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Essentials of Dentistry

Quick Review and Examination Preparation


Essentials of Dentistry
Quick Review and Examination Preparation

Rushik Dhaduk BDS


Tutor, Dharmsinh Desai University
Nadiad, Gujarat, India

Forewords
Mahesh Verma
Bimal S Jathal
NJ Nirmal
Amish Mehta
Rahul K Thakkur

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD


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contact the manufacturer of the drug or device.

Publisher: Jitendar P Vij


Publishing Director: Tarun Duneja
Editor: Richa Saxena
Cover Design: Seema Dogra

Essentials of Dentistry—Quick Review and Examination Preparation


First Edition: 2012

ISBN 978-93-5025-368-7

Printed in India
Affectionally dedicated to
my parents and my dearest bhai and bhabhi

"When emotions are profound, words sometimes are not sufficient to


express our thanks and gratitude"

With these few words, I am trying to express my feelings towards


my family members for their dedication for my happiness. No words can ever express
what their constant undemanding love, sacrifice and prayers have done to help me
achieve whatever I am today.

My father's dedication to his work has stirred my mind all the time to work restlessly.
His few enforcing words during my childhood have always enforced me during
muddling time in my life. He has always stood next to me with elucidation to all
problems.

My mother's soothing voice and caring nature has always been booster in my life.
She has put piles of efforts and dedications to mould me. I lay this book at her feet.

My brother Mr Bhavikkumar Dhaduk’s words are hard to find, when it comes to


highlight his role, in my life. I express my thanks to him for his physical presence and
sentimental support at very critical times often encountered in my life. I thank him for
always standing by aside. He is a friend and a guide, who stood by me as a pillar of
strength, shielding and taking care of all my weaknesses. This book bears an
indelible imprint of his meticulous work.

And at last but not the least comes my dearest bhabhi. My day doesn't start without
pulling her hair. She is more like a friend to me and takes special care of me. Her
gleaming smile relaxes mind after taxing day activity.
Foreword

I am very delighted to write the foreword for the book titled Essentials of Dentistry—Quick
Review and Examination Preparation by Dr Rushik Dhaduk.
The book covers varied important topics pertaining to different specialties especially
Oral Radiology, Conservative Dentistry, Periodontics, Oral Pathology, Pediatric Dentistry
and Oral Surgery. The book is targeted at young graduates and students preparing for
examinations and clinical practice. The book carries basic and clinical sciences topics
with illustrations, tables and charts in order to make it userfriendly and attractive. Extensive
coverage of important subject matter has been done so as to reduce the task of searching
and referring multiple books by the reader. The material has been presented in a very
precise and lucid manner so that it could be easily memorized and recollected during
the examinations. The undergraduate students would surely find the contents very easy
to assimilate and reproduce. The point-wise articulation and self-explanatory diagrams
would surely help students cracking the examinations easily.
I congratulate Dr Rushik Dhaduk who is one of the youngest authors for this novel
and creative endeavor. I wish him a great future and many editions of the publication.

Prof Mahesh Verma


Director–Principal
Maulana Azad Institute of Dental Sciences
New Delhi–110002, India
Vice President, Dental Council of India
Foreword

I am very delighted to write foreword for the book titled Essentials


of Dentistry—Quick Review and Examination Preparation by Dr
Rushik Dhaduk. The book is most comprehensive text of its kind.
Carefully designed diagrams are easy to follow. The book is
targeted to undergraduate dental students and it comprises of
some of the essential topics from different dental subjects. I
wholeheartedly admire Dr Rushik Dhaduk for his hard work and
creativity. Today, as he paints his masterpiece in this book, he puts
his years of hard work, learning and dedication into it. I wish him
a great future ahead.

Dr Bimal S Jathal MDS (Periodontics)


Dean, Faculty of Dental Sciences
Dharmsinh Desai University
Nadiad, Gujarat, India
Foreword

It gives me immense pleasure to know that one of my students


Dr Rushik Dhaduk has written a book titled as Essentials of
Dentistry—Quick Review and Examination Preparation for
undergraduate dental students. This book can be helpful to them
for examination purpose. Various topics are selected and detailed
by him after referring various journals and articles. I wish him all
the best for his future.

Dr NJ Nirmal MDS (Prosthodontics)


Dean, Manubhai Patel Dental College
Baroda, Gujarat, India
Foreword

Rushik, as I have always known him, came across my attention


not only as a student but also as an innovator and orator in
extracurricular activities. While in our department, he was a master
juggler of wire bending. His constant perseverance towards
academic excellence has always impressed me. Spending even
a few minutes with him one cannot avoid being motivated even
as a teacher. That he has put on paper his knowledge, to share
with peers, and juniors is a very commendable task. While proofing
the book, I realized the simplicity in the approach to thoroughly
prepare students for the examination. There is no ambiguity that this compilation will enable
the students to take up the challenges of a drilling examination with confidence. Dear
students, Godspeed.

Dr Amish Mehta MDS (Orthodontics)


Professor and Head
Department of Orthodontics and Dentofacial Orthopedics
Faculty of Dental Sciences, Dharmsinh University
Nadiad, Gujarat, India
Foreword

This new book by Rushik Dhaduk is a well-organized, well-written


and up-to-date treatise. This book is unique as it has a specific
intention of helping the hugely burdened final year dental students
to finish the last lap with ease. The lucid language and illustrations
certify this fact and the page on “Instructions to the reader” would
be useful to students. This huge volume was created by Rushik’s
untiring efforts. The ultimate beneficiaries of the ideas expressed
in the book, of course, are the exam-going students. I have had
the pleasure of knowing Rushik, right from his undergraduate days
and now as a consultant in implantology. His approach to the art
and science of dentistry is very unique and I am sure that it will
rub upon the readers as they go across this book.

Dr Rahul K Thakkur MDS (OMFS)


Facial Plastic (KEM), Head Neck Surgery (TMH)
Professor, Oral and Maxillofacial Surgery
Manubhai Patel Dental College and Hospital, Baroda
Director, Shubhechha Hospital, Baroda, Gujarat, India
Preface

Essentials of Dentistry—Quick Review and Examination Preparation is a unique blend of


essences from numerous publications and from various standard sources. In a novel
approach, special emphasis has been laid down to arrange reading material in a precise
manner that can easily be memorized and recollected during the stressful exam hours.
Illustrations have been enriched and arranged in the best possible manner. The layout
is made more userfriendly and attractive.
My personal experience during exam preparation and studies helped me a lot to develop
the book in a very friendly manner. I was preparing for this book since my college days
and it carries my efforts in a very simple language with useful contents. It took years to
shape this book in the best possible manner. The book is my little effort to lend a hand
to the undergraduate students and it could be a real comrade to the students for exam
preparation.
When I look at this publication, I see many hearts and hands to mould this into shape.
I hope that the book will help the students to cope up the tight exam schedule by quick
review of important topics. Basic topics and frequently asked questions are prepared in
a more simplified and comprehensive manner. Various mnemonics will be much useful
to memorize and reproduce the details. I am sure that the book will find its own place
among undergraduate dental student community.
As no one is perfect in absolute sense, I also humbly accept my shortcomings while
writing this book and therefore I sincerely welcome the valuable suggestions from my
senior colleagues, students and other readers. As you walk through the pages of this
book, you might come across certain errors and mistakes or in the treatment of a subject
as a whole. Your suggestions are always welcomed at [email protected] for improving
the next edition.

Rushik Dhaduk
Acknowledgments

First of all, I would like to convey my sincere thanks to all my teachers, my college; Manubhai
Patel Dental College and Oral Research Centre, Baroda, Gujarat, India and the Chairman
of the college Dr Rajendrasinh Rathore; Dean of the College Dr NJ Nirmal, and the Ex
Dean Dr Ramesh Suchde, for taking me to this stand. It is a well-known fact that God
comes to us in various forms, as parents and as teachers. Some teachers treat us as
if we were their own children and they do take personal care of us. I would always remain
grateful and obliged to my teachers for their sincere efforts and keen interest since budding
stage of my undergraduate studies. It is my honor to thank every teacher of this institute.
The word TEACHER refers not only to the person who teaches you in the school or
college but also to the person who teaches you in one or another way at any point of
life. In this context, I would like to express my sincere thanks to Dr Bimal S Jathal for
giving me the opportunity to be a part of the teaching faculty of well reputed institution
and to all the members of the Faculty of Dental Sciences, Dharmsinh Desai University,
Nadiad, Gujarat, India for corroborating me and improving my knowledge and skill.
I strongly believe in saying, "Tell me your friends and I will tell you your future". My
special thanks to all my dearest friends Dr Vipul Munia, Dr Megha Patel, Dr Brijesh Patel,
Dr Khushal Dodiya, Dr Dilesh Bagadiya, Dr Jignesh Patel, Dr Dhaval Patel, Dr Bhargav
Patel and Dr Deval Patel, without their wholehearted support and encouragement this would
not have been possible. The erudition of my friends and colleagues has been a constant
source of inspiration to me. They worked with me night and day throughout the making
of this book.
Dr Brijesh Patel (Ahmedabad), a leading Dental Implant Surgeon and guide to my
practice deserves special thanks for his continuous support and encouragement extended
as ever during the course of this work, which has converted this “idea” of my mind into
a “book”.
My regards to Mr Tarun Duneja (Director-Publishing), Mrs Samina Khan (PA to Director),
Mr KK Raman (Production Manager), Mr Akhilesh Kumar Dubey, Hemant Kumar and
production staff of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, for their
support, devotion and keen interest in shaping the book.
I am also much obliged to Mr Abhijit Bose, Branch Manager and other staff, Jaypee
Brothers Medical Publishers (P) Ltd, Ahmedabad, Gujarat, India for their support in making
this book published to you.
Contents

1. Rubber Dam Isolation ............................................................................................ 1


Introduction 1; Goals of Isolation 1; Advantages 2; Disadvantages 2; Materials 3;
Sizes 3; Thickness 3; Color 3; Uses 3; Holder 3; Retainer/Clamp 5; Punch 7;
Retainer Forcep 7; Napkin 7; Lubricant 9; Sealants 9; Rubber Dam Template 10;
Placement of Rubber Dam 10; Removal of Rubber Dam 11; Contraindications 11
2. Retention Form of Amalgam Preparation ........................................................... 12
Tooth Preparation 12; Stages and Steps for Tooth Preparation 12
3. Wedges ................................................................................................................ 15
Purpose 15; Requirement 15; Parts of Wedges 15; Types 15; Sizes 16; Shapes
16; Function 16; Methods of Insertion 17
4. Gates Gliddens and Peeso Reamers .................................................................. 20
Sizes of Gates Glidden Drill 20; Sizes of Peeso Reamer 21; Parts 22; Usefulness
in Preparing Root Canals 22; Straightening the Canal 23; Main Uses 25;
Flexogates 25
5. Dental Caries Classifications .............................................................................. 26
Based on Anatomic Site 26; Based on Severity 27; Based on Progress 27; Based
on Chronology 28; Based on Direction of Spread 28
6. Differences Between the Inlay and Amalgam Restorations .............................. 29
7. Electric Pulp Testing ............................................................................................ 33
Principle 33; Electrolyte 33; Types of Pulp Testers 33; Site 33; Procedure 34;
Precautions 35; Contraindications 36; Responses 36
8. Dental Adhesion .................................................................................................. 38
Adhesion 38; Adhesive Joint 38; Micromechanical Bonding 38; Bonding
Systems 38; Adhesive Considerations for Direct Composite Restorations 39;
Dental Adhesive Systems 40; Rationale of Adhesive Systems 43; Newer Adhesive
Developments 45; Key Points to Ensure Effective Bonding with Total Etch
System 46; Key Points to Ensure Effective Bonding with Self-etch System 47
9. Bleaching ............................................................................................................. 48
Introduction 48; Classification of Bleaching Agents 48; Hydrogen Peroxide 49;
Bleaching Techniques 51; Factors Affecting Bleaching 53; Disadvantages of
Bleaching 54; Advantages of Bleaching 55
10. Endodontic Hand Instruments and Instrumentation ......................................... 56
Classifications of Endodontic Instruments 56; Standardization 57; Materials Used
for Manufacturing Instruments 59; Manufacturing of Endodontic Instruments 59;
Features of Endodontic Instruments 60; Barbed Broach 61; Rasp 62; Reamers 62;
Files 64; K-file 64; K-flex File (D-type File) 66; Flexo File 66; Flex-R File 66;
H-file (Hedstrom File) 67; Uni File 69; S-file 69; Safety Hedstrom File 69
11. Hand Instruments in Conservative Dentistry and Some
Considerations for Viva Voce .............................................................................. 70
Basic Classification of Dental Instruments 70; Dental Instruments can be Grossly
Divided into Following Two Categories 71; Instrument Nomenclature 72;
xviii Essentials of Dentistry

