneficial during healing. However this is just Surgical: gut
a hypothesis, which needs further investigation. Until now, to- Plain gut: monofilament (30 days)
tal removal of the granulation tissue has been the time-tested Chromic gut: monofilament (45-60 days)
concept and will remain so. Synthetic
Polyglycolic: braided (16-20 days)
Vicryl
Osseous Management Dexon
Poliglecaprone: monofilament (90-120 days)
The osseous shape and contour is examined, and the neces- Monocryl
sary osseous correction is accomplished. Often bony defects Polyglyconate: monofilament
are discovered only after flap elevation. These are managed by
FIGURE 45.22 Placement of sutures in the interdental space below

the base of an imaginary triangle in the papilla.
tissue, where it follows the needle's curvature. The knot

should not be placed over the incision.
The periodontal flap is closed either with independent su-
tures or with continuous, independent sling sutures. The lat- FIGURE 45.23 Placement of sutures to close a palatal flap. For slight-
ter method eliminates the pulling of the buccal and lingual or ly or moderately elevated flaps, the sutures are placed in the shaded ar-
eas. For the more substantial elevation of the flap, the sutures are placed
palatal flaps together and instead uses the teeth as an anchor in the central (unshaded) areas of the palate.
for the flaps. The flaps are less likely to buckle and the forces
on the flaps are better distributed.
Sutures of any type that are placed in the interdental papil-
lae should enter and exit the tissue at a point located below
the imaginary line that forms the base of the triangle of the Ligation
interdental papilla (Fig. 45.22). The location of sutures for the
closure of a palatal flap depends on the extent of flap elevation lnterdental Ligation
that has been performed. The flap is divided into four quad- Two types of interdental ligation can be used; the direct loop
rants as depicted in Fig. 45.23. suture (Fig. 45.24) and the figure-eight suture (Fig. 45.25).
If the elevation of the flap is slight or moderate, the sutures With the figure-eight suture, thread is placed between the
can be placed in the quadrant closest to the teeth. If the flap two flaps. This suture is used when the flaps are not in close
elevation is substantial, the sutures should be placed in the apposition as a result of apical flap position or nonscalloped
central quadrants of the palate. incisions. This is simpler to perform than the direct ligation.
The clinician may or may not use periodontal dressings. The direct suture allows for a better closure of the interdental
When the flaps are not apically displaced, it is not necessary papilla. It should be performed when bone grafts are used or
to use dressings other than those needed for patient comfort. when close apposition of the scalloped incision is required.
(A)
(C)
FIGURE 45.24 Simple loop suture is used to approximate the buccal and lingual flaps. A, The needle penetrates the outer surface of the first flap.
B, The undersurface of the opposite flap is engaged, and, C, the suture is brought back to the initial side, where, D, the knot is tied.
FIGURE 45.25 Interrupted figure-eight suture is used to approximate the buccal and lingual flaps. A, The needle penetrates the outer surface of
the first flap and, B, the outer surface of the opposite flap. C, The suture is brought back to the first flap, and, D, the knot is tied.
FIGURE 45.26 Single, interrupted sling suture is used to adapt the flap around the tooth. A, The needle engages the outer surface of the flap and,
B, encircles the tooth. C, The outer surface of the same flap of the adjacent interdental area is engaged. D, The suture is returned to the initial site, and
the knot is tied.
Sling Ligation the interdental papilla properly against the bone. Two sutures
The sling ligation can be used for a flap on one surface of a are often necessary. The horizontal mattress suture can be in-
tooth that involves two interdental spaces (Fig. 45.26). corporated with the continuous, independent sling sutures
(Fig. 45 27)
The penetration of the needle is performed in such a way
Types of Sutures that the mesial and distal edges of the papilla lie snugly against
the bone. The needle enters the outer surface of the gingiva
Horizontal Mattress Suture and crosses the undersurface of the gingiva horizontally. The
The horizontal mattress suture is often used for interproxi- mattress sutures should not be close together at the midpoint
mal areas of diastemata or for wide interdental spaces to adapt of the base of the papilla. The needle reappears on the outer
FIGURE 45.27 A, Continuous, independent sling suture with the use of a horizontal mattress suture around, B, diastemata or, C, wide interdental
areas. This mattress suture is used on both the, D, buccal and, E and F, lingual surfaces. G, H, and I, Continuation of suture on the lingual surfaces.
J, Completed suture.
surface at the other base of the papilla and continues around Anchor Suture
the tooth with the sling sutures. The closing of a flap mesial or distal to a tooth, as in the mesial
or distal wedge procedures, is best accomplished by the an-
Continuous, Independent Sling Suture
chor suture. This suture closes the facial and lingual flaps and
A sling suture is used when both a facial flap and a lingual adapts them tightly against the tooth. The needle is placed at
flap are used and when they involve many teeth. The con- the line-angle area of the facial or lingual flap adjacent to the
tinuous, independent sling suture is initiated on the facial tooth, anchored around the tooth, passed beneath the oppo-
papilla closest to the midline, because this is the easiest place site flap, and tied. The anchor suture can be repeated for each
to position the final knot. A continuous sling suture is laced area that requires it (Fig. 45.29).
for each papilla on the facial surface. When the last tooth
is reached, the suture is anchored around it to prevent any Closed Anchor Suture
pulling of the facial sutures when the lingual flap is sutured
around the teeth in a similar manner. The suture is again Another technique to close a flap that is located in an eden-
anchored around the last tooth before the final knot is tied tulous area mesial or distal to a tooth consists of tying a di-
(Fig. 45 28) rect suture that closes the proximal flap, carrying one of the
This type of suture does not pull on the lingual flap when threads around the tooth to anchor the tissue against the
this flap is sutured. The facial and lingual flaps are completely tooth, and then tying the two threads (Fig. 45 30)
independent of each other as a result of the anchoring around
both the initial tooth and the final tooth. The flaps are tied to Periosteal Suture
the teeth and not to each other because of the sling sutures. The periosteal suture is used to hold the apically displaced
Continuous, independent sling suturing is especially ap- partial-thickness flaps on the periosteum. There are two types
propriate for the maxillary arch. This is true because the pala- of periosteal sutures, the holding suture and the closing suture.
tal gingiva is attached and fibrous, whereas the facial tissue is The holding suture is a horizontal mattress suture that is placed
thinner and mobile. at the base of the displaced flap to secure it into the new position.
FIGURE 45.28 Continuous, independent sling suture is used to adapt the buccal and lingual flaps without tying the buccal flap to the lingual flap.
The teeth are used to suspend each flap against the bone. It is important to anchor the suture on the two teeth at the beginning and end of the flap so
that the suture will not pull the buccal flap to the lingual flap.
FIGURE 45.29 Distal wedge suture. This anchor suture is also used to FIGURE 45.30 The closed anchor suture, which is another technique
close flaps that are mesial or distal to a lone standing tooth. that can be used to suture distal wedges.
depends on the purpose for which it is being performed and the

final outcome the clinician desires. Accordingly, various clini-
cians have devised techniques over the period of time and several
names have been given, such as Newman flap, Kirkland flap, flap
curettage, open-flap curettage, and so on. But the most common-
ly practiced techniques today are the modified-Widman flap, the
conventional or the access flap, undisplaced flap (also called in-
verse bevel gingivectomy), and the apically displaced flap.
The modified-Widman flap has been described for exposing
the root surfaces for meticulous instrumentation and for the
removal of the pocket lining. Again, it is not intended to elimi-
FIGURE 45.31 Periosteal sutures for an apically displaced flap. Hold- nate or reduce pocket depth, except for the reduction that
ing sutures, which are shown at the bottom, are placed first. This is fol- occurs during healing as a result of tissue shrinkage.
lowed by the closing sutures, which are shown at the coronal edge of The conventional or access flap attempts to conserve the tis-
the flap.
sues as much as possible so as to ensure optimal coverage of
graft materials and barrier membranes that might have to be
Closing sutures are used to secure the flap edges to the perios- placed for the regeneration of the periodontal tissues.
teum. Both types of periosteal sutures are shown in Fig. 45.31. The undisplaced (unrepositioned) flap improves accessibil-
ity for instrumentation, but it also removes the pocket wall,
thereby reducing or eliminating the pocket. This is essentially
Healing After Flap Surgery an excisional procedure of the gingiva.
Immediately after suturing (:c::,24 h), a connection between the The apically displaced flap provides accessibility and elimi-
flap and the tooth or bone surface is established by a blood nates the pocket, but it does the latter by apically positioning
clot, which consists of a fibrin reticulum with many polymor- the soft-tissue wall of the pocket. Therefore, it preserves or in-
phonuclear leukocytes, erythrocytes, debris of injured cells, creases the width of the attached gingiva by transforming the
and capillaries at the edge of the wound. Bacteria and an exu- previously unattached keratinized pocket wall into attached tis-
date or transudate also result from tissue injury. sue. This increase in the width of the attached gingiva is based
One to three days after flap surgery, the space between the on the apical shift of the mucogingival junction, which may
flap and the tooth or bone is thinner. Epithelial cells migrate include the apical displacement of the muscle attachments.
over the border of the flap and usually contact the tooth at this
time. When the flap is closely adapted to the alveolar process, Incisions
there is a minimal inflammatory response.
One week after surgery, an epithelial attachment to the root All of the three flap techniques that were just discussed in-
has been established by means of hemidesmosomes and a volve the use of the basic incisions described earlier in this
basal lamina. The blood clot is replaced by granulation tissue chapter. The internal bevel incision, the crevicular incision,
derived from the gingival connective tissue, the bone marrow, and the interdental incision. However, there are important
and the periodontal ligament. variations in the way these incisions are performed for the dif-
Two weeks after surgery, collagen fibers begin to appear par- ferent types offlaps (Figs. 45.32 and 45 33) The internal bev-
allel to the tooth surface. Union of the flap to the tooth is still eled incision for the modified-Widman flap closely follows the
weak because of the presence of immature collagen fibers, al- scalloped outline of the dentition to minimize the loss of the
though the clinical aspect may be almost normal. attached keratinized gingiva. This incision is made 1-2 mm
One month after surgery, a fully epithelialized gingival crevice from the teeth. The gingival margin is removed, and the flap is
with a well-defined epithelial attachment is present. There is reflected to gain access for root therapy.
a beginning functional arrangement of the supracrestal fibers. The technique that is used to achieve reconstructive and
Full-thickness flaps, which denude the bone, result in a regenerative objectives is the conventional flap with or without
superficial bone necrosis after 1-3 days. Osteoclastic resorp- papilla preservation, which involves only the crevicular or sec-
tion follows and reaches a peak at 4-6 days and then declines ond incision. This will allow the clinician to retain the maxi-
thereafter. This results in a loss of bone of about 1 mm3; the mum amount of gingival tissue, including the papilla, which
bone loss is greater if the bone is thin. is essential for graft or membrane coverage.
A loss of bone occurs during the initial healing stages both For the undisplaced flap, the internal bevel incision is ini-
in the radicular bone and in the interdental bone areas. How- tiated at or near a point just coronal to where the bottom of
ever, in the interdental areas, which have cancellous bone, the the pocket is projected on the outer surface of the gingiva
subsequent repair stage results in total restitution without any (Fig. 45 32). This incision can be accomplished only if suf-
loss of bone; in radicular bone (particularly if it is thin and ficient attached gingiva remains apical to the incision. There-
unsupported by cancellous bone), bone repair results in the fore, the two anatomic landmarks-the pocket depth and the
loss of marginal bone. location of the mucogingival junction-must be considered to
evaluate the amount of attached gingiva that will remain after
Different Flap Techniques the surgery has been completed. Because the pocket wall is
not displaced apically, the initial incision should eliminate the
Whereas the basic principles of flap surgery remain the same, pocket wall. Thus, an incision should not be made too close
slight variations and modifications are required to deal with dif- to the tooth, because it will not eliminate the pocket wall, and
ferent situations. The design of the flap and the extent to which it may result in the recreation of the soft-tissue pocket. If the
tissues are resectecl/conserved and the amount of flap reflection tissue is too thick, the flap margin should be thinned with the
There is no need to determine where the bottom of the pocket

is in relation to the incision for the apically displaced flap as one
would for the undisplaced flap. The flap is placed at the tooth-
bone junction by apically displacing the flap. Its final position is
MGJ not determined by the placement of the first incision.
If the surgeon contemplates osseous surgery, the first inci-
sion should be placed in a way to compensate for the removal
1. Undisplaced of the bone tissue; so that the flap can be placed at the tooth-
BP = Bottom of Pocket bone junction.
MGJ = Mucogingival Junction
The Flap Technique for Pocket

Therapy
Modified Widman Flap
(A)
In 1965, Morris revived a technique described early during the
20th century in the periodontal literature; he called it the "un-
repositioned mucoperiosteal flap." Essentially, the same proce-
dure was presented in 1974 by Ramfjord and Nissie, who called
it the "modified-Widman flap" (Fig. 45 34). This technique of-
fers the possibility of establishing an intimate postoperative ad-
aptation of healthy collagenous connective tissue to tooth sur-
faces, and it provides access for adequate instrumentation of the
MGJ 1. Modified Widman root surfaces and immediate closure of the area. The following
2. Apically Displaced steps outline the modified-Widman flap technique.
BP = Bottom of Pocket
Step 1: The initial incision is an internal bevel incision to the al-
MGJ = Mucogingival veolar crest starting 0.5-1 mm away from the gingival margin
Junction (Fig. 45 34C) Scalloping follows the gingival margin. Care
should be taken to insert the blade in such a way that the
papilla is left with a thickness similar to that of the remaining
(B) facial flap. Vertical relaxing incisions are usually not needed.
Step 2: The gingiva is reflected with a periosteal elevator
FIGURE 45.32 Locations of the internal bevel incisions for the dif- (Fig. 45.34D)
ferent types of flaps.
Step 3: A crevicular incision is made from the bottom of the
pocket to the bone in such a way that it circumscribes the
triangular wedge of tissue that contains the pocket lining.
Step 4: After the flap is reflected, a third incision is made
in the interdental spaces coronal to the bone with a cu-
rette or an Orban knife, and the gingival collar is removed
(Fig. 45.34E and F)
Step 5: Tissue tags and granulation tissue are removed with a
curette. The root surfaces are checked and then scaled and
planed, if needed (Fig. 45.34G and H). Residual periodontal
fibers attached to the tooth surface should not be disturbed.
Step 6: Bone architecture is not corrected unless it prevents good
tissue adaptation to the necks of the teeth. Every effort is made
to adapt the facial and lingual interproximal tissue adjacent to
FIGURE 45.33 Scalloping required for the different types of flaps.
each other in such a way that no interproximal bone remains
exposed at the time of suturing. The flaps may be thinned
to allow for close adaptation of the gingiva around the entire
circumference of the tooth and to each other interproximally.
initial incision. The proper placement of the flap margin at
Step 7: Continuous, independent sling sutures are placed in
the tooth-bone junction during closure is important to pre-
both the facial and palatal areas (Fig. 45.341 andj) and cov-
vent either recurrence of the pocket or the exposure of bone.
ered with a periodontal surgical pack.
The internal bevel incision should be scalloped into the in-
terdental area to preserve the interdental papilla (Fig. 45.33). Ramfjord and Nissie performed an extensive longitudinal
This will allow better coverage of the bone at both, the radicu- study that compared the Widman procedure (as modified by
lar and interdental areas. them) with the curettage technique and the pocket elimina-
The apically displaced flap technique is selected for cases tion methods, which include bone contouring when needed.
that present a minimal amount ofkeratinized, attached gingiva. The patients were assigned randomly to one of the techniques
For this reason, the internal bevel incision should be made as and results were analyzed yearly for up to 7 years after ther-
close to the tooth as possible (ie, 0.5-1.0 mm) (Fig. 45 32). apy. The researchers reported similar results for each of the
FIGURE 45.34 Modified-Widman flap technique. A, Facial view before surgery. The probing of pockets revealed interproximal depths that ranged
from 4-8 mm and facial and palatal depths of 2-5 mm. B, Radiographic survey of the area. Note the generalized horizontal bone loss. C, Facial internal
bevel incision. D, Palatal incision. E, Elevation of the flap, which left a wedge of tissue still attached to its base. F, Removal of tissue. G, Tissue removed
and ready for scaling and root planing. H, Scaling and root planing of exposed root surfaces. 1, Continuous, independent sling suture of facial portion of
surgery. J, Continuous, independent sling suture of palatal portion of surgery. K, Postsurgical result. (Courtesy Dr Kitetsu Shin, Saitama, Japan.)
three methods tested. Pocket depth was initially similar for problem, the clinician should determine that enough attached
all methods but it was maintained at shallower levels with the gingiva will remain after removal of the pocket wall. The follow-
Widman flap; the attachment level remained higher with the ing steps outline the undisplaced flap technique.
Widman flap.
Step 1: The pockets are measured with the periodontal probe
and a bleeding point is produced on the outer surface of the
gingiva to mark the pocket bottom.
Undisplaced Flap Step 2: The initial or internal bevel incision is made
Currently, the undisplaced flap may be the most frequently per- (Fig. 45.35) after scalloping the bleeding marks on the gin-
formed type of periodontal surgery. It differs from the modified- giva (Fig. 45.36). The incision is usually carried to a point
Widman flap in that the soft-tissue pocket wall is removed with apical to the alveolar crest depending on the thickness of
the initial incision; thus, it may be considered an "internal bevel the tissue. The thicker the tissue is, the more apical the end-
gingivectomy." The undisplaced flap and the gingivectomy are ing point of the incision (Fig. 45.35). In addition, thinning
the two techniques that surgically remove the pocket wall. of the flap should be performed with the initial incision,
To perform this technique without creating a mucogingival because it is easier to accomplish at this time than it is later
(A) MGJ = Mucogingival Junction
(B) MGJ = Mucogingival Junction
FIGURE 45.35 Diagram showing the location of two different areas where the internal bevel incision is made in an undisplaced flap. The incision
is made at the level of the pocket to discard the tissue coronal to the pocket if there is sufficient remaining attached gingiva.
with a loose, reflected flap that is difficult to manage. (The Palatal Flap
use of this technique in palatal areas is considered in the
discussion that follows this list.) The surgical approach to the palatal area differs from that used
Step 3: The second or crevicular incision is made from the for other areas as a result of the character of the palatal tissue
bottom of the pocket to the bone to detach the connective and the anatomy of the area. The palatal tissue is all attached,
tissue from the bone. keratinized tissue and has none of the elastic properties asso-
Step 4: The flap is reflected with a periosteal elevator (blunt ciated with other gingival tissues. Therefore, the palatal tissue
dissection) from the internal bevel incision. Usually there cannot be apically displaced and a partial-thickness (split-
is no need for vertical incisions, because the flap is not dis- thickness) flap cannot be accomplished.
placed apically The initial incision for the palatal flap should allow the
Step 5: The third or interdental incision is made with an in- flap, when sutured, to be precisely adapted at the root-bone
terdental knife to separate the connective tissue from the junction. The flap cannot be moved apically or coronally to
bone. adapt to the root-bone junction, as can be done with the flaps
Step 6: The triangular wedge of tissue created by the three in other areas. Therefore, the location of the initial incision is
incisions is removed with a curette. important for the final placement of the flap.
Step 7: The area is debrided to remove all tissue tags and gran- The palatal tissue may be thin or thick and it may or may
ulation tissue with the use of sharp curettes. not have osseous defects. The palatal vault may be high or low.
Step 8: After the necessary scaling and root planing, the flap These anatomic variations may require changes in the loca-
edge should rest on the root-bone junction. If this is not the tion, angle, and design of the incision.
case as a result of the improper location of the initial inci- The initial incision for a flap varies with the anatomic situa-
sion or the unexpected need for osseous surgery, the edge tion. As shown in Fig. 45.37, the initial incision may be the usual
of the flap is scalloped again and trimmed to allow the flap internal bevel incision, which will then be followed by crevicular-
edge to end at the root-bone junction. and interdental incisions. If the tissue is thick, a horizontal gingi-
Step 9: A continuous sling suture is used to secure the fa- vectomy incision may be made, and this may be followed by an
cial and lingual or palatal flaps. This type of suture, which internal bevel incision that starts at the edge of this incision and
makes use of the tooth as an anchor, is advantageous to ends on the lateral surface of the underlying bone. The placement
position and hold the flap edges at the root-bone junction. of the internal bevel incision must be done in such a way that the
The area is covered with a periodontal pack. flap fits around the tooth without exposing the bone.
FIGURE 45.36 Undisplaced flap. A and B, Preoperative facial and palatal views. C and D, Internal bevel incisions in the facial and palatal aspects.
Note the deeper scalloping palatally for the replaced flap. E and F, Flap elevated to show osseous defects. G and H, Osseous surgery has been per-
formed. I and J, Flaps have been placed in their original sites and sutured. Kand L, Postoperative results. (Courtesy Dr Paulo Camargo, University of
California, Los Angeles.)
Before the flap is reflected to the final position for scaling

and management of the osseous lesions, its thickness must
be checked. Flaps should be thin to adapt to the underlying
osseous tissue and provide a thin, knife-like gingival margin.
Flaps-particularly palatal flaps-are often too thick; they
may have a propensity to separate from the tooth, which may
delay and complicate healing. It is best to thin the flaps be-
fore their complete reflection because a free, mobile flap is
difficult to hold for thinning (Fig. 45 38) A sharp, thin pa-
pilla positioned properly around the interdental areas at the
tooth-bone junction is essential to prevent the recurrence of
soft-tissue pockets.
The purpose of the palatal flap should be considered be-
fore the incision is made. If the intent of the surgery is de-
bridement, the internal bevel incision is planned so that the
flap adapts at the root-bone junction when sutured. If osse-
ous resection is necessary, the incision should be planned to
compensate for the lowered level of the bone when the flap
is closed. Probing and sounding of the osseous level and the
depth of the intrabony pocket should be used to determine
the position of the incision.
The apical portion of the scalloping should be narrower
FIGURE 45.37 Examples of two methods for eliminating a palatal
pocket. One incision is an internal bevel incision made at the area of the
than the line-angle area because the palatal root tapers apical-
apical extent of the pocket. The other procedure involves a gingivectomy ly. A rounded scallop results in a palatal flap that does not fit
incision, which is followed by an internal bevel incision. snugly around the root. This procedure should be done before
1/
(8)
(A)
FIGURE 45.38 Diagrams that illustrate the angle of the internal bevel
incision in the palate and the different ways to thin the flap. A, The FIGURE 45.39 A, Distal view of incisions made to eliminate a pocket
usual angle and direction of the incision. B, Thinning of the flap after it distal to the maxillary second molar. B, Two parallel incisions and the
has been slightly reflected with a second internal incision. C, Beveling removal of the intervening tissue. C, Thinning of the flap and contouring
and thinning of the flap with the initial incision if the position and con- of the bone. D, Approximation of the buccal and palatal flaps.
tour of the tooth allow. D, The problem encountered when thinning the
flap after it has been reflected. The flap is too loose and free for proper
positioning and for the making of the incision. 1 mm from the crest of the gingiva and directed to the crest
of the bone. The incision is made after the existing scallop-
the complete reflection of the palatal flap because a loose flap ing and there is no need to mark the bottom of the pocket
is difficult to grasp and stabilize for dissection. in the external gingival surface, because the incision is un-
It is sometimes necessary to thin the palatal flap after it has related to pocket depth. It is also not necessary to accentu-
been reflected. This can be accomplished by holding the inner ate the scallop interdentally because the flap is displaced
portion of the flap with a mosquito hemostat or Adson for- apically and not placed interdentally
ceps as the inner connective tissue is carefully dissected away Step 2: Crevicular incisions are made and is followed by the
with a sharp no. 15 scalpel blade. Care must be taken to not initial elevation of the flap. Interdental incisions are then
perforate or overthin the flap. The edge of the flap should be performed and the wedge of tissue that contains the pocket
thinner than the base; therefore, the blade should be angled wall is removed.
toward the lateral surface of the palatal bone. The dissected Step 3: Vertical incisions are made extending beyond the mu-
inner connective tissue is removed with a hemostat. As with cogingival junction. If the objective is a full-thickness flap,
any flap, the triangular papilla portion should be thin enough it is elevated by blunt dissection with a periosteal elevator.
to fit snugly against the bone and into the interdental area If a split-thickness flap is required, it is elevated via sharp
(Fig. 45 39) dissection with the use of a Bard-Parker knife to split it.
The principles for the use of vertical releasing incisions are This leaves a layer of connective tissue, including the peri-
similar to those for using other incisions. Care must be exer- osteum, on the bone.
cised so that the length of the incision is minimal to avoid the Step 4: After the removal of all granulation tissue, scaling
numerous vessels located in the palate. and root planing, and osseous surgery if needed, the flap
is displaced apically It is important that the vertical inci-
sions-and therefore the flap elevation-reach past the
Apically Displaced Flap mucogingival junction to provide adequate mobility to the
flap for its apical displacement.
With some variants, the apically displaced flap technique can Step 5: If a full-thickness flap was created, a sling suture
be used for pocket eradication, widening the zone of attached around the tooth prevents the flap from sliding to a posi-
gingiva, or both. Depending on the purpose, the apically dis- tion more apical than what is desired, and the periodontal
placed flap can be a full-thickness (mucoperiosteal) flap or dressing can avoid its movement in a coronal direction. A
a split-thickness (mucosa!) flap. The split-thickness flap re- partial-thickness flap is sutured to the periosteum with the
quires more precision and time, as well as, a gingival tissue use of a direct loop suture or a combination of loop and
that is thick enough to split, but it can be more accurately anchor suture. A dry foil is placed over the flap before it
positioned and sutured in an apical position with the use of a is covered with the dressing to prevent the introduction of
periosteal suturing technique, as follows. pack under the flap.
Step 1: An internal bevel incision is made (Fig. 45.40). To After 1 week, dressings and sutures are removed. The area
preserve as much of the keratinized and attached gingiva is usually repacked for another week, after which the patient
as possible (Fig. 45.32), it should be no more than about is instructed to use chlorhexidine mouthrinse or to apply
FIGURE 45.40 An apically displaced flap. A and B, Facial and lingual preoperative views. C and D, The facial and lingual flaps have been elevated.
E and F, After debridement of the areas. G and H, The sutures are in place. 1 and J, Healing after 1 week. K, Healing after 2 months. Note the preserva-
tion of attached gingiva displaced to a more apical position. (Courtesy Dr Thomas Han, Los Angeles, CA.)
chlorhexidine topically with cotton-tipped applicators for an- Step 2: The preserved papilla can be incorporated into the fa-
other 2 or 3 weeks. cial or lingual/palatal flap, although it is most often integrat-
ed into the facial flap. In these cases, the lingual or palatal
incision consists of a semilunar incision across the interden-
Flaps for Reconstructive Surgery tal papilla in its palatal or lingual aspect; this incision dips
In current reconstructive therapy, bone grafts, membranes, or a apically from the line angles of the tooth so that the papillary
combination of these-with or without other agents-are used incision is at least 5 mm from the crest of the papilla.
for a successful outcome. The flap design should, therefore, Step 3: An Orban knife is then introduced into this incision to
be set up so that the maximum amount of gingival tissue and sever half to two-thirds of the base of the interdental papil-
papilla are retained to cover the material placed in the pocket. la. The papilla is then dissected from the lingual or palatal
Two flap designs are available for reconstructive surgery: aspect and elevated intact with the facial flap.
the papilla-preservation flap and the conventional flap with Step 4: The flap is reflected without thinning the tissue.
only crevicular incisions. The flap design of choice is the papilla-
preservation flap, which retains the entire papilla covering the
Conventional Flap/ Access Flap
lesion. However, to use this flap, there must be an adequate
interdental space to allow the intact papilla to be reflected The technique for employing a conventional flap for recon-
with the facial or lingual/palatal flap. When the interdental structive surgery is as follows.
space is very narrow, thereby making it impossible to perform
Step 1: With the use of a no. 12 blade, an incision to the tissue
a papilla-preservation flap, a conventional flap with only ere-
is made at the bottom of the pocket and to the crest of the
vicular incisions is made.
bone to split the papilla below the contact point. Every ef-
fort should be made to retain as much tissue as possible to
Papilla-Preservation Flap protect the area subsequently.
Step 2: The flap is reflected; keeping it as thick as possible
The technique for employing a papilla-preservation flap is as
without attempting to thin it as is done for resective sur-
follows (Figs. 45.41 and 45.42).
gery. The maintenance of a thick flap is necessary to prevent
Step 1: A crevicular incision is made around each tooth, with exposure of the graft or the membrane, which results from
no incisions across the interdental papilla. necrosis of the flap margins.
~t
\ \
(A) \
(C)
FIGURE 45.41 Flap design for a papilla-preservation flap. A, Incisions for this type of flap are depicted by interrupted lines. The preserved papilla
can be incorporated into the facial or the lingual-palatal flap. B, The reflected flap exposes the underlying bone. Several osseous defects are seen.
C, The flap has been returned to its original position, where it covers all of the interdental spaces.
FIGURE 45.42 Papilla-preservation flap. A, Facial view after sulcular incisions have been made. B, Straight-line incision in the palatal area about
3 mm from the gingival margins. This incision is then connected to the margins with vertical incisions at the midpart of each tooth. C, Papillae are
reflected with the facial flap. D, Lingual view after the reflection of the flap. E, Lingual view after the flap is brought back to its original position. It is
then sutured with independent sutures. F, Facial view after healing. G, Palatal view after healing. (Courtesy Dr Thomas Han, Los Angeles, CA.)
Distal Molar Surgery incomplete repair after the extraction of impacted third mo-
lars (Fig. 4543)
The treatment of periodontal pockets on the distal surface of The gingivectomy incision is the most direct approach to
terminal molars is often complicated by the presence of bul- the treatment of distal pockets that have adequate attached
bous fibrous tissue over the maxillary tuberosity or promi- gingiva and no osseous lesions. However, the flap approach
nent retromolar pads in the mandible. Deep-vertical defects is less traumatic postsurgically because it produces a primary
are also often present in conjunction with the redundant fi- closure wound rather than the open secondary wound left
brous tissue. Some of these osseous lesions may result from by a gingivectomy incision. In addition, it results in attached
Technique
Two parallel incisions that begin at the distal portion of the
tooth and extend to the mucogingival junction distal to the
tuberosity or retromolar pad are made (Fig. 45.45). The facio-
I I
I
I
~
/I
1/
1/
I lingual distance between these two incisions depends on the
\ I\
I / I -._ \ I I depth of the pocket and the amount of fibrous tissue involved.
I I I I --- I / I I
The deeper the pocket, the greater is the distance between the
,,
I
\ I I ~ I / 1 I
\ I \ JI I I I A
v ~1 v ~, two parallel incisions. It is important to note that, when the
I I
, I tissue between the two incisions is removed and the flaps are
(A) \ / (B) '' , thinned, the two flap edges must approximate each other at a
new apical position without overlapping.
When the depth of the pocket cannot be easily estimated,
it is better to err on the conservative side to leave overlap-
ping flaps rather than flaps that are too short and that result
I
i ,, in the exposure of bone. When the two flaps overlap after
,I,. , ,
I
I I\
I I \ the surgery is completed, they should be placed one over the
I
,
I I I
I I
I
other. The overlapping portion of one of them is grabbed with
(C)
\ I './ a hemostat and a sharp knife or scissors is then used to cut
the excess.
FIGURE 45.43 A, Impaction of a third molar distal to a second molar
with little or no interdental bone between the two teeth. B, Removal
A transversal incision is made at the distal end of the two
of the third molar creates a pocket with little or no bone distal to the parallel incisions so that a long, rectangular piece of tissue can
second molar. C, This often leads to a vertical osseous defect distal to be removed. These incisions are usually interconnected with
the second molar. the incisions for the remainder of the surgery in the quadrant
involved. The parallel distal incisions should be confined to
gingiva. It also provides access for examination and, if needed, the attached gingiva because bleeding and flap management
correction of the osseous defect. Procedures for this purpose become problems when the incision is extended into the al-
were described by Robinson and Braden and modified by sev- veolar mucosa. If access is difficult-especially if the distance
eral other investigators. Some representative procedures are from the distal aspect of the tooth to the mucogingival junc-
discussed in the following sections. tion is short-then a vertical incision can be made at the end
of the parallel incisions.
When treating the tuberosity area, the two distal incisions
Maxillary Molars are usually made at the midline of the tuberosity (Fig. 45.46).
The treatment of distal pockets on the maxillary arch is usually In most cases, no attempt is made to undermine the underly-
simpler than the treatment of a similar lesion on the mandibu- ing tissue at this time. These incisions are made straight down
lar arch, because the tuberosity presents a greater amount of into the underlying bone, where access is difficult. A no. 12B
fibrous attached gingiva than does the area of the retromolar blade is generally used. It is easier to dissect out the underly-
pad. In addition, the anatomy of the tuberosity that extends ing redundant tissue when the flap is partially reflected. When
distally is more adaptable to pocket elimination than is that the distal flaps are placed back on the bone, the two flap mar-
of the mandibular-molar arch, where the tissue extends coro- gins should closely approximate each other.
nally. However, the lack of a broad area of attached gingiva
and the abruptly ascending tuberosity sometimes complicate Mandibular Molars
therapy (Fig. 45. 44).
The following considerations determine the location of the in- Incisions for the mandibular arch differ from those used for
cision for distal molar surgery: accessibility, amount of attached the tuberosity as a result of differences in the anatomy and
gingiva, pocket depth, and available distance from the distal as- histologic features of the areas. The retromolar pad area does
pect of the tooth to the end of the tuberosity or retromolar pad. not usually present as much fibrous attached gingiva. The
I,.. \ 1' 1'

f
I
I
\
I/ I I I
Ir II I
I 't I
I / I
-
/
f
/
/
,.
r,~
f
I
f \
I I
I
I
I
\.. /
/
/
/I
/
/
.,----- ')..'"' _.1
(, (' r' r'lr•~ I
I I \\ I
~ I
I
11 \f I
If It I f f I I 1/
I
I
I )
I_/
f
:
I_,_
II II I I
V" \ -- .,,,
, ,/
I ---
(A)
(B)
FIGURE 45.44 A, Removal of a pocket distal to the maxillary second molar may be difficult if there is minimal attached gingiva. If the bone ascends
acutely apically, the removal of this bone may make the procedure easier. B, A long distal tuberosity with abundant attached gingiva is an ideal ana-
tomic situation for distal pocket eradication.
FIGURE 45.45 A, A distal pocket eradication procedure with the incision distal to the molar. B, A scalloped incision around the remaining teeth.
C, The flap has been reflected and thinned around the distal incision. D, The flap in position before suturing. It should be closely approximated.
E, The flap sutured both distally and over the remaining surgical area.
I
I
,,
I
,
: ,
~~--- ------
'
---,--- , ,'
,,'
I ,. ' I ,
I' I I , l \ I ,,
I \ I
I I I I I I ' I ,
I I I 'I,'
I I I
\ I I /
I I
FIGURE 45.46 Typical incision design for a surgical procedure distal I I \ I I I
\ I I I
to the maxillary second molar. (A) '~' ,J ,1
keratinized gingiva, if present, may not be found directly dis-

tal to the molar. The greatest amount may be distolingual or I
I
distofacial, and it may not be over the bony crest. The ascend- I
,,
I
ing ramus of the mandible may also create a short, horizontal
area distal to the terminal molar. The shorter this area, the
more difficult it is to treat any deep distal lesion around the
terminal molar. -------
The two incisions distal to the molar should follow the
area with the greatest amount of attached gingiva (Figs. 45.47
and 45.48). Therefore, the incisions could be directed disto-
lingually or distofacially, depending on which area has more (8)
attached gingiva. Before the flap is completely reflected, it is FIGURE 45.47 A, Pocket eradication distal to a mandibular second
thinned with a no. 15 blade. It is easier to thin the flap before molar with minimal attached gingiva and a close ascending ramus is
it is completely free and mobile. After the reflection of the flap anatomically difficult. B, For surgical procedures distal to a mandibular
second molar, abundant attached gingiva and distal space are ideal.
and the removal of the redundant fibrous tissue, any neces-
sary osseous surgery is performed. The flaps are approximated
similarly to those in the maxillary tuberosity area. and minimal postoperative pain. When flaps need to be re-
positioned apically or coronally, they must sit passively at the
appropriate level before suturing. To ensure this, buccal and
Conclusion lingual flaps need to be elevated beyond the mucogingival
Periodontal flap surgery is the most widely used surgical pro- junction so that the elasticity of the mucosa allows for flap
cedure to treat pockets. Periodontal flaps are designed to pre- mobility. Sometimes it may be necessary to extend the flap el-
serve gingival integrity and to gain access to root surfaces for evation apically with a split incision approach to minimize the
residual calculus removal and to thoroughly remove granula- effect of the less elastic periosteum. Vertical incisions can aid
tion tissue so that bone defects can be visualized and treated. in flap positioning by allowing the clinician to suture the flap
Gentle and efficient procedures result in optimum healing at a different level to the adjacent untreated gingiva.
bone margins, flaps for the precise processes of osseous sur-

gery, and flaps for periodontal regeneration. All of these ap-
proaches have specific flap designs and step-by-step elements,
and all of them include calculus removal and root planing as
part of the essential treatment protocol. Flaps should allow
for adequate access and they should be reflected so that at
least 3 mm of crestal bone is exposed. If the flaps are to be
positioned apically, flap mobility is obtained by extending
the facial and lingual flap elevation beyond the mucogingival
junction, which enables the elasticity of the mucosa to be ap-
plied. Palatal flaps are much less mobile; thus, inverse bevel
incisions are used to remove marginal gingival tissues so that,
at the time of suturing, the flap margin is positioned apically,
if so indicated.
Papilla-preservation techniques with various modifications
are applied to those areas in which gingival recession needs to
be minimized. For some esthetic locations, nonsurgical thera-
py may be more appropriate than flap surgery
Adjacent edentulous areas are incorporated into the flap
design with the use of wedge incisions that enable access to
adjacent root surfaces for complete root planing and that al-
low clinicians to visualize and treat the associated bone de-
fects. Postoperative-plaque control is essential for successful
outcomes. Clinicians should ensure that patients have dem-
onstrated adequate oral hygiene during the presurgical phase
and they should emphasize that this must continue this after
surgery
FIGURE 45.48 Incision designs for surgical procedures distal to the SUGGESTED READINGS
mandibular second molar. The incision should follow the areas of great-
Ainamo A, Bergenholtz A, Hugoson A, et al: Location of the mucogingival
est attached gingiva and underlying bone. junction 18 years after apically repositioned nap surgery, J Clin Periodontal
19:49, 1992.
Braden BE: Deep distal pockets adjacent to terminal teeth, Dent Clin North
Palatal flaps are less mobile as a result of the absence of Am 13:161, 1969.
oral mucosa, so the apical position of the flap depends on Caton J, Nyman S: Histometric evaluation of periodontal surgery. I. The mod-
how much marginal gingival tissue is discarded with the ified Widman nap procedure,] Clin Periodontal 7:212, 1980.
use of a reverse bevel incision. The more apical positioning Matelski DE, Hurt WC: The corrective phase: the modified Widman nap.
desired, the more extensive is the reverse bevel cut. Palatal In Hurt WC, editor: Periodontics in general practice, Springfield, IL, 1976,
Charles C Thomas.
flaps are more difficult to position coronally than buccal or Morris ML: The unrepositioned mucoperiosteal nap, Periodontics 3:147, 1965.
lingual flaps. Thus, if it is required to position flaps coro- Olsen C, Ammons WF, van Belle G: A longitudinal study comparing apically
nally or even at their original levels, then a sulcular incision repositioned naps, with and without osseous surgery, Int J Pe,iodontics Re-
is used. During osseous periodontal surgery, flaps are api- storative Dent 5:10, 1985.
cally positioned to minimize postoperative pocket depth. Ramljord SP: Present status of the modified Widman nap procedure, J Peri-
odontal 48:558, 1977.
During regenerative periodontal surgery, soft-tissue coverage Ramljord SP, Nissie RR: The modified Widman nap, J Periodontal 45:601,
of bony defects, graft materials, membranes, and biologic 1974.
agents is important, so sulcular incisions and tight suturing Robinson RE: The distal wedge operation, Periodontics 4:256, 1966.
techniques are crucial. Takei HH, Han TJ, Carranza FA, et al: Flap technique for periodontal bone
implants: papilla preservation technique,] Periodontal 56:204, 1985.
Periodontal flap procedures for pocket therapy include Tavtigian R: The height of the facial radicular alveolar crest following apically
flaps that are created solely for access to root surfaces and positioned nap operation,] Periodontol 41:412, 1970.
46
Treatment of Gingival
Enlargement
PM Camargo • FA Carranza • FQ Pirih • HH Takei • CD Dwarakanath
Chapter Outline
Chronic Inflammatory Enlargement Neoplastic Gingival Enlargements
Gingival and Periodontal Abscesses (Gingival Tumours) and Other Solitary
Drug-Associated Gingival Enlargement Overgrowths
Gingival Enlargement During Pregnancy Recurrence of Gingival Enlargement
The treatment of gingival enlargement is based on an under- Gingival and Periodontal Abscesses
standing of the cause and underlying pathologic changes of
this condition. Gingival enlargements are of special concern The reader is referred to Chapters 32 and 33 for a complete
to the patient and the dentist because they pose problems that discussion of abscess treatment.
involve plaque control, function (including mastication, tooth
eruption, and speech), and aesthetics. As they differ with re-
gard to cause, the treatment of each type is best considered Drug-Associated Gingival
individually. Enlargement
Gingival enlargement has been associated primarily with
Chronic Inflammatory Enlargement the administration of three different types of drugs: anticon-
Chronic inflammatory enlargements, which are soft and discol- vulsants, calcium channel blockers, and the immunosup-
ored and which are caused principally by edema and cellular pressants. Chapter 15 provides a comprehensive review of
infiltration, are treated by scaling and root planing, provided the clinical and microscopic features and the pathogenesis
that the size of the enlargement does not interfere with the of gingival enlargement induced by these drugs. There is
complete removal of deposits from the involved tooth surfaces. limited evidence that other drugs may also induce gingival
When chronic inflammatory gingival enlargements include enlargement, albeit at a lower prevalence and with a lesser
a significant fibrotic component that do not undergo shrink- severity.
age after scaling and root planing or are of such size that they The examination of cases of drug-induced gingival enlarge-
obscure deposits on the tooth surfaces and interfere with ment reveals the overgrown tissues to have two components:
access to them, surgical removal is the treatment of choice. fibrotic, which are caused by the drug, and inflammatory,
Two techniques are available for this purpose: gingivoplasty/ which are induced by bacterial plaque. Although the fibrotic
gingivectomy and the flap operation. and inflammatory components present in the enlarged gin-
The selection of the appropriate technique depends on the giva are the result of distinct pathologic processes, they almost
size of the enlargement and the character of the tissue. When always are observed in combination. The role of bacterial
the enlarged gingiva remains soft and friable even after scaling plaque in the overall pathogenesis of drug-induced gingival
and root planing, a gingivectomy is used to remove it because enlargement is not clear.
a flap requires a firmer tissue in order that the incisions and
the other steps in the technique may be performed. However,
if the gingivectomy incision removes all of the attached gin-
Treatment Options
giva, thereby creating a mucogingival problem, then a flap The treatment of drug-induced gingival enlargement should
operation is indicated. Tumor-like inflammatory enlargements be based on the medication being used and the clinical fea-
are treated by gingivectomy. tures of the case.
529
Patient taking drug known

to cause gingival enlargement
Gingival enlargement present

Gingival enlargement not present
Oral hygiene reinforcement

Oral hygiene reinforcement Chlorhexidine gluconate rinses
Professional recalls Scaling and root planing
Possible drug substitution /
Professional recalls
Gingival enlargement regresses Reevaluation
Maintain good oral hygiene Gingival enlargement persists

Maintain professional recalls
Small areas of enlargement

(6 teeth)
- Periodontal surgery indicated
No attachment loss or
Horizontal bone loss
Large areas of enlargement
Abundance of keratinized tissue
(>6 teeth)
Presence of osseous defects
Limited keratinized tissue
Gingivectomy
Periodontal flap
Maintenance:
Good oral hygiene
Chlorhexidine gluconate rinses
Professional recalls
Use of positive pressure appliance
Consider periodic surgical retreatment
FIGURE 46.1 Decision tree for treatment of drug-induced gingival enlargements.
First, consideration should be given to the possibility of The administration of the antibiotic Azithromycin has been
discontinuing the drug or changing the medication. These shown to decrease the severity of gingival enlargement induced
possibilities should be discussed with the patient's physician by the administration of cyclosporine. A 3-day course of sys-
and the final decision should be made by the latter. Simple temic azithromycin is reported to significantly decrease gingival
discontinuation of the offending drug is usually not practi- enlargement, and the effect is observed as early as 7-30 days
cable, but its substitution with another medication may be an after the initiation of antibiotic therapy The topical administra-
option. The following alternatives may be considered. tion of azithromycin in the form of a toothpaste also decreased
the severity of cyclosporine-induced gingival enlargement.
1. Phenytoin sodium may be replaced by Valproic acid and
In some patients, gingival enlargement persists after careful
Carbamazepine.
consideration of the previous approaches. These patients may
2. Nifedipine may be replaced by Diltiazem or Verapamil or
require surgery, which may involve either gingivectomy or the
other groups of antihypertensives like ~-blockers, ACE in-
periodontal flap.
hibitors etc.
The importance of optimal plaque control in all such cases
3. Cyclosporine can be substituted by Tacrolimus.
need not be over emphasized.
However, the replacement drugs also have shown to cause Fig. 46.1 presents a decision tree that outlines the sequence
gingival overgrowth. Judicial decisions have to be taken keep- of events and options for the treatment of drug-induced gin-
ing basically the patient's medical conditions in mind. gival enlargement.
the basic steps in the technique. Fig. 46.5 shows a patient

treated with the flap technique.
The recurrence of drug-induced gingival enlargement
is a reality in surgically treated cases. As stated previously,
meticulous home care, chlorhexidine gluconate rinses, and
professional cleanings can decrease the speed at which the
degree to which recurrence occurs. A hard, natural rub-
ber, fitted bite guard worn at night may help to control
recurrence.
Although the periodontal flap approach may be techni-
cally more difficult than the gingivectomy procedure, as
indicated previously, the postsurgical healing of the flap tech-
nique presents less discomfort and alleviates hemorrhagic
problems. The primary closure of the surgical site with the
flap procedure is a great advantage over the secondary open
wound that results from the gingivectomy technique. In ad-
FIGURE 46.2 Gingivectomy technique as used to treat patients with dition, postsurgical home care can be instituted earlier with
drug-induced gingival enlargement. The dashed line represents the ex- the periodontal flap.
ternal bevel incision, and the shaded area corresponds to the tissue to Recurrence may occur as early as 3-6 months after surgi-
be excised. The gingivectomy incision may not remove the entire hyper-
plastic tissue (shaded area). This may leave a wide wound of exposed
cal treatment, but, in general, surgical results are maintained
connective tissue. for at least 12 months. In one study, the 6-month postsurgical
examination of the recurrence of cyclosporine-induced gin-
gival enlargement after periodontal flap surgery or gingivec-
tomy determined that the return of increased pocket depth
Gingivoplasty/Gingivectomy was slower with the flap. The recurrence of increased thick-
These procedures have the advantage of simplicity and quick- ness of periodontal tissue, however, has not been objectively
ness but present the disadvantages of more postoperative dis- evaluated.
comfort and an increased chance of postoperative bleeding.
They also sacrifice keratinized tissue and do not allow for os-
seous recontouring. The clinician's decision regarding the sur- Gingival Enlargement During
gical techniques available must consider the extension of the
area to be operated, the presence of periodontitis and osseous
Pregnancy
defects, and the location of the base of the pockets in relation Treatment requires the elimination of all local irritants that
to the mucogingival junction. may be responsible for precipitating the gingival changes that
In general, small areas (ie, up to six teeth) of drug- occur during pregnancy. The elimination oflocal irritants early
induced gingival enlargement with no evidence of attach- in pregnancy is a preventive measure against gingival disease,
ment loss (and therefore no anticipated need for osseous which is preferable to the treatment of gingival enlargement
surgery) can be effectively treated with the gingivectomy after it occurs. Marginal and interdental gingival inflamma-
technique. An important consideration is the amount of tion and enlargement are treated by scaling and curettage (see
keratinized tissue present: remember that at least 3 mm in Chapters 31). The treatment of tumor-like gingival enlarge-
the apicocoronal direction should remain after the surgery ments consists of surgical excision as well as the scaling and
is completed. planing of the tooth surface. The enlargement recurs unless all
Chapter 44 describes the gingivectomy technique in irritants are removed. Food impaction is frequently an incit-
detail. Fig. 46.2 depicts the procedure diagrammatically, ing factor.
and Fig. 46.3 illustrates a case of cyclosporine-induced
gingival enlargement treated with the gingivectomy tech-
Timing of Treatment and Indications
nique.
Gingivectomy or gingivoplasty can also be performed with Gingival lesions during pregnancy should be treated as soon as
electrosurgery or via a laser device (see Chapter 44). There they are detected, although not necessarily by surgical means.
is some preliminary evidence that the recurrence of drug- Scaling and root planing procedures and adequate oral hy-
induced gingival enlargement is slower in patients treated giene measures may reduce the size of the enlargement. Gin-
via laser as compared with conventional gingivectomy or flap gival enlargements do shrink after pregnancy, but they usually
surgery. do not disappear. After pregnancy, the entire mouth should be
reevaluated, a full set of radiographs taken, and the necessary
Flap Technique treatment undertaken.
Larger areas of gingival enlargement (ie, more than six teeth) Lesions should be removed surgically during pregnancy
or areas where attachment loss and osseous defects are pres- only if they interfere with mastication or produce an aesthetic
ent should be treated by the flap technique, as should any disfigurement that the patient wants to be removed.
situation in which the gingivectomy technique may create a During pregnancy, the emphasis should be on (1) prevent-
mucogingival problem. ing gingival disease before it occurs and (2) treating existing
The periodontal flap technique used for the treatment of gingival disease before it worsens. All patients should be seen
gingival enlargements is a simple variation of the one used to as early as possible after becoming pregnant. Those without
treat periodontitis (refer previous chapter). Fig. 46.4 shows gingival disease should be checked for potential sources of
FIGURE 46.3 Surgical treatment of cyclosporin-induced gingival enlargement with the use of the gingivectomy technique on a 16-year-old girl
who had received a kidney allograft 2 years earlier. A, Enlarged gingival tissues and pseudopocket formation. No attachment loss or evidence of
vertical bone loss existed. B, Initial external bevel incision performed with a Kirkland knife. C, lnterproximal tissue release achieved with an Orban
knife. D and E, Gingivoplasty performed with tissue nippers and a round diamond at high speed with abundant refrigeration. F, Aspect of the surgical
wound at conclusion of the surgical procedure. G, Placement of noneugenol periodontal dressing. H, The surgical area 3 months postoperatively.
Note the successful elimination of the enlarged gingival tissue, the restoration of a physiologic gingival contour, and the maintenance of an adequate
band of keratinized tissue.
local irritation and should be instructed with regard to plaque-

control procedures. Those with gingival disease should be
treated promptly, before the conditioning effect of pregnancy
on the gingiva becomes manifest. Chapter 30 presents the
(C) necessary precautions for the periodontal treatment of preg-
FIGURE 46.4 Diagram of periodontal flap treatment for drug- nant women.
induced gingival enlargement. A, Initial reverse bevel incision followed Every pregnant patient should be scheduled for peri-
by thinning of the enlarged gingival tissue; dotted lines represent inci-
sions, and the shaded area represents the tissue portion to be excised.
odic dental visits. The importance of such visits for the
B, After flap elevation, enlarged portion of the gingival tissue is removed. prevention of serious periodontal disturbances should be
C, The flap is placed on top of the alveolar bone and sutured. stressed.
FIGURE 46.5 Treatment of combined cyclosporine and nifedipine-induced gingival enlargement with a periodontal flap on a 35-year-old female
who had received a kidney allograft 3 years earlier. A, Presurgical clinical aspect of the lower anterior teeth, showing severe gingival enlargement.
B, Initial scalloped reverse bevel incision, including maintenance of keratinized tissue and creation of surgical papillae. C, Elevation of a full-thickness
flap and removal of the inner portion of the previously thinned gingival tissue. After scaling and root planing, osseous recontouring can be performed if
necessary. D, The flap is positioned on top of the alveolar crest. E, Postsurgical aspect of the treated area at 12 months. Note the reduction of enlarged
tissue volume and acceptable gingival health.
Neoplastic Gingival Enlargements The recurrence of chronic inflammatory enlargement im-

mediately after treatment indicates that all irritants have not
(Gingival Tumours) and Other been removed. Contributory local conditions (eg, food im-
Solitary Overgrowths paction, overhanging margins of restorations) are often over-
looked. If the enlargement recurs after healing is complete and
Lesions such as peripheral giant cell granuloma, fibroma, pyo-
normal contour is attained, inadequate plaque control by the
genic granuloma, etc. are frequently encountered in practice.
patient is the most common cause.
Such lesions have to be excised and subjected to histopatho-
Recurrence during the healing period is manifested as
logical examination to confirm the clinical diagnosis. While
red, beadlike, granulomatous masses that bleed with slight
excising such lesions, care should be taken to maintain the
provocation. This is a proliferative vascular inflammatory
periodontal architecture as much as possible. Rarely heman-
response to local irritation, which is usually a fragment of
giomas of the gingiva are seen and the clinician has to take
calculus on the root. The condition is corrected by removing
appropriate measures during surgery in order to prevent po-
the granulation tissue and scaling and planing the root sur-
tential bleeding complications.
face. Also, it should be noted that healing tissues are highly
Fig. 46.6 A, B, C, and D show a case of pyogenic granu-
sensitive to plaque buildup and very quickly the gingiva
loma excised completely and resulting in excellent gingival
increases in size. Hence optimal plaque control should be
form observed for a period of 2 years.
stressed to the patients. Further, if the enlargement is pre-
Recurrence of Gingival Enlargement disposed by malalignment of teeth, orthodontic treatment
should be instituted.
Recurrence after treatment is the most common problem in Familial, hereditary, or idiopathic gingival enlargement re-
the management of gingival enlargement. Residual local irrita- curs after surgical removal even if all local irritants have been
tion and systemic or hereditary conditions that cause nonin- removed. The enlargement can be maintained at minimal size
flammatory gingival hyperplasia are the responsible factors. by preventing secondary inflammatory involvement.
FIGURE 46.6 Pyogenic granuloma treated by surgical excision. A, Preoperative photograph; B, lesion excised; C, two- year follow-up photograph
showing excellent gingival contour; D, photomicrograph confirming clinical diagnosis.
SUGGESTED READINGS Margreiter R, Pohanka E, Sparacino V, et al: Open prospective multicenter

study of conversion to tacrolimus therapy in renal transplant patients expe-
Bondo-Guitton E, Bagheri H, Montastruc JL: Drug-induced gingival over-
riencing ciclosporin-related side-effects, Transpl Int 18:816, 2005.
growth: a study in the French Pharmacovigilance Database, J Clin Periodon-
Mavrogiannis M, Ellis JS, Seymour RA, et al: The efficacy of three different
tol 29:513, 2012.
surgical techniques in the management of drug-induced gingival over-
Camargo P, Melnick P, Pirih F, et al: Treatment of drug-induced gingival en-
growth,] Clin Periodontol 33:677, 2006.
largement: aesthetic and functional considerations, Periodontal 27:131,
Pilloni A, Camargo PM, Carere M, et al: Surgical treatment of cyclosporine A-
2001, 2000.
and nifedipine-induced gingival enlargement,] Periodontol 69:791, 1998.
Ciancio SG, Yaffe SJ, Catz CC: Gingival hyperplasia and diphenylhydantoin,
Rostaing L, Sanchcz-Fructoso A, Franco A, et al: Conversion to tacrolimus
once daily from ciclosporin in stable kidney transplant patients: a multi-
Harel-Raviv M, Eckler M, Lalani K, et al: Nifedipine-induced gingival hyper-
center study, Transpl Int 25:391, 2012.
plasia: a comprehensive review and analysis, Oral Surg Oral Med Oral Pathol
Walker RG, Cottrell S, Sharp K, et al: Conversion of cyclosporine to tacrolim-
Oral Radial Endod 79:115, 1995.
us in stable renal allograft recipients: quantification of effects on the sever-
Lopez-Pintor RM, Hernandez G, de Arriba L, et al: Amlodipine and nifcdipine
ity of gingival enlargement and hirsutism and patient-reported outcomes,
used with cyclosporine induce different effects on gingival enlargement,
Nephrology 12:607, 2007.
Transplant Proc 41:2351, 2009.
47
Resective Osseous Surgery
TN Sims • CD Dwarakanath
Chapter Outline
Normal Alveolar Bone Morphology Osseous Resection Technique
Terminology Flap Placement and Closure
Selection of Treatment Technique Postoperative Maintenance
Rationale Specific Osseous Reshaping Situations
Factors in Selection of Resective Osseous Conclusions
Surgery
The damage resulting from periodontal disease manifests in Normal Alveolar Bone Morphology
variable destruction of the tooth-supporting bone. Generally,
bony deformities are not uniform; they are not indicative of Knowledge of the morphology of the bony periodontium in
the alveolar housing of the tooth before the disease process a state of health is required to perform resective osseous sur-
and do not reflect the overlying gingival architecture. Bone gery correctly. The characteristics of a normal bony form are
loss has been classified as either "horizontal" or "vertical," but as follows:
in fact, bone loss is most often a combination of horizontal The interproximal bone is more coronal in position than
and vertical loss. Horizontal bone loss generally results in a the labial or lingual/palatal bone and pyramidal in form.
relative thickening of the marginal alveolar bone because bone The form of the interdental bone is a function of the tooth
tapers as it approaches its most coronal margin. form and the embrasure width. The more tapered the tooth,
The effects of this thickening and the development of verti- the more pyramidal is the bony form. The wider the embra-
cal defects leave the alveolar bone with countless combina- sure, the more flattened is the interdental bone mesiodistally
tions of bony shapes. If these various topographic changes are and buccolingually.
to be altered to provide a more physiologic bone pattern, a The position of the bony margin mimics the contours of
method for osseous recontouring must be followed. the cementoenamel junction. The distance from the facial
Osseous surgery may be defined as the procedure by bony margin of the tooth to the interproximal bony crest is
which changes in the alveolar bone can be accomplished more flat in the posterior than the anterior areas. This "scal-
to rid it of deformities induced by the periodontal disease loping" of the bone on the facial surfaces and lingual/palatal
process or other related factors such as exostosis and tooth surfaces is related to tooth and root form, as well as tooth po-
supraeruption. sition within the alveolus. Teeth with prominent roots or those
Osseous surgery can be either additive or subtractive in displaced to the facial or lingual side may also have fenestra-
nature. Additive or regenerative osseous surgery includes proce- tions or dehiscences. The molar teeth have less scalloping and
dures directed at restoring the alveolar bone to its original lev- a more flat profile than bicuspids and incisors.
el, whereas resective or subtractive osseous surgery is designed Although these general observations apply to all patients,
to restore the form of preexisting alveolar bone to the level the bony architecture may vary from patient to patient in the
present at the time of surgery or slightly more apical to this extent of contour, configuration, and thickness. These varia-
level (Fig. 4 7 .1) tions may be both normal and healthy.
Additive osseous surgery brings about the ideal results of
periodontal therapy. It implies regeneration of lost bone and Terminology
reestablishment of the periodontal ligament, gingival fibers,
and junctional epithelium at a more coronal level. This type of Numerous terms have been developed to describe the topog-
osseous surgery is discussed in Chapter 48. raphy of the alveolar housing, the procedure for its removal,
Resective osseous surgery procedures provide an alterna- and the resulting correction.
tive to additive methods and should be used when additive Procedures used to correct osseous defects have been clas-
procedures are not feasible. These subtractive procedures are sified into two: osteoplasty and ostectomy. Osteoplasty refers
discussed in this chapter. to reshaping the bone without removing tooth-supporting
535
(A)
I I
(B)
(C)
FIGURE 47.2 Diagram of types of bony architecture. A, Positive bony
architecture. B, Flat bony architecture. C, Reversed, or negative, bony
FIGURE 47.1 Additive and subtractive osseous surgery. A, Before, form.
and, B, immediately after subtractive osseous surgery; the osseous wall
of the two adjoining infrabony pockets has been removed. C, Before,
and, D, 1 year after additive osseous surgery; the area has been flapped
and thoroughly instrumented, resulting in reconstruction of the interden-
tal and periapical bone. (Courtesy Ors. E.A. Albano and 8.0. Barletta,
Buenos Aires, Argentina.)
bone. Ostectomy, or osteoectomy, includes the removal of tooth-

supporting bone. One or both of these procedures may be
necessary to produce the desired result.
Terms that describe the bone form after reshaping can
refer to morphologic features or to the thoroughness of the
reshaping performed. Examples of morphologically descrip-
tive terms include negative, positive,jlat, and ideal. These terms
relate to a preconceived standard of ideal osseous form.
Positive architecture and negative architecture refer to the rela-
tive position of interdental bone to radicular bone (Fig. 4 7.2).
The architecture is "positive" if the radicular bone is apical
FIGURE 47.3 Skull photograph of healthy periodontium. Note the
to the interdental bone. The bone has "negative" architecture shape of the alveolar bone housing. This bone is considered to have
if the interdental bone is more apical than the radicular bone. ideal form. It is more coronal in the interproximal areas, with a gradual
Flat architecture is the reduction of the interdental bone to the slope around and away from the tooth.
same height as the radicular bone.
Osseous form is considered to be "ideal" when the bone is
consistently more coronal on the interproximal surfaces than
Selection of Treatment Technique
on the facial and lingual surfaces. The ideal form of the mar- The morphology of the osseous defect largely determines
ginal bone has similar interdental height, with gradual, curved the treatment technique to be used. One-wall angular defects
slopes between interdental peaks (Fig. 47.3). usually need to be recontoured surgically. Three-wall defects,
Terms that relate to the thoroughness of the osseous reshap- particularly if they are narrow and deep, can be successfully
ing techniques include "definitive" and "compromise." Definitive treated with techniques that strive for new attachment and
osseous reshaping implies that further osseous reshaping would bone reconstruction. Two-wall angular defects can be treated
not improve the overall result. Compromise osseous reshaping indi- with either method, depending on their depth, width, and
cates a bone pattern that cannot be improved without significant general configuration. Therefore, except for one-wall defects
osseous removal that would be detrimental to the overall result. and wide, shallow two-wall defects, and interdental craters,
47 Resective Osseous Surgery 537
osseous defects are treated with the objective of obtaining op-

timal repair by natural healing processes.
Rationale
Resective osseous surgery provides the surest method of re-
ducing pockets and is based on the tenet that discrepancies (A) (8)
in level and shapes of the bone and gingiva predispose pa-
tients to recurrence of pocket depth postsurgically. Its goal is
to reshape the marginal bone to resemble that of the alveolar
process undamaged by periodontal disease. The technique is
performed in combination with apically positioned flaps and
the procedure eliminates periodontal pocket depth and im-
proves tissue contour to provide a more easily maintainable
I
environment.
(C) (D)
The conversion of the periodontal pocket to shallow gin-
gival sulcus enhances the patient's ability to remove plaque
and oral debris from the dentition. However this concept has
been questioned in the last two decades as periodontal dis-
ease pathogenesis is very complex and does not solely depend
upon ideal bone form. Hence unless the defects are extreme
as to influence the periodontal status markedly it is better to
leave them as they are if additive/regenerative techniques can- (F)'
not be employed. Its value as a surgical approach is limited
(E)
by the presence, quantity, and shape of the bony tissues and FIGURE 47.4 Effect of correction of craters. A and B, Diagram of fa-
by the amount of attachment loss that is acceptable. Although cial and interproximal bony contours after flap reflection. Note the loss
this concept is not universally accepted and the procedure in- of some interproximal bone and cratering. C and D, Line angles; this is
only osteoplasty and has resulted in a reversed architecture. E and F, Os-
duces loss of radicular bone in the healing phase, recontour-
tectomy on the facial and lingual bone and the removal of the residual
ing of bone is the only logical treatment of choice in some widow's peaks to produce a positive bony architecture.
cases.
Likewise, the ability of dental professionals to maintain the
periodontium in a state free of gingivitis and periodontitis is 2. Gingival recession and its sequelae
more predictable in the presence of shallow sulci. The more 3. Often lengthy unpleasant postsurgical recovery
effective the periodontal maintenance therapy, the greater is 4. Postsurgical mobility
the longitudinal stability of the surgical result. The efficacy
of osseous surgery therefore depends on its ability to reduce
pocket depth and to promote periodontal maintenance.
Factors in Selection of Resective
Indications Osseous Surgery
Resective osseous surgery is indicated in the following situ-
ations: 1. Depth and configuration of bony lesion to root morphol-
ogy and the adjacent teeth (Fig. 474).
1. Inconsistent bone margins 2. Amount of bone that requires removal.
2. Reverse architecture 3. The extent of attachment loss.
3. One-wall defects 4. The number of remaining walls of bony defect.
4. Buttressing bone formation 5. The amount of soft tissue present interproximally.
5. Ledges and plateau
6. Shallow craters Examination and Treatment Planning
7. Furcation defects In addition to the routine clinical and radiographic exami-
8. Crown lengthening for restorative dentistry nation described earlier (Chapter 26), the following factors
should be assessed:
Contraindications
1. The type of bone loss and its configuration by sounding or
1. Extensive bone loss transgingival probing under local anesthesia.
2. High caries activity 2. Evaluation of the esthetics.
3. Existing mobility 3. Restorative/prosthodontic considerations.
4. Esthetic zones 4. Prognosis of the overall dentition.
Advantages 5. The type of periodontitis.
6. Response to phase 1 therapy.
1. Predictability
2. Complete elimination of periodontal pockets Treatment planning should provide solutions for active
3. Obtaining ideal bone form periodontal diseases and correction of deformities that re-
sult from periodontitis. Planning should also facilitate the
Disadvantages performance of other dental procedures included in a com-
1. Loss of valuable supporting bone prehensive dental treatment plan. The extent of periodontal
FIGURE 47.5 Reduction of bony ledges and exposure of caries by osteoplasty. A, Buccal preoperative photograph showing two crowns, exostoses,
and caries. B, Flap reflected to reveal caries on both molars at the restoration margins, interdental cratering, and a facial exostosis. C, After osseous
surgery; the bulk of the bony removal was by osteoplasty, with minor ostectomy between the two molars. The caries is now exposed, and the crowns
are lengthened for restoration. D, Postoperative photograph at 6 weeks. The plaque control is deficient, but the teeth should be readily restorable at
this time. (Courtesy Dr. Joseph Schwartz, Portland, OR.)
involvement can vary significantly from tooth to tooth in the also provide a means of producing optimal crown length for
same patient. The response to therapy from patient to patient cosmetic purposes.
may also vary, as may the treatment objectives for the pa-
tients. Therefore a treatment plan may encompass a number
of steps and combinations of procedures in the same surgical Osseous Resection Technique
area.
Instrumentation
After oral hygiene instruction, scaling and root planing,
and other disease control procedures, the response of the pa- A number of hand and rotary instruments have been used for
tient to these treatment procedures is evaluated by reexamina- osseous resective surgery. Some excellent clinicians use only
tion and recording the changes in the periodontium. Since hand instruments and rongeurs, whereas others prefer a com-
the extent of periodontal involvement can vary significantly bination of hand and rotary instruments. Rotary instruments
from tooth to tooth in the same patient, the local response are useful for the osteoplasty, whereas hand instruments pro-
to therapy is also variable. The resolution of inflammation vide the most precise and safe results for ostectomy.
and decrease in edema and swelling may have resulted in a Recently piezoelectric surgical techniques have also been
return to normal depth and configuration of some pockets, used with success for osseous surgical resection. Regardless
and additional therapy beyond periodic maintenance may not of the type of instruments used, care and precision are re-
be required. However, notwithstanding conscientious efforts quired for each step of the procedure to prevent excessive
during phase 1 therapy, some probing depths may still remain. bone removal or root damage, both of which are irreversible.
Further nonsurgical therapy has little effect on the bony de- Fig. 4 7 .6 illustrates some of the instruments commonly used
formities. In such cases bone has to be exposed and its topog- for osseous resection techniques.
raphy altered. To address the many clinical situations, the following se-
Resective osseous surgery is also used to facilitate certain quential steps are suggested for resective osseous surgery
restorative and prosthetic dental procedures (Fig. 4 7.5). Den- (Fig. 47.7):
tal caries can be exposed for restoration; fractured roots of
1. Vertical grooving
abutment teeth can be exposed for removal; and bony exosto-
2. Radicular blending
ses and ridge deformities can be altered in contour to improve
3. Flattening interproximal bone
the performance of removable or fixed prostheses. Severely
4. Gradualizing marginal bone
decayed teeth or teeth with short anatomic crowns can be
lengthened by resection or by a combination of orthodontic Not all steps are necessary in every case, but the sequenc-
tooth extrusion and osseous resection. Such procedures al- ing of the steps in the order given is necessary to expedite the
low the therapist to expose more tooth for restoration, prevent reshaping procedure, as well as to minimize the unnecessary
an invasion of the biologic width of attachment, and create a removal of bone. Fig. 47.8 illustrates bone reshaping in flap
periodontal attachment of normal dimension. Resection can surgery for specific anatomic defects.
(C) (D) .
(E) (F} (G)

FIGURE 47.6 Instruments often used in osseous surgery. A, Currently, the piezoelectric surgical instrument has been used successfully in osseous
resective surgery. B, Rongeurs: Friedman (top) and 90-degree Blumenthal (bottom). C, Carbide round burs. Left to right, Friction grip, surgical-length
friction grip, and slow-speed handpiece. D, Diamond burs. E, lnterproximal files: Schluger and Sugarman. F, Back-action chisels. G, Ochsenbein chisels.
Vertical Grooving grooving are most apparent with thick bony margins, shallow
crater formations, or other areas that require maximal osteo-
Vertical grooving is designed to reduce the thickness of the plasty and minimal ostectomy. Vertical grooving is contraindi-
alveolar housing and to provide relative prominence to the cated in areas with close roots or thin alveolar housing.
radicular aspects of the teeth. It also provides continuity from
the interproximal surface onto the radicular surface. It is the Radicular Blending
first step of the resective process because it can define the gen-
eral thickness and subsequent form of the alveolar housing. Radicular blending, the second step of the osseous reshap-
This step is usually performed with rotary instruments, such ing technique, is an extension of vertical grooving. Concep-
as round carbide burs or diamonds. The advantages of vertical tually, it is an attempt to gradualize the bone over the entire
(C) (D)
FIGURE 47.7 A, Drawing of bony topography in moderate periodontitis with interdental craters. B, Vertical grooving, the first step in correction by
osseous reshaping. C, Radicular blending and flattening of interproximal bone. D, Gradualizing the marginal bone. Note the area of the furcation on
the first molar where the bone is preserved.
radicular surface to provide the best results from vertical Large hemiseptal defects would require removal of inordi-
grooving. This provides a smooth, blended surface for good nate amounts of bone to provide a flattened architecture, and
flap adaptation. The indications are the same as for vertical the procedure would be too costly in terms of bony support.
grooving (ie, thick ledges of bone on the radicular surface, Compromised osseous architecture is the only logical solution
where selective surgical resection is desired). Naturally, this (Fig. 47.10).
step is not necessary if vertical grooving is very minor or if
the radicular bone is thin or fenestrated. Both vertical groov-
Gradualizing Marginal Bone
ing and radicular blending are purely osteoplastic techniques
that do not remove supporting bone. In most situations, The final step in the osseous resection technique is also an
these two procedures compose the bulk of resective osseous ostectomy process. Bone removal is minimal but necessary to
surgery. Classically, shallow crater formations, thick osseous provide a sound, regular base for the gingival tissue to fol-
ledges of bone on the radicular surfaces, and Class I and early low. Failure to remove small bony discrepancies on the gin-
Class II furcation involvements are treated almost entirely gival line angles (widow's peaks) allows the tissue to rise to a
with these two steps. higher level than the base of the bone loss in the interdental
area. This may make the process of selective recession and
subsequent pocket reduction incomplete. This step of the pro-
Flattening lnterproximal Bone
cedure also requires gradualization and blending on the ra-
Flattening of the interdental bone requires the removal of dicular surface. The two ostectomy steps should be performed
very small amounts of supporting bone (Fig. 47.9). It is in- with great care so as not to produce nicks or grooves on the
dicated when interproximal bone levels vary horizontally. By roots. When the radicular bone is thin, it is extremely easy to
definition, most of the indications for this step are one-walled overdo this step, to the detriment of the entire surgical effort.
interproximal defects or hemiseptal defects. The omission For this reason, various hand instruments, such as chisels and
of flattening in such cases results in increased pocket depth curettes, are preferable to rotary instruments for gradualizing
on the most apical side of the bone loss. This step is typi- marginal bone.
cally not necessary with interproximal crater formations or flat
interproximal defects. It is best used in defects that have a
coronally placed, one-walled edge of a predominantly three-
Flap Placement and Closure
walled angular defect, and it can be helpful in obtaining good After performing resection, the clinician positions and sutures
flap closure and improved healing in the three-walled defect. the flaps. Flaps may be replaced to their original position, to
The limitation of this step, as with resective osseous surgical cover the new bony margin, or they may be apically posi-
therapy in general, is in the treatment of advanced lesions. tioned. Replacing the flap in areas that previously had deep
FIGURE 47.8 Bone contouring in flap surgery. A-C, Bone contouring in interdental craters. D and E, Bone contouring in exostoses. F and G, Bone
contouring in one-wall vertical defect.
pockets may result initially in greater postoperative pocket complications and results in optimal postsurgical pocket
depth, although a selective recession may diminish the depth depths (Fig. 47.11).
over time. Positioning the flap apically to expose marginal Suturing may be accomplished using a variety of differ-
bone is one method of altering the width of the gingiva (denu- ent suture materials and suture knots (see Chapter 43). The
dation). However, such flap placement results in more post- sutures should be placed with minimal tension to coapt the
surgical resorption of bone and patient discomfort than if the flaps, prevent their separation, and maintain the position of
newly created bony margin were covered by the flap. Position- the flaps. Sutures placed with excessive tension rapidly pull
ing the flap to cover the new margin minimizes postoperative through the tissues.
Postoperative Maintenance
Sutures may be removed at various times after placement.
Nonresorbable sutures such as silk are usually removed after
1 week of healing, although some of the newer synthetic ma-
terials may be left for up to 3 weeks or longer without adverse
consequences. Resorbable sutures maintain wound approxi-
mation for varying periods of 1-3 weeks or more, depending
on the type of suture material. After suture removal, the surgi-
cal site is examined carefully, and any excessive granulation
tissue is removed with a sharp curette. The patient is given
instructions on optimal oral hygiene. Supersoft toothbrushes
with chlorhexidine mouthrinse are generally prescribed.
FIGURE 47.9 Diagrammatic representation of bone irregularities in Healing should proceed uneventfully, with the attachment
periodontal disease. The thick line is the proposed correction of the
defect. Note the flattening of the interproximal bone between the mo-
of the flap to the underlying bone completed in 14-21 days.
lars and the protection of the furcal bone on the first molar. Facial crest Maturation and remodeling can continue for up to 6 months.
height is reduced in both interproximal areas to the depth of the defect. It is usually advisable to wait at least 6 weeks after completion
FIGURE 47.10 Compromise osseous surgery. A and B, Preoperative views of the buccal and lingual surfaces. C and D, Preoperative and postoperative
views of the buccal osseous recontouring of Class I buccal furcation defects, a moderate crater between the two molars, and a deep 3 walled defect at
the mesial of the first molar. D, Buccal aspects of these lesions were corrected with osteoplasty and a small amount of ostectomy. E and F, Preoperative
and postoperative views of the lingual osseous management. In E, note the combination 1-3 walled defect between the second bicuspid and first molar,
as well as the irregular pattern of bone loss with ledging. F, These defects were corrected by osteoplasty and ostectomy, except for the deep defect at the
mesial surface of the molar. This area was resected until the residual defect was of two and three walls only and left to repair. G and H, Buccal and lingual
5-year postoperative views of tissue configuration. Note the residual soft-tissue defect between the bicuspid and first molar.
FIGURE 47.11 Ostectomy and osteoplasty to a positive contour with flap placement at the newly created bony crest for minimal pocket depth.
A and B, Buccal and lingual preoperative views. C and D, Buccal preoperative view and postoperative correction. Osteoplasty and ostectomy were
used to produce a positive contour. Note the osteoplasty into the buccal furcation of the first molar. This is about the extent of craters that can be cor-
rected to a positive contour in teeth with moderate root trunk length. E and F, Lingual preoperative view and postoperative correction. Osteoplasty
and ostectomy were done to produce a positive contour. Note the lingual ledge, which was reduced. Such ledges are common in this area. G and
H, Buccal and lingual flaps sutured with continuous sling sutures to allow placement of the flaps to cover the bony margins. Ostectomy and osteo-
plasty performed to a positive contour, with flap placement at the newly created bony crest for minimal pocket depth. Ostectomy and osteoplasty to
a positive contour with flap placement at the newly created bony crest for minimal pocket depth. I and J, Buccal and lingual postoperative views at
1 week. Soft-tissue thickness is minimal, and the interdental areas are granulating in over the positive bony form. Minimal pocket depth results from
such management.
I
I l
I I
I I
I
(A)
I I
I
I I
\
,_, \ I
'~'
FIGURE 47.12 lnterproximal craters. The shaded areas illustrate dif-
ferent techniques for the management of such defects. The technique
that reduces the least amount of supporting bone is preferable.
of healing of the last surgical area before beginning dental res-

torations. For those patients with a major cosmetic concern,
it is wise to wait as long as possible to achieve a postoperative
soft tissue position and a stable sulcus.
Specific Osseous Reshaping

Situations (B)
The osseous corrective procedure previously described is clas- FIGURE 47.13 Reduction of a one-wall angular defect. A, Angular
bone defect mesial to the tilted molar. B, Defect reduced by "ramping"
sically applied to shallow craters with heavy faciolingual ledg-
angular bone.
es (Fig. 47.12). The correction of other osseous defects is also
possible; however, careful case selection for definitive osseous
surgery is extremely important.
Correction of one-walled hemiseptal defects requires that
the bone be reduced to the level of the most apical portion of
the defect. Therefore, great care should be taken to select the
appropriate case. If one-walled defects occur next to an eden-
tulous space, the edentulous ridge is reduced to the level of
the osseous defect (Fig. 4 7 .13).
In the absence of ledges or exostoses, the elimination
of the bony lesion begins with reduction of the interdental
walls of craters, the one-walled component of angular de-
(A) (B)
fects, moats, and grooving into sites of early involvement.
The walls of the crater may be reduced at the expense of
the buccal, lingual, or both (Fig. 4 7 14) The reduction
should be made to remove the least amount of alveolar
bone required to (A) produce a satisfactory form, (B) pre-
vent the therapeutic invasion of furcations, and ( C) blend
the contours with the adjacent teeth. The selective reduc-
tion of bony defects by "ramping" the bone to the palatal or
lingual to avoid involvement of the furcation can be done (C)
(Fig. 47.15) FIGURE 47.14 Diagram of crater-reduction patterns. A, Preoperative
In the presence of heavy ledges of bone, it is usually wise bony form after flap reflection. B, Reduction of craters to the lingual
to do osteoplasty first to eliminate any exostoses or reduce wall. C, Reduction of craters to the facial wall. D, Reduction of craters to
both the buccal and the lingual wall.
the buccal/lingual bulk of the bone (Fig. 47.16). It is a com-
mon practice to incorporate a degree of vertical grooving dur-
ing the reduction of bony ledges, because this facilitates the coronal bony height. This removal of bone may result in a
process of blending the radicular bone into the interproximal significant reduction in attachment on relatively unaffect-
areas at the next step. ed adjacent teeth to eliminate the defect. Hence the clini-
One-walled or hemiseptal defects usually require the cian should take appropriate decision based on the correct
removal of some bone from the tooth with the greatest Judgement.
FIGURE 47.15 Correction of osseous defects largely to the palatal wall. A and B, Buccal and palatal preoperative views, 6 weeks after completion
of scaling and root planing. C and D, Buccal preoperative and postoperative views. In C, note the ledging on the facial wall of molars and the one-
wall defects on both molars. D, Postoperative view shows the elimination of these defects by osteoplasty on the ledges and ostectomy of the one-wall
defects to produce a positive buccal architecture. E and F, Palatal preoperative and postoperative views. In E, note the pattern of bony loss, which is
more severe on the palatal wall. In addition to the facial one-wall defects, there is an incipient furcation defect at the mesial wall of the first molar and
a Class II furcation at the mesial wall of the second molar. F, Configuration of the defects was such that ostectomy was performed on the palatal roots
of both molars to produce a compromise architecture. G and H, Ten-year postoperative views of the buccal and palatal areas showing the pattern of
soft-tissue adaptation to the surgically produced bony form.
FIGURE 47.16 Reduction of bony ledges by osteoplasty before correction of interdental defects. A, Buccal preoperative view. B, Buccal flap
reflection. Note the buccal ledge and the Class II buccal furcation. C, Buccal correction largely by osteoplasty with minor ostectomy over the root
prominence to produce a positive architecture. D, Ten-year postoperative view of soft-tissue form. Minimal pocket depth is present.
Conclusions and periodic maintenance. It also preserves the width of the

attached tissue while removing granulomatous tissue and
Although osseous surgical techniques cannot be applied to providing access for debridement of the radicular surfaces.
every bony abnormality or topographic modification, it has In addition, the osseous resection technique permits recon-
been clearly demonstrated that properly advocated they can touring of bony abnormalities, including hemiseptal defects,
eliminate and modify defects, as well as gradualize excessive tori, and ledges. Its benefits also include facilitating restorative
bony ledges, irregular alveolar bone, early furcation involve- dentistry.
ment, excessive bony exostosis, and circumferential defects.
When properly performed, resective osseous surgery achieves SUGGESTED READINGS
a physiologic architecture of marginal alveolar bone condu-
Carnevale G, Kaldahl WB: Osseous Resective Surgery,] Periodontal 22:59-87,
cive to gingival flap adaptation with minimal probing depth. 2000.
The advantages of this surgical modality include a predictable Dibart S, Dibart J-P: Practical Osseous Surgery in Periodontics and Implant
amount of pocket reduction that can enhance oral hygiene Dentistry, Wiley-Blackwell, Hoboken, New jersey, 2011.
48
Periodontal Regeneration and
Reconstructive Surgery
RT Kao • HH Takei • DL Cochran • ML Nevins • CD Dwarakanath
Chapter Outline
Regeneration and Reconstructive Future Directions for Periodontal
Techniques Regeneration
Graft Materials and Procedures Conclusions
Factors That Influence Therapeutic
Success
Periodontal diseases result in the destruction of the attach- 2. Allografts which are obtained from different individuals of
ment apparatus to a varying degree. Although arrest of further same species.
disease progression is the immediate goal, the ideal outcome 3. Xenografts, meaning bone obtained from different species
would be regeneration and reconstruction of the lost tissues usually bovine or porcine origin.
(Fig. 48.1). This chapter describes the various methods to ob- 4. Alloplasts which are synthetic graft materials/bone substitutes.
tain periodontal regeneration through the use of the different
Bone grafts may also be classified by the mode of their
techniques and biomaterials.
actions as under:
It is presumed that the reader is already acquainted with
the definitions of terms such as repair, regeneration, new at- 1. Osteogenic grafts wherein the grafted tissue contains the
tachment, etc. discussed in Chapter 29 (Fig. 48.2). cells necessary to form new bone. Only autografts have this
capacity and hence are considered as gold standard.
2. Osteoinductive grafts which have the capacity to convert
Regeneration and Reconstructive the surrounding tissue to form osteoblasts through the re-
Techniques lease of bone morphogenic proteins.
3. Osteoconductive which is a physical effect by which the
These techniques may be subdivided as follows:
matrix of the graft forms a scaffold that favors outside
1. Graft-assisted procedures using various types of bone cells and blood vessels to penetrate graft and form new
grafts, enamel matrix derivatives (EMDs), and so on. bone.
2. Nongraft-associated techniques such as guided tissue re- 4. Osteoneutral graft is that which merely fills the bone defect
generation ( GTR), laser-assisted new attachment proce- without producing any effect and often gets encapsulated.
dures (LANAPs), root surface biomodification, etc.
Depending on the rate of their bioresorption, grafts are
3. Advanced techniques such as use of growth factors, stem
classified as follows:
cells, and tissue engineering.
1. Fast resorbing wherein the graft gets resorbed within
8-10 weeks after placement.
Graft Materials and Procedures
2. Slow resorbing in which case the grafted material stays for
Numerous bone grafts have been developed over the last three many months.
decades and wealth of data has been generated. Many of them 3. Nonresorbing are those which do not resorb for years.
have become obsolete and are of only historical interest.
It is important for the clinician to understand the proper-
ties and origin of the materials and the purpose for which
Classification of Bone Grafts the graft material is intended to be used. Also it is the duty
of the clinician to explain to his/her patients the source of
Based on the origin:
the graft since the latter may have religious restrictions as
1. Autografts where in the bone is obtained from the same to the type of the graft material that is been used in their
individual. mouth.
547
{A)
FIGURE 48.1 A, Deep three-wall vertical osseous defect with measuring probe inserted. B, Reentry surgery 9 months after treatment shows repaired
bone defect. C, Radiographs before and after treatment showing fill of angular osseous defect; gutta percha points extend to base of pocket. (From
Glickman I: Clinical periodontology, ed 3, Philadelphia, 7 964, Saunders.)
(A) (8)
FIGURE 48.2 A, Periodontal pocket preoperatively. B, Periodontal pocket immediately after scaling, root planing, and curettage. C, New attach-
ment. The arrow indicates the most apical part of the junctional epithelium. Note regeneration of bone and periodontal ligament. D, Healing by long
junctional epithelium. Again, the arrow indicates the most apical part of the junctional epithelium. Note that the bone is new, but the periodontal
ligament is not.
9. Adequate bone fill and promotion of new attachment in-

Properties of an Ideal Bone Graft Material cluding cementogenesis
1. Nontoxic 10. Cost effective and acceptable to the patient
2. Nonantigenic Table 48.1 provides a list of available periodontal regen-
3. Resistant to infection eration biomaterials. Regardless of the type of graft material
4. Predictability used the basic principles of approach are same. These in-
5. Clinical feasibility clude careful case selection and a meticulous phase-1 ther-
6. Easy adaptability apy and establishment of optimum plaque control. Trauma
7. Readily and sufficiently available from occlusion may impair posttreatment healing of the sup-
8. Minimal operative and postoperative hazards porting periodontal tissues, reducing the likelihood of new
48 Periodontal Regeneration and Reconstructive Surgery 549
TABLE 48.1 Graft Materials and Procedures

COMMERCIALLY AVAILABLE BIOMATERIALS Autogenous Bone Crafts
FOR PERIODONTAL REGENERATION Bone from Intraoral Sites. In 1923, Hegedus attempted to
Biomaterial Commercial Name
use bone grafts for the reconstruction of bone defects pro-
duced by periodontal disease. The method was revived by
Allografts Nabers and O'Leary in 1965 and numerous efforts have been
DFDBA Distributed under various name made since that time to define its indications and techniques.
by tissue banks Sources of bone include bone from healing extraction
FDBA Distributed under various name
wounds, bone from edentulous ridges, bone trephined from
by tissue ban ks
Xenografts
within the jaw without damaging the roots, newly formed
Anorganic bovine bone Bio-Oss, OsteoGraf, Pep-Gen bone in wounds especially created for the purpose, bone re-
P-15 moved from tuberosity or the ramus, bone removed during
HA osteoplasty and ostectomy and the lingual surface of the man-
Alloplasts dible or maxilla at least 5 mm from the roots.
Tricalcium phosphate Synthograft Osseous Coagulum. Robinson described a technique using
Hydroxyapatite Periograf, Osteogen, ProOsteone a mixture of bone dust and blood that he termed "osseous
Bioactive glass polymers PerioGlas, BioGran coagulum." The technique uses small particles ground from
Hard-tissue replacement Bioplant cortical bone. The advantage of the particle size is that it pro-
polymer
vides additional surface area for the interaction of cellular and
Coralline calcium carbonate Biocoral
Polymers and collagens
vascular elements (Fig. 48.3).
Collagen CollaPlug, CollaCote, Gelfoam, Bone is removed with a carbide bur #6 or #8 at speeds be-
Helistat tween 5,000 and 30,000 rpm, placed in a sterile dappen dish
Pol y(lactide-co-po l ygl yco Ii de) and used to fill the defect. The obvious advantage of this tech-
Methylcellulose nique is the ease of obtaining bone from an area already ex-
Hyaluronic acid ester HY posed during surgery. The disadvantages are its relatively low
Chitosan predictability and the inability to procure adequate material
DFDBA, demineralized freeze-dried bone allograft; FDBA, freeze-dried bone for large defects. Although notable success has been reported
allograft; HA, hydroxyapatite. by many individuals, studies documenting the efficacy of the
technique are still inconclusive.
attachment. Occlusal adjustment, if needed, is therefore indi- Bone Blend. Some disadvantages of osseous coagulum de-
cated. It is also preferable to splint mobile teeth before bone rive from the inability to use aspiration during accumulation
graft placement. of the coagulum. Another problem is the unknown quantity
Systemic antibiotics are generally used after reconstructive and quality of the bone fragments in the collected material.
periodontal therapy, although definitive information on the To overcome these problems, the "bone blend technique" has
advisability of this measure is still lacking. been proposed.
FIGURE 48.3 A, Osseous defect mesial to a second premolar. B, Graft material placed in dappen dish before transfer to the graft site. C, Material in
place. D, Reentry 6 months later. (Courtesy Dr E. Earl Robinson.)
(D) (E) (F)

FIGURE 48.4 A, November 1973: radiograph of a patient immediately before placement of a fresh iliac autograft. B, 2 months later, bone repair is
evident. Note the early radiolucent areas on the mesial aspect of the canine. C, After 7 months, "bone fill" is occurring, but obvious root resorption is
present. D, April 1975: root resorption is apparent on all grafted teeth. Note the obvious degree of fill of the original bone defects. E, February 1976:
further involvement. F, October 1977: 4 years later, root resorption has progressed into the pulp of the lateral incisor, causing a periosteal-endosteal
complication.
The bone blend technique uses an autoclaved plastic periodontal osseous defects, using bone from the tibia. Schall-
capsule and pestle. Bone is removed from a predetermined horn and Hiatt revived this approach in the 1960s using the
site, triturated in the capsule to a workable, plastic-like mass iliac crest (Fig. 48.4)
and packed into bony defects. Froum et al found osseous The use of fresh or preserved iliac cancellous marrow, bone
coagulum-bone blend procedures to be at least as effective as has been extensively investigated. This material has been used
iliac autografts and open curettage. by orthopedic surgeons for years. Data from human and ani-
mal studies support its use and the technique has proved suc-
Cancellous Bone Marrow Transplants. Cancellous bone can cessful in osseous defects with various numbers of walls. It
be obtained from the maxillary tuberosity, edentulous areas, has also been successful in furcations and even supracrestally
and healing sockets. The maxillary tuberosity frequently con- to some extent. However, because of numerous problems as-
tains abundant cancellous bone, particularly if the third mo- sociated with its use, the technique is no longer in use. Some
lars are not present. After a ridge incision is made distally from of the problems were postoperative infection, bone exfolia-
the last molar, bone is removed with a curved rongeur. Care tion, sequestration, varying rates of healing, root resorption,
should be taken not to extend the incision too far distally to and rapid recurrence of the defect. Other problems increased
avoid entering the mucosal tissue of the pharyngeal area. Also, patient's expense and difficulty in procuring the donor
the location of the maxillary sinus must be analyzed on the material.
radiograph to avoid entering or disturbing it.
Edentulous ridges can be approached with a flap and can- Bone Allografts
cellous bone and marrow are removed with curettes, back- Obtaining donor material for autograft purposes necessitates
action chisels, or trephine. Extraction sockets are allowed inflicting surgical trauma on another part of the patient's body
to heal for 8-12 weeks before reentering and removing the Obviously, it would be to the patient's and therapist's advan-
newly formed bone from the apical portion, which is used as tage if a suitable substitute could be used for grafting purposes
the donor material. that would offer similar potential for repair and not require
the additional surgical removal of donor material from the
Bone Swaging. The bone swaging technique requires an patient. However, both allografts and xenografts are foreign
edentulous area adjacent to the defect, from which the bone is to the patient and, therefore, have the potential to provoke an
pushed into contact with the root surface without fracturing immune response. Attempts have been made to suppress the
the bone at its base. Bone swaging is technically difficult and antigenic potential of allografts and xenografts by radiation,
its usefulness is limited. freezing, and chemical treatment. Bone allografts are com-
mercially available from tissue banks. They are obtained from
Bone From Extraoral Sites. In 1923, Hegedus also pioneered cortical bone within 12 h of the death of the donor, defatted,
the use of extra oral sites as a source of bone for grafting into cut in pieces, washed in absolute alcohol, and deep-frozen.
The material is then demineralized, ground and sieved to with the adjacent tissues, eliciting no systemic immune re-
a particle size of 250-750 µm and freeze-dried before it is sponse.
vacuum-sealed in glass vials. Several studies have reported successful bone regeneration
Numerous steps are also taken to eliminate viral infectiv- and new attachment with Bio-Oss in periodontal defects, as
ity. These include exclusion of donors from known high-risk well as regeneration around implants and sinus grafting.
groups and various tests on the cadaver tissues to exclude Periodontally, Bio-Oss has been used as a graft material
individuals with any type of infection or malignant disease. covered with a resorbable membrane ( Geistlich Bio-Gide).
The material is then treated with chemical agents or strong The membrane prevents the migration of fibroblasts and con-
acids to inactivate the virus, if still present. The risk of human nective tissues into the pores and between the granules of the
immunodeficiency virus (HIV) infection has been calculated graft. Histologic studies of this technique have shown signifi-
as 1 in 1 to 8 million and is therefore characterized as highly cant osseous regeneration and cementum formation.
remote. Yukna et al have used Bio-Oss in combination with a
cell-binding polypeptide (P-15) that is a synthetic analog of
Freeze-Dried Bone Allograft. Several clinical studies by Mel- a 15-amino acid sequence of type I collagen marketed as
lonig, Bowers, and coworkers reported bone fill exceeding PepGen P-15 (Dentsply/CeraMed). This combination seems
50% in 67% of the defects grafted with freeze-dried bone al- to enhance the bone-regenerative results of the matrix alone
lograft (FDBA) and in 78% of the defects grafted with FDBA in periodontal defects.
plus autogenous bone. FDBA, however, is considered an os-
teoconductive material, whereas demineralized freeze-dried Alloplasts (Synthetic Bone Graft Materials)
bone allograft (DFDBA) is considered an osteoinductive graft. Risk of disease transmission, however remote and religious
Laboratory studies have found that DFDBA has a higher os- constraints of the patients regarding the source of the grafts,
teogenic potential than FDBA and is therefore preferred. How- made the researchers to look for synthetic bone replacement
ever FDBA being slow resorbing is often used in guided bone grafts. Many materials such as plaster of Paris, ceramics, poly-
regeneration. mers, bioactive glasses, coral-derived materials, etc. came into
the market. Many of them disappeared as quickly as they were
Demineralized Freeze-Dried Bone Allograft. Experiments introduced.
by Urist have established the osteogenic potential of DFDBA.
Demineralization in cold, diluted hydrochloric acid exposes Calcium Phosphate Biomaterials
the components of bone matrix, which are closely associated Several calcium phosphate biomaterials have been tested since
with collagen fibrils and have been termed bone morphogenetic the mid-1970s and are currently available for clinical use. Cal-
proteins (BMPs) cium phosphate biomaterials have excellent tissue compatibili-
Studies have provided strong evidence that DFDBA in peri- ty and do not elicit any inflammation or foreign body response.
odontal defects results in significant probing depth reduction, These materials are osteoconductive and, therefore, act as a
attachment level gain, and osseous regeneration. The combi- scaffold for blood clots to be retained to allow bone formation.
nation of DFDBA and GTR has also proved to be very suc- Two types of calcium phosphate ceramics have been used.
cessful. However, limitations of the use of DFDBA include the
1. Hydroxyapatite (HA) has a calcium-to-phosphate ratio of
possible although remote, potential of disease transfer from
1.67, similar to that found in bone material. HA is gener-
the cadaver.
ally nonbioresorbable.
A bone-inductive protein isolated from the extracellular
2. Tricalcium phosphate (TCP), with a calcium-to-phosphate
matrix of human bones, termed osteogenin or BMP-3, has been
ratio of 1.5, is otherwise called whitlockite. TCP is at least
tested in human periodontal defects and seems to enhance
partially bioresorbable.
osseous regeneration.
Case reports and uncontrolled human studies have shown
Xenografts that calcium phosphate bioceramic materials are well toler-
Bone products from other species have a long history of use ated and can result in clinical repair of periodontal lesions.
in periodontal therapy. However, many of them are no longer Several controlled studies were conducted on the use of hy-
in use today. droxyl apatite (Periogral) and Calcitite. Clinical results were
Calf bone (Boplant), treated by detergent extraction, steril- good, but histologically these materials appeared to be encap-
ized and freeze-dried, has been used for the treatment of os- sulated by collagen.
seous defects. Kiel bone is calf or ox bone denatured with
20% hydrogen peroxide, dried with acetone, and sterilized Bioactive Glass
with ethylene oxide. Anorganic bone is ox bone from which Bioactive glass consists of sodium and calcium salts, phosphates,
the organic material has been extracted by means of ethylene- and silicon dioxide. For its dental applications, it is used in the
diamine. It is then sterilized by autoclaving. These materials form of irregular particles measuring 90-170 µm (PerioGlas,
have been tried and discarded for various reasons. Block Drug, Jersey City, NJ) or 300-355 µm (BioGran, Ortho
Currently, an anorganic, bovine-derived bone marketed Vita, Malvern, PA). When this material comes into contact with
under the brand name Bio-Oss (Osteohealth) has been suc- tissue fluids, the surface of the particles becomes coated with
cessfully used both for periodontal defects and in implant hydroxycarbonate apatite, incorporates organic ground pro-
surgery. It is an osteoconductive, porous bone mineral matrix teins such as chondroitin sulfate and glycosaminoglycans, and
from bovine cancellous or cortical bone. The organic compo- attracts osteoblasts that rapidly form bone.
nents of the bone are removed, but the trabecular architecture
and porosity are retained. The physical features permit clot Coral-Derived Materials
stabilization and revascularization to allow for migration of Two different coralline materials have been used in clinical
osteoblasts, leading to osteogenesis. Bio-Oss is biocompatible periodontics: natural coral and coral-derived porous HA. Both
are biocompatible, but natural coral is resorbed slowly (sever- development. The development of a promising system using
al months), whereas porous HA is not resorbed or takes years basic fibroblast growth factor-2 (FGF-2) is completing multi-
for resorption. center clinical trials.
Clinical studies on these materials showed pocket reduction, Because tissue-engineering approaches are likely to im-
attachment gain and bone level gain. Coral-derived materials prove clinical results, clinicians need to understand the biolo-
have also been studied in conjunction with membranes, with gy and clinical parameters and limitations of these techniques.
good results. Both materials have demonstrated microscopic
cementum and bone formation, but their slow resorbability or Enamel Matrix Derivatives for Periodontal
lack of resorption has hindered clinical success in practice. Regeneration
EMD has been effective in the treatment of infrabony de-
Tissue Engineering With Biologic fects. The histological evidence of EMD-induced periodontal
Mediators regeneration has been confirmed in a clinical case report. A
mandibular lateral incisor destined for orthodontic extraction
In wound healing, the natural healing process usually re- was treated with acid etching and EMD. After 4 months, the
sults in tissue scarring or repair. Using tissue engineering, the tooth was extracted and examined histologically. Regenerated
wound healing process is manipulated so that tissue regenera- cementum covered 73% of the defect and regenerated alveolar
tion occurs. This manipulation usually involves one or more bone covered 65%. This histological finding was later con-
of the three key elements: the signaling molecules, scaffold or firmed in other case reports, whereas new connective tissue
supporting matrices, and cells. The use of tissue engineering attachment was reported in another case series where EMD
for periodontal regeneration and dental implant site prepara- was used in combination with a bone-derived xenograft.
tion has recently been reviewed. EMD has been shown to be safe for clinical use. Long-term
Early clinical examples involving tissue-engineering prin- stability of EMD regenerative therapy was reported in a case
ciples include the use of bone allografts and autologous series that followed 106 EMD-treated defects in 90 patients.
platelet-rich plasma (PRP). Investigations indicated that the The data suggest radiographic bone level, clinical attachment
success rates with these materials were inconsistent. With the level (CAL) gain and reduced pocket depth reached near max-
development of recombinant growth factors and morpho- imal response after 1 year and the results remained stable over
gens, and the use of synthetic scaffolds, the level of success 5 years. Other long-term studies have confirmed these find-
has improved. Once considered experimental in nature, tis- ings (Fig. 48.5)
sue engineering is now clinically applicable with two com- There have been several studies comparing the use of EMD
mercially available tissue-engineering systems for periodontal alone or in conjunction with other regenerative approaches.
regeneration which involve the use of EMD and platelet-de- When EMD treatment was compared to GTR using bioresorb-
rived growth factor-BB (PDGF-BB) with beta-tricalcium phos- able membranes, the clinical results were comparable and sta-
phate (~-TCP). The ability of BMP type-I collagen sponge to ble over as much as a 10-year period. In a study comparing
enhance periodontal regeneration has been studied, but the EMD, GTR, EMD + GTR to open flap debridement, all three re-
mixed results and the concern for ankylosis have relegated sulted in superior result to open flap surgery with no additional
this differentiation factor to be used primarily for implant site improvement when EMD was used in conjunction with GTR.
FIGURE 48.5 A, Deep vertical bone loss distal to lower left central incisor. B, Area flapped, root prepared, and defect filled with enamel matrix
protein (Emdogain). C, Postoperative photo 6 months later. D, Reentry surgery showing extensive bone fill. (Courtesy Dr Marco Orsini, Aquila, Italy.)
FIGURE 48.6 A sample case of a patient treated in the pivotal trial. A-C, The pretreatment situation at preop, surgical debridement, and postsurgi-
cal reentry. D-F, The radiographic appearance after 12, 24, and 60 months. Surgical reentry after 12 months indicates good bone fill of the circumfer-
ential intrabony defect (C). The clinical pocket depth was 3mm after 5 years and remained stable.
Recombinant Human Platelet-Derived Growth Factor cases indicates the results were stable after 3 and 5 years.
for Periodontal Regeneration Another case series suggests that rhPDGF with FDBA can be
Platelet-derived growth factor (PDGF) is one of the earliest combined to achieve excellent results in severe periodontal
growth factors studied for its effect on wound healing because intrabony defects (Fig. 48 6).
it is a potent mitogenic and chemotactic factor for mesenchy-
mal cells in cell culture. Histological evidence of periodon- Nongraft-Associated Reconstructive
tal regeneration was first reported in experimental defects in
Procedures
beagle dog. During the development of PDGF for clinical use,
recombinant human platelet-derived growth factor (rhPDGF) The following sections discuss the rationale and techniques
was used in conjunction with allogenic bone to correct class that must be considered for a successful outcome in achiev-
II furcations and interproximal intrabony defects on hopeless ing new attachment or periodontal bone regeneration in re-
teeth. Histological evidence of periodontal regeneration was sponse to nongraft-associated reconstructive surgical therapy.
present with excellent furcation fill. Of these procedures, GTR is the main procedure used in clini-
Recently a biomaterial consisting of 0.3mg/ml of rhP- cal practice. Recent evidences suggest that LANAP may also
DGF + ~-TCP (GEM21S, Osteohealth, Shirley, NY) was found result in new attachment and regeneration but further clinical
to significantly improve attachment level gain, bone level, and trial are needed to test its efficacy and parameter for success.
bone volume compared to ~-TCP alone after 6 months in a
multicenter clinical trial. A subset of these patients was fol- Guided Tissue Regeneration
lowed for 24 months and a representative case series were GTR is used for the prevention of epithelial migration along
reported to be stable with increases in radiographic bone fill the cementa! wall of the pocket and maintaining space for
compared to the end results after 6 months. A review of these clot stabilization. Derived from the classic studies of Nyman,
Lindhe, Karring and Gottlow, this method is based on the and the root surface scaled and root planed. The ePTFE mem-
assumption that periodontal ligament and perivascular cells brane is trimmed to adapt to tooth configuration, secured by
have the potential for regeneration of the attachment appara- ePTFE sutures and the flap repositioned. It is interesting to
tus of the tooth. GTR consists of placing barriers of different note that, although much of the emphasis in the literature is
types (membranes) to cover the bone and periodontal liga- on adapting the membrane to the defect, no membrane can
ment, thus temporarily separating them from the gingival epi- ever be perfectly adapted. Despite gaps, these membranes
thelium and connective tissue. Excluding the epithelium and seem to work. After membrane placement, healing is allowed
the gingival connective tissue from the root surface during the to proceed for 4-6 weeks. Barring any membrane exposure, a
postsurgical healing phase not only prevents epithelial migra- second surgery is performed to remove the membrane. Dur-
tion into the wound but also favors repopulation of the area ing this removal, the healing tissue appears reddish and gran-
by cells from the periodontal ligament and the bone. It should ulomatous. After membrane removal, the area should not be
be noted that in the United States, GTR is often performed probed for 3 months. Radiographic evidence of bone fill is
with some type of bone graft as a scaffolding agent, so it is usually present after 6 months and should continue over the
a combined therapy. In Europe and other parts of the world course of 1 year.
where regulatory and religious constraints makes human graft Clinical studies have shown that ePTFE membranes used
materials unavailable, so it is performed as a traditional GTR in GTR procedures are more effective than surgical debride-
procedure and may be occasionally used in conjunction with ment in correcting intrabony defects. In intrabony and fur-
a other graft materials as a combined therapy. cation defects, there are gains in CAL (3-6 mm), improved
Initial animal experiments using Millipore filters and Tef- bone levels (2.4-4.8 mm), and probing depth reductions
lon membranes resulted in regeneration of cementum and (3.5-6 mm). Studies have demonstrated that these regenera-
alveolar bone and a functional periodontal ligament. Clini- tive results can be maintained over the course of several years.
cal case reports indicate that GTR results in a gain in attach- The advent of titanium-reinforced ePTFE allowed for the
ment level. Histologic studies in humans provided evidence formation of larger spaces, thus permitting correction of larger
of periodontal reconstruction in most cases, even with hori- defects. This resulted in significant clinical improvements us-
zontal bone loss. The use of polytetrafluoroethylene (PTFE) ing titanium-reinforced ePTFE compared to ePTFE.
membranes has been tested in controlled clinical studies in To determine how regeneration can be enhanced with GTR
mandibular molar furcations and has shown statistically sig- technique, the prolonged retention of ePTFE membranes was
nificant decreases in pocket depths and improvement in at- evaluated. After allowing the membrane to be retained for
tachment levels after 6 months, but bone level measurements 4 months, surgical re-entry after 1 year determined that the
have been inconclusive. A study on maxillary molar furca- mean bone fill of intrabony defects was 95%. This suggests
tions did not result in significant gain in attachment or bone that prolonged retention of a barrier membrane is desirable if
levels. With the regenerative success associated with the use no tissue perforation is present. This is consistent with many
of nonresorbable membrane, the advantage and disadvantage clinical reports of the improved bone quality associated with
of this approach became apparent. Notably, problems such as guided bone regeneration in implant site development.
membrane exposure, which resulted in no or limited regen- The major problem with using nonresorbable membranes
eration and the need for a secondary procedure for surgical is that the membrane is exposed to the oral environment dur-
removal resulted in the development of biodegradable mem- ing healing. Upon exposure, the membrane is contaminated
branes. Today in clinical practice, most GTR procedures use and colonized by oral microflora. Several studies have shown
biodegradable membranes while the nonresorbable mem- that contamination of the surgical field can result in decreased
branes are used for implant site development. Nevertheless, formation of new attachment. If the membrane is exposed, the
the historical research using nonresorbable membranes and infection can be temporarily managed with topical application
the development of various types of biodegradable mem- of chlorhexidine. This may minimize the infection and extend
branes is valuable. the time the membrane can be retained in place.
Nonresorbable Membranes. In classic animal and human Biodegradable Membranes. Bioresorbable membranes have
studies demonstrating the efficacy of GTR, cellulose acetate replaced the routine use of ePTFE membranes in GTR. There
filters were used. As this technique became more prevalent, are basically three types of bioresorbable membranes: (1)
the first commercial membrane was produced from expanded polyglycoside synthetic polymers (ie, polylactic acid, polylac-
polytetrafluoroethylene (ePTFE). This membrane has all the tate/polygalactate copolymers), (2) collagen, and (3) calcium
properties necessary for GTR barriers in that it (1) is a cel- sulfate. Polyglycoside membranes degrade as the result of ran-
lular barrier; (2) is biocornpatible; (3) provides space for the dom nonenzymatic cleavage of the polymer, producing poly-
healing tissue; ( 4) permits tissue integration; and (5) is clini- lactide and polyglycolide, which are converted to lactic acid
cally manageable. Much of our current understanding of GTR and pyruvate, respectively, and metabolized by the enzymes of
is based on studies using ePTFE membranes. Although they the Krebs cycle. Porcine collagen membranes are degraded by
are used less frequently now, they are still popular for guided collagenases and subsequently by gelatinases and peptidase.
bone regeneration and ridge preservation, so it is important There has been resurgence in the use of calcium sulfate as a
to understand the clinical procedures for managing these regeneration material because it can be used as a pavable re-
membranes. sorbable barrier when used in combination with bone or bone
The clinical effectiveness of ePTFE membranes is depen- substitutes. The calcium sulfate is bioresorbed through a giant
dent on technique. Preservation of the keratinized gingiva and cell reaction. Several features make these bioresorbable mem-
a relatively thick overlying surgical flap are critical to avoid branes easier to manage clinically: (1) they are more tissue
perforation of the flap by the membrane during healing. After compatible than nonresorbable membranes; (2) the timing for
the surgical area has been flapped, the defect is degranulated resorption can be regulated by the amount of cross-linkage in
the synthetic polymer and collagen membrane or the amount 2 mm or more. In both membrane groups, 83% of the sites im-
of heat-processed calcium sulfate chips in calcium sulfate bar- proved 4 mm or more, which was significantly better than the
rier; and (3) a second surgical procedure is not required to surgical debridement control group. These findings indicate
retrieve the nonresorbable membrane. that GTR procedures are equally effective using resorbable and
A recent GTR study compared the use of bioresorbable nonresorbable membranes. This finding has been confirmed
membranes (polylactate/polygalactate copolymer) versus by other investigators.
ePTFE membranes, with surgical debridement as a control. Af- The search for resorbable membranes has included trials
ter 1 year, significant gains in CAL were observed in all three and tests with numerous materials and collagens from differ-
groups (Fig. 48. 7) There was no difference in CAL gain be- ent species such as bovine and porcine. Cargile membrane
tween the two membrane groups, with both of them gaining derived from the cecum of an ox, polylactic acid, Vicryl
FIGURE 48.7 Clinical photographs and radiographs of a CTR case using ePTFE with titanium-reinforced membrane. A and B, The osseous defect
was along the distal interproximal area wrapping buccally over the furcation. C and D, To prevent the membrane from collapsing over the root surfaces,
DFDBA and adjusting the titanium membrane provide a larger space for regeneration. E, After 1 year, the radiographic findings are consistent with
achieving regeneration in this defect. (Courtesy of Rose L, et al, editor: Periodontics: medicine, surgery, and implants, Elsevier Mosby, 2004.)
(polyglactin 910), synthetic skin (Biobrane) and freeze-dried 3. An early fibrin linkage to collagen fibers exposed by the
duramater. Clinical studies with a mixture of copolymers de- citric acid treatment prevents the epithelium from migrat-
rived from polylactic acid and acetyl tributyl citrate resorbable ing over treated roots.
membranes (Guidor membrane, no longer on the market) and
This technique using citric acid has been extensively inves-
a poly-D,L-lactide-co-glycolide (Resolut membrane, also no
tigated in animals and humans. Studies in dogs have shown
longer on the market) have shown significant gains in clinical
encouraging results, especially for the treatment of furcation
attachment and bone fill.
lesions, but the results in humans have been contradictory.
The potential of using autogenous periosteum as a mem-
The recommended citric acid technique is as follows:
brane and also to stimulate periodontal regeneration has been
explored in two controlled clinical studies, one of grade-II 1. Raise a mucoperiosteal flap and thoroughly instrument the
furcation involvements in mandibular molars and another of root surface, removing calculus and underlying cementum.
interdental defects. The periosteum was obtained from the 2. Apply cotton pledgets soaked in a saturated solution of cit-
patient's palate by means of a window flap. Both studies re- ric acid (pH of 10) for 2-5 min.
ported that autogenous periosteal grafts can be used in GTR 3. Remove pledgets and irrigate root surface profusely with
and result in significant gains in clinical attachment and osse- water.
ous defect fill. 4. Replace the flap and suture.
Laser-Assisted New Attachment Procedure The use of citric acid has also been recommended in conjunc-
The role of laser in periodontal therapy has gained popularity tion with coverage of denuded roots using free gingival grafts.
(see Chapter 51). Nevertheless, the use of neodymium-yttrium- Fibronectin. Fibronectin is the glycoprotein that fibroblasts
aluminum-gamet (Nd:YAG) to perform surgical LANAP has been require to attach to root surfaces. The addition of fibronectin
reported for the management of chronic periodontitis and can po- to the root surface may promote new attachment. However,
tentially result in new attachment and periodontal regeneration. increasing fibronectin above plasma levels produces no obvi-
Many questions remain about LANAP that need to be clari- ous advantages. Adding fibronectin and citric acid to lesions
fied. The first is the exact mechanism and parameter by which treated with GTR in dogs did not improve the results.
healing by new attachment versus regeneration occur with LA- Tetracycline. In vitro treatment of the dentin surfaces with
NAP therapy Additionally, a blinded split mouth study to com- tetracycline increases binding of fibronectin, which in tum
pare LANAP protocol to other existing periodontal therapies is stimulates fibroblast attachment and growth while suppress-
in progress and needs to be completed. This along with other ing epithelial cell attachment and migration. Tetracycline also
randomized controlled trials will be needed for metaanalysis to removes an amorphous surface layer and exposes the dentin
determine if LANAP is equivalent or superior to other conven- tubules. In vivo studies, however, have not shown favorable
tional therapy As with all periodontal therapies, the long-term results. A human study showed a trend for greater connective
stability of the regeneration needs to be explored. tissue attachment after tetracycline treatment of roots. Tetra-
cycline gave better results when used alone than when com-
bined with fibronectin. It has been used as an adjunctive pro-
Biomodification of Root Surface. Changes in the tooth sur- cedure in preparation of the root in regenerative procedures
face wall of periodontal pockets (eg, degenerated remnants of and is a recommended step for use with biologic mediators.
Sharpeys fibers, accumulation of bacteria and their products, Other Techniques. Removal of junctional and sulcular epi-
disintegration of cementum and dentin) interfere with new thelium, intentional interdental denudation, free gingival graft
attachment. Although these obstacles to new attachment can in the interproximal area, excisional new attachment proce-
be eliminated by thorough root planing, the root surface of the dure (ENAP), coronally advanced flap, etc. have been tried
pocket can be treated to improve its chances of accepting the in the past to obtain periodontal regeneration but with little
new attachment of gingival tissues. success and hence are not in vogue today
Several substances have been proposed for this purpose in-
cluding citric acid, fibronectin, and tetracycline.
Citric Acid. There has been a series of studies one of which Combined Techniques
applied citric acid to the roots to demineralize the surface,
Periodontal new attachment and bone reconstruction has
attempting to induce cementogenesis and attachment of col-
been a challenge for the clinicians throughout the history of
lagen fibers.
periodontal therapy To take advantage of the different bone
The following actions of citric acid have been reported:
graft materials and biologic mediators, clinicians have com-
1. Accelerated healing and new cementum formation occur bined these graft materials along with the use of membranes
after surgical detachment of the gingival tissues and de- in an attempt to find a predictable technique to regenerate
mineralization of the root surface by means of citric acid. bone (Fig. 48 8)
Topically applied citric acid on periodontally diseased root Several clinicians have proposed a combination of the tech-
surfaces has no effect on nonplaned roots, but after root niques previously described in an attempt to enhance their re-
planing, the acid produces a 4-µm-deep demineralized zone sults. A classic paper published by Schallhorn and McClain
with exposed collagen fiber. Root planed, noncitric acid in 1988 described a combination technique using graft ma-
treated roots are left with a surface smear layer of microcrys- terial, root conditioning with citric acid and coverage with a
talline debris. Citric acid application not only removes the nonresorbable membrane (the only available one at the time).
smear layer, exposing the dentinal tubules, but also makes More recently, with the advent of osteopromotive agents, such
the tubules appear wider and with funnel-shaped orifices. as the EMD (Emdogain) and osteoconductive bovine-derived
2. Citric acid has also been shown in vitro to eliminate endo- anorganic bone (Bio-Oss) graft materials, other combination
toxins and bacteria from the diseased tooth surface. techniques have been advocated. The combined use of these
(Al
(C)
FIGURE 48.8 Radiographs of a GTR case using a nonresorbable ePTFE membrane. A and B, The mesially inclined molar is associated with a three-
walled intraosseous defect. The defect was filled with DFDBA and ePTFE was used. Membrane was exposed after 8 weeks and removed 2 weeks later.
C, Radiographic "fill" was halfway after 6 months and maximum fill was present after 12 months with minimal probing depth. (Courtesy of Rose L,
et al, editor: Periodontics: medicine, surgery, and implants, Elsevier Mosby, 2004, St Louis.)
products, along with autogenous bone with resorbable mem- regenerative and resective techniques. A clinical decision tree
brane coverage, has resulted in an increased percentage of cases is provided to guide the clinician in deciding the appropriate
with successful new attachment and periodontal reconstruc- situations (Fig. 48. 9). As the new therapeutic approaches are
tion. Many of these combination techniques were reviewed in developed, the clinical decision tree may need to be modified
the previous sections of this chapter. Whereas the use of com- to accommodate for these advances.
bination technique may be appealing, it is important for clini-
cians to remember that these added materials often escalate the Tooth and Defect Selection
cost of the procedure and should be balanced with the quality Therapeutic success is influenced by the tooth's importance in
and the long-term stability of the clinical results. the prosthetic rehabilitation, its endodontic status and defect
characteristics.
Factors That Influence Therapeutic The critical question to be addressed is if the involved
tooth is strategically important. If not, the strategic extraction
Success may avoid potential technical difficulty, postsurgical compli-
Factors that adversely affect periodontal regeneration were re- cations, and expenses. Strategic extraction may also improve
viewed at the 1996 World Workshop in Periodontics and 1997 access of better patient oral hygiene and compliance.
Proceedings of the Second European Workshop on Periodon- Once a tooth is deemed essential, it is important to assess
tology. A number of factors have been implicated or shown its endodontic status. If the tooth is endodontically healthy,
to adversely influence periodontal regenerative therapy. These regeneration may proceed. If not, then treatment of the end-
include site selection for reconstructive therapy, patient selec- odontic component must be performed and resolution of the
tion with consideration for compliance and behavior habits endodontic problem must be ascertained prior to the regener-
such as smoking and surgical management. ative procedure. Given the expense for endodontic treatment,
periodontal regenerative procedures, crown buildup and the
Site Selection for Reconstructive Therapy crown, strategic extraction, and possible replacement with
prosthesis or a dental implant should be seriously considered.
Therapeutic Selection Characteristics of the defect, such as the overall defect
The selection of appropriate therapeutic approach is one that depth, width, and walls, can influence clinical outcome in
is based on accurate assessment of the periodontal defect, response to regenerative surgery. Studies have consistently
one's past clinical experience and familiarity with the various shown that the deeper defect is correlated with increased CAL
Assess periodontal defect

