Mischs Avoiding Complications in Oral Implan 2018

Misch's Avoiding Complications in
Oral Implantology
RANDOLPH R. RESNIK, DMD, MDS

Clinical Professor
Department of Periodontology and Oral Implantology
Kornberg School of Dentistry-Temple University
Philadelphia, Pennsylvania
Adjunct Professor
University of Pittsburgh School of Dental Medicine
Graduate Prosthodontics
Pittsburgh, Pennsylvania
Surgical Director/Chief of Staff
Misch International Implant Institute
Beverly Hills, Michigan
CARL E. MISCH, DDS, MDS, PhD (HC)

Clinical Professor and Past Director
Oral Implant Dentistry
Temple University
Kornberg School of Dentistry
Department of Periodontics and Implant Dentistry
Adjunct Professor
University of Alabama at Birmingham
School of Engineering
Birmingham, Alabama
Founder
Misch International Implant Institute
Beverly Hills, Michigan
Table of Contents
Cover image
Title Page
Copyright
Contributors
Foreword
Preface
Acknowledgments
In Memoriam
Dedication
1 Classification of Dental Implant Complications

Complication Studies
Etiology of Complications
Complication Classification
Legal Ramifications
Complications Prevention
Summary
References
2 Medical/Medication Complications in Oral Implantology

Contraindications to Treatment
Medical History
References
3 Treatment Planning Complications

Type of Prosthesis
Divisions of Available Bone
Key Implant Position
Implant Number
Force-Related Issues
Crown Height Space (CHS)
Arch Position
Opposing Arch
Arch Form
Bone Density
Size of Implants
Splinting Implants to Teeth
Patient Treatment Planning
References
4 Radiographic Complications and Evaluation

Radiographic Modalities
Cone Beam Tomography
CBCT Anatomic Radiographic
Normal Radiographic Anatomy

Pathologic Conditions in the Paranasal Sinuses
Miscellaneous CBCT Complications
Radiology Reports
References
5 Dental Implant Intraoperative Complications

Implant Placement: Surgical Related
Stage II Uncovery Surgery Complications
Anesthesia/Platelet-Rich Fibrin Complications
Severe/Life-Threatening Complications
References
6 Ideal Implant Positioning

Mesial-Distal (“X” Axis): Implant–Natural Tooth
Mesial-Distal (“X” Axis): Implant–Implant
Implant Angulation Positioning (“Y” and “Z” Axis)
Distance From Vital Structures
Malpositioning Complication Summary
References
7 Intraoperative Complications
Evaluation of the Coagulation Process
Techniques to Decrease and Control Bleeding
Prevention/Treatment of Bleeding
Postoperative Bleeding Control
References
8 Intraoperative Complications
Risk of Infection
Diagnosis of an Infection
Significant Complications of Infections
Treatment of Infections
Antibiotics Used in Implant Dentistry (Table 8.4)
Prevention and Treatment of Infection
Therapeutic Antibiotics in Implant Dentistry
Sterile Technique
References
9 Neurosensory Deficit Complications in Implant Dentistry

Anatomy
Nerve Injuries
References
10 Postoperative Complications
Medical Issues
Implant-Related Complications
Displacement or Migration Complications
Summary
References
11 Wound Dehiscence
Classification of Incision Line Opening Complications
Factors That Affect Wound Healing/Incision Line Opening
Prevention of Incision Line Opening
Management of Incision Line Opening
References
12 Bone Grafting Complications
Treatment Planning
Procedural Technique Complications
Intraoperative Complications
Particulate Grafts
Block Grafts: Symphysis Bone Grafts
Block Grafts: Ramus Bone Grafts
Postoperative Complications
Summary
References
13 Posterior Maxilla Complications

Anatomy
Pathology
Treatment Plan Complications
Infections
References
14 Complications Associated With Immediate Implant Placement

General Considerations
Complications Following First Stage
References
15 Removable Implant Complications

Complications of Overdentures for the Edentulous Patient
Mandibuar Overdenture Complications
Maxillary Overdenture Complications
Miscellaneous Removable Complications
References
16 Fixed Prosthodontics Complications

Biomechanics: Force-Related Issues
Prosthesis Complications
Intraoperative Prosthodontic Complications
Fixed Occlusal Complications
Summary
References
17 Occlusion Complications
Differences Between Natural Teeth and Dental Implants
Implant-Protected Occlusion
Summary
References
18 Periodontal and Maintenance Complications

Peri-Implant Disease
References
19 Medicolegal Aspects of Implant Dentistry

Litigation Process Part 1

Avoiding Lawsuits
References
Index
Copyright
3251 Riverport Lane

St. Louis, Missouri 63043
AVOIDING COMPLICATIONS IN ORAL IMPLANTOLOGY ISBN: 978-0-

323-37580-1
Copyright © 2018 by Elsevier, Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or

by any means, electronic or mechanical, including photocopying, recording,
or any information storage and retrieval system, without permission in
writing from the publisher. Details on how to seek permission, further
information about the Publisher's permissions policies and our
arrangements with organizations such as the Copyright Clearance Center
and the Copyright Licensing Agency, can be found at our website:
www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected

under copyright by the Publisher (other than as may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new
research and experience broaden our understanding, changes in research
methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and
knowledge in evaluating and using any information, methods, compounds,
or experiments described herein. In using such information or methods they
should be mindful of their own safety and the safety of others, including
parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are
advised to check the most current information provided (i) on procedures
featured or (ii) by the manufacturer of each product to be administered, to
verify the recommended dose or formula, the method and duration of
administration, and contraindications. It is the responsibility of practitioners,
relying on their own experience and knowledge of their patients, to make
diagnoses, to determine dosages and the best treatment for each individual
patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors,
contributors, or editors, assume any liability for any injury and/or damage to
persons or property as a matter of products liability, negligence or otherwise,
or from any use or operation of any methods, products, instructions, or ideas
contained in the material herein.
International Standard Book Number: 978-0-323-37580-1
Senior Content Strategist: Jennifer Flynn-Briggs

Senior Content Development Specialist: Courtney Sprehe
Publishing Services Manager: Julie Eddy
Project Manager: Abigail Bradberry
Design Direction: Amy Buxton
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1

Contributors
Steven Caldwell DDS
Private Practice – Periodontist
El Paso, Texas
Gregory Caldwell DDS, MS

El Paso, Texas
Joseph E. Cillo Jr., DMD, MPH, PhD

Associate Professor of Surgery and Residency Program Director
Drexel University College of Medicine
Division of Oral & Maxillofacial Surgery
Allegheny General Hospital
Francis R. DeLuca DMD, JD

Practicing Malpractice Attorney
Hollywood, Florida
Jarrett B. Foust DDS

Private Practice – General/Implant Dentistry
Glenn J. Jividen DDS

Dayton, Ohio
H. Ray Hazen DDS, MSD

Private Practice – Prosthodontist
Rochester, Indiana
Allen Liu DMD, MS

Seattle, Washington
John W. Preece DDS, MS
Professor Emeritus
Division of Oral and Maxillofacial Radiology
The University of Texas Health Science Center at San Antonio
San Antonio, Texas
Christopher R. Resnik DMD

University of Pittsburgh School of Dental Medicine
Graduate Prosthodontics
Robert J. Resnik MD, MBA

Internal Medicine
Cary Adult Medicine
Cary, North Carolina
Jon B. Suzuki DDS, PhD, MBA

Professor of Microbiology and Immunology (School of Medicine)
Professor of Periodontology and Oral Implantology (School of Dentistry)
Chairman and Program Director, Graduate Periodontology and Oral
Implantology
Associate Dean for Graduate Education
Temple University
Chairman, Dental Products Panel
Food and Drug Administration
Silver Spring, Maryland
Foreword
Oral Implantology has developed and progressed into a central core of the
art and science of dentistry. This field, over the course of its existence, has
transformed from a modality on the fringes of the profession to being
embraced by virtually every component and aspect of our discipline.
However, as with any clinical dental or medical discipline, patient outcomes
continue to drive improvement of diagnoses, techniques and therapies.
Improved management of patient clinical variations to treatment and
unexpected results fortunately are a product of adverse experiences. Simply
put, the tough cases and negative clinical situations are the best teachers,
and we are wise to grow as clinicians from them.
This textbook specifically addresses implant complications for doctors on
any point of their clinical learning curve, from novices to veteran clinicians
with decades of experience. As our profession continues to grow and share
data on clinical experiences, new complications continue to arise, giving us
all a chance to benefit in knowledge from said complication. Presently, our
profession is producing many excellent meetings and publishing textbooks
related to new concepts in the field of Oral Implantology. However, very little
has been dedicated to complications in the literature and from the podium.
This is understandable, as it is not particularly enjoyable to discuss the
negative consequences that occur during treatment, sometimes even despite
our best efforts. This book will provide the profession with a well-needed,
comprehensive textbook on a subject that is most likely to increase in
frequency in the future because of the ever-growing popularity of dental
implants.
The editors of this text, Professors Randolph R. Resnik and Carl E. Misch,
collectively bring over a half-century of clinical education and experience to
these chapters. Not only have they spent decades as top educators in this
field, they have also spent countless hours mentoring implant clinicians
across the world, reviewing cases and helping to provide counsel for the
management of complications that occur along the way. Those experiences
are what shape the content of this text. The information is presented in a
logical sequence of clinical decision making, yet clearly is literature based on
science and peer-reviewed research. The subject matter is very diverse and
comprehensively encompasses all facets of implant dentistry; diagnosis and
treatment planning, surgical intervention, prosthetic rehabilitation, and the
post-operative and maintenance phases of this discipline. The implant
complications case reports contained in these chapters are well-documented
and well-illustrated to serve as an outstanding guide for patient care.
Professors Resnik and Misch have assembled a wealth of talent in the field
of Oral Implantology which provides a unique blend of clinical, academic,
research, and medico-legal experience. These contributors have spent their
careers on the front lines of this field, encountering many of the situations
that are discussed, either directly or indirectly. Their goal is to reduce the
clinical evidence of avoidable and unavoidable complication episodes that an
implant clinician may encounter in their practice.
The authors took a great deal of care to make this text extremely
comprehensive in scope, and it shows in the delivery of the content. Through
a unique technique of discussing the etiology, prevention, and management
of each complication, the reader is guided by the authors to a better
understanding of the fundamentals of treatment, making them able to obtain
a strong foundation for the understanding and treatment of these adverse
events.
On a personal note, I have had a long relationship with Professors Resnik
and Misch, both professionally and personally. I value the clinical and
research mentorship provided to me by them over the past quarter of a
century, and feel fortunate to call these men professional colleagues and
friends. We who call ourselves practitioners of Oral Implantology have all
been in some way touched by their contributions to the field at large.
Jon B. Suzuki DDS, PhD, MBA
Preface
Dental implants have become an accepted therapeutic approach to
rehabilitate patients with edentulous sites. Vast amounts of time and
resources have been dedicated to research and development within the
discipline, and as a consequence, very high survival rates are reported
throughout the literature with a wide range of implant types and systems.
Despite all of these advances in oral implantology, treatment associated with
dental implants is not free of complications. There is a learning curve
necessary to build clinical competency from both surgical and prosthetic
aspects of treatment, and situations occur that lead to less than ideal
outcomes. Even with a high degree of experience, complications can and will
arise. These complications can occur intra-operatively, post-operatively, or
many years after success. Therefore, it is inevitable that the implant clinician
today will be confronted with some sort of complication during the implant
treatment process.
The genesis of this complications book comes from over 25 years of
teaching at the Misch International Implant Institute. Private practice in oral
implantology and teaching hands-on surgery to doctors taught me that if you
do enough procedures, whether surgical or prosthetic, complications will
arise. What sparked my interest was the understanding that even if a
clinician is as careful as possible, problems associated with the treatment do
occur. Additionally, because more dental implants are being placed and
restored today, this obviously will lead to more complications. Unfortunately,
very little exposure is given to the diagnosis, etiology, prevention, and
management of these complications. Even the most benign procedures may
lead to significant long-lasting devastating complications to the patient.
The lecture podium is an area where more often than not, successes are
discussed. New procedures and protocols are introduced, and examples are
given that outline the utility of the presenter's findings. As an educator that
deals with the reality of complications with students and practicing clinicians
that I mentor, I found that a large opportunity existed to aid in the deeper
understanding of clinical practice by discussing how and why things go
wrong during implant treatment. The popularity of the Complications
seminar over the years and the feedback we received helped solidify the
conviction that I held – facing the sometimes harsh reality of what errors may
occur and focusing on how to prevent them. This ultimately helps instill a
greater sense of confidence going forward in the pursuit of excellent clinical
care.
Because of the popularity of dental implants and the ever-changing
technological atmosphere, the profession is in need of a literature based,
comprehensive summary of possible complications. Technology is a vital
component of the dental implant industry. Because technological advances in
implant dentistry are changing at an alarming rate, procedures are often
recommended without guidelines for evaluation. In the past, our philosophy
would entail no recommendation on a product or technique without at least
five years of data and experience. However, today, dental advertising and
manufacturers often give the industry misleading and inaccurate information
that may be detrimental and lead to complications.
Misch's Avoiding Complications in Oral Implantology is designed to be a
comprehensive guide to the diagnosis, etiology, and management of a wide
range of treatment planning, surgical, prosthetic, and maintenance
complications. The underlying theme of this book is the idea that the best
way to treat complications is to “prevent” them from occurring. Therefore,
this book includes factual information that is literature based which allows
the implant clinician to have a thorough understanding of basic principles
and a strong foundation for the recognition of complications.
The five parts of this book discuss diagnosis and treatment planning,
surgical, prosthetic, periodontal and maintenance, and mediolegal aspects of
dental implants;
• Part 1: The diagnosis and treatment planning chapters include an
understanding of various types of complications, radiographic imaging
complications associated with the implant patient, factors associated with
proper treatment planning, and the medical evaluation of the dental
implant patient.
• Part 2: Surgical complications are discussed, which include the ideal
positioning of implants in all planes along with the treatment of
malpositioned implants. Additional chapters include bone grafting
complications, the treatment and prevention of bleeding issues, the
prevention of nerve injuries along with ideal management, incision line
opening, intra-operative complications, and post-operative problems.
• Part 3: The Prosthodontic complications chapters include a detailed
summary of fixed and removable complications. This encompasses all
aspects of treatment planning, procedural, and post-prosthetic
complications. An entire chapter is dedicated to dental implant occlusion,
specific for various types of prostheses along with biomechanical factors.
• Part 4: The periodontal and maintenance chapter includes a detailed
evaluation to the scientific basis of periodontal related complications. The
etiology, management, and prevention of these complications is discussed.
• Part 5: The last chapter is dedicated to the possible medical-legal aspects of
implant dentistry. The entire legal process from pre-suit to a trial is
reviewed with unprecedented recommendations on the most common
asked questions concerning the legal process.
In summary, Misch's Avoiding Complications in Oral Implantology is
comprised of the most comprehensive, in-depth summaries of possible
complications the implant clinician may encounter. This book is not meant to
scare the implant clinician, but to educate them on what may possibly occur.
My experience over the years has led me to understand that clinicians
actually feel more confident about procedures when they are aware of the
most significant pitfalls that may arise. The reader will build a strong
foundation of knowledge to manage the complication with a fact-based
protocol to decrease morbidity of the situation. Ideally, the implant clinician
will obtain an understanding that the information in this textbook is meant
to elevate the science and discipline of implant dentistry, as its focus is not
specifically on how to perform a procedure, but how to overcome negative
outcomes. As an added benefit, the text reviews a great deal of the
fundamentals of implant surgery and prosthetic care, which only adds to a
clinician's understanding.
My hope is that this book encourages clinicians to be conscious of
potential complications, whether benign or life threatening, so they lead to
better overall treatment outcomes for patients.
Randolph R. Resnik DMD, MDS
Acknowledgments
I would like to express my sincere gratitude to the many people that have
supported me in the writing of this book. First, I would never have had the
insight, ambition, and aspiration to write this book if not for the two mentors
in my life, my late father, Dr. Rudolph Resnik and Dr. Carl Misch.
My father was the perfect father, role model, educator, clinician, and a true
pioneer in the field of fixed prosthetics. He was my hero and my best friend,
and the number one reason I am where I am today. His endless support and
encouragement gave me the strength and motivation to succeed both
personally and professionally. It is through his life-long example that I
emulate his work ethic, tenacity, and drive by giving 110% in all that I do.
Dr. Carl Misch was not only my mentor, but also a very close personal
friend and fellow colleague for 30 years. His endless energy and enthusiasm
inspired me to take on and complete such a laborious task as writing this
book. Carl, the true “pioneer of modern implantology”, allowed me to be at
the forefront of this challenging profession and carry on his unprecedented
principles and teachings in the field of oral implantology.
This journey would not have been possible without the support of my
wonderful family. First, I want to thank my wife Diane, she is my high school
sweetheart, my best friend and number one fan. She has been my rock to
lean on and with her unwavering support I have been able to become the
best at what I do. I also want to thank my two wonderful children,
Christopher and Allison, who have made me so proud of their
accomplishments and have driven me to complete this book. Christopher,
who is following in my footsteps, soon to enter a prosthodontic residency
and Allison who is pursuing her dream in medical school. And last of all, my
two furry companions, Charlie and Nellie, who sat by my side patiently for
endless hours in the writing of this book.
I am sincerely appreciative to all the additional chapter authors for sharing
their expertise with the writing of this book. Their dedication to implant
dentistry, and especially their friendship and personal support to me, is
greatly appreciated: Dean Jon Suzuki, Steven Caldwell, Robert Resnik, Glenn
Jividen, Joseph Cillo, Jarrett Faust, John Preece and Frank DeLuca.
A special note of thanks to the staff at Elsevier for their energy, enthusiasm
and creativity with the content of this book. In particular, Courtney L.
Sprehe, Jolynn Gower, Kathy Falk, Jennifer Flynn-Briggs, and Abigail
Bradberry for their dedication and long hours of work in the development of
this book.
At last but not least, I would like to extend my gratitude to the thousands
of doctors that have trained with Dr. Misch and myself at the Misch
International Institute over the last 25 years. They have given us the desire to
and ambition to write this book and take the academic level of implant
dentistry to the next level.
Randolph R. Resnik DMD, MDS
In Memoriam
The world constantly teaches us lessons along the path of life, and one of its
most bittersweet truths becomes apparent when we are put in the presence
of a genius. Certain individuals enter this world and make such an impact
that we are left in awe of their accomplishments. They truly make a mark on
what we know of life. The last lesson they bring us regards the frailty of life's
gift. These geniuses, like all beings, leave this life, and we are left to wonder
what we will do without their guiding light.
Recently, the medical community at large has lost one of its true geniuses,
Dr. Carl E. Misch. His passion and life-long dream was to elevate the standard
of care in implant dentistry, and he worked tirelessly in the pursuit of that
end. Through the development of various principles and classifications that
have led to the origins of modern implant dentistry, he truly changed the
lives of his students, colleagues, and patients. Along with his gifts as a highly
skilled clinician was an uncanny ability to engage and teach fellow dentists
what he had learned along the way. He unselfishly gave others the gift of his
knowledge, as his true belief was to always “share what you have learned”.
Carl Misch was, in the truest sense of the words, a pioneer, teacher, clinician,
friend, and colleague.
During his dental school years, the inquisitive dental student became
fascinated with the little known field of oral implantology, which was still
considered a discipline on the fringes of contemporary dental practice.
Regardless, Carl aggressively pursued is passion and placed his first implant
as a 4th year dental student. Additionally, he was elected class president by
his classmates and was awarded a main podium position as a dental student
at an International Congress of Oral Implantology in Germany. His
fascination for knowledge in oral implantology led him to travel the world,
seeking knowledge and experience from any of the earlier founders of oral
implantology. This led to his tenacious pursuit of acquiring experience from
some of the true pioneers in implant dentistry include the likes of Leonard
Linkow, Ken Judy, Hilt Tatum, Robert James, P.I. Branemark and Dr. Hans
Grafelman.
In 1984, Dr. Misch founded the “Misch International Implant Institute”,
which was one of the first hands-on, one-year continuums for dental implant
education. The Institutes scientific based curriculum became world-
renowned and remains at the forefront today of implant dentistry through
research, education, and its unique clinical applications. The Misch
philosophy and teachings have evolved and expanded over the years, and has
been taught in many cities in the United States, along with locations in
Brazil, Canada, France, Italy, Japan, Korea, Monaco, Spain, and the United
Kingdom. Through the years, six major universities have used the Misch
Institute exclusively for the implant dentistry curriculum of their oral
surgery, periodontal, or prosthodontic residencies. To date, over 5000 dentists
have been trained by the Misch Institute and is known worldwide as the
premier center for dental implant training.
Dr. Misch, in his life, was awarded numerous post-doctoral degrees and
recognitions. He was bestowed two Ph.D. degrees (honoris causa) from the
University of Yeditepe in Istanbul, Turkey, and Carol Davila University of
Medicine and Pharmacy in Bucharest, Romania. He was awarded an honorary
degree and member of Omicron Kappa Upsilon, the national dental honor
society. Additionally, he has been presented with twelve fellowships in
dentistry, including the American College of Dentists, International College
of Dentists, Royal Society of Medicine, American Association of Hospital
Dentistry and the Academy of Dentistry International. In 2014, the American
Dental Association's Board of Trustees awarded the Distinguished Service
Award to Dr. Misch. This is the highest honor conferred by the ADA.
In the 1990's, Dr. Misch authored the text, Contemporary Implant Dentistry,
which is currently in its third edition and has become one of the most
popular textbooks in dentistry. This book has been translated into 9
languages, including Japanese, Spanish, Portuguese, Turkish, Italian and
Korean. Additionally, his prosthetic text, Dental Implant Prosthetics (Elsevier)
is in its second edition. His books are used in dental schools throughout the
world for graduate and postgraduate programs. In March 2017, the long-
awaited textbook Avoiding Complications in Oral Implantology will be
published by Elsevier, which is co-authored by myself and Dr. Misch. Dr.
Misch authored over 250 articles and repeatedly lectured in every state in the
United States as well 50 different countries throughout the world. Dr. Misch
also held 16 patents in dentistry and was the co-inventor of the BioHorizons
Maestro Implant System.
Dr. Misch held Diplomate status at the American Board of Oral
Implantology / Implant Dentistry and served as Board President and
member of the examining committee. He also served as President of several
implant organizations including the International Congress of Oral
Implantologists, American Academy of Implant Dentistry, Academy of
Implants and Transplants and the American College of Oral Implantologists.
He was a past president and Co-Chairman of the Board of Directors of the
International Congress of Oral Implantologists, the largest global implant
organization. Other accomplishments include being deemed a “Knight” by
the King of Sweden and a chevalier of La Confrérie des Chevaliers du
Tastevin, an esteemed French wine society.
Dr. Misch had an unprecedented impact on the field of implant dentistry,
as most techniques and procedures today are based on his original principles
and classifications. In my opinion, one of the truest signs of a genius is the
ability to foresee the need of technology well before the mainstream of
society even recognizes the concept. He had more to do with the inception,
evolution, and current principles used today in implant dentistry than any
other practitioner in the field. Few people in the field have contributed more
than Dr. Misch. He gave his life to implant dentistry; he had a singular focus
towards the understanding that if properly utilized, dental implants could
have significant positive impacts on the health of civilization at large. His
passion was centered on perfecting that craft to ensure that his vision of
implantology as a common treatment method became reality. He was a true
pioneer, in a time that he went against the odds and encountered much
resistance. He has stimulated a renaissance in implantology that will
continue to touch everyone he met.
Dr. Misch will be remembered as the consummate clinician, researcher,
professor, and father. He lived and taught what he believed, teaching right up
to the end of his life. His fire for sharing his love of our profession pushed
him on and gave him the energy continue, even under the most complicated
of circumstances. That is the beauty of life. Certain geniuses come along with
great gifts. The best of these decide to dedicate their lives to sharing those
gifts with others. That is a great description of Dr. Carl Misch, and I, as well
as the rest of our community, will never forget him. His legacy will live on in
the clinicians he has educated, the teachers he has influenced, and the
patients that will benefit from his tireless and profound work. Carl, rest in
peace.
Randolph R. Resnik
Dedication
This Book is Dedicated in Loving Memory of my father
Rudolph Resnik DDS
1927–1990
1
Classification of Dental Implant
Complications
Randolph R. Resnik
One of the main tenets of dentistry is the restoration of a patient to optimal

form, function, and esthetics. In the history of the profession, few
advancements have facilitated dentists in this pursuit more than the advent
of the dental implant. Though historical evidence reveals humans were
attempting to replace missing teeth with foreign materials since ancient
times, the science of fully replacing teeth with biologically compatible
materials has been a very recent phenomenon. Oral implantology, which
encompasses the replacement of missing teeth and their supporting
structures with biologically compatible materials, has drastically improved
the quality of life for millions of individuals. Patients who were once
hopelessly edentulous now have the opportunity to achieve a full restoration
to full chewing capability. People who were once destined to undergo radical
and continuous loss of the bone that supports esthetically vital facial muscles
now have a chance to maintain a youthful appearance. Young patients who
were born with congenitally missing teeth now can go through life with a
normal esthetic presentation without having to cope with a removable
appliance. Though the study of dental implants is a rather recent
phenomenon compared to other medical subjects, the impact that the field
has had on the quality of life for patients around the world is staggering.
Due to the work of the many pioneers in the field, oral implantology has
become a highly successful and viable option for the treatment of edentulous
areas. High success rates for implant treatment have been shown through
numerous clinical studies. However, as more implants are being placed, the
number of complications are increasing. Even with technologic advances in
oral implantology, this type of treatment is not void of complications, even
many years after completion. These complications appear both surgically and
prosthetically, with varying degrees of severity in consequence. Prosthetic
complications leave patients without the restorations they ultimately desire,
due to functional and esthetic issues stemming from inadequate implant
placement, improper diagnosis, or a lack of understanding about the forces
acting upon the prosthetic components. Surgical complications can lead to
implant failure, neurosensory impairments, infections, significant bleeding
episodes, and possibly death. As oral implantology grows as a discipline, the
field of dentistry will be confronted with these complications, and knowledge
of how to treat them is pivotal to the long-term success of the treatment.
Complication Studies
In review of the literature, many studies have evaluated the prevalence of
complications, both surgically and prosthetically. McDermott et al., in a
retrospective study, evaluated approximately 2400 implant cases and
determined an overall complication frequency of 13.9%.1 Jung et al. reported
a 39% complication rate associated with fixed implant-retained restorations
over a 5-year period.2 Serrano et al. in a multi-center retrospective study
found a 50% complications rate with removable implant prostheses.3 Many
other studies have evaluated the specific complications (Table 1.1).
TABLE 1.1
Summary of Complication Journal Articles
Category Study Findings

CBCT COMP LICATIONS
S c hneider Computer Generated Guide • Meta-regression analysis reported a mean deviation of 1.07 mm at entry point and 1.63
(2009) 1 Ac c urac y mm at the apex
D’haese Immediate Loading Guided • Reviewed six papers with an average c omplic ation rate to 42% when
(2012) 2 S urgery stereolithographic guided surgery was c ombined with immediate loading
Arisan Guide Ac c urac y • Bone-supported guides had the highest mean deviations (5.0° ± 1.66° angular, and 1.70
(2010) 3 ± 0.52 mm and 1.99 ± 0.64 mm for implant shoulder and tip, respec tively
Valente Template Guided Flapless S urgery • Mean lateral deviations c oronal (1.4 mm) and apic al (1.6 mm). Mean depth deviation
(2009) 4 was 1.1 mm and mean angular deviation was 7.9 degrees
BLEEDING COMP LICATIONS
Hong Coumadin • Frequenc y of persistent bleeding (2%) with patients on Coumadin
(2012) 5 • Extrac tions + implant plac ement = bleeding inc reases to 4.8%
Balaguer Mandibular Bleeding • Most c ommon area for heavy bleeding after implant surgery is in the mandible (c anine
Martí > inc isor > first premolar)
(2015) 6 • Most c ommon artery is S ublingual artery, usually from lingual perforation
Zijderveld Lateral Window Bleeding • 2% signific ant bleeding c omplic ations after lateral window preparation
(2008) 7
Goodac re Postoperative Ec c hymosis • 24% of all dental implant sites manifest notic eable ec c hymosis. The loc ation of the
(2003) 8 ec c hymosis is influenc ed by gravity
NERVE COMP LICATONS
Burstein Mandibular Nerve Impairment • Meta-analysis of implant plac ement nerve injury studies show a range of inc idenc e
(2008) 9 from 0% to 13%
Bartling Mandibular Nerve Impairment • An inc idenc e of 8.5% nerve impairment was found at the first postoperative
(1999) 10 appointment
Libersa Temporary vs. Permanent Nerve • Evaluated transient vs. permanent implant-related nerve injuries with 75% of injuries
(2007) 11 Injury being permanent
Pogrel Inferior Alveolar Bloc k Nerve • 1 : 26,762 inferior alveolar nerve bloc ks result in nerve impairment with 36% c ausing a
(2000) 12 Impairment dysesthesia
INFECTION COMP LICATIONS
Powell Dental Implant Infec tion • 1.14% infec tion rate after stage I and stage II surgery
(2005) 13
Gynther Dental Implant Infec tion • 0.7% infec tion rate after surgery
(1998) 14
Greenstein Wound Dehisc enc e • Inc ision line opening prevalenc e ranging from 4.6%–13.7%
(2008) 15
Lekovic Wound Dehisc enc e with • 30% prevalenc e of soft tissue dehisc enc e's was noted when barriers were plac ed as
(1997) 16 Membrane part of guided bone regeneration proc edures
Urban S inus Graft Infec tions • 2.3% developed a sinus graft infec tion post-surgery
(2012) 17
S ic ilia Titanium Alloy S ensitivity • Type IV hypersensitivity reac tion (titanium alloy sensitivity) Ti allergy was reported
(2008) 18 with a 0.6% prevalenc e
Davies Air Embolism • Report of three fatal c ases of air emboli after implant plac ement
(1990) 19
SURGICAL COMP LICATIONS
Hämmerle Guided Bone Regeneration • Retrospec tive studies reporting suc c ess or survival rates for implants in regenerated
(2002) 20 bone ranging from 79.4%–100% after 5 years
Levin Autogenous Onlay Grafts • S urvival rate was 96.9%, marginal bone loss around implants ranged from 0 to 3.3 mm
(2007) 21 Complic ations only 5% of the implants presented marginal bone loss 1.5 mm over the follow-up time
Chiapasc o Allograft and Membrane • In the postoperative period, 20% of the nonresorbable membranes and 5% of the
(2009) 22 resorbable ones underwent exposure/infec tion
Chaushu Canc ellous Bloc k Grafts • Partial and total bone-bloc k graft failure oc c urred in 10 (7%) and 11 (8%) of 137
(2010) 23 augmented sites
Nkenke S inus Graft Complic ations • S inus graft c omplic ations 0%–32%
(2009) 24
Di Benign Paroxysmal Positional • Osteotome sinus tec hnique leading to benign paroxysmal positional vertigo (BPPV)
Girolamo Vertigo with a prevalenc e of 3%
(2005) 25
S c hwartz- S inus Membrane Perforation • Most c ommon c omplic ation during sinus graft proc edures is perforation of the
Arad S c hneiderian membrane during its elevation is 40%
(2004) 26
Chrc anovic Mandibular Frac ture • Mandibular frac ture is most likely to oc c ur in the very atrophic mandible with a
(2009) 27 prevalenc e of 0.2% of the patients with inserted implants in an edentulous mandible
Galindo- Implant Migration • In 80% of the c ases in the reported study was either performed as sinus augmentation
Moreno via osteotome approac h (33.3%) or no augmentation (46.7%) at all
(2012) 28
P ROSTHETIC COMP LICATIONS
Kourtis Prosthetic Complic ations • Prosthetic Complic ation frequenc y: S c rew Loosening – 34%, Broken S c rew – 13%,
(2004) 29 Unc emented Restoration – 20%, Frac tured Prosthesis – 20%
Mc Dermott General Complic ations • 13.9% frequenc y of c omplic ations inc luding inflammatory (10.2%), prosthetic (2.7%),
(2003) 30 and operative (1.0%)
S adid-Zadeh S ingle Implant Restoration & Fixed • Meta-analysis showing an overall inc idenc e of tec hnic al or mec hanic al c omplic ations
(2015) 31 Implant Prosthesis in Partially of 10.8% for single implant c rowns and 16.1% for partially edentulous implants = over a
Edentulous 5 year period
DeBoever S c rew Loosening • 12% inc idenc e of sc rew loosening within 3 years
(2006) 32
Chaar S c rew Loosening • S c rew Loosening – 4.3% less than 5 years, 10% between 5–10 years
(2011) 33
K-T Yao Implant S c rew S ettling Effec t • 2%–10% of the initial preload is lost as a result of settling within the first few sec onds or
(2011) 34 minutes after tightening
Goodac re Overdenture Complic ations • 30% c lip/attac hment loosening, relines required 19%, overdenture frac ture 12%
(2003) 35
Pjetursson Fixed Implant Prosthesis • 5-year – 34% of fixed prosthesis had c omplic ations
(2012) 36 • 10-year survival rate of 77.4% for the gold–ac rylic fixed implant prosthesis
• The survival rate of implant-supported fixed prosthesis (all types) was 95.4% after 5
years and 80.1% after 10 years of func tion
S ailer Fixed Implant Prosthesis • Meta-analysis reported 5-year (94.3%) and 10-year (88.9%) survival rate
(2007) 37
S c hley Zirc onia Restorations • Zirc onia Restorations – 5-year c omplic ation-free rate of 76.41% for tec hnic al
(2010) 38 c omplic ations
Albrektsson Tec hnic al and Esthetic • Despite high survival of single implant c rowns, tec hnic al, biologic al and aesthetic
(2012) 39 Complic ations c omplic ations were reported with a rate of 8.8%, 7.1%, and 7.1%, respec tively
Albrektsson S ingle Crown S uc c ess Rate • S ingle implant c rowns reported a 5-year (96.3%) and 10-year (89.8%) survival rate of
(2012) 40 implants and prosthesis
Goodac re Phonetic Complic ation • Phonetic c omplic ation after implant prosthesis in 4%–8% of patients
(1999) 41
IMP LANT FAILURE COMP LICATIONS
Pjetursson Implant Failure • Meta-analysis revealed an estimated survival of implants supporting fixed prosthesis of
(2012) 42 FDPs 95.6% after 5 years and 93.1% after 10 years
Albrektsson Implant S urvival • 5-year implant survival rate was estimated to be 97.7% and based on four prospec tive
(2012) 43 studies and 10-year implant survival rate was estimated to be 94.9%
Goodac re Implant Loss in Poor Quality Bone • 16% implant loss in poor quality bone (~D4 Bone)
(2003) 35
Lang Immediate Implants • The annual failure rate of immediate implants was 0.82% (95% CI: 0.48%–1.39%)
(2012) 44 translating into the 2-year survival rate of 98.4%
Bulard S mall Diameter Implant Failure • Failure rate average for mini implants used for long-term prosthesis stabilization was
(2005) 45 8.83% from 8 months – 5 years
Proussaefs Implant Failure After Membrane • Implant survival at stage II surgery was 100% for nonperforated sites (100%) and
(2004) 46 Perforation perforated sites (69.6%)
Baig S moking – Implant Failure • Failure rate of implants in smokers = more than twic e that in nonsmokers
(2007) 47 • Failure rate of implants plac ed in grafted maxillary sinuses of smokers is more than
twic e that seen in nonsmokers
Peled Diabetes – Implant Failure • The suc c ess rate was 1 year (97.3%) and 94.4% (5 years) following implantation
(2003) 48
P ERIODONTAL COMP LICATIONS
Pjetursson S oft Tissue Complic ations • After 5 years, peri-implantitis and soft tissue c omplic ations approximately 8.5%
(2012) 49
Jung S oft Tissue Complic ations • Biologic al c omplic ations, 5-year c umulative soft tissue c omplic ation rate of 7.1% on
(2012) 50 single implant c rowns
S c hley S oft Tissue Complic ations • Zirc onia – biologic al c omplic ations, 5-year c omplic ation-free rate was 91.72%
(2010) 51
Quirynen Periapic al Pathosis • 1% of implants plac ed during a 5-year period developed periapic al pathosis
(2003) 52
Marrone Peri-Muc ositis vs. Peri-implantitis • Prevalenc e of peri-implant muc ositis and peri-implantitis was 31% and 37%,
(2013) 53 respec tively
Fransson Peri-Implant Disease • Prevalenc e of peri-implant diseases was reported to be 92%
(2008) 54
S ouza Keritinized Tissue • Cross-sec tional analysis reporting lac k of adequate keratinized tissue leading to poor
(2016) 55 gingival health in 40.3% in posterior regions and 30.4% of implants in the anterior
region
1
Schneider D, Marquardt P, Zwahlen M, et al: A systematic review on the accuracy and the clinical outcome
of computer-guided template-based implant dentistry. Clin Oral Implants Res 20(Suppl 4):73–86, 2009.
2
D'haese J, Van De Velde T, Komiyama AI, et al: Accuracy and complications using computer-designed
stereolithographic surgical guides for oral rehabilitation by means of dental implants: a review of the
literature. Clin Implant Dent and Relat Res 14(3):321–335, 2012.
3
Arisan V, Karabuda ZC, Özdemir T: Accuracy of two stereolithographic guide systems for computer-aided
implant placement: a computed tomography-based clinical comparative study. J Periodontol 81(1):43–51,
2010.
4
Valente F, Schiroli G, Sbrenna A: Accuracy of computer-aided oral implant surgery: a clinical and
radiographic study. Int J Oral Maxillofac Implants 24(2):234–242, 2009.
5
Hong C, Napenas JJ, Brennan M, et al: Risk of postoperative bleeding after dental procedures in patients on
warfarin: a retrospective study. Oral Surg Oral Med Oral Pathol Oral Radiol 114:464–468, 2012.
6
Balaguer-Martí JC, Peñarrocha-Oltra D, Balaguer-Martínez J, et al: Immediate bleeding complications in
dental implants: a systematic review. Med Oral Patol Oral Cir Cucal 20(2):e231–238, 2015.
7
Zijderveld SA, van den Bergh JP, Schulten EA, et al: Anatomical and surgical findings and complications in
100 consecutive maxillary sinus floor elevation procedures. J Oral Maxillofac Surg 66(7):1426–1438, 2008.
8
Goodacre CJ, Bernal G, Rungcharassaeng K, et al: Clinical complications with implants and implant
prostheses. J Prosthet Dent 90:121–132, 2003.
9
Burstein J, Mastin C, Le B: Avoiding injury to the inferior alveolar nerve by routine use of intraoperative
radiographs during implant placement. J Oral Implantol 34(1):34–38, 2008.
10
Bartling R, Freeman K, Kraut RA: The incidence of altered sensation of the mental nerve after mandibular
implant placement. J Oral Maxillofac Surg 57:1408–1410, 1999.
11
Libersa P, Savignat M, Tonnel A: Neurosensory disturbances of the inferior alveolar nerve: a retrospective
study of complaints in a 10-year period. J Oral Maxillofac Surg 65(8):1486–1489, 2007.
12
Pogrel MA, Thamby S: Permanent nerve involvement resulting from inferior alveolar nerve blocks. J Am
Dent Assoc 131(7):901–907, 2000.
13
Powell CA, Mealey BL, Deas DE, et al: Post-surgical infections: Prevalence associated with various
periodontal surgical procedures. J Periodontol 76:329–333, 2005.
14
Gynther GW, Kondell PA, Moberg LE, et al: Dental implant installation without antibiotic prophylaxis. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 85:509–511, 1998.
15
Greenstein G, Cavallaro J, Romanos G, et al: Clinical recommendations for avoiding and managing
surgical complications associated with implant dentistry: a review. J Periodontol 79(8):1317–1329, 2008.
16
Lekovic V, Kenney EB, Weinlaender M, et al: A bone regenerative approach to alveolar ridge maintenance
following tooth extraction. Report of 10 cases. J Periodontol 68:563–570, 1997.
17
Urban IA, Nagursky H, Church C, et al: Incidence, diagnosis, and treatment of sinus graft infection after
sinus floor elevation: a clinical study. Int J Oral Maxillofac Implants 27(2):449–457, 2012.
18
Sicilia A, Cuesta S, Coma G, et al: Titanium allergy in dental implant patients: a clinical study on 1500
consecutive patients. Clin Oral Implants Res 19(8):823–835, 2008.
19
Davies JM, Campbell LA: Fatal air embolism during dental implant surgery: a report of three cases. Can J
Anaesth 37(1):112–121, 1990.
20
Hämmerle CH, Jung RE, Feloutzis A: A systematic review of the survival of implants in bone sites
augmented with barrier membranes (guided bone regeneration) in partially edentulous patients. J Clin
Periodontol 29(Suppl 3):226–231, 2002.
21
Levin L, Nitzan D, Schwartz-Arad D: Success of dental implants placed in intraoral block bone grafts. J
Periodontol 78(1):18–21, 2007.
22
Chiapasco M, Zaniboni M: Clinical outcomes of GBR procedures to correct peri-implant dehiscences and
fenestrations: a systematic review. Clin Oral Implants Res 20(Suppl 4):113–123, 2009.
23
Chaushu G, Mardinger O, Peleg M, et al: Analysis of complications following augmentation with cancellous
block allografts. J Periodontol 81(12):1759–1764, 2010.
24
Nkenke E, Stelzle F: Clinical outcomes of sinus floor augmentation for implant placement using
autogenous bone or bone substitutes: a systematic review. Clin Oral Implants Res 20(Suppl 4):124–133,
2009.
25
Di Girolamo M, Napolitano B, Arullani CA, et al: Paroxysmal positional vertigo as a complication of
osteotome sinus floor elevation. Eur Arch Otorhinolaryngol 262(8):631–633, 2005.
26
Schwartz-Arad D, Herzberg R, Dolev E: The prevalence of surgical complications of the sinus graft
procedure and their impact on implant survival. J Periodontol 75:511–516, 2004.
27
Chrcanovic BR, Custódio AL: Mandibular fractures associated with endosteal implants. Oral Maxillofac
Surg 13(4):231–238, 2009.
28
Galindo-Moreno P, Padial-Molina M, Avila G, et al: Complications associated with implant migration into the
maxillary sinus cavity. Clin Oral Implants Res 23(10):1152–1160, 2012.
29
Kourtis SG, Sotiriadou S, Voliotis S, et al: Private practice results of dental implants. Part I: survival and
evaluation of risk factors—Part II: surgical and prosthetic complications. Implant Dent 13(4):373–385, 2004.
30
McDermott NE, Chuang SK, Woo VV, et al: Complications of dental implants: identification, frequency, and
associated risk factors. Int J Oral Maxillofac Implants 18(6):848–855, 2003.
31
Sadid-Zadeh R, Kutkut A, Kim H: Prosthetic failure in implant dentistry. Dent Clin North Am 59(1):195–214,
2015.
32
De Boever AL, Keersmaekers K, Vanmaele G, et al: Prosthetic complications in fixed endosseous implant-
borne reconstructions after an observations period of at least 40 months. J Oral Rehabil 33(11):833–839,
2006.
33
Chaar MS, Att W, Strub JR: Prosthetic outcome of cement-retained implant-supported fixed dental
restorations: a systematic review. J Oral Rehabil 38(9):697–711, 2011.
34
Yao KT, Kao HC, Cheng CK, et al: The effect of clockwise and counterclockwise twisting moments on
abutment screw loosening. Clin Oral Implant Res 23:1–6, 2011.
35
Goodacre CJ, Bernal G, Rungcharassaeng K, et al: Clinical complications with implants and implant
prostheses. J Prosthet Dent 90(2):121–132, 2003.
36
Pjetursson BE, Thoma D, Jung R, et al: A systematic review of the survival and complication rates of
implant-supported fixed dental prostheses (FDPs) after a mean observation period of at least 5 years. Clin
Oral Implants Res 23(Suppl 6):22–38, 2012.
37
Sailer I, Pjetursson BE, Zwahlen M, et al: A systematic review of the survival and complication rates of all-
ceramic and metal–ceramic reconstructions after an observation period of at least 3 years. Part II: fixed
dental prostheses. Clin Oral Implants Res 18(Suppl 3):86–96, 2007.
38
Schley JS, Heussen N, Reich S, et al: Survival probability of zirconia-based fixed dental prostheses up to 5
yr: a systematic review of the literature. Eur J Oral Sci 118(5):443–450, 2010.
39
Albrektsson T, Donos N: Implant survival and complications. The Third EAO consensus conference 2012.
Clin Oral Implants Res 23(Suppl 6):63–65, 2012.
40
41
Goodacre CJ, Kan JY, Rungcharassaeng K: Clinical complications of osseointegrated implants. J Prosthet
Dent 81(5):537–552, 1999.
42
43
44
Lang NP, Pun L, Lau KY, et al: A systematic review on survival and success rates of implants placed
immediately into fresh extraction sockets after at least 1 year. Clin Oral Implants Res 23(Suppl 5):39–66,
2012.
45
Bulard RA, Vance JB: Multi-clinic evaluation using mini-dental implants for long-term denture stabilization: a
preliminary biometric evaluation. Compend Contin Educ Dent 26(12):892–897, 2005.
46
Proussaefs P, Lozada J, Kim J, et al: Repair of the perforated sinus membrane with a resorbable collagen
membrane: a human study. Int J Oral Maxillofac Implants 19(3):413–420, 2004.
47
Baig MR, Rajan M: Effects of smoking on the outcome of implant treatment: a literature review. Indian J
Dent Res 18(4):190–195, 2007.
48
Peled M, Ardekian L, Tagger-Green N, et al: Dental implants in patients with type 2 diabetes mellitus: a
clinical study. Implant Dent 12(2):116–122, 2003.
49
50
Jung RE, Zembic A, Pjetursson BE, et al: Systematic review of the survival rate and the incidence of
biological, technical, and aesthetic complications of single crowns on implants reported in longitudinal
studies with a mean follow-up of 5 years. Clin Oral Implants Res 23(Suppl 6):2–21, 2012.
51
Schley JS, Heussen N, Reich S, et al: Survival probability of zirconia-based fixed dental prostheses up to 5
yr: a systematic review of the literature. Eur J Oral Sci 118(5):443–450, 2010.
52
Quirynen M, Gijbels F, Jacobs R: An infected jawbone site compromising successful osseointegration.
Periodontol 2000 33:129–144, 2003.
53
Marrone A, Lasserre J, Bercy P, et al: Prevalence and risk factors for peri-implant disease in Belgian
adults. Clin Oral Implants Res 24(8):934–940, 2013.
54
Fransson C, Wennstrom J, Berglundh T: Clinical characteristics at implants with a history of progressive
bone loss. Clin Oral Implants Res 19(2):142–147, 2008.
55
Souza AB, Tormena M, Matarazzo F, et al: The influence of peri-implant keratinized mucosa on brushing
discomfort and peri-implant tissue health. Clin Oral Implants Res 27(6):650–655, 2016.
Etiology of Complications
Increased Demand for Dental Implants
There is an ever-increasing demand for dental implants in the world's
population today. This increased need and use of implant-related treatments
result from the combined effect of several factors, including (1) an aging
population that is living longer and more socially active, (2) tooth loss related
to age, (3) consequences of fixed prosthesis failure, (4) anatomic
consequences of edentulism, (5) poor performance of removable prostheses,
(6) consequences of removable partial dentures, (7) psychologic aspects of
tooth loss and needs and desires of aging baby boomers, (8) predictable long-
term results of implant-supported prostheses, (9) advantages of implant-
supported restorations, and (10) increased public awareness.4
A study by the American Association of Oral and Maxillofacial Surgeons
noted a 69% incidence of at least one missing tooth in the 35- to 44-year
demographic group.5 By the age of 75, at least one quarter of adults will be
completely edentulous. These statistics, when blended in with overall
population studies, begin to paint the picture for implant demand. The
percentage of the population over 65 years is increasing, as is the overall
human population. The population in 2000 was 282 million and is projected
to increase 49% to 420 million by 2050. Considering the effect of both a
population increase and a greater percentage of that population being older
than age 65, a dramatic overall increase in patient numbers can be expected.
In 2003, 35 million people were older than age 65. This number is expected to
increase 87% by 2025, resulting in almost 70 million people being older than
age 65 (Fig. 1.1).4 Therefore, because the older population are more likely to
be missing teeth, the need for implant dentistry will dramatically increase
over the next several decades.
FIG 1.1 By 2050, 20.7% of the population will be older than age 65. In addition to
the increasing percentage of 65-year-olds, the population is also increasing. As a
result, 34.9 million people were older than 65 in 2000, and 86.6 million people will
reach this milestone by 2050. (From Misch CE: Contemporary implant dentistry, ed 3, Mosby,
St. Louis, 2008.)
An Accepted Treatment by the Population

The replacement of edentulous sites with dental implants is one of the most
rapidly progressing disciplines in all of medicine. Advancements in the
modification of soft and hard tissues, implant design, and prosthetic
fabrication are leading to long-term success rates well over 90%. In addition,
a surge of patient education materials for both dentists and their patients has
led to a large increase in the public awareness of implants as a viable
treatment modality. These factors are leading to explosive growth in the
dental implant market.
Straumann corporation performed a penetration study that discussed the
growth of the dental implant market by 2020. As of 2011, 15% to 20% of the
population of patients seeking the replacement of a missing tooth or teeth
received implant therapy as a restorative modality. This number is projected
to increase to around 25% to 30% in just 9 years.6 The implant market is
slated to grow 6% to 8% in this short time frame. TechNavio's analysts
forecast the global dental implant market to grow at a compound annual
growth rate (CAGR) of 8.72% over the period 2014 to 2019. The overall dental
implant market, which grew from $3.2 billion to $4.2 billion in 5 years, is
expected to rise to over 6.5 billion by 2018.7
More Dentists Placing Implants

Due to the aforementioned boom of demand for oral implantology in the
patient population as well as the lucrative nature of the procedure from an
economic standpoint, more dentists are placing implants. Straumann
reported that approximately 18% to 20% of US dentists are placing dental
implants, with an average of 55–60 implants being placed by each clinician in
a year. This is compared to a 2004 study by the American Dental Association
(ADA) that had this number at 11%.8,9 As recently as 10 years ago, oral
implantology was not emphasized in the dental school curriculum, but it is
now being taught as a core component of a student's education. The number
of general practitioners placing implants is growing and will continue to
grow in the future. Additionally, technological advances are making it easier
and more profitable for clinicians to treat advanced cases.
Manufacturers Course Training

In the 2007 ADA survey, general practitioners were asked where they
received their training in dental implant placement. Approximately 66% of
these dentists had received specialty training after completing dental school.
The bulk of the remaining practitioners had received their training in a
course sponsored by a manufacturer. Due to the lack of exposure in the past
to oral implantology in dental school, dentists are seeking quick access into
the discipline for a low cost. Dental implant manufacturers are attempting to
fill this void by hosting continuums in oral implantology for the dental
population that is seeking an introduction to this discipline. Though these
short courses are better than the alternative of having dentists receive no
training at all prior to placing implants, there are definitely inherent
drawbacks.
First, there is a lack of foundational didactic training on dental implant
treatment planning, which is a cornerstone of successful treatment
outcomes. A firm understanding on prosthetic design, force distribution, and
site development is paramount to achieving consistent successful dental
implant treatment outcomes. Secondly, the manufacturers tend to
oversimplify the treatment protocols in an effort to embolden clinicians to
offer implant placement in their respective practices. This places the dentist
in a position of not being fully aware of the potential complications they can
encounter during treatment and how to handle them should they arise.
Implants Being Placed in Compromised Sites

Due to the lack of formal training in comprehensive oral implantology,
dentists may lack a firm appreciation for site development as it pertains to
the hard and soft tissues. Many edentulous sites and prosthetic designs
require modifications to the proposed implant site. There is a tendency for
dentists (early on their learning curve) to develop treatment plans that allow
them to avoid procedures they lack knowledge or comfort in, so implants
may be placed in suboptimal areas, which leads to various negative esthetic,
prosthetic, and surgical complications. Because of bone loss after tooth
extraction, many sites are not ideal for implant placement (surgically and
prosthetically). If the dentist lacks knowledge in bone grafting and site
development, this may lead to alternative treatment options such as severely
angled implant placement, excessively short implant bodies, or the
placement of too few implants for the force requirements of the patient's
proposed prosthetic design. All of these “shortcut” or “non-ideal”
procedures may lead to an increase in complications, lower success rates, and
subsequent legal ramifications.
Financial motivation may also affect decision making as it pertains to site
development. A dentist may feel the pressure to “keep procedures in house,”
which may lead to a deviation of proper treatment planning, especially if the
clinician does not possess the skill or knowledge required to augment hard
and soft tissue. In areas of the mouth that show a lack of bone height, width,
density, or a lack of adequate soft tissue, a practitioner will be required to
have greater education, experience, and skill to navigate a proper treatment
plan from the surgical phases to final prosthetic completion. Cases with
compromised tissue volumes typically require augmentation prior to implant
placement, which requires a separate skill set. If a clinician does not possess
these skills but proceeds with a modified treatment plan to work around the
inherent difficulties that the patient's anatomy presents, numerous
complications and morbidities can occur in all phases of treatment. This will
ultimately lead to embarrassment, increased procedural cost, and possible
legal repercussions.
Medically Compromised Patients

With the continued advent of new technologies, medications, and treatment
options, patients are leading longer lives with higher degrees of social
activity. This phenomenon will continue to increase as the population grows
along with the understanding of disease prevention and treatment. The
impact of this for the modern dentist is the presence of a population of
elderly patients who actively seek comprehensive dental care, in a search for
a return to optimal form, function, and esthetics.
As was previously discussed, oral implantology is becoming a larger part
of this patient population's knowledge base, and they are actively seeking
this therapy to help enjoy a better diet, more active social lifestyle, and
younger appearance. However, this also places a higher demand on the
dentist to understand the medical complexities that are inherent in treating
these patients. Patients present with numerous comorbidities, take many
medications that may affect implant healing, and also pose a significant
challenge for the clinician during the surgical phases of treatment.10
Additionally, significant advances in medicine have led to the advent of new
medications for many diseases. However, the interaction of these
medications on the healing of dental implants can cause many complications
and adverse effects (i.e., bisphosphonates).
A survey study was performed showing that with patients in the 57- to 85-
year range, 81% took at least one prescription drug daily, with 29% taking at
least five medications.11 A practitioner performing implant surgery must
know the patient's medical history, have a firm understanding of each
medication, and be aware of how each of these medications affects not only
the patient's ability to cope with the stresses of surgery but also the healing
and integration of bone grafts and dental implants. Medications that are
prescribed pre- and postoperatively may interact with the patient's existing
drug regimen. These factors must all be taken into consideration before
beginning a treatment protocol. A lack of awareness of the effects of
medication on dental implant treatment may lead to numerous unforeseen
complications.
When planning to begin treatment on an medically compromised patient,
the clinician must also understand how various medical conditions may
affect the final outcome. Cardiovascular and respiratory disease may
complicate surgery. Uncontrolled diabetes has significant effects on surgical
healing and implant integration. Anticoagulant therapies may pose a
significant risk for bleeding episodes during treatment. Long-term steroid
use can affect healing and infection risk. Each affirmative check on a medical
questionnaire should be investigated and evaluated for a risk of possible
complications to surgery.
Lack of Medical Clearance Prior to Surgery

A key to success in treatment for the medically compromised patient is an
area that is sometimes overlooked by the dental professional, and that is a
strong working relationship with the patient's physician. While performing
the medical evaluation on a patient presenting with a positive health history,
the implant dentist should take the time and effort to consult with the
treating physician to establish a pre- and postoperative plan, including drug
protocols, ensuring that the patient experiences an outcome free from drug
interactions and medical complications. Surgical clearances should also be
obtained in an effort to minimize the risk that a patient experiences medical
complications or life-threatening emergencies during implant surgery. A
failure to obtain such clearances puts the implant dentist in a serious
medicolegal risk, should complications occur. (See the Medical Consultation
Form in Chapter 2.)
Immediate Implant Procedures

Throughout the history of the discipline of oral implantology, research
studies have been performed to help practicing clinicians understand all
aspects of implant dentistry, in an effort to provide patients with the best
chances of experiencing a successful outcome. These studies have shaped our
understanding of how the body responds to the different implant and graft
materials, how the forces of mastication act on these materials, and how the
microbial environment affects the long-term success of implant restorations.
As this understanding increased, designs for implants were established,
treatment protocols and healing times were authored, and drug regimens
were established to maximize the chance that treatments were successful.
However, as the demand for implant services has increased, so has
competition in that marketplace. Dental professionals compete for patients,
and dental implant manufacturers compete for market share. This has led to
the advent of more and more dental implant procedures that deviate from
the established clinical guidelines set forth and confirmed by previous
research. Though many of these procedures and treatment protocols can
work and have been shown to be effective in the right hands, the skill
requirements of these procedures may prove to be too high for some
practitioners, especially those early on a learning curve. This leads to
numerous surgical and prosthetic complications.
In an effort to reduce the time in which a patient had to wait for a final
restorative outcome, a movement began to not only immediately place an
implant at the time of extraction but also to load the implants at the same
time. In the right circumstances (proper bone volume, density for rigid
fixation, and lack of infection), this treatment has been shown to be clinically
effective. However, with the confirmation that these procedures can indeed
work, we have seen an exploitation of the treatment protocol to encourage
this type of procedure as a matter of routine. The pressures on implant
dentists to produce “teeth in a day” may predispose them to taking shortcuts
and making surgical compromises that put the patient at great risk for
implant/prosthetic failure. The implant dentist must understand that certain
clinical criteria must be present for these procedures to work, and that
factors such as medical status, the presence of infection, or inadequate bone
volumes contraindicate such shortcuts.
Catering to a larger population of dentists who may not possess the skills
to create adequate bone volumes by grafting, manufacturers have also
pushed the boundaries in implant design in an effort to remove barriers to
entry into the implant field. For example, to avoid the problem of having to
build posterior maxillary bone volumes to ensure proper vertical axis loading
of implants, clinicians have invented techniques involving angled placements
of implants with severely angled abutment interfaces. Although these
techniques have been shown to be successful, surgical experience and case
selection are crucial factors for long-term success.
Overuse of “Mini” Implants

Recently, the use of “mini” dental implants to support removable and fixed
prosthesis has dramatically increased in implant dentistry. Initially, the
intended application of mini implants was for provisional restorations during
the healing phase of conventional endosseous implants (> 3.3 mm diameter).
In time, the use of mini implants was expanded to retain removable and fixed
prostheses, which have become extremely controversial. Manufacturers have
since modified the procedure to include minimally invasive techniques,
which include inserting the implant into the bone via flapless surgery. These
techniques have been marketed toward faster, easier, and less traumatic
procedures. However, this marketing has led to more mini implants being
placed in sites that would be more ideally suited (surgically and
prosthetically) for conventional endosseous implants. This has led to
nonideal implant positioning, neurosensory impairment, atypical implant
prosthesis, poor emergence profiles, biomechanical issues, and implant
fractures.
At this time, there are very few studies evaluating the success of mini
implant under functional biting forces and long-term success. Finite element
stress analyses of mini implants have been shown to exhibit high levels of
risk because stress transmission to bone and fatigue fracture. Bulard and
Vance evaluated over 1000 implants and reported a 13.6% failure rate.12
Shatkin reported more failures in the maxilla with a 17% failure under a
complete denture.13 Other studies have shown fatigue fracture to be
responsible for 5% and 20% of all implants lost during function.14 Therefore,
mini-implants definitely have a place in implant dentistry treatment
planning, however in most cases should not be substituted for conventional
size implants.
Poor Treatment Planning

One of the easiest ways to minimize complications, yet one of the most
overlooked by implant dentists, is the ability to accurately and effectively
treatment plan according to sound scientific principles. Each patient presents
a different challenge for the clinician, which makes detailed knowledge of
dental anatomy as well as the engineering of prosthetic cases so vital to
successful outcomes.
Without significant knowledge of a patient's maxillofacial anatomy, an
implant clinician is placed in a potentially dangerous situation. The implant
dentist must know the volume of bone in a proposed implant site and be
aware of any undercuts that may be present. The presence of vital structures
such as sinuses and nerves must be accurately identified and evaluated.
Without this information, the clinician may perforate bony structures,
causing neurosensory impairment that provides sensation to the face and
oral structures or possibly severing blood vessels that may cause life-
threatening bleeding complications.
Excuses for this lack of detailed knowledge are quickly evaporating, as
radiographic modalities such as cone beam computed tomography (CBCT)
imaging are quickly becoming the standard of care. Having an accurate 3-D
representation of the patient's anatomy along with a firm understanding of
how to read and interpret the image puts the clinician in a much better
position to avoid significant complications.
Using a working knowledge and accurate representation of the patient's
anatomy, the clinician must be aware of overall site selection and implant
positioning as it pertains to the demands of the restoration. If a clinician
does not take into consideration the design and demands of the final
prosthesis, there exists a significant potential to place the implant in a
position that places destructive forces upon it during loading, which will
cause either prosthetic or implant integrative failure.
Protocols have been established featuring key implant positions to assist
the implant dentist in properly selecting sites that optimize safe loading
during function as well as establishing safe distances between the multiple
implants and/or adjacent teeth. Following these guidelines can assist the
clinician in knowing where the optimal site for an implant lies, which then
allows for an evaluation of that exact site as it pertains to the need for
additional bone volume via grafting. Neglecting these rules can place the
patient at significant risk of implant loss, adjacent tooth loss, or prosthetic
failure (see Chapter 6).
Poor Communication With Patients

The implant dentist must understand the demands of the patient's existing
oral condition and their expectations for prosthetic options. Patients who
exhibit parafunction require greater implant numbers or implants of greater
size dimensions. A patient who shows more teeth during smiling may
require a different esthetic presentation than one with a low lip line. Patients
with thin tissue biotypes in an esthetic area may require tissue augmentation
prior to implant placement. All of these factors must be known to the
practitioner prior to beginning treatment to avoid problems.
Armed with all of the knowledge regarding implant treatment planning,
the clinician can and must effectively communicate with the patient
regarding expectations and demands. Many health care providers, including
implant dentists, encounter complications when they acquiesce to the
demands of a patient to perform questionable procedures. This can be
avoided by knowing all of the ramifications of each treatment option and
having the ability to communicate them. The patient must be made aware of
all possible options and the strengths/limitations of each. They must
understand the financial implications of treatment and know how that affects
their treatment outcome. An example of this would be the edentulous
mandible, where the number of implants placed dictates the type and
stability of the final prosthesis. If a patient is made aware initially of their
choice of two implants supporting a denture is much less stable than the
alternative of four, the chances of disappointment are reduced.
Communicating the treatment options clearly and setting clear expectations
can help prevent numerous complications, including medicolegal issues.
Poor Understanding of Complications and Failure

to Refer
No clinician expects to be faced with complications during treatment.
Despite all of the education, experience, and skill they may possess, at some
point the implant dentist will be confronted with a complication. As
important as the prevention of complications is to the discipline of oral
implantology, the quick identification and treatment of these events is
equally important. The implant dentist must understand the myriad of risks
associated with each procedure and how to react to these issues should they
arise. During surgery, the severing of a blood vessel requires a rapid response
to ensure the prompt resolution of the incident. Failing to recognize or
respond to a bleeding incident in a quick manner could lead to life-
threatening complications. If a complication during surgery was noted, such
as the potential severing of a nerve, the clinician does the patient a terrible
disservice by avoiding the situation altogether and “hoping things heal on
their own.” Prompt referrals for imaging and specialty treatment are
necessary and are the responsibility of the practitioner to allow the patient
the best chance of a full recovery.
Even after a seemingly successful surgery, the patient must be monitored
for postoperative complications. Incision line opening, one of the most
common surgical complications, poses a risk to a successful outcome,
especially with grafting. Serious postoperative infections may occur that
require prompt antibiotic therapy and even possible hospitalization. All of
these conditions must be anticipated by the implant dentist prior to the
beginning of treatment, and a plan must be in place ahead of time to safely
navigate the “slippery slope” that these complications present. The clinician
must know how to recognize each complication and what avenues to pursue
to get the situation under control, even if it means referral to another doctor.
Complication Classification
Although quality assessment is gaining increased attention in implant
dentistry, there exists no accepted consensus on how to define and quantify
complications. Because of the absence of a consensus, there is little
continuity in the literature with regards to complications. In medicine,
Clavien et al proposed a classification of complications, which has
subsequently been used in the medical literature for outcome assessment.
However, this classification may not be the most practical for the assessment
of oral implantology complications.15
• Grade 1: Any deviation from the normal postoperative course that does not
require pharmacologic intervention (i.e., pain, swelling)
• Grade 2: Any deviation from the normal postoperative course that does
require pharmacologic intervention (i.e., infection)
• Grade 3: A deviation that requires surgical intervention (i.e., incision and
draining)
• Grade 4: Life-threatening complication requiring hosptitalization (i.e.,
sublingual hematoma)
Because of the wide variation in the field of oral implantology, the authors
have developed various classifications, which is dependent on type and phase
of treatment.
Minor vs. Major

A minor complication is self-limiting and usually of short duration, with no
permanent or lasting deficits. (e.g., swelling and bruising).
A major complication is a more serious complication that is longer lasting,
potentially permanent, with associated possible morbidities (e.g., infection,
nerve impairment).
Unavoidable vs. Avoidable

An avoidable complication is a complication such as a nerve impairment
caused by placing an implant in the mandibular canal, without the use of a
CBCT scan to give the clinician an accurate representation of the proper
nerve location.
An unavoidable complication is a complication that cannot be avoided or
preventable in most instances and is not directly a result of negligence of the
implant clinician. An unavoidable complication does not negate legal
ramifications. However, it does favor the implant clinician, as it is considered
a complication that most likely could not have been avoided (e.g., nerve
impairment secondary to administration of inferior alveolar nerve block).
Reversible vs. Irreversible

Reversible complications are complications that usually resolve on their own
and have no associated long-term morbidity (e.g., improper angulation upon
implant placement after the first drill osteotomy, which may be corrected
easily).
Irreversible complications are complications that are permanent and cannot
be reversed, thus having increased severity and consequences (e.g., mandible
fracture after implant placement).
Legal Ramifications
In the past, legal issues concerning implant dentistry were minimal. In
today's practice, this is becoming an ever-increasing and serious problem.
Many years ago, the majority of complications were basically thought of as
risks of the procedure. Today, such complications are deemed a deviation
from the standard of care by many. It is true that fewer dental lawsuits are
brought before the court system today as compared to in the past, but the
cases that appear before the court today carry enormous awards if
successfully tried for the plaintiff. Additionally, many more cases are being
settled out of court because of the expense of litigation. Today, cases
involving complications such as nerve impairments due to negligence can
settle in the six- to seven-figure range.
Furthermore, with the advent of CBCT technology, the field of oral
implantology is moving more toward “perfection.” For example, if an implant
fails, many possible reasons may be given to explain why this has happened.
Most doctors believe an informed consent will minimize these issues;
however, this is usually not true. If negligence is proven against the clinician,
the informed consent is deemed inadmissible, as a patient cannot consent to
negligence. Most likely, in the future, insurance premiums may become so
high for these procedures that it will limit the use of implants by many
practitioners. For the clinicians who continue to provide implant services, it
will be mandatory that they be vigilant in the prevention and proper
handling of complications.
In all aspects of health care, practitioners discuss the virtues of disease
prevention with their patients. In the practice of implant dentistry, it is vital
that clinicians practice that same philosophy as it pertains to complications.
The best way for the implant dentist to treat complications is to “prevent”
them.
Increase Education
The first method of complication avoidance is the pursuit of education.
Implant dentists must have a firm and deep understanding about a wide
spectrum of subjects ranging from CBCT interpretation and diagnosis,
treatment planning, hard and soft tissue management, prosthetic design,
esthetic presentation, pharmacology, surgical principles, and numerous other
subjects. It is vital that the aspiring or practicing implant clinician achieve a
level of expertise in all aspects of the discipline. Though the level of time and
effort devoted to implant education is increasing in dental schools, the
implant dentist must continue to add to his or her knowledge regarding both
the prosthetic and surgical facets of oral implantology.
Comprehensive postgraduate continuing education courses are available to
dentists seeking a deep understanding of implantology. These typically
consist of a combination of intense didactic and laboratory training sessions.
The courses offer the implant clinician an opportunity to obtain a strong
foundation of the diagnostic, surgical, pharmacologic, and prosthetic
sciences as they pertain to implant treatment. Some courses also offer a
hands-on component to assist dentists early on their respective learning
curves with respect to various procedures they have never been exposed to.
Seek Accreditation
It is also highly recommended for clinicians to test themselves by seeking
accreditation with the various implant boards and groups. Groups such as
the American Board of Oral Implantology/Implant Dentistry (ABOI/ID), the
International Congress of Oral Implantologists (ICOI), and the American
Academy of Implant Dentistry (AAID) offer fellowship and diplomate status
to clinicians who pass various didactic tests, while also presenting their own
cases and research for peer review. This higher level of accreditation is vital
for the implant dentist to perform because it helps to build a deeper
understanding and greater mastery of the various aspects of oral
implantology. The level of competency and credibility, after the many hours
of study and preparation it takes to complete the accreditation process,
cannot help but to make a clinician more knowledgeable about the field,
which is a crucial step toward avoiding complications.
Literature Review Updates

Another way for the prevention of implant complications is to become
familiar with the process of literature review. As the advances in the field of
oral implantology increase, more competition will arise, which will inspire
new advances in the field. While some of these advances will stand the test of
peer review and clinical success, many new procedures and equipment ideas
will push boundaries and make unsubstantiated claims. A good piece of
advice for the avoidance of complications is to “not be the first, nor the last”
to the latest trends or ideas in the field. Before implementing a new
procedure or piece of technology, it is wise to extensively research the subject
to evaluate the validity of the advancement. Be skeptical of manufacturer-
driven studies because they may show a significant bias toward the positives
in the methods or materials they intend to take to market. Be hesitant to
accept any claim made by a company or spokesperson until unbiased
research has tested and proven its validity and the test of time.
Patient Information
In order to prevent complications with the patient relationship, the
practitioner should give all possible treatment plans and options to the
patient. This is absolutely paramount because it builds a set of expectations
and a knowledge base for the patient and provider. An example of this would
be the restoration of a missing single, edentulous site. The patient should be
given an option of no treatment (which must always be offered), removable
prosthetics, fixed prosthetics, or implant retained prosthetics. The patient
should be informed of the advantages, disadvantages, risks, and potential
complications regarding each treatment option. Doing so not only gives the
patient greater peace of mind because they are actively participating in the
choice of treatment but it also gives the clinician the comfort of knowing that
they accurately prepared the patient for the upcoming therapy. Expectations
of compliance for each treatment option should also be discussed and
documented. All medical therapy is a two-way street between patient and
provider, and the patient must be responsible for compliance.
Do Not Rush Treatment

During treatment, the clinician can avoid substantial complications by
avoiding the urge to rush through the proper sequence and timelines for
implant dentistry. Oral implantology is unlike other disciplines in dentistry
because patients often have to cope with the difficulties of transitional
removable prosthetics, perimucosal extensions, sutures, and other items they
may find uncomfortable. The implant dentist may feel some pressure to
lessen graft healing, implant integration, or progressive loading timelines in
an effort to make the patient happy. The clinician must explain to the patient
that these timelines are necessary for proper therapy to be completed, and
there isn't much that can be done to lessen the window and still ensure a
favorable outcome.
Treat for the Long Term, Not the Short Term

The implant clinician may also be faced with the dilemma of a nonideal
outcome (e.g., bone loss upon uncover, open contact, ill-fitting margin).
Though this can be a significant source of embarrassment for the clinician
and stress for the patient, it must be explained that for long-term success, the
situation may require modification. Though the pressure to do so may seem
severe, the clinician must NOT alter their best judgment by putting their
patients at risk. Most of the time-related problems and pressures from
patients in regards to comprehensive implant treatment can be handled on
the front end of treatment with the aforementioned treatment presentation.
The patient who is prepared for what is to come is much less likely to have
problems and try to force the clinician into rushed procedures.
Follow-Up Care
The last aspect of complication prevention is a policy of strong follow-up
care. Keeping communication open with the patient through the phases of
treatment is vital to staying on top of any potential complication issues. The
patient should be instructed to inform the clinician of any difficulties
immediately as they pertain to incision line opening, neurosensory issues, or
possible infection. Postoperative evaluations also provide the implant dentist
with opportunities to evaluate healing, transitional prosthesis fit, incision
line closure, the presence of infection, and the post-prosthetic phase. A good
follow-up care protocol builds strong bonds with patients and also allows the
implant dentist the chance to identify and quickly respond to numerous
complications.
Summary
Oral implantology is a discipline filled with complexity. The field demands its
practitioners to have a high level of expertise in a vast array of areas, many of
which evolve at a fast rate. The oral environment is dynamic, and perfect
healing conditions are not always possible. Complications will inevitably
happen, but steps can be taken to prevent them. These include a thorough
and comprehensive medical/dental history; radiographic survey including
CBCT; a strong working knowledge of head and neck anatomy as well as
surgical, prosthetic, pharmacologic, and follow-up care principles; and the
ability to identify and treat a wide array of complications should they occur.
Every dentist who places or restores implants should be aware of these
complications and know how to manage them. Some of the issues will
require little intervention, while others may require the services of
professionals in other areas of expertise. It is the duty of the implant dentist
to recognize all of these situations and know the proper protocols to follow to
ensure that the patient's chances of success are maximized.
According to numerous market research studies, the future of dental
implants seems to be extremely bright. With no other full-tooth replacement
therapy on the immediate horizon, the implant dentist enjoys the ability to
provide the ideal solution for the restoration of missing teeth. The clinicians
who provide this service can enjoy a good lifestyle while providing patients
with a second chance at regaining ideal form, function, and esthetics.
With the many opportunities that implant dentistry provides comes a
distinct responsibility and a sobering reality. Oral implantology is a difficult
field to master, and the consequences of failure can be catastrophic. Patients
may be at risk for life-threatening complications. The stresses of surgery
during anesthesia pose a life risk for some patients. The various types of
neurosensory impairments that patients have suffered as a complication of
implant treatment are tragic, life changing, and have proven to be costly to
the implant clinician. The professional and financial ramifications of some of
these complications for the implant dentist are staggering.
In the face of these scary realities, groups of well-trained and passionate
professionals continue to provide this wonderful service to thousands of
grateful patients every single day. Oral implantology is a life-changing
discipline, not only for the patients, but for the providers with the skill,
knowledge, and passion to provide the treatment with excellence. It is the
mission of this textbook to provide all of those practitioners with a
comprehensive source material to reference should any form of complication
arise.
References
1. McDermott NE, Chuang SK, Woo VV, et al. Complications of dental
implants: identification, frequency, and associated risk factors. Int J
Oral Maxillofac Implants. 2003;18:848–855.
2. Jung RE, Pjetursson BE, Glauser R, et al. A systematic review of the 5-
year survival and complication rates of implant-supported single
crowns. Clin Oral Implants Res. 2008;19:119–130.
3. Serrano Caturla E, Martín-Granizo López R. A multi-center
retrospective study of lost implants. Rev ESp Cirug Oral Maxillofac.
2006;28:339–348.
4. Misch CE. Contemporary implant dentistry. Mosby: St. Louis; 2008.
5. American Association of Oral and Maxillofacial Surgeons. [website]
http://www.aaoms.org.
6. Karoussis IK, Bragger U, Salvi GE, et al. Effect of implant design on
survival and success rates of titanium oral implants: a 10-year
prospective cohort study of the ITI dental implant system. Clin Oral
Implants Res. 2004;15:8–17.
7. Aging demographics and awareness levels drives the global dental
implants volumes, according to new report by Global Industry Analysts,
Inc. [website] http://www.prweb.com/pdfdownload/9693638.pdf.
8. ADA Survey Center. 2004 Distribution of Dentists in the U.S. by Region
and State. American Dental Association; 2006.
9. Achermann G. How will dentistry look in 2020?. [website]
http://www.straumann.com/content/dam/internet/straumann_com/Resource
relations/publications-and-reports/capital-markets-day-
2012/How%20will%20dentistry%20in%202020%20look_Straumann%20CMD2
10. Qato DM, Alexander GC, Conti RM, et al. Use of prescription and
over-the-counter medications and dietary supplements among older
adults in the United States. JAMA. 2008;300:2867–2878.
11. Cardarelli R, Mann C, Fulda KG, et al. Improving accuracy of
medication identification in an older population using a medication
bottle color symbol label system. BMC Fam Prac. 2011;12:142.
12. Bulard RA, Vance JB. Multi-clinic evaluation using mini-dental
implants for long-term denture stabilization: a preliminary biometric
evaluation. Compend Contin Educ Dent. 2005;26(12):892–897.
13. Shatkin TE, Shatkin S, Oppenheimer BD, et al. Mini dental implants
for long-term fixed and removable prosthetics: a retrospective
analysis of 2514 implants placed over a five-year period. Compend
Contin Educ Dent. 2007;28(2):92–99.
14. 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
Periodontol. 2002;29(Suppl 3):197–212.
15. Clavien P, Sanabria J, Strasberg S. Proposed classification of
complication of surgery with examples of utility in cholecystectomy.
Surgery. 1992;111:518–526.
2
Medical/Medication Complications in
Oral Implantology
Randolph R. Resnik, Robert J. Resnik
A comprehensive preoperative medical assessment of patients considering

implant treatment is vital to successful outcomes as well as the avoidance of
significant complications. Studies have shown that the medical status of
patients (i.e., medical history, American Society of Anesthesiologists [ASA]
category) has a direct correlation with endosseous implant failure.1 The need
for implant-related treatment increases with the age of the patient. As a
result, the implant dentist treats more elderly patients with associated
comorbidities than any other specialist in dentistry. An estimated 12% of the
US population is 65 years of age or older; this number is expected to reach
21% (64.6 million) in the year 2030.2 The increased life span of the population
directly correlates with implant dentistry being one of the fastest growing
areas in medicine. Additionally, studies have shown that 15% to 25% of
patients presenting to dental practices are medically complex, which
encompasses a history of systemic diseases, multiple medications, and age-
related issues.3 Because the number of medically compromised patients
seeking dental implant therapy is increasing, it is paramount the implant
clinician understand the effect of systemic diseases and associated
medications on the intraoperative surgical procedures, which have a direct
relationship with the successful osseointegration of dental implants.
Contraindications to Treatment
Initially, when determining if a patient is a potential candidate for implant
treatment, a thorough medical and physical evaluation must be performed.
From this information, the existence of a possible medical contraindication is
ascertained. In medicine, a contraindication is defined as a condition or
situation that potentially makes the procedure in question inadvisable. There
exist two types of contraindications, absolute and relative, with respect to
dental implant procedures. An absolute contraindication is a condition that
makes the procedure completely inadvisable. A relative contraindication is a
condition that necessitates caution and is acceptable as long as the benefits
outweigh the risks. To further clarify the contraindications in the field of
implant dentistry, they may be classified into three categories.
• Surgical contraindication: A condition that places the patient at risk during
the surgical procedure (e.g., advanced heart disease) and that potentially
could result in a medical emergency. However, the condition does not
impact morbidity or success of the implant procedure.
• Implant contraindication: A condition that places the endosseous implant
healing at risk (e.g., IV bisphosphonates), resulting in a decreased success
rate and increased morbidity. However, the condition does not impact the
intraoperative medical condition of the patient or place the patient as a
medical risk.
• Surgical/implant contraindication: The combination of a surgical procedure
risk along with a risk for the success of implant healing or longevity.
Medical History
A comprehensive method of obtaining and documenting a patient's medical
history is essential to ascertain an accurate diagnosis in order to determine
an effective treatment plan algorithm. A thorough patient evaluation
provides the foundation for determining the patient's surgical, anesthetic,
and prosthetic risk, which directly affects morbidity and associated
complications. The review of the patient's medical history is the first
opportunity for the implant clinician to speak directly with the patient. The
practitioner should not underestimate the value of the medical history
interview. Asking questions that show an understanding of the listed medical
conditions, current medications, and related common problems is
paramount for the safety and well-being of the patient.
The two basic categories of information addressed during the review of the
medical history include the current review of the patient's systemic health
condition and an evaluation of recent and current medications. This detailed
medical history should also address possible allergies, family and social
histories, all of which may impact the future dental implant treatment, both
surgically and prosthetically. Each positive answer on the medical history
may have a direct impact on the care of the patient and proposed treatment.
The implant clinician must have a strong understanding of positive
responses associated with the medical history.
Cardiovascular System
Are you currently being treated for high blood pressure, or have you been
told by a health care professional that you have high blood pressure, or
hypertension? /No?
Hypertension is a highly prevalent cardiovascular disease, affecting over 50
million Americans and 1 billion people worldwide. An estimated 7.1 million
deaths per year are attributable to hypertension, along with 62% of
cerebrovascular disease and 49% of ischemic heart disease. Approximately
30% of adults with hypertension are unaware they have hypertension, and
two thirds of patients treated are not controlled to blood pressure less than
140/90 mm Hg.4 The overall prevalence of hypertension is approximately 30%
to 45% of the general population; however, a steep increase with aging is
present.5 Untreated, undiagnosed, and uncontrolled hypertension is a serious
problem in society today. Because implant dentists treat a high percentage of
elderly patients, coupled with the high prevalence in the general population,
incidence of treating patients with uncontrolled or undiagnosed
hypertension is very high. This places the implant clinician at risk because
intraoperative hypertensive episodes may result in cardiac arrhythmias with
possible myocardial ischemia issues, which may lead to possible
cardiovascular events such as myocardial infarction or cerebrovascular
events.
Classification of Hypertension
In February 2014 the members of the eighth Joint National Committee
(JNC8) on high blood pressure issued new guidelines for the treatment and
management of high blood pressure in adults (Table 2.1). This report
redefined treatment goals and thresholds for initiating treatment as well as a
reevaluation of many common medications used to treat high blood
pressure.6 For years, medical providers treated blood pressure to a goal of
120/80 mm HG based on the recommendations of JNC7. JNC8 examined five
new critical blood pressure trials. The most compelling and reproducible
outcome in all the trials was lowering the diastolic blood pressure to less
than 90, which resulted in fewer cardiac events and a reduction in overall
mortality.
TABLE 2.1
Blood Pressure Treatment Guidelines
Systolic (mm Diastolic (mm TREATMENT

Category
Hg) Hg)
P reoperative Intraoperative
Ideal <120 <80 None None
Prehypertension 120–139 80–89 Rec hec k, possible MD c onsultation Rec hec k, stress reduc tion protoc ol
Grade 1 140–159 90–99 Rec hec k, possible MD c onsultation, Monitor, stress reduc tion protoc ol
hypertension (relative)
Grade 2 160–179 100–109 Rec hec k, MD c onsultation, (absolute) Monitor, disc ontinue proc edure,
hypertension possible
ER referral
Hypertensive c risis >180 >110 Rec hec k, emergenc y c are, (absolute) Monitor, abort immediately, emergenc y
c are
Additionally, JNC8 examined the medications used to treat blood pressure

and concluded first-line treatments should be limited to four classes of
medications; angiotension-converting enzyme inhibitor (ACEs), angiotension
receptor blockers (ARBs), thiazide-type diuretics, and calcium channel
blockers (CCBs). The implant clinician must have a thorough understanding
concerning how hypertensive states may impact both surgical success and
implant longevity.
Surgical/Implant Implications
Intraoperative elevated blood pressure.
The implant dentist and staff must be knowledgeable about the
measurement, detection, and treatment of hypertension. The accurate
measurement of blood pressure, along with a review of all medications
including herbal and over-the-counter medications, should be an integral
part of the implant consultation and examination. This information must be
reviewed in detail with the patient prior to surgery. If an automatic blood
pressure–monitoring system is being utilized, a manual sphygmomanometer
should be available to manually verify abnormal readings. Elevated readings
(>160/100) should be verified by manual techniques and the procedure
discontinued until the blood pressure returns closer to the patient's baseline
or within a more acceptable range.
Orthostatic hypotension.
Hypertensive patients are more susceptible to orthostatic hypotension when
brought from a supine to an upright position. This is caused by an excessive
fall in blood pressure, which results in faintness, light-headedness, dizziness,
confusion, or blurred vision. Resolution of this complication will occur
rapidly upon placing the patient back in a supine position. Allowing patients
to sit upright slowly will minimize these complications, especially after
longer procedures and in susceptible patients. Unless a patient has a serious
medical contraindication (e.g., congestive heart failure, renovascular disease,
chronic edema), they should be instructed to hydrate prior to the surgical
procedure. This may help reduce the occurrence of orthostatic hypotension.
Antihypertensive medications + NSAIDs.

The use of nonsteroidal antiinflammatory drugs (NSAIDs) has been shown
to lessen the effectiveness of various antihypertensive medications by
inhibiting prostaglandin production, leading to intraoperative hypertensive
episodes. Blood pressure regulation is highly prostaglandin dependent,
especially as it relates to kidney function through the vasodilatory effects.
NSAIDs possess a higher degree of interaction with diuretics, ACE
inhibitors, ARB inhibitors, and beta blockers, which may modify
prostaglandin-dependent pathways more than drugs that alter non–
prostaglandin-sensitive pathways such as calcium channel blockers and
central acting drugs. Therefore, the interaction with hypertensive
medications and NSAIDs result in a higher propensity to increase blood
pressure.7 Studies have related approximately 50 million patients are being
treated with antihypertensive therapy, and 12 million use NSAIDs
concomitantly. However, the short-term use of NSAIDs has not been shown
to have a clinically significant effect.8
Beta blockers.
The implant clinician must take into consideration that beta blockers may
potentiate the cardiovascular effects of epinephrine used in local anesthetics.
The nonselective beta-adrenergic drugs, such as propranolol (Inderal) and
nadolol, pose the greatest risk of adverse interactions.9 The cardioselective
beta blockers (Lopressor, Tenormin) carry less risk of adverse reactions.
However, there is competitive clearance through the liver between both
classes of beta blockers and the local anesthetic. This may lead to an increase
in serum levels of the local anesthetic.10 To avoid intraoperative hypertensive
episodes, decreasing the dose and increasing the time interval between
epinephrine-containing injections is recommended.11
Calcium channel blockers.

These medications used to treat hypertension or congestive heart failure may
lead to gingival hyperplasia around natural teeth or implants (similar to
Dilantin). Additionally, this drug classification has been associated with
erythema multiforme (a benign rash characterized by patches of red raised
skin) and other types of oral ulceration. Gingival overgrowth can result in
pain, gingival bleeding, and difficulty in mastication, especially around
implant prostheses. The incidence of gingival hyperplasia is approximately
1.7% to 3.8% of patients taking calcium channel blockers.12
Multiple antihypertensive drugs.

Patients with difficult-to-control blood pressure may be prescribed multiple
classes of antihypertensive medications. Even though these patients are
being treated with various antihypertensive medications, they are prone to
possible elevation and spikes in blood pressure. With these patients, the
clinician should seek medical evaluation and consultation, which may
include a postoperative blood pressure–monitoring plan.
Susceptibility to other cardiovascular events.
Severe hypertension or elevation in blood pressure may lead to angina
pectoris, congestive heart failure, myocardial infarction, retinal hemorrhage,
or even a cerebrovascular episode. These conditions may be precipitated by a
rapid increase in blood pressure during a local anesthetic injection or the
inherent stress associated with the surgical procedure. A stress reduction
protocol is paramount with hypertensive patients.
Implant healing.
Cardiac disease (hypertension) may theoretically affect blood supply to the
implant site and hence reduce survival or success. However, multiple studies
have shown no evidence of early or late failure in hypertensive patients
receiving dental implants.13,14
Complication Prevention
Stress reduction protocol.
With hypertensive patients the blood pressure should be controlled before
and during elective dental implant treatment. Because blood pressure often
rises prior to dental and surgical procedures, a preoperative stress control
protocol is mandatory (Box 2.1).
Box 2.1
Stress Reduction Protocol
• Premedication the night before a procedure (longer-acting benzodiazepine
[diazepam 5–10 mg])
• Early morning appointment
• Explain entire procedure in detail
• Sedation (Oral/IV)
• Minimize waiting-room time
• Duration of treatment not to exceed patient's tolerance

• Profound local anesthesia
• Slow/aspiration LA administration
• Sufficient postoperative pain management
IV, intravenous; LA, local anesthetic.
Monitoring.
Accurate assessment of intraoperative vital sign monitoring is extremely
crucial to prevent complications. If elevated blood pressure (Stage 2) is
present, postponement or medical consultation is indicated. When
measuring blood pressure in the office, adhere to the following:
• Allow the patient to sit for 3 to 5 minutes prior to obtaining blood pressure
measurements.
• If blood pressure is elevated, recheck after 5 minutes, changing arms.
• Automatic blood pressure machines may report inaccurate readings in
patients with a history of cardiac arrhythmia such as atrial fibrillation,
which may also cause an erratic heart rate. Multiple measurements of the
blood pressure should be taken, and if a significant variation exists, the
blood pressure should be checked manually with a stethoscope and
sphygmomanometer.
• Position cuff at the patient's heart level and make sure the cuff is snug,
approximately 3 cm above the elbow.
Maintain antihypertensive therapy.

Patients under a physician's care with antihypertensive medications should
be instructed to comply with their medication protocol, especially the
morning of surgery. If patients do not maintain their medication protocol,
inherent intraoperative vital sign fluctuations may result. A patient should
never alter any physician prescribed medication unless otherwise instructed
by their physician.
Slow administration of local anesthetics.

Control of pain and anxiety is paramount in patients with hypertension
because endogenous catecholamines (adrenaline and norepinephrine) are
released in response to pain and stress. Catecholamines increase blood
pressure and cardiac output, thus placing the patient at risk of a stroke or
cardiac arrest. Slow administration and aspiration of local anesthetics
containing epinephrine also will minimize potential complications. High
blood pressure levels may have direct effects on cardiac output, total
peripheral resistance, and mean arterial pressure. This may result in
lowering of the heart rate (bradycardia), a decrease in blood pressure, and in
extreme conditions cardiovascular failure resulting in cardiac arrest.
Reduction in the use of vasoconstrictors.

Especially in elderly patients, the indiscriminate use of local anesthesia with
vasoconstrictor should be cautioned. Attention should be exercised with
patients having a cardiac history, and the dose of vasoconstrictors like
epinephrine should be reduced (<0.4 mg). This may lead to elevation in vital
signs in hypertensive patients, which may possibly lead to cardiovascular
events. A rule of thumb is 50% of the recommended maximum dose of local
anesthetics can be given after 1 half-life of the local anesthetic.
Angina
Do you have chest pain with exertion or have you been treated for angina?
/No?
Angina is defined as significant, painful chest pain as a consequence of
exertion or stress. Angina pectoris is a form of coronary heart disease that is
usually caused by arteriosclerotic heart disease. However, it may be caused
by coronary artery spasm, severe aortic stenosis, aortic insufficiency, anemia,
emboli, and hereditary connective tissue disease. The cause of angina is a
discrepancy between the myocardial oxygen demand and the amount of
oxygen being delivered through the coronary arteries. The classical symptom
of retrosternal pain that often radiates to the shoulders, left arm, or mandible
or to the right arm, neck, palate, and tongue is usually relieved by rest.
Patients with a history of angina may be taking long-acting nitrates to
prevent the occurrence of acute episodes. Sublingual or spray nitroglycerin is
recommended for the treatment of acute episodes. When retrosternal pain
occurs, myocardial infarction is part of the differential diagnosis. The pain is
similar in region but is more intense and usually will not cease within 3 to 5
minutes. Risk factors for angina pectoris are smoking, hypertension, high
cholesterol, obesity, and diabetes.
Acute angina attack.
In the event of an acute angina attack, immediate discontinuation of the
surgical procedure should be completed with the administration of
nitroglycerin tablets (0.3 to 0.4 mg) or sublingual nitroglycerine spray.
Additionally, 100% oxygen should be given to the patient along with
repositioning in a semisupine (45-degree) position. Vital signs should be
monitored with evaluation for irregular heartbeats, which could indicate
premature ventricular contractions as a result of myocardial ischemia. If the
pulse remains irregular, medical assistance should be sought.
Stable vs. unstable angina.

The difference between stable and unstable angina must be understood.
Stable angina relates to chest pain that is similar to past episodes of angina
and is usually brought on by similar amounts of exertion or activity. It usually
resolves within several minutes of rest or discontinuation of exerted activity.
Nitroglycerin will most often relieve the chest pain.
Unstable angina is classified as chest pain or pressure with or without
shortness of breath that is a change from the typical anginal pain symptoms
the patient has been experiencing with exertion. Chest pain at rest or with
minimal exertional activity can also be classified as unstable angina.
Unstable angina or a myocardial infarction in the last 6 months would be an
absolute contraindication to the use of local anesthetics with
vasoconstrictors.
Complication Implication
Postnitroglycerin issues.
Nitroglycerin is a vasodilator that increases the blood supply to the heart and
may lower systemic blood pressure. The net effect reduces the workload and
oxygen demand of the heart, relieving chest pain. The side effects of
nitroglycerin are important to recognize because the overall decrease in
blood pressure may cause a decreased blood flow to the brain. Flushing of
the face and shoulders along with severe headache is common. After
administration, fainting is possible; therefore the patient should be sitting or
lying in a supine position. As the heart attempts to compensate for decreased
blood pressure, the pulse rate may increase to as much as 160 beats/min.
Decrease dental procedural stress.
It is important to minimize factors that can increase the heart rate, increase
blood pressure, and subsequently increase myocardial oxygen demand.
Stress reduction is critical to reduce catecholamine release, which may
adversely impact the cardiac contributors to angina. It is important to initiate
a stress reduction protocol to help alleviate any cardiac stress factors.
Use of nitrous oxide sedation.

Use of sedation, especially nitrous oxide (N2O), will reduce the possibility of
angina attacks. N2O potentially can decrease coronary blood flow; however,
studies have shown no cardiac morbidity.15 Use of N2O in patients with both a
cardiac and pulmonary history such as chronic obstructive pulmonary
disease (COPD) or emphysema should be avoided.
Hypertension treatment summary

• Mild (relative): May undergo most nonsurgical dental procedures
performed with normal protocol. General cardiac precautions are advised,
such as vital signs monitoring, and patients are instructed to bring their
own nitroglycerin to their appointment. Advanced restorative procedures
and minor implant surgery are performed with stress reduction protocol
and sedation.
• Moderate (absolute): Medical consultation recommended for any elective
implant treatment.
• Severe (absolute): Medical consultation recommended for any elective
implant treatment.
Myocardial Infarction (MI)

Do you have a history of myocardial infarction or heart attack? /No?
Myocardial infarction (MI) is a prolonged ischemia or lack of oxygen
resulting from a deficiency in coronary arterial blood supply that causes
injury to the myocardium. The end result is cellular death and necrosis of the
heart muscle. An acute MI may be precipitated when the patient undergoes
unusual stress, either physical (painful stimuli) or emotional (anxiety).
During an MI episode the patient usually will be symptomatic with severe
chest pain in the substernal or left precordial area that may radiate to the left
arm or mandible. Cyanosis, cold sweat, weakness, nausea or vomiting, and
irregular and increased pulse rate are all signs and symptoms of MI.
Cardiovascular issues.
The intraoperative complications of past MI patients include arrhythmias
and congestive heart failure (CHF). The larger the ischemic area, the greater
the risk of heart failure or life-threatening arrhythmias. Any history of MI
indicates damage to the coronary blood vessels. Therefore, recent infarctions
correspond to higher morbidity and death rates, even with simple elective
surgery. Approximately 18% to 20% of patients with a recent history of MI
will have an increase in complications, which have a high mortality rate of
40% to 70%.16
Medical consultation.
A medical consultation should precede any extensive restorative or surgical
procedure. Even though there are recommendations based solely on the
length of time after an MI, the deciding factor on elective dental implant
treatment is not only time but also the amount of myocardial damage. The
implant clinician should follow the recommendation of the physician
concerning treatment options, modifications, or contraindications.

Dental implant surgery after MI may induce arrhythmias or aggravate cardiac
ischemia. An increased blood pressure is not uncommon in the dental office
setting because stress associated with treatment (i.e., white coat syndrome)
leads to increased levels of catecholamine, which causes an increase in blood
pressure and heart rate. The most important step in decreasing stress in the
dental office is to integrate a comprehensive stress reduction protocol.
Reduction in the use of vasoconstrictors.

Epinephrine and other vasoconstrictors have several properties that can
potentially result in adverse outcomes in patients that have not fully
recovered from a recent myocardial infarction. Epinephrine is chronotropic,
which results in an increased heart rate and force of contraction. Both of
these result in an increased oxygen demand and could potentiate ischemia.
Epinephrine does have some arrhythmogenic properties that could provoke
ventricular fibrillation or tachycardia in recovering myocardial muscle. It is
best to minimize complications by consulting the patient's treating physician
and closely monitoring vital signs when vasoconstrictors are used.
MI treatment summary.
The patient's physician should be consulted prior to elective dental implant
treatment to verify the patient's current cardiac status.
• Absolute (surgical): Recent MI (depending on MD recommendation)
• Relative (surgical): History of MI (depending on MD recommendation)
Cerebrovascular Accident (CVA)

Do you have a history of cerebrovascular accident (stroke)? /No?
A stroke is a cerebrovascular accident (CVA) characterized by a sudden
interruption of blood flow to the brain, causing oxygen deprivation. It is most
frequently seen in patients with current cardiovascular diseases and is the
fourth leading cause of death in the United States and a major cause of adult
disability. The majority of strokes are ischemic resulting from narrowing or
blocking of the blood supply to the brain. The etiology of ischemic strokes is
embolic and thrombotic. Thrombotic strokes are the result of clots that form
inside one of the brain's arteries. The clot blocks blood flow to the brain
causing cell death. Usually, these result from plaque or other fatty deposits
from atherosclerosis, which break off and become lodged in the blood vessel.
Embolic strokes are the results of clots that form in other parts of the body
and travel to the brain via the bloodstream. The clot eventually will lodge in a
blood vessel and block flow of blood to the brain. It is important to ask
patients if they have ever been diagnosed or treated for ministrokes or TIAs
(transient ischemic attacks). These attacks are the result of brief (usually less
than 24 hours) interruptions in blood flow causing strokelike symptoms.
Bleeding.
Although it is important to control blood pressure and treat elevated
cholesterol in the management of individuals with a history of strokes,
caution should be taken because most are on blood-thinning medication.
Antiplatelet agents such as aspirin or clopidogrel may be used as single
agents or in combination as part of stroke prevention treatment. Both of
these medications irreversibly impact platelets' clotting ability and have been
shown to cause increased bleeding. In some cases warfarin (Coumadin) may
also be used, which directly interferes with the body's clotting mechanisms.
Evaluation and bleeding control are essential in these types of patients.
Limited dexterity.
Patients who have suffered a compromise in dexterity as the result of a stroke
require alternative treatment planning for their final prostheses. A fixed
prosthesis is usually the best solution for these patients because an implant
retained prosthesis may lead to the inability to remove for routine hygiene.
Additionally, poor oral hygiene when combined with xerostomia causes
additional oral problems such as candidiasis, dental caries, periodontal
issues, and mucositis lesions, which increase implant prostheses morbidity.
Current anticoagulant medications.
The goal of anticoagulation medication is to keep the blood thinned so
clotting is more difficult. However, it is important to understand these
medications work by various pathways and can impact clotting at different
points in the clotting cascade or by directly inhibiting platelet function. The
antiplatelet agents such as aspirin or clopidogrel have been shown to have a
minimal impact on bleeding both intraoperative and postoperative.17 Several
studies have found no increased risk of bleeding during dental procedures
when patients on Coumadin are within the therapeutic treatment range of an
international normalized ratio (INR) below 3.0. In patients with mechanical
heart valves, the upper limit of the therapeutic range can reach 3.5 to 4.0. In
patients with artificial valves, the INR may be checked 24 hours prior to the
implant surgery. Under no circumstances should a patient with a mechanical
valve on Coumadin be instructed to stop or hold a dose without input from
the patient's treating physician.
Hemostatic agents/surgical technique.

Ideal surgical technique should be followed which consists of nontraumatic
incision and reflection of tissue. The surgical procedures should be
minimized with a decreased surgical duration. The implant clinician must
have experience with the use of active and passive hemostatic agents (see
Chapter 7).
Treatment summary
• Absolute (surgical): Recent CVA incident (MD Consult)
• Relative (surgical): History of CVA + anticoagulants (MD Consult)
Congestive Heart Failure (CHF)

Do you have a history of congestive heart failure? /No?
Congestive heart failure (CHF) is a pathophysiologic state in which an
abnormality in cardiac function is responsible for failure of the heart to
pump blood in adequate volume to meet the needs of the metabolizing
tissues. More than 3 million people in the United States suffer from CHF,
with approximately 400,000 new patients being diagnosed each year. Every
year 30% to 40% of patients with CHF are hospitalized, which accounts for
the leading diagnosis-related group of hospitalized patients older than age
65.18
The heart pumps approximately 2000 gallons of blood per day to other
organs and body tissues. It coordinates the function of two pumps
simultaneously: the left side, the larger of the two sides, pushes the blood
out into the body; the right side sends the blood to the lungs for oxygenation.
When the heart has been damaged, the blood begins to back up in the lungs
or body. The heart will attempt to compensate by increasing the rate of
contraction and stretching the muscle to accommodate a larger volume of
blood to contract with a greater force and eject more blood (Frank-Starling
law). Both of these compensation attempts of the heart maintain circulatory
needs in the short term; however, long term they may be problematic. Less
blood is circulated because, in beating faster, the heart is left with less time
to refill, while the extra effort increases the heart muscle's demand for
oxygen. When this need is not met, the heart rhythms can become
dangerously abnormal (arrhythmic) and may lead to death.
Surgical/Implant Implications.
CHF patients are very susceptible to intraoperative cardiovascular morbidity
issues. Stress reduction protocol and strict monitoring should be followed. It
is advisable to discuss the current condition of the patient with their treating
physician (Box 2.2). Patients with CHF can be classified as compensated or
uncompensated. In uncompensated heart failure, the pulmonary circulation
is expanded and congested because the heart is unable to fully compensate.
The classic symptoms are seen including shortness of breath especially with
exertion, fatigue, or lying supine. When the CHF patient is treated for heart
failure through medical management and the symptoms are controlled, the
patient is referred to as compensated.
Box 2.2
New York Heart Association Cardiac Disease
Classification
NYHA I: (Relative) Patients that have no limitation of physical activity.
NYHA II: (Relative) Patients with cardiac disease that results in slight
limitation to physical activity with symptoms such as fatigue, palpations,
dyspnea, or angina pain.
NYHA III: (Absolute) Patients with cardiac disease who are comfortable at
rest; however, less-than-ordinary activity causes fatigue, palpation,
dyspnea, or angina pain.
NYHA IV: (Absolute) Patients with cardiac disease that results in the
inability to carry on any physical activity.
Recognize CHF symptoms.
Although the treatment of CHF should be left up to the patient's physician, it
is important to realize that CHF can worsen without warning or slowly over
time. It is important to evaluate the patient's breathing at rest and with
minimal exertion upon walking, as well as to determine if breathing has
worsened when the patient is lying down. Changes in any of these patterns of
breathing could indicate a decompensation of their congestive heart failure.
Additionally, it is important to evaluate for neck swelling in the jugular area,
which may indicate right-sided heart congestion.
Patient positioning.
CHF patients should be positioned in the most recumbent position in which
they can breathe comfortably and efficiently. This is usually a semireclined or
sitting upright position. Usually, the more upright the patient, the easier it is
for the patient to breathe.
Oxygen supplementation.
Oxygen supplementation (≈2 L/min) during implant procedures is highly
recommended to minimize the possibility of hypoxia. The use of nitrous
oxide in these patients is not advised.

Previously described to prevent increased myocardial workload with a
damaged heart.
Are you predisposed to infectious endocarditis? /No?
The pathogenesis of infectious endocarditis is complex and associated with
many factors. Vessel turbulence in the endothelium of cardiac vessel or
pulmonary shunts combined with bacteremia (streptococci, staphylococci,
enterococci) from oral surgical procedures may cause bacteria proliferation at
the site resulting in infection. These bacteria may enter the bloodstream and
can infect the heart valves. In time the bacteria can destroy heart valves
resulting in life-threatening cardiac conditions. For this reason, antibiotic
coverage is recommended in high-risk individuals undergoing procedures
that may cause these types of bacteremia. The guidelines issued in 1997 for
endocarditis antibiotic prophylaxis were very broad. In 2007 the guidelines
were updated using recommendations from the American Heart Association
Endocarditis Committee (Box 2.3 and Table 2.2).
Box 2.3
Endocarditis Prophylaxis Recommendation
The American Dental Association, American Medical Association, and the
American Heart Association have recommended antibiotic coverage in
patients with the following conditions receiving elective surgery.
• Artificial heart valves
• Past history of infectious endocarditis
• Cardiac transplant that develops a heart valve problem
• Congenital heart disease with shunts or conduitsa repaired

• Congenital heart defect with residual defect
Able to take oral medication: amoxicillin 2 g (50 mg/kg)
Unable to take oral medication: ampicillin 2 g IM or IV (50 mg/kg IM or IV);

cefazolin or ceftriaxone 1 g IM or IV (50 mg/kg IM or IV)
Allergic to penicillin or ampicillin: cephalexin 2 g (50 mg/kg); clindamycin

600 mg (20 mg/kg); azithromycin or clarithromycin 500 mg (15 mg/kg)
Allergic to penicillin or ampicillin and unable to take oral medication:

cefazolin or ceftriaxone 1 g IM or IV (50 mg/kg IM or IV); clindamycin 600
mg IM or IV (20 mg/kg IM or IV)
IM, intramuscular; IV, intravenous.
a Functional murmurs and organic heart murmurs do not require prophylactic antibiotic.
TABLE 2.2
Additional Cardiovascular Issues and Treatment Implications
P ositive Response Treatment Implications

Abdominal aneurysm Rupture leading to high mortality, MD c onsultation (absolute)
Atrial fibrillation Thrombin inhibitors, hemostatic measures
Prosthetic heart valve Maintained at high INR, hemostatic measures
Pac emaker Cardiovasc ular issue, stress reduc tion protoc ol, no elec trosurgery
Fainting/lightheadedness Orthostatic hypotension
Congenital heart defec t Cardiovasc ular issue, medic al c onsult to determine extent
Ankle edema Congestive heart failure, possible varic ose veins
INR, international normalized ratio.
Cardiovascular disease treatment summary

• Surgery: The above mentioned cardiovascular diseases can have a direct
impact on the intraoperative consequences of dental implant surgery. It is
imperative a thorough evaluation of the cardiovascular history be
completed. Medical consultation is highly recommended to determine a
current cardiac status of the patient. Strict stress reduction protocols are an
essential part of the dental treatment plan for all patients with a cardiac
history.
• Implant: Cardiovascular diseases theoretically will have an impact on the
healing of dental implants. These diseases have a direct effect on blood
tissue supply, which may impair the healing process. For normal healing,
the presence of oxygen will increase fibroblast activity, collagen synthesis,
capillary growth, and macrophage activity. Because cardiovascular diseases
compromise blood flow and reduce oxygen tension and nutrient elements,
osseointegration would most likely be affected. However, many studies have
shown no direct correlation between cardiovascular disease and dental
implant failure.19,20
Endocrine System
Diabetes Mellitus
Do you have diabetes? /No?
Diabetes mellitus is a major endocrine disorder that affects approximately
7% of the population with another 2% to 3% undiagnosed. In patients age 60
years or older, 20.9% of all people in this age group suffer from diabetes
(approximately 1 in 5). Approximately 20.8 million children and adults suffer
from diabetes, which contributes to 225,000 deaths per year. Diabetes ranks
as the sixth leading cause of death in the United States.21
The most current classification of diabetes includes three general clinical
categories: type 1 diabetes, type 2 diabetes, and gestational diabetes
(pregnancy). In type 1 diabetes, insulin is not produced from the pancreas.
This type of diabetes develops most frequently in children. However, the
incidence in the older population is increasing. Type 2 diabetes is much more
common and accounts for approximately 95% of the diabetic cases. This type
of diabetes almost always occurs in adults and results from the body's
inability to respond properly to the action of insulin, which is produced from
the pancreas. The incidence of type 2 diabetes is estimated to double by the
year 2025 because of aging, unhealthy diets, and obesity.22,23 A recent study
revealed a much higher percentage of patients with undiagnosed diabetes
visiting dental clinics than was previously reported.24 An increased body
mass index (BMI) and advanced age can be predictors of undiagnosed
diabetes. In patients for whom the clinician has a higher suspicion of
diabetes, questions concerning frequent urination (polyuria) or excessively
thirst (polydipsia) should be determined. These symptoms have a higher
correlation with diabetes and may require additional workup. Additionally,
diabetics tend to have a higher prevalence of periodontal disease, caries, and
other dental problems such as oral candidiasis, recurrent stomatitis, and
parotid gland dysfunction.25
Surgical/Implant Treatment Implications

Hypoglycemia.
The most serious intraoperative complication for diabetic patients is
hypoglycemia, which usually occurs as a result of excessive insulin level,
hypoglycemic drugs, or inadequate food intake. Weakness, nervousness,
tremor, palpitations, or sweating are all signs of acute hypoglycemia. Mild
symptoms can be treated with sugar in the form of orange juice or candy. If
the symptoms are not addressed, they may evolve from minor symptoms to
seizure, coma, and in rare cases death. In these severe cases, patients may
become unconscious or barely arousable. For these symptoms the emergency
administration of 50% IV dextrose should be completed. Additionally,
glucagon should be available because this hormone may raise blood sugar
through a direct effect on the liver. Glucagon may also be administered
intramuscularly in a dose of 1 mg for adults over 20 kg. Patients taking
sulfonylurea medications for diabetes (including glyburide, glipizide, and
glimepiride) who do not have adequate carbohydrate intake prior to their
procedure are at an increased risk of hypoglycemia. It is important that
patients on these medications follow their regularly prescribed diet prior to
the dental procedure.
Hyperglycemia.
The stress of surgery may provoke the release of counterregulatory hormones
that will impair insulin regulation and may result in hyperglycemia and a
catabolic state. The cause of hyperglycemia is multifactorial and may include
any of several medications such as corticosteroids, beta blockers,
epinephrine, diuretics, and some antipsychotic drugs. Hyperglycemia is
usually slower to develop and may not necessarily demonstrate any physical
symptoms. Patients should be instructed to monitor their blood sugars in the
postsurgical period and contact their physician if their readings remain
elevated from their normal baseline. In the acute setting, hyperglycemia can
be treated with insulin or by increasing fluids in noncardiac patients.
Emergency services should be called for patients who experience erratic
breathing and/or fluctuating levels of consciousness associated with high
blood sugar levels.
Bone formation.
Studies have shown hyperglycemia has a negative effect on bone
metabolism, reducing bone mineral density, affecting bone mechanical
properties, and impairing bone formation leading to poor bone
microarchitecture.26 There is a direct correlation between implant
osseointegration and glycemic control.27 It has been shown that
osseointegration is more predictable in anatomic areas with abundant
cortical bone, which is why the mandible has shown a greater bone formation
than the maxilla.28
Infection.
Diabetic patients are prone to develop infections and vascular complications.
The healing process is affected by the impairment of vascular function,
chemotaxis, and neutrophil function, as well as an anaerobic milieu. Protein
metabolism is decreased, and healing of soft and hard tissue is delayed,
which may lead to the susceptibility of infection. Neuropathy and impaired
nerve regeneration may be altered as well as angiogenesis.29
Implant failure.
Human clinical studies have indicated that no contraindications exist for
patients who are well controlled by diet and oral hypoglycemic. However, for
insulin-controlled patients, a contraindication for implants may exist
depending on the state of control. Researchers have concluded that implants
have a high success rate provided the diabetes is controlled (monitor to
ensure that glycosylated hemoglobin [HbA1c ] <7.0). An increased failure rate
of dental implants has been associated with poor metabolic control.30 It is
imperative that uncontrolled or patients exhibiting an elevated HbA1c be
treated prior to and during the implant surgery healing period.
Understand symptoms of diabetes.
Because of the high incidence of undiagnosed diabetes, the implant dentist
must be aware of the major symptoms such as polyuria, polydipsia,
polyphagia, and weight loss. Therefore, undiagnosed diabetic patients may
predispose the implant procedure with an increased morbidity. In the future,
type 2 diabetes will continue to grow at rates that may reach epidemic
proportions.
Determine glycemic control.

The glycemic control should be evaluated via HbA1c test, (hemoglobin A1c,
glycated hemoglobin, A1c, or HbA1c,) in conjunction with a consultation with the
patient's physician. Ideally, the A1c should be maintained at less than 7%
when appropriate. The HbA1c test is ideal for evaluation of glycemic control
because it will show the glycemic control over the past 3 months. The HbA1c
measures the glucose bound to hemoglobin within the red blood cells. The
test is a weighted average of blood glucose levels during the life of the red
blood cells (120 days). This test is more accurate in the assessment of diabetic
control in comparison to a fasting blood glucose, which can give a false
positive or negative results (Table 2.3).
TABLE 2.3
Hemoglobin–Blood Glucose Treatment Regimen
Blood
Risk Hemoglobin Sugar Treatment P lan
Level
A1c mg/dL
Low <6.0 <140 S tress reduc tion protoc ol, maintain glyc emic c ontrol (relative c ontraindic ation)
Low/Medium 6.0–7.0 140– S tress reduc tion protoc ol, maintain glyc emic c ontrol
180 Patients with neuropathy, nephropathy, peripheral vasc ular disease, history of c oronary disease, or
ophthalmologic manifestation of diabetes (retinopathy) may be at higher risk despite c ontrolled HbA 1c .
Consultation with MD may be appropriate (relative c ontraindic ation)
Medium 7.0–8.0 180– Patients without and sec ondary manifestations of diabetes suc h as neuropathy, nephropathy, peripheral
High 215 vasc ular disease, or ophthalmologic (retinopathy) MD c onsult may be obtained (relative). Patients with
c oronary disease or other diabetic related c onditions require MD c onsult (relative/absolute)
High Risk >8.0 >215 MD referral and better glyc emic c ontrol (absolute c ontraindic ation)
HbA1c, glycosylated hemoglobin.
Medication prophylaxis.
Because of the reciprocal relationship between infection and glycemic
control, the use of antibiotic prophylaxis is highly recommended. Ideally, a
beta-lactam antibiotic should be used pre- and postoperatively. When
antibiotic prophylaxis is administered to diabetic patients, studies have
shown a 10.5% reduction in failure rate. Further reduction is achieved by
maintaining a strict aseptic technique in combination with good surgical
technique. Additionally, it has been reported that the use of a chlorohexidine
gluconate (0.12%) rinse at the time of implant placement reduced the failure
rate from 13.5% to a remarkable 4.4% in type 2 diabetic patients.31 A pre- and
postoperative chlorohexidine regimen will decrease morbidity with implants
in diabetics. These patients must practice meticulous oral hygiene and be
recalled at regular intervals to minimize the possibility of peri-implantitis.
Corticosteroids use.
Even though corticosteroids (e.g., dexamethasone) have been shown to
minimize edema and pain after implant surgery, this medication should not
be used in oral- or insulin-controlled diabetics. Corticosteroids have been
shown to cause hyperglycemic episodes and changes in blood glucose levels
that are difficult to correct.
Treatment summary
• Diet-controlled diabetic: Determine/maintain diabetic control
• Hypoglycemic-controlled diabetic: Determine/maintain diabetic, stress
reduction protocol, A1c-<7%
• Insulin-controlled diabetic: Determine diabetic control, stress reduction
protocol, A1c-<7%
Thyroid Disorders
Do you have a thyroid problem? /No?
Thyroid disorders are the second most common endocrine problem,
affecting approximately 1% of the general population, principally women.
The thyroid gland is one of the larger endocrine glands in the body and is
situated at the level of C5 and T1 vertebral bodies, just below the laryngeal
prominence. The main function of the thyroid gland is to produce hormones,
the most common being thyroxine (T4) and triiodothyronine (T3). Thyroxine
is responsible for the regulation of carbohydrate, protein, and lipid
metabolism. In addition, the hormone potentiates the action of other
hormones such as catecholamines and growth hormones. Abnormalities in
the thyroid gland can result in disorders of thyroxine production. Excessive
production of thyroxine results in hyperthyroidism. Symptoms of this
disorder include increased pulse rate, nervousness, intolerance to heat,
excessive sweating, weakness of muscles, diarrhea, increased appetite,
increased metabolism, and weight loss. Excessive thyroxine may also cause
atrial fibrillation, angina, and CHF. Palpation of the patient's neck often
reveals an enlarged thyroid gland (goiter) between the cricoid cartilage and
the suprasternal notch.
Hyperthyroidism.
High levels of circulating free levels of T4 or T3 result in a very low TSH level
indicating hyperthyroidism. These patients may also complain of fatigue, and
usually have excess sweating or feeling of being hot despite the temperature,
restlessness, loose stools, palpitations or elevated heart rate, weight loss,
increased blood pressure, tremor, and feeling of nervousness or irritability.
Hyperthyroid: catecholamine sensitivity.

Patients with hyperthyroidism are especially sensitive to catecholamines
such as epinephrine in local anesthetics. When exposure to catecholamines is
coupled with stress (often related to dental procedures) and tissue damage
(dental implant surgery), an exacerbation of the symptoms of
hyperthyroidism may occur. This can result in a condition termed
thyrotoxicosis or thyroid storm, which is an acute, life-threatening
hypermetabolic state clinically presenting with symptoms of fever,
tachycardia, hypertension, and neurologic and gastrointestinal
abnormalities. Treatment of thyroid storm in the dental setting includes
immediate medical attention. If left untreated, these symptoms may result in
CHF and life-threatening cardiac arrhythmias.
Bleeding.
The increased blood pressure and heart rate that accompany
hyperthyroidism may increase bleeding at the surgical site and require
additional hemostatic techniques. It is also important to note that PTU or
propylthiouracil is used to treat hyperthyroidism. This drug is an antagonist
of vitamin K that has an adverse impact on the clotting cascade and may
result in significant bleeding or postoperative hemorrhage.
Aspirin/NSAID use.
Use of aspirin or NSAIDs requires extreme caution in the hyperthyroid
patient. Aspirin can increase free levels of the T4 hormone because of an
interaction with protein binding. Additionally, many hyperthyroid patients
are on beta blockers for heart rate and blood pressure control, and the use of
NSAIDs can decrease the efficacy of beta blockers. Alternative pain
medications should be considered in patients with hyperthyroidism (e.g.,
Ultram).
Hypothyroidism.
Underactive or low thyroid production results in hypothyroidism. This
disorder can be caused by the thyroid gland not producing sufficient thyroid
hormone. The related symptoms are a result of a decrease in metabolic rate,
which cause symptoms such as tiredness, cold intolerance, and weight gain.
The diagnosis of hypothyroidism or hyperthyroidism can be confirmed with
blood tests measuring thyroid-stimulating hormone (TSH) and free levels of
T4 or T3. Low levels of circulating T4 and/or T3 will result in the TSH being
elevated, indicating hypothyroidism. These patients usually have symptoms
of fatigue, dry skin, hair loss, constipation, feeling cold, irregular menstrual
cycles, weight gain, and they can have an enlarged thyroid gland (goiter).
Hypothyroid: CNS depressants use.

The hypothyroid patient is particularly sensitive to central nervous system
(CNS)–depressant drugs, especially narcotics and sedative drugs such as
diazepam or barbiturates. The risk of respiratory depression, cardiovascular
depression, or collapse must be considered. Patients with longstanding
hypothyroidism may have prolonged bleeding requiring hemostatic control
for excessive bleeding. Additionally, hypothyroid patients may exhibit
delayed wound healing and predisposition to postoperative infection.
Hypothyroid: bone healing.

T4 affects bone metabolism by decreasing recruitment and maturation of
bone cells and reducing the bone growth factor of insulin-like growth factor.
Studies have shown that medically treated hypothyroid patients exhibit
greater bone loss and a less favorable soft tissue response after stage I
surgery but with no significant increased risk of failure.32
Ideal thyroid control (hypothyroid and hyperthyroid).
To minimize any possible detrimental effects related to implant treatment,
the implant clinician should monitor the patient for ideal thyroid control.
Reducing stress in thyroid patients along with patient education on the
importance of medication control is paramount to decrease procedural
morbidity. Additionally, hypothyroid patients should be well informed of a
possible decreased complication and success rate.
Corticosteroid Treatment
Do you have a history of taking corticosteroids? /No?
Corticosteroids are used in medicine today to treat a host of diseases. They
are responsible for many actions including carbohydrate, protein, and lipid
metabolism, the immune response, and the body's response to stress.
Corticosteroids are highly effective in suppressing or minimizing
inflammation while their pharmacologic and physiologic mechanisms are
potentially detrimental to several metabolic, hormonal, and immunologic
functions in the body. Although corticosteroids are routinely used
prophylactically in the field of dental implantology, long-term use for
treatment of various diseases does pose many possible complications for the
patient undergoing dental implant surgery. Cortisol is the main steroid in the
body and is involved in metabolic processes, inflammatory responses, and
the control of responses to stresses. Secretion of cortisol is regulated via the
hypothalamus-pituitary adrenal axis (HPA) feedback axis; however, for
patients who are taking exogenous steroids, the feedback response may not
occur. In these situations, the patient may be predisposed to acute adrenal
insufficiency (adrenal crisis).
Adrenal insufficiency.
Long-term corticosteroid use may decrease a patient's ability to cope with the
stresses of extensive surgical procedures. This may precipitate an acute
adrenal crisis. Patients who are susceptible to adrenal crisis include those
who:
• are currently on daily systemic corticosteroids of 10-mg equivalent;
• are currently on daily systemic corticosteroids of 5-mg prednisone
equivalent;
• have been taking corticosteroids regularly during the previous 30 days;
• have been taking corticosteroids for more than 1 month during the past
year.33
Signs of acute adrenal insufficiency include hypotension, altered mental
status, pallor, and a rapid but steady weak pulse. Emergency treatment
includes terminating the procedure, summoning medical assistance,
administering supplemental oxygen, and monitoring vital signs. Place the
patient in a supine position and raise the patient's legs, if possible, to
counteract the low blood pressure. If available, administer 100 mg of
hydrocortisone sodium succinate (Solu-Cortef) when it is clear that the
patient's current symptoms are due to adrenal crisis rather than to cardiac,
pulmonary, or other medical etiology.
Implant failure.
Long-term corticosteroid therapy has shown adverse effects such as reduced
bone density, increased epithelial fragility, delayed healing (decreased
protein synthesis), and immunosuppression. Animal studies have shown
osseointegration to be compromised; however, no studies to date have shown
increased morbidity or implant failure in patients under systemic
corticosteroids.34
Supplemental steroid coverage.
For patients who have received supraphysiologic doses of corticosteroids,
their HPA may be suppressed, placing them at risk (adrenal crisis) during
dental implant surgery and requiring supplemental doses of corticosteroids.
Various regimens have been proposed; however, the most accepted protocol
involves doubling the normal daily oral dose on the day of the procedure.35
Modification of systemic steroid use should only be completed after
physician consultation.
Susceptibility to infection.
Systemic corticosteroids (long term) may compromise the patient's ability to
fight infection. By decreasing leukocytosis, the patient is more susceptible to
infection after dental implant procedures. Patients should always receive a
prophylactic administration of systemic antibiotics (pre- and postoperatively)
and an antimicrobial mouth rinse (chlorhexidine gluconate) to reduce the
possibility of infection.
Hyperparathyroidism
Do you have hyperparathyroidsim? /No?
Hyperparathyroidism is an excess of parathyroid hormone (PTH) in the
bloodstream due to overactivity of one or more of the parathyroid glands that
maintain calcium balance. The clinical manifestations of this disease vary
widely depending on the severity. Mild forms may be asymptomatic, whereas
severe hyperparathyroidism can cause bone, renal, and gastric disturbance. It
has been noted that skeletal depletion occurs as a result of stimulation by the
parathyroid gland, which results in alveolar bone being affected prior to
bones such as the ribs, vertebrae, or long bones. In the oral and maxillofacial
regions, altered trabecular bone patterns may be present that result in
mobility of the teeth and compromised bone density.
Hyperparathyroidism falls into three categories: primary, secondary, and
tertiary. Primary hyperparathyroidism involves one of the parathyroid glands
becoming overactive and releasing excess parathyroid hormone. This results
in high levels of calcium being released into the bloodstream from the bone,
which leads to osteoporotic bones.
Secondary hyperparathyroidism is a chronic condition where the
parathyroid glands release excess amount of parathyroid hormone because of
chronically low blood calcium levels. Secondary hyperparathyroidism is
usually due to conditions such as chronic kidney disease, vitamin D
deficiency, and some gastrointestinal issues that impact calcium absorption.
Tertiary hyperparathyroidism can occur when the condition causing
secondary hyperparathyroidism is treated. This is similar to vitamin D
deficiency; however, the parathyroid glands continue to produce excess
parathyroid hormone.
Bone involvement.
Dental implants are contraindicated (absolute) in areas of active bony
lesions. However, implant placement may be initiated after treatment and
healing of the affected areas. Altered trabecular bone pattern with the
appearance of ground glass may also occur. In animal studies, secondary
hyperparathyroidism affects alveolar bone more than any other bone of the
skeleton, and central or peripheral giant cell tumors may be present in active
lesion areas.36
Parathyroid control.
When the PTH is elevated, a serum calcium level is obtained to determine if
the hyperparathyroidism is primary or secondary, and the condition is
usually treated with surgery or medication. In advanced disease, there are
certain oral changes that can be present to suggest hyperparathyroidism.
These patients have an increased risk for tori, and reduction in the radicular
lamina dura is evident on dental radiographs. Many patients with higher
levels of parathyroid hormone develop loose teeth and widening of the
periodontal ligament space surrounding the teeth. Additionally, cortical bone
loss at the angle of the mandible has been noted in this disorder.
Xerostomia
Do you have xerostomia? /No?
Xerostomia (dry mouth) may directly or indirectly have effects on dental
implants. A decrease in salivary flow is also accompanied by a change in its
composition. An increase in mucin and a decrease in ptyalin result in a more
viscous and ropy saliva. Plaque formation is increased, and the reduced
antibacterial action of the saliva results in a favorable environment for
bacteria growth.
Oral complications.
Dental implants are not contraindicated in patients suffering from
xerostomia. Case reports have been documented with successful implant
placement with no increase in failure rate.37 However, with the lack of saliva,
implant patients may be susceptible to more oral lesions and the possibility
of irritation from tissue-borne implant prostheses. Additionally, patients are
at higher risk for incision line opening.
Oral bacterial infections.
Patients with xerostomia are at a higher risk for oral infections such as
periodontitis, caries, and fungal infections. A comprehensive oral and
periodontal examination must be completed with emphasis on a low
periodontal pathogen bacterial count to reduce possible postoperative
complications.
Increase saliva flow.

Stimulation of salivary flow may be achieved either by physiologic or
pharmacologic means. Mouth rinses, chewing gum, or salivary substitutes
may be used (Box 2.4).
Box 2.4
Xerostomia Treatment Regimens
• Drink water frequently: helps moisten mucosa and loosen mucus.
• Gum/candy: the use of sugarless gum or candy helps stimulate saliva flow.
• Avoid commercial mouth rinses containing alcohol or peroxide: further

desiccate the mucosa.
• Avoid salty foods, dry foods (for example, crackers, toast, cookies, dry
breads, dry meats/poultry/fish, dried fruit, bananas) and foods and
beverages with high sugar content.
• Avoid drinks containing alcohol or caffeine. Alcohol and caffeine increase

urination and desiccate the mucosa.
• Over-the-counter saliva substitutes: products containing xylitol (e.g., Mouth

Kote, Oasis Moisturizing Mouth Spray, or ones containing
carboxymethylcellulose)
• Prescription medications, after physician consultation (Evoxas, Salagen,

Pilocarpine, Cevimeline)
Final prosthesis.
When treatment planning patients with xerostomia, a final prosthesis that is
not tissue borne is recommended. A fixed-detachable (FP-3) prosthesis is
highly recommended because of the lack of soft tissue coverage. If a
removable prosthesis is warranted, an RP-4 is recommended because of the
lack of soft tissue coverage. Additionally, removable prostheses worn in
patients with xerostomia are associated with a high prevalence of fungal
infections. If fungal infection is diagnosed, the use of a Nystatin medication
is warranted (for additional endocrine implications see Table 2.4).
TABLE 2.4
Additional Endocrine Issues and Treatment Implications

Frequent urination Diabetes (undiagnosed)
Inc reased thirst Diabetes (undiagnosed)
Rec ent weight loss Anxiety, depression, GI disease, diabetes, hyperthyroidism
Rec ent weight gain Heart failure (water retention), c ortic osteroids, Cushing syndrome, hypothyroidism
Inc reased appetite Diabetes, hyperthyroidism
Fatigue Anxiety, depression, anemia, vitamin B defic ienc y, hyper/hypothyroidism, c hronic
pulmonary/c ardiovasc ular disease
Frequent kidney stones Hyperc alc iuria from hyperparathyroidism
Inc reased head/hand shoe size Paget disease
Nontraumatic bone frac tures Osteoporosis, hyperparathyroidism, myeloma
S low healing infec tions/sores Undiagnosed diabetes, Cushing syndrome, c oagulation fac tor defic ienc y, vitamin C defic ienc y, adrenal
insuffic ienc y
Pigment c hanges in skin (dark Undiagnosed diabetes, Addison disease, melanoma, hemoc hromatosis
spots)
GI, gastrointestinal.
Pulmonary System
Chronic Obstructive Pulmonary Disease (COPD)
Do you have chronic obstructive pulmonary disease? /No?
Chronic obstructive pulmonary disease (COPD) refers to a group of
pulmonary diseases that block airflow, resulting in breathing difficulties. The
two most common conditions that make up COPD are chronic bronchitis and
emphysema. Chronic bronchitis is an inflammation of the bronchial tubes
that produces an increase in mucous production and coughing. Emphysema
occurs when the alveoli in the bronchioles of the lungs become damaged or
destroyed creating symptoms of dyspnea (shortness of breath) that may
worsen with mild activity.
Patients with COPD may have a combination of both conditions. These
patients usually present with fatigue, history of recurrent respiratory
infections, wheezing, and shortness of breath. In advanced disease states,
patients may become oxygen dependent with tachypnea being present with
some audible wheezing and shortness of breath even at rest. The various
levels of COPD are classified via GOLD (Global Initiative for Chronic
Obstructive Lung Disease), which classifies patients on their degree of
airflow limitation. The airflow limitation is measured during pulmonary
function tests (PFTs) measured as forced expiratory volume (FEV1) (Table 2.5).
TABLE 2.5
COPD Stages and Related FEV1 Values
S tage I Mild COPD FEV 1/FVC <0.70 FEV 1 ≥80% normal

S tage II Moderate COPD FEV 1/FVC <0.70 FEV 1 50%–80% normal
S tage III S evere COPD FEV 1/FVC <0.70 FEV 1 30%–50% normal
S tage IV Very severe COPD FEV 1/FVC <0.70 FEV 1 <30% normal, or <50% normal ac c ompanied by c hronic respiratory failure
COPD, chronic obstructive pulmonary disease; FEV1, forced expiratory volume; FVC, forced vital capacity.
Anesthetic selection.
In rare instances, patients with COPD receiving local anesthetics have had
adverse reactions. Increased doses of anesthetic solutions that contain
sulfites may increase the risk of bronchospasm or allergic reactions. Most
local anesthetics that are vasopressor anesthetics (e.g., epinephrine,
levonordefrin), will contain the antioxidant sodium (meta) bisulfite. For
COPD patients with a known allergy to bisulfites a local anesthetic without a
vasopressor (e.g., mepivacaine HCL 3%, prilocaine HCL 4%) should be used.
Adrenal suppression.
Adrenal suppression may occur with long-term corticosteroid treatment,
which is common with more advanced COPD patients.
Cardiovascular event.
For patients who have had a cardiovascular event, the patient's functional
capacity should be ascertained (physician consultation) and a stress
reduction protocol implemented. The implant clinician should avoid long or
extensive surgical procedures.
Oxygen supplementation.
High flow rates of oxygen can result in respiratory depression and should not
be used, especially with patients who require at-home oxygen use. Nitrous
oxide is also contraindicated because of the negative impact on the
respiratory drive. Low–flow rate oxygen supplementation (<2 L/min) during
implant procedures is highly recommended, so as to minimize the possibility
of hypoxia.
Bronchodilators/inhaled corticosteroids.
Bronchodilators and inhaled corticosteroids are the hallmark of treatment for
COPD; however, they have been associated with an adverse impact on oral
tissues.
Beta 2 agonists like albuterol have been associated with a decrease in saliva
production and subsequent secretion resulting in xerostomia. Patients
should always be instructed to bring their rescue inhaler (usually albuterol)
to the procedure or, for more advanced COPD patients, their nebulizer and
albuterol solution in case of an emergency.
Minimize elective procedures.
Dental implant management of patients with COPD is staged according to
the severity of the disease. It is important to understand the severity of the
lung disease before initiating any dental procedure. More advanced COPD
patients have a higher propensity to retain carbon dioxide, which may
directly lead to adverse intraoperative outcomes.
Use of sedation.
Sedation should be carefully evaluated in patients with COPD, and
discussion with their treating physician is recommended. Potent sedatives
such as narcotics and barbiturates should be avoided unless approved by the
treating physician. These drugs can further depress the respiratory drive in
more advanced COPD patients. Antihistamines may desiccate respiratory
secretions, which may lead to compromised air flow. Additionally, nitrous
oxide should not be used in COPD patients as it may lead to further
respiratory depression (Table 2.6).
TABLE 2.6
Additional Pulmonary Issues and Treatment Implications

Asthma Inflammatory proc ess in lung is IgE/allergen mediated
Determination of trigger: asthma or bronc hospasm, inc luding anxiety
Albuterol on hand for surgery
Approximation of severity determined by number of medic ations and frequenc y of use of
albuterol resc ue inhaler
S hortness of breath (dyspnea) Asthma, COPD, heart disease, c ardiomyopathy, CHF, arrhythmias, anemia, obesity, heart valve
disease
Wheezing Allergies, asthma, bronc hitis, GERD, voc al c ord dysfunc tion
Hemoptysis (blood in sputum) Bronc hitis, pulmonary embolism, CHF, lung c anc er, blood thinners, TB
Cough Postnasal drainage, asthma, GERD, ACE/ARB blood pressure meds, c hronic bronc hitis in COPD,
other respiratory like bronc hiec tasis
Change in exerc ise toleranc e Any c hanges walking up stairs or walking more than 50 yards
Cardiovasc ular, pulmonary, poor c onditioning
Weight loss Poorly c ontrolled COPD, malignanc y, TB, hyperthyroid, ethyl alc ohol abuse
Dysphagia from stroke or other Risk of aspiration during dental proc edure
neuromusc ular diseases
ACE, angiotensin-converting enzyme; ARB, angiotensin-receptor blocker; CHF, congestive heart failure;
COPD, chronic obstructive pulmonary disease; GERD, gastroesophageal reflux disease; IgE,
immunoglobulin E.
Hematologic System
Erythrocytic Disorders: Polycythemia
Do you have a bleeding/blood disorder? /No?
Polycythemia is a myeloproliferative bone cancer condition that results in
increased red blood cells and is characterized by an increased hematocrit
(>48% in women, >52% in men) and hemoglobin level (>16.5 g/dL in women
and >18.5 g/dL in men). The health concerns associated with polycythemia
are a direct result of thicker blood due to an increased red blood cell count,
placing the patient at a surgical risk. Primary polycythemia is relatively rare
and caused by overproduction of red blood cells by the bone marrow.
Secondary polycythemia is caused by chronic hypoxemia or an
erythropoietin-secreting tumor. Conditions like COPD, CHF, pulmonary
hypertension, testosterone replacement therapy, and sleep apnea may cause
secondary polycythemia.
Thrombus formation.
Because of the higher viscosity of the blood in polycythemia patients, an
increased possibility of stroke, myocardial infarction, pulmonary embolism
may occur.
Bleeding.
Excessive bleeding and clotting issues are common with polycythemia
patients; good surgical technique and strict hemostatic control measures
must be adhered to in order to minimize intraoperative and postoperative
bleeding episodes.
Treatment summary.
Unless cleared by a physician, polycythemia is an absolute contraindication
for dental implant treatment.
Erythrocytic Disorders: Anemia

Anemia, the most common hematologic disorder, is defined as a deficiency
in red blood cells, resulting in low hemoglobin. The etiology of anemia is
either underproduction of red blood cells or an increased destruction or loss
(usually gastrointestinal or menstrual) of red blood cells. Iron deficiency
anemia results from a lack of iron in the body or excessive loss of red blood
cells. Various other anemias exist that are associated with vitamin
deficiencies such as B12 or folate. Some anemias are the result of destruction
of red blood cells. These are known as hemolytic anemias with sickle cell
anemia as an example. Bone marrow dysfunction may also lead to anemia.
The general symptoms and signs are all a consequence of either a
reduction of amount of oxygen reaching the tissues or alterations of the red
blood cell count. The symptoms of mild anemia include fatigue, anxiety, and
sleeplessness. Chronic anemia is characterized by shortness of breath,
abdominal pain, bone pain, tingling of extremities, muscular weakness,
headaches, fainting, change in heart rhythm, and nausea. The general signs
of anemia may include jaundice, pallor, spooning or cracking of the nails,
hepatomegaly and splenomegaly, and lymphadenopathy.
Bleeding.
Some anemias are associated with abnormal bleeding. During extensive
surgery, the increased bleeding may cause a decreased field of view for the
clinician and possible postoperative issues. Most often iron deficiency
anemia and other vitamin-dependent anemias are associated with increased
bleeding.
Edema.
Increased edema and subsequent increased discomfort postsurgically are
common consequences. In addition, the excess edema increases the risk of
postoperative infection and morbidity. Not only are anemic patients prone to
more immediate infection from surgery, they are also more sensitive to
chronic infection throughout their lives. This may affect the long-term
maintenance of the proposed implant or abutment teeth.
Oral soft tissue issues.

The oral signs of anemia affect the tongue. Symptoms include a sore, painful,
smooth tongue, loss of papillae, redness, loss of taste sensation, and
paresthesia of the oral tissues.
Bone healing.
Bone maturation and development are often impaired in the long-term
anemic patient. A faint, large trabecular pattern of bone may even appear
radiographically, which indicates a 25% to 40% loss in trabecular pattern.
Therefore, the initial quality of the bone required to support the implant can
be affected significantly. The decreased bone density affects the initial
placement and may influence the initial amount of mature lamellar bone
forming at the interface of an osseointegrated implant. The time needed for a
proper interface formation is longer in poor-density bone.38 However, after
the implant is loaded successfully, the local strain environment will improve
the bone density at the interface.
MD consultation/lab tests.
Lab tests for anemia include the hematocrit and hemoglobin. The hematocrit
indicates the percentage of a given volume of whole blood composed of
erythrocytes. An abnormal hemoglobin may result from its combination with
substances other than oxygen (e.g., carbon monoxide) or genetic diseases
(e.g., sickle cell diseases). Normal values for men are 13.5 to 18 g/dL; those for
women are 12 to 16 g/dL. The minimum baseline recommended for surgery is
10 mg/dL, especially for elective implant surgery. For the majority of anemic
patients, implant procedures are not contraindicated.
Medications.
Preoperative and postoperative antibiotics should be administered and the
risk of bleeding in anemic patients should not be potentiated by the
prescription/use of aspirin. Hygiene appointments should be scheduled
more frequently for these patients to decrease possible periodontal issues.
Leukocytic (WBC) Disorders

Leukocyte disorders are an important consideration in hematologic diseases.
The WBC count normally ranges from 4500 to 13,500/mm3 in the adult.
Leukocytosis is an increase in circulating WBCs with various etiologies. There
are multiple components of the white blood cell that can be increased: (1)
neutrophils—main defense against bacterial infections; (2) lymphocytes—
main defense against viral infections; (3) monocytes—largest type of
leucocyte (white blood cell), which differentiates into phagocytes; (4)
eosinophils—combat parasites and associated with allergies; (5) basophils—
type of white blood cell; (6) blast cells—immature cells. Leukocytosis is
defined as an increase in circulating WBCs in excess of 13,500/mm3. The most
common cause of leukocytosis is infection. Leukemia, neoplasms, acute
hemorrhage, and diseases associated with acute inflammation or necrosis
(e.g., infarction, collagen diseases) are more serious causes of leukocytosis.
Physiologic conditions such as exercise, pregnancy, and emotional stress can
also lead to leukocytosis in addition to chronic steroid use.
Leukopenia is a reduction in the number of circulating WBCs to less than
4500/mm3. A decreased leukocyte count may accompany certain infections
(e.g., infectious hepatitis), bone marrow damage (from radiation therapy),
nutritional deficiency (e.g., vitamin B12, folic acid), and blood diseases (e.g.,
anemia).9
Infection.
With patients suffering from leukocytosis or leukopenia, many complications
can compromise the success of the implants and prosthesis. The most
common is infection, not only during the initial healing phase but also long
term, which may compromise the longevity of the implants and the final
prosthesis.
Bleeding.
Thrombocytopenia is caused by decreased production, increased destruction,
or sequestration of platelets in the spleen, which results in potential bleeding
complications during surgery. A platelet count should always be obtained via
MD consultation, and a value lower than 50,000 U/L contraindicates elective
dental surgery because of a significant risk of postoperative bleeding.39
Delayed healing.
Delayed healing is also a consequence of WBC disorders. For most dental
implant procedures, the initial few months are critical for the long-term
success of the implants and/or bone graft. Delayed healing may increase the
risk of secondary infection and possibility of incision line opening.
MD consultation.
Because of the wide spectrum of hematologic disease states, the severity of
the disorder and its associated medications should be evaluated with a
strong recommendation of physician consultation (Table 2.7).
TABLE 2.7
Additional Hematologic Issues and Treatment Implications

S ic kle c ell anemia S ec ondary infec tions are a c ommon c onsequenc e with frequent history of osteomyelitis and bone infec tion.
(absolute c ontraindic ation)
Leukemia Experienc e anemia and thromboc ytopenia. Although the infec tion is less severe than in ac ute leukemia, radioluc ent
lesions of the jaws, oral ulc erations, hyperplastic gingiva, and bleeding c omplic ations develop in these patients.
(absolute c ontraindic ation)
Thalassemia Multiple types (alpha, beta) and degrees of severity (major, minor)
More severe forms c an present some issues erythroid mass expansion direc tly into fac ial bones c ausing
maloc c lusions.
Medic al c onsultation is rec ommended to determine severity of disease.
Major (severe forms)—absolute c ontraindic ation
Minor (less severe)—relative c ontraindic ation
Frequent nosebleeds Hypertension, sinus disease, bleeding disorders suc h as von Willebrand
(epistaxis) S pontaneous or frequent nose bleeds should have bleeding time and INR
Easy bleeding gums Gingival disease, bleeding disorder, thromboc ytopenia, leukemia, liver disease
Further investigation may be warranted with platelet, CBC, bleeding time, PT, PTT
Heavy menstrual Thyroid disease, dysfunc tional uterine bleeding (fibroid, polyps, hormone imbalanc e), bleeding disorders, platelet
periods dysfunc tion. If no obvious medic al reason, c hec k CBC, INR, bleeding time
Family history of If family history of bleeding issues, c hec k CBC, INR, PTT, bleeding time to rule out hereditary bleeding disorders
bleeding disorder suc h as von Willebrand, hemophilia, c oagulation fac tor defic ienc ies
Prolonged bleeding Rule out c oagulation defec t, hereditary bleeding disorder, or platelet dysfunc tion; c hec k CBC, INR, PTT, bleeding
after c uts times
Easy bruising or Platelet defic ienc y, c oagulation fac tor issue, leukemias, vitamin K defic ienc y, c hemotherapy, antic oagulation
spontaneous bruising medic ation
History of exc essive If no definitive diagnosis that c orrelates with prolonged bleeding, c hec k CBC, INR, PTT, bleeding time
bleeding after dental
surgery
CBC, complete blood count; INR, international normalized ratio; PT, prothrombin time; PTT, partial
thromboplastin time.
Digestive System
Inflammatory Bowel Disease (IBD)
Do you have or have you been treated for inflammatory bowel disease?
/No?
Inflammatory bowel disease (IBD) is a chronic inflammation of all or part
of the digestive tract. The number of people afflicted with this condition
continues to increase. The two major forms of IBD are ulcerative colitis and
Crohn disease. Patients will usually have symptoms of chronic or severe
diarrhea, fatigue, rectal bleeding, and anemia. Ulcerative colitis is
characterized as an inflammatory disease of the rectum and large intestine
mainly affecting the mucosal lining. Crohn disease is an inflammatory
disease of the entire digestive tract from mouth to anus, resulting in lesions
of healthy tissue in between areas of inflammation. Most cases of Crohn
disease originate within the terminal ileum.
Surgical/Implant Considerations
Infections.
Patients are susceptible to infections and healing issues usually associated
with the immunosuppressive drugs. As well, their dietary restrictions may
impact both of these issues, and postoperative antibiotics are usually
indicated.
Adrenal issues.
During dental procedures, stress reduction protocol is essential. Excess stress
can impact adrenal function and require additional corticosteroid
augmentation. Postoperative pain episodes may increase stress on the
adrenal gland, resulting in possible adrenal suppression complications.
Bleeding.
Many digestive disorder patients are anemic and, because of malabsorption,
may not absorb all the necessary components of clotting factors as well as
certain vitamins. Care should be taken to minimize bleeding.
Oral lesions.
There are many differences in the oral lesions and that manifest in patients
with Crohn disease and those with ulcerative colitis. Many of these patients
present with a glossitis, aphthous ulcerations, or a more classic marker of
ulcerative colitis, pyostomatitis vegetans. This condition is characterized by
pustules with thickened oral mucosa and surrounding erythema with some
erosions.40 Ulcerative colitis has extragastrointestinal manifestations that
have been associated with erosive temporomandibular joint disease.41 Crohn
disease has been shown to have oral symptoms such as cobblestoning of the
oral mucosa accompanied by ulcerations usually in a linear pattern along
with hyperplastic folds of the buccal vestibules (mucosal tags).42
MD consultation.
A physician consultation is recommended to determine the extent of the
patient's digestive disorder along with the current immune status. Most
notably, an evaluation of delayed wound healing and postoperative infection
susceptibility should be ascertained.
Antibiotics usage.
Antibiotics that have a high incidence of antibiotic-associated diarrhea or
pseudomembranous colitis should be avoided (e.g., amoxicillin/clavulanic
acid, erythromycin, clindamycin).
Use of probiotics.
Patients with IBD, especially those with ulcerative colitis, may benefit from
the use of probiotics, especially when antibiotics are prescribed. Probiotics
are live microorganisms that are added to food to change the intestinal
microbial balance. The mechanism of action is controversial; however,
theories include strengthening of the gut barrier, pathogen growth
inhibition, and enhancement of mucosal and systemic immune responses.
Pain management.
Most NSAIDs may precipitate these disease states and should be avoided
unless authorized by a physician.
Stomach Ulcers
Do you have stomach ulcers? /No?
Approximately 1 in 10 Americans will suffer from a version of gastritis or
ulcer disease during their lifetime. Ulcers form when there is a break or
breach of the lining of the stomach or intestine. Peptic ulcers form in the
duodenum of the small intestine from being in contact with stomach acids.
Duodenal ulcers are the most common type of ulcer. Ulcers that occur in the
stomach are referred to as gastric ulcers. In rare cases, esophageal reflux can
cause esophageal ulcers. There are several main causes for ulcer disease
including excessive alcohol intake, stress, medications (NSAIDs, aspirin),
and a bacterium (H. Pylori).
Medications.
While there are no direct contraindications to the use of prophylactic
antibiotics in patients with ulcer disease (except allergies), some patients
may be more sensitive to certain types of antibiotics that may irritate their
stomach. Pain management may be hampered by the inability to use
NSAIDs or certain narcotics. To prevent bleeding from stomach ulcers,
analgesics and antibiotics should be cautiously used (MD clearance) in the
treatment of implant surgical patients.
Liver Cirrhosis
Do you have liver problems? /No?
Cirrhosis of the liver is characterized by irreversible scarring and is usually
caused by excessive alcohol intake, viral hepatitis B and C, and certain
medications. Although patients with advanced disease can present with
jaundice and itching, the diagnosis is usually confirmed by liver biopsy and
blood tests. Cirrhosis may cause excessive bleeding, mental confusion,
kidney failure, and accumulation of fluid in the abdomen (ascites). Cirrhosis
is irreversible, and transplantation is becoming the most successful
treatment for advanced disease states.
These patients may be predisposed to issues including the synthesis of
clotting factors and the inability to detoxify drugs. Hemostatic defects of liver
disease are not only the reduced synthesis of clotting factors, but also an
abnormal synthesis of fibrinogen and clotting proteins, vitamin K deficiency,
enhanced fibrinolytic activity, and quantitative and qualitative platelet
defects. Of patients with liver disease, 50% have a prolonged prothrombin
time (PT) and possible significant clinical bleeding. The inability to detoxify
drugs may result in oversedation or respiratory depression. The laboratory
evaluation of the implant candidate gives much insight into hepatic function.
A basic panel of liver function tests (LFTs) or a comprehensive metabolic
panel (CMP) can provide the needed information. In most patients with liver
disease, it is recommended that a complete blood count (CBC), LFT, basic
metabolic panel (BMP), bleeding time, and an international normalized ratio
(INR)/PT test should be performed.
Surgery/Implant Implications
Bleeding.
Patients with no abnormal laboratory values for CMP, CBC, partial
thromboplastin time (PTT), and PT are at low risk. A normal protocol is
indicated for all surgical implant procedures. Ideally, INR values should be
below 3.0. Patients with an elevated PT of less than 1.5 times the control value
or bilirubin slightly affected are at moderate risk. Chronic severe liver
disease may increase INR.
Medications.
Many drugs such as local anesthetics (lidocaine, prilocaine, mepivacaine,
bupivacaine), sedatives (lorazepam, valium, alprazolam), and antibiotics
(erythromycin, clindamycin) are metabolized primarily in the liver.
Therefore, in some patients a dosage reduction may be warranted based on
the current liver functioning.
NSAIDs.
NSAIDs should be avoided because they can be associated with renal failure.
Acetaminophen at reduced dose is a possible alternative consideration. An
accepted school of thought is that codeine and opioids should not be used or,
if so, at very infrequent and lower dosages to avoid hepatic encephalopathy.43
Additionally, tetracycline, erythromycin, and metronidazole should never be
used in patients with advanced liver disease.
High risk (absolute).
Patients with a PT greater than 1.5 times the control value, mild to severe
thrombocytopenia (platelets lower than 50,000/mL), or several liver-related
enzymes or chemicals affected (bilirubin, albumin, alkaline phosphatase,
serum glutamic oxaloacetic transaminase, and serum glutamic pyruvic
transaminase) are at high risk. If there are any concerns, consultation with
the patient's physician should be completed.
Strict attention to hemostasis.

Hemostatic agents should be used, such as bovine collagen or topical
thrombin, in addition to good surgical technique and placement of additional
sutures.
Bone Diseases
Osteoporosis
Do you have osteoporosis? /No?
The most common disease of bone metabolism the implant clinician will
encounter is osteoporosis, an age-related disorder characterized by a
decrease in bone mass, increased microarchitectural deterioration, and
susceptibility to fractures. The World Health Organization defines
osteoporosis as bone mineral density levels more than 2.5 standard
deviations below the mean of normal young women.44 Forty percent of
postmenopausal women in the United States have bone mineral density
levels denoting osteopenia, and 7% have scores correlated with
osteoporosis.45 As the population ages, the incidence of osteoporosis will
continue to increase in both women and men.
TABLE 2.8
Additional Digestive Issues and Treatment Implications
P ositive
Treatment Implications
Response
Jaundic e Hepatitis, bile duc t disorders, sic kle c ell anemia, autoimmune hemolytic disease panc reatic c anc er
Hepatitis Medic al c onsultation, aseptic tec hnique, preventive measures
Esophageal Infec tion, inc reased tooth dec ay/erosion
reflux
Hiatal hernia Appointment duration not to exc eed patient's toleranc e
Noc turnal c ough Gastric reflux disease, c hronic sinusitis, allergies
Dark tar-c olored GI bleeding (avoid antic oagulants, NS AIDs; need GI evaluation)
stools
Frequent foul- Crohn disease, panc reatic c anc er (gum disease), lac tose intoleranc e (tooth dec ay, bone demineralization), c eliac (gluten
smelling stools intoleranc e) disease (enamel erosion, aphthous ulc ers)
Dysphagia Reflux, esophageal spasm, stric ture, esophageal mass, multiple sc lerosis, Parkinson disease, stroke, poor oral c learanc e,
(solid/liquid) high-volume suc tion, aspiration during treatment, protec t airway rubber dam
Persistent Celiac disease, liver disease, biliary disease (sc lerosing c holangitis)
pruritus (itc hing) All c an lead to c oagulopathy and exc essive bleeding
GI, gastrointestinal; NSAIDs, nonsteroidal antiinflammatory drugs.
The osteoporotic changes in the jaws are similar to those in other bones in
the body. The structure of the bone is normal; however, because of the
uncoupling of the bone resorption and formation processes with emphasis
on resorption, the cortical plates become thinner, the trabecular bone pattern
becomes more discrete, and advanced demineralization occurs.46 The loss of
trabecular bone is accelerated in the edentulous patient because the factors
involved in resorption are already established. Osteoporosis affects the
trabecular bone mass loss to a greater extent than it does cortical bone.47
Surgical technique.
Underpreparation of the osteotomy site (or use of osteotomes) will result in
the implant having more bone at the implant interface. Although not
contraindicated, immediate stabilization of dental implants is a common
concern because of decreased trabecular bone mass. Healing periods and
implant surface characteristics should be selected for poorer-quality bone.
Bisphosphonates use.
Oral/IV bisphosphonates are common medications for osteoporosis. Studies
have suggested there are different guidelines that should be observed in
patients receiving intravenous bisphosphonate treatments in comparison to
those patients on oral formulations of these medications. With oral
bisphosphonates, a low probability of adverse effects on the success of dental
implants. However, it is advised that a detailed medication history for
patients treated for osteoporosis be completed. It is important to know which
bisphosphonate they are taking along with the time duration. For those
patients receiving treatment for more than 3 years, additional testing may be
considered (C-telopeptide [CTx] test).48 IV forms of bisphosphonate
medications have been shown to have the most devastating effects within the
oral cavity (osteonecrosis), despite similar mechanisms of action for both the
oral and IV formulations. It is advised that all patients currently treated with
bisphosphonates be advised of the possibility of bony necrosis of the jaw and
be part of their informed consent. Intravenous administration of
bisphosphonates has been considered an absolute contraindication for
placement of dental implants with the concern for the increase risk of
developing osteonecrosis of the jaw. This association has been based on
patients who were receiving the IV form in treatment of metastatic cancer or
Paget disease. However, medications like zoledronic acid (Reclast) are now
being used routinely to prevent osteoporosis. The risk of developing
medication-related osteonecrosis of the jaw in these patients is being
investigated, however the patient should be informed of the potential
complications.
Length of healing.
In osteoporotic patients, there is a decrease in cortical and trabecular bone;
the repair process (implant healing) may be compromised. Sufficient time for
healing should be adhered to with progressive prosthetic bone loading is
highly recommended.
Peri-implantitis.
A strong correlation has been shown between periodontal disease and
skeletal osteoporotic changes. Strict postoperative recall and periodontal
evaluation should be adhered to.
Progressive bone loading.
Because of poorer bone quality, healing is compromised, necessitating
progressive bone loading throughout the prosthetic rehabilitation. The
poorer-quality bone is progressively increased to better-quality bone, which
results in better bone quality at the implant interface.
Implant design.
Implant design should include greater width implants. Surface conditions of
implant bodies should be designed to increase bone contact and density.
Bone stimulation to the healed interface will increase bone density, even in
advanced osteoporotic changes.
Understand risk factors.
Most clinical studies show no increased failure rate amongst osteoporotic
patients.49,50 However, patients should be well informed about the possible
complications resulting from the poorer-quality bone. Osteoporosis is a
relative complication and the patient should be instructed of possible
complications.
Osteomyelitis
Do you have a history of osteomyelitis? /No?
Osteomyelitis is an acute or chronic inflammatory bone disease that is
bacterial in nature. The radiographic appearance is a poorly defined,
radiolucent area with isolated fragments of bone (sequestra) that can
exfoliate or become surrounded by bone (involucrum). This disorder can be
caused by odontogenic and periodontal infections, trauma, dental implants,
immunocompromised states, and hypovascularized bone. The treatment
includes aggressive surgical drainage, with possible intravenous antibiotic
intervention. Osteomyelitis usually occurs in the mandible and is rarely seen
in the maxilla, most likely due to the increased vascularization of this area.
Surgery/Implants Implications
Implant placement.
Implant placement in surgical sites that have been previously affected with
osteomyelitis leads to an increased morbidity. Because of the lack of
vascularity, endosseous implants have a greater chance of bone loss,
infection, and failure.
Treatment summary.
Osteomyelitis is usually an absolute contraindication unless the etiologic
factors are corrected and adequate blood supply to the affected area is
restored. A physician clearance should be obtained along with a
comprehensive informed consent on the possible complications that may
arise from implant placement into these sites.
Fibrous Dysplasia (FD)

Do you have fibrous dysplasia? /No?
Fibrous dysplasia (FD) is a rare, nonheritable, genetic disorder
characterized by normal bone being replaced by immature, haphazardly
distributed bone and fibrous tissues. The etiology of this bone disease is a
gene mutation that prevents the differentiation of cells within the
osteoblastic formation. FD can be further classified to involve one site
(monostotic fibrous dysplasia [MFD]), multiple sites (polyostotic fibrous
dysplasia [PFD]), or multiple locations (craniofacial fibrous dysplasia [CFD]).
CFD lesions are usually unilateral and occurs twice as often in the maxilla vs.
mandible. The diagnosis of CFD should be determined from the clinical
evidence, histopathologic analysis of the biopsy specimen, and radiologic
findings.51 Most individuals with this disorder are diagnosed early in
childhood.
Postoperative healing.
Healing after trauma in patients with FD is much different than for those
with normal bone. The tissue is hypocellular, which leads to slow healing and
an increased infection rate. These local infections may spread through the
bone and result in more advanced complications.
Proper diagnosis.
The radiographic appearance is highly variable because of the
disproportionately mineralized tissue and fibrous tissue in the lesion. This
variability results with radiographic images depicting the typical “ground
glass” appearance to early-stage radiolucencies and late-stage radiopacities.52
Additionally, severe malocclusion, dental abnormalities, and facial
asymmetry have been shown to be highly prevalent in CFD patients, which
further complicates the prosthetic rehabilitation of these patients.53
Informed consent.
Because of the lack of research and studies, the patient needs to be well
informed of possible morbidity and complications.
Treatment summary
• Active lesion areas: Absolute contraindication
• Nonlesion areas: Relative contraindication
Paget Disease
Do you have a history of Paget disease? /No?
Osteitis deformans, or Paget disease, is a common metabolic disease
characterized by slow, progressive, uncontrolled resorption and deposition of
bone. This disease is usually seen in Caucasian men older than 40 years. The
etiology is unknown and usually affects the maxillary alveolar ridge twice as
frequently as the mandibular ridge. Because of the enlargement of the
middle one third of the face, the appearance of a “lionlike” deformity is often
noted. Diastemas, tooth mobility, and bone pain are additional
characteristics. Radiographically, a decreased radiodensity, large
circumscribed radiolucencies, patchy areas of coalesced sclerotic bone
(cotton-wool appearance), and marrow spaces that are replaced by fibrous
tissue are observed. This disease has a wide spectrum of treatment ranging
from no treatment or the use of bisphosphonates. For patients who are
symptomatic, IV bisphosphonates are usually the preferred treatments.
These drugs help decrease further bone breakdown, formation, and
remodeling.
Bleeding.
During the active phases of this disease, bone is highly vascular with the
possibility of arteriovenous shunts, which may cause hemorrhagic
complications.
Infection.
Bone areas that are affected by this disorder are predisposed to develop
osteosarcoma and possible osteomyelitis.
Treatment summary.
Oral implants are contraindicated in the regions affected by this disorder or
in patients on IV bisphosphonates for the treatment of their Paget
symptoms. For additional bone disease responses and treatment implication
see Table 2.9.
TABLE 2.9
Additional Bone Disease Responses and Treatment Implications

Orthopedic prosthetic devic e Antibiotic prophylaxis
Ec todermal dysplasia Many studies c ompleted showing suc c essful treatment in ec todermal dysplasia patients
Cemento-osseous dysplasia (periapic al c emental Bone quality is questionable bec ause of avasc ular c ementum–like lesions (relative
dysplasia) c ontraindic ation)
Osteomalac ia Hypomineralized bone, questionable bone quality (relative c ontraindic ation)
Autoimmune Disease
Do you have an autoimmune disorder? /No?
Autoimmune disease refers to a group of more than 80 serious, chronic
illnesses that can affect almost any organ in the body. Approximately 75% of
autoimmune diseases occur in women; these diseases are thought to have a
genetic predisposition. However, autoimmune diseases are among the most
poorly understood diseases, with symptoms extremely variable among
individuals.
Sjögren Syndrome
Sjögren syndrome is an autoimmune disease in which immune cells attack
and destroy exocrine glands that produce saliva and tears. This disorder
affects an estimated 4 million people in the United States, with a gender
distribution of 90% female. The average age of onset for the disease is in the
late 40s. The classic symptoms of Sjögren syndrome are xerostomia and
xerophthalmia (dry eyes). Sjögren syndrome often accompanies other
immune diseases including rheumatoid arthritis and lupus.
Systemic Lupus Erythematosus

Systemic lupus erythematous is a chronic, potentially fatal autoimmune
disease in which the immune system attacks cells and tissue in almost any
part of the body. This disease usually affects women, and approximately 5
million people are afflicted with this disorder. Lupus presents and progresses
with such variability that every case is different. Lupus can affect almost any
part of the body including the kidneys, brain, blood vessels, heart, lungs, and
skin.
The hallmark sign of lupus is a butterfly-shaped rash that often appears
around the nose and extends to the cheeks. Some patients only develop the
rash and this is termed discoid lupus. Oral ulcerations may be found in
patients with lupus as well as silvery white (honeycomb) and raised keratotic
plaques referred to as verrucous lupus erythematous. There is no cure for
lupus, and most patients are treated with corticosteroids and
immunosuppressive drugs.
Scleroderma
Scleroderma is a rare, chronic disease characterized by excessive deposits of
collagen that cause musculoskeletal, pulmonary, and gastrointestinal
involvement. The most common symptom is the hardening of the skin in
which scarring can take place. Scleroderma can be localized or systemic. The
localized version only impacts the skin, whereas the systemic version affects
the skin, blood vessels, and major organs. Many patients also have
concurrent symptoms of Raynaud phenomenon, which involves fingers and
toes and results in vasoconstriction of blood vessels in response to cold.
Esophageal motility issues are also common in the more systemic version.
There is no cure for scleroderma, and various stages of the disease are treated
with NSAIDs and immunosuppressant drugs.54
Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic, inflammatory autoimmune disease
that causes the patient's immune system to attack the muscles and joints of
the body. This disorder is known for its painful and disabling inflammation,
which leads to substantial loss of mobility and dexterity. Rheumatoid
arthritis is treated with a wide range of medications including disease-
modifying antirheumatic drugs, antiinflammatory drugs, and analgesic
medications.55 Rheumatoid arthritis patients in general are
immunocompromised by associated medication treatments.
Implant surgery.
Certain medications may contraindicate implant surgery (steroids,
immunosuppressive medications). Special care should be taken to inquire
about the amount of NSAIDs the patient utilizes for daily pain control prior
to surgical treatment because bleeding complications could occur. In patients
with RA is important to get a comprehensive history of medications they are
taking. Most current treatment regimens for rheumatoid arthritis involve the
use of immunosuppressive medications.
Bone resorption and bleeding.

There appears to be a difference in patients who have isolated RA and those
with RA associated with other connective tissue diseases. In patients with RA
and other connective tissue diseases there is some evidence leading to
increased bone resorption and higher bleeding rates.
Xerostomia.
RA patients are more susceptible to decay and having the mucous
membranes become atrophic and friable. Because of the lack of salivary
secretions, complications may arise with the use of a tissue-borne prosthesis.
A fixed prosthesis is highly recommended.
Treatment summary.
In contrast to isolated RA, in RA patients with concomitant connective tissue
disease (CTD), differences in the periimplant parameters such as
pronounced marginal bone resorption and bleeding may be anticipated and
appear to be significantly influenced by the patients' underlying disease.56
Medical consult and evaluation should be conducted prior to any treatment.
Final prosthesis.
Because of the high incidence of xerostomia with autoimmune diseases, the
final prosthesis should be non–tissue-borne (FP-1, FP-2, FP-3) to minimize
any soft tissue coverage. In patients with limited dexterity, an overdenture
(RP-4, RP-5) is contraindicated because of inability to remove attachment-
secured overdenture.
MD clearance/informed consent.
Patients need to be well informed of the full extent of treatment with
possible complications and alternatives.
Treatment summary (depends on severity of disease)

• No medication: Relative contraindication
• Corticosteroids/immunosupressive drugs: Absolute contraindication
Lifestyle
Smoking
Do you smoke? /No?
In the United States, an estimated 42.1 million people, or 18.1% of all
adults (age 18 years or older) in the United States smoke cigarettes. Overall,
smoking prevalence has declined from 2005 (20.9%) to 2012 (18.1%); however,
tobacco is still the most preventable cause of death and disease in the United
States.57
Smoking has been directly related to many oral diseases including
periodontal disease, malignancies, and dental implant–related
complications.58 Studies have shown that over 7000 different gases and
chemicals are found in cigarette smoke (e.g., nitrogen, carbon monoxide,
carbon dioxide, ammonia, hydrogen cyanide, benzene, nicotine). In tissues,
carbon monoxide displaces oxygen from hemoglobin molecules because of
its stronger affinity.59 Hydrogen cyanide has been shown to cause hypoxia in
tissues. The adverse effects that smoking has on successful outcomes in
implant surgery are well documented. Multiple retrospective studies have
shown that smokers experienced almost twice as many implant failures
compared with nonsmokers.60
Increased incision opening.
Studies have shown that smoking is directly related to increased incision line
opening. Possible mechanisms for poor wound healing include the
vasoconstrictive nature of nicotine; increased levels of fibrinogen,
hemoglobin, and blood viscosity; increased platelet aggregation; and
impaired polymorphonuclear neutrophil leukocyte function.61 Therefore,
added sutures along with tension-free closure is recommended.
Infection.
Tobacco smoke decreases polymorphonuclear leukocyte activity, resulting in
lower motility, a lower rate of chemotactic migration, and reduced phagocytic
activity. These conditions contribute to a decreased resistance to
inflammation and infection.62
Implant/bone grafting failure.

Metaanalysis studies have shown a definite correlation between smoking and
failure rates of implants and bone grafts.
Peri-implantitis.
Studies have shown in smokers a strong correlation between peri-implantitis
and dental implants.
Informed consent.
With the possible detrimental effects of smoking on implants, it is
recommended that patients be informed in detail about the risks of smoking.
These possible consequences include increased marginal bone loss after
implant placement and the presence of peri-implantitis. Additionally, there is
a direct impact on the success rates of bone grafts, with almost double the
failure rate in implants placed in grafted maxillary sinuses.
Smoking cessation.
A strong recommendation on smoking cessation before implant surgery is
recommended because smoking cessation after implant surgery has been
shown to improve implant survival.63 Ideally, the patient is instructed to cease
smoking for 2 weeks before surgery to allow for reversal of increased blood
viscosity and platelet adhesion. Smoking cessation is continued for 8 weeks
after implant surgery, which coincides with the osteoblastic phase of bone
healing.64 This has been shown to increase wound healing capabilities and
reverse subgingival microflora.65
Ideally, smoking cessation should be a gradual process because withdrawal
symptoms are less severe in patients who quit slowly. There exists the
concept of the “five As” in smoking cessation:
(1) Ask—all patients should be asked about possible tobacco use;
(2) Assess—determine if the patient has ever quit smoking or is interested in

smoking cessation;
(3) Advise—every smoking patient should be advised of complications that

may arise from continued smoking;
(4) Assist—the smoking patient must be instructed on ways to quit smoking

or be given a relevant physician referral; and
(5) Arrange—make arrangements to evaluate the success of the smoking

cessation (Table 2.10).66
TABLE 2.10
Smoking Cessation Techniques
Technique Instructions P ossible Side Effects

Nic otine gum (Nic orette) Chewing gum that TMJ, gastric irritation, diffic ulty for patients wearing removable prostheses
releases nic otine
Nic otine inhaler (Nic otrol inhaler) Puffing for Dizziness, nausea/vomiting, c onfusion, blurred vision, palpitations
approximately 20
minutes/hour
Nic otine lozenge (Nic orette) Dissolving Dizziness, nausea/vomiting, c onfusion, blurred vision, palpitations
Nic otine nasal spray (Nic otrol) 1–2 doses per hour for Nasal muc osa irritation, dizziness, nausea/vomiting, c onfusion, blurred
2 months vision, palpitations
Nic orette mic rotab sublingual tablets 1–2 tabs hourly Dizziness, nausea/vomiting, c onfusion, blurred vision, palpitations
Nic otine patc h (Nic oderm CQ) Worn during day S kin irritation, dizziness, nausea/vomiting, c onfusion, blurred vision,
palpitations
Rx Medic ation: bupropion S R (Zyban), As direc ted Bupropion S R: dry mouth, nausea, headac he, dizziness, c hanges in
varenic line tartrate (Chantix) appetite, weight loss or gain, worsening of anxiety, insomnia
Varenic line tartrate: c hest pain, dizziness, severe headac he, easy bruising,
vivid nightmares, sleep disturbanc e
Hypnosis Mixed results N/A
supporting
effec tiveness
Ac upunc ture Mixed results N/A
supporting
effec tiveness
Treatment summary
• Any amount of smoking: Relative contraindication
• Excessive smoking (~ >1.5 packs/day): Absolute contraindication
Alcohol
Do you drink alcohol? /No?
Ethyl alcohol is one of the most widely used mood-altering drugs in the
world. Approximately 17 million adults aged 18 and older have an alcohol
use disorder. This is more common in men than women. Many with alcohol
dependence disorders go undiagnosed. Because of the adverse impact of
alcohol on dental implants, screening for undiagnosed alcohol-related
disorders is beneficial. Excessive alcohol intake has been associated with
surgical and dental implant-related issues such as liver and metabolic
dysfunction, bone marrow suppression resulting in bleeding complications,
predisposition to infection, and delayed soft tissue healing.67
Bleeding problems.
Alcohol interferes with coagulation on multiple levels leading to decreased
platelet production (thrombocytopenia), impaired platelet function
(thrombocytopathy), and diminished fibrinolysis. Patients who abuse alcohol
are more susceptible to intra- and postoperative bleeding complications
associated with dental implant surgery.
Infection.
Alcohol use leads to significant alterations of cell-mediated immune systems.
Alcohol-induced immunosuppression results in a decrease in delayed-type
hypersensitivity (DTH), which is a preoperative indicator for postoperative
infectious complications.68 Therefore, patients consuming alcohol (especially
those who consume it immediately after surgery) are more susceptible to
incision line opening and infection.
Increased bone loss.

Alcohol use also leads to decreased bone formation, increased resorption,
and decreased osteoblast function, resulting in decreased bone density and
integration issues. The use of alcohol has a direct effect on dental implant
healing as studies have shown greater marginal bone loss and implant failure
associated with alcohol consumption.
Informed consent/decrease comorbidities.
The patient must be well informed of potential consequences of alcohol use,
especially immediately after implant surgery.
Cessation program.
Abstinence can reverse many of alcohol's effects on hematopoiesis and blood
cell functioning; the patient should be instructed on possible cessation
treatments and programs. Ideally, patients should refrain from using alcohol
for a minimum of two weeks or after incision line closure occurs.
Radiation Therapy
Have you ever received radiation therapy? /No?
Although the survival rate of patients with head and neck cancer has
increased over the last 20 years, it still remains one of the deadliest forms of
cancer. Aggressive treatment includes surgery, radiation, chemotherapy, or a
combination therapy that inevitably leaves the patient with compromised
anatomy and physiologic functioning. Patients are left with many deficits
including oral mucositis, xerostomia, compromised healing, and reduced
angiogenesis. This is a direct result of changes in the vascularity and
cellularity of hard and soft tissue, damage to the salivary glands, and
increased collagen synthesis that results in fibrosis. Because of these
detrimental effects on the bone, wound repair and healing are significantly
reduced after surgical procedures. When exposed to high levels of radiation,
bone undergoes irreversible physiologic changes that include narrowing of
the vascular channels (endarteritis), diminished blood flow, and loss of
osteocytes. In time the bone becomes nonvital, which leads to limited
remodeling and healing potential.
Osteoradionecrosis.
The most significant risk in placing implants into irradiated bone is
osteoradionecrosis (ORN), which is an irreversible devitalization of
irradiated bone that is characterized by necrotic, soft bone that fails to heal
properly. The pathophysiologic mechanism is an imbalance in oxygen
demand and oxygen availability, which is caused by endarteritis of the blood
vessels. Clinical symptoms include pain, exposed necrotic bone, pathologic
fractures, and suppuration. Studies have shown the overall incidence of ORN
after radiotherapy to be from 3% to 22%.69
Radiotherapy to previously placed implants.

There are very few studies on the effects of radiotherapy on preexisting
dental implants. Short-term data show very minimal complications and
failures. However, in longer-term studies, failure rates seem to be higher.70 At
this time, more studies need to be conducted for conclusive results.
Implant placement after radiotherapy.

The time between radiotherapy to implant placement seems to have effects
on the prognosis of implants. Most studies have shown that the longer the
period for implant placement after radiotherapy, the higher the success rate
and the lower the risk of osteoradionecrosis (Box 2.5).71
Box 2.5
Treatment Protocol for Implant Placement in
Radiation Sites
• For sites that have been previously treated with radiotherapy, the authors
recommend referral to a dental school, hospital, or clinic that has
experience in treating radiotherapy patients.
• If the clinician has experience or can treat the associated complications, the
following is recommended:
Ideal Implant Placement:
• Preradiation: more than 14 days before radiation
• During radiation: absolute contraindicationb

• Postradiation: <6 month or >24 months—
relative/absolute contraindication
• 6–24 months: relative contraindicationa
b Radiationtherapy medical consultation, possible >20 years ago referral to cancer institution or hospital
treatments, for 90 minutes before placement followed by 10 minutes after placement.
a Medical consultation, hyperbaric oxygen, informed consent, aseptic technique (<20 Gy cumulative,
approximately <50 Gy technique fractionation).
Irradiation patient prosthetics.

Because of the oral effects of radiotherapy (mucositis, xerostomia), an
implant-supported prosthesis (FP-1, FP-2, FP-3) is recommended over a soft
tissue prosthesis (RP-4, RP-5). This will reduce the possibility of soft tissue
irritation that is associated with postradiotherapy patients wearing
removable prostheses.
Past radiation treatment.
Caution must be emphasized to patients with past radiation therapy because
earlier forms of radiation therapy (pre-1980s) were of lower energy, in
contrast to current higher-energy levels that are less destructive. Because of
this lower energy radiation and associated higher destructive radiotherapy,
progressive endarteritis has been shown to take place, which increases over
time.72
Amount of radiation exposure.

The presently available literature states that implant placement surgery may
be completed on patients who have been irradiated at doses lower than 50
Gy.73 Unfortunately, very few patients receiving doses above 50 Gy have been
rehabilitated with implants.
Studies have shown that implants placed in patients with a cumulative
radiation effect of 18 to 20 (approximately 48 to 65 Gy standard fractionation)
have a rather high success rate. Other reports have shown that doses above a
cumulative radiation effect of 40 (approximately 120 Gy standard
fractionation) exhibit a high degree of failure.74
Hyperbaric oxygen.
One treatment proposed to minimize the possibility of ORN is the use of
hyperbaric oxygen. Prophylactic hyperbaric oxygen has been advocated to
increase oxygen tension in irradiated bone, which will promote capillary
angiogenesis and bone formation.75 Recent data show that oxygen under
hyperbaric conditions acts synergistically with growth factors, which
stimulates bone growth and turnover and also may act as a growth factor
itself. Hyperbaric oxygen has also been shown to act as a stimulator of
osseointegration by increasing new bone formation, increasing bone
turnover, and increasing the vascular supply to irradiated bone.76
Age Related Factors

Adolescents
Are you under the age of 20? /No?
Dental implants are commonly used to correct the congenital absence of
teeth in adolescents, and studies have shown this to be a very reliable and
predictable treatment option. When a clinician is presented with an
adolescent patient, there must be a degree of caution as to the ideal time that
implant therapy should be commenced. The concern is placement of
implants too early may lead to the implants interfering with normal growth
development and potential esthetic issues.
Surgery.
No age-related surgical issues exist unless systemic contraindications or
psychologic issues.
Implant.
If placement is completed before craniofacial growth is complete, possible
interruption of facial growth and esthetic (infraocclusion or labioversion)
issues can result.
Early consultation.
In determining the ideal time for implant placement, the patient/family must
be educated on craniofacial growth in comparison to chronologic age.
Chronologic age is a poor indicator of dental development/facial growth;
timing of implant placement should coincide with growth cessation.
Determination of growth cessation.

In the literature, there exist many methods of determining completion of
craniofacial/skeletal growth: chronologic age, complete dental development,
voice changes, hand-wrist radiographs, cervical vertebral maturation, and
superimposition of lateral cephalometric radiographs. The most reliable
method and safest (no radiation exposure) has been shown to be when the
patient begins to exhibit a lack of growth in stature (<0.5 cm/year).
Cone beam computed tomography evaluation.

A comprehensive radiographic evaluation should be completed as close to
growth cessation as possible. This is most important in the maxillary anterior
region and congenitally missing edentulous sites to determine the ideal
implant position for prosthetic longevity. Most likely these edentulous sites
will be compromised in bone volume in the vertical and anteroposterior
dimensions, thus requiring osseous augmentation prior to implant
placement. Additionally, intraroot distances should be evaluated via axial
cone beam computed tomography (CBCT) slices at the coronal, midroot, and
apical areas. For longevity and esthetic requirements, implants should be no
closer than 1.5 mm from any tooth structure. The importance of this
evaluation cannot be overstated, including patients who have received
adjunct orthodontic care. A patient may appear to have adequate space for
implant placement in the coronal aspect of the edentulous site, only to have
insufficient room in the apical segment due to orthodontic movement.
Treatment summary.
When implants are treatment planned in adolescents, clinicians must take
into consideration the timing, site development, esthetics, and possible
prosthetic limitations including malposition that may develop with age. Most
importantly, the determination of growth cessation should be determined by
the lack of growth in stature. This method involves no radiographs
(decreased radiation exposure) and is the most benign method. The patient's
pediatrician should be consulted in the determination of growth cessation
(Fig. 2.1).
FIG 2.1 Growth cessation chart. Consultation with the patient's pediatrician should
be completed to ascertain growth cessation, which usually coincides with <0.5 cm
of growth in stature (arrows).
Elderly
Are you 65 years old or older? /No?
According to the World Health Organization (WHO), most developed
countries have accepted the chronologic age of 65 years as the definition of
an “elderly” or “older ” person.77 The treatment of elderly patients is
definitely challenging, and because more patients are living longer and are
socially active, elderly patients will continue to be a significant part of the
implant dentist's practice. Studies have shown that elderly patients are more
prone to systemic diseases, more medically compromised, have potentially
longer healing periods, challenging bone conditions (quality and quantity),
increased susceptibility to drug interactions, and increased dental implant
morbidity.
Decreased renal function.
There is an age-related decline in renal functions that is accelerated by
comorbid conditions like hypertension, heart disease, and diabetes. The age-
related decline is more physiologic while the pathologic decline is associated
with many medical conditions. In elderly patients, the glomerular filtration
rate (GFR) and creatine will give insight into the patient's kidney function. As
kidney function declines especially in Stage 3 (GFR 30–59) and above, there is
a decreased metabolism and excretion of drugs (Table 2.11). Therefore, the
intervals between drug administration should be longer and dosages should
be decreased, except for liposoluble drugs and antibiotics, to compensate for
the increase in body fat and the reduced immune response. In the presence
of significant kidney disease (Stage 4 or above), antivirals (acyclovir), beta-
lactams (amoxicillin), and cephalosporins should be reduced. Nonsteroidal
analgesics should not be prescribed in those with Stage 3 or greater
impairment without consultation with the patient's physician. Caution
should be exercised with the use of sedation drugs because they can have
more pronounced and longer-lasting effects.
TABLE 2.11
Age vs. Glomerular Filtration Rate
Stage GFR Description

1 90+ Normal kidney func tion
2 60–89 Mildly reduc ed kidney func tion
3 30–59 Moderately reduc ed kidney func tion
4 15–29 S everely reduc ed kidney func tion
5 <15 or dialysis End stage kidney failure
Decreased gastric motility.

The decreased gastric motility of the elderly patient affects the use of oral
analgesics such as hydrocodone and oxycodone. In addition, the use of
narcotics in the elderly can cause significant changes in bowel habits
especially constipation. If not contraindicated, a stool softener may be
recommended concurrently with use of analgesics. Also, when using
antibiotics for any prolonged period, the use of probiotics may help maintain
normal gut flora.
Medications.
Medications and the number of prescribed drugs usually increase with age
with over 75% of patients 65 and older taking medications. Many of these
drugs are often the cause of adverse or significant drug reactions. Studies
have shown more than 70% of drugs taken by elderly patients have potential
adverse effects in the dental practice.78 Although the incidence of severe drug
interactions with commonly prescribed pain medications is relatively low,
caution should be used in reviewing the elderly patient's complete
medication history before prescribing any analgesics.
Isolated systemic hypertension.

A major cardiovascular health issue with the elderly is isolated systolic
hypertension (ISH). In ISH, systolic blood pressure elevates above 140 mm
Hg while the diastolic pressure remains below 90 mm Hg. The difference
between the systolic and diastolic is termed the pulse pressure, which is a
significant risk factor for stroke and heart disease. Recent metaanalysis
studies have shown a 10 mm Hg increase in pulse pressure will increase the
risk of major cardiovascular events by 20%.79
Bone healing.
Clinical studies have shown a direct correlation between delayed bone
healing with increasing age. Most likely the etiology results from a reduced
number of osteogenic cells and reduced systemic and localized blood flow to
the healing site.80 Therefore, longer healing periods along with progressive
loading are recommended in older patients.
Bone quality/quantity.
Both the quality and quantity of bone is affected by aging.
Histomorphometric and microradiographic studies have shown after the age
of 50, a marked increase in the cortical porosity leading to decreased bone
mass is present. Loss of bone mineral content has been estimated to be
approximately 1.5% per year in females and 0.9% in males.81
Increased implant failure rate.

Studies have shown an increased risk of implant failure as a result of many
age-related factors including compromised bone quality and quantity,
implant length, treatment protocol, and edentulous locations. Other studies
have shown patients older than 60 years were twice as likely to have adverse
outcomes.82
Prosthetic treatment.
Elderly patients have been shown to have increased difficulty in adapting to
final implant prostheses. Postinsertion issues such as general adaptation,
muscle control, hygiene difficulty, tissue inflammation, and overdenture
seating were significant in the older population study. Patient education and
final expectations should be discussed in detail prior to initiation of
treatment.83
Intraoperative modifications.
A strict stress reduction protocol should be adhered to with elderly patients
due to the potential frailty of their cardiovascular systems. Medication
modifications including sedatives and CNS depressants are most important.
Because of less competent immune systems, broad coverage with antibiotics
is indicated and the use of probiotics should be considered. Elderly patients
are less sensitive to pain, thus less analgesic medication is recommended,
especially because gastric motility is reduced in these patients. Shorter
surgical appointments are necessary to minimize exceeding patient
tolerances.
Treatment summary.
The implant clinician must understand the physical, metabolic, and
endocrine changes and the effects associated with the elderly patient before
initiating implant treatment. Age is most certainly a prognostic factor in
implant failure and morbidity. However, increased age is not an absolute
contraindication to implant therapy. It is imperative the clinician obtain a
detailed medical history and list of medications before devising the dental
treatment plan. Patient education along with modification in medication use,
surgical technique, soft and hard tissue healing times, and careful
assessment of postoperative complications must be strictly enforced.
Psychosocial/Stress Related Factors

Psychological
Have you had any psychological problems? /No?
Providing dental implant care to patients with psychologic problems is
very challenging for clinicians. This group of patients is prone to oral health
issues because of poor oral hygiene, compliance, and medication effects.
Providing comprehensive dental implant care to patients requires good
communication skills, perseverance, and flexibility in both the surgical and
prosthetic phases of treatment. Additionally, many patients are on tricyclic
antidepressants, selective serotonin reuptake inhibitors (SSRIs), and
monoamine oxidase inhibitors, which are associated with many interactions
(see drug interactions). Oral manifestations of these diseases and
medications include an increase in caries and periodontal disease, increased
smoking, xerostomia, chronic facial pain, parafunction (bruxism/clenching),
and temporomandibular joint dysfunction.
Medications.
Many psychotherapeutic drugs interact with medications that are commonly
prescribed in implant dentistry. Clinicians must be aware of drug-drug and
drug-disease interactions with respect to the patient's medical history. Most
interactions are related to the potentiation of the sedative and anticholinergic
actions of the psychotherapeutic drugs. It is important to identify patients
taking monamine oxidase inhibitors or tricyclic antidepressants. Although
these are no longer the mainstay of treatment for psychiatric illness, many
patients will be placed on these medications to potentiate the effect of other
medications. Common examples include amitriptyline, doxepin,
nortriptyline, and imipramine. These medications are also being used to treat
nonpsychiatric illnesses and can be used to treat chronic pain and sleep
disorders. The main concern is the interaction of tricyclic medications and
epinephrine because they produce anticholinergic effects on the heart. There
is no contraindication to using them together, but patients should be
followed more closely for adverse interactions. A physician consult as well as
the implementation of a stress reduction protocol are recommended steps to
follow when initiating treatment with these patients.
Clenching/Bruxism
Have you had any issues with clenching or bruxism? /No?
Parafunctional forces on teeth or implants are characterized by repeated or
sustained occlusion and have long been recognized as harmful to the
stomatognathic system. There are two different types of parafunctional
phenomena, bruxism and clenching. Bruxism primarily concerns the
horizontal, nonfunctional grinding of teeth. The forces involved are in
significant excess of normal physiologic masticatory loads. Clenching is a
habit that generates a constant force exerted from one occlusal surface to the
other without any lateral movement. The clench position most often is the
same and rarely changes from one period to another. The direction of load
may be vertical or horizontal. The forces involved are in significant excess of
normal physiologic loads and are similar to bruxism in amount and duration.
A positive feedback loop occurs with patients exhibiting parafunction
because their muscles of mastication often hypertrophy, increasing the
magnitude of force that they can produce during function. This leads to an
overall musculoskeletal situation that must be closely monitored when
initiating implant treatment with a patient.
Implant healing.
The most common cause of both early and late implant failure after
successful surgical fixation is parafunction. Such complications occur with
greater frequency in the maxilla because of a decrease in bone density and an
increase in the moment of force. The lack of rigid fixation during healing is
often a result of parafunction on soft tissue–borne prostheses overlying the
submerged implant.
Implant prosthesis.
Parafunctional forces are most damaging when applied to implant
prostheses, with lateral (shear) forces being the most catastrophic to the
components of the restoration. This will most likely result in screw
loosening, screw fracture, or prosthesis fracture.
Overengineering treatment.
When a patient is diagnosed as having parafunction, the treatment planning
should include more implants, larger diameter implants, and the concept of
progressive bone loading should be adhered to.
Prosthetic design.
In an effort to minimize the effects of lateral (shear) loads on the implant
system, especially in the posterior teeth, the clinician should seek
restorations with narrow occlusal tables and minimal cusp heights.
Furthermore, by splinting individual posterior implant units together, the
impact of these forces is reduced.
Occlusal guards.
For any patient exhibiting signs or symptoms of parafunction, a hard,
processed acrylic nightguard to dissipate the forces to the implant prostheses
is paramount to protect the prostheses for long-term success (Table 2.12).
TABLE 2.12
Miscellaneous Patient Responses and Treatment Implications

S inus disease Possible sinus pathology leading to postoperative morbidity
Frequent headac hes Anxiety, migraine sinusitis, temporomandibular joint disorder, anemia
Intoleranc e to heat/warm rooms Hypertension, hyperthyroidism
S easonal allergies Possible maxillary sinus disease
Pregnanc y Elec tive treatment (absolute c ontraindic ation)
Medications
Osteoporosis Medications
Have you ever taken bisphosphonates or osteoporosis drugs? /No?
Since the first reported cases of necrotic, exposed bone in patients taking
bisphosphonates, there has been much debate over treatment implications
with regards to dental implants. Bisphosphonates are a group of drugs that
are widely used for several bone disorders and have been approved by the US
Food and Drug Administration for treatment of osteoporosis, metastatic
bone cancer, and Paget disease. However, what was once termed
bisphosphonate osteonecrosis has now been renamed drug-induced osteonecrosis of
the jaws (DIONJ) by the American Medical Association. The reason for this is
the incidence of osteonecrosis cases involving additional drug classifications
such as monoclonal antibody drugs, antiangiogenic drugs, and tyrosine
kinase inhibitors (Table 2.13).
TABLE 2.13
Medications Linked to DIONJ
Drug Classification Use Dose Route

Alendronate (Fosamax) Bisphosphonate Osteoporosis 70 mg/week Oral
Risedronate (Ac tonel) Bisphosphonate Osteoporosis 35 mg/week Oral
Ibandronate (Boniva) Bisphosphonate Osteoporosis 150 mg/month Oral
Zoledronate (Rec last) Bisphosphonate Osteoporosis 5 mg/year IV
Zoledronate (Zometa) Bisphosphonate Osteoporosis 4 mg/month IV
Pamidronate (Aredia) Bisphosphonate Osteoporosis 90 mg/month IV
Denosumab (Prolia, Xgeva) Monoc lonal antibody Osteoporosis, Canc er 60 mg/6 months S ubc utaneous
Bevac izumab (Avastin) Monoc lonal antibody Metastatic c anc er 100–400 mg/14 days IV
S unitinib (S utent) Tyrosine kinase inhibitor Canc er 5 mg/year IV
Etidronate (Didronel) Bisphosphonate Paget disease 300–750 mg/6 months Oral
Tiludronate (S kelid) Bisphosphonate Paget disease 400 mg daily/3 months Oral
Bisphosphonates
Bisphosphonates are mainly used for the treatment of osteoporosis (oral
form) and metastatic cancer (IV form) by inducing osteoclastic death or
apoptosis at the cellular level. As an osteoporosis drug, they reduce bone
resorption via a direct effect on the osteoclast. In osteoporotic patients
undergoing bisphosphonate treatment, old bone is retained because bone
turnover is suppressed, preventing normal remodeling in this area, which
results in the formation of brittle bone. Additionally, bisphosphonates kill
functionally resorbing osteoclasts not only at the peripheral sites but also in
the bone marrow.
Monoclonal Antibodies
Monoclonal antibodies work by inhibiting RANKL (receptor activator of
nuclear factor kappa-B ligand), which is a type II membrane protein that acts
as a primary signal for bone removal. They have a direct effect on the
immune system and control bone regeneration and remodeling. These drug
molecules irreversibly bind to mineral matrix in bone and have a half-life of
approximately 26 days, which is much shorter than bisphosphonates (11
years).
Tyrosine Kinase Inhibitors

Tyrosine kinase inhibitors directly inhibit tyrosine kinase receptors such as
PDGF (platelet-derived growth factor) and VEGF (vascular endothelial
growth factor), which regulate cellular replication in both tumor
angiogenesis and tumor cell proliferation. Inhibiting these receptors reduces
tumor vascularization, leading to tumor shrinkage and death.
Diagnosis of DIONJ.
Marx has defined characteristics of patients who are diagnosed as having
DIONJ. These include: (1) current or previous treatment with a systemic
drug that affects bone homeostasis, (2) exposed alveolar bone in the jaws that
persists for more than 8 weeks, (3) no history of radiotherapy to the jaws, and
(4) no known diagnosis of osteopetrosis or cemento-osseous dysplasia. The
definitive symptom of DIONJ is bone exposure in the mandible or maxilla
that does not heal. Pain and inflammation is present with possible secondary
infection of the soft tissue. In severe cases, drainage and progressive
extension of bone involvement or sequestration results.84
Active lesions.
Osteonecrosis may remain asymptomatic for weeks and possibly months.
Lesions usually develop around sharp, bony areas and previous surgical
sites, including extractions, retrograde apicoectomies, periodontal surgery,
and dental implant surgery. Symptoms include pain, soft tissue swelling,
infection, loosening of teeth, and drainage. Radiographically, osteolytic
changes are seen, and tissue biopsy has shown the presence of actinomyces,
which is possibly caused by secondary infection.
CTx test.
It has been proposed that assays to monitor markers of bone turnover may
help in the diagnosis and risk assessment of developing bisphosphonate-
associated osteonecrosis. CTx are fragments of collagen that are released
during bone remodeling and turnover. Because bisphosphonates reduce CTx
levels, it is believed that serum CTx levels can be a reliable indicator of risk
level. The CTx test (also called C-terminal telopeptide and collagen type 1 C
telopeptide) is a serum blood test obtained by laboratories or hospitals (ICD9
diagnostic code 733.40). However, today, the use of the CTx test to determine
the possibility of osteonecrosis is controversial.85,85a
CTx Value Risk for DIONJ
300 to 600 pg/ml (normal) None
150 to 299 pg/ml None to minimal
101 to 149 pg/ml Moderate
Less than 100 pg/ml High
Drug holiday.
Marx has suggested a preoperative protocol for administering possible
DIONJ drugs to patients who are undergoing oral surgical procedures. This
protocol takes into consideration the type and duration of drug use as well as
radiographic and clinical risk factors. Depending upon the laboratory values
obtained, a “drug holiday” may be indicated, which includes temporary
interruption of bisphosphonate treatment. However, improvement of
bisphosphonate levels may not be observed because measurable levels have
been shown to persist in bone for up to 12 years after cessation of therapy.84
Drug holiday recommendation84a

• Presurgical: Medication stoppage 9 months prior to surgery
• Postsurgical: Medication stoppage 3 months after surgery
Medical history.
A comprehensive medical history is essential before any elective treatment is
initiated. The most important history of bisphosphonates is the use of
intravenous nitrogen-containing bisphosphonates such as pamidronate
(Aredia) and zoledronic acid (Zometa) and new osteoporotic drugs, which
have very limited data on the association with DIONJ.
Bisphosphonate drugs.
In the dental setting, the most common bisphosphonates that implant
dentists are exposed to will most likely belong to the family of oral nitrogen-
containing bisphosphonates such as risedronate, ibandronate, and
alendronate. The latest studies show that oral bisphosphonates has a very
low probability of causing osteonecrosis.86 However, because of the long half-
life and short duration of the studies (3 years), future long-term
complications may be less evident. With this in mind, the implant dentist
should be cautioned regarding the possibility of developing osteonecrosis
side effects. The risks vs. benefits of dental treatment must be discussed with
the patient in detail. A well-documented consent form is recommended with
possible medical consultation if the patient has been on this medication for
more than 3 years.
Reclast.
As stated, most drugs used to treat osteoporosis are oral, nitrogen-containing
bisphosphonate drugs. Recently, Reclast (IV: Zoledronate) is given in 5-mg
intravenous doses once a year. Studies have shown that a significant risk
occurs after the fourth yearly dose. This is due to the accumulation of the
medication and its 11-year half-life. Elective dental implant surgery or bone
graft surgery are best scheduled 9 months after the most recent Reclast dose
and 3 months before the next planned dose. However, at this time, very little
research has been conducted on the relationship between Reclast and
DIONJ.
Comorbidities.
Comorbidities are systemic diseases, medical conditions, medications,
gender, and age, all of which can predispose the patient to a greater chance of
developing DIONJ. Many chemotherapeutic drugs, diabetes, immune
diseases, anemia, smoking, obesity, female gender and renal dialysis have
been noted as comorbidities for DIONJ. Additionally, the use of
glucocorticosteroids may be contraindicated in patients taking the DIONJ
medications discussed above because these drugs have been associated with
an increased occurrence of osteonecrosis.
New therapies for osteoporosis.

One of the newest therapies for osteoporosis is a biyearly subcutaneous
injection of denosumab (Prolia). This is a human monoclonal antibody that
functions as a RANK ligand inhibitor. Inhibition of the RANK ligand results
in diminished osteoclast functional and bone resorption. Denosumab
recognizes the specific protein that normally activates osteoclasts, thus
inhibiting their activation and preventing them from breaking down bone.
Denosumab has also been used to treat metastatic bone disease. These
inhibitors do not bind to bone, and their impact on bone remodeling
decreases after treatment is stopped. Osteonecrosis of the jaw has been
observed in patients receiving denosumab, and all patients should receive an
oral exam prior to therapy. The risk of developing osteonecrosis of the jaw is
less studied in denosumab.
Treatment summary
• Oral bisphosphonates: Relative contraindication (informed consent, good
surgical technique, CTx test, drug holiday)
• IV bisphosphonates: Absolute contraindication; Reclast: relative
contraindication
Have you ever taken anticoagulants? /No?
Oral antithrombotic medications have been used successfully to treat a
variety of thrombotic diseases such as myocardial infarction, stroke, and
deep venous thrombosis, while also having frequent use in the prevention of
cardiovascular diseases. For decades, clinicians and patients have been
conscious of the adverse side effects of these medications, primarily
spontaneous or perioperative bleeding. Many have advocated for years to
temporarily discontinue these medications prior to invasive dental
treatments such as dental implant surgery. However, because discontinuation
of these drugs may result in serious thrombus complications, a thorough
knowledge of the mechanism of action needs to be understood (Table 2.14).
TABLE 2.14
Common Anticoagulant Medications
Drug AS A (81 mg) AS A (325 mg) Clopidogrel Coumadin Dabigatran Rivaroxaban Apixaban
(Plavix) (Warfarin) (Pradaxa) (Xarelto) (Eliquis)
Test to determine S erum thrombin S erum thrombin S erum thrombin INR No testing No testing No testing
c oagulation status time, bleeding time, bleeding time time, bleeding needed needed needed
time time
Mec hanism of ac tion Inhibiting platelet Inhibiting platelet Inhibits platelet Inhibits produc tion Direc t Fac tor Xa Fac tor Xa
generation of generation of aggregation and of vitamin K– thrombin inhibitor inhibitor
thromboxane A2 thromboxane A2 ac tivation dependent c lotting inhibitor
results in inhibition results in inhibition fac tors (II, VII, IX,
of thrombus of thrombus and X)
formation formation
Dietary restric tions None None None Vitamin K None None None
Dosing diffic ulty None None None Diffic ult Reduc e Reduc tion Reduc tion
dose CrCl <50 CrCl <50
CrCl <30 dosing dosing
different for different
different for
indic ations different
indic ations
Need for Usually not Case spec ific Case S pec ific , Case S pec ific , Yes, MD Yes, MD Yes, MD
reduc tion/interruption rec ommended usually not usually not Consult, Consult Consult
rec ommended c an rec ommended c an usually
prec ipitate prec ipitate 48–72 hrs.
signific ant medic al signific ant medic al
c lotting issues c lotting issues
Days of Not required in 10 days or more, MD c onsult MD Consult, Yes, Yes, usually Yes,
disc ontinuation prior most c ases, MD Consult espec ially if given usually 5 days or usually 48–72 usually
to proc edures platelet func tion with AS A more 48–72 hours 48–72
inhibited 10–14 hours hours
days
Restarting Medic ation If disc ontinued, If disc ontinued, If disc ontinued, If disc ontinued, Usually Usually 24– Usually
after hemostasis after hemostasis dependent on MD dependent on MD 24–48 48 hours 24–48
rec ommendation rec ommendation hours and and hours and
disc ussion disc ussion disc ussion
with MD with MD with MD
CrCl, creatinine clearance.
Warfarin Sodium
Warfarin sodium (Coumadin) is used as an anticoagulant in a wide range of
conditions such as ischemic heart disease, deep venous thrombosis,
pulmonary emboli, and artificial heart valves. Warfarin sodium has a half-life
of 40 hours, which has been known to vary among individuals from 20 to 60
hours. The mode of action of warfarin sodium is the interference of the
synthesis of vitamin K, which is a cofactor in many reactions within the
coagulation cascade. Coumadin has been the mainstay of anticoagulant
treatment options; however, in the past 3 years there has been a shift to a
new class of blood thinners in the treatment of nonvalvular atrial fibrillation
and deep venous thrombosis. With an aging population the number of
individuals diagnosed with nonvalvular atrial fibrillation continues to climb
with over 2 million Americans now undergoing treatment. The major
concern of atrial fibrillation is the formation of blood clots, so most of these
patients will be maintained on blood-thinning medications.
Medication modification.
Until recently most medical practitioners have believed that anticoagulants
should be discontinued before dental surgery to prevent possible bleeding
problems. However, there exist many documented cases of embolic
complications in patients who discontinue the use of warfarin sodium and
develop thrombosis from rebound hypercoagulability. In addition, studies
have shown that dental surgery may be performed safely on patients
receiving anticoagulant therapy as long as their INR values are within the
therapeutic range (2.0–3.5). A brief periprocedural interruption of warfarin
therapy is associated with a low risk of thromboembolism (0.7%) and risk of
clinically significant bleeding (1.7%); however, the risk vs. benefit of
interruption is not warranted in most cases.87
MD consultation.
Practitioners should consult with the patient's physician to determine the
most recent INR before the surgery (ideally 24–48 hours before surgery). If
the INR values are within the therapeutic range (2 to 3.5), there is no need to
discontinue use of the anticoagulant. If the INR value is above the
therapeutic range (especially higher than 4.0), the physician should take
appropriate steps to lower the INR to a safer level or possibly discontinue the
warfarin and supplement with heparin therapy or vitamin D. It is important
to remember with all anticoagulant patients, special attention should be
given to good surgical technique and use of appropriate local measures to
control bleeding (hemostatic agents).
Aspirin
Aspirin or salicylic acid has been used as an antiinflammatory, analgesic, and
antipyretic medication. However, in the 1980s it was discovered that aspirin
also had an antiplatelet effect at very low doses (0.5 to 1 mg/kg) vs. higher
doses needed for an antipyretic effect (5 to 10 mg/kg) and antiinflammatory
response (30 mg/kg). Because of this research, low-dose aspirin has become a
secondary preventive drug for patients who have cardiovascular and
peripheral vascular disease. Aspirin works by inhibiting the formation of
prostaglandin thromboxane A2 within the platelet, thus affecting thrombus
formation by irreversibly decreasing platelet aggregation.
Bleeding.
With aspirin there is a risk of potential bleeding from low platelet count.
Studies have shown that this risk is minimal unless a 325-mg aspirin is being
used. In a study of tooth extractions, 36 patients were randomized to 325 mg
of aspirin or placebo for 2 days before and 2 days after. There was no
significant association between those that took the aspirin and peri- or
postoperative bleeding.88
Low dose (81 mg).
There exists no study supporting the recommendation of low-dose (<100 mg)
aspirin discontinuation for routine dental implant procedures. In most
patients, interruption is not warranted because it may expose the patient to
the risk of developing thromboembolism, myocardial infarction, or
cerebrovascular accident.
High dose (325 mg).

When patients are advised by their physician to take 325-mg aspirin or doses
higher than 100 mg, a physician consultation is recommended. This is
especially true of patients on aspirin (any dose) with other anticoagulants
such as clopidogrel or dipyridamole. Bleeding times may be appropriate in
these patients in combination with physician consultation.
Novel Anticoagulants
• Plavix (Clopidogrel): Clopidogrel is a platelet inhibitor that is approved for
the reduction of atherosclerotic events in patients of recent stroke, MI, or
peripheral arterial disease. The recent literature has supported longer
treatment times for patients with coronary stents and acute coronary
syndrome from 3 months to 12 months or more in combination with aspirin.
The literature does not support the routine discontinuation of this
medication in relation to dental implant treatment, but it is important to
remember that many patients treated with clopidogrel will be on aspirin or
another antiplatelet medication, especially those with cardiac stents. This
regimen should never be discontinued unless under the recommendation of
a physician.
• Pradaxa, Xarelto, Eliquis: Orally administered anticoagulants have recently
been developed to eliminate the disadvantages associated with warfarin.
Dabigatran etexilate (Pradaxa) and rivaroxaban (Xarelto) have been shown
to have a more favorable (wider) therapeutic index, fewer drug-drug and
drug-food interactions, and a predictable anticoagulant response without
the need for anticoagulants. Dabigatran reversibly inhibits thrombin, so the
duration of action is predictable and correlates well with plasma drug
concentrations. Rivaroxaban is a factor Xa (FXa) inhibitor that produces
reversible inhibition of FXa activity.89
Bleeding.
In contrast to the many studies on oral surgery and the use of warfarin, no
clinical trials have been completed to offer recommendations on the
management of patients on these newer anticoagulants with relation to
dental implant surgery. However, there exist several case studies suggesting
that, with physician consultation, these drugs can be temporarily
discontinued 24 hours prior to elective oral surgery and restarted the
following day, resulting in minimal complications. Because of these drugs
have a short half-life, brief interruption is usually acceptable. It is imperative
that physician consultation be obtained prior any of these medications being
temporarily discontinued. Good surgical technique and the use of hemostatic
agents should be adhered to.
Treatment summary.
Currently, there is no accepted reduction protocol for these medications.
Based on the information available, the clinician should consult the patient's
physician concerning the proposed implant procedure and the invasiveness
of the surgery, anticipated hemostasis complications, and amount of bleeding
to be expected. If physician recommendation is for the temporary
discontinuation of these drugs, the typical discontinuation recommendation
is for 24 hours prior to surgery, and the drug should not be restarted until the
risk of postoperative bleeding is minimal (usually within 24 hours of
surgery).90
Herbal Supplements
Over-the-counter herbal and dietary supplements are being consumed at a
record pace for general health improvement and treatment of chronic
conditions. Herbs have been known to be associated with unwanted side
effects and cause drug interactions, as well as being associated with surgical
complications. Many of these supplements contain active ingredients that
exhibit strong biologic effects. The doses are usually unregulated and
variable among patients. The Journal of the American Medical Association
estimates that 15 million adults are at risk for adverse interactions between
herbs and prescription medications.91 The risks of these medications
associated with dental implant surgery are increased bleeding, drug
interactions, and possible infection. Patients should discontinue the use of
these herbal supplements for at least 2 weeks prior to implant surgery (Box
2.6).
Box 2.6
Herbal Supplement and Adverse Effects
Increased Bleeding
Arnica
Barberry
Bilberry
Bromelain
Cayenne
Cat's claw
Chamomile
Chestnut
Cinnabar root
Devil's claw
Dong quai
Fennel
Feverfew
Garlic
Ginger
Ginkgo biloba
Ginseng
Grape seed
Green tea
Kudzu
Primrose
Red clover
Turmeric
Sweet woodruff
Vitamin E
Increased Inflammation
Celery
Dandelion
Elder
Goldenseal
Juniper
Interactions With NSAIDs

Feverfew
Gingko
Ginseng
St. John's Wort
Uva-Ursi
Interactions With Anesthesia

Green tea: Decrease effect of oral atropine
Dong quai: Increases sedation and lowers seizure threshold
Kava: Increases sedation
Valerian: Increases sedation, interacts with opioids
Vitamin C: In large doses can weaken anesthesia
Yohimbe: Can interact with some analgesics like morphine
Immunosuppressive Drugs
Have you ever received chemotherapy or been treated with
immunosuppressive drugs? /No?
Immunosuppressive drugs are medications that are used to inhibit or
prevent activity of the immune system. They are usually used to minimize
rejection of transplanted organs and tissues and also for treatment of
autoimmune diseases. These drugs have many side effects, with the majority
of them acting nonselectively (acting on normal cells also). There are four
classes of immunosuppressive drugs: glucocorticoids (prednisone),
cytostatics (chemotherapeutic agents), antibodies (polyclonal antibodies),
and immunophilins (cyclosporine).
Glucocorticoids
Glucocorticoids have potent antiinflammatory and immunosuppressive
properties. Because these drugs are widely used in the treatment of
inflammatory and autoimmune diseases, special attention must be given to
patients who are on long-term, high doses of glucocorticoids. These drugs
impair many healthy anabolic processes in the body and suppress the
immune system, which can lead to severe complications in dental implant
patients.
Cytostatics
Cytostatics are common medications in the treatment of malignant disease.
These drugs cannot discriminate between malignant and normal tissues and
become cytoxic to normal tissue. Most chemotherapeutic agents are known to
have cytoxic effects on bone, especially on grafted bone where the blood
supply is compromised.92 Because chemotherapeutic agents have a high
affinity for cells that have a high turnover rate, the oral mucosa is often
affected. These mucosal ulcerations have been known to become secondarily
infected.
Several studies have shown that cyclosporine may negatively influence
bone healing around dental implants and may even impair the mechanical
retention of dental implants previously integrated in bone.93
Tamoxifen
Tamoxifen is a standard treatment for hormone receptor–positive breast
cancer in premenopausal women. Because tamoxifen mimics the effects of
estrogen, it has a very beneficial side effect that preserves bone mass and
prevents bone loss. However, there exist drug-induced osteonecrosis
concerns with the administration of this drug. However, studies show a very
low prevalence.94
Aromatase Inhibitors
In postmenopausal women diagnosed with estrogen receptor–positive breast
cancer, aromatase inhibitors are the mainstay of adjuvant therapy. These
medications inhibit the conversion of androgens to estrogens, which results
in estrogen deficiency and may accelerate bone loss. There has been an
association with an increase in drug-related osteonecrosis of the jaws with
this class of medications.95 However, in patients on aromatase inhibitors the
incidence of osteonecrosis is still significant, and consultation with the
treating physician should be considered in these patients.
Surgery/Implant Implications
Adverse effects.
Some of the most frequent side effects of chemotherapeutic drugs are bone
marrow suppression, leukopenia, thrombocytopenia, and anemia. Therefore,
patients are susceptible to increased infectious episodes, intraoperative
bleeding, and compromised bone healing.
Medical consultation.
A medical consult and evaluation is highly recommended prior to any
proposed implant treatment. For most chemotherapeutic medications,
concurrent use and the placement of implants is an absolute
contraindication. Additionally, patients on long-term corticosteroid use
should be evaluated for possible adrenal insufficiency symptoms.
Treatment summary
• Past chemotherapy: Relative contraindication after MD consultation
• Concurrent chemotherapy + implant therapy: Absolute contraindication
Titanium Allergies
Do you have a titanium allergy? /No?
Titanium has been regarded as a biocompatible and inert material, though
some studies have shown the material may encourage hematologic and
metabolic toxicity.96 Titanium alloys are commonly used in oral implantology
because of their high strength, biocompatibility, and corrosion resistance.
The most common titanium alloy, TiAl6V4, usually will contain many traces
of other elements such as beryllium, cobalt, chromium, copper, iron, nickel,
and palladium. These impurities are thought to potentially initiate type IV
hypersensitivity allergic reactions.
Many case reports have shown dental implant–related allergic reactions
that have resulted in dermal inflammatory reactions such as facial eczema,
dermatitis, and rashes, along with localized erythema.97 Sensitivity to
titanium alloy has been characterized by the presence of macrophages and T
lymphocytes, with the absence of B lymphocytes.98 Studies have shown the
incidence of this phenomenon to be approximately 0.6%.99 Other reports have
confirmed titanium allergies associated with pacemakers, surgical clips, and
hip prostheses.100 It is also important to note allergies to other metals
because there has been some suggestion that allergy to other metals may
increase the risk of a titanium allergy. This would also be of concern in
patients who may have had a reaction to metals in jewelry. In these patients it
may be advisable to consider additional testing. Unless a patient has direct
exposure to titanium through an orthopedic procedure like hip or knee
replacement or through the use of screws or plates to repair fractures, it is
unlikely they would be aware of a titanium allergy. One study estimated the
overall prevalence of titanium allergies to be very low at 0.6%.101
Evaluation of metal allergies.
A list of allergies must be examined as part of a thorough medical history
evaluation. If an allergy to titanium is discovered, the treatment plan should
be modified to test for titanium allergy or possible use of zirconia implants.
Early study on ceramic implants shows promise because they possess good
mechanical strength and excellent tissue compatibility and exhibit
osseointegration comparable to that of titanium.102
Drug Interactions
Have you every had a drug interaction? /No?
In contrast to many years ago, patients who are seeking implant treatment
are older and more medically compromised. Because of the advancement of
pharmaceuticals, patients are on a wide range of medications that
significantly increase the risk for drug interactions. Additionally, because
oral implantology often involves invasive treatment, patients will require
local anesthesia with vasoconstrictors, analgesics, anxiolytics, corticosteroids,
and antibiotics, any of which on occasion could adversely interact with a
variety of the medications they are on. The implant clinician must have a
thorough understanding of the most common drugs prescribed with
inherent interactions (Table 2.15).
TABLE 2.15
Most Common Medications Prescribed + Interactions104
Interacting Drugs Adverse Effects

All Penic illins S tatic drug will impair ac tion of Penic illin
Bac teriostatic Antibiotic s
Methotrexate (Rheumatrex) Dec reases sec retion of Methotrexate
All Cephalosporins Bac teriostatic Antibiotic s S tatic drug will impair ac tion of Penic illin
Antic oagulants Risk of bleeding disorders might be inc reased
in antic oagulated patients
Linc omyc ins Clindamyc in (Cleoc in) Erythromyc in Possibility of antagonism. AVOID
CONCURRENT US E.
Mac rolides: dirithromyc in (Dynabac ) Antic oagulants Risk of bleeding disorders is inc reased in
c larithromyc in (Biaxin) erythromyc in antic oagulated patients—Monitor patient
Benzodiazepines Possible inc reased benzodiazepine levels
resulting in CNS depression, avoid in elderly
CCBs diltiazem (Cardizem) and verapamil QT interval prolongation, c ould c ause sudden
(Isoptin, Calan, Verelan) death
Cyc losporine (S andimmune, Neoral) Inc reased c yc losporine renal toxic ity
“S tatins” (Lipitor, Zoc or, Mevac or) Inc reased statin levels with possible musc le
toxic ity
Metronidazole (Flagyl) Antic oagulants (Coumadin) Risk of bleeding disorders is inc reased in
antic oagulated patients
Ethanol S evere disulfiram-like reac tions
Tac rolimus (Prograf) Metronidazole doubles Prograf levels
Quinolones: Antac ids Dec reased quinolone absorption
Ciprofloxac in (Cipro) Antic oagulants (Coumadin) Inc reased risk of bleeding disorders. Monitor
Gatifloxac in (Tequin) INR
Levofloxac in (Levaquin) Antineoplastic s Quinolone serum levels may be dec reased
Moxifloxac in (Avelox) Cyc losporine (S andimmune, Neoral) Cyc losporine renal toxic ity may be enhanc ed
NS AIDs Enhanc ed CNS stimulation
Caffeine Inc reased c affeine effec ts
Musc le Weakness—Tendon Damage
NS AIDs and Aspirin Antic oagulants (warfarin, Coumadin) Inc rease risk of bleeding disorders in
antic oagulated patient, possible gastrointestinal
(GI) hemorrhage
Antihypertensives (all but CCBs) (ACEI, beta Dec reased antihypertensive effec t. Monitor
bloc kers, diuretic s) blood pressure
Bisphosphonates GI toxic ity
Cyc losporine (Neoral, S andimmune) Nephrotoxic ity of both agents may be
inc reased
Methotrexate (Rheumatrex, Mexate) Toxic ity of methotrexate may be inc reased, and
inc reased possibility of stomatitis
S S RIs GI bleeding, depletion of platelet serotonin
required for aggregation
NS AID + S alic ylates Bloc kage of antiplatelet ac tion with inc reased
GI effec ts
Ac etaminophen Barbiturates, Carbamazepine, Phenytoin, The hepatotoxic ity of APAP may be inc reased
Rifampin, S ulfinpyrazone by high dose or long-term administration of
these drugs
S edatives/anxiolytic s Inc reased sedation and respiratory depression
Ethanol Inc reased hepatotoxic ity of APAP with c hronic
ethanol ingestion
Tramadol (Ultram, Ultrac et) Any drug that enhanc es serotonin ac tivity Possible serotonin syndrome
(S S RI antidepressants, “triptans” for ac ute
migraine
MAOIs (Marplan, Nardil, Parnate) MAOI toxic ity enhanc ed
Quinidine Tramadol inc reased/metabolite dec reased
All Opioids Alc ohol, CNS depressants, loc al anesthetic s, Inc reased CNS and respiratory depression may
antidepressants, antipsyc hotic s, antihistamines, oc c ur. Use c autiously
c imetidine
Hydroc odone/Codeine 2D6 Inhibitors, Amiodarone, Cimetidine, Inhibition of biotransformation of Codeine to
Desipramine, Fluoxetine, Paroxetine, ac tive analgesic form. Use different narc otic on
Propafenone, Quinidine, Ritonavir 2D6 Inhibitor patients
S S RI antidepressants and bupropion Analgesic effec t reduc ed
Amides (e.g., lidoc aine) Alc ohol, CNS depressants, opioids, Inc reased CNS and respiratory. Depression may
antidepressants, antipsyc hotic s, antihistamines oc c ur
Antiarrhythmic drugs Inc reased c ardiac depression
Beta bloc kers, c imetidine Metabolism of lidoc aine is reduc ed
Bupivac aine Toxic ity is additive, total dose should not
exc eed the c ombined maximum dosages
Vasoc onstric tors (epinephrine, Tric yc lic antidepressants-high dose Inc reased sympathomimetic effec ts possible.
levonordefrin) (amitriptyline, desipramine, imipramine, Limit epi to 0.04 mg with high dose TCA's
nortriptyline, etc )
Beta bloc kers (nonselec tive) (e.g., Hypertensive and/or c ardiac rx possible
propranolol, nadolol) Limit epi to 0.04 mg/2 hr. visit
Phenothiazines (e.g., c hlorpromazine) Vasoc onstric tor ac tion inhibited, leading to
possible hypotensive responses. Use
c autiously
Antihistamines diphenhydramine Antic holinergic s Inc reased dry mouth, tac hyc ardia, urinary
(Benadryl) hydroxyzine (Atarax, Vistaril) retention. Monitor
Promethazine (Phenergan) CNS depressants (alc ohol, narc otic s) Enhanc ed duration and intensity of sedation
Reduc e dosages
Benzodiazepines (Triazolam) Rifampin, c arbamazepine Inc reased metabolism leading to dec reased
sedative response
Most of the reactions are the result of interactions with oral pain
medications and with vasoconstrictors used to enhance local anesthetic pain
control and control bleeding. Some of the more common interactions involve
NSAIDs because these medications reduce the effectiveness of many blood
pressure medications. The use of NSAIDs with anticoagulants can increase
the anticoagulant effect and result in gastrointestinal (GI) bleeding. NSAIDs
may increase the GI toxicity of bisphosphonates and SSRIs prescribed for
patients with mental illness. SSRIs also interfere with the metabolism of
codeine and hydrocodone, so the overall analgesic effect may be reduced
(Table 2.16).103,104
TABLE 2.16
Diagnostic Lab Test Summary
Test Name Description Elevated Levels Decreased Levels

Albumin (blood) Is produc ed by liver and most abundant protein in Dehydration Inflammation, liver disease
blood; c an be used to judge c hanges in overall malnutrition, kidney disease,
health, liver, or kidney func tion malabsorption
Alkaline Produc ed by several organs inc luding liver, Bone disease suc h as metastatic Malnutrition,
phosphatase bone, and kidney c anc er, Paget disease, multiple hypophosphatemia,
myeloma, liver disease hypothyroid, B12 defic ienc y
Alanine Used to ac c ess func tion of the liver Liver disease (hepatitis, nec rosis, N/A
transaminase c irrhosis, tumor); medic ations (statins,
(ALT) antibiotic s, c hemotherapy, narc otic s);
mononuc leosis, obesity (fatty liver)
Amylase Enzyme produc ed by panc reas and used to detec t Panc reatitis N/A
issues with panc reas
Antinuc lear Used as a sc reen for c onnec tive tissue disease; Requires further spec ific tests to N/A
antibody (ANA) positive test oc c urs in some individuals without c onfirm lupus, sc leroderma, S jögren
spec ific disease syndrome, or myositis
Aspartate Used to detec t liver disease and provide Liver disease, medic ations, Ac ute renal disease, beriberi,
aminotransferase assessment of liver func tion mononuc leosis, obesity (similar to diabetic ketoac idosis,
(AS T) AS T) pregnanc y, c hronic renal
AS T:ALT >2 : 1—alc oholic liver dialysis
Basic metabolic Blood panel that measures sodium, potassium, Dependent on test (refer to
panel (BMP) gluc ose, BUN, c reatinine, c hloride, CO 2 eac h c omponent)
Bilirubin indirec t Level of bilirubin that is produc t of liver that is not Hemolytic anemia, c irrhosis, No low results available
c onjugated (have sugar molec ules attac hed) transfusion reac tion, Gilbert disease
(lac k enzyme to c onjugate)
Bilirubin direc t Level of bilirubin that is c onjugated with a sugar Viral hepatitis, drug reac tions, No low results available
molec ule but c annot be sec reted through bloc ked alc oholic liver disease, gallstones,
bile duc ts tumors, bile duc t sc arring
Bleeding time Measure c lot time foc used on func tion of platelets von Willebrand disease, N/A
thromboc ytopenia, DIC, medic ations
Blood urea Measure urea nitrogen formed when protein is Kidney dysfunc tion, GI bleed, Liver disease, S IADH
nitrogen (BUN) broken down. Help measure kidney and liver dehydration, shoc k, medic ations, CHF, (syndrome of inappropriate
func tion or urinary outlet obstruc tion antidiuretic hormone),
malnutrition
BUN/Cr ratio Ratio of BUN to Creatinine, usually between 10 : 1 Dehydration, ac ute kidney failure or N/A
and 20 : 1 injury, diet high in protein (ratio c an be
normal in c hronic kidney disease)
Calc ium (Ca) Chec ks blood level c alc ium not in bones and Hyperparathyroidism, lung/breast Chronic renal failure, vitamin
parathyroid func tion c anc er metastasis to bone, Paget D defic ienc y, magnesium
disease, exc essive intake of vitamin D defic ienc y, bisphosphonate
therapy
Carbon Dioxide Level of c arbon dioxide in the blood and Vomiting, COPD, anorexia, Diarrhea, hyperventilation,
(CO 2) important buffer of ac id/base regulation dehydration, hypoventilation kidney or liver disease
Chloride (Cl) Important in the monitoring of ac id/base disorders Dehydration, diarrhea, renal tubular Overhydration (S IADH),
ac idosis, diuretic s, Addison disease, c hronic
hyperparathyroidism vomiting, heart failure
Creatinine (Cr) Important measurement of kidney func tion Kidney disease, dehydration, diuresis, Dec reased musc le mass
medic ation, radioc ontrast induc ed,
hypertensive kidney disease
Creatinine Used to estimate glomerular filtration rate and 90+: S tage 1 (normal kidney func tion)
c learanc e (CrCl) overall kidney func tion 60–89: S tage 2 (mildly reduc ed
kidney func tion)
30–59: S tage 3 (moderately reduc ed
kidney func tion)
15–29 S tage 4 (severe kidney
disease)
<15: End-stage kidney disease
Erythroc yte Nonspec ific marker for inflammation Collagen vasc ular disease (lupus, Polyc ythemia, sic kle c ell
sedimentation rheumatoid arthritis), vasc ulitis, anemia, spheroc ytosis
rate (ES R) infec tions, malignanc y, renal failure,
inflammatory bowel disease, anemias
Ferritin Measures amount of iron stored in body Hemoc hromatosis, porphyria, liver Hemodialysis, iron
disease, multiple blood transfusions, defic ienc y anemia
liver disease, Hodgkin lymphoma
Gluc ose Measurement of blood sugar level that is best Diabetes, nonfasting level, illness, Exc ess insulin sec retion,
interpreted fasting <100 infec tion, stress response exc essive alc ohol, Addison
disease (adrenal
insuffic ienc y), reac tive
hypoglyc emia
Hematoc rit Ratio of red blood c ell volume to the total volume Dehydration, diuresis, polyc ythemia Anemia, pregnanc y,
of the blood vera, high altitude exposures exc essive blood loss
Hemoglobin Carries oxygen to tissues Polyc ythemia, high altitude exposure, Anemia, hemolysis,
extreme exerc ise program exc essive blood loss
Hemoglobin Measurement of perc entage of hemoglobin Poorly c ontrolled diabetes, iron Hemolysis, rec ent blood
A1C (HbA 1c ) c oated with sugar and provides average of blood defic ienc y anemia, vitamin B12 transfusion, c hronic liver
sugar over 3-month period defic ienc y, uremia, alc oholism disease, exc ess treatment of
diabetes,
hypertriglyc eridemia
Iron level (Fe) Measures amount of iron in blood Hemoc hromatosis, hemolysis, liver Low dietary intake, heavy
nec rosis, hepatitis, vitamin B12 menstrual bleeding, GI blood
defic ienc y, exc essive blood loss, intestinal malabsorption,
transfusions pregnanc y
Lipase (LPL) Enzyme produc ed by panc reas to help Panc reatitis, tumors of panc reas, gall May indic ate c hronic damage
breakdown fats and used to help determine bladder infec tion, high triglyc erides, to panc reas
disease of the panc reas exc essive alc ohol, gallstones or
infec tion of gallbladder
Liver func tion Can give measurement of liver func tioning (AS T,
tests (LFT) ALT, bilirubin, albumin, alkaline phosphatase)
Mean Red blood c ell average size Vitamin B12 or folic ac id defic ienc y, Anemias, iron defic ient,
c orpusc ular ETOH abuse, liver disease, bone c hronic disease, sideroblastic ,
volume (MCV) marrow dysfunc tion, hypothyroidism c hronic renal failure, lead
poisoning, thalassemia
Partial Measures time for blood to c lot for intrinsic S imilar to prothrombin time (PT) S imilar to prothrombin time
thromboplastin pathway (fac tors IX, X, XI, XII) (PT)
time (PTT)
Platelets Number of c irc ulating platelets Ac ute bleeding, c anc er, renal failure, Hemolytic uremic syndrome,
infec tions, iron defic ienc y, autoimmune disease,
splenec tomy, inflammatory bowel pregnanc y, ITP, TTP
disease, lupus
Potassium (K) Measure level of potassium in blood, essential for Ac ute/c hronic kidney disease, Diabetic ketoac idosis,
proper func tion of organs and all c ells Addison disease (adrenal diarrhea, exc essive alc ohol or
insuffic ienc y) rhabdomyolysis laxative use, hyperhidrosis
(breakdown of musc le), HTN (exc essive sweating),
medic ations (ACE/ARB), exc essive diuretic s, folic ac id
intake, burn injury defic ienc y, primary
aldosterone tumor, vomiting
Prostate-spec ific Measure blood level of PS A released by prostate Prostate c anc er, prostatitis, c atheter <0.1 in patients treated for
antigen (PS A) gland; PS A normally inc reases with age as insertion, BPH, UTI, age-related, prostate c anc er
prostate enlarges prolonged bike riding
Prothrombin Measures time for blood to c lot by the extrinsic Liver disease, alc ohol abuse, DIC, Vitamin K supplementation,
time (PT) pathway (tissue fac tor, Xa); INR is standard vitamin K defic ienc y, c lotting fac tor estrogen therapy,
measure defic ienc y, medic ation induc ed thrombophlebitis
RBC Measures number of red blood c ells Thalassemia trait, altitude exposure, Anemia (inc luding
c igarette use, polyc ythemia hemolytic ), ac ute blood loss,
bone marrow dysfunc tion
Rheumatoid Measure autoantibody (RF antibody) level that Rheumatoid arthritis, c anc er, c hronic N/A
fac tor (RF) attac ks own tissue and c an indic ate rheumatoid infec tions or liver disease, lupus,
arthritis sc leroderma, S jögren syndrome; also
found in individuals with no disease
S odium (Na) Measure level of c irc ulating sodium (important Inc reased dietary intake, Cushing Medic ations (diuretic s), CHF,
for fluid balanc e and func tioning of nerves and syndrome liver disease, S IADH,
musc les) c hronic vomiting, adrenal
insuffic ienc y, drinking too
muc h water
Thyroid- Released by pituitary and c auses thyroid gland to Hypothyroidism, Hashimoto Hyperthyroidism, subac ute
stimulating release thyroxine (T4) and triiodothyronine (T3); thyroiditis (antibody attac h thyroid), thyroiditis (inflammation
hormone (TS H) used to diagnosis thyroid disease lithium, amiodarone thyroid), exc ess thyroid
replac ement therapy, thyroid
c anc er (low normal)
Thyroxine (T4) Total T4 measures the amount of T4 in blood Hyperthyroidism (Graves disease), Hypothyroidism, pituitary
free or total released by thyroid and used to diagnose pituitary adenoma, exc essive thyroid insuffic ienc y, malnutrition,
hyper/hypothyroid disease and respond to replac ement therapy, thyroiditis, birth c hronic illness, low intake of
thyroid replac ement; total T4 is protein bound and c ontrol pills, pregnanc y, exc essive iodine
c an be abnormal bec ause of protein levels; free iodine intake
T4 more ac c urate and not influenc ed by protein
levels
Triiodothyronine Measure the amount of c irc ulating T3 produc ed Hyperthyroidism (Graves disease), Hypothyroidism, pituitary
(T3) free or total by thyroid; T3 is bound to thyroxine binding pituitary adenoma, exc essive thyroid insuffic ienc y, malnutrition,
globulin; T3 not bound to protein is free T3 and replac ement therapy, thyroiditis, birth illness, medic ations
this is thought to be responsible for biologic c ontrol pills, pregnanc y, exc essive (amiodarone, phenytoin)
ac tivities in the body iodine intake; free T3 levels stable in
pregnanc y and with birth c ontrol pills
WBC Measures total number of white blood c ells Bac terial infec tion, sepsis, steroids Immunosuppression, viral
very high in CLL infec tions, c hemotherapy,
antibiotic s
Types of White Blood Cells
Neutrophils Most abundant type of white blood c ell Bac terial infec tions “shift to left” more Malignanc ies, aplastic anemia,
neutrophils ac ute infec tion severe infec tions
Lymphoc ytes Made up of B c ells that produc e antibodies and T Viral infec tions inc luding Bone marrow dysfunc tion,
c ells produc ed in thymus and are part of immune mononuc leosis and hepatitis c hemotherapy, TB, lupus,
response rheumatoid arthritis, drug
induc ed
Monoc ytes Partic ipate in phagoc ytosis; produc e TB; c hronic inflammatory disorders Vitamin B12 defic ienc y, bone
mac rophages to help fight bac teria, fungi, and suc h as Crohn disease, ulc erative marrow dysfunc tion, c ertain
viruses c olitis, lupus leukemias
Eosinophils produc ed in response to allergens and diseases Allergic reac tions, parasites Cushing disease, treatment
with steroids, stress reac tions
Basophils Least abundant WBC; c ontain heparin and Viruses, lymphoma, hypothyroidism, Pregnanc y, steroid use,
histamine related to hypersensitivity reac tions inflammatory bowel disease hyperthyroidism
Medical Consultation and Clearance

Oral implantology is a complex specialty with many factors that must be
taken into consideration to decrease morbidity and increase the probability
of successful treatment. Medical clearance is a necessity with respect to
patients who present with complicated systemic conditions, medications, and
predisposing factors that may lead to complications. The implant clinician
must relay to the physician all necessary information, including: (1) a
detailed summary of what the patient related as their medical history, (2) list
of all current and recent medications, (3) allergies, (4) any medications that
will be prescribed by the implant dentist, and (5) the invasiveness of the
intended procedure (Fig. 2.2). The physician will provide answers to;
1. Most Recent Physical Exam: to determine if the patient is compliant with

keeping up with their medical health.
2. Documentation of Medical Health: very important to determine if there

exists any misinformation or missing health issues that the patient failed to
represent on the medical/dental history.
3. Medication Modification: The physician will recommend any modifications

to physician prescribed medications or dental surgery proposed medications.
4. Acceptable Candidate: The physician will clear the patient for dental
implant treatment in writing.
5. Contacting the Physician: The physician will document whether their

recommendation is for the implant dentist to contact them prior to
treatment. And lastly, make sure the physician signs and dates the form.
FIG 2.2 Medical consultation form.
References
1. Weijant RJ. Characteristics associated with the loss and peri-implant
tissue health of endosseous dental implants. Int J Oral Maxillofac
Implants. 1992;7:367–372.
2. Dycht K. Age wave: the challenges and opportunities of an aging America.
St. Martin's Press: New York; 1988.
3. Silverman S, Eversole LR, Truelove EL. Essentials of oral medicine.
PMPH-USA; 2001.
4. World Health Organization. World Health Report 2002: Reducing risks,
promoting healthy life. WHO: Geneva, Switzerland; 2002.
5. Pereira M, Lunet N, Azevedo A, et al. Differences in prevalence,
awareness, treatment and control of hypertension between
developing and developed countries. J Hypertens. 2009;27:963–975.
6. James PA, Oparil S, Carter BL, et al. Evidence-based guideline for the
management of high blood pressure in adults; report from the panel
members appointed to the eighth joint national committee. JAMA.
2014;311:507–520.
7. Polonia J. Interaction of antihypertensive drugs with anti-
inflammatory drugs. Cardiology. 1997;88(Suppl 3):47–51.
8. Herman WW, Konzelman JL, Prisan M. New national guidelines on
hypertension: a summary for dentistry. J Am Dent Assoc. 2004;135:576–
584.
9. Becker DE. Drug interactions in dental practice: a summary of facts
and controversies. Compend Cont Educ Dent. 1994;15:1228–1244.
10. Naguib M, Magboul MMA, et al. Adverse effects and drug
interactions associated with local andregional anesthesia. Drug Saf.
1998;18:221–250.
11. Yagiela JA. Adverse drug interactions in dental practice: interactions
associated with vasoconstrictors part V of a series. JADA.
1999;130:701–709.
12. Ellis JS, Seymour RA, Steele JG, et al. Prevalence of gingival
overgrowth induced by calcium channel blockers: a community-
based study. J Periodontol. 1999;70:63–67.
13. Alsaadi G, Quirynen M, Komárek A, et al. Impact of local and
systemic factors on the incidence of oral implant failures, up to
abutment connection. J Clin Periodontol. 2007;34:610–617.
14. Alsaadi G, Quirynen M, Komárek A, et al. Impact of local and
systemic factors on the incidence of late oral implant loss. Clin Oral
Implants Res. 2008;19(7):670–676.
15. DiSesa VJ, et al. Nitrous oxide for blood pressure control after
coronary artery surgery: a dose-response hemodynamic study in
postoperative patients. Ann Thorac Surg. 1987;44:189–191.
16. Pell S, D'Alonzo CA. Immediate mortality and five-year survival of
employed men with a first myocardial infarction. N Engl J Med.
1964;270:915.
17. Ardekian L, Gaspar R, Peled M, et al. Does low-dose aspirin therapy
complicate oral surgical procedures? J Am Dent Assoc.
2000;131(3):331–335.
18. WebMD. Heart disease health center (website).
http://www.webmd.com/heart-disease/default.htm.
19. Khadivi V, Anderson J, Zarb GA. Cardiovascular disease and
treatment outcomes with osseointegration surgery. J Prosthet Dent.
1999;81:533–536.
20. Alsaadi G, Quirynen M, Komarek A, et al. Impact of local and
systemic factors on the incidence of oral implant failures, up to
abutment connection. J Clin Periodontol. 2007;34:610–617.
21. Centers for Diseases Control and Prevention. Diabetes 2014 report card
(website). http://www.cdc.gov/diabetes/data/statistics.
22. World Health Organization. Diabetes (website).
http://www.who.int/nmh/publications/fact_sheet_diabetes_en.pdf.
23. Alsaadi G, et al. Impact of local and systemic factors on the incidence
of late oral implant loss. Clin Oral Implants Res. 2008;19:670–676.
24. AlGhamdi AS, Merdad K, Sonbul H, et al. Dental clinics as potent
sources for screening undiagnosed diabetes and prediabetes. Am J
Med Sci. 2013;345:331–334.
25. Al-Maskari AY, Al-Maskari MY, Al-Sudairy S. Oral manifestations and
complications of diabetes mellitus: a review. Sultan Qaboos Univ Med
J. 2011;11:179–186.
26. Retzepi M, Donos N. The effect of diabetes mellitus on osseous
healing. Clin Oral Implants Res. 2010;21:673–681.
27. Mellado-Valero A, Ferrer Garcia JC, Herrera Ballester A, Labaig Rueda
C. Effects of diabetes on the osseo-integration of dental implants.
Med Oral Patol Oral Cir Bucal. 2007;12:E38–E43.
28. McCracken M, Lemons JE, Rahemtulla F, et al. Bone response to
titanium alloy implants placed in diabetic rats. Int J Oral Maxillofac
Implants. 2000;15:345–354.
29. Marchand F, Raskin A, Dionnes-Hornes A, et al. Dental implants and
diabetes: conditions for success. Diabetes Metab. 2012;38:14–19.
30. Javed F, Romanos GE. Impact of diabetes mellitus and glycaemic
control on the osseointegration of dental implants: a systematic
literature review. J Periodontol. 2009;80:1719–1730.
31. Michaeli E, Weinberg I, Nahlieli O. Dental implants in the diabetic
patient: systemic and rehabilitative considerations. Quintessence Int.
2009;40:645–649.
32. Attard NJ, Zarb GA. A study of dental implants in medically treated
hypothyroid patients. Clin Implant Dent Relat Res. 2002;4:220–231.
33. Fonseca RJ, Marciani RD, Turvey TA. Oral and maxillofacial surgery. ed
2. Saunders: St Louis; 2009.
34. Keller JC, Stewart M, Roehm M, et al. Osteoporosis-like bone
conditions affect osseointegration of implants. Int J Oral Maxillofac
Implants. 2004;19:687–694.
35. Gibson N, Ferguson JW. Steroid cover for dental patients on long-
term steroid medication: proposed clinical guidelines based upon a
critical review of the literature. Br Dent J. 2004;197:681–685.
36. Henrikson P. Periodontal disease and calcium deficiency: an
experimental study in the dog. Acta Odontol Scand. 1968;26(Suppl
50):1–132.
37. Binon PP, Fowler CN. Implant-supported fixed prosthesis of four
osseointegrated oral implant systems. J Mat Sci Mater Med. 1993;8:54–
60.
38. Misch CE. Density of bone: effect on treatment plans, surgical
approach, healing and progressive bone loading. Int J Oral Implant.
1990;6:23–31.
39. Marder MZ. Medical conditions affecting the success of dental
implants. Compendium. 2004;25:739–764.
40. Fatahzadeh M. Inflammatory bowel disease. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 2009;108:e1–e10.
41. Daley TD, Armstrong JE. Oral manifestations of gastrointestinal
diseases. Can J Gastroenterol. 2007;21:241–244.
42. Fatahzadeh M. Inflammatory bowel disease. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 2009;108:e1–e10.
43. Chandok N, Watt K. Pain management in the cirrhotic patient: the
clinical challenge. Mayo Clin Proc. 2010;85:451–458.
44. US Department of Health and Human Services. Bone health and
osteoporosis: a report of the surgeon general, Rockville, MD. 2004.
45. Chestnut CH. Osteoporosis an undiagnosed disease. JAMA.
2001;286:2865–2866.
46. Dempster DW. Bone remodeling. Coe FL, Favis MJ. Disorders of bone
and mineral metabolisms. Raven Press: New York; 1992:355–380.
47. Wakley GK, Baylink DJ. Systemic influences on the bone response to
dental and orthopedic implants. J Oral Implant. 1988;14:285–311.
48. Grant B, et al. Outcomes of placing dental implants in patients taking
oral bisphosphonates: a review of 115 cases. J Oral Maxillofac Surg.
2008;66:223–230.
49. August M, Chung K, Chang Y, et al. Influence of estrogen status on
endosseous implant integration. J Oral Maxillofac Surg. 2001;59:1285–
1289.
50. Friberg B, Ekestubbe A, Mellstrom E, et al. Brånemark implants and
osteoporosis: a clinical exploratory study. Clin Impl Dent Relat Res.
2001;3:50–56.
51. Valentini V, Cassoni A, Marianetti TM, et al. Craniomaxillofacial
fibrous dysplasia: conservative treatment or radical surgery? A
retrospective study on 68 patients. Plast Reconstr Surg. 2009;123:653.
52. Ricalde P, Magliocca KR, Lee JS. Craniofacial fibrous dysplasia. Oral
Maxil Surg Clin. 2012;24:427–441.
53. Bajwa MS, Ethunandan M, Flood TR. Oral rehabilitation with
endosseous implants in a patient with fibrous dysplasia (McCune-
Albright syndrome): a case report. J Oral Maxillofac Surg.
2008;66:2605–2608.
54. Klippel J. Systemic sclerosis and related syndromes: Primer on the
rheumatic diseases. ed 11. The Arthritis Society: New York; 1997.
55. Hasler P. Biological therapies directed against cells in autoimmune
disease. Springer Semin Immun. 2006;27:443–456.
56. Krennmair G, Seemann R, Piehslinger E. Dental implants in patients
with rheumatoid arthritis: Clinical outcome and periimplant
findings. J Clin Periodontol. 2010;37:928–936.
57. Centers for Disease Control and Prevention. Current cigarette
smoking among adults—United States, 2005–2012. MMWR Morb
Mortal Wkly Rep. 2014;63:29–34.
58. Atieh MA, Alsabeeha NH, Faggion CM Jr, et al. The frequency of
periimplant diseases: a systematic review and meta-analysis. J
Periodontol. 2013;84:1586–1598.
59. Leow YH, Maibach HI. Cigarette smoking, cutaneous vasculature, and
tissue oxygen. Clin Dermatol. 1998;16:579–584.
60. Cavalcanti R, et al. The influence of smoking on the survival of dental
implants: a 5-year pragmatic multicentre retrospective cohort study
of 1727 patients. Eur J Oral Implantol. 2010;4:39–45.
61. van Steenberghe D, Jacobs R, Desnyder M, et al. The relative impact of
local and endogenous patient-related factors on implant failure up to
the abutment stage. Clin Oral Implants Res. 2002;13:617.
62. Jones JK, Triplett RG. The relationship of cigarette smoking to
impaired intra-oral wound healing. J Oral Maxillofac Surg.
1992;50:237–239.
63. Bain CA. Smoking and implant failure—benefits of a smoking
cessation protocol. Int J Oral Maxillofac Implants. 1996;11:1667–1674.
64. Bain CA, Moy PK. The association between the failure of dental
implants and cigarette smoking. Int J Oral Maxillofac Impl.
1993;8:609–615.
65. Grossi SG, Zambon J, Machtei EE. Effects of smoking and smoking
cessation on healing after mechanical periodontal therapy. J Am Dent
Assoc. 1997;128:599–607.
66. Scully C. Scully's medical problems in dentistry. ed 7. Churchill
Livingstone: London; 2014.
67. Rees TD. Oral effects of drug abuse. Crit Rev Oral Biol Med.
1992;3:163–184.
68. Tonnesen H. Alcohol abuse and postoperative morbidity. Dan Med
Bull. 2003;50:139–160.
69. Altasalo K. Bone tissue response to irradiation and treatment model
of mandibular irradiation injury. Acta Otolaryngol. 1986;428:1–54.
70. Granstrom G. Osseointegration in irradiated tissues. Experience from
our first 100 treated patients. J Oral Maxillofac Surg. 1996;63:579–585.
71. Granstrom G. Hyperbaric oxygen as a stimulator of osseointegration.
Adv Otorhinolaryngol. 1988;54:33.
72. Jacobsson M. On behavior after irradiation (master's thesis), Goteborg,
Sweden, University of Goteborg. 1985.
73. Keller EE. Placement of dental implants in irradiated mandible. A
protocol without adjunctive hyperbaric oxygen. J Oral Maxillofac
Surg. 1997;55:972.
74. Granstrom G. Osseointegration in irradiated tissues. Experience from
our first 100 treated patients. J Oral Maxillofac Surg. 1996;63:579–585.
75. Albrekttson T. A multicenter report on osseointegrated oral implants.
J Prosthet Dent. 1988;60:75–84.
76. King MA, Casarett GW, Weber DA. A study of irradiated bone: I.
Histopathologic and physiologic changes. J Nucl Med. 1979;20:1142–
1149.
77. World Health Organization. Health statistics and information systems
(website). http://www.who.int/healthinfo/survey/ageingdefnolder/en/.
78. Heeling DK, Lemke JH, Semla TP, et al. Medication use characteristics
in the elderly. The Iowa 65+ rural health study. J Am Geriatr Soc.
1987;35:4–12.
79. Blacher J, Staessen JA, Girerd X, et al. Pulse pressure not mean
pressure determines cardiovascular risk in older hypertensive
patients. Arch Intern Med. 2000;160:1085–1089.
80. Skak SV, Jensen TT. Femoral shaft fracture in 265 children. Log-normal
correlation with age of speed of healing. Acta Orthop Scand.
1988;59:704–747.
81. Hildebolt CF. Osteoporosis and oral bone loss. Dentomaxillofac Radiol.
1997;26:3–15.
82. Moy PK, Medina D, Shetty V, et al. Dental implant failure rates and
associated risk factors. Int J Oral Maxillofac Implants. 2005;20:569–577.
83. Jemt T. Implant treatment in elderly patients. Int J Prosthodont.
1993;6:456–461.
84. Marx RE. Oral and intravenous bisphosphonate-induced osteonecrosis of the
jaws. Quintessence: Hanover Park, Illinois; 2007.
84a. Black DM, et al. Effects of continuing or stopping alendronate after 5
years of treatment: the fracture intervention trial long-term extension
(FLEX): a randomized trial. JAMA. 2006;296(24):2927–2938.
85. Greenspan Sl, Rosen HN, Parker RA. Early changes in serum N-
telopeptide and C-telopeptide cross-linked collagen type 1 predict
long-term response to alendronate therapy in elderly women. J Clin
Endocrinol Metab. 2000;85:3537–3540.
85a. Marx RE. Bisphosphonates and bisphosphonate-induced
osteonecrosis of the jaws. Bagheri SC, Bell RB, Kahn HA. Current
therapy in oral and maxillofacial surgery. Saunders: St. Louis; 2012.
86. Jeffcoat MK. Safety of oral bisphosphonates: controlled studies on
alveolar bone. Int J Oral Maxillofac Implants. 2006;21:349–353.
87. Garcia DA, Regan S, Henault LE, et al. Risk of thromboembolism with
short-term interruption of warfarin therapy. Arch Intern Med.
2008;168:63–69.
88. Brennan MT, et al. Aspirin use and post-operative bleeding from
dental extractions. J Dent Res. 2008;87:740–744.
89. Gomez-Moreno G, Aguilar-Salvaterra A, Martin-Piedra MA, et al.
Dabigatran and rivaroxaban, new oral anticoagulants, new
approaches in dentistry. J Clin Exp Dent. 2010;2:e1–e5.
90. Firriolo JF, Hupp WS. Beyond warfarin: the new generation of oral
anticoagulants and their implications for the management of dental
patients. Oral Surg Oral Medicine O. 2012;113:431–441.
91. Phillips KA, Veenstr DL. Potential role of pharmocogenics in reducing
adverse drug reactions. JAMA. 2001;286:2270–2279.
92. Blanchaert RH. Implants in the medically challenged patient. Dent
Clin N Am. 1998;42:1.
93. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial
endocarditis. Recommendations by the American Heart Association.
J Am Med Assoc. 1997;277:1794–1801.
94. Hess LM, Jeter J, Benham-Hutchins M, et al. Factors associated with
osteonecrosis of the jaw among bisphosphonate users. Am J Med June.
2009;121:475–483 [e3].
95. Shapiro CL. Bisphosphonate-related osteonecrosis of jaw in the
adjuvant breast cancer setting: risks and perspective. J Clin Oncol.
2013;31:2648.
96. Luckey TD, Veugapal B. Metal Toxicity in mammals. ed 11. Plenum
Press: New York; 1979.
97. Egusa H, et al. Suspected association of an allergic reaction with
titanium dental implants: a clinical report. J Prosthet Dent.
2008;100:344–347.
98. Hallab NJ, Mikecz K, Vermes C, et al. Orthopaedic implant related
metal toxicity in terms of human lymphocyte reactivity to metal-
protein complexes produced from cobalt-base and titanium-base
implant alloy degradation. Mol Cell Biochem. 2001;222:127–136.
99. Sicilia A, et al. Titanium allergy in dental implant patients: a clinical
study on 1500 consecutive patients. Clin Oral Implants Res.
2008;19:823–835.
100. Siddiqi A, et al. Titanium allergy: could it affect dental implant
integration? Clin Oral Implants Res. 2011;22:673–680.
101. Sicilia A, et al. Titanium allergy in dental implant patients: a clinical
study on 1500 consecutive patients. Clin Oral Implants Res.
2008;19:823–835.
102. Gahlert M, Gudehus T, Eichhorn S, et al. Biomechanical and
histomorphometric comparison between zirconia implants with
varying surface textures and a titanium implant in the maxilla of
miniature pigs. Clin Oral Implants Res. 2007;18:662–668.
103. Baker K. Treating the new millennium dental patient: medicated and
complicated! (website). http://www.iowadental.org/Baker%20-
%20Sun%20PM2.pdf.
104. Hersh EV, Moore PA. Adverse drug interactions in dentistry.
Periodontol 2000. 2008;46:109–142.
3
Treatment Planning Complications
Randolph R. Resnik, Carl E. Misch
The introduction of the dental implant has greatly expanded the scope of
services that clinicians can provide to restore patients to optimal form,
function, and esthetics. Patients presenting with missing teeth or pathology
that necessitate tooth extraction now have a wide range of treatment options
beyond fixed bridges or removable prosthetics. The progressive loss of bone
as a consequence of tooth extraction can now be minimized. Implant
technology has allowed clinicians to come much closer to the ideal goal of
restoring patients' dental health.
Patients present to dental offices every day with either an edentulous
condition or pathology that necessitates tooth removal. Prior to the
beginning of treatment, the clinician has an ethical and legal obligation to
educate the patient as to the advantages and disadvantages of every
therapeutic option available. The goal of this chapter is to provide clinicians
with a comprehensive treatment protocol for the major edentulous
conditions, including advantages and disadvantages of each. By informing
the patient of each option available (including no treatment), the dental
professional can aid the patient in forming an educated choice for treatment
that meets their needs and values.
In this chapter the various aspects of treatment planning will be discussed.
These include the prosthesis type, available bone, key implant positions,
implant size, and force factors.
Type of Prosthesis
Treatment Planning
In implant dentistry, when a specific prosthetic result is desired, additional
foundation units (support) may be created to obtain the end result. Both the
psychologic and anatomic needs and desires of the patient should be first
evaluated and determined. The prosthesis that satisfies the intended goals
and expectations may then be designed.
Complications often arise when only one implant approach is used for all
patients because the same surgical and prosthetic scenarios and flaws are
invariably repeated. The benefits of implant dentistry can be realized only
when the prosthesis is first discussed and determined in detail by the
clinician and patient. An organized treatment approach based on the
prosthesis permits predictable therapy results. Misch has postulated there
are basically five various prosthetic options available in implant dentistry.
Three restorations are fixed and vary in the amount of hard and soft tissue
replaced; two are removable and are based on the amount of support for the
restoration.1
The amount of support required for an implant prosthesis should initially
be similar to that used in traditional tooth-supported restorations. After the
intended prosthesis is designed, the implants and treatment surrounding
this specific result can be established. The prosthetic option is the first factor
to determine in the overall implant treatment plan.
Not Understanding and Communicating the Types of

Prostheses
Complication.
When treatment planning for a fixed prosthesis, many inherent
complications may occur. It is crucial for the clinician to have a thorough
understanding of how the final fixed prosthesis is directly related to the
amount of hard and soft tissue remaining, position of the implant, and the
anatomic area of the oral cavity. If this is not understood, miscommunication
may result leading to possible esthetic, biomechanical, or periodontal issues.
Prevention
Prosthesis treatment planning first.
To satisfy predictably a patient's needs and desires, the prosthesis should
first be designed. In the stress treatment theorem postulated by Misch, the
final restoration is first planned in a way similar to an architect designing a
building before setting the foundation.2 Implant dentistry is analogous to
constructing a building. Prior to construction, detailed blueprints are
obtained that explain in detail every aspect of the project. Similar guidelines
should be used in implant dentistry treatment planning. Only after the
prosthesis is envisioned and determined can the final abutments, implant
size and location, and available bone requirements be determined to support
the specific predetermined restoration.
Treatment plan according to finances.

Patients are too often treated as though cost is the primary factor in
establishing a treatment plan. Patients should be presented with all viable
treatment plans, regardless of cost. To determine the ideal final prosthetic
design, the existing anatomy is evaluated after it has been determined
whether a fixed or removable restoration is required to address the patient's
desires. An axiom of implant treatment is to provide the most predictable,
treatment that will satisfy the patient's anatomic needs and personal desires.
Patient should be educated on all viable treatment plans.

It is the clinician's obligation to educate the patient on the various treatment
plans that are possible. In edentulous cases, fixed vs. removable should be
explained. It is imperative that patients understand the advantages and
disadvantages of each of these treatment modalities. In this way, patient
expectation complications will be prevented. A good source of providing this
information is via presentation books, videos, and online information. The
education process should be documented and be part of the patient's
records.
Understand the differences between the types of prostheses.

To prevent treatment planning complications, the implant clinician must
understand there are three types of fixed prostheses and two types of
removable prostheses, as postulated by Misch in 1989. When evaluating fixed
prostheses, the three options may be used to replace one tooth or multiple
teeth and may be cemented or screw retained. These types of fixed
prostheses depend on the amount of hard and soft tissue structures replaced
and the aspects of the prosthesis in the esthetic zone. Common to all fixed
options is the inability of the patient to remove the implant prosthesis (Table
3.1 and Fig. 3.1).
TABLE 3.1
Prosthodontic Classification
Type Definition
FP-1 Fixed prosthesis; replac es only the c linic al c rown; looks like a natural tooth with ideal c ontours
FP-2 Fixed prosthesis; replac es the c linic al c rown and a portion of the root; c rown c ontour appears normal in the oc c lusal half but is
elongated or hyperc ontoured in the gingival half
FP-3 Fixed prosthesis; replac es missing c linic al c rown and gingival c olor and a portion of the edentulous site; most c ommon prosthesis is
zirc onia
RP-4 Removable prosthesis; overdenture supported c ompletely by implants (usually with a superstruc ture bar) that is c ompletely implant
supported with no soft tissue support
RP-5 Removable prosthesis; overdenture supported by both soft tissue (primary support) and implants, whic h may or may not have a
superstruc ture bar (sec ondary support)
FIG 3.1 Fixed restorations have three categories: FP-1, FP-2, and FP-3. The
restoration type is related to the contour of the restoration. (FP-1 is ideal, FP-2 is
hypercontoured, and FP-3 replaces the gingiva drape with pink porcelain or acrylic.)
The difference between FP-2 and FP-3 most often is related to the high maxillary lip
position during smiling or the mandibular lip position during sibilant sounds of
speech. FP-2 and FP-3 restorations often require more implant surface area support
by increasing implant number or size. (From Misch CE: Dental implant prosthetics, 2e, St
Louis, 2015, Mosby.)
Fixed Prostheses
FP-1
Definition.
An FP-1 is a fixed restoration and appears to the patient to replace only the
anatomic crowns of the missing natural teeth (clinical crown). To fabricate
this restoration type there must be minimal loss of hard and soft tissues. The
volume and position of the residual bone must permit ideal placement of the
implant in a location similar to the root of a natural tooth. The final
restoration appears very similar in size and contour to the clinical crown or
most traditional FPs used to restore or replace natural crowns on teeth (Figs.
3.2 and 3.3).
FIG 3.2 The Misch prosthesis classification is dictated by the amount of clinical
crown height, hard and soft tissue replacement. FP-1 replaces the ideal clinical
crown, FP-2 replaces the clinical crown + a hypercontoured replacement of the lost
hard and soft tissue, and FP-3 that replaces the clinical crown + significant hard and
soft tissue replacement (pink porcelain, acrylic, zirconia). (From Misch CE: Dental implant
prosthetics, 2e, St Louis, 2015, Mosby.)
FIG 3.3 FP-1 prosthesis. (A) Preoperative image of missing # 10 (maxillary left
lateral incisor); (B) Postoperative, depicting final prosthesis that is normal size to the
adjacent clinical crowns.
Implant Criteria.
The FP-1 prosthesis is most often desired in the maxillary anterior region,
especially in the esthetic zone during smiling. The final FP-1 restoration
appears to the patient to be similar to a crown on a natural tooth. However,
the implant abutment can rarely be treated exactly as a natural tooth
prepared for a full crown. The cervical diameter of a natural tooth is
approximately 6.5 to 10.5 mm with an oval-triangular cross-section. However,
the implant abutment is usually 4 to 5 mm in diameter and round in cross
section. In addition, the placement of the implant rarely corresponds exactly
to the crown–root position of the original tooth. For example, the thin labial
bone lying over the facial aspect of a maxillary anterior root remodels after
tooth loss, and the crest width shifts to the palate, decreasing 40% within the
first 2 years.
Complication.
The most common complication with a patient requesting a FP-1 prosthesis
is not recognizing preoperatively the limitations of the hard and soft tissue
anatomy. If the final implant position is nonideal, it will be almost
impossible to obtain a FP-1 prostheses without hard and soft tissue grafting.
Prevention.
The bone loss and lack of interdental soft tissue complicate the final esthetic
result, especially in the cervical region of the crowns. FP-1 prostheses are
especially difficult to achieve when more than two adjacent teeth are missing
because of the need for hard tissue augmentation, soft tissue augmentation,
and optimal implant positioning.
Hard tissue augmentation.

The width or height of the crestal bone is frequently insufficient after the loss
of multiple adjacent natural teeth, and bone augmentation is often required
before implant placement to achieve natural-looking crowns in the cervical
region.
Soft tissue augmentation.

Because there are no interdental papillae in edentulous ridges, soft tissue
augmentation is often required to improve the interproximal gingival
contour. Ignoring this crucial step will result in open “black” triangular
spaces (where papillae should usually be present) when the patient smiles.
Ideal implant positioning.

To obtain an FP-1 prostheses, the implant must be positioned ideally in the
mesial-distal, buccal-lingual, and apicocoronal planes. The center of the
osteotomy should be midway between the mesial-distal distance, provided
the available space is ideal for the tooth being replaced. In a buccal-lingual
position, the implant should be in a plane slightly lingual to the incisal edge
of the tooth being replaced. In the apicocoronal plane, the implant should be
approximately 3 mm apical to the free gingival margin of the adjacent teeth,
provided that the adjacent teeth have ideal hard and soft tissue anatomy.
FP-2
Definition.
An FP-2 fixed prosthesis restores the anatomic crown and a portion of the
root of the natural tooth and, therefore, is hypercontoured. The incisal edge
of the restoration is in the correct position, but the gingival third of the
crown is overextended, usually apical and lingual to the position of the
original tooth. These restorations are similar to natural teeth exhibiting
periodontal bone loss and gingival recession. In most situations an FP-2 is an
acceptable prosthesis for patients. However, in the esthetic zone or in a
patient with a high smile line, this may pose complication issues because the
prosthesis may be deemed unesthetic by the patient (Fig. 3.4).
FIG 3.4 (A) and (B), FP-2 Prosthesis showing a hypercontoured or elongated tooth
in comparison to the adjacent clinical crowns. (C), FP-2 prosthesis showing
associated complications of bone loss and loss of papilla from implant positioning
too deep or apical.
Implant Criteria.
The volume and topography of the available bone are more apical compared
with the ideal bone position of a natural root (1–2 mm below the cement-
enamel junction) and dictate a more apical implant placement compared
with the FP-1 prosthesis. This most commonly occurs because of implant
placement in Division B ridges, and because of the lack of bone width, the
final implant position will be too far apical in comparison to the adjacent
teeth.
Complication.
The most common complications that occur with a FP-2 prosthesis are a
result of not informing the patient of the hypercontouring of the final
prosthesis or the need for the use of pink porcelain. Especially in the
maxillary anterior region, this may pose an esthetic issue with the patient.
The use of pink porcelain also increases laboratory expenses.
Prevention
Patient communication.
The patient should be well informed prior to the initiation of treatment that
the final FP-2 prosthesis will appear longer than healthy natural teeth
(without bone loss). The patient should be shown photo images or diagrams
of an FP-2 prosthesis compared to an FP-1 prosthesis prior to treatment.
Additionally, the surgical informed consent should be modified to explain
and fully inform the patient of the overcontoured prostheses (FP-1 vs. FP-2)
(Fig. 3.5).
FIG 3.5 Consent form for FP-2 or FP-3 prosthesis.
Preoperative smile zone evaluation.
The esthetic zone of a patient is established during smiling in the maxillary
arch. The number of teeth displayed when a patient smiles is highly variable.
Less than 10% of the population limits their smile to the anterior six teeth.
Almost 50% of people show up to the first premolar and approximately 4% of
our patients display almost all the maxillary teeth during a smile.3 The low lip
position is ideally evaluated during sibilant sounds of speech (e.g.,
Mississippi, sixty-six). It is not unusual for patients to show fewer lower
anterior teeth during smiling, especially in younger patients. Older patients
are most likely to show the anterior teeth and gingiva during speech, with
men showing more than women. Likewise, if the high lip line during smiling
or the low lip line during speech does not display the cervical regions, the
longer teeth are usually of no esthetic consequence, provided that the patient
has been informed before treatment (Fig. 3.6).
FIG 3.6 High smile line. (A) Unfavorable smile line showing the entire clinical crown
and tissue. This type of smile may contraindicate implant placement because of
esthetic related issues. (B) Favorable smile line showing only one-half of the clinical
crown and no tissue. This type of smile line is ideal for an FP-2 or FP-3 prosthesis.
Ideal implant position.

A multiple-unit FP-2 restoration does not require as specific an implant
position in the mesial or distal position as does an FP-1 prosthesis. This is
because the cervical contour is not displayed during function. The implant
position may be chosen in relation to bone width, angulation, or hygienic
considerations rather than purely esthetic demands (compared with the FP-1
prosthesis). On occasion, because of available bone, the implant may even be
placed in an embrasure between the two teeth. This often occurs when
replacing mandibular anterior teeth with a full-arch fixed restoration. If this
occurs, the incisal two thirds of the two crowns should be ideal in width, as
though the implants were not present. Only the cervical region is
compromised (i.e., this is most likely out of the esthetic zone). Although the
implant is not positioned in an ideal mesiodistal position, it should be placed
in the correct facial-lingual position to ensure that contour, hygiene, and
direction of forces are not compromised.
FP-3
Definition.
The FP-3 fixed restoration appears to replace the natural teeth crowns and
has pink-colored restorative material (acrylic or pink porcelain) to replace a
portion of the soft tissue, especially the interdental papillae. This is most
commonly indicated when severe bone resorption has occurred.
Implant Criteria.
As with the FP-2 prosthesis, the original available bone height has decreased
by natural resorption or osteoplasty at the time of implant placement. To
place the incisal edge of the teeth in ideal position for esthetics, function, lip
support, and speech, the excessive vertical dimension to be restored requires
teeth that are unnatural in length. The soft and hard tissue loss requires
replacement with pink porcelain or acrylic (Fig. 3.7).
FIG 3.7 A splinted image of #8-#9 implants with pink porcelain. An FP-2 or FP-3
may not be indicated when a high smile line exists.
Complication.
The main complication associated with an FP-3 prosthesis is patient
acceptance because of the hypercontoured crowns (i.e., pink porcelain or
acrylic). Additionally, the clinician must be aware of the added laboratory
costs associated with an FP-3 prosthesis. Most laboratories will charge a
significantly higher fee for the application of pink porcelain. However, the
clinician should be aware there exist various shades of pink porcelain. It is
recommended that the color of the tissue be evaluated similar to tooth shade.
Many pink shade guides are available for use in implant dentistry today (Fig.
3.8).
FIG 3.8 Pink tissue shading. (A) Pink shade guides. (B) Examples of pink porcelain
and pink stained zirconia.
Prevention
The patient should be well informed prior to any treatment that the final FP-
3 prosthetic teeth will appear longer and also have pink restorative material
associated with the prosthesis to replace the loss of hard and soft tissue.
Photos or examples of the pink prosthesis should be shown to the patient.
Understanding of smile zone variations.

The ideal high smile line (i.e., not showing excessive soft tissue) occurs in
almost 70% of the population. The maxillary lip displays the interdental
papilla of the maxillary anterior teeth, but not the soft tissue above the mid
cervical regions. A high smile or “gummy” smile will usually display the
interdental papillae and at least some of the gingival tissues above the free
gingival margin of the teeth. Patients in both of these categories of high lip
line should have the soft tissue replaced by either the prostheses or
augmentation. Additionally, the appearance of the mandibular teeth may be
evaluated during sibilant sounds (Fig. 3.9).
FIG 3.9 The appearance of the lower anterior teeth is primarily evaluated during
sibilant sounds of speech, and older patients show more teeth than younger
patients. (From Misch CE: Dental implant prosthetics, 2e, St Louis, 2015, Mosby.)
Color of the pink tissue.

Because the color characteristics of patient's gingiva vary greatly, the implant
clinician should use a laboratory that has the capability to use a pink
porcelain shade guide to match the tissue. However, patients should be
informed of the tissue color changes that occur over time.
Understand the two types of FP-3 prostheses.

There are basically two approaches for an FP-3 prosthesis. (1) A hybrid
restoration of denture teeth and acrylic with a metal substructure. The
complications associated with this type of prosthesis are excessive wearing of
the denture tooth or debonding from the prosthesis. (2) A porcelain–
metal/zirconia restoration. An FP-3 porcelain-to-metal/zirconia restoration is
more difficult to fabricate for the laboratory technician than an FP-2
prosthesis. The pink porcelain is more difficult to appear as soft tissue and
usually requires more porcelain firing cycles. This increases the risk of
potential porosity or porcelain fracture (Fig. 3.10).
FIG 3.10 FP-3 prostheses. (A) acrylic/denture tooth construction; (B) pink
porcelain; (C) pink zirconia.
Spacing of multiple implants.

For edentulous arches or larger spaces, implants should be placed a
minimum of 3 millimeters apart. If they are less than 3 millimeters apart,
difficulty with hygiene will result along with the possibility that bone loss on
one will extend to the other, compromising both implants.
Tissue space.
In the maxillary arch, wide open embrasures between the implants may
cause food impaction or speech problems. These complications may be
solved by using a removable soft tissue replacement mask or make the
overcontoured cervical restorations. The maxillary FP-3 prosthesis is often
extended or juxtaposed to the maxillary soft tissue so that speech is not
impaired. However, this results in hygiene issues, which place the prostheses
at risk. The mandibular FP-3 restorations may be left above the tissue, similar
to a sanitary pontic. This facilitates oral hygiene in the mandible, especially
when the implant is exposed through the soft tissue drape and is not visible
during speech. However, if the space below the restoration is too great, the
lower lip may lack support in the labio-mental region.
Removable Prostheses
When treatment planning, the patient's prosthetic requirements should be
fully understood and an evaluation of the patient's anatomy is a priority. The
most common removable implant prostheses are overdentures for
completely edentulous patients. Complete removable overdentures have
been reported with predictability and a high success rate for many decades;
however, there is much confusion concerning this type of prosthesis because
of the inherent variations.4,5 Most often, patients do not understand the
associated movement with overdentures (i.e., dependent on number of
implants, attachments, A-P spread, posterior ridge form) because they don't
understand the associated biomechanical factors with an overdenture
prosthesis. The complications that may a occur may be significant.
There exist two types of removable prostheses that are based on support,
retention, and stability of the restoration. Patients are able to remove the
restoration but not the implant-supported superstructure or attachments to
the abutments. The difference in the two categories of removable
restorations are not in appearance (as it is in the fixed categories). Instead,
the two removable categories are primarily determined by the amount of
implant and soft tissue support (Fig. 3.11).
FIG 3.11 Removable restorations have two categories based on implant support.
RP-4 prostheses have complete implant support in both the anterior and posterior
regions. In the mandible, the superstructure bar often is cantilevered from implants
positioned between the foramina. The maxillary RP-4 prosthesis usually has more
implants and no cantilever (usually no palate present). An RP-5 restoration has
primarily anterior implant support and posterior soft tissue support in the maxilla or
mandible. Often fewer implants are required, and bone grafting is less
indicated. (From Misch CE: Dental implant prosthetics, 2e, St Louis, 2015, Mosby.)
RP-4
Definition.
An RP-4 removable prosthesis is completely supported by implants with no
soft tissue support. The RP-4 prosthesis is primarily a totally implant-
supported prosthesis. The restoration is rigid when inserted, and the
overdenture attachments usually connect the RP to single implant
attachments or a low-profile tissue bar with attachments (Fig. 3.12).
FIG 3.12 (A) RP-4—totally implant-supported prosthesis with no soft tissue
support, note the lack of peripheral seal. (B) RP-5 prosthesis—soft tissue–
supported with secondary implant support and peripheral seal.
Implant Criteria.
The implant placement criteria for an RP-4 prosthesis are different than that
for an FP prosthesis. Denture teeth and acrylic require more prosthetic space
for the removable restoration in comparison to a fixed prosthesis. The
implants in an RP-4 prosthesis (and an FP-2 or FP-3 restoration) should be
placed in the mesiodistal position for the best biomechanical and hygienic
situation. Usually, in the mandible, implants are inserted between the two
mental foramens in the A, B, C, D, and E positions.
Complication.
The most common complication occurring with a RP-4 prosthesis is lack of
adequate implant support (e.g., insufficient number of implants) and food
impaction. In the mandibular RP-4 prosthesis, because there exists no
peripheral seal, often food becomes impacted underneath the prosthesis.
Prevention
The patient should have a thorough understanding of the differences
between a RP-4 and a RP-5 prosthesis. There exist distinct differences
between RP-4 and RP-5 prosthesis with respect to number of implants, type
of support, and prosthesis movement.
Treatment denture.
A preimplant treatment denture may be fabricated to evaluate the occlusal
vertical dimension and ensure the patient's esthetic satisfaction. This
technique is especially indicated for patients with demanding needs and
desires regarding the final esthetic result or with severely reduced vertical
dimensions with their present prosthesis. The implant dentist may also use
the treatment denture as a surgical guide for implant placement and for use
during the healing stage. After the implants are uncovered, the
superstructure or prosthetic design is fabricated within the guidelines of the
existing treatment restoration.
Implant position.
The positioning of implants for an RP-4 overdenture is critical to the
successful outcome of the prosthesis. For example, a Hader clip requires the
mesiodistal implant spacing to be greater than 6 mm from edge to edge of
the implant bodies. Because of this space requirement, the number of
implants is reduced, especially if placed between the interforaminal space of
the mandible. Additionally, in the apicocoronal dimension, adequate
interocclusal space is needed to allow for at least 2 mm of acrylic to retain the
denture teeth with overdentures; approximately 15 mm is needed from the
crest of the bone to the incisal edge.
Implant number.
For a totally implant-supported prosthesis (RP-4), four to five implants are
required in the mandible and six to eight implants in the maxilla. Fewer
implants being utilized to support a RP-4 prosthesis will result in possible
overloading of the prosthesis and/or implants leading to complications.
RP-5
Definition.
RP-5 is a removable prosthesis combining implant and soft tissue support.
Predominately, the soft tissue is the primary support (primary stress-bearing
areas) and implants are used for secondary support. The advantage of an RP-
5 restoration is the reduced cost because fewer implants may be inserted
compared with a RP-4 or fixed restoration. Additionally, there is less demand
for bone augmentation, which decreases cost.
Implant Criteria.
Implants in the mandible are inserted within the mandibular interforaminal
space with two, three, or four implants. These correspond to the Overdenture
Treatment Planning options (e.g., OD-1–OD-5). In the maxilla, usually four to
six implants are recommended depending upon force factors.
Complication.
The most common complication occurring with an RP-5 prosthesis is the
associated movement. A common misconception of patients is they believe
that implants, independent of the number, should have no associated
movement. Because an RP-5 relies on the soft tissue for support, there will be
inherent movement within the prosthesis. Additionally, with an RP-5
prosthesis, because of the primary implant support, soft tissue pressure is
present, which may cause sore spots. If a patient's initial complaint is chronic
posterior sore spots, an RP-5 is not the best prosthetic option.
Prevention
The patient should have a thorough understanding of the differences
between an RP-4 and an RP-5 prosthesis. A common problem with an RP-5
prosthesis is the possible associated movement, which some patients may
not tolerate or expect. A preoperative explanation must allow the patient a
full understanding of the advantages and disadvantages of the two types of
prostheses. A common analogy is the use of a chair. A two-implant
overdenture is similar to a chair with only two legs. The chair may be
stabilized; however, it can easily be moved. A three-implant overdenture is
similar to a three-legged chair because it is more stable than two-implant
overdenture; however, it will still have some degree of movement. A four- to
five-implant overdenture is similar to a four-legged chair, which is associated
with minimal movement (Fig. 3.13).
FIG 3.13 Overdenture type analogy; (A) Two-legged chair (2-implants) will rotate
anterior and posterior, (B) Three-legged chair (3-implants) which is more stable than
2-implants, however still has movement, (C) Four-legged chair (4-5 implants) is the
most stable with no movement.
Treatment denture.
A preimplant treatment denture may be fabricated to determine position and
prosthesis thickness. However, this is usually less important than in a RP-4
type prosthesis.
Posterior ridge form.

If the patient has a poor posterior ridge form (mandible), especially in the
posterior area, an RP-5 prosthesis might not be the ideal treatment option. In
these cases, patient education and consent is mandatory so they fully
understand the limitations of this type of prosthesis.
Implant position.
The positioning of implants for an RP-5 overdenture is critical to the
successful outcome of the prosthesis. When a bar is not going to be utilized,
great care should be exercised to make sure that adequate spacing between
the implants is present. Lack of space between implants (<3 mm), will result
in prosthetic attachment complications. Additionally, the implants should be
placed at approximately the same height and as parallel as possible to
prevent path of insertion complications.
Implant number.
For a totally implant-supported prosthesis, a minimum of two to four
implants is required in the mandible and four to six implants in the maxilla.
Fewer implants will result in additional mobility of the prosthesis or occlusal
overloading.
Continuous residual ridge bone loss.

The clinician and the patient should realize that the residual bone will
continue to resorb in the soft tissue–borne regions of the prosthesis. Relines
and occlusal adjustments every few years are common maintenance
requirements of an RP-5 restoration. Bone resorption in the posterior regions
with RP-5 restorations may occur two to three times faster than the
resorption found with full dentures.6 This may be a determining a factor
when considering this type of treatment in younger patients despite the
decreased cost and lower failure rate (Fig. 3.14).
FIG 3.14 Mandibular RP-4/RP-5 prosthesis treatment plans. (A) RP-4; 5 implants
between the mandibular foramen regions. (B) RP-5; 2 implants. (C) RP-5; 3
implants. (D) RP-5; 4 implants.
Divisions of Available Bone
Quantity of Available Bone
After the type of prosthesis is determined, the available bone for implant
placement is evaluated to determine the surgical approach necessary (i.e.,
bone augmentation, implant insertion, or both) to support the intended
prosthesis. The available bone concept describes the amount of bone in the
edentulous area considered for implantation. Available bone is measured in
width, height, length, and angulation and crown height space (CHS) in
relation to the remaining bone (Fig. 3.15). If the bone is inadequate to
predictably support an implant, a bone graft is considered in the ideal site(s),
or alternative sites may be considered when additional implant numbers are
necessary.
FIG 3.15 Available bone is measured in height (H), width (W), and length (L). Also
considered are crown height space and angulation of bone (which is related to the
direction of force to the implant body). (From Misch CE: Dental implant prosthetics, 2e, St
Not Understanding the Parameters of the Available Bone

To avoid complications in assessing the available bone present, the implant
clinician must understand the correct parameters in determining the bone
height, width, and length.
Available Bone Height.

The available bone height is first determined by radiographic evaluation
(preferably cone beam computed tomography [CBCT]) in the edentulous
region by measuring from the crest of the edentulous ridge to the opposing
anatomic landmark. The anterior regions of the jaws have the greatest height
due to the pneumatization of the maxillary sinus and the inferior alveolar
nerve limits this dimension in the mandibular posterior regions. The
maxillary canine eminence region, just lateral to the lateral piriform rim of
the nose, often offers the greatest height of available bone in the maxillary
anterior (Fig. 3.16).7
FIG 3.16 The height of available bone is measured from the crest of the edentulous
ridge to the opposing landmark. The opposing landmark may be in the maxillary
canine region (A), floor of the nares (B), maxillary sinus (C), tuberosity (D),
mandibular canine region (G), anterior mandible (F), or bone above the inferior
mandibular canal (E). (From Misch CE: Dental implant prosthetics, 2e, St Louis, 2015, Mosby.)
As a general rule, the anterior mandible has the greatest bone height.
There is more bone apical to the mandibular anterior teeth than any other
region. Even after the resorption of the residual ridge after tooth loss, there is
usually adequate bone to insert dental implants (Fig. 3.17). However, the
crown height of the prosthesis may be extensive (e.g., FP-2, FP-3) because of
the loss of bone. This region often has the most available bone but also may
have the greatest crown height space.
FIG 3.17 The anterior mandible has the greatest bone height of any region of the
jaws. However, because of the variable osseous angulation in the anterior mandible,
the implant often engages the lingual plate of bone.
The anterior bone region in the mandible extends between the right and
left mental foramens. The mental foramen is most often found in close
proximity to the two premolars. The anterior region of bone extends beyond
the canines and to the first premolar region most often. The initial
mandibular bone height is influenced by skeletal anatomy, with Angle Class
II patients having shorter mandibular height and Angle Class III patients
exhibiting the greatest height.
The opposing landmarks for both the maxilla and mandible of the initial
available bone height are more limiting in the posterior regions distal to the
first premolar. In the maxillary posterior jaw region, there is usually greater
bone height in the first premolar than in the second premolar, which has
greater height than the molar sites because of the concave morphology of the
maxillary sinus floor. As a consequence, the existing bone anatomy of the
implant patient often requires modification (e.g., sinus augmentation) to
enhance long-term implant success (Fig. 3.21).
FIG 3.21 Available bone length. (A) Evaluation of available bone length between two
teeth is most accurately determined with axial views. (B) In determining available
bone length, a minimum of 3 mm is required for hard and soft tissue health.
The posterior height of bone in the mandibular region is reduced because

of the presence of the mandibular canal, situated approximately 12 mm
above the inferior border of the mandible (Fig. 3.18). Generally, less available
bone is present in the higher force areas of the posterior mandible and
maxilla; however, many treatment plans include shorter and fewer number of
implants. Oikarinen et al found that more than 6 mm of bone height is found
in less than 50% of posterior mandibles and 40% of posterior maxillae in
partially edentulous patients.8
FIG 3.18 The posterior mandible has less bone height because the variable
position of the inferior alveolar canal which dictates the size and positioning of the
implant.
In the literature, the suggested minimum bone height for predictable long-
term endosteal implant survival approaches 12 mm. Failure rates reported in
the literature for implants shorter than 9 mm tend to be higher, independent
of the manufacturer design, surface characteristic, and type of application.9,10
The available bone height in an edentulous site is the most important
dimension for implant consideration because it affects both implant length
and associated crown height. Crown height space directly affects force factors
and esthetics. In addition, bone augmentation is more predictable in width
than height, so even when the width is inadequate for implant placement,
bone grafting may be used to create a site ideal for restorative and implant
insertion requirements.
Available Bone Width.

The width of available bone is measured between the facial and lingual plates
at the crest of the potential implant site. The crestal aspect of the residual
ridge in the mandible is often cortical in nature and exhibits greater density
than the underlying trabecular bone regions. This mechanical advantage
permits immediate fixation of the implant, provided this cortical layer has
not been removed by osteoplasty.
The crest of the edentulous ridge is most often supported by a wider base
in the anterior mandible. In most mandibular situations, because of this
triangular cross-section, an osteoplasty provides greater width of bone,
although of reduced height (Fig. 3.19).
FIG 3.19 (A) The anterior mandible usually has a wider base than the crest of the
ridge and often forms a triangular-shaped cross-section. (B) An osteoplasty to the
narrow ridge in the anterior mandible increases the width of crestal bone (and
reduces the available bone height). (From Misch CE: Dental implant prosthetics, ed 2, St
It should be noted that crest reduction (osteoplasty) affects the location of

the opposing landmark, with possible surgical consequences, including
implant size selection, implant position, and final prosthesis design. This is
particularly important when a FP-1 prosthesis is planned, with the goal of
obtaining a normal contour and proper soft tissue drape around a single
tooth replacement.
Unlike the anterior mandible, the anterior maxilla often does not follow
the triangular anatomy. The palatal plate of bone is more parallel to the facial
plate in the maxilla (Fig. 3.20). In addition, many edentulous ridges exhibit a
labial concavity in the incisor area, with an hourglass configuration. As a
result, osteoplasty does not increase the width of bone as much as in the
mandible. As a consequence, bone augmentation for width is more often
indicated in the maxilla.
FIG 3.20 The anterior maxilla most often has the palatal wall of bone parallel to the
facial cortical plate. Osteoplasty is less effective to increase the bone width.
Augmentation procedures are most often warranted. (From Misch CE: Dental implant
prosthetics, ed 2, St Louis, 2015, Mosby.)
After adequate height is available, the next most significant factor affecting
the long-term survival of endosteal implants is the width of the available
bone. Root form implants with crestal diameters of 4 mm usually require
more than 6 mm of bone width to ensure sufficient bone thickness and blood
supply around the implant for predictable survival. This dimension provides
more than 1 mm of bone on each side of the implant at the crest. Because the
bone usually widens apically in the mandible, this minimum dimension
rapidly increases. For root form implants, the minimum bone thickness is
located in the midfacial and midlingual contours of the crestal region
exclusively (Fig. 3.21).
Available Bone Length.

The mesiodistal length of available bone in an edentulous area is often
limited by adjacent teeth or implants. As a general rule, the implant should
be at least 1.5 to 2.0 mm from an adjacent tooth and 3 mm from an adjacent
implant. This dimension not only allows minor surgical error but also
compensates for the width of an implant or tooth that acquires a crestal
defect, which is usually less than 1.4 mm. As a result, if bone loss occurs at
the crest module of an implant or from periodontal disease with a tooth, the
vertical bone defect will not spread to a horizontal defect and cause bone loss
on the adjacent structure.11 In the case of a single-tooth replacement, the
minimum length of available bone necessary for an endosteal implant
depends on the width of the implant. For example, a 5-mm–diameter implant
should have at least 8 mm of mesiodistal bone, so 1.5 mm is present on each
side of the implant. A minimum mesiodistal length of 7 mm is usually
sufficient for a 4-mm–diameter implant.
The diameter of the implant is also related to the width of available bone
and, in multiple adjacent sites, is primarily limited in this dimension. For
example, a width of bone of 4.5 mm without augmentation requires a 3.5-mm
or smaller implant, with inherent compromises (e.g., less surface area and
greater crestal stress concentration under occlusal loads on abutment screw
and marginal bone). In narrow ridges, it is often indicated to place two or
more adjacent narrow-diameter implants (when possible) to obtain sufficient
implant–bone surface area to compensate for the deficiency in width of the
implant. Because the implants should be 3 mm apart and 1.5 to 2.0 mm from
each tooth, 13 mm or more in available bone mesiodistal length may be
required when the narrower implant dimensions are used to replace a
posterior tooth.
The ideal implant mesiodistal width for single-tooth replacement is often
related to the natural tooth being replaced in the site. The tooth has its
greatest width at the interproximal contacts, is narrower at the
cementoenamel junction (CEJ), and becomes even narrower at the initial
crestal bone contact, which is 2 mm below the CEJ.12 The ideal implant
diameter corresponds to the width of the natural tooth, which may be
measured 2 mm below the CEJ of the adjacent tooth. In this way the implant
crown emergence (emergence profile) through the soft tissue may be similar
to that of a natural tooth. For example, a maxillary first premolar is
approximately 8 mm at the interproximal contact, 5 mm at the CEJ, and 4 mm
at a point 2 mm below the CEJ. A 4-mm–diameter implant (at the crest
module) would be the ideal if it is positioned at least 1.5 mm from the
adjacent roots (2 mm below the CEJ).
Available Bone Angulation.

Bone angulation is the fourth determinant for the evaluation of available
bone. The alveolar bone angulation represents the natural tooth root
trajectory in relation to the occlusal plane. Ideally, this angulation is
perpendicular to the plane of occlusion, which is aligned with the forces of
occlusion and is parallel to the long axis of the prosthodontic restoration. The
incisal and occlusal surfaces of the teeth follow the curve of Wilson and curve
of Spee. As such, the roots of the maxillary teeth are angled toward a
common point. The mandibular roots flare, so the anatomic crowns are more
lingually inclined in the posterior regions and labially inclined in the anterior
area compared with the underlying roots. The first premolar cusp tip is
usually vertical to its root apex.
The maxillary anterior teeth are the only segment in either arch that does
not receive a long-axis load to the tooth roots but instead are usually loaded
at an approximate 12-degree angle. As such, their root diameter is greater
than the mandibular anterior teeth. In all other regions of the mouth, the
teeth are loaded perpendicular to the curves of Wilson and Spee.
Rarely does the bone angulation remain ideal after the loss of teeth,
especially in the anterior edentulous arch. In this region, labial undercuts
and resorption after tooth loss often mandate greater angulation of the
implants or correction of the site before insertion (osseous augmentation).
For example, in the anterior mandible, the implant insertion often engages
the lingual cortical plate, rather than the inferior border of the mandible, as a
consequence of the position of the incisal edge and the angulation of bone.
In the posterior mandible, the submandibular fossa mandates implant
placement with increasing angulation as it distally progresses. Therefore, in
the second premolar region the angulation may be 10 degrees to a horizontal
plane; in the first molar areas, 15 degrees; and in the second molar region, 20
to 25 degrees.
The limiting factor of angulation of force between the body and the
abutment of an implant is the width of bone. In edentulous areas with a wide
ridge, wider root form implants may be utilized. Implants may allow up to 30
degrees of divergence with the adjacent implants, natural teeth, or axial
forces of occlusion with minimum compromise. However, angled loads to an
implant body increases the crestal stresses to the implant components and
bone, but the greater-diameter implant decreases the amount of stress
transmitted to these structures. In addition, the greater width of bone offers
some latitude in angulation at implant placement. The implant body may
often be inserted so as to reduce the divergence of the abutments without
compromising the permucosal site.
An acceptable bone angulation in the wider ridge may be as much as 30
degrees. The narrow yet adequate width ridge often requires a narrower
design root form implant. Compared with larger diameters, smaller-diameter
designs result in greater crestal stress to the system (abutment screws,
crestal bone) and may not offer the same range of custom abutments. In
addition, the narrower width of bone does not permit as much latitude in
placement regarding angulation within the bone. This limits the acceptable
angulation of bone in the narrow ridge to 20 degrees from the axis of the
adjacent clinical crowns or a line perpendicular to the occlusal plane (Fig.
3.22).
FIG 3.22 As bone resorbs from the buccal, the mandible will become more angled
toward the lingual, resulting in an angulation complication for implant placement.
Crown Height Space.

The crown height space (CHS) is defined as the vertical distance from the
crest of the ridge to the occlusal plane. It affects the appearance of the final
prosthesis and may affect the amount of movement force on the implant and
surrounding crestal bone during occlusal loading. Esthetically, the prosthesis
is less likely to replace the sole anatomic crowns of natural teeth when a
greater CHS is present.
The CHS may be considered a vertical cantilever. Any direction of load that
is not in the long axis of the implant will magnify the crestal stresses to the
implant-bone interface and to the abutment screws in the restoration. The
greater the CHS, the greater the moment force or lever arm with any lateral
force or cantilever (Fig. 3.23).
FIG 3.23 Crown height space. (A) Lateral CBCT view of maxilla and mandibular
edentulous areas in relation to the incisal edge. The incisal edge does not change
position; however, as bone loss advances, the CHS increases leading to greater
potential for force-related complications. (B) Ideal crown height space varies with
respect to the intended prosthesis (i.e., FP-3, RP-4, RP-5).
The absence of a periimplant ligament means that the bone-implant

stresses cannot be reduced by increasing the implant height. Therefore, as
the CHS increases and a cantilever or a lateral load is planned on the
restoration, a greater number of implants or wider implants should be
inserted to counteract the increase in stress. For an ideal treatment plan, the
CHS should be equal to or less than 15 mm under ideal conditions.
Not Understanding the Divisions of Bone: Division A

(Abundant Bone)
The Division A edentulous ridge exhibits abundant bone in all dimensions of
height, width, and length. Division A root form implants are optimal and
most often used as independent support for a fixed or removable prosthesis.
Division A bone is the ideal type of bone to provide a natural looking FP-1
prosthesis.
Criteria Division.
Division A bone corresponds to abundant available bone in all dimensions;
the height of 12 mm or more, width of >6 mm, angulation <30 mm, and crown
height space of <15 mm. Osteoplasty may often be performed to obtain
additional bone width in the mandible when a larger diameter implant is
desired. In rare instances, an angle abutment will be required; however, the
direction of load is not excessive (Box 3.1).
Box 3.1
Division A Bone Dimensions
Width >6 mm
Height >12 mm
Mesiodistal length >7 mm
Angulation of occlusal load (between occlusal plane and implant body) <30
degrees
Crown height space ≤15 mm
(From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Surgical Treatment.
The implant choice in Division A bone is a Division A root form that is 4 mm
or greater in diameter and 12 mm or longer in height (length). A larger-
diameter implant is suggested in the molar regions (5 to 6 mm in diameter).
Longer implants are suggested in immediate loading treatment options or
when an implant is immediately inserted after the extraction of the tooth. As
a general rule, Division A bone should not be treated with smaller-diameter
implants for the final prosthesis, unless dictated by the specific tooth
replacement (e.g., maxillary lateral incisors or mandibular incisors) (Fig.
3.24). There are several advantages to the use of implants equal to or greater
than 4 mm in diameter compared with smaller-diameter implants (Box 3.2).
FIG 3.24 (A) Division A bone. (B) Treatment plan includes placement of
conventional size implant.
Box 3.2
Division A Root Form Implant Advantages
• The larger the diameter of an implant, the greater the surface area and the
less stress distributed through the crestal bone region.
• The larger-diameter implants are closer to the lateral cortical plates of

bone, which have greater density and increased strength, modulus of
elasticity, and bone-implant contact percentages.
• The larger-diameter implants are less likely to fracture because the

strength of the material is increased by a power of four related to the
radius of the implant (e.g., a 4-mm-diameter implant is 16 times stronger
than a 2-mm-diameter implant).
• The smaller-diameter implants are often one-piece implants to decrease the

risk of fracture.
• The one-piece implants require an immediate restoration rather than a

submerged or one-stage approach. As such, micromovement may occur at
the bone-implant interface, with an increased risk of crestal bone loss and
implant failure.
• The emergence profile angle of the crown is related to the implant

diameter. The larger-diameter teeth can be most esthetically restored with
a wider-diameter implant.
• The larger the implant diameter, the less stress applied to the abutment
screw, and complications such as screw loosening or fracture are less likely.
• The larger-diameter abutment provides greater cement retention for the

final restoration crown.
• Oral hygiene procedures are more compromised around smaller-diameter

implants restored with greater emergence profile angles and over
contoured restorations.
• The crest module and crestal portion of many two-piece, smaller-diameter

implants are smooth metal to increase the interbody wall thickness, thus
creating shear loads to the crestal bone and an increased risk of bone loss.
• Implant costs to the patient are related to implant number, not diameter.
Increases in implant numbers for smaller-diameter implants increase the
cost to the patient (and clinician).
• Division A root form implants can provide the greatest range of prosthetic
options.
Prosthetic Treatment
Fixed.
FP-1 restorations require a Division A ridge. However, a FP-2 prosthesis most
often also requires a Division A bone. A FP-2 restoration is the most common
posterior restoration supported by multiple adjacent implants in partially
edentulous patients because of either bone loss or osteoplasty prior to
implant placement. A FP-3 prosthesis is most often the option selected in the
anterior Division A bone when multiple adjacent teeth are missing and the
maxillary smiling lip position is high, or a mandibular low lip line during
speech exposes regions beyond the natural anatomical crown position.
Removable.
For removable implant overdentures in Division A bone, the final position of
the tooth and superstructure bar must be evaluated before surgery. A limited
CHS is more common in Division A bone, and an RP-4 or RP-5 restoration
may require osteoplasty before implant placement. Division A bone may
represent a contraindication for high-profile O-ring attachments or
superstructures placed several millimeters above the tissue. This may result
in difficulty in prosthesis fabrication, esthetics, hygiene, adequate strength of
the prosthesis.
Complications.
Complications with Division A bone are minimal. The most common
complication is not assessing the crown height space, which may impinge on
the prosthetic rehabilitation. Many clinicians fail to educate the patient about
the rapid decrease in bone volume width and the consequences of delaying
treatment. When the bone volume is Division A, there is a decrease in
treatment costs, with a reduction in the number and complexity of surgeries
to the edentulous area (Fig. 3.25).
FIG 3.25 The resorption of bone in the maxilla results in the ridge becoming more
narrow because it resorbs toward the midline. The initial mandibular bone loss also
resorbs toward the midline. However, moderate to severe bone loss conditions
result when the mandible is wider than the original mandibular crest. (From Misch CE:
Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Not Understanding the Divisions of Bone: Division B (Barely
Sufficient Bone)
The decreased width and surface area usually require additional implants to
be included in the final prosthesis design. Division B may be changed to
Division A by augmentation or osteoplasty. The treatment options may be
selected in light of the area to be treated. For example, in the anterior maxilla,
augmentation is most often selected because of esthetics. In the anterior
mandible, osteoplasty is common because of the available bone height and
low esthetic concerns. In the posterior mandible, multiple Division B
implants may be used when the bone density is favorable, the available bone
height is limited, and esthetics are not a primary factor. When stress factors
are a concern, bone augmentation precedes Division B root form implants
regardless of the anatomic location (Box 3.3).
Box 3.3
Division B Dimensions
2.5–6 mm wide
B+: 4–6 mm
B−w: 2.5–4 mm
Height >12 mm
Mesiodistal length >6 mm
Angulation <20 degrees
Crown height space <15 mm
As the bone resorbs, the width of available bone first decreases at the
expense of the facial cortical plate because the cortical bone is thicker on the
lingual aspect of the alveolar bone, especially in the anterior regions of the
jaws. This may result in a 25% decrease in bone width the first year and a
40% decrease in bone width within the first 1 to 3 years after tooth
extraction.13 The resulting narrower ridge is often inadequate for most 4-mm-
diameter root form implants (Box 3.4).
Box 3.4
Disadvantages of Division B Root Forms
1. Almost twice the stress is concentrated at the top crestal region around the
implant.
2. Reduced overall surface area results in increased lateral loads causing

three times greater stress on the implant in comparison to Division A root
form implants. This means the lateral loads on the implant are tripled.
3. Fatigue fractures of the implant, abutment, and abutment screw post are
increased, especially under lateral loads.
• The crown emergence profile is less esthetic (except for

maxillary lateral or mandibular incisors).
4. Periodontal conditions for daily care are compromised around the cervical
aspect of the crown.
5. The implant design is most often poor in the crestal region. To increase
implant body wall thickness and to reduce fracture, no threads or
compressive force design are present; however, this further increases stress
and the amount of shear loads to bone.
6. The angle of load must be reduced to less than 20 degrees to compensate

for the small diameter biomechanical disadvantage.
7. Two implants are often required for proper prosthetic support unless
anterior single-tooth replacement for maxillary laterals or mandibular
incisors, thus surface area will be greater because of implant number, not
diameter.
8. Implant costs are not related to diameter, so an increase in implant

number results in greater cost to the doctor and patient.
Complications
Division B root forms.
Division B bone offers sufficient available bone height with compromised
bone width. The Division B available bone width may be further classified
into ridges 4 to 6 mm wide and B minus width (B−w) 2.5 to 4 mm wide, where
bone grafting is indicated most likely (Fig. 3.26). Because the ridge width and
implant diameter are narrower, and forces increase as the angle of load
increases, the angulation of occlusal load is also less and should be ideally
within 20 degrees from the axis of the adjacent teeth or occlusal plane. A CHS
of 15 mm or less (similar to Division A) is necessary in Division B to decrease
the moment of forces with lateral or offset loads, especially because of the
smaller width dimension.
FIG 3.26 In 1985 Misch and Judy presented a classification of available bone
(Divisions A, B, C, D), which is similar in both arches. Implant, bone-grafting
methods, and prosthodontic-related treatment was suggested for each category of
bone. A, Abundant; B, barely sufficient; C, compromised; D, deficient; h, inadequate
height; w, inadequate width. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Not understanding the need for modification.
Three treatment options are available for the Division B edentulous ridge:
1. Modify the existing Division B ridge to Division A by osteoplasty to permit

the placement of root form implants 4 mm or greater in width. When more
than 12 mm of bone height remains after osteoplasty, the Division B bone
is converted to Division A. When less than 12 mm of bone height remains
after osteoplasty, a biomechanical disadvantage results due to the ridge
being changed to a Division C−h (Fig. 3.27).
FIG 3.27 Changing Division B to Division A. (A) Because of the resorptive process,
compromise in width occurs rather quickly. (B) Conversion to Division A via
osteoplasty in the anterior mandible acquiring a minimum of 6 mm of width for
placement of a 4 mm diameter implant.
2. The second treatment option is the placement of a narrow diameter

implant (3–4 mm diameter and 12 mm or more in length; Fig. 3.28).
Smaller-diameter root form implants (3.0–3.5 mm) are designed primarily
for Division B available bone. Because Division B bone is compromised in
width, there exists less margin of error in the ideal placement. The Division
B root form implants present several inherent disadvantages compared
with the larger-diameter implants.14 As a result of these concerns for the
Division B root form, this option is most often used for single-tooth
replacement of a maxillary lateral incisor or mandibular incisors, where the
restricted available bone is in mesiodistal width, or with multiple implants
in the posterior mandible, where bone density is good and esthetic
requirements are limited.
FIG 3.28 Options to treat a Division B ridge in the anterior mandible include a
narrow implant with a final prosthesis closer to anatomic dimensions (FP-1) (left), or
osteoplasty with Division A root forms and extended crown heights (FP-2 or FP-3)
(right). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
3. The third alternative treatment for Division B bone is to change the

Division B ridge into a Division A by grafting the edentulous ridge with
autogenous bone or allogenic bone (Fig. 3.29). A disadvantage of this
treatment plan includes the need for adequate bone healing. The
emergence profile angle of the final crown, which does not compromise
hygiene, requires a Division A root form implant (with the exception of
maxillary lateral incisors or mandibular incisors). Stress factors may also
dictate the augmentation approach to Division B bone in order to utilize
larger-diameter implants. In the presence of unfavorable stress factors, the
number and width of abutments should be increased without increasing
the CHS to provide a greater surface area of resistance to the magnified
forces, which most likely will require augmentation. To accomplish this
goal, augmentation is most ideal in Division B bone.
FIG 3.29 Ideal Division B option. A Division B bone may be modified to Division A
by doing a bone augmentation. This treatment option is most often required for a FP-
1 prosthesis. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Modification from Division B to Division A may lead to a change in

prosthesis.
When a Division B ridge is changed to a Division A by osteoplasty
procedures, the final prosthesis design has to compensate for the increased
CHS. For example, before surgery, the available bone height may be
compatible with an FP-1 prosthetic design. If, at the time of surgery, the ridge
is found deficient in width for implant placement, it is not unusual to remove
crestal bone before reaching a Division A width. This means the final
restoration will require an additional height. It may result in an extended
tooth (FP-2, FP-3) restoration, which may not be acceptable to the patient.
Insufficient osteoplasty.
The most common approach to modify the narrower Division B ridge into
another bone division by osteoplasty is when the final restoration is a
mandibular implant overdenture. Because of the resorptive process that
occurs in the anterior mandible, an osteoplasty is usually indicated to allow
for adequate bone width if the CHS is less than 15 mm; this maybe be
advantageous for a fixed prosthesis and problematic for a removable
prosthesis. When a RP-4 or RP-5 is planned, care should be noted to make
sure adequate CHS is available. If insufficiency osteoplasty is performed, lack
of space will be available for the prosthesis, which may lead to prosthesis
fracture, tooth fracture, or tooth delamination. Ideally, greater than 2 mm of
acrylic is required to secure an attachment or a denture tooth (Fig. 3.30).
FIG 3.30 Mandibular overdenture with inadequate osteoplasty leading to decreased

crown height space.
Not Understanding the Divisions of Bone: Division B−w (B

Minus Width)
The distinction between Division B and Division B−w is especially important
when augmentation is the method of choice. Bone augmentation is more
predictable when the volume to augment is minimal and is for width and
least predictable when additional bone height is desired. For example, a
width increase of 1 to 2 mm may be obtained with an alloplast and guided
bone regeneration, but more than 2 mm of width is more predictable with
autologous bone as part of the graft.
Complications
More bone augmentation required.
The Division B−w ridge will usually require more than 2 mm of width
increase, and therefore autologous bone or an autologous/allogenic graft is
beneficial to predictably grow the additional bone width. If the Division B−w
ridge contour requires alteration altered for improved prosthodontic
relationships, an onlay particulate or block graft of autogenous bone is
indicated. The autograft may be harvested from an intraoral region (e.g., the
mandibular symphysis or ramus) and placed along the lateral aspect of the
ridge that corresponds to ideal arch form. The implant placement is usually
delayed for 4 to 6 months after the augmentation process to permit ideal
implant placement and to ensure complete bone formation before placing
the implant.
Bone resorption progression.

The patient delaying treatment with a Division B bone situation should be
informed of the future bone volume resorption that presents from disuse
atrophy. The augmentation of bone in height is much less predictable and
requires more advanced techniques than augmentation of bone width alone
(Fig. 3.31). For example, the patient may not be experiencing problems with a
maxillary denture, but the Division B bone will resorb in height and decrease
the stability and retention of the removable soft tissue–supported prosthesis.
When treatment is delayed until patient problems begin, the overall result
may be more difficult to achieve and more costly to the patient.
FIG 3.31 Bone rapidly resorbs from Division A to Division B then plateaus for many
years before it is Division C−w. From Division C−w to C−h, it resorbs rapidly. Long
plateaus are found for both Division B and Division C−h. (From Misch CE: Dental implant
Final prosthesis.
The final prosthesis type for Division B ridges is dependent on the surgical
option selected. Whereas grafted ridges will more often be used when a fixed
prosthesis is desired, ridges treated with osteoplasty before implant
placement are likely to be supporting removable prostheses. The treatment
option may be influenced by the region to be restored. For example, in a
partially edentulous anterior maxilla, augmentation is most often selected
because of esthetics, and the parallel bony anatomy of the residual ridge is
not conducive for osteoplasty to gain bone width. In the edentulous anterior
mandible, osteoplasty is common. In the premolar region of the posterior
mandible, Division B root form implants are often used because the bone
density is adequate, available bone height is limited and may be reduced
after osteoplasty, and esthetics are often not a major factor.
Not Understanding the Divisions of Bone: Division C

(Compromised Bone)
The Division C edentulous ridge exhibits moderate resorption and presents
more limiting factors for predictable endosteal implant placement. The
decision to restore with endosteal implants or to change to a more favorable
bone division via augmentation before implant placement is influenced by
the prosthesis, patient force factors, and patient's desires.
The Division C ridge is deficient in one or more dimensions (width, length,
height, or angulation) (Box 3.5) regardless of the position of the implant body
into the edentulous site. The resorption pattern of bone occurs first in width
and then in height. As a result, the Division C ridge continues to resorb in
width, until it becomes inadequate for any design of endosteal implant.
Box 3.5
Division C Bone
Width (C−w bone): 0–2.5 mm
Height (C−h bone) <12 mm
Angulation of occlusal load (C−a bone) >30 degrees
Crown height space >15 mm
Division C−w
The Division C-w is significantly compromised in width, and usually requires
augmentation (facial and lingual) or osteoplasty to convert the ridge to C−h
(adequate height). On occasion, the C−w ridge may be treated by osteoplasty
in the anterior mandible, which converts the ridge to C−h and, in the anterior
mandibular region, most often to a width suitable for root form implants.
The most common available bone division after osteoplasty of C−w is C−h
available bone, not Division A, because the CHS is greater than 15 mm. On
occasion, the C−w osteoplasty may convert the ridge to Division D, especially
in the posterior mandible or maxilla, which most likely contraindicates
implant placement. Care should be exercised to prevent this from occurring
because bone grafting procedures will be more challenging after the height
has been reduced.
After the C−h ridge is augmented, it is treated with the options available in
the acquired bone division. A patient who desires a fixed prosthesis often
requires an autogenous graft before implant placement to acquire proper lip
support and ideal crown height.
Augmentation of C−w is most often used when prosthetic guidelines
require a fixed restoration or excess force factors require greater surface area
implants and improved biomechanics for the prosthesis (Fig. 3.32).
FIG 3.32 (A) and (B) Division C−w.
Complications of C−w
More difficult surgery.
The C−w augmentation is more difficult than for Division B bone because the
need for bone volume is greater, yet the recipient bed is more deficient.
Because less host bone is present, more difficulty in using fixation screws
results. Additionally, there exists a decreased blood supply, which may
compromise healing. Usually, block bone grafts are indicated with the use of
bone graft factors. Soft tissue complications, such as incision line opening,
are also more common in C−w augmentations than Division B because of
compromised attached tissue (Fig. 3.33).
FIG 3.33 Division C augmentation. (A) Preoperative Division C defect. (B)
Recipient site preparation. (C) Augmentation. (D) Five-month postoperative depicting
bone growth on the buccal and lingual. (E) Ideal implant placement.
Fast resorption.
The clinician must be aware that the C−w bone will resorb to a C−h ridge as
fast as A resorbs to B and faster than B resorbs to C−w. In addition, without
implant or bone graft intervention, the C−h available bone will eventually
evolve into Division D (severe atrophy). Care should be noted to prevent
excessive force or pressure on the ridge via a removable prosthesis.
Division C-h
The Division C-h bone exhibits moderate to advanced atrophy vertical height
of bone of 7 to 9 mm, or the crown height space of greater than 15 mm.
Moderate to advanced atrophy may be used to describe the clinical
conditions of Division C. The posterior maxilla and mandible are common
areas for Division C−h bone. This is due to vital structures such as the
maxillary sinus or mandibular canal, which limits vertical height sooner than
the opposing cortical plates in the anterior regions.
The Division C edentulous ridge does not offer as many elements for
predictable endosteal implant or prosthesis success as in Divisions A or B.
Anatomic landmarks to determine implant angulations or positions in
relation to the incisal edge are usually not present, and greater surgical skill
is required. The clinician must realize that Division C ridge implant–
supported prostheses are more complex and have slightly more
complications in healing, prosthetic design, or long-term maintenance. On
the other hand, the patients will usually have greater need for increased
prosthodontic support. Despite the reduced bone volume, modifications of
the treatment plan and prosthesis that decrease stress can provide
predictable, long-term treatment (Fig. 3.34).
FIG 3.34 Division C−h. (A) Posterior maxilla depicting minimal bone below the
sinus. (B) Posterior mandible, premolar area depicting minimal bone above the
mandibular canal.
Complications C−h
Mandible-floor of mouth.
When the anterior mandible is C−h, the floor of the mouth is often level with
the residual mandibular crest of the ridge, which present many potential
complications. Additionally, less attached tissue is present, which may cause
chronic tissue-related issues. During swallowing, it may prolapse over the
residual crest and implant sites, causing constant irritation of the permucosal
implant posts and impairing proper design of the prosthetic superstructures.
Short implants.
In C−h ridges, a common treatment option is the use of short implants. A C
−h root form implant is usually 4 mm or greater in width at the crest module
and 10 mm or less in height. Several studies indicate that implant survival is
decreased when an implant is less than 10 mm in height. For example, a large
multi-center study of 31 different sites and six different implant designs
observed 13% failure with 10-mm implants, 18% failure with 8-mm implants,
and 25% failure with 7-mm implants.15 The implant failure did not occur after
surgery but rather after prosthetic delivery. The loading failure is most likely
due to an inadequate implant support combined with a magnification of
force resulting from excessive CHS.
When endosteal root form implants are used in Division C−h bone with
greater crown heights, additional implants should be placed to increase the
overall implant-bone surface area, and the prosthesis should load the
implants in an axial direction. Additionally, a narrow occlusal table is
indicated to decrease force-related complications. Because the CHS is most
likely greater than 15 mm, the design of a removable prosthesis should often
reduce or eliminate cantilever length and incorporate a stress relief
mechanism. Reduced long-term predictability is usually expected if
additional implants or less stressful prostheses are not used because a
greater moment force is transmitted to the implants and/or prosthesis.
Posterior maxilla: implant placement without sinus graft.

In addition to the residual alveolar bone resorption, the maxillary sinus
expands after tooth loss (pneumatization). As a result, the available bone
height is decreased from both the crestal and apical regions. Placing
implants in the posterior maxilla predisposes the patient to increased
morbidity and possible displacement of the implant into the maxillary sinus.
Sinus grafting is often prescribed before placing endosteal implants in the C
−h posterior maxilla.
Posterior mandible: vertical bone grafting.

In adequate available bone, height is often found in the posterior mandible
because of residual bone loss and the position of the mandibular nerve (i.e.,
especially with type 1 nerve position). Additionally, muscle pull from the
buccinator muscles along with compromised interocclusal space make this
area one of the most difficult to restore with dental implant prostheses.
Fixed prosthesis: excessive crown height space.

A fixed restoration in the Division C−h mandible may require both anterior
and posterior implant support when force factors are greater than usual. The
fixed prosthesis in Division C−h bone with greater than 15 mm CHS is most
often a hybrid device, with denture teeth attached to a precious metal
substructure with acrylic resin. In this way, the complications and costs of a
porcelain-metal fixed restoration may be reduced and repair is easier.
Additionally, fixed prosthesis with excessive CHS tend to be much heavier,
which leads to common patient complaints.
Biomechanical disadvantages.
In general, Division C−h presents less favorable biomechanical factors to the
implant support. Additional implants, cross-arch stabilization, soft tissue
support, or an opposing removable prosthesis, often need to be considered in
the prosthetic design to improve the long-term prognosis. The treatment of
Division C−h ridges require greater clinician experience and training because
the surgical and prosthetic principals are much different than Division A and
B.
Division C−a
In the Division C−a category, available bone is adequate in height and width,
but angulation is greater than 30 degrees. Mraiwa et al found that 28% of
edentulous anterior mandibles had an angulation of 67.6 ± 6.5 degrees.16 This
condition is not uncommon and should be evaluated prior to any treatment.
When present, this excessive angulation condition is most often found in the
anterior mandible. Root form implants placed in this bone category may have
the abutments positioned within the floor of the mouth and compromise
prosthetic reconstruction, speech, and comfort. Other less observed regions
for Division C−a include the maxilla with severe facial undercut regions or
the mandibular second molar with a severe lingual undercut (Fig. 3.35).
FIG 3.35 Division C−a.
Complications C−a
Malpositioned lingually.
When the anterior bone angulation is unfavorable, root form implants may
be positioned too far lingually for prosthodontic support, speech, or hygiene.
The patient will often complain of lack of tongue space and chronic tissue
inflammation and soreness.
Perforate lingual plate.

Another complication related to the Division C–a is placement of implants
that perforate the bony plates. The Division C−a anterior mandible is angled
more than 30 degrees. If the clinician is unaware of this angulation, the
implants may perforate the lingual plate and irritate the tissues of the floor
of the mouth or cause significant bleeding episodes. If the clincian places the
implants within the bone, they may enter the crest of the ridge at the floor of
the mouth and make it almost impossible to restore (Fig. 3.36).
FIG 3.36 (A) Implant placed lingually in poorly angled mandible (e.g., sublingual
undercut), which may lead to severe bleeding episodes. (B) Implant attachments
protruding lingually in poor position for prosthetic rehabilitation and resulting in tongue
impingement.
Difficult prosthetic rehabilitation.

The prosthetic options for Division C ridges more often consist of removable
prostheses in the completely edentulous maxillary arch. A maxillary
overdenture in a Division C ridge supports the upper lip without hygiene
compromise. Ideally, an RP-5 prosthesis (full palate) is recommended to
decrease biomechanical forces on the implants. In the Division C mandible,
the greater CHS often mandates an overdenture design with some soft tissue
support (RP-5). With the buccal shelf mandibular support, less force will be
placed on the implant prosthesis.
Not Understanding the Divisions of Bone: Division D

(Deficient Bone)
The Division D edentulous ridge corresponds to basal bone loss and severe
atrophy, resulting in dehiscent mandibular canals or a completely flat
maxilla. The patient often requires augmentation with autogenous bone
before implant and prosthodontic reconstruction. Severe atrophy describes
the clinical condition of the Division D ridge.
Division D Maxilla.
The Division D maxilla occurs when 6 mm or less of bone exists in the
anterior maxilla below the floor of the nose, or less than 6 mm of posterior
bone is present below the maxillary sinus. In the maxilla, basal bone loss
eventually results in a completely flat maxilla. The partially or completely
edentulous patient with a posterior Division D maxilla and healthy anterior
teeth or implants may undergo sinus augmentation procedures to increase
bone volume for implant placement. The CHS may be insufficient for onlay
grafts in the posterior maxilla despite a lack of available bone height because
the sinus expands faster than the crest of the ridge resorbs. Endosteal
implants of adequate height can rarely be positioned in the posterior maxilla
with Division D bone without a sinus graft. After 6 months post–sinus graft,
the Division D posterior maxilla is restored to Division A or C−h, and root
form implants may be inserted for posterior prosthodontic support (Box 3.6
and Fig. 3.37).
Box 3.6
Division D Bone
Severe atrophy
Basal bone loss
Flat maxilla
Pencil-thin mandible
>20 mm crown height

FIG 3.37 Division D maxilla. Coronal CBCT image depicting no available bone
below the sinus.
Complications – maxilla.
The anterior maxilla rarely provides sufficient support in the Division D
ridge for implants of any design. Autogenous iliac crest bone grafts to
improve the anterior Division D are strongly recommended before any
implant treatment is attempted.73 After autogenous bone grafts are
completed and allowed to heal for 5 or more months, the bone division is
usually Division C−h (or possible Division A), and endosteal implants may
be inserted.
The autogenous bone grafts are not intended for improved denture
support (without future implant placement). If soft tissue–borne prostheses
are fabricated on autogenous grafts, the bone will resorb at an accelerated
rate. Additional augmentation to compensate for this resorption is not
indicated. Repeated relines, highly mobile tissue, sore spots, and patient
frustration are all consequences. However, autogenous bone grafts are
maintained long term in conjunction with implant placement. Because of the
stimulation of the augmented bone, bone supporting the implants will be
maintained. The completely flat anterior Division D maxilla should not be
augmented with only hydroxyapatite (nonresorbable) to improve denture
support. Inadequate ridge form usually exists to guide the placement of the
material. As a result, migration of the graft at the time of surgery or in the
future after soft tissue loading is a frequent sequela leading to significant
complications.
Division D Mandible
Complications – mandible.
In the Division D mandible, the superior genial tubercles become the most
superior aspect of the ridge. The mentalis muscle loses much of its
attachment, even though the superior portion of the muscle attaches near the
crest of the resorbed ridge. In the posterior mandible, the buccinator muscle
may approach the mylohyoid muscle and form an aponeurosis above the
body of the mandible. The mandibular arch also presents with mental
foraminae and portions of the mandibular canal dehiscent. It is not
infrequent that these patients develop neurosensory impairment of the lower
lip, especially during mastication. The CHS is usually greater than 20 mm,
which results in a significant force multiplier and can rarely be reduced
enough to render long-term success of the prosthesis.
Prosthesis type.
The prosthetic result for anterior ridges with Division D without
augmentation is the poorest treatment outcome of all the divisions of bone.
Fixed restorations are nearly always contraindicated because the CHS is so
significant resulting in a biomechanical disadvantage. When treated without
augmentation, completely implant-supported overdentures are indicated
whenever possible to decrease the soft tissue and nerve complications. An
RP-5 restoration is not suggested because bone loss will continue in the soft
tissue–supported region of the overdenture; usually there is lack of a buccal
shelf (primary stress bearing area).
Pathologic fracture.
The mandibular completely edentulous Division D patient is the most
difficult to treat in implant dentistry. Benefits must be carefully weighed
against the risks associated with augmentation procedures. Although the
clinician and patient often regard this condition as the most desperate, these
patients may easily end up with pathologic fracture complications. If implant
failure occurs, the patient may become a dental cripple—unable to wear any
prosthesis. Idiopathic fracture during surgery or from implant failure or
removal is a more likely complication than in other bone divisions. Clinicians
treating anterior Division D mandibles should be able to manage future
complications, which may be extensive.
Implants without bone grafting.
Endosteal root form implants without autogenous grafts may be used on rare
occasions in the anterior Division D mandible when the remaining bone is
dense and the opposing arch is edentulous. Care must be taken during
placement because mandibular fracture at insertion or during postoperative
healing is a possible complication. Under these conditions the CHS is very
great, and the number of implants is often four or fewer. Implant failure after
loading is a greater risk. Implant failure results with circumferential bone
loss, which may be associated with mandibular fracture through the implant
site. An RP-5 removable restoration is usually indicated for Division D with
only anterior implants. However, the RP-5 restoration allows continued bone
resorption and atrophy to continue in the posterior regions. The prudent
therapy is to educate the patient as to the risks of the situation and offer an
autologous bone graft and implants to support a RP-4 restoration (Fig. 3.38).
FIG 3.38 Division D Mandible: (A) Panoramic image. (B) Cephalometric image
showing minimal available bone.
Lack of early treatment.

The Division D arch requires greater clinician training and results in more
frequent complications related to grafting, early implant failure, and soft
tissue management, and treatment options include a more guarded
prognosis. It should be the goal of every clinician to educate and treat the
patient before a Division D bone condition develops. For example, the
profession treats periodontal diseases before pain in the region occurs, and
carious lesions are removed from teeth before abscess formation. Bone loss is
monitored around teeth in millimeters and requires continued care to reduce
the risks of future tooth and bone loss. Likewise, prudent practitioners
monitor bone loss in edentulous sites and offer education and treatment
before deleterious effects occur.
Key Implant Position
Treatment Planning
Implant positions are an important component of the dental implant
treatment planning process, which is crucial to reduce force reduction to the
implant system. The maximum number of potential implants that may be
used in a fixed prosthesis is usually determined by allowing 1.5 to 2.0 mm or
more from each natural tooth and a 3-mm space between each implant and
adding the diameter of the implant (Fig. 3.39). This results in dividing the
length of the span by 7 mm for the maximum number of implants (when the
implants are 4 mm in diameter − 14 mm space divided by 7 = 2 × 4.0 mm
implants). Hence, a 21- to 27-mm span may have three implants, and a 28- to
34-mm span may have four implants. The key implant positions are more
important sites than the others to reduce biomechanical forces. When
utilized, the key implant abutment locations will decrease biomechanical
complications.
FIG 3.39 The maximum number of implants in an edentulous span may be
determined by allowing 1.5 mm or more from an adjacent tooth and 3 mm between
each implant and adding the diameter of the implants. (From Misch CE: Dental implant
Misch has postulated four general guidelines to determine key implant

positions for a fixed prosthesis in the edentulous site with multiple adjacent
teeth missing:17
1. Cantilevers on prostheses designed for partially edentulous patients or

completely edentulous maxillae should preferably be eliminated; the
terminal abutments in the restoration are key positions.
2. Three adjacent pontics should not be designed in the prosthesis, especially

in the posterior regions of the mouth.
3. When the canine is missing, the canine site is a key position, especially
when other adjacent teeth are missing.
4. When the first molar is missing, the first molar site is a key implant
position for all partially edentulous patients and completely edentulous
maxillae.
No Cantilevers
The first rule for ideal key implant positions is that no cantilever should be
designed in the fixed prosthesis for partially edentulous patients or full-arch
maxillary fixed restorations (unless favorable force factors). Cantilevers are
significant force magnifiers, which result in excessive force to the cement or
prosthesis screws, prosthesis superstructure, abutment screws, implant-bone
interface, and the implants.18
Cantilevers on fixed partial dentures (FPDs) supported by teeth have a
higher complication rate than prostheses with terminal abutments.19 The
primary causes of traditional three-unit FPD failure with natural tooth
abutments are caries and endodontic complications (often related to the
tooth preparation or decay). The 5-year survival rate of the traditional FPD is
often above 95%.20 However, when a cantilevered three-unit FPD supported
by two teeth is used to replace a missing tooth, the failure rate is over 25%
within the first 5 years, and the complication rate increases to 40% by 10
years; the primary cause of failure is biomechanics.21
When a load is placed on the cantilever portion of a prosthesis, the
abutment farthest from the cantilevered pontic has a tensile and shear force
applied to the cement seal because the tooth adjacent to the pontic acts as a
fulcrum (Fig. 3.40). Cements are 20 times weaker to tension and shear
compared with forces in compression.22 Therefore, with a cantilevered
prosthesis, the cement seal breaks on the most distal abutment, and then the
abutment often decays. The abutment closest to the cantilever becomes
mobile or fractures (especially when endodontics was performed) because it
is the only retained abutment for the prosthesis. These biomechanical-
related complications usually occur in a relatively shorter period of time
compared with biologic complications (e.g., decay or periodontal disease).
FIG 3.40 When a compressive force is placed on a cantilever from two (or more)
natural teeth, the closest tooth acts as a fulcrum, and the distal tooth from the
cantilever has a shear and tensile load applied to the cement seal. In this example,
the compressive load is applied to a first premolar, the second premolar acts as a
fulcrum, and the shear and tensile load is applied to the first molar. (From Misch CE:
One Missing Tooth

Ideal placement.
When one tooth is replaced with an implant, the implant should be inserted
into the mesiodistal center of the site. If the implant is positioned in the
mesial-distal center, a cantliever will result. As a general rule, the implant
should be 1.5 to 2 mm from an adjacent tooth. Care should be exercised to
decrease the possibility of placing the implant too far from the natural teeth.
This will also result in a cantilevered prosthesis.
Implant size.
A 4-mm implant requires 7 mm of space (4 mm + 1.5 mm + 1.5 mm). When a
molar (∼10–12 mm) is replaced, the implant should be larger in diameter to
decrease the mesial and distal cantilever and placed in the mesiodistal center
of the edentulous site. This decreases the biomechanical-related risks to the
implant system. A common treatment planning problem is when the implant
size is selected on the available bone with no emphasis on the space being
replaced (Figs. 3.41 and 3.42).
FIG 3.41 (A) An implant was placed in the distal position to restore a first molar. A
mesial 7-mm cantilever was used to restore the crown. (B) The first molar implant
fractured within a few years. Two implants should have been used to replace a
molar tooth this large. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 3.42 Cantilever. (A) Implant distally placed in mandibular right first molar
position that resulted in a mesial cantilever. (B) Focre-related fatigue resulted in
fracture of the implant body.
Two Missing Teeth.

When two adjacent teeth are missing, two implants should ideally support
the implant restoration. As a result, whenever two adjacent teeth are missing
and the space is 12 mm or more, two adjacent implants should be inserted,
even in the esthetic zone.
To enforce the rule of no cantilever, the key implant positions indicate one
implant per tooth when one or two adjacent teeth are missing with a span of
more than 12 mm (when the implant diameter is 3 mm), 13 mm (when one
implant is 3 mm and the other 4 mm), and so on (Fig. 3.43).
FIG 3.43 When two adjacent teeth are missing in the esthetic zone, the implants
should be 1.5 mm from the teeth and 3 mm (or more) apart. This means a 12-mm
space is required when the implants are 3 mm in diameter, and 14 mm is required
for two 4-mm-diameter implants. A-P, anteroposterior. (From Misch CE: Dental implant
When one of the two (or more) missing teeth include a molar, one of the
terminal implants should be positioned 1.5 mm from the anterior adjacent
tooth and the other terminal implant at the distal of the last molar, not in the
middle of the molar. In this fashion, the 3-mm cantilever from the midmolar
to the marginal ridge is eliminated when the implants are splinted together.
When the implant is not positioned in the distal molar position, the size of
the last molar should be reduced to eliminate the cantilever. The clinician
should be aware that the last molar should ideally be a premolar-size crown
when the distal implant is positioned in the mesial to midmolar position.
Lower incisor option.

When missing two mandibular incisors, usually one implant may be placed
interproximally, slightly lingual with a screw-retained prosthesis. If all four
lower incisors are missing, two implants may be placed interproximally,
distributing the cantilever amount equally (Fig. 3.44). This area involves
lower force factors.
FIG 3.44 Mandibular anterior treatment planning. (A) Missing two mandibular
incisors are ideally restored with a single implant. (B) Missing four mandibular
incisors are ideally replaced with two implants and a screw-retained prosthesis.
Three Missing Teeth.

When three adjacent teeth are missing, the key implant positions include the
two terminal abutments, one on each end of the prosthesis (Fig. 3.45). A
three-unit prosthesis may be fabricated with only these abutments when
most of the force factors are low to moderate and the bone density is
favorable. A cantilevered restoration on multiple splinted implants may be
compared to a class I lever.18 The extension of the prosthesis from the last
abutment is the effort arm of the lever. The last abutment next to the
cantilever acts as a fulcrum when a load is applied to the lever. The distance
between the last abutment and the farthest abutment from the end of the
cantilever represents the resistance arm, and the distance between the
implants may be called the anteroposterior distance, or A-P spread.
FIG 3.45 A three-unit prosthesis has key implant positions at each terminal end of
the restoration. If force factors are high, a third implant is recommended.
The length (usually in millimeters) of the cantilever (effort arm) divided by

the resistance arm represents the mechanical advantage. Therefore when two
implants are 10 mm apart with a cantilever or extension of 20 mm, the
mechanical advantage is 2 (20 mm/10 mm). In this example, a 25-lb force on
the cantilever results in a 50-lb tensile force on the farthest abutment from
the cantilever (25 lb × 2 = 50 lb). The abutment closest to the cantilever
(fulcrum) receives a compressive force equal to the sum of the other two
forces, or, in this example, 75 lb (25 lb + 50 lb). In other words, the force on
the cantilever increases the force on the implants by two to three times (Fig.
3.46). Cantilevers magnify forces to all the abutments supporting the
prosthesis.
FIG 3.46 A cantilever on two implants may be considered a class I lever. When the
implants are 10 mm apart, with a 20-mm cantilever, a mechanical advantage of 2 is
created. A load on the cantilever will be multiplied by 2 on the most distal implant,
and the implant close to the cantilever receives the sum total stress of the two other
loads. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
When a cantilevered force exists, a greater load to the implant farthest

from the cantilever results in a tensile or shear type of force, and any part of
the implant system is at an increased risk of biomechanical failure (e.g.,
porcelain fracture, uncemented prosthesis, abutment screw loosening, crestal
bone loss, implant failure, implant component or body fracture). This is
especially observed when parafunction or increased CHS exists.
To eliminate posterior cantilevers, bone augmentation is often indicated to
increase bone volume for implant placement. However, there does exist
disadvantages of bone augmentation procedures. Bone augmentation often
requires an additional surgery before implant placement. Additional training
is required to learn bone augmentation procedures, the learning curve is
longer, and it is more difficult to become accomplished in these techniques.
Complications related to bone augmentation are more common than implant
surgery in existing bone volumes and may be more extensive and even
debilitating to the patient. However, cantilevered implant prostheses have a
more frequently observed biomechanical risk than the surgical risks of
augmentation, and these risks can cause the loss of the entire implant
support and prosthesis. Additionally, bone loss and resultant defects from
implant failure may make the following bone augmentation procedures even
more difficult to perform than when treatment was rendered in the original
condition.
Four or More Adjacent Teeth Missing.