Instrument Formula 72; Exploring Instruments 72; Instruments for Tooth Structure
Removal 74; Restorative Instruments 74; Hand Instruments 76; Considerations
for Operative Dentistry and Endodontia Viva Voce 81; Clinical Classification of
Traumatic Dental Injuries Including Codes of WHO International Classification 83
12. Gingiva in Health and Disease ............................................................................ 88
13. Dentogingival Junction ....................................................................................... 95
Definition 95; Components 95; Development 95; Mechanism of Attachment of
the Dentogingival Junction 96; Age and Inflammation Changes 97; Clinical
Implication 97
14. Cementum In Disease ......................................................................................... 98
Structural Changes 98; Chemical Changes 99; Physical Changes 100
15. Tooth Mobility .................................................................................................... 101
Introduction 101; Types 101; Causes 102; Factors Affecting Tooth Mobility 102;
Increased vs Increasing Mobility 103; Miller’s Classification (1950) 104;
Glickman’s Classification (1972) 104; Lindhe’s Classification 104; Stages of Tooth
Mobility 104; Measurement of Tooth Mobility 104; Generalized Treatment of
Mobility 106
16. Food Impaction .................................................................................................. 107
Definition 107; Types 107; Factors Affecting Food Impaction 107; Plunger Cusp 108;
Classification of Factors Causing Food Impaction 108; Signs and Symptoms 111;
Prevention and Treatment 111
17. Halitosis ............................................................................................................. 114
Definition 114; Clinical Features 114; Primary Factors Affecting Halitosis 115;
Microbiota in Halitosis 115; Mechanisms 115; Etiology 116; Diagnosis 119;
Prevention 121; Management of Oral Malodor 121
18. Periodontal Probe .............................................................................................. 123
Definition 123; Design 123; Functions 123; Classification of Probes 124
19. Probing ............................................................................................................... 129
Definition 129; Probing Technique 129; Interpretation 131; Limitations 132; Factors
Affecting Probing 132; Probing at Various Times 132
20. Scalers and Curettes ......................................................................................... 134
Differences of Gracey Curette and Universal Curette 137; Comparison of Scalers 138;
Areas of Instrumentation of Gracey Curettes 141
21. Gingival Curettage ............................................................................................. 143
Definition 143; Rationale 144; Indications 144; Contraindications 144; Limitations 144;
Procedures 145; Other Techniques 145; Healing after Curettage 146
22. Infrabony Pocket ................................................................................................ 147
Signs 147; Symptoms 147; Classifications of Pockets 148; Classifications of
Periodontal Pockets 148; Classifications of Infrabony Defects 148; Etiology of
Infrabony Pocket and Infrabony Defect 151; Incidence 151; Diagnosis of Infrabony
Defect 151; Treatment 152
23. Bone Replacement Grafts ................................................................................. 157
Extra and Intraoral Donor Sites for Autogenous Bone Grafts 157; Osseous
Coagulum 158; Bone Blend 158; Bone Swaging 158; Allogenic Bone Grafts 158;
Alloplastic Materials 160; Xenografts 160
Contents xix

24. Hypersensitivity ................................................................................................. 162


Definition 162; Basic Concepts of Tooth Sensitivity 162; Pain Mediators 162;
Neurophysiology 162; Other Theories of Dentin Hypersensitivity 163;
Prevalence 163; Highest Incident Site 164; Pathophysiology 164; Causes 165;
Clinical Implications 165; Diagnostic Methods 165; Conditions to Rule Out
Hypersensitivity 166; Ways to Rule Out 166; Occurrence of Pain 166; People at
Risk 166; Treatment Strategies 167; Management of Hypersensitivity 167
25. Definitions and Questionnaire for Periodontia Viva Voce ............................... 173
Gingiva 173; The Tooth-supporting Structure 178; Epidemiology of Periodontal
Disease and Gingival Disease 180; Periodontal Microbiology 180; Dental Calculus
181; Role of Iatrogenic and Other Local Factors 181; Dental Occlusion 181;
Influence of Systemic Diseases on Periodontium 184; Clinical Features of
Gingivitis 184; Gingival Enlargement 185; Acute Gingival Infections 185;
Desquamative Gingivitis and Oral Mucous Membrane Diseases 186; Periodontal
Pocket 186; Bone Loss and Pattern of Bone Loss 187; Periodontal Response to
External Forces 188; Prepubertal and Juvenile Periodontitis 188; Other 188; Rationale
for Periodontal Treatment 189; Principle of Periodontal Instrumentation 189; Plaque
Control 190; Questionnaire for Periodontia Viva Voce 191; Scaling and Root
Planing 208; History 209; Few Points about Intraoral Examination 209
26. Ameloblastoma .................................................................................................. 226
Tumors 226; Odontogenic Tumors 226; Classification 226; Ameloblastoma 227;
History 227; Definition 227; Etiology 227; Classification 228; Pathogenesis 228;
Incidence 228; Age 228; Sex 229; Site 229; Size 229; Race 229; Preceding
Factors 229; Onset 229; Clinical Features 229; Spread 230; Radiographic
Features 230; Diagnostic Aids 231; Histological Features 231; Management 233;
Specific Principles 233
27. Properties of X-rays ........................................................................................... 234
Radiation 234; X-radiation 234; Properties of X-rays 234
28. Considerations for Oral Medicine Viva Voce .................................................... 238
Types of Geographic Tongue 245; Syndromes with Characteristic Features 256
29. Orbital Blow Out Fracture ................................................................................. 265
Definition 265; Etiology 265; Types 265; Sites 265; Clinical Signs 267; Diagnosis 267;
Management 268
30. Considerations for Oral Surgery Viva Voce ...................................................... 273
Leukoplakia (WHO—1975) 273; Oral Submucous Fibrosis (OSMF) 273;
Sialosis 273; Sialadenitis and Sialodochitis 273; Sialadenosis 273;
Xerostomia 273; Sialolithiasis 273; Sialectasis 273; Sialorrhea/Ptylism 273;
Trigeminal Neuralgia 274; Pain 274; Local Anesthesia 274; Ludwig’s Angina 274;
Bell’s Palsy 274; Osteomyelitis 274; Cyst 274; Marsupialization 274;
Neuralgia 275; Tumors/Neoplasm 275; Some Considerations for Viva Voce 275;
Some Commonly Used Compositions 278; Classifications 278; Tooth
Impaction 284
31. Morphological Differences between Primary and Permanent Teeth ............... 286
32. Definitions in Pedodontia .................................................................................. 293
Pedodontics 293; Psychology 293; Child Psychology 293; Child Management 293;
Emotion 293; Behavior 293; Fear 293; Anxiety 293; Phobia 294; Behavioral
Science 294; Behavior Management 294; Behavior Shaping 294; Behavior
xx Essentials of Dentistry

Modification 294; Nursing Caries 294; Rampant Caries 294; Plunger Cusp 294; Pit
and Fissure Sealants 294; Indirect Pulp Capping 294; Direct Pulp Capping 295;
Pulpotomy 295; Pulpectomy 295; Apexogenesis 295; Apexification 295; Preventive
Orthodontics 295; Interceptive Orthodontics 295; Space Control 295; Space
Maintenance 295; Space Maintainer 295; Habit 296; Thumb Sucking 296; Tongue
Thrusting 296; Mouth Breathing 296; Bruxism 296; Self-injurious Habit 296;
Handicapped Person 296; Mental Retardation 296; Cerebral Palsy 296

Index ........................................................................................................................ 299


CHAPTER

1 Rubber Dam Isolation

INTRODUCTION
The rubber dam is the most effective way for controlling the field of operation. The goals
achieved by rubber dam application in isolating the field of operation are a combination
of most of the goals achieved by all other isolation methods. Rubber dam ensures
appropriate dryness of teeth and improves the quality of restorative material (Fig. 1.1).

Fig. 1.1: Armamentarium

GOALS OF ISOLATION

Moisture Control
• Rubber dam excludes the sulcular fluid, saliva and gingival bleeding from the operating
field.
• It prevents the swallowing of handpiece spray and restorative debris.
• It helps in maintaining the operative field dry, and prevents the mirror fogging due to
breathing.
• Rubber dam produces a water tight seal that allows the safe use of sodium hypochlorite,
other disinfectants and irrigants.

Retraction and Access


• Soft tissues retraction by rubber dam protects them from injuries during treatment.
The inquisitive tongue is kept out of the operating field.
Essentials of Dentistry 2 Rubber Dam Isolation

Fig. 1.2: Retraction and access

• It provides maximum exposure of operating site by maintaining open mouth with


retraction of gingival tissue, tongue, lips, and cheeks (Fig. 1.2).
• It allows unimpeded vision of the tooth during treatment.

Harm Prevention
• It prevents aspiration of small instruments and restorative debris and also the soft tissue
injuries.
• It prevents the aspiration of the aerosol of microbes and saliva produced by turbine
handpiece. In addition, the patient does not have a mouth full of water.

Local Anesthesia
• It eliminates discomfort of patient during treatment and controls moisture.
• It reduces salivation, blood flow and gives more comfort to patient.
• Treatment is quicker and more pleasant for both the patient and the clinician.

ADVANTAGES
• Dry, clean operative field.
• Improves access and visibility.
• Potentially improved properties of dental materials.
• Protection of patient and operator.
• Operating efficiency.

DISADVANTAGES
• It is time consuming procedure (for tyro clinicians).
• Some patients may have objection for the rubber dam application.
• Certain oral conditions precluding the use of rubber dam are;
1. Teeth that aren’t sufficiently erupted
2. Some third molars
3. Extremely malpositioned teeth
4. Patient suffering from asthma.
Rubber Dam Isolation 3

MATERIALS
Rubber dam material is usually latex rubber. For patients who have an allergy to latex,
a silicone (nonlatex) rubber dam is available. They are available in variety of thicknesses,
colors, sizes and materials (Figs 1.3A to C).

Essentials of Dentistry
Sizes

5 × 5 inch For children


6 × 6 inch For adult

Thickness
The medium thickness is commonly used for general purpose. It nicely adapts to the cervical
area of the tooth, providing fluid tight seal without use of floss or ligature ties. It doesn’t
tear easily and provides improved visibility. However, thin materials are recommended for
isolation of mandibular anterior teeth and partially erupted teeth. As being less bulky, they
exert less dislodging forces on the clamp.

Thin 0.006 inch/0.15 mm


Medium 0.008 inch/0.20 mm
Heavy 0.010 inch/0.25 mm
Extra heavy 0.012 inch/0.30 mm
Special heavy 0.014 inch/0.35 mm

Color
• Dark brown
• Green
• Black
• Blue.
They are available in dark and light shades with different flavors and aromas. Dark-colored
material provides a contrasting color as a background. It has shiny and dull side. Dull
side is less light reflective so it is placed facing the occlusal side.

Uses
Thicker dam is more effective in retracting tissue and more resistant to tearing so it is
recommended for class V lesions.
Thinner dam easily passes through the contacts so it is helpful in tight interdental
contacts.

Holder
Variety of holders is available to support the dam. They keep the peripheries of the dam
out of the mouth. They are of mainly two types:
1. Strap type: It is anchored on back of the patient’s head and attached to the corners
and sides of the dam. The dam is stretched and pulled toward the occipital parts of
the head, e.g. Woodburry holder, Wizard holder.
2. Hanging frame holder: There is variety of dental dam frames to meet the requirement
of clinician. Young’s frame is a “U” shaped, elliptical or rectangular metal/plastic frames
with multiple prongs at periphery securing the borders of the rubber dam (Fig. 1.4).
Essentials of Dentistry 4 Rubber Dam Isolation

C
Figs 1.3A to C: Rubber dam sheets

Frames were originally constructed from metal and were radiopaque, so that they
needed to be removed to avoid obscuring important details on radiographs. However,
they are most popular because of ease of application and minimal contact of dam
Rubber Dam Isolation 5

Essentials of Dentistry
Fig. 1.4: Hanging frame holder

Fig. 1.5: Plastic rubber dam holder

with skin. Other is Nygaard-Østby dental dam frame which is shield-shaped to fit the
face. It is made up of radiolucent nylon material (Fig. 1.5).
Various articulated hinged frames and frames made up of soft metal are also available.

Retainer/Clamp
• The retainer secures the dam to the tooth and helps in soft tissue retraction.
• The rubber dam retainer/clamp has four prongs and two jaws connected by a bow.
Most rubber dam clamps are now manufactured from stainless steel as this resists
corrosion much better than plated steel (Figs 1.6A to C).
• Specific retainers are designed for certain teeth. However, teeth that are rotated, partially
erupted, fractured, unusual crown form or with severe carious involvement require special
clamps (Fig. 1.7).
• Properly selected retainer should contact the tooth in four areas. Thus, it prevents rocking/
tilting of retainer.
• It shouldn’t extend beyond the mesial and distal line angles of the tooth because:
– It may interfere with matrix and wedge placement.
– Gingival trauma may occur.
– Complete seal around the anchored tooth becomes difficult.
6 Rubber Dam Isolation

• Some retainers have processes which are gingivally directed. They help to anchor the
partially erupted tooth and provide additional soft tissue retraction.
• Retainers are available in two forms; wingless and winged.
• The advantage of a winged clamp on a molar tooth is that both clamp and dam can
be placed on the tooth simultaneously. Wings allow a more rapid, efficient means of
Essentials of Dentistry

applying dam. In addition, it gives broader buccolingual deflection of the dam. When
a wingless clamp is used on a molar tooth, it is normal to place the clamp first, and
place the dam over it.
• Most of the anterior teeth can be isolated with a small winged clamp but if stability
is a problem, a wingless clamp is almost always successful.
• Winged retainer has 2 wings—Anterior and lateral. They provide extra retention and
allow the attachment of the dam to the retainer before its placement. Wing may interfere
with the placement of the matrix band, band retainers and wedges. Sometimes, anterior
wing can be cut away, if not required. However, generally in such condition wingless
retainers are preferred (Figs 1.6A to C).
• Bow is tied with dental floss of approximately 12 inches in length before the retainer
is placed in the mouth.
For maximum protection floss is tied with both holes. Floss allows retrieval of the
retainer/its broken parts, if it is accidentally swallowed or aspirated.
• Jaw is sometimes re-contoured according to the shape of the tooth by grinding with
mounted stone.
• In case of treatment of anterior teeth except class-V restoration, a retainer is usually
not required.

B C
Figs 1.6A to C: Rubber dam clamp
Rubber Dam Isolation 7

Essentials of Dentistry
Fig. 1.7: Rubber dam clamps

• Wedges or strips of rubber dam can be used to retain the dam instead of a clamp
in the front of the mouth. This is especially useful in the anterior region, when it is
necessary to use a split-dam technique.