• Pocket depth
• Attachment level
• Furcation involvement
• Endodontic status
• Radiographic assessment
of osseous architecture
Reevaluate systemic
issues, endodontic status,
and tooth morphology
Evaluate restorative
significance
Regenerate Pocket elimination

Nonsurgical surgery
Pocket elimination,
management, Extract and consider
maintenance, and Extract
maintenance, dental implant
monitoring Reevaluate after
and monitoring
12+ months
Nonmaintainable Maintenance
results and monitoring
FIGURE 48.9 Clinical decision tree for the management of advanced periodontitis.
and probing depth. One is more likely to achieve improved enthusiastic about oral hygiene and compliant with periodon-
regenerative results in narrow and circumferential, three- or tal maintenance.
two-walled configuration. Conversely, horizontal, one-walled,
and wide defects are less amenable to regenerative procedures. Smoking
Barring early reports on the use of iliac and autologous grafts, Smoking is a behavioral challenge that the therapist must
current regenerative approaches have not been consistently always assess. Smoking not only promotes disease progres-
successful in regenerating horizontal and one-walled defects. sion but also results in adverse therapeutic outcomes. It has
been implicated as having a detrimental effect on periodontal
wound healing following surgical procedures and to adversely
Patient Selection influence periodontal regeneration.
Poor Plaque Control and Compliance
Surgical Factors. The following principles play an important
Classical studies on of poor plaque control and poor post-
role in the success of periodontal regeneration techniques.
operative recall compliance have indicated that much of the
therapeutic gain from periodontal surgery will deteriorate. 1. Correct incisions: Usually access flaps with maximum tis-
Similarly, the positive results from GTR regenerative proce- sue conservation for optimal closure later are indicated.
dure have been shown to deteriorate with poor compliance. Particular care should be taken to retain the entire inter-
Progressive deterioration in these patients has been demon- dental papilla in order to obtain close approximation.
strated to possess a higher incidence of infection with puta- 2. Thorough debridement: It is important to thoroughly de-
tive periodontal pathogens (P gingivalis, P intermedia, and A bride the area free of diseased tissue and local irritants.
actinomycetemcomitans). Areas that are difficult to maintain, 3. Decortication: Often following removal of granulation tis-
such as furcation and root proximity situations, have also been sue the osseous defects become dry. In such situations,
shown to be difficult to be maintained. As a result, risk for healthy bleeding should be promoted by decortication us-
deterioration is higher. It is important to remember that the ing small round burs with copious irrigation.
patient came in with behavioral and anatomical issues, which 4. Presuturing: It is always preferable to place presutures so
resulted in the periodontal defect. After therapy, the hard- as to prevent displacement of the graft material during su-
est challenge is to continue to motivate patients to be highly turing.
5. Graft placement: The bony defects should never be over- • Scaffold or supporting matrice
filled. The clinician has to be realistic as over enthusiastic • Allogenic and alloplastic bone-grafting materials
placement of graft material results in poor outcome. • Collagen carriers
6. Optimal closure: Graft materials and membranes should • Calcium sulfate
be completely covered as exposure of the same leads to • Substrate modification to enhance cell selection
infections and consequently failure.
Wealth of information is available some of which are excit-
7. Periodontal dressing: It is recommended that periodontal
ing and mind boggling. Total periodontal reconstruction may
dressings are avoided following GTR membrane placement
be a reality in the near future.
as it may result in collapse of the membrane into the defect.
8. Postoperative care and maintenance: Ideally the patients are
advised not to brush on the grafted region for 3-4 weeks. Conclusions
They can instead be advised to use chlorhexidine mouth
Over the past 3 decades, the periodontal literature has been
rinses. The importance of optimal plaque control need not
filled with numerous reports related to periodontal regen-
be over emphasized.
eration. This therapeutic goal, although ideal, is difficult to
achieve. A variety of graft materials and regenerative strategies
are now available; however, they all have limitations. The sur-
Future Directions for Periodontal gical procedure can be technically demanding and when suc-
Regeneration cess is achieved, the maintenance of positive results is highly
dependent on patients' oral hygiene habits and compliance
In wound healing, the natural healing process usually re-
with periodontal maintenance. Despite all these difficulties,
sults in tissue scarring or repair. Using tissue engineering
periodontal regeneration is a clinical possibility that can be
(Fig. 48 10), the wound healing process is manipulated so
offered to patients. The clinician must carefully evaluate the
that tissue regeneration occurs. This manipulation usually in-
various regenerative and reparative approaches and decide
volves one or more of the three key elements: the signaling
which technique may result in the best clinical outcome. With
molecules, scaffold or supporting matrices, and cells. There is
the advent of new regenerative approaches, such as biological
an interplay among the following factors.
modifiers such as EMD and growth factors, one must criti-
• BMPs for periodontal and implant site regeneration cally evaluate how they may improve our ability to regenerate
• The use of recombinant human fibroblast growth factor 2 periodontal defects.
for periodontal regeneration Treatment planning in periodontics also has changed dra-
• Cell therapy matically in the past decade because of the acceptance of den-
• Gene therapy tal implants as a viable long-term option for replacing missing
Tissue engineering concept
Signaling molecules,
eg, PDGF, BMP
Time
Regeneration of
tissue/organs
Appropriate
environment
Cells,
eg, osteoblasts Scaffolds,
fibroblasts eg, CaP04, collagen
FIGURE 48.10 Tissue engineering is the manipulation of one or more of the three elements: signaling molecules, scaffolds, or cells. (Courtesy
Dr Samuel Lynch.)
teeth. With the increased predictability of implants, the ques- SUGGESTED READINGS
tion arises as to when to treat severe periodontal defects with Alger FA, Solt CW, Vuddahanok S, et al: The histologic evaluation of new at-
regenerative procedures and when to perform strategic extrac- tachment in periodontally diseased human roots treated with tetracycline
tion in preparation for implant placement. Sometimes the best hydrochloride and fibronectin,J Periodontol 61:447, 1990.
Bowers GM, Chadroff B, Carnevale R, et al: Histologic evaluation of new attach-
management of a periodontal defect may be extraction in lieu ment apparatus formation in humans. Part III,] Periodontol 60:683, 1989.
of periodontal regeneration or when regenerative efforts have Camelo M, Nevins ML, Schenk RK, et al: Periodontal regeneration in hu-
been unsuccessful. Extraction would minimize further bone man class II furcations using purified recombinant human platelet-derived
loss and provide the maximum volume of bone at the future growth factor-BB (rhPDGF-BB) with bone allograft, Int] Periodontics Restor-
ative Dent 23:213-225, 2003.
implant healing site. This paradigm shift has complicated our Caton JC: Overview of clinical trials on periodontal regeneration, Ann Peri-
views about regeneration. With dental implants as a viable odontal 2:215, 1987.
alternative, we need to redefine periodontal prognosis and Giannobile WV, Hollister SJ, Ma PX: Future prospects for periodontal bioen-
consider strategic extraction more often. Conversely, heroic gineering using growth factors, Clin Ad Periodontics 1:88, 2011.
regenerative procedures would be contraindicated. Kao RT, Murakami S, Beirne OR: The use of biologic mediators and tissue
engineering in dentistry, Periodontal 2000 20:127, 2009.
Periodontal regeneration continues to be one of the pri- Murphy KG, Gunsolley JC: Guided tissue regeneration for the treatment of
mary therapeutic approaches toward the management of periodontal intrabony and furcation defects. A systematic review, Ann Peri-
periodontal defects. Although evidence suggests that present odontal 8:266-302, 2003.
regenerative techniques can lead to periodontal regeneration, Needleman I, Tucker R, Giedrys-Leeper E, et al: Guided tissue regeneration
for periodontal intrabony defects-a Cochrane Systematic Review, Peri-
the use of GTR, and biological modifiers can enhance these odontal 2000 37:106-123, 2005.
results. The crucial challenge for the clinician is to critically Nevins M, Camelo M, Nevins ML, et al: Periodontal regeneration in humans
assess whether a periodontal defect can be corrected with a using recombinant human platelet-derived growth factor BB (rhPDGF-BB)
regenerative approach or whether it would be better managed and allogenic bone,] Periodontol 74:1282, 2003.
with osseous resection for the slight periodontal defect and Nevins M, Giannobile WV, McGuire MK, et al: Platelet-derived growth factor
stimulates bone fill and rate of attachment level gain: results of a large mul-
with strategic extraction for the advanced diseased state. In ucenter randomized controlled trial,] Periodontal 76:2205, 2005.
this assessment, the clinician should attempt to differentiate Nevins M, Kao RT, McGuire MK, et al: PDGF promotes periodontal regenera-
between techniques that have been studied in depth and with tion in localized osseous defects: 36 month extension results from a random-
acceptable results and those that are still experimental and ized, controlled, double-masked clinical trial,] Pe1iodontol 84:456, 2013.
Reynolds MA, Aichclmann-Reidy EM, Branch-Mays GL, et al: The efficacy of
promising. Research papers must be critically evaluated for bone replacement grafts in the treatment of periodontal osseous defects. A
adequacy of controls, selection of cases, methods of evalu- systematic review, Ann Periodontal 8:227-265, 2003.
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clinician should remember that we treat patients on the basis tioning, and guided tissue regeneration, Int J Periodont Restor Dent 8:8, 1988.
of "clinical" success and not "statistical" success. A resulting Sculean A, Alessandri R, Miron R, et al: Enamel matrix proteins and peri-
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49
Furcation Involvement
and Treatment
TN Sims • HH Takei • CD Dwarakanath
Chapter Outline
Etiologic Factors Indices of Furcation Involvement
Diagnosis and Classification of Furcation Treatment
Defects Nonsurgical Therapy
Local Anatomic Factors Surgical Therapy
Anatomy of the Bony Lesions Prognosis
The progress of inflammatory periodontal disease, if unabat- the diagnosis, treatment planning, and therapy of the patient
ed, ultimately results in attachment loss sufficient enough to with furcation defects.
affect the bifurcation or trifurcation of multirooted teeth. The
furcation is an area of complex anatomic morphology that
Diagnosis and Classification of
may be difficult or impossible to debride by routine periodon-
tal instrumentation. Routine homecare methods may not keep Furcation Defects
the furcation area free of plaque. A thorough clinical examination is the key to diagnosis and
The presence of furcation involvement is one clinical find- treatment planning. Careful probing is required to determine
ing that can lead to a diagnosis of advanced periodontitis and the presence and extent of furcation involvement, the posi-
potentially to a less favorable prognosis for the affected tooth tion of the attachment relative to the furca, and the extent and
or teeth. Furcation involvement, therefore, presents both di- configuration of the furcation defect. The Nabers probe may
agnostic and therapeutic dilemmas. be helpful to enter and measure difficult-to-access furcal ar-
eas (Fig. 49.1). Transgingival sounding may further define the
anatomy of the furcation defect. The goal of this examination
Etiologic Factors is to identify and classify the extent of furcation involvement
The primary etiologic factor in the development of furcation and to identify factors that may have contributed to the devel-
defects is bacterial plaque and the inflammatory consequences opment of the furcation defect or that could affect treatment
that result from its long-term presence. The extent of attach- outcome. These factors include: (1) the morphology of the
ment loss required to produce a furcation defect is variable affected tooth, (2) the position of the tooth relative to adja-
and related to local anatomic factors (eg, root trunk length cent teeth, (3) the local anatomy of the alveolar bone, ( 4) the
and root morphology) and local developmental anomalies [eg, configuration of any bony defects, and (5) the presence and
cervical enamel projections (CEPs)]. Local factors may affect extent of other dental diseases (eg, caries and pulpal necrosis).
the rate of plaque deposition or complicate the performance The dimension of the furcation entrance is variable but
of oral-hygiene procedures, thereby contributing to the de- usually quite small; 81 % of furcations have an orifice of 1 mm
velopment of periodontitis and attachment loss. Studies in- or less, and 58% are 0. 75 mm or less. The clinician should
dicate that prevalence and severity of furcation involvement consider these dimensions and the local anatomy of the furca-
increase with age. Dental caries and pulpal death may also tion area, when selecting instruments for probing. A probe of
affect a tooth with furcation involvement or even the area of small cross-sectional dimension is required if the clinician is
the furcation. All of these factors should be considered during to detect early furcation involvement.
561
(A) (B) (C) (D)

FIGURE 49.3 Different anatomic features that may be important in
prognosis and treatment of furcation involvement. A, Widely separat-
ed roots. B, Roots are separated but close. C, Fused roots separated only
in their apical portion. D, Presence of enamel projection that may be
conducive to early furcation involvement.
moderate root trunk length, or roots that may be fused to a

point near the apex (Fig. 49.3). The combination of root trunk
length with the number and configuration of the roots affects
the ease and success of therapy. The shorter the root trunk,
the less attachment needs to be lost before the furcation is
involved. Once the furcation is exposed, teeth with short root
trunks may be more accessible for maintenance procedures
and the short root trunks may facilitate some surgical proce-
(B) dures. Alternatively, teeth with unusually long root trunks or
fused roots may not be appropriate candidates for treatment
FIGURE 49.1 A, The Nabers probe is designed to probe into the furca- once the furcation has been affected.
tion. B, The probe placed into a Class II furcation of a dried skull.
Root Length
Local Anatomic Factors Root length is directly related to the quantity of attachment
supporting the tooth. Teeth with long root trunks and short
Clinical examination of the patient should allow the therapist roots may have lost a majority of their support by the time
to identify not only the furcation defects but also many of that the furcation becomes affected. Teeth with long roots and
the local anatomic factors that may affect the result of ther- short-to-moderate root trunk length are more readily treat-
apy (prognosis). Well-made dental radiographs, although do ed because sufficient attachment remains to meet functional
not allow a definitive classification of furcation involvement, demands.
provide additional information vital for treatment planning
(Fig. 49.2). Important local factors include anatomic features
of the affected teeth, as described next. Root Form
The mesial root of most mandibular first and second molars
and the mesiofacial root of the maxillary first molar are typi-
Root Trunk Length cally curved to the distal side in the apical third. In addition,
A key factor in both the development and the treatment of fur- the distal aspect of this root is usually heavily fluted. The cur-
cation involvement is the root trunk length. The distance from vature and fluting may increase the potential for root perfora-
the cementoenamel junction to the entrance of the furcation tion during endodontic therapy or complicate postplacement
can vary extensively. Teeth may have very short root trunks, during restoration. These anatomic features may also result
FIGURE 49.2 Different degrees of furcation involvement in radiographs. A, Grade I furcation on the mandibular first molar and a grade Ill furca-
tion on the mandibular second molar. The root approximation on the second molar may be sufficient to impede accurate probing of this defect. B,
Multiple furcation defects on a maxillary first molar. Grade I buccal furcation involvement and grade II mesiopalatal and distopalatal furcations are
present. Deep developmental grooves on the maxillary second molar simulate furcation involvement in this molar with fused roots. C, Grades Ill and
IV furcations on mandibular molars.
49 Furcation Involvement and Treatment 563
in an increased incidence of vertical root fracture. The size of Anatomy of the Bony Lesions
the mesial radicular pulp may result in removal of most of this
portion of the tooth during preparation. Pattern of Attachment Loss
The form of the bony lesions associated with the furcation can
lnterradicular Dimension vary significantly. Horizontal bone loss can expose the furca-
The degree of separation of the roots is an important factor tion as thin facial/lingual plates of bone that may be totally lost
also in treatment planning. Closely approximated or fused during resorption. Alternatively, areas with thickened bony
roots can preclude adequate instrumentation during scal- ledges may persist and predispose an individual to the de-
ing, root planing, and surgery. Teeth with widely separated velopment of furcations with deep vertical components. The
roots present more treatment options and are more readily pattern of bone loss on other surfaces of the affected tooth
treated. and adjacent teeth must also be considered during treatment
planning. The treatment response in deep, multiwalled bony
defects is different from that in areas of horizontal bone loss.
Anatomy of Furcation Complex multiwalled defects with deep, interradicular verti-
The anatomy of the furcation is complex. The presence of bi- cal components may be candidates for regenerative therapies.
furcational ridges, a concavity in the dome, and possible ac- Alternatively, molars with advanced attachment loss on only
cessory canals complicates not only scaling, root planing, and one root may be treated by resective procedures.
surgical therapy, but also periodontal maintenance. Odon-
toplasty to reduce or eliminate these ridges may be required Other Dental Findings
during surgical therapy for an optimal result.
The dental and periodontal condition of the adjacent teeth
must be considered during treatment planning for furcation
Cervical Enamel Projections involvement. The combination of furcation involvement and
CEPs are reported to occur on 8.6-28.6% of molars. The root approximation with an adjacent tooth represents the
prevalence is highest for mandibular and maxillary sec- same problem that exists in furcations without adequate root
ond molars. The extent of CEPs was classified by Masters separation. Such a finding may dictate the removal of the
and Hoskins in 1964 (Box 49 1). Figure 49.4 provides an most severely affected tooth or the removal of a root or roots
example of a grade llI CEP. These projections can affect (Fig. 49 5)
plaque removal, can complicate scaling and root planing, The presence of an adequate band of gingiva and a moder-
and may be a local factor in the development of gingivitis ate to deep vestibule will facilitate the performance of a surgi-
and periodontitis. CEPs should be removed to facilitate cal procedure, if indicated.
maintenance.
Indices of Furcation Involvement
The extent and configuration of the furcation defect are criti-
cal factors for both diagnosis and treatment planning. This
has led to the development of a number of indices to record
Grade /: The enamel projection extends from the
furcation involvement. These indices are based on the hori-
cementoenamel junction of the tooth toward the furcation zontal measurement of attachment loss in the furcation, on
entrance. a combination of horizontal and vertical measurements, or a
Grade II: The enamel projection approaches the entrance to combination of these findings with the localized configuration
the furcation. It does not enter the furcation and therefore,
no horizontal component is present.
Grade Ill: The enamel projection extends horizontally into the
furcation.
From Masters DH, Hoskins SW:/ Periodontol 35:49, 1964.
FIGURE 49.5 Advanced bone loss, furcation involvement, and root

approximation. Note the buccal furcation, which communicates with
the distal furcation of a maxillary first molar that also displays advanced
attachment loss on the distal root and approximation with the mesial
root of the maxillary second molar. The patient with such teeth may
benefit from root resection of the distobuccal root of the first molar or
FIGURE 49.4 Furcation involvement by grade Ill CEPs. extraction of the molar.
FIGURE 49.6 Glickman classification of furcation involvement. A, Grade I furcation involvement. Although a space is visible at the entrance to
the furcation, no horizontal component of the furcation is evident on probing. B, Grade II furcation in a dried skull. Note both the horizontal and the
vertical component of this cul-de-sac. C, Grade Ill furcations on maxillary molars. Probing confirms that the buccal furcation connects with the distal
furcation of both these molars, yet the furcation is filled with soft tissue. D, Grade IV furcation. The soft tissues have receded sufficiently to allow direct
vision into the furcation of this maxillary molar.
of the bony deformity. Glickman classified furcation involve- through the furcation because of interference with the bifur-
ment into four grades (Fig. 49.6): cational ridges or facial/lingual bony margins. However, if the
clinician adds the buccal and lingual probing dimensions and
obtains a cumulative probing measurement that is equal to
Grade I
or greater than the buccal/lingual dimension of the tooth at
A grade I furcation involvement is the incipient or early stage the furcation orifice, the clinician must conclude that a grade
of furcation involvement (Fig. 49.6A). The pocket is suprabo- III furcation exists (Fig. 49 6C). Properly exposed and angled
ny and primarily affects the soft tissues. Early bone loss may radiographs of early Class III furcations display the defect as a
have occurred with an increase in probing depth but radio- radiolucent area in the crotch of the tooth.
graphic changes are not usually found.
Grade IV
Grade II
In grade IV furcations, the interdental bone is destroyed, and the
A grade II furcation can affect one or more of the furcations of soft tissues have receded apically so that the furcation opening
the same tooth. The furcation lesion is essentially a cul-de-sac is clinically visible. A tunnel, therefore, exists between the roots
(Fig. 49.6B) with a definite horizontal component. If multiple of such an affected tooth. Thus, the periodontal probe passes
defects are present, they do not communicate with each other readily from one aspect of the tooth to another (Fig. 49.6D).
because a portion of the alveolar bone remains attached to the
tooth. The extent of the horizontal probing of the furcation
Other Classification Indices
determines whether the defect is early or advanced. Vertical
bone loss may be present and represents a therapeutic com- Hamp et al modified a three-stage classification system by at-
plication. Radiographs may or may not depict the furcation taching a millimeter measurement to separate the extent of
involvement, particularly with maxillary molars, because of horizontal involvement. Easley, Drennan, Tarnow, and Fletch-
the radiographic overlap of the roots. In some views, however, er described classification systems that consider both hori-
the presence of furcation "arrows" indicates possible furcation zontal and vertical attachment loss in classifying the extent of
involvement (see Chapter 26). furcation involvement. The Tarnow and Fletcher article uti-
lizes a subclassification that measures the probeable vertical
depth from the roof of the furca apically. The subclasses being
Grade Ill
proposed are: A, B, and C. "A" indicates a probeable vertical
In grade III furcations, the bone is not attached to the dome of depth of 1-3 mm, "B" indicates 4-6 mm, and "C" indicates
the furcation. In early grade III involvement, the opening may > 7 mm of probeable depth from the roof of the furca apically.
be filled with soft tissue and may not be visible. The clinician Furcations would thus be classified as IA, IB, and IC; IIA, IIB,
may not even be able to pass a periodontal probe completely and IIC; and IIIA, IIIB, and IIIC.
Consideration of defect configuration and the vertical com- Nonsurgical Therapy

ponent of the defect provide additional information that is
useful in planning therapy. Oral-Hygiene Procedures
Furcal management is difficult at best. Therapeutic modali-
Treatment ties for the treatment and maintenance of furcations have long
been a dilemma amongst periodontists and restorative den-
The objectives of furcation therapy are to (1) facilitate mainte- tists. Nonsurgical therapy is a very effective way of produc-
nance, (2) prevent further attachment loss, and (3) obliterate ing a satisfactory stable result. Ideal results with furcations are
the furcation defects as a periodontal maintenance problem. impossible to obtain. Once furcation breakdown has begun,
The selection of therapeutic mode varies with the class of fur- there is always a fairly compromised result clinically Both
cation involvement, the extent and configuration of bone loss, surgical and nonsurgical therapies have been shown to work
and other anatomic factors. effectively over time. Nonsurgical therapy, a combination of
oral-hygiene instruction, scaling, and root planing, has pro-
Therapeutic Classes of Furcation Defects vided excellent results in some patients. The earlier the furca-
tion is detected and treated, the more likely a good long-term
Class I: Early Defects result can be obtained. Nonetheless, even advanced furcation
Incipient or early furcation defects (Class I) are amenable to lesions can have successful long-term treatment. Several oral-
conservative periodontal therapy. Since the pocket is suprabony hygiene procedures have been used over time. All include
and has not entered the furcation, oral hygiene, scaling, and root access to the furcation. Obtaining access to the furcation re-
planing are effective. Any thick overhanging margins of restora- quires a combination of the awareness of the furcation by the
tions, facial grooves, or CEPs should be eliminated by odonto- patient and an oral-hygiene tool that facilitates that access.
plasty, recontouring, or replacement. The resolution of inflam- Many tools, including rubber tips; periodontal aids; tooth-
mation and subsequent repair of the periodontal ligament and brushes, both specific and general; and other aids have been
bone are usually sufficient to restore periodontal health. used over time for access to the patient (Fig. 49.8).
Class II
Once a horizontal component to the furcation has devel-
oped (Class II), therapy becomes more complicated. Shallow Nonsurgical maintenance by the clinician has also improved
horizontal involvement without significant vertical bone loss over time as instrumentation has improved. In recent decades,
usually responds favorably to localized flap procedures with instruments beyond simple curettes have been used to instru-
odontoplasty, osteoplasty, and ostectomy. Isolated deep Class ment the furcation. The frustration of instrumentation of the
II furcations may respond to flap procedures with bone grafts furcation was illustrated beautifully by Bower in 1979 in his
and guided tissue regeneration (Fig. 49. 7). This reduces the articles showing that only 58% of furcations could be entered
dome of the furcation and alters gingival contours to facilitate typically using curettes. Subsequently, other instrumenta-
the patient's plaque removal. tion has evolved, including DeMarco curettes, diamond files,
Quetin furcation curettes, and Mini Five Gracey Curettes. See
Classes 11 to IV: Advanced Defects Chapter 36 for a detailed discussion on this subject.
The development of a significant horizontal component to Svardstrom and Wennstrom illustrated that in the long
one or more furcations of a multirooted tooth (late Class II, term, furcations could be maintained using nonaggressive
Class III, or Class IV) or the development of a deep vertical techniques over a 10-year period in patients who were par-
component to the furca poses additional problems. Nonsur- ticipants in consistent maintenance. Other studies also il-
gical treatment is usually ineffective because the ability to lustrate that maintenance therapy is useful for patients to
instrument the tooth surfaces adequately is compromised. facilitate furcation cleanliness. Chemotherapy has proven
Periodontal surgery, endodontic therapy, and restoration of disappointing. Ribeiro et al found that nonsurgical therapy
the tooth may be required to retain the tooth. can effectively treat Class II furcation involvements but using
FIGURE 49.7 Treatment of a grade II furcation by osteoplasty and odontoplasty. A, This mandibular first molar has been treated endodontically
and an area of caries in the furcation repaired. A Class II furcation is present. B, Results of flap debridement, osteoplasty, and severe odontoplasty
5 years postoperatively. Note the adaptation of the gingiva into the furcation area. (Courtesy Dr Ronald Rott, Sacramento, CA.)
these surgical techniques have been used. The immediate goal

with these surgical approaches is to create access for the pa-
tient to maintain good hygiene.
Regeneration
In furcal lesions, bone regeneration is often thought to be rela-
tively futile. The periodontal literature has well-documented
therapeutic efforts designed to induce new attachment and
reconstruction on molars with furcation defects. Many surgi-
cal procedures using a variety of grafting materials have been
tested on teeth with different classes of furcation involvement.
Some investigators have reported clinical success, whereas
others have suggested that the use of these materials in Class
II, III, or IV furcations offers little advantage compared with
surgical controls.
Furcation defects with deep two-walled or three-walled
components may be suitable for reconstruction procedures.
These vertical bony deformities respond favorably to a variety
of surgical procedures, including debridement with or with-
out membranes and bone grafts. Chapter 41 addresses thera-
pies designed to induce new attachment or reattachment.
Tsao et al have shown that the furcation defect is a graftable
lesion. They found that lesions that were grafted had a great-
er vertical fill than areas treated with open-flap debridement
alone. Bowers et al have shown that furcation bone grafting us-
ing various membranes can improve the clinical status of these
lesions. Nonetheless, bone grafting remains an elusive goal with
variable results in furcation lesions. Another area of interest has
been barrier-membrane technology. Analysis of published stud-
FIGURE 49.8 A, The utilization of a Perio-Aid into the furcation for ies demonstrated a great variability in the clinical outcomes in
plaque removal. B, Proxy brush is used for plaque removal into the furca- mandibular grade II furcations treated with different types of
tion lesion. (Courtesy Karen OeYoung, ROH, and Janet Shigekawa, ROH.)
nonbioabsorbable and bioabsorbable barrier membranes.
Although many barrier-membrane studies show a slight
clinical improvement after treatment in both maxillary and
mandibular furcations, the results are generally inconsistent.
povidone-iodine did not provide additional benefits to sub-
gingival instrumentation.
The area most critical in furcation management is main- Root Resection
taining a relatively plaque-free status of the furcation. Root resection may be indicated in multirooted teeth with
Attaining access is a problem in this regard, but with the grades II-IV furcation involvements. Root resection may be
previously mentioned instruments and an effective nonsurgi- performed on vital teeth or endodontically treated teeth. It is
cal approach, much can be accomplished. The most critical preferable, however, to have endodontic therapy completed
component of multirooted-tooth maintenance is always the before resection of a root(s). If this is not possible, the pulp
successful reduction or elimination of plaque-retention areas should be removed, the patency of the canals determined, and
from the furcation area; meticulous oral hygiene by the pa- the pulp chamber medicated before resection. It is distressing
tient; and an effective nonsurgical therapy can play a major for both the patient and the clinician to perform a vital root
role in attaining this goal. resection and subsequently have an unfavorable event occur,
such as perforation, fracture of the root, or an inability to in-
Surgical Therapy strument the canal.
The indications and contraindications for root resection
Osseous Resection were well summarized by Bassaraba. In general, teeth planned
for root resection include the following points.
Osseous surgical therapy can be divided into resective and
regenerative therapy. This also applies to the furcation areas 1. Teeth that are critically important to the overall dental
when surgical therapy is contemplated. For many years, os- treatment plan. Examples are teeth serving as abutments
teoplasty and ostectomy have been used to make the furcation for fixed or removable restorations for which loss of the
areas cleansable. In the advanced cases, techniques were used tooth would result in loss of the prosthesis and entail ma-
to open the furcation into a Class IV from a severe Class II or jor prosthetic retreatment.
III case. This would allow easier hygiene into the furcation 2. Teeth that have sufficient attachment remaining for func-
area for the patient. These techniques have limited usefulness tion. Molars with advanced bone loss in the interproxi-
today, but in the compromised individual in whom teeth can- mal and interradicular zones, unless the lesions have three
not be extracted or in whom conservative therapy has failed, bony walls, are not candidates for root amputation.
FIGURE 49.9 Resection of a root with advanced bone loss. A, Facial osseous contours. There is an early grade II furcation on the facial aspect of
the mandibular first molar and a Class Ill furcation on the mandibular second molar. B, Resection of the mesial root. The mesial portion of the crown
was retained to prevent mesial drift of the distal root during healing. The grade II furcations were treated by osteoplasty. C, Buccal flaps adapted and
sutured. D, Lingual flaps adapted and sutured. E, Three-month postoperative view of the buccal aspect of this resection. New restorations were sub-
sequently placed. F, Three-month postoperative view of the lingual aspect of this resection.
3. Teeth for which a more predictable or cost-effective meth- root resection and the identification of which root to remove
od of therapy is not available. Examples are teeth with before surgery (Fig. 49.9). Every attempt should be made to
furcation defects that have been treated successfully with determine this prior to surgical exposure.
endodontics but now present with a vertical root fracture, The following is a guide to determine which root should
advanced bone loss, or caries on the root. be removed.
4. Teeth in patients with good oral hygiene and low activity
1. Remove the root(s) that will eliminate the furcation and
for caries are suitable for root resection. Patients unable
allow the production of a maintainable architecture on the
or unwilling to perform good oral hygiene and preventive
remaining roots.
measures are not suitable candidates for root resection or
2. Remove the root with the greatest amount of bone and
hemisection. Root-resected teeth require endodontic treat-
attachment loss. Sufficient periodontal attachment must
ment and usually cast restorations.
remain after surgery for the tooth to withstand the func-
These therapies can represent a sizable financial invest- tional demands placed on it such as bridge abutments and
ment by the patient in an effort to save the tooth. Alterna- in bruxers. Teeth with uniform advanced horizontal bone
tive therapies and their impact on the overall treatment plan loss are not suitable for root resection.
should always be considered and presented to the patient. 3. Remove the root that best contributes to the elimination
of periodontal problems on adjacent teeth. For example,
Criteria for Root Removal a maxillary first molar with a Class llI buccal-to-distal
A tooth with an isolated furcation defect in an otherwise intact furcation is adjacent to a maxillary second molar with a
dental segment may present few diagnostic problems. How- two-walled intrabony defect between the molars and an
ever, the existence of multiple furcation defects of varying early Class II furcation on the mesial furcation of the sec-
severity combined with generalized advanced periodontitis ond molar. There may or may not be local anatomic factors
can be a challenge for treatment planning. Careful diagno- affecting the teeth. The removal of the distobuccal root of
sis usually allows the therapist to determine the feasibility of the first molar allows the elimination of the furcation and
management of the two-wall intrabony lesion and also fa- facial and lingual/palatal flaps. Typically, a root cannot be re-
cilitates access for instrumentation and maintenance of the sected without elevating a flap. The flap should provide ad-
second molar. equate access for visualization and instrumentation and mini-
4. Remove the root with the greatest number of anatomic mize surgical trauma.
problems, such as severe curvature, developmental grooves, After debridement, resection of the root begins with the ex-
root flutings, or accessory and multiple root canals. posure of the furcation on the root to be removed. The remov-
5. Remove the root that least complicates future periodontal al of a small amount of facial or palatal bone may be required
maintenance. to provide access for elevation and to facilitate root removal. A
cut is then directed from the apical to the contact point of the
tooth, through the tooth, and to the facial and distal orifices
Hemisection
of the furcation. This cut is made with a high-speed, surgical-
Hemisection is the splitting of a two-rooted tooth into two length fissure or crosscut fissure carbide bur. The placement
separate portions. This process has been called bicuspidi- of a curved periodontal probe into or through the furcation
zation or separation because it changes the molar into two aids in orienting the angle of the resection. For hemisection, a
separate roots. Hemisection is most likely to be performed vertically oriented cut is made faciolingually through the buc-
on mandibular molars with buccal and lingual Class II or III cal and lingual developmental grooves of the tooth, through
furcation involvements. As with root resection, molars with the pulp chamber, and through the furcation. If the sectioning
advanced bone loss in the interproximal and interradicular cut passes through a metallic restoration, the metallic portion
zones are not good candidates for hemisection. After section- of the cut should be made before flap elevation. This prevents
ing of the teeth, one or both roots can be retained. This decontamination of the surgical field with metallic particles.
cision is based on the extent and pattern of bony loss, root If a vital root resection is to be performed, a more horizontal
trunk and root length, ability to eliminate the osseous defect, cut through the root is advisable. An oblique cut exposes a large
and endodontic and restorative considerations. The anatomy surface area of the radicular pulp and/or dental pulp chamber.
of the mesial roots of mandibular molars often leads to their This can lead to postoperative pain and can complicate end-
extraction and the retention of the distal root to facilitate both odontic therapy. A horizontal cut, although may complicate
endodontic and restorative therapy. root removal, has fewer postoperative complications. This root
The interradicular dimension between the two roots of a stump can be removed by odontoplasty after the completion of
tooth to be hemisected is also important. Narrow interradicu- endodontic therapy or at the time of tooth preparation.
lar zones can complicate the surgical procedure. The reten- After sectioning, the root is elevated from its socket. Care
tion of both molar roots can complicate the restoration of the should be taken not to traumatize bone on the remaining
tooth, since it may be virtually impossible to finish margins roots or to damage an adjacent tooth. Removal of the root
or to provide an adequate embrasure between the two roots provides visibility to the furcation aspects of the remaining
for effective oral hygiene and maintenance (Fig. 49 .10). There- roots and simplifies the debridement of the furcation with
fore, orthodontic separation of the roots is often required to hand, rotary, or ultrasonic instruments. If necessary, odonto-
allow restoration with adequate embrasure form (Fig. 49.11). plasty is performed to remove portions of the developmental
The result can be the need for multiple procedures and exten- ridges and prepare a furcation that is free of any deformi-
sive interdisciplinary therapy. In these patients the availability ty that would enhance plaque retention or adversely affect
of other treatment alternatives should be considered, such as plaque removal.
guided tissue/guided bone regeneration or replacement by os- Patients with advanced periodontitis often have root resec-
seointegrated dental implants. tion performed in conjunction with other surgical procedures.
Figure 49.13 provides an example of combining root resection
Root Resection/Hemisection Procedure and periodontal osseous surgery. The bony lesions that may
be present on adjacent teeth are then treated using resective
The most common root resection involves the distobuccal or regenerative therapies. After resection, the flaps are then
root of the maxillary first molar, as diagrammed in Fig. 49 .12. approximated to cover any grafted tissues or slightly cover the
After appropriate local anesthesia, a full-thickness mucoperi- bony margins around the tooth. Sutures are then placed to
osteal flap is elevated. Root resection or hemisection of teeth maintain the position of the flaps. The area may or may not be
with advanced attachment loss usually requires opening both covered with a surgical dressing.
FIGURE 49.10 A, Grade Ill furcation lesion. B, Hemisection to divide the tooth into mesial and distal portions. C, Postoperative view of a hemisected
mandibular with new crowns for both roots.
FIGURE 49.11 Hemisection and interradicular dimension. A, Buccal preoperative view of a mandibular right second molar with a deep grade II
buccal furcation and root approximation. B, Buccal view of bony lesions with flaps. Note the mesial and distal one-wall bony defects. The lingual
furcation was similarly affected. C, The molar has been hemisected and partially prepared for temporary crowns. Observe the minimal dimension be-
tween the two roots. D, Buccal view 3 weeks postoperatively. Because the embrasure space is minimal, these roots will be separated with orthodontic
therapy to facilitate restoration. (Courtesy Dr Louis Cuccia, Roseville, CA.)
FIGURE 49.12 Diagrams of distobuccal root resection of maxillary first molar. A, Preoperative bony contours with grade II buccal furcation and
a crater between the first and second molar. B, Removal of bone from the facial side of the distobuccal root and exposure of the furcation for instru-
mentation. C, Oblique section that separates the distal root from the mesial and palatal roots of the molar. D, More horizontal section that may be
used on a vital root amputation because it exposes less of the pulp of the tooth. E, Areas of application of instruments to elevate the sectioned root. F,
Final contours of the resection.
FIGURE 49.13 Hemisection combined with osseous surgery to treat furcation defects. A, Buccal preoperative view with provisional bridge. B,
Lingual view with provisional bridge in place. C, Radiograph of bony defects. Note the deep mesial bony defect, largely of one wall, and the radiolu-
cent area in the furcation of the first molar, indicating a grade II defect. D, Buccal view before osseous surgery. In addition to the furcation involvement,
a root separation problem exists between the two roots of the first molar. Class II furcations are present on the second molar. E, Buccal view after os-
seous surgery. Mesial root hemisected and removed. The other defects were treated by osteoplasty and ostectomy. F, Lingual preoperative view. Note
the heavy bony ledging at the lingual surface of these first and second molars. G, Lingual postoperative view. The mesial root has been resected, the
bony ledging recontoured, and the grade II furcations treated by osteoplasty. H, Buccal view 10 years after treatment. I, Lingual view 10 years after
treatment. (Courtesy Dr Louis Cuccia, Roseville, CA.)
FIGURE 49.14 Mesial root resection in the presence of advanced bone loss. A and B, Buccal and lingual preoperative views. Note the soft-tissue
contours that are predictive of the bony defects. C, Radiograph of extent of furcation involvement of the first and second molars. D and E, Buccal
preoperative and postoperative views. The mesial root of the second molar was resected and the interproximal craters treated by osteoplasty and minor
ostectomy. F and G, Lingual preresection and postresection views. The heavy ledges and horizontal bone loss on the lingual surface were managed by
osteoplasty. H and I, Buccal and lingual views 6 weeks postoperatively. A temporary wire splint has been bonded to the molars to prevent tipping of
the distal root of the mandibular second molar. (Courtesy Dr Louis Cucci, Roseville, CA.)
FIGURE 49.15 A, Clinical picture of a Class Ill furcation involvement. B, Radiographic appearance is far more grave than the clinical appearance.
C, After the tooth is removed, a computed tomography (CT) radiograph is taken to plan treatment for implant replacement. D, The implant restored.
(Courtesy Dr Sarvenaz Angha, Los Angeles.)
The removal of a root alters the distribution of occlusal antibacterial therapies, and delay extraction until the tooth
forces on the remaining roots. Therefore, it is wise to evaluate becomes symptomatic. Although additional attachment loss
the occlusion of teeth, from which roots have been resected may occur, such teeth may survive a significant number of
and, if necessary, adjust the occlusion. Centric holds should years.
be maintained but eccentric forces should be eliminated from
the area over the root that was removed. Patients with ad-
Dental Implants
vanced attachment loss may benefit from temporary stabiliza-
tion of the resected tooth to prevent movement (Fig. 49 .14 ). The advent of osseointegrated dental implants as an alterna-
tive abutment source has had a major impact on the retention
Extraction of teeth with advanced furcation problems. The high level of
predictability of osseointegration may motivate the therapist
The extraction of teeth with through-and-through furcation and the patient to consider removal of teeth with a guarded or
defects ( Classes Ill and IV) and advanced attachment loss may poor prognosis and to seek an implant-supported prosthetic
be the most appropriate therapy for some patients. This is par- treatment plan. Therefore, careful evaluation of the long-term
ticularly true for individuals who cannot or will not perform periodontal, endodontic, and restorative prognosis must be
adequate plaque control, who have a high level of caries activ- considered before invasive surgical therapy is undertaken to
ity, who will not commit to a suitable maintenance program, save a tooth with an advanced furcated lesion (Fig. 49 .15).
or who have socioeconomic factors that may preclude more
complex therapies. Some patients are reluctant to accept peri-
odontal surgery or even allow the removal of a tooth with
Prognosis
advanced furcation involvement, even though the long-term For many years the presence of significant furcation in-
prognosis is poor. The patient may elect to forego therapy, opt volvement meant a hopeless long-term prognosis for
to treat the area with scaling and root planing or site-specific the tooth. Clinical research, however, has indicated that
furcation problems are not as severe a complication as orig- to long-term success appear to be (1) thorough diagnosis,
inally suspected if one can prevent the development of car- (2) selection of patients with good oral hygiene, (3) excel-
ies in the furcation. Relatively simple periodontal therapy lence in nonsurgical therapy, and ( 4) careful surgical and
is sufficient to maintain these teeth to function for long restorative management.
periods. Other investigators have defined the reasons for
clinical failure of root-resected or hemisected teeth. Their
SUGGESTED READINGS
data indicate that recurrent periodontal disease is not a
deSanctis M, Murphy KG: The role of resective periodontal surgery in the
major cause of the failure of these teeth. Investigations of treatment of furcation defects,] Periodontol 22:154-168, 2000.
root-resected or hemisected teeth have shown that such Newell DH: The diagnosis and treatment of molar furcation invasions, Dent
teeth can function successfully for long periods The keys Clin North Am 42(2):301-337, 1998.
50
Periodontal Plastic and Esthetic
Surgery
HH Takei • ET Scheyer • RR Azzi • EP Allen • TJ Han • CD Dwarakanath
Chapter Outline
Terminology Techniques to Deepen the Vestibule
Objectives Techniques to Remove the Frenum
Etiology of Marginal Tissue Recession Techniques to Improve Esthetics
Factors That Affect Surgical Outcome Criteria for Selection of Techniques
Techniques to Increase Attached Gingiva Conclusions
Techniques to Treat Gingival Recession
In the last three decades, the scope and ambit of periodontal • esthetic surgical correction around implants
therapy has gone far beyond arresting the disease and elimi- • surgical exposure of unerupted teeth for orthodontics
nating the pockets. Increasing patient awareness has resulted
Periodontal plastic surgery is defined as the surgical pro-
in a big demand for restoration and augmentation of esthet-
cedures performed to correct or eliminate anatomic, devel-
ics. Further, the periodontist is now an important member of
opmental or traumatic deformities of the gingiva or alveolar
the interdisciplinary team, which aims at overall maintenance
mucosa. Mucogingival therapy is a broader term that includes
of the dentition in a state of health, function, and esthetic
nonsurgical procedures such as papilla reconstruction by
harmony.
means of orthodontic or restorative therapy. Periodontal plas-
tic surgery includes only the surgical procedures of mucogin-
Terminology gival therapy.
This chapter discusses the periodontal plastic surgical tech-
The term mucogingival surgery was initially introduced in the
niques included in the traditional definition of mucogingival
literature by Friedman to describe surgical procedures for the
surgery (1) widening of attached gingiva, (2) deepening of
correction of relationships between the gingiva and the oral
shallow vestibules, and (3) resection of the aberrant frena. In
mucous membrane with reference to three specific problem
addition, esthetic surgical therapy around the natural denti-
areas: attached gingiva, shallow vestibule, and frenum inter-
tion and tissue engineering (biologic mediator) are included in
fering with the marginal gingiva. With the advancement of
this chapter. Other aspects of periodontal plastic surgery, such
periodontal surgical techniques, the scope of nonpocket sur-
as periodontal-prosthetic surgery, esthetic surgery around im-
gical procedures has increased, now encompassing a multi-
plants, and surgical exposure of teeth for orthodontic therapy,
tude of areas that were not addressed in the past. Recognizing
are covered in other areas in this book.
this, the 1996 World Workshop in Clinical Periodontics re-
named mucogingival surgery as "periodontal plastic surgery,"
a term originally proposed by Miller in 1993 and broadened Objectives
to include the following areas:
The five problems for which periodontal plastic surgery pro-
• periodontal-prosthetic corrections
vides solutions described in this chapter are as follows:
• crown lengthening
• socket preservation 1. inadequate or lack of attached gingiva
• ridge augmentation 2. gingival recession
• esthetic surgical corrections 3. shallow vestibule
• coverage of the denuded root surface 4. aberrant frenum
• reconstruction of papillae 5. various esthetic deformities of the gingiva.
573
Problems Associated with Attached depth, which is measured from the gingival margin to the bot-
Gingiva tom of the vestibule. As indicated previously, with minimal
vestibular depth, proper hygiene procedures are jeopardized.
One of the goals of mucogingival surgical procedures is the The sulcular brushing technique requires the placement of the
creation or widening of attached gingiva around teeth and im- toothbrush at the gingival margin, which may not be possible
plants. The width of the attached gingiva varies in different with reduced vestibular depth.
individuals and on different teeth of the same individual. At- Minimal attached gingiva with adequate vestibular depth
tached gingiva is not synonymous with "keratinized gingiva" may not require surgical correction if proper atraumatic hy-
because the latter also includes the free gingival margin. giene is practiced with a soft brush. Minimal amounts of kera-
The width of the attached gingiva is determined by sub- tinized attached gingiva with no vestibular depth benefit from
tracting the depth of the sulcus or pocket from the distance mucogingival correction. Adequate vestibular depth is also
between the crest of the gingival margin and the mucogingival necessary for the proper placement of removable prostheses.
junction.
The original rationale for mucogingival surgery was pred-
Problems Associated with Aberrant
icated on the assumption that a minimal width of attached
gingiva was required to maintain optimal gingival health. Frenum
However, several studies have challenged the view that a wide, Another important objective of periodontal plastic surgery is to
attached gingiva is more protective against the accumulation correct frenal or muscle attachments that may extend coronal
of plaque than a narrow or a nonexistent zone. No minimum to the mucogingival junction. If adequate keratinized, attached
width of attached gingiva has been established as a standard gingiva is present coronal to the frenum, it may not be neces-
necessary for gingival health. People who practice good and sary to remove the frenum. A frenum that encroaches on the
atraumatic oral hygiene may maintain excellent gingival margin of the gingiva may interfere with plaque removal, and
health with almost no attached gingiva. the tension on the frenum may tend to open the sulcus. In such
However, those individuals whose oral hygiene practices cases, surgical removal of the frenum is indicated (Fig. 50 .1).
are less than optimal can be helped by the presence of keratin-
ized gingiva and vestibular depth. Vestibular depth provides
space for easier placement of the toothbrush and prevents Esthetic Deformities
brushing on mucosa! tissue. To improve esthetics, the objec- As indicated earlier, the recession of the facial, gingival margin
tive is the coverage of the denuded root surface. The maxillary will alter the proper gingival symmetry and result in an es-
anterior area, especially the facial aspect of the canine, often thetic problem. The presence of the interdental papilla is also
presents extensive gingival recession. In such cases, the cover- important to satisfy the esthetic goals of the patient. A missing
ing of the denuded root surface not only widens the zone of papilla creates a space that many address as a "black hole."
attached gingiva but also creates an improved esthetic result. The regeneration of the lost or reduced papilla is one of the
This recession and the resultant denuded root surface have most difficult goals in esthetic periodontal plastic surgery An-
special esthetic concerns for individuals with a high smile other area of concern is the patient who presents an excessive
line. A wider zone of attached gingiva is also needed around amount of gingiva in the visible area. This condition is often
teeth that serve as abutments for fixed or removable partial addressed as a "gummy smile" and may be corrected surgi-
dentures, as well as in the ridge areas bearing a denture. Teeth cally by crown lengthening. The correction of these anatomic
with subgingival restorations and narrow zones of keratinized defects has become an important part of periodontal plastic
gingiva have higher gingival inflammation scores than teeth surgery Also gingival asymmetry needs to be corrected to im-
with similar restorations and wide zones of attached gingiva. prove the smile profile of the patient. The esthetic demands of
Widening the attached gingiva accomplishes the following the patients today have increased to such an extent that black
four objectives: or brownish discoloration of the gums-"physiologic hyper
1. enhances plaque removal around the gingival margin melanin pigmentation" is unacceptable. Gingival depigmen-
2. improves esthetics tation, although provides only a temporary relief, is widely
3. reduces inflammation around restored teeth performed nowadays.
4. gingival margin binds better around teeth and implants
with attached gingiva.
Etiology of Marginal Tissue Recession
Gingival Recession The most common cause of gingival recession and the loss
of attached gingiva is abrasive and traumatic tooth brush-
Exposed roots besides being unaesthetic also cause additional ing habits (Fig. 50.2). The bone and soft tissue anatomy of
problems like dentinal hypersensitivity, pulpal hyperemia be- the buccal, radicular surface of the dentition is usually thin,
sides being prone for caries. Hence root coverage has become especially around the anterior area. Teeth positioned buc-
a very important procedure in Periodontics today cally may have an even thinner bone and gingiva. In many
instances, such areas may have a complete absence of bone
Problems Associated with Shallow beneath the thin overlying gingival tissue. Such defect in the
Vestibule bone is called a dehiscence. This anatomic status combined
with external trauma from overzealous brushing can lead to
Another objective of periodontal plastic surgery is the creation the loss of gingival tissue. Recession of the gingival tissue and
of vestibular depth when it is lacking. Gingival recession dis- bone exposes the cementa! surface of the root, which results
places the gingival margin apically, thus reducing vestibular in abrasion and "ditching" of the cementa! surface apical to
50 Periodontal Plastic and Esthetic Surgery 575
FIGURE 50.1 A-D, Examples of frenum attached to the gingiva.
the cementoenamel junction (CEJ). The cementum is softer width of the attached gingiva after mucogingival surgery are
than enamel and will be destroyed before the enamel surface affected as much by tooth alignment as by variations in treat-
of the crown. ment procedures.
Another cause for gingival recession is periodontal disease Orthodontic correction is indicated when mucogingival
and chronic marginal inflammation. The loss of attachment surgery is performed on malposed teeth in an attempt to wid-
caused by the inflammation is followed by the loss of bone en the attached gingiva or to restore the gingiva over denuded
and gingiva. Advanced periodontal involvement in areas of roots. If orthodontic treatment is not feasible, the prominent
minimal attached gingiva results in the base of the pocket ex- tooth should be reduced to within the borders of the alveolar
tending close to or apical to the mucogingival junction. Peri- bone, with special care taken to avoid pulp injury
odontal therapy of these areas also results in gingival recession Roots covered with thin bony plates present a hazard in
caused by the loss of gingiva and bone (Fig. 50.2D and E). mucogingival surgery. Even the most protective type of flap,
Frenal and muscle attachments that encroach on the mar- a partial-thickness flap, creates the risk of bone resorption on
ginal gingiva can distend the gingival sulcus, which creates the periosteal surface. Resorption in amounts that ordinarily
an environment for plaque accumulation. This condition are not significant may cause loss of bone height when the
increases the rate periodontal recession and will contribute bone plate is thin or tapered at the crest.
to the recurrence of the recession even after treatment These
problems are more common on facial surfaces, but may also
Mucogingival Line (Junction)
occur on the lingual surface.
Orthodontic tooth movement through a thin buccal osse- Normally, the mucogingival line in the incisor and canine ar-
ous plate may lead to a dehiscence beneath a thin gingiva, eas is located approximately 3 mm apical to the crest of the al-
which can lead to recession. veolar bone on the radicular surfaces and 5 mm interdentally.
In periodontal disease and on malposed disease free teeth, the
bone margin is located farther apically and may extend be-
Factors That Affect Surgical Outcome yond the mucogingival line. The distance between the muco-
Irregularity of Teeth gingival line and the CEJ before and after periodontal surgery
is not necessarily constant. After inflammation is eliminated,
Abnormal tooth alignment is an important cause of gingival the tissue tends to contract and draw the mucogingival line in
deformities that require corrective surgery and also an impor- the direction of the crown.
tant factor in determining the outcome of treatment. The lo-
cation of the gingival margin, width of the attached gingiva,
and alveolar bone height and thickness are all affected by Techniques to Increase Attached
tooth alignment. On teeth that are tilted or rotated labially, Gingiva
the labial bony plate is thinner and located farther apically
To simplify and better understand the techniques and the re-
than on the adjacent teeth; therefore the gingiva is recessed so
sult of the surgery, the following classification is presented.
that the root is exposed. On the lingual surface of such teeth,
the gingiva is bulbous and the bone margins are closer to the • Gingival augmentation apical to the area of recession. A graft,
CE]. The level of gingival attachment on root surfaces and the either pedicle or free, is placed on a recipient bed apical to
FIGURE 50.2 A, Gingival recession and extreme inflammation around a lower central incisor. B, Advanced recession of mesial root of a first lower
molar, C, Gingival recession caused by faulty tooth brushing. D, Preoperative view showing deep periodontal pocket between the maxillary central
incisors. E, Recession following periodontal flap surgery.
the recessed gingival margin. No attempt is made to cover Gingival Augmentation Apical
the denuded root surface. to Recession
• Gingival augmentation coronal to the recession (root cover-
age). A graft (either pedicle or free) is placed covering Techniques for gingival augmentation apical to the area of re-
the denuded root surface. Both the apical and the coro- cession include free gingival autograft, Free Connective Tissue
nal widening of attached gingiva enhance oral hygiene Autografts and the apically positioned flap.
procedures, but only the latter can correct an esthetic
Free Gingival Autografts
problem. For preprosthetic purposes, the combination
of widening keratinized gingiva apical and coronal to the Free gingival grafts are used to create a widened zone of at-
recession would satisfy this objective. Consideration of tached gingiva. They were initially described by Bjorn in 1963
the objectives as apical, coronal, or both provides a bet- and have been extensively investigated since that time.
ter understanding of the techniques required to achieve
the goals. The Classic Technique (Fig. 50.3). Step 1: Prepare the recipi-
ent site. The purpose of this step is to prepare a firm connec-
Widening of the keratinized attached gingiva (apical or tive tissue bed to receive the graft. The recipient site can be
coronal to the area of recession) can be accomplished by nu- prepared by incising at the existing mucogingival junction
merous techniques, such as the free gingival autograft, free with a No. 15 blade to the desired depth, blending the inci-
connective tissue autograft and lateral pedicle flap, which can sion on both ends with the existing mucogingival line. Perios-
be used for either objective. teum should be left covering the bone (Fig. 50.4).
FIGURE 50.3 Free gingival graft. A, Before treatment; minimal keratinized gingiva. B, Recipient site prepared for free gingival graft. C, Palate will
be donor site. D, Free graft. E, Graft transferred to recipient site. F, At 6 months, showing widened zone of attached gingiva. (Courtesy Dr. Perry Klok-
kevold, Los Angeles.)
An aluminum foil template of the recipient site can be

made to be used as a pattern for the graft.
Grafts can also be placed directly on bone tissue. For this
technique, the flap should be separated by blunt dissection
with a periosteal elevator. The advantages of this variant are
less postoperative mobility of the graft, less swelling, better
hemostasis and 1.5-2 times less shrinkage. However, there is
a healing lag period that is observed for the first 2 weeks.
Step 2: Obtain the graft from the donor site. The classic or con-
ventional free gingival graft technique consists of transferring
a piece of keratinized gingiva approximately the size of the
recipient site. To avoid the large wound that this procedure
sometimes leaves in the donor site, some alternative methods
have been proposed. The original technique is described first,
followed by several of the most common variants.
For the classic technique, a partial-thickness graft is used.
FIGURE 50.4 Diagram of graft bed suture.
The palate is the usual site from which the donor tissue is
removed. The graft should consist of epithelium and a thin
Another technique consists of outlining the recipient site layer of underlying connective tissue. Place the template over
with two vertical incisions from the incised gingival margin the donor site, and make a shallow incision around it with
into the alveolar mucosa. Extend the incisions to approxi- a No. 15 blade. Insert the blade to the desired thickness at
mately twice the desired width of the attached gingiva, allow- one edge of the graft. Elevate the edge and hold it with tissue
ing for 50% contraction of the graft when healing is complete. forceps. Continue to separate the graft with the blade, lifting
The amount of contraction depends on the extent to which the it gently as separation progresses to provide visibility Plac-
recipient site penetrates the muscle attachments. The deeper ing sutures at the margins of the graft helps control it during
the recipient site, the greater is the tendency for the muscles separation and transfer and simplifies placement and suturing
to elevate the graft and reduce the final width of the attached to the recipient site.
gingiva. The periosteum along the apical border of the graft Proper thickness is important for survival of the graft. It
is sometimes penetrated in an effort to prevent postoperative should be thin enough to permit diffusion of fluid from the
narrowing of the attached gingiva. recipient site, which is essential in the immediate post trans-
The No. 15 blade is used to incise along the gingival mar- plant period. A graft that is too thin may necrose and expose
gin to separate a flap consisting of epithelium and underlying the recipient site. If the graft is too thick, its peripheral layer
connective tissue without disturbing the periosteum. Extend is jeopardized because of the excessive tissue that separates it
the flap to the depth of the vertical incisions. Suture the flap from new circulation and nutrients. Thick grafts may also cre-
where the apical portion of the free graft will be located. Three ate a deeper wound at the donor site, with the possibility of
to four independent gut sutures are placed. The needle is first injuring major palatal arteries. The ideal thickness of a graft is
passed as a superficial mattress suture perpendicular to the between 1.0 and 1.5 mm. After the graft is separated, remove
incision and then on the periosteum parallel to the incision. the loose tissue tags from the undersurface. Thin the edge to
avoid bulbous marginal and interdental contours. Special pre- The graft is initially maintained by a diffusion of fluid from
cautions must be taken with grafts from the palate. the host bed, adjacent gingiva, and alveolar mucosa. The fluid
The submucosa in the posterior region is thick and fatty is a transudate from the host vessels and provides nutrition
and should be trimmed so that it will not interfere with vas- and hydration essential for the initial survival of the trans-
cularization. Grafts tend to reestablish their original epithe- planted tissues. During the first day, the connective tissue
lial structure, so mucous glands may occur in grafts obtained becomes edematous and disorganized and undergoes degen-
from the palate. eration and lysis of some of its elements. As healing progresses,
A thick graft can be thinned by holding it between two wet the edema is resolved and degenerated connective tissue is
wooden tongue depressors and slicing it longitudinally with a replaced by new granulation tissue.
sharp No. 15 blade. Revascularization of the graft starts by the second or third
Step 3: Transfer and immobilize the graft. Remove the sponge day. Capillaries from the recipient bed proliferate into the graft
from the recipient site, reapply it with pressure if necessary to form a network of new capillaries and anastomose with pre-
until bleeding is stopped. Remove the excess clot. A thick clot existing vessels.
interferes with vascularization of the graft. Many of the graft vessels degenerate and are replaced by
Position the graft and adapt it firmly to the recipient site. A new ones, and some of these participate in the new circula-
space between the graft and the underlying tissue (dead space) tion. The central section of the surface is the last to vascular-
impairs vascularization and jeopardizes the graft. Suture the ize, but this is complete by the tenth day.
graft at the lateral borders and to the periosteum to secure it The epithelium undergoes degeneration and sloughing,
in position. The graft must be immobilized. Any movement with complete necrosis occurring in some areas. It is replaced
interferes with healing. Avoid excessive tension, which can by new epithelium from the borders of the recipient site. A thin
distort the graft from the underlying surface. Every precaution layer of new epithelium is present by the fourth day, with rete
should be taken to avoid trauma to the graft. Tissue forceps pegs developing by the seventh day. Heterotopically placed
should be used delicately and a minimum number of sutures grafts maintain their structure (keratinized epithelium), even
used to avoid unnecessary tissue perforation. after the grafted epithelium has become necrotic and has been
Step 4: Protect the donor site. Cover the donor site with a replaced by neighboring areas of nonkeratinized epithelium,
periodontal pack for 1 week and repeat if necessary. Retention which suggests that a genetic predetermination of the specific
of the pack on the donor site can be a problem. If facial at- character of the oral mucosa exists that depends on stimuli
tached gingiva was used, the pack may be retained by locking originating in the connective tissue. This is the basis for the
it through the interproximal spaces onto the lingual surface. technique that uses grafts composed only of connective tis-
If there are no open interdental spaces, the pack can be cov- sue obtained from areas in which it is covered by keratinized
ered by a plastic stent wired to the teeth. A modified Hawley epithelium.
retainer is useful to cover the pack on the palate and over As seen microscopically, healing of a graft of intermediate
edentulous ridges. thickness (0.75 mm) is complete by 10 weeks; thicker grafts
(1. 75 mm) may require 16 weeks or longer. The gross ap-
Variant Techniques. The free gingival graft technique is a pearance of the graft reflects the tissue changes within it. At
predictable procedure, but the donor site (palate) is left with transplantation, the graft vessels are empty and the graft is
an open wound that must heal by secondary intention. The pale. The pallor changes to an ischemic grayish white during
following variant techniques attempt to minimize the donor the first 2 days until vascularization begins and a pink color
site wound by removing the donor tissue in a different con- appears. The plasmatic circulation accumulates and causes
figuration and altering the shape to maximize coverage over softening and swelling of the graft, which are reduced when
the recipient site. These techniques are (1) the accordion tech- the edema is removed from the recipient site by the new blood
nique, (2) the strip technique (Fig. 50.5), and (3) the com- vessels. Loss of epithelium leaves the graft smooth and shiny.
bination epithelial-connective tissue strip technique. All are New epithelium creates a thin, gray, veillike surface that devel-
modifications of the free gingival grafts. ops normal features as the epithelium matures.
The accordion technique, described by Rateitschak et al, Functional integration of the graft occurs by the seven-
attains expansion of the graft by alternate incisions in opposite teenth day, but the graft is morphologically distinguishable
sides of the graft. This technique increases the donor graft tis- from the surrounding tissue for months. The graft eventually
sue by changing the configuration of the tissue. blends with adjacent tissues, but sometimes although pink,
The strip technique, developed by Han et al, consists of firm, and healthy, it is somewhat bulbous. This usually pres-
obtaining two or three strips of gingival donor tissue about ents no problem, but if the graft traps plaque or is esthetically
3- 5 mm wide and long enough to cover the entire length of unacceptable, thinning of the graft may be necessary. Thin-
the recipient site. These strips are placed side by side to form ning the surface of the grafted tissue does reduce the bulbous
one donor tissue and sutured on the recipient site. The area is condition because the surface epithelium tends to proliferate
then covered with aluminum foil and surgical dressing. again. The graft should be thinned by making the necessary
incisions to elevate it from the periosteum, removing tissue
Healing of the Graft. The success of the graft depends on from its undersurface, and suturing it back in place.
survival of the connective tissue. Sloughing of the epithelium
occurs in most cases, but the extent to which the connective Accomplishments. Free gingival grafts effectively widen the
tissue withstands the transfer to the new location determines attached gingiva. Several biometric studies have analyzed the
the fate of the graft. Fibrous organization of the interface be- width of the attached gingiva after the placement of a free gin-
tween the graft and the recipient bed occurs within two to gival graft. After 24 weeks, grafts placed on denuded bone
several days. shrink 25%, whereas grafts placed on periosteum shrink
FIGURE 50.5 Free gingival graft: strip technique. A-D, Mucosa[ tissue around implants. E and F, Recipient site prepared. G, Donor site with strips of
free graft removed. H, Donor strips of free graft. I and J, Strips placed side by side on recipient site. K, Donor area 1 week after graft removal. L, Healing
of recipient site after 3 months. Note good keratinized, attached gingiva. (Courtesy DrT Han and Dr P Klokkevold, Los Angeles.)
50%. The greatest amount of shrinkage occurs within the first tooth surface not previously exposed to the oral environment
6 weeks. and found in the course of flap surgery
The placement of a gingival graft does not "improve" the The use of free gingival autografts to cover denuded roots
status of the gingiva. Therefore the indication for a free gingi- is described later in this chapter.
val graft should be based on the presence of progressive gingi-
val recession and inflammation. When recession continues to Allografts as Donor Tissue (Fig. 50.6). Another technique
progress after a few months with good plaque control, a graft to minimize the use of the palate as a donor site is the use
can be placed to prevent further recession and loss of attached of acellular dermal matrix (ADM) as a substitute for palatal
gingiva. donor tissue. The use of the palate as a donor site for gingival
Other materials have been used to replace gingival tissue augmentation has numerous disadvantages, for not only are
in gingival extension procedures. Attempts with lyophilized the patients fearful of palatal surgery from where the donor
duramater and sclera have not been satisfactory The use of tissue is procured but there is also a limitation on the amount
irradiated free gingival allograft showed satisfactory results, of tissue that can be removed. Currently, there are numerous
but further research is necessary before it can be considered clinicians who advocate the use of ADM as a substitute for
for clinical use. palatal donor tissue. This product is commercially available
Free autogenous gingival grafts have been found to be use- under the name AlloDerm and is derived from donated human
ful for covering nonpathologic dehiscences and fenestrations. skin. Commercial preparation of this tissue includes a multi-
Nonpathologic refers to openings of the bone through the step proprietary process that removes both the epidermis and
FIGURE 50.6 A, Preoperative view. B, lntrasulcular incision. C, AlloDerm on the surface before insertion into the pouch. D, AlloDerm sutured within
the pouch. E, Pouch coronally positioned and sutured. F, Postoperative view after 1 month. G, Postoperative view after 1 year.
FIGURE 50.7 Free connective tissue graft. A, Lack of keratinized, attached gingiva buccal to central incisor. B, Vertical incisions to prepare recipient
site. C, Recipient site prepared. D, Palate from which connective tissue will be removed for donor tissue. E, Removal of connective tissue. F, Donor site
sutured. G, Connective tissue for graft. H, Free connective tissue placed at donor site. I, Postoperative healing at 10 days. J, Final healing at 3 months.
Note wide, keratinized, attached gingiva. (Courtesy Or. M. Orisini, Italy.)
the cells that can lead to tissue rejection and graft failure with- intention. The patient has less discomfort postoperatively at
out damaging the matrix. The remaining ADM consists of a the donor site (Fig. 50. 7).
nondenatured three-dimensional arrangement of intact colla- Another advantage of the free connective tissue autograft is
gen fibers, ground substance, and vascular channels. Random- that, improved esthetics can be achieved because of a better
ized, controlled clinical trials have demonstrated outcomes color match of the grafted tissue to the adjacent areas.
with ADM equivalent to palatal donor tissue in treatment of
gingival recession Apically Displaced Flap
This technique uses the apically positioned flap, either partial
Free Connective Tissue Autografts thickness or full thickness, to increase the zone of keratinized
The connective tissue autograft technique was originally de- gingiva. Chapter 45 provides a step-by-step description of the
scribed by Edel and is based on the fact that the connective surgical technique for apically displaced flaps, and illustrates
tissue carries the genetic message for the overlying epithelium the procedure (Fig. 50 8)
to become keratinized. Therefore only connective tissue from
beneath a keratinized zone can be used as a graft. Accomplishments. The apically displaced flap technique in-
The advantage of this technique is that the donor tissue is creases the width of the keratinized gingiva but cannot pre-
obtained from the undersurface of the palatal flap, which is dictably deepen the vestibule with attached gingiva. Adequate
sutured back in primary closure, therefore healing is by first vestibular depth must be present before the surgery to allow
the flap at the crest of the bone. New tissue covers the crest
of the bone to produce a firm, tapered gingival margin.
Placing the flap short of the crest increases the risk of a
slight reduction in bone height, but the advantage of a well-
formed gingival margin compensates for this.
Techniques to Treat Gingival

Recession
Gingival Augmentation Coronal
to Recession (Root Coverage)
Understanding the different stages and conditions of gingival
recession is necessary for predictable root coverage. Several
classifications of denuded roots have been proposed. In the
1960s, Sullivan and Atkins classified gingival recession into
four anatomic categories: (1) shallow-narrow, (2) shallow-
wide, (3) deep-narrow, and (4) deep-wide.
This early classification helped categorize the lesion but did
not enable the clinician to predict the outcome of therapy. The
predictability of root coverage can be enhanced by the presur-
gical examination and the correlation of the recession by using
the classification proposed by Miller, as follows (Fig. 50 9):
Class I. Marginal tissue recession does not extend to the mu-
cogingival junction. There is no loss of bone or soft tissue
in the interdental area. This type of recession can be narrow
or wide.
Class II. Marginal tissue recession extends to or beyond the
mucogingival junction. There is no loss of bone or soft tis-
sue in the interdental area. This type of recession can be
subclassified into wide and narrow.
Class III. Marginal tissue recession extends to or beyond the
mucogingival junction. There is bone and soft tissue loss
interdentally or malpositioning of the tooth.
Class IV Marginal tissue recession extends to or beyond the
mucogingival Junction. There is severe bone and soft tissue
loss interdentally or severe tooth malposition.
In general, the prognoses for Classes I and II are good to
FIGURE 50.8 Apically displaced partial-thickness flap. A, Internal excellent whereas, for Class III, only partial coverage can be
bevel incision (I) separates inner wall of periodontal pocket. MC, Muco- expected. Class IV has a very poor prognosis with current
gingival junction; V, vestibular fornix. B, Partial-thickness flap (F) sepa-
techniques.
rated, leaving periosteum and a layer of connective tissue on the bone.
The inner wall of the periodontal pocket (I) is removed, and the tooth is The following is a list of techniques used for root coverage.
scaled and planed. C, Partial-thickness flap (F) displaced apically, with
edge of the flap at crest of the bone. Note that the vestibular fornix is
1. free gingival autograft
also moved apically. D, Partial-thickness flap (F) displaced apically, with 2. pedicle graft (laterally or horizontally displaced flap)
edge of the flap several millimeters below crest of the bone. 3. coronally advanced flap; includes semilunar pedicle graft
(Tarnow)
4. subepithelial connective tissue graft (Langer)
apical positioning of the flap. The edge of the flap may be 5. guided tissue regeneration (GTR)
located in three positions in relation to the bone as follows: 6. pouch and tunnel technique (coronally advanced tunnel
technique)
1. Slightly coronal to the crest of the bone. This location attempts
7. other techniques
to preserve the attachment of supracrestal fibers. It may
also result in thick gingival margins and interdental papil- Some of the techniques used for widening the attached
lae with deep sulci and may create the risk of recurrent gingiva apical to the area of recession can also be used for
pockets. root coverage. Both the free gingival and the connective tissue
2. At the level of the crest. This results in a satisfactory gingival autograft used for apical widening can be used for coronal
contour, provided that the flap is adequately thinned. augmentation by incorporating some modifications. In using
3. Two millimeters short of the crest. This position produces the the free grafts for root coverage, the recipient bed surrounding
most desirable gingival contour and the same posttreat- the denuded root surface must be extended wider to allow for
ment level of gingival attachment as obtained by placing better blood supply to the donor free graft. This is necessary
II
Ill
Attached gingiva
- Mucosal tissue
FIGURE 50.10 Laterally displaced flap for coverage of denuded root.
Top, Incisions removing the gingival margin around the exposed root
and outlining the flap. Bottom, After the gingiva around the exposed root
IV is removed, the flap is separated, transferred, and sutured.
Step 5: Transfer the graft. Transfer the graft to the recipient site
and suture it to the periosteum with a gut suture. Good
stability of the graft must be attained with adequate sutures.
Step 6: Cover the graft. Cover the grafted site with dry alumi-
num foil and periodontal dressing.
Attached gingiva
Pedicle Autograft
~ Mucosal tissue Laterally (Horizontally) Displaced Pedicle Flap. The dis-
placed pedicle flap technique, originally described by Grupe
FIGURE 50.9 P.O. Millers classification of denuded roots.
and Warren in 1956, was the standard technique for many
years and is still indicated in some cases. The laterally po-
because a portion of the donor tissue overlies the root surface, sitioned flap can be used to cover isolated, denuded root
which does not have blood supply. surfaces that have adequate donor tissue laterally. Adequate
vestibular depth must also be present.
Free Gingival Autograft The following is a step-by-step surgical description:
Successful and predictable root coverage has been reported (Figs. 50.10 and 50.11)
using free gingival autografts.
Step 1: Prepare the recipient site. Epithelium is removed around
the denuded root surface. The exposed connective tissue
The Classic Technique. Miller applied the classic free gingi-
will be the recipient site for the laterally displaced flap. The
val autograft described previously with a few modifications.
root surface will be thoroughly scaled and root planed.
Step 1: Root planing. Root planing is performed with the ap- Step 2: Prepare the flap. The periodontium of the donor site
plication of saturated citric acid for 5 minutes on the root should have a satisfactory width of attached gingiva and
surface. The application of this acid has not been validated minimal loss of bone, without dehiscence or fenestration. A
by some studies, but numerous clinicians practice this tech- full-thickness or partial-thickness flap may be used, but the
nique. latter is preferable because it offers the advantage of rapid
Step 2: Prepare the recipient site. Make a horizontal incision in healing at the donor site and reduces the risk of loss of fa-
the interdental papillae at right angles to create a margin cial bone height. This is especially important if the bone is
against which the graft may have a butt joint with the inci- thin or a dehiscence or fenestration is suspected. However,
sion. Vertical incisions are made at the proximal line angles if the gingiva is thin, even a partial-thickness flap may not
of adjacent teeth and the retracted tissue is excised. Main- be sufficient for flap survival.
tain an intact periosteum in the apical area. With a No. 15 blade, make a vertical incision from the gin-
Steps 3 and 4. Refer to the step-by-step technique described for gival margin to outline a flap adjacent to the recipient site.
the classic gingival graft earlier in this chapter. This tech- Incise to the periosteum, and extend the incision into the
nique results in predictable coverage of the denuded root oral mucosa to the level of the base of the recipient site. The
surface but may present esthetic color discrepancies with flap should be sufficiently wider than the recipient site to
the adjacent gingiva because of a lighter color. cover the root and provide a broad margin for attachment
FIGURE 50.11 Laterally displaced flap. A, Preoperative view, maxillary bicuspid. B, Recipient site is prepared by exposing the connective tissue
around the recession. C, Incisions are made at the donor site in preparation of moving the tissue laterally. D, Pedicle flap is sutured in position. E, Post-
operative result at 1 year. (Courtesy Dr. E.B. Kenney, Los Angeles.)
to the connective tissue border around the root. The in- cover roots denuded by isolated gingival defects with a flap
terdental papilla at the distal end of the flap, or a maJor formed by Joining the contiguous halves of the adjacent inter-
portion of it, should be included to secure the flap in the dental papillae. Results with this technique are unpredictable
interproximal space between the donor and the recipient because blood supply is impaired by suturing the two flaps
teeth. over the root surface.
Make a vertical incision along the gingival margin and inter-
dental papilla, and separate a flap consisting of epithelium Accomplishments of Pedicle Autograft. Coverage of the ex-
and a thin layer of connective tissue, leaving the periosteum posed root surface with the sliding-flap technique has been
on the bone. reported to be 60, 61, and 72%. Histologic studies in animals
A releasing incision is sometimes needed to avoid tension have reported 50% coverage.
on the base of the flap, which can impair the blood supply The extent to which the flap establishes a new attach-
when the flap is moved. To do this, make a short oblique ment to the root with the formation of new cementum and
incision into the alveolar mucosa at the distal corner of the the embedding of new connective tissue fibers has not been
flap, in the direction of the recipient site. established. New attachment on artificially denuded roots in
Step 3: Transfer the flap. Slide the flap laterally onto the ad- experimental animals and in some clinical studies of humans
jacent root; making sure that it lies flat and firm without has been reported, but it does not occur consistently enough
excess tension on the base. Fix the flap to the adjacent gin- to be predictable.
giva and alveolar mucosa with interrupted sutures .A sus- In the donor site, there is uneventful repair and restoration
pensory suture may be made around the involved tooth to of gingival health and contours, with some loss of radicular
prevent the flap from slipping apically. bone (0.5 mm) and recession (1.5 mm) reported with full-
Step 4: Protect the flap and donor site. Cover the operative field thickness flaps.
with aluminum foil and a soft periodontal dressing, extend-
ing it interdentally and onto the lingual surface to secure it. Coronally Advanced Flap. The purpose of the coronally dis-
Remove the dressing and sutures after 1 week. placed flap procedure is to create a split-thickness flap in the
area apical to the denuded root and position it coronally to
Variant Techniques. There are many variations in the inci- cover the root. Two techniques are available for this purpose.
sions for the laterally displaced flap. A common alternative
is the use of converging oblique incisions over the recipient Classic Technique (Fig. 50.12)
site and a vertical or oblique incision at the distal end of the Step 1. With two vertical incisions, delineate the flap. These
donor site so that the transposed flap is slightly wider at its incisions should go beyond the mucogingival junction.
base. In another modification, the marginal attachment at the Make a crevicular incision from the gingival margin to the
donor site is preserved to reduce the likelihood of recession bottom of the sulcus. Elevate a mucoperiosteal flap using
and marginal bone resorption, but this requires a donor site careful sharp dissection.
with a wider zone of attached gingiva. Step 2. Scale and plane the root surface.
Sliding partial-thickness grafts from neighboring eden- Step 3. Return the flap and suture it at a level coronal to the
tulous areas (pedicle grafts) can be used to restore attached pretreatment position. Cover the area with a periodontal
gingiva on teeth adjacent to edentulous spaces with denuded dressing, which is removed along with the sutures after
roots and a small, vestibular fornix, often complicated by ten- 1 week. The periodontal dressing is replaced for an addi-
sion from a frenum. The "double-papilla flap" attempts to tional week if it is necessary.
FIGURE 50.12 Coronally displaced flap. A, Preoperative view. Note the recession and the lack of attached gingiva. B, After placement of a free
gingival graft. C, Three months after placement of the graft. D, Flap, including the graft, positioned coronally and sutured. E, Six months later. Note the
root coverage and the presence of attached gingiva. Compare with A. (Courtesy Dr T./. Han, Los Angeles.)
FIGURE 50.13 Semilunar coronally positioned flap. A, Class 1 recession on the facial surface of the maxillary right central incisor. B, A semi lunar
incision is made and tissue separated from the underlying bone. C, Crevicular incision. D, The flap collapses covering the incision, no sutures given.
E, Appearance after 7 weeks showing complete root coverage. (Courtesy Dr/./. Elbaz, Beverly Hills, California.)
Variations to Classic Technique A significant degree of reduction in recession treated by

Results with the coronally displaced flap technique are often this double-step procedure was reported after 2 years by Ber-
unfavorable because of insufficient keratinized gingiva apical nimoulin et al and confirmed by others.
to the recession. To overcome this problem and to increase the Semilunar Flap Technique
chances of success, a gingival augmentation procedure with a
Tarnow has described the semilunar coronally repositioned
free autogenous graft can be performed before the coronally
flap to cover isolated denuded root surfaces (Fig. 50.13).
positioned flap, as described earlier in this chapter. This cre-
ates several millimeters of attached keratinized gingiva apical Step 1. A semilunar incision is made following the curvature
to the denuded root. of the receded gingival margin and ending about 2-3 mm
Two months after this surgery, a second-stage procedure short of the tip of the papillae. This location is very im-
is performed, coronally positioning the flap that includes the portant because the flap derives its blood supply from the
free autogenous graft. The use of citric acid or tetracycline for papillary areas. The incision may need to reach the alveolar
conditioning the root surface has been suggested. mucosa if the attached gingiva is narrow.
Step 2. Perform a split-thickness dissection coronally from the gingival thickness to allow a split-thickness flap to be elevated.
incision and connect it to an intrasulcular incision. Adjacent to the denuded root surface, the donor connective
Step 3. The tissue will collapse coronally, covering the de- tissue is sandwiched between the split flap. This technique
nuded root. It is then held in its new position for a few was described by Langer and Langer in 1985. Similar ap-
minutes with moist gauze. Many cases do not require either proaches had been previously reported by Perez-Fernandez
sutures or periodontal dressing. This technique is simple and Raetzke.
and predictably provides 2-3 mm of root coverage. It can The following is the step-by-step surgical description
be performed on several adjoining teeth. This technique is (Figs. 50.14 and 5015):
indicated where the recession is not extensive (3 mm) and
Step 1. Raise a partial-thickness flap with a horizontal incision
the facial gingival biotype is thick. It is successful for the
2 mm away from the tip of the papilla and two vertical inci-
maxilla, particularly in covering roots left exposed by the
sions 1-2 mm away from the gingival margin of the adjoin-
gingival margin receding from a recently placed crown mar-
ing teeth. These incisions should extend at least one tooth
gin. It is not recommended for the mandibular dentition.
wider mesiodistally than the area of gingival recession. Ex-
Subepithelial Connective Tissue Graft (Langer tend the flap to the mucobuccal fold.
and Langer) Step 2. Thoroughly plane the root, reducing its convexity.
Step 3. Obtain a connective tissue graft from the palate by
The subepithelial connective tissue procedure is indicated for
means of a horizontal incision 5-6 mm from the gingival
larger and multiple defects with good vestibular depth and
FIGURE 50.14 Subepithelial connective tissue graft for root coverage. A, Preoperative view: recession on mandibular 1st premolar, B, Graft site
prepared, C, Graft placed on the recipient site. D, Flap replaced and covered over the graft. E, Postoperative view showing complete root coverage.
Mucogingival junction Incision
Gingival line
(F)
FIGURE 50.14 (cont.) F-J, Schematic representation of Sub-epithelial connective tissue graft technique.
margin of molars and premolars. The palatal wound is su- root surface and covers at least 2 mm of marginal perios-
tured in a primary closure. teum.
Step 4. Place the connective tissue on the denuded root(s). Step 3. A suture is passed through the portion of the mem-
Suture it with resorbable sutures to the periosteum. brane that will cover the bone. This suture is knotted on the
Step 5. Cover the graft with the outer portion of the partial- exterior and tied to bend the membrane, creating a space
thickness flap and suture it interdentally. between the root and the membrane. This space allows for
Step 6. Cover the area with dry foil and surgical dressing. After the growth of tissue beneath the membrane.
7 days, the dressing and sutures are removed. The esthetic re- Step 4. The flap is then positioned coronally and sutured.
sults are favorable with this technique since the donor tissue is Four weeks later, a small envelope flap is performed, and
connective tissue. The donor site heals by primary intention, the membrane is carefully removed. The flap is then again
with considerably less discomfort than after a free gingival graft. positioned coronally, to protect the growing tissue, and su-
tured. One week later these sutures are removed.
Other techniques have been described to harvest subepi-
thelial connective tissue from the palate. Tinti and Vincenzi used titanium-reinforced membranes to
A variant of the subepithelial connective tissue graft, called create space beneath the membrane. Resorbable membranes
a subpedicle (bilaminar) connective tissue graft, was described by have also been used to achieve root coverage. The inability
Nelson in 198 7. This technique uses a pedicle over the con- to create space between the resorbable membrane and the
nective tissue that covers the denuded root surface. Therefore, denuded root because of its softness may present a problem,
the blood supply is increased over the donor tissue and the even though not needing a second surgery is an advantage.
gingival margin is thickened for better marginal stability. Clinical studies comparing this technique with the coronal-
ly displaced flap have shown that the GTR technique is better
Guided Tissue Regeneration Technique for Root when the recession is greater than 4. 98 mm apicocoronally.
Coverage Histologically, one case reported 3.66 mm of new connective
Pini Prato et al described a technique based on the principle tissue attachment associated with 2.48 mm of new cementum
of GTR (Chapter 48) Theoretically, GTR should result in the and 1.84 mm of bone growth.
reconstruction of the attachment apparatus, along with cover-
age of the denuded root surface. Pouch and Tunnel Technique (Coronally Advanced
The following is a step-by-step description of the surgery Tunnel Technique)
(Fig. 50 16):
To minimize incisions and the reflection of flaps and to provide
Step 1. A full-thickness flap is reflected to the mucogingival abundant blood supply to the donor tissue, the placement of
junction, continuing as a partial-thickness flap 8 mm apical the subepithelial donor connective tissue into pouches beneath
to the mucogingival junction. papillary tunnels allows for intimate contact of donor tissue to
Step 2. A membrane is placed over the denuded root surface the recipient site (Fig. 50.17) The positioning of the graft in
and the adjacent tissue. It is trimmed and adapted to the the pouch and through the tunnel and the coronal placement of
FIGURE 50.15 Langer technique for root coverage. A, Preoperative view. Note the recession on teeth #6 to #8. B, Split-thickness flap elevated on
teeth #6 and 117. Note that the interdental papillae are neither included in the flap, nor is the gingival margin area of tooth 118, which was treated by
means of a coronally displaced flap. C, Connective tissue from palate. D, graft placed under the flap and covering receded areas approximately to the
cementoenamel junction. Sutures in place. E, Roots covered after complete healing. Note the thickness of the tissue in the area covered and excellent
color. (Courtesy Dr T.J. Han, Los Angeles.)
the recessed gingival margins completely covers the donor tis- Step 1. Preparation of the patient includes plaque control in-
sue. Therefore the esthetic result is excellent. The technique is struction and careful scaling and root planing several weeks
especially effective for the anterior maxillary area in which ves- before the surgical procedure. The patient is instructed to
tibular depth is adequate and there is good gingival thickness. rinse for 3.0 s with chlorhexidine gluconate solution 0.12%.
One of the advantages to this technique is the thicken- Step 2. After adequate anesthesia of the region, the surgical
ing of the gingival margin after healing. The thicker gingival procedure, as follows, is performed.
margin is stable to allow for the possibility of "creeping reat- Step 3. Composite material stops are placed at the contact
tachment" of the margin. The use of small, contoured blades points (temporary) to prevent the collapse of the suspended
enables the surgeon to incise and split the gingival tissues to sutures into the interproximal spaces before the surgery
create the recipient pouches and tunnels. The work by Azzi Step 4. Root planing of the exposed root surfaces is performed
et al in this area of surgery has contributed to a better un- using Gracey curettes.
derstanding of the technique and outcome of this procedure. Step 5. Initial sulcular incisions are made using 15c and 12d
This surgery is also referred to as the coronally advanced tunnel blades. Small, contoured blades (Fig. 50.17) and mini cu-
technique. rettes are used to create the recipient pouches and tunnels.
Following is a step-by-step description of the surgical pro- Step 6. On the buccal aspect, an intrasulcular incision is made
cedure as outlined by Azzi: around the necks of the teeth. The incision is extended to
FIGURE 50.16 Guided tissue regeneration technique for root coverage. A, Marked recession of maxillary left cuspid. B, Vertical incisions made
and membrane placed over recession. C, Flap sutured over the membrane. D, Postoperative result. Note complete coverage of recession. (Courtesy
Dr Zoran Aleksic, Belgrade, Serbia.)
one adjacent tooth both mesially and distally using a 15c pushed into the pouch and tunnel using tissue forceps and
blade. This incision maintains the full height and thickness a packing instrument. The graft is pushed from the adjacent
of the gingival component and enables access beneath the tooth on one side of the surgical area to the adjacent tooth
buccal gingiva with Gracey curettes. The cutting edge is on the other side.
directed toward the bone to dissect the connective tissue Step 13. A mattress suture placed on one end of the graft will
beyond the mucogingival line and free the buccal flap from help maintain the graft in position while the buccal tissue
its insertions to the bone around each tooth. covers the connective tissue graft. This connective tissue
Step 7. Muscle fibers and any remaining collagen fibers on the graft is anchored to the inner aspect of the buccal flap in the
inner aspect of the flap, which prevent the buccal gingiva interdental papilla area. A vertical mattress suture is used
from being moved coronally, are cut using Gracey curettes. to hold the connective tissue in position beneath the gin-
Step 8. The papillae are kept intact and undermined to main- giva. The connective tissue graft is completely submerged
tain their integrity and carefully released from the underly- beneath the buccal flap and the papillae.
ing bone, which allows the coronal positioning of the pa- Step 14. The entire gingivopapillary complex (buccal gingiva
pillae. with the underlying connective tissue graft and papillae)
Step 9. An envelope, full-thickness pouch and tunnel are cre- is coronally positioned using a horizontal mattress suture
ated and extended apically beyond the mucogingival line by anchored at the incisal edge of the contact area. The contact
blunt dissection for the insertion of the free connective tis- areas are splinted presurgically using a composite material.
sue graft through the intrasulcular incision. Saline-moistened Step 15. Other holding sutures may be placed through the
gauze is placed over the recipient site. overlying gingival tissue and donor tissue to the underlying
Step 10. The size of the pouch, which includes the area of periosteum to secure and stabilize the donor tissue and the
the denuded root surface, is measured so that an equiva- overlying gingiva in a coronal position.
lent size donor connective tissue can be procured from the
The area is not covered with periodontal dressing.
tuberosity
The patient is instructed to rinse daily with chlorhexidine
Step 11. A second surgical site is created to obtain a connec-
gluconate and to avoid touching the sutures during oral hy-
tive tissue graft of adequate size and shape to be placed at
giene procedures.
the recipient site. The connective tissue harvested from the
Antibiotics can be administered (Amoxicillin 500 mg 3
tuberosity area is contoured to fit into the recipient tunnel
times a day), if deemed necessary
and pouch.
Step 12. A mattress suture placed at one end of the graft is Other Techniques. In the last few years, a number of new
helpful in guiding the graft through the sulcus and beneath techniques have developed particularly for multiple root cov-
each interdental papilla. The border of the tissue is gently erage. Some of them have been enumerated later. The reader
FIGURE 50.17 Pouch and tunnel technique for root coverage. A, Preoperative view. Note gingival recession. B, Sulcular incision is made from the
mesial to the facial line angles. C, A tunnel is made through the papilla using a blunt incision. D, A connective tissue graft is taken from the palate.
E, The connective tissue is placed through the papillary tunnel and apically beneath the pouch. F, The facial gingival margin covers the connective
tissue using horizontal mattress sutures interdentally. G, Postoperative view. Note complete root coverage and thickened gingival margin at 3 months.
(Courtesy Dr Robert R. Azzi, Paris.)
is encouraged to go through the relevant literature from vari- tissue. If there is a lack of periosteal connective tissue, the do-
ous standard international journals for detailed information. nor tissue may be placed over bone. The donor tissue may be
either free gingival or connective tissue, but it must be placed
• vestibular incision subperiosteal tunnel access (VISTA)
over a nonmobile recipient site.
• the Pinhole approach
• Zuchellis technique
• use of a cellular dermal matrix (Fig. 50 .18).
• <lento gingival transfer Techniques to Remove the Frenum
• periosteal transfer A frenum is a fold of mucous membrane, usually with en-
closed muscle fibers, that attaches the lips and cheeks to the
Techniques to Deepen the Vestibule alveolar mucosa and/or gingiva and underlying periosteum.
A frenum becomes a problem if the attachment is too close to
The presence of adequate vestibular depth is important for the marginal gingiva. This anatomic situation may be a genetic
both oral hygiene and retention of prosthetic appliances. Nu- condition of the individual or the result of recession of the
merous surgical techniques have been proposed to accomplish gingival margin reaching the area of the frenum. Tension on
the objective of deepening the vestibule. The classic clinical the frenum may pull the gingival margin away from the tooth.
studies in the early 1960s by Bohannan indicated that deep- This condition may be conducive to plaque accumulation and
ening of the vestibule not involving use of a free gingival graft inhibit proper placement of the toothbrush at the gingival
were not successful when evaluated years later. Predictable margin. These hygiene problems are most often encountered
deepening of the vestibule can only be accomplished by the in the mandibular anterior areas. The maxillary anterior vesti-
use of free autogenous graft techniques and their variants, as bule is deep and the frenum is usually located in the midline
covered in this chapter. The important clinical aspect in deep- between the two central incisors. The aberrant frenum located
ening the vestibule is the proper preparation of the recipient between the maxillary central incisors may present an esthetic
site. The recipient site must be covered by immobile periosteal problem in a patient with a high lip line.
FIGURE 50.18 A, Preoperative view showing multiple gingival recessions. B, Incisions placed. C, Recipient site preparation. D, AlloDerm placed.
E, Postoperative view showing root coverage.
Frenectomy and Frenotomy premolar areas. They occur less often on the lingual surface
of the mandible.
Frenectomy and frenotomy refer to surgical procedures that
differ in degree. Frenectomy is complete removal of the fre- Procedure
num, including its attachment to underlying bone and may be
required in the correction of an abnormal diastema between If the vestibule is deep, the procedure is confined to the fre-
the maxillary central incisors. Frenotomy is the relocation of num. It is often necessary to deepen the vestibule to provide
the frenum, usually in a more apical position. space for the repositioned frenum. This is accomplished as
Frenectomy and frenotomy can be performed in conjunc- follows (Fig. 50.19):
tion with other periodontal treatment procedures, such as Step 1. After anesthetizing the area, engage the frenum with a
during a free gingival graft procedure to deepen the vestibule hemostat inserted to the depth of the vestibule.
in the mandibular anterior area, but most often they are ac- Step 2. Incise along the upper surface of the hemostat, extend-
complished as a separate surgical procedure. Frenal problems ing beyond the tip.
occur most often on the facial surface between the maxil- Step 3. Make a similar incision along the undersurface of the
lary and mandibular central incisors and in the canine and hemostat.
FIGURE 50.19 Removal of the frenum. A, Preoperative view of frenum between the two maxillary central incisors. B, Removal of the frenum from
both the lip and gingiva. C, Site is sutured after it is placed over the wound. D, Postoperative view at 2 weeks. (Courtesy Dr J./. Elbaz, Beverly Hills,
California.)
Step 4. Remove the triangular resected portion of the frenum 3. therapy to correct excessive gingival display
with the hemostat. This exposes the underlying fibrous at- 4. procedure to correct gingival asymmetry
tachment to the bone. 5. gingival depigmentation
Step 5. Make a horizontal incision, separating the fibers and
bluntly dissect to the bone.
Step 6. If necessary, extend the incisions laterally and suture Root Coverage (Gingival Augmentation
the labial mucosa to the apical periosteum. A gingival graft Coronal to the Recession)
or connective tissue graft is placed over the wound.
Step 7. Clean the surgical field with gauze sponges until bleed- The surgical correction of root coverage is discussed in detail
ing stops. in the section on gingival augmentation coronal to the reces-
Step 8. Cover the area with dry aluminum foil and apply the sion.
periodontal dressing.
Step 9. Remove the dressing after 2 weeks and redress if neces- Papilla Reconstruction
sary. One month is usually required for the formation of an
intact mucosa with the frenum attached in its new position. As previously indicated in this chapter, the loss of the inter-
dental papilla is a major esthetic problem for many patients. It
is often referred to as the "black triangle or hole" (Fig. 50.20).
Techniques to Improve Esthetics The reconstruction of the lost or reduced interdental papilla
is the most difficult and unpredictable problem in esthetic
The maxillary anterior area in a patient with a high lip line
periodontal therapy. The interdental papilla is gingival tissue
presents a visible area in which patients are concerned with
supported and created by two adjacent teeth in contact and
the esthetic appearance of the gingival tissues. This area is ad-
the underlying bone beneath this tissue. The loss of this bone
dressed as the "esthetic zone," which requires special consid-
as the result of periodontal disease or the loss of the contact
eration in restorative, periodontal and implant therapy. The
alters the support of the interdental tissue, which can lead to
symmetry of the facial gingival margin from canine to canine
the loss or the reduced height of the papilla. Tarnow in his
is altered with the recession of the gingival margin, the loss
study of this area stated the distance from the crest of the in-
of the interdental papilla or if there is excessive amount of
terdental bone to the apical portion of the contact above this
gingival tissue creating a "gummy smile." The therapy to cor-
bone determines whether the interdental papilla is absent or
rect these gingival conditions is discussed under the following
present (Fig. 50.21). Therefore, the predictable reconstruction
topics:
of the papilla is determined not only by the augmentation of
1. root coverage the gingival tissue but also by the presence or absence of the
2. papilla reconstruction underlying bone and the contact of the two adjacent teeth.
incorporates several of the concepts indicated earlier for pa-

pilla reconstruction. These concepts are (1) semilunar pedicle
design, (2) both connective tissue (Fig. 50.22) and bone graft-
ing into the interdental area, and (3) the use of restorative
dentistry to place the apical portion of the contact closer to
the crestal bone.
The future of papilla reconstruction will involve tech-
niques developed by tissue engineering using biologic media-
tors. In a study reported by McGuire and Scheyer, autologous
fibroblasts were injected into the interdental papilla to atrau-
matically augment the deficient interdental papilla. Further
discussion of this topic is presented in Section "Soft Tissue
Regeneration." The exciting field of tissue engineering will
FIG U RE 50.20 The loss of the interdental papilla and the esthetic allow the clinician to use minimally invasive procedures to
problem . The black triangle or hole. reconstruct the lost papilla.
Therapy to Correct Excessive Gingival

Display
Excessive gingival display, commonly called a "gummy smile,"
represents an esthetic concern for many patients. This ap-
Crest of bone pearance may be caused by a skeletal problem called vertical
maxillary excess, by dentoalveolar extrusion, or by incomplete
exposure of the anatomic crown, often referred to as altered
passive eruption. It may be associated with a short upper lip
or excessive lip translation. There may be a combination of
Apical portion causative factors requiring more than one treatment option.
of contact Even in patients with excessive gingival display, the pri-
mary esthetic feature is the appearance of the teeth. If the
cause of the "gummy" appearance is incomplete exposure of
the anatomic crown, the teeth will appear short and unattract-
FIGURE 50.21 The distance from the crest of the interdental bone ive. This appearance is often noticed in adolescent patients
to the apical portion of the contact, which determines the absence or during orthodontic treatment. It has been found that if there
presence of the papilla as indicated by Tarnow et al.
is a need for esthetic crown lengthening before orthodontic
therapy, there will still be a need after orthodontic therapy
Orthodontics and restorative therapy also play an important and likely still a need 5 years later. Although patients may
role in the loss and reconstruction of the papilla since they can complain of the gummy exposure, the real esthetic issue is the
determine the location of the contact position in the dentition. altered tooth form. Surgical crown lengthening addresses both
We have also learned from experience that grafting bone or concerns, but its focus should be the exposure of a properly
gingiva of minimal size to a small recipient site is unpredict- proportioned tooth.
able because of the lack of blood supply from the recipient Ideally, the width/length ratio of a maxillary central inci-
site to the donor tissue. Therefore bone grafting or free gin- sor clinical crown should fall between 0. 78 and 0.85. Thus a
gival grafting of interdental areas to reconstruct the papilla is central incisor with a width of 8.5 mm should have a length
not a predictable procedure. There have been numerous case between 10 and 11 mm. The length of the maxillary canine is
reports of different techniques to augment gingival tissue into equal to or slightly less than the central incisor and its gingi-
the interdental area. All of these techniques must be based on val margin should be aligned with the central incisor gingival
the principle of adequate blood supply to the donor tissue. margin. The gingival margin of the lateral incisor is usually
Of the many gingival grafting procedures used in periodontal about 1.0 mm coronal to the margins of the adjacent teeth,
therapy, the technique that offers the best blood supply to the although in patients with a high lip line, it is generally more
donor tissue is the pedicle graft because it maintains a con- pleasing to have the lateral incisor gingival margin equal to the
nection between the donor tissue and the origin of the graft. central incisors and canines.
The pouch and tunnel surgical procedure also creates the ideal
blood supply for the recipient site to accept the donor tissue. Surgical Techniques
Han et al reported a technique using a semilunar pedicle graft Exposure of the full anatomic crown is necessary to achieve a
and pouch to gain papillary height, but without bone support smile with minimal gingival exposure. Measurements before
this technique was able to only reduce the interdental space. surgery should include clinical crown width and length, ana-
Azzi et al have also reported successful results with numerous tomic crown length and height of keratinized tissue.
cases using different surgical techniques to regain the lost pa- Surgical crown lengthening may be accomplished by soft
pilla. All of these cases employ different grafting techniques, tissue excision alone or by flap surgery with or without osse-
using not only connective tissue and bone but also a surgical ous surgery The determinates for choice of surgical procedure
flap design applying the principle of the pouch and tunnel are (1) the need to leave a minimum of 3.0 mm of keratinized
to maximize the blood supply to the grafted tissue. The case marginal tissue and (2) the possible need for osseous surgery
If excision of soft tissue for full anatomic crown exposure Gingival Depigmentation. Gingival pigmentation is depen-
would leave at least 3.0 mm ofkeratinized marginal tissue and dent on many factors including racial background. The ac-
there is no need for osseous surgery, soft tissue excision alone tivity of the melanocytes which are nonkertinocytes present
is the treatment of choice. If less than 3.0 mm of keratinized in the gingival epithelium varies among individuals. Physi-
marginal tissue would remain after the necessary excision, an ological gingival hyperpigmentation can be treated albeit the
apically positioned flap would be required. fact that the results last for anywhere from 6 to 36 months
Figure 50.23 demonstrates a clinical case of esthetic crown (Fig. 50.25).
lengthening to correct the "gummy appearance" in the maxil- Gingival depigmentation involves the removal of the su-
lary esthetic zone. perficial epithelium by one of the following methods.
Procedure to Correct Gingival Asymmetry. The clinician 1. mucosal excision/stripping by a BP blade
should have the precise idea of the normal contour, zenith, 2. rotary instruments
and curvature of the gingiva of the teeth in the esthetic zone. 3. electrosurgery
The gingiva can be reshaped either by Gingivoplasty or mini- 4. cryosurgery
mally invasive flap surgery (Fig. 50.24). 5. lasers
FIGURE 50.22 A, Preoperative view. Note the loss of the interdental papilla and the extensive recession of the facial marginal gingiva. B, lntrasulcular
incision is made around the neck of the right lateral incisor and central incisors. A horizontal incision starting at the mucogingival junction, extending
into the alveolar mucosa and apically up to the labial fold is performed to elevate a split-thickness flap. C, Mucogingival flap is elevated coronally
and secured with a horizontal mattress suture anchored to the interdental contact point of the central incisors, exposing the interdental bone. D, Con-
nective tissue removed from the tuberosity to be placed over the bone graft in the interdental area. E, Bone graft removed from the tuberosity, which
will be grafted in the interdental area. F, Diagram of the bone fixed to the alveolar crest using a titanium screw. a, Saddle-shaped graft fits over the
interdental bone crest. b, Internal view of the osseous graft. c, Profile view of the osseous graft. G, Diagram of the flap returned and sutured over the
grafted materials to obtain complete closure.
FIGURE 50.22 (cont.) H, Crushed cancellous bone is packed around the grafted bone in the shape of the reconstructed interdental bone. I, Ara-
diograph indicating the titanium screw that is used to hold the grafted bone in place. J, Coronal positioning of the entire gingivopapillary unit by the
use of a horizontal mattress suture anchored over the splinted incisal portion of the contact. The rnucosal portion of the flap is approximated to the
gingivopapillary edge of the flap and sutured using 4.0 sutures. K, Three-month postoperative healing. Normal anatomy and shape with complete root
coverage on the right lateral incisor, partial root coverage on the central incisors, and reconstruction of the interdental papilla. L, Preoperative view.
Compare with the reconstructed papilla. M, One-year postoperative view with two porcelain veneers bonded on the central incisors. The contact is
placed apically to help reduce the interdental space. (Courtesy Dr R. Azzi, Paris.)
Maximum care should be taken not to completely remove Criteria for selection of mucogingival techniques are as fol-
the gingiva and exposing the root and/or bone. This can hap- lows:
pen particularly when the gingival biotype is thin.
1. Surgical site free of plaque, calculus, and inflammation.
The results obtained by cryosurgery and lasers appear to
2. Adequate blood supply to the donor tissue.
sustain for a longer time than surgery by scalpel blade. Rotary
3. Anatomy of the recipient and donor sites.
instruments produce the least satisfactory outcome whereas
4. Stability of the grafted tissue to the recipient site.
electrosurgery is not indicated because of its inability to con-
5. Minimal trauma to the surgical site.
trol the extent of tissue destruction.
It should be clearly understood that mentioned procedures
are for only physiological hyperpigmented gingiva and not for Surgical Site Free of Plaque, Calculus,
pathologically discolored gums. and Inflammation
Periodontal plastic surgical procedures should be undertaken
Criteria for Selection of Techniques in a plaque-free and inflammation-free environment to enable
Different techniques are presented for solving mucogingi- the clinician to manage gingival tissue that is firm. Meticulous,
val problems outlined in this chapter. The proper selection precise incisions and flap reflection cannot be achieved when
of the numerous techniques must be based on the predict- the tissue is inflamed and edematous. Thorough scaling and
ability of success, which in turn is based on the criteria de- root planing, as well as meticulous plaque removal by the pa-
scribed next. tient, must be accomplished before any surgical procedure.
FIGURE 50.23 A, Pretreatment view showing short clinical crowns. B, Excess tissue removed by a diode laser. C, Gingiva recontoured. D, Postopera-
tive view showing improved gingival form.
Adequate Blood Supply depth and widen the zone of attached gingiva. Other tech-
niques require vestibular depth to be present before the
To obtain the maximum amount of blood supply to the donor surgery, including pedicle grafts (lateral and coronal), subepi-
tissue, gingival augmentation apical to the area of recession thelial connective tissue graft (Langer), and pouch and tunnel
provides a better blood supply than coronal augmentation, procedures.
since the recipient site is entirely periosteal tissue. Root cover- The availability of donor tissue is another anatomic factor
age procedures present a portion of the recipient site (denud- that must be considered. Pedicle displacement of tissue neces-
ed root surface) without blood supply. Therefore, if esthetics sitates the presence of an adjacent donor site that presents
is not a factor, gingival augmentation apical to the recession gingival thickness and width. Palatal tissue thickness is also
may be more predictable. A pedicle-displaced flap has a better necessary for the connective tissue donor autograft. Gingival
blood supply than a free graft, with the base of the flap intact. thickness is required at the recipient site for techniques us-
In root coverage, therefore, if the anatomy is favorable, the ing split-thickness, sandwich-type flap or the pouch and tun-
pedicle flap or any of its variants may be the best procedure. nel techniques. In fact, inferior results are obtained when the
The subepithelial connective tissue graft (Langer and periodontal biotype is thin.
Langer) and the pouch and tunnel techniques use a split flap
with the connective tissue sandwiched between the flaps. This
flap design maximizes the blood supply to the donor tissue. If Stability of the Grafted Tissue
large areas require root coverage, these sandwich-type recipi- to the Recipient Site
ent sites provide the best flap design for blood supply.
Good communication of the blood vessels from the grafted
donor tissue to the recipient site requires a stable environ-
Anatomy of the Recipient and Donor Sites ment. This necessitates sutures that stabilize the donor tissue
The presence or absence of vestibular depth is an important firmly against the recipient site. The least amount of sutures
anatomic criterion at the recipient site for gingival augmenta- and maximum stability should be achieved.
tion. If gingival augmentation is indicated apical to the area of
recession, there must be adequate vestibular depth apical to
Minimal Trauma to the Surgical Site
the recessed gingival margin to provide space for either a free
or a pedicle graft. If a vestibule is necessary, only a free graft As with all surgical procedures, periodontal plastic surgery is
can accomplish this objective apical to the recession. based on the meticulous, delicate, and precise management
Mucogingival techniques, such as free gingival grafts and of the oral tissues. Unnecessary tissue trauma caused by poor
free connective tissue grafts, can be used to create vestibular incisions, flap perforations, tears or traumatic, and excessive
FIGURE 50.24 A, Pretreatment view showing gingival asymmetry and hyper pigmentation. B, Superficial epithelium excised for de-pigmentation
C, Gingiva recontoured. D, Postoperative view showing pleasing gingival appearance.
FIGURE 50.25 A, Hyperpigmented gingiva. B, Following gingival depigmentation with cryosurgery.
placement of sutures can lead to tissue necrosis. The selec- Conclusions

tion of proper instruments, needles, and sutures is mandatory
to minimize tissue trauma; sharp contoured blades, smaller- As defined in this chapter, periodontal plastic surgery refers
diameter needles, and resorbable monofilament sutures all are to soft-tissue relationships and manipulations. In all of these
important factors in achieving atraumatic surgery. procedures, blood supply is the most significant concern and
must be the underlying issue for all decisions regarding the
Smoking individual surgical procedure. A major complicating factor is
the avascular root surface and many modifications to exist-
Periodontal plastic surgical procedures in smokers produce
ing techniques are used to overcome this. Diffusion of fluids
inferior results.
is short term and of limited benefit as tissue size increases.
Thus the formation of a circulation through anastomosis and
Microsurgery angiogenesis is crucial to the survival of these therapeutic pro-
Enhanced vision by either surgical loupes or microscope gives cedures. The formation of vascularity is based on growth mol-
distinctively superior results (see Chapter 51). ecules, such as vascular endothelial growth factor (VEGF) and
cellular migration, proliferation, and differentiation. As tissue- Azzi R, Takei H, Etienne D, et al: Root coverage and papilla reconstruction
engineering techniques improve, the success and predict- using autogenous osseous and connective tissue grafts, Int] Peria Rest Dent
2141-147, 2001.
ability of mucogingival surgery should dramatically increase. Becker BE, Becker W: Use of connective tissue autografts for treatment of
Undoubtedly, all advancements will have adequate circulation mucogingival problems, Int] Periodont Restor Dent 6:89, 1986.
and blood supply as their basis. Carranza FA Jr, Carraro JJ: Mucogingival techniques in periodontal surgery,
New techniques are constantly being developed and are J Paiodontol 41:294, 1970.
Cortellini P, Clauser C, Pini-Prato GP: Histologic assessment of new attach-
slowly being incorporated into periodontal practice. The ment following the treatment of a human buccal recession by means of a
practitioner should be aware that, at times, new methods guided tissue regeneration procedure,] Periodontol 64:387, 1993.
are published without adequate clinical research to ensure Hawley CE, Staffileno H: Clinical evaluation of free gingival grafts in peri-
the predictability of the results and the extent to which the odontal surgery,] Periodontol 41:105, 1970.
techniques may benefit the patient. Critical analysis of newly Langer B, Langer L: Subepithelial connective tissue graft technique for root
coverage,] Periodontal 56:715, 1985.
presented techniques should guide our constant evolution to- McGuire MK, Nunn ME: Evaluation of human recession defects treated with
ward better clinical methods. coronally advanced flaps and either enamel matrix derivative or connective
tissue. I. Comparison of clinical parameters, J Periodontal 74:1110-1125,
2003.
McGuire MK, Scheyer ET, Schupbach P: Growth factor-mediated treatment
SUGGESTED READINGS of recession defects: a randomized controlled trial and histologic and mi-
American Academy of Periodontology: American Academy of Periodontology: crocomputed tomography examination,] Periodontol 80:550-564, 2009.
glossary of periodontal terms, ed 3, Chicago, 1992, American Academy of Miller PD Jr: A classification of marginal tissue recession, Int] Periodont Restor
Periodontology. Dent 5:9, 1985.
51
Advances in Periodontal
Surgical Procedures
(Microsurgery and Laser)
DA Shanelec • LS Tibbetts • A McGregor • JD Cross • RT Kao
• B Butler • CD Dwarakanath
Chapter Outline
MICROSURGERY LASERS
Philosophy of Periodontal Laser Application in Periodontics
Microsurgery Physics of Lasers and Their Biological
Advantages of Microsurgery Interactions
Magnification Systems Advantages and Disadvantages of Laser
Microsurgical Sutures Therapy
Esthetic Periodontal Microsurgery Laser Use in Periodontal Procedures
Microsurgical Knots Lasers in the Surgical Management of
Conclusions Periodontitis
Conclusions
Many new technologies are being evolved to assist the clini- Philosophy of Periodontal
cian and to enhance the outcome of periodontal therapy. Mi-
crosurgery, lasers, and peizosurgeries have been increasingly Microsurgery
employed in periodontics. This chapter deals with the vari- Microsurgery is a philosophy that embraces three core values.
ous applications of microsurgeries and lasers in periodontal The first is enhanced motor skill for better surgical perfor-
therapy. By strict definition Microsurgery is defined as a sur- mance. This is accomplished through improved visual acuity
gery performed under magnification of lOx or more using a and the use of a precise hand grip to increase accuracy and
surgical microscope. However periodontal microsurgery in- reduce tremor. The second is minimal tissue trauma, which is
cludes all the procedures done under magnification starting accomplished through smaller incisions and reduced surgical
from 2.5x onwards either using surgical loupes or microscope. field (Fig. 51.2) The third value is primary passive wound
The hallmarks of microsurgery are increased visual acuity closure. This is accomplished by microsuturing to eliminate
and improved manual dexterity when visibility is increased gaps and dead spaces at the wound edge.
10-fold, motor movement precision is increased from 1 mm to Advanced periodontics has an increasing need for
10 µm. This is the approximate size of an epithelial cell. Large clinical procedures that require intricate surgical skills.
incisions for visibility are therefore not necessary. Small surgi- Regenerative procedures, periodontal plastic surgery, and
cal instruments are used to advantage in the reduced surgical dental implants are but a few of the surgical procedures
field (Fig. 51.1) This minimally invasive philosophy results in that demand clinical performance that frequently challeng-
less injury, diminished morbidity, and rapid healing. Central es the skills of periodontal surgeons beyond the range of
to this approach are sharp microsurgical blades to create in- possibility with ordinary vision. Microsurgery establishes
cisions at a virtual cellular level. These incisions are closed a minimally invasive surgical approach to periodontics ex-
with meticulous apposition to eliminate wound edge gaps and emplified by fewer vertical incisions and smaller surgical
dislocations, allowing healing by primary intention to begin sites. Every field of microsurgery has noted the extent to
within hours of microsurgical closure. This circumvents the which reduced incision size and less retraction directly re-
need for an extensive secondary mitotic stage of wound heal- lates to reduced postoperative morbidity and rapid healing
ing to bridge wound gaps and fill surgical voids. (Fig. 51.3)
599
FIGURE 51.1 Side-by-side dimensional comparison of commonly used conventional versus microsurgical instruments. A, No. 15 blade versus
ophthalmic blade. B, Working tip of conventional needle holder versus McGregor microsuturing forceps.
In addition to the use of magnification and reliance on revealed, under the microscope, as gross crushing and tearing
atraumatic technique, microsurgery requires specially con- of delicate tissues. Periodontics has long advocated atraumatic
structed instruments designed specifically to minimize trau- surgery, but the limits of normal vision have made this goal
ma. An important characteristic of microsurgical instruments unattainable.
is their ability to create clean incisions that prepare wounds Proprioceptive guidance is of little value at the microsurgi-
for healing by primary intention. Microsurgical incisions are cal level. Visual guidance is used for midcourse correction of
established at a 90-degree angle to the surface using ophthal- scalpels and instruments to achieve the finest level of skill and
mic microsurgical scalpels. Microscopy permits easy identifi- dexterity. Incisions can be accurately mapped, flaps elevated
cation of ragged wound edges for trimming and freshening. with minimal damage, and wounds closed accurately with-
For primary wound closure, microsutures in the range of 6-0 out tension. Periodontal microsurgery is a natural progression
to 9-0 are needed to approximate the wound edges accurately. from conventional surgical principles to a surgical ethic in
Microsurgical wound apposition minimizes gaps or voids at which the surgical microscope is employed for the most ac-
the wound edges and encourages rapid healing with less post- curate and atraumatic handling of tissue.
operative inflammation and less pain (Figs. 51.4-51.5). The end-point appearance of microsurgery is superior to
that of conventional surgery. The difference is self-evident and
often startling (Fig. 51. 7) As much as judgment and knowl-
Advantages of Microsurgery edge play a role in surgery, in the end surgery is a craft. Sur-
Periodontal microsurgery raises the treatment bar in many geons appreciate this, especially when microsurgery raises
ways. Surgical decision making is enhanced because the qual- their work to the levels of artistic expression. Personal grati-
ity and quantity of visual data reaching the cerebral cortex is fication in performing better surgery leads to acceptance of
increased by a square of the magnification level. Ergonomic periodontal microsurgery by surgeons motivated to improve
and body posture advantages also occur when using the sur- the quality of their work.
gical microscope (Fig. 51.6). Issues, such as neuromuscular Another very important advantage of microsurgery is in
fatigue and occupational skeletal pathology, are reduced. Sit- the area of root preparation. The importance of root debride-
ting comfort, good body posture, arm support, and controlled ment is recognized universally as an essential component of
breathing are inherent to proper microscope use. Motor skills periodontal therapy. Research in clinical dentistry has shown
are enhanced through instruments designed for a precision that microscope-enhanced vision more readily accomplishes
grip of the hand. Titanium instruments are used for strength the long-established clinical goals of endodontic and restor-
and lightness and are made with round handles to permit pre- ative dentistry. In periodontics, studies demonstrated that
cise rotation. This reduces hand fatigue and tremor for pre- root debridement performed without magnification was in-
cise surgical movement. Ergonomic benefit may be one of the complete. When debrided roots were examined with the aid
most significant aspects of microscope use in periodontics. of a microscope, substantial deposits remained. Even in the
An important aspect of periodontal microsurgery is techni- absence of clinical studies, it may be inferred that microscope-
cal improvement in surgical performance. Higher skill levels enhanced vision in periodontics permits more definitive root
have been shown in many surgical disciplines and can be fully debridement.
appreciated when a surgeon tries his or her hand under the The primary goals of periodontal surgery include visual ac-
microscope. Viewing surgery under the microscope impresses cess to the root surface for plaque and calculus removal and
a surgeon with the coarseness of conventional surgical manip- for removing pathologically altered tooth structure. Magnifi-
ulation. What appears to the unaided eye as gentle surgery is cation greatly improves the surgeon's ability to create a clean,
51 Advances in Periodontal Surgical Procedures (Microsurgery and Laser) 601
FIGURE 51.2 Microsurgical connective tissue graft. Minimal tissue trauma during incisions, surgical manipulation, and suturing is accomplished
after microsurgical principles.
smooth root surface. The root surface represents one oppos- With training, the average periodontal microsurgeon can
ing edge of the periodontal wound. Root planing is therefore consistently produce better crafted work than the most tal-
analogous to establishing a clean soft tissue incision. Mag- ented conventional surgeon.
nification permits preparation of both hard and soft tissue
wound surfaces so that they may be joined together according
Magnification Systems
to the accepted microsurgical principle of butt joint wound
approximation. This encourages primary wound healing and A variety of simple and complex magnification systems are
enhanced periodontal reconstruction. Wound healing studies available to dentists, ranging from simple loupes to prism tele-
show epithelial anastomosis of microsurgically joined surgical scopic loupes and surgical microscopes. Each magnification
wounds in animals within 48 h. system has its specific advantages and limitations. Although
FIGURE 51.3 A, Before B, during, and C, 8 weeks after healing of microsurgical connective tissue graft.
FIGURE 51.4 Papilla reconstruction. A, Before surgery. B, Microsurgical view. C, After surgery.
magnification improves the accuracy of clinical and diagnostic must converge to view the operative field. This can result in
skills, it requires an understanding of optical principles that eyestrain, fatigue, and even pathologic vision changes, espe-
govern all magnification systems. The assumption that "more cially after prolonged use.
magnification is better" must always be weighed against the Three types of Keplerian loupes are typically used in peri-
decrease in field of view and depth of focus that can occur as odontics: simple or single-element loupes, compound loupes,
magnification increases, which is a problem more common and prism telescopic loupes. Each type may differ widely in
with dental loupes than operating microscopes. optical sophistication and individual design.
Simple Loupes
Magnifying Loupes
Simple loupes consist of a pair of single meniscus lenses
Dental loupes are the most common system of optical magni- (Fig. 51.8). Simple loupes are primitive magnifiers with lim-
fication used in periodontics. Loupes are fundamentally dual ited capabilities. Each lens is limited to only two refracting
monocular telescopes with side-by-side lenses convergent to surfaces. Their magnification can only increase by increasing
focus on the operative field. The magnified image formed has the lens diameter and thickness. Size and weight constraints
stereoscopic properties by virtue of their convergence. A con- make simple loupes impractical for magnification beyond
vergent lens optical system is called a Keplerian optical system. 1.5 X. Another disadvantage of simple loupes is that they are
Although dental loupes are widely used, they have disad- greatly affected by spherical and chromatic aberration. This
vantages compared with the microscope. The clinician's eyes distorts the image shape and color of objects being viewed.
FIGURE 51.5 A, Mandibular first bicuspid showing class II gingival recession, B, Incisions placed, C, Partial thickness flap reflected, D, pala-
tal incision, E, harvested graft in place, F, 1-week postoperative showing microsutures, G, result after 6 months showing complete root coverage.
(Photographs presented by Dr Ceetha Priyadarshini and Dr C.D. Dwarakanath.)
Compound Loupes
Compound loupes use multielement lenses with intervening
air spaces to gain additional refracting surfaces (Fig. 51. 9).
This allows increased magnification with more favorable
working distance and depth of field. Magnification of com-
pound loupes can be increased by lengthening the distance
between lenses, thereby avoiding excessive size and weight.
In addition to offering improved optical performance,
compound lenses can be achromatic, which is an optical fea-
ture that clinicians should always choose when selecting mag-
nifying loupes. Achromatic lenses consist of two glass lenses
joined together with clear resin. The specific density of each
lens counteracts the chromatic aberration of its paired lens to
produce a color-correct image. However, multielement com-
pound loupes become optically inefficient at magnifications
above 3X.
Prism Telescopic Loupes
The most advanced loupe optical magnification currently
available is the prism telescopic loupe (Fig. 51.10) Such
FIGURE 51.6 Muscle strain and potential career-ending injuries can
loupes employ Schmidt or "rooftop" prisms to lengthen the
be prevented through a more ergonomic position facilitated by the light path through a series of switchback mirrors between
proper use of a microscope. the lenses. This arrangement folds the light so that the barrel
FIGURE 51.7 Microsurgical crown-lengthening procedure. A, Altered passive eruption covering teeth crowns. B, Immediate microsurgical postop-
erative result. C, Three weeks' postoperative healing.
FIGURE 51.8 Simple loupes.