When four adjacent teeth are missing, the terminal abutments are the key
implant positions (Fig. 3.47). Most often, one to two additional implants are
required, especially when the missing teeth include a canine, a posterior
teeth or when the bone density is poor. Restorations of 5 to 14 units require
the key terminal positions plus additional abutments regardless of force
factors or bone density. The number of additional abutments is determined
by many biomechanical factors such as arch form, bone density, opposing
occlusion, parafunctional habits, available bone, and type of prosthesis.
FIG 3.47 When four adjacent teeth are missing, the two terminal abutments are
the key implant positions. Most often, one or two additional implants are required.
Cantilever Options.
The ideal implant treatment plan should eliminate cantilevers in partially
edentulous patients and in complete arch maxillae. However, in completely
edentulous mandibles, a cantilever is often the most prudent treatment
option because of available anatomy. For example, in a completely edentulous
mandible, available bone in the posterior regions may be insufficient for root
form implant placement without advanced procedures (e.g., nerve
repositioning, iliac crest bone grafts).
In addition, the dynamics of bone movement during opening and function
is different for a mandible and maxilla. Upon opening, the mandible flexes
distal to the mental foramen toward the midline (mandibular flexure).
During heavy biting on the side of the jaw, the bottom of the mandible
rotates to the buccal, and the crest slightly rolls toward the lingual, again,
distal to the mental foramen (Fig. 3.48).23 As a consequence of this flexure,
splinting a molar implant across the arch to the contralateral molar may
cause discomfort and lateral forces on the implant sites. With implant
prostheses, uncemented restorations, bone loss, and even implant failure
have been observed when there was cross-arch splinting of molars.
FIG 3.48 The mandibular bone has dynamic movement during function. Upon
opening, the mandible flexes toward the midline. Parafunction or heavy biting on one
posterior side results with a torsion of the mandible with the inferior border rolling
buccal and the crest moving toward the tongue. (From Misch CE: Dental implant
No Three Adjacent Pontics

In most prostheses designs, three adjacent pontics are contraindicated on
natural tooth abutments in the posterior regions of the mouth (Fig. 3.49). The
adjacent abutments are subjected to considerable additional force when they
must support three missing teeth, especially in the posterior regions of the
mouth. When three adjacent posterior teeth are missing between remaining
teeth (and the third molar is absent), the terminal abutments are the second
molar and the canine. The forces in the posterior regions are three to four
times greater than the anterior region, and the force on the canine is two
times greater than on the anterior region. In addition, the canine receives a
lateral load in most excursions. The lateral load increases the intensity of the
force and places the cement seal and porcelain/zirconia under more tensile
and shear loads.
FIG 3.49 A posterior fixed prosthesis with three (or more) pontics is
contraindicated with natural teeth abutments. (From Misch CE: Dental implant prosthetics,
ed 2, St Louis, 2015, Mosby.)
In addition to the greater loads applied to the abutment teeth, all pontic
spans between abutments flex under load. The greater the span between
abutments, the greater the flexibility of the metal in the prosthesis. In a one-
pontic prosthesis, minimal flexure results (8 µm or less with precious metal
under a 25-lb load). In comparison, a two-pontic span flexes eight times more
than a one-pontic span, all other variables being equal. Although the metal
flexure is more for the two-pontic prosthesis, the failure rate of three- or four-
unit prosthesis supported by natural teeth is similar for the first 5 years
because the cause of failure is mostly biologic (e.g., caries).
The metal between abutments for a three-pontic span flexes 27 times more
than that of a one-pontic span if all other factors are equal (Fig. 3.50).24 In
addition, the greater the load, the greater the flexure. With parafunction
patients, the flexure is even greater, with an increased shear and tensile force
on the abutments. The greater the flexure, the greater the risk of porcelain
fracture, uncemented prostheses, and abutment screw loosening. As a result,
not only is the magnitude of the force increased to the adjacent abutments
when the prosthesis has three pontics (because they are supporting two
abutments and three pontics) but the flexure of the metal also increases to a
point that the incidence of complications makes the treatment plan
contraindicated, especially when forces are greater (as in the posterior
region). As a result, a three–adjacent-pontic prosthesis has an increased
failure rate compared with a one- or two-pontic fixed prosthesis. The
increased failure rate of long-span fixed prostheses is due largely to the
increase in biomechanical complications (e.g., unretained restorations and
fracture). As a consequence, it is well accepted in the literature that three
pontics in the posterior regions are contraindicated for natural teeth.
FIG 3.50 (A) A one-pontic fixed partial denture (FPD) has minimal flexure of the
metal. (B) A two-pontic FPD flexes eight times more than a one-pontic span. (C) A
three-pontic FPD has 27 times more flexure than a one-pontic span. (From Misch CE:
The flexure of materials in a long span is more of a problem for implants

than natural teeth. Because natural roots have some mobility both apically
and laterally, the tooth acts as a stress absorber, and the amount of material
flexure may be reduced. Because an implant is more rigid than a tooth (and
has a greater modulus of elasticity than a natural tooth), the risk for
complications of increased load and material flexure are greater for an
implant prosthesis. Because three posterior pontics are contraindicated in a
natural tooth–fixed prosthesis, it is even more important not to have three
pontics in an implant restoration.
The span of the pontics in the ideal treatment plan should be limited to the
size of two premolars, which is 13 to 16 mm. When a molar is one of the teeth
missing between existing teeth, the missing molar space alone may be 10 to
13 mm long. As a result, when a large second premolar and first molar are
missing, this edentulous span is often treatment planned to replace three
teeth, rather than two, and an additional implant is warranted in this span.
This is especially appropriate for greater patient forces (i.e., moderate to
severe parafunction) or softer bone types (i.e., D3 and D4).
To limit the effect of the complications of three adjacent premolar-size
pontics, additional intraimplant key positions are indicated in prostheses
missing five or more adjacent teeth. When 5 to 14 missing adjacent teeth are
to be replaced, key implant positions are located in the terminal abutments,
and additional pier or intermediary abutments are indicated to limit the
pontic spans to two premolar-size pontics. Following this rule, a five- to
seven- premolar–size unit prosthesis has three key abutments (two terminal
and one pier) (Fig. 3.51).
FIG 3.51 When five to seven adjacent teeth are missing, there are three key
implant positions: the terminal abutments and another implant to limit the edentulous
span to two teeth. Note additional implants are usually required, especially for six or
seven missing teeth (translucent implants).
An 8- to 10-premolar–size unit prosthesis has four key implant positions

(two terminal and two pier). An 11- to 13-unit prosthesis has five key
abutments (two terminal and three pier), and a 14-unit prosthesis has six key
abutment positions. In addition to these key abutments, additional
abutments may be required to address patient force factors and bone density.
Rarely is the force factor situation favorable and bone density ideal enough
in a maxilla to be fulfilled with solely key abutments for a fixed prosthesis
replacing more than five teeth.
Three-Pontic Options.
Angled forces to the premaxilla magnify the amount of the force to the
implant system in both centric and excursive occlusal forces. Therefore, most
maxillary anterior prostheses should also limit the number of pontics in the
restoration. The exception to the no three-pontic rule is most often the
anterior mandible, when the three adjacent missing teeth are mandibular
incisors. As long as implants are placed in the canine position, the number of
pontics may be increased because of the long axis angle of force, the reduced
bite force, and the good bone quality. However, when the dentate arch
position is tapered and the three anterior pontics are cantilevered to the
facial, an additional implant is indicated even in the anterior mandible.
Canine Rule
In any arch, certain positions are more important sites than others. In the
dental arch, these more important positions are represented by the canine
and the first molar (Fig. 3.52).25 The canine root has more surface area in
either arch compared with any other anterior tooth, and the molar has more
root surface area than any posterior teeth (Fig. 3.53).26 The canine is a
particularly interesting tooth. When a lateral force is placed on the natural
canine and no posterior teeth are in contact, two thirds of the masseter and
temporalis muscles do not contract, and the resultant force on the anterior
teeth is less. In addition, because the mandible acts as a class III lever, with
the temporomandibular joint behind the muscles of mastication, the force
applied to the anterior teeth is less when the posterior teeth do not occlude.
Therefore, both biologic and biomechanical factors make the canine position
an important site in the dental arch.
FIG 3.52 In a dental arch, the two most important biomechanical positions are
represented by the canine and the first molars. (From Misch CE: Dental implant prosthetics,
FIG 3.53 The canine has more root surface area than any anterior tooth and the
first molar more area than any other posterior tooth. (From Misch CE: Dental implant
A fixed restoration replacing a canine is at greater risk than nearly any

other restoration in the mouth. The maxillary or mandibular adjacent incisor
is one of the weakest teeth in the mouth, and the first premolar is often one
of the weakest posterior teeth. As a consequence, when a canine is missing, a
single tooth implant replacing the canine is the ideal treatment of choice (Box
3.7).
Box 3.7
Arch Position
Canine
• Most surface area of any anterior tooth
• Canine-guided excursion of the mandible reduces masticatory muscle

contraction
• Canine and anterior teeth farthest from the temporomandibular joint (less
force magnitude)
• Adjacent teeth are less ideal for additional force
When two adjacent teeth are missing and include a canine, two implants
are required. Even when a canine and lateral incisor are in the esthetic zone,
it is better to reduce the size of the implants and place two implants with no
cantilever rather than place a larger implant with a cantilever. The implants
should be at least 3 mm apart so the base of the interimplant papilla can
support the soft tissue drape.
A traditional fixed prosthetic axiom on natural teeth indicates it is
contraindicated to replace a canine and two or more adjacent teeth.24 If a
patient desires a fixed prosthesis, implants are required whenever the
following adjacent teeth are missing in either arch: (1) the first premolar,
canine, and lateral incisor; (2) the second premolar, first premolar, and
canine; and (3) the canine, lateral, and central incisors. Whenever these
combinations of teeth are missing, implants are required to restore the
patient because (1) the length of the span is three adjacent teeth, (2) the
lateral direction of force during mandibular excursions increases the stress to
the prosthesis, (3) the magnitude of the bite force is increased in the canine
region compared with the anterior region, and (4) an implant in the canine
region with implant-protected occlusion (mutually protected occlusion)
distributes reduced lateral loads during mandibular excursions.
The canine is the most important position for the occlusal scheme of the
patient. Canine guidance or mutually protected occlusion is the primary
occlusal format in most fixed implant reconstructions or completely implant-
supported removable restorations. The angled force of approximately 22 to 25
degrees in excursions should not be magnified on a canine pontic with an
implant prosthesis supported by fewer implants.27 Although the force
reduction in excursions is not as great with an implant as with a natural
canine tooth, there still is some force reduction as a consequence of the class
III lever effect.28 Whenever the canine and two or more adjacent teeth are
missing, the canine is a critical site along with the terminal positions of the
span (Fig. 3.54).
FIG 3.54 A panoramic radiograph of a patient missing a maxillary right canine,
lateral incisor, and central incisor. The key implant positions are the canine and
central incisor to support a three-unit fixed partial denture. (From Misch CE: Dental
implant prosthetics, ed 2, St Louis, 2015, Mosby.)
When the three adjacent teeth are the first premolar, canine, and lateral
incisors, the key implant positions are the first premolar, the canine, and the
lateral incisor when the overall intratooth space is greater than 19 mm
because three implants with no cantilever reduce any increased force factor
risks. The minimum implant sizes are usually 3.5 mm for the premolar and
canine and 3 mm for the lateral incisor.
When the first premolar, canine, and lateral incisor are missing and the
intratooth span is less than 19 mm, only two implants are used to support the
prosthesis. In this scenario, it is better to place terminal abutments and have
a canine pontic, especially when the prosthesis is within the esthetic zone.
The size of the implants is slightly increased to compensate for the angled
forces during a lateral excursion. In addition, the amount of the incisal
vertical overbite is reduced to decrease the leverage effect on the canine. The
incisal guidance should be as shallow as possible to decrease the force
during excursions. However, it must be steep enough to separate the
posterior teeth in the mandibular excursions.
When there are multiple missing teeth on each side of the canine site, the
canine edentulous site is a key pier abutment position. The canine position is
a key implant position to help disocclude the posterior teeth in mandibular
excursions. As a result, when four or five adjacent teeth are missing,
including a canine and at least one adjacent posterior premolar tooth, the key
implant positions are the terminal abutments and the canine position. For
example, when the first premolar, canine, lateral, and central incisor are
missing, the key implant positions are the first premolar and central incisor
(terminal abutments) and the canine (canine rule) (Fig. 3.55).
FIG 3.55 (A) The patient is missing a maxillary central incisor, lateral incisor,
canine, and first premolar. There is inadequate bone volume in the canine position.
(B) A block bone graft is positioned primarily in the canine region. (C) The block bone
graft matures for 6 months. (D) The key implant positions are the central incisor,
canine, and first premolar. (E) An additional implant was positioned in the lateral
incisor region. (The patient is a man with deep vertical overbite.) (F) A four-unit fixed
partial denture was cemented in place. (From Misch CE: Dental implant prosthetics, ed 2, St
When six or more adjacent teeth are missing, which include both canines,
additional pier abutments (which limit the pontics' spans to no more than
two teeth) are also indicated. For example, when the first premolar to first
premolar are missing, five key implants are indicated, especially in the
maxillary arch—the terminal abutments, the canines, and an additional
implant in one of the central incisor positions. The same five key implant
positions exist for the one-tooth span of second premolar to second premolar
(Fig. 3.56).
FIG 3.56 A panoramic radiograph of 10 anterior teeth missing. There are five key
implants positions for this fixed prosthesis: the second premolars, the canines, and
an anterior implant to limit the pontics to no more than two. (From Misch CE: Dental
First Molar Rule

The molars have the most root surface area of any natural tooth in the mouth
and have two or three roots. The biomechanical rationale for this condition is
that the bite force doubles in the molar position compared with that of the
premolar position in both the maxilla and mandible. In addition, the
edentulous span of a missing first molar is usually 10 to 12 mm compared
with a 7-mm span for a premolar. As a result, the first molar is also a key
implant position.17
As previously presented, cantilevers should not be used in partially
edentulous patients to replace a first molar, especially when patient force
factors are moderate to great (e.g., parafunction, opposing arch). The
cantilever further increases the force of the molar region to the splinted
abutments. As a result, uncemented restorations, bone loss, and failure are
at greater risk.
When a first molar is missing, a 5- to 6-mm-diameter implant is indicated
in the mid mesiodistal position of the edentulous site when the molar is less
than 12 mm wide. When a first molar implant is indicated in the maxilla, a
sinus bone graft is most always required. The maxillary sinus expands rapidly
after tooth loss. More often than not, the sinus floor should be altered and
grafted in conjunction with a first molar implant insertion.
When two adjacent teeth are missing, including a first molar, the key
implant positions include the terminal abutments, including the distal molar
position. When three posterior teeth are missing and include a first molar, a
first molar implant is included. For example, in a patient missing the second
premolar, first molar, and second molar, three key implant positions are
required to restore the full contour of the missing molars teeth: the second
premolar and second molar terminal abutments and the first molar pier
abutment (Fig. 3.57). A similar scenario is present when all four posterior
teeth are missing—first premolar, second premolar, first molar, and second
molar. The key implant positions are the terminal abutments (first premolar
and second molar) and the first molar (Fig. 3.58). In the maxilla, a sinus graft
is most always indicated to replace these four adjacent teeth (Fig. 3.59). When
one implant replaces a molar (with a span of 10–13 mm), the implant should
be at least 5 mm in diameter. When a smaller-diameter implant is selected in
a molar space of 14 mm or more, the molar may be considered the size of two
premolars, and two smaller-diameter implants may be selected.29
FIG 3.57 (A) A panoramic radiograph of a patient missing the second premolar,
first molar, and second molar. There is inadequate bone height because of the
pneumatization of the maxillary sinus. (B) A sinus graft restores the bone height to
favorable limits for future implants in the second premolar, first molar, and second
molar. (C) Three implants are inserted: the second premolar and the second
terminal implants and a first molar implant. (D) The three implants after integration.
(E) A three-unit fixed partial denture supported by three implants. Only the mesial
half of the second molar is restored because there is no opposing mandibular
second molar. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 3.58 (A) A panoramic radiograph of a patient missing mandibular first premolar
to second molar. (B) Four implants were used to restore the missing teeth. (C) The
key implant abutments are the first premolar and second molar (no cantilever) and
the first molar. (D) The four-unit splinted fixed partial denture restores the missing
teeth. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 3.59 A panoramic radiograph replacing the first premolar to second molar. A
sinus graft is most always required to place the molar implants. (From Misch CE: Dental
Four to six implants in the anterior maxilla have been suggested in the
complete edentulous maxilla, with posterior cantilevers (Fig. 3.60). Full-arch
restorations for the edentulous maxillary arch should also have a first molar
implant. In general, density of bone in the maxilla is less than the mandible
in both the anterior and posterior regions. The anterior maxillary implants
receive an angled load (compared with the anterior mandible) in both centric
and mandibular excursions. The anterior maxillary arch usually has shorter
implants than the anterior mandible because the vertical height of bone is
less compared with the anterior mandible. The shorter implants have less
surface area and higher stresses, especially in soft bone. Maxillary fixed
restorations most often oppose an implant prosthesis (usually fixed) or
natural teeth. This increases the force to the maxillary prosthesis. Therefore,
the biomechanical risks associated with full-arch maxillary prostheses with a
molar cantilever are greater than for mandibular restorations. A literature
review of full-arch prostheses reports an implant failure rate three times
higher in full-arch maxillary implant fixed restorations than with mandibular
full-arch implant restorations.30 The treatment plan should be different for
the two arches.
FIG 3.60 (A) Four implants in an edentulous maxilla are suggested in the literature
to support a fixed prosthesis. (B) The fixed prosthesis supported by four anterior
implants most often cantilevers the molars. In addition, there is also an offset
cantilever to the facial in both the anterior and posterior regions. (C) The failure rate
of the maxillary implants usually causes additional bone loss. The maxilla may be
unable to be restored without advanced bone grafts, more implants, and a new
prosthesis. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The key implant positions for an edentulous maxilla are the distal of the
first molars bilaterally, the bilateral canines, and an implant in one of the
central incisor positions between the canines. This permits the five sections
of an arch to be splinted together and take advantage of the biomechanics of
an arch (Fig. 3.61).
FIG 3.61 The key implant positions for an edentulous maxilla to support a fixed
prosthesis (or RP-4 prosthesis) are the bilateral molars, the bilateral canines, and an
implant in one of the central incisor positions. (From Misch CE: Dental implant prosthetics,
Implant Number
Treatment Planning
In the past, the number of implants most often was determined in relation to
the amount of available bone. This concept became popular in the mid 1980s,
when the Brånemark philosophy of osseointegrations was introduced for
completely edentulous arches. In an edentulous arch, four to six anterior
implants were used in available bone situations between the mental
foramina in the mandible and anterior to the maxillary sinuses in the maxilla
for a full-arch fixed prosthesis. The prosthesis cantilevered the molars from
the anterior implant positions. Four implants were used in moderate to
severe atrophic ridges for a fixed full-arch prosthesis.31 This concept has been
expanded to include zygomatic implants in the posterior regions, which
engage the palate and the apical 4 mm of the zygomatic process (passing
through the maxillary sinuses) (Fig. 3.62). This treatment option does not
consider the force magnifiers of CHS or the A-P spread of the implants in
relationship to the anterior cantilever replacing the anterior teeth. In
addition, when four implants support a 12-unit fixed prosthesis, the position
of the implants cannot follow the four key implant position rules, and there
are often no implants in the canine positions and more than three pontics
between the anterior implants or three pontics cantilevered from the most
distal implants.
FIG 3.62 (A) A panoramic radiograph of four zygomatic implants supporting a fixed
prosthesis in the maxilla. (B) The full-arch maxillary prosthesis is cantilevered to the
facial, and there are six adjacent pontics in the anterior region, including a canine
position. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
In full-arch prostheses, studies comparing six implants to four- and three-

implant abutments show better distribution and reduced stress on the six-
implant system components (crown, cement, abutment, abutment screw,
marginal bone, implant-bone interface, and implant components) (Fig.
3.63).32 Silva et al evaluated, with three-dimensional finite element analyses,
the difference in four vs. six implants to support a full-arch cantilevered
prosthesis.29 The cantilever length and crown height were similar in both
models. The six-implant support model reduced the stress to the implant-
bone regions between 7% to 29%, depending on the direction and position of
the applied load.
FIG 3.63 The more implants supporting a fixed prosthesis, the lower the bending
movement and stress in the support system. (From Misch CE: Dental implant prosthetics,
2e, St. Louis, 2015, Mosby; Data from Duyck J, Van Doosterwyck H, Vandersloten J, et al: Magnitude
and distribution of occlusal forces on oral implants supporting fixed prostheses: an in vivo study,
Clin Oral Implants Res 2:465–475, 2000.)
In rare cases, four implants in the mandible between the foramen may be
used to support a full-arch implant-supported prosthesis—fixed or RP-4. The
implants are typically positioned in the first to second premolar positions,
and the canines. However, the other patient force factors should be low (e.g.,
no moderate to severe parafunction, crown height space less than 15 mm,
older woman, and opposing a maxillary complete denture). In addition, the
bone density should be favorable (D2). When all of these conditions are not
present, consideration is given to the five key implant positions, and more
implants are indicated when stress factors are moderate to severe.
When a full-arch fixed implant restoration is the treatment for a maxillary
arch, the suggested number of implants by some authors is often the same as
the mandible. For example, “all on four ” is a common treatment option
presented to the profession in either arch along with similar fees for either
arch to the patient (Fig. 3.64).33 Yet a literature review reveals the failure rate
of the full-arch maxillary restoration is three times greater than the
mandible.30 The hardness of the bone is related to its strength. The mandible
more often has hard (strong) bone, and the maxilla more often has softer
bone. In fact, the posterior maxillary bone may be 5 to 10 times weaker than
the hard bone of the anterior mandible.34 As a result, more implants should
be used in the poorer-quality bone found in the maxilla. Increasing the
implant number decreases the periimplant bone stress.
FIG 3.64 Full-arch implant fixed restoration by many authors uses the same
number of implants in the maxilla and mandible. However, three times greater failure
rates are observed in the maxillary arch. (From Misch CE: Dental implant prosthetics, ed 2, St
The maxillary anterior arch receives a force at a 12- to 15-degree angle

during occlusion and up to a 30-degree angle in excursions. A 15-degree
angled force increases the force component on the implant by 25.9%, and a
30-degree force increases the force by 50%.35 This is a biomechanical rationale
for why maxillary anterior teeth are larger than the mandibular anterior
teeth. Hence, the size or number of implants in the anterior maxilla should
be greater than an anterior mandible.
The excursive forces in a maxillary restoration come from within the arch
to push outside the arch. This force direction on the maxillary arch is more
detrimental than in the mandible. The mandible receives a force from
outside of the arch toward the inside of the arch, which is the mechanism of
force the Roman or gothic arch was designed to resist. As a result of these
biomechanical issues, more implants should be used in maxillary compared
with mandibular restorations. It is probably not a coincidence that there are
more roots for the teeth in the maxillary arch compared with those in the
mandibular arch.
The minimum number of implants used to support a restoration should
include all of the key implant positions. Yet the number of implants in a
treatment plan should rarely be the minimum. There is no safety factor if an
implant fails: the prosthesis becomes partially unretained, or the patient has
a parafunctional episode. For example, if 25 patients receive four implants to
support a fixed prosthesis, there would be 25 fixed prostheses and 100
implants in the report. This type of treatment planning may initially be less
expensive for the patient, but an implant failure any time after implant
surgery places the patient's restoration at considerable risk. If each patient
lost one implant with this implant number per prosthesis, the overall
implant success would be 75%, but there would only remain three implants
in each patient. As a result, all 25 fixed prostheses would be at risk of
overload failure. If 20% of the implants fail (with one failure per patient),
only 5 of the 25 patients would have four implants to support the restoration
(only 20% of the patients would be restored with a fixed prosthesis) (Table
3.2).17
TABLE 3.2
Implants vs. Prosthesis Success: Four Implants per Prosthesis for 25
Patients (100 Implants for 25 Prostheses)
Implant Number Success Rate P rosthesis Number P rosthesis Success Rate

100% 25 100%
90% 15 60%
80% 5 20%
75% 0 0%
If the 25 edentulous patients in this example have eight implants to

support a full-arch, 12-unit fixed prosthesis, the risk of prosthesis failure is
significantly reduced (Table 3.3). If each patient loses one implant, most
likely all patients would still be able to function with their original
prosthesis. Even if all 25 patients lost two implants, the 25 restorations may
still function without risk (depending on the implant failure location). The
additional implants also reduce the cantilever length and reduce the number
of pontics in the prosthesis, providing more abutments for greater retention
of the restoration, with reduced risk of screw loosening or uncemented
prosthesis. As a general rule, it is better to err on the side of safety in
numbers than on the side of too few implants. When in doubt, add an
additional implant to the treatment plan.
TABLE 3.3
Implants vs. Prosthesis Success: Eight Implants per Prosthesis for 25
Patients (200 Implants for 25 Prostheses)
Implant Number Success Rate P rosthesis Number Success Rate

100% 25 100%
87.5% 25 100%
75% 25 100%
Influence of Patient Force Factors on Implant Number

The additional number of implants, after the key implant sites are
established, are related to the patient force factors and the bone density.18
Five patient force factors determine the amount of stress transmitted to the
prosthesis. They are:
1. Parafunction
Bruxism (severe, moderate, mild, absent; this is the most

important stress factor)
Clenching (force magnitude may be as great as bruxism)

2. Masticatory muscle dynamics
Sex (men have greater force)
Age (younger patients have greater force and live longer)
Size (larger patients have greater force)

3. Crown height space
Double the crown height and double the force with any
angled load or cantilever (mesial, distal, facial, or
lingual)
4. Arch position
a. Anterior regions: low forces
b. Canine and premolar: medium forces
c. Posterior regions: high forces

5. Opposing dentition
a. Denture: lowest force
b. Natural teeth: intermediate force
c. Implant fixed prosthesis: higher forces

Not all patient force factors have the same risk.
In conclusion, whenever the patient force factors are greater than usual,
additional implants should be added to support the prosthesis. Of the
patient force factors, severe bruxism is the most significant followed by
clenching and CHS, region of the mouth, masticatory dynamics, and the
opposing arch.
Influence of Bone Density on Implant Number

The additional number of implants after the key implant sites are established
is also related to the density of bone. The softest bone type (D4) has (1) the
lowest strength and may be 10 times weaker than the strongest bone type on
a scale of 1 to 10 for bone strength (D4 bone is a 1 or 2); (2) the greatest
biomechanical mismatch with its modulus of elasticity compared with
titanium; (3) the lowest bone-implant contact (≈25%) and higher stresses
(stress = force/area); and (4) strains in the bone are transmitted not only at
the crest but also along the entire bone-implant surface.
The soft bone type (D3) has (1) a low bone strength, which is 50% weaker
than hard bone (D2) (on a 10-point scale, its strength is a 3 to 4); (2)
intermediate difference of modulus of elasticity compared with titanium; (3)
low bone-implant contact (≈50%); and (4) strain patterns at the crestal half of
the implant.
The hard bone (D2) has (1) ideal strength (a 7 to 8 on a 10-point scale), (2)
high bone-implant contact (≈75%), (3) more stiff modulus of elasticity, and (4)
strain patterns primarily at the crestal region of the implant. The hardest
bone (D1) has the best biomechanical features of (1) strength (9 to 10 on a 10-
point scale), (2) highest bone-implant contact (above 85%), (3) stiffest
modulus of elasticity, and (4) strain values above the first thread.
As the bone quality is reduced, the number of implants to support the
prosthesis should increase. The risk factor scale for bone density is inversely
related to the strength of the bone scale. D4 bone is a 10, D3 bone is an 8, D2
bone is a 4, and D1 bone is a 2. When the implants are inserted into D4 bone,
a larger-diameter or another implant is suggested, depending on the number
of teeth replaced. A full-arch fixed restoration in the mandible with D2 bone
may often have five implants, but in D4 bone, nine implants may be
appropriate. The total number of implants is related to the key implant
positions plus the influence of the patient force factors and the quality of
bone.
In conclusion, the decision for the number of implants in the treatment
plan begins with the implants in the ideal key positions. Additional numbers
are most often required and are primarily related to the patient force factors
or to bone density in the edentulous sites. For example, a young, large man
who bruxes severely with greater-than-normal CHS in the posterior regions
of the mouth opposing an implant restoration will require one implant for
each missing root (two implants for each molar). Likewise, patients with
moderate force factors and poor bone density (D4 bone) in the implant sites
may also require this many implants.
Implant Number: Full-Arch Mandibular Fixed Prosthesis

As a general observation, the number of implants to replace all of the
mandibular teeth ranges from five to nine, with at least four between the
mental foraminae. When the implants are limited to sites anterior to the
mental foraminae to support a fixed prosthesis, a cantilever must be
designed. Cantilevers in the mandible should ideally be projected in only one
posterior quadrant to increase the A-P distance and reduce the force to the
implants (Fig. 3.65). Whenever possible, at least one implant should be
positioned in a first molar site. When implants are positioned in four of the
five open pentagon positions in the mandible, a cantilever is at a reduced risk
of overload because of favorable dynamics of an arch, increased A-P distance,
and usually a more favorable bone density. When seven or more implants are
used in the edentulous mandible with bilateral molar implants, two separate
restorations may be fabricated with no posterior cantilever to permit
mandibular flexure and torsion. Usually, the second molar is not replaced in
the edentulous mandible.
FIG 3.65 The anteroposterior (A-P) spread of implants is determined by drawing a

line from the distal of the last implant on each side and a parallel line through the
middle of the most anterior implant.
Implant Number: Full-Arch Maxillary Fixed Prostheses

The edentulous maxillary fixed prosthesis should usually not have a
cantilever. The first seven ideal sites are often the bilateral first molars,
bilateral second premolars, bilateral canines, and one implant between the
canine positions (Fig. 3.66). These positions satisfy the key implant positions
and add an implant in the posterior region because the bone density is often
poor. Additional implants in the bilateral second molar sites are a benefit to
increase the A-P distance of the implants, which counters the anterior bite
forces that may be increased from parafunction and so on (Fig. 3.67). A
greater number of implants are generally required in the maxilla to
compensate for the less dense bone and more unfavorable biomechanics of
the premaxilla and range from 7 to 10 implants with at least three implants
from canine to canine (Fig. 3.68).
FIG 3.66 In an edentulous maxilla, the most common additional implant site is in
the second premolar region. Seven implants (or more) are most often used to
support a fixed (or RP-4) prosthesis. (From Misch CE: Dental implant prosthetics, ed 2, St
FIG 3.67 In the maxillary arch, secondary implants may be positioned to decrease
the stress in soft bone or in patients with high force factors. (From Misch CE: Dental
FIG 3.68 (A) A panoramic radiograph of a maxillary bilateral sinus graft and
maxillary and mandibular iliac crest bone grafts. Eight implants were used in the
maxilla and seven implants in the mandible. (B) An intraoral view of the maxillary and
mandibular implants. (C) FP-3 fixed restorations in situ. (D) A panoramic radiograph
of the implants and fixed restorations. (From Misch CE: Dental implant prosthetics, ed 2, St
Force-Related Issues
Parafunction
Definition
Parafunctional forces on teeth or implants are characterized by repeated or
sustained occlusion (e.g., habitual movements) and have long been
recognized as harmful to the stomatognathic system. These same forces,
when applied to implant prostheses, have been shown to be very harmful.
General Complications
The lack of rigid fixation during implant healing may be a result of
parafunction on soft tissue–borne prostheses overlying the submerged
implant (e.g., interim prosthesis). The most common cause of both early and
late implant failure after successful surgical fixation is the result of
parafunction. Such complications occur with greater frequency in the maxilla
because of a decrease in bone density and an increase in the moment of
force. The presence of these parafunctional conditions must be carefully
noted during the early phases of treatment planning.
Classification
The classification of parafunction involves (1) bruxism, (2) clenching, and (3)
tongue thrust or increased size. The dental literature usually does not
identify bruxism and clenching as separate entities. Although several aspects
of treatment are similar, their diagnosis and treatment are in some ways
different.
Bruxism and clenching are the most critical factors to evaluate in any
implant reconstruction. Long-term success will not be achieved with severe
parafunction of bruxism or clenching. The implant clinician should always try
to diagnose the presence of these two conditions.
This does not mean that patients with moderate and severe parafunction
are absolute contraindications to implant treatment. Because patients with
moderate to severe parafunction represent so many additional risks in
implant dentistry, one must be aware of these conditions and the methods to
reduce their noxious effects on the entire implant-related system.
Unfortunately, parafunction may be a difficult entity to diagnose, especially if
the patient is completely edentulous and is wearing a recently fabricated
prosthesis.
Bruxism.
Bruxism primarily concerns the horizontal, nonfunctional grinding of teeth.
The forces involved are in significant excess of normal physiologic
masticatory loads. Bruxism may affect the teeth, muscles, joints, bone,
implants, and prostheses. These forces may occur while the patient is awake
or asleep and may generate increased force on the system several hours per
day. Bruxism is the most common oral habit and may be difficult to
diagnosis.
The maximum biting force of bruxing patients is greater than average.
Fortunately, the bite force does not continue to increase in most bruxing
patients. When muscles do not vary their exercise regimen, their size and
function adjust to the dynamics of the situation. As a result, the higher bite
forces and muscle size usually do not continue in an unending spiral.
Diagnosis.
Bruxism does not necessarily represent a contraindication for implants, but it
does dramatically influence treatment planning. The first step is to recognize
the condition before the treatment is rendered. The symptoms of this
disorder may be ascertained by a dental history and may include repeated
headaches, a history (or presence) of fractured teeth or restorations, repeated
uncemented restorations, or jaw discomfort upon awakening. When the
patient is aware of muscle tenderness or the spouse is conscious of the noise
of bruxism during sleep, the diagnosis is readily obtained. However, many
patients do not attribute these problems to excessive forces on the teeth and
report a negative history. A lack of these symptoms does not negate the
possibility of bruxism (Box 3.8).
Box 3.8
Bruxism
Symptoms
Frequent headaches – Pain on opening/closing
History or presence of fractured teeth and/or restorations
Repeated uncemented restorations

Jaw tension and discomfort upon awakening
Muscle soreness and tenderness
Spouse awareness during sleep
Clinical signs.
Fortunately, many clinical signs of bruxism warn of excessive grinding. The
signs of bruxism include an increase in size of the temporalis and masseter
muscles. These muscles and the external pterygoid may also be tender
during palpation. In addition, other signs include deviation of the lower jaw
on opening, limited occlusal opening, increased mobility of teeth, cervical
abfraction of teeth, fracture of teeth or restorations, and uncemented crowns
or fixed prostheses (Box 3.9).
Box 3.9
Bruxism
Clinical Signs of Bruxism
1. Increase in muscle size of temporalis and masseter muscles
2. Temporalis, masseter, or external pterygoid muscles tender to palpation
3. Mandibular deviation while opening
4. Limited occlusal opening
5. Tooth mobility
6. Cervical abfraction of teeth
7. Fracture of teeth or restorations
8. Uncemented crowns or restorations
9. Wearing (attrition) of natural teeth

10. Tooth sensitivity
Clinical exam.
A physical examination for the implant candidate should include palpation of
the muscles of mastication including the masseter, temporalis, and internal
and external pterygoid muscles. Hyperactive or hypertrophied muscles are
the most common sign of bruxing. The lateral pterygoid muscle is more often
overused by the bruxing patient and is often difficult to palpate. The
ipsilateral medial pterygoid muscle provides more reliable information in
this region. It acts as the antagonist to the lateral pterygoid in hyperfunction
and, when tender, provides a good indicator of overuse of the lateral
pterygoid.36 However, the most effective method to diagnose bruxism is to
evaluate the wearing of the natural teeth. Nonfunctional wear facets on the
incisal edges occur most often on natural teeth rather than on crowns made
of porcelain or metal occlusal, especially in the anterior mandible and
maxillary canines. Enamel opposing enamel causes more occlusal material
wear than almost any other combination (e.g., enamel opposing metal, metal
opposing metal, etc.).37 As a result, in a partially edentulous patient, enamel
wear is easily observed in the bruxing patient.
Not only is enamel wear the easiest method to determine bruxism in a
dentate patient but Misch has noted the disorder may also be classified as
absent, mild, moderate, or severe. No anterior wear patterns in the teeth
signifies an absence of significant bruxism. Mild bruxism has slight wearing
of anterior teeth but is not a cosmetic compromise (Fig. 3.69). Moderate
bruxism has obvious anterior incisal wear facets but no posterior occlusal
wear pattern (Fig. 3.70). Severe bruxism has an absence of incisal guidance as
a result of the excessive wear, and posterior wearing of the teeth is obvious
(Fig. 3.71).
FIG 3.69 (A) Mild bruxism. Note the wear facet on the mandibular canine and the
slight notch in the maxillary lateral incisor. (B) Patients often grind their teeth in a
specific, repeated movement of the mandible, called an engram. When the opposing
wear facets of the teeth are in contact, one should note the occlusal position of the
teeth. The patient shown in A has a working contact on the mandibular premolar with
the maxillary canine in this engram position. The slight cervical abfraction of the
mandibular first premolar is a consequence of the parafunction. The patient's
posterior teeth should not occlude in this position to decrease the amount of force on
the anterior teeth. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 3.70 (A) Moderate bruxism of the central incisors (there is an esthetic
consequence). (B) The engram position placed the mandibular anterior teeth
anterior to the maxillary incisal edge and caused the wear of the central
incisors. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 3.71 This patient has severe bruxism because occlusal wear is both anterior
and posterior (right). The incisal guidance should be reestablished before a maxillary
arch fixed reconstruction. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Complications
Posterior wear facets.

Tooth wear is most significant when found in the posterior regions and
changes the intensity of bruxism from the moderate to the severe category.
Posterior wear patterns are more difficult to manage because they are usually
related to a loss of anterior guidance in excursions, and when the posterior
teeth contact in excursive jaw positions, greater forces against the teeth are
generated.38 The masseter and temporalis muscles contract when posterior
teeth contact. With incisal guidance and an absence of posterior contact in a
lateral excursion of this jaw, two thirds of these muscles do not contract and,
as a consequence, the bite force is dramatically reduced. However, when the
posterior teeth maintain contact, the bite forces are similar in excursions, as
during posterior biting. In a patient with severe bruxism, the occlusal plane
or the anterior incisal guidance may need modification to eliminate all
posterior contacts during mandibular excursions before the implant
restoration.
Repeatable movement.
Bruxing patients often repeat the same mandibular movements, which are
different from border movements of the mandible and are in one particular
direction. As a result the occlusal wear is very specific and primarily on one
side of the arch or even on only a few teeth (Fig. 3.72). This engram pattern
usually remains after treatment. If the restoring dentist reestablishes incisal
guidance on teeth severely affected by an engram bruxing pattern, the
incidence of complications on these teeth will be increased. If the patient
wears an occlusal guard, it is usually easy to see the repeatable excursive
movements.
FIG 3.72 This patient exhibits an engram pattern of bruxism primarily toward the
left premolar to central incisors. The right canine and lateral incisor have far fewer
wear facets. Incisal guidance should be restored before any left posterior restoration.
This “pathway of destruction” is specific. (From Misch CE: Dental implant prosthetics, ed 2,
St Louis, 2015, Mosby.)
Component fracture.
Because patients that exhibit bruxism have increased occlusal force, and
much of the force results in lateral (nonaxial) loading, this may be very
damaging to the implant system. An increased probability of crestal bone
loss, implant fracture, abutment screw loosening, porcelain fracture, or
unretained restorations.17
Clenching.
Clenching is a habit that generates a constant force exerted from one occlusal
surface to the other without movement. The habitual clenching position does
not necessarily correspond to centric occlusion. The jaw may be positioned in
any direction and position before the static load; therefore a bruxing and
clenching combination may exist. The clench position most often is in the
same repeated position and rarely changes from one period to another. The
direction of load may be vertical or horizontal. The forces involved are in
significant excess of normal physiologic loads and are similar to bruxism in
amount and duration; however, several clinical conditions differ in
clenching.39
Diagnosis.
Many clinical symptoms and signs warn of excessive grinding. However, the
signs of clenching are often less obvious. The forces generated during
clenching are usually directed more vertically to the plane of occlusion, at
least in the posterior regions of the mouth. Wearing of the teeth is usually
not evident, and clenching often is not diagnosed during the intraoral
examination. As a result, the clinician must be more observant to the
diagnosis of this disorder.
Clinical signs.
Many of the clinical signs of clenching resemble bruxism. When a patient has
a dental history or presence of muscle tenderness (often upon awakening) or
tooth sensitivity to cold, parafunction is strongly suspected. In the absence of
tooth wear, clenching is the prime suspect. Tooth mobility, temporalis, lateral
pterygoid, or masseter muscle tenderness or hypertrophy, deviation of the
mandible during occlusal opening, limited opening, stress lines in enamel,
cervical abfraction, and material fatigue (enamel, enamel pits, porcelain and
implant components) are all associated clinical signs of clenching.40 When
the clinical signs of excessive force appear on the teeth, muscles, or joint in
the absence of incisal wear, clenching is strongly suspected.
A most common clinical finding of clenching is a scalloped border of the
tongue. The tongue is often braced against the lingual surfaces of the
maxillary or mandibular teeth during clenching, exerting lateral pressures
and resulting in the scalloped border. This tongue thrust position may also
be accompanied by an intraoral vacuum, which permits a clench to extend for
a considerable time, often during sleep. When the clinician asks the patient
to open wide to evaluate maximum occlusal opening (while palpating the
temporomandibular joint [TMJ]), the lateral tongue contour is observed to
notice any scalloped border (Box 3.10).
Box 3.10
Clenching: Clinical Signs
• History or presence of temporalis, lateral pterygoid, or masseter muscle
tenderness (often upon awakening)
• Tooth sensitivity
• Tooth mobility
• Temporalis, lateral pterygoid, or masseter muscle hypertrophy
• Deviation of mandible during opening
• Limited opening – pain on opening
• Stress lines in enamel
• Cervical abfraction
• Material fracture (enamel pits, restorations) – porcelain fracture
• Scalloped border of tongue – presence of antegonial notch at the angle of

the mandible
Clinical exam.
Muscle evaluation for clenching (and bruxism) includes deviation during
opening of the jaw, limited opening, and tenderness of the TMJ. Deviation to
one side during opening indicates a muscle imbalance on the same side.36
Limited opening is easily evaluated and may indicate muscular imbalance or
degenerative joint disease. The normal opening should be at least 40 mm
from the maxillary incisal edge to the mandibular incisal edge in an Angle
Class I patient, taking into consideration an overjet or overlap. If any
horizontal overjet or overlap exists, its value in millimeters is subtracted
from the 40-mm minimum opening measurement.41 The range of opening
without regard for overlap or overjet has been measured in the range of 38 to
65 mm for men and 36 to 60 mm for women from incisal edge to edge.42
Increased mobility of teeth may be an indication of a force beyond
physiologic limits, bone loss, or their combination. This requires further
investigation in regard to parafunction and is very important if an implant
may be placed in the region of the mobile teeth. The rigid implant may
receive more than its share of occlusal force when surrounded by mobile
teeth. Fremitus, a vibration type of mobility of a tooth, is often present in the
clenching patient. To evaluate this condition, the dentist's finger barely
contacts the facial surface of one tooth at a time and feels for vibrations while
the patient taps the teeth together. Fremitus is symptomatic of a local excess
of occlusal loads.
Cervical erosion is often a sign of parafunctional clenching (Fig. 3.73). The
notched appearance of the cervical portion of the tooth directly correlates
with the concentration of forces shown in three-dimensional finite analysis
and photoelasticity studies.43 Abfraction of teeth was also observed in cats,
rats, and marmosets and was described in the literature as early as 1930. A
study of a noninstitutionalized older human population revealed that
cervical abrasion was present in 56% of the participants.44
FIG 3.73 Clenching habits are more difficult to diagnose because occlusal wear is
often absent. (A) A common sign is scalloping of the tongue, which results from
tongue protrusion during clenching. (B) Antegonial notch, which results from
massetter hypertrophy. (C) Prosthesis fracture resulting from excessive
biomechanical force.
Complications
Postoperative care.
A common cause of implant failure during healing is parafunction in a
patient wearing a soft tissue–supported prosthesis over a submerged
implant. The tissue overlying the implant is compressed during the
parafunction episode. The premature loading may cause micromovement of
the implant body in the bone and may compromise osteointegration. When
an overlying soft tissue–borne restoration exerts pressure as a result of
parafunction, pressure necrosis causes soft tissue dehiscence over the
implant. This condition is not corrected by surgically covering the implant
with soft tissue, but the soft tissue support region of the prosthesis over the
implant should be generously relieved during the healing period whenever
parafunction is noted. With metal-free partial dentures, this may weaken the
prosthesis leading to possible fractures.
Treatment Planning for Parafunction Patients

(Clenching/Bruxism)
Progressive Bone Loading.

The time intervals between prosthodontic restoration appointments may be
increased to provide additional time to produce load-bearing bone around
the implants through progressive bone-loading techniques.45 By utilizing the
progressive bone loading technique, poorer bone density is transformed into
better quality bone, which is more ideal for excessive occlusal loads.
Greater Surface Area.

Anterior implants that are subjected to parafunctional forces are problematic
because they are usually nonaxial or shear forces. To counteract this excessive
force the use of wider-diameter implants or additional number of implants
(i.e., greater surface area) should be treatment planned.
Occlusion.
With parafunctional habits, the occlusion must be strictly designed and
monitored. Ideally, the patient should be maintained in a canine guided
occlusion, as long as the canines are healthy. Mutually protected occlusion,
with additional anterior implants or teeth distributing forces, is developed if
the implants are in the canine position or if this tooth is restored as a pontic.
The anterior teeth may be modified to recreate the proper incisal guidance
and avoid posterior interferences during excursions.
The elimination of posterior lateral occlusal contacts (i.e., nonaxial loading)
during excursive movements is recommended when opposing natural teeth
or an implant or tooth-supported fixed prosthesis. This is beneficial in two
aspects: (a) because lateral forces dramatically increase stress at the implant-
bone interface, the elimination of posterior contacts diminishes the negative
effect of angled forces during bruxism, and (b) the presence of posterior
contacts during excursions, and almost all fibers of the masseter, temporalis,
and the external pterygoid muscles contract and place higher forces on the
anterior teeth and implants. On the contrary, during excursions in the
absence of posterior contacts, fewer fibers of the temporalis and masseter
muscles are stimulated, and the forces applied on the anterior implant–teeth
system are reduced by as much as two thirds.
Prosthesis Design.
The prosthesis may be designed to improve the distribution of stress
throughout the implant system with centric vertical contacts aligned with the
long axis of the implant whenever possible. Narrow posterior occlusal tables
to prevent inadvertent lateral forces and to decrease the occlusal forces are
beneficial. Enamoplasty of the cusp tips of the opposing natural teeth is
indicated to help improve the direction of vertical forces within the
guidelines of the intended occlusion (i.e., improve plane of occlusion) newer
occlusal materials (e.g., zirconia). Wider implant bodies, harder cement types
(e.g., zinc phosphate vs. zinc oxide), titanium alloy implant bodies, and more
implants splinted together are all beneficial.
Occlusal Guard.
The most important treatment for a patient with parafunctional habits is the
use of an occlusal guard. Ideally, patients should wear a hard, processed
acrylic occlusal guard at night. The guard will absorb the majority of the
parafunctional forces, reducing the damaging forces to the implant system.
Patients should also be instructed to wear the guard during any time they
might exhibit parafunction, such as stressful time periods, driving, and
working at a computer.
Tongue Thrust and Size.

Parafunctional tongue thrust is the unnatural force of the tongue against the
teeth during swallowing. A force of approximately 41 to 709 g/cm2 on the
anterior and lateral areas of the palate has been recorded during
swallowing.46 These forces may cause clinical complications.
Types.
Several different types of tongue thrust have been identified; anterior,
intermediate, posterior, and either unilateral or bilateral, which may be
found and in almost any combination (Fig. 3.74). To evaluate anterior tongue
thrust, the doctor holds the lower lip down, squirts water into the mouth with
the water syringe, and asks the patient to swallow. A normal patient forms a
vacuum in the mouth by positioning the tongue on the anterior aspect of the
palate and is able to swallow without difficulty. A patient with an anterior
tongue thrust is not able to create the vacuum needed to swallow when the
lower lip is retracted because the seal and vacuum for the patient are
achieved between the tongue and the lower lip. As a consequence, the
patient is unable to swallow while the lower lip is withdrawn.
FIG 3.74 Patient with anterior openbite secondary to tongue thrust. Because of the
openbite, the patient has no anterior guidance with mandibular excursions.
A posterior tongue thrust is evaluated by retracting one cheek at a time

away from the posterior teeth or edentulous region with a mouth mirror,
injecting water into the mouth with a water syringe and asking the patient to
swallow. Visual evidence of the tongue during deglutition may also be
accompanied by pressure against the mirror and confirms a lateral force.
Complications
Early loading.
Although the force of tongue thrust is of lesser intensity than in other
parafunctional forces, it is horizontal and can increase stress at the
permucosal site of the implant. This is most critical for one-stage surgical
approaches and immediate restoration of implants in which the implants are
in an elevated position at initial placement and the implant interface is in an
early healing phase. If the natural teeth in the region of the tongue thrust
were lost as a result of an aberrant tongue position or movement, the
implants are at increased risk during initial healing and early prosthetic
loading (Box 3.11).
Box 3.11
Parafunction
Tongue Thrust and Size
1. Tongue thrust
a. Less force than bruxism or clenching
b. Is constant
c. Horizontal direction
2. Several types possible
a. Anterior
b. Intermediate
c. Posterior unilateral or bilateral

3. Incision line opening after surgery
4. Early loading risk for one stage or immediate restorations
5. Prosthetic complications
Incision line opening.

The tongue thrust may also contribute to incision line opening after bone
grafting or implant surgery, which may compromise both the hard and soft
tissues. This is especially noteworthy in a bone augmentation procedure.
Tooth movement.
A tongue-thrust habit may lead to tooth movement or mobility, which is of
consequence when implants are present in the same quadrant. If the
remaining teeth exhibit increased mobility, the implant prosthesis may be
subject to increased occlusal loads.
Inadequate tongue room.

A potential prosthetic complication for a patient with a lateral tongue thrust
is the complaint of inadequate room for the tongue after the mandibular
implants are restored. A prosthetic mistake is to reduce the width of the
lingual contour of the mandibular teeth to give the tongue more space. The
lingual cusp of the restored mandibular posterior teeth should follow the
curve of Wilson and have a proper horizontal overjet to protect the tongue
during function. A reduction in the width of the mandibular posterior teeth
often increases the occurrence of tongue biting and may not dissipate with
time. When the lingual surface of the mandibular restoration is reduced, the
entire prosthesis may need to be refabricated. The restoring dentist should
identify the tongue position before treatment and inform the patient about
the early learning curve for the tongue once the teeth are delivered on the
implants (Fig. 3.75).
FIG 3.75 In a patient with missing teeth and no prosthetic replacement, such as a
complete or partial denture, the tongue often increases in size. The tongue does not
transfer an active lateral force during swallowing. This tongue type will adapt most
often to a mandibular posterior implant prosthesis. (From Misch CE: Dental implant
Complication prevention.
Even in the absence of tongue thrust, the tongue often accommodates to the
available space, and its size may increase with the loss of teeth. As a result, a
patient not wearing a mandibular denture often has a larger-than-normal
tongue. The placement of implants and prosthetic teeth in such a patient
results in an increase in lateral force, which may be continuous. The patient
then complains of inadequate room for the tongue and may bite it during
function. However, this condition is usually short lived, and the patient
eventually adapts to the new intraoral condition. However, it has been
observed a fixed restoration is more advantageous for this type of patient. If
the patient has a RP-5 prosthesis, it should be turned into an RP-4: An RP-5
restoration is much less stable in patients with tongue thrust or size issues,
and patient complaints are more common with removable restorations in
general.
Crown Height Space (CHS)
Definition
The crown height space or interarch distance is defined as the vertical
distance between the maxillary and mandibular dentate or dentate arches
under specific conditions (e.g., the mandible is at rest or in occlusion).47 The
CHS for implant dentistry is measured from the crest of the bone to the
plane of occlusion in the posterior region and the incisal edge of the arch in
question in the anterior region (Fig. 3.76). In the anterior regions of the
mouth, the presence of a vertical overbite means the CHS is larger in the
maxilla than the space from the crest of the ridge to the opposing teeth
incisal edge. In general, when the anterior teeth are in contact in centric
occlusion, there is a vertical overbite. The anterior mandibular CHS is usually
measured from the crest of the ridge to the mandibular incisal edge.
However, the anterior maxillary CHS is measured from the maxillary crestal
bone to the maxillary incisal edge, not the occlusal contact position.
FIG 3.76 The crown height space is measured from the occlusal plane to the crest
of the bone. The ideal space for a FP-1 prosthesis is between 8 mm and 12 mm.
CT, Connective tissue attachment; JE, junctional epithelial attachment. (From Misch
CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The ideal CHS needed for a fixed implant prosthesis should range between
8 and 12 mm. This measurement accounts for the “biologic width,” abutment
height for cement retention or prosthesis screw fixation, occlusal material
strength, esthetics, and hygiene considerations around the abutment crowns.
Removable prostheses often require a CHS greater than 12 mm for denture
teeth and acrylic resin base strength, attachments, bars, and oral hygiene
considerations (Box 3.12).48
Box 3.12
Crown Height Space
• The CHS is measured from the occlusal plane to the crest of the bone.
• CHS does not have a specific ideal dimension. With fixed restorations, the
acceptable range for CHS is between 8 and 12 mm.
• Removable implant restorations often require a CHS of 12 mm or more,

especially when a bar connects the individual implants.
• An increase in prosthetic complications occurs with either limited or

excessive CHS.
CHS, crown height space.

Complications
Increased Force.
By definition, force magnifiers are situations or devices that increase the
amount of force applied to a system and include a screw, pulley, incline plane,
and lever.18 The biomechanics of CHS are directly related to lever mechanics.
The properties of a lever have been appreciated since the time of Archimedes
2000 years ago. (“Give me a lever and a fulcrum and a place to stand and I
can move the world.”) The complex issues of cantilevers and implants have
been demonstrated in the edentulous mandible, where the length of the
posterior cantilever directly related to complications or failure of the
prosthesis.49 Rather than a posterior cantilever, the CHS is a vertical
cantilever when any lateral or cantilevered load is applied and is also a force
magnifier (Fig. 3.77). As a result, because CHS excess increases the amount of
force, any of the mechanical complications related to implant prostheses may
also increase, including uncemented prosthesis, screw loosening (prosthetic
or abutment), overdenture attachment complications, and so on.
FIG 3.77 The crown height space is a vertical cantilever to any angled load or
cantilever. The FP-3 on the right will deliver greater stresses to the implant
compared with the implant on the left. A wider-diameter implant is of benefit to
support the implant restoration on the right. (From Misch CE: Dental implant prosthetics, ed
2, St Louis, 2015, Mosby.)
Cantilevers.
When the direction of a force is in the long axis of the implant, the stresses to
the bone are not magnified in relation to the CHS (Fig. 3.78). However, when
the forces to the implant are on a cantilever or a lateral force is applied to the
crown, the forces are magnified in direct relationship to the crown height.
Bidez and Misch evaluated the effect of a cantilever on an implant and its
relation to crown height.50 When a cantilever is placed on an implant, there
are six different potential rotation points (i.e., moments) on the implant body
(Fig. 3.79; Table 3.4). When the crown height is increased from 10 to 20 mm,
two of six of these moments are increased by approximately 200%.
FIG 3.78 When a long axis load is applied to an implant, the crown height does not
magnify the load. The implant on the left will have similar stress to the one on the
right because the load is in the long axis. (From Misch CE: Dental implant prosthetics, ed 2,
FIG 3.79 Moment loads tend to induce rotations in three planes. Clockwise and
counterclockwise rotations in these three planes result in six moments: lingual-
transverse, facial-transverse, occlusal, apical, facial, and lingual. (From Misch CE:
TABLE 3.4
Moment Load at Crest, When Subjected to Forces Shown in Fig. 3.79
Influences on Mom ent Im posed Mom ents (N/m m ) at Im plant Crow n-to-Crest Interface
Occlusal Height (mm) Cantilever Length (mm) Lingual Facial Apical Occlusal Facial Transverse Lingual Transverse
10 10 100 0 50 200 0 100
10 20 100 0 50 400 0 200
10 30 100 0 50 600 0 300
20 10 200 0 100 200 0 100
20 20 200 0 100 400 0 200
20 30 200 0 100 600 0 300
A cantilevered force may be in any direction: facial, lingual, mesial, or

distal. Forces cantilevered to the facial and lingual direction are often called
offset loads. Because bone resorption proceeds from buccal to lingual and
results in decreased width. Unless bone augmentation is completed,
implants will be often placed more lingual than the center of the natural
tooth root. This often results in a final restoration cantilevered to the facial.
When the crest of the ridge resorbs, available bone height is also decreased,
and the CHS is increased. The potential length of the implant is often
reduced in excessive CHS conditions (i.e., because of vital structures), and
the more lingual implant position results in offset loads (i.e., biomechanical
disadvantage).
The vertical distance from the occlusal plane to the opposing landmark for
implant insertion is typically a constant in an individual (with the exception
of the posterior maxilla because the sinus cavity expands more rapidly than
crestal bone resorption in height). As the bone resorbs, the crown height
becomes larger, but the available bone height decreases (Fig. 3.80). An
indirect relationship is found between the prosthesis and implant height.
Moderate bone loss before implant placement may result in a crown height–
bone height ratio greater than 1, with greater lateral forces applied to the
crestal bone than in abundant bone (in which the crown height is less). A
linear relationship exists between the applied load and internal stresses
within the bone.51 Therefore, the greater the load applied, the greater the
tensile and compressive stresses transmitted at the bone interface and to the
prosthetic components. And yet many implant treatment plans are designed
with more implants in abundant bone situations and fewer implants in
atrophied bone volume. The opposite scenario should ideally exist. The
available bone present, the greater the crown height and the greater the
number of implants indicated (Fig. 3.81).
FIG 3.80 In the past, treatment plans included more and longer implants in
abundant bone (top) but fewer and shorter implants in less available bone (bottom).
However, crown height increases as bone height decreases, and this approach
creates unfavorable mechanics when the bone height is reduced. (From Misch CE:
FIG 3.81 Crown height is a force magnifier to any lateral load or horizontal
cantilever. When available bone height decreases with a greater crown height, more
implants should be inserted and cantilever length reduced. (From Misch CE: Dental
Treatment of Excessive Crown Space

Crown height space greater than 15 mm is considered excessive and is
primarily the result of the vertical loss of alveolar bone from long-term
edentulism. Other causes may include genetics, trauma, and past implant
failure. Treatment of excessive CHS before implant placement includes
orthodontic and surgical methods. Orthodontics in partially edentulous
patients (i.e., especially in the growth and development state) is the method
of choice because other surgical or prosthetic methods are usually more
costly and have greater risks of complications. Several surgical techniques
may also be considered, including block onlay bone grafts, particulate bone
grafts with titanium mesh or barrier membranes, interpositional bone grafts,
and distraction osteogenesis. A staged approach to reconstruction of the jaws
is often preferred to simultaneous implant placement, especially when large-
volume gains are required. Significant vertical bone augmentation may even
require multiple surgical procedures.
In case of excessive CHS, bone augmentation may be preferred to
prosthetic replacement, especially in type C−h or D bone volumes. Surgical
augmentation of the residual ridge height reduces the CHS and improves
implant biomechanics by both position and number. Augmentation often
permits the placement of wider-body implants with the associated benefit of
increased surface area (Fig. 3.82). Prosthetics is the most commonly used
option to address excess CHS; however, it should be the last choice. Using
gingival-colored prosthetic materials (pink porcelain, acrylic resin, or stained
zirconia) on fixed restorations or changing the prosthetic design to a
removable restoration should often be considered when the prosthesis is
used to restore excessive CHS (Fig. 3.83).
FIG 3.82 (A) A panoramic radiograph of a severely resorbed maxilla and mandible.
(B) An autologous bone graft may be used to increase the available bone height and
reduce the crown height in a Division C or D bone volume. (C) A panoramic
radiograph after the iliac crest bone graft to the maxilla and mandible. (D) Implants
may be inserted into the bone graft after 6 months. (E) The implants are prepared to
support a cemented prosthesis. (F) A FP-3 fixed restoration is fabricated. (G) The
maxillary and mandibular FP-3 prosthesis in place. (H) The high smile line of the
patient. (I) A panoramic radiograph of the iliac crest, implants, and prostheses. (From
Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 3.83 When the crown height space is greater than 12 mm, pink porcelain (or
acrylic) is often used to replace the soft tissue drape in the prosthesis. (From Misch
In the maxilla, a vertical loss of bone results in a more palatal ridge

position. As a consequence, implants are often inserted more palatal than the
natural tooth position. Removable restorations have several advantages
under these clinical circumstances. The removable prosthesis does not
require embrasures for hygiene. The removable restoration may be removed
during sleep to decrease the effects of an increase in CHS on nocturnal
parafunction. The removable restoration may improve the lip and facial
support, which is usually deficient because of the advanced bone loss. The
overdenture may have sufficient bulk of acrylic resin to decrease the risk of
prosthesis fracture and allow for ease of repair. The increase in CHS permits
ideal denture tooth placement without infringement of the implant-
prosthetic substructure.
The excessive CHS on a RP-5 prosthesis often makes the restoration more
unstable and often requires more soft tissue support. In RP-5 overdentures,
there are two different components of the CHS: (1) the distance from the
crest of the ridge to the height of the overdenture attachment and (2) the
distance from the overdenture attachment to the occlusal plane. The greater
the distance from the attachment to the occlusal plane, the more force on the
prosthesis to move or rotate on the attachment and the greater the prosthesis
mobility (and less the stability). Therefore, more tissue support, (i.e., buccal
shelf) is required during function. If the prosthesis loads the soft tissue
incorrectly, sore spots may occur and may accelerate the posterior bone loss
(Fig. 3.84).
FIG 3.84 A RP-5 overdenture is usually less stable when the crown height space
(CHS) is large. The CHS of the prosthesis is measured from the occlusal plane to
the height of the overdenture attachments. (From Misch CE: Dental implant prosthetics, ed 2,
An increase in the biomechanical forces is in direct relationship to the

increase in CHS. The treatment plan of the implant restoration should
consider stress-reducing options whenever the CHS is increased. Methods to
decrease stress include:
1. Shorten cantilever length.
2. Minimize offset loads to the buccal or lingual.
3. Increase the number of implants.
4. Increase the diameters of implants.
5. Utilize implants with maximum surface area.
6. Fabricate removable restorations that are less retentive and incorporate

soft tissue support (e.g., buccal shelf).
7. Remove the removable restoration during sleeping hours to reduce the

noxious effects of nocturnal parafunction.
8. Splint implants together, whether they support a fixed or removable

prosthesis.
Crown height space is a considerable force magnifier; the greater the

crown height, the shorter the prosthetic cantilever that should extend from
the implant support system. When the CHS is greater than 15 mm, no
cantilever should be considered unless all other force factors are minimal.
The occlusal contact intensity should be reduced on any offset load from the
implant support system. Occlusal contacts in centric relation occlusion may
even be eliminated on the most posterior aspect (or offset region) of a
cantilever. In this way a parafunction load may be reduced because the most
cantilevered portion of the prosthesis is only loaded during functional
activity (e.g., chewing).52
Arch Position
Posterior Has Higher Forces
The arch position is an important part of the treatment planning process and
has a significant impact on the amount of force generated to an implant
prosthesis. In general, the maximum biting force is greater in the molar
region and decreases as measurements progress anteriorly. Maximum bite
forces in the anterior incisor region correspond to approximately 35 to 50 psi,
those in the canine region range from 47 to 100 psi, and those in the molar
area vary from 127 to 250 psi (Fig. 3.85).53 Mansour et al evaluated occlusal
forces and moments mathematically using a class III lever arm, the condyles
being the fulcrum and the masseter and temporalis muscles supplying the
force.54 The forces at the second molar were 10% higher than at the first
molar, indicative of a range from 140 to 275 psi.
FIG 3.85 The maximum bite forces are greater in the posterior regions of the jaws
compared with the anterior regions. (From Misch CE: Dental implant prosthetics, ed 2, St
Arch position should also consider the anterior maxilla versus the anterior
mandible. Not only is the bone generally denser in the anterior mandible,
but the direction of force is also more in the long axis for the lower anterior
teeth. The angled load of 12 to 15 degrees in maxillary anterior implants
increases the force by approximately 25%. Note that the maxillary anterior
teeth are wider in diameter and have greater surface area compared with the
smallest teeth in the mouth, the mandibular incisors. The amount of force is
similar, but the direction of force places the maxillary teeth more at risk.
Arch position includes the maxillary arch vs. the mandibular arch. As
previously mentioned the bone in the mandible is more often more dense
than that of the maxilla, especially in the posterior regions. The edentulous
maxilla with a poorer bone density requires more implants or larger widths
compared with the edentulous mandible. It is interesting to note that the
maxillary dentition has more roots and greater surface area roots than the
mandibular counterparts (Box 3.13). Yet, in the edentulous maxilla, there is
less available bone height than any region because the maxillary sinus
quickly expands to decrease bone height.
Box 3.13
Arch Position
Posterior Regions
1. Significantly higher biting force in the molar regions.
a. Mechanical component: class III lever
b. Biologic component: amount of muscle mass

contraction
2. Posterior region is associated with long-term crestal bone loss of integrated
implants
3. Bone density poorer than in anterior regions of mouth (e.g., D3/D4 -

maxilla vs. D2 - mandible)
4. Posterior maxilla more at risk than posterior mandible because of poorer

bone quality
5. Posterior maxilla has least bone volume

a. Crestal bone loss
b. Sinus expansion
c. Close approximation and root apexes extending into

maxillary sinus (e.g., palatal and MB root of first
molar)
6. Posterior mandible less bone height than anterior regions
a. Position of mandibular canal and foramen
b. Angulation issues because of the buccal bone

resorption
c. Sublingual undercuts
Complications
Greater Bone Loss.

In a study by Chung et al with 339 implants in 69 patients in function for an
average of 8.1 years (range, 3–24 years), the posterior implants (even with
keratinized mucosa) showed a 3.5-fold greater average bone loss per year
than anterior implants.55 In the region of higher bite forces, greater bone loss
may be evident. The anterior biting force is decreased in the absence of
posterior tooth contact and greater in the presence of posterior occlusion or
eccentric contacts. Besides the mechanical properties of a class III lever
function, there also is a biologic component to decrease bite force in the
anterior regions. When the posterior teeth are in contact, the large
masticatory muscles contract. When the posterior teeth are not in contact,
two thirds of the temporalis and masseter muscles do not contract their
fibers, which result in the biting force being reduced.
Decreased Surface Area.
In the anterior regions with less force, the anterior natural tooth roots are
smaller in diameter and root surface area compared with posterior teeth. The
greatest increase in natural tooth surface area occurs in the molar region,
with a 200% increase compared with the premolars. Yet in implant dentistry,
we primarily determine the implant length by existing bone volume and
place longer implants in the anterior region and shorter implants in the
posterior regions (or cantilever off the anterior implants, which results in
posterior bite forces magnified by the cantilever length). This approach
should be corrected to conform to the biomechanical load similar to that
observed with natural teeth. However, the length of an implant is less
effective to dissipate force. Instead, implant width and design are more
effective. The best option to decrease stress is to increase implant number.
Implants in the posterior regions should often be of greater diameter or
greater number (because molars have more roots), especially in the presence
of additional force factors.
Poorer Bone Density Resulting in Less Support.

The natural teeth are surrounded by a thin cortical plate of bone and
periodontal complex, which is similar for all teeth and arch positions.
However, after the teeth are lost, the bone density in the edentulous site is
reduced and is often different for each region of the mouth. The posterior
regions, in general, form less bone density after tooth loss than the anterior
regions, with the anterior maxilla less dense than the mandible. The
mandibular anterior implant sites benefit from denser bone than the
maxillary anterior implant sites. The denser the bone, the greater its
resistance to stress applied at the implant-bone interface. In other words, the
edentulous bone density is inversely related to the amount of force and
surface area of the natural tooth roots generally applied in that arch position.
As a result, the posterior maxilla is the most at-risk arch position followed by
the posterior mandible and then the anterior maxilla. The most ideal region
for implant stress transfer within the physiologic loading zone for bone is the
mandibular anterior region.56
Opposing Arch
An often overlooked factor in the treatment planning process is the opposing
arch. In general, natural teeth transmit greater impact forces through
occlusal contacts than soft tissue–borne complete dentures. In addition, the
maximum occlusal force of patients with complete dentures is limited and
may range from 5 to 26 psi.57 The force is usually greater in recent denture
wearers and decreases with time. Muscle atrophy, thinning of the oral tissues
with age or disease, and bone atrophy often occur in edentulous patients as a
function of time.58 Some denture wearers may clench on their prosthesis
constantly, which may maintain muscle mass, but will usually result in bone
loss.
The maximum force generated against an implant prosthesis is related to
the number of teeth or implants supporting the prosthesis in the opposing
arch. Partially edentulous dentate patients have less force than dentate
patients with all of their teeth. Patients with partial dentures may have forces
intermediate between those of natural teeth and complete dentures,
depending on the location and condition of the remaining teeth, muscles,
and joints. In partially edentulous patients with implant-supported fixed
prostheses, force ranges are more similar to those of natural dentition, but
lack of proprioception may magnify the load amount during parafunctional
and functional activity (Fig. 3.86).
FIG 3.86 Opposing arch. Greatest forces from high to low. (A) Implant-supported
fixed prosthesis. (B) Conventional fixed porcelain fused to metal. (C) Natural
Dentition. (D) Overdenture/conventional denture.
A complete implant fixed prosthesis does not benefit from proprioception

as do natural teeth, and patients chew food with a force four times greater
than with natural teeth. The highest forces are created with implant
prostheses in the opposing arch. An RP-4 overdenture may have some
movement compared with a fixed prosthesis and is more likely to have acrylic
or resin teeth. Hence, the bite force is slightly less than for a full arch fixed
implant prosthesis. In addition, premature contacts in occlusal patterns or
during parafunction on the implant prostheses do not alter the pathway of
closure because occlusal awareness is decreased with implant prostheses
compared with natural teeth. Continued stress increases can be expected to
occur with the implant restoration (Box 3.14).
Box 3.14
Opposing Arch
Force Generated (Lowest to Highest)
1. Soft tissue–borne denture (conventional complete denture)

2. RP-5 overdenture (primary support - soft tissue)
3. Partially edentulous arch
4. Dentate arch
5. RP-4 overdenture (primary support - implants)
6. Fixed implant prosthesis (full-arch implant-supported)
The opposing arch is not as major a factor to alter an implant treatment

plan as parafunction, masticatory dynamics, or excessive CHS, but is a major
factor for the risk of porcelain or prosthesis fracture. In a report by Kinsel
and Lin, the opposing dentition varies the incidence of porcelain fracture to
an implant crown.59 When the opposing arch was a denture, 0% fracture of
the implant crowns in the opposing arch was found. The opposing dentition
of a natural tooth found 3.2% fracture of implant crowns. The opposing
dentition of a crown on a natural tooth found a 5.7% fracture of the opposing
implant crown. A 16.2% fracture was observed when an implant crown
opposed an implant crown. When the percentage of patients with major
fractures of porcelain were compared to the percentage with no fractures, the
incidence of patients with porcelain fractures of implant crowns was 19.4%
for natural teeth and 69.5% of patients with implant crowns in the opposing
arch. Therefore, the opposing dentition may increase the impact force, and
the greater the force, the higher the risk of porcelain fracture (Box 3.15).
Box 3.15
Implant Crown Porcelain Fracture Related to
Opposing Arch
Least to Highest Risk
1. Complete denture (0%)
2. Natural teeth (3.2%) (19.4% of patients)
3. Crown on a natural tooth (5.7%)

4. Implant crown (16.2%) (69.5% of patients)
As a consequence of the opposing arch affecting the intensity of forces

applied to an implant prosthesis, the treatment plan may be modified to
reduce the risk of fatigue fracture and overload. Rarely should the opposing
arch be maintained in a traditional denture as a method to decrease the
stress to the implant arch. Unfortunately, many edentulous patients opt to
remain in a denture for the maxillary arch as a consequence of the increased
costs associated with implant prostheses. However, the patient should be
aware of the continued bone loss in the maxillary edentulous arch, and a
preferred treatment is an implant-supported prosthesis in both arches in
order to maintain the existing bone volume.
Arch Form
The patient's arch form should always be evaluated in the treatment planning
process, especially in the mandibular arch. There exist many variations on the
size and shape of patients' arch forms. The distance from the center of the
most anterior implant to a line joining the distal aspect of the two most distal
implants on each side is called the anteroposterior (A-P) distance or the A-P
spread (Fig. 3.87).60 The greater the A-P spread (Fig. 3.87),60 theorectically the
farther the distal cantilever may be extended to replace the missing posterior
teeth, which minimizes force-related issues. As a general rule, when five to
six anterior implants are placed in the anterior mandible between the
foramina to support a fixed prosthesis, the cantilever should not exceed two
times the A-P spread, with all other stress factors being low.
FIG 3.87 The anteroposterior (A-P) distance is determined by a line drawn from the
distal portion of the distalmost implant on each side of the arch and another parallel
line drawn through the center of the anteriormost implant from the cantilever. (From
The A-P distance is directly affected by the arch form. The types of arch
forms may be separated into square, ovoid, and tapering. A square arch form
in the anterior mandible has a 0- to 6-mm A-P spread between the most distal
and most anterior implants (Fig. 3.88). An ovoid arch form has an A-P
distance of 7 to 9 mm and is the most common type (Fig. 3.89). A tapering
arch form has an A-P distance greater than 9 mm (Fig. 3.90). Whereas a
tapering arch form may support a 20-mm cantilever, a square arch form
requires the cantilever to be reduced to 12 mm or less. A tapering arch form
is most ideal, and a square arch form is susceptible to force-related
complications.
FIG 3.88 A mandibular square arch form has an anteroposterior (A-P) distance of 0
to 6 mm. As a result, a cantilever is limited. (From Misch CE: Dental implant prosthetics, ed
FIG 3.89 A mandibular ovoid arch form has an anteroposterior (A-P) distance of 7
to 9 mm and is the most common type. A cantilever may extend to 18 mm with the
ovoid-type arch. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 3.90 A mandibular tapered arch form has an anteroposterior (A-P) distance of
greater than 9 mm, and is the type least observed. A cantilever is least at risk for this
arch form. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The A-P spread is only one of the force factors to be considered for the
extent of the distal cantilever. If the stress factors are high (e.g., parafunction,
crown height, masticatory musculature dynamics, opposing arch), the
cantilever length of a prosthesis should be reduced and may even be
contraindicated.
Bone Density
Treatment Planning
The external (cortical) and internal (trabecular) structure of bone may be
described in terms of quality or density, which reflects a number of
biomechanical properties, such as strength, modulus of elasticity, bone-
implant contact (BIC) percent, and stress distribution around a loaded
endosteal implant (Box 3.16). The external and internal architecture of bone
controls and dictates virtually the surgical and prosthetic protocol for the
patient. The density of available bone in an edentulous site is a determining
factor in treatment planning, surgical approach, implant design, healing
time, and the need for initial progressive bone loading during prosthetic
reconstruction.56
Box 3.16
Bone Quality Reflects
• Strength of cortical/cancellous bone
• Modulus of elasticity
• Bone-implant contact percent (interface)
• Stress contours around a loaded endosteal implant
• Surgical protocol
• Healing time
• Need for progressive bone loading
The bone density has a significant impact on the treatment planning of an

implant patient. The initial treatment plan is presented to the patient using
the anatomic location as an index of the bone density: anterior mandible and
single tooth replacement is D2, anterior maxilla and posterior mandible is
D3, and posterior maxilla is D4. After the initial treatment evaluation of the
osseous structures are taken into consideration (e.g., prosthesis type and
design, implant key position, and patient force factors), a more complete
treatment plan relative to bone density is obtained by a CBCT scan or
modified during the surgical procedure using the tactile method to
determine bone density.
Understanding the Basics of Bone

Bone is an organ that is able to change in relation to a number of factors,
including hormones, vitamins, and mechanical influences. However,
biomechanical parameters, such as the amount of strain transmitted to bone,
are predominant. Awareness of this adaptability in the skeletal system has
been reported for more than a century. In 1887, Meier qualitatively described
the architecture of trabecular bone in the femur.61 In 1888 Kulmann noticed
the similarity between the pattern of trabecular bone in the femur and
tension trajectories in construction beam concepts used by Eiffel (Fig. 3.91).62
Wolff, in 1892, further elaborated on these concepts and published: “Every
change in the form and function of bone or of its function alone is followed
by certain definite changes in the internal architecture, and equally definite
alteration in its external conformation, in accordance with mathematical
laws.”63 It has been widely reported that, in the structural skeleton, the
external architecture of bone (cortical bone) changes in relation to function,
and the internal bony structure (trabecular bone) is also modified (Wolff ’s
Law).
FIG 3.91 The proximal head of the femur has trabecular bone aligned along stress
pathways, similar to beams for a bridge or tower. (From Misch CE: Dental implant
The structural changes in bone as a consequence of mechanical influences

have also been noted in the jaws. As an example, both MacMillan and Parfitt
have reported on the structural characteristics and variation of trabeculae in
the alveolar regions of the jaws.64 The maxilla and mandible have different
biomechanical functions (Fig. 3.92). The mandible, as an independent
structure, is designed as a force-absorption unit. When teeth are present, the
outer cortical bone is much denser and thicker, and the trabecular bone is
more coarse and dense (Fig. 3.93). This bony architectural make-up is in
direct relation to the force applied. On the other hand, the maxilla is a force-
distribution unit. Stresses to the maxilla are transferred by the zygomatic arch
and palate away from the brain and orbit. As a consequence, the maxilla has
a thin cortical plate and fine trabecular bone surrounding the teeth (Fig.
3.94). When evaluating bone quality around natural teeth, Neufeld noted that
the bone is most dense around the teeth (cribriform plate) and more dense
around the teeth at the crest compared with the regions around the apices
(Fig. 3.95).65
FIG 3.92 The maxilla and mandible vary in their bony make-up. The maxilla is a
force distribution unit, and the mandible is a force absorption unit. As a
consequence, the cortical and trabecular bone are different. (From Misch CE: Dental
FIG 3.93 The trabecular bone in a dentate mandible is coarser than that in the
maxilla. The cortical bone is thick and dense. The mandible, as an independent
structure, is a force-absorbing element. (From Misch CE: Dental implant prosthetics, ed 2, St
FIG 3.94 The dentate maxilla has a finer trabecular pattern compared with the
mandible. The cortical bone is more thin and porous. The maxilla is a force
distribution unit and is designed to protect the orbit and brain. (From Misch CE: Dental
FIG 3.95 The trabecular bone of each jaw has structural variations. The trabecular
bone is densest next to the teeth, where it forms the cribriform plate. Between the
teeth, the bone is usually densest near the crest and least dense at the apex. (From
Orban demonstrated a decrease in the trabecular bone pattern around a

maxillary molar with no opposing occlusion compared with a tooth with
occlusal contacts on the contralateral side (Fig. 3.96).66 Bone density in the
jaws also decreases after tooth loss. This loss is primarily related to the
length of time the region has been edentulous and not loaded appropriately,
the initial density of the bone, flexure and torsion in the mandible, and
parafunction before and after tooth loss. In general, the density change after
tooth loss is greatest in the posterior maxilla and least in the anterior
mandible.
FIG 3.96 On the left, the opposing mandibular tooth was removed. A lack of
occlusal contact resulted in loss of trabecular bone around the maxillary tooth. The
tooth on the right is from the same monkey, with the opposing mandibular tooth in
place. The trabecular bone is much denser around the tooth. The disuse atrophy
observed on the left is from inadequate microstrain conditions to maintain the
bone. (From Orban B: Oral histology and emb ryology, ed 3, St Louis, 1953, Mosby.)
Cortical and trabecular bone throughout the body is constantly modified

by either modeling or remodeling. Modeling has independent sites of
formation and resorption and results in the change of the shape or size of
bone. Remodeling is a process of resorption and formation at the same site
that replaces previously existing bone and primarily affects the internal
turnover of bone, including that region where teeth are lost or the bone next
to an endosteal implant. These adaptive phenomena have been associated
with the alteration of the mechanical stress and strain environment within
the host bone.67
Stress is determined by the magnitude of force divided by the functional
area over which it is applied. Strain is defined as the change in length of a
material divided by the original length. The greater the magnitude of stress
applied to the bone, the greater the strain observed in the bone.18 Bone
modeling and remodeling are primarily controlled, in part or whole, by the
mechanical environment of strain. Overall, the density of alveolar bone
evolves as a result of mechanical deformation from microstrain.
Frost proposed a model of modeling/remodeling patterns for compact
bone as it relates to mechanical adaptation to strain.68 Spontaneous fracture,
the pathologic overload zone, mild overload zone, adapted window, and
acute disuse window were described for bone in relation to the amount of the
microstrain experienced (Box 3.17). These categories also may be used to
describe the trabecular bone response next to a dental implant in the jaws.
Box 3.17
Mechanical Adaptation of Bone Categories6 8
1. Spontaneous fracture
2. Pathologic overload zone
3. Mild overload zone
4. Adapted window
5. Acute disuse window
With disuse atrophy, bone loses mineral density, and disuse atrophy occurs
because modeling for new bone is inhibited and remodeling is stimulated,
with a gradual net loss of bone. The microstrain of bone for trivial loading is
reported to be 0 to 50 microstrain.68 This phenomenon may occur throughout
the skeletal system, as evidenced by a 15% decrease in the cortical plate and
extensive trabecular bone loss consequent to immobilized limbs for 3
months.69 A cortical bone density decrease of 40% and a trabecular bone
density decrease of 12% also have been reported with disuse of bone (Fig.
3.97).70
FIG 3.97 Four zones for bone related to mechanical adaption to strain before
spontaneous fracture. The acute disuse window is the lowest microstrain amount.
The adapted window is an ideal physiologic loading zone. The mild overload zone
causes microfracture and triggers an increase in bone remodeling, which produces
more woven bone. The pathologic overload zone causes increase in fatigue
fractures, remodeling, and bone resorption. (From Misch CE: Dental implant prosthetics, ed
The adapted window (50–500 microstrain) represents an equilibrium of

modeling and remodeling, and bone conditions are maintained at this level.
Bone in this strain environment remains in a steady state, and this may be
considered the homeostatic window of health. The histologic description of
this bone is primarily lamellar or load-bearing bone. Approximately 18% of
trabecular bone and 2% to 5% of cortical bone is remodeled each year in the
physiologic loading zone, which corresponds to the adapted window.71 This is
the range of strain ideally desired around an endosteal implant after a stress
equilibrium has been established. Bone turnover is required in the adapted
window; Mori and Burr provide evidence of remodeling in regions of bone
microfracture from fatigue damage within the physiologic range.72
The mild overload zone (1500–3000 microstrain) causes a greater rate of
fatigue microfracture and increase in the cellular turnover rate of bone. As a
result, the bone strength and density decrease. The histologic description of
bone in this range is usually woven or repair bone. Woven bone is able to
form faster but is less mineralized and less organized than lamellar bone.
This may be the state for bone when an endosteal implant is overloaded and
the bone interface attempts to adapt to the greater strain environment.
During the repair process, the woven bone is weaker than the more mature,
mineralized lamellar bone.73 Although bone is loaded in the mild overload
zone, care must be taken because the “safety range” for bone strength is
reduced during the repair.
Pathologic overload zones are reached when microstrains are greater than
3000 units. Cortical bone fractures occur at approximately 10,000 to 20,000
microstrain (1%–2% deformation). However, pathologic overload may begin
at microstrain levels of only 20% to 40% of the ultimate strength or physical
fracture of cortical bone. The bone may resorb and form fibrous tissue or,
when present, repair woven bone is observed in this zone because a
sustained turnover rate is necessary. The marginal bone loss evidenced
during implant overloading may be a result of the bone in the pathologic
overload zone. Implant failure from overload may also be a result of bone in
the pathologic overload zone.
Understanding Different Bone Densities

In 1988, Misch proposed four bone density groups independent of the
regions of the jaws based on macroscopic cortical and trabecular bone
characteristics.74 This bone density classification allows for different
treatment protocols according to the type of bony anatomy. Suggested
treatment plans, implant design, surgical protocol, healing time, and
progressive loading time spans have been described for each bone density
type.17 Following this regimen, similar implant survival rates have been
observed for all bone densities.75
Dense or porous cortical bone is found on the outer surfaces of bone and
includes the crest of an edentulous ridge. Coarse and fine trabecular bone
types are found within the outer shell of cortical bone and occasionally on
the crestal surface of an edentulous residual ridge. These four macroscopic
structures of bone may be arranged from the most dense to the least dense,
as first described by Frost and by Roberts: dense cortical bone, porous
cortical bone, coarse trabecular bone, and fine trabecular bone (Fig. 3.98).
FIG 3.98 The macroscopic structure of bone may be described, from the least
dense to the most dense, as (1) fine trabecular, (2) coarse trabecular, (3) porous
cortical, and (4) dense cortical. (Courtesy E. Roberts; from Misch CE: Dental implant
prosthetics, 2e, St Louis, 2015, Mosby.)
In combination, these four macroscopic densities constitute the four bone

categories described by Misch (D1, D2, D3, and D4) located in the edentulous
areas of the maxilla and mandible (Table 3.5; Fig. 3.99). The regional locations
of the different densities of cortical bone are more consistent than the highly
variable trabecular bone.
TABLE 3.5
Misch Bone Density Classification Scheme
Bone Density Description Tactile Analog Typical Anatomic Location

D1 Dense c ortic al Oak or maple wood Anterior mandible
D2 Porous c ortic al and c oarse trabec ular White pine or spruc e wood Anterior mandible
Posterior mandible
Anterior maxilla
D3 Porous c ortic al (thin) and fine trabec ular Balsa wood Anterior maxilla
Posterior maxilla
Posterior mandible
D4 Fine trabec ular S tyrofoam Posterior maxilla
D5 Immature, non-mineralized bone — Early healed grafted bone
FIG 3.99 Misch described four bone densities found in the anterior and posterior
edentulous regions of the maxilla and mandible. D1 bone is primarily dense cortical
bone, D2 bone has dense to thick porous cortical bone on the crest and coarse
trabecular bone underneath, D3 bone has a thinner porous cortical crest and fine
trabecular bone within, and D4 bone has almost no crestal cortical bone. The fine
trabecular bone composes almost all of the total volume of bone. (From Misch CE:
D1 bone is primarily dense cortical bone. D2 bone has dense to porous

cortical bone on the crest and lateral to the implant site. The bone within this
cortical housing has coarse trabecular bone (Fig. 3.100). D3 bone types have a
thinner porous cortical crest and facial/lingual regions, with fine trabecular
bone in the region next to the implant (Fig. 3.101). D4 bone has almost no
crestal cortical bone and porous cortical lateral plates. The fine trabecular
bone comprises almost all of the total volume of bone next to the implant
(Fig. 3.102). A very soft bone, with incomplete mineralization and large
intratrabecular spaces, may be addressed as D5 bone (Fig. 3.103). This bone
type is found often in the immature bone of a developing bone graft site. The
bone density may be determined by the general location, tactile sense during
surgery, or computerized radiographic evaluation.
FIG 3.100 A cross section of a D2 mandible in the region of the midline. A dense to
porous cortical plate exists on the crest and lateral borders, and a coarse trabecular
bone pattern exists within. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
FIG 3.101 A posterior mandible with D3 bone. A thin porous cortical bone is at the
crest and fine trabecular bone is in the body of the mandible. (From Misch CE: Dental
FIG 3.102 An anterior maxilla demonstrating D3 bone with a thin porous cortical
plate on the crest with fine trabecular bone underneath. (From Misch CE: Dental implant
FIG 3.103 In a D4 posterior maxilla, the posterior crestal region has little to no
cortical bone on the crest and is composed primarily of fine trabecular bone. (From
Complications Related to Bone Density
D1.
Dense cortical bone also presents several disadvantages. The implant height
is often limited to less than 12 mm in the atrophic mandible, and the crown
height space is often greater than 15 mm. As a result, additional force-
multiplying factors (such as cantilevers or lateral forces) are further
magnified on the implant-prosthetic system. Stress-reducing factors may be
incorporated in the prosthesis design to reduce these effects, not only on the
bone, but also on the prosthetic components (Fig. 3.104).
FIG 3.104 D1 bone, when present, is almost always in the anterior mandibular
area in the severely atrophic mandible. This type of bone has a high BIC (~80%) and
is susceptible to surgical complications (i.e., overheating the bone during osteotomy
preparation).
D1 bone has a more compromised vasculature with fewer blood vessels

than the other three types, and it is more dependent on the periosteum for
its nutrition. The cortical bone receives the outer one third of all its arterial
and venous supply from the periosteum.76 This bone density is almost all
cortical, and the capacity of regeneration is impaired because of the poor
blood circulation. Delicate and minimal periosteal reflection is indicated.
When D1 density is present, the bone width is usually abundant (i.e., as bone
is lost in height, the mandible exhibits greater width). Fortunately, there are
few occurrences when facial or lingual undercuts are observed with D1 bone
densities, and flap reflection can be safely kept to a minimum. The precise
closure of the periosteum and the overlaying tissue has been shown to help
recover the blood supply and is encouraged (Box 3.18).
Box 3.18
D1 Bone: Surgical Modifications
1. Overheating During Osteotomy
• Abundant external or internal irrigation
• Cooled saline irrigation
• Intermittent pressure on drill (e.g., bone dancing)
• Maintain irrigation while pausing every 3-5 seconds
• Utilize new, sharp drills
• Incremental drill sequence (use more drills; pass same drill more than once
to widen osteotomy)
2. Blood Supply
• Primarily from periosteum, results in longer healing times
• Minimal reflection to decrease blood compromise
3. Final Osteotomy Drill

• Greater width to minimize pressure necrosis
• Greater depth
• Slower drill speed
• Verify no bone debris remaining
4. Bone Tap
• Short of full osteotomy depth
• Allows passive implant fit to minimize pressure necrosis

• Prevents internal implant-body–implant-bone interface microfracture
• Removes drill remnants
5. Final Implant Placement at or Above Bone Level
• After final insertion, unthread turn to relieve internal stresses
6. Slower Healing Rate

• Lamellar bone – fewer blood vessels
• Five months to achieve mature interface – anterior mandible
7. Stage II Uncovery
• May initiate stage II surgery after 3 to 4 months
• May often use immediate loading (when prosthesis is biomechanically

stable)
D2.
D2 bone provides excellent implant interface healing, and osteointegration is
very predictable. There exist basically no disadvantages to this type of bone.
Most implant systems refer to this density of bone for their ideal surgical
protocol. The dense to porous cortical bone on the crest or lateral portions of
the implant site provides a secure initial rigid interface. Osteoplasty to gain
additional width of bone before implant placement or countersinking below
the crestal bone does not compromise support because the lateral cortices
and coarse internal trabecular bone provide rigid fixation. The implant may
even be placed slightly above the crest of the ridge with decreased
compromise or risk of movement at the interface during healing, compared
with softer bone types. The intrabony blood supply allows bleeding during
the osteotomy, which helps control overheating during preparation and is
most beneficial for bone-implant interface healing (Figs. 3.105 and 3.106).
FIG 3.105 D2 bone has a dense to porous cortical crest, and inner trabecular bone
is coarse. It is found most often in the mandible. (From Misch CE: Contemporary implant
dentistry, ed 3, St Louis, 2008, Mosby.)
FIG 3.106 D2 bone. (A) D2 bone is the ideal bone for implant placement and
healing with a high success rate. (B) This type of bone also allows for the
accumulation of bone from the osteotomy that can be used to augment defects.
D3.
D3 bone also presents several disadvantages (Box 3.19). It is more difficult to
manage than the previous two bone density types (D1 and D2) because its
preparation is completed easily. Bone preparation in D3 bone completed with
constant care of direction to avoid enlargement or elliptical preparation of
the site.
Box 3.19
D3 Bone: Surgical and Prosthetic Modifications
1. Bone Anatomy
• Most common in anterior maxilla; usually deficient in width
2. Osteotomy
• Lateral perforation may occur because of width deficiency
• Osteotomy is commonly overprepared
• Ideal angulation to prevent apical perforation
3. Bone-Implant Contact
• Approximately 50%, which compromises initial stability and increases bone
healing
• Additional implant may need to be placed for biomechanical advantage
4. Implant Placement
• One time, no removal and reinsertion
• Level with thin crestal cortical bone or slightly below
• Greater risk of load during healing, verify no interim prosthesis pressure
• Use high-torque handpiece to insert self-tapping threaded implant – avoid

using insertion ratchet as this tends to widen osteotomy or redirect
implant
5. Implant Design
• Titanium plasma spray (TPS) or hydroxyapatite (HA) coated
• Larger-thread design
• Only threaded implants should be placed
• Increased diameter implants, results in greater surface area
6. Healing Period
• Six months to increase lamellar bone and mineralization
• Prosthetic progressive loading more important than for D1 or D2
7. Prosthetic Rehabilitation
• Splint implants for biomechnical stress distribution
• Narrow occlusal table
• Progressive bone loading
A common mistake that causes an elliptical site to form is the use of a

finger rest during the osteotomy. Because the drill is often longer than 20
mm, a finger rest results in an arched pathway of the drill into the bone. In
dense bone, the side of the drill encroaches upon the dense cortical crest,
which opposes the movement and stops the rotation before the crestal
osteotomy is enlarged. In D3 bone the arc pathway is not stopped and the
osteotomy at the level of the crestal bone is of greater diameter than the drill.
If the implant design does not increase at the crestal region, the surgical
defect created around the top of the implant may heal with fibrous tissue
rather than bone and cause an initial bony pocket. Additionally, the direction
for the osteotomy may be changed (see Box 3.19).
To improve rigid fixation of traditional root form designs during healing,
the opposing thin cortical bone of the nasal or antral floor is often engaged in
the maxilla or the apicolingual plate in the mandible, when immediate
loading is considered. If the original implant height determined before
surgery does not engage the opposing cortical bone, the osteotomy is
increased in depth until it is engaged and even perforated. Slightly longer
implants are placed in this approach to further increase surface area of
support with rigid fixation being of utmost importance. However, it should
be noted this technique improves stability during healing but does not
decrease the crestal loads to bone after healing. Instead, implant crest
module design and the crestal one-third of the implant body design are
necessary to decrease stress when the implant prosthesis is loaded (Fig.
3.107).
FIG 3.107 (A) and (B), D3 bone has a thin, porous cortical crest and fine trabecular
bone within the alveolus. It is frequently found in a posterior mandible. (From Misch CE:
Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
D4.
Fine trabecular bone presents the clinician with the most difficult and
greatest possibilty for rigid fixation problems. Bone trabeculae are sparse
and, as a result, initial fixation of any implant design presents a surgical
challenge (Box 3.20). The implant surgeon should not prepare D4 bone with
rotating drills, which use an extraction technique to remove bone preparation
of the osteotomy. The initial drill to determine site depth and angulation is
the only drill to be used in this bone type, after which osteotomes may be
used with a surgical mallet or hand piece to compress the bone site, rather
than remove bone, as the osteotomy increases in size. The compaction
technique of the site is prepared with great care. The bone site is easily
distorted, resulting in reduced initial stability of the implant. The final
osteotomy diameter is similar to the D3 preparation. The residual ridge is
easily expanded in this bone type. The osteotomy may both compress the
bone trabeculae and expand the osteotomy site resulting in an improved
bone density (Fig. 3.108 and Box 3.20).
Box 3.20
D4 Bone: Surgical and Prosthetic Modifications
1. Bone Anatomy
• Location is usually posterior maxilla, which results in surgical difficulty
• No cortical crest results in compromised initial fixation
• Decreased height because of maxillary sinus pneumatization
• Bone augmentation is usually indicated
2. Osteotomy
• Easily overprepared, surgical site should be underprepared
• Use of osteotomes is highly recommended
• Angulation should be strictly monitored and misdirection often occurs
3. Bone-Implant Contact
• Approximately 25% resulting in poor initial fixation
• Additional implant indicated for biomechanical stress distribution
4. Implant Placement
• No removal and reinsertion
• Placement below the crestal bone to minimize loading during the healing
phase
• Implant design with greater surface area
• Placement with handpiece is recommended to maintain path of insertion
• Insertion ratchet should not be used
5. Prosthesis Fabrication
• Progressive loading highly recommended
• Narrow occlusal table decreases force-related issues
• Splinting of implants for force distribution
(From Misch CE: Contemporary Implant Dentistry, ed 3, St Louis, 2008, Mosby.)
FIG 3.108 The posterior maxilla is the most common location for D4 bone.
Because of the poor bone implant contact (∼25%), modifications of the surgical and
prosthetic procedures need to be implemented to decrease complications.
Prevention Of Bone Density Complications
Understanding Bone Strength and Density
To understand how the direct effect bone density has on dental implant
success and morbidity, the clinician must have knowledge of the make-up
and biomechanics of bone. Bone density is directly related to the strength of
bone before microfracture. Misch et al. reported on the mechanical
properties of trabecular bone in the mandible using the Misch bone density
classification.77 A 10-fold difference in bone strength may be observed from
D1 to D4 bone (Fig. 3.109). D2 bone exhibited a 47% to 68% greater ultimate
compressive strength compared with D3 bone (Fig. 3.110). On a scale of 1 to
10, D1 bone is a 9 to 10 relative to strength, D2 bone is a 7 to 8 on this scale,
D3 bone is 50% weaker than D2 bone and is a 3 or 4 on the strength scale,
and D4 bone is a 1 to 2 and up to 10 times weaker than D1 bone. It should be
noted that the studies of bone strength were performed on mature bone
types. Bone is 60% mineralized at 4 months after implant surgery, and the
strength of bone is related to the amount of mineralization. It is prudent to
increase healing time prior to loading in D3 and D4 bone densities. A period
of 3 to 4 months is adequate for D1 and D2 bone. A healing period of 5 to 6
months is beneficial in D3 to D4 bone. The bone densities that originally
relied on clinical impression are now fully correlated to quantitative objective
values obtained from CBCT scans and bone strength measurements. These
values can help prevent failure in specific situations of weak densities.
FIG 3.109 The strength of bone is related directly to the density of bone. (From Misch
FIG 3.110 The ultimate compressive strength of D2 trabecular bone is greater than
D3 trabecular bone, and D4 trabecular bone is the weakest. (From Misch CE: Dental
Elastic Modulus and Density

By definition, elastic modulus describes the amount of strain (changes in
length divided by the original length) as a result of a particular amount of
stress. This has been shown to be directly related to the apparent density of
bone.78 The elastic modulus of a material is a value that relates to the
stiffness of the material. The elastic modulus of bone is more flexible than
titanium. When higher stresses are applied to an implant prosthesis, the
titanium has lower strain (change in shape) compared with the bone. The
difference between the two materials may create microstrain conditions of
pathologic overload and cause implant failure. When the stresses applied to
the implant are low, the microstrain difference between titanium and bone is
minimized and remains in the adapted window zone, maintaining load-
bearing lamellar bone at the interface.79
Misch et al. found the elastic modulus of the trabecular bone in the human
jaw to be different for each bone density (Fig. 3.111). As a result, when a
stress is applied to an implant prosthesis in D1 bone, the titanium-D1 bone
interface exhibits very little microstrain difference. In comparison, when the
same amount of stress is applied to an implant in D4 bone, the microstrain
difference between titanium and D4 bone is greater and may be in the
pathologic overload zone (Fig. 3.112). As a result, D4 bone is more likely to
cause implant mobility and failure. Clinicians must take into consideration
that poorer quality of bone is inherently more susceptible to implant
complications.
FIG 3.111 The elastic modulus for D2 trabecular bone is greater than that for D3
trabecular bone, and D4 trabecular bone has the lowest elastic modulus. (From Misch
FIG 3.112 The microstrain difference between titanium and D4 bone is great and
may be in the pathologic overload zone, whereas at the same stress level, the
microstrain difference between titanium and D2 bone may be within the ideal
adapted window zone. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Bone-Implant Contact Percentage

The initial bone density not only provides mechanical immobilization of the
implant during healing but after healing also permits distribution and
transmission of stresses from the prosthesis to the implant-bone interface.
The mechanical distribution of stress occurs primarily where bone is in
contact with the implant. Open marrow spaces or zones of unorganized
fibrous tissue do not permit controlled force dissipation or microstrain
conditions to the local bone cells. Because stress equals force divided by the
area over which the force is applied, the less the area of bone contacting the
implant body, the greater the overall stress, other factors being equal.
Therefore, the BIC percent has a significant influence on the amount of stress
and strain at the interface.
In 1990, Misch noted that the bone density influences the amount of bone
in contact with the implant surface, not only at first-stage surgery but also at
the second-stage uncovery and early prosthetic loading.80 The BIC percentage
is significantly greater in cortical bone than in trabecular bone. The very
dense D1 bone of a C−h resorbed anterior mandible or of the lingual cortical
plate of a Division A anterior or posterior mandible provides the highest
percentage of bone in contact with an endosteal implant and may
approximate more than 85% BIC (Fig. 3.113). D2 bone, after initial healing,
usually has 65% to 75% BIC (Fig. 3.114). D3 bone typically has 40% to 50%
BIC after initial healing (Box 3.21). The sparse trabeculae of the bone often
found in the posterior maxilla (D4) offer fewer areas of contact with the body
of the implant. With a machined-surface implant, this may approximate less
than 30% BIC and is most related to the implant design and surface
condition. Consequently, greater implant surface area is required to obtain a
similar amount of BIC in soft bone compared with a denser bone quality. As
a result, many anterior mandibles with denser bone have less importance
with respect to the implant number, size, or design compared with posterior
maxillae with less dense bone.
FIG 3.113 Bone-Implant Contact (BIC): (A) D1 Bone - ~85%, (B) D2 Bone - 65–
75%, (C) D3 Bone - 40–50%, (D) D4 Bone - ~30%.
FIG 3.114 Bone density. An alternative material to evaluate bone density is: D1
bone = maple wood; D2 bone = white pine wood; D3 bone = balsa wood; D4 bone =
Styrofoam.
Box 3.21
Initial Bone-Implant Contact Percent (BIC %)
D1: 85%
D2: 65%–75%
D3: 40%–50%
D4: <30% (% = bone-implant contact)
Studies have shown the BIC is directly related to the bone density and the
healing time. For example, in a study by Carr et al.,80a the BIC was greater in
the mandible than the maxilla (i.e., because of the greater bone density in the
mandible in comparison to the maxilla). In addition, the BIC was greater at 6
months compared with 3 months in both jaws (Fig. 3.115). Thus, the healing
time before implant loading is related to the density of bone because the
strength of bone increases and the BIC increases with a longer time period.
Three to 4 months of healing for D1 to D2 bone and 5 to 6 months for D3 to
D4 bone has less risk than a shorter time period for all bone types.
FIG 3.115 The percentage of bone contact after initial healing and before any
occlusal load may be related to bone density (e.g., mandible vs. maxilla) and healing
time. Longer healing periods may increase bone-implant contact. (From Misch CE:
Stress Transfer
Crestal bone loss and early implant failure after loading results may occur
from excess stress at the implant-bone interface. A range of bone loss has
been observed in implants in different bone densities with similar load
condition.81 Bidez and Misch noted in 1990 that part of this phenomenon may
be explained by the evaluation of finite element analysis (FEA) stress
contours in the different volumes of bone for each bone density.82 Each model
reproduced the cortical and trabecular bone material properties of the four
densities described. Clinical failure was mathematically predicted in D4 bone
and some D3 densities under occlusal loads (Fig. 3.116). Other studies using
FEA models with various implant designs and bone quality have also
evaluated the stress-strain distribution in the bone around the implants.83 For
example, Tada et al. evaluated the three-dimensional changes around
different length implants in different bone qualities (Fig. 3.117).84 The type 3
and 4 bone categories had four to six times more strain around all implants,
with the highest strains around the shortest implants. As a result of the
correlation of bone density to the elastic modulus, bone strength, and BIC
percent, when a load is placed on an implant, the stress contours in the bone
are different for each bone density.85 In D1 bone, the highest strains are
concentrated around the implant near the crest, and the stress in the region
is of lesser magnitude. D2 bone, with the same load, sustains a slightly
greater crestal strain, and the intensity of the stress extends farther apically
along the implant body. D4 bone exhibits the greatest crestal strains, and the
magnitude of the stress on the implant proceeds farthest apically along the
implant body.
FIG 3.116 (A) Stress transfer around the implant interface is different for each bone
density. In this two-dimensional finite element analysis, D2 bone has an intermediate
stress intensity around the implant. (B) A two-dimensional finite element analysis
demonstrates that D4 bone has a higher stress intensity around the implant, and the
higher intensity even extends to the zone around the apical threads. (From Misch CE:
FIG 3.117 The softer bone types (types 3 and 4) have higher strain values around
implants regardless of their length compared with harder bone types (types 1 and
2). (From Misch CE: Dental implant prosthetics, 2e, St Louis, 2015, Mosby; Data from Tada S,
Stegaroiu R, Kitamura E, et al.: Influence of implant design and bone quality on stress/strain
distribution in bone around implants: a 3-dimensional finite element analysis, Int J Oral Maxillofac
Implants 18:357–368, 2003.)
As a consequence of different strain regions present around implants with

different bone densities, the magnitude of a prosthetic load may remain
similar, and yet give one of the following three different clinical situations at
the bone-implant interface based on the bone density around the implant: (1)
physiologic bone loads in the adapted window zone and no marginal bone
loss; (2) mild overload to pathologic overload bone loads and crestal bone
loss; or (3) generalized pathologic overload and implant failure. To obtain a
similar clinical result in each implant prosthesis, the variables in each patient
must be either eliminated or accounted for in the treatment plan. Because
the myriad of variables cannot be eliminated relative to bone density, the
treatment plans (including implant number, size, and design) should be
modified.
Bone Density Treatment Planning

The first component of the treatment planning process should include the
use of a radiographic evaluation, preferably a CBCT x-ray. Initially, an idea of
the potential bone density can be determined by the anatomic position;
anterior mandible and single tooth replacement is D2, anterior maxilla and
posterior mandible is D3, and posterior maxilla is D4. Secondly, a more
accurate representation of the bone density may be determined by evaluation
of the hounsfield units (Hu) on a medical CT scan or a CBCT scan (i.e., linear
correlation with the corresponding hounsfield units). A third technique
would be to use prior experience (i.e., if surgery has been completed prior in
the area) as a guideline for the determination of bone density.
Treatment Planning Modification.

When utilizing bone density in the treatment planning process, the clinician
must take into consideration these four facets of bone quality: (1) each bone
density has a different strength; (2) bone density affects the elastic modulus;
(3) bone density differences result in different amounts of BIC percent; and
(4) bone density differences result with a different stress-strain distribution
at the implant-bone interface. Bone density is an implant treatment plan
modifier in several ways—prosthetic factors, implant number, implant size,
implant design, implant surface condition, and the need or method of
progressive loading (Box 3.22).
Box 3.22
Treatment Plan Modifiers
↓Bone density = ↑ Implant area
↑Implant number
↑Implant width
↓Cantilevers
↑Implant body surface area
↑Implant length (D4 bone)
↑Implant surface condition

Increase Surface Area.
As the bone density decreases, the strength of the bone also decreases. In
order to decrease the incidence of microfracture of bone, the strain to the
bone should be reduced. Because strain is directly related to stress, the stress
to the implant system should be reduced as the bone density decreases.
Stress may be reduced by increasing the functional surface area over which
the force is applied. Increasing implant number is an ideal way to reduce
stress by increasing functional loading area. For example, three implants
rather than two may decrease applied implant moments in half and bone
reaction forces by two thirds, depending on implant position and size. An
implant prosthesis with normal patient forces in D4 bone should have at
least one implant per tooth. In the molar region, two implants for each
missing molar may even be appropriate. In D3 bone, one implant per tooth is
often appropriate in the posterior region, where fewer implants are required
in the anterior location. In D2 bone with normal patient forces, one or more
pontic may replace a tooth between two implants in both posterior and
anterior regions.
Implant Design.
The surface area of the implant macrogeometry may be increased to decrease
stress to the implant-bone interface. The easiest technique is to increase the
implant diameter, which will decrease stress by increasing the surface area.
This may also reduce the length requirement. For example, when a 0.5-mm
increase in width occurs, there is an increased surface area between 10% and
15% for a cylinder implant (i.e., even more difference is found with threaded
implant body designs). Because the greatest stresses are concentrated at the
crestal region of the implant in favorable bone types, width is more
significant than length for an implant design after adequate length has been
established. D4 bone should often require wider implants compared with D1
or D2 bone. This may require onlay grafts or bone spreading to increase the
width of bone when other stress factors are high. Based on long-term clinical
experience of V-shaped threaded implant bodies, the minimum bone height
for initial fixation and early loading for D1 bone is 7 mm; for D2 bone, 9 mm;
and for D3 bone, 12 mm using the classic V-thread screw implant design and
titanium surface condition. Because the crestal region is the location of
pathologic overload of bone most often occurs after prosthetic loading, after
initial healing is complete, the length of the implant is not as significant to
solve crestal bone loss (i.e., and the quality of implant health) as other factors
(e.g., implant design, implant width). In contrast, D4 bone benefits from
relatively longer implants for initial fixation and early loading compared with
other bone densities. This is not only for initial fixation but also because the
stress-strain transfer of occlusal forces extends farther down the implant
body.
Implant Coatings.
Coatings or the surface condition on an implant body can increase the BIC
percentage and the functional surface area. A rougher surface is strongly
suggested in soft bone (e.g., D3, D4) and has resulted in improved survival
rates compared with machined titanium. However, after 1 to 2 years, the
mechanical load on the overall implant design is more critical to the amount
and type of bone contact compared with the surface condition on the implant
body. Rough surface conditions also may have some disadvantages. Plaque
retention when exposed above the bone, contamination, and increased cost
are a few of the concerns with roughened surfaces. The benefit and risk of
surface conditions suggests that the roughest surfaces are most often used in
only softer bone types.
Direction of Force.
The consequences of the direction and amount of occlusal force is directly
related to the bone density. A load directed along the long axis of the implant
body decreases the amount of stress in the crestal bone region compared
with an angled load (i.e., nonaxial load). As the bone density decreases, axial
loads on the implant body become more critical as crestal bone loss may
occur. Bone grafting or bone spreading to increase the width of bone and to
better position the implant relative to the intended load is considered for soft
bone types. Additionally, adhering to progressive bone loading in poorer
bone qualities will decrease the possibility of force-related bone loss.
Progressive Bone Loading.

Progressive bone loading provides for a gradual increase in occlusal loads,
separated by a time interval to allow the bone to mature and accommodate to
the local strain environment. If proper techniques are utilized, progressive
bone loading changes the amount and density of the implant-bone contact
(i.e., a D4 bone may be changed to a D3 bone density). The increased density
of bone at the implant interface improves the overall support system
mechanism. The poorer quality of the bone, the more important the need for
progressive loading.
Bone Density Summary

A key determinant for clinical success is the diagnosis of the bone density in
a potential implant site. The strength of bone has been shown to be directly
related to bone density. The modulus of elasticity and the percentage of BIC
is related to bone density. The occlusal force and direction of force with the
consequences are affected by the density of bone. As a consequence, the
clinician must take into consideration altering the protocol of treatment
related to bone density to decrease morbidity and increase survival rates.
Studies and clinical experience has shown that altering the treatment plan to
compensate for soft bone types has provided similar survival rates in all bone
densities. After the prosthetic option, key implant position, and patient force
factors have been determined, the bone density in the implant sites should
be evaluated to modify the treatment plan. The treatment plan may be
modified by reducing the force on the prosthesis or increasing the area of
load by increasing implant number, implant size, implant design, or implant
body surface condition. Of these possibilities, the number of implants (i.e.,
adding additional implants) is often the most effective method to decrease
the stress to the implant system.
Size of Implants
Narrow-Diameter (Mini) Implants
In the 1970s, narrow-diameter implants smaller than 2 mm in diameter were
very popular in Europe and South America. These “pin” implants were often
used in two or three sets for each tooth (Fig. 3.118). They did not maintain
crestal bone, often would fail or fracture, and became unpopular after the
3.75-mm-diameter root form implants were developed. More recently, these
implants have reemerged in the marketplace (Fig. 3.119).
FIG 3.118 Placement of mini-implants for interim prosthesis. (A) O-ring one piece
mini-implant. (B) 3–implants overdenture. (C) 4–implants overdenture. (D) 5–
implants fixed prosthesis.
FIG 3.119 Mini-implants. (A–B) The use of mini-implants for fixed prostheses is
associated with a high surgical and prosthetic morbidity.
The initial reentry of the mini-implant was for a transitional prosthesis; the
diameter of these implants ranged from 1.8 to 2.4 mm. After the final
implant positions and numbers were inserted in a two-stage healing process,
additional mini-implants were used to immediately restore and support a
transitional prosthesis. This approach still has validity when patients do not
want to wear a removable restoration during the initial healing process or to
protect a bone graft site during augmentation. Although the transitional
mini-implants may fail in some clinical situations, the regular-size implants
are not affected, and the final restoration is not at risk.
After a few years, the mini-implants were suggested for implant
overdenture support. The concept (as presented) places multiple mini-
implants with O-ring or other overdenture attachment systems and
immediately is used to retain and support the prosthesis (Fig. 3.120). It is
also presented as a “simple solution for denture comfort because of flapless
implant installation.” This concept also encourages a reduced fee to have
greater patient acceptance.
FIG 3.120 (A–B) Mini-implants being used for retention of an overdenture.
Disadvantages of “Mini” Implants

Compared with implants 3.75 mm or larger, with thousands of clinical
reports, the small-diameter implant has almost no long-term studies. Even
studies longer than 3 years are limited in numbers. Because implants smaller
than 3 mm in diameter are usually too narrow for a two- or three-piece
implant body abutment design, a one-piece implant is most often designed
(Fig. 3.121). This requires the implant abutment portion to extend into the
mouth upon insertion. Hence, the implant most often is immediately placed
into more function compared with the one- or two-stage approach. This
increases the risk of failure during the healing period of bone because the
surgical healing and the early loading period occur at the same time.
FIG 3.121 Most mini-implants are too narrow for a separate abutment-to-implant
connection. As a result, they are one-piece implants with the abutment connected to
the implant body and often placed in function after insertion. (From Misch CE: Dental
An implant has an increased risk of healing and early loading failure of 5%

to 30% when used for an immediate restoration, in part related to a number
of factors, including the implant diameter and design. The mini-implant is
usually less than 2 mm in width. In a study by Misch, the small-diameter
implant (2.2–2.4 mm) had a 75.7% survival rate after 6 weeks when used
immediately for retention of a mandibular denture using four to five
implants per patient.86
To decrease the risk of healing and early loading failure, a wider-diameter
implant with an implant body with more surface area is of benefit. Because
the mini-implants are too narrow to increase the depths of each thread, they
act more as a “nail” than a screw. The surface area for initial fixation, early
loading, and mature loading is reduced.
The mini-implant designs are usually deficient in seven ways: (1) decreased
diameter and less surface area for loading; (2) a decreased thread depth; (3)
less initial fixation; (4) greater risk of fracture; (5) narrow range of prosthetic
abutment options; (6) difficult to splint implants together; and (7) immediate
restoration often required (Box 3.23).
Box 3.23
Narrow “Mini” Diameter Implants
Disadvantages
1. Few long-term studies
2. Immediate restoration often required
3. Less surface area for loading
4. Decreased initial fixation
5. Higher associated failure rates
6. Poor emergence profile for fixed prosthesis
7. Greater risk of fracture
8. Higher risk procedure
9. Often associated with flapless surgery resulting in increased morbidity
10. Removal process of fractured implants more difficult

The “flapless” surgical approach is often suggested with the mini-implant
and has a perceived benefit of surgical ease and less patient discomfort.
However, there is an increased risk of bone perforations in the areas of
concavities or minimal thickness regions of the crestal bone. If a CBCT scan
is not performed before surgery, it is almost impossible to evaluate most
edentulous maxillae and many edentulous mandibles without reflecting the
tissue. Additionally, this places the patient at risk in the posterior mandible
for possible neurosensory impairment issues. In a study by Misch, there was
no difference in the postoperative pain medication requirements of patients
with a “flapless” surgery compared with the regular reflection surgical
technique. It is suggested to directly observe the bone region before and
during implant insertion unless abundant bone and CT scans are available.
Less risk of early implant failure is present when the implants can be
splinted together. The mini-implant is most often used as an independent
unit because angled abutments are not available (because the implant-
abutment is all one piece). Therefore, the stresses are generally greater and
the failure rate risk is greater because the implants are independent units.
In addition to a higher risk of failure, the bending fracture resistance and
fatigue fracture of the mini-implant is 16 times less than that of a regular 4-
mm-diameter implant. Cycles to fracture may be as few as 11,000 to 20,000
cycles at 200 N (1350 lb). The teeth often have 440 cycles/day of function and
parafunction with 314 cycles/day of maximum bite force.87 Thus, the mini-
implant is at risk of fracture even within the first year of loading (Fig. 3.122).
FIG 3.122 Fractured mini-implants. Biomechanical failure of mini-implants resulting

fractured implant bodies.
A mini-implant is often promoted as a less expensive option for the

patient. The product cost to the clinician of a “mini” implant is
approximately half that of a regular-size implant. It is safer to reduce the fee
in half and then add the extra cost of a regular implant than to reduce the fee;
use a mini-implant; and have a greater risk of early failure, greater risk of
fracture, greater risk with independent units, and limited prosthetic options.
A two-stage implant system may have confirmation of successful integration
healing without a prosthetic load. A range of abutments permits individual
loading or splinting the implants together after integration is confirmed.
However, the mini-implants do have a benefit for transitional prostheses and
transitional solutions to protect a bone graft, especially when the patient
does not accept a transitional removable restoration. The clinician must be
conscious of the type of removable prosthesis used with mini implants either
on a intreim basis or for the final prosthesis. An RP-5 prosthesis should
always be used (i.e., completely soft tissue–supported) to minimize stress on
the implants.
Ideal Implant Width

The natural teeth may be used as a guideline to determine the ideal implant
width for function loads and esthetics. The roots of the natural dentition
optimize the amount and direction of forces found with the mouth. The
smallest-diameter roots are located in the mandibular anterior region, where
the forces are less and the direction of force is along the long axis of the root.
The maxillary anterior teeth have larger roots and a different cross-section
shape to compensate for the off-axis loading that increases lateral forces on
the structure. The canines have a greater root surface area (i.e., maxilla
compared to mandibular) in response to the higher bite forces (90 lb/in2
compared with 35 lb/in2) and the direction of force during mandibular
excursions.
The premolars have less surface area than the canines because they do not
receive a lateral load in excursions. The molars have multiple roots splinted
together in one crownmainly due to the amount of force received. The
maxillary posterior region has the least bone density; the mandibular
counterpart has coarser trabecular bone. The maxillary molars have more
roots than the mandibular components and have more surface area to
dissipate loads in the fine trabecular bone located in this region of the
mouth. The molar crowns are almost twice as large in diameter, and the root
surfaces are twice those of the premolars. This compensates for the amount
of load increase by two to three times and decreases the risk of damaging
stresses (Fig. 3.123).
FIG 3.123 (A) The root surface area of the mandibular teeth is greater in the
posterior regions, where the bite forces are greater. (B) The root surface area of the
maxillary teeth is greater than that of the mandibular teeth because the surrounding
bone is less dense. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
In this light, the mandibular incisors region and the maxillary lateral
incisor may be replaced with 3- to 3.5-mm-diameter implants; the maxillary
centrals, canines, and premolars in both arches may use 4-mm-diameter
implants. The molars may be restored with 5- or 6-mm-diameter implants in
both arches. When larger-diameter implants cannot be used in the molar
region, two 4-mm-diameter implants for each molar should be considered,
especially in the maxilla (Box 3.24).
Box 3.24
Ideal Implant Diameters
Function and Esthetics (Diameter)
Maxillary centrals: 4.0 mm

Maxillary laterals: 3.0–3.5 mm
Maxillary cuspids and premolars: 4.0 mm
Maxillary molars: 5.0–7.0 mm
Mandibular incisors: 3.0 mm
Mandibular cuspids and premolars: 4.0 mm
Mandibular molars: 5.0–7.0 mm
The ideal size of the implant body should be incorporated into a treatment
plan rather than the surgeon determining this dimension at the time of
surgery. The initial size of an implant is determined in both length and
diameter. In a two-stage healing protocol the ideal implant length should be
at least 12 mm. The poorer quality of the bone, the longer the implant
requirements. The greater the bite force, the longer the implant dimension.
Therefore, the shortest implant length may be treatment planned in the
anterior mandible, the anterior maxilla may have a slightly longer implant,
the posterior mandible may have a longer implant, and the longest implant
requirement for an ideal treatment plan is usually found in the posterior
maxilla.
The diameter of an implant has surgical, loading, and prosthetic
considerations. In the initial treatment plan, the loading and prosthetic
components are most important. The width of the implant is directly related
to the overall functional surface area. Where the forces are greater or the
bone is less dense, the implant is wider, ranging from 3 to 6 mm. As a
general rule, the narrowest implant is found in the anterior mandible
followed by the anterior maxilla and the posterior mandible; the widest-
diameter requirements are found in the molar region of the posterior maxilla.
The prosthetic aspects of the implant width are primarily related to the
esthetics of the emergence profile, the force on an abutment screw, and the
strength of the implant components. As a result, wider-diameter implants
are selected in the molar regions; standard diameters in the canines,
premolars, and maxillary central incisors; and the smallest-size implants in
the maxillary lateral and mandibular incisors.
The natural dentition follows the guidelines established in the implant-
size treatment plan considerations. The correlation is most likely found
because of the biomechanical relationship of the amount and type of the
forces in the location of the jaws and the type of the bone in the region. In
the maxilla, fine trabecular bone is used to dissipate forces, and the amount
of force is the greatest in the molar region. The mandible is a force-absorbing
unit and has coarse trabeculae and dense cortical bone. The tooth size
difference is reflected in the diameter of the tooth, not in the overall length
dimension. These guidelines are consistent for both teeth and implants when
engineering principles determine tooth and implant size.
Splinting Implants to Teeth
Treatment Planning
Treatment planning a splinted implant-tooth prosthesis is very controversial
in implant dentistry today. The connection of a natural tooth (i.e., with a
periodontal ligament) with a dental implant (i.e., direct bone interface) poses
a biomechanical challenge. To date, studies have been equivocal on the
success of this treatment mainly due to the differential support mechanisms.
Although rare, the most common scenario for which a root form implant
may be joined to a natural tooth as a terminal abutment is in the posterior
regions of the mouth. For example, if a patient is missing the first and second
molars in a quadrant (with no third molar present), the segment requires at
least two implants of proper size and design to independently restore these
two teeth. If adequate bone exists in the second molar and distal half of the
first molar but inadequate bone exists in the mesial half of the first molar, a
premolar-size pontic is required. The pontic may be cantilevered from the
anterior natural teeth or the posterior implants. Either of these options may
result in complications because of tensile forces on the cement seal of the
abutment farthest from the pontic.
An alternative may be to join the implant to a natural tooth, if all other
factors are favorable. This plan is more likely in the presence of a Division C
−h ridge in the pontic region, when inadequate bone height adjacent to the
natural tooth decreases the prognosis of a vertical bone graft. Another
scenario in favor of this treatment plan is when the posterior implants are of
a narrower diameter than usual. When two Division B root forms are used in
the posterior mandible to replace molars, there should be no cantilever to
magnify the force on the implants. Posterior pontics should not be
cantilevered from even two splinted Division B root form implants. An
additional root form implant or natural tooth is required as an abutment for
the fixed prosthesis. When an additional implant insertion is not an option,
the posterior implants may be joined by a rigid connector (i.e., a solder joint)
to natural teeth within the prosthesis, provided all dental factors are
favorable (Fig. 3.124).
FIG 3.124 (A) When the inadequate bone adjacent to a tooth can be grafted for
implant placement and an independent prosthesis, this is the treatment of choice.
(B) When the inadequate bone adjacent to a tooth cannot be grafted, one option is to
cantilever the missing tooth from the anterior teeth or from posterior implants. The
posterior implants permit the replacement of more than one tooth but require at least
two implants. (C) When the inadequate bone adjacent to a tooth cannot be grafted,
another option is to insert an implant more distal and make a three-unit fixed partial
denture by connecting the implant to the nonmobile tooth. (D) When the inadequate
bone adjacent to a tooth cannot be grafted and the tooth is slightly mobile, one option
is to insert an implant more distal and make a four-unit fixed partial denture by
connecting the implant to two anterior teeth (when the most anterior tooth is
nonmobile). (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
The connection of natural teeth and osteointegrated implants within a

single rigid prosthesis has generated concern and publications, with studies
and guidelines for both extremes (Fig. 3.125). In other words, some articles
report problems, whereas others state that no problem exists. To be more
specific to a particular situation, more information is required to design a
successful treatment plan. Two designs are available for the connection of
implants and teeth within the same prosthesis: a conventional fixed partial
denture or a fixed partial denture with a nonrigid connector. To address this
issue, the mobility of the natural abutment must be assessed.
FIG 3.125 Splinting a rigid implant to a natural tooth has caused concerns relative
to the biomechanical differential in movement between the implant and tooth.
Because the tooth moves more than the implant, the implant may receive a moment
force created by the “cantilever” of the prosthesis. (From Misch CE: Contemporary implant
Mobility
The mobility of potential natural abutments influences the decision to join
implants and teeth more than any other factor. In the implant-tooth rigid
fixed prosthesis, five components may contribute movement to the system:
the implant, the bone, the tooth, the prosthesis, and implant/prosthetic
components.
Vertical Movement.
A natural tooth exhibits normal physiologic movements in vertical,
horizontal, and rotational directions. The amount of movement of a natural
tooth is related to its surface area, root design, and bone support. Therefore,
the number and length of the roots; their diameter, shape, and position; and
the health of the periodontal ligament primarily influence tooth mobility. A
healthy tooth exhibits no clinical mobility in a vertical direction. Actual
initial vertical tooth movement is about 28 mm and is the same for anterior
and posterior teeth. The immediate rebound of the tooth is about 7 mm and
requires almost 4 hours for full recovery, so additional forces applied within
this time period depress the tooth less than the original force. The vertical
movement of a rigid implant has been measured as 2 to 3 mm under a 10-lb
force, and is due mostly to the viscoelastic properties of the underlying bone
(Fig. 3.126).
FIG 3.126 A three- or four-unit precious metal prosthesis with an implant and a
posterior tooth rigidly splinted has some inherent movement. The implant moves
apically 0 to 5 µm, and the tooth moves apically 8 to 28 µm but can rotate up to 75
µm toward the implant because of a moment force. The metal in the prosthesis can
flex from 12 to 97 µm, depending on the length of the span and the width of the
connecting joints. The abutment-to-implant component movement may be up to 60
µm because of abutment prosthetic screw flexure. As a result, a vertical load on the
prosthesis creates little biomechanical risk when joined to a nonmobile tooth
because of the design. (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008,
Mosby.)
Prosthesis Movement.
The fixed prosthesis that connects a tooth and implant also illustrates
movement. Under a 25-lb vertical force, a prosthesis with a 2-mm connector
fabricated in noble metal results in a 12-mm movement for one pontic and
97-mm movement for a two-pontic span. The fixed partial denture movement
helps compensate for the difference in vertical mobility of a healthy tooth
and implant. A fixed prosthesis supported by one implant and one natural
tooth will have the abutment/gold cylinder screw joint of the system act as a
flexible element. The inherent flexibility will match the vertical mobility of
the natural tooth. The minimal movement of the tooth and the fact that
implant, prosthesis, and abutment components have some mobility indicate
the risk is small in the vertical direction with the biomechanical difference of
implant and tooth in the same prosthesis when one or two pontics separate
these units.
Horizontal Movement.
With natural teeth, horizontal tooth mobility is greater than vertical
movement. A very light force (500 g) moves the tooth horizontally 56 to 108
mm (Fig. 3.127). The initial horizontal mobility of a healthy, nonmobile
posterior tooth is less than that of an anterior tooth and ranges from 56 to 75
mm, which is two to nine times the vertical movement of the tooth. Initial
horizontal mobility is even greater in anterior teeth and ranges from 90 to
108 mm in healthy teeth.
FIG 3.127 A healthy natural tooth may move laterally from 56 to 108 µm, with
anterior teeth moving more than posterior teeth. (From Misch CE: Contemporary implant
Muhlemann found that tooth movement may be divided into initial

mobility and secondary movement.88 The initial mobility is observed with a
light force, occurs immediately, and is a consequence of the periodontal
ligament. If an additional force is applied to the tooth, a secondary
movement is observed, which is related directly to the amount of force. The
secondary tooth movement is related to the viscoelasticity of the bone and
measures up to 40 mm under considerably greater force.
Implant Movement.
The implant-bone interface also exhibits lateral movement. Sekine et al.
evaluated the movement of endosteal implants with rigid fixation and found
a range of 12 to 66 mm of movement in the labiolingual direction.89
Komiyama measured 40 to 115 mm of implant movement in the mesiodistal
direction under a force of 2000 g (about 4.5 psi) and a labiolingual range of 11
to 66 mm.90 The greater implant movement in the mesiodistal dimension
corresponds to the lack of cortical bone between the implants in this
direction compared with the thicker lateral cortical plates present in the
labiolingual dimension. The mobility of implants varies in direct proportion
to the load applied and the bone density and reflects the elastic deformation
of bone tissue.
An interesting note in implant mobility is that no significant difference
was related to implant length. This finding further confirms that implant
length is not the primary factor for implant support, even in the presence of
lateral loads. Bone density affects this condition more than implant length.
These mobility characteristics corroborate the findings of Fenton et al., who
applied a 500-g load for 4 seconds to maxillary anterior teeth and
osseointegrated implants. The implants were displaced a mean 10 mm with a
rapid elastic return (less than 1 millisecond), whereas the teeth showed a
mean displacement of 57 mm with a prolonged viscoelastic return.91 When all
factors are considered, an implant moves vertically and horizontally, the
abutments and prosthesis flex, and the tooth has apical and lateral
movements.
Guidelines for Joining Implants to Teeth

A vertical movement/force placed on a posterior implant joined to a healthy
posterior tooth causes mesial tension on the implant. The implant can move
vertically 3 mm and mesially 40 to 115 mm, and a noble metal-fixed
prosthesis with one pontic allows mesiodistal movement of 6 mm. A natural
tooth with no clinical mobility could be connected rigidly to an
osseointegrated implant because the implant, bone, and prosthesis
compensate for the slight tooth movement. There is extensive documentation
that implants can be connected rigidly to stable teeth. However, the occlusion
should be modified to allow the initial occlusal contacts on the natural tooth
so that the implant does not bear the major portion of the initial load.
No Mobility of Natural Tooth Abutment.

The mobility of healthy anterior incisor teeth often is recorded as 1 with a
range of movement from 90 to 108 mm. Visual clinical evaluation by the
human eye can detect movement greater than 90 mm. When the mobility of a
natural tooth can be observed, mobility is greater than 90 mm and too great
to be compensated by the implant, bone, and prosthesis movement. When
the vertical posterior tooth movement, vertical implant movement,
mesiodistal implant movement, and prosthesis movement are compared
with the same conditions of an anterior tooth with lateral loads, the
biomechanical risk factors do not correlate. One primary condition for
joining an implant to natural teeth is the lack of observable clinical
movement of the natural abutment.
No Lateral Forces on Prosthesis.

Another requisite to join an implant to a natural tooth is that no lateral force
should be designed on the prosthesis. Lateral forces increase the amount of
tooth movement and decrease the amount of implant movement
(faciolingual vs. mesiodistal). Horizontal forces placed on an implant also
magnify the amount of stress at the crestal bone region. Implants should
rarely be connected to anterior teeth because (1) anterior teeth often exhibit
greater clinical mobility than the implant can tolerate and (2) the lateral
forces applied to the restoration during mandibular excursions are
transmitted to the natural tooth and implant abutments (Fig. 3.128).
FIG 3.128 Clinical image of tooth-implant showing failure because of recurrent

decay.
Additional Treatment Options.

When the natural abutment exhibits clinical horizontal movement or
conditions promote horizontal forces against the abutment tooth, two
options can be selected for the final prosthesis. The first, and the option of
choice, is to place additional implants and to avoid the inclusion of natural
abutments in the final prosthesis. The other option is to improve stress
distribution by splinting additional natural abutments until no clinical
mobility is observed.
Guidelines for Splinting Dental Units

Splinting natural teeth does not decrease the mobility of a tooth significantly
after the prosthesis is removed; however, the overall prosthesis movement is
decreased, especially when the splinted units form an arch. If posterior
contacts cannot be eliminated in lateral excursions as a result of skeletal
relationships or when opposing a removable prosthesis, splinting often is
safer to reduce the risk of long-term complications. In addition, splinting
natural abutments also decreases the amount of load to each abutment
(when a 150-psi load is distributed to all splinted abutments, the resultant
force on each abutment is decreased) (Fig. 3.129).
FIG 3.129 (A) Splinting natural teeth together decreases their mobility and reduces
the amount of stress transferred to the support system. (B) When the terminal
natural tooth is slightly mobile, splinting an adjacent tooth is indicated. ([A] Courtesy Y.
Ismail, Pittsburgh, PA. [B] From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The number of teeth to splint together is the number required to eliminate

prosthesis movement. The initial dental evaluation may include acid etching
and bonding potential mobile natural abutments to each other to determine
how many teeth must be joined to reduce the prosthesis clinical mobility to
zero. The dentist applies the following prosthetic guidelines:
1. The last tooth connected in the splint should not be mobile. In other
words, to decrease mobility, at least the last tooth in the splint (and
sometimes more) should be rigid.
2. The terminal abutments in the splint should not have poor retention form.
3. Adjacent teeth splinted together should be parallel enough to have the
same path of insertion for the prosthesis.
4. Adjacent teeth should not be crowded or overlapped and should have

enough room for splinted crowns to have adequate interproximal hygiene.
A classic axiom for splinting teeth in prosthodontics reads, “It is

unadvisable to employ the last tooth as a splinted abutment if it lacks a
degree of firmness comparable to its healthy neighbor because the strain on
the firm abutment could be destructive.”92 Implant prostheses may use
additional secondary natural abutments to decrease the movement of the
prosthesis so that rigid fixation of the implant will not be compromised.
However, if the last abutment is mobile, it does not serve the intended
purpose. A general guideline is to not end a fixed prosthesis on the weakest
splinted abutment. The weak tooth does not offer additional support and
further burdens the healthier abutments. In addition, if cement failure
occurs or the restoration needs retrieval, the partially retained prosthesis is
more difficult to retrieve from the mobile abutment, resulting in more
frequent coronal fracture and other complications.
The natural teeth exhibit some faciolingual movement, which varies from
56 to 108 µm in health. The discussion here is to reduce tooth movement
when it is visible so that the mobile teeth may be connected to the implants.
Although the teeth move in a faciolingual direction, different regions of the
arch have different directions of movement relative to each other. In other
words, the faciolingual direction of the anterior teeth corresponds to the
mesiodistal direction of the posterior teeth, and if these dental units are
splinted to each other, the splint may become nonmobile.
A dental arch may be described as a five-sided structure. The posterior
teeth on one side move in a similar direction to each other, the canine moves
in a different direction, the anterior teeth move in a third direction, the
contralateral canine moves in yet another direction in comparison, and the
other posterior component of the arch moves in a similar direction as the
first. The more dental sections are connected, the more rigid the structure.
As a general rule, three or more sections rigidly connected create an overall
nonmobile dental structure. Even mild to moderate individual mobile dental
units may become a nonmobile single unit.
The approach of joining implants to mobile teeth in several different arch
positions is usually limited to conditions when the multiple sections of the
dental arch already require restoration. Rarely would one consider crowning
eight or more teeth solely to splint to the implant component. Instead, the
use of a natural tooth pier abutment may be indicated.
The last tooth in a splinted prosthesis should not have poor retentive form.
When a force is applied to the terminal region of a multiple-splinted
restoration, the pier abutments may act as a fulcrum. As a consequence,
tensile and shear forces may be applied to the cement seal. Because the
cements are 20 times weaker in shear compared with compressive forces, the
cement seal may break. As a consequence, the natural abutment often decays
and may be lost. The most distal tooth in a splinted restoration should have
adequate height and retentive form.
The adjacent teeth should be able to have the path of insertion as all the
dental units in the prosthesis. It may be necessary to perform endodontics or
even extract an offending tooth to accomplish the goal of splinting across an
arch.
The adjacent teeth that are splinted together should not be overlapped or
crowded. It may be necessary to have orthodontics or selective extractions to
prepare the teeth for a similar path of insertion as the implant prosthesis.
When the adjacent teeth are splinted, enough interproximal tooth tissues
must be removed to permit adjacent metal crowns, connectors, and porcelain
to be applied and maintain interproximal hygiene.
In conclusion, the natural abutment connected to a rigidly fixated implant
should not exhibit clinical mobility or poor retentive form. These same two
criteria should be considered for the natural tooth used as a secondary
abutment when splinting teeth in a FPD.
Nonrigid Connectors.
Although nonrigid connectors have been advocated in the literature,93 a
nonrigid connector in a unilateral prosthesis rarely is indicated for implant-
fixed prostheses and may be detrimental. Nonrigid connection does not
improve the stress distribution between the different abutments94 and has
been reported to have caused migration of the natural teeth.95 If the nonrigid
connector exhibits any clinically observed mobility, it moves more than the
implant. As such, the implant-supported part of the restoration is
cantilevered to the attachment. In addition, the nonrigid (or mobile)
attachment adds cost, creates overcontoured abutments, impairs daily
hygiene, and does not decrease the clinical tooth movement.
Intrusion.
Reports of intrusion of the natural tooth connected to an implant usually
include the use of temporary cement to lute a coping to the natural
abutment, leaving the final restoration uncemented on the coping, or the use
of a nonrigid connector.96 When implants are joined to teeth that act as a
terminal abutment, a definitive cement should be used for the natural tooth.
The tooth cannot intrude unless it becomes unretained from the abutment
(or has a nonrigid connector between the units).
A possible explanation for tooth intrusion may be that the tooth is pushed
vertically 28 µm but wants to rebound only 8 µm. The fixed prosthesis
rebounds immediately and pulls on the tooth. The cement seal eventually
breaks, causing a space to develop, which is first occupied by air. The
prosthesis then acts as an orthodontic appliance and continually pushes the
tooth in a vertical direction. Eventually, the space is occupied by saliva, and
hydraulics continue the downward force during mastication. The tooth
eventually submerges or intrudes from the prosthesis (Fig. 3.130).
FIG 3.130 Splinting implants via intracoronal attachment (A, B). Clinical image of
nonrigid attachment, which is contraindicated. Ideally, the implants should be
splinted together, independent of the natural teeth.
Implant Pier (Intermediary) Abutments

A pier abutment is one between two other abutments, sometimes referred to
as an intermediate abutment. The intermediate abutment may be an implant
or a natural tooth, and each type plays a different role in the overall
treatment. When an implant serves as a pier abutment between two natural
teeth, the difference in movement between implant and tooth may increase
the complication rate compared with one intermediate tooth joined to two
terminal implants (Fig. 3.131). The pier implant abutment exhibits less
movement than the natural teeth terminal abutments and acts as the fulcrum
of a class I lever. As a consequence, a compressive force on one end of the
prosthesis is converted to a tensile or shear force on the other terminal
abutment. The cement tensile strength is often 20 or more times less than the
compressive strength. When the implant acts as a fulcrum, an uncemented
abutment (usually the least mobile tooth or least retentive crown) is a
common consequence, with decay being the next most common occurrence.
FIG 3.131 A pier implant abutment between two natural teeth may cause a cement
seal to break on the teeth, especially if one is more mobile than the other. (From Misch
This problem is magnified by a longer lever arm such as a pontic between
the implant and tooth. When the natural tooth or teeth have clinical mobility,
the force is lateral on the prosthesis, or the forces are greater than usual. A
pier implant abutment may cause complications even when joined to
nonmobile teeth as terminal abutments (Fig. 3.132).
FIG 3.132 When grafting and additional implants are not an option, a mobile
attachment may be used to prevent the pier implant from acting as a fulcrum. (From
Uncemented restorations are a common complication in FPDs even when

all aspects of treatment are within acceptable limits. Any condition that may
increase this problem, such as the one presently addressed, should be
carefully avoided.
Patient Treatment Planning
Failure to Provide to the Patient Comprehensive
Treatment Options
When discussing a treatment plan with a patient, it is quite easy to get
mentally focused on a certain treatment option based on the actual needs
and perceived values of the patient. Implant clinicians sometimes favor
certain treatments (e.g., overdenture vs. fixed prosthesis) according to their
learning curve, training, or their personal preferences. It is imperative from
an ethical and legal perspective that the clinician discuss all treatment
options, including a conversation concerning each option's advantages and
disadvantages. Most state dental boards in the United States require as part
of their dental law code that all patients be given all possible and viable
options, including advantages and disadvantages.
To prevent complications and treatment misunderstandings, a
comprehensive treatment planning protocol should be developed with every
patient. The next section of this chapter will discuss various edentulous site
treatment situations along with the associated advantages and disadvantages
of each treatment.
Single Missing Tooth
No Treatment.
Even though in most cases the option of “no treatment” is not ideal, the
patient should always be given an explanation of the possible ramifications
that may occur if no treatment is rendered. Proposing this treatment option
may seem counterintuitive to clinicians because the goal of dentistry is to
restore a patient to optimal function. However, the presentation of this
option does allow the clinician to enter into a discussion as to the various
consequences of tooth loss, bone loss, and lack of masticatory efficiency.
Advantages.
The only advantages of no treatment are the patient will not have to undergo
further procedures to address the situation, and secondly, there will be no
financial demands for the patient.
Disadvantages
Movement of adjacent teeth.
When a patient loses a single tooth, there are numerous consequences that
may result to create an occlusal disharmony and the potential for further
dental complications. If a tooth is extracted in any position anterior to the
second molars, the patient can expect for the tooth distal to it to begin tilting
mesially into the vacant space. This will most likely result in a change of the
occlusal plane on that side. As the teeth experience this mesial tilt, the
direction of load changes, which may cause excessive stress to the
periodontal ligament. The contacting teeth in the opposing arch will begin to
supraerupt in relation to the changes in the occlusal plane. The correction of
future supraerupted teeth may require orthodontic or endodontic/crown
therapy. In some situations, extraction may be necessary.
Occlusal force issues.

Another consequence of the single missing tooth is the patient will typically
favor the fully dentate side to chew with, due to a decreased masticatory
efficiency on the partially edentulous side. This situation results in the
overuse of the fully dentate side, leading to fatigue-related issues with the
teeth. Examples of these issues would be porcelain fracture of crowns,
fractures of enamel/fillings, significant occlusal wear, or myofascial pain
complications (Box 3.25).
Box 3.25
Missing Single Tooth
No Treatment Option
Advantages
• No treatment time for the patient
• No financial outlay for the patient
Disadvantages
• Supraeruption of the opposing teeth
• Drifting/tilting movement of the adjacent teeth

• Decrease masticatory function
• Food impaction
• Adjacent teeth will receive a higher occlusal load
• Occlusal overuse of contralateral side
Removable Partial Denture
Advantages.
The main advantages of the removable partial denture (RPD) in restoring a
single missing tooth are based on convenience. The patient can receive a
tooth-borne RPD after a few appointments, and there is a lack of invasive
treatment in this modality. There is also a lower associated cost in
comparison to most other treatment options.
Disadvantages
Decreased acceptance.
Removable partial dentures, even those that are primarily tooth borne, have a
low patient acceptance rate compared to other treatment options. Patients
experience difficulty in eating, as food debris may become trapped under the
prosthesis. Speech patterns are often disrupted, as the patient must
acclimate to the partial framework in the mouth. The prosthesis is often
bulky, covering part of the palatal tissue on the maxilla or the lingual tissue
on the mandible.
Increased morbidity to abutment teeth.

Reports of removable partial dentures indicate the health of the remaining
dentition and surrounding oral tissues often deteriorates. In a study that
evaluated the need for repair of an abutment tooth as the indicator of failure,
the “success” rates of conventional removable partial dentures were 40% at 5
years and 20% at 10 years.97 Patients wearing the partial dentures often
exhibit greater mobility of the abutment teeth, greater plaque retention,
increased bleeding upon probing, higher incidence of caries, speech
inhibition, taste inhibition, and noncompliance of use. A report by Shugars et
al. found abutment tooth loss for a removable partial denture may be as high
as 23% within 5 years and 38% within 8 years.98
Increased bone loss.

The natural abutment teeth, on which direct and indirect retainers are
designed, must submit to additional lateral forces. Because these teeth are
often compromised by deficient periodontal support, many partial dentures
are designed to minimize the forces applied to them. The result is an
increase in mobility of the removable prosthesis and greater soft tissue
support. These conditions protect the remaining teeth but accelerate the
bone loss in the edentulous regions.99 It should be noted that bone loss is
accelerated in the soft tissue support regions in patients wearing the
removable prosthesis compared with no prosthesis (Box 3.26).
Box 3.26
Removable Partial Denture Treatment Option
Advantages
• Minimal treatment minimal cost compared to other options
Disadvantages
• Poorly tolerated
• Decreased survival rate
• Increased mobility
• Plaque accumulation
• Bleeding on probing caries on abutment teeth
• Increased need for abutment teeth loss or repair
• Food impaction
• Accelerated bone loss in edentulous area

Fixed Partial Denture
Advantages
Common type of treatment.
A fixed prosthesis is a conventional and common type of procedure that most
clinicians are comfortable performing. The prosthesis can be fabricated
rather quickly because a laboratory can generate a complete restoration in 1
to 2 weeks that satisfies the criteria of normal contour, comfort, function,
esthetics, speech, and health. Most patients have an increased compliance
with this type of treatment, especially because no surgical intervention is
needed.
Minimal need for soft and hard tissue augmentation.

With a fixed partial denture, augmentation of the edentulous area is very
uncommon. Because the pontic may be modified to encompass most defects,
surgical augmentation procedures are usually not indicated. In some
instances, lack of attached tissue will be present on abutment teeth; however,
this is rather rare.
Disadvantages
Increased caries rate.
Despite the many advantages that an FPD has over its removable
counterpart, the treatment modality does have inherent disadvantages.
Caries and endodontic failure of the abutment teeth are the most common
causes of fixed partial denture prosthesis failure.100 Caries occur more than
20% of the time and endodontic complications to the abutments of a FPD
15% of the time. Recurrent decay on the abutment crown primarily occurs on
the margin next to the pontic. Fewer than 10% of patients floss on a regular
basis, and those using a floss threader are even fewer.101 As a result, the
pontic acts as a large overhang next to the crown and a reservoir for plaque
and bacteria. The long-term periodontal health of the abutment teeth may
also be at greater risk as a result of the plaque increase, including bone loss.
Increased endodontic treatment.

When a vital tooth is prepared for a crown, a 3% to 6% risk of irreversible
pulpal injury and subsequent need for endodontic treatment exists.102 Not
only does tooth preparation present a risk for endodontics on each of the
vital abutment teeth, the crown margin next to the pontic is also more at risk
of decay and the need for endodontics as a result. Studies have shown up to
15% of abutment teeth for a fixed restoration require endodontic therapy
compared with 3% to 6% of nonabutment teeth with crown preparations.103
Unfavorable outcomes of FPD failure.

There exist many issues that may result when a fixed partial denture fails.
These may include not only the need to replace the failed prosthesis but also
the loss of an abutment tooth and the need for additional pontics and
abutment teeth in the replacement bridge. Because 15% of FPD abutment
teeth require endodontics, many abutment teeth may be lost. In addition, an
endodontic posterior tooth abutment is at a greater risk of fracture. Reports
indicate that abutment teeth for a FPD fail from endodontic complications
(e.g., fracture) four times more often than those with vital pulps.104 The
fracture of the tooth may result in failure of the prosthesis and abutment
tooth.
The abutment teeth of an FPD may be lost from caries, endodontic
complications, or root fracture at rates up to 30% for 8 to 14 years.105 Recent
reports indicate 8% to 18% of the abutment teeth supporting a FPD are lost
within 10 years. This is most disturbing because 80% of abutments have no
previous decay or are minimally restored before the fabrication of the FPD
(Box 3.27).106
Box 3.27
Fixed Partial Denture Treatment Option
Advantages
• Most common treatment (doctor friendly)
• Reduced time (two appointments, 1 to 2 weeks apart)
• Restores function, esthetics, and intraarch health
• Few bone and soft tissue considerations

• Proven long-term survival
• Reduced cost—dental insurance covers procedure (reduced patient cost)
• Indicated when minimal mesiodistal space (<6 mm space)
• Potential abutments have clinical mobility; will benefit from being splinted
• Increases patient compliance and reduces fear
Disadvantages
• Mean life span approximates 10 to 15 years
• Caries and endodontic failure of abutment teeth most common

complication
• Increased plaque retention of pontic increases caries and periodontal

disease risk
• Hygiene difficulty
• Damage to healthy teeth (removing undamaged tooth structure)
• Failure of prosthesis related to loss of abutment teeth (8% to 18% within 10

years)
• Fracture complications (porcelain, tooth)
• Esthetic complications (crowns less esthetic than natural teeth)
• Uncemented restoration
Single Tooth Implant (Box 3.28)
Advantages
Higher success rate.
The single tooth implant provides numerous advantages when compared to
the other treatment options. Most studies to date have shown a single tooth
implant to be the most predictable method of single tooth replacement. Most
long-term studies report success rates exceeding 90%.
Box 3.28
Dental Implant Treatment Option
Advantages
• Adjacent teeth do not require splinted restorations
• Less risk of caries
• Less risk of endodontics
• Less risk of porcelain fracture
• Less risk of uncemented restoration
• Less fracture of tooth
• Psychologic need of patient addressed: patient does not desire two adjacent
teeth (often virgin) prepared and splinted to restore missing tooth
• Improved hygiene conditions
• Less decay risk
• Floss vs. floss threader
• Less pontic “plaque trap overhang”
• Decreased cold or contact sensitivity
• Prepared teeth more temperature sensitive
• Cementum of tooth removed by tooth preparation; toothbrush or scaler

sensitive
• Maintains bone in site: 30% decreasing bone width within 3 years after
extraction
• Decreases adjacent tooth loss: 30% vs. 0.05% risk at 10 years
Disadvantages
• Increased treatment time
• Need for surgical treatment
• May need hard and soft tissue augmentation
• Possibly less esthetic
• Retained cement
• Peri-implantitis
• Increased laboratory fees
Hygiene.
The dental implant treatment plan will usually allow for easier hygiene
access because the proximal surfaces can be reached for flossing. This acts as
a preventive measure against peri-implatntitis issues.
No alteration of adjacent teeth.

Adjacent teeth do not have to be altered with the implant option, which
decreases the risk of recurrent caries or endodontic possibilities with these
teeth. Because of these advantages the patient is at a much lower risk of
losing further teeth in the future.
Better cost comparison.

Cost comparison studies conclude that the implant restoration demonstrates
a more favorable cost-effectiveness ratio.30 Even when the adjacent teeth are
not lost, the conventional FPD often needs to be replaced more frequently
because of decay, endodontic complications, porcelain fracture, or unretained
restoration (i.e., which most likely results in decay and the need for
endodontic treatment).
Improved maintenance of bone.
With a fixed partial denture replacing a single missing tooth, continued bone
resorption will occur. Therefore, placing an implant into the edentulous site
will help maintain the existing host bone. Additionally, this will decrease the
possibility of soft tissue recession.
Disadvantages
Increased treatment time.
The single tooth implant procedure will take a considerably longer time for
treatment in comparison to a RPD or FPD. From the initial surgical
placement, the average implant will require an average of 4 to 6 months for
osseointegration to occur. This time frame is dependent on the patient's bone
density in that area as well as the volume of bone that was present at
placement. In an effort to address this issue, techniques have been proposed
to immediately place and at times immediately provisionalize implants.
However, in certain circumstances, these techniques present disadvantages,
especially when the patient criteria for these procedures is not met.
Need for additional treatment.

In esthetic areas, modifications to the soft tissue may be necessary as well in
an effort to change the soft tissue drape or to enhance the patient's tissue
biotype. This usually will lead to more complex procedures that are needed
for tissue augmentation. In addition, bone augmentation procedures may be
indicated to increase bone volume for implant placement. In some cases, this
may increase the cost significantly as well as the treatment time.
Esthetics.
Based on available bone and crown height space, the final prosthesis may
feature a traditional tooth contour (FP1), a longer crown form (FP2), or may
require the addition of pink porcelain to mimic normal soft tissue contours
(FP3). The patient must be aware of these possibilities as their esthetic
demands may contraindicate implant placement or will dictate dictate the
need for adjunctive bone grafting procedures.
Multiple Missing Teeth
No Treatment.
The patient should always be given an explanation of the possible
ramifications that may occur if no treatment is rendered. No treatment is
more of a concern in comparison to a single edentulous site as esthetic
issues, decrease in masticatory efficiency, and food impaction issues may
arise.
Advantages.
When a patient is missing multiple teeth, the education and communication
to the patient is even more important. Although there is no financial or time
commitment for the patient, the disadvantages are more significant in
comparison to a single missing tooth.
Disadvantages
Decreased masticatory function.

The main disadvantage of not replacing multiple missing teeth is the
decreased masticatory function. Patients will place more force and stress on
their remaining teeth, which leads to increased morbidity. The forces of
mastication are transmitted to the remaining teeth, which results in a greater
possibility of decay, mobility, periodontal issues, and loss of teeth. The longer
the edentulous ridge remains without stimulation, the greater chance bone
loss will occur. This may lead to the future need for hard and soft tissue
augmentation procedures to increase hard and soft tissue volume for implant
placement.
Tooth movement.
The remaining teeth may continue to shift in relation to the stresses of
mastication, causing movement and tilting. Teeth in the opposing arch will
supraerupt due to the lack of stimulation by an opposing tooth, causing root
exposure and occlusal disharmony. These phenomena combine to potentially
complicate or contraindicate future implant placement.
Esthetics.
If no treatment is rendered for the edentulous area, obvious esthetic issues
will result. In most cases, patient acceptance of the edentulous areas is low,
and esthetics is usually a motivating factor in seeking rehabilitation.
Removable Partial Denture

See the advantages and disadvantages for RPD in Box 3.26.
Implanted-Supported Crowns
See the advantages and disadvantages for RPD in Box 3.28.
Completely Edentulous
No Treatment.
The patient should always be given an explanation of the possible
ramifications that may occur if no treatment is rendered.
Advantages.
There exist few advantages other than no treatment time or financial outlay
for the patient.
Disadvantages
Continued bone loss.

Most clinicians overlook the insidious bone loss that will occur after tooth
extraction. The patient is often not educated about the anatomic changes and
the potential consequences of continued bone loss. The bone loss accelerates
when the patient wears a poorly fitting soft tissue–borne prosthesis. Most
patients do not understand that bone resorption occurs over time and at a
greater rate beneath poorly fitting dentures. Patients do not return for
regular visits for evaluation of their condition; instead, they return after
several years when denture teeth are worn down or can no longer be
tolerated. In fact, studies have shown that the average denture wearer sees a
dentist every 14.8 years after having a complete denture. The traditional
method of tooth replacement (dentures) often affects bone loss in a manner
not sufficiently considered by the clinician and the patient. The clinician
should inform the patient that a denture replaces more bone and soft tissue
than teeth, and every 3 to 5 years a reline, or new denture is suggested to
replace the additional bone loss by atrophy that will occur (Fig. 3.133 and Box
3.29).
FIG 3.133 A dentate mandible on the left and a long-term edentulous mandible on
the right. Note the amount of bone loss in height. Loss of bone height in the mandible
may be measured by the centimeter and often is ignored. Such bone loss is often
more significant than the bone loss (in millimeters) from periodontal disease. The
patient should understand that a denture often replaces more bone than teeth to
restore the proper dimensions of the face. (From Misch CE: Dental implant prosthetics, ed 2,
Box 3.29
Consequences of Bone Loss in Fully
Edentulous Patients
• Decreased width of supporting bone
• Decreased height of supporting bone
• Prominent mylohyoid and internal oblique ridges with increased sore spots
• Progressive decrease in keratinized mucosa surface
• Prominent superior genial tubercles with sore spots and increased denture
movement
• Muscle attachment near the crest of the ridge
• Elevation of prosthesis with contraction of mylohyoid and buccinators

muscles serving as posterior support
• Forward movement of prosthesis from anatomic inclination (angulation of
mandible with moderate to advanced bone loss)
• Thinning of mucosa with sensitivity to abrasion
• Loss of basal bone
• Paresthesia from dehiscent mandibular neurovascular canal
• More active role of tongue in mastication
• Effect of bone loss on esthetic appearance of lower third of face
• Increased risk of mandibular body fracture from advanced bone loss
• Loss of anterior ridge and nasal spine, causing increased denture

movement and sore spots during function
Soft tissue consequences.

As bone loses width, then height, then width and height again, the attached
gingiva gradually decreases. A very thin attached tissue usually lies over the
advanced atrophic mandible or is entirely absent. The increasing zones of
mobile, unkeratinized gingiva are prone to abrasions caused by the overlying
prosthesis, which will lead to bone loss. In addition, unfavorable high muscle
attachments and hypermobile tissue often complicate the situation. The
continued atrophy of the posterior mandible eventually causes prominent
mylohyoid and internal oblique ridges covered by thin, movable, unattached
mucosa. The anterior residual alveolar process also continues to resorb, and
the superior genial tubercles (which are 20 mm below the crest of bone when
teeth are present) eventually become the most superior aspect of the anterior
mandibular ridge. There is little to prevent the prosthesis from moving
forward against the lower lip during function or speech. This condition is
further compromised by the vertical movement of the distal aspect of the
prosthesis during contraction of the mylohyoid and buccinator muscles and
the anterior incline of the atrophic mandible compared with that of the
maxilla.107 The thickness of the mucosa on the atrophic ridge is also related to
the presence of systemic disease and the physiologic changes that
accompany aging. Conditions such as the patient's age, hypertension,
diabetes, anemia, and nutritional disorders have deleterious effects on the
vascular supply and soft tissue quality under removable prostheses. These
disorders result in a decreased oxygen tension to the basal cells of the
epithelium. Surface cell loss occurs at the same rate, but the cell formation at
the basal layer is slowed. As a result, thickness of the surface tissues
gradually decreases, and sore spots and uncomfortable removable prostheses
result. The tongue of a patient with edentulous ridges often enlarges to
accommodate the increase in space formerly occupied by teeth. At the same
time, it is used to limit the movements of the removable prostheses and takes
a more active role in the mastication process. As a result, the removable
prosthesis decreases in stability. The decrease in neuromuscular control,
often associated with aging, further compounds the problems of traditional
removable prosthodontics. The ability to wear a denture successfully may be
largely a learned, skilled performance. An aged patient who recently became
edentulous may lack the motor skills needed to adjust to the new conditions
(Box 3.30).
Box 3.30
Soft Tissue Consequences of Edentulism
• Attached, keratinized gingiva is lost as bone is lost
• Unattached mucosa for denture support causes increased soft spots
• Thickness of tissue decreases with age and systemic disease that causes
more sore spots for dentures
• Tongue increases in size, which decreases denture stability
• Tongue has more active role in mastication, which decreases denture

stability
• Decreased neuromuscular control of jaw in elderly adults
Esthetic consequences.
The facial changes that naturally occur in relation to the aging process can be
accelerated and potentiated by the loss of teeth (Fig. 3.134). There exist many
esthetic consequences that result from the loss of alveolar bone. A decrease
in facial height from a collapsed vertical dimension will causes several facial
changes (Fig. 3.135). The loss of the labiomental angle and deepening of
vertical lines in the area create a harsh appearance. As the vertical dimension
progressively decreases, the occlusion evolves toward a pseudo class III
malocclusion. As a result, the chin rotates forward and creates a prognathic
facial appearance (Fig. 3.136). These conditions result in a decrease in the
horizontal labial angle at the corner of the lips; the patient appears unhappy
when the mouth is at rest (Fig. 3.137). People with short facial types have
higher bite forces, greater bone loss, and more dramatic facial changes with
edentulism compared with others. A thinning of the vermilion border of the
lips results from the poor lip support provided by the prosthesis and the loss
of muscle tone. The maxillary retruded position is related to the loss of the
premaxillary ridge and the loss of tonicity of the muscles involved in facial
expression. The contraction of the orbicularis oris and buccinator muscles in
a patient with moderate to advanced bone atrophy displaces the modiolus
and muscles of facial expression medially and posteriorly. As a result, a
narrowing of the commissure, inversion of the lips, and hollowing of the
cheeks are characteristic findings.
FIG 3.134 Esthetic aspects of the inferior third of the face are not only related to
the position of the teeth but even more important is the position and amount of bone
in the jaws and include the muscles that attach to the bone. (From Misch CE: Dental
FIG 3.135 A patient often wears a denture for more than 15 years. The loss of bone
height during this time is associated with many extraoral facial changes as a closed
bite, a mandible that rotates forward, a receding maxilla, a reverse smile line,
increased number and depth of lines in the face, more acute angle between the
nose and the face, loss of vermilion border in the lips and jowls, and witch's chin
from loss of muscle attachment. (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
FIG 3.136 Loss of bone height can lead to a closed bite with rotation of the chin
anterior to the tip of the nose. This picture represents the face of someone without
teeth and advanced bone loss. (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
FIG 3.137 This patient has severe bone loss in the maxilla and mandible. Although
she is wearing her 15-year-old dentures, the facial changes are significant. The loss
of muscle attachments leads to ptosis of the chin (witch's chin), loss of vermilion
border (lipstick is applied to the skin), reverse lip line (decrease in horizontal angles),
increased vertical lines in the face and lips, increased lip angle under the nose, and
a lack of muscle tonicity in the masseter and buccinator muscles. (From Misch CE:
A deepening of the nasolabial groove and an increase in the depth of other

vertical lines in the upper lip are related to normal aging but are accelerated
with bone loss. This usually is accompanied by an increase in the columella-
philtrum angle. This can make the nose appear larger than if the lip had
more support (Fig. 3.138). Men often grow a moustache to minimize this
effect. The maxillary lip naturally becomes longer with age as a result of
gravity and loss of muscle tone, resulting in less of the anterior teeth shown
when the lip is at rest. This has a tendency to “age” the smile because the
younger the patient, the more the teeth show in relation to the upper lip at
rest or when smiling. Loss of muscle tone is accelerated in edentulous
patients, and the lengthening of the lip occurs at a younger age and is longer
(showing less teeth) than dentate patients of a similar age. The upper lip
often rolls over the incisal edge of the maxillary dentures, which further
decreases the size of the vermilion border.
FIG 3.138 Profile view. Note the maxillary bone loss effect on the lack of vermilion
border of the lip, deep labial folds, and the columella–philtrum angle. Yet the lower lip
has a normal vermillion border and the muscles to the anterior lower jaw are still
attached, providing a normal contour. (From Misch CE: Dental implant prosthetics, ed 2, St
The attachments of the mentalis and buccinator muscles to the body and
symphysis of the mandible also are affected by bone atrophy. This will result
in sagging of the tissue or “jowls” or a “witch's chin.” This effect is
cumulative because of the loss in muscle tone with the loss of teeth, the
associated decrease in bite force, and the loss of bone in the regions where
the muscles used to attach (Box 3.31). Patients are usually unaware the hard
and soft tissue changes are from the loss of teeth. Among denture wearers,
studies have shown that 39% have been wearing the same prosthesis for
more than 10 years.87 The profession is unable to evaluate patients unless
they return yearly. It is important that the consequences of tooth loss be
explained to partially or completely edentulous patients during the early
phases of treatment.
Box 3.31
Esthetic Consequences of Bone Loss
• Decreased facial height
• Loss of labiomental angle
• Deepening of vertical lines in lip and face
• Chin rotates forward—gives a prognathic appearance
• Decreased horizontal labial angle of lip—makes patient look unhappy
• Loss of tone in muscles of facial expression
• Thinning of vermilion border of the lips from loss of muscle tone
• Deepening of nasolabial groove
• Increase in columella-philtrum angle
• Increased length of maxillary lip, so less teeth show at rest and smiling—
ages the smile
• Ptosis of buccinators muscle attachment—leads to jowls at side of face
• Ptosis of mentalis muscle attachment—leads to “witch's chin”
Complete Upper Denture
Advantages.
Compared to no treatment, the complete upper denture will usually satisfy
esthetic and some functional requirements. The patient will have landmarks
to use for pronunciation of words, and they will retain the appearance of
facial height, although superficially.
Disadvantages
Masticatory function.
The difference in maximum occlusal forces recorded in a person with natural
teeth and one who is completely edentulous is dramatic. In the first molar
region of a dentate person, the average force has been measured at 150 to 250
psi.108 A patient who grinds or clenches their teeth may exert a force that
approaches 1000 psi. The maximum occlusal force in an edentulous patient is
reduced to less than 50 psi. The longer patients are edentulous, the less force
they are able to generate. Patients wearing complete dentures for more than
15 years may have a maximum occlusal force of less than 6 psi.57
As a result of decreased occlusal force and the instability of the denture,
masticatory efficiency also decreases with tooth loss. Ninety percent of the
food chewed with natural teeth fits through a no. 12 sieve; this is reduced to
58% in the patient wearing complete dentures.109 A study of 367 denture
wearers (158 men and 209 women) found that 47% exhibited a low
masticatory performance. The 10-fold decrease in force and the 40% decrease
in efficiency affect the patient's ability to chew. In patients with dentures,
29% are able to eat only soft or mashed foods, 50% avoid many foods, and
17% claim they eat more efficiently without the prosthesis.110 Lower intakes
of fruits, vegetables, and vitamin A by females were noted in this group.
Denture patients also take significantly more drugs (37%) compared with
those with superior masticatory ability (20%), and 28% take medications for
gastrointestinal disorders. The reduced consumption of high-fiber foods
could induce gastrointestinal problems in edentulous patients with deficient
masticatory performance. In addition, the coarser bolus may impair proper
digestive and nutrient extraction functions.111
Systemic consequences.
The literature includes several reports suggesting that compromised dental
function causes poor masticatory performance and swallowing poorly
chewed food, which in turn may influence systemic changes favoring illness,
debilitation, and shortened life expectancy.112 In another study, the
masticatory performance and efficiency in denture wearers were compared
with those of dentate individuals. This report noted that when appropriate
corrections were made for different performance norms and levels, the
chewing efficiency of a denture wearer was less than one sixth of a person
with teeth.113
Several reports in the literature correlate a patient's health and life span to
dental health. Poor chewing ability may be a cause of involuntary weight loss
in old age, with an increase in mortality rate.114 In contrast, patients with a
substantial number of missing teeth were more likely to be obese. After
conventional risk factors for strokes and heart attacks were accounted for,
there was a significant relationship between dental disease and
cardiovascular disease, the latter still remaining as the major cause of
death.115
Satisfaction of prosthesis.
A dental survey of edentulous patients found that 66% were dissatisfied with
their mandibular complete dentures. Primary reasons were discomfort and
lack of retention causing pain and discomfort.116 Past dental health surveys
indicate that only 80% of the edentulous population are able to wear both
removable prostheses all the time.117 Some patients wear only one prosthesis,
usually the maxillary; others are only able to wear their dentures for short
periods. In addition, approximately 7% of patients are not able to wear their
dentures at all and become “dental cripples” or “oral invalids.” They rarely
leave their home environment, and when they feel forced to venture out, the
thought of meeting and talking to people when not wearing their teeth is
unsettling.
Speech effects.
A report of 104 completely edentulous patients seeking treatment was
performed by Misch and Misch.118 Of the patients studied, 88% claimed
difficulty with speech, with one fourth having great difficulty. This most
likely occurs with the mandible, which rests upon the buccinator muscle and
mylohyoid muscle when the posterior mandible resorbs. When the patient
opens his or her mouth, the contraction of these muscles acts like a
trampoline and propels the lower denture off the ridge. As a result, the teeth
often click when the patient talks, not from vertical dimension issues, but
from the lack of stability and retention of the prosthesis. Speech problems
may be associated with a concern for social activities. Awareness of
movement of the mandibular denture was cited by 62.5% of these patients,
although the maxillary prosthesis stayed in place most of the time at almost
the same percentage.
Psychologic aspects of tooth loss.

The psychologic effects of total edentulism are complex and varied and range
from very minimal to a state of neuroticism. Although complete dentures are
able to satisfy the esthetic needs of many patients, some believe their social
lives are significantly affected. They are concerned with kissing and romantic
situations, especially if a new partner in a relationship is unaware of their
oral handicap. Fiske et al., in a study of interviews with edentulous subjects,
found tooth loss was comparable to the death of a friend or loss of other
important parts of a body in causing a reduction of self-confidence ending in
a feeling of shame or bereavement (Box 3.32).119
Box 3.32
Negative Effects of Complete Dentures
• Bite force is decreased from 200 psi for dentate patients to 50 psi for
edentulous patients
• 15-year denture wearers have reduced bite force to 6 psi
• Masticatory efficiency is decreased
• More drugs are necessary to treat gastrointestinal disorders
• Food selection is limited
• Healthy food intake is decreased
• The life span may be decreased
• Reduced prosthesis satisfaction
• Speech difficulty
• Psychologic effects
Implant-Supported Overdenture (Removable-RP4/RP5)
Advantages
Reduction in soft tissue coverage.
The overdenture (RP4) may reduce the amount of soft tissue coverage and
extension of the prosthesis. This is especially important for new denture
wearers, patients with tori or exostoses, and patients with low gagging
thresholds. Also, the existence of a labial flange in a conventional denture
may result in exaggerated facial contours for a patient with recent
extractions, which can result in chronic soreness. Implant-supported
prostheses (RP4) do not require labial extensions or extended soft tissue
coverage. Note: An RP-5 prosthesis would have full peripheral acrylic
extensions in the maxilla and mandible (i.e., mandible, buccal shelf support;
maxilla, full palatal coverage).
Increased retention.
In general, an implant overdenture prosthesis will have significant retention
in comparison to a conventional complete removable prosthesis. For
example, a complete mandibular denture moves during most mandibular jaw
movements in function and speech. Studies have shown a mandibular
denture may move approximately 10 mm during function. Under these
conditions, specific occlusal contacts and the control of masticatory forces are
nearly impossible. An IOD provides improved retention and stability of the
prosthesis, and the patient is able consistently to reproduce a determined
centric occlusion.120
Increased biting forces.

Higher bite forces have been documented for mandibular overdentures on
implants. The maximum occlusal force of a patient with dentures may
improve 300% with an implant-supported prosthesis.121 A study of chewing
efficiency compared wearers of complete dentures with wearers of implant-
supported overdentures (IODs). The complete denture group needed 1.5 to
3.6 times the number of chewing strokes compared with the overdenture
group.122 The chewing efficiency with an IOD is improved by 20% compared
with a traditional complete denture.123
Better speech.
The contraction of the mentalis, buccinator, or mylohyoid muscles may lift a
traditional denture off the soft tissue. As a consequence, the teeth may touch
during speech and elicit clicking noises. The retentive IOD remains in place
during most mandibular movements. The tongue and perioral musculature
may resume a more normal position because they are not required to limit
mandibular denture movement. However, most patients will obtain better
speech with a RP-4 prosthesis, as a RP-5 overdenture tends to have longer
flanges, which impinge on the musculature.
Decreased number of implants.
An overdenture also provides some practical advantages over an implant-
supported complete fixed partial denture. Fewer implants may be required
when a RP-5 restoration is fabricated because soft tissue areas may provide
additional support. The overdenture may provide stress relief between the
superstructure and prosthesis, and the soft tissue may share a portion of the
occlusal load. Regions of inadequate bone for implant placement may be
eliminated from the treatment plan rather than necessitating bone grafts or
placing implants with poorer prognosis. As a result of less bone grafting and
fewer implants, the cost to treat the patients is dramatically reduced. An RP-4
prosthesis requires more implants than an RP-5; however, less than a fixed
prosthesis.
Esthetics.
The esthetics for many edentulous patients with moderate to advanced bone
loss are improved with an overdenture compared with a fixed restoration.
Soft tissue support for facial appearance often is required for an implant
patient because of advanced bone loss, especially in the maxilla. Interdental
papilla and tooth size are easier to reproduce or control with an overdenture.
Denture teeth easily reproduce contours and esthetics compared with time-
consuming and technician-sensitive porcelain metal fixed restorations. The
labial flange may be designed for optimal appearance, not daily hygiene. In
addition, abutments do not require a specific mesiodistal placement position
for an esthetic result because the prosthesis completely encompasses the
implant abutments.
Hygiene.
Hygiene conditions and home and professional care are improved with an
overdenture compared with a fixed prosthesis. Periimplant probing is easier
around a bar than a fixed prosthesis because the crown contour often
prevents straight-line access along the abutment to the crest of the bone. The
overdenture may be extended over the abutments to prevent food
entrapment during function in the maxilla. With a fixed implant prosthesis,
hygiene is usually complicated because of the contours of the prosthesis in
comparison to the implant position.
Less trauma from parafunction.

An overdenture may be removed at bedtime to reduce the noxious effect of
nocturnal parafunction, which increases stresses on the implant support
system. In addition, a fixed prosthesis is not desired as often for a long-term
denture wearer. Long-term denture patients do not appear to have a
psychologic problem associated with a removable implant prosthesis vs. a
fixed prosthesis.
Ease of repair.
The overdenture prosthesis is usually easier to repair than a fixed restoration.
Reduced laboratory fees and fewer implants allow the restoration of patients
at reduced costs compared with a fixed prosthesis. If a fixed prosthesis
fractures (i.e., porcelain), remediation usually will include refabrication of
the prosthesis.
Decreased bone loss.

In the areas of implant placement, bone atrophy will be reduced greatly in
comparison to areas of edentulism. It has been shown in numerous studies
that the stimulation from the implants and/or prosthesis maintains posterior
bone volume.
Prosthesis may be upgraded.

In most cases, an overdenture may be upgraded to a fixed prosthesis (i.e., as
long as there exist no positioning or bone deficiency issues) (Box 3.33; Box
3.34). For example, a two-implant RP-5 mandibular overdenture may be
changed to a RP-4 by adding 2 to 3 additional implants or an FP-3 fixed
prosthesis by adding 3 to 4 additional implants in the mandible.
Box 3.33
Mandibular Implant Overdenture Advantages
• Prevents anterior bone loss
• Improved esthetics
• Improved stability (reduces or eliminates prosthesis movement)
• Improved occlusion (reproducible centric relation occlusion)
• Decrease in soft tissue abrasions

• Improved chewing efficiency and force
• Increased occlusal efficiency
• Improved prosthesis retention
• Improved prosthesis support
• Improved speech
• Reduced prosthesis size (reduces flanges)
• Improved maxillofacial prostheses
Box 3.34
Implant Overdenture Advantages vs. Fixed
Prosthesis
• Fewer implants (RP-5)
• Less bone grafting required before treatment
• Less specific implant placement
• Improved esthetics
• Denture teeth
• Labial flange
• Soft tissue drape replaced by acrylic
• Soft tissue considerations
• Improved periimplant probing (follow-up)
• Hygiene
• Reduced stress
• Nocturnal parafunction (remove prosthesis at night)
• Stress relief attachment
• Lower cost and laboratory cost (RP-5)
• Fewer implants (RP-5)
• Less bone grafting (RP-5)
• Easy repair
• Laboratory cost decrease (RP-5)
• Transitional device is less demanding than a fixed restoration
Disadvantages
Patient expectations.
The primary disadvantage of a mandibular overdenture is related to the
patient's desire, primarily when he or she does not want to be able to remove
the prosthesis. A fixed prosthesis often is perceived as an actual body part of
the patient, and if a patient's primary request is not to remove the prosthesis,
an implant-supported overdenture would not satisfy the psychologic need of
the patient.
Food impaction.
Unlike the labial flange of a maxillary denture, the labial flange of a
mandibular overdenture rarely is required for esthetics. A mandibular
overdenture often traps food below its flanges, similar to a denture. Dentures
and RP-5 IODs are border molded to the muscle attachment level to allow
the floor of the mouth to raise during swallowing. As a consequence, food
accumulates below the denture flange while the muscles are at rest and then
is compressed under the restoration during deglutition. The contour of a
fixed restoration is less prone to food entrapment. The daily care for a bar
IOD (RP-4) may be similar to that for a fixed mandibular restoration because
ridge lap pontics are not required for esthetics or speech, as with some
maxillary fixed prostheses.
More maintenance.
Removable overdentures require greater maintenance and exhibit more
frequent prosthetic-related complications than fixed restorations. For
example, Walton and McEntee noted that there were three times more
maintenance and adjustments for removable prostheses compared with fixed
restorations.124 IODs often require attachments to be changed or modified
every 6 months to 2 years, and denture teeth often wear, requiring a new
prosthesis to be fabricated every 5 to 7 years.125 In a review of literature by
Goodacre et al., IODs have retention and adjustment problems 30% of the
time, relines 19% of the time, clip or attachment fracture 17% of the time, and
fracture of the prosthesis 12% of the time.30 Fixed prostheses need less repair
and less maintenance and often last the life of the implant support. Although
porcelain fractures with a fixed restoration may occur and be costly to repair,
over a lifetime the implant-supported removable prosthesis is often more
expensive.
Denture teeth attrition.

Denture teeth wear faster on an IOD (i.e., hybrid) than with a traditional
denture because bite force and masticatory dynamics are improved. A new
overdenture often is required at 5- to 7-year increments because of denture
tooth wear and changes in the soft tissue support. Patient education
regarding the long-term maintenance requirement and the associated costs
should be outlined at the onset of implant therapy (Box 3.35).
Box 3.35
Overdenture Disadvantages
• Psychologic (need for nonremovable teeth)
• Greater abutment crown height space required
• More long-term maintenance required

• Attachments (change)
• Relines (RP-5)
• New prosthesis every 7 years
• Continued posterior bone loss
• Food impaction
• Movement (RP-5)
Implant-Supported Fixed Prosthesis (Fixed)
Advantages
Ideal prosthesis.
The implant-supported fixed prosthesis is the closest available treatment
option for an edentulous patient to return to optimal form, function, and
esthetics. Most patients receiving a fixed prosthesis will state that it “feels
like normal teeth,” which carries a profound psychologic impact. The
prosthesis does not require removal and is less likely to impact food in
comparison to a removable prosthesis.
Less bone loss in cantilevered areas.

Wright et al. have evaluated posterior mandibular bone loss in IODs (type 5
removable prosthesis [RP-5]) compared with cantilevered fixed prostheses
from anterior implants.121 The annual bone loss index observed in the RP-5
overdentures ranged from +0.02 to −0.05 with 14 of 20 patients losing bone in
the posterior regions. The fixed prostheses group had a range from +0.07 to
−0.015 with 18 of 22 patients gaining posterior bone area. Reddy et al. also
found a similar clinical observation in 60 consecutively treated cantilevered
fixed prostheses supported by five to six implants placed between the
foarmina.126 The mandibular body height was measured 5, 10, 15, and 20 mm
distal to the last implant. The baseline measurements up to 4 years after
function increased from 7.25 ± 0.25 mm to 8.18 ± 0.18 mm. Nearly all of the
bone growth occurred during the first year of function. An important role for
the complete implant-supported restoration is the maintenance and even
regeneration of posterior bone in the mandible.
Decreased maintenance.
Because there are no attachments utilized with a fixed implant prosthesis,
there is far less maintenance required. Less maintenance is associated with
less financial outlay that the patient must commit to in comparison to an
overdenture treatment (Fig. 3.139 and Box 3.36).
FIG 3.139 Implant overdentures with posterior soft tissue support lose bone in the
posterior regions almost 75% of the time (purple bars). Fixed prostheses
cantilevered from anterior implants gain bone in the posterior regions more than 80%
of the time (blue bars). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby;
Data from Wright PS, Glastz PO, Randow K, et al: The effects of fixed and removable implant-
stabilized prostheses on posterior mandibular residual ridge resorption, Clin Oral Implants Res
13:169–174, 2002.)
Box 3.36
Advantages of a Full-Arch Fixed Partial
Denture vs. Overdenture
• Psychologic: “feels like teeth”
• Less prosthetic maintenance (e.g., attachments, relines, new overdenture)
• Less food entrapment

• Posterior mandibular bone gain
Disadvantages
Cost.
The cost of a fixed prosthesis is higher than other treatment plans, which
may serve as a barrier to acceptance. In patients with severe parafunction,
the argument does arise for fabrication of a removable overdenture as
opposed to the porcelain fixed restoration as it is removable and is easily
repaired if needed.
Esthetics.
The esthetics for a fixed detachable prosthesis may be inferior to an
overdenture. Because soft tissue support for facial appearance often is
required for an implant patient with advanced bone loss, a fixed prosthesis
will usually not be as soft tissue supportive as an overdenture. Because there
is no labial flange with a fixed prosthesis, compromises in the soft tissue may
result. If overcontouring of the prosthesis is completed by the laboratory, this
will often result in decreased hygiene.
Food impaction.
With a fixed prosthesis, a common complaint exists with an increase in food
impaction. This will most likely result when custom abutments are used to
offset nonideal implant positioning. Because the prosthesis is fixated,
removing the prosthesis, whether cement or screw, is time-consuming and
increases potential complications.
Summary
The foundation of a successful treatment outcome is to fully inform the
patient as to the advantages and disadvantages of every possible treatment
option for their respective condition. Even with superior clinical skill and
perfect execution, a clinician may encounter patient dissatisfaction with the
finished treatment due to unmet expectations. With a firm understanding of
every possible treatment option, the practitioner can effectively educate the
patient, agree on a treatment plan based on the patient's values, and manage
expectations throughout the process. By doing this, both the clinician and
patient will enjoy the benefits of their relationship.
References
1. Misch CE. Prosthetic options in implant dentistry. Int J Oral
Implantol. 1991;7:17–21.
2. Misch CE. Consideration of biomechanical stress in treatment with
dental implants. Dent Today. 2006;25:80 [82, 84, 85; quiz 85].
3. Tjan AH, Miller GD, The JG. Some esthetic factors in a smile. J
Prosthet Dent. 1984;51:24–28.
4. Chan MFW, Johnston C, Howell RA, et al. Prosthetic management of
the atrophic mandible using endosseous implants and overdentures:
a 6-year review. Br Dent J. 1995;179:329–337.
5. Zarb GA, Schmitt A. The edentulous predicament. I. The
longitudinal effectiveness of implant-supported overdentures. J Am
Dent Assoc. 1996;127:66–72.
6. Jacobs R, Schotte A, van Steenberghe D, et al. Posterior jaw bone
resorption in osseointegrated implant overdentures. Clin Oral
7. Razavi R, Zena RB, Khan Z, et al. Anatomic site evaluation of
edentulous maxillae for dental implant placement. J Prosthet Dent.
1995;4:90–94.
8. Oikarinen K, Raustia AM, Hartikainen M. General and local
contraindications for endosseal implants—an epidemiological
panoramic radiograph study in 65-year-old subjects. Community Dent
Oral Epidemiol. 1995;23(2):114–118.
9. Testori T, Younan R. Clinical evaluation of short, machined-surface
implants followed for 12 to 92 months. Int J Oral Maxillofac Implants.
2003;18:894–901.
10. Weng D, Jacobson Z, Tarnow D, et al. A prospective multicenter
clinical trial of 3i machined-surface implants: results after 6 years of
follow-up. Int J Oral Maxillofac Implants. 2003;18:417–423.
11. Tarnow DP, Cho SC, Wallace SS. The effect of inter-implant distance
on the height of inter-implant bone crest. Periodontology. 2000;71:546–
549.
12. Hebel KS, Gajjar R. Achieving superior aesthetic results: parameters
for implant and abutment selection. Int J Dent Symp. 1997;4:42–47.
13. Berg H, Carlsson GE, Helkimo M. Changes in shape of posterior parts
of upper jaws after extraction of teeth and prosthetic treatment. J
Prosthet Dent. 1975;34:262–268.
14. Misch CE, Wang HL. The procedures, limitations and indications for
small diameter implants and a case report. Oral Health. 2004;94:16–
26.
15. Minsk L, Polson A, Weisgold A, et al. Outcome failures of endosseous
implants from a clinical training center. Compend Contin Educ Dent.
1996;17:848–859.
16. Mraiwa N, Jacobs R, van Steenberghe D, et al. Clinical assessment and
surgical implications of anatomic challenges in the anterior
mandible. Clin Implant Dent Relat Res. 2003;5:219–225.
17. Misch CE. Contemporary implant dentistry. ed 3. Mosby: St Louis; 2008.
18. Bidez MW, Misch CE. Force transfer in implant dentistry: basic
concepts and principles. J Oral Implantol. 1992;18:264–274.
19. Pjetursson B, Tan K, Lang N, 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. Clin Oral Impl Res. 2004;15:625–
642.
20. Scurria MS, Bader JD, Shugars DA. Meta-analysis of fixed partial
denture survival: prostheses and abutments. J Prosthet Dent.
1998;79:459–464.
21. Palmquist S, Swartz B. Artificial crowns and fixed partial dentures 18
to 23 years after placement. Int J Prosthodont. 1993;6:179–205.
22. Dykema RW, Goodacre CJ, Phillips RW. Fundaments of fixed prosthetics.
WB Saunders: St Louis; 1986.
23. Abdel-Latif H, Hobkirk J, Kelleway J. Functional mandibular
deformation in edentulous subjects treated with dental implants. Int
J Prosthodont. 2000;13:513–519.
24. Rosenstiel SF, Land MF, Fujimoto J. Contemporary fixed prosthodontics.
ed 4. Mosby: St Louis; 2006.
25. Misch CE, Silc JT. Key implant positions: treatment planning using the
canine and first molar rules. Dent Today. 2009;28(8):66–70.
26. Misch CE. Treatment plans related to key implant locations: the
canine and first molar position. Oral Health. 2008;98(8):43.
27. Dawson PE. Functional occlusion: from TMJ to smile design. Mosby: St
Louis; 2007.
28. Williamson EH, Lundquist DO. Anterior guidance: its effect on
electromyographic activity of the temporal and masseter muscles. J
Prosthet Dent. 1983;49:816–823.
29. Silva GC, Mondonca JA, Lopes LR, et al. Stress patterns on implants in
prostheses supported by four or six implants: a three-dimensional
finite element analysis. Int J Oral Maxillofac Implants. 2010;25:239–
246.
30. Goodacre CJ, Bernal G, Rungcharassaeng K, et al. Clinical
complications with implant and implant prostheses. J Prosthet Dent.
2003;90:121–132.
31. Adell R, Lekholm U, Rockler B, et al. A 15-year study of
osseointegrated implants in the treatment of the edentulous jaw. Int J
Oral Surg. 1981;6:387–416.
32. Balshi TJ, Wolfinger GJ. Two-implant-supported single molar
replacement: interdental space requirements and comparison to
alternative options. Int J Periodontics Restorative Dent. 1997;17:426–435.
33. Maló P, Rangert B, Nobre M. All-on-4 immediate function concept
with Brånemark implants for completely edentulous maxillae: a 1-
year retrospective clinical study. Clin Implants Dent Relat Res.
2005;7:88–94.
approach, healing, and progressive bone loading. Int J Oral Implantol.
1990;6:23–31.
35. Misch CE, Bidez MW. Implant protected occlusion: a biomechanical
rationale. Compend Contin Dent Educ. 1994;15:1330–1343.
36. Dawson PE. Differential diagnosis and treatment of occlusal problems. ed
2. Mosby: St Louis; 1989.
37. Monasky GE, Tough DF. Studies of wear of porcelain, enamel and
gold. J Prosthet Dent. 1971;25:299–306.
38. Misch CE, Palattella A. Bruxism and its effect on treatment plans. Int
Mag Oral Implant. 2002;2:6–18.
39. Misch CE. Clenching and its effect on dental implant treatment plans.
Texas State J. 2003;581–592.
40. Misch CE. Clenching and its effects on implant treatment plans. Oral
Health. 2002;92:11–24.
41. Tanaka TT. Recognition of the pain formula for head, neck, and TMJ
disorders: the general physical examination. Calif Dent Assoc J.
1984;12:43–49.
42. Mezitis M, Rallis G, Zachariatides N. The normal range of mouth
opening. J Oral Maxillofac Surg. 1989;47:1028–1029.
43. Hood JAA. Experimental studies on tooth deformation: stress
distribution in Class V restorations. N Z Dent J. 1968;68:116–131.
44. Hand ASJ, Hunt A, Reinhardt JW. The prevalence and treatment
implications of cervical abrasion in the elderly. Gerodontics.
1986;2:167–170.
45. Misch CE. Progressive bone loading. Dent Today. 1995;14(1):80–83.
46. Winders RV. Forces exerted on the dentition by the peri-oral and
lingual musculature during swallowing. Angle Orthod. 1958;28:226.
47. The glossary of prosthodontic terms. J Prosthet Dent. 1999;81:39–110.
48. Misch CE, Goodacre CJ, Finley JM, et al. Consensus conference panel
report: crown-height space guidelines for implant dentistry—part 1.
Implant Dent. 2005;14:312–318.
49. Bragger U, Aeschlimann S, Burgin W, et al. Biological and technical
complications and failures with fixed partial dentures (FPD) on
implants and teeth after four to five years of function. Clin Oral
Implants Res. 2001;12:26–43.
50. Misch CE. Contemporary implant dentistry. Mosby: St Louis; 1993.
51. Kakudo Y, Amano N. Dynamic changes in jaw bones of rabbit and
dogs during occlusion, mastication, and swallowing. J Osaka Univ
Dent Soc. 1972;6:126–136.
Implant Dent. 2006;15:113–121.
53. Carlsson GE. Bite force and masticatory efficiency. Kawamura Y.
Physiology of mastication. Karger: Basel, Switzerland; 1974.
54. Mansour RM, Reynik RJ, Larson PC. In vivo occlusal forces and
moments: forces measured in terminal hinge position and associated
moments. J Dent Res. 1975;56:114–120.
55. Chung DM, Oh TJ, Shotwell B, Misch CE, et al. Significance of
keratinized mucosa in maintenance of dental implants with different
surface conditions (master's thesis). University of Michigan: Ann
Arbor, MI; 2005.
approach, healing and progressive bone loading. Int J Oral Implantol.
1990;6:23–31.
57. Carr AB, Laney WR. Maximum occlusal forces in patients with
osseointegrated oral implant prostheses and patients with complete
dentures. Int J Oral Maxillofac Implants. 1987;2:101–108.
58. Michael CG, Javid NS, Colaizzi FA, et al. Biting strength and chewing
forces in complete denture wearers. J Prosthet Dent. 1990;3:549–553.
59. Kinsel RP, Lin D. Retrospective analysis of porcelain failures of metal
ceramic crowns and fixed partial dentures supported by 729 implants
in 152 patients: patient-specific and implant-specific predictors of
ceramic failure. J Prosthat Dent. 2009;101:388–394.
60. English CE. The mandibular overdenture supported by implants in
the anterior symphysis: a prescription for implant placement and bar
prosthesis design. Dent Implantol Update. 1993;4:9–14.
61. Meier GH. Die architektur der spongiosa. Arch Anat Physiol Wess Med.
1887;34:615–628.
62. Kulmann C. Die graphische Statik 1. Meyer and Zeller: Aufl, Zurich;
1888.
63. Wolff J. Das Gesetz der Transformation der Knochen. A Hirshwald: Berlin;
1892.
64. Parfitt AM. Investigation of the normal variations in the alveolar bone
trabeculation. Oral Surg Oral Med Oral Pathol. 1962;15:1453–1463.
65. Neufeld JO. Changes in the trabecular pattern of the mandible
following the loss of teeth. J Prosthet Dent. 1958;8(4):685–697.
66. Orban B. Oral histology and embryology. ed 3. Mosby: St Louis; 1953.
67. Currey JD. Effects of differences in mineralization on the mechanical
properties of bone. Philos Trans R Soc Lond B Biol Sci. 1984;1121:509–
518.
68. Frost HM. Mechanical adaptation. Frost's mechanostat theory. Martin
RB, Burr DB. Structure, function, and adaptation of compact bone. Raven
Press: New York; 1989:154–178.
69. Kazarian LE, Von Gierke HE. Bone loss as a result of immobilization
and chelation: preliminary results in Macaca mulatta. Chin Orthop
Relat Res. 1969;65:67–75.
70. Minaire MC, Neunier P, Edouard C, et al. Quantitative histological
data on disuse osteoporosis: comparison with biological data. Calcif
Tissue Res. 1974;17:57–73.
71. Misch CE, Steigenga J, Barboza E, et al. Short dental implants in
posterior partial edentulism: a multicenter retrospective 6-year case
series study. J Periodontol. 2006;77:1340–1347.
72. Mori S, Burr DB. Increased intracortical remodeling following fatigue
damage. Bone. 1993;14:103–109.
73. Roberts WE, Smith RK, Zilberman Y, et al. Osseous adaptation to
continuous loading of rigid endosseous implants. Am J Orthod.
1984;86:96–111.
74. Misch CE. Bone character: second vital implant criterion. Dent Today.
1988;7:39–40.
75. Misch CE, Hoar JE, Hazen R, et al. Bone quality based implant system:
a prospective study of the first two years of prosthetic loading. J Oral
Implantol. 1999;25:185–197.
76. Chanavaz M. Anatomy and histophysiology of the periosteum:
classification of the periosteal blood supply to the adjacent bone with
855r and gamma spectrometry. J Oral Implantol. 1995;21:214–219.
77. Misch CE, Qu Z, Bidez MW. Mechanical properties of trabecular bone
in the human mandible implications of dental implant treatment
planning and surgical placement. J Oral Maxillofac Surg. 1999;57:700–
706.
78. Rice JC, Cowin SC, Bowman JA. On the dependence of the elasticity
and strength of cancellous bone on apparent density. J Biomech.
1988;21:155–168.
79. Misch CE, Bidez MW, Sharawy M. A bioengineered implant for a
predetermined bone cellular response to loading forces: a literature
review and case report. J Periodontol. 2001;72:1276–1286.
approach, healing, and progressive bone loading. Int J Oral Implant.
1989;6(2):23–31.
80a. Misch CE. Dental implant prosthetics. ed 2. Mosby: St Louis; 2015.
81. Manz MC. Radiographic assessment of peri-implant vertical bone loss:
DICRG interim report no. 9. J Oral Maxillofac Surg. 1997;55:62–71.
82. Misch CE, Bidez MW. Bone density and implant dentistry, IIBS abs. Int
J Oral Implant. 1990;7:8.
83. Sevimay M, Turhan F, Kilicarsian MA, et al. Three-dimensional finite
element analysis of the effect of different bone quality on stress
distribution in an implant-supported crown. J Prosthet Dent.
2005;93:227–234.
84. Tada S, Stegaroiu R, Kitamura E, et al. Influence of implant design and
bone quality on stress/strain distribution in bone around implants: a
3-dimensional finite element analysis. Int J Oral Maxillofac Implants.
2003;18:357–368.
85. Ichikawa T, Kanitani H, Wigianto R, et al. Influence of bone quality in
the stress distribution—an in vitro experiment. Clin Oral Implants
Res. 1997;8:18–22.
86. Misch KA. Small diameter dental implants for the stabilization of complete
dentures: outcome assessments of pain, use of pain medication and oral
health–related qualities of life. [master's thesis] University of Michigan;
2008.
87. Misch CE. Contemporary implant dentistry. Implant Dent. 1999;8(1):90.
88. Muhlemann HR. Tooth mobility: a review of clinical aspects and
research findings. J Periodontol. 1967;38:686–708.
89. Sekine H, Komiyama Y, Hotta H. Mobility characteristics and tactile
sensitivity of osseointegrated fixture-supporting systems. van
Steeberghe D. Tissue integration in oral maxillofacial reconstruction.
Excerpta Medica: Amsterdam; 1986:326–332.
90. Komiyama A, Björn K, Hultin M. Treatment outcome of immediately
loaded implants installed in edentulous jaws following computer-
assisted virtual treatment planning and flapless surgery. Clin Oral
Implants Res. 2008;19:677–685.
91. Fenton A. The role of dental implants in the future. J Am Dent Assoc.
1992;123:36–42.
92. Shillinburg HT, Hobo S, Whitsett LD, et al. Fundamentals of fixed
prosthodontics. ed 3. Quintessence: Chicago; 1997.
93. Shillingburg HT, Fisher DW. Nonrigid connectors for fixed partial
dentures. J Am Dent Assoc. 1973;87:1195–1199.
94. Ismail YH, Misch CM, Pipko DJ, et al. Stress analysis of a natural
tooth connected to an osseointegrated implant in a fixed prosthesis. J
Dent Res. 1991;70:460.
95. Rieder CE, Parel SM. A survey of natural tooth abutment intrusion in
implant connected fixed partial dentures. Int J Periodontics Restorative
Dent. 1993;13:335–347.
96. Cho GC, Chee WL. Apparent intrusion of natural teeth under an
implant supported prosthesis: a clinical report. J Prosthet Dent.
1992;68:3–5.
97. Wetherell J, Smales R. Partial dentures failure: a long-term clinical
survey. J Dent. 1980;8:333–340.
98. Shugars DA, Bader JD, White BA. Survival rates of teeth adjacent to
treated and untreated posterior bounded edentulous spaces. J Am
Dent Assoc. 1998;129:1089–1095.
99. Rissin L, House JE, Conway C, et al. Effect of age and removable
partial dentures on gingivitis and periodontal disease. J Prosthet Dent.
1979;42:217–223.
100. Walton JN, Gardner FM, Agar JR. A survey of crown and fixed partial
denture failures, length of service and reasons for replacement. J
Prosthet Dent. 1986;56:416–421.
101. Payne BJ, Locker D. Oral self-care behaviours in older dentate adults.
Community Dent Oral Epidemiol. 1992;20:376–380.
102. Jackson CR, Skidmore AE, Rice RT. Pulpal evaluation of teeth restored
with fixed prostheses. J Prosthet Dent. 1992;67:323–325.
103. Bergenholtg G, Nyman S. Endodontic complications following
periodontal and prosthetic treatment of patients with advanced
periodontal disease. J Peridontol. 1984;55:63–68.
104. Randow K, Glantz PO, Zoger B. Technical failures and some related
clinical complications in extensive fixed prosthodontics: an
epidemiological study of long-term clinical quality. Acta Odontol
Scand. 1986;44:241–255.
105. Bell B, Rose CL, Damon A. The Normative Aging Study: an
interdisciplinary and longitudinal study of health and aging. Int J
Aging Hum Dev. 1972;3:5–17.
106. Misch CE, Misch-Dietsh F, Silc J, et al. Posterior implant single tooth
replacement and status of abutment teeth: multicenter 10-year
retrospective report. J Periodontol. 2008;79:2378–2382.
107. Hickey JC, Zarb GA, Bolender CL. Boucher's prosthodontic treatment for
edentulous patients. ed 10. Mosby: St Louis; 1990:3–27.
108. Howell AW, Manley RS. An electronic strain gauge for measuring oral
forces. J Dent Res. 1948;27:705.
109. Rissin L, House JE, Manly RS, et al. Clinical comparison of
masticatory performance and electromyographic activity of patients
with complete dentures, overdentures and natural teeth. J Prosthet
Dent. 1978;39:508–511.
110. Misch LS, Misch CE. Denture satisfaction: a patient's perspective. Int J
Oral Implant. 1991;7:43–48.
111. Hildebrandt GH, Dominguez BL, Schock MA, et al. Functional units,
chewing, swallowing and food avoidance among the elderly. Prosthet
Dent. 1997;77:588–595.
112. Sheiham A, Steele JG, Marcenes W, et al. The relationship among
dental status, nutrient intake, and nutritional status in older people. J
Dent Res. 2001;80:408–413.
113. Kapur KK, Soman SD. Masticatory performance and efficiency in
denture wearers. J Prosthet Dent. 1964;14:687–694.
114. Sullivan D, Walls R, Lipschitz D. Protein-energy undernutrition and
risk of mortality within 1 year of hospital discharge in a select
population of geriatric rehabilitation patients. Am J Clin Nutr.
1991;43:559–605.
115. Sheiham A, Steele JG, Marcenes W, et al. The relationship between
oral health status and body mass index among older people: a
national survey of older people in Great Britain. Br Dent J.
2002;192:703–706.
116. Berg E. The influence of some anamnestic demographic and clinical
variables on patient acceptance of new complete dentures. Acta
Odontol Scand. 1984;42:119–127.
117. Bergman B, Carlsson GE. Clinical long-term studies of complete
119. Fiske J, Davis DM, Frances C, et al. The emotional effects of tooth loss
in edentulous people. Br Dent J. 1998;184:90–93.
120. Atwood DA, Coy WA. Clinical, cephalometric, and densitometric
study of reduction of residual ridge. J Prosthet Dent. 1971;26:280–295.
121. Wright PS, Glantz PO, Randow K, et al. The effects of fixed and
removable implant-stabilized prostheses on posterior mandibular
residual ridge resorption. Clin Oral Implants Res. 2002;13:169–174.
122. Geertman ME, Slagter AP, van Waas MA, et al. Comminution of food
with mandibular implant-retained overdentures. J Dent Res.
1994;73:1858–1864.
123. Awad MA, Lund JP, Dufresne E, et al. Comparing the efficacy of
mandibular implant-retained overdentures and conventional
dentures among middle-aged edentulous patients: satisfaction and
functional assessment. Int J Prosthodont. 2003;16:117–122.
124. Walton JN, McEntee MI. Problems with prostheses on implants: a
retrospective study. J Prosthet Dent. 1994;71:283–288.
125. Watson RM, Jemt T, Chai J, et al. Prosthodontics treatment, patient
response, and the need for maintenance of complete implant-
supported overdentures: an appraisal of 5 years of prospective study.
Int J Prosthodont. 1997;10:345–354.
126. Reddy MS, Geurs NC, Wang IC, et al. Mandibular growth following
implant restoration: does Wolff's Law apply to residual ridge
resorption? Int J Periodontics Restorative Dent. 2002;22:315–321.
4
Radiographic Complications and
Evaluation
Randolph R. Resnik, John W. Preece
The use of diagnostic imaging in implant dentistry has changed dramatically

over the years. Comprehensive and accurate radiographic assessment is a
crucial aspect of dental implant treatment planning. Various imaging
techniques have been used to evaluate bone quality, quantity, and location of
anatomic structures in relation to proposed implant sites. Traditionally,
implant clinicians have relied on two-dimensional conventional radiographic
modalities in implant dentistry. However, with the advent of computed
tomography (CT) and cone beam computed tomography (CBCT), a new era in
all phases of the radiographic imaging survey of implant patients has
become available. These technologic advances have significantly increased
the level of detailed information available to implant clinicians in the
diagnosis, treatment planning, surgical, and prosthetic phases of dental
implant treatment. This chapter will comprehensively review the use of
various radiographic modalities and technologies to avoid complications
related to the presurgical evaluation, treatment planning, and postoperative
assessment of implant treatment.
Radiographic Modalities
2-Dimensional
Periapical Radiograph
Periapical radiography, one of the most commonly used radiographic
modalities in dentistry, has many advantages such as high resolution, low
radiation, convenience, and image modification via digital software
capability. However, the implant clinician must understand the inherent
disadvantages of this radiologic technique when used in oral implantology.
Limitations
• Image Distortion: Intraoral radiographs are inherently susceptible to image
distortion and magnification because the object of interest does not have
the same focal spot-to-object distance. When determining the location of
anatomic structures, the clinician should note that the image may contain
distortion and that relying on exact measurements from these images
should be cautioned against. If the x-ray beam is perpendicular to the image
receptor (film or sensor) but the object is not perpendicular to the image
receptor and object, dimensional changes such as foreshortening and
elongation will occur (Fig. 4.1). Edentulous sites/quadrants are especially
predisposed to these errors because flat maxillary palatal vaults along with
high muscle attachments in the mandible make accurate positioning of the
image receptor difficult.
FIG 4.1 Film positioning. (A) The central ray is perpendicular to the bone, object,
and film, resulting in no distortion. (B) The central ray is perpendicular to the film, but
not to the implant, resulting in foreshortening. (C) The central ray is perpendicular to
the object, but not the film, resulting in elongation. (From Misch CE: Dental implant
prosthetics, ed 2, St. Louis, 2015, Mosby.)
• Two-Dimensional Radiographic Modality: For ideal site assessment for

dental implants, a true evaluation and determination of the buccal-lingual
available bone must be determined. Because periapical radiography
anatomically compresses the width dimension into a two-dimensional
radiograph, important information cannot be obtained. Therefore when
attempting to estimate width distances in close approximation to maxillary
and mandibular anatomic structures with two-dimensional radiographs, the
implant clinician must be continuously conscious of the inherent
inaccuracies associated with two-dimensional images.
• Identification of Vital Structures: When evaluating the position of vital
structures with intraoral radiographs, extreme caution should be exercised.
In the evaluation of the true location of the mental foramen, studies have
shown less than 50% of periapical radiographs depict the correct location of
the mental foramen.1 Other studies have concluded that, because of
insufficient cortical bone around the mandibular canal, only 28% of
periapical radiographs will accurately identify the mandibular canal.2
Therefore periapical radiographs exhibit high false-positives and false-
negatives with respect to the identification of vital anatomic structures.
Complication Implications.
Periapical radiographs have many inherent disadvantages, the most notable
being that they provide only a two-dimensional image of a three-dimensional
object. The inability to determine the buccal-lingual bony dimensions is a
major shortcoming with respect to implant treatment planning. These
radiographs are of little value in determining quantity and quality of bone,
identifying vital structures, and depicting the spatial relationship between
structures within proposed implant sites. Thus, periapical radiographs
should be limited to an initial evaluation of a proposed implant site,
intraoperative evaluation, and postoperative assessment.
Panoramic Radiograph
Panoramic radiography is a curved-plane tomographic radiographic
technique used to depict the body of the mandible, maxilla, and the maxillary
sinuses in a single image. Its convenience, speed, and ease have made this
type of radiography a popular technique in evaluating the gross anatomy of
the jaws. However, the implant clinician must understand the inherent
fundamental limitations characteristic of this type of radiograph.
Limitations
• Magnification/Distortion: All panoramic radiographs suffer from vertical
and horizontal magnification, along with a tomographic section thickness
that varies according to the anatomic position. Because the x-ray source
exposes the jaws utilizing a negative angulation (~8%) to avoid
superimposing the occipital bone/base of the skull over the anterior dental
region, variable magnification will always be present on panoramic
radiographs. Increased magnification stems from variances in patient
positioning, focal object distance, and the relative location of the rotation
center of the x-ray system and variations in normal anatomic form and size
from one patient to the next. Zarch et al. have shown that 83% of panoramic
measurements are underestimated, with the greatest magnification being
present in the anterior region (Fig. 4.2).3
• Horizontal magnification: Horizontal magnification is

determined by the position of the object within the
focal trough. The degree of horizontal magnification
depends on the distance of the object from the focal
trough center and is influenced by the patient's
anatomy and positioning within the panoramic
machine. In the anterior region the horizontal
magnification will increase significantly as the object
moves away from the focal trough. This results in
anterior magnification being far greater and more
variable than posterior magnification.
• Vertical magnification: Vertical magnification is

determined by the differences between the x-ray
source and object. Because the beam angle is directed
at a negative (upward) angulation, structures
positioned closer to the source are projected higher
within the image in relation to structures positioned
farther from the x-ray source. Therefore the spatial
relationships between objects projected on a
panoramic radiograph are inaccurate (see Fig. 4.3).
FIG 4.2 All panoramic radiographs exhibit magnification, distortion, overlapping of

images, and ghost images, making these images inaccurate as the sole
determination for dental implant diagnosis.
FIG 4.3 Panoramic showing nonuniform magnification in the vertical and horizontal
plane depicting inaccurate measurements. Vertical magnification can be determined;
however, horizontal magnification is entirely inaccurate.
• Two-Dimensional Radiographic Modality: The panoramic radiograph is a

two-dimensional (2-D) image depicting 3-dimensional (3-D) structures.
Accordingly, it does not demonstrate the buccal-lingual dimension of
maxillofacial structures; therefore bone width and vital structures cannot be
determined. Additionally, it produces a flattened, spread-out image of
curved structures, which results in significant distortion of the vital
structures and their relationship in space.
• Identification of Vital Structures: Panoramic radiography does not exhibit
an accurate assessment of bone quality/mineralization, and it does not truly
identify and locate vital structures accurately.
• Visibility of mandibular canal: Lindh has shown that

the mandibular canal cortical walls were visible in
only 36.7% of panoramic radiographs.4
• Mental foramen location: Yosue et al, in evaluation of

the mental foramen, concluded that over 50% of
radiographs will not depict the true location of the
mental foramen.1
• Linear measurements: Sonic et al have shown an

inaccuracy rate of 24% in determination of linear
measurements for bone assessment with respect to
vital structures.5
• Anterior loops: Studies completed by Kuzmanovic et

al of anterior loops (mental nerve courses anteriorly to
the mental foramen), concluded panoramic
radiographs exhibit a high incidence of false positives
and false negatives, making them totally inaccurate.6
• Location of septa: In evaluation of maxillary sinus

floor bony septa by Krenmair et al, correct
identification and location has been shown to be
approximately 21.3%.7
• Identification of accessory foramina: Accessory

(double) foramina have been shown to accurately
identified in less than 50% of panoramic radiographs.8
Complication Implications.
Although panoramic radiographs have historically been the gold standard in
evaluating potential implant sites, many disadvantages are associated with
these types of radiographs. A lower resolution prevents evaluation of the fine
detail that is required for the assessment of osseous structures and anatomy.
The magnification in the horizontal and vertical planes is nonuniform; thus
linear measurements are inaccurate (Fig. 4.3). Often the image has
superimposition of real, double, and ghost images, which result in difficulty
in visualizing anatomic and pathologic details. The true positions of
important vital structures, which are crucial in dental implant treatment, are
not easily seen or incorrectly depicted. Therefore panoramic radiographs
have value for initial evaluation; however, they predispose the implant
clinician to many surgical, prosthetic, and medicolegal complications.
Cone Beam Tomography
3-Dimensional
To overcome some of the disadvantages of two-dimensional radiographs and
conventional medical CT scanners, a new type of computed tomography
specific for dental applications has been developed. This type of advanced
tomography is termed cone beam volumetric tomography (CBVT) or cone
beam computed tomography (CBCT). In the past, conventional computerized
tomography, when used for dental implant treatment planning, has been
underutilized due to concerns related to potentially high radiation dose and
lower resolution. Because of the low radiation dose inherent with cone beam
technology, the limitations of medical computerized tomography have been
overcome. Additionally, this scanning technology has advantages including
potential “in-office” installation and use, which allow the clinician and
patient the convenience of onsite scanning capabilities and treatment
planning. In addition, for clinicians not wishing to invest in a personal CBCT
unit, many major cities have specialized dental scanning centers for referral
for appropriate CBCT imaging.
Today, CBCT imaging has become the gold standard for dental implant
treatment planning. However, many implant clinicians lack the background
and knowledge in evaluating and treatment planning with CBCT, thus
predisposing to possible complications. Therefore the implant clinician must
have a thorough understanding of inherent disadvantages of CBCT scans
along with knowledge of applied head and neck anatomy, anatomic variants,
incidental findings, and pathologic conditions with respect to implant
treatment planning.
CBCT Technology Complications
Sensor (Detector) Type.

The x-ray sensor receives the x-rays and converts them into electrical data
that are then converted to various images via special computer programs.
There exist two types of sensors used today in CBCT technology: (1) image
intensifiers (IIs) with charged coupling devices (CCD) and (2) flat panel
detectors (FPDs). Image intensifiers have many disadvantages in comparison
to flat panel detectors including poorer resolution, larger size, and a higher
patient radiation dose requirement. Flat panel detectors, although more
expensive than image intensifiers, produce images with much higher quality
and resolution. Most FPDs used today in CBCT units utilize cesium iodide
(CsI) as the scintillator crystal screen. Cesium iodide scintillators produce
the highest spatial resolution possible among various CBCT screens.
Voxel Size.
The unit element in the 3-D image is termed the voxel, which is analogous to
the 2-D pixel. Images composed of multiple voxels are stacked in rows or
columns that are isotropic (i.e., they have equal dimensions in the x, y, and z
planes) and range in size from 0.075 to 0.6 mm. Each individual voxel is
assigned a grayscale value that corresponds to the anatomic structures
attenuation value. The smaller the voxel size, the greater the resolution and
quality of the image, but also the greater the resultant radiation dose. A voxel
size of 0.2 to 0.3 mm is considered ideal because it allows for an equitable
trade-off between image quality and absorbed radiation dose (Fig. 4.4).
FIG 4.4 Comparison of volume data sets obtained isotropically (left) and
anisotropically (right). Because CBCT data acquisition depends on the pixel size of
the area detector and not on the acquisition of groups of rows with sequential
translational motion, the compositional voxels are equal in all three dimensions,
rather than columnar, with height being different from the width and depth
dimensions. (From Scarfe WC, Farman AG: What is cone-beam CT and how does it work? Dent
Clin North Am 52(4):707–730, 2008.)
Spatial Resolution.
Spatial resolution is measured in lines/millimeter (lp/mm) and relates to the
ability to distinguish two anatomically close objects. On a CBCT image, the
higher the spatial resolution, the greater the ability to delineate two different
objects from one another. Normally, CBCT scanners (voxel size 0.075–0.6 mm)
are most commonly associated with higher spatial resolution than medical
grade scanners (voxel size 0.6–1 mm). However, decreased spatial resolution
on CBCT images may result from: (1) the use of a higher voxel size (> 0.4)
(i.e., use of voxel sizes > 0.3 mm for implants is not recommended due to the
lower spatial resolution), (2) decreased radiation (kVp or mA), which results
in increased noise, (3) metallic restorations resulting in artifacts, and (4)
increased focal spot size.
Contrast Resolution.
Contrast resolution is defined as the ability to differentiate tissues of
different radiodensities. In implant dentistry, the ability to produce different
shades of gray is important for a clearly diagnostic image. Because CBCT
images utilize less radiation and are produced with lower kVp (peak
kilovoltage) and mA (milliamperage) settings in comparison to MDCT units,
dental CBCT images are associated with slightly higher image contrast,
modifiable through software settings. Dental CBCT images generally have
increased noise and image scatter compared to medical units. To minimize
noise and scatter, a smaller FOV may be used. However, smaller FOVs are
usually associated with slightly higher radiation settings.
Bit Depth.
The quality of CBCT images is directly related to the number of shades of
gray (bit depth). Currently, CBCT units produce up to 16-bit images, which
corresponds to (216) 65,536 shades of gray. However, computer monitors may
display up to only 8 bits (28) 256 shades of gray. To increase the quality of the
image, the monitor brightness and contrast may be adjusted to display 8 bits
per image.
Bone Density: MDCT.

Medical CT data permit differentiating between tissues that have a physical
density of less than 1%. In contrast, conventional radiography requires a
minimum of 10% difference in physical density to be seen.9 Each medical CT
image is composed of pixels and voxels, which are characterized by a given
numeric value, which reflect the x-ray beam attenuation. These values are
directly affected by the density and thickness of the tissue. The Hounsfield
units (HU), or CT numbers, correlate with the density of the medical CT
image and range in value from −1000 (air) to +3000 (enamel). A specific shade
of gray or density number is assigned to each CT number, which ultimately
forms the image. The correlation of these CT numbers has been used to
associate the density of the area of interest with various bone densities used
for surgical and prosthetic treatment planning. Thus the gray values depicted
on medical CT images are considered true attenuation x-ray values (HU) (Fig.
4.5).
FIG 4.5 Hounsfield units correlation with bone density classification.
Bone Density: Dental CBCT.

When evaluating dental CBCT images in regards to bone density, there does
not exist a direct correlation (accuracy of measurement) as compared with
medical CT. Most dental CBCT systems inherently have an increased
variation and inconsistency with density estimates. The density estimates of
gray levels (brightness values) are not true attenuation values (HU); thus,
inaccuracies in bone density estimates result.10 This is mainly due to the high
level of noise in the acquired images and the slight inconsistencies in the
sensitivity of the CBCT detectors. Dental imaging software frequently
provides attenuation values (HU); however, such values should be recognized
as approximations lacking the precision of HU values derived from medical
CT units.
Artifact Complications
Beam Hardening.
Because metallic objects in the oral cavity are associated with higher
attenuation coefficients than soft tissue, dental CBCT images inherently are
predisposed to these artifacts. One of the most common types of artifacts is
termed beam hardening. Beam hardening occurs when x-rays travel through
the bone/implant, resulting in more low-energy photons being absorbed than
high-energy photons. Because of this the image will have compromised
image quality.11 The titanium alloy surface is highly susceptible to these types
of artifacts because of the high-density nature of the metal. This results in
inaccuracies, especially when viewing periimplant bone levels. Conventional
intraoral images will not exhibit these beam-hardening artifacts and may
appropriately be used to better evaluate the quality and quantity of bone
mesial and distal to an implant when beam-hardening artifacts may
obliterate visualization of interproximal bone, especially when multiple
implants are present in the same quadrant. Additionally, higher-density
materials commonly found in the oral cavity (e.g., amalgam, gold) will lead to
complete absorption of the beam and beam-hardening artifacts.12 There exist
two types of beam-hardening artifacts that result in linear areas of dark
bands or streaks between dense objects and cupping artifacts. Cupping
artifacts occur when x-rays pass through the center of a highly dense object
and are absorbed more than the peripheral x-rays. This results in an image in
which a uniformly dense object appears to be less dense (darker, lower CT
numbers) at its center and appears as a “cup” (Fig. 4.6).
FIG 4.6 Beam hardening, which results in radiolucency surrounding the implant
that frequently is misdiagnosed as a failing implant. This is caused by the dense
nature of titanium implants and the exposure of more low-energy photons.
Motion-Related Artifacts.
Motion artifacts are usually the result of patient movement and result in the
inaccurate depiction of bony landmarks, measurements, and implants.13
Patient movements and incorrect patient positioning create blurring
problems, double density line artifacts adjacent to major bony structures that
result in nondiagnostic images. Patients should be instructed to not move
and avoid swallowing throughout the scan. The motion blurring causes
“double contours” of anatomic structures that result in decreased scan
quality and spatial resolution. This may lead to improper implant placement
and possible damage to neural structures.14 Motion-related artifacts may be
decreased by using sit-down CBCT units or head restraints, or by decreasing
scanning times (Fig. 4.7).
FIG 4.7 Motion artifact due to movement of the patient leading to overlapping
“double images.”
Streak Artifacts.
CBCT images are susceptible to streak artifacts caused by x-rays traveling
through objects with a high atomic number (metallic restorations). Streak
artifacts usually are seen as light and dark lines that arise from the source
object, resulting in images with decreased quality and obscuring of anatomic
structures (Fig. 4.9).
FIG 4.9 Scattering artifacts showing “streaks” that result from the metal
restorations.
Scatter.
Another disadvantage inherent with CBCT images is scatter, which is most
commonly produced from metallic restorations. This is caused by photons (x-
rays) that are deflected from their original path by metallic objects. When
these deflected photons reach the sensor (detector), the intensity of the
signal is magnified in a nonuniform magnitude. The end result is an image
with decreased resolution and image quality, which ultimately leads to
inaccuracies in the reconstructed CT number or voxel density.15 The field of
view (FOV) of the CBCT is proportional to the amount of scattering; thus
smaller FOVs are associated with less scattering. CBCT images have
inherently greater scatter radiation than medical-grade CT images (Fig. 4.9).16
Noise.
There are two types of noise associated with CBCT images: additive (results
from electrical noise) and photon-count (quantum noise). Because CBCT
operate at much lower amperage (mA) settings than MDCT scanners, CBCT
images are associated with greater quantum noise. The noise is displayed as
a “graining” of the image and is the result of inconsistent distribution of the
signal, which results in inconsistent attenuation (gray) values in the
projection images (see Fig. 4.8).
FIG 4.8 Image showing resultant noise (grainy appearance).
Bone Dehiscence on 3-D Reformatted Images.

MDCT and dental CBCT data have the ability to be reformatted by software
algorithms to represent 3-D images by only projecting the voxels that
represent the surface of the object (surface rendering), resulting in a
“pseudo-3D rendering of the facial skeleton.” The pixels are illuminated on
the screen as if a light source is present in the front of the object. The closer
the pixels, the brighter they appear. This shading effect allows the object to
be projected as a 3-D object with depth. However, some 3-D images appear to
have large voids or no bone present on the surface because the software
averages volume elements, and the voids appear when the software attempts
to reconstruct portions of the image covered by a very thin layer of bone.
When evaluating the cross-sectional images, bone will be present. This is a
direct result of the reformatting process, which usually selects a higher HU
reformation, resulting in decreased scatter on the 3-D image. Therefore the
implant clinician should be aware 3-D images do not accurately depict the
quantity and quality bone, but provide only a stylized representation of the
facial skeleton (Fig. 4.10).
FIG 4.10 Bone dehiscence on 3-D images caused by reformatting with too high of
Hounsfield unit threshold, which is done to decrease scattering of the image.
Scanning Technique Complications
Imaging Protocol.
The patient should be positioned within the CBCT unit as per manufacturer's
recommendations. When taking the scan, the teeth should be slightly
separated so that the different arches may be easily differentiated upon
reformation. Cotton rolls, tongue depressors, or a bite registration may be
used. Additionally, cotton rolls may be placed in the vestibule to separate the
lips and cheeks from the buccal mucosa. This will allow for a more accurate
representation of the contour and thickness of the gingival tissues.
Position of the Scanning Template.

The position of the scanning template/radiographic markers in the mouth
during CBCT examination is crucial for the accuracy of fabrication of the
surgical template. First, it is recommended that an index be used to position
the scanning template in the correct position. The ideal index includes a
radiolucent bite registration, which will allow for the teeth to be separated
and maintain the patient in centric relation. This will prevent inaccuracies
and help stabilize the template in the mouth. Additionally, denture adhesive
should be used with the CBCT template to keep it in the ideal position.
Mucosal Thickness.
When fabricating mucosa-supported surgical guides, the thickness of the
mucosa may have a direct effect on the accuracy of the of the planning of the
implant sites. Increased mucosa thickness may lead to inaccurate placement
of the mucosa-borne guides during the surgical placement procedure. Vasek
showed a 1.0-mm buccal mucosa thickness may result in a buccal-lingual
deviation of over 0.41 mm.17 This will inevitably cause inaccurate
measurements and possible misalignment of the surgical guide when placing
the implants. When significant atrophy is present in the premaxilla, usually
there will be excessive tissue thickness, which will result in rocking of the
template.
CBCT Anatomic Radiographic
Anatomy
Incidental Findings
The role of CBCT is rapidly emerging in all aspects of diagnosis and
treatment planning with dental implants. Because of varying FOVs, the
implant clinician is placed in a position to evaluate maxillofacial areas that
they may not be familiar with. Therefore it is crucial the implant clinician be
able to interpret anatomic structures and pathology outside their primary
area of interest. In radiology, an incidental finding is defined as an
unexpected discovery found on a radiologic examination performed for an
unrelated reason. Unfortunately, many normal anatomic variants,
developmental anomalies, and imaging artifacts may be misidentified as
possible pathologic conditions by inexperienced clinicians.18 This may lead to
unnecessary concern and stress for patients and embarrassment for the
clinician. Additionally, possible significant pathologies may exist that go
undiagnosed. This problem results in many professional, ethical, clinical, and
potential legal issues for the implant clinician.
Understanding Incidence of Incidental Findings.

Incidental findings on CBCT scans have been well documented in the
literature. The exact frequency of incidental findings varies from study to
study depending on age, gender, race, and FOV. Price et al showed a high
incidence (3.2 findings/scan) of incidental findings with approximately 16%
requiring intervention or referral.19 These incidental findings ranged from
common benign findings to significant pathologic conditions. Miles reported
a minimum of two reportable findings per CBCT and also showed a high
incidence of periapical lesions that went undetected on conventional
radiographs.20 Cha determined after evaluation of 500 scans an incidence of
24.6% of incidental findings, most in the airway region.21 Arnheiter showed
patients 40 to 49 years old had the largest percentage of reportable incidental
findings (70%), with patients aged 20 to 29 years old with the lowest
percentage (40%).22
Obtaining a Radiology Report.

Radiology reports immediately after CBCT exams, prior to surgery, minimize
the liability that may present to the implant clinician. Formal radiology
reports may be obtained from many sources, preferably from an
appropriately qualified, board-certified maxillofacial radiologist.
Unfortunately, the geographic distribution of maxillofacial radiologists is not
uniform within states or regions within a state, and a careful search will be
required. Several, but not all, states require that the report be made by a
maxillofacial radiologist licensed in the state, and it is therefore crucial to
check with your local dental board or dental practice act to determine if in-
state licensure is required. The implant clinician must be able to recognize
and evaluate variations from normal and refer for appropriate medical
consultation any significant incidental finding that may be contained in the
radiology report.
Use of the Smallest FOV as Possible.

Ideally, the smallest FOV should be utilized for scans when treatment
planning for dental implants (Fig. 4.11). A smaller FOV (~Mid FOV) will
reduce radiation dose to the patient, thus adhering to the ALARA (As Low
As Reasonably Achievable) principle. However, caution should be exercised
to not take an inadequate FOV that includes insufficient view of the anatomic
area of concern. The most common anatomic area for this to occur is the
maxillary posterior region because many practitioners will set the limits of
the scan superiorly/coronally to exclude the maxillary ostium. When placing
implants or bone grafting in the posterior maxilla area, confirming the
patency of the ostium is important to minimize complications associated
with an obstructed osteomeatal complex.
FIG 4.11 Examples from the i-CAT FLX Cone Beam 3D system depicting of
different field of views for specific areas of interest. Ideally, the smallest FOV should
be selected as long as the areas of interest are fully depicted on the images.
(Images courtesy Imaging Sciences International, LLC, Hatfield, PA.)
Normal Radiographic Anatomy
Due to the complex nature of implant treatment and the potential for
complications throughout the surgical and prosthetic phases, the clinician
must have a thorough understanding of the normal anatomy of the
maxillofacial region. Traditional dental education has focused on the
interpretation of conventional 2-D radiographic images for diagnosis, but
with the introduction and rise of CBCT images, a deeper understanding of
anatomy is necessary to examine the patient's structures in three dimensions.
This section of the chapter will address the basic radiographic anatomy as
viewed in the three planes (axial, coronal, sagittal) typically seen on a CBCT
image.
Mandibular Anatomy
Location of the Mandibular Canal in the Mandible
The position of the mandibular canal as it courses through the mandible
from posterior to anterior is highly variable. Although the pathway of the
inferior alveolar nerve and the mental nerve have been well described in the
literature, it is paramount that the implant clinician have a clear
understanding of their anatomic features and variations. When evaluating
the intraosseous course of the mandibular canal buccal-lingually and
inferior-superiorly within the mandible, many variations exist based on
gender, ethnicity, amount of bone resorption, and age.
Buccal-Lingual Mandibular Canal Locations

Radiographic evaluation.
In the posterior region of the mandible, the inferior alveolar nerve enters the
mandibular foramen on the lingual surface of the mandible and progresses
anteriorly in the body of the mandible. In between the mandibular canal and
the mental foramen, the buccal-lingual position is extremely variable. Studies
have shown the buccal-lingual location is dependent on such variables as the
amount of bone resorption, age, and ethnicity.23 The buccal-lingual position
of the mandibular canal is easily depicted on cross-sectional images after
canal location is verified and highlighted (Fig. 4.12).
FIG 4.12 Variable buccal-lingual position. (A) Buccal positioned; (B) lingual
positioned.
Clinical significance.
The intraosseous path of the mandibular canal is variable in the buccal-
lingual position within the mandible, and a comprehensive radiographic
survey (CBCT) ideally should be completed prior to implant osteotomy
initiation to determine the anatomic path. A 2-millimeter safety zone
between the implant and the mandibular canal should always be adhered to.
Attempting to place an implant buccal or lingual to the neurovascular bundle
may result in neurosensory impairment.
Inferior-Superior Mandibular Canal Locations

The vertical position of the mandibular canal below the apices of the natural
teeth within the mandible is also highly variable. Therefore, generalizations
cannot be made as to a constant inferior-superior position because the
distance of the canal to the root apices is not consistent.24 An early
classification of the vertical positions of the course of the alveolar nerve was
reported by Carter and Keen.25 They described three distinct types: (1) in
close approximation to the apices of the teeth, (2) a large nerve approximately
in the middle of the mandible with individual nerve fibers supplying the
mandibular teeth, and (3) a nerve trunk close to the inferior cortical plate
with large plexuses to the mandibular teeth. After the mandibular canal is
located and drawn on the reconstructed panoramic image using CBCT
viewing software, the vertical position of the intraosseous path may be
determined by scrolling through the cross-sectional images. The vertical
position is then easily seen on individual cross sections or CBCT-generated
reconstructed panoramic images (Fig. 4.13).
FIG 4.13 Superior-inferior mandibular nerve tracts. (A–B) Type 1: mandibular canal
in close proximity to tooth roots. (C–D) Type 2: mandibular canal in center of
mandible (most common). (E–F) Type 3: mandibular nerve close to inferior border of
mandible.
The intraosseous path of the mandibular canal is variable in the inferior-
superior position within the mandible, and a comprehensive radiographic
survey (CBCT) ideally should be completed prior to implant osteotomy.
Special care should be exercised in type 1 nerves because their close
approximation to the root apexes results in compromised bone height for
implant placement. Immediate implant placement in the mandibular
posterior when a type 1 nerve exists is not recommended. Type 3 nerves are
most favorable for implant placement in the posterior mandible because the
mandibular canal is positioned low in the mandible, therefore having
increased available bone in height.
Mandibular Canal
The inferior alveolar canal (IAC), or mandibular canal (MC), contains the
neurovascular bundle, which consists of the inferior alveolar nerve, artery,
vein, and lymphatic vessels. The inferior alveolar nerve bundle enters the
mandibular foramen, where it transverses anteroinferiorly from lingual to
buccal within the body of the mandible. A 3-D evaluation of the MC position
is recommended when implant placement is going to be completed in
proximity to the nerve. The most accurate assessment of the anatomic
position is with CBCT because images may be enhanced via viewing software
adjustments for contrast, brightness, and gray scale to help depict the
anatomic location of the MC.
Image Evaluation.
Radiographically, the MC appears as a linear, radiolucent shadow with or
without inferior and superior radiopaque borders. Studies have shown the
total length to be approximately 62.5 mm, with slightly longer measurements
in males (+~2.5 mm).26 The average diameter of the MC is approximately 2.0
to 3.4 mm with the diameter being the greatest in the posterior near the
mandibular foramen (entrance of inferior alveolar nerve on the lingual
surface of the ramus).27 The mandibular canal becomes more ovoid as it
progresses anterior towards the mental foramen.28 Location is variable
depending on the patient's race, gender, and amount of bone resorption.
Usually, the MC is located on a bony ledge, the lingula, which is located on
the medial surface of the ramus. Studies have shown the foramen to be
located approximately 19.7 mm from the anterior border of the ramus.29 The
CBCT data are used with appropriate viewing software to identify and trace
the MC. The depiction of the MC enables the implant clinician to assess the
position in various multiplanar and 3-D reformations. Initially, the MC is
most easily drawn on the CBCT reconstructed panoramic view with location
confirmation on the cross-sectional images. In most cases, the endpoints are
first identified (e.g., mandibular foramen, mental foramen), then the location
of the MC is extrapolated between these two landmarks.
Radiographic Complication.
In many instances the mandibular canal may not be easily depicted on the
CBCT image; thus identification can be extremely challenging. The visibility
of the MC varies significantly, even within the same individual.
The mandibular canal walls usually are not made up of compact bone,
showing only a coalescence of trabecular bone with varying degrees of
density.2 This complicates the determination and location of the true
identification of the canal. Studies have shown that the unreliability of
identifying the entire MC course is a direct result of minimal to no dense
cortical plates surrounding the nerve bundle, which has been shown to occur
in approximately 30% of cases. The MC has an increased wall density in the
posterior region (mandibular foramen > third molar region) in comparison to
the anterior region.30
With CBCT, images are susceptible to noise and artifacts, with resulting
low contrast. Because of these inherent quality issues, distinguishing the
mandibular canal from other aspects of the internal trabecular components
of the mandibular image may be difficult. Thus, the clinician should be be
proficient at utilizing available tools within the software programs to be able
to identify the mandibular canal.
Mental Foramen
The mental foramen is an opening in the anterolateral aspect of the
mandible, commonly in the apical space in the first and second premolar
area; however, individuals may rarely exhibit the position of the foramen as
anterior to the cuspid area and as far posteriorly as the bifurcation of the first
molar. One of the two terminal branches of the inferior alveolar nerve is the
mental nerve, which exits the mental foramen with sensory innervation to the
chin, lip, and anterior gingiva. The mental foramen completes in formation
after the 12th gestational week, when the mental nerve separates into several
fascicles. If the mental nerve separates prior to the formation of the mental
foramina, the formation of a accessory foramen may result.31 The mental
foramen location, size, and number is highly variable with many dependent
factors including gender, ethnic background, age, skeletal makeup.
Image Evaluation.
The mental foramen may be most easily identified on axial, coronal and
cross-sectional images. The relationship between the mental foramen and
teeth or vital structures can be evaluated most easily on volumetric 3-D
images.
The location of the mental foramen on 2-D periapical and conventional
panoramic radiographs has been shown to be inaccurate because they do not
show the true location in most cases. Additionally, when placing immediate
implants in the premolar region, angulation and avoidance of the foramen
should be noted because the mental foramen has been shown to be located
coronal to the root apex of premolars in 25% to 38% of patients. In most cases
when an implant is to be treatment planned in approximation of the
foramen, a CBCT evaluation is recommended. A CBCT image will always
provide excellent visualization of the mental foramen because it exits the
buccal cortical plate regardless of how poorly the canal may be visualized
prior to the exit point. The identification difficulty occurs when the canal is
poorly visualized by an absence of cortication or in D3 or D4 bone quality,
where very little internal trabeculation is visible. Such a bony pattern makes
it difficult to trace the canal posterior from the mental foramen (Fig. 4.14).
FIG 4.14 (A) The mandibular canal (arrow) is easily seen when a thick cortical
component is present. (B) However, in 30% of patients, the mandibular canal will not
have a cortical component (arrow). (C) CBCT panoramic view depicting thin cortical
outline with poorly defined internal bony trabecular pattern indicative of
osteoporosis/osteopenia. (D) Poorly defined mandibular canal (arrows).
Mandibular Ramus (Donor Site for Autogenous Grafting)

The mandibular ramus area has become a very popular donor site for
autogenous onlay and trephine bone grafting. This anatomic area of the
mandible is extremely variable in the amount of bone present, as well as the
buccal-lingual and inferior-superior position of the mandibular canal. Most
commonly, the lateral aspect of the ramus is harvested as a block graft, which
is used for ridge augmentation procedures.
Image Evaluation.
The mandibular ramus is quadrilateral and contains two surfaces, four
borders, and two processes. The lateral surface is flat with two oblique
ridges, the external and internal. The masseter muscle attaches on the entire
lateral ramus surface. The medial surface gives rise to the lingula, which is
the entrance of the inferior alveolar nerve and associated vessels. When
present, the antegonial notch, anterior to the angle of the mandible, is
significant for the presence of parafunction.
The relationship between the lateral cortical plate in the ramus area and
the position of the mandibular canal is easily seen on cross-sectional images
after nerve location identification. Additionally, 3-D images and bone models
assist in the determination of the osseous morphology in this region to help
the clinician select the most appropriate graft site.
Historically, standard 2-D radiographs for evaluation of the ramus area as a
donor site included conventional panoramic images, in which the location of
the external oblique and the mandibular canal may be noted. However, 2-D
evaluation of this area can be very difficult to use for determination of the
amount of bone present and position of the mandibular canal. With this
procedure it is vital that the implant clinician be able to completely
determine the exact position of the mandibular canal with respect to the
external oblique ridge and the lateral cortical bone. Overestimation of
available bone can result in increased morbidity, so a more accurate
representation of this area is with the use of CBCT (Fig. 4.15).
FIG 4.15 The mandibular ramus area can be evaluated. (A) Cross-sectional
(outline for ramus block graft) and (B) 3-D images (depicting the ramus area in
relation to the adjacent teeth).
Mandibular Symphysis (Implant Placement and Bone Donor

Site)
The mandibular symphysis area is a common area for implant placement as
well as a donor site for autogenous block grafting. This anatomic region has
been shown to be one of the most ideal intraoral donor sites for bone
harvesting. However, the mandibular symphysis is susceptible to
nonuniform bone resorption and contains various anatomic variations that
may lead to surgical complications.
Image Evaluation.
The anterior surface of the mandible is termed the mandibular symphysis. A
ridge divides the right and left side and inferiorly forms the triangular
eminence of the mental protuberance. The elevated center of this depressed
area forms the mental tubercle, which is the origin of the mentalis muscles.
This area should be evaluated on cross-sectional, axial, and 3-D images.
Radiographic Evaluation.
Two-dimensional imaging of this area should only be used as a preliminary
evaluation for bone quantity determination. Poor angulation, bony
undercuts, and measurements cannot be determined with 2-D radiography.
CBCT imaging is highly recommended to prevent implant malposition or
overestimation of available bone for harvest procedures, which may lead to
increased complications (Fig. 4.16).
FIG 4.16 The symphysial area can be evaluated on (A) cross-sectional image(s)
along with (B) axial slices.
Anatomic Variants of the Mandibular Anatomy

Anterior Loop
As the mental nerve proceeds anteriorly in the mandible, it may on occasion
extend beyond the anterior boundary of the mental foramen. This endosteal
curved loop is proximal to the mental foramen and exits distally through the
mental foramen and is termed an “anterior loop.” Studies have shown a
prevalence of approximately 35% to 50 %, with a mean distance of 1.16 mm
anteriorly to the foramen.32 Clinically, an anterior loop may be determined by
probing within the mental foramen in a posterior direction; however, this
necessitates full reflection of the mental foramen.
An anterior loop is difficult to identify and cannot be determined accurately
with 2-D radiography. High false-positive and false-negative results have
been noted on conventional panoramic and periapical radiographs. To
identify an anterior loop on a reformatted CBCT image, the mandibular canal
must be highlighted, including the cross-sectional image depicting the
mental foramen slice. The anterior part of the mental foramen is marked
with a constant perpendicular line (line will remain constant throughout all
the images). In sequential axial images, scrolling from superior to inferior,
any component of the nerve anterior to the constant line is considered a
anterior extension. If an anterior loop exists, the highlighted nerve will be
anterior to the perpendicular line (Fig. 4.17).
FIG 4.17 An anterior loop is determined by evaluating axial images in a superior to

inferior direction. (A) The anterior aspect of the foramen should be marked (line that
remains constant in the vertical plane). (B) As the axial images are sequentially
evaluated from superior to inferior, if any part of the marked canal extends anterior to
the line (C–D, arrows), a anterior loop exists.
Clinical Significance.
Determining the presence of an anterior loop is critical when placing
implants anterior to the mental foramen. Inability to establish the existence
of an anterior loop may result in implant placement too close to the mental
nerve, resulting in possible neurosensory impairment and related
complications.
Accessory Foramens
In approximately 6.6% to 12.4 % of patients, an accessory (double) foramen is
present with an average diameter of 1.0 mm.33-35 Special care should be noted
to evaluate for an accessory canal because it may contain components of one
of the three branches of the mental nerve. Accessory foramens are believed
to be the result of early branching of the inferior alveolar nerve, prior to
exiting the mental foramen during the 12th week of gestation.36
The ideal technique to determine an accessory foramen is evaluation of
coronal images along with evaluation of the 3-D image. In the coronal image,
the mandibular foramen will be shown bifurcating into two canals, resulting
in the presence of two foramina. The evaluation of 3-D images will easily
depict two canals. Normally, accessory canals are located superior and distal
to the mental foramen (Fig. 4.18).
FIG 4.18 Accessory (double) foramina can be evaluated on (A) 3-D images or (B)
coronal images.
In the majority of patients, small accessory foramina usually contain a small
branch of the mental nerve, which is not problematic because of cross
innervation. However, in some cases, a larger branch of the mental nerve
(equal or larger size foramen) may exit the mental foramen. If a larger
accessory foramen is present and resultant damage to the nerve exists,
possible neurosensory impairment is possible. The larger accessory foramens
are sometimes termed “double foramens.”
Lingual Concavities (Anterior/Posterior)

The trajectory/angulation of the mandible along with inherent undercuts
pose a significant problem to the implant clinician. Lingual concavities may
occur in the anterior region as an hourglass or constriction of the mandibular
bone. Butera has shown the incidence to be approximately 4% of patients,
which is most likely genetic or developmental in origin.37 In the posterior
region, concavities are much more common, resulting in undercuts in
approximately 35% of patients.38 Because of these undercuts, implant
placement may be difficult and perforation of the lingual plate may result.
Anterior
Anterior undercuts are most easily seen in cross-sectional and 3-D images
(Fig. 4.19A).
FIG 4.19 (A) CBCT panoramic view of anterior mandible depicting significant
quantity of bone; (B–C) however, when viewed three-dimensionally, resultant
hourglass concavities present in the anterior mandible; (D) complication of
sublingual perforation which may lead to bleeding complications. (E) 3-D images
depicting sublingual undercut; (F) cross section depicting significant undercut; and
(G) complication of sublingual perforation.
In the anterior region, perforation of the bony plates of the mandible during
implant osteotomies may lead to extensive bleeding from sublingual vessels.
A significant plexus of sublingual and submental arteries may lead to life-
threatening floor-of-the-mouth hematoma formation. Therefore, a thorough
CBCT examination will, with interactive treatment planning, determine the
exact location and angulation for safe implant placement.
Posterior
Posterior undercuts are most easily seen in cross-sectional and 3-D images.
In the posterior region, overestimation of available bone is a common
complication. If an implant osteotomy is completed in this area, perforation
of the lingual plate may result, leading to possible bleeding and possible
implant morbidity. Life-threatening lingual bleeding may occur as a result of
blood vessel injury leading to bleeding into the soft tissues. Additionally,
damage to the lingual nerve may occur upon perforation of the lingual
cortical plate. Case reports have been published revealing loss of the implant
body into the sublingual space when large undercuts are present (see Fig.
4.19B).
Hypomineralization of the Mandibular Canal

Studies have shown in 20.8% of CBCT scans the mandibular canal walls are
hypomineralized.39 This often results in poor localization of the mandibular
canal and is sometimes an early indication of osteopenia or osteoporosis. A
thin cortical outline, poorly defined internal bony trabecular pattern, and
variable density within the cortical layer are potential indications of
osteoporosis/osteopenia. In 30% of cases, no superior cortical plate is
present, which complicates the identification of the true location (see Fig.
4.14 C–D).
The brightness and contrast may be altered using imaging software to more
clearly define the canal walls. Ideally, the mandibular canal may be seen
easiest in the panoramic or cross-sectional images.
Lack of identification of the MC may result in placement of implants too
close to the nerve resulting in possible nerve damage. Additionally, when
hypomineralization is present, usually the bone density throughout the
mandible will be poor and compromised (~D4).
Incisive Canal
The mandibular incisive canal is a bony canal within the anterior mandible
that is a continuation of the MC. This canal contains the terminal branch of
inferior alveolar nerve, which travels inferiorly to the mandibular anterior
teeth and terminates in the midline. In approximately the first molar region,
the inferior alveolar nerve bifurcates into the mental and incisive nerves. The
mandibular incisive canal terminates as nerve endings within the anterior
teeth or bone near the lateral incisor region and will extend only to the
midline in 18% of patients, and in some cases will anastomosis with the
contralateral side.40
The incisive canal is not always seen radiographically on CBCT. The incisive
nerve may be differentiated from the mental nerve by determination of any
canal that is anterior to the mental nerve/foramen exit. When present, this
radiolucent canal will continue anteriorly from the mental foramen and can
be seen as a bifurcation with branches in the superior direction (Fig. 4.20).
FIG 4.20 The incisive canal is a continuation of the inferior alveolar canal, which
contains the incisive nerve, which innervates the mandibular anterior teeth (red
shows the inferior alveolar canal; green shows the incisive canal). (A) CBCT image
showing incisal canal extension from mandibular canal, and (B) CBCT panoramic
image showing branching of incisive canal (arrows).
The incisive canal is often mistaken for an anterior loop of the mental nerve,
but this nerve innervates the anterior teeth and has no sensory innervation to
the soft tissue. However, if the incisive canal is traumatized, cases of
excessive bleeding have been reported. Usually the canal and its branches
will become necrotic after the teeth are extracted.
Retromolar Foramen
The retromolar fossa of the mandible forms a triangular depression that
borders the temporal crest medially and the anterior border of the
mandibular ramus laterally. Within this fossa, an anatomic variant termed the
retromolar foramen (RMF) is present in approximately 14% of patients.41 The
RMF on the alveolar surface is the terminal end to the retromolar canal,
which branches from the mandibular canal.
RMFs are not located in a constant position and usually are not bilateral.
Most commonly, RMFs should be initially evaluated via CBCT sagittal slices
and then verified with cross-sectional images.
It is important to confirm the RMF and canal locations prior to surgical
procedures because this area is a common donor site for bone grafts. If
perforation of the retromolar canal results, excessive bleeding may result.
Lingual Foramen/Canal
The interforaminal region in the anterior mandible is usually a relatively safe
area for implant placement and bone grafting procedures. However, on the
lingual aspect of the mandible, in the midline, lies the lingual foramen or
foramina. This anatomic structure houses the terminal branches of the
lingual artery (sublingual artery), facial artery (submental artery), or the
anastomosis of both. As the blood vessels enter within the mandible, they
are termed the mandibular median vascular canal.
Lingual canals and foramina may be seen radiographically as a radiolucent
canal in the midline of the mandible and easily depicted on cross-sectional or
axial views. Studies have verified the median vascular canal is present in 96%
to 100% of patients. The median vascular canal size is proportional to the
diameter of the arteries entering the foramen. The average diameter has been
shown to be approximately 0.84 mm, with the average distance from the
inferior mandibular border to be 11.2 mm. With consideration to the extent
of penetration within the mandible, 19.4% of canals end within the lingual
third, 52.8% reach the middle one third of the mandible, and 27.8 %
penetrate to the buccal one third (Fig. 4.21).42
FIG 4.21 Mandibular vascular canal. (A) Lingual foramen, where right and left
sublingual arteries enter the mandible (arrow); (B–C) mandibular vascular canal that
contains the sublingual artery anastomosis; and (D) off midline lingual vascular
canal (arrow).
Potentially, these vessels may cause extensive bleeding in the mandible
during endosseous implant placement or symphysial bone grafts. When
larger lingual canals exist (>1.0 mm), significant bleeding issues may present
with a possible compromised integration because of a potential soft tissue
interface with the implant. Usually bleeding may be slowed or stopped by
inserting a surgical drill, direction indicator, or implant into the osteotomy
site.
Calcified Carotid Artery Atheroma

Calcified carotid artery atheromas are calcifications found in the common
carotid usually located near the bifurcation of the internal and external
carotid arteries. These calcifications give radiographic evidence of
atherosclerosis, which is an indicator of possible stroke or metabolic disease.
It has been shown that approximately 80% of strokes are ischemic and due to
atherosclerotic disease in the carotid bifurcation.43
Carotid artery calcifications are small, multiple radiopacities in the carotid
space anterior and lateral to cervical vertebrae C3-C4. These multiple and
irregularly shaped calcifications may be vertical in orientation and are
usually easily distinguished from the adjacent soft tissue. They can be easily
seen on axial and 3-D images (Fig. 4.22 A–B). An additional common site to
evaluate for carotid artery calcifications in large-volume CBCT images is
lateral to the pituitary fossa.
FIG 4.22 (A–B) Carotid calcification atheroma at the level of cervical vertebrae C3-
C4 (arrows).
Because of the significant complications that may arise from the presence of
carotid calcifications (ischemic cerebrovascular disease is the second leading
cause of death in most developed countries), the patient should be referred
to their physician for assessment of carotid artery stenosis and possible
ultrasound evaluation.
Maxillary Anatomy
The maxilla is composed of paired bones (right and left) that unite to form
the upper jaw and is composed of four processes: posterolateral (zygomatic,
horizontal, and medial); palatine, arch and inferior; alveolar; and the superior
projecting frontal process. In oral implantology, the maxilla presents a
difficult and demanding challenge in the treatment and placement of
implants with its complex osseous makeup, anatomy, and anatomic variants.
Premaxilla
The anterior premaxilla is one of the most difficult areas for the implant
clinician in preoperative assessment, surgical placement, and esthetic and
prosthodontic demands. Numerous factors affect the anatomic makeup of
the premaxilla that may predispose to surgical complications and result in a
decrease in implant survival.
The premaxilla is a difficult and complex region of the oral cavity to evaluate
clinically and radiographically. Many factors complicate this area, such as the
trajectory of the anterior maxilla, rapid buccal bone resorption after tooth
loss, decreased bone density, and a highly esthetic demanding area. The
premaxilla may be easily evaluated via cross-sectional, sagittally, and 3-D.
As a result of the alveolar ridge resorption after tooth loss, the residual
available bone migrates to a more palatal position.44 This leads to difficulties
in implant positioning that place the implant clinician at risk due to esthetic
issues. Because bone resorption occurs at the result of the buccal plate,
implant placement usually occurs in a more palatal position. This results in a
greater moment force leverage on the bone-implant interface, abutment
screws, and implants. Coupled with an angled force in both centric and
excursions, more stress is transmitted to premaxillary implants than those in
anterior mandibles. This often dictates more implants and larger-diameter
implants with bone augmentation by bone-spreading or bone graft
procedures before or in conjunction with implant placement.
In most patients, the bone is less dense in the anterior maxilla than in the
anterior mandible. The maxilla most often presents thin porous bone on the
labial aspect, very thin porous cortical bone on the floor of the nasal and
sinus region, and a denser cortical bone on the palatal aspect.45 The
trabecular bone in the premaxilla is usually fine and less dense than the
anterior region of the mandible. Due to this poor bone quality, increased
difficulty in implant placement and a higher probability of overload implant
failures or crestal bone loss may result.
Because of the poor bone quality in the premaxilla, preexisting bone after
extractions is predisposed to significant resorption. After tooth loss, the
facial cortical plate rapidly resorbs during initial bone remodeling, and the
anterior ridge has been shown to lose up to 25% of its width within the first
year, as well as 40% to 50% within the next 3 to 5 years, mostly at the expense
of the labial contour (Fig. 4.23A–B). Therefore, it is imperative that when
radiographically evaluating the premaxilla, a radiopaque template be utilized
to ascertain the ideal implant position with respect to the teeth being
replaced.
FIG 4.23 The premaxilla presents a challenging area for the implant clinician
because of the (A) hard and soft tissue resorption and (B) advanced buccal plate
resorption, which complicates implant placement because of compromised width
and trajectory of bone (arrow).
Nasopalatine Canal/Incisive Foramen

The nasopalatine canal (also termed the incisive canal or anterior palatine
canal) is a passageway within the anterior maxilla midline that connects the
palate to the floor of the nasal cavity. The entrance of the canal into the oral
cavity is via the incisive foramen, which is posterior to the central incisor
teeth. The vital structures passing through the canal include the terminal
branch of the internal maxillary artery and the nasopalatine nerve, which
communicates with the sphenopalatine artery and the greater palatine nerve.
The anatomic structures (e.g., nerve artery, vein) in the nasopalatine canal
may present with wide variation in the location, shape, and dimensions.
The location and dimension of the nasopalatine canal is most likely seen on
axial and coronal images. Cross-sectional and 3-D images may also depict the
size, shape, and location of the nasopalatine canal along with evaluation of
implant impingement on this space.
Determining the morphology of the nasopalatine canal via CBCT images
allows the clinician to ascertain if available bone is present for dental
implantation. Placing implants in the anterior maxilla (central incisor area) is
the most challenging anatomic location for the implant dentist because of
biomechanical, functional, esthetic, and phonetic demands. Especially with
immediate implant placement, consideration must be given to the presence
of the nasopalatine canal, including a careful evaluation of its morphology
and position to minimize implant placement complications.
The incisive foramen often expands laterally within the palatal bone, and
the central incisor implant osteotomy may inadvertently encroach on this
structure, resulting in the formation of fibrous tissue at the interface in the
mesiopalatal region. If the osteotomy invades the incisive canal, treatment
options include tissue removal within the canal with and bone graft and/or
implant placement. When a large nasopalatine canal exists, a more distally
placed implant in the central incisor region prevents encroachment on this
area. Because most restorations in an edentulous premaxilla are FP-2 or FP-3,
the most favorable sites for bone width are selected, even when they are in
the interproximal region of central and lateral incisor sites.
When there exists an enlarged canal, the lack of available bone will most
likely not permit ideal implant placement. However, it is important to
differentiate enlarged canals from incisive canal cysts. Incisive canal cysts are
known to cause localized dilation of the canals with possible displacement of
the teeth. In edentulous patients, the nasopalatine canal has been shown to
be significantly larger in comparison to that of dentate patients (Fig. 4.24).
FIG 4.24 The nasopalatine canal area should be evaluated as to the size and
location because implant placement in this area may predispose to placement within
soft tissue. (A) Implant placement impinging on nasopalatine canal; (B) very large
canal leading to minimal available bone (arrow).
When implants are positioned in contact with neural tissue, lack of

osseointegration and failure of the implant may result. Additionally,
placement of implants in close approximation to nasopalatine blood vessels
may cause excessive bleeding during surgical procedures; however, such
bleeding episodes are usually self-limiting and controlled by local hemostatic
techniques.
Infraorbital Foramen
The infraorbital foramen (IOF) is located in the anterior aspect of the
maxillary bone below the infraorbital margin (IOM) of the orbit. The
infraorbital artery, vein, and nerve exit the foramen. On average, the IOF-IOM
distance is approximately 6.1 to 10.9 mm.46
The infraorbital foramen is easily seen on coronal images along with 3-D
reformatted images.
Anatomic variants have been reported to be as far as 14 mm from the orbital
rim in some individuals. In the severely atrophic maxilla, the infraorbital
neurovascular structures exiting the foramen may be close to the intraoral
residual ridge and should be avoided when performing sinus graft
procedures to minimize possible nerve impairment. This is of particular
concern on soft tissue reflection and the bone preparation of the superior
aspect of the window. Because the infraorbital nerve is responsible for
sensory innervations to the skin of the upper cheek, mucosa of the maxillary
sinus, maxillary incisors, canines, and premolars, as well as of the gingiva,
skin, and conjunctiva of the eyelid, lateral nose, and mucosa of the upper lip,
damage to this nerve may cause significant discomfort to the patient. Most
often, the nerve is not severed, and a neurotmesis presents that usually
resolves within 1 month after the surgery (Fig. 4.25 A–B).
FIG 4.25 (A) Normal location for infraorbital nerve; (B) variation closer to ridge that
may result in neurosensory impairment from retraction or possible transection upon
reflection of the tissue.
Paranasal Sinuses
Frontal.
The frontal sinuses are bilateral and funnel-shaped and located on each side
of the midline superior to the orbital bones. The borders of the frontal sinus
are: inferior (orbital portion of the frontal bone), posterior (separates the
dura of the frontal lobe from the lining mucosa), and posterior (separates the
dura of the frontal lobe from the lining mucosa). The frontal sinuses extend
to the middle meatus and drain through the nasofrontal duct and into the
frontal recess. The frontal ostia are located approximately two-thirds high on
the posterior medial wall, which anatomically complicates clearing of the
sinus after infection.47 The frontal recess, which is the drainage pathway of
the frontal sinus, drains into the middle meatus or ethmoid infundibulum.
On coronal CBCT images the frontal recess is superior and medial to agger
nasi cells.
Ethmoid.
The ethmoid sinuses are within the ethmoid bone and are divided into two
compartments, the anterior and posterior. The anterior ethmoid sinus drains
into the middle meatus, and the posterior ethmoids drain into the
sphenoethmoidal recess. The borders of the ethmoid sinuses include:
anterior ethmoid (lateral): lamina papyracea of the orbit (medial); middle
turbinate (superior): fovea ethmoidalis (cribriform plate); posterior ethmoid
(lateral): lamina papyracea of the orbit (medial); superior turbinate
(superior); fovea ethmoidalis (cribriform plate). The ethmoid sinuses have
various radiographic anatomic markers that are termed air cells. The ethmoid
bulla are the largest and most prominent radiographically in the anterior
region. Agger nasi cells are usually the most anterior of the anterior air cells
and are located in anterior/superior to the middle turbinate. Along the
inferior border of the orbits are the Haller cells, which may impair
mucociliary clearance when they enlarge and impinge of the ethmoid
infundibulum. The Onodi cells derive from the posterior ethmoid and are
located lateral and superior to the sphenoid sinus.48
Sphenoid.
The sphenoid sinus, located within the sphenoid bone, contains superiorly
the pituitary fossa and olfactory nerves. Inferiorly, the pterygoid canal
courses beneath the mucosa with the cavernous portion of the internal
carotid artery within the lateral wall. The ostium lies in the superior aspect
and drains into the sphenoethmoidal recess.49
Maxillary.
The maxillary sinuses are the largest of the paired paranasal sinuses and an
often problematic area for implant clinicians. The posterior maxilla has many
inherent disadvantages including poor bone density, minimal interocclusal
space, and insufficient bone quantity for ideal implant placement. Thus, the
implant clinician must have a comprehensive knowledge of normal vs.
abnormal anatomy in association with the maxillary sinus and paranasal
sinus anatomy. The maxillary sinus has a high prevalence of anatomic
variants and pathology, which predispose the patient to increased morbidity
during procedures in the posterior maxilla. Thus, a comprehensive
knowledge and understanding of this area is important for implant
clinicians. Radiographically, the maxilla sinus has the following borders:
Superiorly, the maxillary sinus is bordered by the orbital floor, which houses
the infraorbital canal. Inferiorly, the floor of the maxillary sinus approximates
the roots of the maxillary teeth. The medial wall coincides with the lateral
wall of the nasal cavity and is the location of the maxillary ostium, the area of
drainage of the ethmoid infundibulum (Fig. 4.26).
FIG 4.26 Normal paranasal sinus anatomy images. (From Misch CE: Contemporary
implant dentistry, ed 3, St. Louis, 2008, Mosby.)
Nasal Cavity
The borders of the nasal cavity are: hard palate (inferior); medial walls of the
right and left maxillary sinus (lateral); nasal, ethmoid, and sphenoid bones
(superior); and nasal septum (medial). The lateral walls of the nasal cavity are
made up of turbinates (concha), which are epithelium-lined bony structures
that protrude into the nasal cavity and function to warm, cool, and filter
inspired air. Below each turbinate are spaces termed meatuses. The middle
meatus is most important because this is the area of drainage for the frontal,
anterior ethmoid, and maxillary sinuses. The inferior meatus is the drainage
site for the nasolacrimal duct. The superior meatus interconnects with the
posterior ethmoid and sphenoid sinuses through the sphenoethmoidal
recess.50
Maxillary Sinus Membrane

The maxillary sinus is lined by the Schneiderian membrane, which is
identical to respiratory epithelium. This pseudostratified columnar
epithelium is continuous with the nasal epithelium through the maxillary
ostium in the middle meatus. The membrane has an average thickness of 0.8
mm and is usually thinner and less vascular than nasal epithelium.51
A CBCT scan of normal, healthy paranasal sinuses reveals a completely
radiolucent (dark) maxillary sinus. Any radiopaque (whitish) area within the
sinus cavity is abnormal, and a pathologic condition should be suspected.
The normal sinus membrane is radiographically invisible, whereas any
inflammation or thickening of this structure will be radiopaque. The density
of the diseased tissue or fluid accumulation will be proportional to varying
degrees of gray values (Fig. 4.27).
FIG 4.27 The maxillary sinus membrane (Schneiderian membrane) in health
should be invisible (red arrow). When inflammation or pathology is present, it will be
depicted as an increase in density/radiopacity or a visible increase in thickness
(green arrow).
Ideally, when evaluating the maxillary sinus, it should be completely
radiolucent. If any radiopaque areas are present, this is most likely the result
of a disease process (e.g., inflammation, cystic, polyps). Therefore, if implant
placement into the maxillary sinus is planned, the degree of radiopacity is
significant to the long-term success and morbidity. In some cases, treatment
may be indicated prior to entry (i.e., implant placement or bone grafting) into
the maxillary sinus.
Ostiomeatal Complex
The ostiomeatal unit is composed of the maxillary ostium, ethmoid
infundibulum, anterior ethmoid cells, uncinate process, and the frontal
recess. This anatomic area allows air flow and mucociliary drainage into the
middle meatus.
The osteomeatal complex can be evaluated radiographically most easily on a
coronal scan, which includes the following structures:
1. Maxillary sinus ostium

2. Infundibulum
3. Ethmoid bulla
4. Uncinate process
5. Hiatus semilunaris
Maxillary Ostium.
The main drainage avenue of the maxillary sinus is through the ostium. The
maxillary ostium is bounded superiorly by the ethmoid sinuses and inferiorly
by the uncinate process. The maxillary sinus ostium is on the superior aspect
of the medial wall of the sinus, approximately half-way between the anterior
and posterior walls. The ostium is usually oval shaped and oriented
horizontally or obliquely.52
The maxillary ostia are visualized on coronal images, usually in the anterior
one third of the maxillary sinus. This opening is located in the superior
aspect of the maxillary sinus medial (lateral wall of nasal cavity). The patency
of the maxillary ostium should always be ascertained when placing implants
or bone grafts into the maxillary sinus. By scrolling through various coronal
images, the opening can be verified (Fig. 4.28).
FIG 4.28 (A) Maxillary sinus ostium patency is the mucociliary drainage area of the
maxillary sinus; (B) nonpatent ostium; (C) suspected nonpatent ostium; (D–E)
scrolling through cross section depicts patency of ostium. Red arrows, patent
ostium; white arrow, membrane inflammation; green arrow, nonpatency.
If the maxillary ostium is nonpatent, the mucociliary clearance of the
maxillary sinus may be affected. This can lead to an increased morbidity in
implant-related procedures.
Infundibulum/Hiatus Semilunaris.
Vital structures within the osteomeatal complex that allow for mucociliary
drainage of the sinuses are the maxillary infundibulum and the hiatus
semilunaris. Drainage through the maxillary ostium enters the maxillary
infundibulum, which is a pathway that leads to the hiatus semilunaris. The
hiatus semilunaris is a crescent-shaped space or opening in the lateral wall of
the nasal cavity, which is inferior to the ethmoid bulla that is the location for
the openings of the frontal sinus, maxillary sinus, and anterior ethmoid
sinus. These sinuses drain through this area into the middle meatus.
Radiographic interpretation.
The maxillary infundibulum and hiatus semilunaris are easily seen on
coronal sections of the patient's maxillary anatomy. These crucial areas of the
maxillary osteomeatal complex is bounded anteriorly and inferiorly by the
uncinate process of the ethmoid bone, superiorly by the ethmoid bulla, and
posterior by the inferior nasal concha.
Any blockage of the infundibulum or hiatus semilunaris will lead to
inflammation, congestion, or infection in the maxillary, ethmoid, or frontal
sinuses. Therefore, prior to any procedures that may violate the maxillary
sinus (e.g., implant, bone graft), the patency of infundibulum and hiatus
semilunaris must be verified to decrease the possibility of postoperative
complications.
Uncinate Process.
The uncinate process is an important structure in the lateral wall of the nasal
cavity. This finger-like bony projection helps form the boundaries of the
hiatus semilunaris and ethmoid bulla, which allow the draining of the frontal
and maxillary sinuses.
On coronal or cross-sectional CBCT images the uncinate process is bordered
by the medial wall of the maxillary sinus and articulates with the ethmoid
process and inferior nasal turbinate. Inferiorly, it borders the semilunar
hiatus and posteriorly it has a free margin.
A deflected uncinate process (either laterally or medially) can narrow the
ethmoid infundibulum, thus affecting the osteomeatal complex. Perforations
may also be present within the uncinate process, leading to communication
between the nasal cavity and ethmoid infundibulum. In addition, the
uncinate process may be pneumatized. Although this is rare, it may
compromise adequate sinus clearance. Uncinate process variations should be
evaluated and treated prior to any procedure in which the physiology of the
maxillary sinus is altered (implant placement or bone grafting).
Ethmoid Bulla: the ethmoid bulla is the largest and most prominent
ethmoid air cell. The ethmoid bulla is caused by bulging of the middle
ethmoidal cells and may be a pneumatised cell or a bony prominence.
Radiographic Interpretation: The ethmoid bulla are usually evaluated on
coronal images. These air cells are part of the anterior ethmoid sinuses and
make up the superior border of the hiatus semilunaris and maxillary
infundibulum and laterally bounded by the lamina papyracea.
Clinical Significance. The degree of pneumatization within the ethmoid
bulla varies. When enlarged, the bulla may encroach upon the uncinate
process and middle turbinate, resulting in nonpatency of the osteomeatal
complex. The patency of this area should be verified prior to any procedures
involving the maxillary sinus.
Anatomic Variants of the Maxillary Anatomy

Concha Bullosa
The middle turbinate plays a significant role in proper drainage of the
maxillary sinus. Normally, the middle turbinate is a thin, boney structure;
however, it can be aerated, in which case it is termed a concha bullosa. This
anatomic variant can be unilateral or bilateral and has been shown to have a
prevalence of up to 53.6% of the population.53 Additionally, there is a strong
association with the concha bullosa and a deviated septum of the
contralateral side.54
Concha bullosa are easily identified on a CT/CBCT coronal image as a
radiolucent air space in the center of the middle meatus and surrounded by
an ovoid bony rim.
In most cases of concha bullosa, no paranasal sinus pathology results. The
larger the concha bullosa, the more likely the probability of compromising
the drainage of the middle meatus. When enlarged, pressure against the
uncinate process may occur, decreasing the infundibulum drainage, and thus
affecting the physiology of the maxillary sinus leading to increased drainage
problems. Caution must be exercised because concha bullosa patients are
more predisposed to postoperative complications from bone grafting and
implants in the sinus area (Fig. 4.29).
FIG 4.29 (A–C) An anatomic variant that may predispose the implant patient to
postoperative mucociliary impairment is a concha bullosa (arrows), which is an
aerated middle turbinate.
Paradoxical Middle Turbinate

A paradoxical middle turbinate is an anatomic variant of the middle
turbinate with a prevalence of approximately 15% of the population.55 This
anatomic variant is a reversal of the normal medially directed convexity of the
middle turbinate (middle turbinate convexity is towards the lateral instead of
medial). The inferior edge of the middle turbinate may have various shapes
exhibiting excessive curvature that may predispose the patient to blockage in
the nasal cavity, infundibulum, and middle meatus.56
A paradoxical middle turbinate is most easily seen on a coronal CT/CBCT
scan image. It may also be seen in certain cross-sectional images. The
convexity of the paradoxical middle turbinate is directed laterally, instead of
medially toward the nasal septum.
When a paradoxical middle turbinate is present, the implant clinician must
take into consideration the possibility of postoperative mucociliary
complications after bone grafting or implant placement in the maxillary
sinus from blockage of the ostium (Fig. 4.30).
FIG 4.30 (A–B) An anatomic variant that may predispose the implant patient to
postoperative mucociliary impairments is a paradoxical middle turbinate. The convex
side of the middle turbinate is directed laterally, instead of medially. Note the concha
bullosa on the left side (arrows).
Deviated Septum
One of the most common anatomic variants in the oral region is a deviated
septum, which may be congenital or traumatic in origin. Studies have shown
a prevalence of 70%, which increases the possibility of osteomeatal complex
blockage. This occurs when the nasal septum is displaced laterally towards
one side of the nasal cavity. When the deviation is severe, the flow of air
through the nasal cavity is redirected and may cause nasal obstruction,
hypoplasia of the ipsilateral turbinates, or hyperplasia of the contralateral
turbinates.
A deviated septum can be seen most easily via the coronal and axial image
scans. Additionally, a 3-D image of the midline structure will allow direct
evaluation. The nasal septum will be displaced toward one side of the nasal
cavity (Fig. 4.31).
FIG 4.31 (A–B) An anatomic variant that may predispose the implant patient to
postoperative mucociliary impairments is a deviated septum. The side of deviation
may cause blockage of the maxillary ostium.
When the deviation is severe, the air flow through the nasal cavity is
compromised, manifesting as nasal congestion. Patients with deviated septa
are predisposed to sinus clearance issues, which increase morbidity of bone
grafting and implant placement procedures in the maxillary posterior area on
the side of deviation. Usually, the contralateral side will have normal
mucociliary clearance.
Haller Cells
Haller cells are infraorbital ethmoidal air cells that project from the maxillary
sinus roof and the most inferior portion of the lamina papyracea. They are
usually present unilaterally with a prevalence of approximately 6% of the
population.57 The origin of Haller cells is the anterior ethmoid (88%) and
posterior ethmoid (12%).58
Haller cells are identified on coronal images that are located inferior to the
ethmoid bulla and adhering to the medial roof of the orbit, lateral to the
uncinate process.
These air cells may expand into the orbit and narrow the ostium of the
maxillary sinus, especially in the presence of an infection. Haller cells have
been associated with a high incidence of chronic rhinosinusitis because they
may impinge on the patency of the maxillary ostium, thus inhibiting ciliary
function. Procedures (implants, bone grafts) that may involve the maxillary
sinus have an increased morbidity when Haller cells are present.
Agger Nasi Cells

Agger nasi cells are the most anterior ethmoidal air cells, extending
anteriorly into the lacrimal bone. They can be identified on CT/CBCT in over
90% of patients and have a high incidence of frontal sinusitis.59
Agger nasi cells are most easily seen in CT/CBCT coronal images as they lie
anterior, lateral, and inferior to the frontal recess and borders the primary
ostium of the frontal sinus (Fig. 4.32).
FIG 4.32 Agger nasi cells that are anterior aerated ethmoid air cells (arrows).
These cells may predispose the patient to postoperative sinus complications.
Their size may directly influence the patency of the frontal recess and the
anterior middle meatus, thus indirectly affecting the patency of the
osteomeatal complex.
Maxillary Sinus Septa

Antral septa (buttresses, webs, and struts) are the most common osseous
anatomic variants seen in the maxillary sinus. Underwood, an anatomist, first
described maxillary sinus septa in 1910. Krennmair et al further classified
these structures into two groups: primary, which are a result of the
development of the maxilla, and secondary, which arise from the
pneumatization of the sinus floor after tooth loss.7 The prevalence of septa
has been reported to be in the range of 33% of the maxillary sinuses in the
dentate patient and as high as 22% in the edentulous patient. The most
common location of septa in the maxillary sinus has been reported to be in
the middle (second bicuspid–first molar) region of the sinus cavity. CT scan
studies have shown that 41% of septa are seen in the middle region, followed
by the posterior region (35%) and the anterior region (24%). For diagnosis
and evaluation of septa, CT scans are the most accurate method of
radiographic evaluation.60
3-D images depict the anatomic features of septa most easily on CBCT
images. They may also be easily seen on reformatted panoramic and axial
and sagittal images (Fig. 4.33).
FIG 4.33 (A–D) The maxillary sinus inferior floor is highly variable and may be
problematic with respect to the sinus graft procedures.
Maxillary septa complicate sinus graft surgery and can prevent adequate
access and visualization to the sinus floor; therefore inadequate or
incomplete sinus grafting is possible. Additionally, a higher incidence of
membrane perforation results when septa are present.
Maxillary Sinus Hypoplasia

Hypoplasia of the maxillary sinus may be a direct result of trauma, infection,
surgical intervention, or irradiation to the maxilla during the development of
the maxillary bone. These or other congenital developmental conditions
interrupt the maxillary growth center, thus producing a smaller-than-normal
maxilla. A malformed and positioned uncinate process is associated with this
disorder, leading to chronic sinus drainage problems.
Smaller-than-normal maxillary sinus volume can be seen on panoramic,
cross-sectional, coronal, axial, or 3-D images.
Most often, these patients have adequate bone height for endosteal implant
placement, and a sinus graft is not required to gain vertical height. If implant
placement or bone grafting involves the maxillary sinus, caution should be
exercised, as this condition has been associated with chronic sinus disease.
(Fig. 4.34A–B)
FIG 4.34 (A–B) Hypoplasia of the maxillary sinus with inflammation (white arrow).
(C) Normal relationship of nasal cavity and maxillary sinus. (D) Big-nose variant,
which results in the nasal cavity extending into the first molar region leaving
inadequate bone for implants in the bicuspid region.
Inferior Turbinate and Meatus Pneumatization (Big-Nose

Variant)
A rather uncommon anatomic variant, the big-nose variant, occurs when the
inferior third of the nasal cavity exhibits pneumatization within the maxilla
and resides over the alveolar residual ridge. Studies have shown an incidence
of approximately 3%. Because the maxillary sinus is lateral to the edentulous
ridge, there exists inadequate bone height.
Big-nose variants may be determined by evaluation on conventional or
reconstructed panoramic images because the nasal cavity will extend distal or
posterior to the premolar area.
If this condition is not taken into account, the implant may be placed into the
nasal cavity above the residual ridge and often may penetrate into the
inferior meatus and contact the inferior turbinate. A sinus graft is
contraindicated with this patient condition because the sinus is lateral to the
position of the implants. Instead, an onlay graft is required to increase bone
height (Fig. 4.34C–D).
Buccal Thickness of Bone in Premaxilla

On average, maxillary buccal cortical plates are less than 1-mm thick,
significantly thinner than the mandibular alveolar bones, which are greater
than 1 mm. Thin cortical plates (similar to voxel size) tend to become
indistinguishable from adjacent cementum or titanium implants on CBCT
images.
Studies have shown that spatial resolution limitations of CBCT limit bone
visibility of thickness less than 0.6 mm, meaning this is the minimum
thickness required for bone to be measureable. Additionally, clinical studies
show that when bone dehiscence is suspected, a true dehiscence is present
only 50% of the time and a fenestration is present 25% of the time.61
Because of the high degree of false positives, diagnosis and treatment
planning can be problematic. The bone thickness should be correlated with
all CBCT images, especially the cross-sectional views (not 3-D views).
Intraosseous Anastomosis
Within the lateral wall of the maxilla sinus is the intraosseous anastomosis,
which is composed of the posterior superior alveolar and infraorbital
arteries. The vertical component of the lateral-access wall (lateral wall
osteotomy) for the sinus graft often severs these blood vessels.
The intraosseous anastomosis is easily seen on cross-sectional or coronal
views of a CBCT scan as a discontinuation of the lateral wall with a
radiolucent notch (opening). On average, this structure is approximately 15
to 20 mm from the crest of a dentate ridge.
When lateral wall sinus augmentation is indicated, evaluation of the CBCT
should be completed to determine location and size. If bleeding does occur
during the lateral wall osteotomy, it can be addressed by cauterization by the
hand piece and diamond bur without water, electrocautery, or pressure on a
surgical sponge while the head is elevated (Fig. 4.35).
FIG 4.35 Intraosseous anastomosis (arrow) shown on a cross-sectional image

seen as discontinuity of the lateral wall.
Canalis Sinuosus
The anterior superior alveolar nerve branches from the infraorbital canal,
just lingual to the cuspid area. This radiolucent canal is called the canalis
sinuosus. The canal runs forward and inferior to the inferior wall of the orbit
and follows the lower margin of the nasal aperture and opens to lateral to the
nasal septum.62 The canalis sinuosus transmits the anterior superior alveolar
nerve, artery, and vein.
If the clinician is unaware of the canalis sinuosus, the anatomic structure
may be misinterpreted as apical pathology on 2-D radiographs. Therefore, on
CBCT scans, the bilateral anatomic structure should be evaluated for its
presence. It may be depicted on axial, cross-sectional or 3-D images. Studies
have shown the canalis sinuosus to be present on 87.5% of CBCT scans (Fig.
4.36).63
FIG 4.36 Canalis sinuosus. (A) Panoramic image depicting the canalis sinuosus
which transmits the anterior superior alveolar vessels; (B–C) cross-sectional image;
(D) 3-D image showing course of the canal.
Because the anterior maxillary region is a common area for dental implant
placement, the presence of canalis sinuosus may lead to a high degree of
implant morbidity. Impingement into the canal may lead to a soft tissue
interface and failure of the implant, as well as temporary or permanent
sensory dysfunction and possible bleeding issues.64 However, significant
sensory impairments are rare because of cross innervation.
Pathologic Conditions in the Paranasal
Sinuses
Rhinosinusitis
Odontogenic Sinusitis (Periapical Mucositis)
Odontogenic rhinosinusitis occurs when the sinus membrane is violated by
infection of teeth and pathologic lesions of the jaws. The intimate
approximation of the roots of the maxillary posterior teeth to the floor of the
sinus results in inflammatory changes of the periodontium or surrounding
alveolar bone, which promotes the development of pathologic conditions in
Radiographic Appearance.
Odontogenic rhinosinusitis will usually produce generalized sinus mucosal
hyperplasia, which is seen as a radiopaque band that follows the contours of
the sinus floor. A localized periapical mucositis reveals a thickening of the
mucous membrane adjacent to the offending tooth and, on occasion, a
perforation through to the floor of the sinus. This radiographic appearance
has been termed a halo effect (Fig. 4.37).
FIG 4.37 Odontogenic rhinosinusitis associated with a pathologic tooth (red arrow
shows the thickened membrane; green arrow shows expansion into sinus cavity
secondary to diseased tooth).
Differential Diagnosis.
This condition may be confused with acute rhinosinusitis or mild mucosal
thickening. However, in odontogenic rhinosinusitis, the patient will most
likely have pathology associated with an existing tooth (e.g., pain from a
posterior tooth or a recent extraction, exudate around the existing natural
posterior teeth) and radiographic evidence of communication between the
teeth and the maxillary sinus.
Acute Rhinosinusitis
A nonodontogenic pathologic condition may also result in inflammation in
the maxillary sinus in the form of a rhinosinusitis. The most common type of
rhinosinusitis in the maxillary sinus is acute rhinosinusitis. The signs and
symptoms of acute rhinosinusitis are rather nonspecific, making it difficult
to differentiate from the common cold, influenza type of symptoms, and
allergic rhinitis. However, the most common symptoms include purulent
nasal discharge, facial pain and tenderness, nasal congestion, and possible
fever. Acute maxillary rhinosinusitis results in 22 to 25 million patient visits
to a physician in the United States each year, with a direct or indirect cost of 6
billion US dollars. Although four paranasal sinuses exist in the skull, the
most common involved in sinusitis are the maxillary and frontal sinuses.65
The radiographic hallmark in acute rhinosinusitis is the appearance of an air-
fluid level. A line of demarcation will be present between the fluid and the
air within the maxillary sinus. If the patient is supine (CBCT), the fluid will
accumulate in the posterior area; if the patient is upright during the imaging,
the fluid will be seen on the floor and accumulate horizontally. Additional
radiographic signs include smooth, thickened mucosa of the sinus, with
possible opacification. In severe cases the sinus may fill completely with
supportive exudates, which gives the appearance of a completely opacified
sinus. With these characteristics, the terms pyocele and empyema have been
applied (Fig. 4.38).
FIG 4.38 Acute bacterial rhinosinusitis. (A) Coronal scan showing bilateral air-fluid
level. (B) Axial image showing air-fluid level on the right side, the scan is most likely
taken with the patient in a supine position. (C) Left-sided air-fluid level. Arrows, air-
fluid level. (From Som PE and Curtin HD: Head and neck imaging, ed 5, St. Louis, 2012, Mosby.)
The differential diagnosis of acute rhinosinusitis and prolonged viral upper
respiratory infection are very similar. However, a classic air-fluid level in the
maxillary sinus will give rise to the confirmation of acute rhinosinusitis.
Additionally, viral rhinosinusitis will usually improve within 7 to 10 days,
whereas acute bacterial rhinosinusitis persists for longer than 10 days.66
Chronic Rhinosinusitis
Chronic rhinosinusitis is a term used for a rhinosinusitis that does not resolve
in 6 weeks and also has recurrent episodes. It is the most common chronic
disease in the United States, affecting approximately 37 million people.
Symptoms of chronic rhinosinusitis are associated with periodic episodes of
purulent nasal discharge, nasal congestion, and facial pain.
Chronic rhinosinusitis has the characteristic feature of sclerotic, thickened
cortical bone from long-lasting mucoperiosteal inflammation. Additionally, it
may appear radiographically as thickened sinus mucosa to complete
opacification of the antrum.
Allergic Rhinosinusitis
Allergic rhinosinusitis is a local response within the maxillary sinus caused
by an irritating allergen in the upper respiratory tract. The allergen may be
the cause of the allergic rhinosinusitis. This category of rhinosinusitis may be
the most common form, with 15% to 56% of patients undergoing endoscopy
for sinusitis showing evidence of allergy. Allergic rhinosinusitis leads to
chronic rhinosinusitis in 15% to 60% of patients.67 The sinus mucosa becomes
irregular or lobulated, with resultant polyp formation.
Polyp formation related to allergic rhinosinusitis is usually characterized by
multiple, smooth, rounded, radiopaque shadows on the walls of the maxillary
sinus. Most commonly, these polyps are located near the ostium and are
easily observed on a CBCT scan. In advanced cases, ostium occlusion, along
with displacement or destruction of the sinus walls, may be present, with a
radiographic image showing a completely opacified sinus (Fig. 4.39).
FIG 4.39 (A) Bilateral polyposis, usually associated with allergies, showing the
circumferential, polypoid nature of the lesions. (B) Bilateral opacified sinuses
representing a severe case of allergic rhinosinusitis; severe cases may lead to
complete opacification.
Although the radiographic signs of allergic rhinosinusitis may be similar to
acute/chronic rhinosinusitis, a thorough medical history may be used to
differentiate. Most patients with allergic rhinosinusitis will have systemic
systems (e.g., bilateral involvement) and also have a past history of allergy
issues.
Fungal Rhinosinusitis (Eosinophilic Fungal Rhinosinusitis)

Granulomatous rhinosinusitis is a very serious (and often overlooked)
disorder within the maxillary sinus. Patients who have fungal sinusitis are
thought to have had an extensive history of antibiotic use, chronic exposure
to mold or fungus in the environment, or are immunocompromised.
Fungal rhinosinusitis is usually unilateral (78% of cases) with bony
destruction very rare. Within the sinuses the presence of mild thickening to
complete opacification may be present. In most cases, varying degrees of
density (“double-densities”) are seen. The majority of maxillary sinuses
exhibiting fungal disease will radiographically show near complete
opacification. Depending on the invasiveness of the disease, expansion of the
involved sinus may occur and possibly remodeling, thinning, or erosion of
the sinus walls may be seen radiographically (Fig. 4.40).
FIG 4.40 Coronal image showing a progressive fungal rhinosinusitis of the left
paranasal sinus area. Note the dense radiopacity, which is termed a fungal ball
(arrow).
Three possible clinical signs may differentiate fungal sinusitis from acute or
chronic rhinosinusitis: (1) no response to antibiotic therapy, (2) soft tissue
changes in sinus associated with thickened reactive bone, with localized
areas of osteomyelitis, and (3) association of inflammatory sinus disease that
involves the nasal fossa and facial soft tissue. In some cases a positive
diagnosis may require mycologic and histologic studies.
Cystic Lesions
Cystic lesions are a common occurrence in the maxillary sinus, and studies
have reported a prevalence range of 2.6% to 20%.68 They may vary from
microscopic lesions to large, destructive, expansile pathologic conditions that
include pseudocysts, retention cysts, primary mucoceles, and postoperative
maxillary cysts.
Pseudocysts (Mucous Retention Cyst)

The most common cysts in the maxillary sinus are mucous retention cysts.
After much controversy, in 1984, Gardner69 distinguished two categories of
these cysts: (1) pseudocysts and (2) retention cysts. Pseudocysts are more
common and of much greater concern during sinus graft surgery compared
with retention cysts. Pseudocysts reoccur in approximately 30% of patients
and are often unassociated with sinus symptoms. As a consequence, many
physicians do not treat these lesions. However, when their size is larger than
10 mm in diameter, pseudocysts may occlude the maxillary ostium during a
sinus graft procedure and increase the risk of postoperative infection.
Pseudocysts are depicted radiographically as smooth, homogenous, dome-
shaped, round-to-ovoid, well-defined homogeneous radiopacities.
Pseudocysts do not have a corticated (radiopaque) marginal perimeter and
are always on the floor of the sinus cavity. As their name states, they are not
true cysts (e.g., pseudocyst), therefore do not have an epithelium lining (Fig.
4.41).
FIG 4.41 (A) Pseudocyst, also termed a mucous retention cyst. (B) Cross
sections showing the dome-shaped lesion on the floor of the maxillary sinus. (C)
Maxillary right large pseudocyst, which has expanded to encompass most of the
sinus proper. Note in the cross sections, a pathologic tooth is present, which is most
likely the etiologic factor because of the communication with the sinus.
The pseudocyst is easily identified in comparison to other cystic lesions (e.g.,
retention, mucocele, polyps) by being dome-shaped and only located on the
floor of the sinus.
Retention Cysts
Retention cysts may be located on the sinus floor, near the ostium, or within
antral polyps. Because they contain an epithelial lining, researchers consider
them to be mucous secretory cysts and “true” cysts. Retention cysts are often
microscopic in size.
Retention cysts are usually very small and not seen clinically or
radiographically. In rare instances, they may achieve adequate size to be seen
in a CT image and may resemble the a small pseudocyst.
Retention cysts are very uncommon, rarely seen clinically or radiographically,
and no treatment is indicated. Therefore, these lesions are of no
consequence.
Primary Maxillary Sinus Mucocele

A primary mucocele is a cystic, expansile, destructive lesion that may include
painful swelling of the cheek, displacement of teeth, nasal obstruction, and
possible ocular symptoms.70
In the early stages, the primary mucocele involves the entire sinus and
appears as an opacified sinus. As the cyst enlarges, the walls become thin
and eventually perforate. In the late stages, destruction of one or more
surrounding sinus walls is evident (Fig. 4.42).
FIG 4.42 Primary mucocele. (A) Expansile nature of lesion causes destruction of
sinus walls. (B) Clinical image depicting right side of a complete radiopaque sinus
with expansion of walls.
The primary maxillary sinus mucocele has clinical and radiographic
similarities to chronic rhinosinusitis, fungal rhinosinusitis, or neoplasm.
Patients that present with these signs and symptoms should be referred for
proper diagnosis and treatment.
Postoperative Maxillary Cyst

A postoperative maxillary cyst of the maxillary sinus is a cystic lesion that
usually develops secondary to a previous trauma or surgical procedure in the
sinus cavity. It has also been termed a surgical ciliated cyst, postoperative
maxillary sinus mucocele, or a secondary mucocele.71
The cyst radiographically presents as a well-defined radiolucency
circumscribed by sclerosis. The lesion is usually spherical in the early stages,
with no bone destruction. As it progresses, the sinus wall becomes thin and
eventually perforates. In later stages, it will appear as two separated
anatomic compartments (Fig. 4.43).
FIG 4.43 (A) Secondary mucocele is a well-defined radiolucent lesion that
separates the sinus cavity into two separate compartments, which is usually fluid
filled. (B) Radiograph depicting cystic area surrounding implant. (C) Blade implant
after removal which is fully encompassed by lesion. (D) Histologic section
confirming secondary mucocele diagnosis.
The postoperative maxillary cyst is easily differentiated from other lesions
present in the maxillary sinus as the patient will have had a past history of
sinus surgery and radiographically there will be two distinct radiolucent
cavities.
Neoplasms
Squamous Cell Carcinoma, Adenocarcinoma
Malignant tumors of the paranasal sinuses are rare, with a poorly
differentiated squamous cell carcinoma comprising approximately 80% of
tumors. Seventy percent of these tumors are found in the maxillary sinus.72
Symptoms can vary; however, neoplasms of the maxillary sinus usually
include nasal obstruction, rhinorrhea, epistaxis, cranial neuropathies, and
pain. Advanced cases may include visual disturbances, paresthesias, and
possible malocclusion.
Radiographic signs of neoplasms may include various-sized radiopaque
masses, complete opacification, or bony wall changes. A lack of a posterior
wall on a radiographs should be a sign of possible neoplasm (Fig. 4.44).
FIG 4.44 (A–B) Squamous cell carcinoma of the right maxillary sinus showing
complete radiopacity with associated expansion and destruction of sinus walls.
A maxillary sinus neoplasm may show signs and symptoms similar to chronic
rhinosinusitis, primary maxillary sinus mucocele, fungal rhinosinusitis, or
allergic rhinosinusitis. An opacified sinus or bony expansion should result in
immediate referral.
Antroliths
Maxillary Sinus Antroliths
Maxillary sinus antroliths are the result of complete or partial encrustation of
a foreign body that is present in the sinus. These masses found within the
maxillary sinus originate from a central nidus, which can be endogenous or
exogenous.73
The radiographic appearance of a maxillary antrolith resembles either the
central nidus (retained root) or appears as a radiopaque, calcified mass
within the maxillary sinus (Fig. 4.45).
FIG 4.45 (A–B) Antrolith or calcified masses present in the sinus (arrows).
Because the calcified antrolith is composed of calcium phosphate (CaPO4),
calcium carbonate salts, water, and organic material, it will be considerably
more radiopaque than an inflammatory or cystic lesion.74 The central nidus of
the antrolith is similar to its usual radiographic appearance (e.g., implant,
tooth root).
Miscellaneous CBCT Complications
Diagnostic Factors
Patient Positioning
Improper positioning of patients during CBCT examinations may lead to
inaccuracies in image quality that can cause incorrect measurements during
interactive treatment planning. Therefore it is important that a standardized
protocol for all patients be completed by staff taking the scans. Especially if
guided surgery is to be utilized, strict evaluation and protocol of patient
positioning must be verified. Additionally, the patient should be instructed
to not move, as any movement (even minor) may lead to blurring and errors
with the interactive treatment planning.
Lack of Radiopaque Template

For ideal implant placement, anatomic and prosthetic considerations of the
planned tooth or prosthesis must be determined. A radiographic template
must be used during the scanning process to simulate the information into
the final treatment plan. There exist various techniques to fabricate
radiographic templates. These include: (1) the existing or duplicate
prosthesis with radiopaque markers, (2) a thermoplastic template with
radiographic markers, and (3) use of radiopaque teeth in a mucosa or tooth-
supported template. Care should be taken if the existing prosthesis is
utilized, and any esthetic or functional changes should be made prior to
scanning.
FIG 4.46 Summary of the most common pathologic conditions occurring in the
paransal sinuses. (From Misch CE: Contemporary implant dentistry, ed 3, St. Louis, 2008,
Mosby.)
Clinical Complication.
If a radiopaque template is not utilized, the ideal positioning may not be
determined. For cases involving minimal edentulous sites, interactive
treatment planning software may be used to fabricate the position of the
replacement teeth (e.g., Virtual Teeth, Materialize Dental). For full-arch
edentulous cases, a radiopaque template or a dual scan protocol should be
utilized (Fig. 4.47 A–B).
FIG 4.47 (A–B) Without a radiopaque template, ideal angulation may not be
determined. (C) A radiopaque template allows for the correct placement of the
implant.
Lack of Radiopaque Template Stability

If any instability is present in the radiopaque template, inaccuracies may
result with the interactive treatment planning. The final positioning of the
implants and the final prosthesis may be compromised. Because of the need
for ideal implant placement, denture adhesive or reline of the prosthesis
should be used for the scan. If not, the prosthesis might be canted, thus
altering the anatomy and placement of the implants. On CBCT images, a
radiolucent space will be present showing a void and improper positioning of
the prosthesis.
Complications Prevention.
The radiopaque template should always be evaluated for midline verification,
ideal occlusal plane, and approved esthetics. This will minimize the
possibility of transferring incorrect information to be used for the implant
placement position and surgical guide preparation. A well-fitting prosthesis
with denture adhesive or reline should be used to help stabilize the
prosthesis along with a bite registration. The patient should maintain the
teeth in together (i.e., slightly out of occlusion) during the scan (Fig. 4.48).
FIG 4.48 Radiolucent air spaces exhibiting improper positioning or ill-fitting of the
prosthesis during the CBCT scan. The air spaces represent no contact between the
prosthesis and the soft tissue.
Inability to Identify Mandibular Canal
Identification of Mandibular Canal Methods.

The accurate identification of the mandibular canal is crucial for preoperative
treatment planning for implant placement in the posterior mandible.
Because the amount of available bone height present between the alveolar
ridge and the mandibular canal dictates the positioning and size of the
dental implant, any inaccuracies may lead to an increased morbidity. Because
of the inability to ascertain cortical borders in the MC and with varying
trabeculation, in some cases it may be difficult to determine the exact
location. Studies have shown the visibility of the MC decreases towards the
mental foramen. This unreliability of visualization of the MC near the mental
foramen is due to the lack of definite walls in the anterior portion of the
canal. Even with the wide variation of CBCT images, the ability to identify
this structure is dependent on the density of the bone and MC.
Lofthag-Hansen et al determined that the mandibular canal is only visible
on one third of cross-sectional images. However, when other images (sagittal
and axial) were evaluated, the visibility of the MC increased significantly to
approximately 87%. Therefore, assessing every sequential image available
increases the localization of the MC (Box 4.1 and Figs. 4.49 and 4.50).75
Box 4.1
Technique to Localize Mandibular Canal
Manipulation of Images (See Fig. 4.50)
1. Select the reconstructed panoramic view using the CBCT software to access
the mandibular canal (MC).
2. If the mandibular canal is not seen clearly, manipulate the mandibular

curve in the axial view buccal-lingually (Fig. 4.49B).
3. When the mandibular canal can be seen clearly, the nerve is drawn (main
nerve canal) from the posterior to the mental foramen.
4. In the cross-sectional views, scroll until the mental canal/foramen is seen.

Draw the first nerve (green) from the mandibular canal to the exit of the
mental foramen. Draw the second nerve (orange) from anterior to posterior.
5. If mandibular canal cannot be seen clearly, mark the posterior and anterior
limits of the mandibular canal and extrapolate via cross-sectional images.
The MC can then be drawn connecting the extrapolating points on the
panoramic image (see Fig. 4.49)
Additional Techniques
If the CBCT examination does not depict the mandibular canal clearly, an
MRI examination may be completed to more easily see the cortical and
cancellous bone, nerve, and blood vessels. Studies have shown that MRI
images provide less variability in determining the locations of the
mandibular nerve, the mental foramen, and the mandibular foramen than
CBCT images. Even though there exists no ionizing radiation, MRI
technology is limited in dentistry due to cost, availability, and no cross
referencing.76
CBCT, cone beam computed tomography; MC, mandibular canal; MRI,
magnetic resonance imaging.
FIG 4.49 (A) Lack of mandibular canal is seen on the right side of the mandible
because the panoramic curve is outside the focal trough of the canal (red arrow). (B)
On the left side, the canal is easily depicted as the panoramic curve is in the center
of the focal trough (blue arrow).
FIG 4.50 (A) Evaluate mandibular canal. (B) Manipulate the panoramic curve until
the entire mandibular canal may be seen clearly. (C) Scroll until cross section
identifies the mental canal/foramen. (D) Draw the mental nerve and extend through
foramen. (E–F) Draw mandibular nerve from anterior to posterior. (G–H) 3-D
images.
Inadequate Field of View (Maxillary Posterior)
It is imperative to determine the patency of the maxillary ostium when
placing implants or bone grafting into the maxillary sinus area. If pathology
exists, there is possible need for referral to an otolaryngologist for
examination and treatment. If the ostium is not seen on the CBCT, this will
result in the need for an additional scan, which ends up being embarrassing
for the implant clinician as a new scan will need to be taken (Fig. 4.51).
FIG 4.51 (A) Incorrect superior scanning limits. Because the limits of the scan
were not high enough, the ostium cannot be evaluated. (B) Correct superior limit
depicting maxillary ostium.
Radiology Reports
Interpretation
In dentistry, a practicing, licensed dentist is considered by the licensing
board to be competent to interpret commonly utilized radiographs. When
evaluating a medium-to-large-volume CBCT capturing more than one
quadrant or one arch above or below the root apices, it is helpful to use some
type of radiographic template as a guide. The use of a report template makes
sure the anatomic structures that have been included within the volume have
been thoroughly evaluated and deviations from normal symmetry
commented upon. In general, the radiologist will be performing an “over
read” of the volume on your behalf, meaning you have looked at the volume
and the radiologist has validated your observations and findings in a formal
report. Each radiologist may use a slightly different reporting form to fit their
style of reporting, but the common elements of a report are described below.
Basic Information Elements

A typical radiographic report template will include the following basic
information elements:
Patient/Office Identification Section.

This section records date of report, patient name, date of birth, gender, name
of the referring doctor, date of the scan, and the name of the scanning center
or dental office taking the scan/volume.
• Clinical Significance: Critical/patient record information.
Images Provided.
Enter the type of images provided for review. A typical entry would be: “Cone
beam CT images with bone window; axial, coronal and sagittal planes.”
Optional information would include: the name of the CBCT unit, pixel
resolution, (e.g., 0.3 mm, size of the volume—small, medium, large).
• Clinical Significance: Critical/patient record information; when volume size
and pixel resolution are included, patient dose reconstruction is possible
when the specific CBCT unit is identified.
Clinical Information.
This section would include a brief relevant history and/or clinical note.
Entries might include such elements as: “Implant evaluation for edentulous
areas of maxilla,” “Relationship of endosseous implant to the mandibular
canal,” etc.
• Clinical Significance: Critical/patient record information providing the
clinician’s rationale for taking the diagnostic image.
Diagnostic Objectives.
The referring clinician enters their specific objectives for the report such as:
1) sinus evaluation; 2) rule out pathology; 3) implant measurements #3, 10,
14, 19, 29, 4) rule out osteomyelitis; 5) mandibular/maxillary pathology.
• Clinical Significance: Clinician’s specific request or potential concern for
the radiologist to look for as a priority.
Radiographic Findings.
This section of the template provides the radiologist/volume interpreter with
a list of specific areas within the volume to be evaluated. A standard listing
would include:
• Maxilla
• Paranasal Sinuses
• Nasal Cavity
• Air Space
• TMJ
• Other Findings
Dental Findings.
The radiologist will provide limited comments in this section and typically
WILL NOT report on caries, calculus, or periodontal disease associated with
individual teeth. Typically, third molar positions will not be reported unless
specifically requested by the clinician because the interpretation of these
anomalies are within the diagnostic skill-set of the dentist.
• Clinical Significance: Provides a summary of radiographic findings for the
clinician to quickly identify areas of normality and abnormality within the
patient volume. Note: With a digital template for reports, these areas may
have a “normal” response listed and subsequently edited as necessary when
variations from the normal appearances are identified. For example, maxilla:
no abnormalities detected; sinuses: no abnormalities detected, the right and
left osteomeatal complexes were patent; nasal cavity: no abnormalities
detected, etc. for each area on the list.
Radiographic Impression.
This section of the report template will identify specific variations and
deviations from “normal” for each of the areas listed under the radiographic
findings and provide the radiologist’s impression of the deviation from
normal.
• Clinical Significance: Provides a summary of radiographic findings
providing the clinician with a differential radiographic interpretation of
deviations from normal.
Recommendations.
This section may be combined with the radiographic impression noted
above. However, it may be separated to provide general recommendations for
clinician guidance related to the findings listed within the radiographic
impression section. The “Recommendations” section would most likely
include statements such as “Physician referral for more thorough evaluation
of ¼.” Included here would be any anomaly NOT within the dental scope of
practice as defined by your state licensing board. Other recommendations
might include: “Biopsy suggested/recommended for more thorough
evaluation of the biologic processes involved in ¼.” For example: a large
cystlike lesion in the anterior dental area could represent a cyst of the
incisive canal/foramen, large radicular/periapical cyst, ameloblastoma, or
central giant cell tumor, and a biopsy would be helpful in identifying the
specific biologic nature of the lesion.
• Clinical Significance: Provides the clinician with general guidance related
to a specific anomaly. Note: In general, the radiologist WILL NOT
recommend a specific type of treatment for any finding because this is a
consultative report that the clinician must integrate into the patient’s overall
treatment plan and outcome assessment.
Radiologist Name and Signature

• Clinical Significance: Critical/patient record information.
Typical Radiographic Descriptions
Mucositis/sinusitis: “The right maxillary and sphenoid sinuses exhibited an
increase in the thickness and density of the sinus lining.”
Mucous retention pseudocyst: “A homogeneous ovoid/dome-shaped increase

in density was noted within the left maxillary sinus.”
Sinusitis: “The right maxillary sinus was partially occupied by homogeneous

area of increased density containing bubbles.”
Osteomeatal complex: if the opening is not clearly visible, it should be

reported as obstructed/blocked.
Other, less common sinus findings: a thickening, irregularity, and sclerosis of

the walls of the sinus may potentially represent a longstanding chronic
inflammation of the sinuses. Small irregular calcifications within the
homogeneous density of the tissues of the sinus may be an indication of
antrolith formation, and an indication of a longstanding chronic sinusitis
and small osteomas within the ethmoid sinus.
Radiographic Findings
Maxilla.
Asymmetries between right and left maxilla or sinuses, changes in bone
pattern or texture.
Typical report findings might read: “An asymmetry was noted between the
right and left maxillary sinuses; the right maxillary sinus and maxilla exhibits
a smaller volume and size than the left, potentially suggestive of maxillary
hypoplasia. Correlation of the radiographic observation with the patient's
clinical evaluation is suggested.”
• Clinical Significance: Identification of possible hemimaxillary hypoplasia,
previous trauma, fibrous dysplasia.
Sinuses.
This section will report on findings within all major sinus groups: right and
left maxillary, ethmoid, frontal and sphenoid sinuses. Under “normal”
circumstances the linings of the sinuses are not radiographically visible and
are reported as “no abnormalities detected.” When the lining becomes
visible, sinus pathology is present and reported if the lining is 3 mm or more
in thickness.
Typical report findings might read: “The radiographic findings appear
consistent with a mild chronic sinusitis of the right and left maxillary
sinuses. Review of patient's history for chronic sinusitis/allergy is suggested.
Physician referral for more thorough evaluation is suggested if merited by
clinical findings and symptoms.”
• Clinical Significance: Identification of potential changes on the sinus
region meriting potential physician referral in the presence of symptoms.
Nasal Cavity.
This section will include any findings of asymmetry associated with the nasal
cavity including: inferior, middle, and superior turbinates; deviations of the
nasal septum; absence of internal nasal structures potentially associated with
previous ENT surgery. A variation in normal anatomy is a dilation within the
middle turbinate referred to as a concha bullosa.
Typical report findings might read: “A mild deviation the nasal septum to
the right; enlargement of the middle turbinate consistent with a concha
bullosa, is considered a variation in normal anatomic form. Deviation of the
nasal septum is considered a variation in normal anatomy; referral and
treatment is not indicated unless the patient provides a history of difficulty
breathing through their nose.”
• Clinical Significance: Identification of possible changes in the nasal cavity
potentially influencing breathing patterns.
Air Space.
Variations in the size of the airway are noted in the section as well as
potential enlargements of the adenoid and pharyngeal tonsils.
Typical report findings might read: “Narrowing of the airway has been
associated with a variety of respiratory disorders including an increased risk
of obstructive sleep apnea. Correlation of the radiographic observation with
the patient's clinical history is suggested. Clinical evaluation of the soft
tissues of the oral pharynx is suggested.”
• Clinical Significance: Identification of possible airway changes affecting
patient breathing patterns.
TMJ.
This section reports on variations and deviations in symmetry between the
right and left condyles, articular fossae, and joint spaces.
Typical report findings might read: “The right condyle, articular fossa, and
joint space exhibited normal bony profiles and contours; the left articular
fossa and joint space exhibited normal radiographic contours; the left
condyle exhibits a localized discontinuity the cortical outline, the presence of
resorption lacunae, and sclerosis of the underlying bony trabecular pattern
consistent with DJD. Correlation of the radiographic observation with the
patient's clinical findings and symptoms, if any, is suggested.”
• Clinical Significance: Identification of possible radiographic changes within
the bony structures of the TMJ region affecting patient symptoms/occlusion.
TMJ-positive findings may predispose the patient to prosthetic
rehabilitation complications.
Other Findings.
This section is used to report radiographic changes in anatomic structures
not associated with the maxilla and mandible but included within the volume
including, but not limited to: calcifications within the carotid artery lateral to
the pituitary fossa and within the lower neck; radiographically visible
changes within the cervical vertebra including osteophyte formation,
sclerosis, narrowing, and irregularity of intervertebral disk space width with
potential bone to bone contact; generalized loss or thinning of cortical bone
and an absence of internal bony trabeculation suggestive of systemic
metabolic disorders of bone/osteoporosis; increased density noted within
one or both mastoid processes. Common incidental radiographic findings
included here would be: calcification the stylohyoid ligament, calcifications
of pineal gland and cavernous sinus (middle cranial fossa area), idiopathic
soft tissue calcifications within the soft tissues of the skin or soft tissues of
the oral pharynx (tonsilloliths), salivary gland/duct calcifications, metallic
foreign bodies, ear wax, etc.
Styles of Radiology Reports

Each radiologist has their own style and format they use to construct a
report, and it is appropriate for the referring clinician to do their “due
diligence” and select the radiologist who will provide the kind of report they
are comfortable using as a basis for treatment planning decisions. Examples
of radiology report templates are shown in Fig. 4.52. For example, some
radiologists specify that their review of the volume is through the assessment
of “axial cross sections only,” which limits the potential of visualization of
radiographic anomalies when CBVT volumes and the software used easily
provide axial, coronal, and sagittal cross sections. Our suggestion is to
identify a radiologist who provides interpretation based on a complete
analysis of the volume utilizing axial, coronal, and sagittal cross sections.
FIG 4.52 Sample radiology report. (A) Minimal information report. (B) Medical style
(written only, no illustrations). (C) Hybrid medical style with illustrations.
Summary
One of the keys to preventing potential complications during the surgical
and prosthetic phases of implant treatment is to have as clear a picture of the
patient's current anatomic makeup as possible. Identifying deficiencies of
bone allows the clinician to modify the bony architecture to achieve optimal
implant location for prosthetic success. Knowing the exact locations of vital
structures allows clinicians to plan safe zones during treatment to avoid
potentially catastrophic complications. Proper planning is absolutely
paramount to success in any endeavor, and having a strong plan in place
prior to the initiation of implant treatment is no exception.
Cone beam technology has ushered in a new era of accuracy in treatment
planning. Clinicians are no longer having to rely on “guesswork” by
extrapolating anatomical measurements from a distorted 2-D image.
Templates may be made based on these new 3-D images to assist clinicians
during tough surgical cases, especially early on respective learning curves.
CBT is closer to becoming the standard of care across the board.
With the combination of 3-D imaging and a thorough knowledge of the
anatomic areas that are focused on in this chapter, a clinician can acquire a
further degree of confidence that the likelihood of complications has been
reduced, which makes the implant treatment process less stressful for both
patient and provider.
References
1. Yosue T, Brooks SL. The appearance of mental foramina on
panoramic radiographs. I. Evaluation of patients. Oral Surg Oral Med
Oral Pathol. 1989;68:360–364.
2. Denio D, Torabinejad M, Bakland LK. Anatomical relationship of the
mandibular canal to its surrounding structures in mature mandibles.
J Endod. 1992;18:161–165.
3. Hoseini ZSH, Bagherpour A, Javadian LA, et al. Evaluation of the
accuracy of panoramic radiography in linear measurements of the
jaws. Iran J Radiol. 2011;8:97.
4. Lindh C, Petersson A, Klinge B. Measurements of distances related to
the mandibular canal in radiographs. Clin Oral Implants Res.
1995;6:96–103.
5. Sonick M, Abrahams J, Faiella RA. A comparison of the accuracy of
periapical, panoramic, and computerized tomographic radiographs in
locating the mandibular canal. Int J Oral Maxillofac Implants.
1994;9:455–460.
6. Kuzmanovic DV, Payne AG, Kieser JA, Dias GJ. Anterior loop of the
mental nerve: a morphological and radiographic study. Clin Oral
Implants Res. 2003;14:464–471.
7. Krennmair G, Ulm GW, Lugmayr H, et al. The incidence, location, and
height of maxillary sinus septa in the edentulous and dentate maxilla.
J Oral Maxillofac Surg. 1999;57:667–671.
8. Naitoh M, Yoshida K, Nakahara K, et al. Demonstration of the
accessory mental foramen using rotational panoramic radiography
compared with cone-beam computed tomography. Clin Oral Implants
Res. 2011;22:1415–1419.
9. Gulsahi A. Bone quality assessment for dental implants. Turkyilmaz
I. Implant dentistry—The most promising discipline of dentistry. InTech:
Rijeka, Croatia; 2011:456–478.
10. Angelopoulos C, Aghaloo T. Imaging technology in implant
diagnosis. Dent Clin North Am. 2011;55:141–158.
11. Schulze RK, Berndt D, d'Hoedt B. On cone-beam computed
tomography artifacts induced by titanium implants. Clin Oral
Implants Res. 2010;21:100–107.
12. Haramati N, Staron RB, Mazel-Sperling K, et al. CT scans through
metal scanning technique versus hardware composition. Comput Med
Imaging Graph. 1994;18:429–434.
13. Pettersson A, Komiyama A, Hultin M, et al. Accuracy of virtually
planned and template guided implant surgery on edentate patients.
Clin Implant Dent Relat Res. 2012;14:527–537.
14. Visconti MAPG, Verner FS, Assis NMSP, et al. Influence of
maxillomandibular positioning in cone beam computed tomography
for implant planning. Int J Oral Maxillofac Surg. 2013;42:880–886.
15. Wang J, Mao W, Solberg T. Scatter correction for cone-beam computed
tomography using moving blocker strips. SPIE Medical Imaging.
International Society for Optics and Photonics; 2011:796125.
16. Tamimi D. Specialty imaging: Dental implants. Amyrsis Publishing: Salt
Lake City, UT; 2015.
17. Vasak C, Watzak G, Gahleitner A, et al. Computed tomography–based
evaluation of guided surgery template (NobelGuide)–guided implant
positions: a prospective radiological study. Clin Oral Implants Res.
2011;22:1157–1163.
18. Scarfe WC. Incidental findings on cone beam computed tomographic
images: a Pandora's box? Oral Surg Oral Med Oral Pathol.
2014;117:537–540.
19. Price JB, Thaw KL, Tyndall DA, et al. Incidental findings from cone
beam computed tomography of the maxillofacial region: a descriptive
retrospective study. Clin Oral Implants Res. 2012;23:1261–1268.
20. Miles DA. Clinical experience with cone-beam volumetric imaging
report of findings in 381 cases. Comp Tom. 2005;20:416–424.
21. Cha JY, Mah J, Sinclair P. Incidental findings in the maxillofacial area
with 3-dimensional cone-beam imaging. Am J Orthod Dentofacial
Orthop. 2007;132:7–14.
22. Arnheiter C, Scarfe WC, Farman AG. Trends in maxillofacial cone-
beam computed tomography usage. Oral Radiol. 2006;22:80–85.
23. Kim ST, Hu KS, Song WC, et al. Location of the mandibular canal and
the topography of its neurovascular structures. J Craniofac Surg.
2009;20:936–939.
24. Anderson LC, Kosinski TF, Mentag PJ. A review of the intraosseous
course of the nerves of the mandible. J Oral Implantol. 1991;17:394–
403.
25. Carter RB, Keen EN. The intramandibular course of the inferior
alveolar nerve. J Anat. 1971;108(Pt 3):433–440.
26. Liu T, Xia B, Gu Z. Inferior alveolar canal course: a radiographic study.
Clin Oral Implants Res. 2009;20:1212–1218.
27. Ikeda K, Ho KC, Nowicki BH, et al. Multiplanar MR and anatomic
study of the mandibular canal. AJNR Am J Neuroradiol. 1996;17:579–
584.
28. Sutton JP. The practical significance of mandibular accessory
foramina. Aust Dent J. 1974;19:167–173.
29. Hayward J, Richardson ER, Malhotra SK. The mandibular foramen: its
anteroposterior position. Oral Surg Oral Med Oral Pathol.
1997;44:837–843.
30. Gowgiel JM. The position and course of the mandibular canal. J Oral
Implantol. 1992;18:383–385.
31. Naitoh M, Hiraiwa Y, Aimiya H, et al. Accessory mental foramen
assessment using cone-beam computed tomography. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod. 2009;107:289–294.
32. Filo K, Schneider T, Locher MC, et al. The inferior alveolar nerve's loop
at the mental foramen and its implications for surgery. J Am Dent
Assoc. 2014;145:260–269.
33. Hanihara T, Ishida H. Frequency variations of discrete cranial traits in
major human populations. IV. Vessel and nerve related variations. J
Anat. 2001;199:273–287.
34. Singh R, Srivastav AK. Study of position, shape, size and incidence of
mental foramen and accessory mental foramen in Indian adult
human skulls. Int J Morphol. 2010;28:1141–1146.
35. Juodzbalys G, Wang HL, Sabalys G. Anatomy of mandibular vital
structures. Part II: Mandibular incisive canal, mental foramen and
associated neurovascular bundles in relation with dental
implantology. J Oral Maxillofac Res. 2010;1:e3.
36. Serman NJ. The mandibular incisive foramen. J Anat. 1989;167:195–
198.
37. Butura CC, Galindo DF, Cottam J, et al. Hourglass mandibular
anatomic variant incidence and treatment considerations for all–on–
four implant therapy: report of 10 cases. J Oral Maxillofac Surg.
2011;69:2135–2143.
38. Watanabe H, Mohammad AM, Kurabayashi T, et al. Mandible size and
morphology determined with CT on a premise of dental implant
operation. Surg Radiol Anat. 2010;32:343e349.
39. Leite GMF, Lana JP, de Carvalho Machado V. Anatomic variations and
lesions of the mandibular canal detected by cone beam computed
tomography. Surg Radiol Anat. 2014;36:795–804.
40. Jacobs R, Mraiwa N, Van Steenberghe D, et al. Appearance of the
mandibular incisive canal on panoramic radiographs. Surg Radiol
Anat. 2004;26:329–333.
41. Athavale SA, Vijaywargia M, Deopujari R. Bony and cadaveric study of
retromolar region. People's J Sci Res. 2013;6:17–25.
42. Babiuc I, Tarlungeanu I, Pauna M. Cone beam computed tomography
observations of the lingual foramina and their bony canals in the
median region of the mandible. Rom J Morphol Embryol. 2011;52:827–
829.
43. Almog DM, Tsimidis K, Moss ME, et al. Evaluation of a training
program for detection of carotid artery calcifications on panoramic
radiographs. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2000;90:111–117.
44. Atwood DA, Coy WA. Clinical cephalometric and densitometric study
of reduction of residual ridges. J Prosthet Dent. 1971;26:200–295.
approach, healing and progressive bone loading. Int J Oral Implantol.
1991;6:23–31.
46. Macedo VC, Cabrini RR, Faig-Leite H. Infraorbital foramen location in
dry human skulls. Braz J Morphol Sci. 2009;26:35–38.
47. DelBalso AM. Maxillofacial imaging. Saunders: Philadelphia; 1990.
48. Kantarci M, Karasen R, Alper F, et al. Remarkable anatomic variations
in paranasal sinus region and their clinical importance. Eur J Radiol.
2004;50:296–302.
49. Tami T. Anatomy and physiology. Seiden A, Tami T, Pensak M, et al.
Otolaryngology: the essentials. Thieme Medical Publishers: New York;
2002:77–118.
50. Parks ET. Cone beam computed tomography for the nasal cavity and
paranasal sinuses. Dent Clin North Am. 2014;58:627–651.
51. Bergh J, Bruggenkate CM, Disch FJ. Anatomical aspects of sinus floor
elevations. Clin Oral Implants Res. 2000;11:256–265.
52. Prasanna LC, Mamatha H. The location of maxillary sinus ostium and
its clinical application. Indian J Otolaryngol Head Neck Surg.
2010;62(4):335–337.
53. Zinreich S, Albayram S, Benson M, et al. The ostiomeatal complex and
functional endoscopic surgery. Som P. Head and neck imaging. ed 4.
Mosby: St Louis; 2003:149–173.
54. Stallman JS, Lobo JN, Som PM. The incidence of concha bullosa and
its relationship to nasal septal deviation and paranasal sinus disease.
AJNR Am J Neuroradiol. 2004;25:1613–1618.
55. Llyod GA. CT scan of the paranasal sinuses: Study of a control series
in relation to endoscopic sinus surgery. J Laryngol Otol. 1990;4:477–
481.
56. Wani AA, Kanotra S, Lateef M. CT scan evaluation of the anatomical
variations of the ostiomeatal complex. Indian J Otolaryngol Head Neck
Surg. 2009;61:163–168.
57. Arslan H, Aydinlioğlu A, Bozkurt M. Anatomic variations of the
paranasal sinuses: CT examination for endoscopic sinus surgery.
Auris Nasus Larynx. 1999;26:39–48.
58. Kainz J, Braun H, Genser P. Haller's cells: morphologic evaluation and
clinico-surgical relevance. Laryngorhinootologie. 1993;72:599–604.
59. Brunner E, Jacobs JB, Shpizner BA, et al. Role of the agger nasi cell in
chronic frontal sinusitis. Ann Otol Rhinol Laryngol. 1996;105:694–700.
60. Kim MJ, Jung UW, Kim CS, et al. Maxillary sinus septa: prevalence,
height, location and morphology: a reformatted computed
tomography scan analysis. J Periodontol. 2006;77:903–908.
61. Leung CC, Palomo L, Griffith R. Accuracy and reliability of cone-beam
computed tomography for measuring alveolar bone height and
detecting bony dehiscences and fenestrations. Am J Orthod
Dentofacial Orthop. 2010;137:S109–S119.
62. Neves FS, Souza MC, Franco LCS, et al. Canalis sinuosus: a rare
anatomical variation. Surg Radiol Anat. 2012;34:563–566.
63. Wanzeler AMV, Marinho CG, Junior SMA. Anatomical study of the
canalis sinuosus in 100 cone beam computed tomography
examinations. Oral Maxillofac Surg. 2014;19:49–53.
64. Jacobs RL, Martens W, Mraiwa N, et al. Neurovascularization of the
anterior jaw bones revisited using high resolution magnetic
resonance imaging. Oral Surg Oral Med Pathol Oral Radiol Endod.
2007;103:683–693.
65. American Academy of Otolaryngology. Head and Neck Surgery
(website). http://www.entnet.org/content/sinus-headaches.
66. Rosenfeld RM, Andes D, Bhattacharyya N, et al. Clinical practice
guideline: adult sinusitis. Otolaryngol Head Neck Surg. 2007;137(Suppl
3):S1–S31.
67. Beninger MS, Mickleson SA. Functional endoscopic sinus surgery,
morbidity and early results. Henry Ford Hosp Med J. 1990;38:5.
68. Yoshiura K, Ban S, Hijiya K, et al. Analysis of maxillary sinusitis using
computed tomography. Dentomaxillofac Radiol. 1993;22:86.
69. Gardner DG. Pseudocysts and retention cysts of the maxillary sinus.
Oral Surg Oral Med Oral Pathol. 1984;58:561–567.
70. Kudo K, Fujioka Y, Ohashi Y. Clinicopathological study of
postoperative maxillary cysts. J Jpn Stomatol Soc. 1972;21:250–257.
71. Misch CM, Misch CE, Resnik RR, et al. Postoperative maxillary cyst
associated with sinus elevation procedure: a case report. J Oral
Implantol. 1991;18:432–437.
72. Tiwari R, Hardillo JA, Mehta D, et al. Squamous cell carcinoma of
maxillary sinus. Head Neck. 2000;22:164–169.
73. Blaschke FF, Brady FA. The maxillary antrolith. Oral Surg Oral Med
Oral Pathol. 1979;48:187–191.
74. Karges MA, Eversol LR, Poindexter BJ. Report of case and review of
literature. J Oral Surg. 1971;29:812–814.
75. Lofthag-Hansen S, Gröndahl K, Ekestubbe A. Cone-beam CT for
preoperative implant planning in the posterior mandible: visibility of
anatomic landmarks. Clin Implant Dent Relat Res. 2009;11:246.
76. Chau A. Comparison between the use of magnetic resonance imaging
and conebeam computed tomography for mandibular nerve
identification. Clin Oral Implant Res. 2012;23:253–256.
5
Dental Implant Intraoperative
Complications
Randolph R. Resnik
The surgical placement of dental implants, once a very specialized treatment

modality, has become a very mainstream component of contemporary
dentistry. This has been made possible by advancements that have made
dental implant procedures very predictable with high success rates. Despite
this level of success, there still exist many potential complications that can
occur at any phase of the implant surgical procedure. During any implant
surgery the potential for a complication exists, ranging from simple issues to
situations that could potentially place the patient at increased risk. The goal
of this chapter is to provide the implant clinician with a knowledge base to
properly address many of the common and uncommon complications that
may occur during the implant surgical phase.
Implant Placement: Surgical Related
Placement of Implants Into Sites With
Preexisting Pathology
Infection or bacteria at or adjacent to a potential implant site is a significant
source for future implant morbidity. Placement of an implant close to an
infected site or into a previous extraction site with bacterial contamination
may lead to the loss of the implant and/or loss of the adjacent tooth. Ayangco
et al reported that teeth with failed endodontic lesions that were extracted,
debrided, and sufficiently healed, are at risk of possible retrograde peri-
implantitis after implant placement.1
Etiology
Bacteria present at the time of surgery places the implant at risk.
Endodontically infected teeth have involved bacteria, which are most
commonly Propionibacterium acnes, Staphylococcus epidermidis, Streptococcus
intermedius, Wolinella recta, and Porphyromonas and Prevotella spp.2 Bacteroides
spp bacteria have been shown to inhabit natural tooth periapical lesions that
are encapsulated in a polysaccharide that enhances its virulence and survival
ability. Bacteroides forsythus has been shown to be present in asymptomatic
periradicular endodontic lesions and may survive encapsulated in bone even
after extraction and debridement.3
Prevention
The surgical site should be evaluated radiographically prior to the surgery for
any possible apical pathology. The adjacent teeth should be assessed for the
presence of periodontal ligament (PDL) thickening or radiolucent areas that
may impinge on the area of implant placement. Brisman et al reported that
even asymptomatic endodontically treated teeth with normal radiographic
appearance could result in implant morbidity. They relate the possibility of
inadequate obturation with an incomplete seal on the tooth root that may
contain bacteria, even when they are free of symptoms.4 Nelson and Thomas
revealed in studies that bacteria persist and are reactivated upon implant
placement even after debridement of apical infection, complete extraction
socket healing, and alveolar bone remodeling.5 Kassolis et al reported that
edentulous jaws will contain regions of bacterial biofilm and nonvital bone
for over 1 year after extraction, and healing may pose a significant risk for
future implant failure.6
Treatment
Endodontic therapy, apical surgery, or extraction of the adjacent tooth should
be completed prior to placement of dental implants in this area. Even in the
absence of infection, extraction sites should be thoroughly debrided and
bleeding initiated to reduce the bacteria count and increase bone growth
factors to the site. If granulation tissue remains, bacteria and a resultant
inflammatory response will persist. Special curettes may be used to assist in
the removal of the granulation tissue and small round burs (#2 or #4) can be
used to perforate the alveolar walls to increase bleeding areas (Fig. 5.1).
FIG 5.1 Postextraction socket. (A) With existing pathology. (B) Removal of fibrous
and granulation tissue with serrated spoon curette. (C) Walls of extraction site are
decorticated with #2 or #4 round bur to initiate regional acceleratory phenomenon
(RAP). (D) After complete removal of all bacteria and tissue, implant placement. (E)
If the extraction site is compromised, a bone graft procedure is recommended.
Retained Root Tips in Implant Site

Placement of dental implants into extraction sites that contain retained tooth
roots may lead to inflammation and retrograde peri-implantitis.
Unfortunately, in some cases, root tips are difficult to diagnosis
preoperatively, the condition may go unnoticed until after implant
placement.
Etiology
Placement of dental implants, especially after immediate extraction, may lead
to undiagnosed retained root tips at the site of implantation. Gray et al, in an
animal study, evaluated the intentional placement of dental implants into
tooth roots. Histologically, there was no inflammation, and in some of the
specimens a calcified material was deposited on the implants. Buser et al also
supported the same findings in animal studies. However, implants should
never be placed in contact with tooth structure because this may be a source
of infection and place the practitioner at risk for possible medicolegal issues.
Prevention
To prevent retained tooth roots, atraumatic and careful extraction of teeth
should be completed. Special care should be exercised with multirooted teeth
and tooth roots with dilacerations. Preoperative evaluation should include a
CT evaluation with the following Hounsfield numbers as a guide (Fig. 5.2):
Air = − 1024 Hu
Water = 0 Hu
Trabecular bone ≅ 200 Hu
Cortical bone ≅ 1500 to 2000 Hu
Tooth structure—Enamel ≅ 3072 Hu

FIG 5.2 Retained root tips. (A–B) All root tips should ideally be removed prior to
bone graft or implant placement. (C) Retained bacteria, granulation tissue, or tooth
root may lead to increased morbidity after implant placement.
Treatment
Prior to Placement.
Root tips should be removed and the site evaluated for implant placement. If
an inadequate amount of bone is present, grafting should be completed
followed by implant placement at a later date.
After Implant Placement.

If a root tip is discovered after implant placement, the site should be
evaluated on a strict recall basis. If any signs of inflammation develop, the
implant and root tip should be removed, grafted, with implant placement at
a later date (Figs. 5.2 and 5.3).
FIG 5.3 Evaluation of different densities. (A) Retained root tip. (B) Difference in
host bone vs. grafted bone utilizing medical grade CT imaging (Hounsfield units) and
showing different bone densities.
Flapless Surgery
Flapless surgery has become very popular today in implant dentistry. This
technique entails no reflection of the crestal soft tissue and placement of the
implant through the opening for the osteotomy. The advantages of flapless
surgery are: (1) no soft tissue reflection, decreasing the invasiveness of the
surgery; (2) minimizes bleeding; (3) reduces inflammation and pain; (4) hard
and soft tissue preservation, which maintains vascular supply and soft tissue
drape; and (5) no suturing.
Etiology
However, flapless surgery does have disadvantages that may be detrimental
to the prognosis of dental implants. These include: (1) inability to assess the
bone volume before or during the implant osteotomy and insertion; (2)
inability to ascertain perforation of the cortical plates; (3) tissue punches are
often used, which may result in decreased keratinized tissue; (4) difficulty in
visualizing crestal bone area, resulting in the inability to determine
apicocoronal positioning; (5) possibility of overheating the bone and causing
thermal damage, especially if a tissue borne surgical template is used; and (6)
possibility of soft tissue entrapment into the osteotomy site, which may lead
to a retrograde infection (Fig. 5.4).
FIG 5.4 Flapless surgery. (A) Drill sequence and implant placement after tissue
punch. (B) Osteotomy preparation and implant placement through surgical template.
(C) Flapless surgery leading to lingual position of implant, with the complication of
traumatizing the lingual tissue and vital structures in the mandible. (D) Maxillary
anterior flapless surgery leading to implant placed facially, completely out of the
bone. (E) Tissue surgical templates should be fixated with bone screws to minimize
possibility of malposition.
Prevention
A thorough preoperative evaluation should be completed including a three-
dimensional analysis of the available bone and anatomic variants. Use of
cone beam computed tomography (CBCT)–generated surgical templates is
recommended. Care should be noted in Division B or Division C ridges
because ideal placement is difficult.
Treatment
Flapless implant placement should only be completed in the presence of
adequate keratinized tissue and sufficient bone quantity and angulation,
where root approximation is not an issue. If bone quantity is compromised,
the surgical approach should be changed to an exposure (flap) procedure to
verify ideal placement and angulation.
Malpositioned Initial Osteotomy Site

In certain initial osteotomies, the initial implant position may not be placed
in the ideal location. The osteotomy may need to be repositioned to allow for
ideal placement. The use of a Lindemann bur is ideal for the repositioning of
an osteotomy because of its side-cutting capabilities. Lindemann burs are
side-cutting burs, which allow easy positional change with minimal trauma
to the bone.
Etiology
Once the initial osteotomy is prepared, it is assessed for proper position with
a direction indicator. If incorrect, the osteotomy site may need to be
“stretched” or repositioned to a more ideal location.
Prevention
Use of surgical templates or implant-positioning devices for ideal implant
positioning to decrease the possibility of changing the osteotomy position.
Treatment
To horizontally reposition an osteotomy site, the use of conventional drills is
difficult because of the end-cutting capabilities of the burs. The use of a side-
cutting Lindemann bur will allow for repositioning to a new, corrected site.
The new osteotomy position should be deepened so that subsequent end-
cutting drills will not reposition back into the original osteotomy site.
However, when using the Lindemann bur, always use copious amounts of
saline because this bur will generate a significant amount of trauma and heat
to the bone7 (Fig. 5.5).
FIG 5.5 Malpositioned initial osteotomy site (i.e., not equidistant between implants).
(A) Implant position too close to center implant. (B) Use of Lindemann bur to move
the implant site posteriorly. (C) Side-cutting Lindemann bur. (D) Lindemann bur used
to reposition osteotomy site by increasing osteotomy depth to prevent from entering
back into original malpositioned site.
Lack of Keratinized Tissue at Surgical Site

The presence of keratinized tissue is a controversial subject in oral
implantology. However, there appear to be greater benefits with having this
tissue in relation to an implant when compared to a natural tooth. Some
reports indicate the lack of keratinized tissue may contribute to implant
failure.8
Etiology
Mobile, nonkeratinized mucosa has been shown to exhibit greater probing
depths, which has been confirmed histologically. The absence of keratinized
mucosa also increases the susceptibility of periimplant regions to plaque-
induced destruction.9 Additional studies have shown that mobile mucosa
may disrupt the implant-epithelial attachment zone and contribute to an
increased risk of inflammation from plaque.10 For larger edentulous ridges,
the zone of attached tissue on the facial flap (mandible) provides greater
resistance for the sutures against tension of the mentalis muscle in the
anterior region and the buccinator muscle in the molar-premolar regions,
which often cause incision line opening. As a result, an incision made facial
to the attached tissue may cause partial ischemia to some of the crestal
tissue. In addition, the incision in unkeratinized facial tissue also severs
larger blood vessels, which increases bleeding and decreases vision during
surgery, while also potentially complicating final suturing (Fig. 5.6).
FIG 5.6 (A) Ridge with lack of keratinized tissue. (B) Incision made to the lingual to
maintain as much attached tissue on facial as possible. (C) Dermal accelular matrix
(e.g., OraCELL [Salvin Dental Specialties, Inc.]) modified with a tissue punch. (D)
Dermal matrix placed over implants prior to closure.
Prevention
A thorough clinical examination to determine the amount of host-attached
tissue prior to surgery and the possible implementation of tissue grafting
prior to implant placement.
Treatment
For implant sites intended for crown restorations, an evaluation of attached
tissue should be done. If insufficient attached tissue is present, tissue
augmentation procedures should be completed prior to implant placement.
For larger edentulous sites, especially in the mandible, the incision may be
modified to maintain the attached tissue in some cases. If the crest of the
ridge is above the floor of the mouth, and there exists greater than 3 mm of
attached, keratinized gingiva on the crest of the ridge, a full-thickness
incision is made, bisecting the attached tissue. If less than 3 mm of attached
gingiva exists on the ridge, the full-thickness incision is made more to the
lingual so that at least 1.5 mm of the attached tissue is to the facial aspect of
the incision line. Additionally, AlloDerm may be used as a membrane and to
increase the amount of attached tissue.
Bur “Stuck” in Bone During Osteotomy

Etiology
Often in hard bone (≈D1–D2 bone), if the handpiece is stopped with the
surgical drill in the bone, it may be difficult to remove out of the osteotomy.
Attempting to remove the bur with the handpiece (either forward or reverse)
will result in damage to the handpiece gears (Fig. 5.7).
FIG 5.7 Bur lodged in the bone. (A) Osteotomy preparation in dense bone may
result with internal stress within the prepared site leading to difficulty in bur removal.
(B) When bur cannot be removed, do not attempt to use handpiece in reverse
direction because this may cause damage to the handpiece. (C) Handpiece
disengaged from bur. (D) Bur gently removed with forceps in counterclockwise
direction. (E) Bur removed carefully to minimize possibility of fracturing buccal plate.
Prevention
To avoid this complication, in dense bone small (minimal) increments of
bone should be removed at a time. When performing the osteotomy, “bone
dancing” should be performed, which will result in less stress to the bone
and will allow for ease of widening the osteotomy. Also, by using
intermediate burs (more burs close in diameter), smaller amounts of bone
are removed at a given time, decreasing the possibility of burs being lodged
in the bone (“bur integration”).
Treatment
If a bone drill becomes lodged in the bone during preparation, the hand
piece should not be wiggled back and forth to disengage the drill. This may
increase the size of the bone preparation, cause injury and necrosis to the
bone, or separate the drill above or below the bone. Instead, the drill is
disengaged from the handpiece and gently rotated counterclockwise with
forceps or rongeurs.
Overpreparation of Final Drill

Etiology
The final drill is the most critical surgical step in the osteotomy preparation.
The bone surrounding this drill will be in direct contact with the implant.
When the final drill preparation is not precise, the implant-bone region may
be irregular with gaps that may decrease initial stability and lead to early
implant failure. A decreased initial bone contact of the host bone and dental
implant also decreases the percentage of new bone-implant contact
formation (Fig. 5.8).
FIG 5.8 (A) Overpreparation of the osteotomy site that results in mobility and lack
of bone implant contact. (B) Irregular osteotomy site showing overpreparation of site.
(C) In less dense bone (lack of cortical bone), no crestal bone drill should be used
because this will result in lack of stability of the implant.
Prevention
A constant pressure and angulation is used with the final drill to ensure that
a precise, round osteotomy is prepared. The most important factor is the use
of the final drill only once to avoid over preparation, most importantly in less
dense bone (≈D3–D4). In D4 bone the final bur is often not used to increase
bone-implant contact (BIC) around the implant. Additionally, in less dense
bone a crestal bone drill should never be used because of increased loss of
initial fixation.
Treatment
If overpreparation of the osteotomy site occurs, clinical evaluation should be
completed to determine if mobility of the implant exists. If mobility does
exist, the following are possible options; however, it is imperative that the
final placement of the implant not have any micromovement:
Compress Buccal and Lingual Cortical Plates.

In less dense bone, the buccal and lingual cortical plates can be depressed to
reduce movement of the implant. The implant should then be evaluated for
micromovement. If movement exists, the implant should be removed.
Remove Implant, Deepen Osteotomy.

The mobile implant may be removed, and the osteotomy deepened so that
rigid fixation is obtained. However, care should be exercised to not allow
encroachment on any vital structures (e.g., mandibular canal) or compromise
the prosthesis by increasing the crown-implant ratio.
Remove Implant, Place Wider Implant.

If sufficient width of bone is present, the implant may be removed and a
wider implant placed to obtain rigid fixation. Usually, the osteotomy site does
not need to be further prepared for the wider implant. However, a minimum
of 1.5 mm of bone should be present on the facial aspect of the ridge after
implant placement.
Remove Implant, Graft, Let Heal.

Usually, the ideal technique for a mobile implant, which will lead to
decreased implant morbidity, is to remove the mobile implant, graft the site,
and allow for sufficient healing prior to implant placement.
Remove Implant, Graft, Replace Implant.

An often-used technique, which has the highest possibility of complications,
is removing the mobile implant, replacing the implant, and grafting the areas
with little bone contact.
Facial Dehiscence After Implant Placement

After implant placement, it is not uncommon to have facial plate dehiscence
on the buccal aspect of the implant. Because bone resorbs from the facial
aspect, usually less than 1.5 mm of facial bone is present after final implant
placement. Thus, if inadequate bone is present, this may lead to future soft
tissue complications and increased implant morbidity.
Etiology
Bony defects at the crest after implant placement will usually result in lack of
available bone width at the ridge level (Fig. 5.9) (e.g., a division B ridge that is
compromised in width ∼<6 mm).
FIG 5.9 Facial dehiscence after implant placement. (A) Ideal implant position in
relation to ridge. (B) When lingual bone is higher than buccal bone, implant
placement will result in a facial bony dehiscence. (C) 3-D image of implant
placement in division B bone. (D) Autograft from osteotomy site. (E) Defects packed
with autograft. (F) All sites grafted with bone retained within surgical drills prior to
closure.
Prevention
All ridges should be modified to obtain a division A bone (e.g., >6 mm width
and >12 mm of bone height) before osteotomy initiation. After implant
placement, 1.5 mm of facial bone should be present or the area should be
grafted.
Treatment
After implant placement, if there exists less than 1.5 mm of bone on the
facial aspect of the ridge, the site may be grafted with autogenous bone
(ideally). The autogenous bone may be obtained from fragments gathered
from the flutes of the surgical drills during the osteotomy preparation. The
consistency of this bone allows for ease of packing, and the graft will have
less of a chance of migrating. Allograft bone is not preferred because it tends
to migrate easily after placement and is an added expense.
Loss of Facial Plate When Placing an Implant

When placing implants in bone that is compromised in width (∼division B),
it is not uncommon to fracture or lose the facial plate of supporting bone.
This leads to a compromise in the healing of the implant and the longevity of
the implant and prosthesis.
Etiology
Ideally, the width of bone needs to exceed 6.0 mm for placement of a 4.0-mm
diameter implant. When compromised width of bone exists, the trauma of
the osteotomy or the placement of the implant may fracture or “pop off ” the
buccal plate. This is most likely the result of the buccal plate being thinner
than the lingual plate, which results in the facial plate being more
susceptible to fracture (Fig. 5.10).
FIG 5.10 (A) Facial plate fracture leading to exposure of the implants after
placement. (B) Prevention includes grafting site prior to implant placement to restore
site to ideal dimensions prior to implant placement. (C–D) Grafting facial aspect of
implant with autogenous bone harvested from surgical burs.
Prevention
Determine the available bone prior to implant placement. If nonideal width
of bone is present, site development, including grafting, is indicated to
obtain a division A bone. The osteotomy preparation should be in one plane,
and care should be exercised to not deviate from the original angulation. If
division B bone is present, ridge augmentation is recommended to achieve a
division A ridge prior to implant placement.
Treatment
After implant placement, if a fracture or loss of the buccal plate exists,
treatment will depend on the extent of the deficit.
Loss of Entire Buccal Plate.

If the entire buccal plate is lost or if mobility of the implant exists, the ideal
treatment should include grafting then allowing for sufficient healing before
implant placement.
Partial Buccal Plate Still Intact.

If no mobility of the implant is present and the facial plate is partially intact,
the facial area can be grafted, ideally with autogenous bone from the
osteotomy site (e.g., surgical drill).
Not Altering Surgical Protocol in Poorly Dense

Bone
Many studies have shown the greatest risk of surgical failure is observed in
the softest bone type (D4), especially when found in the maxilla. To combat
this problem, Misch developed a different surgical protocol for the various
bone qualities in 1988. The implant design, surgical protocol, healing times,
treatment plans, and progressive loading time spans are unique for each
bone density type.
Etiology
Fine trabecular (D4) bone has very little density with minimal to no cortical
crestal bone. The most common locations for this type of bone are the
posterior molar region of the maxilla in a long-term edentulous patient, in an
augmented ridge (grafted for height and width with particulate bone or
substitutes), or in a sinus graft.
The tactile sense during osteotomy preparation of this bone is similar to
stiff, dense Styrofoam or soft balsa wood. The bone trabeculae may be up to
10 times weaker than the cortical bone of D1. The BIC after initial loading is
often less than 25%. A CBCT scan with reformatted images of D4 bone has a
Hounsfield number (or equivalent) of less than 375 units (Fig. 5.11).
FIG 5.11 Implant placement in less dense bone. (A) D3 to D4 type of poor bone
density showing lack of cortical bone and fine trabeculae. (B) Osteotomes to
compact the existing bone, increasing bone implant contact, should be used in D3
and D4 bone quality of bone. (C) Implant in D4 type of bone should be countersunk
in comparison to better-quality bone (D2). (C, From Misch CE: Contemporary implant
Prevention
Osteotomy Drills.
The implant surgeon should not prepare D4 bone with rotating drills, which
use an extraction technique to remove bone during preparation of the
osteotomy. These types of drills in D4 bone will result in distortion of the
osteotomy site (enlargement). Ideally, a compaction technique should be
used with osteotomes, which expands the bone by compressing the
trabecular bone.
Insertion With Handpiece.

The implant should be allowed to self-tap with the use of a slow-speed, high-
torque hand piece. A hand wrench is contraindicated because it will widen
the osteotomy (i.e., make elliptical) and possibly result in a lack of rigid
fixation of the implant. The pressure on the implant during insertion
corresponds to the speed of rotation, and the implant proceeds to self-tap the
soft bone.
One-Time Placement.
Once inserted, the implant should not be removed and reinserted. Instead, a
one-time placement is mandatory because removal of an implant in this bone
will lead to less bone at the interface.
Countersink.
The implant is countersunk in this bone if any risk of loading is expected
during healing (e.g., under a soft tissue–borne denture). Countersinking the
implant below the crest reduces the risk of micromovement during healing
in this very soft bone. No countersink drill is used before implant placement
because this decreases the density of bone at the crestal area.
Treatment
When a poorer type of bone exists, increased healing times and progressive
bone loading should be adhered to. Increased healing time is indicated to
allow for more bone to remodel at the surface and to intensify its trabecular
pattern. The additional time also allows a more advanced bone
mineralization and increased strength. Six or more months of undisturbed
healing is suggested. The compression technique for surgery (e.g.,
osteotomes), the extended healing time, and progressive bone loading
protocol allow the remodeling of the poor quality bone into a more organized
and load-bearing quality similar to D3 bone before the final prosthetic
loading of the implants.
Overheating the Bone
One of the most common complications that has been associated with early
implant failure and bone loss is overheating of the bone during osteotomy
preparation. This usually is a result of the surgical osteotomy protocol.
Etiology
The amount of heat produced in the bone is directly related to the amount of
bone removed by each drill.11 A 3-mm pilot drill has been shown to generate
greater heat than a 2-mm pilot drill.12 As a result most manufacturers suggest
the first drill be 2 mm or less in diameter. In a similar fashion, the amount of
heat generated by successive drills is also directly related to the increase in
drill diameter. A 3-mm drill after a 2-mm drill removes 0.5 mm of bone on
each side of the drill. A 2.5-mm drill after a 2-mm drill removes only 0.25 mm
of bone on each side of the osteotomy. The smaller incremental drill size
allows the surgeon to prepare the site faster, with less pressure and less heat.
In addition, when large increases in drill diameter are used to prepare bone,
the surgeon may inadvertently change the angulation of the drill because the
larger drill is removing a greater bone volume and the tactile sense is
decreased. As a result, an elliptical osteotomy may be prepared that does not
correspond accurately to the round implant diameter. The gradual increase in
osteotomy size also reduces the drill chatter at the crestal opening, which can
inadvertently chip away pieces of bone on the crest, where complete bony
contact is especially desired. The gradual increase in drill diameter also
keeps each drill sharper for a longer period, which also reduces the heat
generated (Fig. 5.12).
FIG 5.12 Overheating bone. (A) D1 type of bone: highest amount of bone is
present at the interface, which predisposes to heat generation. (B) Area of bone
necrosis from overheating around implant (arrow). (C) Devitalized bone (D) and
vitalized bone (V). (D) Use copious amount of irrigation during osteotomy
preparation to avoid overheating the bone. (E) Caution should be exercised with the
use of surgical templates because minimal irrigation enters the osteotomy site and
overheating the bone is a common problem. (F) Modification (removal of buccal
flange) of the template to allow for increased irrigation (i.e. external irrigation;
arrow). (A and C, From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
Prevention
Intermediate Drills.
Some manufacturers do not utilize an intermediate drill in their drilling
protocol. However, a decrease in the heat and trauma generated is found with
the intermediate drill. Gradual increases in drill diameter reduce the amount
of pressure and heat transmitted to the bone, especially in the presence of
dense and thick cortical bone.
Copious Amounts of Saline.