Punch
This instrument is used to cut the holes in the rubber. It has a rotating disc/table with
six holes of varying sizes and a tapered, sharp pointed plunger. Edges of the holes are
angular to provide a sharp clean hole (Figs 1.8A and B).
Holes Teeth
Larger Molars
Medium Premolars
Upper canines
Sometimes for upper incisors
Small Lower incisors

Plunger should be centered in the cutting holes so that edges of the hole don’t get
chipped by the plunger tip otherwise cutting quality of the punch will be ruined. This results
in poor seal at the time of placement and may make the dam susceptible to tearing.

Retainer Forcep
• It is a modified forcep which retracts the jaws of a clamp away from each other allowing
the clamp to overcome the occlusal diameter of the tooth. Two commonly used designs
are Ash- or Ivory-style clamp forceps (Figs 1.9A to C).
• Each clamp has holes/grooves in each of its jaw to accommodate this forceps.
• It helps in placement and removal of clamp from the tooth.

Napkin
The rubber dam napkin is placed between rubber dam and patient’s skin. They are absorbent
papers or cloth towels (disposable) (Fig. 1.10).
Essentials of Dentistry 8 Rubber Dam Isolation

A B
Figs 1.8A and B: Ainsworth rubber dam punch

B C
Figs 1.9A to C: Rubber dam forceps

Fig. 1.10: Napkin


Rubber Dam Isolation 9

Advantages
• It prevents skin contact with rubber to reduce the possibility of allergic reactions in
sensitive patients.
• It absorbs any saliva seeping at the corners of the mouth.

Essentials of Dentistry
• It acts as a cushion.
• It provides a convenient method of wiping the patient’s lip on removal of the dam.
• It adds to the comfort of the patient.

Lubricant
It is a water-soluble solution which is applied in the area of punched holes to facilitate
the passing of the dam septa through the proximal contact, e.g. Commercially available
solutions:
• Soap slurry
• Shaving cream
• Silicone lubricant
• Cocoa butter/petroleum jelly is applied at the corner of patient’s mouth to prevent irritation.
Dental tape can be used to take rubber dam through a contact point and can then
act as a retainer.

Sealants
Modeling Compound
Low fusing modeling compound is used to secure the retainer to the tooth to prevent
its movement during operative procedure. Compound must not cover the holes in the
retainer to have ready access to the retainer for rapid removal with forceps.
Anchors other than retainer are:
• Waxed dental tape (floss) (Figs 1.11A and B)
• Small piece of rubber dam.

A B
Figs 1.11A and B: Waxed dental floss
10 Rubber Dam Isolation

Others
Various caulking agents have been marketed to help seal around rubber dam. For example,
OraSeal caulking (Ultradent, South Jordan, UT, USA), rubber base adhesive, cavit and
periodontal pack. For larger deficiencies or in the absence of a commercial caulking agent
Essentials of Dentistry

Cavit (ESPE, Seefeld, Oberlay, Germany) or Kalzinol (Dentsply) are useful. On occasions,
some elastomeric impression material can be used.

RUBBER DAM TEMPLATE


Rubber dam template is a square sheet with four quadrants. It is of two different sizes-
5 × 5 inch, 6 × 6 inch (Figs 1.12 and 1.13).

Placement of Rubber Dam


General rule for limited isolation is to include one tooth posterior and two teeth anterior
to the tooth being operated.
Steps for placement of rubber dam are:
1. Testing and lubricating the proximal contacts.
2. Punching the holes.
3. Lubricating the dam.
4. Selecting the retainer.
5. Testing the retainers.
6. Positioning the dam over the retainer.
7. Applying the napkin.
8. Positioning the napkin.
9. Attaching the frame.
10. Attaching the neck strap.
11. Passing the dam through posterior contact.
12. Applying compound.
13. Applying the anterior anchor.
14. Passing the septa through the contacts.
15. Confirming a properly applied rubber dam.
16. Checking access and visibility.
17. Inserting the wedges.

Fig. 1.12: Universal rubber dam template Fig. 1.13: FDI rubber dam template
Rubber Dam Isolation 11

Removal of Rubber Dam


• Cutting the septa.
• Removing the retainer.
• Removing the dam.

Essentials of Dentistry
• Wiping the lips.
• Rinsing the mouth and massaging the tissue.

Contraindications
• A child with upper respiratory infections and nasal obstruction.
• Presence of some fixed orthodontic appliances.
• Recently erupted tooth.
• Patient with allergy to latex.
CHAPTER

2 Retention Form of
Amalgam Preparation

TOOTH PREPARATION
“Tooth preparation is defined as the mechanical alteration of a defective, injured or diseased
tooth to best receive a restorative materials that will reestablish a healthy state for tooth,
including esthetic correction where indicate along with normal form and function.”

STAGES AND STEPS FOR TOOTH PREPARATION

Initial Tooth Preparation Stage


1. Outline form and initial depth
2. Primary resistance form
3. Primary retention form
4. Convenience form.

Final Tooth Preparation Stage


1. Removal of any remaining infected dentin and/or old restorative material, if indicated.
2. Pulp protection, if indicated.
3. Secondary resistance form and retention form.
4. Procedure for finishing external walls.
5. Final procedures:
– Cleaning
– Inspection
– Sealing.

Retention Form for Amalgam

Primary Retention Form


Design of the cavity preparation must provide retention of the restorative material especially
in case of nonbonded restorations. Features of the retention form also enhance the
resistance form.

Definition
“Primary retention form is that shape/form of the conventional preparation that resist
displacement or removal of the restoration from tipping/lifting forces.”
Retention Form of Amalgam Preparation 13

Principles
For class-I and class-II preparations:
1. External wall should be converging occlusally.
• Facial and lingual walls of occlusal portion as well as that of proximal portion should

Essentials of Dentistry
converse occlusally.
• In addition to retention, proximal convergence conserves the marginal ridge and
reduces forces of mastication on the restoration.
2. Adhesive systems provide some retention by micromechanically bonding amalgam
to tooth structure. It also reduces microleakage.

Additional Features for Class-II Preparation


CL-II tooth restoration may displace four ways.
1. Proximal displacement of entire restoration
When force is applied obliquely to the tooth, it has two components.
i. Horizontal component (H)
ii. Vertical component (V)
Vertical component will seat restoration into the tooth but horizontal component will
tend to rotate the restoration proximally at gingival cavosurface margin. This is prevented
by facial and lingual retention grooves and occlusal dovetail (Figs 2.1A and B).
2. Proximal displacement of proximal portion
If restoration is considered as being L-shaped, long arm will remain occlusally and
short arm remains proximally.
When the long arm is loaded by vertical force (v), it will seat the restoration more into
the pulpal floor will change the location as indicated by dotted line in Figure 2.2. The
short arm of L will move proximally which is prevented by facial, lingual and/or gingival
grooves.
3. Lateral rotation around hemispherical floor
Lateral rotation is prevented by definite line angles, point angles and ledges.
4. Occlusal displacement
It is prevented by directing occlusal force in such a way that it will seat the restoration
(Fig. 2.3).
These four displacements are repeated thousands of times per day and to counteract
these movements all parts of the cavity preparation should be self-retaining.

A B

Figs 2.1A and B: (A) Components of forces, (B) Retention grooves and occlusal dovetail
Essentials of Dentistry 14 Retention Form of Amalgam Preparation

Fig. 2.2: Proximal displacement

Fig. 2.3: Occlusal displacement

Secondary Retention Form


Secondary retention form is of two types:
1. Mechanical features.
2. Placement of etchant, primer or adhesive on prepared walls.
Mechanical features
Retention locks, grooves and coves
• Various type of retention grooves and retention locks provide retention for proximal
portion of preparation.
• Horizontal retention grooves are useful in class III and IV preparation.
• Retention coves are appropriately placed undercuts for the incisal retention of class
III amalgams.
Groove extensions
• Extension of the preparation onto facial/lingual fissures provides additional retention.
• Skirts, beveled enamel margins.
• Pins, slots, steps.
When there is great need of increased retention form, pins and slots are incorporated
into the preparation.
Placement of etchant, primer or adhesive on prepared walls
In addition to mechanical features, certain alterations in the preparation walls increase retention.
Enamel wall etching
Enamel walls are etched for bonded restorations. Etching of enamel by appropriate acid
increases the total surface area and improves the bonding of material to the tooth structure.
Dentin treatment
Dentinal surfaces may require etching and priming when using bonded amalgam restorations.
Sometimes, a glass ionomer is used as a base before the restoration of tooth with amalgam.
CHAPTER

3 Wedges

Wedges are third component of matrix system. The invention of dental wedges (Fig. 3.1)
was carried out primarily for achieving anatomical contours of restorations in hollow spaces
between neighboring teeth associated with caries. They can be triangular or trapezoidal
in cross-section.

PURPOSE
Purpose of wedge is to support the filling material during entering the hollow space and
also during subsequent hardening of material in such a way that the filling material can
adapt exactly to the healthy part of the tooth without undesirable overhang.

REQUIREMENT
• For the matrix band to fulfill its function, the matrix band has to be approached as
far possible to the shape of the tooth and has to be fixed in the position such that
the filling material corresponds to the outer face of the healthy tooth and does not
protrude into the embrasures. Over extension of filling material favors the formation
of new carious lesions and periodontal pathologies.
• The dental wedge has to be absolutely immovable in its position between two teeth
during treatment and therefore it has to be pressed with a force, usually generated
with the aid of a special instrument, until the dental wedge is maintained in position
between the teeth based on friction.

PARTS OF WEDGES
It is comprised of two major parts:
1. A rigid body configured to be inserted within an interproximal space between two adjacent
teeth, which tapers from a proximal end to a distal end.
2. Flexible members protruding away from the rigid body.

TYPES
Wedges are made up of different materials.
Wood or plastic
Advantages of wooden wedges are:
• They are easy to trim with a scalpel and they adapt well to the tooth surface.
• Wooden wedges are more stable compared to plastic wedges.
• On contact with saliva, they swell and firmly wedge between the teeth.
Advantage of plastic wedge is:
• Transparent plastic wedge transmit the light and useful for composite fillings.
Essentials of Dentistry 16 Wedges

Fig. 3.1: Dental wedge

SIZES
The dental wedges are offered also in different sizes such that the selection can be made
corresponding to the respective anatomy.

SHAPES
Wedges can be triangular or trapezoidal in cross section. The side view of the dental wedge
is comparable to a long extended, pointed converging triangle where the cross-section of
the dental wedge resembles a turned over V, which is downwardly open. The open side
of V (dental wedge) comes in contact with the interdental papilla and other side walls with
greater elasticity aids in easy insertion, firm support and good adaptation to the tooth surfaces.
Dental wedges may exhibit a dice-(cube) shaped prolongation at their broad end, inclined
remote from the tip. The base of the wedge should be slightly larger than the space between
the adjacent teeth in order to separate them apart for easy insertion of matrix.
The two lower longitudinal edges are obtusely angled off for the better adaptation to
the anatomy of interdental surfaces of tooth and also to prevent the injury to the interdental
papilla.
Some additional features:
• The edge is bent upward like a saber which takes care of gingival papilla at the exit
point of the dental wedge. It prevents the wedge from piercing the papilla or rubber
dam during placement.
• The base face and the side faces of the edge are arched concavely inwardly. This
curved underside leaves room for the papilla, causing less compression.
• The impact edges of the base face and of the side faces of the dental wedge are rounded.
This soft radius of the edge prevents trauma to the papilla during insertion and removal
of wedge.
The dental wedge with these characteristic features is ideal for proper adaptation to the
proximal surfaces of teeth and helps is restoring tooth with anatomically best adapted shape.

FUNCTION
When dental wedge is pressed between the neighboring teeth and the gums, it pushes
the matrix band against the tooth to be treated and simultaneously presses the teeth
somewhat apart. It creates the cervical constriction to prevent the overhang of restoration.
After hardening of restorative material, when the matrix band is removed, the teeth can
support each other mutually by returning into their starting position and the space previously
claimed by the matrix band does not remain as a gap or as a slot opening.
Wedges 17

METHODS OF INSERTION (FIGS 3.2 TO 3.4)


• Correct wedge selection will supply proper seal and separation while helping to prevent
the wedge from loosening or backing-out during the procedure. Select the largest wedge
that will fit the interproximal space. The flexible, compressible material will allow a larger

Essentials of Dentistry
wedge to adapt the tooth surface during placement. It is not necessary to bend the
wedge for placements at anterior teeth.
• Continue to hold the wedge and simultaneously place your index finger or the back,
flat end of metallic instrument close to the wedge head.
• Use your index finger to apply force to the wedge head, inserting it into the interproximal
space to the desired position.
• In case of wedge with wand (handle), once the proper placement has been achieved,
twist the handle with your fingers and separate it from the wedge head without damaging
surrounding tissues (Fig. 3.5)
Removal of the handle from the wedge is optional. Depending on the procedure,
you may wish to leave the wand attached to the wedge head for easy removal of the
wedge, when the procedure is complete.
• If you wish to drive the wedge further, after removing the handle, use a hemostat or
sturdy cotton plier to correct the placement.

Fig. 3.2: Wedge insertion

Fig. 3.3: Insertion of wedge


Essentials of Dentistry 18 Wedges

Fig. 3.4: Insertion of wedge

Fig. 3.5: Wedge design

Fig. 3.6: Piggy back


Wedges 19

(The decision whether the wedge should be inserted from buccally or lingually depends upon
the two main factors;
1. Location of retainer
2. Design of cavity preparation.
Generally, wedge is inserted from the lingual or palatal side as the lingual embrasure is larger

Essentials of Dentistry
than the buccal. If it interferes with the tongue, it is preferred to insert from the buccal side).