FIGURE 51.10 Eyeglass-mounted prism loupes.
of the loupes can be shortened. Prism loupes produce better

magnification, wider depths of field, longer working distances,
and larger fields of view than other types of loupes. The bar-
rels of prism loupes are short enough to be mounted on either
eyeglass frames or headbands. However, increased weight of
prism telescopic loupes with magnification above 4 X makes
headband mounting more comfortable and stable than eye-
glass frame mounting. Recent innovations in prism telescopic
loupes include coaxial fiber optic lighting incorporated in the
lens elements to improve illumination (Fig. 51.11).
Magnification Range of Surgical Loupes
Dental loupes provide a limited range of magnification, 1.5 X
FIGURE 51.9 Compound loupes. to -6X. Loupes delivering magnification of less than 3X are
lateral illumination from side-mounted dental lights or head-

lamps. Fiberoptic coaxial illumination is a major advantage
because it focuses light parallel to the microscope's optical
axis, which eliminates shadows. Surgeons can visualize the
deepest reaches of the oral cavity, including subgingival pock-
ets and angular bony defects. Definitive visualization of the
root surface to detect deposits and irregularities is possible.
Surgeons can view anatomy to make clinical decisions based
on the accurate assessment of pathology rather than blind,
educated guesses.
Documentation is important for patient and professional
education and for dental legal reasons. The surgical operating
microscope is an ideal platform for documenting periodon-
FIGURE 51.11 Coaxial lighted prism loupes. tal pathology and clinical procedures. Digital images can be
captured using a beam splitter and camera attachment. A foot
control switch permits a surgeon to record, as the procedure
usually inadequate for the visual acuity necessary for clini- unfolds, without interrupting surgery. These images represent
cal periodontics. Surgical loupes providing magnification of the surgical field exactly as the surgeon sees it, as opposed
more than 4 X are impractical because of their small field of to a camera view over the surgeon's shoulder. High-definition
view, shallow depth of focus, and excessive weight. Exces- video cameras capture both still and video images simultane-
sively heavy loupes can make it difficult to maintain a stable ously to permit documentation of periodontal procedures for
visual field. educational purposes.
For some periodontal procedures, prism telescopic loupes
with magnification of 4 X provide an adequate combination
of magnification, field of view and depth of focus. However,
the surgical microscope offers much higher magnification and
Microsurgical Sutures
superior optics compared to any of the loupe optical systems To achieve ideal microsurgical wound closure, a surgeon de-
mentioned. For some periodontal procedures, prism tele- pends on how the incisions were planned and executed, how
scopic loupes with magnification of 4X provide an adequate the surgery was performed, and the suturing technique. Se-
combination of magnification, field of view, and depth of lection of proper suture needles and materials is essential for
focus. However, the surgical microscope offers much higher successful microsurgical wound closure. The choice of suture
magnification and superior optics compared to any of the and needle size is critical for atraumatic tissue passage. Suture
loupe optical systems mentioned. material must maintain wound closure until healing is suffi-
ciently advanced to withstand functional stress.
Sutures are classified according to structure as mono-
The Surgical Microscope
filament or braided, according to surface as coated or un-
The surgical microscope offers greater versatility than dental coated, and according to biologic properties as absorbable
loupes, by providing a range of magnification with superior or nonabsorbable. The suture of choice in microsurgery is
optical performance. A surgical microscope can last an en- a monofilament suture material such as polypropylene or
tire career, making its long-term expense practical. Proficient polydioxanone. These materials are bacteriostatic and non-
use of the microscope requires training and practice. Surgical inflammatory, hold a knot extremely well, and are easily re-
microscopes designed for dentistry employ Galilean optics, moved. The purpose of sutures is to provide initial wound
which have binocular eyepieces joined by offset prisms, to es- support. They are chosen to appropriate wounds based on the
tablish a parallel optical axis and permit stereoscopic vision fragility of the tissue. The smallest suture capable of support-
without eye convergence or eyestrain. An additional binocular ing the wound produces the least tissue trauma and the least
eyepiece can aid the microsurgical assistant. interruption of the blood supply.
Surgical microscopes have coated achromatic lenses and In periodontal microsurgery the suture size ranges from
high optical resolution, as well as a rotating magnification ele- 6-0 (diameter of a human hair) to 9-0. The size and shape of
ment that allows the microsurgeon to easily change magni- the needle used is essential for the atraumatic passage of the
fication to a value appropriate for the surgical task at hand. suture. The needle diameter is ideally slightly larger than the
Since the optical elements of surgical microscopes are more suture size. Sutures used in microsurgery are swaged, making
advanced than those in loupes, depth-of-focus and field- the needle and the suture continuous. Penetration and pas-
of-view characteristics are greatly enhanced. Surgical micro- sage of the needle depends on the angle of entry of needle
scopes have objective lenses with various working distances. point. Cutting needles pass through gingival tissue easily but
A useful range in dentistry is 250-350 mm. For practical use, can tear tissue. Tapered needles are less traumatic and less
a surgical microscope must have both maneuverability and likely to tear tissue.
stability. Mountings are available for the ceiling, wall, or floor. An important component to needle design is the chord
Adjustable inclining eyepieces enhance postural flexibility for distance. The chord of a needle is the length of a line drawn
various procedures. This maneuverability provides visual ac- between the cutting point and the swaged end. The radius of a
cess to every area of the mouth and is an important factor in needle is the arc of its circumference. A one-half round needle
choosing to use a surgical microscope. has an arc of 180 degrees. The chord determines the ease in
Illumination of the microsurgical field is also an impor- passing a suture between adjacent teeth. The arc determines
tant consideration. Dentists are accustomed to working with the bite size and angle of entry taken by the needle. These
needle dimensions are important when selecting sutures for 5. Symmetry. The distance between the bite sizes on either
periodontal microsurgery. side of the wound edge should be the symmetrical as
should the distance between sutures.
6. Frequency. Smaller suture material and smaller bite size
Esthetic Periodontal Microsurgery makes it necessary to place more microsutures at fre-
Esthetic periodontal microsurgery to reconstruct gingival tis- quent intervals along the wound edge. This supports
sue over denuded roots is routine and predictable using sub- wound closure and avoids stress breakage of sutures or
epithelial connective tissue grafting. The color match, esthetic tissue tearing.
appearance, and lack of scarring of these grafts are ideal. Mi-
crosurgical closure of the palatal donor site allows healing by
primary intention without a painful period of open granula- Microsurgical Knots
tion. This greatly reduces postoperative pain. Two basic knots are employed in microsurgery. The square
To achieve optimal wound healing, three basic microsurgi-
knot, or reef knot, is composed of two single loops thrown in
cal principles are needed: (1) precision tailoring, (2) delicate
opposite directions. The reef knot has more internal stability
tissue manipulation, and (3) passive primary wound closure.
than any other knot. For this reason, it has been employed for
centuries in nautical applications. It lies flat when tied well
Precise Tailoring and is ideal for passive wound closure. As postsurgical edema
occurs, the reef knot opens slightly then becomes self-locking.
An important feature of microsurgery is the ability to create
It maintains wound-edge support without ligation caused by
clean incisions. Design of incisions has a significant impact
excessive tension. If, in tying a knot, both loops are thrown
on how the wound edges fit together. A fundamental prin-
in opposite directions, it becomes the granny knot and unties
ciple of microsurgery is making incisions perpendicular to easily The English surgeon's knot is composed of two double
the tissue surface, creating "butt joint" edges that easily ap-
loops thrown in opposite directions. The first double throw
proximate for wound-edge stability and maintain blood sup-
is less likely to loosen when performing the second throw,
ply patency making it is easier to control tissue apposition. The English
surgeon's knot requires, however, a larger bite size. Both knots
Delicate Tissue Manipulation are tied with instruments.
The microsurgical philosophy is based on minimal invasive-

ness and minimal trauma. This premise extends to the ma- Conclusions
nipulation of gingival tissues during surgery Gentle handling As medicine and dentistry continue the pursuit of minimally
is necessary to reduce cellular injury and subsequent necrosis invasive treatment, periodontal microsurgery and its princi-
and inflammation. It is also necessary to maintain tissue hy- ples will emerge as the methodology to meet both professional
dration and color to maximize healing. and public demand. The microscope provides a tremendous
platform from which the microsurgical clinician can gather
Passive Primary Wound Closure and observe detailed and precise amounts of information for
the diagnosis and treatment of patients with skill and accu-
After precision tailoring and gentle tissue manipulation, the racy. Microsurgery leads to improved esthetics, rapid healing,
final and critical element of microsurgery is achieving pas- reduced morbidity, and enhanced patient acceptance.
sive primary wound closure. There is a specific geometry of
the suturing required, with the following six well-defined
components: Laser Application in Periodontics
1. Angle of entry and angle of exit. The needle should penetrate Lasers are currently available for clinical use to incise soft and
the tissue at a 90-degree angle, perpendicular to the tissue hard tissues. In periodontics, lasers have potential application
surface. Passing the needle at an oblique angle causes tear- in multiple areas such as areas: (1) surgical procedures such as
ing when the knot is tied. gingivectomy and osseous crown lengthening, (2) scaling and
2. Bite size. Proper bite size is between 1 and 1.5 times the root planing, and (3) the management of pathological changes
tissue thickness. Too small a bite size can tear the wound resulting from periodontal disease. ( 4) Gingival depigmenta-
edges. Too large a bite size can cause underriding or over- tion (5) as an aid in healing of wounds, (6) Management of
riding of wound edges. Both outcomes result in impaired dentinal hypersensitivity.
healing and unsightly scarring.
3. Direction of passage. Once the needle has penetrated one Physics of Lasers and Their Biological
edge of the wound, it must exit the opposing side of
the wound with a direction of passage perpendicular to
Interactions
the incision line. This directs the suture force vectors at Laser is an acronym for light amplification by stimulated emis-
90 degrees and prevents lateral dislocation at the wound sion of radiation and functions by transmitting light energy to
edge. tissues. It is a collimated, focused monochromatic ray of light.
4. Tension. Suturing should be accomplished with minimal The energy beam reacts with a target material by being absorbed,
tension. Gentle passage of the suture, in a perpendicular reflected, or scattered. A target tissue absorbs the light. If it is
direction of passage, sets the stage for a microsurgical knot well absorbed, the energy virtually explodes the cell (and ex-
that does not cause tissue strangulation through ligation. tracellular matrix) in a process called ablation. The efficiency of
Good suturing, however, will never save poor tailoring. ablation is related to the wavelength and the affinity of the target
Visible light
(400-700 nm)
X-ray Ultraviolet Infrared Microwave
Wavelength 1 ()2 103 104 105 106 107

10
(nm)
Excimer CO 2
(193-350) (10,600)
Frequency-doubled Er:YAG
Alexandrite (2,940)
(337)
Argon
(438-515)
He-Ne
(637)
Diode Ho:YAG
Nd:YAG
(655-980) {2,100)
(1,064)
FIGURE 51.12 Laser wavelengths.
tissue. If the wavelength is not well absorbed, there is scattering lasers, considerations that each type of wavelength, which the
and a thermal reaction occurs with carbonization, charring, and laser functions with, will have its own set of characteristics
melting. The clinician must understand how this energy is af- (Fig. 5112)
fecting the target tissue and the adjacent tissues as well. Lasers were first used in the 1960s for dental applications
Lasers are named in relation to the active element(s) that They were initially used for removing hard tissue and caries
when stimulated, generate the energy beam. The range of but offered little benefit over standard rotary instruments.
lasers used in dentistry consist of CO2, Nd:YAG, HO:YAG, Recent advances in new wavelengths, delivery units, and
Er:YAG, Er, CT:YSGG, Nd:YAP, GaAs (diode), and argon lasers power maximums have refocused the use of lasers on both
with the wavelengths delivered as either a continuous, pulsed the soft and/or hard tissues (Table 51.1).When applied to the
(gated), or running pulse waveform. Reported periodontal ap- various periodontal tissues such as the gingiva, periodontal
plications for these lasers include soft tissue incision and abla- ligament, cementum, dentin, and bone, the biological inter-
tion; subgingival curettage, scaling of root surfaces, bacterial actions will be unique for that wavelength. Gingiva, dentin,
elimination, osteoplasty, and ostectomy. Because of the vary- enamel, and bone are all composite structures of inorganic
ing absorption spectrum for each tissue type, each laser has and organic elements. Gingiva is comprised of fibrous con-
its unique wavelength spectrum. In understanding the use of nective tissue, extracellular matrix components (including
TABLE 51.1
TYPES OF LASERS CURRENTLY USED IN DENTISTRY

Laser Medium Wavelength (nm) Dental Uses
Argon 488-514 Tooth bleaching and advanced curing lights
Carbon dioxide (CO2) 10,600 Gingivectomy/gingivoplasty, second-stage implant exposure, periodontal curettage (advocated
but not evidence based)
Diode 655-980 Gingivectomy/gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies, dentinal
desensitizing), second-stage implant exposure, periodontal curettage (advocated but
not evidence based)
Neodymium : yttrium- 1,064 Gingivectomy/gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies, dentinal
aluminum-garnet desensitizing), second-stage implant exposure, periodontal curettage (advocated but not
(Nd YAG) evidence based)
Erbium:YAG (Er:YAG) 2,940 Gingivectomy/gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies, dentinal
desensitizing), second-stage implant exposure, periodontal curettage (advocated but
not evidence based), hard tissue cutting (dentin and osseous)
Erbium, 2,780 Gingivectomy/gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies, dentinal
chromium:yttrium desensitizing), second-stage implant exposure, periodontal curettage (advocated but not
(Er,CrYSGG) evidence based), hard tissue cutting (dentin and osseous)
melanin pigmentation), and 70% water. Bone is comprised As such, it has been the basis for malpractice suits. Misuse
of 67% inorganic minerals (calcium hydroxyapatite) and 33% of new technologies can result in "cutting-edge" clinicians
organic elements (collagen, noncollagenous proteins, and finding their early experiences resulting in disastrous re-
water). Other factors to consider are the textures and the den- sults. To avoid these negative results, knowledge of the
sities of these structures. An example is the varying percentage laser mechanics and technique are essential to avoid caus-
of mineralized structures, blood vessels, and fluid found with ing damage to the adjacent tissues. Once mastery of the
cortical and cancellous bone. With the differences in tissue information has been achieved, it is critical to identify the
makeup, the laser energy beam will encounter many fluctua- desired laser application(s) and the fashion in which it will
tions in absorption and scattering, regardless of the wave- be used.
length. Therefore, when considering clinical application, it is
important to appreciate not only what can be accomplished
clinically but also the type of laser being used. Laser Use in Periodontal Procedures
The affinity of the wavelength for the target tissue is
critical. The wavelengths of the diode (655-980 nm) and Currently, lasers are used in periodontal therapy for (1) sur-
Nd:YAG (1064 nm) are well absorbed by pigment. They gical procedures such as gingivectomy and osseous crown
are better suited for soft tissue resective procedures than lengthening, (2) nonsurgical therapy, and (3) the surgical
for hard tissue procedures. The CO2 laser has a very long management of pathological changes resulting from periodon-
wavelength (10,600 nm) with an affinity for water. The CO2 tal disease.
laser should only be used with soft tissue procedures. It is
interesting that the CO2, diode, and Nd:YAG lasers have very Periodontal Esthetic Applications and
different wavelengths, but none have a favorable wavelength Functional Crown Lengthening
for hydroxyapatite.
The wavelengths of erbium:YAG (Er:YAG) (2790 nm) and Several types of laser wavelengths have been reported to be
erbium, chromium:yttrium (Er,Cr:YSGG) (2780 nm) lasers effective for soft tissue procedures. Appropriate use of laser for
have a positive affinity for both water and hydroxyapatite. The procedures such as frenectomy, gingivectomy/gingivoplasty,
specificity for hydroxyapatite also allows cutting hard tissues recontouring of drug-induced gingival overgrowth, short
such as bone, dentin, or enamel. The selection of the type of crowns associated with altered/delayed passive eruption, and
laser is ultimately based on the amount of energy transmitted management of mucosa! tissue/pericoronitis situations distal
to that tissue during a procedure. of mandibular second molars have been well documented.
Photothermal energy is measured in watts (W = joules/ One positive aspect of laser therapy is good visibility during
second). There are other factors to consider besides the the surgical procedure due to minimal bleeding. Minimal tis-
amount of watts being delivered. The amount of energy de- sue damage adjacent to the laser wound is another benefit.
livered to the target can be altered if it is continuous, gated, Additionally, laser therapy can potentially offer extreme preci-
and/or pulsed. A continuous laser transmits more energy than sion and may be easier than using a scalpel.
a pulsed laser to the target tissues. Hertz (Hz) is the cycle/ Esthetic applications for gingivectomy and gingivoplasty
second of a pulsed laser. The benefits of using a laser can be procedures allow delicate tissue shaping. The laser is effec-
compromised if the energy is excessive. Care must be taken tive for the removal of pigmentation from the gingival tissues,
to avoid the transmission of excessive thermal energy to the which can significantly improve the esthetics of highly pig-
tissues adjacent to the target because it can result in cellular mented areas. The CO2, diode, and Nd:YAG lasers have been
damage. used for depigmentation (Fig. 51.13)
Some clinicians advocate the use of lasers for crown-
lengthening procedures (Fig. 51.14). Whereas crown length-
ening involving only soft tissue can be effectively performed
Advantages and Disadvantages with a wide variety of lasers, lasers may be somewhat advanta-
geous for hemostatic control during tissue removal. For func-
of Laser Therapy tional crown lengthening involving osseous contouring, the
There are many advantages to using laser therapy, including use of laser is controversial (see Chapter 50, for a discussion
better visualization of cutting, patient acceptance, and the de- of crown-lengthening surgery). The Er:YAG and Er,Cr:YSGG
toxification of a wound. Other advantages are less invasive lasers have been advocated as one approach for clinical crown
surgery to gain access and minimal wound contraction and lengthening without gingival flap reflection. The Er,Cr:YSGG
scarring. Many of these concepts of laser therapy are positive laser can safely cut bone without burning or altering the
although others still require research. Although different clini- calcium-to-phosphate ratio of the irradiated bone. This ap-
cians have proposed various applications for lasers in peri- proach has been described in case technique reports and case
odontal therapy, further studies and systematic metaanalysis series, but there are no controlled longitudinal or cohort stud-
are required to substantiate their use. ies supporting the use of lasers for clinical crown lengthening
While there are advantages, conversely, lasers can also using the closed-flap technique.
generate excessive temperature changes in hard tissues as re- Decision making for the use of lasers in crown lengthening
ported from the studies by Eriksson and Albrektsson. The ex- in an open or closed approach is based on osseous biotypes.
posure of bone to temperatures ;:,:4 7°C (116.6°F) can induce In the closed approach, the Er,Cr:YSGG or Er:YAG laser can
cellular damage and osseous resorption. Extreme temperature be used only in the medium gingival biotype cases in which
levels of ;:::60°C (l 40°F) result in tissue necrosis. the width of the osseous crest is approximately 1 mm in thick-
Overexposure of laser energy has been the basis for re- ness and may be limited to situations where only 1-2 mm
ports of tissue damage and destruction of the periodontium. of osseous removal is required. In this technique, sounding
FIGURE 51.13 Crown-lengthening procedure by Diode laser. A, Preoperative photograph, B, laser application, C, 6-months postoperative showing
crown in place.
FIGURE 51.14 Gingival depigmentation using diode laser. A, Preoperative photograph showing hyper pigmented gingiva, B, laser application,
C, postoperative photograph after 6 months.
is indicated after the external gingivectomy to determine the decreasing subgingival pathogenic bacteria. In the clinical
thickness of the osseous biotype and to determine the amount situation, periodontal pathogenic bacteria exist in a protec-
of bone removal that is required. The laser tip is placed in tive biofilm in a periodontal pocket. In vitro laboratory analy-
contact with the bone, and the laser is fired for 1-2 s. The tip sis of laser bactericidal properties is not clinically relevant in
is moved slowly around the tooth until the biologic width is that these bacteria do not exist as a suspension or monolayer.
achieved. The osseous removal is verified by sounding, and The protective nature of the biofilm and the disruption of this
detailing is performed with a small chisel. This technique can biofilm result in renewal microbial colonization of this micro
be surgically conservative and result in symmetric gingival niche. In addressing these issues for each laser type, one needs
levels in the esthetic zone. to ask the following questions:
Case selection based on osseous biotypes is critical for the
1. Do the in vivo studies indicate reduction in pathogenic
success of this closed approach for crown lengthening. In a
bacteria as compared to conventional scaling and root
thick biotype, the laser creates a "trough" or an intrabony de-
planing?
fect. Since inadequate bone removal was performed, the soft
2. Are the microbial changes sustained or does microbial col-
tissue will often rebound within a few weeks. With the thick
onization re initiate 7
osseous biotype, the open-flap approach is indicated so ap-
3. Are there any differences in clinical parameters following
propriate osseous contouring can be performed. With thin os-
laser-mediated versus conventional scaling and root plan-
seous or gingival biotypes, laser should absolutely be avoided.
ing' When evaluating nonsurgical periodontal therapy,
Given the thin gingival and osseous structure with the thin
gain in clinical attachment level (CAL) represents the gold
biotype, laser use presents a high risk of overheating the tissue
standard. Pocket depth (PD) and levels of subgingival mi-
and the unpredictable healing response can result in poor or
crobes are important because they correlate with changes
disastrous clinical outcomes.
in CAL
Further issues of concern include: (1) ls there sufficient
4. Are there changes in root surface in vitro conditions?
tactile sense to permit adequate osseous contouring with
properly defined osseous anatomical dimension required for In evaluating laser (ie , Nd:YAG, Er:YAG, and diode lasers)
crown lengthening? (2) ls there any root surface damage? used for nonsurgical periodontal therapy, these questions
Given these concerns and the possible retreatment because need to be addressed. Three recent reviews on the effect of la-
of tissue rebound or poor tissue healing suggest that this is ser therapy as an adjunct of nonsurgical periodontal treatment
not a superior or equivalent technique as compared to train patients with chronic periodontitis have been published.
ditional functional crown lengthening that requires osseous
contouring. Photodynamic Therapy
The use of lasers for photodynamic therapy has recently been
reviewed. This therapy uses a photosensitizer (a nontoxic
Nonsurgical Laser Periodontal Therapy
dye), which specifically targets microorganisms and is activat-
Two of the purported benefits of using laser-mediated peri- ed by a low-level laser light. Photosensitizer activation can be
odontal therapy are for subgingival curettage and significantly achieved by various light sources including argon, Nd:YAG,
FIGURE 51.15 A case treated with LANAP procedure whereby good resolution was obtained and results can be maintained with conventional
periodontal supportive therapy. Resolution was comparable with conventional flap osseous surgery.
and diode lasers. The introduction of a photosensitizer can in histological studies, hence one can only surmise with
greatly increase the bacteriocidal ability of a laser. This is sup- the findings of radiographic fill of the intrabony defects
ported by an in vitro study using methylene blue with a diode that is consistent with possible periodontal regeneration. In
laser to destroy black-pigmented bacteria (Porphyromonas gin- a split-mouth design, the use of ER,Cr:YSGG laser versus
givalis and Prevotella intermedia); 99-100% of bacteria were open-flap debridement was compared. The laser-assisted
eliminated. Disrupting the biofilm may also be effective using pocket therapy was found to provide similar CAL gains
the photodynamic therapy. Anecdotally, lasers can be used to with similar reduction in pocket depth, GI and sulcular
target pigments (ie, Nd:YAG) and have the potential to target bleeding index. These findings were similar to the findings
pigmented P gingivalis. Studies are available on the use of pho- that compared a split-mouth design with three closed ap-
todynamic therapy (PDT) as adjunct to scaling and root plan- proaches, which included SRP, diode laser curettage with
ing, which reported significant clinical and microbiological SRP, and laser-assisted curettage with SRP and laser sealing,
improvements in the PDT + SRP as compared to SRP alone. versus an open approach of papilla reflection with SRP and
One study found the results to be comparable. More clinical flap closure. In comparing these open and closed protocols,
trials are required prior to clinical implementation. all treatments resulted in a reduction in PD and bleeding
on probing. Consistent with the previous study, closed pro-
tocols all resulted in less gingival recession. These authors
Lasers in the Surgical Management concluded that if esthetics is a concern, laser curettage is
of Periodontitis a viable option. Since this is an issue of concern in the
maxillary anterior region, the caveat is that the clinician
The role of laser therapy in the surgical management of peri- must be appropriately trained and familiar with the laser
odontitis remains controversial. At the center of this contro- being used. There are clinical instances where mismanage-
versy is the apparent potential for the Nd:YAG laser to result ment with laser resulted in irreversible hard and soft tissue
in new attachment and regeneration when used with the damage.
LANAP protocol (see Chapter 48). The patented LANAP pro-
cedure consists of a first pass with a Nd:YAG laser at a setting
of 4.0 Wand energy density of 1965 m]/mm2, 100-µs pulse Conclusions
duration, and 20 Hz applied. The first pass deepithelializes
the sulcular epithelium, the underlying connective tissue is The literature has numerous positive findings for the use of
spared, and purportedly kills pigmented bacteria. The teeth lasers in the management of periodontal and periimplant
are then scaled and root planed with piezo ultrasonic instru- disease. The quality of the literature is largely dominated by
mentation. A second pass was performed with similar output case reports and series. The problem is that there are limited
but with a 650-µs pulse duration and 20 Hz. The second pass well-designed random clinical trials and with the various laser
creates a blood clot and if kept stable, it acts as the foundation types, no single laser has been well researched as to the exact
for periodontal wound healing. parameter for use. Therefore, laser use for the treatment of
Since the initial description of LANAP, most evidence periodontal disease presents numerous unknowns.
was based on case reports (Fig. 51.15). Recent publications As in all professions, technology is constantly advancing
suggest that this protocol may have merits. This is based on with new research to provide the clinician with better equip-
two histological studies that report LANAP can result in the ment, drugs, and techniques to improve the therapy rendered
formation of new attachment and periodontal regeneration. to patients. Lasers in periodontics may become an integral
More recently, the effectiveness of LANAP was examined in part of periodontal therapy, but at the present time, further
the treatment of 107 consecutive patients presenting with research as to the parameters for clinical efficacy and biologi-
moderate-to-advanced chronic periodontitis. The main crite- cal basis for laser therapy are required. Clinician considering
rion for determining treatment success over time was mea- incorporating laser therapy should be familiar with what is
sured by tooth loss. Tooth loss per patient treated by LANAP known, the appropriate parameter for use, and receive ad-
was 0.4 3 teeth over the average of 6.2-years posttreatment. equate training to master the laser of interest.
Although a direct comparison with classic studies is not pos-
sible due the shorter time frame for posttreatment evaluation, SUGGESTED READINGS
the trend suggests LANAP compares favorably with conven-
tional surgical treatment modalities and may be a less invasive Microsurgery
treatment alternative. Barraquer JI: The history of microsurgery in ocular surgery,] Microsurg 1 :288,
1980.
There are limited studies on the surgical management of Hoerenz P: Optical principles, illumination systems and support systems,
chronic periodontitis with other laser types. Given the pos- J Miuosurg 1:367, 1980.
itive histological evidence of new attachment and regenera- Shanelec D: Current trends in soft tissue grafting,] Calif Dent Assoc 19:57, 1991.
tion associated with LANAP performed with the Nd:YAG, Shanelec D: Optical principles of dental loupes,] Calif Dent Assoc 20:25, 1992.
Shanelec D, Tibbetts L: An overview of periodontal microsurgery, Curr Sci
the question remains: Can Er:YAG or the Er,Cr:YSGG laser 2:187, 1994.
reproduce similar results' The advantage is that there is
less risk associated with this wavelength. Putative peri-
odontal regeneration of a maxillary intrabony defect based Lasers
on radiographs following Er,Cr:YSGG treatment has been Cobb CM: Lasers in periodontics: a review of the literature, J Periodontal
77(4):545-564, 2006.
recently reported. The difficulty is that periodontal regen- de Paula Eduardo C, De Freitas PM, Esteves-Oliveira M, et al: Laser photo-
eration requires histological evidence of new PDL, cemen- therapy in the treatment of periodontal disease. A review, Lasers Med Sci
tum, and bone formation. This has not been demonstrated 25:781-792, 2010.
Harris OM, Gregg RH, McCarthy DK, et al: Laser-assisted new attachment Sgolastra F, Severino M, Petrucci A, et al: Effectiveness of diode laser
procedure in private practice, Gen Dent 52:396-403, 2004. as adjunctive treatment to scaling root planning in the treatment of
Nevins ML, Camelo M, Schubach P, et al: Human clinical and histologic chronic periodontitis: a meta-analysis, Lasers Med Sci 28(5):1393-
evaluation of laser-assisted new attachment procedure, Int J Periodontics 1402, 2013a.
Restorative Dent 32:497, 2012. Sgolastra F, Severino M, Petrucci A, et al: Nd:YAG laser as an adjunctive treat-
Schwarz F, Jepsen S, Herren M, et al: Influence of different treatment ment to nonsurgical periodontal therapy: a meta-analysis, Lasers Med Sci
approaches on non-submerged and submerged healing of ligature induced 29 887-895, 2013b.
periimplantitis lesions: an experimental study in dogs, J Clin Periodontal Tilt LV: Effectiveness of LANAP over time as measure by tooth loss, Gen Dent
33:584-595, 2006. 60:143-146, 2012.
Sgolastra F, Petrucci A, Gatto R, et al: Efficacy of Er:YAG laser in the treatment Yukna RA, Carr RL, Evans GH: Histologic evaluation of an Nd:YAG laser-
of chronic periodontitis: systematic review and meta-analysis, Lasers Med assisted new attachment procedure in humans, Int] Paiodontics Restorative
Sci 27 661-673, 2012. Dent 27(6):577-587, 2007.
SECTION VI
Multidisciplinary Approach for the

Management of Periodontal Diseases
Section Outline
52 Diagnosis and Management of 54 Adjunctive Role of Orthodontic
Endodontic-Periodontic Lesions Therapy
53 Periodontal-Restorative
Interrelationships
52
Diagnosis and Management
of Endodontic-Periodontic
Lesions
KC Trabert • MK Kang • N Ambalavanan
Chapter Outline
Anatomic Considerations of the Pulpal Differential Diagnosis of Pulpal and
and Periodontal Continuum Periodontal Infection
Factors Initiating Pulpal and Apical Classification of Endodontic-Periodontic
Diseases Lesions
Biologic Effects of Pulpal Infection on Treatment Considerations of
Periodontal Tissues Endodontic-Periodontic Lesions
Biologic Effects of Periodontal Infection Conclusion
on the Dental Pulp
Anatomic Considerations of the length of the root canals, albeit to varying frequencies de-
Pu/pal and Periodontal Continuum pending on their location. Root-canal therapies (RCTs) fail
frequently in maxillary molars because of unidentified second
Persistent infection in the pulp tissue leads to secondary in- mesial canals. These canals are found in a surprisingly high
fection and breakdown of tissues in the periodontium. Con- percentage (80 .8%) of teeth. Clearly, accessory canals can lead
versely, severe periodontal disease may initiate or exacerbate to asymptomatic apical periodontitis resulting from chronic
inflammatory changes in the pulp tissue. This mutuality of in- pulpal diseases. This can be readily detected in periapical ra-
fection between pulp and periodontium is mediated through diographs (Fig. 52 3) and the periodontal lesions usually heal
physical routes, allowing for communication between the two after the successful completion of endodontic therapy. How-
structures. The main and obvious route of communication is ever, the likelihood of primary periodontal infections reaching
the apical foramina. Advanced pulpitis will lead to pulp ne- the dental pulp through accessory canals is rare.
crosis, which often is accompanied by inflammatory bone The third route of communication between the periodon-
resorption at the root apex, as found in cases of apical peri- tium and the pulp is through the dentinal tubules. Dentin is
odontitis or an apical abscess (Fig. 52.1). This is also known a permeable structure and the permeability changes at dif-
as retrograde periodontitis because it represents the periodontal ferent locations along the root surface according to the size
tissue breakdown from an apical to a cervical direction and and density of the dentinal tubules. Bacterial colonization
is the opposite of orthograde periodontitis that results from a in the tubules from infected root canals has been well docu-
sulcular infection. This is typically identified as a periapical mented. Also, bacterial invasion into dentinal tubules from
radiolucency (PARL) (Fig. 52 2). Retrograde periodontitis is the periodontal pocket has been demonstrated, suggesting
the most common example of pulpal diseases leading to sec- that dentinal tubules may allow pulpal irritation from chronic
ondary periodontal breakdown. The presence of patent apical periodontal infections.
foramina can also lead to pulpal inflammatory changes sec- In addition to the aforementioned routes of anatomical
ondary to a severe periodontitis in cases where the periodon- communication between pulpal and periodontal tissues, there
tal defect reaches the apical foramina. are instances in which communication is established between
Alternatively, lateral or accessory canals may also be the the pulp and periodontium by iatrogenic defects, such as ver-
routes of periodontal and pulpal communications. Prevalence tical root fractures and tooth perforations. Both of these situ-
of accessory root canals in various human teeth and their ations represent nonanatomic communication between the
contribution to the complexity of the root canal system has pulp and periodontium and result in the spread of infection
been well established. Accessory canals are found along the from one compartment to the other.
615
(A) (B) (C) (D)

FIGURE 52.1 Classification of endodontic-periodontic lesions. A, Primary pulpal infection can lead to chronic periradicular periodontitis by which
a periapical radiolucency (PARL) can develop and migrate cervically. Mandibular molars can also have accessory canals in lateral orientation or in
the furcation area. These accessory canals can allow migration of the primary pulpal infection and cause secondary breakdown of the periodontium
at their respected loci. B, Primary periodontal infection can lead to extensive breakdown of alveolar crest bone that migrates from the cervical area
to the apex. In these lesions, one would find generalized bone loss around a single tooth or often might involve multiple adjacent teeth. Since the
pulpal-periodontal continuum is present through main root canal foramina or through accessory canals, extensive periodontal infection can cause
irritation in the pulp tissues. C, Both primary pulpal and primary periodontal infection can occur simultaneously in an "independent" endodontic-peri-
odontic lesion, exhibiting the characteristics of both. D, Primary pulpal and primary periodontal infections can occur extensively in this "combined"
endodontic-periodontic lesion.
FIGURE 52.2 Retrograde periodontitis. A, Large periapical lesion extending around the periapex of tooth#47. No visible fractures were detected on
the mesial or distal marginal ridges. The tooth tested nonvital. A sinus tract was visible on the buccal gingiva. B, Endodontic therapy was completed in
two visits, and the canals were obturated. C, Healing of the periradicular bone is evident at 6 months, and a crown providing complete coverage has
been placed. (Courtesy Dr Thomas Rauth.)
FIGURE 52.3 Lateral canal-led periodontal defect from a primary endodontic infection. A, Bone loss is present in the furcation with sinus tract
present on the buccal mucosa. Tooth #46 tested nonvital. B, During condensation, a large amount of sealer was expressed through a large lateral canal
in the distal root. C, Sealer was removed after obturation by curettage of the furcation and irrigation with anesthetic solution through the sinus tract.
D, Healing at 12 months demonstrates complete repair of periradicular bone. (Courtesy Dr Thomas Rauth.)
52 Diagnosis and Management of Endodontic-Periodontic Lesions 617
Factors Initiating Pu/pal sealers invariably cause severe inflammatory reactions in the
apical tissues even though patients may be completely asymp-
and Apical Diseases tomatic. Thus, dental materials often contain chemical irri-
Pulpal and apical diseases are initiated by numerous external tants that affect both the pulpal and periodontal tissues and
factors that may include microorganisms, trauma, excessive one must be cognizant of the potential iatrogenic endodontic
heat, restorative procedures, restorative agents, and malocclu- pathosis associated with their misuse.
sion. These insults lead to inflammatory changes in the pulp, The diagnosis of endodontic lesions that may often have a
starting from a reversible or irreversible pulpitis and ultimate- periodontal component can be confusing (Table 52.1).
ly progressing to pulpal necrosis and subsequent breakdown To make a proper endodontic diagnosis, the clinician must
of the periodontium. Dental caries is a prominent cause of evaluate the symptoms of the patient; the radiographic and
pulpal disease and bacterial infection is the primary form of clinical findings; and the presence, absence, and location of
microbial insult to the pulp. any swelling or drainage. Given all of these variables, it is easy
Thermomechanical irritants can alter pulpal circulation to understand why a lack of clarity exists to ascertain whether
and induce pulp-tissue damage. Earlier studies demonstrated the lesion is primarily endodontic, periodontal, or a true com-
that thermal changes caused by dental procedures, such as bined lesion and why mistakes are made in their diagnosis
tooth preparation, led to marked diminution of pulpal blood (Table 52.2)
flow and plasma extravasation, resulting in an inflammatory
response. Pulpal necrosis will eventually lead to apical peri- Biologic Effects of Pu/pal Infection
odontitis. Likewise, chemical irritants impose measurable
changes in the pulp status. Etching the dentin surface with
on Periodontal Tissues
a high phosphoric acid content yields deleterious effects on The effects of the pulpal disease on the surrounding periodon-
dental pulp. Also, bonding resins used as pulp-capping ma- tal tissues are widely accepted by both clinicians and research-
terials leads to acute pulpitis and varying degrees of necrosis ers, which have been studied for more than 50 years. Early
in human teeth. Root canal overfills with gutta-percha and inflammatory changes in the pulp exert very little effect on the
TABLE 52.1
CLASSIFICATION OF PULPAL DISEASESa

Pulpal State Symptom Vitality Response to Cold
Normal pulp Asymptomatic Vital Within normal limits
Reversible pulpitis Sensitive to pressure or temperature" Vital Hypersensitivity to cold
Symptomatic irreversible pulpitis' Spontaneous, throbbing pain Vital Hypersensitivity to cold and lingering response
Asymptomatic irreversible pulpitis'' None Vital Within normal limits
Pulp necrosis' Asymptomatic' Nonvital No response
Previously treated Variable Nonvital No response
Previously initiated therapy Variable Variable Variable
'Different pulpal conditions cannot be discerned by periapical radiographs. Symptoms and responses to cold explained herein are the general findings but excep-
tions can occur.
'Patients' response to pressure may be due to hyperocclusion in reversible pulpitis cases. In the absence of such factors, patients' complaints mainly revolve
around thermal sensitivity.
'Symptomatic irreversible pulpitis may be symptomatic and painful as described or may be asymptomatic and nonpainful.
"Asympromatic irreversible pulpitis is based on the presence of pulpal inflammation, for example, extensive caries, hyperemia, or traumatic injuries, in the ab-
sence of patients' subjective symptoms.
'Necrotic pulp may cause acute exacerbation of symptom, including spontaneous throbbing pain. However, such sensitivity results from periradicular inllam-
mation.
This diagnostic terminology is based on the recommendations of the AAE Consensus Conference, as shown in the Journal of Endodontics, 35'1634, 2009.
TABLE 52.2
DIFFERENT CHARACTERISTICS OF PULPAL AND PERIODONTAL LESIONSa

Independent Endodontic- Combined Endodontic-
Primary Pulpal Primary Periodontal Periodontic Periodontic
Patient symptom varies" Mild discomfort Varies" Varies"

Coronal integrity Compromised Intact Compromised Compromised
Radiographic lesions PARL Cresta! bone loss Separate PARL and crestal Continuous bony lesions from
lesions alveolar crest to apex
Vitality Nonvital Vital Nonvital Nonvital
Periodontal probing Narrow probing to apex' Generalized bone loss Generalized bone loss Generalized bone loss with
narrow probing to apex
'These are generalized summaries and deviations can occur.
"Patient symptom for pulpal lesions may vary, depending on the type of pathosis. Chronic lesions can be completely asymptomatic, whereas acute symptoms
without any radiographic lesions can trigger pain.
'Primary pulpal lesions may not present with any periodontal defect. Narrow probing in pulpal lesions may indicate sinus tract through sulcus.
periodontium. Even a pulp that is significantly inflamed may tionally impair wound healing and aggravate the development
have little or no effect on the surrounding periodontal tissues. and progression of the periodontal disease state.
It is thought that this initial pulpal inflammatory response is It is clearly apparent that the endodontium and periodon-
an attempt by the body to prevent the spread of infection to tium are closely related and that microorganisms and nonliving
the apical tissues. pathogens play an important role in both infections. Diseases in
When the pulp becomes necrotic, however, it produces a one area can lead to a secondary disease in the other. Diagnosis
significant inflammatory response involving extremely com- therefore is critically important and will dictate the appropriate
plex inflammatory and immune reactions. This response course of treatment.
can traverse the apical foramen, the furcation, lateral canals,
dentinal tubules, or areas of trapped necrotic tissue along the
surface of the root that extend past the periodontal ligament Biologic Effects of Periodontal
(PDL) and into the surrounding apical tissues. This initial
Infection on the Dental Pulp
inflammatory response of the pulp and subsequent necro-
sis that permeates through the numerous spaces of the canal The effects of periodontal disease on the dental pulp appear
system includes various bacterial strains, Spirochetes, fungi, to be more controversial compared to the effects of pulpal
yeasts, and viruses. The nature and extent of the periodontal disease on the periodontium. Although inflammation and
destruction that follows depends on the virulence of the localized pulpal necrosis have been observed next to lateral
pathogens in the canal system, the duration of the disease, canals exposed by periodontal disease, a correlation between
and the defense mechanisms of the host. periodontal disease and changes within the pulp had not been
Bacteria play a critical role in both endodontic and peri- confirmed. When pathologic changes do occur in the pulp of
odontal disease. Proteolytic bacteria predominate in early a tooth as a result of advanced periodontal disease, the pulp
root-canal infections and then change over time to a flora that does not usually undergo degenerative changes as long as the
contains a greater number of anerobes. Fungi and yeasts are main canal has not been involved.
also present in pulpal infections. Current evidence suggests However, the spread of advanced periodontal lesions that
the important role that viruses may play in the pathogenesis extend to the apical foramen can result in pulpal necrosis.
of both periodontal and endodontic disease. Several nonliv- This retrograde infection may proliferate through large acces-
ing pathogens have also been implicated in the inflammatory sory canals on the lateral surfaces of the tooth, canals posi-
process as well. These include foreign bodies, epithelial rests, tioned closer to the apical foramen, and the area where the
cholesterol crystals, Russell bodies, Rushton hyaline bodies, main canal exits the tooth apex. Protection and preservation
and Charcot-Leyden crystals. of the cementum and dentin surrounding the tooth also play
As the degree of pulpal inflammation becomes more ex- important roles in preserving the health of the pulp and pre-
tensive, a greater amount of destruction of the periodontal venting the ingress of periodontal pathogens. The presence
tissues ensues. Extension of the infection through the PDL of an intact layer of cementum is important in protecting the
space, tooth socket, and surrounding bone occurs and the pa- pulp from dental plaque and other periodontal pathogens that
tient begins to experience a localized or diffuse swelling that migrate along the root surface during the development of ad-
may result in cellulitis that invades the various facial spaces. vanced periodontal disease. Excessive root planing and curet-
Most often, however, the infection erupts through the labial, tage that remove the cementum and dentin from the root sur-
buccal, or lingual mucosa and results in a draining sinus tract. face, encourages narrowing of the pulp canals. This process
In cases where the path of least resistance for the infectious is thought to be reparative rather than inflammatory. Several
process is along the attached gingiva, the infection may dis- studies also suggest that periodontal disease is degenerative
sect the PDL space and result in the formation of a deep but to pulpal tissues resulting in continued calcification, fibrosis,
narrow periodontal pocket. This pocket usually extends to the collagen resorption, and inflammation.
main site of the infection when probed or traced with a gutta- Dentin thickness also contributes to the protection of the
percha point. Confusion often results among both general dentists pulp. Some precautions that can be taken during the course of
and specialists as to whether the probing defect is the result of an periodontal therapy are: (1) avoidance of the use of irritating
endodontic or periodontal problem. In general, a narrow probing chemicals on the root surface, (2) minimization of the use of
defect combined with a non vital pulpal response indicates that the ultrasonic scalers when there is less than 2 mm of remaining
problem is usually of endodontic origin rather than periodontal. dentin, and (3) subsidence of minor pulpal irritations before
When endodontic therapy is the main cause of the swell- completion of additional procedures. When these precautions
ing or breakdown of the periodontium, successful endodontic are not followed, and the microvasculature of the pulp is dam-
treatment usually results in healing of both the periapical and aged during periodontal procedures that involve deep curet-
periodontal tissues. There are times, however, when trauma tage or periodontal surgical efforts to save the tooth, necrosis
to the tooth, severe loss of adjacent periodontal tissues, con- may result.
tinued tooth mobility, and occlusal trauma do not provide an It appears, therefore, that both the pulp and periodontal
environment that allows for apical healing to occur. In these compartments influence the other. Periodontal disease, how-
cases, splinting is sometimes necessary to help stabilize the ever, seems to have less of an influence on the pulpal tissues
tooth and allow for potential repair of the apical tissues. compared to the influence of pulpal disease on the periodon-
If an endodontic infection is left untreated, the progression tium. Clearly, advanced periodontal disease has some effect
of periodontal disease continues. Untreated and unresolved on the pulpal state (Fig. 52.4). Unless the microvasculature of
infections of endodontic origin can sustain the growth of vari- the pulp is compromised during aggressive periodontal pro-
ous endodontic pathogens that may lead to increased pocket cedures or excessively deep curettage severs the apical ves-
formation, bone loss, calculus deposition, osteoclastic activity, sels, most periodontal interventions result in only a localized
and subsequent bone and tooth resorption. They may addi- pulpal response and dentin hypersensitivity.
(A)
FIGURE 52.4 Primary periodontal defects causing periradicular bony lesions and pulpal irritation. A, Primary periodontal lesion is evident on the
distal of tooth #47. The defect was probed to a depth of 7 mm and the tooth tested vital to both thermal and electrical pulp testing. The defect was most
likely the result of the impacted third molar and formation of a chronic periodontal abscess. B, Primary periodontal lesions both probing 12 mm into
the furcation. Teeth #26 and #27 tested vital to thermal and electrical testing. The patient's chief complaint was discomfort to cold, thus exemplifying
pulpitis secondary to the primary periodontal infection. (8, Courtesy Dr Gregory Kolber.)
Differential Diagnosis of Pu/pal distinction between pulpal or periodontal infection requires

collectively dissecting the multiple findings and synthesizing
and Periodontal Infection the most probable diagnosis (Table 52.2).
Acute infection of both the periodontium and the pulp must
be differentiated from one another for clinicians to establish
a correct diagnosis with reasonable certainty and to initiate
Patients' Subjective Symptoms
appropriate therapy. A thorough understanding of both dis- Patients suffering from the acute phase of pulpal infection
ease processes and the correct interpretation of clinical and display symptoms that are generally absent in chronic peri-
radiographic findings will aid the dentist in establishing a di- odontal infection. During the initial stage of pulpitis, patients
agnosis that results in the rapid relief of the acute and painful may complain about sensitivity and pain exacerbated by cer-
condition. tain stimuli, including temperature changes, pressure, and/or
When the pulpal and periodontal abscesses are separate biting. If the symptoms result from reversible pulpitis, they
from one another, the diagnosis is usually easier. There are will usually resolve spontaneously with time as the result of
instances, however, when each primary disease may have a various mechanisms, such as the closure of dentinal tubules,
similar clinical characteristic, which makes the diagnosis clearance of microbial irritants and toxins, and reparative
more difficult. In other situations, there may be no demarca- dentin formation. Persistent inflammation leads to a symp-
tion between the two areas of pathosis that both clinically and tomatic irreversible pulpitis, which is often associated with
radiographically appear as one large and continuous lesion sharp and spontaneous pain, although asymptomatic irrevers-
with extreme pain and swelling. When this occurs, it is better ible pulpitis may also occur as described previously. Acute
to avoid classifying these continuous lesions as true combined pain to thermal stimuli may subside after several days as the
lesions. One must rely on all available clinical testing methods pulp becomes necrotic, and the bacteria and their by-products
to help clarify the correct clinical diagnosis prior to the initia- migrate down the complex canal system. As the infection ex-
tion of treatment. tends to and then past the apical foramen or a lateral root
Making the accurate differentiation between pulpal and canal, the tooth becomes particularly sensitive to bite pressure
periodontal lesions can be challenging. If the lesion originates and percussion. After several days, the necrotic tooth may de-
from a pulpal infection and yet was treated by extensive peri- velop an acute apical abscess that results in the elevation of
odontal therapy, it will not resolve. Conversely, performing the tooth from the dentoalveolar complex. Patients frequently
endodontic therapy on a tooth that has an extensive periodon- report that the tooth feels "high" on occlusion. However, pa-
tal defect and a vital pulp will result in the persistence of the tients with irreversible pulpitis or a necrotic pulp may be as-
periodontal infection. Thus, identifying the primary cause of ymptomatic. Thus, making the diagnosis of primary pulpal
infection is a critical determinant for the treatment outcome. infection must be based on multiple objective findings, such
Perhaps the most important consideration when making such as the patients' responses to percussion, palpation, biting,
a distinction is to base the diagnosis on multiple findings. periodontal probing, and vitality testing, as well as thorough
Those include patients' symptoms, coronal integrity, shape evaluation of the patients' subjective symptoms.
and size of the radiographic lesions, periodontal probing, and In apical and periodontal abscesses, the extent of pain
tooth vitality. It is possible that one or more of these findings may vary. In general, an acute apical abscess causes extreme
suggest a pulpal or periodontal infection, whereas others point pain to pressure, bite, percussion, and at times, to palpation
to the contrary. For example, a tooth may exhibit extensive if the infection has penetrated the cortical bone. Periodontal
failing restorations, recurring decay, and radiographic lesions, abscesses are thought to cause less pain because there is little
suggesting probable pulpal involvement. However, the tooth or no elevation of the periosteum. Edema and swelling are
may test completely vital and lack any evidence of an irrevers- characteristics that may be shared by both conditions. The
ible pulpitis upon thermal testing. Under these circumstances, swelling and edema with a periodontal abscess is generally
one would rule out the primary pulpal infection and examine confined to the cervical portion of the tooth. An apical abscess
the patient for periodontal involvement. Thus, making the is usually more sensitive to palpation around the tooth apex if
the infection has penetrated through the bony cortical plate. Radiographic Appearance
Redness and a smooth appearance of the marginal gingival
tissues is more common with abscesses of periodontal ori- Periapical radiographs can provide distinguishing informa-
gin, whereas redness can be detected more apically if a pulpal tion whether the lesion is of pulpal or periodontal origin.
abscess has started to swell and elevate surrounding tissues. It is important to understand to focus on specific entities
Objective findings in periodontal abscesses include bleeding on a radiograph. These should include the coronal sta-
on probing, suppuration, increased pocket depth, increased tus, crestal bone height and shape, presence of an apical
tooth mobility, and occasionally, lymphadenopathy. Abscesses or lateral radiolucency, bony trabeculation, integrity of the
of endodontic origin usually probe normally but may also dis- lamina dura, and careful evaluation of the obturation of
play increased mobility, depending on the amount of bone the root canal if present. Coronal status as revealed on a
loss. Patients may describe the tooth as feeling longer or high- radiograph can also help in the differential diagnosis as de-
er than the adjacent teeth. scribed previously. Also, apical lesions originating from a
Suppuration and drainage from periradicular and peri- primary pulpal infection lead to a retrograde periodontitis
odontal abscesses may also differ. Periodontal abscesses are that migrates from the root apex in a cervical direction. On
associated with severe periodontal destruction and a sup- the contrary, periodontal infections will lead to the loss of
purative exudate that is evident during probing. Bleeding crestal bone from the cervical area of the tooth in an api-
on probing, severe edema, redness and swelling, and some cal direction. Thus, radiographic lesions appear different
degree of mobility may also be present. Some patients also in endodontically treated teeth compared to periodontal
suffer from lymphadenopathy. Aspects of periodontal ther- lesions and the shape of the bony lesions can help distin-
apy that correlate highly with the development of acute guish between the two. For example, radiographic lesions
periodontal abscess formation are (1) patients undergoing representing severe periodontitis will appear wider at the
current periodontal treatment, (2) incomplete removal of cervical end than the apical portion of the lesion. Apical
calculus, (3) a history of a previous abscess at the same site, or lateral radiolucencies may also result from differences in
and ( 4) the previous use of antibiotics for dental or nonden- trabeculation patterns not associated with pulpal infection.
tal reasons. For this reason, it is critical to consider the integrity of the
Drainage from apical abscesses usually comes from one of lamina dura. A break in the lamina dura, accompanied by
two sites. The most prevalent area of drainage is a sinus tract an apical or lateral radiolucency, is usually indicative of a
that develops when the area of swelling breaks through the chronic or acute pulpal infection. If the tooth had been
mucoperiosteum and exits the mucosa! tissue either near or endodontically treated, assessment of the previous obtura-
at some distance from the site of the infection. Additionally, tion qualities (ie, voids, short fills or overfills, missed ca-
the path of least resistance may be along the PDL and the nals, etc.) is also important. These radiographic features
infection may dissect the ligament along the surface of the will provide very useful and often accurate distinguishing
root and exit the tooth at the height of the epithelial attach- information in making the differential diagnosis between
ment. This results in a periodontal defect that probes along a pulpal and periodontal lesions.
narrow path to the apex of the root as previously discussed.
Both the sinus tract and narrow sulcular lesions can usu- Vitality
ally be traced to the infected tooth or offending root using a
gutta-percha point. Testing of tooth vitality often becomes one of the most im-
portant tests that can differentiate between periodontal and
endodontic infections. Teeth with periodontal infection usu-
Coronal Integrity
ally test vital to thermal testing unless the acute condition is
Periodontal infection without pulpal involvement may present a combined lesion in which both endodontic and periodon-
with intact crown structure and absence of coronal defects. tal compartments have become diseased. Teeth with both
Conversely, endodontic infection is almost always associated endodontic infection and periodontal abscess usually test
with the loss of coronal integrity, such as caries, failing resto- nonvital. Exceptions to this are extremely calcified canals,
rations, extensive restorations, and the existence of cracks or extensively restored teeth, or multirooted teeth where canals
fractures that extend to the pulpal tissues. However, this does may be partly necrotic as a result of either pulpal or peri-
not mean that all periodontal infections are devoid of coronal odontal disease. Other canals may still retain vital tissue that
defects or that all endodontic lesions exhibit loss of coronal responds to thermal or electric pulp testing. Thermal testing
integrity. When pulp tissue is severed by trauma, for example, is usually the most reliable way of determining pulpal health
one might expect to find a necrotic pulp in the absence of or disease. Patients with symptomatic irreversible pulpitis of-
coronal defects. If left untreated, such lesions originating from ten report a lingering painful response to a thermal stimulus.
primary pulpal infection lead to the breakdown of the peri- In later stages of pulpitis, heat exacerbates the symptom more
odontium as in asymptomatic apical periodontitis or apical than the cold, and the application of cold may even cause
abscess. Of course, primary periodontal lesions can develop short-term pain relief. Although thermal testing can be in-
in teeth with coronal defects. Furthermore, combined lesions formative as to the status of the pulp, a patient's response to
(so-called endo-perio lesions) would present with a peri- thermal stimuli may be confused with hypersensitivity result-
odontal infection and extensive coronal destruction. However, ing from exposed dentin and patent dentinal tubules in the
careful examination of the coronal status either during the in- absence of pulpitis. Therefore, thermal testing must be com-
traoral or radiographic examination can provide supportive bined with other diagnostic criteria as discussed previously
information in deciding whether the lesion originates from an to distinguish between the lesions originating from pulpal or
endodontic or a periodontal infection. periodontal infection.
Case no. 1
n.A)
Case no. 2
FIGURE 52.5 Independent and combined endodontic-periodontic lesion. Case 7. "Independent" endodontic-periodontic lesion. A, "Truly sepa-
rate" endodontic-periodontic lesions. Vertical periodontal bone loss can be seen at the mesial surface of both teeth #37 and #36. A large endodontic
lesion extends around the apex and into the bifurcation of 36. An apical and furcal defect is evident radiographically. B, Final condensation film
2 weeks after initiating treatment. C, Nearly complete healing of the endodontic lesion at 6 months and restoration of the tooth with a porcelain-fused-
to-metal crown. The areas of vertical bone loss from the periodontal lesions are still present. Case 2. "Combined" endodontic-periodontic lesion.
A, Nonvital tooth with a narrow 9-mm probing defect in the bifurcation of tooth #36 and a large periapical lesion. Normal probing depths were found
on the remaining tooth surfaces. B, 9-month healing demonstrates significant bone repair in the furcation and periapical areas. A small amount of bone
loss in the furcation still remains because of a persistent periodontal defect. (Case 7, Courtesy Dr Thomas Rauth.)
Classification of Endodontic- involving the furcal defect. In fact, this type of lesion and the
healing pattern are observed in almost all secondary peri-
Periodontic Lesions odontal defects resulting from primary pulpal infection and
A simple classification of perio-endo lesions was given by rapid bone loss in the periodontal tissues.
Simon, Glick, and Frank in 1972, as follows: Lesions originating from pulpal infections require endodon-
tic therapy and would not resolve from periodontal treatment
1. Primary endodontic lesions alone. This is exemplified in Fig. 52 .5, a preoperative radio graph
2. Primary periodontal lesions of an "independent" endodontic-periodontic lesion (Case 1)
3. Primary endodontic lesion with secondary periodontal in- shows an apical radiolucency spanning the entire length of the
volvement distal root of tooth #36 and moderate bone loss at the mesial
4. Primary periodontal lesion with secondary endodontic aspect. On completion of endodontic therapy, the periodontal
involvement breakdown around the distal root completely resolved, whereas
5. True combined lesion the mesial bony defect remained unchanged. Case 2 shows a
"combined" endodontic-periodontic lesion involving extensive
Treatment Considerations apical defects around the apices of tooth #36 and a periodontal
defect in the bifurcation. After successful endodontic therapy
of Endodontic-Periodontic Lesions alone, the apical lesions and the furcation defect have resolved,
In managing the lesions of pulpal or periodontal origin, mak- but incomplete healing is noted in the coronal aspect of the
ing an accurate diagnosis as to the source of infection is a furcation. This finding presumes that the unhealed defect origi-
critical determinant of the treatment outcome. Primary pulpal nates from a primary periodontal infection.
lesions combined with secondary periodontal defects would Therefore, endodontic-periodontic lesions require both
completely resolve by conventional RCT alone. Fig. 52.3 endodontic and periodontal therapies for complete healing
shows a chronic pulpal infection associated with a necrotic to occur. This is true whether the endodontic-periodontic
pulp that led to a periodontal defect via the apical foramen. lesions are independent or combined. One important con-
This is a classic example of primary pulpal infection caus- sideration is the sequence of therapies: Which of the two
ing a secondary periodontal defect. In this case, RCT alone should be performed first? As discussed earlier, endodontic
led to complete resolution of the chronic apical periodontitis lesions are often associated with more pronounced symptoms
than periodontal lesions. More importantly, in combined encountered conditions result in the progression of the dis-
endodontic-periodontic lesions, some periodontal defects ease, continued loss of bone and periodontal attachment ap-
will resolve on completion of the endodontic treatment, paratus, a poor prognosis, and possible loss of the tooth.
whereas the opposite would not be the case. After resolution
of the secondary periodontal defect stemming from a primary
pulpal infection, the residual periodontal disease may be more
Conclusion
accurately and predictably managed. These considerations in- Bacterial-induced inflammations of the pulpal and periodon-
dicate that combined endodontic-periodontic lesions are best tal tissues often occur together. Endodontic lesions are more
treated by first performing the necessary endodontic treat- likely to spread to surrounding periodontal tissues with sub-
ment followed by periodontal therapy sequent bone and tissue destruction compared to the less
When patients present with an abscess, the periodontal frequent involvement of periodontal infections on the pulpal
and apical abscesses are managed differently. Previous studies tissues resulting in a retrograde pulpitis.
have suggested that the treatment of the patient with an acute The etiology and diagnosis of dental abscesses are based
periodontal abscess should be performed in two stages. In the on patient history and clinical and radiographic findings.
first stage, the management of the acute lesion is performed. Pulpal pathosis often results in significant pain to thermal
In the second stage, a more comprehensive treatment of the stimuli, tissue swelling, or may be totally asymptomatic. Ra-
original and any residual lesions are accomplished. The man- diographic evaluation may demonstrate a circumscribed peri-
agement of the acute periodontal abscess involves establishing apical lesion when the tooth tests necrotic and the origin of
drainage via the periodontal pocket and subgingival scaling the lesion is pulpal. Vitality testing can detect changes of sen-
and root planning. sation caused by pulpal inflammation and necrosis. If there
Curettage of the epithelium lining, the pocket, and sur- is evidence of pulpal disease and the possibility of associated
rounding connective tissue is then accomplished followed by periodontal bone loss, the endodontic treatment should be
compression of the pocket wall. If the swelling is large and completed first and then the patient should be reevaluated.
fluctuant, flap surgery or incision and drainage may be neces- In many cases, apparent periodontal pathology, including
sary to relieve the pressure. In cases in which the bone loss bone loss, suppuration, and pocket depth resolves if there
is too extensive and the prognosis for the tooth is hopeless, has been a pulpal lesion that has been successfully treated
extraction may be required. endodontically.
Rationale use of antibiotics should be considered in acute Residual periodontal problems can be treated after comple-
periodontal abscesses. The use of systemic antibiotics may tion of successful endodontic treatment and, in many cases, suc-
be indicated when patients have elevated temperatures, eel- cessful regeneration of periodontal defects is possible in end-
lulitis, or systemic disease, and are immunocompromised. In odontically treated teeth. Knowledge of these two disciplines is
the management of acute apical abscesses, the abscess should necessary for a successful treatment outcome for the patient.
first be drained by performing a pulpectomy or incision and
drainage. The choice of which technique to use may be based
on time constraints. Incision and drainage procedures require SUGGESTED READINGS
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141. Takahashi N, Nyvad B: Caries ecology revisited: microbial dynamics tures: value of CT in detection, Radiology 210:545-549, 1999.
and the caries process, Cahes Res 42:409-418, 2008. 171. Zach L, Cohen G: Pulp response to externally applied heat, Oral Surg
14 2. Tamse A, Fuss Z, Lustig J, et al: An evaluation of endodontically treated Oral Med Oral Pathol 19:515-530, 1962.
vertically fractured teeth,] Endod 25:506-508, 1999. 172. Zadik Y, Sandler V, Bechor R, et al: Analysis of factors related to ex-
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53
Periodontal-Restorative
Interrelationships
FM Spear • JP Cooney • PR Melnick • N Ambalavanan
Chapter Outline
Preparation of the Periodontium for Biologic Considerations
Restorative Dentistry Esthetic Tissue Management
Rationale for Therapy Occlusal Considerations in Restorative
Sequence of Treatment Therapy
Control of Active Disease Conclusions
Preparation of the Periodontium Noninflamed, healthy tissues are less likely to change (eg,
shrink) as a result of subgingival restorative treatment or
for Restorative Dentistry postrestoration periodontal care. In addition, tissues that
Periodontal health is a prerequisite for successful comprehen- do not bleed during restorative manipulation allow for a
sive dentistry. To achieve the long-term therapeutic targets of more predictable restorative and esthetic result.
comfort, good function, treatment predictability, longevity, 2. Certain periodontal procedures are designed to provide
and ease of restorative and maintenance care, active periodon- for adequate tooth length for retention, access for tooth
tal infection must be treated and controlled before the initia- preparation, impression making, tooth preparation, and
tion of restorative, esthetic, and implant dentistry. In addition, finishing of restorative margins in anticipation of restor-
the residual effects of periodontal disease or anatomic aberra- ative dentistry. Failure to complete these procedures before
tions inconsistent with realizing and maintaining long-term restorative care can add to the complexity of treatment and
stability must be addressed. More recently, this phase of treat- introduce unnecessary risk of failure.
ment includes techniques performed in anticipation of esthet- 3. Periodontal therapy should antecede restorative care be-
ic or implant dentistry, such as clinical crown lengthening, cause the resolution of inflammation may result in the re-
covering denuded roots, alveolar ridge retention or augmenta- positioning of teeth or in soft-tissue and mucosa! changes.
tion, and implant site development. Failure to anticipate these changes may interfere with pros-
The relationship between periodontal health and the resto- thetic designs planned or constructed before periodontal
ration of teeth is intimate and inseparable. For restorations to treatment.
survive long term, the periodontium must remain healthy so 4. Traumatic forces placed on teeth with ongoing periodon-
that the teeth are maintained. For the periodontium to remain titis may increase tooth mobility, discomfort, and possibly
healthy, restorations must be critically managed in several ar- the rate of attachment loss. Restorations constructed on
eas so that they are in harmony with their surrounding peri- teeth free of periodontal inflammation, synchronous with
odontal tissues. To maintain or enhance the patient's esthetic a functionally appropriate occlusion, are more compatible
appearance, the tooth-tissue interface must present a healthy with long-term periodontal stability and comfort.
natural appearance, with gingival tissues framing the restored 5. Quality, quantity, and topography of the periodontium
teeth in a harmonious manner. may play important roles as structural defense factors in
maintaining periodontal health. Orthodontic tooth move-
ment and restorations completed without the benefit of
Rationale for Therapy periodontal treatment designed for this purpose may be
subject to negative changes that complicate construction
The many reasons for establishing periodontal health before
and future maintenance.
performing restorative dentistry include the following:
6. Successful esthetic and implant procedures may be diffi-
1. Periodontal treatment is undertaken to ensure the establish- cult or impossible without the specialized periodontal pro-
ment of stable gingival margins before tooth preparation. cedures developed for this purpose.
623
pockets (> 5 mm), plaque control measures alone are insuf-

ficient in resolving subgingival infection and inflammation.
CONTROL OF ACTIVE DISEASE

1. Emergency treatment
2. Extraction of hopeless teeth Scaling and root planing combined with oral hygiene mea-
3. Oral hygiene instructions sures have been demonstrated to significantly reduce gingi-
4. Scaling and root planing val inflammation and the rate of progression of periodontitis.
5. Reevaluation
This applies even to patients with deep periodontal pockets.
6. Periodontal surgery
7. Adjunctive orthodontic therapy
PREPROSTHETIC SURGERY Reevaluation
1. Management of mucogingival problems After 4 weeks the gingival tissues are evaluated to determine
2. Preservation of ridge morphology after tooth extraction oral hygiene adequacy, soft-tissue response, and pocket depth
3. Crown-lengthening procedures (see Chapter 34). This permits sufficient time for healing, re-
4. Alveolar ridge reconstruction
duction in inflammation and pocket depths, and gain in clini-
cal attachment levels. In deeper pockets (>5 mm), however,
plaque and calculus removal is often incomplete, with risk of
future breakdown. As a result, periodontal surgery to access
Sequence of Treatment the root surfaces for instrumentation and to reduce periodon-
tal pocket depths must be considered before restorative care
Treatment sequencing should be based on logical and may proceed.
evidenced-based methodologies, taking into account not only
the disease state encountered but also the psychologic and es-
Periodontal Surgery
thetic concerns of the patient. Because periodontal and restor-
ative therapy is situational and specific to each patient, a plan Periodontal surgery may be required for some patients. This
must be adaptable to change depending on the variables en- should be undertaken with future restorative and implant
countered during the course of treatment. For example, teeth dentistry in mind. Some procedures are intended to treat ac-
initially determined to be salvageable may be judged "hope- tive disease successfully, and some are aimed at the prepara-
less," thus altering the established treatment scheme. tion of the mouth for restorative or prosthetic care.
Generally, the preparation of the periodontium for restor-
ative dentistry can be divided into two phases: (1) control of
Adjunctive Orthodontic Therapy
periodontal inflammation with nonsurgical and surgical ap-
proaches and (2) preprosthetic periodontal surgery (Box 53 .1). Orthodontic treatment has been shown to be a useful ad-
junctive to periodontal therapy. It should be undertaken
Control of Active Disease only after active periodontal disease has been controlled.
If nonsurgical treatment is sufficient, definitive periodontal
Periodontal therapy is intended to control active disease. In pocket therapy may be postponed until after the comple-
addition to the removal of root surface accretions that are pri- tion of orthodontic tooth movement. This allows for the
mary etiologic agents, secondary local factors, such as plaque- advantage of the positive bone changes that orthodontic
retentive overhanging margins and untreated caries, must be therapy can provide. However, deep pockets and furcation
addressed. invasions may require surgical access for root instrumenta-
tion in advance of orthodontic tooth movement. Failure to
Emergency Treatment control active periodontitis can result in acute exacerbations
and bone loss during tooth movement. As long as they are
Emergency treatment is undertaken to alleviate symptoms periodontally healthy, teeth with preexisting bone loss may
and stabilize acute infection. This includes endodontic as well be moved orthodontically without incurring additional at-
as periodontal conditions. tachment loss.
Soft tissue-grafting procedures are often indicated in an-
Extraction of Hopeless Teeth ticipation of orthodontic therapy to increase the dimension of
attached tissue.
Extraction of hopeless teeth is followed by provisionalization
with fixed or removable prosthetics. Retention of hopeless
teeth without periodontal treatment may result in bone loss Biologic Considerations
on adjacent teeth. Restorative margins are refined and provi- Margin Placement and Biologic Width
sional restorations refitted after the completion of active peri-
odontal therapy. One of the most important aspects of understanding the
periodontal-restorative relationship is the location of the re-
storative margin to the adjacent gingival tissue. Restorative
Oral Hygiene Measures
clinicians must understand the role of biologic width in pre-
Oral hygiene measures, when properly applied, have been serving healthy gingival tissues and controlling the gingival
shown to reduce plaque scores and gingival inflammation form around restorations. They must also apply this informa-
(see Chapter 35). However, in patients with deep periodontal tion in the positioning of restoration margins, especially in the
53 Periodontal-Restorative Interrelationships 624.el
FIGURE 53.1 Connective tissue graft placed under a double-papilla flap has been used to provide root coverage for a maxillary right canine.
A, Maxillary canine before therapy. B, Connective tissue graft placed over denuded root surface. C, Papilla placed over connective tissue. D, Final
result.
Preprosthetic Surgery has shown an average depth of 0.69 mm (Fig. 53 3) It has

been theorized that infringement on the biologic width by
Management of Mucogingival Problems the placement of a restoration within its zone may result
in gingival inflammation, pocket formation, and alveolar
Periodontal plastic surgical procedures may be undertaken for bone loss (Fig. 53.4). Consequently, it is recommended that
a variety of reasons. The most common techniques include there be at least 3.0 mm between the gingival margin and
those that increase gingival dimensions and achieve root cov- bone crest. This allows for adequate biologic width when
erage. These procedures are often indicated before restoration the restoration is placed 0.5 mm within the gingival sulcus
for prosthetic reasons and in conjunction with orthodontic (Fig. 53 5).
tooth movement. Root coverage procedures may also be un- Surgical crown lengthening may include the removal of
dertaken for purposes of comfort and esthetics (Fig. 53.1). soft tissue or both soft tissue and alveolar bone. Reduction of
At least 2 months of healing is recommended after soft- soft tissue alone is indicated if there is adequate attached gin-
tissue grafting procedures before initiating restorative den- giva and more than 3 mm of tissue coronal to the bone crest
tistry. (Fig. 53 6). This may be accomplished by either gingivectomy
or flap technique. Inadequate attached gingiva and less than
Preservation of Ridge Morphology after 3 mm of soft tissue require a flap procedure and bone recon-
touring (Fig. 53. 7). In the case of caries or tooth fracture, to
Tooth Extraction
ensure margin placement on sound tooth structure and re-
Alveolar ridge resorption is a common consequence of tooth tention form, the surgery should provide at least 4 mm from
loss. Ridge preservation procedures have been shown to be the apical extent of the caries or fracture to the bone crest
useful in anticipation of the future placement of a dental im- (Fig. 53.8).
plant or pontic, as well as in cases where unaided healing With the advent of predictable implant dentistry, it is im-
would result in an unesthetic deformity. portant to weigh carefully the value of crown lengthening for
restorative ease as opposed to tooth removal and replacement
with a dental implant (Box 53 2).
Crown-Lengthening Procedures
Surgical crown-lengthening procedures are performed to Alveolar Ridge Reconstruction
provide retention form to allow for proper tooth prepara-
tion, impression procedures, and placement of restorative Patients are frequently seen after tooth loss and alveolar ridge
margins (Fig. 53 2) and to adjust gingival levels for esthet- resorption have occurred. To provide for adequate anatomic
ics. It is important that crown-lengthening surgery is done in dimensions for the construction of an esthetic pontic or the
such a manner that the biologic width is preserved. The bio- placement of dental implants, alveolar ridge reconstruction is
logic width is defined as the physiologic dimension of the undertaken. In the case of esthetic pontic construction, small
junctional epithelium and connective tissue attachment. defects may be treated with soft-tissue ridge augmentation
This measurement has been found to be relatively constant (Fig. 53.9). For larger defects and in those sites receiving den-
at approximately 2 mm (±30%). The healthy gingival sulcus tal implants, hard tissue modalities are used.
FIGURE 53.2 Surgical crown lengthening has provided these otherwise unrestorable mandibular molars with improved retention and restor-
ative access for successful restorations. A, Before crown lengthening. B, Crown-lengthening surgery completed. Note increased clinical crown.
C, Buccal view after surgery. D, Final restorations.
Gingival sulcus
0.69 mm
Biologic Junctional
width epithelium
2.04 mm 0.97 mm
Connective tissue
attachment
1.07 mm
Periodontal __...__-1
ligament
Cementum
FIGURE 53.4 Importance of considering infringement of biologic

FIGURE 53.3 Estimation of biologic width that comes out to be width must even though gingival inflammation around crowns may have
about 2 mm. Efforts should be made to preserve its integrity. a variety of causes.
53 Periodontal-Restorative Interrelationships 624.e3
Gingival sulcus Bone Bone

0.69 mm
FIGURE 53.7 With less than 3 mm of soft tissue between the bone
Junctional and gingival margin, or less-than-adequate attached gingiva, a flap
Biologic epithelium procedure and osseous recontouring are required for crown length-
width 0.97 mm ening.
2.04 mm . r
Connective issue
attachment
1.07 mm
Periodontal
a1---.--- ---1'!:i:\
-j
f \ Bone
ligament
FIGURE 53.5 Placement of the restorative margin 0.5 mm into the

sulcus, which allows for the maintenance of the biologic width.
Bone
FIGURE 53.8 In the case of caries or fracture, at least 1 mm of sound
tooth structure should be provided above the gingival margin for
proper restoration.
fJ
}mm __O INDICATIONS
Lengthening
1. Subgingival caries or fracture.

2. Inadequate clinical crown length for retention.
3. Unequal or unesthetic gingival heights.
CONTRAINDICATIONS
1. Surgery would create an unesthetic outcome.
Bone 2. Deep caries or fracture would require excessive bone
FIGURE 53.6 Greater than 3 mm of soft tissue between the bone removal on contiguous teeth.
and gingival margin, with adequate attached gingiva, allowing crown 3. The tooth is a poor restorative risk.
lengthening by gingivectomy.
FIGURE 53.9 A, Loss of the maxillary left central incisor has resulted in an unesthetic alveolar ridge defect. B-E, An incision is made at ridge crest,
a pouch is created, and a soft tissue graft harvested from the palate is placed into the pouch. F-H, A removable appliance with an ovate pontic is
placed in light contact with the grafted site. Swelling around the pontic apex results in a tissue concavity from which the more natural-appearing final
restoration emerges.
53 Periodontal-Restorative Interrelationships 625
esthetic zone where a primary treatment goal is to mask the

junction of the margin with the tooth.
A clinician is presented with three options for margin place-
ment: supragingival, equigingival (even with the tissue), and
subgingival. The supragingival margin has the least impact on
the periodontium. Classically, this margin location has been
applied in unesthetic areas because of the marked contrast
in color and opacity of traditional restorative materials against
the tooth. With the advent of more translucent restorative
materials, adhesive dentistry, and resin cements, the ability to
place supragingival margins in esthetic areas is now a real-
ity. Therefore, whenever possible, these restorations should be
chosen not only for their esthetic advantages but also for their
FIGURE 53.10 Ramifications of a biologic width violation if a re-
favorable periodontal impact.
storative margin is placed within the zone of the attachment. On the
The use of equigingival margins traditionally was not desir- mesial surface of the left central incisor, bone has not been lost, but
able because they were thought to retain more plaque than gingival inflammation occurs. On the distal surface of the left central
supragingival or subgingival margins and therefore result in incisor, bone loss has occurred, and a normal biologic width has been
greater gingival inflammation. There was also the concern that reestablished.
any minor gingival recession would create an unsightly mar-
gin display. These concerns are not valid today not only be- biologic width. Two different responses can be observed from
cause the restoration margins can be esthetically blended with the involved gingival tissues (Fig. 53 10).
the tooth but also because restorations can be finished easily One possibility is that bone loss of an unpredictable nature
to provide a smooth, polished interface at the gingival margin. and gingival tissue recession occurs as the body attempts to
From a periodontal viewpoint, both supragingival and equig- recreate room between the alveolar bone and the margin to
ingival margins are well tolerated. allow space for tissue reattachment. This is more likely to oc-
The greatest biologic risk occurs when placing subgingival cur in areas in which the alveolar bone surrounding the tooth
margins. These margins are not as accessible as supragingival is very thin in width. Trauma from restorative procedures can
or equigingival margins for finishing procedures. In addition, play a major role in causing this fragile tissue to recede. Other
if the margin is placed too far below the gingival tissue crest, factors that may impact the likelihood of recession include (1)
it violates the gingival attachment apparatus. whether the gingiva is thick and fibrotic or thin and fragile
The dimension of space that the healthy gingival tissues and (2) whether the periodontium is highly scalloped or flat
occupy between the base of the sulcus and the underlying in its gingival form. It has been found that highly scalloped,
alveolar bone is comprised of the junctional epithelial attach- thin gingiva is more prone to recession than a flat periodon-
ment and the connective tissue attachment. The combined at- tium with thick fibrous tissue.
tachment width is now identified as the biologic width. It was The more common finding with deep margin placement is
found that, in the average human, the connective tissue at- that the bone level appears to remain unchanged, but gingival
tachment occupies 1.07 mm of space above the crest of the inflammation develops and persists. To restore gingival tissue
alveolar bone and that the junctional epithelial attachment be- health, it is necessary to establish space clinically between the
low the base of the gingival sulcus occupies another 0.97 mm alveolar bone and the margin. This can be accomplished ei-
of space above the connective tissue attachment. The combi- ther by surgery to alter the bone level or by orthodontic ex-
nation of these two measurements, averaging approximately trusion to move the restoration margin farther away from the
1 mm each, constitutes the biologic width. bone level.
The biologic, or attachment, width can be identified for
the individual patient by probing to the bone level (referred Biologic Width Evaluation
to as "sounding to bone") and subtracting the sulcus depth
from the resulting measurement. This measurement must be Radiographic interpretation can identify interproximal viola-
done on teeth with healthy gingival tissues and should be re- tions of biologic width. However, with the more common
peated on more than one tooth to ensure an accurate assess- locations on the mesiofacial and distofacial line angles of
ment. The technique allows the variations in sulcus depths teeth, radiographs are not diagnostic because of tooth su-
found in individual patients to be assessed and factored into perimposition. If a patient experiences tissue discomfort
the diagnostic evaluation. The information obtained is then when the restoration margin levels are being assessed with
used for definitive diagnosis of biologic width violations, the a periodontal probe, it is a good indication that the margin
extent of correction needed, and the parameters for placement extends into the attachment and that a biologic width viola-
of future restorations. tion has occurred.
Restorative considerations frequently dictate the placement A more positive assessment can be made clinically by
of restoration margins beneath the gingival tissue crest. Res- measuring the distance between the bone and the restora-
torations may need to be extended gingivally (1) to create ad- tion margin using a sterile periodontal probe. The probe is
equate resistance and retentive form in the preparation, (2) to pushed through the anesthetized attachment tissues from
make significant contour alterations because of caries or other the sulcus to the underlying bone. If this distance is less than
tooth deficiencies, or (3) to mask the tooth-restoration inter- 2 mm at one or more locations, a diagnosis of biologic width
face by locating it subgingivally. When the restoration margin violation can be confirmed. This assessment is completed
is placed too far below the gingival tissue crest, it impinges circumferentially around the tooth to evaluate the extent of
on the gingival attachment apparatus and create a violation of the problem.
Correcting Biologic Width Violations violation is across the facial surface and the gingival tissue lev-
el is correct, orthodontic extrusion is indicated. The extrusion
Biologic width violations can be corrected either by surgically can be performed in two ways. (1) By applying low orthodon-
removing bone away from proximity to the restoration margin tic extrusion force, the tooth will erupt slowly, bringing the
or by orthodontically extruding the tooth and thus moving alveolar bone and gingival tissue with it. The tooth is extruded
the margin away from the bone. Surgery is the more rapid of until the bone level has been carried coronal to the ideal level
the two treatment options. It is also preferred if the resulting by the amount that needs to be removed surgically to correct
crown lengthening creates a more pleasing tooth length. In the attachment violation. The tooth is stabilized in this new
these situations, the bone should be moved away from the position and then is treated with surgery to correct the bone
margin by the measured distance of the ideal biologic width and gingival tissue levels. Another option is to perform rapid
for that patient, with an additional 0.5 mm of bone removed orthodontic extrusion where the tooth is erupted to the de-
as a safety zone. sired amount over several weeks. During this period, a supra-
There is a potential risk of gingival recession after removal crestal fiberotomy is performed circumferentially around the
of bone. If interproximal bone is removed, there is a high like- tooth weekly in an effort to prevent the tissue and bone from
lihood of papillary recession and the creation of an unesthetic following the tooth. The tooth is then stabilized for at least
triangle of space below the interproximal contacts. If the bio- 12 weeks to confirm the position of the tissue and bone, and
logic width violation is on the interproximal side, or if the any coronal creep can be corrected surgically.
Margin Placement Guidelines dentist, which forces the technician to produce a bulky resto-
ration to provide room for the restorative material. In areas of
When determining where to place restorative margins rela- the mouth in which esthetic considerations are not critical, a
tive to the periodontal attachment, it is recommended that flatter contour is always acceptable.
the patient's existing sulcular depth be used as a guideline
in assessing the biologic width requirement for that patient.
The base of the sulcus can be viewed as the top of the attach- Subgingival Debris
ment, and therefore the clinician accounts for variations in Leaving debris below the tissue during restorative procedures
attachment height by ensuring that the margin is placed in the can create an adverse periodontal response. The cause can be
sulcus and not in the attachment. The variations in sulcular retraction cord, impression material, provisional material, or
probing depth are then used to predict how deep the mar- either temporary or permanent cement. The diagnosis of de-
gin can safely be placed below the gingival crest. With shal- bris as the cause of gingival inflammation can be confirmed
low probing depths (1.0-1.5 mm), extending the preparation by examining the sulcus surrounding the restoration with an
more than 0.5 mm subgingivally risks violating the attach- explorer, removing any foreign bodies, and then monitoring
ment. This assumes that the periodontal probe will penetrate the tissue response. It may be necessary to provide tissue an-
into the junctional epithelial attachment in healthy gingiva an esthesia for patient comfort during the procedure.
average of 0.5 mm. With shallow probing depths, future re-
cession is unlikely because the free gingival margin is located
close to the top of the attachment. Deeper sulcular probing Hypersensitivity to Dental Materials
depths provide more freedom in locating restoration margins Inflammatory gingival responses have been reported relat-
farther below the gingival crest. In most circumstances, how- ed to the use of nonprecious alloys in dental restorations.
ever, the deeper the gingival sulcus, the greater is the risk of Typically, the responses have occurred to alloys containing
gingival recession. nickel although the frequency of these occurrences is con-
troversial. Hypersensitivity responses to precious alloys are
Provisional Restorations extremely rare, and these alloys provide an easy solution
to the problems encountered with the nonprecious alloys.
Three critical areas must be effectively managed to produce More importantly, tissues respond more to the differences in
a favorable biologic response to provisional restorations. The surface roughness of the material rather than to the compo-
marginal fit, crown contour, and surface finish of the interim sition of the material. The rougher the surface of the restora-
restorations must be appropriate to maintain the health and tion subgingivally, the greater are the plaque accumulation
position of the gingival tissues during the interval until the and gingival inflammation. In clinical research, porcelain,
final restorations are delivered. Provisional restorations that highly polished gold, and highly polished resin all show
are poorly adapted at the margins, that are overcontoured similar plaque accumulation. Regardless of the restorative
or undercontoured, and that have rough or porous surfaces material selected, a smooth surface is essential on all materi-
can cause inflammation, overgrowth, or recession of gingival als subgingivally.
tissues. The outcome can be unpredictable, and unfavorable
changes in the tissue architecture can compromise the success
of the final restoration. Esthetic Tissue Management
Managing lnterproximal Embrasures
Marginal Fit
Current restorative and periodontal therapy must consider
Marginal fit has clearly been implicated in producing an in- a good esthetic result, especially in the maxillary anterior
flammatory response in the periodontium. It has been shown "esthetic zone." The interproximal papilla is a very impor-
that the level of gingival inflammation can increase corre- tant part in creating this esthetic result. The interproximal
sponding with the level of marginal opening. Margins that are embrasure created by restorations and the form of the in-
significantly open (several tenths of a millimeter) are capable terdental papilla have a unique and intimate relationship.
of harboring large numbers of bacteria and may be respon- The ideal interproximal embrasure should house the gingi-
sible for the inflammatory response seen. However, the qual- val papilla without impinging on it and should also extend
ity of marginal finish and the margin location relative to the the interproximal tooth contact to the top of the papilla so
attachment are much more critical to the periodontium than that no excess space exists to trap food and to be esthetically
the difference between a 20- and a 100-µm fit. displeasing.
Papillary height is established by the level of the bone,
the biologic width, and the form of the gingival embrasure.
Crown Contour
Changes in the shape of the embrasure can impact the height
Restoration contour has been described as extremely impor- and form of the papilla. The tip of the papilla behaves dif-
tant to the maintenance of periodontal health. Ideal contour ferently than the free gingival margin on the facial aspect of
provides access for hygiene, has the fullness to create the de- the tooth. Whereas the free gingival margin averages 3 mm
sired gingival form, and has a pleasing visual tooth contour in above the underlying facial bone, the tip of the papilla aver-
esthetic areas. Evidence from human and animal studies clear- ages 4.5-5.0 mm above the interproximal bone (Fig. 53.31).
ly demonstrates a relationship between overcontouring and This means that if the papilla is farther above the bone than
gingival inflammation, whereas undercontouring produces no the facial tissue but has th e same biologic width, the inter-
adverse periodontal effect. The most frequent cause of over- proximal area will have a sulcus 1.0-1.5 mm deeper than that
contoured restorations is inadequate tooth preparation by the found on the facial surface.
Clinical Procedures in Margin Placement

The first step in using sulcus depth as a guide in margin place-
ment is to manage gingival health. Once the tissue is healthy,
the following three rules can be used to place intracrevicular
margins:
Rule 1: If the sulcus probes 1. 5 mm or less, place the restora-
tion margin 0.5 mm below the gingival tissue crest. This is
especially important on the facial aspect and will prevent a
biologic width violation in a patient who is at high risk in
that regard.
Rule 2: If the sulcus probes more than 1.5 mm, place the mar-
gin half the depth of the sulcus below the tissue crest. This
places the margin far enough below tissue, so that it will
still be covered if the patient is at higher risk of recession. FIGURE 53.12 Depth from the attachment to the level of the prepa-
ration margin is greater than 3 mm. This patient in Figure 53.11 had an
Rule 3: If a sulcus greater than 2 mm is found, especially on altered eruption pattern and a sulcus depth of more than 3 mm when
the facial aspect of the tooth, evaluate to see if a gingivec- these restorations were placed.
tomy could be performed to lengthen the teeth and cre-
ate a 1.5-mm sulcus. Then the patient can be treated using
Rule 1.
The rationale for Rule 3 is that deep margin placement
is more difficult and the stability of the free gingival margin
is less predictable when a deep sulcus exists. Reducing the
sulcus depth creates a more predictable situation in which to
place an intracrevicular margin. The clinician cannot be sure
that the tissue will remain at the corrected level, however, be-
cause some gingival rebound can occur after gingivectomy.
However, sulcular depth reduction ensures that the restorative
margins will not be exposed and visible in the patient's mouth
(Figs. 53 11-5315)
The placement of supragingival or equigingival margins
is simple because it requires no tissue manipulation. With
regard to overall tooth preparation, the amount reduced in-
cisally or occlusally, facially, lingually, and interproximally
is dictated by the choice of restorative materials. Before ex-
tending subgingivally, the preparation should be completed FIGURE 53.13 Two available options to manage treatment appro-
to the free gingival margin facially and interproximally. This priately. (1) place the original margins to half the depth of the sulcus, in
which case the recession that occurred would not have exposed them.
allows the margin of the tooth preparation to be used as
(2) Perform a gingivectomy, creating a 1- to 1.5-mm sulcus. The sec-
a reference for subgingival extension once the tissue is re- ond option was chosen when the restorations were redone. The margins
tracted. were then placed 0.5 mm below the tissue after the gingivectomy (see
Figures 53.12 and 53.14).
FIGURE 53.11 A 78-year-old woman presents with the maxillary an- FIGURE 53.14 At 6 weeks after the gingivectomy and preparation of
terior restorations placed 6 months earlier. She is unhappy with the the teeth. Note the tissue level and that the tissue is rebounding coro-
exposed margins and notes that the margins were covered the day the nally over the margins. This is a common finding when a pure gingivec-
restorations were placed (see Figs. 53.11-53.15). tomy is done.
\~
·~,\ '
\
\\
' I
I
FIGURE 53.15 A 4-year recall photograph after placement of the

final restorations for patient in Figure 53.11. Note the tissue level has FIGURE 53.17 Margin of the preparation extended apically to the
been maintained, with a sulcus depth of 2 mm on the facial surface. top of the retraction cord. This represents the correct placement of the
margin below the previously nonreflected, free gingival margin.
Tissue Retraction
Once the supragingival portion of the preparation is complet-
ed, it is necessary to extend below the tissue. The preparation
margin must now be extended to the appropriate depth in the
sulcus, applying the guidelines presented previously In this
process the tissue must be protected from abrasion, which will
cause hemorrhage and can adversely affect the stability of the
tissue level around the tooth. Access to the margin is also re-
quired for the final impression, with a clean, fluid-controlled
environment. Tissue management is achieved with gingival
retraction cords using the appropriate size to achieve the dis-
placement required. Thin, fragile gingival tissues and shallow
sulcus situations usually dictate that smaller diameter cords be ' ~,
FIGURE 53.18 Placing a second impression cord on top of the first
chosen to achieve the desired tissue displacement.
deflection cord to provide space for impression material. This impres-
For a Rule 1 margin (sulcus depth 1.5 mm or less), the sion cord is placed so that it is between the margin of the preparation
cord should be placed so that the top of the cord is located and the gingiva to create adequate space for impression material after
in the sulcus at the level in which the final margin is to be removal of the cord.
established, which will be 0.5 mm below the previously pre-
pared margin (Fig. 53.16). On the interproximal aspects of tooth so that it does not abrade the tissue (Fig. 53 17) This
the tooth, the cord is usually 1.0-1.5 mm below the tissue process protects the tissue, creates the correct axial reduction,
height because the interproximal sulcus is often 2.5-3.0 mm and establishes the margin at the desired subgingival level. To
in depth. With this initial cord in place, the preparation is create space and allow access for a final impression, it is now
extended to the top of the cord, with the bur angled to the necessary to pack a second retraction cord. The second cord
is pushed so that it displaces the first cord apically and sits
between the margin and the tissue (Fig. 53.18). For the final
impression, only the top cord is removed, leaving the mar-
gins visible and accessible to be recorded with the impression
material (Fig. 53.19). The initial cord remains in place in the
sulcus until the provisional restoration is completed.
As an alternative to additional retraction cords, electrosur-
gery can be used to remove any overlying tissue in the retrac-
tion process. A fine-wire electrode tip is held parallel to the
tooth and against the margin in the sulcus and moved through
the overhanging tissue, opening up the margin and the retrac-
tion cord to visual access (Figs. 53.20-53.23). The electrosur-
gery tip sits on top of the retraction cord in place in the sulcus.
This controls the vertical position of the tip and results in the
removal of the least tissue needed for access.
' ~, For Rule 2 situations in which the sulcus is deeper, two
FIGURE 53.16 Second step in margin placement. This step includes
larger-diameter cords are used to deflect the tissue before ex-
placing a single layer of deflection cord below the previously prepared
margin to the desired final margin level. Here, a single cord has been tending the margin apically (Figs. 53.24-53.26). The top of
placed 0.5 mm below the previously prepared margin. the second cord is placed to identify the final margin location
53 Periodontal-Restorative Interrelationships 626.e3
\
',
FIGURE 53.19 Ideal situation after removal of impression cord. The
deflection cord is still in place maintaining the open sulcus but has been
displaced apically another 0.5 mm by the placement of the impression FIGURE 53.22 Using electrosurgery, the fine-wire electrode tip held
cord, exposing tooth structure apical to the margin so that it can be parallel to the tooth preparation and rests on the cord as the tip is
captured in the impression. moved around the tooth.
FIGURE 53.20 Deflection cord and impression cord are in place. The
soft tissue is falling over the margins of the preparation. In this situation,
FIGURE 53.23 After removal of the impression cord, an adequate
if the impression cord were removed, the impression would not capture
space is created for the impression material, with no soft tissue over-
the margins in the areas in which the tissue is overhanging.
hanging the margins to trap or tear the impression material. Note the
first cord, or deflection cord, is still in place.
FIGURE 53.21 Overhanging tissue has been removed and space cre-
ated for the impression material with electrosurgery. Note that the de-
flection cord and the impression cord are still in place. The impression •.. .. I
cord is now visible completely around the tooth, allowing easy access FIGURE 53.24 First step in margin placement for the patient with
for the impression material to the margin after removal of the impression altered eruption or a deep sulcus is to prepare to the existing free
cord. gingival margin, as in the "Rule 111 patient (see text).
at the correct distance below the previously prepared margin,

which was at the gingival tissue crest level. The margin is low-
ered to the top of the second cord (Fig. 53 27), then a third
cord is placed in preparation for the impression (Figs. 53.28
and 53.29). In the patient with a deep sulcus in which the
margin may be 1.5-2.0 mm below the tissue crest, electrosur-
gery is often required to remove overhanging tissue. To avoid
altering the gingival tissue height, it is important to hold the
electrosurgery tip parallel to the preparation (Fig. 53 30)
' ,,
FIGURE 53.27 Preparation is now extended to the top of the second
deflection cord, finalizing margin location.
',
FIGURE 53.25 Second step for the patient with altered eruption is to
place the deflection cord. Note that the placement of a single deflection
cord does not provide adequate deflection of the tissue to allow the mar-
gin to be carried below tissue without abrading the gingiva with the bur. ' ',
FIGURE 53.28 After extension of the margin to the top of the deflec-
tion cord, a third layer of cord is applied that will act as the impression
cord. This impression cord should be placed so that it fits between the
free gingival margin and the margin of the preparation. Its placement will
also apically displace the two previously positioned deflection cords.
I
1, I
I, I
I:
\\.t ,' '\
',
FIGURE 53.26 Third step for the patient with altered eruption and a ' ',
deep sulcus is to place a second, larger-diameter deflection cord on FIGURE 53.29 Removal of the impression cord creates an adequate
top of the first deflection cord. Combined, these two cords allow ad- space for the impression material to capture the margin and 0.5 mm
equate deflection to open up the sulcus so that the margin can be carried of tooth structure below the margin in which the impression cord had
below tissue without abrading the gingiva. displaced the first two cords.
53 Periodontal-Restorative Interrelationships 626.eS
(A)
(B)
FIGURE 53.30 If it is necessary to use electrosurgery, either in the
normal or altered-eruption patient, the correct inclination of the elec-
trosurgery tip is important. A, Electrosurgery tip being held parallel to
the preparation and resting on the previously placed retraction cord. This
removes a minimal amount of tissue, and the presence of the retraction
cord protects the attachment from the electrosurgery. B, Incorrect incli-
nation of electrosurgery tip. The tip is leaning away from the preparation.
This inclination results in excess tissue removal.
Bone _
scallop
3.0 mm avg.
1 - _,_ -r- Soft tissue
scallop
4.5 mm avq,
--------~ .
(A) (B)
FIGURE 53.32 Relationship between gingival embrasure volume and
papillary form. A, gingival embrasure of the teeth is excessively large as
FIGURE 53.31 Comparison of the behavior of the interproximal pa- the result of a tapered tooth form. Because of the large embrasure form,
pilla relative to bone and the free gingival margin relative to bone in the volume of tissue sitting on top of the attachment is not molded to the
the average human. There is a 3-mm scallop from the facial bone to the shape of a normal papilla but rather has a blunted form and a shallower
interproximal bone. However, on average, a 4.5- to 5.0-mm gingival sulcus. B, Ideal tooth form in which the same volume of tissue sits on top
scallop exists between the facial tissue height and the interproximal pa- of the attachment as in A. Because of the more closed embrasure form
pilla height. This extra scallop of 1.5-2.0 mm of gingiva compared with from the teeth in B, however, the papilla completely fills the embrasure
bone is the result of the extra soft-tissue height above the attachment and has a deeper sulcus, averaging 2.5-3.0 mm. Note that the ideal
interproximal ly. contact position is 3 mm coronal to the attachment.
When the gingival level of the interproximal tooth contacts the facial and lingual, form a col, and become inflamed. This
measured 5 mm or less to the alveolar bone, the papilla al- information is applied when evaluating an individual papilla
ways filled the space. When the contact was 6 mm from bone, with an open embrasure. The papilla in question is compared
only 56% of the papillae could fill the space. Finally, when the to the adjacent papillae. If the papillae are all on the same
contact was 7 mm from bone, only 37% of the papillae could level, and if the other areas do not have open embrasures, the
fill the spaces. problem is one of gingival embrasure form. If the papilla in
Knowing that there is individual variability to the required the area of concern is apical to the adjacent papillae, however,
biologic width, this information relative to the papilla is ap- the clinician should evaluate the interproximal bone levels.
plied by locating the lowest point of the interproximal contact If the bone under that papilla is apical to the adjacent bone
in relation to the top of the epithelial attachment. The ideal levels, the problem is caused by bone loss. If the bone is at
contact should be 2-3 mm coronal to the attachment, which the same level, the open embrasure is caused by the embra-
coincides with the depth of the average interproximal sul- sure form of the teeth and not a periodontal problem with the
cus. As in assessing the facial tissues for margin location, this papilla.
technique requires that the tissue is healthy to allow accurate
probing. If the sulcus measures greater than 3 mm, there is
some risk of papillary recession with restorative procedures. Pontic Design
The clinician most frequently confronts a normal or shal- Classically, there are four options to consider in evaluating
low sulcus with a papilla that appears too short rather than a pontic design: sanitary, ridge-lap, modified ridge-lap, and
tall papilla with a deep sulcus. Management of this situation is ovate designs (Fig. 53.34). Regardless of design, the pontic
best approached by viewing the papilla as a balloon of a cer- should provide an occlusal surface that stabilizes the oppos-
tain volume that sits on the attachment. This balloon of tissue ing teeth, allows for normal mastication, and does not over-
has a form and height dictated by the gingival embrasure of load the abutment teeth. The restorative material for all four
the teeth. With an embrasure that is too wide, the balloon flat- designs can be glazed porcelain, polished gold, or polished
tens out, assumes a blunted shape, and has a shallow sulcus resin. The biologic response of the tissue in contact with the
(Fig. 53.32). restoration is no different in regard to the material chosen, as
If the embrasure is the ideal width, the papilla assumes long as it has a smooth surface finish.
a pointed form, has a sulcus of 2.5-3.0 mm, and is healthy. The key differences between the four pontic designs re-
If the embrasure is too narrow, the papilla may grow out to late to the esthetics and access for hygiene procedures. The
(A) (B) (C) (D)

FIGURE 53.34 Four options to designing the shape of a pontic. A, Sanitary pontic. tissue surface of the pontic is 3 mm from the underlying ridge.
B, Ridge-lap pontic. Tissue surface of the pontic straddles the ridge in saddlelike fashion. The entire tissue surface of the ridge-lap pontic is convex and
very difficult to clean. C, Modified ridge-lap pontic. Tissue surface on the facial is concave, following the ridge. However, the lingual saddle has been
removed to allow access for oral hygiene. D, Ovate pontic. The pontic form fits into a receptor site within the ridge. This allows the tissue surface of
the pontic to be convex and also optimizes esthetics.
Correcting Open Gingival Embrasures