Along with external irrigation from the surgical drills, increased irrigation
may be obtained by using internal irrigation (through the surgical bur) or
with supplemental irrigation via a syringe.
Bone Dance.
The bone-dancing technique was introduced by Misch in 1988 to reduce the
amount of heat generation. When preparing the osteotomy, small increments
of bone should be removed, and by using the up-and-down motion of the
drill, irrigation may enter the osteotomy site easier.
Use of Sharp, New Drills.

Drills that are dull will increase heat generation, causing the possibility of no
bone integration. On average, surgical drills should be replaced
approximately every 20 to 30 autoclave cycles.
Drill Speed.
Sharawy and Misch have shown that the drill speed in hard, dense bone
should be approximately 2000 to 2500 RPM. Osteotomy preparation at higher
speeds with sharp drills elicits less risk of osseous damage and a decreased
amount of devitalized zone adjacent to the implant.12 Yeniyol et al have
shown that drilling at very slow speeds results in a higher degree of bone
fragmentation.13
Surgical Templates.
Surgical templates often result in overheating of the bone because of the
decreased space between the guide tubes in the template and the drill size.
Ideally, the template should be modified to open up the facial aspect of the
template so supplemental irrigation may be utilized.
Treatment
If known excess heat generation occurs during implant placement, ideally the
implant should be removed, regional acceleratory phenomenon (RAP)
initiated, and the site grafted for future implant placement. If bone width is
available after sufficient RAP is completed, a wider implant may be placed.
Implant Pressure Necrosis

A possible cause of early implant failure is pressure necrosis.
Overcompression of the crestal bone has been shown to be a contributing
factor in implant failure.14 It is postulated that excessive tightening of the
implant creates compression forces within the crestal bone around the
implant. This may impair the microcirculation and lead to bone resorption.
Etiology
Pressure necrosis from implant placement may increase the devital zone of
bone around the implant or even cause short-term neurosensory impairment
when the implant site is in the vicinity of the mandibular canal. This most
often occurs where there exists a cortical component of bone in the crestal
region (∼D1–D2 bone). If a crestal bone drill is not used in higher bone
density with a cortical component, excess stress will be generated upon
insertion of the implant, which will lead to a devitalized zone (Fig. 5.13).
FIG 5.13 Pressure necrosis. (A) Normal implant placement level to the ridge. (B)
To decrease pressure necrosis in highly dense bone (~D1), the implant is
unthreaded ≈1 mm after insertion.
Prevention
Torque.
The implant should not be tightened into the osteotomy, such as a nut onto a
bolt. A torque value up to 35 N/cm is considered safe with most threaded
implant designs.
Crestal Bone Bur.
Because most implants have a wider crest module (wider diameter of the
neck of implant in comparison to implant body), greater stress can be
concentrated upon placement in D1 and D2 types of bone. To decrease crestal
pressure, the implant may be placed to ideal position, then backed off
approximately 1 mm to avoid pressure necrosis.
Treatment
Ideally, the thickness of crestal bone and bone quality type should be
ascertained prior to implant osteotomy preparation. This is easily evaluated
on a CBCT radiographic examination. If a large cortical component of bone is
present and the implant placed is known to contain excess pressure, the
implant should be removed and the crestal bone modified. The implant
should be then reinserted.
Bone Spreading Complications

Bone spreading has become a popular surgical technique to expand the
available bone width prior to implant placement. Since Tatum developed the
bone spreading technique in the early 1970s, the expansion technique has
been primarily used in regions of division B bone to increase the bony width.
However, the easiest edentulous ridges to expand are division A bone volume
with associated D3 or D4 bone densities. The narrower the bone, the greater
the risk of fracture of the facial plate. The softer the trabecular bone quality,
the lower the elastic modulus and the greater the viscoelastic nature of the
ridge. Therefore, the less dense the bone, the easier and more predictable the
bone expansion. There exist three main complications that may occur during
bone spreading.
Splintering of Facial Plate
Etiology.
The most common complication of bone spreading, especially in division B
bone that is D2 quality, is splitting the facial plate during the procedure.
Once this occurs the surgeon must decide whether to continue, place the
implant, and perform a barrier membrane layered bone graft, or abort the
procedure and place only a bone graft (Fig. 5.14).
FIG 5.14 Bone spreading complications. (A) Facial dehiscence after implant
healing. (B) Autogenous and allograft bone graft with tent screws. (C) Barrier
membrane is placed (e.g., accelular dermal matrix). (D) A second complication
occurs with the bone grafting being too facial leading to a facial plate fracture,
incision is made slightly lingual to center of ridge. (E) Osteotomy is made lingual to
center of ridge. (F) Bone spread maintaining buccal plate. (G) Care should be
exercised to minimize compromising facial plate thickness. (H) Implant placement
with maintaining buccal plate intact.
Prevention.
Make sure there exists sufficient bone for bone spreading and good surgical
technique. A common misconception is that division C minus width (C−w)
ridges may be spread with simultaneous implant placement. This often
results in fracturing the facial plate. Bone spreading should be restricted to
division A and B ridges.
Treatment.
The implant may be inserted when the following factors are positive: (1) the
implant is rigid at the proper depth, (2) the implant is in a favorable
angulation, and (3) the facial plate is farther facial than the implant (it is
fractured, but expanded). Under these conditions the barrier membrane
layered graft procedure will predictably restore the facial bone, and the
implant is not compromised. If one of these three factors is negative, it is
more prudent to remove the implant, harvest additional autograft, and
perform the bone graft without the implant in situ.
Dehiscence
Etiology.
Another complication of bone spreading is the dehiscence of the labial plate
after healing and bone remodeling around the implant. This results from
insufficient bone quantity preoperatively. Because of its modulus of elasticity
the expansion of the labial plate is not beyond the point of permanent
deformation, and the bone does not fracture. It will attempt to rebound to its
original size during remodeling. As a result, during bone remodeling the
bone does not heal in its expanded position, instead returning to its initial
narrow dimension, and the implant fenestrates the labial plate. When bone
expansion is performed at implant placement, a stage II uncovery with
reflection of the facial soft tissue is advantageous to evaluate the facial plate.
Prevention.
To decrease the possibility of bone dehiscence after bone spreading, the
technique should be restricted to division A and B ridges.
Treatment.
When a dehiscence is observed, a barrier membrane with layered graft
approach is indicated to restore the facial plate. Because the implant is
integrated to the remaining bone, the implant may be progressively loaded
after a 3- to 4-month period, rather than waiting 6 to 9 months, as with
augmentation by barrier grafts alone.
Poor Position
Etiology.
The third complication of bone expansion is a poor final implant position,
usually more facial than ideal. The thicker palatal cortical plate tends to push
the osteotomes to the facial; if the implant surgeon is unaware of this
malpositioning, the end result will be an implant that is too facial and will be
problematic esthetically and functionally.
Prevention.
Constant attention of angulation and modification of the palatal bone with
side-cutting drills (Lindemann drills) is necessary to prevent this problem.
Treatment.
The final prosthesis should not be compromised for the advantage of placing
the implant during the surgery. Bone augmentation and reentry 6 months
postoperatively often improve the implant position and, as a result, the final
restoration.
Inability to Determine True Location of Mental

Foramen on CBCT
If the true position of the mental foramen cannot be determined from the
CBCT, reflection of the foramen is recommended to determine the exact
position.
Etiology
Although rare, sometimes it is difficult to determine the exact location of the
mental foramen or if an anterior loop exists from a CBCT. Because of the
possible consequences of placing an implant too close to the mental foramen,
care must be exercised to prevent impingement.
Prevention
A CBCT evaluation utilizing the cross-sectional and 3-D images should be
used to clearly identify the mental foramen. In some cases, the brightness
and contrast will need to be altered to depict the mental foramen.
Treatment
The primary incision is extended anterior and posterior with releases to
minimize stretching of the tissue so the foramen may be identified. The
location of the foramen is variable, depending on age, ethnic background,
amount of resorption, and skeletal relationship. Initially, the periosteum is
reflected off the residual crest, and a moist surgical sponge can be used to
wipe the periosteum off the dense labial cortical plate to identify the superior
aspect of the foramen. After the superior aspect of the foramen is identified,
the tissue is reflected anterior and posterior to confirm the exact location of
the foramen (Fig. 5.15).
FIG 5.15 Mental foramen reflection. (A) When reflecting the mental foramen, a 3-D
CBCT image is used to determine position in reference to an adjacent tooth
(arrows). Reflection should be initiated anteriorly and posteriorly (green arrows) to
allow for access to the foramen. (B) Full-thickness reflection exposing the superior
aspect of the mental foramen. (C) Mental foramen exposure (blue arrow).
Incisive Foramen Implant Placement Complications

The incisive foramen region, rather than a central incisor site, may also be
used to insert an endosteal implant, especially when an overdenture is the
intended final prosthesis.15 The incisive canal ranges in length from 4 to 26
mm and is directly related to the height of bone in the premaxilla. As
alveolus height is resorbed, the canal reduces in length; therefore division A,
B, and C−w bone have greater canal length than division C−h and D. The
incisive canal has an average axis of 70 degrees with a range of 57.0 to 89.5
degrees from the horizontal plane.16 This structure contains terminal
branches of the nasopalatine nerve, the greater palatine artery, and a short
mucosal canal (i.e., Stensen duct). A vertical projection above the incisive
canal along the nasal floor is called the premaxillary wing. The nasal process
of the premaxilla rises 2 to 3 mm above the nasal floor. As a result, when 7 to
11 mm of bone is present below the nasal floor, a large osteotome may create
a greenstick fracture in this process above the foramen and permit the
placement of a 9- to 14-mm implant. The foramen is usually 4 to 6 mm in
diameter at the crest and narrows down to 4 mm at the apex. Implants
inserted at the same time as the soft tissue is curetted are usually 5 to 6 mm
in diameter.
Prevention/Treatment
There exist many possible complications with incisive foramen implants.
The first surgical complication of an incisive foramen implant is the result
of an implant that is too small for the foramen and not properly fixated. The
implant may be inadvertently pushed through the incisive canal and into the
nares proper. Because the patient is lying on their back during the surgery,
the implant may fall back into the soft palate, then into the trachea or
esophagus. If the implant disappears from the oral site, the patient's head
should be turned to the side immediately, then down and forward. A nasal
speculum and tissue forceps may then be used to recover the implant.
A second surgical complication may include bleeding from the incisive
foramen. Although this complication is very rare, it is possible. When
reflection of the palatal tissue off the incisive canal is associated with arterial
bleeding, a blunt bone tap (mirror handle) may be placed over the canal and
a mallet used to hit the instrument firmly, crushing the bone over the artery.
After several minutes the procedure may continue, and the implant insertion
will obdurate the site and arrest the bleeding.
The short-term complication of an incisive foramen implant is associated
with enucleation of the soft tissue from the foramen. Although the author
has not witnessed this complication, neurologic impairment of the soft
tissues in the anterior palate may exist. This may lead to paresthesia to the
soft tissue or a dysesthesia, with a report of a burning/painful sensation. It is
logical to include this risk in an informed consent. If it should occur, removal
of the implant for dysesthesia is warranted, whereas paresthesia of the palate
most likely is a condition the patient can tolerate without significant issues.
In many cases the patient will regain neurosensory feeling from collateral
innervation.
A long-term complication that has been observed twice by the author is the
regeneration of the soft tissue in the incisive canal, resulting in bone loss
around the implant. When the implant is removed and the soft tissue
biopsied, nerve fibers can be seen reinvading the site. This most likely occurs
because the implant was too small for the size of the foramen, and the soft
tissue can reform around the implant. Treatment of this complication
includes removing the implant and, if necessary for the treatment plan,
regrafting and/or reimplantation (Fig. 5.16).
FIG 5.16 Incisive foramen implant failure. (A) Bone loss and probing depths
resulting from not removing all soft tissue from the incisive foramen implant. (B)
Removal of implant with trephine bur. (C) Implant removed with soft tissue interface.
(D) Histologic examination of the soft tissue around the implant reveals the contents
of the incisive canal are reforming around the implant. (E) Histologic examination
demonstrates nerve fibers in the soft tissue around the implant.
Implant Placement Impinging on the Nasopalatine

Canal
There exists a close anatomic relationship between the nasopalatine canal
and the maxillary central incisor area. The anterior maxillary area has high
esthetic importance, and ideal implant placement is mandatory. The
nasopalatine canal is located in the maxillary palatal midline, just posterior
to the central incisor area. There is a funnel-shaped opening of the canal into
the oral cavity, which is known as the incisive foramen. The canal divides into
two canaliculi towards the nasal cavity, and terminates at the nasal floor as
the foramina of Stensen. The canal contains the nasopalatine (incisive) nerve
and the terminal branch of the descending nasopalatine artery.
Etiology
When the maxillary teeth are lost, the buccal plate anterior to the canal will
lose up to 60% of its width. Also, the canal diameter of the canal and
foramina (nasopalatine foramina and incisive foramen) will increase in size.17
When implants are placed in this area, they may impinge upon the area and
be in contact with soft tissue, which may lead to a soft tissue interface or
implant failure. (Fig. 5.17).
FIG 5.17 Implant impingement on the nasopalatine canal. (A) Axial image depicting
a very large nasopalatine canal. (B) 3-D interactive treatment planning showing
implant impingement into the canal. (C) Implant violating the nasopalatine canal
resulting in soft tissue interface.
Prevention
To prevent implant placement into the nasopalatine area, CBCT imaging is
recommended to determine the dimensions and morphology of the
nasopalatine canal. The nasopalatine canal has many variations ranging from
one canal to various types of “Y” configurations.
Treatment
When it is determined that an implant will impact upon the nasopalatine
canal, alternative procedures must be considered. One such treatment is for
enucleation of the canal, then bone grafting, with subsequent implant
insertion. Alternatively, implants may be placed directly into the canal,
usually for overdenture treatment plans.18
Stage II Uncovery Surgery Complications
Tissue Punch Reducing Amount of Attached
Tissue
A common technique to uncover or expose a healed implant (stage II
surgery) is the use of a tissue punch that is slightly larger than the implant
placed. The tissue punch is preferred by many practitioners because it is
quick and easy; however, it may be detrimental to the soft tissue health of the
implant.
Etiology
A tissue punch is often used because it is fast and simple and can be used
without reflecting the periosteum. However, this may lead to potential
prosthetic and long-term complications because it decreases the available
amount of attached tissue. The tissue punch is placed directly over the top of
the implant and pressure is exerted to remove the tissue, exposing the
implant cover screw. However, the disadvantage of this technique is the
keratinized tissue that is sacrificed, which is often much larger than the
diameter of the implant (Fig. 5.18).
FIG 5.18 Tissue punch. (A–B) Tissue punch used when inadequate attached
tissue will often result in a mucogingival defect. (C) Lack of sufficient attached tissue
for the final prosthesis because of excessive tissue removal. (D) Care should be
exercised in using high speed handpiece and diamond bur as damage to the implant
body can result.
Prevention
If inadequate keratinized tissue is present (<3 mm), a tissue punch should
not be used to uncover an implant. A tissue punch that is significantly larger
than the implant crest module should not be used because excessive tissue
will be removed.
Treatment
In cases of inadequate keratinized tissue, a slightly lingual incision is made
to create a soft tissue flap to uncover the implants. Tissue grafting with
autograft or AlloDerm may be used to increase attached tissue volume
surrounding the implant.
Bony Defects at Uncovery

On occasion, a vertical or horizontal defect may be revealed around the
uncovered implant at the second stage surgery. This often presents a very
difficult decision for the clinician as to the course of action.
Etiology/Prevention
The etiology for this type of defect are often similar to those of premature
implant exposure and include crestal bone trauma during surgery,
inadequate bone volume prior to placement, excess torque from implant
insertion (especially with wider crest modules), bone flexure or torsion in the
posterior mandible, local patient habits that load the implants during
healing, incision line opening, postoperative infection, implant surface
contamination, idiopathic bone loss, or healing factors related to systemic
disease. Proper treatment planning and good surgical technique is
recommended to minimize bone loss after implant placement.
Vertical Defects
Treatment.
If a vertical defect filled with soft tissue is identified anywhere around the
implant, a curette is used to eliminate the tissue. When soft tissue is
removed from around a tooth, the root is scraped because the tissue attaches
to the cementum. The fibrous tissue in a vertical defect around an implant is
not attached to the implant. Therefore, the bone is scraped, but not the
implant. This loosely bound and unorganized tissue is relatively easy to
remove at this time. The implant surface should not be scratched or
contaminated during this procedure. If soft tissue is present around the
threads, a wire brush bur maybe used to remove the tissue. The extent of
bone loss is assessed and should be less than 3 mm if the implant is to be
uncovered at this appointment. Special brush burs (Salvin) may be used to
remove tissue from the implant surface (Fig. 5.19).
FIG 5.19 Removing tissue from defect. (From Misch CE: Contemporary implant dentistry,
Defect greater than 3.0 mm.

If the vertical defect around the implant is of moderate depth (greater than 3
mm) for more than 25% of the circumference, a bone graft/barrier membrane
is placed over the grafted defect, and the soft tissue is reapproximated. This
prevents soft tissue ingrowth into the defect and provides an improved
environment for the bone graft healing time against the implant surface. In
this scenario the second stage uncovery is delayed for approximately 2 to 4
months, depending on the size of the defect.
When bone loss exposes the threads of the implant body, the ability to
reform bone in the defect when the implant is uncovered and loaded is
reduced. When the implant has not been exposed before the uncovery
procedure, the implant body is usually not contaminated by microorganisms
because it has been under soft tissue. The full-thickness reflection of the
region has exposed areas of vital bone not involved in the implant support.
This bone may be harvested and packed into the vertical defect (after the soft
tissue in the defect has been thoroughly removed). The defect and
surrounding area are overpacked. When the implant defect is larger than 3
mm, the most predictable method to correct the condition is with a
particulate autologous bone graft covered by a resorbable membrane (e.g.,
AlloDerm, Biomend), and the soft tissue is reapproximated over the
membrane, bone graft, and implant for an additional 8 to 12 weeks of
healing. A vertical defect greater than 3 mm is usually grafted unless it
represents half or more of the total implant height, in which case the implant
should be removed.
Defect less than 3.0 mm.

When the vertical bone defect around an implant is less than 3 mm, the
implant may be uncovered and used in the current condition for the
prosthetic abutment. After the soft tissue is removed from a defect, the
surrounding bone is again evaluated. In the case of a vertical bone defect of
less than 3 mm, there are three surgical options:
First, an osteoplasty may eliminate the vertical defect when the reduced
bone-implant interface does not compromise the prosthetic support or
esthetics. The permucosal abutment (PME) is placed at the same
appointment (Fig. 5.20).
FIG 5.20 Osteoplasty with bur. (From Misch CE: Contemporary implant dentistry, ed 3, St
A second method to correct a vertical defect less than 3 mm is to curette

the defect and overfill the region with an autograft. The PME may be added
at the same appointment and the tissue approximated around the site. When
there is a desire to have thicker soft tissue around the site, a barrier
membrane (e.g., AlloDerm) may be used over the implant site and covered
with soft tissue (Fig. 5.21).
FIG 5.21 A method to correct a vertical defect less than 3 mm (A) is to curette the
defect and fill the region with an autograft (B). The implant may be exposed with a
permucosal extension or covered by a membrane when additional soft tissue
thickness is desired. (C) The implant on the left has a vertical defect less than 3 mm
deep. (D) A wedge is driven into the bone in the appropriate side, and vital bone is
pushed up against the implant. (From Misch CE: Contemporary implant dentistry, ed 3, St
A third alternative to correct a vertical defect on the mesial and distal

region is to drive a wedge into the bone several millimeters away from the
implant body. Tapping a wedge-shaped osteotome into the distal bone
compresses vital bone up against the implant body. The wedge-shaped defect
created in the ridge as a result of the osteotome is several millimeters away
from the implant and is surrounded by bone; this defect will heal without
consequence. A facial or lingual vertical defect may be corrected by taking a
blunt instrument with a mallet and compressing the facial or lingual bone
against the implant body. This technique also places live, viable bone
(autogenous) adjacent to the implant body. The PME is placed at this
appointment.
Horizontal Defects
Treatment.
A horizontal bony defect of bone around the implant body may also be
treated in several ways.
Greater than one-half length.

When horizontal bone loss around an implant is more than half of the
implant body, the implant should be surgically removed and the site grafted
at the uncovery appointment for future implant placement.
Less than one-half length.

The most predictable method to treat horizontal bone loss that is less than
50% of the implant body is to reduce the soft tissue thickness to decrease the
probing depth around the implant. The soft tissue may be apically
repositioned, exposing a portion of the implant body into the oral cavity. If
threads or a rough surface are present above the bone, an aluminum oxide
(“white”) stone and rubber wheel are used under copious irrigation to
smooth the region and limit plaque accumulation. A cement-retained
prosthesis on an implant with horizontal bone loss may be placed on the
implant body in esthetic regions.
Another option to address horizontal bone loss is to grow bone above the
defect, and this method is used when the final prosthesis is a fixed-prosthesis
1 (FP-1) or additional bone-implant interface is required to withstand the
forces exerted on the prosthesis. To improve the amount of bone formation,
several steps may be taken. The first is to use autogenous bone for the graft.
In most cases, bone is harvested and placed on the crest after the region has
been curetted to increase blood supply and increase the regional acceleratory
phenomenon. A barrier membrane is also placed over the site to prevent
fibrous tissue ingrowth into the region. Anaerobic bacteria are often growing
on the implant body when bone loss is present and should be mechanically
removed. In addition, before grafting the first-stage cover screws are
removed, and the internal cavity of the implant body is thoroughly flushed
with chlorhexidine 0.12% before replacing the screws into the implant body.
The tissues are reapproximated over the bone graft and membrane with
primary closure. The second stage uncovery is delayed for approximately 3 to
4 months, depending on the size of the horizontal defect and bone graft.
Excessive Tissue Thickness at Stage II Surgery

The thickness of the overlaying crestal tissue is evaluated once it is reflected.
Soft tissue greater than 4 mm in thickness will result in a less-than-ideal
pocket depth around the implant.19,20
Etiology
It is not uncommon when implants are placed in edentulous ridges to have
excessive tissue thickness before and after implant surgery. This is most
common in the posterior maxilla and patients with a thick biotype (Fig. 5.22).
FIG 5.22 (A) An incision is made on the periosteal side of the palatal flap, and the
excessive connective tissue is excised to decrease the overall palatal tissue
thickness. (B) The tissue with a reduced thickness may then be approximated
around permucosal extensions 3 to 5 mm in height. (C) A gingivoplasty is often
performed in abundant areas of keratinized, attached tissue, such as on the palate,
to reduce sulcus depth around the implant. (From Misch CE: Contemporary implant
Prevention
Preoperative assessment of tissue should be conducted or the tissue maybe
thinned out at the implant placement appointment.
Treatment
The tissue is relieved from the periosteal surface, especially in the labial flap,
until it is less than 3 mm thick. If abundant attached tissue is present in the
palatal region of the maxillary implants, a gingivoplasty may be performed.
When the tissue requires apical repositioning or when it is 3 to 4 mm thick
and may grow over the healing abutment, the suture groove may be used. A
suture is placed next to the healing abutment (PME) and is tied to lower the
tissue level. Tissue forceps lift the suture from the incision line, and the
suture is then rotated to form a loop. The loop is placed over the enlarged
healing abutment and into the suture groove or under the healing cap. The
suture may then be tied, securing the tissue at the height of the suture
groove. A similar technique is used on the other side of the healing
abutment. These two sutures (one on each side) hold the tissue at the level of
the suture groove and prevent it from lifting up and over the healing cap
during soft tissue healing (Fig. 5.23).
FIG 5.23 (A) The suture groove helps to apically reposition the tissue so it will
remain less than 3 to 5 mm thick to reduce the sulcus depth. (B) The suture groove
in the permucosal extension may be used to loop the suture around the groove and
tie the tissue at a more apical position. (C) The most distal implant to the right has
mobile tissue around it, which is difficult to reposition apically. The suture is placed
on the distal aspect and looped over the suture groove to act as a soft tissue
retainer. (D) When the suture is tied around the permucosal extension, it apically
positions the tissue around the implants. (From Misch CE: Contemporary implant dentistry,
Loss of Papilla After Uncovery (Split-Finger

Technique)
When the implant-bone interface is acceptable, the exposure of the implant
body should be accomplished with the soft tissue final architecture in mind.
To achieve and maintain the proper soft tissue architecture, several options
are available, depending on the soft tissue appearance before stage II
uncovery. It is imperative, especially in the maxillary anterior region, that
exposure of the implant does not lead to gingival recession or loss of papilla.
Prevention
An ideal stage II uncovery procedure developed by Misch is called the split-
finger technique.21 This technique is utilized to increase the amount of papilla
height around the implant body.
Treatment
Maintain Papilla.
An incision is made in the gingival sulci of the adjacent teeth. The incision is
started at the distolingual line angle of the adjacent teeth and forms a loop at
the facial emergence location of the implant crown. This creates two
“fingers” at least 2 mm in width adjacent to each natural tooth. Once
elevated, these two facial fingers will become the facial aspects of the
interdental papillae. A central palatally supported finger is also created. The
tissues are then elevated, and the implant cover screw is exposed and
replaced with an abutment. The palatal finger may then be split into two
segments (i.e., the split-finger approach). Each segment is rotated to the
interproximal region to support the elevated facial fingers. A 4-0 or 5-0
modified mattress suture positions the papillae in the proper location, next
to a transitional crown (Fig. 5.24).
FIG 5.24 (A) When the desired papilla height is almost perfect, a split-finger
technique may be used. (B) An incision is made in the sulcus of the adjacent teeth
and continues from the palatal aspect of each tooth for 1.5 to 2.0 mm and loops to
the facial, parallel to the adjacent interproximal teeth. The incisions then connect on
the facial aspect at the desired midfacial emergence of the crown. (C) The facial
fingers are elevated facially. (D) The palatal finger is reflected palatally. (E) The
palatal finger is split into two sections (mesial and distal). (F) This creates four
interfacing fingers (two on the facial and one toward the palate). (G) The implant
abutment (or permucosal extension) is added, and each split palatal finger is
positioned under the facial corresponding finger. (H) The split palatal fingers are
rotated and support the appropriate facial finger. (I) The implant abutment and
elevated facial fingers are in position. (J) The temporary crown is cemented, and the
fingers are sutured into position. (K) After soft tissue maturation, the final crown is
fabricated. (L) The final crown in position with properly developed interdental
papillae. (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
Increase Papilla Height.

When additional height is required, the split-finger technique may be used in
conjunction with a connective tissue graft or AlloDerm to further augment
the tissue height. This procedure may also be performed at insertion surgery,
when a one-stage approach is desired.
Once the soft tissues are subtracted or added to obtain the desired
emergence contour, the surgeon has basically two options to maintain this
region. The first option is that a PME abutment may be inserted. Its size and
shape should be smaller than the cervical contour of the final crown and
extend through the tissue 1 to 2 mm. The emergence of the PME abutment
will develop the initial soft tissue form. A wide-profile PME abutment should
not be used because it may cause gingival shrinkage and limit the restoring
dentist's ability to shape it into its ideal form. A transitional prosthesis is
recontoured to fit over the healing cap for the next few weeks, until the
patient is seen for the first prosthetic appointment. The soft tissue heals and
is allowed to contour to the healing abutment or permucosal device. Usually,
4 to 6 weeks is needed for ideal tissue maturation.
Reverse Torque Testing Complications

Reverse torque testing (RTT), used as verification for rigid fixation, involves
placing a defined reverse torque (counterclockwise) to the implant (via
mount) at stage II uncovery surgery. The level of applied torque ranges from
10 to 20 N/cm. Implants failing such testing are presumed to be
nonintegrated, likely to become early loading failures, and are not
recommended for use as prosthetic abutments. Reports in the literature have
suggested RTT at stage II surgery or to assess an implant suitability for
immediate loading.22 Two alleged advantages are its use as a biomechanical
measure of initial stability and its use as a definitive verification of initial
osteointegration.
Etiology
The RTT is suggested to be most beneficial in less dense bone, yet bone of
this density is most at risk of failure during the RTT evaluation. In addition,
bone is often only 60% mineralized at stage II uncovery after the surgical
trauma from stage I surgery. According to computer densitometry reports,
bone may be more dense and the bone interface stronger on the day of
surgery, compared with the stage II uncovery date.23,24 It takes 52 weeks after
initial surgery for bone to be completely mineralized. The mineralization of
bone is related to its strength. Using RTT at stage II uncovery evaluates the
interface when it is weak and more at risk to fracture from overload. In
addition, at 4 months the bone is often still histologically woven bone rather
than lamellar bone. Woven bone is unorganized and weaker than the load-
bearing lamellar bone, which is more desirable at the implant interface. An
RTT at uncovery does not permit this improved interface to develop before
testing. RTT of implants too early in the healing process (relative to bone
density) is more likely to lead to the removal of implants that would
otherwise be integrated.
Prevention
In the author's opinion RTT presents too many subjective variables.
Misjudgment can damage the bone-implant interface and prolong treatment
and increase costs associated with the extra reparative treatment. The desire
for objective standards for clinical verification of osteointegration is
understandable. The most common methods of clinical verification used
today, radiographs and manual mobility testing, have an admittedly
subjective component. However, they do not place the implant at risk and
have stood the test of time.
Treatment
It is recommended not to utilize a reverse torque test in the evaluation of the
dental implant integration.
Anesthesia/Platelet-Rich Fibrin
Complications
Inability to Obtain Mandibular Block
With the placement of implants in the mandible, profound anesthesia is a
crucial component of surgical success. In edentulous mandibles or patients
being treated with sedation, this may be difficult, and alternative anesthesia
techniques are warranted. The Misch Implant Institute has recommended for
years a rarely used technique in obtaining profound anesthesia in the
mandible, the Akinosi technique.
Etiology
With edentulous patients the Akinosi technique is preferred because
traditional techniques (Halsted block) require the use of reference points
(occlusal plane), which are not present in edentulous patients. Additionally,
many dental implant patients are sedated, which results in difficulty for the
patient to open fully for the injection.
Prevention
The implant clinician must understand and utilize profound, alternative
anesthesia techniques such as the Akinosi technique.
Treatment
The Akinosi block procedure is administered with the mouth in an almost
closed position or, because the patients often wear a denture, in an
approximate occlusal vertical dimension. In addition, it is a benefit when the
patient positions the jaw toward the side of the injection (e.g., slides the jaw
to the right for a right mandibular block-teeth edge to edge). A long, 27-
gauge needle is used in the syringe. The needle is bent 30 degrees near the
base, so the needle direction on a horizontal plane will be away from the
midline. This is advantageous because the ramus flares laterally as it
proceeds distal. The syringe and needle are placed parallel to the occlusal
plane, at the height of the maxillary mucogingival junction. The needle
penetrates approximately half its length (25 to 30 mm) before aspiration and
injection of anesthetic. For this technique, no bony landmark is used. The
Akinosi block is usually less painful for the patient because the anesthetic
fluid is injected into the top of the pterygoid triangular space, which has
more room for the solution. In addition, the top of this triangular space has
fewer muscle fibers in the pathway of the injection compared to the
penetration site of the Halsted block and is associated with less discomfort
(Fig. 5.25).
FIG 5.25 (A) The Akinosi block procedure for local anesthesia is more effective
than the traditional dental injection in the edentulous patient. (B) Akinosi technique:
The patient's mouth is almost completely closed or at the approximate occlusal
vertical dimension in a denture wearer. The cheek is retracted with the free hand to
expose the posterior teeth. The syringe is aligned parallel to the occlusal plane of the
maxillary molars, and the needle is positioned level with the mucogingival junction of
the maxillary second and third molars. The needle is inserted into the buccal
mucosa as close as possible to the medial surface of the mandibular ramus to a
depth of 25 to 30 mm without contacting bone. After careful aspiration, the
anesthetic solution is deposited approximately halfway between the mandibular
foramen and the neck of the condyle into the middle of the pterygomandibular
space. (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
Inadequate Blood Spin for Platelet-Rich Fibrin

Platelet-rich fibrin (PRF), described by Choukran et al, has become very
popular in the field of implant dentistry.25 The obtained fibrin platelet matrix
contains numerous growth factors that are responsible for cell mitosis,
increasing collagen production, recruiting cells to the injury site, initiating
angiogenesis, and inducing cell differentiation. After drawing the patient's
blood, a centrifuge process allows the formation of a fibrin mesh that is
enriched with platelets and growth factors. This natural fibrin matrix
concentrates platelets and growth factors and allows for enhanced hard and
soft tissue healing. Within the tube the fibrin clot is formed in the middle
layer. The upper layer contains the acellular plasma, and the bottom part
contains red corpuscles.
Etiology
When the centrifuge process does not work properly, a distinct middle layer
(PRF) will not be present. This may happen because of numerous
possibilities including:
• Delay in centrifuging blood (the longer the delay, the less clot formed)
• Insufficient time in the centrifuge
• Inadequate centrifuge RPM (3000 rpm)
• Test tube contains anticoagulant (e.g., chloral hydrate)
Prevention
The blood sample should be immediately placed in the centrifuge without
delay and spun for a minimum of 12 minutes.
Treatment
If the fibrin clot is not present, a new blood sample should be obtained and
the process is repeated (Fig. 5.26).
FIG 5.26 Inadequate PRF coagulant. (A) No distinct fibrin clot formed. (B) Ideal
spin includes the three distinct layers. (C) PRF clot.
Difficulty in Obtaining Blood Sample for PRF

Process
A failed blood draw is most commonly caused by improper needle position.
Ideally, with the use of a vacutainer, after penetration into the vein, negative
pressure allows for the rapid filling of the sample tube.
Etiology
If free flow of the blood into the tube is not present, it is most commonly due
to one of the following improper needle positions: (1) needle insufficiently
deep enough to penetrate vessel; (2) needle too deep, resulting in perforation
of vessel; (3) needle bevel against the wall of the blood vessel; (4) venospasm
resulting in the collapse of the vessel; (5) hematoma formation at the site of
needle entry; (6) intraarterial insertion (Figs. 5.27 and 5.28).
FIG 5.27 Ideal venipuncture technique. (A) Vacutainer armamentarium. (B) Enter
vessel with bevel up and at a 30-degree angle. (C) Once the vessel has been
entered, decrease angle slightly while advancing. (D) Press collection tube to
perforate, negative pressure will allow tube to fill with blood. The tube will fill until
pressure decreases (≈10 mL). The vacutainer is removed. (E) Final tube with blood
specimen. (F) Pressure is placed over venipuncture site.
FIG 5.28 Venipuncture troubleshooting. (A) Ideal needle placement. (B) Needle too
shallow, needs to be placed deeper into the tissue to perforate vessel. (C) Needle
too deep, should be removed and a new venipuncture site selected. (D) Vein
collapse, replace tourniquet, if still no flow, remove and select new site. (E) Bevel
against vein wall, increase angle and place needle slightly deeper. (F) Hematoma
formation, remove needle and select new site, pressure and ice. (G) Intraarterial
entry, remove needle and select new site.
Prevention
Follow the ideal protocol for a venipuncture:
1. Place tourniquet approximately 5 inches above proposed entry site.

2. Identify vein and alcohol antiseptic swab.
3. Skin pulled in opposite direction of needle.
4. With bevel up, enter at a 30-degree angle.
5. Perforate vein and decrease angle with slight advancement.
6. Remove tourniquet.
7. Remove needle.
Treatment
If there is an unsuccessful blood draw, the process should be repeated,
usually on the opposite arm. If a hematoma results, the following treatment
should be rendered:
1. Immediate pressure and ice application.
2. Moist heat to decrease pain after 4 hours of venipuncture.
3. Analgesics for pain.
4. Usually requires 10 to 14 days for subcutaneous blood to resolve.

Severe/Life-Threatening Complications
Swallowing/Aspiration of Implant Components
Unfortunately, any type of dental procedure may result in the aspiration or
ingestion of dental parts or materials. Accidental inhalation of dental
instruments (drills, burs, direction indicators, root tips, crowns, etc.) can
result in many complications, including life-threatening situations. When
this complication occurs, the implant dentist must act proactively to avoid
complications and medicolegal issues.
Etiology
Because of the small size of abutments, screws, drivers, and other implant
components, a significant risk for the implant clinician exists. This may occur
during any dental implant procedure, including the surgical and prosthetic
phases.
There are two possibilities: the patient may swallow the foreign object into
the stomach or aspirate the foreign material into the lungs.
Swallow.
If the object is swallowed, usually the patient will be asymptomatic. However,
depending on the shape and size of the object, it may need to be removed
because of the complication of blockage or not passing through the
gastrointestinal system.
Aspiration.
The object may end up in the lungs, in which case the patient will be
symptomatic. The patient will exhibit signs of coughing, wheezing,
hoarseness, choking, stridor, or cyanosis.
Prevention
Various techniques are available for the implant clinician to prevent
aspiration or swallowing of a foreign object. There is no one technique that
will guarantee that this complication will be avoided; however, extreme
caution should always be exercised. Techniques to prevent swallowing or
aspiration include:
• Floss ligatures to all possible implant components
• Use AS123 prosthetic tool
• Use throat packs (4 × 4 gauze) or pharyngeal screens
• High-vacuum function
• Use curved hemostats
Treatment
If an instrument is lost in the mouth, the patient should first be instructed to
not sit straight up because this will ensure the swallowing or aspiration of
the instrument. The patient should turn to the side and attempt to “cough”
the instrument up. If the instrument is lost, symptoms usually will
determine if aspiration into the lungs or swallowing into the stomach has
occurred. If the instrument has been swallowed into the stomach, usually the
patient will exhibit no symptoms. If the patient has aspirated the instrument,
this will most likely be accompanied with coughing, wheezing, pain, and
cyanosis. This may be life-threatening and should be treated accordingly as a
medical emergency. In all swallowing/aspiration situations, the patient
should be referred to their physician or emergency room for an immediate
chest x-ray. If the instrument has been aspirated, it is usually located in the
right bronchus because the right main bronchus has a more acute angle than
the left. Rigid bronchoscopy is usually used for the removal of the instrument
under general anesthesia (Fig. 5.29).
FIG 5.29 Swallowing/aspiration of objects. (A) Objects that are aspirated are most
likely to enter the right bronchi because it is more vertical than the left. (B) Chest x-
ray of implant hex driver in lungs. (C) Floss ties used to prevent aspiration. (D)
Extraoral prosthetic tool allows for safer placement of abutments/screws. (E) 4 × 4
gauze throat pack. (F) 2 × 2 throat packs should never be used during implant
surgery because they can be easily aspirated, swallowed, or left under a soft tissue
flap. (G) Curved hemostats should always be available to retrieve any implant
components in the oral cavity.
Air Emphysema
Subcutaneous air emphysema can lead to many devastating complications
during and after dental implant surgery. Early recognition and management
of this condition is crucial to preventing progression of the problem. As the
air accumulates subcutaneously, dissection occurs along the connective tissue
that joins the adjacent muscle planes. Via the fascial spaces, air from the oral
cavity may extend into the mediastinum space, where it may communicate
with parapharyngeal and retropharyngeal spaces, which lead to airway
compromise. From the retropharyngeal space, air may lead into the pleural
space and pericardium, which could result in heart and lung failure.
Etiology
Because of the attachment apparatus difference between implants and teeth,
air extruded into the sulcular area around implants may lead to air
emphysema. The two most common ways for this to occur is the use of an air-
driven handpiece or an air-water syringe in which air is forced into the
sulcular area. Symptoms will include swelling that increases over time with a
“crackling” feeling with pain. Crepitus to palpation will confirm the
diagnosis of air emphysema. The patient will usually be apprehensive with a
feeling of difficulty in breathing.
Prevention
When placing implants, modifying abutments with the mouth, or removing
bone around an implant body, an electric handpiece should always be used
(i.e., never use a air-driven handpiece). Additionally, an air-water syringe
should never be used to place air into the sulcular area parallel to the long
axis of the implant.
Treatment
Usually symptoms arise immediately; however, cases have been described
that have occurred minutes to hours after a procedure. Patients with
significant emphysema should be monitored closely prior to discharge for
respiratory or cardiac distress. Treatment should include supportive therapy
with heat and analgesics. Antibiotic therapy should always be given because
infection may result from bacteria being induced into the fascial spaces with
resultant cellulitis or necrotizing fascitis. Resolution usually occurs in 4 to 7
days with minimal morbidity. In isolated cases, exploratory surgery,
emergency tracheotomy, and the placement of chest tubes have been
reported (Fig. 5.30).26
FIG 5.30 Air emphysema. (A) Patient with air emphysema extending into the orbital
region. (B) Air-driven handpieces (air used to turn turbines) should be used with
extreme caution around implants. Electric handpieces can be used because there is
no chance of expelling air into the fascial spaces. (C) the air-water syringe should
never be directed into the sulcular area (i.e. parallel to the long-axis of the implant as
an air emphysema may result, (D) air-water syringe can be used with caution
perpendicular to the abutment/implant. (E) Internal irrigated burs are a common way
to expel air into the marrow spaces and should be used with caution.
Soft/Hard Tissue Complications

Electric Handpieces
Electric handpieces, the most common type of handpieces used in implant
dentistry today, have a tendency to overheat, which may result in significant
soft tissue complications. In 2007 and 2010, the FDA released warnings to
health professionals concerning possible serious burns related to electric
dental handpieces. The FDA has requested manufacturers to decrease these
issues by design modification, overheating alarms, warning labels, and
clinician training to avoid overheating.
Etiology.
Because electric handpieces have insulated housings, the clinician may not
be aware of the extent of the heat generated in the handpiece. Compounding
the problem is that the patient may be anesthetized and unaware of the
thermal injury. Injuries have been reported ranging from first- to third-
degree burns and may require reconstructive surgery. Unlike conventional
air-driven handpieces that decrease efficiency when overworked, electric
handpieces will maintain higher efficiency, thus generating a greater amount
of heat.
Prevention.
Awareness is most crucial for avoiding this complication. The clinician
should be conscious of the possibility of handpiece overheating, take
frequent breaks during treatment, and check continuously for the implant
motor becoming hot during treatment. The electric handpieces should have
routine maintenance according to manufacturer's recommendations.
Treatment.
If a burn occurs, treatment will vary depending on the severity usually.
Treatments range from OTC ointment to a physician referral. For severe
burns, systemic antibiotics are warranted. If the burn does not penetrate the
vermillion border, healing will usually result without a defect (Fig. 5.31).
FIG 5.31 Soft tissue burns. (A) Soft tissue burns will usually occur with an electric
handpiece (e.g., 1 : 1 straight handpiece). (B) Handpiece in contact with
anesthetized tissue (arrow). (C) Soft tissue injury from implant handpiece in contact
with anesthetized tissue (arrow).
Monopolar Electrosurgery Units
Monopolar electrosurgical units are a common soft tissue modality used in
dentistry today. However, in implant dentistry, when these units are used
around dental implants, significant complications may arise. Monopolar
electrocautery should never be used in the proximity of a dental implant or
implant prosthesis.
Etiology.
Electrosurgery is defined as the controlled passage of high-frequency
waveforms, or currents, for the purpose of altering the surrounding soft
tissue. The action of monopolar electrocautery is cutting the tissue by means
of advancing spark with a grounded patient. This results in sparking, current
spread, and thermal damage in the tissues because of the generation of heat.
Prevention.
In implant dentistry, monopolar electrosurgery units are contraindicated. The
monopolar electrodes cannot contact an implant or electrical shock
osteoradionecrosis and possible implant loss may result (Fig. 5.32). However,
bipolar electrosurgical units have been shown to be effective around dental
implants. Bipolar electrocautery utilizes molecular resonance with a sine-
wave current that prevents sparking and thermal damage. These types of
units may be used continuously because they produce progressive
coagulation rather than a single high-output discharge, thus creating no
spark.27
FIG 5.32 Soft tissue burns. (A) Electrosurgery (monopolar) used around implant
with associated thermal damage. (B) Injury one week after electrosurgery. (C) Injury
two weeks after surgery. (D) Failure of implant.
Treatment.
Treatment is usually palliative in nature as electrosurgery damage is usually
irreversible.
Salivary Gland Injury

The sublingual gland may be injured when an implant is placed in the
posterior mandible, which may cause the formation of a ranula. Ranulas are
defined as an accumulation of extravasated salivary secretions that form
pseudocysts in the submandibular area. When the ranula form above the
mylohyoid muscle, they appear as a translucent, bluish swelling in the
sublingual space. Most ranulas are visible on a clinical examination and are
considered “plunging” when they extend inferiorly from the sublingual
space into the neck area. Ranulas are usually not fixed, and they are very
rarely painful unless they become secondarily infected. In some cases, they
develop into larger lesions and may compromise the airway.
Etiology
The proximity of the sublingual gland to the lingual cortical plate of the
mandible makes it susceptible to injury. If the gland is traumatized, a ranula
may result. Trauma usually occurs from improper angulation during dental
implant surgery, which perforates the lingual cortex and causes damage to
the sublingual gland. Additionally, the gland may be injured during
aggressive reflection and retraction when working in the sublingual area.
Prevention
To prevent damage to salivary glands, ideal preoperative treatment planning,
good surgical technique, proper implant angulation, and careful retraction
will avoid these complications. Additionally, the anatomy of the sublingual
area must be understood. The sublingual gland is positioned adjacent to the
lingual cortex and seated below the mylohyoid muscle. The submandibular
duct is positioned inferior and medial to the sublingual gland. The lingual
nerve will cross the submandibular duct from medial to lateral and then
cross back at the first premolar area, where it branches into the tongue
musculature.
Treatment
Treatment should include referral to an oral and maxillofacial surgeon, which
usually involves the complete removal of the sublingual gland. In some
cases, where the ranulas are very small and asymptomatic, no surgery may be
indicated or marsupialization to reestablish connection with the oral cavity
(Fig. 5.33).28
FIG 5.33 Salivary gland damage. (A) Sublingual gland anatomy. The
interrelationships between the ductal systems of the submandibular and the
sublingual glands and the relationship of the lingual nerve to Wharton's duct are
demonstrated. (B) Sublingual ranula after implant placement in premolar area. (C)
Dissection including the retraction of the lingual nerve, which transverses the
sublingual gland. (D) Treatment included complete removal of sublingual gland. (E)
Sublingual closure after removal. (F) Close approximation of sublingual gland (70),
submandibular gland (73), and submandibular duct (71). (A, From Fehrenbach MJ,
Herring SW: Illustrated anatomy of the head and neck, ed 5, St. Louis, 2017, Elsevier; B–D, From
David J. Datillo, DDS, Allegheny General Hospital, Pittsburgh, PA; F, From Logan BM, Reynolds P,
Hutchings RT: McMinn’s color atlas of head and neck anatomy, ed 4, Philadelphia, 2010, Mosby.)
Anesthetic Toxicity
A serious complication, local anesthetic overdosage is of great concern in
implant dentistry. Because many implant-related surgeries are of longer
duration, a greater amount of anesthetic is often administered. Special
attention must be taken during implant surgery as to the number of
cartridges and type of anesthetic used during a procedure.
Etiology
The maximum number of cartridges that can be administered safely to a
patient is time dependent. The elimination half-life is not indicative of
anesthetic duration; however, it may be used as a guide for repeated
anesthetic administration during a lengthy procedure. After one half-life, as
much as 50% of the permissible dose can be administered with reasonable
safety if liver function is normal. Special care must be given to the use of
combination local anesthetics. In implant dentistry, it is common to use two
amide anesthetics together—lidocaine and bupivacaine. Although
acceptable, total doses should not exceed combined maximum recommended
doses. Calculations should factor in the total dose of the combination and
whether sufficient time has elapsed for elimination of the initial dose.29
Treatment
Most amide anesthetics (except for articaine) are metabolized by the liver by
a microsomal enzyme system. Special attention should be given to patients
with decreased liver function (e.g., as a result of chronic alcoholism,
hepatitis), especially elderly patients. The half-life of lidocaine has been
shown to be greater than 2.5 times the normal values in patients with hepatic
disease.30 Special attention must be given to the amount of anesthetic used,
and concern for reinjection (i.e., amount of anesthetic administered after
initial block) must be strictly evaluated in these patients. In addition to the
liver, the kidneys are the primary organs responsible for excretion of the local
anesthetic and its metabolites. Patients with significant renal impairment
will also have difficulty in removing the anesthetic from the blood, resulting
in an increased chance of toxicity.
Patients with cardiovascular disease should be well evaluated before the
use of epinephrine-containing anesthetics, and care should be taken as to the
amount of epinephrine administered. Recommendations on the maximum
safe dose for a healthy patient are 0.2 mg epinephrine vs. 0.04 mg
epinephrine for the cardiac-impaired patient. It should be noted that when
epinephrine is not included in the anesthetic, the systemic uptake of the
drug is more rapid and the maximum number of carpules given is
significantly less in comparison to anesthetics with vasoconstrictors.
If local anesthetic toxicity reactions occur,31 central nervous system
excitation, convulsions, respiratory depression, and cardiac arrest may occur.
Appropriate emergency medical care should be administered immediately
(Box 5.1 and Table 5.1).
Box 5.1
Signs and Symptoms of Local Anesthetic
Toxicity
Mild Symptoms
• Talkativeness
• Slurred speech
• Apprehension
• Localized muscle twitching
• Lightheadedness/dizziness
• Tinnitus
• Disorientation
Progressive Symptoms
• Lethargy
• Unresponsiveness
• Drowsiness/sedation
• Lack of muscle tone
• Mild drop in blood pressure, heart, and respiratory rate

From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby; Adapted from Bennett CR:
Monheim's local anesthesia and pain control in dental practice, ed 7, St Louis, 1984, Mosby.
TABLE 5.1
Maximum Manufacturer-Recommended Number of Anesthetic Capsules
Weight of P atient 2% Lidocaine 1/100 K 2% Mepivacaine 1/20 K 4% Articaine 1/100 K 5% Bupivacaine 1/200 K
(lb) Epinephrine Neocobefrin Epinephrine Epinephrine
80 6.5 6.5 3.5 5
100 8 8 4.5 6.5
120 10 10 5.5 8
140 11.5 11 6 9
160 13 11 7 10
180 13.5 11 7 10
200 13.5 11 7 10
From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby; Data from Malamed SF:
Handbook of local anesthesia, ed 6, St Louis, 2013, Mosby.
Surgical (Anesthesia) Fires

Dental surgical fires are rather rare; however, with the increased use of
sedation in implant dentistry, this potentially devastating complication may
occur. The FDA receives reports of approximately 500 to 600 surgical fires
each year in the United States. Deaths are rare except for fires that occur in
the airway. Clinicians need to be aware of the possibility and take steps to
prevent this complication.
Etiology
Surgical fires occur in dental surgery when the following three elements of
the fire triangle are present:
1. Ignition source (e.g., electrosurgery, lasers, fiberoptic light sources)
2. Fuel source (e.g., surgical drapes, alcohol-based skin preparation agents

such as chlorhexidine)
3. Oxidizer (e.g., oxygen, nitrous oxide)
The most significant risk for a dental surgical fire occurs when laser or
electrocautery units are use in an oxygen-rich environment such as when
supplemental oxygen is administered via a nasal cannula. The spark from the
electrocautery unit or laser in the presence of oxygen or highly inflammable
anesthetic gases may cause the explosion or surgical fire.32
Prevention
The FDA recommends the following steps to prevent dental surgical fires33:
1. Determine which procedures carry high risk, which will include any
procedure requiring the use of supplemental oxygen and the operation of an
ignition source near the oxygen.
2. Use supplemental oxygen safely. Deliver the minimum concentration of

oxygen needed to maintain adequate oxygen saturation for your patient. If
any type of ignition source is required, oxygen should be decreased or shut
off.
3. Use alcohol-based (flammable) skin preparation agents safely. Prevent

alcohol-based antiseptics from pooling in the surgical area (mouth). Remove
alcohol-soaked materials from the prep area, such as 4 × 4 gauze that is used
for intra or extra oral scrub. Allow adequate time for the alcohol-based
antiseptic to dry.
4. Use surgical equipment safely and consider alternatives to using an

ignition source for dental implant surgery. If an ignition source must be
used, know that it is safer to do so after allowing time for the oxygen
concentration to decrease. It may take several minutes for a reduction of
oxygen concentration in the area even after stopping the gas or lowering its
concentration.
5. Understand that surgical drapes and other fuel sources (e.g., patient
napkins, surgical table covers) can ignite easily and burn in an oxygen-
enriched environment, even if the products are described as “flame-
resistant.”
Treatment
In case of an airway fire, immediately halt the procedure and stop the flow of
any gases (e.g., oxygen) and ventilate the operatory. Remove any flammable
material such as gauze and patient drapes. Saline may be used to extinguish
an airway fire. Assess the patient; medical assistance should be summoned
in most cases (Boxes 5.2 and 5.3).
Box 5.2
Surgical Fire Sources in Oral Implantology
IGNITION (HEAT) SOURCES
• Electrosurgery
• Lasers
• Fiberoptic cables and lights
• Heat and spark from tooth/implant abutment preparation from high-speed

handpiece
• Defibrillators
OXYGEN (OXIDIZERS)
• Oxygen – usually via nasal cannula
• Nitrous oxide – via nasal hood, nitrous oxide releases oxygen when heated
FUEL
• Gauze and cotton rolls
• Surgical gowns and blankets
• Petrolatum (petroleum jelly)
• Chlorhexidine
• Alcohol-based skin prep solutions
• Facial hair, epithelium, and so forth
• Vellus hair
• Rubber and plastic goods
• Nasal cannula and nasal hood

• Latex
From Bosack RC, Bruely ME, VanCleave AM, et al: Patient fire during dental care: a case report and call
for safety. J Am Dent Assoc 147(8): 661–666, 2016.
Box 5.3
Surgical Fire Treatment Algorithm
PREVENT
• Fire drills with surgical staff
• “Time out” after use of certain fuels (i.e., sufficient drying time for alcohol-
based prep solutions)
• Follow all safety practices when using potential ignition sources
• Coat hair around the mouth with water-soluble surgical jelly; keep fuels
moist
• Open-face surgical draping
• Stop flow of oxidizers for at least 1 minute before the use of potential
ignition sources
RECOGNIZE
• Any unexpected patient movement, odor, unexpected discomfort/pain,

discoloration, heat, or smoke
MANAGE
• Immediately remove burning materials that should be extinguished by

another team member
• Stop the flow of oxygen or nitrous oxide to the patient
• Smother or pour sterile saline or water on small patient fires
• Care for the patient: airway, ventilation, and immediate emergency medical
service
From Bosack RC, Bruely ME, VanCleave AM, et al: Patient fire during dental care: a case report and call
for safety. J Am Dent Assoc 147(8):661–666, 2016.
Oral/Conscious Sedation Toxicity

It has been estimated that as many as 75% of adults in the United States have
some degree of dental fear, ranging from mild to severe,34 and that
approximately 5% to 10% avoid dental care because of anxiety.35 In implant
dentistry the use of conscious sedation is a valuable adjunct. The American
Dental Association defines conscious sedation as a minimally depressed level
of consciousness that retains the patient's ability to independently and
continuously maintain an airway and respond appropriately to physical
stimulation or verbal command and that is produced by a pharmacologic or
nonpharmacologic method or combination thereof.36 Several sedative agents
are currently available for oral and intravenous sedation. Table 5.2 lists the
most commonly used oral and intravenous sedative agents.
TABLE 5.2
Most Commonly Used Oral and Intravenous Sedative Agents
Half-
Sedative Onset Duration Active
Class Administration Life Oral Dose IV Dose Amnesia Analgesia
Agent (min) (hr) Metabolites
(hr)
Triazolam Benzodiazepine PO 60 1–2 2–3 No 0.125–0.25 mg — Yes No
Diazepam Benzodiazepine PO/IV PO: 0.25–0.5 21–37 Yes 0.2–0.5 mg/kg; 0.1 mg/kg Yes No
60 maximum 15 mg
IV: 1–
2
Lorazepam Benzodiazepine PO/IV PO: IV: 1–2 10–20 No 0.053 mg/kg; 0.03–0.04 Yes No
120– maximum 4 mg mg/kg
240
Brevital Barbiturate IV 0.5 0.3 4 No — 0.2–0.4 Yes No
mg/kg
Fentanyl Narc otic IV 0.5 0.75–1 3–4 No — 1–2 µg/kg No Yes
Propofol S edative IV 0.2–0.5 3–8 min 0.5–1.5 No — 25–100 Yes No
hypnotic µg/kg/min
Midazolam Benzodiazepine PO/IV 0.5–1 0.25– 1–4 No 0.5 mg/kg 0.01–0.1 Yes No
1.25 mg/kg
IV, intravenous; PO, oral.

From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.
Benzodiazepines
Etiology.
Benzodiazepines are the most effective drugs available for dental-related
anxiety used in private practice today. Benzodiazepines mainly produce
anxiolysis and anterograde amnesia, which are extremely useful for patients
undergoing conscious sedation for dental implant procedures. The exact
mechanism is not known; however, benzodiazepines are thought to have an
effect on the limbic system and the thalamus, which are involved with
emotions and behavior.37 Unfortunately, in the field of sedation dentistry, the
use of oral sedative agents is often misused, which may lead to significant
complications.
Triazolam.
One of the most common benzodiazepines used today in implant dentistry is
triazolam (Halcion), which is an orally administered and short-term hypnotic
drug. In addition to its hypnotic properties, triazolam also has the
advantages of anterograde amnesia, anxiolytic, sedative, and anticonvulsant
properties. When given orally, this drug is fast acting with short duration and
has been shown to be safe and effective for dental procedures. Studies have
shown that triazolam given in doses of 0.25 to 0.5 mg does not produce
adverse effects in respiration, heart rate, or arterial pressure.37
Diazepam.
Diazepam (Valium) is a long-acting drug that for years has been the most
commonly used form of benzodiazepine. Basically, in low doses, diazepam
reduces anxiety without sedation and in high doses it acts as a sedative and
promotes sleep. Diazepam has anxiolytic, anticonvulsant, sedative, hypnotic,
skeletal muscle relaxant, and amnestic properties. It is mainly used in
dentistry to reduce tension and anxiety and induce retrograde amnesia.
When given orally, it is rapidly absorbed and has a fast onset of action within
60 minutes. The bioavailability after oral administration is 100%, and the
peak plasma levels occur between 30 minutes and 90 minutes after
administration. Diazepam has the disadvantage of pharmacologically active
metabolites, which may interact with other medications. Because of the active
metabolites, diazepam has a biphasic half-life of about 1 to 2 days and 2 to 7
days for the active metabolite desmethyldiazepam, which results in
prolonged action, causing drowsiness and lethargy for up to 48 hours.38
Additional Conscious Sedation Medications

Fentanyl is a synthetic opioid agonist narcotic that produces analgesia,
drowsiness, sedation, and euphoria, but no amnesia. All opioid agonists
produce dose-dependent depression of ventilation. Respiratory depression is
a result of a decreased response of the ventilatory centers to carbon dioxide.
For this reason, care should be taken when administering opioid agonists,
especially in combination with other sedatives. Nausea and vomiting are
another undesirable effect of opioid agonists. Opioid-induced nausea and
vomiting are caused by direct stimulation of dopamine receptors in the
chemoreceptor trigger zone in the fourth floor of the fourth ventricle.
Propofol (Diprivan) is an intravenous sedative-hypnotic agent commercially
introduced in the United States in 1989 by Zeneca Pharmaceuticals. It was the
first of a new class of intravenous anesthetic agents: the alkylphenols.
Propofol is an ideal sedative anesthetic for dentistry because it is fast-acting
and possesses a short half-life. The elimination half-life of propofol has been
estimated to be between 2 and 24 hours. However, its duration of clinical
effect is much shorter because propofol is rapidly distributed into peripheral
tissues. Because of its pronounced respiratory depressant effect and its
narrow therapeutic range, propofol should be administered only by
individuals trained in airway management. There is no reversal agent at this
time for Propofol.
Prevention
The first key to prevention is obtaining adequate training in the use of
conscious sedation. The implant dentist must acquire sedation skills from
both a theoretical and a practical standpoint. The second key to prevention is
preparedness, which first includes an up-to-date emergency kit containing
emergency drugs (including reversal agents) and an airway kit that enables
them to deliver oxygen under positive pressure. Oxygen is the first line of
defense in a sedation emergency, and proper administration must be
understood. The office should have an emergency plan in place. The third
key of prevention is the use of sedative medications within maximum doses
with strict protocol to patient monitoring.39
Treatment
Besides maintaining the patient's airway and an emergency protocol, implant
dentists must have ideal reversal agents for benzodiazepines. Flumazenil
(Anexate, Lanexat, Mazicon, Romazicon) is a benzodiazepine antagonist used
as a reversal agent for the treatment of benzodiazepine overdose. It reverses
the effects of benzodiazepines by competitive inhibition at the
benzodiazepine binding site on the GABAA receptor.
The onset of action is rapid, and effects are usually seen within 1 to 2
minutes. The peak effect is seen at 6 to 10 minutes. The recommended dose
for adults is 200 mg every 1 to 2 minutes until the effect is seen, to a
maximum of 3 mg per hour. It is available as a clear, colorless solution for
intravenous injection, containing 500 mg in 5 mL. It is hepatically
metabolized to inactive compounds, which are excreted in the urine.40 Many
benzodiazepines have longer half-lives than flumazenil. Repeated doses of
flumazenil may be required to prevent recurrent symptoms of overdosage
after the initial dose of flumazenil wears off (Fig. 5.34). Reversal drug of
choice is naloxone HCl (Narcan 0.4 mg/ml). The initial naloxone dose is 0.4
mg that can be repeated every 2 to 3 minutes depending on the patient's
respiratory status. The duration of action of naloxone is shorter than most
opioids, so the patient should be closely monitored for recurrence of opioid
toxicity.
FIG 5.34 Reversal agents. (A) Flumazenil—benzodiazepine reversal agent, given

in 2-mL doses (0.2 mg/mL) to a maximum of five doses. (B) Narcan—narcotic
reversal agent, given in 0.4 mg/mL doses.
There exists numerous routes of pharmacologic administration for medical

emergency episodes. The most ideal site for administration is intravenous
(IV) because this method has direct access to the bloodstream. In most
nonsedation cases, this is route is impractical. Another option for the
implant clinician for the administration of an injectable emergency drug is
the sublingual approach. This method allows for fast, easy access for the
administration below the tongue, which allows for the medication to diffuse
into the bloodstream. The insertion point is the sublingual midline to avoid
damage to the salivary ducts.
The deltoid approach (intramuscular) utilizes the deltoid muscle site
(upper arm), which is recommended for injections of smaller volume. To
locate this administration site, the acromian process is palpated as the
superior landmark and the axilla is the inferior landmark with the injection
site in the middle. The deltoid technique has slower uptake than the
sublingual approach.
The last approach utilizes the lateral vastus lateralis muscle (IM injection)
corresponds to the lateral thigh. This site has slower uptake than the deltoid;
however, faster than the gluteal. The lateral thigh is divided into thirds, from
the anterior knee to the posterior gluteal region. The entry point is in the
center of the middle third (Fig 5.35).
FIG 5.35 Emergency medication administration. (A) Sublingual—fast, easy
access. (B) Deltoid—slower uptake, not as convenient as sublingual. (C) Thigh—
fast, access more difficult than sublingual.
Summary
Over the course a career as an implant surgeon, regardless of skill level or
experience, a clinician will undoubtedly come across some form of
complication during the placement of a dental implant. Regardless of the
severity of the complication, the proper means of remediation must be called
upon at a moment's notice. With a vast, detailed knowledge of the many
intraoperative complications reported during implant surgery, a plan to
prevent them, and a protocol to treat them should they arise, the surgeon will
provide a much safer and predictable surgical outcome for every patient.
References
1. Ayangco L, Sheridan PJ. Development and treatment of retrograde
peri-implantitis involving a site with a history of failed endodontic
and apicoectomy procedures: a series of reports. Int J Oral Maxillofac
Implants. 2001;16:412–417.
2. Shaffer MD, Juruaz DA, Haggerty PC. The effect of periradicular
endodontic pathosis on the apical region of adjacent implants. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod. 1998;86:578–581.
3. Siqueira JF Jr, Rijas IN, Oliveria JC, et al. Molecular detection of
black-pigmented bacteria in infections of endodontic origin. J Endod.
2001;27:563–566.
4. Brisman DL, Brisman AS, Moses MS. Implant failures associated with
asymptomatic endodontically treated teeth. J Am Dent Assoc.
2001;132:191–195.
5. Nelson S, Thomas G. Bacterial persistence in dentoalveolar bone
following extraction: a microbiological study and implications for
dental implant treatment. Clin Implant Dent Relat Res. 2010;12:306–
314.
6. Kassolis JD, Scheper M, Jham B, et al. Histopathologic findings in
bone from edentulous alveolar ridges: a role in osteonecrosis of the
jaws? Bone. 2010;47:127–130.
7. Simonetti M, Facco G, Barberis F, et al. Bone characteristics following
osteotomy surgery: an in vitro SEM study comparing traditional
Lindemann drill with sonic and ultrasonic instruments. Poseido Jl.
2013;1:187–194.
8. Kirsch A, Ackermann KL. The IMZ osteointegrated implant system.
Dent Clin North Am. 1989;33:733–791.
9. Warrer K, Buser D, Lang NP, et al. Plaque-induced peri- implantitis in
the presence or absence of keratinized mucosa: an experimental
study in monkeys. Clin Oral Implants Res. 1995;6:131–138.
10. Listgarten M, Lang NP, Schroeder HE, et al. Periodontal tissues and
their counterparts around endosseous implants. Clin Oral Implants
Res. 1991;2:81–90.
11. Cordioli G, Majzoub Z. Heat generation during implant site
preparation: an in vitro study. Int J Oral Maxillofac Implants.
1997;12:186–193.
12. Sharawy M, Misch CE, Weller N, et al. Heat generation during implant
drilling: the significance of motor speed. J Oral Maxillofac Surg.
2002;60:1160–1169.
13. Yeniyol S, Jimbo R, Marin C, et al. The effect of drilling speed on early
bone healing to oral implants. Oral Surg Oral Med Oral Pathol Oral
Radiol. 2013;116:550–555.
14. Bashutski JD, D'Silva NJ, Wang H-L. Implant compression necrosis:
current understanding and case report. J Periodontol. 2009;80:700–704.
15. Scher ELC. Use of the incisive canal as a recipient site for root form
implants: preliminary clinical reports. Implant Dent. 1994;3:38–41.
16. Hovorka O. Die aussere nase. Hohler: Vienna; 1893.
17. Mardinger O, Namani-Sadan N, Chaushu G, et al. Morphologic
changes of the nasopalatine canal related to dental implantation: a
radiologic study in different degrees of absorbed maxillae. J
Periodontol. 2008;79:1659–1662.
18. Bornstein MM, Balsiger R, Sendi P, et al. Morphology of the
nasopalatine canal and dental implant surgery: a radiographic
analysis of 100 consecutive patients using limited cone-beam
computed tomography. Clin Oral Implants Res. 2011;22:295–301.
19. Alsaadi G, Quirynen M, Michiels K, et al. A biomechanical assessment
of the relation between the oral implant stability at insertion and
subjective bone quality assessment. J Clin Periodontol. 2007;34:359–
366.
20. Noguerol B, Munoz R, Mesa F, et al. Early implant failure. Prognostic
capacity of Periotest: retrospective study of a large sample. Clin Oral
Implants Res. 2006;17:459–464.
21. Misch CE, Al-Shammari KF, Wang HI. Creation of interimplant
papillae through a split-finger technique. Implant Dent. 2004;13:20–27.
22. Sullivan DY, Sherwood RL, Collins TA, et al. The reverse torque test—
a clinical report. Int J Oral Maxillofac Implants. 1996;11:179–185.
23. Albrektsson T, Jacobsson M. Bone-metal interface in osseointegration.
J Prosthet Dent. 1987;57:587–607.
24. Brånemark PI. Introduction to osseointegration. Brånemark PI, Zarb
GA, Albrektsson T. Tissue-integrated prostheses: Osseointegration in
clinical dentistry. Quintessence: Chicago; 1985.
25. Choukroun J, et al. Platelet-rich fibrin (PRF): a second-generation
platelet concentrate. Part IV: clinical effects on tissue healing. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod. 2006;101:e56–e60.
26. McKenzie WS, Rosenberg M. Iatrogenic subcutaneous emphysema of
dental and surgical origin: a literature review. J Oral Maxillofac Surg.
2009;67:1265–1268.
27. Shuman IE. Bipolar versus monopolar electrosurgery: clinical
applications. Dent Today. 2001;20:74.
28. Newlands C, Kerawala C. Oral and maxillofacial surgery. Oxford
University Press: Oxford; 2010.
29. Moore PA. Adverse drug interactions in dental practice: interactions
associated with local anesthetics, sedatives and anxiolytics. J Am Dent
Assoc. 1999;130:541–554.
30. Thomson PD, Melmo KL. Lidocaine pharmacokinetics in advanced
heart failure, liver disease, and renal failure in humans. Ann Intern.
1973;78:499–513.
31. Moore PA. Prevention of local anesthesia toxicity. J Am Dent Assoc.
1992;123:60–64.
32. VanCleave AM, Jones JE, McGlothlin JD, et al. Factors involved in
dental surgery fires: A review of the literature. Anesth Prog.
2014;61:21–25.
33. US Food and Drug Administration. Preventing surgical fires: FDA
Safety communication. [(website)]
http://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/ucm275189.htm
34. Kleinknecht RA, Thorndike RM, McGlynn FD, et al. Factor analysis of
the dental fear survey with cross-validation. J Am Dent Assoc.
1984;108:59–61.
35. Gatchel RJ, Ingersoll BD, Bowman L, et al. The prevalence of dental
fear and avoidance: a recent survey study. J Am Dent Assoc.
1983;107:609–610.
36. American Dental Association. American Dental Association guidelines
for the use of sedation and general anesthesia for dentists. [(website)]
http://www.ada.org/en/about-the-ada/ada-positions-policies-and-
statements/#Anesthesia.
37. Stoelting RK. Pharmacology and physiology in anesthetic practice. ed 4.
Lippincott Williams & Wilkins: Philadelphia; 2006.
38. Riss J, Cloyd J, Gates J, et al. Benzodiazepines in epilepsy:
pharmacology and pharmacokinetics. Acta Neurol Scand. 2008;118:69–
86.
39. Ogle OE, Hertz MB. Anxiety control in the dental patient. Dent Clin
North Am. 2012;56:1–16.
40. Mosby's dental drug reference. ed 8. Mosby: St Louis; 2008.
6
Ideal Implant Positioning
Randolph R. Resnik
To obtain proper esthetics and function of an implant supported prosthesis,

the three-dimensional positioning of the dental implant is critical. The
malposition of the implant can lead to significant implant complications and
morbidity. In order to achieve an ideal result for the patient, a clinician must
initially place implants in a correct orientation for the prosthesis design.
Nonideal implant positioning may result in undesirable outcomes that may
affect the success and longevity of prosthetic rehabilitation.1 Optimal dental
implant positioning should consider the three-dimensional placement of
implants with respect to the biomechanical and prosthetic principles related
to the final implant prosthesis. Recently, advances in implant dentistry have
created a greater appreciation for the esthetic results of the implant
restoration. Implant dentistry has experienced a profound shift: from a
functional thought process with a surgical approach to esthetics, with a
prosthetically and biologically driven approach.2 The implant should be
positioned in ideal relation to existing teeth, vital structures, and other
implants as well as in buccolingual, mesiodistal, and apicocoronal
dimensions. When implants are malpositioned, any of the following
detrimental effects may occur (Fig. 6.1):
• Increased implant morbidity
• Increased prosthetic complications (e.g., esthetics, prosthesis)
• Increased prosthetic costs
• Increased periodontal complications
• Decreased longevity of prosthesis
The ideal three-dimensional positioning of a dental implant needs to be
addressed prior to the surgical procedure. Lack of proper planning leads to
malpositioning in the three spatial planes (Fig. 6.1). The placement of a
dental implant in available bone is comparable to an object in space that is
defined by “x,” “y,” and “z” coordinates. In implant dentistry, the x-axis is
defined by the mesiodistal plane, the y-axis is the buccolingual dimension,
and the z-axis is known as the apicocoronal (length of implant body in
relation to the osseous crest).3 Placement of dental implants ideally in the
available bone does not necessarily prevent complications from arising. Not
only does the implant need to be placed in the ideal three-dimensional
position but also according to the type of final prosthesis. In this chapter the
proper positioning of implants will be discussed according to the final
prosthetic demands of the patient.
FIG 6.1 (A–D) Various examples of malpositioned implants leading to increased
morbidity.
Mesial-Distal (“X” Axis): Implant–Natural
Tooth
Insufficient Implant–Root Apex Distance
Etiology
Implants placed too close to an adjacent tooth root are usually the result of
poor treatment planning (inadequate space), poor surgical technique
(improper angulation), or placement of too wide of an implant body. This
may occur when there are root dilacerations of an adjacent tooth or if a tooth
has been orthodontically repositioned to where the tooth root has
encroached on the intraroot space (Fig. 6.2A).
FIG 6.2 Root-implant approximation. (A) Implant ideally needs to be >1.5 mm from
root apex. (B) Implant impingement causing apical pathology encompassing the root
and implant. (C) Root apex damaged by implant surgical drill. (D) Resultant
irreversible root damage. (E) Example of a time-related complication involving an
implant placed too close to a tooth root (i.e. immediate post-operative radiograph),
(F) Pathology present four years later resulting in the loss of the tooth and implant.
Complications
Damage to Adjacent Periodontal Ligament.

Implants positioned too close to a tooth risk damage to the periodontal
ligament and surrounding structures. This may cause displacement of bone
into the periodontal ligament (PDL) space and result in altered blood supply
to the adjacent tooth, loss of tooth vitality, apical periodontitis, and internal
or external resorption.4
Loss of Implant.
Implants that are placed too close to an adjacent tooth may fail due to
infection or bone resorption. If more than 1.5 mm of space exists between the
implant and the adjacent tooth, any bony defect around an implant will
remain a vertical defect and will ususally not cause bone loss on the adjacent
natural tooth. If bone loss around an implant is less than 1.5 mm then the
bone on the adjacent tooth will maintain the interdental papilla height.
Loss of Tooth.
If adequate space is not maintained between a tooth and an implant, the
adjacent tooth may be irreversibly traumatized and may be lost to a fracture
or to internal or external resorption (Fig. 6.2B–D).
Prevention
Ideal Position.
The ideal position is to maintain at least 1.5 mm from the adjacent tooth root
or tooth structure. Ideal angulation should be strictly adhered to by
evaluating initial osteotomy position via a radiograph of a direction indicator
after the first pilot drill (Fig. 6.3A).
FIG 6.3 Ideal Implant Positioning (A) 3-D image depicting implant >1.5 mm for
tooth roots. (A) Ideal positioning. (B–C) Errors in positioning are often a result of
using study casts or two-dimensional radiographs (which do not show the true root
position) for implant placement planning. Without evaluating the third dimension, it is
impossible to determine the exact root position.
Proper Treatment Planning.

The exact measurement of intraroot distance should be determined to
prevent implant approximation to the root. Additionally, evaluation for
anatomic variants such as dilacerations of adjacent teeth should always be
radiographically diagnosed. The use of CBCT images should be utilized to
confirm exact space available between the root and intended implant
position. The most accurate CBCT image is the axial slice, which can be easily
used to verify measurements.
Use of Study Casts.

Study casts should not be used as the sole determinate of implant position.
In most cases, root position and angulation cannot be determined from study
casts. A common problem is when positional (fully limiting) surgical guides
are made from study casts without three-dimensional evaluation (Fig. 6.3B–
C).
Two-Dimensional Radiographs.
In evaluation of intraroot distances, caution must be used in using two-
dimensional radiographs as the sole determinants of implant positioning.
Both periapical and panoramic radiographs have inherent disadvantages in
providing accurate measurements (Fig. 6.4A). Ideally, to verify adequate
intraroot distance, a three-dimensional (computed tomography [CT] or cone
beam computed tomography [CBCT]) scan should be performed. Accurate
measurements may be made in the axial images at three locations: the
cementoenamel junction (CEJ), midroot, and root apex (Fig. 6.4B–E).
FIG 6.4 An often problematic positioning area involves the replacement of the
maxillary lateral incisor. This situation often results after orthodontic treatment (A)
when there is close proximity of roots (converging). Ideal computed tomography
evaluation should include evaluation of the axial images at the (B) crestal, (C)
midroot, and (D) root apex. (E) Illustration depicting ideal apical spacing with
nonideal crestal positioning. (F) Caution should be exercised in using two-
dimensional radiographs because of their inherent positioning complications.
Caution With Orthodontic Implants.

A popular relatively new implant modality is the use of orthodontic implants
temporary anchorage devices (TADs) for anchorage. Orthodontic implants
utilize the use of smaller diameter implants, which are inserted
perpendicular to the long axis of the tooth in the interradicular spaces of the
maxilla and mandible. TADs are utilized for tooth movement (e.g., labial
segment retraction or mesial movement of teeth) or for intraoral anchorage,
in which tooth movement in all three planes may be accomplished.
Interradicular orthodontic implant complications include loss of tooth
vitality, tooth loss, osteosclerosis, and dentoalveolar ankylosis.5,6 These
implants should be cautiously placed because they often are placed in areas
of minimal intraroot distance and above the mucogingival line in attached
tissue, which often leads to detrimental effects on adjacent tooth structure
(Fig. 6.5A–B).7
FIG 6.5 Implant-root impingement. (A) Orthodontic implants are often problematic
because of their intended position between tooth roots within attached tissue. (B)
Temporary anchorage device (TAD) placement in close approximation to an adjacent
tooth. (C) A maxillary canine root is often slanted 11 degrees distally and has a distal
curvature 32% of the time. When the implant is placed parallel to the first premolar, it
may inadvertently encroach upon the canine root. (D) A maxillary first premolar
implant may need to be parallel to the canine. (C–D, From Misch CE: Contemporary implant
Maxillary Lateral Incisor Region.

In regards to implant position, one of the most common problematic areas is
the replacement of congenitally missing lateral incisors. Often after
orthodontic treatment, there exists a normal mesiodistal distance of the
clinical crowns; however, compromised intraroot distance will result. This is
most likely to occur in the apical area. Lack of space may contraindicate
implant placement or require orthodontic treatment for repositioning of the
roots (see Fig. 6.4).
Maxillary First Premolar Site.

Another common area for root approximation problems is in the maxillary
first premolar edentulous site. Careful consideration for the angulation of a
natural canine must be evaluated. The 11-degree average distal inclination
and distal curvature of the canine root frequently place the apex of the root
into the first premolar implant area. The implant should be angled to follow
the root of the canine and prevent contact with or perforation of the natural
root. A shorter implant often is indicated, especially when a second premolar
is also present (Fig. 6.5C–D).
FP-2, FP-3, RP-4, and RP-5.

More latitude exists with the mesiodistal positioning of implants for FP-2, FP-
3, RP-4, and RP-5 prostheses; however, the anteroposterior (A-P) spread
should always be maximized. Because the soft tissue is replaced in these
types of prostheses (pink acrylic or porcelain), implants need not be placed
in specific tooth positions. Implant positioning is usually dictated by 3-mm
spacing between implants and maximizing the A-P spread whenever
possible.
Treatment
Initial Placement.
If there is insufficient space between an implant and a natural tooth, the
implant should be removed and repositioned, especially if the adjacent tooth
is symptomatic. If space is compromised (<6.0 mm), the roots should be
repositioned via orthodontics or treatment plan changed to a different type
of prosthesis.
Past Placement.
If an implant has been restored and root approximation (<1.5 mm) exists, the
tooth/implant should be monitored on a regular basis and the patient
informed of the possible morbidity. If symptomatic or radiographic
pathology is present, the implant should be removed and repositioned along
with vitality testing of the tooth.
Lack of Implant–Coronal Distance

Etiology
Lack of space between the implant platform and the coronal aspect of the
adjacent tooth occurs most likely from poor initial osteotomy positioning,
poor treatment planning, or the use of too large of an implant body, leading
to a situation where the implant encroaches upon the adjacent tooth. Implant
clinicians must be aware that most implant crestal platforms are larger than
the implant body, which will result in decreased space between the adjacent
tooth (e.g., a 3.8-mm implant may have a 4.1-mm platform) (Fig. 6.6 and Table
6.1).
FIG 6.6 Mesiodistal distance. Implant body diameter vs. implant crest module. The
crest module of an implant is often wider than the implant body dimension. (Pictured:
External hex implants. Courtesy BioHorizons Implant Systems, Inc.)
TABLE 6.1
Average Mesiodistal Width of Permanent Teeth
Tooth Mandibular (mm) Maxilla (mm)

Central inc isor 5.3 8.6
Lateral inc isor 5.7 6.6
Cuspid 6.8 7.6
First bic uspid 7.0 7.1
S ec ond bic uspid 7.1 6.6
First molar 11.4 10.4
S ec ond molar 10.8 9.8
From Hebel MKS, Gajjar R: Anatomic basis for implant selection and positioning. In Babbush C, editor:
Dental implants: the art and science, ed 2, Philadelphia, 2001, Saunders.
Complications
If implants are positioned too close to the coronal portion of the tooth, many
complications can result.
Interproximal Bone Loss.

When there is a lack of space between the tooth and implant, bone
resorption will occur due to lack of a sufficient blood supply. Esposito has
shown a correlation between increased bone loss and decreased distance of
the implant from the adjacent tooth.8
Compromised Emergence Profile.

Due to a lack of space between the adjacent clinical crown and implant, it
may be difficult, if not impossible, to form an ideal emergence profile in the
new final prosthesis. Lack of proper emergence profile leads to esthetic,
hygienic, and soft tissue complications, which increases implant morbidity
(Fig. 6.7A–C).
FIG 6.7 Coronal positioning. (A) Ideal positioning 1.5 to 2.0 mm from tooth. (B)
Implant/abutment too close to adjacent crown exhibiting bone loss. (C) Abutment in
close approximation to adjacent tooth. (D) Lack of papilla height resulting from lack
of space from implant to adjacent tooth.
Hygiene Difficulties.
Because of the unnatural contours of the prosthesis and the lack of space for
cleansibility, proper hygiene techniques will be difficult. This will result in
plaque buildup and related periodontal complications.
Reduced Papilla Height.

Because of interproximal bone loss due to the proximity of the implant to the
coronal portion of the tooth, a lack of or reduction in the size of papilla will
be present. This will result in periodontal conditions and esthetic issues (Fig.
6.7D).
Prevention
Treatment Planning.
The use of an accurate radiographic modality (CBCT) is paramount in
determining if sufficient space exists for ideal clinical crown size
(measurement on axial slices). Additionally, a study cast and diagnostic wax-
up may be utilized. Ideally, 1.5 to 2.0 mm should be present from the implant
neck to the adjacent tooth (Fig. 6.8).
FIG 6.8 Prevention. (A) The use of CBCT with interactive treatment planning allows
for the accurate placement and positioning of the implant for ideal prosthetic
replacement. (B) Study cast may be used in conjunction with CBCT to evaluate
coronal space available.
Preoperative Modification.
Upon preoperative evaluation, if inadequate space exists for implant
treatment, the following options may be completed to increase mesiodistal
distance:
1. Enameloplasty (modification of the interproximal contact areas) may be

completed on the proximal contours of the adjacent teeth to increase
mesiodistal dimensions. However, aggressive modification may lead to
hypersensitivity and possible endodontic intervention (Fig. 6.9A).
FIG 6.9 Possible treatment options for inadequate spacing. (A) Enameloplasty of
adjacent tooth allows for additional space for prosthesis emergence. (B) Orthodontic
repositioning allowing more space additional spacing (when 12 to 14 mm of space is
available, the mesial and distal contour of the adjacent teeth is modified to gain
addition space). (C) A periapical radiograph of two 3.7-mm implants to replace one
molar, in which the proximal contours of adjacent teeth were reduced. (D) An
intraoral view of two osteotomy sites for the replacement of a mandibular first molar.
(E) When the mesiodistal space is 12 to 14 mm, the implants may be offset to
increase space between the implants. (F) In the mandible, the distal implant is
positioned more buccal and the mesial implant more lingual. In the maxilla, the
mesial implant is more buccal and the distal implant is more lingual. (G) Intraoral
view of mandibular molar with offset implants, the distal implant being more lingual to
facilitate easier flossing (hygiene). (C–G, From Misch CE: Contemporary implant dentistry, ed
3, St. Louis, 2008, Mosby.)
2. Orthodontic intervention may be utilized to upright a tilted adjacent tooth

to increase the intratooth space. For larger spaces (multiple spaces), one
implant may be placed and an orthodontic spring incorporated in the
transitional crown. The spring pushes the distal tooth more distal and, after
orthodontic movement, the second implant may be inserted with less risk
and improved hygiene between each implant. Another option is to reduce
the space orthodontically and place only one implant and crown (Fig. 6.9B).
3. For larger spaces (multiple implants) the implants may be offset with one
implant placed buccal and the other implant on a diagonal toward the
lingual.9 The diagonal dimension increases the mesiodistal space by 0.5 to 1
mm. In the mandible, the most anterior implant is placed to the lingual
aspect of the midcrest and the more distal implant is placed to the facial
aspect to facilitate access of a floss threader from the vestibule into the
intraimplant space. The occlusal contacts also are slightly modified on the
buccal aspect of the mesial implant to occlude over the central fossa. In the
maxilla, the anterior implant is placed facially and the distal implant palatally
to improve esthetics. The distal occlusal contact is placed over the lingual
cusp, and the mesial occlusal contact is located in the central fossa position.
The cervical esthetics of the maxillary molar are compromised on the distal
half of the tooth to achieve greater intratooth distance and easier access for
home care. This maxillary implant placement requires the intraimplant
furcation to be approached from the palate, rather than the buccal approach,
as for the mandible (Fig. 6.9C–D).
Surgical Adjuvants.
A large number of implant clinicians are utilizing positioning devices that
allow for ideal osteotomy preparation and adherence to an implant
placement at least 1.5 to 2.0 mm from the adjacent tooth. A surgical spacer
may be used, which enables the initial osteotomy site to be placed at the
correct position, allowing for adequate space between the tooth and final
implant position (Fig. 6.10A–B). Surgical guidance systems (Salvin) may also
be used to ensure ideal implant placement (buccal-lingual and mesial-distal
spacing) and may be used with any surgical drill system (Fig. 6.10C–D). The
most accurate positioning adjunct is the use of CBCT-generated surgical
templates (tooth supported) (Fig. 6.10E).
FIG 6.10 Ideal placement. (A–B) Positioning device placed on the distal contact of
adjacent tooth allowing for ideal osteotomy site in the edentulous space. (C–D)
Surgical guidance systems may be used for various situations and spacing between
teeth. (E) Tooth-supported surgical template allowing for accurate implant
positioning. (C, Courtesy Salvin Dental Specialties, Inc., Charlotte, NC.)
Treatment
Initial Placement.
If the position of the implant is less than 1.0 mm from the adjacent clinical
crown, removal and reposition of the implant should be completed. If the
implant is positioned 1.1 to 1.5 mm from adjacent tooth, removal or
modification (enameloplasty) of the adjacent tooth may be completed, as
long as irreversible damage to the tooth is not done.
Past Placement.
If implant has been restored and root approximation (<1.5 mm) exists, the
tooth/implant should be monitored. If symptomatic, the implant should be
removed and repositioned along with vitality testing of the tooth.
Too Great a Distance Between Implant and Tooth

Etiology
Too much space between an implant and adjacent tooth is the direct result of
poor treatment planning and/or surgical technique (Fig. 6.11). When
implants are placed more than 2 mm from an adjacent tooth, a cantilever
effect will result on the marginal ridge of the implant crown. In some cases,
this may lead to biomechanical overload or esthetic issues with resulting
bone loss and increased morbidity.
FIG 6.11 Illustration depicting implant placement too far from a tooth (mesial)
leading to a cantilever effect and biomechnical issues.
Complications
Overcontoured Crowns.
Because of the excessive space between the implant and tooth,
overcontouring of the final prosthesis is required to achieve a contact area
with the adjacent tooth. This results in biomechanical issues as well as
esthetic complications.
Atypical Prosthesis.
Because of the need to obtain interproximal contact, the final prosthesis will
be atypical, which may lead to increased difficulty in prosthetic impression,
laboratory, and insertion procedures (Fig. 6.12).
FIG 6.12 Implant positioning too far from tooth. (A) Implant placement too far from
adjacent crown resulting in an excessively large, cantilevered crown. (B) Resultant
prosthesis gives rise to overcontouring/cantilever effect. (C–D) Atypical prosthesis
because of nonideal implant placement and need to obtain contact area, which
results in biomechanical complications and food impaction.
Cantilever Effect (Biomechanics).

The resultant cantilever from a malpositioned implant results in a
biomechanical disadvantage with damaging moment forces, which may
result in bone loss. Cantilevers present on implant prostheses are more
problematic than on natural teeth for several reasons. Forces are magnified
to the entire implant system, which may result in implant screw loosening,
cement retention failure, or even possibly the mobility and failure of the
implant itself. Secondly, because the implant is void of a periodontal
ligament, there is no stress release system in place to protect the implant.
Weinberg et al have shown a 10-degree increase in cusp inclination leads to a
30% increase in the force applied to the restoration. Additionally, studies
have shown that a 10-degree increase in implant inclination can lead to a 5%
increase in force-related function.10 A 1-mm increase in the horizontal offset
of an implant restoration may produce a 15% increase in torque during
function, and a 1-mm increase in the vertical offset introduces a 5% increase
(Fig. 6.13).11 The overcontoured crown leads to resultant shear forces, which
may lead to component failure (i.e., screw loosening, screw fracture, implant
fracture).
FIG 6.13 (A) A posterior implant with a cantilevered crown to the mesial. (B) The
implant fractured within a few years. It is often more predictable to join an implant to
a natural tooth than to cantilever from one implant. (From Misch CE: Dental implant
Food Impaction.
Food impaction is a common complaint from patients with an increased
implant-tooth distance because periodontal maintenance is difficult as a
result of related soft tissue complications.
Periodontal Complications.
Because of difficulty in hygiene, chronic tissue problems often result, which
may cause perimucositis or peri-implantitis, leading to implant morbidity
(see Figs. 6.11–6.12).
Prevention
Positioning Devices.
Prevention for malpositioning may include the use of special positioning
devices that allow for ideal osteotomy placement and adherence to the ideal
placement of 1.5 to 2.0 mm from the adjacent tooth. These predetermined
distance spacers will minimize the possibility of placing the implant too
close or too far from the adjacent tooth (Fig. 6.14).
FIG 6.14 Ideal calculation for implant spacing.
Surgical Templates.
A CBCT-generated template may be used to accurately place the implant.
When an implant is to be placed adjacent to a tooth, a tooth-supported guide
is the most accurate in comparison to bone- or tissue-borne guides (see Fig.
6.10A–B, E).
Treatment
Initial Placement.
If nonideal placement is determined during surgery, the implant should be
repositioned in the ideal position (i.e., 2 mm from adjacent tooth). The
osteotomy should be initiated with the following formula:
In other words, a 4.0-mm implant pilot osteotomy would be 2.0 mm + 2.0 mm

= 4.0 mm from the adjacent tooth. If the initial osteotomy is not ideal, a
Lindemann drill (side cutting) is used to reposition the osteotomy into the
correct position.
Past Placement.
If the implant has already been placed and is ready to be restored, the
amount of occlusal force should be assessed to determine the ideal
treatment:
Minimal Occlusal Forces: If favorable force factors exist, then a cantilever

(overcontoured crown) may be fabricated with (Fig. 6.15A):
• Narrow occlusal table
• Minimal cusp height: It has been reported that every

10-degree increase in cusp inclination leads to a 30%
increase in the torque applied to the restoration during
function10
• No lateral contacts
FIG 6.15 Treatment of excessive distance. (A) Prosthesis with narrow occlusal
table, minimal cusp height and no lateral contacts. (B) To decrease implant-tooth
distance, the natural tooth may be elongated or overcontoured by the use of a crown
or bonding (arrow).
High Occlusal Forces: If unfavorable forces are present, a cantilever is

contraindicated and the mesiodistal distance is reduced by either:
• Overcontouring adjacent crown (e.g., crown,

composite) (Fig. 6.15B)
• Remove implant and reposition

Mesial-Distal (“X” Axis): Implant–Implant
Lack of Implant-Implant Distance
Etiology
When implants are placed too close together, it is usually the result of poor
treatment planning or surgical technique (Fig. 6.16). Treatment planning
issues can be prevented by using ideal spacing rules. The guidelines include
approximately 3.0 mm between implants, and >1.5 to 2.0 mm from adjacent
teeth.
FIG 6.16 Illustration depicting inadequate space between two implants.
Complications
Bone Loss.
Because of the lack of interproximal bone a decreased blood supply will
result in bone loss. Tarnow et al have shown that implants placed less than
3.0 mm apart may have adequate stability and function; however, this
placement will likely result in crestal bone loss. In this study, implants with
greater than 3 mm distance between implants resulted in a 0.45 mm bone
loss, while implants positioned less than 3 mm had over twice the amount of
bone loss, or approximately 1.04 mm.12
Lack of Interimplant Papilla.

When lack of space exists between the implants, the resultant bone loss will
be responsible for the loss of the papilla. As the bone resorbs, the distance
between the contact point of the crowns and the bone level increases. As this
distance increases (i.e., above 5 mm), the papilla will become smaller in size
and contour.
Hygiene Difficulty.
Because of the lack of space, difficulty in hygiene access will result in poor
tissue health. The resultant tissue condition will most likely lead to
perimucositis or peri-implantitis.
Prosthetic Issues.
Inability or difficulty in obtaining a final impression (placement of
impression transfer copings) may result from lack of space between
implants. With some implant systems the transfer copings may be adjusted
to allow for impression of the implant bodies. Additionally, an
unconventional implant prosthesis (irregularly contoured) will most likely
need to be fabricated (Fig. 6.17).
FIG 6.17 Implant-implant distance. (A) Ideal spacing of 3 mm. (B) Lack of implant-
implant distance showing minimal space for prosthesis and maintaining bone health.
(C) Lack of space results in difficulty in hygiene with resultant soft tissue
complications. (D) When implants are placed too close together, difficulty in
obtaining accurate transfer impressions results. In some cases, the transfer
impression copings may be altered to obtain final seating. A radiograph confirming
the complete seating of the transfer copings should be completed prior to the
impression.
Prevention
Ideal Distance.
It is important to maintain 3 mm or more space between final implant
positions. This will allow adequate room for interdental papilla and tissue
health, cleansibility, transfer copings during prosthetic impressions, and
minimizing horizontal bone loss.
Osteotomy Measurement.
A formula exists for ideal placement of initial osteotomies in anticipation of
the final implants. For example, when placing 5.0 mm and 4.0 mm implants,
add diameter of implant + 3.0 mm between implants and 2.5 mm + 2.0 mm
+ 3.0 mm = 7.5 mm between osteotomy sites. Additionally, special spacing
guides may be used for ideal positioning.
Treatment
Initial Placement.
If implants are not ideally positioned (see Figs. 6.10 and 6.14), the osteotomy
should be repositioned to ideal positions (3 mm between implants). The
implant positions may be altered with the side-cutting Lindemann drill (Fig.
6.18A–B).
FIG 6.18 (A) The prevention of multiple implants being placed too close together
includes the use of interactive treatment planning to ensure ideal spacing. (B)
Inadequate space between implants; ideally one of the implants should be removed
and replaced in a more ideal position. (C) When implants are already restored, a
strict recall should be adhered to monitor bone loss and related periodontal
complications.
Past Placement.
If implants have been restored, removal of implants and repositioning
should be completed if the patient cannot adequately clean the prosthesis. In
some situations, the abutment/implant body may be minimally modified to
gain extra space, usually with a flame-shaped diamond bur. This is best
completed with external hex implants because modification of internal hex
implants may alter structural integrity of the implant leading to possible
fracture (Fig. 6.18C).
Implant Angulation Positioning (“Y” and “Z”
Axis)
Buccolingually (“Y-Axis”)
The buccolingual positioning of the dental implant is crucial to the esthetic
and biomechanical effectiveness of the final prosthesis. Frequently, implant
positioning is dictated by the resulting available bone, leading to angulation
complications. Bone remodeling after tooth extractions is common with
resorption occurring from the buccal plate initially, thereby decreasing the
width of bone. Ideally, the implant position is in the center of the ridge, with
a minimum of 1.5 mm present on the buccal and 0.5 mm on the lingual
aspects of the ridges (Fig. 6.18). When present, adequate cortical bone
minimizes future hard and soft tissue recession. In this scenario, if bone loss
occurs on the implant, the facial plate will remain intact and minimal
recession on the facial aspect of the implant will result. Spray et al have
shown if the facial bone is more than 1.8 mm in thickness (after implant
placement), recession infrequently results. However, if the facial plate is less
than 1.8 mm, vertical resorption occurs quickly, mainly because of the lack of
blood supply (Fig. 6.19).13 Improper buccal-lingual positioning has a direct
impact on the type prosthesis, and resultant complications are prosthesis-
dependent.
FIG 6.19 Ideal implant placement for anterior implants. (A) Cement retained
through the incisal edge. (B) Ideal Positioning. (C) Screw retained through the
cingulum area. (D–E) Ideal posterior implant placement with buccal-lingual
placement in line with the central fossa of adjacent teeth. (From Misch CE: Dental implant
Fp-1 and Fp-2 Prosthesis
Prevention
Cement-retained (anterior).
When a FP-1 prosthesis is indicated, precise implant placement is necessary
to obtain an ideal result. In the anterior region, the ideal implant position
allows the placement of a straight abutment directly under the incisal edge of
the final crown for a cemented prosthesis. The resulting forces are
concentrated along the long axis of the implant, minimizing damaging shear
forces. For example, the natural maxillary anterior teeth are loaded at a 12- to
15-degree angle, mainly because of their natural angulation in comparison
with the mandibular anterior teeth. This is one reason the maxillary anterior
teeth are wider in diameter than mandibular anterior teeth (which are loaded
in their long axis). The facial angulation position of the implant body often
corresponds to an implant body angulation, with 15-degree off-axial loads.
The angled load will result in an approximate 25% increase in force to the
implant prosthesis. Many complications may occur from the offset loads,
which include abutment screw–implant–bone complex by 25.9% compared
with a long-axis load.14 Abutment screw loosening, crestal bone loss, and
cervical soft tissue marginal shrinkage.15 As a result, implants angled facially
may compromise the esthetics and increase the risk of technical
complications.
Screw-retained (anterior).
For screw-retained prostheses the implant should emerge toward the
cingulum of the anterior tooth so that the access hole does not affect the
esthetics of the restoration. If the implant is placed too facially, the access
hole will impinge on the esthetics of the restoration (screw hole through the
facial of the restoration). If the implant is placed too far lingually,
overcontouring of the final crown may result in biomechanical issues and
possible occlusal interferences (Fig. 6.19A–C).
Posterior region (cement- or screw-retained).

In the posterior region, the long axis of the implant should emerge within the
approximate center (central fossa) of the prosthesis for a screw- or cement-
retained FP-1 or FP-2. This allows occlusal forces to be directed ideally along
the long axis of the implant (Fig. 6.19D–E).
Complications
Facial.
If the implant is placed too facial for an FP-1 or FP-2 prosthesis, esthetic
issues will result due to overcontouring of the prosthesis. Bone dehiscence
usually will be accompanied by tissue recession and this complication is
more pronounced in thin biotype patients. Facial positioning is often a
complication when implants are placed in immediate extraction sites.
To correct the facial position of the implant, an angled abutment must be
used. However, because of the access hole, the facial of the abutment is more
bulky. This results in overcontouring of the facial aspect, which will lead to
tissue recession and bone loss (Fig. 6.20).
FIG 6.20 Facially placed complications. (A) Facial positioning, lack of bone
present. (B–C) Resultant prosthetic and periodontal complications. (D) Severely
facial-positioned implants predisposing to prosthetic rehabilitation issues. (E–F) An
angled abutment has an access hole for the fixation screw, which exits the facial of
the abutment. As a result, less metal is on the facial. The manufacturer usually
increases the metal thickness to improve the strength (E). As a result of the facial
flare of metal on an angled abutment, the abutment is more facial than the implant
body (F). (G) The angled abutment is usually wider on the facial than the implant to
increase the metal thickness on the facial of the abutment. (E–G, From Misch CE: Dental
Lingual.
Implants placed too far to the lingual can result in facial overcontouring of
the final prosthesis (ridge lap) for esthetic reasons. The prosthetic
impression and placement of the prosthesis is also complicated, which
results in difficulty with the seating of the abutments. Because of the
overcontouring of the lingual contours, patients often complain of lack of
space for the tongue, which may impede speech. In the anterior region, a
lingual placed implant may make the implant nonrestorable if the patient
has a deep bite occlusion and insufficient interocclusal space (Fig. 6.21).
FIG 6.21 Lingual placed complications. (A) Lingually placed abutment showing
overcontouring and possible tongue impingement. (B) Lingually placed implant
showing biomechanical offset loading (cantilever). (C) FP-3 prosthesis showing
ridge lap of prosthesis, complete lingual version.
FP-3 Prosthesis
Prevention
Screw-retained.
After evaluation of the articulated setup, arch form, available bone, and force
factors, the FP-3 prostheses should be determined to be either screw retained
or cement retained. For screw-retained prostheses, ideal positioning should
be slightly lingual to the denture or porcelain teeth to minimize tooth
fractures and delamination.
Cement-retained.
For cement-retained restorations, implant positioning should be located
along the incisal edge in the anterior region and in the central fossa area in
the posterior. If force factors are a concern, ideal implant placement is crucial
to minimize biomechanical overload. However, if force factors are low,
nonideal placement is less of a problem with cement-retained prostheses
because abutment angulation may be modified (Fig. 6.22).
FIG 6.22 Ideal implant placement for removable prosthesis. (A) Occlusal view. (B)
Anterior view. (From Misch CE: Dental implant prosthetics, ed 2, St. Louis, 2015, Mosby.)
Complications
Facial.
Implants positioned too facially will impinge on the esthetics, complicate
screw insertion, and result in increased prosthesis component fractures.
Every 10-degree increase in implant inclination may lead to a 5% increase in
the torque applied to the restoration during function.10
Lingual.
Implants placed too far lingually will result in an overcontoured prosthesis,
resulting in possible speech problems in the maxilla and crowding of the
tongue in the mandible.
RP-4 and RP-5
Prevention.
Implants placed for removable overdentures should be positioned to emerge
within the body of the denture base. This is important so the components
that are attached to the implant do not impinge on the ideal setting of the
denture teeth. Denture acrylic requires a minimum of 2.0 mm of bulk for
strength and resistance form to prevent fractures and delamination.
Complications
Lingual.
Implants that are positioned too far lingually for an overdenture will result in
overcontouring the lingual surface of the denture. This may interfere with
phonetics, and often patients will complain of lack of space for the tongue. If
the lingual aspect of the denture is thinned too much during adjustment, this
will result in an area of possible fracture.
Facial.
Implants placed too far facially will interfere with ideal denture tooth
placement, leading to possible denture tooth “pop offs.” In addition, facially
positioned implants often result in lack of adequate attached tissue and
potential periodontal concerns because gingival irritation and recession are
more likely to result. This may lead to chronic pain, and remediation is
usually unsuccessful (Fig. 6.23).
FIG 6.23 Removable prosthesis complications. (A–B) Facial placed implants with
resultant soft tissue complications leading to tissue soreness. (C) Lingually placed
implants resulting in tongue space impingement. (D–E) Lingually placed implants
leading to overdenture attachment complications and fracture of the denture base
because of minimal acrylic thickness.
Apicocoronal (Z-Axis)
The depth of implant placement is significant in relation to complications.
Whether placed too deep or not apical enough, prosthetic and periodontal
complications may increase implant morbidity.
There exists much controversy in implant dentistry regarding the
placement level of an implant. Some authors have suggested that the implant
be countersunk below the crestal bone more than 4 mm below the facial CEJ
of the adjacent teeth to develop a crown emergence profile similar to a
natural tooth, to prevent soft tissue recession, and to support the tissue of
the adjacent natural teeth.16,17 In theory, this provides an emergence
transition of approximately 5 mm on the facial aspect to obtain the width of
the natural tooth (the ideal free gingival margin on the facial is 1 mm above
the CEJ).
The ideal crown height space (CHS) for a fixed prosthesis is between 8 and
12 mm, accounting for an ideal 3 mm of soft tissue, 2 mm of occlusal material
thickness, and a 5 mm or greater abutment height. A CHS greater than 12
mm may be of concern in fixed restorations. The replacement teeth are
elongated (FP2 or FP3) and often require the addition of gingival tone
materials in esthetic regions. The greater impact force on implants compared
with teeth, combined with the increased crown height, creates increased
moment forces on implants and carries the risks of uncemented or
unretained prostheses as well as component and material fracture. These
problems are more problematic when associated with less favorable
biomechanics on cantilevered sections of fixed restorations.18 In case of
excessive CHS, bone augmentation may be preferred to prosthetic
replacement, especially in type C−h or D bone volumes. Surgical
augmentation of the residual ridge height reduces the CHS and improves
implant biomechanics by both position and number. Augmentation often
permits the placement of wider-body implants with the associated benefit of
increased surface area. Prosthetics is the most commonly used option to
address excess CHS; however, it should ideally be the last choice. Using
gingival-colored prosthetic materials (pink porcelain or acrylic resin) on fixed
restorations or changing the prosthetic design to a removable restoration
should often be considered when the prosthesis is used to restore excessive
CHS with unfavorable conditions.
In regards to the effects of CHS on papilla form, Tarnow et al have shown
that if the bone level to the contact area is less than 5 mm, 98 % of the time
the embrasure space will be filled in. If the distance increases to 6 and 7 mm,
the presence of a papilla reduces to 56% and 27%, respectively (Fig. 6.24).19
FIG 6.24 Ideal and nonideal apicocoronal positioning. The literature usually reports
two positions for the depth of the implant. The facial bone of a healthy natural tooth is
about 2 mm below the cement-enamel junction (CEJ), and the soft tissue from the
free gingival margin to the bone is 3 mm. An implant inserted 4 mm or more below
the facial CEJ often is countersunk below the crestal bone 2 mm or more (A). This
gives “running room” for the porcelain on the crown to create a natural-looking
emergence profile. However, bone loss is likely to occur beyond the implant
abutment connection and often proceeds to the first thread beyond the crest module.
As a result, an increase in probing depth and growth of anaerobic bacteria are more
likely. (B) An implant placed 2 mm below the adjacent facial CEJ provides 3 mm of
soft tissue drape to develop with a natural appearance and is best. An implant
placed too shallowly causes severe emergence profile angles and compromises
esthetics. (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
Fp-1, Fp-2, Fp-3
Complications
Placement too deep.
When implant placement results in positioning 2 mm below CEJ or 3 mm
below free gingival margin, many complications may result:
• Unfavorable crown height space (crown-implant ratio).
• Periodontal complications because of inability to perform proper hygiene
and bone loss on adjacent teeth
• Higher moment forces may cause biomechanical overload with resultant
crestal bone loss
• Prosthetics are more complicated with difficulty in impression taking,
placing abutments, and seating the prosthesis.
• With deeply placed implants, often the facial plate will resorb, especially if
facial inclination is present.
• Long-term sulcular health is decreased because the trabecular bone around
the crest module is weaker against occlusal loads.
• Resultant initial crown height is increased, as are moment forces. A further
increased risk of soft tissue shrinkage occurs long term, with additional
bone loss at the crest module. The result is longer clinical crowns, which
also decrease gradually in width (as the narrowing dimensions approach the
implant body), with resultant black triangular spacings in lieu of interdental
papillae and compromised long-term esthetics (Figs. 6.25–6.26).
FIG 6.25 (A) Implant placed greater than 3.0 mm from free gingival margin. (B) The
crown height is not a multiplier of force when the load is in the long axis of the
implant. However, any angled force or cantilever increases the force and the crown
height magnifies the effect. (From Misch CE: Contemporary implant dentistry, ed 3, St Louis,
2008, Mosby.)
FIG 6.26 (A) Too deep implant positioning leading to impingement on the inferior
alveolar canal. (B) Resultant periodontal and increased crown-implant ratio. (C)
Unfavorable crown-implant ratio with implant placed too deep and lingually positioned
with unfavorable biomechanics.
Treatment
Treatment planning phase.
If during the treatment planning phase it is determined there exist no
alternatives to placing the implants at a compromised depth (i.e., bone
grafting contraindicated), the following can be completed to decrease the
possible of complications:
• Increase the number of implants.
• Increase the diameters of implants.
• Design implants to maximize the surface area.
• Fabricate removable restorations (less retentive) and incorporate soft tissue
support.
• Remove the removable restoration during sleeping hours to reduce the
noxious effects of nocturnal parafunction.
• Splint implants together, regardless of whether they support a fixed or
removable prosthesis (Fig. 6.27).
FIG 6.27 Treatment planning for apicocoronal issues. The greater the crown height
space (CHS), the more implants are required to restore the patient (right side of
drawing). The less the CHS (left side), the fewer the implants to restore the
patient. (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
At time of surgery.
If an implant is inserted and the position is known to be excessively deep,
ideally the implant should be removed, bone graft the site, and then replace
the implant at an ideal position after sufficient healing. If rigid fixation
cannot be accomplished, the implant should be removed and grafting
allowed to heal with future implant placement.
Integrated implant.
If it is determined after integration that the implant position is
compromised, then the risk vs. benefit of removing the implant needs to be
determined. If the morbidity of removing the implant is too significant, then
the implant may be be restored with the following guidelines:
• Shorten cantilever length.
• Minimize buccal and lingual offset loads.
• Ideal emergence profile.
• Occlusal contact load should be reduced on any offset load from the
implant support system.
• Occlusal contacts in centric relation (CR) occlusion may be eliminated on
the offset load area. A parafunction load may be reduced because the most
cantilevered portion of the prosthesis is loaded only during functional
activity while eating food.20
Note: Questionable treatments including segmental osteotomies are not
recommended due to the invasiveness, length of treatment time, and
questionable prognosis.
Complications
Placement with inadequate depth
• When implant positioning is not deep enough (<3 mm from CEJ, <2 mm
from free gingival margin).
• Inadequate emergence profile (transition from the narrower diameter of
the implant compared with the wider dimension of the crown)
• Decreased retention of the implant, which may lead to uncementable
restorations or component fracture
• Poor resultant esthetics because implant abutment or implant body will
show through resulting in cervical darkness, and if this occurs in the
anterior region, it may be unpleasant for the patient. Normally, the facial
margin of the crown will not be able to be placed subgingival enough to
mask the titanium color of the abutment below the margin.
• Inadequate running room because the location of the crest module will
leave inadequate room for adequate hygiene. An abrupt change from the
prosthetic platform to the diameter of the restoration will result. Normally,
this will most likely result in hygiene difficulty.
Treatment
Treatment planning phase.
If it is determined during the treatment planning phase that implant
positioning would result in an implant being in a nonideal location with
respect to the free gingival margin, modifications to the treatment plan or
final prosthesis may be indicated. Skeletal discrepancies (deep bite), reduced
occlusal vertical dimension (OVD) from attrition or abrasion, minimal bone
atrophy after tooth loss, and supraeruption of unopposed teeth may all result
in less-than-ideal space for prosthetic replacement of the dentition.
Traditional prosthetic and restorative procedures are indicated to restore the
proper OVD and plane of occlusion and increase the crown height space.
• Modification or adjustment of opposing occlusion should always be
explained to the patient at the initiation of treatment to prevent
miscommunication issues. This is extremely important, especially if
alteration of the opposing tooth would result in the need for endodontic
therapy.
• Ideally, 8.0 mm of space is required for a cementable prosthesis. The 8-mm
requirement for CHS consists of 2 mm of occlusal material space, 4 mm
minimum abutment height for retention, and 2 mm above the bone for the
biologic width dimension (which does not include the sulcus because a
crown margin may be 1 mm subgingival for retention or esthetics). If this
cannot be accomplished, a screw-retained prosthesis or change to a fixed
partial denture treatment plan is indicated.
At time of surgery.
If the implant is inserted and the position is known to be excessively shallow,
removal of the implant is indicated, the osteotomy should be deepened if
available bone is present, and the implant is reinserted at a more favorable
depth. The location of vital structures should always be determined prior to
deepening of the osteotomy.
Integrated implant.
After implant integration, if the implant is determined to be of inadequate
depth, the implant should be ideally removed. However, if the morbidity of
removing the implant is too significant, then the following may be evaluated
as possible treatment options:
• A screw-retained prosthesis
• Shorten cantilever length
• Minimize buccal and lingual offset loads
• Ideal emergence profile (Fig. 6.28)
FIG 6.28 Implant placement too shallow. (A–B) Too high above the free gingival
margin (FGM) and cemento-enamel junction (CEJ). (C) Resultant fracture screws.
(D) Poor emergence profile because of lack of crown height space.
• Increase mechanical and chemical retention of the abutment by roughening

the abutment surface.
RP-4 and RP-5

Prevention (RP-4, RP-5).
Caution must be exercised to ensure there is adequate interocclusal space for
the overdenture prosthesis, especially if a connecting bar is used. For a bar
and overdenture with attachments, at least 15 mm from the crest of the ridge
to the incisal edge is suggested. If interocclusal space is needed, an
osteoplasty at the time of surgery should be completed to increase space for
the final prosthesis. Interactive treatment planning may be used to fabricate
a reduction guide, which will allow the implant clinician to remove the ideal
amount of bone. A minimum of 2.0 mm of acrylic is required to adequately
retain denture teeth and maintain structural integrity of the prosthesis.
Complications
More than 15 mm.
For an RP-5 prosthesis, greater interocclusal space is usually not problematic
because of the soft tissue support. However, with an RP-4 (implant
supported)prosthesis, greater interocclusal space may pose a problem with
increased “rocking” of the prosthesis because of the lack of soft tissue
support (i.e., RP-4 is completely implant supported). With removable
prostheses, two prosthetic levels of height should be taken into
consideration. The first is the height of the attachment system to the crest of
the bone. The greater the height distance, the greater the forces applied to
the bar, screws, and implant structures. The second CHS to consider is the
distance from the attachment to the occlusal plane. This distance represents
the increase in prosthetic forces applied to the attachment. For example, in a
CHS of 15 mm, a locator attachment may be 7 mm from the crest of bone,
resulting in a lever action of 7 mm applied to the implants. The distance from
the rotation point of the locator attachment to the occlusal plane may be an
additional 8 mm. Under these conditions, a greater lever action is applied to
the prosthesis than to the implant interface. This results in increased
instability of the restoration under lateral forces.20
Treatment.
If more than 15 mm of space is present, a RP-5 prosthesis should have ideal
interocclusal space for the final prosthesis. Peripheral extension and the
primary stress-bearing area support (maxilla—horizontal palate; mandible—
buccal shelf) should be utilized to decrease excessive loading force. The
occlusion should include bilateral balanced contacts with no occlusal
prematurities. If excessive force exists, (i.e., excessive CHS and/or
parafunction) an RP-4 (totally implant supported) may be changed to an RP-5
(soft tissue supported) to decrease the force.
Complications
Less than 15 mm.
When sufficient CHS is lacking and the prosthesis is more prone to
component fatigue and fracture, an overdenture is more difficult to fabricate
than a porcelain-to-metal fixed prosthesis. The 15-mm minimum CHS
provides adequate bulk of acrylic to resist fracture, space to set denture teeth
without modification, and room for attachments, bars, soft tissue, and
hygiene. In the mandible, the soft tissue is often 1 to 3 mm in thickness
above the bone, so the occlusal plane to soft tissue should be at least 9 to 11
mm in height. An osteoplasty to increase CHS before implant placement or a
fixed restoration is often indicated when abundant bone height and width
are present (Fig. 6.29).
FIG 6.29 Lack of interocclusal space for removable prosthesis. (A) Evaluation in
the treatment planning phase. (B) Complication resulting from lack of interocclusal
space, patient in rest position showing bar (suprastructure). (C–D) Decreased
interocclusal space should be diagnosied preoperatively and treated with aggressive
osteoplasty. (E) Lack of acrylic bulk leads to poor retention of denture teeth and
possible fracture of denture base (<2 mm); at least 2 mm of acrylic is needed for
strength. (F) For a bar-retained overdenture, approximately 15 mm (from alveolar
ridge to incisal edge) is required for adequate space of teeth, acrylic, bar, and soft
tissue space. (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
Treatment.
If less than 15 mm of CHS is present, an RP-4 and RP-5 may present issues.
Without sufficient space for tissue health, attachment space, bulk of acrylic,
and nonmodified denture teeth, the overdenture may undergo fatigue and
possible fractures. An RP-4 may be changed to an RP-5 to obtain soft tissue
support to minimize forces to the attachments. Additionally, the overdenture
prosthesis should be changed to a metal base, metal reinforced, or fiber
mesh to increase the strength of the prosthesis to prevent prosthesis
fracture.
Distance From Vital Structures
Implant Position
Inferior Alveolar Nerve Canal or Mental Foramen
Accurate positioning of implants in approximation to the inferior alveolar
canal and mental foramen is crucial in preventing neurosensory impairment.
The correct location of the nerve and canal should ideally be ascertained via
three-dimensional imaging, especially when the implant may be within 2 mm
of the nerve. After identification of the vital structures, the implant should
be placed greater than 2 mm from the inferior alveolar canal or mental
foramen. Implant placement less than 2 mm increases the risk of
compression or traumatic injuries to the nerve trunk, which may result in
neurosensory deficits (Fig. 6.30).
FIG 6.30 Distance from the (A) inferior alveolar nerve canal or mental foramen. (B)
Placement of implant too deep, violating the inferior alveolar canal.
Inferior Border of Mandible

Placement of dental implants in the anterior mandible can lead to significant
and even life-threatening complications. Care should be noted to evaluate the
angulation and trajectory of the anterior mandible with three-dimensional
imaging to minimize the possibility of perforating the lingual cortex. Two-
dimensional radiographs (i.e., panoramic) may lead to false representation of
the amount of bone available. If the inferior border of the mandible is
perforated, bleeding may become evident from the sublingual and
submental blood vessels. Because this area is difficult to obtain access to,
dangerous sublingual bleeding complications may arise (See Chapter 7) (Fig.
6.31).
FIG 6.31 (A–B) Over preparation in the anterior mandible leading to possible
sublingual bleeding.
Nasal Cavity
The anterior maxilla is often a very challenging area to place implants.
Because of the compromised bone in width and height, along with
angulation issues, implants are often malpositioned. Placement of implants
in the anterior maxilla may be very challenging, especially when minimal
height of bone is present. Ideally, implants should be positioned just short of
the nasal floor, without engaging the thin inferior floor of the nasal cavity.
There does exist more advanced surgical techniques where the implants may
extend into the nasal cavity 2 to 4 mm via a subnasal graft; however, these
procedures should only be completed in ideal circumstances (Fig. 6.32).21
FIG 6.32 Anterior maxilla. (A) Ideal placement (arrow). (B–C) Penetration into the
nasal cavity.
Distance From the Maxillary Sinus (Inferior Border)

One of the more challenging areas for implant placement involves the
posterior maxilla. The implant dentist often encounters compromised bone
height and poor bone quality in this area because of bone loss and
pneumatization of the maxillary sinus. There are four treatment options
(Misch Classification) for implants placed in this area with respect to the
quantity of bone from the crest of the ridge to the inferior border of the sinus
(Fig. 6.33)15:
1. SA-1: Greater than 12 mm of bone; a standard implant placement protocol

is indicated
2. SA-2: When 10 to 12 mm of bone is present and the implant is placed along

with antral floor elevation through the osteotomy site 0 to 2 mm
3. SA-3: When 5 to 10 mm of bone is present, sinus grafting is indicated with

(SA-3I) or without (SA-3D) simultaneous implant placement.
4. SA-4: Less than 5 mm of bone is present, which necessitates a lateral wall

sinus augmentation procedure before implant placement.
FIG 6.33 (A–B) Implant penetration into the sinus cavity. (C) Implant-induced
rhinosinusitis. (D–G) Posterior maxilla treatment planning: SA-1 and SA-2 (D and E),
SA-3 (F), and SA-4 (G). (D–G From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Malpositioning Complication Summary
Prevention
Ideal Treatment Planning
The surest way to minimize prevent errors in angulation during implant
surgery is to develop a comprehensive strategy during the preoperative
assessment phase of treatment. CBCT analysis offers the clinician an
excellent evaluation of the patient's anatomy to properly plan implant
position, diameter, and length helping prevent positional, spacing, and depth
issues.
Ideal Available Bone

The amount of available bone width (faciopalatal) should be at least 2.0 mm
greater than the implant diameter at implant insertion. A 3.5-mm implant
requires at least 5.5 mm of bone width (minimum). Augmentation has
become very predictable and accepted in the profession, therefore the
clinician should never compromise when adequate bone is not available.
Various bone grating techniques and materials are available that the clinician
should implement in treating these compromised cases.
Understanding the Prosthesis Type and Associated Ideal

Positioning
When treatment planning, the final prosthesis should always be evaluated
first, prior to implant placement. The implant clinician must have a strong
understanding of the various prosthesis types (e.g., FP-1, FP-2, FP-3, RP-4, RP-
5) along with the positional and prosthesis demands and needs. The
prosthesis type (fixed [FP-1, FP-2, FP-3] or removable [RP-4, RP-5]) dictates
the ideal placement of implants. The implant clinician must understand that
positioning changes as per the type of prosthesis.
Soft Tissue Evaluation

The biotype (thin vs. thick) bone should always be evaluated prior to implant
placement. Thin biotypes are at higher risk of gingival recession and esthetic
issues, especially in the anterior part of the mouth. Thin biotype patients are
more susceptible to malpositioning issues and greater emphasis should be
noted on ideal conditions. If needed, soft tissue augmentation should be
completed prior to implant placement.
Condition of the Adjacent Teeth

Prior to implant placement in edentulous sites, the adjacent natural teeth
should be evaluated for restorability and existing pathology that may be
present. A 5- to 10-year prognostic window should be established for each
natural tooth prior to the completion of an implant treatment plan. If a tooth
does not possess a favorable 5- to 10-year prognosis, extraction should be
discussed or alternative treatment options.
Presence of Pathology
The intended implant site should be carefully evaluated for the presence of
pathology at the site or latent adjacent pathology associated with natural
teeth, which may lead to increased implant morbidity. It is common to have
residual bacteria still present, especially if a recently infected natural tooth
extraction was performed. Additionally, the adjacent teeth should be
evaluated for periapical pathology, as this may lead to a retrograde peri-
implantitis.
Good Surgical Technique

To minimize the possibility of improper angulation, the implant clinician
should evaluate the osteotomy angulation after the use of the first pilot drill.
Usually, the pilot drill is used to a depth of 6 to 8 mm. A direction indicator is
placed, and should be evaluated both radiographically and with a surgical
template for proper positioning. The position can also be evaluated by having
the patient close lightly to determine the interocclusal positioning with the
direction indicator. Any modifications of the angulation should be completed
with a Lindemann drill.
Poorly Dense Bone

In poorly dense bone (≈D4), overpreparation of the osteotomy site may lead
to redirection of the implant upon placement. Additionally, implants should
be inserted with a handpiece instead of by hand ratcheting. When implants
are placed in poorly dense bone with a ratchet, the implant may be easily
redirectioned by placing in a more elliptical direction.
Understand the True Location of Vital Structures

Knowing the exact location of the vital structures is paramount in avoiding
complications. Impinging on vital structures such as the mandibular canal,
maxillary sinus, or nasal cavity may increase morbidity and place the patient
at risk for irreversible complications.
Use of Surgical Templates

A surgical template is defined by the prosthodontics glossary as a guide used
to assist in ideal surgical placement and angulation of dental implants.22 The
objective of using a surgical template is to provide accurate placement of the
implant according to a surgical treatment. There are many different types of
surgical templates used today. Stumpel classified surgical templates
according to the amount of surgical restriction that is utilized in the
template. The categories are: (1) nonlimiting, (2) partial limiting, and (3)
complete limiting design.23
Nonlimiting Design.
The nonlimiting template allows the implant surgeon dimensional variability
in the implant location because the template indicates the ideal space
(location) for the final restoration, not the actual mesiodistal angulation. The
nonlimiting template has become popular because of the ease in fabrication
and the low cost involved.
Complication.
These templates allow the implant surgeon only an initial location of the
proposed prosthesis, not the correct angulation (buccal-lingual) and position
(mesiodistal). A great deal of flexibility and latitude regarding the final
position of the implant is inherent with this type of template (Fig. 6.34).
FIG 6.34 (A–D) Examples of nonlimiting surgical templates, which do not allow for
accurate mesial-distal or buccal-lingual positioning of the patient. (From Misch CE:
Partial Limiting Design.

The partial limiting design incorporates a guided sleeve or a slot that allows
for angulation of one drill size, usually the pilot drill. After the first drill is
used, the rest of the osteotomy sites are completed freehand. Various
techniques can be utilized in fabricating a partial limiting template including
manual laboratory-fabricated templates or templates fabricated from a
radiographic template, which is then converted into a surgical guide
template.
Complication.
Although the partial limiting design is more accurate than a nonlimiting
design, these templates still do not allow for final, accurate positioning of the
implant. Clinical studies have shown these types of templates to have high
degree of error in the buccal-lingual orientation (Fig. 6.35).24
FIG 6.35 (A–D) Examples of partial limiting templates, which have the
disadvantage of not allowing for final positioning or placement of the implant. (From
Complete Limiting Design.

With the complete limiting template design, the position, angulation, and
depth of the osteotomy are dictated by the guided tubes or sleeves, thus
restricting any variation by the implant surgeon. This type of guide prevents
any osteotomy error in the bucco-lingual and mesiodistal planes.
Additionally, drill stops can be incorporated to prevent overpreparation of
the site. Basically, with the complete limiting design, the final position of the
implant is known before the actual surgery. This technique is becoming
popular because the prosthetic final abutment or provisional restoration can
be prefabricated for immediate provisionalization after implant placement.
Complication.
The use of complete limiting surgical templates that are fabricated from
interactive treatment planning with cone beam technology has been shown
to be highly accurate. However, caution must be used when employing
surgical templates that are fabricated conventionally (not from CBCT) on
dental study casts, which are rigid, nonfunctional surfaces without
information of the soft tissue thickness and bone morphology. These types of
surgical templates allow for placement of implants according to an estimate
of location of teeth, soft and hard tissue, and vital structures without three-
dimensional guidance (Figs. 6.36–6.37).25
FIG 6.36 (A–B) Tooth-supported complete limiting templates. (C–D) Bone-

supported complete limiting templates. (From Misch CE: Dental implant prosthetics, ed 2, St
FIG 6.37 CBCT Surgical Templates, (A) Tooth-Supported, (B) Bone-Supported, (C)
Tissue-Supported, (D) CBCT surgical templates allow for accurate placement of
implants.
Use of CBCT Surgical Guides

To overcome the limitations and complications inherent with conventional
surgical templates, the use of CBCT-generated templates has evolved in
implant dentistry today. A computer-generated surgical guide (partial
limiting or complete limiting) provides a link between the CBCT treatment
plan and the actual surgery by transferring the interactive plan accurately to
the surgical site. The two most common surgical templates are those from
Materialise (SimPlant), which are termed surgiguides, and those from Nobel
Biocare (NobelGuide), which are termed surgical templates. Other
commercially available software programs include ImplantMaster (I-Dent
Imaging, Ltd., Hod Hasharon, Israel), Easy Guide (Keystone Dental,
Burlington, MA), and coDiagnostiX (IVS Solutions AG, Chemnitiz,
Germany).
With the use of CBCT-generated software programs (e.g., SimPlant), this
anatomic relationship can be predictably determined before surgery. After
the scan is completed with the radiopaque template, the data must be
converted into a format that can be used by the scanning software. Every
treatment-planning software program has its own specific protocol, but all
software is compatible with DICOM (digital imaging and communication in
medicine) files that are generated and downloaded from the scanner.
Although third-party vendors have integrated a interactive treatment
planning for the placement of the implants, it is highly recommended that
the implant dentist be involved in this planning process.
After the files have been converted into the software program, evaluation
of potential implant sites in the desired prosthetic locations can be
completed. Virtual implants may be placed via comprehensive implant
libraries, which include the implant brand, type, diameter, and length. The
available bone dimensions may be ascertained along with the density and
angulation with respect to the planned prosthesis. After completion of the
final implant positions, the treatment plan is saved, and the surgical
template is designed.20
Complications.
Even though CBCT surgical templates are highly accurate, there are inherent
errors that may occur when placing dental implants, which will result in
malpositioning of the implants. Studies have shown that tooth-supported
guides are the most accurate, followed by bone supported, with the least
accurate being soft tissue–supported. This is mainly due to the questionable
stability of the template during the CBCT scan and the implant placement
with tissue supported templates. Bone-supported templates frequently result
in malpositioning because of bony interferences and inability to seat the
template completely. Soft-tissue templates result in errors because of
nonuniform tissue thickness and incorrect positioning because of decreased
retention. Studies have shown implant placement after virtual planning of
implant position using cone beam CT data and surgical templates is
significantly more accurate than free-hand insertion.26 With all types of
guides the implant clinician must show good judgment as to the accuracy of
the template and must be able to determine any discrepancies (especially in
bone volume) between the intended osteotomy site and the actual current
bony architecture of the patient.
Summary
One of the most critical skills in the practice of implant dentistry is the
ability to place an implant in the ideal and correct position. The complexity of
this skill set is underrated, as the clinician needs to understand the three
planes of placement along with maintaining a safe distance from vital
structures. Malpositioning may result in a successful integration of the
implant, but may place the intended restoration at significant risk for
complication and/or failure. Technological advances such as guided surgery
and surgical templates have proven to be helpful to implant clinicians,
especially those early on their surgical learning curve or in cases where space
tolerances are low. However, even these techniques have margins of error and
tolerances that need to be fully understood.
With a combination of proper treatment planning and ideal positioning
guidelines (Table 6.2), the implant clinician can ensure a predictable surgical
and prosthetic outcome.
TABLE 6.2
Ideal Distances and Positional Measurements
Distances
Implant–tooth >1.5–2.0 mm
Implant–implant 3.0 mm
Crown height spac e >8 mm (c ementable prosthesis)
Interoc c lusal distanc e ~15 mm (removable prosthesis)
Mandibular nerve >2.0 mm
Nasal c avity < engaging c ortic al plate
Maxillary sinus Misc h S A Classific ation
Bone Thickness: (After Implant P lacement)
Buc c al >1.5 mm
Lingual >0.5 mm
P ositioning
Anterior
Cement-retained S lightly lingual to inc isal edge
S c rew-retained Cingulum area
Posterior
Cement/S c rew-retained Central fossa
Apic oc oronal 2–3 mm below free gingival margin
References
1. Katona TR, Goodacre CJ, Brown DT, et al. Force-moment systems on
single maxillary anterior implants: effects of incisal guidance, fixture
orientation, and loss of bone support. Int J Oral Maxillofac Implants.
1993;8:512–522.
2. Priest GF. The esthetic challenge of adjacent implants. J Oral
Maxillofac Surg. 2007;65(Suppl 1):2–12.
3. Stumpel L. Model-based guided implant placement; planned
precision. Inside Dent. 2008;4(9):72–77.
4. Margelos JT, Verdelis KG. Irreversible pulpal damage of teeth
adjacent to recently placed osseointegrated implants. J Endod.
1995;21:479–482.
5. Asscherickx K, Vannet BV, Wehrbein H, et al. Root repair after injury
from miniscrew. Clin Oral Implants Res. 2005;16:575–578.
6. Kravitz ND, Kusnoto B. Risks and complications of orthodontic
miniscrews. Am J Orthod Dentofacial Orthop. 2007;131:S43–S51.
7. Brisceno CE, Rossouw PE, Carrillo R. Healing of the roots and
surrounding structures after intentional damage with miniscrew
implants. Am J Orthod Dentofacial Orthop. 2009;135:292–301.
8. Esposito M, Ekestubbe A, Grondahl K. Radiological evaluation of
marginal bone loss at tooth surfaces facing single Branemark
implants. Clin Oral Implants Res. 1993;4:151–157.
9. Bell FA 3rd, Jones AA, Steward KL. A clinical implant program in the
predoctoral curriculum. J Dent Educ. 1991;55:169–171.
10. Weinberg LA, Kruger B. A comparison of implant/prosthesis loading
with four clinical variables. Int J Prosthodont. 1995;8:421–433.
11. Rieger MR, Mayberry M, Brose MO. Finite element analysis of six
endosseous implants. J Prosthet Dent. 1990;63:671–676.
on the height of inter-implant bone. J Periodontol. 2000;71:546–549.
13. Spray JR, Black CG, Morris HF. The influence of bone thickness on
facial marginal bone response: stage 1 placement through stage 2
uncovering. Ann Periodontol. 2000;5:119–128.
14. Misch CE, Bidez MW. Occlusion and crestal bone resorption: etiology
and treatment planning strategies for implants. McNeil C. Science and
practice of occlusion. Quintessence: Chicago; 1997:473–486.
15. Ha CY, Lim YJ, Kim MJ, et al. The influence of abutment angulation
on screw loosening of implants in anterior maxilla. Int J Oral
Maxillofac Implants. 2011;26:45–55.
16. Perel S, Sullivan P. Esthetics and osseointegration. Quintessence:
Chicago; 1994.
17. Saadoun AP, Sullivan DY, Krischek M, et al. Single tooth implant
management for success. Pract Periodontics Aesthet Dent. 1994;6:73–82.
Implant Dent. 2005;14:312–318.
19. Tarnow DP, Magner AW, Fletcher P. The effect of the distance from the
contact point to the crest of bone on the presence or absence of the
interproximal dental papilla. J Periodontol. 1992;63:995–996.
20. Misch CE, Goodacre CJ, Finley JM, et al. Consensus Conference Panel
Report: Crown-height space guidelines for implant dentistry—part 2.
Implant Dent. 2006;15:113–121.
21. Naitoh M, Ariji E, Okumura S, et al. Can implants be correctly
angulated based on surgical templates used for osseointegrated
dental implants? Clin Oral Implants Res. 2000;11:409–414.
23. Stumpel LJ 3rd. Cast-based guided implant placement: A novel
technique. J Prosthet Dent. 2008;100:61–69.
24. Almog DM, Torrado E, Meitner SW. Fabrication of imaging and
surgical guides for dental implants. J Prosthet Dent. 2001;85:504–508.
25. Ramasamy M, Giri, Raja R, et al. Implant surgical guides: From the
past to the present. J Pharm Bioallied Sci. 2013;5(Suppl 1):S98–S102.
26. Nickenig HJ, Wichmann M, Hamel J, et al. Evaluation of the difference
in accuracy between implant placement by virtual planning data and
surgical guide templates versus the conventional free-hand method—
a combined in vivo—in vitro technique using cone-beam CT (Part II).
J Craniomaxillofac Surg. 2010;38(7):488–493.
7
Bleeding
Randolph R. Resnik
During dental implant and bone graft procedures, persistent minor bleeding
is a common sequela. However, on occasion a significant bleeding episode
may occur. The most common sources of intraoperative bleeding include
incision into highly vascularized areas of the mucosa or periosteum,
anatomic vascular variants, areas of infection, and trauma to nutrient arteries
in the alveolar bone. The implant clinician must be able to identify and
understand the source of the bleeding, which may occur from many different
types of bleeding episodes. These include hemorrhage from small vessels,
large vessels, oozing, medication-induced bleeding, or coagulopathies.
The management of hemostasis during dental implant surgery has many
key factors, the first of which is an accurate preoperative assessment of the
patient followed by good surgical technique. If a bleeding episode occurs, the
implant clinician must be able to utilize various hemostatic agents if
traditional methods fail. These agents may range from absorbable hemostats,
such as gelatins and collagens, to biologically active topical hemostats, such
as thrombin and combined agents. However, the implant clinician must first
have a thorough understanding of all aspects of hemostasis cycle. With this
knowledge the clinician will be in a better position to avoid bleeding
episodes and more importantly, will also have the ability to act decisively and
skillfully during a potential “slippery slope” and scenario with significant
medical implications. It is not always possible to avoid bleeding
complications, but it is of paramount importance to be able to treat them
effectively.
Risk of Bleeding
Bleeding during dental implant surgery poses many potential complications
for the patient and the dental implant surgeon. These include an obscured
surgical field, prolonged surgical time, increased the risk of physiologic
complications, and increased procedural morbidity (Fig. 7.1). Surgical
bleeding may be classified in various ways according to the source or onset
(Box 7.1).
FIG 7.1 Extensive bleeding during dental implant surgery may cause many
complications that lead to surgical and implant morbidity.
Box 7.1
Classification of Surgical Hemorrage
Bleeding According to Source
Arterial hemorrhage: bright red, spurting/pulsatile
Venous hemorrhage: dark red, continuous
Capillary hemorrhage: bright red, continuous
Bleeding According to Onset

Primary hemorrhage: This type of bleeding occurs during surgery and is
usually the result of the incision, retraction, or preparation of the soft or
hard tissue. It is usually controlled with conventional mechanical methods
or with local hemostatic agents.
Reactionary hemorrhage: This type of bleeding usually will occur within hours
after surgery. Reactionary hemorrhage most likely occurs in patients who
exhibit systemic bleeding issues, are on anticoagulant therapy, or
experience postoperative trauma to the surgical area that disturbs the clot.
Additionally, reactionary bleeding may also occur up to 24 hours after
surgery, which is most likely the result of complete arterial sectioning
causing vasospasm. The vasospasm, coupled with the use of
vasoconstrictors, may delay bleeding for hours in the postoperative period.
Secondary hemorrhage: This type of bleeding occurs 7–10 days after surgery
and is most likely the result of an infection. Secondary hemorrhage is very
rare with dental implant procedures.
Mechanism of Hemostasis
Understanding the mechanism of hemostasis is crucial to the surgical
treatment of the dental implant patient. Hemostasis is defined as a highly
regulated process that maintains blood flow through the vasculature
simultaneously as a thrombotic response to the tissue damage.2 Biologically,
hemostasis requires a complex cascade of interactions involving the vessel
wall, platelets, and fibrin coagulation and fibrinolytic systems. For this to
occur, there are three reactions—primary, secondary, and tertiary—that act
simultaneously (Fig. 7.2).
FIG 7.2 Summary of hemostasis. (A-C) Primary hemostasis: vascular and platelet
activity. (C-D) Secondary hemostasis: blood coagulation phase. (E) Tertiary
hemostasis: fibrinolysis. (From Applegate E: The anatomy and physiology learning system, ed
4, St Louis, 2011, Saunders.)
Vascular and Platelet Activity (Primary Hemostasis).

The first phase of hemostasis occurs immediately after blood vessel damage
as a result of vasoconstriction. This reduces blood flow, limits the amount of
blood loss, enhances platelet adherence, and activates coagulation.3
Vasoconstriction is triggered by direct injury to vascular smooth muscle,
chemicals released by endothelial cells and platelets, and reflexes initiated by
pain receptors. This spasm response becomes greater as injury increases and
is more effective on smaller blood vessels.4 Mechanical blockage occurs by
platelets adhering to exposed collagen (platelet adhesion), which release
cytokines (serotonin, thromboxane A2, and endothelin1) into the area of
tissue injury.3 This plug formation is activated by von Willebrand factor
(vWF), a glycoprotein found in plasma. The platelets forming the plug will
release chemical messengers such as adenosine diphosphate (ADP),
fibronectin, thrombospondin, fibrinogen and PDGF, which causes more
platelets to aggregate and enhance vascular spasms.5 As more platelets
adhere and release their chemicals, a positive feedback loop results, which
ends in the formation of a platelet plug. Drugs that affect primary
hemostasis include aspirin and clopidogrel, which affect platelet function
and prevent thrombosis.
Blood Coagulation (Secondary Hemostasis).

The second step in the process of hemostasis occurs when the clotting factors
within the blood plasma form a collagen fiber called fibrin. This fibrin forms
a mesh, collecting red and white blood cells that strengthen the clot, which is
termed the coagulation cascade.6 The coagulation cascade is divided into three
pathways, the intrinsic pathway, extrinsic pathway, and coagulation cascade.
The intrinsic pathway (contact activation pathway) requires clotting factors
VII, IX, X, XI, and XII as well as proteins and calcium ions and phospholipids
secreted by platelets. This pathway has a less significant effect on hemostasis
in comparisons to the extrinsic pathway under normal physiologic
conditions.
The extrinsic pathway (tissue factor pathway) is the main pathway that
generates a “thrombin burst,” which involves a feedback activation role
where thrombin is released rapidly. Thrombin activates factors V and VII,
which in turn activate other factors to continue the coagulation process.
Common pathway involves factor X generation of thrombin from
prothrombin. Thrombin then activates factors XI and VIII, which amplify the
coagulation cascade, releasing more thrombin. Thrombin then causes
fibrinogen to form, which results in cross-linked fibrin. Drugs that effect
secondary hemostasis include warfarin, the direct thrombin inhibitors, and
heparin5,7 (Fig. 7.3).
FIG 7.3 Summary of coagulation cascade (intrinsic and extrinsic pathways). The
coagulation process results in hemostasis which involves a complex set of
reactions. These reactions end by converting fibrinogen into insoluble strands of
fibrin which form a stable clot. (From Huether S, McCance K: Understanding pathophysiology,
Fibrinolysis (Tertiary Hemostasis).

The last phase of hemostasis involves the formation of plasmin from
plasminogen. Plasmin lyses fibrinogen and fibrin. This releases fibrin
degradation products, which are cleared by the kidney and liver. Thus the
fibrin clot, the final product of coagulation, is broken down (fibrinolysis). A
drug that inhibits the tertiary hemostasis is tranexamic acid.8
Factors Contributing to Intraoperative Bleeding

Many factors may contribute to intraoperative bleeding. The incidence of
bleeding episodes during dental surgery has been shown to be up to 4% of
patients exhibiting normal hemostasis. In chronically anticoagulated
patients, studies have shown bleeding episodes to be in the range of 8.6% to
32.1%.9 Although rare, bleeding during dental implant surgery may be life
threatening. The implant clinician must be conscious of the signs and
symptoms of a potential bleeding emergency. If the patient displays any
signs of shock (tachycardia, hypotension, cold/clammy skin, lethargy),
immediate medical assistance is recommended along with immediate
intravenous fluid replacement to replenish the intravascular volume and
reestablish tissue perfusion.
The first step in preventing bleeding issues is with the medical history (see
Chapter 2). A thorough review of the medical history may alert the clinician
to many factors that may ultimately potentiate intraoperative bleeding. A
detailed medical history screening should evaluate current and past systemic
disorders, medication list, and history of past bleeding episodes.
Medications
Anticoagulants.
The most common class of medications that predispose patients to bleeding
problems is the anticoagulants. These may include Coumadin derivatives,
antiplatelets, direct thrombin inhibitors, and herbal supplements. In most
cases of Coumadin-based medications, discontinuation is not recommended
for routine dental implant procedures because local hemostatic measures are
effective in managing hemorrhage. Stopping these medications may have
deleterious effects and have a greater chance of creating complications for
the patient. The patient's physician should always be consulted and the
implant clinician should NEVER unilaterally cease or modify any medication
that was prescribed by a physician (Table 7.1).
TABLE 7.1
Common Anticoagulants54
Coumadin (warfarin) P radaxa (dabigatran) Xarelto (rivaroxaban) Eliquis (apixapan)

Mode of action Four vitamin K–dependent Thrombin-fibrin c lot Fac tor Xa–fibrin c lot Fac tor Xa–fibrin c lot
fac tors
Testing Requires regular blood tests None None None
(PT/INR)
Diet restrictions Many diet restric tions None None None
DOSE (daily) Varies ac c ording to PT/INR 75–150 mg twic e/day 10–15 mg 2.5–5 mg twic e/day
Elimination half-life 20–60 hr 12–17 hr 5–13 hr 6–12 hr
Reversal agent Vitamin K None None None
plasma
Modification for implant Not rec ommended MD c onsult; usually MD c onsult; usually MD c onsult; usually
surgery disc ontinuation disc ontinuation disc ontinuation
INR, international normalized ratio; PT, prothrombin time.
Novel Oral Anticoagulant (NOACs).

Because of the disadvantages of Coumadin-based medications, new
anticoagulant drugs have recently come to the market without the associated
disadvantages of warfarin. The direct thrombin inhibitors have a wide
therapeutic index, less complex pharmacodynamics, fewer drug and food
interactions, and a very predictable response that makes routine blood
testing unnecessary.10 These targeted anticoagulants bind directly to
thrombin and block the interaction with its substrates. Unfortunately, there
is no reversal agent or antidote for these drugs to counteract the
anticoagulant effect at this time, which may lead to serious issues when
uncontrolled bleeding occurs (Table 7.2).
TABLE 7.2
Medications That Increase Bleeding7
Medication Effect on Bleeding

Alc ohol Warfarin enhanc ed by large amounts of alc ohol
Analgesic s Bleeding enhanc ed by aspirin effec t on platelets
Antibac terials Warfarin enhanc ed by c ephalosporins, erythromyc in and metronidazole. Ampic illin and amoxic illin may inc rease
bleeding
Antifungals Warfarin enhanc ed by azoles, inc luding mic onazole topic ally
Antiinflammatories Bleeding enhanc ed by antiplatelet ac tivity of NS AIDs; warfarin may also be enhanc ed. Cortic osteroids may alter
warfarin ac tivity
NSAID, nonsteroidal antiinflammatory drug.
Antiplatelet Medications.
Antiplatelet medications affect clotting by inhibiting platelet aggregation;
however, this occurs by many different mechanisms. Aspirin irreversibly
acetylates cyclooxygenase, thus inhibiting the production of thromboxane A2,
and clopidogrel (Plavix) selectively inhibits ADP. Thus both have the end
result of reducing platelet aggregation. Both of these drugs will affect the
platelet function for the life of a platelet, which is 7–10 days. The synthesis of
new platelets will overcome the platelet dysfunction, and in 50% to 80% of
cases, platelet aggregation returns to normal (Table 7.3).11
TABLE 7.3
Medications That Impair Platelet Function7
Class Medication
Alc ohol
Analgesic s and other platelet inhibitors Aspirin and other NS AIDs
Clopidogrel
Antibiotic s Amoxic illin
Ampic illin and derivatives
Azithromyc in
Benzylpenic illin (penic illin G)
Carbenic illin
Cephalosporins
Gentamic in
Methic illin
Rifampic in
S ulphonamides
Trimethoprim
Antidiabetic s Tolbutamide
Cardiovasc ular drugs Digitoxin
Heparin
Methyldopa
Oxprenolol
Quinine
Cytoxic drugs Many
Diuretic s Ac etazolamide
Chlorothiazide
Furosemide
General anesthetic agents Halothane
Psyc hoac tive drugs Antihistamines (some)
Chlorpromazine
Diazepam
Haloperidol
Tric yc lic antidepressants
Valproate
NS AIDs Celec oxib (Celebrex)
Dic lofenac (Voltaren Cataflam)
Diflunisal (Dolobid)
Etodolac (Lodine)
Fenoprofen (Nalfon)
Ibuprofen (Motrin, Advil, Nuprin)
Indomethac in (Indoc in)
Ketoprofen (Orudis, Ac tron)
Ketorolac (Toradol)
Meloxic am (Mobic )
Nabumetone (Relafen)
Naproxen (Naprosyn, Aleve)
Oxaprozin (Daypro)
Piroxic am (Feldene)
S ulindac (Clinoril)
NSAID, nonsteroidal antiinflammatory drug.
The combination of aspirin and clopidogrel produces additive and possible

synergistic effects because the two medications block complementary
pathways in the platelet aggregation cascade. Rarely will physicians allow the
complete withdrawal of both of these medications as the cardioprotective
benefits outweigh the potential for bleeding episodes in at-risk patients with
cardiovascular disease.
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs).
NSAIDs have a reversible effect on platelet aggregation, and platelet
function is restored once the drug effects are gone. Minor dental implant
surgical procedures can be safely performed without altering the NSAID
dose.12
Herbal Supplements.
Herbal supplements studies have shown as many as 70% of patients do not
reveal they are taking herbal supplements and 40% will take herbal
supplements within 2 weeks of surgery.13 Some herbal remedies are fairly
safe and have been supported by sound medical research. Thus many
PATIENTS believe that, because a medication is termed “natural,” it is safe.
However, the majority of supplements have no research on their safety and
efficacy action because of product variability and minimal regulation. This
has led to many natural plant products on the market that are addictive and
highly toxic and can complicate surgical procedures. Some of these
supplements may prolong bleeding and impair the coagulation process,
which may lead to intraoperative and postoperative bleeding episodes (Table
7.4). Supplements should be withdrawn for a minimum of 2 weeks prior to
surgery.
TABLE 7.4
Herbal Supplements That Inhibit Hemostasis7
Herbal Source
Bilberry Va ccinium myrtillus
Bromelain Ana s comosus
Cat's c law Unca ria tomentosa
Devil's c law Ha rpa gophytum procumbens
Dong quai Angelica sinensis
Evening primrose Oenothera biennis
Feverfew Ta na cetum pa rthenium
Garlic Allium sa tivum
Ginger Zingiber officina le
Ginkgo biloboa Ginkgo biloba
Ginseng Pa na x ginseng
Grape seed Vitis vinifera
Green tea Ca mellia sinensis
Horse c hestnut Aesculus hippoca sta num
Turmeric Curcuma longa
Systemic Bleeding Disorders

Factor Disorders.
Bleeding disorders may directly or indirectly affect the intrinsic or extrinsic
pathways of the hemostasis process. The intrinsic pathway affects the
activated partial thromboplastin time (aPTT) via factors VII, IX, XI, XII and
the extrinsic pathway involves factor VII, which affects the prothrombin time
(PT). Any of these intrinsic or extrinsic factors may affect the common
pathway, which alters the formation of the fibrin clot. Usually laboratory tests
such as partial thromboplastin time (PTT) and PT will reveal the factor
deficiency.
Besides factor disorders, there are also congenital disorders that impact
hemostasis. Hemophilia is a bleeding disorder that may be very minor or can
be a more severe type leading to significant complications. Hemophilia can
be classified into type A (Factor VIII) or type B (Factor IX). von Willebrand
disease is an inherited disorder that results from the lack of von Willebrand
factor, which is a protein within the blood that assists with blood clotting and
carrying clotting factors.11 With any type of systemic bleeding disorder,
physician consultation is highly recommended (Box 7.2).
Box 7.2
Recommendations for Anticoagulant Patients
1. MEDICATIONS (BASED ON PHYSICIAN RECOMMENDATION)
• In most cases, do not interrupt thrombocyte aggregate

inhibitors (e.g., aspirin, clopidogrel).
• Do not interrupt warfarin if INR <3.0.
• Physician consult for direct thrombin inhibitors (e.g.,

apixaban, dabigatran, and rivaroxaban). Physician
consultation should be completed in writing.
2. PRESURGICAL INTERVENTION
• Inform patients of the entire procedure and not to
interrupt any of their medications unless they receive
physician approval.
• Warfarin patients should have their INR checked

within 48 hours of the surgical procedure unless they
have stable values. INR above 3.0 should be a relative
contraindication to the surgical procedure requiring
physician consultation.
3. INTRAOPERATIVE MEASURES
• Minimize surgical trauma and utilize good surgical

technique.
• Reduce surgical time and minimize surgical sites to be

treated (schedule into multiple surgeries).
• Good suturing technique to include primary closure

with high–tensile strength suture (e.g., Vicryl).
• Minimize trauma on surgical site from prosthesis.

4. POSTOPERATIVE RECOMMENDATIONS
• Utilize pressure packs and hemostatic agents if

necessary.
• Minimize the use of aspirin, NSAIDs, and COX-2

inhibitors as analgesics.
• Provide detailed oral and written postoperative

instructions.
• More frequent postoperative appointments.

COX-2, cyclooxygenase-2; INR, international normalized ratio; NSAID,
nonsteroidal antiinflammatory drug.
Liver Disorders.
Liver disease (e.g., cirrhosis, acute liver failure) is associated with many
significant abnormalities of the coagulation system. The coagulation system
and the interrelationship with liver function is very complex. Because most
patients exhibiting liver disease have impaired production of coagulation
factors and thrombocytopenia, medical consultation before any dental
implant procedure is recommended.
Evaluation of the Coagulation Process
Laboratory Tests
There are many tests of the coagulation system that determine the
susceptibility of the patient to a bleeding episode during or after dental
implant surgery.
Prothrombin Time (PT)

The PT test is performed routinely for many patients prior to surgery or to
monitor the effects of the anticoagulant warfarin (Coumadin). Basically, this
test of the extrinsic pathway measures the time it takes for the patient's
plasma to form fibrin. Usually, the patient's warfarin dose will be altered
depending on PT times. The prothrombin time reference range will depend
on the analytical method used; however, it is usually 12-13 seconds. The
results should always be interpreted using the reference range from the
laboratory.
International Normalized Ratio (INR)

Because of the poor standardization of the prothrombin time, a wide
variation in values obtained by laboratories resulted in inconsistent test
values. It has become a standard in most laboratories to perform a correction
of the prothrombin time, or to “normalize” the result. This normalized test is
called the INR (international normalized ratio), and it is much more accurate
in the assessment of a patient's bleeding time. A normal INR is 1.0 %.
However, in anticoagulated patients, the INR will be higher, usually within
the therapeutic range of 2.0% to 3.5%. The target anticoagulation level differs
for each patient because the anticoagulation will require different
therapeutic INR levels. Prolonged INR and PT values are indicative of liver
disease, warfarin treatment, or vitamin K deficiency.
Partial Thromboplastin Time (PTT)

The PTT test is usually performed for many patients prior to surgery and to
monitor the effect of anticoagulation using heparin. The test measures the
intrinsic pathway and factors V, VIII, IX, X, and XI. The formation of the
blood clot requires the participation of a series of proteins, and deficiency of
any of these will result in abnormal values. The test is expressed in seconds
compared to the number of seconds it takes a control normal plasma sample
to clot. The most common causes of an abnormal PTT are a hereditary
deficiency of Factor XI and von Willebrand disease. Ideally, the PTT value
should be approximately 1.5 to 2.5 times the mean normal value.
Bleeding Time
The bleeding time test is a rather old method of determining platelet
function. The Ivy method is the most common technique, which involves a
superficial (less than 1 mm deep), small (1 cm long) cut made on the skin of
the forearm using a special instrument. The time it takes for the cut to stop
bleeding is a test of the function of the platelets. The normal value is usually
less than minutes. A prolonged bleeding time is a result of decreased
number of thrombocytes or impaired blood vessels.
Platelet Count
A platelet count is a test that calculates the number of platelets. Normally,
the platelet count should be 100,000–400,000 cells/mm3. Counts less than
100,000 mm3 (thrombocytopenia) can be associated with significant intra- and
postoperative bleeding.
The platelet is synthesized by the bone marrow and broken down by the
spleen. Abnormalities that would cause a decreased number of platelets are
either inherited or acquired, with acquired being rather rare.
Interuption of Anticoagulant Therapy13a

General Approach
With dental implant patients, interruption of anticoagulation temporarily
increases thromboembolic risk. However, continuing the anticoagulation
medication may increase the risk of bleeding episodes for the patient
(depending on the procedure). The PHYSICIAN should be consulted and
perioperative management of anticoagulation should be based on their
recommendations. Unfortunately, most anticoagulation interruption
approaches are based on expert opinion. Thrombotic and bleeding risks may
vary depending on patient and procedure as data from randomized trials are
not available to generally guide practices. Most physicians will take the
following factors in consideration prior to recommendation:
• Estimate thromboembolic risk. When a higher thromboembolic risk exists,
the importance of minimizing the interval without anticoagulation is
critical. Most patients being treated for atrial fibrillation, recommendations
are based on age and comorbidities. If thromboembolic risk is transiently
increased (e.g., recent stroke, recent pulmonary embolism), usually elective
surgery is delayed until the risk returns to baseline. The most common
issues that increase thromboembolic risk are atrial fibrillation, prosthetic
heart valves, and recent venous or arterial thromboembolism (e.g., within
the preceding three months).
• Estimate bleeding risk. When the procedure is classified as a higher
bleeding risk, there is a greater need for perioperative hemostasis measures
and a longer period of anticoagulant interruption. The risk of bleeding is
usually determined by the type of surgery and invasiveness of the
procedure. Patient comorbidities (e.g., older age, decreased renal function)
and current medications that affect hemostasis should also be taken into
consideration. Usually with dental implant surgery, bleeding risk is most
likely to be classified as “low risk.”
• Determine the timing of anticoagulant interruption. The timing of
anticoagulant interruption depends on the specific anticoagulant the
patient is receiving. For example, warfarin and aspirin usually requires
earlier discontinuation than the shorter-acting direct oral anticoagulants
(e.g., dabigatran, rivaroxaban, apixaban, edoxaban).
Techniques to Decrease and Control
Bleeding
The need to control gross bleeding is paramount for successful surgery
because insidious and continuous loss of blood from arteries, veins, or
capillaries can become significant if bleeding is not controlled. Dental
implant clinicians have numerous options for maintaining hemostasis, which
include mechanical, thermal, pharmacologic, and topical agents.
Mechanical Methods
The most common primary mechanical method to control bleeding is to
apply direct pressure or compression on the bleeding site along with
repositioning the patient. Secondary mechanical methods include suturing,
clamping the blood vessel with hemostats, and ligating the bleeding vessel
with suture material.
Positional Changes
When significant bleeding occurs, maintaining the patient in a supine
position is not recommended because of increased bleeding (head below the
heart). Hydrostatic pressure occurs within the vascular system because of the
weight of the blood vessels and is dependent on gravity. The pressure is
decreased in any vessel above the heart and increased in blood vessels below
the heart. Studies have shown that in an upright position, the average
pressure at the level of the heart is 100 mm Hg. Vessels in the head and neck
averaged 49 mm Hg and 186 mm Hg at the foot level.14 Repositioning the
patient to an upright position (head above the heart) will not stop the
bleeding; however, it will significantly decrease the hemorrhage (studies
have shown a decrease up to 38%) (Fig. 7.4).15
FIG 7.4 Repositioning a patient to decrease bleeding. (A) Supine position results in
increased bleeding. (B) Upright position leads to less bleeding and anxiety for the
patient.
Direct Pressure
If significant intraoperative bleeding occurs, the ideal treatment should
involve immediate application of pressure to the surgical site. Pressure or
compression directly on the blood vessel will allow for platelet aggregation
and initiation of the coagulation cascade. Pressure may be applied manually
or by the patient biting forcefully on a gauze dressing. Pressure should be
maintained for at least 3 to 5 minutes to allow the formation of a blood clot.
Caution should be exercised to not remove the gauze too early because this
may dislodge the clot. Ideally, 3 × 3 or 4 × 4 gauze should be utilized because
2 × 2 gauze may be accidentally aspirated. In primary bleeding, pressure is
the simplest and fastest method to control bleeding prior to the use of
hemostatic measures.
Suturing
Suturing plays a significant role not only in obtaining primary closure for
ideal healing but also for maintaining hemostasis (direct vs. indirect). Direct
placement of a suture (ligation) is used when there is access to a deep
bleeding vessel. The suture is placed by entering the tissue at least 4 mm
from the bleeding vessel, 3 mm below the vessel, and 4 mm exiting the
tissue. This will ligate or occlude the vessel as long as it is placed proximal to
the bleeding area. A figure-eight suture technique is ideally utilized (Fig.
7.5A).
FIG 7.5 Suturing. (A) Direct ligation with figure-eight suturing technique. (B–C)
Indirect tie-back of the mandibular lingual tissue from cuspid-molar contralaterally,
which decreases bleeding, allows for ease of retraction, and prevents tissue
trauma.
Indirect suture placement is utilized to retract the tissue and minimize

bleeding via pressure from the accumulated tissue. This is most often used
as tie-backs when reflecting an edentulous mandible (cuspid to molar
bilaterally). And lastly, good suturing technique is paramount for preventing
reactionary bleeding after surgery. Ideally, interrupted or mattress sutures
should be placed in conjunction with continuous sutures to maintain closure.
A suture material that exhibits high tensile strength is recommended, such
as polyglycolic acid (e.g., Vicryl) (Fig. 7.5B–C). The interim prosthesis should
be modified to have no direct pressure on the wound site and this may
dislodge the sutures.
Clamped Vessel With Hemostat Forceps

When local measures are not successful in controlling bleeding, a hemostat
may be utilized to clamp the blood vessel. Usually a curved Kelly hemostat
may be used to clamp the vessel to control the bleeding via two mechanisms:
1. Occluding the vessel and damaging the blood vessels wall to stimulate
clotting. This clamping pressure should be maintained for approximately 2–3
minutes, which will usually allow for hemostasis. However, this method may
be unreliable because the clot may become dislodged and postoperative
bleeding may occur after removal of the hemostat.
2. A more successful technique in controlling bleeding is to use fine-pointed

hemostats (Kelly hemostats) and ligate the bleeding vessel with suture
material. The vessel should be clamped to obtain immediate hemostasis with
the tip of the hemostat extending beyond the vessel. A clamped vessel may
be ligated with suture material such as an absorbable suture with high
tensile strength (e.g., Vicryl). A tie should be placed around the hemostat,
extending to the vessel. The hemostats are then removed, and two additional
throws are made with the suture. Usually, bleeding from vessels of 2 mm or
greater diameter should be ligated. Direct ligation of the bleeding blood
vessel is usually the most effective technique in stopping arterial blood flow.
However, exposure and identification may sometimes be extremely difficult
(Fig. 7.6).
FIG 7.6 Ligation from a clamped vessel. (A) When a bleeding vessel is identified, a
Kelly hemostat is used to clamp the vessel. A suture (preferably Vicryl) is placed
around the hemostats. (B) A knot is tied around the hemostat and slid to the end of
the hemostat tips. (C) The suture is tightened. (D) the hemostats are removed and
two more throws may be added to the original knot.
Thermal Techniques
The use of electrosurgery or lasers to reduce bleeding is a common
alternative technique to mechanical methods. However, thermal techniques
do have drawbacks, such as episodes where bleeding is present in deeper
tissue with limited access or from multiple capillaries, in which maintaining
hemostasis may be very difficult.
Electrocautery
Electrocauterization, developed in the 1930s, has been one of the most
common hemostatic techniques because of its low cost, accessibility, ease of
use, and effectiveness. Electrocautery is the process of destroying tissue
using heat conduction with a probe that is heated by an electric current.
Different procedures may be completed with the use of high–radio frequency
alternating current for cutting, coagulating, and vaporizing tissues.
Electrocautery is most effective on small vessels and may be utilized in two
modes: monopolar and bipolar (Fig. 7.7).
FIG 7.7 Electrocautery. (A) Monopolar electrocautery, which utilizes current to
establish hemostasis. A ball electrode is the most common to be used; however,
access is sometimes difficult. (B) A battery-operated disposable cautery unit that
does not use current, however generates heat to ligate the blood vessel.
Monopolar electrosurgery delivers current using different types of

waveforms (i.e., modes). The coagulation mode utilizes an interrupted
waveform, which generates heat, thereby coagulating a cell, a phenomenon
also termed fulguration. The cutting mode is low energy, which produces a
cutting effect to vaporize tissue with minimal hemostasis. The blend mode
simultaneously cuts tissue and coagulates bleeding. This technique is often
difficult to use in implant surgery because access and a relatively dry field is
needed to cauterize the vessel. A dry field is needed for the effective
electrical current to pass through the tissues. A high-speed plastic, not metal,
suction tip should be used to maintain a dry field.
Buzzing the Hemostat: (Electrocautery + Hemostat Ligation)
Usually on larger vessels, the combination of a clamped vessel (with curved
hemostat) and electrocautery will allow for the cauterizing of the blood
vessel, thus stopping blood flow in the vessel. The protocol is as follows:
1. Use the lowest possible setting to achieve the desired effect.
2. Use the CUT mode, not the COAG mode. COAG has a higher peak-to-peak
voltage and is more prone to alternate (small) current pathways.
3. After clamping the vessel, touch the active electrode to the hemostat closer
to the patient (below the hand holding the hemostat) and then activate the
electrode. This minimizes sparking and the subsequent demodulation of
current while encouraging a path of least resistance.
Note: Care should be exercised because the implant clinician may receive
burns or be shocked even when wearing protective gloves. When the surgeon
clamps a bleeding vessel and the electrode is touched to the hemostat, the
tissue between the clamped hemostat is coagulated. The “buzzing” may
cause high-voltage breakdown of the surgeon's glove, leading to a burn. To
minimize this possibility the surgeon's glove should be changed if wet
because hydrated gloves show a lower resistance. Additionally, the electrode
should be placed in contact with the hemostat prior to activation of the
electrosurgical current to minimize the production of a spark (Fig. 7.8).
FIG 7.8 (A–C) “Buzzing the hemostat” usually used for larger vessel ligation
(arterial). The vessel is clamped with the hemostat and the electrocautery unit is
placed on CUT mode and lightly touches the hemostat. A spark will usually result
(arrow). Prior to its use, supplemental oxygen (nasal cannula) should be
discontinued to prevent a patient fire.
Lasers
Lasers, which are gaining popularity as a tool in dental surgery, may also be
used to achieve hemostasis. Laser is an acronym for “light amplification by
stimulated emission of radiation,” which produces laser light energy. Laser
energy delivered to an area of bleeding may be reflected, scattered,
transmitted, or absorbed. The extent of the tissue reaction depends on the
laser wavelength, power settings, spot size, and length of contact time with
the bleeding area. Lasers have been shown to be a safe or useful modality in
treating dental surgery patients with bleeding disorders.16
Pharmacologic Techniques
Although pharmacologic techniques may be utilized in implant dentistry to
control bleeding, the success of maintaining hemostasis is questionable, with
varying results.
Epinephrine
Epinephrine may be used to enhance hemostasis in combination with local
anesthesia (e.g., 2% Lidocaine epi or epi). When locally placed,
epinephrine will reduce bleeding, slow the absorption of the local anesthetic,
and prolong the anesthetic and analgesic effect. The hemostatic properties
are related to platelet aggregation, which leads to a decrease in the
adenoreceptors within the vessel walls, thus producing vasoconstriction.
However, rebound hyperemia may result postoperatively, which will increase
bleeding. Various studies have shown that topical application of 1/100,000
concentration of epinephrine creates vasoconstriction and controls
hemostasis with sinus graft procedures with no appreciable changes in
systemic hemodynamics (Fig. 7.9).17
FIG 7.9 (A) Epinephrine-impregnated gauze achieving the benefit of pressure and
vasoconstriction. Lidocaine 2% epinephrine is ideally used because of its
greater vasoconstrictive properties. (B) Gauze impregnated with lidocaine, which
may be used as a pressure dressing to decrease bleeding. (C) Epinephrine gauze
placed over wound site with constant pressure.
Tranexamic Acid Solution

Tranexamic acid 4.8% is an antifibrinolytic oral rinse that facilitates clot
formation by inhibiting the activation of plasminogen to plasmin. Plasmin
prevents the clotting process from initiating fibrinolysis. Tranexamic acid
solution may be used as a mouthwash postoperatively and has been shown to
enhance clotting in patients with coagulopathies or anticoagulant therapy.
Ramstrom et al showed a significant reduction in postoperative bleeding
with a 10-mL rinse, four times a day for 7 days postoperatively.18 Choi et al
showed a significant decrease in bleeding during maxillary surgery after a
bolus of tranexamic acid was given preoperatively (Fig. 7.10).19
FIG 7.10 (A) Tranexamic Acid Injection. (B) Injectable tranexamic acid placed
under bleeding flap. (A, Courtesy X-GEN Pharmaceuticals, Inc., Horseheads, NY.)
Topical Hemostatic Agents

Absorbable topical hemostatic agents are used when conventional methods
of hemostasis are ineffective. These agents may be placed directly into the
bleeding site to decrease bleeding during the procedure or during the
postoperative interval. These agents work either mechanically or by
augmenting the coagulation cascade. The topical hemostatic agents have the
added benefit of minimizing the possibility of systemic blood clots, which
are drawbacks of systemic hemostatic agents.20 There are two types: active
and passive (Table 7.5).
TABLE 7.5
Common Hemostatic Agents55,11
Type P roduct Advantages Disadvantages

COLLAGEN OraTape, Inexpensive, resorbs in 10–14 days, None
S timulates platelet adherenc e OraPlug highly absorbent to many times its
(S alvin) own weight
Collatape,
Collaplug
(Zimmer)
MICROCELLULAR COLLAGEN Avitene (Davol) Good applic ation for large surfac es, Diffic ult to handle, expensive
Provides meshwork for platelet Helitene superior hemostasis to gelatin and
adherenc e (Integra) c ellulose
Instat (Ethic on)
GELATIN GelFoam S welling after applic ation results in May c ause tissue/neural damage due to
Mec hanic al matrix that inc reases (Baxter) tamponade effec t, neutral pH c ompression from swelling. Possible
c lotting, absorbs 40 times its S urgifoam dislodgement from bleeding site
weight, resorbs in 4–6 weeks (Ethic on)
CELLULOSE S urgic el Easy to handle, low pH provides Possible foreign body reac tion, low pH may
Provides a platform for platelet (Ethic on) antimic robial c overage, expands 3– lead to possible postoperative irritation, needs
aggregation and ac tivation with a Blood S top 4 times its original size and to be removed
low pH (S alvin) c onverts to a gel
Oxyc el (Bec ton
Dic kinson)
Ac tc el (Coreva
Health
S c ienc es)
THROMBIN Thrombin-JMI Can be added to c ollagen produc ts, Bovine has been shown to be immunogenic ,
Converts fibrinogen to fibrin, bovine (Pfizer) very good for small vessel leads to severe c oagulopathy
forming stable c lots Evithrom-human bleeding
(Ethic on)
Rec othrom-
rec ombinant
(ZymoGenetic s)
THROMBIN + GELATIN FloS eal (Baxter) Very good for arterial bleeding Can result in signific ant swelling from the
Converts fibrinogen into fibrin to bec ause it has a tamponade effec t c ompression, c an c ause neural disturbanc e
form c lot and gelatin ac ts as
sc affolding for c lot formation
FIBRIN SEALANT Tisseel (Baxter) Good for larger bleeding areas Expensive, preparation time
Thrombin and fibrinogen are Evic el (Ethic on) bec ause it ac ts as an adhesive
c ombined with an applic ator to
form a fibrin c lot
KAOLINITE QuikClot (Z- Kaolin is a naturally oc c urring Limited use in dental surgery, needs to be
Naturally oc c urring mineral; when Medic a) mineral poured into wound, exothermic reac tion
exposed to human plasma, fac tors c auses heat
XI and XII ac tivate the intrinsic
pathway
SYNTHETIC BONE Bone wax Ostene is soluble, it dissolves in 48 Bone wax is insoluble, must be removed or
HEMOSTATIC AGENTS Ostene hours, is not metabolized, with a will c ause inflammation and a foreign body
Tamponades the osseous vasc ular (Ceremed) low bac terial adhesion and infec tion giant c ell reac tion, should not be used in
spac es rate implant dentistry
Active Hemostatic Agents
Thrombin
Active topical hemostatic agents have biologic activity that induce clotting at
the end of the coagulation cascade. Most active agents used in dental implant
surgery contain the coagulant thrombin. Thrombin is a naturally derived
enzyme that is formed from prothrombin and acts as the basis for a fibrin
clot by converting fibrinogen to fibrin. It is mainly used as a topical
hemostatic agent in 5000- to 10,000-unit solutions, which accelerate capillary
bleeding. It may be used as a powder or combined with a gelatin sponge
during surgical procedures.
Thrombin bypasses the initial enzymatic process, thereby exerting its
effect by impairing aspects of the coagulation cascade. For thrombin to
maintain hemostasis, circulating fibrinogen is needed because it is necessary
for the formulation of a clot. Therefore, when a patient exhibits the absence
of fibrinogen, thrombin will not be effective. Fibrinogen is less susceptible to
coagulopathies caused by clotting factor deficiencies and platelet
dysfunction.21 However, thrombin does work in the presence of antiplatelet
and anticoagulation medications, which are quite prevalent in the population
(Fig. 7.11).
FIG 7.11 (A–B) Thrombin, the most utilized active hemostatic agent.
Types of Thrombin.
Thrombin is available in many forms as a hemostatic agent and has been
purified from numerous sources and classified according to the plasma used
to create it.
Bovine thrombin (eg. Thrombin-JMI) is available as a powder that may be
used dry, reconstituted with sterile saline, or added to gelatin sponges or
collagen. Antibody formation has been associated with bovine thrombin, and
this may lead to coagulopathies. 23
Human plasma thrombin (e.g., Evithrom) is available as a frozen liquid that
can be reconstituted via an absorbable gelatin sponge. Human plasma
thrombin has been associated with the potential risk of viral or disease
transmission.24
Recombinant thrombin (e.g., Recothrom) is a genetically engineered
thrombin available in a powder form. It may be applied via a spray kit or with
an absorbable gelatin sponge. The use of recombinant thrombin eliminates
the risk of antibody formation and disease and virus transmission.25
Advantages.
Thrombin use is advantageous in patients receiving antiplatelet or
anticoagulation medications. Thrombin does not need to be removed from
the bleeding site because degeneration and reabsorption of the fibrin clot is
achieved during the normal healing process. Usually, thrombin-containing
active agents have a rapid onset of action, providing hemostasis within 10
minutes in most patients.22
Disadvantages.
Thrombin is ineffective in patients who suffer from afibrinogenemia because
fibrinogen will not be present in the patient's blood. Care should be
exercised to not use thrombin directly on larger vessels because systemic
absorption may lead to intravascular thrombosis.
Passive Hemostatic Agents

Passive hemostatic agents provide hemostasis by accelerating the
coagulation process. These agents form a physical, latticelike matrix, which
activates the extrinsic clotting pathway and provides a platform for platelets
to aggregate and form a clot. Passive hemostatic agents are effective only on
patients who have an ideal coagulation process. If the patient suffers from a
any type of coagulopathy, other hemostatic techniques should be utilized.
These types of agents are available in many different forms (e.g., bovine
collagen, cellulose, gelatins) and application methods (e.g., absorbable
sponge, foam, pads that may absorb several times their own weight).
Expansion may lead to complications, specifically pressing on neural tissue
(e.g., inferior alveolar nerve). Therefore after hemostasis is obtained, passive
hemostats should be removed to minimize postoperative complications.
Passive hemostatic agents are readily available and inexpensive.
Collagen
Collagen-based hemostatic agents work by contact activation and promotion
of platelet aggregation, which occurs as a result of contact between blood and
collagen. Collagen is available in many carrier forms such as a powder, paste,
or sponge. Studies have shown that between 2% to 4% of the total population
are allergic to bovine collagen.26
Bovine Collagen (OraPlug, OraTape [Salvin Dental Specialties,

Inc.]).
Products such as OraPlug and OraTape are soft, white, pliable, nonfriable,
coherent, spongelike structures that are fabricated from bovine collagen
(usually from deep flexor tendons). They are nontoxic, nonpyrogenic, and
highly absorbent. Indications include the control of oozing or bleeding from
clean oral wounds. They help control bleeding, by stabilizing blood clots, and
protect the wound bed to facilitate the healing process. When applied, the
products should be held in place for approximately 2 to 5 minutes to achieve
ideal hemostasis and then may be removed, replaced, or left in place. Most
collagen materials are completely resorbed within 14 to 56 days (Fig. 7.12A–
B).27
FIG 7.12 Collagen hemostatic agents. (A) OraTape. (B) OraPlug. (C) Avitene. (D)
Collagen hemostatic agent placed to control bleeding. (A–B, Courtesy Salvin Dental
Specialties, Inc., Charlotte, NC. C, Courtesy C. R. Bard, Murray Hill, NJ.)
Microfibrillar Collagen (Avitene Microfibrillar Collagen

Hemostat [Davol Inc.]).
Microfibrillar collagen was first introduced in the 1970s. This hemostatic
agent is fabricated by purifying bovine collagen and processing it into
microcrystals. Avitene was first launched in a flour form, and it is still
commonly used in the topical powder form. Collagen-based products activate
the intrinsic pathway of the coagulation cascade.28 Avitene produces a large
surface area, which acts as a matrix for platelet activation, aggregation, and
thrombus formation. Advantages include a rapid onset of hemostasis,
minimal tissue reactivity, low infection rate, and ability to be reabsorbed.29 In
vitro studies have shown microfibrillar collagen to be the most effective in
maintaining hemostasis, followed by collagen, sponge, and then oxidized
cellulose (Fig. 7.12C).20 The disadvantage of microcellular collagen products is
they are extremely expensive with a short shelf life.
Cellulose
The most common cellulose-based hemostatic agent is regenerated oxidized
cellulose that initiates clotting via contact activation. Oxidized cellulose has
been shown to be poorly absorbed and may cause healing complications
postoperatively.
Resorbable Oxidized Cellulose/Fabric Meshwork (Surgicel

[Ethicon US]).
Surgicel is a resorbable oxidized cellulose material in a sterile fabric
meshwork. When Surgicel is applied to the bleeding area, it swells into a
brownish/black gelatinous mass that aids in the clotting process. Because
this agent lowers the pH of the surrounding tissue, red cell lysis occurs,
accounting for the dark discoloration. This caustic material should ideally be
removed because it may delay healing and interfere with osteogenesis (Fig.
7.13A).
FIG 7.13 (A–B) Oxidized regenerated cellulose (Surgicel). (C) Surgicel placed
underneath reflected flap for hemostatis, this should be removed prior to flap
closure. (D–E) BloodSTOP Hemostatic Agent. (F) BloodSTOP placed in extraction
site. (D–E, Courtesy LifeScience PLUS, Inc., Mountain View, CA.)
Cellulose Fabric Meshwork (ActCel [Coreva Health Science,

LLC]).
ActCel is a cellulose fabric meshwork similar to Surgicel. When the
meshwork comes into contact with blood, it expands to 3 to 4 times its
original size and is almost immediately converted to a gel. It will undergo
complete dissolution within 1 to 2 weeks.30 This material has the advantage
over Surgicel that it degrades rapidly into biocompatible end products
(glucose, water) and thus does not adversely affect wound healing or bone
formation. The mechanisms of action will enhance the coagulation process
biochemically by increasing platelet aggregation and physically by initiating
clot stabilization.
Regenerated Cotton Cellulose (BloodSTOP [LifeScience PLUS

Inc.]).
BloodSTOP is a biocompatible, nonirritating, water-soluble, regenerated
cotton cellulose hemostatic agent that resembles traditional gauze. When
applied to a bleeding surgical site, BloodSTOP quickly absorbs blood and
transforms into a gel to seal the wound with a protective transparent layer,
actively aids in blood coagulation, and creates a positive environment for
wound healing. Because BloodSTOP is 100% natural cellulose and is water
soluble, it is easliy removed without disruption of the wound surfaces after
hemostasis. It is manufactured in a single-use, sterile package with a 0.5- × 2-
in size (Fig. 7.13).
Gelatin
Gelatin-based hemostatic agents possess the ability to conform to irregular
wound geometries. Gelatin conforms to the wound and will increase in size,
providing a tamponade effect in the confined spaces. The gelatin particles
restrict blood flow and provide a matrix for clot formation.
Gelatin-Based Hemostatic Agents (Gelfoam [Pfizer Inc.]).

Gelfoam, which was first introduced in the 1940s, is the most common type of
gelatin-based hemostatic agents. Gelfoam is a porous, pliable sponge made
from dried and sterilized porcine skin gelatin. Gelfoam will liquefy in 7 days
and is completely resorbed in 4 to 6 weeks. This material is hygroscopic,
absorbing many times its weight in water and allowing the concentration of
platelets, clotting factors and the gelatin to swell, which provides additional
mechanical hemostatic action through compression (Fig. 7.14).29
FIG 7.14 Gelfoam.
Chitosan
Chitosan is a biocompatible, naturally occurring, positively charged
polysaccharide derived from arthropod skeletons. The positive charge
attracts the negatively charged red blood cells, forming a viscous coagulum,
which seals the bleeding tissue. This material is advantageous due to its
ability to maintain hemostasis independent of coagulation factors. Chitosan
is useful in patients with coagulopathies or patients on anticoagulants.
Chitosan-Based Hemostatic Agents (HemCon Dressing [Tricol

Biomedical, Inc.]).
HemCon dressing is a chitosan-based hemostatic agent that is specifically
made for dental use. Studies have shown hemostasis may be achieved with
HemCon dressings in less than 60 seconds in comparison to a control of 9½
minutes (Fig. 7.15).31 HemCon dental dressings mode of action is an
adhesive-like action, which provides a physical protective barrier. Because
chitosan has a positive charge, it will attract red blood cells, which have a
negative charge. The accumulated red blood cells create a physical barrier.
This dressing will usually dissolve in 48 hours, so no removal is needed.
FIG 7.15 (A) HemCon dressing. (B) HemCon placed under bleeding flap. (C)
Hemostasis achieved, dressing should be removed prior to flap closure. (A,
Courtesy Tricol Biomedical, Inc., Portland, OR.)
Mechanical
Beeswax.
Bone wax, a soft, malleable, nonbrittle wax, was invented in 1886 by Sir Victor
Horsley. The material is a combination of beeswax, salicylic acid, and almond
oil.32 It is most commonly used when the bleeding is visualized as having an
origin from within the bone. This type of bleeding most commonly occurs
during osteotomy preparation and extractions. Bone wax exhibits no
hemostatic quality it obliterates the vascular spaces in cancellous bone.
However, caution should be exercised with the use of bone wax because it is
water insoluble and will not be absorbed. It may predispose the area to
infection or inhibit bone healing. Studies have shown that bone wax, when
removed from an osseous defect after 10 minutes, completely inhibited
further bone regeneration.33 Bone wax also increases inflammation, which
may cause a foreign body giant cell reaction and infection at the site (Fig.
7.16).34
FIG 7.16 Bone wax.
Synthetic Bone Hemostat Material (Ostene [Ceremed Inc.).

Ostene is a synthetic bone hemostat material approved in 2004 by the FDA
for use in cranial and spinal procedures. This material is a mixture of water-
soluble alkylene oxide copolymers that elicits minimal postoperative
inflammation. It has many advantages over bone wax because it is water
soluble and dissolves in 48 hours. It has been associated with a decreased
infection rate and positive bone cultures.35 Ostene is supplied in sterile peel
pouches and is applied in a manner similar to bone wax without the
associated disadvantages. (Fig. 7.17).
FIG 7.17 Ostene. OSTENE (Bone Hemostatis Material). OSTENE material is a
sterile water-soluble surgical implant material. It can be used for the control of
bleeding from bone surfaces by acting as a mechanical barrier. (Courtesy Baxter
Healthcare Corporation, Deerfield, IL. Baxter is a registered trademark of Baxter International Inc.
OSTENE is a registered trademark of Apatech Limited. Copyright © 2017 Baxter Healthcare
Corporation. All rights reserved.)
Combination Agents
Thrombin is used mostly in combination with numerous passive hemostatic
agents such as collagen, gelatin, and fibrin sealant sponges. When fibrinogen
and thrombin is combined, thrombin modifies the fibrinogen into
monomers that polymerize and form a soft plug. The soluble fibrin is then
converted into insoluble fibrils, which form a stable clot.
Combination Hemostatic Agents (FloSeal Matrix Hemostatic

Sealant [Baxter Healthcare Corporation]).
FloSeal was approved in 1999 and is a fast, effective, and proven hemostatic
agent. FloSeal is a combination of two independent hemostatic agents,
combining human-derived thrombin with bovine-derived gelatin matrix
granules, which are mixed at the time of use.36 This hemostatic agent is of
liquid nature, which encompasses crosslinking of the gelatin matrix granules
that minimizes in vivo expansion.37 The gelatin granules swell approximately
10% to 20% when exposed to blood, which helps to seal off the area of
bleeding. This agent works very well on wet, bleeding areas and has been
shown to stop 96% of bleeding with 10 minutes. FloSeal is absorbable within
6–8 weeks, well tolerated, and useful for hard and soft tissues (Fig. 7.18).
FIG 7.18 (A) FLOSEAL Hemostatic Matrix dispensed in a syringe form. (B)
FLOSEAL is indicated in surgical procedures (other than in ophthalmic) as an
adjunct to hemostasis when control of bleeding by ligature or conventional
procedures is ineffective or impractical. (Courtesy Baxter Healthcare Corporation, Deerfield,
IL. Baxter and FLOSEAL are registered trademarks of Baxter International Inc. Copyright © 2017
Baxter Healthcare Corporation. All rights reserved.)
Advantages.
FloSeal is a passive topical hemostatic agent that can be used when
hemostatic control is needed during dental implant procedures. It has been
shown to be effective when more significant and heavier bleeding occurs
because of the larger absorption capacity and greater mass. These agents
may absorb several times their own weight with bleeding. For example,
oxidized cellulose can absorb 7 times its weight, and collagen may absorb 32
times its own weight.20
Disadvantages.
The expansion of FloSeal can result in complications if placed in close
approximation to a vital structure (e.g., inferior alveolar canal) because
neuropraxia type of nerve impairments may result. Additionally, in arterial
bleeds, passive hemostatic agents may not be completely effective. If a
significant arterial bleed occurs, ligation of the artery is usually the ideal
treatment. Caution should be noted on the use of nonabsorbable passive
agents, which can potentiate a foreign-body reaction resulting in chronic
inflammation, infection, or granuloma formation.
Summary of Techniques to Decrease and Control

Bleeding
Intraoperative bleeding episodes during dental implant surgery are most
likely to increase in the future as more medically compromised and elderly
patients are being treated, including patients utilizing anticoagulant
medications. In rare situations, these bleeding episodes may be life
threatening, which necessitates the dental implant surgeon having
knowledge of fast and effective techniques to achieve hemostasis. The use of
topical agents has been shown to improve blood conservation, avoid
potential adverse effects, and decrease surgery time. The dental implant
clinician must be familiar with products that help to achieve hemostasis in
case of complications that may arise.
Prevention/Treatment of Bleeding
Anatomic Areas
The ideal management of intraoperative hemorrhage is prevention. Though
the clinician should be capable of handling potential bleeding complications,
the best course of action is to avoid them as much as possible, which is aided
by taking the appropriate preventive measures. A preoperative assessment of
the patient is mandatory, including a thorough preoperative patient history,
medical consultation when indicated. The clinician should also be familiar
with managing patients on anticoagulants and those who have bleeding
issues, utilize meticulous intraoperative surgical technique, and provide
appropriate postoperative instructions, care, and follow-up. Patients need to
be instructed on the importance of compliance with prescribed medication
and proper postoperative instructions and care.
Incision/Reflection of Tissue
The dental implant clinician must carefully plan the location of incisions with
respect to surgical anatomy to maintain hemostasis and minimize bleeding.
Ideally, incisions should always be made over bony support when possible.
This will allow for pressure to be applied over bone in the event of
uncontrolled bleeding. The flap design should incorporate release incisions
so that excessive pressure and stretching is reduced in order to decrease
possible tearing of the tissue. Elevation of the mucosa and periosteum
should be carefully completed with full-thickness and atraumatic reflection.
Split-thickness flaps should be avoided to minimize potential bleeding sites.
Anatomic areas containing vital structures, that may be highly vascular,
should be carefully evaluated and avoided if possible (Fig. 7.19).
FIG 7.19 (A–B) Ideal incision location and full-thickness reflection will reduce
bleeding with atraumatic reflection of the tissue. Incisions should ideally be over
bone to minimize trauma to the tissue.
Anatomy/ Anatomic Variants

Strategic planning of potential implant sites is mandatory, with a thorough
understanding of anatomic structures and variants with the use of a cone
beam computed tomography (CBCT). The lack of distortion of the CT images
allows the clinician to better plan surgical sites while maintaining relative
safe zones from anatomic structures.
Mandibular Anterior: Intraosseous Vessels

Median Vascular Canal
On occasion, in the mandibular midline, copious bleeding may be present
(e.g., “C” position, even though no bone perforation has occurred). Bilateral
sublingual arteries enter through the lingual foramen within the lingual
plate below the genial tubercles within the mandible. As this anastomosis
transverses within the anterior mandible, the canal is termed the median
vascular canal. Bleeding in this area may be significant; however, it is not
associated with any type of neurosensory impairment.
Prevention.
The presence and size of the sublingual anastomosis and the median
vascular canal is easily seen on a cross-sectional or axial image of a CBCT
scan. The position of the planned osteotomy may need to be modified if a
significant anastomosis is present.
Management.
If significant bleeding occurs after implant osteotomy, a direction indicator
or surgical bur can be placed in the osteotomy site to apply pressure. If the
osteotomy is completed, an implant may also be introduced into the site,
which will compress the walls of bone, thus slowing the bleeding process
(Fig. 7.20). In most cases, intraosseous bleeding is more easily controlled in
comparison to soft tissue hemorrhage.
FIG 7.20 Median vascular canal. (A) Canal exhibiting the anastomosis of the right
and left sublingual arteries. (B) Implant placed in the midline area may cause
significant intraosseous bleeding. (C) Treatment includes placing in the osteotomy
site the surgical drill, direction indicator, or implant to stop the bleeding.
Inferior Alveolar Artery

The inferior alveolar artery is a branch of the maxillary artery, one of the two
terminal branches of the external carotid. Prior to entering the mandibular
foramen, it gives off the mylohyoid artery. In approximately the first molar
region, it divides into the mental and incisal branches. The mental branch
exits the mental foramen and supplies the chin and lower lip, where it
eventually will anastomose with the submental and inferior labial arteries.
Prevention.
The exact location of the inferior alveolar artery is easily determined via a
CBCT evaluation in the panoramic or sagittal views.
Management.
Normally, the inferior alveolar artery is located superiorly to the inferior
alveolar nerve within the bony mandibular canal. Drilling or placing an
implant into the inferior alveolar canal may predispose to significant
bleeding. Hemorrhage may be controlled by placement of an implant or
direction indicator short of the canal. A 2.0-mm safety zone should be
adhered to. If bleeding does occur, follow-up postoperative care is essential
because hematoma formation within the canal may lead to a neurosensory
impairment. This condition should be monitored because it may progress to
respiratory depression via a dissecting hematoma in the floor of the mouth
(Fig. 7.21).
FIG 7.21 Inferior alveolar artery. (A) Penetration within the inferior alveolar canal.
(B) May cause profuse bleeding. (C) Treatment includes placing the drill, direction
indicator, or implant to stop the bleeding.
Incisive Artery
The incisive artery is the second terminal branch of the inferior alveolar
artery, which is a branch of the maxillary artery. The incisal branch continues
anteriorly after supplying in the mandibular first molar area, where it
innervates the incisor teeth and anastomoses with the contralateral incisal
artery. In rare cases, the incisive canal is large, lending to greater bleeding
during osteotomy preparation or bone grafting procedures.1
Prevention.
The exact location of the incisive canal is easily determined via a CBCT
evaluation in the panoramic or sagittal views.
Management.
Bleeding complications can occur when implants are placed into the
mandibular incisive canal, which contains the incisive artery. If bleeding does
occur during placement of the implant, a direction indicator or surgical bur
can be placed into osteotomy to apply pressure (Fig. 7.22).
FIG 7.22 Incisive canal. Placement of implants in the interforaminal area may lead
to increased bleeding; it is usually self-limited.
Mandibular Anterior: Extraosseous Vessels

The anterior mandible is usually known as a safe area for implant placement,
but in certain situations, it may present with a significant undercut on the
lingual aspect between the foramina. Life-threatening hemorrhage has been
reported when a drill perforates the lingual plate of the sublingual region of
the mandible and traumatizes a sublingual or submental artery, especially in
the canine region.38,39 If perforation of the lingual cortical plate is associated
with arterial bleeding, it is critical to identify its origin and treat aggressively.
The origin of bleeding in the floor of the anterior region of the mouth may be
from the lingual artery, facial artery, or one of its branches. The submental
artery originates from the facial artery and courses along the inferior border
of the mandible. The sublingual artery, a branch of the lingual artery, runs
along the inferior border of the mandible and terminates in the midline.
Perforation in this area may lead to bleeding, causing an expanding
ecchymosis (sublingual hematoma) and compromising the airway.
Sublingual Artery (Lingual Artery)

The lingual artery is a branch of the external carotid artery between the
superior thyroid and facial arteries. The lingual artery courses medially to the
greater horn of the hyoid bone and crosses inferiorly and facially around the
hypoglossal nerve. It then transverses deep to the digastric and stylohyoid
muscles and courses between the hyoglossus and genioglossus muscles.
There exist four main branches of the lingual artery: the suprahyoid, dorsal
lingual, deep lingual, and sublingual. Of clinical significance to oral
implantology is the sublingual artery, which supplies the sublingual salivary
gland, mylohyoid and surrounding muscles, and the mucous membranes
and gingiva of the mandible. A distal branch runs medially in the anterior
lingual mandibular gingiva and anastomoses with the contralateral artery. An
additional branch connects with the submental artery under the mylohyoid
muscle.40 The lingual artery will anastomose throughout the tongue area,
with more anastomoses occurring anteriorly.41
Submental Artery (Facial Artery)

The most important branch of the facial artery associated with oral
implantology is the submental branch, which is the largest of the branches of
the facial artery. The submental branch exits the submandibular gland and
proceeds anteriorly on the surface of the mylohyoid muscle, just inferior to
the body of the mandible. The submental branch terminates as an
anastomosis with the sublingual branch of the lingual artery and the
mylohyoid branch of the inferior alveolar artery.40
Studies have shown that the floor of the mouth and lingual gingiva is
supplied approximately 53% by the submental artery and the remaining by
the sublingual artery.42 Perforation of the lingual cortical plate may result in
trauma to the submental artery. Treatment should include immediate
repositioning of the patient in an upright position followed by the
application of bimanual pressure. This should be immediately applied,
followed by airway management and emergency protocol. Bleeding from the
submental artery may be decreased by applying finger pressure over the
lower border of the mandible. Doppler ultrasonography studies have shown
this to reduce the arterial blood by 25% to 50% at the oral commissure level
and 33% to 50 % at the inferior border of the nares.43
Katsumi et al described four types of sublingual and submental arteries:
Type 1: Sublingual artery, no submental artery (63%)
Type 2: Sublingual and submental present (5.6%)
Type 3: Submental, no sublingual (29.6%)
Type 4: Submental with no deep lingual artery (1.8%)
In Types 2, 3, and 4 vessel anatomy are associated with sublingual bleeding

issues.44 There also exists a relationship of the submental and sublingual
arteries in dentate vs. edentulous patients. Usually the sublingual arteries
course above the mylohyoid line and the submental arteries run below or
within the muscle.45,46 In dentate patients hemorrhage risk is high with
vessels above the mylohyoid. In edentulous patients the mylohyoid line
approaches the alveolar crest, thus lending to high risk of hemorrhage, which
may result in arterial damage in the submandibular space.
Prevention.
Clinical and radiographic evaluation should be completed to ascertain the
amount of available bone and osseous angulation in the anterior mandible.
The length of implants should be carefully evaluated because bicortical
stabilization (which may lead to perforation of the lingual plate) is no longer
advocated for implant success. This is most important in the mandibular
canine position. Additionally, care should be exercised in elevation of the
lingual flap and manipulation of the lingual tissue.
Bleeding into the sublingual and submaxillary spaces will cause elevation of
the tongue and floor of the mouth. Bleeding in these spaces will proceed to
airway obstruction because the anterior extension of the hematoma is limited
by the superficial layers of the cervical fascia.47 The signs and symptoms of
sublingual swelling include immediate or delayed (up to 4–8 hours after
surgery) elevation of the floor of the mouth, protrusion of the tongue,
profuse intraoral bleeding, difficulty in swallowing, and respiratory
depression. The submandibular swelling may dislocate the trachea to the
contralateral side and compromise the airway.48 Additionally, pulsatile
hematomas (pseudoaneurysms) of the lingual artery may result from the
injury (Fig. 7.23).49
FIG 7.23 (A) Sublingual and submental arteries showing proximity to inferior border
of mandible. (B) Perforation of the lingual cortical plate. (C) Perforation into
sublingual space may traumatize the sublingual and submental vessels leading to
significant bleeding. (D) To slow sublingual bleeding, apply bimanual pressure with 4
× 4 gauze on lingual surface of mandible and superior pressure extraorally. (A, From
Loukas M, Kinsella CR Jr, Kapos T, et al: Anatomical variation in arterial supply of the mandible with
special regard to implant placement. Int J Oral Maxillofac Surg 37(4):367–371, 2008.)
Management.
Immediate bimanual pressure should be applied to the bleeding area if
location can be determined. A 4 × 4 gauze may be used to apply the bimanual
compression downward from floor of the mouth (lingual surface of the
mandible) and in an upward direction from the submental skin area. The
patient should be repositioned from a supine to an upright position. A Young
forceps may be used to pull the tongue outward, which will slow the
bleeding. Airway obstruction should be of vital concern because this may
lead to a life-threatening situation. If any clinical signs of airway obstruction
exist (e.g., dyspnea, dysphagia, wheezing, stridor, cyanosis), emergency
intervention should be summoned immediately. Ligation of the bleeding
vessel is the ideal treatment to control the hemorrhage. This may be very
difficult in an office setting due to the location and surgical access of the
bleeding vessel. To obtain definitive control of sublingual artery bleeding,
surgical intervention with selective ligation of the branches along with
arterial embolization via interventional angiography is indicated (Fig. 7.24).50
FIG 7.24 Sublingual hematoma. (A) Four implants placed flapless in the anterior
mandible. (B) Resultant sublingual hematoma with airway compromise. (C) Axial CT
images showing extent of hematoma (blue arrows) with airway compromise. Note
perforation of lingual cortical plate (red arrow). (D) Young forceps may be used to pull
tongue out to decrease the bleeding and helps maintain airway until medical
assistance arrives. (From Limongelli L, Tempesta A, Crincoli V, et al: Massive lingual and
sublingual haematoma following post extractive flapless implant placement in the anterior
mandible. Case Rep Dent, vol. 2015, Article ID 839098, 4 pages, 2015.)
Mandibular Posterior: Extraosseous Vessels

Lingual Undercut
In the mandibular posterior area a lingual undercut may be problematic and
difficult to manage. In this area, perforation of the lingual plate can occur
very easily, thereby causing bleeding episodes, with an origin that may be
difficult to locate. Life-threatening situations may result from sublingual
bleeding. Violation of this area may cause infection or constant irritation
from the extruded implant in the soft tissue. If the perforation were to occur
above the mylohyoid muscle, damage to the lingual nerve could result in a
neurosensory impairment.
Prevention.
A clinical exam should always be carried out to determine if an osseous
undercut exists. This may be confirmed with a CBCT examination because
cross-sectional images are a very effective way of observing lingual
undercuts. Additionally, angulation and positioning must be continuously
verified to prevent inadvertent perforation. Studies have shown that lingual
undercuts occur in approximately 66% of the population with a mean
undercut of 2.4 mm.51 Accurate measurements must be made to prevent
overpreparation of the osteotomy site in the anterior mandible. This is most
easily completed with a CBCT examination. Osteotomy angulation should
always be carefully evaluated because improper drilling angulation may lead
to perforations. Additionally, hourglass mandibles, which have been shown
to have an incidence of approximately 4%, should always be concerning
because perforation will occur.52 Palpation of the ridge during osteotomy
preparation will minimize perforations and decrease complications.
Management.
If sublingual posterior bleeding (submental or sublingual arteries) occurs,
the patient should be repositioned in an upright position and bimanual
pressure should be applied to the area of bleeding. If the airway is
compromised, immediate emergency assistance should be summoned (Fig.
7.25).
FIG 7.25 (A) CBCT 3-D image of posterior undercut. (B) Interactive treatment
planning showing implant placement into sublingual undercut, in this case an implant
would most likely be contraindicated. (C) Cross-section of implant perforation that
may lead to pain, bleeding, and implant morbidity.
Mylohyoid Artery
The mylohyoid artery branches from the inferior alveolar artery and courses
along the medial surface of the mandible in the mylohyoid groove, which
supplies the mylohyoid muscle.
Prevention.
This artery is very rarely involved in bleeding episodes with oral
implantology procedures, but an episode may occur from lingual cortical
perforation in the molar region or aggressive reflection of the lingual tissue.
Management.
Bleeding may be controlled locally by applying finger pressure along the
medial side of the mandible (Fig. 7.26).
FIG 7.26 Most common arteries of the head and neck region.
Buccal Artery
A common donor site for autogenous grafting is the lateral ramus area in the
posterior mandible. When making the incision lateral to the retromolar pad,
a common blood vessel to damage is the buccal artery. The buccal artery is a
branch of the maxillary artery and will most likely cause a significant
bleeding episode. This artery runs obliquely between the internal pterygoid
and the insertion of the temporalis on the outer surface of the buccinator.
Prevention.
In most cases, damage to the buccal artery is impossible to avoid. Incision
and reflection will usually encompass the area of buccal artery location.
When performing surgery in this area, a hemostat should always be available
for immediate access in order to clamp the vessel.
Management.
A curved hemostat should be utilized to control the bleeding. It should be
left in place for 3–5 minutes. If bleeding persists, a ligature may be placed
with Vicryl suture material (see Fig. 7.26).
Facial Artery
The facial artery is a branch of the external carotid, lying superior to the
lingual artery and medial to the ramus of the mandible (Fig. 7.27). It courses
below the digastric and stylohyoid muscles and passes through a groove in
the submandibular gland before it becomes superficial around the inferior
border of the mandible. There are two main branches of the facial artery: the
facial and cervical. The facial branch encompasses five branches, which
supply the eye, nose, and lips. There are four branches of the cervical region
supplying the pharynx, soft palate, auditory tube, and submandibular gland.
FIG 7.27 Facial artery. (A) Location in the facial notch in the angle of mandible. (B)
Care should be exercised when using retraction in this area because damage to the
facial artery could occur. (A, From Loukas M, Kinsella CR Jr, Kapos T, et al: Anatomical variation
in arterial supply of the mandible with special regard to implant placement. Int J Oral Maxillofac Surg
37(4):367–371, 2008.)
Prevention.
Trauma to the facial should always be avoided as the clinician should refrain
from excessive retraction in this area.
Management.
If bleeding from the facial artery exists, pressure should immediately be
applied to the angle of the mandible over the vessel. Usually, medical
assistance will need to be summoned.
Maxilla: Lateral Wall/Nasal Bleeding

Significant bleeding from the lateral-approach sinus elevation surgery is
rather rare; however, it has the potential to be troublesome. Three main
arterial vessels should be of concern with the lateral-approach sinus
augmentation. Because of the intra- and extraosseous anastomoses that are
formed by the infraorbital and posterior superior alveolar arteries,
intraoperative bleeding complications of the lateral wall may occur. In some
cases, this bleeding may be significant.
Extraosseous Anastomosis
The soft tissue vertical-release incisions of the facial flap in a resorbed
maxilla may sever the extraosseous anastomoses during lateral wall
osteotomy preparation for sinus graft surgery. The extraosseous anastomosis
on average is located 23 mm from the crest of the dentate ridge; however, in
the resorbed maxilla, it may be within 10 mm of the crest. When this artery is
severed, significant bleeding has been observed. These vessels originate from
the maxillary artery and have no bony landmark to compress the vessel.
Vertical release incisions in the soft tissue should be kept to a minimum
height with delicate reflection of the periosteum. Hemostats are usually
difficult to place on the facial flap to arrest the bleeding. Significant pressure
at the posterior border of the maxilla and elevation of the head to reduce the
blood pressure to the vessels usually slows the bleeding. The elevation of the
head may reduce nasal mucosal blood flow by 38%.15
The vertical component of the lateral-access wall for the sinus graft often
severs the intraosseous anastomoses of the posterior alveolar artery and
infraorbital artery, which is on average approximately 15 to 20 mm from the
crest of a dentate ridge. Methods to limit this bleeding, which is far less of a
risk, include cauterization with the use of a hand piece and diamond bur
without water, electrocautery, or pressure on a surgical sponge while the head
is elevated. In some cases, a second window is made distal to the bleeding
area source for access to ligate (Fig. 7.28).
FIG 7.28 Intraosseous anastomosis. (A) Cross-sectional image showing

radiolucent notch on the lateral wall of the sinus (red arrow). (B) Intraosseous notch
(white arrow). (C) Clinical view of lateral wall removed showing size of intraosseous
anastomosis (blue arrow). (D) Intraosseous anastamosis pulsating bleed.
Posterior Lateral Nasal Artery
The third artery implant surgeons should be cautious of is the posterior
lateral nasal artery (Fig. 7.29). This artery is a branch of the sphenopalatine
artery, which is located within the medial wall of the antrum. As it courses
anteriorly, it anastomoses with terminal branches of the facial artery and
ethmoidal arteries. A significant bleeding complication may arise if this
vessel is severed during elevation of the membrane off the thin medial wall.
FIG 7.29 (A) Posterior lateral nasal artery (red line) in close approximation to the
lateral wall of the nasal cavity (medial wall of maxillary sinus). (B) Nasal bleed during
sinus augmentation procedure.
If the excessive bleeding occurs while the medial wall is elevated, the sinus
may be packed with hemostatic agents, followed by packing with large 4 × 4-
inch surgical sponges, and elevation of the head. Once the bleeding is
arrested, the sponges are removed, the layered graft materials may be
inserted, and the procedure completed.
Epistaxis (active bleeding from the nose) following sinus graft surgery is
rather common. This may occur with or without a membrane perforation.
Usually epistaxis is limited to the first 24 hours after surgery, and the patient
should always be warned of this potential complication.
If bleeding should occur through the nose, there exist numerous
techniques to obtain hemostasis. Placing a cotton roll, coated with petroleum
jelly with dental floss tied to one end, within the nares may obtund nose
bleeding after the surgery. After 5 minutes the dental floss is gently pulled
and the cotton roll removed. The head is also elevated, and ice is applied to
the bridge of the nose. If bleeding cannot be controlled, reentry into the graft
site and endoscopic ligation by an ENT surgeon may be required.
If the orbital wall of the sinus is perforated or if an opening into the nares
is already present from a previous event (i.e., previous sinus surgery), the
sinus curette may enter the nares and initiate bleeding. The arteries involved
in this site are composed of branches of the sphenopalatine and descending
palliative arteries, which are branches of the internal maxillary artery. The
posterior half of the inferior turbinate has a venous network, the Woodruff
plexus, which is highly vascular. A cotton roll with silver nitrate or lidocaine
with 1 : 50,000 epinephrine is also effective in obtaining hemostatis.
Postoperative Bleeding Control
Patient Education
It is imperative that patients understand that minor oozing may persist for
up to 24 hours after dental implant surgery. If the patient is on
anticoagulants, this may persist for up to 48 hours. The patient should be
instructed on the use of pressure dressings, and special care should be taken
to minimize any trauma to the surgical site (e.g., eating, pulling on lip to see
surgical site). The patient should avoid rinsing the mouth vigorously. All
postoperative instructions should be reviewed with the patient and given in
writing prior to surgery.
Patients should be instructed to limit their activities for a minimum of 24
hours depending on the extent of the surgery. The head should be elevated as
much as possible during the daytime hours and the use of two pillows (i.e.,
elevate head) during sleeping will reduce secondary bleeding episodes.
Postoperative hemorrhage in the anticoagulated patients may lead to
significant issues. Studies have shown bleeding episodes in anticoagulant
patients will most likely occur within 6 days of the surgery.53 In patients who
have exhibited significant bleeding during surgery, hemorrhagic shock,
although rare, should be evaluated. If the patient displays any signs or
symptoms of shock (e.g., tachycardia, hypotension, lethargy, disorientation,
cold/clammy skin), immediate medical assistance should be summoned.
Treatment would include intravenous fluid replacement to replenish the
intravascular volume and restore tissue perfusion.
Finally, caution should be exercised on the postoperative use of
medications that may increase bleeding. A comprehensive review of the
patient's medications should be completed to determine if any drug
interactions may exist that would increase bleeding. Agents that interfere
with platelet function should be avoided for routine analgesia (e.g.,
nonsteroidal antiinflammatory drugs [NSAIDs], aspirin) unless the benefit
outweighs the increased risk of bleeding. The routine perioperative use of
aspirin should usually be avoided due to an increased risk of bleeding and
lack of benefit. However, if these medications are administered for a separate
indication under the recommendation of a physician (e.g., recent stroke,
acute coronary syndromes, implanted coronary stent) they should be
continued.
Summary
During the course of any dental implant surgery, the opportunity for a
bleeding episode exists. The network of vascular structures coursing through
the maxillofacial region is extensive, and many of these structures lie
extremely close to the surgical site, regardless of procedure. Damaging these
vessels may cause bleeding episodes that range from very benign to life-
threatening events, and the ability to achieve hemostasis is of paramount
importance. Maintaining hemostasis during the surgical procedure is crucial
to preserving the physiologic functions of the patient, providing the implant
clinician with a clear operating field, and allowing for successful
postoperative wound healing. Understanding factors that predispose the
patient to bleeding issues should be evaluated for each patient. The arterial
vs. venous bleeding is much different and should be able to be differentiated
to determine the origin of the bleeding and treated accordingly. The clinician
must be able to eliminate potential risks that increase bleeding and to utilize
various techniques to maintain hemostasis throughout the intra- and
postoperative time periods.
References
1. Loukas M, Kinsella CR, Kapos T, et al. Anatomical variation in arterial
supply of the mandible with special regard to implant placement. Int
2. Lundblad RL, Bradshaw RA, Gabriel D, et al. A review of the
therapeutic uses of thrombin. Thromb Haemost. 2004;91:851–860.
3. Moake JL. Overview of hemostasis. [The Merck Manual Professional
Version; Available at:]
http://www.merckmanuals.com/professional/hematology-and-
oncology/hemostasis/overview-of-hemostasis.
4. Marieb EN, Hoehn K. Human anatomy & physiology. ed 8. Benjamin
Cummings: San Francisco; 2010:649–650.
5. Ogle OE, Swantek J, Amandip K. Hemostatic agents. Dent Clin North
Am. 2011;55:433–439.
6. Clemetson KJ. Platelets and primary haemostasis. Thromb Res.
2012;129:220–224.
7. Scully C. Scully's medical problems in dentistry. ed 7. Churchill
8. Cesarman-Maus G, Hajjar KA. Molecular mechanisms of fibrinolysis.
Brit J Haematol. 2005;129:307–321.
9. Kazmi RS, Lwaleed BA. New anticoagulants: how to deal with
treatment failure and bleeding complications. Brit J Clin Pharmacol.
2011;72:593–603.
10. Weitz JI. Meeting the unmet needs in anticoagulant therapy. Eur J
Haematol. 2010;85(Suppl 72):1–3.
11. Kamoh A, Swantek J. Hemostasis in oral surgery. Dent Clin North Am.
2012;56:17–23.
12. Servin F. Low-dose aspirin and clopidogrel: how to act in patients
scheduled for day surgery. Curr Opin Anaesthesiol. 2007;20:531–534.
13. Rowe DJ, Baker AC. Perioperative risks and benefits of herbal
supplements in aesthetic surgery. Aesthet Surg J. 2009;29:150–157.
13a. Lip GY, Douketis JD. Perioperative management of patients receiving
anticoagulants. Leung LLK. UpToDate.com. 2016 [Waltham, MA;
(website)] www.UpToDate.com [Accessed on 08.09.16].
14. Martin-Du Pan RC, Benoit R, Girardier L. The role of body position
and gravity in the symptoms and treatment of various medical
diseases. Swiss Med Wkly. 2004;134:543–551.
15. Gurr P, Callahan V, Baldwin D. Laser-Doppler blood flowmetry
measurement of nasal mucosa blood flow after injection of the
greater palatine canal. J Laryngol Otol. 1996;110:124–128.
16. Horch HH, Deppe H. Laser in der Zahnärztlichen Chirurgie und
Mund-, Kiefer-und Gesichtschirurgie. Angew. Lasermedizin. Lehr-
und Handbuch für Praxis und Klinik. Losebl.-Ausg. Landsberg.
Ecomed. 2004;3:1.
17. Degerliyurt K, Denizci S. Does the topical use of epinephrine for sinus
floor augmentation affect systemic hemodynamics? Implant Dent.
2013;22(3):289–294.
18. Sindet-Pedersen S, Ramstrom G. Hemostatic effect of tranexamic acid
mouthwash in anticoagulant-treated patients undergoing oral
surgery. New Engl J Med. 1989;320:840–843.
19. Choi WS, Irwin MG, Samman N. The effect of tranexamic acid on
blood loss during orthognathic surgery: a randomized controlled
trial. J Oral Maxillofac Surg. 2009;67:125–133.
20. Tomizawa Y. Clinical benefits and risk analysis of topical hemostats: a
review. J Artif Organs. 2005;8:137–142.
21. Oz MC, Rondinone JF, Shargill NS. FloSeal Matrix: new generation
topical hemostatic sealant. J Card Surg. 2003;18:486–493.
22. Bochicchio G, Dunne J, Bochicchio K, Scalea T. The combination of
platelet-enriched autologous plasma with bovine collagen and
thrombin decreases the need for multiple blood transfusions in
trauma patients with retroperitoneal bleeding. J Trauma. 2004;56:76–
79.
23. Pfizer Injectables product fact sheet. Thrombin-JMI syringe spray kit
thrombin, topical (bovine origin). [USP Not for Injection; Available at:]
http://www.pfizerinjectables.com/factsheets/Thrombin-
JMI_all%20SKUs.pdf.
24. Evithrom. [Available at:] http://www.ethicon.com/healthcare-
professionals/products/biosurgery/evithrom-thrombin-topical-
human.
25. Recothrom. [Available at:] http://www.recothrom.com.
26. Lynn AK, Yannas IV, Bonfield W. Antigenicity and immunogenicity of
collagen. J Biomed Mater Res B Appl Biomater. 2004;71:343–354.
27. Ogle OE. Perioperative hemorrhage. Dym H, Ogle OE. Atlas of minor
oral surgery. Saunders: Philadelphia; 2010.
28. Sirlak M, Eryilmaz S, Yazicioglu L, et al. Comparative study of
microfibrillar collagen hemostat (Colgel) and oxidized cellulose
(Surgicel) in high transfusion-risk cardiac surgery. J Thorac Cardiovasc
Surg. 2003;126:666–670.
29. Achneck HE, Sileshi B, Jamiolkowski RM, et al. A comprehensive
review of topical hemostatic agents: efficacy and recommendations
for use. Ann Surg. 2010;251:217–228.
30. Gupta G, Prestigiacomo CJ. From sealing wax to bone wax:
predecessors to Horsley's development. Neurosurg Focus. 2007;23:E16.
31. Malmquist JP, Clemens SC, Oien HJ, et al. Hemostasis of oral surgery
wounds with the hemcon dental dressing. J Oral Maxillofac Surg.
2008;66:1177–1183.
32. Tan TC, Black PM. Sir Victor Horsley (1857–1916): Pioneer of
neurological surgery. Neurosurgery. 2002;50:607–611 [discussion 611–
612].
33. Ibarrola JL, Bjorenson JE, Austin BP, et al. Osseous reactions to three
hemostatic agents. J Endod. 1985;11:75–83.
34. Allison RT. Foreign body reactions and an associated histological
artifact due to bone wax. Br J Biomed Sci. 1994;51:14–17.
35. Wellisz T, Yuehuei H, Wen X, et al. Infection rates and healing using
bone wax and a soluble polymer material. Clin Orthop Relat Res.
2008;466:481–486.
36. Baxter FLOSEAL. (Hemostatic matrix) instructions for use. [Available at:]
http://www.floseal.com/us/about.html.
37. Renkens KL Jr, Payner TD, Leipzig TJ, et al. Multicenter, prospective,
randomized trial evaluating a new hemostatic agent for spinal
surgery. Spine. 2001;26:1645–1650.
38. Laboda G. Life-threatening hemorrhage after placement of an
endosseous implant. Report of a case. J Am Dent Assoc. 1990;121:559–
600.
39. Kalpidis CE, Konstantinidis AB. Critical hemorrhage in the floor of
the mouth during implant placement in the first mandibular
premolar position: a case report. Implant Dent. 2005;14:117–124.
40. Flanagan D. Important arterial supply of the mandible, control of an
arterial hemorrhage, and report of a hemorrhagic incident. J Oral
Implantol. 2003;29:165–173.
41. Vujaskovic G. Anastomosis between the left and the right lingual
artery in Serb-Croatian (Roman). Stomatol Glas Srb. 1990;37:267–274.
42. Bavitz JB, Harn SD, Homze EJ. Arterial supply to the floor of the
mouth and lingual gingiva. Oral Surg Oral Med Oral Pathol.
1994;77:232–235.
43. Zhao Z, Li S, Xu J, et al. Color Doppler flow imaging of the facial
artery and vein. Plast Reconstr Surg. 2000;106:1249–1253.
44. Katsumi Y, Tanaka R, Hayashi T. Variation in arterial supply to the
floor of the mouth and assessment of relative hemorrhage risk in
implant surgery. Clin Oral Implants Res. 2013;24(4):434–440.
45. Sterne GD, Januszkiewicz JS, Hall PN. The submental island flap.
British J Plast Surg. 1996;49:85–89.
46. Quirynen M, Mraiwa N, van Steenberghe D. Morphology and
dimensions of the mandibular jaw bone in the interforaminal region
in patients requiring implants in the distal areas. Clin Oral Implants
Res. 2003;14:280–285.
47. Rosenbaum L, Thurma P, Krantz SB. Upper airway obstruction as a
complication of oral anticoagulation therapy. Arch Intern Med.
1979;139:1151–1153.
48. Saino M, Akasaka M, Najajima M, et al. A case of a ruptured lingual
artery aneurysm treated with endovascular surgery. No Shinkei Geka.
1997;25:835–839 [in Japanese].
49. Mitchell RB, Pereira KD, Lazar RH, et al. Pseudoaneurysm of the right
lingual artery: an unusual cause of severe hemorrhage during
tonsillectomy. Ear Nose Throat J. 1997;76:575–576.
50. Lee CYS, Yanagihara LC, Suzuki JB. Brisk, pulsatile bleeding from the
anterior mandibular incisive canal during implant surgery: a case
report and use of an active hemostatic matrix to terminate acute
bleeding. Implant Dent. 2012;21:368–373.
51. Chan HL, Brooks SL, Fu JH. Cross-sectional analysis of the
mandibular lingual concavity using cone beam computed
tomography. Clin Oral Implants Res. 2011;22:201–206.
52. Butura CC, et al. Hourglass mandibular anatomic variant incidence
and treatment considerations for all-on-four implant therapy: report
of 10 cases. J Oral Maxillofac Surg. 2011;69:2135–2143.
53. Morimoto Y, Niwa H, Minematsu K, et al. Risk factors affecting
postoperative hemorrhage after tooth extraction in patients receiving
oral antithrombotic therapy. J Oral Maxillofac Surg. 2011;69:1550–1556.
54. Firriolo JF, Hupp WS. Beyond warfarin: the new generation of oral
anticoagulants and their implications for the management of dental
patients. Oral Surg Oral Med Oral Pathol Oral Radiol. 2012;113:431–
441.
55. Kitchens CS, Konkle BA, Kessler CM. Consultative hemostasis and
thrombosis: Expert consult—online and print. Elsevier Health Sciences:
Philadelphia; 2013.
8
Infection
Randolph R. Resnik, Joseph E. Cillo
Among the numerous potential complications that clinicians face during

implant or bone grafting surgery, the possibility of infection by
microorganisms carries some of the most significant ramifications. Infection
can lead to a multitude of problems, including pain, swelling, loss of bone,
possible failure of the implant, and patient morbidity issues. Studies have
shown that infection after implant surgery occurs approximately 4% to 10%
of the time with over 66% of implants failing.1 It is crucial for the implant
clinician to prevent, diagnose, and treat infections associated with implant
procedures.
There is a large contingent of factors that may promote the occurrence of
infection during the surgical implant process. Given that dental implants and
bone graft materials are placed in an entirely nonsterile environment, the
clinician must pay attention to every aspect that may hinder the healing
process and promote infection at the surgical site. In this regard, the clinician
must obtain a detailed history of the patient's past and current medical
histories and any medications/supplements. This will allow the clinician to
obtain the best possible environment to achieve surgical implant success.
Some of the systemic conditions that clinicians placing implants may
encounter, such as diabetes, may contribute to an increased chance of
infection in the implant and bone graft patient. Uncontrolled diabetes has
long been known as a potential source of infection in dental implant surgery.2
Additionally, two often overlooked medical conditions that have recently
been shown to increase the occurrence of infection and failure in implant and
bone graft surgery are the high levels of low-density lipoprotein (LDL)
cholesterol and low levels of serum vitamin D. These and other biologic
conditions highlight the importance of a comprehensive medical history to
ascertain the risk of infection in the dental implant patient (Box 8.1).3
Box 8.1
Factors Associated With Increased Risk of
Infection for Dental Implant Procedures
Systemic Factors
• Diabetes
• Long-term corticosteroid use
• Smoking
• Immunocompromised systemic disorders
• Malnutrition, obesity
• Elderly population
• ASA 3 or ASA 4
Local Factors
• Use/type of grafting material (autogenous, allograft, alloplast)
• Periodontal disease
• Tissue inflammation
• Odontogenic infections
• Ill-fitting provisional prosthesis
• Incision line opening
• Inadequate hygiene
Surgical Factors
• Poor aseptic technique
• Skill/experience of the surgeon
• Increased duration of surgery
• Wound contamination during surgery
• Foreign body (implant)
ASA, American Society of Anesthesiologists, physical status classification.

(From Misch CE: Contemporary implant dentistry, ed 3, St. Louis, 2008, Mosby.)
Patients with one or more of the above diseases need to be evaluated as

high risk for postoperative infection and delayed healing. A medical
clearance from the patient's physician along with antibiotic prophylaxis is
highly recommended.
Risk of Infection
Even under ideal conditions a dental implant or bone graft is basically placed
into a contaminated field due to the natural flora of the oral environment.
The amount of bacteria required to cause an infection is far less than that
required in a clean surgical wound. For example, when a suture is placed
through the tissue, the amount of bacteria that is needed to cause an
infection is reduced by a factor of 1000. Thus not only are these procedures
complicated by the initial bacterial load but also by an inoculation of the
implant or bone graft area by oral bacteria.4
To evaluate the risk for postoperative wound infection, a classification of
operative wounds and risk of infection was developed by the American
College of Surgeons Committee on Control of Surgical Wound Infections. All
surgical procedures were classified according to four levels of contamination
and infection rates. Within these classifications, it is generally accepted that
all class 2, class 3, and class 4 procedures warrant the use of prophylactic
antibiotics (Box 8.2).5
Box 8.2
Surgical Wound Classifications With
Associated Infection Rates
Class 1: Clean (<2%)
• Elective, nontraumatic surgery; no acute inflammation, respiratory,
gastrointestinal, and biliary tracts not entered
Class 2: Clean-Contaminated (10% to 15%)

• Elective opening of the respiratory, gastrointestinal, and biliary tracts
entered
• Elective dental implant and bone procedures
Class 3: Contaminated (20% to 30%)

• Inflammation; gross spillage from gastrointestinal and biliary tracts along
with fresh traumatic injuries
Class 4: Dirty/Infected (50%)
• Established clinical infection; perforation of respiratory, gastrointestinal,
and biliary tracts
(Adapted from American College of Surgeons Committee on Control of Surgical Infections. Manual on
control of infection in surgical patients, ed 2, Philadelphia, 1984, JB Lippincott.)
By definition, elective dental implant surgery falls within the class 2 (clean-
contaminated) category. Class 2 medical and dental surgical procedures have
been shown to have an infection rate of 10% to 15%. However, with proper
surgical technique and prophylactic antibiotics, the incidence of infection
may be reduced to less than 1%. In a healthy patient, risk of infection after
dental implant surgery is influenced by numerous factors such as type and
location of surgery, skill of the surgeon, methods of intraoperative
management, patient factors, and aseptic technique.6,7 Moreover, additional
patient-related (systemic and local) risk factors that are not addressed in
these classifications and mentioned above have also been correlated with
increased susceptibility to infection.
One of the most significant surgical factors that may contribute to
infection is poor aseptic technique. Various routes of transmission of virulent
bacteria include (1) direct contact with the patient's blood or other body
fluids; (2) indirect contact with contaminated objects; (3) contact of infected
nasal, sinus, or oral mucosa; and (4) inhalation of airborne microorganisms.
To prevent these conditions a controlled, well-monitored aseptic setting
should be achieved for the surgical procedure. The aseptic surgical site
includes proper disinfection and draping procedures of the patient, hand
scrubbing, sterile gowns worn by all surgical members, and maintenance of
complete sterility of the instrumentation.
Another important surgical factor related to postoperative infection is the
duration of the surgical procedure. This factor has been shown to be the
second most critical risk factor (after wound contamination) affecting
postoperative infection rates. In general, surgical operations lasting less than
1 hour have an infection rate of 1.3%, whereas those lasting 3 hours have a
rate of more than 4%.8 It is postulated that the rate of infection doubles with
every hour of the procedure.9
The skill and the experience of the surgeon with the placement of implants
have been shown to be significant in postoperative infections and implant
failures. A recent study has shown that less experienced surgeons (<50
implants placed) have 7.3% more failure rates than do experienced
surgeons.10 Clinicians early on their learning curve must adhere to strict
aseptic protocol and good surgical technique to reduce the possibility of
infections.
In the medical literature, it is well documented that the insertion of any
prosthetic implant or device increases the chance of infection at the surgical
site. A dental implant can act as a foreign body, and the host's defenses may
be compromised. The surface of the implant has been shown to facilitate
bacterial adherence, and the presence of an implant can compromise the
host's defenses. This may result in normal flora with low virulence potential
causing infections at the implant-host interface, which has been shown to be
very difficult to treat.11
The probability of risk for infection for a given procedure is related to
local, systemic, and surgical factors. The patient's American Society of
Anesthesiologists (ASA) score may be used as the systemic baseline and
then can be correlated with various local and surgical factors. A risk index
may then be modified from the literature to correlate these factors to dental
implant surgeries. The probability of wound infection may then be correlated
with the type of wound contamination (class 1 to 4) and the risk index. A
class 2 wound and a risk index 2 has a greater risk of complications, and a
class 1 wound and risk index 0 has the least risk of postoperative infection
(Table 8.1).12
TABLE 8.1
Probability of Wound Infection by Type of Wound, Risk Index, and ASA
Status
RISK INDEX
Operation Classification 0 1 2
Clean 1.0% 2.3% 5.4%
Clean-c ontaminated 2.1% 4.0% 9.5%
ASA, American Society of Anesthesiologists, physical status classification; 0; ASA 1 or ASA 2: As the
number of local and surgical risk factors increase, the probability of wound infection increases significantly.
(From Misch CE: Contemporary implant dentistry, ed 3, St. Louis, 2008, Mosby; data from Cruse PJ Foord
R: A five year prospective study of 23,649 surgical wounds, Arch Surg 107:206–210, 1973.)
Diagnosis of an Infection
Etiology of the Infectious Process
In order to determine if an infection is present the clinician must evaluate
various factors, which include the host, environment, and the organism. In
health, there exists a balance between the three. In a diseased state, there is
an imbalance between the three, with the host usually being the most
important factor in determining the outcome of the infection. There exists an
adversarial relationship between infectious microbes and the host (Box 8.3).
Box 8.3
Microorganisms Most Commonly Associated
With Periimplant Complications
Staphylococcus spp
Actinomyces spp
Surface translocating bacteria
Wolinella spp
Capnocytophaga spp
Fusobacterium spp
Entamoeba gingivalis
Motile rods
Fusiforms
Spirochetes
Enteric gram-negative bacteria
Candida albicans
The pathologic potential of microbes depends on three factors4:
1. Virulence: the degree of pathogenicity of a microorganism, which includes

the pathogen's genetic, biochemical, and structural features.
2. Pathogenicity: the potential or capacity of a pathogen to cause disease.
3. Infectivity: the ability or level at which a pathogen may infect the host and
cause an infection.
In normal conditions the host factors will predominate, and a greater

number of host factors present will increase the ability to fight infection. If
the microbial load increases, an imbalance occurs until the microbial factors
predominate, which results in infection. During a dental implant procedure,
usually there is a breakdown in the local natural barrier, which may lead to
microbes obtaining an advantage over the host defenses. This will result in
the host mobilizing humoral and cellular factors.
Humoral immunity is mediated by macromolecules, which are found in
extracellular fluids such as antibodies, proteins, and antimicrobial peptides.
Humoral immunity substances are found mainly in bodily fluids. Antibodies
or immunoglobulins are glycoproteins that are found in the blood and tissue
fluids. An antibody identifies and neutralizes the bacteria by binding to the
antigens and causing agglutination, which allows for phagocytosis to break
down the bacteria.
Cellular immunity is the body's immune response that does not involve
antibodies, but utilizes phagocytes, T lymphocytes, and cytokines in
response to an antigen. Cellular immunity protects the body from infection
via three mechanisms:
1. activating T lymphocytes that are antigen specific to induce apoptosis

within the body's cells;
2. activate macrophages that destroy pathogens and debris;
3. stimulate cells to secrete a variety of cytokines that influence the functional

aspects of cells in adaptive immune responses.
In most hosts, these humoral and cellular defenses are sufficient to
prevent dissemination of the pathogens and allow for normal healing, free of
infections. However, in some instances, the presence of foreign bodies
(implants, bone grafts) and a breakdown in local defenses will result in an
infectious process.13,14
Host Response to Infection

When the infectious pathogens overcome the host defenses and result in an
infection, the host will trigger a series of reactions in response to the
infectious insult. The first initial reaction is the inflammatory reaction, which
consists of a release of mediators, vascular changes (vasodilation or
hyperemia and increased vascular permeability), and mobilization and
activation of leukocytes. This is the body's physiologic response to the
antigenic stimulation to rid itself of the infectious stimulus, which is
localized to the site of the infectious pathogen. Normally, the initial
inflammatory response to infection is rapid, usually within minutes of the
pathologic stimulus.
The inflammatory response is designed to eliminate the infectious
pathogens and allow for tissue healing. In a healthy individual, there are six
phases of the inflammatory response:
1. hyperemia, which is caused by vasodilation of the arterioles and capillaries,

and increased permeability of venules with the slowing of the venous blood
flow;
2. exudate that is rich in plasma proteins, antibodies, nutrients, and

leukocytes enters into the surrounding tissue;
3. leukotaxin, a permeability factor, is released, which is essential for the

migration of polymorphonuclear leukocytes toward the infected area;
4. fibrin synthesis from the exudate, which walls off the area of infection;
5. phagocytosis of the bacterial and dead cells;
6. macrophages dispose of the necrotic debris.
In addition to the inflammatory reaction they cause, pathogens may attack

the host by direct injury to the host cells, enhancement of the pathogen's
invasiveness, and neutralization of the host defenses. Systemic effects may
result such as fever, shock, hypersensitivity reactions, and autoimmune
responses and may be life threatening.4
Impaired Host Defenses

As stated previously, the host defenses are the most important aspect in the
resolution of the infection. With the inflammatory response a migration of
the white blood cells and the production of antibodies results, which may
resolve the infection allowing for normal tissue healing. However, if the host
defenses are impaired in any way, the host will not be able to overcome the
infectious process. Peterson has shown that depressed defenses are divided
into four categories: physiologic, disease-related, impaired immune system,
and drug suppression–related.4
Physiologic.
The patient has the inability to deliver white blood cells, antibodies, and
complements to act against the bacterial insult. This may be related to
increased age, obesity, lifestyle issues, and fluid imbalances. Also, stress and
many psychologic disorders have been associated with this immune
suppression.
Disease Related.
Several diseases may affect the defense system, such as malnutrition, cancers
(e.g., leukemia, lymphoma, multiple myeloma), uncontrolled diabetes,
pulmonary diseases, and human immunodeficiency virus (HIV).
Impaired Immune System.

The immune system may be suppressed in congenital defects (e.g.,
agammaglobulinemia) in combination with health issues such as multiple
myeloma and radiation therapy.
Drug Related.
There are numerous drug-related groups that may affect the defense
systems.
Cytoxic drug group.

These drugs (e.g., alkylatine, antimetabolite drugs) exert their cytotoxic effect
on the DNA or RNA, which results in protein synthesis and cell division. The
end result will be the impaired proliferation of fibroblasts and collagen
formation, which predisposes implant patients to poor wound healing and
increased infection rate.
Glucocorticosteroids.
The use of glucocorticoids (e.g., prednisone, dexamethasone) suppresses the
inflammatory response, which may result in wound healing complications
and possible infection. The exogenous corticosteroids decrease collagen
formation, vascularity, and fibroplasia. The fibroblasts are decreased by
approximately 30%, thus delaying epithelialization and wound contraction.15
Antibodies (e.g., mono- and polyclonal).

Mono- and polyclonal antibodies are lab-produced molecules that are
specifically engineered to attach to specific defects in cancer cells. They
mimic the antibodies your body naturally produces in response to bacterial
infections.
Drugs acting on immunophilins.

Cyclosporine, which is used in organ transplantation, depresses the T cells
while allowing the B cells to continue their antibacterial activity. Additional
drugs, which affect immunophilins, are interferons, opioids, and tumor
necrosis factor (TNF)–binding proteins.
Signs of Infection
To ascertain if an infection is present, it is crucial to evaluate the patient for
local signs that may include pain, swelling, erythema, presence of exudate,
and limitation in motion. Systemically, the patient may present with fever,
lymphadenopathy, malaise, and an elevated white count.
Vital Signs
The patient's vital signs should be obtained, including blood pressure, pulse
rate, respiratory rate, and temperature.
With infection, the following will be noted:
• Temperature: >101°F (38°C) (normal: 98.6°F [37 °C])
• Pulse Rate: >100 beats/min (normal: 60–100 beats/min)
• Blood Pressure: Systolic will be elevated if there is pain/anxiety
• Respirations: >18 breaths/min (normal: 14–16 breaths/min)
Objective Signs
There are five cardinal signs of inflammation:
1. Rubor: tissue redness, which is caused by arterial vasodilation.
2. Tumor: swelling, which is the accumulation of pus or fluid exudate.
3. Calor: heat, which is the result of inflow of warm blood from deeper
tissues, increased quantity of blood from the vasodilation, and increased rate
of metabolism.
4. Dolor: pain, which results from pressure on sensory nerve endings caused
by the distention of the tissue.
5. Functio laesa: loss of function, which is difficulty in chewing, swallowing,

and breathing.
A common acronym used to describe inflammation is PRISH: Pain,

Redness, Immobility (loss of function), Swelling, and Heat.
Mild vs. Severe Infection
Mild Infection.
Normal vital signs with slight elevation of temperature. Usually associated
with one of the following:
• Fatigue: extreme tiredness
• Malaise: a general feeling of discomfort, illness, or uneasiness
• Lethargy: lack of energy or enthusiasm
Severe Infection.
Elevated pulse, blood pressure, and respirations along with temperature and
any of the following.4
Trismus.
Limited or reduced opening of the jaws caused by spasm of the muscles of
mastication. This is usually painful and distressing to the patient, often
interfering with eating, speech, and oral hygiene and causing an altered facial
appearance. When the etiologic factor is infection, it is usually from a
masticatory space or lateral pharyngeal space complication. Untreated, this
may lead to spread of infection to various facial spaces that may lead to
cervical cellulitis and mediastinitis. Trismus is classified as per the
interincisal opening16:
• Normal (vertical): 35–45 mm
• Normal (lateral): 8–12 mm
• Mild: 20–30 mm
• Moderate: 10–20 mm
• Severe: <10 mm
Lymphadenopathy.
In general, palpable lymph nodes greater than 1 cm in diameter are
considered to be abnormal and should be subject to further evaluation.
Lymphadenopathy is referred to nodes that are abnormal in either size,
consistency, or number. The lymphadenopathy is classified as generalized if
lymph nodes are enlarged in two or more noncontiguous areas or localized if
only one area is involved.17 In acute infection the lymph nodes are enlarged,
soft, and tender, and the skin is red. With chronic infection the enlarged
nodes are less firm, not tender, and edema of the surrounding area exists.
Dysphagia.
Symptoms of dysphagia include difficulty in chewing, initiating swallowing,
difficulty in moving food or liquids from the mouth to the throat, and pain
during swallowing. Dysphagia requires immediate medical care.
Dyspnea.
Dyspnea is difficult or labored breathing, requiring immediate medical care.
Additional symptoms may include respiratory impairment, difficulty in
swallowing, impaired vision, severe headache, stiff neck, vomiting, and
decreased level of consciousness, which all would necessitate immediate
medical care.
Definitions of Terms Related to Postoperative Infection

The definitions of specific terms that describe infections of the head and
neck provide keys to the methodology of treatment and improved
communications (Box 8.4 and Table 8.2).
Box 8.4
Common Terms Related to Postoperative
Infection
Abscess: most commonly has distinct and well-defined borders, usually very
soft and doughy. Will be fluctuant to palpation because of fluid
involvement. The presence of pus will most likely indicate the body has
walled off the infection and the body's host defenses are controlling the
infection.
Cellulitis: is typically larger and more widespread than an abscess or edema.

Its borders are more diffuse; thus the clinician cannot determine borders.
Is usually indurated or hard to palpation and contains no pus. The severity
of the infection is proportional to the firmness.
Chronic skin fistula: is a sign of retained focus of infection and, in some

cases, a more serious condition of bone and bone marrow inflammation
called osteomyelitis. This is most likely observed in the mandible and is
associated with infection of both endosteal and subperiosteal implants in
patients who have poor dental hygiene awareness and lack of implant
maintenance.
Edema: is characteristic of the inoculation stage and is the easiest stage to

treat. Is more diffuse and jelly-like with minimal tenderness to palpation
Lymphadenitis: is a condition in which the regional lymph nodes become

inflamed, enlarged, and tender. The node may become suppurated, break
through the capsule, and involve the surrounding tissues.
Noma: starts as a gangrenous stomatitis and spreads to adjacent bone and

muscles, causing lysis and necrosis of tissue. This rare condition perforates
the cheek, floor of the mouth, or both, and is usually seen in debilitated
individuals.
Phlegmon: is any cellulitis that does not go on to suppuration. In this
condition the inflammatory infiltration of the subcutaneous tissue leads to
accumulation of foul-smelling brownish exudate. Hemolytic streptococci
are usually present.
Sepsis: is a whole body inflammatory reaction to infection. The signs and

symptoms include fever, increased heart rate, increased respiration, and
confusion. Sepsis is usually caused by an immune response triggered by a
bacterial infection and is treated with intravenous antibiotics and fluids. If
the patient does not respond to intravenous fluid treatment, the patient
may go into septic shock, which is characterized by severe hypotension.
These patients are usually treated in an intensive care unit in a hospital.
TABLE 8.2
Edema vs. Cellulitis vs. Abscess
Characteristic Edema (Inoculation) Cellulitis Abscess

Duration 0-3 days (ac ute) 1-5 days (ac ute) 4-10 days (c hronic )
P ain, borders Mild-moderate S evere, loc alized Moderate, loc alized
Size S mall Large S maller
Color Normal Reddened S hiny c enter, peripheral reddened
Consistency Jelly-like Doughy, indurated Fluc tuant
P rogression Inc reasing Inc reasing Dec reasing
Exudate None None Present
Bacteria Aerobic Mainly aerobic Anaerobic
Surface temperature S lightly heated Hot Moderately heated
Levels of malaise Mild S evere Moderately severe
Seriousness Minimal Greater Less
Stages of Infection
There are two main stages of clinical infection, a cellulitis stage and an
abscess stage.
Cellulitis Stage
The initial stage of clinical infection is the cellulitis stage, which exhibits
classic signs of inflammation: heat, pain, redness (erythema), and swelling
(edema) (Fig. 8.1). These are sometimes referred to in the Latin as calor, dolor,
rubor, and tumor, respectively. Heat (calor) is the result of the inflow of blood
and an increased local metabolic rate in attempts by the body to both fight
and localize the infection. Pain (dolor) results from the increasing pressure on
local sensory nerve endings caused by the release of endogenous
inflammatory mediators, such as histamine, and the resulting edema. Edema
(tumor) is this associated swelling as well as the influx of blood and fluid
exudate into the local area. Redness (rubor) is the result of vasodilation close
to the mucosa/skin surface as a combined result of the other signs. Once the
body begins to successfully wall off and fight the developing infection or the
use of medications, such as antibiotics, is initiated, the clinical stage of the
infection may progress to the abscess stage.
FIG 8.1 Cellulitis Stage of Infection: the initial stage of infection characterized by
edema (tumor) that is associated with swelling caused by an influx of blood and fluid
exudate (arrow).
Abscess Stage
The abscess stage is the last stage of an infection. An abscess is an enclosed
collection of liquefied tissue, or pus, that is the result of the body's defensive
reaction to foreign materials or organisms (Fig. 8.2). The abscess will form
once the cellulitis stage begins to consolidate through the body's immune
system response through the use of appropriate antibiotics. Once an abscess
is formed, the purulence that produced it will migrate by the path of least
resistance. This may be either through the mucosa or skin or through the
fascial pathways of the head and neck. An abscess that migrates through the
deeper layers of the head and neck, through the lingual mandibular plate to
the sublingual space for example, may block respiration (as in Ludwig's
angina) or enter the brain (as in cavernous sinus thrombosis or meningitis).
This may be life threatening and require immediate surgical and medical
attention. When an abscess spontaneously drains to an area outside the body,
an orocutaneous fistula for example, it will continue until the source of the
infection is treated.
FIG 8.2 Abscess Stage of Infection. The infection has resulted in the formation of
an orocutaneous fistula (arrow), in which purulence drains via the path of least
resistance.
Determination of infection stage.

One of the primary ways to distinguish among the various stages of infection
is to palpate the area in question. The following should be noted:
Temperature: evaluate warmth or heat, which is sign of infection
Consistency of the swelling:
Soft to firm (doughy): usually inoculation stage
Hard (indurated): cellulitis stage
Fluctuance fluid (pus): abscess stage
Routes of Infection
The principal routes for the spread of infection are through the following
four mechanisms:
1. Vascular System: The vascular system of the head and neck allows for the
spread of infection because pathogens may travel via the venous system,
which drains into other tissues or organs (Fig. 8.3).
FIG 8.3 Veins implicated in the spread of infection. 1, angular vein connecting to
ophthalmic vein and then to cavernous sinus; 2, facial vein to deep facial vein (3)
connecting to pterygoid plexus of veins; 4, emissary veins; 5, maxillary vein; 6,
pterygoid plexus of veins.
2. Thrombophlebitis: Infection may spread to the walls of the veins, which may
also thrombose and create a condition referred to as thrombophlebitis. A lack
of valves in the head and neck's venous system allows retrograde flow of
blood and may involve the cavernous sinus, pterygoid, and pharyngeal
plexuses with infected thrombi.
3. Lymph Vessels: The lymph vessels are very prevalent in the head and neck
(Fig. 8.4). They commonly drain the infected site and carry the infection to
regional lymph nodes. The nodes become tender, enlarged, soft, and mobile
on palpation. This is termed lymphadenitis.
FIG 8.4 Lymph Nodes: Parotid - 6, Submental - 12, Submandibular - 11, Posterior
Auricular - 3, Occipital - 1, Deep Cervical - 2, 18.
4. Fascial Spaces: Once the infection is outside the bone, the loose areolar
connective tissue produces a path of least resistance into the various surgical
spaces of the head and neck, including the thoracic mediastinum (Fig. 8.5).
The muscle attachments to the maxilla, mandible, and fascial compartments
limit or direct the path of infection. Infections that may occur after surgeries
involving reflection of muscle attachments may permit the infection to
spread more easily into these surgical spaces. It is prudent to
prophylactically cover patients with antibiotics when larger regions of soft
tissues are reflected beyond the facial vestibule or mucobuccal fold, which
violate the muscle attachments and invade the subcutaneous tissues.
FIG 8.5 (A) Fascial space anatomy of the face including the Temporal,
Pterygomandibular, Masseteric, Parotid, Canine, and Buccal spaces. (B) Fascial
spaces of the neck. (From Kademani D, Tiwana P: Atlas of oral and maxillofacial surgery, St.
Louis, 2016, Saunders.)
Lymphatic Spread of Infection

The lymphatic system is a part of the greater lymphoid system and is a part
of the body's immune system. It is an accumulation of small vessels
connected by lymph nodes that function as a fluid return system for the
body. A filtrate of the blood plasma flows out of the capillaries into the
surrounding tissues, where it becomes extracellular fluid and is eventually
gathered by the lymphatic vessels. Through a continuous circulation process,
the lymph nodes filter the extracellular fluids, while lymphocytes, produced
within the lymph nodes, fight infectious organisms that are acquired
throughout the system.
The head and neck region has a vast network of lymphatic drainage that
aids in the fight of foreign microorganisms. There are approximately 600
lymph nodes in the body, but only the submandibular, axillary, or inguinal
regions are palpable in the healthy patient. In the head and neck area the
retropharyngeal, submental, submandibular and cervical lymph nodes are
the most important to be evaluated in the diagnosis of infections. The
retropharyngeal nodes are located behind the pharyngeal wall and drain to
the upper deep cervical lymph nodes. The submental nodes are located
under the chin, are small in number, and drain the anterior mandible and
associated structures (mandibular incisors, the tip of the tongue, and the
midline of the lower lip and chin), which then drain into the submandibular
nodes or directly to the cervical nodes. The submandibular nodes are located
around the submandibular gland, the areas of the maxillary teeth, maxillary
sinus (except the maxillary third molars area), the mandibular canines, all
mandibular posterior teeth, floor of the mouth, most of the tongue, the
cheeks, the hard palate, and the anterior nasal cavity all drain to these nodes.
As the submandibular lymph nodes drain a large and extensive area, they are
usually the first to be noticed in the occurrence of oral infections. The
cervical lymph nodes are divided into upper and lower divisions and are
located deep in the neck. The upper deep cervical nodes are located on the
lateral surface of the internal jugular vein and lie just beneath the anterior
border of the sternomastoid muscle. They receive drainage from the
submandibular and retropharyngeal nodes. The lower deep cervical nodes
are also found on the lateral surface of the internal jugular vein and beneath
the anterior border of the sternomastoid muscle (but lower, approximately 2
inches above the clavicle) and drain the upper deep cervical nodes and many
of the nodes at the back of the neck. Both the upper and lower cervical lymph
nodes are impractical to palpate.
Lymph Node Examination.

Ideally, in a lymph node examination, always examine both sides of the head
simultaneously with the pads of the fingertips (most sensitive part of the
hands) (Fig. 8.6). Use steady, gentle pressure to determine enlargement,
inflammation, or pain with respect to the contralateral side. Evaluate for:
• Mobility (mobile vs. fixed)
• Consistency (soft vs. firm)
• Tenderness (tender vs. nontender)
• Shape (regular vs. irregular)
FIG 8.6 Palpating the deep cervical lymph nodes by having the patient's head
turned. (From Fehrenbach MJ, Herring SW: Illustrated anatomy of the head and neck, ed 5, St.
Louis, 2017, Elsevier.)
Fascial Spaces of the Face (see Fig. 8.5)

The fascial spaces of the face are subdivided into five spaces: the canine
space, the buccal space, the masticatory space (further divided into the
masseteric, pterygomandibular, and temporal spaces).
Canine Space.
The canine space is located between the levator anguli oris and the levator
labii superioris muscles. Infection spreads to this space through the root
apices of the maxillary teeth, usually the canine. Direct surgical access is
achieved via incision through the maxillary vestibular mucosa above the
mucogingival junction.
Buccal Space.
The buccal space is bounded anterior to the masticator space and lateral to
the buccinator muscle with no true superior or inferior boundary and
consists of adipose tissue (the buccal fat pad that fills the greater part of the
space), the Stensen duct, the facial artery and vein, lymphatic vessels, minor
salivary glands, and branches of cranial nerves VII and IX. When infection is
involved in the buccal space, the space can serve as a conduit for spreading
disease between the mouth and the parotid gland. Surgical access to the
buccal space infections may be easily accomplished through the intraoral
approach. More complicated infections, directed by location within the
buccal space, may require a preauricular and/or submandibular approach.
Masticatory Spaces
Masseteric space (and submasseteric space).
The fascia that forms the borders of the masticator space is a well-defined
fibrous tissue that surrounds the muscles of mastication and contains the
internal maxillary artery and the inferior alveolar nerve. It is bounded
anteriorly by the mandible, posteriorly by the parotid, medially by the lateral
pharyngeal space, and superiorly by the temporal space. Infections in this
space may be misdiagnosed as a parotid abscess or parotitis.18
The most pronounced clinical feature of infection in this space is trismus.
Computed tomography (CT) scan or magnetic resonance imaging (MRI) may
be an invaluable resource to distinguish abscess from cellulitis and the
surgical course required for treatment.19
Intraoral surgical access to this space for simple, isolated abscesses is
generally adequate to allow for drainage but with extension into adjacent
spaces, an external approach may be required.
Pterygoidmandibular space.
The pterygoidmandibular space is bounded by the mandible laterally and by
the medial pterygoid muscle medially and inferiorly. The posterior border is
formed by parotid glandular tissue, which curves medially around the
posterior mandibular ramus and anteriorly by the pterygomandibular raphe,
the fibrous junction of the buccinator and superior constrictor muscles.
Surgical access to this space may be achieved intraoral in the case of simple
infections, but may require extraoral access when multiple adjacent spaces
are involved.20
Temporal space.
The temporal fascia surrounds the temporalis muscle in a strong fibrous
sheet that is divided into clearly distinguishable superficial and deep layers
that originate from the same region with the muscle fibers of the two layers
intermingled in the superior part of the muscle. Infections of odontogenic or
implant treatment origin are rare in this space but may occur. If an abscess
does develop in this space, intraoral incision and drainage is difficult and
usually requires an extra oral approach. Communicating facial-
zygomaticotemporal nerve branches piercing through the fascial and
muscular planes of the temporal fascia in the superior part of the muscle are
important landmarks to prevent temporal hollowing that may occur due to
surgical access procedures.21
Sublingual Space.
The sublingual space is bounded between the mylohyoid muscle and the
geniohyoid and genioglossus muscles. This space contains the lingual artery
and nerve, the hypoglossal nerve, the glossopharyngeal nerve, Wharton's
duct, and the sublingual salivary gland, which drains into the oral cavity
through several small excretory ducts in the floor of the mouth and a major
duct known as Bartholin's duct. Infectious spread to this space is through
perforation of the lingual mandibular cortical plate (Fig. 8.7). Incision and
drainage of abscesses in this area are generally adequately treated through a
simple intraoral approach.
FIG 8.7 Sublingual abscess spreading into right and left sublingual surgical spaces
and into the tongue. (From Hupp JR, Tucker MR, Ellis E: Contemporary oral and maxillofacial
surgery, ed 5, St. Louis, 2009, Mosby.)
Submental Space.
The submental space is bounded anteriorly by the symphysis of the
mandible, laterally by the anterior bellies of digastric muscles, superiorly by
the mylohyoid muscle, and inferiorly by the superficial fascia of the platysma
muscle. There are no vital structures that traverse the submental space. This
space is usually involved in odontogenic infections from the anterior
mandibular teeth as benign or malignant lesions in this area are rare.
Surgical access for drainage of infection is generally through an extraoral
incision below the chin (Fig. 8.8).
FIG 8.8 Failing mandibular anterior implant. (A) Submandibular abscess formation
depicted as a submandibular swelling. (B) Incision and drainage. (C) Penrose drain
placed.
Submandibular Space.
The submandibular space extends from the hyoid bone to the mucosa of the
floor of the mouth, and is bound anteriorly and laterally by the mandible and
inferiorly by the superficial layer of the deep cervical fascia. The mylohyoid
muscle separates it superiorly from the sublingual space, which
communicates with it freely around the posterior border of the mylohyoid.
The mylohyoid muscle also plays a key role in determining the direction of
spread of oral infections. As it attaches to the mandible at an angle,
infections that perforate the mandible on the lingual side above the
mylohyoid line will involve the sublingual space below.
Surgical access for abscess drainage may be either intraoral or extraoral,
but is generally more suited for the extraoral approach. When infection has
spread to the bilateral submandibular spaces, it represents one of the
components (along with submental and bilateral sublingual space
involvement) of Ludwig's angina (Fig. 8.9). Surgical drainage in these
situations is almost always through multiple extraoral incisions.
FIG 8.9 Ludwig's angina. (A) Schematic diagram of the three facial spaces of
involvement. (B) Fascial space infection with bilateral involvement of the
submandibular, sublingual and submental spaces. (A, From Fehrenbach MJ, Herring SW:
Illustrated anatomy of the head and neck, ed 5, St. Louis, 2017, Elsevier. B, Auerbach FP:
Wilderness Medicine, ed 6, Philadelphia, 2012, Mosby.)
Lateral Pharyngeal Space.
The lateral pharyngeal space is an inverted cone with its base at the base of
skull and apex at the hyoid bone and is bounded posteriorly by the
prevertebral fascia, anteriorly by the raphe of the buccinator and superior
constrictors muscles, and laterally by the mandible and parotid fascia.
Infections present with pain, fever, neck swelling below the angle of the
mandible and trismus (Fig. 8.10). Rotation of the neck away from the side of
swelling causes severe pain from tension on the ipsilateral
sternocleidomastoid muscle.
FIG 8.10 The patient had trismus and pain on swallowing following the
development of submandibular abscess. The infection spread to the
pterygomandibular, parapharyngeal spaces. The patient needs to be hospitalized for
multiple incisions and drainage. (From Hupp JR, Tucker MR, Ellis E: Contemporary oral and
maxillofacial surgery, ed 5, St. Louis, 2009, Mosby.)
Spread of oral infection to this space may produce an ominous sign.

Airway impingement due to medial bulging of the pharyngeal wall and
supraglottic edema may occasionally occur, which may require the
procurement of a stable airway by either tracheotomy or intubation. The
treatment of lateral pharyngeal space infections requires surgical drainage
through either a transoral or extraoral approach.22 While an intraoral
approach may reach the anterior compartment, extraoral access through a
submandibular approach will allow for adequate access.
Significant Complications of Infections
Head And Neck
Osteomyelitis
Osteomyelitis is an inflammatory condition of the bone that originates as an
infection of the medullary space and eventually extends into the cortical bone
and periosteum. The bone infection becomes active in the calcified portion of
the bone and will produce pus in the medullary cavity and beneath the
periosteum, which compromises the blood supply. This initiates ischemia of
the bone, which results in necrosis. Osteomyelitis of the jaws has two main
classifications, acute and chronic, based on the duration of the disease.
Chronic osteomyelitis has classically been defined as a condition that has
lasted over 1 month.23 While there are many subclassifications, acute and
chronic osteomyelitis are generally subclassified as suppurative or
nonsuppurative and usually is different in the etiology, microbiology,
pathogenesis, and treatment in comparison to long bone osteomyelitis.24
Osteomyelitis has been associated with dental implants, usually starting as
a periimplant radiolucency with eventual osteolytic changes. Case reports
have also shown that implants placed in association with retained tooth roots
have caused osteomyelitis infections.25Left untreated, osteomyelitis may
become refractory with bacteria induced peri-implantitis that may lead to
deep bone invasion of bacteria, and the spread of infection into deeper
tissues. 26
Accurate diagnosis of mandibular osteomyelitis is based on clinical,
radiographic, histologic, and microbiologic findings followed by surgical
debridement of the infected area and a long-term antibiotic regimen (Figs.
8.11 to 8.13). Radiographic changes show a poorly defined, radiolucent bone
loss with intermixed radiopaque areas, which show the classic signs of
sequestrum. Conventional radiography of mandibular osteomyelitis has a
higher specificity than its sensitivity, which makes early detection difficult.
Radiographic signs of mandibular osteomyelitis are generally not apparent
until they extend at least 1 cm in bone and compromise 30% to 50% of bone
mineral content and may not be radiographically apparent in adults for up to
two weeks.27 Typical early bony changes seen on conventional radiography
may include: periosteal thickening, lytic lesions, endosteal scalloping, loss of
trabecular architecture, and new bone apposition.28 This gives the classic
“moth-eaten” appearance that is diagnostic for osteomyelitis.
FIG 8.11 Osteomyelitis. (A) Panoramic radiograph depicting delayed healing post-
implant removal. (B) Intraoral photo showing nonhealing, postimplant removal. (C)
Surgical resection. (D) Postoperative bone graft.
FIG 8.12 Osteomyelitis. (A–B) Radiographic images of bone destruction. (C)
Multiple sinus tracts from osteomyelitis of the mandible from a subperiosteal
implant.
FIG 8.13 Post-Implant Osteomyelitis: (A) CBCT panoramic view depicting post-
implant removal in the anterior mandible, (B) Axial image, depicting postimplant
failure and associated osteomyelitis. (C–D) Defect from infection. (E–F) Surgical
reconstruction. (G) Postoperative radiograph showing bone graft. (Courtesy David
Datillo, DDS, Chairman OMFS, Allegheny General Hospital, Pittsburgh, PA.)
Given the difficulty of detecting early stage osteomyelitis with

conventional radiography, CT scanning and MRI are considered standard of
care in the diagnosis of osteomyelitis because they are sensitive and specific.
CT provides excellent delineation of even the most subtle osseous changes
such as abnormal thickening of the affected cortical bone with sclerotic
changes, encroachment of the medullary cavity, and chronic draining fistulas.
Although CT may show these changes earlier than do conventional
radiographs, CT is less desirable than MRI because of decreased soft tissue
contrast as well as exposure to ionizing radiation. A T1-weighted short
inversion time recovery (STIR) MRI has been shown to be able to detect bony
changes indicating osteomyelitis as early as the subacute phase.29
Histologically, suppurative osteomyelitis is characterized by intense
microorganism-provoked marrow inflammation and marrow vessel
thrombosis with retention of viable osteoclasts and periosteum, which
creates an environment conducive to continual bacterial proliferation.30 In
the past, Staphylococcus aureus was thought to be the main causative organism
of osteomyelitis. However, given the unique environment of the oral cavity,
there tends to be a mixed infection with hemolytic streptococci and a
predominance of oral anaerobes (e.g., Peptostreptococcus, Fusobacterium, and
Bacteroides). Additionally, various other organisms, such as Actinomyces spp
and Treponema pallidum, cause other types of osteomyelitis.31
Treatment of osteomyelitis usually involves removal of the suspected
source, antibiotic therapy, medical treatment, and surgical intervention.
Topazian has established the principles of treatment for osteomyelitis to
include: (1) evaluation and correction of host defense deficiencies; (2) Gram
staining, culture, and sensitivity; (3) radiographic imaging; (4) administration
of stain-guided empirical antibiotics; (5) removal of mobile teeth/implants
and sequestra; (6) administration of stain-guided antibiotics; (7) possible
placement of irrigating drains; (8) and sequestrectomy, debridement,
decortication, resection, and reconstruction.1 The complete resolution of the
infection should be the main focus of management in patients with chronic
osteomyelitis of the mandible, and aggressive surgical management is more
likely to result in an ideal outcome.
Medication-Related Osteonecrosis of the Jaws (MRONJ)

In 2003 simultaneous and independent reports were published by Marx32 and
Ruggiero33describing nonhealing exposed bone cases in the oral-facial region
in patients treated with oral and intravenous bisphosphonate drugs. Shortly
thereafter the manufacturers of intravenous bisphosphonates pamidronate
(Aredia) and zoledronic acid (Zometa) notified health care professionals
concerning the risk of developing osteonecrosis of the jaws in patients using
these medications.34
Most recently, the American Association of Oral and Maxillofacial
Surgeons (AAOMS) recommended changing the terminology of this
condition. Previously termed bisphosphonate-related osteonecrosis of the jaw
(BRONJ), the condition is now referred to as medication-related osteonecrosis of
the jaws (MRONJ). This was related to the fact there is a growing number of
osteonecrosis cases involving the maxilla and mandible associated with other
intravenous antiresorptive, antiangiogenic, and monoclonal antibody
medications, such as Denosumab (Prolia, Xgeva), which is a fully human
monoclonal antibody used for the treatment of osteoporosis, treatment-
induced bone loss, bone metastases, and giant cell tumor of bone.
AAOMS has recently initiated guidelines on the signs and symptoms of
MRONJ in comparison with other nonhealing issues.35 Treatment guidelines
have also been established which relate to various stages of the condition
(Table 8.3). (The preoperative management of patients on bisphosphonates
and antiresorptive medications is discussed in Chapter 2). Current or
previous treatment with antiresorptive or antiangiogenic agents:
• Exposed bone or bone that can be probed through an intraoral or extraoral
fistula(e) in the maxillofacial region that has persisted for more than 8
weeks; and
• No history of radiation therapy to the jaws or obvious metastatic disease to
the jaws.
TABLE 8.3
Staging and Treatment Strategies for MRONJ
MRONJ Staginga Treatment Strategiesb

At risk c ategory: No apparent nec rotic bone in patients who have been treated with either oral or IV • No treatment
bisphosphonates indic ated
• Patient educ ation
S tage 0: No c linic al evidenc e of nec rotic bone, but nonspec ific c linic al findings, radiographic c hanges, and • S ystemic
symptoms management,
inc luding the use of
pain medic ation and
antibiotic s
S tage 1: Exposed and nec rotic bone, or fistulae that probes to bone, in patients who are asymptomatic and have no • Antibac terial mouth
evidenc e of infec tion rinse
• Clinic al follow-up on
a quarterly basis
• Patient educ ation and
review of indic ations
for c ontinued
bisphosphonate
therapy
S tage 2: Exposed and nec rotic bone, or fistulae that probes to bone, assoc iated with infec tion as evidenc ed by • S ymptomatic
pain and erythema in the region of the exposed bone with or without purulent drainage treatment with oral
antibiotic s
• Oral antibac terial
mouth rinse
• Pain c ontrol
• Debridement to
relieve soft tissue
irritation and infec tion
c ontrol
S tage 3: Exposed and nec rotic bone or a fistula that probes to bone in patients with pain, infec tion, and one or • Antibac terial mouth
more of the following—exposed and nec rotic bone extending beyond the region of the alveolar bone (i.e., rinse
inferior bone and ramus in the mandible, maxillary sinus and zygoma in the maxilla) resulting in pathologic • Antibiotic therapy and
frac ture, extraoral fistula, oral antral/oral nasal c ommunic ation, or osteolysis extending to the inferior border of the pain c ontrol
mandible of sinus floor • S urgic al
debridement/resec tion
for longer term
palliation of infec tion
and pain
a
Exposed or probably bone in the maxillofacial region without resolution for more than 8 weeks in patients
treated with an antiresorptive and/or an antiangiogenic agent who have not received radiation therapy to the
jaws.
b
Regardless of the disease stage, mobile segments of bone sequestrum should be removed without
exposing uninvolved bone. The extraction of symptomatic teeth within exposed, necrotic bone should be
considered because it is unlikely that the extraction will exacerbate the established necrotic process.
(From Ruggiero SL, Dodson TB, Fantasia J, et al: American Association of Oral and Maxillofacial Surgeons
position paper on medication-related osteonecrosis of the jaw—2014 update, J Oral Maxillofac Surg
72(10):1938–1956, 2014.)
Although the true pathophysiology of MRONJ is not yet fully understood,

decreased bone turnover (altered bone remodeling or over suppression of
bone resorption) and infection are thought to be central to the pathogenesis
of MRONJ.36
Histologically, MRONJ is characterized by marrow spaces with empty
Howship lacunae and an absence of osteoclasts and viable periosteum. This
suggests a noninflammatory drug toxicity to bone by osteoclastic death
leading to oversuppression of bone renewal. Many additional hypotheses
have been proposed such as angiogenesis inhibition, constant microtrauma,
suppression of innate or acquired immunity, vitamin D deficiency, soft tissue
toxicity to bisphosphonates, and inflammation (Fig. 8.14).37-40
FIG 8.14 Medication related osteonecrosis of the jaws (MRONJ). (A) Implant
related MRONJ. (B) Multiple areas of nonhealing exposed bone. (B, From Marx RE: Bone
and bone graft healing. Oral Maxillofac Surg Clin North Am 19(4):455–466, 2007.)
Bisphosphonates prevent the renewal of old and injured bone because they
make it brittle and prone to fracture, have a half-life in bone of 11 years due
to irreversible binding to bone, and (when administered intravenously)
accumulate in bone 142.8 times faster than oral bisphosphates.41
Additionally, osteoclastic resorption of bisphosphonate-loaded bone results
in osteoclast death in which the cell bursts and releases retained
bisphosphonate molecules inside the cell that redistribute in the local bone
or bone marrow in a redosing effect.
Recently, the presence of biofilm has emerged to explain the etiology of
many chronic infections, and this may be a contributing factor in the
development and proliferation of MRONJ. Biofilm is an aggregation of
bacterial colonies and other microorganisms such as yeast, fungi, and
protozoa that have established a microenvironment from the secretion a
mucilaginous protective coating in which they are encased that may be
extremely difficult to treat with medications alone.
Sedghizadeh et al looked at biofilm composition on specimens from
individuals who had sequestrectomy of bone for MRONJ.42 They found that
bone specimens from affected sites in all patients revealed large areas
occluded with biofilms comprising mainly bacteria and occasionally yeast
(Candida spp). The specimens included a large number of bacterial
morphotypes and included species from the genus Fusobacterium, Bacillus,
Actinomyces, Staphylococcus, and Streptococcus. Bacterial colonization of the
denuded bone in MRONJ has suggested that bisphosphonates may increase
bacterial adhesion and biofilm formation. Kos et al discovered an up to a
seven-fold increase in bacterial colonization on pamidronate-coated
hydroxyapatite disc compared to controls.43 They postulated that the nitrogen
group on pamidronate may act as a steric factor that facilitates anchoring of
bacteria to the hydroxyapatite surface or may attract bacteria by direct
electrostatic interaction. These studies lay credence to the high probability
that increased bacterial adhesion in the presence of bisphosphonates may
promote MRONJ and osteomyelitis development.
Individuals taking oral bisphosphonate therapy for short durations of
time, less than 3 years, do not appear to have significantly higher rates of
implant failure or infection.44 However, for patients taking long-term oral
bisphosphonate therapy (exceeding 3 years) with concomitant prednisone
treatment, there may be a significant increase in the incidence of both
implant failure and infection. This phenomenon may be location specific
because implants placed in the posterior mandible or maxilla in patients with
a history of long-term oral bisphosphonate have a greatly increased risk of
MRONJ development.45 Individuals who have received at least three or more
doses of any intravenous antiresorptive medication (e.g., Reclast) may be
considered an absolute contraindication to dental implant therapy with an
almost guaranteed development of MRONJ.46
Cavernous Sinus Thrombosis

Cavernous sinus thrombosis is a very rare but extremely dangerous major
complication of head and neck infections. Although the advent of antibiotics
has decreased the incidence of the condition, a clinician should be able to
recognize its signs and immediately refer the patient to the proper
specialists.
The cavernous sinuses are trabeculated sinuses located at the base of the
skull that drain venous blood from valveless facial veins. Infections may be
delivered to this location from sources of infection in the vicinity of this vein,
most likely those located in the midface. Initial symptoms are progressively
severe headache or facial pain, usually unilateral and localized to retroorbital
and frontal regions with high fever. Eventually, paralysis of the ocular
movements in the eye on lateral gaze is a classic sign of this condition. This is
termed ophthalmoplegia because it is due to compression of the sixth cranial
nerve (lateral ocular gaze) from the pressure of purulence in the confined
space of the sinus. Proptosis (anterior bulging of the eye) and eyelid edema
also develop and may occur bilaterally. As the condition progresses, facial
sensation may diminish confusion, and seizures, and a decreased level of
consciousness may develop. Treatment involves removal of the infection
source as well as administration for weeks of intravenous antibiotics and
fluids because surgery is considered difficult and problematic (Fig. 8.15).
FIG 8.15 Cavernous sinus thrombosis. (A) Seventy-two hours post dental
treatment, patient presented with severe headache, high fever (104°F), chills,
parasthesia of upper and lower eyelids, inability to move her right eye around and
little hemorrhagic spots (petechea) on edematous skin of nose and eyelids. She was
diagnosed with having cavernous sinus thrombosis. (B) Chemosis, proptosis, and
ophthalmoplegia from cavernous sinus thrombosis infection. (B, From Del Brutto OH:
Infections and stroke. Semin Cereb rovasc Dis Stroke 5(1):28–39, 2005.)
Brain Abscess
Transmission of oral infection and the development of brain abscess are a
rare but extremely dangerous and life-threatening situation. Oral
microorganisms may enter the cranium by several pathways including by
direct extension, by hematogenous spread, by local lymphatics, and,
indirectly, by extraoral odontogenic infections.47 Similar to the treatment of
cavernous sinus thrombosis, several weeks of intravenous antibiotics and
fluids are recommended (Fig. 8.16).
FIG 8.16 Brain abscess. (A) CT axial image depicting abscess (arrow). (B) Dry
specimen. (A, From Laban JT, O’Neill K: CNS infection. Surgery (Oxford) 25(12):517–521, 2007. B,
From Damjanov I: Pathology for the health professions, ed 4, St. Louis, 2012, Saunders.)
Neoplasms
Although rare, the development of neoplasms in association with dental
implants has been reported (Figs. 8.17 and 8.18). To date, squamous cell
carcinoma is the most common cancer that has been reported to involve
dental implants.48,49 Other reports have reported dental implant failure
related to the development of a plasmacytoma50 and in association with
breast and lung metastasis.51,52
FIG 8.17 (A) CT scan showing a mixed radiopaque/radiolucent lesion of the right
maxilla associated with the dental implant. The tumor has infiltrated the periodontal
ligament space of the second premolar. (B) CT scan showing the osteosarcoma
eroding the buccal cortex of the maxilla with extension into adjacent soft tissue
(arrow). (From McGuff HS, Heim-Hall J, Holsinger FC, et al: Maxillary osteosarcoma associated
with a dental implant: report of a case and review of the literature regarding implant-related
sarcomas. JADA 139(8):1052–1059, 2008.)
FIG 8.18 (A) Squamous cell carcinoma located on the alveolar ridge and floor of
mouth. (B) Panoramic radiograph showing erosion of lesion into bone (arrows). (C)
Intraoperative photograph after mandible and surrounding soft tissues were
resected, and a free fibular bone flap and reconstruction bone plate have been used
to reconstruct the mandible. Note the venous anastomosis (white arrow). The arterial
supply to the flap is also shown (black arrow), but the actual anastomosis is located
more proximally, under the tissue, and is not visible. (D) After the bone graft has
healed, dental implants are inserted. (E) Panoramic radiograph showing the
reconstructed mandible after implants have been inserted. (F) Intraoral view of
prosthetic reconstruction of dental implants. The white tissue surrounding the
implants is skin that was transferred with the bone flap. (Courtesy Dr. Remy Blanchaert, Jr.
In Hupp JR, Tucker MR, Ellis E: Contemporary oral and maxillofacial surgery, ed 6, St. Louis, 2014,
Mosby.)
In most cases, the clinical signs and symptoms are consistent with peri-
implantitis, which leads to a delay in diagnosis. The pathophysiology of the
carcinogenesis has not been determined, but implant biomaterials,
persistent inflammation, and chronic osteomyelitis have been theorized as
contributing factors.53
The implant biomaterial, along with tumor induction, has been shown to
be related to the development of sarcoma in association with dental
implants. This is thought to be mediated by the toxic and mutagenic
properties of titanium alloy.54 Although more commonly associated with
orthopedic appliances, it has been shown that metallic corrosion occurs with
dissolution into periimplant tissues. Titanium levels have been shown to
reach up to 300 parts per million in tissues around implants, which produces
discoloration.55
Although there are many case reports of neoplasms and dental implants,
this is a relatively rare occurrence. It is difficult to determine a direct cause-
and-effect relationship with the use of titanium and cancer. The most likely
scenario is when an implant exhibits chronic inflammation and peri-
implantitis does not respond to any treatment.
Treatment of Infections
The management of infections can be associated with a high degree of
morbidity and should be related to the comfort level and the training of the
implant clinician. If the implant clinician is unfamiliar or early on their
learning curve with treatment of infections, the patient should be referred to
a specialist.
Normally, the first goal of treatment is to treat or remove the cause of the
infection. This could be an implant, bone graft, or tooth. The secondary goal
is to allow drainage of accumulated pus and bacteria.
Incision and Drainage

This procedure includes the incision of the abscess or cellulitis, which results
in the removal of the accumulated pus and bacteria from the underlying
tissue. The opening of the abscess cavity will decrease the load of bacteria,
reduce the hydrostatic pressure in the region by decompressing tissues, and
allow for the introduction of a local blood supply that increases the delivery
of host defenses and antibiotics to the infected area.
Incision and drainage of a cellulitis serves to prevent the spread of the
infection into deeper anatomic spaces. This usually includes the insertion of
a drain to prevent the closure of the incision line, which prevents the
infection from reforming.
Procedure
An incision with a #15 scalpel blade is made through the mucosa into the
infected cavity. The incision is usually less than 1 cm in length but should be
sufficiently long to allow for adequate access into a gravity-dependent area of
the abscess to allow for drainage. A closed curved hemostat is inserted into
the incision and opened in several directions. The hemostat should be
removed in the open position and never in the closed position to avoid
inadvertent clamping of possible vital structures in the area. This is
completed to break open any small loculations or cavities of purulence. The
area should then be copiously irrigated with sterile saline solution until the
fluid runs clear, an indication that all gross evidence of infection has been
removed. After all visible purulence has been removed, a small drain may be
placed into the opening. The most common drain is a quarter-inch Penrose
drain, which is a soft rubber tube placed in a wound area to prevent the fluid
or purulence accumulation (see Fig. 8.8). Incision and drainage of surgical
spaces such as the sublingual, submandibular, pterygomandibular, and
parapharyngeal spaces that require an extraoral approach and careful
dissection are commonly done under general anesthesia in a hospital setting
with the appropriate preoperative, operative, and postoperative care by a
surgical specialist.
Culture and Sensitivity

In some cases a culture and sensitivity (C&S) test is administered before the
drainage of an abscess. This should ideally be completed at the beginning of
the procedure (Box 8.5).
Box 8.5
Indications for Culture and Antibiotic
Sensitivity Testing
• Infection spreading beyond the alveolar process into fascial spaces
• Symptomatic, rapidly progressive infection
• Nonresponsive infection (after more than 48 hours) with the use of

antibiotics
• Multiple doses of antibiotic therapy
• Chronic, recurrent infection
• Patients who have compromised immune system and comorbidities
(From Hupp JR, Tucker MR, Ellis E: Contemporary oral and maxillofacial surgery, ed 6, St. Louis, 2014,
Mosby.)
Procedure
After adequate anesthesia, the surgical area is disinfected and dried with
sterile gauze. With the use of an 18-gauge needle or the cotton applicator, a
specimen is collected. The needle or cotton-tipped applicator is inserted into
the abscess or cellulitis, and 1–2 mL of pus or tissue fluid is aspirated. The
specimen should include pus, blood, tissue fluid, or necrotic tissue. The
specimen is placed (inoculated) directly into aerobic and anaerobic
culturettes, which are sterile tubes containing a swab and bacterial transport
medium (Fig. 8.19). Culturettes usually have a short shelf life, so the
expiration date should be checked before use. The clinician should request in
writing a Gram stain, aerobic and anaerobic cultures, and antibiotic
sensitivity testing.
FIG 8.19 Culture and sensitivity test. (A) Method to determine which antibiotics are
effective against the specific bacteria. Various antibiotic agents are impregnated and
inoculated with the microorganism. Note the areas of no colonization around the
antibiotic spheres. (B) Anaerobic specimen collector, (C) Remove Handle and cotton
applicators, (D) Inoculate the area of infection, (E) Place cotton tip specimen
collector into agar, (F) Sample sent to lab for culture and sensitivity tests. Culturette
used for C&S test. (A, From Goering R, Dockrell H, Wakelin D et al: Mim's medical microb iology,
ed 4, St Louis, 2008, Mosby. B, Courtesy GettyImages.com.)
After the C&S is completed, an incision with a #15 scalpel blade is made
through the mucosa into the infected cavity. The incision is usually less than
1 cm in length. A closed curved hemostat is inserted into the incision and
opened in several directions. This is completed to break open any small
lobulations or cavities of pus. After all pus has been removed, a small drain
may be placed into the opening. The most common drain is a Penrose drain.
Incision and drainage of surgical spaces such as the buccal, sublingual,
submandibular, pterygomandibular, and parapharyngeal spaces require skin
incision and careful dissection commonly done under general anesthesia in a
hospital setting with the appropriate preoperative, operative, and
postoperative care by a specialist (Fig. 8.20).
FIG 8.20 A, Vestibular mandibular implant infection extending through buccal plate
and creates sizable vestibular abscess. B, Abscess is incised with #11 blade. C,
Beaks of hemostat are inserted through incision and opened so that beaks spread to
break up any loculations of pus that may exist in abscessed tissue. D, A small drain
is inserted to depths of abscess cavity with a hemostat. E, The drain is sutured into
place with a single black silk suture. Note that pus usually flows out along, rather
than through, a tubular drain. (Adapted from Hupp JR, Tucker MR, Ellis E: Contemporary oral
and maxillofacial surgery, ed 6, St. Louis, 2014, Mosby.)
Antibiotics Used in Implant Dentistry (Table
8.4)
Beta-Lactam Antibiotics
The most common beta-lactam antibiotics used in dentistry are the
penicillins and cephalosporins. These antibiotics have similar chemical
structures, and the mechanism of action is the inhibition of bacterial cell wall
synthesis (bactericidal) via the interruption of the cross linking between
peptidoglycan molecules.
TABLE 8.4
Commonly Used Antibiotics in Oral Implantology
THERAPEUTIC
Maximum Adult
Generic Name Brand Name Bactericidal/Bacteriostatic Usual Adult Dose P rophylactic Doses
Dose
Amoxic illin Amoxil Bac teric idal 250–500 mg TID 4 g/day S BE: 2 g 1 hr before
Polymax S urgic al: 1 g 1 hr
Trimax before
Amoxic illin/c lavulanic Augmentin Bac teric idal 250–500 mg TID or 825 4 g/day S urgic al: 825 mg
ac id mg BID
Cephalexin Bioc ef Bac teric idal 250 mg QID or 500 mg 4 g/day S BE: 2 g 1 hr before
Cefanex BID S urgic al: 1 g 1 hr
Keftab before
Keflex
Cefadroxil Duric ef Bac teric idal 500 mg BID 4 g/day S BE: 2 g 1 hr before
Ultrac ef S urgic al: 1 g 1 hr
before
Azithromyc in Zithromax Bac teriostatic 500 mg immediately, 1000 — S BE: 500 mg 1 hr
mg/day before
Clarithromyc in Biaxin Bac teriostatic 250 mg — S BE: 500 mg 1 hr
before
Erythromyc in E-myc in Bac teriostatic 250 mg QID 4 g/day —
E-tab
Tetrac yc line Ac hromyc in Bac teriostatic 250 mg QID 4 g/day —
S umyc in
Clindamyc in Cleoc in HCI Bac teriostatic 150–300 mg TID or QID 1.8 mg/day S BE: 600 mg 1 hr
hydroc hloride before
S urgic al: 600 mg 1 hr
before
Metronidazole Flagyl Bac teric idal 250 mg TID or QID 4 g/day —
Levofloxac in Levaquin Bac teric idal 500 mg/day 500 mg/day S urgic al: 500 mg
Moxifloxac in Avelox Bac teric idal 400 mg/day 400 mg/day —
Trimethoprim/ Bac trim Bac teriostatic 160 mg (DS ) BID — —
sulfamethoxazole S eptra 80 mg BID
SBE, Subacute bacterial endocarditis; DS, double strength.

Penicillins
Penicillin V.
Penicillin V is the oral form of penicillin (penicillin G being the intravenous
form) that is one of the more common antibiotics used in dentistry today. It
is bactericidal, well absorbed, and will achieve peak serum levels within 30
minutes of administration with detectable blood levels for 4 hours. Penicillin
and all its derivatives produce bactericidal effects by inhibition of bacterial
cell wall synthesis. Penicillin V is effective against most Streptococcus species
and oral anaerobes. The main disadvantages of penicillin are four times per
day dosing due its very short half-life and susceptibility to resistant bacteria
(β-lactamase–producing bacteria).
Amoxicillin.
Amoxicillin, an ampicillin analog, is a penicillin-derived, broad spectrum,
bactericidal, semisynthetic beta-lactam antibiotic, with superior absorption,
high bioavailability, and very low toxicity. It acts through the inhibition of cell
wall biosynthesis during bacterial multiplication that leads to the bacterial
death and has excellent diffusion in infected tissues where high tissue
concentrations are easily achieved. Schüssl et al showed that a single dose of
oral amoxicillin (2 grams) leads to concentrations in teeth that exceed the
minimal inhibition concentration of some oral bacteria within 1 hour of
administration.56 It is effective against gram-negative cocci and gram-
negative bacilli, having a greater activity than penicillin V against
streptococci and oral anaerobes.
Amoxicillin/Clavulanic Acid (Augmentin).

This antibiotic is a combination of amoxicillin, a β-lactam antibiotic, and
clavulanic acid, a β-lactamase inhibitor. Certain bacteria, such as Streptococcus
aureus, may produce the enzyme beta-lactamase, which acts to hydrolyze, or
disrupt, the beta-lactam ring that permits penicillin-derivative antibiotics to
function. This may lead to decreased efficacy of the antibiotic and
development of antibiotic resistance. Penicillinase is a specific type of beta-
lactamase that has a specificity for penicillin and penicillin-derived
antibiotics. To counteract the activity of beta-lactamase destruction,
clavulanic acid was added to amoxicillin to form Augmentin (trade name),
which has an affinity for penicillinase-producing bacteria. Clavulanic acid
functions as a “suicide molecule” that inactivates the resistant bacteria
through disruption of penicillinase function, which makes the bacteria more
susceptible to the effects of the accompanying amoxicillin. An increase in the
prevalence of penicillinase-producing bacteria (especially in the sinus), has
made this antibiotic combination popular in oral implantology. This
antibiotic is used mainly in cases in which penicillinase bacteria is suspected
(or known by culture) and is very practical as a perioperative antibiotic for
sinus augmentation (Fig. 8.21).
FIG 8.21 Beta-lactamase inactivation by the clavulanic acid to amoxicillin

(Augmentin). Because of the high binding affinity of clavulanic acid, beta-lactamase
will be inactivated, allowing penicillin to destroy the bacteria. (From Misch CE:
Contemporary implant dentistry, ed 3, St. Louis, 2008, Mosby.)
Cephalosporins
Cephalexin/Cefadroxil.
The first-generation cephalexin/cefadroxil antibiotics have an antibacterial
spectrum similar to amoxicillin. However, they have the advantage of not
being susceptible to beta-lactamase destruction by S. aureus. They are often
used in dentistry as an alternative for the penicillin-allergic patient, although
cross-reactivity between these two drugs may occur. The cross-reactivity rate
to first-generation cephalosporins with penicillin-allergic patients has been
found to be approximately 1%.57
Caution must be exercised because Food and Drug Administration (FDA)
guidelines report a 10% cross-reactivity. The most recent studies have shown
only patients who have had type I (immunoglobulin E: immediate
hypersensitivity reactions) should not be administered a cephalosporin. If
the patient has a previous history of a reaction that was not immunoglobulin
E–mediated (types II, III, IV, or idiopathic reactions), a first-generation
cephalosporin may be administered. Newer second- and third-generation
cephalosporins exhibit a broader spectrum, less cross-reactivity, and a greater
resistance to beta-lactamase destruction.58
Macrolides
The most common macrolide used in dentistry is erythromycin. It is active
against most streptococci, staphylococci, and some anaerobes, and it is an
alternative for patients who are allergic to penicillin. Erythromycin has the
advantage of excellent absorption and, unlike many drugs, is affected by the
presence of food. It is administered primarily by the oral route and has a
relatively low toxicity. This antibiotic has a high incidence of nausea and is
bacteriostatic rather than bactericidal. It is therefore not an ideal first-line
choice for infections in the oral cavity.
These characteristics are also unattractive when either high doses are
required, severe infection exists, or the patient is immunocompromised and
requires bactericidal activity. Even more disturbing is its implication in
numerous drug interactions, including its proclivity for elevating serum
levels of digoxin, theophylline, and carbamazepine. Erythromycin has also
been found to prevent conversion of terfenadine (Seldane), a nonsedating
antihistamine, to its active metabolite. As a result, elevated serum
concentrations of the predrug may result and lead to cardiotoxicity,
presenting a particular form of ventricular tachycardia called torsades de
pointes that may lead to sudden cardiac death.
During the past several years, three novel macrolides have been
introduced that offer advantages over erythromycin (i.e., clarithromycin
[Biaxin], azithromycin [Zithromax]). Unlike other macrolides, they do not
appear to inhibit hepatic cytochrome P450 isozymes, which account for most
drug interactions of erythromycin. Biaxin produces less nausea and has
better Gram activity; Zithromax appears to be more effective against
Haemophilus influenza. A detailed medical and medication history should be
obtained prior to the administration of either clarithromycin or azithromycin
as potentially lethal cardiac rhythms such as QT prolongation, torsades de
pointes, arrhythmia, and even cardiovascular death have been reported,
particularly in individuals with a family history of these conditions or who
are already at a higher risk of cardiovascular events.
Clindamycin
Clindamycin (Cleocin Phosphate), a semisynthetic bacteriostatic derivative of
lincomycin, is a bacterial protein synthesis inhibitor through inhibition of
ribosomal translocation at the 50s RNA subunit. The use of clindamycin has
increased for the treatment of dental infections primarily because of its
activity against anaerobic bacteria. It is most effective against aerobic gram-
positive cocci, such as Staphylococcus and Streptococcus species, and anaerobic
gram-negative rod-shaped bacteria, such as some Bacteroides, Fusobacterium,
and Prevotella.
Clindamycin is also supplied in an aqueous 300-mg/2-mL solution that is
sometimes used in the incorporation of graft material for sinus
augmentation procedures. It is bacteriostatic in normal concentrations and
has a rather high toxicity in larger concentrations. The main disadvantage of
clindamycin is the occurrence of diarrhea in 20% to 30% of patients treated.
This antibiotic also has a higher incidence of antibiotic-associated
pseudomembranous colitis (PMC) caused by C. difficile when administrated
for extended periods. PMC has been reported to occur with most long-term
antibiotics.
The toxicity of antibiotics related to PMC is elevated with ampicillin,
amoxicillin, cephalosporin, and clindamycin. Penicillin, erythromycin, and
quinolones are moderate risk, and the lowest risk is with tetracycline,
metronidazole, and vancomycin. The latter group is often used to treat PMC
conditions.
The patient should be informed that if either diarrhea or abdominal
cramping occurs during or shortly after antibiotic therapy, the drug should
be discontinued and the doctor should be notified.
Antidiarrheal medications should be avoided in these cases because they
hinder the fecal elimination of the pathogen. If it is necessary to continue
management of the dental infection, imidazole or vancomycin is most logical
(if not the original cause of the complications). Metronidazole is not only
effective against anaerobes contributing to the dental infection but also
against C. difficile, the causative agent. If the condition persists after 3 days,
the patient should be assessed by an internist for fluid and electrolyte
imbalance.
Tetracyclines
Tetracyclines have been available since the 1950s and have a wide spectrum
of activity against streptococci, staphylococci, oral anaerobes, and gram-
negative aerobic rods. Because this antibiotic has been so extensively used in
the past, there is a high degree of bacterial resistance. Tetracycline is an
attractive adjunct for the treatment of gingival and periodontal disease with a
high bioavailability in the gingival sulcus. For these reasons, tetracyclines are
used by some practitioners as primary agents for treating implant disease
and infections around implant posts. Their efficacy for managing infrabony
infections is questionable, considering their inactivity when chelated with
calcium complexes. The disadvantages of this antibiotic include a high
incidence of promoting Candida spp infections and the fact that it may be
associated with photosensitivity reactions.
Fluoroquinolones
A recent classification of antibiotics has had a definite impact on the
treatment of infections in dentistry and medicine. Fluoroquinolones are
bactericidal antibiotics and have a broad antibacterial spectrum, which may
be used either orally or parenterally. Ciprofloxacin was one of the first-
generation quinolones and is the prototype for this antibiotic classification.
Newer third- and fourth-generation quinolones have been developed with
great activity against resistant bacteria and anaerobic bacteria. In implant
dentistry, fluoroquinolones are used mainly in the prophylactic and
therapeutic treatment of sinus augmentation procedures. Care should be
exercised with the use of Levaquin and Avelox as they have been associated
with tendon damage.
Metronidazole
Metronidazole is a bactericidal antibiotic that is most often used for
anaerobic infections. Because metronidazole has no activity against aerobic
bacteria, it is seldom used for mixed infections unless it is combined with
another antibiotic. It may be combined with penicillin when managing
severe infections. Patients should be cautioned against drinking alcoholic
beverages while taking this medication because disulfiram-like reactions
have been reported. These consist of severe nausea and abdominal cramping
caused by the formation of a toxic compound resembling formaldehyde.
Metronidazole should not be prescribed for patients taking the oral
anticoagulant warfarin (Coumadin).
Prevention and Treatment of Infection
Because of the risk of morbidity from infections, antimicrobial therapy is an
essential component of the surgical protocol. Although adverse effects are
associated with antibiotic therapy, these are usually mild and infrequent. The
antimicrobials most commonly used in implant dentistry are antibiotics
(local and systemic) and antimicrobial rinses (0.12% chlorhexidine
gluconate).
The use and understanding of the various antibiotic regimens available in
implant dentistry are beneficial for the initial success and long-term
maintenance of implant therapy. Antibiotic therapy utilized in implant
dentistry may be classified as either prophylactic (to prevent infection) or
therapeutic (to treat infection).
Prophylactic Antibiotics
A landmark study by Burke defined the scientific basis for the perioperative
use of antibiotics to prevent surgical wound infection.59 From this work,
Peterson established principles on the perioperative use of prophylactic
antibiotics.60
In general surgery (including its subspecialties), the principles of
antibiotic prophylaxis are well established. Guidelines are specifically related
to the procedure, the type of antibiotic, and the dosage regimen. The use of
prophylactic antibiotics in dentistry has also been documented in the
prevention of complications for patients at risk of developing infectious
endocarditis and immunocompromised patients. In oral implantology, there
is no consensus on the use and indications for prophylactic antibiotics.
Disadvantages of the use of antibiotics include the development of resistant
bacteria, adverse reactions, and possible resultant lax surgical technique. As
a result, the need for prophylactic antibiotics in healthy patients, type of
antibiotic, dosage, and duration of coverage is controversial. On the other
hand, postoperative surgical wound infections can have a significant impact
on the well-being of the patient and the survival of the implant. Documented
cases of potential consequences of infection range from increased pain and
edema to patient death. According to Esposito and Hirsch, one of the main
causes of dental implant failure is bacterial contamination at implant
insertion.61
A local inoculum must be present for a surgical wound infection to occur,
to overcome the host's defenses, and allow growth of the bacteria. This
process has many variables including various host, local tissue, systemic, and
microbial virulence factors. Antibiotic prophylaxis is only one component of
this complex cascade, but the efficacy and impact of antimicrobial
prophylaxis has been proven to be significant.62
Several studies have concluded there is benefit from using preoperative
antibiotics for dental implantology.63,64 In the most comprehensive and
controlled study to date, over 30 VA hospitals and dental schools formed the
Dental Implant Clinical Research Group and concluded the use of
preoperative antibiotics significantly improved dental implant survival, both
in early and later stages. In the evaluation of 2973 implants a significant
difference was found with the use of preoperative antibiotics (4.6% failure)
compared with no antibiotics (10% failure).63
The main goal of the use of prophylactic antibiotics is to prevent infection
during the initial healing period from the surgical wound site, thus
decreasing the risk of infectious complications of the soft and hard tissues.
Although there is no conclusive evidence on the mechanism of preoperative
antibiotics, most likely a greater aseptic local environment is achieved.
The Appropriate Antibiotic for the Surgical Procedure Must Be

Selected60
The prophylactic antibiotic should be effective against the bacteria that are
most likely to cause an infection. In the majority of cases, infections after
surgery are from organisms that originate from the site of surgery. Most
postoperative infections are caused by endogenous bacteria including
aerobic gram-positive cocci (streptococci), anaerobic gram-positive cocci
(peptococci), and anaerobic gram-negative rods (bacteroides).6
Although oral infections are mixed infections in which anaerobes
outnumber aerobes 2:1, it has been shown that anaerobes need the aerobes
to provide an environment to proliferate.65 Subsequent studies have shown
that the early phase of intraoral infections involves streptococci that prepare
the environment for subsequent anaerobic invasion.66 The ideal antibiotic
must be effective against these pathogens.
Least Toxic Antibiotic Should Be Selected

The second factor in selecting the correct antibiotic is to use the antibiotic
with the least amount of adverse effects. These effects may vary from mild
nausea to an extreme allergic reaction.
The final selection factor is that the antibiotic should ideally be
bactericidal. The goal of antibiotic prophylaxis is to kill and destroy the
bacteria. Bacteriostatic antibiotics work by inhibiting growth and
reproduction of bacteria, thus allowing the host defenses to eliminate the
resultant bacteria. However, if the host's defenses are compromised in any
way, the bacteria and infection may flourish. Bactericidal antibiotics are
advantageous over bacteriostatic antibiotics in that (1) there is less reliance
on host resistance, (2) the bacteria may be destroyed by the antibiotic alone,
(3) results are faster than with bacteriostatic medications, and (4) there is
greater flexibility with dosage intervals.
An Appropriate Tissue Concentration of the Antibiotic Must

Be Present at the Time of Surgery60
For an antibiotic to be effective a sufficient tissue concentration must be
present at the time of bacterial invasion. To accomplish this goal, the
antibiotic should be given in a dose that will reach plasma levels that are
three to four times the minimum inhibitory concentration (MIC) of the
expected bacteria.67 The MIC is the lowest antibiotic concentration sufficient
to destroy the specific bacteria. Usually, to achieve this cellular level the
antibiotic must be given at twice the therapeutic dose and at least 1 hour
before surgery.68 It has been shown that normal therapeutic blood levels are
ineffective to counteract bacterial invasion. If antibiotic administration
occurs after bacterial contamination, no preventive influence has been seen
as compared with taking no preoperative antibiotic.
Use of the Shortest Effective Antibiotic60

In a healthy patient, continuing antibiotics after surgery often does not
decrease the incidence of surgical wound infections.69 A single dose of
antibiotics is usually sufficient. However, for patients or procedures with
increased risk factors, a longer dose of antibiotics is warranted.60 With the
high degree of morbidity associated with dental implant infections, one must
weigh the benefits vs. risk involved for the extended use of antibiotics.
Complications of Antibiotic Prophylaxis.

It is estimated that approximately 6% to 7% of patients taking antibiotics will
have some type of adverse event.70 Incidence of significant complications
with the use of prophylactic antibiotics is minimal; however, a small
percentage can be life threatening. The risks associated with antibiotics
include gastrointestinal tract complications, colonization of resistant or
fungal strains, cross-reactions with other medications, and allergic reactions.
Allergic reactions have a wide range of complications, ranging from mild
urticaria to anaphylaxis and death. Studies have shown that 1% to 3% of the
population receiving penicillin will exhibit urticaria type of reactions, with
0.04% to 0.011% having true anaphylactic episodes. Of this small percentage
of anaphylactic reactions, 10% will be fatal.71
An unusual but increasing complication in the general population after
antibiotic use is pseudomembranous colitis. This condition is caused by the
intestinal flora being altered and colonized by Clostridium difficile. Penicillin
and clindamycin use has been significantly associated with
pseudomembranous colitis. All antibiotics have been shown as potential
causative agents. The most common treatment for antibiotic-induced colitis
is vancomycin or metronidazole.
The most recent concern with respect to antibiotic use is the development
of resistant bacteria. It has been observed that the overgrowth of resistant
bacteria begins only after the host's susceptible bacteria are killed, which
usually takes at least 3 days of antibiotic use. Short-term (1-day) use of
antibiotics has been shown to have little influence on the growth of resistant
bacteria.
Use of Prophylactic Antibiotics in Oral Implantology.

Postoperative wound infections can have a significant effect on the success of
dental implants and bone grafting procedures. The occurrence of surgical
host defenses allows an environment conducive to bacterial growth. This
process is complex, with interactions of host, local tissues, and systemic and
microbial virulence factors. Various measures attempt to minimize infection
by modifying the host and local tissue factors. The use of antimicrobials has
been shown to be significant in reducing postoperative infections.
The antibiotic chosen for prophylaxis should encompass the bacteria most
known to be responsible for the type of infection found with the surgical
procedure. The following antibiotics are suggested against pathogens known
to cause postoperative surgical wound infections in bone grafting or implant
surgery:
• Amoxicillin is the drug of choice. If the patient is allergic, alternative drugs
are:
Cephalexin (nonanaphylactic allergy to penicillin)
Clindamycin (anaphylactic allergy to penicillin)

• Sinus involvement procedures (e.g., sinus grafts)
Augmentin
Levaquin (if history of recent use of Augmentin [within 4

weeks])
Treatment.
When surgical wound infections arise, a specific diagnosis is advantageous to
treat the complication. When evaluating the various antibiotics possible that
are effective against the bacteria in question, a broad-spectrum beta-lactam
antibiotic is most often the first-line medication. The duration of treatment
should include antibiotic administration for 3 days beyond the occurrence of
significant clinical improvement, (usually at the fourth day) for a minimum
of 7 days.72
Therapeutic Antibiotics in Implant Dentistry
The recommended treatment for intraoral infections associated with grafting
or implant therapy include the following:
1. Surgical drainage
2. Systemic antibiotics
• Amoxicillin (500 mg)/two immediately, then one tablet

three times daily for 1 week; or if penicillin allergy exists
Clindamycin (300 mg)/two immediately, then one
tablet three times daily for 1 week.
• Note: If no improvement is seen after 4 days, a culture

and sensitivity test can be administered to select the
antibiotic most effective against the responsible
organisms.
• Until culture and sensitivity test results are obtained,

change antibiotic to Levaquin (500 mg)/one tablet
daily for 1 week and 0.12% chlorhexidine gluconate
rinse ( oz twice daily for 2 weeks).
Chlorhexidine
Another modality for antimicrobial prophylaxis for implant surgery is the
use of an oral rinse, 0.12% chlorhexidine digluconate (Peridex; Procter &
Gamble). Chlorhexidine gluconate is a potent antibacterial that causes lysis
by binding to bacterial cell membranes. It has high substantivity that allows
it, at high concentrations, to exhibit bactericidal qualities by causing bacterial
cytoplasm precipitation and cell death.73 In the oral cavity, chlorhexidine has
been shown to have a slow release from tissue surfaces over a 12-hour
period.74
In vitro studies have shown an inhibitory effect of chlorhexidine on
cultured epithelium and cell growth; however, clinical studies have not
shown this effect.75 To the contrary, the use of chlorhexidine has been shown
to be an effective adjuvant in reducing plaque accumulation, enhancing
mucosal health,76 improving soft tissue healing,77 treating periodontal
disease, preventing alveolar osteitis,78 improving tissue healing after
extractions,79 reversing peri-implantitis,80 and it has been shown to have no
adverse effect on implant surfaces.81
When evaluating the effect of preoperative chlorhexidine before dental
implant surgery, a significant reduction in the number of infectious
complications (2 to 1) and a sixfold difference in implant failures compared
to no use of chlorhexidine has been shown.82
Use of Chlorhexidine in Oral Implantology

As a consequence of many reported benefits of chlorhexidine, the use of this
antiseptic is suggested in many ways in oral implantology as follows:
• Patient presurgical rinse. It can be used in the aseptic protocol before
surgery for reduction of bacterial load
• Surface antiseptic. It can be used in the intra- and extraoral scrub of
patient, scrubbing of hands before gowns and gloves
• Postsurgical rinse. Patient should rinse twice a day until incision line
closure
• Periimplant maintenance on daily basis. Treatment of postoperative
infections.
Sterile Technique
Ideally, any surgical procedure where there may be an increased bacterial
insult should utilize a sterile technique. There is much misunderstanding
though, when it comes to the terms clean, aseptic, and sterile.
• Clean technique: The clean technique includes the routine hand washing,
hand drying, and use of nonsterile gloves.
• Aseptic technique: The aseptic technique is used for short invasive
procedures. It includes antiseptic hand wash, sterile gloves, antiseptic rinse,
and use of a clean, dedicated area.
• Sterile technique: The sterile technique includes measures to prevent the
spread of bacteria from the environment to the patient by eliminating all
microorganisms in that environment. This is mainly used for any procedure
in which the bacterial count needs to be lowered and an increase in
infection rate will lead to significant morbidity. This will include surgical
hand scrub, hands dried with sterile towels, complete sterile field, sterile
gown, mask, and gloves (Table 8.5, Boxes 8.6 and 8.7).
TABLE 8.5
Clean vs. Aseptic vs. Sterile
Clean Aseptic Sterile

Proc edure spac e Dental operatory S urgic al suite S urgic al suite
Gloves Nonsterile S terile S terile surgic al
Hand hygiene before the proc edures Routine Aseptic (e.g., alc ohol) S urgic al sc rub lodophors, c hlorheximide
S kin antisepsis No Alc ohol Chlorhexidine
S terile field No No Yes
S terile gown, mask, head c overing No No Yes
Box 8.6
General Considerations of a Sterile Technique
• Only sterile materials and instruments are placed within the sterile field.
• Check for chemical indicators to verify sterility of

items placed onto the sterile field along with package
integrity and package expiration (if appropriate).
• Above and below the sterile field table is considered
“nonsterile.”
• Materials that display a manufacturer's expiration date should be
considered unsafe for use after that date. (Rationale: Expiration dates do
not guarantee either sterility or lack of sterility.)
• If any sterile item (material, instrument, gown, glove) has been

compromised, the package contents, gown, or the sterile field is considered
contaminated. This may happen when:
• nonsterile items contact sterile items;
• liquids or moisture soak through a drape, gown, or

package (strikethrough).
• Single-use materials should only be used on an individual patient for a
single procedure and then discarded.
• Reusable medical devices shall be reprocessed and sterilized according to

the manufacturer's directions.
• Any item that falls below table level is considered unsterile (see Fig. 8.22).
Box 8.7
Sterile Technique
Step 1: Prescrub Wash (see Fig. 8.23)
A short prescrub wash is completed including the hands up to the elbow.
This is to remove superficial microorganisms and gross debris. (Duration =
1 minute)
• Prior to the scrub, make sure surgical attire is worn

and remove all jewelry. Glasses (loops, lights, etc.)
should be placed in the ideal position.
• Perform a rinse from the finger tips to the elbows so

the water flows from the cleanest area (finger tips) to
the less clean area (elbows). Utilize a sink that is wide
and deep so that both arms are contained within the
borders so that water is not splashed out of the sink.
• The next part of the prescrub is to clean the subungal

area of each cuticle. With the disposable nail cleaning
device, remove any debris from under each cuticle.
Step 2: Primary Scrub (see Fig. 8.24)
Depending on the hospital or surgical center, scrubbing methods and
protocol will vary. The counted stroke method seems to be the most
efficient to guarantee sterility. This involves 10 strokes for each side of each
finger (four sides), 10 strokes for each side of the hand, and 10 strokes for
each forearm side. Rinse hands and arms under running water in only one
direction, from finger tips to elbows. Care must be exercised to ensure
fingers, hands, and arms do not touch any nonsterile surface (e.g., faucet).
The hands should remain above the waist and below the axilla. If the water
is controlled by hand-control levers, a nonsterile surgical assistant should
turn the water off.
Step 3: Gowning (see Fig. 8.25A–D)

The hands should be dried with a sterile towel. Care should be exercised to
prevent the sterile gown or gloves from water contamination. When
moving from the scrub sink to the sterile area, keep hands in front of the
body, above the waist, and below the axilla. The neckline, shoulders,
underarms, and sleeve cuffs are considered nonsterile.
The sterile gown should be immediately donned after complete drying of the
hands and forearms, before gloving. Even though the complete gown is
sterile when placed on the sterile table, once the gown is donned, only the
front from the waist to the axilla is sterile. The gown should be lifted
upward and away from the table and allowed to open by locating the
neckline and armholes. Hold the inside front of the gown at the level of the
armholes to allow the gown to unfold. Do not touch the outside of the
gown with bare hands. Extend both arms into the armholes, and the gown
and sleeves will unfold. The gown is pulled onto the body with the cuffs of
the sleeves extended over the hands. Do not push the hands completely
through the cuffs.
Surgical gowns establish a barrier that minimizes the possibility of

contamination from nonsterile to sterile areas, which is commonly referred
to as a “strikethrough” barrier. They are made of a material that is resistant
to blood and fluid penetration.
Step 4: Sterile Gloves (see Fig. 8.25E–I)

Sterile gloves are packaged in a sterile package. The closed-gloving technique
is most widely used. It ensures the hands only touch the inside of the gown
and gloves. With the dominant hand, pick up the nondominant glove by
the inner wrap straight up, placing it on the nondominant hand. Guide and
wiggle the fingers into the glove. Using the gloved hand, pick up the
remaining glove and guide it on the nondominant hand, making sure the
gown cuff is covered. The nondominant glove will then pull the dominant
glove cuff over the gown.
Step 5: Tying of the Gown (see Fig. 8.26)

After the gown and gloves are in place, the front tie of the gown must be
secured. The surgeon holds the left string with the left hand and holds the
right large string and tag with the right hand. The tag is separated from the
small string and handed to an assistant. The surgeon rotates 360 degrees
and the assistant tears off the tag, leaving the right and left for the surgeon
to tie.
Achieving surgical asepsis requires multiple steps including surgical

gloving and gowning along with maintaining a sterile field. Each member of
the team involved in a sterile procedure is responsible for maintaining the
aseptic environment.
Sterile Field
Sterile drapes are most often used within the sterile field to cover any
surgical area utilized during the surgery (Fig. 8.22). Drapes come in various
sizes and are most easily purchased in a kit. The inner surface of the sterile
field, except for a 1-inch border, is considered the sterile field that may be
used to add sterile items. This 1-inch border may also be used to position the
drape within the surgical field. When placing sterile items onto the surgical
field, items may be “dropped” from approximately 6 inches above the sterile
field.
FIG 8.22 (A) Sterile surgical field; blue table drapes are considered sterile. (B)
Sterile technique includes all doctors and staff to be wearing a surgical hat, mask,
glasses, and gown as well as the sterile patient drape. (C) The chair should be
covered, but it is considered nonsterile.
Surgical Scrub
The surgical scrub is the process that removes as many microorganisms from
the nail beds, hands, and forearms by mechanical washing and chemical
antisepsis for a surgical procedure. This will result in a decrease in microbial
count and inhibits the regrowth of bacteria. There are two different types of
scrubbing techniques, a sterile sponge/brush with antimicrobial agent or a
brushless technique with alcohol/chlorhexidine gluconate (Figs. 8.23 and
8.24).
FIG 8.23 Prescrub. (A) Make sure hat, mask, glasses are worn and in place prior
to the initiation of scrubbing. (B) A prescrub brush. (C) Prerinse from finger tips to
elbows. (D) Open prescrub brush. (E) Clean under all fingernails.
FIG 8.24 Primary scrub. (A) With the scrub brush, do a preliminary wash from
finger tips to elbow and then rinse. Brush each side of finger (B), each side of the
hand (C), and each side of both forearms with 10 strokes (D–E). (F–G) Rinse from
the finger tips to the elbows.
All rings, watches, bracelets, and jewelry should be removed prior to

starting the hand scrub. Surgical hats, protective eyewear, headlights, and
surgical mask must be donned prior to surgical hand asepsis. Drying of the
hands and arms is a priority because moist surfaces allow bacteria to
multiply. Gowning, gloving, and tying the front tie of the gown occur after the
handscrub (Figs. 8.25 and 8.26).
FIG 8.25 (A) Sterile gown and gloves. (B) Dry hands thoroughly, moist hands will
impair glove positioning. (C) Pick up the gown from the sterile field from the inside
surface of the gown, step back from the sterile field allowing the gown to unfold from
the body, place arms into the sleeves of the gown. (D) When gown is in the ideal
position, hands are at the seam of the inside cuff. Keep hands between waist and
neck level. (E) With the hands covered by the sleeve of the gown, use the dominant
hand to grasp the folded cuff of the glove for the non-dominant hand. (F) The
dominant hand pulls the glove completely on the hand from the cuff. (G) Place the
second glove on via the same method. (H) Place glove completely over gown. (I)
Use the nondominant glove, under the cuff, to fold over the cuff of the gown.
FIG 8.26 Gown tying. (A) The surgeon holds left string (short) with left hand, holds
tag and right string (long) with right hand, then pulls off tag with right hand. (B) The
surgeon hands the tag to the assistant. (C) The surgeon spins around 360 degrees
and the assistant hands the long string to the surgeon who ties the front of the gown.
(D) The assistant or circulator ties the velcro back. (E) The surgeon is gowned and
the hands are below the sterile area. (F) The sterile area is below the axilla and
above the waist.
Summary
During the course of a career placing dental implants or performing bone
grafting procedures, a clinician will most likely encounter situations where a
patient presents with infection. As illustrated in this chapter, a seemingly
small infection of an implant or graft has the potential to involve the surgical
spaces of the head and neck, causing life-threatening episodes. The early
signs of infection need to be recognized and considered urgently, especially
when the patient's swallowing or breathing is compromised. Also, early signs
of cavernous sinus thrombosis need to be recognized and the patient
referred immediately to a specialist.
Endosteal implants are usually inserted beyond the apex position of
natural teeth. Subperiosteal implants traverse natural barriers of infection
when extended beyond muscle attachments (Fig. 8.27). Intraoral infections
may extend to the base of implants, which may cause more concern than
infections of natural teeth. Placement of medical devices into a patient allows
for the possibility of infection and places the procedure, patient, and doctor
at risk.
FIG 8.27 Subperiosteal failure and infection. (A) Panoramic image depicting bone
resorption and related infection. (B) Preoperative intraoral view showing anterior
teeth and failing circumferential subperiosteal implant. (C) Surgical removal of
subperiosteal. (D) Postoperative treatment involved placement of six implants and a
fixed prosthesis.
The implant dentist must be aware of the changes in the patient's

symptoms as infection progresses and, when indicated, refer the patient
immediately to a specialist for treatment. As discussed in this chapter, the
infection may start as a painful swelling in the face region with little or no
change in the ability of the patient to open the mouth, swallow, or breathe,
and with only mild signs of toxemia. The dentist has to be extremely alert to
the possibility of a progression of the infection to involve the masticatory,
parapharyngeal, perivertebral, and perivisceral spaces and similar areas, with
accompanying signs and symptoms, such as the inability to open the mouth
and the compromise of vital signs, such as breathing. When this occurs, the
patient should be hospitalized without hesitation. It is important that
extraoral incisions and management of infection of the head and neck be
handled by the appropriate specialists.
References
1. Camps-Font O, Figueiredo R, Valmaseda-Castellón E, et al.
Postoperative infections after dental implant placement: prevalence,
clinical features, and treatment. Implant Dent. 2015;24(6):713–719.
2. Chrcanovic BR, Albrektsson T, Wennerberg A. Diabetes and oral
implant failure: a systematic review. J Dent Res. 2014;93(9):859–867.
3. Choukroun J, Khoury G, Khoury F, et al. Two neglected biologic risk
factors in bone grafting and implantology: high low-density
lipoprotein cholesterol and low serum vitamin D. J Oral Implantol.
2014;40(1):110–114.
4. Topazian RG, Goldberg MH, Hupp JR. Oral and maxillofacial
infections. Saunders: St Louis; 2002.
5. Woods RK, Dellinger MD. Current guidelines for antibiotic
prophylaxis surgical wounds. Am Fam Physician. 1998;57:2731–2740.
6. Peterson LJ. Antibiotic prophylaxis against wound infections in oral
and maxillofacial surgery. J Oral Maxillofac Surg. 1990;48:617.
7. Page CP, Bohnen JMA. Antimicrobial prophylaxis for surgical
wounds: guidelines for clinical care. Arch Surg. 1993;128:79.
8. Garibaldi RA, Cushing D. Risk factors for post-operative infection.
Am J Med. 1991;91(Suppl 3B):158S–163S.
9. Rider CA. Infection control within the oral surgeon's office. Compend
Contin Educ Dent. 2004;25:529–534.
10. Dent CD, Olson JW, Farish SE, et al. Influence of preoperative
antibiotics on success of endosseous implants up to and including
stage 2 surgery. J Oral Maxillofac Surg. 1997;55:19–24.
11. Drake DR, Paul J. Primary bacterial colonization of implant surfaces.
Int J Oral Maxillofac Implants. 1999;14:226.
12. Cruse PJ, Foord R. A five-year prospective study of 23,649 surgical
wounds. Arch Surg. 1973;107:206–210.
13. Quintiliani R, Maderazo EG. Infections in the compromised patient.
Topazian RG, Goldberg MH. Oral and maxillofacial infections. WB
Saunders: Philadelphia; 1995:537–556.
14. Pier GB, Lyczak JB, Wetzler LM. Immunology, infection, and immunity.
ASM Press: New York; 2004.
15. Anstead GM. Steroids, retinoids, and wound healing. Adv Wound Care
(New Rochelle). 1998;11(6):277–286.
16. Scully C. Oral and maxillofacial medicine: the basis of diagnosis and
treatment. ed 2. Churchill Livingstone: Edinburgh; 2008.
17. Ferrer R. Lymphadenopathy: differential diagnosis and evaluation. Am
Fam Physician. 1998;58(6):1313–1320.
18. Rai A, Rajput R, Khatua RK, Singh M. Submasseteric abscess: a rare
head and neck abscess. Indian J Dent Res. 2011;22(1):166–168.
19. Schuknecht B, Stergiou G, Graetz K. Masticator space abscess derived
from odontogenic infection: imaging manifestation and pathways of
extension depicted by CT and MR in 30 patients. Eur Radiol.
2008;18(9):1972–1979.
20. Bratton TA, Jackson DC, Nkungula-Howlett T, et al. Management of
complex multi-space odontogenic infections. J Tenn Dent Assoc.
2002;82(3):39–47.
21. Odobescu A, Williams HB, Gilardino MS. Description of a
communication between the facial and zygomaticotemporal nerves. J
Plast Reconstr Aesthet Surg. 2012;65(9):1188–1192.
22. Dzyak WR, Zide MF. Diagnosis and treatment of lateral pharyngeal
space infections. J Oral Maxillofac Surg. 1984;42(4):243–249.
23. Marx RE, Baltensperger M, Eyrich GK. Osteomyelitis of the jaws.
Springer: New York; 2008.
24. Topazian RG, Goldberg MH. Management of infections of the oral and
maxillofacial regions. WB Saunders Company: Philadelphia; 1981.
25. Park SH, Sorensen WP, Wang HL. Management and prevention of
retrograde peri-implant infection from retained root tips: two case
reports. Int J Periodontics Restorative Dent. 2004;24:422–433.
26. Lindhe J, Berglundh T, Ericsson I, et al. Experimental breakdown of
peri-implant and periodontal tissues. A study in the beagle dog. Clin
Oral Implants Res. 1992;3:9–16.
27. Pineda C, Espinosa R, Pena A. Radiographic imaging in osteomyelitis:
the role of plain radiography, computed tomography,
ultrasonography, magnetic resonance imaging, and scintigraphy.
Semin Plast Surg. 2009;23(2):80–89.
28. Kothari NA, Pelchovitz DJ, Meyer JS. Imaging of musculoskeletal
infections. Radiol Clin North Am. 2001;39(4):653–671.
29. Ariji Y, Izumi M, Gotoh M, et al. MRI features of mandibular
osteomyelitis: practical criteria based on an association with
conventional radiography features and clinical classification. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod. 2008;105(4):503–511.
30. Marx RE, Tursun R. Suppurative osteomyelitis, bisphosphonate
induced osteonecrosis, osteoradionecrosis: a blinded histopathologic
comparison and its implications for the mechanism of each disease.
Int J Oral Maxillofac Surg. 2012;41(3):283–289.
31. Peterson LJ. Microbiology of head and neck infections. Oral Maxillofac
Clin North Am. 1991;3:247–257.
32. Marx RE. Pamidronate (Aredia) and zoledronate (Zometa) induced
avascular necrosis of the jaws: a growing epidemic. J Oral Maxillofac
Surg. 2003;61:1115.
33. Ruggiero SL, Mehrotra B, Rosenberg TJ, et al. Osteonecrosis of the
jaws associated with the use of bisphosphonates: a review of 63 cases.
J Oral Maxillofac Surg. 2004;62:527.
34. Hohnecker JA. Novartis “Dear Doctor” precautions added to the label of
Aredia and Zometa. Novartis Oncology: East Hanover, NJ; 2004
[September 24].
35. Ruggiero SL, Dodson TB, Fantasia J, et al. American Association of
Oral and Maxillofacial Surgeons position paper on medication-related
osteonecrosis of the jaw—2014 update. J Oral Maxillofac Surg.
2014;72(10):1938–1956.
36. Katsarelis H, Shah NP, Dhariwal DK, et al. Infection and medication-
related osteonecrosis of the jaw. J Dent Res. 2015;94(4):534–539.
37. Bamias A, Kastritis E, Bamia C, et al. Osteonecrosis of the jaw in
cancer after treatment with bisphosphonates: incidence and risk
factors. J Clin Oncol. 2005;23:8580.
38. Hokugo A, Christensen R, Chung EM, et al. Increased prevalence of
bisphosphonate-related osteonecrosis of the jaw with vitamin D
deficiency in rats. J Bone Miner Res. 2010;25:1337.
39. Wood J, Bonjean K, Ruetz S, et al. Novel antiangiogenic effects of the
bisphosphonate compound zoledronic acid. J Pharmacol Exp Ther.
2002;302:1055.
40. Ruggiero SL, Fantasia J, Carlson E. Bisphosphonate-related
osteonecrosis of the jaw: background and guidelines for diagnosis,
staging and management. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2006;102:433.
41. Marx RE. A decade of bisphosphonate bone complications: what it has
taught us about bone physiology. Int J Oral Maxillofac Implants.
2014;29(2):e247–e258.
42. Sedghizadeh PP, Stanley K, Caligiuri M, et al. Oral bisphosphonate
use and the prevalence of osteonecrosis of the jaw: an institutional
inquiry. J Am Dent Assoc. 2009;140(1):61–66.
43. Kos M, et al. Pamidronate enhances bacterial adhesion to bone
hydroxyapatite. Another puzzle in the pathology of bisphosphonate-
related osteonecrosis of the jaw? J Oral Maxillofac Surg.
2013;71(6):1010–1016.
44. Grant BT, Amenedo C, Freeman K, Kraut RA. Outcomes of placing
dental implants in patients taking oral bisphosphonates: a review of
115 cases. J Oral Maxillofac Surg. 2008;66(2):223–230.
45. Jacobsen C, Metzler P, Rössle M, et al. Osteopathology induced by
bisphosphonates and dental implants: clinical observations. Clin Oral
Investig. 2013;17(1):167–175.
46. Nisi M, La Ferla F, Karapetsa D, et al. Risk factors influencing BRONJ
staging in patients receiving intravenous bisphosphonates: a
multivariate analysis. Int J Oral Maxillofac Surg. 2015;44(5):586–591.
47. Li X, Tronstad L, Olsen I. Brain abscesses caused by oral infection.
Endod Dent Traumatol. 1999;15(3):95–101.
48. Czerninski R, Kaplan I, Almoznino G, et al. Oral squamous cell
carcinoma around dental implants. Quintessence Int. 2006;37(9):707–
711.
49. Block MS, Scheufler E. Squamous cell carcinoma appearing as peri-
implant bone loss: a case report. J Oral Maxillofac Surg.
2001;59(11):1349–1352.
50. Poggio CE. Plasmacytoma of the mandible associated with a dental
implant failure: a clinical report. Clin Oral Implants Res.
2007;18(4):540–543.
51. Dib LL, Soares AL, Sandoval RL, Nannmark U. Breast metastasis
around dental implants: a case report. Clin Implant Dent Relat Res.
2007;9(2):112–115.
52. Verhoeven JW, Cune MS, van Es RJ. An unusual case of implant
failure. Int J Prosthodont. 2007;20(1):51–54.
53. Saglik Y, Arikan M, Altay M, Yildiz Y. Squamous cell carcinoma arising
in chronic osteomyelitis. Int Orthop. 2001;25(6):389–391.
54. Keel SB, Jaffe KA, Petur Nielsen G, Rosenberg AE. Orthopaedic
implant-related sarcoma: a study of twelve cases. Mod Pathol.
2001;14(10):969–977.
55. Esquivel-Upshaw J. Dental implants. Anusavice KJ. Phillips' science of
dental materials. ed 11. Saunders: St Louis; 2003:187–204.
56. Schüssl Y, Pelz K, Kempf J, et al. Concentrations of amoxicillin and
clindamycin in teeth following a single dose of oral medication. Clin
Oral Investig. 2014;18(1):35–40.
57. Campagna JD, Bond MC, Schabelman E, et al. The use of
cephalosporins in penicillin-allergic patients: a literature review. J
Emerg Med. 2012;42(5):612–620.
58. Pichichero ME. Prescribing cephalosporins to penicillin-allergic
patients. North Am Pharmacother. 2006;54:1–4.
59. Burke JF. The effective period of preventive antibiotic action in
experimental incisions and dermal lesions. Surgery. 1961;50:161.
60. Peterson LJ. Antibiotics: their use in therapy and prophylaxis. Kruger
GO. Oral and maxillofacial surgery. Mosby,: St. Louis; 1984:45–89.
61. Esposito M, Hirsch JM. Biological factors contributing to failure of
osseointegrated oral implants. Eur J Oral Sci. 1998;106:721–764.
62. Peterson LJ, Booth DF. Efficacy of antibiotic prophylaxis in intraoral
orthognathic surgery. J Oral Surg. 1976;34:1088.
63. Laskin D, Dent C, Morris H. The influence of preoperative antibiotics
on success of endosseous implants at 36 months. Ann Periodontol.
2000;5:166–174.
64. Dent CD, Olson JW, Farish SE, et al. Influence of preoperative
antibiotics on success of endosseous implants up to and including
stage 2 surgery. J Oral Maxillofac Surg. 1997;55:19–24.
65. Greenberg RN, James RB, Marier RL, et al. Microbiologic and
antibiotic aspects of infections in the oral and maxillofacial region. J
Oral Surg. 1979;37:873–884.
66. Lewis MA, MacFarlane TW, McGowan DA. Quantitative bacteriology
of acute dento-alveolar abscesses. J Med Microbiol. 1986;21:101–104.
67. Norris LH, Doku HC. Antimicrobial prophylaxis in oral surgery. Oral
Maxillofacial Surg Infect. 1992;2:85–92.
68. Page CP, Bohnen JMA. Antimicrobial prophylaxis for surgical wounds:
guidelines for clinical care. Arch Surg. 1993;128:79.
69. Hossein K, Dahlin C. Influence of different prophylactic antibiotic
regimens on implant survival rate: a retrospective clinical study. Clin
Implant Dent Relat Res. 2005;7:32–35.
70. Alanis A, Weinstein AJ. Adverse reactions associated with the use of
oral penicillins and cephalosporins. Med Clin North Am. 1983;67:113.
71. Parker CW. Allergic reactions in man. Pharmacol Rev. 1982;34:85–104.
72. Newman MG, Van Winkehoff AJ. Antibiotic and antimicrobial use in
dental practice. ed 2. Quintessence: Chicago; 2001.
73. Hugo WB, Longworth AR. The effects of chlorhexidine on the
electrophoretic mobility, cytoplasmic constituents, dehydrogenase
activity and cell walls of E. coli and S. aureus. J Pharm Pharmacol.
2001;18:569–578.
74. Schiott C, Loe H. The effect of chlorhexidine mouthrinses on the
human oral flora. J Periodont Res. 1970;5:84–89.
75. Goldschmidt P, Cogen R. Cytopathologic effects of chlorhexidine on
human cells. J Periodontol. 1977;48:212–215.
76. Sanz M, Newman MG. Clinical enhancement of postperiodontal
surgical therapy by a 0.12% chlorhexidine gluconate mouthrinse. J
Periodontol. 1989;60:570–576.
77. Beiswanger DD, Mallat ME. Clinical effects of a 0.12% chlorhexidine
rinse as an adjunct to scaling and root planning. J Clin Dent.
1992;3:33.
78. Larson PE. The effect of a chlorhexidine rinse on the incidence of
alveolar osteitis following the surgical removal of impacted third
molars. J Oral Maxillofac Surg. 1991;49:932.
79. Lang NP, Schild U. Effect of chlorhexidine (0.12%) rinses on
periodontal tissue healing after tooth extraction. I. Clinical
parameters. J Clin Periodontol. 1994;21:422.
80. Hammerle CHF, Fourmousis I. Successful bone fill in late peri-
implant defects using guided tissue regeneration: a short
communication. J Periodontol. 1995;66:303.
81. Thomson-Neal D, Evans GH. Effects of various prophylactic
treatments on titanium, sapphire and hydroxyapatite-coated
implants: an SEM study. Int J Perodontics Restorative Dent. 1989;9:300.
82. Lambert PM, Morris HF. The influence of 0.12% chlorhexidine
digluconate rinses on the incidence of infectious complications and
implant success. J Oral Maxillofac Surg. 1997;55:25–30.
9
Neurosensory Deficit Complications
in Implant Dentistry
Randolph R. Resnik
Iatrogenic injury with resultant sensory impairment of the skin and mucosa
innervated by branches of the trigeminal nerve is a major concern in
association with dental implant surgery. With the increase in the number of
implants being placed and more practitioners becoming involved with dental
implant surgery, nerve damage will most likely be a continued problem in
implant dentistry. The reported incidence of such nerve injuries following
dental implant procedures is highly variable (0% to 44%) in the literature.1
Studies have shown that approximately 73% of doctors who perform implant
surgery have experienced postoperative nerve complications.2 Libersa et al
evaluated transient vs. permanent nerve injuries after implant placement and
determined a 75% incidence of permanent injury (Fig. 9.1).3
FIG 9.1 Neurosensory impairment of the inferior alveolar nerve. (A) Placement of
two implants, completely transecting the mandibular canal. (B–C) Implant placement
impinging on the mental foramen. (D) Immediate placement implant after premolar
extraction causing nerve impairment. (E) CBCT image depicting implant placement
through mandibular canal.
When a nerve injury occurs, it is paramount the dental implant surgeon be

able to recognize the type and extent of injury and provide the most
appropriate postoperative care. Traumatic and iatrogenic nerve complications
may involve total or partial nerve resection, crushing, thermal, stretching, or
entrapment injuries. The resulting sensory deficits may range from a
nonpainful, minor loss of sensation (hypoesthesia), to a more permanent and
severe debilitating pain dysfunction (dysesthesia). Patients with
neurosensory deficits often complain of symptoms that include interference
with function, speaking, eating, kissing, facial soft tissue dysfunction, and
inability to complete everyday tasks such as shaving and placing make-up.
The sensory problems often result in an overall decreased quality of life and
long-standing psychological problems.4 Most patients find accepting and
coping with even minimal nerve injuries difficult to live with. The clinician is
usually affected by increased complaints from the patients, embarrassment,
with significant medicolegal implications.
In the field of oral implantology today, the clinician must have a thorough
understanding of the etiology, prevention, and treatment of neurosensory
impairments. The authors have developed postoperative guidelines for
diagnosis and possible management of neurosensory deficits following
dental implant surgery that are dependent on the history, type, and nature of
the injury.
Anatomy
Peripheral Nerve Fiber Anatomy
The individual nerve fibers of peripheral nerves are situated in fascicles,
which are bundles or groups of nerve fibers. For example, the inferior
alveolar nerve is classified as polyfascicular, meaning that it contains more
than 10 fascicles surrounded by an abundance of interfascicular connective
tissue. Within the fascicles, there are approximately 7000–12,000 axons in
various fascicular arrangements.5 The number of fascicles varies along the
intramandibular course of the inferior alveolar nerve because there are
approximately 18–21 fascicles in the third molar region, decreasing to 12
fascicles in the mental foramen area.6 Because of the polyfascicular nature of
the inferior alveolar nerve, it is better able to regain sensation after injury via
compensatory innervation from the uninjured fascicles. Surrounding the
polyfascicular makeup of this nerve is the perineurium, which consists of
dense, multilayered connective tissue. The perineurium functions to
maintain intrafascicular pressure and acts as a diffusion barrier in the
protection of the individual nerve fibers. Two types of connective tissue, the
inner and outer epineurium, surround the fascicles. The inner epineurium is
composed of loose connective tissue with longitudinal collagen bundles. This
tissue protects the nerve fibers against compressive and stretching forces,
thus maintaining the structural continuity of the nerve. The outer
epineurium is continuous with the mesoneurium, which is the outer loose
areolar tissue that suspends the nerve trunk within the soft tissue and
contains the blood supply to the nerve. The mesoneurium allows the nerve to
have longitudinal movement within the surrounding tissue.
If any of these extraneural tissues (epineurium, perineurium,
endoneurium, or mesoneurium) is injured, impaired neural transmission by
the individual nerve fibers may result in a sensory disturbance. The
neurosensory impairment is dependent on the individual fiber type that is
involved. The A-alpha fibers are the largest fibers; mediate position and fine
touch through muscle spindle afferents and skeletal muscle efferents. The A-
beta fibers are solely for proprioception, and the A-delta carries the initial
pain impulses along with temperature information. Unmyelinated C-fibers
are slow conducting and function for the perception of “second” or slow pain
with an additional temperature component. For dental implant surgeons the
primary concern is loss of sensory functions such as touch, pressure, pain,
and temperature following trauma (Fig. 9.2).
FIG 9.2 Nerve fiber anatomy showing polyfascicular nature of inferior alveolar
nerve. (From Canale ST, Beaty JH editors: Campb ell's operative orthopaedics, ed 11, Philadelphia,
2008, Mosby.)
Trigeminal Nerve
The trigeminal nerve is the fifth cranial nerve and largest of the 12 cranial
nerves. This nerve originates from the brainstem at the midlateral surface of
the pons with its afferent fibers transmitting innervation from the face, oral
and nasal cavity, as well as the scalp. The trigeminal nerve also has visceral
efferent fibers for lacrimal, salivary, and nasal mucosa glands. Somatic
efferent fibers are present that innervate the masticatory muscles. The
trigeminal nerve has three main branches: V1 (ophthalmic); V2 (maxillary);
and V3 (mandibular).
V1: Ophthalmic
The uppermost branch is the ophthalmic nerve, V1, which is the smallest of
the three divisions of the trigeminal nerve. It supplies sensory branches to
the ciliary body, cornea, conjunctiva, lacrimal glands, and nasal mucosa as
well as to the skin of the nose, eyelid, and forehead. The ophthalmic division
structures are rarely involved in neurosensory disturbances associated with
dental implant procedures.
V2: Maxillary
The middle branch of the maxillary nerve (V2) exits the middle cranial fossa
through foramen rotundum and enters the pterygopalatine fossa, where it
gives off branches to the maxillary teeth and gingiva, maxillary sinus, upper
lip, lateral surface of the nose, the lower eyelid, the skin of the cheek and side
of the forehead, nasal cavity, and mucosa of the hard and soft palate (Fig. 9.3).
FIG 9.3 Maxillary nerve (V2) and its associated branches: infraorbital nerve,
posterior, middle, and anterior superior alveolar nerves. (From Rodella LF, Buffoli B,
Labanca M, et al: A review of the mandibular and maxillary nerve supplies and their clinical
relevance. Arch Oral Biol 57:323–334, 2012.)
Nasopalatine Nerve.
The incisive canals fuse and form a common Y-shaped canal that exits lingual
to the central incisor teeth (incisive foramen or incisive fossa). The
nasopalatine nerve passes through these canals and provides sensation to the
anterior palate. These nerves (also termed incisive nerves) terminate at the
nasal floor and enter the oral cavity via the incisive canal, which is
underneath the incisive papilla. To prevent trauma to these nerves, ideal
presurgical planning of implant placement in the maxillary incisor region
should be carefully evaluated (Fig. 9.4).
FIG 9.4 Nasopalatine nerve and canal. (A) Cross-sectional image depicting large
nasopalatine canal. (B) Axial CBCT image. (C–D) Placement of implant into the
nasopalatine canal after removal of soft tissue contents.
Removing the contents of the nasopalatine canal and grafting has been
reported to have a high success rate.7,8 Although this nerve is often affected
by the placement of implants or bone grafting in the incisor region, sensory
disturbances are rare. Nerve damage reported in the literature caused by
complete removal9 or flap surgery10 is of short duration. This is most likely
due to cross innervation of the greater palatine nerve on the anterior palatal
area.
Infraorbital Nerve.
The infraorbital nerve emerges from the infraorbital foramen and gives off
four branches: the inferior palpebral, external nasal, internal nasal, and the
superior labial branches, which are sensory to the lower eyelid, cheek, and
upper lip. The inferior palpebral branches supply the skin and conjunctiva of
the lower eyelid. The nasal branches supply the lateral nose soft tissue and
the movable part of the nasal septum, and the superior labial branches
supply the skin of the cheek and upper lip. Normally, the average distance of
the inferior border of the orbital rim to the infraorbital foramen is 4.6 mm to
10.4 mm (Fig. 9.5).
FIG 9.5 Infraorbital nerve. (A) Anatomic variants showing close proximity to the
residual ridge. (B) Minnesota retractor in close proximity to the infraorbital nerve.
Impairment of the infraorbital nerve may be very traumatic to patients.
Damage to branches of the infraorbital nerve usually will result from
retraction-related trauma (neuropraxia). Procedures involving the maxillary
cuspid-bicuspid area are most susceptible to injuries. Anatomic variants of
the infraorbital foramen have been shown to be up to 14 mm from the orbital
rim. This is most likely seen in elderly female patients with extensive alveolar
atrophy.
Anterior Superior Alveolar Nerve.