Different Wedging Methods


Piggy back (Fig. 3.6) A second smaller wedge is placed on the first wedge to prevent gingival
overhanging. It is useful in patients with gingival recession.
Double wedging Wedges are placed from both lingual and facial surfaces. It is useful in
case of wide proximal box.
Wedge wedging It is used in cases of maxillary 1st premolar due to presence of mesial
concavity; a second wedge is inserted between the first wedge and band.
CHAPTER

4 Gates Gliddens and


Peeso Reamers

Gates Glidden and peeso reamer drills are one piece rotary cutting instruments used in
root canal preparations.
Structural features that make gates and peeso unique are:
• Bud-(flame) shaped cutting point mounted on a fine shaft attached to a latch type shank.
• Non-end-cutting: Fine blunt nipple which acts as a pathfinder in canal without damaging
the canal walls by creating ledge and apical perforation.
• Reliable and relatively inexpensive.
• They break so high up on the shaft next to the part that fits into the slow handpiece
so usually very easy to remove from the tooth.
(They are designed such that the amount of torque required to break the shaft of
the instrument is greater than the amount of torque required to separate the handle
from the shaft. This means the handle will virtually always separate from the shaft before
the shaft itself breaks).
• Non-end-cutting makes them by definition reamers not drills (Fig. 4.1).

SIZES OF GATES GLIDDEN DRILL


• They are available in two lengths; 38 mm for anterior teeth and 28 mm for posterior
teeth (Fig. 4.4).
• They are available in six different sizes from 1 to 6 depending on tip diameter (Fig. 4.2).
• Tip diameter ranges from 0.5–1.5 mm.

Fig. 4.1: Noncutting end


Gates Gliddens and Peeso Reamers 21

SIZES OF PEESO REAMER


• They are also available in size 1–6 (Figs 4.3 to 4.5).
ISO sizes: 50–170
• Tip diameter ranges from 0.7–1.7 mm.

Essentials of Dentistry
For example, the numbers on both the Gates and the Peeso are denoted by the number
of circumferential grooves located on the shaft just below the cutout for the latch.

Fig. 4.2: Gates glidden drill

Fig. 4.3: Peeso reamer

Fig. 4.4: Gates drills

Fig. 4.5: Peeso reamers


22 Gates Gliddens and Peeso Reamers

PARTS
Essentials of Dentistry

Fig. 4.6: Structural comparison of Gates Glidden drill and peeso reamer

Figure 4.6 shows the main parts of each instrument. The differences are:
1. The cutting head is much smaller on the Gates compared to that of Peeso.
2. The shaft is thinner on the Gates compared to that of the Peeso.
3. Peeso reamer have parallel cutting sides rather than elliptical shape of Gates.
4. The diameters of the heads are different for the same number instrument.

USEFULNESS IN PREPARING ROOT CANALS


• Gates-Glidden drills are side cutting instruments with safety tips. They should be used
at 750-1500 rpm (Fig. 4.7).
• They can be used with both crown down as well as step back fashion.
• It is used to remove the lingual shoulder during access cavity preparation and to enlarge
the canal orifice.
Not only are these instruments good for making post-holes but they are exceptionally
good for preparing root canals in an easy and reliable manner. They are especially good
to use in a modified crown-down technique.
In essence, the Peeso and Gates Glidden drills represent the rotary instrumentation
sequence in the Simplified Endodontic Technique (SET). In the SET sequence, we first clean
and shape the apex to a size number 20 (yellow) stainless steel instrument. If we would
continue instrumentation without altering the canal at this stage, it would become more and
more difficult to manipulate the larger number files or reamers in the canal. This would occur
because the coronal end of the canal would still be narrow and the larger files would bind
and work along their entire length, both at the apical and coronal ends.
The file binds over almost the entire length of the canal and it is bent or curved in
that canal (Fig. 4.9). Binding and bending are two situations that lead to instrumentation
breakage. To lessen the chance of breakage, the file should only “work” or bind in the
apical 2-3 mm of its flutes at any one time.
Gates Gliddens and Peeso Reamers 23

Essentials of Dentistry
Fig. 4.7: Features of Gates Glidden drill

Fig. 4.8: Curvature of canal Fig. 4.9: Bending of file

This can easily be accomplished by using the Peeso or Gates to open up the coronal
end of the canal to let the subsequent endodontic instruments work properly. In essence,
we are doing a modified crown-down technique, using the Peeso or Gates.
Figures 4.8 to 4.10 show the typical mesial canal of a mandibular molar.

STRAIGHTENING THE CANAL


• Once the apex has been instrumented to a size — 20 stainless steel instrument, a
number 2 Peeso or number 3 Gates is introduced into the canal. These instruments
cut much better and more easily in wet environment. If you do not have a slow speed
with water spray, use xylocaine or water from the triple syringe or even irrigating solution.
24 Gates Gliddens and Peeso Reamers

• Cut only 2-3 mm in depth, and then remove the drill from the canal. Clean the flute
and now go back into the canal and cut another 2-3 mm deeper (Fig. 4.11).
• Continue in this manner till one-third to one-half of the way down the canal wall. The
result will be that you have done two very good things:
Essentials of Dentistry

1. You have lessened the curvature of the canal; usually from a 60° curve to roughly
a 45° curve (Fig. 4.10).
2. You have straightened out the canal, so there is less of a radius and the endodontic
instruments do not have to bend as much. Figures 4.12A and 4.13A show the typical
mesial canal of a mandibular molar. Direction of file is shown by black lines. Figures
4.12B and 4.13B show the canal after preparation.

Fig. 4.10: Reduction of canal curvature Fig. 4.11: Always cut wet

Figs 4.12A and B: The canal (A) before (B) after preparation
Gates Gliddens and Peeso Reamers 25

MAIN USES
• To widen the coronal 2/3rd of the canal quickly and safely.
• Peeso reamer is used mainly in postpreparation to remove the gutta-percha.
• To widen the canal during retrieval of the broken instrument.

Essentials of Dentistry
Figs 4.13A and B: The canal (A) before and (B) after preparation

FLEXOGATES
• They are derivatives of Gates glidden drill.
• Used to enlarge the apical region of the canal.
• Less likely to cause apical transportation.
• Less fracture resistant but has breakage point approximately 16 mm form the tip making
its retrieval easier when broken.
• Have noncutting guiding tip.
CHAPTER

Dental Caries
5 Classifications

BASED ON ANATOMIC SITE

Occlusal/Pit and Fissure Caries


It is the caries that results in pit and fissures which are developed by the imperfect
coalescence of the enamel during developmental stage of the tooth. This caries can be
represented as cone with base towards dentinoenamel junction and apex towards enamel
surface.

Smooth Surface Caries


The carious lesion on the smooth surface of tooth is called as smooth surface caries.
It doesn’t begin in the clean enamel but rather in an area that is habitually unclean. The
base of the cone is towards enamel surface and apex is towards dentinoenamel junction.

Root/Senile Caries
Dental caries occurring on tooth that has been exposed to oral environment and it is called
as root or senile caries. This is usually more rapid than other forms of caries especially
in older patients.

Surface texture Surface defect Pigmentation

Grade 1 Soft and can be Variable,


(Initial) penetrated with – Light tan
the explorer to brown
Soft, irregular,
Grade 2 rough. Can be < 0.5 mm Variable,
(Shallow) penetrated with in depth Tan to dark
explorer brown
Grade 3 Soft and can be > 0.5 mm
(Cavitation) penetrated with in depth Variable,
the explorer Light brown
Grade 4 Deeply penetrating to dark
(Pulpal) lesion with pulpal – brown
involvement
Dental Caries Classifications 27

Site and Size (Latest Classification)

Site
Site 1 Lesions originating in the pit and fissure and smooth surface of enamel of tooth crown.

Essentials of Dentistry
It includes the buccal pits on mandibular molars and lingual pits of maxillary molars,
erosion lesions on incisal edges and occlusal surfaces.
Site 2 All lesions involving contact areas, i.e. proximal surfaces of anterior and posterior teeth.
Site 3 All lesions at gingival areas in either enamel or dentin around the whole circumference
of tooth.

Size
Size 1 Localized to the point where it is just beyond demineralization.
Size 2 Larger lesions where there is sufficient sound tooth structure remaining to support the
restoration.
Size 3 Remaining tooth structure is weak to support the restoration. Cavity design has to be
modified.

BASED ON SEVERITY

Incipient Caries
Incipient caries is an early caries lesion which is seen on the smooth surfaces of the teeth
as a “White spot”. It occurs due to subsurface demineralization below the intact surface
layer and can undergo remineralization. It may be confused with developmental defects
of enamel. The incipient caries disappear on wetting, while the developmental defect persists.

Occult (Hidden) Caries


Occult caries is not clinically diagnosed but can be seen on the radiographs. Caries usually
increase with time, if untreated. Increase in fluoride exposure inhibits the superficial enamel
caries but the caries underneath the enamel spreads in dentin. The lesion is covered by
relatively intact layer of enamel. Therefore, such hidden lesions are called as “Fluoride
bombs or Fluoride syndrome”.

Cavitation
Once the caries reaches to the dentinoenamel junction, it spreads rapidly to the pulp along
the tubules and is seen as a definite cavitation on the clinical examination.

BASED ON PROGRESS

Arrested Caries
With change in the oral echo system, the carious lesion may become arrested. The arrested
carious lesion of dentin appears as a dark brown pigmentation.

Recurrent/Secondary Caries
The caries occurring at the borders or underneath the restoration is called as secondary
caries. It occurs due to the poor marginal adaptation of the restoration and subsequent
marginal leakage.
28 Dental Caries Classifications

BASED ON CHRONOLOGY

Acute/Rampant Caries
Acute carious lesion is infectious, light-colored lesion which spreads rapidly.
Essentials of Dentistry

Chronic/Slow Caries
Chronic carious lesion is discolored and fairly hard. Slow destruction rate allows for extrinsic
pigmentation.

BASED ON DIRECTION OF SPREAD

Forward Caries
Caries cone in the enamel is larger or same than that of dentin. It spreads in forward
direction from enamel to dentin.

Backward Caries
Once enters the enamel, caries spread along the dentinoenamel junction rapidly and again
extends towards the enamel in backward direction.

Residual Caries
The caries that remains in a completed cavity preparation whether by operational intention or
by accident is called as residual caries.
CHAPTER
Differences between the

6 Inlay and Amalgam


Restorations

Cast inlay Amalgam restoration


Cast inlay is an indirect procedure requiring Amalgam restoration is direct procedure
two appointments. One for tooth preparation that can be finished in one appointment.
and the other for delivering restoration.

Minimum thickness of restorative material Requires at least 1.5 mm thickness of


required to resist deformation is 1-2 mm. amalgam to resist deformation.

Instruments used for cavity preparation

No. 271 bur is mostly used. No. 245 bur is mostly used.

Cavity preparation (Figs 6.2, 6.3, 6.4, 6.6 and 6.7)

Axial walls should be parallel or slightly Retention form is achieved through axial
divergent occlusally (2-5° taper per wall) walls that converge occlusally.
for achieving primary retention

An occlusal bevel of 30-40° is placed Bevels are not indicated as amalgam has
for proper adaptation of the inlay low tensile strength

Gingival bevel of 30° is placed in the Gingival bevel of 15-20° is placed in the
gingival wall to gingival wall to remove the unsupported
1. Remove the weak enamel to improve enamel rods thereby improving the
resistance form. resistance form.
2. To provide a lap sliding fit of the casting. Gingival bevel is not required in
3. To allow burnishing of the metal margin deciduous teeth as there are no unsupported
to improve the adaptation (Fig. 6.1). enamel rods in this region.

Proximal portion is box-shaped Proximal box has an inverted trunk shape.

The isthmus width should not exceed 1/3rd The isthmus width should not exceed 1/4th
of intercuspal distance. of intercuspal distance (Figs 6.5A and B).

Flares (Primary + Secondary) prepared Flares are not indicated


on the facial and lingual proximal walls
carries the same function as that of bevels
on occlusal and gingival walls.

Cavosurface angle is 130-140° (Lap joint) Cavosurface angle is 90-100° (Butt joint)
Marginal metal is 30-40° Metal margin is 90°

(Contd.)
30 Differences between the Inlay and Amalgam Restorations

Contd....

Cast inlay Amalgam restoration

Retention grooves are placed on the Retention locks are prepared on the
Essentials of Dentistry

axiofacial and axiolingual line angles to axiofacial and axiolingual angles for
provide secondary resistance form secondary retention
Indications
It is appropriate for moderate to extensive It is appropriate for conservative
cavity preparations. preparations.
Contraindications
In young patients, due to presence of large Contraindicated in extensive carious
pulp chambers and in old patients, due to lesions and indicated in young patients
lengthy and multistep procedures.
Advantages
Superior control of contours and contacts There is less control on the placement
can be achieved. of proper contours and contacts.
Disadvantages
More cost to the patient Less cost to the patient
Requires at least two appointments Treatment can be completed in one
appointment most of the time.

Fig. 6.1: Preparation for cast restoration

Fig. 6.2: Inlay


Differences between the Inlay and Amalgam Restorations 31

Essentials of Dentistry
Fig. 6.3: Onlay preparation

Fig. 6.4: Inlay preparation

A B
Figs 6.5A and B: Amalgam cavity preparation
Essentials of Dentistry 32 Differences between the Inlay and Amalgam Restorations

Fig. 6.6: Cavity preparation for cast restorations

B
Figs 6.7A and B: Cast restorations
CHAPTER

7 Electric Pulp Testing

Electric pulp testing (EPT) is based on relative conductivity of dental hard tissues. The
objective of electric testing is to determine the sensibility of each tooth at the lowest sensory
response threshold. It doesn’t provide information regarding the health of pulp, status
of inflammation or integrity of a vital pulp but it suggests whether pulp is vital or nonvital.
Electric pulp testers use an electric current (AC or DC) to stimulate a response from the
nerve tissue in the pulp.

PRINCIPLE
Electric pulp testing depends on the nerve supply of the pulp whereas the pulp vitality
depends on blood supply of tooth. Thus, it is not the actual test for tooth vitality. Electric
pulp tester produces a response by electric excitation of neural elements within the pulp
by subjecting tooth to increasing degree of electric current.