Restoratively
There are two causes of open gingival embrasures: (1) the
papilla is inadequate in height because of bone loss or (2)
the interproximal contact is located too high coronally. If a
high contact has been diagnosed as the cause of the problem,
there are two potential reasons. If the root angulation of the (B) (C)
teeth diverges, the interproximal contact is moved coronally,
resulting in the open embrasure. However, if the roots are FIGURE 53.33 Methods of altering gingival embrasure form. A, Typi-
cal open gingival embrasure caused by excessively tapered tooth form.
parallel, the papilla form is normal, and an open embrasure B, Common method employed by restorative dentists to correct the
exists, then the problem is probably related to tooth shape, embrasure, in which material is added supragingivally. This closes the
specifically an excessively tapered form. Restorative dentistry embrasure by moving the contact to the tip of the papilla but results in
can correct this problem by moving the contact point to the overhangs that cannot be cleaned using dental floss. Removing these
overhangs restoratively reopens the embrasure. C, Correct method of
tip of the papilla. To accomplish this, the margins of the res-
closing the gingival embrasure, in which the margins of the restoration
toration must be carried subgingivally 1.0-1.5 mm, and the are carried 1 .0-1 .5 mm below the tip of the pap ii la. Note that this does
emergence profile of the restoration is designed to move the not encroach on the attachment because the average interproximal sul-
contact point toward the papilla while blending the contour cus probes 2.5-3.0 mm. This allows easy cleaning because of the convex
into the tooth below the tissue (Fig. 53.33). This can be ac- profile. It also reshapes the papilla to a more pleasing profile esthetically.
complished easily with direct bonded restorations because
the soft tissue can clearly be seen. For indirect restorations, interproximal contacts apically toward the papilla to eliminate
the desired restoration contours and embrasure form should the presence of large, open embrasures. With multiple-unit
be established in the provisional restorations, and the gin- restorations, it is also possible with tissue-colored ceramics
gival tissues are allowed to adapt for 4-6 weeks before the to bake porcelain papillae directly on the restoration. In the
tissue contour information is relayed to the laboratory for use posterior areas where the interroot widths are significantly
in the final restorations. greater, it is often impossible to carry the proximal contacts
to contact the tissue without creating large overhangs on the
Managing Gingival Embrasure Form restorations. In these situations, the contact should be moved
far enough apically to minimize any large food traps while still
for Patients with Gingival Recession
leaving an embrasure of a convenient size to be accessed with
Management of the gingival embrasure form for patients who an interdental brush for hygiene. It should be noted that de-
have experienced gingival recession varies, depending on veloping excessively long interproximal contacts, whether on
whether the treatment is in the anterior or posterior regions anterior or posterior teeth, always creates rectangular, some-
of the mouth. In esthetic areas, it is necessary to carry the what unesthetic, tooth forms.
-y Pontic to bone
minimum of
--~- 2 mm
Receptor tapers _,
- - .1 Receptor
1-1.5
site
mm
lo level of tissue deep in esthetic
on the palate for areas
ease of hygiene.
FIGURE 53.36 Option for creating an ovate pantie receptor site in

less esthetic areas of the mouth. Rather than creating the receptor site
FIGURE 53.35 Ideal shape and form of an ovate pantie in the es- so that the pontic extends into the ridge, it is possible to create a flat-
thetic area. The receptor site has been created 1.0-1.5 mm apical to the tened receptor site in which the pontic sits flush with the ridge. This
free gingival margin on the facial aspect. This creates the illusion of the facilitates oral hygiene.
pontic erupting from the tissue. On the palatal side, the pontic is tapered
so that the receptor site is not extended below tissue; this allows easier
access for oral hygiene. Note that when the receptor site is created, the dentist wanting a high degree of predictability in the final re-
bone must be a minimum of 2 mm from the most apical portion of the sult, understanding occlusion is critical. The clinician must
pontic. know how to create an occlusion, with the following guide-
lines as a goal:
1. There should be even, simultaneous contacts on all teeth
primary method for cleaning the undersurface of panties is to during centric closure. This distributes the force of closure
draw dental floss mesiodistally along the undersurface. The over all the teeth instead of the few teeth that may touch
shape of this undersurface determines the ease with which first.
plaque and food debris can be removed in the process. The 2. When the mandible moves from centric closure, some
sanitary and ovate panties have convex undersurfaces, which form of canine or anterior guidance is desirable, with no
makes them easiest to clean. The ridge-lap and modified posterior tooth contacts. This combination of anterior
ridge-lap designs have concave surfaces, which are more diffi- guidance and posterior disclusion reduces the ability of
cult to access with the dental floss. Although the sanitary pan- the elevator muscles to contract and distributes the force
tie design provides the easiest access for hygiene procedures, of the movement onto the anterior teeth, which receive less
it is rarely used because of its unesthetic form and a variable force because of the Class-III lever system being applied
acceptance of the open contour by patients. in this situation. It has been shown that, as a result of the
The ovate pantie is the ideal pantie form. It is created by Class-III lever action, the anterior teeth receive approxi-
forming a receptor site in the edentulous ridge with a dia- mately one-ninth the force of a second molar.
mond bur or by electrosurgery. The site is shaped to create 3. The anterior guidance needs to be in harmony with the
either a flat or a concave contour so that when the pantie is patient's neuromuscular envelope of function. Harmony of
created to adapt to the site, it will have a flat or convex out- this relationship is demonstrated by a lack of fremitus and
line. The depth of the receptor site depends on the esthetic mobility on the anterior teeth, by the ability of the patient
requirements of the pantie. In highly esthetic areas such as to speak clearly and comfortably, and by the patient's gen-
the maxillary anterior region, it is necessary to create a recep- eral sense of comfort with the overbite, overjet, and guid-
tor area that is 1.0-1.5 mm below the tissue on the facial as- ance created during chewing and when holding the head
pect. This creates the appearance of a free gingival margin and upright.
produces optimal esthetics (Fig. 53.35). This site can then be 4. The occlusion should be created at a vertical dimension
tapered to the height of the palatal tissue to facilitate hygiene that is stable for the patient. It is generally accepted that
access from the palatal side. In the posterior areas, a deep re- the patient's existing vertical dimension is at equilibrium
ceptor site can complicate hygiene access. In these situations, between the eruptive forces of the teeth and the repeti-
the ideal site has the facial portion of the pantie at the same tive contracted length of the elevator muscles. It has been
level as the ridge, and then the site is created as a straight line demonstrated that vertical dimension can be altered with
to the lingual side of the pantie. This removes the convexity no sense of pain from muscles and joints. However, if this
of the ridge and produces a flat, easily cleanable tissue surface alteration lengthens the pterygomasseteric sling beyond its
on the pantie (Fig. 53.36) ability to adapt, the patient will not maintain the vertical
change and will close the occlusal vertical dimension back
Occlusal Considerations down by intruding the teeth.
in Restorative Therapy 5. When managing a pathologic occlusion or when restor-
ing a complete occlusion, the clinician needs to work with
Occlusion plays an important role in restorative dentistry. a repeatable condylar reference position. Centric relation,
The increased use of dental implants and nonmetallic cos- defined as the most superior condylar position, provides
metic restorations has resulted in greater concern over force such a starting point. Centric relation has been shown to
management. These restorations are more sensitive to occlu- be reproducible over multiple appointments, allowing the
sal trauma, with subsequent structural failure, than are tradi- clinician to create the occlusion indirectly on an articu-
tional restorations on teeth. Consequently, for the restorative lator and return it to the same reference position in the
Ridge Modification Procedures for Ideal

Pontic Contours
When the ridge is being surgically modified, it is important
to know the thickness of soft tissue above the bone. This
measurement is obtained by probing to the bone through the
anesthetized tissue. If the tissue is removed to less than 2 mm
in thickness, significant rebound in ridge height may occur. If
it is necessary to reduce the tissue height to less than 2 mm
above the bone to create the desired pontic form, some bone
will need to be removed to achieve the desired result.
It is important when considering an ovate pontic to realize
that certain soft-tissue ridge parameters must exist to opti-
mize the ovate pontic form. First, the ridge height needs to
match the ideal height of the interproximal papillae where in- FIGURE 53.37 Ridge considerations when an ovate pontic is desired.
For an ovate pontic to be properly created, the soft-tissue ridge must be
terproximal embrasures are planned, either between pontics labial to the desired cervical portion of the pontic. When the pontic is
or next to abutment teeth. Second, the gingival margin height facial to the ridge, it is not possible to create what appears to be a "free
must also be at the ideal level, or the pontic will appear too gingival margin" correctly. The shaded area represents the necessary
long. Third, the ridge tissue must be facial to the ideal cervical amount of tissue that would be augmented to produce an ideal ovate
pontic in this particular site.
facial form of the pontic so that the pontic can emerge from
the tissue. If any of these three areas is inadequate, some form
of ridge augmentation is needed to produce a ridge that can the gingival embrasure form and papilla can be maintained.
have an adequate receptor site created (Fig. 53.37). Any ridge At 4 weeks, the 2.5-mm extension can be reduced to a 1.0-
augmentation procedures should be completed before, or in to 1.5-mm extension to facilitate hygiene. This procedure can
conjunction with, fabricating an ovate pontic. When con- maintain the papilla next to the abutment teeth as long as the
structing the final restorations, the contours of the developed bone on the abutment tooth is at a normal level.
ovate pontic receptor site can be conveyed to the laboratory The "full ridge-lap pontic" is an outdated design that strad-
by capturing a soft-tissue impression 4-6 weeks after the site dles the convexity of the ridge buccolingually and creates an
has been created. undersurface that is entirely concave and cannot be cleaned.
The ovate pontic can serve another important periodontal It is not recommended for use in any situations. However, a
function by maintaining the interdental papilla next to abut- modified ridge-lap pantie can be an acceptable design if inad-
ment teeth after extraction. When a tooth is removed, the gin- equate ridge exists to create an ovate pontic. With the modi-
gival embrasure form is lost. The normal response of the papilla fied ridge-lap design, the pontic follows the convexity of the
to this loss of embrasure form is to recede 1.5-2.0 mm, which ridge on the facial aspect but stops on the lingual crest of the
corresponds to the additional soft tissue that exists above bone ridge without extending down the lingual side of the ridge.
on the interproximal versus the facial aspect. However, this re- Although the facial aspect of the undersurface has a concave
cession can be prevented. By inserting the correct pontic form shape, the more open lingual form allows adequate access for
2.5 mm into the extraction site the day the tooth is removed, oral hygiene.
mouth. It is the only position that has been shown to shut Gracis S, Fradeani M, Celletti R, et al: Biological integration of aesthetic resto-
off lateral pterygoid muscle contraction. Because it is a bor- rations: factors influencing appearance and long-term success, Peliodontol
2000 27:29-44, 2001.
der position, any mandibular movement will result in the Gunay H, Seeger A, Tschernitschek H, et al: Placement of the preparation line
condyle moving inferiorly Therefore, centric relation is the and periodontal health: a prospective 2-year clinical study, Int J Periodont
only position from which an interference-free occlusion Restor Dent 20:173, 2000.
can be created. Kois JC The restorative-periodontal interface: biological parameters, Peri-
odontal 2000 11:29, 1996.
Kois JC Clinical techniques in prosthodontics: relationship of the periodon-
tium to impression procedures, Compend Cantin Educ Dent 21:684, 2000.
Conclusions Kois JC, Spear FM: Periodontal prosthesis: creating successful restorations,
J Am Dent Assoc 123:108, 1992.
The therapeutic goals of patient comfort, function, esthetics, Kokich VG: Esthetics: the orthodontic-periodontic restorative connection,
predictability, longevity, and ease of restorative and main- Semin Orthodont 2:21, 1996.
tenance care are attainable only by a carefully constructed Melnick PR, Camargo PM: Alveolar bone reservation following tooth extrac-
interdisciplinary approach, with accurate diagnosis and com- tion in the esthetic zone. In Fugazzotto P, editor: Implant and ,·egenerative
therapy in dentistry: a guide to decision making, Hoboken, 2009, Wiley-
prehensive treatment planning serving as cornerstones. The Blackwell.
complex interaction between periodontal therapy and success- Spear FM: Maintenance of the interdental papilla following anterior tooth
ful restorative dentistry only serves to underscore this premise. removal, Pract Periodontics Aesthet Dent 11:21, 1999.
Studer S, Zellweger U, Scharer P: The esthctic guidelines of the mucogingi-
val complex for fixed prosthodontics, Prnct Periodontics Aesthet Dent 8:333,
SUGGESTED READINGS 1996.
Camargo PM, Melnick PR, Camargo LM: Clinical crown lengthening in the Tarnow DP, Magner AW, Fletcher P: The effects of the distance from the con-
esthetic zone, J Calif Dent Assoc 35(7):487-498, 2007. tact point to the crest of bone on the presence or absence of the interproxi-
Felton DA, Kanoy Be, Bayne SC, et al: Effect of in vivo crown margin discrep- mal dental papilla,] Peliodontol 63:995, 1992.
ancies on periodontal health,] Prosthet Dent 65:357, 1991. Vacek JS, Gher ME, Assad DA, et al: The dimensions of the human dentogin-
Fradeani M: Esthetic rehabilitation in fixed prosthodontics, volume 2: prosthetic gival junction, Int] Periodont Restor Dent 14:155, 1994.
treatment: a systematic approach to esthetic, biologic, and Junctional integrntion, Van der Yeldon U: Regeneration of the interdental soft tissue following denu-
Chicago, 2004, Quintessence. dation procedures,] Clin Periodontol 9:455, 1982.
54
Adjunctive Role of Orthodontic
Therapy
VG Kokich • N Ambalavanan
Chapter Outline
Benefits of Orthodontic Therapy Fractured Teeth and Forced Eruption
Preorthodontic Osseous Surgery Orthodontic Treatment of Gingival
Orthodontic Treatment of Osseous Discrepancies
Defects Conclusion
Orthodontic tooth movement may be of substantial benefit embrasures are located in the maxillary anterior region,
to the adult periorestorative patient. Many adults who seek they can be unesthetic. In most patients, these areas can be
routine restorative dentistry have problems with tooth mal- corrected with a combination of orthodontic root move-
position that compromise their ability to clean and maintain ment, tooth reshaping, and restoration.
their dentitions. If these individuals also are susceptible to 6. Orthodontic treatment could improve adjacent tooth posi-
periodontal disease, tooth malposition may be an exacerbat- tion before implant placement or tooth replacement. This
ing factor that could cause premature loss of specific teeth. is especially true for the patient who has been missing
Many adults undergo orthodontic treatment to have their teeth for several years and has drifting and tipping of the
teeth aligned and to improve the esthetics of their smiles. If these adjacent dentition.
individuals also have underlying gingival or osseous periodontal
defects, these defects often can be improved during orthodontic
therapy if the orthodontist is aware of the situation and designs Preorthodontic Osseous Surgery
the appropriate tooth movement. In addition, implants have The extent of the osseous surgery depends on the type of
become a major part of the treatment plan for many adults with defect (eg, crater, hemiseptal defect, three-wall defect, or fur-
missing teeth. If adjacent teeth have drifted into edentulous cation lesion).
spaces, orthodontic therapy is often helpful to provide the ideal
amount of space for implants and subsequent restorations.
Osseous Craters
Benefits of Orthodontic Therapy An osseous crater is an interproximal, two-wall defect that
does not improve with orthodontic treatment. Some shallow
Orthodontic therapy can provide several benefits to the adult craters ( 4-5-mm pocket) may be maintainable nonsurgically
periodontal patient. The following six factors should be con- during orthodontic treatment. However, if surgical correction
sidered: is necessary, this type of osseous lesion can easily be elimi-
1. Aligning crowded or malposed maxillary or mandibular nated by reshaping the defect and reducing the pocket depth.
anterior teeth permits adult patients better access to clean This in turn enhances the ability to maintain these interproxi-
all surfaces of their teeth adequately. mal areas during orthodontic treatment. The need for surgery
2. Vertical orthodontic tooth repositioning can improve cer- is based on the patient's response to initial root planing, the
tain types of osseous defects in periodontal patients. patient's periodontal resistance, the location of the defect, and
3. Orthodontic treatment can improve the esthetic relation- the predictability of maintaining defects nonsurgically while
ship of the maxillary gingival margin levels before restor- the patient is wearing orthodontic appliances.
ative dentistry.
4. Orthodontic therapy also benefits the patient with a severe Three-Wall Intrabony Defects
fracture of a maxillary anterior tooth that requires forced
eruption to permit adequate restoration. Three-wall defects are amenable to pocket reduction with
5. Orthodontic treatment allows open gingival embrasures to regenerative periodontal therapy. Bone grafts using either
be corrected to regain lost papilla. If these open gingival autogenous bone from the surgical site or allografts along with
631
FIGURE 54.1 A, This patient had a significant periodontal pocket distal to the mandibular right first molar. B, Periapical radiograph confirmed the
osseous defect. C, A flap was elevated revealing a deep, three-wall osseous defect. D, Freeze-dried bone was placed in the defect. Six months after
the bone graft, orthodontic treatment was initiated. E, The final periapical radiograph shows that F, the preorthodontic bone graft, helped to regenerate
bone and eliminate the defect distal to the molar.
the use of resorbable membranes have been successful in fill- In the periodontally healthy patient, orthodontic brackets
ing three-wall defects. If the result of periodontal therapy is are positioned on the posterior teeth relative to the marginal
stable 3-6 months after periodontal surgery (Fig. 54.1), orth- ridges and cusps. However, some adult patients may have
odontic treatment may be initiated. marginal ridge discrepancies caused by uneven tooth erup-
tion. When marginal ridge discrepancies are encountered, the
Orthodontic Treatment of Osseous decision as to where to place the bracket or band is not deter-
mined by the anatomy of the tooth. In these patients, it is
Defects important to assess these teeth radiographically to determine
the interproximal bone level.
Hemiseptal Defects If the bone level is oriented in the same direction as the mar-
Hemiseptal defects are one- or two-wall osseous defects that ginal ridge discrepancy, leveling the marginal ridges will level
often are found around mesially tipped teeth or teeth that the bone. However, if the bone level is flat between adjacent
have supererupted (Fig. 54 2) Usually, these defects can be teeth (Fig. 54.2) and the marginal ridges are at significantly
eliminated with the appropriate orthodontic treatment. In the different levels, correction of the marginal ridge discrepancy
case of the tipped tooth, uprighting and eruption of the tooth orthodontically produces a hemiseptal defect in the bone. This
levels the bony defect. If the tooth is supererupted, intrusion could cause a periodontal pocket between the two teeth.
and leveling of the adjacent cementoenamel junctions (CEJs) If the bone is flat and a marginal ridge discrepancy is pres-
can help level the osseous defect. ent, the orthodontist should not level the marginal ridges
It is imperative that periodontal inflammation be controlled orthodontically. In these situations, it may be necessary
before orthodontic treatment. This usually can be achieved to equilibrate the crown of the tooth (Fig. 54.2). For some
with initial debridement and rarely requires any preorthodon- patients, the latter technique may require endodontic therapy
tic surgery. After the completion of orthodontic treatment, and restoration of the tooth because of the required amount of
these teeth should be stabilized for at least 6 months and reas- reduction of the length of the crown. This approach is accept-
sessed periodontally. Often, the pocket has been reduced or able if the treatment results in a more favorable bone contour
eliminated, and no further periodontal treatment is needed. between the teeth.
It would be injudicious to perform preorthodontic osseous Some patients have a discrepancy between both the mar-
corrective surgery in such lesions if orthodontics is part of the ginal ridges and the bony levels between two teeth. How-
overall treatment plan. ever, these discrepancies may not be of equal magnitude;
54 Adjunctive Role of Orthodontic Therapy 633
FIGURE 54.2 A, This patient showed overeruption of the maxillary right first molar and a marginal ridge defect between the second premolar and first
molar. B, Pretreatment periapical radiograph showed that the interproximal bone was flat. To avoid creating a hemiseptal defect, the occlusal surface
of the first molar was equilibrated, C and D, and the malocclusion, E and F, was corrected orthodontically.
orthodontic leveling of the bone may still leave a discrep- will also be at the same level. This relationship creates a flat,
ancy in the marginal ridges (Fig. 54.3). In these patients, bony contour between the teeth. However, if a patient has
the crowns of the teeth should not be used as a guide for underlying periodontal problems and significant alveolar
completing orthodontic therapy. The bone should be leveled bone loss around certain teeth, using the anatomy of the
orthodontically and any remaining discrepancies between crown to determine bracket placement is not appropriate
the marginal ridges should be equilibrated. This method pro- (Fig. 544).
duces the best occlusal result and improves the patient's peri- In a patient with advanced horizontal bone loss, the bone
odontal health. level may have receded several millimeters from the CE]. As
During orthodontic treatment, when teeth are being this occurs, the crown-to-root ratio becomes less favorable.
extruded to level hemiseptal defects, the patient should be By aligning the crowns of the teeth, the clinician may perpet-
monitored regularly. Initially, the hemiseptal defect has a uate tooth mobility by maintaining an unfavorable crown-
greater sulcular depth and is more difficult for the patient to to-root ratio. In addition, by aligning the crowns of the teeth
clean. As the defect is ameliorated through tooth extrusion, and disregarding the bone level, significant bone discrepan-
interproximal cleaning becomes easier. The patient should be cies occur between healthy and periodontally diseased roots.
recalled every 2-3 months during the leveling process to con- This could require periodontal surgery to ameliorate the
trol inflammation in the interproximal region. discrepancies.
Many of these problems can be corrected by using the
bone level as a guide to position the brackets on the teeth.
Advanced Horizontal Bone Loss
In these situations, the crowns of the teeth may require con-
After orthodontic treatment has been planned, one of the siderable equilibration. If the tooth is vital, the equilibration
most important factors that determine the outcome of orth- should be performed gradually to allow the pulp to form sec-
odontic therapy is the location of the bands and brackets on ondary dentin and insulate the tooth during the equilibra-
the teeth. In a periodontally healthy individual, the position tion process. The goal of equilibration and creative bracket
of the brackets is usually determined by the anatomy of the placement is to provide a more favorable bony architecture,
crowns of the teeth. Anterior brackets should be positioned as well as a more favorable crown-to-root ratio. In some of
relative to the incisal edges. Posterior bands or brackets these patients, the periodontal defects that were apparent ini-
are positioned relative to the marginal ridges. If the incisal tially may not require periodontal surgery after orthodontic
edges and marginal ridges are at the correct level, the CEJ treatment.
FIGURE 54.3 A, Before orthodontic treatment, this patient had significant mesial tipping of the maxillary right first and second molars, causing mar-
ginal ridge discrepancies. B, The tipping produced root proximity between the molars. C, To eliminate the root proximity, the brackets were placed
perpendicular to the long axis of the teeth. D-F, This method of bracket placement facilitated root alignment and elimination of the root proximity, as
well as leveling of the marginal ridge discrepancies.
FIGURE 54.4 A and B, This patient had a class Ill furcation defect before orthodontic treatment. C, Orthodontic treatment was performed and the
furcation defect was maintained by the periodontist on 2-month recalls until after orthodontic treatment. D, After appliance removal, the tooth was
hemisected, E, and the roots were restored and splinted together. F, The final periapical radiograph shows that the furcation defect has been eliminated
by hemisecting and restoring the two root fragments.
FIGURE 54.5 A and B, Before orthodontic treatment, this patient had a class Ill furcation defect in the mandibular left second molar. C, Since the
patient had an edentulous space mesial to the molar, the tooth was hemisected and, D, the root fragments were separated orthodontically. E and F,
After orthodontic treatment, the root fragments were used as abutments to stabilize a multiunit posterior bridge.
Furcation Defects procedures, bands or brackets can be placed on the root frag-
ments and coil springs used to separate the roots. The amount
Furcation defects can be classified as incipient (class I), moder- of separation is determined by the size of the adjacent eden-
ate (class II), or advanced (class III). These lesions require spe- tulous spaces and the occlusion in the opposing arch. About
cial attention in the patient undergoing orthodontic treatment. 7-8 mm may be created between the roots of the hemisected
Often, the molars require bands with tubes and other attach- molar. This process eliminates the original furcation problem
ments that impede the patient's access to the buccal furcation and allows the patient to clean the area with greater efficiency
for homecare and instrumentation at the time of recall. Fur- In some molars with class III furcation defects, the tooth
cation lesions require special consideration because they are may have short roots, advanced bone loss, fused roots, or
the most difficult lesions to maintain and can worsen during other problems that prevent hemisection and crowning of
orthodontic therapy These patients need to be maintained on a the remaining roots. In these patients, extracting the root
2-3-month recall schedule. Detailed instrumentation of these with a furcation defect and placing an implant may be more
furcations helps minimize further periodontal breakdown. advisable. If this type of plan has been adopted, the timing
If a patient with a class III furcation defect will be under- of the extraction and placement of the implant can occur
going orthodontic treatment, a possible method for treating at any time relative to the orthodontic treatment. In some
the furcation is to eliminate it by hemisecting the crown and patients, the implant can be used as an anchor to facilitate
root of the tooth (Fig. 54.5). However, this procedure requires prerestorative orthodontic treatment.
endodontic, periodontal, and restorative treatment. If the The implant must remain embedded in bone for
patient will be undergoing orthodontic treatment, it is advis- 4-6 months after placement before it can be loaded as an
able to perform the orthodontic treatment first. This is espe- orthodontic anchor. It must be placed precisely so that it not
cially true if the roots of the teeth will not be moved apart. only provides an anchor for tooth movement but also may
In these patients the molar to be hemisected remains intact be used as an eventual abutment for a crown or fixed bridge.
during orthodontics. This patient would require 2-3-month If the implant will not be used as an anchor for orthodontic
recall visits to ensure that the furcation defect does not lose movement, it may be placed after the orthodontic treatment
bone during orthodontic treatment. Keeping the tooth intact has been completed. Considerations regarding timing are
during the orthodontic therapy simplifies the concentration of determined by the restorative treatment plan.
tooth movement for the orthodontist. After orthodontic treat-
ment, endodontic therapy is required (followed by periodon-
Root Proximity
tal surgery) to divide the tooth.
In some patients requiring hemisection of a mandibular When roots of posterior teeth are close together, the ability to
molar with a class Ill furcation, pushing the roots apart dur- maintain periodontal health and accessibility for restoration of
ing orthodontic treatment may be advantageous (Fig. 54.5). If adjacent teeth may be compromised. However, for the patient
the hemisected molar will be used as an abutment for a bridge undergoing orthodontic therapy, the roots can be moved
after orthodontics, moving the roots apart orthodontically per- apart and bone formation will occur between the adjacent
mits a favorable restoration and splinting across the adjacent roots (Fig. 54.3). This opens the embrasure beneath the tooth
edentulous spaces. In these patients, hemisection, endodontic contact, provides additional bone support, and enhances the
therapy, and periodontal surgery must be completed before patient's access to the interproximal region for hygiene. This
the start of orthodontic treatment. After completion of these approach generally improves the periodontal health of this area.
If orthodontic treatment will be used to move roots apart, fracture may extend beneath the level of the gingival margin
this plan must be known before bracket placement. It is advan- and terminate at the level of the alveolar ridge (Fig. 54.6);
tageous to place the brackets so that the orthodontic move- restoration of the fractured crown is impossible because the
ment to separate the roots will begin with the initial archwires tooth preparation would extend to the level of the bone. This
(Fig. 54.3). Therefore, brackets must be placed obliquely to overextension of the crown margin could result in an invasion
facilitate this process. Radiographs are needed to monitor the of the biologic width of the tooth and cause persistent inflam-
progress of orthodontic root separation. In general, 2-3 mm of mation of the marginal gingiva. It may be beneficial in such
root separation provides adequate bone and embrasure space cases to erupt the fractured root out of the bone and move the
to improve periodontal health. During this time, the patient fracture margin coronally so that it can be properly restored.
should be maintained to ensure that a favorable bone response However, if the fracture extends too far apically, it may be bet-
occurs as the roots are moved apart. In addition, these patients ter to extract the tooth and replace it with an implant or bridge.
need occasional occlusal adjustment to recontour the crown The following six criteria are used to determine whether the
because the roots are moving apart. As this occurs, the crowns tooth should be forcibly erupted or extracted:
may develop an unusual occlusal contact with the opposing
1. Root length. Is the root long enough so that a one-to-one
arch. This should be equilibrated to improve the occlusion.
crown-to-root ratio is preserved after the root has been
erupted? To answer this question, the clinician must know
how far to erupt the root. If a tooth fracture extends to
Fractured Teeth and Forced Eruption the level of the bone, it must be erupted 4 mm. The first
Occasionally, children and adolescents may fall and injure their 2.5 mm moves the fracture margin far enough away from
anterior teeth. If the injuries are minor and result in small frac- the bone to prevent a biologic width problem. The other
tures of enamel, these can be restored with light-cured com- 1.5 mm provides the proper amount of ferrule for ade-
posite or porcelain veneers. In some patients, however, the quate resistance form of the crown preparation. Therefore,
FIGURE 54.6 A and B, This patient had a severe fracture of the maxillary right central incisor that extended apical to the level of the alveolar crest
on the lingual side. C, To restore the tooth adequately and avoid impinging on the periodontium, the fractured root was extruded 4 mm. D, As the
tooth erupted, the gingival margin followed the tooth. E, Gingival surgery was required to lengthen the crown of the central incisor so that F, the final
restoration, had sufficient ferrule for resistance and retention and the appropriate gingival margin relationship with the adjacent central incisor.
if the root is fractured to the bone level and must be As the root erupts, the gingiva moves coronally with the
erupted 4 mm, the periapical radiograph must be evalu- tooth. As a result, the clinical crown length becomes shorter
ated (Fig. 54 6B) and 4 mm subtracted from the end of after extrusion (Fig. 54.6). In addition, the gingival margin
the fractured tooth root. The length of the residual root may be positioned more incisally than the adjacent teeth. In
should be compared with the length of the eventual crown these patients, gingival surgery is necessary to create ideal gin-
on this tooth. The root-to-crown ratio should be about 1: 1. gival margin heights. The type of surgery varies, depending
If the root-to-crown ratio is less than this amount, there on whether bone removal is necessary If bone has followed
may be too little root remaining in the bone for stability the root during eruption, a flap is elevated, and the appropri-
In the latter situation, it may be prudent to extract the root ate amount of bone is removed to match the bone height of
and place a bridge or implant. the adjacent teeth. If the bone level is flat between adjacent
2. Root form. The shape of the root should be broad and non- teeth, a simple excisional gingivectomy corrects the gingival
tapering rather than thin and tapered. A thin, tapered root margin discrepancy
provides a narrower cervical region after the tooth has been After gingival surgery, an open gingival embrasure may exist
erupted 4 mm. This could compromise the esthetic appear- between the erupted root and adjacent teeth (Fig. 54 6) The
ance of the final restoration. The internal root form is also space occurs because the narrower root portion of the erupted
important. If the root canal is wide, the distance between tooth has been moved into the oral cavity This space may be
the external root surface and root canal filling will be nar- closed in two ways: (1) by overcontouring the replacement
row In these patients, the walls of the crown preparation restoration and (2) by reshaping the crown of the tooth and
are thin, which could result in early fracture of the restored movement of the root to close the space. The second method
root. The root canal should not be more than one-third of often helps improve the overall shape of the final crown on
the overall width of the root. In this way, the root could still the restored tooth.
provide adequate strength for the final restoration.
3. Level of the fracture. If the entire crown is fractured 2-3 mm
apical to the level of the alveolar bone, it is difficult, if not Hopeless Teeth Maintained
impossible, to attach it to the root to erupt it. for Orthodontic Anchorage
4. Relative importance of the tooth. If the patient is 70 years
Patients with advanced periodontal disease may have specific
of age and both adjacent teeth have prosthetic crowns, it
teeth diagnosed as hopeless, which would be extracted before
would be more prudent to construct a fixed bridge. How-
orthodontic therapy (Fig. 54.7). However, these teeth can be
ever, if the patient is 15 years of age and the adjacent teeth useful for orthodontic anchorage if the periodontal inflam-
are unrestored, forced eruption would be much more con-
mation can be controlled. In moderate-to-advanced cases,
servative and appropriate.
some periodontal surgery may be indicated around a hope-
5. Esthetics. If the patient has a high lip line and displays
less tooth. Flaps are reflected for debridement of the roots to
2-3 mm of gingiva when smiling, any type of restoration in
control inflammation around the hopeless tooth during the
this area will be more obvious. Keeping the patient's own
orthodontic process. The important factor is to maintain the
tooth would be much more esthetic than any type of im-
health of the bone around the adjacent teeth. Periodontal
plant or prosthetic replacement. recall is imperative during the process.
6. Endodontic/periodontal prognosis. If the tooth has a signifi-
After orthodontic treatment, there is a 6-month period of
cant periodontal defect, it may not be possible to retain the
stabilization before reevaluating the periodontal status. Occa-
root. In addition, if the tooth root has a vertical fracture,
sionally, the hopeless tooth may be so improved after orth-
the prognosis would be poor and extraction of the tooth
odontic treatment that it is retained. In most cases, however,
would be the proper course of therapy the hopeless tooth requires extraction, especially if other res-
If all these factors are favorable, forced eruption of the torations are planned in the segment. Again, these decisions
fractured root is indicated. The root may be erupted rapidly require reevaluation by the clinician.
or slowly If the movement is performed rapidly, the alveo-
lar bone will be left behind temporarily, and a circumferential
fiberotomy may be performed to prevent bone from follow- Orthodontic Treatment of Gingival
ing the erupted root. However, if the root is erupted slowly, Discrepancies
the bone follows the tooth. In this situation, the erupted root
requires crown lengthening to expose the correct amount of Uneven Gingival Margins
tooth to create the proper ferrule, resistance form, and reten-
The relationship of the gingival margins of the six maxillary
tion for the final restoration.
anterior teeth plays an important role in the esthetic appear-
After the tooth root has been erupted, it must be stabi-
ance of the crowns. The following four factors contribute to
lized to prevent it from intruding back into the alveolus. The
ideal gingival form:
reason for reintrusion is the orientation of the principal fibers
of the periodontium. During forced eruption, the periodon- 1. The gingival margins of the two central incisors should be
tal fibers become oriented obliquely and stretched as the at the same level.
root moves coronally These fibers eventually reorient them- 2. The gingival margins of the central incisors should be po-
selves after about 6 months. Before this occurs, the root can sitioned more apically than the lateral incisors and at the
reintrude significantly Therefore, if this type of treatment is same level as the canines.
performed, an adequate period of stabilization is necessary 3. The contour of the labial gingival margins should mimic
to avoid significant relapse and reintrusion of the root. the CEJs of the teeth.
FIGURE 54.7 A, This patient had an impacted mandibular right second molar. B-D, The mandibular right first molar was periodontally hopeless
because of an advanced class Ill furcation defect. The impacted second molar was extracted, but the first molar was maintained as an anchor to help
upright the third molar orthodontically. E and F, After orthodontic uprighting of the third molar, the first molar was extracted and a bridge was placed
to restore the eden tu lous space.
4. A papilla should exist between each tooth, and the height The third step is to evaluate the relationship between the
of the tip of the papilla is usually halfway between the shortest central incisor and the adjacent lateral incisors. If the
incisal edge and the labial gingival height of contour over shortest central incisor is still longer than the lateral incisors,
the center of each anterior tooth. Therefore, the gingival the other possibility is to extrude the longer central incisor and
papilla occupies half of the interproximal contact and the equilibrate the incisal edge. This moves the gingival margin
adjacent teeth form the other half of the contact. coronally and eliminates the gingival margin discrepancy. How-
ever, if the shortest central incisor is shorter than the lateral inci-
However, some patients may have gingival margin dis-
sors, this technique would produce an unesthetic relationship
crepancies between adjacent teeth. These discrepancies may
between the gingival margins of the central and lateral incisors.
be caused by abrasion of the incisal edges or delayed migra-
The fourth step is to determine whether the incisal edges
tion of the gingival margins. When gingival margin discrep-
have been abraded. This is best accomplished by evaluating the
ancies are present, the proper solution for the problem must
teeth from an incisal perspective. If one incisal edge is thicker
be determined: orthodontic movement to reposition the
labiolingually than the adjacent tooth, this may indicate that
gingival margins or surgical correction of gingival margin
it has been abraded and the tooth has overerupted. In such
discrepancies.
cases, the best method of correcting the gingival margin dis-
To make the correct decision, it is necessary to evaluate the
crepancy is to intrude the short central incisor. This method
four criteria. First, the relationship between the gingival mar-
moves the gingival margin apically and permits restoration of
gin of the maxillary central incisors and the patient's lip line
the incisal edges. The intrusion should be accomplished at
should be assessed when the patient smiles. If a gingival mar-
least 6 months before appliance removal. This allows reorien-
gin discrepancy is present, but the discrepancy is not exposed,
tation of the principal fibers of the periodontium and avoids
it does not require correction.
reextrusion of the central incisor(s) after appliance removal.
If a gingival margin discrepancy is apparent, the second
step is to evaluate the labial sulcular depth over the two central
incisors. If the shorter tooth has a deeper sulcus, excisional Significant Abrasion and Overeruption
gingivectomy may be appropriate to move the gingival margin
of the shorter tooth apically. However, if the sulcular depths Occasionally, patients have destructive dental habits, such as
of the short and long incisors are equivalent, gingival surgery a protrusive bruxing habit, that can result in significant wear
does not correct the problem. of the maxillary and mandibular incisors and compensatory
overeruption of these teeth. The restoration of these abraded often difficult to resolve with periodontal therapy. However,
teeth is often impossible because of the lack of crown length to orthodontic treatment can correct many of these open gingival
achieve adequate retention and resistance form for the crown embrasures. This open space is usually caused by (1) tooth
preparations. Two options are available. One option is exten- shape, (2) root angulation, or (3) periodontal bone loss.
sive crown lengthening by elevating a flap, removing sufficient The interproximal contact between the maxillary central
bone, and apically positioning the flap to expose adequate incisors consists of two parts: the tooth contact and the
tooth length for crown preparation. However, this type of pro- papilla. The papilla/contact ratio is 1: 1. Half the space is occu-
cedure is contraindicated in the patient with short, tapered pied by papilla and half is formed by the tooth contact. If the
roots because it could adversely affect the final root-to-crown patient has an open embrasure, the first aspect that must be
ratio and potentially open gingival embrasures between the evaluated is whether the problem is caused by the papilla or
anterior teeth. the tooth contact. If the papilla is the problem, the cause is
The other option for improving the restorability of these usually a lack of bone support because of an underlying peri-
short abraded teeth is to intrude the teeth orthodontically and odontal problem.
move the gingival margins apically. It is possible to intrude In some situations, a deficient papilla can be improved
up to four maxillary incisors by using the posterior teeth as with orthodontic treatment. By closing open contacts, the
anchorage during the intrusion process. The patient's poste- interproximal gingiva can be squeezed and moved incisally.
rior occlusion resists the eruption of the posterior teeth, and This type of movement may help create a more esthetic papilla
the incisors gradually intrude and move the gingival margins between two teeth despite alveolar bone loss. Another possi-
and the crowns apically. This creates the restorative space nec- bility is to erupt adjacent teeth when the interproximal bone
essary to restore the incisal edges of these teeth temporarily level is positioned apically.
and then eventually place the final crowns. Most open embrasures between the central incisors are
When abraded teeth are significantly intruded, it is neces- caused by problems with tooth contact. The first step in the
sary to hold these teeth for at least 6 months in the intruded diagnosis of this problem is to evaluate a periapical radio-
position with orthodontic brackets, archwires (or both), or graph of the central incisors. If the root angulation is diver-
some type of bonded retainer. The principal fibers of the peri- gent, the brackets should be repositioned so that the root
odontium must accommodate to the new intruded position, a position can be corrected (Fig. 54.8). In these patients the
process that could take a minimum of 6 months in most adult incisal edges may be uneven and require restoration with
patients. Orthodontic intrusion of severely abraded and over- either composite or porcelain restorations. If the periapical
erupted teeth is usually a distinct advantage over periodontal radiograph shows that the roots are in their correct relation-
crown lengthening, unless the patient has extremely long and ship, the open gingival embrasure is caused by a triangular
broad roots or has had an extensive horizontal periodontal tooth shape (Fig. 54 9)
bone loss. If the shape of the tooth is the problem, two solutions are
possible: (1) restoration of the open gingival embrasure or
(2) reshaping of the tooth by flattening the incisal contact
Open Gingival Embrasures
and closing the space (Fig. 54. 9). This second option results
The presence of a papilla between the maxillary central inci- in lengthening of the contact until it meets the papilla. In
sors is a key esthetic factor in any individual. Occasionally, addition, if the embrasure space is large, closing the space
adults have open gingival embrasures or lack gingival papil- squeezes the papilla between the central incisors. This helps
lae between their central incisors. These unesthetic areas are create a 1: 1 ratio between the contact and papilla and restores
FIGURE 54.8 A, This patient initially had overlapped maxillary central incisors and after initial orthodontic alignment of the teeth, B, an open gingi-
val embrasure appeared between the centrals. C, Radiograph showed that the open embrasure was caused by divergence of the central incisor roots.
D, To correct the problem, the central incisor brackets were repositioned and the roots were moved together. E, This required restoration of the incisal
edges after orthodontic therapy because these teeth had worn unevenly before therapy. F, As the roots were paralleled, the tooth contact moved gin-
givally and the papilla moved incisally, resulting in the elimination of the open gingival embrasure.
FIGURE 54.9 A and B, This patient initially had triangular-shaped central incisors, which C, produced an open gingival embrasure after orthodontic
alignment. D, Since the roots of the central incisors were parallel with one another, the appropriate solution for the open gingival embrasure was to
recontour the mesial surfaces of the central incisors. E, As the diastema was closed, the tooth contact moved gingival ly and the papilla moved incisal ly,
resulting in F, the elimination of the open gingival embrasure.
uniformity to the heights between the midline and adjacent SUGGESTED READINGS
papillae. Brown IA: The effect of orthodontic therapy on certain types of periodontal
defects. I. Clinical findings,] Periodontol 44:742, 1973.
Ingber J: Forced eruption. Part I. A method of treating isolated one and two
Conclusion wall infrabony osseous defects: rationale and case report, J Peliodontol
45:199, 1974.
There are many benefits to integrating orthodontics and peri- Kokich V: Enhancing restorative, esthetic and periodontal results with orth-
odontics in the management of adult patients with underlying odontic therapy. In Schluger S, Youdelis R, Page R, et al, editors: Periodontal
periodontal defects. The key to treating these patients is com- therapy, Philadelphia, 1990, Lea and Febiger.
Kokich V: Esthetics and vertical tooth position: the orthodontic possibilities,
munication and proper diagnosis before orthodontic therapy, Compend Cantin Educ Dent 18:1225, 1997.
as well as continued dialog during orthodontic treatment. Not Kokich V, Nappen D, Shapiro P: Gingival contour and clinical crown length:
all periodontal problems are treated in the same way. This their effects on the esthetic appearance of maxillary anterior teeth, Am J
chapter provides a framework for the integration of orthodon- Orthod 86:89, 1984.
tics to solve periodontal problems.
SECTION VII
Section Outline
55. Supportive Periodontal Treatment
55
Supportive Periodontal
Treatment
RL Merin • DG Naik • A Uppoor
Chapter Outline
Rationale for Supportive Periodontal Referral of Patients to the Periodontist
Treatment Tests for Disease Activity
Maintenance Program Maintenance for Dental Implant Patients
Classification of Posttreatment Patients
Preservation of the periodontal health of the treated patient The maintenance phase of periodontal treatment starts im-
requires as positive a program as that required for the elimi- mediately after the completion of Phase I therapy (Figs. 55.1
nation of periodontal disease. After Phase I therapy is com- and 55.2). While the patient is in the maintenance phase, the
pleted, patients are placed on a schedule of periodic recall necessary surgical and restorative procedures are performed.
visits for the maintenance phase to prevent recurrence of the This ensures that all areas of the mouth retain the degree of
disease (Figs. 55.1 and 55 2). The third World Workshop of health attained after Phase I therapy.
the American Academy of Peridontology 1989 has renamed
the maintenance phase as supportive periodontal therapy (SPT). Rationale for Supportive Periodontal
This term was devised to express the essential need for thera-
peutic measures to support the patient's own efforts to control
Treatment
the periodontal infection and to avoid reinfection. Studies show that even with appropriate periodontal therapy,
Transfer of the patient from active treatment status to a some progression of disease is possible. One likely explanation
maintenance program is a definitive step in total patient care for the recurrence of periodontal disease is incomplete subgingi-
that requires time and effort on the part of the dentist and val plaque removal. If subgingival plaque is left behind during
the staff. Patients must understand the purpose of the main- scaling, it regrows within the pocket. The regrowth of subgin-
tenance program and the dentist must emphasize that preser- gival plaque is a slow process compared to that of supragingival
vation of the teeth depends on maintenance therapy. Patients plaque. During this period (perhaps months), the subgingival
who are not maintained in a supervised recall program sub- plaque may not induce inflammatory reactions that can be dis-
sequent to active treatment show obvious signs of recurrent cerned at the gingival margin. The clinical diagnosis may be
periodontitis (eg, increased pocket depth, bone loss, or tooth further confused by the introduction of adequate supragingival
loss). The more often patients present for recommended sup- plaque control because the inflammatory reactions caused by
portive periodontal treatment, the less likely they are to lose the plaque in the soft-tissue wall of the pocket are not likely to
teeth. One study found that treated patients who do not re- be manifested clinically as gingivitis. Thus, inadequate subgin-
turn for regular recalls are at 5.6 times greater risk for tooth gival plaque control can lead to continued loss of attachment
loss than compliant patients. Another study showed that pa- even without the presence of clinical gingival inflammation.
tients with inadequate SPT after successful regenerative ther- Bacteria are present in the gingival tissues in chronic and
apy have a SO-fold increase in risk of probing attachment loss aggressive periodontitis cases. Eradication of intragingival mi-
as compared to those who have regular recall visits. croorganisms may be necessary for a stable periodontal result.
Motivational techniques and reinforcement of the impor- Scaling, root planing, and even flap surgery may not eliminate
tance of the maintenance phase of treatment should be consid- intragingival bacteria in some areas. These bacteria may re-
ered before performing definitive periodontal surgery. Studies colonize the pocket and cause recurrent disease.
show that few patients display complete compliance with rec- Bacteria associated with periodontitis can be transmitted be-
ommended maintenance schedules (Fig. 55.3). It is meaning- tween spouses and other family members. Patients who appear to
less simply to infarm patients that they are to return for periodic be successfully treated can become infected or reinfected with
recall visits without clearly explaining the significance of these visits potential pathogens. This is especially likely in patients with
and describing what is expected of patients between visits. remaining pockets.
643
Phase I
Reevaluation
•complete
DNone
- Erratic
Phase II (periodontal surgery)
34.13%
Phase Ill (restorative)
FIGURE 55.3 Compliance with maintenance therapy in 961 patients

studied for 1 to 8 years. (Modified from Wilson TC Jr, Clover ME, Schoen
/, et al: J Periodontal 55:468, 1984.)
Phase IV (maintenance)
FIGURE 55.1 Incorrect sequence of periodontal treatment phases.
Maintenance phase should be started immediately after the reevaluation
of Phase I therapy. or months. The return of pathogens to pretreatment levels
generally occurs in approximately 9-11 weeks but can vary
dramatically among patients.
Phase I Both the mechanical debridement performed by the thera-
pist and the motivational environment provided by the ap-
pointment seem to be necessary for good maintenance results.
Patients tend to reduce their oral hygiene efforts between ap-
Reevaluation
pointments. Knowing that their hygiene will be evaluated mo-
tivates them to perform better oral hygiene in anticipation of
the appointment.
In one study, the proportion of Spirochetes obtained in
baseline samples of subgingival flora is highly correlated with
Phase IV (maintenance) clinical periodontal deterioration over 1 year. However, sub-
sequent reports in the same longitudinal study concluded that
II
Phase II Phase Ill
the arbitrary assignment of treated periodontitis patients to
3-month maintenance intervals appears to be as effective in
preventing recurrences of periodontitis as assignment of recall
intervals based on microscopic monitoring of the subgingi-
(periodontal surgery) (restorative) val flora. Microscopic monitoring was found not to be a reli-
FIGURE 55.2 Correct sequence of periodontal treatment phases. able predictor of future periodontal destruction in patients on
3-month recall programs, presumably because of the altera-
tion of subgingival flora produced by subgingival instrumen-
Another possible explanation for the recurrence of peri-
tation.
odontal disease is the microscopic nature of the dentogingival
In conclusion, there is a sound scientific basis Jor recall main-
unit healing after periodontal treatment. Histologic studies
have shown that after periodontal procedures, tissues usually tenance because subgingival scaling alters the pocket micro.flora for
variable but relatively long periods.
do not heal by formation of new connective tissue attachment
to root surfaces but result in a long junctional epithelium. It
has been speculated that this type of dentogingival unit may Maintenance Program
be weaker and that inflammation may rapidly separate the
long junctional epithelium from the tooth. Thus, treated peri- Periodic recall visits form the foundation of a meaningful
odontal patients may be predisposed to recurrent pocket for- long-term prevention program. The interval between visits is
mation if maintenance care is not optimal. initially set at 3 months but may be varied according to the
Subgingival scaling alters the micro.flora of periodontal pock- patient's needs.
ets. In one study, a single session of scaling and root planing Periodontal care at each recall visit comprises three parts
in patients with chronic periodontitis resulted in significant (Box 55.1). The first part involves examination and evaluation
changes in subgingival microflora. Reported alterations in- of the patient's current oral health. The second part includes
cluded a decrease in the proportion of motile rods for 1 week, the necessary maintenance treatment and oral hygiene rein-
a marked elevation in the proportion of coccoid cells for forcement. The third part involves scheduling the patient for
21 days, and a marked reduction in the proportion of Spiro- the next recall appointment, additional periodontal treatment,
chetes for 7 weeks. or restorative dental procedures. The time required for a recall
Although pocket debridement suppresses components of visit for patients with multiple teeth in both arches is approxi-
the subgingival microflora associated with periodontitis, peri- mately 1 h, which includes time for greeting the patient, set-
odontal pathogens may return to baseline levels within days ting up, and cleaning up.
55 Supportive Periodontal Treatment 645
PART I: EXAMINATION
(Approximate time: 14 min)
Patient greeting
Medical history changes
Oral pathologic examination
Oral hygiene status
Gingival changes
Pocket depth changes
Mobility changes
Occlusal changes
Dental caries
Restorative, prosthetic, and implant status
PART II: TREATMENT
Oral hygiene reinforcement
Scaling
Polishing
Chemical irrigation or site-specific antimicrobial placement
PART Ill: REPORT, CLEANUP, AND SCHEDULING
Write report in chart
Discuss report with patient FIGURE 55.4 A, Hyperplastic gingivitis related to crown margins and
Clean and disinfect operatory plaque accumulation in a 27-year-old woman. B, 4 months after treat-
Schedule next recall visit ment, there is significant improvement. However, some inflammation
Schedule further periodontal treatment around crown margins still exists, which cannot be resolved without
Schedule or refer for restorative or prosthetic treatment replacing the crowns.
Treatment
Examination and Evaluation The required scaling and root planing are performed, fol-
lowed by an oral prophylaxis. Care must be taken not to
The recall examination is similar to the initial evaluation
instrument normal sites with shallow sulci (1-3 mm deep)
of the patient. However, because the patient is not new to
because studies have shown that repeated subgingival scal-
the office, the dentist primarily looks for changes that have
ing and root planing in initially normal periodontal sites
occurred since the last evaluation. Analysis of the current
result in significant loss of attachment. Irrigation with anti-
oral hygiene status of the patient is essential. Updating of
microbial agents or placement of site-specific antimicrobial
changes in the medical history and evaluation of restora-
devices is performed in maintenance patients with remaining
tions, caries, prostheses, occlusion, tooth mobility, gingival
pockets.
status, and periodontal and periimplant probing depths are
important parts of the recall appointment. The oral muco-
sa should be carefully inspected for pathologic conditions Recurrence of Periodontal Disease
(Figs. 55.4-55.9)
Occasionally, lesions may recur, which often can be traced to
Radiographic examination must be individualized, de-
inadequate plaque control on the part of the patient or failure
pending on the initial severity of the case and the findings at
to comply with recommended SPT schedules. It should be
the recall visit (Table 55.1) These are compared with findings
understood, however, that it is the dentist's responsibility to
on previous radiographs to check the bone height and look
teach, motivate, and control the patient's oral hygiene tech-
for repair of osseous defects, signs of trauma from occlusion,
nique, and the patient's failure is the dentist's failure. Surgery
periapical pathologic changes, and caries.
should not be undertaken unless the patient has shown profi-
ciency and willingness to cooperate by adequately performing
Checking of Plaque Control his or her part of therapy.
Other causes for recurrence include the following points:
To assess the effectiveness of their plaque control, patients
should perform their hygiene regimen immediately before 1. Inadequate or insufficient treatment that has failed to re-
the recall appointment. Plaque control must be reviewed and move all the potential factors favoring plaque accumula-
corrected until the patient demonstrates the necessary pro- tion (Fig. 55.4). Incomplete calculus removal in areas of
ficiency even if additional instruction sessions are required. difficult access is a common source of problems.
Patients instructed in plaque control have less plaque and 2. Inadequate restorations placed after the periodontal treat-
gingivitis than uninstructed patients and the amount of supra- ment was completed.
gingival plaque affects the number of subgingival anaerobic 3. Failure of the patient to return for periodic checkups
organisms. (Fig. 55.6). This may be a result of the patient's conscious
FIGURE 55.5 A, Patient was 38 years old when these original radiographs were taken and was treated with a combination of surgical and nonsurgi-
cal therapy. This individual is a classic class C maintenance patient. B, Pretreatment photograph. Note the inflammation and heavy calculus deposits.
C, Photograph taken 1 0 years after treatment. D, Radiographs taken 5 years after treatment. E, Radiographs taken 1 0 years after treatment. The radio-
graphic appearance is as good as can be expected in such a severe case. Teeth #15 and #17 were extracted 8 years after treatment.
(A)
FIGURE 55.6 This series of radiographs clearly shows the importance of maintenance therapy. A, Original radiograph of a 58-year-old male.
Note the deep distal bone loss on tooth #18 and the moderate distal lesion of tooth #19. Surgical treatment included osseous grafting. B, Radiograph
14 months after surgical therapy. The patient had recall maintenance performed every 3-4 months. C, Appearance 3 years after surgery, with regular
recalls every 3-4 months. D, Appearance after 2 years without recalls (7 years after surgery). Note the progression of the disease on the distal surfaces
of teeth #18 and #19.
FIGURE 55.7 Advanced cases sometimes do better than expected when the patient complies with maintenance therapy. A, Initial radiographs
showing a very advanced case. The maxillary arch had extractions and nonsurgical treatment. A plastic partial denture was placed and was expected
to grow into a full denture within a few years. The mandibular arch was treated with periodontal surgery, and a permanent, metal and plastic, remov-
able partial denture was placed. B, Radiographs taken 8 years later. The patient performed good oral hygiene and had 3-month recalls. Teeth #12 and
#15 required extraction.
FIGURE 55.8 A, Initial radiographs. The patient was advised to have localized areas of periodontal surgery and periodontal recall every 3 months.
However, the patient did not comply and only had dental cleanings once or twice yearly. B, Radiographs 4 years later. Note the loss of teeth #5 and
#15 and the increased bone loss of several premolars and molars.
or unconscious decision not to continue treatment or the Classification of Posttreatment

failure of the dentist and staff to emphasize the need for
periodic examinations. Patients
4. Presence of some systemic diseases that may affect host The first year after periodontal therapy is important in
resistance to previously acceptable levels of plaque. terms of indoctrinating the patient in a recall pattern and
A failing case can be recognized by the following signs: reinforcing oral hygiene techniques. In addition, it may
take several months to evaluate the results of some peri-
1. Recurring inflammation revealed by gingival changes and odontal surgical procedures accurately. Consequently, some
bleeding of the sulcus on probing. areas may have to be retreated because the results may not
2. Increasing depth of sulci, leading to the recurrence of be optimal. Furthermore, the first-year patient often has
pocket formation. etiologic factors that may have been overlooked and may
3. Gradual increases in bone loss, as determined by radio- be more amenable to treatment at this early stage. For these
graphs. reasons, the recall interval for first-year patients should not be
4. Gradual increases in tooth mobility, as ascertained by clini- longer than 3 months.
cal examination. The patients who are on a periodontal recall schedule are
Cases that do not respond to adequate therapy or recur a varied group. Table 55.3 lists several categories of mainte-
for unknown reasons are referred to as refractory cases, nance patients and a suggested recall interval for each. Pa-
which may be seen in chronic or aggressive periodontitis. tients can improve or may relapse to a different classification,
The decision to retreat a periodontal patient should not be with a reduction in or exacerbation of periodontal disease.
made at the preventive maintenance appointment but should When one dental arch is more involved than the other, the
be postponed for 1-2 weeks. Often the mouth looks much patient's periodontal disease is classified by the arch with the
better at that time because of the resolution of edema and the worse condition.
resulting improved tone of the gingiva. Table 55.2 summa- In summary, maintenance care is a critical phase of therapy.
rizes the symptoms of recurrence of periodontal disease and The long-term preservation of the dentition is closely associ-
their probable causes. ated with the frequency and quality of recall maintenance.
FIGURE 55.9 A, Initial radiographs. The patient was advised to have localized areas of periodontal surgery and periodontal recall every 3 months.
However, the patient did not comply and had no treatment other than emergency care and occasional dental cleanings. B, Radiographs 7 years later.
Note the advanced bone loss and caries on many teeth.
TABLE 55.1
RADIOGRAPHIC EXAMINATION OF RECALL PATIENTS FOR SUPPORTIVE PERIODONTAL TREATMENTa

Patient Condition/Situation Type of Examination
Clinical caries or high-risk factors for caries Posterior bite-wing examination at 6-18-month intervals
No clinical caries and no high-risk factors for caries Posterior bite-wing examination at 24-36-month intervals
Periodontal disease not under good control Periapical and/or vertical bite-wing radiographs of problem areas every 12-24 months
History of periodontal treatment with disease under Bite-wing examination every 24-36 months
good control
Root form dental implants Periapical or vertical bite-wing radiographs after prosthetic placement and at 12 and
24 months, then every 24-36 months unless clinical problems arise
Transfer of periodontal or implant maintenance Full-mouth series if a current set is not available.
patients If full-mouth series has been taken within 24 months, radiographs of implants and
periodontal problem areas should be taken
Radiographs should be taken when they are likely to affect diagnosis and patient treatment. The recommendations in this table are subject to clinical judgment
and may not apply to every patient.
'Adapted from American Dental Association: Guide to patient selection and limiting radiation exposure (website). http://ada.org/2760/aspx. Accessed May 24, 2013.
Referral of Patients periodontal disease and systemic diseases, such as heart

disease, stroke, diabetes, and adverse pregnancy outcomes.
to the Periodontist Therefore, the prevalence of patients requiring SPT is likely to
Many periodontal patients can be well managed by the gen- increase in the future.
eral dentist as more people retain their teeth throughout their This expected increase in the number of periodontal pa-
lifetime and as the proportion of older people in the popula- tients will necessitate a greater understanding of periodontal
tion increases, more teeth will be at risk of periodontal dis- problems and an increased level of expertise for the solution
ease. Considerable research shows possible links between of such problems on the part of the general practitioner of
TABLE 55.2 It is immediately obvious that some patients should be

referred to a specialist, whereas most patients clearly have
SYMPTOMS AND CAUSES OF RECURRENCE problems that can be treated by a general dentist. For a
OF DISEASE third group of patients, however, it will be difficult to de-
Symptom Possible Causes cide whether treatment by a specialist is required. Any pa-
tient who does not clearly belong in the second category
Increased mobility Increased inflammation (Table 55.3) should be considered a candidate for referral
Poor oral hygiene to a specialist.
Subgingival calculus The decision to have the general practitioner treat a
Inadequate restorations
patient's periodontal problem should be guided by a con-
Deteriorating or poorly designed
prostheses
sideration of the degree of risk that the patient will lose a
Systemic disease modifying host tooth or teeth for periodontally related reasons or the risk of
response to plaque the periodontal disease contributing to their general health
Recession Toothbrush abrasion problems.
Inadequate keratinized gingiva The most important factors in the decision are the extent and
Frenum pull location of the periodontal deterioration. Teeth with pockets of
Orthodontic therapy 5 mm or more, as measured from the cementoenamel junc-
Increased mobility Occlusal trauma caused by lateral tion, may have a prognosis of rapid decline. The location of
with no change in occlusal interference, bruxism, and the periodontal deterioration is also an important factor in
pocket depth and no high restoration
determining the risk of tooth loss. Teeth with furcation lesions
radiographic change Poorly designed or worn-out prosthesis
Poor crown-to-root ratio
may be at risk even when more than 50% of bone support
Increased pocket depth Poor oral hygiene remains. Therefore, patients with strategically important
with no radiographic Infrequent recall visits teeth that fall into these categories are usually best treated by
change Subgingival calculus specia !is ts.
Poorly fitting partial denture An important question remains: Should the maintenance
Mesia! inclination into edentulous space phase of therapy be perfarmed by the general practitioner or the
Failure of new attachment surgery specialist? This should be determined by the amount of peri-
Cracked teeth odontal deterioration present. Class A recall patients should
Grooves in teeth be maintained by the general dentist, whereas Class C pa-
New periodontal disease
tients should be maintained by the specialist (Table 55.3).
Gingival overgrowth caused by
medication
Class B patients can alternate recall visits between the general
Increased pocket depth Poor oral hygiene practitioner and the specialist (Fig. 55.10). The suggested
with increased Subgingival calculus rule is that the patient's disease should dictate whether the gen-
radiographic bone Infrequent recall visits eral practitioner or the specialist should perform the maintenance
loss Inadequate or deteriorating restorations therapy.
Poorly designed prostheses
Inadequate surgery
Systemic disease modifying host
response to plaque Tests for Disease Activity
Cracked teeth Even though periodontal patients have received effective peri-
Grooves in teeth
odontal therapy, they are at risk of disease recurrence for the
New periodontal disease
rest of their lives. In addition, many pockets in furcation areas
may not have been eliminated by surgery. The best way of
determining areas that are losing attachment is to use a well-
dentistry. General dentists must know when comanagement organized charting system. Some computerized systems allow
with a periodontist is indicated. Specialists are needed to easy retrieval and comparison of past findings.
treat particularly difficult periodontal cases, patients with Comparison of sequential probing measurements gives
systemic health problems, dental implant patients, and those the most accurate indication of the rate of loss of attachment.
with a complex prosthetic construction that requires reliable A number of other clinical and laboratory variables have been
results. correlated with disease activity.
The question of where to draw the line between the cas- No accurate method of predicting disease activity exists,
es to be treated in the general dental office and those to be and clinicians rely on the information provided by combin-
referred to a specialist varies for different practitioners and ing probing, bleeding on probing, and sequential attachment
patients, and the American Academy of Periodontology has measurements. Patients whose disease is clearly refractory are
issued guidelines to help the general practitioner decide when candidates for bacterial culturing and antibiotic therapy in
comanagement with a periodontist is indicated. The diagnosis conjunction with additional mechanical therapy.
indicates the type of periodontal treatment required. If peri- New methods will undoubtedly be developed in the future
odontal destruction necessitates surgery on the distal surfaces to help predict disease activity. The clinician must be able to
of second molars, extensive osseous surgery, or complex re- interpret whether a test may be useful in determining disease
generative procedures, the patient is usually best treated by a activity and future loss of attachment. Tests should be adopted
specialist. On the other hand, patients who require localized only when they are based on research that includes a critical
gingivectomy or flap curettage usually can be treated by the analysis of the sensitivity, specificity, disease incidence, and
general dentist. predictive value of the proposed test.
55 Supportive Periodontal Treatm ent 651
TABLE 55.3
RECALL INTERVALS FOR VARIOUS CLASSES OF RECALL PATIENTS

Merin Classification Characteristics Recall Interval
First year First-year patient: routine therapy and uneventful healing 3 months
First-year patient: difficult case with complicated prosthesis, furcation 1-2 months
involvement, poor crown-to-root ratios, or questionable patient cooperation
Class A Excellent results well maintained for 1 year or more 6 months to 1 year
Patient displays good oral hygiene, minimal calculus, no occlusal problems, no
complicated prostheses, no remaining pockets, and no teeth with less than
50% of alveolar bone remaining
Class B Generally good results maintained reasonably well for 1 year or more, but 3-4 months (decide on recall
patient displays some of the following factors: interval based on number
1. Inconsistent or poor oral hygiene and severity of negative
2. Heavy calculus formation factors)
3. Systemic disease that predisposes to periodontal breakdown
4. Some remaining pockets
5. Occlusal problems
6. Complicated prostheses
7. Ongoing orthodontic therapy
8. Recurrent dental caries
9. Some teeth with less than 50% of alveolar bone support
10. Smoking
11. Positive family history or genetic test
12. More than 20% of pockets bleed on probing
Class C Generally poor results after periodontal therapy and/or several negative factors 1-3 months (decide on recall
from the following list: interval based on number
1. Inconsistent or poor oral hygiene and severity of negative
2. Heavy calculus formation factors; consider retreating
3. Systemic disease that predisposes to periodontal breakdown some areas or extracting
4. Many remaining pockets severely involved teeth)
5. Occlusal problems
6. Complicated prostheses
7. Recurrent dental caries
8. Periodontal surgery indicated but not performed for medical, psychologic,
or financial reasons
9. Many teeth with less than 50% of alveolar bone support
10. Condition too far advanced to be improved by periodontal surgery
11. Smoking
12. Positive family history or genetic test
13. More than 20% of pockets bleed on probing
confined to the soft tissues surrounding a dental implant with

no signs of loss of supporting bone beyond biologic bone
remodeling. Periimplantitis is defined as a process around an
Periodontitis implant that includes both soft-tissue inflammation and pro-
gressive bone loss beyond biologic bone remodeling. A system
Class A Mild or localized
A C systematic review showed a frequency of periimplant muco-
B Moderate sitis of 30. 7% of implants and a frequency of periimplantitis
C Advanced of 9 .6% of implants. Patients with periodontitis-associated
tooth loss are at a significantly increased risk of developing
periimplantitis.
General dentist Specialist
The overall periodontal condition in partially edentulous
FIGURE 55.10 Scheme for determining which practitioner should implant patients can influence the clinical condition around
perform periodontal maintenance in patients with different degrees of implants. The microflora of implants in partially edentulous
periodontitis.
patients differs from that in edentulous patients. The im-
plant microflora is similar to tooth microflora in the partially
Maintenance for Dental Implant edentulous mouth. Periodontal and implant maintenance are
Patients linked because maintenance of a tooth microflora consistent
with periodontal health is necessary to maintain implant mi-
According to the American Academy of Periodontology re- croflora consistent with periimplant health. Since periim-
port, periimplant diseases present in two forms-periimplant plantitis is difficult to treat, it is extremely important to treat
mucositis and periimplantitis. Periimplant mucositis is de- periodontal disease before implant placement and to provide
fined as a disease in which the presence of inflammation is good supportive therapy with implant patients.
In general, procedures for maintenance of patients with When prosthetics must be unscrewed and removed for
implants are similar to those for patients with natural teeth maintenance, it is best done in the office responsible for
except for the following three differences: placing the prosthetics. Each time the prosthetic appliances
are reattached, a slight change in the occlusion occurs. Time
1. Special instrumentation that will not scratch the implants
must be allowed for occlusal corrections.
is used for calculus removal on the implants.
2. Acidic fluoride prophylactic agents are avoided.
3. Nonabrasive prophy pastes are used. SUGGESTED READINGS
During the phase after uncovering the implants, patients American Academy of Periodontology: Position paper: periodontal mainte-
nance,] Peliodontol 74:1395, 2003.
must use ultrasoft brushes, chemotherapeutic rinses, tartar- American Academy of Periodontology: Peri-implant mucositis and peri-
control pastes, irrigation devices, and yarnlike materials to implantitis: a current understanding of their diagnoses and clinical impli-
keep the implants and natural teeth clean. Patients are often cations,] Periodontol 84:436, 2013.
reluctant to touch the implants but must be encouraged to Becker W, Becker BE, Berg LE: Periodontal treatment without maintenance: a
retrospective study in 44 patients,] Periodontol 155:505, 1984.
keep the areas clean.
Costa FO, Lages EJ, Cota LO, et al: Tooth loss in individuals under peri-
Special instruments should be used on the implants during odontal maintenance therapy: 5-year prospective study, J Periodontal Res
recall appointments. Metal-hand instruments and ultrasonic- 49:121, 2014.
and sonic tips should be avoided because they can alter the ti- Hirschfeld L, Wasserman B: A long-term survey of tooth loss in 600 treated
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Lang NP, Joss A, Orsanic T, et al: Bleeding on probing, J Clin Periodontal
gold-plated curettes should be used for calculus removal 13590, 1986.
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ber cup with flour of pumice, tin oxide, or special implant- J Clin Peliodontol 9:415, 1982.
polishing pastes should be used on abutment surfaces with Wilson TG Jr, Glover ME, Malik AK, et al: Tooth loss in maintenance patients
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Wilson V: An insight into peri-implantitis: a systematic literature review, Prim
Although, the daily use of topically applied antimicrobials Dent] 2:69, 2013.
is advised, acidic fluoride agents should not be used because
they cause surface damage to titanium abutments.
55 Supportive Periodontal Treatment 652.el
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Part Outline
56 Biological Aspects of Dental Implants 58 Surgical Concepts of Implant Therapy

57 Diagnosis and Treatment Planning 59 Periimplant Disease and Management
in Implantology 60 Supportive Implant Treatment
56
Biological Aspects
of Dental Implants
JP Fiorellini • K Wada • PG Stathopoulou • PR Klokkevold • A Jain
Chapter Outline
Implant Geometry (Macrodesign) Soft Tissue Interface
Implant Surface Characteristics Clinical Comparison of Teeth and
(Microdesign) Implants
Hard Tissue Interface Conclusions
Attempts to replace lost dentition by means of implanted Today, implant designs, surgical placement techniques,
materials can be traced back to the ancient Egyptians, who healing times, and restorative protocols continue to evolve
hammered shaped seashells directly into the Jaws for the pur- with the goal of improving outcomes. It is important for
pose of replacing teeth. Over the past few centuries, a variety clinicians to know periimplant anatomy, to understand the
of materials have been implanted into jaws in an attempt re- biology, and to appreciate the functional capacity of osseoin-
place missing teeth. The success of these early implants was tegrated implants. This chapter reviews implant geometry and
extremely poor primarily because they never achieved a stable surface characteristics, as well as the anatomical and biological
state of integration with the supporting tissues. The typical relationship of periimplant tissues.
outcome, regardless of material or design, was healing with a
soft tissue layer interposed between the implant and bone (ie,
fibrous encapsulation). Consequently, implants became mo-
Implant Geometry (Macrodesign)
bile, infected, and painful, which led to failure. Numerous implant systems with various geometric (macrode-
The history of modern implant dentistry began with the sign) designs have been developed and used before the current
introduction of titanium implants. In the 1950s, Per-Ingvar implant systems in use today Previous implant designs includ-
Branernark, a Swedish professor of anatomy, had a serendip- ed blade vents (narrow, flat shape; tapped into boney trough
itous finding while studying blood circulation in bone that prepared with rotary burs), press-fit cylindrical (bullet shape;
became a historical breakthrough in medicine. He discovered pressed or tapped into prepared hole), subperiosteal (custom-
an intimate bone-to-implant apposition with titanium that of- made framework; adapted to the surface of jawbone), and
fered sufficient strength to cope with load transfer. He called transmandibular (long rods or posts; placed through the an-
the phenomenon "osseointegration" and developed an im- terior mandible). Some of these implant systems were initially
plant system with a specific protocol to predictably achieve stable and appeared to be successful over short-term periods
it. The implants were used to anchor prosthetic replacement (eg, 5 years) but failed to remain stable, became symptomatic
teeth in the edentulous jaw, and the first patient was success- and/or loose, and failed over longer periods. Lacking predict-
fully treated in 1965. Subsequent clinical studies proved that ability, these implant systems are no longer used.
commercially pure (CP) titanium implants, placed with a Since the time of the Branernark studies, millions of pa-
strict protocol, including an unloaded healing period, could tients have been treated worldwide using variations of these
predictably achieve osseointegration and retain a full-arch techniques with implants of different geometries and sur-
prosthesis in function with a long-term success (15 years). face characteristics. Similar research including that of Andre
Since that time, millions of patients worldwide have had Schroeder in Switzerland in the mid-l 970s contributed to
missing teeth replaced with implants based on this original the success of endosseous dental implants. The serendipitous
concept. Over the years, implant systems with variations in finding of Branernark was that when a hole is prepared into
design (geometric and surface characteristics) and modified the bone without overheating or otherwise traumatizing the
protocols have been developed and used with equal or better tissues, an inserted biocompatible implantable device would
long-term success. predictably achieve an intimate bone apposition, as long as
655
656 PART 3 Oral lmplantology
BOX 56.1 cannot simply be extracted or removed by a trephine, as with

a cylindrical or screw-shaped implant.
1. Endosseous implants The interface between blade vent implant and bone was
• Bladelike called fibroosseous integration, which was defined as a tissue-
• Pins to-implant contact: interposition of healthy dense collagen
• Cylindrical (hollow and full)
fibers at the interface between the implant and bone. At that
• Disklike
• Screw shaped
time, the fibrous tissue was thought to be the replacement of
• Tapered and screw shaped the periodontal ligament; however, it was fibrous scar tissue
2. Subperiosteal framelike implants produced following the bone necrosis initiated by high-speed
3. Transmandibular implants drilling. This allows epithelial downgrowth around the post
caused by the bacterial infection, which leads to encapsulation
of blade implant with the fibrous scar tissue.
Most of the studies reported less than 50% success rate for
micromovements at the interface were prevented during the 5-year duration with the complication of pocket formation ex-
early healing period. The history of the research endeavors in ceeding 6 mm, followed by the significant alveolar bone loss
Sweden provides a better understanding of the relevant bio- around the implant. It was also a more complicated and inva-
logic parameters involved. sive surgery to remove the failed implant, which was sacrific-
The macroscopic configuration of implants has varied ing significant surrounding jawbone. As a result of the poor
widely; the most common types are listed in Box 56.1. Cur- long-term success, as well as the high complication rate, the
rently, most endosseous implants have a cylindrical or ta- use of blade vent implants has been significantly reduced. Re-
pered, screw-shaped/threaded design. The disastrous results moval of failed blade implants often requires significant cut-
with other implant configurations were largely responsible for ting and bone removal despite being mobile.
the evolution toward the current popular designs.
Pins
Although seldom used at present, in the classic technique,
Endosseous Implants three diverging pins were inserted either transgingivally or af-
Blade Implants ter reflection of mucoperiosteal flaps in holes drilled by spiral
Blade implants were designed and developed by Linkow and drills. At the point of convergence, the pins were intercon-
used clinically in 1960s and 1970s. Blade implants were in- nected with cement to ensure the proper stability because of
serted into the jawbone after mucoperiosteal flap elevation their divergence. On top of this arrangement, a single tooth
and preparation of a channel with a high-speed rotary bur. could be installed. In edentulous jaws, several of these pin
They were tapped into the narrow trench. One or several triads could be used to interconnect with a fixed prosthesis.
posts pierced through the mucoperiosteum after suturing of As with blade implants, the bone necrosis during drilling
the flaps. After a few weeks of healing, a fixed prosthesis was leads to fibrous encapsulation, marsupialization, and loss of
fabricated by a classic method and cemented on top of it. the implants because of infections. A positive aspect, however,
Since the high-speed drilling leads to extensive bone ne- is that when such implants must be removed, removing the
crosis at the histologic level, fibrous scar tissue formation oc- connection at the place of convergence is sufficient to allow
curs. This allows downgrowth of the epithelium, which leads easy extraction of each individual pin. Thus, bone loss from
to marsupialization of the blade implants (Fig. 56.1) If a bac- removal is minimal.
terial infection occurs, it can lead to an intractable periimplan- Disk Implants
titis with ample bone loss. More importantly, removal of such
implants after complications implies sacrificing the surround- Disk implants are rarely used at present. The concept devel-
ing jawbone. Due to its retentive geometry, the blade implant oped by Scortecci is based on the lateral introduction into the
jawbone of a pin with a disk on top. Once introduced into the
bone, the implant has strong retention against vertical extrac-
tion forces. Implants have been used with one, two, and even
three disks. Unfortunately, as mentioned previously for blade
implants, the cutting of the bone by means of high-speed
drills leads to a fibrous scar tissue surrounding the implant,
as revealed frequently by periimplant radiolucencies. Data on
the clinical success of disk implants are mostly anecdotal.
Root Form (Cylindrical) Implants

The first implant in this category, designed and developed by
Schroeder and coworkers between 1974 and 1985, was called
III (International Team for Implantology) hollow-cylinder, plas-
ma-sprayed, one-stage implant (Fig. 56.2). It was thought that
the hollow geometry should provide large bone-to-implant
contact and holes would favorable for the additional fixation
FIGURE 56.1 Blade implant shows a large radiolucency, indicating
that the fibrous encapsulation has led to deep pocketing and sub-
of the implant. However, the survival rates were less favorable
sequent bone loss. Neighboring teeth bear the load of the implant compared to the other system. Thus, this system was with-
restoration. drawn from clinical use.
56 Biological Aspects of Dental Implants 657
tooth. The system presented successful results in the short

term, but long-term success rates were unacceptable (38% in
10 years), leading to the limited use of this implant design.
For this reason, this implant is rarely seen in the market.
Even when an intimate bone apposition is achieved, extrac-
tion forces on such cylindrical implants lead to strong shear
forces at the bone-to-implant interface. Only the microscopic
surface irregularities offer some mechanical retention by inter-
digitation of bone growing onto the implant surface. With a
screw-based geometry, forces acting parallel to the long axis of
the implants are dispersed in many directions.
Transmandibular Implants
Transmandibular implants were developed to retain dentures
in the edentulous lower jaw. They were indicated for use in
the extremely resorbed edentulous mandible with a minimal
alveolar ridge height less than 10 mm. The implant was insert-
FIGURE 56.2 International Team for lmplantology (ITI) hollow cyl-
inder implant. Note the hollow geometry, which should provide large
ed through a submandibular skin incision and required gen-
bone-to-implant contact, and holes that theoretically should be favor- eral anesthesia. Two models were available in the 1960s. The
able for the additional fixation of the implant. first, called the staple-bone implant, was developed by Small. It
consisted of a splint adapted to the lower border of the man-
dible, to which it is fixed by stabilizing pins. Two transman-
When discussing cylindrical implants, it is important to dibular screws were driven transgingivally into the mouth.
distinguish between hollow and full cylindrical implants. The reported implant survival rate was 93% after 5 years and
Straumann and coworkers introduced hollow cylinders in the continued to exceed 90% after 15 years. The other model,
mid-1970s with the III system. The idea was that implant introduced by Bosker, has two metal splints, one below the
stability would benefit from the large bone-to-implant sur- lower border of the mandible and one intraorally to connect
face provided by means of the hollow geometry It was also the four posts piercing through the soft tissues. The Bosker
thought that the holes (vents) would favor the ingrowth of implant seemed less reliable than the staple-bone implant,
bone to offer additional fixation. The same concept was used achieving only 70% survival after 5 years in the mandibular
in the Core-Vent system developed by Niznick. Although it symphyseal area. Both transmandibular implants presented
was not clarified whether the cause was geometry or the as- with the gingival hyperplasia or infection with the incidence
sociated surface characteristics (titanium plasma-sprayed sur- of 10-15% of all cases. Despite the good long-term survival
face, titanium alloy), survival statistics were disappointing for data reported (especially for the staple implant), the high inci-
hollow cylinder implants. dence of complications and the necessity of using general an-
Solid cylindrical implants were used by Kirsch and be- esthesia for implant placement, the transmandibular implant
came available under the name IMZ, referring to the internal design is rarely used today
mobile shoch absorber. The IMZ system, developed by Kirsch,
prevailed in the market (Fig. 56.3). The characteristic func-
tion of this system was the internal mobile element (IME) shock Subperiosteal Implants
absorber, which was able to connect with the adjacent natural Subperiosteal implants are customized according to a plaster
model derived from an impression of the exposed jawbone,
before the surgery planned for implant insertion. The implant
was designed with several posts, typically four or more for
an edentulous jaw, which passed through the gingival tissues.
Subperiosteal implants are designed to retain an overden-
ture although fixed prostheses have also been cemented onto
the posts. As a result of epithelial migration, the framework
of subperiosteal implants usually becomes surrounded by fi-
brous connective tissue (scar), including the space between
the implant and the bone surface. The marsupialization, as
described earlier, often leads to infectious complications,
which often necessitates removal of the implant. Furthermore,
while being loaded by jaw function, jawbone resorption oc-
curs rapidly, resulting in a lack of adaptation of the frame to
the bone surface. As a result of this type of outcome, subperi-
osteal implants are now rarely used.
The subperiosteal implant was used in the treatment of
atrophic mandibles. The implant is custom designed to fit the
FIGURE 56.3 The IMZ implants. The roughened surface of the fixture
had an advantage of higher integration of bone. Conversely, the surface
mandibular jaw bone using a plaster model obtained from
characteristic added to the high frequency of periimplantitis in long-term an impression of the exposed mandible. It consisted of a cast
use. metal framework with a subperiosteal component in contact
FIGURE 56.4 A, illustration of a paral-

lel, threaded implant. B, Illustration of
a tapered, threaded implant. (Copyright
2012 BIOMET 3i, LLC. Used by permis-
sion, all rights reserved.)
with the bone and a transgingival component (posts), which

were used to retain the dental prosthesis. The number of
transgingival posts on the implants depend on the number of
missing teeth, averaging four to six for the totally edentulous
jaw. Several clinical studies reported poor survival rates of less
than 50% for 5-10 years, with the frequent complication of
gingival inflammation, involving tissue reaction around the
post caused by the lack of soft tissue attachment to the metal
post. These complications led to the development of sinus
tract resorption of the cortical bone and exposure of frame-
work. As a result of this higher rate of failure, as well as the
significant complications and surgical invasion, subperiosteal
implants are rarely used.
The most common implant design being used today is the
screw-shaped or threaded cylindrical implant (Fig. 56.4A). A
threaded implant design is preferred because it engages bone FIGURE 56.5 A tapered, threaded implant design is helpful to mini-
mize apical bone fenestration in areas such as the anterior maxilla, as
well and is able to achieve good primary stabilization. Even the result of the presence of labial concavities. Tapered implant designs
systems that started with cylindrical press-fit (nonthreaded) are also advantageous for immediate implant placement into extraction
designs progressively evolved to a threaded geometry. The sockets.
(longitudinal) shape of implants may be parallel or tapered
(Fig. 564B) Although a vast majority of all implants have
been parallel walled, the use of a tapered implant design has a major area of research interest and development over the
recently been advocated because it requires less space in the past 15-20 years. Modifications in surface energy, chemical
apical region (ie, better for placement between roots or in composition, and surface topography are known to influence
narrow anatomic areas with labial concavities). Tapered im- cellular activity and tissue responses leading to enhanced
plants have also been advocated for use in extraction sockets osteogenesis. At the molecular level, modified implant sur-
(Fig. 56 5) faces increase adsorption of serum proteins, mineral ions,
and cytokines, which subsequently promote cellular migra-
Implant Surface Characteristics tion and attachment. Implant surface characteristics can also
(M icrodesign) aid in the retention of a fibrin clot, thus providing a migratory
pathway for the differentiating osteogenic cells to reach the
Implant surface characteristics (microtopography) have been implant surface. Today, implants are treated with a variety
shown to positively influence the healing process. Accord- of technologies to modify surface characteristics (microscale
ingly, modification of implant surface characteristics has been or nanoscale) to enhance bone formation.
Additive Processes
The additive process modifies the microstructure/macrostruc-
ture and chemical nature of the implant surface by adding
materials or chemicals to the existing surface. There are sev-
eral methods used to add materials and/or chemicals to the
implant surface, such as inorganic mineral coatings, plasma
spraying, biocoating with growth factors, fluoride, and partic-
ulates or cements containing calcium phosphates, sulfates, or
carbonates. The addition of materials, such as hydroxyapatite
(Fig. 56.6), to the implant surface has been shown to enhance
or accelerate the initial bone cells adaptation or proliferation.
In general, additive surface modifications tend to increase the
surface texture greater than subtractive surface modifications,
which results in topographically "rougher" implant surfaces
(Fig. 56. 7). Surface roughness can also be increased by oxidiz-
ing or adding an oxide layer (Fig. 56.8)
Subtractive Processes
The subtractive process modifies the microstructure and
chemical nature of the implant surface by removing or alter-
ing the existing surface. The roughness of implant surface can
FIGURE 56.6 High magnification (acid fuchsin-toluidine blue; x100)
be modified by machining, acid etching, blasting, or a com- of hydroxyapatite-coated implant with intimate bone approximation.
bination of these processes to enhance the amount or speed Parts of the hydroxyapatite coating are observed on the surface.
FIGURE 56.7 Scanning electron mi-

croscope (SEM) image of titanium
plasma-sprayed surface implant with
rough surface characteristics. A, Im-
plant with titanium plasma-sprayed
surface (X40). B, Notably complex
macrotopography on titanium plasma-
sprayed surface (Xl 00). C, Titanium
plasma-sprayed surface with 1-25-µm
particles (XS00). D, Titanium plasma-
sprayed surface with 1-25-µm particles
(X1000).
of osseointegration. The changes are most notable at the mi-

croscopic level (Figs. 56. 9 and 56 10) Implant surfaces that
are modified at the microscopic level with techniques such
as acid-etching are thought to promote favorable cellular re-
sponses and increased bone formation in close proximity to
the surface (Fig. 56 11)
Hard Tissue Interface

The primary goal of implant installation is to achieve and
maintain a stable bone-to-implant connection (ie, osseoin-
tegration). Histologically, osseointegration is defined as the
direct structural and functional connection between ordered,
living bone and the surface of a load-bearing implant without
intervening soft tissues (Fig. 56.12). Clinically, osseointegra-
tion is the asymptomatic rigid fixation of an alloplastic mate-
FIGURE 56.8 Roughened surfaces are achieved by plasma spraying,
rial (implant) in bone with the ability to withstand occlusal
by acid etching, or as shown here by oxidizing (Ti Unite surface). (Cour- forces. The hard tissue interface is a fundamental requirement
tesy Nobel Biocare Services AC, Zurich, Switzerland.) for and an essential component of implant success.
(C) (0)
FIGURE 56.9 SEM image of machined surface implant with characteristic grooved pattern. A, Implant with machined surface (X40). B, Grooved
pattern apparent on machined surface (X100). C, Machined surface with distinct ridges and grooves (XS00). D, Machined surface with distinct ridges
and grooves (X 1000). (Courtesy Nobel Biocare Services AC, Zurich, Switzerland.)
FIGURE 56.10 SEM image of acid-etched surface implant with typical microscopic peak-valley appearance. A, Implant with acid etched surface
(X40). B, Microtextured surface alteration on acid-etched surface (Xl 00). C, Acid-etched surface with micropits of 1-3 µm (X XS00). D, Acid-etched
surface with micropits of 1-3 µm surrounded by larger areas with 6-10 µm peak-valley pits (Xl 000).
Initial Bone Healing osteoblasts and fibrous scar tissue will form between the bone
and implant surface. Therefore, it is important to avoid exces-
The osseointegration process observed after implant inser- sive forces, such as occlusal loading, during the early healing
tion can be compared to bone fracture healing. Implant site period.
osteotomy preparation (bone wounding) initiates a sequence Bone tissue damage and debris created by the osteotomy
of events, including an inflammatory reaction, bone resorp- site preparation must be cleared up by osteoclasts for normal
tion, release of growth factors, and attraction by chemotaxis bone healing. These multinuclear cells, originating from the
of osteoprogenitor cells to the site. Differentiation of osteopro- blood, can resorb bone at a pace of 50-100 µm per day. There
genitor cells into osteoblasts leads to bone formation at the is a coupling between bone apposition and bone resorption
implant surface. Extracellular matrix proteins, such as osteo- (Fig. 56.13). Preosteoblasts, derived from primary mesenchy-
calcin, modulate apatite crystal growth. Specific conditions, mal cells, depend on a favorable oxidation-reduction (redox)
optimal for bone formation, must be maintained at the healing potential of the environment. Thus, a proper vascular supply
site to achieve osseointegration. and oxygen tension are needed. If oxygen tension is poor, the
Immobility of the implant relative to the bone must be primary stem cells may differentiate into fibroblasts, form scar
maintained for bone formation at the surface. A mild in- tissue, and lead to implant failure (nonintegration).
flammatory response enhances the bone healing, but mod- If bone is overheated or crushed during preparation, it will
erate inflammation or movement above a certain threshold become necrotic and may lead to nonmineralized (soft tissue)
is detrimental. When micromovements at the interface ex- scar formation or be sequestered. The critical temperature for
ceed 150 µm, the movement will impair differentiation of
FIGURE 56.11 Histologic appearance of bone apposition. A, At 2 weeks, bone is deposited on the bony wall of the tissue chamber and on the
implant surface. Both layers are connected by a scaffold of tiny trabeculae. Woven bone is characterized by the intense staining of the mineralized
matrix and the numerous osteocytes located in large lacunae (undecalcified ground section, surface-stained with toluidine blue and basic fuchsin).
B, At 4 weeks, the volume density of this scaffold has increased both by the formation of new trabeculae and by deposition of more mature, parallel-
fibered bone onto the primary scaffold. Woven bone is mainly recognized by the numerous large osteocytic lacunae (bright). The gap between bone
and implant surface is an artifact. C, At 8 weeks, growth and reinforcement result in a further increase in bone density and an almost perfect coating
of the implant surface with bone. Remodeling has started, replacing the primary bone by secondary osteons (arrows).
bone cells that should not be exceeded is 4 7°C (116.6°F) at an and the bone; it grows fast, up to 100 µm per day, and in
exposure time of 1 min. Thus, preparation of implant osteoto- all directions. Characterized by a random orientation of its
my sites require profuse irrigation (cooling) along with gentle, collagen fibrils, high cellularity, and limited degree of miner-
intermittent, moderate-speed drilling using sharp drills. An- alization, the biomechanical capacity of woven bone is poor
other complicating factor, well recognized from open wound (Fig. 56.14A) Thus, any occlusal load should be well con-
fractures, is that microbial contamination jeopardizes the trolled or avoided in the early phase of healing. After several
normal bone healing. Accordingly, strict aseptic techniques months, woven bone is progressively replaced by lamellar
should be maintained. bone with organized, parallel layers of collagen fibrils and
New bone formation follows a specific sequence of events. dense mineralization. Contrary to the fast-growing woven
Woven bone is quickly formed in the gap between the implant bone, lamellar bone formation occurs at a slow pace (only a
FIGURE 56.12 A, Three-dimensional diagram of the tissue and titanium interrelationship showing an overall view of the intact interfacial zone
around the osseointegrated implant. B, Physiologic evolution of the biology of the interface over time.
Osteciblasts
Blood supply
Osteoclasts
FIGURE 56.13 The basic multicellular unit is the basic remodeling
process for bone renewal. Osteoclasts are imported by the vascular
supply, and the resorption lacunae are soon filled by the lining osteo-
blasts.
few microns per day). Ultimately, after 18 months of healing,

a steady state is reached where lamellar bone is continuously
resorbed and replaced (Fig. 56 14B) At the light microscopic FIGURE 56.14 A, After initial healing, woven bone, as characterized by
level, an intimate bone-to-implant contact has been extensive- its irregular pattern, is laid down. B, After weeks or months, progressively
ly reported (Fig. 56.15). Once the bone-to-implant interface a lamellar bone is laid down, with regular concentric lamellae. B, Bone;
/, implant. (Courtesy Professor T /slbrektsson, Gothenburg, Sweden.)
has reached a steady state, it can maintain itself over decades,
as ascertained by human histology from implants retrieved be-
cause of hardware fractures.
(macrodesign), as well as the quality and quantity of bone
Bone Remodeling and Function available for implant anchorage at a specific site. Secondary
stability, achieved over time with healing, depends on the im-
Clinically, both primary and secondary stability of an implant surface (microdesign), as well as the quality and quantity
plant are critical to success. Primary stability, achieved at the of adjacent bone, which will determine the percentage of con-
time of surgical placement, depends on the implant geometry tacts between the implant and bone. For example, areas such
SIEMENS
+ oooJ
...
....... .
·····
.. ...
FIGURE 56.15 Once a steady state has been achieved at the bone-
to-implant interface, an intimate contact can be observed, with some
marrow spaces seen in between at the light microscopic level.
as the anterior mandible have dense cortical bone and provide

rigid primary stabilization and good support throughout the
healing process. Conversely, areas such as the posterior max-
illa have thin cortical bone and large marrow spaces provide
less primary stability. For this reason, the posterior maxilla has
been associated with lower success rates compared to other
sites with greater bone density and support.
Once osseointegration is achieved, implants can resist and
function under the forces of occlusion for many years. Lon-
gitudinal biomechanical assessments seem to indicate that
during the first weeks after placement of one-stage implants,
decreased rigidity is observed. This may be indicative of bone
resorption during the initial phase of healing. Subsequently,
rigidity increases and continues to increase for years. Thus,
when a prosthesis is installed immediately (in 1 day) or early
(in 1-2 weeks), care must be taken to control against over-
load. It is important to recognize that sites with limited pri-
mary stability or less bone-to-implant contact (eg., posterior FIGURE 56.16 A, Periotest electronic apparatus (presently made by
Gulden, Bensheim, Germany) provides objective means to measure en-
maxilla) will likely go through a period of even less bone sup-
dosseous implant rigidity. B, Periotest measurement performed at surgery
port in the early stages of bone healing due to the initial phase to evaluate the increasing rigidity at future control visits.
of bone resorption.
Asessment of implant biomechanics can easily be done at
the clinical level by noninvasive devices such as the Periotest
(Fig. 56.16) and the Ostell (Fig. 56 17). The Periotest (Gul- These noninvasive tests reflect the rigidity of the bone to im-
den, Bensheim, Germany) projects a rod against the implant plant interface.
or abutment using a magnetic pulse at a certain speed. The The strength of the bone to implant interface cannot be clin-
apparatus measures the deceleration time needed before the ically assessed. Some investigators have measured the force
rod comes to a standstill. This is transformed in an arbitrary needed to undo the tight adhesion of bone tissues. This has
unit, which reflects the rigidity of the bone-to-implant con- often been done by counter torque force measurements to de-
tinuum values should be below + 7, the minimum with the termine the threshold at which loosening, or often fracturing,
most rigid being -8. Osseointegrated implants are thought to is observed. This methodology is questionable because it does
demonstrate an increased rigidity over time. The resonance fre- not reveal the strength of the biologic interface as such, but
quency analysis (RFA) offers an alternative measurement. With rather the congruency of the implant surface irregularities with
the Ostell device, a small transducer attached to the implant the surrounding bone. Indeed, a very roughened surface, such
imposes a series of frequencies and measures the overeall res- as that achieved with a titanium plasma-sprayed implant, will
onance frequency, because the transducer and the structure demonstrate a higher torque resistance than a turned one,
are constant, any change in the resonance frequency reveals where the grooves are much smaller in scale and run paral-
a change in the implant-bone interface, either in quality or in lel to the applied removal force. When the surface roughness
quantity. Primary stability measurements reveal a frequency is microscopic, such as that achieved with an acid-etched or
range of 6-9 kHz, with higher values in the mandible. The blasted implant, the bone adaptation to the microtopography
measures are transformed into arbitrary values where mea- will increase the shear strength needed to fracture the bone
surements should exceed 56, which indicate a level of bone from the surface to a level that is greater than a turned surface
support that is consistent with osseointegration (Fig. 56.18). but lesser than a plasma-sprayed surface.
is detached from the adhering bone. This is a difficult experi-

mental model that is seldom used.
Soft Tissue Interface

Not surprisingly, for two decades, research and clinical interest
focused on the bone-to-implant interface of osseointegrated
implants and the overlying soft tissues were largely ignored.
Except for a few descriptive sentences, the classic handbook
by Branernark et al presented no data or information about the
soft tissue interface. This may be due in part to the fact that
most patients were fully edentulous and the Branernark sys-
tem implants had turned (machined) surfaces, which are less
likely to be associated with soft tissue inflammatory problems.
Today, there is greater interest in and appreciation for periim-
plant soft tissues and the soft tissue-to-implant interface as
a function of esthetics and maintenance of a seal or barrier
against microbial invasion.
Periimplant soft tissues are similar in appearance and
structure to periodontal soft tissues (see Chapter 1). Clearly,
both implants and teeth emerge through the soft tissues on
the alveolar ridge. The soft tissues consist of connective tissue
covered by epithelium. There is a gingival/mucosal sulcus, a
long junctional epithelial attachment, and a zone of connec-
tive tissue above the supporting bone (Fig. 56.19). Despite
the apparent similarities in soft tissues around teeth and im-
plants, the presence of a periodontal ligament around teeth
and not around implants is an important, distinct difference.
Whereas natural teeth have a periodontal ligament with con-
nective tissue fibers suspending them in the alveolar bone,
osseointegrated implants do not. There are no inserting col-
lagen fibers anywhere along the interface of osseointegrated
implants. Bone is in direct contact with the implant surface
without intervening soft tissues.
Clinically, the thickness of the periimplant soft tissues
varies from 2 to several millimeters (Fig. 56.20). An animal
study determined the total height of the periimplant "biologic
FIGURE 56.17 A, Ostell device measures changes in resonance fre- width" to be approximately 3-4 mm where about 2 mm is
quency over time. B, Stimulator is fixed on the implant or abutment
the epithelial attachment and about 1-2 mm is the supra-
to transmit energy in a series of frequencies. Use of the Ostell allows
measurement of the primary stability at surgery. crestal connective tissue zone. Consistent with this finding, a
human histologic study determined the height of the periim-
plant "biologic width," consisting of an epithelial attachment
and supracrestal connective tissue, to be about 4-4.5 mm
Time At 1 2 3 4 5 6 (Fig. 56.21).
Abutment year years years years years years
Connection
Epithelium
Mean -2.16 -2.80 -2.92 -3.30 -3.90 -4.75 -5.50
*------------- •ir. As in the natural dentition, the oral epithelium (OE) around
implants is continuous with a sulcular epithelium that lines
*-----------------* the inner surface of the gingival sulcus; the apical part of the
~-----*
*---------* gingival sulcus is lined with long JE. Ultrastructural exami-
·:- ...
nation of the long junctional epithelial attachment adjacent
*---------------* to dental implants has demonstrated that epithelial cells at-
tach with a basal lamina and hemidesmosomes (Fig. 56.22).
FIGURE 56.18 Over time, Periotest values (PTVs, arbitrary units) in-
Histologic studies indicate that these epithelial structures and
dicate increasing rigidity, which parallels the increased bone density
over time. the surrounding lamina propria cannot be distinguished from
those structures around teeth. In health, the dimension of the
sulcular epithelium is about 0.5 mm, and the dimension of
Others have used pullout tests of the implants as a whole the epithelial attachment is about 2 mm, which is higher than
in a coronal direction. For screw-shaped implants, which are that of the periodontal epithelial attachment.
very retentive in this axis because of the threads, this approach The apical edge of the epithelial attachment is about
apparently cannot assess the biologic adhesion force. The real 1.5-2.0-mm above the bone margin. In healthy periimplant
test should be "pull-off' test in which a nonretentive surface tissues, progressive epithelial downgrowth does not occur,
56 Biological Aspects of Dental Implants 665.el
Implant Surface Chemical Composition molecules and the cells that will subsequently adhere to this
surface are influenced by the surface characteristics of this pel-
There have been unsuccessful trials with oral implants made licle layer. The composition and structure of the initial layer
of carbon or hydroxyapatite. The lack of resistance, because are largely determined by the underlying surface. Thus, the
of material properties, to occlusal forces led to frequent frac- three-dimensional shape of the molecules will be modified
tures. The so-called noble metals or alloys, however, do not during their adherence to this pellicle layer and will unveil
resist corrosion and have thus been abandoned. Today, the vast different radicals, depending on this metamorphosis.
majority of oral implants are made of CP titanium or titanium The surface free energy, often called wettability, is an im-
alloys. The following discussion relates to titanium implants. portant parameter for these interactions. It can be assessed
Titanium is a very reactive metal that oxidizes within nano- through the shape of a standardized drop of liquid put on the
seconds when exposed to air. Due to this passive oxide layer, clean implant surface. The angle of this drop toward the un-
the titanium then becomes very resistant to corrosion in its CP derlying surface reveals that the cohesive forces between liq-
form. Some alloys, such as titanium-aluminum 6%, vanadium uid molecules are stronger than the adhesive forces between
4% (Ti6Al4V), are known to provoke bone resorption as the the liquid and the surface. Thus, a ball-shaped drop would
result of leakage of some toxic components. The oxide layer reveal a low surface free energy.
of CP titanium reaches 10 nm of thickness. It grows over the Surface topography at the cellular and molecular level
years when facing a bioliquid. It consists mainly of titanium means microscopic roughness. Surface roughness can be mea-
dioxide (TiO2). sured with a profilometer, a stylus that follows the surface
All titanium oxides have dielectric constants, which are and measures the peak-to-valley dimensions (expressed as
higher than most other metal oxides. This factor may explain Ra values) or the spacing between irregularities (expressed as
titanium's tendency to adsorb biomolecules, as seen during S,x values). Wennerberg and Albrektsson provide guidelines
surgery when the blood creeps up the surface during implant for topographic evaluation of implant surfaces. No implant
insertion. The biomolecules normally appear as folded-up surface is smooth although several reports have incorrectly re-
structures to hide their insoluble parts, while putting water- ferred to the "turned" (machined) implant surface as "smooth"
soluble radicals on their surface. Thus, they will adhere to (see Fig. 56.9). Roughened implant surfaces speed up the
the TiO2 surface after displacing the original water molecules bone apposition; as demonstrated in vitro, more prostaglan-
sitting on its surface. Although initially attracted by weak van din E2 (PGE2) and transforming growth factor beta 1 (TGF-
der Waals forces, the high dielectric constant of titanium ox- ~1) are produced on rough than on smooth surfaces. Rough
ides and the polarizability of the molecules after adsorption surfaces may show some disadvantages, such as increased ion
will lead to high bond strengths, which are considered irre- leakage and increased adherence of macrophages and subse-
versible when they surpass 30 kcal/mo!. In fact, because of quent bone resorption.
its propensity for being covered by an uninterrupted oxide It was also reported that in vitro adsorption of fibronectin
layer, which has ceramic-like properties similar to other metal was higher on smooth than on rough, CP titanium surfaces.
oxides (eg, aluminum oxides), titanium makes the coating of Fibronectin is a glycoprotein quickly adhering on hard sur-
implants superfluous. This should be stressed because many faces and known to determine subsequent cell adhesion. Mi-
authors hope for even better osseointegration potential with crotopography also influences the number and morphology of
calcium phosphate (CaP)-coated surfaces and strongly advo- cell adhesion pseudopods and cell orientation. Grooves in an
cate their use. To date, clinical results with CaP-coated im- implant surface will guide the cell migration along their direc-
plants have not been encouraging in a long-term perspective. tion. Bone growth can enter altered microtopographic features
Thus, the overall view of potential advantages for different such as pits and porosities with internal dimensions that are
implant surface characteristics is complex, and only clinical only a few microns.
observations can determine their validity. For good-quality Lack of load can also be detrimental and can lead to corti-
bone, after 15 years of follow-up, clinical success rates of 99% cal bone resorption. This is well documented in orthopedics
have been reported for implants with a turned surface. En- and is termed stress shielding. This phenomenon has not been
hanced implant surface characteristics are likely to be most properly evaluated for oral implants in which marginal bone
beneficial for the more challenging situations, such as poor resorption is thought to be associated with chronic inflamma-
quality bone and early and immediate loading. tion of the overlying soft tissues.
The use of finite element analysis (FEA) has become popu-
Implant Surface Free Energy lar but lacks value by itself; invalid assumptions, such as the
isotropic nature of the bone, must be used in the modeling.
and Micro-Roughness
The deviation of FEA data from in vivo data has been well
When an implant is brought into contact with bodily tissues documented. FEA data should be considered as "descriptive"
and fluids, in this case mostly bone, it faces a "bioliquid," an models that require confirmation by biologic data. However,
aqueous environment. Within milliseconds, water, ions, and as with photoelastic studies, FEA analyses do provide some
small biomolecules are absorbed. One could imagine that this insight on stress concentrations and their relation to implant
absorbed layer renders all surfaces equal. However, the large geometry and the prosthetic superstructures.
,._ Sulcular
(crevicular) +----------Sulcular
epithelium epithelium
--------Junctional
epithelium --------Junctional
epithelium
'\" ...: Connective

tissue
(A) (B)
FIGURE 56.19 Schematic illustration of hard and soft tissue around a tooth and an implant. A, Hard and soft tissue anatomy around a natural tooth
demonstrates bone support with a periodontal ligament, a connective tissue zone above the crest of bone with connective tissue fibers (Sharpey) insert-
ing into dentin, a long junctional epithelial attachment, a gingival sulcus lined with sulcular epithelium, and oral gingival epithelium (outer surface of
gingiva). B, Hard and soft tissue anatomy around an implant demonstrates some similarities and some distinct differences. There is supporting bone
in direct approximation to the implant surface without any intervening soft tissues (ie, no periodontal ligament). A connective tissue zone is present
above the level of bone with fibers running parallel to the implant surface and no inserting fibers. There is a long junctional epithelial attachment, a
gingival/mucosal sulcus lined with sulcular epithelium and oral gingival/mucosal epithelium (outer surface of soft tissue). (From Rose LF, Mealey BL:
Periodontics: medicine, surgery, and implants, St. Louis, 2004, Mosby.)
ligament, cementum, and inserting fibers (Fig. 56.23). No

significant differences were found at the biochemical level
between the periimplant and the periodontal soft tissues,
while the dimension of the periimplant connective tissue is
1-2 mm, which is higher than that of the periodontal con-
nective tissue.
The zone of supracrestal connective tissue has an important
function in the maintenance of a stable soft tissue-implant
interface and as a seal or barrier to the "outside" oral environ-
ment. The orientation of connective tissue fibers adjacent to
an implant differs from that of periodontal connective tissue
fibers. In the absence of cementum and inserting connective
FIGURE 56.20 Clinical appearance of normal, healthy periimplant tissue fibers (ie, as in a natural tooth), most periimplant con-
tissue with implant restoration removed. Soft tissue thickness varies nective tissue fibers run in a direction more or less parallel to
from site-to-site, depending on quantity and quality of tissue, as well as
the implant surface. Even when the fiber bundles are oriented
the anatomy of the surrounding area (eg, adjacent to natural teeth with
healthy periodontal attachment versus adjacent to a space). Note that perpendicularly, which occurs more often in the gingiva than
the intrasulcular tissue appears more erythematous as the result of the in the mucosa surrounding implants, the bundles are never
thin, nonkeratinized layer of epithelium overlying the connective tissue. embedded in the implant surface.
(Courtesy Dr Stuart Froum, New York, NY) The fiber bundles can also have a "cuff-like" circular ori-
entation. The role of these fibers remains unknown, but it ap-
indicating that factors other than inserted collagen fiber bun- pears that their presence helps to create a soft tissue "seal"
dles (ie, Sharpey fibers in natural dentition) prevent it. around the implant. The adaptation of the connective tissue
to an implant surface may also be affected by the mobility of
the soft tissue around the implant. The connective tissue in
Connective Tissue
direct contact with the implant surface is characterized by an
Periimplant connective tissue morphology closely resembles absence of blood vessels and an abundance of fibroblasts in-
that of the natural dentition except that it lacks a periodontal terposed between collagen fibers. Several animal and human
FIGURE 56.22 A, Overview of ground section showing periimplant

tissues covered with keratinizing oral epithelium. JE is interposed be-
tween connective tissue and alveolar bone crest (BC). Apical end of JE
FIGURE 56.21 Buccolingual section (basic fuchsin stain; original
(arrow). Toluidine blue stain. (Bar= 200 µm.) B, Transmission electron
magnification X12.5; one-part SLA implant, 3 months unloaded)
microscopic view of sulcular epithelium showing tightly sealed inter-
showing the gingiva and the most coronal part of alveolar bone. Rete
cellular spaces by numerous spot desmosomes (arrows), contributing
peg formation is only apparent in the area of the keratinized oral gingi-
to low permeability of this portion of periimplant mucosa. Bar= 3 µm.
val epithelium. The oral sulcular epithelium exhibits no keratinization.
In the area of the most coronal point of the junctional epithelium (cJE),
the soft tissues are slightly torn away (artifact) because of nondecalcified
histologic processing. The most apical point of the junctional epithelium
UE) is indicated (aJE). No rete peg formation is evident adjacent to the studies have shown that the alignments of connective fibers
basal cell layer of the JE, all showing healthy and physiologic soft tissue were circular and horizontal around the implants (Fig. 56.24).
structures. In addition, the area of connective tissue contact (CTC) adja- More recent studies have shown histologic evidence of con-
cent to the machined titanium surface is marked. A slight round cell in-
filtrate in the connective tissue indicates a mild inflammation. Note bone
nective tissue attachment perpendicular to the microgrooved
remodeling/new bone formation in the crestal bone region indicated by implant surface on both animal and human studies. This la-
saturated, dark-red stained areas. ser-microtextured grooves (Fig. 56.25) have been shown to be
FIGURE 56.23 A, SEM image of the JE. Note the neutrophils located between the cells (red arrows). Bar= 40 µm. B, Higher magnification of
Fig. 56.22 with polarized light showing the apical extent (red arrow) of the JE. Note the dense collagen fibers running apicocoronal (ie, parallel to
the implant surface).
a b
,
i
Dk%-' ~· MR
Bo
(A) (B) (C)
FIGURE 56.24 A, Histologic scheme of epithelial attachment (EA) (identical for tooth and implant). Tl/, Titanium implant; BC, basal complex; LB/,
lamina basal is interna; LBE, lamina basal is externa (only location where cell divisions occur); a, long junctional epithelial attachment zone; b, sulcular
epithelial zone; c, oral epithelial zone. B, At electron microscopic level, basal complex at epithelial attachment (three most apical cells) and con-
nection with stroma. HD, Hemidesmosomes; 0, desmosome; LL, lamina lucida; LO, lamina densa; C, cuticle. C, Implant, abutment (Ab), and crown
within alveolar bone and soft tissues. Im, Endosseous part of implant; MR, margin of gingiva/alveolar mucosa; Bo, marginal bone level; l, implant
crown; 2, vertical alveolar-gingival connective tissue fibers; 3, circular gingival connective tissue fibers; 4, circular gingival connective tissue fibers; 5,
periosteal-gingival connective tissue fibers; a, junctional epithelium; b, sulcular epithelium; c, oral epithelium; All, abutment/implant junction; aAE,
apical (point) of attached epithelium.
FIGURE 56.25 A, Laser-microtextured surface; B, machined collar, SOOx. (Botos et al: Int J Oral Maxil/ofac Implants 26:492-498, 2011. With the
permission of Dr Spyros Botos.)
able to stop the epithelial downgrowth and establish connec- measurement performed with a periodontal probe may be
tive tissue insertion right at the most coronal part of the la- about 1.5-mm higher above the bone level in healthy tissues.
ser microgrooved area. (Fig. 56.26). A prospective controlled At inflamed sites, the probe may penetrate to the bone with
clinical study showed that laser-grooved surface resulted in probing depth measurement reflecting the total soft tissue
shallower probing depth and lesser periimplant crestal bone thickness above bone. In cases with inflammatory periimplant
loss than that seen around implants with machined collars. tissue disease, increasing probing depth and reduced attach-
This connective tissue interface has been examined by ment levels have been reported.
probing attachment level measurements in patients. Probing
attachment levels were consistently found coronal to the al-
Keratinized Tissue
veolar crest in patients with periimplant tissue health, indicat-
ing the presence of a zone of direct connective tissue contact Questions emerged decades ago, as it did for the natural
to the implant surface. This means that the probing depth dentition, about the need for keratinized tissue to surround
frequently when alveolar mucosa surrounds the implant as

compared to when keratinized mucosa surrounds the implant.
Keratinized mucosa tends to be more firmly anchored by
collagen fibers to the underlying periosteum than nonkera-
tinized mucosa, which has more elastic fibers and tends to
be moveable relative to the underlying bone. In clinical stud-
ies evaluating intraoral implants, with or without periimplant
keratinized mucosa, no clinically significant difference in im-
plant success was reported. However, when there is a lack of
keratinized tissue, patients tend to complain about pain and
discomfort while performing oral hygiene procedures or other
functions in the area. The symptoms are alleviated by increas-
ing the amount of keratinized (firmly bound) tissue around
the implant(s) via soft tissue grafting (see Fig. 50 5A-L)
Finally, although it may not be comparable to intraoral im-
plants, mobility of soft tissues surrounding extraoral implants
is associated with a higher incidence of implant failure.
Vascular Supply and Inflammation