The anterior superior alveolar nerve branches from the infraorbital canal on
the lateral face. This small canal may be seen lingual to the cuspid and is
denoted as the canalis sinuosus. The canal runs forward and downward to the
inferior wall of the orbit and, after reaching the edge of the anterior nasal
aperture in the inferior turbinate, it follows the lower margin of the nasal
aperture and opens to the side of the nasal septum.11 Studies have shown
that in approximately 15% of the population, this area is described as
foramina that are 1–2 mm in diameter. The canals present as a direct
extension of the canalis sinuosus and may be clinically relevant when greater
than 2.0 mm12 (Fig. 9.6).
FIG 9.6 (A) Anterior superior alveolar nerve. (B) Canalia sinuosus is an anatomic
variant leading to placement of implants into the canal leading to a soft tissue
interface. Axial CBCT image showing location in center of residual ridge. (C) Cross-
sectional CBCT image depicting the canalia sinuosus. (A, From Wells M: Local and
regional anaesthesia in the emergency department made easy, Edinburgh, 2010, Churchill
Livingstone.)
Clinical relevance.
Because the canine pillar region is a common area for dental implants, care
should be taken to check for the presence of neurovascular bundles of the
infraorbital canal. Insertion of implants in approximation to the canal may be
problematic. Impingement into the canal may lead to a soft tissue interface
and failure of the implant and temporary or permanent sensory dysfunction
and possible bleeding issues.13 However, significant sensory impairments are
rare because of cross innervation. Many clinicians are unaware of the canalia
sinuosus and may misdiagnose this radiolucency as apical pathology of the
maxillary cuspid.
V3: Mandible
The mandibular nerve is the largest of the trigeminal branches and is the
most common branch involved with neurosensory disturbances following
dental implant surgery. The mandibular nerve is the lowest branch of the
trigeminal nerve, which runs along the floor of the cranium, exiting through
the foramen ovale into the infratemporal fossa. It has two branches, the first
being a smaller anterior branch containing the buccal and masseteric nerve.
A larger posterior component divides the mandibular nerve into three main
branches, the auriculotemporal, inferior alveolar (IAN), and lingual nerves
(LN).
This nerve innervates the temporomandibular joint, skin above the ears,
auricle, tongue and its adjacent gingiva, floor of the mouth, mandibular teeth
and associated gingiva, mucosa and skin of the cheek, lower lip and the chin
and the muscles of mastication.
Inferior Alveolar Nerve.

The inferior alveolar nerve is the largest branch of the mandibular nerve.
Before entering the mandibular foramen on the lingual surface of the
mandible, the mylohyoid nerve branches, giving innervation to the
mylohyoid and anterior belly of digastric muscles. In the mandibular canal it
runs downward and forward before dividing, in approximately the first molar
region, into two terminal branches; the incisive and mental nerves.14 The
mental nerve courses anteriorly until it exits through the mental foramen,
which is sensory to the soft tissues of the chin, lip, and anterior gingiva. The
incisive nerve continues anterior and innervates the mandibular anterior
teeth. Accurately determining the exact location of the inferior alveolar nerve
as it courses through the body of the mandible is imperative to avoid
neurosensory disturbances secondary to implant placement (Fig. 9.7).
FIG 9.7 (A) Mandibular nerve and its branches. (B) 3-D image of the intraosseous
course of the mandibular nerve. (A, From Wells M: Local and regional anaesthesia in the
emergency department made easy, Edinburgh, 2010, Churchill Livingstone.)
Histologically, this IAN consists of connective tissue and neural

components in which the smallest functional unit is the individual nerve
fiber. The IAN fibers may be either myelinated or unmyelinated. The
myelinated nerve fibers are the most abundant; they consist of a single axon
encased individually by a single Schwann cell. The individual nerve fibers
and Schwann cells are surrounded by the endoneurium, which acts as a
protective cushion made up of a basal lamina, collagen fibers, and
endoneurial capillaries.
Clinical relevance.
Nerve impairment to the inferior alveolar nerve (mental nerve) is a common
clinical complication with major medicolegal implications. Because of its
anatomic location, the mental nerve is the most common nerve to be
damaged via implants or bone graft procedures. Trauma usually occurs from
placement of implants directly into the foramen or into the inferior alveolar
canal in the posterior mandible. Sensory nerve injury may result in altered
sensation, complete numbness, and/or pain, which may interfere with
speech, eating, drinking, shaving, or make-up application and lead to social
embarrassment.
Lingual Nerve.
Within the infratemporal fossa, the lingual nerve divides from the posterior
division of the mandibular nerve (V3) as a terminal branch. As the lingual
nerve proceeds anteriorly, it lies against the medial pterygoid muscle and
medial to the mandibular ramus. It then passes inferiorly to the superior
constrictor attachment and courses anteroinferiorly to the lateral surface of
the tongue. As it runs forward deep to the submandibular gland, it
terminates as the sublingual nerve.
The lingual nerve is sensory to the anterior two thirds of the tongue, floor
of the mouth, and lingual gingiva. It also contains visceral afferent and
efferent fibers from cranial nerve seven (facial nerve) and from the chorda
tympani, which relays taste information. With the prevalence of second molar
implants, care should be taken to note the possible position of the lingual
nerve on the medial ridge of the retromolar triangle, where it courses
anteriorly along the superior lingual alveolar crest, which is slightly lingual
to the teeth (Fig. 9.8).15
FIG 9.8 (A–B) Lingual nerve anatomy and variant positions. Note the proximity to
the crest of the ridge in the “high” variant position. A lingually placed incision or
excessive retraction may cause damage to the lingual nerve. (From Benninger B,
Kloenne J, Horn JL: Clinical anatomy of the lingual nerve and identification with ultrasonography, Brit
J Oral Maxillofac Surg 51:541–544, 2013.)
Clinical relevance.
Due to the lingual nerve's variable anatomic location, it may be iatrogenically
traumatized during various implant surgical procedures. Usually the lingual
nerve is not damaged from the actual osteotomy preparation of implants
unless the lingual plate is perforated. This sensory nerve is most likely
traumatized during soft tissue reflection during implant placement in the
second molar area or incision/reflection over the retromolar pad for bone
graft procedures. Additionally, the lingual nerve can suffer damage from
lingual flap retraction and inferior alveolar nerve blocks. Studies have shown
that lingual nerve impairment after nerve blocks occurs twice as often as
inferior alveolar nerve damage.16 This is most likely due to the fact the lingual
nerve is most commonly unifascular at the site of the injection. Sensory
damage to the lingual nerve may cause a wide spectrum of complications
ranging from complete anesthesia to paraesthesia, dysesthesia, drooling,
tongue biting, change in taste perception, and change in speech pattern.
Nerve Injuries
Etiology
Most implant-related nerve impairments are the direct result of poor
treatment planning and inadequate radiographic evaluation. Nerve trauma
occurs when the implant clinician is not aware of the amount of bone or does
not know the location of nerve canals or foramens. Preoperative planning is
crucial to determine the amount of available bone in approximation to a
nerve structure, location of vital structures, bone density, and location for
proper placement of implants. A cone beam computed tomography (CBCT)
examination is most commonly used for the three-dimensional planning in
these areas.
Nerve injuries may result from various intraoperative and postoperative
complications. Nerves may be mechanically injured by indirect or direct
trauma via retraction, laceration, pressure, stretching, and transection.
Thermal trauma may cause inflammation and secondary ischemia injuries
with associated degeneration. And lastly, peripheral nerves have been shown
to be susceptible to chemical injuries, where the nerve is directly traumatized
by chemical solutions.
Administration of Local Anesthesia

Adequate local anesthesia is paramount for successful dental implant
surgery and stress reduction protocol. However, although rare, the use of
nerve blocks may result in trauma to various branches of the trigeminal
nerve. The exact etiology of local anesthesia nerve damage is unclear, and
various theories such as injection needle trauma, hematoma formation, and
local anesthetic toxicity have been discussed. Although the true incidence is
difficult to quantify, studies have shown permanent injury occurs in
approximately 1 in 25,000 inferior nerve blocks. Most patients do recover fully
without deficits, with full recovery in 85% of patients with complete
remission in 8–10 weeks.17
Needle.
Complications resulting from needle trauma are likely the most common
theory on why nerve injury results after administering nerve blocks. First, it
is not uncommon for the tip of the needle to become barbed (damaged)
when contacting bone. Stace et al showed that 78% of needles became barbed
after initial injection, increasing the possibility of damaging the nerve. Two-
thirds of the needles developed outward-facing barbs, which have been
shown to rupture the perineurium, damage the endoneurium, and cause
transection of nerve fibers.18 The lingual nerve has been associated with the
highest percentage of nerve impairment cases as a result of an anesthetic
injection (∼70%)19. Because of the lingual nerve's anatomic location, it is
predisposed to nerve injuries because it is commonly contacted when using
the pterygomandibular raphe as an injection landmark due to the nerve
being positioned shallow in the tissue (∼3–5 mm from the mucosa).20
Hematoma.
The anesthetic needle may also cause damage to the epineurial blood vessels,
which may result in hemorrhage-related compression on the nerve fibers.
The accumulation of blood may lead to fibrosis and scar formation, which
may cause pressure-related trauma.21 The extent of impairment to the nerve
is directly related to the amount of pressure exerted by the hematoma and
recovery time of the axonal and connective tissue damage.
Anesthetic Toxicity.
If the anesthetic is injected within the fascicular space, chemical irritation
and damage may occur. Studies have shown articaine to comprise 54% of
mandibular nerve block injuries,22 and it is 21 times more likely to cause
injury in comparison to other nerve injuries.23 Theories concerning articaine
toxicity include the high concentration of articaine solution24 and the
increased resultant inflammatory reaction.25 Lidocaine has been shown to be
the least toxic anesthetic followed by articaine, mepivacaine, and
bupivacaine.26 Chemical trauma from local anesthetics has been shown to
cause demyelination and axon degeneration of nerve fibers.27
Soft Tissue Reflection

Injury to nerves and nerve fibers may occur during the reflection, retraction,
or suturing of the soft tissue. This is most noted when the mental nerve is
dehiscenced or exposed on the mandibular ridge. Special caution should be
exercised when making incisions over these areas because complete
transection injuries may occur from incisions through the nerve or foramen.
Stretching injuries (neuropraxia) may occur from excessive retraction, so care
should be noted as to the proximity of neural vital structures within the
retracted tissue. Complete transection of the nerve results from stretching
the tissue to reduce tension over the flap without regard to the anatomic
location of the nerve (Fig. 9.9).
FIG 9.9 Periosteal release of the tissue to obtain tension-free closure. (A) The use
of a #15 blade to release the periosteal fibers. (B) Blunt dissection to release tissue
with Metzenbaum scissors.
Implant Drill Trauma

Neurosensory impairment may result from direct or indirect trauma from
the osteotomy sites. Direct trauma may occur from overpreparation of the
osteotomy site or lack of knowledge of the true bur length. The implant
clinician must know and understand the true length of the surgical burs used
in the osteotomy site preparation. The marked millimeter gauge lines
inscribed on the shank of the drills most often do not include the cutting
edge of the drill and do not correspond to the actual depth of the drill. Most
drills have a sharp, V-shaped apical portion to improve their cutting
efficiency. The V-shaped apical portion of the drill (termed the “Y” dimension
in engineering) is often not included in the depth measurements of the
commercial drills and may measure as much as 1.5 mm longer than the
intended depth.
When the bone is less dense, slippage of the handpiece may occur, leading
to overpenetration. The implant clinician should use the initial implant
osteotomy twist drill as a gauge for bone density type and for an evaluation
of the position of the surgical drill relative to the mandibular canal. In
implant dentistry today the overzealous use of immediate implants has been
associated with an increase of drilling-related trauma. To gain primary
stability, most immediate implant osteotomy sites require drill preparation
and implant placement apical to the extraction site. When placing implants
in the mandibular premolar area, violation of the canal may occur, causing
nerve damage. Therefore in this anatomic area, immediate implant
placement is not recommended unless adequate bone is available below the
root apex.
The following are the types of surgical drill trauma that may lead to a
neurosensory impairment:
Drill Encroachment.
The surgical drill may cause a nerve impairment from thermal damage even
though the surgical drill does not violate the mandibular canal. Most
commonly, this is the result of insufficient irrigation, which leads to
overheating the bone. Thermal trauma may lead to nerve impairment via
bone necrosis from overheating the bone during preparation. Nerve tissue
has been shown to be more sensitive to thermal trauma than bone (osseous)
tissue. Excessive temperatures have been shown to produce necrosis,
fibrosis, degeneration, and increased osteoclastic involvement.28 To minimize
this complication the bone density should be evaluated preoperatively via
CBCT examination, tactile evaluation, and by location.
Partial Penetration.
The surgical drill may also cause direct trauma to the neurovascular bundle
by penetrating the mandibular canal or mental foramen. The neurosensory
impairment will be directly proportional to the specific nerve fascicles that
are damaged. Normally, the vein and artery, which are positioned more
superiorly than the nerve, will be damaged when penetration of the canal
results. Indirect trauma may also cause nerve damage from the excessive
bleeding (hematoma), as well as thermal and chemical injuries from the
penetration into the canal.
Transection.
The most severe type of nerve injury, with the lowest probability of
regeneration, is when the implant drill transects the canal. Because the nerve
is usually completely severed, repair and regeneration is highly variable. This
type of injury will usually result in anesthesia-type symptoms and neuroma
formation with possible dysesthesia symptoms (Fig. 9.10).
FIG 9.10 Drill impingement trauma. (A) Encroachment: even though surgical drill is
short of canal, thermal damage and bone necrosis (brown/green) result in nerve
damage. (B) Partial penetration (hematoma): the surgical drill partially penetrates the
superior aspect of the canal resulting in bleeding and hematoma formation. (C)
Partial penetration (laceration): the surgical drill penetrates deeper into the canal,
which results in laceration of nerve fibers. (D) Transection: the surgical drill may
penetrate the entire canal leading to complete transection of the nerve fibers.
Implant Encroachment on the Mandibular Canal.

Injuries to vital nerve structures due to implant positioning are most
common in the posterior mandible. These may be caused by direct trauma
(mechanical) and indirect trauma or infection (pressure). Placement of an
implant into or near the mandibular canal is associated with many types of
neurosensory impairments (Fig. 9.11).
FIG 9.11 Implant impingement trauma. (A) Encroachment: even though the implant
body is short of the canal, thermal damage may occur from overheating the bone.
(B) Bone fragments (trabeculae) may be pushed apically resulting in a pressure
necrosis nerve injury. (C) Partial penetration (hematoma): the implant body may
partially penetrate the superior aspect of the canal resulting in bleeding and
hematoma formation. (D) Partial penetration (laceration): the implant body may
penetrate deeper into the canal, which results in laceration of nerve fibers. (E)
Transection: the implant body may penetrate the entire canal leading to complete
transection of the nerve fibers.
Placement of an implant close to the mandibular canal may cause trauma

due to compression or secondary ischemia. A 2.0-mm safety zone of the
implant in proximity to the canal should always be adhered to. Studies have
shown that implant pressure on the canal occurs with increasing stress as the
bone density decreases.29 Khaja and Renton showed that placement of an
implant too close to the canal may cause hemorrhage or deposition of debris
into the canal, causing ischemia of the nerve. Even removing the implant or
repositioning may not alleviate and decrease pressure-related symptoms.
Additional studies have shown the presence of postoperative severe pain
after implant placement in close approximation to the canal resulting in
chronic stimulation and debilitating chronic neuropathy.30
Partial Penetration Into Mandibular Canal.

Placement of the implant body into the mandibular canal is associated with a
high degree of morbidity. The sensory nerve fascicles are usually inferior to
blood vessels within the canal, and the type and extent of injury is
proportional to the fibers that are damaged. This is why in some cases the
implant is directly within the canal; however, no neurosensory symptoms
exist. Additionally, implant placement into the canal may cause hematoma
formation (severing of the inferior alveolar artery or vein), leading to a nerve
impairment.
Perforation Through the Entire Canal.

Complete transection of the nerve occurs when surgical error involves the
preparation of an osteotomy too deep due to inaccurate measurements or
slippage of the handpiece. This type of injury results in the most severe of
response, a total nerve impairment (anesthesia) and neuroma formation.
Usually this type of nerve injury results in a complete anesthesia and
retrograde degeneration resulting in future dysesthesia.27 The extent of
neurosensory impairment is proportional to the extent of fascicle injury and
is dependent upon the time the implant is left to irritate the nerve fibers.
Infection.
Placement of implants in approximation to the canal may cause neurosensory
impairments via periimplant infections. Infectious processes after implant
placement may result from heat generation, contamination, or prior existence
of bone pathology. This may lead to spread of infection that may extend into
the neural anatomy. Case reports have shown nerve impairment issues
resulting from an implant infected by chronic peri-implantitis.31
Mandibular Socket Grafting.

After mandibular tooth extractions, grafting into the socket may effectively
expose the inferior alveolar nerve to socket medicaments. This may lead to
chemical neuritis and, if the irritation persists, an irreversible neuropathy
may occur (Fig. 9.12). Additionally, care should be exercised when removing
pathology and granulation tissue from extraction sockets in close proximity
to the nerve canal (type 1 nerve).32 Overzealous curretting of the socket apex
may lead to direct traumatic injury of the canal.
FIG 9.12 Postextraction site. (A) Care should be taken when grafting an extraction
site in close approximation to the inferior alveolar nerve. (B) A curette should be used
with caution because direct damage to the nerve may occur. (C) Grafting in close
approximation to the canal may lead to nerve trauma.
Delayed Nerve Damage (Canal Narrowing).

Nerve damage may result even when ideal implant placement is performed
(>2.0 mm from the nerve canal). Shamloo et al reported an implant
placement case in which the implant body caused compression and bone to
be forced into the superior aspect of the mandibular canal (canal narrowing).
This led to delayed healing and remodeling within the canal and resulted in
excessive narrowing of the canal with compression of the nerve fibers. The
narrowed aspect of the canal was shown to be approximately 0.2 mm, with an
average diameter in the nonaffected sites being approximately 3.2 mm.33 The
nerve impairment (paresthesia and anesthesia) occurred 2 years after
implant placement surgery.
Physiologic Response
The incidence of nerve impairment has been shown to be patient specific.
Studies have shown that females and older patients are at greater risk of
nerve deficits. As patients age, neural cell body regeneration has been shown
to be much slower.34 Women have been shown to have greater associated pain
and nerve impairment in comparison to men because of lower pain
thresholds, greater chance of seeking treatment in comparison to men, and
an increased tendency to communicate their problems.35
There are many local and host-related factors that determine the
neurologic response to a nerve injury. Older individuals exhibit slower and
less dramatic cell body regeneration in comparison to younger individuals.
The type of injury is the most significant local factor relating to the
neurologic response after trauma. Injuries that occur at the proximal site of
the peripheral nerve are usually more significant in comparison to those that
occur at distal sites.9 In the event any of the extraneural tissues (epineurium,
perineurium, endoneurium, or mesoneurium) are injured or traumatized,
impaired neural transmission may result in a sensory disturbance. The
resultant neurosensory impairment is dependent on the varying functional
units of the individual fiber type involved. A-alpha fibers are the largest
fibers and mediate position and fine touch by way of muscle spindle
afferents and skeletal muscle efferents. The A-beta fibers are mainly
proprioceptive in nature, and A-delta fibers mediate initial pain impulses
along with temperature information. The C-fibers are unmyelinated and slow
conducting, which allow the perception of pain and temperature.4
When complete transection of a nerve occurs, within 96 hours the proximal
end of the nerve fiber shrinks approximately 20% to 50% in diameter and
usually will not recover more than 80% of its original size.10 Shortly
thereafter, axonal nerve sprouts will seek and extend out to the degenerating
distal branch. Each axon may contain up to 50 collateral sprouts and advance
approximately 1–3 mm per day and eventually attempt to reinnervate the
target tissue. If the nerve sprouts are unable to reconnect, forward progress
is stopped and Wallerian degeneration will occur. Wallerian degeneration is
the process resulting from a damaged nerve fiber in which part of the axon is
separated from the neurons cell body. This may also be known as
anterograde or orthograde degeneration.35a Wallerian degeneration usually
results in neuroma (benign growth) formation, which is associated with
increased mechanical and chemical sensitivity, resulting in chronic
neurosensory deficits.11
Quick, immediate treatment is highly recommended in neurosensory
impairment cases. Nerve fiber atrophy has been shown to occur with trauma
over 6 hours.36 After 3 months, permanent central and peripheral changes
occur that make it unlikely the nerve will respond to surgical treatment
intervention.37 Injuries older than 6 months rarely respond to any treatment
and are usually permanent.38
Nerve Healing
After nerve injury, there exist two phases of healing, degeneration and
regeneration.
Degeneration.
There are two types of nerve degeneration: segmental degeneration and
Wallerian degeneration. Segmental demyelination occurs when the myelin
sheath is damaged and causes a slowing of the conduction velocity, which
may prevent the transmission of nerve impulses. The resulting effects will
clinically be paresthesia, dysesthesia, or hyperesthesia. The second type of
degeneration is termed Wallerian degeneration, in which the axons and myelin
sheath distal (away from central nervous system [CNS]) to the injury
undergo complete disintegration (Fig. 9.13). The axons proximal to the site of
injury (towards the CNS) undergo less degeneration, but many nodes of
Ranvier (periodic gaps in the myelin sheaths of axons that facilitate the rapid
conduction of nerve impulses) are affected. Wallerian degeneration usually
occurs after complete transection of the nerve and results in dysesthesia type
of symptoms.
FIG 9.13 Wallerian degeneration resulting with inadequate nerve repair. (From Daroff
RB, Jankovic J, Mazziotta JC, et al editors: Bradley's neurology in clinical practice, ed 7, London,
2016, Elsevier.)
Regeneration.
Usually, regeneration occurs immediately after nerve injury. The proximal
nerve area sprouts out new fibers that grow at a rate of 1.0–1.5 mm per day.
This will continue until the site innervated by the nerve is reached or blocked
by fibrous connective tissue, bone, or object (e.g., dental implant). During
the regeneration process, new myelin sheaths form as axons increase in size.
In some situations the continuity of the Schwann cells is disrupted, and
connective tissue may enter the area. The growth may find an alternative
path, or it may form a traumatic neuroma, which is usually characterized by
significant pain. Studies have shown that the administration of steroids may
minimize the formation of neuromas, especially the administration of high
doses within the first week of nerve injury (Fig. 9.14).2
FIG 9.14 Normal and abnormal nerve responses (degeneration, regeneration) to

nerve injury. (From Hupp JR, Tucker MR, Ellis E: Contemporary oral and maxillofacial surgery, ed
6, St. Louis, 2014, Mosby.)
Neurosensory Deficit Classification
There are two widely accepted classifications of nerve injuries. In 1943
Seddon postulated a three-stage classification, which was later reclassified by
Sunderland in 1951 into five different subclassifications. These nerve injury
classifications are described by the resultant morphophysiologic type of
injury, which is based on the time course and amount of sensory recovery
(Fig. 9.15).
FIG 9.15 Seddon/Sunderland Neurosensory Impairment Classification with

description of nerve damage. (From Ellenbogen RG, Sekhar LN, editors: Principles of
neurological surgery, ed 3, Philadelphia, 2012, Saunders.)
Neuropraxia, or first-degree injury, is characterized by a conduction block

with no degeneration of the axon or visible damage of the epineurium.
Usually, this type of injury is consistent with stretching or manipulation
(reflection of tissue) of the nerve fibers, which results in injury to the
endoneurial capillaries. The degree of trauma to the endoneurial capillaries
will determine the magnitude of intrafascicular edema, which results in
various degrees of conduction block. Usually, resolution of sensation and
function will occur within hours to weeks.
Axonotmesis (second-, third-, or fourth-degree injury) consists of
degeneration or regeneration axonal injuries. The injury classification
depends on the severity of axonal damage. This type of injury involves the
endoneurium, with minimum disruption to the perineurium and
epineurium. The most common type of injuries are traction, stretching, and
compression, which can lead to severe ischemia, intrafascicular edema, or
demyelination of the nerve fibers. Initially, complete anesthesia is most
common, which is followed by paresthesia as recovery begins. Improvement
of the related sensory deficits occurs within approximately 2–4 months with
complete recovery usually within 12 months. In some cases, painful
dysesthesias are possible with resulting neuroma formation.
Neurotmesis (fifth-degree injury) is the most severe type of injury, resulting
from severe traction, compression, or complete transection injuries. Initially,
patients exhibit anesthesia, followed by paresthesia with possible
dysesthesia. A very low probability of neurosensory recovery exists, with
immediate referral for a neurosurgical evaluation recommended.39,40 The axon
and encapsulating connective tissue will lose their continuity. There is
usually complete loss of motor, sensory and autonomic function. Neuroma
formation is common if transection has occurred.
Classification of Sensory Symptoms

The literature involving peripheral nerve injuries is vast, with a significant
variation in the nomenclature used to describe the associated clinical signs
and symptoms. Neurosensory impairments are classified from complete
numbness to severe pain of the facial soft tissues to the intraoral anatomy.
Because of these deficits, severe complications result for the patient and the
clinician. A thorough understanding of the associated classifications and
definitions is necessary (Tables 9.1 and 9.2).
TABLE 9.1
Neurosensory Impairment Classification and Injury Response5,6
Recovery
Sunderland Seddon Description Causes Responses
Rate
I Neurapraxia Temporary interruption of nerve transmission (Conduc tion Nerve Compression • Neuritis Complete
Bloc k) Edema • Paresthesia (Fast—
Hematoma days to
Minor S tretc hing weeks)
Thermal
II Axonotmesis Endoneurium, perineurium, and epineurium remain intac t. Nerve Compression • Paresthesia Complete
S ome axon degeneration may oc c ur Trac tion • Episodic (S low—
Hematoma • Dysesthesia weeks)
Partial Crush
Edema
S tretc hing
III Disruption of axon and c onnec tive tissue (endoneurium) Crush • Paresthesia Variable
c ausing disorganized regeneration. Punc ture • Dysesthesia (S low—
Wallerian degeneration oc c urs S evere Hematoma weeks to
S tretc hing months)
IV Damage involves entire fasc ic le. Axonal, endoneurium, Full Crush • Unlikely
and perineurium c hanges oc c ur. The epineurium is intac t. Extreme S trec thing Hypoesthesia
S c ar tissue formation. High Thermal • Dysesthesia
Direc t Chemic al Trauma • Neuroma
formation
V Neurotmesis Complete transac tion or tear of the nerve with amputation Complete Transec tion • Anesthesia None
neuroma forming at injury site (overpreparation with • Intrac table
implant drill) Pain
• Neuroma
Formation
TABLE 9.2
Description of Neurosensory Impairment Deficits7
Anesthesia Total Loss of Feeling or Sensation

Dysesthesia Abnormal sensation that is unpleasant
Allodynia Pain due to a stimulus that does not normally provoke pain
Hyperpathia Abnormally painful reac tion to a stimulus
Causalgia Persistent burning pain
Anesthetic Dolorosa Pain in an area that is anesthetic
Hyperesthesia Inc reased sensitivity to stimulation
Hyperalgesia Inc reased response to a stimulus that is normally painful
Paresthesia Abnormal sensation that is not unpleasant
Hypoesthesia Dec reased sensitivity to stimulation
Hypoalgesia Dec reased response to a stimulus that is normally painful
S ynesthesia S ensation felt in an area when another area is stimulated
To standardize the nomenclature concerning nerve injuries, the

International Association for the Study of Pain reduced sensory impairment
into three categories: anesthesia, paresthesia, and dysesthesia.40a Anesthesia is
characterized by the complete lack of “feeling,” which is usually consistent
with complete transection of the nerve. This type of altered sensation is most
severe because anesthesias are the most difficult and unpredictable to treat
with a high incidence of neuroma formation. Paresthesia is defined as an
altered sensation that is not unpleasant. It is usually characterized as a “pins
and needles” feeling. Within the paraesthesia category, many subcategories
exist including hypoesthesia (decreased sensitivity to stimulation),
hypoalgesia (decreased response to a stimulus that is normally painful), and
synesthesia (sensation in an area when another is stimulated). Dysesthesias
are classified as an altered sensation that is unpleasant. Usually pain is
associated with this type of impairment, which may be spontaneous or
mechanically evoked. Subcategories include hyperalgesia (painful response
to nonpainful stimuli), hyperpathia (delayed or prolonged painful response),
anesthetic dolorosa (pain in an area that is anesthetized), causalgia
(persistent burning pain), and allodynia (pain in response to a stimulus that
usually does not provoke pain).
Treatment
Nerve Impairment at Time of Surgery
During surgery, if known traction or compression of the nerve trunk has
occurred, the topical application of Dexamethasone may be used to minimize
deficits. Upon removal of an encroaching implant on the mandibular canal,
1–2 mL of the intravenous form of Dexamethasone (4 mg/mL) is topically
applied (Fig. 9.16). This direct steroid application will reduce neural
inflammation and may enhance recovery from neurosensory deficits. Studies
have shown no morbidity associated with the topical application of
glucocorticoids at the injury site and postsurgical recovery has also been
shown to improve significantly.12 No bone grafting or implant should be
placed that may lead to irritation of the traumatized nerve fibers.
FIG 9.16 (A) Dexamethasone 4 mg/mL. (B–C) 1–2 mL of dexamethasone placed
into osteotomy site.
Nerve Impairment Postoperatively

When a neurosensory deficit occurs postoperatively, a comprehensive
sensory evaluation must be completed. This initial examination is used to
determine whether a sensory deficit exists, to quantify the extent of injury,
document a baseline for recovery, and to determine if referral for
microneurosurgery is indicated.
Step 1: Clinical Assessment.

The implant clinician must first determine if a neurosensory deficit exists by
mapping the area of deficit. This diagnostic examination consists of objective
and subjective findings to determine the extent of impairment, to use as a
baseline for future evaluation, and to determine when referral for surgical
intervention is required.
The subjective clinical sensory tests involve nociceptive and
mechanoceptive examinations. Nociceptive tests trigger a variety of
autonomic responses that result in the subjective experience of pain.
Mechanoceptive tests utilize mechanical stimuli to trigger sensory neurons
that elicit various responses such as touch, position and motion (Table 9.3
and Fig. 9.17).
TABLE 9.3
Nociceptive and Mechanoceptive Diagnostic Tests
Diagnostic Test Description

Nociceptive
Pin pressure (A- Determination of feeling from pin pressure using a blunted explorer. A normal response (distinc t sharp pain) is a positive
Delta, C-Fiber) sign of feeling (in relation to an unaffec ted area) with no pain. If no feeling is present in c omparison to an unaffec ted side,
the area is termed hypoa lgesia . If an exaggerated response is noted in relation to an unaffec ted side, the area is termed
hypera lgesia .
Thermal Ic e c hips or ethyl c hloride spray and a heated mirror handle (warmed to 43°C) are used to determine the patient's ability to
disc rimination feel c old and hot.
(warm: A-Delta:
c old: C-Fibers)
Mechanoceptive
S tatic light touc h Cotton tip applic ator with the patient's eyes c losed to test tac tile stimulation by gently touc hing the skin and determining
the threshold of the patient. (A-beta afferent axons.)
Direc tional S oft brush is used to determine the patient's ability to detec t both sensation (A-beta and A-alpha axons) and direc tion of
movement movement. The soft brush is swiped from left to right, as well as in the reverse direc tion.
Two-point With the patient's eyes c losed, the patient's ability to disc riminate varying (myelinated A-alpha fibers) distanc es between
disc rimination two points is determined using a c aliper. The normal values vary signific antly, with the average being approximately 5
mm.71
FIG 9.17 Sensory testing. (A) Mapping out deficit with eyeliner. (B) Light touch with
cotton applicator. (C) Directional test with brush. (D) Two-point discrimination
utilizing calipers. (E) Thermal test with mirror handle. (F) Pin-point tests with
explorer or dull needle.
Clinical examination complications.

There exist many inherent problems with relying on the credibility of the
patient's subjective responses. Because there may exist a high degree of false-
positive and false-negative results, clinicians should utilize clear and concise
instructions when administering these tests. For instance, when
administering the “directional movement” test, the clinician should
complete this test on the contralateral side first so the patient understands
the technique and response. The results of the subjective clinical examination
will depend on good communication between the implant clinician and the
patient, with the outcome of the results related to the patient's perceived
interpretation and how to relate their perceptions. Additionally, the tests
should be administered with the patient's eyes closed, so as to minimize the
possibility of incorrect responses.
Step 2: Radiographic Evaluation/Removal or Repositioning of

the Implant.
A thorough and comprehensive radiographic examination should be
completed including (ideally) a CBCT radiograph. If the implant (or bone
screw) is in close approximation of the nerve bundle, removal or
repositioning should be completed. Care should be exercised in “backing”
the implant out (repositioning farther from the nerve) because trauma to the
nerve may still be present from hematoma formation or pressure from
cancellous bone crushed into the neural space. Additionally, backing the
implant out may lead to the implant being positioned undesirably because of
lack of interocclusal space for the restoration (i.e., too coronally positioned).
In these cases, the implant should be removed and the osteotomy site
irrigated with 4% Dexamethasone (1–2 mL). No graft materials should be
added to the osteotomy site because they may interfere with the
reinnervation and repair of the nerve trunk.41
Step 3: Pharmacologic Intervention.

Immediately after the nerve is traumatized, the inflammatory process begins
with the activation of cytokines and inflammatory mediators. These
inflammatory mediators will contribute to the development of nerve trauma
by activating the neurons and their nociceptors.42
With any type of nerve impairment, corticosteroids or nonsteroidal
antiinflammatory agents should be used immediately. Studies have shown
that the use of systemic adrenocorticosteroids (e.g., Dexamethasone)
minimizes neuropathic symptoms following nerve trauma if administered in
high doses within 1 week of injury.43 It has been advocated that a tapering
dose of a corticosteroid for 5–7 days following trigeminal nerve injury is
beneficial.44 Dexamethasone (∼8 mg) is specifically recommended because
of its greater antiinflammatory effects in comparison to other corticosteroids
such as methylprednisolone or prednisone. Additional pharmacologic agents
include antidepressants, neurologic drugs, antisympathetic agents, and
topical agents.
Additionally, cryotherapy (ice packs) should be applied to the paraneural
tissues intensely for the first 24 hours and then episodically for the first
week. Cryotherapy has been shown to be beneficial in minimizing secondary
nerve injury from edema-induced compression, decreasing the metabolic
degeneration rate of trigeminal ganglion cells and slowing potential neuroma
formation.45 Additional physiologic agents include transcutaneous electric
nerve stimulation, acupuncture, and low-level laser therapy.
Step 4: Possible Referral.

In certain situations, patients may need to be referred in a timely manner to
a practitioner experienced in nerve injury assessment and repair. The
decision and timing to refer should be based on the patient's symptoms and
the type of injury, along with the experience of the implant dentist in treating
nerve injuries. Usually, sufficient time is given for neurosensory recovery. In
cases of dysesthesia, anesthesia, or known nerve transection, prompt surgical
intervention may allow for the best chance of neurosensory recovery. Early,
aggressive treatment has been shown to minimize possible transition to
chronic refractory neuropathies (Table 9.4).16
TABLE 9.4
Neurosensory Deficit Treatment Algorithms
P harmacologic
P ostsurgery Documentation Treatment Referral
Intervention
≈48 hr 3-D radiographic examination (CBCT); Cortic osteriods Implant evaluation: None, unless unfamiliar
neurosensory examination (Dexamethasone 4 Removal or reposition if with neurosensory
mg) impingement within the testing
2 tabs AM for 3 days mandibular c anal
1 tab AM for 3 days No bone grafting
Cryotherapy (1 week)
1 week Neurosensory examination (Testing High-dose NS AIDs Palliative Refer to Oral S urgeon
postoperative should be c ontinued every 2 weeks (600–800 mg ibuprofen or Neurosurgeon if:
thereafter) TID) • Known nerve
transec tion
• Dysesthesia
• Complete anesthesia
8 weeks Neurosensory examination NS AIDs (PRN) Palliative IF NO S IGN OF
postoperative IMPROVEMENT
Refer to OMFS or
mic roneurosurgeon
Step 5: Follow-Up Care.

Follow-up care should always be a component of the treatment of a nerve
impairment patient. The interval between appointments is determined by the
extent and type of nerve injury (see Table 9.4). Usually, after the one week
postoperative, patients are seen every 2 weeks with mapping and
documentation of the deficits noted.
Surgical Intervention
In some cases of neurosensory impairment, surgical repair is indicated. In
general, early treatment is crucial to success and decreased morbidity.
Microneurosurgical procedures include direct nerve repair via primary
anastomoses of the two severed ends for transection injuries. For nerve
splits, reestablishment and proper alignment of nerve stumps will allow for
the best chance to correct regeneration of the damaged nerves (Fig. 9.18).
FIG 9.18 Nerve repair. (A) Mandibular internal fixation screws in a 29-year-old
patient with right inferior alveolar nerve (IAN) sensory dysfunction after sagittal split
ramus osteotomy. (B) The IAN was not directly contacted by any of the screws, but
there is a proximal stump neuroma (arrow) and a thin stalk of scar tissue, containing
no viable nerve tissue, which extends between the proximal and distal nerve
(supported by nerve hook) stumps. (C) The proximal stump neuroma has been
excised and the two nerve stumps have been prepared for microsurgical repair. (D)
The right IAN has been reconstructed with an autogenous right great auricular nerve
graft (arrows at sutured areas). (From Bagheri SC, Meyer RA, Khan HA, et al: Microsurgical
repair of the peripheral trigeminal nerve after mandibular sagittal split ramus osteotomy, J Oral
Maxillofac Surg 68:2770–2782, 2010.)
Prevention
Iatrogenic injuries to the third division of the trigeminal nerve pose a
common and complex problem in implant dentistry today. Neurosensory
impairment in the head and neck region may affect the patient's quality of
life and can present potentially significant medicolegal problems for the
clinician. To prevent damage to vital nerve structures, it is imperative for the
implant dentist to have a comprehensive radiographic survey of the region, a
thorough knowledge of the normal vs. variant anatomy, and awareness of
intraoperative surgical techniques to minimize the possibility of nerve
impairment.
Radiographic Considerations
Understand Disadvantages and Limitations of Two-

Dimensional Radiography.
Today, the sole use of two-dimensional radiography is becoming less
common for treatment planning of dental implant patients. Two-dimensional
radiographs, mainly panoramic, have many inherent disadvantages in
evaluating potential implant sites. All panoramic (2-D) radiographs exhibit
some degree of distortion, nonuniform magnification, and image
superimposition, which can potentially lead to incorrect measurement and
assessment of neural structures. Studies have shown periapical and
panoramic radiography to be unreliable in assessing the true location of the
inferior alveolar canal and the mental foramen.46 Extreme caution should be
exercised when using two-dimensional radiography as the only modality for
implant site evaluation (Fig. 9.19A–B).
FIG 9.19 (A) 2-D panoramic radiographs exhibit many inherent inaccuracies and
should never be solely relied upon in making measurements because they provide
nonuniform magnification. (B) Magnification may be determined in the vertical plane.
Horizontal magnification is completely unreliable and inaccurate. (C) Magnification
(25%) guides are superimposed over two-dimensional radiographs, but they often
lead to misrepresentation of available bone.
Do Not Use Two-Dimensional Magnification Guides.

Manufacturers have made available to implant dentists magnification guides
and digital software programs for intraoral radiographs to assist in the
placement of implants over vital structures. Caution should be noted that
panoramic radiographs have variable magnification (i.e., not 25% as related
by many implant and panoramic companies), and even calibrated intraoral
software programs cannot accurately assess true distances because of their
two-dimensional origin. Both periapical and panoramic radiography are
associated with magnification that is inconsistent and difficult to determine.
Schropp et al have shown that over 70% of cases in which implant size was
initially determined via panoramic radiographs the size had to be altered
after CBCT evaluation.47 Magnification guides should never be used as the
sole criteria for implant site evaluation because they may lead to
overestimation of available bone dimensions (Fig. 9.19C).
Three-Dimensional Radiography Is the Most Accurate Type of

Radiographic Modality.
In most cases, a three-dimensional radiographic modality is recommended
for evaluation of the mandibular arch and related nerve anatomy. To
determine the ideal location and measurement parameters associated with
the dental implant placement, the clinician must be able to accurately
measure the distance between the alveolar crest and the superior border of
the mandibular canal, as well as the width of bone in the proposed implant
site. Medical slice computed tomography (MSCT) and CBCT images have
been shown to be the most accurate radiographic modalities in the
assessment of available bone and identification of the inferior alveolar
nerve.1,48 A thorough knowledge of the relative three-dimensional (3-D)
position of the inferior alveolar nerve is crucial in preventing mandibular
nerve impairment prior to implant placement (Fig. 9.20A).
FIG 9.20 (A) CBCT images have no magnification and are 1 : 1 and can be relied
upon for measurements that approximate vital structures. (B–C) Third-party
interactive software programs showing implant placement via integrated software
program.
Use Interactive Treatment Planning Software for Evaluation of

the Posterior Mandible.
Because MSCT and CBCT have been proven to be 1 : 1 (no magnification), the
implant dentist has the ability to place implants, measure available bone,
evaluate bone density, and order surgical templates directly from their
computerized treatment plan. Interactive treatment planning software
programs available today contain libraries of most implants systems, which
allow the clinician to accurately access the size, type, and ideal placement of
the implant in relation to anatomic structures. This virtual treatment plan
may then be transferred to the patient's surgery by means of a surgical
template or computer-assisted navigation system (Fig. 9.20B–C).
Use of Bone Models.

For implant dentists early on their learning curve, the fabrication of a bone
model can be an invaluable preoperative diagnostic tool. Bone models are
made directly from the CT Dicom data, which involves a third-party vendor
fabrication through some type of 3-D printer, such as stereolithography. The
clinician is able to evaluate the exact osseous morphology (width of bone,
undercuts, bony landmarks) and location of vital structures (color coded
within the model) prior to the actual surgery. Implant osteotomies may be
performed in a laboratory setting to allow the implant dentist to complete
the procedure prior to surgery.
Use of Surgical Templates.

Neurosensory impairment issues are most frequently an inadvertent sequela
of improper diagnosis, treatment planning, or surgical technique. Many of
these complications can be overcome by using three-dimensional surgical
guides for the ideal positioning and placement of implants. Basically, the
surgical guide is the conduit for transferring the interactive treatment plan
from the computer to the patient's actual surgical procedure. This allows the
implant dentist to be able to place the implants in the exact location as per
the treatment plan. Surgical guides are categorized based on method of
retainment: tooth, bone, or mucosa supported. SIMPLANT Safe Guide
(DENTSPLY Implants) gives the practitioner the ability to place the implant
via an interactive treatment plan in the mesiodistal, buccal-lingual, and
apicocoronal dimensions via three types of guides. Guided surgery with
surgical templates has been reported to improve the accuracy of implant
placement in clinical situations in comparison to conventional surgical
methods (Fig. 9.21).49 Nickenig et al showed that implants placed with
surgical templates were within 0.9 mm of the planned positions, whereas
free-hand placement resulted in deviations of approximately 2–3 mm.49a
FIG 9.21 Stereolithographic bone models. (A) Depicting exact location of IAN canal
and mental foramen for implant placement. (B) Bone-supported SurgiGuide
(Materialise Dental) placing posterior mandibular implant. (C–D) Simplant Safe
Guide; implant being placed through guide. (E) Bone model showing ramus bone
graft with the IAN depicted in red. (C, Courtesy Dentsply Sirona Implants, Waltham, MA.)
Anatomic Considerations: Mandible
The Position of the IAN is Variable and Not Consistent in the

Vertical (Inferior-Superior) Plane.
There is a common belief that the vertical position of the inferior alveolar
nerve is relatively constant within the mandible. Normally, the IAN runs a
concave path from posterior to anterior, with anterior segments exiting the
mental foramen and a branch that ascends to the midline of the mandible.
However, studies have confirmed the inferior-superior (vertical) positions of
the inferior alveolar nerve are not consistent.50,51 An early classification of the
vertical positions of the course of the alveolar nerve was reported by Carter
and Keen.52 They described three distinct types: (1) in close approximation to
the apices of the teeth, (2) a large nerve approximately in the middle of the
mandible with individual nerves supplying the mandibular teeth, and (3) a
nerve trunk close to the inferior cortical plate with large plexuses to the
mandibular teeth. In type 1 nerves, impairment is very common because of
the close proximity to the nerve bundle. Three percent of patients can have
the IAN directly contacting one or both of the roots of the mandibular first
molar.53 It is highly recommended that a comprehensive radiographic survey
be completed to evaluate the IAN in a vertical plane, especially with type 1
and 2 nerves (Fig. 9.22).
FIG 9.22 (A) Inferior alveolar nerve. (B) Type 1 nerve (arrow). (C) Type 2 nerve. (D)
Type 3 nerve.
The Position of the IAN is Variable and Not Consistent in the

Buccal-Lingual Plane.
Studies have shown the buccal-lingual location of the IAN as it progresses
anteriorly is not constant. The nerve paths have been described in a buccal-
lingual direction with a high degree of variability and are dependent on the
amount of bone resorption as well as age and race variables.54 Additionally,
older and Caucasian patient groups have shown less distance between the
buccal aspect of the nerve and the inferior border of the mandible.55 Other
studies have shown the most common area for the IAN to be in the middle
of the buccal and lingual cortical plates is the first molar region.56 Thus, in
the buccal-lingual plane, three-dimensional cross-sectional images should be
utilized to determine the true position of the nerve (Fig. 9.23).
FIG 9.23 Cross-sectional image showing variability of the IAN in buccal-lingual

position. (A) Buccal orientation. (B) Lingual orientation.
Understand the Variations of the Mental Foramen Location.

Determining the exact location of the mental foramen is crucial when placing
implants in the posterior mandible. Although the foramen has been shown
to be symmetrical to the contralateral side in most patients, the location has
been shown to be highly variable.57 The mental nerve passes through the
mental foramen with three nerve branches. One innervates the skin of the
mental area, and the other two proceed to innervate the skin of the lower lip,
mucous membranes, and the gingiva as far posteriorly as the second
premolar. Any trauma to this nerve will result in neurosensory impairment in
this area. Clinically, there are many different techniques in identifying the
foramen with a wide variation of predictability.
Palpation.
In rare cases, the implant dentist may be able to palpate the location of the
mental foramen. Most notably, when bone resorption has caused the nerve to
be exposed on the residual ridge, the concavity formed by the exposure of the
nerve can be determined. In these cases, the location of the mental foramen
may be marked with a surgical pen. When the nerve is located on the buccal
surface of the mandible, the palpation method of identification has very low
utility (Fig. 9.24A).
FIG 9.24 Location of the mental foramen. (A) Palpation can be misleading and
should not be used as the sole technique of mental foramen identification. (B)
Anatomic location with respect to the teeth apices is highly variable—cuspid/molar
position (green circles); first premolar (red circle); first/second premolar (yellow
circle); second premolar (blue circle)—and is dependent on gender, age, and race.
(C) Anatomic location: a vertical line through pupils of eyes and infraorbital foramen
or a finger width lateral to ala of the nose. (D) Direct exposure of the foramen with
the use of calipers to measure distance.
Anatomic landmarks.
In the literature, many authors have postulated that landmarks such as teeth
and mandibular bony areas may help identify the location of the mental
foramen. With respect to teeth, the location cannot conclusively be associated
with a particular tooth (e.g., first premolar, second premolar, between apices
of the premolars) because studies have shown the location to be dependent
on gender, age, and race.58 Certain bony landmarks (e.g., alveolar ridge,
mandibular symphysis, infraorbital foramen) have been associated with a
general location of the foramen, although these measurements are extremely
variable and dependent on the extent of bone resorption, skeletal
relationships, and anatomic variants (Fig. 9.24B–C).
Two-dimensional radiographs.
Studies have shown that in over 50% of periapical and panoramic
radiographs, the mental foramen is not in the location depicted on the two-
dimensional image.46 Conventional two-dimensional radiography should
never be used as the sole diagnostic modality in evaluating the foramen
position.
Three-dimensional radiography.
The literature has shown that 3-D imaging is the most accurate tool to
ascertain the exact location of the mental foramen. CBCT panoramic images
and 3-D images are the easiest and most accurate technique in determining
the exact foramen location.
Direct evaluation.
The most precise technique available today to find the exact location of the
mental foramen is by direct evaluation. Exposing the mental foramen may be
intimidating to some clinicians, especially early on their learning curve. This
can be accomplished with very low morbidity; however, the technique's
success depends on the implant dentist's training and experience (Fig.
9.24D).
3-D ultrasound.
The most promising imaging technique for the future is ultrasound.
Ultrasound has the advantage of no ionizing radiation and the ability to
reconstruct 3D images of bone surfaces to within an accuracy level of 24 µm.
At this time, ultrasound units are not available specifically for dental use.
Always Evaluate for an Accessory (Double) Foramen.

Studies have shown that in approximately 10% of patients, an accessory
(double) foramen is present.58 In the majority of cases, small accessory
foramina usually contain a small branch of the mental nerve and are not
problematic because of cross innervation or actually contain nutrient
branches. However, in a small percentage of cases, a larger branch of the
mental nerve (equal or larger size foramen) may exit the second mental
foramen. Special care should be extended in this situations because it may
contain components of one of the three branches of the mental nerve.
Accessory foramina are believed to be the result of early branching of the
inferior alveolar nerve, prior to exiting the mental foramen during the 12th
week of gestation.59 Double foramens are easily seen in the 3-D or the coronal
CBCT images (Fig. 9.25).
FIG 9.25 (A) Accessory nerve anterior to main foramen. (B) Double foramens
showing two large foramens. (C) Coronal image showing two nerve foramina.
Evaluate for Anterior Loops of the Mental Nerve.

As the mental nerve proceeds anteriorly in the mandible, it sometimes runs
below the lower border and the anterior wall of the mental foramen. This
anterior and caudal component of the mental nerve will curve cranially back
to the mental foramen. This anterior and caudal part of the mental nerve is
termed the anterior loop.59 Recently, studies have shown a higher percentage
(70%) prevalence of anterior loops with a mean of 1.16 mm distance
anteriorly. The anterior loop may be depicted most predictably on axial CBCT
images, with 2-D radiographs being totally unreliable.
Determining the presence of an anterior loop is critical when placing
implants anterior to the mental foramen. Inability to ascertain the presence
of an anterior loop may result in damage to the mental nerve (Fig. 9.26). The
anterior loop measurement should be added to the safe zone to avoid
damaging the mental nerve.
FIG 9.26 (A) An anterior loop showing nerve anterior to foramen. (B) Modification of
safe zone with consideration of anterior loop. The anterior loop measurement is
added to the 2-mm safe zone.
Do Not Confuse the Incisive Nerve Branch as an Anterior

Loop.
The incisive nerve branch, a continuation and terminal branch of the IAN,
supplies the mandibular canine and incisor teeth. Because there is no
sensory innervation with this nerve, implants may be placed in proximity to it
without nerve impairment. Studies have shown incisive canals have a mean
diameter of 1.8 mm and location 9.7 mm from the lower cortical border.60 The
incisive nerve has been recognized as an important anatomic structure that
must be taken into consideration when performing surgery in this area. It is
frequently mistaken as an anterior loop in the mandible. Excessive bleeding
has been reported as a significant intraoperative complication in this area
when it is perforated during osteotomy preparation (Fig. 9.27).
FIG 9.27 CBCT panoramic image depicting incisive branch of IAN (arrow).
Intraoperative Considerations
Utilize the Misch “Zone of Safety” Principle.

To determine the ideal position of implants with respect to the inferior
alveolar or mental nerve, Misch, in 1990, identified the “zone of safety”
concept. With this technique the mental foramen is directly identified and a
measurement from the superior aspect of the foramen to the residual ridge is
determined. Research has shown that implants can be placed at this height
measurement 100% of the time posterior to the middle half of mandibular
first molar and 97.5% of the time to the distal of the first molar. The
corresponding safety height measurement extends posterior to the mesial
half of the second molar 43% of the time.61
Maintain a Safety Zone of 2 mm Upon Osteotomy Preparation

and Final Implant Positioning.
A 2-mm safety zone with osteotomy preparation and final implant placement
is paramount in preventing neurosensory impairments.41 Compression-
related injuries (neuropraxia) can occur by encroaching on the IA nerve
without actual contact. Nerve impairments have been reported when
implants are placed less than 2 mm from the canal without invasion of the
canal. Bleeding and resultant hematomas have been shown to cause nerve
damage because of final positioning too close to the neurovascular canal.62
Additionally, the IAN superior to cortical bone can be compressed, causing
pressure necrosis with resultant nerve impairment.63 Interactive treatment-
planning software programs allow the implant clinician to accurately assess
the ideal placement with respect to this vital structure (Fig. 9.28).
FIG 9.28 (A) Ideal placement >2.0 mm from nerve. (B) Simplant Software with 2.0-
mm safety zone for interactive planning. (C) Nerve impairment can be caused from
compression necrosis (arrow).
Understand the “True” Implant Bur Drilling Depths.

Care should always be exercised when performing osteotomies over vital
structures, especially in the posterior mandible. The implant clinician should
double-check the marking depth on the burs prior to initiating the
osteotomy. The principle of “MEASURE TWICE, DRILL ONCE” should be
followed to prevent iatrogenic overpreparation of the implant site.
Additionally, the “Y” dimension of the implant system being used must be
known. As noted earlier, the depth of the millimeter lines inscribed on
surgical drills do not always coincide with the actual depth of the drill. Most
drills contain a V-shaped apical portion designed for cutting efficiency (“Y”
dimension). Usually, the wider the drill, the greater the “Y” dimension. The
implant clinician should always evaluate the manufacturer's drill length with
respect to the length of the implant prior to performing the osteotomy. If this
concept is not adhered to, overpreparation of the site may occur, resulting in
nerve damage (Fig. 9.29).
FIG 9.29 (A) Ideally, measure all burs before performing osteotomy. (B) “Y”
diameter of surgical burs. (C) CBCT image showing penetration from “Y” dimension
into mandibular canal. (A, From Misch CE, editor: Contemporary implant dentistry, St. Louis,
2008, Mosby.)
Use Drill Stop Burs to Prevent Overpreparation.

An additional technique to prevent overpreparation of the osteotomy site is
the use of stop drills. These drills have a predetermined depth marking that
prevents overpreparation. Stop drills are very beneficial in the mandibular
posterior area, especially when visibility and access is compromised. Generic
drill stop kits are also available that may be used with most implant surgical
systems (Salvin Dental Corp.). These autoclaveable, reusable kits may be
used for any size length implant and corresponding drill (Fig. 9.30).
Additionally, some surgical implant systems have specific depth burs that
coincide with the actual implant depth (e.g., Hahn Implants, Glidewell
Corp.).
FIG 9.30 (A) Drill Stop Kit. (B) Sequential surgical drills with stops that prevent
overpreparation. (A, Courtesy Salvin Dental Specialties, Inc., Charlotte, NC. B, Courtesy Dentsply
Sirona Implants, Waltham, MA.)
Understand Bony Crest Anatomy.

Due to resultant bone resorption after extraction, the alveolar ridge becomes
compromised in width (Division B bone) at the expense of the buccal plate.
When measuring available bone height, special consideration should be
given to the final location of the superior aspect of the implant platform, not
the crest of the ridge. It will often appear that there is adequate vertical
height for implant placement; however, when the osteotomy is initiated, the
thin crest will be lost and the implant will be placed inferior to where it was
originally intended. This can lead to unexpected depth drilling and an
implant that is placed too close to the vital structure. The clinician should
either augment the ridge to maintain vertical height or reduce the height
calculation by the amount of osteotomy induced osteoplasty (Fig. 9.31).
FIG 9.31 (A) Panoramic showing available bone above the IAN canal; however, it
does not depict the width of bone. (B) If ridge is Division B (compromised in width)
after osteotomy the crestal bone will be removed. (C) Implant placed at position that
has adequate width; however, it will impinge on the vital structure. (D) Ideal selection
of implant (decreased length) to maintain 2-mm safety zone.
Maintain Total Control of the Handpiece.

When performing osteotomies in the posterior mandible, special care should
be noted to maintain complete control of the surgical handpiece. Large
marrow spaces (i.e., where there is a lack of or thin trabecular bone) are often
present, which may allow the osteotomy site to become deeper than
intended. This will result in the implant being placed more apically, leading
to neurosensory impairment. A MSCT or CBCT comprehensive evaluation
allows the implant dentist to view the bone quality prior to surgery. Many
third-party implant-planning programs allow the clinician to ascertain the
density in the intended site. The implant clinician may also determine the
bone density by tactile sensation when drilling. Additionally, when drilling
the osteotomy near the mental foramen, care should be exercised not to bend
the wrist. This can potentially redirect the drill or implant placement in an
unwanted direction (e.g., near the mental foramen, into a tooth root).
Surgical templates and guides are beneficial in preventing this
malpositioning complication (Fig. 9.32).
FIG 9.32 (A) Ideal placement with respect to the nerve. (B) Misdirection of the
implant from improper drilling technique. (C) When drilling osteotomy, wrist should
never be bent.
Do Not Place Bone Graft Material in Close Approximation to

Nerve.
After tooth extractions, especially in the mandibular premolar areas, care
should be exercised in placing bone graft material (autologous, allogenic,
xenogenic) in direct contact with an exposed IAN. Whether socket grafting or
in conjunction with implant placement, case studies have shown resultant
neurosensory impairment from bone graft material causing compression,
crushing, or chemical burn injuries.64 When socket grafting in this area,
excessive pressure should be avoided.
Use Copious Amounts of Irrigation.

Overheating the bone during osteotomy preparation may produce thermal
stimuli that may lead to periimplant necrosis and secondary postoperative
nerve damage. Neural tissue is extremely sensitive and damaged by heat
stimuli. The thickness of the necrotic area is proportional to the amount of
heat generated during preparation.65 The implant dentist must be cautious to
not overheat the bone. This can be minimized by “bone dancing,” which
involves drilling in short intervals and allowing irrigation to enter the
osteotomy, preventing heat generation. Additionally, new (sharp) and
intermediate-sized drill burs may be used to reduce heat generation. This is
more crucial with harder bone density (e.g., D1 or D2) or bone with
compromised vascularity (Fig. 9.33).
FIG 9.33 (A) During osteotomy preparation, copious amounts of irrigation must be
used to decrease heat most commonly with the use of a SurgiGuide. (B) Internally
cooled drill. (B, Courtesy FFDM PNEUMAT—Département Dentaire THOMAS, Bourges Cedex,
France.)
Avoid Incision-Related Injuries.

There should be an awareness when making incisions near the location of the
mental foramen and associated nerve structures in the posterior mandible.
In cases of severe bone atrophy, the presence of nerve dehiscence may
inadvertently result in a transected nerve during the initial incision (i.e.,
making incision on the crest of the ridge). Anatomic landmarks, 3-D models,
accurate measurements from CBCT scan, or palpation of the nerves are ways
to avoid this complication. Additionally, incisions in the posterior of the oral
cavity should never be made over the retromolar pad. This can result in
possible injury to the lingual nerve, which in 10% of cases transects this area
(Fig. 9.34).
FIG 9.34 Incision-related injury. (A) Bilateral nerve dehiscence. (B) Incision needs
to be modified to decrease chance of nerve damage as crestal incision will transect
nerve. (C) Incision should be made lingual when nerve dehiscence is present.
Avoid Flap/Retraction-Related Injuries.

Neurosensory impairments may also occur from overzealous use or incorrect
placement of retractors. Broad base (not sharp) retractors should be used to
retract tissue that is not directly over the mental foramen because excessive
stretching of the nerve trunk may cause irreversible damage. It is imperative
that the mental foramen and associated branches of the mental nerve be
identified in this area when placing retractors. Retractors should always be
placed and held on the bone to prevent slippage or excessive soft tissue
pressure, which can lead to a neuropraxia type of nerve damage (Fig. 9.35).
Excessive stretching of the tissue may also lead to neurosensory
impairments. It has been shown the perineurium protects the fascicles;
however, if greater than 30% elongation of the nerve occurs, structural
damage will occur to the nerve fibers.65a
FIG 9.35 (A) Avoid direct pressure on mental foramen from retractor. (B) Be
cautious when stretching tissue near the branches of the mental nerve. Note the
sharp damaged retractors that may cause tissue damage.
Use Special Care When Releasing Periosteum Over Mental

Foramen.
It is a common procedure during closure after implant placement or bone
grafting to stretch the periosteal tissue to allow primary and “tension-free”
closure. Various techniques are used to “release” the tissue to improve
vascularization of the incision line and adhesion of the margins to prevent
incision line opening. The submucosal technique developed by Misch in 1988
is an effective method to expand the tissue. This procedure involves the use
of a #15 scalpel blade and soft tissue scissors (i.e., Metzenbaum) to create a
blunt dissection. Knowledge of the location of the three mental nerve
branches is necessary because inadvertent incisions over the mental nerve
branches may result in neurotmesis (transection) type of nerve injuries.
Careful Suturing.
When the mental nerve is exposed, care should be exercised to prevent nerve
tissue from being entrapped within the sutures. The mental nerve emerges
from the mental foramen and divides into three branches below the
depressor anguli oris muscle. Caution must be exercised to prevent any of
the mental nerve branches from becoming entrapped within in the suture
material, potentially causing a neuropraxia (compression) type of nerve
injury. Additionally, nerve fibers may be damaged from the passage of the
extremely sharp suture needle through the tissue (Fig. 9.36).
FIG 9.36 Placement of suture should be carefully assessed to prevent nerve tissue
from becoming entrapped within suture line.
Verify Correct Positioning of CBCT SurgiGuides.

Studies have shown that the most precise and accurate surgical templates are
tooth supported. When using bone- or tissue-supported surgical guides, care
must be exercised to correctly position the guide because an error in
placement may result in direct damage to the IA nerve. Tooth-supported
guides should always be the first choice if possible because they are clinically
proven to give rise to the fewest positioning errors. The least accurate is the
mucosa supported, which are most utilized for flapless surgery.66 Studies
have shown that flapless surgical guides consistently show deviations of
implant positions from ideal locations. Perforations of the buccal plate can be
found in over 50% of the flapless cases.67 A very minor discrepancy
(anterioposterior) in the placement of the guide can lead to impingement on
vital structures (Fig. 9.37). Therefore, surgical templates should always be
fixated and ideal position verified.
FIG 9.37 Tissue-borne surgical template fixated with palatal screw to prevent
movement of the template.
Miscellaneous Alternative Surgical Techniques
Avoid Immediate Implants in the Mandibular Premolar Area.

Immediate implants have gained overwhelming popularity in implant
dentistry today. Extreme caution must be exhibited when extracting and
immediately placing implants in the mandibular premolar area. As noted,
there are many variables that dictate the position of the mental foramen, with
the foramen being highly variable. Studies have shown that 25% to 38% of
the time the mental foramen is superior to the premolars apex.58 Because
most immediate implant osteotomy sites involve drilling the osteotomy site
deeper for stability, chances of nerve trauma are greatly increased. Because of
this the implant clinician must be very selective in cases involving extraction
and immediate implant placement in this anatomic area (Fig. 9.38).
FIG 9.38 (A) CBCT revealing close proximity of root apex to mental foramen. The
root apex is inferior to the mental foramen. (B) Complications arising from
simultaneous extraction and implant placement in premolar area. (C) Implant placed
into mental foramen location.
“Drill Until the Superior Cortical Plate Is Felt.”

It has been advocated in the literature that the osteotomy depth maybe
determined by “feeling” the superior cortical plate of the inferior alveolar
canal. A 2-mm safety zone should always be adhered to because research has
shown in approximately 28% of posterior mandibles, there is no superior
cortical plate over the inferior alveolar canal.68 Additionally, studies have
shown it to be impossible to use tactile sense to ascertain the presence of
superior cortical bone surrounding the mandibular canal.58 Clinical reports
have revealed hemorrhage into the canal or bone fragments may cause
compression or ischemia of the nerve from engaging the superior cortical
plate. Dependence on the ability to “feel” the superior cortical plate through
tactile sense increases the likelihood of nerve complications (Fig. 9.39).
FIG 9.39 (A) In approximately 28% of patients, no superior cortical plate is present.
(B) Even when present, cortical plate is very thin, which makes tactile sensitivity
extremely difficult.
Infiltration Technique.
An alternative technique in placing implants in the posterior mandible is not
utilizing mandibular nerve block anesthesia. Instead, infiltration is
accomplished in the soft tissue surrounding the osteotomy site, and the
patient is asked to alert the implant clinician on the proximity of the drill to
the nerve bundle.69
This alternative technique results in a very high degree of subjectivity
concerning patient's responses due to varying degrees of pain thresholds.
Additionally, disadvantages of this surgical method include inconsistent
mandibular nerve anatomy with varying locations of dental-alveolar nerve
branches. With the success of CBCT radiography in implant dentistry today
in determining the exact location of the inferior alveolar nerve, this technique
should be avoided because of the high degree of false-negative and false-
positive results from patients. Etoz et al showed this supraperiosteal
infiltartion technique to be safe in 91% of cases. However, this results in
approximately one patient in ten ending up with a neurosensory deficit.70
“Place Implants Buccal or Lingual to the IAN Canal or

Foramen.”
Many authors have advocated placing implants buccal or lingual to the
neurovascular bundle. (Kumar; Stellar) As stated previously, the buccal-
lingual nerve position within the mandible is extremely variable along with
the incidence and trajectory of lingual osseous concavities. Attempting to
place implants buccal or lingual to the inferior alveolar canal or mental
foramen is associated with a high degree of morbidity, even with the use of
CBCT-guided surgery. Additionally, perforation of the cortical plate can occur,
which may lead to sublingual bleeding or formation of a sublingual
hematoma (Fig. 9.40).
FIG 9.40 (A–B) Placing implants lingual increases chances of nerve impairment or
perforation of the lingual cortical plate.
“Place Implants at the Depth of the Adjacent Root Apexes.”

Many implant clinicians use the location and length of the adjacent teeth as a
guide in determining the size (length) implant to be placed. Usually a
panorex or periapical radiograph is utilized in determination of this length.
When this technique is used in anatomic type 2 or 3 (i.e., more apically
positioned in the vertical dimension) nerve courses, incidence of nerve
impairment is low. However, in mandibles that exhibit a type 1 nerve course
(close to root apex), close approximation of the implant to the canal is likely
leading to a higher probability of neurosensory impairment. Ideally, the
implant clinician should ascertain the available bone above the mandibular
canal via three-dimensional radiographic analysis (Fig. 9.41).
FIG 9.41 (A) Placement of implants at the level of the adjacent roots is ideal when
an anatomic type 2 or 3 nerve is present (arrow). (B) However, in type 1 nerve
courses, this principle will lead to a greater chance of nerve impairment because of
approximation of the implant and mandibular canal.
“As Long as There Is Not Excessive Bleeding, the Mandibular

Canal Has Not Been Violated.”
Another unconventional technique in avoiding nerve impairment is the
evaluation of the amount of bleeding from the osteotomy site. Many
practitioners correlate the amount of hemorrhage with the proximity of the
neurovascular bundle (inferior alveolar nerve, artery, vein, and lymphatic
vessels). Anatomic studies have shown the inferior alveolar artery may lie
parallel to the nerve and lingual as it traverses anteriorly. Its position varies
with respect to the inferior alveolar nerve within the mandibular canal. Other
studies show the inferior alveolar artery appears to be solitary and lies
superior and lingual to the inferior alveolar nerve, slightly above the
horizontal position.12 Additionally, there exists multiple inferior alveolar
veins positioned superior to the nerve, which may cause venous oozing if
directly traumatized.11 A false positive may occur if this area is damaged as
large marrow spaces, which can cause excessive bleeding, are common in the
posterior mandible (D4 bone). The degree of bleeding should not be used as
an indication of nerve proximity or violation of the mandibular canal (Fig.
9.42).
FIG 9.42 (A–B) The degree of bleeding within the osteotomy is not an indicator of
proximity or violation of the neurovascular canal. (C) Although variations exist,
multiple smaller veins (blue) are usually present superior to the polyfascicular inferior
alveolar nerve (brown) with the inferior alveolar artery (red) superiorly and lingually
positioned.
“Replacing Second Molars.”

There are many prosthetic and surgical disadvantages when evaluating
edentulous second mandibular molar sites for implant placement.
Disadvantages include high incidence of sublingual bony undercuts, which
can result in perforation of the lingual plate or angulation issues, decreased
interocclusal space (especially with supraeruption of the adjacent tooth),
difficult access for surgery and prosthetic component insertion, and the fact
there is 10% greater occlusal force on the second molar vs. the first molar.
Function is not a primary reason for replacement because 90% of masticatory
efficiency is generated anterior to the mesial half of the mandibular first
molar, and cheek biting is more common in this area because of the
proximity of the buccinators muscle. One of the most important
disadvantages is the close approximation of the mandibular canal in the
second molar area, which leads to difficulty in placement of implants in this
area. When implants are placed, usually the available bone present is
compromised in height. As a result, the second molar is often not replaced
when the only posterior teeth missing are the second and third molars. The
primary disadvantage of not replacing the second molar is extrusion of the
opposing maxillary second molar. If extrusion is a significant concern, a full-
coverage crown on the mandibular first molar may include an occlusal
contact on with the mesial marginal ridge of the maxillary second molar (Fig.
9.43).
FIG 9.43 (A–B) Because of the curvature of the mandible in the ramus area, the
mandibular canal is in close approximation to the second molar tooth roots in all
types of nerve courses.
“Nerve Repositioning”.
Patients who exhibit compromised alveolar crest height in the posterior
mandibular area can be very challenging. Techniques include the use of
shorter implants, which become biomechanically compromised, or the use of
bone grafting to increase available bone for future implant placement. An
alternative technique is to reposition the inferior alveolar nerve laterally,
either by nerve lateralization or nerve transposition. In nerve lateralization,
the inferior alveolar nerve is exposed and retracted laterally while the dental
implants are placed. The transposition technique, first published in 1987 by
Jenson and Nock, includes the mental foramen in the osteotomy resulting in
the inferior alveolar nerve being positioned more posterior.71 The inherent
risk with these complex procedures is neurosensory impairment (anesthesia,
paresthesia, or dysesthesia) to the mental nerve branch. Although this is a
valid treatment option in significantly atrophied cases, this technique should
be reserved for practitioners with advanced training and experience with
these procedures (Fig. 9.44).
FIG 9.44 Nerve repositioning in which the IAN is positioned facially and implants
placed in the prior position of the nerve bundle.
Summary
In implant dentistry today, one of the most serious complications is
neurosensory impairment associated with implant placement or bone
grafting. To avoid nerve damage a thorough understanding of the
radiographic anatomy is paramount. If nerve impairment does occur, quick
recognition and treatment is crucial to decreasing long-term morbidity. The
nerves associated with the maxilla and mandible are associated with
inconsistent anatomic locations. The implant clinician should understand the
limitations of two-dimensional radiology and the importance of a
comprehensive radiographic evaluation of the neural anatomy of the maxilla
and mandible. Additionally, the clinician must understand the complications
that may arise from unconventional surgical techniques that may increase
the morbidity of the procedure.
References
1. Alhassani AA, AlGhamdi AS. Inferior alveolar nerve injury in
implant dentistry: diagnosis, causes, prevention, and management. J
Oral Implantol. 2010;36:401–407.
2. Misch CE, Resnik R. Mandibular nerve neurosensory impairment
after dental implant surgery: management and protocol. Implant
Dent. 2010;19:378–386.
3. Libersa P, Savignat M, Tonnel A. Neurosensory disturbances of the
inferior alveolar nerve: a retrospective study of complaints in a 10-
year period. J Oral Maxillofac Surg. 2007;65:1486–1489.
4. Abarca M, van Steenberghe D, Malevez C, et al. Neurosensory
disturbances after immediate loading of implants in the anterior
mandible: an initial questionnaire approach followed by a
psychophysical assessment. Clin Oral Investig. 2006;10:269–277.
5. Day RH. Diagnosis and treatment of trigeminal nerve injuries. J Calif
Dent Assoc. 1994;22:48–51 [53–54].
6. Svane TJ, Wolford LM, Milam SB, Bass RK. Fascicular characteristics
of the human inferior alveolar nerve. J Oral Maxillofac Surg.
1986;44:431–434.
7. Artzi Z, Nemcovsky CE, Bitlitum I, Segal P. Displacement of the
incisive foramen in conjunction with implant placement in the
anterior maxilla without jeopardizing vitality of nasopalatine nerve
and vessels: a novel surgical approach. Clin Oral Implants Res.
2000;11:505–510.
8. Scher EL. Use of the incisive canal as a recipient site for root form
implants: preliminary clinical reports. Implant Dent. 1994;3:38–41.
9. Filippi A, Pohl Y, Tekin U. Sensory disorders after separation of the
nasopalatine nerve during removal of palatal displaced canines:
prospective investigations. Br J Oral Maxillofac Surg. 1999;37:134–136.
10. Magennis P. Sensory morbidity after palatal flap surgery–fact or
fiction? J Ir Dent Assoc. 1990;36:60–61.
11. Neves FS, Crusoé-Souza M, Franco LC, et al. Canalis sinuosus: a rare
anatomical variation. Surg Radiol Anat. 2012;34(6):563–566.
12. de Oliveira-Santos C, Rubira-Bullen IR, Monteiro SA, et al.
Neurovascular anatomical variations in the anterior palate observed
on CBCT images. Clin Oral Implants Res. 2013;24:1044–1048.
13. Jacobs RL, Martens W, Mraiwa N, et al. Neurovascularization of the
anterior jaw bones revisited using high resolution magnetic
resonance imaging. Oral Surg Oral Med Pathol Oral Radiol Endod.
2007;103:683–693.
14. Wadu SG, Penhall B, Townsend GC. Morphological variability of the
human inferior alveolar nerve. Clin Anat. 1997;10:82–87.
15. Benninger B, Kloenne J, Horn JL. Clinical anatomy of the lingual nerve
and identification with ultrasonography. Br J Oral Maxillofac Surg.
2013;51:541–544.
16. Pogrel MA, Thamby S. Permanent nerve involvement resulting from
inferior alveolar nerve block. J Am Dent Assoc. 2000;131:901–907.
17. Bagheri SC, Bell B, Khan HA. Nerve damage in dentistry. Pogrel MA.
Current therapy in oral and maxillofacial surgery. Elsevier Health
Sciences: Philadelphia; 2011:421–468.
18. Stacy GC, Hajjar G. Barbed needle and inexplicable paresthesias and
trismus after dental regional anesthesia. Oral Surg Oral Med Oral
Pathol. 1994;77:585–588.
19. Malamed SF. Handbook of local anesthesia. ed 4. Mosby: St Louis; 1997.
20. Smith MH, Lung KE. Nerve injuries after dental injection: a review of
the literature. J Can Dent Assoc. 2006;72:559.
21. Harn SD, Durham TM. Incidence of lingual nerve trauma and
postinjection complications in conventional mandibular block
anesthesia. J Am Dent Assoc. 1990;121:519–523.
22. Hillerup S, Jensen R. Nerve injury caused by mandibular block
analgesia. Int J Oral Maxillofac Surg. 2006;35:437–443.
23. Haas DA, Lennon D. A 21 year retrospective study of reports of
paresthesia following local anesthetic administration. J Can Dent
Assoc. 1995;61:319–320 [323–326, 329–330].
24. Simon MA, Vree TB, Gielen MJ, Booij MH. Comparison of the effects
and disposition kinetics of Articaine and lidocaine in 20 patients
undergoing intravenous regional anaesthesia during day case
surgery. Pharm World Sci. 1998;20:88–92.
25. Kanaa MD, Whitworth JM, Corbett IP, Meechan JG. Articaine buccal
infiltration enhances the effectiveness of lidocaine inferior alveolar
nerve block. Int Endod J. 2009;42:238–246.
26. Ribeiro PD Jr, Sanches MG, Okamoto T. Comparative analysis of
tissue reactions to anesthetic solutions: histological analysis in
subcutaneous tissue of rats. Anesth Prog. 2003;50:169–180.
27. Juodzbalys G, Wang HL, Sabalys G. Injury of the inferior alveolar
nerve during implant placement: a literature review. J Oral Maxillofac
Res. 2011;2:e1.
28. Fanibunda K, Whitworth J, Steele J. The management of
thermomechanically compacted gutta percha extrusion in the inferior
dental canal. Br Dent J. 1998;184:330–332.
29. Sammartino G, Marenzi G, Citarella R, et al. Analysis of the occlusal
stress transmitted to the inferior alveolar nerve by an osseointegrated
threaded fixture. J Periodontol. 2008;79:1735–1744.
30. Al-Ouf K, Salti L. Postinsertion pain in region of mandibular dental
implants: a case report. Implant Dent. 2011;20:27–31.
31. Kim JE, Shim JS, Huh JB, et al. Altered sensation caused by peri-
implantitis: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol.
2013;116(1):e9–e13.
32. Renton T. Oral surgery: part 4. Minimising and managing nerve
injuries and other complications. Br Dent J. 2013;215:393–399.
33. Shamloo N, Safi Y, Fathpour K, et al. Lower lip numbness due to the
mandibular canal narrowing after dental reimplantation: a case
report. Dent Res J (Isfahan). 2015;12:386.
34. Bruce RA, Frederickson GC, Small GS. Age of patients and morbidity
associated with mandibular third molar surgery. J Am Dent Assoc.
1980;101:240–245.
35. Hurley RW, Adams MC. Sex, gender, and pain: an overview of a
complex field. Anesth Analg. 2008;107:309–317.
35a. Coleman MP, Freeman MR. Wallerian degeneration, wld(s), and
nmnat. Annu Rev Neurosci. 2010;33(1):245–267.
36. Shimpo T, Gilliatt RW, Kennett RP, Allen PJ. Susceptibility to pressure
neuropathy distal to a constricting ligature in the guinea-pig. J Neurol
Neurosurg Psychiatry. 1987;50:1625–1632.
37. Yekta SS, Smeets R, Stein JM, Ellrich J. Assessment of trigeminal
nerve functions by quantitative sensory testing in patients and
healthy volunteers. J Oral Maxillofac Surg. 2010;68:2437–2451.
38. Rood JP, Shehab BA. The radiological prediction of inferior alveolar
nerve injury during third molar surgery. Br J Oral Maxillofac Surg.
1990;28:20–25.
39. Seddon JJ. Three types of nerve injury. Brain. 1943;66:237.
40. Sunderland S. A classification of peripheral nerve injuries produced
by a loss of function. Brain. 1951;74:491.
40a. Merskey H, Bogduk N. Classification of chronic pain: descriptions of
chronic pain syndromes and definitions of pain terms/prepared by the
International Association for the Study of Pain, Task Force on Taxonomy.
ed 2. IASP Press: Seattle; 1994.
42. Costigan M, Scholz J, Woolf CJ. Neuropathic pain: a maladaptive
response of the nervous system to damage. Annu Rev Neurosci.
2009;32:1–32.
43. Vecht CJ, Haaxma-Reiche H, Van Putten WL. Conventional versus
high-dose dexamethasone in metastatic spinal cord compression.
Neurology. 1989;39(Suppl 1):220.
44. Seo K, Tanaka Y, Terumitsu M, et al. Efficacy of steroid treatment for
sensory impairment after orthognathic surgery. J Oral Maxillofac
Surg. 2004;62:1193.
45. Olson J. A review of cryotherapy. Phys Ther. 1972;52:840.
46. Yosue T, Brooks SL. The appearance of mental foramina on panoramic
and periapical radiographs. II. Experimental evaluation. Oral Surg
Oral Med Oral Pathol. 1989;68:488–492.
47. Schropp L, Wenzel A, Kostopoulos L. Impact of conventional
tomography on prediction of the appropriate implant size. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 2001;92:458–463.
48. Ylikontiola L. Comparison of three radiographic methods used to
locate the mandibular canal in the buccolingual direction before
bilateral sagittal split osteotomy. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod. 2002;93:736–742.
49. Fortin T, Bosson JL, Coudert JL, Isidori M. Reliability of preoperative
planning of an image-guided system for oral implant placement
based on 3-dimensional images: an in vivo study. Int J Oral Maxillofac
Implants. 2003;18:886–893.
49a. Nickenig H-J, et al. Evaluation of the difference in accuracy between
implant placement by virtual planning data and surgical guide
templates versus the conventional free-hand method—a combined in
vivo–in vitro technique using cone-beam CT (Part II). J Cranio-
Maxillofacial Surg. 2010;38(7):488–493.
50. Anderson LC, Kosinski TF. A review of the intraosseous course of the
nerves of the mandible. J Oral Implantol. 1991;17:394–403.
51. Narayana K, Vasudha S. Intraosseous course of the inferior alveolar
(dental) nerve and its relative position in the mandible. Indian J Dent
Res. 2004;15:99–102.
52. Carter RB, Keen EN. The intramandibular course of the inferior dental
nerve. J Anat. 1971;108(Pt 3):433–440.
53. Simonton JD. Age- and gender-related differences in the position of
the inferior alveolar nerve by using cone beam computed
tomography. J Endod. 2009;35:944–949.
54. Kim ST, Hu KS, Song WC, et al. Location of the mandibular canal and
the topography of its neurovascular structures. J Craniofac Surg.
2009;20:936–939.
55. Levine MH, Goddard AL, Dodson TB. Inferior alveolar nerve canal
position: a clinical and radiographic study. J Oral Maxillofac Surg.
2007;65:470–474.
56. Miller CS, Nummikoski PV, Barnett DA, Langlais RP. Cross-sectional
tomography. A diagnostic technique for determining the buccolingual
relationship of impacted mandibular third molars and the inferior
alveolar neurovascular bundle. Oral Surg Oral Med Oral Pathol.
1990;70:791–797.
57. Narayana K, Vasudha S. Intraosseous course of the inferior alveolar
(dental) nerve and its relative position in the mandible. Indian J Dent
Res. 2004;15:99–102.
58. Juodzbalys G, Wang HL, Sabalys G. Anatomy of mandibular vital
structures. Part II: Mandibular incisive canal, mental foramen and
associated neurovascular bundles in relation with dental
implantology. J Oral Maxillofac Res. 2010;1:e3.
59. Apostolakis D, Brown JE. The anterior loop of the inferior alveolar
nerve: prevalence, measurement of its length and a recommendation
for interforaminal implant installation based on cone beam CT
imaging. Clin Oral Implants Res. 2012;23:1022–1030.
60. Mraiwa N, Jacobs R, Moerman P, et al. Presence and course of the
incisive canal in the human mandibular interforaminal region: two-
dimensional imaging versus anatomical observations. Surg Radiol
Anat. 2003;25:416–423.
61. Misch CE, Crawford EA. Predictable mandibular nerve location—a
clinical zone of safety. Int J Oral Implantol. 1990;7:37–40.
62. Lamas Pelayo J, Peñarrocha Diago M, Martí Bowen E, Peñarrocha
Diago M. Intraoperative complications during oral implantology. Med
Oral Patol Oral Cir Buca. 2008;13:E239–E243.
63. Khawaja N, Renton T. Case studies on implant removal influencing
the resolution of inferior alveolar nerve injury. Br Dent J.
2009;206:365–370.
64. Bagheri SC, Meyer RA. Management of mandibular nerve injuries
from dental implants. Atlas Oral Maxillofac Surg Clin North Am.
2011;19:47–61.
65. Tehemar SH. Factors affecting heat generation during implant site
preparation: a review of biologic observations and future
considerations. Int J Oral Maxillofac Implants. 1999;14:127–136.
65a. Hubbard JH. The quality of nerve regeneration. Factors independent
of the most skillful repair. Surg Clin North Am. 1972;52(5):1099–1105.
66. Turbush SK, Turkyilmaz I. Accuracy of three different types of
stereolithographic surgical guide in implant placement: an in vitro
study. J Prosthet Dent. 2012;108:181–188.
67. Van de Velde T, Glor F, De Bruyn H. A model study on flapless implant
placement by clinicians with a different experience level in implant
surgery. Clin Oral Implants Res. 2008;19:66–72.
68. Khawaja N, Renton T. Case studies on implant removal influencing
the resolution of inferior alveolar nerve injury. Br Dent J.
2009;206:365–370.
69. Heller AA, Shankland WE II. Alternative to the inferior alveolar nerve
block anesthesia when placing mandibular dental implants posterior
to the mental foramen. J Oral Implantol. 2001;27:127–133.
70. Etoz OA, Er N, Demirbas AE. Is supraperiosteal infiltration
anesthesia safe enough to prevent inferior alveolar nerve during
posterior mandibular implant surgery? Med Oral Patol Oral Cir Bucal.
2011;16(3):e386–e390.
71. Jensen O, Nock D. Inferior alveolar nerve repositioning in
conjunction with placement of osseointegrated implants: a case
report. Oral Surg Oral Med Oral Pathol. 1987;63:263–268.
10
Randolph R. Resnik
Dental implant surgery comprises many diverse procedures that are

considered in dentistry to be relatively safe with a high success rate.
However, implant clinicians must be aware and take into consideration
numerous postoperative complications that may follow dental implant
surgery. Most postoperative complications resolve with minimal intervention,
but some situations may predispose implants to failure or even subject the
patient to life-threatening situations. Understanding the possibility and
magnitude of postoperative complications is crucial for today's clinicians
practicing implant dentistry. In this chapter a wide range of postoperative
complications will be discussed according to the etiology, prevention, and
management to decrease implant and patient morbidity.
Medical Issues
Edema (Postoperative) Surgical Swelling
Postoperative edema is a direct result of tissue injury and is defined as an
accumulation of fluid in the interstitial tissue. Two variables determine the
extent of edema: (1) the amount of tissue injury is proportional to the
amount of edema; (2) the more loose the connective tissue at the surgery site,
the more edema is most likely to be present.1 Because postoperative swelling
can adversely affect the incision line (i.e., result in incision line opening),
measures should be taken to minimize this condition. Usually, edema will
peak at approximately 48–72 hours, therefore patients should always be
informed. Increased swelling after the fourth day may be an indication of
infection, rather than postsurgical edema.
Etiology
The mediators of the inflammatory process include cyclooxygenase and
prostaglandins, which play a significant role in the development of
postoperative inflammation and pain. When tissue manipulation or damage
occurs, phospholipids are converted into arachidonic acid by way of
phospholipase A2. Arachidonic acid, which is an amino acid, is released into
the tissue, which produces prostaglandins via enzymatic breakdown via
cyclooxygenases. The end result is the formation of leukotrienes,
prostacyclins, prostaglandins, and thromboxane A2, which are the mediators
for inflammation and pain.
Prevention
To minimize postoperative swelling, good surgical technique must be used
with minimal tissue trauma. Additional factors include patient systemic
disorders, excessive retraction, and long surgical duration, which will all
contribute to increased inflammation after surgery. Postoperative
prophylactic medications such as ibuprofen (nonsteroidal antiinflammatory
drugs [NSAIDs]) and glucocorticosteroids (steroids) are utilized as
prophylactic medications, which counteract the negative effects of the edema
cascade (Fig. 10.1).
FIG 10.1 Mechanism of action for nonsteroidal antiinflammatory drugs (NSAIDs)
and steroids in the reduction of inflammation. Steroids block arachidonic acid and
NSAIDs interfere with cyclooxygenase in the reduction of edema. (From Misch CE:
Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
Nonsteroidal Antiinflammatory Drugs.

NSAIDs have an analgesic effect as well as an antiinflammatory effect. This
drug class reduces inflammation by inhibiting the synthesis of
prostaglandins from arachidonic acid. Therefore the use of the popular
analgesic drug ibuprofen has a secondary beneficial antiinflammatory effect.
NSAIDs do not have a ceiling effect for inflammation (i.e., ceiling effect for
analgesia is 400 mg); however, higher doses to achieve antiinflammatory
qualities are accompanied by serious side effects.
Recommendation: Ibuprofen 400 mg for Type 1–4 procedures (see Misch
Prophylactic Medication Protocol, Table 10.1).
TABLE 10.1
Procedure-Specific Pharmacologic Protocol for Oral Implantology
Category P atient Selection P rocedures Antibiotic Glucocorticoid Antimicrobial Analgesic

Category AS A1/AS A2 • S ingle implants with Amoxicillin 1 gm None Chlorhexidine: Pain
1 >AS A2 = Category 2 minimal reflec tion One hour before surgery oz. BID for c ontrol
protoc ola
two weeks P CP 1–2
Category AS A1/AS A2 • Traumatic extrac tions Amoxicillin 1 gm Decadron 4 Chlorhexidine: Pain
2 >AS A2 = Category 4 with pathology One hour before surgery, mg oz. BID for c ontrol
• S oc ket grafting then 500 mg 6 hours after • 1 tab AM protoc ol
• S ingle tooth implants day of two weeks P CP 1–2
with extensive surgery
reflec tion
• Multiple implants with
minimal tissue reflec tion
• S A1 sinus proc edures
• Immediate implants
without pathology
Category AS A1/AS A2 • S ingle implants with Amoxicillin 1 gm Decadron 4 Chlorhexidine: Pain
3 >AS A2 = Category 4 bone grafting and One hour before surgery, mg oz. BID for c ontrol
exc essive tissue then 500 mg TID for 3 days • 1 tab AM protoc ol
reflec tion day of two weeks P CP 2–3
• Multiple implants with surgery
extensive reflec tion • 1 tab AM
• Bone grafting day after
(Allograft/Autograft) surgery
• S A2 sinus proc edures • 1 tab AM
two days
after
surgery
Category Any of the following: • Any Category 3 Amoxicillin 1 gm Decadron 4 Chlorhexidine: Pain
4 • >AS A2 proc edures with One hour before surgery, mg oz. BID for c ontrol
• Long duration surgic al or patient then 500 mg TID for 5 days • 2 tab AM protoc ol
surgery fac tors day of two weeks P CP 3–4
• Less experienc ed • Immediate implants with surgery
surgeon pathology • 2 tabs AM
• • Autogenous onlay day after
Immunoc ompromised grafting surgery
• Ac tive periodontal • 1 tab AM
disease two days
after
surgery
Category All All Augmentin Decadron 4 Chlorhexidine: Pain
5 S A3/S A4 S A3/S A4 (875 mg/125 mg): 1 tab BID mg oz. BID for c ontrol
S inus patients S inus proc edures starting one day before, then • 2 tab AM protoc ol
1 tab BID for 5 days day before two weeks P CP 2–3
surgery
• 2 tabs AM
day of
surgery
• 1 tab AM
day after
surgery
• 1 tab AM
two days
after
surgery
a
See Table 10.5 for pain control protocols.
ASA, American Society of Anesthesiologists; NSAID, nonsteroidal antiinflammatory drug; SA, subantral.
Alternative Medications:
Amoxicillin (1 gm) = Cephalexin (1 gm), Clindamycin (600 mg)
Augmentin (875/125) = Ceftin (500 mg) = Doxycycline (100 mg)
(Note: SBE Prophylaxis : change preoperative antibiotic dose to Amoxicillin [2 gm], Cephalexin [2 gm], or
Clindamycin [600 mg])
Ibuprofen (400 mg) > Acetaminophen (500 mg) or Naproxen Sodium (375 mg)
Hydrocodone (5 mg/500 mg) > Tylenol # 2/Tramadol (50 mg)
Hydrocodone (7.5 mg/750 mg) > Tylenol # 3/Tramadol (100 mg)/Nucynta (50, 75, 100 mg)
Hydrocodone (10 mg/660 mg) > Oxycodone (Percocet) 7.5/500 mg
(Note: If patient cannot take medication by mouth, [1] Ibuprofen Oral Suspension (OTC); [2] Lortab Elixar
[7.5 mg hydrocodone/500 mg APAP/15 ml])
Glucocorticosteroids.
The adrenal cortex, which uses cholesterol as a substrate, synthesizes and
secretes two types of steroid hormones—the androgens and corticosteroids.
The corticosteroids are classified additionally by their major actions: (1)
glucocorticoids, which have effects on carbohydrate metabolism and have
potent antiinflammatory actions, and (2) mineralocorticoids, which have
sodium-retaining qualities. The use of synthetic glucocorticosteroids has
become very popular in the postoperative management of inflammation after
oral surgical procedures. These synthetic glucocorticoids have greater
antiinflammatory potency in comparison to natural steroids with very little
sodium and water retention. Most steroids have similar chemical structures;
however, they differ in their milligram potency.2 The antiinflammatory effects
are achieved by altering the connective tissue response to injury, causing a
decrease in hyperemia, which results in less exudation and cellular migration
along with infiltration at the site of injury.3
Glucocorticoids bind to glucocorticoid receptors within cells and form a
glucocorticoid-GR complex. This complex alters the synthesis of mRNA from
the DNA molecule, affecting the production of different proteins. By
suppressing the production of proteins that are involved in inflammation,
glucocorticoids also activate lipocortins, which have been shown to inhibit
the action of phospholipase A2 (PLA2). PLA2 is a key enzyme involved in the
release of arachidonic acid from cell membranes.
Arachidonic acid is an omega-6 fatty acid that is incorporated into cell
membranes. When a cell is damaged, arachidonic acid is released from cell
membranes and is converted into inflammatory and pain prostaglandins by
cyclooxygenase (COX)-2 enzymes. The release of arachidonic acid requires
the activation of enzyme PLA2. However, lipocortins, which cause the
inhibition of PLA2, prevent the release of arachidonic acid, thereby reducing
the amounts of inflammatory prostaglandins.
There is a wide range of glucocorticoid preparations available for local,
oral, and parenteral administration. In relation to the naturally occurring
cortisol (hydrocortisone), synthetic glucocorticoids are longer acting and
more potent. The main differences are based on the classification as short
acting (<12 hours), intermediate acting (12–36 hours), and long acting (>36
hours). A summary of the most common glucocorticosteroids is shown in
Table 10.2.
TABLE 10.2
Synthetic Glucocorticoids
Glucocorticoids Antiinflammatory P otency Equivalent Dose (mg) Duration (h)

Short Acting
Hydroc ortisone 1.0 20 <12
Cortisone 0.8 25 <12
Intermediate Acting
Prednisone 4.0 5 24 to 36
Prednisolone 4.0 5 24 to 36
Long Acting
Dexamethasone 25 0.75 >48
The ideal synthetic glucocorticoid for dental implant surgery should

maintain high antiinflammatory potency with minimal mineralocorticoid
effects. The glucocorticoid that best suits the requirements is the long-acting
glucocorticoid dexamethasone (Decadron). It is imperative this drug be
administered before surgery so that adequate blood levels are obtained.
Also, it should be given in the morning in conjunction with the natural
release of cortisol (~8:00 am). This timing will interfere the least with the
adrenocortical system. Because inflammation usually peaks between 48 and
72 hours, the postoperative regimen of dexamethasone should not exceed 3
days after surgery. This high-dose, short-term glucocorticoid therapy has
been shown not to significantly affect the hypothalamic–pituitary–adrenal
axis (HPA axis), which controls many of the bodies processes, including
reactions to stress.4
A significant additional benefit of the administration of dexamethasone is
the potent antiemetic effects for the prophylactic treatment of postoperative
nausea and vomiting. This is now an accepted medication for hospital-based
outpatient surgery, usually given in doses of 8–10 mg intravenously.5
Contraindications to the use of corticosteroids include active infections
(viral, bacterial, fungal), tuberculosis, ocular herpes simplex, primary
glaucoma, acute psychosis, and diabetes mellitus. Special attention must be
given to diabetic patients because glucocorticoids have an antiinsulin action
that results in increased serum glucose and glycosuria.6 Usually,
corticosteroids are contraindicated with insulin dependent diabetics. For oral
and diet controlled diabetics, a medical consult should be completed prior to
any treatment.
Recommendation: Decadron 4 mg for Type 1–4 procedures (see Table 10.1,
Misch Prophylactic Medication Protocol).
Cryotherapy.
Cryotherapy (application of ice) is one of the simplest and most economical
modalities in the management of postoperative soft tissue inflammation. The
use of ice to reduce pain and swelling dates back to the ancient Egyptians,
over 4000 years ago.7
The use of cryotherapy is highly advised in any dental implant procedure
in which excessive inflammation is expected. The mechanism of action
involves a reduction in fluid accumulation within the body tissues, slowing of
metabolism, control of hemorrhage, and a decrease in the excitability of
peripheral nerve fibers leading to an increase in pain threshold.8
Caution must be taken to limit the application of ice to no longer than 2
days because prolonged use may cause rebound swelling and cell
destruction. Improper and prolonged use of ice may result in cell death due
to prolonged vasoconstriction, ischemia, and capillary thrombosis.9
After 2 to 3 days, moist heat may be applied to the region to increase blood
and lymph flow to help clear the area of the inflammatory consequences.
This also helps reduce any ecchymosis that may have occurred from the
tissue reflection. Although usually safe, the application of ice is cautioned in
patients suffering from cold hypersensitivities and intolerances and
peripheral vascular diseases. Additionally, ice application may be
problematic in patients who are elderly or very young because they may have
impaired thermal regulation and limited ability to communicate. Care should
be exercised in using facial bandages because prolonged ice administration
may result in soft tissue injury.
Recommendation: Cold dressings (ice packs) should be applied extraorally
(not directly on skin: place a layer of dry cloth between ice and skin) over the
surgical site for 20 minutes on/20 minutes off for the first 24–36 hours (Fig.
10.2).
FIG 10.2 Postoperative edema. (A) Postoperative edema after dental implant
surgery, which peaks at 48–72 hours. (B) Cryotherapy to decrease swelling with the
use of ice packs. (C) Facial wrap bandages should be used with caution because
they may cause prolonged exposure and trauma to the skin area. (A, From Torabinejad
M, Fouad A: Endodontics: principles and practice, ed 4, St Louis, 2009, Saunders; B and C, courtesy
of Salvin Dental Specialties, Inc., Charlotte, NC.)
Decrease Activities.
Patients should be instructed to decrease activities after surgery because this
will minimize swelling postoperatively. The more active the patient and the
more strenuous activity the patient engages in, the greater the extraoral
swelling.
Recommendation: Activities should be limited for the first 3 days. Elevation
of the head (sitting upright) and sleeping on multiple pillows will minimize
the postoperative swelling.
Treatment
Swelling is self-limiting and, once it occurs, it is usually difficult to treat
(time-dependent). The above mentioned medications/therapy (Decadron,
NSAIDs, cryotherapy) will help to reduce postoperative inflammation.
Ecchymosis (Bruising)
Ecchymosis is subcutaneous extravasation of blood within the tissues, which
results in discoloration of the skin from the seepage of blood in the tissues.
The location of the ecchymosis may be distant to the surgical site because of
gravity (i.e., always inform patients preoperatively). Ecchymosis that presents
in the inferior mandibular area or neck may be from bleeding under the flap
and traveling via fascial spaces due to gravity (Fig. 10.3).
FIG 10.3 Ecchymosis. (A) Postoperative bruising. (B) Ecchymosis extending into
the neck area. (C) Resolution of the ecchymosis will result in varying degrees of
yellow to golden-brown.
Etiology
The cause of ecchymosis (bruising) is not confined to an existing hematologic
disease or to medication induced bleeding. Moderate bruising should be
expected after dental implant surgery, especially after longer, more invasive
surgeries. Female and elderly patients are more susceptible to bruising. The
ecchymosis cascade includes:
1. Blood vessels rupture
2. Red blood cells die and release hemoglobin
3. Macrophages (white blood cells, [WBCs]) degrade hemoglobin via

phagocytosis
4. Hemo > bilirubin = bluish-red color
5. Bilirubin > hemosiderin = golden-brown color
Ecchymosis may appear as bright red, black, blue, purple, or a combination

of the above colors. It usually consists of nonelevated, rounded, and irregular
areas that increase in intensity over 3–4 days postoperation and will diminish
and become yellow as they disappear. It may take 2–3 weeks for complete
resolution.
Prevention
Unfortunately, even with gentle handling of tissues and good surgical
technique, ecchymosis may be unavoidable. To minimize ecchymosis, avoid
postoperative aspirin, herbal remedies, and food supplements that may
increase bleeding. Always inform the patient preoperatively (preferably in
written postoperation instructions) that bruising may occur. Elderly patients
are more susceptible to ecchymosis because of decreased tissue tone and
weaker intracellular attachment.
Treatment
Ecchymosis is self-limiting and usually resolves without treatment. However,
the patient may treat the ecchymosis in the following ways:
Rest/avoid strenuous activity: promotes tissue healing and decreases
inflammation.
Elevation: helps decrease inflammation, facilitates proper venous return,
and improves circulation to the site.
Analgesics: helps reduce pain associated with the onset of ecchymosis.
Sun exposure: inform patient to avoid sun exposure to the area of bruising
as excessive sunlight may cause permanent discoloration.
Trismus
Trismus refers to reduced opening of the jaws, which is caused by trauma or
spasm to the muscles of mastication. The limited opening may result in an
interference with eating, speech, and hygiene and may cause pain.
Etiology
Trismus after implant surgery can be due to multiple factors. The most likely
etiologic factor is local anesthetic, secondary to an inferior alveolar nerve
block that penetrates the medial pterygoid muscle. Also, complicated or
prolonged surgical procedures that require full-thickness mucoperiosteal
flaps with resultant edema can lead to trismus. Normal interincisal opening
is approximately 35–45 mm, with mild trismus being classified as 20–30 mm
and severe trismus less than 10 mm (Fig. 10.4).1
FIG 10.4 Trismus. (A) Commonly caused by prolonged opening resulting in
spasms of the muscles of mastication. Care should be exercised in using surgical
templates for the placement of implants in the posterior region as access is often
compromised. (B) Measurement of maximum opening, which is normally 35–45
mm.
Prevention
When placing implants, especially in the posterior region, care should be
taken to minimize excessive opening of the patient to where spasm of the
muscles of mastication would result. Bite blocks, short duration treatment,
and sedation may decrease the possibility of trismus complications. When
using CBCT surgiguides, lateral access openings should be utilized in the
guide to prevent extensive opening to accommodate the guide and surgical
bur. This mainly occurs in the posterior region of the oral cavity.
Treatment
Usually trismus will resolve with time; however, patients should maintain a
soft diet and minimize overactivity. Additional treatment includes the use of
physical therapy, passive range of motion exercises, splint therapy, and
medications such as NSAIDs, muscle relaxants, and steroids (Medrol
Dosepak, Decadron).
Postsurgical Pain
Pain has been documented to be inadequately treated in 50% of all surgical
procedures.10 Oral surgical studies have shown pain in the oral cavity to reach
its maximum intensity within the first 12 hours after surgery, and 97% of
patients reporting postoperative pain being the greatest during the first day
of surgery.11
Postsurgical painful experiences predispose the patient to amplification of
noxious stimuli (hyperalgesia) and cause typically painless sensations to be
experienced as pain (allodynia). Patients who have had painful experiences
(surgery) may have increased pain and the need for additional analgesic use
in future surgeries. The goal for pain control in oral implantology is to have
adequate analgesic levels before the cessation of local anesthesia and a well-
administrated postoperative analgesic regimen for patient comfort.
Etiology
The mechanism of painful stimuli is modulated by the peripheral and central
nervous systems. Noxious stimuli (e.g., tissue damage or bone preparation)
cause peripheral nociceptors to transmit signals along nerve fibers lying in
the dorsal root ganglion. Their axons synapse in the dorsal horn of the spinal
cord and then travel along the spinothalamic tract of the spinal cord to the
thalamus and the cortex. Within the cortex and thalamus, signals originating
from tissue damage form the subjective interpretation of pain.
With repeated noxious stimuli, peripheral nociceptors become more
responsive. The sensitivity to these receptors is further enhanced by tissue
factors and inflammatory mediators released in the course of tissue damage.
Numerous inflammatory mediators are present, including prostaglandins,
kinins, leukotrienes, substance P, and histamine. These mediators initiate
and magnify the nociceptive impulses that are transmitted to the central
nervous system for the perception of pain.
The most important mediators, prostaglandins, are extremely important in
sensitizing peripheral neurons to the local stimuli. Prostaglandins are also
synthesized in the spinal cord and brain and enhance pain sensitivity by
recruiting secondary neurons to respond to the primary stimulus.12
One of most commonly used analgesics, NSAIDs, work at the site of tissue
damage, preventing prostaglandin formation by inhibiting cyclooxygenase
(COX). COX is an enzyme that breaks down arachidonic acid for
prostaglandin synthesis. In the tissue there are two well-identified
cyclooxygenases, COX-1 and COX-2. COX-1 enzymes support hemostasis
(platelet degranulation and adhesion), stomach mucosal integrity, and
regulation of kidney function. COX-2 enzymes are an inducible form whose
synthesis is activated in damaged tissue, which leads to the formation of
proinflammatory prostaglandins that play a major role in inflammation,
pain, and fever. A relatively new COX has been described (COX-3) that is
found in the brain and is thought to be the site of action of acetaminophen.13
In contrast to NSAIDs, opioids have a different mechanism of action to
reduce pain. Opioids act on the central nervous system by binding to specific
receptors (m-opioid), thus preventing transmission of nociceptive pathways
while also activating inhibitory pathways that descend to the spinal cord. By
binding to these m-opioid receptors, substance P is prevented from being
released, thus preventing painful stimuli (Fig. 10.5).14
FIG 10.5 Pain cascade depicting the breakdown of arachidonic acid into the
various forms of prostaglandins.
Prevention
The following may be used to prevent postoperative pain:
1. Good surgical technique
2. Surgery duration not to exceed patient's tolerance
3. Postoperative long-acting anesthetics
4. Adequate postoperative pain control and instructions
5. Limitation of patient activities post-operatively.
Treatment
The implant clinician must understand the various aspects of pain control
after dental implant surgery. In most cases: (1) pain is not severe and mild
OTC analgesics can manage the discomfort, (2) peak pain occurs
approximately 12 hours after surgery and diminishes over time, and (3) pain
will persist no longer than 2 days. However, this is patient specific.1
The most important principle with pain management after implant surgery
is the timing of the medication. Ideally, analgesic medications should be
taken before the effects of the local anesthetic subside. With this approach
postoperative pain is easier to control, and the patient is less likely to
experience the acute, severe pain. If the patient takes medication after pain is
present, the patient will inevitably have to take more medication to control
the pain, increasing the likelihood of analgesic side effects.
In implant dentistry, different classifications and mechanisms of pain
suppression may be used. A pain control protocol has been established that
simplifies and standardizes the various aspects of pain relief (Table 10.3):
1. Nonopioid analgesics (nonnarcotics)
2. Opioid analgesics (narcotics)
3. Adjuvants
TABLE 10.3
Analgesic Agents Used to Control Postoperative Surgical Pain
Analgesic Brand Name Onset (hr) P eak (hr) Duration (hr) Recommended Dose Dosing Interval (h) Maximum Dose/Day
Nonopioid
Ac etaminophen Tylenol 0.5 0.5–2 4–6 650–1000 mg 4–6 4000 mg
Ibuprofen Motrin 0.5 1–2 4–6 400 mg 4–6 2400 mg
Advil
Naproxen Anaprox 1 2–4 5–7 275–550 mg 6–8 1375 mg
Tramadol Ultram 0.5 1–2 4–6 50–100 mg 4–6 400 mg
Opioid
Codeine Tylenol with c odeine 0.1–0.3 0.5–1 4–6 60 mg 3–4
Hydroc odone Dic odid 0.25–0.5 0.5 4–8 5–10 mg 4–6
Oxyc odone Perc oc et 0.25–0.5 1 4–6 5–10 mg 4–6
Meperidine Demerol 0.1–0.45 0.5–1 2–4 50–100 mg 6
Propoxyphene Darvon 0.5–1 2–2.5 4–6 65–130 mg 4–6
Nonopioid Medications.
The nonopioid analgesics used in implant dentistry include acetaminophen,
NSAIDs, COX-2 inhibitors, and tramadol.
Acetaminophen.
The mode of action of acetaminophen is not known; however, it is believed to
involve the prostaglandin pathways within the central nervous system with
little influence on peripheral prostaglandin synthesis. COX-3 enzymes have
been described as being fully expressed in the brain, spinal cord, and heart.
The primary function is to regulate pain responses and fever, and COX-3 has
been postulated to be the site of action of acetaminophen.15
Acetaminophen is indicated for mild to moderate pain and as a safe
alternative to NSAIDs. It has excellent analgesic and antipyretic properties
and is void of side effects that are associated with NSAIDs. Like NSAIDs,
acetaminophen also has a ceiling dose (4 g/day) for analgesic effects.
However, unlike NSAIDs, acetaminophen has the drawback of having
minimal antiinflammatory qualities. The main side effect of acetaminophen
is liver damage, which is associated with excessive and long-term use of this
drug.
Nonsteroidal antiinflammatory drugs.

The NSAIDs are one of the most commonly used analgesic families in
implant dentistry today. Clinical trials have shown that NSAIDs are effective
in all levels of pain (mild, moderate, severe).16 The mechanism of action of
NSAIDs is thought to arise from the inhibition of the synthesis of
prostaglandins from arachidonic acid. With the inhibition of COX,
conversion of arachidonic acid to the immediate precursors of prostaglandins
is prevented. Thus, with the lack of prostaglandins in the tissue, the
hyperanalgesia and edema associated with acute inflammation is
minimized.17
The main reasons that NSAIDs are so widely used is the fact that they
work very well as analgesics and have variable effects on inflammation (drug
and dose dependent). Inflammation and pain are two separate entities, with
analgesic doses having a ceiling effect18 and antiinflammatory doses not
having a ceiling effect. In regards to the analgesic effect, there is no reason to
exceed the analgesic ceiling for the treatment of acute pain because higher
doses give no additional pain relief while increasing the likelihood of side
effects.
The side effects of NSAIDs are numerous, including gastrointestinal (GI)
disturbances (dyspepsia, erosions, ulcerations) and liver, renal, and cardiac
effects.19 This group of medications is responsible for the largest number of
serious drug-related complications, surpassing all other drugs by a wide
margin.20 In 2005 GI-related deaths from NSAIDs were the 14th leading
cause of death in the United States, ranked after homicides (13th) and before
atherosclerosis (15th).21
NSAIDs have very little effect on platelet aggregation because bleeding
times are not prolonged. With prolonged use of NSAIDs, interference with
most classes of antihypertensives has been noted. If patients take NSAIDs
for more than 5 days postoperatively, blood pressure should be monitored.
Ibuprofen.
Ibuprofen was first introduced in 1969 as a new NSAID and has since been
the most popular prescribed NSAID. Ibuprofen is used to treat mild to
moderate pain and has been proven to significantly reduce postoperative
dental pain in clinical studies. The analgesic ceiling dose is 400 mg/dose and
1200 mg/day.22 At these doses it has been shown to be as safe as
acetaminophen, while achieving better analgesia with less nausea and
cramping.
Aspirin.
Acetylsalicylic acid (ASA) was the first prototypical NSAID. It has analgesic,
antiinflammatory, and antipyretic properties. However, at analgesic doses its
relative risk for GI complications is high. Acetylsalicylic acid is not a drug of
choice in the management of dental implant surgical patients because of its
very significant antiplatelet effects.
Tramadol.
Tramadol represents a unique classification of analgesic because it is a
centrally acting analgesic with two complementary characteristics: opioid and
antidepressant. It works by inhibition of norepinephrine and serotonin
reuptake within pain pathways of the central nervous system and also by its
relatively weak affinity for the m-opioid receptor. Tramadol is a nonscheduled
drug and is associated with fewer opioid-like side effects, such as
dependence, sedation, respiratory depression, and constipation. Tramadol's
analgesic efficacy is similar to that of codeine (60 mg) and is indicated for
moderate to moderately severe pain management. This drug is an
appropriate analgesic alternative for the treatment of postoperative pain in
patients who have NSAID-related GI and opioid intolerance. Tramadol has
been shown to be effective in the reduction of pain when used in
combination with acetaminophen. Ultracet (tramadol/acetaminophen) has
demonstrated excellent efficacy in pain studies and is supplied as a
combination analgesic containing 37.5 mg tramadol and 325 mg
acetaminophen.23
Narcotics (Opioids).
Narcotics (opioids) are the primary medications for analgesia of moderate to
severe pain from dental origin. They are centrally acting analgesics that act as
agonists at µ- and κ-opioid receptors. Morphine, which is a naturally
occurring opioid, is generally accepted as the prototypical narcotic. All other
narcotics on the market today are compared in potency to morphine.
Unlike nonopioids, opioids do not have a ceiling effect for analgesia. As
the dose increases, the analgesic effect increases. However, in addition to
relieving pain by m-receptor binding, euphoria, nausea, vomiting, and
constipation may occur. With high doses, sedation and respiratory
depression are possible. With chronic use, physical and psychologic
dependence are common.
The following section discusses the most commonly used narcotics in oral
implantology. Structurally, these narcotics are similar to morphine and
provide the same degree of pain relief and unlimited efficacy at equipotent
doses.
Codeine.
Codeine is a naturally occurring alkaloid that is classified as a mild analgesic.
Codeine has excellent antitussive properties; however, it is associated with
high degrees of nausea and constipation. Orally administered codeine is only
60% bioavailable, which results in only 10% being demethylated to morphine.
This 10% is the only part responsible for analgesic properties, thus 90% or
the drug has no analgesic efficacy. Because of the side effects and low potency
compared with other opioids, codeine is usually not the first choice of
narcotics used in oral implantology.
Hydrocodone.
Hydrocodone bitartrate is a semisynthetic narcotic analgesic and antitussive
with multiple actions qualitatively similar to codeine. It is usually used as a
combination analgesic, being combined with either acetaminophen or
ibuprofen. For several years, this narcotic has been the most frequently
dispensed prescription medication in the United States. Hydrocodone is
habit forming, and the most frequent adverse reactions are dizziness,
sedation, nausea, and vomiting.
Oxycodone.
Oxycodone is a semisynthetic opioid with analgesic action similar to
morphine. It is recommended for moderate to severe pain with its principal
actions being analgesia and sedation. It has excellent oral bioavailability
because it retains half of its analgesic activity when administered orally.
Oxycodone has the same adverse effects as most other opioids, with an
increased potential for abuse and drug dependence. Oxycodone is marketed
as a combination narcotic, combined with either acetaminophen (Percocet) or
aspirin (Percodan). A slow-release oxycodone (OxyContin) has been shown to
have a high abuse potential.
Combination Analgesic Therapy for Postoperative Pain.

A pain management strategy using multiple analgesics with different
mechanisms of action is termed combination analgesic therapy. The goal of
combining different types of analgesics is to increase the analgesic effect
while decreasing possible side effects. When multiple drugs are used in
combination, synergistic and additive effects allow for the use of lower doses
of each individual drug (Table 10.4).
TABLE 10.4
Combination Analgesics
Generic Name Brand Name Average Adult Dose Schedule

5 mg c odeine/300 mg ac etaminophen Tylenol #1 1–2 tablets every 4 h III
60 mg c odeine/300 mg ac etaminophen Tylenol #4 1 tablet every 4 h III
5 mg hydroc odone/500 mg ac etaminophen Vic odin/Lortab 5/500 1–2 tablets every 4–6 h (maximum 8 tablets/24 h) III
7.5 mg hydroc odone/750 mg ac etaminophen Vic odin ES 1 tablet every 4–6 h III
7.5 mg hydroc odone/650 mg ac etaminophen Lorc et 1 tablet every 4–6 h III
10 mg hydroc odone/660 mg ac etaminophen Vic odin 1 tablet every 4–6 h III
10 mg hydroc odone/650 mg ac etaminophen Lorc et 10/650 1 tablet every 4–6 h III
7.5 mg hydroc odone/200 mg ibuprofen Vic oprofen 1–2 tablets every 6 h III
5 mg oxyc odone/325 mg ac etaminophen Perc oc et 5/325 1 tablet every 4–6 h II
7.5 mg oxyc odone/500 mg ac etaminophen Perc oc et 7.5/500 1 tablet every 4–6 h/maximum 8/day II
10 mg oxyc odone/650 mg ac etaminophen Perc oc et 10/650 1 tablet every 4–6 h II
5 mg oxyc odone/400 mg ibuprofen Combunox 1 tablet every 6 h/maximum 4/day II
With combination therapy, acetaminophen or NSAIDs are used with an

opioid. Because of the ceiling effects of acetaminophen and NSAIDs, further
increases in dosage will not provide any additional analgesia; however, they
will increase side effects.
Analgesic Agents in Oral Implantology.

The selection of an analgesic or analgesic regimen for management of
postsurgical pain is ideally based on the expected pain intensity. This may be
based on the patient's medical history, past pain threshold, type of
procedure, extent of tissue reflection, and duration of procedure. Because of
the various agents and numerous options for the treatment of postsurgical
pain after dental implant surgery, a pain control protocol was formulated to
aid in the proper administration of these agents. According to the World
Health Organization guidelines, the procedure and patient must be
evaluated and classified as mild, moderate, or severe (Table 10.5).
TABLE 10.5
Recommended Pain Control Protocol (PCP)
Drug Dose
P CP 1: Mild P ain Expected
Ibuprofen 400 mg 1 h before
P CP 2: Mild to Moderate P ain Expected
Ibuprofen + hydroc odone (Vic odin) 400 mg 1 h before surgery + c ontinue 4 times daily for 2 days
5 mg/300 mg as needed
P CP 3: Moderate P ain Expected
Ibuprofen + hydroc odone (Vic odin ES ) 400 mg 1 h before surgery + c ontinue 4 times daily for 2 days, then as needed
7.5 mg/300 mg 4 times daily for 2 days, then as needed
P CP 4: Severe P ain Expected
Ibuprofen + hydroc odone (Vic odin HP) 400 mg 1 h before surgery + c ontinue 4 times daily for 4 days, then as needed
10 mg/300 mg 4 times daily for 2 days, then as needed
Mild pain.
Mild pain is self-limiting and usually will be resolved with normal
recommended doses of NSAIDs.
Moderate pain.
Moderate pain is more intense pain than mild and usually will not be
resolved totally by NSAIDs. It will interfere with function and disrupt the
activities of daily living.
Severe pain.
Severe pain is defined as pain that interferes with some or all of the activities
of daily living. The patient may be confined to bed, and strong opioid
treatment will need to be continued for days. Adjuvant drug therapies may
be needed for supplementation (Table 10.5).
Control of Postoperative Surgical Pain.

The goal of postsurgical pain management is to optimize patient comfort
through pharmacologic and behavioral strategies. The World Health
Organization formulated an analgesic “ladder ” for the treatment of pain
management. The following protocol describes three steps in the treatment
of acute pain.24
1. The first step is to maximize the use of NSAIDs (acetaminophen,

ibuprofen) for mild to moderate pain. Adjuvant medications such as
glucocorticoids and cryotherapy are often suggested.
2. When moderate pain is expected or persists, an opioid (hydrocodone,
codeine) should be added to the NSAID. The fixed dose of opioids with the
NSAIDs provides additive analgesia. Glucocorticoids and cryotherapy are
encouraged.
3. Moderate to severe pain that is expected or persists should be treated by

increasing the dosage of the opioid. Glucocorticoids and cryotherapy are of
particular benefit when not contraindicated.
With the guidelines from the World Health Organization, a pain control
protocol was formulated for treatment of procedures based on the expected
postoperative pain (Box 10.1).
Box 10.1
World Health Organization Pain Relief Ladder
Three-Step Conceptual Model
1. Nonopioid + adjuvant
2. Nonopioid + adjuvant + opioid (moderate)
3. Nonopioid + adjuvant + opioid (severe)
Adjuvants: long-acting anesthetics, glucocorticoids, tricyclic

antidepressants. © Copyright World Health Organization (WHO), 2016. All
Rights Reserved.
Treating Each Patient/Procedure the Same

Pharmacologically
Complication
Many clinicians treat all dental implant patients with the same prophylactic
protocol, irrespective of the patient's ASA classification and type of
procedure. For example, a sinus bone graft has much higher morbidity than a
single tooth implant, therefore, a different pharmacologic protocol is
indicated. The complications and morbidity of the surgical procedure are
proportional and directly related to the medical status of the patient, surgical
procedure, length of surgery, and the extent of tissue reflection. The authors
have developed a pharmacologic approach that recommends different
protocols based the factors mentioned (see Table 10.2).
Prevention
Clinicians should have a clear understanding of all prophylactic medications
(antibiotics, antiinflammatories, analgesics) that are indicated to minimize
postoperative complications and decrease morbidity. Additionally, the
implant clinician must be aware of all drug interactions and
contraindications to the use of these agents.
Treatment
Because of the many variables (e.g., local, systemic, surgical) that need to be
considered with the use of pharmacologic agents in implant dentistry, a
protocol has been developed to standardize the prophylactic use of these
agents. A four-category pharmacologic classification is proposed based on
the patient's ASA status, type of surgical procedure, and invasiveness of the
surgery (see Table 10.2).
Not Giving Adequate Postoperative Instructions

Patients should always receive postoperative instructions both verbally and
in writing. Failure to do so may increase the possibility of postoperative
complications and loss of confidence in the doctor and place the doctor at
risk for medicolegal issues.
Etiology
Unfortunately, many doctors do not have a consistent protocol for the
administration of pre- and postoperative instructions. This leads to patient
misunderstanding about expectations after surgery, after-hours phone calls,
and increased stress for the patient. Additionally, many clinicians have one
generic or generalized instruction protocol. Ideally, there should exist an
instruction protocol that is specific for the type and invasiveness of the
procedure.
Prevention
Detailed postoperative instructions should be given orally and in writing to
the patient before and after surgery. The instructions should also be available
for the patient on the office website if possible.
Treatment
Comprehensive review of all postoperative instructions is an important part
of treatment. Some of the more common topics for which instructions should
be presented to patients include the following:
Bruising.
The possibility of bruising or ecchymosis should always be explained to the
patient, even for shorter-duration and less invasive surgeries. It is crucial the
patient understand the possibility of bruising because this may lead to
embarrassment and esthetic issues for the patient. The patient should be
made aware that bruising can appear 3–4 days postoperatively and may take
up to 10–14 days for complete resolution. Additionally, patients should be
informed about the possibility of bruising extending into the submandibular
and neck area (because of fascial planes and gravity) because this will
minimize the possibility of patients questioning either an aggressive or poor
surgical technique by the doctor.
Bleeding.
The incidence of bleeding postoperatively is extremely high after dental
implant surgery. Patients should be cautioned on the potential for bleeding
during the first 24 hours and instructed on techniques to decrease the
bleeding. Patients should always be given gauze (3 × 3 or 4 × 4 gauze is
recommended because 2 × 2 pads may result in inadvertent aspiration by the
patient) for use as pressure dressings. Recommendations should be given to
minimize wearing an interim prosthesis because this may result in increased
bleeding. For significant or prolonged bleeding, the patient should be
instructed to contact the doctor (see Chapter 7). The patient should also be
instructed not to use a straw when drinking fluids because this may create a
negative pressure and increase bleeding. Also, spitting and vigorous rinsing
may open the surgical wound and cause bleeding.
Swelling.
The patient should be informed that swelling is most likely to occur after
implant surgery and will peak at 48–72 hours. Often, patients will exhibit
minimal swelling the day of surgery; however, it will most likely increase 2–3
days postoperatively. This will prevent the patient from misinterpreting the
swelling as a postoperative infection. The patient should be instructed to use
multiple pillows because sleeping with the head elevated decreases head and
neck swelling.
Hygiene.
Patients may gently brush their teeth during the first day; however, they
should avoid the surgical site. Gentle rinsing with chlorhexidine may be
initiated the day after surgery. Potent antiseptics (e.g., Listerine) should be
avoided until incision line closure.
Diet.
The patient should be counseled that following dental implant surgery, the
body requires adequate fluids and nourishment. Ideally, at least 2 liters of
fluids (milk, water, nonacidic juice) should be consumed within the first 24
hours. The patient should gradually progress to more solid foods. A high-
calorie diet with increased volume of liquid and soft foods for the first 24
hours is recommended. Soft foods are usually tolerated well. These include
milkshakes (use a spoon: NO straw), ice cream, applesauce, pudding, jello,
yogurt, mashed potatoes, scrambled eggs, pasta (no tomato sauce). Hot
liquids (coffee, tea, soup, etc.) should be avoided until local anesthesia has
worn off (~4–8 hours).
If the patient was administered intravenous sedation, the patient should
be instructed to have some food intake after surgery because they have been
NPO for a minimum of 6 hours prior to surgery. This should be in the form of
a soft food such as yogurt, jello, soup, or ice cream.
No Smoking or Alcohol Use.

Patients should have a thorough understanding of the effects of smoking and
alcohol use postoperatively on incision line opening and implant/bone
grafting morbidity. Smoking cessation should be initiated a minimum of 2
weeks prior to surgery and 6 weeks (ideally) postsurgery. The use of alcohol
prior to complete incision line healing should be discussed because this may
lead to an increased possibility of incision line opening and possible
infection.
Nerve Impairment.
Patients should have an understanding of the possible consequences of nerve
damage, which may include paresthesia, dysesthesia, and anesthesia. If this
occurs and is present after 24 hours, the patient should be instructed to
inform the doctor to be seen immediately for evaluation and treatment (see
Chapter 9).
Infection.
Although postoperative infections are rare, the patient should be informed
of the signs of infection, which may include sudden increase of swelling,
pain, elevated temperature, and lethargy. If any of these should occur, the
patient should inform the office of their symptoms.
Interim Prosthesis.
If the patient has an interim prosthesis, they should be instructed on its use
after surgery. Ideally, the prosthesis should not be worn until incision line
closure and inflammation is not present. If the patient is to wear the
prosthesis for social esthetic concerns, the doctor should adjust the
prosthesis to preserve the primary stress-bearing areas so the surgical area
has no pressure areas.
Postoperative Follow-Up.
Patients should have an understanding of the importance of postoperative
follow care. Usually, the patient is seen within 2 weeks of the surgery for
evaluation and suture removal.
Discontinuation of Current Medications.

Patients should fully understand that they should never discontinue or
modify any medication prescribed by their physician. This may result in a
serious complication if the patient fails to take medication such as
antihypertensives, hypoglycemics, or anticoagulants.
Nausea After Surgery

Nausea is not uncommon after dental implant surgery. Postoperative nausea
is usually brief and resolves within several hours. It may be very distressing
to the patient, though, especially if they have been NPO (nothing by mouth)
prior to the procedure.
Etiology
The etiology of nausea after surgery may be a direct result from prophylactic
medications or the swallowing of excessive amounts of blood, especially after
longer procedures. The most common prophylactic medications to cause
nausea are antibiotics. When patients are NPO for IV sedation, many
antibiotics have a high incidence of causing nausea (e.g., Augmentin,
clindamycin).
Prevention
Narcotic pain medications are the most frequent cause of nausea and should
be avoided until the nausea subsides. Nausea can be reduced by preceding
each pain pill with a small amount of soft food, and taking the medication
with a large volume of water. The prophylactic steroid recommended for
most implant surgeries, Decadron, has been shown to be an excellent
medication for prevention of postoperative nausea and vomiting (PONV).
Additionally, minimizing the swallowing of excessive amounts of blood will
reduce the possibility that the blood will irritate the stomach mucosa. The
meticulous removal of blood from the surgery site via suctioning and the use
of gauze throat packs will minimize the swallowing of blood. Yankauer
suctions are especially efficient with removing blood from the oropharynx
area (Fig. 10.6).
FIG 10.6 (A) Clostridium difficile (C. diff), normal bacteria present in the gut, may
cause infection resulting from antibiotic use. (B) Yankauer suction allows for efficient
and easy removal of blood from the surgical site and oropharynx. (C) Clinical image
depicting the use of the Yankauer suction. (A, Courtesy Dr. Clarence Wong. In Walsh TC,
Caraceni AT, Fainsinger R, et al, editors: Palliative medicine, Philadelphia, 2009, Saunders.)
Treatment
If nausea is extensive after surgery, OTC antiemetics may be used or
prescription medications (e.g., ondansetron [Zofran] 4-mg sublingual tablets)
may be prescribed.
Antibiotic-Associated Diarrhea
Antibiotic-associated diarrhea (AAD) is usually a benign, self-limiting
disorder. The frequency of this complication varies among antibiotics. In
most cases, no pathogens are identified and the diarrhea is caused by
alterations in the composition and function of the intestinal flora. AAD has
been defined as a minimum of three watery stools per day. This diarrhea may
occur from a few hours to up to 2 months after antibiotic intake. Studies have
shown the incidence of AAD after antibiotics is between 5% to 25%.25
Etiology
AAD results from an imbalance in the colonic bacteria. The alteration in the
microbiota will change carbohydrate metabolism and fatty acid absorption
resulting is osmotic diarrhea. Almost all groups of antibiotics may cause
AAD, but those with broad-spectrum coverage—in particular,
cephalosporins, fluoroquinolones, extended-coverage penicillins, and
clindamycin—are known to have the highest frequency.26
Prevention
Taking antibiotics with food helps to minimize AAD. Also, many studies
have shown that the use of probiotics decreases the incidence of AAD.27
These techniques are extremely helpful if the dental implant patient presents
with a past history of AAD.
Treatment
Patients with mild diarrhea not caused by C. difficile usually will not require
any treatment other than antibiotic cessation. Lost fluids and electrolytes
should be substituted and poorly absorbable carbohydrates avoided. If a
substitute antibiotic is required, consultation with the patient's physician is
recommended. If the patient exhibits any signs of dehydration they should
be referred to their physician or emergency room.
Pseudomembranous Colitis
In some cases of AAD, colitis (inflammation of the colon) will result. This
may lead to a condition called pseudomembranous colitis. Symptoms usually
include profuse diarrhea associated with cramps, abdominal pain, nausea,
vomiting, and fever. In severe cases, pseudomembranous colitis may be fatal
if not treated aggresively.
Etiology
An additional consequence of antibiotic therapy that causes diarrhea is the
overgrowth of the pathogen Clostridium difficile.28 More commonly known as
C. diff, it may account for up to 10% to 20% of AAD cases. This occurs when
inflammatory colitis results in the destruction of a significant amount of the
normal gut flora. With the decreased amount of “healthy” bacteria, C. diff
will flourish, causing signs of pseudomembranous colitis (see Fig. 10.6).
Prevention
Dental implant patients who present with a past history of AAD or C. diff
infection should not be administered any antibiotics until medical
consultation with the patient's physician. Additionally, patients who are
predisposed to C. diff infection include the elderly population. Patients older
than 65 have a 10 times greater chance of a C. diff infection than younger age
groups. Patients with a past history of a C. diff infection are at a 20% greater
risk of contracting C. diff after antibiotic administration.29
Treatment
Discontinuation of the antibiotic regimen is highly recommended along with
referral to the patient's physician for treatment. Severe cases of C. difficile–
positive diarrhea require oral antibiotic treatment of Vancomycin (125 mg
four times daily), metronidazole (250 mg three times daily), or bacitracin
(25,000 units four times daily).30 These medications should always be
prescribed by the patient’s physician.
Implant-Related Complications
Injury to Adjacent Teeth
Damaging adjacent natural teeth during dental implant placement may lead
to adverse effects on adjacent tooth structures and can result in dental
implant failure. The injury to the root structure of adjacent teeth may be
direct (damage to tooth by the drill or implant) or indirect (thermal damage
from the osteotomy process). Damage may result in bone loss, natural tooth
or implant loss, infection, internal or external resorption, loss of tooth vitality,
or prosthetic failure.
Etiology
Trauma to adjacent teeth may occur upon the placement of dental implants
because of improper angulation, implant sites with insufficient available
space or bone quantity, or by placement of implants with an incorrect
diameter. Dilacerated roots and excessive tilting in the mesiodistal direction
may impinge on the implant space and prevent ideal placement.
Additionally, available space discrepancies often exist between the coronal
space and the apical space. Studies of orthodontic mini-implants placed in
contact with teeth (<1.0 mm) have been shown to cause root resorption.
However, if the implant is removed in a timely fashion, cementum repair will
result.31
Prevention
The location of adjacent teeth to the implant site should be evaluated prior to
implant placement. The angulation should always be evaluated after the
initial osteotomy with a direction indicator (i.e., radiograph with known
diameter and length guide pin in osteotomy) to assess proper positioning.
Cone beam computed tomography (CBCT) surgical templates may be used to
avoid damaging adjacent root surfaces. Ideally, a minimum of 1.5 mm of
space between the implant and root surface is recommended (Figs. 10.7 and
10.8).
FIG 10.7 Prevention of damaging adjacent teeth. (A) Cone beam computed
tomography (CBCT) used to identify the actual space available between adjacent
tooth roots. (B) Ideally, a minimum of 1.5 mm space should exist between the
implant and tooth structure. (C) Positioning device to prevent improper placement
and ideal osteotomy location.
FIG 10.8 (A) Implant placement too close to tooth root resulting in root damage. (B)
Resultant loss of tooth. (C–D) Tooth and implant pathology from implant placement
too close to tooth. (E) A strict postoperative recall should be adhered to when
implant is in close approximation to root. Dilacerated root decreasing intraroot
distance for dental implant.
Treatment
Perioperative.
If the implant is encroaching on the periodontal ligament (PDL) or tooth
structure, ideally it should be removed and repositioned.
Postoperative/Posthealing.
If the implant has been previously placed and is not encroaching on the
PDL/tooth (asymptomatic) structure, strict monitoring should be done with
regular vitality testing. If the tooth is sensitive to thermal stimulation of
percussion, the implant should be removed immediately.
Implant Periapical Lesion
Following implant placement and recall examinations, case reports have
shown the genesis of periapical lesions (radiolucency), which may suggest a
possible precursor to failure of the endosseus implant.32 These periapical
lesions have been termed apical peri-implantitis and retrograde peri-
implantitis.33 The lesions have been defined as a symptomatic or
asymptomatic periapical radiolucency developing after implant placement
with a normal coronal bone to implant interface.
Etiology
Asymptomatic.
A clinically asymptomatic periapical radiolucency is considered to be inactive
when radiographically there exists evidence of bone destruction with no
clinical symptoms. This may result from placing an implant into a site in
which the osteotomy was prepared deeper than the implant length, resulting
in an apical space. Also, when implants are placed adjacent to a tooth with an
apical scar, this may result in a radiolucency. Inactive lesions may be caused
by thermal bone necrosis, which is a direct result of overheating the bone.
The thermal injury may result in a fibrous tissue interface, which may
compromise the prognosis of the implant.34
Symptomatic.
A clinically symptomatic lesion is most commonly caused by bacterial
contamination during implant placement. This may occur when an implant is
placed into a preexisting area with bacteria (existing infection, cyst,
granuloma, or abscess). When lesions are initiated at the apex, they may
spread coronally or facially. Clinical symptoms with active lesions include
intense pain, inflammation, percussion, mobility, or possible fistulas tract
formation (Fig. 10.9).34
FIG 10.9 Retrograde periapical lesion. (A–B) Apical pathology on integrated dental
implants. (C) Apical radiolucency from osteotomy preparation exceeding implant
length.
Prevention
Prevention includes the following:
1. Clear evaluation of adjacent tooth structure to rule out preexisting

infection or pathology
2. Pulp testing of adjacent teeth
3. Caution when placing immediate implants into sites with possible

pathology
4. Extensive debridement of pathologic tissue and decortication of immediate

extraction sites
Treatment
Because of the multifactorial etiology of periapical lesions around dental
implants, there is no accepted general consensus on the treatment.
Nonsurgical antibiotic treatment of periapical lesions has been shown to be
unsuccessful.35 The following has been shown to be effective treatments of
periapical lesions:
Exposure: Tissue reflection is completed to expose the apical implant area

(buccal or lingual access).
Debridement: The granulation tissue is completely removed to expose the

bony walls of the apical area.
Removal of implant apex (elective): The apical portion of the implant may be
removed to gain better access to the bony walls. This should be completed
only if there is no biomechanical compromise for the implant.
Surface decontamination: The implant surface may be detoxified with various

chemicals such as tetracycline (250 mg) grafting,36 citric acid (40%),37
chlorhexidine, and hydrogen peroxide.38,39
Allograft: The defect area is grafted with allograft material along with a
resorbable membrane. A local antibiotic (e.g., Ancef, Cleocin) should be
added to the graft for additional antimicrobial coverage.
Systemic antibiotics: Systemic prophylactic antibiotics (e.g., amoxicillin)

should be used along with 0.012% chlorhexidine oral rinse.
Titanium Allergy/Hypersensitivity
Hypersensitivity to titanium is an ever-increasing reportable complication in
medicine today that has been associated with a wide range of situations.
In orthopedic medicine, there are many case reports of titanium alloy
hypersensitivity. Witt and Swann reported 13 cases of failed total hip
prostheses and concluded the tissue reaction in response to metal-wear
debris may have been the etiology of the failed implants. This process has
been termed repassivation and may produce an oxide that surrounds and
turns the periimplant tissues black.40
Yamauchi et al reported a titanium-implanted pacemaker developing an
allergic reaction. The patient developed a distinct erythema over the
implantation site, which resulted in a generalized eczema. Titanium
sensitivity was confirmed by intracutaneous and lymphocyte stimulation
testing.41
In the dental literature, allergic reactions to pure titanium are rare.
However, many authors have suggested there is a higher incidence of
titanium alloy allergy with respect to dental implants; and is most likely
underreported because of a poor understanding of failure or allergy.42 Preez
et al have reported a case of implant failure due to a suspected titanium
hypersensitivity reaction around a dental implant. Histologic results showed
a chronic inflammatory reaction with concomitant fibrosis.43 Egusa et al
reported a titanium implant overdenture case that resulted in generalized
eczema that fully resolved after implant removal.44 Sicilia et al, in a clinical
study of 1500 consecutive implant patients, reported approximately nine
implants with a positive reaction to titanium allergy.45
Etiology
Sensitivity to titanium has been shown to be a result of presence of
macrophages and T lymphocytes with the presence of B lymphocytes, which
result in a type IV hypersensitivity reaction.46 All metals, when in a biologic
environment, undergo corrosion, which may lead to the formation of metallic
ions and trigger the immune system complex with endogenous proteins.47
Titanium alloy dental implants have been shown to contain many
“impurities” that may trigger type IV hypersensitivity reactions. Harloff used
spectral analysis to investigate various Ti alloy implants. The results showed
that all the Ti alloy samples contained small amounts of other elements such
as beryllium (Be), cobalt (Co), chromium (Cr), copper (Cu), iron (Fe), nickel
(Ni), and palladium. These impurity elements have been shown to be the
etiology of the hypersensitivity reactions.48
Prevention
Thorough medical history involving any past history of titanium
hypersensitivity.
Treatment
When titanium hypersensitivity is suspected, the implants should be
removed and the patient should be referred to their physician for
appropriate testing. Case reports have shown that, after complete removal of
the implants, complete resolution results.44 Metal sensitivity is usually
diagnosed using a “patch-test,” which involves placement of titanium
(allergen) to the skin for approximately 3–4 days. A positive test would
include the appearance of an erythematous reaction. However, there is a
possibility of false negatives because the sealing qualities of the skin against
direct contact may make the test unreliable (Fig. 10.10).
FIG 10.10 Titanium dental implant allergy. (A) Facial eczema after implant
placement. (B) Intraoral view of type IV hypersensitivity reaction. (C) Complete
resolution after implant removal. (From Egusa H, Ko N, Shimazu T, et al: Suspected
association of an allergic reaction with titanium dental implants: a clinical report. J Prosthet Dent
100(5):344–347, 2008.)
Fractured Mandible After Implant Placement

Mandibular jaw fractures after implant placement, although rare, may lead to
devastating complications for the patient. The fracture may be early (at the
time of surgery) or late (during the postoperative period). Most likely,
patients will appear postoperatively with severe pain, inflammation, and
limited opening. The incidence of mandibular fractures after implant
placement is approximately 0.2%.49 The most common location for fractures
to occur after implant placement (late fracture) is near the location of the
most distal implant.50
Etiology
Fractured mandibles most likely occur from attempting to place implants in
patients with severely resorbed ridges, especially when monocortical grafts
and ridge-splitting surgeries are completed. Patients who are predisposed to
fractures include those with highly excessive occlusal forces, or with division
C−w and D mandibles. Studies have shown a higher incidence of fractures in
patients who present with osteomalacia or osteoporosis. This is due to the
brittle bone being subject to loading forces with insufficient support.
Additional causes of mandibular fractures include placing implants that are
too wide or too long, which compromises the host bone and requires
excessive tightening of implants.50 Late (after surgery) mandibular fractures
most likely are caused by an increased stress at the implant site. The implant
generates a concentration of tensile stress that weakens the bone. Repeated
functional forces placed on the implant eventually lead to the fracture of the
bone.51
Prevention
The prevention of mandibular fractures includes proper treatment planning
and diagnosis, which involves the contraindication of implants placed in
division D mandibles. Division D patients should be referred for possible
iliac crest grafting. When drilling osteotomy sites in severely resorbed
mandibles, care should be exercised to not overheat the bone. This is most
easily completed by using intermediate drills, removing less bone with each
drill size. Additional techniques include bone plates and simultaneous
implant placement.
Treatment
The treatment of a fractured mandible after implant placement is referral to
an oral and maxillofacial surgeon for definitive care and possible removal of
the offending implants, along with reduction and stabilization of the
mandible. Treatment of mandibular fractures is usually based on the type
and location of the fracture as well as the extent of atrophy. Treatment
options include lag screws, wires, and plates (Fig. 10.11).
FIG 10.11 Fractured mandible. (A) Panoramic radiograph showing early implant
failure. (B) Panoramic radiograph depicting pathologic graft and osteomyelitis. (C)
Cone beam computed tomography (CBCT) 3-D image depicting fracture. (D) CBCT
3-D showing bone plate. (E) Resection of fracture and necrotic bone. (F) Bone graft
basket encompassing bone graft. (G) Final panoramic image depicting final bone
graft. (Courtesy David J. Dattilo, DDS, Chief OMFS Allegheny General Hospital, Pittsburgh, PA.)
Benign Paroxysmal Positional Vertigo

Benign paroxysmal positional vertigo (BPPV) is a disorder arising in the inner
ear that presents with symptoms of repeated episodes of positional vertigo.
Vertigo is most often characterized by the feeling of a spinning or swaying
movement when the patient is stationary. Often BPPV is associated with
nausea, vomiting, sweating, and difficulties in walking. BPPV is an
unexpected complication that has been reported after dental implant and
bone grafting surgery.
Etiology
The etiology of BPPV has been related to the use of specific surgical
techniques, prolonged patient positioning (supine), and hyperextension of
the neck. BPPV occurs by dislodgement calcium carbonate crystals that are
normally embedded in the utricle. The crystals migrate into the semicircular
canal. The crystals are not only sensitive to dislodgement but also to
prolonged static head positioning. They strike against sensitive nerve
endings (cupula) within the balance apparatus in the semicircular canal
(ampulla), which results in position- or motion-induced vertigo and
disequilibrium.52
Prevention
Do not allow patients to maintain hyperextension of the neck for an extended
amount of time. During maxillary posterior surgery, be conscious of the
possibility of dislodgement of the crystals with the use of osteotomes and a
mallet.
Treatment
The only successful treatment for BPPV is referral to an otolaryngologist
(ENT) physician or health care provider with knowledge of the Epley
procedure (canalith repositioning). This treatment consists of several slow
head position maneuvers (Box 10.2 and Fig. 10.12). The goal is to move the
dislodged particles from the semicircular canals of the inner ear to the
vestibule.
Box 10.2
The Epley Maneuver Procedure (See Fig. 10.12)
1. The patient is positioned in an upright sitting posture, legs fully extended
and the head rotated 45 degrees towards the side.
2. The patient is then quickly and passively forced down backwards by the
clinician performing the treatment into a supine position with the head
held approximately in a 30-degree neck extension for 1–2 minutes.
3. The patient's head is then rotated 90 degrees to the opposite direction,

while maintaining a 30-degree neck extension for 1–2 minutes.
4. With the head and neck in a fixed position relative to the body, the patient
rolls onto the shoulder, rotating the head another 90 degrees in the
direction that they are facing. The patient is now looking downwards at a
45-degree angle for 1–2 minutes.
5. The patient is slowly brought up to an upright sitting posture while

maintaining the 45-degree rotation of the head, and the patient holds the
position for 30 seconds.
6. The entire procedure may be repeated two more times, for a total of three
times.53
FIG 10.12 Vertigo after dental implant surgery. (A) Most common cause is the use
of osteotomes. (B) Epley maneuver. (B, From Beck RW: Functional neurology for practitioners
of manual medicine, ed 2, Edinburgh, 2011, Churchill Livingstone.)
Cover Screw Not Fully Seated

With two-stage dental implant surgery, localized superficial infections
including a fistulas tract may occur postoperatively. After implant placement,
if the cover screw is not adequately tightened, postoperative infections may
result, leading to possible implant morbidity.
Etiology
Because of the micro gap between the implant and cover screw, trapped
bacteria will colonize, which results in a possible irritation and infection.
This may occur from improper placement of the cover screw or excessive
force over the submerged implant.
Prevention
Tighten the cover screw at the time of placement so no micro gap exists. Care
should be noted to remove any tissue or bone that may impinge on the
proper seating of the cover screw. Caution should be exercised to not
overtighten the cover screw in D4 bone (Misch classification) because this
will result in the possibility of reducing the initial fixation of the implant.
Additionally, relieve the prosthesis over the surgical site so no force may be
transmitted to the top of the implant (Fig. 10.13).
FIG 10.13 (A) Inadequate tightening of surgical cover screw on implant after
surgical placement. (B) Resulting swelling with exudate over the cover screw. (C)
Tissue overgrowth of implant body. (D) Latch type tissue punch removal bur. (E)
Treatment includes complete uncovery of the implant and placement of a healing
abutment.
Treatment
Remove the cover screw and, if tissue impingement is the etiologic factor,
remove with a hand tissue punch, tissue punch bur, or laser. If bone is
present, use a profiling bur (end cutting) to remove the bone. A high-speed
handpiece should not be used because implant damage may result. A healing
abutment should be placed to allow for ideal healing of the tissue.
Partial Cover Screw Exposure (Two-Stage)

When the cover screw becomes partially exposed during the healing period
(two-stage technique), the implant is susceptible to premature loading,
increased bone loss, and infection.
Etiology
With two-stage implant surgery, the cover screw may become exposed
because of:
• Incision line opening
• Excess tension on the incision line
• Thin tissue (thin biotype)
• Interim prosthesis pressure
• Immediate implant placement
• Implant design—high surgical cover screw
Prevention
To prevent premature opening, tension should be released from the incision
line. This will allow for tension-free closure and minimal pressure on the
incision line. The interim prosthesis should be adjusted to have no direct
contact on the surgical site.
Treatment
A partially exposed cover screw will retain more bacteria and predispose the
implant to increased bone loss and morbidity. The implant should be
uncovered (tissue punch bur) and the smallest permucosal extension (in
height) should be used. Ideally, the permucosal extension should be 1 mm
above the tissue height. No attempt should be made to resuture and obtain
primary closure. The patient should be instructed on proper hygiene to
include gentle brushing of the abutment along with the use of chlorhexidine
(Fig. 10.14).
FIG 10.14 Partial cover screw exposure. (A) Incomplete tissue covering of implant
is commonly caused by excessive pressure from prosthesis. (B) Prosthesis not
adjusted, note protrusion that most likely will result in excess pressure on implant
(arrow).
Tissue Impingement Between Abutment and

Implant
In some cases, if the final abutment becomes loose during the healing period
or prosthetic rehabilitation, tissue impingement may result. The excess tissue
can prevent the proper seating of a cover screw, healing abutment,
impression transfer, or final prosthetic abutment (Fig. 10.15).
FIG 10.15 Tissue impingement. (A–B) Tissue prevents complete seating of
abutment.
Etiology
Due to the tissue consistency around implants, relapse of the tissue results
rather quickly, which may result in tissue impingement. This may even occur
from leaving out the healing or prosthetic abutment on the implant for an
extended amount of time.
Prevention
Prior to placing any abutment, make sure all tissue is removed from around
the circumference of the implant. After placement of a prosthetic abutment
or try-in of the final prosthesis, a periapical radiograph is recommended to
confirm complete seating. If a gap is present on the radiograph between
implant components, soft tissue impingement should be assumed.
Treatment
A tissue removal bur in a rotary handpiece, tissue punch, or laser of the
appropriate size should be used to remove any tissue from around the
implant or abutment. A radiograph should always be taken to verify
complete seating.
Bone Impingement Between the Abutment and

Implant
In two-stage implant surgery, it is not uncommon for bone overgrowth to be
present over the top of the implant (cover screw). The excess bone must be
removed to allow for proper seating of a cover screw, healing abutment,
impression transfer, or final prosthetic abutment (Fig. 10.16).
FIG 10.16 Bone impingement. (A) Mesial bone (arrow) preventing crown from
complete seating. (B) End-cutting profiling bur is used to remove bone. (C) Removal
of bone, complete seating of crown.
Etiology
Bony overgrowth or interference is most likely to occur when the implant is
placed slightly below the crest of the bone. In some cases, when the ridge is
uneven (higher lingual plate vs. buccal plate), the implant is placed at the
level of the buccal bone; however, the lingual plate of bone will impinge on
the abutment or cover screw. This will result in improper seating of the
implant components.
Prevention
The implant should be placed at the level of the buccal and lingual heights of
bone. If bone is present above the implant, the circumferential bone should
be removed. Care should be exercised to avoid damaging the implant.
Treatment
A profiling bur to reduce the bone height easily removes the bone that
prevents the proper seating of the abutment. A rotary handpiece with
profiling bur (with cover screw attached) should not be used because damage
to the implant body may result. A periapical radiograph will verify the proper
seating of the implant.
Excessive Chronic Pain Around Implant Area

Chronic pain after implant placement that does not resolve will most likely
have an inflammatory, nociceptive, or neuropathic component. Nociceptive
and inflammatory pain will most likely occur in response to a noxious
stimulation of sensory receptors by mechanical, thermal, or chemical trauma
(e.g., osteotomy). Neuropathic pain, on the other hand, may be initiated or
caused by a primary lesion or dysfunction in the nervous system. This may
occur even in the absence of any noxious stimuli. Chronic neuropathic pain
most likely involves both peripheral and central mechanisms.54
Etiology
Because the exact pathophysiology of chronic neuropathic pain is not known,
many etiologic factors have been associated with this complication. Factors
such as preoperative pain, preexisting pain conditions, and impairment in
general physical features have been documented with persistent
postoperative pain. Many psychologic factors such as anxiety, depression, fear
of surgery, and psychic vulnerability have been related with the development
of chronic pain. Additionally, many studies have shown women to be more
likely to experience chronic pain syndromes, as well as patients above the age
of 40, those with smaller-sized mandibles, smokers, diabetics, and those with
advanced bone resorption (Fig. 10.17).
FIG 10.17 Chronic neuropathic pain most commonly occurs when implants are
placed in close approximation to vital structures. (A) Inferior alveolar nerve (arrow).
(B) Failing implant that may cause chronic severe pain.
Prevention
To minimize the possibility of nerve damage during dental implant surgery,
the implant dentist must be cautious around all vital structures (e.g., mental
nerve). CBCT-based radiography should be used to determine the exact
amount of available bone to avoid damage to nerve tissue.
Another complication that may lead to nerve injury is thermal damage
produced by an implant drill. Significant care must be taken to minimize
heat generation. The clinician should use minimal pressure, a sharp drill, and
“bone dancing” when performing osteotomies, as well as copious irrigation.
Neural tissue has been shown to be easily damaged by heat stimuli, reducing
the ability of bone tissue to repair and regenerate.55
Management
The treatment of neuropathic pain is complicated and is not well understood.
There exist many types of treatment modalities to manage chronic
neuropathic pain.
Removal of Implant.
Renton et al showed that implants should be removed within 24 hours of
placement if patients exhibit neuropathic pain. The early removal increases
the probability of resolution of symptoms. In comparison, implants removed
3 to 90 days after placement showed no resolution of the neurosensory
complications.56
Psychologic.
The psychologic status of the patient needs to be evaluated, ideally with a
consultation by a clinical psychologist or psychiatrist. Psychologic variables
may include depression, distress, ADHD, unrealistic treatment expectations,
and background environmental factors.
Pharmacologic.
In the literature, there are various pharmacologic agents that have been
attributed to the treatment of neuropathic pain.57
Tricyclic Antidepressants (amitriptyline, desipramine, and nortriptyline):
The mechanism of action of these drugs is to inhibit the reuptake of
monoamines and to block sodium channels along with exerting
anticholinergic effects.
Serotonin and Norepinephrine Reuptake Inhibitors (duloxetine,
venlafaxine): (SNRIs) are potent inhibitors of the reuptake of serotonin and
norepinephrine, which are neurotransmitters that play an important role in
the mood of the patient. They are popular in the treatment of major
depression disorders and chronic neuropathic pain.
Anticonvulsants (gabapentin and pregabalin): The main mechanism of
action is the decrease of central sensitization and nociceptive transmission.
Local Anesthetics: Although usually used as a diagnostic tool, local
anesthetics have been shown to have therapeutic value in some instances of
chronic neuropathic pain because of their membrane stabilization potential.
Local anesthetics suppress sympathetic sprouting, which has been associated
with NP.58
Topical Medications (lidocaine or benzocaine): Other medications, such as
amitriptyline, carbamazepine, and ketamine, can be added to the mixture
(with lidocaine) by a compounding pharmacy with the local anesthetics.
Opiates/Analgesics: Opiates have been shown to be ineffective in the
treatment of neuropathic pain. Because this pain is chronic, the use of
opiates is not recommended because of possible addiction.59
Pain Specialist.
Patients with the neuropathic pain that cannot be resolved surgically,
pharmacologically, or psychologically should be encouraged to be evaluated
at a chronic pain clinic or pain specialist.
Fractured Implant
Although rare with today's dental implants, fractured implant bodies may
cause significant problems for both clinicians and patients. Dental implant
fractures may be one of the major causes of late implant failures and may
include possible medicolegal issues. Studies by Goodacre et al relate the risk
of implant body fracture in the early to intermediate period for implants 3.75
mm in diameter to be approximately 1%, the abutment screw fracture risk at
2%, and the prosthetic screw risk at 4% (Fig. 10.18).60
FIG 10.18 Fractured implant. (A) Implant body fracture. (B–C) Implant neck
fracture. (D) Small diameter implant placed in a nonideal position, note mesial
cantilever. (E) Because of small diameter implant, presence of mesial cantilever,
internal hex neck fracture. (F) Two mini-implants fractured in the posterior mandible
in close proximity to the mandibular canal.
Etiology
The incidence of implant body fracture dramatically increases when force
conditions are greater. Cantilevers, angled loads, and parafunction increase
the risk of fracture. The risk of fracture also increases over time. Typical
mechanical failures are due to either static loads or fatigue loads. Static load
(i.e., one load cycle) failures cause the stress in the material to exceed its
ultimate strength after one load application. Fatigue load failures occur if the
material is subjected to lower loads but repeated cycles of that load. The
endurance limit or fatigue strength is the level of highest stress a material
may be repetitively cycled through without failure. The endurance limit of a
material is often less than one-half its ultimate tensile strength. Therefore,
fatigue and ultimate strength values are related, but fatigue is a more critical
factor, especially for patients with parafunction because they impose higher
stress magnitude and greater cycles of load. Different materials have varying
degrees of resistance to repeated loading and subsequent fatigue-related
failures. The fatigue strength of titanium alloy (Ti-6Al-4V) is four times
greater (and safer) than grade 1 titanium, and almost two times greater than
grade 4 titanium. Long-term fracture of implant bodies and components may
be dramatically reduced with the use of titanium alloy rather than any grade
of commercially pure titanium (Fig. 10.19 and Table 10.6).
FIG 10.19 (A) Modification of prosthesis to include hollowing out implant site areas
to maintain primary stress-bearing areas. (B) Flange removal and relief made over
implant sites while maintaining primary stress-bearing area.
TABLE 10.6
Mechanical Properties for Different Grades of Titanium
P roperty Grade 1 Grade 2 Grade 3 Grade 4 TI-6A1-4V

Tensile strength, min (MPa) 240 345 450 550 930
Yield strength, 0.2% offset, min (MPa) 170 275 380 483 860
Modulus of elastic ity (GPa) 103 103 103 103 113
Grades 1 to 4, CP titanium; Ti-6AI-4V, titanium-vanadium alloy

Prevention
To reduce the possibility of implant body fracture, a titanium alloy implant
should ideally be used. Parafunctional habits should be addressed with
occlusal guards, narrow occlusal tables, no lateral contacts, and an ideal
occlusal scheme.
Treatment
The ideal treatment for a fractured implant includes the removal and
possible replacement of the implant. Alternative treatments include
modification of the prosthesis to not include the implant and possible
modification of the fractured implant (cementable abutment).
Excessive Pressure From an Interim Prosthesis

If the patient wears an interim prosthesis after implant or bone graft surgery,
excessive pressure may result in the premature loading of the surgical site.
Additionally, denture adhesive may lead to impaired healing with resultant
incision line opening and possible failure of the implant or bone graft.
Ideally, no interim prosthesis should be worn. However, this is unrealistic in
many cases because some patients are more socially active and esthetically
conscious.
Etiology
If the interim prosthesis does not have an occlusal stop (rest stop on teeth) or
is not utilizing the primary stress-bearing areas (maxilla: horizontal palate;
mandible: buccal shelf), normal occlusal forces will overload the surgical site.
This may result in premature loading and implant morbidity including bone
loss or failure of the implant.
Prevention
Patient Education.
If the patient demands to wear the prosthesis, they should be instructed to
wear it as little as possible. Explaining to the patient the inherent
disadvantages of wearing the prosthesis should be addressed. Patients
should also be educated on the complications of the use of denture adhesive,
especially if the adhesive is placed in approximation to the incision line.
Prosthesis Modification.
The labial flange and acrylic overlying the surgical site should be reduced to
minimize any possible pressure on the surgical site. Care should be exercised
to maintain the primary stress-bearing areas within the interim prosthesis to
avoid any pressure to the surgical site.
Selection of Correct Reline Material

Hard reline material.
Generally, hard denture reline materials are made of modified poly (methyl
methacrylate) acrylic (PMMA), which, because of the inherent hardness,
should never be used postsurgically for relines.61 Hard reline material in
approximation to the surgical site may have detrimental effects on the
implant site.
Soft reline material.

Soft relines have been classified as either acrylic or silicone. Silicone soft
liners include heat-cured liners similar to Molloplast-B. This is a gamma-
methacryloxypropyltrimethoxysilane heat-polymerized silicone.61 Soft reline
materials may be used; however, they should be relieved over the surgical
site. Acrylic soft reline materials are usually cold-cured and also should be
relieved over the incision area.
Tissue conditioner.
Tissue conditioners are soft elastomers that are classified as plasticized
acrylics, which are composed of a poly (ethyl methacrylate) mixture of
phthalate plasticizer and up to 25% ethanol. The enclosed plasticizer lowers
the glass-transition temperature so the rigid acrylic resin becomes rubbery
and resilient.
Tissue-conditioning material, when mixed properly, results in a gel of the
polymer and monomer with a resilient consistency. The resilient gel provides
an excellent cushion for traumatized tissue adjacent to the intaglio surface of
the hard, processed denture-base material. When the tissue-treatment liner
is replaced frequently, the damaged intraoral supporting tissues can return to
a state of health. Effective use of any tissue-treatment material may require
replacement every 3 days for up to 30 days depending on the material.
Eventually, these materials will become hard and rough and may harbor
bacteria and fungus.
Before a tissue conditioner is applied, the intraoral tissues must be clean
and dry. Although most dental materials should be mixed according to the
manufacturer's instructions, the mixing instructions of some tissue-
treatment materials can be altered depending on the desired viscosity and
flow needed clinically. After the material is placed on the surface of a
prosthesis and seated intraorally, the material is allowed to flow as the
patient closes their bite into maximum intercuspation or appropriate
interocclusal relation. After the material sets, excess amounts are trimmed
using a sharp, heated knife or scalpel.
Placing a tissue conditioner in a prosthesis for frequent liner replacement
is a relatively simple procedure, but a soft liner material that is not changed
frequently, as per the manufacturer's recommendations, can cause excess
pressure and tissue damage to the surgical site. Plasticizers can leach out,
which will result in a hardened material. Thus the selection of tissue-
conditioning material used is paramount to minimize loading of the implant
or bone graft site.
Some of the most common tissue conditioners are Coe-Comfort (GC
America Inc.), Lynal (DENTSPLY Caulk), and Visco-Gel (DENTSPLY
International). When there is greater tissue mobility and inflammation (post
implant placement or bone grafting), the use of a less viscous material (more
flowable) is indicated. Thus, Visco-Gel is usually the tissue conditioner of
choice because it has favorable flow characteristics, resists bacterial invasion,
and is usually replaced every 30 days compared with other tissue
conditioners, which need to be replaced every 2–3 days.
Treatment
Prosthesis Modification.
The internal surface of the prosthesis is aggressively relieved 3–5 mm over
the surgical site. A common, but incorrect, method is relieving the entire
intaglio surface of the prosthesis. This will result in overloading the surgical
site area. The flanges should also be removed over the surgical site.
Tissue Conditioners.
The proper use of tissue conditioners should be adhered to because a thicker
viscosity should be used to minimize migration of the tissue conditioner
material (Fig. 10.19, see Box 10.3). Migration of the tissue conditioner material
may lead to impingement into the incision line, which may result in impaired
healing.
Box 10.3
Reline Technique
1. Prosthesis preparation: Remove sufficient acrylic from the tissue surface
overlying the surgical site. A minimum of 1–2 mm is required for bulk of
material and the ability for the material to flow. If a flange exists that may
impinge on the surgical site, the flange should be removed.
2. Mix the tissue conditioner: Follow the manufacturer's recommendation for

proper powder-to-liquid ratio. Additional powder may be added to thicken
the mixture, thus reducing the flow of the material when the prosthesis is
inserted. Water-soluble petroleum jelly is applied to facilitate easy removal
of the excess material.
3. Seat the prosthesis in the mouth: Have the patient occlude in centric
occlusion.
4. Trim the excess material: After sufficient setting time (≈10 minutes), the
prosthesis is removed from the patient's mouth, and excess material is
removed with a sharp knife or scalpel.
From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.
Trauma From Explantation of Implants

In some situations a failing implant or the position of the implant
necessitates removal with reinsertion in an ideal position. The following are
possible reasons why dental implants may need to be removed:
• Mobility of the implant
• Extensive bone loss
• Chronic pain
• Advanced peri-implantitis
• Fractured implant
• Malpositioned implant
Complication
Taking an aggressive approach to remove an implant may lead to further
bone loss and jeopardize the future site for reimplantation. Because an
implant does not contain a periodontal ligament, placing too much force and
pressure on it may lead to buccal or lingual plate failure. Loss of bony plates
or excessive bone loss may result in the need for extensive bone
augmentation in the future.
Treatment
The removal of dental implants is dictated by the location, amount of bone
present, type of implant, and presence of mobility.
Mobile Implant.
The loss of the bone-implant integration necessitates immediate removal
because infection and further loss of bone may result. In certain cases, the
implant may migrate within tissue spaces or may be swallowed or aspirated.
Counter-torque Ratchet: This technique involves placing an abutment or an
engaging extraction tool into the implant and reverse torqueing the implant
counterclockwise. This technique is usually very atraumatic.
Convention Extraction Techniques: This method utilizes conventional forceps
and elevators and should be used only with minimal luxation to prevent
possible fracture of the buccal or lingual plate. After removal, all soft tissue
should be removed from the implant site prior to grafting or reimplantation.
Nonmobile Implant.
A partial or fully integrated implant is usually more problematic and can be
rather difficult to remove. Conventional extraction techniques should never
be used because they may lead to significant bone loss or fracture. If a final
crown and abutment is present, they should be removed to allow for easier
access.
Countertorque Ratchet: This technique involves placing an abutment or an
engaging extraction tool into the implant and reverse torqueing the implant
counterclockwise. This should be used only in poorly dense bone (~maxilla).
Care should be exercised in higher-density bone because damage or fracture
of the adjacent bone may occur with this type of removal technique. There
are many factors affecting the ease of implant removal via the countertorque
technique:
Hex (~D1-D2).
An internal hex implant is easier to remove via the countertorque method.
External hex implants, because they engage coronal to the implant body, are
more difficult to remove because of lack of leverage. Trilobe internal
connections, especially those with smaller diameters, have been shown to
fracture when greater than 45 N/cm of torque is applied.62 Care should be
exercised to prevent fracturing the implant upon removal.
Implant thread shape.

There are four types of implant thread designs: buttress, square, V-shaped,
and reverse buttress. The square thread shape has the highest bone-implant
contact (BIC) and will be the most difficult to remove via the countertorque
method.
Implant body design.

A tapered implant design will be easier to remove than a square implant
design. The thread depth and surface area decreases in the apical area, which
minimizes the torque force necessary for removal.
Antirotational design.
Some implant designs contain a vent or opening, usually at the apical end,
that will allow for bone growth integration. This will complicate the removal
of a partially or fully integrated implant. A trephine or surgical bur technique
may be indicated in the removal of these types of implants.
Reverse Screw Techniques: A reverse screw removal drill is utilized when the
internal aspect of the implants (threads) are damaged or when the
countertorque method is unsuccessful. Caution should be exercised with
smaller-diameter internal implants (~3.0 mm) because fracture of the implant
body may occur (Fig. 10.20).
FIG 10.20 Reverse screw techniques. (A) Fixture removal screw. (B) Screw
removal inserted into implant. (C) Counterrotate with torque wrench. (D) Implant will
unscrew. (E) Implant attached to fixture removal screw.
High-Speed Burs: The use of a high-speed bur is a fast, efficient technique to

remove an integrated implant. Ideally, a tapered surgical bur (extra long: 700
XXL) is used to minimize bone removal. The bur is used 360 degrees around
the implant to a depth of one-half to three-fourths the length of the implant
to be removed. Copious amounts of saline should be used to minimize
thermal damage and the possibility of osteomyelitis. This helps to maintain
bone and minimize damage to vital structures. After removal, the implant
site should be irrigated to remove any particles (Fig. 10.21).
FIG 10.21 High-speed burs. (A) 700 XXL. (B) Mesial and distal slots one-half the
depth of the implant. (C–D) Elevator is used with lateral movement to remove
implant.
Piezo Surgical Units: A piezo surgical unit uses piezoelectric vibrations to

cut bone tissue. By adjusting the ultrasonic frequency of the unit, it is
possible to remove hard tissue while leaving soft tissue untouched by the
process. Studies have shown that piezo units cause less soft tissue damage
compared with other extraction techniques (Fig. 10.22).63
FIG 10.22 (A) Piezotome Ultrasonic Surgery Unit. (B–C) Removal of implant with
piezo surgery unit. (A, Courtesy ACTEON North America, Mount Laurel, NJ.)
Trephine Burs: Trephine burs are barrel-shaped burs that have various
diameters. The bur selected should be slightly larger than the implant crest
module because too large of a trephine bur will result in excessive bone
removal. Too small of a trephine may result in implant body particles being
removed and becoming embedded in the implant site. Copious amounts of
saline should be used to minimize thermal damage and the possibility of
osteomyelitis. If the apex of the implant is in approximation to a vital
structure, the trephine bur should not be used at the apex to avoid vital
structure damage. After the implant is removed, the implant site should be
irrigated to remove any retained particles (Fig. 10.23).
FIG 10.23 Trephine burs. (A) Various diameter trephine burs. (B) The smallest
trephine that will encompass the implant should be used. (C) Surgical removal of
implant. (A, Courtesy Société FFDM-PNEUMAT-Département Dentaire THOMAS, Bourges, Cedex
France.)
Combination of Techniques: In some cases, it is prudent to remove bone one-

half to three-fourths the length of the implant (using a trephine, piezo, or
high-speed bur) along with the use of conventional extraction techniques or
countertorque ratchet.
Displacement or Migration Complications
Displacement of Implants: Maxilla
Numerous case reports have been published concerning displacement (at the
time of surgery) or migration (after surgery or prosthetic treatment) of
implants into an adjacent space such as the maxillary sinus, ethmoid sinus,64
sphenoid sinus,65 frontal sinus,66 orbit,67,68 nasal cavity, and the anterior
cranial base.69
Etiology
When dental implants migrate into the maxillary sinus, they may remain
asymptomatic and unknown to the clinician. The timing of implant
displacement into the maxillary sinus proper has been shown to range from
the time of surgery to 10 years after prosthetic rehabilitation.70 When
implants are determined to be displaced into the maxillary sinus, immediate
evaluation and removal should be rendered. If left untreated, the displaced
implants may become calcified (antrolith) or migrate into adjacent anatomic
areas. Case reports in the literature have documented displaced implants in
the maxillary sinus and migrating into the various regions of the head and
neck.
Maxillary Sinus71.
All case reports discussing the migration of implants (either early or late
migration) find that they originate in the maxillary sinus because of its
anatomic location with respect to the maxillary posterior region. After
displacement into the maxillary sinus, the dental implants have been
reported to migrate to various anatomic areas (Fig. 10.24).
Maxillary Sinus Ostium70.

The maxillary ostium is the main drainage location of the maxillary sinus into
the nasopharynx. The mucociliary action of the maxillary sinus cilia propels
any secretions through the ostium, into the infundibulum, through the
hiatus semilunaris, into the middle meatus, and finally into the nasopharynx.
The functional maxillary ostium has been documented to be approximately
2.4 mm in diameter, thus significantly smaller than a regular-sized dental
implant.72 The physiologic action of the maxillary sinus will transport the
dental implant into the ostium area, most likely blocking the area and
causing nonpatency. Nonpatency of the maxillary ostium will lead to
infection or cause the implant to erode through the ostium to other anatomic
areas (see Fig. 10.24).
FIG 10.24 Maxillary sinus. (A–C) Displacement of dental implants into the maxillary
sinus. (D) Displacement into the maxillary ostium causing nonpatency.
Nasal Cavity73.
Dental implants may migrate from the maxillary sinus into the nasal cavity
via extrusion through the ostium or erosion through the medial wall of the
sinus (lateral wall of the nasal cavity). The medial wall of the maxillary is
composed of a very thin layer of cortical bone (<0.5 mm) (Fig. 10.25).
FIG 10.25 Nasal cavity. Implant displaced into the maxillary sinus and eroded
through the medial wall of the maxillary sinus.
Ethmoid Sinus64.
The bilateral ethmoid sinuses arise within the ethmoid bone and form
distinct air cells superior to the maxillary sinus (between the orbits). These
pyramidal air cells are divided by thin septa and bordered by the middle
turbinate and the roof of the maxillary sinus. Dental implants may migrate to
the ethmoid sinus via the ostium or erode through the superior wall of the
sinus (Fig. 10.26A).
FIG 10.26 Migrated implants. (A) Ethmoid sinus. (B–D) Migrated implant into
sphenoid sinus. (A, From Haben M, Balys R, Frenkiel S: Dental implant migration into the ethmoid
sinus, J Otolaryngol 32:342–344, 2003; B–D, From Felisati G, Lozza P, Chiapasco M, et al:
Endoscopic removal of an unusual foreign body in the sphenoid sinus: an oral implant, Clin Oral
Implants Res 18:776–780, 2007.)
Sphenoid Sinus74.
The sphenoid sinus originates in the sphenoid bone in the center of the skull.
The pneumatization of the sphenoid sinus varies and may extend to the
foramen magnum. The cortical walls vary in thickness with the
anterosuperior wall being the thinnest. Dental implants may enter the
sphenoid sinus ostium, which is located on the anterosuperior surface of the
sphenoid bone and medial to the superior turbinate (Fig. 10.26B).
Orbital Area75.
The floor of the orbit coincides with the roof (superior) wall of the maxillary
sinus. The infraorbital nerve and blood vessels transverse this area. Implants
may migrate from the maxillary sinus into the inferior wall of the orbit
(superior wall of maxillary sinus) (Fig. 10.27).
FIG 10.27 (A–B) Migrated implants into the orbital area. (From Griffa A, Viterbo S,
Boffano P: Endoscopic-assisted removal of an intraorbital dislocated dental implant, Clin Oral
Implants Res 21:778–780, 2010.)
Anterior Cranial Base76.

The floor of the cranial cavity forms the skull base, which separates the brain
from other skull structures. The skull base is subdivided into three regions:
anterior, middle, and posterior. The anterior cranial base is formed by the
orbital plates of the frontal bone, the cribriform plate of the ethmoid bone,
and the wings of the sphenoid bone (Fig. 10.28).
FIG 10.28 Migrated implants anterior cranial base. (From Cascone P, et al: A dental
implant in the anterior cranial fossae, Int J Oral Maxillofac Surg 39:92–93, 2010.)
Early Displacement (At the Time of Surgery)
Poor Bone Quality.

In the posterior maxilla it is common for the bone quality to be poor (≈D4),
consisting of very fine trabecular and no cortical bone. Because of the poor
bone quality, the bone lacks density and strength and cannot maintain rigid
fixation of the implant. Forces applied to the area or negative intrasinus
pressure may lead to the migration of the dental implant into the maxillary
sinus proper (Fig. 10.29).
FIG 10.29 Etiology of displaced/migrated implants. (A) Poor bone quality (~D4). (B)
Implant placement without bone graft. (C) Autoimmune/rhinosinusitis. (D) Peri-
implantitis. (E) Implant with minimal surrounding bone that may lead to migration into
the sinus cavity.
Poor Surgical Technique.

Because of the poor bone quality, if the osteotomy is prepared with a
conventional drill sequence (e.g., routine, standard manufacturer's protocol),
overpreparation of the osteotomy site will result. Because of the
overpreparation, there will be insufficient bone at the crestal level to
maintain rigid fixation and migration may occur. Therefore,
underpreparation or the use of osteotomes should be utilized when
preparing osteotomies in these compromised areas.
Implant Placement Without Bone Graft.

Treatment planning in the posterior maxilla should coincide with the Misch
sinus augmentation protocol (SA-1–SA-4). For an implant to be placed
without bone grafting, a minimum of 8–10 mm is required. Less than 8 mm
of bone will predispose the implant to lack of rigid fixation and the
possibility of mobility or migration. For the implant to be placed with bone
grafting, a minimum of 5 mm of host bone is required for initial fixation.
Under-preparation of the osteotomy site is recommended to maintain as
much bone for initial fixation of the implant.
Galindo-Moreno et al completed a retrospective study on migrated dental
implants. They reported in 73% of the migrated implant cases, no bone
grafting was completed in conjunction with implant placement. The average
bone height for implant placement was approximately 5.2 mm. The mean
length of the implants was 13.43 mm, which resulted in no bone contact of
approximately 8.23 mm of the implant surface. Therefore, the main reason
for implant migration was lack of bone grafting with insufficient bone for
initial fixation.76a
Immediate Implant Placement.

With the popularity of immediate implants, there is a greater possibility of
an implant being displaced into the maxillary sinus after the extraction of a
multirooted maxillary molar. This is most critical in the first molar area,
where the defect from the extraction results in minimal bone to maintain
stability of the implant. In over two thirds of maxillary first molars, the
palatal or mesiobuccal root is in approximation of the maxillary sinus floor.
Late (After Surgery) Migration
Negative Pressure.
When initial fixation of the implant is absent, changes in intrasinus and nasal
pressure may intrude the implant into the maxillary sinus proper. Because of
the compromised bone implant contact (BIC), changes in intrasinus and
nasal air pressure may produce a suction effect, causing a negative pressure.
This may result in the displacement of the implant into the maxillary sinus.
Case studies have shown implants that have migrated into the maxillary
sinus and expelled via the maxillary ostium and nose from the negative
pressure.77
Autoimmune Reaction.
Many authors have discussed autoimmune reactions with the dental implant,
which result in bone loss around the implant, loss of integration, and
intrusion into the maxillary sinus.78
Occlusal Overloading.
Because of the poor bone quality in the posterior maxilla, excessive occlusal
force will result in bone loss or loss of fixation of the implant. Sufficient
primary stability is an important factor upon placement of the implant. This
should be followed by sufficient healing time, and strict adherence to
progressive bone loading and implant-protected occlusion (see Chapter 17).
This will involve avoiding shear forces (nonaxial) on the implant prosthesis
and minimizing cantilever effects. In cases of severe parafunction, an
occlusal guard is recommended after prosthetic completion.
Peri-Implantitis.
If peri-implantitis around a maxillary posterior implant is left untreated, loss
of fixation may result, which will lead to insufficient fixation. This may result
in the implant and prosthesis migrating into the maxillary sinus.
Prevention
To prevent displacement and migration of implants into the maxillary sinus,
ideal treatment planning along with surgical technique (modified for the
posterior maxilla) should be adhered to. A comprehensive preoperative
evaluation of the posterior maxilla should be completed and the inherent
unfavorable anatomic and possible pathologic conditions should be
addressed when treatment planning in this area. The Misch sinus
augmentation (SA-1 through SA-4) classification should be adhered to, so as
to minimize the possibility of implant intrusion into the sinus proper.
Treatment
Treatment of migrated or displaced implants includes the immediate
removal, which usually necessitates referral to an oral and maxillofacial
surgeon (OMFS) or otolaryngologist (ENT). The most common approaches
for removal of implants include the traditional Caldwell-Luc procedure,
intraoral approach, or a transnasal approach with functional endoscopic
sinus surgery. Pagella reported the use of an intraoral endoscopic (FESS—
functional endoscopic sinus surgery) extraction of a metallic foreign body
from the maxillary sinus.79 Regev reported the use of the Caldwell-Luc
operation (anterior maxillary wall approach) and also retrieval through an
intraoral preparation site approach.80 A multicenter study compared these
three methods of removing implants from the paranasal sinuses. The
conclusion verified that functional endoscopic sinus surgery in combination
with an intraoral approach is the most ideal for removing implants or
grafting materials.81
If the implant is not removed from the maxillary sinus, it may eventually
exit via the natural ostium by way of the normal physiologic mucociliary
transport. If the dental implant migrates through the ostium, the implant
may be transported through normal physiologic channels in the paranasal
sinuses. Many case reports exist in the literature showing the long-term
effects of dental implants not retrieved, including chronic rhinosinusitis,
fungal infections, and neoplastic changes (Fig. 10.30).82,83
FIG 10.30 (A) Panoramic radiograph depicting migrated dental implant in the right
sinus. (B) Coronal image showing implant in the maxillary ostium area. (C)
Functional endoscopic sinus surgery (FESS) approach to retrieve implant. (D)
Removal of implant from sinus cavity. (From Chiapasco M, Felisati G, Maccari A, et al: The
management of complications following displacement of oral implants in the paranasal sinuses: a
multicenter clinical report and proposed treatment protocols. Int J Oral Maxillofac Surg 38(12):1273–
1278, 2009.)
Displacement of Implants: Mandible

Although uncommon, implants may be displaced and migration may occur
in the mandible. This may occur from two mechanisms: (1) sublingual
osseous undercuts and (2) focal osteoporotic bone marrow defects (Fig.
10.31A).
FIG 10.31 Mandibular displaced implants. (A) Sublingual posterior undercut. (B)
Poor bone quality (marrow spaces). (C) Mandibular implant displaced into sublingual
space.
Sublingual Undercuts
Because of the inherent sublingual undercuts in the posterior mandible,
dental implants may be placed that result in a lack of bone for initial fixation
of the implant. Due to the lack of fixation, the implant becomes displaced
into the sublingual space. To prevent the mandibular displacement, the
osseous contours of the bone should be evaluated with three-dimensional
radiography (Fig. 10.31B). Because of these sublingual undercuts, implants
are often contraindicated when these conditions are present.
Focal Osteoporotic Bone Marrow Defects

In middle-aged women, radiolucent lesions may be present, usually in the
molar area, that are associated with a higher risk of implant displacement.
The defects are generally asymptomatic and are mainly determined during
CBCT evaluation of the posterior mandible. They are isolated or multifocal
radiolucencies, several millimeters to centimeters in diameter, with ill-
defined borders. Most cases are seen in edentulous sites (Fig. 10.31C).84–86
Migration of Allograft
Seok et al reported on a lateral wall sinus graft into a maxillary sinus with
active infection. The allograft was completed with a known membrane
perforation and preexisting maxillary sinus pathology. Shortly after the
surgery the patient reported a submandibular swelling, which required the
removal of the submandibular gland. Upon biopsy the submandibular
lymphatic vessels contained bone graft material that originated from the
maxillary sinus. It was concluded the graft material migrated from the
maxillary sinus to the submandibular lymph nodes through the lymphatic
vessels. The maxillary sinus lymphatic vessels drain through the natural
ostium and via the nasal lymphatic vessels into the submandibular lymph
nodes (Fig. 10.32A).87 Treatment included the complete removal of the
submandibular gland.
FIG 10.32 (A) Migration of allograft material from maxillary sinus to submandibular
gland via lymphatic vessels. (B) Axial radiographic findings depicting enlarged
submandibular lymph nodes (arrow). (C) Macroscopic view of the removed right
submandibular gland and lymph nodes. Necrotic changes in the lymph nodes were
observed (arrow). (D) Periapical radiograph depicting lack of fixation and
radiolucency of the tack migrating posteriorly (arrow). (A–C, From Seok, Hyun, et al:
Migration of alloplastic bone graft material in infected conditions: a case study and animal
experiment. J Oral Maxillofac Surg 72(6):1093, 2014.)
Bone Graft Tack Migration

Bone tacks are often used to fixate membranes, usually in combination with
bone grafting procedures. In many instances, to minimize tissue trauma in
removing the tacks, they are left in place after implant placement.
Unfortunately, tacks can separate from the bone and migrate within the soft
tissue and fascial spaces (Fig. 10.32B–C).88 Therefore, it is recommended to
remove the fixation tacks after bone healing is complete.
Migration of Dental Materials

When extracting maxillary molar teeth, care should be exercised to minimize
the possibility of extruding material (e.g., impression material, reline
material) in the maxillary sinus via an oral-antral communication. When oral-
antral communication exists, dental materials that may be inadvertently
extruded into the sinus proper. When this occurs, the material will become
calcified within the maxillary sinus from the deposition of salt around the
foreign body. The resultant calcified mass is an antrolith, which is a common
cause of chronic rhinosinusitis (Fig. 10.33).89
FIG 10.33 (A) Panoramic radiograph showing radiopaque foreign object in right
maxillary sinus. (B) Coronal view depicting foreign body (reline material) and
radiopaque maxillary sinus. (Evren OK, et al: Evaluation of the relationship between the
maxillary posterior teeth and the sinus floor using cone beam computed tomography, Surg Radiol
Anat 36:907–914, 2014.)
Etiology
After extraction there are two main causes of material being introduced into
the maxillary sinus. When an impression is taken or when a prosthesis is
relined, if the clinician unknowingly places significant pressure upon seating
the impression tray or prosthesis, the material, especially if it has low
viscosity, may flow into the sinus via a communication. With respect to
individual teeth, the first molar is the most common tooth to have roots in
approximation to the sinus cavity. Studies have shown the palatal and
mesiobuccal root to be in contact or perforating into the maxillary sinus
approximately 66% of the time.90 Therefore, after removal of the maxillary
first molar, there is a high probability of communication with the maxillary
sinus and special caution should be exercised prior to impression
completion.
Prevention
When mixing the reline or impression material, an increased viscosity should
be used as this will decrease the possibility of intrusion of material into the
maxillary sinus (See Box 10.3 and Fig. 10.34).
FIG 10.34 (A) Special caution should be used when relining a prosthesis after
maxillary posterior extractions as reline may be extruded into sinus cavity proper. (B)
Ideal mixture consistency for reline material. (C) Final relined prosthesis.
Treatment
If reline material or any other type of dental material is extruded into the
sinus, the patient should be referred to an otolaryngologist for evaluation
and removal of the material. Patients should always be informed of this
complication and the importance of removal.
Summary
When a clinician completes implant therapy with a patient, regardless of the
phase involved, it is paramount that follow-up care be continued. As
described in this chapter, postsurgical complications may arise even in the
best of initial operative situations. Prosthetic complications are also of
concern, which necessitates a comprehensive follow-up program. The
implant clinician who is aware of potential postoperative complications in all
phases of implant therapy will be ready to treat any situation in a rapid and
competent manner. An understanding of the necessity of maintaining close
communication with the patient throughout the entire treatment process is
crucial. Knowing the potential for these complications beforehand and
communicating them to the patient, along with a using a strong follow-up
protocol, gives the patient further confidence in the clinician should any
circumstance arise. This is beneficial to reduce stress for the implant
clinician and the patient, which minimizes the chances of medicolegal issues.
References
1. Hupp JR, Tucker MR, Ellis E. Contemporary oral and maxillofacial
surgery. Mosby: St Louis; 2013.
2. American Dental Association. Accepted dental therapeutics. ed 40.
ADA: Chicago; 1984.
3. Esen E, Tasar F. Determination of the anti-inflammatory effects of
methylprednisolone on the sequelae of third molar surgery. J Oral
Maxillofac Surg. 1999;57:1201–1206.
4. Neuper EA, Lee JW, Philput CB, et al. Evaluation of dexamethasone
for reduction of postsurgical sequelae of third molar removal. J Oral
5. Wang JJ, Ho ST, Lee SC, et al. The prophylactic effect of
dexamethasone on postoperative nausea and vomiting in women
undergoing thyroidectomy: a comparison of droperidol with saline.
Anesth Analg. 1999;89:200–203.
6. Misch CE, Moore P. Steroids and the reduction of pain, edema and
dysfunction in implant dentistry. Int J Oral Implantol. 1989;6:27–31.
7. Bull MJV. Cutaneous cryosurgery: principles and clinical practice. Brit
J Gen Pract. 1995;45:399–566.
8. Forouzanfar T, Sabelis A, Ausems S, et al. Effect of ice compression
on pain after mandibular third molar surgery: a single-blind,
randomized controlled trial. Int J Oral Maxillofac Surg. 2008;37:824–
830.
9. Cameron MH. Physical agents in rehabilitation—from research to
practice. Saunders: Philadelphia; 1999.
10. Carr DB, Jacox AK. Clinical practice guidelines for acute pain
management: operative or medical procedures and trauma. Agency for
Health Care Policy and Research: Washington, DC; 1992.
11. Fisher ES, Frame JW, Rout PG, McEntegart DJ. Factors affecting the
onset and severity of pain following the surgical removal of unilateral
impacted mandibular third molar teeth. Br Dent J. 1988;164:351–354.
12. Huynh MP, Yagiela JA. Current concepts in acute pain management. J
Calif Dent Assoc. 2003;31:1–13.
13. Chandraasekharan NV, Dai H. COX-3, a cyclooxygenase-1 variant
inhibited by acetaminophen and other analgesic/ antipyretic drugs:
cloning, structure, and expression. Proc Natl Acad Sci USA.
2002;99:13926–13931.
14. Basbaum AL, Leveine JD. Opiate analgesia. How central is a
peripheral target? N Engl J Med. 1991;325:1168–1169.
15. Schwab JM, Schluesener HJ. COX-3: just another COX or the solitary
elusive target of paracetamol? Lancet. 2003;361:981–982.
16. Ahmad N, Grad HA. The efficacy of non-opioid analgesics for
postoperative dental pain: a meta-analysis. Anesth Prog. 1997;44:119–
126.
17. Jackson DL, Moore PA. Preoperative nonsteroidal anti-inflammatory
medication for the prevention of postoperative dental pain. J Am Dent
Assoc. 1989;119:641–647.
18. Ruffalo RL, Jackson RL, Ofman JJ, et al. The impact of NSAID
selection on gastrointestinal injury risk for cardiovascular events:
identifying and treating patients at risk. Therapy. 2002;20:570–576.
19. Hernández-Diaz S, García-Rodríguez LA. Epidemiologic assessment
of the safety of conventional nonsteroidal anti-inflammatory drugs.
Am J Med. 2001;110(Suppl 3A):20S–27S.
20. Smalley WE, Griffin MR. The risks and costs of upper gastrointestinal
complications attributable to NSAIDs. Gastroenterol Clin North Am.
1996;25:373–379.
21. Raney LH. Evidence-based use of NSAIDs in the ED. [Available at]
http://www.emedhome.com; 2001.
22. Seymour RA, Ward-Booth P. Evaluation of different doses of ibuprofen
and ibuprofen tablets in postoperative dental pain. Br J Oral
23. Mullican WS, Lacy JR. Tramadol/acetaminophen combination tablets
and codeine/acetaminophen combination capsules for the treatment
of pain: a comparative trial. Clin Ther. 2001;23:1429–1445.
24. United States Department of Health and Human Services. Agency for
Health Care Policy and Research clinical practice guidelines, Number 9. US
Government Printing Office: Washington, DC; 1994.
25. Bartlett JG. Management of Clostridium difficile infection and other
antibiotic-associated diarrhoeas. Eur J Gastroenterol Hepatol.
1996;8:1054–1061.
26. Wiström J, Norrby SR, Myhre EB, et al. Frequency of antibiotic-
associated diarrhoea in 2462 antibiotic-treated hospitalized patients:
a prospective study. J Antimicrob Chemother. 2001;47(1):43–50.
27. Hempel S, Newberry SJ, Maher AR, et al. Probiotics for the prevention
and treatment of antibiotic-associated diarrhea: a systematic review
and meta-analysis. JAMA. 2012;307:1959–1969.
28. Wolfson AB. Harwood-Nuss' clinical practice of emergency medicine. ed 4.
LWW: New York; 2005.
29. C. difficile infection. [Available at] http://www.mayoclinic.org/diseases-
conditions/c-difficile/basics/risk-factors/con-20029664.
30. Högenauer C, Hammer HF, Krejs GJ, et al. Mechanisms and
management of antibiotic-associated diarrhea. Clin Infect Dis.
1998;27:702–710.
31. Kim H, Kim TW. Histologic evaluation of root-surface healing after
root contact or approximation during placement of mini-implants.
Am J Orthod Dentofacial Orthop. 2011;139:752–760.
32. Ayangco L, Sheridan PJ. Development and treatment of retrograde
peri-implantitis involving a site with a history of failed endodontic
and apicoectomy procedures: a series of reports. Int J Oral Maxillofac
Implants. 2001;3:412–417.
33. Quirynen M, Gijbels F, Jacobs R. An infected jawbone site
compromising successful osseointegration. Periodontol 2000.
2003;33:129–144.
34. Temmerman A, Lefever D, Teughels W, et al. Etiology and treatment
of periapical lesions around dental implants. Periodontol 2000.
2014;66(1):247–254.
35. Dahlin C, Nikfarid H, Alsen B, et al. Apical peri-implantitis: possible
predisposing factors, case reports, and surgical treatment
suggestions. Clin Implant Dent Relat Res. 2009;3:222–227.
36. Ashley ET, Covington LL, Bishop BG, et al. Ailing and failing
endosseous dental implants: a literature review. J Contemp Dent Pract.
2003;4(2):35–50.
37. Suarez F, Monje A, Galindo-Moreno P, et al. Implant surface
detoxification: a comprehensive review. Implant Dent. 2013;22(5):465–
473.
38. Meffert RM. How to treat ailing and failing implants. Implant Dent.
1992;1(1):25–26.
39. Artzi Z, Tal H, Chweidan H. Bone regeneration for reintegration in
peri-implant destruction. Compend Contin Educ Dent. 1998;19(1):17–20.
40. Witt JD, Swann M. Metal wear and tissue response in failed titanium
alloy total hip replacements. J Bone Joint Surg Br. 1991;73:559–563.
41. Yamauchi R, Morita A, Tsuji T. Pacemaker dermatitis from titanium.
Contact Dermatitis. 2000;42:52–53.
42. Siddiqi A, Payne AG, De Silva RK, et al. Titanium allergy: could it
affect dental implant integration? Clin Oral Implants Res. 2011;22:673–
680.
43. du Preez LA, Bütow KW, Swart TJ. Implant failure due to titanium
hypersensitivity/allergy? Report of a case. SADJ. 2007;62:24–25.
44. Egusa H, Ko N, Shimazu T, Yatani H. Suspected association of an
allergic reaction with titanium dental implants: a clinical report. J
Prosthet Dent. 2008;100:344–347.
45. Sicilia A, Cuesta S, Coma G, et al. Titanium allergy in dental implant
patients: a clinical study on 1500 consecutive patients. Clin Oral
Implants Res. 2008;19:823–835.
46. Holgers KM, Roupe G, Tjellström A, Bjursten LM. Clinical,
immunological and bacteriological evaluation of adverse reactions to
skin-penetrating titanium implants in the head and neck region.
Contact Dermatitis. 1992;27:1–7.
47. Hallab N, Merritt K, Jacobs JJ. Metal sensitivity in patients with
orthopaedic implants. J Bone Joint Surg Am. 2001;83A:428–436.
48. Harloff T, Hönle W, Holzwarth U, et al. Titanium allergy or not?
“Impurity” of titanium implant materials. Health. 2010;2:306–310.
49. Almasri M, El-Hakim M. Fracture of the anterior segment of the
atrophic mandible related to dental implants. Int J Oral Maxillofac
Surg. 2012;41:646–649.
50. Camargo IB, Van Sickels JE. Surgical complications after implant
placement. Dent Clin North Am. 2015;59(1):57–72.
51. Stellingsma C, Vissink A, Meijer HJ, et al. Implantology and the
severely resorbed edentulous mandible. Crit Rev Oral Biol Med.
2004;15:240.
52. Shivu ME, Billimaga A. Benign paroxysmal positional vertigo during
lateral window sinus lift procedure: a case report and review. Implant
Dent. 2015;24:106–109.
53. Parnes LS, Agrawal SK, Atlas J. Diagnosis and management of benign
paroxysmal positional vertigo (BPPV). CMAJ. 2003;169:681–693.
54. Costigan M, Scholz J, Woolf CJ. Neuropathic pain: a maladaptive
response of the nervous system to damage. Annu Rev Neurosci.
2009;32:1–32.
55. Tehemar SH. Factors affecting heat generation during implant site
preparation: a review of biologic observations and future
considerations. Int J Oral Maxillofac Implants. 1999;14:127–136.
56. Renton T, Dawood A, Shah A, et al. Post-implant neuropathy of the
trigeminal nerve. A case series. Br Dent J. 2012;212:E17.
57. Al-Sabbagh M, Okeson JP, Khalaf MW, et al. Persistent pain and
neurosensory disturbance after dental implant surgery: prevention
and treatment. Dent Clin North Am. 2015;59:143–156.
58. Takatori M, Kuroda Y, Hirose M. Local anesthetics suppress nerve
growth factor-mediated neurite outgrowth by inhibition of tyrosine
kinase activity of TrkA. Anesth Analg. 2006;102:462–467.
59. Rodríguez-Lozano FJ, Sanchez-Pérez A, Moya-Villaescusa MJ, et al.
Neuropathic orofacial pain after dental implant placement: review of
the literature and case report. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod. 2010;109:e8–e12.
60. Goodacre CJ, Bernal G, Runcharassaeng K, et al. Clinical
complications with implants and implant prostheses. J Prosthet Dent.
2003;90:121.
61. O'Brien WJ. Dental materials and their selection. ed 3. Quintessence:
Chicago; 2002:78–85.
62. Froum S, Yamanaka T, Cho SC, et al. Techniques to remove a failed
integrated implant. Compend Contin Educ Dent. 2011;32:22–26.
63. Preti G, Martinasso G, Peirone B, et al. Cytokines and growth factors
involved in the osseointegration of oral titanium implants positioned
using piezoelectric bone surgery versus a drill technique: a pilot
study in minipigs. J Periodontol. 2007;78:716–722.
64. Haben CM, Balys R, Frenkiel S. Dental implant migration into the
ethmoid sinus. J Otolaryngol. 2003;32:342–344.
65. Felisati G, Lozza P, Chiapasco M, Borloni R. Endoscopic removal of an
unusual foreign body in the sphenoid sinus: an oral implant. Clin
66. Chiapasco M, Felisati G, Maccari A, et al. The management of
complications following displacement of oral implants in the
paranasal sinuses: a multicenter clinical report and proposed
treatment protocols. Int J Oral Maxillofac Surg. 2009;38:1273–1278.
67. Griffa A, Viterbo S, Boffano P. Endoscopic-assisted removal of an
intraorbital dislocated dental implant. Clin Oral Implants Res.
2010;21:778–780.
68. Kluppel LE, Santos SE, Olate S, et al. Implant migration into maxillary
sinus: description of two asymptomatic cases. Oral Maxillofac Surg.
2010;14:63–66.
69. Cascone P, Ungari C, Filiaci F, et al. A dental implant in the anterior
cranial fossae. Int J Oral Maxillofac Surg. 2010;39(1):92–93.
70. Ridaura-Ruiz L, Figueiredo R, Guinot-Moya R, et al. Accidental
displacement of dental implants into the maxillary sinus: a report of
nine cases. Clin Implant Dent Relat Res. 2009;11(Suppl 1):e38–e45.
71. Iida S, Tanaka N, Kogo M, et al. Migration of a dental implant into the
maxillary sinus: a case report. Int J Oral Maxillofac Surg. 2000;29:358–
359.
72. Aust R, Drettner B. The functional size of the human maxillary ostium
in vivo. Acta Otolaryngol. 1974;78:1–6 [432–435].
73. Ramotar H, Jaberoo MC, Koo Ng NK, et al. Image-guided, endoscopic
removal of migrated titanium dental implants from maxillary sinus:
two cases. J Laryngol Otol. 2010;124(4):433–436.
74. Felisati G, Lozza P, Chiapasco M, et al. Endoscopic removal of an
unusual foreign body in the sphenoid sinus: an oral implant. Clin
75. Griffa A, Viterbo S, Boffano P. Endoscopic-assisted removal of an
intraorbital dislocated dental implant. Clin Oral Implants Res.
2010;21:778–780.
76. Cascone P, Ungari C, Filiaci F, et al. A dental implant in the anterior
cranial fossae. Int J Oral Maxillofac Surg. 2010;39:92–93.
76a. Galindo-Moreno P, Padial-Molina M, Avila G, et al. Complications
associated with implant migration into the maxillary sinus cavity. Clin
Oral Implants Res. 2012;23(10):1152–1160.
77. Reqev E, Smith RA, Perrott DH, Pogrel MA. Maxillary sinus
complications related to endosseous implants. Int J Oral Maxillofac
Implants. 1995;10:451–461.
78. Galindo P, Sánchez-Fernández E, Avila G, et al. Migration of implants
into the maxillary sinus: two clinical cases. Int J Oral Maxillofac
Implants. 2005;20:291–295.
79. Pagella F, Emanuelli E, Castelnuovo P. Endoscopic extraction of a
metal foreign body from the maxillary sinus. Laryngoscope.
1999;109:339–342.
80. Regev E, Smith RA, Perrott DH. Maxillary sinus complications related
to endosseous implants. Int J Oral Maxillofac Implants. 1995;10:451–
461.
81. Chiapasco M, Felisati G, Maccari A, et al. The management of
complications following displacement of oral implants in the
paranasal sinuses: a multicenter clinical report and proposed
treatment protocols. Int J Oral Maxillofac Surg. 2009;38:1273–1278.
82. Mladina R, Hat J, Klapan I, Heinzel B. An endoscopic approach to
metallic foreign bodies of the nose and paranasal sinuses. Am J
Otolaryngol. 1995;16:276–279.
83. Kobayashi A. Asymptomatic aspergillosis of the maxillary sinus
associated with foreign body of endodontic origin. Report of a case.
Int J Oral Maxillofac Surg. 1995;24:243–244.
84. Bayram B, Alaaddinoglu E. Implant-box mandible: dislocation of an
implant into the mandible. J Oral Maxillofac Surg. 2011;69:498–501.
85. Carvalho A, Barros MM, Garcia FB, et al. Displacement of dental
implant into the focal osteoporotic bone marrow defect [abstracts].
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2014;117:e154.
86. Garcia NG, Barros FBA, Carvalho MMD, et al. Focal osteoporotic bone
marrow defect involving dental implant: a case report. Int J Implant
Dent. 2015;1:1–3.
87. Seok H, Lee SK, Kim SG, et al. Migration of alloplastic bone graft
material in infected conditions: a case study and animal experiment.
Int J Oral Maxillofac Surg. 2014;72:1093–1093.e1.
88. Harrison K, Iskandar I, Chien H-H. Fixation tack penetration into the
maxillary sinus: a case report of a guided bone regeneration
procedure complication. Am J Case Rep. 2013;14:43–47.
89. Brisolla ADOP. Chronic maxillary sinusitis associated with dental
impression material. Med Oral Patol Oral Cir Bucal. 2009;14(4):E163–
E166.
90. Ok E, Güngör E, Çolak M, et al. Evaluation of the relationship between
the maxillary posterior teeth and the sinus floor using cone-beam
computed tomography. Surg Radiol Anat. 2014;36:907–914.
11
Wound Dehiscence
Incision Line Opening

Jon B. Suzuki, Randolph R. Resnik
Primary soft tissue closure is a mandatory condition for the success of

implant and grafting procedures. It ensures healing by primary intention and
requires minimal soft tissue collagen formation and soft tissue remodeling,
which minimizes postoperative discomfort. Incision line opening (ILO) is
one of the most common complications resulting from dental implant
surgery, occurring when a wound dehisces along a suture line (Fig. 11.1).
FIG 11.1 Incision line opening. (A) Incision line opening occurring after implant
placement. (B) Post allograft incision line opening. (C) Membrane graft dehiscence.
(D) Block graft with fixation screw exposure.
The prevalence of ILO has been shown in studies to range from 4.6% to
40% around submerged implants.1,2 In a study by Mendoza, 37% had no ILO,
while 43% had partial ILO, and 20% had complete incision line opening.3 Soft
tissue dehiscences (30%) have been shown to occur around membranes
(barriers) when placed as part of guided bone regeneration procedures
(GBR).4 Therefore, incision line opening is a common postoperative
complication after dental implant and bone grafting surgery. In this chapter
the etiologic factors, prevention, and management of incision line opening
will be discussed along with a treatment protocol that is procedure and time
specific.
Classification of Incision Line Opening
Complications
When placing root form implants with a two-stage approach, spontaneous
early exposure of submerged implants has the potential for complications
that may affect healing and osseointegration of the implants. A classification
and nomenclature system for these exposures is useful for communication
and record keeping. Clinical wound opening has been categorized by Tal et al
(Box 11.1 and Fig. 11.2).2
Box 11.1
Clinical Wound Opening Categories2
Class 0: The mucosa covering the implant is intact (see Fig. 11.2A).
Class 1: A breach in the mucosa covering the implant is observed. Oral

implant communication may be detected with a periodontal probe, but the
implant surface cannot be observed without mechanically interfering with
the mucosa (see Fig. 11.2B).
Class 2: The mucosa above the cover screw is fenestrated; the cover screw is
visible. The borders of the perforation do not reach or overlap the borders
of the cover screw (see Fig. 11.2C).
Class 3: The cover screw is visible. In some areas of the cover screw the
borders of the perforation aperture overlap the borders of the cover screw
(see Fig. 11.2D).
Class 4: Cover screw is completely exposed. When exposure was detected or

observed (Class 1 through 4), the patient was instructed to clean the
exposed site by gently rubbing the mucosa with gauze soaked in 0.2%
chlorhexidine solution twice daily (see Fig. 11.2E).
FIG 11.2 Incision line opening classification. (A) Class 0 wound healing. (B) Class
1 wound opening. (C) Class 2 wound opening. (D) Class 3 wound opening. (E)
Class 4 wound opening.
Considering that spontaneous early exposures are complications that can

potentially lead to mucositis or peri-implantitis, Barbosa proposed
classification for spontaneous early exposure of submerged implants based
on diagnostic methods and treatment modalities to prevent or intercept such
complications. They suggested that implants with spontaneous exposure
should immediately be surgically exposed as early as possible to prevent
mucositis. A healing abutment should be placed after the cover screw is
removed (Fig. 11.3).5
FIG 11.3 Barbosa Incision Line Opening Classification. (From Barboza EP and Caula
AL: Diagnoses, clinical classification, and proposed treatment of spontaneous early exposure of
submerged implants, Implant Dent 11(4):331–337, 2002.)
Morbidity Consequences of ILO With Implants and

Bone Grafting
The resultant consequences of ILO can vary depending on the type of
implant or bone grafting procedure. For implant placement with good initial
fixation, primary closure is favored for one-stage surgery with placement of a
permucosal abutment. For bone augmentation procedures, primary closure
is of paramount importance for clinicians when performing GBR techniques
and autogenous onlay grafting procedures. When incision line opening
occurs during autogenous block grafting, there tends to be a greater
potential for delayed healing, loss of graft particles into the oral cavity, and
increased risk of infection.
Exposure of nonresorbable membranes add additional risk of infection and
unsatisfactory results. If guided bone regeneration is performed in
conjunction with implant placement, ILO may also lead to loss of the
implant. ILO most likely will result in a bacterial smear layer on the implant
body, which may inhibit bone formation. Bone resorption resulting from
infection may require implant removal. The same degree of ILO, without
simultaneous implant placement, could possibly be managed and
compensated for by bone expansion, use of slightly narrower implants,
increased number of implants, and/or additional augmentation.
Immediate Implants
Dental implants have become an accepted treatment modality with
immediate placement into fresh extraction sockets. ILO is typically not an
issue when implants are placed in intact sockets with minimal voids because
primary closure is not necessary. Situations where implants are placed in
nonintact sockets concomitant with bone grafting would be classified
according to the dimension and architecture of osseous defects (similarly to
delayed implant placement). ILO in alveolar ridges with combined implant
placement and significant augmentation may be more vulnerable to
compromised outcomes.
Esthetic Consequences
In addition, ILO can negatively affect esthetic clinical outcomes. The
placement of implants simultaneous with regenerative procedures adds the
risk of a functional and esthetically compromised result. For multistage bone
augmentation procedures, primary soft tissue healing allows for most
predictable outcomes. Incision technique, flap design, soft tissue handling,
and avoidance of transitional prosthesis pressure are key factors in avoiding
ILO.
Postoperative Care
Wound dehiscence may be associated with increased discomfort and the
need for closer monitoring. More postoperative appointments are required.
These are financially nonproductive and negatively impact practice
profitability. Some patients may seek care or a second opinion due to loss of
confidence in the primary clinician. The lack of knowledge or experience on
behalf of the secondary clinician can potentially lead to legal action against
the primary treating doctor. When ILO occurs, the clinician should be
proactive in follow-up care and educating the patient on the complication
consequences.
Classification and Types of Wound Healing

Wound healing is an intricate process in which the body's tissue repairs itself
after injury (surgical wound). Despite having similar healing mechanisms, it
is generally observed that wounds in the oral mucosa heal faster and with
less scarring than extraoral wounds.6
Phases of Wound Healing

Surgical wound healing, whether by normal or delayed healing, will occur in
three phases. Wound healing is not a linear process; rather it progresses
differently depending on many patient-related factors. The three phases of
wound healing are (1) inflammatory phase, (2) proliferation phase, and (3)
maturation phase.
Inflammatory Phase.
The inflammatory phase is the body's natural response to a surgical injury. It
is characterized by a vascular and inflammatory response including local
vasoconstriction for the first 5 to 10 minutes followed by a local vasodilatory
response. This phase takes place the first few days after injury.
Within the first few minutes after injury, platelets adhere to the site,
become activated, and aggregate. These events are followed by activation of
the coagulation cascade, which forms a clot of aggregated platelets in a mesh
of cross-linked fibrin protein. The blood vessels in the wound bed contract,
forming a clot, which promotes hemostasis. The clot formed has two
functions: it temporarily protects the denuded tissues and serves as a
provisional matrix for cell migration.
The blood clot consists of cellular components of blood (including red and
white blood cells and platelets) in a matrix of fibrin, plasma fibronectin,
vitronectin, and thrombosporin.7 Once hemostasis is achieved, dilation of the
blood vessels will result, allowing white blood cells, growth factors,
antibodies, enzymes, and nutrients to invade the surgical wound. At this
stage the characteristic signs of inflammation may be seen: erythema, heat,
edema, pain, and functional disturbances. At the cellular level, neutrophils
and macrophages will initiate a host response, which will lyse and devitalize
the necrotic tissue. The strength of the wound relies mainly on the integrity
of the fibrin clot. Bacteria and cell debris are phagocytized and removed from
the wound by white blood cells.8
Proliferation Phase.
The proliferation phase is characteristic with the formation of new
granulation tissue, which is mainly comprised of collagen and extracellular
matrix. The proliferation phase begins within 24 hours after injury and may
last 3 to 12 days. It is characterized by angiogenesis, collagen deposition,
granulation tissue formation, epithelialization, and wound contraction.
Epithelialization may be completed in 24 to 48 hours in primary closed
wounds or delayed for 3 to 5 days in wounds healing by secondary intention.
In angiogenesis, vascular endothelial cells form new blood vessels. In
fibroplasia and granulation tissue formation, fibroblasts grow and form a
new, provisional extracellular matrix (ECM) by excreting collagen and
fibronectin. Concurrently, reepithelialization of the epidermis occurs, in
which epithelial cells proliferate and migrate over the wound bed, providing
cover for the new tissue.
For healthy granulation tissue to form fibroblasts, there must be adequate
levels of oxygen and nutrients available, which are supplied by the blood
vessels. Characteristics of healthy granulation tissue include a granular and
uneven surface that is pink and does not bleed easily. Epithelial cells will
begin to resurface on the surgical wound, which is termed epithelialization.
Maturation Phase.
Maturation phase is the final phase in the healing process and occurs when
the wound has closed. The remodeling of collagen from type III to type I will
occur. During wound contraction, myofibroblasts decrease the size of the
wound by gripping the wound edges and contracting, using mechanisms that
resemble smooth muscle cell contraction. The wound scar gains strength and
volume, and erythema decreases. Complete scar maturation and final tensile
strength generally take 12 to 18 months. When the cells' roles are close to
complete (no longer needed), they are removed by apoptosis.9 During
maturation and remodeling, collagen is remodeled and realigned along
tension lines. There will also be a reduction in the cellular activity as well as
the number of blood vessels (Fig. 11.4).10,11
FIG 11.4 (A–B) Time-related phases of wound healing showing various

components of the healing process.
Knowledge of the healing rates of the soft and hard tissues is useful to
determine if a patient is healing on schedule. The time for wound repair
subsequent to surgery is tissue specific:
Epithelium: heals at a rate of 0.5 to 1 mm per day (after a 12-hour lag time)
Connective tissue: heals 0.5 mm per day
Bone: heals at a rate of 50 µm per day, 1.5 mm per month

Mucoperiosteal flap: adheres to bone (or soft tissue flap) by a fibrin clot (0 to
24 hours).12
Types of Wound Healing

With respect to wound healing, there exist three types: (1) primary intention,
(2) secondary intention, and (3) tertiary intention.
Primary Intention.
With few exceptions, surgical procedures for dental implantology involve
surgical flaps, which ideally result in healing by primary intention. Healing
by primary intention results when the wound edges are approximated and
stabilized by sutures. Soft tissue flaps are usually maintained in positions
that are “passive” and tension free. A common complication resulting in
incision line opening is for the clinician to utilize sutures to actively
reposition mucoperiosteal flaps. This may result in excessive tension placed
on the flaps and may lead to ischemia and flap necrosis, which will usually
result in incision line opening.
Achieving the goal of primary intention for closure will allow for
hemostasis, less potential for infection and bone necrosis, along with
improved patient comfort. When ILO occurs, the only way for the wound to
heal is via secondary intention, which may lead to increased morbidity.
Wound healing is a complex and intricate process where the skin or tissues
repair after injury. In the case of normal skin, the epidermis and dermis exist
in a steady-state of equilibrium, forming a protective barrier against the
external environment. Once the protective barrier is broken, the physiologic
process of wound healing is immediately set in motion. The general
principles of healing and the cellular and molecular events observed in
extraoral sites also apply to healing processes that take place following oral
surgical procedures.13
Secondary Intention.
When wounds dehisce or ILO has occurred, the wound undergoes healing by
secondary intention. Secondary intention is healing by the body's natural
mechanisms, without surgical intervention. This typically occurs in large
wounds with traumatic tissue loss or avulsion, so that wound edges are
widely separated and cannot be apposed. Healing occurs by clot formation,
granulation, deposition of collagen, and eventual epithelialization. Wound
contracture brings the wound margins together (Fig. 11.5).
FIG 11.5 Secondary intention healing. (A) Larger clot forms in comparison to
primary intention within the first 24 hours. (B) Within 3–7 days, an increase in
inflammation, angiogenesis, macrophages, and fibroblasts are present, which result
in slower healing in comparison to primary intention. (C) Final healing results in
wound contraction. (From Kumar V, Abbas AK, Aster JC: Rob b ins & Cotran pathologic b asis of
disease, ed 9, Philadelphia, 2015, Saunders.)
Tertiary Intention.
A third type of healing has been described as tertiary intention. Tertiary
intention healing occurs when primary closure is delayed, allowing the
wound to granulate for a short period of time. The wound is then
reapproximated manually or by another technique. This method has been
termed delayed primary closure and can be used to debride an infected, acute
wound prior to closure.14 This type of healing is uncommon with respect to
dental implants and bone grafts.
Factors That Affect Wound Healing/Incision
Line Opening
Saliva
As concluded by animal studies, wound healing in oral mucosa is faster and
results in less scarring in comparison to extraoral sites. Oral wound healing
is enhanced by factors present in saliva and by specific microflora of the oral
cavity.15 Additionally, the properties of cells involved in tissue regeneration in
oral mucosa are unique and share properties of fetal cells.16 The observations
suggest that several cell functions important in tissue repair are shared by
fetal and gingival fibroblasts, which differ from dermal fibroblasts.
Gingival fibroblasts are phenotypically unique cells in adult tissue and may
contribute to the rapid healing of oral wounds with minimal scarring in the
gingiva. It is also apparent that saliva provides a unique environment in the
mouth conducive to rapid tissue repair. Reports indicate delayed healing of
oral wounds in patients with xerostomia or sialadenectomized animals.17
There are several physicochemical factors in saliva that favor gingival
wound healing. These include appropriate pH, ionic strength, and presence
of ions such as calcium and magnesium required for healing. Lubrication of
oral mucosa provided by saliva is also beneficial for wound healing.
The advantageous effects of maintaining a moist wound environment
include prevention of tissue dehydration and cell death, accelerated
angiogenesis, and increased breakdown of fibrin and tissue debris. The use
of hydrocolloid occlusive dressings may facilitate cutaneous wound healing.
Saliva-treated wounds undergo shorter inflammatory reactions and faster
epithelial coverage, as well as faster connective tissue regeneration. Moisture
and ionic strength may be primary factors in saliva that promote tissue repair
and are important for overall wound healing. This potential is probably due
to the presence of several elements in saliva including growth factors and
bacteria.18
Saliva is advantageous for wound healing. Patients who exhibit xerostomia or
salivary gland disorders are predisposed to wound healing complications.
Salivary substitutes and more frequent recall examinations are warranted.
Bacteria
The oral cavity harbors larger numbers of bacteria, with over 500 bacterial
species having been identified in the oral cavity. It is clear that bacteria affect
wound healing in the oral cavity, and it is well established that wounds
colonized by pathogenic bacteria have delayed healing.19 Clinicians are aware
of painful complications in extraction wound repair that result from bacterial
infection.
It is well recognized that small concentrations of bacteria may increase
rates of wound healing. In 1921, Carrel reported that wounds of dogs treated
with selected concentrations of Staphylococcus aureus healed faster than
untreated wounds. Several studies have confirmed the observation using
other bacterial species. Larjava found that proliferation of gingival fibroblasts
in culture was increased by Prevotella intermedius but decreased with similar
concentrations of Porphyromonas gingivalis.20 Interestingly, there was great
variation in this effect between fibroblast populations obtained from
different patients. These findings imply that the potential for periodontal
repair depends both on bacterial flora and the individual cell populations of
periodontal wounds.
Wound healing may be delayed and directly influenced by bacteria type. The
use of the antimicrobial 0.12% chlorhexidine rinses is advantageous to
decrease bacterial induced incision related issues. Additionally, the use of
systemic prophylactic antibiotics should be utilized during the pre- and
postoperative treatment phase.
Systemic Diseases
Systemic diseases are a vital component of treatment planning and implant
therapy. Specific systemic diseases and conditions affect wound healing and
bone metabolism, either of which can have a direct impact on the success of
implant therapy. Diabetes mellitus is a major endocrine disorder commonly
reported by approximately 10% patients. With diabetes-associated insulin
deficiency or metabolism defects, glucose remains in the bloodstream and
increases blood glucose levels. Diabetic patients are at risk to develop
infections and vascular complications. The healing process is affected by
impaired vascular function, impaired cell chemotaxis, and impaired
neutrophil function. Protein metabolism is decreased, and healing of soft
and hard tissue is delayed. Nerve regeneration is altered, and angiogenesis is
impaired.
Many non–life-threatening diseases and conditions require medications for
definitive management or control of potential wound healing complications.
Common examples include anticoagulants, immunosuppressants, and
bisphosphonates. Bleeding problems encountered when incising and
reflecting tissue for passive closure may be complicated by anticoagulants.
However, given the potential life-threatening complications of
discontinuing anticoagulants such as warfarin, this is usually not
recommended as long as the therapeutic drug levels are within normal
limits. However, special attention must be devoted to good surgical
technique and use of appropriate local hemostatic measures to control
bleeding.
Two classes of immunosuppressants frequently prescribed for patients are
glucocorticoids (e.g., prednisone) and cytostatics (chemotherapeutic agents).
The negative impact of these medications on wound healing can be mitigated
by appropriate patient selection, timing of treatment, and medical
consultation.
Bisphosphonates can also lead to wound dehiscence following surgery.
These drugs act by suppressing and reducing bone resorption by osteoclasts
and are used to treat bone disorders including osteoporosis, metastatic bone
cancer, and Paget disease (JBS figures on bone metabolism). After surgery
involving the jaws, bone exposure may develop rather than the normal soft
tissue closure healing mechanisms.21 This is common with more potent
nitrogen-containing intravenous bisphosphonates, and the prevalence is
lower with oral bisphosphonates.22 However, the clinician must be able to
differentiate bone exposure of this bisphosphonate origin and insufficient
flap closure or postextraction bony spicule formation.
Systemic diseases play a significant role in the healing process after dental
implant and bone-grafting procedures. The most common systemic disease
that affects healing is diabetes, which, if uncontrolled, may lead to significant
postoperative healing issues. Additionally, many medications including
anticoagulants, immunosuppressants, and bisphosphonates may increase
the risk of surgical wound healing. This underscores the importance of a
thorough medical consultation prior to any implant surgical procedure.
Local/Lifestyle-Related Factors
Smoking
In the United States, approximately 45 million adults and 21% of the
population smokes cigarettes. Approximately 23% of men and 19% of women
smoke cigarettes. Tobacco use has been implicated in many adverse systemic
outcomes, including tooth loss and dental implant failure.23 In fact, the entire
stomatognathic system suffers from the effect of tobacco byproducts.
Tobacco smoke decreases polymorphonuclear leukocyte activity, resulting
in lower motility, a lower rate of chemotactic migration, and reduced
phagocytic activity. These conditions contribute to a decreased resistance to
inflammation, infection, and impaired wound healing potential.24
Smoking is also associated with decreased calcium absorption. Additional
findings demonstrate a reduced mineral content in the bone of aging
smokers and, to a greater degree, in postmenopausal female smokers. The
association of tobacco with intraoral carcinoma is well recognized.
When incision line opening after surgery occurs, smoking delays
secondary wound healing, may contaminate bone grafts, and contributes to
early bone loss during healing. Treatment planning for any type of dental
implant surgery should emphasize the need for smoking cessation protocols.
Alcohol Use
Ethyl alcohol is one of the most widely used mood-altering drugs in the
world. More than 95% of smokers also drink alcohol. Alcoholism has been
associated with diseases such as liver and metabolic dysfunction, bone
marrow suppression resulting in bleeding complications, predisposition to
infection, and delayed soft tissue healing.25 The direct effect on bone includes
decreased formation, increased resorption, decreased osteoblast function,
decreased wound healing, and increased parathyroid hormone secretion,
which leads to lower bone density. However, it has been shown that
withdrawal of alcohol can reverse the negative effects on osteoblast function
in a matter of days.26 Additionally, the use of alcohol immediately after
surgery may predispose the surgical wound to decreased healing.
Obesity
Obesity is a major challenge for health care personnel caring for these
patients. Obesity is a chronic disease, emerging as a major epidemic public
health problem. In 2008, 35% of adults (age 20+) were overweight (body mass
index [BMI] ± 25 kg/m2), and the prevalence of obesity (BMI ≥30 kg/m2) has
doubled since 1980, affecting an estimated 502 million people.
In general, obese patients are at increased risk for wound healing
complications such as seroma, hematoma, infection, and wound dehiscence.
Cardiovascular problems associated with this condition may contribute to
ischemia by providing insufficient oxygen and nutrients to the tissue, which
may lead to tissue necrosis.
Respiratory issues may impair vital capacity and tidal function, which by
compromising tissue oxygenation may adversely affect wound healing. The
higher incidence of infection and the likelihood of other concomitant chronic
nonhealing wounds may diminish immune and healing responses. Oral
wound healing may also be affected by obesity.27 Suvan and coworkers found
that BMI and obesity appeared to be independent predictors of poor
response following periodontal therapy.28 In addition, technical difficulties in
operating on obese patients, including extended operating times, may
increase risk of wound contamination. Because of patient positioning, airway
complications may result.
Treatment Implications.
Lifestyle-related issues such as alcohol use and smoking may decrease
wound healing after dental implant and bone grafting procedures. It is
imperative the patient be informed that these lifestyle issues may lead to
slower wound healing and an increased possibility of incision line opening.
Additionally, physical characteristics may predispose the patient to
complication related issues.
Periodontal Biotype
Although some studies report minimal long-term effects of tissue biotype on
bone grafting and implant success, thicker biotypes may prevent tissue
breakdown or tears during suturing. Tissue augmentation should be
considered for patients with preexisting thin tissue biotypes. With thick
biotype tissue, there exists more keratinized tissue, which results in better
healing, easier suturing, and less likelihood of wound breakdown.
The patient's tissue biotype should always be evaluated prior to surgery.
Patients with a thin biotype may need soft tissue augmentation prior to or in
conjunction with dental implant and bone grafting procedures. Patients with
compromised tissue biotypes may predispose the patient to esthetic related
issues, especially if located in the esthetic zone (e.g., maxillary anterior).
Postoperative Issues
Despite meticulous surgery, deliberate or accidental behavior patterns by
patients may contribute to incision line opening. Failure to modify the diet to
a soft consistency or attempted visualization of surgical sites may traumatize
or place increased tension on the incision, resulting in incision line
dehiscence. It is also paramount that the clinician modify any transitional
prosthesis that may come in close approximation with an incision line, while
also advising the patient on the proper use of these prostheses, which may
include cessation early in the healing process. Poor decision making with
these postoperative issues increases the risk of incision line trauma and
breakdown.
Postoperative instructions should be given in writing and verbally to the
patients before and after surgery to ensure compliance. Patients should be
educated on the use of denture adhesives in approximation to the surgical
wound because this will most likely decrease healing and lead to incision line
opening.
Prevention of Incision Line Opening
Good Surgical Technique
To minimize and promote optimum wound healing and decrease the
possibility of incision line opening, the following surgical principals should
be adhered to.
Incision in Keratinized Tissue

The primary incision should ideally be located be in keratinized tissue
whenever possible. This permits increased wound surface area and a
resultant increase in vascularity to the incision. Not only does this reduce the
initial intraoral bleeding, it also severs smaller blood vessels and reduces
postoperative edema, which may add tension to the incision line. If there is 3
mm or more of attached gingiva on the crest of the edentulous ridge, the
incision bisects this tissue. This places half of the attached gingiva width on
each side of the incision. If there is less than 3 mm of attached keratinized
tissue on the crest, the incision is made more lingually so that at least 1.5 mm
of the attached tissue is placed to the facial aspect of the implant. This
concept is very important in the posterior mandible because attached tissue
is needed to prevent tension and pulling from the buccinator muscle (Fig.
11.6).29
FIG 11.6 Incision bisecting attached tissue.

Broad-Based Incision Design
The apex or tip of the flap should never be wider than the base (e.g., converge
from base to the apex). This will maintain adequate vasculature that will
prevent ischemic necrosis to the flap, decreasing the possibility of incision
line opening. The length of the flap should generally not exceed twice the
width of the base. Additionally, the base of the flap should not have
significant pressure or be excessively stretched or twisted, which may
compromise the blood supply (Fig. 11.7).30
FIG 11.7 Flap design showing a broad-based design allowing for minimal tension
on the flap.
Allow for Adequate Access

The flap should be large enough to provide adequate visualization of the
surgical site and allow for the insertion of instruments to perform the
surgical procedure. If the flap is too small, a retractor will not be able to
maintain the flap without excessive pressure. Excessive retraction pressure
will lead to increased inflammation, which may compromise the healing of
the incision line (Fig. 11.8).
FIG 11.8 Flap should allow for adequate access to decrease tissue trauma with
minimal tissue tension.
Vertical Release Incision to Maintain Blood Supply and

Decrease Tension on Flap
The blood supply to the reflected flap should be maintained whenever
possible. The primary blood supply to the facial flap, which is most often the
flap reflected for an implant or bone graft, is from the unkeratinized mobile
mucosa. This is especially true where muscles of facial expression or
functional muscles attach to the periosteum. Therefore, vertical release
incisions are made to the height of the mucogingival junction, and the facial
flap is reflected only 5 mm above the height of the mucogingival junction.
Both of these incision approaches maintain more blood supply to the facial
flap. In addition, incisions and reflection in the mobile alveolar mucosa
increase flap retraction during initial healing, which may contribute to
incision line opening and may increase risk of scar formation and delayed
healing of the incision line as a consequence of reduced blood supply.
Vertical release incisions should not be made over bony prominences (e.g.,
canine eminence) because this will increase tension on the incision line and
may increase the possibility of incision line opening (Fig. 11.9).
FIG 11.9 (A) Posterior mandibular incision depicting crestal incision with anterior
and posterior release. (B) Clinical image of incision in posterior mandible.
Maintain Flap Margins Over Bone

The soft tissue flap design should also have the margins of the wound over
host bone whenever possible. This is especially important when
approximating tissue over bone grafts or barrier membranes. The host bone
provides growth factors to the margins and allows the periosteum to
regenerate faster to the site. The margins distal to the elevated flap should
have minimal reflection. The palatal flap and the facial tissues distal to the
reflected flap should not be elevated from the palatal bone (unless
augmentation is required) because the blood supply to the incision line will
be delayed. In addition, the unreflected flap does not retract during initial
healing, which could place additional tension on the incision line. The soft
tissue reflection distal to the graft site may be split thickness to maintain
periosteum on the bone around the incision line. This improves the early
vascularization to the incision line and adhesion of the margins to reduce
retraction during initial healing (Fig. 11.10).
FIG 11.10 Broad-based release over bone avoiding boney protuberances.
Clean, Concise Incision

A clean incision is made through the tissue in one direction with even
pressure of the scalpel. A sharp blade of proper size (i.e., #15 blade) should
be used to be make clean, concise incisions without traumatizing the tissue
from repeated passes or strokes. Tentative strokes, especially in different
planes, will increase the amount of damaged tissue and increase the amount
of bleeding. Long, continuous strokes are preferable to shorter, inconsistent,
and interrupted strokes.31
Sharp dissection will minimize trauma to the incision line, which will
result in easier closure. Ideally, the incision should always be over bone. Care
should be noted of vital underlying nerves, blood vessels, and associated
muscles. Scalpel blades dull rather easily, especially when used on bone and
tissue with greater resistance. The clinician should change blades when
dulling is suspected to decrease tissue trauma.
The incision should be made with the blade held perpendicular to the
epithelial surface. This will result in an angle that produces square wound
margins that are easier to reorient during suturing and less likely for surgical
wound necrosis to occur (Fig. 11.11).
FIG 11.11 (A) Ideally, the scalpel is held with a pen grasp and the tissue is incised
perpendicular to the tissue. Sufficient pressure should be used to verify contact with
the bony ridge. (B) Incorrect use of scalpel with the scalpel not perpendicular to the
tissue.
Full Thickness Reflection and Ideal Flap Elevation

Ideally, the flap should be full thickness and include the surface mucosa,
submucosa, and the periosteum. The periosteum is necessary for healing; the
replacement of the periosteum in its original position will increase healing.
Tissue elevation should be completed with extreme care. To minimize
trauma to the soft tissue, meticulous handling is required. Proper use of
appropriate tissue forceps, avoidance of excessive suctioning by the assistant,
and “tieback” sutures all contribute to improved flap management.
Nonlocking tissue pick-ups, also called “thumb forceps,” are commonly held
between the thumb and two or three fingers of one hand. Spring tension at
one end holds the grasping ends apart until pressure is applied. These
forceps are used to hold tissues in place when applying sutures and to gently
retract tissues during exploratory surgery. Dressings or draping flaps may be
relocated without using hands or fingers. Tissue forceps can have smooth
tips, cross-hatched tips, or serrated tips (often called “mouse's teeth”).
Serrated forceps used on tissues will cause less tissue damage than smooth
surface forceps because the surgeon can grasp with less overall pressure.
Smooth or cross-hatched forceps are used to move dressings, remove
sutures, and perform similar tasks.
During flap elevation, elevators should rest on bone and not on soft tissue.
Care should be exercised to not continuously suction the tissue because this
may irritate and traumatize the tissue margins. Use of variable-suction tips
with fingertip control can help minimize tissue damage. After flap
replacement, it is advantageous to apply pressure to the tissue for several
minutes to minimize blood clot thickness and to ensure bleeding has
stopped (Fig. 11.12).
FIG 11.12 (A) Full thickness reflection. (B) The posterior incision line is made on
the crest of the edentulous ridge and often extends to the distal of the canine. (C)
The distal release incision extends lateral to the retromolar pad, along the ascending
ramus. (D) The lingual flap is first reflected off the crest. (E) The facial flap is
reflected and, when a computed tomography scan is not available, usually exposes
the superior aspect of the mental foramen. (B–E, From Misch CE: Contemporary implant
dentistry, ed 3, St. Louis, 2008, Mosby.)
Minimizing surgical operating time will directly benefit soft tissues and
will reduce the risk of infection.32 The tissue retractors should be selected
and placed in a position to prevent undue pressure on tissues. Maintaining
the retractors on bone and not on the tissue will minimize trauma to the
tissue. Excessive pressure and tension on the tissue flap will impair blood
circulation alter the physiologic healing of the surgical wound and
predisposes the wound to bacterial colonization.
Papilla-Saving Incisions
The interproximal soft tissue in sites next to adjacent natural teeth may be
classified into three categories: (1) papillae have an acceptable height in the
edentulous site, (2) papillae have less than acceptable height, or (3) one
papilla is acceptable and the other papilla is depressed and requires
elevation. When the interproximal papilla has an acceptable height, “papilla-
saving” incisions are made adjacent to each neighboring tooth. The vertical
incisions are made on the facial aspect of the edentulous site and begin 1 mm
below the mucogingival junction, within the keratinized tissue. Extending the
vertical incisions beyond the mucogingival junction increases the risk of scar
formation at the incision site. The full-thickness incision then approaches the
crest of the edentulous site, leaving 1.0 to 1.5 mm of the interproximal papilla
adjacent to each tooth. The vertical incisions are not wider at the base than
the crestal width of tissue. This permits the facial flap to be advanced over
the implant or short and adjacent to a permucosal extension (PME) at the
conclusion of the procedure, with no voids at the incision line and primary
closure (Fig. 11.13).
FIG 11.13 When the interdental papillae are in an acceptable position (A), papilla-
saving incisions are made to minimize soft tissue reflection. The incisions are
vertical to allow primary closure. When the papillae are depressed, the vertical
release incisions include the papilla in the edentulous site. In situations with a more
depressed soft tissue, facial soft tissue and papillae over each adjacent tooth are
also reflected. The crestal incision is on the palatal incline on the ridge (B). (C)
Clinical image depicting papilla-sparing incision. (From Misch CE: Contemporary implant
dentistry, ed 3, St. Louis, 2008, Mosby.)
Hemostasis
Hemostasis is important for many reasons, such as providing a clean surgical
field for accurate dissection and flap elevation, along with decreasing trauma.
Bleeding can occur from arteries, veins, or capillaries and may result in
diffuse, continuous oozing. Ideally, complete hemostasis should be achieved
prior to the closure of the wound. If not, the continuous bleeding or
hematoma will prevent the apposition of the surgical wound. There are many
mechanical, thermal, and chemical methods that may be used to achieve
adequate hemostasis. Care should be noted that the use of active or passive
hemostatic agents, along with electrocauterization of the wound margins,
may decrease the normal physiologic healing of the wound margins and
predispose the site to infection and possible wound dehiscence. If
hemostatic agents are used (e.g., cellulose), they should be removed after
hemostasis is accomplished because this may interfere with surgical wound
healing.
Prevent Desiccation of the Tissue

The tissues should be maintained in a moist environment without prolonged
periods of desiccation. If drying of the tissues occurs, there is less likelihood
that complete wound closure will occur. If the tissue margins become
desiccated, periodic irrigations with sterile saline (0.9% sodium chloride) or a
saline-moistened gauze may be used.
Relieving Tissue (Tension Free)

Excessive flap tension is the most frequent etiologic factor causing incision
line opening. This is best prevented by appropriate incision and flap design,
the use of periosteal releasing incisions, and blunt dissection (“tissue
stretching”). Past techniques to expand tissue primarily used a more apical
tissue reflection and horizontal scoring of the periosteum parallel to the
primary incision. Historically, the vestibular approach by Branemark allowed
for optimal visualization of anatomic landmarks, suturing remote from the
surgical area, complete tissue coverage, as well as predictable primary
closure and healing.33 The postoperative disadvantages of this approach
include distortion of the vestibule and other anatomic landmarks, edema,
difficult suture removal, and cumulative patient discomfort.34 Langer and
Langer documented the use of overlapping partial thickness flaps. This
approach results in extension of the coronal aspect of the buccal or palatal
flap, allowing primary intention closure around the site in an overlapping
manner.35 This is usually effective for primary closure when less than 5-mm
advancement of the flap is necessary (Fig. 11.14).
FIG 11.14 Stretchering or relieving the tissue for primary closure. (A) Periosteum
scored with #15 blade. (B) Blunt dissection with Metzenbaum scissors. (C) Relieved
tissue allowing for tension-free closure.
A submucosal space technique developed by Misch in the early 1980s is an

effective method to expand tissue over larger grafts (greater than 15 × 10 mm
in height and width) (Box 11.2).36
Box 11.2
Submucosal Space Technique3 6
Procedure
1. The full-thickness facial flap first is elevated off the facial bone
approximately 5 mm above the height of the vestibule.
2. One incision with a scalpel, 1 to 2 mm deep, is made through the

periosteum parallel to the crestal incision and 3 to 5 mm above the
vestibular height of the mucoperiosteum. This shallow incision is made the
full length of the facial flap and may even extend above and beyond the
vertical release incisions. Care is taken to make this incision above the
mucogingival junction; otherwise, the flap may be perforated and delay
soft tissue healing.
3. Soft tissue scissors (e.g., Metzenbaum) are used in a blunt dissection

technique to create a tunnel apical to the vestibule and above the
unreflected periosteum. The scissors are closed and pushed through the
initial scalpel incision approximately 10 mm deep, then opened slowly.
4. This submucosal space is parallel to the surface mucosa (not deep toward
the overlying bone) and above the unreflected periosteum. The thickness
of the facial flap should be 3 to 5 mm because the scissors are parallel to
the surface. This tunnel is expanded with the tissue scissors several
millimeters above and distal to the vertical relief incisions.
5. The submucosal space is developed and the flap is advanced the distance
of the “tunnel” and draped over the graft to approximate the tissue for
primary closure without tension. Ideally, the facial flap should be able to
advance over the graft and past the lingual flap margin by more than 5
mm. The facial flap may then be returned to the lingual flap margin and
sutured. This soft tissue procedure is performed before preparing the host
region for any type of bone grafting or augmentation around an implant
(Fig. 11.15).
The utility of periosteal incision for gaining flap release was studied by
Park.37 He found flaps could be advanced up to 171.3% (more than one and a
half times longer than its original length) by two vertical incisions and a
periosteal releasing incision (PRI) under a minimal tension of 5 g, while one
or two vertical incisions without PRI could advance the flap only 113.4% and
124.2%, respectively. These results suggested that PRI can be predictably
used to attain tension-free primary closure under a minimal pulling tension
of flaps.
Confirm Cover Screw Completely Tightened (Two

Stage)
A common postoperative complication that leads to incision line breakdown
and infection is the inadequate placement of the cover screw for two-stage
implant procedures. Any microgap between the cover screw and implant
leads to bacterial colonization and tissue irritation. This will most likely
result in swelling directly over the implant. Prior to suturing, the cover screw
should be checked to confirm total seating (Fig. 11.16).
FIG 11.16 (A) Surgical cover screw not fully seated. (B) Radiograph showing
incomplete seating of cover screw. (C–D) Soft tissue swelling with exudate over
implant site.
Utilization of Ideal Suturing Materials and

Techniques
The objective of the proper suturing of the surgical wound is to position and
secure the margins of the incisions to promote ideal and optimal healing.
The goal of the suture material and technique is to hold the margins of the
wound in close apposition until the wound has healed enough to withstand
normal functional tension and stress on the incision line. If surgical wounds
are not properly approximated, separation of the margins will occur, which
leads to increased postsurgical morbidity. The clinician must select a suture
with qualities that include high tensile strength, tissue biocompatibility that
prevents tissue irritation, ease of knot tying, and the ability to prevent
minimal knot slippage (Table 11.1).
FIG 11.15 (A) Incision. (B) Buccal flap elevated with tissue pick-ups. (C)
Periosteum scored with #15 blade (parallel to flap). (D) Blunt dissection with
Metzenbaum scissors (parallel to flap). (E) Tension-free flap.
TABLE 11.1
Various Suture Characteristics58
Tensile
Color of Strength Absorption Tissue
Suture Types Raw Material Contraindications Warnings
Material Retention in Rate Reaction
Vivo
S urgic al Gut Plain Yellowish- Collagen Lost within 3–5 Digested by Moderate S hould not be Absorbs
tan blue derived from days. Individual proteolytic used in tissues relatively
dyed healthy patient body enzymes that heal slowly quic kly
mammals c harac teristic s within 7–10 and require
(i.e., c ow, c an affec t rate of days support or under
sheep) tensile strength high-tension
loss areas
S urgic al Gut Chromic Brown Collagen Lost within 7– Digested by Moderate, Being Protein-
Blue derived from 10 days. body enzymes but less than absorbable, based
dyed healthy Individual within 7–10 plain surgic al should not be absorbable
mammals. patient days gut used where sutures
(i.e., c ow, c harac teristic s prolonged have a
sheep). c an affec t rate of approximation of tendenc y
Treated to tensile strength tissues under to fray
resist loss stress is required when tied
digestion by
body tissues
Coated VICRYL Braided Violet Copolymer Approximately Minimal until Mild Even though a None
(polyglac tin undyed of lac tide and 60% remains at about 40th day. high tensile known
910) (natural) glyc olide 2 weeks. Essentially strength, may not
c oated with Approximately c omplete be suffic ient for
polyglac tin 30% remains at between 60–90 high-stress areas
370 and 3 weeks. days. Absorbed
c alc ium (Dependent on by slow
stearate the type) hydrolysis
PDS Monofilament Violet Polyester Approximately Minimal until S light Being None
(polydioxanone) Clear polyethylene 70% remains at about 90th day. absorbable, known
terephthalate 2 weeks. Essentially should not be
c oated with Approximately c omplete within used where
polybut 50% remains at 210 days. prolonged
4 weeks. Absorbed by approximation of
Approximately slow hydrolysis tissues under
25% remains at stress is required
6 weeks
S urgic al S ilk Braided Blac k Natural Loses all or Usually c annot Ac ute S hould not be S lowly
White protein fiber most in about 1 be found after 2 inflammatory used in any area absorbs,
of raw silk year years. reac tion where suture tissue
spun by Enc apsulation removal would reac tion
silkworm by fibrous be diffic ult
(i.e., fibroin) c onnec tive
tissue may
result
e-PTFE Monofilament White Cytoplast Nonresorbable Nonresorbable Biologic ally None None
inert
Comfortable
to patients
S urgic al S teel Monofilament S ilver An alloy of Indefinite Nonabsorbable: Low S hould not be May
Multifilament Metallic iron-nic kel- remains used when a c orrode
c hromium enc apsulated in prosthesis of and break
body tissues another alloy is at points of
implanted bending,
twisting,
and
knotting
ETHILON Monofilament Blac k Polyamide Loses 15% to Degrades at a Extremely None None
Nylon Green polymer 20% per year rate of about low
Clear 15% to 20% per
year
NUROLON Braided Blac k Polyamide Loses 15% to Degrades at a Extremely None None
Nylon White polymer 20% per year rate of about low
15% to 20% per
year
MERS ILENE Braided Green Polyester Indefinite Nonabsorbable: Minimal None None
Polyester Fiber White polyethylene remains
terephthalate enc apsulated in
body tissues
ETHIBOND Braided Green Polyester Indefinite Nonabsorbable: Minimal None Has not
Polyester Fiber White polyethylene remains been
terephthalate enc apsulated in evaluated
c oated with body tissues in
polybutilate ophthalmic
surgery
PROLENE Monofilament Clear Polymer of Indefinite Nonabsorbable: Minimal None None

Polypropylene Blue propylene remains transient
enc apsulated in ac ute
body tissues inflammatory
reac tion
Suture Type
Absorbable
Absorbable sutures are very popular and advantageous in implant dentistry
because of the elimination of a suture removal appointment. There are two
types of resorbable sutures: natural and synthetic.
Natural.
Natural sutures are mainly broken down by body enzymes. The most
common natural sutures are the plain and chromic gut (Fig. 11.17).
FIG 11.17 (A) Plain gut. (B) Chromic gut.
Plain gut.
Plain gut is a monofilament derived from highly purified collagen from
sheep intestinal submucosa. It is highly antigenic, losing 50% of tensile
strength after 24 hours. Gut has unpredictable absorption because of the
enzymes and macrophages that break it down. This type of suture has been
shown to have a high incidence of tissue reactions, which impede healing.
Chromic gut.
Chromic gut is also derived from purified collagen from sheep intestinal
submucosa that is treated with chromic salts, which decrease absorption.
This material is highly antigenic and loses 50% of tensile strength after 5
days. As a monofilament it causes significant tissue reactivity. Chromic gut
causes inflammation, loses tension, and resorbs too quickly to maintain soft
tissue approximation over an augmented site. It is not recommended when
the tissues are advanced for a bone augmentation.38 Hypersensitivity
reactions have been shown to occur because of the chromate particles
present in the suture.39
Synthetic.
Synthetic sutures are broken down by hydrolysis because of their
hydrophobic nature. The most common synthetic, absorbable suture in
implant dentistry is polyglycolic acid (PGA) (Fig. 11.18).
FIG 11.18 (A) Synthetic absorbable suture: Polyglycolic acid (PGA) sutures which
are supplied in various resorption rates. (B) Clinical image of PGA suture, which has
the advantage of being resorbable and having excellent tensile strength.
Polyglycolic acid (Vicryl).

Because PGA sutures are absorbed by hydrolysis breakdown, they are not
affected by a low pH. Because they are manufactured by synthetic polymers,
their resorption is slower and they will maintain the incision line with a
tensile strength much longer than most suture materials. This suture
material will maintain sufficient tension over the first 2 weeks (75%), 50%
after 3 weeks, and 25% after 2 weeks.40 PGA sutures have varying resorption
rates, which consist of regular breakdown (≈21–28 days) and fast absorbing
(≈7–14 days). The suture material is inert and has a relatively low tissue
reaction.
Nonabsorbable.
Nonabsorbable sutures are composed of manmade materials, which are not
metabolized by the body. The most commonly used nonresorbable suture in
dentistry is a natural fiber, silk, which undergoes a special manufacturing
process to make it adequate for its use in surgery. Other nonabsorbable
sutures are made of artificial fibers (e.g., polypropylene, polyester, nylon),
which may contain coatings to enhance their performance characteristics
(Fig. 11.19).
FIG 11.19 Nonabsorbable sutures. (A) Silk. (B) Wicking present on silk sutures.
(C) Polypropylene. (D) Polyester. (E) Polytetrafluoroethylene (PTFE). (F) Clinical
image of PTFE suture.
Silk: Over time, silk has been the most universally used suture material in
dentistry because of its low cost and ease of handling. However, silk has
many disadvantages with respect to implant dentistry. First, it is
nonresorbable and must be removed. Because silk is a multifilament, is has
been shown to “wick,” which results in accumulating bacteria and fluid to
the surgical wound. And lastly, silk has been shown to release less tension
during early retraction of the flap from healing, along with eliciting greater
inflammation reactions, which may contribute to incision line opening more
often than synthetic materials.41,42
Polypropylene (i.e., prolene): This suture, which is a monofilament, will
not lose tensile strength over time. It is inert, has very little tissue reaction,
possesses a low coefficient of friction, passes through tissue very easily, and
has good knot security. The main disadvantage of this suture material tissue
is irritation from the cut ends of the suture material.
Polytetrafluoroethylene: The polytetrafluoroethylene (PTFE) suture
material is a monofilament, which has a relatively high tensile strength and
is nonwicking (low bacteria accumulation). Additionally, PTFE sutures have
good handling qualities, are easy to tie with excellent knot security, are soft
and comfortable for patients, and are biologically inert. The main
disadvantage of PTFE is that it is very expensive. PTFE sutures are slippery
and have poor frictional resistance to knot loosening. At least seven equally
tensioned, flat square throws are required to produce a secure knot when
using PTFE material.
Suture Qualities
The selection of the suture material should be made with regards to the
location and type of surgical procedure provided. However, an ideal suture
material should exhibit:
High Tensile Strength

High tensile strength is the measured force, in pounds, that the suture will
withstand prior to breaking. A suture material with low tensile strength will
lead to suture breakdown, which will most likely compromise the healing of
the incision line. The tensile strength of the tissue to be sutured will ideally
determine the tensile strength of the suture selected. The tensile strength of
the suture should be at least as strong as the tensile strength of the tissue
being sutured.
Low Tissue Reactivity

Tissue reaction from the suture material has been shown to be exhibited
through an inflammatory response, which will usually develop during the
first 2 to 7 days after suturing the tissue. The suture material selected should
have an inherent low tissue reactivity.42a Low tissue reactivity means that the
suture material should exhibit a minimal inflammatory response, which will
not delay wound healing nor increase infection rate. Tissue reaction is
reflected through an inflammatory response, which develops during the first
2 to 7 days after suturing the tissue.1-3 Several studies published over the past
four decades have reported that synthetic materials exhibit a superior
behavior to oral tissues in terms of tissue inflammatory reactions compared
to nonsynthetic suture material.
Absorbable
Absorbable suture material allows for the convenience of no suture removal.
These types of sutures undergo degradation and absorption in the tissues;
thus the sutures do not have to be removed. There are two mechanisms of
degradation of absorbable sutures: enzymatic breakdown or degradation by
hydrolysis (PGA). Sutures derived from a biologic origin (i.e., plain and
chromic gut) are digested by intraoral enzymes. Usually these types of
sutures lose their tensile strength very fast (within days of surgery) and are
not ideal for dental implant procedures. Secondly, these sutures may break
down even faster when the intraoral pH is low. A decreased pH may result
from infection, medications, metabolic disorders, or dry mouth. Trauma from
suture removal may sometimes lead to incision line opening.
Treatment Implications.
The ideal suture material should exhibit a high tensile strength, low tissue
reactivity, and be absorbable. In implant dentistry, this would include the use
of PGA or polyglycolic acid. A nonresorbable alternative would be a PTFE
suture (e.g., Cytoplast), which exhibit a high tensile strength and is
nonwicking.
Suture Size
Surgical threads are classified by diameter ranging from 1 to 10, with the
highest number being the smallest thread size. In implant dentistry, the most
common diameter is 3-0 for incision lines and 4-0 or 5-0 around tissue release
margins or areas that exhibit thinner tissue. In some situations, a 2-0 suture
will be used, usually as a tie-back for the lingual tissue when performing
mandibular surgery. Ideally, the smallest-diameter suture material that will
adequately hold the tissue in approximation should be used. As diameters of
suture decrease, so do their respective tensile strengths.
Suture Needle
The surgical needle is composed of three parts: (1) point, (2) needle body, and
(3) swaged end. The needle is type is classified by the curvature, radius, and
shape. The most commonly used suture needles in implant dentistry are the
and circle needles.43
The needle allows for the passage of the needle from buccal to lingual in
one pass. The is usually used in more restrictive areas such as maxillary
molars and in periosteal and mucogingival surgery.44 The clinician should
always be aware that there exist two types of needle designs: reverse cutting
and conventional. In implant dentistry, the reverse cutting should always be
used because this will minimize severing of the tissues. The reverse cutting
needle has a smooth inner curvature with its third cutting edge located on its
convex (outer) edge (Fig. 11.20).
FIG 11.20 Various needle sizes used in implant dentistry. (A) 3/8 circle. (B) 1/2
circle. (C) 5/8 circle.
Suturing Technique
Interrupted
Simple Loop.
The simple loop is the most common suture used in implant dentistry. It is
used to approximate mobile surgical flaps in edentulous areas. Each suture is
tied and cut after insertion through the tissue. The disadvantage of this
suture is it is more time consuming than a continuous suture. However, it
does have the advantage that, if one of the sutures would loosen or break, the
remaining sutures would most likely hold the wound together to minimize
wound dehiscence (Fig. 11.21).
FIG 11.21 Simple interrupted suture. (A) Tissue is held with tissue pick-ups. (B)
Enter tissue at a 90-degree angle. (C) Exit tissue at a 90-degree angle. (D) Two
throws over needle holders. (E) Needle holders engage opposite end of suture. (F)
First knot is pulled tight to lay flat. (G) One throw the opposite way from first throw.
(H) Second knot is secured. (I) One throw, the same way as the first throw. (J)
Needle holders engage opposite end of suture. (K) Third knot secured. (L) Suture
ends are cut approximately 3 mm in length.
Figure-Eight.
The figure-eight suture is placed as a simple loop on the buccal; however, on
the lingual, the needle passes through the outer aspect of the flap. The main
disadvantage of the figure-eight is the suture material is interposed between
the flaps after full closure. The figure-eight suture is most commonly used
with extraction sites and around papilla (Fig. 11.22).
FIG 11.22 Figure-eight suture. (A) Enter buccal tissue at 90 degrees. (B) Do not
enter lingual flap. (C) Enter from lingual at 90 degrees. (D) Do not enter buccal flap.
(E) Tie suture ends.
Second Stage Surgery: Permucosal Abutment Suturing.

A modification of the interrupted suture may be completed upon second
stage surgery with a permucosal abutment that has a suture groove. A suture
groove 3 to 5 mm above the platform connection may be incorporated in the
healing abutment (e.g., External implant system, previously known as the
Maestro dental system [BioHorizons IPH, Inc.]) (Fig. 11.23A). When the
tissue requires apical repositioning or when it is 3 to 4 mm thick and may
grow over the healing abutment, the suture groove may be used (see Fig.
11.32). A suture is placed next to the healing abutment. Tissue forceps lift the
suture from the incision line, and the suture is then rotated to form a loop.
The loop is placed over the enlarged healing abutment and into the suture
groove or under the healing cap. The suture may then be tied, securing the
tissue at the height of the suture groove (see Fig. 11.33). A similar technique
is used on the other side of the healing abutment. These two sutures (one on
each side) hold the tissue at the level of the suture groove and prevent it
from lifting up and over the healing cap during soft tissue healing.
FIG 11.23 (A) A suture groove in the permucosal extension may be positioned 3 to
5 mm above the bone. (B) The suture groove helps to apically reposition the tissue,
so it will remain less than 3 to 5 mm thick, to reduce the sulcus depth. (C) The
suture groove in the permucosal extension may be used to loop the suture around
the groove and tie the tissue at a more apical position. (From Misch CE: Contemporary
implant dentistry, ed 3, St. Louis, 2008, Mosby.)
Continuous
Soft tissue spans necessitating four or more interrupted sutures are best
approximated with continuous nonlocking sutures. This suture design places
less tension on the suture line and soft tissue and allows faster vasculariza-
tion of the reflected soft tissue flaps. However, whether locking or
nonlocking, this suture knot has a tendency to loosen with uneven
distribution of tension, which results in a compromise to the integrity of the
suture knot (Fig. 11.24).
FIG 11.24 Simple running or continuous suture: (A–E) Enter tissue at 90 degree
and use the same protocol as a simple interrupted suture. (F) Instead of both
strands (ends) being cut, only cut the short strand leaving a 2–3 mm tail. The
second stitch should be made approximately 3 mm from the first suture. (G–H)
Multiple stitches are made encompassing the entire incision line. (I) The last stitch is
not pulled completely through the tissue. Instead the loop is held with the needle
holder and used as the short strand in order to tie off the distal end of the suture
closure. (J) Clinical Image of Continuous Suture.
Horizontal/Vertical Mattress
Mattress sutures are a variation of the interrupted suture and are used most
commonly where there exists muscle pull or high tension. This type of
suturing technique will evert the surgical wound edges, which keeps the
epithelium away from underlying structures and maintains the tissue flaps to
the underlying structures (i.e., dental implant, graft material, membrane).45
There are two types of mattress suture, horizontal and vertical. Both of
these suture types allow for greater tension to be applied on the soft tissue
closure without risk of tearing the soft tissue flap. It should be emphasized
they are not used to obtain primary closure when tension on the soft tissue
flaps is present at surgery. The tissues should rest passively together before
suturing. However, during functional/parafunctional movement of the
tissues, the tension on the incision line may be reduced with a horizontal
mattress suture. They are often used in the mandible when the floor of the
mouth is in proximity to the lingual flap and the tissue is thin. They may also
be used on a facial flap with a strong muscle pull on the soft tissue. In
addition, horizontal mattress sutures evert the soft tissue margin and ensure
primary closure without epithelium entrapment. A combination of a few
horizontal mattress sutures with a continuous suture may be indicated to
close large soft tissue spans (Figs. 11.25 and 11.26; Box 11.3).
FIG 11.25 Horizontal Mattress Suture: (A) The needle enters the tissue a 90
degrees and exits on the lingual side of the incision. (B–E) The needle is then placed
backwards in the needle holder and is inserted approximately 4 mm farther down
from the first stitch. The needle passes from the far side to the near side (buccal).
(F) The suture is then tied gently on the side of the wound where the suturing
originated.
FIG 11.26 Vertical mattress suture (far-far-near-near). (A) The needle should enter
the tissue a 90 degrees approximately 5–6 mm from the margin of the incision and
exits on the opposite side (same distance on the lingual aspect of the tissue as the
facial). (B–C) The needle is placed backwards in the needle holder and enter the
lingual tissue towards the buccal (approxiamtely ½ the distance from the incision
line. (D–E) The stitch is then tied off on the facial aspect.
Box 11.3
Basic Suturing Principles
1. Suture from mobile to immobile tissues: Allows for better control and
manipulation of the tissue (Fig. 11.27A).
2. Don't hold needle at swage: This may result in bending of the needle (Fig.
11.27B).
3. Enter tissue at 90 degrees: This allows for easier passage of the needle
through the tissue and prevents tearing (Fig. 11.27C).
4. Keep fingers in needle holder (index finger for security): Usually the
thumb and index fingers are used to hold the needle holder. The fingers
should always remain in the needle holders because this will expedite the
suturing process along with allowing for better control (Fig. 11.28A–B).
5. Enter 2–3 mm and exit from tissue margin: Less than 2 mm will lead to
tearing of the tissue margin (Fig. 11.29)
6. Suture 3–5 mm apart: Too many sutures will impair blood supply to the
incision line and increase possibility of ILO (see Fig. 11.29).
7. First throw must lie flat: After the first loop is tied, it is mandatory the loop
lie flat. If folded, the loop will lose tension and knot security will be lost.
Final tension of the first tie should be as horizontal as possible (Fig. 11.30).
8. Avoid excessive tension: Tying knots too tight leads to tissue ischemia and
ILO. Knot tension should not cause tissue blanching. In tying the knot, a
“sawing” motion should be avoided because this will result in weakening
the integrity of the suture,
9. Evert tissue, not invert: This makes it less likely that ILO will occur (Fig.
11.31).
10. Cut sutures approximately 2–3 mm at completion of

knot: Less than 2 mm leads to loss of knot tension and
more than 3 mm leads to patient irritation. When the
ends are too long, patients will tend to irritate the area
with their tongue (Fig. 11.32).
11. Completed knot: The final knot should be tight and firm
so that slippage will not occur. Ideally, the smallest knot
possible should be used to prevent tissue and foreign
body reactions.
Suturing Instruments
It is imperative the implant clinician have a complete understanding of the
instrumentation utilized in the suturing technique.
Tissue Pick-Ups
The goal of the tissue pick-up is to hold tissue (i.e., flap) while suturing. Care
should be exercised not to crush or sever the tissue. There are various types
of tissue pick-ups with the serrated being the most popular. The 1 × 2 tip will
usually result in tearing of the tissue, especially when the tissue is thin (Fig.
11.33).
FIG 11.33 Tissue pick-ups. (A) Serrated. (B) 1 × 2 tips. (Courtesy Salvin Dental
Specialties, Inc., Charlotte, NC.)
Needle Holders
Most needle holders are made from stainless steel, titanium, and tungsten
carbide tipped. The tungsten carbide tipped needle holders tend to deform
the suture needle the least amount. Correct use of needle holders includes:
• Always use the appropriate-size needle holder for the size of the needle.
The larger the needle size, the wider and heavier the needle holders should
be. In contrast, with thinner tissue with a smaller size needle and suture
material, smaller, more delicate needle holders are recommended (e.g.,
Castroviejo).
• Avoid placement of the needle holders near the swage or eye of the needle.
Needles should be grasped approximately to their length from the
swaged area.
• Check the alignment of the needle holder tips, making sure there is no
opening between the tips. The needle should not be able to rock, twist, or
turn within the needle holder tips.
• Always close the needle holder on the first or second ratchet. If the needle
is grasped too tightly, the needle may break or weaken. Hemostats should
never be used as a replacement for needle holders because they will damage
the suture needle and material (Fig. 11.34).
FIG 11.34 (A) Convention Mayo needle holder. (B) Castroviejo needle holder. (C)
Ideal needle holder placement. (A–B, Courtesy Hu-Friedy Mfg. Co., LLC, Chicago, IL.)
Suture Scissors
There exist many different types of scissors that may be used in the suturing
process. There are straight, curved, and special suture scissors that are used
for cutting sutures, especially for removing sutures postoperatively (Fig.
11.35). When using suture scissors to cut the ends of the tied knot, make sure
both tips of the scissors are visible to avoid inadvertently cutting tissue
beyond the suture.
FIG 11.35 (A) Various types of straight vs. curved scissors. (B) Postoperative
scissors. (A, From Trott AT: Wounds and lacerations: emergency care and closure, ed 3,
Philadelphia, 2005, Mosby. B, From Salvin Dental Specialties, Inc., Charlotte, NC.)
Suturing Knots
Surgical suture knot tying is the most important aspect of suturing and often
the most common problematic area. Surgical knots in the oral cavity must be
particularly secure to overcome the potential of loosening with saliva and
normal function.46 There are three components of a sutured knot: (1) loop,
which is created by the knot; (2) knot, which is composed of multiple throws,
each which represents a weave of two strands; and (3) ears, which are
composed of the cut ends of the suture.47 For knots to be effective, they must
contain all three parts and possess attributes of both knot security and loop
security. Knot security is defined as the efficacy of the knot at resisting
slippage when load is applied. This depends on three factors: friction,
internal interference, and slack between suture throws.
Loop security is the ability to maintain a tight suture loop as a knot is
tied.48 Any tied knot may have good knot security but poor loop security (a
loose suture loop). Loose suture loops may be ineffective in approximating
tissue edges to be secured.
Ideally, the knot should have minimal volume and be tied so that it fails
only by breakage, rather than by slippage. A three-throw surgeon's knot
square (2/1/1) should be used.49
Security of the knot will depend on the material used, the depth and
location of the wound, and the amount of stress that will be placed on the
wound postoperatively. Operator experience is an important factor because
considerable variation may result between knots tied by different surgeons
and even between knots tied by the same individual on different occasions
(Fig. 11.36).50
FIG 11.27 (A) Always suture from mobile to immobile tissue. (B) Never hold the
needle at the swage to avoid fracturing the needle. (C) Always enter the tissue at a
90-degree angle.
FIG 11.28 (A) Proper needle holder hand position. Index finger and thumb should
always remain in needle holders. (B) Incorrect hand position using a palm grasp,
which leads to inadequate control.
FIG 11.29 Enter the tissue with greater than 2 mm to avoid tearing. Multiple sutures
should be placed no closer than 3–5 mm apart.
FIG 11.30 (A) Ideal tie (flat) (arrow). (B) Nonideal with the tie folded over, leading to
loss of tension (arrow).
FIG 11.31 Always evert the tissue, not invert.
FIG 11.32 The sutures should be cut approximately 2–3 mm. A suture edge that is
too long will unravel, which can cause irritation for the patient.
FIG 11.36 Various suture knot types.
The type of surgical knot is directly related to the suture material being used.
When using silk, e-PTFE, chromic, or plain gut, a slip (granny) knot should
be used. With synthetic resorbable and nonabsorbable synthetic suture
materials, a modified surgeon's knot is recommended.51 For most dental
implant procedures, the surgical knot of choice is the modified surgeon's
knot. The basic surgeon's knot is composed of two overhand knots. The first
overhand knot is a double (i.e., composed of two loops or throws) and the
second overhand knot is a single (loop) wound in the opposite direction.
Additional knot security can be achieved with the common modification to
the surgeon's knot consisting of the addition of a third knot (composed of
two loops) in the same direction as the first loop.52
Bone Graft (Particulate) Material in Incision Line

No particulate graft material should be present in the incision line during
initial primary closure because this will delay soft tissue healing. Once the
tissues are sutured, the incision line is inspected for any bone graft particles
between the soft tissue margins (Fig. 11.37).
FIG 11.37 Bone graft material must be removed from within the incision line to
prevent wound dehiscence.
Decreasing “Dead Spaces”

Gentle pressure is applied to the reflected soft tissue flaps for 3 to 5 minutes.
This pressure may reduce postoperative bleeding under the flap, which may
cause “dead spaces” and delayed healing. Any stagnant blood under the flap
is “milked” from under the soft tissue by gentle pressure. This also allows
the fibrin formation from the platelets to help “glue” the flap to the graft site
(Fig. 11.38).
FIG 11.38 Gentle light pressure to minimize dead spaces after suture completion
decreases the possibility of bacteria accumulation.
Decrease Inflammation
Systemic corticosteroids or nonsteroidal antiinflammatory medications
(NSAIDs) may be administered before and after surgery to decrease soft
tissue edema because edema has been shown to contribute to incision line
opening.
Transitional and Interim Prosthesis Design

Occlusal forces applied to a removable prosthesis over a healing implant or
graft site may also cause incision line opening of soft tissues and delay
wound healing. Without appropriate adjustment, these forces can easily
result in ILO by compressing the surgical area during function before suture
removal. The potential for crestal bone loss is increased during any graft
healing or around implants during stage I healing, which may lead to
implant failure from early loading. Although use of such prostheses should
be discouraged, other strategies to minimize or eliminate this possibility
would include extensive relief of the intaglio surface, flange elimination, and
use of tissue conditioners. Much more preferable provisional tooth
replacement(s) would be either tooth or implant (transitional) supported
(Fig. 11.39).
FIG 11.39 (A) Pressure on tissue from interim prosthesis. (B) Reline material may
develop fungus growth. (C) Primary stress-bearing area (e.g., maxilla: palate;
mandible: buccal shelf) must be maintained.
Other examples of fixed transitionals would include the bonding of natural

tooth crowns or denture teeth to the teeth bounding the edentulous space
and modification of existing fixed partial denture, i.e., pontic shortening.
Removable transitional prostheses such as an Essix retainer or Snap On
Smile prosthesis are frequently utilized due to their rigid support and
resultant lack of pressure on the incision line. A resin-bonded fixed
restoration can also be fabricated to provide improved function, especially
when crestal bone regeneration is performed.
The prosthesis may depress the interdental papillae of adjacent teeth. As a
result, a resin-bonded fixed prosthesis is fabricated for the extended healing,
and a removable device may be used short term for cosmetic emergencies (if
the prosthesis debonds).
When a resin-bonded restoration is used, the adjacent teeth are not
prepared and the device is bonded to teeth below the centric occlusal
contacts. The interdental papillae are often depressed after initial socket
healing. This type of transitional restoration for the single-tooth implant has
the multiple benefits of being off the soft tissue drape, the developing bone
augmented site, and the healing implant-bone interface. Several options to
the resin-bonded device permit these goals. An Essix appliance is an acrylic
shell, similar to a bleaching tray, that has a denture tooth attached to replace
the missing tooth. This prosthesis is the simplest treatment for tooth
replacement postsurgery.
When an adjacent tooth requires a crown in the overall treatment plan, the
adjacent tooth may be prepared and a cantilevered transitional fixed partial
denture with a pontic over the surgical site may be used. When the patient
requires orthodontics, a denture tooth and an attached bracket may be added
to the orthodontic wire. A cast-clasp RPD with indirect rest seats, which
prevents rotational movements on the surgical site, is an excellent option.
Atraumatic Suture Removal

Etiology
Removing sutures too early or traumatically may result in incision line
opening and causing a delayed healing leading to morbidity of the implant or
bone graft.
Prevention
Normally, nonresorbable sutures or extended absorbable sutures are
removed within 10–14 days after surgery. Suture removal should include the
following steps:
1. Patient rinses lightly with 0.12% chlorhexidine gluconate.
2. With tissue pick-ups, hold up the knot end of the suture and cut the suture
closest to the tissue. Care should be exercised to not traumatize or irritate the
surgical wound.
3. Gently pull the suture out with the knot outside of the tissue. Do not pull
the knot through the tissue to remove.
4. Have the patient rinse with 0.12% chlorhexidine. Evaluate and make sure
the interim prosthesis does not impinge on the surgical wound (Fig. 11.40).
FIG 11.40 Suture scissors to remove sutures atraumatically.
Decrease the Possibility of Infection

Antibiotics
An important complication to prevent after implant surgery is infection.
Infection can lead to a multitude of problems, including pain, swelling, loss
of bone, and possible failure of the implant. Because of the risk of morbidity
from infections, antimicrobial therapy is an essential component of the
surgical protocol. A high microbial burden in a wound increases the host's
inflammatory response to the area.
Bacteria release endotoxins and metalloproteases that destroy the
extracellular matrix of healing connective tissues and cause cell lysis.
Bacterial infection and increased inflammation can lead to further tissue
damage. Bacteria also compromise wound healing by competing with the
healing tissue for nutrients and oxygen.53
It is prudent to address chronic or acute periodontal or endodontic
infections prior to implant surgical procedures. Prophylactic use of
antimicrobials in the form of antibiotics and antimicrobial rinses has
significant benefits for prevention of infections following implant surgical
procedures.
Postoperative surgical wound infections may have a significant impact on
the well-being of the patient and implant survival. Documented cases of
potential consequences of infection range from increased pain and edema to
patient mortality. One of the main causes of dental implant failure may be
bacterial contamination at implant insertion.
Antimicrobial Rinse
Another modality for antimicrobial prophylaxis for implant surgery is the
use of an oral rinse, (e.g., 0.12% or 0.2% chlorhexidine digluconate).
Chlorhexidine gluconate is a potent antibacterial rinse that causes lysis by
binding to bacterial cell membranes. It has high substantivity, which permits
it, at high concentrations, to exhibit bactericidal qualities by causing bacterial
cytoplasm precipitation and cell death.
In the oral cavity, chlorhexidine has been shown to have biologic
substantivity and slow release from tissue surfaces over a 12-hour period. In
vitro studies have reported inhibitory effects of chlorhexidine on cultured
epithelium and cell growth. Clinical studies have not supported the
laboratory findings.
In contrast, chlorhexidine has been demonstrated to be an effective
adjuvant in reducing biofilm, enhancing gingival health, improving soft
tissue healing, treating periodontal disease, preventing alveolar osteitis,
improving tissue healing after extractions, and reversing peri-implantitis,
while showing no adverse effects on implant surfaces. When evaluating the
effect of preoperative chlorhexidine before dental implant surgery, a
significant reduction in the number of infectious complications (2 to 1) is
realized and a sixfold reduction in implant failures in comparison to no use
of chlorhexidine controls has been reported (Fig. 11.41).
FIG 11.41 0.12% Chlorhexidine Gluconate (Courtesy 3M Corporate, St. Paul, MN.)
Aseptic Technique
To prevent conditions likely to result in infection, a controlled, well-
monitored aseptic setting should be achieved for the surgical procedure. The
aseptic surgical site includes proper disinfection and draping procedures of
the patient, hand scrubbing, sterile gowns worn by all surgical members, and
maintenance of complete sterility of the instrumentation.
Decreased Surgical Time
Another important surgical factor related to postoperative infection is the
duration of the surgical procedure. This factor has been shown to be the
second most critical risk factor (after wound contamination) affecting
postoperative infection rates.18 Surgical procedures lasting less than 1 hour
have an infection rate of 1.3%; procedures in excess of 3 hours increase the
infection rate to more than 4%. It is postulated that the rate of infection
doubles with every hour of the procedure.
Clinician Experience and Skill

The skill and the experience of the surgeon with the placement of implants
have been shown to be significant in postoperative infections and implant
failures. A recent study has reported that less experienced surgeons (<50
implants placed) have a 7.3% increase in failure rates in comparison to
experienced surgeons.
Diet and Supplements

Aside from routine postoperative instructions specific to diet, the use and
potential benefits of supplements is a frequent topic of inquiry from patients.
Significant vitamin and trace mineral deficiencies are rarely seen in patients
with acute wounds in whom healing is rapid and uncomplicated. However, in
patients who have chronic disease and who may have inadequate diets,
vitamin deficiencies may play a significant role in delaying wound healing. In
general, if the nutritional status of a patient is in question, supplemental
doses of several key vitamins should be recommended. These medications
are inexpensive and have a very low rate of morbidity if given in therapeutic
doses.
Vitamin C
Vitamin C, oxygen, ketoglutarate, and iron are essential cofactors for the
enzymes prolyl hydroxylase and lysyl hydroxylase, both of which are required
for normal collagen metabolism. Vitamin C is important in aerobic
metabolism. Fibroplasia is especially sensitive to vitamin C deficiency. This is
dramatically demonstrated in patients who suffer from scurvy, in which
wounds fail to heal, fracture nonunions occur, and healed wounds dehisce.
Vitamin A
Vitamin A deficiency is known to impair wound healing even when steroids
are not being used.54 Vitamin A is an important part of wound healing
through cellular reproduction and cellular differentiation. Additionally,
Vitamin A reduces the risk of wound infection as it is essential for proper
immune system function and management of inflammation.
Vitamin B
Vitamin B complex consists of eight water-soluble vitamins found in meat,
dairy, vegetables, fish, and cereals. Vitamin B complex helps to promote cell
proliferation and maintain healthy skin and muscle tone, increase metabolic
rate, and enhance immune and nervous system function. Deficiencies in
vitamin B may impair wound healing, antibody formation, white blood cell
function, and bacterial resistance. They are associated with several disorders,
many of which have skin manifestations.
Thiamine
Thiamine is associated with decreased wound healing and breaking strength.
B-complex vitamins and cobalt are essential cofactors for many enzyme
systems.
Vitamin E
Vitamin E deficiency on wound healing has not been well described.
However, the use of Vitamin E has been shown to improve wound tensile
strength in patients whose wounds had been exposed to ionizing radiation.
Vitamin E may reduce the peroxidation of lipids caused by radiation. In large
doses, vitamin E may be detrimental to wound healing and should not be
given if the patient does not have a clear deficiency.55
Copper
Copper is needed for lysyl amine oxidase, and calcium is needed as a cofactor
for the normal function of granulocyte collagenase and other collagenases.
Zinc
Zinc deficiency retards both fibroplasia and epithelialization. A common
element in numerous enzymes found in the human body, zinc is needed for
DNA replication and is a coenzyme for DNA polymerase and reverse
transcriptase. Cells with a rapid cellular turnover rate are most severely
affected by zinc deficiency.
Reduction of Local Factors

Adverse/destructive oral habits can contribute to wound dehiscence with or
without an interim prosthesis. Patients with parafunctional habits should be
identified during the early phases of treatment planning. Occlusal overload,
even on a well-adjusted interim prosthesis, can transmit harmful forces to
the underlying tissues.
A cascade of complications may result, beginning with wound dehiscence,
and lead to lack of integration or failure of hard and/or soft tissue
augmentation procedures. The causes of parafunction or nonfunctional tooth
contact have been classified into six categories: (1) local, (2) systemic, (3)
psychologic, (4) occupational, (5) involuntary, and (6) voluntary.56 Local
factors include tooth form or occlusion, as well as soft tissue changes such as
ulcerations or pericoronitis.
Psychologic causes occur with the greatest frequency and are associated
with the release of emotional tension or anxiety. Included in this category are
nail biting, cheek biting, and sucking habits. Occupational factors for
professionals such as physicians, dentists, athletes, and precision workers
may lead to parafunction, as well as for the seamstress or musician who
develop altered oral habits. The fifth cause of parafunctional force is
involuntary movement that provokes bracing of the jaws, such as lifting of
heavy objects or sudden stops while driving. Examples of voluntary causes
include chewing gum or pencils, bracing the telephone between the head and
shoulder, and pipe smoking.
In the dental implant literature, there are two treatment recommendations
discussed with respect to incision line opening. The first is to allow the
surgical wound to heal via secondary intention with the use of antimicrobials
and hygiene measures (Box 11.4). The second treatment modality is to
resuture the opened surgical wound, which is not recommended by the
authors (Table 11.2).
Box 11.4
Secondary Intention Protocol
Clinician
1. Relieve prosthesis to have no buccal flange and no contact on the surgical
wound area.
2. Maintain stress-bearing areas on the prosthesis with the use of a tissue

conditioner; however, material should be removed from the dehisced area.
3. Locally clean the dehiscence area with 0.12% chlorhexidine.
4. Closer observation of the patient to include recall appointments a

minimum of once a week for the first month.
Patient Instructions
1. Nonvigorous rinse with 0.12% chlorhexidine twice daily, plaque control.
2. Minimize the use of interim prosthesis.
3. No direct mastication on the area of dehiscence.
4. Avoid smoking and the use of alcohol.
5. Avoid peroxide and alcohol-based mouth rinses.
6. Avoid acidic foods.

7. Avoid inspection of dehiscent site (pulling on lip to see area).
8. Do not use any denture adhesive with the interim prosthesis.
TABLE 11.2
Treatm ent
Surgical P rocedure Early (<1 Week) Late (~>3 Weeks)
Implant: One Stage S ec ondary intention protoc ol (resuture S ec ondary intention protoc ol
ONLY if favorable c onditions)
Two Stage S ec ondary intention protoc ol • Remove overlying tissue with tissue punc h bur or sc alpel
• Plac e permuc osal extension (≈1 mm above tissue; higher extension may
lead to exc essive forc e on the implant) Fig. 11.42
P articulate graft S ec ondary intention protoc ol S ec ondary intention protoc ol
Block graft S ec ondary intention protoc ol • Chec k for mobility of graft
• Reduc e sharp bony edges
• Freshen wound edges with diamond bur
Membrane: collagen S ec ondary intention protoc ol S ec ondary intention protoc ol
(regular)
Collagen (extended) S ec ondary intention protoc ol S ec ondary intention protoc ol
Trim exc ess membrane above tissue level with sc issors
Acellular dermal S ec ondary intention protoc ol S ec ondary intention protoc ol
matrix (Alloderm) Trim exc ess membrane above tissue level with sc issors
Nonresorbable S ec ondary intention protoc ol • Remove membrane if c hronic tissue irritation or infec tion
(cytoplast, titanium) • Ideally, attempt to maintain for at least 6 weeks
To allow the site to heal by secondary intention, there needs to be

significant discipline and patient cooperation for a successful outcome. This
treatment technique is dictated by many variables such as health of the
existing tissue, tissue thickness, location, age of the patient, and size of the
dehiscence. The technique includes the following:
Resuturing Protocol
Resuturing is the more difficult and unpredictable technique. When
attempting to resuture a fresh wound, usually the epithelium is thin and
friable, which often leads to tearing of the incision line. This may result in a
larger dehiscence or infection. If completed, the margins of the tissue should
be “freshened” with a scalpel or a diamond bur. Greenstein has
recommended that, when the dehiscence is small and occurs within 24 to 48
hours, the clinician may immediately resuture the dehiscence. Once the
wound is large (2 to 3 cm) or the time elapsed is more than 2 to 3 days, it
becomes more difficult for the margins of the wound to be excised and
resutured.57 It is the authors' recommendation to be cautious with resuturing
incision lines that may end up resulting in increased morbidity of the
surgical wound.
As stated earlier, there exist many variables when evaluating a wound
dehiscence. Two of the most important factors are the type of surgical
procedure that was completed and the length of time since the dehiscence
occurred. Therefore, a procedure-specific protocol has been established that
is dependent on the timing of the dehiscence (early [within first 2 to 3 days]
vs. late [≈4 weeks after surgery]) (Fig. 11.42).
FIG 11.42 (A) Tissue removal bur that coincides with the implant diameter. (B)
Removing the excess tissue with a latch handpiece.
Summary
The majority of highly experienced implant surgeons will attest that one of
the greatest difficulties that they encountered during their respective
learning curves was the maintenance of incision lines during and after
surgery. Implant surgery, and especially bone grafting procedures, commonly
cause a situation where hard tissue volumes will be larger than the soft tissue
that originally covered the site. This soft tissue must be manipulated to
prevent incision line opening. Managing this phenomenon during surgery is
a skill, and one that requires great surgical fundamentals and practice.
Despite our best efforts, incision line opening does occur from time to
time. When a wound opens and implant/graft contents become exposed to
the oral environment, a situation occurs that demands extreme care in order
to preserve the chances that the overall surgical outcome is a desirable one.
The contents of this chapter will help lay a groundwork for the clinician to
manage these situations in a way that will ensure successful outcomes
despite the complication.
References
1. Adell R, Lekholm U, Rockler B, et al. Marginal tissue reactions at
osseointegrated titanium fixtures (I). A 3-year longitudinal
prospective study. Int J Oral Maxillofac Surg. 1986;15:39–52.
2. Tal H. Spontaneous early exposure of submerged implants: I.
Classification and clinical observations. J Periodontol. 1999;70:213–219.
3. Mendoza G, Reyes JD, Guerrero ME, et al. Influence of keratinized
tissue on spontaneous exposure of submerged implants:
classification and clinical observations. J Osseointegr. 2014;6:47–50.
4. Lekovic V, Kenney EB, Weinlaender M, et al. A bone regenerative
approach to alveolar ridge maintenance following tooth extraction.
Report of 10 cases. J Periodontol. 1997;68:563–570.
5. Barboza EP, Caula AL. Diagnoses, clinical classification, and
proposed treatment of spontaneous early exposure of submerged
implants. Implant Dent. 2002;11:331–337.
6. Hakkinen L, Uitto VJ, Larjava H. Cell biology of gingival wound
healing. Periodontol 2000. 2000;24:127–152.
7. Polimeni G, Xiropaidis AV, Wikesjo UM. Biology and principles of
periodontal wound healing/regeneration. Periodontol 2000. 2006;41:30–
47.
8. Fonseca RJ, Barber HD, Powers MP, et al. Oral and maxillofacial
trauma. Elsevier Health Sciences; 2013.
9. Midwood KS, Williams LV, Schwarzbauer JE. Tissue repair and the
dynamics of the extracellular matrix. Int J Biochem Cell Biol.
2004;36:1031–1037.
10. Leaper DJ, Harding KG. Wounds: biology and management. Oxford
University Press: USA; 1998.
11. Hutchinson J. The wound programme. Centre for Medical Education:
Dundee, Scotland; 1992.
12. Greenstein G, Greenstein B, Cavallaro J, et al. Flap advancement:
practical techniques to attain tension-free primary closure. J
Periodontol. 2009;80(1):4–15.
13. Stadelmann WK, Digenis AG, Tobin AR. Physiology and healing
dynamics of chronic cutaneous wounds. Am J Surg. 1998;176(Suppl
2A):26S–38S.
14. Andrew H, Mustoe TA. The principles of wound healing. Plastic
Surgery Secrets Plus. 2010;3–7.
15. Brand HS, Ligtenberg AJ, Veerman EC. Saliva and wound healing.
Monogr Oral Sci. 2014;24:52–60.
16. Schor SL, Ellis I, Irwin CR, et al. Subpopulations of fetal-like gingival
fibroblasts: characterisation and potential significance for wound
healing and the progression of periodontal disease. Oral Dis.
1996;2(2):155–166.
17. Epstein JB, Scully C. The role of saliva in oral health and the causes
and effects of xerostomia. J Can Dent Assoc. 1992;58:217–221.
18. Zelles T, Purushotham KR, Macauley SP, et al. Concise review: saliva
and growth factors: the fountain of youth resides in us all. J Dent Res.
1995;74(12):1826–1832.
19. Moore WE, Moore LV. The bacteria of periodontal diseases. Periodontol
2000. 1994;5:66–77.
20. Larjava H, Uitto VJ. Effects of extracts from Bacteroides gingivalis,
Bacteroides intermedius, and Bacteroides asaccharolyticus on the
growth of fibroblast lines obtained from healthy and inflamed
human gingiva. Oral Microbiol Immunol. 1987;2:112–116.
21. Marx RE. Pamidronate (Aredia) and zoledronate (Zometa) induced
avascular necrosis of the jaws: a growing epidemic. J Oral Maxillofac
Surg. 2003;61:1115–1117.
22. Jeffcoat MK. Safety of oral bisphosphonates: controlled studies on
alveolar bone. Int J Oral Maxillofac Implants. 2006;21:349–353.
23. Krall EA, Garvey AJ, Garcia RI. Alveolar bone loss and tooth loss in
male cigar and pipe smokers. J Am Dent Assoc. 1999;130:57–64.
24. Noble RC, Penny BB. Comparison of leukocyte count and function in
smoking and nonsmoking young men. Infect Immun. 1975;12:550–555.
25. Rees TD. Oral effects of drug abuse. Crit Rev Oral Biol Med.
1992;3:163–184.
26. Pepersack T, Fuss M, Otero J, et al. Longitudinal study of bone
metabolism after ethanol withdrawal in alcoholic patients. J Bone
Miner Res. 1992;7:383–387.
27. Wilson JA, Clark JJ. Obesity: impediment to wound healing. Crit Care
Nurs Q. 2003;26:119–132.
28. Suvan J, Petrie A, Moles DR, et al. Body mass index as a predictive
factor of periodontal therapy outcomes. J Dent Res. 2014;93:49–54.
29. Gapski R, Wang HL, Misch CE. Management of incision design in
symphysis graft procedures: a review of the literature. J Oral
Implantol. 2001;26:134–142.
30. Hupp JR, Tucker MR, Ellis E. Contemporary oral and maxillofacial
surgery. Elsevier Health Sciences: Philadelphia; 2013.
31. Peterson LJ, Ellis E, Hupp JR, et al. Oral and maxillofacial surgery.
Mosby: St. Louis; 1998.
32. Leong G, Wilson J, Charlett A. Duration of operation as a risk factor
for surgical site infection: comparison of English and US data. J Hosp
Infect. 2006;63:255–262.
33. Zarb GA, Albrektsson T, Branemark PI. Tissue-integrated prostheses:
Osseointegration in clinical dentistry. Quintessence: Illinois; 1985.
34. Buser D, Dahlin C, Schenk R. Guided bone regeneration. Quintessence:
Chicago; 1994.
35. Langer B, Langer L. Overlapped flap: a surgical modification for
implant fixture installation. Int J Periodontics Restorative Dent.
1990;10:208–215.
36. Misch CE. Bone augmentation for implant placement: keys to bone
grafting. Misch CE. Contemporary implant dentistry. ed 2. Mosby: St
Louis; 1999:421–447.
37. Park JC, Kim CS, Choi SH, et al. Flap extension attained by vertical
and periosteal-releasing incisions: a prospective cohort study. Clin
38. Yaltirik M, Dedeoglu K, Bilgic B, et al. Comparison of four different
suture materials in soft tissues of rats. Oral Dis. 2003;9:284–286.
39. Engler RJ, Weber CB. Turnicky R: Hypersensitivity to chromated
catgut sutures: a case report and review of the literature. Ann Allergy.
1986;56:317–320.
40. Selvig KA, Biagiotti GR, Leknes KN, et al. Oral tissue reactions to
suture materials. Int J Periodontics Restorative Dent. 1998;18:474–487.
41. Leknes KN, Roynstrand IT, Selvig KA. Human gingival tissue
reactions to silk and expanded polytetrafluoroethylene sutures. J
Periodontol. 2005;76:34–42.
42. Leknes KN, Selvig KA, Boe OE, et al. Tissue reactions to sutures in the
presence and absence of antiinfective therapy. J Clin Periodontol.
2005;32:130–138.
42a. Lilly GE, Armstrong JH, Salem JE, et al. Reaction of oral tissues to
suture materials, Part II. Oral Surg Oral Med Oral Pathol.
1968;26(4):592–599.
43. Cohen ES. Atlas of cosmetic and reconstructive periodontal surgery.
PMPH-USA: New York; 2007.
44. Silverstein LH. Suture selection for optimal flap closure and tissue
healing. Perio-implant showcase. Pract Periodontics Aesthet Dent.
2005;16:2–3.
45. Silverstein LH, Kurtzman GM. A review of dental suturing for optimal
soft-tissue management. Compend Contin Educ Dent. 2005;26:163–166.
46. Alzacko SM, Majid OW. “Security loop” tie: a new technique to
overcome loosening of surgical knots. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod. 2007;104:e1–e4.
47. Edlich RF, Rodeheaver GT, Morgan RF, et al. Principles of emergency
wound management. Ann Emerg Med. 1988;17:1284–1302.
48. Burkhart SS, Wirth MA, Simonich M, et al. Knot security in simple
sliding knots and its relationship to rotator cuff repair: how secure
must the knot be? Arthroscopy. 2000;16:202–207.
49. Drake DB, Rodeheaver PF, Edlich RF, et al. Experimental studies in
swine for measurement of suture extrusion. J Long Term Eff Med
Implants. 2004;14(3):251–259.
50. Herrmann J. Tensile strength and knot security of surgical suture
materials. Am Surg. 1971;37:209.
51. Silverstein LH. Principles of dental suturing: the complete guide to surgical
closure. Montage Media: New York; 1999.
52. Silverstein LH, Shatz P, Kurtzman D. The suture book: the definitive
guide to dental suturing and surgical flap closure. AEGIS
Communications: New York; 2011.
53. Ulma RM, Aghaloo TL, Freymiller EG. Wound healing. Fonesca RJ.
Oral and maxillofacial trauma. 2013:9–29 [Philadelphia, PA].
54. Hunt TK. Vitamin A and wound healing. J Am Acad Dermatol.
1986;15:817–821.
55. Koch JP, Dunson B. Factors affecting bone healing following implant
surgery. J Oral Implantol. 1996;22:7–11.
56. Nadler SC. Detection and recognition of bruxism. J Am Dent Assoc.
1960;61:472–479.
57. Greenstein G, Cavallaro J, Romanos G, et al. Clinical
recommendations for avoiding and managing surgical complications
associated with implant dentistry: a review. J Periodontol.
2008;79:1317–1329.
58. Dunn DL, Phillips J. Ethicon wound closure manual. Johnson and
Johnson: New York; 2004:1–127.
12
Bone Grafting Complications
Stephen Caldwell
The goal of any dental implant procedure is to restore the patient to optimal
form, function, and esthetics. Through the combined efforts of a great
number of clinicians and researchers, guidelines have been established in
regards to proper implant numbers and positioning based on possible
prosthetic designs. The patient's existing bone volume often makes the
proper placement and positioning of implants difficult, if not impossible.
Ideal treatment planning in implant dentistry often requires the correction of
significant alveolar ridge defects in regions where dental implants are
indicated to support critical prostheses. Alveolar ridge defects are caused by
a variety of factors including developmental anomalies, trauma, and most
commonly, tooth extraction. Following tooth loss, a predictable resorptive
process of the alveolar bone occurs in both a horizontal and vertical
dimension.1,2
The loss of alveolar bone can pose a challenge both from the perspective of
supporting a conventional removable prosthesis or placement of dental
implants in an ideal position for functional and esthetic results. Prior to
development of effective bone grafting techniques, implants were placed in
regions where there was available bony support, often leaving the restorative
dentist with the task of restoring an implant in a less-than-ideal position
within the arch. The success of implant dentistry today has been largely
related to the advent of bone augmentation techniques that allow
regeneration of an ideal ridge form and placement of implants in their ideal
functional and esthetic positions.3-7
The augmentation of bone volumes through grafting is a highly technique-
sensitive process. It requires meticulous surgical skill, practice, and
knowledge to become proficient in creating predictable bone growth prior to
implant placement. Complications are plentiful in this discipline, leading to
treatment delays, patient and provider frustration, as well as possible
neurosensory, vascular, and infectious issues. The dental implant surgeon
must have a firm understanding of the limitations of various bone grafting
techniques to develop appropriate treatment plans. Clinicians must be able
to not only prevent complications during the procedure, but also properly
address these issues should they arise.
Treatment Planning
Failure to Understand Bone Resorption
Etiology.
Treatment planning implant-supported restorations in edentulous spaces
requires a clear understanding of the resorptive patterns of bone loss. As a
ridge resorbs, available bone for support of dental implants disappears,
preventing placement of implants in key locations for restorative success.
After tooth loss, the initial pattern of bone resorption starts with loss of the
lateral (buccal) aspect of the ridge, eventually leading to a decrease in vertical
ridge height. As this resorptive process occurs, the position of implant-
supported restorations can be changed substantially secondary to the new
interarch relationship between the maxilla and the mandible. For instance,
the loss of maxillary posterior teeth with the accompanied loss of the buccal
bony width will often lead to development of a posterior crossbite. This is
compounded as the mandible deteriorates into a division C or D ridge,
resorbing until the remaining mandibular basal bone is actually positioned
laterally, away from the remaining maxillary bone (Fig. 12.1).
FIG 12.1 (A) Bony contours in a normal sagittal view of the maxillary and
mandibular arches. (B) The initial resorption of bone in the lower arch destroys the
lateral aspect of the lower ridge. (C) Further loss in the lower arch leaves the
remaining bone in a more lateral position than the maxillary arch. Lateral resorption
in the maxilla leaves the remaining bone in a more medial position than the lower
arch. (D) The same sagittal view of a patient's CBCT scan depicts the same
resorption pattern that is seen in B.
The treatment planning process must start with a reasonable assessment

of the extent of the bony deficiency and the capacity of a regenerative
procedure to create adequate support for implants in their ideal positions for
comfort, aesthetics, function, and support. As the extent of bone
regeneration is evaluated, care must be taken from the beginning stages to
identify the expected positions of each restoration or prosthesis using
accurate restorative wax-ups. Evaluation of the relationship between the
required restorative positions and the bony deficiency will then provide
insight into the volume and shape of the bone that will need to be generated.
At this stage, the most predictable surgical approach and bone graft material
(e.g., autograft, allograft, xenograft) is selected to ensure adequate bone
support can be developed for ideal implant placement.
Complication.
In site assessment treatment planning, complications often result when the
clinician fails to understand the relationship between the limitations of
various regenerative grafting techniques and the predictable development of
the required bone contours and bone volume needed for overall restorative
success. It is not possible to treat every defect with simple or limited
techniques because this discipline requires a variety of approaches to meet
the reality of advanced bone resorption. When the incorrect technique is
utilized, inadequate bone volume will be regenerated, leading to either
compromised restorative results or a potential failure of the prosthesis.
These problems not only compromise the local grafting site, but they can
also destroy bone around surrounding teeth, creating a worse situation than
was originally encountered.
Prevention.
In an ideal setting, prevention starts with total awareness of ridge
preservation and limiting bone loss before major ridge defects occur. This
starts with atraumatic extraction techniques, aggressive socket grafting, and
communication with the whole implant team in respect to the need for
timely preservation of the ridge. The longer the patient remains without an
implant in an extraction site, the greater the chance that adjunctive grafting
procedures will be necessary. For patients with long-term edentulism, the
surgeon needs to be fully aware of the mechanisms of bone resorption to
understand the current underlying bony architecture and to correctly choose
a grafting protocol that will build the correct volume for the intended
prosthesis. A working knowledge of ridge resorption and expertise in the use
of effective diagnostic imaging to accurately assess bone volumes gives the
clinician the opportunity to correctly organize a reasonable and predictable
implant treatment plan (Fig. 12.2).
FIG 12.2 This series of images presents a decision tree that should be considered
in each case when routes of treatment planning are being considered. For example,
in a Division B ridge, many treatment options are possible, including osteoplasty,
Division B implants, or bone grafting. Each of the treatment options has advantages
and disadvantages that should be evaluated. As one can see, each treatment option
will dictate the final restoration (e.g., FP1, FP2, or FP3).
Failure to Understand the Need for Bone Grafting

Etiology.
Success in any implant prosthesis requires the implants to be placed in
positions that provide ideal aesthetics, function, comfort, and support. To be
successful in the development of a favorable prosthesis, the number and
positions for implants in an edentulous space must be determined with a
careful analysis of the relationship between the restorative prosthesis and
the forces that will be exerted on the final prosthesis. This is then associated
with the functional and esthetic aspects of the case, ultimately dictating the
relationship between the implants, bone, and opposing forces. All of these
factors must be considered in planning support for a prosthesis that
functions well while maintaining the bone volume around its implant
abutments. Clinicians too often try to bypass the grafting process, either to
save time or because they are not experienced in advanced grafting
techniques. Insufficient bone in recipient sites leads to placement of
implants with inadequate diameters, short lengths, or in insufficient
numbers. Compromises like these eventually lead to significant damage
around an implant and the prosthesis it supports. Due to the fact that
resorption occurs in every edentulous site, the need for adjunctive bone
grafting is very common and is often vital for a successful outcome (Fig.
12.3).
FIG 12.3 Maxillary bone loss with respect to prosthesis position. As the bone in the
premaxilla resorbs, the vertical and horizontal soft tissue support around teeth and
implants disappears. This exposes the body of a failing implant or requires the
incorporation of pink porcelain in the treatment plan for a new implant.
Complication.
Failure to recognize the need for bone grafting leads to numerous treatment
issues, ranging from esthetic complications to implant and prosthetic failure.
Placing implants of suboptimal sizes or in less than ideal numbers to bypass
the grafting process is a compromise that often leads to force-related failures
of implant components, the prostheses itself, or accompanied bone loss.
Ultimately, prosthetic and implant morbidities may result.
Prevention.
A multidisciplinary approach should be taken to assess the optimal
prosthetic solution for the patient, based on the patient's wishes, available
bone, and other factors. When the prosthetic plan has been established, the
clinician should begin planning the implant positions required to execute the
prosthetic option. Once the sites for implants have been determined, the
associated sites are evaluated for foundational support in the required
positions. If inadequate bone is available to successfully place an implant in a
key location for the prosthesis, grafting should then be included in the
treatment plan to build the appropriate bone volumes.
Underestimation of Bone Required for Grafting of

the Defect
Etiology.
One of the most difficult components of bone augmentation treatment
planning is learning how to predict the amount of bone that will actually be
required to develop the proper foundational support that the restorative
treatment plan requires. Evaluation of the clinical situation, review of two-
dimensional radiographs, assessment of models with restorative wax-ups,
and information from cone beam computed tomography (CBCT) imaging all
play a role in determining where bone will be required and how much bone
will be needed to successfully graft the site. This is important when
autogenous bone is incorporated into the regenerative process, and failure to
clearly consider the difficulty of this bone harvest can lead to an eventual
shortfall in the graft's success.
Complications.
In cases where the implant clinician fails to properly develop adequate bone
volumes for grafting and implant positioning, reflection of tissue over the
grafted site will reveal inadequate bony support for the intended implant
size and position. At this time, critical decisions must be made to prevent the
chance of compromising the overall case success due to this shortfall. The
best solution is to stop and regraft the site, but this causes inconvenience for
the patient, embarrassment for the surgeon, and an overall increase in the
treatment time and expense. The alternative is to ignore the deficiency,
placing the implant in a deficient site that ultimately limits the implant size
or forces improper placement of the implant in an alternative position.
Successful restorative cases require discipline and cutting corners leads to
disappointed patients.
Prevention.
The use of CBCT imaging along with proper diagnostic casts allow the
clinician to implement a proper prosthetic plan. The restorative wax-up can
easily be interlaced into the CT imaging software for assessment of the bone
volumes needed for proper implant support in key positions. Once the
dimensions and volume of the graft have been determined, proper
application of bone grafting techniques and materials is necessary to ensure
that the intended volume can be achieved. At this point, the patient should
be educated on the details of the regenerative procedures and a timeline of
treatment. Advanced grafting procedures delay completion of the final
prosthesis, and patients should be aware of the extent of the inconvenience
that will need to be tolerated during this surgical sequence. Sites for
autogenous grafts should also be evaluated to ensure there is adequate donor
bone available to produce the bone foundation needed to execute the
treatment plan (Figs. 12.4 and 12.5).
FIG 12.4 (A) Bony topography in severely compromised ridges. When these
regions are being considered for restorations, consideration of the three-dimensional
relationship of bone loss vs. adjacent tooth positioning is important. (B) Severe
vertical resorption requires regeneration to avoid problems with support, aesthetics,
and poor healing. (C) Complete loss of the facial cortical plate requires planning for
support and development of significant width. (D) Defects that destroy both the facial
and palatal cortical plates limit the choice of regenerative procedures that can be
used. (E–F) When there is a sharp declining ridge adjacent to a natural tooth,
placement of an implant 1.5 mm away creates a failing situation beginning at time of
the initial implant placement. As time passes, both the tooth and the implant will be
compromised. Stepping the implant away from the natural tooth can limit this
proximity problem, but then the implant body is too low and the design and loading of
the prosthesis begins to be problematic.
FIG 12.5 (A) CBCT 3-D image depicting the ideal position of the teeth with the use
of a barium sulfate radiopaque template. (B) Sagittal view showing relationship of
ideal implant placement, amount of hard tissue loss, and the ideal position of the
tooth to be replaced.
Failure to Evaluate the Tissue Biotype in Treatment

Planning
Etiology.
Patient-to-patient comparisons of the soft tissue drape surrounding the
natural teeth often demonstrate significant differences in color, surface
consistency, tissue thickness, and overall aesthetics. This is emphasized when
a very thin and friable tissue drape surrounds an anterior tooth.
Differentiation of patients into either a “thick biotype” or a “thin biotype” is
a critical tool that can be used during anterior implant–related treatment
planning. Cook and Mealey demonstrated the most simple way to determine
tissue biotype is through the visibility of a periodontal probe in the sulcus of
an anterior tooth. A patient with a thick biotype will not show any
translucence of the probe through the sulcular tissue. In contrast, a thin
biotype will allow visualization of the coloration of a probe through the
sulcular tissue. A patient with a thick biotype has tissue with a robust pink,
stippled appearance. This dense tissue drape forms a thick layer of tissue
that is very forgiving when dental restorations are placed around natural
teeth and when dental implants are involved. The thin biotype patient,
however, presents a much more difficult challenge. These patients have a
thinner labial plate thickness, a narrower keratinized tissue width, a greater
distance from the CEJ to the initial alveolar crest, and there is visibility of a
periodontal probe through the sulcus. As teeth migrate out of position or
rotate in the arch, the prominence of the roots can increase, complicating the
soft tissue situation even more. Thin layers of tissue around the maxillary
anterior teeth require meticulous planning to hide underlying crown
margins. In the case of implants, problems related to the translucence of the
dark hue of the implant body and the abutment can significantly complicate
the aesthetics surrounding the final restoration (Fig. 12.6).58
FIG 12.6 (A) Thin biotype exhibiting metal show-through. Tissue biotype can be
defined by the translucence of a probe through the sulcus. (B) Thick biotype yellow
probe. (C) Thick biotype with dark probe. (D) Intermediate biotype with visible probe
through sulcular tissue. (E) Thin biotype with probe.
Complication.
When there is no consideration of the biotype of a patient, esthetic
complications can occur, especially in the anterior regions. Thin biotype
patients tend to be more prone to recession, and thin tissue may result in a
bluish-gray hue at the gumline of the implant restored tooth. If recession or
slight bone loss occurs, the facial aspect of the implant can be exposed,
leaving a similar dark hue to the overlying tissue and the patient with a poor
esthetic and embarrassing presentation.
Prevention.
When a clinician is aware of tissue biotype, it is possible to plan ahead
procedurally to maintain or possibly change the biotype, leading to optimal
esthetic outcomes. Patients with a very thin biotype can be evaluated for
intra-operative supplementation using connective tissue grafts and facial
bone grafts to create a more forgiving tissue drape over the implant site. As
thicker cortical bone volumes promote thicker biotypes, the bony
architecture and soft tissue drape may be modified in an esthetic zone prior
to implant placement and restoration. Advance planning also provides the
implant team an opportunity to inform the patient about these issues and to
point out potential esthetic complications prior to commencing treatment. A
patient's expectations must be addressed, especially if they are not interested
in grafting to modify the tissue type (Fig. 12.7).
FIG 12.7 The thick biotype in this case has completely masked the location of the
anterior implant.
Treatment.
Correction of thin biotypes requires tissue augmentation to create a thick,
dense layer of fibrous tissue over the implant body and any deficiencies
involving the adjacent natural teeth. Connective grafting procedures are
readily available to increase the thickness of the tissue drape in situations
like this. Subepithelial connective grafting procedures may utilize either
palatal connective tissue or acellular dermal matrix (i.e., AlloDerm
[BioHorizons IPH, Inc.]) as the source of donor tissue. The thick layer of
connective tissue is inserted into the deficient regions with tunneling
procedures, allowing the repositioned tissue flap to provide the blood supply
to the developing graft site. The use of the subepithelial approach allows the
implant clinician to produce a final tissue tone and color that matches the
adjacent natural tissue. Earlier applications of “free tissue grafting
procedures” utilized the epithelial layer of the palate as the donor site. This
usually creates zones of thicker keratinized tissue with a distinctly white
color that is not acceptable from an aesthetic standpoint when utilized in the
anterior maxilla. Most anterior treatment plans today also incorporate the
addition of layers of allograft or bovine graft particles with membrane
coverage to limit excessive bone remodeling in these critical regions. These
concepts are critical in “immediate implant” cases where many cases require
both soft tissue and hard tissue supplementation (Fig. 12.8).
FIG 12.8 Subepithelial connective tissue grafting to cover grey color translucence
on facial of an implant site. (A) Preoperative. Grey color on facial of implant body. (B)
CT graft. (C) Tissue graft insertion into tissue tunnel on facial of implant site. (D)
Immediate postoperative. (E) Final photo showing resolution of improper tissue
color.
Procedural Technique Complications
Failure to Understand Limitations of
Regenerative Materials
Etiology.
Successful ridge augmentation requires consistent development of bony
foundational support that allows the restorative prosthesis to be placed in an
ideal position for proper aesthetic and functional success. As the
regenerative technique is chosen, grafting materials and isolation techniques
must be clearly understood from the surgeon's standpoint to prevent
inadequate graft development or unpredictable stability of the graft site as
the prosthesis is loaded and maintained. The current approaches to ridge
augmentation consist of a variety of techniques including guided bone
regeneration (GBR), onlay block grafting, ridge splitting, distraction
osteogenesis, or a combination of these techniques.5,6,8,9 GBR with autogenous
bone, bone harvested from the same individual, is considered by some to be
the gold standard for alveolar ridge augmentation.10 The use of allografts
requires timely substitution of these primarily osteoconductive particles with
vital bone, and the consistency of the resulting ridge must be dense enough
to withstand the forces generated during the preparation of the osteotomy
and insertion of the implant. Incorporation of osteoinductive graft materials
into the procedure promotes the development of strong bony ridges, and the
overall substitution process can be shortened. Autogenous bone provides the
most active osteoinductive properties, as does the use of bone morphogenic
protein (BMP) and other growth factors.55
Complications.
A clinician who is not well versed in the limitations of the variety of graft
materials may fall into the trap of a “one size fits all” approach to treatment.
When significant defects require large volumes of bone, autogenous grafting
may also be necessary. Allograft procedures are often used to spare the
patient potential discomfort related to a secondary donor site. However,
allograft in some cases will not develop a sufficient volume of bone to allow
ideal implant placement and an aesthetic restoration. Complications usually
arise when a graft is placed using a technique or with materials unsuited for
the demands of the bone defect. Poor results eventually lead to increased
treatment times, a loss of patient confidence in the surgeon and increased
treatment costs.
Prevention.
The prevention of potential graft failures and poor augmentation volumes
starts with a clear understanding of the anatomical, restorative, and aesthetic
requirements for this specific defect. These factors must be matched to the
best utilization of available grafting materials, membrane choices, techniques
for space maintenance, and site protection. An effective bone regenerative
material that has been matched with a predictable membrane creates the
foundation for the rest of the restorative treatment plan.
GBR Membranes
Nonresorbable.
The ideal GBR membrane is a biocompatible material capable of excluding
epithelium without eliciting an immune reaction that might interfere with
bone regeneration. Membranes are typically classified as resorbable or
nonresorbable. Nonresorbable membranes include titanium foils, expanded
polytetrafluoroethylene (e-PTFE) and dense polytetrafluoroethylene (d-PTFE)
with or without titanium reinforcement. Studies of GBR procedures utilizing
titanium-reinforced nonresorbable membranes have shown great success
with horizontal and vertical alveolar ridge augmentation because of their
ability to maintain space, minimize graft mobility, and exclude epithelium.11-
21
Disadvantages of nonresorbable membranes include the need for reentry
procedures for membrane removal and frequent postoperative infections that
may follow premature membrane exposure.20,22 Various studies have shown
premature membrane exposures typically result in increased morbidity and
decreased bone regeneration in GBR procedures. Recent reports of d-PTFE
use have demonstrated that membrane exposure does not always dictate
failure of the developing graft. If the d-PTFE membrane can be maintained
for at least 6 weeks, removal at that time or later will often be followed with
development of a reasonable bony ridge. This is different than earlier cases,
where e-PTFE membranes allowed bacterial invasion of the entire graft site
through the larger pore sizes found in the e-PTFE membranes. The smaller
pore size in the d-PTFE membrane prevents direct passage of bacteria
through the membrane. Subsequently altered bone development may tend to
be limited to the surrounding margins where the membrane was exposed
(Fig. 12.9).22,54
FIG 12.9 (A–B) Premature membrane exposure resulting in increased morbidity.
Resorbable.
In order to overcome these limitations, resorbable membranes have become
a popular alternative because they are biodegradable and are less likely to
become infected in the event of an exposure.23-26 Resorbable membranes are
typically made of polyesters (e.g., polyglycolic acid [PGA], polylactic acid
[PLA]) or tissue-derived collagens (e.g., AlloDerm GBR, Ossix Plus).
AlloDerm is an acellular dermal matrix originally developed in 1994 to be
used as a skin allograft for burn patients.27 It has been used in the medical
and dental literature as an allograft for various procedures because of its
ability to rapidly vascularize and to increase soft tissue thickness. In the
dental literature, AlloDerm has been successfully used for root coverage,
thickening of soft tissues, and guided bone regeneration.24,28-30 AlloDerm GBR
is a thinner version (thickness ranges from 0.5–0.9 mm) of the original
AlloDerm product (thickness ranges from 0.9–1.6 mm), specifically designed
for GBR. AlloDerm GBR has been successfully used as a barrier membrane
and has also been shown to significantly increase soft tissue thickness by
45% and 73% from baseline at 6 months and 9 months, respectively (baseline
0.55 ± 0.16 mm to 0.80 ± 0.26 mm at 6 months and 0.95 ± 0.28 mm at 9 months;
p < 0.0033), when used as a barrier membrane for GBR of horizontal alveolar
ridge deficiencies.29
Aside from soft tissue exclusion and clot stability, space maintenance is
key to the success of GBR and can be accomplished in various ways using
titanium-reinforced membranes, titanium mesh, particulate graft material,
block grafts, dental implants, or tenting screws/pins.5,31,11,12,32-35
Nonresorbable5,19,34-37 and resorbable tenting screws38 have been used to aid
in space maintenance in various horizontal and vertical ridge augmentation
studies. The tenting screws are typically used as “tent poles” to support the
membrane, decrease graft mobility, and relieve external pressure on the
graft55 (Fig. 12.10).
FIG 12.10 (A) Tent screws used to stabilize membrane in order to achieve desired
contour. (B) Postoperative image depicting bone growth to ideal contours.
Types of Bone Grafting Material

Autogenous Bone.
Autogenous bone is still considered by many to be the gold standard graft
material for GBR because of its osteogenic, osteoinductive, and
osteoconductive properties.6,10,39Autogenous bone is commonly harvested
intraorally from the ramus and symphysis, but is associated with increased
morbidity related to a second surgical site, unpredictable graft resorption,
and graft mobility.5,10,13,40-44 The anatomy of the posterior edentulous ridge can
limit the shape and volume of donor bone available for harvesting
autogenous blocks.44 Many times the autogenous block and recipient site
require such extensive preparation in order to obtain intimate contact
between the graft and recipient site that a large percentage of the harvested
bone cannot be utilized.43 Some clinicians have advocated crushing the
autogenous block graft into a particulate autogenous graft to allow for more
conservative recipient site preparation, complete utilization of the harvested
bone, and a decreased volume of bone that will need to be harvested, thereby
decreasing the morbidity of the procedure (Fig. 12.11).17,45
FIG 12.11 (A) Autogenous ramus harvest block. (B) Harvested cortical ramus
block. (C) Block stored in sterile saline. (D) Block reduced to particulate fragments.
(E) Particulate fragments placed in donor site.
Allografts.
In order to overcome the limitations related to the availability of autogenous
bone volume, various bone substitutes, including xenografts (material
harvested from another species), alloplasts (inert synthetic material), and
allografts (material harvested from another individual of the same species),
are being used as adjuncts for GBR with successful clinical and histologic
outcomes.6,8,13 Some clinicians have advocated combining autogenous bone
with the various bone substitutes.16,23,45,46 The potential benefits of adding
particulate autogenous bone to an allograft are the addition of osteogenic
and osteoinductive growth factors to the osteoconductive properties of a
bone substitute. The use of this combination allows for a reduction in the
amount of autogenous bone harvested, decreasing the morbidity and
postoperative discomfort for the patient.
Xenografts.
Xenografts are graft materials that are taken from a donor of one species and
grafted into a recipient of another species. This type of graft material heals
via osteoconduction. Simian et al found that the addition of deproteinized
bovine bone mineral (Bio-Oss) to autogenous particulate resulted in greater
vertical augmentation than particulate autogenous material alone. Urban has
combined bovine particles with autogenous bone in the development of large
volumes of vertical and horizontal bone in severely compromised
regeneration sites. The incorporation of the bovine product is planned for
extended support of the graft volume, following with a timely turnover into
vital bone as the graft matures (Fig. 12.12).16,47
FIG 12.12 Lack of bone turnover. This mature graft site demonstrates the
presence of bovine particulate graft material that has not been replaced by vital
bone. The goal of any regenerative procedure is to develop as much vital bone as
possible prior to loading an implant.
Alloplasts.
The use of alloplasts is not currently recommended for major ridge
augmentation. Successful grafting requires that the source of the grafting
particles be readily available for consistent replacement with vital bony cells.
Alloplastic approaches tend to leave a very granular ridge form that tends to
fall apart as the osteotomy is prepared and the implant is inserted.
Approaches have been utilized where alloplasts were added to FDBA (freeze
dried bone allograft) or DFDBA (demineralized freeze dried bone allograft),
but overall, the use of alloplasts is not recommended when significant
regeneration is required.55
Incorrect Choice of Regenerative Technique in

Respect to the Severity of the Defect
Etiology.
The literature today provides a multitude of surgical approaches that are
available for regeneration of deficient implant sites. These would typically
include particulate grafts, BMP graft combinations, block grafts, and the use
of ridge-splitting techniques. The implant team must carefully consider each
clinical situation to determine which technique will most predictably develop
the needed bony support for the restorative treatment plan. In this
assessment, the anatomy of the defect will often lead to the choice of a
particular approach due to the ease of graft placement or the limitations of
using a rigid graft in a highly irregular recipient site. Recipient sites with a
very irregular surface are preferably approached with a particulate approach,
and cortical blocks are best utilized where a smooth bed can be prepared for
close adaptation of the block to the underlying defect.
The depth of the vestibule is a significant factor when evaluating defects.
The use of an autogenous block is much easier when the vestibule is very
deep and there is adequate room for adaptation of the entire length of the
cortical graft. Placement of a block in a shallow defect can sometimes be
difficult because of anatomic limits that will force graft placement higher
above the ridge than the bone on the adjacent natural tooth. This can result
in incision line opening, graft exposure, and a compromised healing process
(Fig. 12.13).
FIG 12.13 (A) Incision line opening resulting in autogenous block failure. (B)
Autogenous block failure resulting from nonunion of the blocks and host bone.
If a particulate graft is utilized, lateral support of the graft will need to be

incorporated into the procedure to provide and maintain space for the
regenerative process to be completed. This same spacial support and
protection prevents the graft particles from slipping laterally during the
healing process (Fig. 12.14).
FIG 12.14 Unsupported graft. If particulate grafts are placed with no stabilization
support (i.e., tent screws) results may be unpredictable.
The use of a “ridge splitting” approach should only be considered when

the apical region of the site is thick enough to allow expansion of the cortical
wall laterally without fracturing the expanded cortical plate at the most
inferior point of the split. This is particularly relevant in the maxillary
anterior region where the thin width at the base of the site is often not
substantial enough for a predictable split. Care must be taken to ensure the
ridge split and graft will allow enough width for an implant with the required
diameter. Ridge splits in a maxillary anterior region that is shaped with a
proclined angulation can often lead to the placement of an implant with a
severely angled emergence profile. This emergence angle then requires the
use of an angled abutment to compensate for the malpositioning. Cases like
this are better suited for use of an augmentation approach that thickens the
ridge in both the coronal and apical regions. The additional apical
augmentation developed in these techniques will create a better emergence
profile for the implant and the restoration, leading to better patient
satisfaction (Fig. 12.15).
FIG 12.15 Ridge split technique. Allograft in association with ridge splitting to
increase compromised ridges in width. (From González García R, Monje F, Moreno C:
Alveolar split osteotomy for the treatment of the severe narrow ridge maxillary atrophy: a modified
technique. Int J Oral Maxillofac Surg 40(1):57–64, 2011.)
Complications.
Failure to choose the proper regenerative approach will often result in a poor
postoperative ridge form that will not be amenable to an ideal implant
placement and an acceptable emergence profile. Choice of the incorrect
technique may lead to a graft that is susceptible to complications related to
continuous isolation and stabilization of the graft during the entire healing
process. These problems usually stem from issues related to strain on the
incision line, movement of the temporary prosthesis, migration of the graft
materials, or overzealous attempts to over-grow bone.
Prevention.
The implant clinician must develop a familiarity with the indications for each
of the different types of grafting procedures, and incorporating that
knowledge into a working treatment plan. With the aid of 3-D imaging, the
clinician can complete a comprehensive evaluation of the extent of the bony
defect. A treatment plan must then be developed, taking into consideration
the overall size of the defect, the ability of the recipient site's tissue to be
expanded, and the presence of a temporary prosthesis, and the overall size of
the defect. Included in this strategy would be the choice of possible donor
sites, graft materials, suture type and technique, and the space maintenance
method (Figs. 12.16 to 12.18).
FIG 12.16 Failure to develop adequate ridge width (A) forced placement of this
implant in a very poor occlusal position (B).
FIG 12.17 Deficient ridge width. (A) This ridge has inadequate width and requires
augmentation. (B) Visualization of the required width demonstrates the volume of
bone that will be needed for proper implant placement.
FIG 12.18 (A) Wax-up shows dimensions of required restoration/bone. (B) 3-D
model shows distinct undercut of mandible below implant site.
Poor Incision Line Design
Etiology.
Incision design is one of the keys to a predictable regenerative result. Ideal
incision designs provide complete access to the surgical site without
compromising the integrity of the surrounding tissue. As the incision is
planned, the anatomy of the adjacent papilla must be considered to prevent
any damage that will compromise the aesthetics and function of the tissue
postoperatively. The patient's biotype and the amount of keratinized tissue is
always reviewed, and any deficiencies of attached tissue must be accounted
for in the incision design. The incision must be planned in a way that keeps
incision lines away from critical regions where graft particles or blocks could
become exposed. Observation of sound surgical principles in preparation of
incisions is critical for maintenance of the blood supply to all of the involved
tissues. Wide-based incisions are always important to prevent interruptions
in the vascular supply to the flap.
Complication.
Failure to properly plan the incision design of a flap during grafting can pose
numerous issues, chiefly related to incision line opening postoperatively.
Incision line opening exposes the regeneration site to an influx of oral
pathogens, soft tissue ingrowth, and loss of the graft materials that were
intended to be isolated during the maturation process. Failure to preserve
the integrity of the papilla during incision line design eventually leads to
compromised aesthetics around the final restoration. An initial incision
without a consistent depth may create a split-thickness flap, leading to tissue
shredding and the involvement of vital structures located within the flap.
Incisions through zones with limited keratinized support can leave large
expanses of mucosa along the incision line. Thin mucosa is very difficult to
predictably suture to the adjacent flap, often leading to an open incision days
later. Lastly, failure to make broad-based releasing incisions may compromise
the blood supply to the flap, causing tissue ischemia.
Prevention.
The coronal incision is usually placed on the crest of the ridge, favoring a
location closer to the palatal aspect if possible. In regions where the
keratinized tissue is limited, the incision should at least “split” the distance
between the two edges of the keratinized tissue. It is always best to try to
keep incision lines away from areas that are key to regenerative volume and
protection. When possible, the papillae should be preserved. If there is a
good papilla present, the incision should be designed to avoid involvement
of the papilla or it should be moved to the adjacent interproximal space. If
the papilla is absent or is flat, the incision can be directly adjacent to the root
approximating the graft or it can be moved to the adjacent space. Moving the
releasing incision to the adjacent interproximal space also moves the incision
line away from the grafting site, limiting complications if the wound opens
up postoperatively. Extending to the adjacent interproximal space can
sometimes lead to difficulty in advancement of a tension free flap over the
graft site, but this can be released with additional steps.
The releasing incision should always be prepared with a wider base than
its coronal width to preserve the apical blood supply to the flap. As the flap
is reflected, it is critical that the complete periosteal layer be reflected with
the flap, avoiding maceration of the tissue during the releasing process.
Attention to the thickness of the flap and careful use of the scalpel and
instruments is important at this stage. By keeping instruments firmly against
bone during the flap-releasing process, the clinician ensures a proper full-
thickness flap release.
Incision lines should be prepared with vertical releasing incisions that are
several millimeters away from the lateral border of the graft site. When an
incision line opens around a graft site, the open region can directly
contaminate the underlying graft particles, preventing proper regeneration
of the bony defect. By moving the incision away from the critical regeneration
site, the possibility of this type of contamination can be limited to some
degree (Figs. 12.19 to 12.22).
FIG 12.19 Incision design. (A) Typical crestal incision with keratinized attachment.
(B) Crestal incision, preserving the limited amount of keratinized tissue. (C) Crestal
full arch incision designed to preserve the limited facial zone of keratinized tissue.
FIG 12.20 Release incisions. A papilla sparing incision with vertical releasing
incisions (A) that swing laterally away from the critical graft site (B), limiting the
chance of graft compromise in the case of an open incision line.
FIG 12.21 Alternative release incision. (A–B), The vertical releasing incision is often
moved laterally to the adjacent papilla space. This prevents problems related to
incision line opening from directly complicating the critical graft development in key
positions.
FIG 12.22 Poor release design. Incision line should be moved laterally away from
critical development sites (arrow).
Torn Lingual Flap

Etiology.
The tissue thickness on the lingual aspect of the mandible is very thin and
friable. This tissue can be easily torn during reflection of the flap and
manipulation of the tissue during the grafting procedures. Resultant
“buttonhole” openings may compromise the blood supply to the
surrounding tissue that is needed for coverage over the graft site, leading to
compromised results postoperatively.
Complication.
Tearing or buttonholing the lingual flap leads to exposure of the graft site
and the possibility of margin necrosis coronal to the tear. This exposure may
lead to total graft failure (Fig. 12.23).
FIG 12.23 Lingual flap exposure. (A) Maintaining the integrity of this flap of tissue is
very important in a regenerative procedure because it is very easy to tear the flap
during its initial reflection or to buttonhole the flap during its manipulation over a bulky
graft site. (B) If this occurs, it is very difficult to mend the tear, potentially
compromising the closure of the graft site or predisposing the region to incision line
opening over the healing graft.
Treatment.
If the lingual flap is torn during the procedure it can sometimes be repaired
using 5-0 chromic suture, approximating the edges of the tear and preventing
tension on the weak site. It is recommended to use a collagen membrane
below these fenestrations to assist with healing and to isolate the graft
materials. Maintenance of the blood supply to the tissue flap is important;
thus tension should be minimized to the flap.
Prevention.
Preparation of the initial incision line must be extended completely through
the tissue and through the periosteum. At the time of the initial separation
of the flap margin from the bone, care must be taken to obtain a clean release
of the complete flap margin from the bone. Shredding the flap margin at this
time leads to poor control during the rest of the flap release and ultimately to
increased chances of tearing the partial-thickness flap. Curettes or retractors
must be utilized to create an even release and reflection of the full flap
throughout this process.
Difficulty Releasing the Flap for Tension-Free

Closure
Etiology.
Successful augmentation procedures require maintenance of an intact tissue
closure along the incision line during the healing process. One of the most
common surgical complications that a clinician will experience early in their
learning curve is incision line opening. The failure of maintaining this union
is directly related to an inadequate release of all tension on the tissue flap as
it is stretched over the widened graft space. Clinicians will find that it is
impossible to pull a tissue flap over any sizeable graft site without first
altering the integrity of the flap itself. Examination of the exposed inner
surface of a reflected flap reveals a smooth shiny layer called the periosteum.
The periosteum is comprised of a thin firm layer of dense tissue that has no
elastic fibers. This binding layer limits any significant elongation of the flap
as it is stretched over a graft site. A simple incision through this dense tissue
“releases” this tight band of pressure on the underlying tissue flap. The
tissue directly below the periosteum is primarily comprised of elastic-type
fibers, and once the periosteum has been released, the entire flap can be
stretched. This simple releasing incision ultimately allows tension-free
closure over the graft site.
Complication.
A flap covering a graft that does not have complete release of pressure on the
two margins of the flap will often pull open during the healing process
(incision line opening). Tension on the flap compromises the blood supply to
the tissue along the suture line that is under pressure. This pressure leads to
necrosis and eventual separation of the two edges of the flap closure. Once
this has occurred, the flap cannot be sutured back into place and the graft
site is open for contamination and tissue ingrowth. The success of bone
grafting is largely dependent on the maintenance of space for bone
development and isolation of the graft particles during the slow process of
osteogenesis. Soft tissue ingrowth, bacterial contamination, and migration of
graft particles predictably compromise regenerative results.
Prevention.
The typical graft site requires that the overlying flap be released enough for
extension of the flap at least 5 mm beyond the edge of the adjacent margin
for a tension-free flap closure. The only way to achieve this free flap release is
the use of a shallow incision though the periosteal layer, allowing the elastic
fibers of the underlying flap to stretch over the graft site.
Treatment.
Tension-free flap release technique: A scalpel with a #15 blade is used to
prepare a very shallow incision through the periosteum from the anterior to
the posterior border of the graft site. As the incision is prepared, a clear
separation of the borders of the incision line can be seen. It is not necessary
to make a deeper incision because the underlying tissue can be freely
released with the tip of sharp scissors (e.g., Metzenbaum). The closed scissor
tip is placed into the incision, parallel to the flap itself. The ends are then
opened, spreading the tissue as the ends separate. This is repeated until the
flap can be freely extended at least 5 mm past the border of the lingual
incision line of the graft site. The use of the spreading scissor tips reduces
the need to cut underlying tissue and possibly vital structures like vessels or
nerves. Tissue flaps in the maxillary and mandibular anterior regions usually
require extensive release of the flap for tension-free closure over most graft
sites. The posterior regions do not typically require extensive release and
dissection. Care must be taken to prevent over thinning the flap or
perforating the flap with a “buttonhole” (Figs. 12.24 to 12.26).
FIG 12.24 Tissue release. (A) Adequate flap release around bone graft sites is the
most critical step for tension-free flap closure and predictable graft success. A single
shallow incision through the periosteum is prepared inside the flap. (B) The clear
separation of the periosteal edges as the flap is extended and the elastic fibers allow
the flap to stretch.
FIG 12.25 Extended periosteal release. (A) The incision is extended on the mesial
and distal aspect of the graft site to allow adequate mobility of the flap when it is
extended. (B) After dissection of the periosteal release with sharp scissors, the flap
can be freely extended over the graft site. This release must be completed until the
flap can be moved at lease 5 mm beyond the lingual aspect of the graft site.
FIG 12.26 Lab tissue release example. (A) A #15 blade is used in a pig's foot to
demonstrate the initial incision through the periosteum. (B) The incision is extended
and you can see how the distance between the two edges continues to widen. (C) A
pair of sharp pointed surgical scissors is placed parallel to the flap. They are pointed
into the tissue in a closed position and as they are opened they gently stretch and
release the elastic fibers of the flap. This prevents damage from cutting this tissue
with a scalpel trying to release the flap. (D) As the release is completed, you can see
a clear separation between the thicker layer and the released inner portion of the
flap.
Inadequate Vertical and Horizontal Space

Maintenance in Graft Sites Utilizing Membranes
Etiology.
The field of advanced implant dentistry went through a complete paradigm
shift when the first augmentation procedures were introduced. Until that
time, implants were placed in the islands of bone that were discovered at the
time of flap reflection. This limited preoperative treatment planning to a
great extent and subsequently the role of the restorative dentist was at many
times very difficult. Implants often emerged at odd angles creating a variety
of long-term support and restorative issues. The majority of bone grafts
initially were designed around block grafting techniques where significant
volumes of bone were regenerated horizontally and in limited cases in a
vertical dimension. Block grafting is still used by many surgeons, but these
procedures require surgical expertise and the morbidity can sometimes be an
issue from the patient's standpoint.
Particulate grafting was initially introduced utilizing non-resorbable e-
PTFE membranes. This approach used titanium struts to prevent collapse of
the membrane into the critical regenerative space. The titanium could be
trimmed and shaped into contours that produced the bony support required
for the predetermined restorative plans. Nonresorbable membranes were
used to some extent, but they were generally limited to production of 1–3
mm of bone thickness. These limitations were directly related to the limited
number of ways that the space between the recipient bone and the
suspended membrane could be supported. In most cases, one or two bone
fixation screws were placed in strategic sites, maintaining enough space for
smaller graft sites.
In recent years, alternative approaches have centered around expanded use
of membrane/fixation screw techniques, introduction of nonresorbable d-
PTFE membranes with titanium struts, titanium mesh, temperature molded
and welded membranes, along with other similar approaches. The key
principle in each one of these techniques centers on the use of an occlusive
membrane to maintain a defined space between the recipient bone and the
overlying gingival/connective tissue flap. This space must be isolated from
outside cellular downgrowth, and the flap covering the defined space must
be completely supported throughout the regenerative process. Each
technique has its own advantages in relation to defining the final shape of
the ridge, and each approach has its own issues in respect to maintaining a
sealed layer over the graft site while the bone is developed. All of these graft
techniques require 5 to 6 months for maturation of the graft site. Over this
timeframe various situations contribute to pressure on the graft site and
breakdown of the incision lines and membrane edges.
Deficient ridges occur when one or more of these principles is violated.
Any mobility of the membrane will disrupt the cellular development process,
beginning with interruption of the initial clot stability. Graft particles that are
not confined or protected will tend to shift to a region that has less pressure
or movement. The coronal aspects of all graft sites are very important
because the bone around the platform of an implant carries a great deal of
the occlusal load. Failure to define and maintain this dimension leads to a
narrow width at the coronal aspect. A deficient ridge width like this will
many times create a dehiscence on the facial or lingual aspect of an implant.
This bony deficit subjects the remaining bone to additional stress and also
disrupts the delicate soft tissue attachment around the abutment. Success in
all of these approaches requires development of large volumes of bone,
overbuilding regions where possible. Under-estimation of the required bony
support often leads to thin facial bony coverage over an implant body. It is
our experience that you really never have too much bone. All bone will go
through a constant remodeling process and all too often, facial bone will thin
over time. This facial thickness will eventually tend to thin out over the
threads of the implant, altering aesthetics and possibly implant support.
Membranes that are not rigidly fixed in place tend to move out of position
and some varieties resorb early in the regenerative process, allowing invasion
of tissue, bacteria, or movement of the graft materials. Each one of these
seemingly small issues can compromise the whole regenerative process.
Complication.
Areas where a particulate graft shifts or where a supporting membrane
collapses typically heal in a manner that does not provide the expected ridge
shape and dimension established during the restorative planning process.
The clinician is forced to either compromise the implant position or abort the
implant aspect of the procedure. This delays implant placement until
adequate supporting bone can be developed with additional grafting.
Implants that are placed in compromised recipient sites are prone to
complications when the prosthesis is loaded and bone remodeling occurs.
Prevention.
GBR techniques utilize an occlusive barrier membrane between the alveolar
bone and the gingival epithelium/connective tissue to prevent epithelial
down-growth into the alveolar ridge defect. The occlusive barrier membrane
allows for osteogenic cells from the adjacent alveolar bone to colonize the
blood clot and to induce bone regeneration.31,47 Aside from soft tissue
exclusion and clot stability, space maintenance is the key to the success of
GBR. Screw-supported barrier membranes may be utilized for development
and maintenance of this regenerative space. This same vertical support can
be achieved using titanium-supported membranes, titanium mesh, or any
other approach that creates and holds an open, isolated space for bone to
occupy.
Bone fixation screws.
Space maintenance can be accomplished utilizing bone fixation screws as
vertical and horizontal supports for isolation of bone graft particles and
support of occlusive membranes. The required graft volume and spatial
dimensions determine the number and positioning of these screws. Screws
are anchored in the recipient site as needed to form a dome over the graft
site that matches the height of bone needed for proper implant placement.
Placement of graft materials without defining space maintenance will usually
lead to variable postoperative bone volumes and often deficient bony
support on the facial and lingual aspect of the coronal aspects of the implant
platform. A thin or granular bone consistency at the coronal aspect will lead
to a dehiscence on the facial or lingual aspect of the implant platform.
Titanium supported d-PTFE.

The use of titanium supported d-PTFE membranes has demonstrated
development of significant amounts of bone in everything from minor
defects to extensive vertical defects with through-and-through cortical
destruction. Earlier use of e-PTFE (Gore Tex [W. L. Gore & Associates, Inc.])
membranes showed serious compromises in final graft volumes if any
portion of the membrane was exposed. This failure was largely related to the
large pore size in the e-PTFE membrane. The pores in the e-PTFE were large
enough for bacterial passage through the membrane itself, resulting in
altered bone growth throughout the region (5–25 µ). The success in grafting
with d-PTFE can be related to the small (<2 µ) pore size of d-PTFE, where
bacterial invasion though the membrane itself is blocked.58 Exposed sites in
d-PTFE cases show no side effects related to invasion of bacteria directly
through the membrane and into the developing bone. Exposed sites can still
present problems related to invasion around the edges of the exposed
membranes. It has been described that d-PTFE membrane exposure cases
need to be maintained for at least 6 weeks before the membrane can be
safely removed. Removal of the membranes earlier than this exposes the
contents to bacterial ingrowth and this usually results in a significantly
altered final graft result. Exposed d-PTFE should be maintained with
chlorhexidine rinses and careful hygiene around the exposure sites. Care
should be taken to prevent any movement of the membranes with temporary
appliances.54,56
Titanium mesh.
Mesh support techniques use a piece of thin titanium mesh that is shaped
into the external form of a desired ridge shape required for implant
positioning. The advantage of this technique is directly related to providing
rigid fixation of a formed template over a volume of grafting material,
assuring maintenance of space required for graft development. It is used
with either a particulate graft or with BMP that has been mixed with a graft
and sponge mixture. If the integrity of the soft tissue flap can be maintained
throughout the healing process, significant bone volumes have been
consistently reproduced. If the flap margin or other region of the overlying
flap exposes the titanium mesh, the predictability of the final graft volume
can be compromised.
Treatment.
Treatment for dealing with an inadequate ridge follows one of two
approaches. The first option involves placement of implants in the
compromised bony foundation, grafting additional bone over the exposed
implant threads at the time of implant placement. This technique often leads
to varied results. If the exposure of the implant body is within the contours of
the surrounding basal bone, grafting will be much more predictable than in
cases where the implant contour extends beyond the surrounding basal
bone. The presence of a blood supply, supporting bony protection, and
adequate coverage of the remaining surfaces of the implant are critical. The
second option requires postponement of the implant insertions, attempting
additional augmentation, and placement of the implants after adequate bone
has been regenerated. This approach is the most predictable for a successful
long-term result. (Figs. 12.27 to 12.32).
FIG 12.27 Bone screws for ridge contour. (A) Bone fixation screws are used to
define the topography of the prescribed bony ridge prior to placement of the bone
graft materials. (B) The mature graft postoperatively has grown up to the level of the
heads of the fixation screws. This demonstrates the principle of “space
maintenance,” and the ability of the body to fill in isolated spaces as long as the graft
is supported and tissue ingrowth is prevented during the healing process.
FIG 12.28 Screw positioning. (A) The restorative wax-up and the volume of bone
that will be required to allow proper placement of the implants determine the position
of the screw heads. This approach is very helpful when the recipient site has an
irregular surface like the residual periapical lesion. (B) The screw placed in the deep
defect will assure adequate bone development in this severely compromised area.
(C) Postoperative healed ridge.
FIG 12.29 In this matured graft site, bone has completely filled in the space around
the varied screw positions, creating a substantial bony ridge for implant placements.
FIG 12.30 Postoperative ridge with additional width.