ELECTROLYTE
The electrolytes applied in EPT procedures are Nicholas-colloidal graphite or Grossman
toothpaste. KY jelly is also commonly used as an electrolyte.

TYPES OF PULP TESTERS


Electric pulp testers (EPTs) are widely used diagnostic tools in endodontics. They deliver
a current sufficient to overcome enamel and dentin resistance to stimulate the myelinated
sensory fibers (Ad fibers) at the pulpal-dentinal junction. The unmyelinated C-fibers of
the pulp do not respond as they require greater current for stimulation.
The two main varieties of pulp testers are bipolar and monopolar. Monopolar pulp testers
are commonly used for vitality tests (Fig. 7.1). Electric pulp tester is called as “Vitalometer”.

SITE
• Testing with an EPT requires electrode contact onto tooth surface.
• The best site to apply the probe of tester and electrolyte during EPT is incisal 2/3rd
of labial surfaces and the occlusal 2/3rd of the buccal surface of tooth (Fig. 7.2).
• Placing the electrode at the incisal edge of anterior teeth evokes a response with the
least amount of electrical current.
• There are several considerations regarding optimal placement of the electrode in
assessing the vitality of teeth. The response threshold is reached when an adequate
number of nerve terminals are activated to attain a so-called summation effect.
• The response to a given stimulus will be greatest where the neural density is the highest.
Therefore, an area of high neural density will have a relatively fast and strong response
and requires the least electric current.
Essentials of Dentistry 34 Electric Pulp Testing

Fig. 7.1: Electric pulp tester

Fig. 7.2: Sites for placement of electrode

• In permanent teeth, the highest concentration of neural elements is in the pulp horns
with progressively fewer in the cervical and radicular regions of the pulp.
• The response threshold increases as the electrode is moved apically from the cuspal
tip to the cervical region of the tooth.

PROCEDURES
• Describe the test to the patient to reduce anxiety and to eliminate biased response.
• Isolate the tooth to be tested with cotton rolls and saliva ejector.
• Put small amount of electrolyte (toothpaste is commonly used, other is KY jelly) on
the tip of the electrode of the pulp tester.
• Dry the tooth surface before the procedure to avoid short circuiting through saliva to
the periodontium. Tooth can be isolated with rubber dam. A tooth may also need to
be isolated with strips of rubber dam between the contact points to prevent conduction
through metallic restorations into adjacent teeth.
• Ask the patient to give signal when he/she feels tingling or hot sensation.
• Place the tip of instrument on the facial surface of the tooth with lowest power and
gradually increase the power (Figs 7.3A and B) . (Some newer instruments apply the
Electric Pulp Testing 35

power logarithmically and automatically to the tooth being tested and preclude the
chances of patient receiving full charge on the first application. Such pulp testers turn
on automatically when the probe contacts the tooth and turn off automatically when
the probe is removed from the tooth surface).

Essentials of Dentistry
• If patient feels some sensation, it means tooth is vital and note the power at the same
time.
• Monopolar testers such as the Analytic Technology tester require the circuit to be
completed by the operator or patient. If operator is wearing the rubber gloves, patient
is asked to hold the metal handle to complete the circuit.
• Compare this reading with the normal adjacent and contralateral teeth. If patient doesn’t
feel any sensation, it may indicate necrotic pulp.

PRECAUTIONS
• EPT should first be performed on control teeth favorably an adjacent or contralateral
tooth prior to being performed on the affected tooth to eliminate the bias.
• Gloves should not be worn during EPT as they interfere with completion of circuit. While
using the rubber gloves, one of the two methods must be followed for circuit completion:
i. Use of lip clip (Fig. 7.4)
ii. Contacting the patient’s finger to the metal electrode.
(Later method is more preferred as patient can lift the finger from electrode when a
sensation is felt. This will break the circuit and terminate the stimulus).

B
Figs 7.3A and B: Placement of electrode
36 Electric Pulp Testing

• Multirooted tooth should be tested at more than one location. It may show negative
response at one location and positive response at other location. It indicates that one
canal is necrotic while other contains vital pulp tissues.
• In case of tooth with full coverage restorations, a cavity is prepared through the restoration
Essentials of Dentistry

and dentin is exposed and then the tip of pulp tester is applied on to the dentin.
• Once the assembly is adjusted, current is increased gradually till the patient feels tingling
sensation or pain. Each tooth should be tested two to three times and average reading
is noted.

CONTRAINDICATIONS
• EPT should not be used in patients having cardiac pacemaker as it may interfere with
electric activity of pacemaker.
• It should not be used on recently erupted tooth with immature apex because the
relationship between the odontoblasts and the nerve fibers has not yet developed fully.
It means tooth doesn’t have fully developed sensitivity and may lead to false-negative
reading.
• It should not be used on recently traumatized tooth.

RESPONSES
The ability of electric test to indicate pulp vitality is based on sensitivity of neural transmission,
which can lead to false-positive and false-negative values, but a positive response usually
indicates that there are vital sensory fibers present. Generally, thicker enamel gives delayed
the response.

False-negative
1. Presence of pulp stone.
2. Extensive caries.
3. High amount of reparative dentin.
4. Patients heavily medicated with analgesics, sedatives, narcotics or alcohol.
5. Teeth with large restoration and pulp protective base.
6. Recently erupted tooth with immature root. (It has underdeveloped plexus of Rashkow
as well as greater unmyelinated nerve fibers. Pulp tester is based on excitation of A

Fig. 7.4: Pulp tester with lip clips


Electric Pulp Testing 37

fibers which are not fully developed till the age of adolescent and hence may not respond
in recently erupted tooth).
7. Recently traumatized tooth as nerves fibers are in state of shock.
8. Inadequate contact of electrode with tooth structure due to insufficient conductor or
due to improper placement of tip.

Essentials of Dentistry
9. Low battery of tester. (With battery operated device, if battery is running low, it may
not deliver full current).

False-positive
1. Presence of partially necrotic pulp in one canal of multirooted tooth because partial
necrosis is indicated as total necrosis by pulp tester.
2. Moist gangrenous pulp which requires more current to elicit the response.
3. Electrode contacting any part of oral mucosa allowing current to reach the attachment
apparatus directly.
4. Anxious patient may become hyperactive before perception of the actual sensation.
5. Improper isolation of tooth.
False vitality responses are common in posterior teeth due to presence of vital pulp
tissue in one of the canals.
CHAPTER

8 Dental Adhesion

ADHESION
Adhesion is a process of solid and/or liquid interaction of one material (adhesive or adherent)
with other (adherend) at a single interface. For example, Pit and fissure sealant.
The material or film added to produce the adhesion is known as the “adhesive or
adherent” and the material to which it is applied is called the “adherend”.

ADHESIVE JOINT
It is the result of interaction of a layer of intermediate material (adhesive or adherent) with
two surfaces (adherends) producing two adhesive surfaces.
Adhesion is classified as:

Physical bonding It involves Van der Waals or electrostatic interactions that are relatively
weak. It occurs when the surfaces are smooth and chemically dissimilar.

It involves bonding between atoms formed across the interface from the
Chemical bonding adhesive to the adherent. The extent of this bonding is limited and overall
contribution to the strength is quite low.

It is the result of interface that involves undercuts and rough surface to


Mechanical bonding produce interlocking of materials. Almost every case of dental adhesion
is based primarily on mechanical bonding

MICROMECHANICAL BONDING
It is the microscopically interlocked adhesive and adherent with dimensions of less than
10 m produced by mechanical roughness.
Requirements for adhesion are:
1. To produce good bonding there must be good wetting. 0° contact of adhesive to the
adherent ensures complete wetting.
2. Surfaces being bonded should be clean.

BONDING SYSTEMS
These are classified on the basis of the primary adherent. They are:
• Enamel bonding
• Dentin bonding
• Amalgam bonding.
Dental Adhesion 39

Dentin Bonding Systems (DBS)


• DBS consists of unfilled, liquid acrylic monomer mixture placed onto an acid conditioned
and primed surface.
• Difficulties in dentin bonding are:

Essentials of Dentistry
1. Dentin is living heterogeneous tissue and contains plenty of fluids.
2. Presence of smear layer on the cut dentin surface.
3. The potential biologic side effects that different chemicals can cause within the pulp.
• As most composites are hydrophobic in nature, dentin bonding agent should be
hydrophobic to bond with composite and hydrophilic to interact with dentin.
• Steps of dentin bonding are:
1. Etching/conditioning
2. Application of primer
3. Application of bonding agent

Conditioners
These are the agents which aids in removal or modification of smear layer.
For example, EDTA, 10 percent phosphoric acid, citric acid, maleic acid.

Primers
The primer is used to displace residual moisture, thus creating a surface upon which
the hydrophobic bonding resin can adhere. The primer assists the adhesive to flow
into and penetrate the etched tooth surface. The primer often contains a hydrophilic
portion that interacts with the moisture present in the tooth structure, as well as a
hydrophobic end that provides bonding sites for the methacrylate monomers in the bonding
resin.
For example, 2-HEMA and HEMA dissolved in acetone or alcohol.
Dentin bonding agents are unfilled resins which have a role in formation and stabilization
of hybrid layer (micromechanical attachment between resin and conditioned primed dentin).
Even though tags are formed into tubules, bond strength is mainly due to micro mechanical
bonding of intertubular dentin. Clinical longevity of dentin bonding system is not as long
as enamel bonding due to high water content.
1st generation Uses glycerol-phosphoric acid dimethacrylate

2nd generation Uses chloro substituted phosphate esters of various monomers

3rd generation Three step procedure of conditioning, priming, bonding

4th generation Relies on formation of hybrid layer. Called as self-etching primers as


conditioning and priming are combined in one step.

5th generation Steps two and three are combined.

6th generation One step procedure as all three solutions are in one bottle.

7th generation Fluoride releasing bonding agents.

ADHESIVE CONSIDERATIONS FOR DIRECT COMPOSITE RESTORATIONS


Direct composite resins are the predictable alternative to amalgam or other metal-based
restorations. The clinical success of the direct composite materials is most liked-related
to the improved clinical skills and techniques and dramatic advances in adhesion technology.
40 Dental Adhesion

For this, the dentist is required to understand the rationale for specific clinical techniques,
as well as material idiosyncrasies, in order to optimize the adhesive interface between
the composite restoration and tooth surface.
The actual linkage between composites and the tooth structure is usually mediated
Essentials of Dentistry

through the use of dentin bonding agent. Long-term bonding to phosphoric acid-etched
enamel surfaces has proven to be highly reliable and predictable; long-term bonding to
the dentin is not predictable, regardless of dentin bonding agent. Clinicians can generally
bond predictably to enamel, but not as predictably to dentin because of the morphologic,
histologic and compositional differences between the two substrates. Dentin is highly
variable substrate. Superficial, middle and deep dentin can vary significantly in their structural
and chemical composition. Enamel, on other hand, is quite consistent throughout and
is also considerably more mineralized than dentin.
Factors that further complicate the bonding of dentin are dentin depth, age of the teeth
and history of tooth trauma and/or pathology. This, coupled with very high water content
of dentin, presents a significant challenge for consistent and reliable long-term bonding.
However, it doesn’t mean that stable and strong initial bonds to dentin can’t be attained.
Recent studies have shown that many current adhesive systems are capable of producing
bond strengths to dentin equal or surpass those to acid-etched enamel controls.
Microleakage, nanoleakage, hydrolysis, dentin permeability, pulpal pressure, shrinkage
stress, “water free” formation, phase separation, dentin tubule orientation, occlusion,
enzymes released by bacteria, and operator error have all been implicated as potential
causes of deterioration of the dentin/adhesion interface over time.
The principle mean by which adhesion takes place is by an exchange of calcium and
phosphates (inorganic minerals) from enamel and dentin replacing the same with resins
and nanofillers. The resin-based adhesive systems developed to date can be categorized
as one of two types:
1. Total-etch system
(Etch-and-rinse adhesive systems)
2. Self-etch adhesive systems.
Both systems result in a unique interface at the junction of tooth surface and adhesive.
The difference in the interface that exists for enamel, as compared to dentin, is an important
consideration in the selection of either total etch or a self-etching adhesive system (see
Fig. 8.5). In the last decade, most new developments in dental adhesives have been focused
on simplifying the components required for the bonding systems and improving performance
of the resulting self-etching adhesives.
Careful consideration of several factors is essential in selecting an adhesive system.
Enamel bonding is superior with etch-and-rinse adhesive systems, while self-etch systems may
be more suitable for restorations with large areas of dentin.

DENTAL ADHESIVE SYSTEMS (FIG. 8.1)


Typically, total-etch adhesives produce high and substantive adhesion values for both
enamel and dentin. In comparison, self-etch adhesives generally demonstrate better
adhesion to dentin than to enamel. These are key considerations for anterior restorations.
If the surface to which the adhesive will be applied consists of significantly more enamel
than dentin—and particularly if the surface consists of intact enamel, such as with an anterior
diastema, an unprepared veneer, or a minimally prepared adhesive bridge, an etch-and-
rinse system is preferred.
The main disadvantage of self-etch adhesive systems is that the enamel must be
instrumented to provide an effective etch. Self-etch adhesives typically do not provide as
high an enamel bond compared to etch-and-rinse adhesives.
Dental Adhesion 41

Essentials of Dentistry
Fig. 8.1: Dental adhesive systems

In some cases, self-etch systems demonstrated a higher incidence of marginal staining


on enamel margins, while the dentin margins were acceptable (e.g. posterior/ more extensive
preparations). Self-etch adhesives thus may be preferred over the etch-and-rinse adhesives
if the remaining enamel has been instrumented and if the surface area to be bonded consists
mainly of dentin. They may also be a better choice if sustained isolation from oral fluids
is likely to be a problem.