FIGURE 56.26 Laser-ablated surface: epithelial downgrowth was The vascular supply of the periimplant gingival or alveolar
stopped right at the coronal-most microgrooved area (arrow). Apical to mucosa may be limited, as compared to periodontal gingiva,
the JE, healthy connective tissue fibers attached perpendicularly to the due to the lack of a periodontal ligament (Fig. 56 27) This
laser-ablated channels. (Courtesy Dr Myron Nevins.)
is especially true in the tissue immediately adjacent to the
implant surface. However, capillary loops in the connective
implants. Prospective and cross-sectional studies, evaluating tissue under the junctional and sulcular epithelium around
screw-shaped implants with a machined surface, suggest that implants appear to be anatomically similar to those found in
the presence or absence of keratinized gingiva is not a prereq- the normal periodontium (Fig. 56.28).
uisite for long-term stability. However, it has been suggested Emerging knowledge indicates that the periimplant gingi-
that implants surrounded by mucosa only (ie, nonkeratinized) val or alveolar mucosa has the same morphology as the corre-
are more susceptible to periimplant problems. An animal study sponding tissues around teeth. These soft tissues also react the
observed that ligature-induced periimplantitis occurs more same way to plaque accumulation. Studies investigating the
Abutment
Gingival epithelium
FIGURE 56.27 Schematic illustration of the blood supply in the

connective tissue cuff surrounding the implant/abutment is scarcer
than in the gingival complex around teeth because none originates Mucogingival
from a periodontal ligament. junction
FIGURE 56.28 A, Microvascular topography surrounding a tooth. B, Microvascular topography surrounding an implant. Bar= 5 µm. (Courtesy Dr
N. Selliseth and Or K. Selvig, Bergen, Norway.)
FIGURE 56.29 A, Histologic slide from healthy gingiva surrounding a well-functioning implant in human patient. No morphologic characteristics
differentiate tissue around implant from that around teeth. B, When gingivitis occurs, a profuse migration of inflammatory cells through the pocket
epithelium can be observed. (Courtesy Professor Mariano Sanz, Madrid.)
histology (light microscopic and ultrastructural) of healthy to bone loss and a fibrous inflammatory tissue at the implant
and inflamed tissues surrounding implants in humans have interface.
indicated that the inflammatory response to plaque is similar
to that observed in periodontal tissues. Polymorphonuclear Conclusions
cells and mononuclear cells transmigrate normally through
the periimplant sulcular epithelium (Fig. 56.29). Appreciating the osseointegration process is facilitated by a
good knowledge and understanding of bone healing. Many
factors can interfere with the predictable establishment of a
Clinical Comparison of Teeth and permanent rigid connection between an implant surface and
Implants the surrounding bone that is able to sustain occlusal loads.
Although the soft tissue-to-implant (abutment) interface of- The bone-to-implant interface and its rigidity are a predomi-
fers striking similarities with tissue surrounding the natural nant biomechanical aspect of coping with the time and inten-
dentition, some differences should be considered. At the bone sity of loading. The soft tissue-to-implant interface also plays
level, the lack of a periodontal ligament is the most striking an important role in the long-term maintenance of stable
difference. The following discussion elaborates on the clinical marginal bone levels around implants. Clinicians must famil-
perspectives of these similarities and differences. iarize themselves with the underlying molecular and cellular
At the bone level, the absence of the periodontal liga- events to evaluate the future evolution of implant design and
ment surrounding an implant has important clinical con- implant protocols, including surgical placement, restoration,
sequences. This means that no resilient connection exists and maintenance.
between implants and supporting bone. Implants cannot
intrude or migrate to compensate for the presence of a pre- SUGGESTED READINGS
mature occlusal contact (as teeth can). Implants and the rig- Abrahamsson 1, Soldini C: Probe penetration in periodontal and peri-implant
idly attached implant restorations do not move. Thus, any tissues. An experimental study in the beagle dog, Clin 0ml Implants Res
occlusal disharmony will have repercussions at either the 17:601-605, 2006.
Botos S, Yousef H, Zweig B, et al: The effects of laser microtexturing of the
restoration-to-implant connection, the bone-to-implant in- dental implant collar on crestal bone levels and peri-implant health, Int J
terface, or both. 0ml Maxillofac Implants 26(3):492-498, 2011.
Proprioception in the natural dentition comes from the Buser D, Schenk RK, Steinemann S, et al: Influence of surface characteristics
periodontal ligament. The absence of a periodontal ligament on bone integration of titanium implants. A histomorphometric study in
miniature pigs,] Biomed Mater Res 25:889-902, 1991.
around implants reduces tactile sensitivity and reflex function.
Davies JE: Mechanisms of endosseous integration, Int J Pmsthodont 11:
This can become even more challenging when osseointegrat- 391-401, 1998.
ed, implant-supported, fixed prostheses are present in both Hermann JS, Buser D, Schenk RK, et al: Biologic width around titanium im-
jaws. plants. A physiologically formed and stable dimension over time, Clin Oral
The lack of a periodontal ligament and inability of implants Implants Res 11:1-11, 2000.
Nevins M, Nevins ML, Camelo M, et al: Human histologic evidence of a con-
to move contraindicates their use in growing individuals. nective tissue attachment to a dental implant, Int J Periodontics Restorative
Natural teeth continue to erupt and migrate during growth Dent28:lll-121, 2008.
while implants do not. Implants placed in individuals prior to Nevins M, Kim DM, Jun SH, et al: Histologic evidence of a connective tissue
the completion of growth can lead to occlusal disharmonies attachment to laser microgrooved abutments: a canine study, Int] Periodon-
tics Restorntive Dent 30:245-255, 2010.
with implants. Likewise, it may be problematic to place one Nevins M, Camelo M, Nevins ML, et al: Connective tissue attachment to laser-
or more implants in a location adjacent to teeth that are very microgrooved abutments: a human histologic case report, Int J Paiodontics
mobile from the loss of periodontal support because as the Restorative Dent 32:385-392, 2012.
teeth move in response to or away from the occlusal forces, Pecora GE, Ceccarelli R, Bonelli M, et al: Clinical evaluation of laser micro-
the implant(s) will bear the entire load. texturing for soft tissue and bone attachment to dental implants, Implant
Dent 18 57-66, 2009.
Overload, because of improper superstructure design, Quirynen M, van Steenberghe D, Jacobs R, et al: The reliability of pocket
parafunctional habits, or excessive occlusal load, may cause probing around screw-type implants, Clin Orn/ Implants Res 2:186-192,
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56 Biological Aspects of Dental Implants 670.el
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57
Diagnosis and Treatment
Planning in lmplantology
PR Klokkevold • DL Cochran • S Tetradis
SM Mallya • E Chung • T-L Chang • A Jain
Chapter Outline
Case Types and Indications Clinical Selection of Diagnostic Imaging
Pretreatment Evaluation Patient Evaluation
Risk Factors and Contraindications Prosthetic & Biomechanical
Posttreatment Evaluation Considerations
Radiographic Evaluation of the Implant Biomechanical Considerations
Patient Treatment Planning With Dental
Standard Projections Implants
Cross-Sectional Imaging Strategies to Avoid Implant Overload
Endosseous dental implants and their retained prostheses an esthetic, secure, functional, and long-lasting manner. To
have had a great success over the past few decades follow- achieve this goal, clinicians must accurately diagnose the cur-
ing the landmark research and development of osseointe- rent dentoalveolar condition, as well as the overall mental
grated implants by Branemark et al. Initially, most prosthetic and physical well-being of the patient, to determine whether
reconstructions with osseointegrated implants were limited implant therapy is possible or practical and, perhaps most im-
to use in the edentulous patients, with many reports docu- portantly, whether it is indicated for a particular patient. Local
menting their excellent long-term success of implant-retained evaluation of potential jaw sites for implant placement (eg,
prostheses. measuring available alveolar bone height, width, and spatial
Following much success with implants in edentulous relationship) and prosthetic restorability is an essential part
patients, the original implant treatment protocols were of determining whether an implant(s) is possible. However,
adapted for use in partially edentulous patients. Although determining whether the patient is a good candidate for im-
some transitional problems were associated with the early plants is an equally important aspect of the evaluation pro-
use of dental implants in them, successes were eventually cess. This aspect of the patient evaluation includes identifying
achieved. Subsequently, modifications in implant design, factors that might increase the risk of failure or complications,
procedural techniques, and treatment planning greatly im- as well as determining whether the patient's expectations are
proved implant therapy for the partially edentulous patient. reasonable.
Currently, the long-term success of dental implants used to This chapter presents an overview of the clinical aspects
replace single and multiple missing teeth in the partially of dental implant therapy, including an assessment of pos-
edentulous patient is very good. Additionally, with the sible risk factors and contraindications. It also provides
implementation of bone augmentation procedures, even guidelines for the pretreatment evaluation of potential im-
patients with inadequate bone volume have a good op- plant patients and the posttreatment evaluation of patients
portunity to be successfully restored with implant-retained with implants.
prostheses. Virtually any patient with an edentulous space
is a candidate for endosseous implants and studies suggest
that greater than 90-95% success rates can be expected in Case Types and Indications
healthy patients with good bone health and normal healing
Edentulous Patients
capacity.
The ultimate goal of dental implant therapy is to satisfy The patients who seem to benefit most from dental implants
the patient's desire to replace one or more missing teeth in are those with fully edentulous arches. These patients can be
671
effectively restored, both esthetically and functionally, with

an implant-assisted removable prosthesis or an implant-
supported fixed prosthesis.
The original design for the edentulous arch was a fixed-
bone-anchored bridge that used five to six implants in the
anterior area of the mandible or the maxilla to support a
fixed, hybrid prosthesis. The design is a denture-like com-
plete arch of teeth attached to a substructure (metal frame-
work), which in turn is attached to the implants with cy-
lindrical titanium abutments (Fig. 5 7 .1). The prosthesis is
fabricated without flange extensions and does not rely on
any soft-tissue support. It is entirely implant supported.
Usually, the prosthesis includes bilateral distal cantilevers,
which extend to replace posterior teeth (back to premolars
or first molars).
Another implant-supported design used to restore
an edentulous arch is the ceramic-metal fixed bridge
(Fig. 57.2). Some patients prefer this design because the
ceramic restoration emerges directly from the gingival tis-
sues in a manner similar to the appearance of natural teeth.
Depending on the volume of existing bone, the jaw rela-
tionship, the amount of lip support, and phonetics, some
patients may not be able to be rehabilitated with an implant-
supported fixed prosthesis.
One limitation of both hybrid and ceramometal implant-
supported fixed prostheses is that they provide very little
lip support and thus may not be indicated for patients who
have lost significant alveolar dimension. This is often more
problematic for maxillary reconstructions because lip sup-
port is more critical in the upper arch. Furthermore, for some
patients, the lack of a complete seal (ie, spaces under the
framework) allows air to escape during speech, thus creating
phonetic problems.
Depending on the volume of existing bone, the jaw re-
lationship, the amount of lip support, and phonetics, some
patients may not be able to be rehabilitated with an im-
plant-supported fixed prosthesis. For these patients, a re-
movable, complete-denture type of prosthesis is a better
FIGURE 57.2 A, Clinical photograph of acrylic provisional fixed full-
choice because it provides a flange extension that can be arch prosthesis in the maxilla. B, Clinical photograph of the final cera-
adjusted and contoured to support the lip and there are no mometal restoration, anterior view. C, Occlusal view of final restoration
on master cast. (Courtesy Dr Russell Nishimura, Westlake Village, CA.)
spaces for unwanted air escape during speech. This type of

prosthesis can be retained and stabilized by two or more im-
plants placed in the anterior region of the maxilla or man-
dible. Methods used to secure the denture to the implants
vary from separate attachments on each individual implant
to clips or other attachments that connect to a bar, which
splints the implants together (Fig. 57.3). Advantages and
disadvantages of these attachment designs are discussed in
Chapter 58.
Although the stability of the implant-retained overdenture
does not compare to the rigidly attached, implant-supported
fixed prosthesis, the increased retention and stability over
conventional complete dentures is an important advantage
for denture wearers. Additionally, implant-assisted and im-
plant-Supported prostheses are thought to protect alveolar
FIGURE 57.1 Clinical photograph of patient with a complete maxil-
bone from additional bone loss caused by the long-term use
lary denture opposing a full-arch implant-supported fixed prosthesis of removable prostheses that are bearing directly on the al-
in the mandibular arch. veolar ridges.
57 Diagnosis and Treatment Planning in lmplantology 673
FIGURE 57.3 A, Laboratory view of maxillary overdenture bar attached to four implants with anterior clips and posterior extracoronal resilient at-
tachments (ERAs). B, Clinical view of maxillary overdenture bar. C, Palateless maxillary complete overdenture. D, Tissue surface of same maxillary
implant-assisted overdenture showing clips and ERAs. (Courtesy Dr John Beumer, UCLA Maxillofacial Prosthodontics, Los Angeles.)
Partially Edentulous Patients Early attempts to use endosseous implants to replace

missing teeth in the partially edentulous patient were a chal-
Multiple Teeth lenge partly because the implants and armamentarium were
Partially edentulous patients with multiple missing teeth designed for the edentulous patient and did not have much
represent another viable treatment population for osseointe- flexibility for adaptation and use in the partially edentulous
grated implants but the remaining natural dentition (occlusal patient. Today, clinicians have many choices in terms of im-
schemes, periodontal health status, spatial relationships, and plant length, diameter, and abutment connection to choose
esthetics) introduces additional challenges for successful refor the optimal replacement of any missing tooth, large or
habilitation. The juxtaposition of implants with natural teeth small (Fig. 57 5).
in the partially edentulous patient presents the clinician with The primary challenge with partially edentulous cases is an
challenges not encountered with implants in the edentulous underestimation of the importance of treatment planning for
patient. As a result of distinct differences in the biology and implant-retained restorations with an adequate number of im-
function of implants compared with natural teeth, clinicians plants to withstand occlusal loads. For example, one problem
must educate themselves and use a prescribed approach to the that required correction was the misconception that two im-
evaluation and treatment planning of implants for partially plants could be used to support a long-span, multiunit fixed
edentulous patients (see Chapter 57). In general, endosseous bridge in the posterior area. Multiunit fixed restorations in the
dental implants can support a freestanding fixed-partial den- posterior jaw are more likely to experience complications or
ture. Adjacent natural teeth are not necessary for support, but failures (mechanical or biologic) when they are inadequately
their close proximity requires special attention and planning. supported either in terms of the number of implants, quality
The major advantage of implant-supported restorations in of bone, or strength of the implant material (see Chapter 57).
partially edentulous patients is that they replace missing teeth The use of implants of adequate width and length and better
without invasion or alteration of adjacent teeth. Preparation treatment planning (more implants used to support more re-
of natural teeth becomes unnecessary and larger edentulous storative units), particularly in areas of poor-quality bone, has
spans can be restored with implant-supported fixed bridges. solved many of these problems.
Moreover, patients who previously did not have a fixed op-
tion, such as those with Kennedy Class I and II partially eden- Single Tooth
tulous situations, can be restored with an implant-supported Patients with a missing single tooth (anterior or posterior)
fixed restoration (Fig. 5 7. 4). represent another type of patient who benefits greatly from
FIGURE 57.4 A, Clinical view of partially edentulous posterior mandible (Kennedy Class II distal extension). B, Occlusal view of same patient in A
restored with implant-supported fixed restoration replacing teeth 1118 and 1119. Note that the dimensions of the crowns are smaller than typical man-
dibular molars (ie, closer to bicuspid size). C, Buccal view of same restorations.
1-s-l 1--s-l l-s-1 l-s-1 f-s.s, 1-s-l l--1.s-l

(A) (B)
FIGURE 57.5 Diagram representing the use of wide-, narrow-, and standard-diameter implants for molars, mandibular incisors, and other teeth
(different-sized implants superimposed over various teeth). A, Maxillary teeth. B, Mandibular teeth.
the success and predictability of endosseous dental im- implants often have a wider platform (restorative interface)
plants (see Video 57.1: Single Esthetic Implant Slide Show). that resists tipping forces and thus reduces screw loosening.
Replacement of a single missing tooth with an implant- The wide-diameter implant also provides greater strength
supported crown is a much more conservative approach than and resistance to fracture as a result of increased wall thick-
preparing two adjacent teeth for the fabrication of a tooth- ness (the thickness of the implant between the inner screw
supported fixed-partial denture. It is no longer necessary to thread and the outer screw thread). Implants with an inter-
"cut" healthy or minimally restored adjacent teeth to replace nal connection are inherently more resistant to screw loos-
a missing tooth with a nonremovable prosthetic replacement ening and thus have an added advantage for single-tooth
(Fig. 57.6). Reported success rates for single-tooth implants applications.
are excellent.
Replacement of an individual missing posterior tooth Esthetic Considerations
with an implant-supported restoration has been successful Anterior single-tooth implants present some of the same
as well. The greatest challenges to overcome with the single- challenges as the single posterior tooth supported by an im-
tooth implant restorations were screw loosening and implant but they also are an esthetic concern for patients. Some
plant or component fracture. Due to the increased potential cases are more esthetically challenging than others because of
to generate forces in the posterior area, the implants, com- the nature of each individual's smile and display of teeth. The
ponents, and screws often failed. Both these problems have prominence and occlusal relationship of existing teeth, the
been addressed with the use of wider-diameter implants and thickness and health of periodontal tissues, and the patient's
internal fixation of components (Fig. 57. 7). Wide-diameter own psychologic perception of esthetics, all play a role in
compromised or thin periodontium, inadequate hard or soft

tissues, and high expectations are probably some of the most
difficult challenges in implant dentistry and should not be at-
tempted by novice clinicians.
Pretreatment Evaluation
A comprehensive evaluation is indicated for any patient who
is being considered for dental implant therapy. The evalua-
tion should assess all aspects of the patient's current health
status, including a review the patient's past medical his-
tory, medications, and medical treatments. Patients should
be questioned about parafunctional habits, such as clench-
ing or grinding teeth, as well as any substance use or abuse,
including tobacco, alcohol, and drugs. The assessment should
also include an evaluation of the patient's motivations, level of
understanding, compliance, and overall behavior. For most
patients, this involves simply observing their demeanor and
listening to their comments for an impression of their overall
sensibility and coherence with other patient norms.
An intraoral and radiographic examination must be done
to determine whether it is possible to place implant(s) in the
desired location(s). Properly mounted diagnostic study mod-
els and intraoral clinical photographs are a useful part of the
clinical examination and treatment-planning process to aid in
assessment of spatial and occlusal relationships. Once the data
collection is completed, the clinician will be able to determine
whether an implant therapy is possible, practical, and indi-
cated for the patient.
Conducting an organized, systematic history and exami-
nation is essential in obtaining an accurate diagnosis and
creating a treatment plan that is appropriate for the patient.
FIGURE 57.6 Single-tooth replacement. A, Implant in place. B,
Metalloceramic crown.
Each treatment plan should be comprehensive and provide
several treatment options for the patient, including peri-
odontal and restorative therapies. Then, in consultation,
the clinician can agree on the final treatment plan with the
the esthetic challenge of the case. Cases with good bone vol- patient. Information gathered throughout the process will
ume, bone height, and tissue thickness can be predictable in help the clinician's decision-making process and determine
terms of achieving satisfactory esthetic results (see Fig. 57.6). whether a patient is a good candidate for dental implants. A
However, achieving esthetic results for patients with less- thoughtful and well-executed evaluation can also reveal de-
than-ideal tissue qualities poses difficult challenges for the ficiencies and indicate what additional surgical procedures
restorative and surgical team. Replacing a single tooth with an may be necessary to accomplish the desired goals of therapy
implant-supported crown in a patient with a high-smile line, (eg, localized ridge augmentation, sinus bone augmentation,
FIGURE 57.7 A, Occlusal view of healing abutment, which is attached to a wide-diameter implant used to replace a single missing molar. B, Radio-
graph of same patient depicted in A, showing the wide-diameter implant supporting the final restoration (molar replaced with a single-tooth implant-
supported crown).
etc.). Each part of the pretreatment evaluation is briefly dis- Dental History
cussed here.
A review of a patient's past dental experiences can be a valu-
able part of the overall evaluation. Does the patient report a
Chief Complaint history of recurrent or frequent abscesses, which may indi-
cate a susceptibility to infections or diabetes? Does the patient
What is the problem or concern in the patient's own words? have many restorations? How compliant has the patient been
What is the patient's goal of treatment, and how realistic are with previous dental recommendations? What are the patient's
the patient's expectations? The patient's chief concern, desires current oral hygiene practices?
for treatment, and vision of the successful outcome must be The individual's previous experiences with surgery and
taken into consideration. The patient will measure implant prosthetics should be discussed. If a patient reports nu-
success according to personal criteria. The overall comfort merous problems and difficulties with past dental care, in-
and function of the implant restoration are often the most cluding a history of dissatisfaction with past treatment, the
important factors, but satisfaction with the appearance of the patient may have similar difficulties with implant therapy.
final restoration will also influence the patient's perception of It is essential to identify past problems and to elucidate any
success. Furthermore, patient satisfaction may be influenced contributing factors. The clinician must also assess the pa-
simply by the impact that the treatment has on the patient's tient's dental knowledge and understanding of the proposed
perceived quality of life. Patients will evaluate for themselves treatment, as well as the patient's attitude and motivation
whether the treatment helped them to eat better, look better, toward implants.
or feel better about themselves.
The clinician could consider an implant(s) and the retained
prosthesis a success using standard criteria of symptom-free lntraoral Examination
implant function, implant stability, and lack of periimplant
infection or bone loss. At the same time, however, the pa- The oral examination is performed to assess the current health
tient who does not like the esthetic result or does not think and condition of existing teeth, as well as to evaluate the con-
the condition has improved could consider the treatment as dition of the oral hard and soft tissues. It is imperative that no
a failure. Therefore, it is critical to inquire, as specifically as pathologic conditions are present in any of the hard or soft
possible, about the patient's expectations before initiating im- tissues in the maxillofacial region. All oral lesions, especially
plant therapy and to appreciate the patient's desires and val- infections, should be diagnosed and appropriately treated be-
ues. With this goal in mind, it is often helpful and advisable to fore implant therapy. Additional criteria to consider include
invite patients to bring their spouses or family members to the the patient's habits, level of oral hygiene, overall dental and
consultation and treatment-planning visits to add an indepen- periodontal health, occlusion, jaw relationship, temporoman-
dent "trusted" observer to the discussion of treatment options. dibular joint condition, and ability to open wide.
Ultimately, it is the clinician's responsibility to determine if the After a thorough intraoral examination, the clinician can
patient has realistic expectations for the outcome of therapy evaluate potential implant sites. All sites should be clini-
and to educate the patient about realistic outcomes for each cally evaluated to measure the available space in the bone
treatment option. for the placement of implants and in the dental space for
prosthetic tooth replacement (Box 57.1). The mesial-distal
and buccal-lingual dimensions of edentulous spaces can be
Medical History approximated with a periodontal probe or other measur-
ing instrument. The orientation or tilt of adjacent teeth and
A thorough medical history is required for any patient in need their roots should be noted as well. There may be enough
of dental treatment, regardless of whether implants are part space in the coronal area for the restoration but not enough
of the plan. This history should be documented in writing space in the apical region for the implant if roots are directed
by the patient's completion of a standard health history form into the area of interest (Fig. 57.8). Conversely, there may
and verbally through an interview with the treating clinician. be adequate space between roots but the coronal aspects of
The patient's health history should be reviewed for any condi- the teeth may be too close for emergence and restoration of
tion that might put the patient at risk for adverse reactions or the implant. If either of these conditions is discovered, orth-
complications. odontic tooth movement may be indicated. Ultimately, eden-
Patients must be in reasonably good health to undergo surgi- tulous areas need to be precisely measured using diagnostic
cal therapy for the placement of dental implants. Any disorder study models and imaging techniques to determine whether
that may impair the normal wound-healing process, especially space is available and whether adequate bone volume exists
as it relates to bone metabolism, should be carefully consid- to replace missing teeth with implants and implant restora-
ered as a possible risk factor or contraindication to implant tions. Figure 57.9 diagrams the minimal space requirements
therapy (see section: Risk Factors and Contraindications). for standard-, wide-, and narrow-diameter implants placed
A thorough physical examination is warranted if any between natural teeth, and the minimal interocclusal space
questions arise about the health status of the patient. Ap- needed to restore implants.
propriate laboratory tests (eg, coagulation tests for a patient
receiving anticoagulant therapy) should be requested to
further evaluate any conditions that may affect the patient's Diagnostic Study Models
ability to undergo the planned surgical and restorative pro- Mounted study models are an excellent means of assess-
cedures safely and effectively. If any questions remain about ing potential sites for dental implants. Properly articulated
the patient's health status, a medical clearance for surgery models with diagnostic wax-up of the proposed restora-
should be obtained from the patient's treating physician. tions allow the clinician to evaluate the available space and
Mucli Space Is Required for the Placement of One or More lrnP.lants?'

ALVEOLAR BONE incrementally according to the size of the implant. For
Assuming an implant is 4 mm in diameter and 10 mm long, example, the minimal space needed for the placement of an
the minimal width of the jawbone needs to be 6-7 mm, and implant 6 mm in diameter is 9 mm (7 mm+ 2 mm). Whenever
the minimal height should be 10 mm (minimum of 12 mm in the avai I able space between teeth is greater than 7 mm and
the posterior mandible where an additional margin of safety is less than 14 mm, only one implant, such as placement of a
required over the mandibular nerve). This dimension is desired wide-diameter implant, should be considered. Two narrow-
to maintain at least 1.0-1.5 mm of bone around all surfaces of diameter implants could be positioned in a space that is
the implant after preparation and placement. 12 mm. However, the smaller implant may be more vulnerable
to implant fracture.
INTERDENTAL SPACE
Edentulous spaces need to be measured to determine whether INTEROCCLUSAL SPACE
enough space exists for the placement and restoration with The restoration consists of the abutment, the abutment screw,
one or more implant crowns. The minimal space requirements and the crown (it may also include a screw to secure the crown
for the placement of one, two, or more implants are illustrated to the abutment if it is not cemented). This restorative "stack" is
diagrammatically in Fig. 57.9. The minimal mesial-distal the total of all the components used to attach the crown to the
space for an implant placed between two teeth is 7 mm. The implant. The dimensions of the restorative stack vary slightly
minimal mesial-distal space required for the placement of two depending on the type of abutment and the implant-restorative
standard-diameter implants (4-mm diameter) between teeth is interface (ie, internal or external connection). The minimum
14 mm. The required minimal dimensions for wide-diameter amount of interocclusal space required for the restorative
or narrow-diameter implants will increase or decrease "stack" on an external hextype implant is 7 mm.
'All the minimal space requirements discussed here are generic averages. The actual space limitations for any particular implant system must be determined
according to the manufacturer's specifications.
to determine potential limitations of the planned treatment (Fig. 57.12). Clinical examination of the Jawbone consists
(Fig. 57 10) This is particularly useful when multiple teeth of palpation to feel for anatomic defects and variations in the
are to be replaced with implants or when a malocclusion is jaw anatomy, such as concavities and undercuts. If desired,
present. it is possible with local anesthesia to probe through the soft
tissue (intraoral bone mapping) to assess the thickness of
Hard-Tissue Evaluation the soft tissues and measure the bone dimensions at the pro-
The amount of available bone is the next criterion to evalu- posed surgical site.
ate. Wide variations in jaw anatomy are encountered, and it The spatial relationship of the bone must be evaluated in
is therefore important to analyze the anatomy of the dentoal- a three-dimensional (3D) view because the implant must be
veolar region of interest both clinically and radiographically. placed in the appropriate position relative to the prosthesis.
A visual examination can immediately identify defi- It is possible that an adequate dimension of bone is available
cient areas (Fig. 57.11), whereas other areas that appear in the anticipated implant site (Box 57.1), but that the bone
to have good ridge width will require further evaluation and thus the implant placement might be located too lingual
or too buccal for the desired prosthetic tooth replacement.
Bone augmentation procedures may be necessary to facili-
tate the placement of an implant in an acceptable prosthetic
position despite the availability of an adequate quantity of
bone (ie, the bone is in the wrong location). Indications for
the use of bone-augmentation procedures are discussed in
Chapter 58.
Radiographic Examination
Radiographic assessment of the quantity, quality, and location
of available alveolar bone in potential implant sites ultimately
determines whether a patient is a candidate for implants and if
a particular implant site needs bone augmentation. Appropri-
ate radiographic procedures, including periapical radiographs,
panoramic projections, and cross-sectional imaging, can help
identify vital structures, such as the floor of the nasal cavity,
maxillary sinus, mandibular canal, and mental foramen (see
Chapter 57). In addition to the absolute dimensional mea-
surement of the alveolar bone, it is important to determine
whether the volume of bone radiographically (as well as clini-
FIGURE 57.8 A, Clinical photograph of maxillary premolar space with cally) is located in a position to allow for the proper position of
apparently adequate space between the remaining teeth for an implant-
supported crown. B, Radiograph clearly shows a lack of space between
the implant to facilitate restoration of the tooth/teeth in proper
the roots of the adjacent teeth as a result of convergence into the space esthetic and functional relationship with the adjacent and op-
(same patient as in A). posing dentition. The best way to evaluate the relationship of
(A) (8)
The minimum mesial-distal (d) required for a: The minimum mesial-distal (d) required for two
A. Narrow diameter implant (e.g., 3.25 mm) is 6 mm. standard diameter Implants is 14 mm wide.
B. Standard diameter implant (e.g., 4.1 mm) is 7 mm.
C. Wide diameter implant (e.g., 5.0 mm) is 8 mm.
D. Wide diameter Implant (e.g., 6.0 mm) Is 9 mm.
FIGURE 57.9 A, Minimum amount of mesial-distal space (d) required for placement of single-tooth implant between natural teeth: (A) 6 mm for
narrow-diameter implant (3.25 mm); (B) 7 mm for standard-diameter implant (4.1 mm); (C and D) 8 mm and 9 mm, respectively, for wide-diameter
implants (5.0 mm and 6.0 mm). B, Minimum amount of mesial-distal space (d) required for placement of two standard-diameter (4.1 mm) implants
between natural teeth is 14 mm. This allows approximately 2 mm between teeth/implants and between implant/implant. Minimum amount of space
required between implant/restoration interface and opposing occlusal surfaces for restoration of an implant. This dimension will vary, depending on im-
plant design and manufacturer component dimensions. The minimal dimension of 7 mm is based on an externally hexed implant and UCLA abutment.
available bone to the dentition is to image the patient with a Risk Factors and Contraindications
diagnostically accurate guide using radiopaque markers that
are positioned at the proposed prosthetic locations, ideally Clearly, there are numerous indications for the use of endos-
with appropriate restorative contours (Fig. 5 7 .13). seous dental implants to replace missing teeth. Most patients
who are missing one or more teeth can benefit from the appli-
Soft-Tissue Evaluation cation of an implant-retained prosthesis provided they meet
Evaluation of the quality, quantity, and location of soft tissue the requirements for surgical and prosthetic rehabilitation.
present in the anticipated implant site helps to anticipate the Edentulous patients who are unable to function with com-
type of tissue that will surround the implant(s) after treatment plete dentures and who have adequate bone for the place-
is completed (keratinized vs nonkeratinized mucosa). For ment of dental implants can be especially good dental implant
some cases, depending on the clinician's view of keratinized candidates. Partially edentulous patients are increasingly be-
tissue, evaluation may reveal a need for soft-tissue augmenta- ing treated with dental implant restorations. Many patients,
tion (Box 57.2). Areas with minimal or no existing keratinized whether they are missing one, several, or all of their teeth, can
mucosa may be augmented with gingival or connective tissue be predictably restored with implant-retained prostheses.
grafts. Other soft tissue concerns, such as frenum attachments In this era of high implant success and predictability and
or pulls, should be thoroughly evaluated as well. thus possible complacency, it is imperative for clinicians to
FIGURE 57.10 Photographs of a diagnostic model with proposed lateral incisor and first molar tooth replacement waxed-up to evaluate the
amount of space and contours. A, Diagnostic cast of maxillary arch with missing left lateral incisor and left first molar. B, Diagnostic wax-up of
lateral incisor and first molar in the maxillary arch. C, Diagnostic cast of mandibular arch with missing left first molar. D, Diagnostic wax-up of first
molar. E, Articulated maxillary and mandibular diagnostic models with wax-up of lateral incisor and first molars to evaluate dimensions and contours.
(Courtesy Dr Stacy Yu, University of California, Los Angeles).
recognize risk factors and contraindications to implant ther- be successful in almost all patients; implants may be less pre-
apy so that problems can be minimized and patients can be dictable in some situations, and this distinction should be rec-
accurately informed about risks. As such, the clinician must ognized. Ultimately, it is the clinician's responsibility with the
be knowledgeable in this area and inform patients about risk patient to make decisions as to when implant therapy is not
factors and contraindications before initiating treatment. indicated.
Contraindications for the use of dental implants, although Table 57.1 (online) lists some conditions and factors that
relatively few and often not well defined, do exist. Some con- are thought to increase the risk for implant failure or other-
ditions are probably best described as "risk factors" rather wise deem the patient a poor candidate for implant therapy.
than "contraindications" for treatment because implants can Some of these conditions are briefly discussed online.
FIGURE 57.11 Clinical photographs of edentulous areas with obvious deficient areas of alveolar dimension noted on visual examination.
A, Anterior maxilla; B, Posterior maxilla; C, Anterior mandible; D, Posterior mandible. These clinical images all represent buccal-lingual deficiencies
in the alveolar dimensions.
FIGURE 57.12 Clinical photographs of edentulous areas with apparent good alveolar dimension noted on visual examination. A, Anterior max-
illa; B, Posterior maxilla; C, Anterior mandible; D, Posterior mandible. It is likely that these sites have adequate bone volume for implant placement.
However, it is also possible to find alveolar deficiencies despite the appearance of wide ridges.
FIGURE 57.13 The hammer-and-anvil effect is a useful analogy for the clinician to keep in mind, evoking the combination syndrome, when
planning treatment for an edentulous maxilla opposing a partially dentate mandible. A, Illustration of an edentulous maxilla opposing a mandible
that is missing posterior teeth. The lack of posterior occlusion leads to overclosure of the mandible and results in increased forces being applied to the
anterior maxilla by the mandibular anterior natural dentition. B, Illustration of the hammer-and-anvil effect of combination syndrome.
The debate about whether it is necessary to have a zone of for implant restorations. Keratinized mucosa is typically thicker
keratinized tissue surrounding implants continues. Despite and denser than alveolar mucosa (nonkeratinized). It forms a
strong opinions and beliefs about the need for keratinized strong seal around the implant with a cuff of circular (parallel)
mucosa around implants versus this mucosa being unnecessary, fibers around the implant, abutment, or restoration that is
neither argument has been proved. resistant to retraction with mastication forces and oral hygiene
Some studies have concluded that, in the presence of good procedures. Implants with coated surfaces [ie, hydroxyapatite
oral hygiene, a lack of keratinized tissue does not impair the or titanium-plasma spray coating] demonstrate greater
health or function of implants. Others strongly believe that periimplant bone loss and failures in the absence of keratinized
keratinized mucosa has better functional and esthetic results mucosa.
TABLE 57.1
RISK FACTORS AND CONTRAINDICATIONS FOR IMPLANT THERAPY

Risk Factor Contraindication
Medical and systemic health-related issues

Diabetes (poorly controlled) 77-Possibly Relative
Bone metabolic disease (eg, osteoporosis) 77-Probably Relative
Radiation therapy (head and neck) Yes Relative/Absolute
Bisphosphonate therapy [intravenous (IV)] 77-Probably Relative/Absolute
Bisphosphonate therapy (oral) 77-Possibly Relative
lmmunosuppressive medication ??-Probably Relative
lmmunocompromising disease (eg, HIV and AIDS) 77-Possibly Relative
Psychologic and mental conditions
Psychiatric syndromes (eg, schizophrenia and paranoia) No Absolute
Mental instability (eg, neurotic and hysteric) No Absolute
Mentally impaired and uncooperative No Absolute
Irrational fears and phobias No Absolute
Unrealistic expectations No Absolute
Habits and behavioral considerations
Smoking and tobacco use Yes Relative
Parafunctional habits Yes Relative
Substance abuse (eg, alcohol and drugs) 77-Possibly Absolute
Intraoml examination findings
Atrophic maxilla Yes Relative
Current infection (eg, endodontic) Yes Relative
Periodontal disease 77-Possibly Relative
57 Diagnosis and Treatment Planning in lmplantology 681.el
Medical and Systemic Health-Related Conversely, in a retrospective analysis of 49 patients who re-
Issues ceived sinus-bone augmentation, individuals (11 patients)
with lower bone mass density had significantly lower implant
Although few absolute medical contraindications to implant success rates as compared to age- and sex-matched controls.
therapy exist, some relative contraindications are important Other parameters evaluated in this study did not demonstrate
to consider. The clinician must consider medical and health- any significant differences.
related conditions that affect bone metabolism or any aspect Interestingly, there is a trend in aging adults (men over
of the patient's capacity to heal normally This category in- 50 years and postmenopausal women) for bone mass to de-
cludes conditions, such as diabetes, osteoporosis, immune crease progressively through bone demineralization at a rate of
compromise, medications, and medical treatments such as 1-2% per year and in some individuals as much as 5-8% per
chemotherapy and irradiation. year throughout their later life. If one considers this decline in
bone mass with aging along with a continually increasing life
Diabetes Mellitus expectancy in the population, the number of individuals with
Diabetes is a metabolic disease that can have significant effects osteopenia or osteoporosis will continue to increase, and the
on the patient's ability to heal normally and resist infections. concern about this condition's influence on implant success
This is particularly true for patients whose diabetes is not well will become increasingly more important for clinicians.
controlled. Poorly controlled diabetics often have impaired
wound healing and a predisposition to infections, whereas Medications
diabetic patients whose disease is well controlled experience Some prescribed medications, including steroids and bisphos-
few, if any, problems (see Chapter 12). phonates, may be cause for concern relative to the potential
There is concern about the success and predictability of im- implant patient. Corticosteroid therapy, whether used for hor-
plants in patients with diabetes. Several studies have reported mone replacement, cancer treatment, immune suppression, or
moderate failure rates in patients with diabetes, with implant other chronic condition may suppress the immune response,
success ranging from 85.6-94.3%. A prospective study dem- impair wound healing, or compromise the normal adrenal re-
onstrated 2.2% early failures and 7.3% late failures in diabetic sponse to stress. See the later section: Immune Compromise
patients. After 5 years, the overall success rate for this group and Immune Suppression, as well as Chapters 12, for more
of diabetic patients was 90%. None of these studies were able information on the treatment of patients taking corticoste-
to correlate gender, age, smoking, diabetes type, or level of roids and bisphosphonate medications. Only a brief statement
diabetic control with implant failure. In a metaanalytical re- regarding the risk of bisphosphonate therapy is offered here.
view of implant failures in patients who were not diabetics, Readers are encouraged to review more detailed explanations
the early implant failure rate was 3.2 % and the late implant in Chapters 12 and to consult online information, as well as
failure rate 5.2%. The finding that patients with diabetes ex- other resources, to get updated information about this im-
perience slightly more late failures may be related to less tis- portant subject as more is learned and recommendations are
sue integrity caused by reduced tissue turnover and impaired developed.
tissue perfusion. These results suggest that diabetes may be a Although there is heightened awareness and great con-
risk factor for implants, particularly for late failures. However, cern about risk of bisphosphonate-related osteonecrosis of
the risk does not appear to be particularly high. the jaw (BRONJ), the causal relationship and pathogenesis
of the problem has not been defined. A review of available
Bone Metabolic Disease literature offers information that will help to guide clini-
Osteoporosis is a skeletal condition characterized by de- cians in their decision-making, but it is far from definitive.
creased mineral density The two main classifications are pri- The prevalence and incidence remains uncertain. In general,
mary (three types) and secondary (multiple types) osteopo- the risk of BRONJ is between 1 in 10,000 and 1 in 100,000
rosis. Primary osteoporosis has been attributed to menopausal but may increase to 1 in 300 after an oral surgical procedure.
changes (type I), age-related changes (type II), or idiopathic The great majority of BRO NJ cases will likely remain in the IV
causes (type III). Secondary osteoporosis has been attributed to population. Cofactors, such as smoking, steroid use, anemia,
many different diseases and conditions, including diabetes, hypoxemia, diabetes, infection, and immune deficiency, have
alcoholism, malnutrition, and smoking. not been firmly established but may be important. Rarely does
All the various types of osteoporosis share the same funda- BRONJ in the oral bisphosphonate patient appear to progress
mental problem of decreased bone-mineral density, and the beyond stage 2 and many cases reverses with discontinuation
concern that this condition may impair the patient's ability to of oral medication. Procedures reported to have contributed
achieve and maintain implant osseointegration. The premise to the development of BRONJ include extractions, periodon-
that implants will not perform as well in a patient with os- tal surgery, root-canal treatment, and dental implant surgery
teoporosis is reasonable, given that osseointegration depends Dental implant therapy, as well as other surgical procedures,
on bone formation adjacent to the implant surface and that should be avoided in individuals who have been treated with
success rates are highest in dense bone and lowest in poor- IV bisphosphonate therapy and carefully considered with cau-
quality, loose trabecular bone. However, to date, there is no tion in patients treated with oral bisphosphonate therapy, par-
clear evidence to suggest that implants will not be success- ticularly those with a history of more than 3 years of use.
ful in patients with osteoporosis, so the issue continues to be
debated. On the positive side, although the evidence is weak, Immune Compromise and Immune Suppression
case reports have demonstrated successful implant treatment Individuals undergoing chemotherapy or taking medica-
in patients with osteoporosis. Some investigators advocate tions that impair healing potential (eg, steroids) are probably
the use of longer healing times for osseointegration to occur not good candidates for implant therapy because of the ef-
before loading the implants in patients with osteoporosis. fects these agents have on normal healing. This is especially
true for cancer chemotherapy. A lowered resistance to infec- Smoking and Tobacco Use
tion may also be problematic for these patients. Past history Moderate to heavy smoking has been documented to result
of chemotherapy or immunosuppressive therapy may not be in higher rates of early implant failure and adversely affect
problematic if the patient has recovered from the side effects the long-term prognosis of dental implant restorations. This
of treatment. is particularly true for implants placed in poor quality bone,
Patients with an immunocompromising disease, such as such as the posterior maxilla. The mechanisms of action re-
HIV infection or AIDS, are not good candidates for implants sponsible for higher implant failures associated with smoking
when their immune system is seriously impaired. Patients are not understood. Plausible explanations include the effect
with very low or undetectable viral loads and normal immune of smoking on white-blood cells, vasoconstriction, wound
function (T-cell counts) may be candidates for implant therapy healing, and osteoporosis. Smoking is a known risk factor for
(see Chapter 24). osteoporosis and thus may adversely affect implant success
through its effect on bone metabolism. Smoking cessation
Radiation Therapy
may improve the success rate of implants. In a metaanalyti-
Patients with a history of radiation treatment to the head and cal review, Bain et al found that implants with an altered sur-
neck region may not heal well after surgery. Soft tissue dehis- face microtopography (Biomet 3i, Osseotite; dual acid-etched
cence may follow surgical manipulation, which may lead to surface) seemed to significantly lessen the adverse effects of
osteoradionecrosis (ORN), a serious condition of nonhealing smoking on implant success.
exposure and infection of bone. This is especially problematic
for patients who have received radiation dosages greater than Parafunctional Habits
60 Gy. Surgical procedures, or any procedure that may initi- Parafunctional habits, such as clenching or grinding of teeth
ate a wound, are generally avoided in patients with a history (consciously or unconsciously), has been associated with an
of radiation therapy. If deemed necessary, surgical procedures increased rate of implant failure (eg, failure to integrate, loss
can be done in conjunction with hyperbaric oxygen (HBO) of integration, and implant fracture). Repeated lateral forces
therapy to reduce the risk of ORN. (ie, parafunctional habits) applied to implants can be detri-
Several studies have documented poor success rates for mental to the osseointegration process, especially during the
implants in patients with a history of radiation therapy. In a early healing period. Patients with known parafunctional hab-
literature review, Sennerby and Roos found irradiation to be its should be advised of an increased risk of complications or
associated with high failure rates, as did Esposito et al in their failures as a result of their clenching or grinding. Many con-
review. Beumer et al reported success rates as low as 60.4% in sider bruxism to be a contraindication to implant treatment,
the irradiated maxilla. Granstrom et al reported a significant especially in the case of a short-span, fixed-partial denture or
improvement in survival rates for implants in patients treated a single-tooth implant. If implants are planned for a patient
with HBO. However, in a systematic review, Coulthard et al with parafunctional habits, protective measures should be
concluded that the evidence is lacking to support the clinical employed, such as creating a narrow occlusal table with flat
effectiveness of HBO in irradiated patients receiving implants. cusp angles, protected occlusion, and the regular use of oc-
The application of implants in patients with a history of irra- clusal guards (see Chapter 57).
diation, with or without the use of HBO, is not resolved and
continues to be debated. Clearly, irradiation is a risk factor for Substance Abuse
implant success and may be a contraindication. Drug and alcohol abuse should be considered a contrain-
dication for implant therapy for reasons similar to the psy-
Psychologic and Mental Conditions chologic problems discussed earlier. Patients with drug or
In general, any type of psychologic abnormality can be con- alcohol addictions can be irresponsible and noncompliant
sidered a contraindication to dental implant treatment be- with treatment recommendations. Depending on the severity
cause of the patient's uncooperativeness, lack of understand- and duration of an individual's addiction, some patients may
ing, or behavioral problems. Physiologically, there is no reason be malnourished or may even have impaired organ function
to suspect that implants could not become osseointegrated in and therefore may not be good surgical candidates because of
these patients. However, the patient's ability to tolerate the poor healing capacity. All elective treatments, including im-
number and type of treatment appointments required for implant therapy, should be refused until addictions are treated
plant placement, restoration, and maintenance could be prob- and controlled.
lematic. All psychologic conditions have the potential to be
absolute contraindications to implant treatment depending on
the severity of the condition. The exception might be individ-
uals who demonstrate good cooperative behavior with only
mild psychologic or mental impairment. The clinician should
take great care before accepting a mentally or psychologically
impaired individual for treatment with implants.
Habits and Behavioral Considerations

Patients have a variety of habits and behaviors that may in-
crease the risk of failure for dental implants. Smoking, clench-
ing or grinding of teeth, and drug or alcohol abuse are among
the most well-known habits that should be identified because
of the increased risk for implant failure or complications.
Posttreatment Evaluation Radiographic Evaluation of the

Periodic posttreatment examination of implants, the retained Implant Patient
prosthesis, and the condition of the surrounding periimplant Several radiographic imaging options are available for di-
tissue is an important part of successful treatment. Aberra- agnosis and treatment planning of patients receiving dental
tions and complications can often be treated if discovered implants. Options range from standard projections routinely
early but many problems will go unnoticed by the patient. available in the dental office to more complex radiographic
Thus, periodic examination is essential in discovering prob- techniques typically available only in radiology centers. Stan-
lems early and to intervene and prevent problems from get- dard projections include intraoral (periapical and occlusal)
ting worse. Several parameters are available to evaluate the and extraoral (panoramic and lateral cephalometric) radio-
condition of the prosthesis, the stability of the implant(s), graphs. More complex imaging techniques include cone-beam
and the health of surrounding periimplant tissues after im- computed tomography (CBCT) and multislice computed to-
plant integration and prosthetic restoration. Intraoral radio- mography (MSCT). The CBCT and MSCT image data files
graphs should be taken at the time of placement (baseline), at can be reformatted and viewed on a personal computer us-
the time of abutment connection (confirm seating and serve ing simulation software, making the diagnosis and treatment-
as another baseline), at the time of final restoration deliv- planning process interactive and visually more meaningful.
ery (loading), and subsequently to monitor marginal or pe- Often, combinations of various modalities are used because
riimplant bone changes. Periapical radiographs have excel- no single modality can provide all information pertinent to
lent resolution and provide adequate details for evaluating the radiographic evaluation of the implant patient. Familiar-
bone support around implants if taken at a perpendicular ity with the benefits, limitations of various techniques, and
direction. awareness of the specific clinical questions that need to be
The long-term success of dental implants is dependent answered should guide the decision-making process and se-
on the health and stability of supporting periimplant tissues. lection of radiographic examinations for individual patients.
Good oral hygiene and regular professional care are essential Multiple factors influence the selection of radiographic
in maintaining periimplant health and the importance of good technique(s) for a particular case, including cost, availability,
oral hygiene should be stressed as early as possible. Patients radiation exposure, and case type. The decision is a balance
should be taught to maintain good oral hygiene. Their perfor- between these factors and the desire to minimize risk of com-
mance should be monitored and reinforced at each visit. plications for the patient. Accurately identifying vital ana-
See Chapter 60 for a detailed description of important tomic structures and being able to perform implant placement
clinical and radiographic monitoring methods, as well as oral surgery without injury to these structures are critical to treat-
hygiene and implant-maintenance protocols. ment success. Diagnostic imaging techniques must always be
Hence concluding, dental clinicians can now predictably interpreted in conjunction with a good clinical examination.
replace missing teeth with endosseous dental implants. Most This chapter discusses common imaging techniques used
patients, whether missing a single tooth, several teeth, or all for the evaluation of the implant patient. Indications for each
their teeth, can be candidates for dental implant therapy. How- technique are outlined, along with the advantages and limita-
ever, many factors influence the outcome; the clinician must tions of each technique.
consider the quantity, quality, and location of available bone;
the patient's mental and physical health; as well as risk fac-
tors and contraindications. Patients should be advised about
risk factors and be provided treatment options, both with and
Standard Projections
without dental implants. Periodic evaluation, good oral hy- Standard diagnostic imaging modalities include periapical,
giene, and regular maintenance are important aspects of care panoramic, lateral cephalometric, and occlusal radiographs.
for the long-term success and the prevention of complications Table 57.2 summarizes the advantages and disadvantages of
with dental implants. each modality. Individual modalities are discussed online.
TABLE 57.2
ADVANTAGES AND DISADVANTAGES OF THE VARIOUS RADIOGRAPHIC PROJECTIONS

Modality Advantages Disadvantages
Periapical and occlusal High resolution and detail, easy acquisition, low Unpredictable magnification, small imaged area, and
radiography exposure, and inexpensive 20 representation of anatomy
Panoramic radiography Easy to acquire, images whole ridge, low exposure, Unpredictable magnification, unequal magnification
and inexpensive in vertical and horizontal dimensions, and 20
representation of anatomy, not detailed
Lateral cephalometric Easy to acquire, predictable magnification, low Limited use in area of midline and 20 representation
radiography exposure, and inexpensive of anatomy
MSCT 30 representation, predictable magnification, sufficient Requires special equipment, is expensive, and has a
detail, digital format, and images whole arch high-exposure dose
CBCT 30 representation, predictable magnification, Requires special equipment and is expensive
sufficient detail, digital format, images whole arch,
and low dose
Periapical Radiographs
Periapical radiographs offer great advantages for the evaluation
of the implant patient. They provide an overall assessment of
the quantity and quality of the edentulous alveolar ridge and
the adjacent teeth. They are easy to obtain in the dental of-
fice, are inexpensive, and deliver low radiation to the patient
(Table 57 3) Dentists are familiar with the depicted anatomy
and possible pathology Since these direct-exposure proJec-
tions do not use intensifying screens, intraoral radiographs of-
fer the highest detail and spatial resolution of all radiographic
modalities (Fig. 57.14 ). Thus, intraoral radiographs are the
projection of choice when subtle pathology, such as a retained
root tip, needs to be detected and evaluated.
The most significant disadvantage of periapical radiographs
is their susceptibility to unpredictably magnify anatomic struc-
tures, which does not allow reliable measurements. Foreshort-
ening or elongation can be minimized by the use of paralleling FIGURE 57.14 The periapical radiograph offers a high-resolution, de-
technique. However, distortion is particularly accentuated in tailed image of the edentulous area. Healing of the extraction socket with
edentulous areas where missing teeth and resorption of the dense bone (socket sclerosis) can be seen (small white arrows). Some ana-
alveolus necessitate receptor placement at significant angula- tomic structures, such as the maxillary sinus (large white arrow) and the
zygomatic process of the maxilla (black arrow), can also be visualized.
tion in relation to the long axis of the teeth and the alveolar
bone. Additionally, periapical radiographs are two-dimension-
information of the buccal-lingual dimension of the alveolar
al (2D) representations of 3D objects and do not provide any
ridge. Structures that are distinctly separated in the buccal-lin-
gual dimension appear to be overlapping. Also, the periapical
TABLE 57.3 image is limited by the size of film or sensor being used. Often,
it is not possible to image the entire height of the remaining
RADIATION DOSE (EFFECTIVE DOSE IN µSV) alveolar ridge, and when extensive mesial-distal areas need to
RECEIVED FROM COMMON PROJECTIONS be evaluated, multiple periapical radiographs are required.
DURING EVALUATION OF THE IMPLANT In summary, periapical radiographs are useful screening im-
PATIENT DATN ages that offer a detailed view of a small area of the alveolar arch.
Modality Effective Dose (µSv) Limitations that must be considered include the possibility of
distortion and the 2D representation of anatomic structures.
Full-mouth X-ray (FMX) series 35-388
Panoramic 9-26
Conventional tomography 26-187 Occlusal Radiographs
CT of the head 2000
Occlusal radiographs are intraoral projections that offer easy,
Large FOV CBCT
New Tom 3G 30-68
economic, low-dose, and high-resolution images covering a
i-CAT: next generation portrait mode 74-83 larger area than periapical projections. Depending on recep-
Kodak 9500, 20 cm X 18 cm 93-260 tor placement and the angulation of the X-ray tube, occlusal
Galileos Comfort, 15 cm X 15 cm 70-128 radiographs can provide an image of the mandibular width or
Scanora 3D, 14.5 cm X 13.5 cm 68 can depict an extended area of the edentulous ridge. Occlusal
CB Mercuray, 20 cm diameter 569-1073 radiographs have the same limitations of distortion and over-
Medium FOV CBCT lapping anatomy as periapical radiographs.
Accuitomo 170, 10 cm X 5 cm 54 In summary, occlusal radiographic projections are good
iCat next generation, 16 cm X 6 cm 45 screening images as compared to periapical radiographic pro-
iCat, classic, 16 cm X 8 cm 34-77 jections as they provide an overview of the mandibular width
New Tom 3G, 10 cm diameter 57 and can visualize larger areas of alveolar ridge.
Kodak 9500, 15 cm X 8 cm 76-166
Prexion, 8 cm X 8 cm, low dose 189
Prexion, 8 cm X 8 cm, high dose 389 Panoramic Radiographs
Promax 3D, low dose 28
Promax 3D, high dose 122-652 Panoramic radiographs are often used in the evaluation of the
implant patient because they offer several advantages over
Small FOV CBCT
Accuitomo 3DX, 4 cm X 4 cm 13-44
other modalities. Panoramic radiographs deliver low radiation
Kodak 9000, 5 cm X 3.7 cm 19-40 (Table 57.3) to provide a broad picture of both arches and thus
PaX-Uni3D 44 allow assessment of extensive edentulous areas, angulation of
existing teeth and occlusal plane, and important anatomy in
'Reviewed by Ludlow JB, Davies-Ludlow LE, White SC: Patient risk related
to common dental radiographic examinations: the impact of 2007 Interna- implant treatment planning, such as the maxillary sinus, nasal
tional Commission on Radiological Protection recommendations regarding cavity, mental foramen, and mandibular canal (Fig. 57.15).
dose calculation, J Am Dent Assoc 139:1237, 2008; Ludlow JB, Ivanonic Panoramic units are widely available and easy to operate and
M: Comparative dosimetry of dental CBCT devices and 64-slice CT for dentists are familiar with the anatomy and pathology depicted
oral and maxillofacial radiology, Orn/ Sw·g Orn/ Med Orn/ Pathol Oral Radial
Endod 106 106, 2008; and White SC, Mallya SM: Update on the biological
by the images. Similar to intraoral projections, panoramic im-
effects of ionizing radiation, relative dose factors, and radiation hygiene, ages are 2D and thus do not offer diagnostic information for
Aust Dent] 57(Suppl 1):2, 2012. the buccal-lingual width of the alveolar arch.
implant patient is limited to structures at the midline, with

minimal usefulness for other areas of the jaws.
In summary, lateral cephalometric radiographs have a lim-
ited use in implant treatment planning.
Cross-Sectional Imaging
Cross-sectional diagnostic imaging modalities include MSCT
and CBCT. Conventional tomography also provides cross-
sectional images with predictable magnification and has been
used in the assessment of the implant patient. However, with
the introduction and expansion of CBCT imaging, conven-
FIGURE 57.15 Panoramic radiograph. Both jaws are visualized on the
same image. An overall assessment of superoinferior and mesial-distal di-
tional tomography is becoming progressively infrequent and
mensions of the alveolar ridge can be formulated. Tooth and root positions is not described in this chapter.
relative to planned implant sites can be evaluated. Important anatomic struc-
tures, such as the maxillary sinus and mandibular canal, can be identified.
Multislice Computed Tomography
Panoramic images appear intuitively familiar. However, they CT scanning is widely used in the evaluation of the implant
combine characteristic physical and radiographic principles that patient. The detailed physics behind image acquisition during
make them distinct from other intraoral and extraoral radio- CT scanning are beyond the scope of this chapter. In general,
graphs. Although outside the scope of this chapter, familiarity a fan-beam of X-rays and an array of detectors rotate around
with the principles underlying panoramic radiography is central the patient to generate axial slices of the area of interest
in understanding, and thus compensating for, the limitations and (Fig. 57.16A). Multiple overlapping axial slices are obtained
constraints of the images. The reader is referred to other textbooks by several revolutions of the X-ray beam until the whole area
for detailed discussion of this topic. Briefly, the existence of ghost of interest is covered. These slices are then used to generate
shadows, unpredictable horizontal and vertical magnification, a digital volume of the imaged object with the help of a com-
distortion of structures outside the focal trough, projection ge- puter and sophisticated algorithms. CT's advantage during
ometry generated by the negative vertical angulation of the X-ray evaluation of the implant patient is the construction of this
beam, and propensity to patient-positioning errors do not allow 3D digital map of the jaws. Specialized software can be used
consistent detailed and accurate measurements to be generated. to generate appropriate views that best depict the dimensions
As a result, panoramic radiographs do not provide the highly de- of the jaws and the location of important anatomic structures.
tailed images that are generated by intraoral radiographs. Typical dental views reconstructed from a CT scan include
Measurement distortion is more prevalent and varies axial (Fig. 57.16B), panoramic (Fig. 5716C), and cross-
across the radiographic image. On average, panoramic radio- sectional (Fig. 57.16D) views of the jaws. Appropriate axial
graphs are 25% magnifications of actual size. Implant manu- slices through the alveolar ridge of interest are selected as
facturers often provide transparency sheets with implant size scout views. The curvature of the maxillary or mandibular
outlines of 25% magnification. However, it is important to ridge is then drawn on the axial slices and panoramic images
appreciate that the 25% magnification is an estimate. The ac- along the drawn line are created. Finally, cross-sectional slic-
tual magnification may range from 10-30% in different areas es, every 1-2 mm and perpendicular to the drawn curvature,
within the same image and depends greatly on patient posi- are created. In addition to these flat, 2D views, complex, 3D
tioning during panoramic radiography For this reason, pre- images with surface rendering can also be generated from the
cise measurements on panoramic projections are not possible. CT data (Fig. 57 16E) These images can provide useful infor-
Nonetheless, panoramic radiographs offer an overall view of mation about the alveolar ridge defects that are easy to com-
the maxilla and mandible that can be used to estimate bone prehend. Images can be printed on photographic paper or
measurements and evaluate the approximate relationships transparent film or can be displayed on the computer screen.
between teeth and other anatomic structures. More precise CT scans offer several advantages for evaluation of the implant
diagnostic imaging should be used to measure the proximity patient. True cross-sections offer a precise and detailed evalua-
of critical anatomic structures, such as the maxillary sinus, the tion of the height and width of the alveolar ridge. The images
mandibular canal, or proposed implant positions. can be adjusted and printed without magnification, facilitating
In summary, panoramic projections are useful screening measurements directly on the prints or films with standard rul-
images of the jaws for approximations and relative spatial re- ers (ie, not magnified). Vertical and horizontal rulers adjacent
lationships. However, because of magnification and distortion to each section allow the clinician to check for magnification
errors, panoramic radiographs should not be used for detailed and make direct measurements. The digital format allows for
measurements of proposed implant sites. image enhancement tools, rapid communication between the
radiologist and the surgeon, and generation of multiple copies
Lateral Cephalometric Radiographs of the images. Various anatomic structures can be visualized and
analyzed at all three coordinate axes, so that their superoinfe-
Lateral cephalometric radiographs are occasionally used to rior, anteroposterior, and buccolingual location can be identified
evaluate potential implant patients. These projections pro- with precision. The process of CT-scanning images the entire
vide useful information for the cortical thickness, height, and arch (usually one arch/scan), so several edentulous areas can be
width of the alveolar ridge at the midline, as well as the skel- visualized with a single examination. The bone- and soft-tissue
etal relationship between maxilla and mandible and facial pro- contrast and resolution are excellent for the diagnostic task.
file. Lateral cephalometric radiographs are low in cost, readily CT scanning requires specialized equipment and setting.
available, easy to interpret, and have a predictable magnifi- Radiologists and technicians need to be knowledgeable of the
cation of the depicted structures. However, their use for the anatomy, anatomic variants, and pathology of the jaws, as well
57 Diagnosis and Treatment Planning in lmplantology 682.e3
FIGURE 57.16 Computed tomography (CT) examination for evaluation of edentulous maxilla before implant placement. A, Scout view of the
patient's head; axial sections through the area of interest are indicated. B, Axial slice through the markers is used to display the orientation of the pan-
oramic and cross-sectional images through the alveolar ridge. C, Panoramic views through the alveolar ridge demonstrate the relation of the markers
to adjacent teeth. D, Cross-sectional slices through the area of the markers reveal the height and buccolingual dimension of the alveolar ridge, as well
as the relation of the markers to the ridge. E, 3D reconstructions provide an overall impression of the bone contours and shape of the alveolar ridge.
as, considerations pertinent to implant treatment planning, so An important feature of the various CBCT units is the field
that optimal views will be provided. A CT scan delivers a much of view (FOV) describing the extent of the imaged volume.
higher radiation dose to the patient than other modalities used CBCT units can be distinguished in large-FOV (> 15 cm),
during implant treatment planning (Table 57.3). Since a CT scan medium FOV (5-15 cm), and limited-FOY systems ( <5 cm).
images the whole arch, radiation is delivered to the entire im- Figure 5 7 .17 depicts schematically the anatomic area covered
aged area, regardless of how many or few sites are actually need-
ed. Metallic restorations can cause ring artifacts that impair the
diagnostic quality of the images. This is particularly challenging
in patients with heavily restored dentition. In general, the cost of
CT is significantly higher than that of conventional tomography
or the other standard intraoral and extraoral projections.
In summary, CT scanning offers many advantages during
implant treatment planning, including accurate cross-section-
al imaging and 3D visualization of anatomic structures. High
doses to the patient and ring artifacts caused by metallic resto-
rations are concerns that should be considered.
Cone-Beam Computed Tomography

CBCT is a newer imaging modality that offers significant advan-
tages for the evaluation of implant patients. CBCT was intro-
duced to dentistry in the late 1990s, and currently several CBCT
units are commercially available for imaging of the craniofacial
complex. The X-ray source and the detector are diametrically
positioned and make a 180-360-degree rotation around the
patient's head within the gantry The shape of the X-ray beam
is that of a cone. Thus, at the end of a single complete rotation,
180-500 images of the region of interest are generated. The
computer uses these images to generate a digital, 3D map of the
face. Once this map is generated, multiplanar reconstructions,
as well as axial, coronal, sagittal, or oblique sections of various FIGURE 57.17 Schematic diagram of the anatomic area imaged with
thicknesses, can be reconstructed from the data. large (green), medium (blue), and limited (magenta) FOVCBCT.
FIGURE 57.18 CBCT images for the evaluation of the edentulous space at the area of missing tooth #30 before implant placement using a large
FOV unit (NewTom 3G, Verona, Italy distributed by AFP Imaging, Elmsford, NY). Note the tooth-shaped marker used. A, Series of "panoramic" re-
constructions through the alveolar ridge reveals the relationship of the marker to the adjacent teeth. The top "panoramic" view is 12 mm thick so as
to depict most of the extent of the alveolar ridge and adjacent teeth. The middle "panoramic" image is 1 mm thick through the area of the mandibular
canal. Note that adjacent teeth are out of the plane of the section and thus not depicted on the image. The bottom "panoramic" view is the same as
the middle one but the position of the mandibular canal has been depicted by the red line. B, Scout axial view and series of cross-sections through
the area of the marker. The bottom row shows the same axial slices as the top row. However, the position of the red line drawn on the panoramic view
is also depicted to help localization of the mandibular canal. The height and width of the alveolar ridge have been measured in a selected section.
C, 3D reconstructions provide an overall impression of the bone contours and shape of the alveolar ridge. Note the small exostosis on the lingual
surface of the alveolar ridge.
by large, medium, and limited FOV scans. In general, large from fat or connective tissue compared to CT scans. Fortu-
FOV units image a more extensive anatomic area, deliver a nately, contrast resolution is not a significant concern in im-
higher radiation exposure to the patient, and produce lower plant evaluation. Since bone has a much higher density than
resolution images (Fig. 57 18). Conversely, limited FOV units surrounding soft tissues, both CBCT and CT can clearly depict
image a small area of the face, delivering less radiation and bone shape and architecture. One of the most significant ad-
producing a higher resolution image (Fig. 57 19) vantages of CBCT scanning versus CT scanning is the reduced
CBCT offers the same advantages and disadvantages as CT. amount of radiation dose delivered to the patient (Table 57.3).
However, the two modalities have basic differences that re- In summary, CBCT scanning is a valuable imaging modali-
sult from the different physical principles used during image ty for 3D and cross-sectional evaluation of the implant patient.
acquisition. CT scan offers a greater contrast resolution, or the It has similar advantages and disadvantages as CT scanning.
ability to distinguish two objects with small-density differ- The most significant difference is that CBCT imaging delivers
ences. CBCT scans have a limited capacity to separate muscle much less radiation exposure to the patient.
57 Diagnosis and Treatment Planning in lmplantology 682.eS
FIGURE 57.19 CBCT images for the evaluation of the edentulous space at the area of missing tooth #4 and missing tooth #30 using a limited
FOV scan (3D Accuitomo, J. Morita Corporation, Suita City, Osaka, Japan, distributed by J. Morita USA, Inc., Irvine, CA). Sagittal and cross-sectional
slices are shown. Although the anatomic area imaged is limited, the resolutions of the images are high. A and B, Implant site 114 (maxillary right sec-
ond premolar) in anterior-posterior (AP) and buccolingual cross-sectional views. C and D, Implant site 1130 (mandibular right first molar) in AP and
buccolingual cross-sectional views.
Interactive "Simuletion" Software Software programs specialized in implant treatment plan-

ning, such as SIM/Plant (Materialise/Columbia Scientific,
Programs Glen Burnie, MD), can reformat CBCT- or CT-scan data. The
Implant treatment planning can be greatly enhanced by the use clinician can use the reformatted images on a personal com-
of specialized software. In addition to measuring the quantity puter in an interactive manner to identify anatomic structures,
and quality of bone in potential implant sites, these programs simulate implant placement positions, and better appreciate
use CT- or CBCT-scan data to simulate placement of implant relationships between planned implant positions and teeth
and restorations. Using a database of commercially available or anatomic structures (Fig. 57.20). InVivo5 planning soft-
implant images, the length, width, angulation, and position ware (Anatomage, San Jose, CA) acquires data directly from
of implants can be "simulated" in the desired positions and CBCT- or CT-scan DICOM (Digital Imaging and Communi-
evaluated relative to other structures in 3D. In cases of alveo- cations in Medicine) files without the need for reformatting.
lar ridge deficiency or defects or when sinus-bone augmenta- Once implant positions are confirmed, a computer-generated
tion is indicated, the additional bone volume needed can be surgical guide is produced to facilitate the surgical placement
evaluated and quantified. The restoration of the implants can of implants in the planned positions (Fig. 57.21)
also be simulated and the distribution of mechanical forces
onto the implant and adjacent bone predicted.
FIGURE 57.20 SIM/Plant images. The SIM/Plant software program allows clinicians to measure bone height, width, density, and volume on a per-
sonal computer. Scan data are reformatted for interactive evaluation and manipulation. Implant positions can be simulated on the patient's scan data
before surgery, allowing the surgeon to anticipate areas of deficiency.
FIGURE 57.21 lnVivo5 simulation images. The lnVivoS software program allows clinicians to plan implant treatment and simulate virtual implant
positions directly from DICOM scan data on a personal computer. A, Cross-section and axial images with 3D simulation of implant positions.Band
C, Model mockup for computer generated surgical guide.
FIGURE 57.21 (cont.) D and E, Surgical guide that was created from simulated plan. F-H, Periapical radiographs demonstrating accurate position
and alignment of implants that were placed using computer generated surgical guide.
Clinical Selection of Diagnostic resin. If CT imaging might be performed, the use of metallic
markers should be avoided. The design of such a guide greatly
Imaging enhances the diagnostic information provided by the radio-
Radiography is an important diagnostic tool for the evaluation of graphs because it correlates the radiographic anatomy with
the implant patient. However, radiographic imaging alone is in- the exact position of the proposed implant location.
sufficient. It is important to correlate diagnostic information with
a good clinical examination. Conversely, a clinical examination is Cross-Sectional Tomography
insufficient to provide the information needed to plan implant
treatment for a patient without some radiographic imaging. Some type of cross-sectional imaging, such as conventional
tomography, CT, or CBCT, should be performed before
implant placement in any site of the jaws. The potential mor-
Clinical Examination bidity of a compromised anatomic structure and the poor
Before taking any radiographs, a complete clinical examina- performance and potential failure of a misplaced implant,
tion of the implant patient is required. This should include combined with the wide availability of tomographic facilities,
the etiology and duration of tooth loss, any history of trau- favor the use of cross-sectional imaging in most cases of im-
matic extraction, and a review of records and radiographs, if plant-treatment planning. It is crucial that the cross-sections
available. Clinical assessment of the edentulous area, cover- are perpendicular to the curvature of the mandible and parallel
ing mucosa, adjacent and opposing teeth, and occlusal plane to the planned implant. Improper patient positioning can lead
should be performed. Temporomandibular function, mandib- to an overestimation of the height and width of the available
ular maximal opening, and protrusive and lateral movements bone. If the surgeon believes that sections were performed at
should be evaluated (see Chapter 57) the wrong angulation, new images should be requested. This
might necessitate reexposure of the patient.
Screening Radiographs
lntraoperative and Postoperative
At this point, an overall assessment of the health of the jaws
should be performed. Periapical radiographs provide a high- Radiographic Assessment
resolution image of the alveolus and the surrounding structures, Various radiographic modalities can provide valuable informa-
including adjacent teeth. For extended edentulous areas, pan- tion during implant placement. Due to the ease of acquisition
oramic, lateral cephalometric, and occlusal radiographs can be and high resolution, periapical radiographs are most commonly
used to estimate bone height and width. Any pathology of the used. Intraoperative radiographs can be taken during surgery to
bone at the prospective implant site, as well as of the surround- evaluate proximity to important anatomic structures. Sequential
ing structures, should be identified and treated as indicated. periapical radiographs guide the clinician to visualize changes
in direction and depth of the drilling procedure and parallel-
Fabrication of Radiographic and ism to adjacent teeth and other implants (Fig. 57.22). Digital
radiographs are particularly advantageous during intraoperative
Surgical Guides
assessment of implant placement; images appear on the screen
Once the health of the soft and hard tissues is established, almost instantaneously and can be manipulated to extract the
casts should be taken and detailed analysis performed. The most pertinent diagnostic information (see Chapter 26).
clinician should decide on the number of implants and their Implant osseointegration and the level of periimplant-
desired location. Next, a radiographic guide should be fabri- alveolar bone are major determinants of implant prognosis.
cated, usually with clear acrylic. The position of the desired Panoramic and periapical radiographs offer a fast, easy, and
implants is indicated by the use of radiopaque objects such as low-radiation depiction of the implant and surrounding tis-
metallic balls, cylinders, or rods; gutta-percha; or composite sues and aid in assessment of implant success. To obtain an
FIGURE 57.22 lntraoperative periapical radiographs are valuable in assessing the proximity of adjacent teeth. A, The 2-mm guide pin is used to de-
termine direction of the osteotomy site and its proximity to the adjacent root. B, After angle correction, the osteotomy sites are completed to length with
the final drill. Here the 3-mm guide pins confirm the correct angulation and spacing of the final osteotomy site preparation before implant placement.
FIGURE 57.23 Radiographic follow-up after implant placement in three different patients. A, Periapical radiograph of three implants in the poste-
rior right mandible. "Normal" bone remodeling around anterior two implants and slight horizontal bone loss/remodeling around the molar/posterior
implant is present. B, Periapical radiograph of two implants in the left posterior mandible. Severe bone loss (50% of implant length) is seen around
anterior implant, while mild bone loss/bone remodeling is observed around posterior implant. A moderate buccal cantilever in the restoration likely
contributed to an adverse occlusal load and the resultant bone loss observed in this case. C, Panoramic radiograph of maxillary and mandibular im-
plants in an edentulous patient prior to implant loading. The mandibular implants do not show signs of bone loss and appear to be osseointegrated.
All maxillary show signs of moderate-to-severe periimplant bone loss and the success of osseointegration is questionable.
accurate assessment of periimplant-bone height, the X-ray modalities chosen based on necessary information for the par-
beam should be directed perpendicular to the implant. In the ticular patient. The objectives for any radiographic evaluation,
case of threaded implants, the implant threads should be dis- regardless of imaging technique used, should include an evalu-
tinguishable and not overlapping (Fig. 57.23A) ation to (1) exclude pathology, (2) identify anatomic structures,
A 1.2-mm marginal bone loss during the first year after and (3) measure the quantity, quality, and location of available
implant placement and 0.1 mm/year afterwards are expected; bone.
however, further bone loss is considered abnormal. Pathologic
bone loss could be localized along the full extend of the im-
Exclude Pathology
plant (periimplant-bone loss), or around the crestal part of
the implant ("saucerization"), and could reflect poor osseoin- Healthy bone is a prerequisite for successful osseointegration
tegration, periimplantitis, and/or unfavorable stress distribu- and long-term implant success. The first step in the radio-
tion (Fig. 57.23B and C) graphic evaluation of the implant site is to establish the health
In select cases, when poor implant placement (Fig. 57.24) of the alveolar bone and other tissues imaged within a par-
or compromise of vital anatomic structures (Fig. 57.25) are ticular projection. Local and systemic diseases that affect bone
suspected, advanced imaging (CBCT, CT, or conventional to- homeostasis can preclude, modify, or alter placement of im-
mography) provides a 3D evaluation of the oral structures in plants. Retained root fragments, residual periodontal disease,
relation to the implants. Such information can be very impor- cysts, and tumors should be identified and resolved before im-
tant for proper assessment and treatment planning. The treat- plant placement. Systemic diseases, such as osteoporosis and
ing dentist should recognize relevant signs and symptoms and hyperparathyroidism, alter bone metabolism and might affect
order appropriate imaging as soon as possible after implant implant osseointegration. Areas of poor bone quality should
placement. Implant removal, if necessary, would be less com- be identified and if indicated, adjustments to the treatment
plicated before advanced osseointegration. plan incorporated. Maxillary sinusitis, polyps, or other sinus
pathology should be diagnosed and treated when implants are
Patient Evaluation considered in the posterior maxilla, especially if sinus-bone
augmentation procedures are planned (Fig. 57.26).
Evaluation of the implant patient should be disciplined and
objective. Specific questions that can affect implant placement
Identify Anatomic Structures
and outcome should be considered and examined carefully and
explicitly The advantages and disadvantages of various radio- Several important anatomic structures are found close to de-
graphic projections should be considered and radiographic sired areas of implant placement in the maxilla and mandible
FIGURE 57.24 Radiographic follow-up after implant placement. A, Panoramic radiograph suggests mild-to-moderate bone loss around the neck of
all implants. This is especially true for the implants in the left maxilla. These implants appear to be angled and the distal implant is positioned more api-
cal. The overdenture bar is not completely seated on the left implants. Note superimposed overlapping anatomic structures in this panoramic radiograph
impair the ability to clearly visualize and assess bone loss around implants.Band C, Cross-sectional and sagittal CBCT images of the anterior implant in
the left maxilla. Poor implant placement beyond the buccal cortex of the alveolar ridge (cross-section) and periimplant bone loss (sagittal) are revealed.
FIGURE 57.25 CBCT sagittal and cross-sectional

images clearly demonstrate penetration of the im-
plant into the mandibular canal.
(Box 57.3). Familiarity with the radiographic appearance of and anterior wall of the maxillary sinus, incisive foramen,
these structures is important during treatment planning and floor and lateral wall of the nasal cavity, and canine fossa. Im-
implant placement. Their exact localization is central to pre- portant anatomic structures in the mandible that should be
vent unwanted complication and unnecessary morbidity. Im- recognized include the mandibular canal, anterior loop of the
portant anatomic structures in the maxilla include the floor mandibular canal, mental foramen, anterior extension of the
FIGURE 57.26 CBCT examination of the posterior left maxilla. A, Top row shows reconstructed "panoramic" and coronal sections of the alveolar
ridge. Note the thickened mucoperiosteal lining of the floor of the left maxillary sinus (white arrow). The patient has chronic maxillary sinusitis. B,
Bottom row shows conventional panoramic, reconstructed "panoramic," coronal and axial sections of the alveolar ridge at the area of missing first
maxillary molar. A large radiolucent lesion at the edentulous alveolar ridge elevates the floor of the maxillary sinus and occupies most of the sinus.
Biopsy revealed a keratocystic odontogenic tumor that was an incidental finding in this asymptomatic patient.
of important anatomic structures can lead to unnecessary

complications. For example, inadvertent penetration and
damage to the inferior alveolar nerve can result in serious im-
mediate-term (profuse bleeding), short-term, and long-term
MAXILLA (nerve paresthesia/anesthesia) complications. The height and
1. Maxillary sinus (floor and anterior wall) width of the alveolar bone should be accurately detailed. De-
2. Nasal cavity (floor and lateral wall) pending on the technique, diagnostic imaging can estimate or
3. Incisive foramen measure the coronal-apical height, the buccal-lingual width,
4. Canine fossa and the mesial-distal spacing available for implants that will
5. Canal is sinuosus be placed in proximity to teeth or relative to other planned
MANDIBLE implants.
1. Mandibular canal This task can be simple in cases with good bone quality
2. Anterior loop of the mandibular canal and sufficient bone volume in the desired implant location(s).
3. Anterior extension of the mandibular canal However, in cases with moderate-severe bone resorption,
4. Mental foramen alveolar defects, or recent extraction sites, obtaining a clear
5. Submandibular fossa and accurate diagnostic image can be more challenging. The
6. Retromolar canal diagnostic imaging may reveal inadequate bone volume for
7. Lingual inclination of the alveolar ridge
the proposed implant(s) and indicate a need for bone aug-
mentation or depending on the severity of the deficiency,
preclude the patient from the possibility of implant therapy
canal, and submandibular fossa. The existence of anatomic (Fig. 57.28). When ridge augmentation is deemed neces-
variants, such as incomplete healing of an extraction site, si- sary, radiographic evaluation prior and postsurgery informs
nus loculation, division of mandibular canal (Fig. 57.27), or treatment planning and ensures grafting integrity and quality
absence of a well-defined corticated canal, should also be rec- (Fig. 57 29).
ognized. See Chapter 4 3 for important periodontal and im- In addition to the amount, the quality of the available
plant surgical anatomy. bone should also be evaluated. A uniform, continuous cor-
tical outline and a lacy, well-defined trabecular core reflect
Assess Bone Quantity, Quality, the normal bone homeostasis necessary for appropriate bone
and Volume response around the implant. Thin or discontinuous cortex,
sparse trabeculation, large marrow spaces, and altered trabec-
The primary goal of diagnostic imaging for potential implant ular architecture should be noted because they might predict
patients is to evaluate the available bone volume for implant poor implant stabilization and a less desirable response of the
placement in desired anatomic locations. The clinician wants bone. Poor bone quality may necessitate modifications of the
to estimate and verify exact adequate height, width, and den- treatment planning, such as waiting longer for healing (os-
sity to the recipient bone while avoiding damage to critical seointegration) to maximize bone-to-implant contact before
anatomic structures. Failure to accurately assess the location loading.
FIGURE 57.27 CBCT examination of the area of missing tooth #19 before implant placement. A, Panoramic view of the area of interest depicts an
accessory mandibular canal. B, Same panoramic view with the accessory mandibular canal colored blue and the main canal red. C, Cross-sectional
views through the area of missing tooth 1119. D, Same cross-sectional images depicting the blue and red markings. Note that the position of the mark-
ings coincides with the position of the accessory and main mandibular canals (compare C and D).
FIGURE 57.29 Radiographic evaluation of a patient with missing

FIGURE 57.28 Radiographic evaluation of a patient with congeni- left maxillary second premolar and first molar. Initial CBCT reveals
tally missing maxillary lateral incisors before implant placement. A, A, an atrophic alveolar ridge with, B, an inadequate height for implant
Panoramic radiograph reveals sufficient height and mesial-lateral width placement. Also note the thickened mucoperiosteum at the floor of the
of the alveolar ridge. B, Cross-sectional conventional tomography of the maxillary sinus. CBCT after sinus grafting for ridge augmentation shows,
edentulous areas reveals a narrow ( <4 mm) buccal-lingual width of the C, uniformly opaque grafting area blending with alveolar trabeculation
alveolar ridge that needs to be addressed by modifications in the treat- and a smooth sinus floor elevation, which provides, D, adequate dimen-
ment planning, such as bone augmentation. sions for implant placement.
Evaluate Relation of Alveolar Ridge with Conclusion

Existing Teeth and Desired Implant Position Many radiographic projections are available for the evaluation
Accurate placement (spatial position and angulation relative of implant placement, each with advantages and disadvan-
to adjacent teeth and occlusal plane) will greatly affect the tages. The clinician must follow sequential steps in patient
restorative success and long-term prognosis of the implant evaluation and radiography is an essential diagnostic tool for
(see Chapter 57). A significant variable during the preimplant implant design and successful treatment of the implant pa-
evaluation is the relation of the desired implant position rela- tient. Selection of appropriate radiographic modalities will
tive to the existing teeth, alveolar crest, and occlusal plane. provide the maximum diagnostic information, help avoid
Angled or custom abutments can accommodate slight varia- unwanted complications and maximize treatment outcomes
tions in implant position and implant inclination. However, while delivering "as low as reasonably achievable" radiation
more significant deviations should be avoided. dose to the patient.
Prolonged tooth loss is usually associated with atrophy of
the alveolar ridge and in the case of the maxilla, with pneuma- Prosthetic & Biomechanical
tization of the sinus floor toward the alveolar crest. Traumatic
extractions can compromise the buccal or lingual cortex and
Considerations
alter the shape and buccolingual ridge dimension. Anatomic Clinical research has demonstrated excellent long-term suc-
variants, such as lingual inclination of the alveolus or narrow cess rates for implant-supported restorations in fully and par-
ridges, should be considered during treatment planning of the tially edentulous patients. The replacement of missing teeth
implant patient (Fig. 57.30) with an implant-retained prosthesis restores function and
An important part of diagnostic imaging must include an esthetics, improves confidence and self-esteem, and enhanc-
evaluation of the available bone relative to the "prosthetically es quality of life. However, it is important to recognize that
driven" implant position. This aspect of the patient evalua- implant success is achieved by following certain principles.
tion is best accomplished with diagnostic models, wax-up of Proper treatment planning is essential for predictability and
planned tooth replacement, and radiographic markers in the success. One of the most critical factors in planning is the
desired tooth positions during imaging. Steel balls, brass tubes, control and distribution of stress for preservation of the "bi-
and gutta-percha have all been used to establish the proposed ologic" connection between the implants and bone, as well
tooth positions relative to the existing alveolar bone. The use as the prevention of "mechanical" breakage of implants and
of these nonanatomic markers is helpful for evaluating bone restorative components. The quantity and quality of bone
height and width in specific anatomic locations. However, available to support implants play an important role in stress
they do not accurately represent the tooth contours and do not distribution, maintenance of bone apposition, and support
allow the clinician to estimate variations in implant position under functional loading.
and angulation relative to the position and emergence of the
planned tooth replacement. Therefore, it is more desirable and
beneficial to use radiopaque "tooth-shaped" markers so that Biomechanical Considerations
the existing alveolar bone can be evaluated relative to the entire Osseointegrated dental implants provide a predictable means
tooth position/contours (Figs. 57.18 and 57.31). This is par- of replacing missing teeth and restoring dental function.
ticularly important for anterior, esthetic implant cases. Patients A thorough understanding of implant biomechanics is es-
should always be imaged with radiographic guides (markers). sential if implant-retained restorations are to be employed
FIGURE 57.30 Radiographic evaluation of a patient with edentulous posterior left mandible before implant placement. A and B, Panoramic and
periapical radiographs demonstrate sufficient height of the alveolar ridge with little or no resorption. C and D, CBCT sections reveal significant lingual
inclination of the alveolar ridge with lingual concavity that is not depicted on conventional radiographs.
Clinical Selection of Diagnostic implant. Improper patient positioning can lead to an overes-
timation of the height and width of the available bone. If the
Imaging surgeon believes that sections were performed at the wrong
Radiography is an important diagnostic tool for the evaluation angulation, new images should be requested. This might ne-
of the implant patient. However, radiographic imaging alone cessitate reexposure of the patient.
is insufficient. It is important to correlate diagnostic informa-
tion with a good clinical examination. Conversely, a clinical
examination is insufficient to provide the information needed lntraoperative and Postoperative
to plan implant treatment for a patient without some radio- Radiographic Assessment
graphic imaging. Various radiographic modalities can provide valuable informa-
tion during implant placement. Due to the ease of acquisition
Clinical Examination and high resolution, periapical radiographs are most com-
monly used. Intraoperative radiographs can be taken during
Before taking any radiographs, a complete clinical examina- surgery to evaluate proximity to important anatomic struc-
tion of the implant patient is required. This should include tures. Sequential periapical radiographs guide the clinician to
the etiology and duration of tooth loss, any history of trau- visualize changes in direction and depth of the drilling pro-
matic extraction, and a review of records and radiographs, if cedure and parallelism to adjacent teeth and other implants
available. Clinical assessment of the edentulous area, cover- (Fig. 57.22). Digital radiographs are particularly advanta-
ing mucosa, adjacent and opposing teeth, and occlusal plane geous during intraoperative assessment of implant placement;
should be performed. Temporomandibular function, mandib- images appear on the screen almost instantaneously and can
ular maximal opening, and protrusive and lateral movements be manipulated to extract the most pertinent diagnostic infor-
should be evaluated (see Chapter 57) mation (see Chapter 26).
Implant osseointegration and the level of periimplant-
Screening Radiographs alveolar bone are major determinants of implant prognosis.
Panoramic and periapical radiographs offer a fast, easy, and
At this point, an overall assessment of the health of the jaws low-radiation depiction of the implant and surrounding tis-
should be performed. Periapical radiographs provide a high- sues and aid in assessment of implant success. To obtain an
resolution image of the alveolus and the surrounding struc- accurate assessment of periimplant-bone height, the X-ray
tures, including adjacent teeth. For extended edentulous beam should be directed perpendicular to the implant. In the
areas, panoramic, lateral cephalometric, and occlusal radio- case of threaded implants, the implant threads should be dis-
graphs can be used to estimate bone height and width. Any tinguishable and not overlapping (Fig. 57 23A)
pathology of the bone at the prospective implant site, as well A 1.2-mm marginal bone loss during the first year after
as of the surrounding structures, should be identified and implant placement and 0.1 mm/year afterwards are expected;
treated as indicated. however, further bone loss is considered abnormal. Pathologic
bone loss could be localized along the full extend of the im-
Fabrication of Radiographic and Surgical plant (periimplant bone loss), or around the crestal part of the
implant ("saucerization"), and could reflect poor osseointe-
Guides gration, periimplantitis, and/or unfavorable stress distribution
Once the health of the soft and hard tissues is established, (Fig. 57.23B and C).
casts should be taken and detailed analysis performed. The In select cases, when poor implant placement (Fig. 57.24)
clinician should decide on the number of implants and their or compromise of vital anatomic structures (Fig. 57.25) are
desired location. Next, a radiographic guide should be fabri- suspected, advanced imaging (CBCT, CT, or conventional to-
cated, usually with clear acrylic. The position of the desired mography) provides a 3D evaluation of the oral structures in
implants is indicated by the use of radiopaque objects such as relation to the implants. Such information can be very impor-
metallic balls, cylinders, or rods; gutta-percha; or composite tant for proper assessment and treatment planning. The treat-
resin. If CT imaging might be performed, the use of metallic ing dentist should recognize relevant signs and symptoms and
markers should be avoided. The design of such a guide greatly order appropriate imaging as soon as possible after implant
enhances the diagnostic information provided by the radio- placement. Implant removal, if necessary, would be less com-
graphs because it correlates the radiographic anatomy with plicated before advanced osseointegration.
the exact position of the proposed implant location.
Cross-Sectional Tomography
Some type of cross-sectional imaging, such as conventional to-
mography, CT, or CBCT, should be performed before implant
placement in any site of the jaws. The potential morbidity of
a compromised anatomic structure and the poor performance
and potential failure of a misplaced implant, combined with
the wide availability of tomographic facilities, favor the use
of cross-sectional imaging in most cases of implant-treatment
planning. It is crucial that the cross-sections are perpendicular
to the curvature of the mandible and parallel to the planned
FIGURE 57.31 A, Panoramic view of partially edentulous maxilla with tooth shaped markers in areas of missing teeth (potential implant sites).
B, Cross-sectional views from a CBCT examination before implant placement in the right maxilla. Appropriately sized and shaped tooth markers
placed in the prosthetically desired locations of the planned restorations for the missing teeth help evaluate the existing alveolar ridge relative to the
prospective tooth positions and contours.
predictably The load-bearing capacity of implants supporting is no periodontal ligament and should movement occur, it
the restoration must be greater than the anticipated loads dur- would indicate a loss of osseointegration (eg, fibrous encap-
ing function. If applied loads exceed load-bearing capacity, it sulation). Since excessive forces are destructive, it is crucial to
may lead to mechanical and/or biologic failure. In the case have a good understanding of the biomechanical properties
of mechanical failure, screws that secure the restoration may and the limitations of dental implants to ensure proper treat-
bend, loosen, or fracture. The most devastating type of me- ment planning that will sustain the anticipated occlusal forces.
chanical failure is fracture of the implant. In the case of biologic
failure, a resorptive-remodeling response of the bone around
Load-Bearing Capacity
the implant(s) is provoked, leading to progressive bone loss.
If bone loss around the implant progresses until the implant The load-bearing capacity of implants is influenced by several
is no longer supported, osseointegration may be lost resulting factors, including the number and size of implants, the angu-
in implant failure. lation and arrangement of implant positions, and the quality
The function and support of implant-retained restorations of the bone-to-implant interface (Box 57.4).
is quite different from tooth-retained restorations. Teeth are The number of implants used will influence the load-
suspended within the supporting alveolar bone by a peri- bearing capacity In the 1980s and early 1990s, many poste-
odontal ligament, which allows slight physiologic "move- rior quadrants of the maxilla were restored with one or two
merit" of teeth in function. If forces are excessive, teeth have implants, and in some patients, two implants were used to
the capacity to adjust or move in response to the applied support restorations with three or four dental units. In many
forces. In the absence of an inflammatory periodontal disease, cases, a distinct pattern of bone loss was observed soon af-
teeth will adapt to these forces without appreciable bone loss. ter loading that led to bone loss and failure of the implants
Orthodontic movement of teeth through alveolar bone is the (see Fig. 59 16). Additional implants significantly improved
ultimate example of the capacity of teeth to adapt to excessive the biomechanics of these implant-supported fixed-partial
applied forces. As orthodontic forces move a tooth, bone re- dentures.
sorbs in response to pressure and forms in response to tension Historically, the use of longer(> 7 mm) implants has been
applied by the "attached" periodontal ligament fibers. Osseo- advocated as the result of reported higher rates of failure for
integrated dental implants, by definition, are in direct contact shorter (-5,7 mm) implants. Logic suggests that biomechani-
with the alveolar bone without intervening soft tissues; there cal stress around "short" implants leads to greater bone loss
BOX 57.4
LOAD-BEARING CAPACITY CANTILEVER FORCES

• Implant • Connection to natural dentition
• Number • Size of occlusal table
• Length • Buccolingual dimension
• Angulation • Mesiodistal dimension
• Quality of bone-implant interference • Cantilevered extensions
FACTORS AFFECTING ANTICIPATED LOAD PARAFUNCTIONAL HABITS
• Occlusal factors • Chronic bruxism
• Cusp angles • Clenching habit
• Width of occlusal table • Grinding habit
• Guidance type
• Anterior guidance
• Group function
implants and surrounding bone. Axial loads are tolerated well.

Minor discrepancies in angulation are probably not clinically
significant but if loads are applied at an angle of 20 degree
FEA is a computerized investigative method that uses a
mathematic model to assess stress in various objects and
or more to the long axis of the implant, load magnification
their surroundings when subjected to forces. It is useful in can result, provoking a resorptive-remodeling response of
generating a hypothesis and testing basic biomechanical the adjacent bone. This concept is supported by numerous
mechanisms but cannot be relied on for definitive answers. FEA studies, which clearly demonstrate that nonaxial forces
Only hard clinical evidence is undisputed and any significantly increase the stress concentration to the cortical
assumption or predictions that are made by FEA need to be bone around the neck of the implant (Fig. 57.32). Nonaxial
validated clinically. loads lead to an implant overload through load magnification
at the bone-to-implant interface, which, in turn, precipitates a
resorptive-remodeling response of the bone around the neck
of the implants.
relative to the implant length and a higher rate of implant When excessive loads persist, bone loss continues and may
failure. However, Pierrisnard et al showed that the maximum progress to implant failure. Brunski et al proposed that ex-
implant stress somewhat increased with implant length and cessive occlusal loads lead to microdamage (fractures, cracks,
bicortical anchorage. They also stated that the low anchor- and delamination) of the bone adjacent to the implant, which
age stiffness of shorter implants might reduce the mechanical provokes a resorptive-remodeling response. The bone re-
stress to the implant because of the flexibility of the bone. Us- modeling at the implant surface results in less bone density
ing the finite element analysis (FEA), Pierrisnard et al showed
that greater implant length did not positively affect transfer
of stresses to the implant but that the increasing implant di-
ameter did reduce the intensity of stress along the length of
the implant. Other studies also observed that wider, rather
than longer, implants registered lower stress values to the
whole system, suggesting that the use of short, wide implants
could increase the load-bearing capacity of implants and im-
plant prostheses (Box 57.5). In a recent systematic review of
the literature, Atieh et al concluded that the survival of short
(::;8.5 mm) implants used in the posterior partially edentu-
lous jaw is high and not related to implant surface, design,
or width.
Angulation and Arrangement

The angulation and arrangement of implants used to retain and
support a prosthesis influence the load-bearing capacity of the
system (ie, implants, components, prosthesis, and supporting
bone). In the 1980s, conventional dogma stated that once an
implant became "osseointegrated," it did not matter whether
occlusal loads were applied axially. However, as more clinical
follow-up and animal research data became available, the ad-
verse effect of nonaxial loads on implants became increasingly
more apparent. The angulation of implants in relation to the FIGURE 57.32 Nonaxial loads result in load magnification. Using
plane of occlusion and the direction of the occlusal load is an FEA, Cho and coworkers demonstrated that nonaxial loads concentrated
important factor in optimizing the transfer of occlusal forces to stresses around the neck of the implant. (Courtesy Dr In Ho Cho.)
BOX 57.6
• Excessive occlusal loads

• Load resulting in microdamage: fractures, cracks, and
delam inations
• Resorption-remodeling response of bone
• Loss of bone at the bone-to-implant interface as a result of
remodeling
• Vicious cycle of continued loading, additional
microdamage, and bone loss progressing to implant failure
adjacent to the implant, especially around the coronal aspect

of the implant. This bone has a poor capacity for repair that
is the result in part to the absence of a periodontal ligament
fiber attachment (ie, no bone-forming tension exists). Thus,
a vicious cycle ensues in which continued excessive loading
leads to more microdamage and progressive bone loss until
the implant fails (Box 57 6). FIGURE 57.34 The distal angulation of the implants (posterior man-
Short-span, linear-implant configurations in the posterior dible) and the occlusal loads (arrow) are nonaxial due to the curve of
segments are particularly prone to bone loss when loads are Spee. The nonaxial loading results in implant overload and bone loss
not applied axially. Bone loss in posterior areas can be more around the neck of both implants.
damaging because implants in these areas are often primar-
ily supported by the cortical bone around the most coronal The bone-appositional index (percentage of bone-to-implant
aspect of the implant. In the posterior maxilla, the cortical contact) may be the most important factor to consider when
bone can be very thin, and unless the implant is positioned evaluating the load-bearing capacity of any given implant(s).
to engage the superior cortical bone (floor of maxillary sinus), Less bone density and lower bone-to-implant contact provide
the apical aspect of the implant is usually poorly supported by less support and resistance to occlusal loading. As an example,
loose trabecular bone. The load-bearing capacity is poor and consider the bone support of implants in the posterior max-
nonaxial loads can lead to failure. illa; the bone quality is particularly poor as compared with
Before the widespread use of bone-augmentation procedures the anterior mandible. The trabecular bone is less dense and
in the posterior maxilla (ie, sinus augmentation), many implants the cortical bone layer is thin in the posterior maxilla. As a
were positioned with excessive buccal angulations or were re- result, the bone-appositional index in the posterior maxilla
stored with buccal and/or distal cantilevers. Implant-supported is significantly less than what can be achieved in the ante-
restorations with a cantilevered pontic transfer nonaxial occlu- rior mandible, where the trabecular bone is typically dense
sal forces the adjacent implant and surrounding bone resulting with a thick cortical bone layer. The bone-appositional index
in bone loss. This load magnification causes bone loss around for implants in the posterior maxilla typically ranges from
the neck of the implant closest to the cantilever (Fig. 57.33). 30-60%, whereas the bone-appositional index for implants
Excessive distal angulations, which creates nonaxial loading placed in the anterior mandible typically ranges from 65-90%
is another recognized problem that leads to bone loss. These (Fig. 57.35).
implants often exhibit signs of overload (ie, progressive and ir- Technologic advances in surface modification (as compared
reversible bone loss around neck of implant) when nonaxial to the original machined Branernark surface) may enhance
occlusal loads are applied to the prosthesis (Fig. 57.34). bone apposition and support for implants placed in poor
FIGURE 57.33 Cantilevers in posterior quadrants of partially edentulous patients should be avoided. These radiographs demonstrate two cases of
bone loss (arrows) around the neck of short implants (closest to the cantilever) in which load magnification occurs.
complications and failures have taught clinicians that the "en-

gineering" of implant support for prosthetic appliances is an
essential part of treatment planning and the key to success for
implant-retained restorations (see Chapter 59 for a descrip-
tion of implant complications and failures).
Partially Edentulous Patients

Prosthetic options for patients who are partially edentulous
(missing one to several teeth) include a conventional remov-
able partial denture, a fixed-partial denture (toothborne), or
an implant-supported prosthesis.
Multiple Tooth Sites
Unilateral, implant-supported fixed-partial dentures are pre-
dictable when they are supported by an adequate number of
implants with good quality bone surrounding them. How-
ever, anatomic limitations can prevent the ideal placement
of implants and/or may require the use of shorter implants
in posterior sextants. The lowest success rates for implants
have consistently been reported for short-span (segmental)
restorations in the posterior maxilla. In the posterior maxilla,
the maxillary sinus limits the lengths used, and in the man-
FIGURE 57.35 Bone quality influences the load-bearing capacity. In
these histologic images obtained with light microscopy, note the differ-
dible, the inferior alveolar nerve limits the lengths of the im-
ence in bone-appositional index achieved in A, sparse "poor-quality" plants used. The bone-implant interface for osseointegrated
bone often found in the B, posterior maxilla versus dense bone typical implants in the posterior maxilla is compromised because of
of the anterior mandible. the poor bone quality Anchorage for an implant placed in
this region may be improved by engaging the cortical bone of
the floor of the sinus. Since many patients possess insufficient
quality/quantity bone, thereby gaining anchorage and improv-
bone in the posterior maxilla to receive an implant of suitable
ing the biomechanics. These "rougher" implant surfaces appear
length, bone augmentation of the alveolar ridge or maxillary
to have a significant effect on bone anchorage. Surfaces with
sinus has been suggested. Vertical augmentation of the alveo-
an altered microtopography achieve higher bone-appositional
lar ridge has not been predictable, but the "sinus lift and graft
indices than the machined surfaces and appear to facilitate the
procedure" appears predictable and has achieved wide accep-
biologic processes of bone formation through greater deposition
tance (see Chapter 58).
of bone onto the surface of the implant. In addition, bone depos-
It is imperative to "engineer" the treatment of unilateral,
ited on the surface of acid-etched implants appears to be harder
posterior segments with an implant used to support each
and denser and may be more resistant to resorptive remodeling.
missing tooth that will be restored. If space and available bone
A lack of bone-height limits the amount of available bone for
permits, it is desirable to use a minimum of three implants to
placement of implants and reduces the potential for bone-to-
replace three missing posterior teeth in the maxilla. The same
implant contact. In the posterior mandible the inferior alveolar
rule (one implant for every missing tooth being restored) ap-
nerve and vessels travel through the body of the mandible until
plies to replacing teeth with implants in the posterior man-
exiting the mental foramen in the premolar region (see Chap-
dible as well. However, greater bone density (ie, thickness of
ter 42). The height of bone available for placement of implants
cortical bone) provides better support in the posterior man-
in the posterior mandible is determined by the location of the
dible and sometimes permits the use of fewer implants. A
neurovascular bundle and the resorption of the alveolar ridge.
three-unit bridge supported by two implants in the posterior
Lateral nerve repositioning is possible but has a moderately
mandible is widely accepted. However, the decision to restore
high morbidity rate. In the posterior maxilla, pneumatization of
three missing teeth supported by two implants should always
the maxillary sinus combined with loss of alveolar bone results
be made with consideration for the quantity and quality of
in a decreased total height of available bone in the posterior
bone available to support the implants (ie, effective load-bear-
maxilla, which limits the length of implants that can be used.
ing capacity of the implants).
Sinus-floor elevation and bone-augmentation procedures have
enabled clinicians to increase the height of bone available in Single Tooth Sites
the posterior maxilla, allowing for the placement of longer im-
Implants have been used successfully to replace missing single
plants with improved success (see Chapter 58). Vertical ridge
teeth despite the fact that the loading limit of a single implant
augmentation is challenging and less predictable for all sites.
remains unknown. Single-tooth implant restorations have re-
placed the traditional three-unit bridge and gained acceptance
Treatment Planning With Dental and patient satisfaction.
Implants Standard-diameter implants have been used to restore
single-tooth defects in the posterior quadrants of the maxilla
The success of implant-retained restorations is measured and mandible with mixed results. Solitary implants restor-
not only by successful osseointegration but also by the lack ing maxillary molars have had unpredictable results, whereas
of problems associated in their function over time. Implant single implants used to restore mandibular molars have had
Edentulous Maxilla for implant placement in the posterior region. As a result, im-
plant placement is confined to the anterior region and the AP
Prosthetic options for the patient with an edentulous maxilla spread that can be achieved is often limited (Fig. 57 37). If
include a conventional complete denture, an implant-assisted the AP spread is inadequate to provide support, a full-palatal-
denture, an implant-supported removable prosthesis, or an coverage overlay denture is recommended.
implant-supported fixed prosthesis. For many patients, a con- Most patients are best served with an implant-assisted
ventional complete denture does not provide the comfort and overlay denture. Lower cost, improved hygiene access, and
quality of life that they desire. An implant-assisted or implant- predictable speech articulation are additional benefits that fa-
supported prosthesis can provide stability, retention, comfort, vor the use of an overlay denture in the edentulous maxilla
and restore confidence to the patient, especially in patients over an implant-supported fixed prosthesis. The four-implant-
with one or more of the following conditions. assisted palateless overlay denture ideally addresses the needs
1. Poor ridge form with a marginally stable conventional of most patients (Fig. 57.38). Many patients who are edentu-
maxillary denture. Two or four implants provide greater lous in the maxilla have lost a significant amount of structure
stability and security of a maxillary denture in function in the premaxillary region resulting in a lack of support for
when the maxillary ridge is severely resorbed and lacks the upper lip. An implant-assisted maxillary overdenture is
resistance to lateral forces. preferred over an implant-supported fixed prosthesis because
2. Lack of posterior support with an intact mandibular an- the labial flange can provide the needed lip support. The usual
terior dentition. Implants in the maxilla can offset the resorption pattern of the alveolus places the gingival margin
potentially destructive effects on the premaxillary region of a fixed restoration too far superiorly, too far palatally, or
when a mandible with natural anterior teeth and miss- both. Even if the patient has a low enough smile line to hide
ing posterior teeth opposes an edentulous maxilla. In this the appearance of long crowns and deficient soft-tissue height
situation, the lack of posterior support leads to a condi- (Fig. 5 7 39), a lack of lip support just beneath the nose can be
tion often referred to as combination syndrome in which unsightly with fixed prostheses.
overclosure of the anterior teeth causes a "hammer-and- For those patients who prefer an implant-supported fixed
anvil" type of destruction of the edentulous anterior max- prosthesis (and don't require additional lip support), six or
illa (Fig. 57.36). more implants arranged in an appropriate arc of curvature
3. Palatal coverage is not tolerated. Some patients prefer a with at least 2 cm of AP spread are required (Fig. 57 36) In
palateless denture, which may enhance their sensations of this situation, the fixed prosthesis can be fabricated with distal
taste and texture or may simply provide a psychologic ad- extension cantilevers up to half the AP spread provided it does
vantage. Some patients prefer a palateless denture because not exceed 10 mm.
the proximity of the denture with the soft palate induces a
gag reflex. Patients with large palatal tori (see Fig. 54.19) Edentulous Mandible
can also benefit from a palateless maxillary denture. Min-
imum of four implants with adequate AP spread allows Similar to the edentulous maxilla, prosthetic options for pa-
the fabrication of an implant-assisted overdenture without tients with an edentulous mandible include a conventional
palatal coverage. complete denture, an implant-assisted denture, or an implant-
supported prosthesis. A mandibular complete denture is more
The design of a maxillary implant-retained prosthesis is problematic for patients than a maxillary complete denture,
greatly influenced by the anatomy of the maxilla. Most no- especially for patients with a severely resorbed (atrophic)
tably, the maxillary sinus limits the height of bone available mandibular ridge. The lack of stability and retention makes it
very challenging for patients to control the denture. The addi-
tion of implants offers unprecedented control (ie, stability and
retention) for a complete removable prosthesis.
Implant-assisted overlay dentures are designed so that
most of the masticatory load is borne by the primary denture-
support areas (ie, retromolar pad and buccal shelf). A com-
mon practice is to place two implants in the anterior mandible
with a connecting bar. One or two clips retain the denture to
the bar (Fig. 57.40) When occlusal forces are applied, the
denture rotates around the bar (anterior axis of rotation) and
depresses slightly in the posterior aspect, directing the forces
to the primary denture-bearing areas (Fig. 57.41). Theim-
plants provide stability and retention while bearing minimal
stress from occlusal loads. Individual attachments secured
to each implant can also offer a simple prosthetic alternative
(Fig. 57.42) to the bar and clip design. However, it is more
critical for implants with individual attachments to be parallel
to one another to facilitate a proper path of insertion and to
minimize stress during prosthetic seating and function.
For those patients who prefer an implant-supported fixed
FIGURE 57.36 Diagram demonstrating the AP implant spread. It is
prosthesis, four, five, or six implants arranged in an appropri-
defined as the distance from the middle of the most anterior implant to ate arc of curvature with at least 1 cm of AP spread are re-
the distal edge of the most posterior implant. quired (Fig. 57.36). In this situation, the fixed prosthesis can
FIGURE 57.37 Implant-assisted overlay denture. A, Clinical photograph of four-implant bar in the maxilla designed to retain a palateless overlay
denture. B, Photograph of clip and attachment design of palateless overlay denture. Anterior Hader clip attaches to anterior bar, and posterior ERAs
attach to female connectors at posterior ends of the bar. C, Cross-section of Hader bar clip attached to anterior bar (inset). View of overdenture bar with
Hader clip (left) and ERA (right) attached. These plastic components will be embedded in the overdenture as in B. D, Axis of rotation and function of
resilient attachment. When posterior occlusal forces (solid vertical arrow) are applied, the denture rotates around the bar clip anteriorly (curved arrow)
and resilient attachment (arrow) allows the denture to be compressed to primary denture-support areas posteriorly (open arrow).
be fabricated with distal extension cantilevers up to twice the inclined and distally inclined implants placed in areas with
AP spread (Fig. 57.43). bone (eg, the anterior region) to increase AP spread and used
Many patients prefer a fixed option for psychologic reasons to support a full-arch prosthesis, thus avoiding the need for
but the difference in mastication efficiency provided by a fixed extensive bone augmentation in posterior segments. Early
versus removable prosthesis does not appear to be significant. studies have reported success with initial stability and inte-
Evidence suggests that such fixed restorations tend to stop gration with immediate loading. This technique involves the
resorption of the body of the posterior mandible and in some placement of two dental implants in the anterior region of
cases enable regeneration of the bone in this region. the edentulous jaws in the axial direction and then placement
Regardless of whether implants will retain or support the of two implants, one on each side with a 45-degree distal
prosthesis, every attempt should be made to position pos- inclination to avoid the maxillary sinuses in the maxilla or
terior implants with the long axis directed toward the opmental foramen in the mandible. This technique is appealing
posing stamp cusp and aligned perpendicular to the occlusal to patients because it can decrease the treatment time and
plane. Then, occlusal forces can be directed down the long obviate the need for extensive bone augmentation. However,
axis of the implant, which is tolerated better than nonaxial long-term results are lacking and further research is required
forces. A recent concept is to restore atrophied maxillary and to better understand and assess the risks and benefits of this
mandibular ridges in edentulous patients with both axially technique.
FIGURE 57.38 Three different scenarios of bone level dictating three different fixed restorations. Note that the incisal edge of all the three resto-
rations is at the same level when ideally it should be according to esthetics and phonetics. A, Bone resorption is minimal and no need to replace any
soft tissue. A conventional implant-supported fixed-partial denture is planned. B, Bone resorption is moderate, mainly vertical, and there is a need to
replace soft-tissue loss. To avoid the unesthetic look of a long porcelain restoration, the laboratory technician is asked to add some facial pink porcelain
to mimic the lost soft tissue and reduce the length of the fixed-partial denture visually giving the restoration a more acceptable look. C, Bone resorp-
tion is severe and it is vertical and horizontal. The soft tissue has followed and there is a lack of support of the maxillary lip. The fixed restoration has
to restore esthetics and function and support the I ip; a fixed-removable (hybrid) prosthesis with a metal substructure and a buccal acrylic flange is the
restoration planned in this case.
FIGURE 57.39 Cross-section of a Hader bar with clip. Note that the
minimal height of the Hader bar is 2.5 mm and about 1.2 mm for the
plastic clip and the metal housing. Room should be allowed for acrylic
to set for the retention of these components.
FIGURE 57.40 Implant-assisted overlay denture. A, Clinical view of overdenture in occlusion. B, Photograph of mandibular overlay denture (tissue-
bearing surface) designed for an implant bar attached to two implants in the anterior mandible. Two Hader clips are embedded in the anterior acrylic.
C, Clinical view of bar attached to two implants in the anterior mandible. D, The illustration demonstrates how the axis of rotation allows the denture
to rotate around the bar. When the patient applies occlusal force posteriorly, the overlay denture rotates around the bar and the load is absorbed by
primary denture-bearing surfaces posteriorly.
)
FIGURE 57.41 Individual attachments can be used on each implant to assist in retention of the mandibular overdenture. A, Clinical view of
anterior mandible with individual ball attachments on two implants. B, Tissue-bearing surface of mandibular overdenture showing individual female
attachments embedded in the denture. (Courtesy Dr Sal Esposito, Beachwood, OH.)
57 Diagnosis and Treatment Planning in lmplantology 692.eS
Anterior-posterior spread is
0 I 0 the distance from the
center of the most anterior
implant(s) to the distal
surface of the most
posterior implants
The AP spread required for

an implant-supported
prosthesis is:
1
Maxilla= 2 cm
00 OU vi'
vi'
6+ implants
Mandible = 1 cm
4+ implants
(B)
FIGURE 57.42 Cantilever length relative to AP spread of implant distribution. A, Clinical view of an implant-supported restoration replacing man-
dibular teeth. Notice that the restoration is supported by five implants in the anterior and has cantilever extensions in the posterior segments. B, Study
model view of similar mandibular implant-supported restoration with posterior cantilever extensions. Cantilever length, in the edentulous mandible,
should not exceed twice the AP spread.
FIGURE 57.43 Single-tooth restoration in the posterior mandible supported by a wide-diameter implant. A, Clinical photograph of healing
abutment on wide-diameter implant. B, Photograph of laboratory model with single molar. C, Clinical photograph of molar crown supported by wide-
diameter implant. The use of wide-diameter (external hex) implants eliminates the problem of screw loosening for single-tooth, posterior, implant-
supported crowns. Note that this crown is secured to the abutment via a lingual set screw (small hex driver seen attaching set screw).
FIGURE 57.44 Guidelines for restoring posterior quadrants. Embrasures should be large enough for access with a proxy brush. The occlusal table
must be narrow, cusp angles flattened, and proper emergence profiles developed. Anterior guidance should be restored with the natural dentition
whenever possible. A, Laboratory model and B, clinical photograph of two-unit, fixed-partial denture supported by two implants in the posterior
mandible demonstrates these qualities.
a better prognosis. In the 1980s, clinicians attempted to re- improve biomechanical support and dramatically decrease or
store mandibular first molar sites with conventional implants eliminate rotational forces. (Fig. 57.44).
3. 75 or 4.0 mm in diameter. Unfortunately, the results were Single implants can be used with a high rate of success
quite disappointing. Occlusal overload led to bone loss and, in the anterior and premolar areas. The bone-implant inter-
in some cases, fractured implants, especially for the 3. 75-mm face achieved in this area is good and the size of the occlusal
diameter implant. surface is generally small. Although similar considerations ex-
The most common problem observed, particularly when ist regarding screw loosening for single-implant restorations
external hex-headed implants were used, was loosening of the in the anterior and premolar regions, these concerns are less
screw retaining the restoration. This problem results because significant because of a more anterior position (lesser forces
the diameter of the head of the implant is much smaller than generated). Typically, there is better bone quantity and quality
the size of the occlusal surface. The buccolingual width of the compared with more posterior sites.
crown can be minimized by narrowing the dimension of the
restoration but there is less control over the mesiodistal di-
Strategies to Avoid Implant Overload
mension because contacts need to be established and the space
is most often filled. Consequently, a mesiodistal cantilever, al- Multiunit implant restorations should be splinted to maxi-
beit small, is created. Tipping of the restoration during func- mize implant support by distributing the occlusal loads and
tion eventually leads to stretching and loosening of the screw emergence profiles should be developed with open embrasure
that secures the crown to the implant fixture. If hex-headed spaces to facilitate oral hygiene (Fig. 57 9).
implants are used, the use of wide-diameter implants greatly Implants should be of adequate number, size, and posi-
diminishes the screw-loosening complication (Fig. 57.4 3). tion to sustain the anticipated occlusal loads. Implants with
The larger platform reduces the potential for tipping forces to smaller diameters have a lesser capacity to support bending
stretch or break the screw. The use of implants with internal forces than do implants with larger diameters. Implants with
connections has been shown to be less susceptible to screw a minimum of 4-mm diameter should be used in areas ex-
loosening than implants with an external connection. Implant pected to sustain greater occlusal loads (ie, the posterior re-
systems with internal connections have been introduced to gions). Wider-diameter implants can be used when adequate
lower or eliminate the mechanical complications, such as bone and space exists (Fig. 57.9). Thus, when the residual
abutment screw loosening or even fatigue fracture. A system- ridge and site permits, wide-diameter implants should be
atic review by Gracis et al concluded loosening of abutment used for molar replacement. Wide-diameter implants should
screws was the most frequently occurring technical complica- be avoided at anterior sites because of less bone width and
tion. The type of connection seems to have an influence on the the risk of bone loss, especially along the labial-buccal sur-
incidence of the screw loosening; looser screws were reported face. Standard-diameter ( 4 mm) implants may be best for
for externally connected implant systems for both types of premolar and anterior tooth replacement because they ap-
materials. To minimize the screw-loosening incidence of both proximate the size of these teeth and will provide a better
external and internal connection abutment/reconstructions, it emergence profile.
is highly recommended to tighten the retention screws at the
recommended torque level.
Occlusal Design
If the first molar is lost and suitable abutments are present,
a conventional three-unit, fixed-partial denture is still a viable Occlusal design for implant-supported prostheses is an essen-
option, especially if the adjacent teeth already have large resto- tial and integral determinant of overall treatment planning.
rations or preexisting crowns. However, if adjacent teeth have The risk of implant overload can be minimized by limiting the
small or no restorations, it is more conservative and preferable width of the occlusal table of the implant-supported fixed-
to replace the missing single tooth with an implant. This res- partial denture, flattening the cusp angles, avoiding the use
toration is cost-effective and predictable. In distal extension of cantilevered restorations, and restoring the anterior guid-
areas when restoring a single molar tooth, two conventionally ance (ideally natural tooth). Box 5 7. 7 lists strategies to avoid
sized implants may be placed (with appropriate spacing) to implant overload.
Strategies to t\vo1i::I Implant Overload "nonrigid" and "sernirigid" attachments. In addition, the well-
documented phenomenon of intrusion of the natural tooth
abutment associated with the use of semiprecision attach-
• Place implants perpendicular to the occlusal plane ments is prevented.
• Place implants in tooth positions
• Use an implant for each unit being replaced
• Avoid the use of cantilevers in linear configurations Conclusion
• Avoid connecting implants to teeth
• If connecting implants to teeth, use a rigid attachment The importance of biomechanics and the limitations of im-
• Control occlusal factors, such as cusp angles and width of plant systems were initially underestimated. It was believed
occlusal table that multiunit fixed bridges could be supported by as few as
• Restore anterior guidance if possible two implants, as it was done with the natural dentition. Over
the years, clinical experience and research underscored the
importance of biomechanics in the success and predictability
of implant-retained prostheses. The rigid nature of implant-
The intensity and the vector of the force depend on several retained restorations and the lack of forgiveness in these
variables including the amount of bone contact (osseointegra- systems require proper treatment planning and a good un-
tion), the quality and the quantity of the supporting bone, and derstanding of the biomechanics of implant prostheses. The
the implant surface characteristics. Regardless of the direction principles of biomechanics must be factored into the planning
or the amount of this force, it always leads to micromotion at at the beginning of any implant treatment to achieve long-
the bone-implant interface, which translates as stress to the term, predictable success.
adjacent bone. Splinting implant crowns together and placing When clinicians follow a strategy that avoids implant over-
longer and wider implants, as well as enhanced implant sur- load and place an adequate number of implants in optimal
face features, increase the bone-to-implant contact, or bone- positions, abutment selection is simplified and proper emer-
appositional index, and reduce stress forces, thereby increasing gence profiles can be developed. There should always be suf-
the load-bearing capacity of the implant(s). ficient space in interproximal areas for hygienic access and
tissue health. The clinician will also have better control over
occlusal loads by idealizing the occlusal anatomy with nar-
Cantilevers
rowed occlusal table and flattened cusp angles.
The use of cantilevered implant-supported restorations (ie,
unilateral, linear configurations) in posterior quadrants of the
mandible or maxilla is strongly discouraged and should be
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58
Surgical Concepts of
Implant Therapy
PR Klokkevold • IA Urban • DL Cochran • TJ Han
K-B Park • DA Shanelec • LS Tibbetts • T Vercellotti
DH Etienne • RR Derycke • A Jain
Chapter Outline
General Principles of Implant Surgery Esthetic Management of Difficult
Two-Stage "Submerged" Implant Cases (Minimally Invasive Approach)
Placement Surgical Strategy for Predictable
One-Stage "Nonsubmerged" Implant Esthetics
Placement Immediate Implant Placement for
Localized Bone Augmentation and Predictability and Esthetics
Implant Site Development Dental Implant Microsurgery-
Guided Bone Regeneration Immediate Placement
Localized Ridge Augmentation Implant Microsurgery
Advanced Implant Surgical Procedures Piezoelectric Bone Surgery
Maxillary Sinus Elevation and Bone Clinical Characteristics of Ultrasonic
Augmentation Cutting
Supracrestal/Vertical Bone Augmentation Computer-Assisted Implant Surgery
Growth Factors in Bone Augmentation Conclusions
The surgical procedures for the placement of nearly all endos- (see Video 58.1: Single Tooth Implant). Each implant system
seous dental implants currently used are based on the origi- is designed with specific armamentarium and recommenda-
nal work of Professor Per-Ingvar Branernark and coworkers tions for use (eg, drilling speeds) and it is advisable to follow
in Sweden in the 1960s and 1970s. Their landmark research the detailed protocols provided by the manufacturer.
evaluated the biologic, physiologic, and mechanical aspects
of the titanium screw-shaped implant, subsequently known
General Principles of Implant Surgery
commercially as the Nobelpharma "Branernark" implant
system and currently manufactured by Nobel Biocare. The Patient Preparation
original Branernark implant was a parallel-walled, cylindri-
cally shaped, threaded implant with an external hex connec- Most implant surgical procedures can be done in the office us-
tion and a machined surface. In the past few decades many ing local anesthesia. Conscious sedation (oral or intravenous)
different designs of root form implants have been developed, may be indicated for some patients. The risks and benefits of
modified, and studied. The same fundamental principles of implant surgery specific to the patient's situation and needs
atraumatic, precise implant site preparation applies to all im- should be thoroughly explained prior to surgery. A written,
plant systems. In brief, this includes a gentle surgical tech- informed consent should be obtained for the procedure.
nique and progressive, incremental preparation of the bone
for a precise fit of the implant at the time of placement. Implant Site Preparation
This chapter outlines the basic surgical procedures for the
placement of endosseous dental implants using either one- Some basic principles must be followed to achieve osseo-
stage or two-stage protocols. The principles described here integration with a high degree of predictability (Box 58 1).
are intentionally generic and designed to serve as guidelines The surgical site should be kept aseptic, and the patient
and to be applicable to most of the common implant systems should be appropriately prepared and draped for an intraoral
697
P.rinciples of Implant Therapy

ieve Osseointegration
1. Implants must be sterile and made of a biocompatible
material (eg, titanium).
2. Implant site preparation should be performed under sterile
conditions.
3. Implant site preparation should be completed with an
atraumatic surgical technique that avoids overheating of
the bone during preparation of the recipient site.
4. Implants should be placed with good initial stability.
5. Implants should be allowed to heal without loading or
micromovement (ie, undisturbed healing period to allow
for osseointegration) for 2-4 or 4-6 months, depending on FIGURE 58.1 One-stage implant versus two-stage implant surger-
the bone density, bone maturation, and implant stability. ies. A, One-stage surgery with the implant designed so that the coronal
portion of the implant extends through the gingiva. B, One-stage surgery
with implant designed to be used for two-stage surgery. A healing abut-
ment is connected to the implant during the first-stage surgery. C, In the
surgical procedure. Prerinsing with chlorhexidine gluconate two-stage surgery, top of the implant is completely submerged under
gingiva.
for 1-2 min immediately before the procedure will aid in re-
ducing the bacterial load present around the surgical site. Ev-
ery effort should be made to maintain a sterile surgical field
and to avoid contamination of the implant surface. Implant period of time to allow for osseointegration. In two-stage im-
sites should be prepared using gentle, atraumatic surgical plant surgery, the implant must be surgically exposed follow-
techniques with an effort to avoid overheating the bone. ing a healing period. Some implants are specifically designed
When these clinical guidelines are followed, successful os- with the coronal portion of the implant positioned above the
seointegration occurs predictably for submerged and nonsub- crest of bone and extending through the gingival tissues at
merged dental implants. Well-controlled studies of patients the time of placement in a one-stage protocol (Fig. 58.1, A).
with good plaque control and appropriate occlusal forces have Other implant systems are designed to be placed at the level
demonstrated that root form, endosseous dental implants of bone, require a healing abutment to be attached to the im-
show little change in bone height around the implant over plant at the time of placement to be used in a one-stage ap-
years of function. After initial bone remodeling in the first year proach (Fig. 58.1, B).
(1.0-1.5 mm of resorption described as "normal remodeling A one-stage surgical approach simplifies the procedure
around an externally hexed implant"), the bone level around because a second-stage exposure surgery is not necessary.
healthy functioning implants remains stable for many years. The two-stage, submerged approach is advantageous for situ-
The average annual crestal bone loss after the first year in ations that require simultaneous bone augmentation proce-
function is expected to be 0.1 mm or less. Hence, implants dures at the time of implant placement because membranes
offer a predictable solution for tooth replacement. can be submerged, which will minimize postoperative ex-
Regardless of the surgical approach, the implant must be posure. Mucogingival tissues can be augmented if desired at
placed in healthy bone with good primary stability to achieve the second-stage surgery in a two-stage protocol or as part
osseointegration, and an atraumatic technique must be fol- of the one-stage protocol. Fundamental differences in flap
lowed to avoid damage to bone. Drilling of the bone without management for these two surgical techniques are described
adequate cooling generates excessive heat, which injures bone separately.
and increases the risk of failure. The anatomic features of bone
quality (dense compact vs loose trabecular) at the recipient site
influence the interface between bone and implant. Compact
Two-Stage "Submerged" Implant
bone offers a much greater surface area for bone-to-implant Placement
contact than cancellous bone. Areas of the jaw exhibiting thin In the two-stage implant surgical approach, the first-stage or
layers of cortical bone and large cancellous spaces, such as the implant placement surgery ends by suturing the soft tissues
posterior maxilla, have lower success rates than areas of dense
together over the implant cover screw so that it remains sub-
bone. The best results are achieved when the bone-to-implant
merged and isolated from the oral cavity. In areas with dense
contact is intimate at the time of implant placement. cortical bone and good initial implant support, the implants
are left to heal undisturbed for a period of 2-4 months, where-
One-Stage Versus Two-Stage Implant as in areas of loose trabecular bone, grafted sites, and sites with
lesser implant stability, implants may be allowed to heal for
Placement Surgery
periods of 4-6 months or more. Longer healing periods are
Currently, most threaded endosseous implants can be placed indicated for implants in sites with less bone support. Dur-
using either a one-stage (nonsubmerged) or a two-stage (sub- ing healing, osteoblasts migrate to the surface and form bone
merged) protocol. In the one-stage approach, the implant or adjacent to the implant (osseointegration). Shorter healing pe-
the abutment emerges through the mucoperiosteum/gingival riods are indicated for implants placed in good quality (dense)
tissue at the time of implant placement, whereas in the two- bone and for implants with an altered surface microtopogra-
stage approach, the top of the implant and cover screw are phy (eg, acid etched, blasted, or etched and blasted) Readers
completely covered with the flap closure (Fig. 58.1). Implants are referred to online material and other resources for more
are allowed to heal, without loading or micromovement, for a information about implant surface microtopography.
58 Surgical Concepts of Implant Therapy 699
the buccal mucosa or the opposing teeth to keep the surgical

site open during the surgery. The bone at the implant site(s)
must be thoroughly debrided of all granulation tissue.
For a "knife-edge" alveolar process with sufficient alveolar
bone height and distance from vital structures (eg, inferior al-
veolar nerve), a large round bur is used to recontour or flat-
ten the bone to provide a wider, level surface for the implant
site preparation (Fig. 58.2, B). However, if the vertical height
of the alveolar bone is limited (eg, < 10 mm), the knife-edge
alveolar bone height should be preserved. Bone augmentation
procedures can be used to increase the ridge width while pre-
serving alveolar bone height.
Implant Site Preparation