FIG 12.31 Facial and palatal augmentation. (A) The residual ridge in this
photograph is close to 2 mm in its most narrow region, requiring both facial and
palatal regeneration. The fixation screws define the specific area that will be
regenerated with the grafting process. (B) Strategic positioning of fixation screws
allows the surgeon to outline exactly where bone will be developed. The volume of
the graft is no longer an issue because particulate grafts fill up a defect regardless of
the irregular surfaces involved.
FIG 12.32 Titanium mesh can easily become exposed if a sharp edge works its
way through the soft tissue flap. This can be maintained during the healing process,
but this can often compromise the graft development process.
Particulate Grafts
Exposure of the Bone Fixation Screw During the
Healing Process
Etiology.
Bone fixation screws in regeneration sites sometimes become exposed during
the healing process, potentially leading to bacterial invasion around the neck
of the screw. Careful attention to the timelines of the screw exposure and the
type of regenerative process is important in these situations.
• Block Grafts. Exposures involving a fixation screw in a block graft case do
not allow many options related to screw removal. The most important
concept in block grafting is rigid fixation of the block itself throughout the
regenerative process. Therefore, removal of the exposed screw could result
in a total graft failure. These situations must be maintained as well as
possible with maintenance of the exposed screw.
• Particulate Grafts. Exposure of fixation screws in particulate grafting occurs
when the head of the screw works its way through the overlying membrane
and eventually perforates through the thin layer of the mucosa that covers
the graft site. This typically happens when the screw head has a thin
diameter that perforates through the membrane and eventually through the
tissue. Particulate grafting techniques use these fixation screws to support
the membrane and to define the shape of the desired bony contours. The
use of a screw with a “wide head” is found to be important for predictable
results. The type of membrane used for graft isolation also makes a
significant difference when perforation of the screw through the membrane
is a concern. AlloDerm GBR tends to be very resistant to membrane
perforation during the healing process, whereas collagen membranes are
soft when moistened and tend to perforate and tear if strain is placed on the
hydrated membrane.
Complication.
Perforation of a membrane allows the ingress of foreign matter and fibrous
soft tissue cells into the graft site, causing a disruption in the bone
regeneration process. If the head of the screw pushes through the soft tissue
and is exposed, bacterial contamination may result, potentially leading to
graft infection and possible failure.
Prevention.
The head of the bone fixation screws should have a wide and smooth
diameter that provides enough surface area to support the membrane and to
limit abrasion against the overlying mucosal layer. A small head will tend to
work its way through a membrane when it is placed under tension or where a
delicate membrane is being utilized. The typical bone fixation screw has a
diameter of 1.5 mm, and the head of the screw should be as wide as possible.
Treatment.
Exposed screw heads should be maintained with chlorhexidine rinses until
the surrounding soft tissue has healed. It is recommended that the screws in
particulate techniques be removed at this time to eliminate the possibility of
contamination of the graft through the opening around the shaft of the
screw. If the screw is preventing pressure on the graft in respect to the use of
a removable prosthesis, retention of the screw could be considered. Under no
circumstances should efforts be made to cover the screw by repositioning the
soft tissue (Fig. 12.33).
FIG 12.33 Tent screws. (A) Larger screw heads are more likely to grow bone than
smaller sized screws. Note the lack of bone around the small-headed screw on the
far right side of the photo. (B) Example of “wide headed fixation screw.” (C) Fixation
screws come in various width shanks and lengths. (D) The heads of the fixation
screws are often visible through the thin mucosa covering the healing graft site. This
is not a complication and no special treatment is needed. (E–F) Exposed fixation
screws.
Membrane Placement Too Close to Adjacent Teeth
Etiology.
GBR techniques routinely require placement of occlusive membranes in the
proximity of natural teeth. This requires the implant surgeon to clearly
understand the principles related to the positioning of nonresorbable
membranes and resorbable membranes in relation to natural root surfaces.
• Nonresorbable Membranes. Membranes used in early GBR were
nonresorbable e-PTFE membranes, and these were typically trimmed to
allow 2 mm of space between the GBR membrane and the root of the
adjacent natural tooth. This allows soft tissue attachment around the
biological width of the tooth and anchorage of tissue around the occlusive
barrier. The use of d-PTFE today requires observation of these same rules of
maintenance of 2 mm between the edge of the membrane and the side of an
adjacent root surface. GBR techniques using titanium mesh requires 2 mm
of clearance from the root of a tooth due to similar issues.
• Resorbable Membranes. In GBR techniques utilizing resorbable
membranes, the 2 mm rule is not a critical factor and resorbable
membranes can be placed directly against the roots of the adjacent teeth
without causing a membrane failure. Titanium mesh itself is separated from
the root of a tooth due to similar issues (Fig. 12.34).
FIG 12.34 Titanium resorbable membrane. (A) This defect will require regeneration
of the missing buccal plate, and a nonresorbable membrane will be used for space
maintenance. (B) The support of the titanium struts prevents collapse of the
membrane into the defect during the healing process. (C) Titanium reinforced
membranes are placed with the edges 2 mm away from the adjacent roots to allow
for proper attachment of the soft tissue around the adjacent root. (D) The margin of
the membrane is probably too close to the incision line, potentially leading to
problems with incision line opening.
Complication.
Placing resorbable membranes too close to the adjacent tooth roots can allow
direct contamination of the membrane through the interproximal space,
contributing to tissue ingrowth and bacterial infection of the graft. Titanium
struts that are positioned close to the interproximal root surfaces will often
lead to membrane exposure and a compromised graft volume in the region.
The only complication with placing resorbable membranes directly against
natural roots is related to primary wound closure in the root proximity.
Membranes must be smooth and they should allow the overlying flap to be
adapted evenly around the neck of a tooth root.
Prevention
Nonresorbable membranes.
Nonresorbable membranes should be placed 2 mm from roots of adjacent
teeth if possible. Titanium supported membranes should be selected in a
form that does not have lateral struts that will be positioned in the proximity
of a tooth root. Newer membranes are now being designed in arrangements
that allow support over the interproximal ridge without the need for lateral
struts in these critical interproximal regions.
Resorbable membranes.
Resorbable membranes are not required to be separated from the adjacent
roots in most cases. Acellular dermal matrix does not appear to need to be
separated from root surfaces, keeping in mind that this same membrane is
used in routine periodontal procedures for root coverage.
The most important concept in augmentation procedures is total
membrane coverage of grafting materials from the time of membrane
placement to completion of the graft maturation process. Success is directly
related to the overall management of the soft tissue flap during flap closure.
A successful case starts with the incision, continues with proper flap
reflection of an intact periosteal layer, proper membrane positioning, and
completion with a tension-free flap closure (Fig. 12.35).
FIG 12.35 The use of a resorbable membrane does not require that the edge of the
membrane be separated from the adjacent tooth roots.
Graft Infection
Etiology.
Graft materials resorb very rapidly at a lower pH condition, with
hydroxyapatite crystals dissolving at a pH of 5.5 or less. Infectious
environments may contain a pH of 2 or less, which can cause the rapid
dissolution of a graft. Infection may be caused by lack of aseptic surgical
technique, incision line opening, or infection from adjacent dental infections.
Complication.
The presence of a localized infection in a bone graft will cause dissolution of
the graft material, contributing to a graft failure. The severity of this failure
can vary depending on the duration of the infection and the onset of the
contamination.
Prevention.
The use of proper surgical technique is vital in the preventing surgical
contamination. Preoperative antibiotic regimens, chlorhexidine scrubs, and
aseptic technique will limit bacterial contamination at the time of surgery.
The introduction of antibiotics into the graft medium may also be included
to minimize bacterial invasion. Proper suture technique and flap design are
grafting fundamentals that prevent incision line opening that can also expose
the graft to the oral microflora. Lastly, the clinician should ensure that all
space maintenance components (nonresorbable membranes, titanium mesh,
tenting screws) are free from sharp edges that may perforate the mucosa
postoperatively, allowing the ingress of bacteria into the graft.
Treatment.
Postoperative examinations must be routinely scheduled, especially during
the initial stages of wound healing. The patient must be instructed in
hygiene techniques that minimize strain on the incision line, and
postoperative chlorhexidine rinses can be used to manage the bacterial
microflora. If incision line opening occurs, the patient must be placed on a
chlorhexidine rinsing protocol to keep the graft site clean until the
granulation is complete. If the patient experiences purulence from the site or
general malaise, antibiotic protocols must be commenced immediately. Non-
resorbable membranes can be maintained for an initial 6 week timeframe
unless the site becomes infected. If this occurs, the membrane should be
removed before the situation advances (Fig. 12.36).
FIG 12.36 Exposure of this titanium mesh has been complicated by graft site
infection. Exposed titanium mesh in this situation will greatly complicate proper
development of a normal papilla on the distal of the lateral incisor.
Block Grafts: Symphysis Bone Grafts
Inadequate Symphysis Bone Volume for a Graft
Etiology.
The use of monocortical grafts in the repair of ridge defects usually requires
the harvest of substantial amounts of thick cortical bone to provide a graft
thickness greater than 3 mm. The symphysis provides the potential for
harvesting thicker sections of bone when compared to the ramus, where the
average amount of donor bone does not exceed 3 to 4 mm in thickness.
Normal variations in the cross-sectional anatomy of the symphyseal region in
multiple patients require careful preoperative assessment of the region
before surgical intervention is initiated. Prior to CBCT imaging, clinicians
were generally forced to use lateral cephalograms or early cross-sectional
imaging to predict the thickness of bone in these regions. Today, CBCT cross
sections provide a precise measurement of the thickness of the donor site,
and any anomalies can be identified preoperatively.
Prevention.
Spherical CT imaging or CBCT imaging is the recommended approach for
assessment of the anatomy and thickness of bone in the region of the
symphysis or ramus. It is recommended to measure the actual distance from
the facial cortical plate to the lingual plate to first make sure that this will
provide enough bone for the required recipient site and secondarily to
provide a guide to the surgeon for the depth of the preparation cuts into the
cortical bone during the harvest. If cross-sectional imaging is not available,
use of a lateral cephalogram or a 2-D occlusal film can provide some basic
idea of the anatomy of the region.
Cross-sectional imaging allows a realistic assessment of a potential donor
site, and measurements on the 3-D image can be prepared before surgery is
commenced. Assessment of the thickness of the cortical bone must be
considered, and cases without any medullary bone need to be identified. The
lack of sufficient medullary space may prevent separation of the facial and
lingual cortical plates during the graft harvest and the potential for
sectioning completely through the lingual plate increases as blind harvesting
is attempted.
Complication.
Complications may arise when inadequate donor bone is present. This may
result in inadequate graft volume/thickness, poor density of the graft, and
increased donor site morbidity. Life-threatening situations have been
documented when fractures have occurred, leading to the lingual mandibular
symphysis being displaced into the sublingual space, ultimately interfering
with the airway. When the preparation of a block graft harvest extends
through both the facial and lingual cortical plates, the block is free to be
drawn to the lingual aspect as pressure on the block is applied by muscle
attachments. The region of bone around the genial tubercle is directly
attached to the genioglossus and geniohyoid muscle attachments. If the graft
is no longer attached to the surrounding mandibular bone, it will be drawn
completely through the mandible and into the space below the tongue (Figs.
12.37 to 12.39).
FIG 12.37 (A–B) The lingual concavity in this case greatly limits implant treatment
planning.
FIG 12.38 Variation in mandibular symphysis anatomy. (A–B) Anatomic variants
(hourglass mandible). (C–D) Narrow buccal-lingual width. (E–G) Poor bone density.
FIG 12.39 (A) Cross-sectional image depicts fractured symphyseal plate from poor
patient selection of a symphysis graft. (B) Axial view. (From Cordaro L, Rossini C, Mijiritsky
E: Fracture and displacement of lingual cortical plate of mandibular symphysis following bone
harvesting: case report. Implant dentistry 13(3):202–206, 2004.)
Bleeding/Neurosensory Complications
Complication.
When a cortical graft and the surrounding medullary bone are harvested in
the symphyseal region, the underlying neurovascular components are often
compromised. These disruptions to the nerves and blood vessels may be
accompanied by varied neurologic sensations along with possible significant
bleeding immediately following the graft harvest.
Etiology/Prevention
The incisive canal.

The space between the mental foramina has been known for years to be a
safe zone for bone harvesting because of the lack of vital structures that can
be affected by grafts taken from this region. A thorough understanding of
the neurologic and vascular anatomy in this region is critical for the
prevention of complications during and after surgery in the symphyseal
region. Generally, there is a relative absence of sensory deficit to the lip and
chin after implants are placed in this region as compared to cases involving
the posterior quadrants. However, this can sometimes give rise to a
complication if the lingual plate is perforated or if complications develop
while harvesting large bone grafts from this region.
Studies have shown that, with digital volumetric tomography, in 100% of
the cases reviewed, there is the presence of an “incisive branch” of the
inferior alveolar nerve that branches off at the mental foramen, passing
interiorly to the midline of the symphysis. It has also been commonly
recognized that an “anterior loop” may exist, which is an anterior extension
of the mental nerve in relation to the mental foramen. This anterior loop of
the mental nerve is subject to injury when implants are placed in
approximation to the mental foramen. The “incisive branch” of the inferior
alveolar nerve course veers toward the lingual plate as it approaches the
midsymphyseal region. In the midline area the incisive nerve in most cases
will join the nerve from the contralateral side.48
When block grafts are harvested from the chin, cortical blocks are resected.
In the process, additional medullary bone around the site is scraped out of
the space between the cortical plates. While taking this additional medullary
bone, the clinician may inadvertently resect the incisive nerve and blood
supply. If these neurovascular channels are disrupted, significant bleeding
can occur, and the patient will potentially complain postoperatively about
altered sensation to the incisors. This is not a painful sensation, but it is
disruptive, causing patients to generally describe the incisors as having a
“woody feeling.” This series of complications can usually be avoided by
refraining from aggressive harvesting of medullary bone surrounding the
donor site.
Studies have shown the incidence of neuropraxia following the harvesting
of block grafts from the ramus vs. the symphysis. After 18 months, more
than 50% of the patients with harvest sites in the symphysis still had altered
sensation. None of the patients in the ramus donor group reported any
symptoms at 18 months.48
Lingual artery.
The incisive neurovascular bundle is found to join other vascular structures
in the midsymphyseal region. The genioglossus muscle attaches to the genial
tubercle in the midline, and the lingual artery courses through the lingual
foramen at the genial tubercle. The lingual artery is approximately 1 to 2 mm
in diameter, and cross-sectional views clearly show its anastomosis with the
incisive canal at this point.
The preparation of a grafting osteotomy in the midline can potentially
resect these blood vessels if they fall in the path of the vertical preparation. If
this occurs, the sectioned extension of the lingual artery can prolapse back
into the floor of the mouth. The severed vessel may release arterial blood
flow in the sublingual space, potentially raising the tongue to a point that
compromises the airway. Immediate emergency intervention to maintain the
airway is critical, and in some cases this requires use of a tracheostomy until
the blood flow has been controlled.
Superior genial foramen.

Miller found additional anterior foramina with a diameter of around 2 mm
that anastomosed with the incisive canal. Substantial bleeding reported in
the symphysis during flap reflection may be attributable to these larger
vessels.26 These bleeding points have previously been described as “nutrient
canals,” indicating that they had no sensory component. Injury to these
vessels can be avoided by limiting the apical extension of flaps during
grafting and related procedures close to the symphysis.
Incorrect Size and Shape of Block Graft

Etiology.
The recipient surface anatomy of a bony defect is typically irregular in its size
and shape, which presents the clinician with a challenge as it pertains to
grafting. In areas where block grafts are necessary to build appropriate bone
volume, the clinician must make a choice whether to modify the shape of the
block or the recipient site to ensure a proper integration and resolution of
the defect. An ideal graft/recipient position eliminates as much space
between the two surfaces as possible.
Complication.
Failure to properly adapt a cortical graft to closely approximate the recipient
bed will often lead to a gap that could inhibit early angiogenesis and
eventually osteogenesis. A block that is “inlayed” into the recipient site
limits this gap and allows proper integration of the newly forming bone into
the recipient bed. Rocking of a cortical graft will invariably lead to a failed
union of the cortical graft with the recipient bed. Micromovement of any
graft leads to poor results, if not outright failure.
Prevention.
A thorough examination of the anatomy of the bony defect is required to
determine the dimensional volume of bone needed for proper support of the
implant in the required restorative position. This dimensional volume must
then be realistically assessed to make sure that the donor site will provide a
graft with adequate bone thickness for the size and shape of the defect.
When a recipient site requires more than 4 mm of bone, grafting from the
ramus area is not indicated. Anatomic limitations of the ramus in this region
limit the thickness of the graft to 3 to 4 mm. Larger grafts in the ramus can
impinge on the safety zone around the surrounding vital structures.
All fibrous tissue must be removed from the surface of the recipient site
using a course, round acrylic bur (e.g., 10-12 round bur). The bed of the graft
site is then aggressively shaped to provide a flat-surfaced base for the graft.
If possible, the block should be recessed into the ridge for support and for
improved integration into the native bony ridge. The reshaping of the
recipient bed stimulates a regional acceleratory phenomenon (RAP),
improving the chances of a strong bond between the block and the recipient
bed.
Block preparation.
Preparation of the cortical block should be completed with as little reduction
of the volume of the block as possible. The block not only provides a source
of cells with osteogenic potential, but it also promotes bone development
through the concept of “barrier by bulk.” The natural remodeling of bone
over time will reduce any excess bone bulk, so in this situation, bony excess is
not a problem (Figs. 12.40 to 12.43).
FIG 12.40 (A) Block graft in poor adaptation to donor site leading to increased
chance of nonunion. (B) Recipient site is modified to allow for seating of the cortical,
allowing no movement. (C) The recipient site has been shaped to receive the block
graft in a smooth recipient bed.
FIG 12.41 (A–B) Medullary particles are used to fill the gaps and discrepancies
around a block graft.
FIG 12.42 A very thick graft that has been mortised into a wide buccal defect in the
first molar region.
FIG 12.43 Block graft modification. (A) All sharp edges should be beveled with a
round carbide or diamond bur under copious irrigation. (B) Fixation screws should
always be pre-drilled prior to inserting graft. This will allow for ideal placement and
stability when fixating graft.
Loss of Bone Fragments During Break-Up of

Cortical Blocks
Etiology.
The use of dense cortical bone in ridge augmentations has always presented
a problem when an irregularly surfaced cortical graft needs to be trimmed
and reshaped for adaptation in a graft site. In the case of particulate grafting,
the complete piece of cortical bone must be broken into small pieces before
it can be used. Control of the graft particles during this process is critical
because loose particles can be easily lost or contaminated as the graft is
processed. Autogenous bone harvests are challenging, and loss of critical
bone particles and blocks can cause unnecessary time delays and patient
discomfort if additional bone needs to be harvested to replace a
contaminated block.
Complication.
Pieces of harvested bone can be lost if they are not contained during the
preparation of the cortical grafts. Processing of pieces of bone in these
situations often results in the loss of “bone particles” that fly off the
rongeurs or pieces of the graft that become contaminated as they come in
contact with surrounding surfaces. Entire blocks have fallen out of surgical
fields in the past, totally preventing their use in graft procedures.
Prevention/Treatment.
The particulate grafting technique described in this chapter requires that a
piece of a cortical block be completely broken up into small particles that are
then packed into irregular bony defects. These small particles tend to “shoot
out” of the ronguers if they are not carefully contained. The best way to
eliminate the loss of these cortical particles is to fill a clear, shallow glass
beaker or bowl with saline. The block is then submerged in the saline and
double-action ronguers are used to break it up into the particle size needed
for the procedure. The saline slows escaping particles in the same manner
that water slows the movement of a bullet that is fired into water (Fig. 12.44).
FIG 12.44 (A) Double action ronguers. Cortical bone is broken into small particle
sizes. (B) Use the sides of the ronguers at the end of the beak for larger pieces. Use
the ends for smaller particles that are not too dense. (C) Keep the block under the
water level to prevent loss of particles during this process.
Ultrasonic Piezosurgery–Related Tissue Injury
Etiology.
The use of ultrasound technology in dentistry first began in the 1950s, and in
the last 20 years piezosurgery units have been developed using low-
frequency ultrasound (10–60 kHz) for the selective cutting of bone.
Traditional bone drilling with motorized drills is easily available to clinicians;
however, cutting bone with a drill can generate excessive amounts of heat in
dense bone, potentially damaging the surrounding tissue. A surgical drill
that comes in contact with blood vessels, nerves, or sinus membranes can
also cut or damage adjacent vital structures. The use of piezosurgery in
implant surgery has been a welcome alternative to motorized drills in many
applications. At the lower ultrasonic frequencies used for piezosurgery,
surgical inserts cut through hard, mineralized bone but do not damage the
surrounding soft tissue or generate high amounts of heat. Piezosurgery has
been especially useful in implant surgery, where bone must be cut in close
proximity to a nerve or blood vessel. Use of the piezosurgery inserts
generally allows the clinician to perform these bone alterations without
damaging or cutting delicate tissues that come in direct contact with the
ultrasonic insert.
Complication.
As piezosurgery has been utilized over many years, it has been reported by
practitioners that the inserts should not be allowed to function while in
direct contact with the soft tissue flap. Earlier surgical units were reported to
“heat up the insert tip” during use, and irritations or burns on the soft tissue
flap were sometimes detected.
Prevention.
This altered tissue issue has not been evident in updated piezosurgery units,
but careful attention must be directed to protection of surrounding soft
tissue during ultrasonic insert use. Instructors describe this as an abrasive
phenomenon caused by the rapid ultrasonic movement of the tip against the
soft tissue. Care must be taken to keep the tissue flap away from the
ultrasonic inserts.
Treatment.
Development of any abrasive or burn-type lesion should be treated
symptomatically, just as any other oral burn or abrasive lesion would be
treated. If there are any signs of more serious damage, more involved
treatment may require appropriate referrals for wound care (Figs. 12.45 and
12.46).
FIG 12.45 (A–B) These two photographs show piezo inserts in direct contact with
the adjacent soft tissue flap. The inserts of piezoelectric hand pieces should not be
allowed to lie directly against the adjacent soft tissue during bone preparation.
Damage to the soft tissue related to the vibration of the insert against the tissue has
been reported. (C) Full retraction of the buccal flap provides access for the apical
insert while harvesting a block graft.
FIG 12.46 (A) The piezoelectric inserts are separated from the surrounding soft
tissue with “Pritchard retractors” and wide flap access. (B) Two retractors retract the
tissue while the piezo insert prepares the bone.
Chin Graft Closure Complications

Etiology.
The closure of a chin graft donor site is a very delicate process, with periodic
incidences of incision line opening postoperatively. The chin presents a
unique situation because tension from the surrounding musculature places
constant pressure on the healing wound in a chin graft donor site. The
mentalis has multiple insertions into the symphysis area that predispose the
region to incision line opening.
Complication.
If incision line opening occurs, healing will be compromised, resulting in
pain, inflammation, possible infection, and a potential loss of the graft.
Prevention.
It is recommended that a careful review the thickness and integrity of the
tissue covering the lower incisors be completed before deciding whether to
use a sulcular incision or a vestibular incision for access to the donor site.
The “biotype” of the tissue can provide insight into the best approach for
surgical access and wound closure. If there is bountiful thick tissue around
the teeth with no recession, a sulcular incision provides adequate access for
harvesting the graft and closure is relatively simple. If the incisors have thin
and friable tissue, it is better to utilize a vestibular approach for chin graft
access. This will ultimately prevent any postoperative recession on these
already compromised incisors. Tension on the flap of a patient with a thin
biotype can easily strip the healing tissue away from the teeth, exposing bone
that will then slowly be covered with granulation tissue growth over time.
In cases where a vestibular incision is required, care must be taken to
secure the attachment of the mentalis where possible. This limits direct
tension on the incision line and, subsequently, the incidence of incision line
opening. The type of suturing technique recommended is a two-level
vestibular closure. The muscle is sutured initially, followed by the mucosal
tissue (Fig. 12.47).
FIG 12.47 (A) Two-layer closure. (B) Tension on the flap during chin graft closure
site may be reduced with the use of a two-layer approach. This image shows the
use of suspensory sutures that first pass through the mentalis muscle on each side
of the symphysis and then around the neck of the incisors before tying the knots.
This prevents any strain on the outer portion of the flap closure at the superficial
level. (C) Another example of the superficial layer of the flap closure where the
keratinized tissue around the teeth is used for good anchorage.
Soft Tissue Changes (Ptosis) After Symphysis Graft

Etiology.
One of the main patient concerns when confronted with the prospect of
symphysis grafting is a change in facial or soft tissue appearance. The idea of
having a permanent bony chin defect or ptosis contributes to a patient's
apprehension regarding this procedure.
Complication.
The main concern of patients after a symphysis graft is a postoperative
change in the soft tissue contour of the chin. In the literature, there exists no
evidence of a statistically significant incidence of dehiscence or chin ptosis
after a symphysis graft.
Prevention.
Avoid degloving the mentalis muscle by maintaining the facial and inferior
aspects of the mandible and the lingual aspect of the inferior border of the
mandible during flap refection. Additionally, to prevent lower lip height
reduction and vermilion zone inversion, the integrity of the periosteum to
the inferior reflection should not be deeper than one third of the total
distance from the vermilion border to the mucogingival junction. An
extraoral bandage or pressure dressing may be utilized postoperatively for
support and to help with compression of the wound.
Neurosensory Changes After Symphysis Graft

Complication.
Neurosensory deficits of the third branch of the trigeminal nerve are very
rare in association with symphysis grafts. However, it is a common sequela to
have neurosensory changes in the mandibular anterior teeth.
Etiology.
Because the second terminal branch of the inferior alveolar nerve (incisive
branch) terminates in the anterior mandibular area, it is not uncommon to
sever this section of the nerve during osteotomy preparation. However,
because the incisive nerve is only a sensory nerve to the incisor teeth, this
usually results in only a “dullness” in sensation. Hoppenreijs et al showed a
negative pulpal response in 16% of patients with total resolution in 6 to 12
months.49,50
Prevention.
The superior portion of the harvest site should be prepared at least 5 mm
below the level of the incisor root tips. Care must be taken to avoid the
longer roots of the cuspids as each end of the harvest pattern is prepared.
Aggressive harvesting of the medullary portion of the symphysis should be
minimized in the superior aspects if possible to limit damage to neural
pathways through the region. Most importantly, complete patient education
must be conducted “prior to” the surgery informing the patient about
potential sensory changes that could occur. The patient should be aware that
they could feel a dullness or “woody” feeling of the mandibular anterior
teeth following surgery. This can be temporary or a permanent condition, but
it has never been described as a particularly annoying feeling. Very rarely is
there an indication for endodontic therapy, as the vitality of the teeth returns
to normal (Fig. 12.48).
FIG 12.48 Although the incisive nerve branches are severed with a symphysis
graft, reinnervation usually occurs within 2 to 4 months.
Improper Superior Margin Location: Symphyseal

Graft
Complication.
Devitalization of the lower incisors may occur during preparation of the
superior aspect of the osteotomy for a symphysis graft if it is improperly
positioned (e.g., too close to mandibular incisor root apices).
Etiology.
The superior margin of the block osteotomy should not be placed any closer
than 5 mm below the longest root in the incisor region, and it must avoid
damage to the longer roots of the adjacent cuspids. It is important to
preoperatively assess the thickness of the cortical bone in these cases,
especially with smaller patients and women with osteoporosis. These
patients are more likely to have a very thin cortical plate overlying a
medullary component that is difficult to harvest for grafting.
Prevention.
A CBCT exam will reveal the exact location of the apices of the incisors and
the adjacent cuspids. If the cuspids extend too far apically, the symphysis
graft may be harvested in two blocks, thereby minimizing trauma to the
cuspids (Fig. 12.49).
FIG 12.49 Superior cut location. (A) The osteotomy should be initiated a minimum
of 5.0 mm inferior to any of the natural teeth apexes (arrow). This will avoid
devitalization and trauma to the teeth. (B) Care should be noted with cuspids roots,
which may impinge on osteotomy location. (C) Ideal location of superior cut. (D) The
superior cut must positioned away from the apex of the cuspids.
Block Grafts: Ramus Bone Grafts
Poor Ramus Candidate
Etiology.
The mandibular ramus is a common site for harvesting block grafts because
the area provides a supply of dense cortical bone that can be shaped to fit
numerous defects. Compared to the symphysis region, bone harvests from
the ramus usually results in fewer postoperative complications. Despite this,
there are patients with anatomic restrictions that make them poor candidates
for ramus graft harvesting.
Complication.
The main complication related to ramus grafting is the possibility of
significant damage to the inferior alveolar nerve (IAN) where its course
passes directly adjacent to the external oblique ridge (buccal shelf). Patients
who have an IAN location 10 mm or less from the external oblique have a
much greater chance of a nerve impairment during a graft harvest from that
region. Additionally, this limited dimension limits the amount of bone that is
available for harvesting. The clinician may damage the associated nerves with
an aggressive harvest in an attempt to get an adequate volume of bone.
Prevention.
CBCT analysis can provide the clinician with a clear picture as to how viable
the ramus site is from a nerve injury prevention standpoint as well as the
chance of acquiring a sufficient volume of bone for grafting. Measurements
should be taken to assess the anterior-posterior (A-P) width of the ramus, the
distance from the external oblique and ramus body to the IAN, and the
overall width of the posterior ramus. With these CBCT images, the clinician
can evaluate whether or not the patient has sufficient bone available for
grafting (Fig. 12.50).
FIG 12.50 Mandibular ramus donor site. (A) Assessment of the donor site must
include the amount of available bone, external oblique ridge, and the location of the
mandibular canal. (B) Mandibular ramus graft outline form. (C) Radiolucent image
depicting ramus graft cuts in association with the inferior alveolar canal. (D) Cross-
section anatomy showing nerve location. (E) Complication including inadequate
thickness of graft. (F) More ideal position (~4 mm) from lateral border.
Failure to Decorticate the Host Bone

Etiology.
Detachment of a block graft due to an integration failure may be caused by a
lack of sufficient preparation of the recipient site during the grafting process.
Many recipient graft sites are covered with dense cortical bone, particularly
in the mandible, and proper angiogenesis and eventual osteogenesis requires
passage of the cellular components through this dense bone.
Complication.
As an implant is placed into an osteotomy that has been prepared in a block
graft site, expanding pressure is exerted around the circumference of the
surrounding bone. If a block graft is not fully integrated into the underlying
bone, it will separate and the block will detach. A similar situation is found in
particulate grafting if the developed ridge is not dense and is not fully
integrated to the recipient site. In this situation, the particulate graft does
not have sufficient density to allow for adequate implant support and the
lateral aspect of the newly regenerated ridge will crumble around the coronal
aspect of the implant as the implant is inserted into the osteotomy.
Prevention.
All recipient sites must be thoroughly decorticated with a bur to not only
open a pathway for cellular passage of the osteogenic cells through the dense
cortical bone but also to stimulate the RAP in the region. It is highly
suggested that the same drill size for the fixation screws be used for these
deep penetrating holes and that adequate bleeding be present to ensure
passage of the bone growth factors into the site (Fig. 12.51).
FIG 12.51 Host site decortication. (A) The host site is prepared with a tapered
cross-cut fissure bur (e.g., 169 L) to initiate angiogenesis. (B) The decortication
must be deep enough to cause bleeding, thus allowing blood vessels into the area.
Mobility of the Block (Fig. 12.52 A and B)

Complication.
Mobility of an autogenous or allograft block during the healing process will
almost always result in a graft failure. Mobility of the block prevents proper
integration of the newly forming bone, and eventually it will lead to soft
tissue invasion between the block and the recipient site. Rigid fixation of the
block graft to the recipient bone site is critical for success in the regenerative
process.
FIG 12.52 Bone graft failure. (A) Incision line opening resulting in failure of graft. (B)
Removal of graft after non union and resulting mobility.
Etiology.
Although regeneration with block grafting is related to the concept of
“barrier by bulk,” micromovement will often contribute to a weak bond
between the cortical graft and the recipient site. This will potentially cause
the block to separate from the ridge as pressure is placed on the interface
between the native bone and the integrated block as a result of the implant
being inserted into the osteotomy. The most common cause for graft mobility
is insufficient fixation or pressure from a prosthesis postoperatively.
Prevention.
Initial fixation of a block graft must be attained when the block is originally
placed in the recipient site. Any movement of the block during the healing
process will disrupt the formation of a stable clot around the migrating cells,
and a loose block will not integrate into the host bone. Ideally, two fixation
screws should be used in every block graft, eliminating any micromovement
of the block during the healing process. The recipient site should be
prepared for close approximation of the surface of the block graft to the
recipient site. The block should be inlaid into the recipient site, and particles
of medullary bone or allograft should be packed around the circumference,
filling any discrepancies. The temporary prosthesis should be adjusted to
prevent any contact with the graft site and the buccal flange should be
removed on any removable appliance to limit micromovement.
Fixation screws should be engaged into the underlying bone enough to
provide rigid support of the graft. A longer shaft on the supporting screw
may be necessary to obtain ridge fixation in soft bone. The screws should
have a self-threading tip, and the preparation hole should be prepared deep
enough to prevent the shaft of the screw from bottoming out in dense
cortical bone. Excess insertion pressure on a screw passing into very dense
bone without adequate depth preparation can contribute to the head of the
screw snapping off during its insertion. Most updated fixation screws have a
pointed self-threading screw tip that helps with screw insertion.
Treatment.
If micromovement of the block graft occurs during surgery, the block should
be removed and the screws should be replaced with longer or wider fixation
screws. If the movement occurs during the healing phase, the block should
be monitored carefully to see if by chance it continues to integrate. If the
movement continues, a decision will have to be made to remove the graft,
attempting a second graft at a future time (Figs. 12.53, 12.54, and 12.55).
FIG 12.53 Large donor graft site leading to exposure of the inferior alveolar nerve
(arrow) with associated neurosensory impairment.
FIG 12.54 Prevention of graft mobility. (A) Two screws need to be placed to prevent
micromovement during healing. (B) The donor site needs to be prepared to minimize
“rocking” of the graft when fixated. (C) Block graft securely fit into host site.
FIG 12.55 Modification of the recipient site. (A) Recipient site is modified to allow
passive fit of block graft. (B) Final contoured recipient site prior to fixation of block
graft.
Storing Graft in Incorrect Medium (Fig. 12.56)

Etiology.
During graft surgery an ideal scenario would allow the clinician to
immediately transfer harvested graft material directly into the recipient site.
In many cases, this is not possible, requiring the use of a storage medium to
safely store graft material (autograft or allograft) prior to usage. Due to its
separation from a blood supply, the cells inside of the graft are vulnerable to
death and must be stabilized during storage for the graft to survive.
FIG 12.56 Storage medium for bone. (A) Bone should not be stored dry or in blood
as this will lead to cell death. (B) Ideally, bone should be stored in sterile saline.
Complication.
Storing graft material in a medium that is not isotonic will cause the viable
cells inside of the graft to die. This loss of living cells eliminates many of the
advantages of using autogenous bone in this particular surgical procedure.
Prevention.
Saline provides a perfect isotonic environment for the short-term storage of
bone grafting material. A glass dish of sterile saline (i.e., 0.9% sodium
chloride) should be used for this process. Avoid the use of distilled water
because its hypotonic nature will cause cell lysis within the graft. Another
medium to avoid is the patient's own blood because hemolytic breakdown
products inside the blood will lower the pH of the solution, causing cellular
death.
Soft Tissue Irritation From an Overextended

Fixation Screw
Etiology.
Bone fixation screws are routinely placed in the bony ridge for various
reasons during implant-related surgery. It is not uncommon to find the end
of a screw extending beyond the lingual or palatal cortical plate. When this
occurs, there is a potential for the overextended screw to cause discomfort.
Complication.
Overextended screws can be a source of irritation to the thin soft tissue on
the lingual aspect of the mandible. The movement of the thin mucosa and
tongue against the sharp point of the screw can cause quite a bit of
discomfort. This is not usually an issue in the maxilla, where the thicker
nature of the palatal tissue acts as a protective buffer.
Prevention.
Screw placement should be followed by both a visual inspection of the
opposing surface of cortical bone and a digital review of any potential
problems areas that will need correction.
Treatment.
The only way to treat an overextended screw involves reflection of a flap to
provide access for removal of the overextension or removal of the complete
screw. Screw removal is not usually a reasonable solution because that would
require reflection of the tissue overlying the maturing graft site and
disruption of the graft as the screw is removed (Fig. 12.57).
FIG 12.57 Screw overextension. (A) When screw extends through the lingual plate
(arrow), this will often result in pain and discomfort for the patient. (B) Preoperative
evaluation for fixation screw. (C) Ideally, the fixation screw should exhibit bicortical
stabilization and the length measurements may be determined via CBCT
measurements. (D) The protruding tip of this fixation screw has be visualized.
Block Separation From Bony Ridge During Implant

Placement
Etiology.
Bone grafting always involves the development of newly regenerated bone
into an existing recipient site. In the case of a block graft, the cortical block
assists with the augmentation process through the concept of “barrier by
bulk.” In this process, the block serves a role in maintaining space during
early angiogenesis and osteogenic development into and throughout the
cortical block. As this process occurs, the presence of gaps between the
recipient site and the dense block requires prolific development of bone to
fill the gap and to grow into the donor bone. Failure to fully integrate these
two entities creates a situation where the donor block can fracture off the
ridge as pressure builds during insertion of the implant, spreading the two
sections of bone apart.
Complication.
If the block separates from the ridge during implant placement, the graft
must be replaced. Attempts to place implants in a failed graft site are
doomed to fail because there simply will not be sufficient ridge width for
proper placement of the implants.
Prevention.
The recipient site should be completely cleared of any fibrous tissue
remnants with a coarse bur, and the recipient bone should be aggressively
decorticated to open pathways for osteogenic cellular ingrowth. The dense
recipient site should be recontoured to provide a close adaptation between
the inner surface of the block and the recipient bed where it will be fixed in
place. This disruption of the recipient bone will stimulate the RAP,
promoting good bony integration into the host site (Figs. 12.58 to 12.60).
FIG 12.58 (A) The recipient site is fully decorticated. (B) A block graft is fixed to the
recipient site. Note the adaptation of the graft to the bone. This is necessary to
ensure an ideal integration of the new bone with the autogenous block. (C) The block
has completely integrated with the existing ridge providing a strong foundation that
can resist the strain of separation of the two pieces during implant placement. (D)
Osteotomy preparation including the cortical graft site. To minimize separation, the
block should be stabilized during preparation. (E) Implant insertion.
FIG 12.59 Modification of the recipient site. A pear-shaped cross-cut fissure bur is
used to remove fibrous tissue from the recipient site. This procedure will remove any
soft tissue and also roughen the outer bone surface allowing for a better integration
between the block and host bone.
FIG 12.60 (A) Postoperative image of complete healed autogenous block. (B) The
indicator pins have been inserted in the osteotomies. Because the implant is slightly
larger in diameter than the osteotomy, pressure is exerted around the circumference
of the osteotomy as the implant is inserted. (C) Care is exercised to not undersize
the osteotomy as this may fracture the graft upon insertion.
Nasopalatine Canal/Incisive Foramen Involvement

in Regeneration Sites
Etiology.
Implant restorations in the anterior maxillary region present one of the most
difficult challenges in dentistry today. The combination of aesthetic
demands, biomechanical/functional issues, and phonetic challenges require
implant placement in ideal positions. The incisive foramen is the exit site of
the nasopalatine canal where the terminal branch of the descending palatine
artery and nasopalatine nerve pass into the oral cavity. The proximity of the
incisive foramen and the path of the canal must be evaluated in all maxillary
incisor implant treatment plans because there can be significant variations in
the size, position, and angulation of the nasopalatine canal and the exiting
foramen. As the bone around the maxillary central incisors resorbs, the zone
of available bony support moves palatally, frequently encroaching on the
incisive foramen.
Prevention.
Defining the dimensions and pathway of the nasopalatine canal with CBCT
imaging allows the surgeon to decide if implants can be placed within the
required restorative space or if augmentation will be needed for ideal
placement. This is particularly important in cases involving immediate
implants because the lingual angulation of the immediate implant osteotomy
could potentially fenestrate into the incisive canal. A fenestration in the side
of an osteotomy allows neural/fibrous tissue invasion into the osteotomy,
retarding bone growth and rigid fixation of the implant. Axial CBCT images
provide the most accurate view of the size, shape, and location of the canal in
respect to the possible implant sites. Use of CBCT cross sections and 3-D
images can also help determine the positions and dimensions of this
important anatomic variant. The clinician must be aware of a possible
widening of the canal above the level of the foramen, creating a fenestration
between the canal and the osteotomy in the more apical regions of the
osteotomy. As the cross sections of the CBCT are reviewed, the possible
presence of a nasopalatine cyst should be ruled out, and edentulous arches
should be reviewed for an enlarged foraminal dimension, as is often noted.
The positions of implants in central incisor regions where the foramen is
involved should be adjusted distally where an FP-1 restoration does not
require a specific placement. This slight adjustment distally prevents
fenestration on the mesiopalatal line angle, where this deficiency most likely
will occur (Fig. 12.61).
FIG 12.61 Enlarged incisive foramen. (A) Clinical image of enlarged incisive
foramen. (B) CBCT 3-D image depicting implant placement impinging on the canal.
(C) Cross section of incisal foramen. (D) Enlarged incisive foramen limiting space
for implant placement.
Complication.
Severe bone resorption on the facial aspect of the maxilla reduces the ridge
thickness to surprising extents, often leaving only a thin ridge that is
positioned well to the palatal aspect of the required location for a central
incisor implant. It should be kept in mind that a line between the cingula of
the two cuspids passes directly over the incisal foramen. Subsequently, if an
implant is placed this far palatally, the emergence profile will originate at a
significantly proclined angle and the complete restoration will be palatally
positioned. Cases like this require that the seriously deficient ridge be
regenerated prior to implant placement.
An osteotomy that fenestrates into the nasopalatine canal opens the site to
neural and fibrous tissue invasion at the interface of the implant and the
exposure. This will lead to a failure to integrate and loss of the implant. A
significant invasion into the canal could lead to excessive bleeding during
surgery that is usually self-limiting with pressure and time.
Treatment.
Regions that are determined to be deficient will require facial augmentation
using techniques that are capable of generating enough lateral/vertical bone
volume for proper implant placement and restorative success. Cases where
the implant can be moved slightly in a distal direction can sometimes
prevent the need for major augmentation. Another option is the obliteration
and grafting of the nasopalatine canal, which can aid in providing significant
bone volume for implant placement (Fig. 12.62).
FIG 12.62 Implant placement and grafting into the incisal foramen.
Excessive Pressure on Ridge Augmentation
Sites Caused by Temporary Prostheses
Etiology.
The successful maturation of a bone graft site requires that the area be
completely protected from micromovement and disruption of the covering
membrane or block material. Micromovement of 25 µm can decrease the
final graft volume as much as 40%. The most common source of daily
pressure on a site comes when the patient's transitional appliance has
contact with the surface of the graft site.
Complication.
Micromovement on a localized region of a graft site will consistently yield
compromised results in the mature graft development, if not full graft
failure. It is imperative to take measures to prevent any movement of the
graft during healing.
Prevention.
A transitional appliance (flipper or removable partial denture) must be
modified to eliminate any significant contact with the graft site. It is
recommended that these removable devices be avoided if possible. If a
removable appliance is absolutely necessary, all buccal flanges should be
removed and, if possible, the acrylic should be altered to create regions of
support on the lingual surfaces of the adjacent teeth. Occlusal rests should
be utilized, or in cases where this is not possible, there must be good
adaptation of the prosthesis to direct the forces to alternative stress-bearing
areas (tissue areas away from graft site that take the pressure off the graft
site).
Essix appliances allow at least temporary replacement of teeth in narrow
span regions, allowing long-term appliances to be fabricated after the initial
healing process has been completed. However, the Essix appliance does have
the disadvantage of esthetics, fracture and wear issues, or discoloration. The
Snap-On Smile appliance (Den-Mat Holdings, LLC) has been used
successfully over longer-span edentulous regions with aesthetics that seem
to be acceptable to most patients (Figs. 12.63 to 12.66).
FIG 12.63 (A) Interim prosthesis modified to have no facial flange. (B) Intraoral view
showing no facial impingement. (C) Interim prothesis modified. (D) Postoperative
graft site showing no line of demarcation on tissue.
FIG 12.64 (A) Fixation screw with associated bone loss, (B) caused by interim
prostheses with protrusion placing pressure on graft. (C) Essix appliances allow at
least temporary replacement of teeth in narrow span regions, allowing long-term
appliances to be fabricated after the initial healing process has been completed.
However, the Essix appliances do have disadvantages in respect to limited
esthetics, fractures, and discoloration. If adjusted properly, it will not allow any
pressure on the graft site. (D) Essix appliance with added acrylic that encompasses
soft tissue defect.
FIG 12.65 The Snap-On Smile appliance has been used successfully over longer
span edentulous regions with aesthetics that seem to be acceptable to most
patients. (A–B) Snap-On Smile used to replace teeth #22 to 27. The acrylic
surrounding the adjacent teeth prevents any contact between the anterior pontics
and the underlying graft site.
FIG 12.66 (A) Grafting site. (B) Closure of ridge augmentation. (C) Placement of
Snap-On Smile over the closed graft site to protect augmentation site during the
healing process.
Lack of Attached Tissue Covering the Ridge

Augmentation
Etiology.
Ridge augmentation techniques require that the soft tissue covering the graft
site be released in the buccal vestibule to free the flap for a tension-free
closure over the expanded graft site. In most cases, this will move the
keratinized portion of the tissue flap to the top of the ridge with altered
mucosal positioning. The elevated mucogingival junctional line will often
leave an extension of loose tissue along the facial aspect of the edentulous
ridge that will not be restoratively acceptable. This tissue discrepancy will
need to be addressed before the restorative phase of treatment,
reestablishing the proper arrangement of keratinized tissue along the
restorative margin with the mucosa in its normal apical position. A minor
correction like this not only eliminates an aesthetic problem, but it also
prevents a mucosal tissue band on the facial aspect of the implant
restoration.
Complication.
As the mucogingival junction in a healing augmentations site is evaluated, it
is often noted that the remaining keratinized tissue over the grafted site is
now palatally/lingually positioned. The complete buccal aspect of the ridge in
these cases is covered with loose and mobile mucosa, contributing to
restorative and esthetic issues.
Prevention.
The clinician must be aware of the restorative implications of the soft tissue
related changes that can occur during augmentation procedures. Unattached
mucosa that is stretched over restorative areas provides an esthetically
unacceptable and restoratively difficult situation. This can be addressed with
either preoperative tissue grafting or it can be corrected after the graft site
has completed its healing process. The preoperative approach utilizes a large
autogenous palatal tissue graft over the edentulous region prior to
completion of the ridge augmentation procedure. The newly developed wide
keratinized tissue band usually covers the augmentation site without
requiring extensive movement of the mucogingival junctional level as the
widened graft site is covered. If grafting is not completed preoperatively,
tissue management can be incorporated into the surgical sequencing,
ultimately developing proper tissue aesthetics and attachments. Discussions
with the patient should be conducted prior to implant placement to make
sure they are well informed about the expected need of additional
procedures that could be necessary in correction of soft tissue complications.
Treatment.
Management of high attachment levels of mucosa over previous
augmentation sites requires either pre-operative tissue grafting or
postgrafting tissue management. If there is an expected deficiency, one of
these options will need to be chosen:
• Option 1. Postgrafting approaches are organized around development of a
new zone of thick keratinized tissue that will not only provide a strong
attachment apparatus that will surround the implant abutment but will also
allow a favorable emergence profile and better interproximal tissue papilla
heights. The preferred method in our experience involves use of either
autogenous connective tissue or the thicker type of AlloDerm (acellular
dermal matrix) that is placed during the implant surgery. At the time of
implant placement, a layer of connective tissue or AlloDerm is placed over
the area of concern to prepare a thicker soft tissue foundation. After the
healing process has been completed, a simple split-thickness dissection of
the mucosa is used to expose the underlying layer of dense tissue formed by
the previously grafted connective tissue. The repositioned mucosa is then
sutured apical to the exposed region with 5-0 chromic sutures. The resulting
matured layer of tissue will typically have a normal keratinized consistency
and appearance. In cases where the tissue covering the augmentation site is
very thin, efforts should be made to develop 3 mm of tissue thickness
around the neck of the implant. This may involve use of more than one layer
of connective tissue or AlloDerm on top of the ridge. This is especially
relevant in the upper and lower posterior regions where large amounts of
tissue have been drawn over a wide augmentation site. Tomas Linkevivius
has shown that very thin tissue around implant attachment zones is much
more prone to circumferential bone loss than implants in patients with a
thick biotype and 3 mm or more of tissue thickness around the neck of the
implant.51
• Option 2. Dr. Esteban Urban describes another approach that is completed
after the implants have been placed in a postregeneration site. In his
technique, no grafting is completed at the time of implant placement or
before the grafting procedure. Instead, he describes use of a split-thickness
flap over the zone of mucosal attachment, leaving the periosteum intact. A
large piece of “mucograft” is sutured into place, covering all but a thin zone
at the level of the mucosal suture line. A narrow piece of autogenous palatal
tissue is sutured over this apical zone to create a protective band of
keratinized tissue that limits relapse movement of the mucosa over the
region that was covered with mucograft. This region should granulate in
with keratinized tissue. The thickness of tissue in this approach will not be
as deep as the option 1 approach, where more than one layer of connective
can be placed over the implant site itself.52
• Option 3. Free tissue grafting can be completed prior to augmentation of a
region, using autogenous palatal tissue. In this approach, the recipient site
is prepared with a split-thickness dissection, leaving the periosteum intact.
The palatal graft is harvested from the palatal tissue adjacent to the molars,
avoiding the rugae in the anterior region. One advantage of harvesting
tissue in this manner is the surgeon's ability to gauge how thick the final
tissue needs to be and harvesting an appropriate graft from the donor site.
This creates a wide zone of thick keratinized tissue over the entire region.
Unfortunately, the postgrafted tissue has a white color tone related to the
density and fibrous nature of the palatal graft donor site. This discrepancy
prevents use of this approach in anterior augmentation sites where the
tissue color and surface contour is important (Figs. 12.67 to 12.70).
FIG 12.67 Tissue augmentation. (A) The mucosa in this edentulous graft and
implant site extends to the top of the alveolar ridge (arrow). A layer of AlloDerm
dermal matrix is placed over the implant site at the completion of the stage I
procedure. The mucosa must be repositioned apically prior to the restorative stage
of this implant sequence. (B) A #15 scalpel blade is used to prepare a split-thickness
incision on the buccal aspect between the two natural teeth. This is prepared in a
fashion that separates the mucosa overlying the thick layer of AlloDerm. (C) The
thick nature of the underlying AlloDerm as the elastic fibers are being removed over
its surface is shown. (D) The final restoration in place, and the band of thick,
keratinized tissue along the buccal aspect of the #12 implant.
FIG 12.68 Tissue augmentation. (A) Initial split-thickness dissection of mucosa
covering AlloDerm layer with 5-0 chromic sutures anchoring the mucosa below the
level of the exposed AlloDerm layer. (B) Stage II uncover of two implants in this
same region. (C) Two week postoperative view of the healing zone of AlloDerm.
FIG 12.69 (A) Flap reflection of a postoperative graft site shows very thin tissue
over the ridge with very little remaining keratinized tissue. (B) A blanket of AlloDerm
is placed over the implants like a poncho. The flap is then closed over the AlloDerm,
allowing apical positioning of the tissue at a later date.
FIG 12.70 (A) A free tissue palatal graft is placed on the buccal aspect of two
implants that did not have adequate attached keratinized tissue. (B) Three-week
healing in the grafted site. Note the wide zone of keratinized tissue that is already
developing on the buccal aspect of the implants.
Bone Density Variations in Ridge Augmentations

Etiology.
The sole purpose of ridge augmentation and bone grafting is to develop a
dense stable volume of bony support for implants of appropriate sizes and
numbers that are placed in the locations specified by the restorative plan.
The quality and density of the final graft development is important because a
weak and granular implant osteotomy site is more susceptible to crumbling
during implant insertion. These granular ridges can also resorb when the
implant is loaded and stress is placed on the coronal aspect of the
implant/bone interface. As clinicians plan augmentation procedures, they
must understand the limitations of the materials that they are using and the
techniques that are going to be utilized. Misch created a system of bone
densities for implants, ranging from D1 (hardest) to D4 (softest/most
porous).53 These divisions encompass the acceptable ranges for the
placement and rigid fixation of implants. Successful regeneration procedures
develop a final osteotomy site that provides adequate bone volume in a
dense, firm, manageable form that has a large number of vital bone cells that
will easily integrate with the titanium implant body.
Complication.
When an augmentation procedure is not completed using sound surgical
principles or when an inappropriate graft material is used, the completed
implant site may present with an inadequate bone density for rigid fixation
of the implant. The bone in these compromised sites will have a granular
appearance and feel. This lack of density indicates the lack of adequate bone
turnover from the original nonvital graft particles into a final dense bony
consistency with a high percentage of vital bone cells. Regenerative failures
will have to be regrafted, lengthening the treatment time, the overall costs,
and frustrating the implant patient and the entire implant team.
Prevention.
Success in bone grafting of all types requires a thorough knowledge of the
variety of grafting materials that are available and their capacity to be readily
replaced with vital bone on a timely basis. A clear understanding of the
concepts of osteoinduction and osteoconduction is critical for predictable
grafting success. Use of totally osteoconductive graft materials will
significantly alter the time required for substitution of vital bone for the
nonvital products found in the donor graft. The incorporation of autogenous
bone into this process adds the osteoinductive capacity of autogenous bone
into the osteogenic process, accelerating the turnover into vital bone and
potentially creating a better ridge consistency upon maturation.
Demineralized freeze-dried bone allograft (DFBA) has some osteoinductive
capacities, and the addition of a grafting material with this potential should
improve the outcome of the grafting procedure. The use of bovine products
has similar advantages and can be used to improve outcomes as long as its
properties are understood.
Grafting materials are also categorized into cortical or cancellous particles
and mineralized or demineralized particles. Each type of particle has
properties that can be applied to specific clinical situations, but choosing the
wrong material may compromise the complete grafting result (Figs. 12.71 to
12.74).
FIG 12.71 Bovine augmentation. (A) Poor bone turnover with Pepgen15
(DENTSPLY Tulsa Dental Specialties) ridge augmentation site. (B) Osteograf
300/Grafton Matrix (Osteograf 300/Grafton Matrix) graft site.
FIG 12.72 Poor bone healing. This case involves a combination of two block grafts
in the cuspid positions with particulate grafting using FDBA and a bovine product.
Note the healed ridge consistency and the varied density of the graft. Consistent
turnover of the grafting materials was not predictable.
FIG 12.73 (A) This case shows an autogenous particulate graft site after 5 months
of maturation. (B) Note the very dense consistency of the graft and the lack of any
“grainy” regions in the final ridge form.
FIG 12.74 (A) Vertical defect requiring complete regeneration for reasonable
implant treatment planning. (B) Autogenous particulate graft results in vertical ridge
regeneration.
Difficulty Releasing the Tissue Flap From

Underlying Tenting Screws
Etiology.
Flap reflection is a basic procedure that is common in all surgical
applications. Correct tissue manipulation allows the flap to be released and
reflected without tearing or damaging the underlying periosteal layer. The
use of bone fixation screws in particulate grafting techniques creates a
complicated situation for flap reflection because the fibrous tissue layer of
the periosteum surrounds the head of the screw and any exposed portion of
the neck of the screw. When the flap is drawn away from a screw insertion
site, this fibrous layer must be cut and the binding tissue must be released
before the flap can continue to be drawn away from the region.
Complication.
Flap reflection in screw-supported regeneration sites will reveal tissue that
binds around the heads of the supporting screws. This binding attachment
cannot be easily drawn over the screw heads, and there is a potential to
create perforations or tears in the flap as it is released.
Treatment.
Flap reflection in this situation starts with a simple full thickness crestal
incision that is prepared over the graft site. Flap release is initiated with a
sharp curette that is used to release the flap and to reflect the periosteum,
scraping side to side until the full flap can be elevated. As the flap is
released, the bone fixation screws must be freed from the thick layer of
fibrous tissue that adheres to the screw head. A #12 scalpel is used to cut the
fibrous layer over the screw, and the curette is then used to continue the flap
release until another screw is encountered. Once the flap has been
completely released, the fixation screws are accessible for removal before
placing the implants (Figs. 12.75 to 12.78).
FIG 12.75 Postoperative graft incision. (A) Incision is made to maintain as much
attached tissue of facial of ridge. (B) An incision is made with release incisions. It is
usually advantageous to go over the incision multiple times with a #15 blade to
prevent a split thickness reflection.
FIG 12.76 Reflection. (A–B) A sharp curette or 2-4 Molt is used to release the flap
and to reflect the periosteum, scraping side to side until the full flap can be elevated
(e.g., full thickness).
FIG 12.77 Exposure of bone screws. (A) As the flap is released, the bone fixation
screws must be separated from the thick layer of fibrous tissue that adheres to the
screw head. (B) #12 scalpel is used to sever the fibrous layer over the screws. (C–
D) A curette is then used to continue the flap release until all screws are accessed.
FIG 12.78 (A–B) The flap has been completely released and the fixation screws
are accessible for removal (before placing the implants).
Incision Line Opening in Bone Grafting Sites

Etiology.
Maintenance of complete soft tissue coverage over healing bone grafting
sites is one of the most important principles that must be observed for
predictable grafting success. Any time that the healing graft site is exposed
to the oral flora during the healing process, there will be some type of
compromised change in the final graft site volume and in its overall integrity.
Incision line opening with compromised graft results can often be a major
limiting factor in successful implant placement.
Complication.
Incision line opening can compromise even the most carefully planned
regeneration site, and most of these graft sites will require additional
grafting at a later time if an actual complication develops. An open incision
line introduces numerous potential complications into the healing process.
First, the introduction of microorganisms into a graft site through an open
incision leads to an infection in the healing graft site. Exposure of the graft
particles and the presence of purulence is an indication of impending failure
of the graft. The infection lowers the pH in the graft site, causing a
breakdown of the graft particles and eventually compromising the resulting
ridge volume. Secondly, an open incision line may allow exposure and
breakdown of the barrier membrane, contributing to fibrous tissue ingrowth
into the graft site. Lastly, there exists a potential for particulate graft
materials to escape the graft site, resulting in an inadequate bone volume in
the final proposed implant site.57
Prevention.
Tension-free tissue coverage can be most effectively managed from the
standpoint of overall flap management throughout the surgical procedure. A
clinician's experience in manipulation of soft tissue affects this aspect of
bone regeneration more than any other part of bone regeneration surgery. As
the clinician gains more experience in delicate tissue management and
begins to understand the maintenance of a tension-free flap closure,
problems with graft and membrane exposure will become a very uncommon
occurrence.
Lack of tension-free closure.

The most common cause of an exposed membrane along an open incision
line is directly related to the lack of a tension-free closure of the flap. All
bone graft sites require that the overlying tissue flap be stretched over the
wide bulk of the graft at the completion of the procedure. This stretching
tension places pressure on the sutures along the incision line. If the flap has
not been adequately released, this pressure will eventually lead to necrosis of
the tissue around the sutures, leading to an open incision postoperatively.
The inner surface of a reflected flap is lined with the periosteum: a thin,
dense layer of tissue that cannot be stretched. It is impossible to stretch the
soft tissue flap over a graft site without first severing this layer of tissue. This
“tissue release” is accomplished by preparing a clear and continuous
releasing incision through the periosteum, exposing the underlying elastic
layers of tissue that can then be released for expansion of the flap over the
enlarged graft site. As this incision perforates the periosteal layer, the two
edges clearly separate, allowing the elastic tissue below the periosteum to
stretch. A sharp pair of Metzenbaum scissors is then placed into the space
below the periosteum, and as the scissor tips are opened, the tissue easily
releases and the edges separate farther. This is repeated until the complete
flap is stretched over the graft site and 5 mm beyond the opposite flap
margin.
Treatment.
In the event of an incision line opening, the patient should be placed on a
frequent monitoring protocol to observe the status of the graft material and
any grafting hardware present. The oral microflora must be managed with
the use of daily chlorhexidine rinses. The clinician must not attempt to
suture the site again because healing margins along incision lines feature
tissue that cannot, at that time, support the pressure of another suture under
tension (Figs. 12.79 to 12.82).
FIG 12.79 Incision line opening. (A–B) Postoperative incision line opening with
membrane exposure.
FIG 12.80 Incision line opening. (A) Poor flap preparation and tissue necrosis has
resulted in complete membrane exposure. (B) A lack of tension-free closure and
pressure from an interim prosthesis has resulted in membrane exposure. (C) This
non-resorbable membrane has been exposed. It will need to be maintained for at
least 6 weeks to attempt to salvage the underlying graft.
FIG 12.81 (A) A lower anterior graft site is exposed during the healing process. (B)
The AlloDerm membrane allows maintenance of the exposure site while the tissue
slowly covers the exposed membrane.
FIG 12.82 (A–B) A demonstration of the ability of AlloDerm to promote soft tissue
closure over a significant membrane exposure that occurred while grafting the
maxillary anterior teeth. The patient is instructed to keep the area clean with the use
of chlorhexidine. (C) The mature graft site with complete regeneration of bone to the
level of the fixation screw heads. (D) The exposure in this case did not compromise
the final graft volume at all.
Inadequate Volume of Facial Bone Regeneration

With Particulate Graft
Etiology.
Augmentation of a bony ridge requires assessment of the required position
of the final restoration prior to the regenerative procedure. This dictates how
much bone will be needed to support an implant in the proper position for
an ideal emergence profile of the crown. It is highly recommended that the
augmentation be planned to overbuild the facial bony contour enough to
account for any alterations of the graft volume that may occur during the
healing process and for additional postoperative support on the facial of the
graft site. Thin bone on the facial aspect of any implant site is prone to
remodeling and eventual resorption down the face of the implant body.
Although there is bone on the facial aspect of the implant in a thin graft site,
this bone is susceptible to the natural stresses along the coronal 5 mm of the
implant, potentially leading to future problems.
Complication.
A lack of adequate facial bone regeneration leads to a site that may be prone
to the development of a dehiscence during implant placement or inadequate
support of the implant during loading and long-term use. Continued
breakdown like this eventually leads to the need for repair of the exposed
implant body or possible implant removal.
Prevention.
Planning is a vital ingredient in the prevention of this complication. The site
should be evaluated via CBCT to assess the current volume of bone and to
plan the appropriate implant that will ensure stability and function during
loading. Anterior implant sites should also be assessed for the necessary
angulation required to ensure a proper emergence profile. Once the implant
site and prosthetic design have been chosen, the clinician may choose the
proper graft technique to ensure adequate bone thickness. Ideally, after
implant placement 1.5 mm of bone should be present between the facial
aspect of the implant and the facial plate.
Space maintenance in a graft site is critical for predictable graft
development. The definition of this final graft outer contour must be
established with rigid support using a titanium-supported membrane,
tenting screws, titanium mesh, or other means of space support. Loose graft
particles under a free membrane tend to shift, and the coronal aspect of the
graft site will thin out, leading to a pointed and deficient ridge form.
Knowledge of the properties of membranes used during grafting will
ensure that the graft is free from fibrous tissue ingrowth. It is highly
recommended to use a membrane that has a long lifespan and will stand up
under the pressure of graft coverage, suturing, and postoperative pressure on
the graft site.
Good periosteal flap release and tension-free closure allows the surgeon to
use larger-volume grafts without the fear of incision line opening. Pressure
on a graft site from a temporary removable appliance must be monitored
because it has the potential to reduce the final graft volume secondary to
micromovement of the graft.
Treatment.
If an implant is placed in a regeneration site where the facial bone is thin or
appears to be at risk due to a poor granular consistency, it is recommended
that it be grafted at the time of the implant placement. A layer of allograft or
xenograft should be placed over the entire region of weak bone, and a
collagen membrane should be placed over the particulate graft before
closure. An increased healing time before uncovery and loading should be
considered to allow better graft maturation (Fig. 12.83).
FIG 12.83 Inadequate bone volume. (A–C) An implant in thin bone will be at risk
when strain is directed to the granular facial bone. This has the potential to develop a
dehiscence. (D) An ideal and successful regeneration site provides an excess of
facial bone and the ability of the surgeon to place the implant in an ideal aesthetic
and functional position.
Postgraft Implant Placement: Inadequate Bone

Width at Implant Apex
Etiology.
Regardless of the graft technique or material used, the clinician may
encounter a situation where the apical portion of the implant site is
sometimes deficient due to inadequate development of apical bone or the
lack of apical extension of the bone graft. Implants in typical osteotomy sites
are positioned so the apex of the implant will remain within the bony
architecture. In some cases an apical fenestration will occur, and additional
procedures will be needed to maintain predictable bony support.
Complication.
An apical fenestration in an implant osteotomy occurs when the length of the
osteotomy exceeds the length of available bony support. This creates a
situation that most likely will lead to a lack of fixation, stability under load,
and potential implant morbidity.
Prevention.
Augmentation procedures are designed to add horizontal width to a
deficient ridge. This lateral dimension needs to be regenerated in a manner
that provides support to the entire length of the proposed implant. Whether
an onlay cortical graft is utilized or a membrane procedure is planned, the
length of the graft must extend apically to a level that prevents a fenestration
of the implant at the time of surgical placement. Attention to detail in bone
grafting is important from a three-dimensional standpoint because the
clinician has good visualization in the coronal portion of the graft site, but
the apical region is usually out of sight. It is difficult to extend the bulk of
graft materials into the apical regions during graft placement, and the
maintenance of space in the cramped space is required if any significant
bone volume is to be developed. The quality of bone in the apical region and
over the facial aspect of the implant is very important from a density
standpoint because this critical region of support will bear the strain when
the implant restoration is loaded. Deficiencies or regions of thin bone often
lead to the formation of a dark coloration of the tissue on the facial aspect of
the implant, compromising the aesthetics of the entire case.
Apical fixation.
Many authors have debated the need for fixation of the membrane, but it has
been the experience of the authors that rigid fixation of the membrane is
important for the establishment and maintenance of the apical location of
the graft volume. Membranes are easily fixed into position utilizing bone
tacks or screws, but suturing the membrane to the periosteum is another
technique that can be used. It is important to note that ALL bone tacks
should be removed at the time of implant placement to prevent dislodgment
at a later time. It has been shown that loose tacks have the potential of
migrating through the soft tissue into the proximity of vital structures.
The best sites for anchorage of the membrane are located at the most
apical corners of the membrane, anterior and posterior to the graft site. All
fibrous tissue must be removed from the recipient site, and the tack or
suture fixes the membrane at that point. It is not recommended to anchor the
membrane between these two sites unless the graft involves a very wide
space where the membrane tends to move coronally and the graft could be
exposed. In that case, strategic anchorage is recommended.
Lingual/palatal membrane fixation.

The membrane should ideally be fixed into position on the lingual or palatal
aspect to ensure that there is no movement of the membrane if the incision
line opens up or the graft is shifted by the temporary prosthesis. Fixation
with bone tacks on the lingual aspect is often difficult from an access
standpoint. A lingual or palatal suture can maintain a firm hold on the
membrane from that direction while the flap is closed.
Treatment.
If the initial graft is too short and there is an apical exposure, the apical
region must be augmented with particulate graft or additional cortical bone
with membrane coverage to cover the fenestration. The use of freeze-dried
bone allograft or bovine particulate bone along with a collagen membrane
has been recommended for isolation of the graft (Figs. 12.84 to 12.88).
FIG 12.84 Postgraft apical dehiscence. (A) Implant placement exhibiting apical
dehiscence. It is treated with an allograft and collagen membrane. (B) Grafting
defect with allograft. (From Peñarrocha-Oltra D, Peñarrocha-Diago M, Balaguer-Martínez J, et al:
Full-arched fixed prosthesis supported by four implants in patients with recessive
dystrophicepidermolysis bullosa. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 112(2):e4–10,
2011.)
FIG 12.85 A membrane covering a particulate graft must extend apically enough to
maintain isolation of all graft materials.
FIG 12.86 Apical membrane tacks. (A) Three tacks are anchored into the cortical
bone, apical to the deepest portion of the particulate graft. (B) Demonstration of
volume of bone that needs to be isolated in a membrane procedure. (C–D) Care
must be exercised in making sure adequate graft material is present apically to
prevent implant dehiscence.
FIG 12.87 Alternative membrane fixation technique. Membrane fixation may also be
obtained with apical sutures attached to the periosteum, which help limit any
migration of the membrane or allograft material.
FIG 12.88 Lingual suture membrane fixation. (A) Tack placed in palatal cortical
plate with suture started through the palatal flap, passing below the flap and back
through the membrane. (B) The suture is then passed back from beneath the flap
and out again.
Bone Growth Over Bone Fixation Screws

Etiology.
During particulate grafting or when particulate bone is added over block
grafts, excess amounts of the graft particles can often stimulate formation of
bone over the supporting fixation screws. This is usually a layer of soft bone
that can easily be removed with a curette for access to the screw head.
Location of the various screws can be pinpointed using periapical
radiographs if needed. It is necessary to remove these screws if implants are
treatment planned for that region.
Complication.
If a screw is not removed from the graft site, it may interfere with osteotomy
preparation or implant placement.
Prevention.
There is really no significant problem that is related to bone overgrowth and
no real precautions need to be taken to prevent this situation. Knowledge of
the number and location of the screws along with radiographic evaluation of
the site will prevent the clinician from leaving a graft screw in place.
Treatment.
The location of the hidden screw is confirmed with a radiographic exam and
with a clinical survey of the surface of the mature graft site. The bone directly
over a hidden screw is sometimes slightly discolored by the translucence of
the darker screw through the bone, pinpointing its location. This same bone
is often not quite as dense as the surrounding bone, allowing light dissection
of the region until the head of the screw is located (Fig. 12.89).
FIG 12.89 Bone growth over fixation screws. (A) Bone growth over fixation screw
(arrow). Bone should be ideally removed with an explorer or curette. (B) The location
and number of screws should always be documented. In this example, the screw
was identified only after implant placement.
Summary
To provide optimal treatment to patients on a daily basis, the implant
clinician must become well versed in the concepts of bone regeneration. The
fact is that more patients than not will require some manipulation of bone
volume prior to implant placement if the clinician desires to provide a
restoration with proper form, function, and aesthetics.
The discipline of bone grafting encompasses many different approaches
with varying materials and techniques. As the clinician begins to master the
complete assortment of these techniques, the likelihood of a successful
regeneration outcome will become very predictable. This is based on the fact
that a great variety of bone defects are encountered in a clinical setting
requiring different approaches to ensure that appropriate bone volumes are
achieved.
Along with the knowledge and clinical expertise in these procedures, the
implant clinician must also be equipped with a clear understanding of proper
management of the various complications that may arise during these highly
technique-sensitive operations. The common theme in complication
prevention with bone grafting involves accurate preoperative assessment, a
clear grafting strategy, and sufficient skill during the operation (especially
concerning flap reflection and tension-free closure). This must then be
followed with appropriate postoperative measures including interim
prosthesis modification and monitoring.
The human body is capable of amazing feats as it pertains to the
regeneration of bone volumes; however, conditions must be favorable for the
process to work correctly. These principles of grafting, with minimized
complications, have added a very important skill to the array of techniques
that allow today's patients the opportunity to achieve optimal dental health
and aesthetic restorative care.
References
1. Van der Weijden F, Dell'Acqua F, Slot DE. Alveolar bone dimensional
changes of post-extraction sockets in humans: a systematic review. J
Clin Periodontol. 2009;36:1048–1058.
2. Schropp L, Wenzel A, Kostopoulos L, Karring T. Bone healing and
soft tissue contour changes following single-tooth extraction: a
clinical and radiographic 12-month prospective study. Int J
Periodontics Restorative Den. 2003;23:313–323.
3. Clementini M, Morlupi A, Canullo L, et al. Success rate of dental
implants inserted in horizontal and vertical guided bone regenerated
areas: a systematic review. Int J Oral Maxillofac Surg. 2012;41:847–852.
4. Hammerle CH, Jung RE, Feloutzis A. A systematic review of the
survival of implants in bone sites augmented with barrier
membranes (guided bone regeneration) in partially edentulous
patients. J Clin Periodontol. 2002;29(Suppl 3):226–231 [discussion 232–
223].
5. McAllister BS, Haghighat K. Bone augmentation techniques. J
Periodontol. 2007;78:377–396.
6. Jensen SS, Terheyden H. Bone augmentation procedures in localized
defects in the alveolar ridge: clinical results with different bone grafts
and bone-substitute materials. Int J Oral Maxillofac Implants.
2009;24(Suppl):218–236.
7. Nevins M, Mellonig JT. The advantages of localized ridge
augmentation prior to implant placement: a staged event. Int J
8. Aghaloo TL, Moy PK. Which hard tissue augmentation techniques
are the most successful in furnishing bony support for implant
placement. Int J Oral Maxillofac Implants. 2007;22(Suppl):49–70.
9. Esposito M, Grusovin MG, Felice P, et al. The efficacy of horizontal
and vertical bone augmentation procedures for dental implants—a
Cochrane systematic review. Eur J Oral Implantol. 2009;2:167–184.
10. Misch CM. Autogenous bone: is it still the gold standard? Implant
Dent. 2010;19:361.
11. Pellegrini G, Pagni G, Rasperini G. Surgical approaches based on
biological objectives: GTR versus GBR Techniques. Int J Dent.
2013;2013:521–547.
12. Dahlin C, Linde A, Gottlow J, Nyman S. Healing of bone defects by
guided tissue regeneration. Plast Reconstr Surg. 1988;81:672–676.
13. Buser D, Dula K, Hirt HP, Schenk RK. Lateral ridge augmentation
using autografts and barrier membranes: a clinical study with 40
partially edentulous patients. J Oral Maxillofac Surg. 1996;54:420–432
[discussion 432–423].
14. Buser D, Dula K, Hess D, et al. Localized ridge augmentation with
autografts and barrier membranes. Periodontol 2000. 1999;19:151–163.
15. Chiapasco M, Abati S, Romeo E, Vogel G. Clinical outcome of
autogenous bone blocks or guided bone regeneration with e-PTFE
membranes for the reconstruction of narrow edentulous ridges. Clin
16. von Arx T, Cochran DL, Hermann JS, et al. Lateral ridge augmentation
using different bone fillers and barrier membrane application. A
histologic and histomorphometric pilot study in the canine mandible.
17. Simion M, Dahlin C, Rocchietta I, et al. Vertical ridge augmentation
with guided bone regeneration in association with dental implants:
an experimental study in dogs. Clin Oral Implants Res. 2007;18:86–94.
18. Simion M, Fontana F, Rasperini G, Maiorana C. Vertical ridge
augmentation by expanded-polytetrafluoroethylene membrane and a
combination of intraoral autogenous bone graft and deproteinized
anorganic bovine bone (Bio Oss). Clin Oral Implants Res. 2007;18:620–
629.
19. Fontana F, Santoro F, Maiorana C, et al. Clinical and histologic
evaluation of allogeneic bone matrix versus autogenous bone chips
associated with titanium-reinforced e-PTFE membrane for vertical
ridge augmentation: a prospective pilot study. Int J Oral Maxillofac
Implants. 2008;23:1003–1012.
20. Trombelli L, Farina R, Marzola A, et al. GBR and autogenous cortical
bone particulate by bone scraper for alveolar ridge augmentation: a 2-
case report. Int J Oral Maxillofac Implants. 2008;23:111–116.
21. Langer B, Langer L, Sullivan RM. Vertical ridge augmentation
procedure using guided bone regeneration, demineralized freeze-
dried bone allograft, and miniscrews: 4- to 13-year observations on
loaded implants. Int J Periodontics Restorative Den. 2010;30:227–235.
22. Lindfors LT, Tervonen EA, Sandor GK, Ylikontiola LP. Guided bone
regeneration using a titanium-reinforced ePTFE membrane and
particulate autogenous bone: the effect of smoking and membrane
exposure. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2010;109:825–830.
23. Buser D, Dula K, Belser U, et al. Localized ridge augmentation using
guided bone regeneration. 1. Surgical procedure in the maxilla. Int J
24. Machtei EE. The effect of membrane exposure on the outcome of
regenerative procedures in humans: a meta-analysis. J Periodontol.
2001;72:512–516.
25. Beitlitum I, Artzi Z, Nemcovsky CE. Clinical evaluation of particulate
allogeneic with and without autogenous bone grafts and resorbable
collagen membranes for bone augmentation of atrophic alveolar
ridges. Clin Oral Implants Res. 2010;21:1242–1250.
26. Borges GJ, Novaes AB Jr, Grisi MF, et al. Acellular dermal matrix as a
barrier in guided bone regeneration: a clinical, radiographic and
histomorphometric study in dogs. Clin Oral Implants Res.
2009;20:1105–1115.
27. Feuille F, Knapp CI, Brunsvold MA, Mellonig JT. Clinical and
histologic evaluation of bone-replacement grafts in the treatment of
localized alveolar ridge defects. Part 1: Mineralized freeze-dried bone
allograft. Int J Periodontics Restorative Den. 2003;23:29–35.
28. Sterio TW, Katancik JA, Blanchard SB, et al. A prospective, multicenter
study of bovine pericardium membrane with cancellous particulate
allograft for localized alveolar ridge augmentation. Int J Periodontics
Restorative Den. 2013;33:499–507.
29. Wainwright DJ. Use of an acellular allograft dermal matrix
(AlloDerm) in the management of full-thickness burns. Burns.
1995;21:243–248.
30. Fowler EB, Breault LG, Rebitski G. Ridge preservation utilizing an
acellular dermal allograft and demineralized freeze-dried bone
allograft: Part II. Immediate endosseous implant placement. J
Periodontol. 2000;71:1360–1364.
31. Sudarsan S, Arun KV, Priya MS, Arun R. Clinical and histological
evaluation of alloderm GBR and BioOss in the treatment of Siebert's
class I ridge deficiency. J Indian Soc Periodontol. 2008;12:73–78.
32. Griffin TJ, Cheung WS, Hirayama H. Hard and soft tissue
augmentation in implant therapy using acellular dermal matrix. Int J
33. Polimeni G, Koo KT, Qahash M, et al. Prognostic factors for alveolar
regeneration: effect of a space-providing biomaterial on guided tissue
regeneration. J Clin Periodontol. 2004;31:725–729.
34. Le B, Burstein J, Sedghizadeh PP. Cortical tenting grafting technique
in the severely atrophic alveolar ridge for implant site preparation.
Implant Dent. 2008;17:40–50.
35. Le B, Rohrer MD, Prasad HS. Screw “tent-pole” grafting technique for
reconstruction of large vertical alveolar ridge defects using human
mineralized allograft for implant site preparation. J Oral Maxillofac
Surg. 2010;68:428–435.
36. Hempton TJ, Fugazzotto PA. Ridge augmentation utilizing guided
tissue regeneration, titanium screws, freeze-dried bone, and
tricalcium phosphate: clinical report. Implant Dent. 1994;3:35–37.
37. Simon BI, Chiang TF, Drew HJ. Alternative to the gold standard for
alveolar ridge augmentation: tenting screw technology. Quintessence
Int. 2010;41:379–386.
38. Fugazzotto PA. Ridge augmentation with titanium screws and guided
tissue regeneration: technique and report of a case. Int J Oral
39. Becker W, Becker BE, McGuire MK. Localized ridge augmentation
using absorbable pins and e-PTFE barrier membranes: a new surgical
technique. Case reports. Int J Periodontics Restorative Den. 1994;14:48–
61.
40. Goldberg VM, Stevenson S. Natural history of autografts and
allografts. Clin Orthop Relat Res. 1987;225:7–16.
41. Noia CF, Ortega-Lopes R, Olate S, et al. Prospective clinical
assessment of morbidity after chin bone harvest. J Craniofac Surg.
2011;22:2195–2198.
42. Noia CF, Rodriguez-Chessa JG, Ortega-Lopes R, et al. Prospective
study of soft tissue contour changes following chin bone graft
harvesting. Int J Oral Maxillofac Surg. 2012;41:176–179.
43. Song JM, Lee JY, Kim YD. CBCT morphologic analysis of edentulous
posterior mandible for mandibular body bone graft. J Oral Implantol.
2015;41(4):477–482.
44. Misch CM. Comparison of intraoral donor sites for onlay grafting
prior to implant placement. Int J Oral Maxillofac Implants.
1997;12:767–776.
45. Capelli M. Autogenous bone graft from the mandibular ramus: a
technique for bone augmentation. Int J Periodontics Restorative Den.
2003;23:277–285.
46. Urban IA, Nagursky H, Lozada JL. Horizontal ridge augmentation
with a resorbable membrane and particulated autogenous bone with
or without anorganic bovine bone- derived mineral: a prospective
case series in 22 patient. Int J Oral Maxillofac Implants. 2011;26:404–
414.
47. Urban IA, Nagursky H, Lozada JL, Nagy K. Horizontal ridge
augmentation with a collagen membrane and a combination of
particulated autogenous bone and anorganic bovine bone-derived
mineral: a prospective case series in 25 patients. Int J Periodontics
Restorative Den. 2013;33:299–307.
48. Miller RJ, Edwards WC, Boudet C, Cohen JH. Revised Maxillofacial
Anatomy: the mandibular symphysis in 3D. Int J Dent Implants
Biomaterials. 2009;2:1–7.
49. Hoppenreijs TJM, Nijdam ES, Freihofer HPM. The chin as a donor site
in early secondary osteoplasty: a retrospective clinical and
radiological evaluation. J Cranio Maxillofac Surg. 1992;20(3):119–124.
50. Borstlap WA, Stoelinga PJ, Hoppenreijs TJ, van't Hof MA. Stabilisation
of sagittal split advancement osteotomies with miniplates: a
prospective, multicentre study with two-year follow-up. Part I: clinical
parameters. Int J Oral Maxillofac Surg. 2004;33(5):433–441.
51. Linkevicius T, Puisys A, Steigmann M, et al. Influence of vertical soft
tissue thickness on crestal bone changes around implants with
platform switching: a comparative clinical study. Clin Implant Dent
Relat Res. 2015;17(6):1228–1236.
52. Urban IA, et al. Treatment of severe mucogingival defects with a
combination of strip gingival grafts and a xenogeneic collagen matrix:
a prospective case series study. Int J Periodontics Restorative Dent.
2015;35(3):345–353.
53. Misch CE. Contemporary implant dentistry. ed 3. Mosby: St. Louis; 2008.
54. Bartee BK, Carr JA. Evaluation of a high-density
polytetrafluoroethylene (n-PTFE) membrane as a barrier material to
facilitate guided bone regeneration in the rat mandible. J Oral
Implantol. 1995;21(2):88–95.
55. Caldwell GR, Mealy BL. A prospective study: alveolar ridge augmentation
using tenting screws, acellular dermal matrix and combination particulate
grafts. [A thesis for Master of Science in Periodontics—The University
of Texas Health Science Center at San Antonio Graduate School of
Biomedical Sciences] May 2013.
56. Bartee BK. Implant site development and extraction site grafting:
bone biology and physiology, selection of grafting materials, selection
of barrier membranes, and surgical technique. Osteogenics Clinical
Education. 2012;18–20.
57. Fontana F, Maschera E, Rocchietta I, Simion M. Clinical classification
of complications in guided bone regeneration procedures by means
of a nonresorbable membrane. Int J Periodontics Restorative Dent.
2011;31(3):265–274.
58. Ryan CD, Mealey BL, Verrett RG, et al. Relationship between clinical
periodontal biotype and labial plate thickness: an in vivo study. Int J
Periodontics Restorative Dent. 2011;31(4):344–354.
13
Posterior Maxilla Complications
Randolph R. Resnik
Anatomy
Maxillary posterior partial and complete edentulism are among the most
common conditions in dentistry. Thirty million people in the United States,
or 17.5% of the adult population, are missing all of their maxillary teeth. In
addition, 20% to 30% of the adult partially edentulous population older than
45 years is missing maxillary posterior teeth in one quadrant, and 15% of this
age group is missing the maxillary dentition in both posterior regions.
Approximately 40% of adult patients are missing at least some maxillary
posterior teeth.1
The maxillary posterior edentulous region presents many unique and
challenging situations in implant dentistry. Most noteworthy surgical
methods include maxillary sinus grafts to increase available bone height,
onlay grafts to increase bone width, and modified surgical approaches to
insert implants in areas with poorer bone density. Grafting of the maxillary
sinus to overcome the problem of reduced vertical available bone has become
a very popular and predictable procedure over the last decades. This grafting
procedure has been proven to provide the clinician with adequate bone
volume to place an implant of ideal size and proper orientation. However,
this anatomic area is responsible for more complications in oral
implantology than any other region in the oral cavity.
Anatomic Disadvantages to the Posterior Maxilla

Pneumatization of the Maxillary Sinus
After posterior tooth loss, the maxillary sinuses enlarge, which presents a
unique problem for implant placement. A continued increase of osteoclastic
activity within the periosteum of the maxillary sinus (Schneiderian
membrane) results in expansion. An elevated positive pressure within the
sinus will also increase alveolar bone atrophy allowing for pneumatization,
thus decreasing the available bone for implant placement.2 An inverse
relationship between sinus pneumatization and the remaining alveolar bone
exists due to remodeling and the normal/pathologic status of the
dentoperiodontal apparatus (Fig. 13.1).
FIG 13.1 Pneumatization can be significant even with teeth present as the
maxillary sinus increases in size, leaving less available bone for implant placement.
Clinical Implication.
The net result of maxillary sinus pneumatization is the deficiency in bone
height for implant placement, thus requiring augmentation for increased
bone quantity for future implant placement. With proper grafting techniques
to increase bone volume, this anatomic area may be restored to a more
predictable biomechanical location for future implant placement. If grafting
is not completed where bone quantity is not adequate, an increased
morbidity may result with failure or migration of implants.
Ridge Width/Lingual Repositioning

The maxilla has an inherently thinner facial cortical plate in comparison to
other areas of the mouth (e.g., mandible) because of rapid resorption after
tooth loss. The loss of maxillary posterior teeth results in an initial decrease
in bone width at the expense of the labial bony plate. This process occurs at a
faster rate than in any other region of the oral cavity.3 The resorption
phenomenon is accelerated by the loss of vascularization of the alveolar bone
and existing fine trabecular bone type. However, because the initial residual
ridge is inherently wide in the posterior maxilla, even with a 60% decrease in
the width of the ridge, adequate-diameter root form implants usually can be
placed. As further time passes, the ridge shifts toward the palate until the
ridge is resorbed into a medially positioned narrower bone volume.4 The
posterior maxilla continues to progressively remodel toward the midline as
the bone resorption process continues.
Clinical Implications.
Because of the less than ideal width of bone, buccal-lingual implant
placement may not be ideal. Studies have shown that it is possible to
perform ridge augmentation to increase width at the time of sinus grafting,
but there is an increased rate of morbidity and implant failure when
compared to sinus grafting alone. Due to the more lingual position of the
ridge, implants will be placed more lingual than is ideal. Prosthetically, this
will often result in the buccal cusp of the final restoration being cantilevered
facially to satisfy esthetic requirements at the expense of biomechanics in the
moderate to severely atrophic ridges (Fig. 13.2).1 In some severe resorption
cases, the posterior maxillary implants are more ideally restored in a
crossbite occlusion.
FIG 13.2 In the posterior maxilla the buccal plate resorbs faster than any other area
of the oral cavity. As resorption progresses from division A to B to C to D, the
residual ridge is positioned more lingual. This results in the eventual implant being
placed more lingual, potentially in crossbite with the mandibular posterior teeth or at
a nonideal angle.
Bone Density
The bone quality in the posterior maxilla is usually poorer than in any other
intraoral region. Bone strength is directly related to its density, and the low-
density bone of this region is often five to ten times weaker compared with
bone found in the anterior mandible.5 The various bone densities directly
influence the bone-implant contact (BIC) percent, which accounts for the
transmission of forces to the bone. The posterior maxilla most commonly
exhibits D4 bone (Misch classification), which has the greatest biomechanical
elastic modulus difference when compared with titanium under load. D4
bone is characterized by fine trabeculae with very little cortical bone.
Implants placed into D4 bone are most susceptible to bone loss and
increased morbidity. As such, strategic surgery techniques (e.g., under-
preparation, use of osteotomes) when placing implants in the posterior
maxilla to increase BIC are suggested.
Because the BIC is least in D4 bone, the stress patterns (i.e., from
biomechanical force) in this bone type migrate farther toward the apex of the
implant. As a result, bone loss is more pronounced and occurs more apically
along the implant body, while in denser bone types (D1), one would see only
crestal bone loss. As a result the lateral cortical BIC to stabilize the implant is
often insufficient. To increase BIC and success with posterior maxilla
implants, the surgical and prosthetic technique requires modification; under
preparation of the surgical site, use of osteotomes, greater healing periods,
and progressive bone loading during the prosthetic phase of treatment (Fig.
13.3).
FIG 13.3 Poor bone density. (A) In D4 bone, underpreparation of the surgical site
along with the use of osteotomes increases the BIC of the implant, increasing the
prognosis of the implant. (B) A conventional drilling procedure uses an extraction
technique that removes bone from the site. Note the jagged periphery of the
osteotomy site. (C) With the use of osteotomes, bone compaction results in a better
quality osteotomy and increased BIC for dental implant healing.
Anatomic Location
Because of the anatomic location (posterior maxilla), adequate surgical access
is often a difficult problem because of a lack of interocclusal space. With the
length of the handpiece and surgical drill often exceeding 40 mm, the
posterior maxilla is one of the most difficult areas to complete a successful
osteotomy. The implant clinician is often unable to drill the osteotomy with
the correct angulation (Fig. 13.4) because of the opposing occlusion.
FIG 13.4 (A) Because of the anatomic location, implant osteotomies are often
complicated in the posterior region because of lack of interocclusal space. Nonideal
implant angulation often results. (B) Implant drills + handpiece often exceed 40 mm,
which can make access very difficult.
The implant surgeon is often confronted with lack of interocclusal space,
increasing the difficulty in all aspects of the surgical procedure. Visibility is
diminished in the posterior maxilla, especially when increased bleeding
occurs. This area also becomes very uncomfortable for the patient, especially
if there is a positive gag reflex.
The lack of space also presents an issue with utilizing surgical templates,
especially those guided by cone beam computed tomography (CBCT),
because minimal space is available to accommodate the surgical drill along
with the surgical template. However, newer surgical templates have been
fabricated with the buccal aspect of the drilling tubes removed (buccal
access), which allows the implant clinician additional space to prepare the
osteotomy.
Predisposition to Pathology
The paranasal sinuses, especially the maxillary sinus, have been shown to be
very susceptible to various disease processes. Studies have shown that in
approximately 46% percent of asymptomatic patients requiring
augmentation in the maxillary sinus, some degree of pathology exists.6 The
pathology can range from incipient membrane inflammation to fully
opacified sinuses.
The implant clinician must have a working knowledge of the maxillary sinus
anatomy, anatomic variants, and associated pathology. It is imperative the
patency of the maxillary ostium be determined prior to placement of an
implant or bone graft into the maxillary sinus. To minimize postoperative
morbidity, the clinician must understand the indications for otolaryngologist
(ENT) referral and clearance prior to any procedures that would involve
grafting procedures into the maxillary sinus.
Understanding Paranasal Sinus Anatomy and

Physiology
To decrease the morbidity of treatment in the posterior maxilla, knowledge of
the important structures of the area must be attained. The implant clinician
should evaluate these structures to determine normal anatomy and verify any
presence free of anatomic variants and pathology (Fig. 13.5).
FIG 13.5 Normal paranasal sinus anatomy.
Osteomeatal Complex
The osteomeatal unit is composed of the maxillary ostium, ethmoid
infundibulum, anterior ethmoid cells, hiatus semilunaris, and the frontal
recess, which encompasses the area of the middle meatus. This common
channel allows for air flow and mucociliary drainage of the frontal, maxillary,
and anterior ethmoid sinuses. Blockage in this area leads to impaired
drainage of the maxillary, frontal, and ethmoid sinuses, which may result in
rhinosinusitis and postoperative complications after implant or grafting
procedures.
Radiographic identification of the osteomeatal complex and related
structures must be evaluated to prevent potential postoperative
complications. Pathology or variations within the osteomeatal complex may
lead to postoperative sinus graft morbidity or implant complications due to
compromised mucociliary drainage (alteration of normal sinus physiology) of
Maxillary Ostium
The main drainage avenue of the maxillary sinus is through the maxillary
ostium. The primary ostium is located in the superior aspect of the sinus
medial wall and drains its secretions via the ethmoid infundibulum through
the hiatus semilunaris into the middle meatus of the nasal cavity. The
infundibulum is approximately 5 to 10 mm long and drains via ciliary action
in a superior and medial direction. The ostium diameter averages 2.4 mm in
health; however, pathologic conditions may alter the size to vary from 1 to 17
mm.1
The maxillary ostium and infundibulum are part of the anterior ethmoid
middle meatal complex, the region through which the frontal and maxillary
sinuses drain, which is primarily responsible for mucociliary clearance of the
sinuses to the nasopharynx. As a result, obstruction in one or more areas of
the complex will usually result in rhinosinusitis or lead to morbidity of the
graft or implant.
Patency of the maxillary ostium is most crucial pre- and postoperatively
during maxillary graft sinus surgery to prevent infection and morbidity of the
graft. Evaluating the patency of the ostium via a CBCT is easily accomplished
with evaluation of serial cross-sectional images. A prophylactic regimen
including antibiotics and corticosteroids should always be utilized when
grafting or during implant placement in the sinus proper to maintain
patency of the ostium during the postoperative period.
Schneiderian Membrane
The epithelial lining of the maxillary sinus is a continuation of the nasal
mucosa and is classified as a pseudostratified, ciliated columnar epithelium,
also called respiratory epithelium. The epithelial lining of the maxillary sinus
is much thinner and contains fewer blood vessels than the nasal epithelium.
This accounts for the membrane's pale color and bluish hue. Five primary
cell types exist in this tissue: (1) ciliated columnar epithelial cells, (2)
nonciliated columnar cells, (3) basal cells, (4) goblet cells, and (5)
seromucinous cells. The ciliated cells contain approximately 50 to 200 cilia
per cell. In a healthy maxillary sinus the cilia cells assist in clearing mucus
from the sinus and into the nasopharynx. The nonciliated cells compose the
apical aspect of the membrane, contain microvilli, and serve to increase
surface area. These cells have been theorized to facilitate humidification and
warming of inspired air. The basal cell's function is similar to that of a stem
cell that can differentiate as needed. The goblet cells in the maxillary sinus
produce glycoproteins that are responsible for the viscosity and elasticity of
the mucus produced. The maxillary sinus contains the highest concentration
of goblet cells in comparison with the other paranasal sinuses. The maxillary
sinus membrane also exhibits few elastic fibers attached to the bone7 (no
tenacious attachment is usually present), which simplifies elevation of this
tissue from the bone during grafting procedures. The thickness of the sinus
mucosa in health varies, but is generally 0.3 to 0.8 mm.8 In smokers, it varies
from very thin and almost nonexistent to very thick, with a squamous type of
epithelium.
A CBCT scan of normal, healthy paranasal sinuses reveals a completely
radiolucent (dark) maxillary sinus. Any radiopaque (whitish) area within the
sinus cavity is abnormal, and a pathologic condition should be suspected.
The normal sinus membrane is radiographically invisible, whereas any
inflammation or thickening of this structure will be radiopaque. The density
of the diseased tissue or fluid accumulation will be proportional to varying
degrees of gray values.
Maintaining the integrity of the sinus membrane is crucial in decreasing
postoperative complications, including loss of graft material and the
possibility of infection. Many factors may alter the physiology of the sinus
mucosa such as viruses, bacteria, and foreign bodies (implants). Care should
be taken to minimize membrane perforations during surgery. If perforations
occur, appropriate repair treatment protocols should be adhered to (see
Sinus Perforations).
Mucociliary Drainage
Normal mucociliary flow is crucial to maintaining the healthy physiology of
the maxillary sinus. In a healthy sinus an adequate system of mucus
production, clearance, and drainage is maintained. The key to normal sinus
physiology is the proper function of the cilia, which is the main component
of the mucociliary transport system. The cilia move contaminants toward the
natural ostium and then to the nasopharynx. The cilia of the columnar
epithelium beat toward the ostium at 15 cycles per minute, with a stiff stroke
through the serous layer, reaching into the mucoid layer. They recover with a
limp reverse stroke within the serous layer. This mechanism slowly propels
the mucoid layer toward the ostium at a rate of 9 mm per minute and into the
middle meatus of the nose.8
In health, mucoid fluid is transported toward the ostium of the maxillary
sinus and drains into the nasal cavity, eliminating inhaled small particles and
microorganisms. This mucociliary transport system is an active transport
system that relies heavily on oxygen. The amount of oxygen absorbed from
the blood is not adequate to maintain this drainage system; additional
oxygen has to be absorbed from the air in the sinus. This is why the patency
of the ostium is crucial in maintaining the normal transport system.
Various elements may decrease the number of cilia and slow their beating
efficiency. Viral infections, pollution, allergic reactions, and certain
medications may affect the cilia in this way.9 Genetic disorders (e.g.,
dyskinetic cilia syndrome) and factors such as longstanding dehydration,
anticholinergic medications and antihistamines, cigarette smoke, and
chemical toxins also can affect ciliary action (Fig. 13.6).
FIG 13.6 (A) The pseudostratified columnar epithelium cells have 50 to 200 cilia
per cell that beat toward the ostium to help clear 1 L of mucus from goblet and
mucous glands each day from the sinus. In health the mucous has two layers: a
bottom serous layer and top mucoid layer. The cilia beat with a stiff stroke in the
mucoid layer toward the ostium and a relaxed recovery stroke within the serous
layer. (B) Clinical image depicting the thinness of the lateral wall and showthrough
(dark blue) of the Schneiderian membrane. (C) The bluish hue of the membrane
after lateral wall window preparation.
An alteration in the sinus ostium patency or the quality of secretions can lead
to disruption in ciliary action, which may result in rhinosinusitis.
For clearance to be maintained, adequate ventilation is necessary.
Ventilation and drainage is dependent on the osteomeatal unit, which is the
main sinus opening. Ciliary movements of ciliated epithelial cells dictate
clearance of the maxillary sinus. It is important to maintain the patency of
the maxillary ostium and the osteomeatal complex in the postoperative
period.
The physiologic mucociliary transport system may be compromised by
abnormalities in the cilia, which include a decrease in overall ciliary number
and poor coordination of their movement. This altered physiology may result
in an increased morbidity of implant placement or bone graft healing.
Therefore, it is crucial that the mucociliary drainage mechanism be
maintained throughout the postoperative treatment period. This is most
likely accomplished with good surgical technique, evaluation and treatment
of prior drainage issues, and strict adherence to the use of pharmacologic
agents (e.g., antibiotics, corticosteroids).
Maxillary Sinus Flora

There is much debate on the bacterial flora of the maxillary sinus. Maxillary
sinuses have been considered to be sterile in health; however, bacteria can
colonize within the sinus without producing symptoms. In theory, the
mechanism by which a sterile environment is maintained includes the
mucociliary clearance system, immune system, and the production of nitric
oxide within the sinus cavity. In recent endoscopic studies, normal sinuses
were shown to be nonsterile, with 62.3% exhibiting bacterial colonization.
The most common bacteria cultured were Streptococcus viridans, Staphylococcus
epidermidis, and Streptococcus pneumonia.10 The culture findings for secretions
in acute maxillary sinusitis yielded high numbers of leukocytes, S.
pneumoniae, or Streptococcus pyogenes, with Haemophilus influenzae being
recovered from the purulent exudates with lower numbers of staphylococci.
Other reports have indicated the bacterial flora of the maxillary sinus
consists of nonhemolytic and alpha-hemolytic streptococci, as well as
Neisseria spp. Additional microorganisms identifiable in various quantities
belong to staphylococci, Haemophilus spp, pneumococci, Mycoplasma spp,
and Bacteroides spp. This is important to note because the sinus graft
procedure often violates the sinus mucosa, and bacteria may contaminate the
graft site leading to post-operative complications.1
Clinical Implications
Sterile technique.
The implant clinician must understand the importance of reducing the
bacterial count and possible microorganisms that may initiate infections in
the maxillary sinus. A strict aseptic technique should be adhered to during
any surgical procedures that invade the maxillary sinus proper. This will
minimize the possibility of bacterial colonization within the graft, which may
lead to increased morbidity.
Antibiotic.
The type of bacteria inhabiting the sinus is very important because it dictates
what antibiotic is prescribed preoperatively, postoperatively, and
therapeutically in case of infection. The most common bacteria present in the
sinus must be susceptible to the specific antibiotic to prevent infection and
decrease the morbidity of the graft. The antibiotic selected should not be the
clinician's “favorite” but should be the most ideal antibiotic, which is specific
for the involved bacteria. Ideally, Augmentin (875/125 mg) has been shown to
be most effective in the maxillary sinus.
Blood Supply
The vascular supply in the maxillary sinus is a vital part of the healing and
regeneration of bone after a sinus graft and healing of a dental implant. The
blood supply to the maxillary sinus comes directly from the maxillary artery,
which emanates from the external carotid artery. The maxillary artery
supplies the bone surrounding the sinus cavity and also the sinus
membrane. Branches of the maxillary artery, which most often include the
posterior superior alveolar artery and infraorbital artery, form endosseous
and extraosseous anastomoses that encompass the maxillary sinus. The
formation of the endosseous and extraosseous anastomoses in the maxillary
sinus is termed the double arterial arcade. Studies have shown vascularization
of postgraft material to depend on the intra- and extraosseous anastamoses,
along with the blood vessels of the Schnedierian membrane, which is
supplied by the posterior superior alveolar artery and the infraorbital artery
along the lateral wall.11
There exists different factors that alter the vascularization in this area.
With increasing age the number and size of blood vessels in the maxilla
decrease. As bone resorption increases, the cortical bone becomes thin,
resulting in less vascularization. As the lateral wall becomes thinner, the
blood supply to the lateral wall and lateral aspect of the bone graft comes
primarily from the periosteum, resulting in a compromised vascularization to
the region.
Extraosseous Anastomosis.
Extraosseous anastomosis is found in approximately 44% of the population
and is usually in close approximation to the periosteum of the lateral wall.
The extraosseous anastomosis is superior to the endosseous unit, which is
approximately 15 to 20 mm from the dentate alveolar crest.
To minimize vascular trauma to the extraosseous anastomosis, surgical and
anatomic considerations should be addressed. Ideally, vertical incisions
should be made as short as possible to decrease the possibility of blood
vessel damage. It is crucial to gain adequate access to the lateral aspect of the
maxilla, and the periosteum should be reflected full thickness with great
care. Haphazard reflection may lead to severing or damage to the
anastomosis with resultant postoperative edema.
Treatment implication.
Severing of the extraosseous anastomosis may result in significant increased
bleeding during the surgical procedure. This intraoperative complication
may give rise to impaired visibility for the clinician along with increased
surgery duration. Additionally, postoperative complications such as pain,
edema, and ecchymosis may result from the severing of these blood vessels.
If trauma to these vessels occurs, direct pressure or the use of
electrocautery may be used. However, electrocautery may potentially cause
membrane damage or necrosis. If severe bleeding occurs, curved Kelly
hemostats are used to clamp the bleeding vessel followed by ligature
placement. A slowly resorbable suture with high tensile strength such as
Vicryl is recommended.
Intraosseous Anastomosis.
The intraosseous anastomosis is found within the lateral wall of the sinus,
which supplies the lateral wall and the sinus membrane. In an edentulous
maxilla with posterior vertical bone loss, the endosseous anastamosis may be
5 to 10 mm from the edentulous ridge. The endosseous artery has been
shown to be observed on CBCT scans in approximately one half of the
patients requiring a sinus graft.12 However, anatomic cadaver studies have
shown the prevalence to be 100%.13 In 82% of cases the most common
anatomic location was observed between the canine and second premolar
region.14 However, with a long-term edentulous patient with a thin lateral
wall, the artery may be atrophied and almost nonexistent.
Surgical, radiographic, and anatomic considerations should be addressed to
minimize trauma to these blood vessels. The CBCT radiographic
identification is extremely important in identifying these blood vessels prior
to surgery so preparation may be made. Radiographically, smaller
anastomoses will not be seen if the pixel size (~1.0 mm) is less than one-half
the size of the anastamosis vessel. Using a 0.3 or 0.4 CBCT pixel size for
radiographic evaluation will most likely show the smaller anastomoses.15
Studies have shown that in 20% of lateral wall osteotomies, significant
bleeding complications may occur.16 This is mainly due to the anastomosis
being greater than 1.0 mm in diameter. It has been shown that vessels larger
than 1.0 mm are more problematic and associated with significant bleeding,
whereas smaller vessels (<1.0 mm) are usually insignificant and easily
managed (Fig. 13.7).
FIG 13.7 (A) The extra- and intraosseous anastomosis, which is made up of the
infraorbital and posteriorsuperior artery. (B) Intraosseous notch (arrow) containing
the intraosseous anastomosis, which comprises the posterior superior artery and
infraorbital artery. (C) Cross-sectional CBCT image depicting intraosseous
anastamosis (arrow). (D) Posterior lateral nasal artery location in the medial wall of
In most cases, bleeding is a minor complication and of short duration;
however, in some instances it may be significant and difficult to manage. To
control bleeding, there are many possible treatments: (1) the patient should
be repositioned into an upright position and pressure applied with a surgical
sponge; (2) electrocautery may be used, although this may lead to membrane
necrosis and perforation with possible migration of graft material; (3) a
second window may be made proximal to the bleeding source to gain access
to the bleeding vessel, especially if location cannot be obtained from the
original window; and (4) cutting the bone and vessel with a high-speed
diamond with no irrigation (which cauterizes the vessel). (See Bleeding
Chapter)
Posterior Lateral Nasal Artery.
A posterior lateral nasal artery (branch of the sphenopalatine artery that also
rises from the maxillary artery) supplies the medial aspect of the sinus cavity.
The medial and posterior walls of the maxillary sinus mucosa receive their
blood supply from the posterior lateral nasal artery.
During sinus graft surgery the clinician may be in close approximation to this
artery when elevating the membrane off the medial wall. Care should be
exercised to minimize trauma to this area because aggressive reflection of the
membrane may result in trauma to the blood vessel or perforation into the
nasal cavity.
Trauma to this artery may cause significant bleeding in the sinus proper and
also within the nasal cavity. Because the medial sinus wall is very thin
(usually one-half the thickness of the lateral wall), aggressive membrane
reflection may result in trauma leading to bleeding issues (see Chapter 7).
Sphenopalatine/Infraorbital Arteries.
The sphenopalatine artery is also a branch of the maxillary artery and enters
the nasal cavity through the sphenopalatine foramen, which is near the
posterior portion of the superior meatus of the nose. As the sphenopalatine
artery exits the foramen, it branches into the posterior lateral nasal artery
and the posterior septal artery.17 Additionally, the infraorbital artery enters
the maxillary sinus via the infraorbital fissure in the roof of the sinus and
ascends cranially into the orbital cavity. Because of the anatomic locations of
these blood vessels, it is rarely a concern with respect to sinus graft surgery.
Complication implications.
The sphenopalatine and infraorbital blood vessels are usually not
problematic for bleeding complications during lateral-approach sinus
elevation surgery because of their anatomic locations. However, incorrect
incision locations and aggressive reflection may damage the blood vessels. If
bleeding does occur, it is usually easily controlled with pressure and local
hemostatic agents.
The Anatomic Significance of the Maxillary Sinus
Walls
The maxillary sinus features six bony walls, each of which contain important
anatomic structures that may cause complications during maxillary sinus
graft surgery. The implant clinician should have a strong understanding and
foundation of these structures in the preoperative assessment prior to
surgical procedures (Fig. 13.8).
FIG 13.8 The six bony walls of the maxillary sinus: anterior, medial, lateral,
superior, posterior, and inferior walls.
Anterior Wall
The anterior wall of the maxillary sinus consists of thin, compact bone
extending from the orbital rim to just above the apex of the cuspid. With the
loss of the canine, the anterior wall of the antrum may approximate the crest
of the residual ridge. Within the anterior wall and approximately 6 to 7 mm
below the orbital rim, with anatomic variants as far as 14 mm from the orbital
rim, is the infraorbital foramen. The infraorbital nerve runs along the roof of
the sinus and exits through the foramen. The infraorbital blood vessels and
nerves lie directly on the superior wall of the sinus and within the sinus
mucosa. The infraorbital nerve gives sensory innervation to the soft tissue
from the lower border of the orbit to lateral of the nose to the upper lip (Fig.
13.9A).
FIG 13.9 The six bony walls of the maxillary sinus. (A) Anterior. (B) Superior. (C)
Posterior. (D) Medial. (E) Lateral. (F) Inferior.
Complication Implications
Sinus infection.
Tenderness to pressure over the infraorbital foramen or redness of the
overlying skin may indicate inflammation of the sinus membrane from
infection or trauma, which may contraindicate graft surgery until resolution.
Nerve impairment.
In patients exhibiting anatomic variants, neurosensory impairment may
occur during retraction of this area leading to neurapraxia type injuries. The
use of worn, sharp-edged retractors should be avoided when reflecting tissue
superiorly in this area. Within the anterior wall of the sinus, the thinnest part
is the canine fossa, which is directly above the canine tooth. The anterior wall
of the maxillary sinus may also serve as surgical access during Caldwell-Luc
procedures to treat a preexisting or post–sinus graft, pathologic condition.
Superior Wall
The superior wall of the maxillary sinus coincides with the thin inferior
orbital floor. The orbital floor slants inferiorly in a mediolateral direction and
is convex into the sinus cavity. A bony ridge is usually present in this wall that
houses the infraorbital canal, which contains the infraorbital nerve and
associated blood vessels. Dehiscence of the bony chamber may be present,
resulting in direct contact between the infraorbital structures and the sinus
mucosa (Fig. 13.9B).
Infection.
Ocular symptoms may result from infections or tumors in the superior
aspects of the sinus region and may include proptosis (bulging of the eye)
and diplopia (double vision). When these problems occur, the patient is
closely supervised and a medical consult is advised to decrease the risk of
severe complications that may result from the spread of infection in a
superior direction. Superior-spreading infections may lead to significant
ocular problems or brain abscesses. As a result, when ocular or cerebral
symptoms appear, aggressive therapy to decrease the spread of infection is
indicated. Overpacking the maxillary sinus with bone graft material during a
sinus graft may result in pressure against the superior wall if a sinus
infection develops.
Posterior Wall
The posterior wall of the maxillary sinus corresponds to the pterygomaxillary
region, which separates the antrum from the infratemporal fossa. The
posterior wall usually has several vital structures in the region of the
pterygomaxillary fossa, including the internal maxillary artery, pterygoid
plexus, sphenopalatine ganglion, and greater palatine nerve. The posterior
wall should always be identified on the radiograph. When a posterior wall is
not present, a pathologic condition (including neoplasms) is to be suspected
(Fig. 13.9C).
Bleeding.
Common donor sites to obtain autogenous bone for sinus augmentation
procedures include the tuberosity area. Special consideration should be
taken on the posterior extent of the tuberosity removal. Aggressive
tuberosity removal may lead to bleeding in the infratemporal fossa
(pterygoid plexus), resulting in life-threatening situations.
Pterygoid implants.
It should be noted that pterygoid implants placed through the posterior
sinus wall and into this region might approach vital structures, including the
maxillary artery. A blind surgical technique to place a pterygoid implant
through the posterior wall may have increased surgical risk. However, they
are of benefit primarily when third or fourth molars are needed for
prosthetic reconstruction or sinus grafts are contraindicated and available
bone posterior to the antrum is present.
Medial Wall
The medial wall of the antrum coincides with the lateral wall of the nasal
cavity and is the most complex of the various walls of the sinus. On the nasal
aspect the lower section of the medial wall parallels the lower meatus and
floor of the nasal fossa; the upper aspect corresponds to the middle meatus.
The medial wall is usually vertical and smooth on the antral side. Located in
the superior aspect of the medial wall is the maxillary or primary ostium (Fig.
13.9D).
Verify patency.
The patency of the ostium must be ascertained prior to surgery to prevent
postoperative complications. This is easily verified via coronal or cross-
sectional images on CBCT surveys. Of utmost importance is the patency of
the ostium, which must be maintained throughout the postoperative period.
If ostium patency is compromised, increased morbidity of the graft will occur
as the mucociliary action of the maxillary sinus will be compromised.
Accessory ostia.
Smaller, accessory or secondary ostia may be present that are usually located
in the middle meatus posterior to the main ostium. These additional ostia are
most likely the result of chronic sinus inflammation and mucous membrane
breakdown. They are present in approximately 30% of patients, ranging from
a fraction of a millimeter to 0.5 cm, and are commonly found within the
membranous fontanelles of the lateral nasal wall.18 Fontanelles are usually
classified either as anterior fontanelles (AFs) or posterior fontanelles (PFs)
and are termed by their relation to the uncinate process. These weak areas in
the sinus wall are sometimes used to create additional openings into the
sinus for treatment of chronic sinus infections. Primary and secondary ostia
may, on occasion, combine and form a large ostium within the infundibulum.
Lateral Wall
The lateral wall of the maxillary sinus forms the posterior maxilla and the
zygomatic process. This wall varies greatly in thickness from several
millimeters in dentate patients to less than 1 mm in an edentulous patient. A
CBCT examination will reveal the osseous thickness of the lateral wall, which
is crucial in defining the osteotomy location and preparation technique.
Patients exhibiting increased parafunction forces will have thicker lateral
walls (Fig. 13.9E).
Varying thickness.
The lateral wall thickness of the maxilla has been noted to be extremely
variable, with some cases being nonexistent. This will lead to an increased
possibility of membrane perforation, even occurring on reflection. In
contrast, the lateral wall may be very thick, which is usually seen with
patients that exhibit parafunction and have just recently lost the posterior
teeth. In these situations, lateral wall sinus grafting becomes very difficult
because of the cortical thickness.
Bleeding.
The lateral wall houses the intraosseous anastamosis of the infraorbital and
posterior superior alveolar artery, which may lead to a bleeding complication
because this area is the site for osteotomy preparation of the lateral wall
sinus graft procedure.
Inferior Wall
The inferior wall or floor of the maxillary sinus is in close relationship with
the apices of the maxillary molars and premolars. The teeth usually are
separated from the sinus mucosa by a thin layer of bone; however, on
occasion, teeth may perforate the floor of the sinus and be in direct contact
with the sinus lining. Studies have shown that the first molar has the most
common dehiscent tooth root, occurring up to approximately 30% of the
time.19 In dentate patients the floor is approximately at the level of the nasal
floor. In the edentulous posterior maxilla the sinus floor is often 1 cm below
the level of the nasal floor (Fig. 13.9F).
Irregular floor.
Radiographically, the sinus inferior floor morphology is easily seen via 3-D
imaging. The floor is rarely flat and smooth; the presence of irregularities
and septa should be determined and their exact locations noted. Irregular
floors are most often seen after teeth are extracted, leaving residual bony
crests that increase risk of perforation because of the difficulty in membrane
reflection. In some cases, the bony crests are not even seen on the CBCT
evaluation.
Septa.
Complete or incomplete bony septa may exist on the floor in a vertical or
horizontal plane. Approximately 30% of dentate maxillae have septa, with
three fourths appearing in the premolar region. Complete septa separating
the sinus into compartments are very rare, occurring in only 1.0% to 2.5% of
maxillary sinuses.20 The presence of septa complicate lateral wall sinus graft
procedures, which leads to an increased likelihood of membrane perforation.
Anatomic Variants
Numerous anatomic variants arise that may predispose a patient to
postsurgical complications. When these conditions are noted, a
pharmacologic discipline may be altered and/or implants may be placed after
the sinus graft has matured, rather than predisposing them to an increased
risk by inserting them at the same time as the sinus graft.
Nasal Septum Deviation

The nasal septum is a bony partition and cartilage within the nasal cavity. The
cartilage is termed the quadrangular cartilage and the bones are comprised
of the maxillary alveolar crest, vomer bone, and the perpendicular plate of
the ethmoid. A deviated septum occurs when the cartilaginous ridge leans to
the right or left, resulting in an obstruction of the nasal passages that
separates the right and left nasal cavities. The nasal septum is the bone and
cartilage in the nose that separates the nasal cavity into the two nostrils.
Normally, the septum lies centrally, and thus the nasal passages are
symmetrical.5 Studies have shown a prevalence of septal deviation in up to
70% of the population.21 A deviated septum may be diagnosed by evaluating
the coronal or 3-D CBCT images (Fig. 13.10A).
FIG 13.10 (A) Concha bullosa (arrow) and deviated septum. (B) Large left-sided
concha bullosa (red arrow), deviated septum to the right, and paradoxical middle
turbinate (green arrow). (C) Paradoxical middle turbinate (green arrow) exhibiting
concavity toward the septum, which may lead to clearance issues.
Ostium blockage.
When this bony structure is maligned or deviated, the patient may be at risk
of postoperative complications. This bony variant in extremes may cause
obstruction of the osteomeatal complex, which results in inflammation from
air turbulence, causing increased mucosal drying and particle deposition. If
deviation is significant, or if preoperative sinus pathology is present, an ENT
consultation is recommended. It should be noted that the ipsilateral side
usually will have normal clearance issues and less of a possibility of
postoperative complications.
Concha Bullosa
The middle turbinate plays a significant role in the proper drainage system
of the maxillary sinus. Normally, this bony structure is lined by nasal
respiratory mucosa. A variation of the middle turbinate is a concha bullosa,
which is a pneumatization (air bubble) within the middle turbinate. The
most ideal CBCT image to diagnose a concha bullosa is a coronal image. This
variant has been shown to be present in approximately 4% to 15% of the
population (Fig. 13.10A–B).22
Ostium blockage.
When a concha bullosa is present, the implant clinician should carefully
confirm the patency of the maxillary ostium and any pathology in the
maxillary sinus. A concha bullosa may decrease the size of the middle
meatus, interfering with normal mucociliary flow out of the maxillary sinus.
Normally, this variant does not require surgical correction unless patency
issues are present for which ENT evaluation and correction are indicated.
Usually, corrective surgery includes a turbinectomy, which is the turbinate
being reduced in size by endoscopic nasal surgery.
Paradoxical Middle Turbinate
Another variant within the middle turbinate is a paradoxically curved middle
turbinate, which presents as a concavity toward the septum (backwards),
decreasing the size of the meatus. Normally, the convex side of the middle
turbinate will be oriented towards the midline or septum. A paradoxical
middle turbinate is most easily seen on a CBCT coronal image with a
prevalence of approximately 26% (Fig. 13.10C).
Ostium blockage.
When present, the implant clinician should carefully confirm the patency of
the maxillary ostium and any pathology in the maxillary sinus. The
paradoxical middle turbinate may place pressure on the uncinate process,
leading to a non-patent maxillary sinus ostium. A paradoxical middle
turbinate may decrease the size of the middle meatus, interfering with
normal flow out of the maxillary sinus.
Uncinate Process Variants

A deflected uncinate process (either laterally or medially) can narrow the
ethmoid infundibulum, which affects the patency of the osteomeatal
complex. Perforations may also be present within the uncinate process,
leading to communication between the nasal cavity and ethmoid
infundibulum. In addition, the uncinate process may be pneumatized and is
a common area for ENT intervention in the treatment of chronic
rhinosinusitis.
Ostium blockage.
A deflected uncinate process may lead to narrowing of the flow out of the
ostium, causing patency issues. When present, the implant clinician should
carefully confirm the patency of the maxillary ostium and any pathology in
the maxillary sinus. A deflected uncinate process may decrease the size of the
middle meatus, interfering with normal flow out of the maxillary sinus. This
may lead to post-operative complications after implant or bone graft surgery
in the maxillary sinus.
Haller Cells
Haller cells, also known as infraorbital ethmoidal air cells or
maxilloethmoidal cells, are pneumatized ethmoidal air cells. They project
from the orbital floor and arise most often from the anterior ethmoids in
approximately 34% of the population.23 Hallers cells are most easily seen on
coronal images.
Increased incidence of rhinosinusitis.
In most cases, Haller cells are asymptomatic and generally are associated
with an increased incidence of rhinosinusitis. They may become infected and
potentially extend into the orbit. Additionally, Haller cells may compromise
the patency of the maxillary sinus ostium and also have been associated with
chronic polypoid disease, which both may compromise and predispose to
postsurgical disease (Fig. 13.11).
FIG 13.11 Haller cells. The arrows define Haller cells, which are air cells beneath
the ethmoid bulla and along the roof of the maxillary sinus. This anatomical variant
may compromise the mucociliary drainage of the maxillary sinus.
Supplemental Ostia
A supplemental ostium or secondary ostia may occur between the maxillary
sinus and the middle meatus, which is often found in the posterior
fontanelles (PF). The prevalence of supplemental or accessory ostia is
approximately 18% to 30%. On occasion, these secondary ostia may be
encountered during the membrane elevation off of the medial wall of the
antrum, prior to placement of the sinus graft.
Recirculation.
Because these secondary openings are usually located posterior and inferior
to the natural ostium, they may predispose the patient to rhinosinusitis by
the recirculation of infected secretions from the primary meatus back into
the sinus cavity. The presence of supplemental ostia may increase morbidity
for maxillary sinus graft patients. When observed, a piece of collagen is
placed over the site to prevent graft material from entering the nasal cavity.
Maxillary Hypoplasia
Hypoplasia of the maxillary sinus may be a direct result of trauma, infection,
surgical intervention, or irradiation to the maxilla during the development of
the maxillary bone. These conditions interrupt the maxillary growth center,
which produces a smaller than normal maxilla. The negative pressure within
the maxillary sinus resulting from chronic ostial obstruction impedes the
pneumatization process of the sinus, resulting in hypoplasia. Usually, a
malformed and positioned uncinate process is associated with this disorder,
leading to chronic sinus drainage problems. Maxillary sinus hypoplasia has
been reported in 1.73% to 10.4% of patients with sinus symptoms; however, it
is sometimes asymptomatic.24
Predisposition to disease.
Although patients with hypoplastic maxillary sinuses exhibit a greater
incidence of sinus pathology and clearance issues, the impact on the
placement of implants in this area is negligible. Because of the smaller size of
the sinus, there is a greater volume of available bone, negating the need for
augmentation procedures. Usually, implant placement may be completed
well below the inferior border of the sinus (Fig. 13.12).
FIG 13.12 Hypoplastic maxillary sinus has a high incidence of associated
pathology (arrow); however, it will usually have adequate bone for implant
placement.
Inferior Turbinate and Meatus Pneumatization (Big-Nose

Variant)
A rare anatomic variant, which has a significant impact on implant treatment
planning, is an inferior meatus pneumatization, or big-nose variant. When
the nasal cavity pneumatizes posteriorly, it will reside over the alveolar
residual ridge. This condition is most likely seen on a CBCT panoramic
image. The prevalence of this condition has been documented to be
approximately 3%.
Lack of bone for implant placement.
When the patient has this condition, the maxillary sinus is lateral to the
edentulous ridge. When inadequate bone height is present below this
structure, a sinus graft does not increase available bone height for an
implant. If a clinician is unaware of this variant, the implant may
inadvertently be placed into the nasal cavity above the residual ridge and has
been shown to penetrate the inferior meatus and contact the inferior
turbinate. A sinus graft is usually contraindicated with this patient condition
because the sinus is lateral to the position of the implants. Instead, an onlay
graft is required to increase bone height and width (Fig. 13.13).
FIG 13.13 Inferior meatus pneumatization (big-nose variant) exhibiting extension of
the nasal cavity posterior.
Pathology
Pathologic conditions associated with the paranasal sinuses are common
ailments and afflict more than 31 million people each year. Approximately 16
million people will seek medical assistance related to rhinosinusitis, yet it is
one of the most commonly undiagnosed diseases in clinical practice.
Potential infection in the region of the sinuses may result in severe
complications such as chronic rhinosinusitis, orbital cellulitis, meningitis,
osteomyelitis, and cavernous sinus thrombosis. In fact, paranasal sinus
infections account for approximately 5% to 10% of all brain abscesses
reported each year.25
A preexisting, pathologic, maxillary sinus condition is a contraindication
for many procedures that alter the sinus floor before or in conjunction with
sinus grafting and/or implant insertion. The risk of postoperative infection is
elevated and may compromise the health of the implant and the patient.
Pathologic conditions, either preoperative or postoperative, of a maxillary
sinus should be evaluated, diagnosed, and treated if indicated.
Pathologic conditions of the maxillary sinus may be divided into five
categories: (1) inflammation, (2) cystic conditions, (3) neoplasms, (4) fungal,
and (5) antroliths/foreign bodies. Studies have shown approximately 45% of
the asymptomatic population has a subclinical pathologic condition in the
maxillary sinus. A study completed at the Misch International Implant
Institute evaluated over 1000 consecutive prospective candidates for
maxillary sinus augmentations. The results concluded 32.7% of asymptomatic
patients had maxillary sinus pathologic conditions on CBCT scan evaluation.
Because of this high incidence, it is highly recommended that a thorough
radiographic evaluation be completed on all prospective sinus elevation
patients (Fig. 13.22).
FIG 13.22 Summary of most common pathologic conditions.
Inflammatory
Odontogenic Sinusitis (Periapical Mucositis)
Odontogenic rhinosinusitis occurs when the maxillary sinus membrane is
violated by infection of teeth or pathologic lesions of the jaws. The intimate
approximation of the roots of the maxillary posterior teeth to the floor of the
sinus may result in inflammatory changes of the periodontium or
surrounding alveolar bone. These changes may initiate the development of
pathologic conditions in the maxillary sinus.
Etiology.
Odontogenic rhinosinusitis is caused by a periapical abscess, cyst,
granuloma, or periodontal disease that results in an expansile lesion within
the floor of the sinus. Other causes include sinus perforations during
extractions and foreign bodies (e.g., gutta-percha, root tips, amalgam).
Odontogenic rhinosinusitis is often polymicrobial, with anaerobic
streptococci, Bacteroides spp, Proteus spp, and coliform bacilli being involved.
Studies have reported that approximately 30% to 40% of chronic sinusitis
cases may have some odontogenic origin when teeth are present in the
posterior maxilla.26 Approximately 42% of the time, one or more roots of the
maxillary first molar root will protrude into the sinus cavity along with 40%
of second molars roots.27
Periodontitis may produce generalized sinus mucosal hyperplasia, which is
seen as a radiopaque band that follows the contours of the sinus floor. A
localized periapical mucositis reveals a thickening of the mucous membrane
adjacent to the offending tooth and, on occasion, a perforation through to the
floor of the sinus. This radiographic appearance has been termed a halo
effect (Fig. 13.14A).
FIG 13.14 (A) Odontogenic rhinosinusitis exhibiting mucosa thickening with the
presence of bony septa (arrow). (B) Thickened mucosa generalized on the inferior
floor of the sinus.
Odontogenic rhinosinusitis presents with a thickening of the mucous
membrane adjacent to a diseased tooth exhibiting a radiographic radiopaque
band. This condition may be confused with acute rhinosinusitis or mild
mucosal thickening. However, in odontogenic rhinosinusitis, the patient has
teeth in the posterior maxilla and will usually exhibit symptoms related to
the teeth (e.g., pain from a posterior tooth or a recent extraction, exudate
around the existing natural posterior teeth).
Treatment.
Before sinus augmentation or implant placement, the tooth or teeth involved
should be treated periodontally or endodontically, or extracted. After
intraoral soft tissue healing and resolution of the pathologic condition, the
sinus graft procedure may be performed with minimal risk of postoperative
complications. A CBCT scan should be taken approximately 12–16 weeks
postoperatively to determine sinus status, including sinus ostium patency.
Acute Rhinosinusitis
The most common sinusitis in the maxillary sinus is a nonodontogenic
pathologic condition resulting in inflammation and infection termed acute
rhinosinusitis. The signs and symptoms of acute rhinosinusitis are rather
nonspecific, making it difficult to differentiate from the common cold,
influenza type of symptoms, and allergic rhinitis. Usually patients will
present with symptoms such as purulent nasal discharge, facial pain and
tenderness, nasal congestion, and possible fever. Acute maxillary
rhinosinusitis results in 22 to 25 million patient visits to physicians in the
United States each year, with a direct or indirect cost of 6 billion US dollars.25
Etiology.
Acute rhinosinusitis is an inflammatory process that extends from the nasal
cavity after a viral upper respiratory infection. Microbiologic cultures have
shown the most common pathogens causing acute rhinosinusitis to be
Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.
These pathogens include approximately 20% to 27% beta-lactamase–resistant
bacteria. Staphylococcus aureus has also been cited with the microbiology of
acute rhinosinusitis. However, this pathogen is usually seen only in
nosocomial (hospital-induced) sinusitis and is unlikely to be seen in elective
sinus graft patients.
The most important factor in the pathogenesis of acute rhinosinusitis is
the patency of the ostium.28 Mucous production within the sinus is usually
abnormal in quality or quantity, along with a compromised mucociliary
transport. In an occluded sinus, an accumulation of inflammatory cells,
bacteria, and mucus exists. Phagocytosis of the bacteria is impaired with
immunoglobulin (Ig)-dependent activities decreased by the low
concentration of IgA, IgG, and IgM found in infected secretions.
The oxygen tension inside the maxillary sinus has significant effects on
pathologic conditions. When the oxygen tension in the sinus is altered,
rhinosinusitis occurs. Growth of anaerobic and facultative organisms
proliferate in this environment. Many factors may alter the normal oxygen
tension within the sinuses. A direct correlation exists between the ostium
size and the oxygen tension in the sinus. In patients with recurrent episodes
of sinusitis, oxygen tension is often reduced, even when infection is not
present. As a consequence, a history of recurrent acute rhinosinusitis is
relevant to determine whether an implant may be at increased risk when
inserted at the same time as the sinus graft.
The radiographic hallmark in acute rhinosinusitis is the appearance of an air-
fluid level. A line of demarcation will be present between the fluid and the air
within the maxillary sinus. If the patient is supine (CBCT), the fluid will
accumulate in the posterior area; if the patient is upright during the imaging,
the fluid will be seen on the floor and be horizontal. Additional radiographic
signs include smooth, thickened mucosa of the sinus, with possible
opacification. In severe cases, the sinus may fill completely with supportive
exudates, which gives the appearance of a completely opacified sinus. With
these characteristics the terms pyocele and empyema have been applied (Fig.
13.15A–B).
FIG 13.15 (A) Axial CT scan shows an air-fluid level in the right antrum. The
attenuation of this fluid is less than that of muscle and typically is watery sinus
secretions. This could represent an acutely obstructed sinus, a sinus with poor
drainage in a chronically supine (unconscious) patient, or a patient who had a recent
antral washing for sinusitis. (B) Coronal CT scan shows a typical air-fluid level in the
left antrum with minimal mucosal thickening and obstruction of the ostiomeatal unit.
Some mucosal disease is also present in the left ethmoid and right maxillary
sinuses. Clinically, this patient had acute sinusitis. (C) Chronic rhinosinusitis may
result in a completely opacified maxillary sinus. (A–B, From Som PM, Curtin HD: Head and
neck imaging, ed 5, St. Louis, 2011, Mosby.)
Radiographically, the appearance of an air-fluid level is present with acute
rhinosinusitis. The differential diagnosis of acute rhinosinusitis and
prolonged viral upper respiratory infection are very similar. However, a
classic air-fluid level in the maxillary sinus will give rise to the confirmation
of acute rhinosinusitis. Additionally, viral rhinosinusitis will usually improve
within 7–10 days, whereas acute bacterial rhinosinusitis most likely will
persist for longer than 10 days.29
Treatment.
Because acute rhinosinusitis is one of the most common health problems
today, patients having sinus augmentation procedures should be well
screened for a past history and current symptoms. Even though acute
rhinosinusitis is a self-limiting disease, a symptomatic patient should be
treated and cleared by the physician before grafting procedures. These
patients are also more prone to postoperative rhinosinusitis. As a result, a
more conservative approach is to complete the sinus graft and allow for
several months of healing before the placement of the implant.
Chronic Rhinosinusitis
Chronic rhinosinusitis is a term used for a sinusitis that does not resolve in 6
weeks and also has recurrent episodes. It is the most common chronic
disease in the United States, affecting approximately 37 million people.
Symptoms of chronic sinusitis are associated with periodic episodes of
purulent nasal discharge, nasal congestion, and facial pain.
Etiology.
As maxillary rhinosinusitis progresses from acute to chronic, anaerobic
bacteria become the predominant pathogens. The microbiology of chronic
rhinosinusitis is very difficult to determine because of the inability to achieve
accurate cultures. Studies have shown that possible bacteria include
Bacteroides spp, anaerobic gram-positive cocci, Fusobacterium spp, as well as
aerobic organisms (Streptococci spp, Haemophilus spp, Staphylococcus spp).30 A
recent Mayo Clinic study showed that in 96% of patients with chronic
sinusitis, active fungal growth was also present.31
Chronic rhinosinusitis may appear radiographically as thickened sinus
mucosa, complete opacification of the antrum, and/or sclerotic changes in the
sinus walls (which give the appearance of denser cortical bone in the lateral
walls). Chronic rhinosinusitisis is usually diagnosed from coronal CBCT
images.
Treatment.
Medical evaluation and clearance by a physician experienced in sinus
pathology is highly recommended for patients with chronic maxillary
rhinosinusitis before sinus grafting because significant bacterial resistance
and fungal growth is highly probable. Fungal infections may be difficult to
treat and control, and serious complications may result in postoperative
sinus graft patients. It is imperative that chronic rhinosinusitis patients be
cleared by an ENT because these types of patient may be contraindicated for
sinus graft surgery (Fig. 13.15C).
Allergic Rhinosinusitis
Etiology.
Allergic rhinosinusitis is a local response within the sinus caused by an
irritating allergen in the upper respiratory tract. This allergen may be a cause
of acute or chronic rhinosinusitis. This category of sinusitis may be the most
common form, with 15% to 56% of patients undergoing endoscopy for
sinusitis showing evidence of allergy. This condition often leads to chronic
sinusitis in 15% to 60% of patients.32 The sinus mucosa becomes irregular or
lobulated, with resultant polyp formation.
Polyp formation related to allergic rhinosinusitis is usually characterized by
multiple, smooth, rounded, radiopaque shadows on the walls of the maxillary
sinus. Most commonly, these polyps are located near the ostium and are
easily observed on a CT or CBCT examination. In advanced cases, ostium
occlusion, along with displacement or destruction of the sinus walls may be
present, with a radiographic image of a completely opacified sinus.
Treatment.
Special attention must be given to these patients to ensure a patent ostium
and lack of bacterial resistance. Close postoperative supervision is highly
recommended. The polyp, if enlarged, may be removed before the sinus graft
by an ENT. This may be performed through an anterior Caldwell-Luc
approach or by an endoscopic procedure through the ostium.
Allergic rhinosinusitis patients often have a greater risk of complications
related to an increase in allergen production. Because sinus grafting is an
elective procedure, the time of year for the surgery may be altered to
decrease the postoperative infection risk. For example, if hay fever or a grass
allergy is related to the patient's sinusitis, the sinus graft surgery should be
performed in the season or seasons that have least risk to aggravate the sinus
mucosa (i.e., winter or fall) (Fig. 13.16).
FIG 13.16 (A) Allergic rhinosinusitis with classic polyp formation; polypoid
pathology circumferentially on sinus walls. (B) Surgical removal of polyps.
Cystic Lesions
Cystic lesions are a common occurrence in the maxillary sinus, and studies
have reported a prevalence range of 2.6% to 20%.34 They may vary from
microscopic lesions to large, destructive, expansile pathologic conditions,
which include pseudocysts, retention cysts, primary mucoceles, and
postoperative maxillary cysts.
Pseudocysts (Mucous Retention Cyst)

The most common cysts in the maxillary sinus are mucous retention cysts.
After much controversy, in 1984, Gardner35 distinguished these cysts into two
categories: (1) pseudocysts and (2) retention cysts. Pseudocysts are more
common and are of much greater concern during sinus graft surgery,
compared with retention cysts. Pseudocysts reoccur in approximately 30% of
patients and are often unassociated with sinus symptoms. As a consequence,
many physicians do not treat these lesions. However, when their size is larger
than 10 mm in diameter, pseudocysts may occlude the maxillary ostium
during a sinus graft procedure and increase the risk of postoperative
infection.
Etiology.
A pseudocyst is caused by an accumulation of fluid beneath the periosteum
of the sinus mucosa, which elevates the mucosa away from the floor of the
sinus, giving rise to a dome-shaped lesion. Pseudocysts have also been
termed mucosal cysts, serous cysts, and nonsecreting cysts. Damage to the
capillary walls from bacterial toxins (e.g., diseased tooth) results in the loss of
intravascular proteins and fluid. The accumulation of the exudate in the
connective tissue forms areolar spaces that will coalesce into a single cavity
that is lined by fibroblasts, not from epithelium. Thus, pseudocysts are not
true cysts because they lack an epithelial lining. The cause of the fluid is
bacterial toxins from the sinus mucosa or from odontogenic sources.
Histologically, the pseudocyst appears as a smooth, light blue, translucuent
structure filled with a thin, clear, yellowish fluid.35a
Pseudocysts are depicted radiographically as smooth, homogenous, dome-
shaped, round to ovoid, well-defined radiopacities. Pseudocysts do not have a
corticated (radiopaque) marginal perimeter and are always located on the
floor of the sinus cavity (Fig. 13.17A–B). In rare cases, the pseudocyst can
completely opacify the sinus cavity.
FIG 13.17 (A–B) Pseudocyst depicting classic dome shaped lesion on the sinus
floor.
Treatment.
Pseudocysts are usually not a contraindication for sinus graft surgery. If a
large pseudocyst is present, the elevation of the membrane during a sinus
graft may raise the cyst to occlude the ostium. In addition, on elevation or
placement of the grafting material, the cyst may be perforated, allowing fluid
within the cyst to contaminate the graft. Large cysts of this nature should be
drained and allowed to heal before or in conjunction with sinus elevation
surgery. Most often, an ENT physician should evaluate this condition before
the sinus graft. If a pseudocyst is less than 8 mm, less concern is needed and
the fluid may be drained in conjunction with sinus grafting, depending on
the surgeon's experience in the treatment of this condition. This should be
accomplished with care to prevent membrane perforation. A strict recall
evaluation of these previously infected areas following sinus graft surgery is
in order because reoccurrence of a pseudocyst is common. Many studies have
shown the successful placement of dental implants in conjunction with the
presence of pseudocysts.35b-d In rare cases, the pseudocyst may present with
clinical symptoms such as headache or pain that may require surgical
intervention.
Retention Cysts
The second type of mucous retention cyst is termed a retention cyst.
Retention cysts may be located on the sinus floor, near the ostium, or within
antral polyps. Because they contain an epithelial lining, researchers consider
them to be mucous secretory cysts and “true” cysts. Retention cysts are often
microscopic in size.
Etiology.
Retention cysts result from partial blockage of seromucinous gland ducts
located within the connective tissue underlying the sinus epithelium. As the
secretions collect, they expand the duct, producing a cyst that is
encompassed by respiratory or cuboidal epithelium. They may be caused by
sinus infections, allergies, or odontogenic conditions.
Retention cysts are usually very small and not seen clinically or
radiographically. In rare instances, they may achieve adequate size to be seen
in a CT image and may resemble the appearance of a small pseudocyst.
Treatment.
No treatment for retention cysts exists before or in conjunction with a sinus
graft and/or implant insertion.
Primary Maxillary Sinus Mucocele

A primary mucocele is a cystic, expansile, destructive lesion that may include
painful swelling of the cheek, displacement of teeth, nasal obstruction, and
possible ocular symptoms.36
Etiology.
The primary mucocele arises from blockage of the maxillary ostium by
fibrous connective tissue. Because of the compromised drainage, the mucosa
expands and herniates through the antral walls. The primary mucocele is
classified as a cyst because of the epithelial lining, which contains mucin. As
the mucoid secretions increase, the protein content of the cyst results in the
molality increasing, which attracts more fluid to the lesion. As the
hydrostatic pressure increases, the mucocele becomes elevated, resulting in
pressure necrosis and bony erosion.35a
In the early stages, the primary mucocele involves the entire sinus and
appears as an opacified sinus. As the cyst enlarges, the walls become thin
and eventually perforate. In the late stages, destruction of one or more
surrounding sinus walls is evident (Fig. 13.18).
FIG 13.18 (A) Primary maxillary sinus mucocele. Classic radiographic signs of
opacified sinus with expansion of the bony walls. (B) Secondary mucocele (surgical
ciliated cyst). (C) Blade implant removed with cystic tissue identified to be a surgical
ciliated cyst.
Treatment.
This type of lesion requires ENT evaluation and treatment. Surgical removal
(e.g., enucleation) of this cyst is indicated before any bone augmentation
procedures.
Postoperative Maxillary Cyst (Secondary Mucocele)

A postoperative maxillary cyst of the maxillary sinus is a cystic lesion that
usually develops secondary to a previous trauma or surgical procedure in the
sinus cavity. It has also been termed a surgical ciliated cyst, postoperative
maxillary sinus mucocele, or a secondary mucocele.37
Etiology.
A postoperative maxillary cyst develops as a direct result of trauma or past
history of surgery within the maxillary sinus. The cyst is derived from the
antral epithelium and mucosal remnants that previously were entrapped
within the prior surgical site. This separated mucosa results in an
epithelium-lined cavity in which mucin is secreted. The antrum becomes
divided by a fibrous septum in which one part drains normally, whereas the
other part is composed of the mucocele. It is relatively rare in the United
States; however, it constitutes approximately 24% of all cysts in Japan, mainly
due to a high incidence of rhinosinusitis.
The cyst radiographically presents as a well-defined radiolucency
circumscribed by sclerosis. The lesion is usually spherical in the early stages,
with no bone destruction. As it progresses, the sinus wall becomes thin and
eventually perforates. In later stages, it will appear as two separated
anatomic compartments (Fig. 13.18B–C).
Treatment.
Surgical ciliated cysts should be enucleated before any bone augmentation
procedures. If observed after the sinus graft, they should be enucleated and
regrafted for future implant placement.
Neoplasms
Maxillary sinus neoplasms are relatively rare in United States and are more
common in Asia and Africa. They comprise less than 1% of all malignancies,
with poorly differentiated squamous cell carcinoma being the most common.
Most neoplasms of the maxillary sinus remain asymptomatic and sometimes
will mimic rhinosinusitis.37a
Etiology.
Primary malignant tumors within the maxillary sinus are usually caused by
squamous cell carcinomas or adenocarcinomas. Signs and symptoms of
malignant disease are related to the surrounding sinus wall that the tumor
invades and includes swelling in the cheek area, pain, anesthesia or
paresthesia of the infraorbital nerve (e.g., anterior wall), and visual
disturbances (e.g., superior wall). These tumors in the sinus are usually
nonspecific and give rise to a variety of consequences, including opacified
sinuses, soft tissue masses in the sinus, as well as sclerosis, erosion, or
destruction of the walls of the sinus. Sixty percent of squamous cell
carcinomas of the paranasal sinuses are located in the maxillary sinus,
usually in the lower one half of the antrum. Clinical signs in the oral cavity
reflect the expansion of the tumor and an increased mobility of the involved
teeth. Invasion of the infratemporal fossa is also possible. 25
Radiographic signs of neoplasms may include various-sized radiopaque
masses, complete opacification, or bony wall changes. A lack of a posterior
wall on a radiograph should be a sign of possible neoplasm (Fig. 13.19).
FIG 13.19 Squamous cell carcinoma. (A–B) Carcinomas showing radiopaque
lesions extending into the walls.
Treatment.
Any signs or symptoms of a lesion of this type should be immediately
referred for medical consultation. Implant placement or sinus grafts in areas
affected by neoplasms are contraindicated.
Fungal Rhinosinusitis (Eosinophilic Fungal

Rhinosinusitis)
Granulomatous rhinosinusitis is a very serious (and often overlooked)
disorder within the maxillary sinus. Patients who have fungal rhinosinusitis
are thought to have had an extensive history of antibiotic use or chronic
exposure to mold or fungus in the environment, or are
immunocompromised. The most common classification of fungal
rhinosinusitis includes: (1) invasive and (2) noninvasive, which is based on
histopathological evaluation of the fungi. The invasive classification includes:
(1) acute invasive (fulminant), (2) granulomatous invasive, and (3) chronic
invasive. The noninvasive diseases include: (1) saprophytic fungal infestation,
(2) fungal ball, and (3) fungus-related eosinophilic.37b
Etiology.
Fungal infections are usually caused by aspergillosis, mucormycosis, or
histoplasmosis.33 Chronic rhinosinusitis patients should always be evaluated
for granulomatous conditions, because a high percentage of fungal growth
exists in this patient population. Of concern in these patients is that
eosinophils are activated that release major basic protein (MBP) into the
mucus, which attacks and destroys the fungus. However, this results in the
membrane being irritated and possibly irreversibly damaged, which allows
bacteria to proliferate.
Three possible clinical signs may differentiate fungal sinusitis from acute or
chronic rhinosinusitis: (1) no response to antibiotic therapy; (2) soft tissue
changes in sinus associated with thickened reactive bone, with localized
areas of osteomyelitis; (3) association of inflammatory sinus disease that
involves the nasal fossa and facial soft tissue. In some cases, a positive
diagnosis may require mycologic and histologic studies.
Fungal rhinosinusitis is usually unilateral (78% of cases) with bony
destruction being very rare. Within the sinuses, the presence of mild
thickening to complete opacification may be present. In most cases, varying
degrees of density (“double-densities”) are seen (Fig. 13.20).
FIG 13.20 Fungal rhinosinusitis with radiopaque fungal ball (arrow).
Treatment.
Patients with a history or current knowledge of fungal rhinosinusitis should
be referred to their physician or otolaryngologist for treatment and surgical
clearance. Treatment usually involves debridement and therapy with an
antifungal agent, such as amphotericin B. The history of fungal rhinosinusitis
contraindicates elective sinus graft surgery in many cases.
Antroliths
Maxillary Sinus Antroliths
Maxillary sinus antroliths are the result of complete or partial encrustation of
a foreign body that is present in the sinus. These masses found within the
maxillary sinus originate from a central nidus, which can be endogenous or
exogenous.38
Etiology.
The majority of endogenous sources are of dental origin, including retained
roots, root canal sealer, fractured dental instruments, and dental implants.
Additionally, bone spicules, blood, and mucus have been reported to cause
antroliths. Reports in the literature of exogenous sources include paper,
cigarettes, snuff, and glue.39 Although most antroliths are asymptomatic,
they often are associated with rhinosinusitis.
The radiographic appearance of a maxillary antrolith resembles either the
central nidus (e.g., retained root, dental implant) or appears as a radiopaque,
calcified mass within the maxillary sinus (Fig. 13.21A–B).
FIG 13.21 Antroliths. (A) Foreign body (reline material) that has become calcified.
(B–E) Tooth root antrolith. (F) Migrated implant into the maxillary sinus proper.
Because the calcified antrolith is composed of calcium phosphate (CaPO4),
calcium carbonate salts, water, and organic material, it will be considerably
more radiopaque than an inflammatory or cystic lesion.40 The central nidus of
the antrolith is similar to its usual radiographic appearance.
Treatment.
Before sinus augmentation and implant placement, the antrolith should be
surgically removed. If rhinosinusitis exists, the sinus cavity should be
allowed to heal completely before sinus augmentation procedures. In rare
asymptomatic situations, the antrolith may be removed, sinus membrane
opening sealed, and sinus graft performed at the same surgery.
Treatment Plan Complications
Not Taking CBCT
In implant dentistry today, a thorough CBCT evaluation of the paranasal
sinuses should be completed before placement of implants in the posterior
maxilla that violates the maxillary sinus. Of utmost importance is the
evaluation and confirmation of ostium patency. Many factors may preclude
the sinus to ostium blockage, including pathology, anatomic variants, and
foreign bodies. An implant clinician performing sinus augmentation
procedures should become well versed in identifying these occurrences
during CBCT examination.
If implant placement or bone graft procedures are indicated in the posterior
maxilla that will violate the maxillary sinus proper, the superior limits of the
CBCT should include the ostium to verify patency. If the scan is limited in the
superior positioning, ostium patency cannot be accurately ascertained. If
pathology is present, the scan will be useless for ENT evaluation if the
ostium evaluation is inadequate. This will most likely necessitate a new scan
ordered by the ENT.
Treatment Planning Away From Augmentation

Many doctors place themselves at risk when they treatment plan “away” from
the maxillary sinus. Because of the inherent disadvantages of the posterior
maxilla (e.g., poor bone density, inadequate bone quantity, higher occlusal
forces), a decreased success rate and increased implant morbidity exists,
especially if treatment plans are compromised. Some of the most common
treatment options that would be a compromise would include mini-implants,
shorter implants, placing implants at a nonideal angle to avoid the sinus, and
zygomatic implants.
These methods are not without their own pitfalls because they pose
biomechanical dilemmas to the implant in the prosthetic phase (Fig. 13.23).
FIG 13.23 Treatment planning to avoid the sinus. (A) Avoiding the sinus via
posterior placement and angulation resulting in a significant cantilever which
predisposes to a biomechanical failure. (B) Shorter implants. (C) Placement into the
sinus without grafting.
In 1984, Misch postulated various treatment approaches to the posterior
maxilla based on the amount of bone below the antrum, and later to include
the available bone width that was related to implant design (Fig. 13.24).41 In
the Misch SA (Sinus Augmentation) classification, the treatment modality is
dependent on the available bone height between the floor of the antrum and
the crest of the residual ridge in the region of the ideal implant locations. The
SA protocol also suggested a surgical approach, ideal bone graft material
(layering technique), and a timetable for healing before prosthetic
reconstruction.
FIG 13.24 Misch sinus grafting treatment plans. (A) SA-1: implant placement
without entering the maxillary sinus proper (blue), SA-2: implant placement with
minimal penetration into the maxillary sinus, (B) SA-3I: Implant placement at the
same time as sinus augmentation, (C–D) SA-4: lack of host bone (<5 mm) requires
bone grafting prior to implant placement.
SA-1.
The first Misch SA treatment option, SA-1, occurs when sufficient bone
height is available to permit the placement of endosteal implants following a
conventional surgical protocol. Because the quality of bone in the posterior
maxilla often is D3 or D4 bone (poorer quality), bone compaction to prepare
the implant site is common. The use of osteotomes allow for the osteotomy
site to be increased in size while allowing for the bone to be laterally
compacted. This permits a more rigid initial fixation of the implant and also
increases the bone implant contact (BIC) after initial healing.
Because the maxillary sinus is not violated and the physiology is not
changing during an SA-1 approach, it is less critical to evaluate the sinus
before implant insertion. The contraindications for sinus graft surgery (e.g.,
maxillary sinus pathology) do not apply for implant insertion when adequate
bone is present below the sinus for implants of adequate size to support the
load of the prosthesis. Although a common axiom in implant dentistry is to
remain 2 mm or more from an opposing landmark, this is not necessary in
the SA region.
Endosteal implants in the SA-1 category are allowed to heal in a
nonfunctional environment for approximately 4 to 8 months, which mainly is
dependent on the bone density, type of bone graft material, and quantity of
graft needed. Special care should be utilized in preventing premature
loading of the implants in the posterior maxilla because of the poor bone
quality. Therefore, the prosthetic interim prosthesis should be adjusted to
prevent overloading. After healing, the prosthetic phase of treatment should
include progressive loading, especially if the bone present is D3 or D4.
SA-2.
The second SA option in the Misch SA classification, SA-2, is selected when
10 to 12 mm of vertical bone is present (2 mm less than the minimum height
in SA-1). To obtain the 12 mm of vertical bone necessary for improved
implant survival (ideal implant length = 12 mm) in ridges of adequate width
(division A), the antral floor is partially elevated through the implant
osteotomy. The SA-2 surgical approach elevates the floor of the maxillary
sinus from 0–2 mm. Even though the sinus floor is minimally altered, this
will still change the physiology mucociliary clearance within the maxillary
sinus. A preexisting pathologic condition or nonpatent ostium of the sinus
should be addressed prior to implant placement because the implant site
may be subject to retrograde infection.
The endosteal implant osteotomy is prepared as determined by the density
of bone protocol, which is most commonly D3 bone. The depth of the
osteotomy is prepared approximately 1 to 2 mm short of the inferior floor of
the maxillary sinus. When in doubt of the height dimension, the osteotomy
should err on a shorter length to prevent the possibility of membrane
perforation. The implant osteotomy procedure should be continued to the
same depth (short of the antral floor), until the final width is obtained for
implant placement.
A flat-end or cupped-shape osteotome of the same diameter as the final
osteotomy is selected to infracture the floor of the sinus. Caution should be
exercised when selecting the appropriate osteotomes as sinus osteotomes are
a different shape than osteotomes used for bone spreading. The osteotome is
inserted and tapped firmly into the osteotomy in 0.5- to 1.0-mm increments
beyond the initial depth before reaching its final vertical position. This
should not extend more than 2 mm beyond the prepared implant osteotomy.
A slow, careful elevation of the sinus floor is less likely to perforate the sinus
mucosa. Because this technique ends with a greenstick-type of fracture, the
unprepared bone and sinus membrane over the broad-based osteotome will
be elevated to form the new sinus floor.
SA-3.
The third approach to the maxillary posterior edentulous region, SA-3, is
indicated when a minimum of 5 mm of vertical bone and sufficient width are
present between the antral floor and the crest of the residual ridge. SA-3
sinus augmentation consists of utilizing the Tatum lateral maxillary wall
approach and is performed superior to the residual alveolar bone within the
confines of the maxillary sinus. After the lateral-access window and
membrane are rotated in and upward to a superior position, a mixture of
autogenous bone and allograft (layered technique) material are placed in the
space previously occupied by the sinus. There are two types of sinus
augmentation techniques, the SA-3I (immediate) and SA-3D (delayed) (Box
13.1).
Box 13.1
SA-3 Immediate Vs. SA-3 Delayed Technique
Immediate Implant Placement (SA-3I)
When the endosteal implants are inserted at the same time as the sinus
graft, the following conditions should exist:
• Greater than 5 mm bone height
• Greater than 6 mm bone width

• D3 bone quality or better
• No sinus pathologic condition
• No history of recurrent sinusitis
• No relative contraindications
• No or small sinus membrane tear during surgery, completely sealed with

collagen
• No parafunction on removable soft tissue-borne prosthesis
Delayed Implant Placement (SA-3D)

Implants should not be inserted at the same time as the sinus graft when the
following conditions exist:
• Less than 6 mm bone width
• D4 bone quality
• Treated sinus pathologic condition within last few months
• History of recurrent sinusitis (especially when treated with recurrent

antibiotic medications)
• Relative contraindications (smoking, medically compromised patient)
• Medium to large tear in the sinus membrane during the graft surgery
• Parafunction on overlying removable prosthesis
SA-4.
In the fourth option for implant treatment of the posterior maxilla, SA-4, the
SA region for future endosteal implant insertion is first augmented, allowed
to heal, then implants are placed at a later date. This option is indicated
when less than 5 mm remains between the residual crest of bone and the
floor of the maxillary sinus. The SA-4 corresponds to a larger sinus cavity
along with less host bone on the lateral, anterior, and distal regions of the
graft because the antrum generally has expanded more aggressively into
these regions. The inadequate vertical bone in these conditions decreases the
predictable placement of an implant (i.e., insufficient bone for initial implant
fixation) at the same time as the sinus graft, and less recipient bone exists to
act as a vascular bed for the graft. Therefore, with fewer bony walls, a less
favorable vascular bed, minimal local autologous bone, and larger graft
volume, a longer healing period is mandated with a slightly altered surgical
approach.
Systemic Issues: Smoking

Smoking is known to be associated with an increased susceptibility to allergy
and infections because it interferes with the ciliary function and secretory
immunity of the nasorespiratory tract. In the maxillary sinus, this may have
effects on both immune exclusion and suppression because IgA and IgM
responses are reduced, whereas IgE responses are increased. Smoking is
believed to disturb bone graft healing because it reduces local blood flow by
increasing peripheral resistance and by causing increased platelet
aggregation.42 By-product chemicals of smoking, such as hydrogen cyanide
and carbon monoxide, have been shown to inhibit wound healing, as does
nicotine, which inhibits cellular proliferation. Tobacco may interfere directly
with osteoblastic function, and strong evidence exists of decreased bone
formation in smokers. In addition, smokers have a significant reduction of
bone mineral content. Bone mineral density can be reduced two to six times
in a chronic smoker. Overall, smoking may contribute to poor available bone
quality and poor healing capacity resulting from vascular and osteoblastic
dysfunction.
Smoking is a relative risk factor and has been linked to reduced implant
survival outcomes. In an 8-year follow-up study of 13,147 implants placed in
4316 patients, Busenlechner and colleagues43 found a threefold failure rate
increase in smokers compared with nonsmokers. In a recent systematic
review, Pjetursson and colleagues found there was almost twice the rate of
implant failures in smokers as compared with nonsmokers.44
Smoking may represent a relative contraindication because of the risk of
wound dehiscence, graft infection and/or resorption, and a reduced
probability of osseointegration. It is recommended, however, that if a
decision to proceed with surgery has been made, that patients refrain from
smoking at least 14 days before surgery (the time it takes for nicotine to be
cleared systemically) and 4 to 6 weeks after surgery. Patients may be referred
to their primary physician for the implementation of a smoking cessation
program. Moreover, smokers should sign a detailed informed-consent form
(both verbally and written) in which risks connected to smoking are clearly
explained (See Smoking Cessation Techniques in Chapter 2).
Inadequate Anesthesia: V2 Block
In sinus graft surgery, it is advantageous to anesthetize all structures in the
general area for the comfort of the patient and hemostasis. The maxillary
division of the trigeminal nerve (V2) exits through the foramen rotundum,
transverses in the pterygopalatine fossa anterior though the inferior orbital
fissure into the posterior maxilla. This nerve innervates all maxillary teeth,
gingival tissue, soft tissue of the midface, nasal cavity, and maxillary sinuses,
thus encompassing the entire area of interest for sinus graft surgery.
Technique
The technique for achieving anesthesia to all of the above structures with one
injection is via the greater palatine canal. The anesthetic needle is inserted
through the greater palatine foramen and is advanced into the inferior
portion of the pterygopalatine fossa. To assist in locating the greater palatine
foramen, an open-bore instrument (e.g., the rounded back end of a mouth
mirror handle) can be used to mark the location over the foramen. Pressure
is applied with this instrument along the palatal tissue, at the union of the
residual ridge and hard palate, in the region of the second molar
(approximately 1 cm lingual). The instrument will “fall into” a concavity,
which will mark the area over the foramen opening. A long, -inch needle is
introduced into the foramen from the opposite side of the mouth and
negotiates the canal for approximately 1 inch (depending on length of canal)
as anesthetic is slowly administered (Fig. 13.25).
FIG 13.25 (A) Greater palatine foramen. (B) Identification of the greater palatine
foramen via the end of a mirror handle, (C) V2 block anesthesia.
If improper needle positioning occurs, many complications may arise. Errors
in medial positioning can lead to nasal bleeding; a needle placed too superior
can cause diplopia; incorrect posterior placement can cause coughing;
incorrect placement also results in insufficient anesthesia at the surgical site.
Care should be made to prevent intravascular injections (aspiration), which
may lead to systemic effects and possible hematoma formation.
Incorrect Window Osteotomy Location

The overall design of the lateral-access window is determined after the
review of the CBCT scan, which helps determine the thickness of the lateral
wall of the antrum, the position of the antral floor from the crest of the ridge,
the location of teeth, as well as the presence of septa on the floor and/or walls
of the sinus. The main goal of window design and location is that the graft
MUST encompass the area in which future implants will be placed.
Lack of Grafting Area

If the outline of the window is not ideal, the final location of the graft
material will not encompass the area needed for future implant placement.
Implant placement will result in voids and lack of bone surrounding the
implants. This may lead to inadequate integration, loss of implants, or
migration of implants into the sinus proper.
Osteotomy Window Made Over Host Bone

If the window location and osteotomy is not made within the confines of the
sinus proper, the lateral window will not be able to be infractured. Therefore,
osteotomy preparation over host bone will not allow access to the sinus
cavity and membrane (Figs. 13.26 and 13.27). This results in extended surgical
time and removal of valuable host bone needed for initial implant stability
(e.g., inferior border).
FIG 13.26 (A) A panoramic radiograph of missing posterior teeth in the maxillary
left region; 5 to 10 mm of bone exists below the maxillary sinus floor. (B) The lateral
maxilla is reflected and reveals the zygomatic process, tuberosity, and lateral
maxilla. The Tatum access window is 2 to 5 mm above the antral floor, 2 to 5 mm
from the anterior wall, 15 mm long and 10 mm in height. (C) The carbide drill should
not perforate the lateral maxilla, which will tear the sinus membrane. A paintbrush
stroke is used to outline the access window. (D) A #4 to #6 diamond is used in a
straight or contraangle handpiece and deepens the score line of the access window
until a bluish hue or bleeding is observed.
FIG 13.27 Correct osteotomy location. (A) Implant sites should be planned out prior
to window osteotomy. Superior window cut should be 15 mm and parallel to the
residual ridge, and care should be taken to not remove the tuberosity less than 5
mm from the distal aspect of the most distal implant. (B) Osteotomy should always
be placed within the confines of the sinus; if made over host bone, window infracture
will not be able to be accomplished. (C) Always note the location of the adjacent
roots (arrow) to avoid damage and devitalization.
Damage to Existing Tooth Root

Caution should be exercised to make the window at least 2 millimeters from
any adjacent tooth root and within the sinus proper. Encroaching on a tooth
root may devitalize the tooth, leading to possible endodontic treatment or
internal/external resorption. It is not uncommon for this to occur with
dilacerations or multiple-rooted premolar teeth (see Fig. 13.27C).
Prevention
To ensure ideal bone grafting placement, an ideal window outline must be
performed.
Inferior.
The inferior score line of the rectangular access window on the lateral maxilla
is placed approximately 1–2 mm above the level of the antral floor. If the
inferior score line is made at or below the level of the antral floor, infracture
of the lateral wall will be very difficult, leading to possible membrane
perforation. If the inferior score line is made too high (>5 mm) above the
sinus floor, a ledge above the sinus floor will result in a blind dissection of
the membrane on the floor. This will lead to a higher incidence of membrane
perforation. The inferior osteotomy should follow the outline of the maxillary
sinus inferior border (Fig. 13.28B).
FIG 13.28 Inadequate fill. (A) Lack of anterior grafting resulting in a compromised
anterior site for implant placement. (B) Inferior, superior and medial defect. (C–D)
Lack of medial grafting resulting in implant placement in soft tissue. (E) Lack of
posterior bone grafting. (F) Lack of lateral bone grafting.
Superior.
The most superior aspect of the lateral-access window should be
approximately 15 mm superior to the alveolar crest. This will allow a buffer
zone of 3 mm, as the ideal length of an implant placed in a sinus graft is 12
mm. A soft tissue retractor (Seldin) placed above the superior margin of the
lateral-access window helps retract the facial flap and prevents the retractor's
inadvertent slip into the access window, which may damage the underlying
membrane of the sinus. The superior score line should always be parallel to
the alveolar crest (Fig. 13.28B).
Anterior.
The anterior vertical line of the access window is scored approximately 2–3
mm distal to the anterior vertical wall of the antrum. If the sinus access
window outline is difficult to determine in relation to the sinus cavity, it
should err over the antrum rather than over the bone around this structure.
Additionally, the anterior wall should always be identified to minimize a void
in the area of future implant placement. If the membrane is not released
from the anterior wall, an anterior defect may result. If a defect results,
remediation in this area is very difficult with a high degree of morbidity.
When teeth are present anteriorly, they made be used to determine the
exact location of the anterior vertical osteotomy location (Fig. 13.28A).
Posterior.
If the window location is not extended far enough posterior, future implant
placement may result in inadequate bone fill, leading to remediation or
change of implant site location to a less favorable location. The posterior
score line should extend approximately 5 mm distal to the last implant being
proposed. Care should be noted to make sure the window is far enough
distal to allow the implant to be encompassed in bone. Additionally, the
extent of tuberosity removal used for donor bone should be determined in
relation to the most distal implant site. The tuberosity harvest, if made too
close to the implant site, may compromise placement (Fig. 13.28E).
Aggressive Osteotomy Preparation

The osteotomy window should be prepared with either a #6 or #8 carbide or
diamond bur, or with a Piezosurgery unit. Care must be taken to slowly score
the outline of the osteotomy window while looking for the appearance of the
bluish-hued membrane. Once the membrane has been visualized, light
tapping on the bony window with the end of a mirror handle can alert the
clinician to areas where the lateral wall is still attached.
Complication
Not pausing to check for the mobility of the bony window can place the
clinician in danger of penetrating too deep within the lateral wall and
perforating the membrane. Perforating the membrane complicates the
procedure and increases the morbidity (Fig. 13.29A–B).
FIG 13.29 (A) Osteotomy outline with #8 diamond bur. The procedure should
include the use of a feather touch to minimize perforation. (B–D) A safer technique,
that minimizes perforation, is the use of piezosurgical unit.
Prevention
To prevent overpreparation of the osteotomy, the implant clinician should
select the ideal instrumentation for procedure. Usually, clinicians early on
their learning curve should utilize a piezotome unit for osteotomy
preparation. This technique has the least possibility of perforating the sinus
membrane. A carbide bur should be cautiously utilized, as this technique has
the highest possibility of membrane perforation.
Overfilling of the Sinus
The goal of the sinus bone graft is to obtain adequate vertical height of bone
to place endosteal implants with long-term success. The maximum length
requirement of an implant with adequate surface of design is rarely more
than 12 mm, and as a result the goal of the initial sinus graft is to obtain at
least 12 mm of vertical bone from the crest of the ridge. This usually requires
the bottom one half to one third of the sinus to be filled with graft material
because most sinuses approximate 35 mm in height. A CBCT scan (i.e., and
interactive treatment planning) of the sinus prior to surgery may be used to
estimate the amount of graft material required for the ideal volume of sinus
graft material. The average volume of the maxillary sinus is approximately 15
ml.45 Care should be noted to the amount of graft material placed into the
sinus.
Complication
Overfilling the sinus can result in blockage of the ostium, especially if
membrane inflammation or the presence of a thickened sinus mucosa exists.
This may lead to a chronic rhinosinusitis.
The majority of sinus graft overfills do not have postoperative
complications. If, however, a postoperative sinus infection occurs without
initial resolution, reentry and removal of a portion of the graft and changing
the antibiotic protocol may be appropriate (Fig. 13.30).
FIG 13.30 Overfilling of the sinus cavity with bone graft material may lead to
blockage of the ostium causing a rhinosinusitis.
Inadequate Fill: Density (Voids)

Postoperatively, voids in sinus grafts complicate and increase implant
placement morbidity. This situation may result in a soft tissue interface with
the implant and a decreased likelihood of success may result.
Prevention
When grafting after elevation of the membrane, a sinus syringe (or 1- or 3-ml
syringe) may be used to introduce the material into the sinus. The material
should be introduced in an inferior-anterior angulation in small increments
(most distant first). This will ensure the graft material is introduced to all
reflected areas. Introducing increments of a larger volume may result in
voids. Additionally, a serrated packing instrument should be used to pack the
bone until push-back resistance is achieved. Insufficient packing results in
voids, and excessive pressure results in too dense of a fill for blood vessel
integration and angiogenesis to occur.
Medial.
If the medial wall is not reflected, a resultant defect will result. Since implant
placement trajectory is usually angled to the medial, implant placement may
result in lack of bone around the implant. Additionally, the medial wall is a
significant resource for blood supply, allowing for better healing of the graft.
Care should be noted to make sure graft material is packed in a medial
direction to have contact with the medial wall.
Lateral.
The lateral wall should be grafted to at least the original contour. If not, a
defect will result in tissue invagination, which increases morbidity and
possible infection. This is why a membrane is placed over the lateral wall
after sinus graft augmentation: to minimize loss of graft material and
osseous regeneration to the original bony contour (Fig. 13.31).
FIG 13.31 Bone grafting voids. (A) Void in the center of the graft. (B) Void on the
floor of the sinus. (C) Graft material should be placed incrementally and packed
firmly with a serrated sinus graft packer. (D) Prevention of voids include grafting with
a syringe in an “inferior” and “anterior” direction, which minimizes the possibility of
intruding the graft material. (E) Incorrect technique grafting in a superior direction
which may lead to intruding the lateral wall with resultant grafting voids.
Aggressive Tuberosity Removal

The tuberosity is a common donor site to be used as a source of autogenous
bone with the layering technique of bone grafting. The use of autogenous
bone allows for more predictable bone growth and decreases healing time.
The addition of an autogenous component in sinus grafting is most
important when a lack of sufficient host bone is present (SA-4) because the
less host bone there is, the less blood will be supplied to the region for
healing. Tuberosity bone is ideal for sinus grafting because the cancellous
nature of this bone allows it to be moldable with less chance to migrate.
Correct Location.
The thicker soft tissue in the tuberosity region can mislead the assessment of
this donor site. The tuberosity area should be evaluated with a CBCT
examination, most easily measured on the coronal or panoramic image. The
anatomic limits of this area include the maxillary sinus, pterygoid plates,
adjacent teeth when present, and the greater palatine canal. A vertical
incision is made posteriorly at the lateral aspect of the maxilla. It extends
anteriorly across the tuberosity into the molar region. After reflection of a
mucoperiosteal flap, bone may be harvested from the tuberosity with a
rongeur, chisel, or trephine drill.
Exposure of Posterior Sinus Cavity.

Care should be used to not inadvertently expose the posterior sinus cavity
because of excessive bone removal. This may lead to oroantral
communication and possibly an opening for bacterial contamination, which
may increase the morbidity of the graft area.
Harvest Too Far Posterior.

Harvesting the tuberosity too far posterior may lead to potential bleeding
issues. This aggressive harvest may result in hemorrhage from the tributary
vessels of the pterygoid plexus, such as the deep facial vein or posterior
superior alveolar vessels. This can result in bleeding into the
pterygomaxillary and infratemporal spaces, which may result in a hematoma
via the inferior orbital fissure (Fig. 13.32).46
FIG 13.32 Tuberosity graft. (A) Bone is easily removed with double-action
rongeurs. (B) Cancellous bone grafted from tuberosity. (C) Note demarcation of the
donor site. Care should be exercised not to harvest too close to a planned implant
site. A bone track is placed in the location of the most distal implant site for ease of
site identification after graft healing. (D) Posterior area depicting the close
approximation of the infratemporal fossa, medial and lateral pterygoid plates.
SA-2 (Osteotome Technique) Complications

The SA-2 approach (also termed transalveolar approach, osteotome sinus floor
elevation, Summers technique, or the Crestal approach) may be considered a
more conservative and less invasive sinus grafting technique (Fig. 33.33). This
procedure is performed through the alveolar crest of the edentulous ridge at
the inferior border of the maxillary sinus. It involves elevating the sinus
membrane, creating a “tent” and providing space for graft placement. The
membrane is elevated and the area is grafted blindly, with the disadvantage
of an uncertainty of possible perforations of the sinus floor (Schneiderian)
membrane. The following are complications of this technique.
Patient Selection: Inadequate Bone

It is recommended that at least 10 mm of host bone be present below the
sinus for this technique. If inadequate height and width of bone is present,
rigid fixation is compromised, and the implant may become mobile and
possibly migrate into the sinus proper. Additionally, an oblique sinus floor,
septa, pathology, or nonpatent ostium may increase possible morbidity or
may contraindicate the osteotome technique.
Overpreparation of Osteotomy
Because of the poor bone quality present in the posterior maxilla (D4 Bone),
D4 type of bone, inadequate bone strength, along with lack of cortical bone,
alters the initial primary stability. Lack of stability leads to possible migration
or displacement of the implant into the maxillary sinus or surrounding areas.
Sinus Membrane Perforation

Because of the closed nature of this technique, perforation of the membrane
is usually impossible to determine (i.e., unless a postoperative CBCT
examination is performed). Because of irregular antral floors, septa,
adhesions, and pathology, tears in the membrane are definitely more
frequent than what most report. Perforation leads to possible infection and
morbidity of the graft and implant.
Access
Because of compromised interocclusal space, in some patients, closed sinus
graft procedures may be problematic because of access problems. To make
the surgery easier, bite blocks along with the use of off-angle osteotomes may
be used. Patient opening for a long period of time may lead to muscle
trismus or complications within the temporomandibular joint (TMJ).
Use of Incorrect Osteotomes
The use of straight osteotomes is not ideal because specially made (maxillary
posterior) offset osteotomes are designed to be more user-friendly and work
more efficiently. The use of piezoelectric osteotomy preparation allows for a
more controlled osteotomy with low perforation risk (Fig. 13.33).
FIG 13.33 SA-2 technique. (A) The subantral (SA)-2 technique begins with a pilot
bur to mark the implant site. (B) A 2-mm twist drill prepares the osteotomy 1 to 2
mm short of the sinus floor. (C) A final osteotomy width is sequentially obtained,
remaining 1 to 2 mm short of the antral floor. (D) A flat-ended osteotome, the same
diameter as the final osteotomy size, is used within the site. (E) A surgical mallet is
used to gently and slowly tap the osteotome 1 to 2 mm through the sinus floor. The
osteotome raises the floor and 1 to 2 mm of bone with the sinus mucosa over the
implant site. (F) An implant is inserted into the osteotomy and extends 0 to 2 mm
above the surgical sinus floor.
Final Osteotome Should Only Be Used Once
Entering the osteotomy multiple times leads to increasing the diameter of
the osteotomy and causing decreased primary stability. Usually, undersizing
the osteotomy allows for better fixation along with increasing the amount of
bone present at the implant interface. Poor bone quality (e.g., D4) can be
changed to a D3 or D2 via the osteotome technique.
Graft With Small Increments of Material

Grafting too much material at once will prevent the placement of the implant
into the osteotomy to full length. Ideally, no more than 0.2 cc of bone should
be placed at once, necessitating multiple osteotome grafting techniques.
Benign Paroxysmal Positional Vertigo

Benign paroxysmal positional vertigo (BPPV) has been shown to have a direct
correlation with osteotome sinus floor elevation.47 Studies have shown this
postoperative complication to be relatively high at 3%.48 From the pounding
and repeated force from the osteotomes, calcium carbonate crystals are
dislodged and settle in on the cupula of the semicircular canal
(cupulolithiasis). They strike nerve endings in the semicircular canals, which
produces position- or motion-induced vertigo.49
Diagnosis.
The symptoms associated with BPPV include vertigo and nausea, which are
precipitated by positional changes of the head. This disorder may resolve in
days or may prolong for months.
Management.
Many treatments have been proposed for the treatment of BPPV including
drugs, surgery, and vestibular rehabilitation exercises. However, one of most
common and predictable procedures is the Epley procedure, which is usually
performed by an ENT physician. While sitting on the examination table, the
patient's head is rotated in various directions. The result of this procedure is
that the calcium carbonate crystals are dislodged from the semicircular canal
to the utricular cavity, resolving the BPPV (See Chapter 10).
Membrane Perforations
The most common complication during sinus graft surgery is tearing or
creation of an opening in the sinus membrane, which has been reported in a
wide range of 10% to 60% of surgeries.50 Perforation of the sinus membrane
may predispose the patient to additional complications such as infection,
migration/loss of graft material, and possible loss of implants.
Etiology
The etiology of sinus membrane perforation includes: (1) lack of membrane
present, (2) preexisting perforation, (3) tearing during scoring of the lateral
window, (4) tearing during elevation of the membrane, (5) adhesions, (6) poor
technique and access osteotomy sites, (7) narrow sinus in buccal-lingual
dimension, and (8) previous pathologic condition.
Prevention
Surgical Armamentarium.
There are many different techniques when scoring the lateral wall during the
sinus graft procedure. The use of round carbide burs (#6 or #8) has the
advantage of increased efficiency and speed of window preparation.
However, round carbide burs have the disadvantage of chattering and
increased perforation. Using a round diamond bur (#6 or #8) is a much safer
technique because perforation of the membrane is less common, which may
be advantageous to surgeons early on their respective learning curves.
However, because this technique reduces the bone more slowly, surgery time
is increased. The use of a piezotome will decrease chances of perforation and
is the safest technique with the least amount of morbidity available for
scoring of the window.
Size of Access Window.

In general, the larger the window size, the less chance of membrane
perforation. However, in some cases, the size of the window is dictated by
adjacent teeth or anatomic variants. If the window needs to be increased in
size, a second window can be made or the use of Kerrison rongeurs utilized.
The increased size window allows for easier reflection of the membrane.
Narrow Sinuses.
In general, the more narrow the sinus, the more difficult the graft process
and the greater the chance of perforation. Usually the narrowest part of the
sinus is in the anterior region; however, some sinuses are inherently small in
a buccal-lingual dimension. To prevent perforation, the lateral wall may be
removed to minimize trauma to the membrane.
Osteotomy Line Angles.

The corners of the access window should always be rounded, rather than at
right or acute angles. If the corner angles are too sharp, membrane
perforation may occur when elevating the window. Additionally, the
osteotomy cuts should be deep enough that the window is free, prior to
elevation of the membrane.
Thickness of Membrane.
On average the Schneiderian membrane is approximately 1.0 mm in
thickness. In general, the thinner the membrane, the greater chance of
perforation. The thickness of the membrane should be ascertained prior to
the surgery to determine the exact areas of concern or caution. On a CBCT
scan, the thickness of the membrane will be depicted as varying levels of grey
around the periphery of the sinus. In health the membrane will not be seen
on a CBCT scan. Studies have shown that membranes less than 1.5 mm in
thickness have a 31% perforation rate in comparison to thicker membranes
with a rate of 16.6%.51 Additional studies show a direct relationship between
thicker periodontal biotypes and increased membrane thickness, which lead
to a decreased perforation rate.52
Keep Curette on Bony Floor.

When reflecting the membrane off the floor of the sinus, always keep the
curette on bone because this will reduce the chance of perforation. If you
place pressure directly on the membrane, the chances of perforation will
increase (Fig. 13.34), especially when the membrane is thinner.
FIG 13.34 Perforation prevention. (A) Window osteotomy should be completely
through the bone to prevent perforations. (B–D) The currette should alway be kept
on the bone. The membrane does not have a tenacious adherence to the bone,
therefore it is easily elevated.
Treatment
Alter Surgery Technique.

Once the tear or perforation is identified, the continuation of the sinus
elevation procedure is modified. The sinus membrane should be elevated off
all the bony walls of the antrum, despite the mucosal tear. If a portion of the
membrane is not elevated away from a sinus wall, the graft material will be
placed on top of the membrane, preventing the bone graft from
incorporating with the bony wall. The perforation of the sinus membrane
should be sealed to prevent contamination of the graft from mucus and
contents of the sinus proper while preventing the graft material from
extruding into the sinus proper.
Small Perforation.
The surgical correction of a perforation is initiated by elevating the sinus
mucosal regions distal from the opening. Once the tissues are elevated away
from the opening, the membrane elevation with a sinus curette should
approach the tear from all sides so that the torn region may be elevated
without increasing the opening size. The antral membrane elevation
technique decreases the overall size of the antrum, “folding” the membrane
over on itself and resulting in closure of the perforation. A piece of
resorbable collagen membrane (e.g., CollaTape [Zimmer Dental Inc.]) is
placed over the opening to ensure continuity of the sinus mucosa before the
sinus bone graft is placed. The collagen adheres to the membrane and seals
the SA space from the sinus proper (Fig. 13.35).
FIG 13.35 (A) The bony opening in the lateral maxilla contributes to a maxillary
sinus membrane tear on reflection of the soft tissue. (B) The lateral-access window
is designed and elevated distal to the mucosal opening. (C) The sinus membrane
elevation peripherally around the tear makes the opening smaller (green arrow). (D)
A piece of collagen is placed over the membrane. (E) The sinus graft procedure is
completed. Care is taken to prevent overfilling the sinus. (F) The tuberosity is
harvested. (G) The tuberosity is placed on the sinus floor and lateral wall.
Large Perforation.
If the sinus membrane tear is larger than 6 mm and cannot be closed off with
the circumelevation approach, a resorbable collagen membrane of a longer
resorption cycle (BioMend Extend— ~4 months) may be used to seal the
opening. The remaining sinus mucosa is first elevated as described
previously. A piece of collagen matrix is cut to cover the sinus tear opening
and overlap the margins more than 5 mm. Once the opening is sealed, the
sinus graft procedure may be completed in routine fashion. However, care
should be exercised when packing the sinus with graft material. After a
perforation, the graft is easily pushed through the collagen-sealed opening
and into the sinus proper, so a periosteal elevator may be placed at the top of
the graft site and under the perforation. The graft material is then gently
inserted and pushed toward the sinus floor and sides but not toward the top
of the graft (Figs. 13.36 and 13.37).
FIG 13.36 (A) When the opening in the sinus mucosa is greater than 6 mm, the
tissues distal are elevated, but often the remaining mucosal margins do not
approximate each other. (B) A dry piece of extended resorbing collagen (BioMend
[Zimmer Dental Inc.]) is placed over the sinus membrane opening. (C) A parenteral
form of antibiotic moistens the membrane along with antibiotic being added to the
allograft material decreases the potential for infection.
FIG 13.37 (A) Fixated extending resorbing membrane superiorly prevents migration
of the grafting material. (B) Large perforation, (C) Membrane sutured with 6-0 vicryl
suture material.
Local Antibiotic.
A greater bacterial risk of penetration into the graft material exists through
the torn membrane. It is imperative that local antibiotic (pure form) be
added to the particulate graft material. In addition, mucous may invade the
graft and affect the amount of bone formation. Graft material may leak
through the tear into the sinus proper, migrate to and through the ostium,
and be eliminated through the nose or obstruct the ostium, preventing or
altering normal sinus drainage.
Monitor Postoperatively.
Care must be exercised to minimize potential postoperative complications.
The patient should be instructed to refrain from drinking through a straw
and sneezing or blowing their nose. They must take all prophylactic
medications as prescribed and be warned of possible bleeding/graft material
through the nostril within the first 24 hours.
Abort Implant Placement in SA-3I Patients.

When a sinus membrane perforation has occurred during a SA-3 immediate
(sinus graft + implant placement) approach, it is prudent to delay implant
insertion. Placement of implants is deferred for at least 2 months (in an SA-3
option) to allow for healing of the membrane and the gingival tissues on the
edentulous crest. Risks of the sinus graft entering the sinus proper increase
when implants are inserted into the grafted site. The waiting period before
implant insertion permits assessment of postsurgical complications and graft
consolidation before the implants are inserted.
Antral Septa
Antral septa (buttresses, webs, and struts) are the most common osseous
anatomic variants present in the maxillary sinus. Underwood, an anatomist,
first described maxillary sinus septa in 1910, and these bony variants are
sometimes called Underwood septa. Septa vary in location, orientation,
number, size, and thickness, and may influence the positioning of dental
implants in the posterior maxilla. They complicate the creation of the lateral
window along with reflection of the membrane. The presence of antral septa
has been reported to increase the risk of membrane perforation
significantly.53 The presence of septa, along with the determination of their
location and orientation, is most easily seen via a CBCT survey. Evaluation of
the 3-D or cross-sectional images give the clinician the most accurate
information.
Etiology
Underwood postulated the etiology of these bony projections derived from
three different periods of tooth development and eruption. Krennmair et al54
further classified these structures into two groups: primary, which are a
result of the development of the maxilla, and secondary, which arise from the
pneumatization of the sinus floor after tooth loss.
The septa may be complete or incomplete on the floor, depending on
whether they divide the bottom of the sinus into compartments. The shape of
an incomplete maxillary sinus septum often resembles an inverted gothic
arch that arises from the inferior or lateral walls of the sinus. In rare
instances, they may divide the sinus into two compartments that radiate
from the medial wall toward the lateral wall.
The most common location of septa in the maxillary sinus has been
reported to be in the middle (second bicuspid–first molar) region of the
sinus cavity. CT scan studies have shown that 41% of septa are seen in the
middle region, 35% in the posterior region, and 24% in the anterior region.
Complication
Sinus septa may create added difficulty at the time of surgery. Maxillary sinus
septa can prevent adequate access and visualization to the sinus floor, and
inadequate or incomplete sinus grafting is possible. These dense projections
complicate the surgery in several ways. After scoring the lateral-access
window in the usual fashion, the lateral-access window may not greenstick
fracture and rotate into its medial position. The strut reinforcement is also
more likely to tear the membrane during the releasing of the access window.
The sinus membrane is often torn at the apex of the buttress during sinus
membrane manipulation because it is difficult to elevate the membrane over
the sharp edge of the web, and the curette easily tears the membrane at this
position. However, because septa are mainly composed of cortical bone,
immediate implant placement may engage this dense bone, allowing for
strong intermediate fixation. Moreover, septa allow for faster bone formation
because they act as an additional wall of bone for blood vessels to grow into
the graft.
Management
The modification to the surgery is variable depending on its location. The
septum may be in the anterior, middle, or distal compartment of the antrum.
Anterior.
When the septum is found in the anterior section, the lateral-access window
is divided into sections: one in front of the septa and another distal to the
structure. This permits the release of each section of the lateral wall after
tapping with a blunt instrument. The elevation of each released section
permits access into the exact location of the septum to continue the mucosal
elevation. The window (lateral wall) may also be removed to prevent trauma
to the membrane.
The mucosal tissue may often be elevated from the lateral walls above the
septum. The curette may then slide down the side walls and release the
mucosa from the bottom half of the septum on each side. The sinus curette
should then approach the crest of the buttress from both directions, up to its
sharp apex. This permits elevation of the tissue over the web region without
tearing the membrane (Fig. 13.38).
FIG 13.38 (A–B) Window made anterior to septum, (C–F) Membrane is elevated to
completely expose anterior part of sinus, (H) Second window is made as far
posterior to include most distal implant. (I–K) Second part of sinus is elevated, (L–M)
The posterior wall does not need to be exposed unless most distal implant
encroaches upon it. (N) Clinical image depicting two sinus windows.
Middle.
When the septum is located in the middle region of the sinus, it is more
difficult to make two separate access windows within the direct vision of the
surgeon. As a result, one access window is made in front of the septum. The
sinus curette then proceeds up the anterior aspect of the web, toward its
apex. The curette then slides toward the lateral wall and above the septum's
apex. The curette may then slide over the crest of the septum approximately 1
to 2 mm. A firm, pulling action fractures the apex of the septum. Repeated
similar curette actions can fracture the web off the floor. Once the septum is
separated off the floor, the curette may proceed more distal along the floor
and walls (Fig. 13.39).
FIG 13.39 (A) A maxillary septum found on the floor in the middle of the sinus. (B–
E) An access window and curette elevates the mucosa anterior to the septum. (F)
The curette slides over the top of the septum and pulls it off by greenstick fracture.
(G) Once the septum is removed, the rest of the sinus mucosa may be elevated. (J)
The posterior wall does not need to be exposed unless the most distal implant
encroaches upon it.
Posterior.
When the septum is in the posterior compartment of the sinus, it is often
distal to the last implant site. When this occurs, the posterior septum is
treated as the posterior wall of the sinus, containing the graft material. The
sinus membrane manipulation and sinus graft is placed up against and
anterior to the posterior septum (Fig. 13.40).
FIG 13.40 (A) A maxillary septum found on the floor in the posterior of the sinus.
(B) An access window and curette elevates the mucosa anterior to the septum. The
posterior septa is used as a posterior wall to contain the graft material.
Bleeding
Bleeding from the lateral-approach sinus elevation surgery has the potential
to be problematic. Three main arterial vessels should be of concern with the
lateral-approach sinus augmentation. During this surgery, there exist
multiple arteries which may cause an increase in bleeding issues (see
Chapter 7).
Extraosseous Anastomosis
The soft tissue vertical-release incisions of the facial flap in a resorbed
maxilla may sever the extraosseous anastomoses. The extraosseous
anastomosis on average is located 23 mm from the crest of the dentate ridge.
However, in the resorbed maxilla, it may be within 10 mm of the crest. When
this anastomosis is severed, significant bleeding has been observed. These
vessels originate from the maxillary artery and have no bony landmark to
compress the vessel. Vertical release incisions in the soft tissue should be
kept to a minimum height with delicate reflection of the periosteum.
The vertical component of the lateral-access wall osteotomy for the sinus
graft often severs the intraosseous anastomoses of the posterior alveolar
artery and infraorbital artery, which is on average approximately 15 to 20 mm
from the crest of a dentate ridge. Because of the intra- and extraosseous
anastomoses that are formed by the infraorbital and posterior superior
alveolar arteries, intraoperative bleeding complications of the lateral wall
may occur.
Management
If intraosseous bleeding becomes problematic, a high-speed diamond used
to score the window may be utilized without irrigation to polish the bleeding
site, which cauterizes the vessel from the heat on the bony wall.
Electrocautery may also be used on these vessels if necessary. It also has been
reported that the use of a sterile cotton applicator soaked with epinephrine (1
: 100,000) can also be used to control bleeding. A hemostat to crush the artery
may be less effective because it may fracture the lateral wall and/or perforate
the sinus mucosa. Elevating the head may help reduce bleeding, as studies
have shown that blood flow may be reduced by 38%.55 If the excessive
bleeding occurs while the medial wall is elevated, the sinus may be packed
with gauze or a hemostatic agent such as BloodSTOP or HemCon.
(A) Intrassous anastamosis bleed (arrows). (B) A curved Kelly hemostat is used to
clamp the bleeding vessels.
Posterior Lateral Nasal Artery

The third artery of which the implant clinician should be cautious is the
posterior lateral nasal artery. This artery is a branch of the sphenopalatine
artery that is located within the medial wall of the antrum. As it courses
anteriorly, it anastomoses with terminal branches of the facial artery and
ethmoidal arteries. A significant bleeding complication may arise if this
vessel is severed during elevation of the membrane off the thin medial wall.
The most common site (90%) of nasal bleeding is from a plexus of vessels at
the anteroinferior aspect of the nasal septum and the anterior nasal cavity
(which is anterior to the sinus cavity and within the anterior projection of the
nose). The posterior nasal cavity accounts for 5% to 10% of epistaxis events
and is in the region of the sinus graft. If the medial wall of the sinus is
perforated, a curette may enter the nares and cause bleeding.
Excess Pressure on Graft Site

The stabilization of the sinus graft material is paramount to predictable bone
growth because it ensures blood clot adhesion and the associated growth
factors for predictable healing. Graft immobility is vital to capillary ingrowth
and graft revascularization. The implant clinician must take great care in
preventing any excess pressure over the graft site.
Complication
One of the most common and challenging roadblocks to implant treatment
acceptance is the patient's perception of the temporization
(provisionalization) of the edentulous areas after bone grafting. In most
cases, pressure directly or indirectly on the surgical site can lead to bone loss
and increased morbidity of the graft site.
Prevention
Ideally, no provisionalization after surgery is the best treatment. However, if
the patient is going to wear a removable prosthesis (flipper), the prosthesis
must be modified and relieved in the area of the graft. The flange of the
prosthesis along with the ridge area should be hollowed out so no pressure
from occlusal forces will result in trauma to the graft. The primary stress-
bearing area of the maxilla (horizontal palate) must not be modified. It is
imperative that all forces are concentrated on this area when the patient is
masticating on the prosthesis (Fig. 13.41).
FIG 13.41 Relief of the prosthesis. (A) It is crucial the flange be removed from the
prosthesis and (B) the ridge area be hollowed out so the primary stress-bearing area
(horizontal palate—arrow) takes the majority of the occlusal load upon mastication.
Nerve Impairment
The infraorbital nerve is of concern in sinus elevation surgery because of its
anatomic position. This nerve enters the orbit via the inferior orbital fissure
and continues anteriorly. It lies in a groove in the orbital floor (which is also
the maxillary sinus superior wall) before exiting the infraorbital foramen. The
infraorbital nerve exits the foramen approximately 6.1 to 7.2 mm from the
orbital rim.
It is of note that anatomic variants have been reported to include
dehiscence and malpositioned infraorbital foramina, along with the nerve
transversing the lumen of the maxillary sinus rather than coursing through
the bone within the sinus ceiling (orbital floor). Malpositioned nerves have
been reported as far as 14 mm from the orbital rim in some individuals. In
the severely atrophic maxilla, the infraorbital neurovascular structures
exiting the foramen may be close to the intraoral residual ridge and should
be avoided when performing sinus graft procedures to minimize possible
nerve impairment. This is of particular concern on soft tissue reflection and
the bone preparation of the superior aspect of the window. Special
considerations should be taken during reflection of the superior flap and
sharp-ended retractors should be avoided. Usually, those most at risk have a
small cranial base (i.e., elderly females).
Complication
Because the infraorbital nerve is responsible for sensory innervations to the
skin of the molar region between the inferior border of the orbit and the
upper lip, iatrogenic injury to this vital structure can result in significant
neurosensory deficits of this anatomic area. Most often the nerve is not
severed, and a neuropraxia results. Even though this injury is sensory and
there is no motor deficit, patients usually have a difficult time adapting to
this neurosensory impairment (Fig. 13.42).
FIG 13.42 Nerve impairment. (A) Infraorbital foramen anatomic variants that are
close to the residual ridge. (B) V2 sensory impairment. (C) Broad-based retractor to
avoid nerve trauma.
Management
If an infraorbital nerve impairment occurs, the implant clincian should
immediately follow the clincial and pharmacologic neurosensory impairment
protocol (i.e., outlined in Chapter 9).
Revision Surgery
When failure or compromise of the sinus graft occurs, reentry procedures are
sometimes required to correct deficits. Failed or compromised sinus grafts
result in altered soft and hard tissue characteristics, mainly the formation of
adhesions of the Schneiderian membrane to the buccal flap. This results in
difficulty with reflecting the buccal flap during the reentry procedure.
Studies have shown that separation of the adhesions from the sinus mucosa
led to a 47% perforation rate.
In addition, it has been shown that altered characteristics of the
Schneiderian membrane result in a nonflexible thick fibrotic membrane. In
some cases, where voids are present but have difficult access, regrafting
procedures may need to be accomplished via a closed approach through the
osteotomy site.56
Because of access issues, along with the higher perforation rate and fibrotic
changes in the Schneiderian membrane, patients need to be informed of a
higher postoperative complication rate involving questionable reentry bone
growth and implant success. If reentry is necessary, usually bony adhesions
and bony fenestrations of the lateral walls will be present.
The combination of fibrotic changes of the Schneiderian membrane,
increased chance of perforation, and altered sinus physiology lead to a high
complication rate. The continuation of the sinus mucosa and oral mucosa
make reentry revision surgery problematic and difficult (Fig. 13.43). This will
require the separation of the oral and sinus mucosa to gain access to the
sinus proper.
FIG 13.43 Post–sinus graft infections. (A) Post-sinus infection resulting in fibrous
tissue growth and migration of graft material, (B) Post-op infection with the sinus and
vestibular mucosa being continuous, (C) To gain access to the sinus cavity,
separation of the two tissues is accomplished with a 15 blade.
Edema
Because of the extent of tissue reflection and manipulation, sinus graft
surgery often results in significant edema. The resultant postoperative
swelling can adversely affect the incision line, leading to greater morbidity.
Prevention
The use of good surgical technique that involves careful reflection and
retraction will decrease the amount of postoperative edema.
Minimize Surgical Duration.

The greater the surgery duration, the greater the chance of edema. Caution
should be noted to decrease the amount of surgical duration and should not
exceed the patient's tolerance.
Corticosteroid Treatment.
To minimize edema, corticosteroid use is utilized 1 day prior to and 2 days
after surgery. This short-term prophylactic steroid use will allow for adequate
blood levels to combat edema, which usually will peak at 48 to 72 hours.
Dexamethasone is the ideal drug of choice because of its high
antiinflammatory potency.
Cryotherapy.
Application of an ice pack, along with elevation of the head and limited
activity for 2 to 3 days, will help minimize the postoperative swelling. This
cryotherapy will cause vasoconstriction of the capillary vessels, reducing the
flow of blood and lymph and resulting in a lower degree of swelling. Ice or
cold dressings should only be used for the first 24 to 48 hours. After 2 to 3
days, heat (moist) may be applied to the region to increase blood and lymph
flow to help clear the area of the inflammatory consequences. This will also
help reduce the possibility of ecchymosis that may result.
Ecchymosis
Sinus graft surgery also increases the possibility of bruising or ecchymosis.
Because of the extent of reflection, bone preparation, and the highly vascular
surgical area, ecchymosis will occur more often with this procedure in
comparison to other implant related surgeries.
Etiology
The etiology of ecchymosis includes the following: blood vessels rupture →
red blood cells die and release hemoglobin → macrophages degrade
hemoglobin via phagocytosis → production of bilirubin (bluish-red) →
bilirubin is broken down to hemosiderin (golden-brown).
Prevention
In most cases, ecchymosis will not be able to be completely prevented;
however, the goal should be to minimize the extent of bruising. Additionally,
good surgical technique, shorter surgical duration, the avoidance of
anticoagulant analgesics, and postoperative cryotherapy all aid in the control
of this phenomenon (Fig. 13.44). Patients should always be informed of the
possibility of ecchymosis. This is easily accomplished by having it be part of
the postoperative instructions.
FIG 13.44 Ecchymosis. (A) Swelling and bruising is very common after sinus graft
procedures because of the amount of tissue stretching and reflection. (B) It will most
likely extend into the neck because of gravity.
Pain
Minimal discomfort and pain is usually associated with sinus graft surgery.
However, if narcotics are indicated, any analgesic combination containing
codeine, such as Tylenol 3, is prescribed postoperatively because codeine is a
potent antitussive, and coughing may place additional pressure on the sinus
membrane and introduce bacteria into the graft. The patient is instructed to
cough (if necessary) with the mouth open to minimize possible air pressure
changes within the sinus cavity.
Nasal Bleeding
Epistaxis (active bleeding from the nose) is a common complication following
sinus elevation surgery, especially when a membrane perforation has been
noted. Usually, this occurs within the first 24 hours after surgery.
Treatment
Treatment options to treat epistaxis include nasal packing, electrocautery, and
the use of vasoconstrictive drugs. Placing a cotton roll (coated with
petroleum jelly with dental floss tied to one end) into the nares may obtund
nose bleeding after the surgery. After 5 minutes the dental floss is gently
pulled to remove the cotton roll. The head is also elevated, and ice is applied
to the bridge of the nose. If bleeding cannot be controlled, reentry into the
graft site and endoscopic ligation by an ENT surgeon may be required.

Incision line opening is uncommon for this procedure because the crestal
incision is most likely in attached gingiva and is usually at least 5 mm away
from the lateral-access window. Routinely, the soft tissue requires release
before primary approximation and suturing. Incision line opening occurs
more commonly when lateral-ridge augmentation is performed at the same
time as sinus graft surgery or when implants are placed above the residual
crest and covered with the soft tissue. It may also occur when a soft tissue–
supported prosthesis compresses the surgical area during function before
suture removal.
Complication
The consequences of incision line opening are delayed healing,
contamination of the graft, and increased risk of infection. However, if the
incision line failure is not related to a lateral augmentation graft and is only
on the crest of the ridge and away from the sinus access window, the
posterior crestal area is allowed to heal by secondary intention.
Prevention
Usually, when a collagen membrane is placed over the window, the soft tissue
will not approximate without tension release with the surgeon expanding the
facial flap by releasing the periosteum above the mucogingival junction
(where the tissue becomes thicker). It is imperative that tension-free closure
be completed.
Management
If incision line opening occurs, the soft tissue–borne restoration should be
aggressively relieved, with no reline material in contact with the ridge. If
incision line opening includes a portion of a nonresorbable membrane (e.g.,
for lateral-ridge augmentation), the membrane should be cleaned at least
twice daily with an abrasive device and oral rinses of chlorhexidine. If the
incision line is not closed after 2 months, a surgical procedure should reenter
the site, expand the tissues, remove the bone regeneration membrane, and
reapproximate the tissue.
Oroantral Fistulae
Oroantral fistulae may develop postoperatively, especially if the patient has a
history of past sinus pathology or infection. Small oroantral fistulae (<5 mm)
usually will close spontaneously after treatment with systemic antibiotic
drugs and daily rinses with chlorhexidine. However, larger fistulae (>5 mm)
will normally require additional surgical intervention (Fig. 13.45). Larger
fistulae are associated with an epithelialized tract, which is the result of the
fusion of the sinus membrane mucosa to the oral epithelium. When this
occurs, patients will most likely complain of fluids entering the nasal cavity
upon eating or drinking. Caution should be exercised in using the nose
blowing test to confirm the presence of a oral-antral fistula. The patient is
asked to pinch their nostrils together to occlude the nose. The patient blows
gently to see if air escapes into the oral cavity via the sinus. This is not
recommended as this test may create an opening or make a small opening
larger.
FIG 13.45 Oroantral communications. (A) Small communication. (B) Large

communication.
Management
Closure of oroantral fistulae can be accomplished by using broad-based
lingual or facially rotated flaps (Figs. 13.46 and 13.47). Buccal flaps to close
the fistula may be more difficult after a sinus graft because of the location of
the graft site. In addition, the buccal tissue is very thin, and rotated or
expanded buccal flaps usually result in loss of vestibular depth. Before the
initiation of the flap design, the soft tissue around the fistula is excised and
the sinus floor curetted to ensure direct bone contact. A tension-free rotated
flap is then made for complete covering of the communication. For oroantral
closure after sinus graft procedures, a lingual flap is recommended because
of the abundance of keratinized mucosa with an adequate blood supply. Flap
designs include island flaps, “tongue-shaped” flaps, or rotational and
advanced flaps, depending on the size of the exposure.
FIG 13.46 Buccal flap closure of oroantral fistula. (A) Cross-section of oroantral
fistula in the molar region. (B) The buccal flap has been elevated. (C) The epithelium
lining the fistula has been excised, the periosteum has been released at the
vestibular height of the dissection, and the tension-free flap has been closed across
the defect, with the margins of the flap resting over bone. (From Hupp JR, et al:
Contemporary oral and maxillofactal surgery, 5 ed, St. Louis, 2009, Elsevier.)
FIG 13.47 Membrane-assisted closure of oroantral communications. (A)
Diagrammatic illustration of oroantral fistula in the right maxillary alveolar process in
the region of the missing first molar, which is to be closed with subperiosteal
placement of alloplastic material such as gold or titanium foil or a resorbable
collagen membrane. Facial and palatal mucoperiosteal flaps are developed.
Extension of the flaps along the gingival sulcus one or two teeth anterior and
posterior allows some stretching of the flap to facilitate advancement for closure
over the defect. The fistulous tract is excised. Osseous margins must be exposed
360 degrees around the bony defect to allow placement of the membrane beneath
the mucoperiosteal flaps. The flap is supported on all sides by underlying bone. (B)
Diagram of closure. Ideally, the flaps can be approximated over the defect. In some
cases, a small gap between the flaps will heal over the membrane by secondary
intention. Even if the intraoral mucosa does not heal primarily, the sinus lining usually
heals and closes, and the membrane is then exfoliated or resorbed, and mucosal
healing progresses. (C) Cross-sectional diagram of membrane closure technique.
Buccal and palatal mucoperiosteal flaps are elevated to expose osseous defect and
large area of underlying alveolar bone around the oroantral communication. The
membrane overlaps all the margins of the defect, and the facial and palatal flaps are
sutured over the membrane. (From Hupp JR, et al: Contemporary oral and maxillofactal
surgery, 5 ed, St. Louis, 2009, Elsevier.)
A key to closing the oroantral opening is the dissection of the buccal flap
lateral to the fistula. An incision that extends 15 mm anterior and posterior
to the fistula is of benefit. The fistula then has an elliptical incision on each
side of the opening. The core of tissue and the fistulous tract are excised. The
facial flap is undermined and expanded well into the tissues of the cheek.
The palatal aspect of the incision is adjacent to the tongue-shaped flap.
Placement of the incision for the pedicle flap should be split thickness and
take into account the location and depth of the greater palatine artery. Once
the attached palatal pedicle graft is rotated to the lateral and attached to the
facial flap, horizontal mattress sutures are placed to invert the flap to achieve
a watertight seal. Sutures with high tensile strength (Vicryl) should be used
and allowed to remain in place for at least 2 weeks (Fig. 13.48).
FIG 13.48 (A) An oroantral fistula after sinus graft infection is evident on the
patient's left side. (B) An elliptical incision is made around the fistula and extends
both anterior and posterior to the site. (C) The tissues are reflected. (D) The
fistulous tract is removed, complete with the epithelial lining. (E) The facial flap is
undermined, and a submucosal space is created. (F) Horizontal mattress sutures
are used for the watertight closure.
Infections
When evaluating postsurgical infectious complications after sinus graft
procedures, the implant clinician must differentiate the type, location, and
etiology of the infectious episode. The infection may originate within the
graft site or may originate in the maxillary sinus proper. It could also be a
combination of both (Table 13.1). Very few studies have evaluated these
different processes. Postsurgically, there exist many reports with varying
results (~0%–27%) on the incidence of infection leading to acute
rhinosinusitis.56a Postoperative infections after sinus graft surgery may result
from the following:
• Acute rhinosinusitis: infection within the sinus proper
• Graft site: infection within the graft area (Fig. 13.49)
• Combination infection: from acute rhinosinusitis or graft site
Fig. 13.50 shows preoperative and postoperative infection rates, and
infection rates after 4 weeks.
TABLE 13.1
Postoperative Infections
Acute Rhinosinusitis Graft Site Infection Combination

Etiology Preexisting pathology Pre-existing pathology Primary site c ould be sinus
Nonpatent ostium Oral pathogens proper or graft site
Anatomic variants c ontamination
Graft overfill Untreated periodontitis
Postsurgery physiologic alteration Perforation
S pread of infec tion from graft site Lac k of asepsis
History of c hronic rhinosinusitis Long duration surgery
Preexisting odontogenic or allergic rhinosinusitis S imultaneous ridge
augmentation
S imultaneous implant
plac ement
Lac k of prophylac tic
medic ation
Lac k of loc al graft antibiotic s
S ystemic diseases,
smoking/alc ohol
Bac teria Aerobic gram-positive c oc c i (Streptococcus pneumonia e) Aerobic gram-positive c oc c i Any c ombination of
Aerobic gram-negative rods (Ha emophilus influenza e) (Streptococcus virida ns) pathogens
(Sta phylococcus epidermidis, Streptococcus virida ns, B ca ta rrha lis) Aerobic gram-positive c oc c i
(Sta phylococcus a ureus)
Aerobic gram-negative rods
(Ba cteroides)
Aerobic gram-positive c oc c i
(peptostreptoc oc c us)
Prevention CBCT: Prophylac tic medic ation Any c ombination of
Confirmation of ostium patenc y Good surgic al tec hnique preventive measures
Confirmation of no pathology or anatomic variants Aseptic tec hnique
Prophylac tic medic ations S hort surgic al duration
No membrane perforation
S ymptoms Mild S ite pain/edema Any c ombination of
Fac ial pain/edema Inc ision line opening symptoms
Congestion Exudate
Nasal drip/bloc kage Bad taste
Cough Bleeding
Severe Intra-oral swelling
S ignific ant fac ial pain/edema
Fever
Headac he
Proptosis/diplopia
Malaise
Ideal Beta-lac tam Beta-lac tam Beta-lac tam
Antibiotic Quinolone Linc osamide Quinolone
Initial Antibiotic : Antibiotic : Antibiotic :
Treatment 1. Augmentin 1. Augmentin 1. Augmentin
2. Levaquin 2. Clindamyc in 2. Levaquin
Nasal saline Chlorhexidine Nasal saline/rinse
S ec ondary Referral, espec ially if c erebral/oc ular symptoms Debridement/irrigation Debridement
Treatment Possible c ulture Possible c ulture
Referral, espec ially if
c erebral/oc ular
symptoms
FIG 13.49 Coronal CBCT image depicting infection after implant placement and
sinus graft (SA-3 Immediate).
FIG 13.50 Post–sinus graft infection. (A) Preoperative. (B) Postoperative graft. (C)
Infection 4 weeks after graft showing sinus radiopacity and nonpatent ostium.
Graft Site Infections

Etiology of Graft Site Infection
The graft site may become infected from many sources: (1) preexisting site
bacteria, (2) bacterial contamination of the surgical site, (3) graft material, (4)
surgical technique, (5) bacterial contamination from acute rhinosinusitis, (6)
lack of systemic and local prophylactic antibiotics, and (7) systemic,
mediation, or lifestyle factors.
Additionally, studies have shown a direct correlation between an increased
infection rate with simultaneous implant placement as well as with
simultaneous ridge augmentation. One such study showed that
simultaneous ridge grafting increased the infection rate significantly (15.3%)
vs. sinus grafting alone (3%).57 Most often, the infection begins more than 1
week after surgery, although it may begin as soon as 3 days later.
Diagnosis
The most common sign of graft site infection is swelling, pain, dehiscence, or
exudate near or including the grafting surgical site. Patients may complain of
poor taste and loss of graft particles in their mouth. Incision line opening is a
common sequalae with exudate discharge. Graft site infections usually occur
within days to weeks of the surgery and are less common as a late infection.
Initially, the infection may start as a graft site infection (localized to the
graft), which then leads to an acute maxillary rhinosinusitis.
Prevention
The prevention of graft site infection includes:
Good Surgical Technique.

Good surgical technique involves the use of a true aseptic technique
consisting of sterile drapes and gowning. A clean surgery will decrease the
possibility of contamination of the graft site from many of the pathogens that
predispose to this type of infection. Additionally, aseptic care in the handling
of graft materials is crucial. As such, a surgical environment that includes
intraoral and extraoral scrubbing with chlorhexidine, scrubbing and draping
the patient, as well as gowning the doctor and assistant should be considered
in addition to sterile gloves and sterile instruments. The risk of postoperative
sinus infection is generally less than 5% when these procedures, combined
with a preoperative and postoperative pharmacologic regimen, are used.57
Prophylactic Medications.
The risk of bacterial contamination during and after sinus graft procedures is
much different than regular implant surgical procedures. The pharmacologic
protocol should be effective against the organisms in this surgical site. The
pharmacologic regimen includes an antibiotic drug, antiinflammatory
medications, antimicrobial rinse, and analgesic medications.
Antibiotics.
Following the principles of prophylactic antibiotic administration, the
antibiotic should be effective against the bacteria most likely to cause
infection. The most likely contaminating organisms after transoral surgery
are primarily streptococci, anaerobic gram-positive cocci, and anaerobic
gram-negative rods. Streptococcus pneumoniae, Haemophilus influenzae, and
Moraxella catarrhalis are the three most common pathogens found with acute
sinus infections.58 Staphylococcus aureus along with anaerobic bacteria have a
significant role in causing chronic rhinosinusitis disease. The organisms
associated with infection of allografts such as demineralized bone in oral
surgery include alpha-hemolytic streptococci and S. viridans.59 S. aureus,
Bacteroides spp, and endogenous bacteria cause the vast majority of
postoperative infections. A pharmacologic protocol effective against these
organisms is appropriate.
Bacterial resistance.
When evaluating various classes of antibiotic medications used for treatment
of maxillary sinus infections, the antibiotic class of choice is beta-lactam
antibiotic drugs. However, bacterial resistance has become a significant
problem in the treatment of these pathogens. With the wide range of
possible routes of bacterial invasion and types of bacteria, the antibiotic drug
must be broad spectrum to account for all these possibilities. Bacterial
resistance is initiated by two common mechanisms: (1) production of
antibiotic-inactivating enzymes (S. aureus, H. influenzae, and M. catarrhalis)
and (2) alteration in target site (S. pneumoniae). Studies have shown the
following resistance results60:
H. influenzae: 36.8%
M. catarrhalis: 98%
S. pneumoniae: 28.6%
Ideal antibiotic.
Because of the high rate of bacterial resistance, amoxicillin (the drug of
choice for many years) is no longer used for antibiotic prophylaxis for the
sinus graft surgery. Instead, amoxicillin-clavulanate (Augmentin) is
recommended because of the addition of clavulanic acid, which enhances
amoxicillin's activity against the beta-lactamase–producing strains of
bacteria. The clavulanate acid, which is also an antibiotic, has an affinity to
the beta-lactamase. Because of this interaction, the beta-lactamase is
inactivated. Additionally, Augmentin has a very good, broad spectrum of
bacteria that may cause oral infections.
Alternative antibiotics.
The patient with a history of nonanaphylactic allergic reaction to penicillin
may take cefuroxime axetil (Ceftin), which is a second-generation
cephalosporin, as an alternative.61 Ceftin possesses good potency, efficiency,
and strong activity against resistant S. pneumoniae and H. influenzae bacteria.
If a patient has a history of an anaphylactic reaction to penicillin, recurrent
sinus infections, or a recent history of antibiotic use, levofloxacin (Levaquin)
may be indicated. This newer type of quinolone antibiotic exhibits superior
activity against most types of involved bacteria, along with resistant strains.
Early administration.
Maximum effectiveness of prophylactic antibiotic drugs occurs when the
antibiotic is in adequate concentrations in the tissue prior to bacterial
invasion. Because the sinus mucosa has limited blood supply to combat
possible bacterial invasion from the sinus surgery, along with a high
incidence of tissue inflammation, antibiotic medications should be
administered at least 1 full day before surgery and extended for 5 days after
surgery.
Local antibiotic medications.

The antibiotic concentration within a blood clot of the sinus graft depends on
the systemic blood titer. After the clot stabilizes, further antibiotic drugs do
not enter the area until revascularization.62 The bone graft is a dead space
with minimum blood supply and the absence of protection by the host's
cellular defense mechanisms. This leaves the graft prone to infections that
would normally be eliminated by either the host defenses or the antibiotic.
The osteogenic induction of autografts and allografts is greatly retarded
when contaminated with infectious bacteria.63 To ensure adequate antibiotic
levels in a SA graft, it is recommended to add antibiotic (e.g., pure form) to
the graft mixture.64 The local antibiotic may protect the graft from early
contamination and infection. Numerous studies have shown that an
antibiotic added to graft material has no deleterious effects on bone growth.
Antibiotic drugs such as penicillin, cephalosporin, and clindamycin, even in
high concentrations, have not been found to be destructive to bone-inductive
proteins.65
The locally delivered antibiotic should have efficacy against the most likely
organisms encountered. Because the incidence of allergy is so high with beta-
lactam antibiotic drugs, the parenteral form of cefazolin (Ancef) or
clindamycin is selected. Orally administered capsules and tablets should not
be used within the graft because they contain fillers that are not conducive to
osteogenesis. When the parenteral form of antibiotic is a liquid, the volume
of liquid added to the graft should be minimized to allow adequate handling
of the graft mixture.
(A) Ansef (1 gm) is diluted with 2 ml of saline, 0.2 ml added to membrane and 0.8 ml
added to the graft. (B) Cleocin (300 mg/2 mg), 0.2 ml added to membrane and 0.8
ml added to the graft.
Clinical experience indicates that less risk of infection exists when

preoperative and postoperative antibiotic drugs are used both orally and in
the graft. Because infection considerably impairs bone formation for patients
undergoing sinus graft procedures, oral antibiotic coverage is continued for 5
days after the surgery.
Oral antimicrobial rinse.

An additional antimicrobial medication that is recommended is
chlorhexidine gluconate. This category of mouth rinse has been shown to
successfully decrease infectious episodes and minimizes postoperative
complications from the incision line. Gentle oral rinses of chlorhexidine
gluconate 0.12% should be used twice daily for 2 weeks after surgery.
Glucocorticoid medications.
The decrease in inflammation of the soft tissue decreases postoperative pain,
swelling, and incision line opening. In addition, the clinical manifestations of
surgery on the sinus mucosa can also be decreased by use of a steroid.66 The
usual surgical protocol for most implant surgeries, including sinus grafts,
includes a short-term dose of dexamethasone (Decadron). To ensure patency
of the ostium and minimize inflammation in the sinus before surgery, steroid
medications are initiated 1 full day before surgery. This medication should
also be extended 2 days postoperatively because edema peaks at 48 to 72
hours.
Decongestant medications.
Sympathomimetic drugs that influence alpha-adrenergic receptors have been
used as therapeutic agents for the decongestion of mucous membranes. Both
systemic and topical decongestant medications have been used in reversing a
nonpatent ostium. However, recent recommendations from the
otolaryngology literature discourage the use of these medications. Topical
decongestant drugs can cause a rebound phenomenon and the development
of rhinitis medicamentosa if used more than 3 to 4 days. It should also be
noted that the pulse amplitude and blood flow in the sinus mucosa is
reduced with decongestant drugs such as oxymetazoline. This may, in turn,
decrease the defense mechanism of the tissues.67 Oxymetazoline 0.05% (Afrin
or Vicks Nasal Spray) and phenylephrine 1% should not be used
prophylactically or for therapeutic purposes.
Treatment
Although the incidence of infection after the procedure is usually low, the
damaging consequences on osteogenesis and the possibility of serious
complications require that any infection be aggressively treated. In case of
postoperative infection, it is recommended that the clinician perform a
thorough examination of the area by palpation, percussion, and visual
inspection to identify the area primarily affected. Infection will usually follow
the path of least resistance and is observed by changes in specific anatomic
sites to which it spreads.68
Early, aggressive treatment is crucial for graft site infections to prevent the
loss of graft or extension of the infection into the sinus proper causing an
acute rhinosinusitis or spread of infection to other vital areas. Initially,
systemic antibiotics along with antimicrobial rinses should be used. If
infection persists, debridement and drainage should be completed along
with the use of sterile saline and chlorhexidine. A Penrose drain may also be
used in cases that do not respond to systemic antibiotics. In some instances,
oroantral fistulas result after infection cessation (see the section on oroantral
fistula).
Antibiotic treatment in the maxillary sinus, both prophylactically and
therapeutically, is much different than for most oral surgical procedures.
When selecting antibiotic medications for sinus infections, a variety of
factors must be evaluated. These include the most common type of
pathogens involved, antimicrobial resistance, pharmacokinetic and
pharmacodynamic properties, and the tissue (sinus) penetration of the
various antibiotic drugs. The antibiotic medication of choice should be
effective against respiratory and oral pathogens while exhibiting known
activity against resistant strains of the common pathogens. Two such factors
are used when evaluating sinus antibiotic medications: (1) the minimum
inhibitory concentration (MIC) and (2) the concentration of antibiotic drugs
penetrating inflamed diseased sinus tissue. The MIC is the lowest
concentration of the antimicrobial agent that results in the inhibition of
growth of a microorganism. The MIC is usually expressed by MIC 50 or MIC
90, meaning that 50% or 90% of the microbial isolates are inhibited,
respectively.
Previous studies and treatment modalities used amoxicillin as the first
drug of choice. However, with the increasing prevalence of penicillinase- and
beta-lactamase–producing strains of Haemophilus influenzae and Moraxella
catarrhalis, along with penicillin-resistant strains of Streptococcus pneumoniae,
other alternative antibiotic drugs should be selected.
Beta-Lactam Medications.
The most common beta-lactam antibiotic drugs used in the treatment of
rhinosinusitis and graft site infections are penicillin (amoxicillin,
Augmentin) and cephalosporin (Ceftin, Vantin). Amoxicillin has been the
drug of choice for years to combat the bacterial strains associated with
rhinosinusitis and infections in the oral cavity. However, its effectiveness has
been questioned recently because of the high percentage of beta-lactamase–
producing bacteria and penicillin-resistant S. pneumoniae. Augmentin
(amoxicillin-clavulanate) has the added advantage of activity against beta-
lactamase bacteria. It has been associated with a high incidence of
gastrointestinal side effects. However, with the dosing regimen (twice a day
[bid]), these complications have been significantly decreased.
Two recommended cephalosporin medications have also been suggested to
treat rhinosinusitis: cefuroxime axetil (Ceftin) and cefpodoxime proxetil
(Vantin). Other cephalosporin drugs fail to achieve adequate sinus fluid
levels against the causative pathogens. Ceftin and Vantin have good potency
and efficacy while exhibiting strong activity against resistant S. pneumoniae
and H. influenzae.
Fluoroquinolone Medications.
Fluoroquinolone drugs are bactericidal antibiotic medications that are
classified into four different generations. The third-generation quinolone
drugs are well-suited, broad-spectrum antibiotic medications and have been
labeled by the US Food and Drug Administration (FDA) for use against sinus
and oral pathogens. They exhibit excellent absorption and achieve very
significant sinus blood levels, even in pathologic conditions. Quinolone
drugs are distributed extensively throughout the sinus, with high levels
being found in inflamed tissue and maxillary sinus cysts. The tissue/blood
ratio is approximately 4 : 1, making it extremely potent within the diseased
sinus. The three most common quinolone medications used for sinus
treatment include levofloxacin (Levaquin), gatifloxacin (Tequin), and
moxifloxacin (Avelox).
Macrolide Medications.
Macrolide drugs are bacteriostatic agents that include erythromycin,
clarithromycin (Biaxin), and azithromycin (Zithromax). Macrolide
medications have good activity against susceptible pneumococci; however,
with the increasing rate of macrolide resistance, their use in combating sinus
pathogens is becoming associated with a high likelihood of clinical failure.
These antibiotic drugs are very active against M. catarrhalis, although their
activity on H. influenzae is questionable. These antibiotic medications are not
suggested to treat postoperative sinus infections.
Lincosamide Medications.
Clindamycin (Cleocin) is the primary lincosamide drug used in clinical
practice today that is considered to be bacteriostatic. However, in high
concentrations, bactericidal activity may be present. Clindamycin is mainly
used for the treatment of gram-positive aerobes and anaerobes. With acute
sinus disease, clindamycin is usually not indicated because it exhibits no
activity against H. influenzae and M. catarrhalis. This drug may be used in
chronic sinus conditions because anaerobic organisms play a much larger
role in the disease process.
Tetracycline Derived Medications.

Doxycycline (Vibramycin) is a bacteriostatic agent with adequate activity
against penicillin-susceptible pneumococci and M. catarrhalis. This drug does
not exhibit any activity against penicillin-resistant bacteria and is not
effective against H. influenzae. However, doxycline may be used as an
alternative antibiotic for the treatment of acute rhinosinusitis infections.
Sulfonamide Medications.
The most common sulfonamide drug, trimethoprim-sulfamethoxazole
(Bactrim) is bacteriostatic. Recently, a high rate of resistance to these drugs
has been seen with S. pneumoniae, H. influenzae, M. catarrhalis, and other
sinus pathogens. This drug should not be considered to treat postoperative
infections, unless a culture and sensitivity test has been performed and
susceptibility is shown.
Metronidazole Medications.
Metronidazole is the most important member of the nitroimidazole group. It
is bactericidal and is effective against gram-positive and gram-negative
anaerobic bacteria. Its main use would be in the treatment of chronic sinus
(not acute) conditions. The medication should be used with another
antibiotic drug to be effective against aerobic bacteria.
Antibiotic Conclusion
In the evaluation of different antibiotic drugs used for the treatment of
pathologic conditions of the sinus, meticulous analysis of the activity against
the most common pathogens must be evaluated. With all of the antibiotic
medications evaluated, amoxicillin-clavulanate, cefuroxime axetil,
levofloxacin, and moxifloxacin showed significant sinonasal and MIC 90
blood levels against the most common pathogens associated with sinus
infections. Moxifloxacin, a third-generation fluoroquinolone drug, has been
shown to have superior qualities compared with many other antibiotic
medications. It shows extensive distribution throughout the sinuses in both
inflamed and noninflamed sinus tissue, with significantly high concentration
within maxillary sinus cysts. The tissue/blood ratio is 4 : 1, with blood levels
occurring 3 to 4 hours after administration. Because of the potency and
expense of this medication, it is used only in the treatment of severe
infections.
Decongestant Medications.
Recent recommendations in the medical literature state that nasal
decongestants (sympathomimetic drugs) should not be used except in severe
cases of congestion and infection. Nasal decongestants have been shown to
impair blood flow, thus decreasing antibiotic levels to the site. Additionally, it
may cause a rebound phenomenon and the development of rhinitis
medicamentosa. This rebound phenomenon has been theorized to occur as a
negative feedback vasodilation after repeated introductions of the
sympathomimetic (vasoconstricting) drug.
Saline Rinses.
An important treatment for the patient with the presence of acute
rhinosinusitis and graft infections is the use of saline rinses with a bulb
syringe or a squeeze bottle in the nostril used to lavage the sinus through the
ostium. The nasal saline rinse has a long history for treatment of sinonasal
disease. Hypertonic and isotonic saline rinses have proven to be effective
against chronic rhinosinusitis. These techniques of nasal irrigation have been
evaluated, with the best option of a positive-pressure irrigation using a
squeeze bottle that delivers a gentle stream of saline to the nasal cavity
(NeilMed's Sinus Rinse [NeilMed Pharmaceuticals Inc.]). The syringe or
squeeze bottle should not seal the nasal opening because this may force
bacteria up toward the ethmoidal sinus. Instead, a gentle lavage with sterile
saline rinses the sinus and flushes out the mucus and exudate. Ideally, the
head is placed down and forward so that the saline can reach the ostium in
the superior and anterior portion of the sinus. The course of therapy should
continue for at least 7 days.69 Another option is for the use of a Neti-Pot,
which is very common amongst chronic rhinosinusitis patients (Fig. 13.51).
FIG 13.51 (A) Saline rinse should be directed toward the ostium (arrow). (B) Neti-
Pot used to clear nasal passages. (B, From GettyImages.com.)
Acute Rhinosinusitis Infections

Etiology of Acute Rhinosinusitis
There are two causes of acute maxillary rhinosinusitis after sinus graft
surgery: (1) preexisting maxillary sinus pathology, or (2) progression of sinus
graft surgery to involve the maxillary sinus proper.
Diagnosis
Maxillary rhinosinusitis is a complication that arises when the patient
postoperatively complains of any of the following symptoms: (mild)
headache, pain, or tenderness in the area of the maxillary sinus, rhinorrhea,
or (severe) fever, headache, or ocular symptoms. Studies have supported the
fact that patients who had predisposing factors for rhinosinusitis were more
at risk of developing postoperative transient rhinosinusitis. The wide range
of reported percentages (3% to 20%) may be the result of different methods
used for diagnosis (i.e., clinical, radiographic, endoscopic).
Cases of maxillary sinusitis after dental implant surgery have rarely been
reported in the dental literature. However, recently in the medical literature,
numerous cases of minor to severe complications after sinus surgery have
been documented. Although very infrequent, severe infections may lead to
more severe complications, such as orbital cellulitis, optic neuritis, cavernous
sinus thrombosis, epidural and subdural infection, meningitis, cerebritis,
blindness, osteomyelitis, and, although rare, brain abscess and death.70
Prevention
The prevention of acute rhinosinusitis after sinus graft surgery includes:
CBCT Examination.
The paranasal sinus area must be determined to be void of preexisting
pathology, anatomic variants, and a patent ostium. The superior limits of the
CBCT survey must include the maxillary ostium. Evaluation of this anatomic
area is most important in preventing postoperative sequelae. Additionally,
evaluation of the paranasal sinus anatomy for anatomic variants, pathology,
or any preexisting condition that would lead to clearance morbidity issues
must be determined prior to surgery.
Prophylactic Antibiotics.
Prophylactic antibiotic medications and sound surgical principles minimize
postoperative infections and complications. The resistance of the sinus to
contamination is low, and the chances of this happening are easily increased
with contamination by intraoral or sinus pathogens. The use of systemic
antibiotics, antimicrobial mouth rinses, and corticosteroids will help
maintain the patency of the ostium.
Treatment
If infection occurs postoperatively, treatment must be aggressive because of
the possible complications that may arise to close anatomic structures.
Systemic antibiotic therapy is the first line of treatment along with close
observation of symptoms. Recent medical literature discourages the use of
systemic decongestants and highly recommends the use of saline lavage and
rinses. Systemic decongestants have been shown to impair site antibiotic
delivery and also have a high degree of rebound effect (rhinitis
medicamentosa).
If symptoms are not alleviated with antibiotic and decongestant
medications, possible referral to the patient's physician or otolaryngologist is
warranted. Emergency consultation should be considered if the patient
complains of a severe headache that is not relieved by mild analgesics, as
well as persistent or high fever, lethargy, visual impairment, or orbital
swelling.
The authors highly recommend that a professional association with an
otolaryngologist be obtained. Because the possible morbidity of these
infections and causative pathogen is not easily determined, referral is
sometimes needed. Additionally, if mild sinus symptoms persist or signs of
severe infection are present, immediate referral is recommended. Resolution
of these conditions has been accomplished with the use of antibiotic drugs,
endoscopic treatment, or Caldwell-Luc procedures.
Combination (Graft Site Infections/Acute

Rhinosinusitis)
Etiology
The etiology of a combination infection can either be initiated from the graft
site or the sinus proper.
Diagnosis
The diagnosis for a combination type infection can parallel a combination of
graft site symptoms and/or acute rhinosinusitis.
Prevention
Same preventive techniques discussed previously for graft site infections and
acute rhinosinusitis.
Treatment
The treatment of a combination type infection should include the use of a
beta-lactam antibiotic (e.g., Augmentin) followed by the use of debridement
and nasal saline rinses. If ocular or cerebral symptoms persist, or the patient
does not respond to antibiotic treatment, referral is recommended.
Postoperative CBCT Mucosal Thickening (False-

Positive for Infection)
Immediate postoperative radiographs may reveal significant mucosal
thickening within the sinus. The clinician should not determine this to be
infection unless the above signs of infection are noted. Normally, elevation of
the sinus mucosa and bone grafting does alter the overall maxillary sinus
environment by reducing the size of the sinus and repositioning the
mucociliary transport system. In spite of this, only short-term clearance
impairment exists, resulting in only subclinical effects on the sinus
physiology. However, in cases of preoperative sinusitis histories, elevation
surgery may predispose a patient to sinus-related complications. It has been
shown that these procedures do alter the microbial environment. Studies
reveal at 3 months after surgery, positive sinus cultures were present
compared with cultures taken for the same patients preoperatively. However,
after 9 months the cultures were similar to the preelevation results. The key
is maintenance of the osteomeatal opening between the maxillary sinus and
the nasal cavity.
Migration/Displacement of Implant
In 1995 the first case of a displaced (migrated) implant into the maxillary
sinus was documented. Since then, an increased number of reports are
coming to light, documenting an ever-increasing problem. Reports have
shown that implants migrating from the maxillary sinus have been found in
the sphenoid sinus, ethmoid sinus, orbit, nasal cavity, and anterior cranial
base.
Etiology
The etiology of implant displacement or migration from the maxillary sinus
includes many possibilities. The timing of implants ending up in the
maxillary sinus proper varies from intraoperative displacement to migration
years later. Many etiologic factors have been suggested according to the
timing (early vs. late) (Table 13.2).
TABLE 13.2
Migration/Displacement of Implants
Early Late
• Poor initial stability • Too early loading
• Overpreparation of osteotomy site • Changes in intranasal or intrasinus pressure
• Poor quality of bone • Peri-implantitis
• No c restal c ortic al bone • Autoimmune reac tion
• Implant plac ement into sinus without bone graft
• Inc orrec t treatment planning
• S urgic al inexperienc e
• Untreated antral preparation
• Postoperative sinus infec tion
• Immediate plac ement implants
Prevention
For early migration/displacement complications, most likely the cause is
surgical error or incorrect treatment planning. When evaluating late
migration/placement complications, the majority of issues are a direct result
of postoperative prosthetic errors (too early loading) or factors that are
precipitated by lack of integration or minimal bone at the implant interface.
Management
The management of displaced or migrated implants into the maxillary sinus
should be treated with urgency. Leaving implants in the maxillary sinus may
lead to acute rhinosinusitis complications. Additionally, implants left in the
maxillary may become calcified (antrolith) or become displaced into other
anatomic areas (e.g., sinuses, orbit, nasal cavity, brain). The patients should
be referred as soon as possible for removal via a Caldwell-Luc approach or
endoscopy (FESS) (Fig. 13.52).
FIG 13.52 FESS. (A) FESS scope. (B) Surgical placement of FESS.
Postoperative Fungal Infection

Fungal infection after sinus bone grafting is rarely reported; however, with
the increased number of sinus graft procedures being performed, inevitably
more will be reported in the literature. Fungal sinusitis is a destructive,
invasive disease which is mostly caused by Aspergillus. Aspergillus spp is a
fungus of the Ascomycetes class, which is one of the most commonly
encountered in the human environment.
In the diagnosis of fungal sinusitis, there exist two forms: noninvasive and
invasive. The invasive form is rare and is almost always associated with
immunocompromised patients. Erosion and osseous destruction occurs that
may be fatal. However, this form has not been associated with dental
implants or sinus graft surgery.
Case studies have shown postoperative complications after sinus graft
surgery71 and overextension of root canal filling involving the noninvasive
form.72 This type of fungus growth is also termed fungus balls or asperilloma
and is associated with immunocompetent patients.
Diagnosis
Usually, the patient will present with clinical symptoms of frontal headache,
orbicular pain, nasal congestion, and bleeding with signs of chronic
rhinosinusitis. Radiographically, a distinctly increased soft tissue density
mass (radiopacity) is seen on CBCT scans.
Management
Referral to an ENT for evaluation and confirmation of diagnosis. Usually,
treatment involves surgical removal via Caldwell-Luc or FESS techniques
because systemic antimycotic drugs are ineffective.
Postoperative Maxillary Surgical Cysts

Postoperative maxillary surgical cysts have been reported in the literature
after sinus graft surgery. However, they are extremely rare. In 1927, Kubo
reported a postoperative maxillary cyst arising in the maxilla as a delayed
complication of radical surgical intervention in the maxillary sinus.36 In 1992,
Misch et al reported one incidence of a maxillary surgical cyst associated with
a past sinus graft and blade implant. Complete enucleation was
accomplished, and healing was uneventful.37 Incidence reports are more
common in Japan, where sinus disease is often treated aggressively with
surgery, but are rare in other parts of the world.73
References
2. Raja SV. Management of the posterior maxilla with sinus lift: review
of techniques. J Oral Maxillofac Surg. 2009;67(8):1730–1734.
3. Pietrokovski J. The bony residual ridge in man. J Prosthet Dent.
1975;34:456–462.
4. Misch CE. Divisions of available bone in implant dentistry. Int J Oral
Implantol. 1990;7:9–17.
5. Misch CE, Qu Z, Bidez MW. Mechanical properties of trabecular bone
in the human mandible: implications for dental implants treatment
planning and surgical placement. J Oral Maxillofac Surg. 1999;57:700–
706.
6. Manji A, Faucher J, Resnik RR, Suzuki JB. Prevalence of maxillary
sinus pathology in patients considered for sinus augmentation
procedures for dental implants. Implant Dent. 2013;22(4):428–435.
7. Sharawy M, Misch CE. The maxillary sinus membrane—a histologic
review (unpublished data. 2007.
8. Morgensen C, Tos M. Quantitative histology of the maxillary sinus.
Rhinology. 1977;15:129.
9. Scadding GK, Lund VJ, Darby YC. The effect of long-term antibiotic
therapy upon ciliary beat frequence in chronic rhinosinusitis. J
Laryngol Otol. 1995;109:24–26.
10. Jiang RS, Liang KL, Jang JW. Bacteriology of endoscopically normal
maxillary sinuses. J Larynogol Otol. 1999;113:825–828.
11. Traxler H, Windisch A, Geyerhofer U, et al. Arterial blood supply of
the maxillary sinus. Clin Anat. 1999;12(6):417–421.
12. Elian N, Wallace S, Cho SC, et al. Distribution of the maxillary artery
as it relates to sinus floor augmentation. Int J Oral Maxillofac
Implants. 2005;20:784–787.
13. Rosano G, Taschieri S, Gaudy JF, Del Fabbro M. Maxillary sinus
vascularization: a cadaveric study. J Craniofac Surg. 2009;20:940–943.
14. Nicolielo LFP, Van Dessel J, Jacobs R, et al. Presurgical CBCT
assessment of maxillary neurovascularization in relation to maxillary
sinus augmentation procedures and posterior implant placement.
Surg Radiol Anat. 2014;36(9):915–924.
15. Apostolakis D, Bissoon AK. Radiographic evaluation of the superior
alveolar canal: Measurements of its diameter and of its position in
relation to the maxillary sinus floor: a cone beam computerized
tomography study. Clin Oral Implants Res. 2014;25:553–559.
16. Zijderveld SA, van den Bergh JP, Schulten EA, ten Bruggenkate CM.
Anatomical and surgical findings and complications in 100
consecutive maxillary sinus floor elevation procedures. J Oral
17. Solar P, Geyerhofer U, Traxler H. Blood supply to the maxillary sinus
relevant to sinus floor elevation procedures. Clin Oral Implants Res.
1999;10:34–44.
18. Rice DH, Schaefer SD. Endoscopic paranasal sinus surgery. ed 3.
Lippincott Williams & Wilkins: Philadelphia; 2003.
19. Kilic C, Kamburoglu K, Yuksel SP, Ozen T. An assessment of the
relationship between the maxillary sinus floor and the maxillary
posterior teeth root tips using dental cone-beam computerized
tomography. Eur J Dent. 2010;4(4):462.
20. Ulm CW, Solaur P, Krennmar G, et al. Incidence and suggested
surgical management of septa in sinus lift procedures. Int J Oral
21. Bolger WE, Butzin CA, Parsons DS. Paranasal sinus bony anatomic
variations and mucosal abnormalities: CT analysis for endoscopic
surgery. Laryngoscope. 1991;101:56–64.
22. McKenzie M. Manual of diseases of the nose and throat. Churchill
23. Stackpole SA, Edelstein DR. The anatomic relevance of the Haller cell
in sinusitis. Am J Rhinol. 1997;11(3):219–223.
24. Erdem T, Aktas D, Erdem G, et al. Maxillary sinus hypoplasia.
Rhinology. 2002;40(3):150–153.
25. American Academy of Otolaryngology—Head and Neck Surgery. Fact
sheet: 20 questions about your sinuses. [Available at: URL]
http://www.entnet.org/healthinfo/sinus/sinus_questions.cfm.
26. Simuntis R, Kubilius R, Vaitkus S. Odontogenic maxillary sinusitis: a
review. Stomatologija. 2014;16(2):39–43.
27. Jeong SS, Yoo ES, Goong HS, et al. A computed tomographic study of the
relationship between the inferior wall of the maxillary sinus and maxillary
molar root. [KAID conference (autumn), poster presentation] 2007.
28. Daley DL, Sande M. The runny nose infection of the paranasal
sinuses. Infect Dis Clin North Am. 1988;2:131.
29. Rosenfeld RM, Andes D, Bhattacharyya N, et al. Clinical practice
guideline: adult sinusitis. Otolaryngol Head Neck Surg. 2007;137(Suppl
3):S1–S31.
30. Bolzer WE, Kennedy DW. Changing concepts in chronic sinusitis.
Hosp Pract. 1992;27:20.
31. Ponikau JU, Sherris DA, Kern EB. The diagnosis and incidence of
allergic fungal sinusitis. Mayo Clin Proc. 1999;74:877–884.
32. Beninger MS, Mickleson SA. Functional endoscopic sinus surgery,
morbidity and early results. Henry Ford Hosp Med J. 1990;38:5.
33. Dufour X, Kauffmann-Lacroix C, Ferrie JC, et al. Paranasal sinus
fungus ball: epidemiology, clinical features and diagnosis. A
retrospective analysis of 173 cases from a single medical center in
France, 1989-2002. Med Mycol. 2006;44:61–67.
34. Yoshiura K, Ban S, Hijiya K, et al. Analysis of maxillary sinusitis using
computed tomography. Dentomaxillofac Radiol. 1993;22:86.
35. Gardner DG. Pseudocysts and retention cysts of the maxillary sinus.
Oral Surg Oral Med Oral Pathol. 1984;58:561–567.
35a. Barnes L. ed 2. M. Dekker: New York; 2001:1477–1481. Surgical
pathology of the head and neck. vol 2.
35b. Kara İM, Dervişhan K, Serkan P. Experience of maxillary sinus floor
augmentation in the presence of antral pseudocysts. J Oral Maxillofac
Surg. 2010;68(7):1646–1650.
35c. Tang ZH, Wu MJ, Xu WH. Implants placed simultaneously with
maxillary sinus floor augmentations in the presence of antral
pseudocysts: a case report. Int J Oral Maxillofac Surg. 2011;40(9):998–
1001.
35d. Lin Y, Hu X, Metzmacher AR, et al. Maxillary sinus augmentation
following removal of a maxillary sinus pseudocyst after a shortened
healing period. J Oral Maxillofac Surg. 2010;68(11):2856–2860.
36. Kudo K, et al. Clinicopathological study of postoperative maxillary
cysts. J Jpn Stomatol Soc. 1972;21:250–257.
37. Misch CM, Misch CE, Resnik RR, et al. Postoperative maxillary cyst
associated with sinus elevation procedure: a case report. J Oral
Implantol. 1991;18:432–437.
37a. Jham BC, Mesquita RA, Ferreira MC, et al. A case of maxillary sinus
carcinoma. Oral Oncology Extra. 2006;42(4):157–159.
37b. Chakrabarti A, Denning DW, Ferguson BJ, et al. Fungal
rhinosinusitis: a categorization and definitional schema addressing
current controversies. The Laryngoscope. 2009;119(9):1809–1818.
38. Blaschke FF, Brady FA. The maxillary antrolith. Oral Surg Oral Med
Oral Pathol. 1979;48:187–191.
39. Crist RF, Johnson RI. Antrolith: report of case. J Oral Surg.
1972;30:694–695.
40. Karges MA, Eversol LR, Poindexter BJ. Report of case and review of
literature. J Oral Surg. 1971;29:812–814.
41. Misch CE. Maxillary sinus augmentation for endosteal implants:
organized alternative treatment plans. Int J Oral Implantol. 1987;4:49–
58.
42. Levin L, Schwartz-Arad D. The effect of cigarette smoking on dental
implants and related surgery. Implant Dent. 2005;4:357–361.
43. Tawil G, Mawla M. Sinus floor elevation using a bovine bone material
(Bio-Oss) with or without the concomitant use of a bilayered collagen
barrier (Bio-Gide): a clinical report of immediate and delayed implant
placement. Int J Oral Maxillofac Implants. 2001;16:713–721.
44. Boyne PJ, James RA. Grafting of the maxillary sinus floor with
autogenous marrow and bone. J Oral Surg. 1980;38:613–616.
45. Lang J. Clinical anatomy of the nose, nasal cavity and paranasal sinuses.
Medical Publishers: New York; 1989.
46. Warburton G, Brahim JS. Intraorbital hematoma after removal of
upper third molar: a case report. J Oral Maxillofac Surg. 2006;64:700–
704.
47. Peñarrocha M, Pérez H, Garciá A, Guarinos J. Benign paroxysmal
positional vertigo as a complication of osteotome expansion of the
maxillary alveolar ridge. J Oral Maxillofac Surg. 2001;59:106–107.
48. Di Girolamo M, Napolitano B, Arullani CA, et al. Paroxysmal
positional vertigo as a complication of osteotome sinus floor
elevation. Eur Arch Otorhinolaryngol. 2005;262:631–633.
49. Schuknecht HF. Pathology of the ear. ed 2. Lea & Febiger: Philadelphia;
1993:248–253.
50. Oh E, Kraut RA. Effect of sinus membrane perforation on dental
implant integration: a retrospective study on 128 patients. Implant
Dent. 2011;20(1):13–19.
51. Cho SC, Yoo SK, Wallace SS. Correlation between membrane thickness and
perforation rates in sinus augmentation surgery. [Presented at Academy
of Osseointegration Annual Meeting, Dallas, March 14–16,] 2002.
52. Aimetti M, Massei G, Morra M, et al. Correlation between gingival
phenotype and Schneiderian membrane thickness. Int J Oral
Maxillofac Implants. 2007;23(6):1128–1132.
53. Betts HJ, Miloro M. Modification of the sinus lift procedure for septa
in the maxillary antrum. J Oral Maxillofac Surg. 1994;52:332.
54. Krennmair G, Ulm CW, Lugmayr H, et al. The incidence, location and
height of maxillary sinus septa in the edentulous and dentate maxilla.
55. Flanagan D. Arterial supply of maxillary sinus and potential for
bleeding complication during lateral approach sinus elevation.
Implant Dent. 2005;14:336–339.
56. Mardinger O, Moses O, Chaushu G, et al. Challenges associated with
reentry maxillary sinus augmentation. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 2010;110(3):287–291.
56a. Guerrero JS. Lateral window sinus augmentation: complications and
outcomes of 101 consecutive procedures. Implant Dent.
2015;24(3):354–361.
57. Barone A, Santini S, Sbordone L, et al. A clinical study of the
outcomes and complications associated with maxillary sinus
augmentation. Int J Oral Maxillofac Implants. 2006;21(1):81–85.
58. Peterson LJ. Antibiotic prophylaxis against wound infections in oral
and maxillofacial surgery. J Oral Maxillofac Surg. 1990;48:617–620.
59. Marx RE, Kline SN, Johnson RD, et al. The use of freeze-dried
allogenic bone in oral and maxillofacial surgery. J Oral Surg.
1981;39:264–274.
60. Jacobs MR, Felmingham D, Appelbaum PC, et al. The Alexander
Project 1998-2000: susceptibility of pathogens isolated from
community-acquired respiratory tract infection to commonly used
antimicrobial agents. J Antimicrob Chemother. 2003;52:229–246.
61. Snydor A, Gwaltney J, Cachetto DM, et al. Comparative evaluation of
cefuroxime axetil and cefaclor for treatment of acute bacterial
maxillary sinusitis. Arch Otolaryngol Head Neck Surg. 1989;115:1430.
62. Gallagher DM, Epker BN. Infection following intraoral surgical
correction of dentofacial deformities: a review of 140 consecutive
cases. J Oral Surg. 1980;38:117–120.
63. Urist MR, Silverman BF, Buring K, et al. The bone induction principle.
Clin Orthop Relat Res. 1967;53:243–283.
64. Beardmore AA, Brooks DE, Wenke JC, et al. Effectiveness of local
antibiotic delivery with an osteoinductive and osteoconductive bone-
graft substitute. J Bone Joint Surg Am. 2005;87:107–112.
65. Mabry TW, Yukna RA, Sepe WW. Freeze-dried bone allografts
combined with tetracycline in the treatment of juvenile periodontitis.
J Periodontol. 1985;56:74–81.
66. Mabry RC. Corticosteroids in rhinology. Goldsmith J. The principles and
practice of rhinology. John Wiley & Sons.: New York; 1987:147–162.
67. Falck B, Svanholm H, Aust R. The effect of xylometazoline on the
mucosa of human maxillary sinus. Rhinology. 1990;28:239–477.
68. Sandler NA, Johns FR, Braun TW. Advances in the management of
acute and chronic sinusitis. J Oral Maxillofac Surg. 1996;54:1005–1013.
69. Olson DEL, Rosgon BM, Hilsinger RL. Radiographic comparison of
three nasal saline irrigation. Laryngoscope. 2002;112:1394–1398.
70. Smith D, Goycollea M, Meyerhoff WL. Fulminant odontogenic
sinusitis. Ear Nose Throat J. 1979;58:411.
71. Sohn DS, Lee JK, Shin HI, et al. Fungal infection as a complication of
sinus bone grafting and implants: a case report. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod. 2009;107(3):375–380.
72. Khongkhunthian P, Reichart PA. Aspergillosis of the maxillarysinus as
a complication of overfilling root canal material into the sinus: report
of two cases. J Endod. 2001;27:476–478.
73. Lockhart R, Ceccaldi J, Bertrand JC. Postoperative maxillary cyst
following sinus bone graft: report of a case. Int J Oral Maxillofac
Implants. 2000;15:583–586.
14
Complications Associated With
Immediate Implant Placement
Glenn J. Jividen, Carl E. Misch
The placement of endosseous implants at the time of tooth extraction has

been shown to be a viable protocol.1-5 The objectives of immediate implant
placement are the same as for staged treatment: achievement of implant
primary stability, sufficient rigid fixation after healing, proper prosthetic
location, and an esthetic result. Immediate implant placement has the
potential to accomplish these objectives with fewer procedures, less
treatment time, and less cost. Although complications can occur with any
particular technique or protocol, this technique adds multiple variables that
cumulatively place the clinician more at risk of having an adverse result
(Table 14.1). Extraction and immediate implant placement may also be
combined with immediate provisionalization (either nonfunctional or
loaded). This chapter will address complications specifically related to
immediate implant placement at the time of extraction.
TABLE 14.1
Implant Placement in Extraction Site
Immediate Delayed
Advantages
↑ S urgery ↑ S urgic al c ontrol, position, angulation
↑ Time ↑ Hard tissue quality
↓ Maintenanc e of soft tissue ↑ S uc c ess, less risk of infec tion
Intraosseous bone graft
Disadvantages
↑ Fac ial bone loss after loading or during healing Extended time for transitional
Implant too fac ial and/or angled abutment Onlay graft may be needed at surgery
(From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)

General Considerations
Immediate implant placement after tooth extraction has the potential to
decrease the number of appointments as well as treatment time. Patient
acceptance of this technique is high. Optimal esthetics in many cases is
possible along with hard and soft tissue preservation (Figs. 14.1, 14.2, and
14.3). The caveat relates to case selection and changing medicolegal
standards. Before discussing immediate placement complications, a review of
alternative (staged) placement is presented, with contrasts to immediate
placement where applicable.
FIG 14.1 Hard and soft tissue preservation with immediate implant placement can
result in optimum esthetic outcomes.
FIG 14.2 (A) Carious mandibular molar is planned for extraction and immediate
implant placement. (B) Molar is sectioned to minimize extraction-related bone loss.
Premolar implant has been placed in healed site with force direction indicator in
place. (C) Bone allograft used to fill in voids. (D) Vicryl mesh used as GBR
membrane.
FIG 14.3 Outcome 21 years post immediate implant placement. (A) Complete
bone fill around immediately placed implant. (B) Occlusal view of final restoration.
(C) Radiograph of splinted prosthesis. (D) Buccal view of splinted prosthesis.
Available Bone
Available bone describes the amount of bone in the edentulous extraction
site considered for implantation. It is measured in width, height, length,
angulation, and crown height space (Fig. 14.4). As a general guideline, 1.5 to 2
mm of surgical error is maintained between the implant and any adjacent
landmark. This is especially critical when the opposing landmark is the
mandibular inferior alveolar nerve. However, the implant may be placed
without complication through the cortical plate of the maxillary sinus or
inferior border of the mandible. The implant may also be positioned closer to
the cribriform plate of a natural tooth.6 When placing an implant in an
immediate-extraction site, the surgeon needs to consider the socket
dimension and the defect between the labial plate of bone and the implant.
The faciopalatal dimension of an anterior tooth, for example, is often greater
than its mesiodistal dimension. When an anterior tooth requires extraction,
during the extraction process the thin facial cortex often becomes
compromised or lost. As a result, it is most always several millimeters apical
to the palatal cortical plate, and frequently bone grafting and/or membrane
placement in conjunction with the implant insertion are needed. Immediate
implant placement in the anterior region using a round implant often
requires that the osteotomy and implant insertion engage the lingual wall of
the alveolus and penetrate halfway to two thirds of the way down the
extraction site into the remaining lingual apical bone for rigid fixation (Fig.
14.5). This surgical approach is more challenging than preparing the
osteotomy in a homogenous bone density. The best implant size is often 4 to
5 mm in diameter for a central incisor because the associated extraction
socket is often greater than 6 mm (especially in the faciopalatal dimension),
so a surgical defect as large as 2 mm remains around the implant. More or
less broad, oval, or kidney-shaped spaces have been described to run
coronoapically along the entire surface of the socket next to the implant.7 The
natural resorption of the facial plate may not be halted by implant insertion,
and bone implant contact may be reduced when the facial plate resorbs.8
FIG 14.4 The height of available bone is measured from the crest of the edentulous
ridge to the opposing landmark. The opposing landmark may be in the maxillary
canine region (A), floor of the nares (B), maxillary sinus (C), tuberosity (D),
mandibular canine region (G), anterior mandible (F), or bone above the inferior
mandibular canal (E). (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008,
Mosby.)
FIG 14.5 Multiplanar drilling technique. (A) Extraction socket whose walls have
been evaluated and confirmed to be intact and free from infection. (B) 2-mm pilot drill
first prepares the initial osteotomy two thirds of the way down from the crest and
through the thick palatal cribriform plate. (C) The implant site prepared to the
opposing landmark or preplanned length. (D) The osteotomy is kept in an angulation
aligned with the incisal edge of the adjacent teeth. (From Misch CE: Contemporary implant
Available Bone Height

The height of available bone is measured from the crest of the edentulous
ridge to the opposing landmark. The anterior regions are limited by the
maxillary nares or the inferior border of the mandible. The anterior regions
of the jaws have the greatest height because the maxillary sinus and inferior
alveolar nerve limit this dimension in the posterior regions. The maxillary
canine eminence region often offers the greatest height of available bone in
the maxillary anterior.9 In the posterior jaw region, there is usually greater
bone height in the maxillary first premolar than in the second premolar,
which has greater height than the molar sites because of the concave
morphology of the maxillary sinus floor. Likewise, the mandibular first
premolar region is usually anterior to the mental foramen and provides the
most vertical column of bone in the posterior mandible. However, on
occasion, this premolar site may present a reduced height compared with the
anterior region because of the presence of an anterior loop of the mandibular
canal. The nerve courses anteriorly below the foramen and proceeds
superiorly, then distally, before its exit through the mental foramen. Posterior
nerve anatomy has particular significance with regard to immediate implant
placement. Primary stability for immediately placed implants is frequently
achieved using bone apical to the extraction site. In the posterior mandible,
the course of the inferior alveolar nerve can vary from Type 1 to Type 3 with
associated available apical bone ranging from nonexistent to sufficient and
surgical risk varying accordingly. In addition, variants of the mental foramen
exist that can increase the possibility of injury to the inferior alveolar nerve
during immediate implant placement in the region (Fig. 14.6). The available
bone height in an edentulous site is the most important dimension for
implant consideration because it affects both implant length and crown
height. Crown height affects force factors and esthetics. In addition, vertical
bone augmentation, if needed, is less predictable then width augmentation.
FIG 14.6 Variation of mental foramen positions. (A) 3-D image depicting premolar
root located in mental foramen. (B) In 25% to 38% of patients, the mental foramen is
superior to the root apex of the premolar. (C) Proximity of mandibular canal to the
premolar apex.
Available Bone Width

The width of available bone is measured between the facial and lingual plates
at the crest of the potential implant site. It is the next most significant
criterion affecting long-term survival of endosteal implants. The crestal
aspect of the residual ridge is often cortical in nature and exhibits greater
density than the underlying trabecular bone regions, especially in the
mandible.
Accordingly, the lack of crestal bone at an extraction site makes the
achievement of primary stability more challenging for immediate implant
placement. Facial dehiscence defects commonly found after tooth extraction
and immediate implant placement have been shown to have more
compromised healing as compared to infrabony defects.10
Available Bone Length

Bone length is defined as the mesiodistal length of bone in a postextraction
area. It is most often limited by adjacent teeth or implants. As a general rule
the implant should be at least 1.5 mm from an adjacent tooth and 3 mm from
an adjacent implant. This dimension not only allows surgical error but also
compensates for the width of an implant or tooth crestal defect, which is
usually less than 1.4 mm and may vary with implant diameter and thread
design. As a result, if bone loss occurs around the crest module of an implant
or around a tooth with periodontal disease, the associated vertical bone
defect will not typically expand into horizontal defect and thereby cause bone
loss on the adjacent structure.
Bone Angulation
Bone angulation is an additional determinant for available bone. The initial
alveolar bone angulation represents the natural tooth root trajectory in
relation to the occlusal plane. Ideally, it is perpendicular to the plane of
occlusion, which is aligned with the forces of occlusion and is parallel to the
long axis of the prosthodontic restoration. The incisal and occlusal surfaces
of the teeth follow the curve of Wilson and curve of Spee. As such, the roots
of the maxillary teeth are angled toward a common point approximately 4
inches away. The mandibular roots flare, so the anatomic crowns are more
lingually inclined in the posterior regions and labially inclined in the anterior
area compared with the underlying roots. The mandibular first premolar
cusp tip is usually vertical to its root apex. The maxillary anterior teeth are
the only segment in either arch that does not receive a long axis load to the
tooth roots but instead are usually loaded at a 12-degree angle. As such, their
root diameter is greater than the mandibular anterior teeth. In all other
regions the teeth are loaded perpendicular to the curves of Wilson or Spee.
The anterior sextants may have labial undercuts that often mandate greater
angulation of the implants or concurrent grafting of the site after insertion.
The narrower width ridge often requires a root form implant design that is
likewise narrower. Compared with larger diameters, smaller-diameter
designs cause greater crestal stress and may not offer the same range of
custom abutments. In addition, the narrower width of bone does not permit
as much latitude in placement regarding angulation within the bone. This
limits the acceptable angulation of bone in the narrow ridge to 20 degrees
from the axis of the adjacent clinical crowns ora line perpendicular to the
occlusal plane.6 The angulation of available bone in the maxillary first
premolar region may place the adjacent cuspid at risk during implant
placement (Fig. 14.7).
FIG 14.7 Angulation of available bone adjacent to maxillary canine possess
increase risk for tooth injury. The maxillary first premolar is often angled distally to
remain parallel to the canine root. A shorter implant or tapered implant may be of
benefit. This limitation of bone-implant contact could compromise primary stability
for immediate implant placement. (From Misch CE: Contemporary implant dentistry, ed 3, St
Type of Prosthesis
The clinician must always be aware of the anticipated final prosthesis and its
associated dimensions of crown-height space, whether for a single tooth
crown or full arch prosthesis. In cases where tooth extraction will result in an
edentulous arch, the frequent need for alveoloplasty may result in almost
complete elimination of the residual socket, thus making it comparable to an
implant placement protocol for a healed site.
When considering immediate implant placement for partially edentulous
patients, the dimension of the tooth space(s) being replaced, in the context of
the desired final tooth positioning within and between the arches, may
require orthodontic evaluation and treatment. Typical examples would be
extruded and tipped teeth.
Bone Density
Bone quality or density refers to the internal structure of bone and reflects a
number of its biomechanical properties, such as strength and modulus of
elasticity. The density of available bone in a potential implant site is a
determining factor in treatment planning, implant design, surgical approach,
healing time, and initial progressive bone loading during prosthetic
reconstruction. The quality of bone is often dependent upon the arch
position. The most dense bone is usually observed in the anterior mandible,
with less dense bone in the anterior maxilla and posterior mandible, and the
least dense bone typically found in the posterior maxilla. In addition to arch
location, several independent groups have reported different failure rates
related to the quality of the bone. Johns et al reported 3% failure of implants
in moderate bone densities, but a 28% implant failure in the poorest bone
type.11 Smedberg et al reported a 36% failure rate in the poorest bone
density.12 The reduced implant survival most often is more related to bone
density than arch location. In a 15-year follow-up study, Snauwaert et al
reported early annual and late failures were more frequently found in the
maxilla.13 Hermann et al14 found implant failures were strongly correlated to
patient factors, including bone quality, especially when coupled with poor
bone volume. Bone quality is directly related to the ability to achieve an
acceptable level of primary fixation for immediate implant placement as well
as long-term success for all placement protocols.
Anatomic Location
For immediate implant placement, an awareness of the bone characteristics
of the proposed anatomic location will help dictate the appropriate treatment
plan modifications for short- and long-term success. Regional variations in
both available bone and bone density have already been described. The
initial treatment plan prior to surgery suggests the anterior maxilla be
treated as D3 bone, the posterior maxilla as D4 bone, the anterior mandible
as D2 bone, and the posterior mandible as D3 bone. Bone remodeling,
including loss of bone density, is primarily related to the length of time the
region has been edentulous and therefore not loaded, the initial density of
the bone, and mandibular flexure and torsion. Immediate implant placement
can take advantage of the fact that implant placement can be performed
before the bone density in the jaws begins its usual decline after tooth loss.
Presence of Bacteria/Existing Pathology

Immediate implant placement is generally recognized as a more complex
procedure in contrast to implant placement in a healed ridge of adequate
bone quality. The presence of infection adds an additional variable to this
complexity. A site can be classified as having either periapical, endodontic,
perioendodontic, or periodontal infection. Multiple studies have found the
survival rates for implants immediately placed in infected sockets similar to
those placed in noninfected sockets or healed ridges.15-17 These reviews,
however, should be interpreted taking into account the classification of
infection was often vague and varied among the studies.
Biomechanical Overload Issues

Immediate occlusal loading on temporary crowns positioned immediately on
implants placed in fresh extraction sockets have been shown to reduce
treatment time. A number of different immediate load protocols have been
described in the literature (Schnitman, Tarnow, Misch).18-20 An acknowledged
common concern, however, is the risk of occlusal overload. Often the risks of
this procedure are perceived to be highest during the first week after the
implant insertion surgery. In reality, the bone interface is stronger on the day
of implant placement than it is 3 months later.21 As a result of the surgical
placement, organized, mineralized lamellar bone in the preparation site
becomes unorganized, less mineralized, woven bone of repair next to the
implant.22 The implant-bone interface is weakest and most at risk of overload
at 3 to 6 weeks after surgical insertion because the surgical trauma causes
bone remodeling at the interface that is least mineralized and unorganized
during this time frame. A clinical report by Buchs et al23 found immediately
loaded implant failure occurred primarily between 3 and 5 weeks after
implant insertion from mobility without infection. In addition to procedures
and techniques needed to manage the immediate implant placement, the
desire to add immediate load requires the clinician to address and control
the issues of occlusal overload and bone remodeling.
Learning Curve
Clinical experience has been shown to affect the outcomes of dental implant
treatment. Lambert reported surgical experience may influence the success
or failure of dental implants from initial placement to second-stage surgery.24
Preiskel et al concluded that a 2-year differential of surgical experience can
have a major impact on the failure probability of unloaded implants.25 Geckili
noted a decrease in failure rate from 4.6% to 1.6% owing to the presumptive
improvement in the skill of the surgeon over a 5-year period.26 The added
variable of perioperative bone grafting, frequently performed during
immediate implant placement, was thought to negatively affect implant
success rates in a 6-year study by Smith. That study reported an overall 1-year
survival of 94% and a 5-year survival of 92.8%. In addition, there were a
relatively high proportion of technical failures due to errors in treatment
planning or surgical technique, which accounted for the intraoperative
failures (33%) and late failures (14%) that were attributed to the experience
levels of the surgical trainees.27
Implant Size
Length Relative to Tooth or Teeth Being Replaced
Prosthesis type, bone density, and anticipated load factors are treatment plan
modifiers affecting implant size, design, number, surface condition, and the
need/method of progressive loading.
The implant dimension of width is often limited by adjacent teeth or
implants. As a general rule the implant should be at least 1.5 mm from an
adjacent tooth and 3 mm from an adjacent implant. This dimension not only
allows for surgical error but also compensates for the width of an implant or
tooth crestal defect, which is usually less than 1.4 mm. As a result, if bone
loss occurs at the crest module of an implant or from periodontal disease
with a tooth, the vertical bone defect will not spread horizontally and cause
bone loss on the adjacent structure.28 The ideal implant width for single-
tooth replacement or multiple adjacent implants is often related to the
natural tooth that is being replaced in the site. The tooth has its greatest
width at the interproximal contacts, is narrower at the cement-enamel
junction (CEJ), and is even narrower at the initial crestal bone contact, which
is 2 mm below the CEJ. The ideal implant diameter corresponds to the width
of the natural tooth 2 mm below the CEJ, if it also is 1.5 mm from the
adjacent tooth. In this way the implant crown emergence through the soft
tissue may be similar to that of a natural tooth (Table 14.2).6 The ability to
select the most ideal implant size based on these parameters is much less
difficult in a healed site as compared to an extraction site. An ideal treatment
plan would include implant length of 12 mm or greater with a 4-mm
diameter for most anterior implant sites and 5 mm or greater in the molar
regions.29 When the ideal implant size cannot be inserted because of
inadequate bone, an alternative to bone augmentation may be to increase the
surface area of the implant by modifying the implant body design.6
TABLE 14.2
Maxillary Anterior Teeth Dimension
Type and Number of Mesiodistal Crown Mesiodistal Cervix Mesiodistal Cementoenamel Faciolingual Crown Faciolingual Cervix
Teeth (mm) (mm) Junction (−2 mm) (mm) (mm)
Central 8.6 6.4 5.5 7.1 6.4
Lateral 6.6 4.7 4.3 6.2 5.8
Cuspid 7.6 5.6 4.6 8.1 7.6
(From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008, Mosby.)
Implant Design
The most predictable aspect of implant dentistry appears to be the surgical
success rate from implant insertion to uncovery; it is usually higher than 98%
regardless of implant design or size.30-36 Implant design considerations,
however, should be made with intent of successful long-term outcomes, not
just short-term surgical success; designing an implant for surgical ease does
not appear to be the most important aspect of the long-term overall implant
prosthodontic-related process to reduce the incidence of complications.
Given the desire for long-term implant survival and health, careful selection
of implant design should include the features of titanium alloy material,
roughened surface treatment, tapered crest module, and square thread
design.37,38
Many biocompatible materials are unable to withstand the type and
magnitude of loads that may be imposed on dental implants. Titanium and
titanium alloys have a long history of successful use in dental and orthopedic
applications. The excellent biocompatibility of titanium and its alloy has
been well documented. Titanium-aluminum-vanadium alloy (Ti-6Al-4V) has
been shown to exhibit the most attractive combination of mechanical and
physical properties, corrosion resistance, and general biocompatibility of all
metallic biomaterials.39,40 The primary advantage of titanium alloy as
compared with other grades of titanium is its strength. Ultimate strength and
fatigue strength are primary considerations given the ramifications of the
loading profiles to which dental implant bodies are subjected and that can
still place an alloy at fracture risk (Fig. 14.8).
FIG 14.8 Fractured 5.0-mm ext hex implant. (BioHorizons IPH, Inc.)
Crest module design has a significant influence in regard to overall

implant body design. There are at least six causes of marginal bone loss at
the crestal bone region of implants, including the formation of a “biologic
width” and occlusal overload after the implant is in function.6 Ultimate
strength and fatigue strength are primary considerations given the
ramifications of the loading profiles to which dental implant bodies are
subjected and that still can place an implant of ideal dimensions at fracture
risk. The crest module of an implant should be slightly larger than the outer
thread diameter of the implant body (Fig. 14.9). In this way the crest module
may completely seal the osteotomy, providing a barrier and deterrent for the
ingress of bacteria or fibrous tissue during initial healing after insertion in a
healed site. The contact created by the larger crest module may also provide
for greater initial stability of the implant following placement, especially in
softer unprepared bone, because it compresses the crestal bone region. In
the case of immediate implant placement, the crestal bone contact, if any, will
usually be on the lingual or palatal aspect and can contribute to initial
stabilization. The next consideration of the crest module is related to occlusal
loading. Most of the occlusal stress occurs at the crestal region of an implant
design (Fig. 14.10). A smooth, parallel-sided crest module will increase the
risk of bone loss after loading, whereas any crest module design that
incorporates an angled geometry or grooves to the crest module, coupled
with a surface texture that increases bone contact, will impose a beneficial
compressive component to the contiguous bone and decrease the risk of
bone loss (Fig. 14.11).
FIG 14.9 Fracture of a 5.0-mm diameter implant of alloy construction. This
complication can be minimized with a less complicated selection of ideal implant
dimension possible in a healed or augmented site. (From Misch CE: Contemporary implant
FIG 14.10 Stresses around implants are higher near the crest.
FIG 14.11 The crest module with a cylinder metal collar transfers primarily shear
forces to the bone (left). (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008,
Mosby.)
The surface condition of the implant is particularly important for healing

of immediately placed implants. The bone-implant contact (BIC) of
roughened implants has been shown to be increased during initial healing as
compared to smooth metal.41 Lastly, although selection of thread shape
should be optimized for long-term load function, thread shape may have an
influence on the initial healing phase of osseointegration. An animal study
by Steigenga et al compared three thread shapes with identical implant
width, length, thread number, thread depth, and surface condition. The V-
shaped and reverse buttress thread shapes had similar BIC percent and
similar reverse torque values to remove the implant after initial healing. The
square thread design (Fig. 14.12) had a higher BIC percent and a greater
reverse torque test value.38
FIG 14.12 Standard thread shapes in dental implant design. The V, square, reverse
buttress threads, and non-threaded. (From Steigenga J, et al: J Periodontol 75(9):1233–1241,
2004.)
Potential Complications Related to Immediate Placement

Protocol
In cases where the facial bone is missing, the bone regenerated over the
facial aspect of the implant with guided bone regeneration (GBR) is often
immature woven bone, which is more prone to resorption because of occlusal
overload. To improve GBR success, techniques for immediate implant
placement after extraction typically include countersinking the implant 2 mm
or more below the facial plate (which is already more apical than the palatal
plate) and placing a biomaterial such as deproteinized bovine bone, calcium
phosphate (CaPO4), resorbable hydroxyapatite (HA), allograft, and/or
autologous bone to fill the labial defect, with or without the addition of
connective tissue grafts and/or membranes. Many classifications and
protocols have been published with regard to immediate implant placement.
The implant will obtain rigid fixation with nearly all of these techniques.
However, the goal of implant therapy is not limited solely to rigid fixation.
The inability to achieve proper esthetic and health parameters constitutes a
compromised result and increased risk of esthetic or implant failure.42 When
the implant is countersunk below the facial bone, the implant platform may
be as much as 4 mm apical to the CEJ of the adjacent teeth, which increases
the anatomic crown height and the pocket depth, especially after crestal bone
loss during the first year. In addition, synthetic grafts, if used, placed around
the titanium implant grow less dense quality bone that is also limited in
implant contact. The capacity of this less dense bone promoted by barrier
membranes around implants to withstand loading seems to be limited, and
animal studies indicate as much as 85% may be lost after loading.43 An
explanation may be that no blood vessels arise from the implant; to the
contrary, it reduces the number of bony walls of the defect and limits blood
supply to the facial bone graft. As a result, bone is less likely to form, and
when it forms it is less dense and more at risk of resorption once the implant
is loaded. Although primary closure of the soft tissue provides a more
predictable result when bone grafting is performed, it may be more difficult
with an immediate extraction technique. Although not advocated, the labial
tissue is often reflected to approximate the tissue over the socket defect. This
technique further compromises the blood supply to the labial cortical bone
and also decreases the amount of facial keratinized gingiva because the facial
tissues are placed over the extraction socket. As a consequence, some type of
mucogingival corrective surgery may be indicated after stage I healing to
restore the facial attached and keratinized tissue. The labial bone usually
remodels to 0.5 mm below the abutment-implant connection (which was, in
most cases, already countersunk below the facial bone and several
millimeters below the palatal bone). Bone loss may continue in the region to
the first thread (as a result of the implant crest module design), then
stabilize in a region of greater bone density. As a consequence, reports often
illustrate soft tissue pocket depths greater than 7 to 8 mm at the midfacial
tooth position. The presence of anaerobic microorganisms in soft tissue
pockets of 5 mm or more has been documented. With good hygiene the soft
tissue often recedes, with a resulting lengthened clinical crown and “black
triangles” in the interproximal areas caused by the absence of properly
developed interdental papillae, which compromises long-term esthetics
and/or contributes to soft tissue complications. When judicious case
selection has not been exercised and thorough debridement has not been
performed, an increased risk of postoperative infection exists around the
implant with an immediate insertion owing to the presence of bacteria that
were part of the cause of tooth loss. The presence of exudate lowers the pH,
which causes a solution-mediated resorption of the grafted bone and
contaminates the implant body with a bacterial smear layer, which in turn
reduces bone contact. An improved bone interface may be obtained if the
large-diameter extraction site is grafted before implant placement. If the
labial plate is compromised, additional intraorally harvested bone and/or
GBR are indicated. The delayed implant insertion method appears to enhance
capillary propagation and trabecular formation before implant placement,
facilitating the formation of an implant-bone interface.44 A staged protocol
allows the soft tissue to granulate over the augmented extraction site,
creating an increased zone of attached gingiva. The result of the
augmentation can be evaluated before implant placement, rather than
dealing with compromises after implant integration. In this way the implant
may be placed in an ideal position in relation to the crestal bone and the
adjacent teeth and within the exact contours of the final restoration.6
Prevention Related to an Immediate Placement
Protocol
Presence of Nonintact Alveolar Socket
Bone fill around an implant in an extraction site is most favorable when an
intact socket is present. A nonintact socket may be encountered, either
related to a preexisting condition or the tooth extraction process. This
unanticipated loss of bone may have an extent and anatomy that the clinician
may be unprepared to address if expectations were only of an intact socket.
Prevention
Thorough Pretreatment Evaluation.

The type of extraction defect (e.g., walls of bone present) can be anticipated
with careful preoperative clinical exam that includes periodontal probing
along with two- and three-dimensional radiographs. This clinical data,
including attachment levels, is useful in accessing the periodontium for bone
defects such as dehiscences.
Atraumatic Tooth Extraction.

Once the extraction of a natural tooth is indicated, methods to maintain or
obtain the needed surrounding hard and soft tissues are indicated. Avoiding
soft tissue injury reduces dimensional loss of the underlying bone because
the periosteum supplies more than 80% of the blood supply to cortical
bone.45 The extraction of a natural tooth begins with an incision within the
sulcus, preferably with a thin scalpel blade rather than a blunt periotome,
360 degrees around the tooth, to cut the connective tissue attachment fibers
above the bone. The next step in an atraumatic extraction process is to
observe the crown and root anatomy, especially in multirooted teeth.
Proximal reduction may be indicated to prevent damage to adjacent teeth
and provide space for bone expansion around the root(s). If the roots of the
tooth to be extracted are divergent, they should be sectioned and removed as
individual units, rather than risking fracture of the roots or surrounding
bone. Periotomes and dental elevators, which both use the mechanical
advantage of a wedge, can then be used to initiate the luxation of teeth for
their removal. A traditional dental forceps can then be used to grasp the
tooth for any needed additional luxation prior to tooth removal. Alternatively,
a biomechanically based forceps (physics forceps) can be used. Its increased
mechanical advantage may allow for tooth removal without application of
rotational forces, minimizing potential fracture of the facial plate of bone.46
Treatment Options
Abort Procedure.
Depending on the extent of the residual socket defect, the clinician may
consider aborting the procedure if there is concern or doubt regarding the
skill set needed for bone grafting.
Bone Grafting.
The grafting materials and techniques are based on the number of bony walls
that remain after the tooth is removed (Fig. 14.13).47
FIG 14.13 The graft materials and techniques for socket grafting are related to the
remaining number of bony walls. (A) A thick five-wall bony defect may use any
resorbable graft material (RGM). (B) Four-wall defects require an autograft or
mineralized alloplast, allograft, and barrier membrane. (C) A two- or three-wall bony
defect may use some alloplast/mineralized allograft but should use autograft and a
barrier membrane as well. (D) A one-wall bony defect is most predictable with a
cortical autograft fixated to the host bone. (From Misch CE: Contemporary implant dentistry,
Thick five bony wall defect.

Regeneration restores complete morphology and bone volume to the residual
ridge. This most often occurs when there are five thick, bony walls around
the extraction site. Most of the keys for predictable bone formation are
present under these conditions, and the socket often forms bone in the
extraction socket without loss of width or height. The atraumatic extraction of
a tooth without pathology provides many of the keys necessary for
predictable bone regeneration. The soft tissue around the extraction site
begins to grow over the clot and granulation tissue of the socket and within 2
to 3 weeks covers the site.
Four- to five-wall bony socket.

When a labial plate around a socket is missing, the absence of the wall
prevents space maintenance, reduces host bone vascularization, and replaces
it with soft tissue vascularization. The facial bone level will never grow above
the height of bone on the facial cortical plate of the tooth. Bone
augmentation procedures must be used to obtain an ideal volume and
contour of bone. Sockets with a missing lateral wall are significantly
compromised and heal by repair rather than regeneration. The first
determination after the tooth extraction is complete is the assessment of the
thickness of labial and palatal plates of bone and their relative height to the
ideal volume desired. When one of the lateral plates of bone is thinner than
1.5 mm or when height is desired, a socket graft is indicated, even in the
presence of five bony walls. A similar socket augmentation procedure also
may be used when the labial plate of bone is missing. The two techniques of
choice are a barrier membrane (BM) with a mineralized alloplast/freeze-dried
bone (FDB) socket fill or a modified socket seal surgery.
Barrier membrane with alloplast/freeze-dried bone.

An acellular dermal matrix is selected for a BM when soft tissue
augmentation is also desired, or a collagen membrane is used when the soft
tissue drape is not an issue. A periotome or thin periosteal elevator is used to
tunnel under the final bone periosteum and lift the soft tissue off the bone
over the thin bony wall. This tunnel should extend several millimeters
beyond the desired augmentation site. A BM is then slid into the “pocket”
created under the tissue and extends apical, mesial, and distal beyond the
extraction site. Approximately 6 to 8 mm of the BM should extend above the
marginal tissue. When the facial plate is thin, the socket may be filled with
FDB (e.g., MinerOss, Puros) or a mineralized HA source (e.g., BioOss,
Osteograf-N). When the labial plate is missing, the FDB may be placed in the
apical portion, but particulate autologous bone should be placed in the
crestal half of the socket. The walls of bone on the mesial, distal, and palatal
provide bone blood vessels to this autograft. The extension of collagen or
AlloDerm then covers the top of the socket and is tucked below the palatal
tissue. Sutures are then placed over the top of the BM. Primary closure of the
soft tissues is not obtained because the tissues would need to be reflected
and advanced over the socket, which would affect the soft tissue drape. The
extraction site may be reentered after 4 to 6 months. The clinical time for
reentry is determined by the absence of the cortical lining of the socket
(cribriform plate) on a periapical radiograph. Once this has occurred, the
implant may be inserted and followed by a regular healing and restoration
protocol.
Socket seal surgery.

A composite graft socket seal surgery has been developed by Misch et al48,49
composed of connective tissue, periosteum, and trabecular bone used to seal
a fresh extraction socket. A connective tissue graft has the advantage over a
keratinized graft of blending into the surrounding attached gingival regions,
offering similar color and texture of the epithelium. This is most
advantageous in the maxillary anterior region and other aesthetic areas. The
composite graft also contains autogenous bone. The major advantage of
autologous bone is a more rapid and predictable bone formation via
osteogenesis. This technique may be used any time a tooth is extracted and
an implant is planned as replacement. It employs the use of a 6- to 10-mm
trephine burr (corresponding to the extraction site diameter) in a slow-speed,
high-torque handpiece to harvest a gingival graft with underlying bone. The
most common site for the intraoral composite graft harvest is the maxillary
tuberosity region. The bone core (usually 5 to 10 mm in height) and the
attached soft tissue (about 3 mm in height) are trimmed of their epithelium
with a tissue scissors, leaving 3 to 6 mm of connective tissue attached to the
bone core. A mallet and blunt instrument should be used to tap it into place
and compress the bony core to conform to the crestal contour of the socket.
The connective tissue portion of the graft is then sutured to the surrounding
gingival tissue with facial and palatal interrupted 4-0 Vicryl sutures. A
removable transitional prosthesis should not be permitted to load the tissue
during the first few weeks after extraction; otherwise, the composite graft
may become mobile and sequestrate. The transfer of the bone graft with an
intact periosteal layer expedites revascularization and may decrease the
healing time.50,51 As a result, reentry may be in 4 to 5 months, and placement
of an ideal implant diameter is often made possible.
Two to Three Bony Wall Defects.

A two to three bony wall defect is treated very similarly to a four bony wall
defect. However, because the defect size is larger, more autograft is required
in the bone graft. Rather than using the autograft primarily in the crestal
region, it is of benefit that the entire first layer of the resorbable graft
materials be an autograft. As a consequence, more often a donor site from
the mandible is required. The most common two to three bony wall defects
are extraction sites missing more than the labial bony wall. Because the
mesial distal bony walls are usually present, the host site is more predictable
than a one bony wall defect. Incision line opening is less of a complication
because the residual ridge form has soft tissue support around the defect.
One Bony Wall Defects.

Bone augmentation for these types of defects typically uses GBR or block
graft techniques. Several methods have already been discussed regarding
edentulous site augmentation. There are advantages and disadvantages to
each of the bone regeneration techniques. Although this discussion will
focus on particulate grafting techniques, the clinician needs to carefully
discern the scope and objectives of an augmentation case in the context of
defect size, anticipated soft tissue contours, healing time, and
skill/experience level.
Barrier membranes and guided bone regeneration.

There are disadvantages to using GBR procedures for all host defects or
deficiencies. Bone height and width augmentation with BM are usually
limited to less than 3 to 4 mm. Soft tissue contours are more difficult to
predict. Extended healing times are necessary. The bone quality is often less
than ideal. The concept for GBR is to place a BM directly over a bone defect
and under the soft tissue (including the periosteum) before primary closure.
It has been accepted that the periosteum is a source of osteoblasts for bone
formation and takes part in the bone augmentation process. However, this
apparently is incorrect. When the periosteum is placed directly over a
particulate bone graft, bone does not form under the periosteum. Instead,
fibrous tissue is observed on the surface. When a barrier membrane is placed
over the particulate graft, bone is found. The new bone forms from the
surrounding walls of host bone and follows the invading blood vessels from
the host bone, which grows into the space provided by the membrane or
particulate graft. A wide range of BM exists for GBR. There are three primary
categories of absorbable BM for GBR: collagen membranes,
polylactic/polyglycolic acid membranes, and acellular dermal matrix. The
ideal BM should be absorbable (but last long enough for predictable bone
formation), decrease tissue movement and, when necessary, increase the
tissue thickness over the bone graft. Clinical studies of GBR with different
resorption rates, from 6 weeks to 6 months, often demonstrate similar bone
augmentation results. This includes Biomend, which absorbs over 4 to 8
weeks. Bio-Guide is a bilayer collagen membrane from types I and III porcine
collagen and absorbs over a 2- to 4-week period. Ossix is a porcine barrier
membrane that may take more than 6 months to absorb. It appears that once
the blood vessels from host bone invade the bone graft space, the other key
factors are more relevant (e.g., graft immobilization). Another type of barrier
membrane is AlloDerm (LifeCell Corporation). This dermal allograft is
deepithelialized skin tissue processed to remove all cells, leaving an acellular
dermal matrix. The collagen, elastin, and proteoglycans are still present and
allow for an inert avascular connective tissue to be obtained.52 As a result, the
acellular allograft tissue material may become completely and permanently
incorporated into the soft tissue after 6 weeks rather than resorbing as a
collagen BM; thus it may increase tissue thickness over the graft site. This is
beneficial in esthetic zones when the soft tissue drape needs to be developed.
Because it binds to the overlying soft tissue, it may create a zone of immobile
tissue. This is a benefit for particulate graft immobilization and for implant
soft tissue maintenance after the prosthesis delivery.
Implant insertion and guided bone regeneration.

Guided bone regeneration has been successfully reported at the time of
implant insertion in both animal and human trials.43,53 In most of these
reports, the threads of the implant were exposed on only one side. The
procedure is less at risk when the GBR is for width only, not for both width
and height. The technique is very similar to that already presented. The
osteotomy of the implant site is prepared to the opposing landmark (when
possible), and the bone debris is harvested from the drills. The implant
length does not need to be as deep as the osteotomy, but the extra depth
allows more bone to be harvested. Holes in the cortical bone distal to the
implant (not directly over the intact lateral bone), tent screws, autograft, the
second layer of demineralized freeze dried bone (DFDB) (30%), freeze dried
bone (FDB) (70%), platelet rich plasma (PRP), and the top of the graft are
covered with a barrier membrane with primary closure of the soft tissue. The
most difficult part of GBR at the time of implant insertion is to ensure that
the implant is positioned for the prosthesis without compromise, rather than
positioned more palatal (lingual) or angled to engage more host bone. The
position of the implant should not be compromised so as to improve the
success of the bone graft or to improve the osteointegration rate. The
implants are useful for the prosthesis, not the bone graft. When the implant
cannot be inserted in the correct position (in all three planes) because of the
inadequate host bone, only the bone graft should be performed. Only after
graft maturity can the implant be inserted. It should be noted that in the
anterior regions of the mouth the GBR procedure (with acellular dermal
matrix) is used over the labial plate whenever it is less than 1.5 mm thick.
This reduces the risk of marginal bone loss on the facial, which would result
in shrinkage or recessing of the soft tissue at the cervical of the implant
crown (Fig. 14.14).
FIG 14.14 An implant may be inserted in the correct position, but the labial plate is
less than 1.5 mm thick. A graft and a barrier membrane on the facial of an implant
are indicated when the facial plate is thin and bone loss increases the risk of an
esthetic compromise. (From Misch CE: Contemporary implant dentistry, ed 3, St Louis, 2008,
Mosby.)
The GBR procedure may be used when an implant is immediately placed

after a tooth extraction when conditions permit the implant to be positioned
without compromise to the prosthesis. The osteotomy for the implant is
made to the opposing landmark. The autograft is positioned over the implant
and completely fills the extraction defect. The second layer of graft material
is placed over the facial thin or missing bone. The barrier membrane is
placed over the missing (or thin) bony wall, usually the facial. When a facial
plate of the bone is missing, primary closure of the soft tissue is preferred
(Fig. 14.15). Inability to maintain primary closure will directly influence the
success of the bone graft (Figs. 14.16 and 14.17).
FIG 14.15 (A) Immediate implant placed in cuspid extraction site with
compromised facial plate. (B) Six-month regenerative result with primary closure
maintained.
FIG 14.16 Immediate implant placement in molar position. (A) Implant countersunk
with no encroachment on buccal plate. (B) Mineralized allograft used to fill voids. (C)
Guided bone regeneration membrane in place. (D) Initial primary closure.
FIG 14.17 (A) Incision line opening with complete exposure of cover screw after 6
months. (B) Resultant partial absence/loss of crestal bone.
Inability to Achieve Primary Stability

Implant stability plays an important role in determining treatment
outcome.54 Primary stability is the absence of mobility in the bone after the
implant has been placed. The phenomenon behind this is the same as that
applied for reduction of fractured long bones; that there should be absolutely
no movement between the fragments when the ends of a fractured long bone
are reduced to enable fracture healing.55 This is because movements even in
the micrometer range can induce a stress or strain that may hinder the
formation of new cells in the gap. Likewise, during implant healing a
micromotion between 50 and 150 µm may negatively influence
osseointegration and bone remodeling by forming fibrous tissues at the
bone-to-implant interface thereby inducing bone resorption.55
Primary implant stability may be difficult to achieve in extraction sites
where the trabecular bone density is less than ideal. Even for healed sites,
there are examples of implant displacement into or excessively close to vital
structures such as the mandibular nerve canal56 or the maxillary sinus.57 The
displacement or migration of dental implants into the ethmoid sinus, nasal
floor, or anterior cranial fossa has also been reported.58-60
Unlike a healed ridge of desirable bone volume, primary stability in fresh
extraction sites is more difficult to achieve in general due the lesser quantity
of native bone present as well as the fact that the anatomic challenge of the
coronal aspect of the extraction site is often wider than the implant being
placed. Potential variations in bone density may necessitate multiple
modifications to osteotomy preparation and implant placement protocols as
compared to procedures performed in homogeneous bone density. As a
result, after attempted implantation, the clinician may be faced with a mobile
implant with a questionable level of primary stability.
Prevention
Complete Osteotomy Preparation in Appropriate Location and

Sequence.
Depending on the size of the extracted tooth and the implant to be placed,
somewhere along the surface of the original tooth socket the implant will
extend past the original dimensions of the root and provide mechanical
retention of the implant.61 As described in the general considerations section,
immediate implant placement in the anterior region often requires that the
osteotomy and implant insertion engage the lingual wall of the alveolus and
penetrate halfway to two thirds of the way down the extraction site into the
remaining lingual apical bone for rigid fixation. For maxillary posterior teeth
the initial bur should be positioned off center toward the lingual side of the
interradicular septum. For mandibular posterior teeth initial bur should be
positioned on the mesial aspect of the interradicular septum. A Lindemann
bur is very useful for initiating and modifying osteotomies. The objective of
this multiplane preparation process is to create an osteotomy in a
prosthetically correct position without compromising the buccal wall of bone.
Underprepare Osteotomy Width and Over Prepare Osteotomy

Length.
Misch initially outlined a protocol that adapts the treatment plan, implant
selection, surgical approach, healing regimen, and initial prosthetic loading
to all bone densities and all arch positions and that resulted in similar
implant success for all bone densities.6 To assist in bone quality evaluation,
Cavallero advises clinicians to determine the degree of osseous density with a
2-millimeter twist drill and describes ways in which they can use this
information to alter osteotomy development and subsequent prosthetic
design.62 These concepts can also be applied to immediate implant
placement.
The density of the residual native bone can influence the ability to achieve
adequate primary fixation. With anterior single-rooted teeth, using bone
beyond the apex and the lateral engagement of the some or all of the tooth
socket walls is instrumental in obtaining sufficient primary stability. With
posterior implants, vital structures such as the inferior alveolar nerve and the
maxillary sinus limit stability derived from bone beyond the tooth apices.
Furthermore, the limited native bone present undergoes remodeling after
the surgical trauma of osteotomy preparation and implant insertion. This
trauma leads to a weakening of the bone-implant interface and may have an
adverse effect on implant stability. Often, inadequate primary stability may
only manifest itself after 4 to 6 weeks; the bone interface is stronger on the
day of implant placement compared with 3 months later. The surgical process
of the implant osteotomy preparation and implant insertion cause a regional
acceleratory phenomenon of bone repair around the implant interface. As a
result of the surgical placement, organized, mineralized lamellar bone in the
preparation site becomes unorganized, less mineralized, woven bone of
repair next to the implant. The implant-bone interface is weakest and most at
risk of overload at 3 to 6 weeks after surgical insertion because the surgical
trauma causes bone remodeling at the interface that is least mineralized and
unorganized during this time frame. A clinical report by Buchs et al23 found
immediately loaded implant failure occurred primarily between 3 and 5
weeks after implant insertion from mobility without infection. At 4 months
the bone is still only 60% mineralized, organized lamellar bone. With time,
bone formation and mineralization will lead to increased interlocking with
the implant surface and a stronger implant/bone interface. However, this has
proved to be sufficient in most bone types and clinical situations for two-
stage healing and delayed implant loading. The relative lack of native bone
(compared to a healed site) suggests the osteotomy should frequently be
undersized in width, the degree of which is dependent on bone density. In
addition, for less dense bone, immediate implant fixation can be facilitated if
the clinician can use osteotomes for radial compaction.
Dependent on tooth socket size and anatomy, sufficient implant stability
can sometimes be achieved by lateral wall engagement only. Extending the
osteotomy 3 to 5 mm past the socket apex (without encroaching on vital
structures) is more commonly done for primary stability.61
Clinically Confirm Primary Stability.

Accurate assessment of primary stability is crucial in the immediate
placement protocol. Methods of measuring implant stability include the
percussion testing, insertion torque (IT), percussion testing, reverse torque
testing, resonance frequency analysis (RFA), and surgical experience.
Instrumented percussion testing has utilized the Periotest system. Periotest
evaluations have been useful to gauge primary stability.55,63,64 It is composed
of a metallic tapping rod in a handpiece, which is electromagnetically driven
and electronically controlled. Signals produced by tapping are converted to
unique values called Periotest values. These results are expressed in arbitrary
units with acceptable Periotest values in the ranges of −4 to −2 and −4 to +2.55
This device has been supplanted by RFA due to the lack of reproducibility of
results derived from Periotest measurements. These measurements are
subject to a number of factors such as the vertical position of the measuring
point on the abutment, angulation of the handpiece, and horizontal distance
of the handpiece from the abutment.65
Reverse torque testing (RTT) has been said to be beneficial at stage II
surgery as a definitive clinical verification of initial integration66 or
“adequacy” of the implant-bone interface.67 Given the potential for early
crestal bone loss and early implant failure as a result of this test, especially in
less dense bone types, RTT is not advisable for evaluating healed bone-
implant interfaces.68 This author has found a variation of RTT useful in the
determination of sufficient primary fixation. Some implant systems are sold
with preaffixed abutments, with the abutment screw tightened as per
manufacturer's specifications (e.g., BioHorizons external hex system
abutment screw is pretightened to 6–10 N/cm). The ability to untighten the
abutment screw without countertorque and without any associated implant
movement has been found by these authors to be an additional affirmation
of sufficient primary stability.
More commonly used methodologies for primary stability assessment are
IT measurement and RFA. Interestingly, IT and RFA appear as two
independent features of primary stability. Data in a study by Degidi showed
that IT is only influenced by bone density and that RFA is only correlated to
the length of implants used.69 Insertion torque values also have shown good
correlation with calibrated bone mineral density values as assessed through
CT scans70 and may be considered as a valid measure for determining bone
quality at an implant site. Some studies have determined that implant
stability associated with torque values of 32, 35, 40 N/cm and higher are
preferred thresholds for immediate loading.55,71,72
Resonance Frequency Analysis (RFA) (Fig. 14.18) is a testing method that
provides objective and reliable measurements of lateral micromobility at
various stages of the implant treatment process. The method analyzes the
first resonance frequency of a small transducer attached to an implant or
abutment. It can be used to monitor the changes in stiffness and stability at
the implant-tissue interface and to discriminate between successful implants
and clinical failures. Integration diagnostics developed the Implant Stability
Quotient (ISQ) as a scale of measurement for use with the RFA method. This
more objective assessment of stability may help improve a clinician's
learning curve and is useful for future comparison. Multiple studies73,74 have
determined that an acceptable stability range lies between 55 and 85 ISQ,
with an average ISQ level of 70.75
FIG 14.18 Radiofrequency analysis testing. (A) Osstell transducer. (B) Transducer
placed into immediately placed implant. (C–D) Implant Stability Quotient (ISQ)
readings on various surfaces of the transducer. (E) ISQ reading of 70, which relates
to high stability for an immediate implant.
The information provided by RFA is useful; however, the clinician should

be wary of relying completely on a general standardized range of ISQ
readings due to variations that may exist for different implant designs and
surface conditions as well as the inability to correlate RFA with
histomorphometric data of bone anchorage or with the torque required to tap
the bone for implant placement. The study concluded that validity of the
individual measurement of implant stability using RFA should be considered
with caution because the boundary height, width, and density factors can
influence the resonance frequency of dental implants. However, there is no
clinical study today that proves the RFA level for implants surviving long-
term and the necessary minimum RFA threshold needed for the success of
immediate loaded (IL) implants. These data seem to confirm that RFA and IT
represent two different features of primary stability, with the first indicating
the resistance to bending load and the latter indicating the resistance to
shear forces.76
Degiti conducted a clinical study to (1) evaluate the Osstell as a diagnostic
tool capable of discriminating between stable and mobile ITI (Straumann)
implants, (2) to evaluate a threshold ISQ value obtained at implant
placement (ISQitv) that might be predictive of osseointegration when
assessed after 1 year of loading, and (3) to compare the predictive ISQitv of
IL and DL implants. Degidi's study in 2006 demonstrated a surgeon's
capability to predict IT but at the same time have poor accuracy in prediction
of RFA values. Despite these findings, an experienced surgeon's perception of
primary stability under no circumstances should be discounted.75
Implant design and initial stability.

The clinical perception of primary implant stability is frequently based on
the cutting resistance of the implant during its insertion. The feeling of
“good” stability may be accentuated if there is the sense of an abrupt stop at
the seating of the implant. Although root form tapered implants often have a
geometry that will provide a firm stop, the resultant stability may be a false
perception.77 In addition, in a tapered, threaded implant, threads at the apical
half are often less deep because the outer diameter of the implant body
continues to decrease. This limits the initial fixation of the implant and
further reduces the functional surface area. For immediate implant
placement, the tapered/conical body design may be of benefit during initial
insertion because it is positioned within the osteotomy halfway before
engaging bone.36 The choice of implant body with regard to primary
stabilization is equivocal and may be more influenced by osteotomy
preparation than implant body design. A study by Sakoh concluded the
combination of both conical implant design and the procedure of
underdimensioned drilling appeared to be associated with increased primary
stability.78
Treatment Options
Bone Density.
Dependent on bone density, the implant can sometimes be redirected into
more dense bone; the redirection may be needed in more than one plane and
kept within the needed three-dimensional boundaries for prosthetic
reconstruction. Often a subtle tap of the (threaded) implant in an axial
direction will gain the needed initial primary stability without putting the
implant at risk from excessive apical positioning relative to the osseous crest
and any adjacent teeth. A straight or offset osteotome can be utilized (Fig.
14.19).
FIG 14.19 Use of press fit technique to gain/improve primary stability with a
threaded implant. (A) Prior to osteotome use. (B) After osteotome use.
Use of Larger Implant.
The dimensions, longer and/or wider, of the “rescue” implant may allow for
satisfactory primary fixation; however, it must still be in an acceptable
position in relation to the crestal bone, adjacent teeth, and planned final
prosthesis.79 This may be placed in a redirected manner described above. An
increased implant surface area can engage more cortical bone. It has also
been shown in an experimental study in rabbit tibia that wider implant
diameters resulted in increased removal torque values.80 Matsushita et al81
employed a two-dimensional finite element method to analyze the effect of
different implant diameters on stress distribution within the alveolar bone
using HA-coated implants. They found that stress in cortical bone decreased
with increased implant diameter. Ivanhoff, however, reported a lower survival
rate and a tendency for higher bone loss for 5.0-mm diameter implants, as
compared to 3.75-mm- or 4.0-mm diameter implants.82 Resultant decreased
facial bone dimensions associated with wider implant dimensions increase
the probability of soft tissue recession.
Leave Implant in Place.

An implant with loss of rotational stability (spinner) and minimal, if any,
surrounding ridge deficiencies may be left in place. If replacement is not
possible (for example, in cases of inadequate bone dimensions or where a
larger implant is unavailable), the surgeon must then decide whether to leave
the implant in place or remove it and reevaluate the site for further implant
therapy after healing is complete. Some studies have found that primary
stability, while desirable, may not be an absolute requirement to achieve and
maintain osseointegration.83
Ivanhoff reported osseointegrated implants that have been mobilized due
to a traumatic disruption of the bone-implant interface may reintegrate if
allowed to heal for an additional period of time.84 Orenstein reported a 79.8%
survival rate after 3 years of implants that were mobile at placement. A
significant factor for most of these implants was the presence of a HA
coating. Almost one half of the noncoated, initially mobile, implants failed
by 3 years postplacement. Even if initially mobile implants are found to
integrate, precautions are advised to avoid implant overload. Clinicians may
want to employ strategies such as long-term temporization to promote bone
maturation and evaluate the viability of initially mobile implants in function
prior to inserting the definitive prosthesis.83
Abort the Procedure.
The clinician may consider aborting the procedure and proceeding only with
the bone graft.
Implant Malposition.
Often there are visual cues for immediate implant placement, such as
adjacent and opposing teeth and tooth sockets. Deviations from normal
anatomy and cases of multiple implant placement, however, can be deceptive
and lead to implant malpositioning (Fig. 14.20). Dependent on the experience
level of the clinician, a surgical template can help facilitate more precise
placement in the buccolingual, mesiodistal, and apicocoronal directions.85
Intraoperative imaging with force direction indictors in place is beneficial in
evaluating current osteotomy development vs. planned locations. The
combined use of intraoperative radiographs and surgical template (clinical
visualization) maximizes feedback to the implant surgeon and allows for
corrective measures to be undertaken prior to osteotomy completion and
implant placement.
FIG 14.20 Implant malposition following immediate implant placement for a first
molar. (A–B) Mandibular implant placement too far distal. (C–D) Maxillary implant
placement too far distal. (C) Preoperative of non-restorable molar, (D) Implant
improper placement resulting in placement too far posterior.
Transitional Prosthesis Impingement
The transitional prosthesis over a particulate graft or healing implant should
not rest on the soft tissue over the site. Although the tent screws provide
some protection to a graft site, a fixed transitional prosthesis is more
predictable for the process. Particulate grafts are more prone to movement
during healing, which prevents blood vessels from entering and forming
bone in the site. Patient compliance is improved with fixed provisionals.
Neurosensory Impairment
The close proximity of inferior alveolar nerve to the apices of the mandibular
posterior teeth poses the possibility of neurosensory impairment when
preparing osteotomies and during implant insertion. Not infrequently, the
immediate implant gains its primary stability from the bone beyond the root
apices. This risk is higher in the posterior mandible extraction site than in a
healed site with its increased volume of bone and associated likelihood of the
more abundant bone achieving primary stability without nerve
encroachment. If the surgeon suspects a nerve injury, the algorithms outlined
in the Chapter 9: Neurosensory Deficit Complications in Implant Dentistry
should be followed. Preventive strategies include preoperative three-
dimensional imaging, guided surgery, and having a heightened awareness of
local anatomy.
Excessive Postoperative Pain

If a clinician's patient base has an otherwise unremarkable history of
postoperative discomfort with two-stage implant procedures, an increase in
postoperative symptoms such as discomfort and edema with immediate
placement techniques may be reflective of increased surgical time and
additional gingival flap manipulation of a less experienced operator.
Preoperative communication with the patient regarding posttreatment
expectations, treatment phasing, and appropriate choice of pharmacologic
agents can help minimize or eliminate this sequela. Not infrequently,
removal of a tooth as part of treatment may place some of the remaining
teeth in traumatic occlusion. Occlusal adjustment via selective grinding
frequently results in rapid resolution of this problem. Although not a
frequent occurrence, the clinician should always be aware of patients whose
histories suggest they may present with atypical facial pain.86
Patient Management: Medicolegal Considerations

When anticipating immediate implant placement, the patient should be
informed that the procedure may need to be aborted with only a bone graft
placed. The surgeon does not want to compromise a 30-year prosthesis
simply to avoid waiting an additional 3 to 6 months.6

Primary closure is typically desired when attempting regeneration in other
than simple three-wall defects (with or without the presence of an implant).
Incision line opening (ILO) following implant placement and simultaneous
complex augmentation can have a devastating outcome, whereas, in other
cases, primary closure is not necessary dependent on the defect size and
anatomy (see Fig. 14.14). Strategies for ILO management are discussed in
Chapter 11: Wound Dehiscence: Incision Line Opening. Although some
authors describe the need for primary flap closure, survival of implants is not
dependent on primary closure in all cases.87,88
Complications Following First Stage
Bone Healing
Compromised Implant Position
This common complication of immediate implant placement may not be
readily apparent until the restorative process has been initiated (Fig. 14.21).
For this discussion, care must be taken to distinguish between a
compromise(s) that could be present following a delayed/two-staged
procedure (e.g., increased final crown height) vs. a compromise that could be
solely attributed to implant placement at the time of extraction. Examples of
the later are characterized by excessive positions in one or more of the
potential three reference planes. Nonideal positioning can also result after
multistage procedures; however, the need for native bone for primary
stability in immediate placement cases increases the likelihood of
positioning error. Management of cases with resultant excessive mesial-distal
space/length can be frequently treated by placement of additional (usually
narrower-diameter) implants. Use of surgical templates or guided surgery are
recommended for clinicians desiring physical reference points during
surgery.
FIG 14.21 Management of malpositioning error by addition of narrow implant.
Long-Term Results
The success rate and radiographic results of immediate restorations of dental
implants placed in fresh extraction sockets were comparable to those
obtained in delayed loading group.89
A prospective cohort study by Rodrigo with a 5-year follow-up has shown
that, in the same patients, implants placed immediately upon tooth
extraction behave similarly to implants placed with a delayed protocol. Both
showed similar clinical characteristics, although the implants placed with the
immediate protocol demonstrated a higher tendency for crestal bone loss
and incidence of peri-implantitis.90
Lang found a high survival rate although soft tissue issues were apparent.5
In particular, soft tissue recession was found to be associated with thin tissue
biotype, facial malpositioning, and/or a thin or damaged buccal bone plate
(Figs. 14.22 and 14.23). About 20% of patients who underwent immediate
implant placement and delayed restorations suffered from suboptimal
aesthetic outcomes due to buccal soft tissue recession in studies with
observation period of 3 years or more.
FIG 14.22 Immediate maxillary anterior implants. (A) Compromised facial bone. (B)
Rigidly fixated implants with excellent zone of attached tissue. (C) Provisionalization
of implants. (D) Radiographs of implants during provisionalization stage. (E)
Radiographs after 7 years in function. (F) Facial soft tissue recession after 7 years
in function.
FIG 14.23 Staged maxillary anterior implants. (A) Healed ridge with no facial
defects. (B) Implant placement in intact ridge. (C) Radiograph of implants at time of
placement. (D) Final prosthesis shortly after delivery. (E) Radiograph of splinted
implants after 10 years in function. (F) Final prosthesis after 10 years in function.
Summary
Implant placement in general involves multiple steps and decision points. As
a distinct procedure, the technique of immediate implant placement adds
multiple additional decision points, making it a technique-sensitive modality.
It can have equivalent success rates to staged implant placement if the
implant surgeon has an awareness of the potential pitfalls and the ability to
deal with its unique complications.
References
1. Lazzara RJ. Immediate implant placement into extraction sites:
surgical and restorative advantages. Int J Periodontics Restorative Dent.
1989;9(5):332–343.
2. Gelb DA. Immediate implant surgery: three-year retrospective
evaluation of 50 consecutive cases. Int J Oral Maxillofac Implants.
1993;8(4):388–399.
3. Schwartz-Arad D, Chaushu G. Placement of implants into fresh
extraction sites: 4 to 7 years retrospective evaluation of 95 immediate
implants. J Periodontol. 1997;68(11):1110–1116.
4. Rosenquist B, Grenthe B. Immediate placement of implants into
extraction sockets: implant survival. Int J Oral Maxillofac Implants.
1996;11(2):205–209.
5. Lang NP, et al. A systematic review on survival and success rates of
implants placed immediately into fresh extraction sockets after at
least 1 year. Clin Oral Implants Res. 2012;23(Suppl 5):39–66.
7. Schwartz-Arad D, Chaushu G. The ways and wherefores of immediate
placement of implants into fresh extraction sites: a literature review. J
Periodontol. 1997;68(10):915–923.
8. Araujo MG, Lindhe J. Dimensional ridge alterations following tooth
extraction. An experimental study in the dog. J Clin Periodontol.
2005;32(2):212–218.
9. Razavi R, et al. Anatomic site evaluation of edentulous maxillae for
dental implant placement. J Prosthodont. 1995;4(2):90–94.
10. Schropp L, Kostopoulos L, Wenzel A. Bone healing following
immediate versus delayed placement of titanium implants into
extraction sockets: a prospective clinical study. Int J Oral Maxillofac
Implants. 2003;18(2):189–199.
11. Johns RB, et al. A multicenter study of overdentures supported by
Branemark implants. Int J Oral Maxillofac Implants. 1992;7(4):513–522.
12. Smedberg JI, et al. A clinical and radiological two-year follow-up study
of maxillary overdentures on osseointegrated implants. Clin Oral
Implants Res. 1993;4(1):39–46.
13. Snauwaert K, et al. Time dependent failure rate and marginal bone
loss of implant supported prostheses: a 15-year follow-up study. Clin
Oral Investig. 2000;4(1):13–20.
14. Herrmann I, et al. Evaluation of patient and implant characteristics as
potential prognostic factors for oral implant failures. Int J Oral
15. Waasdorp JA, Evian CI, Mandracchia M. Immediate placement of
implants into infected sites: a systematic review of the literature. J
Periodontol. 2010;81(6):801–808.
16. Crespi R, Cappare P, Gherlone E. Immediate loading of dental
implants placed in periodontally infected and non-infected sites: a 4-
year follow-up clinical study. J Periodontol. 2010;81(8):1140–1146.
17. Crespi R, Cappare P, Gherlone E. Fresh-socket implants in periapical
infected sites in humans. J Periodontol. 2010;81(3):378–383.
18. Schnitman PA, et al. Ten-year results for Branemark implants
immediately loaded with fixed prostheses at implant placement. Int J
Oral Maxillofac Implants. 1997;12(4):495–503.
19. Tarnow DP, Emtiaz S, Classi A. Immediate loading of threaded
implants at stage 1 surgery in edentulous arches: ten consecutive case
reports with 1- to 5-year data. Int J Oral Maxillofac Implants.
1997;12(3):319–324.
20. Misch CE, Wang HL. Immediate occlusal loading for fixed prostheses
in implant dentistry. Dent Today. 2003;22(8):50–56.
21. Strid KG. Radiographic results. Tissue-integrated prostheses:
Osseointegration in clinical dentistry. Quintessence: Chicago; 1985:187–
198.
22. Frost HM. The regional acceleratory phenomenon: a review. Henry
Ford Hosp Med J. 1983;31(1):3–9.
23. Buchs AU, Levine L, Moy P. Preliminary report of immediately loaded
Altiva Natural Tooth Replacement dental implants. Clin Implant Dent
Relat Res. 2001;3(2):97–106.
24. Lambert P, Morris HF, Ochi S. Relationship between implant surgical
experience and second-stage failures: dicrg interim report No. 2.
Implant Dent. 1994;3(2):97–101.
25. Preiskel HW, Tsolka P. Treatment outcomes in implant therapy: the
influence of surgical and prosthodontic experience. Int J Prosthodont.
1995;8(3):273–279.
26. Geckili O, et al. Evaluation of possible prognostic factors for the
success, survival, and failure of dental implants. Implant Dent.
2014;23(1):44–50.
27. Smith LP, et al. Outcomes of dental implants placed in a surgical
training programme. Aust Dent J. 2009;54(4):361–367.
on the height of inter-implant bone crest. J Periodontol.
2000;71(4):546–549.
29. Misch CE. Wide-diameter implants: surgical, loading, and prosthetic
considerations. Dent Today. 2006;25(8):66 [68–71].
30. Golec TS, Krauser JT. Long-term retrospective studies on
hydroxyapatite coated endosteal and subperiosteal implants. Dent
Clin North Am. 1992;36(1):39–65.
31. McGlumphy EA, et al. Prospective study of 429 hydroxyapatite-coated
cylindric omniloc implants placed in 121 patients. Int J Oral
32. Winkler S, Morris HF, Ochi S. Implant survival to 36 months as related
to length and diameter. Ann Periodontol. 2000;5(1):22–31.
33. Lekholm U, et al. Survival of the Branemark implant in partially
edentulous jaws: a 10-year prospective multicenter study. Int J Oral
34. Buser D, et al. Long-term evaluation of non-submerged ITI implants,
Part 1: 8-year life table analysis of a prospective multi-center study
with 2359 implants. Clin Oral Implants Res. 1997;8(3):161–172.
35. Misch CE, et al. A bone quality-based implant system: a preliminary
report of stage I & stage II. Implant Dent. 1998;7(1):35–42.
36. Misch CE. Dental implant prosthetics. ed 2. Mosby: St Louis; 2014.
37. Chang PK, et al. Distribution of micromotion in implants and alveolar
bone with different thread profiles in immediate loading: a finite
element study. Int J Oral Maxillofac Implants. 2012;27(6):e96–e101.
38. Steigenga J, et al. Effects of implant thread geometry on percentage of
osseointegration and resistance to reverse torque in the tibia of
rabbits. J Periodontol. 2004;75(9):1233–1241.
39. Williams DF. CRC Press: Boca Raton, FL; 1981. Biocompatibility of
clinical implant materials. vol 1.
40. Luckey HA, Kubli F Jr. Titanium alloys in surgical implants. AMTM
STP: Philadelphia; 1983.
41. Rasmusson L, Kahnberg KE, Tan A. Effects of implant design and
surface on bone regeneration and implant stability: an experimental
study in the dog mandible. Clin Implant Dent Relat Res. 2001;3(1):2–8.
42. Schropp L, Isidor F. Timing of implant placement relative to tooth
extraction. J Oral Rehabil. 2008;35(Suppl 1):33–43.
43. Becker W, et al. The use of e-PTFE barrier membranes for bone
promotion around titanium implants placed into extraction sockets: a
prospective multicenter study. Int J Oral Maxillofac Implants.
1994;9(1):31–40.
44. Ogiso M, et al. Delay method of implantation enhances implant-bone
binding: a comparison with the conventional method. Int J Oral
45. Roberts WE, et al. Implants: bone physiology and metabolism. CDA J.
1987;15(10):54–61.
46. Misch CE, Perez HM. Atraumatic extractions: a biomechanical
rationale. Dent Today. 2008;27(8):98 [100–101].
47. Misch CE, Dietsh F. Bone-grafting materials in implant dentistry.
Implant Dent. 1993;2(3):158–167.
48. Misch CE, Dietsh-Misch F, Misch CM. A modified socket seal surgery
with composite graft approach. J Oral Implantol. 1999;25(4):244–250.
49. Tischler M, Misch CE. Extraction site bone grafting in general
dentistry. Review of applications and principles. Dent Today.
2004;23(5):108–113.
50. Knize DM. The influence of periosteum and calcitonin on onlay bone
graft survival. A roentgenographic study. Plast Reconstr Surg.
1974;53(2):190–199.
51. Zucman J, Maurer P, Berbesson C. The effect of autografts of bone and
periosteum in recent diaphysial fractures: an experimental study in
the rabbit. J Bone Joint Surg Br. 1968;50(2):409–422.
52. Rothamel D, et al. Biodegradation of differently cross-linked collagen
membranes: an experimental study in the rat. Clin Oral Implants Res.
2005;16(3):369–378.
53. Dahlin C, et al. Generation of new bone around titanium implants
using a membrane technique: an experimental study in rabbits. Int J
54. Sennerby L, Roos J. Surgical determinants of clinical success of
osseointegrated oral implants: a review of the literature. Int J
Prosthodont. 1998;11(5):408–420.
55. Javed F, Romanos GE. The role of primary stability for successful
immediate loading of dental implants. A literature review. J Dent.
2010;38(8):612–620.
56. Bayram B, Alaaddinoglu E. Implant-box mandible: dislocation of an
implant into the mandible. Int J Oral Maxillofac Surg. 2011;69(2):498–
501.
57. Borgonovo A, et al. Displacement of a dental implant into the
maxillary sinus: case series. Minerva Stomatol. 2010;59(1–2):45–54.
58. Haben CM, Balys R, Frenkiel S. Dental implant migration into the
ethmoid sinus. J Otolaryngol. 2003;32(5):342–344.
59. Dimitriou C, et al. Foreign body in the sphenoid sinus. J
Craniomaxillofac Surg. 1992;20(5):228–229.
60. Cascone P, et al. A dental implant in the anterior cranial fossae. Int J
Oral Maxillofac Surg. 2010;39(1):92–93.
61. Greenstein G, Cavallaro J. Immediate dental implant placement:
technique, part I. Dent Today. 2014;33(1):98 [100–104; quiz 105].
62. Cavallaro J Jr, Greenstein B, Greenstein G. Clinical methodologies for
achieving primary dental implant stability: the effects of alveolar
bone density. J Am Dent Assoc. 2009;140(11):1366–1372.
63. Romanos GE, Nentwig GH. Immediate functional loading in the
maxilla using implants with platform switching: five-year results. Int J
64. Romanos GE, Nentwig GH. Immediate versus delayed functional
loading of implants in the posterior mandible: a 2-year prospective
clinical study of 12 consecutive cases. Int J Periodontics Restorative
Dent. 2006;26(5):459–469.
65. Derhami K, et al. Assessment of the periotest device in baseline
mobility measurements of craniofacial implants. Int J Oral Maxillofac
Implants. 1995;10(2):221–229.
66. Pebe P, et al. Countertorque testing and histomorphometric analysis
of various implant surfaces in canines: a pilot study. Implant Dent.
1997;6(4):259–265.
67. Sullivan DY, et al. The reverse-torque test: a clinical report. Int J Oral
68. Jividen G Jr, Misch CE. Reverse torque testing and early loading
failures: help or hindrance? J Oral Implantol. 2000;26(2):82–90.
69. Degidi M, Daprile G, Piattelli A. Primary stability determination by
means of insertion torque and RFA in a sample of 4,135 implants. Clin
Implant Dent Relat Res. 2012;14(4):501–507.
70. Turkyilmaz I, et al. Biomechanical aspects of primary implant
stability: a human cadaver study. Clin Implant Dent Relat Res.
2009;11(2):113–119.
71. Lorenzoni M, et al. Immediate loading of single-tooth implants in the
anterior maxilla, Preliminary results after one year. Clin Oral Implants
Res. 2003;14(2):180–187.
72. Degidi M, Piattelli A. 7-year follow-up of 93 immediately loaded
titanium dental implants. J Oral Implantol. 2005;31(1):25–31.
73. Bischof M, et al. Implant stability measurement of delayed and
immediately loaded implants during healing. Clin Oral Implants Res.
2004;15(5):529–539.
74. Sennerby L, Meredith N. Resonance frequency analysis: measuring
implant stability and osseointegration. Compend Contin Educ Dent.
1998;19(5):493–498 [500, 502; quiz 504].
75. Konstantinović VS, Ivanjac F, Lazić V, et al. Assessment of implant
stability by resonant frequency analysis. Military Medical and
Pharmaceutical Journal of Serbia. 2015;72(2):169.
76. Degidi M, Daprile G, Piattelli A. Determination of primary stability: a
comparison of the surgeon's perception and objective measurements.
Int J Oral Maxillofac Implants. 2010;25(3):558–561.
77. Sennerby L, Meredith N. Implant stability measurements using
resonance frequency analysis: biological and biomechanical aspects
and clinical implications. Periodontol 2000. 2008;47:51–66.
78. Sakoh J, et al. Primary stability of a conical implant and a hybrid,
cylindric screw-type implant in vitro. Int J Oral Maxillofac Implants.
2006;21(4):560–566.
79. Langer B, et al. The wide fixture: a solution for special bone situations
and a rescue for the compromised implant: Part 1. Int J Oral
80. Ivanoff CJ, et al. Influence of implant diameters on the integration of
screw implants: an experimental study in rabbits. Int J Oral
Maxillofac Surg. 1997;26(2):141–148.
81. Matsushita Y, et al. Two-dimensional FEM analysis of hydroxyapatite
implants: diameter effects on stress distribution. J Oral Implantol.
1990;16(1):6–11.
82. Ivanoff CJ, et al. Influence of variations in implant diameters: a 3- to 5-
year retrospective clinical report. Int J Oral Maxillofac Implants.
1999;14(2):173–180.
83. Orenstein IH, et al. Three-year post-placement survival of implants
mobile at placement. Ann Periodontol. 2000;5(1):32–41.
84. Ivanoff CJ, Sennerby L, Lekholm U. Reintegration of mobilized
titanium implants: an experimental study in rabbit tibia. Int J Oral
Maxillofac Surg. 1997;26(4):310–315.
85. Cavallaro J, Greenstein G. Immediate dental implant placement:
technique, part 2. Dent Today. 2014;33(2):94 [96–98; quiz 99].
86. Ferreira JN, Figueiredo R. Prevention and management of persistent
idiopathic facial pain after dental implant placement. J Am Dent
Assoc. 2013;144(12):1358–1361.
87. Wagenberg B, Froum SJ. A retrospective study of 1925 consecutively
placed immediate implants from 1988 to 2004. Int J Oral Maxillofac
Implants. 2006;21(1):71–80.
88. Chen ST, Wilson TG Jr, Hammerle CH. Immediate or early placement
of implants following tooth extraction: review of biologic basis,
clinical procedures, and outcomes. Int J Oral Maxillofac Implants.
2004;19(Suppl):12–25.
89. Crespi R, et al. Immediate versus delayed loading of dental implants
placed in fresh extraction sockets in the maxillary esthetic zone: a
clinical comparative study. Int J Oral Maxillofac Implants.
2008;23(4):753–758.
90. Rodrigo D, Martin C, Sanz M. Biological complications and peri-
implant clinical and radiographic changes at immediately placed
dental implants: a prospective 5-year cohort study. Clin Oral Implants
Res. 2012;23(10):1224–1231.
15
Removable Implant Complications
Randolph R. Resnik
The rate and pattern of edentulism in the United States has certainly shifted
over the years. There is a distinct overall trend toward a decrease in
edentulism; however, the group in need of this rehabilitation is rapidly
growing. It has been estimated over the past 30 years there has been a 10%
decrease in edentulism. However, this has been offset by an increase of 79%
in the adult population over 55 years of age.1 According to the literature, age
is directly related to tooth loss.2 This aging population is an important factor
when evaluating the need for removable implant-retained prostheses. With
tooth loss in this age group, many negative consequences related to
conventional dentures such as decreased masticatory function, systemic
consequences, patient dissatisfaction, and speech and psychologic effects
may result (Box 15.1).
Box 15.1
Negative Effects of Complete Dentures
• Bite force is decreased from 200 psi for dentate patients to 50 psi for
edentulous patients
• 15-year denture wearers have reduced bite force to 6 psi
• Masticatory efficiency is decreased
• More drugs are necessary to treat gastrointestinal disorders
• Food selection is limited
• Healthy food intake is decreased
• The life span may be decreased
• Reduced prosthesis satisfaction

• Psychologic effects
With the growing number of implants being placed, even with the
advances that have been seen in implant dentistry, complications do occur
with implant-retained removable prostheses. The complications may arise
from the treatment planning phase, implant positioning, implant number,
selection of attachments, and the insertion of the prosthesis. This chapter
discusses various complications that may arise with implant-retained
removable prostheses and various techniques to prevent and treat the
complications if they occur (Fig. 15.1 and Fig. 15.2).
FIG 15.1 By 2050, 20.7% of the population will be older than age 65 years. In
addition to the increasing percentage of 65-year-old adults, the population is also
increasing. As a result, 34.9 million people were older than 65 years in 2000, and
86.6 million people will reach this milestone by 2050. (From Misch CE: Dental implant
FIG 15.2 The adult population older than the age of 60 years old will increase by
87% from the year 2000 to the year 2025. (From Misch CE: Dental implant prosthetics, ed 2,
Complications of Overdentures for the
Edentulous Patient
Not Understanding the Disadvantages of
Edentulism
When evaluating an edentulous patient, it is the clinician's responsibility to
explain to the patient the disadvantages that may result from edentulism.
The following are consequences of edentulism that play a significant role in
treatment planning (Box 15.2).
Box 15.2
Disadvantages of Edentulism
• Continued bone loss
• Decreased occlusal biting force
• Decreased masticatory function
• Increased soft tissue discomfort
• Systemic consequences
• Lack of prosthesis satisfaction
• Psychologic
Continued Bone Loss

One of the most common issues of edentulism that is not commonly
explained to patients is the continued loss of bone. Alveolar bone requires
constant stimulation to maintain its form, strength and density. Roberts et al
reported that a 4% strain to the skeletal system maintains bone and helps
balance the resorption and formation phenomena.3 The forces applied to
teeth transmit compressive and tensile forces to the surrounding bone.
However, when a tooth is lost, the lack of stimulation to the residual bone
causes a decrease in trabeculae and bone density in the area, with loss in
external width, then height of the bone volume.4 Studies have shown a 25%
decrease in width of bone during the first year after tooth loss and an overall
4-mm decrease in height during the first year after extractions for an
immediate denture.5 In a longitudinal 25-year study of edentulous patients,
Tallgren demonstrated continued bone loss during this time span, with a
fourfold greater loss observed in the mandible.6 In 1963 Atwood introduced
five different stages of bone loss in an anterior mandible after tooth loss
showing the resorptive process over time.7 Even though the mandibular bone
resorbs faster than the maxillary bone, the mandible has almost twice the
bone initially available.
When patients wear a removable prosthesis, the bone is not stimulated in
the same fashion that a tooth does. The load placed on the removable
prosthesis is transferred to the bone surface, not the internal structure of the
bone. This causes the blood supply to be reduced to the bone resulting in
total bone volume being lost.8 The bone loss accelerates when the patient
wears a poorly fitting soft tissue–borne prosthesis. The average denture
wearer sees a dental professional approximately every 14.8 years after having
a complete denture. Ideally, edentulous patients should be seen every 1 to 2
years and should be informed that every 3 to 5 years a reline or new denture
is suggested to replace the additional bone loss by atrophy that naturally will
occur.
The rate and amount of bone loss may be influenced by many factors such
as gender, hormones, metabolism, parafunction, and ill-fitting dentures.
Studies have shown almost 40% of denture wearers have been wearing an ill-
fitting prosthesis for more than 10 years.9 Patients wearing dentures day and
night place greater forces on the hard and soft tissues, which accelerates
bone loss. Nonetheless, 80% of dentures are worn both day and night.9 Loss
of bone in the maxilla or mandible is not limited to alveolar bone; portions of
the basal bone may also be resorbed, especially in the posterior aspect of the
mandible, where severe resorption may result in the mental foramen or
mandibular canal becoming dehiscent. This may result in significant pain
and discomfort, leading to the inability to wear a removable prosthesis. In
the maxilla, the complete anterior ridge and nasal spine may be resorbed,
causing pain and an increase in maxillary denture movement during function
(Fig. 15.3 and Box 15.3).10
FIG 15.3 A dentate mandible (left) and a long-term edentulous mandible on the
(right). Note the amount of bone loss in height. Loss of bone height in the mandible
may be measured by the centimeter and often is ignored. Such bone loss is often
more significant than the bone loss (in millimeters) from periodontal disease. The
patient should understand that a denture often replaces more bone than teeth to
restore the proper dimensions of the face. (From Misch CE: Dental implant prosthetics, ed 2,
Box 15.3
Anatomic Consequences of Edentulism
• Decreased width of denture-supporting bone
• Decreased height of denture-supporting bone
• Prominent mylohyoid and internal oblique ridges with increase in denture

sore spots
• Progressive decrease in keratinized attached mucosa
• Prominent superior genial tubercles with increased denture movement
• Muscle attachments near crest of edentulous ridge
• Posterior elevation of prosthesis with contraction of mylohyoid and

buccinator muscles during function
• Forward movement of prosthesis from anatomic inclination with moderate

to advanced bone loss
• Thinning of surface mucosa with increased sensitivity to abrasion
• Loss of basal bone
• Paresthesia from dehiscent mental foramen and neurovascular canal
• Increased risk of mandibular body fracture from advanced bone loss
Decreased Occlusal Biting Force

The biting force of edentulous patients is a significant factor that patients
must be educated about concerning various treatment plans. The difference
in maximum occlusal forces recorded in a patient with natural teeth and one
who is completely edentulous is dramatic. In the first molar region of a
dentate person, the average force has been measured to be approximately 150
to 250 psi.11 A parafunction patient who grinds or clenches their teeth may
exert a force that approaches 1000 psi. In edentulous patients the maximum
occlusal force approaches less than 50 psi. This is very important when
explaining various treatment plans to patients, especially with expectations.
The longer patients are edentulous, the less occlusal force they are able to
generate. Studies have shown that patients wearing complete dentures for
more than 15 years have been shown to exhibit a maximum occlusal force of
less than 6 psi.12 This is a significant disadvantage that patients need to be
educated about, especially when patients decline implant treatment plans in
favor of conventional removable dentures. In comparison, the maximum
occlusal force may improve upwards of 300% with an implant-supported
prosthesis.13
Decreased Masticatory Efficiency

As a result of decreased occlusal force and the instability of the complete
denture, masticatory efficiency will decrease with tooth loss. Rissen et al
showed that 90% of food chewed with natural teeth fits through a no. 12
sieve; this is reduced to 58% in the patient wearing complete dentures.12 A
study of 367 denture wearers (158 men and 209 women) found that 47%
exhibited a low masticatory performance.14 In patients with dentures, 29% are
able to eat only soft or mashed foods, 50% avoid many foods, and 17% claim
they eat more efficiently without the prosthesis.15 Lower intakes of fruits,
vegetables, and vitamin A by women were noted in this group. Denture
patients also take significantly more drugs (37%) compared with those with
superior masticatory ability (20%), and 28% take medications for
gastrointestinal disorders. The reduced consumption of high-fiber foods
could induce gastrointestinal problems in edentulous patients with deficient
masticatory performance. In addition, the coarser bolus may impair proper
digestive and nutrient extraction functions.16
Increased Soft Tissue Discomfort

Mandibular discomfort was listed in a study by Misch and Misch with equal
frequency as movement (63.5%), and, surprisingly, 16.5% of the patients
stated they never wear the mandibular denture. In comparison, the maxillary
denture was uncomfortable half as often (32.6%), and only 0.9% were seldom
able to wear the prosthesis. Function was the fourth most common problem
reported by these 104 denture wearers. Half of the patients avoided many
foods, and 17% claimed they were able to masticate more effectively without
the prostheses. The psychologic effects of the inability to eat in public can be
correlated with these findings. Other reports agree that the major motivating
factors for patients to undergo implant-related treatment were related to the
difficulties with eating, denture fit, and discomfort.15
Systemic Consequences
The literature includes several reports suggesting that compromised dental
function causes poor masticatory performance and swallowing poorly
chewed food, which in turn may influence systemic changes favoring illness,
debilitation, and shortened life expectancy.17,18 In a study evaluating the
ability to eat fruit, vegetables, and other dietary fiber in edentulous subjects,
10% claimed difficulty, and blood tests demonstrated reduced levels of
plasma ascorbate and plasma retinol compared with dentate subjects. These
two blood tests are correlated to an increased risk of dermatologic and visual
problems in aging adults. In another study the masticatory performance and
efficiency in denture wearers were compared with those of dentate
individuals. This report noted that, when appropriate corrections were made
for different performance norms and levels, the chewing efficiency of a
denture wearer was less than one sixth of a person with teeth.19
Several reports in the literature correlate a patient's health and life span to
dental health. Poor chewing ability may be a cause of involuntary weight loss
in the elderly population, with an increase in mortality rate.20 In contrast,
persons with a substantial number of missing teeth were more likely to be
obese. After conventional risk factors for strokes and heart attacks were
accounted for, there was a significant relationship between dental disease
and cardiovascular disease, the latter still remaining as the major cause of
death.21 It is logical to assume that restoring the stomatognathic system of
these patients to a more normal function may indeed enhance the quality
and length of their lives.
Lack of Prosthesis Satisfaction

A dental survey of edentulous patients found that 66% were dissatisfied with
their mandibular complete dentures. Primary reasons were discomfort and
lack of retention causing pain and discomfort. Past dental health surveys
indicate that only 80% of the edentulous population are able to wear both
removable prostheses all the time. Some patients wear only one prosthesis,
usually the maxillary; others are only able to wear their dentures for short
periods. In addition, approximately 7% of patients are not able to wear their
dentures at all and become “dental cripples” or “oral invalids.” They rarely
leave their home environment, and when they feel forced to venture out, the
thought of meeting and talking to people when not wearing their teeth is
unsettling.22
Speech Difficulty
A report of 104 completely edentulous patients seeking treatment was
performed by Misch and Misch. Of the patients studied, 88% claimed
difficulty with speech, with one fourth having great difficulty. The lower
prosthesis rests upon the buccinator muscle and mylohyoid muscle when the
posterior mandible resorbs. When the patient opens their mouth, the
contraction of these muscles acts like a trampoline and propels the lower
denture off the ridge. As a result, the teeth often click when the patient talks,
not from too much of the vertical dimension restored but from the lack of
stability and retention of the prosthesis. Speech problems may be associated
with a concern for social activities. Awareness of movement of the
mandibular denture was cited by 62.5% of these patients, although the
maxillary prosthesis stayed in place most of the time at almost the same
percentage.
Psychologic Impact of Edentulism
The psychologic effects of total edentulism are complex and varied and range
from very minimal to a state of neuroticism. Although complete dentures are
able to satisfy the esthetic needs of many patients, some believe their social
lives are significantly affected. They are concerned with kissing and romantic
situations, especially if a new partner in a relationship is unaware of their
oral handicap. Fiske et al, in a study of interviews with edentulous subjects,
found tooth loss was comparable to the death of a friend or loss of other
important parts of a body in causing a reduction of self-confidence ending in
a feeling of shame or bereavement.23
The psychologic needs of edentulous patients are expressed in many
forms. For example, in 1970, Britons used approximately 88 tons of denture
adhesive.24 In 1982, more than 5 million Americans used denture adhesives
(Ruskin Denture Research Associates: AIM study, unpublished data, 1982),
and a report shows that in the United States, more than $200 million is spent
each year on denture adhesives, representing 55 million units sold.27 Patients
are willing to accept the unpleasant taste, need for recurring application,
inconsistent denture fit, embarrassing circumstances, and continued expense
for the sole benefit of increased retention of the prosthesis. Clearly, the lack
of retention and psychologic risk of embarrassment in the denture wearer
with removable prostheses is a concern the dental profession must address.
Advantages of an Implant-Supported Prosthesis

(Box 15.4)
Maintenance of Existing Bone
The use of dental implants to provide support for prostheses offers many
advantages compared with the use of removable soft tissue–borne
restorations. A primary reason to consider dental implants to replace missing
teeth is the maintenance of alveolar bone. It is well accepted that dental
implants placed in the anterior mandible help retain a lower denture and are
a benefit over a complete denture. However, the posterior bone loss will
continue and may eventually lead to significant complications. Instead, when
sufficient implants are inserted, the restoration is not only retained but it
also is completely supported and stabilized off the tissue and bone. The
implants also stimulate and maintain the bone of the mandible as well as
serve as an anchor for the prosthetic device. As a result, dental implants are
one of the better preventive maintenance procedures available in dentistry.
Box 15.4
Advantages of an Implant-Supported
Prosthesis
• Maintenance of existing bone
• More ideal occlusion
• Increased masticatory function
• Less morbidity in comparison to teeth
• Increased biting force
• Increased retention and stability
• Enhanced phonetics
• Improved psychologic health
More Ideal Occlusion

One of the main complications of wearing a lower removable denture is the
associated movement and lack of security. A mandibular denture often moves
when the mylohyoid and buccinator muscles contract during speech or
mastication. Occlusion is difficult to establish and stabilize with a completely
soft tissue–supported prosthesis. Because the mandibular prosthesis may
move as much as 10 mm or more during function, proper occlusal contacts
occur by chance, not by design. In comparison, an implant-supported
restoration is much more stable.25 The patient can more consistently return
to centric relation occlusion rather than adopt variable positions dictated by
the prosthesis' instability. Proprioception is awareness of a structure in time
and place. The receptors in the periodontal membrane of the natural tooth
help determine its occlusal position. Although endosteal implants do not
have a periodontal membrane, they provide greater occlusal awareness than
complete dentures. Whereas patients with natural teeth can perceive a
difference of 20 µm between the teeth, implant patients can determine a 50-
µm difference with rigid implant bridges compared with 100 µm in those
with complete dentures (either one or two).26 As a result of improved occlusal
awareness, the patient functions in a more consistent range of occlusion.
With an implant-supported prosthesis, the direction of the occlusal loads is
controlled by the restoring dentist. Horizontal forces on removable
prostheses accelerate bone loss, decrease prosthesis stability, and increase
soft tissue abrasions. The decrease in horizontal forces that are applied to
implant restorations improves the local parameters and helps preserve the
underlying soft and hard tissues.
Increased Masticatory Function

In a randomized clinical trial comparing conventional vs. implant-supported
prostheses by Kapur et al, the implant group of patients demonstrated a
higher level of eating enjoyment and improvement of speech, chewing ability,
comfort, denture security, and overall satisfaction.27 The ability to eat several
different foods among complete denture vs. mandibular overdenture
patients was evaluated by Awad and Feine. The implant overdenture was
superior for eating not only harder foods, such as carrots and apples, but also
softer foods, such as bread and cheese. Geertman et al evaluated complete
denture wearers with severely resorbed mandibles before and after
mandibular implant overdentures. The ability to eat hard or tough foods
significantly improved.28
Researchers at McGill University evaluated blood levels of patients who
had complete dentures and 30 maxillary dentures and mandibular implant
prostheses 6 months after treatment. Within this rather short period, implant
patients had higher vitamin B12 hemoglobin (related to iron increase) and
albumin levels (related to nutrition). These patients also had greater body fat
in their shoulders and arms, with decreased body fat in their waists.29
Less Morbidity in Comparison to Teeth

The success rate of implant prostheses varies depending on a host of factors
that change for each patient. However, compared with traditional methods of
tooth replacement, the implant prosthesis offers increased longevity,
improved function, bone preservation, and better psychologic results.
According to 10-year survival surveys of fixed prostheses on natural teeth,
decay is indicated as the most frequent reason for replacement; and survival
rates are approximately 75%.30 In a partially edentulous patient, independent
tooth replacement with implants may preserve intact adjacent natural teeth
as abutments, further limiting complications such as decay or endodontic
therapy, which are the most common causes of fixed prosthesis failure. A
major advantage of the implant-supported prosthesis is that the abutments
cannot decay and never will require endodontics. The implant and related
prosthesis have been shown to attain a 10-year survival rate of more than
90%.
Increased Biting Force

Patients with an implant-supported fixed prosthesis may increase their
maximum bite force by 85% within 2 months after the completion of
treatment. After 3 years the mean force may reach more than 300% compared
with pretreatment values. As a result, an implant prosthesis wearer may
demonstrate a force similar to that of a patient with a fixed restoration
supported by natural teeth. Chewing efficiency with an implant prosthesis is
greatly improved compared with that of a soft tissue–borne restoration. The
masticatory performance of dentures, overdentures, and natural dentition
were evaluated by Rissin et al. The traditional denture showed a 30%
decrease in chewing efficiency; other reports indicate a denture wearer has
less than 60% of the function of people with natural teeth. The tooth-
supported overdenture loses only 10% of chewing efficiency compared with
natural teeth. These findings are similar with implant-supported
overdentures. In addition, rigid, implant-supported fixed bridges may
function the same as natural teeth.31
Improvement of Retention and Stability

Stability and retention of an implant-supported prosthesis are great
improvements over soft tissue–borne dentures. Mechanical means of implant
retention are far superior to the soft tissue retention provided by dentures or
adhesives and cause fewer associated problems. The implant support of the
final prosthesis is variable, depending on the number and position of
implants, yet all treatment options demonstrate significant improvement
over conventional prosthesis treatment options.
Enhanced Phonetics
Phonetics may be impaired by the instability of a conventional denture. The
buccinator and mylohyoid muscles may flex and propel the posterior portion
of the denture upward, causing clicking, regardless of the vertical dimension.
As a result, a patient in whom the vertical dimension already has collapsed
10 to 20 mm may still produce clicking sounds during speech. Often the
tongue of the denture wearer is flattened in the posterior areas to hold the
denture in position. The anterior mandibular muscles of facial expression
may be tightened to prevent the mandibular prosthesis from sliding forward.
The implant prosthesis is stable and retentive and does not require these oral
manipulations. The implant restoration allows reduced flanges or palates of
the prostheses. This is of special benefit to new denture wearers, who often
report discomfort with the bulk of the restoration. The extended soft tissue
coverage also affects the taste of food, and the soft tissue may be tender in
the extended regions. The palate of a maxillary prosthesis may cause gagging
in some patients, which can be eliminated in an implant-supported
overdenture.
Improved Psychologic Health

Patients treated with implant-supported prostheses judge their overall
psychologic health as improved by 80% compared with their previous state
while wearing traditional, removable prosthodontic devices. They perceived
the implant-supported prosthesis as an integral part of their body.32 For
example, Raghoebar et al evaluated 90 edentulous patients in a randomized
multicenter study. Five years after treatment, a validated questionnaire
targeted patient esthetic satisfaction, retention, comfort, and the ability to
speak and eat with either a complete mandibular denture, complete
mandibular denture with vestibuloplasty, or mandibular two-implant
overdenture. Implant overdentures had significantly higher ratings, but no
significant difference was found between the two complete-denture groups.33
Geertman et al reported similar results comparing chewing ability of
conventional complete dentures with mandibular implant overdentures.34
Not Understanding the Disadvantages of a

Removable Implant Prosthesis (Overdenture)
Although dental implant overdentures are successful in many situations,
patients should be informed of the inherent disadvantages and
complications that may occur. Many studies have shown a rather high
incidence of complications. Goodacre et al have shown overdenture
complications to include clip/attachment loosening (30%), clip/attachment
fracture (17%), and overdenture fracture (12%). In a study by Bilhan et al on
59 patients, two thirds of implant-supported overdenture (IOD) patients had
prosthetic-related complications the first year. For example, relines were
necessary in 16%, loss of retention in 10.2%, fracture of the IOD in 8.5%,
pressure spots in 8.5%, dislodged attachment in 6.8%, and screw loosening in
3.4%.35 Other studies have shown up to 18% of overdentures requiring a
reline of the prosthesis within the first year.36 It is imperative that patients
understand fully the basis and long-term issues that may be associated with
implant-retained overdentures.
Not a Fixed Prosthesis

Many patients are not educated in the inherent mechanics of overdentures
and the various levels of support that exist, which are dependent on the
position, number, and types of retentive mechanisms. The most common
misconception that may lead to patient disapproval is an overdenture is not a
“fixed prosthesis.” With that, the patient must understand the decreased
occlusal force in comparison to fixed prosthesis. An overdenture is
considered a prosthesis, whereas a fixed prosthesis is considered a body part.
Fixed implant prostheses are often considered by patients to be similar to
their natural teeth in esthetics and function. With an overdenture, movement
of the prosthesis is usually noted by the patient along with decreased
masticatory function (Fig. 15.4).
FIG 15.4 (A) Fixed prosthesis, which exhibits greater masticatory efficiency. (B)
Removable implant prosthesis, which has many disadvantages in comparison to a
fixed prosthesis.
Need of Adequate Crown Height Space (CHS)

A greater crown height space (CHS) is required for an implant-retained
overdenture in comparison to other types of implant prostheses. With an
overdenture prosthesis, there is often a lack of space that results in a
prosthesis fracture or loss of denture teeth. When space is compromised,
inadequate room results in modification of the materials (reduction of acrylic
from denture base or hollowing out of denture teeth) to obtain room for
attachment mechanisms. In these situations, the appropriate attachment
(e.g., Locator 6–low profile) must be selected to minimize these
complications. When abundant bone is present and implants are already
inserted, a compromised CHS may indicate a change in treatment planning
to a fixed prosthesis if adequate number and position of implants are present
(Fig. 15.5).
FIG 15.5 (A) For a removable implant-supported overdenture to be successful,
adequate space is needed for the attachments and denture teeth. Sagittal CBCT
view depicting the available space between the bone level and incisal edge. (B)
When inadequate space is available (arrow), the denture base or denture is
weakened (i.e., inadequate acrylic thickness) leading to possible fracture. (C)
Fractured denture base due to lack of acrylic bulk. (D) Articulated setup of
overdenture case exhibiting lack of interocclusal space with bar contacting maxillary
posterior teeth. (E) Panorex showing lack of prosthetic space due to inadequate
amount of osteoplasty (arrow).
Maintenance
An increased maintenance protocol is often required for an overdenture.
Denture teeth wear more rapidly on an IOD in comparison to a denture (i.e.,
increased occlusal force). As a result, a new IOD may need to be fabricated
on a more continuous basis depending on the amount of wear. The patient
should be informed at the beginning of treatment of the need for
maintenance to avoid patient complications. Although the initial cost of
treatment may be less for an IOD, overdenture wearers often incur greater
long-term expenses than those with fixed restorations. Attachments (i.e., O-
rings or clips) regularly wear and must be replaced, which in some cases is
very time consuming. Walton and McEntee noted there were three times
more maintenance and adjustments issues for overdentures compared with
fixed restorations.37
Food Impaction
A common complaint with IODs is food impaction under the prosthesis.
When the denture is fabricated, border molding captures the muscles in
their contracted position. In the relaxed muscle state, food will sometimes
become displaced under the denture border. For example, when the patient
swallows, the food is pushed under the denture. Because the IOD moves less
than a denture, the food remains under the IOD and becomes lodged,
usually requiring the patient to physically remove the irritants (Fig. 15.6).
FIG 15.6 A removable implant prosthesis tends to impact food more than a
conventional removable prosthesis. An RP-4, totally implant-supported prosthesis,
will tend to accumulate food more than an RP-5 (soft tissue support with secondary
implant support).
Loss of Posterior Bone

Most mandibular IODs used by the profession are supported by implants
anterior to the mental foramina and soft tissue support in the posterior
regions. The anterior implants allow improved anterior bone maintenance,
and the prosthesis benefits from improved function, retention, and stability.
Dental implants placed in the anterior mandible help retain a lower denture
and are certainly a benefit over a complete denture. The posterior bone loss
will continue and may eventually lead to significant complications with
respect to lack of soft tissue support (i.e., RP-5 prosthesis). Studies have
shown posterior bone loss to occur four times faster than anterior bone
loss.38 The lack of posterior support in two- and three-implant overdentures
allows continued posterior bone loss. A primary concern for RP-5
overdentures (soft tissue support in the posterior regions) compared with
RP-4 or fixed restorations (restorations completely supported, retained, and
stabilized) should be the continued bone loss in the posterior regions.
Wright et al evaluated the change in the posterior mandibular residual
ridge over time comparing patients wearing mandibular IOD with bar
attachments or mandibular fixed cantilever prostheses stabilized on five or
six implants. Bone measurements were made by digitizing tracings of
panoramic radiographs. The mandibular fixed cantilever prostheses
demonstrated bone growth in the posterior mandibular residual ridge while
IOD showed bone resorption in the same area (Fig. 15.7).39
FIG 15.7 Posterior ridge resorption. Anterior bone is retained due to the presence
of implants; however, posterior ridge resorption will occur.
Reddy et al also confirmed this finding with the measurement of bone

height under a fixed detachable cantilever restoration supported by five or
six endosseous implants. A computer-enhanced method was used to measure
mandibular height distal to the last implant, which showed a significant
bone growth in the mandible the first year of function.40
Not Understanding the Wide Range of Overdenture
Retention
Etiology
A common complication that arises with overdenture treatment planning is
utilizing the same or “favorite” treatment plan (i.e., implant number and
position) for all patients. The clinician must understand there exists a
significant difference between overdenture treatment plans including
number of implants, implant positioning, opposing dentition, and patient
expectations.
Prevention
Understand Overdenture Mechanics.