Mechanisms of Action
The basic mechanism for enamel and dentin bonding using etch-and-rinse systems consists
of the following steps (Fig. 8.2):
• Demineralization of the surface by the acid (etchant)
• Penetration of the adhesive monomers into the microscopic spaces created by the
etchant
• Curing of the adhesive monomers to form resin tags that microscopically provide a
mechanical bond and seal to dentin and enamel.
The etchant creates a demineralized surface 3 mm to 5 mm in depth that is available
for resin penetration while also removing the smear layer debris created during
instrumentation. Failure to remove the smear layer reduces the dentin permeability, as
that layer acts as a barrier and prevents adhesion to the underlying intact tooth structure.
Demineralization results in the exposure of the collagen contained in the dentin. Macroresin
tags are created peripherally around the demineralized surface of the hydroxyapatite
crystals, and microtags are formed by resin penetration into demineralized crypts within
the crystals.
The primer and adhesive (or combined primer-adhesive, in the case of two-step systems)
then interpenetrates the exposed collagen and remaining mineral, penetrating to the residual
intact mineralized dentin within this microscopic etched surface and providing retention
upon curing of the adhesive. This newly created interface is referred to as the “hybrid
layer” and is observed in three distinct areas (Fig. 8.3):
• Within the dentinal tubules
• In the microscopic branches lateral to the tubules
• In the intertubular dentin.
Essentials of Dentistry 42 Dental Adhesion

Fig. 8.2: Mechanism of action

Fig. 8.3: Formation of hybrid layer

Accordingly, they treat cut dentin surface in two fundamentally different ways. The clinical
picture stands in stark contrast to the dematerialized, highly permeable condition of the
dentin that exists after the removal of smear layer by phosphoric acid needed for fourth-
generation bonding systems. One could conclude that the significantly reduced outcome
than what is generally produced by the more technique sensitive total etch adhesives.

One key performance factor that influences the success of etch-and-rinse systems includes the
thorough removal of the etchant prior to bonding.

An important consideration when selecting between etch-and-rinse and self-etch systems


is the condition of the enamel that will be bonded. If the enamel comprises mostly intact
or uninstrumented enamel, the choice of an etch-and-rinse system is preferred. If the tooth
surface to be etched consists mainly of dentin, self-etching systems may be a better choice
in order to avoid the need to reinfiltrate the dentin after exposing the dentinal tubules with
the etchant of the etch-and-rinse system.
Self-etch adhesives modify the layer and then penetrate through it to further demineralize
the superficial layer of the dentin and combine with collagen and the remaining
hydroxyapatite to form a hybrid layer of not more than 0.5–1 micron. This depth of 1 micron
is much lesser than 4–5 micron depths of total etch (Fig. 8.4).
Dental Adhesion 43

Essentials of Dentistry
Fig. 8.4: Penetration of adhesive

Three-step etch-and-rinse systems contain an etchant, a primer and a bonding resin


(adhesive). The primer is used to displace residual moisture, thus creating a surface upon
which the hydrophobic bonding resin can adhere. The primer assists the adhesive to flow
into and penetrate the etched tooth surface. The primer often contains hydrophilic portion
that interacts with the moisture present in the tooth structure, as well as a hydrophobic
end that provides bonding sites for the methacrylate monomers in the bonding resin. The
subsequently applied bonding resin (adhesive) fills the residual space and seals the dentinal
tubules. Polymerization of the bonding resin stabilizes the hybrid layer and also provides
a polymerized surface layer upon which the final composite resin is bonded. Two-step
systems combine the primer and adhesive materials into one component, thus condensing
that application process into only one step. Several authors have suggested that the two-
step systems may introduce greater variability into bonding results. However, these systems
have exhibited excellent clinical performance over the years.
While it has been suggested that self-etch adhesive systems result in less postoperative
sensitivity, a recent study shows that there is no differences in postoperative sensitivity
between patients treated with self-etch adhesives and those treated with etch-and-rinse
adhesives nor have any differences been discovered in marginal integrity. It was concluded
that restorative technique influences postoperative sensitivity.

RATIONALE OF ADHESIVE SYSTEMS


Primers of total etch system are far less acidic, and consequently require a preliminary
treatment with 32 percent phosphoric acid to change the dentin surface in a way that
facilitates a strong dentin bond. This phosphoric-acid treatment completely removes the
smear layer formed during cavity preparation, a layer that otherwise would block the dentin
tubules, thus resulting in increased dentin permeability and, within potential for postoperative
sensitivity. This smear layer removal is necessary for the fourth generation primer and
the bond to penetrate the tubules and form the hybrid zone. The self-etch technique, on
the other hand leaves smear layer in place. The self-etch system is based on infiltration
and modification of the smear layer by an acidic monomer. Intact smear layer impedes
the fluid movement within the dentinal tubules and thus reducing postoperative sensitivity.
All dentin bonding systems employ acids of one type or another type to facilitate adhesion
to the tooth tissues. Acidic treatment of enamel and/or dentin creates a zone of
demineralization, which is subsequently (i.e. total-etch) or concurrently (i.e. self-etch)
infiltrated with various bi-functional primers and resins. While many adhesive systems are
capable of providing acceptable clinical results if used in a knowledgeable fashion with
attention to detail, all have their particular idiosyncrasies.
44 Dental Adhesion

The fourth generation, or three step total-etch systems generally have good long-term
clinical track records and perhaps the most versatile of all the adhesive categories because
they can be employed for virtually any bonding protocol (i.e. direct, indirect, self cure,
dual cure). These systems are still the “gold standard” by which the newer systems are
Essentials of Dentistry

judged. Indeed, none of the newer systems in the marketplace today perform any better,
and often perform worse, than the original multiple component total etch systems of 15
years ago, if bond strength to dentin/enamel, microleakage and long-term durability are
used as the evaluation criteria.
The fifth generation, or two step total-etch system, evolved from the desire to simplify
the three step total-etch system protocol. As a group, these are among the most popular
systems presently being utilized in dentistry. They have generally proven to be highly
effective, simpler and faster than the multiple component predecessors. On the down side,
many in this category, with some exception, are not as predictable as the three step total-
etch systems when it comes to bonding to self- and dual-cure composites. It has been
suggested that a small amount of residual acidic resin monomer can deactivate the tertiary
amine that promotes the dark-cure polymerization of the resin cement or restorative. It
is for this reason that it is suggested that, unless specifically designed for use with dual-
and/or self-cure resin cement or restorative, self-etching adhesives should be avoided.
In fact, even with etch-and-rinse adhesive systems, mixing different manufacturers’ materials
should be avoided to prevent incompatibility issues between the interface of the adhesive
and the dual- and/or self-cure restorative or cement material.
In addition, the two-step total-etch systems may be more susceptible to water
degradation over time than three-step total-etch systems. This is because the polymerized
primer of the two-step systems tends to be hydrophilic in nature. When using a three-
step system, the hydrophilic primer is covered by a more hydrophobic resin, making it
less susceptible to water sorption.
Majority of studies show that fourth generation and fifth generation total-etch system
in the placement of a direct composite perform best when placed on moist dentin. This
has been termed as “wet” bonding, although the moist bonding may be a more accurate
description of the phenomena. Dentin exposed to phosphoric acid results in dissolution
of the inorganic hydroxyapatite matrix. As the matrix dissolves, the collagen fibrils, which
are inherent in dentin, become exposed as they are no longer supported and surrounded
by their inorganic scaffolding. The phosphoric acid treatment leaves the protein component
of dentin completely unsupported, literally floating in the rinse water. If the surface is too
much dried, collapsed collagen fiber network creates an impermeable organic barrier for
primer penetration. This leads to gaps formation and bond strength decreases. On another
side, if excessive water left on the substrate creates a different problem in that the primers
do not remain dissolved in their solvents. Consequently, resin globules and water trees
can form, interfering with bond strength and creating fluid movement within the tubules,
promoting postoperative sensitivity.
It is this friable “collagen network” that must be infiltrated by subsequently placed primers
and resins to ensure good bonding. Air-drying of acid-etched dentin causes collapse of
collagen network and interferes with subsequent primer/resin infiltration. In dentin that
is left moist (after acid etching) the collagen fibrils remain in a relatively “open” state and
appear to be more permeable to subsequently placed primers and resins. The
recommended technique when utilizing a total-etch protocol on unlined dentin is not air
dry the dentin once the phosphoric acid conditioner is washed off. The excess water is
simply blotted out with moist cotton pellets prior to placing the primer. This leaves a visibly
moist dentin surface. It warrants noting that some total-etch systems, usually those that
are acetone-based, appear to be more sensitive to this wet/dry dentin issue than others
(e.g. alcohol/water-based systems). It is mandatory to follow moist bonding with acetone
Dental Adhesion 45

containing adhesives. This highlights an inherent ambiguity many have with the concept
of wet bonding, namely exactly how wet is?
Perhaps the biggest advantage of the sixth generation or two component, self-etching
systems is that their efficacy appears to be less dependent on the hydration state of dentin
that total etch systems. Since dentin is not pretreated with phosphoric acid as in the case

Essentials of Dentistry
with total-etch systems- no exposed collagen layer is present to collapse on air drying
prior to placement of self etching primers. Clinically, this means that “wet” bonding is not
a concern and the tooth surface can be briefly air-dried prior to placing self-etching primer.
This is not to say that self-etch systems perform any better than total etch system, but
they need to be less technique sensitive in this regard. One could also argue that a possible
advantage of self-etching system is that demineralization of the dentin occurs concurrently
with primer infiltration. If the tooth surface to be etched consists mainly of dentin, self-
etching systems may be a better choice in order to avoid the need to reinfiltrate the dentin
after exposing the dentinal tubules with the etchant of the etch-and-rinse system thus
eliminating the potential for over-etching when treating dentin.
In principle, this helps ensure that the entire zone of demineralization is saturated with
primer where it can then be polymerized in situ. On the down side, many products in
this category do not etch enamel as well as their total-etch cousins and many are not
compatible with self- and dual-cure composites. A common clinical technique that can
be used is to first etch the enamel with traditional phosphoric acid prior to using self-
etching system. This ensures good bond strength to enamel but it does require an additional
step in the bonding protocol. Those utilizing this technique should take care to confine
the phosphoric acid solely to enamel. Additional etching of the dentin with phosphoric
acid could, in principle create an “over etch” situation where the demineralization zone
is too deep for subsequently placed primers to completely penetrate.
The seventh generation or one bottle self-etching systems represents the latest
simplification of adhesive systems. With these systems all the ingredients required for bonding
are placed in and delivered from, a single bottle. This greatly simplifies the bonding protocol.
Incorporating and placing all of the chemistry required for a viable adhesive system into
a single bottle and having it remain stable over a reasonable period of time, poses a significant
challenge. These inherently acidic systems tend to have a significant amount of water in
their formulations and may be prone to hydrolysis and chemical breakdown. In addition,
once placed and polymerized, they are generally more hydrophilic than two-step self-etching
systems, which makes them more prone to water sorption. This could contribute to hydrolysis
and degradation of the adhesive interface, as well as a reduction in mechanical properties
of the composite restoration. The acidic nature of the polymerized primers in seventh
generation adhesives generally makes them unsuitable for use with self-cure composites
since their acidic nature degrades the tertiary aromatic amines required for chemical
polymerization of self-cure composites. According to some author’s opinion, while offering
ease and simplicity, seventh generation adhesive systems should be used cautiously until
more independent research clearly demonstrate their short- and long-term effectiveness.
In principle, the “ideal” adhesive system would be one that is hydrophilic when first
placed in order to interact with dentin, which inherently has high water content, but then
becomes completely hydrophobic once polymerized in order to discourage water sorption
and hydrolysis. Unfortunately, no such chemistry currently exists. A new recently introduced
total-etch system among the first to address this issue by utilizing chemistries that are
less hydrophilic in nature.

NEWER ADHESIVE DEVELOPMENTS


In the last decade, most new developments in dental adhesives have been focused on
simplifying the components required for the bonding systems and improving performance
46 Dental Adhesion

of the resulting self-etching adhesives. The true one-bottle self-etch systems have now
evolved to only one material. This is applied to the tooth with no mixing required. Some
of the newer systems have modified the self-etch ingredients so as to result in improvements
in the product’s shelf lives, with diminished hydrolysis in the package. As noted above,
Essentials of Dentistry

while the quality of dentin adhesion with these self-etch systems is comparable to the
etch-and-rinse adhesives, the enamel bonding of these systems still falls short of values
for bond strengths achieved in the laboratory using a phosphoric acid etch system.
The self-etch systems remain popular due to the lack of concern regarding the technique
used with moist dentin. The moist bonding technique has been repeatedly shown to
augment bond strengths of ethanol- and acetone-based etch-and-rinse adhesives, while
low bond strengths have been associated with excessively air-dried dentin in the etch-
and-rinse materials. The major reason for this is presumed to be the effect of collapsing
the collagen network at the bonding interface. The collapsed collagen prevents complete
infiltration of the resin monomers into the demineralized dentin, leading to gaps and voids
within the adhesive interface.