Once the flaps are reflected and the bone is prepared (ie, all
granulation tissue removed and knife-edge ridges flattened),
the implant osteotomy site can be prepared. A series of drills are
used to prepare the osteotomy site precisely and incrementally
for an implant (Fig. 58.5). A surgical guide or stent is inserted,
checked for proper positioning, and used throughout the pro-
cedure to direct the proper implant placement (Fig. 58.4, E).
Round Bur
A small round bur (or spiral drill) is used to make the ini-
FIGURE 58.2 Tissue management for a two-stage implant placement. tial penetration into bone for the implant site(s). The surgi-
A, Cresta I incision made along the crest of the ridge, bisecting the existing cal guide is removed, and the initial marks are checked for
zone of keratinized mucosa. B, Full-thickness flap is raised buccally and
their appropriate buccal-lingual and mesial-distal location, as
lingually to the level of the mucogingival junction. A narrow, sharp ridge
can be surgically reduced/contoured to provide a reasonably flat bed for well as the positions relative to each other and adjacent teeth
the implant. C, Implant is placed in the prepared osteotomy site. D, Tissue (Fig. 57 9). Slight modifications may be necessary to adjust
approximation to achieve primary flap closure without tension. spatial relationships and to avoid minor ridge defects. Any
changes should be compared to the prosthetically driven sur-
gical guide positions. Each marked site is then prepared to a
In the second-stage (exposure) surgery, the implant is uncov- depth of 1-2 mm with a round drill, breaking through the
ered and a healing abutment is connected to allow emergence of cortical bone and creating a starting point for the 2-mm twist
the abutment through the soft tissues. Once healed, the restorative drill (Fig. 58.3, A)
dentist then proceeds with the prosthodontic aspects of the im-
plant therapy (impressions and fabrication of prosthesis). The 2-mm Twist Drill
The following paragraphs describe the steps for osteotomy A small twist drill, usually 2 mm in diameter and marked to in-
preparation and the first-stage implant placement surgery of dicate various lengths (ie, corresponding to the implant sizes),
the two-stage protocol. Figures 58.2 and 58.3 illustrate the is used next to establish the depth and align the long axis of the
procedures via diagrams, and Fig. 58.4 depicts the procedures implant recipient site (Fig. 58.3, B) This drill may be externally
with clinical photographs. or internally irrigated. In either case, the twist drill is used at a
speed of approximately 800-1500 rpm, with copious irrigation
to prevent overheating of the bone. Additionally, drills should
Flap Design, Incisions, and Elevation
be intermittently and repeatedly "pumped" or pulled out of the
Flap management for implant surgery varies slightly, depend- osteotomy site while drilling to expose them to the water cool-
ing on the location and objective of the planned surgery. There ant and to facilitate clearing bone debris from the cutting sur-
are different incision/flap designs but the most common is the faces. In other words, clinicians should pump the drill (up and
crestal flap design. The incision is made along the crest of down) intermittently and avoid using a constant "push" of the
the ridge, bisecting the existing zone of keratinized mucosa drill in the apical direction only.
(Figs. 58.2, A, and 58.4, B). When multiple implants are being placed next to one an-
A remote incision with a layered suturing technique may other, a guide pin should be placed in the prepared sites to
be used to minimize the incidence of bone graft exposure check alignment, parallelism, and proper prosthetic spacing
when extensive bone augmentation is planned. The crestal throughout the preparation process (Fig. 58.3, C). The rela-
incision, however, is preferred in most cases because closure tionship to neighboring vital structures (eg, nerve and tooth
is easier to manage and typically results in less bleeding, less roots) can be determined by taking a periapical radiograph
edema, and faster healing. with a guide pin(s) or radiographic marker(s) in the osteot-
A full-thickness flap is raised (buccal and lingual) up to omy site(s) (Fig. 57 22) Implants should be positioned with
or slightly beyond the level of the mucogingival junction, approximately 3 mm between one another to ensure sufficient
exposing the alveolar ridge of the implant surgical sites space for interimplant bone and soft-tissue health and to fa-
(Figs. 58.2, B, and 58.4, C). Elevated flaps may be sutured to cilitate oral hygiene procedures. Therefore, the initial marks
FIGURE 58.3 Implant site preparation (osteotomy) for a 4.0-mm diameter, 10-mm length screw-type, threaded (external hex) implant in a sub-
crestal position. A, Initial marking or preparation of the implant site with a round bur. B, Use of a 2-mm twist drill to establish depth and align the
implant. C, Guide pin is placed in the osteotomy site to confirm position and angulation. D, Pilot drill is used to increase the diameter of the coronal
aspect of the osteotomy site. E, Final drill used is the 3-mm twist drill to finish preparation of the osteotomy site. F, Countersink drill is used to widen
the entrance of the recipient site and allow for the subcrestal placement of the implant collar and cover screw. Note: An optional tap (not shown) can
be used following this step to create screw threads in areas of dense bone. G, Implant is inserted into the prepared osteotomy site with a handpiece
or handheld driver. Note: In systems that use an implant mount, it would be removed prior to placement of the cover screw. H, Cover screw is placed
and soft tissues are closed and sutured.
should be separated by at least 7 mm (center to center) for during the initial ridge preparation, this must be taken into
4 mm standard-diameter implants. Incrementally more space account when preparing the site for a predetermined implant
is needed for wide-diameter implants (Fig. 57.9). length. For example, if it appears that the implant will be too
The 2-mm twist drill is used to establish the final depth close to a vital structure, such as the inferior alveolar nerve
of the osteotomy site corresponding to the length of each canal, the depth of the implant osteotomy site and length of
planned implant. The clinician should also evaluate the bone the implant may need to be reduced.
quality (density) with this drill while preparing the osteotomy The next step is to use a series of drills to incrementally
to assess the need for modification of subsequent drills used increase the width of the osteotomy site to accommodate the
(Box 58.2). If the vertical height of the bone was reduced planned implant diameter. The styles, shapes, and final diameter
FIGURE 58.4 Clinical view of stage one implant placement surgery. A, Partial edentulous ridge; presurgical and prosthodontic treatment has been
completed. B, Mesial sulcular and distal vertical incisions are connected by a crestal incision. Notice that bands of gingival collars remain adjacent
to the distal molar tooth. C, Minimal flap reflection is used to expose the alveolar bone. Sometimes a ridge modification is necessary to provide a
flap recipient bed. D, Buccal flap is partially dissected at the apical portion to provide a flap extension. This is a critical step to ensure a tension-free
closure of the flap after implant placement. E, It is important to use the surgical stent to determine the mesial-distal and buccal-lingual dimensions and
proper angulation of the implant placement. F, Frequent use of the guide pins ensures parallelism of the implant placement. G, After placement of two
Nobelpharma implants, the cover screws are placed. The cover screws should be flushed with the rest of the ridge to minimize the chance of exposure.
This is especially important if the patient will wear a partial denture during the healing phase. H, Suturing completed. Both regular interrupted and
inverted mattress sutures are used intermittently to ensure tension-free, tight closure of the flaps.
of the drills will differ slightly among different implant systems,

but their general purpose is to prepare a recipient site with a
precise diameter (and depth) for the selected implant without
unduly traumatizing the surrounding bone. It is important to
use copious irrigation and a "pumping" action for all drilling.
Pilot Drill
Following the 2-mm twist drill, a pilot drill with a noncutting
2-mm diameter "guide" at the apical end and a cutting 3-mm
diameter (wider) midsection is used to enlarge the osteotomy
site at the coronal end, thus facilitating the insertion of the
subsequent drill in the sequence (Fig. 58.3, D).
The 3-mm Twist Drill

The final drill in the osteotomy site preparation for a standard-
diameter (4.0 mm) implant is the 3-mm twist drill. It is the
last drill used to widen the site along the entire depth of the
FIGURE 58.5 Sequence of drills used for standard-diameter (4.0 mm) osteotomy from the previous diameter (2 mm) to final diam-
implant site osteotomy preparation: round, 2-mm twist, pilot, 3-mm eter (3 mm). This final drill in the sequence finishes preparing
twist, and countersink. Bone tap (not shown here) is an optional drill
that is sometimes used in dense bone before implant placement. the osteotomy site and consequently is the step that dictates
whether the implant will be stable or not (Fig. 58.3, E). It is
critically important that the final diameter drilling be accom-
plished with a steady hand, without wobbling or changing di-
rection so that the site is not overprepared. Finally, depending
on bone density, the diameter of this final drill may be slightly
increased or decreased to enhance implant support (Box 58.2).
Countersink Drill (Optional)

CLINICAL SITUATION 1 When it is desirable to place the cover screw at or slightly be-
If the final drill hits the bottom of the recipient site before low the crestal bone, countersink drilling is used to shape or
reaching the desired depth, the added hand pressure flare the crestal aspect of the osteotomy site allowing the coro-
necessary to achieve the proper depth often causes wobbling nal flare of the implant head and cover screw to fit within the
and funneling of the recipient site. This is especially true with osteotomy site (Fig. 58.3, F). As with all drills in the sequence,
"cannon" drills (used for cylindrical implants). To minimize copious irrigation and gentle surgical techniques are used.
this effect, a smaller-diameter drill should be used to prepare
the site slightly deeper (eg, 0.5 mm or less). This narrower Bone Tap (Optional)
drill allows the desired depth to be reached without affecting
the side walls and facilitates a more precise osteotomy As the final step in preparing the osteotomy site in dense corti-
preparation with the final drill. cal bone, a tapping procedure may be necessary (not shown).
With self-tapping implants being almost universal, there is
CLINICAL SITUATION 2
less need for a tapping procedure in most sites. However,
If the final drill is inserted at an inaccurate angle, the result
in dense cortical bone or when placing longer implants into
is funneling of the coronal portion of the implant site. To
minimize this potential problem, when drilling multiple
moderately dense bone, it is prudent to tap the bone (create
implant sites, the operator should always keep a direction threads in the osteotomy site) before implant placement to
indicator in an adjacent site. For single-implant sites, the facilitate implant insertion and to reduce the risk of implant
adjacent teeth and surgical guide should serve as direction binding (Fig. 58.3, G).
indicators. When dealing with dense bone, a precise
recipient site can be achieved more predictably if there is Clinical Comment. When faced with a very soft, poor-quality
minimal diameter change from drill to drill. For example, bone (eg, loose trabecular bone in the posterior maxilla), tap-
switching from 3.0 to 5.0 mm is much less precise than ping is not necessary or recommended (Box 58.2). It is better
proceeding from 3.0 to 3.3 to 4.2 to 5.0 mm. to allow the threaded implant to "cut" its own path into the
CLINICAL SITUATION 3 osteotomy site.
If the bone is "soft" (eg, loose trabecular bone), it may be Bone tapping and implant insertion are both done at very
advantageous to underprepare the osteotomy site. A slightly slow speeds (eg, 20-40 rpm). All other drills in the sequence
underprepared site can be accomplished by using the final are used at higher speeds (800-1500 rpm).
drill to a shallower depth than the previous drill (eg, half It is important to create a recipient site that is very accurate
the depth of the osteotomy site). This avoids removing too in size and angulation. In partially edentulous cases, limited
much bone and increases the implant stability or tightness jaw opening or proximity to adjacent teeth may prevent appro-
at the time of placement. Another method to achieve an
priate positioning of the drills in posterior edentulous areas. In
underprepared site is to use a drill with a slightly smaller
diameter as the final drill in the preparation (eg, a 2.75-mm
fact, implant therapy may be contraindicated in some patients
drill as the final drill rather than a 3.0 mm or a 3.25 mm as because of a lack of interocclusal clearance, lack of interdental
the final drill for a 4.0-mm implant). space, or a lack of access for the instrumentation. Therefore, a
combination of longer drills and shorter drills, with or without
extensions, may be necessary Anticipating these needs before BOX 58.3 Objectives of Second-Stage Implant
surgery facilitates the procedure and improves the results. Surgery
Implant Placement 1. To expose the submerged implant without damaging the
Implants are inserted with a handpiece rotating at slow speeds surrounding bone.
2. To control the thickness of the soft tissue surrounding the
(eg, 25 rpm) or by hand with a wrench. Insertion of the implant
implant.
must follow the same path or line as the osteotomy site. When 3. To preserve or create attached keratinized tissue around the
multiple implants are being placed, it is helpful to use guide pins implant.
in the other sites to have a visual guide for the path of insertion. 4. To facilitate oral hygiene.
5. To ensure proper abutment seating.
6. To preserve soft-tissue esthetics.
Flap Closure and Suturing
Once the implants are inserted and the cover screws secured
(Fig. 58.4, G), the surgical sites should be thoroughly irrigat- the objectives for second-stage implant exposure surgery. The
ed with sterile saline to remove debris and clean the wound. need for a zone of keratinized tissue surrounding implants is
Proper closure of the flap over the implant(s) is essential. One desirable, as one long-term study indicated that the presence
of the most important aspects of flap management is achiev- of keratinized tissue is strongly correlated with soft- and hard-
ing good approximation and primary closure of the tissues in tissue health.
a tension free manner (Fig. 58.3, H). This is achieved by in-
cising the periosteum (innermost layer of full-thickness flap), Simple Circular "Punch" or Cresta! Incision
which is nonelastic. Once the periosteum is released, the In areas with sufficient zones of keratinized tissue, the gingiva
flap becomes very elastic and is able to be stretched over the covering the head of the implant can be exposed with a cir-
implant(s) without tension. One suturing technique that con- cular or "punch" incision (Fig. 58.6). Alternatively, a crestal
sistently provides the desired result is a combination of alter- incision through the middle of the keratinized tissue and full-
nating horizontal mattress and interrupted sutures (Fig. 58.4, thickness flap reflection can be used to expose implants.
H). Horizontal mattress sutures evert the wound edges and
approximate the inner, connective tissue surfaces of the flap Partial-Thickness Repositioned Flap
to facilitate closure and wound healing. Interrupted sutures If a minimal zone of keratinized tissue exists at the implant
help to bring the wound edges together, counterbalancing site, a partial-thickness flap technique can be used to fulfill the
the eversion caused by the horizontal mattress sutures. objective of the second-stage surgery (exposing the implant)
The clinician should choose an appropriate suture for the while increasing the width of keratinized tissue. The initial
given patient and procedure. For patient management, it is incision is made within the zone of keratinized tissue so that
sometimes simpler to use a resorbable suture that does not it becomes the outer edge of the reflected split-thickness flap.
require removal during the postoperative visit (eg, 4-0 chromic Vertical releasing incisions are used on both the mesial and the
gut suture). However, when moderate-to-severe postoperative distal end of the flap (Fig. 58.7, A and B). A partial-thickness
swelling is anticipated, a nonresorbable suture is recommend- flap is then raised in such a manner that a nonmobile, firm
ed to maintain a longer closure period (eg, 4-0 monofilament periosteum remains attached to the underlying bone. The flap,
suture). These sutures require removal at a postoperative visit. containing a narrow band of keratinized tissue, is then repo-
sitioned to the facial side of the emerging head of the implant
and sutured to the periosteum with a fine needle and resorb-
Postoperative Care able suture such as a 5-0 gut suture (Fig. 58.8). If the initial
Simple implant surgery in a healthy patient usually does not amount of keratinized tissue is less than 2 mm, the flap may
require antibiotic therapy However, antibiotics [eg, amoxicillin, be started at the labial edge of the keratinized tissue allowing
500 mg three times a day (tid)] can be prescribed if the surgery that zone to remain on the lingual aspect of the implant. A
is extensive, or if the patient is medically compromised. Post- partial-thickness flap is apically displaced and sutured to the
operative swelling is likely after flap surgery This is particularly periosteum without exposing the alveolar bone (Fig. 58. 7, C).
true when the periosteum has been incised (released). As a pre- A free gingival graft may be harvested from the palate and su-
ventive measure, patients should apply cold packs over the first tured to the periosteum on the labial surface of the implants to
24-48 h. Chlorhexidine gluconate oral rinses can be prescribed increase the zone of keratinized tissue (not shown).
to facilitate plaque control, especially in the days after surgery After the flap is repositioned and secured with periosteal
when oral hygiene is typically poorer. Adequate pain medica- sutures, the excess tissue coronal to the cover screw is ex-
tion should be prescribed (eg, ibuprofen, 600-800 mg tid) cised, usually with a surgical blade (Fig. 58.8, B). However,
Patients should be instructed to maintain a relatively soft if removal of this tissue would jeopardize the amount of re-
diet after surgery. Then, as healing progresses, they can gradu- maining keratinized tissue around the lingual aspect of the
ally return to a normal diet. Patients should also refrain from implant(s), a similar partial-thickness flap can be elevated and
tobacco and alcohol use after surgery Provisional restorations, repositioned on the lingual side as well. Extra care must be
whether fixed or removable, should be checked and adjusted taken when creating a split-thickness flap on the lingual sur-
to minimize trauma to the surgical area. face of mandibular sites because the tissue is often very thin.
Alternatively, a full-thickness lingual flap will be safer and will
serve a similar purpose of preserving keratinized tissue on the
Second-Stage Exposure Surgery lingual surface of the implant(s).
For implants placed using a two-stage "submerged" protocol, When the excess tissue over the cover screw is removed
a second-stage exposure surgery is necessary. Box 58.3 lists or displaced, the outline of the cover screw is visible. A sharp
FIGURE 58.6 Clinical view of second-stage implant exposure surgery in a case with adequate keratinized tissue. A, Simple circular "punch" inci-
sion used to expose implant when sufficient keratinized tissue is present around the implant(s). B, Implant exposed. C, Healing abutment attached. D,
Final restoration in place, achieving anesthetic result with a good zone of keratinized tissue.
FIGURE 58.7 Clinical view of second-stage implant exposure surgery in a case with inadequate keratinized tissue. A, Two endosseous implants
were placed 4 months previously and are ready to be exposed. Note the narrow band of keratinized tissue. B, Two vertical incisions are connected by
crestal incision. If facial keratinized tissue is insufficient, it is necessary to locate the crestal incision more lingually so that there is at least 2-3 mm of
keratinized band. C, Buccal partial-thickness flap is sutured to the periosteum apical to the emerging implants. D, Gingival tissue coronal to the cover
screws is excised using the gingivectomy technique. E, Cover screws are removed, and heads of the implants are cleared. F, Abutments are placed.
Visual inspection ensures intimate contact between the abutments and the implants. G, Healing at 2-3 weeks after second-stage surgery. H, Four
months after the final restoration. Note the healthy band of keratinized attached gingiva around the implants.
FIGURE 58.8 Illustration depicting the use of a split-thickness flap

that is repositioned to the labial surface in order to preserve and in-
crease the amount of keratinized tissue. A, Partial-thickness flap is cre-
ated from the lingual aspect of the crest toward the labial surface in
order to preserve the keratinized tissue on the crest (over the implant).
Note: This tissue might be excised in a simple implant exposure. B, The
split-thickness flap is repositioned to the labial surface. C, The flap is su-
tured to the periosteum at a more apical position preserving the amount
of keratinized tissue (arrows). Finally, the remaining connective tissue
over the cover screw (B) is excised with a sharp blade to expose the
implant. Care should be taken to avoid removing keratinized tissue from
the lingual aspect of the implant.
blade is used to eliminate all tissues coronal to the cover screw

(Fig. 58.7, D). The cover screw is then removed, the head of FIGURE 58.9 Tissue management for a one-stage implant place-
the implant is thoroughly cleaned of any soft- or hard-tissue ment. A, Crestal incision made along the crest of the ridge, bisecting
overgrowth, and the healing abutments or standard abut- the existing zone of keratinized mucosa. B, Full-thickness flap is raised
buccally and lingually to the level of the mucogingival junction. A nar-
ments are placed on the implant (Fig. 58.7, E and F). The fit
row, sharp ridge can be surgically reduced or contoured to provide a
of the healing abutments to the implants can often be visually reasonably flat bed for the implant. C, Implant is placed in the prepared
evaluated. However, if it is not possible to visualize clearly the osteotomy site. D, Tissues are adapted around the neck of the implant to
intimate connection between the implant and the abutment, achieve flap closure with the implant protruding through the soft tissues.
an intraoral periapical X-ray film should be taken to confirm
complete seating. Bone may need to be removed around the support, the implants are left to heal undisturbed for a pe-
top of the implant to get the abutment to seat properly. Read- riod of 2-4 months, whereas in areas of loose trabecular bone,
ers are referred to online material for a discussion of bone grafted sites, and/or minimal implant support, they may be
profiling. allowed to heal for periods of 4-6 months or more).
Postoperative Care
In the one-stage surgical approach, the implant or the heal-
ing abutment protrudes approximately 2-3 mm from the bone
Once the implant is exposed and soft tissues are sutured, it crest, and the flaps are adapted around the implant/abutment.
is important to remind the patient of the need for good oral As with the second-stage surgical procedures described, the
hygiene around the implant and adjacent teeth. Care should soft tissues may be thinned, repositioned, or augmented at the
be taken during oral hygiene procedures to avoid dislodging implant placement surgery to increase the zone of keratinized
any repositioned or grafted soft tissues. Direct pressure or tissue surrounding the implant(s).
movement directed toward the soft tissue from a provisional
prosthesis can delay healing and should be avoided. Tissues
should be monitored regularly and the provisional prosthesis Flap Design, Incisions, and Elevation
should be adjusted as needed. Impressions for the final pros- The flap design for the one-stage surgical approach is always
thesis fabrication can begin about 2-6 weeks after implant ex- a crestal incision bisecting the existing keratinized tissue
posure surgery, depending on healing and maturation of soft (Fig. 58.9). Vertical incisions may be needed at one or both
tissues. Figure 58. 7, G and H, shows the postoperative results ends to facilitate access to the bone or osteotomy site. Tissues
in a clinical case after 2-3 weeks and 4 months, respectively. can be thinned in posterior areas if desired but are generally
not thinned in anterior esthetic areas. Full-thickness flaps are
One-Stage "Nonsubmerged" Implant elevated facially and lingually.
Placement
In the one-stage implant surgical approach, a second im-
plant exposure surgery is not needed because the implant is Implant site preparation for the one-stage approach is identi-
exposed (per gingival) from the time of implant placement cal in principle to the two-stage implant surgical approach.
(Fig. 58.9). In the standard (classic) implant protocol, the im- The primary difference is that the coronal aspect of the im-
plants are left unloaded and undisturbed for a period simi- plant or the healing abutment (two-stage implant) is placed
lar to that for implants placed in the two-stage approach (ie, approximately 2-3 mm above the bone crest and the soft tis-
in areas with dense cortical bone and good initial implant sues are approximated around the implant/implant abutment.
Flap Closure and Suturing prevent alveolar ridge deficiencies for the optimal placement
of dental implants.
The keratinized edges of the flap are sutured with single inter-
rupted sutures around the implant. Depending on the clini-
cian's preference, the wound may be sutured with resorbable Guided Bone Regeneration
or nonresorbable sutures. When keratinized tissue is abun- Much of what can be achieved with implant surgery and spe-
dant, scalloping around the implant(s) provides better flap cifically with bone augmentation procedures is directly related
adaptation. to the achievements and understanding of guided bone regen-
eration (GBR). Historically, augmentation or "regeneration" of
Postoperative Care alveolar bone that was lost following tooth removal, or from
alveolar bone resorption or traumatic injury, presented a sig-
The postoperative care for one-stage surgical approach is simi- nificant challenge for clinicians. Allowed to heal without the
lar to that for the two-stage surgical approach except that the intervention of regenerative procedures, extraction site defects
cover screw or healing abutment is exposed to the oral cav- (especially those lacking a self-supporting bone structure)
ity. Patients are advised to avoid chewing in the area of the heal with fibrous connective tissue or scar formation and often
implant(s). Prosthetic appliances should not be used if direct did not fill completely with bone. The surrounding soft tis-
chewing forces can be transmitted to the implant, particularly sues collapsed into the bone defect, leaving an alveolar ridge
in the early healing period (first 4-8 weeks). When removable deficiency with respect to the natural tooth position and jaw
prosthetic appliances are used, they should be adequately reshape. Over time, the alveolar ridge continued to resorb, espe-
lieved and a soft-tissue liner should be applied. cially when removable prosthetic appliances are used.
Periodontal studies during the past several decades have
Conclusions led to new techniques and a new treatment approach referred
to as guided tissue regeneration (GTR). In brief, this concept
It is essential to understand and follow basic guidelines to
is based on the principle that specific cells contribute to the
predictably achieve osseointegration. Fundamental protocols
formation of specific tissues. Exclusion of the faster-growing
must be followed for implant placement (stage one) and im-
epithelium and connective tissue from a periodontal wound
plant exposure surgery (stage two). These fundamentals apply
for a minimum of 6-8 weeks allows the slower-growing tis-
to all implant systems.
sues to occupy the space adjacent to the tooth. Osteoblasts,
cementoblasts, and periodontal ligament cells then afforded
Localized Bone Augmentation and the opportunity to regenerate a new periodontal attachment
Implant Site Development (defined by new bone and new connective tissue fibers insert-
ed into newly formed cementum) on the previously diseased
One of the most critical aspects of creating anesthetic implant root surface. Chapter 48 includes a discussion on the concepts
restoration is surgical placement of the implant in a "pros- of GTR as related to periodontal regeneration.
thetically driven" position to restore the tooth in a natural The same basic principle of GTR has been applied to al-
position and to emulate the natural emergence of the tooth veolar bone defects to regenerate new bone. Using a canine
from the soft tissues. Implants placed without regard for pros- model, Schenk et al demonstrated with histology that bone
thetic position often lead to dental restorations that are func- regeneration in membrane-protected defects healed in a se-
tionally and esthetically compromised, and patients are left quence of steps that simulated bone formation after tooth
with a less-than-optimal reconstruction. Placement of dental extraction. They found that after blood clot formation, bone
implant(s) in an esthetically and functionally optimal position regeneration was initiated by the formation of woven bone
requires reconstruction of deficient alveolar ridges (or preser- initially along new blood vasculature at the periphery of the
vation of ridges when teeth are to be extracted). defect. The new vascular supply emanated from the existing
Periodontal bone loss, gingival recession, tooth loss, and bone bed (recipient site). Cortical perforations surgically cre-
long-term use of removable appliances typically result in al- ated in the recipient site are thought to enhance the blood
veolar defects that prevent the placement of implants in an supply and cellular access to the bone grafted area. The woven
optimal prosthetic position. It also leads to soft-tissue defi- bone, which is formed quickly with a disorganized, immature
ciencies that are unacceptable. Fortunately, continuous inno- structure, was subsequently replaced by lamellar bone with
vations in surgical techniques and advances in the biologic an organized, mature structure. Over time, bone remodeling
understanding of bone-regenerative techniques have led to continued with new, secondary osteons being formed.
advanced implant procedures and an increased predictability This concept employed the same principles of specific tis-
in the reconstruction of alveolar ridge defects. sue exclusion but was not associated with teeth. Rather, it was
Standard implant placement surgery, as described in this bone that was being isolated from the surrounding soft tis-
chapter, is based on adequate bone volume and quality in the sues. Thus the term applied to this technique was GBR. Since
desired implant location. The time-tested standard protocol the objective of GBR is to regenerate a single tissue, namely
allows for adequate remodeling and maturation of bone, with bone, it is theoretically easier to accomplish than GTR, which
healing periods of 3-6 months. Recent implant procedures strives to regenerate multiple tissues simultaneously in a com-
often challenge these original conventions by placing implants plex relationship.
in areas with inadequate bone volume, simultaneous with Interestingly, long before the current concepts of GBR were
bone augmentation, and restoring or loading implants after introduced, Murray and coworkers demonstrated that when
shorter healing periods. This chapter presents an overview of a cavity with a source of osteoblasts and a blood supply was
surgical bone augmentation procedures used to correct or to isolated from adjacent soft tissues, it could fill with bone,
TABLE 58.1 some bone along the entire vertical length. Dehiscence defects
can usually be managed during implant placement because
BIOLOGIC REQUIREMENTS FOR BONE most of the implant is covered and stabilized by native bone.
REGENERATION If the horizontal deficiency is large and the implant placement
would result in significant exposure (ie, implant body is sig-
Requirement Surgical procedure
Blood supply Cortical perforations
nificantly outside the alveolar bone), it may be better to recon-
Stabilization Fixation screws, membrane tacks struct the bone first, in a staged approach, with a subsequent
Osteoblasts Autogenous bone (graft or recipient site) surgery for implant placement.
Confined space Barrier membrane Although reconstruction of deficient ridges with bone
Space maintenance Tenting screws, bone graft materials grafts alone (ie, without barrier membrane) has proved to
Wound coverage Flap management, tension-free suturing be effective, variable resorption of the grafted bone has been
reported. Preliminary results in a 1- to 3-year study using au-
tografts harvested from the maxillary tuberosity showed an in-
whereas if the space were not protected, it would fill with fi- creased ridge width, but resorption of 50% of the graft volume
brous connective tissue. In addition to this observation, they was also noted. Buser et al investigated the lateral ridge aug-
suggested that a bone graft placed in the space might interfere mentation procedure using an autograft from the retromolar
with bone formation because the graft would need to be re- or symphysis area covered by a membrane in 40 consecutively
sorbed before bone could occupy the space. treated patients and noted no clinical signs of resorption of
Bone is a unique tissue that has the capacity to regener- the block graft. The researchers emphasized a remote inci-
ate itself completely Due to its rigid calcified structure, how- sion technique, perforation of the cortex, stable placement
ever, bone has specific requirements that must be respected to of corticocancellous autografts, precise adaptation and stabi-
achieve regeneration. Since the calcified structure of bone is lization (with miniscrews) of the ePTFE membranes, and a
not conducive to perfusion, new bone formation is critically tension-free primary soft tissue closure. After 7-13 months,
dependent on establishing an adequate blood supply through the sites were reopened for membrane removal and implant
the ingrowth of new vasculature while maintaining rigid fixa- placement. Of the 40 patients, 38 exhibited excellent ridge
tion or stabilization for bone formation. Any movement of the augmentation, whereas 2 sites showed some soft tissue encap-
segments of bone relative to one another (even micromotion) sulation of the grafted bone.
during healing results in disruption of the blood supply and a Nevins and Mellonig and Doblin et al reported an increased
change in the type of tissue formed in the site from mineral- amount of new bone using freeze-dried bone allografts (FD-
ized bone to fibrous connective tissue. Table 58.1 lists the bio- BAs) with membranes, even in the presence of membrane
logic requirements for bone regeneration and the associated exposure. The biopsies showed viable bone cells and visible
component of GBR surgical procedures needed to accomplish osteocytes in lacunae, and a 9-month specimen showed no
bone regeneration. remaining allograft material.
On the other hand, there are some contradictory results
Localized Ridge Augmentation using DFDBA and membrane combinations. In a human
study, seven paired extraction sockets were grafted with ei-
Patients often present for implant planning after tooth loss and ther DFDBA or autologous bone. Sites were reentered and
alveolar ridge resorption. In these cases, the clinician is obli- biopsied after 3-13 months to evaluate bone formation. His-
gated to perform augmentation procedures to reconstruct lost tologic specimens revealed dead particles of DFDBA with no
bone and place implants in a prosthetically driven position. evidence of bone formation on the surface and no evidence of
Surgical reconstructive procedures for the preparation and osteoclastic resorption. Conversely, the autogenous sites re-
placement of dental implants have become more numerous vealed vascular channels with woven and lamellar bone. Some
and complex. Depending on the size and morphology of the nonvital, cortical bone chips were observed with osteoclastic
defect, various augmentation procedures can be used. These resorption.
procedures have been categorized according to the deficient Figure 58.10 shows an example of the lack of bone forma-
dimension: horizontal or vertical. Methods used to augment tion around DFDBA particles used in a ridge augmentation
horizontal, as well as vertical, bone deficiencies include par- procedure after more than 20 months of healing under a non-
ticulate bone grafts and monocortical block grafts. Barrier resorbable ePTFE barrier membrane.
membranes can be used with bone grafts to reconstruct all
types of alveolar bone defects. See further in this chapter for
Simultaneous Implant Placement
a review of procedures used to achieve vertical augmentation.
All the proven principles of GBR and flap management must Large alveolar bone defects need to be augmented before im-
be followed to achieve good results. These include an ade- plant placement and require a healing period of 6 months
quate blood supply; maintaining a stable, protected space for or longer. In selected cases, it is possible to perform a bone
bone growth; and achieving tension-free flap wound closure. augmentation procedure simultaneously with the implant
placement. It is essential to achieve good implant stability in
Horizontal Bone Augmentation the existing native bone so that endosseous integration can
occur.
A deficiency in the horizontal dimension of bone may be A very predictable osseous defect to manage with simul-
minimal, such as a dehiscence or fenestration of an implant taneous implant placement is the implant dehiscence or
surface, or it may be more significant, such that the implant fenestration defect. Fenestration defects are exposures of the
would have more than one axial surface exposed while having implants axial surface that do not include the coronal aspect
58 Surgical Concepts of Implant Therapy 707 .el
Barrier Membranes degradation process may produce varying degrees of inflam-

mation. Recent developments include cross-linking of colla-
Barrier membranes are biologically inert materials that serve gen to increase resistance to biodegradation and thus increase
to protect the blood clot and prevent soft-tissue cells (epithe- longevity of the barrier function. Fortunately, the mild inflam-
lium and connective tissue) from migrating into the bone de- matory reaction caused by bioresorbable membranes does not
fect, allowing osteogenic cells to be established. Membranes seem to interfere with osteogenesis. Another disadvantage is
have been manufactured from biocompatible materials that that resorbable barrier membranes are quite pliable. The lack
are either nonresorbable and resorbable. The ideal proper- of stiffness often results in collapse of the membrane into the
ties of a barrier membrane are (1) biocompatibility, (2) space defect area. Thus resorbable membranes are best suited for
maintenance, (3) cell occlusiveness, ( 4) good handling prop- situations that allow the graft material or hardware (tenting
erties, and (5) resorbability or ease of removal (nonresorb- screws, plates) or the adjacent alveolar bone to maintain the
able). Advantages and disadvantages of the resorbable versus desired dimensions.
nonresorbable membranes are outlined next. Human histology has demonstrated that resorbable barrier
membranes support the growth of new bone when used in
Nonresorbable Barrier Membranes
GBR procedures for horizontal, vertical, sinus, and extraction
Various nonresorbable materials have been used as barrier socket defects. They have also been shown to reduce bone
membranes, including latex and Teflon. Teflon, an expanded resorption when used over a monocortical bone block to aug-
polytetrafluoroethylene membrane (ePTFE, Gore-Tex Peri- ment horizontally deficient ridges. Geurs et al demonstrated
odontal and Bone Regenerative Membranes, Gore and Asso- that a bioabsorbable barrier membrane, used in a GBR proce-
ciates, Flagstaff, AZ), has been used extensively as a barrier dure along with an allograft, was able to facilitate new bone
membrane in both GTR and GBR procedures. A variety of formation. At present, it can be stated that biodegradable
shapes and sizes have been designed to be custom-fit around membranes have the potential to support bone formation if
teeth and osseous defects. These barrier membranes are non- they are supported by bone graft material to resist collapse and
resorbable and thus require a subsequent surgical procedure if they are long-lasting enough to maintain their barrier func-
to remove them. The advantage of a nonresorbable barrier tion for extended periods in small to moderate bone defects.
membrane is its ability to maintain separation of tissues over
an extended time. Unless the barrier is exposed, it can remain
in place for several months to years. Typically, GBR mem- Bone Graft Materials
branes are removed after 6-12 months. Unlike other tissues, bone has the unique capacity to com-
The disadvantage of a nonresorbable barrier membrane is pletely regenerate itself. The major limiting factors are main-
that if it becomes exposed, it will not heal (ie, wound will tenance of space and structure for bone formation. Bone graft
remain open) spontaneously and may become progressively materials have been used to facilitate bone formation within a
more exposed. Exposed membranes become contaminated given space by occupying that space and allowing the subse-
with oral bacteria, which may lead to infection of the site and quent bone growth (and graft replacement) to take place on
result in bone loss. Therefore, exposed membranes must be the structure. The biologic mechanisms that support the use
removed. Contamination or early removal may also result in of bone graft materials are osteoconduction, osteoinduction,
less bone regeneration. and osteogenesis.
Space can be maintained under a barrier membrane with Osteoconduction is the formation of bone by osteoblasts
bone graft material or tenting screws, thereby facilitating the from the margins of the defect on the bone graft material. Ma-
regeneration of increased bone volume. Stiffer or titanium-re- terials that are osteoconductive serve as a scaffold for bone
inforced (TR) membranes (Gore and Associates, Flagstaff, AZ) growth. They neither inhibit nor induce bone formation. They
with space-maintaining capabilities can regenerate bone without simply allow the normal formation of bone by osteoblasts into
the need for bone grafts or tenting apparatus. Stiffer membranes the grafted defect along the surface of the graft material. Os-
are able to promote significant amounts of new bone and main- teoconductive bone graft materials facilitate bone formation
tain sufficient space without the addition of supportive devices. by bridging the gap between the existing bone and a distant
Ridge augmentation can be enhanced with a TR membrane in location that otherwise would not be occupied by bone.
conjunction with implant placement in localized bone defects. Osteoinduction involves new bone formation through
stimulation of osteoprogenitors from the defect (or from the
Resorbable Barrier Membranes vasculature) to differentiate into osteoblasts and begin form-
The use of resorbable membranes continues to attract wide- ing new bone. This induction of the bone-forming process
spread interest primarily because it eliminates the need for an by cells that would otherwise remain inactive occurs through
additional surgery to be removed. Copolymers of polylactide cell mediators that "turn on" these bone-forming cells. The
and polyglycolide have been used to construct biodegrad- most widely studied of these mediators is the family of bone
able membranes. Today, collagen-based resorbable barrier morphogenic proteins (BMPs). See further in this chapter for
membranes are used extensively. The primary advantage of a review of BMP use in bone augmentation.
a resorbable membrane is the elimination of surgical reentry Osteogenesis occurs when living osteoblasts are part of
for membrane removal. In the case of a subsequent implant the bone graft, as in autogenous bone transplantation. Given
placement procedure (or exposure surgery), this may not be an adequate blood supply and cellular viability, these trans-
a significant advantage. The other advantage is that resorb- planted osteoblasts form new centers of ossification within the
able membranes are less likely to become exposed and are less graft. Thus, in addition to the bone formation from osteoblasts
problematic if they do become exposed. that already exist in the defect, osteoblasts added as part of the
A possible disadvantage is that many resorbable mem- bone graft also form ossification centers and contribute to the
branes degrade before bone formation is completed, and the total capacity for bone formation.
TABLE 58.2 called osteons with a central blood supply. The dimension of
these cones (100-µm radius) is determined by the distance
BIOLOGIC PROPERTIES OF VARIOUS BONE that the central vasculature supply can provide nutrients to
GRAFT MATERIALS cells at the edges of the osteon.
Source Osteoconductive Osteoinductive Osteogenic
Alloplast Yes No No
Autogenous Bone
Xenograft Yes No No Compared with other bone graft materials, autogenous bone
Allograft Yes Yes/No7 No is thought to be the best bone graft material because, in addi-
Autograft Yes Yes Yes
tion to being osteoconductive, it is osteoinductive and osteo-
genic. Furthermore, barring contamination, there is no risk
of rejection or adverse reaction to the autogenous graft mate-
TABLE 58.3
rial. Intraoral sources of autogenous bone include edentulous
ROOT EXTRACTION SURGICAL CLASSIFICATION spaces, maxillary tuberosity, mandibular ramus, mandibular
BY TOMASO VERCELLOTTI symphysis, and extraction sites. Bone harvested from a recent
extraction site (eg, approximately 6-12 weeks healing) may
Periodontal Alveolar Surgery have the advantage of increased osteogenic activity compared
Biotype Ligament Difficulty Technique with other sites, which are more static and undergoing little
Type 1 Normal Normal Easy Standard or no osteogenesis. The maxillary tuberosity provides a more
Type 2 Thin Normal Medium Advanced' cellular source of autogenous bone compared with other sites.
Type 3 Normal Ankylotic Complex Advanced" However, the trabecular nature of this site provides a lesser
Type 4 Thin Ankylotic Severe Advanced' quantity of mineralized matrix, and the resultant total volume
'Advanced technique involves cutting root into fractions, internal luxation, of bone available for grafting is often inadequate. For greater
and removal. amounts of bone, it is more desirable to harvest bone from the
"Advanced technique involves roor-plasry to reduce size, internal luxation, mandibular ramus or symphysis. This bone, which is typically
and removal.
'Advanced technique involves root-plasry, cutting root into buccal slice frac-
more cortical, can be harvested and used as a monocortical
tions, internal luxation, and removal. block graft or it can be ground or shaved into small fragments
and used as a particulate graft.
Although the mandibular ramus and symphysis offer good
Numerous bone graft materials have been used to aid in sources of bone for grafting, clinicians are sometimes reluctant
the reconstruction of bone defects. These range from allografts to harvest bone from these sites because of an increased risk of
(derived from the same species) to xenografts (derived from a morbidity from the surgical procedure. Risks of surgery in the
different species) and alloplast or synthetic graft materials. At mandibular symphysis region include postoperative bleeding,
a minimum, bone graft materials should be osteoconductive. bruising, wound dehiscence, damage to lower incisors, disfig-
Bone graft materials that are also osteoinductive are believed urement, and injury to nerves. Nerve injury may be the most
to be more advantageous than those that are only osteocon- significant concern because it can be a long-term (possibly
ductive. Table 58.2 lists the properties of different classes of permanent), annoying alteration in sensation of the lower lip,
bone graft materials (Table 58.3) chin, anterior teeth, and gingiva for the patient. A more se-
Demineralized freeze-dried bone allograft (DFDBA) is rious risk is the alteration of facial appearance, particularly
thought to have osteoinductive effects because viable BMPs when the facial muscles are completely elevated from the bone
within the donor tissue matrix are exposed by the decalcifica- beyond the inferior border of the mandible. A condition re-
tion process. In contrast to this view, more recent reports sug- ferred to as "witch's chin" can occur when the facial muscles
gest that bone augmentation with DFDBA is not osteoinduc- and overlying skin of the chin fall, causing a disfiguring sag of
tive because it does not contain the BMPs necessary to induce facial tissues after surgery.
bone formation. Schwartz et al reported that variations in the A retrospective analysis of 48 chin graft-harvesting pro-
amount of bone formation induced by BMPs in DFDBA may cedures, suggests that maintaining a 5-mm margin of safety
be related to the source (ie, donor tissue) of the bone and the between graft harvest sites and vital structures (eg, lower inci-
techniques used to process it. In addition to processing varia- sors, the inferior border of the chin, and the mental foramen)
tions, it has been demonstrated that young donor bone results will minimize postoperative complications. In the 48 proce-
in significantly greater quantities of BMPs retained in the bone dures, postoperative sequelae included bruising of the lower
allograft matrix compared with older donor bone. Therefore, face (48/48), bruising of the upper neck (6/48), and pares-
the source of donor bone can greatly influence its osteoinduc- thesia of the lower lip and incisors (6/48). No patient experi-
tive capacity. enced facial disfigurement or muscle prolapse (chin droop).
Bone graft materials help maintain space under a barrier Three of the six patients with paresthesia experienced tran-
membrane to facilitate the formation of bone within a con- sient symptoms and recovered completely within 2 months,
fined space. Perhaps more importantly, bone graft materials whereas symptoms persisted longer than 6 months in the
should facilitate neovascularization and the migration of os- other three patients. Not surprisingly, the larger harvest de-
teoprogenitors. Since the size of the bone graft particles defects (trephined six-ring sites) resulted in a higher incidence of
termines the resultant space available (between particles) for paresthesia, which was longer lasting than that of the smaller
osseous formation, particle size has been carefully selected ac- defects (trephined four-ring sites). Harvesting bone in a cus-
cording to this concept. The typical size of bone graft particles tom-shaped "block" did not result in paresthesia, presumably
ranges from 100 to 1000 µm, which is conducive to neovas- because these harvest sites were smaller than the four-ring and
cularization and the ingrowth of bone. Bone forms in cones six-ring trephine-harvested sites.
58 Surgical Concepts of Implant Therapy 707.e3
Observation of the following basic principles can minimize the mental foramen. Do not extend cuts or harvest bone
the risk of postoperative morbidity: deeper than 6 mm, and do not include both labial and
lingual cortical plates.
1. Carefully evaluate the harvest site for potential risks. A
5. Suture the wound in layers (muscle and overlying mucosa
critical radiographic evaluation before surgery can identify
separately) to prevent postoperative wound separation.
individuals with inferior alveolar nerve branches that ex-
tend anterior beyond the mental foramen. When harvesting autogenous bone, regardless of site or
2. Use extreme care in making incisions laterally toward the method used, it is important to use techniques that prevent
mental nerve, and dissect the area with blunt instruments overheating and maintain viability of the bone cells. Exceeding
to locate the foramen. 4 7° C (116.6°F) is known to cause bone necrosis. Thus the use
3. Do not elevate and reflect muscle attachments beyond the of drills, trephines, or saws to cut bone should always be done
inferior border of the mandible. with profuse irrigation to keep instruments and bone cooled.
4. Limit bone cuts to an area at least 5 mm away from the Precision of osseous cuts can be facilitated with new technolo-
tooth apices, the inferior border of the mandible, and gies such as piezoelectric bone surgery.
Flap Management General concepts for flap management associated with

ridge augmentation include the following:
Soft-tissue management is a critical aspect of bone augmen-
tation procedures. Incisions, reflection, and manipulation 1. It is desirable to make incisions remote relative to the
should be designed to optimize blood supply and wound placement of barrier membranes (eg, vertical releasing in-
closure. The design and management of mucoperiosteal flaps cisions at least one tooth away from the site to be grafted).
must consider the increased dimensions of the ridge after In the anterior maxilla, keeping vertical incisions remote is
augmentation as well as esthetics and approximation of the also an esthetic advantage.
wound margins. The surgical procedure must be executed 2. Full mucoperiosteal flap elevation at least 5 mm beyond
with the utmost of care in order to preserve the vascularity of the edge of the bone defect is desirable.
the flap and to minimize tissue injury. 3. The use of vertical incisions, although often required for
Several flap techniques maintain a "submerged" position of surgical access, should be minimized.
bone grafts and barrier membranes during the entire healing 4. Use of a periosteal releasing incision to give the flap elas-
process, including a remote or displaced incision. The advan- ticity and permit tension-free suturing is essential. This
tage of a remote incision is that the wound opening is posi- permits complete closure without stress on the wound
tioned away from the graft. A conventional crestal incision can margins.
be used, even in large supracrestal defects, as long as a periosteal 5. Removable appliance should not be inserted over the
releasing incision and coronal advancement of the flap achieve wound for 2 weeks or more to avoid postoperative trauma
a tension-free closure. Most reports suggest removing sutures to the surgical site.
approximately 10-14 days after surgery. It is also suggested that 6. Wound closure should incorporate a combination of mat-
no prosthesis be inserted for 2-3 weeks after surgery to avoid tress sutures to approximate connective tissues and inter-
pressure over the wound during the early healing phase. rupted sutures to adapt wound edges.
Particulate Bone Graft environment that is stable and supports new bone formation.
Advantages of particulate bone grafts (or bone chips) are that Figure 58.12 depicts the use of a barrier membrane in com-
the smaller pieces of bone demonstrate more rapid ingrowth bination with a particulate bone graft to treat a mandibular
of blood vessels (revascularization), larger osteoconduction horizontal defect.
surface, more exposure of osteoinductive growth factors, and
easier biologic remodeling compared with a bone block for re- Monocortical Block Graft
construction of large defects. However, particulate grafts often Horizontal alveolar deficiencies that might be challenging to
lack a rigid, supportive structure and are much more easily reconstruct with particulate grafts can easily be reconstructed
displaced than block grafts. with a monocortical block bone graft. The technique uses a
Autologous particulated bone grafts can be harvested cortical block of bone harvested from a remote site and used
from any edentulous jaw site, either in smaller "particle" to increase the width of bone. The block graft taken from an
or in a larger "block" of bone. If the bone has been harvest- intraoral (eg, mandibular symphysis or ramus) or extraoral
ed in a block, a bone mill is necessary to "particulate" the (eg, iliac crest or tibia) site is fixated to the prepared recipient
bone and prepare it for transplantation into the bone defect site with screws. The overlying soft tissues can be separated
(Fig. 58 11) from the bone graft with a barrier membrane or simply cov-
Particulate grafts are indicated (1) in defects with multiple ered with the mucoperiosteal flap. Fixation hardware (screws
osseous walls that will contain the graft or (2) in dehiscence or and plates) should be removed after an adequate period of
fenestration defects when implants are placed during the bone healing (approximately 6 months). The disadvantage of this
augmentation procedure. If a bone defect does not have suffi- technique is the biologic limitation of revascularizing large
cient osseous walls to contain the graft, the barrier membrane bone blocks. It therefore is crucial to have sufficient osteo-
(placed in contact with the native bone) should be secured genic cells in the residual surface of the surrounding bone and
along the periphery with tacks, screws, or sutures. This bone to limit this technique to horizontal augmentation and only
graft and secured barrier membrane combination becomes an minimal vertical defects.
FIGURE 58.11 A, R. Quetin bone mill (assembled). B, R. Quetin bone mill (disassembled). C, Ground bone observed in blades of bone mill. D,
Autogenous block bone ground into evenly sized particulate bone with bone mill suitable for bone grafting
Figure 58.13 shows the use of a monocortical block graft to The autogenous monocortical block graft was harvested from
reconstruct a horizontal deficiency in the posterior right man- the mandibular symphysis. It was cut to an appropriate size and
dible. The patient presented with a loss of the buccal cortical mortised to intimately fit the recipient defect site. Once properly
plate of bone after a traumatic extraction of endodontically positioned, the graft was fixated with two fixation screws (Leib-
treated tooth #29. The surgical extraction also resulted in a inger, Kalamazoo, MI) that passed through the graft and into
nonrestorable cut into the mesial root of tooth #30. Recom- the existing native alveolar bone. A periosteal releasing incision
mended treatment included extraction of tooth #30, mono- was used to sever the periosteum from anterior to posterior and
cortical block graft reconstruction of the buccal defect at site facilitate coronal advancement of the mucogingival flap.
#2 9, and bone augmentation of the extraction socket #30. The After 6 months of healing, a full-thickness mucoperiosteal
procedure for this case follows. flap was elevated to expose the alveolar bone sites #29 and
30. Mild resorption of the monocortical block graft is evident.
Procedure. After local anesthesia, an incision was made in Notice that the position of the head of the fixation screws (es-
keratinized tissue along the crest and around the molar tooth pecially the posterior screw) is more protruded than the graft-
(#30) with a vertical releasing incision mesial to the first bi- ed bone as a consequence of bone remodeling and resorption
cuspid (#28). A full-thickness flap was elevated to expose the (Fig. 58.13, Hand I).
alveolar bone (Fig. 58.13, D). All soft tissues were thoroughly The fixation screws are removed, and the sites are prepared
removed from the recipient site before bone grafting. After in the usual manner for the placement of two screw-type,
simple forceps delivery of tooth #30, the defect to be grafted wide-diameter implants (Implant Innovations, Palm Beach
was measured to determine the size of block graft to harvest Gardens, FL). Care is taken to avoid preparing the grafted site
from the mandibular symphysis. Several bleeding points were too wide or too far labially because the grafted bone may be
created using a small round bur. vulnerable to fracture or additional resorption (Fig. 58.13, J).
58 Surgical Concepts of Implant Therapy 707.eS
FIGURE 58.12 Horizontal bone augmentation with expanded polytetrafluoroethylene (ePTFE) barrier membrane. Bone graft consists of a mix-
ture of autogenous particles harvested from the alveolar ridge and Bio-Oss (Osteohealth Company, Luipold Pharmaceuticals, Inc., Shirley, NY). A,
Partially edentulous posterior mandible with narrow buccolingual dimensions. B, Cortical perforations made in buccal bone with small round bur
to enhance blood supply to grafted area. C, Placement of ePTFE barrier membrane and mixture of autogenous and Bio-Oss particulate bone graft.
D, View of "C" from occlusal perspective to visualize horizontal augmentation. E, Barrier membrane secured to native bone with fixation screws. F,
Clinical photograph of healed site prior to membrane removal. Soft-tissue closure maintained throughout healing without membrane exposure. G,
Clinical photograph of healed ridge after membrane removal. Dimensions of alveolar ridge are significantly wider as demonstrated with periodontal
probe. H, Two standard-diameter implants placed in "prosthetically driven" ideal position. Notice there are no implant exposures. (Images courtesy
Dr Istvan A. Urban, Budapest, Hungary.)
FIGURE 58.13 Use of a monocortical block graft to reconstruct a horizontal deficiency in the posterior right mandible. A, Periapical radiograph
shows missing tooth #29 and damaged (ie, cut) mesial root #30. Band C, Labial and occlusal views, respectively, of site reveal deficient alveolar ridge
on buccal side of #29. D, Full-thickness flap reflection reveals the extent of missing bone in the buccal aspect of site #29, as well as the periodontal de-
fect and damaged mesial root #30. E and F, Autogenous monocortical bone block graft secured to native alveolar bone with fixation screws. G, Good
tissue healing after block graft, with evidence of a widened alveolar ridge. H, After 6 months of healing, posterior fixation screw is observed protruding
through the mucosa. 1, Full-thickness flap reveals that bone resorption has resulted in exposure of part of the fixation screw. J, Osteotomy prepared for
wide-diameter implants, taking care to avoid making the labial bone "graft" too thin. K, Complete closure and good healing of wound after implant
placement.Land M, Clinical photographs of completed restorations. N, Final radiograph shows good restoration contours on wide-diameter implants.
FIGURE 58.10 A, Clinical view of maxillary alveolar ridge after removal of a failed implant (center defect) and placement of two implants in the bone
adjacent to this site. B, The narrow ridge was grafted with decalcified freeze-dried bone allograft (DFDBA) particulate bone graft material. The graft
material was completely covered by a nonresorbable, expanded polytetrafluoroethylene (ePTFE) barrier membrane. C, The ePTFE barrier membrane
was secured with the cover screw of one implant and sutures that were secured to the periosteum. D, Clinical view of DFDBA-augmented ridge after
more than 20 months healing under a nonresorbable ePTFE barrier membrane. The membrane remained submerged throughout the entire healing
period. E, Hematoxylin-eosin (H&E) light microscopic view of specimen harvested from the DFDBA-augmented ridge. Note there are no bone cells
(osteoblasts, osteoclasts, or osteocytes), no bone formation, and no osteoclastic resorption of DFDBA particles. There is no evidence of inflammation.
Fibroblasts and connective tissue surround the "dead" DFDBA particles. F, Polarized light microscopic view of the same specimen (E) harvested from
the DFDBA-augmented ridge. Note the appearance of lamellar layers demonstrating the presence of the DFDBA particles.
of the implant (Fig. 58.14). Dehiscence defects expose a part coverage of exposed implant surfaces in humans demonstrat-
of the axial surface, including the coronal aspect of the im- ed that the membrane treatment was far superior with regard
plant, while maintaining sufficient bone volume around all to bone fill. Another controlled study in humans showed bet-
remaining implant surfaces (Fig. 58.15). In a dehiscence deter results in the membrane groups; four of six sites (67%)
fect the implant remains within the confines of the existing treated with a membrane resulted in 95-100% elimination
bone. of the dehiscence and total coverage of the threads. In the
Fenestration and dehiscence defects have been managed control sites, only two of six sites (33%) showed moderate-
with barrier membranes or simply with flap closure. Bone to-complete bone fill. All other clinical studies are in the form
grafts have also been used. The only controlled comparison of case reports. Figure 58.16, M, demonstrates coverage of
studies between membrane treatment and periosteal flap an implant dehiscence using a barrier membrane. Admittedly,
healing found complete bone coverage over all implants. Ra-

diographic evaluation demonstrated the implants functioning
with normal crestal bone support after 1 year.
No clinical comparisons are available in the literature eval-
uating the placement of bone grafts with or without barrier
membranes on implant dehiscence defects. Most evidence
supports the use of graft materials in conjunction with mem-
brane treatment, especially the use of FDBA in conjunction
with GBR. In a study with 40 patients, 110 implants were
placed in conjunction with barrier membranes and FDBA; a
success rate of 96.8% was achieved with complete bone fill
(defined as >90% fill of dehiscence). This study reported a
membrane exposure rate of 29%, but noted little adverse ef-
fect on the bone regeneration.
FIGURE 58.14 Fenestration defect observed in very thin maxillary With respect to ridge preservation, Becker et al reported
anterior sites. Implants placed in the maxillary lateral incisor positions the effect of barrier membranes and autogenous bone grafts on
demonstrating fenestration defects caused by the concavities in the api- the preservation of ridge width around implants. They evalu-
cal area. Notice that the natural teeth (centrals and cuspids) also dem- ated the ridge width around 76 implants in 61 patients from a
onstrate fenestrations. Bone will grow across this type of defect in a very
predictable manner because the implants are stable; the defect is small
case series database. Three groups were compared, including
and surrounded by bone. 34 implants treated with GBR (barrier membranes), 27 im-
plants treated with autogenous bone grafts, and 15 implants
placed without the need for ridge preservation/augmentation
procedures (control group). The results revealed that implant
sites treated with barrier membranes and autogenous bone
grafts lost an average of 0.1 and 0.8 mm, respectively, more
than the no augmentation group.
Another study evaluated the possibility of regenerating
bone around implants placed in extraction sockets. Bone aug-
mentation was achieved with human DFDBA particles mixed
with tetracycline packed around the exposed implant surfaces.
Implants and graft material were covered with ePTFE barrier
membranes with complete flap closure for 4-6 months. The
results demonstrated complete bone regeneration in all cases
except when barrier membranes were prematurely exposed
and removed. One-year posttreatment histologic evaluation
of regenerated bone revealed remnants of the DFDBA graft
particles in direct contact with vital bone tissue (woven and
lamellar bone). Osteoblasts were observed and appeared to be
actively engaged in bone formation adjacent to graft particles.
FIGURE 58.15 Dehiscence defect observed during placement of an Figure 58.16, Land M, demonstrates a simultaneous GBR and
implant in the maxillary central incisor position. Note that the implant implant placement in a dehiscence defect.
is completely surrounded by existing native bone except for the facial
surface, which is exposed. Bone will grow across this type of defect in a
very predictable manner because the implant is stable and the exposed Complications
surface is relatively flat with bone on all surfaces.
Bone augmentation procedures used to increase the bone
volume in deficient alveolar ridges have been successful and
without a biopsy, it cannot be determined whether the tissue have enabled the placement of implants into prosthetically
covering the implant is bone or firm connective tissue. driven positions. Unfortunately, these augmentation proce-
A 1-year multicenter study evaluating 55 Branernark dures carry an increased risk of morbidity and can require
implants (ie, machined-surface, external hex) with bone de- secondary surgeries to correct problems resulting from the
hiscence in 45 patients, treated by ePTFE membrane alone, procedure. The subsequent corrective surgeries required to
demonstrated an average bone fill of 82 % . The average initial correct problems add surgical time and complexity to the im-
defect height was 4.7 mm. The 1-year follow-up of these implant therapy.
plants demonstrated a favorable response to loading. Of the Surgical complications are reported for a variety of bone
55 implants, a total of 6 failed, corresponding to a cumulative reconstructive techniques. A review assessed the number and
survival rate of 84.7% in the maxilla and 95.0% in the man- types of complications associated with bone reconstructive
dible, which is similar to previously published results for this procedures for endosseous implants. The review of literature
implant design. (1976-94) included 2315 implants in 733 autogenous blocks,
A clinical report on the use of TR membranes demonstrat- particulate, and various other bone graft materials. Compli-
ed the biologic potential to fill a large protected space in four cations reported included bleeding, postoperative infection,
patients. Bone dehiscence at implant sites ranged from 5 to bone fracture, nerve dysfunction, perforation of the mucosa,
12 mm (mean: 8.2 mm). They were covered with a TR mem- loss of a portion of the bone graft, pain, decubital ulcers, si-
brane alone (no graft). Reentry after 7-8 months of submerged nusitis, and wound dehiscence. Wound dehiscence seemed
FIGURE 58.16 Use of staged (A-H) and delayed (1-0) implant placement after extraction of two maxillary lateral incisors in one individual. A,
Preoperative photograph of tooth #7 with gingival recession and marginal inflammation. B, Atraumatic extraction or tooth #7 without tissue incision
or tissue elevation. Palpation reveals no facial bone present at the time of extraction. C, Decalcified freeze-dried bone allograft condensed into extrac-
tion site. D, Expanded polytetrafluoroethylene (ePTFE) barrier membrane positioned over graft and held in place with sutures. E, Six months after the
extraction/graft, the implant is placed. Notice the implant is completely covered with bone. F, Final restoration. G, Preoperative photograph of tooth
#10 with exposed gingival margin. H, Atraumatic extraction of tooth #10 without tissue incision or tissue elevation. Palpation reveals no facial bone
present, and deh iscence is expected.
to have the most deleterious effect on implant survival. This the regeneration varied between 42% and 62%. The authors
finding emphasizes the importance of flap management. concluded that the length of membrane healing and size of
Typical findings include less bone fill with early exposure the defect played a significant role in the amount of new bone
and membrane removal versus retaining the membrane with- formation.
out exposure for 6-8 months. Buccolingual ridge deficiencies Other authors have reported successful bone fill in situa-
were treated in a prospective study involving 19 patients using tions in which the membranes had to be removed because of
ePTFE membranes and miniscrews as fixation and tenting dean early exposure. A significantly greater fill of the osseous
vices. The group of defects, which healed uneventfully, yield- defects at the grafted sites was noted. The authors concluded
ed on reentry 90-100% bone regeneration compared with that the regeneration of bone around the implants appeared
the maximal volume of the space defined by the membrane most dependent on the anatomy of the bony defect at the time
placement. In the exposed-membrane group, the percentage of implant placement.
of regenerated bone ranged from 0-62%. When a late mem- Although the effect or amount of regenerated bone with
brane removal was performed (3-5 months postsurgically), regard to membrane exposure is somewhat contradictory,
FIGURE 58.16 (cont.) I, Two months after extraction, the implant is placed with dehiscence defect. J, Guided bone regeneration accomplished
with ePTFE barrier membrane positioned over the dehiscence. K, Final restoration. L, Periapical radiograph of tooth 117 with a large radiolucent le-
sion around the apex and periodontal bone loss along the distal interproximal area. M, Final radiograph of delayed implant placement. N, Periapical
radiograph of tooth 1110.0, Final radiograph. (Figs. A, B, C, F, C, /, M, N, and O from Klokkevold PR, Han TJ, Camargo PM.: Aesthetic management of
extractions for implant site development: delayed versus staged implant placement. Pract Periodontics Aesthet Dent 11 :603, 1999.)
the goal should be to keep the membranes covered during Conclusions

the healing period so that the risk of infection and soft tis-
sue and esthetic problems can be minimized or eliminated. Localized bone augmentation procedures allow clinicians
Again, the importance of flap management for ridge aug- to reconstruct horizontal alveolar ridge deficiencies and re-
mentation procedures should be stressed. See Chapter 59 for place missing teeth with dental implants in a prosthetically
more information and details regarding surgical complica- driven position with natural appearance and function. In
tions and failures. many cases, implants can be placed simultaneously with the
58 Surgical Concepts of Implant Therapy 711.el
Alveolar Ridge Preservation/ saline. Finally, the clinician can evaluate the bone level and
socket anatomy to determine whether to bone-graft the site
Management of Extractions and when to place the implant (immediate, delayed, or staged
Since tooth extraction (or tooth loss) often results in alveolar placement).
ridge resorption or collapse, preservation of bone volume at
the time of extraction is a desirable goal. Most bone loss after Delayed Implant Placement
extraction occurs in the first 6-24 months. Therefore, when
clinicians are afforded the opportunity to intervene at the time Delayed implant placement shares some advantages of im-
of extraction, preservation of alveolar bone should be initi- mediate implant placement, including extraction site pres-
ated. A conservative approach to the management of extrac- ervation, and offers additional advantages. Unlike immedi-
tion sites can eliminate or significantly reduce the necessity of ate implant placement, which is deficient of soft tissue for
advanced bone augmentation procedures. coverage, the delayed-implant placement technique allows
When extracting a tooth and preparing for implant place- time for soft-tissue healing to close the wound. The delayed-
ment, alveolar bone resorption should be prevented. Experi- placement technique still reduces the length of treatment by
mental animal studies show that the use of a barrier mem- several months because it is not necessary to wait for com-
brane enhances the predictability of bone fill in the extraction plete bone healing. Furthermore, because bone formation is
site and therefore maintains original bone volume when com- active within the first few months after tooth extraction, the
pared with mucoperiosteal flap coverage alone. Clinical stud- delayed technique may facilitate more osteogenesis adjacent
ies also demonstrate the benefits of a regenerative approach to the implant.
to tooth extraction. These authors found that a nonresorbable The primary advantage of delayed implant placement
barrier membrane results in minimal resorption of alveolar is that by allowing for soft-tissue healing and closure of the
ridge size and shape. extraction site, mucogingival flap advancement is not neces-
Although earlier studies have proposed the concept of sary. This alleviates the need for additional surgeries to correct
treating extraction sites without flap closure (ie, an exposed mucogingival discrepancies. Delayed implant placement also
membrane used to cover the graft), more recent studies con- allows time for resolution of infections that may have been
clude that complete wound closure over the physical barrier present within the extraction site.
might be associated with greater bone fill. The decision about As with immediate implant placement, similar limitations
whether to advance a flap to achieve wound closure must be of bone support and implant stability exist for delayed place-
weighed against the soft-tissue changes that will be created ment. The normal osseous healing that occurs within the first
and may need to be corrected (ie, mucogingival junction dis- 2 months does not significantly affect the anatomy of the
crepancies and esthetic problems). alveolar bone. Therefore, limitations in bone support after
The timing of implant placement relative to the time of ex- 2 months of healing are similar to those that exist at the time
traction has been widely debated. Depending on the quantity, of extraction.
quality, and support of existing bone, as well as the prefer-
ences of the clinician and patient, the placement of implants Staged Implant Placement
after tooth extraction can be immediate, delayed, or staged.
By definition, immediate implant placement occurs at the time Staged implant placement allows adequate time for osseous
of extraction. Delayed implant placement is performed ap- healing. This may be complete osseous healing of an extrac-
proximately 2 months after extraction to allow for soft tissue tion site without a bone graft (if circumferential bone support
healing. Staged implant placement allows for substantial bone is good) or with a bone graft. Staged implant placement, by
healing within the extraction site, which typically requires definition, allows for complete hard and soft-tissue healing
4-6 months or longer. and permits the placement of implants into healed bone sites
Tooth extraction is managed with an atraumatic surgical with adequate coverage by hard and soft tissues. This elimi-
technique that uses a narrow, flat instrument (eg, Periotome, nates the necessity of mucogingival flap advancement, allows
Hu-Friedy, Chicago) directed apically into the sulcus to sever for the resolution of preexisting infections, and prevents soft-
the periodontal ligament and slightly expand the adjacent tissue invasion. Furthermore, by using an extended healing
periodontal tissues. The tooth is elevated and removed with period, the grafted bone also has the opportunity to become
forceps using a gentle, rotational movement. Chapter 80 de- vascularized. Bone grafts performed simultaneously with im-
scribes new techniques for atraumatic extraction. Buccolin- plant placement do not share this advantage.
gual forces are avoided to prevent damaging the integrity of The primary disadvantage of staged implant placement is
the labial bone. No incisions are made, and care is taken to the length of time required for bone healing.
avoid soft-tissue reflection. In this manner, soft tissues main-
tain their structural anatomy, and the periosteum (blood sup-
Delayed Versus Staged Technique
ply to the bone) remains intact. If the tooth has multiple roots,
curved roots, or other anatomic features that make removal Delayed and staged techniques for implant placement are
difficult, it may be necessary to cut the tooth using a high- demonstrated here in one individual using two extraction
speed rotary drill or other cutting device and remove it in sites with similar bone morphologies in the anterior maxilla
smaller pieces. It is important to cut only tooth structure and (Fig. 58.16). Both techniques facilitate the esthetic placement
avoid cutting (overheating) bone when using high-speed roof implants into prosthetically driven positions. Delayed and
tary drills. The bone within the extraction site is completely staged approaches maintain alveolar bone volume, reduce
debrided of soft tissue with surgical curettes. After debride- the need for advanced bone augmentation, and eliminate the
ment, the extraction site is thoroughly irrigated with sterile need for subsequent mucogingival surgery. The timing and
management of delayed versus staged implant placement is soft-tissue invasion around the implant. A 1-year study of 49
described in the next section. immediate extraction site implants treated by a membrane
To decide which implant placement method to use, the alone demonstrated a 93.6% bone fill. After 1 year (postload-
quantity and location of bone surrounding the tooth should ing), the implant success rate was 93.9%.
be assessed. Once the patient has been anesthetized, a peri- Although some have advocated submerging implants
odontal probe can be used to "sound" for the level of bone placed in extraction sockets with flap advancement, others
support through the soft tissue. Using this method, the bone have demonstrated success with a nonsubmerged approach.
levels surrounding the tooth can be mapped. Bone support Implants may be placed in extraction sockets along with bone
that surrounds the extraction site can also be evaluated and augmentation without flap advancement using a one-stage
confirmed after tooth removal by palpation, probing, and di- implant placement approach. Clinical studies evaluating the
rect (internal) visualization. outcome of bone augmentation around implants placed in ex-
If the tooth to be extracted has sufficient bone support on traction sockets reveal good bone fill. The placement of 21
all surfaces, the extraction site can be expected to fill with transmucosal implants in immediate extraction sites treated
bone without additional augmentation procedures, except with a barrier membrane were tested for the implant success
when the labial bone is very thin. A simple extraction fol- rate and the percentage of bone fill. Of 21 transmucosal im-
lowed by a healing period of 4-6 months could be sufficient plants, 20 yielded complete bone fill and coverage of the en-
for complete osseous healing. Subsequently, an implant could tire plasma-coated implant surface.
be placed in the usual manner without the need for bone aug- A clinical report on the use of resorbable collagen mem-
mentation. Conversely, if little or no bone exists on the labial branes around extraction site implants demonstrated a vari-
surface, it should be anticipated that the site would require able degree of bone fill in nine patients. More clinical review
bone augmentation to facilitate placement of the implant. In of the use of resorbable membranes for GBR is required be-
this case, bone grafting at the time of extraction can be used cause evidence is insufficient to evaluate the predictability
to maintain the alveolar ridge dimensions occupied by the In a study of 30 patients, the use of autografts alone in 54
tooth. extraction sites was highly effective for simultaneously placed
implants completely within the envelope of bone. The study
showed that extraction sites, including those with a buccal
Immediate Implant Placement
dehiscence, could be treated with autografts alone. However,
The primary advantage of immediate implant placement is the because ungrafted sites were not included, the absolute need
reduction of the healing time, which translates to an earlier to graft small defects adjacent to implants was not ascertained
restorative time (ie, shorter time to completion for the pa- by this study. In another study, implants placed in extraction
tient). Since the implant is placed at the time of extraction, the sockets were tested for their potential to regenerate bone with
bone-to-implant healing begins immediately with extraction allograft alone, a membrane alone, and a combination treat-
site healing. Another advantage is that the normal bone heal- ment. Reentry confirmed 100% thread coverage in all but one
ing, which generally occurs within the extraction site, takes implant in the "no-wall" group treated with DFDBA alone.
effect around the implant. This bone-forming activity may en- A clinical study of five patients evaluated different treatment
hance the bone-to-implant contact compared with an implant modalities for extraction site implants together with bone
placed in a less osteogenically active site. graft combinations. This small study supported the concept
Possible disadvantages of immediate implant placement that "nonspace-making defects" are best treated with a com-
include the need for subsequent mucogingival surgeries to bination of barrier membrane and an autograft or allograft as
correct tissues moved by repositioned flaps and the need for compared to treatment with a nonreinforced membrane alone
bone grafting to fill extraction site defects around the implant. (without a graft).
If inadequate bone exists to stabilize the implant, immediate Immediate placement of an implant into the extraction
implant placement is not recommended. socket in a one-stage approach along with immediate provi-
When a two-stage implant is placed at the time of tooth sionalization is perhaps the best way to manage the hard and
extraction, the mucogingival flap is advanced, with releasing soft tissues following extraction (Fig. 58.17). The immediate
incisions, to cover the implant completely (exception: one- placement of a provisional restoration is the best way to sup-
stage implants). It may also be necessary to graft bone into the port the soft tissues (papilla and marginal gingiva) following
extraction site in areas that do not contact the implant to avoid tooth extraction.
FIGURE 58.17 Immediate implant placement after extraction of a maxillary first premolar. A, Preoperative clinical photograph of tooth #12, which
fractured and was deemed nonrestorable. B, Periapical radiograph of tooth 1112. It is root canal-treated and has a full-coverage porcelain-fused-to-
metal crown. C, Atraumatic extraction of tooth 1112 without incisions or tissue elevation. D, Extracted tooth. E, Palpation and examination with probe
reveals intact bony walls around the extraction socket. The facial bone wall is observed to be about 2 mm below the facial gingival margin. F, The
palatal aspect of the extraction socket is prepared, and a tapered implant is placed to emerge through the central fossa. Autogenous bone chips (har-
vested from the maxillary tuberosity) are condensed into the labial aspect of the extraction socket to support the facial bone and soft tissue contours.
G, An immediate provisional restoration is fabricated (indirectly in the laboratory) and delivered at the time of implant placement. The palatal cusp is
not replaced in this provisional to avoid function and the occlusion is checked for light centric contacts only. H, Facial view of provisional restoration
at the time of delivery. Notice how the interdental papilla and facial gingival margin is well supported by the contours of the provisional restoration. I,
Final restoration at time of delivery (approximately 4 months after implant placement). J, Final radiograph of definitive restoration.
augmentation procedure. In cases of advanced bone resorp- osteotomy and a variety of techniques to lift the sinus floor
tion, ridge augmentation before implant placement may be a from a crestal approach.
better choice. Bone augmentation procedures can also be used Various bone graft materials have been used to augment
to preserve alveolar dimensions following tooth extraction. If the maxillary sinus. The 1996 Consensus Conference on Max-
adequate bone exists to stabilize an implant, these procedures illary Sinus Bone Grafting reviewed available data and con-
may be combined. The predictable outcome of these proce- cluded that allografts, alloplasts, and xenografts, alone or in
dures depends on several biologic principles that must be fol- combination with autogenous bone, can be effective as bone
lowed. Diagnosis, treatment planning, careful execution of the substitute graft materials for sinus bone augmentation. More
surgical treatment, postoperative follow-up, and appropriate importantly, it was concluded that the sinus graft procedure
implant loading are all important factors in achieving success. with implant placement is a highly predictable and effec-
tive therapeutic modality for the rehabilitation of the poste-
rior maxilla. Sinus floor elevation with bone augmentation
Advanced Implant Surgical of the maxillary sinus is now a well-accepted procedure used
Procedures to increase bone volume in the posterior maxilla. Numerous
reports have validated the safety and efficacy of this proce-
The high predictability of endosseous dental implants has
dure. Implant success rates are equal to or better than that
led to routine use and an expectation for success. However,
of implants placed in nongrafted maxillary bone (ie, areas of
the ultimate success for any patient or any particular implant
the posterior maxilla with adequate height of existing native
relies on several factors, the most important of which is the
bone). Thus bone augmentation of the maxillary sinus is a
availability of bone. The loss of teeth, whether caused by dis-
viable option for the vertically deficient posterior maxilla in
ease or trauma, can result in severe deficiency of the alveolar
which the interocclusal dimension is normal or only moder-
bone. Horizontal bone deficiencies are managed quite predict-
ately increased.
ably with localized bone augmentation procedures. However,
vertical bone deficiencies are much more challenging. The
edentulous posterior maxilla is challenging as the result of a Indications and Contraindications
general lack of bone volume and the omnipresent poor bone
As with any therapeutic procedure, treatment success de-
quality of the area; that is, posterior maxillary bone often con-
pends on appropriate patient selection, careful evaluation of
sists of a thin cortical shell filled with sparse trabecular bone.
the anatomy, identification and management of any pathology,
Edentulous sites, in any anatomic location, that have suffered
sound surgical procedures, and appropriate postsurgical man-
significant vertical alveolar bone loss are especially challeng- agement. The primary indication for maxillary sinus elevation
ing to reconstruct.
and bone augmentation, specific for the placement of endos-
This chapter reviews advanced surgical procedures used
seous dental implants, is an alveolar bone height in the pos-
to treat the most challenging type of bone loss, which is a
terior maxilla that is deficient (eg, less than 7 mm of existing
deficiency in vertical bone height. Maxillary sinus elevation and
vertical bone height). Other factors that must be considered
bone augmentation, vertical bone augmentation, and distrac-
include the health of the patient, the condition of the remain-
tion osteogenesis are reviewed. The role of growth factors in ing dentition, and the likelihood of a beneficial outcome. A
bone augmentation procedures is also discussed.
thorough evaluation of the patient and the judgment of the
clinician ultimately determine whether the procedure is indi-
Maxillary Sinus Elevation and Bone cated for any particular individual.
Contraindications to maxillary sinus elevation and bone
Augmentation augmentation are similar to contraindications for other surgi-
Rehabilitation of the edentulous posterior maxilla with en- cal procedures, with the added consideration of the maxillary
dosseous dental implants often represents a clinical challenge sinus (Box 58.4). Patients must be in good general health and
because of insufficient bone volume resulting from pneumati- free of diseases that affect the maxilla or maxillary sinus. Local
zation of the maxillary sinus and resorption or loss of alveo-
lar crestal bone. Before the utilization of bone augmentation
procedures, patients with missing teeth and deficient bone in
the posterior maxilla could only be rehabilitated with remov-
able prostheses, short implants, or cantilevered restorations
LOCAL FACTORS
(ie, supported by adjacent teeth or implants). Historically, the
failure rate for implants in the posterior maxilla has been sig- 1. Tumors or pathologic growth in the sinus
2. Maxillary sinus infection
nificantly higher than failure rates for implants in all other
3. Severe chronic sinusitis
anatomic locations. Consequently, procedures such as the 4. Surgical scar/deformity of sinus cavity
maxillary sinus elevation and bone augmentation are needed 5. Dental infection involving or in proximity to sinus
to increase the amount of vertical bone height in the posterior 6. Severe allergic rhinitis/sinusitis
maxilla for the placement of implants. 7. Chronic topical steroid use
In 1980, Boyne and James first described a procedure to
SYSTEMIC FACTORS
graft the maxillary sinus floor with autogenous marrow and
1. Radiation therapy involving the maxillary sinus
bone for placing an implant (blade type). Access to the maxil-
2. Metabolic disease (eg, uncontrolled diabetes mellitus)
lary sinus was gained through a "Caldwell-Luc" procedure (ie , 3. Excessive tobacco use
an opening into the maxillary sinus created at the anterior- 4. Drug/alcohol abuse
superior aspect). Since then several other techniques have 5. Psychological/mental impairment
been described, including variations on the lateral window
factors that are considered contraindications to maxillary si- particular treatment for each patient. The rate of complica-
nus elevation and bone augmentation include the presence tions associated with vertical bone augmentation procedures,
of tumors, maxillary sinus infection, severe chronic sinusitis, including membrane exposure and/or postoperative infection,
scar or deformity of the sinus cavity from previous surgery, is reported to range from 2. 78% to 17%. Alternative treatment
dental infection, severe allergic rhinitis, and chronic use of options, albeit with limited outcomes, need to be considered.
topical steroids. Systemic contraindications to treatment in- For example, regenerating a vertically deficient defect may not
clude radiation therapy, uncontrolled metabolic disease (eg, be necessary if (1) implants can be placed in adjacent sites,
diabetes), excessive tobacco use, drug or alcohol abuse, and (2) short implants can be used, or (3) pink ceramic can be
psychologic or mental impairment. used to create an illusion of "normal" soft-tissue anatomy.
Historical attempts to vertically increase alveolar bone
Risks and Complications height using modalities such as onlay bone grafting have
failed. More recent treatment modalities developed for verti-
The maxillary sinus elevation and bone augmentation pro- cal bone growth include distraction osteogenesis and vertical
cedure is technique sensitive, requiring meticulous surgical guided bone regeneration (GBR). The techniques and evi-
skills. Risks and complications of the procedure include tear- dence of success are presented online.
ing or perforation of the schneiderian membrane, intraopera-
tive/postoperative bleeding, postoperative infection, and loss
of bone graft or implants (see Chapter 59). Growth Factors in Bone
The reported incidence of perforation or tearing of the Augmentation
schneiderian membrane varies greatly (up to 60%) and de-
pends largely on the anatomy of the sinus and the skill and Current research is exploring the use of various growth factors
experience of the operator. The presence of septa in the maxil- to induce bone formation. These bone-inductive mediators are
lary sinus increases the likelihood of membrane perforation. powerful modifiers of the healing process. Incorporation of
Positioning of the sinus window within 2-4 mm from the osteoinductive mediators into bone graft material or other car-
anterior and inferior borders of the sinus makes it easier to get riers can be applied to sites in conjunction with conventional
direct access to the bony walls. This may lessen the amount bone augmentation procedures to enhance the outcome.
of membrane perforation during the elevation of the sinus Most of the clinical techniques available to try and stimu-
membrane. late new bone growth at such sites use some type of bone
If the perforation is small, it can often be managed with replacement graft, including autograft, allograft, xenograft,
a resorbable barrier membrane placed over the opening, fol- or alloplast. These bone graft materials have both advantages
lowed by careful packing of the bone augmentation material. and limitations. Consequently, attempts have been made to
If a perforation or tear is extensive (Fig. 59.18, A online), it improve bone grafting by either using growth factors alone
may be necessary to abort the procedure, close the wound, or growth factors combined with a bone replacement graft.
and attempt it again at a later date. The rationale is that bone formation can be further enhanced
Infections have been reported in a small but significant when a growth factor is used to stimulate osteoblast precursor
number of cases (up to 10%) after maxillary sinus elevation or osteoblast cells and hence to push the bone formation/bone
and bone augmentation procedures. Prevention of infection resorption balance in favor of bone formation.
is crucial for bone augmentation procedures. Surgery should
always be performed using sterile technique. Patients should Conclusions
use a presurgical antimicrobial mouth rinse (eg, chlorhexi-
dine), and postoperative antibiotics should be prescribed. Bone augmentation and advanced implant surgery proce-
The signs and symptoms of sinus graft infection as well as a dures allow clinicians to reconstruct vertical alveolar bone
detailed protocol for its treatment was described in a recent deficiencies and replace missing teeth with endosseous dental
clinical study. implants. As stated in this chapter, the predictable outcome
Opening a window through the lateral wall is accomplished of these procedures depends on several biologic principles
by completely cutting through the bone of the lateral wall up that must be followed. Diagnosis, treatment planning, careful
to the schneiderian membrane. The membrane is highly vas- execution of the surgical treatment, postoperative follow-up,
cularized and may bleed significantly. However, a more serious and appropriate implant loading are all important factors in
bleeding problem can arise if an intraosseous artery is severed achieving success. Sinus elevation and bone augmentation has
in the process. Bone wax and topical hemostatic agents must become a widely used and predictable procedure to augment
be available to manage such an urgent surgical complication. the deficient posterior maxilla (ie, pneumatized maxillary si-
If a medium-to-large vascular channel is identified (with CT nus). Reconstruction of vertically deficient ridges remains a
or CBCT scan) presurgically, it can usually be avoided. significant challenge despite the reported progress and suc-
cess of new techniques.
Supracrestal!Vertical Bone
Augmentation Esthetic Management of Difficult
Supracrestal or vertical bone augmentation presents one of
Cases (Minimally Invasive Approach)
the greatest challenges of bone regeneration in implant den- In recent years, implant dentistry has been increasingly in-
tistry. This is primarily a result of the difficulty of the surgical fluenced by esthetic considerations. In addition to success-
procedure and its potential complications. Since vertical aug- ful osseointegration, harmonious soft and hard tissues must
mentation can be a very challenging procedure with a rela- surround the implant restorations so that they look natural
tively high rate of complications, it is necessary to justify this and healthy. A major challenge in implant dentistry is that, in
Surgical Procedures for Sinus Elevation It has been suggested that a minimum of 5 mm of exist-
ing native bone in the alveolar crest is required for simultane-
The goal of sinus elevation and bone augmentation is to lift ous implant placement. However, some clinicians claim that
the schneiderian membrane from the floor of the sinus, rais- it is possible to place implants simultaneously with as little
ing it up into the sinus cavity to create a new, more superiorly as 1 mm of remaining bone. The most important factor in
located sinus floor with a space between it and the deficient determining whether implant(s) can be placed at the time of
alveolar ridge. The newly created space can then be filled with sinus bone augmentation is the ability to achieve implant sta-
bone (or a suitable bone substitute material) to increase the bility in the existing bone rather than any measure of bone
total vertical height of bone in the posterior maxilla for the height. Factors that influence implant stability include bone
placement of endosseous implants. height, bone quality, precision of osteotomy preparation, and
The maxillary sinus bone augmentation procedure was first the surgeon's skill and experience. If inadequate native bone
described in the 1960s by Boyne (unpublished oral presenta- exists to place implants at the time of the bone augmentation
tions to United States Navy Dental postgraduates, 1965-68) procedure, they can be placed at a subsequent surgery after an
and originally used as a preprosthetic surgical procedure for appropriate healing period (Fig. 58.20).
patients with large tuberosities and pneumatized sinuses. To
reduce the size of the tuberosity without creating an oral-an- Bone Craft Materials
tral defect, bone was grafted into the sinus cavity to increase Autogenous bone is often considered the "gold standard" for
the volume of bone within the maxillary tuberosity. After a bone augmentation because of its osteoconductive, osteoin-
period of healing, the tuberosity was able to be reduced surgi- ductive, and osteogenic properties. However, harvesting au-
cally from the alveolar ridge crest. As stated earlier, Boyne and togenous bone from intraoral or extraoral locations creates
James were the first to describe the use of the maxillary sinus a second surgical site with additional morbidity. Numerous
bone-grafting procedure for placement of an implant (blade studies have demonstrated clinical success using many varia-
type) to retain a prosthesis. Greater use and further develop- tions of bone graft materials and combinations.
ment of this procedure evolved along with the success of en- Several recent clinical studies and reports have attempted
dosseous dental implants and the desire to replace missing to evaluate the maxillary sinus augmentation procedures us-
posterior maxillary teeth with implant-retained restorations. ing a variety of bone-grafting materials, including autogenous
The techniques used for sinus elevation and bone augmen- bone from the iliac crest or oral cavity and bone substitutes
tation are primarily differentiated by the anatomic location such as freeze-dried demineralized bone, resorbable and non-
of the osteotomy used to gain access to the maxillary sinus. resorbable hydroxyapatite, and xenografts. However, only a
Specifically, four different anatomic locations have been de- few studies have critically evaluated the long-term clinical
scribed: (1) the superior lateral wall, or "Caldwell-Luc," open- outcome of this procedure, and most have used a small study
ing, which is located just anterior to the zygomatic arch; (2) population. Short- to long-term clinical studies of dental
the middle lateral wall opening, which is located midway be- implants placed into grafted sinuses demonstrate an equiva-
tween the alveolar ridge and the zygomatic arch; (3) the in- lent or higher survival rate as compared to implants placed
ferior lateral wall opening, which is located at the level of the in native maxillary bone (ie, without the need of sinus aug-
alveolar ridge; and ( 4) the crestal osteotomy approach, which mentation). The results of these studies support the clinical
is an opening through the alveolar bone crest superiorly to- predictability of maxillary sinus augmentation procedures for
ward the floor of the sinus. At present, the most common pro- the rehabilitation of the edentulous posterior maxilla with
cedures used for sinus elevation and bone augmentation are implant-supported prostheses (Fig. 58.21).
the lateral wall antrostomy (middle or inferior approach) and The use of bone-substitute graft materials can reduce the
the crestal approach osteotomy. morbidity introduced by a second surgical site while main-
taining equally good implant success rates. Anorganic bovine
Presurgical Evaluation of Maxillary Sinus
bone-derived mineral (ABBM; ABBM has also been referred to
Presurgical evaluation of the maxillary sinus is primar- in the literature as deproteinized bovine bone mineral, deprotein-
ily accomplished using radiographic examination techniques ized anorganic bovine bone, and anorganic bovine bone) has also
(Fig. 58.18). Several observations about the anatomy can be been used successfully for sinus augmentation. This graft ma-
made with a periapical or panoramic projection, but the in- terial has demonstrated good dimensional stability and high
ternal anatomy is more accurately assessed with a three-di- implant survival rates. These materials form an osteoconduc-
mensional (3D) scan, such as computed tomography (CT) or tive scaffold for bone growth but do not have any osteoinduc-
cone-beam CT (CBCT) scan. The maxillary sinus should be tive properties. A possible exception is demineralized freeze-
evaluated for any pathology, masses, or the presence of septa. dried bone allograft (DFDBA). This material has demonstrated
If 3D scans are available, the lateral wall should also be evalu- osteoinductive potential but has not proved to be particularly
ated for the presence of medium or large intraosseous vascular advantageous in the maxillary sinus bone augmentation. In
channels (Fig. 54.15). Medium- to large-sized vessels occa- fact, the bone volume gained with the use of DFDBA is less
sionally traverse the lateral wall of the maxillary sinus, and than that achieved with mineralized graft materials as a result
identifying them is helpful in avoiding a bleeding problem of moderate postoperative shrinkage of DFDBA-grafted bone.
during surgery (see Chapter 42).
Crestal Osteotomy Technique
Simultaneous Implant Placement In cases with moderate bone height (eg, 7-9 mm) that re-
Simultaneous implant placement is possible with sinus eleva- quire limited sinus bone augmentation, a crestal approach to
tion and bone augmentation procedures as long as the implant elevation may be desirable. The osteotome technique is a pro-
can be stabilized in the desired location with the existing na- cedure that uses osteotomes (Fig. 58.22) to compress bone
tive bone (Fig. 58.19). (internally from the alveolar crest upward) against the floor
FIGURE 58.18 Presurgical evaluation of the maxillary sinus. A, Periapical radiograph. B, Panoramic projection from cone-beam scan. Note the
presence of maxillary septa in the premolar region. C, Cross-sectional image in premolar region showing about 6 mm of bone height and presence of
maxillary septa. D, Cross-sectional image in molar region showing about 2 mm of bone height.
FIGURE 58.19 Simultaneous implant placement

with maxillary sinus elevation and bone augmenta-
tion procedure. A, Preoperative periapical radiograph.
B, Preoperative, cross-sectional image in premolar re-
gion demonstrating 10.6 mm of vertical bone height.
C, Preoperative, cross-sectional image in molar region
demonstrating 5.3 mm of vertical bone height. D, Post-
surgical radiograph of graft and implants in place.
FIGURE 58.20 Staged implant placement after sinus elevation and bone augmentation procedure. Same patient as in Figure 58.1. See preopera-
tive radiograph and preoperative cross-sectional images. A, Postsurgical panoramic view of bone-augmented maxillary sinus. The maxillary left cuspid
has been extracted because of a vertical fracture. B, Postsurgical cross-sectional image in premolar region demonstrating more than 17-mm vertical
bone height. C, Postsurgical cross-sectional image in molar region demonstrating 19.1-mm vertical bone height. D, Postsurgical radiograph of implants
placed in the previously grafted maxillary sinus (and cuspid site).
FIGURE 58.21 Long-term follow-up of patient presenting with minimal residual crestal bone height. A, Preoperative radiograph demonstrates
minimal residual crestal bone height. B, Postoperative radiograph demonstrates sinus graft healing after 6 months. C, Abutment connection of implants
after 6 months of submerged healing. The three distal implants were placed into augmented bone. D, Periapical radiograph demonstrates stability
of crestal bone around implants at 10 years loading. (From Urban IA, Lozada JL. A prospective study of implants placed in augmented sinuses with
minimal and moderate residual crestal bone: results after 1 to 5 years. Int J Oral Maxillofac Implants 25(6): 1203-7 212, 20 70.)
be contraindicated for sinuses that have an acutely sloped

floor or septa in the location of the planned osteotomy. An
acutely sloped sinus floor will tend to deflect the osteotome in
an undesirable direction rather than allowing the osteotome
to penetrate into the sinus space, and the presence of septa
makes it virtually impossible to fracture the sinus floor in-
ward. Box 58.5 provides additional precautions and clinician
comments on using the osteotome technique. Several new
instruments and techniques have emerged that improve the
ability to create a crestal approach osteotomy while avoiding
trauma or injury to the schneiderian membrane. These in-
struments/techniques vary from drill systems to piezoelectric
bone surgery.
Lateral Window Technique
The lateral window technique is probably the most effective
and efficient way to access the maxillary sinus and elevate the
sinus floor. In this procedure, an opening into the maxillary
sinus is created to elevate the schneiderian membrane and to
place bone graft in the space immediately above the existing
alveolar bone. The osteotomy can be prepared with a high-
FIGURE 58.22 Osteotome instruments. A, Straight osteotomes. B, speed round diamond or a piezoelectric bone surgery device.
Offset osteotomes.
Some clinicians prefer to cut the lateral window (outline cut
through to the membrane) and use the impacted bony wall
as the superior wall of the space created for bone grafting
of the sinus, ultimately leading to a controlled "inward frac- (Fig. 58.24, A-C), and others prefer to eliminate the bony
ture" of the sinus floor bone and the schneiderian membrane, window entirely by reducing it to a paper-thin layer, which is
which should remain intact above the inward-fractured bone. easily removed (Fig. 58.24, D-F) With the former technique,
The osteotome sinus floor elevation technique was de- it is important to create a window that is small enough, rela-
scribed by Summers. It is considered to be a "conservative" tive to the mediolateral width of the maxillary sinus, to allow
approach to sinus elevation, but it is also a "blind" technique the "window" to be pushed completely into the sinus cavity.
because it does not allow the operator to visualize the schnei- If the window cannot be inserted completely, it must be care-
derian membrane during the osteotomy. For this reason, it is fully separated from the membrane and removed. The bone
a technique-sensitive procedure as well (ie, the operator must removed from the lateral window osteotomy can be harvested
"feel" the bone fracture and the membrane elevation). Verifi- and incorporated into the bone graft.
cation of success can only be observed with radiographs and Elevation of the schneiderian membrane is accomplished
visualization of the bone graft material in the sinus cavity. with hand instruments that are inserted along the internal as-
pect of the bony walls of the sinus (Fig. 58.25)
Procedure. An osteotomy site is prepared with a series of Great care is taken to avoid perforation of the membrane.
drills (eg, initial drills used for implant site preparation) to Small instruments, such as the De Marco curette, are intro-
a depth that is approximately 1-2 mm from the floor of the duced along the inferior, anterior, posterior, and superior as-
maxillary sinus. Osteotomes are used to increase compressive pects of the prepared antrostomy window, gradually inserting
forces gradually against the floor of the sinus by adding incre- further along the bone until the membrane begins to separate
mental quantities of graft material until the floor of the sinus and lift away from the bone. Subsequently, larger instruments,
fractures inward (Fig. 58.23). After the controlled inward frac- such as the Gracey 13/14 curette, are gently introduced along
ture of the maxillary sinus floor, bone graft materials continue the bone to continue lifting the membrane to the desired levels
to be slowly introduced, through the osteotomy site and into (height, width, and depth). Instruments must always be kept
the maxillary sinus, which continues to elevate the membrane in contact with the bone surface while elevating the schnei-
and thus allows a vertical expansion of the bone height in a lo- derian membrane to avoid perforation. Regardless of whether
calized area of the maxillary sinus. Once the sinus membrane implants are being placed simultaneously or not, it is useful
is elevated with bone graft material to the desired height, the to estimate the dimensions of the augmentation needed by
implant osteotomy can be completed, with a final drill used to inserting a surgical guide with holes or markers indicating the
finish preparation of the site, and an implant can be inserted. ideal location for planned implants. Once elevated, the space
Multiple individual sites can be elevated and prepared simul- can be grafted with bone (autogenous, bone substitute, or a
taneously through separate osteotomy sites. combination). If implants are being simultaneously placed,
Published reports of this technique have demonstrated in- the implant osteotomy sites should be prepared, and implants
creased bone height from 2 to 7 mm (average: 3.8 mm). Thus placed after the medial, anterior, and posterior aspects are
the crestal approach is a useful technique for increasing the filled with bone, thereby supporting the schneiderian mem-
vertical height of bone up to approximately 4 mm. If more brane up and away from the drills and implants. After implant
vertical bone height is needed, the lateral wall osteotomy ap- placement, the remaining lateral aspect is packed with bone
proach may be more advantageous. In addition to the usual graft. Finally, the antrostomy and bone graft is covered with
precautions and contraindications for sinus elevation and a barrier membrane (eg, resorbable membrane) and the flap
bone augmentation procedures, the osteotome technique may is sutured.
FIGURE 58.23 Illustration of the osteotome sinus floor elevation (OSFE) technique. A, Osteotomy prepared with drills to a depth that is near the
maxillary sinus floor. B, Graft material introduced into osteotomy and condensed with osteotome. C, Additional bone graft material is added to the
osteotomy. D, Bone graft continues to be condensed by osteotomes. E, This process is continued until floor of sinus is "fractured" up internally and the
floor is lifted with the bone graft material. F, Continuation of process shown in E for second site. G, Bone graft material continues to be added gradu-
ally to both sites with osteotome condensation to elevate the schneiderian membrane away from the bone (maxillary sinus walls) until sufficient height
and volume are created for the placement of implants. H, The coronal aspect of the osteotomy is carefully prepared for the placement of implants
(instrumentation not shown) and the implant is placed. I, Final view of two implants placed in the grafted maxillary sinus using the OSFE technique.
ifechni~ue
CLINICAL PERSPECTIVE 1
The osteotome procedure involves repeated tapping of osteotomes with a mallet to create the necessary pressure to fracture the floor of
the maxillary sinus. This tapping can be bothersome to some individuals, especially those patients who are not sedated for the procedure.
The tapping procedure tends to be more bothersome for patients with dense cortical bone than for those with loose trabecular bone. In
fact, a specific postoperative complication, called benign paroxysmal positional vertigo (BPPV), has been associated with the osteotome
sinus elevation technique. During the osteotomy preparation and sinus floor elevation, the trauma induced by percussion of the osteotome
with the surgical hammer, along with hyperextension of the neck during the operation, can displace otoliths in the inner ear and induce
BPPV (see Chapter 59).
CLINICAL PERSPECTIVE 2
The osteotome technique requires that the osteotome be properly aligned in the direction of the long axis of the planned implant. Thus
patients must be able to open wide enough to allow a direct insertion of the osteotome into the osteotomy site. Offset osteotomes are
available that can facilitate the correct angulation (Figure 58.4, B).
(A)
(D)
FIGURE 58.24 Illustrations showing two techniques for the lateral window procedure to access the maxillary sinus for bone augmentation. The
first technique (A-C) preserves the bone of the lateral window elevating it up into the sinus cavity to create a new sinus floor. The second technique
(D-F) completely removes the lateral window as part of the preparation. A, Lateral window is cut at the periphery of the access window, leaving the
lateral bony wall in the center of the window intact. The bony window is then pushed inward to become the new, elevated sinus floor/superior wall
of the grafted maxillary sinus space. B, Bone graft material is packed into the newly created space. C, A barrier membrane is placed over the lateral
window and bone graft material. The full-thickness flap is sutured over the barrier membrane. D, Lateral window is removed entirely during the prepa-
ration of the osteotomy. The schneiderian membrane is elevated inward and upward to become the superior containment of the grafted maxillary sinus
space without a superior bony wall. E, Bone graft material is packed into the newly created space. F, A barrier membrane is placed over the lateral
window and bone graft material. The full-thickness flap is sutured over the barrier membrane.
FIGURE 58.25 Instruments used to elevate the schneiderian membrane through lateral window antrostomy. A, De Marco curettes. B, Gracey
13/14 curette. C, Universal curettes. D, Large spoon curettes. E, Medium-size curved membrane elevators.
Guided Bone Regeneration and bone augmentation of the posterior maxillary ridge was done
Augmentation simultaneously with sinus bone augmentation (Fig. 58.27).
At membrane removal, the mean vertical bone augmenta-
The surgical technique of GBR for supracrestal regeneration tion was 5.5 mm (±2.29 mm). The mean combined crestal
was described in the 1990s. Both animal and human studies remodeling was 1.01 mm (±0.57 mm) at 12 months, which
demonstrated successful vertical bone augmentation with his- remained stable through the 6-year follow-up period. There
tologic evidence. The available evidence describing and sup- were no statistically significant differences between the treat-
porting the use of supracrestal GBR is limited. Some studies ment groups in mean marginal bone remodeling. The overall
have evaluated the effect of space creation by a membrane implant survival rate was 100% with a cumulative success
alone, whereas others have used an autogenous bone graft to rate of94.7%.
maintain space under the membrane. Animal (dog) studies The efficacy of a 1:1 mixture of ABBM and autogenous par-
demonstrated the ability to gain about 2.7 mm (0.4-4.0 mm) ticulated bone graft using ePTFE membranes was evaluated
of vertical bone height around simultaneously placed im- histologically and histomorphometrically in 8 patients (10
plants. In one clinical study, 5 patients were treated with a ridge defects). After a healing period of 6 to 9 months, a mean
supracrestal exposure of 3-7 mm (average: 4.67 mm) and vertical gain of 3.15 mm (SD ±1.12 mm) was achieved. In a
showed a clinical bone gain of 0.5-4 mm (average: 2.97 mm) recent clinical and histologic study evaluating the same graft
after 9 months. These studies suggest that supracrestal bone material and using dense PTFE membranes in 19 patients,
formation up to 3 mm is predictable using the GBR technique an average bone gain of 5.45 mm (SD 1.93) was achieved.
with a membrane-blood clot combination. In both studies histologic evaluation showed that ABBM was
Simion et al and Jovanovic et al used a titanium-reinforced connected with a dense network of newly formed bone of
(TR) membrane for vertical bone regeneration around dental varying degrees of maturation. However, long-term results are
implants without the placement of supportive bone substrates. not available to confirm the predictability of the procedure or
Instead, the space was filled with a blood clot facilitated by implant success. More long-term studies are needed.
perforating the cortical bone surface or by injecting the space
with venous blood. Supracrestal bone regeneration achieved
Distraction Osteogenesis
was 3.3 mm and 1.82 mm in these studies, respectively Re-
cent studies showed that supracrestal bone formation is more Distraction osteogenesis is a surgical technique that has been
predictable using a bone graft filler material placed under the developed to increase vertical bone height in the deficient jaw
TR membrane. Therefore, at present, advanced surgical GBR site and contrasts with the more conventional method of bone
augmentation for vertical bone gain should be achieved with grafting with or without membranes. Under the proper cir-
a nonresorbable TR membrane that is supported by a bone cumstances, most cells in bone can differentiate into osteo-
graft (Fig. 58 26) genic (or chondrogenic) cells needed for repair. Ilizarov popu-
The long-term results of vertical GBR after 1-5 years of larized the concept of distraction osteogenesis in the 1980s by
prosthetic loading were examined in a retrospective multi- developing a protocol for "cutting" long bones and "stretch-
center study evaluating 123 implants. Three treatment modal- ing" them during the healing process.
ities (nonresorbable regenerative membranes in combination Based on experimental and clinical studies over 35 years,
with blood clot only, DFDBA, and autogenous bone chips) distraction osteogenesis can provide a surgeon with the abil-
were studied, and the results from this investigation revealed ity to treat small bones in the hands and feet using external
that vertical bone regeneration greater than 4 mm could only fixation devices. Recently, new intraoral devices for vertical
be achieved with the use of autogenous bone chips. These bone growth of the alveolar process have been developed and
authors reported an overall success rate of 97.5%, leading successfully applied in preparation for the placement of dental
them to conclude that vertically augmented bone using GBR implants. Other important advantages of distraction osteogen-
techniques supports implant placement in a fashion similar to esis are that it may avoid the need for a second surgical site
native, nonregenerated bone. to harvest bone, and the newly created bone has native bone
Urban et al used TR membranes with autogenous par- at the crest, which is thought to withstand forces better than
ticulated bone for vertical bone augmentation before implant regenerated bone.
placement. The study included 35 patients with 36 vertical One of the most significant disadvantages of the distraction
bone defects. Eighty-two implants were placed in a staged osteogenesis procedure for intraoral application is the unidi-
approach and a resorbable collagen membrane (Bio-Gide Re- rectional limitation of current devices. The application of dis-
sorbable Bilayer Membrane, Osteohealth, Shirley, NY) was traction osteogenesis for vertical bone growth has shown good
placed over the newly formed crestal bone at the implant predictability However, limitations have been encountered in
placement surgery to protect the graft from early resorption achieving horizontal bone growth with this method. Second-
after removal of the expanded polytetrafluoroethylene (ePT- ary bone grafting is frequently needed following vertical dis-
FE) membrane. Implants were followed from 1 to 6 years after traction osteogenesis, especially for the extremely resorbed
prosthetic loading. (narrow) ridges. Consequently, distraction osteogenesis can-
Treatment groups included single and multiple tooth sites, not be expected to solve vertical ridge defects without the use
as well as vertical defects in the posterior maxilla. Vertical of additional augmentation procedures.
FIGURE 58.26 Representative case of a posterior mandibular vertical ridge augmentation. A, Atrophic posterior mandibular area. B, Particu-
lated chin bone graft is placed on the ridge. Cortical bone was perforated and guided tissue regeneration membrane/titanium-reinforced (GTRM-TR)
membrane was secured on the lingual side before applying bone graft. C, GTRM-TR membrane is secured over the graft with titanium pins. D, Three
implants are in place in the newly formed posterior mandibular ridge. Note the well-integrated bone graft. E, Periapical radiograph at abutment con-
nection. F, Periapical radiograph at 8-year follow-up with implants in function. G, Clinical picture demonstrates healthy periimplant mucosa. (From
Urban IA, Jovanovic SA, Lozada JL: Vertical ridge augmentation using guided bone regeneration (CBR) in three clinical scenarios prior to implant place-
ment: a retrospective study of 35 patients 12 to 72 months after loading. Int J Oral Maxillofac Implants 24(3):502-510, 2009.)
FIGURE 58.27 Simultaneous vertical ridge and sinus bone augmentation. Representative case requiring posterior maxillary vertical and sinus aug-
mentation. A, Failing implant and severe periimplant bone defect on the right maxillary premolar area. B, Radiograph 3 months after implant removal
demonstrates vertical deficiency and sinus proximity. C and D, Remote full-thickness flap is elevated exposing the facial bone of the posterior maxillary
region. Buccal and occlusal views of esthetically and functionally demanding vertical defect. E, The lateral window of the sinus is outlined and frac-
tured inward. The schneiderian membrane is carefully elevated until the correct vertical height is reached. F and G, Anorganic bovine-derived bone
mineral (ABBM) and autogenous bone was applied and packed to the subantral space of the elevated sinus. Guided tissue regeneration membrane/
titanium-reinforced (GTRM-TR) membrane was fixated on the palatal bone and a titanium tenting screw is placed protruding to the desired vertical
position. Autogenous particulated bone was applied to the vertical defect.
Bone Morphogenetic Proteins product has been cleared for oral cavity use in both sinus lift
augmentation therapy and for ridge augmentation in maxil-
Perhaps the most studied of all the osteoinductive growth lary anterior extraction sites with bone loss.
factors are the bone morphogenetic proteins (BMPs), which The BMPs are a group of related proteins that are found in
belong to the transforming growth factor beta (TGF-~) super- the body and are important for skeletal development. Each of
family Of this family, recombinant human bone morphogenetic the proteins has relatively specific functions, and BMP-2 has
protein-2 (rhBMP-2) has shown significant signs of bone-en- been shown to have some of the strongest bone-producing
hancing potential. activity. BMP-7 [also called osteogenic protein-] (OP-1)] and
One commercial bone growth factor product has been BMP-3 (also known as osteogenin) have also been shown to
approved by the FDA for use in the oral cavity to stimulate stimulate bone formation. The BMPs were originally isolated
bone formation. As was noted in the use of growth factors for from bovine bone by Marshall Urist. As a growth factor, the
periodontal regeneration, the growth factor protein must be BMPs induce the differentiation of mesenchymal stem cells
combined with a carrier to have activity and be used clinically. to become bone-producing osteoblast cells. Thus, unlike pro-
The commercially available bone growth product contains rh- liferation factors that increase the number of cells, the BMPs
BMP-2 combined with a bovine type I collagen sponge. This are differentiation factors that stimulate cells to produce bone
58 Surgical Concepts of Implant Therapy 713.el 1
FIGURE 58.27 (cont.) H and I, Buccal and occlusal views of GTRM-TR membrane secured over the graft with titanium pins. J, After 9 months of
uneventful healing, the GTRM-TR membrane has maintained its position. Kand L, Buccal and occlusal views of the regenerated alveolar bone crest.
M, The final reconstruction demonstrates a functional and esthetic outcome. N, Stable crestal bone around the implants after 10 years of loading.
tissue. Many carriers have been tested with the BMPs, but the and showed a bony union of the defects for rhBMP-treated
binding and release kinetics using bovine type I collagen have sites. The control sites were not closed at the same intervals.
proved to be the most useful clinically. BMP binds tightly to The clinical results of using rhBMP-2 and collagen in pa-
the collagen within minutes and has been shown to be re- tients are remarkable considering that only one bone differ-
leased over time for 2-3 weeks at the defect site. The extended entiation agent is being delivered to the bone site and it is
release kinetics likely allow the undifferentiated mesenchymal only delivered at the time of the surgical procedure. Relatively
cells migrating into the wound site over time to be exposed to high doses of the protein are often used in some sites however,
the growth factor. These BMPs have been extensively studied possibly as the result of the need to release effective doses
and have been shown to stimulate bone formation in many at later times. Future research directions will likely focus on
animal models and in humans under a variety of conditions more targeted delivery of the bone growth factor at specified
and indications. In fact, the same product approved for use in times during the wound healing process.
the oral cavity had previously been approved by the FDA for The use of growth factors for bone augmentation has the
use in single-level spine fusion procedures and in open tibial potential to completely eliminate the need of bone harvesting
fractures in humans. and any bone filler materials, and preliminary results are en-
The BMPs have specific receptors on the surfaces of cells. couraging. However, the clinician must recognize that there is
Binding of the BMP causes dimerization of the receptor pro- limited clinical information available on these new modalities,
teins, which in turn stimulates a cascade of events intracellu- and no information on resorption of the regenerated bone,
larly involving a set of proteins called SMADs. The end result implant survival, or bone remodeling around implants. Fur-
of the intracellular cascade is the activation of genetic activity ther documentation from long-term, randomized, controlled
and bone cell differentiation. clinical studies are necessary.
The preclinical results of using rhBMP-2 in animals with
critical-sized defects have reported rapid new bone forma-
Autologous Platelet Concentration
tion. The inductive capacity of rhBMP-2 was demonstrated by
impregnating a polymer carrier and placing the substrate in In recent years, a new approach to enhance the vitality of
critical-sized rat mandibular defects with or without a barrier bone grafts has been introduced by using platelet concen-
membrane. The study evaluated 12- and 24-day healing times trate or platelet-rich plasma (PRP). PRP is an autologous
source of platelet-derived growth factors and transforming graft and has been shown to increase the quality of and re-
growth factors that is obtained by sequestering and concen- duce the time needed for bone regeneration. Clinical and ex-
trating platelets by centrifugation. The patient's own blood is perimental studies are scarce but suggest that this technique
withdrawn and separated into platelet-rich and platelet-poor holds promise for large bone defects and bone defects with
components. The PRP is the important content, containing a low osteogenic potential. Extrapolation to the possible effect
high-level mixture of platelets and a concentration of growth of PRP on other bone-filler materials cannot be made at this
factors. This PRP mixture is added to the autologous bone time.
FIGURE 58.28 Implant sites in the anterior, esthetic zone with extensive bone loss. A, Anterior mandibular site showing extensive bone loss fol-
lowing extraction of hopelessly infected mandibular incisors. B, Extremely narrow (labial-palatal) ridge width in the anterior maxilla that was missing
centrals and laterals for many years. C, Moderate bone loss associated with the extraction socket of a maxillary cuspid.
many instances, dental implants need to be placed in an es- pushing the art and science of dentistry, it is necessary more
thetic zone in which there is extensive alveolar bone deficien- than ever for clinicians to fully understand all the available
cy from tooth loss, dentoalveolar infection, or other pathology options of treatment and decide appropriately which, where,
(Fig. 58.28, A-C) Gingival morphology follows the shape of when, and how to use these options for each patient.
the underlying bone, and it is difficult to build esthetically An important recent clinical development in dental implant
acceptable gingiva in areas with deficient supporting bone. surgery is the concept of "minimally invasive" approaches to
Furthermore, using conventional surgical approaches to ac- treatment. Specifically, there is a new drive toward minimally
complish the goal in a patient-friendly manner with minimal invasive implant placement. With advances in technologies,
trauma and clinical predictability is an extremely demanding materials, and biologic sciences in dentistry, this approach to
task. implant surgery is becoming more popular among clinicians
Treatment planning in a complex implant case today is of- and will most likely dominate the way dental implants will be
ten confusing because there are many different surgical and placed in the near future.
restorative approaches to solve the same problem. Many times Minimally invasive surgery in implant dentistry implies a
these procedures seem to conflict. When considering the sur- surgical approach that minimizes the extent and number of
gical placement of implants, clinicians must consider the ap- surgeries while providing esthetics, predictability, and longevi-
proach (conventional two-stage approach vs a one-stage ap- ty with minimal surgical morbidity and discomfort to patients.
proach) and the timing of implant placement (immediate vs The surgical approach most often required to achieve these
delayed or staged placement). For bone augmentation proce- goals for anterior implant therapy involves immediate implant
dures, there is the more conventional approach of augmenting placement, one-stage surgical approach, with or without flap,
the ridge first and placing the implant(s) after healing, or the and simultaneous bone grafting. Furthermore, these surgical
simultaneous implant placement with bone augmentation ap- techniques need to be guided by a consistent surgical strategy
proach in which bone grafting is done at same time as implant that provides predictable esthetic results in implant dentistry.
placement. All of these approaches can provide a successful A minimally invasive approach to implant therapy in posterior
outcome if patient selection is appropriate and techniques are sextants in which esthetics is not a major concern can be pre-
performed properly. However, depending on the situation, dictably achieved with the use of short wide implants.
some of these techniques are more advantageous than others This chapter introduces surgical strategies that enhance
in achieving esthetic results with better predictably and less the esthetic predictability in implant dentistry. The minimally
patient discomfort. invasive surgical approach to manage difficult esthetic and
It is easy for a clinician to "dogmatically" choose one ap- anatomically deficient cases is discussed with examples. The
proach, usually choosing the one that the clinician feels most one-stage, immediate implant placement technique, which is
comfortable with, and to treat all patients with the same ap- the foundation of a patient-friendly approach to esthetic im-
proach. However, with heightened expectations of esthetics plant dentistry, is presented in detail. The thought processes
involved in case selection, their scientific rationale, and proper stability in an extraction socket, often without elevating a flap.
techniques of soft and hard tissue management are described The alveolar architecture in relation to the angle of the im-
with cases. plant to be inserted; the presence or absence of a bone concav-
ity apical to the extracted tooth; the amount of existing bone
Surgical Strategy for Predictable apical and palatal to the extraction socket, which can provide
primary stability for the immediate implant; and the quality of
Esthetics the bone and soft tissues of the ridge should all be thoroughly
Observation of and adherence to the following surgical strate- evaluated clinically and radiographically before surgery. Many
gies enhance predictability and outcomes for esthetic dental clinicians perform successful immediate implant placement
implant surgeries with minimal discomfort to patients: without the aid of 3D scans [eg, computed tomography (CT)
or cone-beam CT (CBCT)]. However, if the tooth involved is
1. Determine the level of surgical esthetic goal to be achieved. long and large or if there is an alveolar concavity or other ana-
2. Visualize the final outcome. tomic variations, the use of a CT/CBCT scan is advised.
3. Preserve existing tissues important for esthetics. A major disadvantage of placing implants immediately in
4. Always overbuild bone and soft tissue in augmentation the changing alveolar bone of an extraction socket is that it may
surgeries. result in progressive recession of the gingival labial margin over
the implant restoration. Therefore, when placing an immediate
Immediate Implant Placement implant with one-stage surgical approach in anesthetic zone, a
prudent strategy would be to improve the quality and quantity
for Predictability and Esthetics of labial gingival tissue, which seems to be vital for the stabil-
Immediate implant placement in a one-stage approach, in ity of the labial gingival margin involving immediate implants.
which a healing abutment or provisional restoration is at- One of the most effective ways to keep the implanted socket
tached to the implant and remains exposed, provides more from collapsing and improve the labial gingival biotype is to
predictable preservation of the interproximal periimplant gin- simultaneously fill the labial socket void with particulate bone
gival tissue with less patient discomfort and treatment time. and augment the labial gingival tissue with soft tissue.
This approach to implant placement is the foundation of a An effective bone and gingival tissue augmentation tech-
minimally invasive approach to esthetic implant dentistry. nique used with flapless immediate implant placement in a
However, as with any surgical technique, it takes learning and one-stage approach is the bone and crescent-shaped free gin-
practice to perform it properly. The criteria and techniques for gival grafting technique. In this technique, the space between
proper immediate implant placement have previously been the inner surface of the labial bony wall and the labial surface
established and reported with successful long-term outcomes. of the implant is filled with slow-resorbing mineralized, freeze-
One of the more difficult aspects of immediate implant dried particulate bone allograft or particulate xenograft to help
placement is positioning the implant with sufficient primary preserve the horizontal dimension of the ridge (Fig. 58.32, A).
FIGURE 58.32 A, Bone graft material is lightly packed

into the extraction socket gap between the labial wall and
the implant surface. B, Diagram of crescent-shaped, free
gingival graft tissue being harvested from the palate. C,
Clinical photograph of crescent-shaped, free gingival graft
tissue positioned over the bone graft to fit snuggly in the
gap between the gingival wall and the implant surface. D,
Crescent-shaped, free gingival graft is sutured in place us-
ing 5-0 gut sutures. The sutures pass through the gingival
graft toward the labial gingival margin and are tied. Then,
without cutting the ends, the suture is passed over the
graft and tied to the palatal gingival tissue. Three sutures
are needed to keep the graft in position.
Determine the Level of Surgical