To develop a mandibular IOD with reduced complications, the final
prosthesis should be predetermined and related to three factors:
1. Retention: retention is related to the vertical force necessary to dislodge the

prosthesis. The amount of overdenture retention is dictated by the number,
location, and type of attachments.
2. Support: the support of a prosthesis is related to the amount of vertical

movement of the prosthesis toward the tissue. This will vary greatly
depending upon the patient's ridge form. Support is primarily related to
implant number, independent attachments or presence of a bar design in the
posterior region.
3. Stability: stability of a prosthesis is evaluated with horizontal or

cantilevered forces applied to the restoration. The stability of the IOD is
more related to implant (attachment and bar) position. This is often a
misconception of patients because they believe there should exist no
movement of the prosthesis.
Treat According to Patient's Desires.

The patient's initial complaints, hard and soft tissue anatomy, prosthetic
desires, and financial commitment determine the amount of implant
support, retention, and stability. Because different anatomic conditions and
patient force factors influence these factors for an IOD, not all prostheses
should be treated in the same manner. In other words, the two-implant
overdenture should not be the only treatment plan offered to a patient. One
should emphasize that most mandibular overdentures should be designed to
eventually result in a RP-4 prosthesis (e.g., totally implant supported). If the
patient wishes for a less retentive prosthesis, a prosthesis with less support,
and with minimal stability, the patient needs to understand the inherent
disadvantages. It is highly recommended that the clinician furnish all
patients with ALL possible overdenture treatment plans. This is important
for two reasons. First, the patient will be well aware of the type of prosthesis
they have selected, and, secondly, this allows for the patient to understand
they can “upgrade” to a prosthesis at a later time that will have increased
retention, support, and stability. This will prevent unacceptable expectations
from the patient following the insertion of the prosthesis.
Understand Prosthesis Movement.

The most common complications found with mandibular IODs are related to
the prosthetics and a misunderstanding of retention, support, and stability of
the prosthesis. When a fixed restoration is fabricated on implants, it is rigid,
and cantilevers or offset loads are clearly identified. For example, rarely will a
practitioner place a full-arch fixed restoration on three implants, especially
with excessive cantilevers because of implant positioning. However, three
anterior implants with a connecting bar may support a completely fixed
overdenture, solely because of attachment design or placement. The
restoring clinician believes the three-implant overdenture has less prosthetic
occlusal load but does not realize that a three-implant overdenture may
become “fixed” just by the design of the attachments. A complete
understanding of the concept of prosthesis movement (PM) is needed by the
clinician (Fig. 15.8).
FIG 15.8 Example of improper use of the bar/attachment system. Because the
attachments are not in the same plane, the prosthesis will become fixed instead of
allowing for rotational movement (arrows).
Not Understanding the Concept of Prosthesis

Movement
An overdenture is by definition a removable prosthesis; however, in function
or parafunction the prosthesis may not move (e.g., because of the retentive
mechanism, it may become fixed). Clinicians need to understand that an
attachment may be classified as having movement in all directions; however,
using it incorrectly or in combination with other attachments may actually
change the range of motion. This may result in damaging forces to the
implant or the prosthesis.
Prosthesis Movement
Many precision attachments with varying ranges of motion are used in IODs.
The motion may occur in zero (rigid) to six directions or planes: occlusal,
gingival, facial, lingual, mesial, and distal.41 For example, a type 2 attachment
moves in two planes and a type 4 attachment in four planes. Attachment and
the prosthesis movement are independent from each other and should be
evaluated as such. An important item for the IOD treatment plan is to
consider how much prosthesis movement the patient can adapt to or tolerate
with the final restoration. It was to address this need that Misch has
formulated the concept of prosthesis movement instead of the classification
of the individual attachment. The PM classification encompasses movement
from PM-0 to PM-6 (Fig. 15.9).
FIG 15.9 Prosthesis movement. Hinging action of the prosthesis resulting from
anterior implants and lack of posterior soft tissue support (i.e., primary stress
bearing area – buccal shelf). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
PM-0.
A PM-0 attachment exhibits no movement in any direction. For example, if
the prosthesis is rigid (i.e., movement in no direction) when in place but can
be removed, the PM is labeled PM-0 regardless of the attachments used. If an
O-ring is used individually, they may provide motion in six different
directions. However, if four O-rings are placed along a complete arch bar, the
prosthesis rests directly on the bar and result in a PM-0 restoration. Because
of the design of the attachments and prosthesis, the end result would be a
fixed prosthesis (Fig. 15.10).
FIG 15.10 Prosthesis movement PM-0.
PM-2.
A hingelike PM permits movement in two planes (PM-2) and most often uses
attachments that have the capability to hinge. The most common examples of
PM-2 attachments are the Dolder bar and clip without a spacer or Hader bar
and clip. A Dolder bar is egg shaped in cross section, and a Hader bar is
round. A clip attachment may rotate directly on the Dolder bar. A Hader bar
is more flexible because round bars flex (x4) related to the distance between
the abutments and other bar shapes flex (x3). As a result, an apron often is
added to the tissue side of the Hader bar to limit metal flexure, which might
contribute to unretained abutments or bar fracture.42 A cross section of the
Hader bar and clip system reveals that the apron, by which the system gains
strength compared with a round bar design, also limits the amplitude of
rotation of the clip (and prosthesis) around the fulcrum to 20 degrees,
transforming the prosthesis and bar into a more rigid assembly. The Hader
bar and clip system may be used for a PM-2 when posterior ridge shapes are
favorable and soft tissue is stable enough to limit prosthesis rotation (Fig.
15.11).
FIG 15.11 Prosthesis movement PM-2, 3, or 4 depending on the number and types
of attachments placed.
It should be noted that for these systems to function as designed, the

hinge attachment needs to be perpendicular to the axis of prosthesis rotation
so the PM also will be in two planes (i.e., PM-2). If the Hader or Dolder bar is
at an angle or parallel to the direction of desired rotation, the prosthesis is
more rigid and may resemble a PM-0 system. As a consequence, the implant
system may be overloaded and cause complications such as prosthetic screw
loosening or fracture, implant crestal bone loss, and even implant failure. A
Hader bar-clip system is an ideal low-profile attachment for a RP-4 prosthesis
with PM-0. Usually, these clips are placed on the bar in different planes of
rotation around the arch.
PM-3.
A prosthesis with an apical and hinge motion is defined as a PM-3. An
example is a Dolder bar with a space provided over the bar. As a result, the
prosthesis moves toward the tissue and then rotates.
PM-4.
PM-4 allows movement in four directions.
PM-6.
PM-6 has a range of PM in all six directions. The most common overdenture
attachments for a PM-6 are independent O-rings or Locator attachments (Fig.
15.12).
FIG 15.12 Prosthesis movement PM-6. O-Ring with a single implant may move in
all six directions.
Height of the Attachment

An important aspect of overdenture PM is also related to the height of the
attachment connection. There are two crown height dimensions for
overdentures: (1) the occlusal plane to the height of the attachment rotation
and (2) the height of the attachment to the level of the bone. The occlusal
plane to attachment height is a force magnifier to the overdenture with any
lateral or cantilevered force. When an attachment is connected to an implant
directly, the crown height above the attachment is greater than when the
attachment is placed on a bar. If you double the crown height, the force is
increased 200%. Hence, the individual implant attachment has a greater
crown height above the attachment and greater lateral force to the
prosthesis. Therefore, the overdenture is less stable (Fig. 15.13).
FIG 15.13 There are two crown height space aspects for an implant overdenture.
The occlusal plane to the attachment is a crown height force magnifier to the
overdenture. Any lateral or offset load will be magnified in relation to the crown height
above the attachment.
When the attachment is placed on a bar, the stability of the prosthesis is

improved because less lateral force is applied to it (i.e., the crown height
above the attachment is reduced). Whenever possible, the implant should be
connected with a bar and an attachment placed on top of the bar. Rotation of
the prosthesis should be as far off the bone as practical. However, there
should be a minimum of 2 mm or more of acrylic space between the
attachment and the denture teeth. This allows adequate bulk of material to
decrease prosthesis fracture or dislodgement of teeth.
The second CHS is the height of the attachment to the bone level. The
greater the attachment-to-bone level, the greater the force placed on the
implant abutment screw, marginal bone, and implant-bone interface with any
lateral load. When the attachment-to–bone height distance is greater than 7
mm, the implants should be splinted together to decrease the risk of
complication of the implant system.
Too Large of a Cantilever (“Hidden Cantilever”)

The hidden cantilever was postulated by Misch in 1993 and describes the
portion of the removable prosthesis that extends beyond the last implant or
connecting bar.43 When hidden cantilevers exist, they may result in lack of
support for the prosthesis, excessive wearing of attachments, increased stress
to the bar-implant interface, and possible fracture of the prosthesis. In many
of these cases, the attachment system does not wear because the removable
prosthesis is PM-0 (i.e., no prosthesis movement); however, the excessive
resultant forces place the prosthesis, abutment screws, and marginal bone at
risk.
Etiology
If the bar/attachment is not designed correctly, the removable prosthesis
does not rotate at the end of the implant or bar to load the soft tissue. This
results in a “hidden cantilever.” For example, if a cantilevered bar extends to
the second premolar but forces on the second molar of the restoration do not
result in movement of the restoration (i.e., posterior-inferior movement,
anterior-superior movement), the cantilever extends to the second molar
position. The cantilever length is measured to the point of PM, not to the end
of the bar and attachment system.
Prevention
With most overdentures, the final restoration should not include extension
beyond the first molar. This will minimize the hidden cantilever and will
decrease the possibility of excessive force. The design of the overdenture
system should have the proper movement, and care should be exercised to
not induce a PM movement, especially when minimal number of implants
exist. (Fig. 15.14).
FIG 15.14 The hidden cantilever is that portion of the removable prosthesis that
extends beyond the connecting bar, which does not rotate. If the prosthesis rotates
at the first molar position and the bar extends to the premolar, the true cantilever
length is the first molar position. (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
Mandibuar Overdenture Complications
In 1985 Misch presented five organized treatment options for implant-
supported mandibular overdentures in completely edentulous patients. With
these mandibular overdenture treatment options, studies have shown less
than 1% implant failure and no prosthesis failure over a 7-year period with
147 mandibular overdentures (IOD) when using the organized treatment
options and prosthetic guidelines presented in this chapter.43 Kline et al
reported on 266 implants for mandibular splinted implant-supported
overdentures for 51 patients with the Misch protocol. An implant survival
rate of 99.6% and a prosthesis survival rate of 100% were reported.44
When evaluating a patient for a mandibular overdenture, ideal treatment
planning and overdenture mechanics must be considered. A determination
of the final prosthesis being totally implant supported or soft tissue
supported must be ascertained. Misch has determined the IOD treatment
options to range from primarily soft tissue support and secondary implant
retention (RP-5) to a completely implant-supported prosthesis (RP-4) with
rigid stability and retention gained primarily from overdenture attachments
(no soft tissue support). The prostheses are usually supported by two to five
anterior implants for these five treatment options between the mental
foraminal area. There are four RP-5 options that have a range of retention,
support, and stability. The RP-4 restoration is defined as a rigid cantilevered
bar that completely supports, stabilizes, and retains the restoration (Fig.
15.15).
FIG 15.15 RP-4/RP-5 prosthesis. Five prosthetic options are designed for the
mandibular overdentures. Four options are RP-5 (posterior soft tissue support) and
one option is RP-4 (prosthesis completely supported by implants and connective
bar). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Complications arise when patients are treated with the same protocol
without regard to the patient's needs and expectations. For example, a two-
implant overdenture may work very well with some patients; however, for
others it tends to work very poorly. There are many factors that need to be
evaluated prior to implementing an overdenture treatment plan. A thorough
understanding of the positioning, number, and type of implants along with
patient expectations should be ascertained according to various treatment
plans. In addition, reports indicate that RP-5 mandibular IODs may cause a
combination-like syndrome, with increased looseness, subjective loss of fit,
and midline fracture of the upper denture.45
Inadequate Crown Height Space

Etiology
Implant overdentures may exhibit significant complications when reduced
CHS (i.e., interocclusal space) exists. When sufficient CHS is lacking, the
prosthesis is more prone to component fatigue and fracture and has more
complications in comparison to porcelain-to-metal fixed prostheses.1
Prevention
Removable prostheses have space requirements for elements such as a
connecting bar, type, and position of attachments and restorative material
(metal vs. resin). According to English, the minimum CHS for individual
attachments is 10 mm of CHS for Locator-type attachments and between 12
and 15 mm for a bar and O-rings.14 The ideal CHS for removable prostheses is
greater than 14 mm, and the minimum height is 10.5 mm.46 The lowest
possible profile attachment should be used in situations of reduced CHS to
fit within the contours of the restoration, provide greater bulk of acrylic resin
to decrease fracture, and allow proper denture tooth position without the
need to weaken the retention and strength of the resin base.16
The minimum CHS provides adequate bulk of acrylic to resist fracture;
space to set denture teeth without modification; and room for attachments,
bars, soft tissue, and hygiene. In the mandible the soft tissue is often 1 to 3
mm thick above the bone, so the occlusal plane to soft tissue should be at
least 12 mm in height (Fig. 15.16).
FIG 15.16 The mandibular overdenture requires at least 12 mm between the soft
tissue and the occlusal plane to provide sufficient space (15 mm from bone level to
occlusal plane) for the bar, attachments, and teeth. (From Misch CE: Dental implant
An osteoplastic procedure to increase CHS before implant placement is

often indicated, especially when abundant bone height and width are
present. The crown height space should be evaluated and properly treatment
planned prior to implant placement. Otherwise, a fixed porcelain-metal
restoration should be considered (Fig. 15.17).
FIG 15.17 Osteoplasty. (A) increase crown height space. (B) Difference in amount
of osteoplasty for a FP-3 vs. RP-4/5 prosthesis.
The most common method of bar retention by almost the same percentage
for overdentures is screw retention. In minimum CHS situations, the screw-
retained bar has a clear advantage, but in ideal to excessive CHS situations,
the cemented bar may be considered. A combination of screw retention on
some abutments and cement retention on others offers an advantage for
many RP-4 prostheses, especially when implants are placed in the posterior
region.
Poor Osseous Angulation (C-A)

Etiology
With increased bone resorption, the mandible resorbs from a division A to
division C, eventually being compromised in angulation (division C−a). The
division C−a is defined as an anterior mandible that is angled more than 30
degrees. If the clinician is unaware of this angulation, the implants may
perforate the lingual plate and irritate the tissues of the floor of the mouth. If
the implants are within the confines of the bone, they may enter the crest of
the ridge at the floor of the mouth and make it almost impossible to restore
(Fig. 15.18). In a study by Quirynen et al of 210 computer tomogram images,
28% of the anterior mandibles were lingually tilted −67.6 degrees ± 5.5
degrees.47 The mandibles with less than −60 degree tilt represent about 5% of
the cases (Fig. 15.19).
FIG 15.18 C−a mandible. (A) CBCT examination exhibiting significant angulation.
(B) Cross-section CBCT exhibiting angulation from extensive buccal bone
resorption.
FIG 15.19 Implant placement in angle mandible. Angulation overcorrection leading
to possible perforation of lingual plate.
Almost 10% of patients may have a greater than 30-degree angle to the
occlusal plane. When present, this condition is most often found in the
anterior mandible. Root form implants placed in this bone category (i.e.,
within the cortical plates) may have the abutments positioned within the
floor of the mouth and compromise prosthetic reconstruction, speech, and
comfort.
Prevention
In patients with division C−a, implants may be contraindicated to prevent
surgical and prosthetic complications. In some cases, conventional
removable prosthetics may be indicated or extensive bone grafting may be
warranted to transform the division C−a into a division A.
Treatment
If implants have been placed prior to restoration, it may be the implants are
nonrestorable. If the implants are nonrestorable, treatment options include:
1. Removal of the implants followed by bone grafting, placement of new
implants in a more ideal position.
2. Surgical cover screws are placed in the implants, thus “sleeping” the
implants followed by fabrication of a conventional prosthesis.
Nonideal Implant Positioning

Etiology
Usually, the greatest available bone height in an edentulous mandible is
located in the anterior region between the mental foraminae. This location
most likely exhibits optimal density of bone for implant support and ease of
implant placement. The implant overdenture treatment options presented
are designed for anterior implant placement between the mental foramina
because the prostheses movement will be more limited and available bone
volume and density is more favorable than posterior implants.
Nonideal implant positioning leads to many complications, which include
hard and soft tissue complications, prosthesis dissatisfaction or fracture, and
questionable long-term implant health.
Prevention
The available bone in the anterior mandible (between the mental foramen) is
divided into five equal columns of bone serving as potential implant sites,
labeled A, B, C, D, and E, starting from the patient's right side (Fig. 15.20).48
The mean interforaminal distance has been shown to be approximately 53
mm.49 Five implants of 4 to 5 mm diameter can usually be placed with
general placement guidelines of 3 mm between implants and 2 to 3 mm from
the mental foramen.
FIG 15.20 (A) The interforaminal space is selected for placement of mandibular
implants for overdentures. (B) Five implants sites are easily selected labeled A, B,
C, D, E starting from the right side.
When placing implants, regardless of the treatment option being executed,

all five implant sites should be ideally located at the time of treatment
planning and surgery. There are three reasons for this treatment approach:
1. The patient always has the option to obtain additional implants and
prosthesis support and stability in the future if all five sites were not initially
used for implant support. For example, a patient may receive adequate
retention, stability, and support for an IOD with four implants. However, if
the patient desires a fixed prosthesis in the future, the four implants most
likely will be inadequate for the new prosthetic requirements. If the clinician
does not plan an additional implant site during the initial surgery, but
instead placed the four implants an equal distance apart, the additional
interimplant space may not be available without removing one of the
preexisting implants.
2. A patient may desire a completely implant-supported restoration (e.g., RP-

4 implant supported overdenture or FP-3—fixed prosthesis), but for financial
reasons may not able to enter into the treatment at that time. Three implants
in the A, C, and E positions and an IOD may be provided first. This is the
initial or first phase of the treatment, which has many advantages over a
conventional complete denture. Two more implants may be added in the B
and D locations at a later date, and a completely implant-supported
overdenture or fixed restoration may then be fabricated (Fig. 15.21).
FIG 15.21 (A) Patient presented with two-implant overdenture with inadequate
retention. (B) Three additional implants placed in the B, C, D positions. (C) Final RP-
4 prosthesis.
3. If an implant complication occurs, the preselected option sites permit

repeatable corrective procedures. For example, if implants were placed in the
A, B, D, and E positions and an implant fails to achieve rigid fixation, the
failed implant may be removed and an additional implant placed in the C
position at the same time. This saves an additional surgery and eliminates
the time required for bone grafting and healing before another implant could
be reinserted.
Not Understanding Mandibular Overdenture

Treatment Plans
The five treatment options proposed for mandibular implant–supported
overdentures provide an organized approach to solving a patient's
complaints that takes into consideration various anatomic limitations. The
treatment options initially proposed are designed for completely edentulous
patients with division A or B anterior bone who desire an overdenture. These
options are modified when the CHS is excessive (as when the anterior bone is
division C−h) and eliminated for division D. The implants are placed
between the foramens in the A through E positions (Fig. 15.22).
FIG 15.22 (A) There are five treatment options for a mandibular implant
overdenture. Two implants in the B, D position may be independent (OD-1) or
splinted together (OD-2). (B) Three implants may be used, splinted together with a
bar (OD-3). (C) Four implants with a cantilevered bar (OD-4) or five implants and a
cantilevered bar (OD-5) may have a RP-5 or RP-4 restoration. C–h, division C
minus height bone class; OD, overdenture option; PM, prosthesis movement
class. (From Misch CE: Misch Implant Institute manual, Dearborn, MI, 1984, Misch Implant
Institute.)
Overdenture Option 1 (OD-1)

The overdenture option 1 (OD-1) must be a RP-5 (soft tissue supported with
secondary implant support), which means it must be able to rotate and load
the posterior soft tissue regions of the mandible. The stability and support of
the prosthesis are gained primarily from the anatomy of the mandible and
prosthesis design, which is similar to a complete denture.
Advantages.
The primary advantage with treatment option OD-1 is reduced cost to the
patient. The two implants are usually the fewest implant number, and no
connecting bar reduces the prosthetic appointments and the laboratory costs.
Indications.
The first treatment option for mandibular overdentures (OD-1) is indicated
primarily when cost is the most significant patient factor. However, it is
important to note the patient's desires should also be minimal (i.e., patient
must understand the limitations of the treatment plan), and the bone volume
in both the anterior and posterior regions should be abundant (division A or
B). The posterior ridge form should be an inverted U shape, with high
parallel walls for good to excellent anatomic conditions for conventional
denture support and stability. The problem associated with the existing
denture should relate primarily to the amount of retention, not stability or
support. In addition, the opposing arch should ideally be completely
edentulous and restored with a traditional complete denture (Box 15.5).
Box 15.5
Patient Selection Criteria: OD-1
• Opposing a maxillary full denture
• Anatomic conditions are good to excellent (division A or B anterior and

posterior bone)
• Posterior ridge form is an inverted U shape
• Patient's needs and desires are minimal, primarily related to lack of

prosthesis retention
• Edentulous ridge not square with a tapered dentate arch form
• Cost is the primary factor

• Additional implants will be inserted within 3 years
Anatomic Position.
Usually, two implants are placed in the B and D positions. The implants
remain independent of each other and are not connected with a
superstructure. The overdenture attachment primarily improves retention
and gives little additional support or stability to the prosthesis. The stability
of the restoration is slightly improved in the anterior section by the implants,
and the posterior inverted U shape regions from the ridge form are required
to improve this factor (Fig. 15.23).
FIG 15.23 Overdenture option 1 consists of two independent implants. These are
best inserted in the B and D positions to limit the forward rocking of the restoration
during function. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
In the past, most two-implant overdentures positioned the implants

immediately anterior to the mental foramen in the A and E positions.
Positioning of the implants in the B and D position is a much better
prosthetic option in OD-1 than positioning in the A and E regions.
Independent implants in the A and E positions are usually implant locations
in the first premolar region, which is more posterior to the anterior fulcrum
line of the anterior teeth and allows a greater amplitude of rocking of the
restoration. When using B and D implants (with positions similar to the
natural canines), the anterior movement of the prosthesis is reduced (Fig.
15.24).
FIG 15.24 Care should be exercised to not prevent rotational movement of an RP5
prosthesis. In this example, two implants in the B and D position are accurately
placed, however because the attachments are in different planes, the prosthesis
becomes a fixed prosthesis.
Support.
The support of the OD-1 restoration is provided primarily from the buccal
shelf in the posterior and the ridge in the anterior, similar to a traditional
denture. The IOD must be RP-5 with preferably a PM-3 or more, which allows
for rotation and loading of the posterior soft tissue regions of the mandible
(Fig. 15.25).
FIG 15.25 A and E Implants. (A) Independent implants in the A and E positions
allow a greater anterior rocking of the restoration and place greater leverage forces
against the implants (arrows). (B) Resultant prosthesis will have an associated
anterior and posterior cantilever (arrows).
Attachment.
The most common type of attachment used in OD-1 is an O-ring or Locator
design. The implant support mechanism is poor because stress relief of the
attachment is permitted in any plane. In other words, the stability and
support of the prosthesis are gained primarily from the anatomy of the
mandible and prosthesis design, which is similar to a complete denture.
Complications of OD-1
Lack of posterior support.
If the posterior area is not supported (buccal shelf) adequately, the prosthesis
will be loaded mainly from the implants. This will lead to excessive forces
being applied to the implants, which may result in bone loss. As the
posterior ridge resorbs, the patient will gradually lose posterior occlusion,
leading to a posterior open bite.
Positioning.
The two independent implant retention systems often have more prosthetic-
related complications in comparison to other treatment plans. There are
several reasons the complication risk is increased (Fig. 15.26A).
FIG 15.26 (A) Poor positioning. (B) Ideal positioning, same height.
Perpendicular to occlusal plane.

The two implants should be perpendicular to the occlusal plane to allow the
posterior regions of the overdenture to move downward and load the soft
tissue over the mandibular buccal shelves for support. The hinge rotation
should be at 90 degrees to the rotation path; otherwise, one side is loaded in
a different manner than the other. In addition, because only two implants
sustain the occlusal load during function or parafunction, minimization of
the forces to the implant components and crestal bone is achieved by placing
the implants in the long axis of the implant body and perpendicular to the
occlusal plane (Fig. 15.26B).
Height parallel to occlusal plane.

The two independent implants should be positioned at the same occlusal
height parallel to the occlusal plane. If one implant is higher than the other,
the prosthesis will disengage from the lower implant during function and
rotate primarily on the higher implant. This situation will accelerate the wear
of the O-rings or Locator attachments. In addition, because the higher-
positioned implant receives the majority of the occlusal load, an increased
risk of complications may occur, including abutment screw loosening,
marginal bone loss around the implant, and implant failure (Fig. 15.27). If the
implant bodies are positioned at different heights, the use of different size
abutments should be used to make them as level as possible.
FIG 15.27 Implants placed in ideal position with abutments at the same height.
Distance from midline.

The implants should be equal distance off the midline. If one implant is
more distal (farther from the midline), it will serve as the primary rotation
point or fulcrum when the patient occludes in the posterior segments. In
such a case, the more medial implant attachment will wear faster, and the
more distal implant will receive a greater occlusal load when the patient
occludes in the anterior region (Fig. 15.27).
Implant parallelism.
The two implants in this treatment option should be parallel to each other.
The path of insertion of the prosthesis should also be similar to the path of
insertion of the attachments. When the implants are not parallel, the first
attachment to engage wears less, and the second attachment rubs along the
side of the male and increases the wear rate. When the path of insertion of
the restoration is different than the attachments (as when a facial undercut
below the crest exists), the attachments will wear prematurely (Fig. 15.27).
Angulation.
If a facial undercut exists, the path of insertion of the restoration may not
coincide because of the implant position. This may lead to chronic sore spots
and the need for multiple adjustments. This most often occurs when there
has been extensive atrophy (buccal resorption) from a division A to a division
B or C (Fig. 15.28).
FIG 15.28 When an anterior undercut is present it determines the pathway of
insertion of the restoration and should be similar to the pathway of the insertion into
the attachment. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Arch form.
There are two types of arch forms: the tooth position arch form and the
edentulous ridge arch form. It should be noted that the edentulous residual
ridge may be square, ovoid, or tapering. The dentate arch form is also divided
into square, ovoid, and tapering categories and may be different than the
ridge form. When a tapered tooth position arch form is supported by two
independent implants in a square residual ridge form, the anterior teeth are
cantilevered anteriorly from the implant retentive system. More implants are
required in this type of tooth-supported ridge form combination to help
stabilize the prosthesis, and the OD-1 option will have a considerable
disadvantage.
Decreased support.
Individual implants have more prosthetic complications than when the
implants are joined by a bar. When implants are supported by a bar, the
individual implants have less force and stress applied to the system.
Attachments are easily made parallel with a bar-fabricated prosthesis by the
laboratory in similar horizontal, vertical, and axial planes. This is much easier
and more predictable than relying on the surgical placement making the
implants completely parallel in all planes.
The opposing arch for an OD-1 mandibular treatment option should be a
traditional complete denture. The bite forces are reduced when the patient is
completely edentulous. The maxillary denture has some movement during
function and acts as a stress reliever. The instability of the maxillary denture
and mandibular OD-1 overdenture is shared. The support requirements of
the posterior regions of the mandible are reduced when opposing a complete
denture. Ideally, the opposing arch should be a complete denture when OD-1
is the treatment option.
Patient misconceptions.
The OD-1 is used as a treatment option when patients understand that a
connecting bar or additional implants are beneficial but financial constraints
require a transition period. However, many patients do not realize the lack of
support that is associated with two implants. The ultimate long-range goal in
the treatment plan is to convert OD-1 patients to a RP-4 or FP with more
implant support and stability before the loss of the posterior bone in the
mandible occurs posterior to the foramina. Future modification of the
treatment plan results in implant placement in the A and E positions. This
will allow the four implants (A, B, D, E positions) to be connected with a bar
that may be cantilevered to the posterior. Additionally, an increased surface
area for support helps reduce the posterior bone loss.
Abutment height.
The two independent implants most often use a Locator system or O-ring
attachment. After healing, the permucosal extensions and premanufactured
titanium alloy Locator or O-ring abutments are inserted into the implant
bodies. The abutment for attachment replaces the permucosal extension. The
attachments should be parallel to each other and at the same occlusal height.
The higher the abutment, the more the lateral stability of the prosthesis.
However, at least 2 mm of acrylic should be present between the teeth and
borders of the denture around the encapsulator of the attachment (Fig.
15.29).
FIG 15.29 Attachment heights. (A) Locator attachment. (B) O-ring attachment.
The abutments for attachments are provided in different heights. The

abutment should be ideally 2 mm above the tissue and 2 mm below the
denture teeth so adequate thickness of acrylic is present. The attachment and
encapsulator are placed into the implants. The abutments are then tightened
with a torque wrench at 20 to 35 N/cm (depending on the manufacturer). Too
high of an abutment placement will lead to increased torqueing forces and
instability.
Indications.
The second treatment option for a mandibular overdenture (OD-2) is
selected when more support is indicated in comparison to OD-1 (Box 15.6).
The anatomic needs and patient desires are similar to the first option, OD-1.
A bar is designed to position the attachments for added retention at an equal
distance off the midline parallel to each other at the same occlusal height and
in a similar angulation. The ideal distance between the implants is in the 14-
to 16-mm range or B and D positions.
Box 15.6
• Opposing arch is a maxillary denture
• Anatomic conditions are good to excellent (division A or B bone in anterior

and posterior regions)
• Posterior ridge forms an inverted U shape
• Patient's needs and desires are minimal, primarily related to lack of

retention
• Patient can afford a new prosthesis and connecting bar
• Additional implants will not be inserted for more than 3 years
• Low patient force factors (e.g., parafunction)
• The mandibular residual ridge form is square to ovoid, and the dentate
arch form is square to ovoid
Anatomic Position.
The implants in OD-2 are also positioned in locations B and D, but with this
option, they are splinted together with a superstructure bar without any
distal cantilever. Reduced loading forces are exerted on two anterior implants
when splinted with a bar compared with individual implants.50,51 The
implants should not be positioned in the A, E position even when connected
with a bar. The A, E position is most often the first premolar and may even be
in the second premolar position (depending on sex and race). When the
implants are joined with a straight bar, the connecting bar is lingual to the
anterior ridge. The overdenture flange is often too bulky and may impinge on
the sublingual area and affect speech. The denture teeth are anterior to the
residual ridge and act as a lever on the bar, and the prosthesis is not stable
(i.e., anterior cantilever). The connecting bar between A and E implants flexes
five times more than when the bar connects B and D implants; therefore
screw loosening is more of a risk. When a curved bar is used to position it
more anterior, the prosthesis often rides along the sides of the bar and limits
PM. If the prosthesis rests against the sides of the curved bar, the PM may
even be reduced to PM-0. This places a much greater vertical and lateral load
on the implant system. There are greater lateral forces on the A, E implant
position, which may increase screw loosening. If the patient has implants
already inserted into the A and E positions, the best treatment option is to
insert another implant in the C position and connect the three implants with
a bar (Figs. 15.30 and 15.31).
FIG 15.30 Treatment option 2 has implants in the B and D positions, and a bar
joins the implants. Attachments such as an O-ring or a Hader clip, which allow
movement of the prosthesis, can be added to the bar. The attachments are placed
at the same height at equal distances off the midline and parallel to each other. (From
FIG 15.31 A bar splinting the A and E positions will flex five times more than a bar
connecting implants in the B and D positions. As a consequence, screw loosening
risk is increased. Implants in positions A and E should not be splinted together.
Instead, an implant in the C position should first be inserted. (From Misch CE: Dental
Bar/Attachment.
When attaching two implants together, reduced loading forces are exerted on
the two anterior implants when splinted together with a bar. This may result
in less screw loosening and crestal bone loss than OD-1. Secondly, the
laboratory may position the attachments parallel to each other at the same
height and equal distance from the midline regardless of the corresponding
implant positions, thus reducing prosthetic complications. The retentive
element on the splinted bar may be an O-ring or clip design depending on
the crown height distance available. The bar can be similar to those designed
by Dolder or Hader. The bar cross section is ideally ovoid (Dolder) or round
with an apron so as to increase the strength of the bar and reduce its
flexibility. Ideally, the bar should be a minimum of 1 mm away from the soft
tissue to provide easy access for hygiene aids.
Compromised bone.
Two implants often work well in cases when there is abundant bone.
However, two implants are not indicated in division C−h bone, division D
bone, or when there is parafunction and opposing anterior or posterior
natural teeth. The resulting increase in crown height, poor posterior ridge
form, and masticatory forces, as well as the natural opposing arch, place
additional stresses on the implant system and will most likely increase
complications. When these situations are present, additional implants
should be used to decrease the possible prosthetic risks.
Connecting bar complications.

One of the most common complications with an implant connecting bar is
insufficient space between the bar and the soft tissue. This will most likely
impair oral hygiene procedures and may also be the cause of food debris
impaction and soft tissue inflammation. The success of the bar may be
achieved more easily by the selection of the proper height implant
abutments and an accurate master cast. The abutment height should be a
minimum of 1 mm above the tissue and no greater than 2 mm. Too high of an
abutment will increase force and stress on the prosthesis components. The
prosthesis attachment system to the superstructure bar is closely scrutinized
when Hader and Dolder clips are used for retention. The connecting bar and
clips should be perpendicular to the path of rotation and parallel to the
occlusal plane. This usually requires a straight bar perpendicular to the
midline. A curved bar often places the clips closer to the implants and
prevents rotation of the prosthesis, therefore becoming more of a fixed
prosthesis (Fig. 15.32).
FIG 15.32 Two-implant bar with implants too close together.
The connecting bar of the restoration should always be fabricated after the
final contours and teeth position are ascertained for the overdenture.
Otherwise, compromises of inadequate room for denture teeth or
overcontoured restorations (most often on the lingual surface) result. The bar
may be connected on the facial aspect of each implant coping. In this way the
lingual flange of the prosthesis remains within the contour of a traditional
denture.
Positioning.
It should be noted implants placed closer than the B, D position will result in
reduced prosthesis stability during function, whether they are connected or
independent units. When a bar is going to be fabricated, implants positioned
too close together will impede the use of an attachment. Additionally, the
nonideal positioning may lead to future issues if additional implants are
treatment planned. By placing implants in a differing position than B and D
will result in future inability to place implants in the A, B, or C position.
Lever arm.
The higher the attachment position, the more stable the overdenture will be.
However, CHS above the attachment will act as a lever arm. The greater the
occlusal height, the greater the force and the less stable the overdenture to
any lateral force. However, the height of the attachments on the connecting
bar should allow a minimum of 2 mm of acrylic space between the denture
teeth and attachment to permit adequate dimension for strength. The
internal aspect of a bar-retained overdenture should not be processed against
the sides of the abutment or bar because this will limit rotation and increase
the possibility of fractures (Fig. 15.33).
FIG 15.33 (A) This denture is processed with the acrylic receptor sides over the
copings and bar too close and will limit (or prevent) rotation of the implant
overdenture during function. (B) The clip should engage the bar, and the denture
should not rest on the sides of the implant abutments or bar. (From Misch CE: Dental
Cantilever.
The connecting bar should not be cantilevered to the distal when only two
implants are placed. When a bar is cantilevered from anterior implants, there
is insufficient anteroposterior (A-P) distance between the two implants to
counter the effect of the cantilever. An increased risk of prosthetic and
abutment screw loosening exists with the cantilever (Fig. 15.34).
FIG 15.34 The connecting bar between implants B and D should not be
cantilevered to the distal (arrow). (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
Increased fee.
Because a bar is indicated in OD-2, the clinician must take into consideration
the increased associated expense. A laboratory fabricated bar/attachment can
be costly. The patient should be well aware of this prior to the initiation of
treatment.
Indications.
The third treatment option may be used when the opposing arch is a denture
and the patient has moderate to low retention, support, and stability needs.
With an opposing complete denture, the amount of force on the prosthesis is
minimized. When the posterior ridge form is poor (division C−h or D bone),
the OD-3 is the lowest treatment option suggested.
The OD-3 treatment option is usually the first option presented to a
patient with minimal complaints and is concerned primarily with retention
and anterior stability of the IOD when cost is a moderate factor. The
posterior ridge form should be evaluated because it determines the posterior
lingual flange extension of the denture (buccal shelf), which limits lateral
movement of the restoration in this treatment option (Box 15.7).
Box 15.7
• Opposing arch is a maxillary denture
• Anatomic conditions are moderate to excellent
• Posterior ridge forms an inverted U shape
• The patient's needs and desires require improved retention, support, and
stability
• Cost a moderate factor
• The patient may have moderate force factors (e.g., parafunction)
Position.
Three root form implants are placed in the A, C, and E positions for OD-3. A
superstructure bar connects the implants but with no distal cantilever. A PM-
2 or greater can be designed with three A, C, and E anterior implants. In the
future, when more retention, support, and stability is warranted, additional
implants may be placed in the B and D positions. If the posterior ridge form
is poor (division C–h), the lack of lateral stability places additional forces on
the anterior implants. Implants then are best placed in the B-C-D position to
allow greater freedom of movement of the prosthesis. The greater the stress
to the system, the greater prosthesis movement/stress relief indicated. This
increases the posterior movement of the restoration, but decreases the
amount of stress placed on the implants and screw-retained bar (Fig. 15.35).
FIG 15.35 (A) Overdenture option 3 corresponds to implants in the A, C, and E
positions connected with a bar. The attachments should be positioned to allow
movement of the distal section of the prosthesis. (B) Minimum bone width for a 4-
mm-diameter root form is 6 mm in the midfacial and lingual regions because the
round implant design results in more bone in all other dimensions (width and
height). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Advantages.
There are many advantages of splinting A, C, and E implants compared with
implants in the B and D positions. The implants splinted in the A, C, and E
positions usually do not form a straight line. The C implant is most often
anterior to the more distal A and E implants (in the premolar regions) and
ideally directly under the cingulum position of the anterior incisor denture
teeth (increased A-P spread). The restoration benefits from direct occlusal
load to the implant support in the anterior arch, which reduces tipping and
improves stability. As a consequence, when more than two implants are
placed in the anterior mandible, a tripod support system may be established.
To determine the amount of benefit of an A-P distance, the distal of the most
posterior implants on each side are connected with a straight line. The
distance from this line to the perpendicular position of the center implant is
termed the A-P spread. The greater the A-P spread of the A, C, and E
implants, the greater the biomechanical advantage of the bar to reduce stress
on the implants because they are splinted together. The splinted A-C-E
implant and bar position is more stable than the B-D position for the
prosthesis. The lateral stability of the overdenture system is improved
because the implants are in the A and E positions and the attachments are in
the B and D positions and more distal than OD-2. In addition, the connecting
bar can be higher off the tissue when the interocclusal space permits, and the
attachment-to–bone height dimension can be greater. As a result, rotation of
the prosthesis is more limited compared with OD-1 and OD-2. Therefore, the
third implant for OD-3 for a division C–h mandibular edentulous patient is a
considerable advantage because of the compromised height.
Bar/Attachment System.
O-rings/Locators attached to the connecting superstructure offer greater
leeway in bar design and position. An O-ring is often used when CHS
permits to increase the crown height attachment–to-bone dimension and
decrease the occlusal plane–to-attachment dimension. The smaller the
occlusal plane–to-attachment distance, the more stable the overdenture is to
lateral forces. The intaglio surface of the prosthesis should not contact the
sides of the connecting bar because this would result in too rigid a system,
placing too much force on the bar system.
The connecting bar should be parallel to the plane of occlusion, and the
attachments should be placed at the same height along the bar. Such
placement is needed for the prosthesis to rotate effectively during function.
No cantilever of the bar should be designed within this three-implant
system. However, the attachments may be placed on the distal of the A and E
abutments, similar to a Kennedy class 1 partial denture design (if positive
force factors).
Improper attachment design.
The IOD option 3 usually does not use two Hader clips for the attachment.
Because the two clips do not rotate in the same plane, the prosthesis is
usually too rigid, and the clips do not rotate unless they expand, making
wearing of the clip and bar a common complication. If a clip attachment is
designed for the prosthesis, the bar may connect the facial of the A and E
implant copings and the lingual of the C coping. As a result, a straight bar
may be fabricated perpendicular to the path of rotation (Fig. 15.36).
FIG 15.36 An implant overdenture option 3 should rarely use a Hader clip for the
attachment system. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Fabricating a RP-4 prosthesis.

With a three-implant overdenture, an RP-5 prosthesis should always be
fabricated because of the need for soft tissue support. Often an RP-4
prosthesis is fabricated with a three-implant treatment plan, leading to
overloading the implants. This may result in excessive attachment wear or an
accelerating wear of attachments.
Indications.
The patient's indications for the OD-4 treatment option as a minimum
requirement include moderate to poor posterior anatomy that causes a lack
of retention and stability of the IOD, history of recurrent soft tissue soreness,
or difficulty with speech. The clinician must understand the edentulous
posterior mandible resorbs four times faster than the anterior mandible. In
the C−h posterior mandibles, the external oblique and mylohyoid ridges are
high (in relation to the residual ridge) and often correspond to the crest of
the residual ridge. The muscle attachments are at or near the crest of the
posterior ridge. Another condition that indicates an OD-4 as a minimum
treatment option is when the patient's complaints and desires are more
demanding than for the previous treatment options (Box 15.8).
Box 15.8
• Moderate to severe problems with traditional dentures
• Needs or desires are demanding
• Need to decrease bulk of prosthesis
• Inability to wear traditional prostheses
• Desire to abate posterior bone loss
• Unfavorable anatomy for complete dentures
• Problems with function and stability
• Posterior sore spots
• Opposing natural teeth
• C−h bone volume
• Unfavorable force factors (parafunction, age, size six, crown height space
>15 mm)
Positions.
With the fourth mandibular overdenture option (OD-4), four implants are
placed in the A, B, D, and E positions. This is often the minimum number of
implants when the patient has opposing maxillary natural teeth, or C−h
anterior bone volume with CHS greater than 15 mm. The implants usually
will provide sufficient support to include a distal cantilever up to 10 mm on
each side if the stress factors are intermediate to low (i.e., parafunction, CHS,
masticatory dynamics, and opposing dentition) (Fig. 15.37).
FIG 15.37 In overdenture option 4, four implants are placed in the A, B, D, and E
positions. The implants usually provide sufficient support for a distal cantilever up to
10 mm. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Cantilever.
The cantilevered superstructure (bar) is a feature of the four or more implant
treatment options in a completely edentulous arch for three reasons:
1. Increase in implant support compared with OD-1 to OD-3.
2. Biomechanical position of the splinted implants is improved in an ovoid or

tapering arch form compared with OD-1 or OD-2.
3. Additional retention is provided by the fourth implant for the

superstructure bar, which limits the risk of prosthetic screw loosening and
other related complications of cantilevered restorations.
In considering a distal cantilever for a mandibular overdenture bar, the
implant position is the primary local determinant. Cantilevers may be
compared to a class 1 lever in mechanics. The distalmost implant on each
side acts as a fulcrum when occlusal forces are applied to the distal
cantilever. The amount of the occlusal force is magnified by the length of the
cantilever, which acts as a lever. For example, a 25-lb load to a 10-mm
cantilever results in a 250-lb mm force.
This moment force is resisted by the length of the bar anterior to the
fulcrum. If the two anterior implants (B and D) are 5 mm from the fulcrum
(distal implants A and E), the effect of the posterior cantilever is reduced. If
the implants are 5 mm apart, the mechanical advantage of the lever is the 10-
mm cantilever divided by the 5-mm A-P spread, which equals 2. Because the
implants are splinted, a 25-lb distal force is magnified to 50 lb to the anterior
implant and 75 lb (50 + 25 = 75) to the distal (fulcrum) implant.
Arch form.
As a general rule the posterior cantilever from anterior implants may be
equal to the A-P distance when other stress factors are low to moderate. The
mandibular residual ridge arch form may be square, tapering, or ovoid. The
arch form relates to the A-P distance of A-E and B-D implants. Square arch
forms limit the A-P spread between implants and may not be able to
counteract the effect of a distal cantilever.
A square arch form often results in an A-P distance of 4 mm or less. Under
these conditions a minimum cantilever should be designed, and a PM-3 to
PM-6 restoration is indicated. The distal cantilevers are significantly reduced
for square arch forms. In a mandibular ovoid to tapering arch form, the A-P
spread between implants in the A, E and D, B positions is greater and
permits a longer distal cantilever. This A-P spread is usually 8 to 10 mm in
these arch forms and often permits a cantilever up to 10 mm from the A and
E positions.
It should be emphasized that the A-P spread is only one factor to
determine the length of the cantilever. When stress factors such as occluding
forces are greater, the cantilever is decreased. Parafunction, opposing arch,
masticatory dynamics, and CHS affect the amount of force on the cantilever.
For example, when the crown height is doubled, the moment forces are
doubled. Under ideal, low-force conditions (crown height less than 15 mm,
no parafunction, older female patient, opposing a maxillary denture), the
cantilever may be up to 1.5 times the A-P spread for OD-4 overdentures.
When the force factors are moderate, the cantilever should be reduced to 1
times the A-P spread. The amount of distal cantilever is related primarily to
the force factors and to the arch form, which corresponds to the A-P spread
(Fig. 15.38).
FIG 15.38 (A) Arch shape affects the anteroposterior (A-P) distance. The square
arch form is less than 5 mm. (B) The ovoid arch form often has an A-P distance of 5
to 8 mm. (C) A tapered arch form has the greatest A-P distance, larger than 8
mm. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Attachments.
The most common attachment type is an O-ring or Locator because its
position allows the most freedom. The usual O-ring positions are on the
distal aspect of each bar and in between the A-B and D-E positions. An
alternative is to position one O-ring in the C implant position (because no
implant is at this site). The two distal O-rings permit rotation of the
restoration toward the buccal shelf, and the anterior O-rings permit the
restoration to rotate up toward the incisal. The connecting bar gives implant
support from the premolar region forward and lateral stability. The O-rings
provide adequate retention. A smaller-size O-ring or less retentive material
usually is positioned in the anterior, especially when two anterior O-rings are
used.
Advantages.
The patient benefits from the four-implant option because of greater occlusal
load support, lateral prosthesis stability, and improved retention. The
prosthesis loads the soft tissue over the buccal shelf and the first and second
molars and retromolar pad regions. The amount of occlusal force on the
implant system is reduced (compared with a fixed restoration or RP-4
prosthesis) because the bar does not extend to the molar position, where the
forces are greater.
The OD-4 treatment option is usually the lowest treatment rendered when
the patient has maxillary teeth. The greater vertical and horizontal forces to
the mandibular IOD require anterior disclusion in excursions to decrease the
bite force. As such, more anterior implants are required under these
conditions.
Complications/Disadvantages of OD-4
Hidden cantilever.
To reduce the hidden cantilever effect, the second molar is not restored in the
mandibular overdenture. In addition, the overdenture must contain
movement when loads are placed in the molar region. The position and type
of attachments on the connecting bar are important. The OD-4 prosthesis is
indicated to obtain greater stability and a more limited range of prosthesis
motion. The overdenture attachments often are placed in the distal
cantilevers with an O-ring attachment in the midline. The prosthesis is still
RP-5 but with the least soft tissue support of all RP-5 designs. The anterior
attachment must allow vertical movement for the distal aspect of the
prosthesis to rotate toward the tissue.
Hader bar/clip positioning.

The use of Hader bar/clips, which permit rotation, are difficult to use on
cantilevered superstructures. To allow movement, the clip must be placed
perpendicular to the path of rotation, not along the cantilevered bar where its
only function then is retention (and limits rotation). When Hader bar/clips
are made nonperpendicular to the path of insertion, the prosthesis becomes
fixed, which results in increased force to the bar/attachment system.
Indications.
The fifth mandibular overdenture option (OD-5) is designed for two types of
patients. Most important, this is a minimum treatment option for patients
with moderate to severe problems related to a traditional mandibular
denture. The needs and desires of the patient are often most demanding and
may include limiting the bulk or amount of the prosthesis, major concerns
regarding function (mastication and speech) or stability, posterior sore spots,
or the inability to wear a mandibular denture. This option is often indicated
when maxillary teeth or a fixed implant restoration is in the opposing arch
(especially with parafunction) (Box 15.9).
Box 15.9
• Moderate to severe problems with traditional dentures
• Needs or desires are demanding
• Need to decrease bulk of prosthesis

• Inability to wear a traditional prosthesis
• Desire to abate posterior bone loss
• Unfavorable anatomy for complete dentures
• Problems with function and stability
• Posterior sore spots
• Moderate to poor posterior anatomy
• Lack of retention and stability
• Soft tissue abrasion
• Speech difficulties
• More demanding patient type
• Maxillary teeth or fixed implant prostheses
• Angle's class II division I mandible restored to class I
The second patient condition that determines this option is for the
treatment to stop the continued bone loss in the posterior mandible. If no
prosthetic load is on the posterior bone, the resorption process is delayed
considerably and often reversed. Even when no posterior implants are
inserted, the cantilevered bar and overdenture avoid load to the posterior
residual ridge and often halt its resorption process. Recent studies show that
completely implant-supported prostheses often increase the amount of
posterior bone height even when no posterior implants are inserted.52
However, it should be noted that a better option to prevent this posterior
bone loss and increase the A-P spread is the insertion of one or more
posterior implants before the bone atrophy has occurred. The OD-5
treatment option is also indicated when the patient desires a RP-4 or fixed
restoration, the arch form is square for a RP-5 prosthesis, or the maxillary
arch has natural teeth (especially in a young patient or male).
Position.
In the OD-5 treatment option, five implants are inserted in the A, B, C, D,
and E positions. The superstructure is usually cantilevered distally up to two
times the A-P spread (when favorable force factors) and averages 15 mm,
which places it under the first molar area (Fig. 15.39).
FIG 15.39 Overdenture option 5. (A) Implants placed in the A, B, C, D, E positions,

which are splinted together with a distal cantilever. The size of the cantilever is
based on many factors including size of implants, position, A-P spread, bone
density, parafunction, and opposing occlusion. (B) Clinical image of five implant
splinted bar.
Forces/A-P Spread.
The amount of the distal bar cantilever is related (in part) to the A-P distance.
The forces exerted on cantilevered bar designs and implants have been
studied by several authors. A constant finding is that the most distal
implants receive stresses two to three times greater than the other implants.
The highest concentration of stresses is at the level of the crest distal to the
most distal implant on the loaded side. No statistical differences were found
between different implant lengths. The stresses increase with the length of
the cantilever. Stress factors need to be evaluated carefully and pondered
before an extended cantilever is designed.
Stresses are magnified in direct proportion to the length of cantilever and
should be planned carefully based on the patient's force factors and the
existing anatomy. The A-P distance is greater than in OD-4 because the C
implant is often more anterior than the B and D implant sites. A square ridge
form usually has an A-P spread of less than 5 mm and should have a
minimum cantilever even with five implants joined together. An ovoid arch
has an A-P spread from 5 to 8 mm and a tapered arch form more than 8 mm.
In these situations a cantilever of two times this distance is indicated when
force factors are not excessive (see Fig. 15.39).
If any major stress factors (e.g., parafunction, opposing arch) are not
favorable, the cantilever should be reduced. The patient force factors are as
important as the A-P spread. In a study in which the failure criterion was the
failure of the screw joint with arrangements of three, four, five, and six
implants with a similar A-P spread submitted to forces from 143 to 400 N, the
greater transmitted forces to the prosthetic connection always exceeded the
yield strength of the system. This study emphasizes the fact that the amount
and duration of occlusal load is even more important than the A-P spread to
be considered for cantilever length determination.53
The superstructure bar may be cantilevered up to two times the A-P
distance with low stress factors for three reasons. The additional C implant
increases the implant–bone surface area of the system, adds another
retentive element to the bar to reduce screw loosening, and increases the A-P
dimension. This helps counter act the class 1 lever action created by the
distal cantilever.
Five implants also allow the superstructure and prosthesis to be
cantilevered forward from the anterior ridge. This is of particular benefit for
Angle's skeletal class II patients. The lower lip is supported by the maxillary
teeth when the jaw is at rest. Traditional mandibular dentures reconstruct the
original horizontal overjet, so the lower anterior teeth position does not
infringe on the neutral zone during rest or function. However, in an RP-4
restoration, the teeth may be set in a skeletal class I pattern, where they
provide the best esthetic result. This also increases the amount of function in
the anterior region. Because these patients are skeletal class II, the forward
anterior tooth position also places the molars forward, reducing the need for
a more distal cantilever. The distal cantilever reduction also decreases the
posterior lever force.
Attachments.
Usually four to six retentive attachments are included in the cantilevered bar
design. The attachments are typically O-rings, Locators, or Hader clips.
Because of their number and distribution, the attachments provide retention
and oppose PM. Typically, four O-rings are distributed evenly (two anterior
and two posterior to the distal implants). If the OVD is limited or
parafunction is present, the IOD may use a metal framework within the
prosthesis (similar to a partial denture). This design reduces the risk of IOD
fracture.
A Hader bar clip may be placed distal to the last O-rings on each
cantilevered section. At delivery, the O-rings may be the only attachments
used. The Hader clip may be added as a backup system for additional
retention in case an O-ring stud breaks or when the vertical dimension of
occlusion does not permit the use of high-profile retentive O-rings and
causes repeated fracture of the overlying acrylic denture. It can also provide
additional retention to prevent sticky food from lifting the posterior aspect of
the denture.
The six-attachment bar design also permits a method to decrease stress to
the bar and implants if screw loosening or bone loss around the implants is
noticed. The Hader clip and bar may be sectioned off the connecting bar. The
RP-4 prosthesis then is converted to a RP-5 restoration because it may rotate
on the two O-rings placed just distal to the posterior implants.
Maxillary Overdenture Complications
The maxillary overdenture concept is much different in comparison to
mandibular overdentures in many aspects. Fewer reports have been
published for maxillary IOD compared with mandibular overdentures.
According to Goodacre et al, mandibular overdentures have one of the
highest implant success rates, and the restoration with the highest implant
failure rate is a maxillary overdenture (19% failure rate).54 A prospective
study by Johns et al reported on maxillary IODs at 1 year, 3 years, and 5
years.55 Sixteen patients were followed throughout the study with a
cumulative success rate of 78% for prostheses and 72% for implants.
Not Understanding the Advantages Associated With

a Maxillary Overdenture
Facial Esthetics May Be Enhanced
The loss of facial esthetics often occurs first in the maxillary arch, with the
loss of vermilion border of the lip, increased length of the maxilla lip, and
lack of facial bone support. However, patients may not realize these changes
are related and are accelerated because of the loss of teeth and bone. The use
of implant-retained prosthesis has the advantage of decreasing the continued
bone loss and prevent the later complications found in the maxillary arch.
Although difficult because of the premaxillary bone loss, a maxillary
overdenture may eliminate the complications.
Less Soft Tissue (Palatal) Coverage

The extended soft tissue coverage of a maxillary denture negatively affects
the taste of food and acts as an insulator to temperature. The soft tissue may
become tender in the extended vestibular borders as the crest of the ridge
resorbs. The palate of a maxillary prosthesis may cause gagging in some
patients. Most of these disadvantages of a complete maxillary denture may be
eliminated in an implant-supported overdenture, especially with an RP-4
horseshoe overdenture. Reducing the bulk of the prosthesis, especially when
the palate is eliminated from the overdenture, is more of a patient benefit in
comparison to the mandibular overdenture. Eliminating the palate reduces
the gagging effect from some patients and improves the taste of food in some
individuals. In some patients, an anatomic variant is present that includes
taste factors from the 11th nerve that innervate taste buds in the palate.
Although unusual, these patients benefit from the reduction of the palate of
their overdenture.
Decreases Premaxillary Resorption

When the resorption of the premaxilla increases, the maxillary denture will
become unstable. The maxillary anterior teeth will become positioned more
facially with respect to the residual bone. As a result, the denture will rotate
up in the anterior, resulting in rotation in a downward direction in the
posterior. The denture will lose the posterior valve seal as a consequence. In
the maxillary arch an implant-retained overdenture should be considered
before significant bone is lost in the premaxilla. The complete anterior ridge
and even the nasal spine may be resorbed in the maxilla, causing pain and an
increase in maxillary denture movement during function.56
Several factors affect the condition of the premaxilla and may result in a
decrease in implant survival or an increase in prosthetic complications. The
completely edentulous anterior bony ridge is often inadequate for endosteal
implants. The facial cortical plate may be resorbed from periodontal disease
or often is lost during the extraction of teeth. In addition, the facial cortical
plate resorbs during initial bone remodeling, and the anterior ridge loses
25% of its width within the first year after tooth loss and 40% to 60% over 3
years, mostly at the expense of the labial plate. As a result, the maxillary
denture migrates to a more palatal position.57
In the maxilla, horizontal and vertical loss of bone results in a more palatal
ridge position. As a consequence, implants are often inserted more palatally
than the natural tooth position. With overdentures, this is an advantage.
Removable restorations have several advantages under these clinical
circumstances. The removable prosthesis does not require embrasures for
hygiene. The facial cantilevered fixed prosthesis may make it impossible to
perform sulcular hygiene. The removable restoration may be removed during
sleep to decrease the effects of an increase in CHS on nocturnal parafunction.
The removable restoration may improve the lip and facial support, which is
deficient because of the advanced bone loss. The overdenture may have
sufficient bulk of acrylic resin to decrease the risk of prosthesis fracture. The
increase in CHS permits denture tooth placement without infringement of
the implant-prosthetic substructure.
Ability to Increase Soft Tissue Support

The primary advantages of a maxillary IOD compared with a fixed prosthesis
is the ability to provide a flange for maxillary lip support, the improved
sulcular hygiene, and the reduced laboratory fee compared with a fixed
restoration. As a consequence, before the selection of a specific prosthesis
type and to facilitate the diagnosis, the labial flange above the maxillary teeth
of the existing denture (or wax try-in of a new prosthesis) may be removed
and the facial appearance of the maxillary lip without labial support
assessed. A common complication after the placement of a fixed prosthesis in
the maxillary arch is to have insufficient soft tissue support leading to
dissatisfaction from patients. If labial lip support is not satisfactory, two
options are available:
1. A bone or soft tissue graft to the premaxilla is performed before or in

conjunction with implant insertion or at uncovery for a fixed implant
prosthesis.
2. A maxillary IOD is fabricated with a labial flange on the prosthesis.
Possible Maxillary Overdenture Complications

Compromised Crown Height Space
Removable prostheses often require a CHS greater than 12 mm for denture
teeth and acrylic resin base strength, attachments, bars, and oral hygiene
considerations.58 The amount of CHS in an edentulous region greatly varies.
The larger CHS may facilitate the fabrication process of removable
overdentures because it is easier for denture tooth setup and greater bulk of
acrylic can be used to strengthen the prosthesis. The inadequate CHS may
make an overdenture contraindicated. In these situations the denture tooth
position may be affected, the prosthesis may repeatedly fracture, and the
attachments may be compromised. This often occurs in the maxilla because
of the available bone and trajectory. When less than 12 mm of CHS is present,
an osteoplasty is considered before implant insertion. However, rarely can an
osteoplasty be completed because insufficient bone will be available for
implant placement (Fig. 15.40).
FIG 15.40 Less than 15 mm crown height space (CHS) for an implant overdenture
may compromise the position of the overdenture teeth and increase the risk of
prosthesis fracture. An insufficient CHS is a major problem for the fabrication of a
prosthesis (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Hidden Cantilever
A rigid overdenture (RP-4) has identical requirements for implant support in
position and number as a fixed prosthesis because it is rigid during function.
Soft tissue support in addition to implant-supported removable implant
restorations with an excessive CHS are recommended when it is not possible
to adequately engineer the implant support system. Misch has described the
“hidden cantilever ” beyond the cantilevered bar with a rigid IOD.59 When
the overdenture has no movement during function, the cantilever does not
stop at the end of the cantilevered substructure but ends at the last occlusal
contact position on the prosthesis, often the distal of a second molar. This
can lead to occlusal overload and overstress to the implant system.
Poor Treatment Planning Options

When the premaxilla is compromised with regards to available bone, some
clinicians will treatment plan posterior implants (premolar and molar)
without implant support in the canine regions. The prosthetic design is to
connect the implants with a full-arch bar for a maxillary overdenture. This is
not indicated when a bar extends from premolar to premolar around an arch
because the overdenture prosthesis is completely implant supported (RP-4)
and will not move (PM-0) during function or parafunction. As such, the
overdenture acts as a fixed restoration with less support and without
implants in the key implant positions.
Another poor treatment option for fully edentulous maxillae is the
placement of implants in each posterior quadrant (no canine position) with
independent bar segments and an overdenture (Fig. 15.41). This treatment
option is prone to failure for the following reasons:
1. If the IOD in the maxilla has only posterior implants and is not rigid, the
prosthesis rocks forward and up every time the patient bites into food or the
mandible moves into excursions. The rigid, posterior implants act as
fulcrums, and the restoration is not stable.
2. The implants in the premolar regions act as the fulcrum, and the incisal
edge of the prosthesis is cantilevered from this position. As a result, the
attachment system repeatedly fails. This type of prosthesis resembles a
Kennedy class IV partial denture and is the least stable restoration in
prosthetics. In fact, it is usually less stable than a conventional denture.
3. The posterior implants in this type of restoration are in a straight line and
do not resist the lateral forces as well. Often the attachments repeatedly need
replacement, and all the implants on one side of the arch may fail.
FIG 15.41 Posterior implants with individual bars allow rocking of the prosthesis,
which accelerated attachment wear and prosthetic screw loosening. (From Misch CE:
Not Taking Into Consideration Treatment Planning Factors.

To increase implant and prosthesis survival rates, treatment for maxillary
overdentures with division A bone is planned similarly to treatment for
mandibles with C minus height (C−h) bone and greater factors of forces. In
other words, four or more implants are inserted from first premolar to first
premolar. In addition, subantral augmentation often is performed to place
more distal implants and dramatically improve the A-P distance when the
anterior and posterior implants are splinted with a bar. This treatment
approach has proved successful in yielding success rates similar to those for
mandibular overdentures.
From a biomechanical perspective the implant-restored anterior maxilla is
often the weakest section compared with other regions of the mouth.
Compromised anatomic conditions and their consequences include the
following factors.
Poorer bone quality.

In the majority of patients with available bone in the maxilla, the bone is less
dense in the anterior maxilla than in the anterior mandible. In the mandible
a dense cortical layer is coupled with coarse trabecular bone strength and
permits implants to be supported by a denser bone quality. The maxilla
presents thin, porous bone on the labial aspect, very thin, porous cortical
bone in the floor of the nasal region, and denser cortical bone on the palatal
aspect. The trabecular bone is usually fine and is also less dense than the
anterior region of the mandible.
Force issues.
In the premaxilla, esthetics and phonetics dictate that the replacement teeth
be placed at or near their original position, often cantilevered off the residual
ridge, which usually is resorbed palatally and superiorly. Crown height as a
force magnifier is of paramount importance in the anterior maxilla, where
the natural crown height is already greater than in any other region even
under ideal conditions. The arc of closure is anterior to the residual ridge; as
a consequence, the moment force is greatest against the maxillary anterior
crowns supported by implants and directed against the thinner facial bone.
All mandibular excursions place lateral forces on the maxillary anterior teeth,
with resulting increased stress on the crestal bone, especially on the labial
aspect of the implant.
Available bone.
The narrow ridge of a premaxilla has parallel walls of bone, so an osteoplasty
to increase width is less effective. Because of the compromised bone width,
smaller-diameter implants will result in increased stress concentrations in
the implant and contiguous interfacial tissues, particularly at the crestal
region.
Cantilevers.
The use of facial cantilevers result in increased moment loads at the implant
crest, often leading to localized crestal remodeling and implant or abutment
fracture.
Occlusion.
Oblique centric contacts result in potentially harmful, off-axis load
components, and lateral forces in excursion resulting in greater moment
loads applied to the implant.
Buccal plate thickness.

The premaxilla has inherently minimal buccal plate thickness. Absence of
thick cortical plate at the crest results in the loss of high-strength implant
support and less resistance to angled loads, which increase stress.
Bone loss.
After loss of teeth in the premaxilla, bone volume loss in the incisor region
accelerates, often resulting in the inability to place central and lateral incisor
implants without substantial augmentation procedures. In the posterior
maxilla, compromised bone quantity is also an issue resulting in the need for
subantral augmentation.
Maxillary Overdenture Treatment Options

Whereas there are five overdenture treatment plans for the mandible, there
are only two options for the maxilla (Box 15.10). The difference is primarily
due to biomechanical disadvantages of the maxilla compared with the
mandible. Independent implants are unpredictable with a higher incidence
of morbidity and are completed with caution. In addition, the attachment is
closer to the tissue, and the CHS from the attachment is greater, so the
prosthesis has more movement. As such, the two treatment options are
limited to a removable prosthesis RP-5 restoration with 4 to 6 implants with
some posterior soft tissue support, or an RP-4 restoration with 6 to 10
implants (which is completely supported, retained, and stabilized by
implants).
Box 15.10
Maxillary Implant Overdenture Options
1. RP-5 prosthesis: four to six implants in three to five arch positions
2. RP-4 prosthesis: 6 to 10 implants in all five key implant arch positions
Option 1: Maxillary RP-5 Implant Overdenture
Indications.
The first treatment option with a maxillary implant-retained overdenture is
an RP-5 prosthesis. This option is not as beneficial to the patient compared
with mandibular RP-5 restorations. A RP-5 maxillary IOD may have
associated movement and may even rock more than a denture because the
anterior implants act as a fulcrum under the prosthesis. The major
advantages of an RP-5 maxillary IOD is the maintenance of the anterior bone
and the cost (a less expensive treatment option than an RP-4 or fixed
prosthesis). The RP-5 overdenture treatment is less expensive than an RP-4
overdenture because fewer implants are required and bilateral sinus grafts
and ridge augmentation are not required to support molar implants. The RP-
5 treatment plan is often used as a transition to an RP-4 prosthesis when
financial considerations of the patient require a staged treatment.
Implant Number/Position.
The maxillary OD-1 treatment plan for a completely edentulous maxilla uses
four to six implants supporting an RP-5 prosthesis, of which three are usually
positioned in the premaxilla. Based on the poor success rates reported in the
literature, specific biomechanical requirements, and poor bone quality, the
fewest number of implants for a RP-5 maxillary overdenture should be four,
with a wide A-P spread (Fig. 15.42). Implant number and location are more
important than implant size, but the implants should ideally be a minimum
of 9 mm in length and 3.5 mm in body diameter. An improved and more
predictable number of implants for an RP-5 prosthesis is five. The key
implants are positioned in the bilateral canine regions and at least one
central incisor position. Other secondary implants may be placed in the first
or second premolar region (five-sided arch of treatment planning).
FIG 15.42 At least four implants, splinted together, are indicated for a maxillary
implant overdenture, at least three of which are placed in the premaxilla. (From Misch
Alternative positioning includes placing an implant in the incisive foramen

or lateral incisor area. When an implant cannot be placed in at least one
central incisal position, the incisive foramen may be considered for implant
insertion. Another alternative is the use of a lateral incisor implant. In such
cases, owing to the reduced A-P spread of the lateral incisor in the anterior
most implant site, the second premolar position also should be used on the
contralateral side (along with the canine) to improve the A-P spread. Six
implants are often indicated for an RP-5 prosthesis when force factors are
greater (Fig. 15.43).
FIG 15.43 An alternate design with six implants includes key implants in the canine
regions, implants in the lateral incisor regions, and secondary implants in the second
premolar regions to improve the anterior-posterior spread. Dolder clips or O-rings
can be used in such a way as to allow two directions of prosthesis movement. (From
Prosthetic Design.
The implants are always ideally splinted together with a rigid bar. There is no
distal cantilever, and the bar design should follow the dental arch form but
slightly lingual to the maxillary anterior teeth. This will allow for more room
of acrylic for strength and retention. The prosthesis should have at least two
directions of movement; however, three or more are preferred. A Dolder clip
or O-ring may be used if it is placed in the center of the arch and
perpendicular to the midline. A Dolder clip has a spacer over the clip to allow
some vertical movement before rotation. When O-rings are used to retain the
restoration, they may be positioned more distal than a center Dolder clip,
often immediately distal to the canine position. O-rings may also be used just
distal to the last abutment on each side or between the implants. When
intermediate O-rings are used, relief is provided distal to the bar to allow
prosthesis movement toward the tissue under posterior occlusal forces.
Support.
The maxillary RP-5 IOD is designed exactly as a complete denture with fully
extended palate and flanges. The restoration should be allowed to move
slightly in the incisal region during function so that the restoration may
rotate toward the posterior soft tissue around a fulcrum located in the canine
or premolar position. The prosthesis is soft tissue–supported with secondary
retention from the implants. Ideal support on the primary stress-bearing
area of the maxilla must be utilized (horizontal palate).
Advantages.
The benefits of a RP-5 maxillary overdenture are retention and stability from
the implants. Posterior support is obtained from the soft tissue. The other
primary benefit is the maintenance of the premaxillary bone because of
implant force stimulation to the bone. There is also a reduced fee compared
with a RP-4 prosthesis because bilateral sinus grafts are not required for
molar implants, and the number of implants may be as few as four.
Option 2: Maxillary RP-4 Implant Overdenture
Indications.
The second option for a maxillary IOD is a RP-4 prosthesis with 6 to 10
implants that is rigid during function (Fig. 15.44). This option is the preferred
IOD design because it maintains greater bone volume and provides
improved security and confidence to the patient compared with a denture or
RP-5 prosthesis. The loss of bone width in the premaxilla does not require a
bone graft or hydroxyapatite graft for lip support as for a fixed prosthesis.
However, the cost of treatment parallels that of a fixed hybrid prosthesis. The
RP-4 restoration most often still requires sinus grafts and posterior implants.
In some instances, extensive bone grafting may be indicated for the entire
premaxilla for a fixed prosthesis. The RP-4 restoration may be required for
facial esthetics if augmentation procedures are not performed.
FIG 15.44 A maxillary overdenture bar and RP-4 prosthesis is supported by 7 to 10

implants and is rigid during function. (From Misch CE: Dental implant prosthetics, ed 2, St
Unfortunately, many practitioners believe that the RP-4 overdenture

requires fewer implants and less attention to the biomechanics of occlusal
load compared with a fixed restoration just because the restoration is
removable. This is a primary cause of implant failure in maxillary IODs.
When the IOD is completely supported, retained, and stabilized by the
implant support, it acts as a fixed prosthesis. The number of implants is
similar to that of a fixed prosthesis.
Implant Number/Positions.
Treatment planning for RP-4 maxillary overdentures is very similar to fixed
prosthesis because the IOD is fixed during function. Two of the key implant
positions for the RP-4 maxillary IOD are in the bilateral canines and distal
half of the first molar positions. These positions usually require sinus grafts
in the molar position. Additional posterior implants are located bilaterally in
the premolar position, preferably the second premolar site (greater force
than first premolar). In addition, at least one anterior implant between the
canines often is required. The anterior implant often may be placed in the
incisive canal when inadequate bone width is present (Fig. 15.45). Six
implants is the minimum suggested number for a RP-4 treatment option, and
seven implants are used more often. When force factors are greater, the next
most important sites are the second molar positions (bilaterally) to increase
the A-P spread and improve the biomechanics of the system. A 10th implant
may be placed in the premaxilla for a tapered arch form.
FIG 15.45 Incisive canal implant.

Prosthesis Design.
The 6 to 10 implants are splinted together around the arch with a rigid bar
(five-sided arch in treatment planning). Four or more attachments are usually
positioned around the arch. This provides a retentive, stable overdenture
prosthesis. Usually palatal coverage is maintained with a horseshoe design.
This helps prevent speech problems and allows for greater patient comfort.
Occlusal Scheme.
The occlusal scheme for this RP-4 restoration is similar to that for a fixed
prosthesis: centric occlusion around the arch and only anterior contact
during mandibular excursions (unless opposing a mandibular complete
denture). The maxillary overdenture should be removed during sleep to
prevent nocturnal parafunction. If the patient wears maxillary and
mandibular overdentures, only the mandibular restoration needs to be
removed. However, the maxillary overdenture should be removed for a short
interval during the day.
Attachments.
The position and type of overdenture attachments may render an
overdenture rigid during function even in the absence of distal cantilevers on
the bar. For example, when three anterior implants are splinted together and
a Hader clip is used to retain the prosthesis, if the Hader clips are placed at
angles to the midline, the attachments have limited movement and result in
a rigid overdenture during function.
Advantages.
The main advantage of an RP-4 maxillary prosthesis is the minimal palatal
coverage. Because the prosthesis is horseshoe shaped, patient satisfaction is
much higher, especially if the patient has a gagging habit.
Understanding Maxillary Arch Forms

When evaluating arch forms for implant prostheses, the clinician should
evaluate two distinct forms: the edentulous and dentate. The residual
edentulous bone determines the A-P distance for implant support. The
dentate arch form will determine the arch form for the final prosthesis. Both
arch forms may be described as ovoid, tapering, or square.
Types of Arch Forms
Ovoid.
The ovoid arch form is the most common followed by the square and then
the tapered form. The ovoid arch form has qualities of both tapered and
square arches.
Square.
The square arch form may result from the residual formation of the basal
skeletal bone. However, the presence of a square arch form is more common
in maxillary implant patients as a result of labial bone resorption of the
premaxilla region when anterior teeth are lost earlier than the canine. The
square dental arch form is preferred when canine and posterior implants are
used to support anterior teeth in either arch.
Tapering.
The tapering arch form is often found in skeletal class II patients as a result
of parafunctional habits during growth and development. It is not
uncommon to find different arch forms in the upper and the lower arches.
The tapering residual ridge arch form is favorable for anterior implants
supporting posterior cantilevers.
Importance of Arch Form

The dentate and edentulous arch forms are not necessarily related, and the
worst situation in the maxilla corresponds to a square residual arch form that
supports a tapered dental restoration. The prosthesis cantilever off the
anterior available bone is greatest in this combination (Fig. 15.46).
FIG 15.46 The dental arch form may be different than the arch form of the residual
arch. A tapered dentate arch form on a square residual bone form is the worst
combination because the anterior teeth are cantilevered from the implant
abutments. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The arch form is a critical element when anterior implants are splinted
together and support a posterior cantilever restoration. For these conditions,
a square arch form provides a poorer prognosis than a tapered arch form.
The A-P distance or A-P spread is the distance from the center of the most
anterior implant to a line joining the distal aspect of the two most distal
implants.60 It provides an indication as to the amount of cantilever that can
be reasonably planned. When five anterior implants in the mandible are
used for prosthesis support, the cantilevered posterior section of the
restoration should not exceed two times the A-P spread when all patient
force and stress factors are low and bone density is favorable. The actual
length of the cantilever depends not only on implant position but also on
other stress factors, including parafunction, crown height, implant width,
and number.
The predominant factors to determine the cantilever length are related to
stress, not only the A-P distance. For example, the distance between two
implants supporting a cantilever (C) forms a class I lever. For implants 10
mm apart and a 10-mm posterior cantilever, the following forces are applied:
a 25-lb force on cantilever C results in a 25-lb force on the most anterior
implant from the cantilever (A) and 50 lb for the nearest implant to the
cantilever (B), which acts as a fulcrum. An interimplant distance of 5 mm
with the same 10-mm cantilever and a 25-lb force applied on C results in a 50-
lb force on A and a 75-lb force on B. The distance between implants
significantly increases the forces to both implants. But in the first example, if
a patient with parafunction bites with a 250-lb force on C, the force on
implant A is 250 lb, and the force on implant B is 500 lb. In other words,
parafunction is much more meaningful in terms of force than the
interimplant distance (A-P distance) when designing a cantilever. A-P
distance is only one stress factor to evaluate for cantilever length.
Parafunction, crown height, masticatory dynamics, arch position, opposing
arch, direction of force, bone density, implant number, implant width,
implant design, and A-P distance are all factors to be considered. When the
force factors are low and the area factors (implant number, width, and
design) are high, the cantilever length may be as much as two times the A-P
distance in good-quality bone.
As mentioned previously, anterior endosteal implants often may not be
inserted in their ideal location in the maxilla as a result of labial plate
resorption and inadequate bone width at the implant site. This not only
requires implant placement more palatally compared with the original
natural teeth, but it may also negate the lateral and central positions and
require the use of the canine regions in more advanced atrophic arches. The
resulting restoration is a fixed, anteriorly cantilevered prosthesis to restore
the original arch form. Under these conditions, greater stresses are placed on
the dentate-tapered arch forms compared with dentate square arch forms, all
other factors being identical.60
The maxillary anterior cantilever to replace teeth in a dentate-tapered arch
form requires the support of additional implants of greater width and
number to counteract the increase in lateral load and moment force. For
example, not only are the canine implants necessary, but two more additional
anterior implants are also suggested even if bone grafting is required before
their placement. In addition, additional posterior implants in the first to
second molar region splinted to the most anterior implants are highly
suggested. If a maxillary tapered arch form requires this treatment approach,
at least eight implants (four on each side) and an increased A-P distance
from molar implants splinted to incisor implants is suggested. In addition,
second molar implants should be splinted to the anterior implants to
increase the A-P distance. In the maxilla the recommended anterior
cantilever dimension is less than for the posterior cantilever in the mandible
because of poor bone density and forces directed outside the arch during
excursions.
Overdenture Attachment Complications

The selection of the overdenture attachment system is often a confusing part
of the prosthetic rehabilitation of the patient. Clinical studies concerning the
attachments are scarce and difficult to evaluate. Usually, attachment selection
is based on the clinician's personal preference, laboratory preference, expert
opinion, or empirical information. An ideal overdenture attachment should
have basic features to minimize and decrease clinical complications. An
overdenture attachment main goal is to retain the prosthesis and allow
movement during function or removal of the prosthesis. As a consequence of
forces applied to the prosthesis, all overdenture attachments wear and
become less retentive over time. The clinician should understand the positive
and negative inherent factors associated with attachments.
Ideal Attachment
Ease of Replacement.
Ideally, the attachment selected should allow ease of replacement. A chair
side, cold-cure acrylic procedure should not have to be used every time the
attachment needs replaced. This leads to nonproductive time for the clinician
and also places the prosthesis at risk of being altered. Additionally, this will
result in considerable time, risk, and frustration every time the attachment is
changed. To prevent this issue, an attachment should be selected that allows
for easy replacement and long-term use.
Ability to Control Retention.

The ideal overdenture attachment should also offer many options to control
the degree of retention. A mobile or minimally retentive attachment at the
initial delivery ensures improper fit leading to prosthesis movement and
possible screw loosening. Adequate retention should be ascertained prior to
the final insertion of the prosthesis. A gradual increase in retentive capability
may be achieved later by replacing the component within the encapsulator
by a more retentive attachment. Likewise, if more retention is required in the
future, a stiffer element, which is held by the same encapsulator, easily solves
the problem (Fig. 15.47).
FIG 15.47 Control of retention. (A) Locator: various colored inserts with varying
degrees of retention. (B) O-rings: retention varies with the type of material.
Male Attached to Implant/Female in Prosthesis.

Most attachments used in implant dentistry today have the male component
in the oral cavity and the female in the prosthesis. The male can be more
easily cleaned while in the mouth, and the more difficult component (i.e.,
female) may be cleaned with direct vision via access outside of the mouth
(i.e., within the prosthesis). When the female component is part of the
implant or connecting bar, if any plaque or food accumulates within the
component, the overdenture will not seat completely. This will lead to patient
frustration because of occlusal disharmonies, lack of retention, and possible
tissue impingement (Fig. 15.48).
FIG 15.48 Female attachment in prosthesis. When the female attachment is in the
prosthesis, it is easier to clean. When female attachments are placed intraorally,
food impaction is common, which prevents complete seating of the prosthesis.
Adequate Retention for the Prosthesis.

The retention and stability are significant factors that affect the type of
attachment system. For a single unsplinted attachment, 4 N has been
suggested as the minimum retentive force.61 Other studies have shown a
cumulative force of 20 N of retentive force needed for a two-implant
mandibular overdenture.62 When evaluating the retentive capabilities of
attachment systems, the term peak load is used to define the maximum force
that is developed before complete separation of the attachment components
from the implant abutments. When evaluating peak load, various attachment
systems have been classified as: (1) high (e.g., ERA gray), (2) medium (e.g.,
Locator LR white, Spheroflex ball, Hader bar and metal clip, ERA white), (3)
low (e.g., Locator LR pink), and (4) very low (e.g., Shiner magnet, Maxi
magnet, Magnedisc magnet) retention groups.63
Alsabeeha et al showed that Locator attachments white, pink, and blue
connectors have demonstrated higher retentive forces than either a 7.9-mm
prototype ball attachment design or the standard 2.25-mm ball attachment.64
Other studies have shown the attachment with the highest peak load was the
Zest Anchor Advanced Generation (ZAAG) attachment (Zest Dental
Solutions), in comparison to the Nobel Biocare ball, the Zest Anchor, and the
Sterngold ERA (Sterngold Dental, LLC).65 The ZAAG attachment showed
significantly the highest retentive vertical and oblique forces under
dislodging tensile forces applied to the housings in the vertical and oblique
directions.
Ideal Attachment Summary.

In implant dentistry today the two most common attachment systems to use
are the Locator system and the O-ring attachment system. They have the
universal advantage of different retention strengths, utilize metal
encapsulators, are easy to change and replace, and have the male component
in the oral cavity. The Locator and O-ring have been shown to be long lasting
through numerous clinical studies. And lastly, both of these attachments can
be used independently or attached and incorporated into a bar via cast-to or
cemented protocols (Fig. 15.49).
FIG 15.49 Attachment location. (A) Independent attachments. (B) Incorporated into
a bar. (C) The abutment height is dictated on the tissue depth. The attachment
needs to be slightly above the highest area of tissue depth.
Complications of Dental Implant Attachments
Retention Loss Over Time.

The main complication over time with dental implant attachments is the loss
of retention. Depending on the situation, this is highly variable and
dependent on many factors. Retention loss over time studies show the wear-
induced structural changes inherent with every attachment system will
inevitably lead to a reduction or total loss of retention. Mechanical action
alone or a combination of chemical and mechanical actions will induce loss
of material from the surface, which is defined as wear. Wear has been shown
to decrease the attachment's retention, lead to deterioration and
deformation, work hardening, and can also lead to attachment fracture.66
Factors that predispose to loss of retention and wear include the following:
Mastication wear.
The attachment wear from occlusal forces is much different from insertion-
removal cycles. In most overdentures (RP-5), the amount of occlusal load
applied to the attachment is dictated by the resiliency of the tissue. The
amount of mucosa displacement will reduce the denture movement and less
force on the attachment. Studies showing simulated masticated Locator
attachment retention to be reduced by 40% with a nonlinear descending
curve. This correlates with maintenance issues being directly related to
masticatory forces. In this study, only minor changes were found for ball type
attachments.67
Insertion-removal wear.
Mechanical fatigue has been shown to reduce retention on almost all
attachment systems after 15,000 fatigue cycles.62 Studies have shown
approximately 800 cycles are needed to attain relatively stable retention of
overdenture attachments.68 The Locator pink attachment remained the most
retentive after fatigue, compared to the ERA orange and white. However,
researchers concluded that implant parallelism has more impact on
complications that occur than the choice or type of attachments.69 When
directly picking up the attachment, care should be exercised not to place too
much force on the denture (i.e., displacement force). Any installation load
greater than 0 N will have a resultant force acting on the prosthesis/implant.
Other studies have evaluated the force-related issues with the insertion
and removal consequences of attachment systems. Alsabeeha et al submitted
various attachment systems to either axial or paraxial forces in the range of
540 to 10,000 cycles from repeated insertion and removal of the prosthesis.
This would represent 6 months to 9 years of clinical function, on the basis of
three daily overdenture removals and insertions for hygienic purposes. A
common trend toward reduction or total loss in retentive force was found
across the majority of the attachment systems.70 Rutkunas et al concluded
that ball-socket attachments have a gradual and continuous loss of retention
after repeated insertion-removal cycles. This loss can be abrupt after
approximately 500 cycles and may reach 80% of the initial value after 2000
cycles.68
Types of Attachment Systems

O-Ring Attachment System
The O-ring attachment system is composed of an elastic O-ring, a metal
encapsulator, and a metal post. It may be used as an independent unit or part
of a connecting bar that joins the implants together (Fig. 15.50). O-rings are
doughnut-shaped, synthetic polymer gaskets that possess the ability to bend
with resistance and then return to their approximate original shape. In part,
this feature results from a three-dimensional network of flexible elastomeric
chains. The O-ring attaches to a post with a groove or undercut area within
the O-ring. The O-ring is compressed radially between two mating surfaces
consisting of a post and a metal encapsulator into which the O-ring is
installed. The O-ring has been used primarily in removable prosthetics as a
retentive device and has seen a resurgence in popularity with overdentures
supported by endosteal implants and is widely available in a variety of
implant systems.71 The advantages of O-rings are ease in changing the
attachment, the wide range of movement, low cost, different degrees of
retention, and possible elimination of the time and cost of a superstructure
for the prosthesis.
FIG 15.50 An O-ring attachment has a resilient O-ring gasket (top right), a metal
encapsulator (top left), and a male post (middle). (From Misch CE: Dental implant
Range of Motion.
All O-ring applications are categorized in terms of relative motion. In
situations that require few or no moving parts or movement, the O-ring is
classified as static (e.g., gasket or washer). In situations involving
reciprocation, rotation, or oscillating motion relative to the O-ring, it is
classified as dynamic. The dynamic movement of the O-ring allows it to be
one of the most resilient or mobile types of attachments.
O-rings may allow motion in six different directions. However, if a
superstructure connects the implants, the range of motion decreases. If the
O-ring is placed on a complete arch bar in four different sites and the
prosthesis rests on the superstructure bar, the restoration may have PM of 0
(PM-0). Two O-rings placed on a bar perpendicular to the midline may have
two to six directions of PM, depending on the resilient depression of the O-
rings, whether a spacer is over the post head, or space is over the connecting
bar.
Encapsulator.
A metal or plastic encapsulator permits the easy replacement of the O-ring
after wearing or damage. This eliminates the need for chairside cold curing
of a new attachment in place. Virtually every O-ring encapsulator has an
undercut region that houses the O-ring, called the internal cavity. The O-ring
volume must be larger than the internal cavity. As a result, the O-ring is
compressed into position in the encapsulator and prevents the ring from
moving or rolling while in place, which prematurely damages and wears the
ring. The overall size of the encapsulator is larger than the O-ring and should
be placed with the O-ring on the O-ring post during fabrication of the
prosthesis to ensure adequate space (>2 mm of acrylic) (Fig. 15.51).
FIG 15.51 The metal encapsulator of the O-ring should fit within the contours of the
implant overdenture, so at least 2 mm of acrylic exists around this structure. (From
O-Ring Post.
The O-ring post usually is made of machined titanium alloy when used as an
independent attachment or a Delrin post that is waxed and cast in metal alloy
along with the connecting superstructure bar joining root forms. The three
components of the post are a head, neck, and body. The head is wider than
the neck, and the O-ring is compressed over the head during insertion.
Under the head of the post there is an undercut region called the neck or
groove that the ring engages after it stretches over the head. The body of the
post is connected to the implant abutment or superstructure bar.
Complication.
Overpolishing of a cast post head or neck region may unwittingly cause a
decrease in retention of the system. When the attachment is fabricated and
cast within the bar system, care should be exercised to not overpolish when
finishing.
O-Ring Size.
The inside surface of the O-ring slides over the post neck or groove. The
internal diameter (hole diameter) of the O-ring must be smaller than the post
neck and fit snugly in the groove diameter. The O-ring inside diameter will
be stretched to 1% to 2% (not to exceed 5%) when in place against the post
neck.72 If not, the O-ring will roll or wobble over the post and increase wear
and tear of the attachment. O-rings and posts may come in a variety of
diameters depending on the space available within the volume of the
prosthesis. The larger the diameter of the O-ring system, the easier it is to
place the O-ring within the encapsulator. Troubleshooting retention
complications is also easier, and greater retention is possible with a larger-
diameter system. Typically, three sizes of O-rings are used in implant
prostheses (small, medium, and large) (Fig. 15.52).
FIG 15.52 O-ring size identification. Red line: the height of contour of the ball
attachment. Usually the ring selection will be approximately 0.5 mm larger than the
measurement. Blue line: the diameter of the retentive zone, which correlates to the
size of the O-Ring. (Courtesy Preat Corporation, Grover Beach, CA.)
Complication.
The manufacturer's size protocol should be adhered to for all O-ring systems.
Too large of an O-ring size will result in compromised retention and too
small of an O-ring will prevent full seating of the prosthesis. Most O-rings
are specifically made (e.g., size, retention) for the specific implant and
abutment system.
O-Ring Height.
The O-ring attachment system needs a minimum of 5 mm or more height,
which is the greatest of any attachments for overdentures. In addition, a
space of 1 to 2 mm above the O-ring post is suggested to ensure the ring
seats completely over the head of the post. This space also prevents the post
from penetrating or fracturing the prosthesis over the head and allows apical
movement for a partial soft tissue–supported removable prosthesis (RP-5).
Complications.
The height requirements of the O-ring attachment present several
disadvantages. A decreased CHS, which is often present in overdenture cases,
may require a lower-profile attachment. A denture tooth, O-ring, post, bar,
and hygiene clearance often require at least 12 to 15 mm of CHS to allow
sufficient room for the acrylic base of the restoration to resist fracture. In
addition, the higher the freedom of movement of a stress-relief attachment
(required for all partial soft tissue–supported prostheses), the greater the
moment of force on the attachment. Because the rotation point of O-rings is
at the neck of the O-ring post, the point of rotation is not as high as first
perceived. However, if the prosthesis is made incorrectly and places lateral
forces on the post, the lever arm of the post height can increase the force to
the bar, screws, implants, and bone.
O-Ring Hardness.
O-ring hardness can be measured with a durometer, which measures surface
resistance to the penetration of an indentation point. The resultant numerical
rating of hardness ranges from 0 to 100. The softest O-rings will range from
30 to 40, and the hardest are 80 to 90. Color is not indicative of hardness as
this is dependent on the manufacturer.72
O-Ring Materials.
The US Food and Drug Administration has issued guidelines for O-rings
used in medicine. The elastomeric materials meeting these requirements
include silicone, nitrile, fluorocarbon, and ethylene-propylene. The materials
are available from a variety of industrial manufacturers.72
Complications.
The clinician should be aware of the type of O-ring material used. Silicone is
composed of a group of elastomers made from silicone, oxygen, hydrogen,
and carbon. Silicones are known for their retention of flexibility and low-
compression set characteristics. Silicones are also fungus resistant, odorless,
tasteless, and nontoxic. However, poor tensile and tear strength, low abrasion
resistance, and high friction characteristics preclude silicones from effective
O-ring use in most implant dynamic situations. In addition, silicone is not
compatible with petroleum-based products such as petroleum jelly.73
Ethylene-propylene is a copolymer of ethylene and propylene, sometimes
combined with a third comonomer. Similar to silicone, this elastomer
performs poorly when exposed to petroleum-based products.
Nitrile is one of the more widely used elastomers for implant O-ring use.
Nitrile combines excellent resistance to petroleum-based products, silicone
greases, water, and alcohols, with a good balance of desirable properties such
as high tensile strength and high abrasion resistance. Fluorocarbon also
combines excellent resistance to petroleum products with outstanding
chemical resistance. Fluorocarbon-based compounds approach the ideal for a
universal O-ring material.74
Surface treatment of O-rings with lubricants helps protect them from
abrasion, pinching, and cutting during performance. External lubrication also
helps seat the O-rings easily into the metal encapsulator with minimal
twisting or damage and maximal assembly speed. In all cases requiring O-
ring lubrication, a lubricant should be selected that is compatible with the O-
ring compound and the oral environment. Nitrile O-rings may be lubricated
with petroleum jelly or petroleum-based ointments. Petroleum-based
products will damage silicone O-rings, so a water-based lubricant (e.g., KY-
Jelly [Johnson & Johnson]) that has a glycerin component should be used.
O-Ring Failure.
O-rings typically fail in their application because of the combined adverse
effects of stress and environmental elements (i.e., friction, heat, and
swelling).75 Such environmental factors may be compounded by incorrect O-
ring size, improper laboratory technique, installation damage during final
component assembly, and failure to properly maintain or lubricate the O-
ring.
Extrusion and nibbling.

Extrusion and nibbling occur with forced extension of part of the O-ring into
the clearance gap of the metal encapsulator. The problem is identified by O-
ring diameter enlargement or many small bites (nibbles) taken from the
internal diameter of the O-ring. This results when O-ring materials are too
soft, oral fluids degrade the O-ring, or the O-ring is too large for the metal
encapsulator. The clinical solution for this problem is to use a harder O-ring
material or install a properly sized O-ring.
Spiral failure.
A spiral failure results when certain segments of the O-ring slide while other
segments simultaneously roll (Fig. 15.53). At a single point on its periphery,
the O-ring gets caught on an eccentric component or against the metal
encapsulator wall, causing twisting, spiraling, or surface cuts. Problem
sources include an uneven surface or finish of the post by the laboratory,
inadequate lubrication, or excessive O-ring material softness. The suggested
solutions are evaluation of the post to ensure that it is not out of round,
increasing O-ring hardness, and making sure the patient uses a lubricant
daily.
FIG 15.53 (A) Spiral failure of an O-ring exhibits a series of deep spiral cuts on the
surface. (B) Clinical image of O-ring failure. (From Misch CE: Dental implant prosthetics, ed
Abrasion.
Abrasion may occur in dynamic O-rings involved in reciprocating, oscillating,
or rotary motion. This failure pattern can be identified by a flattened, worn
surface on the inner diameter of a cross section of the O-ring. The most
common cause is bruxism by the patient or lifting and seating of the
overdenture as a nervous habit. Another source of the problem includes a
rough metal surface on the post (acting as an abrasive). The suggested
recommendations are to use metal finishes; change to a more abrasion-
resistant O-ring material (nitrile); or eliminate abrasive contamination, which
may be found in the diet (e.g., the abrasive particles found in chewing
tobacco).76
Compression set.
Compression set failure produces flat surfaces on both sides of the cross
section of the O-ring (Fig. 15.54). The most common cause of this type of
failure is parafunctional clenching on the prosthesis. Other problem sources
include selection of an elastomer with poor compression set properties or
excessive “squeezing” or biting of the prosthesis into place to seat the
restoration. The suggested solution is to make sure the prosthesis is removed
at night or to reduce the O-ring hardness, which reduces the compression
required to insert the prosthesis.
FIG 15.54 (A) Compression set failure is demonstrated as flat surfaces on the top
and bottom of the O-ring. (B) Clinical image of O-ring failure. (From Misch CE: Dental
Installation damage.
Installation damage is one of the most common types of O-ring
complications. This failure mode is marked by short cuts, notches, or a
skinned or peripherally peeled surface. The problem sources include sharp
edges on the encapsulator from poor laboratory technique, sharp edges on
the O-ring post head, too large an O-ring for the encapsulator, twisting or
pinching of the O-ring into the encapsulator, attempting to insert the O-ring
with a sharp instrument, too small an O-ring for the post, or lack of O-ring
lubrication during installation. The suggested solutions include installing
properly sized O-rings, using a blunted insertion instrument, and using
lubrication during assembly (Fig. 15.55).
FIG 15.55 Ideal replacement of an O-Ring. (A) Old o-ring is removed with explorer,
(B) Water soluble lubricant is added to metal encapsulator, (C) O-ring is squeezed
and easily slips into encapsulator.
Locator Attachment
The Locator attachment system (Zest Anchors) has been available in implant
dentistry since 2000. The Locator attachment has become one of the most
popular attachments in implant dentistry today. The advantages of the
Locator include the ease of insertion and removal, dual retention capabilities,
low vertical profile, ability to pivot, toleration of implant divergence, and
increased resiliency. Although this attachment system is associated with a
similar incidence of prosthodontic complications as other attachment
systems, these problems seem to be simpler and easier to resolve. Studies
have shown the most common issues that dentists report concerning the
maintenance and repair of Locator attachments were inadequate
remuneration, lack of training, experience, and equipment.77 The inherent
advantages of the Locator attachment include:
Self-Alignment.
One of the most common complications of Locator implant attachments
involves distortion of the overdenture attachments from malalignment of the
male and female components. Many patients prefer to “bite” the overdenture
into place, causing damage to the attachments. To avoid this complication,
the locator was designed to be self-aligning. This is accomplished by the
rounded contours of the female attachment (in the mouth) and the nylon
male (in the overdenture). The skirt of the male attachment is guided into
position, similar to guide planes on a partial denture.
Dual Retention.
Another important quality of the Locator attachment is the “dual retention”
of the attachment. The nylon male attachment engages both the inside and
outside of the female attachment. The retentive surface area is doubled with
respect to other types of attachments. This feature allows for greater
longevity of retention (Fig. 15.56).
FIG 15.56 (A) Dual retention of the Locator attachment. (B) Self-aligning advantage
of Locator.
Attachment Divergence.
A common complication of overdenture attachments is a divergence between
implants that prevent the prosthesis from seating completely. With the
Locator attachment, the nylon male insert is allowed to pivot within the
metal housing. The pivotal advantage allows the standard male to
accommodate 10 degrees each, for a total of 20 degrees between implants. In
cases with extended divergence, there are extended range male attachments
that allow for divergence of 20 degrees each or a total of 40 degrees. Studies
have shown with this tolerance for divergence, retention may reach up to
60,000 insertion/removals.78
Resilient Function.
The locator is one of the most resilient attachments used in implant dentistry.
The resiliency allows movement between the prosthesis and the implant,
allowing and transferring stress from the implants to the tissue bearing
areas. The male remains in static contact with the female socket while the
metal housing has a full range of rotational movement over the male.
Use in Cases With Lack of Interocclusal Space.

A common problem that leads to prosthesis fracture is the lack of
interocclusal space. If insufficient space is available, increased complications
will result. This occurs because of inadequate acrylic thickness,
overcontoured prosthesis, and increased susceptibility to breakage. The
Locator metal housing with nylon male inset requires approximately 2.27 mm
above the tissue, and the female abutment needs to extend only 1.5 mm
above the tissue for the male element to seat without impinging on the
tissue. With external hex implants a minimum of 3.2 mm is required; 2.5 mm
is required for internal hex implants. Locator female abutments are also
available in 0 mm connections for flat-top connection implants.79 With a total
attachment height of only 3.17 mm (male plus 1-mm collar abutment) for an
externally hexed implant, the Locator attachment has been shown to save a
minimum of 1.68 mm to 3.05 mm of interocclusal space compared to other
implant overdenture attachments (Fig. 15.57).
FIG 15.57 Locator impression pick-up technique. (A) Remove the healing
abutments and confirm that the prosthetic platforms are free of any bone debris or
soft tissue. (B) Place Locator abutment onto each implant using the Locator hand
driver with a Locator abutment holder. Hand tighten. (C) Each Locator abutment is
torqued to 30 Ncm using a calibrated torque wrench and a Locator square drive tool.
(D) Impression coping snapped onto each Locator abutment. (E) Impression is
made to pick up the impression copings and to record all soft tissue contours for the
new denture fabrication. The impression copings will remain in the impression when
it is removed. (F) Denture base is relieved, must have verification that abutment has
no contact with denture base. (G) The Locator female analogs are placed into the
impression. (H) Final master cast.
Available in Multiple Abutment Heights.

The abutment should be selected that results in a minimum of 1.5 mm above
the tissue. If less height is available, the male attachment will not be able to
seat completely. The clinician should measure the deepest portion of the
implant to tissue crest in determining the height selection. The Locator
attachment is available for use with most implant systems. The abutments
are available in numerous tissue heights ranging from 0 to 6 mm in 1-mm
increments. Ideally, 1.5 mm of the abutment should be above the tissue. The
tissue cuff height measurement must be taken at each implant site using the
deepest side of the tissue for measuring from the apical shoulder of the
implant to the crest of the tissue. The working portion of the Locator
abutment is at or slightly above the gingival level.
Locator Core Tool.

When replacing Locator attachments, care should be exercised to use the
Locator tool. Use of any other type of placement tool will lead to damage to
the attachments. The Locator Core Tool may be utilized for three different
purposes:
1. Insertion the female abutments: The abutment retention sleeve is used to

secure the female abutment during insertion. The sleeve is placed over the
end of the abutment driver and the Locator female is then placed through
the sleeve.
2. Removal of processing males (used during the retrofitting step to lock the
position of the metal housing inside a denture base): To remove processing
or worn nylon males, the male removal tool is slightly unscrewed from the
middle section of the male removal tool.
3. Removal of worn males and insertion of new male attachments: The

inverted conical tip is inserted into the worn male and pulled straight back
for removal. The male removal tool is then screwed completely into the
middle section to protrude the plunger and kick off the male insert. A new
nylon male is placed on the middle male seating section and inserted into the
metal housing (Fig. 15.58).79
FIG 15.58 Chairside pick-up of locator attachment. (A) Locator abutment placed
onto each implant using the Locator hand driver with a Locator abutment holder.
Hand tighten. (B) A white block-out spacer is placed over the head of each Locator
abutment. This blocks out the area immediately surrounding the abutment allowing
the full resilient function of the pivoting metal denture cap over the Locator male. A
Locator cap with a black processing insert is placed on each Locator abutment. (C)
Denture base is hollowed out to accommodate the protruding Locator males. There
must be no contact between the denture and the titanium caps. If the denture rests
on the metal cap, excess pressure on the implant will result and the prosthesis will
be ill-fitting. Lingual vent holes should be made for excess acrylic to escape. (D) A
chairside light cure acrylic resin or a permanent self-curing acrylic is used to bond
the denture caps to the denture. A small amount of a material of choice is placed into
the recessed area of the denture and around the denture caps. Seat the prosthesis,
verify occlusion. (E) After the acrylic has cured, the denture is removed and the
white spacer is discarded. Voids are filled with acrylic and the excess is removed.
(F) The black processing male is removed from the denture cap with the use of the
Locator male removal tool. (G) The Locator core tool is used to firmly push a Locator
male retention insert into the denture cap. The retention insert must seat securely
into place, level with the rim of the cap. (H) Removal of the prosthesis, verify
occlusion, and polish.
Hader Bar and Clip

Helmut Hader, a master dental technician, developed the Hader bar and
rider system in the late 1960s, and this system was unchanged for almost 30
years. English, Donnel, and Staubli modified the system in 1992 to form the
Hader EDS system.80 The Hader bar system involves a semiprecision bar
attachment that provides hinge movement. The function of the bar is based
on the principle of mechanical snap-retention technology (Fig. 15.59).
FIG 15.59 (A) Hader Bar. RP-4 bar with posterior cantilever Hader bars. (B) Hader
clips. (B, Courtesy Preat Corporation, Grover Beach, CA.)
Complications
Bar position.
A common complication arises when two implants are positioned in the A
and E positions and connected with a bar. Because the implants are placed
farther distally than the ideal B and D position, the bar will need to be placed
lingually and possibly would interfere in the tongue space. This may create
problems with speech and possible fracture of the prosthesis. If implants are
placed in a diagonal position (A → D or B→ E), friction-free movement will
not be possible, which will result in excessive pressure and force on the
implants. Ideally, the bar should be perpendicular to the line that bisects the
angle formed by the most distal implants.
Clip assembly.
The ideal length for a clip bar is 20–24 mm to accommodate two clips and
housings. If less space is available, inadequate retention will result. The clips
have three different retention strengths and a 20-degree clip rotation, which
greatly improves the flexibility of the system for a range of patient needs or
desires. In addition, a gold-plated stainless steel housing maintains the clip,
which reduces the need to cold cure new attachments in place. This is a
significant advantage because the gold plating minimizes the color bleeding
through the prosthesis. The Hader bar and clip is a type 2 attachment and
may be used for PM-0 or PM-2 treatment plans.
The standard or EDS Hader bar has a round superior aspect and an apron
toward the tissue below. The apron acts as a stiffener to improve the strength
of the bar and limit its flexibility. Round bar designs flex in relation to x4 (x to
the 4th power). In other words, a bar twice as long flexes 2 × 2 × 2 × 2 = 16
times more. Other bar shapes flex to x3 or 2 × 2 × 2 = 8 times more. This is a
considerable improvement. The height of the apron or stiffener is related to
the amount of clearance between the bar and gingiva.
There are three color-coded clips/riders with three retentive strengths. In
order, from lightest to strongest, they are white, yellow, and red. The use of
metal housings with Hader plastic clips/riders is recommended. In addition
to plastic clips/riders, the adjustable gold alloy clips/riders are an available
option.
Design/movement.
Because of poor design, Hader clips may wear prematurely. The clip rotation
compensates for the resilience of the posterior soft tissue, which is usually
0.5 to 1 mm in the mandible. Highly mobile tissue, more often seen in the
maxilla, requires a greater range of clip movement. For a bar and clip to
rotate, several important design features must be considered. For example,
the bar should be aligned perpendicular to a line bisecting the angle between
the posterior arches and should be parallel to the plane of occlusion.81
Interocclusal space.
Whereas the EDS bar is only 3 mm high, the original was 8.3 mm in height.
The total height of the Hader bar and clip assembly may be as low as 4 mm
rather than the 5 to 7 mm required for an O-ring system. A greater moment
of force is placed on the bar during rotation, and clearance is required under
the denture base. However, the increase in CHS above the attachment may
make the prosthesis less stable to lateral loads for PM-2–type prostheses (Fig.
15.60).
FIG 15.60 Chairside Hader clip instructions. (A) Intraorally, place blockout
compound and the green processing spacers. (B) Relieve denture and prepare a
lingual escape vent. (C) Place self-cure acrylic in the prosthesis (only about 1/4 of
the relief area should be filled) and on the housings. Seat the prosthesis. Do NOT
have the patient bite the prosthesis into place as this may displace tissue and distort
attachment alignment. (D) Prosthesis with cured green processing spacers. (E)
Remove green spacers and place clip into metal housing. (F) Note: right side has
room for clip to flex (green spacer used) and left side does not allow clip to flex,
which will prevent proper seating (no green space used).
Dolder Bar
The Dolder bar is a prefabricated precision bar attachment developed by Dr
Eugen Dolder in Switzerland. This bar system comes in two different forms:
(1) rigid: a U-shaped bar with parallel walls; and (2) resilient: egg-shaped
form in cross section, which provides vertical and hinge resiliency.
The Dolder bar and its metal sleeve are made of gold alloy (Elitor) and is
adjustable so the clinician can control the amount of retention provided by
the bar. The Dolder bar is usually soldered to the abutments, and the sleeve
should be secured in the denture base with self-cure acrylic.
The Dolder bar is usually used in patients who have increased crown
height space and when a minimum resiliency and maximum retention is
indicated. There are various sizes ranging in height from 2.3 to 3.0 mm and in
width from 1.6 to 2.2 mm (Fig. 15.61).
FIG 15.61 Dolder bar. Multiple Dolder bars turning prosthesis into a PM-0.
Complications.
The complications associated with a dolderbar/clip are similar to the Hader
bar/clip.
Miscellaneous Removable Complications
Bar Try-in Resulting in Pain
In certain clinical situations, when trying in the bar, the patient may
experience pain. The pain may originate from many different areas (Fig.
15.62).
FIG 15.62 Bar try-in may cause pain upon insertion.
Etiology
Nonpassive Prosthesis.
Nonpassive prosthesis (i.e., ill-fitting) can be due to poor impression
technique, laboratory error, or milling or casting discrepancy.
Incorrect Placement.
Incorrect insertion placement can occur, especially when placing the bar
where there is deep sulcular tissue present. This will result in the bar not
being able to be seated fully.
Loose Abutment.
If the abutment is loose or not fully seated, trying-in the bar may result in
pain.
Poor Bone-Implant Interface.

Although there is no innervation to the implant, if the implant is failing, pain
may result from the infected or inflamed fibrous tissue interface.
Impingement on Tissue.
Trying-in a bar with tissue collapse (i.e., soft tissue impeding the seating) will
result in pain from the tissue (Fig. 15.63).
FIG 15.63 Bar insertion. Screws should be initially inserted the length of the
screw in the following order: # 1, center; # 2 and # 3, terminal abutments; # 4 and #
5, in between the center and terminal abutments.
Prevention
Always tighten abutments prior to try-in, making sure no tissue collapse is
present that would impede placement.
The bar should be tried-in in the following sequence:
1. Place bar over abutments or implant bodies and evaluate for stability
2. With insertion driver, hand tighten center screw ( screw length)
3. Hand tighten terminal screws ( screw length)

4. Place and hand tighten the remainder of screws ( screw length)
5. Evaluate margins between bar/abutment
6. All screws should then be sequentially tightened and torqued to

manufacturer's recommendations (Fig. 15.64)
FIG 15.64 The bar casting should always be evaluated for irregularities.
Note: If there is any rocking present or open margins, the bar is nonpassive
and should be sectioned /soldered or redone.
Treatment
Nonpassive Bar.
Fabricate new bar or solder (e.g., bar is sectioned, all screws fixated, luted
together with GC Pattern Resin or impression plaster, pick-up impression).
Incorrect Placement.
Reinsert with ideal path of insertion.
Loose Abutment.
Tighten abutments prior to bar try-in; verify with radiographs to ensure
complete seating.
Poor Bone-Implant Interface.

Evaluate implants for possible failure (i.e., radiographic evaluation).
Impingement on Tissue.
Remove tissue with tissue punch bur.
Gingival Inflammation Around Bar

When a bar is fabricated and placed too close to the tissue, gingival
hyperplasia may result. This will lead to a chronic inflammatory complication
that may be painful and result in bleeding with possible bone loss (Fig.
15.65).
FIG 15.65 Hyperplastic tissue. Excessive tissue growth due to lack of space
between bar and tissue.
Etiology
Ideally, there should exist 1 to 2 mm or more of space between the bar and
the tissue surface. This will allow for adequate space for hygiene. Less than 1
to 2 mm of space results in plaque and calculus accumulation and will
complicate oral hygiene maintenance. If the bar is fabricated to be in direct
contact with the tissue, compression of the mucosa will initiate a hyperplastic
response.
Prevention
To prevent this complication, a minimum of 1 to 2 mm is needed between the
bar and soft tissue. This will allow for self-cleansing of the area along with
decreasing the possibility of tissue inflammation and discomfort.
The ideal spatial relationship of the bar should be over the crest of the
ridge. If the bar is positioned facial, this will result in possible prosthesis
fracture. Bulk acrylic (2 mm) is required for minimal strength. Additionally, if
the implants are positioned too far labial, there will be lack of attached
tissue, which may result in chronic tissue soreness. A lingual positioned
prosthesis will result in interference with the tongue space leading to speech
and mastication complications.
Treatment
The hyperplastic tissue should be removed with a scalpel (gingivectomy) or
laser. Care should be exercised to not use an electrosurgery unit because this
will result in sparking and resultant hard and soft tissue damage.
Additionally, iatrogenic damage of the implant titanium surface should be
avoided because it could harbor plaque and enhance gingival tissue
inflammation.
Prosthesis With Lack of Soft Tissue Support for RP-

5
The clinician must understand the inherent differences between a RP-4 and
an RP-5. Because the RP-5 is soft tissue–supported (buccal shelf), it is
mandatory the prosthesis have adequate flange support, mainly in the
primary stress bearing area (maxilla: horizontal palate; mandible: buccal
shelf). If the primary stress-bearing area is not utilized, the prosthesis will be
loaded as an RP-4, completely soft tissue–supported (Fig. 15.66).
FIG 15.66 RP-5 lack of tissue support. No buccal shelf support increases
movement and rocking of the prosthesis.
Etiology
If extension is not utilized in the prosthesis to encompass the primary stress-
bearing areas, the implants will be overloaded. A common error is an RP-5
mandibular treatment plan (two or three implants) that has insufficient soft
tissue support. This will result in overstressing the implants, leading to
increased morbidity and/or bone loss.
Prevention
Maxillary.
For RP-5 prostheses the horizontal palate should have ideal primary stress-
bearing coverage. An RP-5 must be a full-coverage prosthesis (no horseshoe
design) (Fig. 15.67). A RP-4 (i.e., more implants) would be indicated if a
horseshoe palate is required.
FIG 15.67 Maxillary RP-5 should always have full palatal support.
Mandibular.
For mandibular RP-5 prostheses, the buccal shelf should have adequate
coverage because this is the primary stress-bearing area. The buccal shelf is a
flat area in the mandible bounded by the crest of the ridge (medially),
external oblique ridge (laterally), and retromolar pad (distally; Fig. 15.68).
This area has a thick submucosa and lies perpendicular to the occlusal plane.
FIG 15.68 Mandibular RP-5 should have peripheral extensions similar to a

complete denture.
Denture Teeth Fractures/Debonding
With overdentures, if insufficient space exists, the prosthesis is more prone
to fracture. Denture or composite teeth may “pop-off ” for a number or
reasons (i.e., most common is the lack of sufficient acrylic). Repairing a
fracture or adding a denture tooth is often a time-consuming and difficult
procedure.
Etiology
When insufficient space is available for acrylic (<2 mm), this will result in
denture base fracture or teeth debonding. It is common for laboratory
technicians to hollow out denture teeth to gain additional space. However,
this results in the possibility of the denture teeth fracturing or debonding
from the prosthesis. Denture teeth may become debonded from lack of
mechanical retention (Fig. 15.69).
FIG 15.69 Denture teeth debonding. When there is a lack of acrylic, denture teeth
may fracture or become unbounded from prosthesis.
Prevention
Bulk of Acrylic.
Acrylic is always stronger in bulk. A minimum of 2 mm of acrylic should be
maintained. In some situations a different attachment system may need to be
removed. Approximately 15 mm of space is needed for an implant bar
overdenture with Hader bar or O-Rings.
Verify Occlusion.
The occlusion should always be verified to maintain an even distribution of
masticatory force. Any prematurities should be eliminated and frequent
recall examinations should be part of the postoperative care.
Increase Mechanical Retention.

Usually, it is difficult to add mechanical retention into a denture tooth as this
will lead to stress fractures. Diatoric retention may be utilized with PERMA
RET system, which involves placing a metal wire into the denture tooth for
mechanical retention (Fig. 15.70).
FIG 15.70 Mechanical retention for denture teeth include the use of pins placed into
the lingual aspect of the teeth. (Courtesy Preat Corporation, Grover Beach, CA.)
Overdenture Fractures
A significant and often embarrassing complication that may occur is the
fracture of an overdenture base. This often will result in loss of confidence in
the doctor by the patient.
Etiology
Occlusal Force.
Excessive occlusal force may result in fracture of the denture base. Ideal
occlusion and even distribution of force is mandatory. If warranted, an
occlusal guard should be fabricated.
Thin Acrylic Base.

When compromised acrylic thickness is present, this will most likely result in
microfractures and resultant denture base fracture.
Prevention
Strengthen the Denture Base.

The denture base may be strengthened with the use of acrylic or meshwork.
This will result in fewer fractures to the denture base (Fig. 15.71).
FIG 15.71 (A–B) Prosthesis support. To increase the strength of the denture base,
fiber mesh or rods may be processed inside the prosthesis. (Courtesy Preat Corporation,
Grover Beach, CA.)
Treatment Planning.
For an overdenture, always make sure there is sufficient room for attachment
or bar with adequate acrylic thickness (Fig. 15.72).
FIG 15.72 Overdenture fracture due to lack of acrylic support.
“Locking” Denture Under Bar Locking Prosthesis in

When picking up attachments (i.e., cold or light cure) for an overdenture,
sometimes locking the prosthesis under the bar will occur. This may lead to
significant complications and morbidity.
Prevention
A block-out material should always be used. It is recommended to use a
cellulose-based caulking and block-out material that is syringe delivered
(e.g., Perma Block [Preat Corporation]). These materials will adhere to wet
surfaces such as gingival and mucosal tissues.
This material will block-out the undercuts during attachment pick-up or
impression procedures. Its heavy body will prevent displacement, which may
allow encroachment of the autopolymerizing material into the sulcus. An air-
water syringe along with a brush will assist in removal (Fig. 15.73).
FIG 15.73 Block-out compound should be used anytime attachments are cold
cured within the mouth. The compound works very well in moist conditions.
Treatment
If the denture is locked under the bar/attachment, careful access to the
undercut can be obtained via the use of a diamond bur with excess irrigation.
This is most likely in the lingual aspect of the flange, directly over the
attachment in question.
Food Impaction
Etiology
A common compliant of mandibular overdentures is food impaction. Because
the flanges of the prosthesis do not extend to the floor of the mouth in the
rest position (to eliminate sore spots caused by elevation of the floor of the
mouth during swallowing), openings allow for food accumulation under the
prosthesis. During mastication, food debris migrates and become impacted
under the prosthesis during swallowing. A similar condition is found with a
traditional denture. When a lower denture “floats” during function, the food
more readily goes under and then through the prosthesis; however, the IOD
will trap the food debris against the implants, bars, and attachments.
Highly polished borders of the prosthesis should be completed because less
food will tend to accumulate. The patient should be informed of food
impaction prior to implant placement. An RP-4 will tend to accumulate more
food impaction because of more implants, larger space at the tissue level,
and the ease of food accumulating around the bar (Fig. 15.74).
FIG 15.74 Food impaction. (A) Because of the space from an overdenture, food
may easily accumulate underneath. (B) Food debris is difficult to remove from under
the bar.
References
1. Douglass CW, Shih A, Ostry L. Will there be a need for complete
dentures in the United States in 2020? J Prosthet Dent. 2002;87(1):5–8.
2. Marcus SE, Drury JF, Brown LS, et al. Tooth retention and tooth loss
in the permanent dentition of adults: United States, 1988–1991. J Dent
Res. 1996;75(spec issue):684–695.
3. Roberts WE, Turley PK, Brezniak N, et al. Implants: bone physiology
and metabolism. Cal Dent Assoc J. 1987;15:54–61.
1975;34:456–462.
5. Carlsson G, Persson G. Morphologic changes of the mandible after
extraction and wearing of dentures: a longitudinal clinical and x-ray
cephalometric study covering 5 years. Odont Rev. 1967;18:27–54.
6. Tallgren A. The reduction in face height of edentulous and partially
edentulous subjects during long-term denture wear: a longitudinal
roentgenographic cephalometric study. Acta Odontol Scand.
1966;24:195–239.
7. Atwood DA. Postextraction changes in the adult mandible as
illustrated by microradiographs of midsagittal section and serial
cephalometric rootsenograms. J Prosthet Dent. 1963;13:810–824.
8. Gruber H, Solar P, Ulm C. Maxillomandibular anatomy and patterns
of resorption during atrophy. Watzek G. Endosseous implants: scientific
and clinical aspects. Quintessence: Chicago; 1996:29–62.
9. Brodeur JM, Laurin P, Vallee R, et al. Nutrient intake and
gastrointestinal disorders related to masticatory performance in the
edentulous elderly. J Prosthet Dent. 1993;70:468–473.
10. Misch CE. Dental implant prosthetics. Mosby: St Louis; 2015.
11. Howell AW, Manley RS. An electronic strain gauge for measuring oral
forces. J Dent Res. 1948;27:705.
12. Carr A, Laney WR. Maximum occlusal force levels in patients with
osseointegrated oral implant prostheses and patients with complete
dentures. Int J Oral Maxillofac Implants. 1987;2:101–110.
13. Sposetti VJ, Gibbs CH, Alderson TH, et al. Bite force and muscle
activity in overdenture wearers before and after attachment
placement. J Prosthet Dent. 1986;55:265–273.
14. Carlsson GE, Haraldson T. Functional response. Brånemark PI, Zarb
GA, Albrektsson T. Tissue integrated prostheses: osseointegration in
clinical dentistry. Quintessence: Chicago; 1985:55–87.
16. Hildebrandt GH, Dominguez BL, Schock MA, et al. Functional units,
chewing, swallowing and food avoidance among the elderly. Prosthet
Dent. 1997;77:588–595.
17. Joshipura KJ, Wilkett WC, Douglass CW. The impact of
edentulousness on food and nutrient intake. J Am Dent Assoc.
1996;127:459–467.
18. Sheiham A, Steele JC, Marcenes W, et al. The impact of oral health on
stated ability to eat certain food; findings from the National Diet and
Nutrition Survey of Older People in Great Britain. Gerontology.
1999;16:11–20.
19. Kapur KK, Soman SD. Masticatory performance and efficiency in
20. Sullivan D, Walls R, Lipschitz D. Protein-energy undernutrition and
risk of mortality within 1 year of hospital discharge in a select
population of geriatric rehabilitation patients. Am J Clin Nutr.
1991;43:559–605.
21. Chen MK, Lowenstein F. Masticatory handicap, socio-economic status
and chronic conditions among adults. J Am Dent Assoc. 1984;109:916–
918.
22. Bergman B, Carlsson GE. Clinical long-term studies of complete
23. Fiske J, Davis DM, Frances C, et al. The emotional effects of tooth loss
in edentulous people. Br Dent J. 1998;184:90–93.
24. Adisman IK. The use of denture adhesive as an aid to denture
treatment. J Prosthet Dent. 1989;62(6):711–715.
25. Sheppard IM. Denture base dislodgement during mastication. J
Prosthet Dent. 1963;13:462–468.
26. Lundqvist S, Haraldson T. Occlusal perception of thickness in patients
with bridges on osteointegrated oral implants. Scand J Dent Res.
1984;92:88.
27. Kapur KK, et al. A randomized clinical trial comparing the efficacy of
mandibular implant-supported overdentures and conventional
dentures in diabetic patients. Part I: methodology and clinical
outcomes. J Prosthet Dent. 1998;79(5):555–569.
28. Awad MA, Feine JJ. Measuring patient satisfaction with mandibular
prostheses. Community Dent Oral Epidemiol. 1998;26:400–405.
29. McGill University. Health and Nutrition Letter 2. [21, April] 2003.
30. Walton JN, Gardner FM, Agar JR. A survey of crown and fixed partial
denture failures, length of service and reasons for replacement. J
Prosthet Dent. 1986;56:416–421.
31. Rissin L, House JE, Manly RS, et al. Clinical comparison of masticatory
performance and electromyographic activity of patients with
complete dentures, overdentures and natural teeth. J Prosthet Dent.
1978;39:508–511.
32. Blomberg S. Psychological response. Brånemark PI, Zarb GA,
Albrektsson T. Tissue integrated prostheses: osseointegration in clinical
dentistry. Quintessence: Chicago; 1985:243–248.
33. Raghoebar GM, Meijer HJ, Steigenga B, et al. Effectiveness of three
treatment modalities for the edentulous mandible: a five-year
randomized clinical trial. Clin Oral Implants Res. 2000;11:195–201.
34. Geertman ME, Boerrigter EM, van't Hof MA, et al. Two-center clinical
trial of implant-retained mandibular overdentures versus complete
dentures—chewing ability. Community Dent Oral Epidemiol.
1996;24:79–84.
35. Bilhan H, et al. Maintenance requirements associated with
mandibular implant overdentures: clinical results after first year of
service. J Oral Implantol. 2011;37(6):697–704.
36. Cune MS, de Putter C. A comparative evaluation of some outcome
measures of implant systems and suprastructures types in
mandibular implant overdenture treatment. J Oral Maxillofac
Implants. 1994;9:548–555.
37. Walton JN, MacEntee MI. Problems with prostheses on implants: a
retrospective study. J Prosthet Dent. 1994;71(3):283–288.
38. Mericke-Stern R. The forces on implant supporting overdentures: a
preliminary study of morphologic and cephalometric considerations.
Int J Oral Maxillofac Implants. 1993;8:256–263.
39. Wright PS, Glantz PO, Randow K, Watson RM. The effects of fixed and
removable implant-stabilised prostheses on posterior mandibular
residual ridge resorption. Clin Oral Implants Res. 2002;13(2):169–174.
40. Reddy MS, Geurs NC, Wang IC, et al. Mandibular growth following
implant restoration: does Wolff's law apply to residual ridge
resorption? Int J Periodontics Restorative Dent. 2002;22(4):315–321.
41. Preiskel HW. Quintessence: Chicago; 1984. Precision attachments in
prosthodontics: the applications of intracoronal and extracoronal
attachments. vol 1.
42. English CE. Bar patterns in implant prosthodontics. Implant Dent.
1994;3:217–229.
43. Misch CE. Treatment options for mandibular implant overdentures:
an organized approach. Misch CE. Contemporary implant dentistry.
Mosby: St Louis; 1993:489–502.
44. Misch CE. Mandibular overdenture treatment options. Misch Implant
Institute manual. Misch International Implant Institute: Dearborn,
MI; 1985.
45. Narhi TO, Geertman ME, Hevinga M, et al. Changes in the edentulous
maxilla in persons wearing implant-retained mandibular
overdentures. J Prosthet Dent. 2000;84:43–49.
46. Misch CE. What you don't know can hurt you (and your patients).
Dent Today. 2000;19(12):70–73.
47. Awad MA, Lund JP, Shapiro SH, et al. Oral health status and
treatment satisfaction with mandibular implant overdentures and
conventional dentures: a randomized clinical trial in a senior
population. Int J Prosthodont. 2003;16:390–396.
48. Misch CE. Implant overdentures relieve discomfort for the edentulous
patient. Dentist. 1989;67:37–38.
49. Park J. Analysis of the mandibular symphysis of participants with a normal
occlusion population using cone-beam–computed tomography. 2014 [Wiley
Online Library, pp 1–12].
50. Mericke-Stern R, Piotti M, Sirtes G. 3-D in vivo force measurements on
mandibular implants supporting overdentures: a comparative study.
51. Bidez MW, Misch CE. The biomechanics of interimplant spacing. [In
Proceedings of the Fourth International Congress of Implants and
Biomaterials in Stomatology, Charleston, SC, May 24–25] 1990.
52. Wright PS, Glantz PO, Randow K, et al. The effects of fixed and
removable implant-stabilized prostheses on posterior mandibular
residual ridge resorption. Clin Oral Implants Res. 2002;13:169–174.
53. McAlarney ME, Stavropoulos DN. Determination of cantilever length:
anterior posterior spread ratio assuming failure criteria to be the
compromise of the prosthesis retaining screw prosthesis joint. Int J
54. Goodacre CJ, et al. Clinical complications with implants and implant
prostheses. J Prosthet Dent. 2003;90(2):121–132.
55. Johns RB, Jemt T, Heath MR, et al. A multicenter study of
overdentures supported by Branemark implants. Int J Oral Maxillofac
Implants. 1992;7:513–522.
56. Gruber H, Solar P, Ulm C. Maxillomandibular anatomy and patterns of
resorption during atrophy. Watzek G. Endosseous implants: scientific
and clinical aspects. Quintessence: Chicago; 1996:156–163.
1975;34:456–462.
58. Wright PS, Watson RM. Effect of prefabricated bar design with
implant-stabilized prostheses on ridge resorption: a clinical report.
59. Misch J. Lehrbuch der Grenzgebiete der Medizin und Zahnheilkunde.
[Leipzig, Germany] 1922 [FC Vogel].
60. Misch CE. Premaxillary implant considerations, treatment planning
and surgery. Misch CE. Contemporary implant dentistry. Mosby: St
Louis; 1999:509–520.
61. Lehmann KM, Amin F. Studies on the retention forces of snap-on
attachments. Quintessence Dent Technol. 1978;7:45–48.
62. Setz I, Lee S, Engel E. Retention of prefabricated attachments for
implant stabilized overdentures in the edentulous mandible: an in
vitro study. J Prosthet Dent. 1998;80:323–329.
63. Chung KH, Chung CY, Cagna DR, Cronin RJ Jr. Retention
characteristics of attachment systems for implant overdentures. J
Prosthodont. 2004;13:221–226.
64. Alsabeeha NH, Payne AG, Swain MV. Attachment systems for
mandibular two-implant overdentures: a review of in vitro
investigations on retention and wear features. Int J Prosthodont.
2009;22:429–440.
65. Petropoulos V, Smith W. Maximum dislodging forces of implant
overdenture stud attachments. Int J Oral Maxillofac Implants.
2002;17:526–535.
66. Anusavice KJ. Phillips' science of dental materials. WB Saunders:
Philadelphia; 1996:709.
67. Abi Nader S, de Souza RF, Fortin D. Effect of simulated masticatory
loading on the retention of stud attachments for implant
overdentures. J Oral Rehabil. 2011;38:157–164.
68. Rutkunas V, Mizutani H, Takahashi H. Evaluation of stable retentive
properties of overdenture attachments. Stomatologija. 2005;7:115–120.
69. van Kampen F, Cune M, van der Bilt A, Bosnian F. Retention and
postinsertion maintenance of bar-clip, ball and magnet attachments
in mandibular implant overdenture treatment: an in vivo comparison
after 3 months of function. Clin Oral Implants Res. 2003;14:720–726.
70. Alsabeeha NH, Payne AG, Swain MV. Attachment systems for
mandibular two-implant overdentures: a review of in vitro
investigations on retention and wear features. Int J Prosthodont.
2009;22:429–440.
71. Kline KW, Misch CE: Elastometric O-ring implant design principles
(in press).
72. American Society for Testing and Materials. Medical devices. ASTM:
Philadelphia; 1990.
73. Zetpol hydrogenated nitrile rubber [brochure BJ-004], White Plains,
NY, Nippon Zeon of America.
74. Morton M. Rubber technology. ed 3. Van Nostrand Reinhold: New York;
1987.
75. Machine design: Compilation of articles on seal performance. [Cleveland]
1980 [Penton/IPC].
76. Bowles WH, Wilkinson MR, Wagner MJ, et al. Abrasive particles in
tobacco products: a possible factor in dental attrition. J Am Dent
Assoc. 1995;126:327–331.
77. Vere JW, Eliyas S, Wragg PF. Attitudes of general dental practitioners
to the maintenance of Locator retained implant overdentures. Br Dent
J. 2014;216(3):E5.
78. Delsen Testing Laboratories. Insertion and extraction test of retention
loss: test report 3-30. 2000:1–7.
79. Agarwal R. Principles of Attachment Selection for Implant-supported
Overdentures and Their Impact on Surgical Approaches, AAOMS 95th
Annual Meeting, Aaoms. 2013.
80. English CE. Bar patterns in implant prosthodontics. Implant Dent.
1994;3:217–229.
81. Preiskel HW. Quintessence: Chicago; 1984. Precision attachments in
prosthodontics: the applications of intracoronal and extracoronal
attachments. vol 1.
16
Fixed Prosthodontics Complications
Randolph R. Resnik
Dental implants have been shown to have excellent clinical survival; however,
many longitudinal studies have shown an increased incidence of biologic and
technical complications when compared with tooth-borne full coverage
restorations.1 As dental implants are becoming more and more popular, the
implant clinician must be cognizant of potential prosthetic complications
that may ensue. In this chapter, a wide range of fixed prosthetic
complications will be discussed. These include biomechanical force–related
complications, prosthesis complications, intraoperative complications,
esthetic complications, and postoperative complications. By having an
understanding of the guidelines established to prevent, identify, and treat
these numerous fixed prosthetic complications, an implant dentist can
significantly improve clinical outcomes while reducing the overall stresses of
daily practice life.
Biomechanics: Force-Related Issues
Biomechanical stress, which is responsible for a majority of dental implant
complications, most commonly occurs from occlusal function. Most
biomechanical complications do not occur as a result of a single force event
because they typically develop over time. This repetitive force, which is
applied to the various dental materials that make up the prosthesis, follows a
fatigue curve. The fatigue curve is directly related to the number of cycles
and the intensity of the force.2 When lower-force magnitudes repeatedly
contact an object, the force can eventually exceed the endurance limit and
fracture of the material will result (Fig. 16.1). For example, a wire coat hanger
that is bent does not break the first time, but repeated bends will fracture the
material—not because the last bend was more forceful but because of the
resultant fatigue. This same principle applies to dental implants and is why
the most common cause of implant and prosthesis component complications
are related to biomechanical conditions that give rise to fatigue.3
FIG 16.1 (A) When stress is plotted on the y-axis and cycles to failure are plotted
on the x-axis, the fatigue curve of a material may be established. Any stress
condition above the endurance limit will eventually cause fracture when enough
cycles are applied. (B–C) Force-related fractured implant (i.e., cantilevered
prosthesis and small diameter implant).
Screw Loosening
Abutment screw loosening has been shown to be associated with an overall
average of 6% of implant prostheses fabricated.3 Screw loosening is the most
common implant prosthetic complication, accounting for approximately 33%
of all postimplant prosthodontic complications.4 More recent studies indicate
this complication occurs in approximately 8% of single crowns, 5% of
multiple-unit fixed prostheses, and 3% of implant overdentures. De Boever
has shown that 12% of prostheses exhibit loosening within 3 years,5 while
Chaar has shown an incidence of 4.3% within 5 years and approximately 10%
long term (5–10 years).6
Screw loosening may cause considerable complications. A loose screw may
contribute to crestal bone loss because bacteria are able to colonize and
harbor in the open interface. When an abutment screw becomes loose on a
cemented crown, the crown may need to be cut off the abutment to gain
access to the abutment screw, which results in patient disappointment and
unproductive clinician time. If a loose abutment screw is not treated
appropriately, fracture of the prosthesis, implant components, or the implant
body may occur.
Etiology
External Force Factors (Box 16.1).

External forces that act on a screw joint greatly increase the risk of screw
loosening. These forces may be called joint-separating forces when related to
screw loosening; however, they are the same forces that are risk factors for
implant failure, crestal bone loss, and component fracture. When the external
joint-separating forces are greater than the force holding the screws together
(called clamping forces), the screw will become loose. The external forces from
parafunction, crown height, masticatory dynamics, position in the dental
arch, and opposing dentition are factors that can dramatically increase the
stress to the implant and the screw joint. In addition, conditions that
magnify or increase these factors are cantilevers, angled loads, and poor
occlusal designs.
Box 16.1
External Forces That Increase Screw Loosening
1. Parafunction
2. Crown height space
3. Masticatory musculature dynamics
4. Arch position (anterior, middle, posterior)
5. Opposing arch
6. Cantilevers
7. Angled loads
8. Poor occlusal designs
9. Lack of key implant positions
a. Canine
b. First molar
10. Inadequate implant number
a. No three adjacent pontics
11. Nonpassive prostheses
12. Inadequate Screw Torque

13. Excessive Screw Torque
14. Improper Prosthesis Insertion Technique

External forces applied to the joint system are important to account for
when the aim is to decrease the incidence of screw loosening. The endurance
limit of a material is the amount of force required to fracture the object when
enough cycles are applied. The greater the force, the fewer cycles required
before fracture occurs. It is the combination and relationship of both the
amount of force and the number of cycles that is the cause of the screw
loosening complication.
Cantilevers/Increased Crown Height Space.

One of the most common etiologic factors that results in screw loosening is
excessive continuous occlusal forces. The most common example occurs in
prostheses with improper occlusal contacts. The greater the stress applied to
the prostheses, the greater the risk of abutment screw loosening. A nonideal
prosthetic design may potentiate the force applied. Cantilevers increase the
risk of screw loosening because they increase the magnitude of forces to the
implant system: there is a direct relationship between the length of the
cantilever and force applied to the prosthesis.7 Any of these external forces
applied to a cantilever will further magnify the joint-separating forces. For
example, cantilevers on prostheses lead to uneven occlusal loads. Uneven
occlusal loads cause repeated cycles of compression and then tension and
shear of implant components. Screws are especially vulnerable to tensile and
shear forces. Both of these are dramatically increased with cantilever forces
or angled loads. Because the screw is an inclined plane, the continued
vibration causes it to unthread. The greater the range of external forces, the
fewer the number of cycles necessary before screw loosening.
When an increased crown height space exists (poor crown-implant ratio),
there is a resultant greater force applied to the screw. This usually results in a
greater risk of screw loosening (or fracture). Boggan et al demonstrated that
the force that is applied to the screw is directly related to the crown height.
The crown height acts as a vertical cantilever, which magnifies the force on
the abutment screw (Fig. 16.2).8
FIG 16.2 (A) Excessive crown height space comparing an FP-3 to a FP-1, which
leads to a vertical cantilever to any angle load. (B) Apical placement of implant
results in greater force to the prosthesis and abutment screw leading to an
increased incidence of screw loosening. (C) Poor implant positioning (e.g., implant
placement too far posterior) leading to excessive resultant force from cantilever
effect and greater stress on the screw system. Note the significant cusp height and
opposing cusp concavity, which increases the shear component of force on the
implant system. ([A] From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Parafunction.
Of all the external forces that cause screw loosening, the primary factor is
parafunction related. A horizontal bruxing patient loads the implant crown
with an angled force repeatedly. This increases the magnitude of force, cycles
to fatigue failure, and the angle of the force that places shear on the interface.
Abutment screw loosening can be expected in a patient with a severe bruxing
habit. A parafunction patient increases the amount of force to the system
while also increasing the number of cycles to the system. Hence, fractures of
porcelain and cement seals and screw loosening or fracture are inevitable.
When the adjacent natural teeth are mobile to lateral or angled forces, the
rigid implant and implant crown may be overloaded. A heavy bite force
occlusal adjustment, which allows the adjacent teeth to move before implant
crown contact, is recommended to reduce the risk of overload.
Continuous occlusal loads can have a cumulative effect on the preload, and
the screw material may undergo deformation.9 When the force exceeds the
yield strength, plastic deformation occurs, and the screw begins to deform.
This material deformation causes the screw to loosen and leads to potential
failure of the prosthesis.
Screw loosening is also affected by the amount of the force and the
number of cycles and is similar to fatigue. External methods to limit screw
loosening include factors that reduce the biomechanical stress. These include
key implant positions (i.e., to distribute forces evenly), sufficient number of
implants (i.e., adequate surface area), passive frameworks, and adequate
occlusal schemes.10
Splinted vs. Nonsplinted Crowns.

Screw loosening of abutment or prosthetic screws occurs more often on
individual implant crowns than on crowns that are splinted together. For
example, in a report for single molar replacement, the abutment screw-
loosening rate was 40% during a 3-year period. When two splinted implants
were used to replace the molar space, the screw loosening was reduced to
8%.11 The stress distribution of splinted prosthetic units results in less force
applied to the screw system. Studies have shown splinted implant-retained
overdentures have far less screw loosening in comparison to fixed
prostheses.12
Crown/Abutment Not Fully Seated.

If the abutment is not fully seated because of improper abutment placement,
tissue impingement, or bone impingement, a poor distribution of force in the
screw system will result, which leads to increased screw loosening. When the
abutment is not seated fully and completely tightened, the prosthetic screw
will be distorted, which leads to inadequate preload and subsequent screw
loosening or fracture (Fig. 16.3).
FIG 16.3 (A) Nonpassive or improperly seated screw-retained restorations may be
distorted when seated into position when the prosthetic screw is threaded. The
distortion of the superstructure causes stresses that are concentrated at the crestal
bone level and may result in bone loss. (B) Radiographic image depicting incomplete
seating of abutment, which predisposes prosthesis to screw loosening. ([A] From
Insufficient/Excessive Torqueing.
When improper preload via the torqueing process is applied to the abutment
screw, screw loosening will often occur. This may be caused by either
excessive or insufficient tightening of the abutment screw. An implant screw
is similar to a bolt joint in engineering. There is a preload (tightening force)
placed on the screw, which develops a force within the screw. As the screw is
tightened, it elongates, producing tension, which results in the implant screw
acting like a spring. The preload stretch of the screw is maintained by
frictional force, and the tension between the screw and the implant/abutment
is termed a clamping force. When insufficient preload is applied to the screw,
there is insufficient clamping force, which ultimately leads to screw
loosening, especially under occlusal loading. When excessive force is applied,
the clamping force is easily released, and screw loosening will occur (Fig.
16.4).
FIG 16.4 (A) Insufficient torque applied to the screw leads to a greater incidence of
screw loosening. If the screw is not torqued sufficiently or overtorque occurs,
insufficient preload will result, which will most likely result in screw loosening. (B)
The proper torque wrench and technique should be used according to the
manufacturers' specifications as implant systems have various recommended
torque values. ([A] From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby. [B]
Courtesy BioHorizons Implant Systems, Inc.)
Screw Diameter.
The diameter of the abutment screw may have a significant effect on the
amount of preload applied to the system before deformation occurs. The
greater the screw diameter, the higher the preload that may be applied,
which results in a greater clamping force on the screw joint. However, the
coping and prosthetic screws vary greatly according to the type, size, and
material. The strength of the material increases by a power of four when the
diameter of the screw doubles (a screw with twice the diameter is 16 times
stronger). As a result, abutment screws loosen less often because they can
take a higher preload compared with coping and prosthetic screws. Some
companies offer similar diameters for abutment and prosthetic screws. As a
result, a similar clamping force may be used for either component (Fig. 16.5).
FIG 16.5 Screw sizes vary according to manufacturers. In general, the larger the
screw diameter, the greater preload that may be applied. Care should be exercised
to not place too high of a torque as this will lead to screw deformation and screw
loosening.
Screw Material.
The composition of the screw is another factor that modifies its performance.
The composition of the metal may influence the amount of strain in the
screw from preload and the point of fracture, directly affecting the amount of
preload that can be safely applied. Screw material and yield strength vary
greatly when all other factors are similar (e.g., 12.4 N for a gold screw to 83.8
N for a titanium alloy screw fixation).13
The deformation or permanent distortion of the screw is the end point of
the elastic modulus. Titanium alloy has four times the bending fracture
resistance of grade 1 titanium. Abutment screws made of grade 1 titanium
deform and fracture more easily than the alloy. Titanium alloy is 2.4 times
stronger than grade 4 titanium. As such, a higher torque magnitude can be
used on the titanium alloy abutment screw and female component (found
within the implant body), less on grade 4 titanium, less on grade 1 titanium,
and the least on gold screws.
The elongation of metal is related to the modulus of elasticity, which
depends on the type of material, width, design, and the amount of stress
applied. The material of which the screw is made (e.g., titanium alloy,
titanium, or gold) has a specific modulus of elasticity. A prosthetic gold screw
exhibits greater elongation than a screw made of titanium alloy but has a
lower yield strength.
Although the strengths of titanium grades are dramatically different, the
modulus of elasticity is similar for grade 1 to 4 titanium. Hence, the strain of
the abutment screw is similar with each grade of titanium, but the safety load
relative to fracture is different. Titanium alloy (grade 5) has a slightly higher
modulus of elasticity. Although not clinically relevant to metal-bone
osseointegration, the titanium alloy screw should have a slightly higher
preload value. This is not a consequence relative to permanent deformation
or fracture because it is more than twice as strong as the other grades of
titanium.
The metal for the screwdriver used in the torque wrench is also important
to consider. Stripping of the screw head prevents the clinician from
tightening or removing the screw. Some manufacturers make the torque
wrench driver out of titanium alloy, and the screw is made of gold or
titanium. The concept is that the torque wrench will not deform the hexagon
and will not strip, so the device lasts longer. However, this is not ideal. It is
easier to replace the torque wrench driver than the abutment or prosthetic
screw. Because of this, the torque wrench should be made of titanium and the
screw of titanium alloy.
From a clinical standpoint the receptor site for the torque wrench is also a
feature of the screw head to consider. The screw head has a rotation feature,
most commonly a hexagonal design. The more sides to the rotation feature,
the more often the head will strip. A slot or triangular feature will strip less
than a hexagon (Fig. 16.6).
FIG 16.6 Variation of abutment screw threads. (A) The more threads present on an
abutment screw the less chance of screw loosening. (B) Material. Ideally, screw
material should be titanium alloy, as gold alloy screws have a higher incidence of
loosening and fracturing. (Courtesy BioHorizons Implant Systems, Inc.)
Component Fit.
In the science of machining metal components, there is a range of
dimensions that manufacturers use. For instance, an implant 4 mm in
diameter may actually range from 3.99 mm to 4.01 mm. Likewise, the
abutment and prosthetic coping connection also has a range. As a result, if a
smaller implant body hex dimension is mated with a larger abutment
connection, the components may not ideally fit together. Most implant
manufacturers allow for a misfit range that results in the abutment or coping
being able to rotate ±10 degrees on the implant body. Components between
the abutment and implant body may have a misfit of 10 degrees in a
rotational dimension, and horizontal discrepancies have been reported up to
99 µm.14,15 These ranges are different with respect to each implant system.
The more accurate the component fit, the less force applied to the abutment
or prosthetic screw (Fig. 16.7).
FIG 16.7 The rotational fit of the abutment-to-implant body is variable from one
manufacturer to another. The greater the rotational misfit (red line and dotted line),
the more force is applied to the abutment screw. (From Misch CE: Dental implant
The incidence of screw loosening is also a function of the accuracy of fit of

the flat-to-flat connection of the implant and abutment or prosthetic
component. Implant abutment connections or prosthetic connections with an
unstable mating interface place undue stress on the screw that connects the
components. Mechanical testing has demonstrated a direct correlation
between the tolerance of the flat-to-flat dimension of the external hexagon
and the stability of the abutment or prosthetic screw. Binon showed that a
mean flat-to-flat range of less than 0.005 mm exists on the hexagon, and a
flat-to-flat range of less than 0.05 mm for the entire sample would result in a
more stable screw joint.16 Studies have shown plastic castable patterns, which
can be highly inaccurate, to have a vertical misfit as high as 66 µm.17
The same manufacturing conditions apply to impression transfer copings
and analogs. Many manufacturers have a wider machining range (+ or −
variance) for the prosthetic components to reduce the cost of manufacturing.
When transfer copings and analogs are used in impressions and then to
fabricate the prosthesis in the laboratory and the implants are splinted
together, the prosthesis may not passively seat.
Many manufacturers recommend the use of plastic (non-metal) burn-out
posts. Plastic burnout prosthetic copings cost less, but they exhibit much
greater laboratory variance and poor fit because of irregularities and settling
of the superstructure. Besides cost, another advantage of a plastic burnout
pattern for a coping is that one type of metal is used for the coping and
superstructure, lessening the risk of metal corrosion or separation between
the coping and superstructure.
To reduce settling a machined coping may be used to fit the implant
abutment more accurately. Some manufacturers suggest a titanium coping to
reduce the risk of misfit. However, oxides form on the titanium-machined
coping surface and impair metal adherence when the prosthesis or abutment
metal work is cast to the coping. Mechanical retentive features on the coping
improve this metal-to-metal attachment.
Laboratory studies demonstrate that an alloy-cylinder compatibility exists
when noble metal alloys are used rather than titanium for a superior metal-
to-metal connection. A machine coping connection is still present, so it is
superior to the plastic components used to cast one metal.18 The risk of
oxides forming between the coping and metal of the prosthesis is also
reduced (Fig. 16.8).
FIG 16.8 (A) Plastic castable vs. metal coping abutments. The plastic castable
abutments often lead to significant discrepancies in fit after casting. (B) Nonpassive
casting resulting from incomplete seating of prosthesis.
Implant Design.
The type and design of the dental implant has a significant impact on screw
loosening. As a general rule, most implant bodies have an antirotational
feature for the abutment connection. The most common designs are an
external hexagon, an internal hexagon, a Morse taper, and a Morse taper with
threads.
Factors that affect the abutment screw connection and screw loosening
include the height (or depth) of the hexagon and the platform diameter.
Boggan et al studied the influence of design factors on the mechanical
strength and quality of fit of the implant abutment interface. Whereas failure
mode for static test samples was bending or deformation of the abutment
screw, fracture of the abutment screw was the common failure mode for the
fatigue test samples. The static failure load was greater for the external hex
implants of 1 mm in height compared with implants with an internal
hexagon of 1.7 mm. The larger-diameter implant had the greatest static load
before failure (Table 16.1).8 As the hexagon height (or depth) increases, the
load on the abutment screw decreases. Likewise, as the diameter of the
implant platform increases, the force on the abutment screw decreases.
Reduction of the lateral load (P) on the abutment screw is crucial to prevent
the load on the screw to be beyond the yield strength of the material.
TABLE 16.1
Failure Loads of Various Implant Types
Implant Type Static Failure Load (N)

1.0 mm external hexagon, 4 mm 966
1.0 mm external hexagon, 5 mm 1955
0.7 mm external hexagon 756
0.6 mm internal oc tagon 587
1.7 mm internal hexagon 814
The height (or depth) of the antirotational hexagon is directly related to the
force applied to the abutment screw with any lateral load. Because the crown
is connected to the abutment and the abutment rests on the implant
platform, a lateral force on the crown creates a tipping force on the
abutment. This tipping force is resisted by the hexagon height or depth, the
platform, and the abutment screw. When the arc of rotation is above the
hexagon height, all of the force is applied to the abutment screw. For the
hexagon height to be above the arc of tipping forces, the hexagon height
must be at least 1 mm for a 4-mm-diameter implant. Yet many implant
manufacturers feature a hexagon height of only 0.7 mm, so almost all of the
force is directed to the abutment screw, increasing the occurrence of screw
loosening and fracture (Fig. 16.9).
FIG 16.9 The higher (or deeper) the antirotational hexagon component (x
component on the graph), the less the force applied to the abutment screw (Fs) on
the y-axis. A 0.7-mm hexagon height is standard in the industry and was used first
by Nobel Biocare. A 1-mm hexagon height has less risk of screw loosening because
the force on the screw is decreased. (From Misch CE: Dental implant prosthetics, ed 2, St
The difference between external vs. internal connections has been well
documented. Studies have shown the incidence associated with external-
connection (EC) implants was 18.3% at a mean of 5.3 years (217 of 1183
restorations; maximum, 59.9%).19,20 The complication rate with internal-
connection (IC) implants was 2.7% at a mean of 4.5 years (142 of 5235
restorations; maximum, 31.6%).21,22 Other studies have shown the external hex
to have a significantly higher incidence of screw loosening than internal hex
(MA-EC, 15.1%; Zr-EC, 6.8%; MA-IC, 1.5%; Zr-IC, 0.9%).23
The platform dimension upon which the abutment is seated is also an
important factor in screw loosening. Larger-diameter implants, with
associated larger platform dimensions, reduce the forces applied to an
abutment screw and change the arc of displacement of the abutment on the
crest module. For example, in a report by Cho et al, abutment screw
loosening over a 3-year period was almost 15% for a 4-mm implant diameter
but less than 6% for the 5-mm implant diameter (Fig. 16.10).24
FIG 16.10 To reduce forces on the abutment screw, the platform diameter of the
implant is more important than the hexagon height. The larger the diameter (x-axis),
the less the force applied to the screw (y-axis). (From Misch CE: Dental implant prosthetics,
Screw vs. Cement Retained.

When evaluating the prosthesis type (cement vs. screw), studies have shown
screw-retained (8.5%) had a much higher incidence of screw loosening in
comparison to cement retained (3.1%). These complications have a greater
incidence with screw-retained restorations compared with cement-retained
restorations because cement-retained restorations are more passive and have
less strain on the implant system.25 Although a cement-retained restoration
is more common, screw-retained restorations are indicated when low-profile
retention is necessary on a short abutment or when the implant bodies are
more than 30 degrees from each other and splinting is required to restore the
patient. Additionally, a screw-retained prosthesis has the advantage of less
chance of tissue irritation because of the high incidence of retained cement
with a cement retained prosthesis.
Screw loosening and partially unretained restorations are common
complications of nonpassive castings. The more passive the fit on the
implant abutment for screw retention and the more controlled the occlusal
forces, and the more secure the prosthesis. The repeated compressive and
tensile forces from nonpassive castings under occlusal loads cause vibration
and loosening of the screw components. Accuracy in design and fabrication
of the metal superstructure are determining factors for the reduction of
forces at the implant abutment and implant-bone interface.
Passive screw-retained restorations are more difficult to fabricate than
passive cement-retained restorations. When the screw is threaded into
position, the superstructure may distort, the implant may move within the
bone, or the abutment screw may distort. The distortion of the
superstructure and implant system may reach a level such that a 500-µm
original gap may not be detectable.26 As a result, the casting may appear to fit
the implant abutment for screw retention. However, the superstructure,
bone, and components do not bend beyond their elastic limit, and
compression, tensile, and shear forces are placed on the bone-implant
interface.27 The bone must remodel to eliminate these forces. If the forces are
beyond physiologic or ultimate strength limits, resorption of the bone-
implant interface occurs. As a result, greater crestal bone loss has been
associated with nonpassive castings. Creep (a constant force applied over
time on a material) or fatigue also can contribute to fracture of the
components over time because of a constant load or cyclic load frequency
(Figs. 16.11 to 16.13).
FIG 16.11 When a screw-retained restoration (yellow) is fixated in place,

compressive, tensile, and shear forces are present with the screw components
(blue). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 16.12 When the prosthesis is not passive (yellow), the compressive tensile
and shear forces are directly applied to the implant system (i.e., Red Arrows:
abutment, implant body, abutment screw, marginal bone, implant-bone
interface). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 16.13 An improper fit between the abutment and the implant will lead to
stresses that are applied throughout the implant concentrated at the crestal bone
level, which may cause bone loss. In this example, a 50-µm misfit may force the
implant body to move approximately 200 µm at the apex. (From Misch CE: Dental implant
Anatomic Location.
The location of the prosthesis in the oral cavity is also a significant factor in
the incidence of screw loosening. Sadid-Zadeh showed a significant incidence
difference with respect to anatomic locations; anterior (12.8%; 51 of 398
restorations) and posterior positioning (4.8%; 144 of 2972 restorations).
However, when evaluating internal connection implants, they had an
associated higher incidence of screw loosening in the posterior region (4.3%)
than the anterior region (0.7%).28
Prevention
Decreased Force.
Because of the directional relationship between force and screw loosening,
the evaluation, diagnosis, and modification of treatment plans related to
stress conditions are of considerable importance. After the clinician has
identified the source of excessive force on the implant system, the treatment
plan is altered in an attempt to minimize the negative impact on the
longevity of the implant, bone, and final restoration.
Prosthetic Design.
The prosthetic design may be altered to minimize the possibility of screw
loosening. Ideal implant placement in the key implant positions should be
adhered to. Cantilevers should be eliminated or reduced, especially when
high occlusal forces are present. Additionally, implant protection principles
should be adhered to including reduction of cuspal inclines of the prosthesis
(decreased cusp height), decreased occlusal table, and no lateral contacts,
especially in the posterior.
Ideal Preload.
The ideal torque force on an abutment screw varies by manufacturer and may
range from 10–35 N/cm. This preload is determined by many variables
including the screw material, screw head design, abutment material,
abutment surface, and possible lubricant. To reduce the incidence of screw
loosening, the abutment screw should be torqued by the following protocol:
1. Light finger tighten with driver (~10 N/cm)
2. Maximum finger tighten with driver (~20 N/cm)

3. Implant screw should be torqued to the manufacturer specifications
4. After 5–10 minutes, the screw should be retorqued to the same

manufacturer specifications.
Note: For cases of expected increased force, the implant

screw may be retorqued a third time after 30–60 days.
Screw Tightening Sequence.

When screw tightening a multi-unit fixed implant prostheses, a proper
sequence and technique is crucial to obtain the correct torque. The torque
should be applied incrementally amongst all screws so that not one screw is
tightened fully. This is based on the fact that a multi-unit prosthesis is
unlikely to be “completely” passive. A nonideal tightening sequence will lead
to either an insufficient or excessive amount of torque placed onto a specific
screw thread. Undertorque will lead to insufficient clamping force and lack of
ideal stretching of the screw. This will most often lead to screw loosening.
Overtorque will lead to permanent deformation of the screw which may lead
to screw fracture (Fig. 16.14).
FIG 16.14 Screw tightening sequence. (A) Incorrect tightening sequence for bar,
leading to uneven distribution of stress to the screw system. (B) Correct sequence,
which should be completed with light finger tightening, then maximum finger
tightening, and lastly final torque wrench. (C) Incorrect tightening sequence for a
fixed prosthesis. (D) Correct sequence, which should be completed with light finger
tightening, then maximum finger tightening, and lastly final torque wrench.
Settling Effect.
Settling is a term used to describe the effect of various implant parts wearing
and fitting closer together. Minor irregularities on or within a casting that
incorporates the top of an abutment or screw can cause slight elevation of the
casting or the screw head. Over time, micromovement wears down the
irregularities, and the parts fit closer together. However, this settling relaxes
the preload force on the prosthetic screw and is more likely to cause screw
loosening. This embedment relaxation or loss of preload has been shown to
be approximately 2% to 10 % of the initial preload within the first few
seconds or minutes after tightening. This is the reasoning for the above
protocol to include a second retorque after 5–10 min to regain the lost
preload due to settling (Fig. 16.15).29
FIG 16.15 (A) Final ideal torque technique (after hand tightening). Phase 1 final
torque, then, after 5–10 minutes, phase 2 final torque. (B) Settling effect of the
abutment screw occurs after the initial preload. A final torque is needed to maintain
the initial preload. (Courtesy BioHorizons Implant Systems, Inc.)
Torque Under Moist Conditions.

Studies have shown when placing and torqueing abutment screws, more
accurate torque values result under wet conditions vs. dry.30 Saline may be
used to lubricate the screw prior to placement of preload to maximize the
accuracy of the preload.
Wider Implant Bodies.

The use of wider implant bodies results in decreased force on the screw.
Graves has shown increasing implant size from 3.75 mm to 5.0 mm results in
20% greater strength, while increasing implant size from 3.75 mm to 6.0 mm
to increases the strength by 33%.31
Treatment
When confronted with a mobile prosthesis, it is important to determine if the
mobility is a result of screw loosening or the actual implant being mobile
(implant failure). Box 16.2 shows a technique to determine the etiology of the
prosthesis movement (Fig. 16.16).
Box 16.2
Technique to Determine the Etiology of the
Prosthesis Movement (see Fig. 16.16)
Step 1: Movement of crown. With the use of two mirror handles placed on
the buccal and lingual aspect of the crown, a buccal-lingual force is applied
to evaluate the mobility of the prosthesis. This will result in a subjective
response from the patient experiencing either pain or no pain.
No pain: if no pain is present, then it is most likely the

abutment screw is loose.
Pain: if pain is present, it may be the result of either the

abutment loosening or implant failure. With respect to
the abutment screw, the pain will originate from the
movement of the crown, most likely resulting from
tissue impingement. In some situations, this can be
verified by a radiograph showing incomplete seating
of the prosthesis with the abutment. If the pain
originates from the implant, this will usually indicate
failure of the implant.
Step 2: Palpation of buccal/lingual cortical plates. A second test is to palpate
the buccal and lingual cortical plates over the implant body. If no pain is
present, then it is most likely the abutment. If pain is present, it is usually
a sign the implant has failed.
FIG 16.16 (A–B) Checking buccal-lingual mobility of prosthesis with a mirror
handle. (C–D) Palpation of buccal and lingual cortical plates to assess the presence
of pain.
Implant Movement.
Mobility of the implant indicates failure of the implant and necessitates
immediate removal. A radiograph may reveal a circumferential radiolucency.
The site should then be reevaluated after adequate healing for the need of
bone grafting, implant placement, or change in prosthetic treatment
planning (Fig. 16.17).
FIG 16.17 Implant body movement. When buccal-lingual movement of the implant
body is present, usually radiographic signs will be present confirming implant failure
(i.e., circumferential radiolucency).
Abutment Screw Movement

Option 1.
Removing a cemented crown from a mobile abutment is very challenging
with crown removal techniques (e.g., crown bumper). The impact force that is
applied to the mobile crown is dissipated because of the loose screw. This
may result in damage to the internal threads of the implant body. In addition,
when an implant crown margin is subgingival, it is often difficult to obtain
access for the crown remover. In poorer bone densities, overzealous use of a
crown remover may result in loss of bone-implant interface.
Option 2.
The safest and most predictable treatment option to treat abutment
movement is accomplished with making an occlusal access, and turning the
cement-retained crown into a screw-retained crown (Fig. 16.18).
FIG 16.18 Technique for removing a screw. (A) Occlusal opening to obtain access
to abutment screw with #8 diamond round bur. (B) Hex driver engages abutment
screw. (C) Reverse torque removes the screw. (D) Implant-retained crown is
removed along with screw. (E) Implant crown with abutment retained within the
crown. (F) A new screw should always replace the old screw. The old screw is most
likely deformed and will have a high incidence of chronic loosening. Screw is
discarded; new screw is used to fixate implant crown. (G) PTFE tape is used to
protect the screw head. (H) Opaque composite used to occlude access hole.
The following are the steps for completing this procedure:
1. Evaluate and determine the location and angulation of the implant

abutment screw (buccal-lingually and mesial-distally). An intraoral
radiograph is often helpful.
2. With a round diamond bur (≈#8 round), access is made through the
occlusal surface to remove the abutment screw (i.e., central fossa: posterior
teeth and lingual aspect of crown in anterior teeth).
3. After the screw is located, the screw is engaged with the appropriate hex
driver, reverse-torqued, and the screw is removed.
4. Discard old screw and place new screw.
5. Torque to the manufacturer specifications with ideal protocol.
6. Cover access hole with filler (polytetrafluoroethylene [PTFE]) and opaque

composite.
In situations where the access hole is through the facial aspect of the
prosthesis (i.e., anterior crowns), the crown will need to be removed and a
new crown fabricated. Care should be exercised when cutting the crown off
because in most cases it is difficult to determine the cement location (Fig.
16.19). This may result in sectioning the crown too deep causing damage to
the abutment, abutment screw, or implant body (Fig. 16.20). A safer method
includes the above technique (access with screw removal) with fabrication of
a new prosthesis. If the abutment remains fixated to the prosthesis, the
prosthesis can be easily removed by gently heating the prosthesis with a
Bunsen burner.
FIG 16.19 Screw access. (A) Ideally, the screw will be able to be removed without
compromising esthetics (i.e., anterior teeth—lingual, posterior teeth—central fossa).
(B) Anterior crown where screw has to be removed via the facial surface, resulting in
the need to remake crown.
FIG 16.20 (A–B) Ideally, the crown should not be sectioned or “cut-off.” This often
leads to trauma to the abutment screw because of the very thin cement margin.
Screw Fracture
Etiology
The etiologic factor most likely to cause screw fractures is biomechanical
stress to the implant system. The biomechanical stress leads to partially
unretained restorations or fatigue, which is directly related to an increased
amount of force. Prosthesis screw fracture has been shown to occur with a
mean incidence of 4% with a range of 0% to 19%. Abutment screw fracture is
directly related to the screw diameter, with larger-diameter screws fracturing
less often, with a mean incidence of 2% and a range of 0.2% to 8%3 (Fig.
16.21).
FIG 16.21 Abutment screw fractures. (A) Fractured screw; note the large facial
overcontouring resulting in a shear load to the screw. (B) Implant with screw
fractured; space can be identified between the screw and the threads of the implant
body, which result from loss of preload. (C) Prosthesis fracture leading to multiple
fractured screws. (D) In some instances, the screw will fracture with the retained
preload, which makes removal very difficult.
The etiology of abutment screw fracture is the same for screw loosening
(see above).
Prevention
Immediate Treatment of Loose Screw.

If an abutment screw is determined to be mobile, immediate treatment is
recommended. The longer the time period that force is applied to a mobile
prosthesis, the greater the chance the abutment screw will be deformed and
possibly fracture. The loose screw follows a fatigue curve that is related to the
number of cycles and the intensity of the repeated forces.
Treatment
Explorer.
The easiest method to remove a screw is to rotate the screw counterclockwise
with a sharp explorer tip. Because a loose screw has no preload, the fractured
component remains passive in the implant body. If the screw has been
deformed or debris has been introduced between the screw and implant
body, this technique may not be successful (Fig. 16.22).
FIG 16.22 Explorer technique to remove screw. (A) Screw has lost its preload, can
easily be unscrewed (counterclockwise). (B) Screw removal.
Ultrasonic/cavitron Device.
If debris is present between the threads, an ultrasonic or cavitron device may
be used. The vibration (≈20,000–30,000 rpm) will usually dislodge the debris,
and the screw can then be removed via the explorer method.
Round Bur (205LN).

A very small round bur or 205LN can be used in a slow-speed handpiece or
AS123 screwdriver. The tip of the bur is placed at the seam of the fractured
screw and abutment (implant). As the bur spins clockwise, the friction
placed on the screw makes it turn counterclockwise, and the screw unthreads
(Fig. 16.23).
FIG 16.23 Round bur (205LN). (A) A fractured abutment screw in a bruxing patient.
(B) A very small round bur is used in a slow handpiece. (C) The bur is positioned in
the seam of the screw and implant and as it rotates clockwise, friction unthreads the
screw. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Inverted Cone Bur (≈ Bur).

With an inverted cone bur in a high-speed handpiece (ideally electric
handpiece in reverse), gently touch the top of the screw. This will usually
result in the screw being extruded from the implant body. Care should be
exercised to not touch the implant body with the bur because this will result
in damage to the implant body threads. With this technique, always use a
throat pack to prevent loss (Fig. 16.24).
FIG 16.24 Inverted cone ( carbide bur) with handpiece. (A) Screw fractures
off within the abutment for screw. (B) inverted cone. (C) The fractured screw
is lightly tapped in the center of the screw, care must be exercised to not touch the
internal walls/threads of the implant.
Slot the Top of Screw.

A slot 1 mm deep is made through the center of the screw with a high-speed
handpiece and a very narrow fissure bur (or bur). A small screwdriver is
then used to unthread the screw. Be careful using this technique because the
bur may inadvertently perforate the side of the implant body. There is no
predictable method to repair the implant body if this occurs. The patient
should be informed that implant failure may result as a consequence of this
technique (Fig. 16.25).
FIG 16.25 (A) Slot the top of screw. A slot is made in the screw with a high-speed
handpiece and narrow fissure bar. A screwdriver is then used to unthread the screw.
(B) Use of an ultrasonic scaler to loosen debris between the screw and the internal
threads of the implant. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Manufactured Retrieval Instruments.

There are multiple retrieval kits on the market that are used to remove
fractured screws. These are usually specific for the type of implant body type
(internal, external, trilobe, etc.) (Fig. 16.26).
FIG 16.26 Salvin Implant Rescue Kit. (A) Place guide on implant and hold with
stabilizing handle. Insert drill into implant handpiece. Set motor to REVERSE at
1000–1250RPM and 50–70 N-cm torque. (B) Drill in REVERSE using “up and down”
motion to prepare 1- to 2-mm deep dimple into top of broken screw. (C) Insert tap
into implant handpiece set motor to REVERSE at 70–80 rpm and 50–70 N-cm
torque. (D) Insert tap into the 1- to 2-mm dimple in the top of the broken screw. Use
the tap in REVERSE to remove broken screw. (E) Screw removed. (Courtesy Salvin
Dental Specialties, Inc., Charlotte, NC.)
Excessive Torque Applied to the Abutment

Screw/Prosthesis
Etiology
The amount of force applied to tighten a screw joint is related to the success
and technique in placement of the screw preload. Torque rotational forces on
a screw may be measured in newton-centimeters (N-cm). Too large of a
torque (exceeding manufacturers' recommendations) leads to a low clamping
force, which increases the risk of loosening. The clamping forces on a metal-
to-metal screw component are one of the more important considerations for
long-term screw fixation. The joint strength is improved the most by
achieving ideal clamping forces. The clamp force is directly proportional to
the force used to tighten the screw or the preload.
The torque applied to a screw component affects both the compressive
forces in the threads and the compressive force applied to the head of the
screw on the recipient component. The torque applied to the screw will also
result in tensile forces within the male component of the screw. The
compressive and tensile forces from the torque forces are magnified because
they are applied to the inclined plane of the screw components. The tensile
forces attempt to lengthen (strain) the screw when adequate torque is
applied. The strain (change in length divided by original length) of the screw
is also related directly to the amount of torque force. The higher the force,
the greater the strain. Too great a torque force causes plastic or permanent
deformation or a permanent change in the material, at which point the screw
is no longer retrievable and additional force causes fracture of the screw. Too
large a torque results in fracture of the screw or stripping of the thread
components (Fig. 16.27).
FIG 16.27 The abutment screw male (light gray) engages the female receptor site
(blue arrow), and as it rotates in position, the male component is stretched (strain) in
relation to the preload force. If too large force is applied, the screw will be deformed
leading to fracture or screw loosening. (From Misch CE: Dental implant prosthetics, ed 2, St
Prevention
Ideal Torque.
The suggested amount of the torque for a preload should be 75% of the value
to reach permanent deformation of the screw material.32 The amount of
preload applied to a screw joint should be consistent and adequate enough to
cause deformation (strain) within the screw thread. In the original screw
retention system of Nobelpharma from 1980 to 1990, only finger pressure
from a handheld screwdriver was used to tighten screws. However, a hand
screwdriver has been shown to produce an inconsistent torque value. In a
study by Misch with 136 dentists, the average torque placed on a screw joint
with a hand screwdriver was 11 N-cm and ranged from 5 to 21 N-cm. As a
consequence, abutment and screw loosening during that era was observed in
almost 50% of the restorations.
Consistent Torque.
A torque wrench is required to obtain a consistent value of torque. However,
several reports have shown that most torque wrenches are not completely
accurate and components may corrode after autoclaving many times, which
may increase the torque applied to the system.33,34 There exist two types of
torque wrenches, friction and spring. Studies have shown that spring-type
wrenches are more accurate and have less chance of over-torquing the
abutment screw.
Autoclaving hand torque wrenches in the open position and the clinician
testing the torque wrench before use are suggested to make sure the
components are not frozen in place, which will increase overtorque.
Periodically, the torque wrench should be recalibrated or replaced (≈ after 100
autoclave cycles) by the implant company or manufacturer (Fig. 16.28).
FIG 16.28 Torque wrenches. (A) Various types of torque wrenches, friction
wrenches, and spring wrenches. (B) If the torque wrench is a preset release type,
make sure it is autoclaved in the open position (arrow). (C) A torque wrench, which
has significant debris and corrosion (arrow). This can lead to incorrect torque
values.
Prostheses Fractures/Occlusal Material Fracture

In a retrospective analysis by Kinsel and Lin, porcelain failures of metal
ceramic crowns and fixed partial dentures supported by implants ranged
from 0% to 53% of patients and were directly related to force factors.35 For
example, whereas 35% of patients with bruxism (and 19% of the implant
crowns) experienced porcelain fracture with implant-supported prostheses,
17% of patients without bruxism had at least one of the porcelain units
fractured. When implant prostheses opposed a denture, no fracture was
observed. When implant prostheses opposed each other, 16% of the dental
units experienced a fracture of porcelain. The higher forces in the implant
system (including the occlusal porcelain) were related to a dramatic increase
in biomechanical complications. The fracture rate was greatest for bruxism
patients or group function occlusal patients with 34.9% and 51.9% of patients,
respectively, affected. The percentage of porcelain units that fractured in
these two conditions were 18.9% and 16.1%, respectively. Note that the
incidence of porcelain fracture, even in patients without higher force
conditions, is greater than observed with natural teeth.
Etiology
The second most common complication for fixed prostheses on natural teeth
is porcelain fracture. Occlusal material fracture is more common with
implants than natural teeth because of the lack of periodontal stress relief
with implants and a resultant higher impact force to the occlusal material.36
Material.
Porcelain, acrylic, and composite fractures may occur under excessive loads
or even with a lesser load of longer duration, angulation, or frequency.
Acrylic or composite materials fracture more easily than porcelain, metal, or
enamel. The compressive strength of acrylic resin is 11,000 psi compared with
40,000 psi for enamel.37 Composite resin is three times stronger than acrylic.
Acrylic fractures more often occur when used as a crown and bridge occlusal
veneer than does porcelain fused to gold.
Acrylic fracture is a much more common complication for fixed
reconstructions than for removable prostheses. Acrylic denture teeth on
traditional dentures do not sustain the forces developed in implant-
supported restorations. In addition, unlike porcelain, acrylic obtains its
strength by bulk. Mechanical retention must be incorporated in the metal
superstructure with proper resistance to the forces of occlusion. Posterior
acrylic or composite facings often fracture because of the inadequate bulk
and inadequate yield and fatigue strengths compared with the bite force
developed under parafunction or on cantilevers for fixed restorations (Figs.
16.29 to 16.31).
FIG 16.29 Acrylic fracture. (A) Cantilevered acrylic FP-3 fracture. (B–C) The
etiology of fracture is lack of metal extension leading to unsupported acrylic.
FIG 16.30 Metal substructure fracture. (A) FP-3 fracture through the most distal
abutment. (B) FP-3 cantilever fracture. Note the attrition of the acrylic from
excessive, repeated forces. (C) Resultant metal substructure fracture.
FIG 16.31 (A) Porcelain fracture on posterior implant. (B) Anterior porcelain implant
prosthesis fracture.
Monolithic zirconia is a relatively new restorative material with exceptional

mechanical properties in comparison to ceramics available today in dentistry.
Zirconia exhibits very high flexural strength (i.e. 900–1200 MPa) and fracture
resistance and toughness (i.e. 9–10 MPa). Additionally, monolithic zirconia
has solved many of the chipping problems associated with zirconia veneer
ceramics as studies have show a complication rate of for single crowns after
2–3 years and 3%–36% for fixed prostheses after 1–5 years.37a (Fig. 16.32).
FIG 16.32 (A) Zirconia Veneer—common complication is chpping and fracture, (B)
Monolithic Zirconia—material has been shown to be superior to other implant
restorative materials as it exhibits high fracture resistance and exceptional flexural
strength.
Cement vs. Screw.

A decreased incidence of porcelain or acrylic fracture of the prosthesis has
been observed with cement-retained restorations when compared with
screw-retained prostheses. The screw hole may increase stress concentration
to the restoring material and more often leads to unsupported porcelain. For
example, a study presented by Nissan et al examined the porcelain fracture
incidence of screw-retained restorations compared with cemented
prostheses. The study used a split-mouth evaluation for bilateral edentulous
sites in partially edentulous patients. Ceramic fracture was 38% for screw-
retained vs. 4% for cemented prostheses. The mean loading period for these
restorations was 5 years (Table 16.2).38
TABLE 16.2
Occlusal Material Characteristics
P orcelain Gold Resin Zirconia

Esthetic s + − + +/−
Impac t forc e − + + +
S tatic load + + + +
Chewing effic ienc y + + − +
Frac ture − + − +
Wear + + − +
Interarc h spac e − + − +
Ac c urac y − + − +
+, Favorable; −, unfavorable.
Reduce Force.
Implants, components, and the prosthesis are subjected to loads with a
broad range of magnitude, duration, direction, and frequency. As a result,
permanent deformation may result, and fatigue fracture and creep are
expected conclusions after years of function. These effects relate to factors of
force. Force-related issues need to be addressed. A common treatment that is
most widely underutilized is the use of occlusal guards. It is highly
recommended to treat all patients with an occlusal guard who exhibit
symptoms of parafunction and prosthesis situations that are prone to
fracture (implant prosthesis against implant prosthesis).
Ideal Porcelain Thickness.

The ideal thickness of porcelain to minimize the possibility of breakage is
approximately 2 mm.39 When the metal superstructure is not designed
properly, unsupported areas of porcelain may occur. This is especially true
with FP-2 or FP-3 prostheses due to their large volume of metal and
porcelain. Many dental laboratories fabricate thin metal copings over the
implants and teeth and then add porcelain to the final contour and occlusal
table. As a result, FP-2 or FP-3 restorations may have significantly more
unsupported porcelain (>2 mm). To limit the amount of unsupported
porcelain, the incisal edge and occlusal table position of the prosthesis must
be planned before fabrication of the metal superstructure. The technician
then may fabricate a full-contour wax-up of the final prosthesis and afterward
reduce the contour by 2 mm in the regions where porcelain is to be added. A
common error is to fabricate the metal framework, then determine the incisal
position (Fig. 16.32).
Uncemented Prosthesis
Uncemented prostheses are the third most common cause of fixed
prostheses failure on natural teeth.40 This complication is even more common
with implant abutments because they are more rigid and higher forces are
transmitted to the cement interface. Kourtis has reported an uncemented
prosthesis to be the second most common implant prosthetic complication,
which compose 25% of the documented complications.4
Etiology
Implant Abutment.
An implant prosthesis is most often susceptible to loss of cementation when
chronic loads or shear forces are applied to the prosthesis, which eventually
weakens the cement interface. With dental implants an uncemented
restoration is more common because of the inherent qualities that an
implant abutment exhibits. The implant abutment is usually made of
titanium alloy, which predisposes the restoration to inferior cement
adherence in comparison to a natural tooth. In dentistry today, most cements
are made to adhere to the interface with the dentin of a natural tooth. The
porosity of a natural tooth is far greater than most machined and lab-
fabricated abutments. Additionally, an implant abutment is usually smaller
in diameter than a natural tooth, resulting in less surface area. With less
surface area, a greater possibility of loss of retention may result. To
complicate the situation further, many clinicians often desire to make
implant restorations retrievable to more easily handle future complications.
A softer cement (temporary implant cement) is often used for implant
crowns, which additionally predisposes to uncemented restorations (Fig.
16.33).
FIG 16.33 (A) Implant abutment often has decreased surface area and nonideal
taper. (B) Most stock abutments have a smooth surface leading to possible
uncemented restoration. (C) Ideal preparation of the abutment leads to roughened
surface and increased cement retention.
Prevention
Retention/Resistance Form.
The tenets of retention and resistance of fixed prosthodontics are directly
applicable to implant abutments and include taper, surface area, height, the
geometry of the abutment preparation, surface roughness, and luting agents
(Box 16.3).
Box 16.3
Properties of Various Restorative Materials
Material Yield Strength (N/mm2) Tensile Strength (N/mm2) Elastic Modulus (N/mm2) Shear Modulus (N/mm2)
Titanium Alloy (TI-6AL-4V) 827 1050 1.048 × 10 6 4.428 × 10 3
Denture (Ac rylic ) 45 73 3000 1.2 × 10 3
Monolithic Zirc onia 1000 1300 2.1 × 10 5 6.06 × 10 3
Bullis G, Jokada M: Finite element analysis of the BruxZir full-arch implant prosthesis vs. the titanium-
bar-supported acrylic denture, Inclusive Magazine-Glidewell Laboratories, 6(1):42–47.
Abutment Taper.
The retention of a crown has been shown to rapidly decrease as the taper is
increased from 6 to 25 degrees.41 Taper degree is defined as the sum of both
sides of the preparation. A typical tapered diamond bur is ideally fabricated
to exhibit a taper of about 3 degrees on each side, or a 6-degree total taper.
The parallelism of the axial walls has been recognized to be the single most
effective factor for retention.42 The ideal taper originally was recommended to
be within 2 to 5 degrees of parallelism of the path of insertion, which also
places minimal stress concentrations on prepared abutments.43
Unfortunately, most manufactured stock implant abutments for cement
exhibit total tapers ranging from 10 to over 30 degrees. As a result, the
retentive surfaces of the more tapered, unprepared implant abutments
provide less retention than natural abutments. The preparation in the
cervical third of the abutment near the crown margins may be indicated in
the more tapered implant abutments to reduce the taper even when the path
of insertion is satisfactory (Fig. 16.34).
FIG 16.34 As the taper of an implant abutment is increased from 6 to 25 degrees,

the retention of the crown is rapidly decreased. (From Misch CE: Dental implant prosthetics,
Abutment Surface Area.

The surface area of an implant abutment influences the amount of retention.
The parameters of retention are similar for a tooth or implant and mainly are
influenced by the diameter and height of the abutment. Studies have shown
a linear increase in retention occurs as the diameter increases for
preparations with identical height, and a wider abutment offers greater
retention than a narrower abutment.44
The diameter of an implant abutment for cement retention is often less
than 5 mm (posterior region), which is comparable to that of a prepared
lateral incisor. The decreased surface area results in poorer retention than
most natural abutments. Wider implant abutments usually have more
retention than standard-size abutments. A wider abutment can be obtained
by two methods. First, a wider implant body has a corresponding wider
abutment for cement than a smaller-diameter implant. Second, the abutment
may have a wider emergence design than the implant body (or abutment
flare). The greater-diameter abutment has many advantages including
providing a greater taper, a thicker outer body wall, and more surface area for
retention (Fig. 16.35).
FIG 16.35 The greater the surface area of an abutment, the greater the retention.
Wider implant abutments (left) have greater retention than narrow-diameter implant
abutments (right). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Additionally, preparing or roughening the abutment surface will result an

increased surface area. The surface of stock or premanufactured abutments
should be modified with a diamond bur, cross-cut fissure carbide, or a
heatless stone. This will also increase mechanical retention for cementation
(Fig. 16.36).
FIG 16.36 (A) Stock abutments depicting smooth surface and significant taper. (B)
To increase surface area, abutments are roughened with heatless stone. (C)
Abutments roughened with cross-cut fissure bur. (D) Grooves may be placed within
the abutment, which increases retention and resistance form.
Abutment Height.
With dental implant abutments, the longer (increased height) the abutment,
the greater the retention, which results in fewer uncemented restorations.
The increase in height and the height-to-width ratio are determinants for
retention. Studies have shown a 2-mm increase in height will increase
retention up to 40%, especially when the abutment is only 4 mm in diameter.
An increase in height from 4 to 7 mm results in a 67% increase in retention.45
When the height of the implant abutment is less than 5 mm, the diameter of
the implant abutment is more critical to improve cement retention or
resistance. A customized abutment, larger in diameter than the stock
abutment, may be necessary to retain the restoration. In these instances,
additional abutment height not only increases the surface area but also
results in increased retention and resistance form. The longer axial walls
allow for more compressive and tensile force, rather than damaging shear
stress.
Geometry of Abutment.
Manufactured implant abutments for cement are usually circular in cross
section, providing little resistance to shear forces, especially on individual,
unsplinted crowns. The surface area of an abutment exposed to shear forces
is more critical than the total surface area under tensile force.46 The strength
of the cement interface is weakest under the shear component of a force. A
flat side on the implant abutment preparation decreases shear forces on the
cement interface. Whenever possible, a preparation with one or two flat sides
should be made on circular abutments for cemented prostheses (Fig. 16.37).
FIG 16.37 When the path of insertion is similar to the forces of mastication, sticky
food may place shear and tensile forces on the restoration and contribute to
uncemented prostheses. The implant body should receive a long-axis load to reduce
crestal stress. A path of insertion different from the occlusal force direction is
selected to decrease the shear loads to the cement seal from the sticky foods. A
path angle to the mesial facilitates preparation of the abutment and seating of the
restoration. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
A tapered implant abutment post may provide multiple paths of insertion

or removal. The addition of one or more parallel-sided grooves to an
abutment limits the path of withdrawal of the crown to one direction.47
Whenever possible, retentive elements such as grooves parallel to the path of
insertion should be added to a short or excessively tapered implant abutment
for cement. Additional grooves parallel to the path of insertion mechanically
resist rotational forces, place compressive forces on the cement in these
regions, and dramatically improve cementation.48 However, caution should
be exercised on the outer walls of two-piece abutments. These abutments
most likely have thin walls, and a groove may perforate or weaken the
abutment (Figs. 16.38 and 16.39).
FIG 16.38 A tapered abutment (left) has multiple paths of insertion or removal.
Grooves in the axial walls of the abutment limit the path of removal and decrease
uncemented restorations. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
FIG 16.39 Short abutments may increase retention and resistance by preparing
parallel grooves in the axial walls and by having a subgingival margin that increases
abutment height. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Abutment Surface Texture.

The surface texture of the abutment increases the retention of a restoration
by creating microretentive irregularities into which the luting agent projects.
The surface retention depends on the surface texture, the type of burs used
for the preparation, and the type and thickness of the luting agent.49 The
clinician may use a coarse diamond over the surface of the implant abutment
to increase the amount and depth of microscopic scratches on the surface to
more than 40 µm. The internal aspect of the casting can also be air abraded
with 50 µm of alumina to enhance its retention for cementation by as much
as 64%.50
Abutment Resistance Form.

The resistance form of an abutment opposes the uncementation of the
prosthesis against forces directed in apical, oblique, or horizontal
directions.46 Forces most likely to cause uncemented restorations related to
resistance are associated with parafunction, long spans, cantilevers, mobile
natural abutment teeth joined to implants, offset loading, and horizontal
loads from occlusal contacts.
When a force is directed within the margins of the abutment crowns,
leverage or tipping forces are limited. However, for implant-supported
prostheses, forces often are projected away from the abutment, usually
facially. In addition, excursive movements generate a leverage force,
especially on maxillary anterior abutments. The forces affect not only the
bone-implant interface but also the cemented abutment crown. The arc of
rotation of the crown influences the dislodging forces and is affected by the
direction of forces. The surface design and conditions of the preparation
farthest from the fulcrum or rotation point provide the resistance to
uncementation. The greatest resistance factors of the abutment for cement
retention to a moment force are a minimum abutment taper and maximum
abutment height. The higher the abutment, the greater its resistance to
lateral forces. The height of the abutment should ideally be greater than the
arc formed by the crown rotating about a fulcrum at the margin of the
opposite side of the restoration (Fig. 16.40).43
FIG 16.40 The dislodging force to a crown is related to the arc of rotation and is a
radius of a circle determined by the edge of the crown margin to the base of the
abutment (P3). The taller the abutment, the more resistance to the lateral
force. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Most implant abutment heights range from 4 to 10 mm. Some

manufacturers only supply ≈5-mm abutments to save the clinician
preparation time. Although this may be adequate in some situations, a
cantilever or fixed prosthesis with a large crown height often may require
longer implant abutments to resist the arc of removal or to resist lateral
forces in the anterior regions of the mouth. In cases with insufficient height,
ideally a custom abutment should be fabricated to increase retention and
resistance form (Fig. 16.41).
FIG 16.41 An increase in abutment height increases resistance to a lateral force
because more of the axial walls are placed under compressive forces (A). A short
abutment height has less resistance to a lateral force or cantilever force (B). (From
A wider-diameter implant abutment provides greater retention but may

offer less resistance to moment forces than a narrow abutment for a similar
height and degree of taper. The wider abutment for cement has a longer axis
of rotation and provides a reduced area of resistance at the opposite side of
the preparation. The worst resistance form is with a short, wide abutment,
for example, in a molar region (Fig. 16.42).
FIG 16.42 When a crown receives a lateral force, it tends to rotate upward on one
side of the implant. The arc of rotation is related to the diameter of the implant. The
greater the width, the greater height the arc of rotation. The abutment should be
higher than the arc of rotation. A wider implant requires a taller abutment than a
smaller-diameter implant (top). The arc of rotation is decreased when directional
grooves are prepared into the abutment (bottom). When abutment height is
questionable, directional grooves decrease the risk of uncementation (bottom
right). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Since the introduction of implant-supported cantilevered prostheses for

completely edentulous arches (i.e., Brånemark approach), the cantilever has
gained acceptance in implant dentistry. A cantilevered restoration also forms
an arc of removal when force is applied on the cantilevered portion. The
radius of the arc of displacement is equal to the anterior to posterior
contacts, not the A-P distance of the implants. The height of the implant
abutment farthest from the fulcrum or cantilever is the primary element for
resistance (Fig. 16.43).43
FIG 16.43 In a cantilevered prosthesis, tensile forces (F) are applied on the crown
farthest from the cantilever. The height of the implant abutment should be greater
than the arc of displacement of the prosthesis to increase the amount of resistance
and compressive forces to the cement seal below the arc of displacement. The
abutment farthest from the cantilever has the greatest height requirement. (From
Torque or bending moments placed on implants as a result of, for example,

cantilever bridges or bar sections may result in interface breakdown, bone
resorption, prosthetic screw loosening, and fracture of the implant,
components, or prostheses. However, one of the most common complications
of cantilevers is an uncemented restoration, which may occur as often as 60%
of the time in three-unit restorations. Proper restorative designs must
include features to resist such forces. The tensile and shear forces on the
abutment for cement retention from the posterior cantilever bar or pontics
may be reduced by vertical grooves on the buccal and lingual aspects of the
posterior abutments. As a result, the arc of displacement and the moment
force on the restoration are mechanically reduced (Fig. 16.44). Implants often
are placed more medial than the occlusal or incisal contacts of the overlying
prostheses. Both of these conditions create offset loads on the implant
abutments and greater tensile and shear forces on cement or screw fixation
devices. Buccolingual offset loads place the cement under tension, which may
increase uncementation. When the implant crown has an offset load to the
facial or lingual, the radius of rotation for dislodging forces is increased.
Additional resistance features are indicated on the mesial or distal of the
abutment (Fig. 16.45). These loads may be reduced on a cement-retained
prosthesis by placing vertical grooves on the mesial and distal aspects of the
restoration (Fig. 16.46). The same features are beneficial when horizontal
forces are introduced from a mutually protected occlusion or bruxism.
FIG 16.44 Buccal or lingual vertical directional grooves (or both) may be used with
a mesial or distal cantilever to modify the arc of displacement and decrease the risk
of uncementation. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 16.45 (A) An offset load is often placed on an implant crown. (B) This load acts
as a cantilever force and increases the radius of the arc of rotation for dislodging
forces. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 16.46 Mesial and distal vertical directional grooves decrease tensile and shear
forces on a prosthesis subjected to buccal or lingual offset loads. (From Misch CE:
In summary, when the cantilever is to the mesial or distal, the grooves or

boxes in the abutment preparation should be on the facial or lingual of the
preparation. When the cantilever is to the facial or lingual, the groove or box
should be placed on the mesial or distal of the abutment.
Prosthesis Complications
Improper Crown Margin
Etiology
Position.
The indications for subgingival margins described for teeth may be adapted
to implants and are only indicated for two reasons: increased retention and
esthetics. The advantages of supragingival margins suggest their use on
implants in the majority of situations that are out of the esthetic zones. Often
clinicians use the prefabricated abutments with a built-in flare. This is most
likely 1 mm above the implant body connection, which is often near the crest
of the bone, resulting in a deep subgingival margin.
Margin type.
Implant abutments are a common indication for minimum abutment margin
reduction because they are usually smaller in diameter than a prepared
natural tooth for a crown (5 mm or less). Reduction of the abutment diameter
to achieve room for porcelain or a beveled margin further decreases the
surface area for retention. Additional space for metal and porcelain in the
region of the margins typically is not required because the implant is already
smaller in diameter than the cervical aspect of the tooth and sufficient
volume is available for the restorative materials (Fig. 16.47).
FIG 16.47 Porcelain may be bonded to the knife-edge margin when additional bulk
and contour are necessary to develop the emergence of the crown. The porcelain
applied to the knife-edge margin may extend from the metal coping to any
emergence contour desired. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Position.
The subgingival margin for teeth or implants should not proceed further
than 1.5 mm below the free gingival margin even in the interproximal region.
It is important to note that the implant abutment flare is often 1 mm above
the implant body connection, which is often at the crest of the bone. When
the tissues are 2.5 mm thick (or more), the abutment flare is apical to the
crown margin location.
Margin Type.
Traditional preparations on teeth usually restrict the use of knife-edge
margins (minimum tooth preparation) to avoid overcontouring of the final
restoration. No scientific studies have stated that chamfers or chamfer and
aprons are superior to other finish lines, but the ease of preparation has
made them desirable and avoids excessive bulk of restorations. However,
whenever minimum implant abutment or tooth preparation is indicated, a
knife-edge finish line should be considered (Box 16.4).
Box 16.4
Indications for a Knife-Edge Margin
1. Implant abutments
2. Furcation regions
3. Interproximal region mandibular incisors
4. Lingual surface of mandibular posterior teeth
5. Convex axial surfaces
6. Abutment tilted more than 15 degrees
A knife-edge finish line also is indicated on the side of the implant or

natural abutment tilted more than 15 degrees. The amount of abutment
material removed for parallelism jeopardizes the width of the implant
abutment. Minimum structure removal of the implant or natural tooth on the
side toward the angulation is suggested to reduce these complications.
An exception to a knife-edge abutment margin is when the implant is too
facial or too close to an adjacent tooth and a porcelain crown margin is
desired. Crown margin designs such as a shoulder or chamfer can be selected
in cases in which the implants are placed too facially so as to create sufficient
space for the restoration and avoid overcontouring (Fig. 16.48). Another
indication for greater reduction is to allow for sufficient space in a
mesiodistal dimension for the prosthesis when two implants are too close to
each other. Preparation will need to be made to allow for ideal hygiene
practices.
FIG 16.48 The facial position of two of these implant abutments requires a chamfer
preparation to provide greater room for porcelain. (From Misch CE: Dental implant
Nonpassive Prosthesis
The passive fit of a prosthesis was first described by Brånemark to be
approximately 10 µm between the prosthesis and the implant or abutment.51
Other authors have shown marginal fits up to 100 µm are clinically
acceptable, with larger gaps having a greater chance of bacterial colonization
and increasing inflammation around the implants.52 The definition of passive
fit has evolved to be a clinical “acceptable fit in which the stress/strain
conditions are within the physiologic range that enables immature bone to
mature and remodel in response to occlusal loads following physiologic
connection.”53 A horizontal fit discrepancy leads to binding of the screws and
bending stresses in the implant system. A vertical fit discrepancy results in
the preload bringing the mating surfaces together, which predisposes the
screw to fatigue fractures and loosening.54
Ideally, when a prosthesis is retained by prosthetic (coping) screws, the
restoration passively sits on top of the abutments, and the prosthetic screws
fixate the two components together. When the prosthesis fits passively, the
screws place a compressive or tensile force on the abutments, but no force is
transmitted to the implant bodies (Fig. 16.49). If, however, the casting of the
prosthesis does not sit passively on the abutments for screws, the force of the
prosthetic screws is then transmitted to the implant bodies (Fig. 16.50).
FIG 16.49 (A) A screw-retained prosthesis ideally sits passively on the abutments,
and the prosthetic screws are held in place by compressive, tensile, and shear
forces. (B) Passive fit of the prosthesis occurs when no microgap is present and the
abutment is fully seated. ([A] from Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
FIG 16.50 If the prosthesis is not passive, the torque force placed on the prosthetic
screw is transferred to the implant body. (From Misch CE: Dental implant prosthetics, ed 2, St
A screw is a combination of inclined planes and wedges and is one of the

most efficient machine designs. A torque force of 20 N-cm applied on a screw
can move two railroad cars. This same force applied to a nonpassive casting
tends to distort the superstructure, underlying bone, and implant
components (Fig. 16.51). Because the force is constant, it can introduce
biomechanical creep into the system, which can fatigue materials and bone.
An implant does not predictably move within bone, yet retained stresses
from nonpassive castings must be accommodated through a bone
remodeling process.
FIG 16.51 A nonpassive casting will distort, and the implant may move or strain the
bone when the screw is torqued into position. (From Misch CE: Dental implant prosthetics,
As a result of all these variables, implant prosthesis distortions ranging

from 291 to 357 µm may be observed during the fabrication of the
restoration.55 Passive final restorations are highly unlikely when more than
two implants are splinted together and support a prosthesis with screw
retention as the method of fixation. If a casting has a 50-µm misfit, the
casting and implant may have to move 200 µm before the system is
completely passive (Fig. 16.52). This is a considerable risk to create crestal
bone loss, loose prosthetic screws, and implant failure.
FIG 16.52 A misfit of 50 µm of casting may require the prosthesis and implant to
move 200 µm before becoming passive. (From Misch CE: Dental implant prosthetics, ed 2,
Etiology
When the screw-retained prosthesis is attached to the abutment for screw
retention of the implant, no space exists between the crown and abutment.
Instead, a metal-to-metal system with zero tolerance for error is created.
Nonpassive screw-retained restorations may create permanent strain
conditions on the implant system that can be many times greater than that of
cemented prostheses. The microstrain applied to the bone may fall beyond
the overload zone and into the pathologic zone in which bone remodeling
occurs with crestal bone loss or even implant failure.
Nonpassive prostheses have been shown to be a primary cause of
unretained restorations, crestal bone loss, implant component fracture, and
implant mobility. A truly passive screw-retained dental restoration is virtually
impossible to fabricate on multiple splinted implants.56 There are too many
variables that are out of the clinician's control when attempting to fabricate a
prosthesis. Unfortunately, this process allows for zero tolerance for error, and
laboratory procedures may lack the precision needed for such an exact result.
Full-arch restorations more often are not passive despite an acceptable
metal try-in because the volume of porcelain or acrylic shrinkage may have
caused material distortion. Porcelain and acrylic shrinkage also is related
directly to material volume and may distort the superstructure even though
the superstructure was initially passive.
The “clamping down” while tightening the prosthetic screws of an
inaccurate structure may lead to screw loosening and fracture. After
prosthesis delivery, an abutment for screw retention or prosthesis screw may
loosen between appointments. This usually indicates that the casting is not
seated passively, yet the cause often is overlooked. Instead, the screws are
tightened again (often with more torque), and the bone must remodel to
release the strain in the implant system. This strain may lead to crestal bone
loss and possibly even implant failure.
Indirect Transfer Copings.

The use of indirect transfer copings on multiunit implant cases is a
significant source of nonpassive restoration. An indirect-transfer coping
utilizes the elastomeric properties of impression material. The indirect-
transfer coping is screwed into the abutment or implant body and remains in
place when a traditional “closed-tray” impression is set and removed from
the mouth. The indirect-transfer coping is removed from the implant
body/abutment in the mouth, connected to an implant body analog, and then
reinserted into the closed-tray impression. The copings usually have
undercuts that engage the elastic impression material when reinserted, are
slightly tapered to allow ease in removal from the impression, and often have
flat sides or smooth undercuts to facilitate reorientation in the impression
after it is removed.
The disadvantages of this technique include inaccuracies within the
elastomeric impression material, inability to insert the implant into the
correct position, and micromovement of the implant components. The
indirect impression transfer copings remain in the mouth when the
impression is removed and are replaced into the impression before pouring
the working or master cast. The greater the permanent deformation, the less
retentive the impression pin and the more variable its position in the
distorted receptor site. As stone is vibrated around the indirect transfer, the
attached abutment analog may move, and the final position may not be
accurate relative to the intraoral abutment position.
Another source of impression transfer error may occur when the
impression is made. An air bubble inadvertently may be present on the top
of the transfer coping; as a result, the transfer may be reinserted into this
void beyond its initial position. Some manufacturers have incorporated a
screw hole or slot in the top of the transfer coping, which should be blocked
out before making the impression. Otherwise, the positive replica in the
impression may prevent the indirect transfer from seating completely in the
impression before the pouring of the master model. This will result in
definite inaccuracies of the true position of the implant bodies.
Prevention
Impression Material.
Clinicians must understand the advantages and disadvantages of impression
materials. The dimensional change of the impression material from 2
minutes after it leaves the mouth to 24 hours later is an important property.
The amount of change can be used as a gauge to evaluate other properties of
the material. All elastic impression materials shrink after they are removed
from the mouth.57 The rate of shrinkage is not uniform. In general, about half
of the shrinkage occurs during the first hour after removal from the mouth.
The greatest accuracy occurs if impressions are poured soon after they are
made. Polyethers absorb water, which increases dimensional change, and
should not be stored in this medium. In addition, most impression materials
continue to change after the 24-hour period. The exception to this rule is
addition silicones, which are stable and may not change for many days. The
greatest dimensional change occurs with condensation silicones (Table 16.3),
which exhibit more than a 0.5% dimensional change. This change is clinically
relevant. Superstructures fabricated from these models will be less precise.
The use of condensation silicone should be avoided. Polysulfide has about
half the amount of shrinkage as the condensation silicones (0.2%). This also
may be clinically relevant. Polysulfide continues to shrink dramatically after
24 hours.58 Pouring of the impression as early as possible is strongly advised.
In a study comparing tray and impression material performance over time,
addition silicone impression materials exhibited the longest stability, with up
to 720 hours.59 Although varied results have been published, the vast
majority of studies appear to conclude that the least amount of dimensional
change occurs with addition silicones (0.06%) and polyethers (0.1%). The use
of these materials to make the final impression for a screw-retained
restoration is strongly suggested (Fig. 16.53).
TABLE 16.3
Setting Properties of Elastic Impression Materials
P ermanent Deformation (%) Dimensional Change at 24 Hours (%)

Polysulfide 3.0 0.22
S ilic one 0.4 0.58
Condensation 0.07 0.06
Addition
Polyether 1.1 0.10
FIG 16.53 Impression materials. All impression materials shrink after setting. This
results in the implant analogs being in a different position than in the mouth.
Silicones and polyethers are the most dimensionally stable materials for final
impressions.
Laboratory Process/Materials.
Almost all laboratory materials will have associated inaccuracies. Dental
stone has been shown to expand 0.01% to 0.1% and does not correlate to the
dimensional changes of impression materials.60 In addition, the wax patterns
distort while setting or spruing, and the investment material expands a
variable amount.61 The metal castings shrink when cooled, and the shrinkage
does not permit an accurate metal-to-metal connection.55 The metal
superstructures are often thicker and larger in implant prostheses than in
traditional prostheses because the implant abutment is of reduced diameter,
and bone loss volume often is replaced by the final prosthesis. Dimensional
changes during metalwork fabrication are correlated directly with the size of
the casting. The marginal fit and tolerance between the implant analog and
implant abutment are often different from actual implant and abutment
components.62 Implant components are not all fabricated to exact
dimensions, and each transfer of an implant component has a slightly
different size, which leads to misfit and is magnified by the number of
different pieces used during the fabrication steps.
As a result of all these variables, implant prosthesis distortions ranging
from 291 to 357 µm may be observed during the fabrication of the
restoration.55 Passive final restorations are highly unlikely when more than
two implants are splinted together and support a prosthesis with screw
retention as the method of fixation. If a casting has a 50-µm misfit, the
casting and implant may have to move 200 µm before the system is
completely passive. This is a considerable risk to create crestal bone loss,
loose prosthetic screws, and implant failure (Fig. 16.54).
FIG 16.54 (A) Metal shrinkage may lead to a nonpassive casting. When the bar is
fabricated in two or more sections, the volume of metal is reduced, and the amount
of shrinkage is minimized. (B) When the casting is made in sections, it then may be
laser soldered together. The two-step cross section results in a stronger union than
when the sections are split in one dimension. (From Misch CE: Dental implant prosthetics,
Impression Technique.
Various techniques have been suggested to achieve an accurate master cast.
The precise transfer of the spatial relationships of implants from the mouth
to the master cast with an impression is the first and critical step to ensure
passive fit of implant framework. To maximize the accuracy of the impression
process, an understanding of direct vs. indirect and open vs. closed
impression technique must be understood. A direct-transfer impression
coping consists of two components, a hollow transfer coping (often square)
and a long central screw to secure it to the abutment or implant body. An
“open-tray” impression tray is used to permit direct access to the long central
screw securing the direct-transfer coping. After the impression material is set
in the mouth, the direct-transfer coping screw is unthreaded to allow removal
of the impression from the mouth. The square coping remains in the
impression, seated on the implant without fixation. This technique utilizes
the advantages of impression material with rigid properties and eliminates
the error of permanent deformation because the transfer coping remains
within the impression until the master model is poured and separated. They
are also less likely to be rotated or moved during the model fabrication
compared with the indirect techniques.
Impression Recommendation.
Square impression coping with a direct open-tray technique has been shown
to be much more accurate than a tapered impression coping and stock
tray.63,64
When evaluating the splinting of impression copings as per the Brånemark
et al recommendation, there have been many controversies.65 The basis of
joining transfer copings together with acrylic resin is to stabilize and prevent
any micromovement of the copings during the impression process. The
problem in the past with autopolymerizing resin is the inherent shrinkage of
the material. Acrylic resin has been shown to have a total shrinkage of acrylic
resin between 6.5% and 7.9% in the first 24 hours, with 80% of shrinkage
occurring in the first 17 minutes after mixing.66 Another material that has
been shown to be superior is impression plaster, which has a setting
expansion of 0.01% and 0.12%.67 Impression plaster is quick setting, very rigid
with no distortion, easy to manipulate, and inexpensive. If acrylic resin is
used, a resin scaffold should be fabricated 24 hours in advance and then
separated and fused together with a low shrinkage resin (e.g., Pattern Resin
[GC America Inc.]).
Treatment
Modification.
If a cemented prosthesis is not passive, the casting or abutment may be
modified slightly at the same try-in appointment. High-speed carbides with
copious amounts of water may be used to modify the abutment, adjust the
internal aspect of the casting, or both, and may provide an immediate
solution. The internal aspect of the casting should always be evaluated for
any distortions.
Soldering.
A screw-in prosthesis that is not clinically passive requires casting separation
and soldering of the casting or a new impression. The separation of the metal
superstructure must respect specific dimensions to ensure the precision of
the soldering (0.008 inch). Too much space causes solder shrinkage and a
weak joint; too little space may cause distortion from expansion during
heating of the casting.68 Indexing the separate pieces also requires greater
time, and the patient must return for another appointment after the
laboratory process of soldering, which includes an additional laboratory fee
(Figs. 16.55 to 16.57).
FIG 16.55 Long screws from the impression transfers are used to secure the
sectioned bar. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 16.56 Indirect technique. (A) After soft tissue healing, the permucosal
extension is removed from the implant body. (B) An “indirect” impression transfer
coping is inserted into the implant body. (C) A “closed-tray” impression is made of
the indirect impression transfer coping. (D) The indirect impression transfer coping
is removed from the mouth and attached to the implant body analog. (Two-piece
transfer and ball-top screw allow the hex of the implant module to be transferred to
the analog.) (E) The implant body analog and indirect impression transfer is
reinstated into the impression. (F) The indirect impression transfer is reinserted into
the impression. (G) A working model is made with dental stone. A soft tissue replica
may be used around the implant body. (H) A patient model with implant abutment
inserted into the implant analog replacing the first molar. (I) The prosthesis is made
and inserted into the mouth. ([A–G] Courtesy BioHorizons Implant Systems, Inc.; [H–I] From
FIG 16.57 Direct technique. (A) A permucosal extension is removed after initial soft
tissue healing. (B) A “direct” impression transfer coping is inserted into the implant
body. (C) An “open” impression tray with an opening over the impression transfer is
positioned over the implant to verify its position. (D) An impression is made of the
impression transfer coping and (E) allowed to set. (F) After the impression sets, the
screw is unthreaded and removed from the transfer coping. (G) An implant analog is
attached to the transfer coping while it remains in the impression. (H) The implant
body analog is a direct transfer because the transfer coping is never removed from
the impression. (I) A soft tissue replica material is often used around the implant
transfer before the stone model is poured. (Courtesy BioHorizons Implant Systems, Inc.)
Splinted vs. Independent Implant Crowns
Etiology
In implant dentistry today, many clinicians use the same concepts and
protocols for implant prosthetics that they do with prosthetics on natural
teeth. However, there are many misconceptions concerning splinting vs.
nonsplinting of implants. The clinician must have a complete and
comprehensive understanding of the differences and misconceptions
between prosthetic rehabilitation of implants vs. natural teeth.
Independent Crowns (Natural vs. Implants).

The primary advantages for independent crowns are related to biologic
complications on natural teeth. A single crown has a caries risk of less than
1% within 10 years. However, when natural teeth are splinted together, decay
at the interproximal margin often occurs at a rate of more than 20%.69 In
addition, the endodontic risk is increased when crowns are splinted. Whereas
a single crown has an endodontic risk of 3% to 5.6%, splinted teeth have an
endodontic risk of 18%. Independent units reduce the incidence of
complications and allow the practitioner to more readily treat these
complications. However, implants do not decay or need endodontic therapy.
As a result, independent units on implants would not be required to address
these complications.
Splinted Crowns (Natural vs. Implants).

The primary perceived advantage of restoring implants as independent units
is interproximal hygiene. When natural teeth crowns are splinted,
interproximal aids are difficult to use. This is because the roots of the teeth
are often less than mm apart. However, in ideal placement of implants,
there will be a ≈3 mm separation. Most interproximal aids (e.g., floss
threader, proxy brush) can easily reach and clean an intraimplant region.
Unfortunately, fewer than 8% of our patients floss daily, and an even lower
percent use any interproximal aid when their natural teeth are splinted
together.70 Because more than 90% of patients do not floss and those who do
can more easily use an interproximal device between implants, the perceived
advantage of improved hygiene is not a relative concept for most implant
prostheses. Additionally, implants do not have the inherent disadvantages of
natural teeth, in that they do not decay and are less prone to bone loss from
bacterial plaque than natural teeth (Fig. 16.58).
FIG 16.58 Individual vs. splinted implant crowns. (A) Individual implant crowns in
the posterior mandible with associated crestal bone loss. (B) Individual implant
crowns further compromised by an increased crown-implant ratio, large cusp height,
and anterior cantilever. (C–D) Ideally splinted crowns, which are significantly
stronger and distribute force much better than individual crowns.
Porcelain Repair.
Many clinicians will recommend the use of independent crowns on dental
implants so they may repair porcelain fracture if it occurs. An evaluation of
the forces on the porcelain of splinted vs. nonsplinted implants must be
understood. When implants are independent, the margins of porcelain-to-
metal crowns are most often placed over unsupported porcelain with shear
loads, which increases the risk of porcelain fracture (interproximal). When
dental implants are splinted together, the implants are supported by metal,
which results in the porcelain being placed under compressive forces.
Splinting Is More Difficult.
Another perceived reason for independent implant crowns is the belief that
splinting makes the case more technically challenging. As individual units,
the interproximal contacts can be modified to seat the individual crowns.
Fully seating all the implant crowns, although more time consuming, is
supposedly a more accurate technique. The authors disagree with this
thought process. The cause of casting misfit is related to impression material
shrinkage, stone expansion, and analog variance of the abutment or implant
body. Although this may have been an issue in the past, advancements with
dental materials and techniques have led to the ability to obtain an accurate
prosthesis.
Planning for Failure.

Another perceived advantage of independent implant units is if one implant
fails, the clinician needs to replace only one implant and crown. However, the
implant failure often causes bone loss, which then requires bone
augmentation, implant reinsertion, and crown refabrication. These
procedures are usually more difficult to perform around existing teeth and
implants than the original implants.
Advantages of Splinted Implant Crowns.

There are many advantages to splinting dental implants together. To
maximally benefit from an increased number of implants, the implants
should be splinted together. Splinted implants have the following advantages
over independent units:
Increase the functional surface area of prosthesis support.

Splinted implants increase the functional surface area to the support system.
When implants are independent, they cannot share the occlusal load from
one implant to another.71 As a consequence, with splinted implant crowns,
the risks associated with the biomechanical overload to the implant system
are reduced (occlusal porcelain, cement, screw, marginal bone loss, implant-
bone interface stress, and implant components failure). If a maxillary second
molar implant is connected to a maxillary first molar implant, it can share an
occlusal load to the first molar even when the second molar has no direct
occlusal load. As a consequence of splinting, implant survival may be greater.
For example, Quiryman et al72 reported success rates of 90% for single
implants, 97% for two splinted implants, and 98% for three splinted
implants.
Increase the A-P distance (A-P spread) to resist lateral loads.

An anteroposterior (A-P) distance between two or more implants is a benefit
for any angled load or cantilever, especially when three or more implants are
not in a straight line. The biomechanics of an arch is of most benefit because
there are five different planes connected together (bilateral molar, bilateral
premolar, bilateral canines, and an anterior implant). Rotational forces,
angled forces, and cantilevers to the facial or lingual (offset loads) are all
reduced when splinted implants are not in the same plane and receive a load
comparable to individual units (Fig. 16.59).73
FIG 16.59 A-P splint. (A–C) The mandible may have a square, ovoid, or tapering
shape. The anteroposterior distance between the most distal implant on each side
and most anterior implant is variable and directly related to the shape of the arch. (D)
The anteroposterior (A-P) distance is determined by a line drawn from the distal
portion of the distalmost implant on each side of the arch and another parallel line
drawn through the center of the anteriomost implant from the cantilever. (From Misch
Increased retention and resistance form of the prosthesis.
Splinted implant crowns provide greater abutment surface area and
resistance form; thus the prosthesis has more retention. For a cementable
prosthesis, there is less force transferred to the cement interface, which
results in less likelihood of uncementation. This is especially significant
when the abutments are short or lateral forces are present. Both cement
retention and resistance form are increased with splinted crowns. The
prosthesis is less likely to become uncemented, so less hard cements or
temporary cements may be used, which allows the restoration to be more
easily removed when necessary (Fig. 16.60).
FIG 16.60 Splinted implant crowns have more abutment surface area and
improved retention and resistance form. (From Misch CE: Dental implant prosthetics, ed 2, St
Ease of removing the prosthesis for abutment screw loosening.

If a prosthesis does become partially retained or an abutment screw becomes
loose, a splinted restoration is much easier to remove than individual
nonsplinted units. The impact removal force to an individual crown is
decreased by the loose abutment screw. This results in difficulty in removing
the crown and possible damage to the internal threads of the implant body.
In addition, attempting to engage a single crown margin is often difficult for
the crown remover, especially when a subgingival margin is present. As a
consequence, the crown may need to be cut off and destroyed to gain access
to the loose abutment screw. With a splinted prosthesis, a crown remover is
easily engaged into the interproximal space of the prosthesis.
Decrease the risk of marginal bone loss because of better force

distribution.74
Splinted implants have less stress transmitted to the crestal marginal bone.
Force distribution is more beneficial with a splinted prosthesis; thus less
force is transmitted to the osseous tissue. Increased stress to the prosthesis
is related to marginal bone loss around an implant.
Decrease the risk of porcelain fracture.

Splinted crowns have less risk of porcelain fracture. The marginal ridges (and
often buccal mandibular cusps) of implant crowns are usually unsupported
by the metal work. As a consequence, the load on a marginal ridge is a shear
load, with porcelain weakest to shear loads. In a report by Kinsel and Lin,
porcelain fractures occurred in 35% of patients with implant crowns,
especially when bruxing patients were restored in group function. Splinted
implant crowns have the metal connectors of the casting below the marginal
ridges. The interproximal porcelain has a compressive force on the porcelain,
and porcelain is strongest to compressive loads.75
Decrease the risk of abutment screw loosening.

Splinted implants reduce the risk of screw loosening. One of the highest
prosthetic complications with single tooth or independent implant crowns is
abutment screw loosening. In a review of the literature by Goodacre et al,
independent crowns had a screw loosening rate of 8%, with a range as high
as 22%.3 In a report by Balshi and Wolfinger, single-tooth implants replacing
a molar had 48% screw loosening over a 3-year period. When two implants
were splinted together to replace a molar, the incidence of screw loosening
was reduced to 8% over the same time period.76
Decrease the risk of implant component fracture.

Splinted implants distribute less force to the implant bodies, which
decreases the risk of implant body fracture. In a report by Sullivan and
Siddiqui, a 4-mm single implant replacing a molar had implant body fracture
in 14% of the cases. In comparison, multiple implants splinted together
report a 1% implant body fracture rate.3,77
Easier to treat upon implant failure.

When an independent implant fails, the implant most likely will need to be
removed, which usually indicates bone grafting prior to the reimplantation.
This may require multiple surgeries over a long time period with great
expense to the clinician. In contrast, when multiple crowns are splinted and
an implant fails, the affected implant may often be removed and the implant
crown converted to a pontic using the same prosthesis. As a result, rather
than several surgical and prosthetic procedures over an extended period
when independent units are restored, the problem may be solved in one
relatively short appointment.
Mandibular Full-Arch Splinting—Flexure

In the mandible, full-arch splinting with implants distal to the mental
foramen may lead to significant complications with the patient. Patients may
exhibit myofascial pain complications along with limited opening from a full-
arch splint.
Etiology
Medial Movement.
The body of the mandible flexes distal to the foramen upon opening and has
torsion during heavy biting with potential clinical significance for full-arch
implant prostheses. Many reports have addressed the dimensional changes
of the mandible during jaw activity as a result of masticatory muscle action.
Five different movements have been postulated. Medial convergence is the
one most commonly addressed.78 The mandible between the mental
foramina is stable relative to flexure and torsion. However, distal to the
foramina, the mandible exhibits considerable movement toward the midline
on opening.79 This movement is caused primarily by the attachment of
internal pterygoid muscles on the medial ramus of the mandible. The
distortion of the mandible occurs early in the opening cycle, and the
maximum changes may occur with as little as 28% opening (or about 12 mm).
This flexure has also been observed during protrusive jaw movements.80 The
greater the active opening and protrusive movements, the greater the
amplitude of mandibular flexion. The amount of movement varies among
individuals and depends on the density and volume of bone and the location
of the site in question. In general, the more distal the sites, the more medial
flexure. The amplitude of the mandibular body flexure toward the midline
has been measured to be as much as 800 µm in the first molar–to–first molar
region to as much as 1500 µm in the ramus-to-ramus sites (Fig. 16.61A).
FIG 16.61 Flexure of mandible. (A) The flexure of the mandible during opening and
protrusive movements occurs distal to the mental foramina. The amount of flexure
depends on the amount of the bone volume and the sites in question. The medial
movement from the first molar to the first molar region may be 800 µm. (B) Unilateral
molar biting causes the mandible to undergo torsion with the bottom of the mandible
expanding outward and the crest of the mandible rotating medially. (Adapted from
Hylander WL: Mandibular function in Galago crassicaudatus and Macaca fascicularis: an in vivo
approach to stress analysis of the mandible, J Morphol 159:253–296, 1979.)
Torsion.
Torsion of the mandibular body distal to the foramina has also been
documented in both animal and human studies. Hylander evaluated larger
members of the rhesus monkey family (macaque) and found the mandible
twisted on the working side and bent in the parasagittal plane on the
balancing side during the power stroke of mastication and unilateral molar
biting (Fig. 16.61B).81 Parasagittal bending of the human jaw during unilateral
biting was confirmed by Abdel-Latif et al, who showed patients with implant
prostheses measured up to 19 degrees of dorsoventral shear.82 The torsion
during parafunction is caused primarily by forceful contraction of the
masseter muscle attachments (Fig. 16.62A). Parafunctional bruxism and
clenching may cause torsion-related problems in the implant support system
and prosthesis when the mandibular teeth are splinted from the molar-to-
molar regions.
FIG 16.62 Flexure of mandible. (A) The mandible flexes toward the midline on
opening or during protrusive movements as a result of the internal pterygoid muscle
attachments on the ramus. The mandible also torques, with the inferior border
rotating out and up and the crestal region rotating lingually. The movement is caused
by the masseter muscles during forceful biting or parafunction. (B) Some authors
propose that the ideal implant positions to support a mandibular full-arch prosthesis
are the bilateral molars and bilateral canines splinted together with a rigid structure.
These positions are not ideal because of the mandibular dynamics during opening
and function. (C) Panorex showing ideal treatment planning with implants between
the foramen. (D) Prosthesis. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Implants placed in front of the foramina and splinted together or implants

in one posterior quadrant joined to anterior implants have not shown these
complications related to the flexure or torsion of the mandible. Complete
implant-supported fixed restorations can halt the posterior bone loss
associated with edentulism, improve psychologic health, and produce fewer
prosthetic complications than removable restorations. All edentulous
mandibular patients should be given the option of having a fixed prosthesis.
However, the increase in forces of mastication, increase in force with patients
of greater force factors (e.g., parafunction, crown height space, opposing arch
type), or reduced bone density in the implant sites warrants an increase in
implant number or implant position in anterior and posterior implant sites.
Prevention
The concept of flexure and torsion does not affect the maxilla, where all
implants are often splinted together, regardless of their positions in the arch.
Prevention of mandibular flexure should include the following treatment
plans:
Bilateral Posterior Implants: If implants are positioned bilaterally in the

premolar/molar regions of the mandible, the final prosthesis should be
splinted with two sections. This will minimize the possibility of
flexure/torsion issues.
Anterior Implants with Unilateral Implants Posterior: Full-arch splinted

prostheses may be fabricated without concern regarding flexure/torsion
problems.
Anterior Implants with No Posterior Implants: Full-arch splinted prostheses

may be fabricated without concern regarding flexure/torsion problems.
Treatment
If a full-arch splinted prosthesis is fabricated and the patient exhibits
complications related to the flexure/torsion of the mandible, the prosthesis
needs to be remade or modified so that it is not fabricated in one piece (Fig.
16.62B).
Connecting Implants to Teeth

Prior to 1988, many practitioners connected an implant to one or two natural
teeth. These implants were designed to have either a fibrous tissue or a direct
bone interface. When the root form osseointegration concept of Brånemark
for full-arch edentulous fixed prostheses became more dominant in the mid-
1980s, these implants came to be used in partially edentulous arches. It was
hypothesized at the time that joining a rigid implant to a natural tooth would
cause biomechanical complications on the implant, implant prosthesis, or
both. Since that time, several reports have indicated that a rigid implant may
be joined to a natural tooth in the same prosthesis.83,84 In fact, implant-
cantilevered prostheses in partial edentulous patients have more reported
complications than when implants are joined to teeth.
There are more partially edentulous patients missing posterior teeth than
anterior teeth. As a result, the most common scenario for which a root form
implant may be joined to a natural tooth is in the posterior regions. Of these
cases, the most common scenario is as a terminal abutment in a patient
missing the molars. For example, if a patient is missing the first and second
molars in a quadrant (with no third molar present), the segment requires at
least two implants of proper size and design to independently restore these
two teeth. If adequate bone exists in the second molar and distal half of the
first molar but inadequate bone exists in the mesial half of the first molar, a
premolar-size pontic is required. The pontic may be cantilevered from the
anterior natural teeth or the posterior implants. Either of these options may
result in complications because of tensile forces on the cement seal of the
abutment farthest from the pontic.
The connection of natural teeth and osseointegrated implants within a
single rigid prosthesis has generated concern in publications, with studies
and guidelines for both extremes. In other words, some articles report
complications, but others state that no problem exists. To be more applicable
to a particular situation, more information is required to design a successful
treatment plan. Two prosthetic designs are available for the connection of
implants and teeth within the same prosthesis: a conventional fixed partial
denture (FPD) or an FPD with a nonrigid connector. To address this issue, the
mobility of the natural abutment should be assessed (Fig. 16.63).
apically 0 to 5 mm, and the tooth moves apically 8 to 28 mm but can rotate up to 75
mm toward the implant because of a moment force. The metal in the prosthesis can
flex from 12 to 97 mm, depending on the length of the span and the width of the
prosthesis creates little biomechanical risk when joined to a nonmobile tooth. (From
Etiology
The mobility of potential natural abutments influences the decision to join
implants and teeth more than any other factor. In the implant-tooth rigid
fixed prosthesis, five components may contribute movement to the system:
the implant, the bone, the tooth, the prosthesis, and implant and prosthetic
components.
Existing Tooth Mobility.

The tooth exhibits normal physiologic movements in vertical, horizontal, and
rotational directions. The amount of movement of a natural tooth is related
to its surface area and root design. The number and length of the roots; their
diameter, shape, and positions; and the health of the periodontal ligament
primarily influence tooth mobility. A healthy tooth exhibits no clinical
mobility in a vertical direction. Actual initial vertical tooth movement is
about 28 µm and is the same for anterior and posterior teeth.85 The
immediate rebound of the tooth is about 7 µm and requires almost 4 hours
for full recovery, so additional forces applied within 4 hours depress the tooth
less than the original force.86 The vertical movement of a rigid implant has
been measured as 2 to 5 µm under a 10-lb force and is mostly attributable to
the viscoelastic properties of the underlying bone (Fig. 16.64).87 The implant
movement is not as rapid as the tooth movement because the tooth
movement is a consequence of the periodontal ligament, not the surrounding
bone elasticity.
FIG 16.64 Whereas a vertical force on a tooth results with 28-µm movement, an
implant moves only 2 to 5 µm. (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
Horizontal tooth mobility is greater than vertical movement. A very light

force (500 g) moves the tooth horizontally 56 to 108 µm (Fig. 16.65). The
initial horizontal mobility of a healthy, nonmobile posterior tooth is less than
that of an anterior tooth and ranges from 56 to 75 µm, which is two to nine
times the vertical movement of the tooth.88 Initial horizontal mobility is even
greater in anterior teeth and ranges from 90 to 108 µm in healthy teeth.88
FIG 16.65 A healthy natural tooth may move laterally from 56 to 108 µm, with
anterior teeth moving more than posterior teeth. (From Misch CE: Dental implant
Muhlemann found that tooth movement may be divided into initial

mobility and secondary movement.88 The initial mobility is observed with a
light force, occurs immediately, and is a consequence of the periodontal
ligament. If an additional force is applied to the tooth, a secondary
movement is observed, which is related directly to the amount of force. The
secondary tooth movement is related to the viscoelasticity of the bone and
measures up to 40 µm under considerably greater force (Fig. 16.66). The
secondary tooth movement is similar to implant movement.
FIG 16.66 Teeth have a primary tooth movement related to a periodontal ligament.
This accounts for the 28-µm apical and 56- to 108-µm lateral movement. They also
have a delayed secondary mobility related to the viscoelastic nature of bone. (From
Prosthesis Movement.
A fixed prosthesis that connects a tooth and implant also illustrates
movement. Studies have shown that with a 25-lb vertical force, a prosthesis
with a 2-mm connector fabricated in noble metal results in a 12-µm
movement for one pontic and 97-µm movement for a two-pontic span (Fig.
16.67).89 The FPD movement helps compensate for some difference in vertical
mobility of a healthy tooth and implant.
FIG 16.67 Bridge flexure is related to the cube of the span between abutments.
Whereas a one-pontic prosthesis may flex 12 µm, a two-pontic prosthesis flexes up
to 97 µm. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Rangert et al reported an in vitro study of a fixed prosthesis supported by

one implant and one natural tooth and showed that the abutment or gold
cylinder screw joint of the system also acts as a flexible element. The inherent
flexibility matched the vertical mobility of the natural tooth. The minimal
movement of the tooth and the fact that implant, prosthesis, and abutment
components have some mobility indicate that the risk is small in the vertical
direction with the biomechanical difference of an implant and a tooth in the
same prosthesis when one or two pontics separate these units.90
Implant Mobility.
The implant-bone interface also exhibits lateral movement. Sekine et al
evaluated the movement of endosteal implants with rigid fixation and found
a range of 12 to 66 µm of movement in the labiolingual direction.87 Komiyama
measured 40 to 115 µm of implant movement in the mesiodistal direction
under a force of 2000 g (≈4.5 psi) and a labiolingual range of 11 to 66 mm (Fig.
16.68).91 The greater implant movement in the mesiodistal dimension
corresponds to the lack of cortical bone around the implants in this direction
compared with the thicker lateral cortical plates present in the labiolingual
dimension. The mobility of implants varies in direct proportion to the load
applied and the bone density, which reflects the elastic deformation of bone
tissue.
FIG 16.68 Implant movement is more mesiodistal than faciolingual, reaching

values between 40 and 115 µm. (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
Although the implant has a range of mobility, the mobility is related to the
viscoelastic component of bone, not the physiologic aspect of a periodontal
membrane. As such, when the implant and tooth are loaded in the same
prosthesis, the tooth immediately moves (primary tooth movement), and
then the tooth and implant move together. In other words, secondary tooth
movement is similar to implant movement because they both depend on the
viscoelasticity of the bone. In a study by Sekine et al, when a tooth was
gradually loaded over a 2-second period, the tooth immediately moved 36 µm
and then gradually moved an additional 6 µm. The implant gradually loaded
had movement directly related to the amount of load and eventually moved
as much as 22 µm. The secondary tooth movement was similar to the implant
movement (Fig. 16.69).87
FIG 16.69 Sekine compared tooth movement with a gradual load over 2 seconds
(left) with implant movement. The secondary tooth movement was similar to implant
movement. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
In summary, when all factors are considered, an implant moves vertically

and horizontally, the abutments and prosthesis flex, and the tooth has apical
and lateral movements. However, the major difference in movement between
implants and teeth is more related to the direction of movement (the
horizontal dimension is more compared to much less difference in the
vertical dimension).
Guidelines for Joining Implants to Teeth

No lateral force on prosthesis.
To decrease biomechanical conditions, which increase the risk of
complications, a requisite to join an implant to a natural tooth is that no
lateral force should be designed on a unilateral prosthesis. Lateral forces
increase the amount of tooth movement and decrease the amount of implant
movement (faciolingual vs. mesiodistal). Horizontal forces placed on an
implant also magnify the amount of stress at the crestal bone region.
Natural tooth with no clinical mobility.

A vertical movement or force placed on a posterior implant joined to a
healthy posterior tooth causes mesial tension on the implant. The implant
can move vertically 3 to 5 µm and mesially 40 to 115 µm, and a noble metal–
fixed prosthesis with one pontic allows mesiodistal movement of 6 µm (Fig.
16.70). A natural tooth with no clinical mobility could be connected rigidly to
an osseointegrated implant with no lateral forces because the implant, bone,
and prosthesis compensate for the slight tooth movement. Finite element,
photoelastic, and clinical documentation confirm that implants can be
connected rigidly to stable teeth.92 However, the occlusion should be
modified to allow the initial occlusal contacts on the natural tooth so that the
implant does not bear the major portion of the initial load.93
apically 0 to 5 mm, and the tooth moves apically 8 to 28 mm but can rotate up to 75
mm toward the implant because of a moment force. The metal in the prosthesis can
flex from 12 to 97 mm, depending on the length of the span and the width of the
prosthesis creates little biomechanical risk when joined to a nonmobile tooth. (From
The lateral mobility of healthy anterior incisor teeth often is recorded as (+)
with a range of movement from 90 to 108 µm. Visual clinical evaluation by
the human eye can detect movement greater than 90 µm. When the
horizontal mobility of a natural tooth (anterior or posterior) can be observed,
mobility is greater than 90 µm and too great to be compensated by the
implant, bone, and prosthesis movement. When the vertical posterior tooth
movement, vertical implant movement, mesiodistal implant movement, and
prosthesis movement are compared with the same conditions of a “mobile”
tooth with lateral loads, the biomechanical risk factors are not the same. One
of the primary conditions for joining an implant to natural teeth is the lack of
observable clinical movement of the natural abutment during functional
movement. Nonmobile posterior teeth with no lateral forces on the
prosthesis may join rigid implants. However, implants rarely should be
connected to an individual anterior tooth because (1) anterior teeth exhibit
more than tenfold greater clinical mobility than the implant, and (2) the
lateral forces applied to the restoration during mandibular excursions are
transmitted to the natural tooth and implant abutments.
When the natural abutment exhibits clinical horizontal movement or
conditions promote horizontal forces against the abutment tooth, two
options can be selected for the final prosthesis. The first, and the option of
choice, is to place additional implants and to avoid the inclusion of natural
abutments in the final prosthesis. This may include the extraction of the
mobile tooth and replacement with an implant. The other option is to
improve stress distribution by splinting additional natural abutments until
no clinical mobility of the splinted units is observed.
Rigid connectors are contraindicated.

Implants should not be joined to mobile teeth with rigid attachments, which
basically adds a cantilever on the implant (the tooth acting as a living pontic).
If the natural teeth are too mobile in relation to the implant in the same
prosthesis, several complications may occur that may be detrimental to the
tooth and implant. If the prosthesis is cemented, movement may break the
cement–implant abutment seal. Cement does not adhere as well to titanium
as to dentin. In addition, the mobile tooth will move (which decreases the
impact force) rather than break the cement seal on the tooth. However, the
rigid implant will have greater stresses applied to the cement (or screw)
retained crown. After the prosthesis is loose from the implant, greater stress
is applied to the natural mobile tooth. The tooth may increase in mobility as
a result or fracture as a consequence (especially when endodontic procedures
were performed) (Fig. 16.71).
FIG 16.71 Rigid connection implant. (A–B) Treatment plan involving connecting
posterior implant-supported crowns to natural teeth.
Nonrigid connectors are contraindicated.

A mobile attachment between the implant and natural tooth is usually not a
benefit. A mobile attachment moves more than an implant or a tooth.
Therefore, it is not an “attachment.” The pontic is cantilevered from the
implant with little to no support from the tooth. It is usually better to have a
rigid connector between implants and teeth than a mobile attachment.
Although nonrigid connectors have been advocated in the literature, a
nonrigid connector in a unilateral prosthesis rarely is indicated for implant-
fixed prostheses and may be detrimental.94 Nonrigid connection does not
improve the stress distribution between the different abutments and has
been reported to have caused migration of the natural teeth.95,96
If the nonrigid connector exhibits any clinically observed mobility, it moves
more than the implant. As such, the implant-supported part of the
restoration is cantilevered to the attachment. In addition, the nonrigid (or
mobile) attachment adds cost, creates overcontoured abutments, impairs
daily hygiene, and does not decrease the clinical tooth movement.
Prevent Tooth Intrusion.

When implants are joined to teeth that act as a terminal abutment, a
definitive cement should be used for the natural tooth. The tooth cannot
intrude unless it becomes unretained from the abutment (or has a nonrigid
connector between the units).
Reports of intrusion of the natural tooth connected to an implant usually
include the use of temporary cement to lute a coping to the natural
abutment, leaving the final restoration uncemented on the coping, or the use
of a nonrigid connector.97
A possible explanation for tooth intrusion may be that the tooth is pushed
vertically 28 µm but wants to rebound only 8 µm. The fixed prosthesis
rebounds immediately and pulls on the tooth. The cement seal eventually
breaks, causing a space to develop, which is first occupied by air. The
prosthesis then acts as an orthodontic appliance and continually pushes the
tooth in a vertical direction. Eventually, the space is occupied by saliva, and
hydraulics continue the downward force during mastication. The tooth
eventually submerges or intrudes from the prosthesis.
Ideal, Favorable Conditions.

An alternative may be to join the implant(s) to a natural tooth if all other
factors are favorable. This treatment option is more likely in the presence of a
division C−h ridge in the pontic region when inadequate bone height
adjacent to the natural tooth decreases the prognosis of a vertical bone graft.
This option is also available when a posterior implant is positioned too distal
to restore with a single crown. It is almost always better to splint the implant
to the adjacent tooth rather than fabricating a cantilevered crown from one
implant, especially when parafunction is present.
Narrow-Diameter Implants.
Another scenario in favor of this treatment plan is when the posterior
implants are of a narrower diameter than usual. When two division B root
forms are used in the posterior mandible to replace molars, there should be
no cantilever to magnify the force on the implants. Posterior pontics should
not be cantilevered from even two splinted division B root form implants
because they will have a greater biomechanical risk. An additional root form
implant or a natural tooth is usually required as an abutment for the fixed
prosthesis. When an additional implant insertion is not an option, the
posterior implants may be joined by a rigid connector (e.g., a solder joint) to
a natural tooth or teeth within the prosthesis, provided all dental factors are
favorable.
Intraoperative Prosthodontic Complications
Abutment Not Seated
If an abutment is not fully seated within the implant, the preload placed on
the screw will be insufficient. This will lead to an increased possibility of
screw loosening and prosthesis mobility. An opening or microgap will lead to
bacterial accumulation, which will result in soft tissue infection and
irritation. If left untreated, fracture of the screw or implant may occur (Fig.
16.72).
FIG 16.72 Abutment not seated. (A) Radiograph verifying space between abutment
and implant. (B) After correction, no space present between abutment and implant.
Etiology
When an abutment is torqued into an implant, care must be noted to fully
seat the abutment into the hex of the implant. In some situations, tissue or
bone may impede the full seating of the prosthesis, causing a microgap to
exist, which may lead to complications.
Prevention
When placing the abutment, insert the abutment into the implant until it is
fully seated. When the implant is significantly subgingival, this may be
difficult to determine. A radiograph should always be taken to confirm
complete seating.
Treatment
If the abutment is not seated via the radiograph, it should be treated in the
following ways:
Improper Placement.
Remove abutment, replace, then verify seating with a new radiograph.
Tissue Impingement.
Remove tissue with a tissue punch bur or scalpel, then verify seating with a
new radiograph (Fig. 16.73).
FIG 16.73 Soft tissue impingement. (A) Excess tissue preventing abutment from
complete seating. (B) Tissue punch bur used in latch handpiece. (C) Removal of
soft tissue impingement.
Bone Impingement.
Remove bone that is preventing the abutment from fully seating. A curette or
a profiling bur may be used. Verify seating with a new radiograph (Fig. 16.74).
FIG 16.74 Bone impingement. (A) Radiograph depicting mesial bone preventing
proper seating of abutment (arrow). (B) Profiling bur to remove bone. (C) Final
radiograph showing complete seating (arrow).
Pain on Abutment Placement

When placing the abutment into the implant body, sometimes pain will
result. This may be due to many reasons.
Etiology
Pain may occur from many possibilities.
Tissue Impingement.
Because of the lack of circular fibers, tissue collapse is very common after
permucosal extension removal. When placing the abutment, the tissue will
become pinched resulting in pain.
Implant Failure.
If the implant becomes infected or loses integration, in some instances when
pressure is placed on the implant, pain will result.
Prevention
Tissue Impingement.
To decrease the possibility of tissue collapse, abutment placement should be
completed without delay after the permucosal extension. The greater the
time period the abutment is out, the greater the chance of tissue
impingement.
Implant Failure.
Prior to abutment placement, clinical and radiographic evaluation of the
integration of the implant should be completed.
Treatment
Tissue Impingement.
Remove excess tissue with a tissue punch bur or a scalpel (see Fig. 16.73).
Implant Failure.
If the implant has mobility or circumferential radiolucency is present, the
implant should be removed (Fig. 16.75).
FIG 16.75 Pathology associated with a failed dental implant. Note the
circumferential radiolucency.
Pain on Application of Torque to Abutment

When applying torque to an implant, on rare occasions, the patient will
complain of pain.
Etiology
Tissue Impingement.
Because of the lack of circular fibers, tissue collapse is very common after
permucosal extension removal. If tissue impinges between the abutment and
the implant, a painful response may occur.
Implant Failure.
If the implant becomes infected or loses integration, in some instances when
pressure is placed on the implant, pain will result.
Poor Bone Quality.

If an abutment screw is torqued into place in poor quality of bone, an
unsupported force may be applied that may eliminate the osseous
integration of the implant.
Tissue Impingement.
Remove any excess tissue prior to abutment placement.
Implant Failure.
If the implant becomes infected or loses integration, removal of the implant
is indicated.
Poor Bone Quality.

When placing torque on an implant, always hold abutment with curved
hemostats or the use of an acrylic verification jig. This will help stabilize the
abutment (Fig. 16.76).
FIG 16.76 Counter-torque to decrease possibility of shear forces on the implant
body. (Courtesy BioHorizons Implant Systems, Inc.)
Abutment Will Not Tighten

In some situations the abutment is tightened onto the implant; however, the
abutment will move in a vertical direction. This is the direct result of the
abutment screw not being fully seated, which may lead to screw loosening or
component fracture.
Etiology
The most common cause of inadequate abutment tightness is debris inside
the base of the implant. It is not uncommon for blood coagulants or excess
debris to accumulate in the base of the implant. Because many implant
systems are designed with minimal space between the end of the screw and
the base of the implant, the screw will be prevented from being fully seated.
This will result in the screw being tight; however, the implant abutment will
move vertically.
This can be easily prevented by irrigation with saline or 0.12% chlorhexidine
with a small tuberculin syringe (Fig. 16.77).
FIG 16.77 (A) Abutment screw fully seated showing minimal space between end of
screw and implant body. (B) Irrigating debris out of implant body with chlorhexidine.
Hex on Abutment Screw Is Stripped

The most common hex insertion tool used in implant dentistry today is the
0.05 (1.25-mm) hex. After extended use, the hex will become stripped, which
will prevent final torque to be applied to the abutment screw (Fig. 16.78).
FIG 16.78 (A) Stripped hex. The more sides a screw has, the greater chance of
stripping. (B) One of the most common causes is the use of a stripped hex driver
(arrow). (C) Hex driver should have a clear delineated hex, not rounded.
Etiology
The most common cause of a stripped hex screw is the placement of the final
torque with the torque wrench not completely seated in the hex screw head
or the use a hex driver that is worn.
Prevention
Always seat the hex driver completely into the hex screw head. This will
minimize the possibility of stripping the hex screw or dulling the hex driver.
When placing torque on the screw, insert the hex driver first, then attach the
torque driver to the hex driver. This will minimize the possibility of not
having the hex driver fully seated.
Treatment
There are three possible treatment options to remove a stripped hex screw.
1. Place and fully seat the hex driver into the hex screw head. With an
osteotome or mirror handle, lightly tap the hex drive to fully seat the driver
into the hex. Ideally, a new hex driver should be used.
2. Add a small amount of autopolymerizing acrylic (GC Pattern Resin) onto
the tip of the hex driver. Seat the hex driver into the hex screw head. Place
constant pressure to hold the hex driver into the fully seated position. After
final curing, with good apical pressure, reverse torque the screw (Fig. 16.79).
FIG 16.79 Treatment of a stripped screw abutment. (A) Insert hex driver, lightly tap
to engage hex fully. (B) Another option includes placing a small amount of acrylic
(Pattern Resin [GC America Inc.]) and hold in place until fully cured, reverse torque.
3. The last option should only be used if #1 and #2 are unsuccessful. The
abutment is sectioned, the screw exposed, and the screw is slotted and
reverse torqued to remove.
Improper Torqueing Technique

The use of a torque wrench improperly may lead to inadequate torque
application, stripping of the hex screw head, and/or dulling of the hex driver.
Etiology
There are numerous errors when using a torque wrench. The first is not
placing apical pressure on the top of the torque wrench. Failure to keep good
apical pressure will lead to a shear force applied to the screw and/or
stripping of the screw. Secondly, the torque wrench can be a significant lever
arm. Thus, the torque wrench should be used with short strokes. And lastly,
the torque wrench should be replaced on a regular basis and maintained in a
good working condition. When autoclaving the torque wrench, make sure the
wrench is in the open position. This will reduce the possibility of excess
residue forming within the torque wrench assembly. Studies have shown
that, on average, clinicians use torque wrenches with deviations of 10% or
greater. Regular recalibration with a torque tester restores the required
torque values.98
Prevention
Finger tighten the hex screw to approximately 10–15 N/cm. Place good apical
pressure with your index finger when torqueing the abutment. Hold the
torque wrench stable to minimize lateral forces. An abutment clamp may be
used to apply countertorque, which is held against the rotation of the wrench
to protect the bone interface from excess lateral stress. Wet torques (implant
screws lubricated with saliva) have a higher mean torque than dry torques
(unlubricated).99 Because of the settling effect, abutment screws should be
retorqued after 10–15 minutes to minimize screw loosening (Figs. 16.80 and
16.81).
FIG 16.80 The torque (T) applied to an abutment screw (which strains the screw
[Fp]) is also applied to the implant-bone interface. (From Misch CE: Dental implant
FIG 16.81 A counter-torque technique (which stops the abutment from rotating) is
used when possible to resist the rotational force applied to the screw being applied
to the implant-bone interface. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Damaging Implant Body
Most implants today are fabricated from grade 5 titanium or Ti6Al4V. This
metal does have the disadvantage of easily being altered or damaged. If an
implant is traumatized with a handpiece and bur, or a sharp instrument,
irreversible damage may be done to the implant (Fig. 16.82).
FIG 16.82 High-speed handpieces may easily damage a titanium alloy implant.
Etiology
When removing tissue or bone around an implant, care should be exercised
to not damage the implant. No high-speed handpiece should be used around
an implant. Another common situation that may damage the implant is the
removal of a fractured screw. Attempting to slot the screw may lead to
damaging the internal threads or walls of the implant.
To prevent damage to the implant, a tissue punch bur or profiling bur should
be used. Alternative techniques to remove a fractured screw should be used
to minimize the possibility of implant damage.
Fixed Occlusal Complications
When two bodies collide in a small interval of time (fractions of a second),
large reaction forces develop. Such a collision is described as impact. In
dental implant systems subjected to occlusal implant loads, deformation may
occur in the prosthodontic restoration, in the implant itself, and in the
contiguous interfacial tissues. The nature of the relative stiffness of these
components in the overall implant system largely controls the response of
the system to impact load. The higher the impact load, the greater the risk of
implant and bridge failure and bone fracture.
Rigidly fixed implants generate a higher interfacial impact force with
occlusion compared with natural teeth, which possess a periodontal
ligament. Soft tissue–borne prostheses have the least impact force because
the gingival tissues are resilient.
The manner in which forces are applied to implant restorations within the
oral environment dictates the likelihood of system failure. The duration of a
force may affect the ultimate outcome of an implant system. Relatively low-
magnitude forces, applied repetitively over a long time, may result in fatigue
failure of an implant or prosthesis. Stress concentrations and, ultimately,
failure may develop if insufficient cross-sectional area is present to dissipate
high-magnitude forces adequately. If a force is applied some distance away
from a weak link in an implant or prosthesis, then bending or torsional
failure may result from moment loads. An understanding of force delivery
and failure mechanisms is critically important to the implant practitioner to
avoid costly and painful complications.
Moment Loads
The moment of a force about a point tends to produce rotation or bending
about that point. A moment force is defined as a vector (M) (vectors are
described in terms of magnitude and direction) the magnitude of which
equals the product of the force magnitude multiplied by the perpendicular
distance (also called the moment arm) from the point of interest to the line of
action of the force. This imposed moment load also is referred to as a torque
or torsional load and may be destructive to the implant system (Fig. 16.83).
FIG 16.83 The moment of a force is defined as a vector (M), the magnitude of
which equals the product of the force magnitude multiplied by the perpendicular
distance (moment arm) from the point of interest to the line of action of the
force. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
A total of six moments (rotations) may develop about the three clinical
coordinate axes previously described (occlusoapical, faciolingual, and
mesiodistal axes). Such moment loads induce microrotations and stress
concentrations at the crest of the alveolar ridge at the implant-tissue
interface, which lead inevitably to crestal bone loss (Fig. 16.84).
FIG 16.84 Moment loads tend to induce rotations in three planes. Clockwise and
counterclockwise rotations in these three planes result in six moments: lingual-
transverse, occlusal, apical, facial, and lingual. (From Misch CE: Dental implant prosthetics,
Three clinical moment arms exist in implant dentistry: (1) occlusal height,
(2) cantilever length, and (3) occlusal width. Minimization of each of these
moment arms is necessary to prevent unretained restorations, fracture of
components, crestal bone loss, and complete implant system failure.
Occlusal Height
The occlusal height serves as the moment arm for force components directed
along the faciolingual axis working or balancing occlusal contacts, tongue
thrusts, or in passive loading by cheek and oral musculature, as well as force
components directed along the mesiodistal axis.
In division A bone, initial moment load at the crest is less than in division
C or D bone because the crown height is greater in division C and D bone.
Treatment planning must take into account this initially compromised
biomechanical environment (Table 16.4). The moment contribution of a force
component directed along the vertical axis is not affected by the occlusal
height because no effective moment arm exists. Offset occlusal contacts or
lateral loads, however, introduce significant moment arms.
TABLE 16.4
Moment Load at Crest When Subjected to Cantilever Forces in Relation
to Crown Height
INFLUENCES ON MOMENT IMPOSED MOMENTS (N/m m ) AT IMPLANT CROWN–CREST INTERFACE

Occlusal Height Cantilever Length Lingual Facial Apical Occlusal Facial-Transverse (mm) Lingual-Transverse (mm)
10 10 100 0 50 200 0 100
10 20 100 0 50 400 0 200
10 30 100 0 50 600 0 300
20 10 200 0 100 200 0 100
20 20 200 0 100 400 0 200
20 30 200 0 100 600 0 300
Cantilever Length
Large moments may develop from vertical axis force components in
prosthetic environments designed with cantilever extensions or offset loads
from rigidly fixed implants. A lingual force component also may induce a
twisting moment about the implant neck axis if applied through a cantilever
length.
An implant with a cantilevered mesobar extending 1, 2, and 3 cm has
significant ranges of moment loads. A 100-N force applied directly over the
implant does not induce a moment load or torque because no rotational
forces are applied through an offset distance. This same 100-N force applied
1 cm from the implant results in a 100 N-cm moment load. Similarly, if the
load is applied 2 cm from the implant, a 200 N-cm torque is applied to the
implant-bone region, and at 3 cm, a 300 N-cm moment load results. For
comparison, recall that implant abutments typically are tightened with 30 N-
cm of torque.
Occlusal Width
Wide occlusal tables increase the moment arm for any offset occlusal loads.
Faciolingual tipping (rotation) can be reduced significantly by narrowing the
occlusal tables or adjusting the occlusion to provide more centric contacts.
In summary, a vicious, destructive cycle can develop with moment loads
and result in crestal bone loss. As crestal bone loss develops, occlusal height
automatically increases. With an increased occlusal height moment arm, the
faciolingual microrotation and rocking increase and cause even more stress
to the crestal bone. Unless the bone increases in density and strength, the
cycle continues to spiral toward implant failure if the biomechanical
environment is not corrected (Fig. 16.85).
FIG 16.85 (A) Three clinical moment arms contribute to torsional (moment) loads
on dental implants: occlusal height, occlusal width, and cantilever length. (B)
Occlusal height serves as moment arm for force components directed along
faciolingual axis and force components directed along mesiodistal axis (C). D,
Lingual force component also may induce twisting moment about the implant neck if
applied through the cantilever length. E, Moment of force along the vertical axis is not
affected by occlusal height because its effective moment arm is zero if positioned
centrically. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Not Utilizing Implant-Protected Occlusion

Etiology
A proper occlusal scheme is a primary requisite for long-term implant
prosthetic survival, especially when parafunction or a marginal foundation is
present. A poor occlusal scheme increases the magnitude of loads and
intensifies mechanical stresses (and strain) to the implant system. These
factors increase the frequency of complications of the prosthesis and bone
support. Crestal bone loss may lead to anaerobic sulcus depths and peri-
implant disease states. These conditions may also cause tissue shrinkage and
loss of interdental papillae and poor esthetic conditions. All of these
complications may be caused by biomechanical stress as a result of occlusal
loads (functional or parafunctional).
Prevention
The implant-protective occlusion (IPO) concept refers to an occlusal plan
specifically designed for the restoration of endosteal implants, providing an
environment for reduced biomechanical complications and improved clinical
longevity of both the implant and prosthesis.93 The biomechanical rationale
for this concept was published by the author after long-term clinical
evaluation and biomechanical studies (and was originally called medial-
positioned, lingualized occlusion). This concept was specifically designed for
fixed prostheses in either partial or complete edentulous patients. Clinical
considerations for this concept are drawn from basic prosthetic concepts,
bone biomechanical principles, and finite element analyses to reduce noxious
occlusal loads and establish a consistent occlusal philosophy.
A primary goal of an occlusal scheme is to maintain the occlusal load that
has been transferred to the implant system within the physiologic and
biomechanical limits of each patient. These limits are not identical for all
patients or restorations. The forces generated by a patient are influenced by
ranges of parafunction, masticatory dynamics, implant arch position and
location, arch form, and crown height. The treatment plan philosophy for
dental implants varies greatly and depends on these several parameters. The
clinician can address these force factors best by selecting the proper position,
number, and implant size, increasing bone density when necessary by
progressive bone loading and selecting the appropriate occlusal scheme
using stress-relieving design elements.
The IPO principles for fixed prostheses address several conditions to
decrease stress to the implant system, including existing occlusion, implant
body angle to occlusal load, cusp angle of implant crowns, mutually
protected articulation, cantilever or offset loads, crown height, crown
contour, occlusal contact position, timing of occlusal contacts, and protection
of the weakest component (Box 16.5).
Box 16.5
Implant-Protective Occlusion Principles
• No premature occlusal contacts or interferences
• Mutually protected articulation
• Implant body positioned perpendicular to occlusal load
• Narrow cusp angle of crowns (cuspal inclination)
• Minimize cantilever or offset loads
• Minimize crown height (vertical offset)
• Ideal implant crown contour
• Ideal occlusal contact positions
• Ideal timing of occlusal contacts
• Protect the weakest component (i.e arch)
• Long, wide contact area
Occlusal Considerations for Fixed Implant

Prostheses
Initial Evaluation
Many clinicians begin to evaluate the occlusion of the patient when the final
implant prosthesis is delivered to the patient. However, this time frame is
often too late to properly restore the patient. The underlying question that
helps determine the need for occlusal correction before restoration of the
implant patient is the observation of negative symptoms related to the
existing condition. This may include temporomandibular joint (TMJ)
conditions, tooth sensitivity, mobility, wear, tooth fractures, cervical
abfraction, or porcelain fracture. The fewer and less significant the findings,
the less likely an overall occlusal modification is required before restoration
of the patient. However, to properly assess these conditions, the clinician
must not ignore them before treatment.
Existing Occlusion
Maximal intercuspation (MI) is defined as the complete intercuspation of the
opposing teeth independent of condylar position, sometimes described as
the best fit of teeth regardless of the condylar position. Centric occlusion
(CO) is defined as the occlusion of opposing teeth when the mandible is in
centric relation (CR).100 This may or may not coincide with the tooth position
of MI. Its relationship to CR (a neuromuscular position independent of tooth
contact with the condyles in an anterior, superior position) is noteworthy to
the restoring dentist. The potential need for occlusal adjustments to
eliminate deflective tooth contacts as the mandible closes in CR and the
evaluation of their potential noxious effects on the existing dentition and the
planned restoration is important to evaluate.
Correction of the deflective contacts before treatment presents many
advantages and may follow a variety of approaches depending on the severity
of the incorrect tooth position: selective odontoplasty (a subtractive
technique), restoration with a crown (with or without endodontic therapy), or
extraction of the offending tooth. The existing occlusion is best evaluated
with facebow-mounted diagnostic casts on an articulator mounted with an
open-mouth bite registration in CR.
Controversy exists as to the necessity to have MI harmonious with CO (CR
occlusion). A vast majority of patients do not have such a relationship, yet
they do not exhibit clinical pathology or accelerated tooth loss. It is difficult
to state that these two positions must be similar. However, it is important to
evaluate the existing occlusion and the mandibular excursions to decide
whether the existing situation should be modified or be maintained. In other
words, clinicians should determine whether they are going to ignore or
control the occlusion of the patient.
As a general rule, the more teeth replaced or restored, the more likely the
patient is restored to CO. For example, if a completely edentulous mandible
is to be restored with an implant-supported fixed prosthesis, CO provides
consistency and reproducibility between the articulator and the intraoral
condition. The slight changes in occlusal vertical dimension (OVD) and its
relationship to the position of anterior implant abutments to the direction of
force may be studied and implemented on the articulator without the need to
record a new occlusal vertical position on the patient. On the other hand,
when one anterior tooth is being replaced, the existing MI position is often
satisfactory to restore the patient even though a posterior interference and
anterior slide into full interdigitation may be present (with little clinical
variance from the ideal conditions). However, in a partially edentulous
patient, the existing occlusion should be evaluated to determine if noxious
conditions are present.
Premature Occlusal Contacts

A fundamental biomechanical formula is stress equals force divided by the
area over which the force is applied (S = F/A). During either maximum
intercuspation or CO, no occlusal contacts should be premature, especially
on an implant-supported crown. Premature occlusal contacts often result in
localized lateral loading of the opposing contacting crowns.101 Because the
surface area of a premature contact is small, the magnitude of stress in the
bone increases proportionately (i.e., S = F/A). All of the occlusal force is
applied to one region rather than being shared by several abutments and
teeth. In addition, because the premature contact is most often on an
inclined plane, the horizontal component of the load increases the shear
crestal stresses and the overall amount of stress to the entire implant system.
The occlusal porcelain, the abutment screw, and the cement retaining the
crown are all at increased risk because shear loads render more
complications.
This is a general criterion for natural teeth, but the concept is much more
important on implant prostheses with their higher impact force and less
occlusal awareness for the several reasons previously addressed. Myata et al
evaluated premature contacts on implant crowns in monkeys (Macaca
fascicularis). The crestal bone was histologically evaluated on implant crowns
with 100 µm, 180 µm, and 250 µm of premature contacts for 4 weeks. The
crowns with 100-µm premature contacts had little bone changes. The 180-µm
group demonstrated a V-shaped pattern of bone loss for several millimeters.
The 250-µm implant crowns for 4 weeks had a large V-shaped defect around
the implants that extended for more than two thirds of the implant body. The
implant is rigid, and the premature implant load cannot be released by
increased mobility or occlusal material wear as with a natural tooth.102 The
premature contact on an implant system contributes to a higher risk of early
abutment screw loosening, porcelain fracture, early loading failure, and
crestal bone loss.
The elimination of premature occlusal contacts is especially important
when habitual parafunction is present because the duration and magnitude
of occlusal forces are increased. The elimination of premature contacts is
more critical than in natural teeth because of the lack of proprioception and
the implant's inability to move and dissipate the forces. Because of increased
proprioception, an initial premature occlusal contact on a tooth often affects
the closure of the mandible to result in an MI position different from CO. A
premature contact on an implant crown does not benefit from such
protective features. As a result, the implant system is at increased risk.
Therefore, occlusal evaluation in CO and MI and adjustment as necessary in
partially edentulous implant patients is more critical than in natural
dentition because the premature contacts can result in more damaging
consequences on implants compared with teeth (Fig. 16.86).33
FIG 16.86 Premature occlusal contacts (i.e. implant prosthesis occluding prior to
natural teeth) are detrimental to the implant leading to possible bone loss or implant
fracture.
Implant Body Orientation

Forces acting on teeth and dental implants are referred to as vectors (defined
in magnitude and direction). Occlusal forces are typically three dimensional,
with components directed along one or more of the clinical coordinate axes.
The primary forces of occlusion can be resolved into a combination of
components in any given plane. The same magnitude of force can have
dramatically different effects on the implant system solely because of the
direction of the applied load. This is especially noted on implant support
systems because they are more rigid. Teeth are naturally designed primarily
for long-axis loads. The natural tooth roots in the majority of the mouth are
perpendicular to the curves of Wilson and Spee. Although chewing is in an
elliptical “tear drop” pattern, when the teeth finally contact, the forces are in
the long axis of the roots, especially during power biting (Fig. 16.87). The
apical movement of teeth is minimal compared with their lateral movement.
The maxillary anterior teeth receive a lateral load. The consequences of a
lateral force to a tooth are reduced because of the increased tooth mobility,
which decreases the effects of the lateral force component of a load.
FIG 16.87 The natural teeth occlude perpendicular to the curves of Wilson and
Spee (arrows). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
An axial load over the long axis of an implant body generates less overall
stress and a greater proportion of compressive stress compared with an
angled force to the implant body. When an implant body is loaded along its
long axis, a 100-N force results with an axial force component of 100 N, and
no lateral force component is observed. The implant body should be
positioned perpendicular to the curves of Wilson and Spee, just as with
natural teeth.
Most anatomic variations of the bone (e.g., bony concavities) are located on
the facial aspect and influence implant body inclination. An implant body
may be positioned with a 15-degree angle to avoid the facial concavity and,
therefore, is positioned at 15 degrees to the occlusal load. This angled
implant may be restored during prosthetic reconstruction with a 15-degree
angle abutment. From the level of the crest of the ridge to the occlusal plane,
the implant abutment looks similar to one in an axial implant body. The
laboratory technician and restoring dentist often treat the angled implant
and axial implant in similar fashion. However, in the 15-degree angled
implant body, the load to the facial bone increases by 25.9% compared with
an axial load (Fig. 16.88). If the implant surgeon places the implant body with
a 30-degree angulation, the buccal force component of any occlusal load will
result in a 50% increase of the load applied to the facial bone.93
FIG 16.88 An implant loaded in the long axis does not increase the buccal force
component of the load (far left). A 15-degree angle increases the buccal force
component by 25.9% (middle). A 30-degree angle load increases the force by 50%.
When the forces are applied along the long axis of an implant body, stresses are
concentrated on the crestal region (far left). The intensity of the stress is not
increased as a result of the position of the implant. The implant body in the center is
15 degrees off the long axis. With an angled abutment of 15 degrees, the implant
restoration is similar to the previous situation. However, now 25.9% greater stress is
on the crestal bone; all other factors are similar. The implant body on the far right is
30 degrees off the long-axis load. With a 30-degree angled abutment, the crown may
appear similar. However, the abutment screw, abutment-implant connection, and
implant-bone interface are subject to a 50% increase in stress on the facial aspect
of the system. (From Misch CE: Contemporary implant dentistry, ed 2, St Louis, 1999, Mosby.)
The risk of crestal bone loss is increased with an angled implant. In

addition, the greater force is applied to most of the implant system. The
occlusal porcelain may be loaded in the long axis with the angled abutment,
but the abutment screw loosening and implant component fracture risks
increase in direct comparison to the load applied to the bone. Although the
restoring dentist may place a 30-degree angled abutment and restore the case
similar to the axial implant, the conditions and risks of early loading failure,
crestal bone loss, and loose abutment screws are dramatically different (Fig.
16.89).
FIG 16.89 As the angle of the implant body load direction increases, the stresses
to the entire crown implant-bone system increase. B, buccal; L, lingual. (From Misch
CE: Contemporary implant dentistry, ed 2, St Louis, 1999, Mosby.)
Force Direction and Bone Mechanics

The noxious effect of offset or angled loads to bone is exacerbated further
because of the anisotropy of bone. Anisotropy refers to the character of bone
whereby its mechanical properties, including ultimate strength, depend on
the direction in which the bone is loaded and the type of force applied. For
example, cortical bone of human long bones has been reported as strongest
in compression, 30% weaker in tension, and 65% weaker in shear.103 Porcelain,
titanium components, and cements are also weakest to shear components of
a load. IPO attempts to eliminate or reduce all shear loads to the implant
system because the bone, porcelain, titanium components, and cement are
weakest to shear loads.
Any occlusal load applied at an angle to the implant body may be
separated into normal (compressive and tensile) and shear forces. As the
angle of load to an implant body increases, the amount of compressive and
tensile forces is modified by the cosine of the angle. Hence, the force is
slightly reduced. However, the angled component of force is a shear force,
and the shear force is the amount of force times the sine of the load, which
considerably increases the load. The force the bone observes is the sum of
the compressive, tensile, and shear forces. For example, a 100-N force applied
at 12 degrees off-axis will increase the total force to the bone by 100 N ×
cosine 12 degrees = 97.81 N + 100 N × sine 12 degrees = 20.79 N. The total
force is 97.81 N + 20.79 N = 118.60 N (or almost a 20% increase in total force).
The greater the angle of load to the implant long axis, the greater the
compressive, tensile, and shear stresses (Fig. 16.90).
FIG 16.90 A 12-degree angled force increases the force to the implant system by
18.6%. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
In finite element analysis, when the direction of the force changes to a

more angled or horizontal load, the magnitude of the stress is increased by
three times or more.104 In addition, rather than a primarily compressive type
of force, tensile and shear components are increased more than tenfold
compared with the axial force. In a photoelastic block with implants inserted,
the strain contours in the bone may be observed (Fig. 16.91). The axial-loaded
implants have less strain in the system (left side and lower right of figure). The
angled implant has more strain lines indicating greater loads (right upper
implant).
FIG 16.91 A photoelastic study of opposing implants in a maxilla and mandible.
One of the maxillary implant bodies is angled in relation to the direction of load. The
number of stress contour lines in the material is similar for the three implants with a
long-axis load. The stress contour lines are increased for the angled implant
body. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
An angled load to the implant long axis increases the compressive forces at
the crest of the ridge on the opposite side of the implant, increasing the
tension component of force along the same side as the load. The greater the
angle of force to the long axis of the implant body, the greater the potentially
damaging load at the crest of the bone. For example, three-dimensional finite
element analysis demonstrates that a vertical load on an implant with 100%
bone contact may have compressive stress of 4000 psi (27.6 MPa) and almost
no tensile stress at the bone-implant crest interface. With a load at a 45-
degree angle on the same implant design, the compressive stress may
increase to 14,000 psi (96.6 MPa), and on the opposite side, tensile stress may
increase to 4000 psi (27.6 MPa). The compressive stresses are tripled, and the
tensile stress increases 1000-fold with a load from a 45-degree angle.
The stress contours in the bone simulant of the three-dimensional studies
resemble the clinical pattern of early crestal bone loss on implants. Not only
does the magnitude of stress increase under angled loads, but it also evolves
into a more noxious shear component, which is more conducive to bone loss
and screw loosening.105 The greater the angle of the force, the greater the
shear component. Bone is 65% weaker to shear load. The amount of the force
increases, and the strength of the bone decreases. It has been reported that
angled occlusal forces decrease the ability of successful bone repair on
natural teeth. It may also impair successful bone remodeling around an
implant.
Not only is the bone weakest to shear loads but forces applied at an angle
to the bone also further affect the physiologic limit of compressive and
tensile strengths of bone. A force applied at a 30-degree angle may decrease
the bone strength limits by 10% under compression and 25% with tension
(Table 16.5). A 60-degree force angle reduces the strength 30% under
compression and 55% under tension. Not only does the crestal bone load
increase around the implant with angled forces but also the amount of stress
the bone may withstand (i.e., the ultimate strength) decreases in shear,
tension, and compression. The greater the angle of load, the lower the
ultimate strength of bone. IPO attempts to eliminate lateral or angled loads
to an implant-supported prosthesis because the magnitude of the force
increases and the strength of the bone decreases.
TABLE 16.5
Cortical Bone Strength Related to Angle of Load
Type Strength (MP a) Direction of Load

Compression 193 Longitudinal
173 30 degrees off axis
133 Transverse
Tension 133 Longitudinal
60.5 60 degrees off axis
51 Transverse
From Reilly DT, Burstein AH: The elastic and ultimate properties of compact bone tissue, J Biomech
80:393–405, 1975.
In conclusion, the microstrain of the crestal bone is increased with an

angled load and may shift from an axial load within physiologic limits to an
angled load in the pathologic overload zone and, as a consequence, result in
bone loss. The greater force, especially in shear, is generated to the entire
implant system. The occlusal porcelain is weaker to shear and may fracture,
the cement that retains the prosthesis is weakest to shear and may become
unretained, the abutment screw more likely becomes loose with shear loads,
the crestal bone region may resorb, and implant components fracture more
often with higher shear loads. When shear forces are increased with an
angled load to the implant system, an attempt should be made to reduce the
negative effect of angled loads.106
The primary component of the occlusal force should be directed along the
long axis of the implant body, not at an angle or following an angled
abutment post. Angled abutments should be used only to improve the path
of insertion of the prosthesis or improve the final esthetic result. The angled
abutment, which is loaded along the abutment axis, transmits a significant
moment load (i.e., tending to rotate or rock the implant) to the entire implant
system.
Prosthetic Angled Loads

Greater crestal bone strains with angled forces have been confirmed with
photoelastic and three-dimensional finite element analysis methods.
Whether the occlusal load is applied to an angled implant body or an angled
load (e.g., premature contact on an angled cusp) is applied to an implant
body perpendicular to the occlusal plane, the results are similar (Fig. 16.92).
A biomechanical risk to the implant system increases.
FIG 16.92 When an angled load is placed on an implant body, the compressive
stresses on the opposite side of the implant increase and the tensile and shear
loads on the same side of the implant increase. Because bone is weaker to tensile
and shear forces, the risks to the bone are increased for two reasons: (1) the
amount of the stress increases, and (2) the type of stress is changed to more
tensile and shear conditions. F, force. (From Misch CE: Dental implant prosthetics, ed 2, St
The implant surgeon may place the implant body ideally, perpendicular to
the occlusal plane, yet the restoring dentist then may load the implant crown
at an angle. Similar noxious forces are increased in shear, and a decrease in
bone strength occurs to the crestal bone, as well as an increase of shear loads
on implant components and the abutment screws. An angled implant body
or an angled load on the implant crown increases the amount of crestal
stresses on the implant system, transforms a greater percentage of the force
to shear force, and reduces bone, porcelain, and cement strength. In contrast,
the surrounding implant system stress magnitude is least, and the strength
of bone, porcelain, and cement is greatest under a load axial to the implant
body and perpendicular to the occlusal plane. All of these factors mandate
the reduction of angled forces to the implant system (Fig. 16.93).
FIG 16.93 The force applied to an implant body with an angled load or angled
direction of force is increased in direct relation to the force angle. The major
increase of force is a result of the offset angle of the load. (From Misch CE: Dental
Most implant bodies inserted at an angle of greater than 12 degrees to the

occlusal plane require an angled abutment. The surgeon and restoring
dentist should understand that angled abutments are fabricated in two
pieces and are weaker in design than a two-piece straight abutment without
an angle. Because less metal flanks the abutment screw on one side of an
angled abutment, it is at more risk of fracture or is less able to be reduced in
width for ideal crown contours. Furthermore, a larger transverse load
component develops at the abutment screw and crest of the ridge as a result
of angled loads and increases the risk of abutment screw loosening. In a
study by Ha et al, the angled abutment was compared with a straight
abutment for screw loosening in the anterior maxilla. The angled abutments
showed more screw loosening with cyclic loading than the straight
abutments.107
Solutions to Angled Loads

When lateral or angled loads cannot be eliminated, a reduction in the force
magnitude or additional surface area of implant support is indicated to
reduce the risk of biomechanical complications to the implant system. For
example, if three adjacent implants are inserted with the first in the long axis
to the load, the second at 15 degrees, and the third implant at 30 degrees, the
surgeon may decrease the overall risk by (1) adding an additional implant in
the edentulous space next to the most angled implant, (2) increasing the
diameter of the angled implants, or (3) selecting an implant design with
greater surface area. Of the three options, increasing the implant number is
most effective to reduce overall stress to the system.108 In addition, a greater
number of implants also has more retention for the restoration.
The restoring dentist may reduce the overload risk by (1) splinting the
implants together, (2) reducing the occlusal load on the second implant and
further reducing the load on the third implant, and (3) eliminating all lateral
or horizontal loads from the most angled implant and completely
eliminating them in all posterior regions.
The anterior mandible (with a force magnitude similar to the anterior
maxilla) often has the implant body positioned perpendicular to the occlusal
plane and restored with a straight abutment. In the anterior maxilla, even
under ideal conditions, the implant should be angled away from the labial
bone and results with the abutment toward the facial crown contour. An
angled prosthetic abutment is required, and these implant bodies are more
frequently loaded at an angle. In fact, maxillary anterior teeth are usually
loaded at a 12- to 15-degree angle to the occlusal plane.
The natural dentition reduces the increased stress to the maxilla by
increasing the size of the roots compared with mandibular incisors and
increasing the mobility of the tooth. In the maxilla, a larger-diameter implant
or a greater number of implants are indicated to minimize the crestal bone
stress on each abutment, especially in patients exhibiting severe bruxism.
Ridge augmentation may be necessary before implant placement to improve
implant position or facilitate the use of a wider-diameter implant. IPO aims
at reducing the force of occlusal contacts, increasing the implant number, or
increasing the implant diameter for implants subjected to angled loads.
Occlusal Contact Timing

Most commonly, clinicians use subjective methods when evaluating and
determining occlusal contact. This may often lead to false-positive or
negative results because of the use of dental anesthesia, the subjective nature
of the method, and questionable awareness of contact timing.
Etiology
Occlusal Awareness.
Jacobs and van Steenberghe evaluated patient occlusal awareness by the
perception of an interference. When teeth oppose each other, an interference
is perceived at approximately 20 µm. An implant opposing a natural tooth
detects an interference at 48 µm; this detection is more than twice as poor.
An implant crown opposing an implant crown perceives the interference at
64 µm, and when a tooth opposes an implant overdenture, the awareness is
108 µm (five times poorer than teeth opposing each other).109 Mericske-Stern
et al measured oral tactile sensitivity with steel foils. The detection threshold
of minimal pressure was significantly higher on implants than on natural
teeth (3.2 vs. 2.6 foils).110 Similar findings also were reported by Hammerle et
al in which the mean threshold value for implants (100.6 g) was 8.75 times
higher than that of natural teeth (11.5 g).111 An occlusal adjustment
performed by occlusal awareness—“How does the bite feel? Is the implant
crown high?”—is a poor indicator for hyper contacts compared with a crown
on a natural tooth. As a consequence of decreased quantity and quality of
occlusal awareness, a premature occlusal contact may remain on an implant
crown after occlusal adjustment.
The biomechanical concern for the difference in tooth movement and
implant movement should not be restricted to situations in which these
entities are directly connected within the same prosthesis. When an implant
is placed in a partially edentulous arch, many similar biomechanical
elements are present, whether the teeth are splinted to the implant or are
independent.
Inherent Laboratory Error.

The laboratory cannot equilibrate the occlusion accurately on the working
casts. The technician taps two stone casts together to evaluate the occlusal
contacts. The stone dies do not move 28 to 108 µm. As a result, the occlusal
adjustment in the mouth compensates for the primary and secondary tooth
movement. When a heavy bite force occlusal adjustment is not performed at
the delivery of an implant crown, the dentist may not be aware that the
implant may be overloaded similar to a new crown on a natural tooth that
has not been equilibrated in the mouth.
Tooth vs. Implant Movement.

The sudden, initial (primary) tooth movement ranges from 8 to 28 µm in a
vertical direction under a 3- to 5-lb load, depending on the size, number, and
geometry of the roots and the time elapsed since the last load application.86
This tooth movement has been called “primary” tooth movement and is a
result of the movement within the periodontal complex. An implant has no
initial or primary vertical tooth movement. An implant with a heavy bite
force may move apically up to 5 µm. When the initial tooth movement
occurs, secondary tooth movement is present during a greater load and
reflects the viscoelastic property of the surrounding bone. The vertical
secondary tooth movement is minimal and may approach 3 to 5 µm for a
natural tooth.
The secondary tooth movement is similar to the bone-implant movement.
In other words, the initial axial movement during a light bite force of an
implant has no initial, sudden movement. Contrary to the teeth that move
immediately, even with light loads, implants only move under a heavy
occlusal load and even under these conditions have almost no mobility. The
implant may move up to 5 µm after additional force causes the bone to
deform, with little correlation of movement to the implant body length.87 In
fact, the mobility of implant “secondary” movement is more related to bone
density than any other factor.
When teeth oppose each other, the combined intrusive movements of the
contacting elements may be 56 µm (28 + 28 µm). When a tooth opposes an
implant, the initial combined intrusive movement is only 28 µm (28 + 0 µm).
In other words, when implant prostheses oppose natural teeth, the difference
in movement between teeth in the rest of the mouth and the implants causes
a condition with greater loads to the implant.
Articulation Protocol
1. The clinician should first evaluate the existing occlusion before implant
reconstruction and ideally eliminate occlusal prematurities on teeth before
the final evaluation of the occlusion for the implant reconstruction.
2. At the delivery of the implant prosthesis, any premature contact on the

implant restoration should be eliminated. It is interesting to note that a
coating of petroleum jelly on the articulating paper will help release the dye
and allow more precise occlusal contact identification on the teeth and
implant restoration (Fig. 16.94). After this step, the clinician uses thin
articulating paper (less than 25-µm thickness tin foil) for the initial implant
occlusal adjustment in occlusion under a light tapping force (Fig. 16.95). The
implant prosthesis should barely contact during this light bite force, and the
surrounding teeth in the arch should exhibit greater initial occlusal contacts.
In other words, only light axial occlusal contacts should be present on the
implant crown.
FIG 16.94 Petroleum jelly applied to articulating paper helps release the dye and
makes the occlusal marks more specific. (From Misch CE: Dental implant prosthetics, ed 2,
FIG 16.95 A light occlusal force is applied first to the implant and teeth. The first
molar implant crown has less initial contact than the teeth. (From Misch CE: Dental
3. After the equilibration, when a light bite force is completed, the patient
applies a heavier occlusal force and grinds on the articulating paper (Fig.
16.96). A plastic articulatory paper is a benefit, so the “paper ” will not tear
during the heavy bite and grind force on the teeth (e.g., 20 µm, Accufilm;
Parkell, Farmingdale, NY). The occlusal contact point on the implant crown
should remain axial over the implant body and may be of similar intensity on
the implant crown and the adjacent teeth. When greater bite forces are used,
all of the occlusal elements react similar under the heavy occlusal load. To
harmonize the occlusal forces between implants and teeth, the dentist
evaluates a heavy bite force occlusal adjustment because it depresses the
natural teeth, positioning them closer to the less depressed implant position,
and permits equal sharing of the occlusal load.45
FIG 16.96 The first molar implant crown is evaluated with a heavy bite force during
grinding movements (especially in a parafunction patient). The implant crown in this
patient needs to be adjusted because the occlusal markings on the lingual cusps
and marginal ridge are offset loads. (From Misch CE: Dental implant prosthetics, ed 2, St
Occlusal Contact in One Quadrant.

When all posterior teeth in one quadrant of the same arch are implant
supported, the same occlusal timing is suggested. Under a light bite force,
the occlusal contacts between the anterior and posterior teeth on the
opposite side are slightly heavier in centric occlusion than the implant
prosthesis. Under a heavy bite force in occlusion, similar contacts are created
around the arch. To evaluate these occlusal contacts, a full-arch articulating
paper is required.
Implant Prostheses Opposing Each Other.

When implant prostheses oppose each other unilaterally, the heavy bite force
occlusal adjustment must account for a 56-µm difference in vertical
movement between the opposing implant crowns and the rest of the natural
teeth. The light bite force occlusal adjustment should again be performed
with a full-arch-size articulating paper, and the implant-implant section
should barely contact, but the tooth-tooth anterior and posterior sections
have more occlusal contact. Under a heavy bite force in occlusion, similar
occlusal contacts are present on both sides of the arch.
Complete Implant-Supported Prosthesis.

A complete-arch implant-supported prosthesis in one arch opposing
complete natural teeth does not require a difference in a light and heavy bite
force occlusal evaluation. Likewise, when implants support both maxillary
and mandibular prostheses, a light and heavy bite force difference in occlusal
timing is not required.
Maxillary Anterior.
When anterior teeth disocclude the posterior teeth in excursions, the lateral
tooth movement of the posterior teeth (56–73 µm) does not have to be
accounted for because no lateral force exists. Because anterior teeth and
implants have lateral movement during mandibular excursion that results in
greater discrepancies, the occlusal adjustment in this direction is more
critical to the implant system. The clinician will first use light force and thin
articulating paper to ensure that little to no implant crown contact occurs
during the initial occlusal or lateral movement of the teeth. A heavier force
during CO and excursions to develop similar occlusal contacts on anterior
implants and natural teeth should then be completed.
To compensate for the difference in 100 µm of horizontal movement
between maxillary anterior implants and anterior teeth, two modifications
are required. The first is to enameloplasty the facial incisal contact of the
mandibular incisal edge. The patient is told the height of the tooth is not
reduced, only the facial incisal edge. Very often, when a maxillary anterior
tooth is lost, the opposing mandibular incisor shifts to the facial and makes
the implant position and occlusal adjustment more critical. The second
modification is often that the lingual contour of a maxillary anterior crown is
more concave than a natural tooth to accommodate the heavy bite force
occlusal adjustment (Fig. 16.97).
FIG 16.97 (A) The occlusal equilibration of an anterior implant crown is made first
with a light occlusal contact in centric occlusion (CO) and during mandibular
excursions. (B) The anterior implant crown then is equilibrated under a heavy bite
force in CO and during mandibular excursions. The difference between primary
tooth movement and implant movement is greater in the anterior regions of the
mouth. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The proposed heavy bite force occlusal adjustment does not encourage
tooth migration or changes in tooth position because regular occlusal
contacts still occur. The teeth opposing implants are not taken out of
occlusion. Brief occlusal contacts on a daily basis maintain the tooth in its
original position (similar to the rest of the mouth). In addition, because most
teeth in a skeletal class I occlusion occlude with two opposing teeth (with the
exception of the mandibular central incisor), the opposing teeth positions are
even more likely to remain the same. In other words, the two opposing
natural teeth to an implant crown still have occlusal contacts on the adjacent
natural teeth to the implant. However, teeth do move over time. Unlike teeth,
implants do not extrude, rotate, or migrate under occlusal forces. As such,
the restoring dentist may vary the intensity of the force applied to an implant
without causing the implant to change its position readily in the bone. On
the contrary, natural teeth do exhibit mesial drift, and slight changes in
occlusal position do occur over time.
Treatment
Recall Examination.
No occlusal scheme will prevent mesial drift and minor tooth movement
from occurring. In addition, enamel may wear approximately 30 µm each
year. An integral part of the implant-protected occlusion philosophy is the
regular evaluation and control of occlusal contacts at each regularly
scheduled hygiene appointment. This permits the correction of minor
variations occurring during long-term function and helps prevent porcelain
fracture and other stress-related complications (abutment screw loosening)
on the implant prostheses.
Occlusal Table Too Large

Etiology
The occlusal table of the crown should also be modified in nonesthetic
regions to conform to the implant size and position and to direct vertical
forces to the implant body. For example, posterior mandibular implant-
supported prostheses have narrower occlusal tables at the expense of the
buccal contour because the implant is smaller in diameter and placed in the
central fossa region of the tooth. Maxillary posterior teeth often have reduced
occlusal tables from the palatal aspect because the buccal cusp is often
within the esthetic zone (Fig. 16.98).
FIG 16.98 This full-arch prosthesis has posterior crown contours that are narrower
than natural teeth because the implant is smaller in diameter than the tooth. As a
general rule, the maxillary arch has reduced lingual contours and the mandibular
posterior prosthesis has reduced buccal contours. (From Misch CE: Dental implant
A buccal or lingual cantilever in the posterior regions is called an offset

load, and the same principles of force magnification from class 1 levers apply.
In other words, the greater the offset, the greater the load to the implant
system.112 Offset loads may also result from buccal or lingual occlusal
contacts and create moment forces, which increase compressive, tensile, and
shear forces to the entire implant system (Fig. 16.99).
FIG 16.99 An occlusal contact to a buccal cusp of an implant crown is often an

offset load to the implant, which increases the shear component of a load. (From
The laboratory technician often attempts to fabricate an implant crown

with occlusal facial and lingual contours similar to those of natural teeth. The
posterior implant crown should have a reduced occlusal width compared
with a natural tooth when out of the esthetic zone. A wide occlusal table
favors offset contacts during mastication or parafunction. The narrower
occlusal contour of an implant crown also reduces the risk of porcelain
fracture.
A facial profile similar to a natural tooth on the smaller-diameter implant
(e.g., 10-mm tooth vs. a 4- to 6-mm implant) results in cantilevered restorative
materials. This cantilever crown contour is often designed as a ridge lap
pontic of an FPD (Fig. 16.100). The facial porcelain most often is not
supported by a metal substructure because the gingival region of the crown
is also porcelain. As a result, shear forces result on the buccal cusp of the
mandibular crown or lingual cusps in the maxillary crown and are more
likely to increase the risk of porcelain fracture. This risk is compounded
further by the higher impact force developed on implant abutments
compared with natural teeth.
FIG 16.100 (A) Facial cantilever on lingually placed implant. (B) Posterior occlusal
table is narrowed to minimize shear forces.
The extended crown contours not only increase offset loads but also often
result in ridge laps or porcelain extension at the facial gingival margin of the
implant abutment. As a result, home care in the sulcular region of the
implant is impaired by the overcontoured crown design. The dental floss or
probe may reach under the ridge lap to the FGM, but it cannot enter the
gingival sulcus, making daily hygiene almost impossible to perform. The
narrower posterior occlusal table facilitates daily sulcular home care.
In conclusion, a narrow occlusal table combined with a reduced contour
facilitates daily care, improves axial loading, and decreases the risk of
porcelain fracture. However, in the esthetic zone, the ridge lap design may be
necessary to restore the implant rather than removing it, bone grafting, and
replacing the implant in a more ideal position for esthetics.
Mandibular Posterior Crowns.

The posterior mandible resorbs lingually as the bone resorbs from division A
to B. As a result, endosteal implants are also more lingual than their natural
tooth predecessors. The division C−h and D mandibular ridge shifts to the
buccal compared with the maxillary arch. However, endosteal implants
typically cannot be inserted because the available bone above the mandibular
nerve is inadequate for endosteal implants.
The mandibular implant crown should be reduced from the buccal (and
the maxillary crown reduced from the lingual). The “stamp cusp” offset load
is reduced. The reduced buccal contour in the posterior mandible is of no
consequence to cheek biting because the buccal horizontal overjet is
maintained (and increased). The lingual contour of the mandibular implant
crown is similar to a natural tooth (Fig. 16.101). This permits a horizontal
overjet to exist and push the tongue out of the way during occlusal contacts
(just as natural teeth). As with the natural tooth, the lingual cusp has no
occlusal contact.
FIG 16.101 (A) A mandibular first molar implant and abutment. (B) The implant
crown is reduced in width on the buccal. The lingual contour is similar to the
adjacent teeth to prevent biting the tongue during occlusion. (From Misch CE: Dental
In the posterior mandible, as the implant diameter decreases, the buccal

cusp contour is reduced. This decreases the offset length of cantilever load.
The lingual contour of the crown remains similar regardless of the diameter
of the implant. The lingual contour permits a horizontal overlap with the
maxillary lingual cusp, so the tongue is pushed away from the occlusal table
during function. The mandibular lingual cusp is not occlusally loaded (as
with natural teeth).
Maxillary Posterior Crowns.

In the esthetic zone (high lip position during smiling), the buccal contour of
the maxillary implant crown is similar to a natural tooth. This improves
esthetics and maintains the buccal overjet to prevent cheek biting. But just as
with the natural teeth, there is no occlusal contact on the buccal cusp. Ideally,
when maxillary posterior implants are in the esthetic zone, they are
positioned more facial than the center of the ridge. The lingual contour of a
maxillary implant crown should be reduced because it is out of the esthetic
zone and is a stamp cusp for occlusion (which is an offset load).
The ideal functional position for the maxillary posterior implant is under
the central fossa when the cervical region is not in the esthetic zone. The
lingual cusp is cantilevered from the implant similar to the buccal cusp of the
posterior mandible. The reduced lingual contour reduces the offset load to
the lingual (Fig. 16.102).
FIG 16.102 The posterior maxillary first molar implant crown has primary contact
over the implant. When the implant is under the central fossa to lingual cusp, the
crown contour is reduced on the lingual, and occlusal load is directed along the long
axis of the implant. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The maxillary dentate posterior ridge is positioned slightly more facial

than its mandibular counterpart because the teeth have a maxillary overbite.
When the maxillary teeth are lost, the edentulous ridge resorbs in a medial
direction as it evolves from division A to B, division B to C, and division C to
D. As a result, the maxillary permucosal implant site gradually shifts toward
the midline as the ridge resorbs. Sinus grafts permit the placement of
endosteal implants in the posterior maxilla even in previous division D
ridges. However, because of resorption in width, the maxillary posterior
implant permucosal site may even be palatal to the opposing natural
mandibular tooth.
In the esthetic zone, many of the crown contours are made to resemble the
natural tooth as closely as possible. However, out of the esthetic zone, in the
posterior regions of the mouth, the crown contour should be different than a
natural tooth. The implant body buccolingual dimension is smaller than the
natural tooth. The center of the implant most often is placed in the center of
the edentulous ridge. Because the crest of the ridge shifts lingually with
resorption, the implant body is most often not under the opposing cusp tips
but rather near the central fossa or even more lingual and in the maxilla may
even be under the lingual cusp of the original natural tooth position. Most
often, the laboratory fabricates a posterior implant crown that is similar in
size to a natural tooth, with a cantilevered facial contour. In addition, the
occlusal contacts are often on the “stamp cusp” of the mandible (buccal
cusps). However, these “stamp cusps” are often offset loads (buccal
cantilevers).
When the maxillary posterior teeth are out of the esthetic zone, the crown
may be designed for a crossbite (Fig. 16.103). The lingual overjet prevents
tongue biting, the buccal overjet (from the mandibular tooth) prevents cheek
biting, the implant is axial loaded by the lingual cusp of the mandible, and
hygiene is improved.
FIG 16.103 When the implant site is out of the esthetic zone and the implant is
positioned more lingual, a crossbite may be designed in the implant crown. B,
buccal; L, lingual. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Summary.
Restorations mimicking the crown contour and occlusal anatomy of natural
teeth often result in offset loads (increased stress and risk of associated
complications), complicated home care, and an increased risk of porcelain
fracture. As a result, in nonesthetic regions of the mouth, the occlusal table
should be reduced in width compared with natural teeth.
Increased Posterior Cusp Angle
The angle of force to the implant body may be influenced by the cusp
inclination of the implant crown in similar fashion as an angled load to an
implant body. The posterior natural dentition often has steep cuspal inclines,
and 30-degree cusp angles have been designed in denture teeth and natural
tooth prosthetic crowns to fulfill the same contours (Fig. 16.104).
FIG 16.104 A 30-degree cusp angle is often used to restore an implant

crown. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Etiology
The greater cusp angles are often considered more esthetic and may even
incise food more easily and efficiently. However, to negate the negative effect
of an angle cusp contact, the opposing teeth need to occlude at the same time
in two or more exact positions on the ipsilateral cusp angles of the crowns
(Fig. 16.105). This is usually not possible in a clinical setting with a dynamic
dentition.
FIG 16.105 To negate an angled load to the implant body from a crown with cusp
angles, two or more simultaneous contacts are necessary. (From Misch CE: Dental
The occlusal contact along only one of the angled cusps results in an
angled load to the implant system even when it is not premature to other
occlusal contacts (Fig. 16.106). The magnitude of the force is minimized when
the angled occlusal contact is not a premature contact but instead is a
uniform load over several teeth or implants. However, the angled cusp load
does increase the resultant tensile and shear stress with no observable
benefit. No advantage is gained, but the biomechanical risk is increased (e.g.,
increased abutment screw loosening, porcelain fracture, and unretained
restoration).
FIG 16.106 An occlusal contact on an angled cusp results in an angled load to the
implant system. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The occlusal contact over an implant crown should ideally be on a flat surface
perpendicular to the implant body. This occlusal contact position usually is
accomplished by increasing the width of the central fossa to 2 to 3 mm in
posterior implant crowns, which is positioned over the middle of the implant
abutment. The opposing cusp is recontoured to occlude the central fossa of
the implant crown directly over the implant body (Fig. 16.107). The laboratory
technician should identify the middle of the implant body and then make a
central fossa 2 to 3 mm wide over this position parallel to the curve of Wilson
and Spee (Fig. 16.108). The buccal and lingual contours of the crown may
then be established (reduced on the buccal for the posterior mandible and
the lingual for the posterior maxilla). The opposing tooth may require
recontouring of an opposing cusp to help direct the occlusal force along the
long axis of the implant body.
FIG 16.107 A posterior crown usually has a widened central fossa positioned over
the implant abutment. This directs the occlusal load along the long axis of the
implant body. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 16.108 The dental laboratory technician determines the position of the implant
related to occlusal load on the implant crown. (From Misch CE: Dental implant prosthetics,
Poor Emergence Profile
Etiology
The “emergence profile” concept was first introduced in 1977 by Stein et al to
describe tooth and crown contours from the soft tissue to the contact area
interproximally.113 When a restoration is fabricated with an unnatural
contour, esthetics and soft tissue health will be compromised. The successful
restoration of lost teeth in the anterior region of the mouth has to meet both
aesthetic and functional parameters. In addition to the correct placement of
the implant fixture, it is essential to achieve a soft tissue morphology as
physiologically realistic as possible.
Prevention
Ideal Implant Placement.

The most important factor in obtaining an ideal emergence profile is the
correct and ideal placement of the implant. Implants should be placed
approximately 2.0 mm from a natural tooth, 3.0 mm between implants, and in
the ideal buccal and lingual orientation with respect to the incisal edge and
occlusal table.
Implant Size.
An implant with too small of a diameter will lead to a nonideal emergence
profile. The larger the implant diameter, the more closely the emergence
profile resembles the natural tooth, especially in the posterior region of the
jaws. Most natural roots are greater than 4 mm in cross section. The closer
the implant diameter to the root diameter (2 mm below the cementoenamel
junction [CEJ], where the ideal crestal bone level resides), the more similar
the crown emergence profile to a natural tooth. This is especially noted in the
maxillary first molar region because the root diameter approaches 8 mm, or
twice the size of a 4-mm implant. The wider crown contour also decreases the
interproximal space of the crown and decreases the incidence of food
impaction during function. The wide-diameter implant may also improve
sulcular daily oral hygiene by improving the crown emergence, avoiding the
need for a prosthetic ridge lap of the crown. The improved contour also
allows access to the sulcus for periodontal probing depths (Fig. 16.109).
FIG 16.109 The diameter of a tooth is often larger than an implant to replace it. As
such, the larger the implant, the more the emergence profile at the cervical region
resembles a tooth. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Abutments.
Most healing abutments and stock abutments have a cylindrical shape that
does not reproduce correctly the emerging profile of the natural teeth. The
final tissue heights of the papillae and gingival margins are ultimately
dictated by the posthealing levels, type of abutment, and position of the
interproximal and facial bone. Special emergence profile abutments are often
advocated by the manufacturers; however, this is usually not necessary
because the emergence profile can be developed with the restoration on a
stock abutment.
Modification of Soft Tissue.

The easiest technique to achieve the emergence profile is to sculpture the
peri-implant mucosa with the use of a provisional prosthesis. This is most
successful with a thick biotype tissue because it may be easily manipulated.
With a thin biotype, there is a high risk of soft tissue collapse and gingival
recession.
Laboratory.
The emergence profile can sometimes be improperly fabricated based on a
final cast with nonideal soft tissue foundation. The dental technician should
model an implant-supported prosthesis with an ideal emergence profile (Fig.
16.110).
FIG 16.110 (A–B) Poor emergence profile. (C) Emergence profile is easily obtained
via the prosthesis, (D) not necessarily a flared prefabricated abutment.
Because of its characteristics, the peri-implant mucosa can be modified by

a sculpting process based on the principle that soft tissue becomes
modifiable after controlled, constant compression. Especially in patients with
a thick gingival biotype, this tissue can be manipulated to reproduce the
normal scalloped, parabolic gingival contours. Different approaches have
been suggested by the current literature on the soft tissue profiling.
An emergence profile that mimics the natural tooth should be obtained by
successful intraoral soft tissue modifications. Prefabricated provisional
crowns cannot mimic the complexity and the variations of the soft tissue that
occurs during the healing process. Usually, a chairside modification of the
provisional restoration can accomplish the optimal result. Moreover, it is
advantageous if the provisional restoration screw is retained to prevent
irritating side effects of provisional cement on the peri-implant soft tissues,
especially in situations where frequent removals of the provisional
restoration are required. However, in some instances, the screw access hole
will be facially oriented which may compromise the esthetics.
In highly demanding areas, specially where the esthetic outcome is a
priority, the soft tissue should be modified to obtain an optimal emergence
profile and gingival contours with physiologic appearance as realistic as
possible. The previously described method allows for most accurate
duplication of the conditioned soft tissue when the final impression is taken;
thus their reproduction on the definitive restoration is possible.
Parafunction: No Occlusal Guard

Etiology
When an implant reconstruction is considered in a bruxing patient, a patient
with significant occlusal force, or an irregular plane of occlusion, occlusal
analysis is warranted. Premature and posterior contacts during mandibular
excursions increase stress conditions.
Prevention
An elimination of eccentric contacts in a patient with myofascial pain
dysfunction may allow recovery of periodontal ligament health and muscle
activity within 1 to 4 weeks. Occlusal harmony does not necessarily eliminate
bruxism; however, it will usually decrease the occurrence and magnitude of
parafunction.
Forces from moderate to severe parafunction are the most difficult to
address on a long-term basis. Education and informed consent of the patient
are helpful to gain cooperation in eliminating or reducing the noxious effects.
If the opposing arch is a soft tissue–supported removable prosthesis, the
effects of the nocturnal habit may be minimized if the patient removes the
prosthesis at night. The use of a night guard is helpful for a patient with a
fixed prosthesis in order to transfer the weakest link of the system to the
removable acrylic device. Centric contacts in centric relation occlusion and
anterior-guided disocclusion of the posterior teeth in excursions are strongly
suggested.
Treatment
An occlusal guard can be a useful diagnostic tool to evaluate the influence of
occlusal disharmony and parafunction. A flat plane, hard-processed night
guard exhibits even occlusal contacts circumferentially in centric relation
occlusion and provides posterior disocclusion with anterior guidance in all
excursions of the mandible.114 This device may be fabricated with 0.5- to 1-
mm colored acrylic resin on the occlusal surface. After 4 weeks of nocturnal
wear, the muscles and periodontal ligament are restored. If the patient wears
this device for an additional month or more, the influence of occlusion on the
bruxism may be directly observed because there are no premature contacts
while the device is worn. If the colored acrylic is still intact, the nocturnal
parafunction has been reduced or eliminated. Occlusal reconstruction or
modification may proceed. If the colored acrylic on the night guard is ground
through, an occlusal adjustment will have little influence on decreasing this
parafunctional habit. The night guard is still indicated to relieve stresses
during nocturnal parafunction, but the prosthetic reconstruction treatment
plan should account for the greater forces (Fig. 16.111).
FIG 16.111 (A–B) Parafunction treatment includes the use of a hard, processed
night guard.
Not Utilizing Progressive Bone Loading

Poor bone density may compromise implant success even when key implant
position and number are satisfactory. In addition, crestal bone loss may be
reduced with progressive loading.
Etiology
As a general rule, the higher the risk factors, the more progressive the
recommended loading. The principles of gradual loading are demonstrated
best in a cement-retained prosthesis. A longer healing time between stage I
and stage II is suggested when forces are greater or bone is softer. This time
allows greater mineralization of bone and a more mature lamellar bone
interface to form next to the implants before the load of the screws is applied
to the implant bodies.
Prevention
The concept of progressive loading is to allow the bone to adapt to increasing
amounts of biomechanical stress. Rather than immediately loading the bone-
implant interface, methods to slowly increase the stress over time are a
benefit. The progressive loading protocol uses a cement-retained prosthesis
when implants are splinted together. Because a screw-retained splinted
restoration is not completely passive and a torque force applied to a screw is
greater than a bite force, a traditional screw-retained restoration cannot use
progressive loading to gradually load the bone.
The progressive loading protocol has six different methods to gradually
load the bone or to increase the bone density around the implant (Box 16.6).
These elements help give the implant clinician the ability to evaluate the
gradual loading progress (Table 16.6).
Box 16.6
Elements of Progressive Loading
Time interval
Diet
Occlusal material
Occlusal contacts
Prosthesis design
Bone Density
TABLE 16.6
Treatment Times for Progressive Bone Loading for Cement-Retained
Prostheses
Bone Density Initial Healing (months) Interval Between Appointments (weeks) Reconstruction (weeks) Total Time (months)
D1 3 1 3 4
D2 4 2 6 5.5
D3 5 3 9 7
D4 6 4 12 9
Time: Initial Healing.

The histologic type of bone in contact with the implant varies and can affect
the amount of stress the bone can sustain within physiologic limits. The ideal
bone for implant prosthetic support is lamellar bone. Lamellar bone is highly
organized but takes about 1 year to mineralize completely after the trauma
induced by implant placement.115 Woven bone is the fastest and first type of
bone to form around the implant interface; however, it is mineralized only
partly and demonstrates an unorganized structure less able to withstand full-
scale stresses. At 16 weeks, the surrounding bone is only 70% mineralized
and still exhibits woven bone as a component. Computer-aided radiographic
densitometry studies have confirmed that the bone-implant interface
decreases the first several months after surgical insertion of an implant.116
The percentage of bone mineralization and the type of supporting bone
influence whether a load to the bone-implant interface is within its
physiologic limits.
It has been reported that the bone-implant contact (BIC) is related to the
bone density and the healing time. For example, in a study by Carr et al the
BIC was greater in the mandible than the maxilla (the mandible is usually
more dense).117 In addition, the BIC was greater at 6 months compared with 3
months in both jaws. An increase in BIC occurred in both the maxilla and
mandible between 3 and 6 months and ranged from a 7% to 9%.90 The healing
time before implant loading may be related to the density of bone because
the strength of bone increases and the BIC increases with a longer time
period. Hence, 3 to 4 months of healing for D1 and D2 bone and 5 to 6
months for D3 and D4 bone have less risk than a shorter time period for all
bone types. The time period between surgical placement and full occlusal
loading is variable, depending on the bone density.
The macroscopic coarse trabecular bone heals about 50% faster than dense
cortical bone. Although it heals more slowly, D1 bone has the greatest
strength and greater lamellar bone contact. The suggested healing time
between the initial and second-stage surgeries is kept similar for D1 and D2
bone and is 3 to 4 months. A longer time is suggested for the initial healing
phase of D3 and D4 bone (5 and 6 months, respectively) because of the lesser
bone contact and decreased amount of cortical bone to allow for the
maturation of the interface and the development of some lamellar bone. In
very immature bone, the healing time may be as long as 8 months.
The D4 implant-bone interface typically found in posterior regions of the
maxilla exhibits minimum initial bone contact, with little to no cortical bone
at the crest or apex. An implant surgery initially may trigger an increase in
the amount of bone in the region. The initial increase of bone cell activity
most likely results from the surgical trauma and the regional acceleratory
phenomenon.74 A longer initial healing time is most beneficial to the poorest
bone density types.
In softer bone, a longer period of time of initial healing and gradual
loading is suggested. As a general rule, D1 bone uses a 3-month (or more)
period before loading, D2 bone a 4-month (or more) period, D3 bone a 5-
month (or more) initial healing period, and D4 bone uses a 6-month (or
more) period.
The combined observations of the macroscopic amount of bone in contact
with a nonloaded implant and the microscopic type of bone at the stage II
surgery of the implant demonstrates a wide difference in D1 to D4 bone
densities. However, the major improvement in bone density and strength
long term occurs as a consequence of loading the implant.
Four prosthodontic steps are suggested for the reconstruction of a partially
or completely edentulous patient, with endosteal implants supporting a
cemented prosthesis. Each of the four major prosthodontic appointments
also are separated by a period of time related to the bone density observed at
the initial time of surgery. In addition, the dentist attempts to gradually
increase the load to the implant at each prosthetic step.
The four prosthetic steps are: (1) abutment insertion, preparation, final
impression and temporary (of the esthetic zone); (2) a metal try-in and new
bite registration; (3) initial delivery of the prosthesis; and (4) final evaluation
of the restoration and hygiene appointment.
In simple restorative cases, the prosthetic appointments may be reduced to
three appointments: (1) abutment selection, preparation, final impression,
opposing impression, and closed-mouth bite registration; (2) initial delivery
of the restoration; and (3) final evaluation stage (accompanied by a hygiene
appointment).
Type D1 bone benefits from the greatest amount of lamellar bone contact
at the beginning of the restoration process. As a result, gradual loading of
the implant interface through spacing of the prosthodontic appointments is
least important, and the restorative appointments can be separated by as
little as 1 week. Type D2 bone responds favorably to physiologic loads. The
four prosthetic appointments during which the implant body is loaded
sequentially are separated by 2 weeks or more. As a result, the initial 4
months of healing after surgery and 2 months for prosthesis fabrication
make the overall treatment time 5.5 months.
The prosthodontic appointments for D3 bone are separated by at least 3
weeks, and overall treatment takes about 7 months to complete, including
the 5 months of initial healing. During this time the bone contact percentage
can increase, and the fine woven bone trabeculae can mature into coarser
lamellar trabeculae, with an increase in mineral content. The progressive
loading process is more critical for D3 bone than for D2 or D1 bone because
of its weakness and less initial bone contact.
In D4 bone the progressive bone loading protocol is most critical. The
scheduling of restorative appointments err on the side of safety, separated by
at least 4 weeks. As a consequence, the overall treatment time for D4 bone is
twice that of D1 or D2 bone and requires at least 9 months (including 6
months of initial healing). This schedule allows sufficient time for mature
lamellar, mineralized bone to develop at the interface and increases the
numbers of trabeculae in direct contact and within the network region of the
implant (see Table 16.5).
When the dentist uses multiple implants, the weakest bone area
determines the gradual load protocol. If the anterior maxilla and posterior
maxilla are restored together, the posterior maxilla would determine the
initial healing period and the time period between each prosthetic
appointment.
Diet.
The implant clinician controls the diet of the patient to prevent overloading
during the early phases of the restorative process. During the initial healing
phase, the clinician instructs the patient to avoid chewing in the area,
especially when the implants are placed in a one-stage approach with an
exposed healing abutment. After being uncovered, the implant connected to
an abutment for cement retention is at greater risk of loading during
mastication. The patient is limited to a soft diet such as pasta and fish from
the final impression stage until the initial delivery of the final prosthesis. The
masticatory force for this type of food is about 10 psi. This diet not only
minimizes the masticatory force on the implants but also decreases the risk
of temporary restoration fracture or a partially uncemented restoration.
Either of these consequences can overload an implant and cause unwanted
complications.
The diet should not be overlooked during the restorative phase of
treatment. Most dentists have observed the fracture of an acrylic prosthesis
with harder foods and greater occurrence of uncemented restorations when
they ignore the type of diet during the transitional prosthesis stages.
After the initial delivery of the final prosthesis, the patient may include
meat in the diet, which requires about 21 psi in bite force. The final
restoration can bear the greater force without risk of fracture or
uncementation. After the final evaluation appointment, the patient may
include raw vegetables, which require an average 27 psi of force. A normal
diet is permitted only after evaluation of the final prosthesis function,
occlusion, and proper cementation.
It should be noted that the most damaging forces to a transitional (or final)
restoration is parafunction, not the function of eating. After the prosthesis is
placed into occlusion, the evaluation of parafunction and methods to reduce
its negative side effects are critical to the loading process.
Occlusal Material.
The occlusal material may be varied to gradually load the bone-implant
interface. During the initial steps, the implant has no occlusal contact and in
essence has no material over it. At subsequent appointments, the clinician
may use acrylic as the occlusal material, with the benefit of a lower impact
force than metal or porcelain. Either metal or porcelain can be used as the
final occlusal material.
If parafunction or cantilever length causes concern relative to the amount
of force on the early implant-bone interface, the dentist may extend the softer
diet and acrylic restoration phase several months. In this way, the bone has a
longer time to mineralize and organize to accommodate the higher forces.
Occlusion.
The clinician gradually intensifies the occlusal contacts during prosthesis
fabrication. No occlusal contacts are permitted during initial healing (step 1).
The first transitional prosthesis is left out of occlusion in partially edentulous
patients (step 2). The occlusal contacts then are similar to those of the final
restoration for areas supported by implants. However, no occlusal contacts
are made on cantilevers or offset loads (step 3). The occlusal contacts of the
final restoration follow the implant-protective occlusion concepts.
Prosthesis Design.
There are four potential prosthesis designs in a restorative process. During
initial healing, the clinician attempts to avoid any load on the implants,
including soft tissue loads. In a completely edentulous patient, relief and a
soft tissue conditioner (also relieved) may be used. The first transitional
acrylic restoration in partially edentulous patients has no occlusal contact
and no cantilevers. Its purpose is to splint the implants together and reduce
stress by the mechanical advantage and to have implants sustain masticatory
forces solely from chewing. The second acrylic transitional restoration has
occlusal contacts placed over the implants with occlusal tables similar to the
final restoration but with no cantilevers in nonesthetic regions. The final
restoration has narrow occlusal tables and cantilevers designed with occlusal
contacts following implant-protective occlusion guidelines.
Progressive Loading Phases.

After the surgical stage II uncovery procedure or one-stage implant healing,
the implant clinician evaluates clinical mobility, bone loss (horizontal and
vertical), proper placement in reference to prosthetic design and angulation
to load, zones of attached gingiva, and gingival thickness. The surgeon
usually attaches a low-profile permucosal extension (PME) to the implant
body at the end of this appointment. This component extends through the
tissue about 2 mm and is protected from early loading.
In selected cases, often when the implant surgeon and restoring dentist are
the same person, one may obtain the preliminary impression during this
appointment if the soft tissues are outside the esthetic areas and if no bone
recontouring or grafting has been performed or a one-stage surgical
approach was used during initial healing. The dentist instructs the patient
with a posterior implant in a partially edentulous arch not to wear any
removable restoration. If anterior teeth are part of the removable prosthesis,
a 7-mm-diameter hole is placed completely through the partial denture
framework around each PME so it will not load the implant. In completely
edentulous patients, the tissue surface of the denture is relieved at least 5
mm over and around the implants and is replaced by a tissue conditioner.
The conditioner also is relieved a few millimeters. The patient returns in 2
weeks for suture removal and to replace the tissue conditioner with a soft
liner.
The procedures for a partially edentulous Kennedy class I or II patient are
first presented. The progressive bone-loading appointment sequence for
cement-retained prostheses is as follows (Table 16.7).
1. Initial abutment selection, final impression, and transitional prosthesis I
2. Metal superstructure try-in and transitional prosthesis II
3. Initial insertion of final prosthesis
4. Final evaluation and hygiene
TABLE 16.7
Progressive Loading Appointments for a Cement-Retained Prosthesis
Occlusal
Step P rocedure Diet Occlusal Contracts
Material
1 Final abutments S oft Ac rylic 1; none
Final impression 2; no c antilever
Transitional
prosthesis
2 Transitional S oft Ac rylic 1 and 2; c ontac ts only on implant; no c ontac ts on c antilevers or pontic s; oc c lusal table
prosthesis II same as final prosthesis
Metal try-in
3 Final prosthesis Harder Metal or Oc c lusion follows implant-protec tive oc c lusion guidelines; narrow oc c lusal table
Adjust oc c lusion porc elain
4 Final evaluation Normal Metal or S ame as above
Hygiene porc elain

Food Impaction
Etiology
Food impaction after placement of a fixed implant restoration can be a
significant complication that is troublesome to the patient and the soft
tissues. There are many reasons for the prosthesis to accumulate food.
Improper Implant Placement.

When implant placement is nonideal, a compromised prosthesis must be
fabricated. This leads to improper contours that compromise esthetics and
the soft tissue health.
Inadequate Contact Area.

If inadequate contact exists, food accumulation will result. This most often
occurs when the restoration is fabricated with angled or tilted adjacent teeth,
which prevent a long contact area.
Prevention
Improper Implant Placement.

Implant placement should be ideal, if conditions (lack of bone) do not allow
this, hard and soft tissue augmentation should be completed to provide a
more ideal condition for implant placement.
Inadequate Contact Area.

When angled or tilted adjacent teeth are present, prior to the fabrication of
the prosthesis, guide planes should be made to allow for a long contact area
in the prosthesis. This also allows for the greater force distribution, which is
advantageous, especially in high stress areas (Fig. 16.112).
FIG 16.112 Food impaction. (A) Usually, it is the result of tilting the adjacent teeth
leading to a point contact. (B) By modifying the adjacent teeth, long contact areas
may be utilized to prevent food impaction and help distribute forces.
Treatment
If food impaction occurs on a chronic basis, the prosthesis should be
modified or refabricated, especially if soft tissue complications arise.
Cement Retention
Cemented implant prostheses have become popular because of the lower
cost, relative simplicity, more passive fit, improved esthetics, and similarity to
traditional prosthetics. However, with all of these advantages comes a
significant disadvantage, the retention of postoperative cement. The retained
cement has been shown to retain bacteria (similar to calculus with a natural
tooth), which leads to peri-implant disease (Fig. 16.113).
FIG 16.113 Cement retention. (A) Cement present in sulcus (arrows). (B) Bone
loss. (C) Failure of implant. (D) Dark hue present 6 months post implant crown
insertion, (E–F) Etiologic complication resulting from sulcular retention of
impression.
Etiology
The etiology of cement-retained peri-implantitis is the following:
Cement.
The retained cement acts as a nidus for bacterial accumulation and
proliferation. The roughened surface of the cement inhibits the hygienic
removal of the bacteria, which leads to peri-implant disease. Cement acts the
same way that as the etiologic factor in periodontal disease.
Timing.
Wilson has shown that the time it takes for retained cement to become
problematic and to eventually be diagnosed is in a range of 4 months to 9.3
years, with an average of 3 years.118
Sulcus Teeth vs. Implant.

Around natural teeth the junctional epithelium and connective tissue
attachment insert perpendicularly into the cementum, which tends to
prevent the flow of excess cement into the sulcus. In contrast, the connective
tissue around dental implants runs parallel, with no attachment into the
implant surface. The flow of cement is not restricted, and it easily migrates
apically (Fig. 16.114).
FIG 16.114 Different attachment systems for implant vs. tooth. (A) Circular fibers
attach into the cementum minimizing the possibility of cement retention, (B)
Because an endosseous implant does not contain an attachment system with the
tissue, retained cement can be easily extruded into the sulcular area. (Adapted from
LeBeau J: Maintaining the long-term health of the dental implant and the implant-borne restoration,
Compend Contin Educ Oral Hyg 3[3]:3–10, 1997.)
Submucosal Margins.
Margins of implant restorations are often placed more than 2 mm
subgingivally for a better emergence profile and esthetics. However, studies
have shown the deeper the margins, the more difficult the removal of
cement. In margins that are greater than 1.5 mm subgingivally, it is almost
impossible to remove the cement totally.119
Location.
Retained cement may attach to the following: (1) crown, (2) abutment, and (3)
bone. If the cement is pushed into the sulcular area and reaches the bone,
significant chronic issues will arise (Fig. 16.115).
FIG 16.115 Residual cement retention; can attach to crown, tissues, or bone.
Many clinicians believe that two-dimensional radiographs will depict
retained cement. However, radiographs are unpredictable because only
cement that is present on the mesial or distal surfaces will be shown.
Additionally, many cements are not radiopaque and need an adequate
thickness to be seen on a radiograph.120 Linkevicius et al have shown in a
clinical study that dental radiographs should not be considered as a reliable
method for cement excess evaluation because results show that cement
remnants are seen less than 10% of the time mesially and distally and 0% of
the time buccally and lingually (Fig. 16.116).121
FIG 16.116 (A–C) Radiographic evaluation of cement retention; can only be seen
on mesial and distal.
Type of Cement.
There are many types of cement used today in implant dentistry to retain
implant-supported crowns. Agar et al have shown that cement with resin
components is the most difficult to remove from the abutment surface after
cementation.122 Cements containing zinc have been shown to be ideal for
cementing implant crowns as they are the easiest to see radiographically.
Zinc phosphate is a well-known popular cement choice, which makes
retrievability very difficult. Additionally, because of its solubility in the oral
environment, a dry field is definitely needed.
Provisional cements are also popular in cementing implant crowns as they
allow for retrieval. However, because provisional cements exhibit weaker
retentive strengths, uncementation of the implant prosthesis may be
problematic.
Radiopacity of Cement.
There is a large variation in the radiographic detection ability of cements.
Some cements have a very high radiographic density, which allows for
detection on radiographs. However, many cannot be detected, even at greater
thickness (≈2 mm).
Cementation Technique.
A common reason for retained cement is the cervical cementation technique,
which usually parallels the technique for cementation on natural teeth. Most
clinicians place an excessive amount of cement within the internal surface of
the crown, which leads to extrusion in the sulcular area. Techniques using
different amounts of cement have been evaluated with mixed results (Fig.
16.117).
FIG 16.117 Cervical cementation technique. (A) Example using a clear cup with
shaving cream placed in the cervical one-third. (B) The cement proceeds up the
sides; however, excess cement still extrudes from the margins.
Prevention
Supragingival Margins.
Excess retained cement may be minimized by designing the abutment
margins supragingivally. However, dentists are reluctant to place the margins
at this level if the crowns are in the esthetic zone. Studies have shown
margins placed 1 mm supragingival or at the gingival margins allow for ease
of cement removal without a decreased chance of retention.123
Ideal Application of Cement.

Controlling the amount of cement that is placed in the implant crown will
allow for a decreased possibility of cement retention. Clinicians are reluctant
to use a small amount of cement because this translates into the possibility
of leakage and loss of retention. Excess cement may lead to improper seating,
alteration of occlusion, and difficulty in cement removal. Ideally, a uniform
thickness of 40 µm over the intaglio surface is ideal; however, in a clinical
setting, this is very difficult. The internal surface of the crown may
sometimes be irregular, and unequal flow patterns may exist between
parallel and nonparallel surfaces. Additional factors that complicate ideal
cementation are the cement's flow properties, viscosity, dimensional stability,
and wettability of the surfaces.
Screw-Retained Prostheses.
Although screw-retained implant prostheses have the disadvantages of
higher cost and compromised esthetics, the lack of cement is a significant
advantage (Fig. 16.118).
FIG 16.118 Prevention of cement retention. (A) Supragingival margins. (B)

Duplicate abutment technique. (C) Screw-retained prosthesis. (D) Cement on
supragingival margin.
Implant Abutment Modification.

To reduce the amount of excess cement, studies have shown that
modification of the abutment leads to less pressure and extruded cement.
Ideally, the abutment should be vented with two 0.75-mm radius vent holes
placed 3 mm apical to the occlusal area of the abutment and 180 degrees
apart. This technique by Wadhwani has shown to limit the amount of cement
extruded into the gingival sulcus of implant-retained crowns (Fig. 16.119).124
FIG 16.119 To minimize excess cement, maintain an open access and two holes
maybe placed 180 degrees apart in the abutment.
Techniques.
Various techniques in the literature have been discussed to reduce retained
cement. A popular technique is the abutment copy technique, which utilizes
Teflon tape inside the intaglio surface prior to copying the abutment with a
polyvinyl siloxane (PVS) material. The cement-filled final implant crown is
seated on the copied abutment for excess cement removal before it is quickly
transferred intraorally to be fully seated. This technique minimizes the
possibility of retained cement; however, it has limitations when cementing a
multiple splinted implant prosthesis.125
The author has developed a technique (lubrication technique), which
utilizes water-soluble petroleum jelly placed on the outer surfaces of the
crown or prosthesis and below the implant margin (i.e., sulcular area). This
prevents any cement from adhering to the crown, sulcus, or underlying bone
(Box 16.7 and Fig. 16.120).
Box 16.7
Reducing Chance of Cement Retention With
Copy Abutment: Lubrication Technique
Step 1: Apply water-soluble petroleum jelly to the outer margin of the crown
with a 1 cc tuberculin syringe.
Step 2: Seal the abutment screw (cotton ball, Teflon tape) without sealing the
entire access.
Step 3: Place a thin layer of petroleum jelly 360 degrees within the sulcus and
around the implant.
Step 4: Apply a thin layer (≈40 µm) of cement to the intaglio surface of the
crown abutment.
Step 5: Seat crown, remove crown, remove excess cement adhered to the
outer margin surface, remove any sulcular excess cement and Vaseline with
a brush.
Step 6: Reseat crown.