KEY POINTS TO ENSURE EFFECTIVE BONDING


WITH TOTAL ETCH SYSTEM
1. Etch the enamel first for at least 15 seconds, followed by etching the dentin for a maximum
of 15 seconds. This will ensure that the demineralized areas created during etching
will be filled through capillary action, subsequently forming resin tags.
Enamel should not be under-etched (less than 15 seconds) and dentin should not
be over-etched (more than 15 seconds) — either of which could result in a reduced
bond strength because deeper demineralization of dentin makes it difficult to infiltrate
it completely with the adhesive. Also, the presence of some hydroxyapatite within the
exposed collagen fibrils will provide some protection from hydrolysis. Ensure that the
dentin is slightly moist after rinsing-off the etchant and ‘drying’ the dentin. This “moist
bonding” helps prevent exposed collagen from collapsing and forming coagulate, which
could prevent adhesive penetration into the dentin. Bonding is impaired, if the dentin
is either too dry or too moist.
Different methods recommended in order of preference are:
• Take a small piece of cotton, roll it into a small pellet, dip it in sterile water, squeeze out the
excess water and wipe of the cavity in such a way that no excess water remains on enamel
or dentin.
• Take a small piece of dry cotton and remove the excess water from cavity. Care should be
taken not desiccate the preparation.
• Use air syringe taking care to see that no oil or water is spurting out and gently dry for not
more than 3 seconds. (Least preferred)

Fig. 8.5: Self-etching vs etch and rine


Dental Adhesion 47

2. Dispense the etch-and-rinse primer or primer-adhesive combination immediately prior


to placement, so as to avoid evaporation of the solvents contained therein. Use of
delivery system that results in simultaneous dispensing is preferable.
3. Apply an amount of adhesive sufficient to thoroughly coat and penetrate the entire
etched surface. If using a two-step system, several layers of the primer-adhesive should

Essentials of Dentistry
be applied to ensure an adequately thick layer of adhesive—solvent present in the
primer-adhesive can otherwise result in a layer that is too thin. Because etching dentin
removes the smear layer, a larger surface area for adhesion is exposed, thus requiring
more adhesive than is necessary for the etched enamel surface.
4. Thoroughly air-dry the adhesive to remove the ethanol, acetone, or hydrophilic solvent
carrier, reducing the potential for interference with the polymerization process and to
spread the adhesive evenly on prepared surface. Solvent chase out the water from
the dentinal tubules so that resins can penetrate deeper inside so after this work is
over its presence dilute the bonding agent and weakens the bond. Air drying removes
the solvent and concentrates the resin in hybrid zone and strengthens it.
5. Ensure that the adhesive is thoroughly light-cured prior to composite restoration
placement to avoid displacement of uncured adhesive during placement.
Flowable resins have low physical properties and exhibits high polymerization
shrinkage. They are used in thin layers and should be cured for 10–15 seconds more
because of increased presence of polymerizable resins.

KEY POINTS TO ENSURE EFFECTIVE BONDING


WITH SELF-ETCH SYSTEM
1. Enamel, if present, should be beveled to improve retention. Some authors prefer to place
bevel as long as the cavity for better esthetics and bonding especially in class V.
2. The surfaces to be bonded should be clean and debris-free to prevent contamination
of the adhesive, since there is no rinsing step that would remove any contaminants.
3. If using a multidose, single-bottle adhesive, the amount required should be dispensed
immediately prior to use in order to reduce the risk of solvent loss, which could potentially
result in phase separation of monomer and water. Using a unit-dose package helps
to avoid this problem and also provides an appropriate amount of adhesive for use.
4. Apply the self-etch adhesive to the enamel first, followed by application to the dentin.
Some products recommend agitation of the adhesive to enhance its penetration.
5. Do not use a separate etchant on the dentin prior to using self-etch adhesives. While
it may be believed that this would improve the bond to dentin, self-etch adhesives
are not designed to work on etched dentin. The result would be clinically undesirable
and could potentially result in catastrophic failure of the restoration. If using a separate
etchant on enamel, great care must be taken to avoid its contact with dentin and to
thoroughly rinse it off prior to the use of self-etch adhesives.
6. If using a one-step self-etch adhesive, apply multiple applications (as recommended
by manufacturer) to help ensure adequate coating and penetration.
7. Thoroughly dry the adhesive (with a gentle stream of air) once it has been placed,
to ensure removal of any volatile solvent and prevent interference with polymerization.
8. Light-cure the adhesive prior to placing the composite.
CHAPTER

9 Bleaching

The lightening of color of tooth through application of chemical agent to oxidize/reduce


the organic pigmentation in the tooth is known as bleaching.

INTRODUCTION
It was 1st advocated by Dr JA Chapple (1877). He used oxalic acid. Harlan used hydrogen
peroxide for bleaching first time in 1884, which he called hydrogen dioxide.
Although many mechanisms by which bleaching removes discoloration are not fully
understood, the basic process involves oxidation, in which the bleaching agent enters
the enamel/dentin of discolored tooth and releases the molecules that removes the stains.
The effectiveness of bleaching procedure broadly depends upon the cause of the stain,
location and depth of the stain, length of period the stain permitted to retain on the structure
of tooth and depth of penetration and period of retention of bleaching agent inside the
tooth to release the deep stains.
The process of bleaching for superficial stains is fairly simple. However, deep stains
may require mild etching to remove the superficial organic materials and to expose the
deeper areas of enamel. Once hydrogen peroxide was established as a most effective
bleaching agent, attempts were put to facilitate its absorption and penetration to speed
the procedure of oxidation. In 1918, Abbot discovered what the basic combination today
remains: A high intensity light that produces the rapid rise in the temperature of hydrogen
peroxide to accelerate the procedure of bleaching. Since then there is continuous
improvement in the effectiveness and the ease of use of bleaching agents, heat and light
catalyst devices, and the alternative methods.
Three most prominent bleaching processes are peroxide, chlorine and chloride. Peroxide
requires least time and it is most commonly used.

CLASSIFICATION OF BLEACHING AGENTS


a. Oxidizing agents:
Sodium peroxide
30-35% H2O2 Toxic free radicals, perhydroxyl anions or both
E.g. Pyrozone, Superoxol, Perhydral
95% sodium perborate Sodium metaborate, H2O2, Nascent O2
10% Carbamide peroxide Urea, ammonia, CO2,
(Urea hydrogen peroxide) 3.5% H2O2

b. Reducing agents:
• Sulphur dioxide
• Sulphurous acid
• Sodium thiosulphate
Bleaching 49

(c) Chlorine bleaching agent:


Chlorinated lime + Acetic acid
(d) Decalcifying agent:
• HCl
• H2PO4

Essentials of Dentistry
Products Based on H2O2

Superoxol 30% watery solution


Pyrozone 25% H2O2 in ether
Perhydral 30% H2O2 in water
Starbrite 35% H2O2 gel
Dentalite plus 25% solution

Recently 1-10% H2O2 Solutions Marketed are:


Peroxyl—1-5% gel (Colgate)
Brite smile—1-10% solution (Brite smile)
Natural white—6% gel

HYDROGEN PEROXIDE
Hydrogen peroxide bleaching requires least time and it is most commonly used. The low
molecular weight hydrogen peroxide and its capability to denature the proteins probably
enhance its ability to penetrate teeth. Volume of the oxygen released determines the strength
of the solution rather than the concentration. Volume indicates the amount of oxygen
released by one volume of designated hydrogen peroxide.

Concentration Volume

27.5% 100
35% 130
50% 200

Mechanism of Action of H2O2


• The exact mechanism is not known. It includes oxygen releasing, mechanical cleansing
and oxidation/reduction (redox) reactions (Fig. 9.1).
• It differs according to type of discoloration and physical and chemical environment
present at the time of reaction.
• In redox reaction, the oxidizing agent (H2O2) has free radicals with unpaired electrons.
On giving them, it becomes reduced and reducing agent (tooth) accepts the electrons
and becomes oxidized.
• Depending upon condition, H2O2 is capable of releasing free radicals and
H2O2  H + OOH/H2O2  HO + OH
Perhydroxyl anions
H2O2  H+ + :OOH– or
A combination of both free radicals and anions
HOO + OH–  O2 + H2O in a basic solution
HOO  O2 + H+ in an acidic solution
50 Bleaching

These compounds are attracted towards the electron rich alkenes bonds

Form unstable epoxides

Essentials of Dentistry

Form alcohol

Double bond creates discoloration thus breaking them often eliminates discoloration.
• Moreover, H2O2 increases permeability of tooth and movement of ions through it. Initially,
highly pigmented carbon ring compounds are opened and converted into lighter colored

Fig. 9.1: Hydrogen peroxide bleaching


Bleaching 51

chains. These carbon double bonds, usually pigmented yellow are converted into
hydroxyl group which are colorless. “As these processes continue tooth continually
lightens”.
• The point at which only the hydrophilic colorless structure exists is called as “Saturation
point”. At this point optimal amount of bleaching has occurred.

Essentials of Dentistry
• Bleaching process must be stopped at this point as further bleaching leads to tooth
structure loss making tooth more porous and brittle.

Carbamide Peroxide
• Carbamide peroxide is available at concentration 3 to 15 percent but usually used at
a concentration of 10 to 15 percent.
• It breaks down into hydrogen peroxide. 10 percent Carbamide peroxide produces 3.6
percent hydrogen peroxide.
• Carbamide peroxide product contains either carbopol or glycerin base.

BLEACHING TECHNIQUES
Broadly divided into:
I. Nonvital bleaching:
Out office — Walking bleach using sodium perborate with either
30 percent H2O2 or distilled water
In office — Thermocatalytic bleaching
II. Vital bleaching:
Out office — Night guard vital bleaching (10-15% Carbamide peroxide)
In office — Using Superoxol
- Modified mc Inne’s solution
- 35 percent Carbamide peroxide gel

In Office Bleaching
Vital Bleaching
Step 1:
• Teeth must be cleaned of all surface stains and plaque. Isolate and protect the teeth
and mouth.
• Soft tissues can be protected by applying Vaseline or Oraseal (ultradent).
Step 2:
• Teeth to be bleached should be isolated with rubber dam. If floss is to be used as
ligature around the teeth, waxed floss is preferred as unwaxed floss may absorb the
hydrogen peroxide and burn the tissue.
• Prepare the tooth by cleaning with pumice.
Step 3:
• Some clinicians prefer to etch the severely stained tooth with 35 percent of phosphoric
acid for 5-7 seconds as it enhances the penetrability of bleaching solution and greatest
amount of immediate stain reduction can be made possible.
Step 4:
• Dry the teeth thoroughly and apply the 35 percent of hydrogen peroxide bleaching
solution such as superoxol with help of gauze piece.
Step 5:
• Bleaching can be done with heat, without heat or by dual application.
52 Bleaching

• In case of with heat, place the bleaching light at a distance of approximately 30cm
from the teeth to be bleached. Direct the light to the labial surface of teeth.
• Gradually increase the temperature by adjusting rheostat from 46°C (115°F) as long
as patient feels no sensitivity.
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• Temperature recommended for vital teeth bleaching varies from 46°C to 60°C.
Care must be taken to prevent the irreversible thermal damage to the teeth.
Patient’s comfort is used as a guide for adjusting the temperature. The thumb rule
is adjusting temperature at least 10 degree below the temperature at which patient
feels discomfort.
Step 6:
• Keep the teeth saturated with bleaching solution for 20 to 30 minutes.
Step 7:
• Flush the teeth with copious amount of warm water before removing the dam.
Step 8:
• In case of uneven discoloration, apply 35 percent hydrogen peroxide to the severely
stained areas of tooth and allow it to remain on tooth for 5–10 minutes. Enamel surface
can be disked with abrasive in case of severe staining.
Step 9:
• Polish the bleached teeth using the aluminum oxide abrasive disks and wheels (3M
soflex system, Shofu cosmetic contouring kit). If patient feels sensitivity than 1.1 percent
neutral sodium fluoride or desensitizing paste can be applied in between the
appointments.

Out Office Bleaching


Nonvital Bleaching
Step 1:
• Check the vitality of tooth with thermal or electric pulp testing. Sometimes the access
cavity preparation without anesthesia is used to determine the vital status of tooth.
If the tooth is previously endodontically treated, check the adequacy of obturation
and health of surrounding bone.
Step 2:
• Through prophylaxis of nonvital tooth and the adjacent healthy tooth helps in revealing
the true color of the tooth. Shade is recorded with the help of shade guide for future
reference.
Step 3:
• Isolate only the tooth to be bleached or the two adjacent teeth as well for comparison
of shade.
• Ligate the cervical region of tooth with floss to protect the gingival region and it also
permits the accurate observation of the critical cervical region of tooth during bleaching
process.
Step 4:
• Endodontic access cavity is prepared according to normal guidelines. And after the
obturation, the access cavity is thoroughly cleaned to remove the any remaining root
canal filling material and endodontic sealer.
• Place the barrier material either GI or Cavit against the gutta percha and condense
it thoroughly so that no voids remain in between them.
Bleaching 53

Step 5:
• Place the bleaching solution inside the prepared cavity. A cotton pellet saturated with
Superoxol or a syringe of 35 endodontic hydrogen peroxide is placed on to the labial
wall or in the pulp chamber.
• Thermocatalytically activate the bleaching solution with heated instrument. If free bleach

Essentials of Dentistry
liquid is present inside the prepared cavity, don’t use the heated pluggger as excess
temperature may make the solution to boil out of the access cavity (Fig. 9.2).
• Cotton saturated with the solution is pressed against the cavity wall with the help of
heated pluggger.
Step 6:
• Thermocatalytic and walking bleach may be used separately or in combination.
• At the end of heating, rinse the cavity thoroughly and place the walking bleach inside
the cavity.
• Solution used is a thick mix of sodium perborate and superoxol or sodium perborate
and water inside the cavity and press against the wall (Fig. 9.3).
• Evaluate after 3-7 days and repeat the procedure if necessary.
Step 7:
• Seal the access cavity with temporary and leave it for 2-7 days.
Step 8:
• When the desired results are achieved, remove the material from the access cavity
and restore the tooth with permanent filling material.

FACTORS AFFECTING BLEACHING


1. Surface debridement: Thorough scaling and polishing removes the superficial debris
and enhance the effectiveness.
2. Hydrogen peroxide concentration: The higher the concentration, greater the effect of
oxidation process. The highest concentration used is 35 percent. (Addition of gelling
agent reduces the concentration to 25 percent).