Esthetic Goal
In dental implant therapy, it is important to determine from
the onset the level of surgical esthetic goal. To determine the
treatment needs, it is important to assess the patient's esthetic
expectations and to consider their age, medical condition,
time constraints, and finances as well as the status of existing
soft and hard tissue. The ability and experience of the clini-
cian must also be factored into the determination.
The surgical esthetic goal can be ideal, acceptable, or com-
promised. An ideal surgical esthetic goal (Fig. 58.29) implies
an ideal, complete surgical reproduction of periimplant tissue
around an implant restoration. An acceptable surgical esthetic FIGURE 58.31 Compromised surgical esthetic goal. Severe ridge
goal (Fig. 58 30) implies that the esthetics of the final implant deficiency resulted in long implant-supported fixed restoration and dif-
restoration and the periimplant tissue is not ideal, but both ficult oral hygiene access. Notice the pink porcelain used to mask the
the patient and the clinician accept it. Also, the hygiene and increased length of the crowns. Soft tissues are obviously compromised
and completely lack any semblance of normal.
the long-term health of the restoration are not compromised.
A compromised surgical esthetic goal (Fig. 58.31) implies that
the esthetic, hygiene, and long-term health of the implant are
far below what is acceptable in today's clinical standard. treatment so that the patient is well informed about treatment
In general, more surgeries are required to achieve esthetic costs and time requirements. Many clinicians feel it is over-
results that are close to ideal. The treatment time is usually treatment to attempt ideal esthetics for all patients.
much longer and the cost is much higher. There is more surgi-
cal morbidity for the patient, and the ideal esthetic outcome Visualize the Final Outcome
remains elusive and often is not achieved. Once the level of the esthetic goal is determined, the next step
Due to the logistic consequences of this decision, the level is to visualize the final outcome. Determination of the vertical
of the esthetic goal should be determined at the beginning of position of the implant, quantity and quality of the soft and
hard tissue augmentation needed, components of the alveolar
tissue that need to be preserved in surgery, and what surgical
approach is most appropriate for the patient cannot be ac-
complished without first visualizing the final esthetics of the
implant restoration(s) involved. In simple cases, the visualiza-
tion can be done mentally or with the aid of computer graphic
simulation. In more complex cases, a diagnostic wax-up may
be necessary.
Preserve Existing Tissues Important

for Esthetics
Once what needs to be accomplished surgically is decided
through visualization of the esthetics of the final restorations,
the next step is determining what aspects of the soft and hard
tissues need to be preserved for a predictable esthetic result.
FIGURE 58.29 Ideal surgical esthetic goal. Clinical photograph of an
For example, if the initial vertical position of the interdental
implant-supported crown replacing maxillary right cuspid in a 20-year- papilla is esthetically compatible with the image of the final
old female with a high smile line. Soft tissues are full and contours ap- restorations, it is prudent to preserve them rather than need-
pear natural. ing to rebuild them after they are lost. Knowing what needs
to be preserved will help assist in choosing an appropriate
. . ,. ~ • -:-- J'.:'..,,~-
surgical approach.
•.
•.. ,...
...,.
· ,,
.•..... .
- Always Overbuild Bone and Soft Tissue
···--· .
in Augmentation Surgeries
Many studies have shown that there is rapid labial and vertical
-'•- --~ •.
~·~
bone loss after extractions, and immediate implant placement
~· : 4
_ ..
,,
it' _
• ·!J, .. "
i :.~
J t -
.
·,
, ·., does not stop the resorption process. Furthermore, it has
. -
been demonstrated that soft and hard tissues grafted in aug-
mentation procedures to enhance esthetics undergo extensive
shrinkage within 3-6 months. Therefore, the deficient ridge
FIGURE 58.30 Acceptable surgical esthetic goal. Clinical photograph
of implant-supported crowns replacing multiple missing maxillary ante-
needs to be overbuilt by approximately 30-40% at the time of
rior teeth in a 63-year-old female with a low smile line. Soft tissues are surgery to be esthetically sufficient after the expected primary
nearly full and contours appear fairly normal but not ideal. and secondary tissue shrinkage.
Then, a crescent-shaped soft-tissue graft is harvested from Certainly, these techniques require learning and practice to
the ipsilateral palate (Fig. 58.32, B) and transplanted into make them effective in each clinician's hands. However, they
the labial recipient site coronal to the particulate bone graft present a sound approach to what is possible in hard- and
(Fig. 58.32, C) To provide/maintain the blood supply to soft-tissue management for esthetic implant surgery and pro-
the donor tissue, it is important that the outer surface of the vide effective strategies and techniques for solving many dif-
crescent graft fits with an intimate contact with the bleeding ficult esthetic cases in a patient-friendly manner.
lamina propria of the labial gingiva. Proper suturing ensures
good proximity and prevents the graft from being displaced
coronally out of the recipient site (Fig. 58.32, D)
Dental Implant Microsurgery-
The advantage of this approach to gingival augmentation Immediate Placement
is simplicity and minimal surgical morbidity. In addition to The success of dental implants in extraction sites combined
providing a sealed protection for the bone graft, it prevents with immediate provisionals for newly placed dental implants
resorption of the sensitive labial crestal bone. Preparation has brought a convergence in restorative and surgical prac-
of the recipient site involves no surgical manipulation other tice for treatment planning of dental implants. This conver-
than deepithelialization as described. Gingival walls are com- gence reaches its summit in the approach to failing teeth in the
pletely intact with a full blood supply. The donor site wound maxillary esthetic zone. For anatomic reasons, maxillary an-
is small (approximately 3 mm depth X 3 mm height at the terior teeth are at high risk for traumatic injury (Fig. 58.36).
widest point) with intact epithelium around the wound, Traumatized teeth frequently receive endodontic treatment
which epithelializes within a week and causes minimal dis- that may be followed by horizontal or vertical root fracture.
comfort for the patient. Since each donor tissue graft is small, Dentistry's historic answer to tooth loss has been the fixed
multiple grafts can be harvested from a single palate so that bridge. Tooth preparation necessary for a fixed bridge often
multiple immediate implants can be augmented at same results in significant reduction of tooth structure. Inherent
time. Furthermore, this gingival augmentation technique esthetic limitations of fixed bridges include loss of gingival
frequently improves an unfavorable initial gingival margin papillae and resorption of the buccal alveolar plate. For these
because the grafted gingival margin is always coronal to the reasons, dental implants are a preferred choice for tooth re-
existing gingival margin. This minimizes a need for other placement in the maxillary esthetic zone.
time-consuming techniques, such as orthodontic extrusion,
or a delayed approach to implant placement when the initial
gingival margin is not esthetic or ideal, as recommended by Implant Microsurgery
many authors. Microsurgery is associated with enhanced soft-tissue proce-
The risk-to-benefit ratio of the crescent grafting technique dures and fine suturing. This is part of the scope of implant
is favorable enough that if the graft does not survive, or if microsurgery but additional benefits include dental implant
more than expected horizontal resorption of the ridge occurs, drilling precision. The ability to discern minute dimensional
traditional techniques (eg, subepithelial connective tissue differences permits implant osteotomy preparations centered
graft) can be performed to augment the results. This is usu- exactly between reference points such as adjacent teeth, adja-
ally possible without refabrication of the implant restoration cent implants, or buccal and lingual ridge anatomy More pro-
because the vertical height of the interdental papilla is suffi- foundly, the microscope allows immediate detection of subtle
ciently preserved with immediate implant placement in a one- changes in drill position so appropriate feedback corrections
stage approach. can be applied to the handpiece. Enhanced angular percep-
tion is also important. The drill's angular position can be ori-
Conclusions ented relative to small landmarks such as the implant platform
The clinical science in dentistry has evolved to where place-
ment of dental implants and restoring them requires sufficient
knowledge in several disciplines of dentistry. In addition to
mastering surgical objectives and techniques, periodontists
must be able to evaluate and accurately diagnose (and treat
or refer) a wide range of related "restorative" issues including
but not limited to esthetics, occlusion, temporomandibular
joint function, vertical dimension, and dental-skeletal re-
lationships. These "other" aspects of diagnosis are essential
for the development of an appropriate treatment plan, which
is necessary for a successful outcome in esthetic implant
dentistry.
In addition, with heightened expectations of esthetics
pushing the art and science of dentistry, it is necessary more
than ever for clinicians to fully understand all the available
treatment options and to be able to appropriately determine
which option to choose, when to use certain techniques, and
how to apply them for each patient scenario.
The minimally invasive approach and techniques present-
ed in this chapter are not the only ways to manage difficult
esthetic cases, and some may consider them controversial. FIGURE 58.36 X-ray of typical fractured central incisor.
Surgical Management of Difficult Radiographic evaluation demonstrates moderate-to-severe

vertical and horizontal periodontal bone loss. The osseous
Cases (Minimally Invasive Approach) crest position, in relation to the gingival margins, appears too
The cause of the failure to satisfy the esthetic needs of a pa- apical to provide adequate gingival support (Fig. 58.33, B).
tient frequently starts with an inadequate examination of the The restorative and periodontal status of the canines is healthy.
soft and hard tissues surrounding the surgical site and the nat-
Treatment Objectives
ural dentition. This can result in an incorrect diagnosis, which
leads to incorrect treatment plan. The wrong treatment plan Considering her age, reasonable esthetic expectation, concern
combined with selection of inappropriate surgical approaches for surgical morbidity, and a lack of willingness to wear a re-
or techniques can result in a disastrous esthetic outcome and movable provisional prosthesis, the treatment objective for
unnecessary patient suffering. The first two case presentations this patient would be to use a surgical approach that mini-
describe the examination and thought processes involved in mizes the extent and number of surgical procedures while
determining the diagnosis and treatment planning of complex providing predictability, longevity, and acceptable esthetics.
anterior cases with extensive alveolar bone loss. The proper Recommending orthodontic extrusion or multiple surgeries
application of the surgical strategies and the minimally inva- to achieve ideal esthetics on this patient would be considered
sive techniques, previously described, are illustrated. The final an excessive treatment plan and would not provide any ad-
case presentation illustrates the minimally invasive approach ditional value or benefits for her.
to posterior implant therapy with the use of short wide im-
Treatment Options
plants, in which esthetics is not the major concern.
Considerations for extracting four maxillary incisors include
the need to remove sound porcelain-fused-to-metal crowns
Components of Esthetic Examination from the canines to replace them as part of a 6-unit fixed pros-
The patient's chief complaint, esthetic zone, tooth positions, thesis. This option has questionable long-term functional and
gingival form, osseous crest position, biotype, tooth shape, esthetic prognosis. Her dentition exhibits evidence of excessive
overbite and parafunctional habit, which may have contribut-
horizontal and vertical ridge deficiency, and occlusal status all
play an important role in deriving an accurate esthetic treated to the alveolar bone loss of the incisors in the first place. The
ment plan for the patient. Therefore, developing the necessary convex shape of the ridge and the lack of osseous support most
skill and knowledge to examine and recognize problems of likely result in substantial horizontal and vertical resorption
these components is an essential first step to clinical success. of the edentulous ridge under the panties of the fixed bridge,
even with extraction socket grafting and ovate provisionaliza-
tion. This will compromise the long-term esthetics.
Case Presentation 1 Even if this patient can tolerate the temporary removable
partial denture, which she said she could not, this option pos-
The first case presented is a simultaneous bone and soft-tissue es a considerable esthetic challenge. The ridge surrounding
augmentation with multiple maxillary anterior immediate im- the extraction sockets will rapidly lose vertical and horizon-
plants placed in a one-stage, flapless approach. tal dimensional soon after the extractions. The loss of vertical
height in the interproximal gingival areas creates an esthetic
Patient Dental History and Chief Complaint
problem that is very difficult to correct. It often requires mul-
The patient is a 70-year-old female with severe mobility and tiple surgeries that have a high incidence of surgical morbidity
discomfort of the maxillary four incisors. Except for a general- and rarely achieves the desired ideal esthetic result. This is
ized feeling of weakness, she is healthy and does not have any especially true in a case like this in which there is extensive
medical contraindications for dental treatment. She presented periodontal vertical and horizontal bone loss. The anticipated
with a desire to replace her maxillary incisors with dental im- vertical ridge collapse after the extraction is substantial, even
plants, but she is very concerned about the physical discom- with bone grafting of the extraction sockets. More importantly,
fort she may experience from the implant surgery. She does the need for multiple surgeries to achieve "acceptable" esthetic
not want to wear a removable prosthesis at all, not even for a results for this patient may be too traumatic for her.
short time. She is content with her present dental esthetics. Extracting four maxillary incisors, immediately placing two
implants, and replacing the teeth with a 4-unit provisional fixed
Examination and Diagnosis partial denture supported by two implants is an acceptable but
The maxillary incisors exhibit moderate-to-severe periodonti- risky treatment option. Immediate provisionalization of the two
tis with 4- to 7-mm periodontal probing depths. They exhibit immediately placed implants, with her occlusion and suspected
severe (2+) mobility with fremitus. The periodontal and re- parafunctional habit, carries the risk of early excessive loading
storative prognosis of these teeth is poor. She has an excessive and implant failure. Additionally, it will be challenging to main-
overbite with evidence of moderate mandibular incisor wear, tain the vertical and horizontal ridge dimensions in the edentu-
indicating possible parafunctional habits. Her incisors are lous area under the panties. Most likely it will require additional
slightly elongated, but the dentogingival symmetry is accept- soft-tissue augmentation procedure(s) to achieve "acceptable"
able (Fig. 58.33, A) The shape of the incisors is slightly tri- esthetics in the pantie area (ie, missing central incisor area).
angular with sufficient interdental papilla volume and height. Extracting four maxillary incisors, immediately placing
Interproximal gingival tissue is not swollen or edematous. four implants in the sockets, and replacing the missing teeth
Her gingival biotype appears to be on the thin side with slight with a 4-unit provisional fixed partial denture supported by
marginal inflammation, and the position of the labial gingival four implants is another acceptable option. Splinting four
margins is already high (ie, maximal apical position). Any fur- provisionals together should provide sufficient resistance and
ther recession will be unaesthetic. protection to the implants from early excessive loading. Some
FIGURE 58.33 A, Clinical photograph of periodontally compromised maxillary anterior teeth with long clinical crowns. The presenting esthetic
status is not ideal. However, the dentogingival symmetry is fair as the gingival margin is approximately the same for all incisors (cuspids, laterals, and
centrals). B, Periapical radiographs of the maxillary anterior teeth reveal moderate to severe horizontal periodontal bone loss with vertical intrabony
defects. C, Simple, atraumatic extraction of the maxillary incisors reveals sockets with unsupported interdental tissues. Note that there are no incisions
or flap reflection, which has preserved the blood supply and integrity of the interdental soft tissues. D, Guide pins placed in prepared implant sites
reveal good position within the extraction sockets achieving good primary stability from the palatal aspect of the socket. E, Implants with temporary
abutments and crescent shaped, free gingival grafts (not yet sutured). F, Implant provisional abutments are prepared and provisional restorations are
fabricated using conventional methods. G, One-year postloading results show nearly complete preservation of the interproximal papilla height and
improved labial gingival biotype. Labial gingival margins are substantially coronal in position as compared to the initial levels. H, The final restorations
have a more normal length offering the patient a much more youthful smile. Preexisting moderate to severe attrition is noted on the incisal edges of
the mandibular anterior teeth. I, Periapical radiographs at 1 year of the implants with final restorations reveal good preservation of interproximal bone
height with minimal saucerization. The platform-switched implant restorations likely contribute to the preservation of bone.
clinicians do not recommend placing implants next to each Treatment Sequence

other in the lateral and central incisor positions because they In complex treatment involving dental implants, the treat-
are often positioned too close and it is very difficult to create ment plan must be sequenced and coordinated between the
or maintain an interdental papilla that emulates an interden- restorative dentist and the surgeon before starting the treat-
tal papilla between an implant and a tooth or between two ment. This is especially true when immediate provisionaliza-
natural teeth. However, the more recent use of implants with tion is planned. This will enhance success and help make the
a platform-switching design may change the spatial require- treatment more patient friendly.
ments for achieving an interdental papilla between implants.
The bone between implants appears to be better protected, Surgical Procedure
and as a result, the vertical height of the interproximal tissue
Once the patient is anesthetized, the incisors are extracted
may be better preserved. If procedures are carried out proper-
atraumatically, ensuring that gingival tissues, especially the in-
ly, this option can provide a long-term functional and esthetic
terdental papilla are not damaged (Fig. 58.33, C). The sockets
result, with minimal discomfort to the patient.
are prepared to receive implants by removing the sulcular epi-
1. Extract four maxillary incisors and replace them with a thelium, and by completely and thoroughly removing all granu-
conventional (6-unit) fixed prosthesis supported by the lation tissue. Immediately placed implants must have complete
canines. primary stability at the time of placement. Proper vertical posi-
2. Extract four maxillary incisors and wait for healing of the tion, buccolingual position, and mesiodistal position, as well as
sockets and ridge while temporarily replacing the missing buccolingual angulation, are all critical factors for a successful
teeth with a removable partial denture. Plan to place two outcome. Implants in anterior sockets are prepared and placed
or four implants after 3-6 months of healing using either a toward the palate (Fig. 58.33, D) to ensure sufficient labial
one- or two-stage approach. bone thickness for labial margin stability. Once the provisional
3. Extract four maxillary incisors, immediately place two im- healing abutments are accurately seated (may require bone pro-
plants in the lateral positions and replace the missing teeth filer), the labial void of the sockets are grafted with particulate
with a 4-unit provisional fixed partial denture supported bone and a crescent-shaped free gingival tissue graft is harvest-
by two implants. ed and placed over the graft (Fig. 58.33, E) as described previ-
4. Extract four maxillary incisors, immediately place four im- ously and in the literature. Using this technique, all four teeth
plants in the sockets and replace the missing teeth with a can be augmented in one surgery with minimal discomfort to
4-unit provisional fixed partial denture supported by four the patient. Once the soft-tissue crescent grafts are secured with
implants. sutures, the provisional abutments are prepared for provisional
crowns. The provisional crowns (splinted) are fabricated using
Surgical Strategy for Predictable Esthetics conventional methods (Fig. 58.33, F). Contours of the provi-
Due to the patient's age and reasonable expectation, the level sional crowns may need to be modified as the healing and re-
of the esthetic goal determined for this patient is not ideal modeling occurs. Impression taking for the final restoration is
but is acceptable. This level of esthetics can be predictably relatively easy because the provisional abutments placed at the
achieved in a minimally invasive, patient-friendly manner. time of surgery and modified during healing nicely shape the
By mentally visualizing the surgical and prosthetic goal, an tissues for an optimal prosthetic emergence profile.
acceptable esthetic outcome can be achieved for this patient
if the existing heights of the interproximal gingival tissues Results
can be maintained. Additionally, if the existing biotype and The 1-year result shows nearly complete preservation of the
the level of the labial gingival margin can be overbuilt with interproximal papilla height, an improved labial biotype with
hard and soft-tissue augmentation, the final esthetic outcome labial gingival margins that are substantially coronal to the
is enhanced. If this can be accomplished with simultaneous original gingival margin level (Fig. 58.33, G) The final re-
implant placement, it minimizes the number of surgeries result is crowns with a more normal incisor length and a more
quired. In this case, especially as the patient appears to have youthful smile (Fig. 58.33, H). There is some gingival irregu-
parafunctional habits, it is desirable to place more implants larity noted, which appears to be a result of the soft-tissue
and use them to support the immediate provisionalization. grafting. These areas could easily be smoothed with gingivo-
Considering all of these treatment options, the treatment plasty, but the patient refused. Radiographs reveal preserva-
that is most compatible with this patient's surgical strategy for tion of interproximal bone with minimal saucerization around
predictability, acceptable esthetics, and long-term results is the implants with a platform-switch design (Fig. 58.33, I)
treatment option 4, extraction of the incisors followed by im- After the surgical strategies described and using minimally
mediate placement of four implants with an immediate provi- invasive surgical techniques, this 70-year-old patient received
sional restoration supported by the implants. immediate implant-supported replacement of severely compro-
mised maxillary incisors with an acceptable (or better) esthetic
Treatment Plan and Rationale result and minimal treatment discomfort. With one surgery, in-
Four maxillary incisors are to be extracted, and four implants cluding the extractions, she was provided with a fixed implant
placed immediately in a one-stage approach with simultaneous restoration on four implants. In the same surgery, the bone and
bone and soft-tissue grafting. The bone and crescent-shaped soft tissue was augmented while preserving the interdental pa-
free-gingival grafting technique is used to overbuild labial gingi- pilla. She experienced very little postoperative pain and was
val biotype. A tapered implant with platform-switching design pleased with her new, more youthful-looking smile. The treat-
is to be used. The tapered design has shown to promote prima- ment time was only 6 months from extraction to final restora-
ry stability in sockets, and the platform-switching design bet- tion. She was never without teeth and never wore a removable
ter maintains the interimplant bone. An immediate provisional prosthesis. The improvement of the labial gingival margin was
restoration without centric contacts is attached to the implants. achieved without orthodontic extrusion or multiple surgeries.
Case Presentation procedure(s) and concerned the procedures will interfere with
her busy schedule. She prefers a fixed provisional during the
Case presentation 2 is a simultaneous extensive bone augmen- healing period if possible.
tation with multiple mandibular anterior immediate implants
placed in a one-stage approach with labial flap reflection. Examination and Diagnosis
The patient's mandibular incisors exhibit severe periodontal
Dental History and Chief Complaint
and endodontic infections with periodontal pockets extend-
The patient is a 41-year-old female with severe periodontal ing to the apex on several of her teeth. Porcelain-fused-to-
and endodontic infection affecting her mandibular anterior metal crowns with overhanging margins are splinted together.
teeth. She is experiencing pain, halitosis, and a bad taste in The gingival tissue is swollen, erythematous, and heavy exu-
her mouth. She is healthy and does not present with any dation is expressed from the gingival margins with palpation
medical contraindications for dental treatment. She is frus- (Fig. 58.34, A) She has a difficult time brushing because of
trated by her current dental condition because she recently re- the pain from the infection. Radiographic evaluation reveals
placed the crowns on the involved teeth. She understands the severe generalized vertical and horizontal periodontal bone
hopeless condition and would like to replace the teeth with loss around the incisors with endodontic involvement. Exist-
dental implants, but she is apprehensive about the surgical ing endodontic treatment showed inadequate obturation and
FIGURE 58.34 A, Splinted porcelain-fused-to-metal crowns with overhanging margins on mandibular incisors that are infected. The gingival tis-
sues are swollen with moderate to severe inflammation. B, Radiograph reveals severe generalized vertical and horizontal bone loss from periodontal
and endodontic infections. C, Alveolar bone shows extensive destruction from periodontal and endodontic infections. D, With a surgical stent, the
proposed implant sites are visualized and the surrounding bone is evaluated. E, Visualizing how the adjacent bone topography (socket walls) will con-
tribute to bone formation around the implants, it is evident that even without grafting, most of the implant surface will become integrated with bone.
F, Layers of resorbable collagen membrane cover the bone graft material.
FIGURE 58.34 (cont.) G, Full-thickness periosteal flaps are released, adapted around the healing abutments and sutured. H, Three months after
surgery, the provisional restoration shows healing gingival tissues with sufficient ridge height and volume. I, Four-year results show acceptable esthetic
implant restorations in a stable ridge with a wide zone of keratinized, attached gingiva. J, Periapical radiographs at 4 years demonstrate good bone
regeneration and maintenance with osseointegration of all implants.
apical seal (Fig. 58.34, B). These mandibular incisors have It is common to expect a loss of vertical height ranging from
poor periodontal and endodontic prognosis. The remaining 5 to 10 mm after extraction of multiple mandibular inci-
dentition is stable. She is not overtly concerned with esthetics, sors with severe bone loss. Surgical procedures used in an
but desperately wants relief from pain, halitosis, and the bad attempt to regain the vertical height of the ridge for accept-
taste in her mouth. able esthetics in this region carry substantial risk and mor-
bidity Once the ridge collapses, any vertical ridge augmen-
Treatment Objectives tation procedure requires extensive labial flap releasing to
The immediate focus for this patient is to make her comfort- close over the grafting material and membrane. These large
able by eliminating the source of infection as soon as possible. flaps often dehisce from the tension caused by the lower lip
However, considering her esthetic requirements, concern for muscle movements and require more time to heal by sec-
surgical morbidity, and preference for a fixed provisional, an ondary intention with potentially compromised outcome.
important treatment objective for this patient would be to Even when flap closure is maintained, extensive labial
identify a surgical approach that minimizes the extent and flap releasing frequently results, obliterates the vestibu-
number of surgeries while providing predictability, longev- lar space, and creates mucogingival problems, which may
ity, and acceptable esthetics. Getting into a situation in which require additional surgery to correct. The ridge augmen-
multiple extensive surgeries are necessary to achieve accept- tation procedure can be done on an incremental basis to
able esthetics would be difficult for both the clinician and the minimize surgical complications, but the patient is sub-
patient. jected to multiple surgeries and prolonged treatment time.
Distraction osteogenesis is an option to gain back the lost
Treatment Options ridge height, but there are other problems associated with
1. Extracting six mandibular incisors and replacing missing this approach, and it also requires multiple patient visits
teeth with a removable provisional prosthesis immediately with extended use of a removable provisional prosthesis.
addresses the patient's chief complaints, but because of the However, the biggest disadvantage to this direction of
anticipated severe ridge collapse after the extractions, this treatment is that whichever ridge augmentation procedure
approach will most likely result in a situation in which is used to reconstruct the ridge, it is extremely difficult to
multiple extensive surgeries will be necessary to achieve gain back the vertical ridge height that was lost. The final
acceptable esthetics. esthetic result is usually disappointing.
2. Extracting six mandibular incisors and augmenting the alveolar bone height by acting as tent poles to support the
ridge/sockets with particulate bone graft using a labial flap grafting material and membrane. The ridge will be overbuilt
approach to completely remove granulation tissues and ex- in anticipation of augmentation tissue/material shrinkage. If
pose healthy alveolar bone is better than the first but still the implant-bone relationship is favorable, a one-stage ap-
requires considerable labial flap releasing to close over the proach can be used and an immediate fixed provisional resto-
grafting material and barrier membrane. ration can be delivered at the time of surgery.
There is risk of flap dehiscence during healing for the rea- Considering all of these treatment options, the treatment
son mentioned previously. Due to the postoperative swell- that is most compatible with this patient's surgical strategy for
ing and ridge dimensional changes, maintaining the flap predictability, acceptable esthetics, and long-term results is
closure under a removable provisional prosthesis is diffi- treatment option 3, extraction of the mandibular incisors, im-
cult. Complete bone regeneration will take 6-10 months, mediate placement of implants (provided the implant-bone
depending on the type of bone grafting material used, and relationship is favorable), bone augmentation with particulate
the total treatment time will be prolonged. Most often, bone graft and barrier membrane, and immediate fixed provi-
multiple surgeries are required with several provisional sional restoration supported by the implants. Again, provided
modifications to obtain the desired esthetics. However, the the implant-bone relationship is favorable).
biggest disadvantage of this treatment option is the inabil-
ity to predictably reconstruct the lost vertical ridge height. Treatment Plan and Rationale
The final esthetic result is typically disappointing, espe- To decrease the infectious process, alleviate symptoms,
cially considering the enormous time and effort invested in and improve tissue quality, initial therapy consisted of pa-
treatment. tient education, oral hygiene instructions with an ultrasoft
3. Extracting six mandibular incisors, immediately placing toothbrush, chlorhexidine rinses, and 1 week of antibiotic
four implants, augmenting the alveolar defects with par- therapy [eg, Augmentin 500 mg, by mouth (PO), every 8 h
ticulate bone graft and resorbable membranes, and replac- (q8h) X 7 days]. Six mandibular incisors will be extracted
ing the missing teeth with a 6-unit provisional fixed partial using a labial full-thickness flap reflection to ensure complete
denture supported by four implants is the third option. removal of the granulation tissue and to visualize the bony
(Note: It is preferable to place implants in a one-stage ap- architecture. If the implant-bone relationship is favorable for
proach and to restore them with a provisional restoration, bone regeneration around the restoratively determined im-
but the decision depends on the relationship of the implant positions (canines and laterals), implants are immedi-
plants to the surrounding bone.) ately placed in a one-stage approach with simultaneous bone
If implants are placed immediately using a two-stage ap- augmentation, which allows immediate provisionalization of
proach (ie, flap release with primary closure), there will be these implants. Since the bone in the anterior mandible is
similar surgical risks and esthetic limitations as described dense, sufficient primary stability for immediate provisional-
for treatment option 2. However, this option has some ad- ization can be easily achieved. If the bone architecture is unfa-
vantages over treatment option 2. The implants placed at vorable for a one-stage approach, the implants are placed in a
the time of extractions will function as tent poles to sup- two-stage approach with simultaneous bone grafting, barrier
port the bone graft materials and membrane and will be membrane, and primary flap closure. If a one-stage implant
osseointegrated and able to support a fixed provisional placement is achieved, the implant position is recorded (ie,
restoration in approximately 6 months. This will minimize indexed) at the time of surgery for the purpose of laboratory
the required time that the patient will have to endure a provisional fabrication, and the provisionals are delivered
removable provisional prosthesis. If the implant-bone re- within 1-2 weeks after surgery. The bulk of the surgical swell-
lationship is favorable enough to place the implants in a ing should have subsided at that time. An Essex provisional
one-stage approach (ie, the implant will be positioned in is delivered at the time of surgery for temporary esthetic re-
an intraosseous location or within the bony envelope and placement of the missing teeth. The patient is in provisional
not supracrestal or outside the bony envelope), the surgi- restoration for 6 months to ensure implant integration and
cal risks and morbidity will be less and an immediate fixed periimplant tissue stabilization. A final restoration can be fab-
provisional restoration can be delivered at the time of the ricated and delivered at that time.
surgery. This treatment option more predictably preserves
the vertical height of the ridge, and avoids the likelihood Treatment Sequence
of severe ridge collapse following extractions. Only this Impressions are taken at the initial oral hygiene appointment
treatment option offers a reasonable possibility of provid- and used to fabricate a surgical guide and an Essex provisional
ing anesthetic implant restoration; it is accomplished with restoration.
a minimal number of surgeries and less surgical risk. During the surgical appointment, the anterior mandibu-
lar teeth are extracted, and the surgical treatments are carried
Surgical Strategy for Predictable Esthetics out as outlined in the treatment plan. The Essex provisional
Due to the patient's reasonable expectation, the level of the is delivered, and patient is dismissed. If all goes as planned
esthetic goal selected for this patient is not an ideal level but and implants are immediately placed in a one-stage approach,
an acceptable level. This level of esthetics can be predictably the fixed provisionals are delivered in 1-2 weeks. The fixed
achieved in a minimally invasive, patient-friendly manner. provisional restoration is replaced with the final restoration in
Mentally visualizing the final result with clinical and radio- approximately 6 months.
graphic data, an acceptable esthetic outcome can be achieved
for this patient if the existing heights of the lingual and inter- Surgical Procedure
proximal bone can be preserved with grafting. If the implants Once the patient is anesthetized, the incisors are extracted
can be placed immediately, they will assist in preserving the with minimal damage to the delicate gingiva. The interdental
papillae are severed at the crest, and a full-thickness labial flap bone was harvested, the donor surgical site was minimized
is reflected. The flap is designed with divergent vertical inci- and postoperative discomfort was minor. The grafted material
sions at the mesial line angles of the first premolars to facilitate was covered with two layers of resorbable collagen membrane
surgical access and wound closure. A lingual full-thickness (Bio-Gide, Osteohealth, Shirley, NY) to isolate and protect the
flap is reflected just enough to expose the crest of the lingual graft material (Fig. 58.34, F). The labial flap periosteum was
bony wall. Granulation tissue is thoroughly debrided to pre- adequately released to minimize flap tension during closure
pare the bone for implant placement and bone augmentation and healing. The flaps were adapted around the healing abut-
(Fig. 58.34, C) ments and sutured with interrupted 4-0 chromic gut sutures
The initial impression of the extensive bony destruction (Fig. 58.34, G) The mucogingival junction and the vestibular
observed after complete debridement suggests that immediate depth were not appreciably altered because it was not neces-
implant placement may not be possible and certainly immedi- sary to advance the flap significantly The Essex provisional
ate implant placement in a one-stage approach is doubtful. was delivered to the patient, making sure that the apical edges
However, when the surgical guide is put in position, the bony did not cut the sutures or impinge on the wound during the
architecture surrounding the proposed implant sites indicates postoperative healing and probable swelling. The patient was
a favorable implant-bone relationship (Fig. 58.34, D) and a dismissed with postoperative instructions.
good potential for bone regeneration around the immediately Ten days after the surgery and after the postoperative swell-
placed implants, even in a one-stage approach. Mentally vi- ing has mostly subsided, the lightly secured healing abut-
sualizing the final result again with the bone exposed con- ments were removed. The laboratory-fabricated provisionals
firms that an acceptable esthetic result can be achieved for were carefully placed; making sure to avoid tissue impinge-
this patient because the existing heights of the lingual and ment. Provisional bridges should be sectioned before placing
interproximal bone can be preserved with immediate implant and rejoined after the placement on the implants. The joined
placement and bone augmentation. contacts should be strong enough to avoid being separated
It has been documented in the literature and confirmed during mastication. The patient should be seen on a monthly
with clinical cases that if implant(s) are placed within the basis to enforce good oral hygiene and to evaluate tissue heal-
bony envelope of the ridge (ie, in an intraosseous relation- ing and provisional stability (Fig. 58.34, H) The provisional
ship with the surrounding bone), the bone regeneration po- restoration is replaced with a final restoration in approximate-
tential around immediately placed implant(s) is favorable ly 6 months.
even when there is a labial dehiscence. Furthermore, when
the implant head is positioned at or below the crest of bone Results
in an intraosseous relationship to the surrounding bone and The 4-year result demonstrates an acceptable esthetic implant
bone grafts are used with barrier membranes, bone will pre- restoration in a stable ridge with sufficient vertical height and
dictably fill to the top of the implant and integrate with the horizontal volume. There is a wide zone of keratinized, at-
implant surface. tached gingiva (Fig. 58.34, I) Periapical radio graph ( 4 years)
Therefore, the four implants are placed, according to these indicates bone regeneration and maintenance at the top of the
principles, in the sites determined by the surgical guide. The implants. All implants are stable and appear to be osseointe-
apical-coronal position of the implant is partially dictated by grated (Fig. 58 34, J).
the adjacent level of the bony wall, but care is taken to avoid By following the surgical strategies described and using
placing them more than 4 mm below the anticipated labial minimally invasive techniques, this 41-year-old patient was
gingival margin of the final restorations. The implants are provided with esthetic dental implant restoration with a mini-
placed as far lingual as reasonably possible to maximize the mal number of surgeries and treatment time. Her immediate
distance from the implant to the labial envelope of the residual complaints were addressed without the need for multiple
ridge to enhance the likelihood of achieving an intraosseous extensive surgeries. She did experience some postoperative
relationship with the surrounding bone. Imagining how the pain and swelling, but her entire treatment required only
adjacent bone topography (socket walls) contributes to bone one surgery and the total treatment time was only 6 months
formation around the implants, it is evident that even without from extractions to the final restoration. She was provided im-
grafting, most of the implant surfaces will become integrated mediately with an Essex provisional restoration, which was
with bone (Fig. 58.34, E). Once a favorable potential for bone replaced with a laboratory-fabricated fixed provisional resto-
regeneration around the implants was ascertained, the deci- ration attached to the implants 10 days after surgery. She was
sion to proceed with a one-stage implant placement approach comfortable throughout the duration of the treatment.
was confirmed. Long implants (15 mm length) were placed This surgery may appear very extensive and at first impres-
to ensure sufficient primary stabilization that, when splinted sion not minimally invasive. However, any treatment option
together, would be capable of withstanding occlusal loads. A other than this approach would most likely require multiple,
rapid setting registration material was used to register the im- more extensive surgeries with higher surgical morbidity and
plant position for provisional fabrication. Healing abutments much longer treatment time. More critically, because it is dif-
(5 mm tall) were lightly secured to the implants for the initial ficult to reconstruct vertical ridge height after it is lost, the
postoperative healing phase. biggest disadvantage of the other treatment options is that
For more complete bone regeneration around the implants the final esthetic result is more often than not disappointing.
and to overbuild the ridge dimensions, the site was aug- Therefore, even with the extensive bone loss observed in this
mented with particulated autogenous graft and mineralized case, immediate implant placement in a one-stage approach
allograft. A thin layer of particulated autogenous bone har- with simultaneous bone augmentation and immediate provi-
vested from the ramus area was placed directly on the implant sionalization is considered by many to be a minimally invasive
surfaces to enhance integration, and the allograft was layered and patient-friendly approach to providing esthetic dental im-
to overbuild the ridge. Since only a small piece of the ramus plant therapy.
Case Presentation 3 recipient site to maximize bone contact between it and the
donor bone. Even in the cases in which the graft has sur-
Case presentation 3 illustrates the use of short wide-diameter vived, there is substantial vertical height loss as the result
implants to treat a severely resorbed mandibular posterior of postsurgical resorption. As with the other two options,
ridge. the final ridge height is often insufficient to place implants
Dental History and Chief Complaint with longer lengths.
4. Vertical ridge augmentation with particulate bone and
The patient is a 65-year-old female with a severely resorbed membrane has provided vertical height gains up to several
mandibular posterior ridge. She is frustrated with her partial millimeters, but depending on the type of bone graft used,
denture and wants dental implants to give her better "chew- it can increase treatment time substantially. If autogenous
ing" ability. She does not present any medical contraindication bone graft is used, there will be increased postoperative
for dental treatment, but she is anxious about extensive dental surgical morbidity as the result of the donor site wound.
surgeries. The esthetic outcome is not a concern for her. Maintaining the flap closure over the grafted ridge and
Examination and Diagnosis membrane is difficult, and clinicians have experienced in-
creased surgical complications. It is a technique-sensitive
The patient's posterior ridge of the mandible shows exten-
and skill-dependent procedure. Furthermore, the verti-
sive vertical ridge resorption with a narrow band of keratin-
cally augmented bone can be unstable, and the resulting
ized gingiva at the crest. The ridge height is near the floor of
ridge is often insufficient to place implants with longer
the mouth, with frenum and muscle pull on the buccal side
lengths.
(Fig. 58.35, A). The radiographic vertical height of the ridge
5. Vertical augmentation using bone morphogenetic pro-
measured from the crest to the mandibular canal is approxi-
teins (BMPs) and space-maintaining membrane or tita-
mately 7 mm (Fig. 58.35, B). Clinical examination shows
nium mesh has the advantage of limiting or eliminating
what appears to be a narrow ridge, but the horizontal width
the need for donor sites to harvest autogenous bone.
of the ridge measured at the bony crest with a caliper is ap-
However, many clinically important questions related to
proximately 8 mm. A 3D scan (eg, CT or CBCT) can confirm
the predictability of augmentation with biologic mediators
this finding. The typical anatomy of mandibular and maxillary
such as BMPs remain unanswered. As with other vertical
posterior segments after severe vertical resorption cases often
augmentation procedures, the surgical challenge of main-
has sufficient ridge width for implant placement.
taining flap closure over the grafted ridge and membrane
Treatment Objectives or titanium mesh is difficult. The commercially available
biologic mediator such as BMP is expensive, and the surgi-
Considering her concerns about surgical morbidity, the treat-
cal procedure is a technique-sensitive and skill-dependent
ment objective would be to identify a surgical approach that
procedure.
minimizes the extent and number of surgeries while provid-
6. Implant placement with mandibular nerve reposition-
ing predictability and longevity. Attempting to reconstruct the
ing can provide the opportunity for placement of longer
vertical height of the deficient posterior ridge with multiple
implants by repositioning the inferior alveolar nerve, but
extensive surgeries would be difficult for both the clinician
there is an increased surgical morbidity and complications
and the patient.
associated with it. Also, it is a technique-sensitive and
Treatment Options skill-dependent procedure.
7. Placing multiple, short wide-diameter implants. Since
1. Distraction osteogenesis can provide sufficient vertical examination of the alveolar dimensions reveals an 8-mm
height for normal implant placement, but it most likely horizontal width and a 7-mm vertical height, it is possible
requires multiple surgeries, may be associated with high to plan for the placement of four short wide-diameter im-
surgical morbidity, and certainly increases treatment time. plants. To increase the biomechanical stability, the restora-
Furthermore, performing this procedure in a severely re- tions are splinted together. Since bone dehiscence is not
sorbed posterior mandible area is challenging, technique- anticipated, these implants can be placed using either a
sensitive, and skill-dependent. one-stage or two-stage approach, depending on the cli-
2. Interpositional bone augmentation can provide sufficient nician's preference. A one-stage approach would further
vertical height for normal implant placement, but as with reduce the number of required surgeries and treatment
the distraction osteogenesis approach, it requires multiple time. Preparation of precise osteotomy sites is important
surgeries, longer treatment time, and high surgical mor- for short implants to ensure good stability. A mild-to-mod-
bidity of both the donor and recipient sites. Performing erate amount (eg, two threads) of bone loss around short
this procedure in a severely resorbed posterior mandibular implants is more significant than the same amount of bone
area is challenging, technique-sensitive, and skill-depen- loss around longer implants because it results in a greater
dent. Furthermore, the ridge height initially gained using percentage of lost support relative to the implant length.
interpositional grafts has been shown to decrease during
healing, and often, the resulting ridge is insufficient to Treatment Plan and Rationale
place implants with longer lengths. Since there is an 8-mm horizontal width and only a 7-mm
3. Vertical ridge augmentation with autogenous monocorti- vertical ridge height at the three distal implant sites, three
cal bone block can provide vertical ridge height gain, but 5-mm diameter X 5-mm long implants are placed. A 4-mm
as with the other two options, there is increased surgical diameter X 7-mm long implants are placed in the most an-
morbidly of both the donor and recipient sites. It will re- terior site because the ridge is narrower ( "'6 mm) and taller
quire multiple surgeries and longer treatment time. This ("'9 mm). These implants will be placed in a two-stage ap-
surgical approach often requires extensive reshaping of the proach to accommodate the clinician's preference, but with
FIGURE 58.35 A, Severely resorbed ridge in the posterior mandible in a 65-year-old female. Examination reveals a narrow band of keratinized, at-
tached gingiva at the ridge crest. B, Panoramic radiograph of patient in (A) showing a limited vertical height of bone above the inferior alveolar nerve of
approximately 7 mm. C, Clinical view of prepared implant osteotomy sites in the posterior mandible. Despite the severe vertical ridge resorption, most
of the time there is sufficient ridge width in posterior sites to accommodate wide-diameter implants. D, One 4-mm-diameter short (7-mm) implant and
three 5-mm-diameter short (5-mm) implants were placed with good initial stability. The bone width was adequate, and there were no implant thread
exposures. E, The final implant restorations were fabricated with gold occlusal surfaces and splinted together. Adequate interproximal spaces were
created for oral hygiene access. F, Periapical radiograph (13 months postloading) reveals stable crestal bone height despite the long crown-to-implant
ratio. G, Another follow-up periapical radiograph (30 months postloading) reveals continued stability of the crestal bone height. Platform-switched
abutment/restorations, adequate biomechanical support, and careful occlusal design contributes to bone preservation and maintenance.
precise surgery, they could be placed in a one-stage approach. E). The restorations have a platform-switching configuration
This surgery does not require special skills, and if the restor- to enhance crestal bone preservation, and they are splinted
ative treatment plan is properly executed, the use of short im- together with sufficient embrasure for proper oral hygiene.
plants will provide predictability and longevity
Results
Treatment Sequence A periapical radiograph, taken 13 months after loading,
No special treatment sequencing is necessary This procedure shows a stable crestal bone level despite the long crown-to-
is facilitated, like all implant surgeries, by using a surgical implant ratio of the restorations (Fig. 58.35, F). The implant
stent and following a proper restorative treatment plan. abutments have platform-switching design, which has been
shown to preserve crestal bone. A periapical radiograph, taken
Surgical Procedure 30 months after loading, shows long-term crestal bone stabil-
Once the patient is anesthetized, a crestal incision is made, ity without further bone loss around the short wide-diameter
bisecting the existing band of crestal keratinized tissue. Buccal implants (Fig. 58.35, G)
and lingual full-thickness flaps are reflected to clearly visual- This patient was provided with a very functional stable im-
ize the full width of the ridge. Sutures can be used to keep plant restoration in just 3 months using short wide-diameter
the flaps away from the surgical site. Properly spaced oste- implants. The other possible treatment options for this pa-
otomy sites are prepared to accommodate one 4-mm diameter tient would have required multiple surgeries and would have
and three 5-mm diameter implants (Fig. 58.35, C). Implants increased the risk of surgical morbidities and complications.
are placed with very good primary stability and no bone Treatment time would have been much longer and the re-
dehiscence(s) (Fig. 58.35, D) The flaps are closed with a com- sults may have fallen short of the treatment goal. This case
bination of mattress and interrupted sutures. The exposure of offers a sound example of how patients with extensive verti-
the implants and the fabrication of the restorations are done cal bone loss in posterior regions can be treated using short
3 months after the implant placement. Since the esthetic is not wide-diameter implants with a minimally invasive, patient-
the major concern for the patient, the clinician elected to use friendly surgical approach, without sacrificing predictability
gold metal occlusal surfaced implant restorations (Fig. 58.35, and longevity
FIGURE 58.37 Flapless dental implant microsurgery.

-
---·
surface level or the angle of adjacent implant healing caps.
This permits optimal parallel positioning and depth of adja- FIGURE 58.51 Piezosurgery device by Mectron Medical Technology.
cent implants. The implant drill angle can also be accurately

oriented to root surface angulation using just 3-4 mm of root clinical applications to other fields of medicine. The extraor-
anatomy exposed between the cementoenamel Junction and dinary cutting properties of piezoelectric bone surgery have
the osseous crest. These reference points are simply not vis- been introduced and applied in maxillofacial surgery, cranial
ible without a microscope. The detection of subtle angulation and spinal neurosurgery, and hand-foot surgery.
reference points and changes in drill position permit feedback The most compelling characteristics of piezoelectric bone
correction, which is important for osteotomy preparation in surgery are low surgical trauma, exceptional control dur-
extraction sockets. The microscope-enhanced accuracy of os- ing surgery, and a fast healing response of tissues. Clinical
teotomy microsurgery permits socket implant placement in studies demonstrate that the specificity of operation and the
an ideal position followed by an esthetic implant-supported techniques employed with piezoelectric bone surgery make
provisional (Fig. 58.37). As a flapless procedure, this is ac- it possible to advantageously exploit differences in hard- and
complished with minimal patient morbidity. soft-tissue anatomy. This not only increases treatment effec-
tiveness but it also improves postoperative recovery and heal-
ing. Experimental studies on animals have shown faster tissue
Conclusions healing when compared to traditional cutting instruments.
Some of the advantages of microsurgery for extraction and Ideally, surgical trauma should be minimized to obtain the
implant placement have been described with an emphasis on optimal healing, which depends on gentle management of soft
tissue management and the ability to enhance visualization of and hard tissues. Surgery, by definition, alters normal physiol-
details, which translates into better results. This microsurgery ogy by interrupting the vascular supply of tissues. The degree
protocol advances dentistry from an era of traumatic tooth of surgical invasiveness is extremely important for the quality
extraction to one of seamless immediate tooth replacement of tissue healing and may effect whether wounds heal by re-
using implant microsurgery. pair or regeneration. Indeed, when surgical trauma is kept to
a minimum it generates enough stimulation to favor healing
mechanisms that lead to regeneration. On the other hand, sur-
Piezoelectric Bone Surgery gical techniques that are more traumatic often lead to greater
inflammatory responses with slow healing that may lead to
Ultrasound has been used for many years in periodontics to repair and scarring rather than regeneration. For this reason, it
remove tartar, debride root surfaces, and to degranulate peri- is desirable to choose the least-traumatic surgical instruments
odontal defects. In the past decade, a novel family of ultrason- and techniques for any surgical procedure. Piezoelectric bone
ic-powered devices has been developed that is revolutionizing surgery was conceived and developed precisely to overcome
maxillofacial bone surgery. the limits of traditional bone-cutting instruments and to
A new surgical technique, known as piezosurgery, was in- achieve the most effective treatment with the least morbidity.
vented by Vercellotti and developed by Mectron Medical From a mechanical standpoint, the effect of burs or twist
Technology. The piezosurgery device (Fig. 58.51) consists of a drills on bone is characterized by lamellar fracturing in areas
piezoelectric ultrasonic transducer powered by an ultrasonic adjacent to the cut surface and the deposition of large bone
generator, capable of driving a range of specially designed cut- fragments and debris in the endosteal spaces. This finding is
ting inserts (Fig. 58.52). Box 58.6 describes the main cutting thought to be, at least in part, responsible for the inflamma-
properties of piezosurgery by Mectron, and Box 58. 7 describes tory process that takes place in the immediate postsurgical
piezosurgery inserts. Piezoelectric bone surgery techniques wound healing and for the delay of osteogenesis observed in
have been developed for clinical applications in dentistry these wounds. On the other hand, the micromechanical cut-
and are becoming state of the art for a variety of procedures. ting action of piezoelectric bone surgery results in microniza-
Recently, Piezosurgery Medical expanded development of tion of the cut bone and does not cause lamellar fracturing in
58 Surgical Concepts of Implant Therapy 717 .el
FIGURE 58.38 A, Periotome extrac-

tion of lateral incisor. B, Noninvasive
extraction of lateral incisor.
Microsurgical Tooth Extraction

Tooth extraction has been traumatic for centuries. Conven-
tional tooth extraction may require mucogingival flaps and
bone removal, resulting in compromised esthetics. Employ-
ing a microscope with minimally invasive principles reduces
trauma and results in predictable esthetic outcomes. Instru-
ment selection influences the trauma of tooth removal. Peria-
tome luxation or leveraged mechanical extraction employing
tapped root anchorage systems can carefully separate a tooth
from its surrounding ligament and lift it vertically from the
socket. This limits injury to papillae and preserves natural
gingival anatomy (Fig. 58 38). Subtle nuances in luxation di-
rection can be microscopically detected for root removal in a
proper anatomic path of extraction. Increased visibility under
the microscope permits most extractions without mucogin-
gival flaps. Greater visibility also permits atraumatic section-
ing of ankylosed roots to leave alveolar bone and soft tissue FIGURE 58.39 Palatal wall socket osteotomy.
uninjured. Apical granulomatous lesions can be completely
debrided with full visibility Such minimally invasive micro-
surgical techniques translate into reduced patient morbidity
with enhanced healing.
proper pressure and rotational speed are applied to varying
Implant Drilling in the Extraction Site bone densities encountered in the socket. The angular veloc-
ity at the cutting edge of a 4-mm drill is several times faster
Microsurgical implant drilling in the extraction socket is than the velocity at the cutting edge of a 2-mm drill. For this
unique. Under the microscope, a socket appears as large as a
reason, pressure and rotation of larger diameter drills must be
room with its apex and walls clearly visible. A different set of
decreased to compensate for their faster cutting speed. En-
skills is required for socket drilling. For placement of maxil-
hanced visual feedback for speed and pressure correction is
lary anterior implants, the most favorable bone lies to the pal-
accomplished through directly viewing the advancing drill
atal (Fig. 58.39). Drilling therefore must be done at an angle
under the microscope.
to the palatal socket wall. Twist drills innately track toward
the direction of less dense bone and into the open socket.
Bone Grafting
Drilling sockets under a microscope utilizes visual feedback to
constantly redirect the drill to the correct position and angu- The osteotomy in an extraction socket is prepared in the pala-
lation. This avoids the common mistake of an implant being tal wall. This placement results in a gap between the implant
placed too far toward the buccal. With the magnification and and the buccal socket wall. To avoid displacing a particulate
lighting a microscope provides, implants can be placed in the graft, the provisional is finished before a socket bone graft is
palatal socket wall with good initial stability and ideal esthetic placed. The socket is filled with xenograft to within a millime-
position. Microscope-enhanced dimensional and angular per- ter of its crest. Xenograft is selected to reduce remodeling re-
ceptions allow adjustments to correct drilling speed. Too little sorption of the buccal bone. Filtered bone from the osteotomy
or too much drill pressure or excessive drill speed causes fric- preparation is rinsed with 3% tetracycline solution then con-
tional heat. This adversely affects implant osteointegration. densed on the top of the xenograft. Finally, it is covered with a
Detecting micromovement of the advancing drill ensures that layer of microfibrillar collagen to contain the graft.
FIGURE 58.40 Facial connective tissue graft.
FIGURE 58.41 A, Screw-retained provisional before finishing. B,

Screw-retained provisional after finishing.
Buccal Gingival Grafting
Recession on the buccal gingival margin around anterior im- (Fig. 58.41). Subgingival provisional contours created under
plants placed in extraction sockets has been well documented. the microscope provide tissue support and well-finished mar-
Multiple factors, such as the periodontal biotype, presence or gins. The provisional crown on the implant serves a number
absence of the buccal cortical plate, surgical trauma, implant of functions as follows:
position, and the emergence profile of both the provisional
and final restorations, are associated with such recession. A 1. It provides optimal esthetics and function.
subepithelial connective tissue graft is therefore harvested 2. It minimizes tissue collapse by supporting the gingival
from the palate and transferred into a split-thickness envelope tissue .
incision on the buccal of the implant. A connective tissue graft 3. It obturates the surgical extraction socket to contain par-
is done to maintain or augment gingival height and thickness ticulate and soft-tissue grafts.
that may have been lost as the result of injury (Fig. 58.40). Creating an implant provisional crown begins before
Even gingival tissue at a normal height can be expected to re- the tooth is removed. A clear silicone impression captures
cede as much as 1.5 mm unless gingival grafting is performed. the dentogingival junction and its proximal tooth contours
Placing a subepithelial connective tissue graft concurrent with (Fig. 58.42). Tooth color-matching is done and a light-cured
implant placement insures stability of the postoperative gin- flowable composite resin duplicate of the tooth is created
gival level. using the impression (Fig. 58.43). The duplicate crown is
trimmed to the exact location of the dentogingival junction
Immediate Provisional Fabrication then hollowed to create a shell crown. It is fitted to a screw-
retained titanium provisional abutment that is opaque for a
To preserve natural esthetics and provide support for gingi- color match (Fig. 58.44). Great attention is paid to the incisal
val anatomy, an implant provisional must emerge from the edge position of the shell crown before luting it to the abut-
surrounding gingival tissue exactly like the extracted tooth. ment with flowable composite resin. Screw access for removal
The surgical microscope gives dentists the visibility neces- of the provisional is accomplished by drilling through the in-
sary to fabricate ideal anatomy for implant provisional crowns cisal one-third of the provisional crown.
.
FIGURE 58.42 A, Clear silicone impression of failing tooth crown. B, Clear silicone impression filled with composite.
58 Surgical Concepts of Implant Therapy 717 .e3
The luted abutment and crown are removed and placed machined titanium provisional abutment ensures good mar-
on a laboratory handle to facilitate shaping and polishing (see ginal fit and reduces the possibility for the loosening.
Figs. 58.4 7 and 58.48) Each provisional crown has a unique-
ly shaped subgingival emergence profile that duplicates the Immediate Implant Occlusion
original tooth. Voids and rough edges are eliminated, and the
provisional is carefully shaped under the microscope to pro- Early loading bone trauma is minimized in multiple immedi-
vide gingival support (Fig. 58.45). Shaping the provisional is ate implant provisional cases by splinting. Early loading bone
accomplished with a 12-fluted finishing bur, glass nail file, trauma in single implant cases is reduced by lessening oc-
and a prophylaxis cup with pumice. Attention to detail is clusal forces. Symmetric and light mesial and distal proximal
critical. As a final step, the provisional crown is glazed and contacts are established and the provisional is taken out of
thoroughly cured. Light curing the composite ensures that no centric and lateral occlusal contact using 1-mm green occlusal
free monomer is present to irritate soft tissue or bone. The indicator wax. This technique allows patients to leave the den-
tal office with a nonloaded esthetic provisional tooth securely
anchored to the implant (Fig. 58.46)
Custom Impression Transfer Coping

A custom impression transfer coping is necessary to pre-
serve and communicate gingival supporting contours to the
ceramicist. The chairside-created provisional anatomy must
be precisely reproduced for the dental laboratory via the cus-
tom impression transfer coping. To make the custom transfer
coping, an impression of the gingival third of the provisional
crown is made with an implant analog attached (Fig. 58.4 7).
This registers the implant platform orientation and preserves
the provisional anatomy The crown is removed, and a stan-
dard impression coping is attached to the implant analog.
Acrylic powder is filled into the gap between the impression
coping and the clear silicone impression. Monomer liquid is
FIGURE 58.43 Shell composite crown created from impression. then infused into the powder to create a hard acrylic copy of
FIGURE 58.44 A, Opaque titanium temporary abutment. B, Composite crown luted to opaque titanium temporary abutment.
FIGURE 58.45 Provisional supporting gingival tissue. FIGURE 58.46 Provisional 1 week after implant microsurgery.
FIGURE 58.47 Clear silicon impression of provisional.
provisional anatomy. Using a 25-gauge needle to apply mono-

FIGURE 58.48 Custom impression transfer coping reproducing
mer to the powder from the base up minimizes inclusion of emergence profile.
air bubbles in the custom transfer coping. For orientation, a
mark is initially applied to the labial of the provisional impres-
sion. It is transferred to the custom transfer coping to provide
Final Implant Restoration
orientation for the restorative dentist during final impressions
(Fig. 58.48). This technique allows precise communication Final impressions are taken, using the custom impression
from the surgeon to the restorative dentist to the ceramicist transfer coping. Computer-assisted scanning and machining
of the anatomy required for a final restoration that esthetically creates a zirconia abutment and zirconia coping for an all-
supports gingival tissue. ceramic crown (Fig. 58.49). Zirconia has the benefit of tissue
FIGURE 58.49 A, Before microsurgery. B, Immediately after microsurgery. C, Provisional 8 weeks after microsurgery.
FIGURE 58.50 A, Before microsurgery. B, Immediately after microsurgery. C, Final restoration.
biocompatibility and light translucency. The sequence de- original tooth shape. Working as a team, surgeon, restorative
scribed ensures a final implant abutment and crown that ex- dentist, and laboratory technician can create a final restoration
actly matches both the provisional emergence profile and the in harmony with preserved gingival architecture (Fig. 58.50).
-s
I
r-- V)
1-- r--
C) 1--
C)
(A) (B)·~ (C). ·i, (D) •._ :.
~
V)
I
o...
(E) (F) (G) (H)-
-
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LJ.J
(I)
FIGURE 58.52 Specially designed cutting inserts. A, Piezosurgery osteotomy 7 insert: OT7 (0.5 mm thick). B, Piezosurgery osteotomy 7 special
insert: OT7S (0.35 mm thick). C, Piezosurgery osteoplasty 1 insert: OPl. D, Piezosurgery osteoplasty 3 insert: OP3. E, Piezosurgery implant site prepa-
ration 1 insert: lMl. F, Piezosurgery implant site preparation 2 insert: IM2. G, Piezosurgery implant site preparation 3 insert: IM3. H, Piezosurgery
periodontal surgery 2 insert: PS2. I, Piezosurgery elevation (of schneiderian membrane) 1 insert: EL 1.
ana Cutting Properties of Piezosurgery by Mectron

Piezosurgery is an electronic device that generates ultrasonic microvibrations at variable frequency. Its technology is unique in the
world (US Patent 6,695,047B2) for the characteristic vibrations generated in parallel and variable frequency modulation for precise
cutting of bone with different degrees of density.
The unit has a display that allows the operator to select either the BONE or ROOT operating modes. The BONE cutting mode is
used to cut bone with selections that are specific to bone type or density. The ROOT mode is used to shape, debride, and smooth root
surfaces (both external: periodontal and internal: endodontic).
BONE OPERATING MODE
Cortical Bone
The basic low ultrasonic frequency (30 kHz) is overmodulated by sound waves for cutting and removing small cortical bone fragments.
Spongy Bone
The basic low ultrasonic frequency is overmodulated by sound waves that are slower than those for cortical bone, which is better for
cutting and removing cancellous bone fragments.
ROOT OPERATING MODE
Periodontal Surgery
The low ultrasonic frequency without overmodulation is set at an ideal power level for scaling, debridement, and root planing.
Endodontic Surgery
The ultrasonic frequency is set at an ideal power level for retrocanal and intracanal debridement after root canal treatment.
The mechanical action of bone cutting takes place thanks to the linear microvibrations of inserts with a variable range from 20 to
80 µm, depending on efficiency. Piezosurgery inserts are classified based on their functional and clinical characteristics.
FUNCTIONAL CLASSIFICATION
1. Sharp: These inserts have sharp ends for osteotomy and osteoplasty. They are made of nitride titanium steel and they are gold in
color.
2. Smoothing: These nitride titanium inserts are diamond coated and gold in color. Their different granulometry produces a
smoothening action that is generally used to complete the cut near soft tissue.
3. Blunt: These steel color inserts are characterized by rounded ends and are generally used to refine the cut in contact with soft
tissue.
The inserts described in the functional classification as sharp, smoothing, and blunt have clinical classification codes that relate to
their specific use.
CLINICAL CLASSIFICATION
1. OT: The identification code for inserts used to perform osteotomy is OT followed by a number.
2. OP: The identification code for inserts used to perform osteoplasty is OP followed by a number.
3. EX: The identification code for inserts used to perform extraction is EX followed by a number.
4. IM: The identification code for inserts used to perform implant site preparation is /M followed by a number.
adjacent bone, which may favor exposure and release of bone range of approximately 80 µm and a frequency of 30,000
morphogenetic proteins and be responsible for the early onset times a second. A sound wave is overmodulated on this base
of osteogenesis at these sites (see later). Furthermore, there frequency, which generates a hammering action with very lit-
may be a diminished inflammatory response since there is tle heat because the mechanical energy necessary to produce
little or no need to remove damaged bone and surgical debris the microvibrations is very low. This action, along with the
as compared to conventional rotary-drilled sites. water spray, facilitates removal of bone debris.
Piezoelectric osteotomies are easy to create, but it is impor-
tant to recognize that the technique and instrument handling
Clinical Characteristics of Ultrasonic are different than the technique using a traditional handpiece
Cutting with rotary instruments. The piezosurgery insert is applied to
The primary clinical characteristics of the piezosurgery cut- the bone with a relatively light stroke similar to the smooth
ting action include microprecision, selective cutting, maxi- precision used to draw a picture. Heavy pressure or force is
mum visibility, and excellent healing. not required. Indeed, the pressure applied by the surgeon to
the piezosurgery handpiece is much lower than the pressure
typically applied to a rotary or oscillating type handpiece,
which uses mechanical macrovibrations for cutting. This
Microprecision
characteristic provides maximum control during surgery and
Piezosurgery cuts mineralized tissues with microprecision. makes this technique unique especially in areas with delicate
The cut is made by mechanical microvibrations at a linear anatomy
Selective Cutting with increasing diameters under profuse irrigation to create a

precise osteotomy site in the bone for the placement of a den-
Piezosurgery ultrasonic microvibrations are low frequency tal implant. The site is prepared, and the implant positioned
and selective for cutting mineralized tissue only. These mi- to avoid important anatomic structures, such as the inferior
crovibrations are physically unable to cut soft tissue. Clearly, alveolar nerve, sinus cavities, and teeth, and to optimally sup-
the most significant demonstrated benefit of piezosurgery se- port and emulate the planned prosthetic tooth replacement(s).
lective cutting is the ability to preserve the integrity of soft Proper implant position is important for optimal function and
tissues, such as the alveolar nerve, the infraorbital nerve, the es the tics.
maxillary sinus membrane, and the dura mater, while effec- Clinicians determine implant positions based on presurgi-
tively cutting the mineralized tissue (bone) in close proximity cal diagnostic imaging, study models, and the use of a diag-
to these tissues. nostic wax-up of the planned tooth replacement(s). The actual
or final position of the implant(s) results from the surgeon's
Maximum Visibility interpretation of diagnostic information and his or her ability
to translate that information to the patient at surgery. Most
Piezosurgery creates a surgical field that is blood free during often, the surgical "guide" between the diagnostic information
cutting because of its cavitation effect. Cavitation is a physi- and the patient is an acrylic stent, fabricated by a laboratory
cal phenomenon that, from a clinical standpoint, happens technician that may or may not have precise guide channels
with the nebulization of the saline solution. The slight hy- for implant positioning. Consequently, inaccuracies in the
dropneumatic pressure applied by piezosurgery temporarily stent fabrication and movement of the stent during surgery,
stops bleeding from both hard and soft tissues. It is important as well as variations in the use of the stent during surgery, can
for the liquid pump to be flowing properly and for the cut- lead to imprecise implant positioning.
ting action to be intermittent to maintain optimal surface mi- Recent advances in implant surgical technology include the
crocirculation, especially for long surgical procedures. Tissue following:
perfusion resumes shortly after cutting (and cavitation action)
is stopped. • Computer-imaging software used preoperatively to "simu-
late" the implant position(s) into a virtual patient, that is,
a 3D computer image of the patient's jaw created from the
Excellent Healing computed tomography (CT) scan data.
Clinical studies comparing use of piezoelectric bone surgery • Computer-generated surgical guides with drill sleeves based
with traditional rotary instruments for third molar extractions on the presurgical "virtual" implant positioning are used to
and periodontal surgery have reported better recovery and place implants more accurately in the "planned" locations.
fewer postoperative symptoms in those treated with piezo- • Computer-assisted implant surgery (CAIS) uses simultane-
surgery. Postoperative healing after piezoelectric bone sur- ous tracking and "guidance" of the implant instrumentation
gery is characterized by minimal swelling and little bleeding to accurately follow the planned treatment during surgery.
and postoperative morbidity is lower compared to traditional The actual trend is to use two different approaches:
techniques. Gingival tissue is typically light in color when
compared to the appearance of autogenous gel of platelet-rich • CT based images where the correlation with the patient
plasma. anatomy is done with radiomarkers.
• Novel real-time ultrasound or contact probe 3D mapping,
which captures positional data at the time of patient posi-
Conclusions tioning. There is no need for image matching or fusion.
Piezosurgery is a new surgical technique for bone surgery with CAIS is the most sophisticated and perhaps the most
many clinical applications in dentistry. The extraordinary cut- promising of these technologies because it has the greatest po-
ting properties and applications of piezoelectric bone surgery tential to reduce surgical time, minimize surgical invasiveness,
were described. The most compelling characteristics of piezo- and result in a more precise translation of implant planning to
electric bone surgery are low surgical trauma, exceptional pre- the actual surgical procedure. CAIS immediate mapping has
cision, and fast healing response. As a result, piezosurgery has the advantage of an immediate chairside procedure, which
the ability to increase treatment effectiveness while improving can be performed without CT scan images. Understandably,
postoperative recovery and healing. CAIS is also the technique that requires the greatest amount of
Although a great deal of scientific research focuses on new preparation and coordination of the patient, image data, and
products for tissue engineering and bone regeneration, the surgical instrumentation. This chapter provides a conceptual
importance of minimal surgical trauma for optimal bone heal- overview of the techniques and terminology used in CAIS.
ing and regeneration should not be overlooked. A new appre-
ciation for the effectiveness of piezosurgery has the potential
to redefine the concept of minimally invasive surgery in oste- Uses and Requirements
otomy and osteoplasty procedures. Computerized navigation surgery evolved from early appli-
cations in neurosurgical procedures and continues to evolve
Computer-Assisted Implant Surgery today with applications in many surgical specialties. Clearly,
the advantage of using a computer to assist surgery is the pre-
Implant surgical procedures have more or less remained the cision that it offers. There is also a real-time safety control ob-
same since the introduction of osseointegrated dental im- tained with multiple imaging sources facilitating a minimally
plants. In brief, implant placement surgery involves the use of invasive approach to surgical procedures. As in medicine, 3D
a full-thickness flap elevation and a sequential series of drills imaging is used in dentistry to facilitate presurgical planning
Clinical Applications the periodontal bone and soft tissues to a more apical position
with appropriate biologic dimensions and minimal periodon-
There are many important clinical applications of piezoelectric tal inflammation.
bone surgery in dentistry. In fact, nearly all techniques previ- The clinical crown lengthening technique entails perform-
ously performed with burs, twist drills, chisels, or oscillating ing a periradicular ostectomy of a few millimeters, which al-
saws have the potential to be performed with piezosurgery. lows repositioning of the periodontal flap in a more apical
For 10 consecutive years the author Tomaso Vercellotti has position. The positive result obtained is that the health of
used piezosurgery on a daily basis for oral, periodontal, and the treated part is preserved even though the normal gingi-
implant surgical procedures, enabling him to develop tech- val morphology is altered. Clinical application must include
niques and protocols for each. Readers are referred to online esthetic assessment, as well as an assessment on the position
materials and other publications for detailed descriptions and and health of the adjacent periodontium.
step-by-step instructions on these piezosurgery protocols. A The traditional surgical technique entails raising a full-
brief overview of basic clinical applications using piezoelectric thickness flap, performing the ostectomy with manual in-
surgery is described here. struments, osteoplasty with a bur for crest bone architecture
recontouring, periradicular bone removal, root planing, and
Periodontal Surgery finally replacing the flap in an apical position.
The ostectomy is simple to perform using piezosurgery
The use of piezosurgery in periodontal surgery simplifies and in direct contact with the root surface because control of the
improves handling of soft and hard tissues. In resective peri- instrument during surgery is precise, even in very difficult
odontal surgery, for example, after raising the primary flap proximity cases (piezosurgery OP3 insert). The root planing
with a traditional technique, using a scaler-shaped insert (PS2) phase can be performed very effectively using blunt ultrasonic
(Fig. 58.53, A) or an insert in the shape of a rounded scalpel inserts (piezosurgery PP 1 insert).
(OP3) makes it easier to detach the secondary flap and remove Saline solution cavitation reduces bleeding during surgery
inflammatory granulation tissue. This phase has little bleeding and facilitates debridement of the surgical area. This effect is like-
as the result of the cavitation of the saline solution (coolant). ly responsible for the excellent soft-tissue healing result, which
With the right inserts and power mode, the ultrasound de- is always characterized by a light color and without edema.
vice facilitates effective scaling, debridement, and root planing A histologic study conducted by Harvard University
(Fig. 58.53, B and C). In particular, debridement with a spe- showed a better healing response for bone and root cemen-
cial diamond-coated insert enables thorough cleaning even for tum in teeth that were crown lengthened using piezosurgery
interproximal bone defects (Fig. 58.53, D) The mechanical as compared to teeth that were crown lengthened with tradi-
action of ultrasonic microvibrations, together with cavitation tional rotary instruments. Concerning the latter, the tungsten
of the irrigation fluid (pH neutral; isotonic saline solution) carbide bur is more favorable than the diamond-coated bur
eliminates bacteria, toxins, dead cells, and debris, which cre- for the bone healing process.
ates a clean physiology for healing. Healing is improved by The crown lengthening technique performed with piezo-
applying ultrasound to produce micropits at the base of the surgery using appropriate inserts makes it possible to effec-
defect to activate cellular response of healing mechanisms. tively reduce bone while preserving root surface integrity.
Autogenous bone-grafting material consists of bone chips that
are collected during the piezoelectric osteoplasty operation
for recontouring bone irregularities (Fig. 58.53, E). The result Tooth Extraction Techniques
is that this technology reduces the invasiveness of traditional Today, tooth extraction is often the first step in the prepara-
surgery by making surgery faster and by ensuring thorough tion for implant placement. Maintaining the integrity of the
cleaning of the periodontium. It also favors tissue healing by alveolar bone walls is an essential part of this process. Con-
using bone removed in the osteoplasty procedure to graft os- sequently, whether an implant is being placed at the time of
seous defects. extraction or not, the selection of instruments and techniques
Piezosurgery in periodontal surgery redefines the guide- that minimize trauma to socket walls is critical.
lines that mark the border between resective treatment and Anatomic differences greatly influence the difficulty of ex-
regenerative treatment. Indeed, the choice between a resective traction and the challenge of maintaining alveolar bone walls.
technique and a regenerative technique generally depends on A new bone classification system has been developed that
the depth of the bone defect, whether it is higher or lower makes it easier to choose the best surgical tooth extraction
than 3.5 mm. technique for different anatomic situations (Table 58.1). The
The ability to work on the bone defect with magnifying aim is always to preserve the integrity of the alveolar walls
systems makes it possible to exploit the benefits of piezosur- and the morphology of soft tissue. This classification divides
gery microprecision in preparing the recipient site and stabi- anatomy into four types depending on the anatomic charac-
lizing micrografts (Fig. 58.53, F-H) teristics of periodontal biotype and anatomy/pathology of the
periodontal ligament. Classifying anatomy into type 1, 2, 3,
Crown Lengthening or 4 simplifies the diagnosis and the subsequent surgical de-
cision. Each type corresponds to a different anatomic issue,
Clinical crown lengthening is the most common periodon- which requires a specific extraction technique and determines
tal surgical (ostectomy) operation performed in otherwise the most effective surgical instruments.
healthy periodontal conditions. The indication for this proce- Type 1 anatomy describes a normal periodontal biotype
dure is usually associated with a need or desire to expose more and a normal periodontal ligament (ie, no pathology). This
tooth structure because of short clinical crowns and/or loss of anatomic condition poses little surgical difficulty. A traditional
clinical tooth structure. In general, the goal is to reposition extraction technique using manual instruments is sufficient.
FIGURE 58.53 Clinical case demonstrating the use of piezoelectric bone surgery for periodontal surgery. A, Ultrasonic scaling using piezosurgery
PS2 insert. B, Root surface debridement using piezosurgery diamond-coated OPS insert. C, Ultrasonic root planing using piezosurgery blunt insert:
PP1. D, lnterproximal infrabony defect with probe. E, Autogenous bone chip-harvesting technique using piezosurgery osteoplasty insert: OP3. F, Au-
togenous bone grafting technique. G, Collagen membrane stabilizing microbone grafting. H, Flap repositioned and sutured.
Type 2 anatomy describes a thin periodontal biotype with a preservation of alveolar crestal bone while achieving maxi-
normal periodontal ligament. The surgical difficulty for tooth mum primary stability
removal is minimal. However, preserving the integrity of the The second advantage of UISP is the fast clinical healing of
thin alveolar walls makes the extraction more complex. In this both soft and hard tissue. Animal research demonstrates that
situation, the normal displacement operation runs the risk of new bone formation (neoosteogenesis) is active at implant
creating a dehiscence from fracturing the thin buccal corti- sites prepared with piezoelectric bone surgery earlier than at
cal plate. To avoid this risk, a root fractioning technique that sites prepared with traditional techniques. A histomorpho-
makes it possible to obtain root mobility inside the alveolus to metric study on mini-pigs showed more bone formation and a
eliminate the risk of damaging the thin labial and crestal bone greater density of periimplant osteoblasts at implant sites pre-
is recommended. pared with piezosurgery as compared to sites prepared with
Type 3 anatomy describes a normal periodontal biotype twist drills.
with an ankylotic periodontal ligament. The surgical difficulty The improved healing response observed at piezoelectric
for tooth removal is high because it is not possible to obtain bone surgery-treated sites (compared to sites prepared with
the mobility necessary for displacement. The traditional tech- traditional drills) may be explained by differences in the level
nique uses a periradicular osteotomy with burs. This is pos- of bone morphogenetic proteins (BMPs), growth factors, and
sible without much consequence for mandibular third molars cytokines. In an animal study comparing the biomolecular pro-
but results in serious damage to the alveolar walls of all the file of sites prepared with piezoelectric bone surgery or rotary
other teeth. The recommended technique creates the space drills, BMP-4 increased earlier at implant sites prepared with
necessary for extraction by operating only on the root surface piezoelectric bone surgery As compared to drilled sites, the lev-
through a root-plasty maneuver. The tooth is removed from els of BMP-4 at piezoelectric bone surgery-treated sites were
the socket by cutting the root surface without touching the al- 18.5 times higher at 7 days, 15 times higher at 14 days, and 2
veolar bone. This technique is easy to perform with excellent times lower at 56 days. The peak levels of BMP-4 were observed
control using specific piezosurgery inserts. at 14 days for piezoelectric bone surgery-treated sites. The level
Type 4 anatomy describes a thin periodontal biotype and an of BMP-4 at drilled sites did not reach the same level of BMP-4
ankylotic periodontal ligament, which is a combination of the achieved at piezoelectric bone surgery-treated sites until day
challenging aspects of type 2 and type 3 anatomy The surgi- 56. There was also a greater increase in the level of transforming
cal difficulty for tooth removal is the highest. In the anterior growth factor p2 (TGF-P2) cytokine at implant sites prepared
maxilla, where esthetics are important, a root-sectioning tech- with piezoelectric bone surgery techniques. As compared to
nique that divides the root into segments with a mesial-dis- drilled sites, the levels of TGF-P2 at piezoelectric bone surgery
tal cut is recommended. This allows the separate pieces (eg, treated sites were 3. 5 times higher at 7 days, 19 times higher at
buccal and palatal) to be removed internal to the socket with 14 days, and diminished below baseline at 56 days. The level of
minimal force applied to the socket walls. TGF-P2 at drilled sites never exceeded baseline levels.
Proinflammatory cytokine tumor necrosis factor a, proin-
Simplified Tooth Extraction flammatory and bone-resorbing cytokine interleukin-If (IL-
In addition to the techniques described, there is a simplified lP), and antiinflammatory cytokine IL-10 were also measured.
version to assist most extraction operations. This technique In general, the expression of these proinflammatory cytokines
consists of cutting the root surface with a thin, cone-shaped was higher in the early experimental phases of drilled sites
diamond-coated insert that cuts the outer circumference only, which also showed more inflammatory cells. The piezo-
of the tooth in manner similar to a crown preparation electric bone surgery-treated sites showed a higher expression
(Fig. 58.54). This operation, performed under magnification, of the proinflammatory and bone-resorbing cytokine IL-lP at
enables preservation of the alveolar bone, which is important 56 days. This latter finding might be indicative of bone re-
for the placement of dental implants. The reader is referred modeling at day 56 in piezoelectric bone surgery treated sites
to other publications for more information and details on this (IL-lP is involved in osteoclast differentiation).
technique. It is assumed that the micronization of the bone reduces
cut trauma while saline solution cavitation produces debride-
ment of the osteotomy surfaces with exposure and preserva-
tion of a high number of BMPs and growth factors. These
Special piezosurgery inserts developed for bone perforation proteins are capable of increasing the mitosis of stromal stem
have enabled the development of a new technique for ultra- cells and osteoblasts.
sonic implant site preparation (UISP). Extensive experience The surgical technique entails an osteotomy preparation us-
gained over 5 years using the technique to prepare more than ing a series of piezosurgery insert. The preparation is initiated
1500 implant sites has culminated in the development of a with the narrow, pointed IMl insert (Fig. 58.56, A). Parallel
protocol with significant clinical advantages. pins are used throughout the procedure to check alignment
The first advantage of UISP is related to the cutting char- (Fig. 58.56, B). The 2-mm-diameter IM2 insert is used to fur-
acteristics of piezosurgery, which facilitate differential prepa- ther prepare the osteotomy (Fig. 58.56, C). The coronal as-
ration of the cortical and cancellous bone. A surgical bone pect of the preparation is widened with the pilot 2/3 insert
classification system was developed that simplifies the diagno- (Fig. 58.56, D), and the osteotomyis finished with the IM3 insert
sis and surgical decision-making process by exploiting differ- (Fig. 58.56, E) Final cortical preparation is accomplished with
ences in bone anatomy (Fig. 58.55). The differential implant the IM4 insert (Fig. 58.56, F). After pilot 3/4 insert (Fig. 58.56,
site preparation (DISP) technique can be used within the ini- G), the implant osteotomy is completed (Fig. 58.56, H) If de-
tial osteotomy site to correct the implant axis by selectively sired, before implant placement, osteoplasty of the crestal bone
directing the cutting action in the desired direction. DISP is possible with the OP3 insert (Fig. 58.56, I). Final occlusal
can also be used in combination with twist drills to facilitate view of implant placed in a narrow ridge (Fig. 58.56, J).
FIGURE 58.54 Case demonstrating use of piezoelectric bone surgery for tooth extraction. A, Radiograph of mandibular incisors with severe
periodontal bone loss that are to be extracted because of a hopeless prognosis. B, The piezosurgery insert operates only on the root surface without
cutting, damaging, or overheating the surrounding bony walls of the extraction socket. C, The piezosurgery insert is directed at cutting the root surface
only (root-plasty) without cutting, damaging, or overheating the surrounding bony walls of the extraction socket in this simplified extraction technique.
D, Mobility is obtained with an elevator in a mesial-distal direction. E, Teeth are extracted with forceps after displacement. F, Notice the preservation
of the alveolar bone. The narrow socket walls are completely intact after this root-plasty extraction technique. G, Implant placement and particulate
bone grafting of extraction socket defects. H, Flap closure and suturing.
0 2 ~3
(A)
H M L
(B)
FIGURE 58.55 Surgical bone classification by Tomaso and Giuseppe Vercellotti. A, Cortical crestal thickness in millimeters. B, Radiographic can-
cellous bone classification.
FIGURE 58.56 Implant site preparation and placement. A, Piezosurgery insert (IMl) used to start the implant site preparation. B, Parallel pin in place
to check the direction of osteotomy. C, Piezosurgery 2-mm diameter insert (IM2) for pilot osteotomy. D, Piezosurgery insert for cortical preparation (pilot
2/3). E, Cancellous bone preparation with piezosurgery insert IM3. F, Piezosurgery diamond-coated insert (IM4) for final cortical bone preparation.
FIGURE 58.56 (cont.) G, Piezosurgery pilot insert 3/4 in action. H, Occlusal view of completed implant site preparation. I, Osteoplasty of crestal
bone in the periimplant area using piezosurgery insert OP3. J, Occlusal view of well-placed implant despite the narrow ridge.
Advanced Clinical Applications

Sinus Lift
Procedures used to lift the floor of the maxillary sinus for
bone augmentation make it possible to use dental implants to
replace teeth in the atrophied posterior maxilla. Approaches
to sinus lift techniques typically involve the use of a lateral
window or crestal osteotomy. The lateral window approach
enables the surgeon to visually see and monitor the integrity
of the sinus membrane at each step in the process. The crestal
osteotomy approach is a blind technique because it is not pos-
sible to visually observe the schneiderian membrane during
preparation (ie, the orifice is limited in size if being used for
implant placement). In some cases, when the crestal window
FIGURE 58.57 Schneiderian membrane observed through the crest-
is slightly larger (eg, when simultaneous implant placement is
al osteotomy prepared for sinus lift with piezosurgery inserts. Notice
not anticipated), the schneiderian membrane can be observed the membrane is exposed through the crestal bone and elevated without
during the lift procedure (Fig. 58.57). perforation.
The lateral window approach entails the opening of a bony
window through the lateral wall of the maxillary sinus cavity.
This window is generally prepared in the premolar to first mo- the average of 30% with rotary instrumentation to only 7%
lar area. The traditional technique using a high-speed rotary with piezosurgery. The authors stated that all incidences of
bur to remove bone runs a high risk of damaging the schnei- membrane perforation occurred during hand instrumentation
derian membrane, which often results in membrane perfora- and were not caused by the piezosurgery inserts. The use of
tion (approximately 14-56% incidence). piezosurgery for lateral window osteotomy has greatly reduced
In 2000, a new technique was developed that entails cutting the incidence of membrane perforation even in cases of par-
an antrostomy (lateral window) using piezosurgery. This tech- ticularly difficult anatomy with thin schneiderian membranes.
nique has greatly reduced the risk of membrane perforation The surgical technique entails a lateral window osteotomy
(approximately 5-7%). In a series of 100 consecutive cases, that traces the frame of the bony window, which is then re-
Wallace et al reported the perforation rate was reduced from moved (Fig. 58.58, A and B). Separation of the membrane
FIGURE 58.58 Sinus bone augmentation using a lateral window approach. A, Lateral window osteotomy outline created using a piezosurgery
diamond-coated scalpel (OT1 ). B, Complete bony wall removal to expose the schneiderian membrane. Notice the membrane is completely intact
without damage or perforations. C, Initial membrane separation from the edges of the lateral window using a noncutting piezosurgery insert (EL 1 ). D,
Membrane elevation with a manual instrument. E, Schneiderian membrane completely elevated. Ball probe used to evaluate adequate height of sinus
lift. F, Implant site is prepared with piezosurgery inserts after sinus membrane elevation for simultaneous bone augmentation and implant placement.
G, Bone augmentation material is inserted and packed to fill prepared sinus cavity.
from the inner wall is made using an inverted cone insert that Ridge Expansion
detaches the membrane around the perimeter of the bony
window (Fig. 58.58, C). This reduces membrane tension fa- Horizontal alveolar ridge expansion is an extremely useful
cilitating further separation and lifting with piezoelectric or technique for increasing bone width and simultaneously plac-
manual instruments (Fig. 58.58, D-F). Once completely eling implants in narrow ridges. The great advantage is that
evated, bone augmentation material is inserted and packed both augmentation and implant placement are accomplished
and the bony window is closed with a collagen membrane in one surgical procedure. A possible disadvantage is that
(Fig. 58.58, G). crestal bone loss may be greater in cases that begin with very
Piezosurgery simplifies the sinus lift technique and in- narrow ridges.
creases predictability with its selective cutting action, which Clinical and radiographic evaluation of the size, shape, and
enables surgeons to maintain membrane integrity. This has morphologic characteristics of the alveolar bone in the ridge
resulted in a considerable reduction in patient morbidity in is necessary to determine whether to use a ridge expansion
maxillary sinus surgery. or a traditional bone augmentation technique (Fig. 58.59, A).
FIGURE 58.59 Ridge expansion. A, Evaluation of narrow (3-mm wide) posterior mandibular ridge with a periodontal probe. B, Horizontal and
vertical osteotomies prepared with narrow (0.35 mm) piezosurgery insert (OT75). C, Initial implant site preparation started with piezosurgery insert
IM1. D, Screw expanders used to separate bone segments and begin expanding alveolar ridge. E, Differential implant site preparation (DISP) using
piezosurgery insert OT4. F, Mandibular ridge expanded, implant sites prepared, and three implants simultaneously placed. Periodontal probe dem-
onstrates final ridge width.
In brief, it can be said that this technique exploits bone elas- There are two piezosurgery inserts used for performing this
ticity so it is necessary to know the bone anatomy of each bone chip-harvesting technique. Osteoplasty insert 1 (OPl)
implant site. In particular, the morphology of the crestal bone is the most effective because it is large and quickly harvests
and the thickness of the buccal cortical and lingual cortical bone fragments. However, the size and surgical movement re-
plates in relation to the amount of cancellous bone present in quires donor sites with ample surface area. It is generally used
the ridge greatly influences the ease and ability to prepare an in bone grafting techniques for implant surgery Osteoplasty
osteotomy and to expand the ridge. The technique requires insert 3 (OP3) is smaller and tends to harvest smaller bone
preservation of periosteum integrity while elevating mucogin- fragments in any anatomic situation. It can be used in any site
gival flaps enough for access to create the appropriate oste- to collect bone for any bone grafting technique, but is best
otomy Piezosurgery is an indispensable tool used to create a used in limited areas to harvest smaller quantities of bone for
horizontal osteotomy through the alveolar bone crest caused periodontal osseous defects.
by its precise (narrow) cutting action. In some cases (eg, areas
of dense bone with little elasticity), it may also be necessary Clinical Note. It is advantageous to use 0Pl/OP3 inserts
to make one or two vertical cuts in the alveolar bone to al- to collect bone (for grafting defects) while performing other
low ridge expansion. The horizontal osteotomy is expanded procedures (eg, in maxillary sinus lift surgery while remov-
in subsequent steps using piezoelectric inserts for implant site ing bone from the lateral window osteotomy or in periodontal
preparation together with screw-type or fan-type expanders surgery while recontouring bone with osteoplasty/ostectomy).
for increasing the diameter or section, respectively
Expanding a narrow ridge by the entire width (diameter) Block Harvesting Technique
of the planned implant(s) may be challenging because of the Choosing an appropriate donor site and selecting the best in-
density of cortical bone and limited elasticity The need to ex- struments and technique for harvesting block bone are im-
pand or displace the buccal cortical bone can be reduced (ie, portant decisions in the success of bone augmentation with
less than the implant diameter) with rigorous application of monocortical bone block grafts. Harvesting block bone with
DISP to the lingual cortical bone (ie, preferential preparation piezosurgery is extremely simple, precise and fast.
of the lingual side), which is generally thicker than the buc- The most common donor sites for harvesting monocorti-
cal cortical. This is difficult to do with traditional twist drills cal-cancellous block bone are the mandibular ramus and sym-
because they cannot limit cutting to one side and tend to get physis (chin). The surgical operation with piezosurgery offers
displaced by areas of dense bone into areas of loose or missing considerable precision and operating sensitivity during sur-
bone (ie, twist drills are deflected away from dense cortical gery so that the operator is able to easily recognize differences
bone). In fact, attempting to prepare the site (between sepa- in cortical and cancellous bone allowing him/her to preserve
rated cortical plates) with traditional drills can fracture the the integrity of important structures.
weaker, inelastic buccal cortical bone, making simultaneous Harvesting a monocortical-cancellous bone block from the
implant placement impossible. mandibular ramus is generally preferable to the symphysis re-
Piezoelectric bone surgery has radically simplified the gion because of the reduced level of morbidity Evaluation of
ridge expansion technique in the horizontal osteotomy presurgical 3D scan images facilitates measurements and deter-
phase, which can be performed with micrometric precision, mines how much bone can be harvested with respect to the po-
and in the site preparation phase, which exploits the differ- sition of the inferior alveolar nerve canal, the position of molar
ent degree of cortical resistance compared to cancellous bone roots, and the width of the mandible in the ramus area. Osteot-
(Fig. 58.59, B-F) omies performed with piezosurgery allow an extremely precise,
clean, and smooth vertical cut through bone with excellent vis-
Bone Harvesting ibility The result is that a cortical block can be removed with
a portion of spongy bone and its surface is extremely regular
The bone harvesting technique using piezosurgery is effec- compared to blocks harvested from the chin.
tive for harvesting bone fragments and for removing blocks of This technique is very predictable because it facilitates
monocortical-cancellous bone. harvesting the maximum amount of bone with respect to the
donor site. By comparison, bone blocks harvested using tradi-
Particulate Bone Chip-Harvesting Technique tional rotary cutting instruments reduce the width of the corti-
Particulate bone chips are harvested using special osteoplasty cal bone by at least 1 mm circumferentially around the entire
inserts to scrape the bone surface. The flow of the irrigation graft. Furthermore, traditional cutting instruments are unable
fluid should be reduced to prevent particles from being dis- to effectively cut the internal cancellous bone. The result is
persed after harvesting. The end of the aspirator tip should that the block is detached by using scalpels or chisels to break
be kept away from the collecting particles or placed in the it away, which makes the width irregular. Subsequently, it be-
opposite direction of the insert movement. comes necessary to further reduce the block width.
and to guide the surgical placement of dental implants. This tracking of the patient position. If no teeth are available, a
allows precise positioning while avoiding injury to nearby mini implant can be placed to hold a bracket. Any other
important anatomic structures. Several different approaches tool with its tracking device will be localized, in real time, with
to computers have been used in dental implant surgery, from the patient position. These tools and patient position will
simple imaging software to visualize the implant positions generate data in the same referral time and 3D space.
in a 3D virtual patient to more complex, simultaneous im- 2. Chairside JD mapping data acquisition.
age monitoring and instrument navigation used to perform a. Anatomical 3D contouring with a contact probe or a
surgery similar device. Tracking cameras are scanning in an
The use of CAIS requires precise and continuous coordina- infrared light environment, while reflecting markers
tion of the patient, the image data, and the surgical instrumen- (rigid body) are connected to a contra angle through
tation. Therefore, CAIS requires an accurate alignment (iden- a rigid mount. The contact probe can be a regular drill
tification and registration) of the patient with the patient's and its tip will draw lines to contour teeth surfaces or a
image data (contact probe or ultrasound 3D mapping CT scan bone socket in case of extraction. Since a 3D mapping
data) and a system of tracking the precise movements of the is recorded at the same time as the patient is positioned,
surgical instrumentation (eg, handpiece, drills) in relation to the inaccuracy is limited to the maximum deviation
the actual patient. A variety of systems have been developed (0.3 mm) of the camera's tracking systems.
to acquire and register image data and to coordinate and track b. 3D Ultrasound bone and root contour acquisition. An
movements. These methods are described in the following ultrasound probe depth provides a bone surface map-
sections. ping, point by point, with a maximum deviation of
0.2 mm for 10 mm of soft-tissue thickness. With this
Sequence of Steps technology of 3D bone and soft-tissue mapping there is
no need to match images.
The clinical sequence of steps required for conventional CAIS c. Navigation. Can be performed immediately after chair-
is as follows: side acquisition.
1. Data acquisition. The patient is scanned for image data ac- d. Accuracy. Sustained accuracy procedures are easily
quisition (eg, CT scan) with fiducial (artificial) radiograph- performed in a 3D mapping real-time system by a
ic markers (eg, stent with markers or intentionally placed contact on a tooth or a bone surface. In case of dis-
pins or screws into jaw) or anatomic (natural) markers crepancy the system can be reset rapidly to provide a
such as teeth or bony landmarks. If fiducial markers are real-time safety
placed in a stent, the patient must have it in place when
scanned.
2. Identification. The anatomic or fiducial markers will be Advantages and Disadvantages
identified with a probe tracked by the system. If markers Benefits and advantages of CAIS include the following:
were incorporated into a radiographic stent, the stent will
again be placed in the mouth and the markers identified by 1. CAIS 3D mapping provides real-time matching position
hand with a probe tracked by the stereovision system. with the patient.
3. Registration. After identification of the predetermined 2. CAIS 3D mapping provides chairside accurate 3D bone
markers, the software will indicate the best localization or surface, which will allow an immediate surgical proce-
"match" on the arch between the image data and the pa- dure in most cases.
tient. If registration is not validated, matching can be im- 3. Security features can stop the rotary instrument in prox-
proved with additional points. An invalidated registration imity to important structures.
may be caused by an improper initialization or CT scan 4. Simulation can be visualized before surgery A real 3D
data. simulation with a 3D projected screen can be visualized
4. Navigation. Ultimately, the operator will be able to visualize before and during surgery
surgical instrument navigation (movement). The drilling 5. Implant position can be planned before surgery
instruments will be guided to a target point of impact with 6. Real-time information is provided to the surgeon.
a 3D spatial orientation. 7. Inexperienced surgeons will improve their skill with
5. Accuracy. Sustained accuracy procedures are critical during training.
surgery and should prove reliability in regard to the sys- 8. Experienced surgeons can treat more challenging cases
tem's overall accuracy This sustained accuracy procedure with greater comfort and confidence.
will be done through contact of the drill on the handpiece 9. Surgical time is reduced using a surgical guide.
with selected teeth, by visualization of markers, which can 10. Noninvasive surgery is possible; some cases may be per-
be viewed by the stereovision system, or repositioning of formed with minimal or no flap reflection.
the radiomarker stent. Limitations and disadvantages of CAIS include the following:
6. Feedback. Variations from the ideal position can be restrict-
ed by the software through inactivation of the drill (stop- 1. initial cost of the system.
and-go action) or by an audible or visual cue. 2. increased installation time for surgery
3. training time is mandatory
The clinical sequence of steps required for CAIS immediate 4. accuracy depends on the various components of the
mapping is as follows: system.
1. Preparation for JD mapping data acquisition. A removable at- 5. inaccurate data (eg, CT scan, displaced markers) can lead
tachment (bracket or similar device) is stuck on a nonmo- to difficulties in registration.
bile tooth to support infrared markers for a 3D real-time 6. three anatomic or fiducial markers must be visible.
Data Acquisition image data and the intraoperative patient anatomy: (1) point-
based, (2) line-based or curve-based, (3) surface-based, ( 4)
CAIS CT-Based Technology volume-based, and (5) projective methods. Point- and line-
CT scans and the more-recent cone-beam CT (CBCT) scans are based methods are described here to illustrate the require-
widely used for 3D patient imaging (see Chapter 57). Factors ments for an adequate registration.
that must be considered when deciding to use a CT scan include In the point-based method, a few particular points are
radiation exposure, limitations in accuracy, and the possibil- identified in the preoperative image data and the patient
ity of diffracted images as a result of metallic restorations. The anatomy. These can be natural (anatomic points) or artificial
evolution of scanner technology (spiral CT scan, CBCT scan) (fiducial) markers. In either case, points must be well defined
has made it possible to reduce the radiation dose to the level and stable so that they can be precisely measured. The opera-
of a conventional panoramic radiograph while maintaining ad- tor can manually click, with a tracking device, on the point
equate diagnostic quality for preoperative implant planning. in the patient corresponding to the image point. After several
Similar to implant planning using conventional diagnostic points are matched, the computer calculates a transformation
methods, radiographically identifiable markers are important equation that minimizes the mean distance between matched
for CAIS. However, unlike conventional planning, in which ori- points to complete the registration. Three nonaligned points
entation and simulation of implant positions are related to the are necessary to obtain a nonambiguous result. The registra-
planned prosthetic crown positions, CAIS markers must relate tion accuracy can be predicted, depending on the distribution
the image data to the actual patient anatomy In other words, the of points (eg, an equilateral tripod will give more accurate re-
position of the surgical instrumentation (and ultimately the im- sults than three colinear points).
plant) must be related to the scan image data of the patient's jaw The most intuitive algorithm may be the Hough transfor-
morphology Thus it is critically important to scan the patient mation, in which the most simple geometric invariant, the dis-
with markers that are identified in the scan and correlated to tances between points, are computed, compared, and used to
the patient at surgery Markers can be anatomic markers, such as find a triangle in the preoperative set of points and a triangle in
teeth or specific bony landmarks, or artificial markers (fiducial), the intraoperative set of points that shares similar edge lengths.
such as small tacks or screws that are secured in the bone. The triangle points are then registered using the best-fit algo-
rithm. Once a first estimate of the transformation has been
CAIS Immediate Mapping computed, the clinician can apply the transformation to the in-
Chairside real-time synchronization between 3D images (con- traoperative points. An average accuracy is around 0.5-1 mm.
tact probe and ultrasound) and patient position allows a real- Line-based or curve-based methods are derived from
time accuracy and, in case of mismatch, the ability to perform a point-based methods but require a few lines or curves to be
new chairside 3D acquisition at any time during the procedure. measured and identified. Artificial lines can be extracted from
This accuracy depends on a rigid body tracking system with a the CT scan image data and measured intraoperatively by
maximum deviation around 0.3 mm without artifacts or devia- the operator with the tracking device. All lines and surfaces
tions that can occur with CT scan or CBCT. An ultrasound sur- measured on image planning (after segmentation of anatomic
face mapping will not provide internal structure images, except structure of the jawbone in the CT scan), and the points taken
root contours and the sinus floor. However, the distance from on the patient anatomy by the tracking device are known as
the alveolar crest to the nerve canal can be evaluated on two- a set of points. These sets may be dense or sparse; a segment-
dimensional (2D) X-ray, transferred precisely to the extracted ed bone surface may have hundreds or thousands of points.
2D image from a 3D mapping image. If needed 3D X-ray im- However, it is not practical to measure hundreds of points.
ages can be superimposed on the ultrasound or probe mapping. When the segmented surface is dense, one can assume
that almost all points measured with the tracking device will
Identification and Registration be identified as points of the segmented surface. Thus, algo-
rithms developed for the point-based registration, based on
After scan acquisition, the 3D image data of the patient's jaw(s) identification of matching between the preoperative and the
are interpreted by software as anatomic geometric elements. As intraoperative data, can be easily adapted. However, the num-
previously stated, a sufficient number of markers (anatomic or ber of possible errors in the identification process increases
fiducial) must be identified in the patient's mouth to correlate dramatically in line-based or curve-based methods.
the image data with the patient anatomy. Several devices have
been used to capture the actual patient anatomy for registra-
Navigation and Positional Tracking
tion with the scan data, including a touch pointer and an ultra-
sound probe. The touch pointer allows the operator to touch Numerous commercial products exist for navigation or positional
specific anatomic points (or fiducial markers) while a tracking tracking, but few meet the computer-aided surgery (CAS) require-
device "sees" the instrument and records each point of refer- ments in terms of accuracy (approximately 1 mm in 1 m3), reli-
ence. This device is fairly accurate, but if the clinician is not ability, and clinical usability The "real-time" navigational technol-
careful, there is a tendency to define points that are not in con- ogy is based on the global positioning system technology Some
tact to a real surface, thus creating a false mapping. The ultra- of the technologies used in medical CAS to track movement in-
sound probe has a lower accuracy than the touch pointer but clude mechanical, magnetic, and optical tracking systems.
has the advantage of being able to capture continuous data of Mechanical tracking systems use a six-axis coding robot with
bone morphology through the mucosa or gingiva. Echo qual- a passive arm. The system is very reliable and highly accurate
ity is subject to variations with the type of penetrated tissue. but has limitations when more than one instrument or patient
Matching between the geometry of the image data with the marker needs to be located. Thus mechanical tracking is less
patient anatomy is called registration. Five registration meth- desirable for CAIS, which requires the use of several different
ods are used to compare anatomic points of the preoperative instruments and multiple markers.
Magnetic tracking systems use a magnetic source and a field External Viewer, Augmented Reality, and
receiver. The system loses accuracy in the presence of magnet- 3D Projection Screens
ic field interference. Relative inaccuracies result from changes
in the magnetic field, which may be caused by any metallic Once registration between the data and the actual patient has
mass that may be present, such as a drill motor (with or with- been established, the instrumentation can be coordinated with
out activation). Thus the obligatory presence of drill motors in the system and observed by the surgeon/operator (Figs. 58.60
the operatory during implant surgery makes magnetic track- and 58.61). Instrument movement relative to the image data
ers impractical for CAIS. (and through registration to the patient) may be viewed on
Optical tracking systems are recognized for their dependabil-
ity and accuracy. Positioning is made by intersecting the vision
plane between two or three cameras to locate markers with
stereovision. A passive system absorbs and processes ambient
light, whereas an active system interprets reflected light.
Active markers with infrared light-emitting diodes (IREDs)
have been widely used with superb accuracy but are sensitive
to reflections and interference with the line of sight between
the IRED markers and the cameras. Although variations in
optical localizers are adequate for medical applications, they
need to be improved for use in dental implant surgery. This
is particularly problematic with the typical seating arrange-
ment of surgeon and assistant (ie, the direct line of sight to the
cameras may be interrupted by the operators). A stereovision
with natural-light cameras is a less expensive alternative com-
pared with IREDs. However, natural-light systems are more
sensitive to surrounding light, background, and the shape of
markers. In comparison, infrared cameras are less sensitive to
these light variations.
With optical tracking devices, the surrounding light in FIGURE 58.60 Global setup for surgical navigation. The basic setup
the operatory is important, and a headset light is preferred for a navigation system consists of stereovision cameras with several
with a camera sensitive to natural light. Patient motion will tools. The contra-angle probe, the ultrasound probe and the patient jig
need to have markers, which are tracked by the cameras. The occlusal
be tracked efficiently if the marker is stable during surgery. In
stent, with markers in the standard process and without markers in ultra-
case of loose teeth or unstable markers, cortical bone screws sound registration, used during computed tomography scan acquisition
should be used. will be recognized in its three dimensions for prosthetic planning.
FIGURE 58.61 Images of computer screen and surgeon's view of computer-aided implant surgery navigation simulated with dry mandible. Dur-
ing navigation, the surgeon concentrates on visual cues seen on the eye viewer.
the surgical field continuously. An augmented-reality viewer

allows the surgeon to see target data in three dimensions, su-
perimposed over the surgical site through projected images in
both eyes. The augmented-reality method allows the opera-
tor to adapt to the system more naturally and therefore more
rapidly, but there do not appear to be advantages over the use
of a 2D side-viewer devices in terms of accuracy. Both systems
allow simultaneous viewing of virtual information of the im-
plant (axis and target) and a real vision of the surgical site.
Augmented-reality devices are very sensitive to calibration be-
fore surgery and require care and monitoring intraoperatively
to prevent misalignment during the surgery. The relative sta-
bility of a headset is critical to maintaining accuracy.
Alternatively, 3D projection screens provide a "real 3D vi-
sion" viewed on a specialized monitor (Fig. 58.62) without
the need for viewers (ie, operator glasses).
FIGURE 58.62 Dental implant real-time navigation system with in-

frared stereovision cameras and a 3D monitor display showing the re-
construction of a computed tomography scanned mandible.
an external monitor, visually projected in the surgeon's field

of vision (resulting in a superimposed visual image seen over
the surgical field) using a head-mounted projection system or FIGURE 58.64 Screen views available during surgery. Upper left,
projected on a 3D projection screen (Fig. 58.62). In this man- Simulated implants in green and red. The computed tomography (CT)
scan reconstruction of the mandible and teeth is observed in yellow.
ner, the image on the external monitor (Fig. 58.61), the surgi- Surface mapping of bone and crown morphology (dark green/blue) ob-
cal field, or the 3D projection screen (Figs. 58.63 and 58.64) tained from ultrasound or optical scanner. The computer compares the
will guide the surgeon to perform the planned procedure. data from the 3D topography to the 2D X-ray. Lower left, The 2D X-ray is
Side viewers display target data in two dimensions and re- matched to a 3D topography of the patient "matrix" with the simulated
quire the surgeon to look away from the surgical field. How- implant positions in green and red. Upper right, The target and position
of the drill/implant are observed. Lower right, Real-time navigation with
ever, see-through viewers display target data transparently in a combination of superimposed images from a 2D X-ray, optical scanner,
the surgeon's field of view and allow the operator to observe CT scan, and 3D ultrasound.
FIGURE 58.63 Conventional X-ray and ultrasound acquisition for alveolar bone topography (light brown, lower left) combined with an optical
scan image showing crown and alveolar bone morphology (dark green). The implant position is shown in red. This two-dimensional view is obtained
without a computed tomography scan.
Two types of 3D projection screens are available as follows: This 3D projection screen technology cannot provide a
true holographic 3D view because of the eye's plane of focus
1. The multiplane device has a screen that provides three
on a flat screen, but it does provide a 3D "real volumetric
simulated real-time planes. The object is projected in the
view." The actual 3D projected screen technology does not
screen with a backfield simulated projection. A plane with-
provide enough high-quality texture, but it is overviewed with
in the screen surface and the forward plane are at a maxi-
simple shape symbols (eg, cross, circle). Another difficulty is
mum focus of 10-20 cm. This device provides a 3D view
introduced by the nonlinear depth scale of the screen, which
that is extremely dependent on the shape.
is perceived by the operator's brain as nonlogical and induces
2. A new generation device uses nanolenses on each pixel of
a decrease in intuitive hand localization. In addition to this
screen resolution. It provides a natural light-splitting effect
improvement in 3D vision, a 3D sequence of images can be
similar to the effect of a natural eye separating the three
modified for specific applications such as navigation. For ex-
basic colors. Consequently, it is perceived as a natural view.
ample, a 3D sequence of 8 views can be modified to facilitate
A lateral displacement of the operator's head provides 8-12
the observation of a projected view of the object at 90 degree
simulated views, which together create a natural "volume"
with a minimal head side shift of only 5 degree. These real-
effect. No adaptation time is required and viewing is
time, 3D front and side views provide intuitive 3D data views
intuitive.
in spite of the 2D parameters used to visualize them.
Geurs NC, Wang IC, Shulman LB, et al: Retrospective radiographic analy-
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59
Periimplant Disease and
Management
SJ Froum • PR Klokkevold • S-C Cho • SH Froum • A Jain
Chapter Outline
Definition of Implant Survival and Biologic Complications
Implant Success Conclusions
Types and Prevalence of Implant
Complications
Patients have experienced much success with endosseous Prosthetic or mechanical complications and failures typically
dental implants. Yet, despite the long-term predictability and occur in the form of material failure such as abutment and
success of implants, complications do occur in a percentage prosthetic screw loosening or fractures. The patient can recov-
of cases. Some complications are relatively minor and easy er from many of these mechanical problems if they are minor
to correct, but others are more significant, resulting in loss of and recognized early However, some complications, such as
implants, failure of prostheses, and occasionally in severe loss implant fractures, are not salvageable.
of tissues in the area of implant failure. Complications may be Esthetic complications arise when patient expectations
surgical, biologic, mechanical, or esthetic. are not met. Patient satisfaction with the esthetic outcome
Biologic complications are those that involve the periim- of the implant prosthesis will vary from patient to patient,
plant supporting hard and soft tissues. Changes in the peri- depending on several factors. The risk for esthetic complica-
implant soft tissues may be minor, such as inflammation and tions is increased for patients with high esthetic expectations
proliferation, or more significant, involving progressive bone and less-than-optimal patient-related factors (eg, high smile
loss. The ultimate biologic complication is implant loss or line, thin gingival tissues, or inadequate bone quantity and
failure, which may also result in soft and hard-tissue defects. quality).
Biologic loss of implants may be caused by a lack of osseoin- This chapter reviews several of the more common
tegration in the early stages before restoration or by a loss of implant-related complications. A summary of findings
osseointegration as a result of bone loss after the restoration is from the literature is presented to offer some insight into
installed and functioning. the prevalence of various types of implant-related complica-
Surgical complications are those problems or adverse out- tions. Implant failure, surgical complications related to site
comes that result from surgery, including procedures used development, and different implant placement protocols are
for implant placement, implant exposure, and augmentation discussed as well.
procedures. One of the more prevalent types of implant com-
plications are those arising from implant malposition or those
arising from an implant being placed in a nonideal position. Definition of Implant Survival
Malpositioned implants, which usually are the result of poor
and Implant Success
presurgical treatment planning and/or surgical technique, can
lead to an array of implant problems ranging in severity from Implant success (or failure) is reported in many ways. Case
minor to major. These complications include compromised reports, case series, retrospective studies, controlled studies,
esthetic and/or prosthetic results, soft-tissue and bone dehis- and prospective studies, all report levels of success and fail-
cences, impingement on anatomic structures, and possibly ure as related to the population being evaluated. Each type of
implant failure. Unfortunately, the extent of the problems that report or study has recognized limitations. However, recog-
arise from implant malposition are often not recognized until nizing the tremendous variation in the way individual investi-
the time of implant restoration or years after insertion. gators measure and interpret success may be more important.
725
At times, outcomes are measured simply by the presence or score (PES) is an index proposed by Furhauser et al that con-
absence of the implant(s) at the time of the last examination, siders seven soft-tissue parameters, including an evaluation of
which is only a measure of implant survival and should not be the color, contour, and texture of the surrounding soft tissues
confused with implant success. In contrast to this simplified (papilla and facial mucosa). Each parameter is given a score
assessment, some investigators use detailed criteria to mea- of O, 1, or 2, which allows the best score of 14 to determine
sure implant success and failure, with variations of successful the highest level of esthetics. Other indices were proposed
outcomes separated and defined by additional criteria. for single-tooth implant restorations in the esthetic zone. The
Implant survival is simply defined as any implant that re- most recent, proposed by Belser et al, combines a modified
mains in place at the time of evaluation, regardless of any un- PES index with a white esthetic score (WES) focusing on the
toward signs, symptoms, or history of problems. Clearly, there visible part of the implant restoration scoring five parameters
is a difference between implants that are present and function- from general tooth form to hue, value, surface texture, and
ing under an implant-retained restoration and implants that translucency. The maximum possible WES score is 10. These
are present but not connected to any restoration and not pro- indices are aimed at quantifying the esthetic result, which
viding support or function. These implants are sometimes re- could then present an objective method of judging "implant
ferred to as "sleepers" and should not be considered successful es the tic success."
merely because they are present and remain osseointegrated.
Rather, sleeper implants should be included in the discussion
as "surviving" but counted as "failures" because they failed to Types and Prevalence of Implant
fulfill the originally intended treatment.
Complications
Implant success, conversely, is defined not only by the
presence of the implant but also by the criteria evaluating the The prevalence of implant-related complications has been re-
condition and function of the implant at the time of examina- ported in several reviews. However, until recently, a system-
tion. Criteria for implant success and failure have been de- atic review of the incidence of biological and technical com-
fined over the years, but not all investigators use them. In the plications in studies of at least 5 years revealed that biological
classic definition, Albrektsson et al defined implant success as complications were considered in only 40-60% and techni-
an implant with no pain, no mobility, no radiolucent periim- cal complications in only 60-80% of the studies. One of the
plant areas, and no more than 0.2 mm of bone loss annually few conclusions of this review indicated that the incidence of
following the first year of loading. Roos-Jansaker et al added technical complications related to implant components and
to this definition by defining a successful implant as one that suprastructures was higher in overdentures than in fixed res-
lost no more than 1 mm of bone during the first year in func- torations. In a systematic review of reports on the survival
tion. Sometimes these criteria are used as proposed, whereas and complication rates of implant-supported FPDs, Pjeturs-
at other times, they are used by investigators with modifica- son et al found that the most common technical complication
tions and new criteria. Consequently, it is inherently difficult was fracture of veneers (13.2% after 5 years), followed by
to make comparisons between studies and often impossible to loss of the screw access hole restoration (8.2% after 5 years),
make absolute conclusions about any aspect of implant suc- abutment/occlusal screw loosening (5.8% after 5 years), and
cess or failure based on one or a few studies. abutment/occlusal screw fracture (1.5% after 5 years; 2.5%
If one considers "success" using a strict definition as the after 10 years). Fracture of implants occurred infrequently
outcome without any adverse effects or problems, then "im- (0.4% after 5 years; 1.8% after 10 years). A retrospective
plant success" should be defined as any implant-retained evaluation of 493 7 implants by Eckert et al found that im-
restoration in which (1) the original treatment plan is per- plant fractures occur more frequently in partially edentulous
formed as intended without complications, (2) all implants restorations (1.5%) than in restorations of completely eden-
that were placed remain stable and functioning without prob- tulous arches (0.2%), and all observed implant fractures oc-
lems, (3) periimplant hard and soft tissues are healthy, and curred with commercially pure 3. 75-mm diameter threaded
( 4) both the patient and the treating clinician(s) are pleased implants.
with the results. When these strict criteria are used, implant In a literature review that included all types of implant-
success (ie, absence of complications) is projected to be only retained prostheses, Goodacre et al found that the most
about 61 % after 5 years for implant-supported fixed partial common technical complications were loosening of the over-
dentures (FPDs) and 50% after 10 years for combined tooth/ denture retentive mechanism (33%), resin veneer fracture
implant FPDs. with FPDs (22%), overdentures needing to be relined (19%),
An additional criteria of implant success that is often un- and overdenture clip/attachment fracture (16%). Their review,
reported but must be considered is the "esthetic" success with the inclusion of edentulous patients having overdentures,
or patient satisfaction with the outcome. There have been a seemed to indicate a significantly higher percentage of com-
number of proposed methods to evaluate esthetic results. A plications than Pjetursson systematic review of patients with
restorative index was proposed by Jensen et al to appraise the implant-supported FPDs. Goodacre et al found it impossible
esthetics of the final restoration. The index uses a scale from to calculate an overall prosthesis complication rate because
1 to 10 with 1 being an extremely poor result and 10 being a most studies included in their review did not report on several
superlative esthetic result. The index, based on both subjec- of the complication categories.
tive and objective criteria, evaluates the size and shape of the The most common complication reported for single crowns
implant restoration in comparison to the equivalent contralat- was abutment or prosthesis screw loosening. Abutment screw
eral tooth, blending into the arch, as well as the presence of loosening varied dramatically from one study to another,
the papillae, gingival form, color, and other factors considered ranging from 2% to 45%. The highest rate of abutment screw
essential in determining an esthetic result. The pink esthetic loosening was associated with single crowns, followed by
59 Peri implant Disease and Management 727
overdentures. The rate of prosthesis screw loosening was simi- In Pjetursson systematic review of survival and complica-
lar, ranging from 1 % to 38% in various studies. A higher fre- tion rates for implant-supported FPDs, biologic complications,
quency was reported for single crowns in the posterior areas such as periimplantitis and soft-tissue lesions, occurred in
(premolar and molar) than in the anterior region. 8.6% of implant-supported FPDs after 5 years. However, in a
Implant fracture is an uncommon but significant complica- more recent literature review of the prevalence of periimplant
tion. Goodacre et al reported a 1.5% incidence in their litera- diseases, Zitzmann and Berglundh reported that although
ture review. The incidence of implant fracture was higher in cross-sectional studies are rare, data from the only two stud-
FPDs supported by only two implants. Consistent with this ies available showed that periimplant mucositis occurred in
finding, Rangert et al reported that most fractured implants 80% of the subjects and 50% of implant sites. Periimplantitis,
occurred in single- and double-implant-supported restora- conversely, was identified in 28 and 56% or more of subjects
tions. They also indicated that most of these fractures were and in 12 and 43% of implant sites in the two studies that
in posterior partially edentulous segments, in which the gen- followed subjects with implants in function at least 5 years.
erated occlusal forces can be greater, as opposed to anterior A critical review of the literature by Esposito et al included
segments (Fig. 59.1) 73 publications reporting early and late failures of Branemark
In a systematic review of prospective longitudinal studies implants; biologically related implant failures were relatively
(minimum of 5 years) reporting both biologic and technical low at 7. 7%. The treatments involved all anatomic areas and
complications associated with implant therapy (all restoration all types of prosthetic design. The authors concluded that the
types included), Berglundh et al found that the incidence of predictability of implant treatment was especially good for
technical complications was consistent with Pjetursson find- partially edentulous patients compared with totally edentulous
ings, with implant fracture occurring in less than 1 % (0.08- patients, with failures in the latter population being twice as
0. 74%) of cases. Interestingly, consistent with the findings in high. Also, the incidence of implant failure was 3 times higher
Goodacre review, technical complications were higher for im- for the edentulous maxilla than for the edentulous mandible,
plants used in overdenture therapy than implants supporting whereas failure rates for the partially edentulous maxilla were
fixed prostheses. similar to those for the partially edentulous mandible.
Risk factors, such as smoking, diabetes, and periodontal
disease, may contribute to implant failure and complications.
Several studies with numerous implants and years of follow-
up have concluded that smoking is a definite risk factor for
implant survival. A systematic review of the effect of risk fac-
tors on implant outcomes concluded that smoking has an ad-
verse effect on implant survival and success, with the effects
being more pronounced in areas of loose trabecular bone (ie,
posterior maxilla). The review suggested that type 2 diabe-
tes may have an adverse effect on implant survival rates but
did not have enough studies to permit a definitive conclusion.
Finally, the same review also concluded that while patients
with a history of treated periodontitis did not show any de-
crease in implant survival, they did experience more biologic
implant complications and lower success rates.
Biologic Complications
Biologic complications involve pathology of the surrounding
periimplant hard and soft tissues. Frequently, soft-tissue prob-
lems are an inflammatory response to bacterial accumulation.
The cause of bacterial accumulation around implants is key
to understanding the problem. For example, bacteria may ac-
cumulate at the junction of an ill-fitting implant-abutment or
abutment-crown connection. Some of the highly textured,
macroscopically rough implant surfaces [eg, titanium plasma-
sprayed (TPS) or hydroxyapatite (HA) coated] may also per-
petuate the accumulation of bacteria on the implant surface.
Inflammation and Proliferation