FIG 16.120 Lubrication cementation technique. (A) 1 cc Tuberculin syringe filled
with water-soluble petroleum jelly. (B) Water-soluble lubricant is applied to underside
of crown (to prevent cement from adhering to crown). (C–D) Water soluble lubricant
is syringed in sulcus area (to prevent cement from adhering to bone or sulcular
area). (E) Lubricant is placed 360 degrees around abutment. (F) Cement is placed
into crown (marginal area is avoided). (G) Crown is completely seated onto
abutment. (H) Crown is removed. (I) Excess cement is removed from undersurface
of crown. (J) Excess cement is removed in sulcular area with brush. (K) Crown is
reseated for final cementation. (L) Crown is flossed on mesial and distal to the
implant neck to remove final cement.
Treatment
Even the most diligent and skilled implant clinician may leave residual
cement in the sulcular area of implant crowns. The importance of
postoperative appointments for implant patients following cementation of
the restoration cannot be overemphasized. Regular maintenance is extremely
crucial for cement-retained crowns. Some of the symptoms that may warrant
an evaluation for retained cement are localized inflammation, bleeding on
probing, exudate, progressively increased probing depths, and radiographic
bone loss.
Nonsurgical.
Regular curettage with hand instruments.
Surgical.
In many cases, surgical access is necessary for complete cement removal,
which includes flap, curettage, and detoxification with possible grafting (Fig.
16.121).
FIG 16.121 Treatment for retained cement. (A) Soft tissue irritation with chronic
inflammation. (B) Radiographic confirmation of retained cement. (C) Treatment
included surgical access for cement removal that included curettage, detoxification,
and grafting.
Summary
As outlined in this chapter, the principles utilized in dentistry for natural
teeth do not necessarily apply to the practice of implant dentistry as it
pertains to prosthetics. A dental implant exhibits different attachment
mechanisms to the host bone, which changes the force dynamics presented
to their respective prostheses. The intricate component mechanisms of a
dental implant prosthesis react to forces placed upon them, requiring greater
care and attention when designing occlusal schemes. It is paramount that the
implant surgeon and restoring dentist have a clear plan in place based on
sound fundamentals to ensure that the placement of the necessary implants
falls in line with proper biomechanical principles. Steps may be taken to
prevent unnecessary loads on the implant prosthesis, from occlusal scheme
and design to the fabrication of bruxism guards for patients exhibiting
parafunction.
In the prosthetic phase of treatment, possibly more than in any other
phase, prevention may be the easiest to achieve. By using sound
biomechanical principles, the implant dentist may prevent many of the
prosthetic and implant complications that can occur over the life span of a
restoration.
Should complications arise, such as screw loosening, porcelain fracture, or
retained cement, this chapter has provided protocols to safely and
predictably manage these events.
References
1. Pjetursson BE, Bragger U, Lang NP, Zwahlen M. Comparison of
survival and complication rates of tooth-supported fixed dental
prostheses (FDPs) and implant-supported FDPs and single crowns
(SCs). Clin Oral Implants Res. 2007;18(Suppl 3):97–113.
2. Bidez MW, Misch CE. Forces transfer in implant dentistry: basic
3. Goodacre CJ, Bernal G, Rungcharassaeng K. Clinical complications
with implants and implant prostheses. J Prosthet Dent. 2003;90:121–
132.
4. Kourtis SG, Sotiriadou S, Voliotis S, Challas A. Private practice results
of dental implants. Part I: survival and evaluation of risk factors—Part
II: surgical and prosthetic complications. Implant Dent.
2004;13(4):373–385.
5. De Boever AL, Keersmaekers K, Vanmaele G, et al. Prosthetic
complications in fixed endosseous implant-borne reconstructions
after an observations period of at least 40 months. J Oral Rehabil.
2006;33(11):833–839.
6. Chaar MS, Att W, Strub JR. Prosthetic outcome of cement-retained
implant-supported fixed dental restorations: a systematic review. J
Oral Rehabil. 2011;38:697–711.
7. Kallus T, Bessing C. Loose gold screws frequently occur in full-arch
fixed prostheses supported by osseointegrated implants after 5 years.
8. Boggan S, Strong JT, Misch CE, et al. Influence of hex geometry and
prosthetic table width on static and fatigue strength of dental
implants. J Prosthet Dent. 1999;82:436–440.
9. Wie H. Registration of localization occlusion and occluding material
for failing screw joints in the Brånemark implant system. Clin Oral
10. Hurson S. Practical clinical guidelines to prevent screw loosening. Int J
Dent Symp. 1995;3(1):23–25.
11. Balshi TJ, Hernandez RE, Pryszlak MC, et al. A comparative study of
one implant versus two replacing a single molar. Int J Oral Maxillofac
Implants. 1996;11:372–378.
12. Hemming KW, Schmitt A, Zarb GA. Complications and maintenance
requirements for fixed prostheses and overdentures in the
edentulous mandible: a 5-year report. Int J Oral Maxillofac Implants.
1994;9:191–196.
13. McGlumphy EA, Elfers CL, Mendel DA. A comparison of torsional
ductile fracture in implant coronal screws (abstract), Academy of
Osseointegration Proceedings. Int J Oral Maxillofac Implants.
1992;7:124.
14. Binon PP, McHugh MJ. The effect of eliminating implant/ abutment
rotational misfit on screw-joint stability. Int J Prosthodont. 1996;9:511–
519.
15. Binon PP. The evolution and evaluation of two interference fit implant
interfaces. Postgrad Dent. 1996;3:3–13.
16. Binon PP. The effect of implant/abutment hexagonal misfit on screw
joint stability. Int J Prosthodont. 1996;9:149–160.
17. Binon PP. Evaluation of three slip fit hexagonal implants. Implant
Dent. 1996;5:235–248.
18. Carr AB, Brantley WA. Characterization of noble metal implant
cylinders: as received cylinders and cast interfaces with noble metal
alloys. J Prosthet Dent. 1996;75:77–85.
19. Bonde MJ, Stokholm R, Isidor F, et al. Outcome of implant-supported
single-tooth replacements performed by dental students. A 10-year
clinical and radiographic retrospective study. Eur J Oral Implantol.
2010;3:37–46.
20. Jemt T. Single implants in the anterior maxilla after 15 years of follow-
up: comparison with central implants in the edentulous maxilla. Int J
Prosthodont. 2008;21:400–408.
21. Mangano C, Mangano F, Piattelli A, et al. Prospective clinical
evaluation of 307 single-tooth Morse taper-connection implants: a
multicenter study. Int J Oral Maxillofac Implants. 2010;25:394–400.
22. Duncan JP, Nazarova E, Vogiatzi T, et al. Prosthodontic complications
in a prospective clinical trial of single-stage implants at 36 months.
23. Sadid-Zadeh R, Ahmad K. Hyeongil Ki: Prosthetic Failure in Implant
Dentistry. Dent Clin North Am. 2015;59(1):195–214.
24. Cho SC, Small PN, Elian N, Tarnow D. Screw loosening for standard
and wide diameter implants in partially edentulous cases: 3- to 7-year
longitudinal data. Implant Dent. 2004;13(3):245–250.
25. Clelland NL, Van Putten MC. Comparison of strains produced in a
bone stimulant between conventional cast and resin-luted implant
frameworks. Int J Oral Maxillofac Implants. 1997;12:793–799.
26. Clelland NL, Papazoglou E, Carr AB, et al. Comparison of strains
transferred to a bone stimulant among implant overdenture bars
with various levels of misfit. J Prosthodont. 1995;4:243–250.
27. Jemt T. In vivo measurement of precision fit involving implant
supported prostheses in the edentulous jaw. Int J Oral Maxillofac
Implants. 1996;11:151–158.
28. Sadid-Zadeh R, Ahmad K. Hyeongil K: Prosthetic failure in implant
dentistry. Dent Clin North Am. 2015;59(1):195–214.
29. Yao K-T, Kao H-C, Cheng C-K, et al. The effect of clockwise and
counterclockwise twisting moments on abutment screw loosening.
30. Nigro F, Sendyk CL, Francischone CE Jr, Francischone CE. Removal
torque of zirconia abutment screws under dry and wet conditions.
Braz Dent J. 2010;21(3):225–228.
31. Graves SL, Jansen CE, Saddiqui AA, et al. Wide diameter implants:
indications, considerations and preliminary results over a two-year
period. Aust Prosthodont J. 1994;8:31–37.
32. Jorneus L. Loads and designs for screw joints for single crowns
supported by osseointegrated implants. Int J Oral Maxillofac
Implants. 1992;7:353–359.
33. Goheen K. Torque generated by handheld screw drivers and
mechanical torquing devices for osseointegrated implants. Int J Oral
34. Gutierrez J, Nicholls JI, Libman WJ, et al. Accuracy of the implant
torque wrench following time in clinical service. Int J Prosthodont.
1997;10:562–567.
in 152 patients: patient specific and implant specific predictors of
ceramic failure. J Prosthet Dent. 2009;101(6):388–394.
36. Goodacre CJ, Kan JYK, Rungcharassaeng K. Clinical complications of
osseointegrated implants. J Prosthet Dent. 1999;81:537–552.
37. Leinfelder KF, Lemons JE. Clinical restoration materials and techniques.
Lea & Febiger: Philadelphia; 1988.
37a. Malkondu Ö, Tinastepe N, Akan E, et al. An overview of monolithic
zirconia in dentistry. Biotechnol Biotec Eq. 2016;30(4):1–9.
38. Nissan J, Narobi D, Gross D, et al. Long-term outcome of cemented
versus screw retained implant supported partial restorations. Int J
39. Seghi RR, Daher T, Caputo A. Relative flexural strength of dental
restorative ceramics. Dent Mater. 1990;6:181–184.
40. Goodacre CJ, Bernal G, Rungcharassaeng K, et al. Clinical
complications in fixed prosthodontics. J Prosthet Dent. 2003;90:31–41.
41. Malone WFP, Koth DL. Tylman's theory and practice of fixed
prosthodontics. ed 8. Ishiyaku EuroAmerica: St Louis; 1989.
42. Goodacre CJ, Campagni WV, Aquilino SA. Tooth preparations for
complete crown: an art form based on scientific principles. J Prosthet
Dent. 2001;85:363–376.
43. Shillinburg HT, Hobo S, Whitsett LD, et al. Fundamentals of fixed
prosthodontics. ed 3. Quintessence: Chicago; 1997.
44. Gilboe DB, Teteruck WR. Fundamentals of extracoronal tooth
preparation. 1. Retention and resistance form. J Prosthet Dent.
1974;32:651–656.
46. Dykema RW, Goodacre CJ, Phillips RW. Johnston's modern practice in
fixed prosthodontics. ed 4. WB Saunders: Philadelphia; 1986.
47. Potts RG, Shillingburg HT, Duncanson MG. Retention and resistance
of preparations for cast restorations. J Prosthet Dent. 1980;43:303–308.
48. Woolsey GD, Matich JA. The effect of axial grooves on the resistance
form of cast restorations. J Am Dent Assoc. 1978;97:978–980.
49. Juntavee N, Millstein PL. Effect of surface roughness cement space on
crown retention. J Prosthet Dent. 1992;68:482–486.
50. Tuntiprawon M. Effect of surface roughness on marginal seating and
retention of complete metal crowns. J Prosthet Dent. 1999;81:142–147.
51. Brånemark PI. Osseointegration and its experimental background. J
Prosthet Dent. 1983;50:399–410.
52. Kan JY, Rungcharassaeng K, Bohsali K, et al. Clinical methods for
evaluating implant framework fit. J Prosthet Dent. 1999;81(1):7–13.
53. Lee S-J, Cho S-B. Accuracy of five implant impression technique:
effect of splinting materials and methods. J Adv Prosthodont.
2011;3(4):177–185.
54. Millington ND, Leung T. Inaccurate fit of implant superstructures.
Part 1: Stresses generated on the superstructure relative to the size of
fit discrepancy. Int J Prosthodont. 1995;8:511–516.
55. Tan K, Rubenstein JE, Nicholls JI, et al. Three dimensional analysis of
the casting accuracy of one piece osseointegrated implant retained
prostheses. Int J Prosthodont. 1993;6:346–363.
56. Pietrabissa R, Gionso L, Quaglini V, et al. An in vivo study on
compensation mismatch of screwed vs cement-retained implant
supported fixed prostheses. Clin Oral Implants Res. 2000;11:448–457.
57. Lewinstein I, Craig RG. Accuracy of impression materials measured
with a vertical height gauge. J Oral Rehabil. 1990;17:303–310.
58. Dounis GS, Ziebert GJ, Dounis KS. A comparison of impression
materials for complete arch fixed partial dentures. J Prosthet Dent.
1991;65:165–169.
59. Thongthammachat S, Moore BK, Barco MT, et al. Dimensional
accuracy of dental cast influence of tray—material, impression
material and time. J Prosthodont. 2002;11:98–108.
60. Linke B, Nicholls J, Faucher R. Distortion analysis of stone casts made
from impression materials. J Prosthet Dent. 1985;54:794–802.
61. Phillips RW. Skinner's science of dental materials. ed 9. WB Saunders:
Philadelphia; 1991.
62. Binon PP. Evaluation of machining accuracy and consistency of
selected implants, standard abutments and laboratory analogs. Int J
Prosthodont. 1995;8:162–178.
63. Carr AB, Stewart RB. Full-arch implant framework casting accuracy:
preliminary in vitro observation for in vivo testing. J Prosthodont.
1993;2:2–8.
64. Gordon GE, Johnson GH, Drennon DG. The effect of tray selection on
the accuracy of elastomeric impression materials. J Prosthet Dent.
1990;63:12–15.
65. Zarb GA, Albrektsson T, Brånemark P-I. Tissue-integrated prostheses:
osseointegration in clinical dentistry. Quintessence: New York; 1985.
66. Mojon P, Oberholzer JP, Meyer JM, Belser UC. Polymerization
shrinkage of index and pattern acrylic resins. J Prosthet Dent.
1990;64:684–688.
67. American Dental Association Council on Dental Materials and
Equipment. ANSI-ADA Specification No.25 Dental gypsum products.
[Chicago] 2000.
68. Willis LM, Nicholls JI. Distortion in dental soldering as affected by
gap distance. J Prosthet Dent. 1980;43:272–278.
69. Palmquist S, Swartz B. Artificial crowns and fixed partial dentures 18
to 23 years after placement. Int J Prosthodont. 1993;6:179–205.
70. Segelnick S. A survey of floss frequency, habit and technique in a
hospital dental clinic and private periodontal practice. N Y State Dent
J. 2004;70:28–33.
71. Yilmaz B, Seidt JD, McGlumphy ED, Clelland NL. Comparison of
strains for splinted and nonsplinted screw-retained prostheses on
short implants. Int J Oral Maxillofac Implants. 2011;26:1176–1182.
72. Quiryman M, Naert Z, van Steenberghe D, et al. A study on 589
consecutive implants supporting complete fixed prosthesis. J Prosthet
Dent. 1992;8:655–663.
73. Hobkirk JA, Havthoulas TK. The influence of mandibular
deformation, implant numbers, and loading position on detected
forces in abutments supporting fixed implant superstructures. J
Prosthet Dent. 1998;80:169–174.
in 152 patients: patient specific and implant specific predictors of
ceramic failure. J Prosthet Dent. 2009;101(6):388–394.
76. Balshi TJ, Wolfinger GJ. Two-implant-supported single molar
replacement: interdental space requirements and comparison to
alternative options. Int J Periodontics Restorative Dent. 1997;17:426–435.
77. Sullivan D, Siddiqui A. Wide-diameter implants: overcoming
problems. Dent Today. 1994;13:50–57.
78. Hylander WL. The human mandible: lever or link? Am J Phys
Anthropol. 1975;43:227–242.
79. Osborne J, Tomlin HR. Medial convergence of the mandible. Br Dent J.
1964;117:112–114.
80. De Marco TJ, Paine S. Mandibular dimensional change. J Prosthet
Dent. 1974;31:482–485.
81. Hylander WL. Mandibular function in Galago crassicaudatus and
Macaca fascicularis: an in vivo approach to stress analysis of the
mandible. J Morphol. 1979;159:253–296.
82. Abdel-Latif HH, Hobkirk JA, Kelleway JP. Functional mandibular
deformation in edentulous subjects treated with dental implants. Int
J Prosthodont. 2000;13:513–519.
83. Cavicchia F, Bravi F. Free standing vs tooth connected implant
supported fixed partial restoration: a comparative retrospective
clinical study of the prosthetic results. Int J Oral Maxillofac Implants.
1996;9:711–718.
84. Astrand P, Borg K, Gunne J, et al. Combination of natural teeth and
osseointegrated implants as prosthesis abutments: a 2-year
longitudinal study. Int J Oral Maxillofac Implants. 1991;6:305–312.
osseointegrated implant in the treatment of the edentulous jaw. Int J
Oral Surg. 1981;6:387.
86. Parfitt GS. Measurement of the physiologic mobility of individual
teeth in an axial direction. J Dent Res. 1960;39:608–612.
87. Sekine H, Komiyama Y, Hotta H, et al. Mobility characteristics and
tactile sensitivity of osseointegrated fixture-supporting systems. van
Steenberghe D. Tissue integration in oral maxillofacial reconstruction.
Elsevier: Amsterdam; 1986.
89. Bidez MW, Lemons JE, Isenberg BF. Displacements of precious and
nonprecious dental bridges utilizing endosseous implants as distal
abutments. J Biomed Mater Res. 1986;20:785–797.
90. Rangert B, Gunne J, Sullivan DY. Mechanical aspects of a Brånemark
implant connected to a natural tooth: an in vitro study. Int J Oral
91. Komiyama Y. Clinical and research experience with osseointegrated
implants in Japan. Albrektsson T, Zarb G. The Brånemark
osseointegrated implant. Quintessence: Chicago; 1989.
92. Ismail YH, Misch CM, Pipko DJ, et al. Stress analysis of a natural
tooth connected to an osseointegrated implant in a fixed prosthesis. J
Dent Res. 1991;70:460.
93. Misch CE, Bidez MW. Implant protected occlusion, a biomechanical
rationale. Compendium. 1994;15:1330–1342.
94. Shillingburg HT, Fisher DW. Nonrigid connectors for fixed partial
dentures. J Am Dent Assoc. 1973;87:1195–1199.
95. Misch CM, Ismail YH. Finite element analysis of tooth to implant
fixed partial denture designs. J Prosthodont. 1993;2:83–92.
96. Pesun IJ. Intrusion of teeth in the combination implant-to- natural-
tooth fixed partial denture: a review of the theories. J Prosthodont.
1997;6:268–277.
97. Cho GC, Chee WL. Apparent intrusion of natural teeth under an
implant supported prosthesis: a clinical report. J Prosthet Dent.
1992;68:3–5.
98. Rajatihaghi H, Ghanbarzadeh J, Daneshsani N, et al. The accuracy of
various torque wrenches used in dental implant systems. J Dent
Materials Techniques. 2013;2(2):38–44.
99. Nigro F, Sendyk CL, Francischone CE, et al. Removal torque of
zirconia abutment screws under dry and wet conditions. Braz Dent J.
2010;21(3):225–228.
100. Dawson PE. Functional occlusion—from TML to smile design. Mosby: St
Louis; 2007.
101. Abrams L, Coslet JG. Occlusal adjustment by selective grinding.
Cohen DW. Periodontal therapy. ed 4. Mosby: St Louis; 1968.
102. Miyata T, Kobayashi Y, Araki H, et al. The influence of controlled
occlusal overload on peri-implant time. 4. A histologic study in
monkeys. Int J Oral Maxillofac Implants. 2002;17:384–390.
103. Reilly DT, Burstein AH. The elastic and ultimate properties of
compact bone tissue. J Biomech. 1975;80:393–405.
104. Misch CE. Three-dimensional finite element analysis of two plate form
neck designs, master's thesis. University of Pittsburgh; 1989.
105. Papavasiliou G, Kamposiora P, Bayne SC, et al. Three dimensional
finite element analysis of stress distribution around single tooth
implants as a function of bony support prosthesis type and loading
during function. J Prosthet Dent. 1996;76:633–640.
106. Ko CC, Kohn DH, Hollister SJ. Micromechanics of implant/tissue
interfaces. J Oral Implantol. 1992;18:220–230.
107. Ha C-Y, Lim Y-J, Kim M-J, et al. The influence of abutment angulation
108. Duyck J, Van Oosterwyck H, Vander Sloten J, et al. Magnitude and
distribution of occlusal forces on oral implants supporting fixed
prostheses: an in vivo study. Clin Oral Implants Res. 2000;11:465–475.
109. Jacobs R, van Steenberghe D. Comparison between implant
supported prostheses and teeth regarding passive threshold level. Int
J Oral Maxillofac Implants. 1993;8:549–554.
110. Mericske-Stern R, Assal P, Mericske E, et al. Occlusal force and oral
tactile sensibility measured in partially edentulous patients with ITI
implants. Int J Oral Maxillofac Implants. 1995;19:345–353.
111. Hammerle CH, Wagner D, Bragger U, et al. Threshold of tactile
sensitivity perceived with dental endosseous implants and natural
teeth. Clin Oral Implants Res. 1995;6:83–90.
112. Belser UC, Hannam AG. The influence of working-side occlusal
guidance on masticatory muscles and related jaw movement. J
Prosthet Dent. 1985;53:406–413.
113. Stein RS. A dentist and dental technologist analyze current ceramo
metal procedures. Dent Clin North Am. 1977;21:729–749.
114. Borchers L, Reichart P. Three-dimensional stress distribution around
a dental implant at different stages of interface development. J Dent
Res. 1983;62:155–159.
115. Roberts EW, Turley PK, Brezniak N, et al. Bone physiology and
metabolism. J Calif Dent Assoc. 1987;15:54–61.
116. Strid KG. Radiographic results of tissue integrated prostheses.
Brånemark P-I, Zarb GA, Albrektsson T. Tissue integrated prostheses:
osseointegration in clinical dentistry. Quintessence: Chicago; 1985.
117. Carr AB, Larsen PE, Gerard DA. Histomorphometric comparison of
implant anchorage for two types of dental implant after 3 and 6
months' healing in baboon jaws. J Prosthet Dent. 2001;85:276–280.
118. Wilson TG Jr, Thomas G. The positive relationship between excess
cement and peri-implant disease: a prospective clinical endoscopic
study. J Periodontol. 2009;80(9):1388–1392.
119. Present S, Levine RA. Techniques to control or avoid cement around
implant-retained restorations. Compendium. 2013;34(6):432–437.
120. Linkevicius T, Vindasiute E, Puisys A, et al. The influence of the
cement margin position on the amount of undetected cement. A
prospective clinical study. Clin Oral Implants Res. 2013;24(1):71–76.
121. Wadhwani C, Rapoport D, La Rosa S, et al. Radiographic detection
and characteristic patterns of residual excess cement associated with
cement-retained implant restorations: a clinical report. J Prosthet
Dent. 2012;107(3):151–157.
122. Agar JR, Cameron SM, Hughbanks JC, Parker MH. Cement removal
from restorations luted to titanium abutments with simulated
subgingival margins. J Prosthet Dent. 1997;78:43–47.
123. Linkevicius T, Vindasiute E, Puisys A, Peciuliene V. The influence of
margin location on the amount of undetected cement excess after
delivery of cement-retained implant restorations. Clin Oral Implants
Res. 2011;22(12):1379–1384.
124. Wadhwani C, Piñeyro A, Hess T, et al. Effect of implant abutment
modification on the extrusion of excess cement at the crown-
abutment margin for cement-retained implant restorations. Int J Oral
125. Wadhwani C, Piñeyro A. Technique for controlling the cement for an
implant crown. J Prosthet Dent. 2009;102:57–58.
17
Occlusion Complications
Randolph R. Resnik, Carl E. Misch
The clinical success and longevity of endosteal dental implants as load-

bearing abutments are controlled largely by the mechanical setting in which
they function. The treatment plan is ultimately responsible for the design of
the prosthesis along with the position and number of the implants. The most
common complications of implant prostheses relate to biomechanical factors
such as porcelain fracture, unretained prostheses (cement or screw),
abutment screw loosening, early implant failure after loading, and implant
component fracture.1-4
Studies have shown that after an implant achieves rigid fixation with
proper crestal bone contour and gingival health, the mechanical stress or
strain beyond the physical limits of hard tissues is a primary cause of bone
loss around loaded implants.5-8 After successful surgical and prosthetic
rehabilitation with a passive prosthesis, noxious stresses and loads applied to
the implant and surrounding tissues result primarily from nonideal occlusal
contacts. Complications (prosthetic or bony support) reported in follow-up
studies underline occlusion as a determining factor for success or failure.9,10
However, the choice of an occlusal scheme for implant-supported prostheses
is broad and often controversial. The occlusal scheme is especially important
during parafunctional activity of the jaws because the magnitude and
duration of the parafunctional occlusal stresses are greater than functional
stress. It is also more important when the implant foundation is not ideal in
number or location to the implant-bone interface, where the overall surface
area of load is reduced.
Almost all implant occlusal concepts are based on the concepts developed
with natural teeth and are transposed to implant support systems with little
to no modification. This approach has some justification. Wearers of
complete dentures are reported to exhibit mandibular movement and
velocity different from patients with natural dentitions. However, Jemt et al11
found that after fixed implant reconstructions are placed into previously
edentulous patients, the displacement of the jaw during mandibular opening
and function is similar in velocity and movement to that in patients with
natural teeth. Gartner et al12 also demonstrated similar habitual chewing for
patients with implants and patients with natural teeth. During maximal
occluding forces, electromyograms demonstrated that the implant patient
group activated similar working and nonworking muscles as patients with a
natural dentition. It appears logical to derive implant occlusion from occlusal
principles for the natural dentition. However, several conditions indicate that
implant prostheses are at greater biomechanical risk than natural teeth,
which may lead to complications in both the prosthetic components and the
overall health of the implants that support them. As a result, some of the
occlusal concepts for implants should be modified from concepts for the
natural dentition. With a knowledge of the fundamentals of dental implant
occlusion, a clinician may significantly impact the longevity of successful
implant treatment for his or her patient, while avoiding many complications.
Differences Between Natural Teeth and
Dental Implants
The differences between natural teeth and dental implants are numerous.
Most importantly, a natural tooth has a support system that allows for a
reduction of forces to the surrounding bone. A natural tooth is encompassed
and suspended by a periodontal ligament (PDL), and force and stress are
dissipated and distributed away from the axis of natural teeth (Fig. 17.1).
Because an implant has no PDL, the concentration of force and stress is at
the crestal region (Table 17.1).
FIG 17.1 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) inserting 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 (i.e., 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.)
TABLE 17.1
Occlusal Overload in Comparing Natural Teeth vs. Dental Implants
Characteristic Natural Teeth Dental Implants

Interface Periodontal membrane Direc t bone
Junctional Hemidesmosomes and basal lamina (lamina luc ida Hemidesmosomes and basal lamina (lamina luc ida and lamina densa
epithelium and lamina densa zones) and sublamina luc ida zones)
Connective 12 groups: 6 insert perpendic ular to tooth surfac es; Only 2 groups: parallel and c irc ular fibers; no attac hment to implant
tissue ↓ c ollagen, ↑ fibroblasts surfac e; ↑ c ollagen, ↓ fibroblasts
Vascularity Greater; supraperiosteal and PDL Less; mainly periosteal
Biologic width 2.04–2.91 mm 3.08 mm
Mobility + −
P ain +/− (tooth may be hyperemic ) −
Attrition + wear fac ets, abfrac tion, fremitus − (~ porc elain frac ture, possible sc rew loosening)
Radiographic + inc reased radiopac ity and thic kness of c ribriform Crestal bone loss
changes plate
Interference + (proprioc eption) − (osseoperc eption)
awareness
Nonvertical Relatively tolerated Results in bone loss
forces
Force related Primary: movement of PDL Primary: osseous movement
movement S ec ondary: osseous movement
Lateral force Apic al of root surfac e Crestal bone
Lateral 56–108 µm 10–50 µm

movement
Apical 25–100 µm 3–5 µm
movement
Tactile High Low
sensitivity
Signs of PDL thic kening, fremitus, mobility, wear fac ets, pain S c rew loosening, sc rew frac ture, abutment frac ture, implant body
overloading frac ture, bone loss
PDL, Periodontal ligament.
Peripheral Feedback System

The control of the muscles of mastication is directly related to a peripheral
feedback system that includes the enamel-dentin-pulp complex and
mechanoreceptors in the dentate dentition. However, endosseous implants
lack the periodontal proprioception feedback system, resulting in less fine
motor control and alteration of the awareness of force.
Teeth
Natural teeth have a unique sense of occlusal awareness in the control of
mastication, force, and control of muscles during swallowing. The role of the
enamel-dentin-pulp complex has been shown in the control of oral function
via the peripheral feedback system.13 In combination with the periodontal
mechanoreceptors (PMRs), afferent information is sent to the brain on the
horizontal and vertical forces applied to teeth. The mechanoreceptors are
very sensitive to low forces and allow for the recognition of occlusal force and
the discrimination of load magnitude and direction. The sensitivity of teeth
varies with anterior teeth being most sensitive to low forces (<1 N), whereas
posterior teeth exhibit sensitivity to forces in the range of less than 4 N.
The number of mechanoreceptors have been shown to be more numerous
around anterior teeth compared with posterior teeth. The anterior receptors
relay information concerning forces in all directions because they have
greater sensitivity to occlusal loading. These teeth contribute to the
positioning of food in the oral cavity and manipulation of objects between
the teeth.14
In comparing individual teeth, the cuspid plays a dominant role in the
control of function. Anatomy (large crown and long root) and location in the
dental arch (cornerstone position) allow for the cuspid to have an ideal
physiologic feedback system from the mechanoreceptors. Additionally, the
morphologic makeup of the cuspid, featuring a lingual contour that divides
the mesial and distal via an axial ridge, allows for crown strength for
anterolateral guidance. Because of the contour, arch location, and root length,
this allows for the preferred mesial (not distal) canine guidance in
mastication to confirm there is a distinct anterior component of the jaw and
ipsilateral condylar movement.14
The posterior teeth in comparison have fewer mechanoreceptors, which
results in a lower static and dynamic sensitivity allowing for posterior teeth
to accommodate higher forces during mastication. The posterior teeth are
strategically located with large clinical crowns and multiple roots (increased
surface area) to sustain the increased posterior forces. Additionally, the first
molars provide guidance during the eruption process and are functionally
positioned in the center of the occlusal table.14
Implants
With dental implants, studies have shown that the lack of mechanoreceptors
may influence jaw motor control because of a peripheral feedback system.15
Because of the absence of these mechanoreceptors, there is lack of afferent
information to be relayed to the central nervous system (CNS) during biting
and chewing with dental implants. The proprioception associated with dental
implants is similar to natural teeth that are blocked by local anesthesia.16
However, the term “osseoperception” has been used to describe a different
type of mechanical stimulation specific to dental implants. This type of
sensation has been associated with mechanoreceptors in the orofacial tissues
(e.g., most likely present in muscle, joint, mucosa, periosteal tissues).17 PMRs
have been described to react to very low levels of force, and the detection of
static force is approximately 10 times greater for patients with implants
compared with dentate patients.18 The mechanoreceptors that are
responsible for osseoperception have been shown to be located a distance
from the actual implant and qualitatively remit different sensory signals to
static and dynamic loads.
Force-Related Factors
Many differences exist in comparing clinical aspects of force-related factors
between natural teeth and dental implants.
Vertical Occlusal Loads
Tooth.
When a vertical occlusal load is applied to a natural tooth, a normal
physiologic movement exists that is related to the surface area and root
morphology. Therefore, the number, length, diameter, position, surrounding
bone density, and health of the PDL has a primary influence on a tooth's
mobility. A healthy tooth under normal conditions exhibits zero clinical
mobility in a vertical direction. Actual initial vertical tooth movement has
been shown to be approximately 28 µm and is the same for anterior and
posterior teeth (Fig. 17.2).19
FIG 17.2 Physiologic movement of a healthy natural tooth has been measured as
28 µm in the apical direction and up to 108 µm in the horizontal direction. (From Misch
Implant.
Rigid fixation is a clinical term used to describe the absence of clinical
mobility of an implant tested with vertical or horizontal forces less than 500
g. Osseointegration is a histologic term that is used to define bone in direct
contact with an implant surface at the magnification of a light microscope
(Fig. 17.3). Over the years, these two terms have been used interchangeably,
and implant abutment support is most predictable with rigid fixation. Lack
of implant mobility does not always coincide with a direct bone-implant
interface.20 However, when observed clinically, rigid fixation usually means
that at least a portion of the implant is in direct contact with bone, although
the percentage of bone contact cannot be specified.21 A mobile implant
usually indicates the presence of connective tissue between the implant and
bone and soft tissue interface.
FIG 17.3 Osseointegration is a histologic term that describes a direct bone-to-
implant contact at the level of magnification of a light microscope. (From Misch CE:
Lack of clinically observable movement does not mean the true absence of
any movement. A healthy implant moves less than 73 µm; it appears as zero
clinical mobility (rigid fixation). Sekine et al22 applied a gradually increasing
load over a 2-second period to a tooth and an implant. The teeth moved
immediately with a light load (primary tooth movement) and less with an
additional load (secondary tooth movement). The implant, in contrast to the
natural tooth, did not feature primary tooth movement. A heavier force
caused the implant to move gradually, similar to the secondary tooth
movement (Fig. 17.4).
FIG 17.4 A gradually increasing load over a 2-second period was applied to a tooth
(left) and an implant (right). The natural tooth has two phases of movement which
correlates to the compression of the periodontal ligament and then compression of
the bone. The implant lacks the initial movement and movement is proportional to
the movement of the bone. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Nonvertical Occlusal Loads (Horizontal)
Tooth.
When evaluating horizontal mobility on natural teeth, it is often difficult to
determine the true movement. For example, a “nonmobile” posterior natural
tooth actually moves horizontally 56–73 µm. The human eye does not
perceive this movement. The anterior teeth, which often have slight clinically
observable movement, actually can move approximately 0.1 mm.
With nonvertical loading, forces on natural teeth are better tolerated and
will adapt to the force much more favorably than dental implants. Studies
have shown that lateral forces on a healthy natural tooth are rapidly
dissipated away from the bone crest toward the apex of the tooth. This is
because natural teeth may move 56–108 µm with rotation around the apical
one-third of the root. Muhlemann23 found that horizontal tooth movement
may be divided into initial mobility and secondary movement. The initial
mobility is observed when a light force is applied, will occur immediately,
and is a consequence of the PDL. Initial horizontal tooth mobility is greater
than initial vertical movement. A very light force (500 g) horizontally moves
the tooth. The initial horizontal mobility of a healthy, “nonmobile” posterior
tooth is less than that of an anterior tooth and ranges from 56–75 µm, which
is two to nine times the vertical movement of the tooth. Initial horizontal
mobility is even greater in anterior teeth and ranges from 70–108 µm in
health.24
The secondary tooth movement described by Muhlemann occurs after the
initial movement when greater forces are applied. When an additional force
is applied to the tooth, a secondary movement is also observed, which is
related directly to the amount of force. The secondary tooth movement is
related to the viscoelasticity of the bone and can measure 40 µm under
considerably greater force (Fig. 17.5).
FIG 17.5 A secondary horizontal movement of a tooth occurs after the initial tooth
movement when a greater force is applied and is related to the deformation of the
alveolar bone. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Implant.
With dental implants, the nonvertical stress will most likely result in trauma
to the supporting bone. An implant will gradually move and may move 10–50
µm.19 An implant will have greater forces around the crest of the bone
because an implant does not pivot as much as a tooth does, and all the forces
are generated at the crest, which usually will result in bone loss.
Sekine et al25 evaluated the movement of endosteal implants with rigid
fixation and found a range of 12–66 µm of movement in the labiolingual
direction. Komiyama26 reported 40–115 µm of implant movement in the
mesiodistal direction under a force of 2000 g (≈4.5 psi) and a labiolingual
range of 11–66 µm. The greater implant movement in the mesiodistal
dimension corresponds to the lack of cortical bone between the implants in
this direction compared with the thicker lateral cortical plates present in the
labiolingual dimension. Rangert et al27 suggested that part of this implant
movement may also be due to component flexure of the implant abutment
and screw. The mobility of implants varies in direct proportion to the load
applied and the bone density, reflecting the elastic deformation of bone
tissue.
Excessive Contacts/Occlusal Overloading

When premature contacts or excessive contacts occur on a natural tooth, the
tooth will often become mobile, become hyperemic, or fracture. The
associated proprioception will allow the neuromuscular system and
peripheral feedback system to control the occlusal forces during function.
This will minimize the possibilities of prematurities and interferences. In
comparison, when a premature contact is associated with a dental implant,
the patient usually is asymptomatic, and the implant will have no mobility.
Because of the lack of PMRs, there is no feedback system present. This will
most likely result in crestal bone loss or mechanical failure will result
because there is no feedback system to make the patient aware of a
prematurity.
Prematurities on natural teeth are less common and may be uneventful for
years. Natural teeth may orthodontically reposition themselves or become
symptomatic. However, excessive contacts on dental implants are more
damaging because they will usually result in a force overload with resultant
crestal bone loss (Fig. 17.6).
FIG 17.6 Implant exhibiting bone loss from excessive force. Note the high cusps
and concavity for the maxillary plunging cusp.
Masticatory
With a natural tooth, the specialized PMRs are responsible for providing
neural information to the muscles during mastication. Several hundred of
these specialized receptors are present, which are used for fine motor control
and conscious perception of tactile forces when applied to the teeth.17
The compression of the collagen fibers in the PDL will send nerve signals
to the CNS. These receptors surrounding teeth have different sensitivities to
the force applied, and each individual receptor is stimulated independently
depending on the position within the PDL. The resultant force vectors have
varying numbers depending on the anatomic location within the oral cavity.
Usually, the number of force vectors decreases from anterior to posterior
teeth. The anterior natural teeth may perform very delicate tasks, whereas
the posterior teeth are less sensitive. This is why the anterior teeth can split
food very precisely, whereas the posterior teeth are mainly used to grind
food.28
Masticatory Efficiency
Many studies have evaluated the masticatory efficiency between teeth and
implants. Svensson et al29 completed studies on the mastication effectiveness
of food between (1) natural teeth, (2) natural teeth with full coverage
restorations, and (3) implant-supported restorations. Results showed that
natural teeth were far superior in the refined action of splitting or incising
food. Natural teeth were shown to be significantly better able to position the
food boluses between the teeth and be able to fine-tune the direction of the
bite force. This is most likely the result of the signal of the PMRs to the CNS
on the spatial location and direction of forces needed to chew the food.
However, with splinted fixed crowns and implant prostheses, the results
showed inconsistent and poor incising of food. With tooth-supported
prostheses, even though PMRs are present, the tooth-supported prosthesis
(splinted crowns) dissipates the force, and the PMRs are not activated. With
an implant prosthesis, because no PMRs are present, no peripheral feedback
system exists to allow for the refined motor movement (Fig. 17.7). These
findings are consistent with studies by Trulsson and Gunne,30 in which
prostheses supported by the oral mucosa (removable complete dentures) or
dental implants (fixed prostheses) had difficulty in holding and splitting
food, similar to patients with natural teeth and profound anesthesia. The
afferent information is blocked by the local anesthesia (Fig. 17.8).
FIG 17.7 (A) Examples of subjects with natural dentition or tooth- or implant-
supported fixed prostheses trying to split a spherical piece of chocolate hard candy
into two parts of equal size with the anterior teeth. (B) The mandibular movements
(frontal view) of these same subjects during a representative “first chewing cycle” of
eating a hazelnut. (A, From Svensson KG, Trulsson M: Physiological Considerations of Oral
Implant Function. In Klineberg I, Eckert S: Functional occlusion in restorative dentistry and
prosthodontics, St Louis, 2016, Mosby. B, Modified from Grigoriadis J, Trulsson M, Svensson KG:
Motor behavior during the first chewing cycle in subjects with fixed tooth- or implant-supported
prostheses, Clin Oral Implants Res 27:473–480, 2016.)
FIG 17.8 Illustration of the “hold-and-split” task developed by Trulsson and
Johansson.16 (A) The handheld apparatus employed to record the bite forces
exerted on the morsel of food. This morsel rested on the upper horizontal plate, and
the apparatus was positioned between the upper and lower teeth. (B)
Representative force profile (upper trace) and predicted response (in impulses/s) by
the periodontal mechanoreceptors (lower trace) for a subject with natural teeth while
holding and splitting a peanut. (C) Representative force profile (upper trace) and
predicted receptor response (lower trace) for a subject with natural teeth while
splitting a peanut. (From Svensson KG, Trulsson M: Physiological Considerations of Oral Implant
Function. In Klineberg I, Eckert S: Functional occlusion in restorative dentistry and prosthodontics, St
Natural teeth are associated with greater masticatory efficiency, and less
trauma to the dental complex will be present. Patients are able to refine their
masticatory movements because of the mechanoreceptors that are present.
However, with dental implant prostheses (also tooth-supported prostheses),
the masticatory refinement is much poorer, leading to the greater possibility
of angled- or force-related complications to the implant or prosthesis.
Speed of Mastication
Patients with natural teeth take longer to masticate food compared with
tooth-supported and implant prostheses. This is most likely due to natural
teeth requiring time for the PMRs to signal the CNS. This slow and delayed
response is the result of the timing required to collect and process the spatial
information and stimulate the appropriate motor program and efferent
output to manipulate the muscles to fire with respect to the direction and
amount of bite forces. The processing of PMRs requires time for the central
processing, resulting in a longer contact phase of mastication. These results
are consistent with other studies that have shown patients with natural teeth
will initially hold the food under low force directly after contact and then will
apply greater biting forces. There is a delay between the contact of the food
and the splitting of the food.
Patients with a tooth-supported fixed prosthesis and implant prosthesis have
altered spatial information. Although patients with tooth-supported fixed
partial dentures (FPDs) have PMRs, because of the rigid connection, minimal
signals to the CNS exist to initiate motor function. In patients with an
implant-supported prosthesis, osseoperception must occur. This involves
signaling sensory information concerning contact forces (dynamic loading) to
the artificial teeth in an osseointegrated dental implant fixed prosthesis from
remote receptors in other tissues activated by vibrations transmitted via the
jawbone.31 The sensory information of PMRs is significant with respect to
masticatory efficiency and protection of the dentition. Impairment (tooth-
supported FPD) or absence (implant-supported prosthesis) results in poorer
performance and altered motor activity. Patients with tooth-supported and
implant-supported prostheses also have a compromised protective
mechanism in which they masticate their food with higher force, less delay
(i.e., may not be able to comprehend that the food is too hard), and less
precision. With increased speed of mastication, the greater possibility of
damage to the prosthetic system exists.
Biting Force
PMRs present in natural teeth provide proprioception and early detection of
occlusal forces and interferences. Bite forces on natural teeth during
mastication and parafunction are not as strong because of the fine motor
control of the mandible. Trulsson and Johansson16 showed that the lack of
proprioception leads to a heavier bite in patients with implants compared
with natural dentition. Mericske-Stern et al32 measured the oral tactile
sensibility with test steel foil and showed that minimal pressure was
significantly higher with implants than with natural teeth (3.2 vs. 2.6 steel foil
sheets). Jacobs and van Steenberghe33 evaluated occlusal awareness and
found that interference perceptions of natural teeth, implants with opposing
teeth, and implants opposing implants were approximately 20 µm, 48 µm,
and 64 µm. Hämmerle et al34 also concluded the mean threshold value of
tactile perception for implants (100.6 g) was ninefold higher than that of
natural teeth (11.5 g).
Biting forces are significantly higher with an implant-supported prosthesis
compared with natural teeth, and this may lead to excessive forces on the
implant system because of lack of awareness. The sensory feedback system
present in teeth cannot be modulated the same around dental implants. The
increased biting force may lead to abnormal forces on the dental implant
system, which may lead to crestal bone loss, screw loosening, or component
fracture (Fig. 17.9).
FIG 17.9 Excessive biting force often leads to prosthesis failure (i.e., porcelain
fracture).
Implant-Protected Occlusion
Because of the biomechanical differences between teeth and implants,
modifications must be made in the development of occlusal schemes for
prosthetic rehabilitation. An ideal occlusal scheme is a primary requisite for
long-term implant prosthetic survival, especially when parafunction or a
marginal foundation is present. A poor occlusal scheme increases the
magnitude of loads and intensifies mechanical stresses (and strain) to the
implant system. These factors increase the frequency of complications of the
prosthesis and bone support. Crestal bone loss most likely leads to an
increase in peri-implantitis. The conditions may also cause tissue shrinkage
and loss of interdental papillae and poor esthetic results. All these
complications may be initiated by biomechanical stress as a result of
excessive occlusal loads (functional or parafunctional).
The concept of implant-protected occlusion (IPO) was developed by Misch.
It is unique and specifically designed for the prosthetic rehabilitation of
dental implants. This protocol provides for an environment to reduce the
biomechanical stress to the implant and prosthesis. Minor modifications
from conventional prosthodontic occlusal concepts have been established
with the sole purpose of reducing stress on the prosthesis.
The ideal occlusion for an implant prosthesis is to control the stress on the
implant system, provide a prosthetic and biologically acceptable implant
interface, and maintain long-term stability of the marginal bone and
prosthesis. The occlusal scheme should maintain the occlusal load that has
been transferred to the implant system within the physiologic and
biomechanical limits of each patient. However, these principles are not
identical for all patients or restorations. The forces generated by a patient are
influenced by ranges of parafunction, masticatory dynamics, implant arch
position and location, arch form, crown height, and crown morphology. The
treatment planning philosophy for dental implants varies greatly and
depends on these several parameters. The implant dentist can address these
force factors best by selecting the most ideal implant position, number, and
size; using the progressive bone loading concept in poorer bone densities;
and selecting the appropriate occlusal scheme using stress-relieving design
elements.
The following guidelines and principles have been established to restore
fixed and removable implant-supported prostheses. The IPO principles for
fixed and removable prostheses address several conditions to decrease stress
to the implant system, including existing occlusion, implant body angle to
occlusal load, cusp angle of implant crowns, mutually protected articulation,
cantilever or offset loads, crown height, crown contour, occlusal contact
position, timing of occlusal contacts, and protection of the weakest
component (Box 17.1).
Box 17.1
Principles of Implant Protected Occlusion
1. Evaluate existing occlusion before treatment
2. Ideal treatment plan before treatment
3. No premature contacts
4. No nonaxial loading
5. Shallow anterior guidance
6. Minimal posterior cusp angle
7. Minimize cantilevers
8. Increase surface area
9. Narrow occlusal plane
10. Ideal occlusal contact
Preimplant Occlusal Principles

Evaluate Existing Occlusion Before Dental Treatment
The first step in the process of treatment planning for dental implants is the
fabrication of accurate diagnostic casts for the evaluation of the patient's
existing occlusion. The value of diagnostic casts or study models is crucial in
all phases of dentistry, especially in oral implantology. When edentulous sites
exist, the combination of continued bone loss and dentition changes related
to missing teeth greatly increases the number of factors that must be
considered for oral rehabilitation compared with traditional prosthodontic
treatment. The implant dentist must determine the type of implant
prosthesis initially (i.e., FP-1, FP-2, FP-3, RP-4, RP-5), followed by the number
and location of ideal and optional abutment sites and the final occlusal
scheme.
Diagnostic casts must be accurate reproductions of the maxillary and
mandibular arches with complete representation of the edentulous areas
(Fig. 17.10). Diagnostic casts mounted on an articulator allow for an initial
evaluation for implant site selection, angulation requirements, prosthesis
selection, existing occlusion, and fabrication of a surgical template. In
addition, these study casts allow for a preoperative assessment of treatment
options that may be discussed with other practitioners and laboratory
technicians and during patient consultations.
FIG 17.10 It is paramount that diagnostic casts be an accurate representation of

the entire dental anatomy including the edentulous ridges. (From Misch CE: Dental
To accurately assess the maxillomandibular relationship of the implant

patient, proper mounting of the study casts must be completed using an
articulator. An articulator is defined as a “mechanical instrument that
represents the temporomandibular joints (TMJs) and jaws, to which
maxillary and mandibular casts may be attached to simulate some or all
mandibular movements.”35 Today, the use and indications for the various
types of articulators employed in prosthetic dentistry are very controversial.
At the present time, wide arrays of articulator types are available, with
multiple ranges of movements and adjustments, making classification and
nomenclature very confusing. In the dental literature, many different
classifications exist; however, today the most simplistic and most often used
classification parallels the “Glossary of Prosthodontic Terms.” Articulators
maybe categorized into four groups according to the adjustability of the
articulators. This classification is based on the ability of the articulator to
accept the five most common patient records: (1) facebow transfer, (2) centric
jaw record, (3) protrusive record, (4) lateral records (Bennett movement), and
(5) intercondylar distance (Table 17.2 and Fig. 17.11).36
TABLE 17.2
Articulator Options
Hinge Axis (Facebow) CR Record P rotrusive Movement Lateral Excursion Bennett Movement
Nonadjustable (Simple and Average) No Yes No No No
Semiadjustable Approximate (arbitrary) Yes Yes (straight line) Yes (straight line) Approximate
Fully Adjustable Yes (kinematic ) Yes Yes (c urved) Yes (c urved) Yes
CR, Centric relation.

FIG 17.11 Examples of various articulators used in implant dentistry. (A) Simple
hinge. (B) Arbitrary plane line. (C) Semiadjustable. (D) Fully adjustable. (From Misch
To evaluate the patient's occlusion, an accurate mounting of diagnostic

casts with an open-bite registration and facebow transfer allows for the static
and dynamic (semi or fully adjustable articulators) relationships of the teeth
and edentulous ridges, without interference from protective neuromuscular
reflexes. By evaluating the articulated study casts, abnormalities or
interferences that are not easily detectable intraorally can be determined
along with comprehensive information that is paramount in dental implant
treatment planning (Box 17.2).37,38
Box 17.2
Diagnostic Information Obtained From Proper
Mounting of Study Casts in Implant Dentistry
1. Occlusal centric relation position, including premature occlusal contacts
2. Edentulous ridge relationships with respect to adjacent teeth and opposing

arches
3. Position and location of potential natural abutment sites including

inclination, rotation, extrusion, spacing, parallelism, and esthetic
considerations
4. Tooth morphology and signs of parafunction (e.g., wear facets, fractures)
5. Evaluation of potential force direction in future implant sites
6. Present occlusal scheme including the presence of balancing or working

contacts
7. Edentulous soft and hard tissue angulation, length, width, locations,

permucosal esthetic position, muscle attachments, and bony
protuberances (tori, tuberosities)
8. Interarch space
9. Occlusal curve of Wilson and curve of Spee
10. Skeletal arch relationships
11. Evaluation of opposing dentition
12. Potential future occlusal schemes
13. Site evaluation of edentulous sites
14. Arch location of future abutments

15. Arch form and symmetry
16. Interdental contact location
17. Used for a diagnostic wax-up

From Misch, CE: Dental implant prosthetics, ed 2, St. Louis, 2015, Mosby.
Ideally, all abnormal contacts should be identified and eliminated before

the implant prosthodontic phase. However, to evaluate the patient's current
dental status, the implant clinician must have a thorough understanding of
the various types of occlusion and interferences that patients may have (Box
17.3).
Box 17.3
Occlusal Terms
Occlusal Planes
Curve of Spee—the anatomic curve of the occlusal surfaces, beginning with
the cusp tip of the mandibular canine and following the buccal cusp tips of
the premolar and molar teeth, continuing through to the anterior border of
the mandibular ramus. In natural dentition, the curve must be sufficiently
low in the posterior to allow for disocclusion of the posterior teeth during
protrusive movement. In edentulous patients with complete dentures, the
curve must be higher to maintain posterior tooth contact in protrusive
excursions.109
Curve of Wilson—the curve in the frontal plane that is formed by an
imaginary line of the buccal and lingual cusp tips of similar teeth on each
side of the arch. In theory, the occlusion should be spherical, the curve in the
lower arch being concave and the curve in the upper arch being convex. The
curvature in the lower arch is affected by an equal lingual inclination of the
right and left molars so that the tip points of the corresponding cross-
aligned cusps can be placed into the circumferences of a circle. The
transverse cuspal curvature of the upper teeth is affected by the equal buccal
inclinations of their long axes. That curve, as viewed in the frontal plane, is
formed by an imaginary line touching the buccal and lingual cusp tips of
similar teeth on each side of the mandibular arch. The curve is concave in
the lower arch and should be in harmony with lateral anterior guidance to
provide disocclusion of the maxillary lingual cusps on the nonworking side
during lateral excursions.110
(A) Curve of Spee. (B) Curve of Wilson. (From Bath-Balogh MB, Fehrenbach MJ: Illustrated
dental emb ryology, histology, and anatomy, ed 3, St Louis, 2011, Saunders.)
Teeth Relationships
Centric occlusion—the occlusion of opposing teeth when the mandible is in
centric relation. This may or may not coincide with the maximal intercuspal
position.109
Centric relation—the maxillomandibular relationship in which the condyles
articulate with the thinnest avascular portion of their respective discs with
the complex in the anterosuperior position against the shapes of the
articular eminencies. This position is independent of tooth contact. Also,
centric relation is the most retruded relation of the mandible to the maxillae
when the condyles are in the most posterior unstrained position in the
glenoid fossae from which lateral movement can be made at any given
degree of jaw separation.
Maximum intercuspation—the complete intercuspation of the opposing
teeth independent of condylar position, sometimes referred to as the best fit
of the teeth regardless of the condylar position.
Occlusion Types
Group function occlusion—a type of occlusion involving multiple contact
relations between the maxillary and mandibular teeth in lateral movements
on the working side whereby simultaneous contact of several teeth act to
distribute occlusal forces.109
All facial (buccal) cusps on the working side contact the opposing
dentition, and no contact is made on the nonworking side. Schuyler first
observed that nonworking side contacts were destructive, resulting in
neuromuscular disturbances, temporomandibular joint dysfunction,
accelerated or increased periodontal breakdown and excessive wear.111 This
“unilateral” balanced occlusion or “group function” allows for working side
contacts to distribute the occlusal load. The absence of nonworking side
contacts prevents destructive, obliquely directed forces.
Ideally, in this occlusal scheme, the implant-supported prosthesis should
receive stress along the long axis of the implant. In lateral movement, the
total stress should be transmitted among the implant or tooth segments.
There should be no interferences during closure into the maximum
intercuspal position, proper interocclusal clearance should be maintained,
and the teeth should contact in lateral movement without interferences.
Group function.
Mutually protected occlusion—mutually protected occlusion is an occlusal

scheme in which the posterior teeth prevent excessive contact of the anterior
teeth in maximum intercuspation, and the anterior teeth disengage the
posterior teeth in all mandibular excursive movements. An alternative
occlusal scheme is one in which the anterior teeth disengage the posterior
teeth in all mandibular excursive movements, and the posterior teeth
prevent excessive contact of the anterior teeth in maximum intercuspation.109
In mutually protected occlusion, also termed canine protected occlusion,
maximum intercuspation coincides with the optimal condylar position of the
mandible (centric relation). Forces applied to the posterior teeth are directed
along their long axis. During lateral and protrusive excursions, the maxillary
and mandibular anterior teeth guide the mandible so that no posterior
occlusal contacts occur. This results in a decrease in frictional wear. The
posterior teeth protect the anterior teeth in centric relation, whereas anterior
teeth protect the posteriors in protrusion, and canines protect the incisors
and posterior teeth during lateral excursive movements. Centric relation will
coincide with maximum intercuspation. Ideally, there should be stable
posterior tooth contacts with vertically directed resultant forces.
Mutually protected occlusion.
Bilateral balanced occlusion—a type of occlusion that has bilateral,

simultaneous, anterior, and posterior occlusal contacts of teeth in centric
and eccentric positions.109 Working and nonworking contacts are present.
This type of occlusion is present in the construction of complete dentures to
prevent tipping of the denture. A balanced occlusion in natural dentition
with normal periodontium is very rare and if present is most likely the result
of advanced attrition. This type of occlusion is based on the theory that
forces are generated horizontally instead of vertically. Wide, maximum
contacts in intercuspation and eccentric movements are needed.
Bilateral balanced occlusion.
Medial-positioned lingualized occlusion—lingualized occlusion was first

postulated by Gysi and further modified by Payne (maxillary buccal cusps of
posterior teeth are reduced) and Pound (placed the lingual cusp of
mandibular posterior teeth between lines drawn from the canine to each
side of the retromolar pad). This occlusion is designed to narrow the occlusal
table to reduce the forces to the bone and stabilize the lower denture (see
Fig. 17.84).
Implant protected occlusion—this type of occlusion was developed by Misch
and is defined as techniques that allow for the implants to have an increased
longevity. The concept includes the use of implants of the greatest width, the
anterior teeth should disclude the posterior teeth, absence of lateral contacts
in excursions, occlusal contacts more medial than the natural teeth, and a
reduced occlusal table width.
Interferences
Occlusal prematurity—any contact of opposing teeth that occurs before the
planned intercuspation.109
Deflective occlusal contact—a contact that displaces a tooth, diverts the
mandible from its intended movement, or displaces a removable denture
from its basal seat.
Occlusal disharmony—occlusal surfaces are not in harmony with other
tooth contacts or the anatomic and physiologic components of the
craniomandibular complex.
Interferences may also be classified according to the effect the
interference has on a particular part of occlusion.112
Centric Occlusal Interferences
With a centric occlusal interference, the premature contact causes the
mandible to deflect forward or laterally from the optimal superior position
of the mandibular condyles in the glenoid fossa. These types of interferences
may cause parafunctional habits such as clenching or bruxism with
associated muscle fatigue and temporomandibular joint pain.113 There are
two types:
1. Arc of closure interference—a tooth contact that interferes with closure to

maximum intercuspation in centric relation by causing the mandible to
deflect forward.
2. Line of closure interference—a tooth contact that interferes with closure to

maximum intercuspation in centric relation by causing the mandible to
deviate to the right or left.
Centric interferences.
Working Occlusal Interferences
A working occlusal interference occurs between the contacting maxillary and
mandibular teeth during lateral movement on the side that corresponds to
the direction in which the mandible is moving.
Working occlusal interferences.
Nonworking Occlusal Interferences

A nonworking occlusal interference is a deflective contact that occurs on the
opposite side of the direction of mandibular movement. These types of
forces are potentially damaging to the masticatory apparatus (especially with
implants) because they place shear forces outside the long axis of the teeth
(or implants) and may cause bone loss and disruption of normal muscle
function. They also increase the amount of force to the dentition during the
excursions because more muscle mass fires in the masseter and temporal
musculature.
Nonworking occlusal interferences.
Protrusive Occlusal Interferences

A protrusive occlusal interference occurs during deflective contact between
the mesial aspects of the mandibular posterior teeth and the distal aspects
of maxillary posterior teeth on protrusive mandibular movement. This is not
considered a border movement and is usually less damaging to the
stomatognathic system. However, these types of interferences may be
damaging to teeth and implants because they result in shear forces because
they prevent the posterior teeth from being disoccluded by the incisors.
Protrusive occlusal interferences.
Diagnostic Wax-Up Before Treatment

Techniques used to determine the location, angulation, and contours of the
final prosthesis are initiated by the completion of a diagnostic wax-up.
Procedures range from simplistic (single missing tooth) to complex (full-
mouth rehabilitation).
Partially Edentulous
Diagnostic wax-up.
Duplicate diagnostic casts are mounted on an articulator, and a diagnostic
wax-up is completed for the desired contour, occlusal scheme, and esthetic
aspects of the final restoration. Attention should be given to individual tooth
morphology, tooth axis, gingival contours, and interdental contacts. The
diagnostic wax-up technique is especially recommended when full-mouth
rehabilitation is indicated, particularly if a change in vertical dimension is
desired (Fig. 17.12 and Box 17.4).
FIG 17.12 (A–C) Diagnostic wax-up for a partially edentulous patient. (From Misch
Box 17.4
Diagnostic Wax-Up
1. Fabrication of diagnostic casts: Impressions are made of the maxillary and
mandibular ridges. It is more important that the impressions have no
voids, as opposed to the dental casts, because they result in a positive
mistake compared with a negative representation. If indicated, a facebow
transfer is completed to relate the maxillary cast to the articulator along
with a centric relation interocclusal record. The impressions should be
poured in dental stone with the proper water-to-powder ratio.
2. Selection of an articulator: Select the desired articulator as per the

complexity of the case. Ideally, a semiadjustable articulator is used to
simulate the jaw movements of the patient when any occlusal disease is
present.
3. Mounting of the diagnostic casts: The maxillary and mandibular diagnostic

casts are mounted with the facebow transfer and the centric bite.
4. Diagnostic wax-up completed: Future implant sites are evaluated for ideal
implant placement, spacing, and contour restrictions. The edentulous
spaces are waxed to replicate ideal positioning of the teeth and contours.
Denture teeth may be used as a substitute for the wax.
5. Duplication of the final diagnostic wax-up: The final diagnostic cast is

duplicated to allow for laboratory-fabricated surgical templates, or a fully
edentulous setup may be processed and used as an interim prosthesis.
A common clinical situation that may become problematic is when a

posterior tooth is missing and the opposing tooth supraerupts into the space.
The plunging cusps of the opposing dentition usually will cause either a
premature contact or an angled load. Management should include informing
the patient before treatment so as to prevent complications from
modifications of the offending tooth (i.e., enameloplasty leading to tooth
sensitivity) or possible endodontic therapy and full coverage restorations.
Completely Edentulous
No modification to existing prosthesis is indicated.
For fully edentulous cases, duplication of the patient's existing prosthesis (if
esthetically and functionally ideal) may be used for the mounting of the
diagnostic casts. The simplest technique is the use of a denture duplicator
(Fig. 17.13).
FIG 17.13 If the patient's existing prosthesis is esthetically and functionally

acceptable, the prosthesis may be used in the diagnostic process. (A) Denture
duplicator. (B) Duplication is completed with the use of alginate and acrylic. (A,
Courtesy Lang Dental Manufacturing Company, Inc., Wheeling, IL. B, From Misch CE: Dental implant
Modification to existing prosthesis is indicated.

If modification of the existing prosthesis is required because of a change in
esthetics or function, a traditional complete denture setup is indicated. After
the try-in approval appointment, the prosthesis may be duplicated to be used
as a radiographic or surgical template fabrication (Fig. 17.14).
FIG 17.14 Diagnostic wax-up for a fully edentulous patient. (From Misch CE: Dental
Management.
The evaluation of the patient's existing occlusion is crucial to the long-term
success of the implants and implant prosthesis. Maximal intercuspation (MI)
is defined as the complete intercuspation of the opposing teeth independent
of condylar position, sometimes described as the best fit of teeth regardless
of the condylar position.39 Centric occlusion (CO) is defined as the occlusion
of opposing teeth when the mandible is in centric relation.40 This may or may
not coincide with the tooth position of MI. Its relationship to centric relation
(a neuromuscular position independent of tooth contact with the condyles in
an anterosuperior position) is noteworthy to the restoring dentist. The
potential need for occlusal adjustments to eliminate deflective tooth contacts
as the mandible closes in centric relation and the evaluation of their potential
noxious effects on the existing dentition and the planned restoration is
important to evaluate.
In implant dentistry today, many clinicians begin to evaluate the occlusion
of the patient when the final implant prosthesis is delivered to the patient.
However, this time-frame is often too late for proper restoration of the
patient (Fig. 17.15). The underlying question that helps determine the need
for occlusal correction before restoration of the implant patient is the
observation of negative symptoms related to the existing condition. This may
include TMJ conditions, tooth sensitivity, mobility, wear, tooth fractures,
cervical abfraction, or porcelain fracture. The fewer and less significant the
findings, the less likely an overall occlusal modification is required before
restoration of the patient. However, in most cases, to properly assess these
conditions, the clinician should perform these diagnostic techniques to
minimize future complications.
FIG 17.15 (A) A maxillary first molar is replaced with an implant. The lateral forces
should be applied to the anterior teeth during mandibular excursions. (B) The implant
crown is seated, and the right mandibular excursion is evaluated. The premolars
exhibit a slight working interference on the buccal cusps. The maxillary premolars
have slight gingival recession and initial cervical abfraction regions below the
cementoenamel junction. The excursive force is reduced when the posterior teeth
do not interfere during excursions. The buccal cusp inclines of the premolars should
be reduced. If the incisal edge of the canine continues to wear in the future, the
occlusal contacts will need to be modified further when the posterior teeth contact
during excursions. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
As a general rule, the more teeth replaced or restored, the more likely the
patient is restored to CO. For example, if a completely edentulous mandible
is to be restored with an implant-supported fixed prosthesis, CO provides
consistency and reproducibility between the articulator and the intraoral
condition. The slight changes in occlusal vertical dimension and its
relationship to the position of anterior implant abutments to the direction of
force may be studied and implemented on the articulator without the need to
record a new occlusal vertical position on the patient. When one anterior
tooth is being replaced, the existing MI position is often satisfactory to
restore the patient even though a posterior interference and anterior slide
into full interdigitation may be present (with little clinical variance from the
ideal conditions). However, in a partially edentulous patient, the existing
occlusion should be evaluated to determine if noxious conditions are present.
A considerable prosthetic advantage is present when centric relation
occlusion is harmonious with maximal intercuspal position. Lack of change
in the occlusal vertical dimension permits a closed-mouth centric recording
during prosthetic reconstruction for the fabrication of the prosthesis without
the need for an accurate hinge axis recording of the condyles or fully
adjustable articulators. When the incisal edge position of the maxilla is
determined, its position usually causes a steeper protrusive or excursive
position than the condylar disc assembly on semiadjustable articulators. As a
result, posterior disocclusion can be easily established. These conditions
permit the prosthetic reconstruction to be fabricated in the laboratory and
transferred accurately to the patient.
Correction of the deflective contacts before treatment has many
advantages and may follow a variety of approaches depending on the severity
of the incorrect tooth position: selective odontoplasty (a subtractive
technique), restoration with a crown (with or without endodontic therapy), or
extraction of the offending tooth. Premature contacts may be ascertained
after proper mounting of the study casts with the use of a wax spacer or bite
registration (open-mouth bite). On removal of the occlusal records that
separate the teeth, the premature or irregular contacts may be determined
and verified when the casts are closed and then modified intraorally.40
The occlusion may require complete rehabilitation to eliminate potential
unfavorable forces to the implant restoration. In some complex cases, both
arches may require prosthodontic treatment to establish the desired occlusal
schemes. Parafunctional bruxism with loss of incisal guidance from attrition
and an opposing single denture are the most common conditions that
mandate more comprehensive opposing dentition modification (Box 17.5).
Box 17.5
Common Occlusion Definitions Used in
Prosthodontic Dentistry
Centric relation: The maxillomandibular relationship in which the condyles
articulate with the thinnest avascular portion of their respective discs with
the complex in the anterosuperior position against the shapes of the
articular eminences. This position is independent of tooth contact.
Centric occlusion: The occlusion of opposing teeth when the mandible is in

centric relation. This may or may not coincide with the maximal
intercuspal position.
Maximal intercuspal position: The complete intercuspation of the opposing

teeth independent of condylar position; sometimes referred to as the best
fit of the teeth regardless of the condylar position.
Anterior (incisal) guidance: The influence of the contacting surfaces of the

mandibular and maxillary anterior teeth on mandibular movements.
Data from The glossary of prosthodontic terms, J Prosthet Dent 94:10–92, 2005.
Ideal Treatment Planning—Implant Positioning

The positioning of the implant within the bone is vitally important to
minimize stress to the implant system. When a force is placed on a tooth or a
dental implant, it is referred to as a vector (i.e., defined in magnitude and
direction).41 Occlusal forces are typically three-dimensional, with components
directed along one or more of the clinical coordinate axes. The primary forces
of occlusion can be resolved into a combination of components in any given
plane. The same magnitude of force can have dramatically different effects
on the implant system, solely because of the direction of the applied load.
This is especially noted on implant support systems because they are more
rigid.
Natural teeth are designed primarily to be able to withstand long-axis
loads. The natural tooth roots in most of the oral cavity are positioned
perpendicular to the curves of Wilson and Spee. Although chewing is in an
elliptical “teardrop” pattern, when the teeth finally contact, the forces are
directed along the long axis of the roots, especially during power biting (Fig.
17.16). The apical movement of teeth is minimal compared with their lateral
movement. Lateral loads are significant in the maxillary anterior teeth. The
consequences of a lateral force to a tooth are reduced because of the
increased tooth mobility, which decreases the effects of the lateral force
component of a load. However, an implant does not withstand this lateral
load like a tooth.
FIG 17.16 The natural teeth occlude perpendicular to the curves of Wilson and
Spee. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Implants are also designed for long-axis loads. Two-dimensional finite

element analysis by Binderman42 in 1970 evaluated 50 endosteal implant
designs and found that all designs sustained stress contours concentrated
primarily at the transosteal (crestal) region. In addition, less stress was
observed under a long-axis load compared with angled loads. Since then,
two-dimensional and three-dimensional finite element analyses by several
authors have yielded similar results (Fig. 17.17).43,44
FIG 17.17 A three-dimensional finite element analysis of an implant with a long-axis
load. The stresses are mainly at the crestal region and primarily have compressive
forces. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
An axial load over the long axis of an implant body generates less overall
stress and a greater proportion of compressive stress compared with an
angled force to the implant body. For example, when an implant body is
loaded along its long axis, a 100-N force results with an axial force component
of 100 N, and no lateral force component is observed. The implant body
should be positioned perpendicular to the curves of Wilson and Spee, just as
with natural teeth.
However, most anatomic variations of the bone (e.g., bony concavities) are
located on the facial aspect and influence implant body positioning. An
implant body may need to be positioned with a 15-degree angle to avoid the
facial concavity and is positioned at 15 degrees to the occlusal load. This
angled implant may be restored during prosthetic reconstruction with a 15-
degree angle abutment. From the level of the crest of the ridge to the occlusal
plane, the implant abutment looks similar to one in an axial implant body.
The laboratory technician and restoring clinician often treat the angled
implant and axial implant in similar fashion. However, in the 15-degree
angled implant body, the load to the facial bone increases by 25.9% compared
with an axial load (Fig. 17.18).45 Additionally, if the implant clinician places
the implant body with a 30-degree angulation, the buccal force component of
any occlusal load will result in a 50% increase of the load applied to the facial
bone.
FIG 17.18 An implant loaded in the long axis does not increase the buccal force
component of the load (far left). A 15-degree angle increases the buccal force
component by 25.9% (middle). A 30-degree angle load increases the force by 50%.
When the forces are applied along the long axis of an implant body, stresses are
concentrated on the crestal region (far left). The intensity of the stress is not
increased as a result of the position of the implant. The implant body in the center is
15 degrees off the long axis. With an angled abutment of 15 degrees, the implant
restoration is similar to the previous situation. However, now 25.9% greater stress is
on the crestal bone; all other factors are similar. The implant body on the far right is
30 degrees off the long-axis load. With a 30-degree angled abutment, the crown may
appear similar. However, the abutment screw, abutment-implant connection, and
implant-bone interface are subject to a 50% increase in stress on the facial aspect
of the system. B, Buccal; CL, Crown long axis; L, Lingual. (From Misch CE: Dental
Prevention.
The clinician should always adhere to the ideal implant positioning
principles as discussed in Chapter 6 to prevent poor force distribution.
Ideally, dental implants should be placed perpendicular to the curve of Spee
and the curve of Wilson. This will minimize the possibility of angled forces,
which may lead to force-related bone loss and component failure.
Additionally, implants should be placed parallel to the adjacent natural tooth
root with ideal spacing (i.e., 3.0 mm between implants and >1.5 mm from
adjacent tooth). The possible exception to this rule is the mandibular
posterior area because of the curvature of the mandible (i.e., mandibular first
molar replacement should bisect the long axis of the second premolar and
second molar) (Fig. 17.19).
FIG 17.19 As the angle of the implant body load direction increases, the stresses
to the entire crown implant-bone system increase. B, Buccal; L, lingual. (From Misch
Postimplant Occlusal Principles

No Premature Contacts/Hyperocclusion on Implant Prostheses
A premature contact occurs when an occlusal contact on closure interferes
with the normal movement and positioning of the mandible. Studies have
shown that premature contacts may cause bone loss or implant failure.6,46
Etiology.
A fundamental biomechanical formula is stress equals force divided by the
area over which the force is applied (S = F/A).41 During either maximum
intercuspation or CO, no occlusal contacts should be premature, most
importantly on implant-supported crowns or prosthesis. Premature occlusal
contacts often result in localized lateral loading of the opposing contacting
crowns.
The surface area of a premature contact is usually minute; however, the
magnitude of stress to the bone will increase proportionately (i.e., S = F/A).
When a premature contact occurs, the occlusal force will be applied to one
region rather than being shared by several abutments and teeth. In addition,
because the premature contact is most often on an inclined plane, the
horizontal component of the load increases the shear crestal stresses and the
overall amount of stress to the entire implant system. The implant system
(occlusal porcelain, abutment screw, and cement retaining the crown) is at
increased risk because shear loads increase the possibility of complications.
This is a general criterion for natural teeth, but the concept is much more
important on implant prostheses with their higher impact force and less
occlusal awareness for the several reasons previously addressed. Miyata et
al47 evaluated premature contacts on implant crowns in monkeys (Macaca
fascicularis). The crestal bone was histologically evaluated on implant crowns
with 100 µm, 180 µm, and 250 µm of premature contacts for 4 weeks.48 The
crowns with 100-µm premature contacts had little bone changes. The 180-µm
group demonstrated a V-shaped pattern of bone loss for several millimeters.
The 250-µm implant crowns had a large V-shaped defect around the implants
for 4 weeks that extended for more than two-thirds of the implant body (Fig.
17.20).
FIG 17.20 (A) An implant crown with 100-µm premature contact for 4 weeks
displayed little crestal bone change. (B) An implant crown with a 180-µm premature
contact for 4 weeks had 2–3 mm of crestal bone loss. (C) An implant crown with
250-µm premature contact for 4 weeks had marginal bone loss of more than two-
thirds of the implant length. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Isidor9 evaluated excessive premature contacts on implants in monkeys

over a 20-month period on eight integrated implants. Implant failure
occurred in six of eight implants between 2 and 14 months. The implants that
did not fail had greater bone density and crestal bone loss with osteoclastic
activity within the threads of the implants (Fig. 17.21). The premature contact
on an implant system contributes to a higher risk of early abutment screw
loosening, porcelain fracture, early loading failure, and crestal bone loss (Fig.
17.22).
FIG 17.21 (A) Three-fourths of integrated implants with premature occlusal
contacts failed 2 to 14 months after loading. (B) The implants that did not fail had
crestal bone loss. (C) The implants that did not fail had osteoclastic activity within
the threads. (From Isidor R: Histological evaluation of peri-implant bone at implants subjected to
occlusal overload or plaque accumulation, Clin Oral Implants Res 8:1–9, 1997.)
FIG 17.22 Premature contact on central incisor (implant), which is more
susceptible to increased biomechanical stress at the implant crest because of
increased horizontal movement of the natural teeth.
Prevention.
The elimination of premature occlusal contacts is especially important when
habitual parafunction is present because the duration and magnitude of
occlusal forces are increased. The elimination of premature contacts is more
critical with dental implants because of the lack of proprioception and the
inability of the implant to move and dissipate the forces. With the natural
dentition and its increased proprioception, an initial premature occlusal
contact on a tooth often affects the closure of the mandible to result in an MI
position different from CO. A premature contact on an implant crown does
not benefit from such protective features; as a result, the implant system is at
increased risk. Occlusal evaluation in CO and MI and adjustment as
necessary in partially edentulous implant patients are more critical than in
natural dentition because the premature contacts can result in more
damaging consequences on implants compared with teeth.49
Additionally, occlusal contacts should allow for a wide freedom (1.0–1.5
mm) in centric relation and MI position. This will minimize the possibility of
premature contacts and allow for a more favorable force distribution.50
Timing.
The occlusal contact in CO on implant prostheses with adjacent natural teeth
requires a reduced initial mechanical load on the implants. The most
common method an implant clinician uses to determine the timing of
occlusal contacts at the implant prosthesis delivery is to ask the patient,
“How does the bite feel? Is the crown too high?” This is not the ideal
technique to ascertain the ideal occlusion for the patient. Jacobs and van
Steenberghe51 evaluated occlusal awareness by the perception of an
interference. When natural teeth oppose each other, an interference is
perceived at approximately 20 µm.39 An implant opposing a natural tooth
detects an interference at approximately 48 µm; therefore, it is more than
twice as poor. An implant crown opposing an implant crown perceives the
interference at 64 µm, and when a tooth opposes an implant overdenture, the
awareness is 108 µm (five times poorer than teeth opposing each other).
Mericske-Stern et al52 measured oral tactile sensitivity with steel foils. The
detection threshold of minimal pressure was significantly higher on implants
than on natural teeth (3.2 foils vs. 2.6 foils). Similar findings were reported by
Hämmerle et al34 in which the mean threshold value for implants (100.6 g)
was 8.75 times higher than that of natural teeth (11.5 g). The use of subjective
questions (e.g., “How does the bite feel?”; “Is the implant crown high?”) is a
poor indicator for hypercontacts compared with a crown on a natural tooth.
As a consequence of decreased quantity and quality of occlusal awareness, a
premature occlusal contact may remain on an implant crown after occlusal
adjustment.
The procedure to obtain ideal contact is as follows (Fig. 17.23):
1. Patient bites into centric relation with a very light force. An extra thin
articulating paper (<10 µm shimstock) is used, and any contact on the
implant is removed. The patient should be able to bite lightly and the
shimstock removed unobstructed. GOAL: Natural tooth to take the greater
force so this will coincide with the PDL being compressed.
2. The patient is then instructed to bite with heavy force; the shimstock
should be placed between the implant prosthesis and opposing dentition
with difficulty in removal. GOAL: The heavy force exerted equals the
compression of the PDL, resulting in an even contact between the natural
tooth and implant.
3. In patients with parafunctional habits, extra care should be exercised to
prevent premature loading of the implant.
FIG 17.23 Occlusion timing. (A) In light occlusion, no contact should exist on the
implant prosthesis as shimstock (approximately 10 µm) is easily pulled through. (B)
On heavy occlusion (clenching), the teeth will move apically (periodontal ligament),
and the implant crown will have light contact (i.e., shimstock having resistance when
pulled through). (C) If implant prosthesis and natural teeth occlude evenly with light
occlusion, the implant will be in hyperocclusion and subject to biomechanical
overload. (Courtesy Glidewell Dental.)
Even though the patient “feels” the occlusion to be ideal, premature contacts
may still occur because of the difference in the vertical movement of teeth
and implants in the same arch. Ideally, the natural teeth should exhibit
greater initial contacts compared with implants through “timed” contacts.
When hard or parafunctional bite forces cause depression of the natural
teeth, they are closer to the implant, possibly overloading the implant. In
cases where implant restorations oppose each other, the implant prostheses
must account for the vertical movement of the teeth. An important
component of occlusal harmony is the periodic reevaluation of occlusal
contacts to ensure longevity and decrease morbidity of the prosthesis (Fig.
17.24).
FIG 17.24 Tooth vs. implant occlusal markings. (A) Occlusal marks on natural
tooth in light contact, no contact on implant (second bicuspid). (B) Heavy occlusal
marks on heavy occlusion (first bicuspid and first molar) and minimal markings on
implant (second bicuspid).
No Angled Occlusal Loads

Ideally, the implant prosthesis should have no angled occlusal loads. This is
based on the anisotropy of bone, which refers to the character of bone
whereby its mechanical properties, including ultimate strength, depend on
the direction in which the bone is loaded and the type of force applied. For
example, studies have shown that the cortical bone of human long bones has
been reported as strongest in compression, 30% weaker in tension, and 65%
weaker in shear (Fig. 17.25).53
FIG 17.25 The strength of the bone before fracture depends on the type of force
applied to the bone. Bone is strongest to compression forces, 30% weaker to tensile
forces, and is only 35% as strong to shear loads. Whenever possible, bone should
be loaded with compressive loads. (From Misch CE: Contemporary implant dentistry, ed 2, St
Etiology.
Similar to bone, porcelain, zirconia, titanium components, and cements are
also weakest to shear components of a load. The elimination or reduction of
all shear loads to the implant system is mandatory because of the inherent
weakness of bone, porcelain, titanium components, and cement to shear
loads. Occlusal loads applied at an angle to the implant body may be
separated into normal (compressive and tensile) and shear forces. As the
angle of load to an implant body increases, the amount of compressive and
tensile forces is modified by the cosine of the angle. The force is slightly
reduced. However, the angled component of force is a shear force, and the
shear force is the amount of force times the sine of the load, which
considerably increases the load. The force the bone observes is the sum of
the compressive, tensile, and shear forces. For example, a 100-N force applied
at 12 degrees off-axis will increase the total force to the bone by 100 N Å~
cosine 12 degrees = 97.81 N + 100 N Å~ sine 12 degrees = 20.79 N. The total
force is 97.81 N + 20.79 N = 118.60 N (or almost a 20% increase in total force).
The greater the angle of load to the implant long axis, the greater the
compressive, tensile, and shear stresses (Fig. 17.26).
FIG 17.26 A 12-degree angled force increases the force to the implant system by
18.6%. (From Misch CE: Contemporary implant dentistry, ed 2, St Louis, 2015, Mosby.)
In finite element analysis, when the direction of the force changes to a

more angled or horizontal load, the magnitude of the stress is increased by
three times or more.54,55 In addition, rather than a primarily compressive type
of force, tensile and shear components are increased more than ten-fold
compared with the axial force. Studies have shown that in a photoelastic
block with implants inserted, the strain contours in the bone may be
observed (Fig. 17.27). The axial-loaded implants have less strain in the system
(left side and lower right of Fig. 17.27). The angled implant has more strain
lines indicating greater loads (right upper implant).
FIG 17.27 A photoelastic study of opposing implants in a maxilla and a mandible.
One of the maxillary implant bodies is angled in relation to the direction of load. The
number of stress contour lines in the material is similar for the three implants with a
long-axis load. The stress contour lines are increased for the angled implant
body. (From Misch CE: Contemporary implant dentistry, ed 2, St Louis, 2015, Mosby.)
An angled load to the implant long axis increases the compressive forces at
the crest of the ridge on the opposite side of the implant, increasing the
tension component of force along the same side as the load. The greater the
angle of force to the long axis of the implant body, the greater the potentially
damaging load at the crest of the bone. For example, three-dimensional finite
element analysis demonstrates that a vertical load on an implant with 100%
bone contact may have compressive stress of 4000 psi (27.6 MPa) and almost
no tensile stress at the bone-implant crest interface.54 With a load at a 45-
degree angle on the same implant design, the compressive stress may
increase to 14,000 psi (96.6 MPa), and on the opposite side, tensile stress may
increase to 4000 psi (27.6 MPa). The compressive stresses are tripled, and the
tensile stress increases 1000-fold with a load from a 45-degree angle.
The stress contours in the bone simulant of the three-dimensional studies
resemble the clinical pattern of early crestal bone loss on implants. Not only
does the magnitude of stress increase under angled loads, but it also evolves
into a more noxious shear component, which is more conducive to bone loss
and screw loosening.56 The greater the angle of the force, the greater the
shear component. Bone is 65% weaker to shear load. The amount of the force
increases, and the strength of the bone decreases. It has been reported that
angled occlusal forces decrease the ability of successful bone repair on
natural teeth. It may also impair successful bone remodeling around an
implant.57
Not only is the bone weakest to shear loads, but also forces applied at an
angle to the bone further affect the physiologic limit of compressive and
tensile strengths of bone. A force applied at a 30-degree angle may decrease
the bone tension (Table 17.3). A 60-degree force reduces the strength 30%
under compression and 55% under tension. Not only does the crestal bone
load increase around the implant with angled forces, but also the amount of
stress the bone may withstand (i.e., the ultimate strength) decreases in shear,
tension, and compression. The greater the angle of load, the lower the
ultimate strength of bone. Therefore, IPO attempts to eliminate lateral or
angled loads to an implant-supported prosthesis because the magnitude of
the force increases and the strength of the bone decreases. Barbier and
Schepers58 histologically evaluated implants loaded in the long axis vs. off-
axis loading in dogs. The long-axis–loaded implants had lamellar bone at the
interface. Lamellar bone is mineralized and organized and is called load-
bearing bone in orthopedics. The off-axis–loaded implants had woven bone
at the interface, which is a weak, embryonic type of bone. It is less
mineralized, unorganized, and weaker than lamellar bone (Fig. 17.28). The
greater strains in the bone with off-axis loading may cause the bone to repair
and places it at a higher risk of overload and resorption.
TABLE 17.3
Cortical Bone Strength Related to Angle of Load
Type Strength (mP a) Direction of Load

Compression 193 Longitudinal
133 Transverse
Tension 133 Longitudinal
60.5 60 degrees off axis
51 Transverse
From Reilly DT, Burstein AH: The elastic and ultimate properties of compact bone tissue, J Biomech
80:393–405, 1975.
FIG 17.28 (A) A long-axis load to an implant found lamellar bone at the interface.
(B) An off-axis load to an implant found woven bone (bone of repair) at the interface,
indicating higher strain conditions than ideal. (From Barbier L, Schepers E: Adaptive bone
remodeling around oral implants under axial and nonaxial loading conditions in the dog mandible,
Int J Oral Maxillofac Implants 12:215–223, 1997.)
The microstrain of the crestal bone is increased with an angled load and
may shift from an axial load within physiologic limits to an angled load in the
pathologic overload zone and, as a consequence, result in bone loss. The
greater force, especially in shear, is generated to the entire implant system.
The occlusal porcelain is weaker to shear and may fracture, the cement that
retains the prosthesis is weakest to shear and may become unretained, the
abutment screw more likely becomes loose with shear loads, the crestal bone
region may resorb, and implant components fracture more often with higher
shear loads. When shear forces are increased with an angled load to the
implant system, an attempt should be made to reduce the negative effect of
angled loads.59
The primary component of the occlusal force should be directed along the
long axis of the implant body, not at an angle or following an angled
abutment post (Fig. 17.29). Angled abutments should be used only to
improve the path of insertion of the prosthesis or improve the final esthetic
result. The angled abutment, which is loaded along the abutment axis,
transmits a significant moment load (i.e., tending to rotate or rock the
implant) to the entire implant system.
FIG 17.29 (A) Poor implant positioning results in the need for (B) an excessive
angled abutment (>30 degrees), which is a significant biomechanical disadvantage.
Prosthetic Angled Loads
Etiology.
Greater crestal bone strains with angled forces have been confirmed with
photoelastic and three-dimensional finite element analysis methods.
Whether the occlusal load is applied to an angled implant body or an angled
load (e.g., premature contact on an angled cusp) is applied to an implant
body perpendicular to the occlusal plane, the results are similar (Fig. 17.30).
Biomechanical risk to the implant system is increased. The implant surgeon
may place the implant body ideally, perpendicular to the occlusal plane, but
the restoring dentist then may load the implant crown at an angle. Similar
noxious forces are increased in shear, and a decrease in bone strength occurs
to the crestal bone, along with increase of shear loads on implant
components, and the abutment screws. An angled implant body or an angled
load on the implant crown increases the amount of crestal stresses on the
implant system; transforms a greater percentage of the force to shear force;
and reduces bone, porcelain, and cement strength. In contrast, the
surrounding implant system stress magnitude is least, and the strength of
bone, porcelain, and cement is greatest under a load axial to the implant
body and perpendicular to the occlusal plane. All these factors mandate the
reduction of angled forces to the implant system (Fig. 17.31).
FIG 17.30 When an angled load is placed on an implant body, the compressive
stresses on the opposite side of the implant increase, and the tensile and shear
loads on the same side of the implant increase. Because bone is weaker to tensile
and shear forces, the risks to the bone are increased for two reasons: (1) the
amount of the stress increases, and (2) the type of stress is changed to more
tensile and shear conditions. F, Force. (From Misch CE: Dental implant prosthetics, ed 2, St
FIG 17.31 The force applied to an implant body with an angled load or angled
direction of force is increased in direct relation to the force angle. The major
increase of force is a result of the offset angle of the load. (From Misch CE: Dental
To decrease the force concentrated to the surrounding bone, the implant

should ideally have sufficient surface area to combat the forces. It is well
accepted in the literature that implants with decreased surface area that are
subject to angled loads are magnified if there is deficient implant surface
area.10,60
Ideally, there should be no clinical nonaxial loading of the implant system. If
this cannot be achieved, modifications need to be made such as increased
implant number, larger implant diameter (i.e., increased surface area),
splinted implants, and a narrow occlusal table. In some cases, the prosthesis
may be modified from a fixed to a removable prosthesis to incorporate
increased soft tissue support to share the distribution of forces.
Management: Angled Loads.

Most implant bodies inserted at an angle of greater than 12 degrees to the
occlusal plane require an angled abutment. The implant clinician should
understand that angled abutments are fabricated in two pieces and are
weaker in design than a two-piece straight abutment without an angle.
Because less metal surrounds the abutment screw on one side of an angled
abutment, it is at more risk of fracture or is less able to be reduced in width
for ideal crown contours. Furthermore, a larger transverse load component
develops at the abutment screw and crest of the ridge as a result of angled
loads and increases the risk of abutment screw loosening. In a study by Ha et
al,61 the angled abutment was compared with a straight abutment for screw
loosening in the anterior maxilla. The angled abutments showed more screw
loosening with cyclic loading than the straight abutments.
Surgical Management.
When lateral or angled loads cannot be eliminated, a reduction in the force
magnitude or additional surface area of implant support is indicated to
reduce the risk of biomechanical complications to the implant system. For
example, if three adjacent implants are inserted with the first implant in the
long axis to the load, the second at 15 degrees, and the third at 30 degrees,
the implant clinician may decrease the overall risk by (1) adding an
additional implant in the edentulous space next to the most angled implant,
(2) increasing the diameter of the angled implants, or (3) selecting an implant
design with greater surface area. Of the three options, increasing the implant
number is most effective to reduce overall stress to the system. In addition, a
greater number of implants has more retention for the restoration and
greater surface area.62
Prosthetic Management.
The restorative clinician may reduce the overload risk by (1) splinting the
implants together, (2) reducing the occlusal load on the second implant and
further reducing the load on the third implant, and (3) eliminating all lateral
or horizontal loads from the most angled implant and completely
eliminating them in all posterior regions.
The anterior mandible (with a force magnitude similar to the anterior
maxilla) often has the implant body positioned perpendicular to the occlusal
plane and restored with a straight abutment. In the anterior maxilla, even
under ideal conditions, the implant should be angled away from the labial
bone, which results in the abutment being angled toward the facial crown
contour. An angled prosthetic abutment is required, and these implant
bodies are more frequently loaded at an angle. Maxillary anterior teeth are
usually loaded at a 12- to 15-degree angle to the occlusal plane (Fig. 17.32).
FIG 17.32 Maxillary anterior implants most often are placed at an angled load to the
lower anterior teeth. As a result, the amount of the load should ideally be reduced.
Clenching patients may develop a considerable anterior bite force. Occlusal contact
reduction, larger diameter implants, increasing implant number, splinting implants,
and night guards are possible solutions.
The natural dentition reduces the increased stress to the maxilla by

increasing the size of the roots compared with mandibular incisors and
increasing the mobility of the teeth. In the maxilla, a larger diameter implant
or a greater number of implants are indicated to minimize the crestal bone
stress on each abutment, especially in patients exhibiting severe bruxism.
Ridge augmentation may be necessary before implant placement to improve
implant position or facilitate the use of a wider diameter implant. IPO aims
at reducing the force of occlusal contacts, increasing the implant number, or
increasing the implant diameter for implants subjected to angled loads.
Shallow Anterior Guidance

With healthy natural anterior teeth, apical and lateral movements are
significantly larger compared with implant movements, with a larger
difference being seen for the lateral movements. Because the differences in
lateral movement are greater, this allows for occlusal adjustment. As most
ideal occlusal schemes with natural teeth suggest, the anterior teeth
disocclude the posterior teeth during eccentric excursion. This is based on
the concept of electromyographic studies, which show that the
stomatognathic system elicits significantly less force when the posterior
segments are not in contact in the lateral mandibular position.63 Other
studies have shown that for every 10-degree change in the angle of
disclusion, there is a 30% difference in load (Fig. 17.33).64
FIG 17.33 The incisal guidance for a patient with moderate to severe bruxism
should be shallow (but steeper than the angle of the eminentia of the joint) to reduce
the force on the anterior teeth during excursive movement of the mandible. (From
If healthy anterior teeth or natural canines are present, the mutually

protected occlusion scheme allows those teeth to distribute horizontal
(lateral) loads during excursions, while the posterior teeth disocclude during
excursions (e.g., canine guidance or mutually protected articulation) (Fig.
17.34). The posterior teeth are protected from lateral forces by the anterior
guidance during excursions, and the anterior teeth have lighter forces in
excursions because the posterior teeth do not contact.
FIG 17.34 In the implant protected occlusion concept, in all mandibular excursions,
the anterior teeth should disocclude the posterior teeth. (From Misch CE: Dental implant
When lateral or angled forces are applied to the anterior teeth, the
magnitude of the stress is increased. However, when mutually protected
occlusal philosophies are applied, the consequences of the lateral forces are
reduced. The mutually protected articulation concept is used in the implant-
protected concept. In protrusive mandibular movements, the central and
lateral incisors disocclude the posterior teeth. In lateral excursions, the
canine (and lateral incisor when possible) disocclude the posterior teeth. In
CO, the posterior and canine teeth occlude. When the central and lateral
incisors are natural, they may also occlude in CO (or MI). When the anterior
teeth are implants, they may not occlude in centric occlusion, especially when
the opposing dentition is also implant supported.
Group function (or unilateral balance) has been suggested with
periodontal bone loss on the remaining teeth. The concept in theory is to
allow for the sharing of lateral loads during excursions with more teeth. For
example, with this philosophy, a mandibular excursion to the right contacts
as many anterior and posterior teeth on the right as possible. This is not
indicated in implant-protected occlusion. The lateral posterior forces increase
the moment loads to posterior implants. The posterior contacts during
excursions also have greater forces to the posterior implants because more
muscle mass contracts, and the occlusal contacts are closer to the TMJ (class
3 lever). In addition, the posterior lateral loads increase the force to the
anterior teeth or implants during the excursions. As a result, both the
anterior and the posterior implant components receive a greater force (Fig.
17.35).
FIG 17.35 (A) This patient was restored in group function. (B) Posterior maxillary
right two implants fractured. (C) Posterior mandibular right two implants fractured.
(D) The maxillary anterior implants lost integration. (From Misch CE: Dental implant
In a study by Jemt et al,11 when implant-supported restorations were used

in the maxilla opposing natural dentition, the velocity of the mandible during
excursions was greater with group function than when incisal guidance was
present. The force to the implant system was greater with group function.
Kinsel and Lin65 reported that group function in patients with implant-
supported prostheses had a porcelain fracture rate of 16.1% and occurred in
51.9% of implant patients. When anterior disclusion was the occlusal scheme
in excursions, the fracture rate on implant crowns was 5.3%, and this
complication affected 15.9% of patients (more than a threefold difference).
The steeper the incisal guidance, the greater the force on the anterior teeth
or implants. The anterior guidance of an implant prosthesis with anterior
implants should be as shallow as practical. According to Weinberg and
Kruger,64 for every 10-degree change on the angle of disclusion, there is a 30%
difference in load (Fig. 17.36). A 10-degree force on the anterior implants with
a 68-psi load will increase to 100 psi when the incisal guidance is 20 degrees
and will further increase to 132 psi if the incisal guidance is 30 degrees. As a
consequence, the impression by these authors is that the incisal guidance
should be less than 20 degrees. However, because the condylar disc assembly
is usually 20–22 degrees, the incisal guidance should be greater than this
amount to separate the posterior teeth.40 When the incisal guidance is less
than the angle of the eminentia of the TMJ, the posterior teeth will still
contact in excursions. In most patients, an incisal guidance of at least 23–25
degrees is suggested in IPO.
FIG 17.36 For every 10-degree change on the angle of disclusion, there is a 30%
difference in load. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The increase in load that occurs from the incisal guidance angle is further
multiplied by the crown height above the initial occlusal contact (the vertical
overbite) because it acts as a lever arm while the mandible slides down the
incline plane (Fig. 17.37). An ideal vertical overbite in prosthetics has been
reported to be 5 mm and often is more, especially in Angle Class II, division
II patients. However, especially in parafunctional patients, incisal guidance
should be as shallow as possible in implant prostheses (23–25 degrees) and
the vertical overbite reduced to less than 4 mm, yet the posterior teeth
should disocclude in the excursions (Figs. 17.38 and 17.39).
FIG 17.37 The anterior load during excursions is increased from the centric
occlusal contact (far right) to the incisal edge (far left). (From Misch CE: Dental implant
FIG 17.38 The vertical overbite in the implant prosthesis should be reduced to 4
mm or less. When implants oppose each other, there is no occlusal contact
between the canines in centric occlusion. (From Misch CE: Dental implant prosthetics, ed 2,
FIG 17.39 (A) Full-arch maxillary and mandibular implant prosthesis with a vertical
overbite of 3 mm. (B) The incisal guidance is 25 degrees, so the posterior teeth
separate in any mandibular excursion. (From Misch CE: Dental implant prosthetics, ed 2, St
Cuspid Implant.
A clinical condition that sometimes causes confusion is the occlusal scheme
for a single-tooth implant replacing a maxillary canine. A missing maxillary
canine is indicated for a single-tooth implant crown. The lateral incisor is the
weakest anterior tooth, and the first premolar is often the weakest posterior
tooth. These abutments are not great candidates for a three-unit prosthesis,
especially because lateral forces would be placed on the premolar.
The proprioceptive mechanism of the natural canine in excursions blocks
approximately two-thirds of the activity of the masseter and temporalis
muscles and decreases the bite force when posterior teeth disocclude.63 An
anesthetized canine has more muscle mass that contracts both in clenching
and in the lateral excursion compared with the same patient before
anesthesia.66 The natural canine PDL nerve complex helps decrease the force
in excursions. The anesthetized natural canine has been compared with the
proprioception of an implant.67 Proprioception is transmitted through the
bone from an implant but in a reduced amount compared with a natural
tooth. A mutually protected occlusion is still a benefit when a single-tooth
canine implant is restored. In other words, a greater decrease in lateral forces
occurs when a natural anterior tooth root is involved in the excursion
compared with an implant crown, but an implant crown also can decrease the
force and is better than a pontic in the canine position. In addition, the class
3 lever mechanism of the canine position still is able to reduce the force in
excursions when the posterior teeth do not contact.
No occlusal contact occurs on the single-tooth canine implant crown
during mandibular excursions to the opposite side. During protrusion, no
contact on the canine implant crown is ideal. If a contact is necessary, it is
adjusted so that a light bite force has no occlusal contact on the implant
crown. Under a heavy bite force in protrusive movements, the canine implant
crown may contact.
The occlusion during the working excursion toward the canine implant
crown is of particular concern. The dentist should make an attempt to
include a natural tooth in the lateral excursion because teeth have greater
proprioception than implants. To create a mutually protected articulation
scheme that includes a lateral incisor is preferable because this tooth is
farther from the TMJ. With a light working lateral excursion, the lateral
incisor occludes first and moves 97 µm (when in health), and then the canine
implant crown engages and helps disocclude the posterior teeth. During a
heavy bite force excursion, the lateral incisor and implant crown contact with
similar magnitude (Fig. 17.40). However, in Angle Class II, division I
patients, the first premolar may need to be included in the excursion process,
rather than the lateral incisor because the horizontal overjet may be
excessive.
FIG 17.40 (A) A maxillary right canine is replaced with an implant. This patient is an
Angle Class II, division 2 patient and has a deep vertical overbite. A steep incisal
guidance places greater force than a shallow incisal guidance, which may be why
the canine tooth fractured after endodontic therapy. (B) The right mandibular
excursion is evaluated first with a light and then a heavy bite force. Ideally, the lateral
incisor should contact first and then the canine. The first premolar contact should be
eliminated to decrease the force to the implant. (From Misch CE: Dental implant prosthetics,
All lateral excursions in the concept of implant-protected occlusion opposing
fixed prostheses or natural teeth use anterior teeth or implants whenever
possible to disocclude the posterior components. The resulting lateral forces
are distributed to the anterior segments of the jaws, with an overall decrease
in force magnitude. This occlusal scheme should be followed whether or not
anterior implants are in the arch. However, if anterior implants must
disocclude posterior teeth, natural teeth (whenever possible) are first used
during the initial primary tooth movement. When multiple anterior teeth are
missing, two or more implants splinted together (when possible) should help
dissipate the lateral forces. The anterior guidance of implant-supported
prostheses should be as shallow as possible to minimize forces on the
anterior implants.
Decreased Posterior Crown Cusp Angle
The angle of force to the implant body may be influenced by the cusp
inclination of the implant crown in similar fashion as an angled load to an
implant body. The posterior natural teeth often have steep cuspal inclines,
and 30-degree cusp angles have been designed in denture teeth and natural
tooth prosthetic crowns (Fig. 17.41). The greater cusp angles are often
considered more esthetic and may even incise food more easily and
efficiently.68 To negate the negative effect of an angle cusp contact, the
opposing teeth need to occlude at the same time in two or more exact
positions on the ipsilateral cusp angles of the crowns, which is highly
unlikely to be achieved in a clinical setting (Fig. 17.42).
FIG 17.41 Natural teeth often have cusp angles of 30 degrees. If a premature
contact occurs on a cuspal incline, the direction of load may be 30 degrees to the
implant body if the implant crown duplicates a natural tooth cusp angle. (From Misch
FIG 17.42 When opposing crowns occlude, the three cuspal inclines must hit at
the same time to result in a long-axis load. (From Misch CE: Dental implant prosthetics, ed 2,
The occlusal contact along only one of the angled cusps results in an
angled load to the implant system even when it is not premature to other
occlusal contacts (Fig. 17.43). The magnitude of the force is minimized when
the angled occlusal contact is not a premature contact but instead is a
uniform load over several teeth or implants. However, the angled cusp load
does increase the resultant tensile and shear stress with no observable
benefit. No advantage is gained, but the biomechanical risk is increased (e.g.,
increased abutment screw loosening, porcelain fracture, unretained
restoration).
FIG 17.43 The mandibular buccal cusp incline is occluding with the lingual incline
of the maxillary cusp. An occlusal contact on a cusp angle transmits an angled load
to the implant body. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Occlusal contact position determines the direction of force, especially

during parafunction. A cantilevered load is a force applied on the mesial or
distal from the implant, which acts as a fulcrum. An offset load is a force
applied to the buccal or lingual and increases the stress to the implant
system. An occlusal contact on a buccal cusp of a mandibular premolar and
molar or lingual cusp in the maxilla is usually an offset load when the
implant is positioned under the central fossa because the occluding cusp is
cantilevered from the implant body (Fig. 17.44). In addition, the angle of the
cusp tip introduces an angled load to the implant body.
FIG 17.44 An offset load to the implant body increases the stress to the implant
system. A buccal cusp occlusal contact in the posterior mandible or lingual cusp
contact in the maxilla is an offset load to the implant. B, Buccal; Fi, central fossa
contact; Fn, buccal cusp contact; L, lingual. (From Misch CE: Dental implant prosthetics, ed
Studies have investigated various occlusal designs and bone remodeling.

When evaluating cusp inclinations (0, 10, and 30 degrees) and loading
locations (central fossa, 1- and 2-mm offsets horizontally), the load
concentration was mainly at the crestal part of the implant system. The load
concentration increased with steeper cuspal inclinations and broader
occlusal tables. This increased shear stress, which can potentially lead to
damage of the bone-implant interface and progressively induces
micromotion.14 A more concentrated central fossa loading with a narrow
occlusal table is ideal.69,70
Prevention.
The occlusal contact over an implant crown should ideally be on a flat surface
perpendicular to the implant body. This occlusal contact position usually is
accomplished by increasing the width of the central fossa to 2–3 mm in
posterior implant crowns, which is positioned over the middle of the implant
abutment. The opposing cusp is recontoured to occlude the central fossa of
the implant crown directly over the implant body (Fig. 17.45). The laboratory
technician should identify the middle of the implant body and then make a
central fossa 2–3 mm wide over this position parallel to the curves of Wilson
and Spee (Fig. 17.46). The buccal and lingual contour of the crown may then
be established (reduced on the buccal for the posterior mandible and the
lingual for the posterior maxilla). The opposing tooth may require
recontouring of an opposing cusp to help direct the occlusal force along the
long axis of the implant body.
FIG 17.45 (A) A posterior implant crown should have a wider central fossa
perpendicular to the implant body and parallel to the occlusal plane. The opposing
tooth occluding cusp should be modified to occlude with the widened central fossa.
(B) Posterior occlusion displaying minimal cusp height (monoplane occlusal
plane). (A, From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 17.46 The laboratory technician usually will place the implant abutment under
the central fossa of the implant crown. (From Misch CE: Dental implant prosthetics, ed 2, St
Ideal Posterior Occlusal Contacts

The ideal number of occlusal contacts in different occlusal schemes varies.
For example, Thomas'71 occlusal theories suggest that there should be a
tripod contact on each occluding cusp (stamp cusp), on each marginal ridge,
and in the central fossa with 18 and 15 individual occlusal contacts on a
mandibular and maxillary molar, respectively (Fig. 17.47).
FIG 17.47 The ideal number of occlusal contacts varies in the literature. As many
as 15 to 18 tripod occlusal contacts have been designed. (From Misch CE: Dental implant
Other occlusal contact schemes indicate that the number of occlusal

contacts for molars may be reduced to five or six contacts, including the
dominant cusp (stamp cusp) of the buccal cusps in the mandible and the
lingual cusps in the maxilla, the marginal ridges, and the central fossa. When
a crown morphology is designed, usually no thought is given to how many
contacts should be present or where they should occlude. It is almost
impossible for the clinician to control the number and locations of occlusal
contacts.
The average number of occlusal contacts found on natural posterior teeth
of individuals never restored or equilibrated by a dentist and with no
occlusal-related pathologic condition has been observed to average only 2.2
contacts (Fig. 17.48) with a range of one to three occlusal contacts per tooth.72
If the tooth had an occlusal restoration, the occlusal contact number was
reduced to an average of 1.6 occlusal contacts. The number of occlusal
contacts on a natural tooth apparently may be reduced to one to three
contacting areas without consequence. A more simplified occlusal approach
than often taught is logical. If the ideal occlusal contacts per tooth should
have minimum offset loads to the implant body, the central fossa is the
logical primary occlusal contact position when the implant is positioned in
this region. The central fossa of an implant crown should be 2–3 mm wide in
posterior teeth and parallel to the occlusal plane. The ideal implant body
position for function is most often directly under the central fossa in the
mandible and maxilla. The ideal primary occlusal contacts will reside within
the diameter of the implant within the central fossa. Secondary occlusal
contacts should remain within 1 mm of the periphery of the implant to
decrease moment loads. Marginal ridge contacts usually should be avoided
unless implants are splinted together. When the implant is positioned closer
to a stamp cusp (buccal in the mandible and lingual cusp in maxilla), the
cusp angle is flat, and the contact is over the implant (Fig. 17.49).
FIG 17.48 (A–C) An average of 2.2 occlusal contacts (range, 1–3) usually is found
on natural posterior teeth. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
FIG 17.49 (A) The occlusal contact position is ideally directly over the implant.
When under a cusp tip, the cusp angle is more flat. (B) The implant crowns are
reduced from the lingual compared with the natural tooth molar crown. (From Misch
Posterior Implant Position.

The most common implant body position for a posterior implant is in the
middle of the buccolingual dimension of the bone. The implant surgeon
begins the osteotomy in the middle of the ridge, and the implant diameter
maintains 1.5 mm or more of bone on each side. The center of an edentulous
ridge more often corresponds to the central fossa of a posterior crown in
either arch. Occasionally, it may correspond to the natural tooth lingual cusp
region but less often is under the buccal cusp in either arch.
The marginal ridge contacts are also a cantilever load on the single-tooth
implant crown because the implant is not under the marginal ridge but may
be several millimeters away. If the implant body is 5 mm in diameter and
replaces a 12-mm molar in the mesiodistal dimension, a marginal ridge
contact may create a magnified moment load equal to 3.5 mm times the
amount of the force. A 100-N load will be multiplied to a 350–N-mm force on
the marginal ridge (Fig. 17.50).
FIG 17.50 (A–B) The ideal occlusal contact on a single-tooth implant crown is
directly over the implant. A marginal ridge occlusal contact is an offset load similar to
the lingual cusp in the posterior maxilla. (From Misch CE: Dental implant prosthetics, ed 2, St
The mesiodistal dimension of the molar crown often exceeds the

buccolingual dimension, so the marginal ridge contact may contribute more
to the biomechanical risk. In addition, laboratories often create an all-
porcelain marginal ridge completely unsupported by the metal substructure,
which places a shear load on the porcelain. The shear loads further increase
the risk of porcelain fracture. The moment forces on marginal ridges also
may contribute to forces that increase abutment screw loosening. Marginal
ridge contacts on individual implant crowns or the most mesial or distal
splinted crown should be avoided whenever possible.
Splinted Implants.
The marginal ridge occlusal contact is not a cantilevered load when located
between two implants splinted to each other. In addition, the metal/zirconia
framework that splints the implants supports the porcelain/zirconia in the
marginal ridge region and minimizes the risks of fracture. The splinted
crowns decrease occlusal forces to the crestal bone, reduce abutment screw
loosening, decrease the force to the cement interface, increase retention of
the crowns, and reduce the force to the bone-implant interface. Adjacent
implant crowns should most often be splinted together, and the occlusal
contact position may be extended from the most mesial to most distal
implants (minus the marginal ridges at each extreme) (Fig. 17.51).
FIG 17.51 When the implants are splinted together, the occlusal contacts ideally
should be in the central fossa, over the implant bodies, and in a zone extending
between the implants. The marginal ridges between the implants may also have a
secondary occlusal contact. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Screw-Retained Prosthesis.
A posterior screw-retained restoration often requires cantilevered occlusal
contacts. The occlusal screw hole rarely is loaded because the filling material
easily wears or fractures. As a result, the occlusal contacts of screw-retained
crowns are not often directed over the top of the implant but are offset
several millimeters away. This results in a higher moment load to the implant
system, yet the occlusal access hole is the best position for the occlusal
contact.
Occasionally, when a maxillary posterior tooth is in the esthetic zone, the
implant may be 1–2 mm to the facial aspect of the midcrest (when bone is
abundant) to be closer to the buccal cusp to improve the esthetic emergence
of maxillary implant crowns. Under these conditions, the central fossa is
positioned more facial, the lingual contour of the crown is reduced, and the
occlusal contact is over the lingual aspect of the implant body (which is
under the central fossa).
Minimize Cantilevers
A cantilever in implant dentistry is to be considered a class 1 lever.41
Cantilevers, especially with nonideal crown-implant ratios, may result in
peri-implant disease and prosthetic failure (i.e., porcelain fracture, prosthetic
screw loosening or fracture).
A cantilever may be present in implant dentistry in many situations (Fig.
17.52):
1. Single implant crown between natural teeth (buccal-lingual, mesial distal)
2. Malpositioned implant resulting in an atypical prosthesis
3. Prosthesis with distal extension
4. Bar for an overdenture

FIG 17.52 Possible cantilevers in implant dentistry. (A) Between natural teeth with
marginal ridge occlusal forces. (B) Implant splinted prosthesis with mesial and distal
cantilevers. (C) Cantilevered forces on a bar-retained overdenture. (D) Fixed
prosthesis with bilateral cantilevers.
Length of Cantilevers.
Studies have proven the detrimental effects of cantilevers. Longer cantilevers
(>15 mm) have been shown to be associated with greater prosthesis failure
than shorter (<15 mm) cantilevers.42 When a biting force is applied to a distal
cantilever, the highest axial forces and bending moment forces are on the
distal abutment. For example, if two implants are 10 mm apart and are
splinted with a cantilever of 20 mm, the following mechanics result: the
mechanical advantage of the cantilever is 20 mm/10 mm, or 2. Whatever force
is applied to the cantilever, a force twice as great will be applied to the
farthest abutment from the cantilever.
Occlusal Contact on Cantilevers.

The occlusal contact on a cantilever may result in the overloading of the
implants. For example, when a crown is placed over an implant with a buccal
cantilever (i.e., 5-mm implant body replacing a mandibular molar with an 11-
mm diameter), the angled buccal cusp will act as a cantilever. A marginal
ridge contact may also cause overloading because this is a force-related
cantilever.
Forces on Cantilevers.
Although the force on the cantilever is compressive in nature, the force to the
distal abutment is a tensile and shear force. The load on the abutment closest
to the cantilever (which acts as a fulcrum) is the sum of the other two
components and is a compressive force (Fig. 17.53). In this example, a 100-N
force on the cantilever equals a 200-N tensile or shear force on the most distal
abutment and a 300-N compressive force on the abutment (the fulcrum) next
to the lever.
FIG 17.53 A cantilever on two implants may be considered a class I lever. When
the implants are 10 mm apart, with a 20-mm cantilever, a mechanical advantage of
2 is created. The load on the cantilever will be multiplied by 2 on the far implant, and
the implant close to the cantilever receives the total stress of the two loads. (From
Because cement and screws are weaker to tensile loads, the implant
abutment farthest from the cantilever often becomes unretained, resulting in
the fulcrum abutment bearing the entire load. Because the implant is more
rigid than a tooth, it acts as a fulcrum with higher force transfer and is at
higher risk (Fig. 17.54). As a consequence, crestal bone loss, fracture, and
implant failure are often imminent after the distal abutment loses support to
the prosthesis.
FIG 17.54 (A) A tooth is more mobile than an implant. An implant as a fulcrum
transmits more tensile and shear load to the distal abutment from the cantilever than
a tooth. (B) The cantilever to the mesial caused the cement seal to break in the
distal molar. The fulcrum implant carried all the load, and the implant failed. (From
Cantilevers increase the amount of stress to the implant system. The greater
the force on the cantilever, the even greater the forces on the implants
because the cantilever is a force magnifier. Parafunctional loads are
particularly dangerous for biomechanical overload. The greater the length of
the cantilever, the greater the mechanical advantage and the greater the loads
on the implants. The shorter the distance between the implants, the greater
the mechanical advantage and the greater the force on the implant system
(Fig. 17.55).
FIG 17.55 (A) Panoramic radiograph of a maxillary and mandibular implant fixed
prosthesis. The mandibular restoration is cantilevered from implants positioned
between the mental foramina. (B) Lateral cephalogram demonstrates that the
anteroposterior distance of the implants is approximately 6 mm. The prosthesis is
cantilevered more than four times the anteroposterior distance. The posterior
occlusal load is magnified more than four times to the anterior implants, and the
most distal implants receive the total sum of the loads. In addition, the opposing arch
is implant supported and with less proprioception and higher bite forces than natural
teeth. All these risk factors make this mandibular restoration less predictable. The
cantilever should be reduced, the posterior occlusal contacts should be reduced, an
anterior contact occlusal night guard should be worn, and preventive changes of the
prosthetic screws should be done every few years. (From Misch CE: Dental implant
The goal for cantilevers is to reduce the force on the pontics of the lever
region compared with that over and between the implant abutments. To
reduce the amount of force that is magnified by the cantilever, the occlusal
contact force may be reduced on the cantilevered portion of the prosthesis. A
gradient of force type of load that gradually decreases the occlusal contact
force along the length of the cantilever is beneficial. In addition, no lateral
load is applied to the cantilever portion of the prosthesis (whether it is in the
posterior or anterior region). Although the functional forces of occlusion
during mastication may not be significantly altered by this technique,
parafunctional forces (which are the most damaging) are significantly
reduced with a gradient of force occlusal adjustment.
Avoid Excessive Crown Height Space

The interarch distance is defined as the vertical distance between the
maxillary and mandibular dentate or dentate arches under specific
conditions (e.g., the mandible is at rest or in occlusion).35 A dimension of
only one arch does not have a defined term in prosthetics; therefore, Misch
proposed the term “crown height space” (CHS).73 The CHS for implant
dentistry is measured from the crest of the bone to the plane of occlusion in
the posterior region and the incisal edge of the arch in question in the
anterior region (Fig. 17.56). In the anterior regions of the mouth, the presence
of a vertical overbite means the CHS is larger in the maxilla than the space
from the crest of the ridge to the opposing teeth incisal edge. In general,
when the anterior teeth are in contact in CO, there is a vertical overbite. The
anterior mandibular CHS is usually measured from the crest of the ridge to
the mandibular incisal edge. However, the anterior maxillary CHS is
measured from the maxillary crestal bone to the maxillary incisal edge, not
the occlusal contact position. The ideal CHS required for a fixed implant
prosthesis should be between 8 and 12 mm. This measurement accounts for
the “biologic width,” abutment height for cement retention or prosthesis
screw fixation, occlusal material strength, esthetics, and hygiene
considerations around the abutment crowns (Fig. 17.57).
FIG 17.56 The crown height space is measured from the occlusal plane to the
crest of the bone. The ideal space for an FP-1 prosthesis is between 8 mm and 12
mm. CT, Connective tissue attachment; JE, junctional epithelial attachment. (From
FIG 17.57 Excessive crown height space leading to occlusal overload. The
increased crown height space acts as a vertical cantilever.
Removable prostheses often require a CHS greater than 12 mm. The CHS is
measured from the crest of the bone to the plane of occlusion in the posterior
region and the incisal edge of the arch in question in the anterior region. The
implant crown height is often greater than the original natural anatomic
crown even in division A bone. If the implant is loaded ideally on the long
axis, crown height does not magnify the force (Fig. 17.58). However, crown
height is a force magnifier (vertical cantilever) when any lateral load, angled
force, or cantilever load is applied (Fig. 17.59).41 A crown height with any of
these conditions acts as a magnifier of stress to most of the implant system
(i.e., cement or screw retaining the crown, abutment screw, marginal bone,
and implant-bone interface). The greater the crown height, the greater the
resulting crestal moment with any lateral component of force, including
forces that develop because of an angled load. Angled abutments loaded in
the direction of the angled abutment with an increase in crown height are
subject to similar greater crestal moment loads because of the lateral load to
the implant body and the increased lever effect from the crown height.
FIG 17.58 Crown height does not magnify the stress to the implant system when
the force is applied in the long axis of the implant body. (From Misch CE: Dental implant
FIG 17.59 A cantilever load on an implant results in six different moments applied
to the implant body. An increase in crown height directly increases two of six of the
moment forces. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Occlusal loads may be directed to the implant system with an increased

CHS if the following occur: a 30-degree angled load to an implant body, an
implant crown with a 30-degree load, or a 30-degree cusp angle contact
results in a similar condition. In this situation, 50% of the occlusal load is
transformed into a horizontal or shear component to the implant system.
However, the angled load on an implant crown is at greater risk to the crestal
bone than the angled implant body because the crown height acts as a
vertical cantilever. Whatever load is applied to the occlusal table (or cusp
angle) is magnified by the crown height. For example, a 12-degree angled
load of 100 N on the implant crown results in 21 N of additional load as a
lateral force component. However, if the crown is 15 mm high, the final load
to the crest of bone and abutment screw is 21 N Å~ 15 mm = 315 N-mm
moment force. The dentist should be aware of the noxious effects of a poorly
selected cusp angle, or an angled load to the implant crown will be magnified
by the crown height measurement (Fig. 17.60).
FIG 17.60 The crown height directly increases the effect of an angled force. For
example, a 100-N load at a 12-degree angle increases the lateral or shear force
component by 21 N. A crown height of 15 mm increases the 21-N force to a 315–N-
mm moment force. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
If a load perpendicular to the curves of Wilson and Spee is applied to an

angled implant body, the increase in load is not magnified by the crown
height. The angled implant will increase the force components but will not
be magnified by the crown height. The angle of load to the occlusal surface is
more important to control than the angle of the implant body position.
Axial loading of the implant is especially critical when the crown height
increases, intensity of force increases, or duration of force increases (i.e.,
parafunction). The crown height is not a force magnifier (lever) when there is
no cantilever or lateral load. A long-axis load of 100 N is similar to the
implant system, whether the crown height is 10 mm or 20 mm. Occlusal
schemes and crown occlusal anatomy should incorporate axial loads to
implant bodies and, when not applicable, should consider mechanisms to
decrease the noxious effect of lateral loads. Because horizontal or lateral
loads cause an increase in the amount of tension and shear forces to the
implant system, these loads should be reduced within the occlusal scheme,
especially in mechanical systems that increase the magnitude of the
biomechanical load.
Maintain Narrow Posterior Occlusal Tables

In the posterior region, large occlusal table designs present many inherent
complications. A buccal or lingual cantilever in the posterior regions is called
an offset load, and the same principles of force magnification from class 1
levers apply. The greater the offset, the greater the load to the implant
system. Offset loads may also result from buccal or lingual occlusal contacts
and create moment forces, which increase compressive, tensile, and shear
forces to the entire implant system (Fig. 17.61).
FIG 17.61 A cantilever occlusal contact to the facial or lingual is called an offset
load. Cantilever or offset loads increase the force by the length of the lever and
increase the shear component of the force. A posterior implant most often is placed
under the central fossa of the implant crown. A buccal cusp contact is an offset or
cantilever load. The ideal occlusal contact is over the implant body. B, Buccal; F,
force; L, lingual. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Etiology
Mandibular posterior crowns.
After tooth loss in the posterior mandible, the resorption process leads to the
residual ridge being positioned more lingual. As the ridge resorbs lingually,
the bone division will shift from a division A to B. As a result, dental
implants (without bone grafting) will be more lingually placed than their
natural tooth predecessors. Care should be taken in the placement of dental
implants in this area because this may lead to nonaxial loading and
impingement on the tongue space.
As the mandible resorbs more, the ridge will shift from a division B to a
division C-h and then to a division D. However, because of the angulation of
the mandible and the sublingual undercuts, the ridge will actually shift back
toward the buccal. However, endosteal implants typically cannot be inserted
in these cases because inadequate bone is available above the mandibular
nerve (Fig. 17.62).
FIG 17.62 The posterior maxillary and mandibular edentulous arches resorb
lingually as bone volumes change from division A to B to B minus width to C minus
width. The mandibular posterior arch resorbs facially as the edentulous site
becomes C minus height and D bone volume. (From Misch CE: Dental implant prosthetics,
To prevent the nonaxial loading and linguoversion of the implant and
implant prosthesis, the implant clinician to should evaluate via cone beam
computed tomography interactive treatment planning the position of the
implant and final prosthesis. If the implant cannot be placed in an ideal
position, bone augmentation to restore the lost buccal bone should be
completed before implant placement.
Maxillary posterior crowns.

The maxillary dentate posterior ridge is positioned slightly more facial than
its mandibular counterpart because the teeth have a maxillary overbite.
When the maxillary teeth are lost, the edentulous ridge resorbs in a medial
direction as it evolves from division A to B, division B to C, and division C to
D. As a result, the maxillary permucosal implant site gradually shifts toward
the midline as the ridge resorbs. However, because of resorption in width,
the maxillary posterior implant permucosal site may even be palatal to the
opposing natural mandibular tooth.
In the esthetic zone (high lip position during smiling), the buccal contour
of the maxillary implant crown is similar to a natural tooth. This improves
esthetics and maintains the buccal overjet to prevent cheek biting and retains
cheek fullness. However, just as with the natural teeth, there is no occlusal
contact on the buccal cusp. Ideally, when maxillary posterior implants are in
the esthetic zone, they are positioned more facial than the center of the ridge.
The ideal functional position for the maxillary posterior implant is under the
central fossa when the cervical region is not in the esthetic zone.
Although sinus augmentation permits the placement of endosteal implants
in the posterior maxilla, there is often a ridge discrepancy. The clinician
should evaluate the axial positioning of the proposed implant site, and in
some cases horizontal (width) augmentation may need to be completed in
association with sinus grafting.
The lingual contour of a maxillary implant crown should be reduced
because it is out of the esthetic zone and is a stamp cusp for occlusion (which
is an offset load) (Fig. 17.63). The lingual cusp is cantilevered from the
implant similar to the buccal cusp of the posterior mandible. The reduced
lingual contour reduces the offset load to the lingual aspect of the implant
(Fig. 17.64).
FIG 17.63 (A) A maxillary posterior implant in the esthetic zone is positioned slightly
more to the facial position than the central fossa. (B) The facial contour of the
maxillary first molar implant crown is contoured similar to the adjacent teeth. (C) The
lingual crown contour of the maxillary first molar crown is reduced compared with
the natural tooth. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
FIG 17.64 Posterior maxillary implants most often are positioned under the central
fossa when the cervical region is not in the esthetic zone. The posterior maxillary
lingual contours of implant crowns usually are reduced for improved hygiene and
less offset loads to the implants. B, Buccal; L, lingual. (From Misch CE: Dental implant
Prevention
Larger implant body.
Wider root form implants can accept a broader range of vertical occlusal
contacts while still transmitting lesser forces at the permucosal site under
offset loads. Narrower implant bodies are more vulnerable to occlusal table
width and offset loads. With the implant protected occlusion concept, the
width of the occlusal table is related directly to the width of the implant body
(Fig. 17.65).74
FIG 17.65 Narrow diameter implant showing significant discrepancy between

occlusal table and implant body dimension.
Prosthesis fabrication.
The laboratory technician often attempts to fabricate an implant crown with
occlusal facial and lingual contours similar to that of natural teeth. When out
of the esthetic zone, the posterior implant crown should have a reduced
occlusal width compared with a natural tooth (Fig. 17.66). The narrower
occlusal contour of an implant crown also reduces the risk of porcelain
fracture because of a decreased possibility of unsupported porcelain. A facial
profile similar to a natural tooth on the smaller diameter implant (e.g., 10-
mm tooth vs. 4- to 6-mm implant) results in cantilevered restorative materials
in four areas: buccal, lingual, mesial, and distal. Thus, the cantilevered crown
contour is often designed as a ridge lap pontic of a fixed partial denture (Fig.
17.67). The facial porcelain most often is not supported by a metal
substructure because the gingival region of the crown is also porcelain. As a
result, shear forces result on the buccal cusp on the mandibular crown or
lingual cusps in the maxillary crown and are more likely to increase the risk
of porcelain fracture. The extended crown contours not only increase offset
loads but also often result in ridge laps or porcelain extension at the facial
gingival margin of the implant abutment. This risk is compounded further by
the higher impact force developed on implant abutments compared with
natural teeth (Fig. 17.68).
FIG 17.66 (A) Mandibular posterior crowns with an occlusal table that is too large.
(B–C) Narrow occlusal table decreases amount of force applied to the implant.
FIG 17.67 (A) Cantilevered buccal ridge lap is the result of buccal plate resorption
and the implant placed more lingual than the natural tooth. (B) Where implants
supporting a fixed prosthesis lie palatal or lingual to the occlusal platform, vertical
forces on the teeth will tend to rotate the prosthesis around its fixing points on the
implants. (B, From Hobkirk JA: Occlusion and Principles of Oral Implant Restoration. In Klineberg I,
Eckert S: Functional occlusion in restorative dentistry and prosthodontics, St Louis, 2016, Mosby.)
FIG 17.68 (A) Posterior mandibular implant in the second premolar position. A
posterior implant (in the position of the second premolar in this case) often is
inserted under the central fossa position. (B) The implant body is more narrow than
the natural tooth. When the laboratory fabricates an implant crown the same size as
the missing tooth, a facial ridge lap crown often results so as to restore the complete
tooth contour. The ridge lap crown does not allow sulcular hygiene or facial probing.
A ridge lap crown contour was made by the laboratory to restore the full contour of
the missing teeth. (C) In situ, the crown appears as a crown on a natural tooth, but
the cervical aspect is not in the esthetic zone. Offset loads, porcelain fracture, and
abutment screw loosening risk are increased. (D) The ridge lap was eliminated, and
the buccal contour was reduced. (Note there was no metal work to support the
cantilevered porcelain.) (E) The modified crown in situ. Daily hygiene is improved,
and biomechanical risk is reduced. The second premolar implant crown restores the
function and occlusal aspect of the missing tooth. The esthetic facial cervical region
is compromised to improve hygiene and force resistance because this region is not
seen during function, speech, or smiling. (From Misch CE: Dental implant prosthetics, ed 2,
Management.
As a result of the ridge laps or porcelain extensions, home care in the
sulcular region of the implant is impaired by the overcontoured crown
design. The dental floss or probe may reach under the ridge lap to the free
gingival margin, but it cannot enter the gingival sulcus. Daily hygiene is
almost impossible to perform. The narrower posterior occlusal table
facilitates daily sulcular home care. A narrow occlusal table combined with a
reduced buccal contour (in the posterior mandible) facilitates daily care,
improves axial loading, and decreases the risk of porcelain fracture. However,
in the esthetic zone, the ridge lap design may be necessary to restore the
implant rather than removing it, bone grafting, and replacing the implant.
An increased frequency of hygiene may be indicated.
The mandibular implant prostheses should be reduced from the buccal
and the maxillary crown reduced from the lingual. The “stamp cusp” offset
load is reduced. The reduced buccal contour in the posterior mandible is of
no consequence to cheek biting because the buccal horizontal overjet is
maintained (and increased). The lingual contour of the mandibular implant
crown should be similar to a natural tooth (Fig. 17.69). This permits a
horizontal overjet to exist and push the tongue out of the way during occlusal
contacts (just as natural teeth). As with the natural tooth, the lingual cusp
has no occlusal contact.
FIG 17.69 (A) Mandibular implant in the first molar position. (B) The first molar
crown in situ. The lingual contour is similar to the natural tooth. The buccal contour
is reduced in width. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
In the posterior mandible, as the implant diameter decreases, the buccal

cusp contour is reduced. This decreases the offset length of cantilever load.
The lingual contour of the crown remains similar regardless of the diameter
of the implant. The lingual contour permits a horizontal overlap with the
maxillary lingual cusp, so the tongue is pushed away from the occlusal table
during function. The lingual cusp is not occlusal loaded (as with natural
teeth) (Fig. 17.70). During mastication, the amount of force used to penetrate
the food bolus may be related to occlusal table width. For example, less force
is required to cut a piece of meat with a sharp knife (narrow occlusal table)
than with a dull knife (wider occlusal table). The greater surface area of a
wide occlusal table requires greater force to achieve a similar result. The
wider the occlusal table, the greater the force developed by the biologic
system to penetrate the bolus of food. Although these functional forces are
typically less than 30 psi, with parafunction they can be 10 to 20 times greater.
FIG 17.70 The wider the implant body, the wider the occlusal table width of the
implant crown. As the mandibular bone width decreases, the implant body may
decrease in width. The lingual contour of the implant crown remains similar
regardless of the width of implant. The buccal contour is reduced as the implant
diameter decreases. A narrow ridge in an esthetic zone may require bone
augmentation, so a wider implant may be used to support an implant crown, which
appears as a natural tooth. B, Buccal; CF, central fossa; L, lingual. (From Misch CE:
In the esthetic zone, many of the crown contours are made to resemble the
natural tooth as closely as possible. However, out of the esthetic zone, in the
posterior regions of the mouth, the crown contour should be different than a
natural tooth. The implant body buccolingual dimension is smaller than the
natural tooth. The center of the implant most often is placed in the center of
the edentulous ridge. Because the crest of the ridge shifts lingually with
resorption, the implant body is most often not under the opposing cusp tips
but rather near the central fossa or even more lingual and in the maxilla may
even be under the lingual cusp of the original natural tooth position (Fig.
17.71). Most often, the laboratory fabricates a posterior implant crown that is
similar in size to a natural tooth, with a cantilevered facial contour. In
addition, the occlusal contacts are often on the “stamp cusp” of the mandible
(buccal cusps).
FIG 17.71 The implants in the second premolar and first molar are positioned
under the lingual cusps. The laboratory made the buccal crown contour similar to
the missing teeth. A facial offset load is present. The cantilever force should not be
compounded by occlusal loads in the central fossa from a mandibular buccal
cusp. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
However, these “stamp cusps” are often offset loads (buccal cantilevers)
(Fig. 17.72). When the maxillary posterior teeth are out of the esthetic zone,
the crown may be designed for a crossbite (Fig. 17.73). The lingual overjet
prevents tongue biting, the buccal overjet (from the mandibular tooth)
prevents cheek biting, the implant is axial loaded by the lingual cusp of the
mandible, and hygiene is improved (Fig. 17.74).
FIG 17.72 In the maxillary posterior region, the implant may be positioned under the
lingual cusp (arrow). The laboratory often cantilevers the facial crown profile, to make
it appear as a natural tooth. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
FIG 17.73 When maxillary posterior implants are placed in division B to D bone
volumes out of the esthetic zone, the implant crown often is restored in posterior
crossbite. The maxillary lingual horizontal overjet prevents tongue biting, the
mandibular buccal overjet prevents cheek biting, and the primary occlusal contact is
in the central fossa over the implant body. B, Buccal; L, lingual. (From Misch CE: Dental
FIG 17.74 Mandibular first molar implant crown. The lingual contour is similar to the
adjacent teeth, but the lingual cusp tip is not loaded. The buccal contour is reduced
compared with the adjacent teeth. (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
Staggered Implants.
Alternative techniques exist in the literature that propose staggering of
posterior implants (i.e., buccal-lingual dimension) to improve biomechanical
resistance to loads.75 This concept is most effective and indicated when more
narrow implants are positioned in wider ridges so that the staggered position
is increased. However, a disadvantage of this technique includes the
fabrication of an atypical prosthesis, which results in hygiene difficulty and
esthetic issues. Additionally, implants placed more lingual may result in
lingual overcontouring and impingement on the tongue space, resulting in
speech and mastication issues. Compared with placing implants with
increased diameter and splinting, the staggering concept will decrease crestal
loads and is a better mechanism of stress reduction.
Increased Proximal Contact Area

The proximal contact area is highly variable in patients depending on many
factors such as age, sex, past orthodontic treatment, parafunction, and
missing teeth. Most commonly, the contact area is oval and is usually found
toward the buccal aspect of interproximal areas.76 In the incisal region, the
contacts are more vertically oriented and in the posterior are more
horizontally oriented. The proximal contacts usually increase in size from
anterior to posterior.77
When adjacent teeth shift with respect to a single edentulous space, this
poses multiple issues. Because of the shifting teeth, only a “point” contact
can be accomplished. This not only poses problems in food impaction,
formation of a black triangle, increased caries, and periodontal issues, but
also complicates the seating of the final prosthesis.
A common problem in the replacement of posterior teeth is lack of
sufficient interproximal contact or loss of contact over time. This is most
commonly seen with single edentulous sites in which the adjacent teeth have
rotated, tilted, or migrated. This results in the fabrication of a prosthesis that
has many disadvantages (Fig. 17.75).
FIG 17.75 When adjacent teeth are tilted or have migrated, it often results in a point
contact. An enameloplasty should be completed to allow for one path of insertion
and a long contact area.
Difficulty in Seating Prosthesis.

When the interproximal surfaces are not parallel to each other, two paths of
insertion are often required to seat the prosthesis properly (i.e., or may
prevent complete seating of the restoration). When the two adjacent teeth
have interproximal surfaces that parallel each other, only one path of
insertion exists, making the seating much easier.
Prevention.
Before the final impression, the adjacent proximal areas should be adjusted
with guide planes so that they are parallel. This is most often achieved with
the use of a diamond bur (i.e., flat-end cylinder). This will allow for a broader
contact area and one path of insertion for the final placement of the
prosthesis. Before implant placement (i.e., treatment planning phase), the
patient should be informed of the modifications of the adjacent teeth. This
communication with the patient will prevent patient questions and possible
dissatisfaction later in the prosthodontic process.
Food Impaction.
Point contacts are more prone to impacting food and developing a “black
triangle,” which can lead to difficulty in hygiene and esthetic compromises.
Prevention.
By increasing the proximal contact areas via guide planes on the adjacent
teeth, there is a decreased possibility of spaces for food impaction. The
laboratory must be instructed to fabricate an ideal emergence profile for the
prosthesis (Fig. 17.76).
FIG 17.76 Food impaction resulting from inadequate contact areas and poor
emergence profile.
Lack of Force Distribution.
With longer contact areas, a better force distribution (i.e., adjacent tooth will
absorb more of the force) is present, which decreases the offset loads
associated with the cantilevered mesial and distal marginal ridge areas.
Prevention.
Because of the cantilevered and offset loading of the mesial and distal
proximal areas, a wider proximal contact area is highly advantageous. There
will be greater surface area to distribute the force that is applied (i.e., force
distribution to the adjacent tooth because of broader contact) (Fig. 17.77).
FIG 17.77 Placing guide planes on adjacent teeth allows for a long proximal
contact area, which will allow for better force distribution.
Development of Open Contacts.

The etiology of acquired open contacts is unclear, and they are most likely
caused by many factors. Studies have confirmed the complication of open
contacts. Byun77a showed that open contacts (no resistance) occur 38% of the
time, and loose contacts (minimal resistance) occur 20% of the time over a
mean time of 57 months. Koori et al78 showed interproximal gaps
approximately 43% of the time over a period of 1 to 123 months. Wei et al79
reported an even higher incidence of 58% with the average time period being
2.2 years. Wong et al80 showed no difference in open contact areas among
screw vs. cement prostheses. Several possible factors contribute to open
contacts.
Inadequate proximal contact.

A small proximal contact area will most definitely impact this complication.
Open contacts usually do not occur between natural teeth because of
physiologic drift. When an implant is adjacent to a natural tooth, the osseous
interface will not allow for the implant to move in association with the
natural tooth. When natural teeth move through natural physiologic
movement, attrition, and parafunctional forces, with an implant having an
osseous interface, the teeth will not move.
Acquired contact area opening.

Usually, a contact area that opens after some time (e.g., originally strong
contact area present) originates from occlusal forces, mainly from the
mandibular closure muscles (i.e., lateral and medial pterygoid, masseter,
temporalis). The forces directed to the teeth are mainly dictated by inclined
cusp planes. Forces exist that push teeth mesial and distal; however, the
anterior, forward vector is five times stronger than the posterior force.80,81
Additionally, studies have shown the anterior component of force is
transmitted via the interproximal contacts and that its strength will decrease
with increased distance from the posterior teeth.82 Another possible reason
for the loss of contact area is craniofacial growth. Facial growth has been
reported in some patients well beyond adulthood. Even minor facial growth
may allow for mesial, buccal, or vertical growth leading to opening of
occlusal contacts (Fig. 17.78).83
FIG 17.78 Open contact area after prosthesis insertion.
Management and Prevention

Enameloplasty.
To prevent this complication, before the final impression for a crown, an
enameloplasty should be completed to allow for parallel interproximal
contact areas. The longer and wider contact areas will allow for better force
distribution, especially if there is a significant mesial or distal cantilever over
the marginal ridge area. This concept has been advocated in natural dentition
via large interproximal contacts to increase tooth position stability.77
Occlusal guard.
To maintain a strong contact and prevent this complication, an occlusal guard
is warranted to minimize stress to the system.
Occlusal adjustment.
Occlusion is modified to have even contacts on all incline planes, decreasing
the distal vector forces on the natural tooth (Fig. 17.79).
FIG 17.79 Contact Area Opening. (A) If occlusal forces are directed distally via
cuspal inclined planes, the natural tooth may become distally oriented. (B) By
decreasing the cuspal inclinations along with more favorable contacts, the natural
tooth will be less susceptible to movement.
Treatment: if open contact occurs after insert.

Treatment includes remaking the prosthesis or adding a contact to the
adjacent tooth via a new crown or composite bonding.
Mutually Protected Articulation

Numerous philosophies exist on the occlusal schemes for natural teeth. One
such scheme is termed “mutually protected occlusion,” in which the anterior
teeth disocclude the posterior teeth during excursions (i.e., incisal guidance
steeper than the condylar disc assembly).84-87 The posterior teeth protect the
anterior teeth in CO, and the anterior teeth protect the posterior teeth in
mandibular excursions. This occlusal design is based on the concept of using
the maxillary canine as the key of this occlusion scheme to avoid lateral
forces on the posterior teeth.88
Anterior, compared with posterior, bite force measurements and
electromyographic studies provide evidence that the stomatognathic system
elicits significantly less force when the posterior segments are not in contact
when the anterior teeth occlude.89 For example, the maximum bite force in
the posterior regions of the mouth (with no anterior occlusal contact) is 200–
250 psi. The maximum bite force in the anterior region (with no posterior
occlusal contact) is 25–50 psi. This difference results from a biologic response
and a mechanical condition when the posterior teeth do not contact. Almost
two-thirds of the temporalis and masseter muscles do not contract when
posterior teeth do not occlude.90 In addition, the TMJ and teeth complex form
a class 3 lever condition (i.e., the nutcracker).40 As a result, the closer the
object is placed toward the hinge (TMJ), the greater the force on the object.
In addition, the greater lateral mobility of the anterior teeth compared with
the posterior teeth (108 µm vs. 56 µm) also decreases the consequences of the
lateral forces during excursions.
In CO, the anterior teeth contacts are shared and protected by the occlusal
contacts of the posterior teeth. When the canine separates the posterior teeth
in right or left lateral excursions, the term “canine” or “cuspid protected
occlusion” may be used. If healthy anterior teeth or natural canines are
present, the mutually protected occlusion scheme allows those teeth to
distribute horizontal (lateral) loads during excursions, while the posterior
teeth disocclude during excursions (e.g., canine guidance or mutually
protected articulation) (see Fig. 17.34). The posterior teeth are protected from
lateral forces by the anterior guidance during excursions, and the anterior
teeth have lighter forces in excursions because the posterior teeth do not
contact. In other words, when lateral or angled forces are applied to the
anterior teeth, the magnitude of the stress is increased. However, when
mutually protected occlusal philosophies are applied, the consequences of
the lateral forces are reduced.
The mutually protected articulation concept is used in the implant protected
occlusion technique with the following designs:
• In protrusive mandibular movements, the central and lateral incisors
disocclude the posterior teeth.
• In lateral excursions, the canine (and lateral incisor when possible)
disocclude the posterior teeth.
• In CO, the posterior and canine teeth occlude. When the central and lateral
incisors are natural, they may also occlude in CO (or MI). When the anterior
teeth are implants, they should not occlude in centric occlusion, especially
when the opposing dentition is also implant supported.
Group function (or unilateral balance) has been suggested with
periodontal bone loss on the remaining teeth. The concept was to share the
lateral loads during excursions with more teeth. For example, in this
philosophy, a mandibular excursion to the right contacts as many anterior
and posterior teeth on the right as possible. This is not indicated in IPO. The
lateral posterior forces increase the moment loads to posterior implants. The
posterior contacts during excursions also have greater forces to the posterior
implants because more muscle mass contracts and the occlusal contacts are
closer to the TMJ (class 3 lever). In addition, the posterior lateral loads
increase the force to the anterior teeth or implants during the excursions. As
a result, both the anterior and the posterior implant components receive a
greater force (see Fig. 17.35).
In a study by Jemt et al,11 when implant-supported restorations were used
in the maxilla opposing natural dentition, the velocity of the mandible during
excursions was greater with group function than when incisal guidance was
present. The force to the implant system was greater with group function.
Kinsel and Lin91 reported that group function in patients with implant-
supported prostheses had a porcelain fracture rate of 16.1% and occurred in
51.9% of implant patients. When anterior disclusion was the occlusal scheme
in excursions, the fracture rate on implant crowns was 5.3%, and this
complication affected 15.9% of patients (more than a threefold difference).
All lateral excursions in IPO opposing fixed resulting lateral forces are
distributed to the anterior segments of the jaws, with an overall decrease in
force magnitude. This occlusal scheme should be followed whether or not
anterior implants are in the arch. However, if anterior implants must
disocclude posterior teeth, natural teeth (whenever possible) are first used
during the initial primary tooth movement. When multiple anterior teeth are
missing, two or more implants splinted together (when possible) should help
dissipate the lateral forces. Prostheses or natural teeth use anterior teeth or
implants whenever possible to disocclude the posterior components. The
resulting lateral forces are distributed to the anterior segments of the jaws,
with an overall decrease in force magnitude.
Use Progressive Bone Loading for Poor Bone Quality
Complication.
In poorer quality of bone, occlusal overload is a potentially damaging
complication for an implant prosthesis. When unfavorable force magnitude
and direction is coupled with poor bone quality, an increase in implant
failure results.92,93 The bone density is a critical factor in the determination of
the healing time and the type of prosthesis, and it is paramount that a
separate surgical and prosthetic technique be given for each bone density
type.
Prevention and Treatment.

Misch94 first proposed the concept of progressive bone loading, which allows
for modified prosthetic techniques to increase the bone-implant interface.
This is accomplished via principles associated with Wolff's law, where bone
mass increases in response to controlled stresses placed on the prosthesis. By
gradually increasing the load applied, implants in poor bone quality are
allowed to establish increased bone mass and density. The different elements
of progressive bone loading include treatment time intervals (approximately
3–8 months), modified diet (softer food), occlusion (gradually intensify the
occlusal contacts), and allowing loading to gradually increase during
prosthesis construction and a gradual increase in the strength of prosthesis
materials (from resin to metal to porcelain).
Rationale for Bone Density: Bone Physiology.

Cortical and trabecular bone throughout the body are constantly modified by
either modeling or remodeling.95 Modeling has independent sites of
formation and resorption and results in the change of the shape or size of
bone. Remodeling is a process of resorption and formation at the same site
that replaces previously existing bone and primarily affects the internal
turnover of bone, including the region where teeth are lost or the bone is
next to an endosteal implant. These adaptive phenomena have been
associated with the alteration of the mechanical stress and strain
environment within the host bone.96
Bone responds to hormonal and biomechanical regulation and in some
instances in which the demand for calcium is great (the primary objective for
hormonal regulation), functional loading can compete and maintain bone
mass.97 The stress applied to bone is measured by the magnitude of force
divided by the functional area over which it is applied. Strain is defined as
the change in length of a material divided by the original length.
The greater the magnitude of stress applied to the bone, the greater the
strain observed in the bone.64 Bone modeling and remodeling are primarily
controlled, in part or in whole, by the mechanical environment of strain.
Overall, the density of trabecular bone evolves as a result of mechanical
deformation from microstrain. The deformation of the alveolar bone by
mechanical forces is also related to the thickness of the bony plate.
Clinical evaluation confirms an increase in the amount of trabecular bone
and cortical plate thickness in patients with natural teeth exhibiting
parafunction. A dentist can observe these bone density changes when
attempting to extract teeth. In a severely parafunctional patient, the tooth
usually fractures when attempting to remove it because the surrounding
bone is stronger than the tooth. In a maxillary posterior second molar
unopposed by any mandibular tooth, the bone is so soft that the complete
tuberosity and surrounding bone fractures and the tooth and attached
surrounding bone are removed as one piece. Frost98 proposed that bone mass
is a direct result of the mechanical usage of the skeleton. He redeveloped a
mechanical adaptation chart relating trivial loading, physiologic loading,
overloading, and pathologic loading zones to ranges of microstrain. His
studies demonstrated increases in cortical bone mass related to strains
applied to the bone (Fig. 17.80).
FIG 17.80 The microstrain conditions applied to bone determine the cellular
events. The ideal loading zone is the adapted window. The pathologic overload zone
causes bone resorption. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Bone cells and the extracellular matrix comprise the strain-sensitive
population, and each plays a vital role in the mediation of the interface. A
review of the literature of in vivo and in vitro studies has shown that dynamic
or cyclic loading is necessary to cause a significant metabolic change in the
bone cell population.99 The greater the rate of change of applied strain in
bone, the more bone formation is increased.100 The effect of applied strains
on bone is dictated not only by the rate of the applied load but also by the
magnitude and duration.
In other words, the prosthetic loading of the dental implant changes the
number and density of bone cells. Cyclic loading is necessary to cause a
significant metabolic change in bone cell population. Lower magnitude loads
applied for many cycles can cause the same anabolic effects of larger loads
applied for a limited number of cycles.101 A range of clinical conditions may
equate to an increase in bone density, with prosthetic loading a logical
condition for a dental implant.
Clinical Studies Supporting Progressive Loading.

The biomechanical environment plays an intricate role in the quality and
compositional outcome of the new implant-bone interface. Under loading,
bone behaves as a structure with material and architectural properties and as
a biologic system.102 Functional loading of the implant brings additional
biomechanical influences, which greatly affect its maturation.
Computer-aided assessment of fixated implants through digital
subtraction radiographic image analysis and an interactive image-analysis
system demonstrate an increase in density of peri-implant bone structures
over a 6-month to a 4-year period after the implant was placed.103 The major
changes of bone condensation around the implants occurred after the first 2
years they were loaded (Fig. 17.81). Bone density increase is primarily
reflective of the local stress factors, and endosteal implants are the major
method to alter the strain and increase bone density in the edentulous jaws.
Continuously loaded implants remain stable within the bone with bone
formation in areas under compression and the orientation of trabeculae
corresponding to lines of stress.104 As bone responds to physiologic forces, a
gradual increase in loads during prosthetic fabrication stimulates an increase
in density. The implementation of progressive loading is more critical for
lesser bone densities because they are several times weaker than loads with
significant cortical bone. Parafunction, cantilevers, and other stress
magnifiers can increase the forces applied to the prosthesis and their shear
components and cause bone microfracture or microstrains in the pathologic
zone around the implant.105 Progressive bone loading aims at increasing the
density of bone, decreasing the risk of implant-bone failure, and decreasing
crestal bone loss.
FIG 17.81 (A) An implant interface after initial healing is weaker than the day of
surgery because woven bone is primarily present next to the implant. (B) After
loading, the implant-bone interface is stronger than the original bone condition
because the bone remodels in relation to the local strain condition. (From Misch CE:
Dental implant prosthetics, ed 2, St Louis, 2015, Mosby; data from Brägger U, Bürgin W, Lang NP, et
al: Digital subtraction radiography for the assessment of changes in peri-implant bone density, Int J
Oral Maxillofac Implants 6:160–166, 1991.)
Progressive Loading Protocol

Full-arch prostheses with little or no cantilever and adequate implant
number, position, and size rarely require progressive loading unless the bone
density is poor. The favorable biomechanics of an arch are even compatible
with immediate occlusal load applications.100 However, the fewer the number
of implants or the softer the bone types, the more progressive loading is
needed and recommended.
Cantilevers, patient force factors, and implant position may influence risk
factors in implant dentistry. Poor bone density may compromise implant
success even when key implant position and number are satisfactory. In
addition, crestal bone loss may be reduced with progressive loading.
The concept of progressive loading is to allow the bone to adapt to
increasing amounts of biomechanical stress. Rather than immediately
loading the bone-implant interface, methods to slowly increase the stress
over time are beneficial. The progressive loading protocol uses a cement-
retained prosthesis when implants are splinted together. Because a screw-
retained splinted restoration is not completely passive and a torque force
applied to a screw is greater than a bite force, a traditional screw-retained
restoration cannot use progressive loading to gradually load the bone.
As a general rule, the higher the risk factors, the more progressive loading
is recommended. The principles of gradual loading are demonstrated best in
a cement-retained prosthesis and are least applicable for the screw-retained
bar of a mandibular removable prosthesis type 5 (RP-5) restoration. In
addition, gradually loading an RP-4 or RP-5 prosthesis with a screw-retained
superstructure bar is difficult because the transitional prosthesis often
remains removable during the prosthesis fabrication. In addition, most of the
forces placed onto the implants for a screw-retained bar or prosthesis are
generated at the delivery from nonpassive superstructures. As a result,
screw-retained prostheses do not use a progressive loading protocol.
A longer healing time between stage I and stage II is suggested when
forces are greater or bone is softer. This time allows greater mineralization of
bone and a more mature lamellar bone interface to form next to the implants
before the load of the screws is applied to the implant bodies.
The progressive loading protocol has five different methods to gradually
load the bone or to increase the bone density around the implant (Box 17.6).
These elements help the dentist evaluate the gradual loading progress.
Box 17.6
Elements of Progressive Loading
• Time interval
• Diet
• Occlusal material
• Occlusal contacts
• Prosthesis design
Time
Initial healing.
The histologic type of bone in contact with the implant varies and can affect
the amount of stress the bone can sustain within physiologic limits. The ideal
bone for implant prosthetic support is lamellar bone. Lamellar bone is highly
organized but takes approximately 1 year to mineralize completely after the
trauma induced by implant placement. Woven bone is the fastest and first
type of bone to form around the implant interface; however, it is mineralized
only partly and demonstrates an unorganized structure less able to
withstand full-scale stresses. At 16 weeks, the surrounding bone is only 70%
mineralized and still exhibits woven bone as a component. Computer-aided
radiographic densitometry studies confirm that the bone-implant interface
decreases the first several months after surgical insertion of an implant.106
The percentage of bone mineralization and the type of supporting bone
influence whether a load to the bone-implant interface is within its
physiologic limits.
It has been reported that the bone-implant contact is related to the bone
density and the healing time. For example, in a study by Carr et al,107 the
bone-implant contact was greater in the mandible than the maxilla (the
mandible is usually more dense). In addition, the bone-implant contact was
greater at 6 months compared with 3 months in both jaws. An increase in
bone-implant contact occurred in both the maxilla and the mandible between
3 and 6 months and ranged from a 7% to 9% increase (Fig. 17.82). The healing
time before implant loading may be related to the density of bone because
the strength of bone increases and the bone-implant contact increases with a
longer time period. A period of 3–4 months of healing for D1 and D2 bone
and a period of 5–6 months for D3 and D4 bone have less risk than a shorter
time period for all bone types. The time period between surgical placement
and full occlusal loading is variable, depending on the bone density.
FIG 17.82 The percentage bone area is greater at 6 months compared with 3
months in both the maxilla and the mandible. (From Misch CE: Dental implant prosthetics,
The macroscopic coarse trabecular bone heals approximately 50% faster

than dense cortical bone. Although it heals more slowly, D1 bone has the
greatest strength and greater lamellar bone contact. The suggested healing
time between the initial and second-stage surgeries is similar for D1 and D2
bone and is 3–4 months. A longer time is suggested for the initial healing
phase of D3 and D4 bone (5 and 6 months, respectively) because of the lesser
bone contact and decreased amount of cortical bone to allow for the
maturation of the interface and the development of some lamellar bone. In
very immature bone, the healing time may be 8 months.
The D4 implant-bone interface typically found in posterior regions of the
maxilla exhibits minimum initial bone contact, with little to no cortical bone
at the crest or apex. An implant surgery initially may trigger an increase in
the amount of bone in the region. For example, bone has been shown to grow
in contact with a submerged titanium screw inserted into an open marrow
chamber of the femur.108 The initial increase of bone cell activity most likely
results from the surgical trauma and the regional acceleratory phenomenon.
The longer initial healing time is most beneficial to the poorest bone density
types. In softer bone, a longer period of time of initial healing and gradual
loading is suggested. Generally, D1 bone uses a period of 3 or more months
before loading, D2 bone uses a period of 4 or more months, D3 bone uses a
period of 5 or more months, and D4 bone uses a period of 6 or more months.
The combined observations of the macroscopic amount of bone in contact
with a nonloaded implant and the microscopic type of bone at the stage II
surgery of the implant demonstrates a wide difference in D1 to D4 bone
densities. However, the long-term major improvement in bone density and
strength occurs as a consequence of loading the implant.
Four prosthodontic steps are suggested for the reconstruction of a partially
or completely edentulous patient, with endosteal implants supporting a
cemented prosthesis. Each of the four major prosthodontic appointments
also are separated by a period of time related to the bone density observed at
the initial time of surgery. In addition, the dentist attempts to gradually
increase the load to the implant at each prosthetic step. The four prosthetic
steps are (1) abutment insertion, preparation, final impression, and
temporary (of the esthetic zone); (2) a metal try-in and new bite registration;
(3) initial delivery of the prosthesis; and (4) final evaluation of the restoration
and hygiene appointment. In simple restorative cases, the prosthetic
appointments may be reduced to three appointments: (1) abutment
selection, preparation, final impression, opposing impression, and closed
mouth bite registration; (2) initial delivery of the restoration; and (3) final
evaluation stage (accompanied by a hygiene appointment).
Type D1 bone benefits from the greatest amount of lamellar bone contact
at the beginning of the restoration process. As a result, gradual loading of
the implant interface through spacing of the prosthodontic appointments is
least important, and the restorative appointments can be separated by 1
week.
Type D2 bone responds favorably to physiologic loads. The four prosthetic
appointments during which the implant body is loaded sequentially are
separated by 2 weeks or more. The initial 4 months of healing after surgery
and 2 months for prosthesis fabrication result in the overall treatment time
of 5.5 months.
The prosthodontic appointments for D3 bone are separated by at least 3
weeks, and overall treatment takes approximately 7 months to complete,
including the 5 months of initial healing. During this time, the bone contact
percentage can increase, and the fine woven bone trabeculae can mature into
coarser lamellar trabeculae, with an increase in mineral content. The
progressive loading process is more critical for D3 bone than for D2 or D1
bone because of its weakness and less initial bone contact.
In D4 bone, the progressive bone loading protocol is most critical. When
scheduling restorative appointments, one should err on the side of safety; the
appointments should be separated by at least 4 weeks. As a consequence, the
overall treatment time for D4 bone is twice that of D1 or D2 bone and at least
9 months (including 6 months of initial healing). This schedule allows
sufficient time for mature lamellar, mineralized bone to develop at the
interface and increases the numbers of trabeculae in direct contact and
within the network region of the implant (Table 17.4).
TABLE 17.4
Treatment Times for Progressive Bone Loading for Cement-Retained
Prostheses
Bone Density Initial Healing (months) Interval Between Appointments (weeks) Reconstruction (weeks) Total Time (months)
D1 3 1 3 4
D2 4 2 6 5.5
D3 5 3 9 7
D4 6 4 12 9
When the dentist uses multiple implants, the weakest bone area
determines the gradual load protocol. If the anterior maxilla and posterior
maxilla are restored together, the posterior maxilla would determine the
initial healing period and the time period between each prosthetic
appointment.
Diet.
The dentist controls the diet of the patient to prevent overloading during the
early phases of the restorative process. During the initial healing phase, the
dentist instructs the patient to avoid chewing in the area, especially when the
implants are placed in a one-stage approach, with an exposed healing
abutment.
After being uncovered, the implant connected to an abutment for cement
retention is at greater risk of loading during mastication. The patient is
limited to a soft diet such as pasta and fish from the final impression stage
until the initial delivery of the final prosthesis. The masticatory force for this
type of food is approximately 10 psi. This diet not only minimizes the
masticatory force on the implants but also decreases the risk of temporary
restoration fracture or a partially uncemented restoration. Either of these
consequences can overload an implant and cause unwanted complications.
The diet should not be overlooked during the restorative phase of
treatment. Most dentists have observed the fracture of an acrylic prosthesis
with harder foods and greater occurrence of uncemented restorations when
they ignore the type of diet during the transitional prosthesis stages.
After the initial delivery of the final prosthesis, the patient may include
meat in the diet, which requires approximately 21 psi in bite force. The final
restoration can bear the greater force without risk of fracture or
uncementation. After the final evaluation appointment, the patient may
include raw vegetables, which require an average 27 psi of force.
A normal diet is permitted only after evaluation of the final prosthesis
function, occlusion, and proper cementation. The most damaging forces to a
transitional (or final) restoration are from parafunction, not the function of
eating. After the prosthesis is placed into occlusion, the evaluation of
parafunction and methods to reduce its negative side effects are critical to
the loading process.
Occlusal Material.
The occlusal material may be varied to gradually load the bone-implant
interface. During the initial steps, the implant has no occlusal contact and in
essence has no material over it. At subsequent appointments, the dentist
uses acrylic as the occlusal material, with the benefit of a lower impact force
than metal or porcelain. Either metal or porcelain can be used as the final
occlusal material.
If parafunction or cantilever length causes concern relative to the amount
of force on the early implant-bone interface, the dentist may extend the softer
diet and acrylic restoration phase several months. In this way, the bone has a
longer time to mineralize and organize to accommodate the higher forces.
Occlusal Contacts.
The dentist gradually intensifies the occlusal contacts during prosthesis
fabrication. No occlusal contacts are permitted during initial healing (step 1).
The first transitional prosthesis is left out of occlusion in partially edentulous
patients (step 2). The occlusal contacts then are similar to those of the final
restoration for areas supported by implants. However, no occlusal contacts
are made on cantilevers or offset loads (step 3).
Prosthesis Design.
There are four potential prostheses designs in a restorative process. During
initial healing, the dentist attempts to avoid any load on the implants,
including soft tissue loads. In a completely edentulous patient, relief and a
soft tissue conditioner (also relieved) may be used. The first transitional
acrylic restoration in partially edentulous patients has no occlusal contact
and no cantilevers. Its purpose is to splint the implants together and reduce
stress by the mechanical advantage and to have implants sustain masticatory
forces solely from chewing.
The second acrylic transitional restoration has occlusal contacts placed
over the implants with occlusal tables similar to the final restoration but with
no cantilevers in nonesthetic regions. The final restoration has narrow
occlusal tables and cantilevers designed with occlusal contacts following
implant-protective occlusion guidelines.
Progressive Loading Phases.

After the surgical stage II uncovery procedure or one-stage implant healing,
the surgeon evaluates clinical mobility, bone loss (horizontal and vertical),
proper placement in reference to prosthetic design and angulation to load,
zones of attached gingiva, and gingival thickness. The surgeon usually
attaches a low-profile permucosal extension to the implant body at the end of
this appointment.
This component extends through the tissue approximately 2 mm and is
protected from early loading (Fig. 17.83). In selected cases, often when the
surgeon and restoring dentist are the same person, one may obtain the
preliminary impression during this appointment if the soft tissues are
outside the esthetic areas and if no bone recontouring or grafting has been
performed or a one-stage surgical approach was used during initial healing.
The dentist instructs the patient with a posterior implant in a partially
edentulous arch not to wear any removable restoration. If anterior teeth are
part of the removable prosthesis, a 7-mm-diameter hole is placed completely
through the partial denture framework around each permucosal extension so
that it will not load the implant. In completely edentulous patients, the tissue
surface of the denture is relieved at least 5 mm over and around the implants
and replaced by a tissue conditioner. The conditioner also is relieved a few
millimeters.
FIG 17.83 A permucosal extension was placed by the surgeon at the implant
insertion or at stage II uncover. Ideally, the soft tissue is healed before prosthetic
reconstruction. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The patient returns in 2 weeks for suture removal and to replace the tissue
conditioner with a soft liner. The procedures for a partially edentulous
Kennedy Class I or II patient are first presented. The progressive bone-
loading appointment sequence for cement-retained prostheses is as follows
(Table 17.5):
1. Initial abutment selection, final impression, and transitional prosthesis I
2. Metal superstructure try-in and transitional prosthesis II
3. Initial insertion of final prosthesis
4. Final evaluation and hygiene

TABLE 17.5
Progressive Loading Appointments for a Cement-Retained Prosthesis
Step P rocedure Diet Occlusal Material Occlusal Contacts

1 Final abutments S oft Ac rylic None
Final impression No c antilever
Transitional
prosthesis
2 Transitional
prosthesis II
Metal try-in S oft Ac rylic Contac ts only on implant; no c ontac ts on c antilevers or pontic s; oc c lusal table
same as final prosthesis
Bite registration
3 Final prosthesis Harder Metal porc elain, or Oc c lusion follows implant-protec tive oc c lusion guidelines; narrow oc c lusal table
zirc onia
Adjust oc c lusion
4 Final evaluation Normal Metal porc elain, or S ame as above
zirc onia
Hygiene
From Misch, CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.

Summary
The prosthodontic rehabilitation of patients with dental implants is one of
the most complicated and complex parts of dentistry. The occlusal loading of
the implant prosthesis is much different than traditional prosthetic
principles on natural teeth. In the earliest years of the discipline, implant
dentistry primarily existed as a multidisciplinary, team-based practice.
Surgical principles were followed for implant placement, and restorative
concepts were then put into action that created prostheses for the integrated
implants. In many instances, the surgical and prosthetic plans lacked
cohesiveness in design and planning, resulting in numerous complications
and failures.
As knowledge regarding implant dentistry has increased, we now see the
importance of blending these phases together. The occlusion scheme for
implant-supported prostheses becomes most important to the longevity of
the restoration because that scheme will dictate biomechanical stress
placement along integrated implants. Failure to account for these
fundamentals of implant occlusion will result in numerous complications in
both the prosthesis and the implants proper.
It is paramount that any clinician, whether on the surgical, restorative, or
both ends of implant treatment, be well versed in occlusal design before
commencing with therapy. Force factors may need to be addressed, bone
volumes may need to be augmented to allow for larger diameter (or more)
implants, and key implant positions may need to be modified to offset
potential loads. Knowing the optimal occlusal concept for a specific
treatment plan will also assist the surgical phase of treatment because the
surgeon has a clearer understanding of the demands of each implant as it
pertains to function and optimal direction of force within the arch (Figs. 17.84
to 17.87, Boxes 17.7 to 17.11, and Table 17.6). The concepts in this chapter will
allow for practitioners in all phases of implant dentistry to gain a clearer
understanding of the prosthetic concepts that ensure stable, successful long-
term dental implant restorations.
FIG 17.84 (A) Only the lingual cusps of the maxillary anatomic posterior teeth
occlude with the mandibular teeth. This brings the occlusal contact closer to the
crestal bone support and helps stabilize the denture. (B) The mandibular teeth have
occlusal contact in the central fossa; the buccal cusps are reduced in height, with no
occlusal contact in centric occlusion. (From Misch CE: Dental implant prosthetics, ed 2, St
FIG 17.85 When multiple adjacent implants are placed in a premaxilla, the arch
dimension often does not allow implant placement in the original teeth location
without placing the implants closer than 3 mm apart (left). When multiple anterior
teeth are missing, most often only two implants can be positioned to replace the
three anterior teeth (on the right). (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
FIG 17.86 When four anterior incisors are missing, most often three smaller
diameter implants are used as prosthetic support. (From Misch CE: Dental implant
FIG 17.87 There are often facial cantilevers on anterior implants (points A and B).
The crown height is also larger than the natural tooth (C in centric occlusion and D in
protrusive). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Box 17.7
Occlusal Recommendations for Single
Implant-Supported Prostheses
• Implant diameter—correspond as closely to the mesial-distal diameter of
edentulous space. A mandibular first molar has an average mesial-distal
diameter of 11 mm. A 3- to 4-mm implant is usually contraindicated.
Ideally, a 5- to 6-mm implant should be placed.
• Implant length—longer implants (i.e., >12 mm indicated in patients with

poorer bone quality).
• Narrow occlusal table—minimize nonaxial loading forces (i.e., cantilever

effect).
• Implant angulation—ideally perpendicular to curve of Spee and curve of

Wilson; less than 30 degrees is contraindicated.
• Centered contacts in maximum intercuspation—to be in centric fossa with

a larger contact area (approximately 2–3 mm; e.g., centric contacts to be
avoided on marginal ridge because of cantilever effect).
• Minimal cusp height (i.e., monoplane occlusion).
• No contact with light biting force/light contact at heavy biting force—

maximize force to adjacent teeth.
• No offset excursive contacts
• Increased interproximal contact area—dissipate occlusal forces
• Occlusal guard when parafunction present
• Progressive bone loading in poorer bone quality
Box 17.8
Occlusal Recommendations for Multiple
Implants—Anterior Implant-Supported
Restorations (Kennedy Class IV [Anterior
Edentulous])
• Number of implants: In most cases, fewer implants are placed because of
decreased length present (e.g., as bone resorbs from buccal, length of bone
decreases, resulting in less space for implants).
Examples:
Replacing No. 6–11: Implants usually placed at No. 6, 8,

9, 11.
Replacing No. 23–25: Two implants placed between No.

23–24 and No. 25–26 (see Figs. 17.85 and 17.86).
• Canine position (if missing) is the most important position for implant
placement.
• Implant diameter should correspond to diameter of natural tooth that is

being replaced. Bone augmentation is often indicated.
• Implants should always be splinted together to distribute forces. Most

often facial cantilevers are present because of the residual ridge resorption,
which increases the moment force (see Fig. 17.87).
• Crown height space should always be evaluated in the anterior region

because it is a force magnifier, which increases the cantilever effect.
• Progressive bone loading is often indicated because of inherent poor bone

quality in the premaxilla (approximately D3 bone quality).
• Occlusal guard is indicated when parafunction is present.
Box 17.9
Occlusal Recommendations for Multiple
Implants—Posterior Implant-Supported
Restorations
• Number of implants: Usually one implant for each tooth replacement (e.g.,
fewer implants indicated when favorable force factors are present).
• Interbone distance between implants: approximately 3 mm.
• Splinting of implants indicated to increase force distribution.
• Narrow occlusal table.
• Minimal cusp height.
• Avoid nonaxial loading.

• Avoid cantilevers when possible (e.g., biomechanically a mesial cantilever
is more favorable than a distal cantilever).
• Infraocclusion on cantilever part of occlusal table.
• Maintain excursive guidance on healthy natural teeth while discluding the

posterior implant segment.
• Centric contacts should be evenly placed over occlusal table corresponding

to implant positions.
• Crossbite may be used when indicated.
• Use of occlusal guards is indicated especially when parafunctional forces

are present.
• Kennedy Class I (bilateral posterior edentulous) and II (unilateral posterior

edentulous): No protrusive contacts, narrow occlusal table, minimal cusp
height, timed occlusal contacts.
• Kennedy Class III (edentulous space with anterior and posterior natural
teeth): Timed occlusal contacts, disclusion is determined by natural tooth
incisal guidance.
Box 17.10
Occlusal Recommendations for Fully
Edentulous Implant Fixed Prosthesis
• Implant number:
Maxilla: 6–9 implants (e.g., <6 implants is controversial)
Mandible: 5–7 implants (e.g., <5 implants is

controversial)
• Angulation—implant position to be lingual to incisal edge.
• Splinting—should always be completed on maxilla and mandible except on
mandible when bilateral implants posterior to the mental foramen (i.e.,
separate prosthesis usually separated distal to the cuspid on one side).
• Cantilever—amount of cantilever depends on force factors; cantilever

should be in infraocclusion (approximately 100 µm).
• Occlusion—is dependent on opposing arch, skeletal relationship, and force

factors; however, anteroposterior simultaneous contacts in centric relation
and maximal intercuspation position.
• Shallow anterior guidance when opposing natural teeth.
• Freedom in centric relation (1–1.5 mm).
• Occlusal guard when parafunction is present.
Box 17.11
Occlusal Recommendations for Fully
Edentulous Implant Removable Prosthesis
• Implant number:
Maxilla: 4–8 implants depending on RP-4 or RP-5 (e.g.,

<4 implants is controversial).
Mandible: 2–5 implants depending on RP-4 or RP-5 (e.g.,

2 implants is controversial).
• Angulation—implant position to be center of ridge.
• Implant position—dependent on number of implants and anteroposterior

spread.
• Anteroposterior simultaneous contacts in centric relation and maximal

intercuspation position.
• Occlusion—bilateral balance occlusion (i.e., medial positioned lingualized
occlusion), true balanced occlusion opposing natural teeth may be difficult
to obtain (i.e., minimum of three-point balance contacts on lateral and
excursions). For poor ridge form (i.e., Division D, severe posterior ridge
resorption), monoplane occlusion may be used.
• Support—usually bar-retained implant overdentures are implant

supported (RP-4), and stud attachments usually exhibit primary soft tissue
support (RP-5).
TABLE 17.6
Recommended Occlusion for Implant Prosthesis and Opposing Dentition
Implant P rosthesis Opposing Dentition Ideal Occlusal Scheme Additional Information

Edentulous FP-3 Natural dentition Mutually protec ted S hallow inc isal guidanc e
FP-3 Complete denture Bilateral balanc ed Lingualized oc c lusion
FP-3 FP-3 Mutually protec ted
FP-3 Overdenture Bilateral balanc ed
Edentulous Overdenture Natural dentition Mutually protec ted
Overdenture Complete denture Bilateral balanc ed Lingualized oc c lusion
Overdenture Overdenture Bilateral balanc ed
Overdenture FP-3 Mutually protec ted
Dentate Kennedy Class I/II FPD Natural dentition Mutually protec ted Ideal splinting c rowns
FPD Complete denture Balanc ed Lingualized oc c lusion
Dentate Kennedy Class III/IV FPD Natural dentition Mutually protec ted Ideal splinting c rowns
FPD Complete denture Balanc ed Lingualized oc c lusion
Single tooth S ingle implant c rown Any Mutually protec ted
FPD, Fixed partial denture.

References
1. Goodacre CJ, Kan JK, Rungcharassaeng K. Clinical complications of
osseointegrated implants. J Prosthet Dent. 1999;81:537–552.
2. Misch CE. Progressive bone loading. Misch CE. Contemporary implant
dentistry. Mosby: St Louis; 1993.
3. Jemt T, Linden B, Lekholm U. Failures and complications in 127
consecutively placed fixed partial prostheses supported by
Brånemark implants: from prosthetic treatment to first annual
checkup. Int J Oral Maxillofac Implants. 1992;7:40–44.
4. Naert I, Quirynen M, van Steenberghe D, et al. A six-year
prosthodontic study of 509 consecutively inserted implants for the
treatment of partial edentulism. J Prosthet Dent. 1999;67:236–245.
5. Misch CE. Early crestal bone loss etiology and its effect on treatment
planning for implants. Postgrad Dent. 1995;3:3–17.
6. Isidor F. Loss of osteointegration caused by occlusal load of oral
implants. Clin Oral Implants Res. 1996;7:143–152.
7. Hansson S. The implant neck: smooth or provided with retention
elements. Clin Oral Implants Res. 1999;10:394–405.
8. Misch CE, Bidez MW. Occlusion and crestal bone resorption: etiology
and treatment planning strategies for implants. McNeil C. Science and
practice of occlusion. Quintessence: Chicago; 1997.
9. Isidor R. Histological evaluation of peri-implant bone at implants
subjected to occlusal overload or plaque accumulation. Clin Oral
10. Rangert B, Krogh PH, Langer B, et al. Bending overload and implant
fracture: a retrospective clinical analysis. Int J Oral Maxillofac
Implants. 1995;7:40–44.
11. Jemt T, Lindquist L, Hedegard B. Changes of the general chewing pattern
in complete denture wearers after insertion of bridges on osseointegrated
oral implants in the lower jaw. [In] Proceedings of the Symposium on
Prosthetic Reconstructions on Osseointegrated Implants, Goteborg,
Sweden. 1983:143–150.
12. Gartner JL, Mushimoto K, Weber HP, et al. Effect of osseointegrated
implants in the coordination of masticatory muscles: a pilot study. J
Prosthet Dent. 2000;84:185–193.
13. Farahani RM, Simonian M, Hunter N. Blueprint of an ancestral
neurosensory organ revealed in glial network in human dental pulp. J
Comp Neurol. 2011;519:3306–3326.
14. Klineberg IJ, Trulsson M, Murray GM. Occlusion on implants—is
there a problem? J Oral Rehabil. 2012;39:522–537.
15. Svensson KG, Trulsson M. Force control during food holding and
biting in subjects with tooth- or implant-supported fixed prosthesis. J
16. Trulsson M, Johansson RS. Forces applied by the incisors and roles or
periodontal afferents during food-holding and -biting tasks. Exp
Brain Res. 1996;107:486–496.
17. Klineberg I, Eckert S. Functional occlusion in restorative dentistry and
prosthodontics. Mosby: St Louis; 2016.
18. Yoshida K. Tactile threshold for static and dynamic loads in tissue
surrounding osseointegrated implants. Jacobs R. Osseoperception.
Catholic University of Leuven, Department of Periodontology:
Leuven; 1998:143–156.
20. McKinney RV, Koth DC, Steflik DE. Clinical standards for dental
implants. Clark JW. Clinical dentistry. Harper & Row: Hagerstown,
MD; 1984.
21. Steflik DE, Koth DC, McKinney RV Jr. Human clinical trials with the
single crystal sapphire endosteal dental implant: three year results,
statistical analysis, and validation of an evaluation protocol. J Oral
Implantol. 1987;13:39–53.
tactile sensitivity of osseointegrated fixture-supporting systems. Van
Excerpta Medica: Amsterdam; 1986.
24. Rudd KD, O'Leary TJ, Stumpf AJ. Horizontal tooth mobility in
carefully screened subjects. Periodontics. 1964;2:65–68.
Excerpta Medica: Amsterdam; 1986.
osseointegrated implant. Quintessence: Chicago; 1989.
27. Rangert B, Gunne J, Sullivan DY. Mechanical aspects of Brånemark
28. Türker KS, Sowman PF, Tuncer M, et al. The role of periodontal
mechanoreceptors in mastication. Arch Oral Biol. 2007;52:361–364.
29. Svensson KG, Grigoriadis J, Trulsson M. Alterations in intraoral
manipulation and splitting of food by subjects with tooth- or
implant-supported fixed prostheses. Clin Oral Implants Res.
2013;24:549–555.
30. Trulsson M, Gunne HS. Food-holding and -biting behavior in human
subjects lacking periodontal receptors. J Dent Res. 1998;77:574–582.
31. Klineberg I, Calford MB, Dreher B, et al. A consensus statement on
osseoperception. Clin Exp Pharmacol Physiol. 2005;32:145–146.
33. Jacobs R, van Steenberghe D. Comparison between implant-
supported prostheses and teeth regarding passive threshold level. Int
34. Hämmerle CH, Wagner D, Bragger U, et al. Threshold of tactile
sensitivity perceived with dental endosseous implants and natural
teeth. Clin Oral Implants Res. 1995;6:83–90.
36. Rihani A. Classification of articulators. J Prosthet Dent. 1980;43:344–
347.
37. Laney WR. Critical aspects of removable partial denture service.
Goldman HM. Current therapy in dentistry. Mosby: St Louis; 1968.
38. Desjardins RP. Tissue integrated prostheses for edentulous patients
with normal and abnormal jaw relationships. J Prosthet Dent.
1988;59:180–187.
39. Dawson PE. Functional occlusion—from TML to smile design. Mosby: St
Louis; 2007.
40. Dawson PE. Evaluation, diagnosis, and treatment of occlusal problems. ed
2. Mosby: St Louis; 1989.
concepts and principles. Oral Implantol. 1992;18:264–274.
42. Binderman I. NIH grant study on two-dimensional FEA study of 54
implant body designs. 1973 [(personal communication)].
43. Kinni ME, Hokama SM, Caputo AA. Force transfer by
osseointegration implant devices. Int J Oral Maxillofac Implants.
1987;2:11–15.
44. Cook SD, Klawitter JJ, Weinstein AJ, et al. The design and evaluation
of dental implants with finite element analysis. Gallagher RA. Finite
elements in biomechanics. University of Arizona: Tucson; 1980.
occlusal overload on peri-implant tissue. Part 3: A histologic study in
occlusal overload on peri-implant time. 4. A histologic study in
occlusal overload on peri-implant tissue: a histologic study in
49. Gartner JL, Mushimoto K, Weber HP, et al. Effect of osseointegrated
implants in the coordination of masticatory muscles: a pilot study. J
Prosthet Dent. 2000;84:185–193.
50. Kim Y, Oh TJ, Misch CE, et al. Occlusal considerations in implant
therapy: clinical guidelines with biomechanical rationale. Clin Oral
Implants Res. 2005;16:26–35.
51. Jacobs R, van Steenberghe D. Comparative evaluation of oral tactile
function by means of teeth or implant support prostheses. Clin Oral
53. Reilly DT, Burstein AH. The elastic and ultimate properties of
compact bone tissue. J Biomech. 1975;80:393–405.
54. Misch CE. Three-dimensional finite element analysis of two plate form neck
designs. [master's thesis, Pittsburgh] 1989 [University of Pittsburgh].
55. Clelland NL, Lee JK, Bimbenet OC, et al. A three-dimensional finite
element stress analysis of angled abutments for an implant placed in
the anterior maxilla. J Prosthodont. 1995;4:95–100.
56. Papavasiliou G, Kamposiora P, Bayne SC, et al. Three-dimensional
finite element analysis of stress distribution around single tooth
implants as a function of bony support prosthesis type and loading
during function. J Prosthet Dent. 1996;76:633–640.
57. Qin YX, McLeod KJ, Guilak F, et al. Correlation of bony ingrowth to
the distribution of stress and strain parameters surrounding a porous
coated implant. J Orthop Res. 1996;14:862–870.
58. Barbier L, Schepers E. Adaptive bone remodeling around oral
implants under axial and nonaxial loading conditions in the dog
mandible. Int J Oral Maxillofac Implants. 1997;12:215–223.
59. Ko CC, Kohn DH, Hollister SJ. Micromechanics of implant/tissue
interfaces. J Oral Implantol. 1992;18:220–230.
60. Akca K, Iplikcioglu H. Finite element stress analysis of the effect of
short implant usage in place of cantilever extensions in mandibular
posterior edentulism. J Oral Rehabil. 2002;29:350–356.
61. Ha C-Y, Lim Y-J, Kim M-J, et al. The influence of abutment angulation
62. Duyck J, Van Oosterwyck H, Vander Sloten J, et al. Magnitude and
distribution of occlusal forces on oral implants supporting fixed
prostheses: an in vivo study. Clin Oral Implants Res. 2000;11:465–475.
Prosthet Dent. 1983;49:816–823.
64. Weinberg LA, Kruger B. A comparison of implant/prosthesis loading
with four clinical variables. Int J Prosthodont. 1995;8:421–433.
in 152 patients: patient-specific and implant-specific predictors of
ceramic failure. J Prosthet Dent. 2009;101:388–394.
66. Pasricha N, Sidana V, Bhasin S, et al. Canine protected occlusion.
Indian J Oral Sci. 2012;3(1):13.
67. Bonte B, Steenberghe D. Masseteric post-stimulus EMG complex
following mechanical stimulation of osseointegrated oral implants. J
Oral Rehabil. 1991;18(3):221–229.
68. Kaukinen JA, Edge MJ, Lang BR. The influence of occlusal design on
simulated masticatory forces transferred to implant-retained
prostheses and supporting bone. J Prosthet Dent. 1996;76:50–55.
69. Rungsiyakull P, Rungsiyakull C, Appleyard R, et al. Loading of single
implant in simulated bone. Int J Prosthodont. 2011;24:140–143.
70. Rungsiyakull C, Rungsiyakull P, Li Q, et al. Effects of occlusal
inclination and loading on mandibular bone remodelling: a finite
element study. Int J Oral Maxillofac Implants. 2011;26:527–537.
71. Thomas PK. Syllabus for full mouth waxing technique for rehabilitation
tooth to tooth cusp-fossa concept of organic occlusion. ed 2. University of
California School of Dentistry, Los Angeles: San Francisco; 1967.
72. Welcott J. A simplified occlusal concept. J Prosthet Dent.
1989;61(3):457–463.
73. Misch CE, Misch-Dietsh F. Pre-implant prosthodontics. Misch CE.
Dental implant prosthetics. Mosby: St Louis; 2005.
74. Misch CE. Occlusal considerations for implant-supported prostheses.
Misch CE. Contemporary implant dentistry. Mosby: St Louis; 1993.
75. Sato Y, Shindoi N, Hosokawa R, et al. A biomechanical effect of wide
implant placement and offset placement of three implants in the
posterior edentulous region. J Oral Rehabil. 2000;27:15–21.
76. Greenstein G, et al. Open contacts adjacent to dental implant
restorations. J Am Dent Assoc. 2016;147:28–34.
77. Sarig R, Lianopoulos NV, Hershkovitz I, et al. The arrangement of the
interproximal interfaces in the human permanent dentition. Clin
Oral Investig. 2013;17:731–738.
77a. Byun SJ, Heo SM, Ahn SG, et al. Analysis of proximal contact loss
between implant-supported fixed dental prostheses and adjacent
teeth in relation to influential factors and effects: a cross-sectional
study. Clin Oral Implants Res. 2015;26:709–714.
78. Koori H, Morimoto K, Tsukiyama Y, et al. Statistical analysis of the
diachronic loss of interproximal contact between fixed implant
prostheses and adjacent teeth. Int J Prosthodont. 2010;23:535–540.
79. Wei H, Tomotake Y, Nagao K, et al. Implant prostheses and adjacent
tooth migration: preliminary retrospective survey using 3-
dimensional occlusal analysis. Int J Prosthodont. 2008;21:302–304.
80. Wong AT, Wat PY, Pow EH, et al. Proximal contact loss between
implant-supported prostheses and adjacent natural teeth: a
retrospective study. Clin Oral Implants Res. 2015;26:e68–e71.
81. Vardimon AD, Beckmann S, Shpack N, et al. Posterior and anterior
components of force during bite loading. J Biomech. 2007;40:820–827.
82. Conroy JJ. An investigation of the posterior component of occlusal force.
[master's thesis, Iowa City, IA] 1994 [University of Iowa].
83. Brash JC. The growth of the alveolar bone and its relation to the
movements of the teeth, including eruption. Int J Orthod. 1928;14:196–
223.
84. Shupe RJ, Mohamed SE, Cristensen LV, et al. Effects of occlusal
guidance on jaw muscle activity. J Prosthet Dent. 1984;51:811–818.
85. Manns A, Chan C, Miralles R. Influence of group function and canine
guidance on electromyographic activity of elevator muscles. J Prosthet
Dent. 1987;57:494–501.
86. Lucia VO. Modern gnathological concepts. Mosby: St Louis; 1961.
87. Alexander PC. Analysis of cuspid protected occlusion. J Prosthet Dent.
1963;13:307–317.
88. D'Amico A. The canine teeth: normal functional relation of the
natural teeth of man. J South Calif Dent Assoc. 1958;26:1–7.
Prosthet Dent. 1983;49:816–823.
90. Belser UC, Hannam AG. The influence of working-side occlusal
guidance on masticatory muscles and related jaw movement. J
Prosthet Dent. 1985;53:406–413.
in 152 patients: patient-specific and implant specific predictors of
ceramic failure. J Prosthet Dent. 2009;101:388–394.
92. Becktor JP, Eckert SE, Isaksson S, et al. The influence of mandibular
dentition on implant failures in bone-grafted edentulous maxillae. Int
93. Esposito M, Thomsen P, Molne J, et al. Immunohistochemistry of soft
tissues surrounding late failures of Branemark implants. Clin Oral
Implants Res. 1997;8:352–366.
approach, healing, and progressive bone loading. Int J Oral Implantol.
1990;6:23–31.
95. Enlow DH. Principles of bone remodeling: an account of post-natal growth
and remodeling processes in long bones and the mandible. Charles C
Thomas: Springfield, IL; 1963.
96. Currey JD. Effects of differences in mineralization on the mechanical
properties of bone. Philos Trans R Soc Lond B Biol Sci. 1984;1121:509–
518.
97. Goldstein GR. The relationship of canine protected occlusion to a
periodontal index. J Prosthet Dent. 1979;41:277–283.
98. Frost HM. Vital biomechanics: proposed general concepts for skeletal
adaptations to mechanical usage. Calcif Tissue Int. 1988;42:145–155.
99. Hasegawa S, Sato S, Saito S, et al. Mechanical stretching increases the
number of cultured bone cells synthesizing DNA and alters their
pattern of protein synthesis. Calcif Tissue Int. 1985;37:431–436.
100. Clinton T, Lanyon KLE. Regulation of bone formation by applied
dynamic loads. J Bone Joint Surg Am. 1984;66:397–402.
101. Duncan RC, Turner CH. Mechanotransduction and functional
response of bone to mechanical strain. Calcif Tissue Int. 1995;57:344–
358.
102. Roesler H. The history of some fundamental concepts in bone
biomechanics. J Biomech. 1987;20:1025–1034.
103. Braggen U, et al. Digital subtraction radiography for the assessment
of changes in peri-implant bone density. Int J Oral Maxillofac
Implants. 1991;6:160–166.
104. Roberts WE, Garetto LP, DeCastro RA. Remodeling of demineralized
bone threatens periosteal implants with threaded or smooth surfaces.
J Indiana Dent Assoc. 1989;68:19–24.
105. Holmes DC, Loftus JT. Influence of bone quality on stress
distribution for endosseous implants. J Oral Implantol. 1997;23:104–
111.
106. Strid KG. Radiographic results of tissue integrated prostheses.
Brånemark P-I, Zarb GA, Albrektsson T. Tissue integrated prostheses:
osseointegration in clinical dentistry. Quintessence: Chicago; 1985.
107. Carr AB, Larsen PE, Gerard DA. Histomorphometric comparison of
implant anchorage for two types of dental implant after 3 and 6
months' healing in baboon jaws. J Prosthet Dent. 2001;85:276–280.
108. Plenk H Jr, Danhel Mayhauser M, Haider R, et al. Histomorphometrical
comparison of 69 Brånemark's and Ledermann's dental screw implants in
sheep (abstract). [In] Proceedings of the First World Congress of
Implants and Biomaterials. 1989 [Paris].
109. Academy of Prosthodontics. [Available at]
http://www.academyofprosthodontics.org/_Library/ap_articles_download/GP
[(Accessed 13.05.16.)].
110. Wilson GH. A manual of dental prosthetics. Lea & Febiger: Philadelphia;
1911.
111. Thornton LJ. Anterior guidance: group function/canine guidance. A
literature review. J Prosthet Dent. 1990;64:479–482.
112. Hobo S, Shillingburg HT Jr, Whitsett LD. Articulator selection for
restorative dentistry. J Prosthet Dent. 1976;36:35–43.
113. Dawson PE. Temporomandibular joint pain-dysfunction problems
can be solved. J Prosthet Dent. 1973;29:100–112.
18
Periodontal and Maintenance
Complications
Jon B. Suzuki, Carl E. Misch
Implant dentistry has evolved into an evidence-based, clinical science with

well-documented research to validate previously unsupported clinical
practice procedures. Significant efforts that focus on the biology and
biomechanics of implant dentistry have helped develop and refine clinical
techniques based on peer-reviewed findings. The evolution of research and
understanding of biologic concepts in implant dentistry has caused many
areas of conflict and controversy. Innovative theories have been developed
that have resulted in technique changes. Science has spurred implant
dentistry to new pinnacles of success.
The tremendous expansion of knowledge in this field has created new
ideas and terminology that is redefined based on new principles. In many
instances, new research may contradict established paradigms. It may be
confusing for clinicians to select correct protocols, procedures, instruments,
and techniques. As materials and techniques are further investigated, dogma
may undergo criticism and controversy. Seasoned clinicians consistently
update and modify techniques and instruments to maintain clinical
excellence as technology and research advance.
One area of expansion of knowledge and conflict of views relates to the
maintenance of dental implants. Early research explored techniques and
instruments that were current for the methods and materials of that time.
Although many of those implants still exist and are functional in patients,
research and advances in technology have given us newer materials and
advances in implant design and structure, minimizing previous challenges
from a maintenance perspective.
An understanding of the mucoepithelial implant attachment is essential
before commencing maintenance procedures. Controversies and parameters
for probing and crestal bone loss are important for clinicians to recognize.
There are anatomic and histologic differences between the attachment
apparatus of teeth compared with implants that have undergone
osseointegration. The bacterial plaque biofilm challenges on these implant-
tissue attachments may be significant to clinical success.
When the clinician understands the parameters of implants and teeth,
specific maintenance plans may be established for the patient. Clinicians
should inform patients of expectations and outcomes during treatment and
demonstrate oral hygiene options appropriate during each stage. Patients
need to recognize the importance of maintenance protocols, and clinicians
should assess compliance to home care routines. Patients also should be
competent to perform home maintenance procedures. As the acceptance of
and demand for dental implants increase, the need to understand the
importance of maintenance as it relates to long-term implant success also
increases. The role of the dental hygienist in implant maintenance and care is
also increasing and becoming more defined.
Implants and associated prostheses are much different than natural teeth
and may require adjunctive procedures and instruments for professional and
patient care. Complications may arise when clinicians fail to comprehend
these differences, which may increase the morbidity of treatment. The
instrumentation utilized must be effective at removing biofilms and
accretions, and procedures performed by patients and clinicians should
avoid damage to all components of the implant, abutment, restoration, and
associated tissue. Establishment and maintenance of the soft tissue seal
around the transmucosal portion of the implant enhances the success of an
implant. This barrier is fundamentally a result of appropriate wound healing
and connection of epithelial attachments. The maintenance of healthy peri-
implant tissues may contribute to implant success. In addition, tissues free
of inflammation and a biofilm-free implant sulcus will support the patient's
general and oral health.
Diagnosis
Complication
One important but often neglected component of comprehensive dental
implant treatment is the postoperative evaluation and treatment of peri-
implant issues. There are many conflicting thoughts and controversies on the
diagnosis and treatment of these complications. Failure to effectively and
promptly diagnose and treat peri-implant disease with dental implants leads
to an increase in implant and prosthetic failure.
Etiology
Dental professionals are initially trained to have a firm understanding of the
disease processes associated with the natural dentition. A variety of tests,
indices, and radiographic signs are used to determine the health of a natural
tooth. Dental implants and their related prostheses have fundamentally
different relationships to the oral environment than teeth, and these
differences necessitate a change in diagnostic protocol for the determination
of health. Failure to understand these differences may lead to a lack of
recognition of early disease processes. Without early intervention, increased
morbidity may result.
Prevention
The following section of this chapter will outline various anatomic and
histologic differences between natural dentition and the dental implant as
they pertain to periodontal structures. By having this background
established, the clinician may appreciate these necessary differences and will
be better equipped to effectively diagnose peri-implant disease processes.
Inflammatory conditions around dental implants or dental implant
prostheses are collectively defined as peri-implant disease. The most
common terms accepted in implant dentistry, peri-mucositis and peri-
implantitis, originated from the First European Workshop on Periodontology
in 1994.1 These terms remain current with slight modifications and have
similar comparisons to periodontal diseases around natural teeth (i.e.,
gingivitis, periodontitis).2 An implant clinician should have a thorough
understanding of the related definitions.
Gingivitis is a bacteria-induced inflammation involving the region of the
marginal gingiva above the crest of bone and next to a natural tooth. It is
always associated with plaque and may be classified as (1) acute necrotizing,
(2) ulcerative, (3) hormonal, (4) drug induced, or (5) spontaneously
occurring.3 These categories also can relate to the gingival tissues around an
implant because the mode of attachment of the gingiva to a tooth and
implant has been reported to be partially similar.4
The bacteria responsible for gingivitis around a tooth may affect the
epithelial attachment without loss of connective tissue attachment. Because
the connective tissue attachment of a tooth extends an average of 1.07 mm
above the crestal bone, at least 1 mm of protective barrier above the bone is
left. In contrast, no connective tissue attachment zone exists around an
implant because no connective fibers extend into the implant surface.
Therefore, no connective tissue barrier exists to protect the crestal bone
around an implant.5
Periodontitis around teeth is characterized by apical movement of
junctional epithelium and periodontal attachment coupled with loss of
alveolar bone. Bacteria is thought to be responsible by stimulating the body's
immune response, which results in an overall resorptive effect on the
periodontal attachment apparatus. The American Academy of
Periodontology recognizes two main types of periodontitis: chronic and
aggressive periodontitis. Each encompasses many specific subtypes for each
category such as adult chronic periodontitis, progressive periodontitis,
localized juvenile, prepubertal, etc.
In contrast to teeth, early crestal bone loss around an implant
postprosthetically usually is not caused by bacteria. Most often the bone loss
results from stress factors too great for the immature, incompletely
mineralized bone-implant interface or an extension of the biologic width
onto a smooth metal crest module.6 An implant may exhibit early crestal
bone loss with a different mechanism or cause compared with natural teeth.
However, on occasion, bacteria may be the primary factor. Anaerobic bacteria
have been observed in the microgap between the implant and the abutment
or in the sulcus of implants, especially when sulcus depths are greater than 5
mm (Box 18.1).7
Box 18.1
Stable Integrated Implants: Bacteria Related to
Pocket Depth Increases
Shallow
Gram-positive facultative cocci, rods
Gram-negative anaerobic cocci, rods
Motile rods
Spirochetes
Black-pigmented Bacteroides
Fusobacterium
Deep
Vibrios organisms
Periodontal disease that develops around dental implants has been

classified into two separate entities: peri-implant mucositis and peri-
implantitis. These classifications were proposed via a consensus report from
the First European Workshop on Periodontology (EWOP). Peri-implant
mucositis was defined as a reversible inflammatory reaction in the peri-
implant tissues surrounding an implant, and peri-implantitis is defined as
inflammatory reactions with loss of supporting bone around an implant.1
Periimplant mucositis is an inflammatory condition of the soft tissue
surrounding an implant, which is similar to gingivitis around a tooth. This
has been defined as a reversible condition with no loss of attachment or bone
loss. The primary etiologic factor has been shown to be plaque biofilm, the
removal of which easily reverses the disease process. If allowed to progress,
peri-implantitis may result, which includes loss of bone and loss of
osseointegration, similar to loss of attachment and bone with periodontitis.
The prevalence of peri-implant mucositis (bleeding on probing and no loss of
bone) has been shown to be approximately 79% to 90% of subjects and 50%
of implants.8
Peri-implantitis exhibits similar microbial flora as adult periodontitis.
Changes involve both the hard and soft tissues surrounding an implant. The
implant may exhibit all the signs of peri-implant mucositis as well as
exudate, increased pocket depth, and bone loss. If left untreated, significant
bone loss, infection, and mobility could result, leading to the failure of an
initially integrated implant. According to Mombelli et al, the microbiota are
site specific and similar to chronic adult periodontitis.9 The clinical signs
include radiographic or probing vertical bone loss, peri-implant pockets,
bleeding upon probing (with or without exudate), mucosal swelling and
redness, and an absence of pain (Box 18.2). The crestal bone loss may be
induced by stress, bacteria, or a combination of both. Stress-induced bone
loss occurs without bacteria as the primary causative agent. However, after
the bone loss from stress or bacteria, the sulcular crevice deepens and
decreases the oxygen tension, and anaerobic bacteria may become the
primary promoters of the continued bone loss. An exudate or abscess
indicates exacerbation of the periimplant disease and possible accelerated
bone loss. The prevalence of peri-implantitis has been found in 28% to 56% of
subjects and 12% to 43% of implant sites (Fig. 18.1).8
Box 18.2
Clinical Signs of Peri-implantitis
• Vertical bone loss (radiographic, probing, or both)
• Periimplant pockets
• Bleeding upon probing
• ± Exudate
• Mucosal swelling
• Erythema
• No pain

FIG 18.1 (A) Spongiotic gingivitis exhibiting erythematous marginal tissue with
cyanotic tissue. (B) Periodontitis: mandibular anterior exhibiting severe horizontal
bone loss. (C) Perimucositis: erythematous buccal gingiva with associated bleeding
around implant crown. (D) Peri-implantitis: significant bone loss with erythematous
tissue with significant plaque accumulation.
Evaluation of Periodontal Indices

Periodontal indices are often used for evaluation of dental implants. A
comparison of natural teeth and implants for each criterion provides insight
into their differences in the health-disease continuum. After one
understands the basis for evaluation, these criteria may then be used to
establish a health-disease implant quality scale related to patient treatment.
Mobility
Natural Tooth vs. Implant Support Systems.

A dental implant and a natural tooth differ in many ways. In general, a
natural tooth is better designed to reduce the biomechanical forces
distributed to the tooth/restoration and the crestal bone region. The
periodontal attachment apparatus, biomechanical design of the tooth root
and material, nerve and blood vessel complex, occlusal material (enamel),
and surrounding type of bone blend to decrease the risk of occlusal overload
to the natural tooth system.10
Tooth movement.
A tooth exhibits normal physiologic movements in vertical, horizontal, and
rotational directions. The amount of movement of a natural tooth is directly
related to its surface area and root design. The factors that dictate the
movement include: the number and length of the root surface, the root
diameter, shape, position, health of the periodontal attachment apparatus,
and the bone density primarily influence a tooth's mobility. A healthy tooth
exhibits zero clinical mobility in a vertical direction. Studies have shown an
initial vertical tooth movement to be about 28 µm and is the same for
anterior and posterior teeth.11 The vertical movement of a rigid, fixated
implant has been measured to be approximately 2 to 3 µm under a 10-lb force
and is due mostly to the viscoelastic properties of the underlying bone.12
Muhlemann found that horizontal tooth movement may be divided into
initial mobility and secondary movement.13 The initial mobility is observed
when there is a light force applied, which occurs immediately, and is a
consequence of the periodontal ligament (PDL). Initial horizontal tooth
mobility is greater than initial vertical movement. A very light force (500 g)
may horizontally move a tooth. The initial horizontal mobility of a healthy,
“nonmobile” posterior tooth is less than that of an anterior tooth and ranges
from 56 to 75 µm, which is two to nine times the vertical movement of the
tooth. Initial horizontal mobility is even greater in anterior teeth and ranges
from 70 to 108 µm in health (Fig. 18.2).14
FIG 18.2 The physiologic movement of a healing tooth has been measured as 28
µm in the apical direction and up to 108 µm in the horizontal direction. (From Misch CE:
The secondary tooth movement described by Muhlemann occurs after the

initial movement when greater forces are applied. When an additional force
is applied to the tooth, a secondary movement is also observed, which is
related directly to the amount of force. The secondary tooth movement is
related to the viscoelasticity of the bone and measures as much as 40 µm
under considerably greater force (Fig. 18.3).13
FIG 18.3 A secondary horizontal movement of a tooth occurs after the initial tooth
movement when a greater force is applied and is related to the deformation of the
alveolar bone. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Implant movement.
The term rigid fixation is used to describe the absence of clinical mobility of
an implant tested with vertical or horizontal forces less than 500 g. However,
rigid fixation is a clinical term. Osseointegration is a histologic term that is
defined as bone in direct contact with an implant surface at the
magnification of a light microscope (Fig. 18.4).15 Over the years, these two
terms have been used interchangeably, and implant abutment support is
most predictable with rigid fixation. Lack of implant mobility (IM) does not
always coincide with a direct bone-implant interface. However, when
observed clinically, rigid fixation usually means that at least a portion of the
implant is in direct contact with bone, although the percentage of bone
contact cannot be specified. When an implant has mobility, there is most
likely connective tissue between the implant and bone.
FIG 18.4 Osseointegration is a histologic term that describes a direct bone-to-
implant contact at the level of magnification of a light microscope. (From Misch CE:
In some situations, the presence of implant mobility may be difficult to

discern. The absence of clinically observable movement does not indicate the
true absence of any movement. For example, a “nonmobile” posterior natural
tooth actually moves horizontally 56 to 73 µm. The human eye does not
perceive this movement. The anterior teeth, which often have slight clinically
observable movement, actually move approximately 0.1 mm. A healthy
implant may move less than 73 µm; it appears as zero clinical mobility (rigid
fixation).
Similar to a natural tooth, the implant-bone interface exhibits more lateral
than apical movement. Sekine et al evaluated the movement of endosteal
implants with rigid fixation and found a range of 12 to 66 µm of movement in
the labiolingual direction.12 Komiyama reported 40 to 115 µm of implant
movement in the mesiodistal direction under a force of 2000 g (≈4.5 psi) and a
labiolingual range of 11 to 66 µm.16 The greater implant movement in the
mesiodistal dimension corresponds to the lack of cortical bone between the
implants in this direction compared with the thicker lateral cortical plates
present in the labiolingual dimension. Rangert et al suggested that part of
this implant movement may also be due to component flexure of the implant
abutment and screw.17 The mobility of implants varies in direct proportion to
the load applied and the bone density and reflects the elastic deformation of
bone tissue.
Sekine et al applied a gradually increasing load over a 2-second period to a
tooth and an implant. The teeth moved immediately with a light load
(primary tooth movement) and less with an additional load (secondary tooth
movement). The implant did not move when the tooth had its primary tooth
movement. A heavier force caused the implant to gradually move, similar to
the secondary tooth movement (see Fig. 18.3).12 These mobility characteristics
corroborate the findings of Fenton et al, who applied a 500-g load for 4
seconds to maxillary anterior teeth and osseointegrated implants.18 Whereas
the implants were displaced a mean of 10 µm with a rapid elastic return (less
than 1 millisecond), the teeth showed a mean displacement of 57 µm with a
prolonged viscoelastic return.
Evaluating Dental Implant Mobility

Mirror handles.
Increased tooth mobility may be caused by many factors including occlusal
trauma or bone loss. Increased tooth mobility alone is not a criterion of
periodontal health or pathology. Unlike a tooth, for which mobility is not a
primary factor for longevity, mobility is a primary determining factor for
implant health.15 Rigid fixation of an implant is also an excellent indicator of
the implant health status because it is an easy, objective test. As such, rigid
fixation is usually the first clinical criterion evaluated for a dental implant.
The techniques to assess rigid fixation are similar to those used for natural
tooth mobility. Two rigid instruments apply a labiolingual force of
approximately 500 g, and no observed mobility indicates rigid fixation (Fig.
18.5).3
FIG 18.5 Evaluation of implant mobility with the use of a mirror handle.
The amplitude of tooth mobility may be rated from 0 to 4, where 0 is

normal mobility from physiologic movement; 1 is detectable increased
mobility; 2 is visible mobility up to 0.5 mm; 3 is severe mobility up to 1 mm;
and 4 is extreme mobility, including vertical movement.3 This same gradient
may be used for oral implants with slight modification. As Table 18.1 depicts,
IM-0 corresponds to the absence of clinical mobility, IM-1 demonstrates
detectable increased movement, IM-2 is visible mobility movement up to 0.5
mm, IM-3 is severe horizontal mobility greater than 0.5 mm, and IM-4 is
visible horizontal and vertical movement. The IM scale was used frequently
for plate (blade) form implants or disc implants because a clinical goal was
for slight mobility when joining the device to natural teeth. However, the
ideal goal for root form implants should always be rigid fixation and IM-0
status (no movement).
TABLE 18.1
Clinical Implant Mobility Scale
Scale Description
0 Absenc e of c linic al mobility with 500 g in any direc tion
1 S light detec table horizontal movement
2 Moderate visible horizontal mobility up to 0.5 mm
3 S evere horizontal movement greater than 0.5 mm
4 Visible moderate to severe horizontal and any visible vertic al movement
From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby; data from Misch CE: Implant
quality scale: a clinical assessment of the health-disease continuum, Oral Health 88:15–25, 1998.
Periotest.
The Periotest (Gulden-Medizinteknik) is a computer-mechanical device,
developed by Schulte, that measures the dampening effect or attenuation
degree against objects by developing a force of 12 to 18 N against a pistonlike
device, which then measures the distance the piston recoils into the chamber
after striking an object.19 A soft surface or mobile object gives higher
recordings than a hard or rigid object. The recordings range from negative 8
to positive 50 numbers.
Teeth with zero clinical mobility have typical Periotest ranges from 5 to 9.
The degree or absence of clinical movement around an implant corresponds
to values ranging from −8 to +9, or a range of 17 units. The bone density
around the implant may be correlated with Periotest numbers. Whereas
softer bone types give higher numbers, harder bone around the implant
results in lower numbers. A nondestructive resonance frequency analysis
technique to measure implant stability and osteointegration has also been
introduced to the profession and provides similar valuable information as to
the clinical movement and bone density around implants (Table 18.2).20,21
TABLE 18.2
Periotest Values vs. Clinical Interpretation
P eriotest Value Clinical Interpretation

−8 to 0 S atisfac tory integration
+1 to +9 Clinic al examination rec ommended bec ause integration is not suffic ient for prosthetic loading
+10 to +50 Integration insuffic ient, progressive bone loading rec ommended
Osstell.
A second device exists to evaluate the implant-bone interface that is
nondestructive and noninvasive. The Osstell (Ostell) is based on resonance
frequency analysis (RFA) and was developed by Huang.22 The Osstell has
been shown to have quantitative and reproducible measurements on the
presence of integration, immediate load feasibility, and follow-up evaluation
at the prediction of an implant failure. RFA is a technique that is based on
continual excitation of the implant interface through the use of dynamic
vibration analysis (piezo effect). A specialized transducer, which contains two
piezoceramic elements, is either attached directly to the implant or
abutment. The first piezo element generates an excitation signal that is a
sinusoidal wave (5–15 kHz), leading to vibration of a whole transducer-
implant-tissue complex. The oscillation response is measured by the second
piezo element.23
The RFA technique measures implant stability as a function of stiffness of
the bone/implant complex. The health of the implant is measured on an
implant stability quotient (ISQ) that is calculated on a scale from 1 to 100.
The full integration of an implant is most usually measured in the range
from 45 to 85 ISQ. Measurements of less than 45 are indicative of implant
failure, whereas an ISQ value of 60 to 70 indicates success.24 Studies have
shown that the Osstell is more reliable than the Periotest in evaluating and
measuring implant stability in hard and soft tissue interfaces (Fig. 18.6 and
Table 18.3).25
FIG 18.6 Implant Stability Quotient (ISQ) is a scale from 1 to 100 that measures
the stability of an implant. The ISQ scale has a nonlinear correlation to micro
mobility. High stability means >70 ISQ, between 60 and 69 is medium stability and
<60 ISQ is considered as low stability. (A) Osstell Smart Peg that is implant specific.
(B) Hand driver that is used to place Smart Peg into implant. (C) Smart Peg hand-
torqued into implant. (D) Handle removed, Osstell reader is placed in approximation
(without touching the Peg). (E) Osstell reading exhibiting high stability.
TABLE 18.3
Osstell Values vs. Clinical Interpretation
Osstell Value (ISQ Score) Clinical Interpretation

<60 Low stability = Implant at risk
60–65 Medium stability = Traditional two-stage loading protoc ol
65–70 Medium to high stability: Early loading
>70 High stability: Immediate loading
Plaque Biofilm
The differences between tooth and implant biologies make dental implants
more susceptible to inflammation and bone loss in the presence of bacterial
plaque accumulation.26 Biofilms are the primary causative factor of
periodontal disease processes. Sticky masses of bacteria with a
polysaccharide matrix, water, and bacteria accumulate on hard and soft
surfaces in the oral cavity and can be disturbed and removed with
mechanical or chemical obliteration. If undisturbed, mature plaque will
form. Current chemotherapeutics cannot penetrate thick biofilm, and rough
surfaces have been found to hold more biofilm than smooth surfaces.27
Bacteria will migrate from teeth to implants and from implant to implant.
Similar to teeth, clinical findings of failing implants include inflammation,
pockets, and progressive bone loss. Another similarity lies in the bacteria
responsible for periodontitis and peri-implantitis.
When evaluating the peri-implant microbiota, Lee et al. compared
microbial changes between patients with a history of periodontal or peri-
implant infections and implants that have been in function for a length of
time.28 This study found a history of periodontitis had a greater impact on the
peri-implant microbiota than implant loading time. The major influence on
the peri-implant microbiota was, however, the microbiota on remaining
teeth. Porphyromonas gingivalis and Bacteroides forsythus (Tannerella
forsythia), red complex periodontal pathogens, colonized several implants,
although all implants were successfully osteointegrated. It is important to
educate patients about their responsibility to decrease plaque effectively,
especially if they have a history of periodontal disease.
Plaque biofilm development and maturation have similarities for natural
teeth and dental implants. The gingival sulcus in periodontal health and the
perimucosal attachment of a successful dental implant are essentially similar.
In a study by Mombelli and Mericske-Stern of the plaque from 18 edentulous
patients with successful dental implants, facultative anaerobic cocci (52.8%)
and facultative anaerobic rods (17.4%) were reported.
However, the pathogens P. gingivalis and spirochetes were absent, and
minimal (7.3%) gram-negative rods were present.29 Generally, pellicle—a
naturally occurring glycoprotein in the saliva—first adheres to the intraoral
structure, whether it be a tooth or an implant. Gram-positive cocci bacteria
are the first “early colonizers,” beginning with single cocci and progressing
to streptococci forms (Box 18.3).
Box 18.3
Plaque Biofilm Development and Colonization
Identify potential implant patients
↓
Bacterial adhesion
↓↓
Supragingival plaque
Gram+, streptococci, Actinomyces
↓↓↓
Plaque maturation (gram−, rods, and filaments)
↓↓↓↓
Well-differentiated subgingival plaque
(Gram−, anaerobes)
From Misch CE: Contemporary implant dentistry, ed 3, St. Louis, 2008, Mosby.
Without appropriate oral hygiene measures (e.g., brushing, flossing,

interdental cleaning), additional bacterial colonies including gram-negative
rod-shaped bacteria synergistically grow with the established gram-positive
bacteria. The gram-negative bacteria are frequently facultative or strict
anaerobic bacteria and are considered “late colonizers.” Many, if not the
majority, of these gram-negative bacteria are black pigmented and are
classified under a number of genera (e.g., Bacteroides, Prevotella,
Porphyromonas, Fusobacterium).
Plaque biofilm reported to be associated with failing dental implants also
consists largely of gram-negative rods.30 Clinically, failing dental implants are
characterized by soft tissue inflammation, increased probing depths,
increased mobility, and peri-implant radiolucency.
Specific pathogens in implant pockets greater than 6 mm include
Actinobacillus actinomycetemcomitans (Aggregatibacter
actinomycetemcomitans), Prevotella intermedia, and P. gingivalis in more than
one third of the sites, as confirmed by DNA analysis.31
In other studies on plaque biofilm around dental diseases and failing
implants, differences in bacterial type have been reported.32,33 Mombelli did
not detect spirochetes in plaque samples from well-maintained and clinically
healthy implants. Rams et al noted higher proportions of staphylococci
(15.1%)19 than usually found in gingivitis (0.06%) and periodontitis (1.2%)
sites.34 This finding suggests that staphylococci may be more significant in
developing peri-implantitis lesions than previously recognized.
Changes involve both the hard and soft tissues surrounding an implant.
The implant may exhibit all the signs of peri-implant mucositis, as well as
exudate, increased pocket depth, and bone loss. If left untreated, significant
bone loss, infection, and mobility could result, leading to the failure of an
initially integrated implant.
Comparisons of plaque biofilms have been reported in a limited study of
Brånemark and ITI (Straumann Institute) implants and are remarkably
similar in controlled studies. Mombelli et al compared 10 patients with
Brånemark implants and 10 patients with ITI implants and sampled the
deepest pockets around the implants.35 After 3 and 6 months, several
periodontal pathogens were cultured and isolated, including P. gingivalis, P.
intermedia, Fusobacterium nucleatum, and various spirochetes. None of the
implants were colonized by A. actinomycetemcomitans. Longer investigations
by Leonhardt et al extended these microflora reports on dental implants in 19
patients. At 3 years, the osteointegrated implants were colonized
predominantly by P. gingivalis, P. intermedia, and A. actinomycetemcomitans.36
Natural dentitions with dental implants appear to increase the risk for
implant infections, compared with completely edentulous patients. This
suggests that natural teeth may serve as a reservoir for periodontal
pathogens that may extend their growth to contiguous implants in the same
oral cavity.37 Quirynen and Listgarten reported that proportions of coccoid
forms (65.8%), motile rods (2.3%), and spirochetes (2.1%) in implant pocket
areas were similar to the microorganisms in natural teeth (55.6%, 4.9%, and
3.6%, respectively). Fully edentulous patients exhibited more coccoid forms
(71.3%), fewer motile rods (0.4%), and no spirochetes.38 They also concluded
that microflora in partially edentulous implant patients were potentially
more pathogenic than they were in fully edentulous patients. Implants with
longevity of more than 3 or 4 years appear to have greater numbers of
bacteria than implants in place for 1 or 2 years.
Clinical Significance
Plaque biofilms are the main reason peri-implantitis treatments fail. Host
tissue is unable to reform attachments onto implant surfaces if titanium
surface is not thoroughly cleaned. Bacterial deposits produce toxins that
prevent fibroblast and osteoblast growth, which prevents proximal
regeneration onto implant surface. To ensure the most optimal condition for
treatment success, plaque biofilms need to be thoroughly removed. It is
important to note that while it is impossible to guarantee 100% sterility of
exposed implant surfaces, the body is capable of removing small amounts of
bacterial deposit via cellular defense mechanisms. Carefully removing macro
deposits of plaque biofilm and irrigating with antimicrobial solution is
generally sufficient to allow a favorable environment for new attachment
formation.
In essence, the patient should have a full-mouth debridement to reduce
overall oral load of bacterial colonies while making an effort to remove all
plaque biofilms on exposed implant surfaces. This gives the body a chance to
reform a healthy-associated colonization of biofilm.
Percussion
Percussion often is used on teeth to determine which tooth is sensitive to
function or if pulpal necrosis is beginning. In the past, percussion was used
to evaluate the presence of rigid fixation for osseointegrated implants.15
However, percussion is an indicator neither of clinical health nor of rigid
fixation for osseointegrated implants. The ringing sound that occurs on
percussion only corresponds to the presence of some amount of bone at the
interface because 2 mm of bone and 16 mm of bone-implant interface sound
almost identical.
Percussion may be used to diagnose pain or tenderness with an implant but
is misleading if used to determine the status of rigid fixation.
Probing Depths
Probing depths around teeth is an excellent proven means to assess the past
and present health of natural teeth. The increasing sulcus depth around
natural teeth is directly related to disease and bone loss. However, probing
depth indices used to evaluate dental implants are more controversial
because implant sulcus depth and health are not always directly related. A
thorough appreciation of the soft tissue interface is needed for the clinician
to understand the inherent differences between natural teeth and dental
implants.
Soft Tissue Interface Around Teeth and Implants

For a natural tooth the surrounding soft tissue has an average biologic width
of 2.04 mm between the depth of the sulcus and the crest of the alveolar
bone. It should be noted the biologic “width” is actually a height dimension
with a greater range in the posterior region compared with the anterior and
may be greater than 4 mm in height.39 With respect to natural teeth, the
biologic width is composed of a connective tissue attachment (1.07 mm
average) above the bone and a junctional epithelial attachment (JEA) (0.97
mm average) at the sulcus base, with the most consistent value among
individuals being the connective tissue attachment (Fig. 18.7).
FIG 18.7 The biologic width for a natural tooth is approximately 1 mm of connective
tissue above the bone and 1 mm of epithelial attachment between the sulcus and
the connective tissue. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The sulcular regions around an implant and around a tooth are similar in
many respects. The rete peg formation within the attached gingiva and the
histologic lining of the gingiva within the sulcus are similar in implants and
teeth.40 A free gingival margin forms around a tooth or implant with
nonkeratinized sulcular epithelium, and the epithelial cells at its base are
also similar to teeth and implants, with junctional epithelial cells for both.
However, a fundamental difference characterizes the base of the gingival
complex around teeth. Whereas a tooth has two primary regions that make
up the biologic width, an implant only has one (Fig. 18.8).
FIG 18.8 The soft tissue around an implant (I) has a sulcular region very similar to
a tooth. A free gingival margin (F) with nonkeratinized sulcular epithelium and cells at
the base (C) have junctional epithelial attachment above the bone (B). CT,
Connective tissue. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
When probing next to a tooth, the probe not only measures the sulcus
depth but also penetrates and measures the JEA.41 The junctional epithelial
“attachment” of a tooth is not a true attachment. It attaches to teeth via
hemidesmosomes, but these attachments are light in general and are easily
disrupted. A periodontal probe, plaque, or impression material can easily
separate the hemidesmosomal attachment. At the apex of the sulcus is the
junctional epithelium, which is a few cells thick and supported by the
connective tissue attachment zone (see Fig. 18.8).
The connective tissue attachment zone of the “biologic width” around a
tooth prevents the probe from penetrating deeper into the sulcus and allows
gingival fibers of the connective tissue attachment zone to establish direct
connection with the cementum of the natural tooth. It acts as a physical
barrier to the bacteria in the sulcus to the underlining periodontal tissues.
Eleven different gingival fiber groups compose the connective tissue
attachment zone observed around a natural tooth and tissue: dentogingival
(coronal, horizontal, and apical), alveologingival, intercapillary, transgingival,
circular, semicircular, dentoperiosteal, transseptal, periosteogingival,
intercircular, and intergingival.3 At least six of these gingival fiber groups
insert into the cementum of the natural tooth: the dentogingival (coronal,
horizontal, and apical), dentoperiosteal, transseptal, circular, semicircular,
and transgingival fibers. In addition, some crestal fibers from the periodontal
fiber bundles also insert into the cementum above the alveolar bone. These
Sharpey fibers form a true attachment to the tooth. They prevent a
periodontal probe from invading the PDL space and delay the ingress of
plaque.
James and Schultz were the first to begin a systematic study to investigate
the biologic seal phenomenon of the soft tissue around dental implants.40
Hemidesmosomes from the JEA region help form a basal lamina-like
structure on the implant, which can act as a biologic seal. However,
collagenous components of the linear body cannot physiologically adhere to
or become embedded into the implant body.26 The hemidesmosomal seal has
a circumferential band of gingival tissue to provide mechanical protection
against tearing. However, the mucopolysaccharide layer is less adherent to an
implant surface than a natural tooth root. The hemidesmosome of the
natural tooth has a lamina lucida and a lamina densa, which are part of the
basement membrane. The hemidesmosome next to an implant has a lamina
lucida, lamina densa, and sublamina lucida (which is less adherent).42
The biologic width for implants has been reported by Cochran et al to be
3.3 mm, but unlike the biologic width dimension for teeth, they also included
the sulcus depth.43 In a typical implant gingival region, only two of the
gingival fiber groups found around a tooth (circular and periosteogingival
fibers) and no periodontal fibers are present.44 These fibers do not insert into
the implant body below the abutment margin as they do into the cementum
of natural teeth. Instead, the collagen fibers around an implant run parallel
to the implant surface, not perpendicular, as with natural teeth.45 Hence, the
implant only has a junctional epithelial “attachment” system.
The gingival and periosteal fiber groups are responsible for the connective
tissue attachment component of the biologic width around teeth, and these
are not present around the transosteal region of an implant. The “biologic
width” around the abutment-implant connection should not be similarly
compared with the connective tissue attachment of a tooth. The biologic seal
around dental implants can prevent the migration of bacteria and endotoxins
into the underlying bone. It is unable, however, to constitute an attachment
component of the biologic width similar to the one found with natural teeth
(Fig. 18.9).
FIG 18.9 The sulcus and epithelial attachment above the implant body do not have
a true connection to the implant. (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
Consequences of Probing Around an Implant

A dental probe introduced into an implant sulcus may proceed through the
junctional epithelial close approximation of tissue and the probe may
proceed to the crestal bone (Fig. 18.10).
FIG 18.10 An implant has no connective tissue fibers in the connective tissue zone
that insert into the implant. The periimplant probe penetrates the sulcus, junctional
epithelial attachment (JE), and most of the connective tissue zone. CT, Connective
tissue; FGM, free gingival margin. (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
The connective tissue zone for an implant has only two fiber groups, and
neither of them inserts into the implant. As a result, with an implant the
probe goes beyond the sulcus, through the JEA, and through the type III
collagen connective tissues and reaches closer to the bone.46 Because the
probe penetrates deeper next to an implant compared with a tooth, one
should take care not to contaminate the implant sulcus with bacteria from a
diseased periodontal site (Table 18.4).
TABLE 18.4
Comparison of Tooth and Implant Support Structures
Structure Tooth Implant

Connec tion Cementum, bone, periodontium Osseointegration, bone func tional ankyloses
to bone
Junc tional Hemidesmoses and basal lamina (lamina luc ida Hemidesmosomes and basal lamina (lamina luc ida, lamina densa, and
epithelium and lamina densa zones) sublamina luc ida zones)
Connec tive 12 groups: six insert perpendic ular to tooth Only two groups: parallel and c irc ular fibers; no attac hments to the implant
tissue surfac es surfac e ↑ c ollagen, ↓ fibroblasts
↓ c ollagen, ↑ fibroblasts
Biologic 2.04–2.91 mm 3.08 mm (inc ludes sulc us)
width
Vasc ularity Greater; supraperiosteal, and periodontal Less periosteal
ligament
Probing 3 mm in health 2.5–5.0 mm (depending on previous soft tissue depth)
depth
Bleeding on More reliable Less reliable
probing
The benefit of probing the implant sulcus has been challenged in the
literature because sound scientific criteria for the rationale are lacking. The
location of the probe tip subgingivally for a tooth depends on the pressure
used, the presence of inflammation, and the angle at which the probe is
introduced in the sulcus depth between the junctional epithelium and the
root surface. The correct pressure recommended for probing is 20 g, yet
conventional probing often exerts a force more than five times this level and
greatly varies. The potential for damage to the fragile hemidesmosome
attachment to the implant or marring of the implant surface exists during
probing. In addition, reports in the literature suggest that the reproducibility
of attachment level measurements may be questionable independently from
the instrument used to perform the measurements.47,48 Many of these
variables are similar for a dental implant. Unlike natural teeth, fixed implant
prostheses with subgingival margins of crowns often have wide emergence
profiles, making probe positioning difficult around most implant bodies.
The implant sulcus depth may be a reflection of the original soft tissue
thickness of the area before implant placement. The posterior maxillary
tissue can be thicker than 4 mm after tooth extraction and subsequent bone
volume loss before implant placement. As a result, the tissue above the bone
before implant insertion may be 4 mm thick or more. As a result of greater
tissue thickness before surgery and a greater probing depth compared with
teeth, the probing depth next to a healthy implant may be greater than that
of a healthy natural tooth.
When the tissues are thick, gingivoplasty to reduce the flap thickness and
pocket depth can be performed at the initial surgery. The advantage of the
reduction in tissue thickness at this time is the tissue heals and matures as
the bone-implant interface develops. However, thinning the flap at the initial
surgery may cause greater loading of the implant body during healing from
an overlying soft tissue–borne temporary prosthesis. After initial bone
healing, the stage II uncovery surgery also may correct tissue thickness.
Lekholm et al found that the presence of deep pockets was not
accompanied by accelerated marginal bone loss.49 Stable, rigid, fixed
implants were reported with pocket depths ranging from 2 to 6 mm. Healthy,
partially edentulous implant patients consistently exhibit greater probing
depths around implants than around teeth. An increasing probing depth
next to an implant is a more significant sign than a probing depth unrelated
to a time interval because it usually signifies bone loss except in cases of
gingival hyperplasia or hypertrophy. Probing using fixed reference points on
the abutment or crown margin allows evaluation of crestal bone loss vs.
tissue hypertrophy.
Despite the limitations, charting the attachment level in implant
permucosal areas does aid the clinician in monitoring these regions. As the
sulcus depth increases, the oxygen tension decreases. The bacteria in an
implant sulcus are similar to those of a natural tooth. A toothbrush and daily
hygiene procedures has been shown to be unable to clean a sulcus greater
than 2 mm.50 Sulcus depths greater than 5 to 6 mm have a greater incidence
of anaerobic bacteria (Table 18.5). As a consequence, this sulcus depth often
requires gingivectomy or bone revision surgery. As a general rule, to enable
the patient to perform effective daily hygiene, the ideal implant sulcus
should be maintained at less than 5 mm.
TABLE 18.5
Subgingival Microflora Associated With Human Dental Implants
Pocket Depth (m m )
Mic roflora <5 >6
S piroc hetes (%) 2 32
Motile rods (%) 16 18
Coc c oids (%) 64 30
From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby; data from Rams TE, Roberts TW,
Tatum H Jr, et al: The subgingival microflora associated with human dental implants, J Prosthet Dent 5:529–
534, 1984.
The monitoring of early crestal bone loss is most important during the first
critical year of stress accommodation of the bone. Minor bone changes are
clinically easier to observe with a periodontal probe than with radiographs.
Early bone loss may occur on the facial aspect of the implant; radiographs
demonstrate clearly only the mesial and distal regions.
Changes in crestal bone levels warrant close monitoring and early
intervention. Patient education to reduce parafunctional stress on the
implant system, the use of parafunctional appliances, and other stress-
reducing methods is required when early crestal bone loss beyond the first
thread is detected.
Despite the uncertain meaning of pocket depth increase, probing is an
appropriate method to assess potential deleterious changes in the
periimplant environment and should be performed every 3 to 4 months for 1
year after prosthesis delivery. After this time, if crestal bone levels are stable,
probing is still relevant. Probing also reveals tissue consistency, bleeding, and
exudate. Probing is important not only to measure increasing sulcus depths
but also to allow the dentist to evaluate several periimplant parameters at the
same time and at the same sites.
Controversy exists as to the material from which the probe should be
fabricated. In theory, different metal types (e.g., stainless steel, titanium)
should not come into contact because of a risk of contamination of the two
metals and the resulting galvanic corrosion that may develop and cause
crestal bone loss. As a result of this concern, the suggestion has been made
that only titanium surgical instruments be used to contact the implant and
that only titanium or plastic instruments be used to probe or scale the
implant (Fig. 18.11).
FIG 18.11 Implant probing. (A) A titanium or plastic periodontal probe to be used to
evaluate pocket depth. (B) Because of nontypical prosthetics, in some cases it may
be difficult to probe along the long axis of the implant because of access. (C)
Impossible to probe.
Touching the surface of the abutment subgingivally with a stainless steel

instrument is not of clinical concern. However, scratching the surface may
contribute to plaque migration following the direction of the scratch. Plaque
follows the direction of scratches on a titanium plate even though right
angles and a maze pattern may be scratched onto the surface. When probing
almost to the bone level around the implant, one should take care not to
scratch the surface because plaque that forms at the surface may follow the
scratch subgingivally to the bone level. This is particularly important during
scaling procedures and during the removal of cement below a crown margin.
One should use semicircular strokes, parallel to the sulcus or crown margin,
to scale the implant above the bone. If a scratch on the implant body occurs,
plaque will not have a direct “highway” below the tissue.
Baseline probing depths should be taken at the time of prosthesis insertion.
The baseline measurement is important because these measurements will be
used as a reference point. The probing depths should be measured as six
points (i.e., mesiobuccal, midbuccal, distobuccal, mesiopalatal, midpalatal,
distopalatal). However, it should be noted that implant type may complicate
the probing process. If the implant is platform switched (abutment smaller
than implant neck), probing may be difficult or misleading because the perio
probe will not show the true extent of the pocket depth. Additionally, an
overcontoured or atypical prosthesis may prevent achieving accurate probing
depths.
Bleeding Index
Gingival bleeding when probing around teeth correlates with sulcular
inflammation and plaque index. Easily ulcerated sulcular epithelium
represents inflammation from plaque and is the primary cause of bleeding
when probing. A bleeding index is an indicator of sulcus health. Bleeding
also can be provoked by undue pressure on the probe.
Controversy surrounds the issue of using bleeding and gingival health as
an implant health indicator. Unlike a natural tooth, implant success in the
first few years is related more often to biomechanical equilibrium than to
gingival health. Compared with a natural tooth, the soft tissue inflammation
from bacteria may be more restricted to above the crestal bone because of
the lack of a periodontal membrane or fibrous tissue between the implant
and the bone interface. As a result, the bleeding index may not be as
important a factor when evaluating the early implant quality of health.
The correlation between gingival health and implant success appears in
part to be related to the cervical surface condition of the implant. Adell et al
found no evidence that gingivitis was a precursor of progressive bone loss.51
Lekholm et al also found that gingivitis and deep sulcular pockets were not
accompanied by accelerated bone loss.49 Both of these reports evaluated a
machined-surface titanium screw design (e.g., Nobel Biocare).
In contrast to the previous reports with machined-surface implants, Kirsch
and Mentag found a correlation between the gingival sulcus depth and
implant failure.52 The implant design studied in this report had an
intramobile element with a larger implant body abutment crevice and a
roughened, titanium plasma spray body (IMZ Maschinen Vertriebs GmbH).
A similar correlation between implant failure and gingival health status was
observed when a porous titanium alloy microball surface was exposed above
the bone (Endopore [Sybron Implant Solutions]).53
In addition to the surface condition of the implant, other studies show a
correlation to gingival health and implant teeth. Jepsen et al identified
elevated levels of proteolytic enzymes in an implant sulcus with
inflammation and bleeding on probing as predictors of implant disease.54
Lekholm et al and Quirynen et al found that plaque and gingivitis around
implants were correlated.55 Steflik et al found that the gingival bleeding index
correlated highly with the plaque index and the crevicular fluid index.56
Bleeding on probing is a simple and accurate indicator of the health of the
peri-implant tissues. The presence or degree of peri-implant mucositis can be
associated by the degree of bleeding and the possibility of progression into
peri-implantitis. The clinician is encouraged to probe the sulcular region to
evaluate crestal bone loss around the implant. Periodontal probing is less
demanding than the determination of a gingival sulcular fluid volume index.
One may observe the bleeding index while probing for sulcus depth and may
record it easily to help evaluate gingival health.
Regardless of whether gingival health is relative to success, all clinicians
agree that the ideal soft tissue condition around an implant is an absence of
inflammation. Radiographic bone loss and increased pocket depth have been
correlated with sulcular bleeding. The gingival status around an implant
should be recorded and used to monitor the patient's daily oral hygiene.
However, surrounding soft tissues around implants have fewer blood vessels
than teeth; therefore, inflammation is typically less around implants than
around teeth.57
The most common bleeding gingival index used for implants is the Loe
and Silness gingival index.3 When used on teeth, this index scores gingival
inflammation from 0 to 3 on the facial, lingual, and mesial surfaces of all
teeth. The symptom of bleeding comprises a score of at least 2 (Table 18.6).
TABLE 18.6
Gingival Index (Loe and Silness)
Normal Description
0 Mild inflammation, slight c olor c hange and edema, no bleeding
1 Moderate inflammation, redness, edema, bleeds on probing
2 S evere inflammation, marked redness and edema ulc eration, spontaneous bleeding
The gingival index scores may also be used on implants to record the
gingival inflammation on the facial, lingual, and mesial surfaces. The facial
and lingual are already being probed to evaluate bone loss that cannot be
seen on a radiograph. Because the bleeding index evaluates inflammation,
the Loe and Silness index is adequate for implants, and because fewer
implants typically are used to restore a region compared with the presence of
natural teeth, one also may evaluate the distal surface when bleeding is
present because the implants are more than 2 mm apart and access often is
unobstructed.
During the first year of clinical examinations for the periimplant tissues,
the clinician should record color, form, and consistency along with bleeding
on probing and should probe depths for all sites. After 1 year of stable
probing depths, the examination may be restricted to facial and lingual
checks at maintenance appointments and may be correlated with
radiographic observation for the mesial and distal surfaces. Removal of the
prosthesis for more accurate probing and evaluation is not indicated unless
warranted by changing conditions. Repeated removal of a screw-retained
fixed prosthesis causes wear of the screw attachment system and causes
more frequent partially unretained restorations over the long term.
Pain
Subjective findings of pain, tenderness, and sensitivity are common dental
conditions that the dentist treats as part of a general practice. Pain and
tenderness are subjective criteria and depend on the patient's interpretation
of the degree of discomfort. Pain is defined as an unpleasant sensation
ranging from mild discomfort to excruciating agony. Tenderness is more an
unpleasant awareness of the area in question. In comparison to an implant, a
natural tooth often becomes hyperemic and sensitive to cold as the first
indicator of a problem. A tooth with a more serious condition becomes
sensitive to heat and painful to percussion, indicating pulpitis. Dental
emergencies usually are associated with pain, and the clinician is adept at its
diagnosis and treatment planning.
Pain is often a poor indicator of the presence of peri-implant disease,
especially in the early stages. In many cases, patients do not experience pain
until sufficient osseous destruction has occurred and/or there exists an active
infection with pus. Because dental implants do not have PDL support and
associated sensory apparatus, low-grade infections and osseous atrophy are
not detected by marginal gingiva. As the disease process begins around an
implant, the patient may feel slight irritation, but normally not enough pain
to cause alarm. It is recommended that the dentist be proactive in evaluating
the status of dental implants with the incorporation of a routine maintenance
protocol for patients.
Marginal Bone Loss

The marginal bone around the implant crestal region is usually a significant
indicator of implant health. Unlike natural teeth, the causes of crestal bone
loss around the implant are multifactorial and may occur at different time
periods. These bone loss types include surgical bone loss, initial “biologic
width” bone loss, early-loading bone loss, intermediate-term bone loss, and
long-term bone loss. Each time period may have a different cause for the
bone loss. Most often the surgical trauma causes little bone loss, but on
occasion, bone loss may reach several millimeters. The clinician may assess
the presence of surgical bone loss when a two-stage surgery is used to obtain
initial rigid fixation. The level of the crestal bone is measured from the
crestal position of the implant at the stage II uncovery surgery. When the
abutment is attached to the implant body, approximately 0.5 to 1 mm of
connective tissue forms apical to this connection.55 This bone loss may be
caused by an “implant biologic width.” Initial bone loss during the surgical
healing phase may vary for submerged and unsubmerged healing protocols.
For example, an implant originally placed 2 mm above the bone and another
countersunk 2 mm below the bone also have a different initial bone loss
history after the abutment is attached to the implant.42 Whenever possible,
the implant should be inserted at or above the bone crest to avoid an
increase in the sulcus depth around the implant related to the crestal bone
loss after abutment placement.
After the implant is connected to a permucosal element, the marginal bone
may be lost during the first month from (1) the position of the abutment-
implant connection or (2) the crest module design of the implant. The
abutment-implant connection will cause 0.5 to 1.0 mm of bone loss when it is
at or below the bone. In addition, when smooth metal is below the abutment-
implant connection and extends onto the neck of the implant, additional
bone loss will occur in direct relation to the smooth metal region. The bone
levels will most often recede to the first thread or at a roughened surface;
after the first month a permucosal element or abutment extends through the
soft tissue (Fig. 18.12).43
FIG 18.12 When an implant is placed with the abutment connection at the crest of
the ridge (left side), after the permucosal abutment is connected, the bone is usually
lost to the first thread, especially when the crest module is machined or smooth
(right side). (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
Crestal bone loss has been observed around the permucosal portion of
dental implants for decades. It has been described in the crestal region of
successfully osteointegrated implants regardless of surgical approaches. It
can range from loss of marginal bone to complete failure of the implant and
dramatically decreases after the first year.
Early Marginal Bone Loss

Adell et al were the first to quantify and report marginal bone loss. The study
also indicated greater magnitude and occurrence of bone loss during the first
year of prosthesis loading, averaging 1.2 mm during this time frame, with a
range of 0 to 3 mm. This report measured bone loss from the first thread as
the 0-mm baseline, not from the original level of crestal bone at insertion,
which was 1.8 mm above this baseline point.15 Thus, the actual first-year
crestal bone loss averaged 3.3 mm around the implants observed. Years
subsequent to the first showed an average of 0.05 to 0.13 mm bone loss per
year. Other studies report an average first-year bone loss of 0.93 mm, with a
range from 0.4 to 1.6 mm and a mean loss of 0.1 mm after the first year.58 The
early crestal bone loss has been observed so frequently that proposed criteria
for successful implants often do not even include the first-year bone loss
amount.
The initial transosteal bone loss around an implant forms a V- or a U-
shaped pattern, which has been described as ditching or saucerization around
the implant. The current hypotheses for the cause of crestal bone loss have
ranged from reflection of the periosteum during surgery, preparation of the
implant osteotomy, the position of the microgap between the abutment and
implant body, micromovement of the abutment components, bacterial
invasion, the establishment of a biologic width, and factors of stress.51,59,60,57
An understanding of the causes of marginal crestal bone loss around dental
implants and early implant failure is critical in preventing such occurrences,
fostering long-term peri-implant health, improving long-term implant
success rates and, foremost, implant prosthesis success. Marginal crestal
bone loss may influence esthetics because the height of the soft tissue (e.g.,
interdental papilla) is directly related to the marginal bone. If the tissue
shrinks as a consequence of the bone loss, the emergence profile of the
crown elongates and the papilla may disappear next to the adjacent tooth or
implant. If the soft tissue does not shrink, the increase in pocket depth may
be related to the presence of anaerobic bacteria and peri-implantitis (Fig.
18.13).
FIG 18.13 Radiographic evaluation of bone loss. (A) Crestal bone loss. (B)
Significant horizontal bone loss, not the ideal angulation as all implant threads are
seen clearly. (C) Bitewing radiograph showing bone loss.
Etiology
There are many theories on the potential etiologic factors that may cause
marginal bone loss around dental implants. These include Periosteal
Reflection Hypothesis, Implant Osteotomy Hypothesis, Autoimmune
Response to the Host Hypothesis, Occlusal Trauma, Cellular Biomechanics,
Engineering Principles, Bone Mechanical Properties, Implant Design
Biomechanics, and Implant Design Mechanics. Limited marginal bone loss
during the first year of function after stage II surgery has been observed
around the permucosal portion of dental implants for decades. Hypotheses
for the causes of crestal bone loss have included the reflection of the
periosteum during surgery, preparation of the implant osteotomy, level of the
microgap between the abutment and implant body, bacterial invasion, the
establishment of a biologic width, the implant crest module design, and
occlusal overload.6,60
Periosteal Reflection Hypothesis.

Periosteal reflection causes a transitional change in the blood supply to the
crestal cortical bone. Ninety percent of the arterial blood supply and 100% of
the venous return are associated with the periosteum in the long bones of the
body.61 When the periosteum is reflected off the crestal bone, the cortical
bone blood supply is affected dramatically, causing osteoblast death on the
surface from trauma and lack of nutrition. These events have fostered the
periosteal reflection theory as a cause for early bone loss around an endosteal
implant.
Although crestal bone cells may die from the initial trauma of periosteal
reflection, the blood supply is reestablished once the periosteum
regenerates. Cutting cones develop from monocytes in the blood and precede
new blood vessels into the crestal regions of bone. Osteoblasts then are able
to remodel the crestal bone anatomy.36 Composite bone forms rapidly on
periosteal surfaces to restore its original condition. In addition, the
underlying trabecular bone is also a vascular source because its blood supply
often is maintained in spite of crestal periosteal reflection. The greater the
amount of trabecular bone under the crestal cortical bone, the less crestal
bone loss is observed. To place the implant in sufficient available bone, an
implant ridge is usually 5 mm or wider at the crest. As a result, trabecular
bone is readily available to assist in cortical blood supply and remodeling
around the implants. The cortical bone is remodeled to its original contour,
without significant loss of height. The periosteal reflection theory would lead
to a generalized horizontal bone loss of the entire residual ridge reflected,
not the localized ditching pattern around the implant that typically is
observed. In addition, generalized bone loss already would be directly
noticeable at the second-stage uncovery of the implant body, 4 to 8 months
after stage I implant placement surgery. Yet generalized bone loss rarely is
observed at the second-stage uncovery surgery. The periosteal reflection
hypothesis does not appear as a primary causal agent of marginal crestal
bone loss around an implant (Fig. 18.14).
FIG 18.14 At stage II uncovery, the marginal bone level most often is similar to the
level the initial day of surgery and may even have grown over the top of the implant.
Because the periosteum is reflected and bone is prepared to insert the implants, the
cause of frequently occurring early crestal bone loss may not be related to the
reflection of the periosteum or the osteotomy preparation. (From Misch CE:
Implant Osteotomy Hypothesis.

Preparation of the implant osteotomy has been reported as a causal agent of
early implant bone loss. Bone is a labile organ and is sensitive to heat. The
implant osteotomy causes trauma to the bone in immediate contact with the
implant, and a devitalized bone zone of about 1 mm is created around the
implant. A renewed blood supply and cutting cones are necessary to remodel
the bone at the interface. The crestal region is more susceptible to bone loss
during initial repair because of its limited blood supply and the greater heat
generated in this denser bone, especially with the less efficient cutting of
countersink drills used in this region.62 This condition supports implant
osteotomy preparation as a causal agent for marginal crestal bone loss
around the implant.
However, if heat and trauma during implant osteotomy preparation were
responsible for marginal crestal bone loss, the effect would be noticeable at
the second-stage uncovery surgery 4 to 8 months later. The average bone loss
of 1.5 mm from the first thread is not observed at stage II uncovery. In fact,
bone often has grown over the first-stage cover screw, especially when level
or slightly countersunk below the bone. Reports in the literature indicate
different surgical trauma causes and numbers for bone loss. For example,
Manz observed that bone loss at second-stage surgery ranged from 0.89 to
0.96 mm regardless of the bone density.63 Hoar et al reported only 0.2-mm
bone loss at stage II uncovery.64 The surgical system or approach may
influence these data, but usually this bone loss remains minimal. One should
remember that these are averages of bone loss reported. If 2 mm of bone loss
is found on one implant and the next nine implants exhibit no bone loss, the
average bone loss would be 0.2 mm. Most implants at stage II uncovery do
not demonstrate any bone loss. The implant osteotomy hypothesis for
marginal crestal bone loss cannot be primarily responsible for this routinely
observed phenomenon.
Autoimmune Response of Host Hypothesis.

The primary cause of bone loss around natural teeth is bacterially induced.
Repeat studies demonstrate that bacteria are the causative element for
vertical defects around teeth. Occlusal trauma may accelerate the process,
but trauma alone is not deemed a determining factor.65 The implant gingival
sulcus in the partially edentulous implant patient exhibits a bacterial flora
similar to that of natural teeth. A logical assumption is that if implants are
similar to teeth, the marginal implant bone loss is caused primarily by
bacteria, with occlusal factors playing a contributing or accelerating role.
In a prospective study of 125 implants, Adell et al reported 80% of implant
sulcular regions were without inflammation.51 Lekholm et al found that deep
gingival pockets around implants were not associated with crestal bone
loss.66 Yet the marginal crestal bone loss to the first thread of screw-type
implants is a common radiologic finding. If bacteria were the causal agent for
the initial bone loss, why does most bone loss occur the first year (1.5 mm)
and less (0.1 mm) each successive year? The implant sulcus depth
progressively increases from the early bone loss, impairing hygiene and
making anaerobic bacteria more likely as the cause of bacteria-related bone
loss. If bacteria are responsible for 1.5-mm early crestal bone loss, what local
environmental changes occur to reduce their effect by 15 times after the first
year? The bacterial autoimmune theory cannot explain the marginal bone
loss condition when it follows the pattern most often reported. Although the
bacteria theory does not explain adequately the marginal crestal bone loss
phenomenon, this does not mean that bacteria are not a major contributor to
bone loss around an implant. Threads and porous implant surfaces exposed
to bacteria are reported to cause a more rapid loss of bone around an
implant.66 Poor hygiene also is reported to accelerate the bone loss observed
around endosteal implants.67 To state that bacteria are never involved in
marginal bone loss around an implant would be incorrect. Bone loss often is
associated with bacteria as a causal agent. However, when most bone loss
occurs in the first year and less bone loss is observed afterward, the
hypothesis of bacteria as the primary causal agent for the early crestal bone
loss cannot be substantiated.
Biologic Width Hypothesis.

The sulcular regions around an implant and around a tooth are similar in
many respects. The rete peg formation within the attached gingiva and the
histologic lining of the gingiva within the sulcus are similar in implants and
teeth. A free gingival margin forms around an implant with nonkeratinized
sulcular epithelium, and the epithelial cells at its base are similar to the
functional epithelial cells described with natural teeth.68 However, a
fundamental difference characterizes the base of the gingival sulcus.
For a natural tooth, an average biologic width of 2.04 mm exists between
the depth of the sulcus and the crest of the alveolar bone. It should be noted
the biologic “width” is actually a height dimension with a greater range in
the posterior region compared with the anterior, and may be greater than 4
mm in height. In teeth, it is composed of a connective tissue (CT) attachment
(1.07 mm average) above the bone and a junctional epithelial attachment
(0.97 mm average) at the sulcus base, with the most consistent value between
individuals being the CT attachment.39
The biologic width allows gingival fibers and hemi-desmosomes to
establish direct contact with the natural tooth and acts as a barrier to the
bacteria in the sulcus to the underlining periodontal tissues. When a crown
margin invades the biologic width, the crestal bone recedes to reestablish a
favorable environment for the gingival fibers (Fig. 18.15).69
FIG 18.15 The biologic width of a natural tooth has a connective tissue zone that
inserts into the cementum of the tooth. A periodontal probe will penetrate the sulcus
and the junctional epithelial attachment. BC, bone crest; GM, gingival margin; aJE,
junctional epithelium attachment; CEJ, cementoenamel junction. (From Misch CE:
Many surgical protocols recommend the placement of endosteal implants

at or below the crest of the ridge during the first-stage surgery. The
abutment-to-implant body connection may be compared with a crown
margin. Berglundh et al observed 0.5 mm of bone loss below the implant-
abutment connection within 2 weeks after stage II uncovery and abutment
connection in dogs.26 Lindhe et al reported an inflammatory connective tissue
extending 0.5 mm above and below this implant abutment connection.70
Wallace and Tarnow stated that the biologic width also occurs with implants
and may contribute to some of the marginal bone loss observed.71 The
biologic width theory seems attractive to explain the lack of bone loss from
the first stage of surgery and the early bone loss seen within the first year
after the second-stage abutment placement. However, it should be noted that
the biologic “width” in implants, as reported, often includes the sulcus
depth, whereas the natural tooth biologic width does not include the sulcus
depth. Eleven different gingival fiber groups are observed around a natural
tooth: dentogingival (coronal, horizontal, and apical), alveologingival,
intercapillary, transgingival, circular, semicircular, dentoperiosteal,
transseptal, periosteogingival, intercircular, and intergingival. At least six of
these gingival fiber groups insert into the cementum of the natural tooth: the
dentogingival (coronal, horizontal, and apical), dentoperiosteal, transseptal,
circular, semicircular, and transgingival fibers. In addition, some crestal
fibers from the periodontal fiber bundles also insert into the cementum
above the alveolar bone.3 However, in a typical implant gingival region, only
two of these gingival fiber groups and no periodontal fibers are present.
These fibers do not insert into the implant body below the abutment margin
as they do into the cementum of natural teeth.72 Instead, the collagen fibers
in the CT attachment around an implant run parallel to the implant surface,
not perpendicular, as with natural teeth.73 The gingival and periosteal fiber
groups are responsible for the connective tissue attachment component of
the biologic width around teeth, and these are not present around the
transosteal region of an implant. The CT attachment around the abutment-
implant connection cannot be compared with the CT attachment of a tooth.
James and Keller were first to begin a systematic scientific study to
investigate the biologic seal phenomenon of the soft tissue around dental
implants.72 Hemidesmosomes help form a basal lamina–like structure on the
implant that can act as a biologic seal. However, collagenous components of
the linear body cannot physiologically adhere to or become embedded into
the implant body as they do in the cementum of the tooth.54 The
hemidesmosomal seal only has a circumferential band of gingival tissue to
provide mechanical protection against tearing.55 The biologic seal around
dental implants can prevent the migration of bacteria and endotoxins into
the underlying bone. It is unable, however, to constitute a junctional
epithelial attachment component of the biologic width similar to the one
found with natural teeth. The amount of early crestal bone loss seems
unlikely to be solely the result of the remodeling of the hard and soft tissues
to establish a biologic width below an abutment connection. No connective
tissue attachment zone or components of the linear body are embedded into
an implant. The importance, amount, and mechanism for these anatomical
structures require further investigation (Fig. 18.16).
FIG 18.16 There are primarily two soft tissue fiber groups around an implant:
circular fibers and crestal bone fibers. Neither of these fiber types insert into the
implant or the abutment. The peri-implant probe penetrates the sulcus, junctional
epithelial attachment, and most of the connective tissue zone. CT, connective
tissue. (From Misch CE: Contemporary implant dentistry, ed 3, St. Louis, 2008, Mosby.)
The crevice between the cover screw and the implant body during initial
healing is similar to the crevice of the abutment-implant connection. Yet
bone can grow over the cover screw, and the crevice, in and of itself, may not
be the cause of bone loss. The crevice between the implant and the abutment
connection has been called a “microgap.” The actual dimension of this
connection is usually 0 mm and has a direct metal-to-metal connection.
However, when the crevice is exposed to the oral environment, bone loss is
usually observed for at least 0.5 mm below the connection.74 The biologic
width hypothesis cannot fully explain the several millimeters of marginal
crestal bone loss, which also has been observed readily with one-stage
implants that extend through the tissue at the initial implant placement
surgery and have no abutment-implant connections. For example, plate form
(blade) implants, transosteal implants, pins, one-piece screw implants, and
even subperiosteal implants demonstrate the marginal crestal bone loss
phenomenon.
It is true that bone loss does occur around an exposed abutment-implant
connection placed below the bone (observed within 2 to 4 weeks) once the
connection is exposed to the oral environment. The bone loss often occurs
before the implant is loaded with the prosthesis. It is logical to call this
marginal bone loss the biologic width. The primary question remains, when
the surgeon places the implant abutment connection below the bone, how
much bone loss is from the implant biologic width and out of the influence
of the dental practitioner? Several reports in the literature note implant
macro- and microgeometry may affect the biologic width dimensions or the
amount of early crestal bone loss.75
The bone loss to the first thread observation implies the amount of bone
loss is similar for different implant designs. However, the first thread is a
different distance from the abutment margin for several implant designs. A
smooth polished 4-mm collar below the bone has been associated with
greater bone loss than a smooth 2-mm collar below the bone. The implant
biologic width concept does not explain completely the total amount of
vertical bone loss observed. In addition, the amount of bone loss from the
biologic width occurs within 1 month whether the implant is loaded or not
and is related to the crest module implant design and the position of the
abutment-implant connection in relation to the bone but is unrelated to the
density of the bone. The concept does not explain why greater crestal bone
loss often is observed in soft bone compared with denser bone after loading,
nor does it explain the higher implant failure rates in lesser-quality bone
after loading.
Occlusal Trauma.
Marginal bone loss on an implant may be from occlusal trauma.60 Occlusal
trauma may be defined as an injury to the attachment apparatus as a result of
excessive occlusal force. A controversy exists as to the role of occlusion in the
bone loss observed after an implant prosthesis delivery. Some articles state
that peri-implant bone loss without implant failure is primarily associated
with biologic formations or complications.76 Other authors suggest a
correlation of crestal bone loss to occlusal overload.57,77 The determination of
the etiology of bone loss around dental implants is needed in order to
minimize its occurrence and foster long-term peri-implant health that may
ultimately determine implant prosthesis survival.
The association of occlusal trauma and bone loss around natural teeth has
been debated since Karolyi claimed a relationship in 1901.78 A number of
authors conclude trauma from occlusion is a related factor in bone loss,
although bacteria is a necessary agent.79 On the other hand, Waerhaug and
many others state there is no relationship between occlusal trauma and the
degree of periodontal tissue breakdown.80 According to Lindhe et al,
“trauma” from occlusion cannot induce periodontal tissue breakdown.81
However, occlusal trauma may lead to tooth mobility that can be transient or
permanent.
To establish further a correlation between marginal bone loss and occlusal
overload, related articles from cellular biomechanics, engineering principles,
mechanical properties of bone, physiology of bone, implant design
biomechanics, animal studies, and clinical reports were procured.60
Cellular biomechanics.
Bone remodeling at the cellular level is controlled by the mechanical
environment of strain.82 Strain is defined as the change in length divided by
the original length, and the units of strain are given in percentages. The
amount of strain in a material is directly related to the amount of stress
applied.10 Occlusal stress applied through the implant prosthesis and
components can transmit stress to the bone-implant interface. The amount of
bone strain at the bone-implant interface is directly related to the amount of
stress applied through the implant prosthesis. Mechanosensors in bone
respond to minimal amounts of strain, and microstrain levels 100 times less
than the ultimate strength of bone may trigger bone remodeling (Fig.
18.17).83
FIG 18.17 Mechanical stress applied to bone cells causes a change in shape or
strain. The microstrains may trigger the release of cytokines and bone
resorption. (From Misch CE: Contemporary implant dentistry, ed 3, St. Louis, 2008, Mosby.)
One of the earliest remodeling theories for a direct relationship between

stress and the magnitude of bone remodeling was proposed by Kummer in
1972.84 More recently, Frost reported on the cellular reaction of bone to
different microstrain levels.85 He observed that bone fractures at 10,000 to
20,000 microstrain units (1% to 2% deformation). However, at levels 20% to
40% of this value (4000 units), bone cells may trigger cytokines to begin a
resorption response. In other words, excessive bone strain may not only
result in physical fracture but may also cause bone cellular resorption. The
hypothesis that occlusal stresses beyond the physiologic limits of bone may
result in strain in the bone significant enough to cause bone resorption is
plausible from a cellular biomechanics standpoint. To date, bone cellular
studies have not replicated this bone condition next to a dental implant.
However, cytokines in the bone-implant interface tissue obtained from failed
hip replacement devices leading to bone loss have been reported in
humans.86
Engineering principles.
The relationship between stress and strain determines the modulus of
elasticity (stiffness) of a material. The modulus conveys the amount of
dimensional change in a material for a given stress level. The modulus of
elasticity of a tooth is similar to that of cortical bone. Dental implants are
typically fabricated from titanium or its alloy. The modulus of elasticity of
titanium is 5 to 10 times greater than that of cortical bone (Fig. 18.18). An
engineering principle called the composite beam analysis states that when two
materials of different elastic moduli are placed together with no intervening
material and one is loaded, a stress contour increase will be observed where
the two materials first come into contact.87 In an implant-bone interface,
these stress contours are of greater magnitude at the crestal bone region.
This phenomenon was observed in both photoelastic and three-dimensional
finite element analysis (Fig. 18.19) studies when implants were loaded within
a bone simulant.88 These authors note that the marginal bone loss observed
clinically and radiographically around implants follows a similar pattern to
the stress contours in these reports.
FIG 18.18 The modulus of elasticity is greater for titanium (Ti) compared with
bone. When stress is plotted on the Y axis and strain on the X axis, the modulus of
elasticity can be obtained. Titanium is 5 to 10 times more rigid than cortical
bone. (From Misch CE: Contemporary implant dentistry, ed 3, St. Louis, 2008, Mosby.)
FIG 18.19 A three-dimensional finite element analysis of a titanium implant in a
bone model after axial loading. The V-shape pattern of strain is greatest at the
crestal region and decreases in intensity as the stress is dissipated throughout the
implant length. (From Misch CE: Contemporary implant dentistry, ed 3, St. Louis, 2008, Mosby.)
Bone mechanical properties.

Bone density is directly related to the strength and elastic modulus of bone.72
In denser bone, there is less strain under a given load compared with softer
bone. As a result, there is less bone remodeling in denser bone compared
with softer bone under similar load conditions. A decrease in bone
remodeling can result in a reduction of bone loss. In a prospective human
study, Manz observed the amount of marginal bone loss next to an implant
was related to the density of bone.63 The initial peri-implant bone loss from
implant insertion to uncovery was similar for all bone qualities. However, 6
months after prosthesis delivery, the additional radiographic-observed peri-
implant bone loss ranged from 0.68 mm for quality 1 to 1.1 mm for quality 2,
1.24 mm for quality 3, and 1.44 mm for quality 4-type bone (Fig. 18.20). In
other words, the more dense the bone, the less peri-implant bone loss was
observed after prosthesis delivery. A clinical report by Appleton et al89
demonstrated that progressively loaded single-tooth implants in the first
premolar region of human beings exhibited greater bone density increase in
the crestal half of the implant interface and less marginal bone loss
compared with nonprogressively loaded implants in the same jaw region and
even the same patient on the contralateral side without progressive loading.
Because an increase in bone density is related to bone strength, elastic
modulus, bone remodeling, and a decrease in marginal bone loss, these
entities may be related to each other.
FIG 18.20 Mean peri-implant vertical bone change for study intervals by bone
quality score. Many observed the amount of bone loss from stage 1 to stage 2 was
similar, regardless of bone quality. However, after 6 months of loading, the amount of
marginal bone loss was directly related to the quality of the bone, with type 4 (the
softest bone) exhibiting the greatest bone loss. (Reproduced from Manz MC: Radiographic
assessment of peri-implant vertical bone loss: DIRG Implant Report No 9, J Oral Maxillofac Surg
55(Suppl):62–71,1997.)
Several animal studies in the literature demonstrate the ability of bone

tissue to respond to a dental implant. For example, Hoshaw et al inserted
dental implants into a dog femur perpendicular to the axis of the long bone
and perpendicular to the direction of the osteons.90 After applying a tensile
load to the implants for only 5 days, the bone cells reorganized to follow the
implant thread pattern and resist the load. This unique bone pattern was
observed for only 3 to 4 mm around the implants. Crestal bone loss was also
noted around these implants and explained as stress overload. To rearrange
its osteal structure, bone must remodel.
Miyata placed crowns on integrated dental implants with no occlusal
contacts (control group), and premature interceptive occlusal contacts of 100
mm, 180 mm, and 250 mm in a monkey animal model.91 After 4 weeks of
premature occlusal loads, the implants were removed in a block section and
evaluated. The crestal bone levels for 100 mm and control implants with no
loading were similar. However, statistically significant crestal bone loss was
observed in the 180-mm group. The 250-mm group experienced two to three
times the bone loss of the crowns with moderate prematurities. Duyck used a
dog model to evaluate the crestal bone loss around screw-type dental
implants with no loads (controls), static loads, and dynamic loads.92 The
dynamic-loaded implants were the only group to demonstrate crestal bone
loss. Because the only variable in these two studies was the intensity or type
of occlusal load applied to the implants, these animal reports imply dynamic
occlusal loading may be a factor in crestal bone loss around rigid fixated
dental implants.
Clinical reports have shown an increase in marginal bone loss around
implants closest to a cantilever used to restore the lost dentition.93 Cantilever
length and an increase in occlusal stress to the nearest abutment are directly
related and point to the fact that the increase in marginal bone loss may be
related to occlusal stress. Quirynen et al evaluated 93 implant patients with
various implant restorations and concluded that the amount of crestal bone
loss was definitely associated with occlusal loading.58 These authors also
reported increased crestal bone loss around implants in patients with no
anterior occlusal contacts and parafunctional habits in full-arch fixed
prostheses in both jaws. These clinical reports do not provide statistical
analyses to demonstrate a clear link between occlusal stress and bone loss.
However, they indicate a consensus by some authors that occlusal overload
may be related to the incidence of peri-implant bone loss around the cervical
aspect of an implant. In fact, in a study of 589 consecutive implants, Naert et
al suggested overload from parafunctional habits may be the most probable
cause of implant loss and marginal bone loss after loading.94
Rangert et al have noted that occlusal loads on an implant may act as a
bending moment, which increases stress at the marginal bone level and can
cause implant body fracture.95 Before the fracture of the implant body,
marginal bone loss was noted in this retrospective clinical evaluation. The
same stress that caused implant fracture is the logical cause of the peri-
implant bone loss before the event. Rosenberg et al found microbial
differences in implant failures from both overload and biologic
complications.96 Uribe et al presented the case of a mandibular implant
crown with a marginal peri-implantitis and osseous defect.97 Histologic
analysis revealed an infiltrate and a central zone of dense fibroconnective
tissue with scanty inflammatory cells. According to the authors, this finding
differs from chronic inflammatory tissue associated with infectious peri-
implantitis and can be directly related to occlusal overload. A clinical report
by Leung et al observed radiographic angular crestal bone loss to the seventh
thread around one of two implants supporting a fixed prosthesis in
hyperocclusion 2 weeks after prosthesis delivery.98 The prosthesis was
removed, and over the next few months radiographic observation showed the
crestal defect was repaired to almost the initial level, without any surgical or
drug intervention. The prosthesis was then seated with proper occlusal
adjustment. The bone levels stabilized at the second thread of the implant
and remained stable over the next 36 months. This report indicates bone loss
from occlusal overload is not only possible but may even be reversible when
found early in the process. Although no prospective clinical study to date has
clearly demonstrated a direct relationship between stress and bone loss
without implant failure, several practitioners agree a causal relationship may
exist.
The fact that occlusal overload may be an etiology for crestal bone loss
does not mean other factors are not present. For example, the microgap
position of the implant platform and abutment and the biologic width often
affect the marginal bone during the first month after the implant becomes
permucosal. However, the clinician has certain variables under their control
that may influence the amount of peri-implant bone loss. The position of the
microgap in relation to the bony crest and the implant crest module design
are primarily under the control of the implant surgeon. On the other hand,
the autoimmune or bacterial response of the patient, the biologic width, and
the patient response to the surgical trauma of implant placement are
variables often escaping the control of the dentist. Once the final prosthesis
is delivered to the patient, many events responsible for marginal bone loss
have already occurred, whereas others such as occlusal overload and its
relationship to the quality of bone persist. Occlusal overload is one factor
most in control of the restoring dentist. If a relationship between occlusal
overload and crestal bone loss exists, approaches to decrease stress to an
implant interface appear appropriate. A puzzling element in the relationship
between occlusal force and peri-implant bone loss is the lack of continued
bone loss until the implant fails. Implant crown height may be measured
from the occlusal plane to the crest of the bone. The crown height is a vertical
cantilever, which may magnify the stresses applied to the prosthesis. As a
result of the greater crown height from the vertical bone loss, occlusal
overload will be increased after crestal bone loss occurs. If occlusal loading
forces can cause crestal bone loss, the resulting increased moment forces
should further promote the loss of bone until the implant fails. Yet most
clinical studies indicate the rate of bone loss decreases after the first year of
loading and is minimal thereafter. There are two reasons why the bone levels
may become stable after initial marginal bone loss, even when the cause is
from occlusal overload: bone physiology and implant design mechanics.
Bone physiology.
The bone is less dense and weaker at stage 2 implant surgery than it is 1 year
later after prosthetic loading.99 Bone is 60% mineralized at 4 months and
takes 52 weeks to complete its mineralization.100 Partially mineralized bone is
weaker than fully mineralized bone. In addition, the microscopic
organization of bone progresses during the first year. Woven bone is
unorganized and weaker than lamellar bone, which is organized and more
mineralized. Lamellar bone develops several months after the woven bone
repair has replaced the devitalized bone caused by the surgical insertion
trauma around the implant.101 The occlusal stress levels may be high enough
to cause woven bone microfracture or overload during the first year, but the
increase in bone strength achieved after complete mineralization and
organization may be able to resist the same stress levels during the
subsequent years.
As functional forces are placed on an implant, the surrounding bone can
adapt to the stresses and increase its density, especially in the crestal half of
the implant body during the first 6 months to 1 year of loading.102 In a
histologic and histomorphometric study of bone, Piatelli et al reported
reactions to unloaded and loaded nonsubmerged implants in monkeys (Figs.
18.21 and 18.22). The bone changed from a fine trabecular pattern after initial
healing to a more dense and coarse trabecular pattern after loading,
especially in the crestal half of the implant interface.103 Hoshaw loaded
threaded implants in dogs with a tensile load and noted that the fine
trabecular bone pattern became coarse trabecular bone around the implant.90
In addition, the bone reorganized to a more favorable condition to assist the
direction and type of occlusal load (Fig. 18.23). Fine trabecular bone is less
dense than coarse trabecular bone. Because the density of bone is directly
related to its strength and elastic modulus, the crestal bone strength and
biomechanical mismatch between titanium and bone may diminish
gradually during the functional loading phase. In other words, the stresses
applied to the peri-implant bone may be great enough to cause bone
resorption during the first year because bone strains are greatest at the crest.
However, the stresses applied below the crest of bone are of less magnitude
and may correspond to the physiologic strain that allows the bone to gain
density and strength. As a result, the occlusal load that causes bone loss
initially (overload) is not great enough to cause continued bone loss once the
bone matures and becomes more dense.
FIG 18.21 In evaluating the bone around an implant after healing in a monkey
model, a fine trabecular pattern is noted. (From Piatelli A, Ruggeri A, Franchi M, et al: A
histologic and histomorphometric study of bone reactions to unloaded and loaded nonsubmerged
single implants in monkeys: a pilot study, J Oral Implantol 19:314–319, 1993.)
FIG 18.22 Once the implant was loaded, the fine trabecular bone became coarse
trabecular bone, especially at the crestal region. When the stresses are too great,
bone loss occurs. When the stresses are within the physiologic range, the bone
density increases. (From Piatelli A, Ruggeri A, Franchi M, et al: A histologic and
histomorphometric study of bone reactions to unloaded and loaded nonsubmerged single implants
in monkeys: a pilot study, J Oral Implantol 19:314–319, 1993.)
FIG 18.23 Researchers loaded threaded implants in dog tibiae and noted the fine
trabecular bone in the apical region (A) became coarse trabecular after loading. In
addition, crestal bone loss was observed on the loaded implant. (From Hoshaw SJ,
Brunski JB, Cochran GVB: Mechanical loading of Brånemark fixtures affects interfacial bone
modeling and remodeling, Int J Oral Maxillofac Implants 9:345–360, 1994.)
A clinical report by Appleton et al demonstrated that progressively loaded

single-tooth implants in the first premolar region of humans exhibited less
bone loss and greater bone density increase in the crestal half of the implant
interface compared with nonprogressively loaded implants in the same jaw
region, and even in the same patient, on the contralateral side.104 (Fig. 18.24).
Marginal bone loss is less in the mandible compared with the maxilla in
several clinical reports. The bone is denser in the mandible than the maxilla.
The reduced crestal bone loss that has been reported in the mandible in
greater bone densities and in progressively loaded implants point to the fact
that stress/strain is a primary etiology of crestal bone loss after the implant is
loaded. The stresses at the crest of the ridge may cause microfracture or
overload during the first year, and the change in bone strength after loading
and mineralization is complete alters the stress/strain relationship and
reduces the risk of microfracture during the following years.105
FIG 18.24 Researchers observed in humans that less crestal bone loss and an
increase in bone density were present around implants progressively loaded in the
maxillary first premolar region. (From Appleton RS, Nummikoski PV, Pigno MA, et al: A
radiographic assessment of progressive loading on bone around single osseointegrated implants
in the posterior maxilla, Clin Oral Implants Res 16:161–167, 2005.)
Implant design biomechanics.

Different amounts of marginal bone loss have been reported for different
implant body designs. The design and surface condition of the implant body
may affect the amount of strain distributed to an implant-bone interface. A
report by Zechner et al evaluated the peri-implant bone loss around
functionally loaded screw-type implants with machined surfaced V-threads or
a sandblasted, acid-etched square-thread design (Fig. 18.25).106
FIG 18.25 Researchers have compared crestal bone loss for the implant design
on the left (a V-shaped machined thread) with the implant design on the right (a
roughened square thread) in the anterior mandible for 3 to 7 years. (From Misch CE:
Both these implant designs had a similar crest module and external hex
connection. Four interforaminal implants were placed in the mandible in 36
patients and followed for 4 years. Over this period, the average bone loss was
2.4 mm (V-thread) versus 1.6 mm (square thread). However, the range of bone
loss in the study was 0.1 to 8.5 mm for machined V-threaded implants and 0.2
to 4.8 mm for rough-surfaced square-threaded implants. Twenty-two V-
threaded implants lost more than 4 mm of bone of less than 1 mm was
reported for 16 rough-surface square-threaded implants compared with only
two machined-surfaced V-threaded implants (Fig. 18.26). There were no
clinical findings of inflammation or exudate. The range of bone loss with the
different implant surface conditions and designs in a clinical report suggests
that more than the biologic width, microgap position, and/or surgical causes
are involved in the individual implant marginal bone loss process. The three
most probable factors that influenced the amount of crestal bone loss in this
report are the amount of force applied to the prosthesis, the quality of the
bone to resist these forces, and the implant body design. All three of these
conditions implicate occlusal overload as the cause of marginal bone loss
around an implant.
FIG 18.26 Most of the implants that lost more than 4 mm of bone were of the
machined V-shaped thread design (MS). The implants that lost less than 1 mm of
bone were primarily roughened square thread designs (SE). (From Misch CE:
A prospective study by Karousis et al also indicated that different implant

designs and surface conditions correspond to different incidences of crestal
bone loss.107 Three different implant designs from the same manufacturer
were evaluated over 10 years in a prospective report. One implant body
design lost more than 5 mm of bone 26% of the time, whereas the other two
designs reported 37% and 39% incidence. More than 6 mm of marginal bone
loss occurred in 22% of the implants with the first design, compared with
35% and 33% for the other two designs. These results indicate that one
implant design may result in less marginal bone loss than another and point
to the fact that clinical reports with similar healing and loading protocols,
but of variable implant body designs and surface conditions, may yield
different amounts of crestal bone loss. Because the implant design and
surface condition affect the amount of stress transferred to the bone, one of
the reasons for a different amount of bone loss for different implant designs
may be related to the stress transmitted to the bone.
In the field of orthopedics, hip joint replacement has several
complications, including wound infection, periprosthetic fracture,
dislocation, mechanical failure, and osteolysis.108 Osteolysis refers to the bone
resorption that occurs around both cemented and uncemented orthopedic
implants. Aseptic loosening from osteolysis of the bone-implant interface is
the leading cause of late joint replacement failure (10% within 10 years).
Mechanical loading factors primarily are associated with this condition.
Patient factors that increase loading failure include body weight and activity
level. An animal model and human report have linked the resorption of bone
at the interface to mechanical overload.109 Treatment of the disorder, if the
patient is asymptomatic with a large osteolytic defect but no implant
mobility, includes curettage of the osteolytic membrane and bone grafting.110
These orthopedic reports accept that mechanical overload can cause bone
resorption at the bone-implant interface. The metal most often used in hip
replacement therapy is titanium alloy, and the bone-implant interface is very
similar to a dental implant. In addition, potential causative elements
encountered intraorally, such as oral bacteria contamination, microgap
position, and microbial-related bone loss, are eliminated in this aseptic
environment. It is logical to assume these studies further support a
relationship between marginal bone loss around implants and biomechanical
stress.
Radiographic Evaluation of Bone Loss.

The radiographic assessment of natural teeth assists in determining the
presence of decay, lesions of endodontic origin, and periodontal bone loss.
Radiographs may be used to evaluate the result of periodontal diseases on
the supporting bone but cannot indicate the presence or absence of the
disease process. Assessments of bone loss for natural teeth may include (1)
the presence or absence of intact lamina dura; (2) the width of the PDL space;
(3) the bone crest morphology (even or angular); and (4) the distance from
the cementoenamel junction (CEJ) and the coronal level of the PDL (normal
or abnormal width). Normal radiographic bone levels next to natural teeth
are typically between 1 to 3 mm from the CEJ.
Implants do not decay and do not develop endodontic-related conditions.
However, the crestal bone region is often the most diagnostic for the ranges
of optimum, satisfactory, and compromised health conditions. Radiographic
interpretation is one of the easiest clinical tools to use to assess implant
crestal bone loss but has many limitations. A radiograph only illustrates
clearly the mesial and distal crestal levels of bone. However, early bone loss
often occurs on the facial aspect of the implant.
An absence of radiolucency around an implant does not mean bone is
present at the interface, especially in the anterior mandible. As much as 40%
decrease in density is necessary to produce a traditional radiographic
difference in this region because of the dense cortical bone.111 When the bone
is wide, a V-shaped crestal defect around an implant may be surrounded by
cortical bone and, as a result, the radiograph is less diagnostic.
Parallel periapical radiographs are more difficult to obtain for implants
than for teeth. An implant is often apical to the apex of the preexisting
natural tooth. As a result, the apex of the implant often is located beyond
muscle attachments or in regions almost impossible to capture with a
parallel radiographic method. A foreshortened image to accommodate the
apical portion of the implant defeats the purpose of radiographic
interpretation of the crestal bone. Crestal bone loss is often best evaluated
with vertical bitewing films or periapical radiographs that do not include the
apical portion of the implant (Fig. 18.27).
FIG 18.27 Vertical bitewings are often more diagnostic to determine radiographic
bone loss compared with radiographs, which attempt to capture the apex of the
implant. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The clear depiction of the threads on the radiograph indicates use of a

proper angulation. If the threads are clear on one side but fuzzy on the other,
the angulation was incorrect at least 10% (Fig. 18.28). If both sides of a
threaded implant are unclear, the radiograph is not diagnostic for crestal
bone loss assessment. Ideally, the abutment-implant connection should
appear as a clear line between the two components. When the top of the
implant is placed at the crest of the regional bone, the amount of crestal bone
loss is easiest to evaluate.
FIG 18.28 On this periapical radiograph, the threads are clear on one side only.
The central ray was not directed completely perpendicular to the implant body but
was within 10 degrees. This film is not ideal but is clinically acceptable in most
situations. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The implant quality of health evaluation protocol depends on clinical and
radiographic observations. A baseline radiograph is obtained at the initial
delivery of the prosthesis. By this time the “biologic width” and influence of
the implant crest module design have already contributed to its influence on
crestal bone loss. Because crestal bone changes often occur during the first
year of loading, preventive maintenance appointments are scheduled every 3
to 4 months, and a periapical/vertical bitewing radiograph at 6 to 8 months
may be compared with the baseline if probing depths increase. Vertical
bitewing radiographs may be taken at 1 year and compared with the previous
two images. If no changes are apparent, subsequent radiographic
examinations may be scheduled for every 3 years unless other clinical signs
warrant more frequent examinations.
If crestal changes are evident by probing or radiographs, stress reduction
and hygiene are modified accordingly. Radiographs are taken and reviewed
every 6 to 8 months until the bone is stable for two consecutive periods. If
bone loss greater than 2 mm is observed from the bone levels noted at the
prosthesis delivery, the dentist should strongly suspect parafunction on too
few implants. Night guards and stress reduction on the affected implants are
indicated.
The following section outlines the major types of peri-implant disease, while
offering a comprehensive treatment and prevention protocol (Table 18.7).
TABLE 18.7
Diagnostic Comparison of Peri-Mucositis vs. Peri-Implantitis
Bleeding on P robing Suppuration P robing Depths Radiographic Bone Loss Implant Mobility
Peri-implant muc ositis + +/− >4 mm + −
Peri-implantitis + +/− <4 mm − +/−
Peri-implant Mucositis
Peri-implant mucositis is an inflammatory condition of the soft tissue
surrounding an implant, which is similar to gingivitis around a tooth. This
has been defined as a reversible condition with no loss of attachment or bone
loss. The prevalence of peri-implant mucositis (bleeding on probing and no
loss of bone) has been shown to be approximately 79% to 90% of subjects and
50% of implants.8
Clinically, peri-implant mucositis may be diagnosed as bleeding on
probing with or without suppuration, probing depths less than 4 mm, with
no evidence of radiographic evidence of bone loss (Fig. 18.29).
FIG 18.29 Peri-mucositis images. (A) Spontaneous bleeding around dental implant
prosthesis. (B) Erythematous marginal diseased tissue with bleeding on probing. (C)
Cyanotic buccal gingiva indicating chronic bacterial challenge.
Etiology.
The primary etiologic factor has been shown to be plaque biofilm, the
removal of which easily reverses the disease process. If allowed to progress,
peri-implantitis may result, which includes loss of bone and loss of
osseointegration, similar to loss of attachment and bone with periodontitis.
The relationship between plaque accumulation and peri-implant mucosal
inflammation has been proven through numerous studies.112,113 Histologically,
peri-implant mucositis is composed of T cells with an apical extension that is
limited to the barrier epithelium.114 Most cases of peri-mucositis are due to
poor oral hygiene, inability to clean the implant or prosthesis, poor implant
position, poor fit of the prosthesis, and retained cement.
Additionally, peri-mucositis may also be caused by titanium alloy
hypersensitivity. Most dental implants today are covered by a titanium
dioxide layer that gives the implant a high surface energy that facilitates the
interaction between the host tissues and the dental implant. When the
implant becomes exposed to the oral environment, a lower surface energy
may provoke a type IV hypersensitivity reaction that may contribute to peri-
mucositis.115
Prevention.
Because of the high prevalence of peri-mucositis, it is imperative the implant
clinician be able to assess the risk profile of each patient and take this into
consideration when treatment planning is initiated. A recent consensus
report by the American Academy of Periodontology has shown risk factors to
include poor oral hygiene, history of periodontal disease, smoking, retained
cement, and occlusal disharmonies. Systemic factors also have been shown to
include such disorders as diabetes and cardiovascular disease.116 The clinician
should be well versed on the role of systemic diseases and medications have
on the soft tissue interface that may result in peri-mucositis.
Another key component of peri-mucositis prevention is ideal implant
placement. The implant should be placed in the ideal buccal-lingual, mesial-
distal, and apical-coronal dimension to ensure soft tissue health. This will
also allow for ideal prosthesis design, which will facilitate ideal hygiene
procedures.
Management.
Peri-implant mucositis has been shown to be a reversible inflammatory
process.8 However, if not treated properly, the persistent inflammatory
condition may progress to peri-implantitis that includes irreversible bone
loss. In most cases, peri-mucositis is required for the development of peri-
implantitis.117,118
Nonsurgical mechanical debridement coupled with antimicrobial rinse
therapies is the primary therapeutic approach for peri-implant mucositis.
Factors contributing to poor management of peri-implant mucositis may
include lack of patient compliance, inconsistent maintenance intervals, and
impairment of implant prosthesis for proper plaque control.119
Because peri-implantitis is reversible, it is imperative the biofilm be
eliminated from the implant surface. If the biofilm remains, peri-mucositis
may progress to peri-implantitis.
The goal of peri-implant mucositis treatment is to reestablish a healthy
peri-implant mucosa by means of removing the peri-implant biofilm and
calculus without damaging or altering the implant surface.
It is crucial to implement a comprehensive patient and professional oral
hygiene program to combat the peri-implant mucositis. Power brushes,
interproximal and irrigation power devices, dentifrices, and antimicrobials
have been recommended in the management of peri-implant mucositis.
Professional Mechanical Debridement.

For the removal of the supra- and subgingival biofilm and bacteria,
debridement of the exposed implant surface and implant abutment must be
completed. There exist many different debridement systems.
Curettes.
The selection of scalers for titanium implant debridement is important to
minimize surface changes following treatment. There are various types of
curettes available for debridement procedures.
• Titanium-coated curettes are specifically made for dental implant
debridement because they have a similar hardness to the titanium surface
and will not scratch or mar the surface.
• Carbon-fiber curettes are softer than the implant surfaces and will not
damage the implant surface. These types of curettes are prone to fracture.
• Teflon curettes are similar to carbon-reinforced curettes and will not scratch
the surface of the implant.
• Plastic curettes have been advocated as the instrument of choice to prevent
damage from the implant surface. However, the efficacy and efficiency of
these instruments are questionable. These types of curettes are also prone
to breaking.
• Stainless steel curettes are much harder than titanium alloy and are not
recommended for use around dental implants because they may alter the
implant surface.
• Amorphous resin scalers come with unfilled or filled resin. Unfilled resin
scalers have no reinforcements for shape or stiffness while filled resin fillers
may use materials like silica, graphite, or glass. These scalers have
replacement tips on a stainless steel handle. Longevity of these curettes
tends to be relatively short.
• Titanium brush burs (Salvin) insert into implant motor. They have a variety of
shapes allowing them to adapt around implant surface circumferentially,
single surface, and groove cleaning. Brushes are used at 600 rpm and
adapted against implant surface to remove debris.
Hasturk et al compared six different types of scaler materials and their
tendency to scratch surfaces of different brands of implants abutments
under scanning electron microscope. The result showed glass-filled resin
curettes caused the most scratches while the unfilled resin scalers had the
least surface alteration. However, these studies are on smooth titanium
abutments and not on the rough implant surface.120 A study by Anastassiadis
suggested that there may not be any clinical relevance on whether curettes
scratch implant surfaces or not. It has been previously demonstrated that
metal scalers do not readily scratch cementum; it is questionable that a
titanium implant surface, which has a higher Mohs hardness, should be of
any concern.121 Furthermore, scalers as a whole may be effective in removing
large calculus particles or granulation tissues but are rather ineffective trying
to navigate the perimeter and grooves of an exposed implant surface. For that
reason, curette material may not be a significant concern, but rather the act
of curetting is (Fig. 18.30).
FIG 18.30 (A) Titanium curette. (B) Carbon-reinforced curette. (C) Teflon/plastic.
(D) Steel curette. (A and B, From Salvin Dental Specialties, Inc., Charlotte, NC.)
Ultrasonic devices.
Ultrasonic devices with special polyetheretherketone-coated tips have been
used to debride the implant surface. This tip is made of a plastic material
with a stainless steel core. This ultrasonic device allows the debridement of
plaque and calculus while leaving a smooth and clean surface.
While metal tips are not recommended, plastic tips may have high chances
of shredding when cleaning around implant grooves and threads. Tips made
of PEEK material by Hu-Friedy have been shown to be resistant to shredding
and may be considered.
Neither the American Dental Association nor American Academy of
Periodontology have released a consensus on the use of ultrasonic devices
around implants. Evidence is currently anecdotal and not sufficient to
support use of devices.
Antimicrobials.
Antiseptics are defined as antimicrobial substances that are nondamaging to
living tissue/skin while reducing the possibility of infection, sepsis, or
putrefaction. There are several types of antiseptics ready for dental use:
sodium hypochlorite 1.0%, hydrogen peroxide 3.0%, chlorhexidine gluconate
0.12% (USA) or 0.2% (Europe, Asia, Canada), citric acid 40.0%, EDTA 24%,
povidone iodine 10%, phenols and essential oils. In regards to peri-
implantitis, several qualities are needed for antiseptics to be effective:
biofilm penetration, long substantivity, tissue biocompatibility, and low
resistance. For these reasons, we recommend the use of citric acid. Removal
of macro deposits should be performed with scalers first. A cotton pellet is
soaked with 40% citric acid. It is gently dabbed to remove excess fluid then
burnished onto exposed implant surfaces for 30 to 60 seconds.122 Although
there are many other potential antiseptics such as povidone iodine, hydrogen
peroxide, chlorhexidine, and saline, citric acid has the most biocompatible
characteristics and ease of use. Citric acid is shown to be able to reduce
bacterial endotoxin, specifically Porphyromonas gingivalis, by up to 90% with 2
minutes of contact.123 The body is capable of handling minimal amount of
bacterial colonies. With mechanical and antiseptic use, it allows cells a
chance to try to regenerate onto clean implant surfaces.
In regards to other antiseptics, chlorhexidine applied on a cotton pellet
and burnished against machined surface has shown a 92.9% Pg endotoxin
reduction but is known to be toxic to fibroblasts.124 Povidone iodine has high
antiseptic capability but has a highly irritating effect if any residue comes in
contact with osseous structure. Bürgers et al studied several of the antiseptics
and their effectiveness on S. epidermis, C. albicans, and S. sanguinis. While
sodium hypochlorite was most effective in the reduction of all three bacterial
biofilms, it has the highest tissue toxicity. Hydrogen peroxide was only active
against C. albicans, while chlorhexidine gluconate, phenols, and essential oils
only had activity against S. sanguinis and C. albicans.125
Not enough supportive studies have deemed any of the listed antiseptics
as the clear choice, but 40% citric acid is recommended for ease of use, tissue
compatibility, and effectiveness in reducing bacterial residue (Fig. 18.31).126
FIG 18.31 0.12% chlorhexidine rinse.
Locally delivered antibiotics.

The recommended locally delivered antibiotic (LDA) is tetracycline at 50
mg/ml solution. Tetracycline capsules can be opened and mixed with small
amounts of saline solution to create a paste. This paste is burnished onto
implant surfaces for 60 seconds then thoroughly rinsed away with saline.
Tetracycline is bacteriostatic because it targets the 30s ribosomal subunit in
the mRNA translation complex of bacterial protein synthesis. It is also found
to have inhibition effect on matrix metalloproteinases; the application of
tetracycline solution needs to be completely removed. A study with pure
tetracycline application showed reosseointegration after 4 months.127 It is
highly recommended to incorporate tetracycline in treatment of peri-
implantitis.
Tetracycline capsules may be mixed with few drops of saline to form a slime
gel consistency. It should stay gelled when scooped up to be delivered to
exposed implant surfaces. The gel is allowed to sit on implant surface for 1 to
5 minutes then thoroughly rinsed off. It allows proximal contact of
antibiotics to implant surface colonies and may assist in success in treatment
of peri-implantitis (Fig. 18.32).
FIG 18.32 (A) Tetracycline 300-mg capsule. (B) Mixed with minute amount of
sterile saline to form a workable paste.
Systemic antibiotics.
The use of systemic antibiotics has been well studied for treatment of
periodontitis.128 However, peri-implantitis treatments with use of systemic
antibiotics are relatively few. It is known that patients with periodontitis are
three times more likely to develop peri-implantitis, but the bacterial colonies
found in peri-implantitis and periodontitis share few characteristics. Still,
many studies have demonstrated the most effective combination as
amoxicillin and metronidazole. Metronidazole is bactericidal to anaerobic
organisms. It disrupts DNA synthesis. This antibiotic has been shown to be
especially effective against A. actinomycetemcomitans and effective against P.
gingivalis and P. intermedia.129 The amoxicillin and metronidazole
combination has also been shown to have long-term effects against A.
actinomycetemcomitans.130 Use of amoxicillin and metronidazole mixture is
recommended. For patients who are allergic to amoxicillin, doxycycline 10%
controlled release gel such as atridox may be considered.
Script formulation:
Amoxcillin 500 mg tid, metronidazole 250 mg, 21 tabs tid till finish
Doxycycline hyclate 10% (atridox) applied subgingivally
Patient At-Home Mechanical Debridement.

The mechanical reduction of supragingival plaque by removal with
toothbrushes (manual or powered) significantly reduces the amount and
composition of subgingival microbiota around teeth. This reduction should
translate to a decreased risk of periodontal disease initiation or recurrence.
Furthermore, the decreased prevalence of periodontal pathogens in
supragingival plaque lowers potential reservoirs of these species (Fig.
18.33).131
FIG 18.33 (A) Prosthesis with significant plaque accumulation; patient home care
instruction is crucial to the long-term health of the soft tissue. (B) Patient home care
is also important during the implant healing phase because plaque and calculus
accumulation results in poor tissue health.
The absence of adequate keratinized mucosa in endosseous dental

implants, especially in posterior implants, was associated with higher plaque
accumulation and gingival inflammation but not with more annual bone loss,
regardless of the implant's surface configurations.132 The implant type, with
the presence or absence of keratinized tissue, may be a challenge for oral
hygiene procedures for many patients. The clinician should stress the
importance of adequately performing plaque control and select products and
procedures that are well suited to the needs and ability of the patient.
Toothbrushing: Manual and Power.

There are many types of toothbrushes available for implant patients to clean
exposed implant surfaces and prostheses. The patient should be instructed to
initially attempt to use a soft, multitufted, nylon toothbrush. Because of often
nonideal implant locations or prostheses, the clinician should choose a
handle that will allow for easy access to all areas. The toothbrush technique
should be the modified Bass technique or a short, horizontal back-and-forth
movement can be utilized. The modified Bass technique allows for the brush
to be held at a 45-degree angle where the abutment post meets the gingival
tissue. A location that is often missed is lingual aspect of the abutments or
prosthesis.
In some instances, patients will be able to use rotary unitufted power
brushes, oscillating-rotating brushes, and sonic brushes. Most available
powered brushes will not damage the exposed implant surfaces or
abutments. Most manufactured power brushes have soft interchangeable
bristle heads (flattened, rubber cup–like, short and long pointed in shape)
that may be used. The short and long pointed tips are ideal for reaching
proximal areas, wide embrasures, and pontic areas under a splinted
prosthesis. The hollowed, rubber cup may be used on the facial and lingual
aspects of the implant and prosthesis (Fig. 18.34).133
FIG 18.34 Toothbrushing aides. (A) Oral-B Superfloss. (B) Oral-B Power Tip. (C)
Interproximal cleaning device (Philips AirFloss Pro). (A and B, Courtesy Oral-B
Laboratories Inc., Iowa City, IA. C, Courtesy Philips Oral Healthcare, Stamford, CT.)
Auxiliary Aids.
Interdental brushes may be used to massage the peri-implant tissue around
an implant, which results in increased blood flow to enhance the tone of the
surrounding gingiva. Instructions should be given to insert the tip
interdentally in an occlusal direction, pressing the side of the tip against the
marginal gingiva and applying a gentle rotary motion. In some cases,
interproximal brushes with small brush heads (e.g., GUM End Tuft [Sunstar
Americas, Inc.]) may be required for easier access. However, caution should
be exercised to use plastic-coated devices because metal may potentially
damage or scar the implant or prosthesis surface.
There are numerous types of floss on the market for implant hygiene use.
A commonly used brand is Oral-B Super Floss, which is a thicker, wide
ribbon that has one end that allows for ease of threading. This type of floss
may also be used in conjunction with an antimicrobial solution (e.g.,
chlorhexidine gluconate), which may be used in a side-to-side motion. This
allows the thick ribbon to clean on both sides of the exposed implant. In
areas with tighter, small openings, a traditional unwaxed floss may be used
with a floss threader.
Oral irrigators may be used as an adjunct for removing supragingival soft
debris around implants and prostheses. However, caution should be
exercised because incorrect use or excessive water pressure may damage the
peri-implant tissues. Patients should be instructed to use these modalities on
low-medium settings, with the irrigator tip placed in the interproximal area
horizontal to the implant and along its gingival margin to avoid subgingival
spray. Additionally, an antimicrobial solution may be used (e.g.,
chlorhexidine gluconate).133
The main goal of auxiliary aids is mechanical debridement. Patient
adherence to home care is essential. Superfloss and interdental brushes work
by physically engaging plaque and tartar. Oral irrigators function by
hydraulic pressure to force fluid into the subgingival space. It functions by
both introduction of oxygen to an anaerobic bacteria dominant space and
removal of debris. In addition, chemical agents may be of benefit (e.g.,
chlorhexidine gluconate, peroxide, low-concentration bleach) and are
advocated. Each of these solutions has high capabilities to penetrate bacterial
biofilm and induce reduction of colonies. Irrigation around implants should
be incorporated into patient's home care regime on a daily basis.
Antimicrobial Agents.
Chlorhexidine gluconate is an antimicrobial safe and nontoxic adjunct to oral
hygiene procedures in the maintenance of dental implants. Chlorhexidine is
effective in reducing peri-mucositis because of its substantivity (i.e., binding
to tissue or implant surfaces). Additionally, it allows for fibroblast
attachment to implant surfaces. It has a long half-life because the pellicle
maintains bacteriostasis.
Although regular use may assist in patient home care, several adverse side
effects may occur for patients on routine use of chlorhexidine. Reports of
alteration of taste and staining of teeth are common. It is not recommended
to put a patient on long-term use of chlorhexidine; prescribing use should be
at the discretion of prescriber. It is recommended to be given postsurgery for
use to assist in soft tissue healing.
Chlorhexidine regimen.
Patients are given scripts for 1 bottle 0.12% or 0.2% chlorhexidine and are
instructed to rinse both in the morning after brushing teeth and at night
before going to sleep. Due to side effects, patients should be under close
monitoring. It should be noted that other countries may have different
concentrations of chlorhexidine.
Peri-Implantitis
Etiology.
Peri-implantitis has been associated with a gram-negative anaerobic
microbiota, similar to that found in severe periodontitis around natural
teeth.134
Peri-implantitis encompasses the criteria of peri-mucositis and the
addition of loss of osseous support. Although some natural bone remodeling
post implant placement is normal, a stabilized implant that continues to
exhibit bone level change is indicative of peri-implantitis.
Although bacterial insult is identified as the main cause of peri-mucositis,
peri-implantitis is considered to be initiated by stress factors caused by a
poor biomechanical environment. In addition, several other factors exist,
such as poor implant placement, poor oral hygiene, residual cement, the
body's rejection, poor implant surface, unfavorable osseous density,
untreated periodontitis, drinking and smoking, untreated endodontic
lesions, diabetes, etc. More etiologies are being identified as studies
continue. Unfavorable stress factors can initiate crestal bone loss, and
bacterial presence can further propagate the rate of osseous destruction. In
recent studies, Rodrigues et al found that bacterial biofilms attached onto the
surface of implants can create a highly acidic environment that causes
corrosion, pitting, cracking, etc.135 Furthermore, new studies have shed light
on the release of titanium ions from the implant surface, which causes a
significant increase in local inflammatory effect.136
Prevention
Home care.
An effective oral hygiene program is paramount to minimize peri-implant
disease. This has been shown through multiple studies. Lindquist found a
direct association between poor oral hygiene and peri-implant bone loss in a
10-year follow-up study.137 Other studies have shown a correlation with poor
oral hygiene and a higher plaque score.138 Additionally, patients who have
lost their teeth to periodontal disease are more susceptible to peri-
implantitis.139
Professional care.
A thorough periodontal charting and review is essential. Patients with
periodontitis need to have this condition controlled before implant
placement. Patients who do not demonstrate the ability to maintain oral
hygiene need to be educated and put on a stringent professional care
regimen.
Prosthetic design.
A thoroughly evaluated cone beam computed tomography (CBCT) scan with
favorable biomechanical design for prosthetics is required. Refer to Misch's
book, Dental Implant Prosthetics, ed 2, for detailed treatment designs and
recommendations in treatment cases.
Cementation technique.
The meticulous use of cements when delivering a prosthesis is imperative, or
the clinician can choose to use screw-retained prostheses. If cementation is
desired, be careful to apply only on the edge of intaglio surfaces of the crown.
Overfilling or complete coverage of all inner surfaces of the crown is not
conducive to avoidance of cement extrusion.
Control of parafunctional forces.
A bite guard is critical to prevent unfavorable occlusal stress. The night
guard is adjusted to be on flat plane occlusion to disperse stress. Careful
discussion should be conducted with the dental laboratory to convey the
desired design for successful application.
Management.
The objective of treatment for peri-implantitis is for osseous regeneration of
the osseous defect. However, this proves to be challenging because the
implant surface needs to be detoxified along with modifying the soft and
hard tissues. This may involve nonsurgical and surgical treatment (Box 18.4).
Box 18.4
Treatment of Peri-Implant Mucositis/Peri-
Implantitis
Patient Self-Administered Mechanical and/or Chemical Plaque
Control
Toothbrushes
Toothpastes
Antimicrobial rinses/flossing/oral irrigators
Topical application of gel
Systemic antibiotics
Probiotic Lactobacillus reuteri–containing tablets
Professional Nonsurgical
Mechanical plaque control
• Hand instruments
• Powered instruments
Chemical plaque control
• Local delivery of antibiotics
• Chlorhexidine
• Phosphoric acid
• Ozone, oxygen, and saline solution

Mucogingival
Prostheses
Peri-Implantitis
Nonsurgical
Different mechanical instruments
• Nonmetal instruments
• Rubber cups
• Air abrasive
• Metal instruments
• Burs
Adjunctive treatments
• Microbiologic test
• Local antimicrobials
• Systemic antimicrobials
Disinfect titanium surfaces
• Antiseptics
• Air polishing
• Laser
Mucogingival
Prostheses
Peri-Implantitis
Surgical
• Animal studies
• Open flap debridement
• Surface decontamination
• Regenerative approach
• Biologics
• Guided tissue regeneration
• Guided bone regeneration

Human studies
• Systemic antibiotics
• Access surgery
• Resective surgery
• Regeneration surgery
Retrograde Peri-Implantitis
Maintenance and Prevention
Patient self-administered preventive regimens
Supportive periodontal therapy/maintenance (professionally)
• Mechanical nonsurgical therapy
• Mucogingival
• Prostheses
Nonsurgical Management of Peri-Implantitis
Whereas the nonsurgical treatment of peri-mucositis is often successful, the
nonsurgical treatment for peri-implantitis has a questionable efficacy. This is
most likely due to the inability to remove the bacterial biofilm from the
exposed implant surface. Usually this is more significant when the implant
design involves a rough surface.140
The nonsurgical treatment of peri-implantitis usually involves the
debridement and detoxification of implant surfaces, similar to the treatment
of peri-mucositis. However, the issue that arises is that these exposed
surfaces usually have concurrent subgingival pockets.
Low-Abrasive Amino Acid Glycine Powder.

Low-abrasive amino acid glycine powder has been shown to be an effective
treatment for removing biofilm without damaging the implant surface, hard,
and soft tissues. This technique uses a special handpiece with a plastic tube
nozzle with three orthogonally oriented holes. An air-powder mixture with
reduced pressure is expelled through the nozzle, which prevents the
formation of air emphysema complications. The nozzle is moved in a
circumferential movement around the implant surface.141
Although more extensive studies need to be conducted as to technique
efficacy, glycine powder can be incorporated into a treatment regimen. The
clinician should be careful to use the powder only in areas where access is
available and a posttreatment rinse can remove any residue. This modality is
best utilized in cases with buccal dehiscence and or horizontal bone loss
without crater or infrabony pocketing. Hu-Friedy/EMS produces a device that
can be used to effectively dispense glycine air-powder mixtures (Fig. 18.35).
FIG 18.35 Low-abrasive powder. Hu-Friedy glycine powder jet used to debride
titanium implant surfaces.
Ultrasonic Devices.
When used for treatment of peri-implantitis, tip modifications (i.e., carbon
fiber, silicone, or plastic) must be made. Care must be exercised to not use
metal tips because they may alter the implant surface.
Ultrasonic devices should be used only when a plastic tip is available.
Irrigation and meticulous cleaning is recommended in treatment for either
open flap debridement or closed flap irrigation.
Laser.
The use of lasers is becoming a more recognized treatment for peri-
implantitis. Although there are many varieties of different wavelength lasers
and each serves different type of purposes, only Nd:YAG laser has been
showing promise. The American Academy of Periodontology (AAP) has
continued to express reservations on use of lasers in treatment of peri-
implantitis disease. There is minimal evidence to support any lasers as the
lone treatment modality, although the Er:YAG laser has been shown to be
effective for root debridement by assisting calculus removal and reducing
endotoxin.142 It is important to note that the Er:Yag is a hard tissue laser and
it is rather damaging when used on implant surfaces without careful
monitoring. The damaging effect that accompanies the use of such lasers
does not warrant recommendation.
Invariably, more studies are starting to gravitate toward the regeneration
capability of the Nd:YAG laser. Nicholson et al published very promising
results of visible osseous regeneration around failing implants.143 In 2016, the
FDA awarded clearance for the Nd:YAG LANAP Protocol for periodontal
regeneration (FDA Clearance 510 (k) 151763). The LANAP Protocol results in
the “true regeneration of the attachment apparatus (new cementum, new
periodontal ligament, and new alveolar bone)” on previously diseased root
surfaces. A companion protocol, LAPIP, may be used to address mild to
moderate peri-implantitis.143a (Fig. 18.36).
FIG 18.36 Laser treatment. (A) Initial evaluation of peri-implantitis. (B) Laser tip
activated around sulcular margins of implant. (C) Immediate postsurgical
appearance. (D) Two-week postoperative with granulation tissue reforming around
implant collar.
Treatment procedure.
If the clinician desires to use lasers, the first step is to verify with
manufacturer whether the specific brand of lasers under consideration is
suitable for implant use or not (e.g., Er-YAG hard tissue lasers are
contraindicated for dental implant use). Further, a detailed treatment
sequence should be acquired from the manufacturer. Each laser has various
settings, different heat dispersions, and other limitations.
In general, the goal of the use of a laser is to detoxify the implant surface,
being careful to not produce heat that may damage the integration of the
implant.
Mild peri-implantitis.
Without flap exposure, the laser may be used to perform a sulcular incision-
like action around implant collar (i.e., neck). Specific soft tissue lasers are
able to ablate diseased tissue around implants and create access for use with
curettes.
Advanced peri-implantitis (crestal bone loss exceed 3 mm or requiring

access).
A sulcular incision is made around the implant (one tooth mesial to one
tooth distal). A full-thickness flap is reflected, exposing the implant surface.
Debridement of the implant surface is performed initially with curettes or
titanium brush. The surface is irrigated with 40% citric acid, 17% EDTA
(ethyl-diamine tetra acetic acid), and/or choice of antimicrobial agent. Laser
settings are specific to each individual laser according to manufacturer
protocol. Care should be exercised to cover all exposed surfaces (i.e., each
exposed thread) for the detoxification process. Use of regenerative material
(allograft and extended resorbable membrane) is highly recommended.
Tissues are modified and sutured to reapproximate tissue for tension-free
primary closure. The Nd:YAG LANAP Protocol (discussed earlier) can also
be used with advanced peri-implantitis. In addition, there are also rescue
approaches which combine laser and surgical therapies.
Note: It is critical to limit time exposure of the implant surface with the
laser application to avoid overheating or charring. This may increase implant
morbidity and possibly lead to premature loss of the implant due to bone
disintegration.
Surgical Management of Peri-Implantitis

Though nonsurgical treatment of peri-implantitis may be effective in some
cases, the majority of cases require a more invasive approach to ensure an
effective treatment outcome. There are various surgical techniques to treat
peri-implantitis, depending on the final objective (Fig. 18.37)144:
• Access flap: for cleaning and decontamination of implants with pus, heavy
bleeding, or with evidence of probing or craterlike radiographic bone loss.
• Regenerative procedures: provides access for cleaning, plus regeneration
procedures for deep crater defects past the first thread of nonmobile
implants.
• Apically positioned flap: provides access for cleaning and decontamination,
and is used for implants showing generalized horizontal bone loss past first
thread.
FIG 18.37 Advanced peri-implantitis. (A) Probing depths result in exudate. (B)
Vertical bone loss. (C) Poor tissue health exhibiting inflammation and bleeding. (D)
Extensive hard and soft tissue loss associated with poor hygiene. (E) Resulting in
failure of the suprastructure and prosthesis.
Access Flap.
This surgical technique is used to maintain the soft tissues around the
implant with the goal of decontamination (Fig. 18.38). A sulcular incision is
made around the implant and extends at least one tooth mesial and one
tooth distal on both the buccal and palatal/lingual side. This allows the
clinician to have proper visualization and access for the next step. A full-
thickness flap reflection is performed to gain access to the implant and bone
surface. Although it is desirable to minimize the incision on healthy tissue, if
access is inadequate, a vertical incision may be included to gain further
access. Degranulation can be completed with curettes, specialized titanium
brushes with an implant handpiece, and/or a glycine polishing handpiece.
Along with mechanical decontamination, a chemical decontamination
process should be followed, using compounds such as doxycycline or citric
acid. The flaps are then reapproximated in their original position using a
horizontal mattress suture, which helps adapt tissue around the implant
while creating a ferrule effect. Interrupted sutures will also serve this
purpose.
FIG 18.38 Access flap. (A) Crestal incision with full thickness reflection. (B) Buccal
and lingual flap to obtain full exposure.
Heitz-Mayfield et al published a 12-month prospective study with

antiinfective surgical therapy outcomes. Thirty-six patients with moderate to
advanced peri-implantitis had access flap disinfection followed with a
combination of systemic antibiotics (amoxicillin and metronidazole). They
found at 1 year the patients were 92% with stable crestal bone height, and all
had a marked reduction of probing depth; 47% had complete resolution of
bleeding on probing.145 It is possible to also complete a subepithelial tissue
augmentation while performing the access flap debridement. Schwarz et al
concluded that simultaneous tissue grafting with debridement had a
significant reduction of bleeding on probing, pocket depth, and clinical
attachment loss at a 6-month postoperative evaluation.146
1. Sulcular incision around desired dentition being careful to extend at least

one tooth mesial and one tooth distal in anticipation to the area of treatment
2. Full thickness flap reflection is complete past the mucogingival junction on

both buccal and palatal/lingual if necessary
3. Implants are detoxified with citric acid, cleaned with curettes and titanium
brush if needed.
4. Flaps are readapted over osseous structure and should be in relatively

similar position
5. Horizontal mattress sutures or interrupted sutures can be used being

careful to not exert too much tension that causes bunching of tissues. Tissue
does not have to be completely approximated; new tissue will form and
granulate in the wound site.
Regenerative Procedures.
For peri-implantitis cases where a craterlike defect is present, regeneration is
recommended (Fig. 18.39). Even though regeneration is an ideal treatment
modality for all peri-implantitis cases, there are many criteria that must be
fulfilled to allow successful treatment. In a similar principle to bone
regeneration for natural teeth, the higher the number of osseous walls
remaining in a defect, the better the anticipated result. Also, the prosthesis
must be free from any premature contacts that may introduce excessive force
to the implant interface. Ideally, especially in single-tooth implant cases,
removal of the crown would be performed to ensure proper healing. A
sulcular incision is performed from one tooth mesial to one tooth distal of
the implant. A full-thickness flap is reflected to gain adequate access to
defect. Thorough removal of granulation tissue is vital. Mechanical
debridement is then begun, using the methods previously outlined in this
chapter. A titanium brush with a small tip may be needed to access the
implant surface if the osseous crater around the implant has very little
access. After thorough mechanical debridement, freeze dried bone allograft
(FDBA) allograft or bovine xenograft can be packed in with a resorbable
membrane layered over. Soft tissue augmentation may also be included,
which will enhance healing. Flap advancement may sometimes be needed to
achieve soft tissue primary closure around implant. A longer-lasting suture is
recommended to ensure the flap does not open prematurely.
FIG 18.39 Regenerative procedures. (A) Radiograph depicting significant bone

loss surrounding implant in the first molar position. (B) Full-thickness reflection
showing extent of defect with retained cement. (C) Detoxification with tetracycline
hydrochloride, after removal of cement. (D) Augmentation with allograft. (E)
Postoperative radiograph two years postoperative. (Courtesy of Dr. Nolen Levine.)
In addition to the steps listed above, Froum and Rosen proposed the use of
enamel matrix derivative, platelet-derived growth factor, and human allograft
or bovine xenograft in conjunction with a collagen membrane or
subepithelial tissue graft. The study followed 51 consecutive patients treated
with up to 7.5-year follow-up, and the result is encouraging.147
Regenerative technique:
1. Sulcular incision around area of interest with one tooth mesial and one
tooth distal
2. Full-thickness flap is reflected past mucogingival junction being careful to

ensure enough tension release from flap tissue. It is essential to produce
adequate release so there is minimal tension when closing flap. Inadequate
reflection will result in incision line opening, which will increase morbidity
of the graft.
3. The bone surface is curetted to clean and remove all soft tissue remnants.
Bone surface is curetted being careful to remove all remnants of soft tissue.
Detoxification:
a. Citric acid is applied to exposed surface for 30 to 60

seconds.
b. Rinse with sterile saline for 30 seconds.

4. Bone graft of choice is placed on defect.
5. A resorbable membrane (extended resorbable collagen membrane: 4–6

months) is then draped over bone graft being careful to cover 3 mm past all
edges of bone graft
6. Tissue tension is reduced via tissue-stretching techniques. Flap is

resutured (i.e., high-tensile strength suture material: vicryl) being careful to
provide tension-free closure to produce maximal contact between tissue
edges (primary closure).
Apically Positioned Flap.

This surgical technique is used for implants that have generalized horizontal
bone loss past the first thread when regeneration is not considered feasible
(Fig. 18.40). An internal bevel incision or sulcular incision following the
implant is made. Two vertical incisions are added on the mesial and distal of
the implant creating a pyramidal flap. The clinician should be mindful of the
blood supply of the flap, and a wide base is necessary to ensure the sulcular
margin of the flap does not necrose. On the lingual/palatal a gingivectomy
may be performed at the level of the anticipated final gingival height. Being
mindful of the attached keratinized tissue, a submarginal incision may be
performed in cases where ample amounts of keratinized tissue are present
(e.g., palate). Ideally, a partial-thickness flap is recommended because it will
help apical flap adaptation; however, a full-thickness flap elevation technique
may be easier in tight-access areas.
FIG 18.40 Apical-positioned flap. (A) Apical repositioning of the tissue to decrease
pocket depth. (B) Closure showing stabilized apically repositioned flap.
Once reflected, similar treatment as the access flap may be performed.

Granulation tissue needs to be completely removed, followed by thorough
cleaning of implant surfaces. A chemical detoxification can similarly be
performed. A decision may be made to remove implant threads with a
handpiece if significant loss of osseous support is present and regeneration
is unlikely.146 The final flap is sutured to the underlying periosteal tissue if a
split-thickness flap was used. If a full-thickness flap was performed, it can be
adapted apically via individual interrupted sutures. The goal is to readapt
tissue back onto remaining osseous support to minimize thickness of a soft
tissue collar, thereby minimizing probing depth. Apically repositioned
surgical technique:
1. Sulcular incision around desired dentition being careful to extend at least

one tooth mesial and one tooth distal in anticipation to the area of treatment
2. Full-thickness flap reflection is complete past the mucogingival junction on

both buccal and palatal/lingual if necessary.
3. Osseous recontouring is complete at this time to create a positive

architecture.
4. Implants are detoxified with citric acid, cleaned with curettes and titanium
brush if needed.
5. Flaps are readapted over remaining osseous structure and should be apical
in comparison to original flap position.
6. Horizontal mattress sutures or interrupted sutures can be used being

careful to not exert too much tension that causes bunching of tissues. Tissue
does not have to be completely approximated; new tissue will form and
granulate in the wound site.
Miscellaneous Soft Tissue Complications

Lack of Keratinized Tissue
The absence or presence of a zone of keratinized gingiva around teeth and
oral implants remains a controversial issue. No direct evidence confirms or
denies the need for nonmobile keratinized tissue next to natural teeth. The
tooth with the least amount of keratinized tissue is often the mandibular first
premolar.3 Yet this tooth is rarely the first tooth lost from periodontal disease.
If all other periodontal indices are normal, the amount or absence of
keratinized gingiva has little to do with the expected longevity of the tooth.
In longitudinal studies, Wennstrom et al demonstrated that the lack of
adequate keratinized and attached tissue does not compromise the long-term
health of soft and hard tissue as long as patients maintain good oral hygiene
(Fig. 18.41).148,149
FIG 18.41 Lack of keratinized tissue. (A) Postimplant placement showing deficient
attached tissue. (B) Postprosthesis chronic pain and soreness from inadequate
attached tissue.
On the other side of the issue, some authors consider keratinized attached
gingiva important. Lang and Loe advocate a minimum of 2 mm of keratinized
gingiva and 1 mm of attached gingiva to maintain gingival health.150 Stetler
and Bissada addressed mucogingival considerations in restorative dentistry
in 1987.151 They concluded that if subgingival restorations were to be placed
in areas of minimally keratinized gingiva and less than optimal plaque
control, augmentation to widen the zone of keratinized tissue may be
warranted. However, they also noted that in unrestored teeth, the difference
in the inflammatory status of sites with or without a wide zone of keratinized
tissue was not significant.
Although keratinized tissue around a tooth may not be mandatory for
long-term health, a number of benefits are present with keratinized mucosa.
The color, contour, and texture of the soft tissue drape should be similar
around implants and teeth when in the esthetic zone. The interdental
papillae should ideally fill the interproximal spaces. A high smile line often
exposes the free gingival margin and interdental papillae zones. The
keratinized tissue is more resistant to abrasion. As a result, hygiene aids are
more comfortable to use, and mastication is less likely to cause discomfort.
The degree of gingival recession appears related to the absence of keratinized
gingiva. Root sensitivity and esthetic concerns may be associated with
gingival recession. From a restorative dental aspect, keratinized mucosa is
more manageable during the retraction and impression-making process.
Subgingival margin placement is improved, as is long-term stability in the
presence of keratinized tissue. Many of these benefits directly apply to the
soft tissue around an implant.
Natural teeth typically have two primary types of tissue: attached,
keratinized gingiva and unattached, nonkeratinized mucosa. The type of
tissue around a dental implant is more varied than natural teeth. After bone
loss in the maxilla, excess tissue is often found, and the tissue is usually
keratinized, unattached gingiva. An implant placed in the region may also
have keratinized, unattached tissue. The tissues around the implant may also
be similar to most natural teeth, surrounded by keratinized, attached gingiva
(Fig. 18.42). The tissues may be nonkeratinized, unattached mucosa, more
often in the mandible after bone height loss or after a bone graft and flap
advancement to approximate the gingiva (Fig. 18.43). The nonkeratinized
tissue may also be attached when acellular tissue (Alloderm [BioHorizons
IPH, Inc.]) is positioned under the periosteum and bounds the overlying
tissues to the bone.
FIG 18.42 The soft tissues around these implants are keratinized, attached
gingiva, similar to natural teeth. (From Misch CE: Dental implant prosthetics, ed 2, St Louis,
2015, Mosby.)
FIG 18.43 The soft tissue on the facial of the implant crown for the maxillary right
central incisor is unkeratinized, unattached mucosa. (From Misch CE: Dental implant
The need for keratinized tissue around dental implants seems more
controversial than that around teeth. In theory, structural differences in
implants compared with teeth make them more susceptible to the
development of inflammation and bone loss when exposed to plaque
accumulation or microbial invasion (e.g., less vascular supply, fewer
fibroblasts, lack of connective tissue attachment to cementation).26,152 Some
reports indicate the lack of keratinized tissue may contribute to implant
failure. Kirsch and Ackermann reported that the most important criterion for
implant health in the posterior mandible was related to the absence or
presence of keratinized gingiva.153 In this report, mobile, nonkeratinized
mucosa exhibited greater probing depths, which was histologically
confirmed. A study by Warrer et al in monkeys found that an absence of
keratinized mucosa increases the susceptibility of peri-implant regions to
plaque-induced destruction.154
The presence of keratinized tissue next to an oral implant presents some
unique benefits compared to natural teeth. Keratinized gingiva has more
hemidesmosomes; the JEA zone may be of benefit when in keratinized
tissue. Whereas the orientation of collagen fibers in the connective tissue
zone of an implant may appear perpendicular to the implant surface, these
fibers in mobile, nonkeratinized tissue run parallel to the surface of the
implant. Schroeder et al, James et al, and Listgarten et al have suggested that
mobile mucosa may disrupt the implant-epithelial attachment zone and
contribute to an increased risk of inflammation from plaque (Fig. 18.44).40,155
In addition to the general advantages of keratinized tissue stated for teeth,
keratinized tissue around implants may also be beneficial in several other
ways. In a two-stage protocol the implant is less likely to become exposed
during the healing process. The formation of an interdental/implant papillae
is completely unpredictable with mobile nonkeratinized tissues. When the
nonkeratinized tissue is mobile, several reports state that this is
unsatisfactory. Ono et al have proposed a classification of attached gingiva
and surgical alternatives to improve soft tissue types in edentulous sites for
implant placement.156 Meffert et al recommend ideally adequate keratinized
tissue before implant placement, especially in the posterior regions.157
FIG 18.44 Mobile mucosa around a dental implant results in more complications
than nonmobile tissues. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015,
Mosby.)
Interestingly, the studies that have advocated the need for keratinized
mucosa around dental implants have primarily investigated implants with
rough surfaces. Failure of rough-surface implants (e.g., hydroxyapatite-coated
and plasma-sprayed cylinder-shaped implants) have been related to a lack of
keratinized mucosa.158 On the other hand, the studies that have questioned
the need of keratinized mucosa around dental implants have examined
implants with smooth surfaces. A meta-analysis of the literature performed
on the subject by Esposito et al reported 20% fewer instances of peri-
implantitis in smooth-surface implants compared with rough-surface
implants.159
Another benefit of keratinized tissue is the clinical ease of treatment to
reduce pocket depths if crestal bone loss occurs. Probing depths 6 mm or
more are more often associated with anaerobic bacteria. If the implant is out
of the esthetic zone, a gingivectomy to reduce pocket depth is very
predictable. An apically positioned flap with nonkeratinized mucosa is less
predictable and is more difficult to perform.
However, it should be noted that several reports demonstrate the long-
term implant survival in the absence of keratinized tissue. Although reports
are more cautious with mobile mucosa next to an implant, nonmobile tissue
rather than keratinized tissue appears to be the primary criterion relative to
tissue type.
A study by Chung et al evaluated the significance of keratinized mucosa in
the maintenance of dental implants with different surface conditions.160 All
69 patients and 339 implants in the study had implant restorations for at
least 3 years and as long as 24 years with an average of 8.1 years. Bleeding
index, modified plaque index, gingival index, probing depth, width of
attached keratinized mucosa, and amount of attached mucosa were recorded.
In addition, average annual bone loss was calculated using past and present
radiographs. Gingival inflammation and plaque accumulation were
significantly higher in patients with less than 2 mm of keratinized mucosa or
1 mm of attached mucosa. The surface condition of the implant was not
statistically significant in this study, although the smooth implants with less
than 2 mm of keratinized mucosa were less stable than other groups relative
to the soft tissue profile.
This study also found the average annual bone loss was not influenced by
the amount of keratinized or attached mucosa or the type of implant surface
configuration (smooth vs. rough). The greatest amount of bone loss was
observed with rough implants in keratinized mucosa of less than 1 mm, but
the difference was not statically relevant. The presence of keratinized mucosa
in this study was most significantly advantageous in the soft tissue health of
posterior implants, as indicated by the gingival index. Posterior implants,
even in the presence of keratinized tissue, had a 3.5-fold higher annual bone
loss than anterior implants in this study (0.14 vs. 0.04 mm).158 Implant
location appears more important than the presence or absence of keratinized
mucosa.
The question relative to the need for keratinized tissue around implants
should be modified to, “Which would you prefer?” No one in the literature
has stated that the nonkeratinized tissue is more preferable than keratinized
tissue; the controversy is abated. Some authors prefer keratinized mucosa
more intensely than others. If one side of the controversy demonstrates
benefits while the other side states that keratinized tissue is not mandatory,
both sides may be correct.
In specific clinical instances, attached, keratinized gingiva is more often
desirable. For example, a fixed prosthesis (FP-1) in the esthetic zone requires
keratinized mucosa to develop the soft tissue drape around the implant
crowns. A second prime example is a mandibular overdenture, which
benefits from a vestibule and zone of nonmobile tissue around the implant
abutments.
Management of Lack of Keratinized Tissue

Tissue augmentation can be completed prior to surgery, concurrent with
surgery, or post implant surgery. The most ideal time to graft is prior to
surgery; however, patients may not like to have additional surgeries. The
treatment at all three timeframes is similar.
Use of Alloderm requires periods of familiarity with material. Prior
experience with handling is recommended.
Presurgical Augmentations.
Presurgical augmentation steps are as follows:
1. A trapezoidal flap is reflected from the desired areas of grafting.
2. Although a split-thickness tissue flap is recommended, a full-thickness

flap will invariably be effective as well.
3. Alloderm (soaked in saline for 20 minutes prior to use) is applied to area.
4. Chromic gut suture is used (5-0 recommended) to secure Alloderm to

attached tissue.
5. Flap is modified to be tension free and pulled over to cover Alloderm and
sutured with 4-0 or 5-0 non-resorbable suture.
Concurrent Augmentation.
Concurrent augmentation steps are as follows:
1. Full-thickness flap is reflected at site of desired implant position (one

tooth mesial and one tooth distal).
2. After implant placement and or bone augmentation, Alloderm can be

layered over desired location.
3. It is critical to have abundant tissue release to allow coverage of soft tissue

over bone graft, and soft tissue. It may be the most difficult task of the entire
procedure; it should be done only after one feels comfortable with tissue
advancement procedures.
4. The flap is sutured with no tension and secured for primary intention
healing.
Postimplant Tissue Augmentation.