Inflammation in the periimplant soft tissues has been found to
be similar to the inflammatory response in gingival and other
FIGURE 59.1 A, Radiograph of a three-unit, posterior, FPO supported periodontal tissues. Not surprisingly, the clinical appearance
by two standard-diameter, screw-shaped threaded implants. Notice long is similar as well. Inflamed periimplant tissues demonstrate
crown height, relatively short implant length, and bone loss around pos-
terior implant. B, Photograph of the ultimate implant-supported restora-
the same erythema, edema, and swelling seen around teeth.
tion failure. The anterior implant fractured between the second and third Occasionally, however, the reaction of periimplant soft tissues
threads, which resulted in loss of the restoration. to bacterial accumulation is profound, almost unusual, with
59 Periimplant Disease and Management 727.el
Surgical Complications
As with any surgical procedure, there are risks involved with
implant surgery. Proper precautions must be taken to prevent
the risk of injury resulting from surgical procedures, including
but not limited to (1) a thorough review of the patient's past
medical history, (2) a comprehensive clinical and radiograph-
ic examination, and (3) good surgical techniques. Surgical
complications include perilous bleeding, damage to adjacent
teeth, injury to nerves, and iatrogenic jaw fracture. Postop-
erative complications include bleeding, hematoma, and infec-
tion. They may be minor, transient, and easily managed or
more serious and require postoperative treatment.
FIGURE 59.3 Clinical photograph of postoperative (extraoral) bruis-
ing indicative of subdermal bleeding into connective tissues spaces.
Hemorrhage and Hematoma This is a normal expectation that resolves within 7-14 days.
Bleeding during surgery is expected and usually easily con-

trolled. However, if a sizable vessel is incised or otherwise
injured during surgery, the hemorrhage can be difficult to connective tissues and soft-tissue spaces can result in hema-
control. Smaller vessels will naturally constrict or retract to toma formation. Postoperative bruising is a typical example of
slow the hemorrhage. If bleeding continues, it may be neces- minor submucosal or subdermal bleeding into the connective
sary to apply pressure or to suture the hemorrhaging vessel. tissues (Fig. 59.3). Bruising and small hematomas typically
This can be especially difficult if there is a vascular injury to an resolve without special treatment or consequence. However,
artery that is inaccessible such as in the floor of the mouth or larger hematomas or those that occur in medically compro-
posterior maxilla. Serious bleeding from an inaccessible vessel mised individuals are susceptible to infection as a result of the
can be life threatening, not by exsanguination but rather as a noncirculating blood that sits in the space. Thus, it is prudent
result of airway obstruction. This is most problematic when to prescribe antibiotics for patients who develop a noticeably
the point of bleeding is inaccessible and internal (within the large hematoma.
connective tissues and soft-tissue spaces). Although the incidence of a life-threatening hemorrhage
Postoperative bleeding is an equally important problem from implant surgery is extremely low, the seriousness of the
to manage (Fig. 59.2). Patients should be given postopera- problem warrants the attention of everyone who participates
tive instructions on normal expectations for bleeding and how in this type of surgery. Potentially fatal complications have
to prevent and manage minor bleeding. Historically, standard been reported for implant surgical procedures in the mandible
practice has recommended that they should be advised, with (especially the anterior region). Massive internal bleeding in
their physician's approval, to discontinue or reduce medica- the highly vascular region of the floor of the mouth can result
tions that increase bleeding tendency 7-10 days before sur- from instrumentation or implants that perforate the lingual
gery. However, recent evidence suggests that this may not be cortical plate and sever or injure the arteries running along
necessary and may increase the risk of hematologic or car- the lingual surface. Depending on the severity and location
diovascular problems (see Chapter 30). Dental healthcare of the injury, bleeding may be apparent immediately or only
providers should consult with medical healthcare providers after some delay. In either case, the progressively increasing
regarding the best management for each individual patient. hematoma dissects and expands to displace the tongue and
Furthermore, dental healthcare providers and patients should soft tissues of the floor of the mouth, ultimately leading to up-
always include the treating medical practitioner in the man- per airway obstruction. Emergency treatment includes airway
agement decisions if postoperative bleeding is excessive or management (primary importance) and surgical intervention
persistent. Submucosal or subdermal hemorrhage into the to isolate and stop the bleeding. Clinicians must be aware of
this risk and must be prepared to act quickly. It is important to
recognize that bleeding, although considered a complication
at the time of surgery, may be a serious complication in the
hours and days after surgery.
Neurosensory Disturbances
One of the more problematic surgical complications is an in-
jury to nerves. Neurosensory alterations caused by damage to
a nerve may be temporary or permanent. Neuropathy can be
caused by a drilling injury (cut, tear, or puncture of the nerve)
or by implant compression or damage to the nerve (Fig. 59.4;
also see Fig. 57.25). In either case, the injury produces neu-
roma formation, and two patterns of clinical neuropathy may
follow. Hypoesthesia is a neuropathy defined by impaired
sensory function that is sometimes associated with phantom
FIGURE 59.2 Clinical photograph of postoperative bleeding around pain. Hyperesthesia is a neuropathy defined by the presence
healing abutments after second-stage implant exposure surgery. of pain phenomena with minimal or no sensory impairment.
Implant Malposition
Many of the aforementioned complications that arise during
implant surgery can be attributed to the dental implant being
placed in an undesired or unintended position. Malposition-
ing of dental implants is usually the result of poor treatment
planning before the implant surgery, lack of surgical skill by
the implant surgeon, and/or poor communication between
implant surgeon and restorative dentist. Optimal implant
esthetics and the avoidance of positional complications can
be achieved by placing the implant in a prosthetically driven
manner. In other words, the implant should be placed with
reference to the three dimensions dictated by the position of
the final restoration and not by the availability of bone. The
angulation is another important determinant (fourth dimen-
sion) of implant position that will affect outcome esthetics.
The ideal implant position entails an accurate preparation,
insertion, and placement of the implant into the alveolus in
a proper three-dimensional geometry according to apicocoro-
nal, mesiodistal, and buccolingual parameters, as well as im-
plant angulation relative to the final prosthetic restoration and
gingival margins. (see Chapter 58).
Apicocoronally, the implant should be placed so the dental
implant platform is 2-3 mm apical to the gingival margin of
the anticipated restoration. The actual implant position varies
slightly from one implant system to another, depending on
FIGURE 59.4 A, Cross-sectional image from computed tomography abutment design and space requirements. If the implant plat-
(CT) scan showing implant impinging on inferior alveolar nerve canal. form is placed too coronal, there will not be sufficient room
B, Panoramic image of CT scan showing implant in lower left first molar to develop a natural-looking emergence profile and the tooth
area impinging on inferior alveolar nerve canal. Nerve is marked by
tracing with software.
may have a squarish, unesthetic contour. If the platform is
placed at or above the level of the gingival margin, a metal
collar or implant exposure can occur yielding an unesthetic
result (Fig. 595) Conversely, if the implant platform is placed
Some neuropathies will resolve, whereas other will persist. too apically, a long transmucosal abutment will be necessary
The type of neuropathy is not indicative of the potential for to restore the implant. This can lead to a deep pocket and dif-
recovery. ficult hygiene access for the patient and clinician.
It is likely that neurosensory disturbances occur more fre- Mesiodistal implants should be placed at a distance of
quently after implant surgery than currently reported in the 1.5-2 mm from a natural tooth and 2-3 mm from an adjacent
literature for several reasons. First, many of these changes implant to maintain an adequate biologic dimension. Similar
are transient in nature, and most patients recover completely to natural teeth, violation of biologic width around an implant
or at least recover to a level that is below a threshold of an- can lead to bone loss. Implants that are placed too close to
noyance or daily perception. Second, wide variation exists in each other (Fig. 59.6) or natural teeth can be difficult to re-
the postoperative evaluation of patients by clinicians. Some store. Impression copings and impression-taking techniques
clinicians do not examine or inquire about postsurgical neu-
rosensory disturbances at all, thus allowing this complica-
tion to go unnoticed. Likewise, some patients may think that
the altered sensation is part of the expected "side effect" of
surgery and may never acknowledge or comment on its pres-
ence, especially if the disturbance is minor. Therefore, it is
likely that minor neuropathies exist but go unrecognized and
unreported.
Neurosensory disturbances reported in the literature are
most prevalent and significant when they are more serious
and occur more frequently, such as those associated with lat-
eral transposition of the mandibular nerve. This relatively un-
common procedure is used to reposition the nerve and allow
longer implants to be placed in the atrophic posterior man-
dible. Lateral nerve transposition procedures are associated
with almost 100% incidence of neurosensory dysfunction im-
mediately after surgery. More than 50% of these neurosensory
FIGURE 59.5 Clinical photograph of gingival recession around a
changes are permanent (ranging from 30% to 80%). Several maxillary anterior implant (left central incisor) resulting in exposure
articles have been written on the treatment of neurosensory of the crown margin, the implant collar, and several threads of the
disturbances. implant.
59 Periimplant Disease and Management 727.e3
loosening, screw fracture, or implant fracture) complications,

as well as difficulties with hygiene.
Ideally, implants should be placed, buccolingually so there
is at least 2 mm of bone circumferentially around the implant.
Implant exposure through the lingual or buccal cortex can
predispose an individual to abscess and/or suppuration. Im-
plants that are placed too far palatally/lingually require pros-
thetic compensation in the form of a buccal ridge lap, which
may be difficult for the patient to clean and could lead to tis-
sue inflammation.
To obtain ideal esthetics, to avoid potential esthetic com-
plications, and to correct bodily placement of the dental im-
plant, the implant must be correctly angulated on insertion.
In most anterior cases, it is desirable to have the implant long
axis directed so it is emerging toward the cingulum. In the
posterior region, the implant axis should be directed toward
the central fossa or the stamp cusp of the opposing tooth. Im-
plants that are placed with mild-to-moderate misangulations
can often be corrected prosthetically with implant abutments.
Minor misangulations (up to 15-20 degrees) can be corrected
with prefabricated stock-angled abutments; moderate mi-
FIGURE 59.6 Radiograph of two mandibular anterior implants sangulations (20-35 degrees) can usually be managed with
placed too close together (no proximal space) resulting in implants
customized UCLA-type abutments; extreme errors in implant
that will be impossible to restore.
angulations (more than 35 degrees) may deem an implant un-
restorable and require it to be left submerged (ie, sleeper) or
to be removed (Fig. 59. 7).
must be modified. Improperly spaced implants invariably lead The ultimate complication of malposed implant(s) is im-
to chronic inflammation and periimplantitis. Conversely, implant or instrument invasion into vital structures. The most
plants placed with excessive distance from an adjacent tooth common violation of neighboring anatomy is the placement
or implant may require prosthetic compensation in the form of the dental implant into the adjacent tooth root. Surgical
of mesial or distal cantilevers, which may predispose the im- procedures used to prepare osteotomy sites and place im-
plant to biologic (eg, bone loss) and mechanical (eg, screw plants adjacent to teeth can injure the teeth either by directly
FIGURE 59.7 Clinical photograph of maxillary anterior implant (left central incisor) placed with an extreme facial angulation resulting in an
implant that emerges through the gingiva at a level that is more apical than the adjacent natural tooth gingival margins. A, Surgical exposure of
malpositioned implant. B, Surgically removed implant. C, Alveolar defect resulting from surgical removal of malpositioned implant.
cutting into the tooth structure or by damaging nearby sup- lower lip, skin, mucosa, and teeth may result, as well as arte-
porting tissues and nerves. Instrumentation (eg, drills) di- rial or venous bleeding. The incidence of sensory disturbanc-
rected at or near the adjacent tooth may cause injury to the es after mandibular implant placement has been reported to
periodontal ligament, tooth structure, and nerve of the tooth. range from 0% to 17.5%.
Depending on the extent of the injury, the tooth may require In the maxilla, care must be taken to avoid dental implant
endodontic therapy or extraction. On insertion, dental im- perforation into the maxillary sinus or nasal cavity. Displace-
plants will follow the trajectory of the osteotomy prepared ment of the entire dental implant into the maxillary sinus cav-
by the surgical drills. Care must be taken when preparing ity may require a Caldwell-Luc procedure for retrieval. See the
the osteotomy to stay true to the planned path of insertion. online section on sinus augmentation for further information
Guidepin location radiographs taken during implant surgery about complications related to the maxillary sinus.
can greatly reduce the potential for damaging adjacent teeth The risks of surgery are always present, but the compli-
(see Fig. 57.22). Radiographic analysis before implant sur- cations can be minimized with an understanding of the eti-
gery should include detection of curved, convergent, and/ ologies and with proper diagnosis and treatment planning.
or dilacerated root structures of adjacent teeth that can limit Three-dimensional imaging [eg, computed tomography (CT)
implant placement. and cone-beam CT (CBCT) scans] provides the surgeon
Particular care must be taken when placing implants in the with useful presurgical information for proper diagnosis and
mandible so as to not encroach on the inferior alveolar ca- treatment planning (see Chapter 57). Careful surgical expo-
nal or the mental foramen. Encroachment on the mandibular sure for direct visualization and identification of the mental
canal or mental foramen during osteotomy or implant place- nerve may be indicated as well. Once identified, it is recom-
ment via direct contact or mechanical compression of bone mended to establish a "zone of safety" and to keep instru-
can result in injury to nerves and blood vessels. Paresthesia, mentation and implants a safe margin away from the nerve
hypoesthesia, hyperesthesia, dysesthesia, or anesthesia of the (eg, ~2 mm).
a dramatic inflammatory proliferation (Fig. 59.8). This type Recession is a common finding after implant restoration and
of lesion is somewhat characteristic around implants and is should be anticipated especially when soft tissues are thin and
indicative of either a loose-fitting implant to abutment con- not well supported (Fig. 59.11). Improper implant position-
nection or trapped excess cement that remains buried within ing also predisposes periimplant tissues to recession. As noted
the soft-tissue space or "pocket." The precipitating local factor earlier, placement or angulation of the implant too far to the
ultimately becomes infected with bacterial pathogens, leading buccal causes the buccal plate to resorb and has been shown
to mucosal hypertrophy or proliferation and possible abscess to result in greater recession. Another factor to consider is
formation (Fig. 59.9). Correction of the precipitating factors the thickness of the buccal plate of bone. Spray et al recom-
(eg, loose connection, retained cement) may effectively resolve mended this thickness to be 2 mm or greater to support the
the lesion. Another type of lesion resulting from a loose abut- buccal soft tissue. If this thickness is not present, presurgical
ment connection is the fistula (Fig. 59 .10). Again, correcting or simultaneous site development using guided bone regen-
the etiologic factor can quickly resolve the fistula. eration is indicated. Recession is a problem that is particularly
disconcerting in anterior esthetic areas. Patients with a high
smile line or high esthetic demands consider such recession a
Dehiscence and Recession
failure (Fig. 59 12)
Dehiscence or recession of the periimplant soft tissues occurs The anatomy and soft-tissue support around implants is
when support for those tissues is lacking or has been lost. different than that around teeth. Specifically, periodontal tis-
sues have the distinct advantage of soft-tissue support from
circumferential and transseptal connective tissue fibers that
FIGURE 59.8 Inflammatory proliferation caused by a loose-fitting

connection between the abutment and the implant. (Courtesy Dr John FIGURE 59.10 Fistula caused by loose implant-abutment connec-
Beumer, UCLA Maxillofacial Prosthetics, Los Angeles, CA.) tion (maxillary left lateral incisor).
FIGURE 59.9 A, Clinical photograph of abscess caused by excess cement trapped within the soft tissues. B, Radiograph of implant with cemented
crown (same patient as in A). Notice the subgingival depth of the crown-abutment (cement line) junction, which is below the level of the adjacent
interproximal bone and therefore impossible to adequately access with explorer to remove excess cement. (Courtesy Dr John Beumer, UCLA Maxil-
lofacial Prosthetics, Los Angeles, CA.)
59 Peri implant Disease and Management 729
FIGURE 59.11 A, Clinical photograph of single-tooth implant crown (maxillary right central) with moderate recession that occurred 1-year after
delivery of final restoration. Recession, in this case, most likely occurred because the labial bone around this wide-diameter implant was very thin or
nonexistent. B, Radiograph of wide-diameter (6 mm) implant supporting maxillary central incisor crown (same patient as in A).
Periimplantitis and Bone Loss

Periimplantitis is defined as an inflammatory process affect-
ing the tissues around an osseointegrated implant in func-
tion, resulting in loss of supporting bone. The prevalence
of periimplantitis has been reported to be controversial de-
pending on the criteria used to define the amount of mar-
ginal bone loss necessary to be present, together with the
evidence of soft-tissue inflammation to determine the exis-
tence of the disease. Reports of prevalence of periimplantitis
have varied from approximately 7% to 37% of implants in
various studies. Recently, a proposed classification for early,
moderate, and advanced periimplantitis based on the de-
gree of bone loss was presented in an attempt to improve
communication when describing prevalence and treatment.
FIGURE 59.12 Poor esthetics resulting from gingival recession and To diagnose a compromised implant site, soft-tissue mea-
exposure of crown margins, implant collars, and threads of several surements using manual or automated probes have been
maxillary and mandibular implants supporting full-arch FPDs. Notice suggested. Although some reports state that probing is con-
the thin labial tissues and erythema (especially around mandibular im- traindicated, careful monitoring of probing depth over time
plant sites).
seems useful in detecting changes of the periimplant tissue.
Standardized radiographic techniques, with or without com-
puterized analysis, have been well documented and found
insert into the cementum at a level that is more coronal than to be useful in evaluating periimplant bone levels. Together
the supporting bone. In the absence of inflammation, these with periodic evaluation of tissue appearance, probing depth
fibers support periodontal soft tissues far above the level of changes, and radiographic assessment are the best means of
crestal bone. As a result, gingival margins and interdental pa- detecting changes in bone support. Clinicians should moni-
pillae are supported and maintained around teeth even when tor the surrounding tissues for signs of periimplant disease
the periodontal tissues are very thin. Periimplant soft tissues, by monitoring changes in probing depth and radiographic
however, are entirely dependent on the surrounding bone for evidence of bone destruction, suppuration, calculus build-
support. Soft-tissue thickness accounts for some soft-tissue up, swelling, color changes, and bleeding. Periimplantitis
height, but there are no supracrestal inserting connective tis- may be perpetuated by bacterial infection that has contami-
sue fibers to aid in the soft-tissue support around an implant. nated a rough (eg, TPS, HA-coated) implant surface and by
Therefore, soft-tissue height around implants typically does excessive biomechanical forces. A classic trough-type defect
not exceed about 3-4 mm, and bone loss around implants is typically associated with periimplantitis (Fig. 59 13). In
often leads to recession. cases with severely reduced bone support extending into
FIGURE 59.13 Moderately advanced bone loss around an implant

with the typical circumferential trough type of boney defect. (From
Garg AK: Implant dentistry: a practical approach, ed 2, Mosby, St. Louis,
2070.)
FIGURE 59.15 A, Radiograph of early failed implant caused by lack

of osseointegration. In addition to the crestal bone loss, notice the ra-
diolucency along the sides of the implant. B, Photograph of the failed
(non integrated) implant (shown in A) that was easily removed along with
surrounding connective tissue.
occur before implant restoration. Late implant failures occur

after the implant has been restored. When an implant fails
before restoration, it probably did not achieve osseointegra-
tion, or the integration was weak or jeopardized by infec-
tion, movement, or impaired wound healing (Fig. 59.15).
Late implant failures occur after prosthesis installation for
a variety of reasons, including infection and implant over-
load (Fig. 59.16). In a review of the literature to evaluate
FIGURE 59.14 Severe horizontal and vertical bone loss around sev-
biologic causes for implant failure, Esposito et al found that
eral mandibular implants.
infections, impaired healing, and overload were the most
important contributing factors. Two systematic reviews of
the literature concluded that a single dose of preoperative
the apical half of the implant (Fig. 59 14) or in cases dem- antibiotic therapy may decrease the failure rate of dental
onstrating mobility, implant removal should be considered. implants.
The number and distribution of implants and the occlusal The risk of implant failure varies among patients and
relationships influence the biomechanical forces applied to patterns of loss tend to cluster within subjects. A second
implants (see Chapter 57). A recent review by Lindhe and attempt at dental implant placement should be approached
Meyle from the Consensus Report of the Sixth European cautiously when attempting to place the implant in the same
Workshop on Periodontology concluded that risk indica- site as the one that previously failed. Oftentimes, it is chal-
tors for periimplantitis included (1) poor oral hygiene, (2) a lenging to achieve adequate diameter, length, and stability
history of periodontitis, (3) diabetes, ( 4) cigarette smoking, of replacement implants due to the residual defect created
(5) alcohol consumption, and (6) implant surface. Most of by removal of the failed implant. In 2007, Grossmann and
these risk factors (1-4) have been recognized and reported Levin reported an overall survival rate of 71 % for dental
in the literature. The report suggests that although data for implants that were placed in sites of previously failed single
the latter two risk factors (5 and 6) are limited, they appear implants. In that study all of the original implants failed
to be relevant to periimplantitis. Another risk factor that has during the early healing phase (mean 2.3-3.2 months post-
been proposed involves gene polymorphism related to an placement). In a similar study in 2008, Machtei reported
individual's genotype. More research is needed to study the an overall survival rate of 83.5% for the second attempt
relationship of this potential risk factor to the development of dental implants. They concluded that replacing failed
of periimplantitis. implants resulted in implants with a lower survival rate
compared with implants placed in pristine sites. A factor
that could not be associated with conventional implant or
Implant Loss or Failure
patient-related implant failures. They suggested a possible
Implant loss or failure is generally considered relative to site-specific negative effect that might be associated with
the time of placement or restoration. Early implant failures this phenomenon.
59 Periimplant Disease and Management 731
In 2011, Machtei reported a lower survival rate of 60%

for the third reimplanted sites. This outcome represents a fur-
ther diminished prognosis compared with implants in original
sites in or even following the first re-do. Their findings dem-
onstrated that the replacement of a failed implant presents a
challenge in achieving osseointegration in a healed bone site
and may result in a decline in the survival rate.
Conclusions
Although implants offer a highly predictable treatment option
for the replacement of single and multiple missing teeth, there
are a variety of potential complications that may be surgical,
biologic, mechanical, prosthetic, or esthetic. Careful diagno-
sis and treatment planning, along with the use of diagnostic
imaging, surgical guides, meticulous techniques, and adher-
ence to proven principles can prevent many of the problems
discussed in this chapter. A thorough understanding of anat-
omy, biology, and wound healing can reduce the incidence of
complications. However, there is no substitute for training,
knowledge, and clinical experience for preventing, recogniz-
ing, and successfully managing complications. This chapter is
a start. The clinician who places and/or restores implants must
be aware of techniques and procedures for early intervention
should a complication arise.
SUGGESTED READINGS
Berglundh T, Persson L, Klinge B: A systematic review of the incidence of
biological and technical complications in implant dentistry reported
in prospective longitudinal studies of at least 5 years, J Clin Periodontal
29(Suppl 3):197-212, 2002, discussion 232-233.
Del Fabbro M, Testori T, Francetti L, et al: Systematic review of survival rates
for immediately loaded dental implants, Int J Periodontics Restorative Dent
26 249-263, 2006.
den Hartog L, Slater JJ, Vissink A, et al: Treatment outcome of immediate,
early and conventional single-tooth implants in the aesthetic zone: a sys-
tematic review to survival, bone level, soft-tissue, aesthetics and patient
satisfaction,] Clin Periodontal 35:1073-1086, 2008.
Esposito M, Hirsch J, Lekholm U, et al: Differential diagnosis and treatment
strategies for biologic complications and failing oral implants: a review of
the literature, Int J Oral Maxillofac Implants 14:4 73-490, 1999.
Goodacre CJ, Bernal G, Rungcharassaeng K, et al: Clinical complications with
implants and implant prostheses,] Prnsthet Dent 90:121-132, 2003.
Lang NP, Pjetursson BE, Tan K, et al: A systematic review of the survival and
complication rates of fixed partial dentures (FPDs) after an observation
period of at least 5 years. II. Combined tooth-implant-supported FPDs,
Clin Oral Implants Res 15:643-653, 2004.
Pjetursson BE, Tan K, Lang NP, et al: A systematic review of the survival and
FIGURE 59.16 Four-unit FPO in the posterior maxilla supported by
complication rates of fixed partial dentures (FPDs) after an observation
only two implants. A, Clinical photograph of implant abutments in the period of at least 5 years, Clin Oral Implants Res 15:667-676, 2004.
posterior maxilla. B, Radiograph taken 30-months after restoration. Note
Roos-jansaker AM, Lindahl C, Renvert H, et al: Nine to fourteen-year follow-
the bone loss around the distal implant. C, Failed distal implant attached to up of implant treatment. Part II: presence of peri-implant lesions, J Clin
failed prosthesis. The biologic failure of one (posterior) implant resulted in
Periodontal 33:290-295, 2006.
a long-span cantilever extension from the other (anterior) implant that ul-
timately led to its mechanical failure (ie, abutment screw fracture). (Cour-
tesy Dr John Beumer, UCLA Maxillofacial Prosthetics, Los Angeles, CA.)
59 Periimplant Disease and Management 731.el
Complications Related after symphysis grafts has been reported to be as high as 4 3%.
Many of these paresthesias are temporary
to Augmentation Procedures In addition, fracture of the mandible has been reported af-
A common problem encountered in implant dentistry is insuf- ter bone graft harvesting from the symphysis. Many of these
ficient bone quantity to allow implant placement according to complications can be avoided by proper surgical technique,
standard procedures. Deficiencies in alveolar bone result from good planning, and an experienced operator.
developmental defects, periodontal disease, tooth loss, and Recipient site complications include wound dehiscence,
trauma. For most cases with alveolar ridge resorption, bone flap necrosis, graft exposure, graft contamination, infection,
regenerative procedures are required to correct the defects be- and problems with bone graft incorporation and resorption.
fore or simultaneous with implant placement. The success of Proper flap reflection, intimate fixation of the graft, and flap
bone augmentation procedures has been assessed by experi- coverage without tension can avoid many of the potential
enced clinicians in several workshops. One systematic review postsurgical complications. Bone graft material including bar-
of literature (the 2003 Workshop on Contemporary Science rier membranes should be immobilized (fixated if possible).
in Clinical Periodontics) found that survival rates of dental Provisional restorations should be adjusted to prevent pres-
implants in augmented bone achieved a high level of predict- sure over grafted areas. Block grafts, as well as other augmen-
ability and showed that these rates were similar to implants tation procedures, require experience in handling hard and
placed in natural bone. However, a more-recent systematic re- soft tissue, as well as a clinician who is prepared to recognize
view of the literature (the 2008 Consensus Report of the Sixth and treat complications should they arise.
European Workshop on Periodontology) concluded that bone
augmentation procedures can fail and that implants placed in
these areas do not enjoy the high long-term survival rates of Guided Bone Regeneration
dental implants placed in pristine sites. The consensus em- Guided bone regeneration (GBR) is a procedure that uses a
phasized that research is needed to answer questions concern- barrier membrane to isolate an area for bone growth. The
ing (1) long-term performance of dental implants placed in technique has been well documented for horizontal (and lim-
augmented bone, (2) the clinical performance of dental im- ited vertical) ridge augmentation (see Chapter 58). The most
plants placed in augmented or pristine sites, and (3) the clini- common complication associated with GBR is premature ex-
cal benefits of bone augmentation with respect to alternative posure of the barrier membrane and necrosis of the overlying
treatments. flap (Fig. 59 .1 7). Exposure rates of expandable polytetrafluo-
The procedures most often used to regenerate bone include roethylene (ePTFE) membranes during various GBR proce-
autogenous bone harvesting and grafting, guided bone regen- dures range from 41 % when the technique was first intro-
eration, and sinus bone augmentation (see Chapters 58 for duced in the early 1990s for horizontal ridge augmentation to
detailed descriptions of these procedures). The following is 12.5% when surgical techniques improved and clinicians be-
a brief review of the most common complications related to came more familiar with handling the material. Once exposed
these three augmentation procedures. to the oral environment, the membrane becomes colonized
with bacteria within 3-4 weeks and the potential for bone
regeneration under the membrane is limited to an area that is
Autogenous Bone Harvesting at least 2-3 mm from the contaminated surface. Topical ap-
and Grafting plication of chlorhexidine to the exposed membrane has been
Autogenous bone from a histologic and biologic point of view advocated as a method of reducing the amount of bacteria,
has been considered the gold standard for osseous reconstruc- but it does not solve the problem and removal of the exposed
membrane is necessary
tion. Bone block grafts of autogenous bone from extraoral
Other complications associated with GBR procedures in-
and intraoral sources have been documented as a predictable
clude soft tissue or bone graft infection, failure to regenerate
procedure for reconstruction of defective or atrophic alveolar
adequate bone volume and mucogingival problems, including
ridges. Complications can occur either at the donor or recipi-
ent sites. The most common extraoral donor sites include the
ilium and tibia. Complications related to extraoral donor sites
are beyond the scope of this chapter. The most common in-
traoral donor sites include the mandibular symphysis, man-
dibular ramus, and maxillary tuberosity Although each donor
area has specific associated complications, the most common
complications of intraoral autogenous harvesting and grafting
concern those from the mandibular symphysis.
The ramus donor site is associated with a much lower in-
cidence of complications compared to the symphysis area.
Potential complications associated with surgical harvesting
of bone from the ramus include damage to the inferior al-
veolar nerve and trismus after surgery Damage to the buc-
cal nerve, although rare, has been reported as well. Surgical
harvesting of bone from the mandibular symphysis region is
associated with a higher incidence of altered neurosensory
disturbances to the mandibular anterior teeth and soft tissues FIGURE 59.17 Clinical view of flap necrosis over area treated with
of the chin area. The incidence of mental nerve paresthesia guided bone regenerative procedure.
FIGURE 59.18 A, Large perforation of the Schneiderian membrane during a sinus elevation procedure. B, Attempts to close or reduce the size of the
perforation with resorbable sutures. C, Use of resorbable barrier membranes to cover the perforation.
loss of keratinized tissue and decrease in the vestibule. Most of "patch" the opening (Fig. 59 .18). Very large membrane tears
these complications are related to insufficient soft-tissue heal- may be too big to repair and require aborting the procedure.
ing after tooth extraction, inadequate flap design, movement Careful surgical technique and the use of newer instruments
of the membrane and/or graft caused by transmucosal loading (eg, piezoelectric surgery) have been shown to significantly
and improper provisionalization, flap suturing under tension, reduce this complication (see Chapter 58).
poor surgical technique, contamination of the membrane The most common, although infrequent, postsurgical com-
or surgical site, compromise of the vascular supply and flap plication associated with sinus bone augmentation is infec-
advancement for graft coverage that reduces the keratinized tion. The incidence of infection has been reported to vary
tissue, and vestibular depth. To prevent complications associ- from 2% to 5.6%. Careful surgical techniques, adherence to
ated with GBR procedures, proper surgical technique should sterility, and the judicious use of antibiotics can minimize the
be employed. risk of postoperative infections. Some infections resolve with
antibiotic treatment alone, whereas others require surgical de-
bridement of the infected area. Consultation or referral to a
Sinus Bone Augmentation
specialist may be indicated for persistent infections.
Lateral Window Sinus Lift
The lateral window sinus lift and bone augmentation proce- Crestal (Osteotome) Sinus Lift
dure has been well documented and reviewed in three pub- Another method of sinus elevation and bone augmentation
lished systematic reviews. Although survival rates of implants involves the use of osteotomes. This technique is indicated
placed in sinus-grafted areas has been shown to be high when there is enough native bone to stabilize the implant and a
(95%), there are intraoperative and postoperative complica- minimal need for sinus floor elevation. Bone is added through
tions associated with this procedure. The most common in- the crestal osteotomy by means of osteotomes and a mallet,
traoperative complications include bleeding and perforation the floor of the sinus is fractured, and the Schneiderian mem-
of the Schneiderian membrane. Bleeding usually occurs when brane lifted by the bone graft (see Chapter 58). This method is
the vascular supply to the lateral wall of the sinus is severed or thought to be a relatively less-invasive technique of great utili-
damaged. In most cases, if the patient does not have an under- ty in certain patients. However, it has been associated with the
lying bleeding problem and is not taking anticoagulants, the complication of benign paroxysmal positional vertigo (BPPV),
bleeding is usually minor and relatively easy to control with which has been described as a consequence of working the
local measures. Perforation of the Schneiderian membrane, as implant bed with osteotomes. During the osteotomy prepara-
reported in the literature, has an incidence that varies from tion and sinus floor elevation using the osteotome technique,
11 % to 56% with most clinicians reporting an incidence of the trauma induced by percussion with the surgical hammer,
approximately 20-30%. Minor membrane perforations can along with hyperextension of the neck during the operation,
be treated by reflection of the membrane that folds on itself, can displace otoliths in the inner ear and induce BPPV It has
whereas medium-to-large membrane perforations require the been reported that 1.25% of the patients treated suffered ver-
use of an absorbable membrane placed over the perforation to tigo when trying to sit up immediately after surgery and were
diagnosed with BPPV Since implant treatment is increasingly a surgical stent, round bur, sharp initial bur, and side cut-
being carried out on older patients, and because of the wide- ting burs can avoid slipping and improve the accuracy of
spread use of bone expansion technique with osteotomes, the implant site preparation (see Chapter 58). Although success
incidence of BPPV can be expected to increase. In suspected rates of implants placed with an IIP are excellent, failure to
cases of BPPV, the patient should be informed about the con- attain primary stability in native bone apical or lateral to the
dition and then referred to an otoneurologic specialist to de- socket may increase failure rates. Inability or lack of thorough
termine which semicircular canal is affected and to carry out debridement of an infected or compromised (eg, tooth with
the appropriate otolithic reinstatement maneuver. an apicoectomy) socket may also increase the risks of failure.
To prevent this complication, care should be taken when Buccal plate resorption and gingival margin recession post-
using the osteotome technique. The application of manual implant placement may expose the implant surface following
force instead of hammer percussion and the use of a surgi- integration of the implant (see Figs. 59.5 and 59 11) This
cal fraise in combination with osteotomes can minimize the may, in turn, compromise the esthetic results or necessitate
trauma to the craniofacial area, especially in older patients. hard- and soft-tissue augmentation procedures to improve the
Many alternative techniques for a crestal approach to sinus esthetic outcome. A recent published case series documented
elevation and bone augmentation have been developed in- this problem for IIP postextraction without flap elevation. The
cluding the use of inflatable balloon techniques, selective risk of the previously mentioned complications may be de-
drill systems, and piezoelectric surgical instruments that cut creased with proper case selection, proper procedures, and
bone while leaving the Schneiderian membrane intact (see experience in using this protocol. Until clinicians have the
Chapters 58). These newer methods should be considered to knowledge and experience to use an IIP protocol, they should
avoid BPPV avoid using it in the esthetic zone.
Complications Related to Placement Immediate Loading After Implant

and Loading Protocols Placement
The traditional implant placement protocol required a healed Branernark established the concept and predictability of the
edentulous ridge into which implants were placed and al- osseointegrated dental implant based on a requirement for an
lowed to osseointegrate for a period of 3-6 months without unloaded healing period of 3-6 months. This original protocol
occlusal loading (see Chapter 58). In contrast to these early purported that premature loading would cause micromotion
standards, some current protocols advocate dramatically dif- of the dental implant leading to fibrous encapsulation and im-
ferent approaches, including (1) implant placement immedi- plant failure. However, several studies in the dental literature
ately after tooth extraction, (2) implant loading immediately have shown that immediately loaded dental implants can have
after placement, and (3) flapless implant placement surgery. success rates similar to that of conventionally loaded dental
Each of these approaches has distinct advantages but are also implants. Whether restoring a single tooth or a complete den-
accompanied by specific risks of complications. The most tition, there are many advantages to early or immediate load-
common complications associated with these newer, developing. It is critical to recognize that these advantages may come
ing protocols are discussed in this section. with increased risks for complications and failures. The most
significant complications are failure to achieve primary stabil-
ity and implant failure.
Immediate Implant Placement
Studies have shown that using longer and wider implants
Immediate implant placement (IIP) is a protocol that places can provide increased success rates when immediately load-
an implant in an extraction socket immediately after tooth re- ing the dental implant. In addition, when placing multiple
moval and socket debridement. This procedure was originally implants in an edentulous area, the implants should be placed
described by Schulte et al and Lazzara and has been reported in a fashion that maximizes the anterior to posterior spread
to have similar implant survival rates as implants placed into leading to a greater distribution of forces over a wider area
healed ridges with long-term survival rates of approximately and a reduction in cantilever forces. Studies have suggested
94%. The advantages of this protocol include fewer surgi- that implants placed around the arch lead to what is known
cal procedures (and decreased morbidity), decreased time of as cross-arch stabilization, which can decrease the individual
treatment, decreased cost, and decreased soft-tissue healing force and motion experienced by any individual implant. For
time by avoiding flap reflection and advancement. However, the fully edentulous case a minimum of four to six implants of
as with any surgical protocol, complications are possible and adequate size, good stability, and properly spaced throughout
there are specific complications associated with IIP These the ridge are recommended to improve success with immedi-
include implant failure, poor implant position, bone loss, re- ate load case. Mandibular cases may require fewer implants
cession of the periimplant marginal soft tissues, and compro- than maxillary cases because of greater bone density, especial-
mised esthetic outcomes. ly in the interforaminal region. If the opposing arch is restored
After tooth extraction, there may be a compromised socket with a removable prosthesis, fewer implants may be needed
as the result of pathology (periodontal, endodontal, or frac- to immediately support a restoration because of a decreased
ture) of the hopeless tooth. Proper implant position may be opposing occlusal force.
difficult to establish when the socket walls are missing or Other contributing factors associated with increased failure
deficient. For example, the implant osteotomy for extracted rates of immediately loaded implants include implant surface
maxillary anterior teeth should be made on the lingual in- and implant design. Lower success rates with immediately
cline of the lingual wall of the socket. Quite often the burs loaded implants have been reported with smooth (ie, turned/
will "slip" buccally causing the osteotomy to be made too far machined) surface implants, especially in cases of single tooth
to the buccal or at an undesired angulation. Careful use of immediately loaded restorations. Studies have also suggested
that the macrodesign features of an implant (eg, threaded

vs cylindrical) can affect initial stability and success rates in
immediately loaded cases. Two studies have concluded that
patient bruxism, clenching, and the posterior maxilla may re-
duce the likelihood of implant success under an immediate
loading protocol.
Complications of immediately loaded implants can also
arise from a poorly constructed or inserted restoration despite
all things going well with the surgical placement. Extreme
care must be taken to achieve a passive fit of restoration and
to eliminate nonworking or balancing contacts on the resto-
ration. In addition, in full arch cases that were immediately
loaded, the restoration must be designed to withstand direct
occlusal force. This can be accomplished via a rigid connec-
tion and splinting the implants together in a cross-arch fash-
ion. Loosening or unseating of the provisional restoration
usually indicates mismanagement of occlusal forces and is an
early predictor of failure.
Immediately loading dental implants is a technique that
offers many advantages but can also increase the incidence
of complications and failure. This technique should only be
performed by an experienced operator who is prepared and
informed. Controlling micromotion postloading is tantamount
to success. Meticulous case selection, which incorporates cross-
arch stabilization, controlling occlusal overload, minimizing
cantilevers, and increasing the anterior-posterior distribution
of implant placement, can significantly increase the success
rates of loading dental implants immediately after placement.
Implant Placement Using a Flapless FIGURE 59.19 A, Removal of small circular section of tissue prior to
Approach osteotomy. B, Dental implant in place.
Flapless implant surgery is the placement of a dental im-

plant without elevation of the epithelium, connective tissue, (Fig. 59 21). These guides are usually used in fully edentu-
and periosteum covering the alveolar bone. It is performed lous arches and have fixation screws that keep them in place.
by either drilling through the soft tissue with twist drills or When using a flapless approach, before initiating the osteoto-
by first removing a small circular section of the soft tissue my, the operator should sound the soft tissue with a periodon-
(Fig. 59. l 9A) and preparing the osteotomy, and placing the tal probe to ascertain the tissue thickness and account for this
implant (Fig. 59 19B) without reflecting a full-thickness flap. dimension when determining the final position of the implant
Flapless surgery has been shown to be successful and has platform in the apical-coronal dimension (Fig. 59.22).
many advantages because it is minimally invasive. The ben- A common complication is placement of the implants
efits of flapless surgery include a decrease in associated surgi- apical to the crestal bone because it is difficult, even with a
cal morbidity, including postoperative pain, ecchymosis, and punch, to visualize the alveolar bony crest in relation to the
swelling, as well as a reduction in surgical time and intraop- platform of the implant. If this occurs, it is difficult to fully
erative bleeding. Studies show that when a full-thickness mu- seat the abutment. Therefore, the relationship between im-
coperiosteal flap is raised, there is loss of bone volume, while plant and abutment connection must be verified by periapical
a flapless approach results in less bone resorption. radiographs. If bone prevents abutment seating, the implant
The lack of operator visualization of the alveolus when must be backed out until it is at the crest or the bone must
preparing osteotomies and placing implants may increase the be removed with a profile drill. If a fenestration occurs when
potential for complications. The most common problems as- placing the dental implant, full flap reflection is required, and
sociated with flap less surgery are the loss of keratinized tissue GBR procedures should be performed to augment the bone
when excising the crestal "circle" of soft tissue and improper and cover the fenestration.
positioning of the dental implant within the bone resulting Although flapless implant surgery has many beneficial fea-
from a lack of direct vision. Improper positioning may result tures, it is a technique-sensitive procedure that requires surgi-
in a dehiscence/fenestration defect (Fig. 59.20) or damage to cal experience, an accurate surgical guide, and knowledge of
adjacent vital structures. the anatomy surrounding the planned implant site.
An anatomically correct computer-generated surgical
guide fabricated from a three-dimensional CT or CBCT scan Prosthetic or Mechanical
is recommended when performing flapless surgery to reduce
potential implant malposition complications. There are sev-
Complications
eral systems (ie, Nobelguide, Materialize SurgiGuide) that can Prosthetic or mechanical complications occur when the
generate a precise surgical guide with metal sleeves of exact strength of materials is no longer able to resist the forces that
dimension that can direct the implant into proper position are being applied. As materials fatigue, they begin to stretch
FIGURE 59.20 A, Preoperative clinical view of missing single tooth #5. There appears to be good alveolar ridge shape with adequate keratinized
gingiva. B, Radiograph showing good bone height and mesial-distal space available for single tooth implant. C, Occlusal view of circular "punch"
incision used to access bone and prepare implant osteotomy. D, Full flap reflection (after noticing suspicious protrusion in labial vestibule) revealed
implant protruding out of alveolar bone on buccal surface.
FIGURE 59.21 A, Clinical view of computer-generated surgical guide showing metal drill sleeves in the position of planned implants. B, Clinical
view (buccal) of implant mounts emerging from gingival showing accurate placement of four implants in the posterior maxilla using the computer-
generated surgical guide. C, Photo of three surgical guides with increasing sleeve diameter that are used in the sequence of implant site preparation.
D, Radiographic view of four implants placed in the planned position using the computer-generated surgical guide.
retained by multiple implants, the ability to detect a loose

screw is greatly diminished and the problem may go unno-
ticed until additional screws stretch, fatigue, and fracture. In
either case, the biomechanical support (and resistance) for the
restoration must be evaluated and if possible, changed to pre-
vent recurrence of the problem.
Implant Fracture
The ultimate mechanical failure is implant fracture because
it results in loss of the implant and possibly the prosthesis
(Fig. 59.23). Furthermore, removal of a fractured implant cre-
ates a large osseous defect. Factors such as fatigue of implant
materials (Fig. 59.24) and weakness in prosthetic design or
dimension are the usual causes of implant fractures. Balshi
FIGURE 59.22 Use of a periodontal probe to sound the bone and listed three categories of causes that may explain implant
measure the soft-tissue thickness over the bone in the proposed im- fractures: (1) design and material, (2) nonpassive fit of the
plant site. prosthetic framework, and (3) physiologic or biomechanical
overload. Patients with bruxism seem to be at higher risk for
such events and therefore need to be screened, informed, and
and bend; ultimately, depending on the applied forces, they
managed accordingly. These patients should be fitted with
will fracture. Material failures, in turn, lead to prosthetic com-
occlusal guards in conjunction with placement of the final
plications such as loose, broken, and failed restorations.
prostheses.
Screw Loosening and Fracture

Screw loosening has been reported to occur quite frequently
in screw-retained FPDs. Screw-retained single crowns at-
tached to externally hexed implants (ie, those with narrow- or
standard-diameter restorative interface connection surfaces)
are particularly prone to this type of mechanical complica-
tion. Studies have reported screw loosening in 6-49% of
cases at the first annual checkup. Screw loosening was a
more prevalent problem with earlier designs. For example,
abutment screws were previously made with titanium, which
did not offer the clamping forces of current materials. Newer
abutment designs and improved abutment screws allow for
an increased clamping force to be achieved without excessive
torque levels, which has helped to reduce the rate of screw
loosening.
Abutment or prosthesis screw loosening is often correct-
ed by retightening the screws. Over time, however, if screws FIGURE 59.24 Implant fractured at internal connection collar result-
ing from fatigue. This collar fracture was caused by rotational forces
continue to be stretched, they become fatigued and eventu- applied to the implant at the time of placement into dense bone. The
ally fracture. This problem is evident in the patient with a fracture was likely the result of a combination of material weakness and
loose single crown. However, in the patient with a prosthesis density of the prepared site.
FIGURE 59.23 A, Radiograph of fractured implant (standard diameter) used to support a molar-sized single crown in the posterior mandible. B,
Crown and coronal portion of implant (same as that shown in A) that fractured between the third and fourth threads.
FIGURE 59.25 Fractured porcelain from incisal edges of implant-

supported FPO.
Fracture of Restorative Materials

Fracture or failure of materials used for implant-retained res-
torations can be a significant problem. This is particularly true
for veneers (acrylic, composite, or ceramic) that are attached
to superstructures (Fig. 59.25).
Esthetic and Phonetic Complications

Esthetic Complications
The challenge of modern implant dentistry is achieving an es-
thetic, as well as a functional, implant restoration. Harmoni-
ous tooth shape, size, and ideal soft-tissue contours are key
factors for successful esthetic outcomes.
Esthetic complications arise when patient expectations
are not met. Patient satisfaction with the esthetic outcome of
the implant prosthesis vary from patient to patient, depend-
ing on a number of factors. As mentioned earlier, the risk
for esthetic complications is increased for patients with high
esthetic expectations and less-than-optimal patient-related
factors (eg, high smile line, thin periodontal soft tissues, or
inadequate bone quantity and quality). In addition to the
actual appearance of the final restoration, individual percep-
tions and desires determine the acceptance of the results.
Esthetic complications result from poor implant position
and deficiencies in the existing anatomy of the edentulous FIGURE 59.26 Poor implant position makes it impossible to restore
sites that were reconstructed with implants. An important with an esthetic, "natural appearing" restoration. A, Anterior view with
prerequisite for achieving optimal gingival tissue contour is removable partial dentures inserted. B, Anterior view without remov-
able partial dentures. Notice the high level of implant cover screw/head
sufficient periimplant bone to support the soft tissues. Hard- exposure (maxillary right lateral incisor) that is significantly apical to the
tissue defects can be treated by a variety of bone augmenta- level of the adjacent natural tooth (cuspid) gingival margin. C, Occlusal
tion procedures. view of same patient. Again, notice the labial projection of same implant
Implant placement in the esthetic zone requires precise (maxillary right lateral incision), as well as the palatal position of the
implant in premolar area. Any attempt to restore the anterior implants
three-dimensional tissue reconstruction and ideal implant
would not be esthetically acceptable.
placement. This reconstructive procedure enables the restor-
ative dentist to develop a natural emergence profile of the im-
plant crown. If the amount of available bone does not allow
for ideal implant placement and if the implant is positioned (Fig. 59.28). These restorations provide numerous advantages
too apical, buccal, or in the proximal space, an unesthetic over conventional restorations, including improved lip sup-
prosthetic profile will be developed (Fig. 59.26). port, masking of interproximal spaces, and restoration of gin-
If crown contours and dimensions are not ideal or if gingival symmetry in selected cases.
gival harmony around the implant restoration is unesthetic, If the patient is truly dissatisfied with the esthetic result
the patient may consider the implants or restorations as com- and there is a problem with the position of the implants that
plications because the outcome does not represent a natural can be corrected (ie, the patient's expectations are reasonable),
appearance (Fig. 59.27). Gingiva-colored materials used to the implants could be removed; the case could be reevaluated
replace lost gingival anatomy can offer an alternative to sur- and possibly retreated. However, the clinician should consider
gical augmentation in patients undergoing implant therapy prosthetic solutions before implant removal. Use of angulated
731.eB PART 3 Oral lmplantology
FIGURE 59.27 High gingival margin on single-tooth implant crown in FIGURE 59.28 Pink porcelain used on implant-supported fixed res-
the maxillary lateral incisor position. Notice the discrepancy between toration to mask the high gingival margin and long implant crowns
gingival margin levels of the implant and the adjacent natural teeth. resulting from an uncorrected alveolar ridge defect.
abutments, superstructures, and gingiva-colored materials Phonetic Problems

may result in an acceptable esthetic result, thus avoiding mul-
tiple surgeries necessary to rebuild hard and soft tissue if an Implant prostheses that are fabricated with unusual palatal
integrated implant is removed. contours (eg, restricted or narrow palatal space) or that have
Careful patient evaluation and treatment planning along spaces under and around the superstructure can create pho-
with a solid understanding and appreciation for the predict- netic problems for the patient. This is particularly problem-
ability and limitations of implant procedures will minimize atic when full-arch, implant-supported, fixed restorations are
esthetic complications. Patients with a high smile line, high fabricated for patients who have a severely atrophied max-
esthetic demands, thin periodontium, or lack of hard- and illa. These patients are probably best served with an implant-
soft-tissue support in the anterior esthetic region are some of assisted maxillary overdenture because the design facilitates
the most difficult cases to treat and should only be treated replacement of missing alveolar structure and avoids creating
after extensive planning by experienced clinicians. spaces that allow air to escape during speech.
59 Peri implant Disease and Management 731.e9
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60
Supportive Implant Treatment
J Do • PR Klokkevold • A Jain
Chapter Outline
Rationale for Supportive Implant Implant Maintenance
Treatment Treatment of Periimplant Diseases
Examination of lmplant(s) Referral of Patients to the Periodontist
Assessment of Periimplant Health
Dental implant therapy does not end with the final prosthetic implants. Periimplantitis is characterized by periimplant in-
restoration of the implant. Predictability and long-term suc- flammation with progressive crestal bone loss beyond the ini-
cess of a dental implant and its restoration require sound tial remodeling. The prevalence of periimplantitis in patients
treatment planning, precise surgical and restorative execution, ranges from 11.2-53%. Poor oral hygiene, residual cement,
and impeccable long-term maintenance, which is contingent current or history of periodontitis, cigarette smoking, and dia-
on patient compliance with home care and professional sup- betes mellitus are risk factors for periimplant diseases.
portive implant treatment. Periimplant maintenance begins as The relationship between periimplant mucositis and pe-
the implant becomes exposed to the oral cavity and continues riimplantitis is similar to that of gingivitis and periodontitis.
at regular intervals during the life of the implant. The recall in- Although periimplant mucositis does not necessarily progress
terval is determined by the patient's oral hygiene and suscep- to periimplantitis, it is likely the precursor to periimplantitis.
tibility to plaque-induced inflammatory diseases. Initially, for The inflammatory response in periimplant disease appears to
the first year after treatment, recall maintenance visits should be similar to that in periodontal disease. However, severity
be scheduled at 3-month intervals and then adjusted to suit and rate of disease progression appear to be more pronounced
the patient's individual needs. Some patients (those who have around implants. This, perhaps, is due to the absence of a "self-
good oral hygiene, minimal deposits, and disease resistance) limiting" process, observed in periodontitis, around implants
will require infrequent professional hygiene maintenance, that separates the inflammatory cell infiltrate from the bone.
whereas others (those who have poor oral hygiene, heavy de- Experimental models demonstrated that periimplant mucositis
posits, and disease susceptibility) will require more frequent is reversible at the biomarker level [matrix metalloproteinase
follow-up care. 8 (MMP-8) and interleukin-If (IL-1~)]. A review of the lit-
erature reported that periimplant mucositis can be effectively
Rationale for Supportive Implant treated with nonsurgical mechanical therapy while such mo-
dalities tend to be ineffective against periimplantitis. Further-
Treatment more, results of surgical treatment for periimplantitis are not
Although dental implants are not vulnerable to dental caries, predictable. For these reasons, the prevention, early detection,
they are still susceptible to mechanical complications and pe- and early treatment of periimplant diseases are critical. Peri-
riimplant plaque-induced inflammatory tissue changes. A 10- odic and well-regimented supportive implant treatment is es-
year retrospective study of 397 fixed-implant reconstructions sential to the long-term success of dental implant therapy.
in 300 patients observed a mechanical complication rate of
2 4. 7%. The most frequent complication was ceramic chipping Examination of lmpfant(s)
(20.31 %), followed by occlusal screw loosening (2.57%), and
loss of retention (2.06%). Although relatively infrequent, oc- The supportive implant-treatment appointment should in-
clusal screw loosening can result in a subgingival gap at the clude: an inquiry of any new concerns, problems, or pain;
implant-abutment junction that retains plaque and stimulates review of changes in the patient's medical and oral status;
an inflammatory reaction in both the soft and hard tissue. evaluation and reinforcement of oral hygiene; examination
Biologically, periimplant-plaque accumulation due to inad- and evaluation of soft and hard tissue health; evaluation of
equate or lack of access for oral hygiene can result in peri- implants and the associated implant restorations' stability and
implant mucositis and periimplantitis. Periimplant mucositis integrity; and professional supportive treatment. Finally, as-
is characterized by inflammation confined to the soft tissue sessment should be made to determine the appropriate recall
and is reported to affect up to 80% of patients with dental interval and plan for the next visit.
733
FIGURE 60.1 Periimplantitis. A and B, Minimal plaque accumulation. Periimplant mucosa exhibits minimal erythema and edema. Note: buccal
placement of implant in B. C, Manipulation of tissue indicates lack of buccal keratinized attached gingiva and exudation from periimplant sulcus
(arrow). D, Periapical radiograph shows periimplant-bone loss to the apex of the implant.
Examination begins with visual inspection for plaque and is no equivalent fiber attachment around implants. Connec-
calculus accumulation; signs of inflammation and swelling; tive tissue fibers around implants generally run parallel to the
periimplant soft-tissue quality, color, consistency, and con- implant or restorative surface and do not have perpendicular
tour; and aberrations in the implant prostheses. Periimplant or inserting fibers (see Chapter 56). The primary source of re-
soft tissue can be digitally palpated to detect edema, tender- sistance to the probe around an implant will differ depending
ness, exudation, or suppuration. Periimplant probing can be on the conditions surrounding the implant. At noninflamed
used to assess the condition and level of soft and hard tissues sites, the most coronal aspect of connective tissue adhesion to
surrounding implants. When indicated, radiographic images the implant will resist the probe. At inflamed sites, the probe
can be obtained to help verify the level of the periimplant tip consistently penetrates farther into the connective tissue
crestal bone. Determination of implant stability (mobility) until less inflamed connective tissue is encountered, which is
and percussion testing can help verify implant osseointegra- often close to or at the level of bone.
tion (Fig. 60.1) The value of periimplant probing is different than peri-
odontal probing and offers very limited information by com-
parison. Probing around implants can measure the level of the
Periimplant Probing
mucosa! margin relative to a fixed position on the implant or
Probing of implants can be done with light force (0 25 N) us- restoration and can also measure the depth of tissue around
ing a traditional steel probe without adverse effects to the pe- the implant. The periimplant probing depth is often a mea-
riimplant mucosa. Implant probing should be recorded at the sure of the thickness of the surrounding connective tissues
time of final restoration delivery as the baseline measurement and correlates most consistently with the level of surround-
and at least annually thereafter. ing bone. However, periimplant probing is affected by several
Clinicians should use caution when evaluating periim- conditions, including the size of the probe, the force and di-
plant probing because these measures cannot be interpreted rection of insertion, the health and resistance of periimplant
the same as probing depths around teeth. While periodontal tissues, the level of bone support, the features of the implant,
probing around natural teeth is very useful to assess the health abutment, and prosthesis design (Fig. 60.2). A comparison of
of periodontal tissues, the sulcus or pocket depth, and the probing pocket depth of implants with periimplantitis before
level of attachment, probing around implants may not provide and after the removal of the prosthetic restorations reported
comparable results. Due to distinct differences in the tissues similar probing depths in only 3 7% of sites. In 39% of sites,
that surround and support teeth compared to those that sur- the difference was ±1 mm, in 15% of sites, it was ±2 mm,
round and support implants, the probe inserts and penetrates and in 9% of sites, it was ±3 mm. In other words, probing
differently. Around teeth, the periodontal probe is resisted by measurements can be an accurate measure of soft-tissue thick-
the health of the periodontal tissues and, perhaps most impor- ness around an implant (ie, periimplant soft tissue above the
tantly, by the insertion of supracrestal connective tissue fibers bone level), but in many cases or sites, the inability to prop-
into the cementum of the root surface. These fibers, unique to erly angle and direct the probe alongside of the implant may
teeth, are the primary source of resistance to the probe. There lead to the inaccurate assessment of soft-tissue thickness. In
60 Supportive Implant Treatment 735
of an overwhelming bacterial insult and subsequent host re-

sponse. Furthermore, human biopsies indicate that periim-
plantitis and periodontitis exhibit similar histologic features
including an inflammatory cell infiltrate in the connective tis-
sue dominated by B lymphocytes and plasma cells, as well
as upregulation of inflammatory biomarkers. No convincing
evidence indicates that laboratory tests for the identification of
suspected periodontal pathogens are of any use in the evalu-
ation of implants. The usefulness of microbial testing may be
limited to the evaluation of periimplant sites that show signs
of infection and bone loss, so the clinician can prescribe ap-
propriate antibiotics.
FIGURE 60.2 Buccal probing of implant impeded by implant resto-
ration. Stability Measures
The assessment of implant stability (or mobility) is an im-
these situations, the clinician must appreciate the limitations portant measure for determining whether osseointegration is
and know that other clinical parameters and radiographs are being maintained. Important as it is, however, this measure
required to help evaluate periimplant condition. Furthermore, has extremely low sensitivity but high specificity; that is, an
probing around implants is likely to be more variable than implant may exhibit significant bone loss and remain stable.
around teeth; studies have shown that a change in probing Stability measure in this case has a low sensitivity for the de-
force around implants results in more dramatic changes than tection of any bone loss. Conversely, if any implant mobility
a similar change in probing force around teeth. The probing is detected, it is likely that the implant is not surrounded by
depth around implants presumed to be "healthy" (and with- bone; mobility is highly specific for the detection of implant
out bleeding) has been documented to be about 3 mm around failure or lack of osseointegration. Mobility must be differ-
all surfaces. The absence of bleeding on probing around teeth entiated between loss of implant osseointegration and loose
has been established as an indicator of health and a predictor implant restoration.
of periodontal stability. Studies comparing bleeding on prob- There is a great interest in evaluating the stability of the
ing around teeth and implants in the same patient have re- bone-to-implant contact in a noninvasive manner. Two
ported that bleeding around implants occurs more frequently. noninvasive techniques that have been used for evaluating
The presence of bleeding on probing at implant sites may implant stability are impact resistance (eg, Periotest) and
indicate inflammation in the periimplant mucosa. However, resonance frequency analysis (RFA). Originally designed to
the ability to use bleeding on probing as an indicator of as- evaluate tooth mobility quantitatively, the Periotest (Gulden,
sessing diseased versus healthy sites around implants has not Bensheim, Germany) is a noninvasive, electronic device that
been established. Due to the potential for false-positive bleed- provides an objective measurement of the reaction of the
ing (ie, provoked-bleeding) with probing, the use of marginal periodontium to a defined impact load applied to the tooth
bleeding, which is a more sensitive indicator of inflammation crown. The Periotest value depends to some extent on tooth
and is less likely to elicit false-positive bleeding, has been pro- mobility but mainly on the dampening characteristics of the
posed to assess periimplant inflammation. Marginal bleeding periodontium. Despite the dependence on the periodonti-
can be evaluated by running a probe circumferentially along um, the Periotest has been used to evaluate implant stability
the coronal portion in the implant sulcus. Overall, the value of as well. However, unlike teeth, the movement of implants
periimplant probing is in monitoring changes in the probing and the surrounding bone are minuscule and therefore the
pocket depth over time rather than the initial value as some Periotest values fall within a much smaller range compared to
implants may be placed apically for esthetics. the range found with teeth. Detection of horizontal mobility
may be a significant advantage for the use of the Periotest be-
Microbial Testing cause it is much more sensitive to horizontal movement than
similar detection by other means, such as manual assessment.
Studies in animals and humans have demonstrated the de- Another noninvasive method used to measure the stability of
velopment of periimplant mucosa! inflammation in response implants is with RFA. This method uses a transducer that is
to the accumulation of bacterial plaque. Microbiologic stud- attached to the implant or abutment. A steady-state signal is
ies suggest that greater probing depths or "pockets" around applied to the implant through the transducer and a response
implants harbor higher levels of pathogenic microorganisms. is measured. The RFA value is a function of the stiffness of
Studies have also documented similarities in the microbial the implant in the surrounding tissues. The stiffness is influ-
composition of plaque in healthy periodontal sites compared enced by the implant, the interface between the implant and
to healthy periimplant sites. Likewise, evidence indicates that bone and soft tissues, as well as the surrounding bone itself.
the microbiota of diseased periodontal pockets harbor the Additionally, the height of the implant or abutment above
same periodontal pathogenic microorganisms as those ob- the bone will influence the RFA value. Unlike the Periotest,
served in inflamed periimplant sites (periimplantitis). How- however, the RFA is not dependent on movement in only
ever, there is no evidence to prove that periodontal pathogens one direction. Thus, the absolute RFA values vary from one
cause periimplant disease and the pathogenesis of inflam- implant design to another and from one site to another but
matory disease around implants has not been defined. A re- there is high consistency for any one implant or location. The
cent report now generally accepts the belief that periimplant value of RFA is most appreciated with repeated measures of
disease, like periodontal disease, occurs primarily as a result the same implant over time because it is very sensitive to
FIGURE 60.3 A, Periapical radiograph capturing the whole implant. B, A second perpendicular periapical is necessary to assess crestal bone level.
Note: platform-switching at implant-abutment junction.
changes in the bone-implant interface. Small changes in tis- evaluate the presence and quality of bone along the length of
sue support can be detected using RFA. An increase in the the implant, as well as to detect any periimplant radiolucen-
RFA value indicates increased implant stability, whereas a cies. Although the predictive value of assessing implant stabil-
decrease indicates loss of stability. However, this is a rela- ity with radiographs is low, films do offer a reasonable method
tive measure and it has not been determined whether RFA to measure changes in bone levels. The predictive value of
is capable of detecting impending failure before the implant detecting implant failure or loss of stability is good when ra-
actually fails. Currently, much interest and research have fo- diolucent lesions are discovered with periapical radiographs.
cused on the use of noninvasive methods to evaluate implant Radiographic identification of unstable implants is reliable
stability. Mobility remains the cardinal sign of implant failure when performed as part of annual examinations and when
and detecting mobility is therefore, an important parameter. examining patients on a routine, long-term basis.
The radiographic examination remains one of the primary
Implant Percussion tools for detecting failed or failing implants in routine clinical
evaluation, even though it is not as accurate as mobility tests.
Tapping of an implant-healing abutment or restoration with In one study designed to evaluate the accuracy and precision
an instrument will produce a sound that can help determine of radiographic diagnosis of mobility, the probability of pre-
implant osseointegration. A solid resonating sound and the dicting implant mobility in a population with a low preva-
absence of pain usually indicate implant osseointegration. lence of implant failures was found to be low. Other studies,
A dull sound may indicate the implant is fibrous encapsu- however, have demonstrated much higher predictive value for
lated; radiographic and other clinical findings are needed for radiographic diagnosis of implant mobility. The authors con-
diagnosis. cluded that the most important factors for making an accurate
radiographic diagnosis are the quality of the radiograph and
the experience of the clinician.
Radiographic Examination
Perpendicular intraoral-periapical radiographs should be
taken at implant placement, at abutment connection, at final Assessment of Periimplant Health
restoration delivery for baseline documentation of bone levels,
Evaluation of Plaque (Biofilm) Control
and annually thereafter to monitor marginal or periimplant-
bone changes. In the presence of periimplant inflammation, Impeccable plaque control or removal of biofilm is crucial
a periapical radiograph is indicated for periimplant-bone for periimplant tissue health. Poor plaque control is associ-
evaluation and disease diagnosis. Periapical radiographs have ated with periimplant diseases with an odds ratio of 14.3. It
excellent resolution and, when taken perpendicular to an im- is advantageous to evaluate plaque control prior to any tissue
plant, can provide valuable details of the implant-abutment manipulation. The amount and location of plaque and cal-
junction, mesial and distal crestal bone level relative to the culus accumulation should be assessed visually. Poor plaque
implant platform, and bone-to-implant interface along the control is typically associated with plaque and calculus reten-
length of the implant (Fig. 60.3). The limitation of periapi- tion and erythematous and edematous gingival tissue. When
cal radiographs is that they are difficult to standardize and plaque control is inadequate, the patient should be asked to
great variability is inherent in the acquisition process. How- demonstrate his or her oral hygiene routine in front of a mir-
ever, periapical radiographs are relatively simple, inexpensive, ror so that the clinician can evaluate the patient's oral hygiene
and readily available in the dental office. It is diagnostically techniques. If the patient fails to remove plaque in any areas,
important to obtain images that clearly show implant threads the patient's attention should be directed to the location of
(ie, not blurred by nonperpendicular angulation) and the the plaque. An instrument can be used to remove the plaque
restorative-implant abutment connection. under the attention of the patient so that he or she can see its
The objective of the radiographic examination is to mea- color and consistency. At this time, oral hygiene instruction
sure the height of bone adjacent to the implant(s) and to should be demonstrated and reinforced.
FIGURE 60.4 A, Subcrestal placement of implant with adequate buccal and lingual bone thickness. B, Periapical radiograph at time of implant place-
ment. C and D, Implant at 5-month osseointegration check exhibiting adequate periimplant keratinized attached tissue and crestal bone remodeling
to the first thread. Arrows indicate mesial-crestal bone level.
Evaluation of Periimplant Health determine periimplant-bone loss. The presence of suppu-

and Disease ration often indicates periimplantitis. Radiographic crestal
bone loss beyond the implant baseline level at the time of
Periimplant mucosal health is characterized by pink, firm, and final prosthesis delivery in conjunction with bleeding on
well-adapted gingival tissue. Periimplant disease is associated probing is characteristic of periimplantitis; due to potential
with clinical erythema, edema, and loss of tissue tightness measurement errors, a threshold of detectable bone loss of
around the implant. Periimplant mucosa can be nonke- 1.0-1.5 mm is recommended for diagnosis of periimplantitis.
ratinized unattached (Fig. 60 .1 C) or keratinized attached In the absence of a baseline radiograph, a vertical distance of
(Fig. 60.4C). In the presence of keratinized attached mucosa, 2 mm from the expected marginal bone level following the
a gingival seal or gingival cuff is established around the im- initial crestal bone remodeling is recommended as the thresh-
plant. The gingival cuff has the potential to protect the under- old for diagnosing periimplantitis. The amount of initial mar-
lying bone and reduce subgingival plaque formation. Due to ginal bone remodeling can vary depending on the design of
the mobile nature of oral mucosa, the protective function of the implant-abutment junction. Platform-switched implants
nonkeratinized unattached periimplant mucosa may not be as (Figs. 60.3 and 60 SC), in which the abutment is internally
effective. However, the presence of keratinized attached gin- offset relative to the implant fixture at the implant-abutment
giva, which can facilitate oral hygiene, is not a requisite for junction, may exhibit less crestal bone remodeling than non-
periimplant health if plaque is well controlled. Nonetheless, platform-switched implants (Fig. 60.4), in which the abut-
sites deficient in keratinized attached tissue typically exhibit ment is flush or even with the implant fixture at the implant-
vertical and/or horizontal ridge deficiencies, shallow vestibu- abutment junction.
lar depths, and long or bulky restorations. All of these factors
can impede oral hygiene access and contribute to plaque ac-
cumulation and periimplant inflammation.
Evaluation of Implant Osseointegration
In the presence of periimplant inflammation, the periim-
plant tissue must be palpated for tenderness and suppura- Implant osseointegration must be determined prior to the
tion, the implant must be probed, and periapical radiographs fabrication and delivery of the final implant prosthesis. Im-
must be obtained and compared to baseline radiographs to plant osseointegration can only be definitively determined
FIGURE 60.5 Restoration designed with adequate hygiene access. A, Lingual view. B, Mesia[ view of buccal contour. C, Periapical radiograph
showing gradual transition from implant fixture to restoration. Note: platform-switching at implant-abutment junction.
histologically, which would require the implant and the sur- replaced and properly torqued down. Worn-out retentive
rounding bone to be removed. Thus, a combination of ra- components must be replaced periodically to ensure proper
diographic and clinical parameters is used to make an as- retention, stability, and function of the removable prostheses.
sessment of implant osseointegration or to rule out lack of Occlusal wear of teeth and fit of tissueborne surfaces of im-
osseointegration. These include absence of periimplant in- plant-tissueborne prostheses should be assessed and correct-
flammation and pain to palpation and percussion, presence ed as indicated. In patients with oral parafunctions and heavy
of a solid resonating sound to percussion, complete radio- occlusal forces, occlusal guards are recommended to protect
graphic bone-to-implant contact along the implant surface implants and restorations.
(ie, absence of radiolucencies along the bone-implant inter-
face), and implant stability.
Implant Maintenance
Methods for Patient Oral Hygiene
Evaluation of Implant Restorations
The importance of good oral hygiene should be stressed even
Implant superstructures, frameworks, and restorations should before implants are placed, and periimplant oral hygiene for
be fabricated to accommodate and facilitate oral hygiene (eg, plaque control should begin as early as possible once the im-
embrasure spaces should be made to allow the passage of a plant is exposed to the oral cavity. A cotton tip, cotton gauze,
proxy brush) (Fig. 60.4). Occlusal schemes of implant resto- or soft toothbrush can be used to gently remove plaque from
rations should provide adequate posterior support, maximize healing abutments or provisional restorations during the early
axial loading, and minimize incline contacts, nonaxial loading, postoperative phase of healing. Products that can be consid-
and interferences in excursive movements. During delivery, ered abrasive or aggressive for plaque control have not been
radiographs perpendicular to the implant should be obtained tested during this phase. Once implant osseointegration has
for baseline documentation and to verify complete seating of been achieved and verified, a comprehensive oral hygiene
the restorations. Following delivery, cement-retained implant regimen is needed. The research in this area is limited and has
restorations should be thoroughly evaluated for residual ex- not lead to a standard protocol or regimen for implant main-
cess cement, which must be removed. During follow-up visits, tenance. Most recommendations are based on expert opinion,
implant restorations should be carefully examined for heavy research of natural teeth, and experience. Evidence from a sys-
contacts, fractures, loose screws, and in removable prostheses, tematic review showed that mechanical plaque control with
worn-out retentive components (ie, Hader clips and locator- either a powered or manual toothbrush can be effective in re-
attachment inserts). Occlusion should be adjusted according- ducing mucositis. Other dental hygiene aids, such as dental
ly to prevent implant overload and fractures of implant parts. floss, rubber tip, and interdental brushes, may also be recom-
Loose abutment and setscrews must be evaluated, possibly mended (Fig. 60.6) but there is no research to demonstrate
FIGURE 60.6 Methods for patient oral hygiene. A, Flossing. B, Bass method of brushing with extra-soft toothbrush. C, lnterproximal brushing.
D, Removal of plaque with a rubber tip. Note: hygiene is targeted at the removal of plaque along the gingival margin.
FIGURE 60.7 Water flosser tip with three tufts of bristles recommended for implants. (Courtesy Water Pik, lnc., Fort Collins, CO, USA.)
their efficacy. A powered water flosser has been studied with Methods for Professional Recall
implants. One study reported subgingival irrigation of 0.06% Maintenance
chlorhexidine gluconate with a Waterpik Water Flosser (Wa-
ter Pik, Inc., Fort Collins, CO, USA) to be more effective at re- Professional maintenance consists of the removal of dental
ducing plaque and mucosa! inflammation and produced less plaque and calculus from implant components exposed to the
stains than rinsing with 0.12% chlorhexidine gluconate once oral environment. Similar to root surfaces, the transmucosal
a day (Fig. 60. 7) Another randomized controlled study com- surfaces of implants should be smooth to minimize plaque
pared a water flosser to string floss over 4 weeks. The water accumulation and to facilitate oral hygiene practices. As such,
flosser group showed an 81 % reduction in bleeding compared at sites with excellent plaque control and periimplant health,
to 33% for string floss, which is a 2.45-fold difference. Pa- the need for professional instrumentation is minimal and
tients require products that they can easily maneuver around should be limited to prevent iatrogenic damage to implant
the prosthetic replacement and access areas susceptible to components that can contribute to plaque and calculus ac-
plaque accumulation to prevent periimplant diseases. cumulation. In the presence of plaque, calculus and tenacious
deposits, care should be taken to minimize damage to trans- consist of antimicrobial rinse and irrigation, local antibiot-
mucosal implant surfaces. However, priority should be placed ics, ultrasonic debridement, mechanical debridement with
on the complete removal of implant surface deposits. air-abrasive devices, and laser therapy. Surgical treatment
All metal instruments, including metal curettes, scalers, includes full-thickness flap elevation for access followed by
and (ultra)sonic scalers, increase surface roughness of pol- degranulation, surface debridement by laser or mechanical in-
ished titanium. As such, the use of plastic, Teflon-coated, struments, surface decontamination with laser or antimicrobi-
carbon- and gold-coated curettes, and nonmetal ultrasonic als, and bone augmentation. Based on two systematic reviews,
tips have been advocated to protect the titanium-implant currently available scientific data is insufficient to suggest
surface and the titanium abutment from contamination by which treatment intervention of periimplantitis is most effec-
other metals and to reduce the likelihood of scratching the tive and which antibiotic should be administered locally or
surface. Unfortunately, the large size and flexibility of non- systematically. Implant-surface decontamination/disinfection
metal curettes may not allow effective plaque and calculus remains challenging especially for implants with roughened
removal; and Teflon- and gold-coated curettes cannot be surfaces. For some treatment modalities, recurrence of periim-
sharpened. Most current implant prostheses are made with plantitis appears to be high (up to 100%) after 1 or more years
gold alloys or ceramic materials, which are usually identical of treatment and retreatment may be necessary. Surgical access
to the materials used in restorations for the natural denti- appears to be necessary to arrest periimplant-bone loss. Surgi-
tion. Furthermore, the location of the connection between cal treatment may result in gingival recession and compromise
these restorative materials and the implant is typically below esthetics. At sites with high esthetic demands, definitive treat-
the mucosa and often near the crest of bone; most calculus ment of periimplantitis may include the removal of the im-
removal occurs above this level. Thus, the fear of contami- plant, grafting of the site, and placement of another implant.
nating the titanium implant is unwarranted. The gold alloy
or ceramic surfaces can be debrided with most scalers and
curettes (plastic, gold-coated, and stainless steel) without Referral of Patients
damaging the surface. Rubber cups and polishing paste can to the Periodontist
be used to remove plaque or biofilm and to enhance surface
smoothness of machined and polished surfaces. Magneto- The guidelines described in this chapter will allow many im-
strictive and piezoelectric ultrasonic instruments with metal plant patients to be maintained very well by their primary
tips (eg, Cavitron) should be used with caution because of dental care provider (ie, general dentists). Referral to a perio-
irregularities that can easily be created in the surface. dontist should be considered if periimplantitis or periimplant
mucositis is diagnosed and not resolved with improved oral
hygiene and professional maintenance care. Early referral is
Treatment of Periimplant Diseases advantageous to stop progression and limit extent of bone
The goals of periimplant disease treatment are elimination of loss.
all periimplant infectious and inflammatory processes, pre-
vention of disease progression, and preservation and restora-
tion of function and esthetics. Treatment begins with patient SUGGESTED READINGS
education in the etiology, disease process, prevention of pe- Academy Report: Peri-implant mucositis and pcri-implantitis: a current
understanding of their diagnoses and clinical implications, J Periodontal
riimplant diseases, and oral hygiene instruction. Although 84(4)436-443, 2013.
bacteria are the main etiologic factor, systemic (eg, smoking De Bruyn H, Vandeweghe S, Ruyffelaert C, et al: Radiographic evaluation of
and poorly controlled diabetes) and local factors (eg, residual modern oral implants with emphasis on crestal bone level and relevance to
excess cements and poorly designed restorations that inhibit peri-implant health, Periodontal 2000 62(1):256-270, 2013.
Esposito M, Grusovin MG, Worthington HV: Interventions for replacing
hygiene access) should be identified and modified.
missing teeth: treatment of peri-implantitis, Cochrane Database Syst Rev Jan
18(1) CD004970, 2012.
Lang NP, Berglundh T: Working Group 4 of Seventh European Workshop
Periimplant Mucositis on Periodontology: Periimplant diseases: where are we now? Consensus
Periimplant mucositis can be effectively treated with non- of the Seventh European Workshop on Periodontology, J Clin Periodontal
38(Suppl 11) 178-181, 2010.
surgical mechanical therapy. Treatment requires complete Lindhe J, Meyle J: Group D of European Workshop on Periodontology. Peri-
removal of supramucosal and submucosal plaque, calculus, implant diseases: Consensus Report of the Sixth European Workshop on
and deposits using curettes, ultrasonic scalers, polishing Periodontology,J Clin Periodontal 35(Suppl 8) 282-285, 2008.
cups, and prophy paste. The use of adjunctive antimicrobials Louropoulou A, Slot DE, Van der Weijden FA: Titanium surface alterations
following the use of different mechanical instruments: a systematic review,
(eg, chlorhexidine irrigation and mouth rinse) to mechanical Clin Oral Implants Res 23(6):643-658, 2012.
debridement can enhance treatment outcome. Salvi GE, Aglietta M, Eick S, et al: Reversibility of experimental peri-implant
mucositis compared with experimental gingivitis in humans, Clin Oral
Implants Res 23(2) 182-190, 2012.
Periimplantitis Serino G, Turri A, Lang NP: Probing at implants with peri-implantitis and
its relation to clinical peri-implant bone loss, Clin Oral Implants Res
The treatment of periimplantitis includes nonsurgical and sur- 24(1) 91-95, 2013.
gical interventions, both of which may be combined with the van Winkelhoff AJ: Antibiotics in the treatment of peri-implantitis, Eur J Oral
adjunctive use of antimicrobials. Nonsurgical interventions Implantol 5(Suppl):S4 3-S50, 2012.
60 Supportive Implant Treatment 740.el
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Index
Page numbers followed by "P' indicate figures, "t" indicate tables, and "b" indicate boxes.
A Acute herpetic gingivostomatitis, 368-370 After Five curette, 409f

Aberrant frenum, problems, 574 treatment, 3 70f Gracey curette, comparison, 408f
Abnormal mobility, 278 Acute leukemia, periodontal ligament/alveolar Mini Five curette, comparison, 409f
Abrasion, 277,638 bone (involvement), 140 Afunctional atrophy, 35
example, 277 Acute myelocytic leukemia, 139 AGEs. See Accumulated glycation end-products
Abrasive dentifrice, usage, 2 77 anterior view/palatal view, l 39f Aggregatibacter actinomycetemcomitans (Aa), 4 7,
Abscesses leukemic gingival enlargement, 86,96, 134,239,242,302,309,317,
periodontal origin, 620 appearance, 17 lf 339,354,451
Absorbable gelatin sponge, 494 Acute myelogenous leukemia colonization, 242
Gelfoam, 549 gingiva/floor, enlargement, 136f complement evasion, 111
Absorbable hemostatic agents, 494, 713 gingival hyperplasia/spontaneous etiologic agent, 309-310
Accessory binocular module, example, 605 bleeding, 157 growth
Accessory pulpal canals, presence, 218 soft/hard tissue destruction, mucormycosis inhibition, tetracyclines (usage), 451
Accessory root canals, prevalence, 615-616 (impact), 133-134 invasion, 90
Accidental damage, 56 Acute necrotizing ulcerative gingivitis involvement, 340
Accidental traumatic lesions, 56 (ANUG), 158 isolates, 111
Accumulated glycation end-products drugs, role, 366 periodontitis, association, 103
(AGEs), 134 first visit, 365-366 prevalence, 239
Acellular afibrillar cementum, 26 gingiva, contouring, 367 primary etiologic agent, 107
Acellular cementum (AC), 25 local therapy, inadequacy, 368 strain JP2, 2 48
arrangement, 26 patient instructions, 366 translocation, 102-103
formation, 26 second visit, 366 Aggressive periodontitis, 58, 60-61, 62, 92, 104,
Acellular extrinsic fiber cementum, systemic disease, 365 105t, 106,111,117,125,128,138,
composition, 26 third visit, 366 141,147, 197,213,215,241-249,
Achromatic compound lenses, 603 treatment, 367f 242t, 276,286,297,303,307,310,
Acquired coatings, 12 considerations, 36 7 317,320,327,353,354,356[,358
Acquired deformities/conditions, 67 gingiva, reshaping, 367f advanced bone loss, 74b, 226
Acquired immunodeficiency syndrome (AIDS), Acute pericoronitis, 368 alveolar bone destruction, 215
237,251,311,365 treatment, 368, 369f antibiotic therapy, 257, 358t
advanced AIDS, periodontal health Acute periodontal abscesses, 2 76, 288f, 289 anti-infective therapy, considerations, 449
(appearance), 259f Acute streptococcal gingivostomatitis, lip/gingiva antimicrobial therapy, 464
HAART, usage, 253 lesions, 180 bacterial challenge, host response, 248
health status, 259-260 Acute trauma, 221,222 chronic periodontitis, differences, 662
infection control measures, 260 Adaptive immunity, 91-93 clinical characteristics, 241-242
maintenance therapy, 2 60 innate immunity, differences, 47, 90, 125 clinical presentation, assessment, 249
therapy, goals, 260 Addison's disease, 159 cyclic neutropenia/agammaglobulinemia,
Acquired pellicle, 44 Additive osseous surgery, 535 presence, 138
Acrylic provisional fixed full-arch prosthesis, impact, 498f dental implants, usage, 324
clinical photograph, 672f Adhesive dentistry, 625 full-mouth disinfection, 358
Actinobacillus actinomycetemcomitans levels, Adipose cells, 14 full-mouth radiographs, 356f
elevation, 4 3 Adjunctive orthodontic therapy, 624 generalized form, 60, 453
Actinomyces odontolyticus (colony Adjunctive therapeutic approaches, 462f genetic features, assessment, 250
morphology), 99t Adjunctive therapy, 453 genetics
Actinomyces ens, 97 Adolescents, mean alveolar bone loss per family studies, 248
Actinomyces viscosus, 105t, 109, 200 patient, 121 polymorphisms, 248
root surface caries microorganism, 200 Adult blood pressure, classification, 338t host defense, assessment, 317
Actinomyces odontolyticus, 99t, 120 Adult periodontitis, 452 host modulation, 258
Active disease Advanced alveolar bone resorption, host response, 248
adjunctive orthodontic therapy, 624 clinical/cone-beam computed implant therapy, 331
control, 624 tomography, 682 intraoral clinical photographs, 356f
emergency treatment, 624 Advanced bone loss, 563f, 649f local delivery, 357
hopeless teeth, extraction, 624 aggressive periodontitis, presence, 52b localized aggressive periodontitis, 297
oral hygiene measures, 624 bacterial plaque, impact, 4 7, 113 localized form, 59b
periodontal surgery, 624 presence, mesial root resection, 5 70f microbial testing, 356-357
reevaluation, 624 Advanced chronic periodontitis, 6lf, microbiology, 247
scaling and root planing 358, 611 pathobiology, 247-249
(SRP), 624 Advanced gingivitis, 156 periodontal maintenance, 260
Actonel, 274 Advanced horizontal bone loss, 56 7, 633 periodontal therapy, 256
Acusection, 416 Advanced periodontitis, pocket wall (bacterial postoperative radiographs, 683
Acute abscess, 331 penetration), 198f, 199 probing depths, 63f
chronic abscess, differences, 3 71 Advanced radiographic alveolar bone, prognosis, 315-325
Acute angina! attacks, nitroglycerin observation, 117 regenerative therapy, 317
(usage), 338 Aerosol production, 349 subgroups, 242
741
742 Index
Aggressive periodontitis (cont.) Anatomic spaces, 483, 489 Aredia, 274

supportive periodontal therapy, Anatomic structures, identification, 682 Arg-gingipains, 112
considerations, 463, 643 Androgenic hormones, changes, 158 Arterial blood supply, 487f
surgical resective therapy, 354 Anemia, 159 Arterioles, 14, 167
surgical therapy, considerations, 280 Anesthesia, 296, 338, 339, 341 Aspirin-induced chemical burn, biopsy, 122
susceptibility, environmental factors, 249 Anginal episode, 338 Association, 120f, 124
therapeutic modalities, 353-354 Angioplasty, 339 Atherosclerosis, 262-265, 263
treatment, 353-354 Angiotensin-converting enzyme (ACE) Atrophic periodontal ligament, 36f
planning/restorative considerations, 353 inhibitors, 339 Atrophy, 35,137,140,224
systemic tetracycline, usage, 3586 Angular bone loss afunctional atrophy, 35
Agranulocytosis, 596, 138 furcation, involvement, 378, 383 disuse atrophy, 35
Air-powder polishing, 415 Angular defects (bone), 536, 544 Attached gingiva, 45, 46f, 74
Albrights syndrome (polyostotic fibrous Angulation, 639, 683, 688 amount, 286
dysplasia), 159 distal angulation, 691 demarcation, 165
Alendronate (bisphosphonate), 328 Animals, mitotic rate, 12 example, 46[
Allergies, 495 Ankylosis, 29 interdental papillae, 139f
outpatient surgery, 493 Anosmia, 4 71 mean width, 4f
Allogenic bone graft, usage, 67, 354 Anoxemia, 153 problems, 557-558
Allografts, 466, 54 7, 549t Anterior gingival tissues, initial view, 366[ stippling, 17
Alpha-defensins, 90 Anterior open bite, 119 width, 4
Alveolar bone, 31,117,120 malocclusion, 13 7 determination, example, 2 72f
aging, impact, 30 Anterior sector, moderate-to-severe periodontitis Attached plaque, 98f, 200
cancellous portion, 23 (therapy), 394t Attachment loss, 21
CEJ (relationship), periapical radiographs Anterior teeth, 405, 410, 418 bone loss, relationship, l 94f
(usage), 82t, 115f mobility, 226 pattern, 563
destruction, 87 pathologic migration, 226, 227 Attrition, 27, 46[, 277
aggressive periodontitis, 215 Antibiotics Atypical ulcers (nonspecific oral
infection, impact, 287 agents, 450 ulcerations), 256
panoramic radiograph, 289 coverage, administration, 346 Augmentation surgeries, 715
development, 29 prophylactic regimens, 340 Autogenic succession, 449
height, 120 serial/combination antibiotic therapy, Autogenous bone grafts, 549
loss, panoramic radiograph, 485f 454-456 Autogenous monocortical block graft,
metabolism, periodontal ligament systemic administration, 450-454 harvesting, 707
(impact), 46-47 background/rationale, 454-455 Autografts, 707
morphologic changes, 4 7 tetracyclines, 454 iliac autograft, placement, 550f
remodeling, 36 therapy, selection (decision tree), 455f Automated periodontal probes, example, 286f
resorption, 88 Antibodies, 40, 43, 52, 90, 92 Automatic cardioverter-defibrillators, 339
stimulation, slightly excessive pressure Anticoagulant medications, 346 Automatic periodontal probing, 341, 365
(impact), 223 Anticoagulant therapy, 346 Avascular necrosis, 462
variation, 157 clinical studies, 346 Avulsed teeth, replantation, 68f
Alveolar crest Anticonvulsants, 158, 163, 164, 166, 529 Azithromycin, administration, 358t, 450t
apical position, 203 Antigen-presenting cells (APCs), 89f, 91
Alveolar dimension, 672, 680f, 712 Anti-infective agent, 450
Alveolar mucosa (AM), 4f, 16, 68, 69f, 256, chemotherapeutic agent, 450 B
258,512 definitions, 450 Bacillary angiomatosis (BA) (epithelioid
Alveolar process, 15, 29, 486, 518, 699 Anti-Inflammatory cytokines, 465f angiomatosis), 254, 256f
knife-edge alveolar process, 699 Antimicrobial agents, 312 Back-action chisel, 417[
sockets, presence, 486 local delivery, 357 Background characteristic, 309-312
Alveolar ridge Antimicrobial peptides, defining, 89 Bacteria-host interactions (modulation), oral
defect, 65, 67[ Antimicrobial resistance, biofilm streptococci (impact), 109
loss, 484[ (relationship), 102 Bacterial challenge
clinical images, 67[ Antiplaque agents, usage, 238 host response, 129
Amalgam Antiplatelet medications, 346 Bacterial DNA, virulence factor, 305, 452
overhang, radiograph, l 18f Antiplatelet therapy, 350 Bacterial enzymes, 86, 102, 112
Ameloblastic epithelium, reduction, 12 Aortocoronary bypass (cardiac bypass), 339 Bacterial pathogens, 134,238, 261, 359
American Academy of Periodontology (AAP), 51, APCs. See Antigen-presenting cells Bacterial plaque, 47,113, 142f, 151,161,
445,456,651 Aphthous lesions, recurrence, 257 212,309
American Dental Association (ADA), 272,383, Apical abscesses, drainage, 620 Bacterial resistance, development (risk), 360,
457,462 Apical diseases, 617 450,452
reports, 340 classification, 617 Bacterial species, summary, 105t, llOt
American Heart Association (AHA), 339 initiation, factors, 619 Bacterial transmission/translocation, 102-103
Arninelluoride, 473 Apical fibers, 21 Bacterium (bacteria)
Amino acids, proteolytic degradation, 468[ Apically displaced nap, 481, 509 adherence, 109
Amlodipine-associated gingival enlargement, 167 facial/lingual preoperative views, 524f ability, 109
Ammonia, production, 86, 102 selection, 529 biofilm mode of living, 96
Amoxicillin, 340t Apical third, tobacco stains, l l 7f initial adhesions/attachment, 99
Amoxicillin-clavulanate potassium, 360, 352 Apical vessels, branches, 36, 618 intraoral translocation, 103
Anaerobic-to-aerobic species, ratio, 107 Apicoectomy, impact, 57[ pathogenic bacteria, 107, 111
Analgesia, levels, 348 Aplastic anemia, appearance, 140, 345t reservoir, subgingival environment, 261
Anamnesis, 470 Arbitrarily primed-polymerase chain reaction, scanning electron micrograph, 7f, 197f
Anatomic area, schematic diagram, 406, 658 105t, 305 secondary colonizers, 99
Anatomic crown/root, distinction, 18 Arbitrary values, 664 species, colonization, 99
Anatomic factors, 310, 3166, 321 Archaea, 96 survival, strategies, 102
Anatomic location, 686, 688, 712 Area-specific curettes, 410 Bad breath
Anatomic morphologic defects, correction, 4 786 curved blade, presence, 406,437 control, chewing gum (usage), 4 73
Anatomic periimplant sulcus, occlusal view, 734f universal curettes, comparison, 406, 408t pathways, 467
Index 743
Baking soda, 4 73 reduction, saline solution cavitation gingival inflammation, impact, 4 78f
Ball sickle scaler, 405 (impact), 720 histopathology, 205
Bard-Parker knife, usage, 513f Blood dyscrasias, 52 mechanisms, 213
Barrier membranes, submerged position, 518, gingival diseases, association, 51 occlusion, trauma (impact), 185
566,707 gingival/periodontal disturbances, patterns, 209-219
Basal cell layer, 9f association, 280 systemic disorders, impact, 213
Basal lamina, 10 Blood pressure (BP), increase, 337 Bone grafts, 354,514,524
internal basal lamina, 10 Blood supply, 351, 487f Bone loss, 565, 567f, 618
Basement membrane, adequacy, 560 advanced bone loss, 74t, 226, 244, 563f
immunolluorescent-labeled Blood vessels, presence, 578, 596, 608 generalized horizontal bone loss, 292f
antibodies, 55f Blood viscosity, 263f horizontal bone loss, 292
Basic life support (BSL), impact, 494 Blotter (Periopaper), usage, 40 mandibular implants, impact, 684f
Bass method, 739f Bone intraoral radiographs, 65f
Bass technique, 388 action radius, 212 periimplantitis, relationship, 104, 114
B-cell activation, endpoint, 92 allografts, 466, 549t, 550 severity, 201
Behavioral considerations, 68lt freeze-dried bone allograft, 551 tooth support, loss, 241
Benign masses, 1 73 angular defects, 212 vertical bone loss, mandibular implants
Benign mucous membrane pemphigoid, 52, 55f appositional index, 691 (impact), 234f
Benzodiazepine, intravenous administration, 499 architecture, correction (absence), 214 vertical movement, 4 38f
Benzothiazine derivatives, 167 blend, 549 Bone morphogenetic proteins (BMPs), 463, 551
Bile pigments, 159 technique, 549 Bone-substitute graft materials, impact, 712
Biofilm bulbous bone contours, 217 Bone-to-implant interface, 657, 663, 6916
accumulation, 144, 145 contour, conformation, 34 Bony architecture, types (diagram), 535, 536f
antimicrobial resistance, relationship, 102 deformities (osseous defects), 214 Bony defect, correction, 537, 544
bacteria distribution, 3 lf Bony depression, l 7f
communication, 102 exposure, 140,503,507 Bony ledges (reduction), osteoplasty
resistance, 102 faciolingual diameter, 289 (usage), 538f
heterogeneity, 124 formation Bony lesions, anatomy, 563
mode of living, 96 buttressing, 213 Bony periodontium, photograph, 535
Biological mediators, 552 periodontal disease, 213 Bony trabeculae, realignment, 30f
Biologic complications, 725, 727 presence, 213 Breastfeeding, 252
Biologic considerations, 624 furcation involvement, 217 Breath malodor, 467-474
Biologic depth, 4, 283 grafting, 66, 493, 712, 714 dental pathologies, 469
Biologic failure, 689 height limits, absence, 692 dry mouth, 469-470
Biologic mediators, usage, 556, 593 inorganic matter/organic matrix, 31 epidemiology, 467
Biologic plausibility, 189 marrow, 33 etiology, 467-470
Biologic pocket depth, 20lf, 232,237 metabolic disease, 681 t intraoral causes, 468-469
Biologic width, 538, 609, 624 morphology, factors, 214, 507 pathways, 467
evaluation, 625 necrosis, 656 periodontal infections, 469
human biologic width, 625 new bone formation, 662 semantics/classification, 467
identification, 625 occlusal forces, transmission, 23 Breath odor, defining, 467
variations, 626 operating mode, 7196 Bristle brushes, 384
violation, ramifications, 625f osteoclasis, mesial root surface, 32f BRON] See Bisphosphonate-related
violation, restoration design/shape osteonectin, expression, 4 lf, 308 osteonecrosis of the jaw
(impact), 626 pocket, relationship, 322 Bruxism, 278
Biomarkers, 94f, 123, 144, 735 quality, 358 Buccal alveolar plate, cervical portion
Biomechanics. See Implants quantity/volume, assessment, 686 (variations), 716
angulation/arrangement, 690 regeneration, 706 Buccal exostosis, clinical photograph, 489f
considerations, 688 remodeling/function, 690 Buccal lower premolar, bone (exposure), 66f
load-bearing capacity, 689 remodeling, regulation, 690 Buccal mucosa, intraoral habitats, 103
Bio-Oss (Osteohealth), usage, 551 removal, osteoplasty/ostectomy (usage), 656 Buccal space, location, 490
Birbeck granules, 8 renewal, remodeling process (multicellular Bulbous bone contours, 217
Bisection-of-the-angle technique, long-cone unit), 663f Bullous lichen planus, consideration, 184
paralleling (comparison), 290f resorption, 661, 6916 Bullous pemphigoid, 188
Bismuth gingivitis, appearance, 14 7f reversed architecture, 21 7 Bundle bone, 20f
Bisphosphonate-associated osteonecrosis of appearance, 217f teeth, physiologic mesial migration
the jaw, 66f sialoprotein, 19, 20, 31,308 (association), 24f
Bisphosphonate-related osteonecrosis of the spatial relationship, 673 Bundles, 25, 26, 30, 165

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C ZA'S

CD DWARAKANATH, MOS DG NAIK, MOS

CARRANZA'S CLINICAL PERIODONTOLOGY, 12rn EDITION, Michael G Newman, Henry

Carranza's Clinical Periodontology, Second South Asia Edition

Copyright© 2016 RELX India Private Limited.

Sr Manager-Education Solutions: Shabina Nasim

Typeset by Thomson Digital

ASSOCIATE AND SECTION EDITORS

E Abt, DDS, MS, MSc MJ Bloom, DMD

RRAzzi, DDS L Chambrone, DDS, MSc, PhD, Pos-Doc

S-C Cho, DDS S De Geest

RD Finkelman, DDS, PhD SK Haake, DMD, MDentSc, PhD

JP Fiorellini, DMD, DMSc TJ Han, DDS, MS, FACD

CA Jahn, RDH, MS M Kebschull, Dr Med Dent

RT Kao, DDS, Phd OA Korczeniewska

F Kuo, MS BL Mealey, DDS, MS

KF Novak, DDS, MS, PhD B Pelsmaekers, DDS

AM Pattison, RDH, MS TD Rees, DDS, MSD

C Rossa, Jr, DDS, MS, PhD G Shklar, DDS, MS

K Shin, DDS, PhD

HH Takei, DDS, MS, FACD IA Urban, DMD, MD, PhD

CONTRIBUTORS TO THE ADAPTATION EDITION

CD Dwarakanath, MOS A Uppoor, MOS

MICHAEL G. NEWMAN, DDS, FACD

HENRY H. TAKEI, DDS, MS, FACD

PERRY R. KLOKKEVOLD, DDS, MS, FACD

FERMIN A. CARRANZA, DR ODONT, FACD

Dr CD Dwarakanath ob- Dr Dilip G Naik obtained

Dr N Ambalavanan ob- Dr Ashita Uppoor graduated

Editors v 8 Biofilm and Periodontal Microbiology 95

About the Authors xvii 9 Microbial Interactions with the Host

11 Smoking and Periodontal Disease 12 7

3 Defense Mechanisms of the Gingiva 39 14 Clinical Features of Gingivitis 155

4 Aging and the Periodontium 45 15 Gingival Enlargement 163

16 Acute Gingival Infections 177

5 Classification of Diseases and Conditions

22 Chronic Periodontitis and Necrotizing 33 Treatment of Periodontal Abscess 371

PART 2 38 Antiinfective Therapy 449

SECTION I 39 Host Modulation C, 461

31 Treatment of Aggressive and Atypical Forms

SECTION Ill 47 Resective Osseous Surgery 535

49 Furcation Involvement and Treatment 561 SECTION VII

51 Advances in Periodontal Surgical Procedures

53 Periodontal-Restorative 59 Periimplant Disease and Management O 725

• N Ambalavanan 60 Supportive Implant Treatment 733

SECTION I Normal Periodontium SECTION IV Periodontal Pathology

Definition and Scope of Oral Mucosa

the probe depends on several factors, such as probe diameter,

FIGURE 1.7 lnterdental papillae (arrow) with a central portion formed

FIGURE 1.8 An absence of interdental papillae and col where the

interdental papillae are formed by the marginal gingiva of the

Gingival Epithelium cell with an increasing prevalence of tonofilaments; (2) the

FUNCTIONS CONSTANT RENEWAL

Modified from Dale BA: Periodontal 2000 30:71, 2002.

membranes of the adjoining cells are thought to be fused.