After flap is allowed to heal post–implant surgery, ideally the soft tissue
augmentation can be performed during the abutment change appointment
or uncovery appointment (3 months healing). The steps are as follows:
1. A full-thickness flap is reflected being wide enough to cover size of

Alloderm membrane.
2. Presoaked Alloderm is applied and sutured to neighboring attached tissue

(chromic 5-0).
3. The flap is advanced over Alloderm being careful to cover entire Alloderm
tissue (nonresorbable suture 4-0 or 5-0).
Note: exposed Alloderm tissue can produce a pungent, necrotic smell that
makes the patient uncomfortable. It is important to notify patient that the
normal transformation of Alloderm may have undesired side effects during
the early stages of healing.
Peri-Implant Mucosal Hyperplasia

Gingival overgrowth (hyperplasia) around the peri-implant mucosa has been
recognized as a significant clinical issue in implant dentistry today. The
hyperplastic161 tissue complication has been also termed in the literature as
implant gingival hyperplasia, mucosal proliferation, proliferative gingivitis, and
implant-related tissue hyperplasia.162 The gingival overgrowth results in
extreme difficulty for the patient to maintain adequate hygiene and the
clinician in performing debridement. When gingival overgrowth is associated
with radiographic bone loss, the resultant periodontal pockets are expressed
as “true” periodontal pockets. If there is no associated bone loss, the pockets
are termed pseudopockets. These hyperplasia-induced pockets may harbor
pathogenic anaerobic bacteria. The plaque biofilm colonization and
maturation in implant pockets initiates inflammation. The resultant
hyperplastic tissue is most commonly composed of compact collagenous
fibers, fibroblasts, and inflammatory cells.163 This may result in osseous
resorption and soft tissue destruction, which can lead to peri-implantitis.
Gingival hyperplasia may also result in an esthetic issue for the patient.
This will require surgical intervention to reduce the tissue. Additionally,
gingival hyperplasia may make it impossible for a prosthesis to be
completely seated (i.e., bar overdenture) or give rise to chronic tissue
soreness.
Etiology.
After clinical diagnosis of implant-related gingival overgrowth, potential
etiologies must be identified such as hormonal, medication induced, allergy
induced, and patient-related habits. Various hormonal factors (e.g., related to
pregnancy or puberty) and medications have been associated with the
gingival overgrowth. Medications such as phenytoin (i.e., Dilantin),
immunosupressants (e.g., cyclosporine), calcium channel blockers, and
amphetamines have been associated with gingival hyperplasia. Gingival
overgrowth has also been associated with patient habits such as mouth
breathing. Allergy-induced hyperplasia is also becoming more prevalent in
implant dentistry. With the use of titanium alloys for the fabrication of the
dental implants and abutments, exacerbated allergic reactions are becoming
a more common problem. Nickel (Ni), combined with titanium or in the final
prosthesis, may exacerbate and cause an acute allergic reaction. Aluminum
(Al) and beryllium (Be) have been associated with eczema and soft tissue
reactions that result in gingival overgrowth.164
Prevention.
If a patient is considered to be at high risk for implant-related gingival
hyperplasia (e.g., because of medications), they should be instructed to
maintain meticulous hygiene. Additionally, a more frequent recall protocol
(3–4 times per year) should be implemented that includes debridement. The
prosthesis should be evaluated and maintained with a minimum of 1 mm of
space between the tissue and the prosthesis for ease of cleaning and
prevention of prosthesis-induced irritation.
Management.
Management of peri-implant gingival overgrowth should include the
determination of the etiology (e.g., medication or humoral). If the etiology is
determined to be medication induced, consultation with the patient's
physician is recommended for possible alternative treatment (Table 18.8).
TABLE 18.8
Peri-Implant Hyperplasia Etiologic Factors
Causative Agent Example

Antic onvulsants Phenytoin
Phenobarbital
Lamotrigine
Vigabatrin
Ethosuximide
Topiramate
Primidone
Calc ium Channel Bloc kers Nifedipine
Amlodipine
Verapamil
Immunosuppressant Drugs Cyc losporine
S ystemic Fac tors Pregnanc y
Puberty
Vitamin C defic ienc y
Leukemia
Neoplasms (fibromas, papillomas, c arc inomas)
The treatment of peri-implant hyperplasia should begin with conventional

periodontal therapies to reduce plaque biofilm and inflammation. The
surgical management of implant gingival overgrowth may require
gingivectomy (if adequate keratinized gingiva is present) or apically
positioned flaps (without adequate keratinized gingiva).
The use of 0.12% chlorhexidine daily has been shown to be successful in
reducing tissue overgrowth and bacteria counts.165 When gingival hyperplasia
is present around implants associated with overdentures, care should be
exercised to minimize further enlargement (Fig. 18.45). Commonly,
practitioners will relieve the denture so the path of insertion does not cause
irritation or mucosal injury. Ideally, the tissue enlargement should be
reduced and the causative agent identified and treated accordingly. It is
important to note that even with meticulous care and removal of etiology,
gingival overgrowth may recur. Communication with the patient is key to
avoid misunderstanding.
FIG 18.45 Hyperplasia. Hyperplastic tissue growth surrounding existing implant
prosthesis resulting in home care difficulty.
Quality Scale
Implant Quality of Health Scale: A Clinical Assessment of the
Health-Disease Continuum
The criteria for success in implant dentistry remain complex. The vast
majority of clinical studies reporting success and failure do not qualify the
type of success achieved. Instead, the term success primarily has been used
interchangeably with survival of the implant. The term failure has been used
to indicate the implant is no longer present in the mouth. Nearly all reports
in the prosthetic literature also report survival as success.
What is success for a natural tooth? In the periodontal literature, a quality
of health is presented, and well-established guidelines based on clinical
criteria describe the ideal health of natural teeth. The general term success in
implant dentistry should be replaced with the concept of quality of health,
with a health-disease continuum describing the status of implants.
Success criteria for endosteal implants have been proposed previously by
other authors, including Schnitman and Shulman,166 Cranin et al,167
McKinney et al,168 Albrektsson et al,169 and Albrektsson and Zarb.170 An
implant quality of health scale with five levels has been established by James
and modified by Misch.171 The James-Misch scale also proposes management
modalities corresponding to these five levels. In 2007, a consensus
conference in Pisa, Italy (sponsored by the International Congress of Oral
Implantologists; www.icoi.org) modified the James-Misch scale to four
conditions that describe success, survival, and failure (Table 18.9).
TABLE 18.9
New Proposed Classification of Peri-Implant Diseases
Implant Quality Scales Clinical Conditions Management

S uc c ess (optimal health) No pain or tenderness upon func tion Normal maintenanc e
Osseointegration/S tage 0 0 mobility
osseoseparation <2 mm radiographic bone loss from initial
surgery
PD <4 mm
No suppuration
No BOP
S urvival (satisfac tory health) No pain Frequent S PT
S tage I osseoseparation 0 mobility Nonsurgic al debridement (hand, mac hine, air powder,
Peri-muc ositis <2 mm radiographic bone loss from initial lasers, etc )
surgery Patient self-administered c are
Peri-muc osal inflammation Adjunc t loc al and systemic antimic robials
PD ± 4 mm (bleeding and/or suppuration on S oft tissue and/or prosthetic c orrec tions if required
probing)
S urvival (potentially No pain
c ompromised) 0 mobility
S tage II osseoseparation 2–4 mm radiographic bone loss
Early peri-implantitis PD ± 4 mm (bleeding and/or suppuration on
probing)
Perimuc osal inflammation
Bone loss <25% of the implant length
S urvival (c ompromised health) Variable pain Treatment as above plus surgic al reentry and revision
S tage III osseoseparation 0 mobility Laser
Moderate peri-implantitis Peri-muc osal inflammation Implant surfac e dec ontamination
PD ≥6 mm (bleeding and/or suppuration on Regeneration
probing)
Bone loss 25% to 50% of the implant length
Failure (c linic al failure) Peri-muc osal inflammation S urgic al reentry and revision
S tage IV osseoseparation Pain upon func tion Lasers
Advanc ed peri-implantitis PD >8 mm (bleeding and/or suppuration on Removal of implant
probing)
Bone loss >50% of the implant length
Mobility
Unc ontrolled exudate
Maybe no longer in mouth
Others (suc h as retrograde peri- Variable perimuc osal inflammation S urgic al reentry and revision or removal of implant
implantitis) Radiographic ally: periapic al lesion around
implant
Clinic al: pain, tenderness, fistula formation or
swelling
BOP, bleeding on probing; PD, probing depth; SPT, supportive periodontal therapy.
(Data from Suzuki JB, Hsiao YJ, and Misch CE: Personal communication, 2017.)
Ideal clinical conditions for natural teeth include absence of pain, less than
0.1 mm of initial horizontal mobility under lateral forces of less than 100 g,
less than 0.15 mm of secondary mobility with lateral forces of 500 g, absence
of observed vertical mobility, periodontal probing depths of less than 2.5
mm, radiographic crestal bone height 1.5 to 2.0 mm below the
cementoenamel junction, intact lamina dura, no bleeding on probing, no
exudate, and absence of recession or furcation involvement on multirooted
teeth (Box 18.5).172
Box 18.5
The Role of the Dental Hygienist in Implant
Maintenance
• Identify potential implant patients
• Education and motivation throughout treatment
• Development, continual assessment, and modification of patient-specific

oral hygiene procedures
• Evaluation of prosthesis (components, attachments, mobility, and

retention)
• Evaluation of peri-implant tissue
• Probing
• Exposing clinically acceptable radiographs
• Removal of biofilms, soft and hard accretions
• Recommendation of oral hygiene implements
• Determine a patient-specific recall interval
• Cotherapist to identify potential problems and complications
• Documentation of implant(s) status
The AAP and ADA defined five periodontal types for diagnosis and
treatment of natural teeth: type I: gingivitis; type II: early periodontitis; type
III: moderate periodontitis; type IV: advanced periodontitis; type V:
refractory and juvenile periodontitis.173 The categories of disease do not
simply indicate success or failure but rather a range from health to disease.
This classification allows a clinical approach to treatment in each category. A
similar scale for implants has been established as an aid to diagnosis and
treatment that also proposes management approaches according to the signs
and symptoms.174
The James-Misch scale presented for implant quality of health based on
clinical evaluation was supported by the International Congress of Oral
Implantologists in 2007 (Table 18.10).172 This quality of health scale allows the
implant dentist to evaluate an implant using the listed criteria, place it in the
appropriate category, and then treat the implant accordingly. The prognosis
also is related to the quality scale.
TABLE 18.10
Human Studies on Peri-Implantitis Treatment
Number of
P atients
and
Implants Treatment Outcome
and Time
of Follow
Up
Leonhardt Ac c ess surgery 9 patients S ystemic antibiotic s (ac c ording to mic robiologic analysis) + Healing: 58% of the implants
et al 2003 26 ac c ess surgery + dec ontamination of the implant surfac e using 7 implants lost
implants 10% hydrogen peroxide 4/19 ongoing bone loss
60 0.2% CHX 2× a day rinse 6/19 bone gain
months Mean gingival bleeding was
reduc ed from 100% to 5%
Disease progression at 2
other implants
Romeo et Apic ally 19 S ystemic antibiotic s (amoxic illin for 8 days) + full mouth Radiographic assessment:
al 2007 repositioned patients disinfec tion Implantoplasty is an effec tive
flap surgery + 38 9 patients with resec tive surgery and 10 with resec tive surgery treatment proc edure
implant surfac e implants and modific ation of surfac e topography S ignific antly better results
modific ation (11 Implant surfac e dec ontamination with metronidazole gel, w/apic al reposition flap
Resec tive hollow tetrac yc line hydroc hloride, and saline surgery + implant surfac e
surgery sc rew modific ation
and 7
solid
sc rew)
12–24–36
months
Behneke Bone grafts and 10 Irrigation with iodine + systemic antibiotic s (Ornidazole 500 mg Clinic al: (6 months/14
et al bone graft patients × 2 for 7 days) implants)
1997a, b substitutes 14 Implant surfac e treated with air powder and irrigation with saline BI: 2.4–0.3
surgery implants 7 implants with 2–3 wall defec ts got bone c hips and 7 implants PD: 5.9–2.3 mm
• 6 with 1 wall defec t got bone bloc ks Clinic al: (2 years/5 implants)
Nonsubmerged months– BI: 2.4–0.4
2 years PD: 5.9–2.5 mm
Radiographic : (3–12
months/14 implants)
Average bone fill: 3 mm
Behneke Bone grafts and 25 Irrigation with iodine for 1 month + debridement with Clinic al: (1 year/18 implants)
et al 2000 bone graft implants muc operiosteal flap surgery PD: 5.3–2.2 mm
substitutes 6 months Implant surfac e dec ontamination with air abrasive instruments Clinic al: (3 year/10 implants)
surgery to 3 for 30 sec ond + saline irrigation + 7 bone c hips and 18 bone PD: 5.3–1.6 mm
• years bloc ks (Metronidazole 400 × 2 for 7 days) Radiographic : (1 year/18
Nonsubmerged implants)
Mean bone fill: 3.9 mm
Radiographic : (3 year/10
implants)
Mean bone fill: 4.2 mm
Aughtun Barrier 12 ePTFE membrane + systemic antibiotic s (tetrac yc line 200 mg × Clinic al:
et al 1992 membranes patients 1 for 12 days) + implant detoxific ation (air powder) + irrigationPI: 1.9–1.0
• 15 with saline BI: 1.1–1.1
Nonsubmerged implants PD: 5.2–4.1 mm
6–12 Radiographic
months Mean bone loss: 0.8 mm
Minor improvements on soft
tissue c onditions
Membrane exposure
Jovanovic Barrier 7 patients ePTFE membrane + systemic antibiotic s (Tetrac yc line 250 mg × Clinic al:
et al 1992 membranes 10 4 for 7 days) + implant detoxific ation (air-powder + c hloramine PI: 1.7–0.6
• implants T + saline irrigation) GI: 2.1–0.3
Nonsubmerged 6 months PD: 6.8–4.1 mm
to 3 All c linic al signs improved
years Radiographic ally:
7 defec ts showed bone fill
3 defec ts: no bone fill
Khoury Grafting materials 25 S ystemic antibiotic s Clinic al:
and + barrier patients Group 1 (12 implants): detoxific ation with c hlorhexidine 1: PD reduc tions: 5.1 mm
Buc hmann membranes 41 irrigation + c itric ac id + hydrogen peroxide + saline + bone 2. PD reduc tions: 5.4 mm
2001 implants bloc ks and partic ulate bone 3. PD reduc tions: 2.61 mm
36 Group 2 (20 implants): treatments as group 1 + ePTFE Radiographic :
months Group 3 (9 implants): treatments as group 1 + c ollagen 1. 2.4 mm bone fill
membrane (submerged) 2. 2.8 mm bone fill
3. 1.9 mm bone fill
58.6% of the barrier treated
implant sites were
c ompromised by early post
therapy c omplic ations
The additional applic ation of
barriers does not improve
the overall treatment
outc omes 3 years following
therapy
Mattout et With and without 19 patients 23 defec ts: ePTFE alone Mean suc c ess rate 68% for the
al 1995 grafting material 11 defec ts: ePTFE + DFDBA + hydrated tetrac yc line membrane group and 90%
Postoperative: 0.1% CHX + amoxic illin 500 mg (2× for 8 days) for the membrane + bone
allograft
S c hwarz Grafting 22 Granulation tissue removed + implant surfac e debridement with Clinic al:
et al 2006 materials + patients plastic c urettes + irrigation with saline 1: PD: reduc tions:
barrier 22 Group 1: Nanoc rystalline HA 2.1 mm
membranes implants Group 2: Bovine xenograft + resorbable c ollagen membrane 2. PD: reduc tions:
• 6 months 2.6 mm
Nonsubmerged “In both groups, radiologic al
observation revealed a
dec reased transluc enc y
within the intrabony
c omponent of the respec tive
periimplant bone defec t.”
Additionally, both treatments
resulted in c linic ally
reduc tions in PD and gains
of CAL at 6 months after
surgery
S c hwarz Grafting 22 Group 1: Ac c ess flap surgery + nanoc rystalline hydroxyapatite 2 patients in NHA: severe pus
et al 2008 materials + patients Group 2: Ac c ess flap surgery + natural bone mineral + c ollagen formation at 12 months
barrier 2 years membrane Clinic ally:
membranes PD:
• Group 1: 1.5 ± 0.6 mm
Nonsubmerged Group 2: 2.4 ± 0.8 mm
CAL gains:
Group 1: 1.0 ± 0.4 mm
Group 2: 2.0 ± 0.8 mm
Both treatment showed
effic ac y over 2 years.
Natural bone mineral +
c ollagen membrane showed
better c linic al improvements
Roos- Grafting 36 S ystemic antibiotic (amoxic illin 375 × 3 + metronidazole 400 Group 1:
Jansaker et materials + patients mg × 2) for 10 days starting 1 day before surgery PD reduc tion: 2.9 mm
al 2007a barrier 65 Debridement of the granulation tissue, implant surfac e Mean bone fill: 1.5 mm
membranes implants dec ontamination with hydrogen peroxide and irrigated with Group 2:
• 12 saline PD reduc tion: 3.4 mm
Nonsubmerged months Group I: Bone substitute + resorbable membrane Mean bone fill: 1.4 mm
Group 2: Bone substitute but no membrane
Roos- Grafting 12 S ystemic antibiotic s (amoxic illin 375 × 3 + metronidazole 400 Clinic al and radiographic
Jansaker et materials + patients mg × 2) for 10 days starting 1 day before surgery improvements were
al 2007b barrier 16 Debridement of granulation tissue. Implant surfac e observed.
membranes implants dec ontamination with hydrogen peroxide and irrigation with PD reduc tion: 4.2 mm
• S ubmerged 12 saline Bone substitute + resorbable membrane Mean bone fill: 2.3 mm
months
Haas et al Diode Laser 17 Implant surfac e dec ontamination with c urettage + laser + defec t Radiographic ally:
2000 treatment during patients filled with autogenous bone + ePTFE membrane + systemic 3 months from time of
surgery 24 antibiotic s for 5 days membrane removal: 21.8%
implants 9.5 months: mean bone gain:
3–9.5 36.4%
months
Bac h et al Diode Laser 30 Group 1: S c aling + 1.5% CHX + open flap debridement, apic al Group 1:
2000 treatment during patients repositioning the flap + osseous augmentation and/or 18 months: no inc reased PD,
surgery 5 years muc ogingival c orrec tions BOP or sign of inflammatory
Group 2: Treatments as group 1 + laser dec ontamination with proc ess
diode laser (810 nm w/6 W) 2 years: 2 patients with
inc rease PD, BOP and
c linic al sign of inflammation
4 years: 5 patients with
inc rease PD, BOP and
c linic al sign of inflammation
Between 3 and 5 years:
4 implants removed
Group 2:
3 years: no relapse
5 years: 5 patients with
inc rease PD and c linic al
signs of inflammation
No implant removed
S ignific ant reduc tion of gram-
negative, anaerobic bac teria
in laser group than
c onventional group
Dortbudak Diode laser 15 Implant surfac e: Curettage + rinsing with saline for 1 minute, TBO alone results in a
et al 2001 treatment during patients then stained with toluidine signific ant bac terial reduc tion
surgery 15 Half of the implants further treated with diode laser for 1 minute of P. intermedia and AA on
implants plasma flame-sprayed
c ontaminated implant surfac es,
while a c ombined treatment
leads to a reduc tion to AA, P.
gingiva lis, and P. intermedia .
Complete elimination of
bac teria was not ac hieved
Romanos CO 2 laser + bone 15 Open flap debridement w/ titanium c urettes + CO 2 laser (2.84 ± PI:
and augmentation + patients 0.83 watts) for 1 minute Preoperative: 1.01 ± 1.37
Nentwig membrane 27.10 ± Bone augmentation (bovine or autogenous bone) and c ollagen Postoperative: 0.98 ± 1.20
2008 17.83 membrane BI:
months No systemic antibiotic s Preoperative: 2.76 ± 0.35
Postoperative: 1.03 ± 0.85
PD:
Preoperative: 6.00 ± 2.03 mm
Postoperative: 2.48 ± 0.63 mm
Keratinized tissue
BI:
Preop: 2.30 ± 1.45 mm
Postop: 2.41 ± 1.39 mm
Deppe et CO 2 laser + bone 32 Group 1 (19 implants): S oft tissue resec tion + c onventional 3 implants lost in group 1
al 2007 augmentation patients dec ontamination 4 implants lost in group 2
73 Group 2 (15 implants): Treatment as group 1 + βTCP + 2 implants lost in group 3
implants autogenous bone grafts 4 implants lost in group 4
4 months Group 3 (22 implants): S oft tissue resec tion + CO 2 laser Beginning of hygiene phase
and 5 dec ontamination PI:
years Group 4 (17 implants): Treatment as group 3 + βTCP + Group 1: 1.8 ± 1.2
autogenous bone Group 2: 1.4 ± 1.2
Group 3: 1.4 ± 0.9
Group 4: 2.6 ± 0.5
BI:
Group 1: 2.7 ± 0.9
Group 2: 2.3 ± 1.4
Group 3: 2.8 ± 1.2
Group 4: 3.3 ± 0.6
PD:
Group 1: 6.2 ± 1.8
Group 2: 5.1 ± 1.7
Group 3: 5.7 ± 1.4
Group 4: 5.7 ± 1.4
Immediately prior to surgery
PI:
Group 1: 0.7 ± 0.8
Group 2: 0.9 ± 0.4
Group 3: 0.7 ± 0.8
Group 4: 0.5 ± 0.6
BI:
Group 1: 0.7 ± 0.8
Group 2: 0.5 ± 0.8
Group 3: 0.6 ± 0.3
Group 4: 1.2 ± 0.6
PD:
Group 1: 5.1 ± 1.3
Group 2: 4.8 ± 1.4
Group 3: 6.1 ± 1.6
Group 4: 5.0 ± 1.3
4 months
PI:
Group 1: 0.6 ± 0.7
Group 2: 0.6 ± 0.6
Group 3: 0.8 ± 0.6
Group 4: 0.5 ± 0.4
BI:
Group 1: 0.9 ± 0.5
Group 2: 0.6 ± 0.6
Group 3: 0.7 ± 0.6
Group 4: 0.9 ± 0.8
PD:
Group 1: 3.2 ± 0.9
Group 2: 2.4 ± 0.7
Group 3: 2.1 ± 1.3
Group 4: 1.0 ± 0.7
5 years
PI:
Group 1: 0.8 ± 0.8
Group 2: 1.1 ± 0.8
Group 3: 1.0 ± 1.3
Group 4: 1.2 ± 1.3
BI:
Group 1: 1.1 ± 1.2
Group 2: 2.1 ± 1.4
Group 3: 1.8 ± 1.1
Group 4: 1.9 ± 1.0
PD:
Group 1: 4.3 ± 1.2
Group 2: 2.5 ± 1.1
Group 3: 3.4 ± 1.5
Group 4: 2.5 ± 1.4
Treatment of peri-implantitis
may be ac c elerated by using
a CO 2 laser + soft tissue
resec tion
Long-term results in
augmented defec ts, no
differenc e between laser and
c onventional
dec ontamination
Froum et Regenerative 51 S ystemic antibiotic s (2000 mg amoxic illin or 600 mg No implant lost
al 2012 approac h implants c lindamyc in) 1 hr prior to surgery and c ontinue 500 mg PD reduc tion:
Biologic s + 38 amoxic illin tid or c lindamyc in 150 mg qid for additional 10 Group 1: 5.4 mm
bone + patients days Group 2: 5.1 mm
membrane 3 to 7.5 S urfac e dec ontamination w/ bic arbonate powder for 60 sec onds Bone level gain:
years (air abrasive devic e), 60-sec ond irrigation with sterile saline, Group 1: 3.75 mm
tetrac yc line (50 mg/mL with c otton pellets or brush for 30 Group 2: 3 mm
sec onds, then sec ond bic arbonate air abrasion 60 sec onds,
applic ation of 0.12% CHX for 30 sec onds, then 60 sec onds
reirrigation with sterile saline + enamel matrix derivatives +
anorganic bovine bone soaked in platelet derived growth
fac tor for at least 5 minutes or mineralized freeze-dried bone +
c ollagen membrane or subepithelial CT graft at area (<2 mm
KG)
Group 1: Greatest defec t depth radiographic ally
Group 2: Greatest bone loss on the fac ial of implant
Group I: Optimum Health

Group I represents implant success with optimum health conditions.
No pain is observed with palpation, percussion, or function. No mobility is
noted in any direction with loads less than 500 g of implant movement (IM).
Less than 2.0 mm of crestal bone has been lost since the placement of the
implant. This bone loss is typically a result of the implant biologic width
below the abutment connection and surface of the implant. The implant has
no history of exudate, and no radiolucency is present around the implant
body (Fig. 18.46). The probing depth is equal to or less than 5 mm and is
stable after the first year. Ideally, the bleeding index is 0 to 1. Group I
implants follow a normal maintenance program every 6 months.
FIG 18.46 (A–B) Group I represents optimum health conditions around an implant.
Less than 1.5 mm of crestal bone loss occurs during the first year of occlusal
loading from the time of prosthesis delivery. (C) A vertical bitewing radiograph can be
obtained to assess mesiodistal bone levels. (From Misch CE: Dental implant prosthetics, ed
The prognosis is very good to excellent.
Group II: Satisfactory Health

Group II implants exhibit satisfactory health and are stable, but tenderness
is observed on palpation, percussion, or function.
No observable mobility exists in the horizontal or vertical direction with
loads less than 500 g. Crestal radiographic bone loss is between 2 and 4 mm
from implant placement (Fig. 18.47). The most common cause is the early
loading bone loss related to the amount of occlusal force and the density of
the bone. No pain or bone. The probing depths may be as much as 5 to 6 mm
because of the original tissue thickness and marginal bone loss but are
stable. Bleeding upon probing index is often 1 or even 2. These implants may
be considered to have peri-implant mucositis. The treatment indicated for
group II implants consists of a stress reduction protocol for the implant
system, shorter intervals between hygiene appointments (e.g., 9 months),
reinforcement of oral hygiene instructions, annual radiographs until the
crestal bone has stabilized, and gingivoplasty or sulcus reduction procedures
where indicated. The prognosis is good to very good depending on the depth
of the implant sulcus.
FIG 18.47 (A) Group II represents satisfactory health around an implant. This
implant has lost 2 mm of crestal bone. (B) The implant crown has bleeding upon
probing index of 2. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
For pockets less than 6 mm in depth, the following can be concluded175:
1. Mechanical therapy alone or combined with chlorhexidine results in the

clinical resolution of periimplant mucositis lesions.
2. Histologically, both treatments result in minimal inflammation compatible

with health.
3. The mechanical effect alone is sufficient to attain clinical and histologic

resolution of mucositis lesions.
Group III: Compromised Survival

Group III implants are classified as compromised survival and exhibit a
slight to moderate peri-implantitis and compromised health status. Peri-
implantitis is defined as an inflammatory process affecting the tissue around
an implant that results in loss of supporting bone.
Group III implants are characterized by radiographically evident vertical
bone loss, periimplant pocket, bleeding on probing (plus occasional
suppuration), and mucosal swelling and redness but no pain upon function
(Fig. 18.48).
FIG 18.48 (A) Group III implants have a compromised health status and warrant a
surgical procedure to decrease the risk of further deterioration. Probing on the facial
of this implant indicates a 6-mm pocket, and exudate is present. (B) This implant
required surgical reentry to decontaminate the surface of the implant and remove the
noxious elements. A reduction of thread depth and a bone graft or apical-positioned
flap was indicated. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
These implants warrant more aggressive clinical therapy. No pain is

apparent in function, but tenderness may be slight on percussion or
function. No vertical or initial horizontal mobility (IM-0) is evident. Greater
than 4 mm of crestal bone loss has occurred since implant insertion but less
than half the length of the implant. Greater than 7 mm and increasing
probing depths are also present, usually accompanied by bleeding when
probing. Exudate episodes may have lasted more than 1 to 2 weeks and may
be accompanied by a slight radiolucency evident around a crestal region of
the implant.
Group III implants warrant aggressive surgical and prosthetic
intervention. Stress factors are also addressed. The prosthesis may be
removed in nonesthetic regions, or the bar may be removed under
overdentures during the surgical therapy. Modification of the occlusal
scheme and methods to decrease the forces in the afflicted regions after hard
and soft tissue surgical treatment include decreasing cantilever length,
occlusal adjustment, and occlusal splint therapy.
In cases of rapid bone changes, the prosthesis design may be modified
completely from a fixed to a removable restoration to stress relief and soft
tissue support. Additional implants to support the restoration may be
indicated, especially if the patient is unwilling to wear a removable
prosthesis.
Systemic and topical antibiotics and local chemical agents such as
chlorhexidine are indicated in the presence of exudate.
However, this method is usually of short-term benefit if the causative
agents of implant failure are not eliminated. Bacterial culture and sensitivity
tests (Oral Microbiology Testing Service, Temple University, Philadelphia;
www.temple.edu) may be indicated, especially if existing signs and
symptoms do not subside within a few weeks. Surgical management most
often consists of soft tissue removal or exposure of a portion of the implant.
Bone grafts may be used along with these approaches around the implant. A
three-step approach is implemented for this category in the following order:
(1) antimicrobial therapy (local or systemic), (2) stress reduction, and (3)
surgical intervention.
The prognosis is good to guarded, depending on the ability to reduce and
control stress after the surgical corrections have improved the soft and hard
tissue health.
Group IV: Clinical Failure

Group IV of implant health is clinical or absolute failure. The implant should
be removed under any of these conditions: (1) pain on palpation, percussion,
or function; (2) greater than 0.5 mm of horizontal mobility; (3) any vertical
mobility; (4) uncontrolled progressive bone loss; (5) uncontrolled exudate; (6)
more than 50% bone loss around the implant; (7) generalized radiolucency;
or (8) implants surgically placed but unable to be restored (sleepers).
Implants that are surgically removed or exfoliated are also in the category of
failure.
This category also includes implants surgically removed or exfoliated and
no longer in the mouth. The remaining edentulous area often is treated with
autogenous or synthetic bone graft procedures, which are performed to
replace the missing bone. After the favorable bony conditions are restored,
implants may be inserted again with a good prognosis (Fig. 18.49).
FIG 18.49 (A) Implants in group IV represent clinical failure and implants no longer
in the mouth. The center implant in this radiograph is an implant with more than 50%
loss; it is category IV. (B) The implant should be removed when group IV exudates
are present. (C) The implant is removed from the site. The implant now is converted
to group V (absolute failure). (D) The prosthesis is modified to become a three-unit
fixed partial denture. (From Misch CE: Dental implant prosthetics, ed 2, St Louis, 2015, Mosby.)
The terminology for implant failure often is confusing, with different

terms describing similar situations. Terminology for implant failure using
the time period of failure has been suggested as a primary criterion. Many
implant failures are not described ideally by the time of the complication and
are not addressed in this nomenclature.
Occasionally, the patient will not permit removal of the implant. Regardless
of whether the patient returns for implant removal, the implant is recorded
as a failure in all statistical data. The patient should be warned against the
irreversible damage to the surrounding bone with implants retained in this
condition. Consideration should be given to their removal because future
treatment may be compromised.
Conclusion
Once the surgical and prosthetic phases of implant therapy have been
completed, the work of the clinician is not over. Patients must be educated in
regards to proper maintenance of their implant-supported restorations, and
routine examinations should be performed to monitor overall health. Many
differences exist in the biologies of natural teeth vs. implants as they pertain
to periodontal status, and it is critically important that the implant dentist
recognize these differences, properly diagnose disease states, and effectively
manage issues should they arise. By understanding the etiologies of the
various peri-implant disease states, a clinician can work with the patient to
build an effective protocol of prevention.
References
1. Albrektsson T, Isidor F. Consensus report: implant therapy. Lang NP,
Karring T. Proceedings of the 1st European Workshop on Periodontology.
Quintessence: Berlin; 1994:365–369.
2. Lindhe J, Meyle J. Peri-implant diseases: Consensus report of the
sixth European workshop on periodontology. J Clin Periodontol.
2008;35:S282–S285.
3. Rateitschak KH, Rateitschak EM, Wolf HF, et al. Color atlas of dental
medicine. ed 2. Thieme: New York; 1989.
4. Listgarten M, Lang NP, Schroeder HE, et al. Periodontal tissues and
their counterparts around endosseous implants. Clin Oral Implants
Res. 1991;2:81–90.
5. Bauman GR, Rapley JW, Hallmon WW, et al. The peri-implant. Int J
6. Oh TJ, Yoon J, Misch CE, et al. The causes of early implant bone loss:
myth or science. J Periodontol. 2002;73:322–333.
7. Rams TE, Roberts TW, Tatum H Jr, et al. The subgingival microflora
associated with human dental implants. J Prosthet Dent. 1984;5:529–
534.
8. Zitzmann NU, Berglundh T. Definition and prevalence of peri-
implant diseases. J Clin Periodontol. 2008;35(8 Suppl):286–291.
9. Mombelli A, Van Oosten MAC, Schurch E, et al. The microbiota
associated with successful or failing osseointegrated titanium
implants. Oral Microbiol Immunol. 1987;2:145–151.
Excerpta Medica: Amsterdam; 1986:241–265.
14. Rudd KD, O'Leary TJ, Stumpf AJ. Horizontal tooth mobility in
carefully screened subjects. Periodontics. 1964;2:65–68.
osseointegrated implants in the treatment of the edentulous jaw. Int J
Oral Surg. 1981;10:387–416.
osseointegrated implant. Quintessence: Chicago; 1989:16–25.
17. Rangert B, Gunne J, Sullivan DY. Mechanical aspects of Brånemark
18. Fenton AH, Jamshaid A, David D. Osseointegrated fixture mobility. J
Dent Res. 1987;66:114.
19. Teerlinck J, Quirynen M, Darius MS, et al. Periotest, an objective
clinical diagnosis of bone apposition towards implants. Int J Oral
20. Meredith N, Alleyne D, Cauley P. Quantitative determination of the
stability of the implant-tissue interface using resonance frequency
analysis. Clin Oral Implants Res. 1996;7:261–267.
21. Lachmann S, Yves Laval J, Jager B, et al. Resonance frequency analysis
and damping capacity assessment. Clin Oral Implants Res. 2006;17:80–
84.
22. Huang HM, Chiu CL, Yeh CY, et al. Early detection of implant healing
process using resonance frequency analysis. Clin Oral Implants Res.
2003;14:437–443.
23. Zix J, Hug S, Kessler-Liechti G, et al. Measurement of dental implant
stability by resonance frequency analysis and damping capacity
assessment: comparison of both techniques in a clinical trial. Int J
24. Sennerby L, Roos J. Surgical determinants of clinical success of
osseointegrated oral implants: a review of the literature. Int J
Prosthodont. 1998;11:408–420.
25. Al-Jetaily S, AlFarraj Al-dosari A. Assessment of Osstell™ and
Periotest® systems in measuring dental implant stability (in vitro
study). Saudi Dent J. 2011;23(1):17–21.
26. Berglundh T, Lindhe J, Ericsson I, et al. The soft tissue barrier at
implants and teeth. Clin Oral Implants Res. 1991;2:81–90.
27. Bollen CM, Papaioanno W, Van Eldere J, et al. The influence of
abutment surface roughness on plaque accumulation and peri-
implant mucositis. Clin Oral Implants Res. 1996;7(3):201–211.
28. Lee KH, Maiden MF, Tanner AC, et al. Microbiota of successful
osseointegrated dental implants. J Periodontol. 1999;70:131–138.
29. Mombelli A, Mericske–Stern R. Microbiological features of stabile
osseointegrated implants used as abutments for overdentures. Clin
30. Mombelli A, Van Oosten MAC, Schurch E, et al. The microbiota
associated with successful or failing osseointegrated titanium
implants. Oral Microbiol Immunol. 1987;2:145–151.
31. Becker W, Becker B, Newman MG, et al. Clinical and microbiologic
findings that may contribute to dental implant failure. Int J Oral
32. Mombelli A, Buser D, Lang NP. Colonization of osseointegrated
titanium implants in edentulous patients: early results. Oral Microbiol
Immunol. 1988;3:113–120.
33. Mombelli A. Microbiology of the dental implant. Adv Dent Res.
1993;7:202–206.
34. Rams TE, Feik D, Slots J. Staphylococci in human periodontal
diseases. Oral Microbiol Immunol. 1990;5:29–32.
35. Mombelli A, Marxer M, Gaberthuel T, et al. The microbiota of
osseointegrated implants in patients with a history of periodontal
disease. J Clin Periodontol. 1995;22:124–130.
36. Leonhardt A, Adolfsson B, Lekholm U, et al. A longitudinal
microbiological study on osseointegrated titanium implants in
partially edentulous patients. Clin Oral Implants Res. 1993;4:113–120.
37. Apse P, Ellen RP, Overall CM, et al. Microbiota and crevicular fluid
collagenase activity in the osseointegrated dental implant sulcus: a
comparison of sites in edentulous and partially edentulous patients. J
Periodontal Res. 1989;24:96–105.
38. Quirynen M, Listgarten MA. The distribution of bacterial
morphotypes around natural teeth and titanium implants ad modum
Brånemark. Clin Oral Implants Res. 1990;1:8–12.
39. Vacek JS, Gher ME, Assad DA, et al. The dimensions of the human
dentogingival junction. Int J Periodontics Restorative Dent. 1994;14:154–
165.
40. James RA, Schultz RL. Hemidesmosomes and the adhesion of
junctional epithelial cells to metal implants: a preliminary report. J
Oral Implantol. 1974;4:294.
41. Ericsson I, Lindhe J. Probing at implants and teeth: an experimental
study in the dog. J Clin Periodontol. 1993;20:623–627.
42. Steflik DE, McKinney RV, Koth DL. Ultrastructural (TEM) observations
of the gingival response to the single crystal sapphire endosteal
implant. J Dent Res. 1982;61:231.
43. Cochran DL, Herman JS, Schenk RK, et al. Biologic width around
titanium implants: a histometric analysis of the implanto-gingival
junction around unloaded and loaded submerged implants in the
canine mandible. J Periodontol. 1997;68:186–198.
44. Schroeder A, Pohler O, Sutter F. Tissue reaction to a titanium hollow
cylinder implant with titanium plasma sprayed surface. Schweiz
Monatsschr Zahnmed. 1976;86:713–727.
45. Abrahamsson I, Berglundh T, Lindhe J. The mucosal barrier following
abutment disreconnection: an experimental study in dogs. J Clin
Periodontol. 1997;24:568–572.
46. Ericsson I, Lindhe J. Probing at implants and teeth: an experimental
study in the dog. J Clin Periodontol. 1993;20:623–627.
47. Best AM, Burmeister JA, Gunsolley JC, et al. Reliability of attachment
loss measurements in a longitudinal clinical trial. J Clin Periodontol.
1990;17:564–569.
48. Page RC. Summary of outcomes and recommendations of the
workshop on CPITN. Int Dent J. 1994;44:589–594.
49. Lekholm U, Adell R, Lindhe J, et al. Marginal tissue reactions at
osseointegrated titanium fixtures. II. A cross-section retrospective
study. Int J Oral Maxillofac Surg. 1986;15:53–61.
50. Stefani LA. The care and maintenance of the dental implant patient. J
Dent Hygiene. 1988;62:447–466.
51. Adell R, Lekholm U, Rockler G, et al. Marginal tissue reactions at
osseointegrated titanium fixtures. I. A 3-year longitudinal prospective
study. Int J Oral Maxillofac Implants. 1986;15:39–52.
52. Kirsch A, Mentag P. The IMZ endosseous two phase implant system: a
complete oral rehabilitation treatment concept. J Oral Implantol.
1986;12:576–589.
53. Deporter HS, Friedland B, Watson P, et al. A clinical and radiographic
assessment of a porous surface titanium alloy dental implant in dogs.
Int J Oral Implantol. 1987;4:31–37.
54. Jepsen S, Ruhling A, Jepsen K, et al. Progressive peri-implantitis.
Incidence and prediction of peri-implant attachment loss. Clin Oral
Implants Res. 1996;7:133–142.
55. Quirynen M, Naert I, Teerlinck J, et al. Periodontal indices around
osseointegrated oral implants supporting overdentures. Schepers E,
Naert J, Theunier G. Overdentures on oral implants. Leuwen University
Press: Leuwen, Belgium; 1991:287–291.
56. Steflik DE, Koth DC, McKinney RV Jr. Human clinical trials with the
single crystal sapphire endosteal dental implant: three year results,
statistical analysis, and validation of an evaluation protocol. J Oral
Implantol. 1987;13:39–53.
57. Misch CE. Early crestal bone loss etiology and its effect on treatment
planning for implants. Postgrad Dent. 1995;2:3–17.
58. Quirynen M, Naert I, van Steenberghe D. Fixture design and overload
influence on marginal bone loss and fixture success in the Brånemark
implant system. Clin Oral Implants Res. 1992;3:104–111.
59. Albrektsson T, Zarb GA, Worthington P, et al. The long-term efficacy
of currently used dental implants: a review and proposed criteria of
success. Int J Oral Maxillofac Implants. 1986;1:11–25.
60. Misch CE, Suzuki JB, Misch-Dietsh FD, et al. A positive correlation
between occlusal trauma and peri–implant bone loss: literature
support. Implant Dent. 2005;14:108–114.
61. Rhinelander FW. Circulation of bone. Bourne GH. The biochemistry and
physiology of bone. Academic Press: New York; 1972:89–91.
62. Brisman EL. The effect of speed, pressure and time on bone
temperature during the drilling of implant sites. Int J Oral Maxillofac
Implants. 1996;11:35–37.
63. Manz MC. Radiographic assessment of peri-implant vertical bone loss:
DIRG Implant Report No 9. J Oral Maxillofac Surg. 1997;55(Suppl
5):62–71.
64. Hoar JE, Beck GH, Crawford EA, et al. Prospective evaluation of
crestal bone remodeling of a bone density based dental system. Comp
Cont Educ Dent. 1998;19:17–24.
65. Glickman I, Samelos JB. Effect of excessive forces upon the pathway of
gingival inflammation in humans. J Periodontol. 1965;36:141–147.
66. Lekholm U, Ericsson I, Adell R, et al. The condition of the soft tissues
of tooth and fixture abutments supporting fixed bridges: a
microbiological and histological study. J Oral Clin Periodontol.
1986;13:558–562.
67. Kent JN, Homsby CA. Pilot studies of a porous implant in dentistry
and oral surgery. J Oral Surg. 1972;30:608.
68. Koutsonikos A. Implants: success and failure—a literature review.
Ann R Australas Coll Dent Surg. 1998;14:75–80.
69. Tarnow D, Stahl S, Maner A, et al. Human gingival attachment:
responses to subgingival crown placement marginal remodeling. J
70. Lindhe J, Berglundh T, Ericsson I, et al. Experimental breakdown of
peri–implant and periodontal tissues. A study in the beagle dog. Clin
71. Wallace S, Tarnow D. The biologic width around implants. [International
Congress Oral Implant Meeting, Munich, Germany] October 1995.
72. James RA, Keller EE. A histopathological report on the nature of the
epithelium and underlying connective tissue which surrounds oral
implant. J Biomed Mat Res. 1974;8:373–383.
73. Gould TRL, Westbury L, Brunette DM. Ultrastructural study of the
attachment of human gingival to titanium in vivo. J Prosthet Dent.
1984;52:418–420.
74. Barboza EP, Caúla AL, Carvalho WR. Crestal bone loss around
submerged and exposed unloaded dental implants: a radiographic
and microbiological descriptive study. Implant Dent. 2002;11:162–169.
75. Van Steenberghe D, Tricio J, Van den Eynde E, et al. Soft and hard
tissue reactions towards implant design and surface characteristics
and the influence of plaque and/or occlusal loads. Davidovitch Z. The
biologic mechanism of tooth eruption, resorption and replacement by
implants. Harvard Society for the Advancement of Orthodontics:
Boston; 1994:111–114.
76. Lang NP, Wilson TG, Corbet EF. Biologic complications with dental
implants: their prevention, diagnosis and treatment. Clin Oral
Implants Res. 2000;11(Suppl):146–155.
77. Hermann JS, Buser D, Schenk RK, et al. Crestal bone changes around
titanium implants: a histometric evaluation of unloaded non-
submerged and submerged implants in the canine mandible. J
Periodontol. 2000;71:1412–1424.
78. Karolyi M. Beobachtungen über Pyorrhea alveolaris. Osterenorichisch-
Ungarische viertel jahresschrift fur Zahnheilkunde. 1991;17:279.
79. Glickman I. Clinical significance of trauma from occlusion. J Am Dent
Assoc. 1965;70:607–618.
80. Waerhaug J. The infrabony pocket and its relationship to trauma from
occlusion and subgingival plaque. J Periodontol. 1979;50:355–365.
81. Lindhe J, Nyman S, Ericsson I. Trauma from occlusion. Lindhe J.
Clinical periodontology and implant dentistry. ed 4. Blackwell: Oxford;
2003.
82. Cowin SC, Hegedus DA. Bone remodeling I: theory of adaptive
elasticity. J Elasticity. 1976;6:313–326.
83. Cowin SC, Moss-Salentign L, Moss ML. Candidates for the
mechanosensory system in bone. J Biomechan Engineer. 1991;113:191–
197.
84. Kummer BKF. Biomechanics of bone: mechanical properties,
functional structure, functional adaptation. Fung YC, Perrone H,
Anliker M. Biomechanics: foundations and objectives. Prentice-Hall:
Englewood Cliffs; 1972:289–299.
85. Frost HM. Bone “mass” and the “mechanostat”: a proposal. Anat Rec.
1987;219:1–9.
86. Chiba J, Rubash JE, Kim KJ, et al. The characterization of cytokines in
the interface tissue obtained from failed cementless total hip
arthroplasty with and without femoral osteolysis. Clin Orthop.
1994;300:304–312.
87. Baumeister T, Avallone EA. Marks' standard handbook of mechanical
engineers. ed 8. McGraw-Hill: New York; 1978.
88. Bidez M, McLoughlin S, Lemons JE. FEA investigations in plate-form
dental implant design. Proceedings of the First World Congress of
Biomechanics. CA: San Diego; 1990.
89. Appleton RS, Nummikoski PV, Pigmo MA, et al. Periimplant bone
changes in response to progressive osseous loading. J Dent Res.
1997;76:412 [Special issue].
90. Hoshaw S. Investigation of bone remodeling and remodeling at a loaded
bone-implant interface [thesis]. Rensselaer Polytechnic Institute: Troy,
NY; 1992.
occlusal overload on peri-implant tissue. Part 3: a histologic study in
92. Duyck J, Ronold HJ, Oosterwyck HV, et al. The influences of static and
dynamic loading on marginal bone reactions around osseointegrated
implants: an animal experimental study. Clin Oral Implant Res.
2001;12:207–218.
93. Lindquist JW, Rockler B, Carlsson GE. Bone resorption around fixtures
in edentulous patients treated with mandibular fixed tissue
integrated prostheses. J Prosthet Dent. 1988;59–63.
94. Naert I, Quirynen M, Van Steenberghe D, et al. A study of 589
consecutive implants supporting complete fixed prostheses. Part II:
prosthetic aspects. J Prosthet Dent. 1992;68:949–956.
95. Rangert B, Krogh PHJ, Langer B, et al. Bending overload and implant
fracture: a retrospective clinical analysis. Int J Oral Maxillofac
Implants. 1995;10:326–334.
96. Rosenberg ES, Torosian JP, Slots J. Microbial differences in 2 clinically
distinct types of failures of osseointegrated implants. Clin Oral
Implants Res. 1991;2:135–144.
97. Uribe R, Penarrocha M, Sanches JM, et al. Marginal periimplantitis
due to occlusal overload: a case report. Med Oral. 2004;9:159–162.
98. Leung KC, Chew TW, Wat PY, et al. Peri-implant bone loss:
management of a patient. Int J Oral Maxillofac Implant. 2001;16:273–
277.
99. Roberts WE, Turley DK, Brezniak N, et al. Bone physiology and
100. Misch CE. Consideration of biomechanical stress in treatment with
dental implants. Dent Today. 2007;25:80–85.
101. Roberts WE, Turley DK, Brezniak N, et al. Bone physiology and
102. Roberts WE, Garetto LP, De Castro RA. Remodeling of devitalized
bone threatens periosteal margin integrity of endosseous titanium
implants with threaded or smooth surfaces: indications for
provisional loading and axially directed occlusion. J Indiana Dent
Assoc. 1989;68:19–24.
103. Piatelli A, Ruggeri A, Franchi M, et al. An histologic and
histomorphometric study of bone reactions to unloaded and loaded
non-submerged single implants in monkeys: a pilot study. J Oral
Implant. 1993;19:314–319.
104. Appleton RS, Nummikoski PV, Pigno MA, et al. A radiographic
assessment of progressive loading on bone around single
osseointegrated implants in the posterior maxilla. Clin Oral Implants
Res. 2005;16:161–167.
105. Rotter BE, Blackwell R, Dalton G. Testing progressive loading of
endosteal implants with the periotest—a pilot study. Implant Dent.
1996;5:28–32.
106. Zechner W, Trinki N, Watzek G, et al. Radiographic follow-up of peri-
implant bone loss around machine-surfaced and rough-surfaced
interforaminal implants in the mandible functionally loaded for 3 to
7 years. Int J Oral Maxillofac Implants. 2004;19:216–222.
107. Karousis IK, Brägger U, Salvi G, et al. Effect of implant design on
survival and success rates of titanium oral implants: a 10-year
prospective cohort study of the ITI Dental Implant System. Clin Oral
Implant Res. 2004;15:8–17.
108. Winemaker MJ, Thorhill TS. Complications of joint replacement in
the elderly. Rosen CJ, Glovacki J, Bilezikian JP. The aging skeleton.
Academic Press: San Diego; 1999:168–178.
109. Hornhill TS, Ozuna RM, Shortkeoff S, et al. Biochemical and
histologic evaluation of the synovial-like tissue around failed (loose)
total joint replacement prostheses in human subject and a canine
model. Biomaterials. 1990;11:69–72.
110. Morrey BF. Difficult complications after hip joint replacement:
dislocation. Clin Orthop Relat Res. 1997;334:179–187.
111. White SC, Pharoah M. Oral radiology: principles and interpretation. ed 5.
Mosby: St Louis; 2004.
112. Pontoriero R, Tonelli MP, Carnevale G, et al. Experimentally induced
peri-implant mucositis. A clinical study in humans. Clin Oral Impl
Res. 1994;5(4):254–259.
113. Salvi GE, Aglietta M, Eick S, et al. Reversibility of experimental peri-
implant mucositis compared with experimental gingivitis in humans.
Clin Oral Impl Res. 2012;23(2):182–190.
114. Zitzmann NU, Berglundh T, Marinello CP, Lindhe J. Experimental
peri-implant mucositis in man. J Clin Periodontol. 2001;28:517–523.
115. Sennerby L, Lekholm U. The soft tissue response to titanium
abutments retrieved from humans and reimplanted in rats. A light
microscopic pilot study. Clin Oral Impl Res. 1993;4:23–27.
116. Rosen P, Clem D, Cochran D, et al. Peri-implant mucositis and peri-
implantitis: a current understanding of their diagnoses and clinical
implications. J Periodontol. 2013;84(4):436–443.
117. Costa FO, Takenaka-Martinez S, Cota LO, et al. Peri-implant disease
in subjects with and without preventive maintenance: a 5-year follow-
up. J Clin Periodontol. 2012;39(2):173–181.
118. Lang NP, Bragger U, Walther D, Beamer B, Kornman KS. Ligature-
induced peri-implant infection in cynomolgus monkeys. I. Clinical
and radiographic findings. Clin Oral Implants Res. 1993;4(1):2–11.
119. Bassetti M, Schär D, Wicki B, et al. Anti-infective therapy of peri-
implantitis with adjunctive local drug delivery or photodynamic
therapy: 12-month outcomes of a randomized controlled clinical trial.
Clin Oral Implants Res. 2014;25(3):279–287.
120. Hasturk H, Nguyen DH, Sherzai H, et al. Comparison of the impact of
scaler material composition on polished titanium implant abutment
surfaces. J Dent Hyg. 2013;87(4):200–211.
121. Anastassiadis PM, Hall C, Marino V, et al. Surface scratch assessment
of titanium implant abutments and cementum following
instrumentation with metal curettes. Clin Oral Investig.
2015;19(2):545–551.
122. Sãnchez-Garcãs M, Gay-Escoda C. Peri-implantitis. Med Oral Pathol
Oral Cir Bucal. 2004;9:63–74.
123. Dennison DK, Huerzeler MB, Quinones C. Caffese RG: Contaminated
implant surfaces: an in vitro comparison of implant surface coating
and treatment modalities for decontamination. J Periodontol.
1994;65(10):942–948.
124. Faria G, Cardoso CR, Larson RE, et al. Chlorhexidine-induced
apoptosis or necrosis in L929 fibroblasts: a role for endoplasmic
reticulum stress. Toxicol Appl Pharmacol. 2009;234(2):256–265.
125. Bürgers R, Witecy C, Hahnel S, Gosau M. The effect of various topical
peri-implantitis antiseptics on Staphylococcus epidermidis, Candida
albicans, and Streptococcus sanguinis. Arch Oral Biol. 2012;57(7):940–
947.
126. Schou S, Holmstrup P, Jørgensen T, et al. Implant surface preparation
in the surgical treatment of experimental peri-implantitis with
autogenous bone graft and ePTFE membrane in cynomolgus
monkeys. Clin Oral Implants Res. 2003;14(4):412–422.
127. Hall EE, Meffert RM, Hermann JS, et al. Comparison of bioactive glass
to demineralized freeze-dried bone allograft in the treatment of
intrabony defects around implants in the canine mandible. J
Periodontol. 1999;70(5):526–535.
128. Loesch WJ. Nonsurgical treatment of patients with periodontal
disease. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
1996;81:533–543.
129. Guerrero A, Griffiths GS, Nibali L, et al. Adjunctive benefits of
systemic amoxicillin and metronidazole in non-surgical treatment of
generalized aggressive periodontitis: a randomized placebo-
controlled clinical trial. J Clin Periodontol. 2005;32(10):1096–1107.
130. Pavicic M, Van Winkelhoff AJ, Dougué NH, et al. Microbiological and
clinical effects of metronidazole and amoxicillin in Actinobacillus
actinomycetemcomitans associated periodontitis: a 2-year evaluation.
J Clin Periodontol. 1994;21(2):107–112.
131. Haffajee AD, Smith C, Torresyap G, et al. Efficacy of manual and
powered toothbrushes (II). Effect on microbiological parameters. J
Clin Periodontol. 2001;28(10):947–954.
132. Chung DM, Oh TJ, Shotwell JL, et al. Significance of keratinized
mucosa in maintenance of dental implants with different surfaces. J
Periodontol. 2006;77(8):1410–1420.
133. Kracher CM, Schmeling Smith W. Oral health maintenance of dental
implants. [Available at] http://www.dentalcare.com.
134. Renvert S, Roos-Jansaker AM, Lindahl C, et al. Infection at titanium
implants with or without a clinical diagnosis of inflammation. Clin
135. Rodrigues DC, Valderrama P, Wilson TG, et al. Titanium corrosion
mechanisms in the oral environment: a retrieval study. Materials.
2013;6:5258–5274.
136. Wachi T, Shuto T, Shinohara Y, et al. Release of titanium ions from an
implant surface and their effect on cytokine production related to
alveolar bone resorption. Toxicology. 2015;327:1–9.
137. Lindquist LW, Carlsson GE, Jemt T. Association between marginal
bone loss around osseointegrated mandibular implants and smoking
habits: a 10-year follow-up study. J Dent Res. 1997;76:1667–1674.
138. Ferreira SD, Silva GLM, Cortelli JR, et al. Prevalence and risk variables
for peri-implant disease in Brazilian subjects. J Clin Periodontol.
2006;33:929–935.
139. Costa FO, Takenaka-Martinez S, Cota LOM, et al. Peri-implant disease
in subjects with and without preventive maintenance: a 5-year follow-
up. J Clin Periodontol. 2012;39:173–181.
140. Renvert S, Polyzois I, Claffey N. How do implant surface
characteristics influence peri-implant disease? J Clin Periodontol.
2011;38(Suppl 11):214–222.
141. Petersilka GJ, Steinmann D, Haberlein I, et al. Subgingival plaque
removal in buccal and lingual sites using a novel low abrasive air-
polishing powder. J Clin Periodontol. 2003;30:328–333.
142. Schwarz F, et al. Laser application in non-surgical periodontal
therapy: a systematic review. J Clin Periodontol. 2008;35(Suppl 8):29–
44.
143. Nicholson D, Blodgett K, Braga C, et al. Pulsed Nd:YAG laser treatment
for failing dental implants due to peri-implantitis Lasers in Dentistry
XX, SPIE Vol. 8929 89290H-1. March 2014.
143a. Suzuki JB. Salvaging implants with an Nd:YAG Laser: a novel
approach to a growing problem. Compend Contin Educ Dent.
2015;36(10):756–761.
144. Figuero E, Graziani F, Sanz I, et al. Management of peri-implant
mucositis and peri-implantitis. Periodontol 2000. 2014;66(1):255–273.
145. Heitz-Mayeld LJA, Salvi GE, Mombelli A, et al. Anti-infective surgical
therapy of peri-implantitis. A 12-month prospective clinical study.
Clin Oral Impl Res. 2012;23:205–210.
146. Schwarz F, Sahm N, Becker J. Combined surgical therapy of advanced
peri-implantitis lesions with concomitant soft tissue volume
augmentation. A case series. Clin Oral Implants Res. 2014;25(1):132–
136.
147. Froum SJ, Froum SH, Rosen P. Successful management of peri-
implantitis with a regenerative approach: a consecutive case series of
51 treated implants with 3- to 7.5-year follow-up. Int J Periodontics
Restorative Dent. 2012;32:11–20.
148. Wennstrom JL. Lack of association between width of attached gingiva
and development of soft tissue recession: a 5-year longitudinal study.
J Clin Periodontol. 1987;14:181–184.
149. Kennedy J, Bird W, Palcanis K, et al. A longitudinal evaluation of
varying widths of attached gingiva. J Clin Periodontol. 1985;12:667.
150. Lang NP, Loe H. The relationship between the width of keratinized
gingiva and gingival health. J Periodontol. 1972;43:623–627.
151. Stetler K, Bissada NF. Significance of the width of keratinized gingiva
on the periodontal status of teeth with submarginal restoration. J
Periodontol. 1987;58:696–700.
152. Berglundh T, Lindhe T, Jonsson K, et al. The topography of the
vascular systems in the periodontal and peri-implant tissues in the
dog. J Clin Periodontol. 1994;21:189–193.
153. Kirsch A, Ackermann KL. The IMZ osteointegrated implant system.
Dent Clin North Am. 1989;33:733–791.
154. Warrer K, Buser D, Lang NP, et al. Plaque-induced peri-implantitis in
the presence or absence of keratinized mucosa: an experimental
study in monkeys. Clin Oral Implants Res. 1995;6:131–138.
implants. Clark JW. Clinical dentistry. Harper and Row: Hagerstown,
MD; 1984:45–47.
156. Ono Y, Nevins M, Cappetta M. The need for keratinized tissue for
implants. Nevins M, Mellonig JT. Implant therapy. Quintessence:
Chicago; 1998:23–28.
157. Meffert RM, Langer B, Fritz ME. Dental implants: a review. J
Periodontol. 1992;63:859–870.
158. Block MS, Kent JN. Factors associated with soft- and hard-tissue
compromise of endosseous implants. J Oral Maxillofac Surg.
1990;48:1153–1160.
159. Esposito M, Coulthard P, Thomsen P, et al. The role of implant surface
modification, shape and material on the success of osseointegrated
dental implants: a Cochrane systematic review. Eur J Prosthodontics
Restorative Dent. 2005;13:15–31.
160. Chung DM, Oh TJ, Shotwell JL, Misch CE, et al. Significance of
keratinized mucosa in maintenance of dental implants with different
surfaces. J Periodontol. 2006;77:1410–1420.
161. Simons AM, Darany DG, Giordano JR. The use of free gingival grafts
in the treatment of peri-implant soft tissue complications: clinical
report. Implant Dent. 1993;2(1):27–30.
162. Payne AG, Solomons YF, Tawse-Smith A, et al. Inter-abutment and
peri-abutment mucosal enlargement with mandibular implant
overdentures. Clin Oral Impl Res. 2001;12(2):179–187.
163. Bhatia V, Mittal A, Parida AK, et al. Amlodipine induced gingival
hyperplasia: a rare entity. Int J Cardiol. 2007;122(3):e23–e24.
164. Javed F, Al-Hezaimi K, Almas K, et al. Is titanium sensitivity
associated with allergic reactions in patients with dental implants? A
systematic review. Clin Impl Dent Rel Res. 2013;15(1):47–52.
165. Pilatti GL, Sampaio JE. The influence of chlorhexidine on the severity
of cyclosporine A-induced gingival overgrowth. J Periodontol.
1997;68(9):900–904 [Erratum in: J Periodontol 1998 69(1):102, 1998].
166. Schnitman PA, Shulman LB. Recommendations of the consensus
development conference on dental implants. J Am Dent Assoc.
1979;98:373–377.
167. Cranin AN, Silverbrand H, Sher J, et al. The requirements and clinical
performance of dental implants. CRC Press: Boca Raton, FL; 1982:42–
45. Smith DC, Williams DF. Biocompatibility of dental materials. vol 4.
implants. Clark JW. Clinical dentistry. Harper and Row: Harperstown,
PA; 1984:78–81.
169. Albrektsson T, Zarb GA, Worthington P, et al. The long-term efficacy
of currently used dental implants: a review and proposed criteria of
success. Int J Oral Maxillofac Implants. 1986;1:1–25.
170. Albrektsson T, Zarb GA. Determinants of correct clinical reporting.
Int J Prosthodont. 1998;11:517–521.
171. Misch CE. Implant quality scale: a clinical assessment of the health-
disease continuum. Oral Health. 1998;88:15–25.
172. Misch CE, Perel ML, Wang HL, et al. Implant success, survival, and
failure: The International Congress of Oral Implantologists (ICOI)
Pisa Consensus Conference. Implant Dent. 2008;17(1):5–15.
173. Council on Dental Care Programs. reporting periodontal treatment
under dental benefit plans. J Am Dent Assoc. 1988;17:371–373.
174. Misch CE. Implant success or failure: clinical assessment in implant
dentistry. Misch CE. Contemporary implant dentistry. Mosby: St Louis;
1993:782–799.
175. Trejo PM, Bonaventura G, Weng D, et al. Effect of mechanical and
antiseptic therapy on peri-implant mucositis: an experimental study
in monkeys. Clin Oral Implants Res. 2006;17:294–304.
19
Medicolegal Aspects of Implant
Dentistry
Randolph R. Resnik, Francis R. DeLuca
In dentistry today, dental practitioners are exposed to an array of possible

legal liability claims. These claims may arise from the various components of
civil, criminal, and administrative legal systems at either the state or federal
level (Fig. 19.1). In the field of oral implantology an ever-increasing number
of legal claims are occurring. For this reason, any discussion of implant
dentistry complications must necessarily include a review of the legal risks
and ramifications associated with this type of treatment. Practitioners
engaged in oral implantology must practice effective risk management, or
they may predispose themselves to the loss of time and money associated
with unwanted litigation and administrative proceedings. Although the
possibility of legal claims may be an accepted risk and complication of
implant dentistry, it is largely an avoidable risk.
FIG 19.1 US legal system. Dental practitioners are subject to a wide array of
potential legal issues within the statutory, civil, and criminal legal systems. The most
common legal action to be brought against a dental practitioner is a civil tort law
negligence claim.
As a dentist, the chances of being named in a medical negligence lawsuit

are approximately 1 : 200 per year depending upon your jurisdiction, and to
some extent, your specialty.1 According to recent data from the National
Practitioner Data Bank (NPDP), 11% of medical malpractice cases involved
the practice of dentistry. NPDP studies show that approximately 8500 dentists
in the United States are named as defendants each year in dental malpractice
suits, with an average payout of approximately $68,000.2 Over 97% of these
payments are from out-of-court settlements prior to trial.3 As the cost of
modern dental care rises, it is likely these numbers will only grow because it
becomes more economically worthwhile to pursue dental malpractice claims.
On the other hand, risk is something that can and should be managed and
avoided. However, in reality, even with the best planning and care, oral
implantology complications may predispose the practitioner to legal action
(Box 19.1).
Box 19.1
Most Common Types of Malpractice in
Dentistry
• Lack of informed consent
• Failure to refer to a specialist
• Failure to properly treat complications of care (e.g., infection, paresthesia)
• Failure to properly perform prosthodontic work, including crown and

bridgework
• Failure to diagnose various conditions, including infection, periodontal

disease, tumors, and cancer
• Failure to properly treat periodontal disease
• Failure to render appropriate endodontic care
• Failure to appropriately place, treat, or follow up with all types of implants
• Failure to appropriately extract teeth or improper extraction of teeth
• Failure to appropriately treat with orthodontics
• Failure to diagnose or treat TMJ dysfunction
• Failure to properly supervise or oversee actions of employees, actual

agents, or apparent agents
• Slips, falls, burns, or cuts while in dental chair or office
• Anesthesia incidents
The prevalence and type of complications in implant dentistry are

increasing and evolving over time. This is most likely due to three factors.
First, there is an increase in the number of implants being placed every year.
Secondly, more complex and difficult procedures with higher morbidity are
being performed. And lastly, more dentists with limited training are
providing implant treatment, including practitioners with a lack of
experience and knowledge in the prevention and treatment of complications.
The standard of care in oral implantology is not precise in part because there
is an absence of a recognized specialty of oral implantology. Yet the standard
of care in oral implantology is an ever-rising bar due to the increasing
complexity of cases and the expertise demanded by patients.
Unfortunately, complications do occur in implant dentistry, and they are
sometimes unavoidable. In the early days of oral implantology, complications
were merely termed “risks” of the procedure. In today's litigious society,
patients often equate complications with “malpractice” or a deviation from
the standard of care by the practitioner. Many patients have invested
substantial amounts of time, energy, and money in their appearance and
dental care. When complications arise or expectations are not met, patients
often demand answers and seek a legal course of action. Strategically and
correctly managing complications is paramount in the prevention of medical
negligence liability claims.
Implant dentistry is an acquired skill requiring extensive training,
continuous practice, and refinement of skills and technique. Some dentists
will take a 2-day weekend course sponsored by a dental implant
manufacturer and assume they have the knowledge and skills necessary to
treat even the most difficult cases and complications. However, they are
mistaken, and this has been substantiated through various studies. Lambert
et al, in a landmark study evaluating inexperienced surgeons (<50 implants
placed), found that doctors early on their learning curve were twice as likely
to have failed implants in comparison to experienced surgeons.4
The authors have noticed a trend in dental malpractice litigation termed
the “500–4000 syndrome.” Dental implant litigation seems to spike in the
first 500 implants placed by a dentist simply because dentists on the front
end of the learning curve are more likely to experience complications. The
good news is that, with additional experience, the number of litigation cases
levels out in the range of 500–4000 implant placements. However, a second
spike of litigation occurs after the placement of approximately 4000 implants.
Clinicians often become complacent, and there is a greater chance to “take
shortcuts” in the treatment of implant patients. They tend to be lax with their
preoperative assessment (clinical and radiographic evaluation), do not keep
current with the literature, and fail to attend appropriate continuing
education programs while managing their busy practices.
The malpractice litigation process is embarrassing, time consuming, and
financially and psychologically draining on the practitioner. This long, drawn-
out malpractice process has been shown to have an average time from injury
to resolution of 5 years, with 33% of cases lasting over 6 years.5 However,
dental implant practitioners can take proactive steps to decrease their risk
liability and to minimize their exposure. In this chapter we will examine the
best ways to avoid lawsuits and also review the litigation process, including
presuit, the discovery process, and malpractice trial (Fig. 19.2).
FIG 19.2 Anatomy of a civil malpractice suit. There are three components of a
dental malpractice case: (1) the presuit period, (2) the discovery period, and (3) trial.
Presuit
When a patient enters into a civil lawsuit, they will initiate a process termed
litigation. Litigation is governed by various rules of civil procedure (i.e., the
court's rules and standards during a lawsuit) in the state and federal courts.
The first part of the litigation is called the “presuit period.” The presuit
period is very important because the clinician will usually receive notice of
commencement of a legal action, and they must react promptly. Most doctors
are not taken by surprise when a patient initiates legal action against them
because there are often subtle signs. These include the patient not returning
for scheduled appointments, failure to return phone calls from the doctor or
the office, or refusing to pay their bill. More significant indications that are
consistent with a patient bringing a legal action include a formal notice or a
request for their dental chart by the patient, another practitioner, or a
patient's lawyer. Most often in such situations verbal communication
between the dentist and patient has deteriorated or may have become
nonexistent.
Notification
Records Request.
The initiation of a lawsuit usually starts with a request for records. When
presented with a records request from a patient, it is imperative that the
practitioner not ignore the request no matter how unfounded the potential
claim may be. In most states, there is a statute (law) that governs the time
period that the dental provider has to comply with the request. Refusing to
fulfill a patient's request for a copy of their treatment record in a timely
manner will only complicate and exacerbate the situation and may prejudice
the dentist's position in future litigation. This will also cast the doctor in a
negative light from the outset of the litigation in the eyes of the court and
also with the state dental board. Although the doctor owns the actual dental
record, the patient owns the diagnostic images, and they are entitled to a
copy of both parts of their dental records. When a patient is denied access to
their records by a dentist, their only recourse may be to file a complaint with
the state board of dentistry. Under those circumstances, it is unlikely the
state board will be sympathetic to the claims or concerns of the practitioner
and may expose the dentist to discipline (Fig. 19.3).
FIG 19.3 Records request form. To ensure compliance with HIPAA laws, the
patient should always sign a patient request form prior to any documents being
released.
Time to respond.
The time to respond to a request by a patient for their records is dictated
specifically by individual state law, with the average deadline to provide
records being approximately 30 days. Some states do not have associated
time periods (e.g., Alaska) or use terminology such as “a reasonable time”
(e.g., Alabama).6 A records request does have to be accompanied by a
HIPAA-compliant medical authorization form.
Documentation of records request.

As a matter of office policy, no records should be provided by a dental office
or its personnel to a patient either “in person” or via written request without
the treating doctor's prior approval. In doing so, the doctor will be able to
ensure the patient is provided with the exact information requested. The
patient chart should be documented accordingly, including notations
documenting the exact records provided (i.e., make an additional copy), the
date the records are delivered, and the manner in which the records were
provided (e.g., US mail, fax, wire, or email). It is best to keep records
establishing the exact date such materials were provided (example, “certified
mail/return receipt requested”). Documenting the date the record request
was made by the patient is especially important where the statute of
limitations (i.e., maximum time after the alleged negligent event to initiate
legal action to pursue a claim relating to it or otherwise it may be deemed
“time barred” by law) may become an issue with respect to the filing of the
lawsuit. The term time-bar refers to a legal claim that is barred by the passage
of time under a statute of limitations.
Official Notice Letter.

The dentist may also receive a letter from the patient's attorney informing
them of their intent to initiate a legal action on behalf of a patient and that
the attorney is investigating the matter. Some states require that the patient
provide a “Presuit Notice” prior to the formal filing of a lawsuit. This will
initiate the presuit period, which allows the patient and doctor the ability to
obtain records and provides both sides an opportunity to settle the matter
prior to litigation. The form and method of the notice of commencing a
presuit is usually dictated by state statute or rule. For example, the state of
Florida requires that notice be provided by certified US mail or return receipt
requested (Fig. 19.4).
FIG 19.4 Official notice letter. In some states an attorney is required to send to the
doctor a letter informing them of an initiation of a legal action.
Requirements After Receiving Notice
The first step or action that an insured dentist should take after receiving
notice is to inform their dental malpractice insurance carrier of the
possibility of a malpractice suit. By placing the dental malpractice insurance
carrier on notice, the dentist will have access to immediate guidance and
legal advice from the carrier or an appointed attorney for all aspects of the
ensuing process. In general, by informing the carrier, no adverse
consequences will result, such as losing coverage or increased premiums.
Responsibility of the Insured Dentist

Proactive response.
If the doctor receives a request for dental records from the patient or their
attorney, a proactive response to inform the insurance carrier is mandatory.
To preserve malpractice coverage, most policies require the insured to inform
the carrier with prompt notice of any potential claims. An insured dentist's
failure to provide notice in a timely manner could potentially jeopardize the
carrier's obligations both to defend and to indemnify (pay for the damage or
loss allegedly suffered by the patient) in the potential lawsuit. The dental
malpractice insurance carrier requires immediate notice to become involved
as early possible in the matter of a dental malpractice claim.
Cooperation.
Most dental malpractice insurance policies contain a “cooperation clause,”
which requires the insured (dentist) to cooperate in the defense of a legal
claim. If the insured dentist fails to cooperate with the defense of the suit,
the malpractice carrier may refuse to indemnify for a lawsuit. No matter how
much of a nuisance or how frivolous a dentist may feel a lawsuit may be, it is
important to take the time to cooperate in defending it.
Responsibility of Insurance Carrier

Defense and indemnity.
The insurance carrier has two main obligations to the insured with respect to
malpractice policies. The “duty to defend” will require the insurance carrier
to retain legal counsel for the insured in the defense against any legal claims
brought against the dentist. There also exists the “duty to indemnify,” which
requires the insurance carrier to pay for any settlement or judgment on
claims within the policy limits.
Assignment of counsel.
An insurance carrier has an obligation to retain legal counsel when a legal
action is brought against a dentist. Typically, the insurance carrier will assign
an attorney who has had past experience with the type of malpractice suit
filed. All attorneys' fees will be paid by the carrier; however, a dental
malpractice insurance carrier will not pay for personal counsel hired by a
dentist. Most insurance carriers will take into consideration a dentist's
recommendation for legal council, as long as the attorney has experience in
dental litigation cases.
Consent to settle.
With most dental malpractice insurance policies, a “consent clause” is
contained within the contract. This requires the insurance carrier to obtain
the dentist's consent in order to settle a case. If the dentist does give the
carrier consent, the dentist will surrender his or her right to the insurance
company on the decision to settle the case. However, for the insurance carrier
to protect their interests, they will include a “Hammer Clause” in the
malpractice policy. This clause will stipulate that if the dentist refuses to
consent to an out-of-court settlement recommended by the insurer, the
insurer's liability for the claim will not exceed the amount for which the claim
could have been settled. Therefore, the dentist may be responsible for any
additional defense costs incurred and any excess amount above the
recommended settlement amount.
Appointment of Legal Council
Defense Counsel Appointment.

The dentist should inquire relative to the assigned attorney's dental
knowledge, how many dental implant malpractice cases the lawyer has
settled or tried to a jury, and the results obtained in such proceedings. If the
doctor is not comfortable with their appointed attorney, they may request
new counsel from their insurance carrier. This request should be made early
in the litigation process. In most cases, a dentist may request a particular
defense attorney, if the attorney has the necessary qualifications or
experience, and in some cases, if counsel is on the carrier's “approved” list,
the dental malpractice insurance provider will most likely approve the
doctor's request.
The defense attorney will handle all matters with respect to the presuit
period and subsequent litigation. Counsel will provide guidance concerning
the discovery process. The defense attorney will be responsible for filing the
appropriate responsive pleadings and ensuring the dentist's legal rights are
protected. Presuit time periods and requirements are dictated by the
applicable state law and vary greatly.
Personal Counsel.
Depending on the significance of the potential claim or issues relating to
insurance coverage, the dentist should consider retaining independent
personal counsel to assist and serve as the doctor's liaison with counsel hired
by the dental malpractice insurance company. The hiring of personal counsel
is particularly important if the claim exposes the doctor to a potential
judgment in excess of their policy limits or if the insurance carrier has
indicated it may not indemnify the doctor against the claims asserted by the
patient. Personal counsel may be particularly helpful in cases where the
doctor's insurance carrier has the right to settle a claim without the doctor's
consent (i.e., no consent to settle clause). However, a personal council should
have a background and experience with dental malpractice cases.
If the dentist's malpractice insurance policy does not contain a deductible,
all legal fees and litigation expenses (except legal fees paid to personal
counsel) will be paid for by the dental malpractice insurance carrier. Despite
this fee arrangement, the defense attorney has a fiduciary duty to the dentist,
not the dental malpractice insurance carrier. The attorney retained on behalf
of the insured has an obligation to preserve the doctor's confidences and may
not allow the dental malpractice insurance carrier to interfere with the
attorney's professional judgment and recommendations (e.g., settlement of a
case because it would be in the best interests of the insurance carrier).
Plaintiff's Requirements for the Filing of a Lawsuit

Prior to initiating a lawsuit against a doctor, the following four elements
must be proven by the patient/plaintiff by a preponderance (greater than
50%) of the evidence.7
1. Existence of Duty: The patient must prove there exists a patient-doctor

relationship, and the doctor had a duty to treat the patient. First, a
professional relationship must be established, which usually involves the
doctor initiating treatment.
2. Breach of Duty: The patient must demonstrate the doctor breached or

deviated from the standard of care (i.e., was negligent). This would include
treatment that is outside the scope of what a prudent practitioner would do
in a similar circumstance. Standard of care is typically determined by the
individual experts retained by each side to give their opinions concerning the
circumstances involving the case.
3. Causation Directly Related to the Treatment: There exists a connection

between the treatment rendered, or failure to render treatment, that failed to
meet the standard of care and as a result caused or contributed to cause
injury.
4. Occurrence of Related Damages: The patient must demonstrate there are

damages that have resulted from the doctor's deviation from the standard of
care. Damages may include physical and/or mental claims.
Affidavit of Merit.
In many states a medical or dental malpractice suit may not be filed until an
expert witness signs an affidavit of merit. To obtain an affidavit of merit, the
plaintiff's council will need to send the pertinent records to a potential expert
witness for evaluation of negligence and proximate cause issues. The expert
witness does have to be familiar with the appropriate standard of care with
regards to the case and be willing to sign an affidavit of merit, which is
usually filed with the complaint. The affidavit of merit in simple terms must
state that in the opinion of the expert witness, the dentist in question
deviated from the standard of care. The reviewing expert does not necessarily
have to agree to testify as an expert witness. This affidavit of merit is a
relatively recent requirement intended to minimize the filing of frivolous
malpractice actions clogging an otherwise overloaded court system (Fig.
19.5).
FIG 19.5 Expert witness affidavit. In certain states a malpractice case may not be
filed until an expert signs an affidavit of merit stating there exists a deviation from the
standard of care.
Statute of Limitations.
In most states a patient must bring a medical malpractice claim fairly quickly
—often between 6 months and 2 years, depending on the state. Generally,
this time period within which to file a lawsuit is termed the statute of
limitations. A failure on the part of the patient to initiate a claim within the
applicable statutory time limit will lead to the claim being “time-barred” or
past the deadline to file a lawsuit (Table 19.1). However, in special
circumstances, the statute of limitations may be extended by three possible
situations:
1. Failure to Discover the Basis of the Lawsuit: When a patient has been unable
to discover the “basis” (cause of injury) of the lawsuit, the patient may be
allowed to file within a “reasonable time” after the discovery of the issue in
question. This may result from “fraudulent concealment by the dentist.”
Most notably, this occurs when the dentist does not inform the patient of a
complication (e.g., broken file or bur, retained cement). In such instances, the
time for calculating the statute of limitations does not begin until the patient
could have reasonably known they were the victim of negligence, and most
often this is when a subsequent doctor is consulted who informs them of the
circumstances.
2. Notice Letter: in most states, the sending of a notice letter will extend the
statute of limitations (e.g., Texas will extend the statute of limitations by 75
days after filing notice). In Pennsylvania, it is the Writ of Summons, which is
filed with the courts to toll the statute of limitations, and this informs the
doctor they are about to be named in a lawsuit. Counsel for the doctor may
then file a Rule to File Complaint, which gives the patient or their lawyer 2
weeks, within which a suit must be filed.
3. Minor Plaintiff: The statute of limitations does not begin to run until the
minor plaintiff is 18 years old. In certain states, this will allow for the delay of
the filing of the lawsuit to the age of 20 (i.e., 18 years of age + 2 years) for a
minor patient and guardian to initiate a legal action.
TABLE 19.1
Statute of Limitations by State
State Statute of Limitation

Alabama* 2 or 4 years
Alaska 2 years
Arizona 2 years
Arkansas 3 years
California* 1 or 3 years
Colorado 2 years
Connec tic ut* 2 or 3 years
D.C. 3 years
Delaware 2 years
Florida* 2 or 4 years
Georgia 2 years
Hawaii* 2 or 6 years
Idaho 2 years
Illinois 2 years
Indiana 2 years
Iowa 2 years
Kansas 2 years
Kentuc ky 1 year
Louisiana 1 year
Maine 3 years
Maryland* 3 or 5 years
Massac husetts 3 years
Mic higan 2 years
Minnesota 4 years
Mississippi* 2 or 7 years
Missouri* 2 or 10 years
Montana 3 years
Nebraska 2 years
Nevada* 2 or 4 years
New Hampshire 3 years
New Jersey 2 years
New Mexic o 3 years
New York 2 and a half years
North Carolina* 3 to 10 years
North Dakota 2 years
Ohio* 1 or 4 years
Oklahoma 2 years
Oregon 2 years
Pennsylvania 2 years
Rhode Island 3 years
S outh Carolina 3 years
S outh Dakota 2 years
Tennessee 1 year
Texas 2 years
Utah 2 years
Vermont 3 years
Virginia* 2 to 10 years
Washington 3 years
West Virginia 2 years
Wisc onsin 3 years
Wyoming 2 years
*
time varies according to type of injury or when injury was discovered.
Filing of the Lawsuit

A malpractice suit will formally begin with the filing of a petition with the
court and service (i.e., delivery to the doctor/defendant or his/her authorized
representative) of the initiating legal pleading.
Complaint.
Once the matter has proceeded through the presuit period, a formal legal
complaint is filed. A “complaint” is a legal document that initiates a lawsuit
and serves to inform the doctor, referred to as the “defendant,” of the
jurisdiction of the court and basis for the requested relief (i.e., negligence).
The complaint includes a concise statement of the claim, the relief
(compensation) and remedies (damages and restitution) requested by the
patient (referred to as the “plaintiff ”), and a demand for judgment. The
complaint usually will contain allegations of facts, which, if proven, entitle
the patient/plaintiff to the damages they are seeking. Often the allegations
within the complaint are very brief and generalized and may omit important,
pertinent information (Fig. 19.6).
FIG 19.6 Complaint. A complaint is a legal document that informs the doctor of the
lawsuit and allegations and damages.
Service of Process.
If a lawsuit is filed, the doctor/defendant should notify their counsel and
request that their attorney contact the lawyer for the patient/plaintiff and
arrange for acceptance of service of process (usually by receipt of a summons
and complaint). Defense counsel should offer to accept service on behalf of
doctor/defendant or offer to schedule a time for service. This alleviates the
stress and embarrassment of a sheriff or process server appearing in the
doctor's waiting room to serve papers in the presence of the doctor's patients.
Most plaintiff attorney firms will comply with this request.
Summons.
The doctor/defendant, or in the alternative, their counsel, will be served with
the complaint together with a legal document called a summons. The
summons is the document that notifies the doctor/defendant a legal action
has been filed. The summons will include the name of the case, location of
the court, and the name and address of the attorney for the patient/plaintiff.
It will also inform the doctor/defendant of the deadline for responding to the
complaint.
It is imperative that upon receipt of the summons and complaint, the
doctor/defendant immediately contact their defense attorney and provide
their attorney with a copy of the summons and complaint, along with any
attached exhibits. In the event the doctor/defendant has had no prior notice
of the impending legal action or has not been appointed insurance defense
counsel, they should immediately contact the professional liability carrier
and provide the insurance carrier with copies of the documents provided.
The fact that counsel has not been appointed by the insurance carrier does
not change the time for responding to the complaint (Fig. 19.7).
FIG 19.7 Summons is a legal document that usually accompanies the complaint
that informs the doctor a legal action has been filed with the court.
Response to the Complaint.
The doctor/defendant's counsel will need to file a response to the complaint.
This response may take a number of forms depending on the legal
sufficiency of the complaint. A typical response is in the form of a pleading
(i.e., formal statement presenting legal documents or arguments) known as
the answer. The answer filed on behalf of the doctor/defendant serves three
functions:
1. It is a response to each of the individual allegations of the complaint. Each

allegation will be either admitted or denied or will state that the
doctor/defendant is without knowledge of the specific assertion.
2. It will contain any affirmative defenses that the doctor/defendant is

interposing to any cause of action alleged in the complaint. An affirmative
defense is a legal reason why doctor/defendant should not be held liable for
the events alleged in the complaint. For example, a cause of action may be
barred by the applicable statute of limitations. This affirmative defense
claims that the lawsuit has not been filed within the time limit provided by
state law.
3. The answer may seek relief against the patient/plaintiff by asserting what
is referred to as a counterclaim. A counterclaim is a claim being redirected
back against the patient/plaintiff. Typically, this occurs when the patient has
failed to pay for their services and has in turn sued for malpractice.
The doctor/defendant should always be consulted by their attorney before

filing of an answer. Any allegations admitted in the answer are established as
a matter of law (i.e., the information may be used at trial). As a consequence,
the doctor/defendant should specifically approve the proposed answer before
it is served on the patient/plaintiff's attorney and carefully review any
proposed admissions. In general, these admissions may not be withdrawn
during the litigation process or trial and are binding on the
doctor/defendant.
In the event that a response is not filed on behalf of the doctor/defendant
in a timely fashion, a default may be entered by the plaintiff's counsel. The
effect of a default is the doctor/defendant admits to the allegations in the
complaint and agrees to the relief (financial claim) requested by the
patient/plaintiff. Unless the default is set aside by the court (reversed), the
only issue at trial will be to determine the amount of the patient/plaintiff's
damages.
Miscellaneous Presuit Recommendations
Discussing the Claim.

Upon receiving a notice letter, a doctor/defendant may attempt to discuss the
situation with other colleagues to obtain their opinions. If a lawsuit is
initiated, the doctor/defendant may be asked to recount the conversations,
even if they are unfavorable to the defense of the case. It is highly
recommended that the doctor/defendant have no discussion of the case with
anyone other than their attorney or insurance carrier.
Do Not Attempt to Communicate With Patient/Plaintiff Lawyer.

Attempting to contact the patient/plaintiff or their attorney is not
recommended. Often, the doctor/defendant may feel the need to plead their
case and dissuade a disgruntled patient or attorney from continuing legal
action. However, this is almost always futile and may have significant
negative ramifications. Another common error made by the
doctor/defendant is to offer the patient a refund in lieu of the filing of the
lawsuit. Although generally inadmissible (i.e., cannot be used against the
doctor/defendant in court) in any subsequent court proceeding, at the very
least it creates the appearance that the doctor/defendant may be guilty of
wrongdoing.
Calling Subsequent Providers.

Similarly, contacting subsequent treating doctors is not recommended. If a
case is brought against a doctor, records of all subsequent treating providers
will be easily obtained through the discovery process. Calling the subsequent
treating provider may potentially result in an uncomfortable situation
wherein the subsequent treating doctor may request that the implant
clinician take financial responsibility for the patient's subsequent medical
needs, no matter how open ended. In turn, the subsequent treating provider
may promise to encourage the patient to drop any legal claims. However, the
payment of remedial medical/dental expenses is rarely successful in
persuading a patient to drop their legal claims.
Secure All Records.

The original chart, radiographs, study casts, surgical templates, laboratory
prescriptions, pharmacy prescriptions, appointment logs, and any other
documents or materials relating to the patient's care should be secured and
copies placed in a safe location (e.g., doctor's home or safe deposit box).
Although only a remote possibility, computer failures do occur (sometimes
without effective backup), as well as fires, floods, or other catastrophes,
resulting in the permanent loss the patient's records.
Uninsured Defendant.
In most states, medical practitioners are required to secure active malpractice
insurance. The fact that a doctor does not have malpractice insurance to
cover a specific claim does not mean that the doctor cannot be sued. If
doctor/defendant is not insured, it is imperative they retain counsel to
represent their interests. The old adage is “a person who acts as their own
lawyer has a fool for a client” applies with equal force to health care
professionals, including doctors. Having no, or inadequate, legal counsel may
be devastating to the defense of an otherwise defensible lawsuit.
Discovery Phase
The second phase of the litigation process is known as the discovery phase. In
this part of the case, each side is afforded the opportunity to acquire
information about the other's case. The defendant/doctor, through the
discovery process, is able to determine the exact nature of the claims of the
patient, the damages allegedly suffered, the names of subsequent treating
practitioners, and names of any supporting witnesses, including experts. The
plaintiff/patient is likewise given the opportunity to obtain information
concerning the case rendered, including access to the records, radiographs,
study casts, photographs, and defenses asserted by the defendant/doctor.
Forms of Discovery
The methods, means, and timing of the various forms of discovery are
governed by the rules of civil procedure (i.e., the body of law that sets the rules
and standards the courts must follow in civil lawsuits) of the particular state.8
Interrogatories.
Interrogatories are written questions that are formally asked by one side to
the other. Answers to interrogatories are usually drafted by the attorney in
consultation with their client. Similar to admissions made in response to the
complaint, interrogatory answers may not be withdrawn during the litigation
process or trial and are binding (i.e., cannot be withdrawn) by the
defendant/doctor.
Interrogatories are most effectively directed to the issue of damages,
including any expenses (i.e., medical and dental bills) the plaintiff/patient
contends were incurred as a result of the alleged negligence by the
doctor/defendant (Fig. 19.8).
FIG 19.8 Interrogatory. An interrogatory is a list of questions that one side sends to
the other side during the discovery process. Each side is required to answer the
questions under oath and within a specified time period.
Requests for Disclosure.
Requests for disclosure are statutorily (i.e., governed by law) predetermined
requests for information that must be produced without objection by either
plaintiff or defendant. Disclosures cover basic information that is involved in
a lawsuit, which includes witnesses, experts, contentions of the parties,
damages incurred, and the identity of any health care providers that treated
the plaintiff.
Production of Documents and Things.

This form of discovery allows either party the opportunity to obtain for
evaluation and/or copying documents, records, bills and other materials. The
production of these documents is not without limitation. The materials
requested must be somehow relevant to the case or potentially applicable to
the pending action (Fig. 19.9).
FIG 19.9 Production of documents and things are requests made by either side for
the disclosure of documents or associated materials (e.g., study casts) dealing with
the case.
Request for Admissions.
In a request for admission, the party served is required to admit or deny or
state that the party lacks sufficient information to respond, concerning
certain facts and contentions of the case. If a responding party gives lack of
information or knowledge as a reason for a failure to admit all or part of a
request for admission, that party shall state in the answer that a reasonable
inquiry concerning the matter in the particular request has been made and
that the information known or readily obtainable is insufficient to enable
that party to admit the matter. The purpose of requests for admissions is to
eliminate unnecessary proof of undisputed facts at trial. Extreme care must
be taken in responding to requests for admissions. A request that has been
admitted may be presented (i.e., read) by the opposing attorney to the jury
during trial and may establish the matter(s) admitted. These requests are
usually time sensitive, and failure to respond in a timely manner will result
in admissions being deemed against the party served (Fig. 19.10).
FIG 19.10 Request for admissions requests to admit or deny any potential
allegations during the discovery process.
Expert Reports.
An expert report is a report written by either side's medical expert stating
their facts and findings within the case. The use of expert reports varies
greatly among states. In some states, either party may request the expert's
opinion and the basis for their opinions. However, in some states, written
expert reports are not required for the filing of a lawsuit (Fig. 19.11).
FIG 19.11 Plaintiff expert report example.
Depositions.
The last and possibly the most important form of discovery is the deposition.
A deposition is a formal question-and-answer session in which the attorney is
given the opportunity to ask questions of the opposing party under oath. The
deposition will also serve as a road map for the trial testimony. Once a
question is answered in a deposition, it is difficult to contradict the testimony
at a later date. A seasoned attorney will readily identify the contradiction and
“impeach” (i.e., discredit the witness) the testimony. Therefore, whatever is
stated in deposition cannot be easily amended or changed during trial.
Preparation for a deposition should occur in the days or weeks prior to the
date of the actual deposition.
Preparation for the Deposition

The doctor/defendant should meet with their counsel and discuss the case in
its entirety prior to the deposition. They should be fully aware of the
allegations of the claim, the alleged damages, specific dates, and the issues of
potential liability.
At the predeposition conference, the doctor/defendant should be
intimately familiar with their care and treatment of the patient, their
justification for the treatment provided, as well all written dental charting,
and the billing ledger. The doctor/defendant should ensure that the dental
charting matches the billing ledger or be prepared to explain any
discrepancies. The chart should be organized in such a fashion as to allow
the doctor/defendant to easily find the various items contained therein.
The objective of the conference is to prepare the doctor/defendant to
testify at deposition. The deposition is under oath, and the doctor will be
expected to tell the truth. In some jurisdictions the deposition may be
videotaped. Often it is not what is said but how it is said that matters most.
If the radiographs are digital, photographic quality prints should be made
available to the attorney for use during the deposition, if necessary. Poor-
quality or copied radiographs often result in possible incorrect testimony and
will often be confusing to the jury (Box 19.2).
Box 19.2
Recommendations/Ground Rules for a
Deposition
• The doctor should be well prepared and have a complete knowledge of the
records.
• Answer only what is asked, do not volunteer information.
• If you do not understand the question, answer as such.
• Keep your answers short, responsive, and to the point.
• Answer the question only after the attorney is done asking it.
• Do not attempt to convince the attorney that you are right and that he or
she and his or her client are wrong.
• If an objection is made by your attorney, do not answer unless instructed to

do so by your counsel.
• Feel free to look at the chart/records and radiographs—it is not a memory

test.
• If you are shown radiographs and need a light box to view them, advise that
one is necessary.
• Do not comment on radiographs that are inadequate or poor copies.
• Do not guess or speculate on questions.
• If you don't know, answer as such.
• Do not discuss any conversations or emails you had with your counsel.
• Be careful not to state that an author, text, or an expert is authoritative. This

places the practitioner at risk because if some component of the treatment
rendered differs from what has been written, the practitioner may be
impeached by anything the author or expert states.
• Always follow your attorney's recommendations or suggestion because

they are required to represent your best interests.
• Do not become argumentative or adversarial with the opposing attorney.

The doctor/defendant should ask their attorney to provide them with a
copy of any depositions taken by the patient's attorney. This is particularly
important if the doctor has never been deposed before. Although it would be
advantageous to have a transcript from a similar case, it is not imperative.
The purpose of reviewing such a transcript is for the doctor/defendant to
become familiar with the process and to obtain an idea of the attorney's
general deposition procedure. Trial attorneys are generally creatures of habit,
and the roadmap they follow in deposition is the same or similar from case to
case. Additionally, this will give the doctor an idea of the dental acuity of
their opponent. Many plaintiff attorneys have limited knowledge with
respect to dental procedures and complications. Do not, however, sell your
adversary short; most jurisdictions now have lawyers who are very seasoned
in handling dental malpractice actions.
Doctor/Defendant Testimony at Deposition.

On the day of the deposition the defendant should dress professionally,
arrive promptly, and be cooperative. Although the doctor may believe
strongly in their position, arguing and fighting the process will accomplish
nothing more that lengthening the duration of the deposition. In some cases
the patient may appear in person to witness the doctor's testimony; however,
there should be no communication with the patient. The patient may not ask
questions and is not permitted to interfere with the doctor's testimony. The
doctor/defendant cannot charge for their time at deposition, and expenses
(e.g., court reporter, videographer) are usually covered by the
patient/plaintiff's attorney.
Patient/Plaintiff Testimony at Deposition.

Just as the patient/plaintiff is entitled to take the doctor's deposition, the
doctor/defendant counsel has the right to depose the patient. As with all
depositions the doctor/defendant has the legal right to appear at the
deposition. The doctor may provide questions to their counsel and may
discuss the testimony but may not interfere with or disrupt the process. All
expenses for the patient/plaintiff's deposition are covered by the
doctor/defendant's malpractice carrier.
If the doctor/defendant elects to attend a treating doctor or expert's
deposition, they should do the following:
1. Do not arrive before your attorney and attempt to engage the witness in
conversation, whether related to the case or not.
2. Be polite and introduce yourself to the plaintiff's attorney.
3. Do not interfere in any way with counsel's questioning. If you believe

information needs to be addressed by your attorney, write the information on
a notepad and wait till a break occurs to discuss.
Mediation
Prior to the 1990s, mediations were essentially nonexistent. Settlements
typically occurred based on telephone conversations between opposing
counsel, similar to the manner in which settlements occurred in routine
personal injury claims. As liability insurance companies became more and
more concerned about attorney fees associated with the defense of medical
malpractice claims, mediation became more prevalent. In recent years, when
settlements of medical malpractice claims occur, the majority of them do so
at mediation conferences.
In most jurisdictions a mediation conference is required prior to trial.
Mediation is a nonbinding alternative dispute resolution process. With time,
it was found that cases often settled on the proverbial “courthouse steps.” In
an effort to facilitate the settlement process and encourage discussion prior
to the day of trial, the mediation process was developed.
Mediation involves a potential settlement process in which a third party
(mediator) attempts to find points of agreement and to resolve conflicted
issues. Usually the mediator (typically an attorney or retired judge) is agreed
upon by both sides or appointed by the trial court. The mediator has been
educated and trained in the art of opening dialogue and addressing
contested issues with the goal of resolving the case and putting an end to the
litigation process. The mediation conference is strictly confidential, and
concessions or resolutions are inadmissible in a court hearing. In most cases
the doctor/defendant will be required to attend. The doctor/defendant should
be prepared to provide guidance to their attorney concerning claims and
allegations that are made in the conference. The doctor may be asked either
at the time of the conference or shortly before to consent to a potential
settlement. In most instances the doctor/defendant must consent to an
agreement in mediation.
A potential tactic that mediators use is to provide a “mediator number ” at
the conclusion of the mediation conference if the mediator believes the case
should be settled but the parties cannot reach an agreed-upon amount. The
mediator provides a settlement figure on a piece of paper, providing each
party with the opportunity to say “yes” or “no” to the suggested number. The
mediator does so after conclusion of the mediation conference, providing a
deadline for the parties to say “yes” or “no.” The parties are told to return
the sheet of paper indicating their response within a certain timeframe. If the
parties agree to the proposed settlement figure, the mediator notifies the
parties of the settlement. After agreement, the mediation settlement is a
binding agreement. When both parties sign the agreement, neither party can
deviate from the mediation settlement agreement. The patient/plaintiff
basically agrees to waive their right to sue the doctor/defendant in exchange
for compensation.
Pretrial Modes of Disposition

If a lawsuit is resolved before trial, the resolution is accomplished by one of
the following methods8:
Motion for Summary Judgment.

A summary judgment is a motion by either party that asserts that all factual
issues in the case are settled, therefore there is no need for a trial. The
motion is supported by affidavits, depositions under oath, and admissions of
fact, as well as a legal argument. This motion has the following components:
Facts: the party initiating the motion will present its version of the facts.
Law: a memorandum discussing the statutes that govern the case.
Summary: the party will summarize and anticipate the opposing counsel's
arguments and will explain why those arguments are not valid.
Opposing Party Response: the opposing counsel will respond to the

information contained within the summary judgment.
Judge's Decision: the judge will review the motion and responses and will
either grant (agree) the motion or deny the motion.
In a dental malpractice suit, this motion is usually filed by the defense to

test the patient/plaintiff's ability to obtain an expert witness that can
establish negligence and proximate cause.
Motion to Dismiss.
Typically, a motion to dismiss is filed in lieu of an answer to test the legal
sufficiency of the plaintiff's complaint. Matters typically raised in a motion to
dismiss include adequacy of the facts alleged. For purposes of motion to
dismiss, all well-pleaded allegations of the complaint are accepted as true. In
such circumstances the plaintiff will generally be given the opportunity to
correct the defect and proceed. A motion to dismiss may also be filed when
the plaintiff cannot produce a qualified expert witness that can establish
negligence and proximate cause. The time period is governed by statutes
with each state. (e.g., Texas = 180 days). Most statutes will provide the
plaintiff an extension to comply with the provision.
Voluntary Nonsuit.
In some situations the patient/plaintiff may elect to drop the lawsuit against
the doctor/defendant. This is most commonly done to simplify and narrow
the case when there are multiple doctor/defendants named in the lawsuit.
However, the voluntarily dismissed claim may be resubmitted if the statute
of limitations period has not expired.
Settlement.
When the plaintiff and defendant parties agree to settle the lawsuit prior to a
trial, a settlement agreement will be filed. This agreement will usually
contain language stating that the doctor/defendant does not admit
negligence and the settlement agreement is agreed upon to avoid the time,
cost, and harassment of defending a lawsuit. Both parties will then mutually
execute an agreed motion for nonsuit to be filed in court, which will be
granted by the judge.
Settling a Lawsuit
Ramification of Settling a Malpractice Case.

The doctor/defendant is often confronted with the difficult question of
whether to settle the lawsuit or continue to litigate with the possibility of a
trial. Studies show that over 70% of cases decided by judge or jury are
resolved in favor of the defendant doctor.9 Many doctors look at this statistic
and believe their chances are very good. However, this statistic is misleading
because most of the strongest cases against doctor/defendants are settled out
of court, prior to a trial.
Whether the doctor/defendant agrees to settlement or suffers an adverse
verdict at trial, the doctor may be subject to a number of possible adverse
consequences:
1. The trial may be personally humiliating to the doctor and their practice. In
some cases the local newspaper or television station have covered the trial
result and even have published the names involved.
2. The malpractice carrier is compelled by law to report the settlement to the

National Practitioner Data Bank (NPDB) and the state dental board.
3. The state licensing division may open a disciplinary investigation against

the dentist's license, and sanctions and fines may be implemented.
4. If the doctor has clinical privileges at a hospital or ambulatory surgical

centers, the malpractice carrier is compelled to report such settlements,
which may affect the doctor/defendant's privileges.
5. If the doctor participates with dental insurance plans, the

doctor/defendant's contract may require them to report the settlement to
these plans, which may affect the status of participation.
6. If the doctor/defendant is board certified in a dental specialty, the

doctor/defendant may be required to report the action to the specialty board,
which may affect the doctor's certification.
Consent to Settle Policy.

Most doctor/defendants do not know what their rights are when it comes to
making a decision on a proposed settlement. Each malpractice policy has a
“consent to settle” provision, which sets forth the rights, duties, and
obligations of both the insurer and the insured with regard to settlement of a
claim. Usually, a consent to settle clause will require the insurance company
to obtain the doctor/defendant's approval before settling any claim. It is
recommended that every doctor check this in their policy because some
provisions will give authority regarding settlement back to the insurance
company. Examples include10:
Hammer Clause: A hammer clause will entitle the insurance company to be
only responsible for the amount of a claim that has been “settled,” even
though the doctor/defendant does not consent. For example, if the
insurance company negotiates a settlement of $100,000 and the doctor does
not give consent for settlement, the doctor would be responsible for any
monies paid on a claim over $100,000, plus attorney fees.
Unreasonable Provision: This clause will override the doctor's consent

authority if the insurance company determines the doctor is unreasonable
in withholding consent. The insurance company may settle the case
without the doctor's permission.
Board Approval Provision: With a board approval provision, the insurance

company's review board has the ability to override the doctor/defendant's
wishes if they agree that the doctor's actions deviated from the standard of
care.
Binding Arbitration: In some insurance policies, if the insurance company

disagrees with the doctor's refusal to consent to settlement, the case must
be sent to binding arbitration. Binding arbitration is when the dispute is
given to an unbiased third party to resolve and their decision is agreed
upon by both parties as final or binding.
No Active Insurance: If the doctor no longer owns an active malpractice policy

with the carrier, this provision causes the doctor/defendant to lose their
ability to withhold consent to settlement.
License Revoked/Deceased: with these provisions, if the doctor has their license
revoked or is deceased, the consent for settlement provision is deemed
null and void.
Potential Nonsettlement Ramifications.

The doctor/defendant should be fully aware of the ramifications of a refusal
to settle. The hammer clause, also known as the “nuclear option,” will
sometimes force a doctor/dependent to settle the lawsuit. If the
doctor/defendant refuses to settle pursuant to the insurance policy, the
insurer's liability for the claim will not be greater than the amount for which
they could have settled the claim. Further, the defendant may be liable for
the defense costs, including attorney's fees, following a refusal to settle.
While the defendant/doctor may feel strongly about their position,
proceeding to trial is not without potential consequences. Confronted with
this situation, it is highly recommended that the doctor/defendant seek
personal council for advice.
Malpractice Trial
When all attempts to resolve the dispute have been futile, the final option for
resolution is a trial. Dental malpractice lawsuits rarely end in a trial. Statistics
show that approximately 7% of malpractice suits are decided by a jury.11 In
the event that settlement negotiations fail and the doctor/defendant is
unable to have the matter thrown out by the court on legal grounds, the
matter will proceed to trial. A malpractice trial may be described as a
“theater with rules.”
The doctor/defendant should ensure they are fully prepared for trial. This
should involve meeting with their attorney a minimum of 1 week before trial
to discuss the process and to rehearse their testimony. The defendant/doctor
should have a complete set of their dental records and be intimately familiar
with the chart's contents. The defendant/doctor should be able to easily
identify and acquire any document, radiograph, scan, or study cast being
discussed. Being disorganized in front of a jury is troublesome because it
gives the appearance of “sloppiness.”
Malpractice trials are often a lengthy process. The doctor/defendant should
be prepared to devote as much time as is necessary to defend the case. This
usually involves at a minimum of 1 week with the possibility of, on rare
occasions, multiple weeks of trial time. The trial duration is usually
dependent on the complexity of the malpractice case. Although attendance of
the doctor/defendant is not mandatory, absence is not recommended because
it gives a negative connotation in the eyes of the jury.
Court Docket
The exact date and time a trial will commence is often not clearly defined.
The court usually places the trial on a “docket,” which is a range of time that
the court may call for the start of the trial. This may happen with as little as
24-hours notice. The doctor/defendant must be prepared to change their
schedule and devote the time necessary for trial. The scheduling of the trial,
which includes coordinating all witnesses, attorneys, judge, and jurors, is not
always easy and often conflicts exist (Fig. 19.12).
FIG 19.12 Court docket. The court will give notice to the doctor/defendant on when
the trial will commence. This will usually be a range of time (≈4–8 weeks).
Continuance
In American procedural court law, a continuance is a postponement of the
trial at the request of either or both the defendant and plaintiff or the judge.
A motion for continuance is usually granted when there is reasonable cause.
In some states “fast-track” rules limit the ability of judges to grant
continuances. There exist many reasons for a continuance:
1. Inadequate time to prepare
2. Conflicting obligations of counsel
3. Illness of any of the involved
4. Expert witness conflict
5. An agreement between the parties
6. Religious holidays
Civil Courtroom Layout

The courtroom layout for a civil malpractice trial includes (Fig. 19.13):
Judge's bench: the presiding judge will sit behind a raised desk, known as the
bench.
Witness stand: adjacent to the judge's bench is the witness stand in which the
various witnesses will present their testimony.
Court reporter: the court reporter usually will sit in front of the judge's bench
and is responsible for recording verbatim all testimony, objections, and
judge's rulings.
Judge's clerk: the clerk is located in front of or to the side of the judge's bench
and will usually administer the oath to jurors and witnesses. The clerk is
also in charge of all physical exhibits that are introduced into evidence.
Bailiff: the bailiff has many duties including calling the witnesses, being in
charge of the jury, and acting as the liaison between the judge and jury.
Council tables: in front of the court reporter table, two tables (plaintiff and
defense) will be present for the plaintiff and defendant and attorneys.
Jury box: on the far side of the courtroom will be the jury box, where the jury
will sit while testimony is given.
FIG 19.13 Civil courtroom layout diagram. Although variations exist, the civil
courtroom is setup with the judge's box in the center, with the witness stand directly
to the judge's left side (closet to the jury box). A court reporter (to the right of the
judge box) and court clerk (front of the judge's box) are positioned around the judge's
bench. The defendant's table (defendant and defendant's attorney) and plaintiff's
table (plaintiff and plaintiff's attorney).
Jury Selection
The first step in the trial process is the jury selection. Also referred to as voir
dire. Voir dire is a Latin phrase that literally means “to say what is true, what
is objectively accurate or subjectively honest.” A group of potential jurors are
summoned to the courthouse to be questioned by the lawyers and judge to
determine their suitability for jury service. The potential jurors may also be
required to complete a questionnaire. The jury pool is usually selected from
the voter registration list or from the driver's license registrations in most
jurisdictions. The attorneys on both sides are given an opportunity to
question the prospective jurors about their backgrounds to determine if they
have any biases or prejudices that would prevent them from being fair and
impartial to either side. During voir dire process, lawyers strive to achieve
four major goals in evaluating the jury candidates: (1) eliciting information
from each potential juror, (2) developing a rapport with the potential juror,
(3) educating potential jurors on the process, and (4) attempting to educate
potential jurors concerning their case.
After questioning is completed, the selection process begins. The court will
take into consideration what is referred to as challenges for cause. The court
will be asked to “strike” (i.e., remove) any potential juror who has indicated
they cannot be fair and impartial or who is otherwise unfit to serve as a juror
on that case. An example of unfitness is being a convicted felon. Once the
for-cause challenges have been addressed, each side is given a certain
number of “peremptory challenges.” A peremptory challenge allows
attorneys to dismiss a prospective juror for any reason they deem necessary.
These challenges are used by each side to eliminate potential jurors who
would be otherwise qualified. After these potential jurors are removed from
the pool, those who remain will become the jury. The rules in each state are
different, with the jury panel usually comprising from 6 to 12 jurors. In most
states, one or more alternate jurors may be selected. Alternate jurors will
attend trial and are called on to replace a juror who is unable to complete
their jury service (e.g., for health reasons).
Opening Statement
Once the juror panel is selected and sworn in, the plaintiff and defense
attorneys for both sides are asked to give an opening statement. The
plaintiff's attorney will be first to give their opening statement, followed by
the defense attorney. The opening statement is an overview or roadmap of
what each side intends on proving and explaining to the jury what they can
expect from each of the witnesses. Attention should be paid to the opening
statements because the opponent's claims will be discussed in detail. It is
bad practice to assert that you intend on proving a particular fact and claim
and then not doing so.
Patient/Plaintiff Case Presentation
Upon completion of the opening statements, the patient/plaintiff will begin
their case. The patient/plaintiff presents their case in the hopes of proving
that the doctor/defendant deviated from the standard of care. The plaintiff
attorney must prove each and every legal aspect of their claim. If each
element is not proven, the court may take the case away from the jury and
enter a judgment (defendant verdict) in favor of the doctor/defendant.
The term standard of care is often used and rarely understood.
Unfortunately, there exists no universal definition. The jury, in some
jurisdictions, will be instructed that the standard of care means what “a
similar practitioner would do under the same or similar circumstances.” In
other states, including Florida, the jury will be instructed that the standard of
care is “reasonable and appropriate care.” This does not mean perfect care,
nor does it mean what another practitioner would have done.
The mere occurrence of a bad outcome or result does not entitle the
patient/plaintiff to a verdict in their favor (i.e., failed dental implant). The tort
system in this country is fault based; some fault or deviation from the
standard of care must be proven by the patient/plaintiff in order for them to
prove their claim.
Proof of a deviation from the standard of care is usually accomplished
through an expert witness or, on occasion, via a subsequent treating doctor.
The term expert is likewise frequently used in the litigation process but is
similarly not well understood by doctors or lawyers. An expert designation
does not mean that the witness is an exceptional dentist, researcher,
instructor, or author. It merely means that the witness possesses specialized
training and education (dental school education at a minimum) on a topic at
issue and will be able to aid the finder of fact (jury) in making its
determination of the ultimate issues.
Specially retained experts are the so-called “hired guns.” They are paid to
review all the documents with respect to the case and testify during trial.
Because “experts” are witnesses for hire, the credibility of a specially retained
expert is always an issue, and the jury is free to believe or not believe the
testimony of any witness, including a specially retained expert.
Subsequent treating doctors tend to be more troublesome when they
provide opinion or expert testimony. Unlike the hired guns, they are not
handpicked like specially retained experts, and they usually testify on the
basis of their clinical evaluation of the patient/plaintiff. They are also not
generally paid a fee for their “expert witness” testimony. Most commonly,
these witnesses will be attacked on the basis that they are testifying on
behalf of a patient who remains under their care. Additionally, a subsequent
treating dentist must defend their own conduct. For example, if the
subsequent treating dentist has removed all or part of the dental work
delivered to the patient by the doctor/defendant, the subsequent treating
dentist must offer a valid reason for removing what is otherwise perfectly
acceptable dental work. The subsequent treating dentist is locked into
testifying there was some deficiency that necessitated the subsequent care
and treatment, including the removal of the dental work. Otherwise, it is the
subsequent treating dentist, and not the defendant, who has subjected the
patient to unnecessary care and treatment.
Witness Order
The general order of witnesses to be called to testify is left to the discretion
of the attorneys. Generally, the plaintiff attorneys will select the
doctor/defendant as the first witness, the treating doctors next, followed by
witnesses to discuss damages, the expert witness, with the patient/plaintiff
generally going last. In some cases, the plaintiff's attorneys may vary this
plan by placing the plaintiff on the stand first with the doctor/defendant
going last.
The doctor/defendant must be completely prepared to testify, and their
answers should be intelligently thought out, given in a concise manner
consistent with the dental chart and the prior testimony (i.e., deposition). A
common pitfall for the doctor/defendant is to argue with the opposing
counsel, which never results in a positive outcome. The questions should be
answered as phrased; however, further explanation may be given. At the very
least it makes it appear that the attorney is not allowing the doctor/defendant
to tell the full story and not given the opportunity to expound on your
response.
Once the plaintiff's attorney has finished asking their questions, the
doctor/defendant's attorney is given an opportunity to question their own
client. This is generally brief and is used as a means of clarifying the doctor's
testimony. The doctor/defendant will be given an opportunity to testify a
second time if their attorney deems it necessary to testify in the defense side
of the case. This is called cross-examination, or simply referred to as “cross.”
On completion of the cross-examination, the patient/plaintiff attorney is
given one more opportunity to question the witness, which is referred to as a
redirect. This inquiry is limited to areas covered in the cross-examination.
After the plaintiff's attorney has presented their case, they will “rest,” and
the defense will be given the opportunity to present their case or move for
dismissal. If the judge does not dismiss the case, the defense will call their
witnesses, with the plaintiff's attorney having the opportunity to cross-
examine.
For a successful verdict against a doctor/defendant, the plaintiff's attorney
must prove there was a deviation from the standard of care. However, they
only need to prove evidence of probability (not necessarily a certainty) of a
breach in the standard of care. This is termed preponderance of evidence. The
legal definition of probability means that, even if the jury has 49% doubt that
the plaintiff's version of the facts is true, they will still find the
doctor/defendant failed to meet the standard of care.12
Expert Witnesses
In a dental implant malpractice suit the jury is requested to determine if the
doctor/defendant violated the standard of care by evaluating the evidence
provided by each side. Usually, with respect to standard of care, the most
compelling evidence is from the expert witnesses. Expert witnesses can be
general dentists, specialists, or other health care professionals. In some
states, the expert is required to have training identical to or greater than that
of the defendant (e.g., Arizona). The jury will evaluate the information
provided by the expert witness to determine their credibility and knowledge
concerning the subject.
There are two types of expert witnesses, nonretained and retained.
Nonretained are usually subsequent care providers who have expressed
criticism and testify on the injuries involved in the defendant's treatment.13
Retained expert witnesses are witnesses who have not necessarily seen the
patient for treatment but are hired by the attorney for their opinions on
standard of care and causation by reviewing the records.14 In most cases, the
doctor/defendant may request their expert witness for testimony on their
behalf.
Impeachment
The doctor/defendant should have a copy of all discovery, including their
deposition, answers to interrogatories, and requests for admissions. The
doctor should be fully prepared to discuss in detail each of these items,
including their deposition testimony. If, during testimony, the
doctor/defendant contradicts themselves, they may be subject to
“impeachment” by the inconsistent statement. This is a process whereby the
opposing attorney is able to bring the inconsistency to the attention of the
jury. It is an unpleasant event and is very embarrassing. The more times a
witness is “impeached,” the more the witness loses credibility with the jury.
It is imperative the doctor/defendant know exactly what was answered in all
interrogatories and deposition testimony.
Inadmissible Information
In most states, peer review records and testimony regarding peer review
activities are immune from discovery and are inadmissible (i.e., not allowed)
as evidence in dental malpractice suits. Additionally, quality assurance
committees, utilization committees, and incident and risk management
reports also are not discoverable or admissible. This information, which may
include findings or retributions against the doctor/defendant, may not be
used against them in a malpractice court hearing.15
Closing Arguments
Once both parties have completed presentation of their cases each will rest
and closing arguments will commence with the plaintiff side going first. The
closing argument or summation is the final opportunity for the attorneys to
persuade the jurors to find in favor of their side. The facts will be
summarized to show their side has proven their case and to point out the
failures of the opponent's claims and contentions. The attorneys may not
discuss or comment about any information that was not presented during the
course of the trial; commentary is limited to the evidence presented. After
the defense presents their closing argument, the plaintiff's attorney is
entitled to make a concluding argument or rebuttal. This is the last
opportunity for the plaintiff to discuss any points made by the defense
attorneys in their final arguments. At the conclusion of closing arguments,
the judge will instruct the jury as to the appropriate rules of the law that they
must follow in reaching a verdict.
Deliberation
After the final arguments and instructions from the judge, the jury will
proceed to the jury room to begin the process of deliberation. The jury will
have all of the items and materials introduced into evidence with them to
consider in the deliberations. Initially, a presiding juror will be elected to
direct over discussions and voting. This juror is referred to as the foreperson.
The bailiff will oversee the jurors and will be the go-between between the
judge and jury.
In the deliberation process the jury will attempt to reach a decision on the
outcome of the case. In most jurisdictions a majority (i.e., over 50%) of the
jurors must agree on a final verdict; in some jurisdictions the verdict must be
unanimous. During this process the jury may ask for the judge to explain or
instruct them on certain aspects of the law. In some jurisdictions it is
permissible for the jury to request that certain aspects of the trial testimony
be read back to them. Once the jury reaches a decision, they will allocate and
decide the amount of the award of damages, if any. Damages may be
categorized as either economic, noneconomic, or punitive (damages awarded
as punishment in excess of the actual damages). The amount and availability
of the various damages is dependent on state laws.
Verdict
After the jury decides on the final verdict, the jury will notify the bailiff, who
will in turn notify the trial judge. All the participants in the trial will then
reconvene in the courtroom for the announcement of the verdict. The judge
will usually read, or “publish,” the verdict in open court. If the verdict is for
the plaintiff, the jury will usually set forth the amount the defendant must
pay the plaintiff for damages. The attorney for either side may ask for the
jury to be polled. When the jury is polled, each juror will be asked if they
agree with the decision announced. The losing party has the right to appeal,
in which they petition a higher court to review various aspects of the case and
trial with the hope that the appellate court may find fault with decisions of
the trial court and reverse the jury verdict. An appelate court, also know as
an appeals court, reviews the decisions and process of a lower court.
Although damages are not paid until the appeal is heard by an appeals court
and a final ruling is completed, a bond may be required to secure the verdict.
Damages
If a doctor/defendant has breached the standard of care, the patient may be
awarded by two types of damages: general or special. General damages are
awarded for physical and emotional pain and suffering. The amount of the
award is solely in the jury's discretion but is subject to statutory caps. Special
damages are provided as compensation for financial loss, such as medical
bills, hotel and travel expenses, lost wages, or loss of future earning capacity.
Comparative Fault
If the patient is found to be negligent or to have caused or contributed to the
adverse event or complication (e.g., failure to take antibiotic, missed
appointments), the award may be reduced or withdrawn. Such comparative
fault reduces or extinguishes the award based on the percentage of patient's
fault. It behooves every practitioner to make detailed notes on missed
appointments, failed instructions, or a false or deceptive history. In some
states the doctrine of contributory negligence is followed, which provides
that if a patient is at fault to any degree, there can be no recovery and the
malpractice claim is dismissed by the court.16
Postverdict Adjustments
In many large verdict cases, upon judicial review, awards are reduced.
Because the jury verdict must be ratified by the trial judge in the form of a
“judgment,” many judges will readjust the damages if they appear excessive.
A higher court may also reduce the award if they feel the evidence does not
support the full amount awarded. And lastly, the damages may be negotiated
between the plaintiff and defense teams. The defense may threaten to appeal
to a higher court, which could overturn the verdict or reduce the award. An
appeal will increase the plaintiff's costs, which will result in many cases the
plaintiff accepting a lesser amount in settlement.
Excess Verdict
Jury awards in liability cases are often unpredictable and may exceed the
doctor/defendant's liability coverage. Most doctors do not realize they or
their corporation are responsible for the excess verdict amount (i.e., reward
amount above the maximum malpractice limits). For example, if the doctor
has a $1 million policy limit and a judgment against the doctor is $2.5
million, the doctor is responsible for the excess $1.5 million. For doctors
concerned about excess verdicts, policy limits may be raised to $3 million or
$5 million. It is highly recommended that if a doctor/defendant has a case
that may potentially result in an excess verdict, personal counsel should be
retained to safeguard the interests of the defendant dentist.
Types of Malpractice Insurance

Occurrence.
Occurrence dental insurance is the most popular dental insurance carried by
dental practitioners. This coverage is based on when the actual dental
treatment in question occurred, not when the claim is made. As long as the
incident in question is made during the active policy period, the malpractice
carrier will adhere to the terms and conditions of the policy. For example, if a
claim against an insured doctor is made in 2015 for treatment rendered in
2012 (i.e., while the policy was active), the malpractice carrier will cover the
claim. The occurrence policy offers permanent coverage for incidents during
the policy period.
Claims-Made.
Claims-made insurance provides coverage when claims occur when both the
alleged incident and resulting claim occur during period the policy is in
force. Claims-made policies provide coverage as long as the doctor continues
to renew the initial policy and any subsequent renewals. Once the doctor
stops paying the premiums, the coverage stops. Claims brought against a
doctor after the coverage ends will not be covered, even if the incident
occurred while the policy was in force.
For claims-made policies, a “tail” coverage (extended reporting
endorsement) must be purchased at the end of the termination of the policy.
This extended policy is needed upon retirement, taking a leave of absence
from practice, joining a group practice with different insurance, or moving to
a different state. Usually, malpractice carriers will offer free tail coverage in
the event of death, disability, and retirement, provided a certain age is
reached. Tail coverage can be expensive, often three times the last premium
paid by the practitioner.
Extreme care must be used if a practitioner switches insurance carriers
with a claims-made policy. The new policy will not generally cover conduct
occurring prior to the date of the new policy. Doctors should request “prior
acts” coverage, commonly referred to as “nose” coverage, to cover this
potential gap. Alternatively, the doctor may purchase prior acts coverage
from the new insurance company. This will cover any incidents which occur
before the date on which the new coverage begins.
Limits of Malpractice Insurance

A policy limit stipulates the maximum amount of compensation an insurance
company will cover upon the result of a claim against a doctor. With an
occurrence policy, a separate set of limits will be given for each year you
purchase the policy. The limits of the policy remain available to pay for future
claims, which are based upon claims that occur during that specific policy
period. With claims-made coverage, only the current limits apply to pay for
claims, which arise from the previous years of practice. For example, a
standard $1 million/$3 million policy limit will allow for $1 million available
to pay any single claim and $3 million total for the span of the policy period.
Entity Coverage
Most doctors do not realize that their practice entity may be named in a
lawsuit along with themselves. If the doctor owns their own practice, there
are two possible forms of coverage.
Separate Limits Coverage.

With most insurers the practice may be eligible for an entity malpractice
policy with separate limits of liability. This will allow for defense costs and
indemnity payments to be covered separately from the individual policy
limits.
Shared Limits Coverage.

Doctors who own 100% of a solo practice may combine their individual policy
limits with their practice policy limits. Defense costs and indemnity
payments will be paid on behalf of both the individual and the practice.
Reporting to National Data Base

The National Practitioner Data Bank (NPDB) was created by Congress as a
federal repository of health care provider information within the United
States. The NPDB was implemented in 1990, and it requires reporting of any
licensure, hospital privileges, and professional society actions against
dentists related to quality of care. Additionally, the NPDB monitors and
provides information on malpractice payments made for all health care
practitioners on settled malpractice cases. The information is not available to
the general public and is only provided to hospitals, health care entities, and
licensing boards.
If a doctor is reported to the NPDB, the doctor is given the opportunity to
respond to the allegations of the reported incident. This statement is
available on the NPDB website. Additionally, there is a self-query service for
health care professionals to view and request information about themselves
contained in the NPDB.
State Dental Licensure Complaints

Complaints against practitioners to state boards are on the rise in most
states. Complaints against dentists to the state board usually occur by two
avenues. First, if money is paid to a patient by an insurance company in
resolution of a claim, the malpractice carrier is in most circumstances
obligated to inform the state board. This report often results in an
investigation by the state licensing board. Secondly, a patient may have
difficulty in obtaining legal representation in pursuing dental malpractice
litigation against a dentist. Many attorneys will not represent patients unless
there is serious injury to the patient. With no other recourse, the patient files
a licensure complaint to the state licensing board.
After the state board is informed or receives a complaint about a licensed
dentist, an investigation will follow. The procedures to be followed will vary
according to a particular state's public health code, dental practice act, or
health department administrative. It is highly recommended that the
practitioner be well versed on the processes and procedures for their own
state.
Additionally, some states may require dentists to self-report any
convictions of crimes, which most likely will result in a board investigation.
Most state legislatures have enacted legislation that mandates the state
dental board to investigate every complaint (e.g., patient insurance carrier,
self-reporting) asserted against a licensed dentist.
The investigation process usually begins with a request for records by the
state board. In some situations, a records request is not the result of a
complaint against the dentist but could involve a complaint against another
licensed practitioner. When sending records, is it imperative to make a
notation of what records were sent and confirmation of their delivery. Most
states have dental investigators who will review the requested records,
radiographs, and other related documents and make a recommendation to
the state board. If the investigation recommends further investigation, the
dentist may be interviewed, and the process will continue according to the
state's dental practice act.
After evaluation by the state board and the investigator, if the board
determines there has been a violation of the state dental practice act, a wide
array of sanctions may be imposed against the dentist. This may include a
monetary fine, restriction of certain practice procedures, continuing
education, restitution in the form of repayment to a patient or third-party
carrier, or licensure suspension or revocation.
Most commonly, the highest expenditures involving a complaint against a
licensed dentist are the legal costs associated with its defense. Most dental
professional liability policies will not provide for coverage for any state board
fines, restitution, continuing education costs, or other discipline that may be
imposed.
Legal Representation.
Although many dentists feel that a state board complaint is not as serious as
a dental malpractice suit, they are often mistaken. It is highly recommended
that the dentist seek legal representation immediately upon being notified of
a state board complaint. Most insurance carriers will provide legal
representation for state board issues if they arise from a dental injury or
incident during an active policy period. An attorney will ensure full
compliance with state laws and will aid in the process.
If the state investigator requests an interview, an attorney is highly
recommended to be present. This will prevent the doctor from putting
themselves in a compromised or a vulnerable position. More importantly, if
the licensing board requests a settlement conference, the practitioner should
be accompanied by legal representation. This will minimize the possibility of
the dentist making ill-advised statements that may be detrimental to the
final outcome of their case.
Avoiding Lawsuits
Maintaining Accurate, Concise Dental Records
The first step in an effective overall risk avoidance philosophy is to maintain
good, accurate, and timely dental records and charting. The dentist with
detailed and complete records has a significant advantage in any litigation or
administrative proceeding.
Proper documentation is important for a number of reasons. First, it is a
legal requirement of the various state licensing boards. Each practitioner
should be familiar with the record-keeping and charting requirements of the
jurisdiction in which they practice. Second, the record is a means of
communication to keep the doctor, as well as other practitioners caring for
the patient, apprised of what treatment has been completed and a summary
of future treatment indicated. Third, charting creates documentation in both
litigation and administrative proceedings. If charting is inadequate, it will
create a negative connotation in the eyes of the court and jury and may
expose the practitioner to discipline.
No practitioners can remember every interaction, phone call, medication,
conversation, and procedure involving every patient. In the event of a legal
action, the practitioner will most likely need to rely upon what has or has not
been documented, to some degree. In addition, in the litigation environment
the practitioner's expert is going to formulate their opinions based upon the
available documents and records. The expert should be able to read the
documentation and understand what treatment has been performed, the
clinical and radiographic basis for the care, and the treatment's final
outcome. The age-old adage “if it's not written it did not happen” still holds
true today. Conversely, it is difficult for a patient's expert to contradict the
documentation in a patient's chart if the record is detailed and accurate both
before and after a complication arises. The logical inference is that a
practitioner who keeps accurate records as a matter of course has records
that are more trustworthy.
The plaintiff's attorney and expert will also scrutinize the patient's records.
If the records are poor, this may have a negative effect on the implant
clinician's credibility. For example, the plaintiff's attorney and expert will
explain to the jury that the records are “sloppy” and a deviation from the
state board's requirements. On the other hand, good records suggest that
appropriate time and care has been devoted to the patient's medical-dental
needs.
One often-overlooked area of documentation is missed or cancelled
appointments. It is crucial, particularly in cases with complications, to note
patient appointment failures or cancellations. It is difficult, if not impossible,
to reconstruct a history of missed or cancelled appointments years after they
occur. This is especially important where the patient's failure to keep
appointments makes it more difficult for the dentist to monitor and treat a
complication.
Additional information that is often overlooked and not documented
includes:
• Medical history updates
• List of current medications
• Medications prescribed (include name of pharmacy/phone number if called
in)
• Consultation referrals
• Recommended posttreatment care
• Postoperative instructions
• Lack of patient compliance
The minimum content of progress notes/treatment notes is generally
governed by the various state dental practice acts. However, some general
principles apply to all such records that extend beyond the minimal
requirements established by the state boards. The SOAP format is a method
of documentation recommended for health care providers for progress notes
in the patient's chart. The SOAP acronym has four components: subjective,
objective, assessment, and plan (Box 19.3).
Subjective: includes the patient's chief complaint and should include

comments, desires, expectations, and physical complaints.
Objective: includes information that the practitioner observes from the

patient's clinical presentation. This may include the medical history review,
physical examination, clinical findings, diagnostic test results, radiographic
evaluation, and observations.
Assessment: should include a summary of the patient's main symptoms and

diagnosis including a differential diagnosis. The assessment should also
include possible and likely etiologies of the patient's problem.
Plan: should include all aspects of the actual treatment plan including:
Patient preparation: includes informed consent,

preoperative medications, NPO status, local
anesthesia, etc.
Patient treatment: includes all aspects of the treatment

performed.
Postoperative instructions and medications prescribed

(prescription and over-the-counter)
Next visit summary: treatment to be performed at the

next visit.
Box 19.3
Ideal Patient Records
1. All entries in the written patient record should be completed by the doctor,
not the assistant or staff member.
2. If a staff member does make an entry into the chart, the information
should be initialed and dated.
3. The record should be completed as soon as possible after treatment is

completed; delays in documentation lead to errors.
4. The record should represent the facts in an objective manner.
5. Document any complication or unexpected event in detail with treatment

and follow-up information.
6. Document any change in the treatment plan and a reason for such change.
7. Document how the patient tolerated the procedure.
8. Document any medications administered including quantity of local

anesthetic.
9. Provide postoperative instructions to patient verbally and in written form;

explain the purpose and proper dosage of any medications prescribed.
10. Document that the patient was discharged in good

condition.
11. Document treatment to be rendered at the next

appointment.
Potential Complications
Inadequate Documentation Concerning Implant Procedures.

Implant-related treatment must to be documented in a comprehensive,
detailed manner with respect to the course of treatment. Some important
documents that are often missing from practitioner's treatment records
include:
Medical history: any changes in the patient's medical history including

medications and recent medical procedures
Implant details: surgery report describing implant location, size

specifications, serial numbers, and manufacturer
Unexpected treatment: documentation of nonideal placement (e.g., anatomic

variants, malposition, grafting)
Anesthesia: type, quantity, and method of administration of anesthesia used

in case of medical emergency or postoperative complication
Bone graft material: type, source, quantity, location, and label in surgery
report
Fixation screws: number, size, and location of bone or tack screws
Membrane: type, source, quantity and size, location and label in surgery
report
Complications: detailed, accurate recording of any intra- or postoperative

complication
Altering, Adding, Deleting Information From the Patient

Records.
When confronted with litigation or a licensing board inquiry, the implant
clinician may often be inclined to make additions or modifications to the
chart. The practitioner will often look back at events or pertinent facts that
were not documented and make alterations to place themselves into a more
favorable position.
Altered records are discovered in a number of ways. Often, unbeknownst
to the dentist, staff has already provided copies of the unaltered chart to the
patient. Staff often view a request for records as an administrative task and
unnecessary burden for the doctor. Secondly, the popularity of electronic
records has raised many validity issues with progress notes and imaging.
Most software programs today contain tracking and theft mechanisms that
will detect if any alterations were made.
There are numerous forensic expert witnesses who are specialists at
analyzing questioned documents. These include document/handwriting
examiners, chemists who analyze ink, and computer specialists. From a legal
perspective, the consequences of altered records can be catastrophic for the
doctor, even where the resulting litigation or administrative proceeding is
otherwise defensible. The practitioner will lose their credibility when found
guilty of document alteration. The practitioner may also lose their
malpractice insurance coverage, as well as the legal representation provided
by their insurance malpractice. They may be subject to court sanctions,
including the striking of legal defenses, and/or subject themselves to claims
for exemplary or punitive damages, or even criminal prosecution.
If a change needs to be made to a patient's record, the added information
should be included as an addendum, not in the original document. When
corrections need to be made, a single line should be made through any
information to be deleted. These changes should be signed and dated
appropriately.
Comprehensive Medical-Dental History Forms
A common problem in many dental offices is the failure of practitioners to
periodically review and amend their forms and record systems. Older, dated
medical histories tend to ask broad-based questions (e.g., “Do you suffer
from any serious medical condition?” or “Are you in good health?”). This is
not a good practice and often results in significant medical issues being
missed. The modern trend in medical histories is towards specific “condition-
based” inquiries. These type of questions are more easily understood by the
patient and are less likely to be overlooked.
A good example are bisphosphonate medications. Most older medical
history forms do not ask whether there is a history of bisphosphonate use
because 20 years ago this entire drug category was in its infancy. Today,
practitioners regularly and routinely encounter patients who have a current
or past history of bisphosphonate use. Where the use of these medications is
not known, implant clinicians place their patients at risk and expose
themselves to potential litigation and administrative action. Herbal remedies
present similar problems. Many supplements affect bleeding, inflammation,
and healing and cause drug interaction complications. As such, questions
about their use should be an integral part of the patient's medical history
form.
Not Updating Forms.

If a medical update is not obtained by the doctor, this may show evidence of
lack of diligence that may support a patient's claim of professional
negligence. Practitioners need to recognize that the practice of dentistry is
always evolving and that forms require periodic updating. In the event
something is missed on the medical history, it is not a valid defense in a legal
action that “it was not on the form” or that “it's the software's fault.” Should
a medical complication occur and litigation result, a patient's lawyer and
expert witness will analyze the patient's past and current medical history
forms with great care. An updated medical history form should be an
essential part of a dentist's office risk management program.
Prior to each appointment the written medical history should be reviewed
along with the patient's current medications and dietary supplements.
Patients should be asked if there have been “any changes in the medical
history since the last appointment.” At a minimum, a notation should be
made in the chart confirming that the patient's health status and medications
were reviewed by the practitioner and discussed with the patient, including
(when applicable) the lack of any changes in the patient's health status or
medications.
At a minimum, patients should have their medical forms reviewed or a
new medical history questionnaire completed on an annual basis. A problem
arises if an older medical history is continuously updated: it may be difficult
to understand because it will be crowded with notations and dates. In such
cases a new questionnaire is always recommended.
Lack of Attention to What the Patient States in the Medical

Forms.
Practitioners must always review the patient's medical history in detail. The
doctor should ask questions about positive responses and inconsistencies.
For example, a patient may list prescription medications on the history form
yet fail to list a treating or primary care physician. Or a patient may indicate
that they are a “controlled” diabetic. If the doctor does not follow up with
questions concerning how the patient's diabetes is being treated and their
A1c level, the doctor places their patient, and ultimately themselves, at
unnecessary risk.
Failure to Obtain Medical Clearance

Another significant area of concern that dentists commonly fail to address is
obtaining medical clearance from the patient's physician. If a practitioner has
any doubts concerning a patient's current medical status or condition,
additional inquiry is required. The patient's primary care physician or
treating medical physician is in the best position to address questions and
issues concerning the patient's care. In the event of an adverse event, the
physician will most likely be supportive. Conversely, should the dentist fail to
consult with the physician, they could be the most harmful witness in any
subsequent litigation or administrative proceeding.17
Not Providing Physician With Adequate Information.

The content of the medical clearance request is extremely important. Over
the years the trend has been to merely request clearance to “perform a dental
procedure” or to “perform dental surgery.” This is completely inadequate
because insufficient information is provided to the physician. The
practitioner's medical clearance request should at a minimum contain the
following18 and should be accompanied by a cover letter (Fig. 19.14).
• A brief description of the procedure(s) to be performed including time
duration and expected estimation of blood loss.
• The patient's current medical conditions and medication list.
• A list of pre- and postoperative medications to be administered and type of
anesthesia (local anesthesia (LA), intravenous sedation (IV), oral sedation,
general anesthesia) to be administered for the procedure.
• A request for any special instructions the physician may have on the
modification of any current or proposed medications.
• Most Important: NO MEDICATION SHOULD EVER BE ALTERED
WITHOUT PHYSICIAN'S CLEARANCE.
FIG 19.14 Medical clearance form. This is a summary of patient-reported medical
issues and a list of medications, list of proposed medications, and questions for the
physician to complete and forward back to the practitioner.
Ordering Lab Tests.
Because of the increased prevalence of patients with systemic diseases,
laboratory tests such as hemoglobin A1c (diabetes), CBC (complete blood
count) and INR (anticoagulant therapy) are often warranted. However, the
tests should always be ordered by the physician and interpreted by the
physician. If the implant clinician orders a test, they are placing themselves
at risk of being responsible for the interpretation and referral when there are
abnormal values.
Not Following Up With Physician's Office.

The implant clinician should follow up on a regular basis with the patient's
physician, especially for patients with multiple comorbidities, to determine if
there is any change in the patient's health or status. A patient may have a
change in health status or prescribed medication, which affects treatment
planning and/or appropriate treatment options.
Verbal Communication.
Care should be taken when obtaining medical clearance via verbal
communication. It is highly unlikely the physician will document the
conversation. If a problem arises and litigation results, testimony most likely
will occur many years later. It is often difficult, if not impossible, for the
physician to remember all the details concerning a phone conversation.
Dentists often are confronted with a physician not responding to a request
for medical clearance. This is not a green light to move forward with
treatment. It is entirely appropriate to have the patient contact the medical
office and insist that the physician complete the clearance. It is simply not a
valid defense to a civil or administrative proceeding to say that “the
physician did not return my calls so I performed the procedure anyway.”
Inadequate Information From Physician.

One must make sure the clearance is complete prior to undertaking a
procedure. If the medical clearance is equivocal in any respect or not
responsive to the practitioner's specific concerns, additional inquiry is
appropriate. If the medical history and/or subsequent clearance reveals a
matter potentially affecting the care or treatment, the practitioner should
have a detailed discussion with the patient and the informed consent should
be modified accordingly. In this situation, the patient will be well aware of
the potential risks and complications of the procedure, not just from the
dentist's standpoint, but from the physician's perspective as well.
Comprehensive, Detailed Treatment Plan

A detailed treatment plan should be thoroughly discussed with the patient,
and the patient should be provided with a copy of the proposed plan in
writing. All possible options, along with the advantages and disadvantages of
each option, should be discussed in a manner that is easily understood by
the patient. Often, practitioners give the patient a single option, which, in
reality, is simply the option preferred by the doctor. Finally, the treatment
plan should include an estimate of the cost and anticipated duration of the
treatment, as well as language addressing the fact that the treatment plan is
“only an estimate” and “additional procedures and expenses may be
necessary” (Fig. 19.15).
FIG 19.15 Treatment plan example.
Unforeseen Treatment.
From time to time, unexpected procedures are necessary in the treatment of
dental implant patients. This may result in a dispute between the patient and
the doctor.
Example: An example of this situation in oral implantology is the extraction
of a tooth along with a socket graft. Caution should be noted to describe the
socket graft as a “preliminary graft.” If a tooth is extracted and no buccal
plate is present, an additional graft may be necessary in the future, prior to
implant placement. By using the term “preliminary graft,” the practitioner
will have informed the patient about the possibility and the need for a
second graft.
Detailed Cost Breakdown.

If the practitioner does not give a detailed fee summary, the patient may not
understand the total extent of treatment. A financial disagreement may very
well lead to the patient pursuing litigation.
Example: Patients often believe the cost of the implant is inclusive of the
restoration. The patient must be informed and understand that separate fees
exist with the implant, abutment post, and implant crown.
Giving Patient One Treatment Option.

Furnishing the patient with all treatment options minimizes the possibility
of miscommunication. The patient should be instructed to initial the plan
selected, and both doctor and patient should sign the form. The document,
including the plans rejected by the patient, should be made part of the chart.
In many instances, this may be beneficial for future treatment if the patient
decides to upgrade to a different prosthesis.
Example: An edentulous patient is interested in an overdenture; however,
after receiving the final prosthesis, the patient is not happy with the
movement associated with the overdenture. The doctor can then show the
patient the other options that were discussed previously with the patient.
This will minimize the possibility of the patient becoming upset over
unreasonable expectations and costs.
Informed Consent
Most practitioners are unaware of the precise language of their informed
consent forms. Ideally, informed consent is an educational process that
includes the following:
• An explanation of the problem, condition, or area of concern
• The consequences of the condition if left untreated
• The proposed treatment plan
• The reasonable expectations for the treatment
• All realistic treatment options, including no treatment
• The risks and potential benefits of your proposed treatment
This information needs to be provided in a form the patient can
understand, and the patient should be given adequate time to evaluate and
ask questions if necessary.
The adequacy of informed consent is in part determined by state dental
board laws. Each practitioner should be familiar with the obligations
imposed by the state board. The standard against which a practitioner's
conduct is measured falls within two broad categories. In the more
traditional approach the dentist's conduct will be measured or evaluated
against what a “reasonably prudent practitioner ” would have told their
patient when presented with the same or similar clinical circumstances. A
newer and evolving approach adopted by a number of states is the
“reasonable patient” standard. The dentist's conduct will be measured
against what a reasonable patient would want to have known prior to
agreeing to undergo a particular procedure.
In summary, the practitioner has a legal obligation to disclose in an
understandable fashion all significant and relevant information necessary for
the patient to make an intelligent and reasonable decision concerning
whether to proceed with the proposed course of treatment. Experience has
shown that a well-informed patient who has been fully advised of what to
expect and what complications can occur is less likely to pursue litigation
when a complication occurs.
Many practitioners also incorrectly believe that an informed consent will
protect them from potential liability. In reality, the fact that the patient
consented to the care and treatment provided is a different question than
whether the practitioner acted within the applicable standard of care.
Patients cannot consent to negligence.
Example: Many practitioners believe that if the patient signs an informed
consent and an adverse complication (nerve impairment from not accessing
the quantity of bone) arises, the practitioner will not be held liable.
Broad Language.
The language of the informed consent form should be clear and direct, with
no room for misinterpretation. Language that is too broad will lead to
impeachment of the informed consent because of misinterpretation.
Example: A consent form states that “excessive smoking” may lead to
complications resulting in implant failure. In this example, a practitioner
would have a very difficult time explaining what “excessive” actually means
(i.e., 10, 20, 25 cigarettes/day?).
Obtaining Consent Day of Surgery.

Consent is best obtained prior to the day of surgery. Ideally, the consent
should be available on the practice's website or given to the patient prior to
the surgical appointment. A good protocol would be to have the patient sign
the consent form during a “work-up” appointment, which is completed prior
to making the surgical appointment.
Example: When a consent form is signed the day of surgery, patients often
state they “did not read” or “were pressured into signing” the consent
document. Additional allegations in informed consent lawsuits include: “I
was sedated when the form was placed in front of me to sign,” “The front
desk handed it to me and said it was nothing,” or “I did not get a chance to
ask questions.”
Not Understanding Various Types of Consent

Implied consent.
This form of consent is based on the words or conduct of the patient.
Conduct often speaks louder than words. A patient seeks out care and
voluntarily submits to the proposed treatment.
Example: A patient who opens his mouth for the administration of local
anesthetic will not be permitted to deny they consented to local anesthesia.
This is by far the weakest form of consent and should never be used as the
sole type of consent.
Written consent form.

Formal written consent documents have been the hallmark of dental consent
for decades. They are often provided from insurance companies or implant
organizations or they are taken from various textbooks or downloaded off the
Internet. The ideal consent form will allow the patient to initial each different
aspect of the consent (Fig. 19.16).
FIG 19.16 Consent form.
Verbal consent.
Ideally, the practitioner should discuss with the patient all of the risks,
benefits, and alternatives to the proposed treatment. This verbal consent will
act to supplement the written form and should not be used as the sole type
of consent. The practitioner should document in the patient's chart that
verbal consent was completed as further evidence that informed consent was
obtained from the patient.
Video consent.
The newest and most comprehensive form of consent is based on a video
review of the procedure by the patient. In the event the patient denies all or
part of what was explained in the video presentation, the video may be
played for the jury.
An area often overlooked by dentists and many seasoned lawyers is the
concept of informed consent as a cause of action. Lawyers often combine a
claim for failure to obtain informed consent together with a standard
negligence claim. In order to prevail on such an informed consent claim, the
patient and lawyer must prove a number of legal and factual elements.
When consent was obtained irregularly, these elements will include:
1. The dentist failed to obtain the consent of the patient at a time and in a
manner consistent with acceptable standards of care among members of the
profession with similar training and experience in the same or similar
medical community;
2. Had the patient been properly informed, the patient would not have
consented to the procedure;
3. As a result, the patient sustained loss, injury, or damages.
When the issue is whether insufficient information was given, these

elements will include:
1. The dentist failed to provide the patient with sufficient information to give
a reasonable person a general understanding of the proposed treatment or
procedure. This may entail failing to provide acceptable alternative
treatments or procedures or failing to advise the patient of the substantial
risks and hazards inherent in the proposed treatment or procedure that are
recognized by other dentists in the same or a similar community who
perform similar treatments or procedures;
2. If the patient had been properly informed, the patient would not have
reasonably consented to the procedure;
3. As a result, the patient sustained loss, injury, or damages.
It is difficult for a patient to prove they would have refused treatment had
they received appropriate consent, and for that reason, attorneys find it
difficult to prove claims based on lack of informed consent.
Not Utilizing Informed Refusal.

If a patient refuses a recommended treatment or procedure, the practitioner
has a legal obligation to advise the patient of the potential adverse
consequences, and to document the patient's refusal to consent. Informed
refusal occurs where a patient refuses to accept recommended treatment,
therapy, or medication. The dentist still has a duty to provide reasonable and
appropriate care consistent with the applicable standards of care. The
practitioner should obtain and clearly document the informed refusal.
However, an informed refusal does not constitute approval to proceed with
treatment when the proposed treatment is against the practitioner's clinical
judgment.
Example: A patient refuses a cone beam computed tomography (CBCT)
scan prior to dental implant surgery. If it is against the dentist's clinical
judgment to proceed without the scan, the practitioner must advise the
patient accordingly and not proceed with the surgery, irrespective of the
patient's “consent” to the procedure.
Not Documenting Refusal for Referral.

In some situations, the implant clinician may recommend referral to another
dentist or specialist. If the patient refuses the referral, the patient's decision
must be well documented.
Particularly in the absence of a referral to a specialist, experts working on
behalf of the patient will most often focus on the implant clinician's failure
to: (1) predict the potential for complications; (2) recognize the occurrence of
a complication and initiate appropriate treatment; or, (3) recognize the
occurrence of a complication and make a timely referral.16
Battery.
Theoretically, if treatment is rendered to a patient without proper informed
consent, in certain states this may be construed as “battery” (i.e.,
intentionally touching a patient without obtaining consent). Battery is a
criminal offense, which can be the basis of a civil lawsuit. The key element of
battery is the touching (treatment) is not authorized by the patient, not that
it be intended to harm the patient. Forcing beneficial or needed care on an
unwilling patient would be considered battery. An example of this is the
performance of a sinus lift and bone graft on a patient who is sedated and
has not consented to such procedures.
Managing Complications
In the event a complication occurs, at a minimum the practitioner should
record:
• What occurred in a detailed, objective manner
• Detailed plan for addressing the event
• Discussions with the patient including comprehensive instructions
The practitioner's response to a complication will likely be a significant
factor in the outcome of any subsequent litigation: it may even determine
whether there is any litigation in the first instance. The dentist should
explain to the patient that complications sometimes arise and they will work
through the situation together. Any discussion with the patient should be
clear and detailed, including the events leading to the complication, and
documented by the dentist.
Placing Blame on the Patient.

Put simply, it is best to avoid blaming the patient for a complication, even in
instances where the patient failed to follow instructions or is otherwise
responsible. Ideally, the complication should be addressed with the patient
and resolved before the dentist-patient relationship is compromised by ill
will or severed completely.
Example: Many dentists will blame a failed implant (early failure) on the
patient's lack of hygiene.
Not Documenting After Hours Phone Calls.

One of the most important aspects of the treatment of complications is the
documentation of “night of surgery” or “after hours” communications. These
communications are particularly important in instances where the
complication results in litigation or administrative proceedings. For this
reason, practitioners should maintain an “After Hours Contact Form” or
alternative method of documenting “after hours” communications with
patients. This includes “night of surgery” postoperative checks, patient calls
regarding complications, and/or medication issues. Such notes should
include specific information (Box 19.4).
Box 19.4
After Hours Contact Form
• Date and time of the call
• Who initiated the call
• Who was spoken to: the patient, family member or other individual
• Any subjective complaints of the patient
• Inquiry as to whether the patient had prescriptions filled and if they are
taking the medications as directed.
• Instructions given, if any
• Prescriptions called in with the name and phone number of the pharmacy
• Any offers to see the patient apart from the scheduled follow up
• Any additional information
Good Rapport With Patient

When adverse complications arise, doctors should be as accommodating as
possible to their patient. Studies have shown the two main reasons patients
take legal action following dental surgery are deviations from the standard of
care and professional attitude.19 If the patient feels betrayed by the doctor or
the doctor is less than receptive to the patient's concerns or complaints, the
patient may seek a second opinion. That, in turn, may lead to the patient
contacting an attorney. For these reasons, spending time with the patient and
discussing the issue and treatment options is far more likely to deter a
patient from seeking legal action than ignoring the patient's concerns or
blaming the patient for the complication. If a patient genuinely feels that
their doctor is compassionate and cares about their well-being and is
committed to achieving a desirable outcome, the threat of litigation
decreases significantly.
Keep Current
All implant clinicians should stay current with the newest research and
protocols within the profession. An excellent avenue is continuing education
from a course not presented by a manufacturer. Practitioners should remain
skeptical of questionable new products, as well as manufacturer-based
studies. In other words, implant dentists seeking to manage their risk should
adhere to the “don't be the first, but don't be the last,” line of logic.
Understand the Basics of CBCT Technology

One of the fastest growing diagnostic areas in implant dentistry is the use of
CBCT. However, as CBCT technology advances, so does the potential for
litigation. There are several factors that predispose a doctor to liability with
CBCT scans.20
Potential Liability
To Take a Scan or Not.

In medicine, radiographic equipment is usually not approved for a particular
purpose or indication. Nor is there any actual “standard of care” or
universally accepted guidelines for the use of CBCT technologies. Instead,
any applicable standard of care is mandated by the legislature, a court, or
dental board.20
On the other hand, even in the absence of an express guideline, an implant
clinician is more likely to be questioned for failing to use available CBCT
technologies preoperatively if a complication arises.21
Technical Parameters.
The doctor ordering the scan must be careful to select the correct parameters
of the scan. Inadequate or improper CBCT settings and parameters may lead
to liability. Examples include ordering a scan with low resolution when a high
resolution is indicated (e.g., tooth fracture).
Field of View.
The field of view (FOV, anatomic limits of the scan) is crucial in the
preoperative assessment of an implant patient. Ideally, the FOV should be
the smallest possible to reduce the patient x-ray dosage and improve spatial
resolution. However, if the FOV is too small, inadequate sufficient evaluation
of the anatomic area will result. This is most commonly seen in the posterior
maxillary augmentation when too small a field of view is used. If there is any
type of pathology in the sinus and the scan is not taken high enough to
determine the patency of the ostium, the doctor is at risk of causing serious
sinus issues because of the inability to determine the patency of the ostium
and the nature of the pathology.
Interpreting the Scan.

There is no current consensus on the legal ramifications of interpreting
CBCT scans. However, as a general proposition the implant dentist remains
responsible for interpreting the entire scan.22 The implant clinician has three
options. The implant clinician may: (1) interpret the scan themselves; (2)
send the CBCT data to a licensed radiologist, or (3) have the CBCT data
evaluated by the hospital or imaging center radiologist.
Referral to Radiologist.
Ideally, most clinicians will decrease their liability by referring their CBCT
scans to a radiologist for evaluation. However, if the doctor sends the scan to
a radiologist who is unqualified to interpret the scan, the dentist may have
liability for the negligent referral.23 Additionally, the CBCT scan must be read
by a radiologist licensed in the same state as the implant clinician.
Otherwise, the dentist may be subject to disciplinary action by the state
dental board for aiding and abetting the radiologist's unlicensed practice of
medicine and for negligent referral of the patient's scan to the unlicensed
provider.24 The implant clinician also should confirm that the radiologist's
malpractice insurance covers the reading of CBCT scans.
Waiver of Liability.
Many implant clinicians who are untrained in CBCT interpretation request
their patients sign a waiver of liability regarding the interpretation of the
CBCT scans or a waiver of the right to have the scan read by a radiologist. In
general, a patient cannot consent to the negligence of their dentist or other
health care provider.25 Waivers of liability typically have no legal effect and
are inadmissible.
Guaranteed Outcome of Treatment

Caution should be exercised to avoid guaranteeing the results of treatment
such as the ability to masticate certain types of food (e.g., eat an apple).
Marketing advertisements may also indirectly be interpreted by patients as
guaranteed results. These issues may be minimized by good verbal
communication prior to treatment on the possible complications and
associated longevity of the prosthesis. Usually, dissatisfaction with esthetics
can be explained by unreasonable expectations by the patient. However, if
the doctor has marketing materials such as before and after photos of
previous cases, this may be construed by the patient as the expected
outcome.
Example: This will most likely occur with maxillary anterior implant in
which the final crown will be elongated or longer than the adjacent teeth.
Ideally, this possibility should be included in the consent form prior to
treatment.
Patient Abandonment
In the medical field a doctor has an obligation to treat the patient once the
dentist-patient relationship has been established. However, there may be
instances where it is unreasonable or impossible to fulfill the demands of the
patient to complete treatment. Sometimes a patient will become
unreasonably demanding or refuse to accept proposed treatment
recommendations. It is prudent to send a letter to the patient indicating that
the dentist-patient relationship is being terminated and clearly outline the
treatment needs of the patient, including follow-up care. To guard against
being accused of abandonment, the dentist should take the following steps:
1. Document completely the noncompliant actions of the patient

2. Send a termination letter (certified) to the patient with the following
information:
• The reason for dismissal from the practice
• The consequences of not seeking treatment by another

practitioner
• An offer to see patient on an emergency basis for a

reasonable period of time (≈30 days)
• Recommendation on possible avenues for the patient to

obtain another dentist (e.g., local dental society)
• Offer to forward progress notes and radiographic

information to the new practitioner upon receipt of a
release (Fig. 19.17).
FIG 19.17 Patient dismissal form.
Summary
Malpractice suits are a feared, often devastating and infuriating, event that
changes a doctor's life. Especially in the field of oral implantology today, the
legal ramifications are significant. Complications do occur and will continue
to occur despite even the best care of the practitioner. With the number of
implants being placed increasing at an alarming rate, along with a wide
spectrum of general dentists and specialists placing implants, legal issues
will most likely increase in the future. Malpractice actions are governed by
the individual state laws and rules; thus the implant clinician must have a
complete understanding of the laws and rules in the state they practice. In
general, however, all states require a malpractice claim to contain the same
elements: (1) duty; (2) breach of duty (i.e., deviation from the standard of
care); (3) legal causation between the deviation from the standard of care and
resulting injury; and (4) damages. The implant dentist should have a strong
understanding the legal system and terminology along with a strong
foundation on how to avoid the possibility of a lawsuit (Box 19.5).
Box 19.5
Common Legal Terminology
Action: Another term for a legal case or lawsuit.
Appeal: A review by a higher court concerning the decision of a malpractice

trial court verdict.
Arbitration: Submitting a case or dispute to designated parties (group of

attorneys) for a decision instead of using a judge or jury.
Claim: The receipt of a demand for money naming the insured and alleging
dental malpractice. Claims may also include dental licensing board
complaints.
Compensatory Damages: Reimbursement for actual loss or injury.
Complaint: A legal document that informs the court of the malpractice case
and is usually served with a summons on the defendant to begin the case.
Continuance: The adjournment or postponement of a court case to another

day.
Counter-Claim: A claim by the defendant in a malpractice case stating the

defendant is entitled to damages or other relief from the plaintiff.
Cross-Examination: The questioning of a witness for a particular party by an

opposing party.
Damages: Money a party receives as compensation for a legal wrong.
Defendant: In malpractice cases, the doctor being sued, also called a

respondent.
Deliberation: The process by which a judge or jury makes a decision or a
verdict.
Deposition: Testimony of a witness taken, under oath, in response to another

party's questions. This testimony is usually given outside the courtroom in
a doctor's office or lawyer's office.
Direct Examination: The questioning of a witness for a particular party by

that party.
Discovery: A formal request or gathering of information by one party in a

lawsuit to disclose information or facts known by other parties or
witnesses.
Finding: The court or jury's decision on issues of fact.
Inadmissible: Evidence that is not allowed to be presented because it is

deemed unreliable.
Interrogatories: Formal, written questions used to get information from

another party in a lawsuit.
Injunction: A court order to stop doing or to start doing a specific act.
Judgment: A court decision. Also called a decree or an order.
Jury Instructions: Statements made by the judge to the jury that instruct the
jurors on the pertinent law in the jurisdiction applicable to the action
about which they will deliberate.
Malpractice: When treatment provided by a dentist falls below or fails to

comply with the standard of care exercised by other similarly trained
dentists in similar situations.
Mediation: A dispute resolution process in which an impartial third party

assists the parties to voluntarily reach a mutually acceptable settlement.
Motion: Request (usually written) to the court in a case. Filed with the clerk's
office.
Motion in Limine: A motion usually made at the start of a trial requesting the
judge rule that certain evidence may not be introduced in trial.
Negligence: Failure to exercise the care similar to what a reasonable or

prudent practitioner would do in the same circumstance.
Notarize: To formally complete a document by acknowledgement or oath.
Perjury: Making false statements under oath.
Plaintiff: The person who sues or starts a civil case; also called the petitioner
or the complainant.
Pleading: A formal statement of the cause of an action or defense.
Preponderance of Evidence: A requirement that states more than 50% of the

evidence is present and is the burden of proof in a civil trial.
Pretrial Hearing: Conference with attorneys to determine scope of possible

trial with view toward resolving issues through agreement.
Recovery: The acquisition of something of value through the judgment of a

court.
Relief: Compensation sought by the plaintiff for their injuries.
Remedies: Is the means with which a court of law enforces a right, imposes a
penalty, or makes a court order to impose its will.
Settlement: The resolution of a lawsuit without going forward to a final court

judgment.
Statute of Limitation: A law that prevents patients from bringing malpractice

claims against a doctor once a specified period of time has passed since
treatment.
Subpoena: Legal process that commands a witness to appear and testify.
Summons: A legal paper used to start a civil case and get jurisdiction over a
party.
Tort: A wrongful act or an infringement of a right, which leads to a civil legal
liability.
Verdict: The determination of a jury on the facts and, usually, the legal
consequences of those facts.
Voir dire: A legal phrase that refers to an oath taken by jurors to tell the
truth. This is the process by which attorneys question, or examine,
prospective jurors to determine whether they are qualified to serve as
jurors.
Writ: An order issuing from a court of justice and requiring the performance
of a specified act, or giving authority and commission to have it done.
References
1. Florida Office of Insurance Regulation: Professional Liability Tracking
System. [Available at]
http://www.floir.com/Sections/PandC/ProfLiab_db/index.aspx.
2. National Practitioner Data Bank Public Use File. [December; Available
at] http://www.npdb.hrsa.gov/resources/publicData.jsp; 2012.
3. Frankel D. What determines malpractice payments? MedMal Reporter.
2007;1:1.
4. Lambert PM, Morris HF, Ochi S. Positive effect of surgical experience
with implants on second-stage implant survival. J Oral Maxillofac
Surg. 1997;55(12 Suppl 5):12–18.
5. Studdert DM, et al. Claims, errors, and compensation payments in
medical malpractice litigation. N Engl J Med. 2006;354(19):2024–2033.
6. Health Information and the Law. [Available at]
http://www.healthinfolaw.org/comparative-analysis/individual-access-
medical-records-50-state-comparison.
7. Oja v. Kin, 229 Mich. App. 184. 1998.
8. Berry DB. The physician's guide to medical malpractice. Proc (Bayl
Univ Med Cent). 2001;14(1):109–115.
9. Odom L, Garcia A, Milburn P. The ethicality of capping economic
damages to control rising healthcare costs: panacea or false and
misleading practice? Internet J Healthcare Admin. 2004;3(1).
10. Tahouni MR, Kahn JH. Professional liability insurance. Emerg Med Clin
North Am. 2009;27(4):569–581.
11. Vidmar N, Lee P, MacKillop K, et al. Jury awards for medical
malpractice and post-verdict adjustments of those awards. DePaul
Law Rev. 2005;54:315–356.
12. Justia. [Available at] http://www.justia.com/trials-
litigation/docs/caci/200/200.html.
13. California Code of Civil Procedure Section 2034. [210(a)] 2010.
14. California Code of Civil Procedure Section 2034. [210(b)] 2010.
15. Ohio Rev: Code §2305.252.
16. Curley AW. The law and dentoalveolar complications: trends and
controversies. Oral Maxillofac Surg Clin North Am. 2011;23(3):475–484.
17. Gary CJ, Glick M. Medical clearance: an issue of professional
autonomy, not a crutch. J Am Dent Assoc. 2012;143(11):1180–1181.
18. Geist SM, Geist JR. Improvements in Medical Consultation Responses
with a Structured Request Form. J Dent Ed. 2008;72(5):553–561.
19. Holmes SM, Udey DK. Risk management in oral and maxillofacial
surgery. Oral Maxillofac Surg Clin North Am. 2008;20(1):119–126.
20. Friedland B, Miles DA. Liabilities and risks of using cone beam
computed tomography. Dent Clin North Am. 2014;58(3):671–685.
21. Pollack A. Medical technology ‘arms race’ adds billions to the nation's
bills. N Y Times Web. 1991;29(A1):B8 [Available at]
http://www.nytimes.com/1991/04/29/us/medical-technology-arms-
race-adds-billions-to-the-nation-s-bills.html.
22. Friedland B. Clinical radiologic issues in orthodontic practice. Semin
Orthod. 1998;4(1):64–78.
23. Estate of Tranor v Bloomsburg Hosp. 60 F. Supp. 2d 412, 416 (M.D. Pa.
1999).
24. Texas Occupations Code, Title 3, Subtitle D, Chapter 251; California
Business and Professions Code x2264.
25. Dahl D. Doctors' ‘no sue’ contracts spark debate. [Lawyers USA May 21]
2007.
Index
Page numbers followed by “f” indicate figures, “t” indicate tables, and “b”
indicate boxes.
A
AAD. See Antibiotic-associated diarrhea
AAID. See American Academy of Implant Dentistry
AAOMS. See American Association of Oral and Maxillofacial Surgeons
Abandonment of patients, 862, 863f
ABOI. See American Board of Oral Implantology/Implant Dentistry
Abrasion, O-rings and, 617
Abscess
brain, 309–310, 311f
infection stage of, 298–299, 299f
terminology and characteristics of, 298b, 298t
Absorbable sutures, 418–420
natural, 418, 418f
synthetic, 418–420, 418f
Abundant bone. See Division A
Access flap, for peri-implantitis management, 802–803, 805f
Accessory foramens
nerve impairment and evaluation for, 351–352, 352f
radiography and, 159–160, 161f
Accreditation, complication prevention and, 11
ACEs. See Angiotension-converting enzyme inhibitors
Acetaminophen (Tylenol), 44t–45t, 369–370, 370t
Achromycin. See Tetracycline
Acrylic fracture, 648, 649f
ActCel, 277t, 279
Actinobacillus actinomycetemcomitans, 777–778
Active hemostatic agents, 277–278, 277t, 278f
Acupuncture, 33t
Acute disuse window, in modeling/remodeling bone, 113–114, 114f
Acute rhinosinusitis, 176–177, 176f, 513
antibiotics for, 551
CBCT examination for, 551–552
differential diagnosis of, 513
etiology of, 513
maxillary sinus grafting infections and, 551–552
radiographic appearance of, 513, 514f
treatment of, 513
ADA. See American Dental Association
Adapted window, in modeling/remodeling bone, 114, 114f
Adenocarcinoma, 180
Adjacent teeth
cantilevers and four or more missing, 81, 82f
GBR membrane placement too close to, 460–462, 462f
injury, 375
etiology of, 375
prevention of, 375, 376f
treatment of, 375
IPO, increased proximal contact area and tilted, 756f
malpositioning of implants and condition of, 260
Adolescents, 34–35
CBCT for, 35
complications prevention with, 35
growth cessation and, 35, 36f
surgical/implant implications with, 35
Adrenal issues
COPD and, 24
corticosteroids and, 22
IBD and, 27
Advil. See Ibuprofen
Affidavit of Merit, 833, 834f
Afrin (oxymetazoline), 550
AFs. See Anterior fontanelles
After hours contact form, 861, 861b
Agger nasi cells, 172, 172f
Aging population. See also Elderly
dental implant demand and, 1–6, 6f, 13
edentulism decreasing in, 580
GFR and, 35, 35t
increases in, 581f
Air emphysema, 223, 224f
Akinosi block technique, 215–218, 218f
Alanine transaminase (ALT), 46t–49t
Albumin, 46t–49t
Alcohol, 33
adverse impact of, 33
bleeding implications with, 33
bone loss implications with, 33
cessation program for, 33
complication prevention with, 33
inadequate postoperative instructions for, 373
infection implications with, 33
wound healing/ILO and use of, 408
Alkaline phosphatase, 46t–49t
Allergic rhinosinusitis, 177, 178f, 514
etiology of, 514
radiographic appearance of, 514
treatment of, 514, 515f
Allergies, metal, 43–44
Alloderm, 198–199, 212, 215, 482, 485f–486f, 567
soft tissue closure promoted with, 491f–492f
Allodynia, 342t
Allograft material, 448
Allograft migration, 396, 397f
Alloplasts, 449, 566–567
ALT. See Alanine transaminase
Alveolar socket, nonintact, 565–573
aborting procedure after discovery of, 566
atraumatic tooth extraction for prevention of, 565–566
bone grafting techniques for, 566–567, 566f
pretreatment evaluation for anticipation of, 565
prevention, 565–566
American Academy of Implant Dentistry (AAID), 11
American Association of Oral and Maxillofacial Surgeons (AAOMS), 1–6,
306–307
American Board of Oral Implantology/Implant Dentistry (ABOI), 11
American Dental Association (ADA), 7
American Society of Anesthesiologists (ASA), 295
Amides, 44t–45t, 225–226
Amitriptyline, 37, 384
Amorphous resin scalers, 796
Amoxicillin (Amoxil, Polymax, Trimax), 313, 316t, 319, 366t, 798
Amoxicillin/clavulanic acid (Augmentin), 313–314, 315f, 316t, 319, 366t, 550
for graft site infection prevention, 548
Amoxil. See Amoxicillin
Amylase, 46t–49t
ANA. See Antinuclear antibody
Analgesic agents, for postsurgical pain treatment, 371–372, 371t–372t, 384
Ancef (cefazolin), 549, 549f
Anemia
antibiotics and, 26
bleeding and, 26
bone healing and, 26
edema and, 26
lab tests for, 26
oral signs of, 26
signs and symptoms of, 26
Anesthesia, 341–342, 342t
Anesthetic Dolorosa, 342t
Anesthetics, 384
Akinosi block technique for, 215–218, 218f
COPD and selection of, 24
fires, 226–228, 229b
hypertension and, 15–16
implant placement in mandible and techniques for, 215–218, 218f
maxillary sinus grafting and V2 block injections of, 523, 524f
nerve impairment and, 335
anesthetic toxicity, 335
hematoma, 335
needle, 335
toxicity and overdosage, 225–226, 228b, 228t
Anexate (flumazenil), 231–232, 231f
Angina, 16
N2O sedation for, 16
nitroglycerin complications with, 16
stable and unstable, 16
stress reduction for, 16
surgical/implant implications of, 16
treatment summary for, 16
Angiotension receptor blockers (ARBs), 14
Angiotension-converting enzyme inhibitors (ACEs), 14
Angled loads
CHS magnifying, 747–748, 749f
cortical bone strength and, 733, 733t
crestal bone strain and, 733–734
FEA and increased stress with, 733
fixed occlusal complications and, 687–688, 688f
solutions to, 688
IPO and no occlusal, 732–734, 732f–734f
management of, 735
prosthetic, 735–736, 736f
surgical, 735
prosthetic, 734–736, 735f
Angulation, available bone, 67, 67f, 558–560, 561f
Anterior cranial base, displacement of implants in, 392–393, 393f
Anterior fontanelles (AFs), 507–508
Anterior guidance, 727b
IPO and shallow, 736–739, 736f–739f
cuspid implant and, 738–739, 740f
vertical overbite and, 738, 738f–739f
Anterior loop
IAN confusion with, 352, 353f
mental nerve evaluation for, 352, 352f
radiography and, 159, 160f
Anterior mandible. See Mandible, anterior
Anterior maxilla
available bone angulation of, 67
available bone height of, 64
available bone width of, 65, 66f
ideal implant positioning distance from, 257–258, 261f
occlusal contact timing prevention in, 690–691, 691f
Anterior palatine canal. See Nasopalatine canal
Anterior superior alveolar nerve, 332, 333f
Anterior wall of maxillary sinus, 506–507, 508f
Anteroposterior distance (A-P spread), 79–80
arch form and, 110, 110f–111f
OD-5 and, 605–606, 605f
Antibiotic-associated diarrhea (AAD), 374–375
Antibiotics See also specific antibiotics
for acute rhinosinusitis, 551
anemia and, 26
beta-lactam, 313–314, 550
clindamycin, 44t–45t, 316–317, 316t
diabetes mellitus and recommendations for, 20
fluoroquinolones, 317, 550
for graft site infection prevention, 547–549
IBD and use of, 28
for ILO infection prevention, 434–435
for infection treatment, 313–317, 316t, 319
prophylaxis, 317–319
infectious endocarditis and recommendations for, 19b
lincosamides, 551
locally delivered, 797–798, 798f
macrolides, 315–316, 550–551
maxillary sinus flora and, 504–505
for maxillary sinus grafting infections, 548–549
metronidazole, 44t–45t, 316t, 317, 551
for peri-implant mucositis debridement, 798
prophylactic, 317–319
complications of, 318–319
MIC of tissue and, 318
in oral implantology, 319
selection of, 318
shortest effective, 318–319
for sinus membrane perforation, 533
sulfonamides, 551
tetracycline, 316t, 317, 551
Anticoagulant medications, 17–18, 40, 44 See also specific types
bleeding and, 42, 269, 269t
types of, 41t
Anticoagulant therapy, interruption of, 272
Anticonvulsants, 384
Antihistamines, 44t–45t
Antihypertensive drugs, 14–15. See also Nonsteroidal anti-inflammatory
drugs
Antimicrobial rinse, 435, 435f
for graft site infection prevention, 549
for peri-implant mucositis debridement, 797, 797f
Antinuclear antibody (ANA), 46t–49t
Antiplatelet medications, 270, 270t
Antirotational design, implant, 388–390
Antral septa
anterior section management of, 536, 537f–538f
complications with, 533–536
etiology of, 533
maxillary sinus grafting and, 533–536
middle section management of, 536, 539f
posterior section management of, 536, 540f
Antroliths, 396
maxillary sinus, 518–520
etiology of, 519
radiography of, 180–181, 182f, 519, 519f
treatment of, 519–520
A-P spread. See Anteroposterior distance
Apical fenestration, 493
Apical fixation, 493–494, 495f
Apical peri-implantitis. See Periapical lesion, implant
Apically positioned flap, for peri-implantitis, 805, 807f
Apicocoronal (“z”-axis) positioning, 252–257
CHS and, 252, 253f
countersinking and, 252
FP-1, FP-2, FP-3 and, 254
complication and treatment for placement too deep, 254f–255f, 255
complication and treatment for placement with inadequate depth, 255–
256, 256f
RP-4 and RP-5 and, 257
CHS less than 15mm, 257, 258f–259f
CHS more than 15mm, 257
complication prevention for, 257
Apixaban (Eliquis), 41t, 42, 269t
ARBs. See Angiotension receptor blockers
Arch forms
maxillary IODs and, 611–612
importance of, 611–612, 612f
types of, 611
OD-4 and, 603, 604f
ovoid, 611
square, 611
tapering, 611
treatment planning with, 110, 110f
Arch position
bone loss and, 108
canines and, 84–85, 84b, 84f
decreased surface area and, 108
first molars and, 84f, 85–91
of maxilla compared to mandible, 108, 108b
maximum bite forces and, 107–108, 108f
poor bone density and, 108–109
posterior regions and, 107–109, 108b, 108f
treatment planning and, 107–109
Aredia (pamidronate), 39, 306–307
Aromatase inhibitors, 43
Arterial hemorrhage, 268b
Articaine, 225–226
Articulation
IPO and mutually protected, 758
occlusal contact timing and protocol for, 689–690, 689f–690f
Articulators, 718–719, 719f, 719t
Artifacts, CBCT, 151–153
beam hardening and, 151–152, 152f
bone dehiscence on 3-D reformatted images, 152–153, 153f
motion-related, 152, 153f
noise, 152, 153f
scatter, 152, 153f
streak, 152, 153f
ASA (American Society of Anesthesiologists), 295
Aseptic technique
clean and sterile techniques compared to, 320t
definition of, 319
for ILO infection prevention, 435
Aspartate aminotransferase (AST), 46t–49t
Aspiration of implant components, 219–221
etiology of, 219–220
prevention of, 220
treatment for, 221, 222f
Aspirin, 40, 270, 370
adverse effects of, 44t–45t
bleeding and, 40
hyperthyroidism and use of, 21
AST. See Aspartate aminotransferase
Atarax (hydroxyzine), 44t–45t
Atraumatic tooth extraction, 565–566
Attachment system, for IODs. See also Dolder bar; Hader bar and clip
system; Locator attachments; O-rings
complications, 612–614
ideal, 612–613
control of retention for, 612–613, 613f
ease of replacement for, 612
location for, 614f
male attached to implant/female in prosthesis for, 613, 613f
retention and stability for, 613
summary of, 613
insertion-removal wear and, 614
mastication wear and, 613–614
for OD-1, 596
for OD-2, 599–600
for OD-3, 602
OD-3 and improper design complication with, 602, 602f
for OD-4, 603
for OD-5, 606
PM and height of, 589, 589f
retention loss over time with, 613–614
for RP-4 option for maxillary IODs, 611
types of, 614–621
Augmentin. See Amoxicillin/clavulanic acid
Autogenous block failure, ILO and, 448, 450f
Autogenous bone grafts. See also Bone grafting
mandibular ramus as donor site for, 158, 159f
material of, 448, 449f
site evaluation for bone needed for, 443, 444f–445f
Autoimmune disease, medical history of, 31–32
Autoimmune reaction, displacement of implants in maxilla and, 394
Autoimmune response of host hypothesis, for marginal bone loss, 786
Available bone
angulation, 67, 67f, 558–560, 561f
CHS, 67–68, 68f
division A (abundant bone), 68–69
advantages of, 69b
complications with, 69, 69f
criteria and dimensions for, 68, 68b
division B (barely sufficient bone) modification to, 71–72, 71f
fixed prostheses and, 68
removable prostheses and, 69
treatment planning for, 68
division B (barely sufficient bone), 69–72
dimensions of, 69, 70b
disadvantages of, 69, 70b
division A (abundant bone) modification from, 71–72, 71f
insufficient osteoplasty and, 72, 72f
root forms of, 70, 70f
treatment options for, 71–72, 71f
division B-w (B minus width), 72–73
bone resorption progression and, 72, 72f
division C (compromised bone), 73
division C-a, 75–76, 75f–76f, 592–593, 592f
division C-h, 73–75, 75f
division C-w, 73, 73f–74f
OD-2 complications with, 600
division D (deficient bone), 76–78
dimensions of, 76b
mandible, 77–78, 77f
maxilla, 76–77, 76f
height, 64–65, 64f–65f
immediate implant placement and, 557–560
angulation, 558–560, 561f
height of, 557–558, 560f–561f
length of, 558
width of, 558
implant number determined by, 91
length, 66–67, 66f
malpositioning of implants and ideal, 259
prostheses and evaluation of, 63–78, 64f
quantity of, 187
width, 65–66, 66f
Avelox (moxifloxacin), 44t–45t, 316t, 550
Avitene, 277t, 279, 279f
Avoidable complications, 10
Axonotmesis, 340–341, 341f, 342t
Azithromycin (Zithromax), 315–316, 316t, 550–551
B
B minus width. See Division B-w
Bacteria
immediate implant placement and presence of, 562
implant placement in sites with preexisting, 194, 195f
wound healing/ILO and, 407–408
Bacteroides forsythus, 776
Bacteroides spp., 503–504, 513–514
Bactrim (trimethoprim/sulfamethoxazole), 316t, 551
Barely sufficient bone. See Division B
“Barrier by bulk”, 466, 474, 476–477
Barrier membrane (BM), 566–567
Basic metabolic panel (BMP), 28, 46t–49t
Basophils, 46t–49t
Battery offense, 861
Beam hardening, CBCT and, 151–152, 152f
Beeswax, 277t, 281–282, 282f
Benadryl (diphenhydramine), 44t–45t
Benign paroxysmal positional vertigo (BPPV)
postoperative complications with, 379–380
etiology of, 379
prevention of, 380
treatment of, 380, 380b, 381f
SA-2 complications with, 529–530, 531f
Benzocaine, 384
Benzodiazepines, 44t–45t
diazepam, 41t, 230t
oral/conscious sedation toxicity and, 229, 230t
reversal agents for, 231–232, 231f
triazolam, 44t–45t, 230t
Beta blockers, 15
Beta-lactam antibiotics, 313–314, 550
Biaxin (clarithromycin), 44t–45t, 315–316, 316t, 550–551
BIC. See Bone-implant contact
Big-nose variant
in maxillary radiography, 172, 174f
maxillary sinus and, 511, 512f
Bilateral balanced occlusion, 722, 722f
Bilirubin, 46t–49t
Binding arbitration, 846
Biocef (cephalexin), 314, 316t, 319
Biologic width hypothesis, for marginal bone loss, 786–788, 787f
Biomechanical force-related complications, fixed prostheses and, 631–656
excessive torque applied to abutment screw/prosthesis, 645–646, 648f–649f
occlusal material fracture, 646–651
cement compared to screw and etiology of, 649, 650t
ideal thickness for prevention of, 650–651, 650f
material and etiology of, 648–649, 649f–650f
reduce force for prevention of, 649–650
screw fractures, 643–645
cavitron device for treatment of, 644
etiology of, 643, 644f
explorer technique for treatment of, 644, 645f
immediate loose screw treatment for prevention of, 643–644
inverted cone bur (33 1/2 bur) for treatment of, 645, 647f
manufactured retrieval instruments for treatment of, 645, 648f
round bur (205LN) for treatment of, 645, 646f
slot top of screw for treatment of, 645, 647f
screw loosening, 631–643
abutment screw movement and treatment for, 640–643, 642f–643f
anatomic location in, 638
cantilevers/increased CHS and, 631–632, 633f
component fit, 635–636, 636f
crown/abutment not fully seated and, 633, 634f
decreased force for prevention of, 638
external force factors of, 631, 632b
ideal preload for prevention of, 639
implant design and, 636–637, 637f, 637t
insufficient and excessive torquing with, 633, 634f
parafunction and, 632–633
PM and treatment for, 640, 640b, 641f
prevention of, 638–640
prosthetic design and prevention of, 638–639
screw compared to cement in, 637–638, 638f
screw diameter in, 633, 635f
screw material in, 633–635, 635f
screw tightening sequence for prevention of, 639, 639f
settling effect and prevention of, 639–640, 640f
splinted implant-tooth prosthesis and, 633
torque under moist conditions for prevention of, 640
treatment for, 640–643, 641f
wider implant bodies for prevention of, 640
uncemented prosthesis, 651–656
abutment height and prevention of, 652
abutment resistance form and prevention of, 653–656, 655f–656f
abutment surface area and prevention of, 652, 652f–653f
abutment surface texture and prevention of, 653
abutment taper and prevention of, 651–652, 652f
geometry of abutment and prevention of, 652, 654f
implant abutment and, 651, 651f
retention/resistance and prevention of, 651, 651b
Biomend, 212, 567
Bisphosphonate osteonecrosis. See Drug-induced osteonecrosis of the jaws
Bisphosphonates, 38–39
osteoporosis and, 29–30
Bit depth, CBCT and, 151
Biting force
edentulism and decreasing, 581
IODs increasing, 584
natural teeth and implant differences with, 717, 717f
Bleeding. See also Hematologic system; Hemostasis
alcohol implications with, 33
anemia and, 26
anticoagulant medication and, 42
aspirin and, 40
cirrhosis of liver and, 28
classification of surgical, 268b
CVA and surgical implications with, 17
epistaxis, 542–543
factors contributing to intraoperative, 268–271
hyperthyroidism and, 21
IBD and, 27–28
from incisive foramen, 209
journal articles on complications with, 2, 2t–6t
laboratory tests of coagulation system and, 271–272
lateral wall of maxillary sinus and, 509
from lateral-approach sinus elevation surgery, 536
extraosseous anastomosis and, 536
intraosseous anastomosis and, 536
management of, 536
posterior lateral nasal artery and, 536
leukocytic disorders and, 26–27
mandible and
anterior, extraosseous vessels, 285–286
anterior, intraosseous vessels, 283–285
buccal artery, 288–289, 288f
facial artery, anterior area, 285–286, 286f–287f
facial artery, posterior area, 289, 289f
incisive artery, 285, 285f
interior alveolar artery, 284, 284f
lingual artery, 285, 286f–287f
lingual undercut, 286–288, 288f
median vascular canal, 283–284, 284f
mylohyoid artery, 288, 288f
posterior, extraosseous, 286–289
mandibular canal violation evaluation by amount of, 359–360, 360f
maxilla and
extraosseous anastomosis, 289
intraosseous anastomosis, 290, 290f
lateral wall/nasal, 289–291
posterior lateral nasal artery, 290–291, 290f
mechanical methods to decrease and control, 272–274
clamped vessel with hemostat forceps, 273–274, 274f
direct pressure, 273
positional changes, 273, 273f
suturing, 273, 274f
medical history and, 269
medications and, 269–271
anticoagulants, 39, 269, 269t
antiplatelet medications, 270, 270t
direct thrombin inhibitors, 269–270, 270t
herbal supplements, 270–271, 271t
NSAIDs, 270
Paget disease and, 31
pharmacologic techniques to control, 273–274
epinephrine, 275–276, 276f
tranexamic acid, 276, 278f
polycythemia and, 25
posterior wall of maxillary sinus and, 507
postoperative control and patient education with, 291
prevention and treatment of, 283–291
CBCT for anatomy/anatomic variants in, 283
incision/reflection of tissue, 283, 283f
RA and, 32
risks and complications of, 267–268, 268f
symphysis bone grafts complications with, 463–464
incisive canal and, 464
lingual artery and, 464
superior genial foramen and, 464
systemic disorders, 271, 271b
techniques to decrease and control, 272–283
thermal techniques to control, 274–275
electrocautery, 274–275, 275f
lasers, 275
topical hemostatic agents to control, 276–277
active, 277–278
cellulose, 277t, 279–280, 280f
chitosan, 277t, 281, 281f
collagen, 277t, 279, 279f
combination, 277t, 282–283, 282f
gelatin, 277t, 280–281, 281f
mechanical, 277t, 281–282, 282f
passive, 278–283
thrombin, 277–278, 277t, 278f
types of, 277t
Bleeding index, 782–783, 783t
Bleeding time test, 46t–49t, 272
Block grafts, 455
bone fixation screw exposure during healing process of, 458
ramus bone grafts, 471–478
block separation from bony ridge during implant placement in, 476–478,
479f–480f
failure to decorticate host bone in, 472–474, 474f
incorrect graft storage medium for, 475–476, 476f
mobility of block in, 474–475, 474f–476f
poor candidates for, 471–472, 473f
soft tissue irritation from overextended fixation screw in, 476, 477f
symphysis bone grafts, 463–471
bleeding, nerve impairment complications with, 463–464
bone fragment loss in break-up of cortical blocks, 467–468, 468f
chin graft closure complications, 468–470, 472f
improper superior margin location in, 470–471, 472f
inadequate bone volume for graft, 463, 464f–465f
incorrect size and shape of, 464–466, 466f–467f
neurosensory changes after, 470, 471f
soft tissue changes (ptosis) after, 470
ultrasonic piezosurgery-related tissue injury, 468, 469f–470f
Block-out material, 627, 628f
Blood coagulation (secondary hemostasis), 267–268, 268f–269f
Blood pressure. See also Hypertension
surgery implications with intraoperative elevated, 14
treatment guidelines, 14t
Blood sample difficulties, with PRF, 218–219, 220f–221f
Blood urea nitrogen (BUN), 46t–49t
BloodSTOP, 277t, 279, 280f
BM. See Barrier membrane
BMP. See Basic metabolic panel; Bone Morphogenic Protein
Board approval provision, 846
Body design, implant, 388
“Bone dancing”, 199, 204
Bone dehiscence on 3-D reformatted images, CBCT and, 152–153, 153f
Bone density, 110–124
arch position and poor, 108–109
BIC percentage and, 120–122, 121b, 121f–122f, 699, 761, 761f
bone strength relation to, 119–120, 120f, 123–124
CBCT technology complications with, 151, 151f
classification groups of, 115, 115f, 115t
D1 bone, 115–117, 117f
D2 bone, 117, 117f
D3 bone, 117–118, 118f–119f
D4 bone, 118–119, 119f
D1 bone
classification of, 115, 115f, 115t
complications with, 115–117, 117f
initial healing time for, 761–762, 762t
surgical modifications with, 117b
D2 bone
classification of, 115, 115f–116f, 115t
D3 bone
complications with, 117–118, 118f–119f
implant placement for, 202–204, 203f
surgical and prosthetic modifications for, 118b
D4 bone
drill preparation for poor, 203
elastic modulus and, 120, 120f–121f
immediate implant placement and, 561
implant number and, 94
implant placement and poor, 202–204
etiology of, 202–203, 203f
treatment for, 204
IPO and progressive bone loading rationale for, 759–760, 759f
in jaws after tooth loss, 113, 113f
malpositioning of implant prevention and poor, 261
modulus of elasticity and, 789–790
in posterior maxilla, 499–500, 501f
primary implant stability redirection based on, 572, 573f
ridge augmentations and variations in, 484–486
complications with, 484
etiology of, 484
prevention of, 484–486, 487f–488f
stress transfer and, 122, 123f
treatment planning and, 110–119, 110b, 122–124
direction of force and, 124
implant coatings and, 124
implant design in, 124
modification with, 123, 123b
progressive bone loading and, 124
summary for, 124
surface area increased in, 123–124
Bone diseases. See also Fibrous dysplasia; Osteomyelitis; Osteoporosis; Paget
disease
medical history of, 29–31
treatment implications for, 31t
Bone fixation screws
block graft healing process and exposure of, 458
bone growth over, 494–496
etiology of, 494
membrane space maintenance with, 457, 458f–460f
for mobility of block in ramus bone grafts, 474–475
particulate graft healing process and exposure of, 458–460
etiology of, 458
treatment of, 459–460, 461f
soft tissue irritation from overextended, 476, 477f
Bone grafting. See also Block grafts; Maxillary sinus grafting; Particulate
grafts; Resorbable graft material; Symphysis bone grafts
for excessive CHS, 105–107, 105f–106f
historical development of, 455–456
incision line and material from, 432–433, 433f
intraoperative complications with, 451–458
difficulty releasing flap for tension-free closure, 453–454, 456f–457f
membrane space maintenance, 455–458, 458f–460f
nasopalatine canal/incisive foramen involvement in regeneration sites,
478, 481f
poor incision design, 451–452, 453f–454f
torn lingual flap, 452–453, 455f
mandibular ramus as site for autogenous, 158, 159f
morbidity consequences of ILO with, 402–403
esthetic outcomes, 402
immediate implants, 402
postoperative care, 402–403
nerve impairment and placement of, 354
for nonintact alveolar socket, 566–567, 566f
bone density variations in ridge augmentations, 484–486, 487f–488f
bone growth over bone fixation screws, 494–496, 496f
difficulty releasing tissue flap from tenting screws, 486–487, 489f–490f
excessive pressure on ridge augmentation from temporary prostheses,
478–480, 482f–484f
ILO, 487–489, 490f–492f
inadequate bone width at implant apex, 491–494, 494f–496f
inadequate volume of facial bone regeneration with particulate graft,
489–491, 493f
lack of attached tissue covering ridge augmentation, 480–484, 485f–487f
smoking and failure of, 32
subepithelial connective tissue, 443–445, 446f
tack migration, 396, 397f
technique complications in, 446–451
failure to understand regenerative material limitations, 446–447
GBR membranes, 447–448, 447f–448f
incorrect choice of regenerative technique in respect to severity of defect,
449–451, 450f–452f
treatment planning for, 440–445
bone resorption understanding, 440–441, 441f–442f
tissue biotype evaluation, 443–445, 445f–446f
underestimation of bone, 442–443, 444f–445f
understanding need for bone grafting, 441–442, 442f
types of material for, 448–449
allografts, 448
alloplasts, 449
autogenous bone, 448, 449f
xenografts, 448, 449f
unsupported, 450, 450f
voids in, 525–528, 528f
Bone impingement
between abutment and implant, 382–383, 384f
etiology of, 382
prevention of, 382
treatment of, 383
in fixed prosthesis with abutment not seated, 675, 676f
Bone loss. See Marginal bone loss
Bone Morphogenic Protein (BMP), 446–447
Bone spreading complications, 206
facial dehiscence, 206, 207f
labial plate dehiscence, 206
poor implant position, 206
Bone wax, 277t, 281–282, 282f
Bone-implant contact (BIC), 110, 199–200, 564
bone density and percentage of, 120–122, 121b, 121f–122f, 699, 761, 761f
in posterior maxilla, 499–500, 501f
Bones. See also Available bone; Marginal bone loss; Trabecular bone
alcohol implications with loss of, 33
anemia and healing of, 26
arch position and loss of, 108
augmentation of
cantilevers and, 80
excessive CHS and, 105–107, 107f
basics of, 112–115
bone grafting and underestimation of required, 442–443
prevention of, 443, 444f–445f
cantilevers and augmentation of, 80
CHS relationship with height of, 104, 104f
diabetes mellitus and formation of, 20
division B-w (B minus width) and resorption of, 72, 72f
early displacement of implants in maxilla and poor quality of, 393, 394f
edentulism and continued loss of, 580, 582b, 582f
edentulism and loss of, 137, 138b, 138f
elderly and, 36
fixed prostheses and loss of, 143
fixed prosthesis with pain on application of torque and quality of, 677, 677f
hyperparathyroidism and involvement of, 23
hypothyroidism and healing of, 22
implant placement and overheating, 204, 205f
implant placement in osteotomy and “stuck”, 199, 200f
interproximal loss of, 236–237
mandibular ramus for harvesting, 471–472
modeling/remodeling, 113
acute disuse window in, 113–114, 114f
adapted window in, 114, 114f
mechanical adaptation categories for, 113, 114b
mild overload zone in, 114, 114f
nerve impairment prevention with, 347
pathologic overload zone in, 114–115, 114f
spontaneous fracture in, 114f
modulus of elasticity of titanium compared to, 788–789, 789f
osteoporosis and healing of, 30
premaxilla and buccal thickness of, 172–173
RA and resorption of, 32
resorption of, 440–441
complications in, 440
RP-5 and residual ridge bone loss, 63, 63f
SA-2 patient selection and inadequate, 529
strength of
angled loads and cortical, 733, 733t
bone density relation to, 119–120, 120f, 123–124
Bony defects, at uncovery, 210–213
etiology and prevention of, 211–213
horizontal defects and, 212–213
vertical defects and, 211–212, 212f–213f
Bony wall defects
five, 566
four, 566
one, 567–568, 568f–570f
two to three, 567
types of, 566f
Bovine collagen, 279
Bovine thrombin (Thrombin-JMI), 278
BPPV. See Benign paroxysmal positional vertigo
Brain abscess, infection complications with, 309–310, 311f
Breach of duty, 832
Brevital, 230t
Bronchodilators, COPD and, 25
Bruising. See Ecchymosis
Bruxism, 37–38
classification of, 95–98
clinical exam for, 97
mild, 97, 97f
moderate, 97, 98f
severe, 97, 98f
clinical signs of, 96–97, 97b
component fracture and, 98
diagnosis of, 96, 97b
evaluation of, 95
posterior wear facets with, 97–98
repeatable movement and, 98, 98f
surgical/implant implications with, 37–38
Buccal artery, bleeding and, 288–289, 288f
Buccal plate
compression of, 200
loss of entire, 202
partially intact, 202
Buccal space, 301f–302f, 302–303
Buccal-lingual mandibular canal locations, 155, 156f
Buccolingual (“y”-axis) positioning, 248–252, 249f, 251f
FP-1, FP-2 and, 248–249, 249f–251f
FP-3 and, 249–252, 252f
IAN position in, 349, 350f
RP-4, RP-5 and, 252, 253f
BUN. See Blood urea nitrogen
BUN/Cr ratio, 46t–49t
Bupivacaine, 225
Bupropion SR (Zyban), 33t
Burs. See also Drills
crestal bone, 206
high speed, 388, 389f
implant placement in osteotomy and removal of “stuck”, 199, 200f
“integration” of, 199
Lindemann, 197, 198f
nerve impairment prevention and length of, 353, 354f
trephine, 388–389, 390f
C
Ca. See Calcium
CAGR. See Compound annual growth rate
Calcified carotid artery atheroma, 163, 165f
Calcium (Ca), 46t–49t
Calcium channel blockers
surgical/implant implications with hypertension and, 15
Calcium channel blockers (CCBs), 14
Canalis sinuosus, radiography and, 174, 175f
Canine space, 301f–302f, 302
Canines
arch positions of, 84–85, 84b, 84f
implant positions and, 84–85, 85f–87f
root surface area of, 84, 84f
Cantilevers
bone augmentation and, 80
CHS and, 102–104
force magnification from, 104, 104f
moment loads and rotations in, 103f, 104t
offset loads from, 103–104
first molars and, 85
forces on, 80, 81f
four or more adjacent teeth missing and, 81, 82f
on FPDs, 78
hidden, 590
etiology of, 590
maxillary IOD complications with, 607
on implant compared to natural tooth, 243–244, 245f
implant positions and, 78–82
IPO and, 744–746
clinical significance of, 745–746, 747f
forces on, 744–746, 746f
length of, 744
occlusal contact on, 744
presence of, 744, 745f
OD-2 complications with, 600–601, 601f
OD-4 and, 602–603
one missing tooth and, 78–79, 79f–80f
screw loosening and, 631–632, 633f
three missing teeth and, 79–80, 81f
treatment options with, 81–82, 82f
two missing teeth and, 79, 80f–81f
Capillary hemorrhage, 268b
Carbamazepine, 384
Carbon dioxide (CO2), 46t–49t
Carbon-fiber curettes, 796, 797f
Cardiovascular system. See also Angina; Congestive heart
failure; Hypertension; Infectious endocarditis; Myocardial
infarction; Stroke
treatment summary for, 19, 19t
Carotid artery calcifications, 163, 165f
Catecholamines, 15–16
hyperthyroidism sensitivity with, 21
Causalgia, 342t
Causation directly related to treatment, 832–833
Cavernous sinus thrombosis, 309, 310f
Cavitron, for screw fracture treatment, 644
CBC. See Complete blood count
CBCT. See Cone beam computed tomography
CCBs. See Calcium channel blockers
CCD. See Charged coupling devices
Cefadroxil (Duricef, Ultracef), 314, 316t
Cefanex (cephalexin), 314, 316t, 319
Cefazolin (Ancef), 549, 549f
Cefpodoxime proxetil (Vantin), 550
Cefuroxime axetil (Ceftin), 550
CEJ. See Cementoenamel junction
Cellular immunity, 296
Cellulitis
infection stage of, 298, 299f
Cellulose, 277t, 279–280, 280f
Cementoenamel junction (CEJ), 67, 235, 562–563, 794
Cement-retention complications, 701–705, 702f
etiology of, 702–703, 702f–704f
ideal application of cement for, 704
implant abutment modification for, 705, 705f
screw-retained prostheses for, 704, 704f
supragingival margins and, 703–704
techniques for, 705, 705b, 706f
Central nervous system depressant drugs. See CNS depressant drugs
Centric occlusal interferences, 723, 723f
Centric occlusion (CO), 683–684, 721, 727b
premature contact in, 730–731
Centric relation (CR), 683, 721, 727b
Cephalexin (Biocef, Cefanex, Keftab, Keflex), 314, 316t, 319
Cephalosporins, 44t–45t, 314, 550
Cerebrovascular accident (CVA)
bleeding and, 17
complication prevention with, 17–18
embolic, 17
limited dexterity and, 17
thrombotic, 17
CFD. See Craniofacial fibrous dysplasia
Chantix (varenicline tartrate), 33t
Charged coupling devices (CCD), 150
Chest x-rays, for swallowing/aspiration of implant components, 221, 222f
CHF. See Congestive heart failure
Chin graft closure complications, 468–470
etiology of, 468
prevention of, 469–470, 472f
Chitosan, 277t, 281, 281f
Chlorhexidine, 319, 366t, 435, 435f, 549, 677, 677f, 800
Chloride (Cl), 46t–49t
Chlorohexidine gluconate, 20
Chromic gut, 416t, 418
Chronic neuropathic pain, around implant area, 383–384
prevention of, 384
treatment of, 384
Chronic obstructive pulmonary disease (COPD), 24–25
adrenal suppression and, 24
anesthetic selection and, 24
bronchodilators/inhaled corticosteroids and, 25
N2O sedation and, 25
oxygen supplementation and, 24–25
stages and FEV1 values for, 24t
symptoms and types of, 24
Chronic rhinosinusitis, 177, 513–514
treatment of, 514
Chronic skin fistula, 298b
CHS. See Crown height space
Ciprofloxacin (Cipro), 44t–45t, 317
Cirrhosis of liver, 28–29
bleeding and, 28
NSAIDs and, 28–29
surgery/implant implications with, 28–29
Cl. See Chloride
Claims-made insurance, 852
Clamped vessel with hemostat forceps, to control bleeding, 273–274, 274f
Clamping forces, 631
Clarithromycin (Biaxin), 44t–45t, 315–316, 316t, 550–551
Clean technique
aseptic and sterile techniques compared to, 320t
definition of, 319
Clearances
medical, 50f, 855–857, 856f
surgical, 8
Clenching, 37–38
clinical exam for, 99, 100f
clinical signs of, 99, 99b
diagnosis of, 99
evaluation of, 95
Cleocin, 549f
Clindamycin (Cleocin), 44t–45t, 316–317, 316t, 319, 551
Clinical failure, in quality scales, 820, 821f
Clopidogrel (Plavix), 41t, 42, 270
Closing arguments, 850–851
Clostridium difficile, 375
CMP. See Comprehensive metabolic panel
CNS (central nervous system) depressant drugs, hypothyroidism and, 22
CO. See Centric occlusion
CO2. See Carbon dioxide
Coagulation system laboratory tests, 271–272
Coated VICRYL, 416t
Codeine, 44t–45t
for postsurgical pain treatment, 370t, 371
coDiagnostiX, 264
Coe-Comfort, 387
Collagen, 277t, 279, 279f
Collatape, Collaplug, 277t, 279
Combination analgesics, for postsurgical pain treatment, 371, 371t
Combination hemostatic agents, 277t, 282–283, 282f
Communication
complications with poor patient, 9
FP-2 and patient, 57, 58f
FP-3 and patient, 59
RP-4 and patient, 62
RP-5 and patient, 62, 63f
Comparative fault, 851
Complaint, in filing lawsuit, 833–835, 836f
Complete blood count (CBC), 28
Complete limiting surgical template design, 261–264, 264f–265f
Complete upper denture
speech effects of, 141
treatment planning with, 140–141
advantages of, 140
disadvantages of, 140–141, 141b
Complications See also specific complications
avoidable, 10
classification of, 10
journal articles and studies on, 1, 2t–6t
bleeding, 2, 2t–6t
CBCT, 2, 2t–6t
implant failure, 2t–6t, 5
infections, 2t–6t, 3
nerve, 2, 2t–6t
periodontal complications, 2t–6t, 5–6
prostheses, 2t–6t, 4–5
surgery, 2t–6t, 3–4
major, 10
medicolegal issues and, 10
prevalence of, 827
minor, 10
preventing, 10–12
accreditation and, 11
education for, 10–11
follow-up care for, 11–12
hypertension and, 15–16
literature review updates for, 11
long term treatment for, 11
not rushing treatment for, 11
patient provided with information for, 11
referral failures and poor understanding of, 9–10
reversible, 10
site development and, 7
unavoidable, 10
Component fracture, bruxism and, 98
Composite beam analysis, 788–789, 789f
Compound annual growth rate (CAGR), 6–7
Comprehensive metabolic panel (CMP), 28
Compression set failure, of O-rings, 617, 617f
Compromised bone. See Division C
Compromised survival, in quality scales, 819, 820f
Concha bullosa
maxillary sinus complications with, 509, 510f
ostium blockage and, 509
Cone beam computed tomography (CBCT), 9. See also Radiography
for acute rhinosinusitis, 551–552
for adolescents, 35
artifact complications with, 151–153
beam hardening and, 151–152, 152f
bone dehiscence on 3-D reformatted images, 152–153, 153f
motion-related, 152, 153f
noise, 152, 153f
scatter, 152, 153f
streak, 152, 153f
for bleeding treatment, anatomy/anatomic sites, 283
complication studies on, 2, 2t–6t
FOV in, 862
historical development of, 150
for ideal clinical crown size, 237, 240f
malpositioning of implant prevention with surgical templates in, 264–265
malpractice litigation avoidance with understanding of, 861–862
mandibular canal location complications with, 183–184, 184f, 186b, 186f
maxillary ostium evaluation complications with, 184, 186f
maxillary sinus grafting complications with, 520
maxillary sinus grafting infections and postoperative mucosal thickening
in, 553
mental foramen location detection on, 206–208, 208f
nasopalatine canal dimensions defined with, 478, 481f
for nerve impairment postoperative treatment, 343
nerve impairment prevention and accuracy of, 347, 348f
nerve impairment prevention and positioning of surgical templates and,
356, 358f
overview of, 150–154
patient positioning complications with, 181
perfectionism with, 10
radiopaque template complications with, 181–183, 183f–184f
referral to radiologist, 862
scanning technique complications with, 153–154
imaging protocol, 153–154
mucosal thickness, 154
scanning template position, 154
technical parameters of, 862
technology complications with, 150–151
bit depth and, 151
bone density and, 151, 151f
contrast resolution and, 151
sensor/detector types and, 150
spatial resolution and, 150–151
voxel size and, 150, 151f
waiver of liability and, 862
Congestive heart failure (CHF), 17–19
classification of, 18b
incidence of, 18
oxygen supplementation and, 18
patient positioning and, 18
stress reduction and, 18–19
symptom recognition and, 18
Connecting bar. See also Dolder bar; Hader bar and clip system
bar try-in resulting in pain, 621–623, 625f
treatment for, 623
gingival hyperplasia around, 623–626, 625f
IODs “locking” under, 627, 628f
OD-2 attachment and, 599–600
OD-2 complications with, 600, 600f
OD-3 attachment and, 602
Connective tissue disease (CTD), 32
Conscious sedation toxicity, 228–232
benzodiazepines and, 229, 230t
common agents in, 230t
fentanyl, 229, 230t
prevention of, 231
propofol, 230t, 231
treatment of, 231–232, 231f–232f
Consent forms, for FP-2 and FP-3, 58f
Continuance, 847
Continuous suture technique, 421, 426f–427f
Contrast resolution, CBCT and, 151
Convention extraction techniques, 388
COPD. See Chronic obstructive pulmonary disease
Copper, 436
Coronal incision design, 452
Coronal-implant distance, lack of, 236–242
etiology of, 236, 237t, 239f
treatment of, 242
Cortical bone
angled loads and strength of, 733, 733t
Cortical plate, “drill until feeling”, 357, 359f
Corticosteroids
adrenal insufficiency and, 22
COPD and inhaled, 25
diabetes mellitus and use of, 20–21
for edema prevention, 541–542
implant failure and, 22
infection susceptibility with, 22–23
treatment with, 22–23
Costs
of fixed prostheses, 144
of mini implants, 127
OD-2 and increased, 601
of single tooth implant, 136–137
site development and, 7
treatment planning and, 54
Coumadin. See Warfarin sodium
Countersinking
apicocoronal (“z”-axis) positioning and, 252
implant placement and, 203
Counter-torque ratchet, 388
Court docket, 847, 848f
Courtroom, layout of, 847, 849f
Cover screw
ILO prevention with fully seated, 414, 415f
not fully seated, 380
etiology of, 380
treatment of, 380
partial exposure of, 380
etiology of, 380
prevention of, 380
treatment of, 380, 383f, 388b
Cr. See Creatinine
CR. See Centric relation
Craniofacial fibrous dysplasia (CFD), 30
CrCl. See Creatinine clearance
Creatinine (Cr), 46t–49t
Creatinine clearance (CrCl), 46t–49t
Crest module, in immediate implant design, 563–564, 563f–564f
Crestal bone
angled loads and strain of, 733–734
burs, 206
nerve impairment prevention with intraoperative consideration of, 354,
356f
occlusal overloading and loss of, 791
pressure necrosis and, 204–206, 205f
Crohn disease, 27
oral lesions and, 28
Crown height space (CHS)
angled loads magnified by, 747–748, 749f
for apicocoronal (“z”-axis) positioning of RP-4, RP-5
less than 15mm, 257, 258f–259f
more than 15mm, 257
available bone, 67–68, 68f
bone augmentation for excessive, 105–107, 107f
bone grafts for excessive, 105–107, 105f–106f
bone height relationship with, 104, 104f
cantilevers and, 102–104, 746–747, 749f
force magnification from, 104, 104f
moment loads and rotations in, 103f, 104t
offset loads from, 103–104
definition of, 102–107, 102b
division C-h and excessive, 75
for ideal apicocoronal (“z”-axis) positioning, 252, 253f
increased force and, 102, 103f–104f, 104
in long axis, 103f
IOD needs with adequate, 585, 586f
IPO and avoiding excessive, 746–748, 748f–749f
mandibular IODs and inadequate, 591–592, 591f–592f
maxillary IODs and compromised, 607, 608f
measurement of, 102, 102f, 746, 748f
occlusal overloading and excessive, 748f
O-rings and, 602
pink porcelain replacing soft tissue in excessive, 107f
RP-5 for excessive, 107, 107f
treatment planning with, 102–107, 105f–107f
Crown margin, fixed prostheses and improper, 656–657
knife edge abutment margin for, 657, 657b
prevention and treatment of, 657, 658f
Crowns
CBCT for ideal size of, 237, 240f
IPO and decreased cusp angle in posterior, 739–741, 740f–742f
mandibular posterior, 692–693, 693f
narrow occlusal tables and mandibular posterior, 749, 750f
narrow occlusal tables and maxillary posterior, 749–750, 750f–751f
overcontoured, 243
posterior maxilla, 693–694, 693f–694f
screw loosening and not fully seated, 633, 634f
splinted vs. independent implant, 662–668
difficulty of splinting, 666
etiology, 662–668
independent crown advantages, 662–665
planning for failure with, 666
porcelain repair and, 665–666
splinted crown advantages, 665–668, 666f–668f
Cryotherapy, 344
edema prevention with, 541
for postoperative edema prevention, 365, 367f
C&S test. See Culture and sensitivity test
CTD. See Connective tissue disease
CTx test, 39
Culture and sensitivity (C&S) test, 313, 313b, 314f–315f
Curette on bony floor, for sinus membrane perforation prevention, 532, 532f
Curettes, 796, 797f
Curve of Spee, 67, 720, 721f
Curve of Wilson, 67, 101, 720–721, 721f
Cusp angles
fixed occlusal complications and increased posterior, 694–695, 694f
etiology of, 694–695, 694f–695f
IPO and decreased posterior crown, 739–741, 740f–742f
load concentration and, 740
of natural teeth, 739, 740f
occlusal contact timing and, 739–740, 740f–741f
Cuspid implant, IPO with shallow anterior guidance and, 738–739, 740f
Cyclosporine, 297
Cystic lesions, 177–180
in maxillary sinus, 514–517
postoperative maxillary cyst, 517, 517f
pseudocysts, 514–516, 516f
retention cysts, 516
postoperative maxillary surgical, 554
primary maxillary sinus mucocele, 179–180, 180f
pseudocysts, 177, 179, 179f
retention cysts, 177–179
Cytostatics, 43
Cytotoxic drugs, 297
D
D1 bone
surgical modifications with, 117b
D2 bone
D3 bone
D4 bone
Dabigatran etexilate (Pradaxa), 41t, 42, 269t
Damages, trial and, 851
“Dead spaces,” suture completion and minimization of, 433, 433f
Debridement, for peri-implant mucositis, 796–798
antimicrobial aids in, 800
antimicrobial rinse in, 797, 797f
at-home, 798, 799f
auxiliary aids in, 799–800
curettes in, 796, 797f
LDAs in, 797–798, 798f
systemic antibiotics in, 798
toothbrushing and, 798–799, 799f
ultrasonic devices in, 796–797
Decadron, 366t
Decongestant medications, for graft site infection prevention, 550–551
Defense council appointment, 832
Deficient bone. See Division D
Deflective occlusal contact, 722
Degeneration, nerve, 339, 339f
Delayed implant placement, SA-3, 521f, 522, 522b
Delayed primary closure, 406
Deliberation, of jury, 851
Demineralized freeze-dried bone allograft (DFBA), 484–486
Denosumab (Prolia, Xgeva), 306–307
Dense polytetrafluoroethylene (d-PTFE), 447, 455
membrane space maintenance with titanium, 457
Dental hygienist, implant maintenance role of, 812b
Dental implants. See also Displacement of implants; Ideal implant
positioning; Implant placement, surgical related; Implant
positions; Implant size; Implant-tooth connection, fixed prostheses
complications with; Life-threatening surgery complications; Mini
implants; Natural teeth and implant differences, occlusion and; Oral
implantology; Prostheses; Single tooth implant; Splinted implant-tooth
prosthesis
adolescents and implications with, 35
anemia implications with, 26
angina and implications of, 16
antirotational design of, 388–390
aspirin implications with, 40
body design of, 388
bone density treatment planning and coatings of, 124
bone density treatment planning and design of, 124
bruxism implications with, 37–38
cantilevers on natural teeth compared to, 243–244, 245f
CHF and implications with, 18
cirrhosis of liver implications with, 28–29
clenching implications with, 37–38
COPD implications with, 24–25
corticosteroid use and implications with, 22
CVA and implications of, 17
diabetes mellitus and implications with, 20
DIONJ implications with, 39
elderly and implications with, 35–37
FD implications with, 30
guidelines for joining teeth to, 131, 131f
hyperparathyroidism and implications with, 23
hypertension and implications of, 14–15
IBD considerations with, 27–28
immunosuppressive drug implications with, 43
increased demand for
aging population and, 1–6, 6f, 13
dentist placements and, 7
general population acceptance and, 6–7
immediate implant procedures and, 8
journal articles on complications and failure of, 2t–6t, 5
leukocytic disorder implications with, 26–27
manufacturer training for, 7
MI and implications of, 17
mobility of natural teeth compared to, 773–775, 774f
morbidity consequences of ILO with, 402–403
osteomyelitis implications with, 30
osteoporosis implications with, 29–30
Paget disease implications with, 31
polycythemia implications with, 25
bone impingement between abutment and implant, 382–383, 384f
BPPV, 379–380, 380b, 381f
chronic neuropathic pain around implant area, 383–384, 385f
cover screw not fully seated, 380, 382f
excessive pressure from interim prosthesis, 367t, 386–387, 387f
fractured implant, 384–386, 385t, 386f–387f
fractured mandible after implant placement, 378, 379f
implant periapical lesion, 375–377, 377f
injury to adjacent teeth, 375, 376f
partial cover screw exposure, 380, 383f, 388b
tissue impingement between abutment and implant, 380–382, 383f
titanium allergy/hypersensitivity, 377–378, 378f
trauma from explantation of implants, 387–390, 389f–390f
psychological problems and implications with, 37
RA implications of, 32
radiation therapy implications with, 34, 34b
smoking and implications with, 32
soft tissue interface around natural teeth compared to, 778–780, 779f–780f
subperiosteal, 320–326, 326f
thread shape of, 388
thyroid disorders and implications with, 21
treatment planning and size of, 124–128
treatment planning and width of, 127–128, 127f, 128b
warfarin sodium implications with, 40
xerostomia implications with, 23
Dental material migration, 396–397, 398f
Dentists/dentistry
advancements in, 1
implant demand and placement by, 7
responsibility of insured, 829–832
Dentures. See also Complete upper denture; Edentulism; Fixed partial
dentures; Implant-supported overdentures; Removable partial
denture; Removable prostheses
complete upper, 140–141
edentulism and dissatisfaction with, 582–583
fractures/debonding of, 626–627, 627f
hybrid restoration of acrylic teeth and, with metal substructure, 60, 61f
negative effects of, 580, 581b
RP-4 and treatment, 62
RP-5 and treatment, 62–63
Deposition, 838–844
preparation, 844–845
doctor/defendant testimony, 844
ground rules for, 844b
patient/plaintiff testimony, 844–845
Desipramine, 384
Deviated septum, radiography and, 170–171, 171f
Dexamethasone, 20–21, 342–344, 343f
Dexterity, CVA and surgical implications with limited, 17
DFBA. See Demineralized freeze-dried bone allograft
Diabetes mellitus
antibiotic recommendations for, 20
bone formation and, 20
corticosteroids use for, 20–21
glycemic control for, 20, 21t
hyperglycemia and, 20
hypoglycemia and, 20
implant failure and, 20
incidence of, 19
infections and, 20
symptoms understood for, 20
Diagnostic casts, IPO evaluation of existing occlusion with, 718–720, 718f,
720b
Diagnostic wax-up, before IPO, 720–727
for completely edentulous patient, 720, 725f
for partially edentulous patient, 720, 724b, 725f
Diazepam (Valium), 230t
Dicodid. See Hydrocodone
DICOM (digital imaging and communication in medicine), 264
Diet
for fixed occlusal complications with progressive bone loading, 699–700
inadequate postoperative instructions, 373
progressive bone loading and, 762–763
Digestive system. See also Cirrhosis of liver; Inflammatory bowl disease
issues and treatment implications for, 29t
Digital imaging and communication in medicine (DICOM), 264
DIONJ. See Drug-induced osteonecrosis of the jaws
Diphenhydramine (Benadryl), 44t–45t
Diprivan (propofol), 230t, 231
Direct impression technique, soldering and, 664f–665f
Direct pressure, to decrease bleeding, 273
Direct thrombin inhibitors, 269–270, 270t
Directional movement test, 344t
Dirithromycin (Dynabac), 44t–45t
Discovery phase, in malpractice litigation, 838–846
deposition preparation in, 844–845
doctor/defendant testimony, 844
ground rules for, 844b
patient/plaintiff testimony, 844–845
forms of discovery in, 838–844
deposition, 838–844
expert reports, 838, 843f
interrogatories, 838, 839f
production of documents and things, 838, 840f
request for admissions, 838, 841f–842f
requests for disclosure, 838
mediation in, 845
pretrial modes of disposition in, 845
motion for summary judgment, 845
motion to dismiss, 845
settlement, 845
voluntary nonsuit, 845
settlement of lawsuit in, 846
Displaced implants, maxillary sinus grafting infection and, 553, 553f, 553t
Displacement of implants
in mandible, 395–396, 396f
focal osteoporotic bone marrow defects and, 396, 396f
sublingual undercuts, 395–396, 396f
in maxilla, 390–395
anterior cranial base, 392–393, 393f
autoimmune reaction and late, 394
ethmoid sinuses, 390, 392f
immediate placement and early, 393–394
implant placement without bone graft and early, 393
maxillary ostium, 390, 391f
maxillary sinus, 390
nasal cavity, 390, 391f
negative pressure and late, 394
occlusal overloading and late, 394
orbital area, 392, 393f
peri-implantitis and, 394
poor bone quality and early, 393, 394f
poor surgical technique and early, 393
sphenoid sinuses, 390–392, 392f
maxillary sinus grafting infections and, 553, 553f, 553t
Disposition, pretrial modes of, 845
Distraction osteogenesis, 446–447
Disuse atrophy, 113–114, 114f
Ditching, 784
Division A (abundant bone), 68–69
advantages of, 69b
criteria and dimensions for, 68, 68b
division B (barely sufficient bone) modification to, 71–72, 71f
treatment planning for, 68
Division B (barely sufficient bone), 69–72
disadvantages of, 69, 70b
division A (abundant bone) modification from, 71–72, 71f
insufficient osteoplasty and, 72, 72f
root forms of, 70, 70f
Division B-w (B minus width), 72–73
bone resorption progression and, 72, 72f
Division C (compromised bone), 73
division C-a, 75–76, 75f–76f
mandibular IODs and, 592–593, 592f
division C-h, 73–75, 75f
division C-w, 73, 73f–74f
Division D (deficient bone), 76–78
dimensions of, 76b
mandible, 77–78, 77f
maxilla, 76–77, 76f
Dolder bar, 588–589
composition and function of, 621, 625f
Doxepin, 37
Doxycycline (Vibramycin), 551
d-PTFE. See Dense polytetrafluoroethylene
Drills. See also Burs
“drill until cortical plate is felt”, 357, 359f
nerve impairment and handpiece control of, 354, 356f
nerve impairment and trauma from, 336–339
canal narrowing, 338–339
drill encroachment, 336, 337f
encroachment on mandibular canal, 336–338, 337f
infection, 338
mandibular socket grafting, 338, 338f
partial penetration, 336, 337f
partial penetration into mandibular canal, 338
perforation through entire canal, 338
transection, 336, 337f
nerve impairment prevention and bur length for, 353, 354f
nerve impairment prevention with stop, 353–354, 355f
in osteotomy
intermediate, 204
overheating bone and, 204
overpreparation of final, 199–200, 200f
poor bone density and, 203
speed of, 204
Drug holiday, 39
Drug interactions, medical history with, 44, 44t–45t
Drug-induced osteonecrosis of the jaws (DIONJ)
classification of drugs linked to, 38, 38t
comorbidities with, 39
diagnosis of, 39
lesions and, 39
Dry mouth. See Xerostomia
Duloxetine, 384
Duricef (cefadroxil), 314, 316t
Dynabac (dirithromycin), 44t–45t
Dysesthesia, 341–342, 342t
Dysphagia, 297–298
Dyspnea, 298
E
Easy Guide, 264
Ecchymosis (bruising), 543f
maxillary sinus grafting and, 542, 543f
postoperative, 367–368, 367f
inadequate instructions for, 373
prevention of, 368
treatment of, 368
Edema
anemia and, 26
corticosteroids for prevention of, 541–542
cryotherapy for prevention of, 541
maxillary sinus grafting postoperative complications with, 541–542
postoperative, 364–365
activities decreased for prevention of, 365
cryotherapy for prevention of, 365, 367f
etiology of, 364
glucocorticoids for prevention of, 364–365, 367t
NSAIDs for prevention of, 364, 365f, 366t
Edentulism
aging population and decreasing, 580
biting force decreasing with, 581
CHS in mandible and maxilla areas with, 68f
continued bone loss with, 580, 582b, 582f
denture dissatisfaction and, 582–583
diagnostic wax-up completion before IPO for complete, 720, 725f
diagnostic wax-up completion before IPO for partial, 720, 724b, 725f
masticatory efficiency decreasing with, 581–582
occlusal schemes for full
fixed prosthesis, 766b
removable prostheses, 766b
psychological problems and, 141, 583
soft tissue discomfort with, 582
speech difficulty with, 583
systemic consequences of, 582
treatment planning for no treatment option with, 137–140
bone loss and, 137, 138b, 138f
esthetic consequences and, 138–140, 139f–140f, 140b
soft tissue consequences and, 137–138, 138b
Education
bleeding postoperative control and patient, 291
for complication prevention, 10–11
prostheses and patient, 54–55
Elastic modulus, bone density and, 120, 120f–121f
Elderly. See also Aging population
bones and, 36
complications prevention with, 37
gastric motility of, 35–36
ISH and, 36
medications for, 36–37
renal function of, 35, 35t
Electric handpieces, soft/hard tissue complications with, 223, 225f
Electrocautery
“buzzing the hemostat” and, 275, 276f
to control bleeding, 274–275, 275f
Electrosurgery, soft/hard tissue complications with, 223, 226f
Eliquis (apixaban), 41t, 42, 269t
Embolic stroke, 17
Emergence profile
compromised, 237, 240f
fixed occlusal complications with poor, 695–696
abutments and prevention of, 696
ideal implant placement for prevention of, 696
implant size for prevention of, 696, 696f
laboratory and prevention of, 696, 697f
soft tissue modification and prevention of, 696
E-mycin (erythromycin), 315–316, 316t, 550–551
Enameloplasty, 100, 237–241, 241f–242f
Encapsulator, of O-rings, 615, 615f
Endocrine system. See also Corticosteroids; Diabetes
mellitus; Hyperparathyroidism; Thyroid disorders; Xerostomia
medical history for, 19–24
Endosteal implant osteotomy, 522
Endurance limit, 631
Eosinophils, 46t–49t
Epinephrine, 21, 44t–45t
maximum safe dose of, 226
Epistaxis, maxillary sinus grafting and, 542–543
Epithelialization, 405
Epley procedure, 380, 380b, 381f
Erythrocyte sedimentation rate (ESR), 46t–49t
Erythrocytic disorders. See Anemia; Polycythemia
Erythromycin (E-mycin, E-tab), 315–316, 316t, 550–551
ESR. See Erythrocyte sedimentation rate
Essix appliances, 478–480, 483f–484f
E-tab (erythromycin), 315–316, 316t, 550–551
ETHIBOND, 416t
ETHILON, 416t
Ethmoid bulla, 169–170
Ethmoid sinuses, 167, 188
displacement of implants in, 390, 392f
Evicel, 277t
Evithrom (human plasma thrombin), 278
Excess verdict, 851
Existence of duty, 832
Expert reports, 838, 843f
Expert witness, 850
Explorer technique, for screw fracture treatment, 644, 645f
External hexagon implants, 636–637
Extraosseous anastomosis
bleeding from lateral-approach sinus elevation surgery and, 536
maxillary sinus blood supply and, 505
Extraosseous anastomosis, bleeding and, 289
Extrusion and nibbling, of O-rings, 616
F
Facial artery
bleeding and
anterior area, 285–286, 286f–287f
mandibular posterior area, 289, 289f
Facial bone regeneration, inadequate volume of, 489–491, 493f
Facial dehiscence
implant placement and, 201, 201f
bone spreading complications and, 206, 207f
Facial plate loss, during implant placement, 201–202, 202f
Failure. See Implant failure
Fascial spaces
buccal space, 301f–302f, 302–303
canine space, 301f–302f, 302
infection routes and, 299–300, 301f–302f, 302–304
lateral pharyngeal space, 301f–302f, 304
masticatory space, 301f–302f, 303
sublingual space, 301f–303f, 303
submandibular space, 301f–302f, 304, 305f
submental space, 301f–302f, 303–304, 304f
FD. See Fibrous dysplasia
FDB. See Freeze-dried bone
FEA. See Finite element analysis
Femur, trabecular bone in, 112, 112f
Fentanyl, 229, 230t
FESS endoscopy, 553, 553f
FEV1. See Forced expiratory volume
Fibrinolysis (tertiary hemostasis), 268, 268f
Fibrous dysplasia (FD), 30
Field of view (FOV), 862
Figure eight suture technique, 421, 424f–425f
Filing lawsuit, 833–835
complaint in, 833–835, 836f
plaintiff's requirements for, 832–833
statute of limitations and, 833, 833t
response to complaint in, 835
service of process in, 835
summons in, 835, 837f
Finite element analysis (FEA), 122
angled loads and increased stress in, 733
three-dimensional, 727, 727f, 788–789, 789f
two-dimensional, 727
Fires, surgical, 226–228, 229b
First molars
arch positions of, 84f, 85–91
cantilevers and, 85
implant positions and, 85–91, 87f–91f
mandible implants for, 85–86, 89f
in maxilla
four implants in edentulous, 86–91, 90f
sinus graft for, 85–86, 90f
root surface area of, 85
First premolars, root approximation problems with, 235, 239f
Fixed occlusal complications, 680–700
angled loads and, 687–688, 688f
solutions to, 688
existing occlusion and, 683–684
force direction and bone mechanics in, 685–687, 686f–687f, 687t
implant body orientation and, 685, 685f–687f
increased posterior cusp angle and, 694–695, 694f
etiology of, 694–695, 694f–695f
initial evaluation for, 682–683
IPO not utilized, 682
etiology of, 682
prevention of, 682, 682b
moment loads and, 680–682
occlusal height moment arm in, 680–682, 681t
occlusal length moment arm in, 682
occlusal width moment arm in, 682, 683f
rotations in three planes from, 681f
torque and, 681f
occlusal contact timing and, 689–691
etiology of, 689
recall examination for, 691
occlusal table size and, 691–694
mandibular posterior crowns for prevention/management of, 692–693,
693f
maxillary posterior crowns for prevention/management of, 693–694,
693f–694f
offset loads and, 691, 692f
parafunction with no occlusal guard, 696–698
prevention of, 697
poor emergence profile and, 695–696
abutments and prevention of, 696
ideal implant placement for prevention of, 696
implant size for prevention of, 696, 696f
laboratory and prevention of, 696, 697f
soft tissue modification and prevention of, 696
premature occlusal contacts and, 684, 684f
diet and prevention of, 699–700
etiology of, 698
occlusal material and prevention of, 700
occlusion and prevention of, 700
prevention of, 698–700, 698b
progressive loading phases in, 700, 701t
prosthesis design and prevention of, 700
Fixed partial dentures (FPDs)
cantilevers on, 78
three-pontic, 82–83, 83f
treatment planning for single missing tooth with, 135–136, 136b
Fixed prostheses, 55–60, 55t. See also Biomechanical force-related
complications, fixed prostheses and
abutment not seated complication with, 674–675, 675f
etiology of, 675
prevention of, 675
treatment for, 675, 675f–676f
abutment tightness complications with, 677, 677f
bone loss and, 143
canines and, 84
cement-retention complications and, 701–705, 702f
etiology of, 702–703, 702f–704f
ideal application of cement for prevention of, 704
implant abutment modification for prevention of, 705, 705f
screw-retained prostheses for prevention of, 704, 704f
supragingival margins and prevention of, 703–704
techniques for prevention of, 705, 705b, 706f
cost of, 144
division A (abundant bone) and, 68
esthetics of, 144
food impaction with, 144, 700–701
treatment for, 701
FP-1, 55–56, 55f
apicocoronal (“z”-axis) positioning and, 254–256, 254f–256f
buccolingual (“y”-axis) positioning and, 248–249, 249f–251f
criteria for, 55
definition of, 55, 56f–57f
hard and soft tissue augmentation and, 56
ideal positioning for, 56
FP-2, 55f, 56–59
buccolingual (“y”-axis) positioning and, 248–249, 249f–251f
consent form for, 58f
criteria for, 56–57
definition of, 56, 57f
ideal position for, 59
mesial-distal positioning of, 235–236
patient communication and, 57, 58f
pre-operative smile zone evaluation for, 57–59, 59f
FP-3, 55f, 59–60
buccolingual (“y”-axis) positioning and, 249–252, 252f
consent form for, 58f
criteria for, 59, 59f
definition of, 59
patient communication and, 59
pink tissue color and, 60
smile zone variations and, 59–60, 60f
spacing of multiple implants with, 60
tissue spacing with, 60
types of, 60, 61f
implant damage complications with, 679, 680f
implant-tooth connection complications with, 669–674
existing tooth mobility in, 670–671, 671f–672f
guidelines for joining implants to teeth, 672–674, 673f–674f
ideal conditions for prevention of, 674
implant mobility in, 672, 672f
narrow-diameter implants for managing, 674
natural abutment mobility assessed in, 670, 671f
prosthesis movement in, 671–672, 672f
tooth intrusion prevention for, 674
improper crown margin and, 656–657
knife edge abutment margin for, 657, 657b
IOD compared to, 142, 143b–144b, 144f
IOD expectations and, 585, 585f
mandibular full arch splinting flexure complications with, 668–669
medial movement and, 668, 669f
prevention of, 669
torsion and, 668–669, 669f–670f
nonpassive prosthesis complications for, 657–661, 658f–659f
impression materials and prevention of, 660, 660f, 660t
impression recommendation for prevention of, 661
impression technique for prevention of, 660–661
indirect-transfer copings and, 659
laboratory process and materials for prevention of, 660, 661f
modification for treatment of, 661
soldering for treatment of, 661, 661f–665f
torque force and, 658, 658f–659f
occlusal schemes for fully edentulous implant, 766b
pain on abutment placement complication with, 675–676
etiology of, 675
prevention of, 676
treatment of, 675f–676f, 676
pain on torque application to abutment complication with, 676–677
prevention of, 677, 677f.
splinted implant-tooth prosthesis and movement of, 129–130
splinted vs. independent implant crowns for, 662–668
etiology, 662–668
stripped hex screw abutment complication with, 677–678, 678f
etiology of, 678
prevention of, 678
torque wrench technique complications, 678–679
etiology of, 678
prevention of, 678–679, 679f–680f.
treatment planning for, 143–144, 144b, 144f
Flagyl. See Metronidazole
Flapless surgery
advantages of, 195–196
disadvantages of, 196
implant placement and, 195–197, 197f
for mini implants, 125–126
Flaps
access, 802–803, 805f
apically positioned, 805, 807f
bone grafting complications with releasing, for tension-free closure, 453–
454, 456f–457f
difficulty releasing, from tenting screws, 486–487, 489f–490f
ILO and tension-free flap closure of, 488
ILO prevention and
adequate access with, 410, 410f
design of, 409–410, 410f
full thickness reflection and ideal elevation in, 411–412, 412f
margins over bone maintained, 410–411, 411f
relieving tissue for tension and, 414, 414f–415f, 427b
vertical release incision maintaining blood supply to, 410, 410f
torn lingual, 452–453, 455f
Flat panel detectors (FPDs), 150
FloSeal, 277t, 282–283, 282f
Flumazenil (Anexate, Lanexat, Mazicon, Romazicon), 231–232, 231f
Fluoroquinolones, 317, 550
Focal osteoporotic bone marrow defects, displacement of implants in
mandible and, 396, 396f
Follow-up care, complication prevention with, 11–12
Fontanelles, 507–508
Food
fixed prostheses and impaction of, 144, 700–701
treatment for, 701
increased proximal contact area and impaction of, 756, 756f
IOD disadvantages with, 585, 586f, 627–628, 628f
Forced expiratory volume (FEV1), 24t
Force-related issues, treatment planning and, 95–101. See also Biomechanical
force-related complications, fixed prostheses and
arch form, 110, 110f–111f
arch position, 107–109
bruxism, 99–101
CHS, 102–107, 105f–107f
clenching, 99–101
opposing arch, 109–110, 109b–110b, 109f
parafunction, 95–101
FOV. See Field of view
FP-1, FP-2, FP-3. See Fixed prostheses
FPDs. See Fixed partial dentures; Flat panel detectors
Frank-Starling law, 18
Free tissue palatal graft, 484, 487f
Freeze-dried bone (FDB), 566–567
Frontal sinuses, 166, 188
Fulguration, 275
Full-arch prostheses. See also Mandibular full arch splinting, flexure
complications with
implant number for, 91, 92f
in mandible, 94, 94f
in maxilla, 91–95, 92f, 95f
Fungal rhinosinusitis, 177, 179f
etiology of, 518
maxillary sinus grafting and postoperative infection of, 552, 554
treatment of, 518
Fusobacterium nucleatum, 778
Fusobacterium spp., 513–514
G
Gastric motility, of elderly, 35–36
Gatifloxacin (Tequin), 44t–45t, 550
GBR. See Guided bone regeneration
Gelatin, 277t, 280–281, 281f
GelFoam, 277t, 280–281, 281f
Gender, nerve impairment and, 339
GFR. See Glomerular filtration rate
Gingival bleeding index, 782–783, 783t
Gingival fibroblasts, 406
Gingival hyperplasia around bar, 623–626, 625f
Gingivitis classification, 772
Glomerular filtration rate (GFR), 35, 35t
Glucocorticoids, 43
for graft site infection prevention, 549–550
for postoperative edema prevention, 364–365, 367t
Glucocorticosteroids, 297
Glucose test, 46t–49t
Gown tying, in sterile technique, 321, 325f
Gowning, in sterile technique, 321, 323f–324f
Graft site infections, 545–551, 548f
amoxicillin/clavulanic acid for prevention of, 548
antibiotics for prevention of, 547–549
antimicrobial rinse for prevention of, 549
decongestant medications for prevention of, 550–551
diagnosis of, 544–554
etiology of, 545
glucocorticoids for prevention of, 549–550
good surgical technique for prevention of, 546
Group function occlusion, 721, 721f
Guaranteed outcome of treatment, 862
Guided bone regeneration (GBR), 402, 446–447. See also Dense
polytetrafluoroethylene
immediate implant placement success with, 564–565
membranes, 447–448
nonresorbable, 447, 447f, 460
placement too close to adjacent teeth, 460–462, 462f
resorbable, 447–448, 448f, 460–462, 462f
space maintenance for, 455–458, 458f–460f
for one bony wall defects, 567–568, 569f
types of material for, 448–449
allografts, 448
alloplasts, 449
autogenous bone, 448, 449f
xenografts, 448, 449f
H
Hader bar and clip system, 588–589, 606
bar position, 619–621
clip assembly, 621
design and movement, 621
interocclusal space, 621, 624f
composition and function of, 619–621, 623f
development of, 619–621
Haemophilus influenzae, 503–504, 513, 547
Haemophilus spp., 503–504
Halcion (triazolam), 44t–45t, 230t
Haller cells
maxillary sinus complications with, 510, 511f
radiography of anatomic variants of maxilla and, 171
Halo effect, in radiography, 175, 176f
Halsted block technique, 215
Hammer clause, 846
Hard reline materials, 386
Hard tissue. See also Soft tissue
life-threatening surgery complications with, 223
electric handpieces and, 223, 225f
monopolar electrosurgery units and, 223, 226f
HbA1c . See Hemoglobin A1C
HbA1c test, 20, 21t
Helitene, 277t, 279
Hematocrit test, 46t–49t
Hematologic system. See also Anemia; Bleeding; Polycythemia
issues and treatment implications with, 27t
Hematoma, nerve impairment and, 335
HemCon dressing, 281, 281f
Hemoglobin A1C (HbA1c ), 46t–49t
Hemoglobin test, 46t–49t
Hemophilia, 271
Hemostasis. See also Bleeding
ILO prevention and, 413
mechanism of, 267–268
blood coagulation (secondary hemostasis), 267–268, 268f–269f
fibrinolysis (tertiary hemostasis), 268, 268f
vascular and platelet activity (primary hemostasis), 267, 268f
Hemostat ligation, “buzzing the hemostat” and, 275, 276f
Hemostatic agents, topical, 276–277
active, 277–278
thrombin, 277–278, 277t, 278f
passive, 278–283
cellulose, 277t, 279–280, 280f
gelatin, 277t, 280–281, 281f
mechanical, 277t, 281–282, 282f
types of, 277t
Herbal supplements
adverse effects with, 42, 42b
bleeding and, 270–271, 271t
Hex implant removal, 388
Hiatus semilunaris, 168
Hidden cantilever
IODs and, 590
etiology of, 590
maxillary IOD complications with, 607
High speed burs, 388, 389f
Horizontal mattress suture technique, 421–425, 428f
Horizontal movement, splinted implant-tooth prosthesis and, 130, 130f
HPA. See Hypothalamus-pituitary adrenal axis
Human plasma thrombin (Evithrom), 278
Humoral immunity, 296
Hybrid restoration of acrylic/denture teeth, with metal substructure, 60, 61f
Hydrocodone (Dicodid), 44t–45t
Hydrocortisone sodium succinate (Solu-Cortef), 22
Hydrogen cyanide, 32
Hydroxyzine (Atarax, Vistaril), 44t–45t
Hygiene
IODs and, 142
lack of coronal-implant distance and, 237
lack of implant-implant distance and, 246
Hyperalgesia, 342t
Hyperbaric oxygen, radiation therapy and, 34
Hyperesthesia, 342t
Hyperglycemia, 20
Hyperparathyroidism, 23
bone involvement and, 23
categories of, 23
Hyperpathia, 342t
Hypertension
anesthetics and, 15–16
antihypertensive drugs and, 14–15
beta blockers and, 15
calcium channel blockers and, 15
classification of, 14–16, 14t
implant healing and, 15
intraoperative elevated blood pressure and, 14
monitoring for, 15
NSAIDs and, 14–15
orthostatic hypotension and, 14
prevalence of, 13–14
stress reduction for, 15, 15b
susceptibility to other cardiovascular events and, 15
vasoconstrictor reduction for, 16
Hyperthyroidism
aspirin/NSAID use and, 21
bleeding and, 21
catecholamine sensitivity and, 21
ideal control of, 22
Hypnosis, 33t
Hypoalgesia, 342t
Hypoesthesia, 342t
Hypoglycemia, 20
Hypoplasia, of maxillary sinus, 172, 174f, 511, 511f
Hypothalamus-pituitary adrenal axis (HPA), 22
Hypothyroidism
CNS depressant drugs and, 22
ideal control of, 22
I
IAN. See Inferior alveolar nerve
IBD. See Inflammatory bowl disease
Ibuprofen (Advil, Motrin), 366t, 370, 370t
ICOI. See International Congress of Oral Implantologists
Ideal contact procedure, 731, 731f
Ideal implant positioning. See also Implant positions; Malpositioning of
implants
anterior maxilla distance in, 257–258, 261f
apicocoronal (“z”-axis), 252–257
CHS and, 252, 253f
FP-1, FP-2, FP-3 and, 254–256, 254f–256f
RP-4 and RP-5 and, 257, 258f–259f
buccolingually (“y”-axis), 248–252, 249f, 251f
FP-1 and FP-2 and, 248–249, 249f–251f
FP-3 and, 249–252, 252f
RP-4, RP-5 and, 252, 253f
guidelines for, 266t
inferior alveolar canal distance in, 257, 260f
inferior border of anterior mandible distance in, 257, 260f
malpositioning of implant prevention by understanding, 259
maxillary sinus distance in, 258–259, 262f
mental foramen distance in, 257, 260f
mesial-distal (“x”-axis): implant-implant, 244–248, 245f–246f
mesial-distal (“x”-axis): implant-natural tooth and, 234–244
excessive space between implant and tooth, 242–244, 244f–246f
insufficient root-implant apex distance, 234–236, 236f–239f
lack of coronal-implant distance, 236–242, 237t, 239f–243f
nasal cavity distance in, 257–258, 261f
osteotomy formula for, 247
ILO. See Incision line opening
IM. See Implant mobility
Immediate implant placement
available bone and, 557–560
angulation, 558–560, 561f
height of, 557–558, 560f–561f
length of, 558
width of, 558
design for, 563–565
crest module in, 563–564, 563f–564f
thread shapes in, 564, 564f
titanium in, 563, 563f
first stage/bone healing complications with, 575, 575f–577f
GBR and success of, 564–565
general considerations in, 557–565
advantages and disadvantages of, 558t
anatomic location and, 562
bacteria/existing pathology and, 562
biomechanical overload issues, 562
bone density and, 561
implant size/length relative to teeth being replaced, 563t
learning curve with, 562
optimal esthetics with, 557, 558f–559f
prosthesis type and, 561
implant malpositioning and, 573, 574f
implant size
length relative to teeth being replaced, 562–563
inability to achieve primary stability with, 568–569
aborting procedure after, 573
bone density and redirection for, 572, 573f
clinical confirmation of primary stability, 570–572, 571f
complete osteotomy preparation in appropriate location and sequence
for, 569–570
implant design and initial stability preventing, 572
larger implant for managing, 572
leaving implant in place after, 572–573
under prepare osteotomy width and over prepare osteotomy length for,
570
intraoperative complications, 565–573
in mental foramen and nerve impairment prevention, 356, 358f
morbidity consequences of ILO with, 402
nonintact alveolar socket and, 565–573
aborting procedure, 566
atraumatic tooth extraction for prevention of, 565–566
bone grafting for, 566–567, 566f
pretreatment evaluation for anticipation of, 565
prevention, 565–566
excessive pain, 574–575
ILO, 575
medicolegal considerations, 575
nerve impairment, 574
transitional prosthesis impingement, 573–574
potential complications related to, 565–573
SA-3 and, 521f, 522, 522b
immunosuppressive drugs
surgery/implant implications with, 43
types of, 42–44
Impeachment, 850
Implant contraindication, 13
Implant design, 563–565
Implant drills. See Drills
Implant failure
corticosteroids and, 22
diabetes mellitus and, 20
fixed prosthesis and
with pain on abutment placement, 675–676, 676f
with pain on application of torque, 677
journal articles and studies on, 2t–6t, 5
Implant malpositioning, immediate implant placement and, 573, 574f
Implant mobility (IM)
mirror handles for evaluation of, 775, 775f
Osstell values for evaluation of, 776, 776t, 777f
Periotest values for evaluation of, 775–776, 776t
Implant number
available bone determining, 91
bone density influence on, 94
for full-arch prostheses, 91, 92f
in mandible, 94, 94f
in maxilla, 91–95, 92f, 95f
patient force factors and, 93–94
prostheses success and, 93, 93t
for RP-4, 62
in RP-4 option for maxillary IODs, 610–611, 611f
for RP-5, 63
in RP-5 option for maxillary IODs, 609–610, 609f–610f
zygomatic implants and, 91, 92f
Implant osteotomy hypothesis, for marginal bone loss, 786
Implant placement, surgical related, 194–210. See also Immediate implant
placement; Life-threatening surgery complications; Stage II uncovery
surgery
anesthetic techniques for mandible and, 215–218, 218f
bone spreading complications and, 206
facial dehiscence, 206, 207f
labial plate dehiscence, 206
poor implant position, 206
emergence profile and ideal, 696
facial dehiscence after, 201, 201f
bone spreading and, 206, 207f
facial plate loss during, 201–202, 202f
final drill overpreparation and, 199–200, 200f
flapless surgery and, 195–197, 197f
incisive foramen complications with, 208–209, 209f
keratinized tissue and, 198–199, 199f
mental foramen location detection on CBCT, 206–208, 208f
nasopalatine canal impinged by, 209–210, 210f
osteotomy and
bur “stuck” in bone during, 199, 200f
malpositioned initial site in, 197–198, 198f
overheating bone and, 204, 205f
poor bone density (D3, D4) and, 202–204
treatment for, 204
in preexisting pathology sites, 194, 195f
pressure necrosis and, 204–206, 205f
PRF and
blood sample difficulties and, 218–219, 220f–221f
inadequate blood spin for, 218, 219f
retained root tips and, 194–195, 196f
Implant positions. See also Ideal implant positioning; Malpositioning of
implants
bone spreading complications and poor, 206
canine rule and, 84–85, 85f–87f
cantilevers and, 78–82
four or more adjacent teeth missing, 81, 82f
one missing tooth, 78–79, 79f–80f
three missing teeth, 79–80, 81f
two missing teeth, 79, 80f–81f
first molar rule, 85–91, 87f–91f
IPO and ideal treatment planning with, 727–728, 727f–729f
mandibular IODs and nonideal, 593–594, 593f–594f
occlusal contact schemes and posterior, 743, 744f
OD-1 complications with, 596–598, 597f
for OD-3, 601, 601f
for OD-4, 602–603, 603f
for OD-5, 605, 605f
with RP-4, 62
in RP-4 option for maxillary IODs, 610–611, 611f
with RP-5, 63
in RP-5 option for maxillary IODs, 609–610, 609f–610f
three adjacent pontics and, 82–84, 82f–83f
treatment planning and key, 78–91, 78f
Implant quality scales, 811–818, 811t
group I: optimum health, 818, 818f
group II: satisfactory health, 818–819, 819f
group III: compromised survival, 819, 820f
group IV: clinical failure, 820, 821f
Implant size, 562–563. See also Mini implants
fixed occlusal complications with poor emergence profile and, 696, 696f
ideal, 128, 128b
immediate implant placement considerations with, 562–563, 563t
width, 127–128, 127f, 128b
Implant Stability Quotient (ISQ), 571–572, 776, 776t, 777f
ImplantMaster, 264
Implant-protective occlusion (IPO), 682, 682b, 717–764
development of, 718, 722
diagnostic casts and existing occlusion evaluation for, 718–720, 718f, 720b
diagnostic wax-up completion before, 720–727
for completely edentulous patient, 720, 725f
for partially edentulous patient, 720, 724b, 725f
ideal treatment planning and implant positioning for, 727–728, 727f–729f
postimplant principles for, 728–764
angled load management, 735–736, 736f
avoid excessive CHS, 746–748, 748f–749f
cantilevers and, 744–746, 745f–747f
decreased posterior crown cusp angle, 739–741, 740f–742f
ideal contact procedure for, 731, 731f
ideal posterior occlusal contact schemes, 741–743, 742f–744f
increased proximal contact area, 755–757, 756f–757f
mutually protected articulation, 758
narrow posterior occlusal tables, 748–755
no angled occlusal loads, 732–734, 732f–734f
no premature contacts on prostheses, 728–731, 729f–732f
progressive bone loading used for poor bone quality, 758–760, 759f–760f
prosthetic angled loads and, 734–736, 735f
shallow anterior guidance, 736–739, 736f–740f
preimplant principles for, 718–728
clinical significance of, 726–727
management and, 725–727, 726f
principles of, 718, 718b
terms for, 720b–724b
Implant-supported overdentures (IODs). See also Attachment system, for
IODs; Mandibular IODs; Maxillary IODs; Removable prostheses
advantages of, 583–584, 583b
biting force increased with, 584
existing bone maintenance with, 583
ideal occlusion with, 583
less morbidity compared to teeth, 584
masticatory function increased with, 584
psychological health improved with, 584
retention and stability improved with, 584
speech enhanced with, 584
bar try-in resulting in pain and, 621–623, 625f
treatment for, 623
disadvantages of, 585–587
adequate CHS needed, 585, 586f
fixed prosthesis expectations, 585, 585f
food impaction with, 585, 586f, 627–628, 628f
maintenance, 585
posterior bone loss, 585–587, 587f
fixed prostheses compared to, 142, 143b–144b, 144f
fractures of, 627, 628f
gingival hyperplasia around bar and, 623–626, 625f
hidden cantilever and, 590
etiology of, 590
hygiene and, 142
“locking” under bar, 627, 628f
maximum bite forces and, 142
mini implants for support of, 125, 126f
parafunction advantages of, 142
PM understanding for, 587–589, 588f
attachment height and, 589, 589f
PM-0, 588, 588f
PM-2, 588–589, 589f
PM-3, 589, 589f
PM-4, 589, 589f
PM-6, 589, 589f
RP-5 lack of soft tissue support and, 626, 626f
speech advantages of, 142
treatment planning with RP-4/RP-5, 141–143
advantages of, 141–142, 142b–143b
wide range of retention complications with, 587
etiology of, 587
prevention of, 587
Implant-tooth connection, fixed prostheses complications with, 669–674
existing tooth mobility in, 670–671, 671f–672f
implant mobility in, 672, 672f
prosthesis movement in, 671–672, 672f
guidelines for joining implants to teeth, 672–674
natural tooth with no clinical mobility, 673, 673f
no lateral force on prosthesis, 672–673
no nonrigid connectors, 674
no rigid connectors, 673–674, 674f
ideal conditions for prevention of, 674
narrow-diameter implants for managing, 674
natural abutment mobility assessed in, 670, 671f
tooth intrusion prevention for, 674
Implied consent, 859
Incision design, poor, 451–452
prevention of, 452, 453f–454f
Incision line opening (ILO). See also Wound healing
alcohol use and, 408
autogenous block failure and, 449–450, 450f
bacteria and, 407–408
in bone grafting sites, 487–489
etiology of, 487
lack of tension-free flap closure in, 488
prevention of, 488
treatment for, 488–489, 490f–492f
classification of, 402–406, 404b, 404f–405f
cover screw fully seated for prevention of, 414, 415f
decreasing infection possibility for prevention of, 434–435
antibiotics for, 434–435
antimicrobial rinse for, 435, 435f
aseptic technique for, 435
clinician experience and skill for, 435
decreased surgical time for, 435
diet and supplements for prevention of, 435–436
immediate implant placement and, 575
management of, 436–438, 437t
maxillary sinus grafting and, 542–543
morbidity consequences of, with implants and bone grafting, 402–403
obesity and, 408–409
oral habits contributing to, 436
periodontal biotype and, 409
postoperative complications and, 409
prevalence of, 402, 403f
resuturing protocol and, 437, 437f
saliva and, 406–407
smoking and, 408
surgical technique for prevention of, 409–414
clean, concise incision, 411, 411f
flap allowing for adequate access, 410, 410f
flap design, 409–410, 410f
flap margins maintained over bone, 410–411, 411f
full thickness reflection and ideal elevation of flap, 411–412, 412f
hemostasis, 413
incision in keratinized tissue, 409, 409f
papilla-saving incisions, 412, 413f
relieving tissue for flap tension, 414, 414f–415f, 427b
tissue desiccation prevention, 414
vertical release incision for blood supply to flap, 410, 410f
sutures for prevention of
absorbability for, 420
atraumatic removal of, 434–435, 434f
bone graft material in incision line and, 432–433, 433f
continuous technique for, 421, 426f–427f
“dead space” minimization for, 433, 433f
decreasing inflammation for, 433
figure eight technique for, 421, 424f–425f
high tensile strength for, 420
knots, 425–432, 432f
low tissue reactivity for, 420
materials and techniques in, 414, 416t
mattress techniques for, 421–425, 428f–429f
needle holders with, 425, 432f
needles for, 420, 421f
PME for, 421, 425f
scissors with, 425–427, 432f
simple loop technique for, 420–421, 422f–423f
size of, 420
tissue pick-ups with, 425, 431f
transitional and interim prosthesis design and, 433–434, 434f
types of, 416t, 418–420
systemic diseases and, 408
Incision-related injuries, nerve impairment and, 355, 357f
Incisive artery, bleeding and, 285, 285f
Incisive canal, 208
symphysis bone graft complications with bleeding, nerve impairment in,
464
Incisive foramen
bleeding from, 209
bone grafting regeneration site involvement of, 478, 481f
implant placement complications with, 208–209, 209f
Incisive nerves, 330–332, 332f
Independent implant crowns, splinted crowns vs., 662–668
etiology, 662–668
Indirect impression technique, soldering and, 662f–663f
Indirect-transfer copings, nonpassive fixed prostheses complications and,
659
Infections. See also Sterile technique
anterior wall of maxillary sinus and, 506–507
corticosteroid use and susceptibility to, 22–23
diabetes mellitus and surgical complications with, 20
etiology of infectious process, 295–297, 296b
host response to infection, 296
impaired host defenses, 296–297
drill trauma, nerve impairment and, 338
face and neck significant complications with, 304–311
brain abscess, 309–310, 311f
cavernous sinus thrombosis, 309, 310f
MRONJ, 306–309, 310f
neoplasms, 310–311, 311f–312f
osteomyelitis, 304–306, 306f–308f
graft site, 545–551, 548f
etiology of, 545
IBD and, 27
ILO prevention and decreasing possibility of, 434–435
antimicrobial rinse for, 435, 435f
aseptic technique for, 435
clinician experience and skill for, 435
decreased surgical time for, 435
implant placement in sites with preexisting, 194, 195f
journal articles on complications with, 2t–6t, 3
leukocytic disorders and, 26
maxillary sinus grafting and, 544–554, 547t, 548f
acute rhinosinusitis, 551–552
combination, 552–553
migration/displacement of implants and, 553, 553f, 553t
postoperative CBCT mucosal thickening and, 553
postoperative fungal rhinosinusitis and, 552, 554
postoperative maxillary surgical cysts, 554
saline rinses for, 551, 552f
Paget disease and, 31
particulate graft, 462–463
etiology of, 462
prevention of, 463
postoperative terms for, 298, 298b, 298t
risk of, 294–295, 295b, 295t
routes of, 299–304
fascial spaces, 299–300, 301f–302f, 302–304
lymphatic system, 299–302, 300f
thrombophlebitis, 299
vascular, 299, 299f
signs of, 297–298
mild compared to severe, 297–298
objective, 297
vital, 297
smoking and, 32
stages of, 298–299
abscess, 298–299, 299f
cellulitis, 298, 299f
palpate area of swelling to distinguish, 299
subperiosteal implants and, 320–326, 326f
superior wall of maxillary sinus and, 507
surgical wound classifications and rates of, 294–295, 295b, 295t
antibiotics used in, 313–317, 316t, 319
culture and sensitivity (C&S) test, 313, 313b, 314f–315f
incision and drainage, 311–313
prophylactic antibiotics, 317–319
Infectious endocarditis, 18, 19b
Inferior alveolar canal. See also Mandibular canal
ideal implant positioning and distance from, 257, 260f
“place implants buccal or lingual to”, 359, 359f
Inferior alveolar nerve (IAN)
anterior loop confusion with, 352, 353f
in mandibular nerve (V3), 333–334, 334f
nerve impairment prevention and position of
in buccal-lingual plane, 349, 350f
in vertical plane, 349, 350f
“place implants buccal or lingual to”, 359, 359f
ramus bone grafts damaging, 472
Inferior meatus pneumatization (big-nose variant), 172, 174f, 511, 512f
Inferior turbinate, 511, 512f
Inferior wall, of maxillary sinus, 508f, 509
Inferior-superior mandibular canal locations, 155–156, 157f
Infiltration surgical technique, 357–359
Inflammation
maxillary sinus and, 512–514
acute rhinosinusitis, 513, 514f
allergic rhinosinusitis, 514, 515f
chronic rhinosinusitis, 513–514, 514f
odontogenic rhinosinusitis, 512–513, 512f
signs of, 297
sutures for ILO prevention and decreasing, 433
Inflammatory bowl disease (IBD), 27–28
adrenal issues and, 27
antibiotics and, 28
bleeding and, 27–28
forms of, 27
infections and, 27
oral lesions and, 28
probiotics and, 28
surgical/implant considerations with, 27–28
Inflammatory phase of wound healing, 403–404
Inflammatory response, 296
Informed consent, 857–861, 860f
Informed refusal, 859
Infraorbital artery, 506
Infraorbital foramen (IOF), 165–166, 166f
Infraorbital nerve
in V2, 332, 333f
maxillary sinus grafting and impairment of, 540–544, 541f
Infundibulum, 168
INR. See International Normalized Ratio
Insertion torque (IT), 570–572
Installation damage, of O-rings, 617–618, 618f
Instat, 277t, 279
Interactive treatment planning software, for posterior mandible evaluation,
347, 348f
Interim prosthesis
excessive pressure from, 386–387
etiology of, 386
treatment of, 367t, 387, 387f
sutures for ILO prevention and, 433–434, 434f
Interior alveolar artery, bleeding and, 284, 284f
Intermediary abutments. See Pier implant abutments
Intermediate drills, 204
Internal hexagon implants, 636–637
International Congress of Oral Implantologists (ICOI), 11
International Normalized Ratio (INR), 17–18, 28, 272
Interocclusal space
Hader bar and clip system complications with, 621, 624f
Locator attachment use with insufficient, 618–619, 620f–621f
Interrogatories, 838, 839f
Interruption of anticoagulant therapy, 272
Intraoperative complications
immediate implant placement, 565–573
Intraosseous anastomosis
bleeding and, 290, 290f
bleeding from lateral-approach sinus elevation surgery and, 536
maxillary sinus blood supply and, 505, 506f
Inverted cone bur (33 1/2 bur), 645, 647f
IODs. See Implant-supported overdentures
IOF. See Infraorbital foramen
IPO. See Implant-protective occlusion
Iron level test, 46t–49t
Irreversible complications, 10
Irrigation, nerve impairment and intraoperative use of, 354–355, 357f
Isolated systolic hypertension (ISH), 36
ISQ. See Implant Stability Quotient
IT. See Insertion torque
J
James-Misch scale, 811–818, 811t
Jaws. See also Drug-induced osteonecrosis of the jaws; Mandible; Maxilla
bone density in, after tooth loss, 113, 113f
trabecular bone in, 112–113, 113f
JEA. See Junctional epithelial attachment
Joint National Committee (JNC8) on high blood pressure, 14
Junctional epithelial attachment (JEA), 778–779, 780f
Jury
deliberation, 851
selection, 847
K
Keflex, Keftab (cephalexin), 314, 316t, 319
Kelly hemostat forceps, 273–274, 274f
Keratinized tissue
benefits of, 807–808
ILO prevention with technique for incision in, 409, 409f
implant placement and, 198–199, 199f
lack of, 806–809, 807f–808f
concurrent augmentation for, 809
management of, 809
postimplant augmentation for, 809
presurgical augmentation for, 809
Ketamine, 384
Knife edge abutment margin, 657, 657b
Knots, suture, 427–432, 432f
L
Labial lip support, with maxillary IODs, 607
Labial plate dehiscence, bone spreading and, 206
Lanexat (flumazenil), 231–232, 231f
Lasers
bleeding control with, 275
for peri-implantitis, 801–802, 803f
Lateral pharyngeal space, 301f–302f, 304
Lateral wall of maxillary sinus, 508–509, 508f
sinus grafting voids and, 528, 528f
Lateral-approach sinus elevation surgery, bleeding from, 536
management of, 536
LDAs. See Locally delivered antibiotics
Legal council appointment, 832
Legal issues. See Medicolegal issues
Legal system, in United States, 827, 828f
Lesions, DIONJ and, 39
Leukemia, 27t
Leukocytic disorders
bleeding and, 26–27
infection and, 26
signs and symptoms of, 26–27
Levaquin (levofloxacin), 44t–45t, 316t, 319, 550
Lever arm, OD-2 complications with, 600, 600f
Lever mechanics, 102
Levofloxacin (Levaquin), 44t–45t, 316t, 319, 550
Levonordefrin, 44t–45t
LFTs. See Liver function tests
License revoked/deceased, 846
Lidocaine, 44t–45t, 225, 384
half-life of, 225–226
Lifestyle, medical history and, 32–34. See
also Adolescents; Alcohol; Bruxism; Clenching; Elderly; Psychological
health; Radiation therapy; Smoking
Life-threatening surgery complications, 219–232
air emphysema, 223, 224f
anesthetic toxicity, 225–226, 228b, 228t
oral/conscious sedation toxicity, 228–232
benzodiazepines, 229, 230t
fentanyl, 229, 230t
prevention of, 231
propofol, 230t, 231
salivary gland injury, 224–225, 227f
soft/hard tissue complications, 223
surgical fires, 226–228, 229b
swallowing/aspiration of implant components, 219–221
prevention of, 220
Lincomycins, 44t–45t
Lincosamides, 551
Lindemann bur, 197, 198f
Lingual artery
bleeding and, 285, 286f–287f
symphysis bone graft complications with bleeding, nerve impairment in,
464
Lingual concavities, radiography and, 160–161, 162f
Lingual flap tears, 452–453, 455f
Lingual foramen/canal, radiography and, 162–163, 164f
Lingual membrane fixation, 494, 496f
Lingual nerve (LN), 334, 335f
Lingual plate, compression of, 200
Lingual undercut, bleeding and, 286–288, 288f
Lipase test, 46t–49t
Literature review updates, for complication prevention, 11
Litigation. See Malpractice litigation
Liver. See Cirrhosis of liver
Liver disease, 271
Liver function tests (LFTs), 28, 46t–49t
LN. See Lingual nerve
Locally delivered antibiotics (LDAs), 797–798, 798f
Locator attachments, 589, 597
abutment height and, 598
attachment divergence, 618
available in multiple abutment heights, 619
dual retention, 618, 619f
insufficient interocclusal space use, 618–619, 620f–621f
resilient function, 618
self-alignment, 618
Locator Core Tool for, 619, 622f–623f
in OD-1, 596
retention control with, 613f
Lorazepam, 230t
Low-abrasive amino acid glycine powder, 801, 802f
Lymph nodes
examination of, 302, 303f
location of, 300–301, 300f
Lymphadenitis, 298b
Lymphadenopathy, 297
Lymphatic system
examination of, 302, 303f
infections routes and, 299–302, 300f
Lymphocytes, 46t–49t
Lynal, 387
M
Macrolides, 44t–45t, 315–316, 550–551
Major complications, 10
Malpositioning of implants, prevention of
adjacent teeth condition for, 260
good surgical technique for, 261
ideal available bone for, 259
ideal treatment planning for, 259
morbidity and, 234, 235f
pathology presence and, 260–261
poor bone density and, 261
prosthesis type and associated ideal positioning for, 259
soft tissue evaluation for, 259–260
surgical templates for, 261–264
CBCT, 264–265
complete limiting design, 261–264, 264f–265f
nonlimiting design, 261, 263f
partial limiting design, 261, 263f
vital structure true location for, 261
Malpractice insurance, 851–852
claims-made, 852
entity coverage in, 852
limits of, 852
occurrence, 851
Malpractice litigation
avoiding, 853–863
abandonment of patients and, 862, 863f
CBCT understanding for, 861–862
complication management, 861, 861b
comprehensive medical-dental history forms for, 854–855
detailed treatment plan for, 857, 858f
good rapport with patients for, 861
guaranteed outcome of treatment and, 862
informed consent and, 857–861, 860f
keeping current for, 861
medical clearance for, 855–857, 856f
patient record maintenance for, 853–854, 854b
discovery phase in, 838–846
deposition preparation, 844–845, 844b
forms of discovery, 838–844, 839f–843f
mediation in, 845
pretrial modes of disposition, 845
settlement of lawsuit in, 846
NPDB reporting and, 852
presuit, 828–838
appointment of legal council, 832
filing lawsuit, 833–835, 836f–837f
notification, 828–829, 831f
plaintiff's requirements for filing lawsuit, 832–833, 833t, 834f
recommendations for, 835–838
requirements after receiving notice, 829–832
process of, 827–828, 829f
state dental licensure complaints and, 852–853
terminology in, 863b–864b
trial phase in, 846–853
closing arguments in, 850–851
comparative fault and, 851
continuance and, 847
court docket and, 847, 848f
courtroom layout for, 847, 849f
damages in, 851
deliberation in, 851
excess verdict and, 851
expert witness in, 850
impeachment in, 850
inadmissible information in, 850
jury selection for, 847
opening statement in, 847
patient/plaintiff case presentation in, 847–850
postverdict adjustments and, 851
verdict in, 851
witness order in, 850
types of, 828b
Mandible
anterior
available bone angulation of, 67, 67f
available bone height of, 64, 65f
available bone width of, 65, 66f
division C-h and, 74
ideal implant positioning distance from inferior border of, 257, 260f
arch position of maxilla compared to, 108, 108b
BIC percentage and bone density in maxilla compared to, 122, 122f
bleeding and
anterior, extraosseous vessels, 285–286
anterior, intraosseous vessels, 283–285
buccal artery, 288–289, 288f
facial artery, anterior area, 285–286, 286f–287f
facial artery, posterior area, 289, 289f
incisive artery, 285, 285f
interior alveolar artery, 284, 284f
lingual artery, 285, 286f–287f
lingual undercut, 286–288, 288f
median vascular canal, 283–284, 284f
mylohyoid artery, 288, 288f
posterior, extraosseous, 286–289
CHS in edentulous areas of, 68f
displacement of implants in, 395–396
division D, 77–78, 77f
first molar implants in, 85–86, 89f
flexure, 81–82, 82f
as force absorption unit, 112–113, 112f
fractured, after implant placement, 378
etiology of, 378
prevention of, 378
ideal implant size in, 128, 128b
implant number for full-arch prostheses in, 94, 94f
implant placement and anesthetic techniques for, 215–218, 218f
incisors, two missing, 79, 81f
nerve impairment prevention considerations with, 349–352
accessory foramens evaluation, 351–352, 352f
anterior loop and IAN confusion, 352, 353f
IAN position in buccal-lingual plane, 349, 350f
IAN position in vertical plane, 349, 350f
mental foramen location identification, 349–351, 351f
mental nerve anterior loop evaluation, 352, 352f
posterior
available bone height of, 64, 65f
interactive treatment planning software for evaluation of, 347, 348f
narrow occlusal tables and crowns of, 749, 750f
radiography and anatomic variants of, 159–163
accessory foramens, 159–160, 161f
anterior loop, 159, 160f
calcified carotid artery atheroma, 163, 165f
incisive canal, 161, 163f
lingual concavities, 160–161, 162f
lingual foramen/canal, 162–163, 164f
mandibular canal hypomineralization, 158f, 161
retromolar foramen, 161–162
radiography and anatomy of, 155–159
mandibular canal image evaluation and complications, 156
mandibular ramus as autogenous grafting donor site, 158, 159f
mandibular symphysis, 158–159, 159f
mental foramen, 156–158, 158f
Mandibular canal (MC)
bleeding as evaluation for violation of, 359–360, 360f
drill trauma and
encroachment, 336–338, 337f
partial penetration, 338
hypomineralization and, 158f, 161
location of, 155–156
buccal-lingual, 155, 156f
CBCT complications identifying, 183–184, 184f, 186b, 186f
inferior-superior, 155–156, 157f
radiographic evaluation and complications of, 156
Mandibular full arch splinting, flexure complications with, 668–669
medial movement and, 668, 669f
torsion and, 668–669, 669f–670f
prevention of, 669
Mandibular IODs. See also Implant-supported overdentures
division C-a, 592–593, 592f
inadequate CHS, 591–592, 591f–592f
nonideal implant positioning, 593–594, 593f–594f
OD-1 option for, 594–598, 595f
abutment height complications with, 598, 598f
advantages of, 594
anatomic position of, 594–595, 596f
attachment for, 596
indications for, 594, 594b
O-rings and Locator attachments in, 596
patient misconceptions with, 598
positioning complications with, 596–598, 597f
posterior support complications with, 596
support of, 595–596, 596f
OD-2 option for, 595f, 598–601
anatomic position for, 598–599, 599f
bar/attachment for, 599–600
cantilever complications with, 600–601, 601f
compromised bone complications with, 600
connecting bar complications with, 600, 600f
increased costs with, 601
lever arm complications with, 600, 600f
positioning complications with, 600
bar/attachment system for, 602
improper attachment design complication with, 602, 602f
position for, 601, 601f
RP-4 fabrication complication with, 602
arch form and, 603, 604f
attachments for, 603
complications and disadvantages of, 604–605
O-rings in, 603
positions for, 602–603, 603f
A-P spread and forces in, 605–606, 605f
O-rings in, 606
Mandibular median vascular canal, 162–163, 164f
Mandibular nerve (V3)
anatomy of, 332–334
IAN in, 333–334, 334f
LN in, 334, 335f
Mandibular posterior crowns, 692–693, 693f
Mandibular ramus. See also Ramus bone grafts
as autogenous grafting donor site, 158, 159f
bone harvesting from, 471–472
Mandibular socket grafting, nerve impairment from, 338, 338f
Mandibular symphysis, 158–159, 159f
Manufacturer training, for dental implants, 7
Marginal bone loss, 784–795
autoimmune response of host hypothesis for, 786
biologic width hypothesis for, 786–788, 787f
early, 784, 784f–785f
implant osteotomy hypothesis for, 786
occlusal trauma hypothesis for, 788–794
bone mechanical properties in, 789–791, 790f
bone physiology and, 791, 792f–793f
cellular biomechanics and, 788, 789f
engineering principles in, 788–789, 789f
implant design biomechanics and, 791–794, 793f
periosteal reflection hypothesis for, 785, 785f
radiographic evaluation of, 785f, 794–795, 794f
Masseteric space, 301f–302f, 303
Mastication speed, natural teeth and implant differences with, 716–717
Masticatory efficiency
edentulism and decreasing, 581–582
IODs and increased, 584
natural teeth and implant differences with, 715–716, 716f–717f
Masticatory space, 301f–302f, 303
Materialise (SimPlant), 264
Mattress suture techniques, 421–425, 428f–429f
Maturation phase of wound healing, 405, 406f
Maxilla. See also Anterior maxilla; Posterior maxilla
arch position of mandible compared to, 108, 108b
BIC percentage and bone density in mandible compared to, 122, 122f
bleeding and
extraosseous anastomosis, 289
intraosseous anastomosis, 290, 290f
lateral wall/nasal, 289–291
posterior lateral nasal artery, 290–291, 290f
CHS in edentulous areas of, 68f
displacement of implants in, 390–395
division D, 76–77, 76f
first molars in
four implants in edentulous, 86–91, 90f
sinus graft for, 85–86, 90f
as force distribution unit, 112–113, 112f
ideal implant size in, 128, 128b
implant number for full-arch prostheses in, 91–95, 92f, 95f
radiography and anatomic variants of, 170–174
buccal thickness of bone in premaxilla, 172–173
canalis sinuosus, 174, 175f
concha bullosa, 170, 170f
deviated septum, 170–171, 171f
Haller cells, 171
inferior turbinate and meatus pneumatization (big nose variant), 172,
174f
intraosseous anastomosis, 173–174, 175f
maxillary sinus hypoplasia, 172, 174f
maxillary sinus septa, 172, 173f
paradoxical middle turbinate, 170, 171f
radiography and anatomy of, 163–170
infraorbital foramen, 165–166, 166f
maxillary sinus membrane, 167–170, 168f
nasal cavity, 167
nasopalatine canal/incisive foramen, 164–165, 166f
ostiomeatal complex, 168–170, 169f
paranasal sinuses, 166–167, 167f
premaxilla, 163–164, 165f
radiography report findings for, 188
Maxillary IODs, 606–621
facial esthetics enhanced by, 606
less soft tissue coverage with, 606–607
arch forms and, 611–612
importance of, 611–612, 612f
types of, 611
compromised CHS, 607, 608f
treatment planning options and factors, 607–609, 608f
hidden cantilever and, 607
labial lip support with, 607
premaxillary resorption decreased with, 607
RP-4 option for, 610–611
advantages of, 611
attachments in, 611
implant number/position in, 610–611, 611f
indications for, 610, 610f
occlusal scheme in, 611
prosthesis design in, 611
RP-5 option for, 609–610
advantages of, 610
implant number/position in, 609–610, 609f–610f
indications for, 609
O-rings in, 610
prosthetic design in, 610
support in, 610
treatment options for, 609–611, 609b
Maxillary nerve (V2)
anatomy of, 330–332, 331f
anterior superior alveolar nerve in, 332, 333f
infraorbital nerve in, 332, 333f
maxillary sinus grafting and block anesthesia injections to, 523, 524f
nasopalatine nerve in, 330–332, 332f
Maxillary ostium
anatomy and physiology of, 501–502
CBCT evaluation complications with, 184, 186f
Maxillary posterior crowns, 693–694, 693f–694f
Maxillary sinus
anatomic variants of, 509–511
Haller cells and, 510, 511f
inferior turbinate and meatus pneumatization (big-nose variant), 511,
512f
nasal septum deviation, 509, 510f
paradoxical middle turbinate, 509–510, 510f
supplemental ostium, 510–511
uncinate process variants, 510
anatomy of, 167
antroliths, 518–520
etiology of, 519
radiography of, 180–181, 182f, 519, 519f
blood supply in, 505–506
intraosseous anastomosis and, 505, 506f
posterior lateral nasal artery and, 505–506, 542
sphenopalatine and infraorbital arteries and, 506
cystic lesions in, 514–517
pseudocysts, 514–516, 516f
displacement of implants in, 390
flora, 503–505
antibiotics and, 504–505
sterile technique for, 504
fungal rhinosinusitis in, 518, 518f
hypoplasia, 172, 174f, 511, 511f
inflammation and, 512–514
acute rhinosinusitis, 513, 514f
allergic rhinosinusitis, 514, 515f
chronic rhinosinusitis, 513–514, 514f
odontogenic rhinosinusitis, 512–513, 512f
membrane, 167–170, 168f
neoplasms in, 517–518, 518f
pathologic conditions of, 511–520
pneumatization of, 499, 500f
primary mucocele of, 179–180, 180f
radiography report findings on, 188
septa, 172, 173f
walls of, 506–509, 507f
anterior, 506–507, 508f
inferior, 508f, 509
lateral, 508–509, 508f, 528, 528f
medial, 507–508, 508f, 527–528, 528f
posterior, 507, 508f
superior, 507, 508f
Maxillary sinus grafting
V2 block anesthesia injections and, 523, 524f
aggressive osteotomy preparation in, 524–525, 527f, 548
aggressive tuberosity removal for, 528–529
correction location in, 528–529
harvesting too far posterior in, 529, 530f
posterior sinus cavity exposure in, 529
antral septa and, 533–536
etiology of, 533
bleeding from lateral-approach sinus elevation surgery, 536
management of, 536
CBCT complications with, 520
excess pressure on graft site in, 536–540, 540f
graft site infections, 545–551, 548f
etiology of, 545
incorrect window osteotomy location in, 523–524
damage to existing tooth root and, 524, 526f
lack of grafting area and, 523
window made over host bone and, 523–524, 525f–526f
infections and, 544–554, 547t, 548f
acute rhinosinusitis, 551–552
combination, 552–553
migration/displacement of implants and, 553, 553f, 553t
postoperative CBCT mucosal thickening and, 553
postoperative fungal rhinosinusitis and, 552, 554
postoperative maxillary surgical cysts, 554
saline rinses for, 551, 552f
membrane perforations in, 530–533
curette kept on bony floor for prevention of, 532, 532f
large perforation surgical correction for, 533, 535f
membrane thickness and prevention of, 532
narrow sinus complications with, 532
osteotomy line angles for prevention of, 532
postoperative monitoring of, 533
SA-3 implant delays after, 533
size of access window for prevention of, 531–532
small perforation surgical correction for, 533, 534f
surgical armamentarium for prevention of, 531
surgical technique alterations for, 532
overfilling sinus and, 525–527, 527f, 548
postoperative complications in, 540–544
ecchymosis, 542, 543f
edema, 541–542
ILO, 542–543
infraorbital nerve impairment, 540–544, 541f
oroantral fistulae, 543–544, 544f–546f
pain, 542
revision surgery, 541, 543f
SA complication prevention for, 520–523
SA-1, 520–522, 521f
SA-2, 521f, 522, 529–530, 531f
SA-3, 521f, 522, 522b
SA-4, 521f, 522–523
smoking complications with, 523
treatment planning complications with, 520–523
voids in, 525–528, 528f
Maximal intercuspation (MI), 683, 727b
Maximum bite forces
arch position and, 107–108, 108f
IODs and, 142
Maximum intercuspation, 721
Mazicon (flumazenil), 231–232, 231f
MC. See Mandibular canal
Mean corpuscular volume (MCV), 46t–49t
Mechanical hemostatic agents, 277t, 281–282, 282f
Mechanoceptive diagnostic tests, 343, 344t, 345f
Medial wall of maxillary sinus, 507–508, 508f
sinus grafting voids and, 527–528, 528f
Medial-positioned lingualized occlusion, 722
Median vascular canal, bleeding and, 283–284, 284f
Mediation, 845
Medical clearance, 50f, 855–857, 856f
Medical history, 13–50
of autoimmune disease, 31–32
bleeding and, 269
of bone diseases, 29–31
of cardiovascular system, 13–19
of digestive system, 27–29
with drug interactions, 44, 44t–45t
of endocrine system, 19–24
of hematologic system, 25–27
lab tests for, 46t–49t
lifestyle and, 32–34
medications and, 38–42
of pulmonary system, 24–25
Medical slice computed tomography (MSCT), 347, 348f
Medical-dental history forms, 854–855
Medication-related osteonecrosis of the jaws (MRONJ)
infection complications with, 306–309, 310f
terminology of, 306–307
treatment and staging guidelines for, 307, 309t
Medicolegal issues. See also Malpractice litigation
complications and, 10
prevalence of, 827
with immediate implant placement, 575
terminology in, 863b–864b
United States legal system and, 827, 828f
Membrane fixation
apical, 493–494, 495f
lingual/palatal, 494, 496f
Membrane space maintenance, 455–458
prevention of complications in, 456–458
bone fixation screws, 457, 458f–460f
titanium d-PTFE, 457
titanium mesh, 457–458, 460f
treatment for, 458, 458f–460f
Mental foramen, 156–158, 158f
ideal implant positioning and distance from, 257, 260f
immediate implants in, 356, 358f
implant placement and CBCT location detection of, 206–208, 208f
location identification for, 349–351
anatomic landmarks, 350, 351f
direct evaluation, 351, 351f
palpation, 350, 351f
radiography, 350–351
ultrasound, 351
periosteal tissue releasing techniques and location of, 355
Mental nerve, anterior loop evaluation for, 352, 352f
MERSILENE, 416t
Mesial-distal (“x”-axis) positioning: implant-implant, 244–248, 245f–246f
Mesial-distal (“x”-axis) positioning: implant-natural tooth, 234–244
excessive space between implant and tooth and, 242–244
for FP-2, FP-3, RP-4, RP-5, 235–236
insufficient root-implant apex distance, 234–236
treatment of, 236
lack of coronal-implant distance and, 236–242
etiology of, 236, 237t, 239f
treatment of, 242
Metal allergies, 43–44
Metal copings, 636, 636f
Metal substructure fracture, 648, 650f
Metronidazole (Flagyl), 44t–45t, 316t, 317, 551, 798
MFD. See Monostotic fibrous dysplasia
MI. See Maximal intercuspation; Myocardial infarction
MIC. See Minimum inhibitory concentration
Microfibrillar collagen, 277t, 279, 279f
Midazolam, 230t
Middle turbinate, paradoxical
maxillary sinus complications with, 509–510, 510f
ostium blockage and, 510
Migration of implants, maxillary sinus grafting infection and, 553, 553f, 553t
Mild overload zone, in modeling/remodeling bone, 114, 114f
Mini implants
cost of, 127
disadvantages of, 73f, 125–127, 126b, 126f
flapless surgical approach for, 125–126
historical development and reemergence of, 124–128, 125f–126f
for IOD support, 125, 126f
overuse and complications with, 8–9
Minimum inhibitory concentration (MIC), 318
Minor complications, 10
Mirror handles, for IM evaluation, 775, 775f
Misch SA classification. See Sinus augmentation
Mobility index
implant mobility evaluation, 775–776, 775f, 775t–776t, 777f
natural tooth compared to implant support systems, 773–775, 774f
Modeling/remodeling bone, 113
acute disuse window in, 113–114, 114f
adapted window in, 114, 114f
categories for mechanical adaptation in, 113, 114b
mild overload zone in, 114, 114f
pathologic overload zone in, 114–115, 114f
spontaneous fracture in, 114f
Modulus of elasticity
bone density and, 789–790
for titanium compared to bone, 788–789, 789f
Molars. See First molars
Moment loads, fixed occlusal complications and, 680–682
occlusal height moment arm in, 680–682, 681t
occlusal length moment arm in, 682
occlusal width moment arm in, 682, 683f
rotations in three planes from, 681f
torque and, 681f
Monoamine oxidase inhibitors, 37
Monoclonal antibodies, 38, 297
Monocytes, 46t–49t
Monopolar electrosurgery
soft/hard tissue complications with, 223, 226f
Monostotic fibrous dysplasia (MFD), 30
Moraxella catarrhalis, 513, 547
Morse taper implant, 636
Motion for summary judgment, 845
Motion to dismiss, 845
Motion-related artifacts, CBCT and, 152, 153f
Motrin. See Ibuprofen
Moxifloxacin (Avelox), 44t–45t, 316t, 550
MRONJ. See Medication-related osteonecrosis of the jaws
MSCT. See Medical slice computed tomography
Mucociliary drainage, 502–503, 504f
Mucograft, 482–484
Mucosal thickness
CBCT scanning technique complications with, 154
maxillary sinus grafting infections and postoperative CBCT, 553
Mutually protected articulation, IPO and, 758
Mutually protected occlusion, 721–722, 722f
Mycoplasma spp., 503–504
Mylohyoid artery, bleeding and, 288, 288f
Myocardial infarction (MI), 16–17
stress reduction for, 17
vasoconstrictor reduction for, 17
N
N2O sedation. See nitrous oxide sedation
Naloxone HCl (Narcan), 231, 231f
Narrow-diameter implants. See Mini implants
Nasal artery. See Posterior lateral nasal artery
Nasal cavity
bleeding in maxilla and, 289–291
radiography and, 167
radiography report findings for, 188
Nasal septum deviation, 509, 510f
Nasopalatine canal
bone grafting regeneration site involvement of, 478, 481f
CBCT defining dimensions of, 478, 481f
implant placement impinging on, 209–210, 210f
National Practitioner Data Bank (NPDB), 852
Natural sutures, 418, 418f
Natural teeth. See Teeth, natural
Natural teeth and implant differences, occlusion and, 711–717
force-related factors, 713–717
biting force, 717, 717f
excessive contacts, 715, 715f
mastication speed, 716–717
masticatory efficiency, 715–716, 716f–717f
nonvertical occlusal loads, 714–715, 715f
occlusal overloads and, 713t, 715
vertical occlusal loads, 713–714, 714f
peripheral feedback system, 711–713
premature occlusal contact prevention and, 729–730
Nausea, after surgery, 374
Nd:YAG laser, 801–802
Needle holders, sutures and, 425, 432f
Needles
nerve impairment and trauma from, 335
suture, 420, 421f
Neisseria spp., 503–504
Neoplasms
infections complications with, 310–311, 311f–312f
in maxillary sinus, 517–518, 518f
Nerve impairment, 329, 330f. See also Peripheral nerve fibers; Trigeminal
nerve
alternative surgical techniques for prevention of, 356–361
bleeding for mandibular canal violation evaluation, 359–360, 360f
immediate implants in mental foramen, 356, 358f
infiltration technique, 357–359
nerve repositioning, 361, 361f
“place implants at depth of adjacent root apexes”, 359, 359f
“place implants buccal or lingual to IAN canal or foramen”, 359, 359f
second molar replacement, 360, 360f
anatomy and, 329–334
anesthetic administration and, 335
anesthetic toxicity, 335
hematoma, 335
needle, 335
anterior wall of maxillary sinus and, 507
drill trauma and, 336–339
drill encroachment, 336, 337f
encroachment on mandibular canal, 336–338, 337f
infection, 338
mandibular socket grafting, 338, 338f
partial penetration, 336, 337f
partial penetration into mandibular canal, 338
transection, 336, 337f
immediate implant placement and postoperative, 574
intraoperative considerations for prevention of, 352–356
bone graft material placement, 354
bur drilling depths, 353, 354f
CBCT surgical templates, 356, 358f
crestal bone anatomy, 354, 356f
drill handpiece control, 354, 356f
incision-related injuries, 355, 357f
irrigation, 354–355, 357f
periosteal tissue releasing techniques, 355
retractor-related injuries, 355, 358f
safety zones, 352–353, 353f
stop drills preventing overpreparation, 353–354, 355f
suturing, 356, 358f
journal articles on, 2, 2t–6t
mandible considerations for prevention of, 349–352
accessory foramens evaluation, 351–352, 352f
anterior loop and IAN confusion, 352, 353f
IAN position in buccal-lingual plane, 349, 350f
IAN position in vertical plane, 349, 350f
mental foramen location identification, 349–351, 351f
mental nerve anterior loop evaluation, 352, 352f
physiologic response to, 339–342
degeneration, 339, 339f
gender and, 339
neurosensory deficit classification, 340–341, 341f
regeneration, 340, 340f
sensory symptoms classification, 341–342, 342t
postoperative treatment of, 342–344
CBCT evaluation, 343
clinical assessment, 343, 344t, 345f
follow-up care, 344, 346t
pharmacologic intervention, 343–344
possible referral, 344, 346t
radiographic considerations for preventing, 344–348
bone models, 347
CBCT and MSCT accuracy, 347, 348f
interactive treatment planning software for posterior mandible
evaluation, 347, 348f
surgical templates, 347–348, 349f
two-dimensional radiography limitations and disadvantages, 344–345,
347f
two-dimensional radiography magnification guides, 345–347, 347f
soft tissue reflection and, 336, 336f
symphysis bone grafts complications with, 463–464
treatment at time of surgery of, 342, 343f, 344, 346f
Nerve repositioning, 361, 361f
Neti-Pot, 551, 552f
Neurapraxia, 340, 341f, 342t
Neurosensory deficit classification, 340–341, 341f
Neurotmesis, 341, 341f, 342t
Neutrophils, 46t–49t
NicoDerm CQ (nicotine patch), 33t
Nicorette (nicotine gum, nicotine lozenge), 33t
Nicorette microtab sublingual tablets, 33t
Nicotine gum (Nicorette), 33t
Nicotine inhaler (Nicotrol inhaler), 33t
Nicotine lozenge (Nicorette), 33t
Nicotine nasal spray (Nicotrol), 33t
Nicotine patch (NicoDerm CQ), 33t
Nicotrol (nicotine nasal spray), 33t
Nicotrol inhaler (nicotine inhaler), 33t
Nitroglycerin, angina complications with, 16
Nitrous oxide (N2O) sedation
angina complication prevention with, 16
COPD and, 25
No active insurance, 846
NOACs. See Novel oral anticoagulants
Nobel Biocare (Nobel-Guide), 264
Nociceptive diagnostic tests, 343, 344t
Noise, CBCT and, 152, 153f
Noma, 298b
Nonabsorbable sutures, 418–420, 419f
polypropylene, 416t, 420
polytetrafluoroethylene, 416t, 420
silk, 416t, 419
Nonlimiting surgical template design, 261, 263f
Nonpassive prosthesis complications, for fixed prostheses, 657–661, 658f–
659f
indirect-transfer copings and, 659
impression materials and, 660, 660f, 660t
impression recommendation for, 661
impression technique for, 660–661
laboratory process and materials for, 660, 661f
torque force and, 658, 658f–659f
treatment of
modification for, 661
soldering for, 661, 661f–665f
Nonresorbable GBR membranes, 447, 447f, 460
Nonrigid connectors, 133, 674
Nonsteroidal anti-inflammatory drugs (NSAIDs), 44
adverse effects of, 44t–45t
bleeding and, 270
cirrhosis of liver and, 28–29
hyperthyroidism and use of, 21
for postoperative edema prevention, 364, 365f, 366t
for postsurgical pain treatment, 370, 370t
surgical/implant implications with hypertension and, 14–15
Nonvertical occlusal loads, 714–715
implants and, 715
natural teeth and, 714, 715f
Nonworking occlusal interferences, 723, 723f
Nortriptyline, 37, 384
Novel oral anticoagulants (NOACs), 269–270, 270t
NSAIDs. See Nonsteroidal anti-inflammatory drugs
NUROLON, 416t
Nystatin, 24
O
Obesity, wound healing/ILO and, 408–409
Occlusal awareness, occlusal contact timing and, 689
Occlusal contact
on cantilevers, 744
deflective, 722
IPO and ideal posterior, 741–743, 742f–743f
implant position and, 743, 744f
screw-retained prosthesis and, 744–746
splinted implants and, 743, 744f
Occlusal contact timing, 689–691
cusp angles and, 739–740, 740f–741f
etiology of, 689
inherent laboratory error and, 689
occlusal awareness and, 689
tooth and implant movement and, 689
articulation protocol and, 689–690, 689f–690f
complete implant-supported prosthesis and, 690
in maxillary anterior, 690–691, 691f
in one quadrant, 690
opposing prostheses and, 690
recall examination for, 691
Occlusal disharmony, 722
Occlusal guards, 38
parafunction and, 100
parafunction with no, 696–698
prevention of, 697
Occlusal height moment arm, 680–682, 681t
Occlusal length moment arm, 682
Occlusal loads. See Angled loads
Occlusal material fracture, 646–651
cement compared to screw and, 649, 650t
material and, 648–649, 649f–650f
reduce force for prevention of, 649–650
Occlusal overloading
crestal bone loss and, 791
displacement of implants in maxilla and, 394
excessive CHS and, 748f
natural teeth and implant differences with, 713t, 715
Occlusal planes, 720–721
Occlusal prematurity, 722
Occlusal schemes. See also Implant-protective occlusion
for fully edentulous implant fixed prosthesis, 766b
goal of, 682
importance of, 682, 711, 764–767
for multiple implants
anterior implant-supported restorations, 765f, 766b
posterior implant-supported restorations, 766b
for prostheses and opposing dentition, 767t
for single implant-supported prostheses, 765b
Occlusal tables
IPO and narrow, 748–755
larger implant body for prevention of, 750–751, 751f
management of, 752–755, 754f–755f
mandibular posterior crowns and, 749, 750f
maxillary posterior crowns and, 749–750, 750f–751f
prosthesis fabrication for prevention of, 751–752, 751f–753f
staggered implants and, 755
size complications of, 691–694
mandibular posterior crowns for prevention/management of, 692–693,
693f
maxillary posterior crowns for prevention/management of, 693–694,
693f–694f
Occlusal terms, 720b–724b
common, 727b
interferences, 722–724
centric occlusal, 723, 723f
nonworking occlusal, 723, 723f
protrusive occlusal, 724, 724f
working occlusal, 723, 723f
occlusal planes, 720–721
occlusion types, 721–722
teeth relationships, 721
Occlusal trauma hypothesis, for marginal bone loss, 788–794
bone mechanical properties in, 789–791, 790f
bone physiology and, 791, 792f–793f
cellular biomechanics and, 788, 789f
engineering principles in, 788–789, 789f
implant design biomechanics and, 791–794, 793f
Occlusal vertical dimension (OVD), 684
Occlusal width moment arm, 682, 683f
Occlusion. See also Fixed occlusal complications; Implant-protective
occlusion; Natural teeth and implant differences, occlusion and
fixed occlusal complications and existing, 683–684
fixed occlusal complications with progressive bone loading and, 700
forces of, 685
IODs and ideal, 583
IPO and diagnostic casts for evaluation of existing, 718–720, 718f, 720b
of natural teeth, 727, 727f
parafunction and, 100
RP-4 for maxillary IOD and scheme for, 611
terms for, 720b–724b
types of, 721–722
bilateral balanced, 722, 722f
group function, 721, 721f
IPO, 722
medial-positioned lingualized, 722
mutually protected, 721–722, 722f
Occurrence insurance, 851
Occurrence of related damages, 833
OD-1. See Overdenture option 1
Odontogenic rhinosinusitis, 175–176, 176f, 512–513
etiology of, 512
treatment of, 513
Official notice letter, 829, 831f
Offset loads
from cantilevers and CHS, 103–104
occlusal contacts and, 748, 749f
occlusal table size complications and, 691, 692f
stamp cusp, 752, 754–755, 755f
Onlay block grafting, 446–447
Opening statement, 847
Ophthalmic nerve (V1), 330
Ophthalmoplegia, 309
Opiates, 384
Opioids, 44t–45t
Opposing arch, treatment planning with, 109–110, 109b–110b, 109f
Optimum health, in quality scales, 818, 818f
Oral implantology. See also Dental implants
complexity of, 12
prophylactic antibiotics in, 319
Oral sedation toxicity, 228–232
benzodiazepines and, 229, 230t
fentanyl, 229, 230t
prevention of, 231
propofol, 230t, 231
OraPlug, OraTape, 277t, 279, 279f
Orbital area, displacement of implants in, 392, 393f
O-rings, 597
CHS permitting, 602
composition and use of, 614–618, 615f
encapsulator of, 615, 615f
failure of, 616–618
abrasion and, 617
compression set, 617, 618f
extrusion and nibbling, 616
installation damage and, 617–618, 618f
spiral, 617, 617f
hardness of, 616
height of, 616
materials for, 616
in OD-1, 596
in OD-4, 603
in OD-5, 606
PM and, 588–589, 589f
post of, 615
range of motion of, 614–615
retention control with, 613f
in RP-5 option for maxillary IODs, 610
size of, 615–616, 616f
ORN. See Osteoradionecrosis
Oroantral fistulae, maxillary sinus grafting and, 543–544, 544f–546f
Orthodontic implants (TADs), 235, 239f
Orthostatic hypotension, 14
Osseointegration, 774
Osstell values, 776, 776t, 777f
Osteitis deformans. See Paget disease
Ostene, 277t, 282, 282f
Osteolysis, 793–794
Osteomyelitis, 30
acute and chronic classification of, 304
diagnosis of, 305
infection complications with, 304–306, 306f–308f
radiography for detecting, 305–306
treatment of, 306
Osteoplasty
division B and insufficient, 72, 72f
vertical defects eliminated in, 212, 212f
Osteoporosis, 29–30. See also Drug-induced osteonecrosis of the jaws
bisphosphonates and, 29–30
complication prevention and, 30
new therapies for, 39–40
Osteoradionecrosis (ORN), 34
Osteotomy. See also Drills, in osteotomy; Implant placement, surgical related
endosteal implant, 522
ideal implant positioning formula for, 247
implant placement with
bur stuck in bone and, 199, 200f
malpositioned initial site for, 197–198, 198f
maxillary sinus grafting and aggressive preparation of, 524–525, 527f, 548
maxillary sinus grafting and incorrect window location in, 523–524
damage to existing tooth root and, 524, 526f
lack of grafting area and, 523
window made over host bone and, 523–524, 525f–526f
overheating bone and, 204, 205f
primary implant stability and
complete preparation in appropriate location and sequence for, 569–570
under prepare width and over prepare length for, 570
SA-2 complications with multiple entries in, 529
SA-2 complications with overpreparation of, 529
sinus membrane perforation prevention and line angles in, 532
Ostiomeatal complex, 501
Ostium
blockage
concha bullosa and, 509
nasal septum deviation and, 509
paradoxical middle turbinate and, 510
uncinate process and, 510
medial wall of maxillary sinus and patency of, 507
supplemental, 510–511
OVD. See Occlusal vertical dimension
Overcontoured crowns, 243
Overdenture option 1 (OD-1), 594–598, 595f
abutment height complications with, 598, 598f
advantages of, 594
anatomic position of, 594–595, 596f
attachment for, 596
O-rings and Locator attachments in, 596
patient misconceptions with, 598
positioning complications with, 596–598, 597f
posterior support complications with, 596
support of, 595–596, 596f
Overdenture option 2 (OD-2), 595f, 598–601
anatomic position for, 598–599, 599f
bar/attachment for, 599–600
cantilever complications with, 600–601, 601f
compromised bone complications with, 600
connecting bar complications with, 600, 600f
increased costs with, 601
lever arm complications with, 600, 600f
positioning complications with, 600
bar/attachment system for, 602
improper attachment design complication with, 602, 602f
RP-4 fabrication complication with, 602
arch form and, 603, 604f
complications and disadvantages of, 604–605
O-rings in, 603
positions for, 602–603, 603f
A-P spread and forces in, 605–606, 605f
O-rings in, 606
Overfills, sinus graft, 525–527, 527f, 548
Overheating bone, implant placement and, 204, 205f
Ovoid arch forms, 611
Oxycodone (Percocet), 370t, 371
Oxygen
CHF and supplementation of, 18
COPD and supplementation of, 24–25
radiation therapy and hyperbaric, 34
Oxymetazoline (Afrin, Vicks Nasal Spray), 550
P
Paget disease, 30–31
bleeding and, 31
infection and, 31
signs and symptoms of, 30–31
Pain, postsurgical, 368–372
control of, 372, 372b
immediate implant placement and excessive, 574–575
maxillary sinus grafting and, 542
prevention of, 369
acetaminophen for, 369–370, 370t
analgesic agents for, 371–372, 371t–372t, 384
codeine for, 370t, 371
combination analgesics for, 371, 371t
hydrocodone for, 370t, 371
NSAIDs for, 370, 370t
opioids for, 370t, 371
oxycodone for, 370t, 371
tramadol for, 370–371, 370t
Pain index, 783–784
Pain specialists, 384
Palatal membrane fixation, 494, 496f
Palpation, mental foramen location identification with, 350, 351f
Pamidronate (Aredia), 39, 306–307
Panoramic radiography, 148–150, 149f
Papilla
ideal CHS for apicocoronal (“z”-axis) positioning and, 252, 253f
ILO prevention and incisions saving, 412, 413f
lack of coronal-implant distance and height of, 237, 240f
lack of interimplant, 246
stage II uncovery surgery and loss of, 213–215, 216f–217f
Paradoxical middle turbinate. See Middle turbinate, paradoxical
Parafunction. See also Bruxism; Clenching
bruxism, 95–98
clenching, 98–99
definition of, 95
greater surface area countering forces of, 100
IOD advantages with, 142
with no occlusal guard, 696–698
prevention of, 697
occlusal guards and, 100
occlusion and, 100
premature occlusal contact prevention and, 729–730
prosthesis design and, 100
screw loosening and, 632–633
tongue thrust and size and, 100–101
complications with, 101, 101b, 102f
types of, 101, 101b, 101f
Paranasal sinuses. See also Ethmoid sinuses; Maxillary sinus; Maxillary sinus
grafting; Sphenoid sinuses
anatomy and physiology of, 500–506, 503f
blood supply in maxillary sinus, 505–506
maxillary ostium, 501–502
maxillary sinus flora, 503–505
mucociliary drainage, 502–503, 504f
ostiomeatal complex, 501
Schneiderian membrane, 502
antroliths and, 180–181, 182f
cystic lesions and, 177–180
pseudocysts, 177, 179, 179f
retention cysts, 177–179
frontal, 166
neoplasms and, 180, 182f
pathologic conditions in, 175–181, 182f, 511–520
radiography and anatomy of, 166–167, 167f
rhinosinusitis and, 175–177
acute, 176–177, 176f
allergic, 177, 178f
chronic, 177
fungal, 177, 179f
odontogenic, 175–176, 176f
Parathyroid hormone (PTH), 23
Paresthesia, 341–342, 342t
Partial limiting surgical template design, 261, 263f
Partial thromboplastin time (PTT), 46t–49t, 272
Particulate grafts, 455, 458–463
bone fixation screw exposure during healing process of, 458–460
etiology of, 458
treatment of, 459–460, 461f
GBR membrane placement too close to adjacent teeth and, 460–462
inadequate volume of facial bone regeneration with, 489–491, 493f
infection, 462–463
etiology of, 462
prevention of, 463
Passive hemostatic agents, 278–283
cellulose, 277t, 279–280, 280f
gelatin, 277t, 280–281, 281f
mechanical, 277t, 281–282, 282f
Pathologic overload zone, in modeling/remodeling bone, 114–115, 114f
Patient records, maintaining ideal, 853–854, 854b
Patients
abandonment of, 862, 863f
bleeding postoperative control and education of, 291
CBCT complications with positioning of, 181
CHF and complication prevention with positioning of, 18
complication prevention with information provided to, 11
complications and
medically compromised patients, 7–8
poor communication, 9
FP-2 and communication with, 57, 58f
FP-3 and communication with, 59
good rapport with, 861
implant number influenced by force factors of, 93–94
OD-1 misconceptions of, 598
postoperative complications and
inadequate instructions, 373–374
patient/procedure treated same pharmacologically, 367t, 372
prostheses and education of, 54–55
RP-4 and communication with, 62
RP-5 and communication with, 62, 63f
SA-2 complications in selection of, inadequate bone, 529
comprehensive options for, 133–144
PDGF (platelet-derived growth factor), 38–39
PDL. See Periodontal ligament
PDS. See Polydioxanone
Penicillin V, 313
Penicillins, 44t–45t, 313–314
Percocet. See Oxycodone
Percussion, 778
Periapical lesion, implant, 375–377
prevention of, 377
treatment of, 377
Periapical radiography, 148, 149f
Peri-implant diseases, 771–820
complications of, 771
new proposed classification of, 811t
types of, 795–805, 795t
Peri-implant mucosal hyperplasia, 809–810
etiology of, 810
management of, 810, 810f, 810t
prevention of, 810
Peri-implant mucositis, 795–800
characteristics of, 772
debridement for, 796–798
antimicrobial aids in, 800
antimicrobial rinse in, 797, 797f
at-home, 798, 799f
auxiliary aids in, 799–800
curettes in, 796, 797f
LDAs in, 797–798, 798f
systemic antibiotics in, 798
toothbrushing and, 798–799, 799f
ultrasonic devices in, 796–797
management of, 796, 800, 801b
peri-implantitis diagnosis compared to, 795t
prevention of, 796
radiographic evidence of, 795, 795f
Peri-implantitis, 800
classification of, 772b
clinical signs of, 772–773, 773b
displacement of implants in maxilla and, 394
etiology of, 800
human studies on treatment for, 812t–817t
nonsurgical management of, 800–802, 801b
lasers for, 801–802, 803f
low-abrasive amino acid glycine powder for, 801, 802f
ultrasonic devices for, 801
peri-implant mucositis diagnosis compared to, 795t
prevention of, 800
smoking and, 32
surgical management of, 800, 801b, 802–805, 804f
access flap for, 802–803, 805f
apically positioned flap for, 805, 807f
regenerative procedures for, 803–805, 806f
Periodontal biotype, wound healing/ILO and, 409
Periodontal complications, 2t–6t, 5–6. See also Peri-implant disease; Peri-
implant mucositis; Peri-implantitis
Periodontal indices
bleeding, 782–783, 783t
evaluation of, 773–776
marginal bone loss, 784–795
autoimmune response of host hypothesis for, 786
biologic width hypothesis for, 786–788, 787f
early, 784, 784f–785f
implant osteotomy hypothesis for, 786
occlusal trauma hypothesis for, 788–794, 789f–790f, 792f–793f
periosteal reflection hypothesis for, 785, 785f
radiographic evaluation of, 785f, 794–795, 794f
mobility
natural tooth compared to implant support systems, 773–775, 774f
pain, 783–784
percussion, 778
plaque biofilm, 776–778, 778b
probing depths, 778–782
consequences of probing around implant, 780–782, 780f, 781t, 782f
for soft tissue interface around teeth compared to implants, 778–780,
779f–780f
Periodontal ligament (PDL), 711
damage to adjacent, 234
Periodontal mechanoreceptors (PMRs), 711, 715–716
Periodontitis, 772
Periosteal reflection hypothesis, for marginal bone loss, 785, 785f
Periosteal releasing incision (PRI), 414
Periosteal tissue releasing techniques, 355
Periotest values, 570–571, 775–776, 776t
Peripheral feedback system, 711–713
implants and, 712–713
natural teeth and, 711–712
Peripheral nerve fibers, anatomy of, 329, 331f
Permucosal extension (PME), 212, 212f–213f, 215, 412
sutures for ILO prevention and, 421, 425f
Personal council appointment, 832
PFD. See Polyostotic fibrous dysplasia
PFs. See Posterior fontanelles
PGA. See Polyglycolic acid
Phenergan (Promethazine), 44t–45t
Phenylephrine, 550
Phlegmon, 298b
Phonetics. See Speech
Pier implant abutments, 133, 134f
Piezosurgery units, 388, 389f
tissue injury related to, 468, 469f–470f
Pin pressure test, 344t
Pink porcelain, 59–60, 60f
excessive CHS and soft tissue replaced with, 107f
Plain gut, 416t, 418
Plaque biofilm, 776–778, 778b
Plasmacytoma, 310
Plastic castable copings, 636, 636f
Plastic curettes, 796
Platelet and vascular activity (primary hemostasis), 267, 268f
Platelet count, 272
Platelet-derived growth factor (PDGF), 38–39
Platelet-rich fibrin (PRF)
blood sample difficulties and, 218–219, 220f–221f
inadequate blood spin for, 218, 219f
Platelets test, 46t–49t
Plavix (Clopidogrel), 41t, 42, 270
PM. See Prosthesis movement
PMC. See Pseudomembranous colitis
PME. See Permucosal extension
PMMA. See Poly methyl methacrylate acrylic
PMRs. See Periodontal mechanoreceptors
Pneumatization of maxillary sinus, 499, 500f
Poly methyl methacrylate acrylic (PMMA), 386
Polyclonal antibodies, 297
Polycythemia
bleeding and, 25
thrombus formation and, 25
Polydioxanone (PDS), 416t
Polydipsia, 19–20
Polyether impression material, 660, 660t
Polyglycolic acid (PGA), 418, 418f
Polymax. See Amoxicillin
Polyostotic fibrous dysplasia (PFD), 30
Polypropylene sutures, 416t, 420
Polysulfide impression materials, 660, 660t
Polytetrafluoroethylene sutures (PTFE), 416t, 420. See also Dense
polytetrafluoroethylene
Polyuria, 19–20
Polyvinyl siloxane (PVS), 705
Porcelain fracture, 646–651
Porcelain repair, for splinted and independent implant crowns, 665–666
Porcelain-to-metal/zirconia restoration, 60, 61f
Porphyromonas gingivalis, 407, 776–778, 797
Porphyromonas spp., 194
Positioning. See Implant positions
Posterior bone loss, IODs and, 585–587, 587f
Posterior fontanelles (PFs), 507–508
Posterior lateral nasal artery
bleeding and, 290–291, 290f
lateral-approach sinus elevation surgery and, 536
maxillary sinus blood supply and, 505–506, 542
Posterior mandible. See Mandible, posterior
Posterior maxilla. See also Maxillary sinus grafting
anatomic disadvantages to
anatomic location, 500
bone density, BIC, 499–500, 501f
maxillary sinus pneumatization, 499, 500f
predisposition to pathology, 500
ridge width/lingual repositioning, 499, 500f
available bone height of, 64
crowns, 693–694, 693f–694f
narrow occlusal tables and crowns of, 749–750, 750f–751f
Posterior ridge form, RP-5 and, 63
Posterior wall of maxillary sinus, 507, 508f
Post-grafting tissue management, 482–484, 485f–487f
Postoperative complications See also specific complications
AAD, 374–375
allograft migration, 396, 397f
bleeding and inadequate instructions, 373
bone graft tack migration, 396, 397f
with bone grafting, 478–496
bone density variations in ridge augmentations, 484–486, 487f–488f
bone growth over bone fixation screws, 494–496, 496f
difficulty releasing tissue flap from tenting screws, 486–487, 489f–490f
excessive pressure on ridge augmentation from temporary prostheses,
478–480, 482f–484f
ILO, 487–489, 490f–492f
inadequate bone width at implant apex, 491–494, 494f–496f
inadequate volume of facial bone regeneration with particulate graft,
489–491, 493f
lack of attached tissue covering ridge augmentation, 480–484, 485f–487f
dental material migration, 396–397, 398f
diet and inadequate instructions, 373
displacement of implants, in mandible, 395–396, 396f
displacement of implants, in maxilla, 390–395
ecchymosis, 367–368, 367f
prevention of, 368
treatment of, 368
edema, 364–365
activities decreased for prevention of, 365
cryotherapy for prevention of, 365, 367f
etiology of, 364
glucocorticoids for prevention of, 364–365, 367t
NSAIDs for prevention of, 364, 365f, 366t
fixed prostheses and, 700–705
hygiene and inadequate instructions, 373
with immediate implant placement, 573–575
excessive pain, 574–575
ILO, 575
medicolegal considerations, 575
nerve impairment, 574
transitional prosthesis impingement, 573–574
implant-related, 375–390
bone impingement between abutment and implant, 382–383, 384f
BPPV, 379–380, 380b, 381f
chronic neuropathic pain around implant area, 383–384, 385f
cover screw not fully seated, 380, 382f
excessive pressure from interim prosthesis, 367t, 386–387, 387f
fractured implant, 384–386, 385t, 386f–387f
fractured mandible after implant placement, 378, 379f
implant periapical lesion, 375–377, 377f
injury to adjacent teeth, 375, 376f
partial cover screw exposure, 380, 383f, 388b
tissue impingement between abutment and implant, 380–382, 383f
titanium allergy/hypersensitivity, 377–378, 378f
trauma from explantation of implants, 387–390, 389f–390f
inadequate postoperative instructions, 373–374
infection and inadequate instructions, 373
interim prosthesis and inadequate instructions, 374
in maxillary sinus grafting, 540–544
ecchymosis, 542, 543f
edema, 541–542
ILO, 542–543
infraorbital nerve impairment, 540–544, 541f
oroantral fistulae, 543–544, 544f–546f
pain, 542
revision surgery, 541, 543f
nausea after surgery, 374
nerve impairment and inadequate instructions, 373
patient/procedure treated same pharmacologically, 367t, 372
postsurgical pain, 368–372
acetaminophen treatment of, 369–370, 370t
analgesic agents for treatment of, 371–372, 371t–372t
codeine for treatment of, 370t, 371
combination analgesics for treatment of, 371, 371t
control of, 372, 372b
hydrocodone for treatment of, 370t, 371
NSAIDs for treatment of, 370, 370t
opioids for treatment of, 370t, 371
oxycodone for treatment of, 370t, 371
prevention of, 369
tramadol for treatment of, 370–371, 370t
treatment of, 369–372, 370t
pseudomembranous colitis, 374f, 375
smoking/alcohol use and inadequate instructions, 373
trismus, 368, 368f
wound healing/ILO and, 409
Postoperative maxillary cyst, 180, 181f, 517, 517f
Postoperative maxillary surgical cysts, 554
Postverdict adjustments, 851
Potassium test, 46t–49t
Pradaxa (dabigatran etexilate), 41t, 42, 269t
Premature occlusal contact, 728–731
etiology of, 728–729, 729f–731f
timing of, 730–731, 731f–732f
Premature occlusal contacts, 684, 684f
Premaxilla
buccal thickness of bone in, 172–173
maxillary IODs decreasing resorption of, 607
radiographic anatomy of, 163–164, 165f
Premaxillary wing, 208
Pre-scrub wash, in sterile technique, 321, 322f
Pressure necrosis, implant placement and, 204–206, 205f
Presuit, in malpractice litigation, 828–838
appointment of legal council in, 832
defense counsel, 832
personal counsel, 832
filing lawsuit in, 833–835
complaint, 833–835, 836f
response to complaint in, 835
service of process in, 835
summons in, 835, 837f
notification in, 828–829
official notice letter, 829, 831f
records request, 828–829, 830f
plaintiff's requirements for filing lawsuit in, 832–833
statute of limitations and, 833, 833t
recommendations for, 835–838
requirements after receiving notice in, 829–832
insurance carrier responsibility, 832
insured dentist responsibility, 829–832
Prevotella intermedia, 777–778
Prevotella intermedius, 407
Prevotella spp., 194
PRF. See Platelet-rich fibrin
PRI. See Periosteal releasing incision
Primary hemostasis, 267, 268f
Primary implant stability, inability to achieve, 568–569
aborting procedure after, 573
bone density and redirection for, 572, 573f
clinical confirmation of primary stability, 570–572, 571f
implant design and initial stability preventing, 572
larger implant for managing, 572
leaving implant in place after, 572–573
osteotomy preparation for prevention of
appropriate location and sequence in complete, 569–570
under prepare width and over prepare length for, 570
Primary intention wound healing, 405
Primary maxillary sinus mucocele, 179–180, 180f
Primary scrub, in sterile technique, 321, 322f–323f
Probing depths, 778–782
consequences of probing around implant, 780–782, 780f, 781t, 782f
for soft tissue interface around teeth compared to implants, 778–780, 779f–
780f
Probiotics, IBD and, 28
Production of documents and things, 838, 840f
Progressive bone loading
appointment sequence for, 764t
bone density treatment planning and, 124
elements of, 760–764, 761b
diet, 762–763
occlusal material, 763
occlusion, 763
prosthesis design and, 763
time interval, initial healing, 761–762, 761f, 762t
fixed occlusal complications and, 698–700
diet and prevention of, 699–700
etiology of, 698
occlusal material and prevention of, 700
occlusion and prevention of, 700
prevention of, 698–700, 698b
progressive loading phases in, 700, 701t
prosthesis design and prevention of, 700
phases of, 763–764, 763f
for poor bone quality in IPO, 758–760
clinical studies supporting, 760, 760f
complication of, 758
prevention with, 759
rationale for bone density, 759–760, 759f
PROLENE, 416t
Prolia (denosumab), 306–307
Proliferation phase of wound healing, 404–405
Promethazine (Phenergan), 44t–45t
Propionibacterium acnes, 194
Propofol (Diprivan), 230t, 231
Prostate-specific antigen (PSA), 46t–49t
Prostheses. See also Available bone; Dental implants; Fixed prostheses; Full-
arch prostheses; Interim prosthesis; Removable prostheses; Splinted
implant-tooth prosthesis
available bone evaluation for, 63–78, 64f
D3 bone modifications for, 118b
D4 bone modifications with, 119b
excessive pressure on ridge augmentation from temporary, 478–480, 482f–
484f
fixed occlusal complications with progressive bone loading and design of,
700
immediate implant placement and type of, 561
implant number and success rate of, 93, 93t
journal articles on complications with, 2t–6t, 4–5
lack of implant-implant distance and, 246, 250f
parafunction and design of, 100
patient education on, 54–55
recommended occlusal schemes for opposing dentition and, 767t
three adjacent pontic, 82–84, 82f–83f
treatment planning and planning of, 54
types of, 54–55
differences between, 55, 55f, 55t
fixed, 55–60, 55f, 55t
malpositioning of implant prevention by understanding, 259
not understanding and communicating, 54–55
removable, 55t, 61–63, 61f
Prosthesis movement (PM)
O-rings and, 588–589, 589f
PM-0, 588, 588f
PM-2, 588–589, 589f
PM-3, 589, 589f
PM-4, 589, 589f
PM-6, 589, 589f
screw loosening treatment and, 640, 640b, 641f
understanding of, 587–589, 588f
attachment height and, 589, 589f
Prosthetic angled loads, 734–736, 735f
Prothrombin time (PT), 28, 46t–49t, 271–272
Protrusive occlusal interferences, 724, 724f
Proximal contact area, IPO and increased, 755–757
food impaction and, 756, 756f
force distribution lacking and, 756, 756f
management and prevention of, 757, 757f
open contact development and, 756–757, 757f
seating prosthesis difficulty and, 756
tilted adjacent teeth and, 756f
PSA. See Prostate-specific antigen
Pseudocysts, 177, 179, 179f, 514–516
Pseudomembranous colitis (PMC), 316
postoperative, 374f, 375
Pseudopockets, 809–810
Psychological health, 37
edentulism and problems with, 141, 583
IODs improving, 584
oral health issues and, 37
PT. See Prothrombin time
Pterygoid implants, posterior wall of maxillary sinus and, 507
Pterygoidmandibular space, 301f–302f, 303
PTFE. See Polytetrafluoroethylene sutures
PTH. See Parathyroid hormone
Ptosis, after symphysis bone grafts, 470
PTT. See Partial thromboplastin time
Pulmonary system. See also Chronic obstructive pulmonary disease
PVS. See Polyvinyl siloxane
Q
QuickClot, 277t
Quinolones, 44t–45t
R
RA. See Rheumatoid arthritis
Radiation therapy, 34
hyperbaric oxygen and, 34
surgical/implant implications with, 34, 34b
Radiography, 154–174. See also Cone beam computed tomography; Two-
dimensional radiographic modalities
acute rhinosinusitis appearance in, 513, 514f
allergic rhinosinusitis appearance in, 514
antroliths and, 180–181, 182f, 519, 519f
chronic rhinosinusitis appearance in, 514, 514f
cystic lesions and
pseudocysts, 177, 179f
fungal rhinosinusitis appearance in, 518, 518f
halo effect in, 175, 176f
mandibular anatomic variants and, 159–163
accessory foramens, 159–160, 161f
anterior loop, 159, 160f
calcified carotid artery atheroma, 163, 165f
incisive canal, 161, 163f
lingual concavities, 160–161, 162f
lingual foramen/canal, 162–163, 164f
mandibular canal hypomineralization, 158f, 161
retromolar foramen, 161–162
mandibular anatomy and, 155–159
mandibular canal image evaluation and complications, 156
mandibular canal location, 155–156, 156f–157f
mandibular ramus as autogenous grafting donor site, 158, 159f
mandibular symphysis, 158–159, 159f
mental foramen, 156–158, 158f
marginal bone loss evaluation with, 785f, 794–795, 794f
maxillary anatomical variants and, 170–174
buccal thickness of bone in premaxilla, 172–173
canalis sinuosus, 174, 175f
deviated septum, 170–171, 171f
Haller cells, 171
inferior turbinate and meatus pneumatization (big nose variant), 172,
174f
intraosseous anastomosis, 173–174, 175f
maxillary sinus hypoplasia, 172, 174f
maxillary sinus septa, 172, 173f
paradoxical middle turbinate, 170, 171f
maxillary anatomy and
infraorbital foramen, 165–166, 166f
maxillary sinus membrane, 167–170, 168f
nasal cavity, 167
nasopalatine canal/incisive foramen, 164–165, 166f
ostiomeatal complex, 168–170, 169f
paranasal sinuses, 166–167, 167f
premaxilla, 163–164, 165f
maxillary ostium and, 168, 169f
neoplasms and, 180, 182f
of neoplasms in maxillary sinus, 517, 518f
nerve impairment prevention and, 344–348
bone models, 347
CBCT and MSCT accuracy, 347, 348f
interactive treatment planning software for posterior mandible
evaluation, 347, 348f
surgical templates, 347–348, 349f
two-dimensional radiography limitations and disadvantages, 344–345,
347f
two-dimensional radiography magnification guides, 345–347, 347f
odontogenic rhinosinusitis appearance in, 512, 512f
osteomyelitis detection with, 305–306
peri-implant mucositis evidence in, 795, 795f
of postoperative maxillary cyst, 517, 517f
pseudocyst appearance in, 516, 516f
reports, 184–189
basic information elements for, 187–188
findings in, 188–189
interpretation of, 184–189
sample, 189f–191f
styles of, 189, 189f–191f
typical descriptions for, 188
retention cysts appearance in, 516
rhinosinusitis and
acute, 176, 176f
allergic, 177, 178f
chronic, 177
fungal, 177, 179f
odontogenic, 175, 176f
for Schneiderian membrane evaluation, 502
Radiopaque template, CBCT complications with, 181–183, 183f–184f
Ramus bone grafts, 471–478
block separation from bony ridge during implant placement in, 476–478,
479f–480f
failure to decorticate host bone in, 472–474, 474f
IAN damage from, 472
incorrect graft storage medium for, 475–476, 476f
mobility of block in, 474–475, 474f
bone fixation screws for prevention of, 474–475
etiology of, 474
treatment of, 475, 475f–476f
poor candidates for, 471–472, 473f
soft tissue irritation from overextended fixation screw in, 476, 477f
RANKL (receptor activator of nuclear factor kappa-B ligand), 38
RAP. See Regional acceleratory phenomenon
RBCs. See Red blood cells
Receptor activator of nuclear factor kappa-B ligand (RANKL), 38
Recirculation, supplemental ostium and, 511
Reclast (Zoledronate), 39
Recombinant thrombin (Recothrom), 278
Records request, 828–829, 830f
Recothrom (recombinant thrombin), 278
Red blood cells (RBCs), 46t–49t
Referrals
of CBCT to radiologist, 862
complications and failures with, 9–10
documenting refusal of, 859–861
Regeneration, nerve, 340, 340f
Regenerative material limitations, in ridge augmentation, 446–447
Regenerative procedures, for peri-implantitis, 803–805, 806f
Regional acceleratory phenomenon (RAP), 466
Releasing incision design, 452, 454f
Reline materials
hard, 386
soft, 387
Reline technique, 388b
Remodeling, bone. See Modeling/remodeling bone
Removable partial denture (RPD), 135, 135b
Removable prostheses, 55t, 61–63, 61f. See
also Dentures; Edentulism; Implant-supported overdentures
disadvantages of, 585–587
division A (abundant bone) and, 69
mini implants and, 127
occlusal schemes for fully edentulous implant, 766b
RP-4, 61–62
apicocoronal (“z”-axis) positioning and, 257, 258f–259f
buccolingual (“y”-axis) positioning and, 252, 253f
criteria for, 61
implant number for, 62
implant position for, 62
OD-3 complication with fabrication of, 602
options for, 590, 591f
patient communication for, 62
treatment denture for, 62
treatment planning for overdenture supported by, 141–143, 142b–143b
RP-4 option for maxillary IODs, 610–611
advantages of, 611
attachments in, 611
implant number/position in, 610–611, 611f
indications for, 610, 610f
occlusal scheme in, 611
prosthesis design in, 611
RP-5
apicocoronal (“z”-axis) positioning and, 257, 258f–259f
buccolingual (“y”-axis) positioning and, 252, 253f
criteria for, 62
excessive CHS and, 107, 107f
implant number for, 63
implant position for, 63
lack of soft tissue support with, 626, 626f
options for, 590, 591f
posterior ridge form and, 63
residual ridge bone loss and, 63, 63f
treatment dentures for, 62–63
treatment planning for overdenture supported by, 141–143, 142b–143b
RP-5 option for maxillary IODs, 609–610
advantages of, 610
implant number/position in, 609–610, 609f–610f
indications for, 609
O-rings in, 610
prosthetic design in, 610
support in, 610
Renal function, of elderly, 35, 35t
Repassivation, 377
Repositioning, to decrease bleeding, 273, 273f
Request for admissions, 838, 841f–842f
Requests for disclosure, 838
Residual ridge bone, RP-5 and loss of, 63, 63f
Resonance frequency analysis (RFA), 570–572, 571f, 776
Resorbable GBR membranes, 447–448, 448f, 460–462, 462f
Resorbable graft material (RGM), 566f
Response to complaint, in filing lawsuit, 835
Resuturing, ILO and, 437, 437f
Retained root tips, implant placement and, 194–195, 196f
Retention cysts, 177–179, 516
Retractor-related injuries, nerve impairment and, 355, 358f
Retrograde peri-implantitis. See Periapical lesion, implant
Retromolar foramen (RMF), 161–162
Reverse screw techniques, 388, 389f
Reverse torque testing (RTT), 215, 571
Reversible complications, 10
RF. See Rheumatoid factor
RFA. See Resonance frequency analysis
RGM. See Resorbable graft material
Rheumatoid arthritis (RA), 31–32
bone resorption and bleeding with, 32
surgical/implant implications of, 32
xerostomia and, 32
Rheumatoid factor (RF), 46t–49t
Rhinosinusitis, 175–177
acute, 176–177, 176f, 513
CBCT examination for, 551–552
etiology of, 513
maxillary sinus grafting infections and, 551–552
treatment of, 513
allergic, 177, 178f, 514
etiology of, 514
radiographic appearance of, 514
chronic, 177, 513–514
treatment of, 514
fungal, 177, 179f
etiology of, 518
maxillary sinus grafting and postoperative infection of, 552, 554
treatment of, 518
Haller cells and, 510, 511f
odontogenic, 175–176, 176f, 512–513
etiology, 512
treatment of, 513
Ridge augmentation
bone density variations in, 484–486
etiology of, 484
lack of attached tissue covering, 480–484
management of, 482–484, 485f–487f
prevention of, 481
regenerative material limitations in, 446–447
temporary prostheses causing excessive pressure on sites of, 478–480,
482f–484f
Ridge splitting, 446–447, 450, 450f
Rigid bronchoscopy, 221, 222f
Rigid connection implants, 673–674, 674f
Rigid fixation, 774
Rivaroxaban (Xarelto), 41t, 42, 269t
RMF. See Retromolar foramen
Romazicon (flumazenil), 231–232, 231f
Root-implant apex distance
insufficient, 234–236
treatment of, 236
“place implants at depth of adjacent”, 359, 359f
Round bur (205LN), 645, 646f
RP-4, RP-5. See Removable prostheses
RPD. See Removable partial denture
RTT. See Reverse torque testing
Rule to File Complaint, 833
S
SA. See Sinus augmentation
Safety zones, nerve impairment prevention and, 352–353, 353f
Saline, 204
Saline rinses, 551, 552f
Saliva, wound healing/ILO and, 406–407
Salivary flow, 23, 23b
Salivary gland injury, 224–225, 227f
Salvin, 211, 242
Satisfactory health, in quality scales, 818–819, 819f
Saucerization, 784
Scanning technique complications, with CBCT, 153–154
imaging protocol, 153–154
mucosal thickness, 154
scanning template position, 154
Scatter, CBCT and, 152, 153f
Schneiderian membrane
anatomy and physiology of, 502
clinical implications of, 502
radiological evaluation of, 502
thickness of, 532
Scissors, for sutures, 425–427, 432f
Scleroderma, 31
Screw fractures, 643–645
immediate loose screw treatment for prevention of, 643–644
cavitron device for, 644
explorer technique for, 644, 645f
inverted cone bur (33 1/2 bur) for, 645, 647f
manufactured retrieval instruments for, 645, 648f
round bur (205LN) for, 645, 646f
slot top of screw for, 645, 647f
Screw loosening, 631–643
anatomic location in, 638
cantilevers/increased CHS and, 631–632, 633f
component fit, 635–636, 636f
crown/abutment not fully seated and, 633, 634f
external force factors of, 631, 632b
implant design and, 636–637, 637f, 637t
insufficient and excessive torqueing with, 633, 634f
screw compared to cement in, 637–638, 638f
screw diameter in, 633, 635f
screw material in, 633–635, 635f
splinted implant-tooth prosthesis and, 633
decreased force for, 638
ideal preload for, 639
prosthetic design and, 638–639
screw tightening sequence for, 639, 639f
settling effect and, 639–640, 640f
torque under moist conditions for, 640
wider implant bodies for, 640
abutment screw movement and, 640–643, 642f–643f
PM and, 640, 640b, 641f
Screw tightening sequence for, 639, 639f
Second molars, alternative surgical techniques for replacing, 360, 360f
Secondary hemostasis (blood coagulation), 267–268, 268f–269f
Secondary intention wound healing, 405, 407f
Segmental degeneration, 339
Selective serotonin reuptake inhibitors (SSRIs), 37
Sensors, CBCT, 150
Sepsis, 298b
Septa
antral, 533–536
etiology of, 533
inferior wall of maxillary sinus and, 509
Septra (trimethoprim/sulfamethoxazole), 316t, 551
Serotonin and norepinephrine uptake inhibitors (SNRIs), 384
Service of process, in filing lawsuit, 835
Settlement
of lawsuit, 846
as pretrial mode of disposition, 845
Settling effect, screw loosening and, 639–640, 640f
Severe surgery complications. See Life-threatening surgery complications
Sickle cell anemia, 27t
Silicone impression materials, 660, 660t
Silk sutures, 416t, 419
SimPlant (Materialise), 264
SimPlant Safe Guide, 347–348, 349f
Simple loop suture technique, 420–421, 422f–423f
Single tooth implant
costs of, 136–137
treatment planning for single missing tooth with, 136–137, 136b
Sinus augmentation (SA)
maxillary sinus grafting complication prevention with, 520–523
SA-1, 520–522, 521f
SA-2, 521f, 522, 529–530, 531f
SA-3, 521f, 522, 522b
SA-4, 521f, 522–523
SA-2 complications, 529–530
access, 529
BPPV, 529–530, 531f
graft with small increments of material, 529
incorrect osteotomes, 529
osteotomy, multiple entries, 529
osteotomy overpreparation, 529
patient selection, inadequate bone, 529
sinus membrane perforation, 529
SA-3 implant delays after sinus membrane perforations, 533
Sinus graft overfills, 525–527, 527f, 548
Sinus grafting. See Maxillary sinus grafting
Sinus membrane perforations, 530–533
curette kept on bony floor for prevention of, 532, 532f
membrane thickness and prevention of, 532
narrow sinus complications with, 532
osteotomy line angles for prevention of, 532
postoperative monitoring of, 533
SA-3 implant deferments after, 533
size of access window for prevention of, 531–532
surgical armamentarium for prevention of, 531
surgical technique alterations for, 532
large perforation, 533, 535f
small perforation, 533, 534f
Sinusitis. See Rhinosinusitis
Site development, 7
Sjögren syndrome, 31
Smile zone
FP-2 and pre-operative evaluation of, 57–59, 59f
FP-3 and variations in, 59–60, 60f
Smoking, 32–33
bone grafting failure and, 32
cessation, 32–33, 33t
diseases attributed to, 32
infections and, 32
maxillary sinus grafting complications with, 523
wound healing/ILO and, 408
Snap-On Smile appliance, 478–480, 483f–484f
SNRIs. See Serotonin and norepinephrine uptake inhibitors
Socket seal surgery, 567
Sodium test, 46t–49t
Soft reline materials, 387
Soft tissue. See also Tissue impingement
Alloderm promoting closure of, 491f–492f
bone fixation screw overextension causing irritation of, 476, 477f
complications with
lack of keratinized tissue, 806–809, 807f–808f
peri-implant mucosal hyperplasia, 809–810, 810f, 810t
edentulism and discomfort in, 582
edentulism without treatment and consequences with, 137–138, 138b
excessive CHS and pink porcelain replacing, 107f
FP-1 augmentation of, 56
life-threatening surgery complications with, 223
malpositioning of implant prevention and evaluation of, 259–260
maxillary IODs and less coverage of, 606–607
natural teeth compared to implant interface with, 778–780, 779f–780f
nerve impairment and reflection of, 336, 336f
RP-5 lack of support of, 626, 626f
stage II uncovery surgery and excessive, 213, 214f
symphysis bone grafts changes to, 470
tissue punch reduction of, 210, 211f
Soldering, for nonpassive prosthesis complications, 661
direct technique for, 664f–665f
indirect technique for, 662f–663f
long screws for, 661f
Solu-Cortef (hydrocortisone sodium succinate), 22
Spatial resolution, CBCT and, 150–151
Speech
complete upper denture impact on, 141
edentulism and difficulty with, 583
IOD advantages of, 142
IODs enhancing, 584
Sphenoid sinuses, 167, 188
displacement of implants in, 390–392, 392f
Sphenopalatine artery, 506
Spiral failure, of O-rings, 617, 617f
Splinted crowns, independent implant crowns vs., 662–668
etiology, 662–668
Splinted implant-tooth prosthesis, 128–133
guidelines for splinting natural teeth, 131–133, 132f
intrusion and, 133, 133f
nonrigid connectors and, 133
mobility of, 129–131
fixed prosthesis movement and, 129–130
horizontal movement and, 130, 130f
implant movement and, 130–131
vertical movement and, 129, 130f
occlusal contact schemes and, 743, 744f
pier implant abutments and, 133, 134f
screw loosening and, 633
treatment planning with, 128–133, 129f–130f
Split-finger technique, 213–215, 216f–217f
Spontaneous fracture, in modeling/remodeling bone, 114f
Squamous cell carcinoma, 180, 182f, 310
Square arch forms, 611
SSRIs. See Selective serotonin reuptake inhibitors
Stage II uncovery surgery, 210–215
bony defects at uncovery, 210–213
etiology and prevention of, 211–213
horizontal defects and, 212–213
vertical defects and, 211–212, 212f–213f
excessive tissue thickness at, 213, 214f
papilla loss after, 213–215, 216f–217f
reverse torque testing complications and, 215
tissue punch reducing attached tissue in, 210, 211f
Stamp cusp offset loads, 752, 754–755, 755f
Standard of care, 849
Staphylococcus aureus, 306, 407, 513, 547
Staphylococcus epidermidis, 194, 503–504
Staphylococcus viridans, 547
State dental licensure complaints, 852–853
Static light touch test, 344t, 345f
Statute of limitations, 833, 833t
Steel curettes, 796, 797f
Sterile field, sterile technique and, 320, 321f
Sterile gloves, in sterile technique, 321, 323f–324f
Sterile technique, 319–326
clean and aseptic techniques compared to, 320t
definition of, 319–320
general considerations of, 320b
for maxillary sinus flora, 504
steps in, 321b
gown tying, 321, 325f
gowning, 321, 323f–324f
pre-scrub wash, 321, 322f
primary scrub, 321, 322f–323f
sterile gloves, 321, 323f–324f
sterile field and, 320, 321f
surgical scrub and, 320, 322f–323f
Stomach ulcers, 28
Storage medium, ramus bone grafts and incorrect, 475–476, 476f
Strain, definition of, 788
Streak artifacts, CBCT and, 152, 153f
Streptococcus intermedius, 194
Streptococcus pneumonia, 503–504, 513, 547
Streptococcus pyogenes, 503–504
Streptococcus viridans, 503–504
Stress
angina and reduction of, 16
CHF and reduction of, 18–19
hypertension and reduction of, 15, 15b
MI and reduction of, 17
Stress transfer, bone density and, 122, 123f
Stripped hex screw abutment, fixed prostheses and, 677–678, 678f
etiology of, 678
prevention of, 678
Stroke, 17. See also Cerebrovascular accident
Study casts, 235, 237f
Subepithelial connective tissue grafting, 443–445, 446f
Sublingual gland injury, 224–225, 227f
Sublingual space, 301f–303f, 303
Sublingual undercuts, displacement of implants in mandible and, 395–396,
396f
Submandibular space, 301f–302f, 304, 305f
Submasseteric space, 301f–302f, 303
Submental space, 301f–302f, 303–304, 304f
Submucosal space technique, for tissue expansion, 414, 415f, 427b
Subperiosteal implants, infection and, 320–326, 326f
Sulfonamides, 551
Summons, in filing lawsuit, 835, 837f
Sumycin. See Tetracycline
Superior genial foramen, 464
Superior margin location, symphysis bone grafts and improper, 470–471, 472f
Superior wall of maxillary sinus, 507, 508f
Supplemental ostium, 510–511
Surgery. See also Flapless surgery; Implant placement, surgical related; Life-
threatening surgery complications; Stage II uncovery surgery
adolescents and implications with, 35
anemia implications with, 26
angina and implications of, 16
aspirin implications with, 40
bruxism implications with, 37–38
CHF and implications with, 18
cirrhosis of liver implications with, 28–29
clenching implications with, 37–38
complications with
clearances and, 8
journal articles on, 2t–6t, 3–4
COPD implications with, 24–25
corticosteroid use and implications with, 22
CVA and implications of, 17
D3 bone modifications for, 118b
diabetes mellitus and implications with, 20
DIONJ implications with, 39
early displacement of implants in maxilla and poor technique in, 393
elderly and implications with, 35–37
FD implications with, 30
graft site infection prevention with good technique in, 546
hyperparathyroidism and implications with, 23
hypertension and implications of, 14–15
IBD considerations with, 27–28
ILO prevention with good technique for, 409–414
clean, concise incision, 411, 411f
flap allowing for adequate access, 410, 410f
flap design, 409–410, 410f
flap margins maintained over bone, 410–411, 411f
full thickness reflection and ideal elevation of flap, 411–412, 412f
hemostasis, 413
incision in keratinized tissue, 409, 409f
papilla-saving incisions, 412, 413f
relieving tissue for flap tension, 414, 414f–415f, 427b
tissue desiccation prevention, 414
vertical release incision for blood supply to flap, 410, 410f
immunosuppressive drug implications with, 43
leukocytic disorder implications with, 26–27
malpositioning of implant prevention with good technique for, 261
MI and implications of, 16
nausea after, 374
nerve impairment prevention and alternative techniques for, 356–361
bleeding for mandibular canal violation evaluation, 359–360, 360f
immediate implants in mental foramen, 356, 358f
infiltration technique, 357–359
nerve repositioning, 361, 361f
“place implants at depth of adjacent root apexes”, 359, 359f
“place implants buccal or lingual to IAN canal or foramen”, 359, 359f
second molar replacement, 360, 360f
nerve impairment treatment at time of, 342, 343f, 344, 346f
osteomyelitis implications with, 30
osteoporosis implications with, 29–30
Paget disease implications with, 31
polycythemia implications with, 25
psychological problems and implications with, 37
RA implications of, 32
radiation therapy implications with, 34, 34b
sinus membrane perforation and technique alterations in, 532
large perforation, 533, 535f
small perforation, 533, 534f
smoking and implications with, 32
thyroid disorders and implications with, 21–22
warfarin sodium implications with, 40
xerostomia implications with, 23
Surgical contraindication, 13
Surgical fires, 226–228, 229b
Surgical hemorrhage classification, 268b
Surgical scrub, sterile technique and, 320, 322f–323f
Surgical steel, 416t
Surgical templates
malpositioning of implant prevention and use of, 261–264
CBCT, 264–265
complete limiting design, 261–264, 264f–265f
nonlimiting design, 261, 263f
partial limiting design, 261, 263f
for nerve impairment prevention, 347–348, 349f
nerve impairment prevention and positioning of CBCT, 356, 358f
overheating and, 204
Surgical wounds, infection rates and classification of, 294–295, 295b, 295t
Surgical/implant contraindication, 13
Surgicel, 277t, 279, 280f
SurgiGuides, 264
Sutures
absorbable, 418–420
synthetic, 418–420, 418f
basic principles of, 430f–431f, 436b
to decrease and control bleeding, 273, 274f
ILO prevention and
absorbability for, 420
bone graft material in incision line and, 432–433, 433f
continuous technique for, 421, 426f–427f
“dead space” minimization for, 433, 433f
decreasing inflammation for, 433
figure eight technique for, 421, 424f–425f
high tensile strength for, 420
knots, 427–432, 432f
low tissue reactivity for, 420
materials and techniques in, 414, 416t
mattress techniques for, 421–425, 428f–429f
needle holders with, 425, 432f
needles for, 420, 421f
PME for, 421, 425f
scissors with, 425–427, 432f
simple loop technique for, 420–421, 422f–423f
size of, 420
tissue pick-ups with, 425, 431f
transitional and interim prosthesis design and, 433–434, 434f
types of, 416t, 418–420
nerve impairment prevention with careful, 356, 358f
nonabsorbable, 418–420, 419f
polypropylene, 416t, 420
polytetrafluoroethylene, 416t, 420
silk, 416t, 419
Swallowing of implant components, 219–221
prevention of, 220
Symphysis bone grafts, 463–471
bleeding, nerve impairment complications with, 463–464
bone fragment loss in break-up of cortical blocks in, 467–468
etiology of, 467
chin graft closure complications and, 468–470
etiology of, 468
improper superior margin location in, 470–471, 472f
inadequate bone volume for graft, 463
complications with, 463, 464f–465f
etiology of, 463
prevention of, 463
incorrect size and shape of, 464–466
block preparation, 466, 466f–467f
prevention of, 466
neurosensory changes after, 470, 471f
soft tissue changes (ptosis) after, 470
ultrasonic piezosurgery-related tissue injury, 468, 469f–470f
Synesthesia, 342t
Synthetic sutures, 418–420, 418f
Systemic diseases, wound healing/ILO and, 408
Systemic lupus erythematous, 31
T
T4. See Thyroxine
TADs. See Orthodontic implants
Tamoxifen, 43
Tapering arch forms, 611
Teeth, natural. See also Adjacent teeth; Implant-tooth connection, fixed
prostheses complications with; Mesial-distal (“x”-axis) positioning:
implant-natural tooth; Natural teeth and implant differences, occlusion
and; Splinted implant-tooth prosthesis
bone density in jaws after loss of, 113, 113f
cantilevers and one missing, 78–79, 79f–80f
cantilevers on implant compared to, 243–244, 245f
cusp angles of, 739, 740f
guidelines for joining implants to, 131, 131f
intrusion and, 133, 133f
nonrigid connectors and, 133
guidelines for splinting, 131–133, 132f
immediate implant placement and size/length relative to, 562–563, 563t
IODs with less morbidity compared to, 584
malpositioning of implants prevention and condition of adjacent, 260
mobility of implants compared to, 773–775, 774f
nonintact alveolar socket prevention with atraumatic extraction of, 565–566
occlusal contact timing and movement of, 689
occlusion of, 727, 727f
soft tissue interface around implants compared to, 778–780, 779f–780f
treatment planning for multiple missing, 137
treatment planning for single missing
FPD for, 135–136, 136b
no treatment option, 134, 135b
RPD for, 135, 135b
single tooth implant for, 136–137, 136b
Teflon curettes, 796, 797f
Temporal space, 301f–302f, 303
Tent screws, 461f
difficulty releasing flaps from, 486–487, 489f–490f
Tequin (Gatifloxacin), 44t–45t, 550
Tertiary hemostasis (fibrinolysis), 268, 268f
Tertiary intention wound healing, 406
Tetracycline (Achromycin, Sumycin), 316t, 317, 551
for peri-implant mucositis debridement, 797–798, 798f
Thalassemia, 27t
Thermal discrimination test, 344t
Thiamine, 436
Thiazide-type diuretics, 14
33 1/2 bur (inverted cone bur), 645, 647f
Thread shape
for immediate implant design, 564, 564f
implant, 388
3-D reformatted images, bone dehiscence on, 152–153, 153f. See also Cone
beam computed tomography (CBCT)
Three-dimensional finite element analysis, 727, 727f, 788–789, 789f
Thrombin, 277–278, 277t, 278f
Thrombin-JMI (bovine thrombin), 278
Thrombophlebitis, infections routes and, 299
Thrombotic stroke, 17
Thrombus formation, polycythemia and, 25
Thyroid disorders, 21–22
aspirin/NSAID use and, 21
bleeding and, 21
catecholamine sensitivity and, 21
CNS depressant drugs and, 22
hyperthyroidism signs and symptoms, 21
hypothyroidism signs and symptoms, 22
Thyroid storm, 21
Thyroid-stimulating hormone (TSH), 46t–49t
Thyrotoxicosis, 21
Thyroxine (T4), 46t–49t
Tisseel, 277t
Tissue biotypes, bone grafting and failure to evaluate, 443–445
Tissue conditioners, 387
Tissue desiccation prevention, 414
Tissue impingement
between abutment and implant, 380–382, 383f
etiology of, 382
prevention of, 382
treatment of, 382
in fixed prosthesis
with abutment not seated, 675, 675f
with pain on abutment placement, 675–676, 675f
with pain on application of torque, 676–677
Tissue pick-ups, sutures and, 425, 431f
Tissue punch, in stage II uncovery surgery, 210, 211f
Titanium
allergies, 43–44
d-PTFE, for membrane space maintenance, 457
immediate implant design with, 563, 563f
mechanical properties for different grades of, 385t
modulus of elasticity of bone compared to, 788–789, 789f
postoperative complications with allergies/hypersensitivity, 377–378
prevention of, 378
Titanium brush bars, 796
Titanium mesh
exposure of, 463f
for membrane space maintenance, 457–458, 460f
Titanium-coated curettes, 796, 797f
Tongue thrust and size, 100–101
complications with, 101, 101b, 102f
types of, 101, 101b, 101f
Toothbrushing, for peri-implant mucositis, 798–799, 799f
Torque
consistent value of, 646
excessive application of, to abutment screw/prosthesis, 645–646, 648f–649f
fixed prostheses and wrench technique complications with, 678–679
etiology of, 678
prevention of, 678–679, 679f–680f.
fixed prostheses pain on application to abutment of, 676–677
ideal preload, 645
moment loads and, 681f
nonpassive fixed prostheses and, 658, 658f–659f
screw loosening and excessive/insufficient, 633, 634f
screw loosening and moist conditions for, 640
Trabecular bone
in femur, 112, 112f
in jaws, 112–113, 113f
in mandible, 112–113, 112f
in maxilla, 112–113, 113f
Tramadol (Ultram, Ultracet), 44t–45t
for postsurgical pain treatment, 370–371, 370t
Tranexamic acid, to control bleeding, 276, 278f
Transitional prosthesis
ILO prevention with sutures and, 433–434, 434f
immediate implant placement and impingement of, 573–574
Treatment See also specific treatments
of acute rhinosinusitis, 513
of adjacent teeth injury, 375
of allergic rhinosinusitis, 514, 515f
angina and summary of, 16
anticoagulant medications summary for, 42
for bar try-in resulting in pain, 623
bleeding prevention and, 283–291
CBCT for anatomy/anatomic variants in, 283
incision/reflection of tissue, 283, 283f
blood pressure guidelines for, 14t
bone disease implications for, 31t
of bone fixation screw exposure during particulate graft healing process,
459–460, 461f
of bone fragment loss in break-up of cortical blocks, 468, 468f
of bone growth over bone fixation screws, 496, 496f
of bone impingement between abutment and implant, 383
of BPPV, 380, 380b, 381f
cantilever options with, 81–82, 82f
cardiovascular system summary for, 19, 19t
for cement-retention complications, 705, 707f
of chronic neuropathic pain around implant area, 384
of chronic rhinosinusitis, 514
complications with
long term treatment for preventing, 11
not rushing for prevention of, 11
poor planning causing, 9
contraindications to, 13
with corticosteroids, 22–23
of cover screw not fully seated, 380
CVA and summary of, 18
of dental material migration, 397
diabetes mellitus and summary of, 21
digestive system issues and implications for, 29t
of displacement of implants in maxilla, 395, 395f
division B (barely sufficient bone) options for, 71–72, 71f
of elderly, 35–37
endocrine system issues and implications for, 24t
of excessive pressure from interim prosthesis, 367t, 387, 387f
for excessive space between implant and tooth, 244, 246f
for fixed prostheses with abutment not seated, 675, 675f–676f
of fixed prostheses with pain on abutment placement, 675f–676f, 676
for food impaction of fixed prostheses, 701
of fractured mandible after implant placement, 378, 379f
of fungal rhinosinusitis, 518
of graft site infection, 550–551
guaranteed outcome of, 862
hematologic system issues and implications for, 27t
for ILO in bone grafting sites, 488–489, 490f–492f
for implant explantation trauma, 388–390, 389f–390f
of implant periapical lesion, 377
for inadequate volume of facial bone regeneration with particulate graft,
491, 493f
of infections, 311–313
antibiotics used in, 313–317, 316t, 319
culture and sensitivity (C&S) test, 313, 313b, 314f–315f
incision and drainage, 311–313
prophylactic antibiotics, 317–319
of insufficient root-implant apex distance, 236
of mandibular full arch splinting flexure complications, 669, 670f
mandibular IOD options for, 594–606, 595f
maxillary IOD options for, 609–611, 609b
of maxillary sinus antroliths, 519–520
for membrane space maintenance, 458, 458f–460f
MI and summary of, 17
of mobility of block in ramus bone grafts, 475, 475f–476f
MRONJ guidelines for, 307, 309t
of neoplasms in maxillary sinus, 517–518
of nerve impairment, at time of surgery, 342, 343f, 344, 346f
of nerve impairment, postoperative, 342–344
CBCT evaluation, 343
clinical assessment, 343, 344t, 345f
follow-up care, 344, 346t
pharmacologic intervention, 343–344
possible referral, 344, 346t
of nonpassive prosthesis complications
modification for, 661
soldering for, 661, 661f–665f
of odontogenic rhinosinusitis, 513
of osteomyelitis, 306
for parafunction with no occlusal guard, 697–698, 698f
of particulate graft infection, 463, 463f
of postoperative maxillary cyst, 517
of postsurgical pain, 369–372, 370t
acetaminophen for, 369–370, 370t
analgesic agents for, 371–372, 371t–372t, 384
codeine for, 370t, 371
combination analgesics for, 371, 371t
hydrocodone for, 370t, 371
NSAIDs for, 370, 370t
opioids for, 370t, 371
oxycodone for, 370t, 371
tramadol for, 370–371, 370t
of pseudocysts, 516, 516f
pulmonary system issues and implications for, 25t
of retention cysts, 516
of screw fractures, 644–645
explorer technique for, 644, 645f
inverted cone bur (33 1/2 bur) for, 645, 647f
manufactured retrieval instruments for, 645, 648f
round bur (205LN) for, 645, 646f
slot top of screw for, 645, 647f
for screw loosening, 640–643, 641f
abutment screw movement and, 640–643, 642f–643f
PM and, 640, 640b, 641f
of stripped hex screw abutment, 678, 679f
of tissue impingement between abutment and implant, 382
of titanium allergies/hypersensitivity, 378, 378f
xerostomia regimens for, 23b
Treatment planning. See also Implant positions
bone density and, 110–119, 110b, 122–124
direction of force and, 124
implant coatings and, 124
implant design in, 124
modification with, 123, 123b
summary for, 124
surface area increased in, 123–124
for bone grafting
bone resorption understanding, 440–441, 441f–442f
tissue biotype evaluation, 443–445, 445f–446f
underestimation of bone, 442–443, 444f–445f
understanding need for bone grafting, 441–442, 442f
with complete upper denture, 140–141
advantages of, 140
cost and, 54
for division A (abundant bone), 68
for edentulism, no treatment option, 137–140
bone loss and, 137, 138b, 138f
esthetic consequences and, 138–140, 139f–140f, 140b
soft tissue consequences and, 137–138, 138b
education and, 54–55
for fixed prostheses, 143–144, 144b, 144f
force-related issues and, 95–101
arch form, 110, 110f–111f
arch position and, 107–109
for bruxism, 99–101
with CHS, 102–107, 105f–107f
for clenching, 99–101
with opposing arch, 109–110, 109b–110b, 109f
parafunction, 95–101
implant number and, 91–95
implant size and, 124–128
implant width and, 127–128, 127f, 128b
IPO and ideal implant positioning in, 727–728, 727f–729f
key implant positions for, 78–91, 78f
for malpositioning of implants, 259
malpractice litigation avoided with detailed, 857, 858f
maxillary IOD complications with, 607–609, 608f
maxillary sinus grafting complications with, 520–523
for multiple missing teeth, 137
with patients, 133–144
comprehensive options for, 133–144
prostheses planning prior to, 54
for RP-4/RP-5 overdenture, 141–143
advantages of, 141–142, 142b–143b
for single missing tooth
FPD for, 135–136, 136b
no treatment option, 134, 135b
RPD for, 135, 135b
single tooth implant for, 136–137, 136b
splinted implant-tooth prosthesis and, 128–133, 129f–130f
Trephine burs, 388–389, 390f
Trial, in malpractice litigation, 846–853
closing arguments in, 850–851
comparative fault and, 851
continuance and, 847
court docket and, 847, 848f
courtroom layout for, 847, 849f
damages in, 851
deliberation in, 851
excess verdict and, 851
expert witness in, 850
impeachment in, 850
inadmissible information in, 850
jury selection for, 847
opening statement in, 847
patient/plaintiff case presentation in, 847–850
postverdict adjustments and, 851
verdict in, 851
witness order in, 850
Triazolam (Halcion), 44t–45t, 230t
Tricyclic antidepressants, 37, 384
Trigeminal nerve
mandibular branch (V3)
IAN in, 333–334, 334f
LN in, 334, 335f
maxillary branch (V2)
anatomy of, 330–332, 331f
anterior superior alveolar nerve in, 332, 333f
infraorbital nerve in, 332, 333f
maxillary sinus grafting and block anesthesia injections to, 523, 524f
nasopalatine nerve in, 330–332, 332f
ophthalmic branch (V1), 330
Trimax. See Amoxicillin
Trimethoprim/sulfamethoxazole (Bactrim, Septra), 316t, 551
Trismus, 297
postoperative, 368, 368f
TSH. See Thyroid-stimulating hormone
Tuberosity, maxillary sinus grafting aggressive removal of, 528–529
correction location in, 528–529
harvesting too far posterior in, 529, 530f
posterior sinus cavity exposure in, 529
205LN (round bur), 645, 646f
Two-dimensional finite element analysis, 727
Two-dimensional radiographic modalities, 148–150. See also Radiography
intraroot distance evaluation with, 235, 238f
limitations and disadvantages of, 344–345, 347f
magnification guides of, 345–347, 347f
panoramic radiography, 148–150, 149f
periapical radiography, 148, 149f
Two-point discrimination test, 344t
Tylenol. See Acetaminophen
Tyrosine kinase inhibitors, 38–40
U
Ulcerative colitis, 27–28
Ultracef (cefadroxil), 314, 316t
Ultracet, Ultram. See Tramadol
Ultrasound
for mental foramen location identification, 351
for peri-implant mucositis debridement, 796–797
peri-implantitis management with, 801
piezosurgery units, 388, 389f
tissue injury related to, 468, 469f–470f
Uncemented prosthesis, 651–656
implant abutment and, 651, 651f
prevention of
abutment resistance form and, 653–656, 655f–656f
abutment surface area and, 652, 652f–653f
abutment surface texture and, 653
abutment taper and, 651–652, 652f
geometry of abutment and, 652, 654f
retention/resistance and, 651, 651b
Uncinate process, 168–170
variants and complications of, 510
Uncovery. See Stage II uncovery surgery
Underwood septa. See Antral septa
Unreasonable provision, 846
Unsupported grafts, 450, 450f
V
V1 nerve (ophthalmic), 330
V2 nerve. See Maxillary nerve
V3 nerve. See Mandibular nerve
Valium (diazepam), 230t
Vantin (cefpodoxime proxetil), 550
Varenicline tartrate (Chantix), 33t
Vascular and platelet activity (primary hemostasis), 267, 268f
Vascular endothelial growth factor (VEGF), 38–39
Vascular system, infection route in, 299, 299f
Vasoconstrictors, 44t–45t
hypertension and reduction of, 16
MI and reduction of, 17
VEGF (vascular endothelial growth factor), 38–39
Venipuncture
difficulty with, 218–219
protocol for ideal, 219
technique for, 220f
troubleshooting for, 221f
Venlafaxine, 384
Venous hemorrhage, 268b
Verbal consent, 859
Verdict, trial, 851
Vertical mattress suture technique, 421–425, 429f
Vertical movement, splinted implant-tooth prosthesis and, 129, 130f
Vertical occlusal loads, 713–714
implants and, 713–714, 714f
natural teeth and, 713, 714f
Vertical overbite, IPO with shallow anterior guidance and, 738, 738f–739f
Vertical release incision, for blood supply to flap, 410, 410f
Vertigo. See Benign paroxysmal positional vertigo
Vibramycin (doxycycline), 551
Vicks Nasal Spray (oxymetazoline), 550
Video consent, 859
Visco-Gel, 387
Vistaril (hydroxyzine), 44t–45t
Vitamin A, 436
Vitamin B, 436
Vitamin C, 435–436
Vitamin E, 436
Voids, in maxillary sinus grafting, 525–528, 528f
Voluntary nonsuit, 845
von Willebrand factor (vWF), 267
Voxel size, CBCT and, 150, 151f
vWF. See von Willebrand factor
W
Waiver of liability, CBCT and, 862
Wallerian degeneration, 339, 339f
Warfarin sodium (Coumadin), 17–18, 41t, 269t–270t
as anticoagulant option, 40
White blood cells (WBCs), 26–27. See also Leukocytic disorders
lab test for, 46t–49t
types of, 46t–49t
Witness order, 850
Wolff's Law, 112
Wolinella recta, 194
Working occlusal interferences, 723, 723f
Wound dehiscence. See Incision line opening
Wound healing. See also Incision line opening
alcohol use and, 408
bacteria and, 407–408
classification and types of, 403–406
primary intention, 405
secondary intention, 405, 407f
tertiary intention, 406
obesity and, 408–409
periodontal biotype and, 409
phases of, 403–405
inflammatory, 403–404
maturation, 405, 406f
proliferation, 404–405
postoperative complications and, 409
saliva and, 406–407
smoking and, 408
systemic diseases and, 408
Writ of Summons, 833
Written consent, 859
X
Xarelto (rivaroxaban), 41t, 42, 269t
“X”-axis positioning. See Mesial-distal (“x”-axis) positioning: implant-
implant; Mesial-distal (“x”-axis) positioning: implant-natural tooth
Xenografts, 448, 449f
Xerostomia (dry mouth), 23–24
RA and, 32
treatment regimens for, 23b
Xgeva (denosumab), 306–307
Y
“Y”-axis positioning. See Buccolingual positioning
Z
“Z”-axis positioning. See Apicocoronal positioning
Zinc, 436
Zithromax (azithromycin), 315–316, 316t, 550–551
Zoledronate (Reclast), 39
Zoledronic acid (Zometa), 39, 306–307
“Zone of safety,” nerve impairment prevention and, 352–353, 353f
Zyban (bupropion SR), 33t
Zygomatic implants, implant number and, 91, 92f

Mischs Avoiding Complications in Oral Implan 2018

Uploaded by

Copyright:

Available Formats

Mischs Avoiding Complications in Oral Implan 2018

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Mischs Avoiding Complications in Oral Implan 2018

Uploaded by

Copyright:

Available Formats

Misch's Avoiding Complications in

RANDOLPH R. RESNIK, DMD, MDS

CARL E. MISCH, DDS, MDS, PhD (HC)

1 Classification of Dental Implant Complications

2 Medical/Medication Complications in Oral Implantology

3 Treatment Planning Complications

Divisions of Available Bone

Key Implant Position

Crown Height Space (CHS)

Splinting Implants to Teeth

Patient Treatment Planning

4 Radiographic Complications and Evaluation

Cone Beam Tomography

CBCT Anatomic Radiographic

Normal Radiographic Anatomy

Miscellaneous CBCT Complications

5 Dental Implant Intraoperative Complications

Stage II Uncovery Surgery Complications

Anesthesia/Platelet-Rich Fibrin Complications

6 Ideal Implant Positioning

Mesial-Distal (“X” Axis): Implant–Implant

Implant Angulation Positioning (“Y” and “Z” Axis)

Distance From Vital Structures

Malpositioning Complication Summary

Techniques to Decrease and Control Bleeding

Postoperative Bleeding Control

Significant Complications of Infections

Antibiotics Used in Implant Dentistry (Table 8.4)

Prevention and Treatment of Infection

Therapeutic Antibiotics in Implant Dentistry

9 Neurosensory Deficit Complications in Implant Dentistry

Displacement or Migration Complications

Factors That Affect Wound Healing/Incision Line Opening

Prevention of Incision Line Opening

Management of Incision Line Opening

Procedural Technique Complications

Block Grafts: Symphysis Bone Grafts

Block Grafts: Ramus Bone Grafts

13 Posterior Maxilla Complications

Treatment Plan Complications

14 Complications Associated With Immediate Implant Placement

Complications Following First Stage

15 Removable Implant Complications

Mandibuar Overdenture Complications

Maxillary Overdenture Complications

Miscellaneous Removable Complications

16 Fixed Prosthodontics Complications

Intraoperative Prosthodontic Complications

Fixed Occlusal Complications

18 Periodontal and Maintenance Complications

19 Medicolegal Aspects of Implant Dentistry

Litigation Process Part 2

3251 Riverport Lane

AVOIDING COMPLICATIONS IN ORAL IMPLANTOLOGY ISBN: 978-0-

No part of this publication may be reproduced or transmitted in any form or

This book and the individual contributions contained in it are protected

International Standard Book Number: 978-0-323-37580-1

Senior Content Strategist: Jennifer Flynn-Briggs

Last digit is the print number: 9 8 7 6 5 4 3 2 1

Gregory Caldwell DDS, MS