Fig. 9.2: Thermocatalytic bleach


Essentials of Dentistry 54 Bleaching

Fig. 9.3: Walking bleach

3. Temperature: Increase in temperature by 10°C doubles the rate of chemical reaction.


Generally, if the temperature is elevated to a point at which the patient doesn’t feel
discomfort, then the procedure is taking place at a safer temperature range.
4. pH: During the storage of hydrogen peroxide, the acidic pH must be maintained to
extend shelf life. The optimum pH of hydrogen peroxide to have its oxidation effect
is 9.5 to 10.8. This gives 50 percent greater results in the same amount of time compared
to lower pH.
5. Time: The effect of bleaching is directly related to time of exposure. Longer the exposure,
greater the color change.
6. Sealed environment: Placing the hydrogen peroxide into sealed environment increases
the bleaching efficacy.

DISADVANTAGES OF BLEACHING
1. The effect of bleaching on natural tooth is not permanent compared to crowns and
veneers which can be restored to their original shade by cleaning and polishing. This
is particularly significant when patient is unwilling to give up the stain promoting habits,
such as smoking or drinking excessive tea or coffee.
2. Many times, it requires two or three sessions more compared to instant veneering.
3. It is not effective for all forms of discolorations, such as banding seen in severe tetracycline
staining. The banding effect will remain, albeit somewhat lighter in color. Furthermore,
bleaching cannot totally correct opacity or white spots frequently seen in fluorosis.
4. Bleaching can be inappropriate or dangerous when the surface, thickness and health
of enamel has been compromised for any reason like microcracks permeating the deeper
penetration of stain or thinned enamel as seen in many systemic disorders and in older
age.
5. Bleaching is somewhat unpredictable to speculate the color change.
6. It can sometimes cause some low-grade reversible pulpal inflammation and may lead
to hard tooth structure damage.
Bleaching 55

7. Seepage of bleaching agent into the surrounding periodontal tissues can lead to gingival
irritation or severe damage.
8. Greatest potential hazard with nonvital bleaching procedure is cervical resorption of tooth.

Essentials of Dentistry
ADVANTAGES OF BLEACHING
1. The chief advantage is its minimal invasiveness, which requires no alteration of tooth
structure and absolute loss of enamel.
2. Relatively low cost compared to other esthetic treatments.
CHAPTER

10 Endodontic Hand
Instruments and
Instrumentation

CLASSIFICATIONS OF ENDODONTIC INSTRUMENTS


According to Function (by Grossman)
Instruments are divided into four groups.
1. Exploring Instruments
To locate the canal orifice or to assist in obtaining patency of the root canal.
– Smooth barbed broach
– DG-16 explorer.
2. Debriding Instruments
To extirpate the pulp and to remove debris and other foreign materials.
– Barbed broach.
3. Shaping Instruments
To shape root canal apically and laterally.
– Reamers
– Files.
4. Obturating Instruments
To pack gutta-percha into root canal.
– Plugger
– Spreaders
– Lentulo spirals.

Harty’s Classification
1. Instrument for access cavity preparation
– Basic instrument pack
– Burs
– Rubber dam.
2. Instruments for root canal preparation
– Hand instruments
– Power assisted root canal instruments
– Electronic canal measuring device
– Measuring instruments, gauges and stands
– Instruments for retrieving broken instruments and posts.
3. Instruments for filling root canals
– Lateral condensation
– Vertical condensation
– Hybrid technique
– Thermoplasticized gutta-percha.
Endodontic Hand Instruments and Instrumentation 57

4. Equipments for storing instruments


5. Sterilization of endodontic instruments
6. Equipments for improving visibility
7. References.

Essentials of Dentistry
ISO and FDI Classification
ISO and FDI grouped root canal instruments according to their method of use.
Group I Group II Group III Group IV
Hand operated Same as group I but the Similar to the Group II type Endodontic points
instrument handles are replaced by having a latch type
latch type of adaptor for attachment but they are
the insertion in the slow fabricated from a single piece
speed handpiece. of metal so latch, shank and
These instruments consist cutting edge are made of one
of 2 parts: piece.
– An operative cutting edge
– Latch type of attachment
E.g. Barbed Ni Ti rotary instruments E.g. Gates Glidden drills. E.g. GP points,
broaches, like profile, pro taper silver points,
K-file, H-file, paper points
Reamer,
pluggers.

Other Classification
1. Instruments used for initial examination
2. Instruments used for diagnosis
3. Instruments used for isolation
4. Instruments used for access cavity preparation
5. Instruments used for working length determination
6. Instruments used for canal preparation
7. Instruments used for irrigation
8. Instruments used for obturation
9. Instruments used for postspace preparation
10. Instruments used for retrieval of broken instrument/post/gutta percha
11. Instruments used for endodontic surgery.

STANDARDIZATION
In the past, instruments were not standardized as regards to the diameter, taper and length.
Later in 1957, INGLE and Le VINE gave the recommendations for having uniformity in
instrument diameter and taper, which were further developed by International Standards
Organization (ISO) (Fig. 10.1).
1. Instruments shall be numbered from 10-100. The numbers are advanced by 5 units
up to 60 and then by 10 up to 100.
2. Each number is the representative of the diameter of the instrument at the tip in the
100th of millimeter.
E.g. No.10 is 10/100 = 0.1 mm at tip.
3. The working blade (flute) should begin at the tip designated site D1 shall extend exactly
16 mm up to the shaft terminating at designated site D2 (D16).
Essentials of Dentistry 58 Endodontic Hand Instruments and Instrumentation

Fig. 10.1: Instrument standardization

Fig. 10.2: Modifications

There is constant increase in taper of 0.2 mm/mm, so the diameter at D2 is 0.32 mm


greater than that at D1.
E.g. For No. 20 reamer
D1 = Diameter at the tip = 0.2 mm
D2 = Diameter 16 mm away from tip (D1) = 0.32 + 0.20
= 0.52 mm
(Later on, they are made available in sizes 6,8,10 up to 150)

Other Specifications Added Later


After several years, the ISO committee made another change in standardization
nomenclature (Fig. 10.2).
• The name of the original point D1 (where the cutting flutes begin) is altered and given
a new identification, D0 (Fig. 10.3).
• Point D2 was given a new identity, D16 (where cutting flutes end).
• An additional diameter measurement point D3 is 3 mm from the tip of the cutting end
of instrument D0 (earlier D1).
• The tip angle of the instrument should be 75° + 15°.
• Size of the instrument should increase by 0.05 mm from No.10 to No. 60 and by 0.1
mm from No. 60 to No. 150.
• Instrument handles have been color coded for easier recognition.
• Color coding facilitates quick picking of instruments during treatments and thereby
saves time (Fig. 10.4).
• They are available in different lengths of 21, 25, 28 and 30 mm. Ordinarily 25 mm
instruments are used.
• Greater taper (0.04, 0.06, 0.08) are available.
21 mm For molars especially when patient cannot open wide
28-30 mm For cuspids and long anteriors
25 mm For anteriors
40 mm For endodontic implant
Endodontic Hand Instruments and Instrumentation 59

Essentials of Dentistry
Fig. 10.3: Comparison of original and present specifications

MATERIALS USED FOR MANUFACTURING INSTRUMENTS


Various materials are used for manufacturing the endodontic instruments depending on
the particular characteristic of the material.
Carbon steel is more brittle and less resistant to corrosion than stainless steel. Stainless
steel is more resistant to corrosion but looses sharpness faster than carbon steel. Nickel-
titanium instruments have superflexibility.
The traditional endodontic instruments made up of stainless steel sustain deformation
and retain permanent shape change. New generation endodontic instruments, made up
of nickel-titanium, have the property called, superelasticity. It allows instruments to return
to its original shape following significant deformation. Nickel-titanium files are more flexible
and better conform to canal curvature, resist fracture and wear less than stainless steel
files. They are biocompatible and extremely resistant to corrosion.
Carbon steel Stainless steel
Fe – 98% Fe – 81%
Composition C – 1-1.2% Cr – 18%
Mn – 0.2% C – 0.6-1%
Si – 0.2%
Corrosion resistance Very low High
Cutting efficiency High Low, so wears rapidly
Stiffer, stronger, harder but brittle. Less hard than carbon steel but
Physical properties
Less heat generation on cutting less brittle. More heat generation
Superior, at high speed and better Superior, at low speed and better
Efficiency
at cutting the enamel at cutting dentin

MANUFACTURING OF ENDODONTIC INSTRUMENTS


Instruments are prepared from round wire by modifying it to form tapered instruments
with cutting edges, of different shapes and sizes. There are two main techniques for
manufacturing these instruments.
Essentials of Dentistry 60 Endodontic Hand Instruments and Instrumentation

Fig. 10.4: Color coding

• By grinding and twisting the metal shaft’s long axis:


The raw metal is ground into tapered blanks and then it is twisted counterclockwise
to form the desired instrument (Fig. 10.5).
K-files
Reamers
K-flexo
Flexo
• By machining the instruments (cutting a solid round metal rod) on lathe machine.
H-file
Flex-R
Uni files
(  —more resistant to fracture, —increased cutting efficiency)

FEATURES OF ENDODONTIC INSTRUMENTS


Cutting Blade
Portion of the file behind the tip (0.16 mm in length) that removes dentin is called cutting
blade.
Endodontic Hand Instruments and Instrumentation 61

Essentials of Dentistry
Fig. 10.5: Cross-sections of instruments

Taper
2° 0.02 mm increase in diameter/mm
4° 0.04 mm increase in diameter/mm
6° 0.06 mm increase in diameter/mm

Rake Angle
More acute the rake angle, the sharper the blade.
• Positive rake angle: Blade turns in the same direction of force applied to the surface
being cut.
• Neutral: Blade is 90° to the surface.
• Negative rake angle:
– Blade is turned opposite to the surface being cut.
– Standard instruments have negative rake angles.
– Such instruments require more energy to cut and they are less efficient.

Instrument Tips
• Cutting tip
• Modified tip (Safe cutting tip)
• Canal master tip (Noncutting tip or Batt tip)
• Precision cutting tip.

BARBED BROACH
Barbed broach is one of the oldest root canal instruments. However, because of its ease
of breakage, it is confined to removal of soft tissues only. It is a short handled instrument
meant for single use. It is made from soft steel wire, and barbs are formed by cutting
into metal and notching the cut portion away from the shaft (Fig. 10.6). It is used in the
straight portion of the canal. Working portion is 10 mm in length.

Methods of Use
• It should be used with caution as it is a fragile instrument.
• It is loose within the canal and engages soft tissues only just short of the apical foramen.
• It is rotated 360° to engage pulp and then withdrawn.
• If the tissue is not removed, the broach is lightly scrubbed along the wall from the
apex outwards.
• When the instrument is forced apically within a tightly fitting canal, the barb is bent
towards the shaft allowing deeper insertion of the instrument. While removing the
instrument from the canal, barb is wedged against the wall of the canal and the sharp
barb tips dig into the canal wall and fracture the shaft.
Essentials of Dentistry 62 Endodontic Hand Instruments and Instrumentation

Fig. 10.6: Barbed broach

Use
Broaches should not be used until the canal is wide enough for insertion, and without
digging the dentin. Care should be taken to use the barbed broach in the narrow buccal
canals of maxillary molars and the mesial canals of maxillary molars.
• Vital pulp extirpation and removal of necrotic debris.
• Retrieval of paper points and cotton dressing from within the root canal.
Broaches are available in different sizes.

0 xxxxf no. 10 Purple


1 xxxf no. 15 White
2 xxf no. 20 Yellow
3 xf no. 25 Red
4 f no. 30 Blue
5 m no. 35 Green
6 st no. 40 Black

RASP
• It is similar to barbed broach except in taper and barb size.
• It has shallower and more rounded barbs.
• They are used to remove the pulpal tissue from the canal.

Broaches Rasps
Barb height • 1/2 tip diameter • 1/3 tip diameter·
• Barbs are derived from core, making • Not as weak as barbed broach
itweaker instrument
Taper 0.007 to 0.010 mm per mm of length 0.015/0.020 mm per mm of length
Numbers of barbs Average 40 Average 50–60

REAMERS
Reamers are K-type instruments which are used to ream the canal. They are symbolized
by .
Endodontic Hand Instruments and Instrumentation 63

Features
• Reamers have fewer blades than K-files. Cutting blades are 1/2 to 1 per mm while
in file, it is 1 1/2 to 2 per mm (Fig. 10.7).
• Angle of blank is 60° creating a sharp knife like edge to shave the canal. Three 60°

Essentials of Dentistry
angles provide superior cutting efficiency.
• Triangular cross section shows less resistance to bending, are more flexible, and there
is less risk to torsional fracture than those made from square blank.
• They are manufactured by twisting triangular blanks and are triangular in cross section
(Fig. 10.8).
• Basic action: Insert into the canal, turn 1/4 to 1/2 clockwise in order that the blades
engage into the dentin and then pull so that the dentin chips from the root canal.
(Insertion-rotation-retraction)
• Reaming is the only action to produce a round, tapered preparation, when used in
straight canals.
• Hand operated instruments are known as type K reamers.
• It is used with pushing rotating motion.
• Engine reamers do not readily follow the course of curved canal and may perforate
the root canal. They are likely to break.
• Angle of blade to the long axis of K-reamer is about 10–30°. Hence, these instruments
are primarily designed to be used in rotary reaming motion.
• Reamers tend to remain self-centered in the canal resulting in less chances of canal
transportation.

Uses
• To enlarge and shape the irregular shapes of root canal into a cavity of rounded cross-
section.
• Cleaning and shaping of root canal during Schilder’s method.
• Though reamer has fewer numbers of flutes than file; cutting efficiency is less than that
of file. More space between flutes provides more room for better removal of debris. They
are used to remove the intracanal debris and old gutta-percha fillings from the canal.

Fig. 10.7: Reamer

Fig. 10.8: Cross-section of reamer


64 Endodontic Hand Instruments and Instrumentation

FILES (FIG. 10.9)


Files are used for cleaning and shaping of the canal by machining the dentin. Various
types of root canal files are;
• K-files
Essentials of Dentistry

• K-flex
• Flexo file
• Flex-R
• Headstrom and safety headstrom
• S-file.
Files are predominantly used with filing or rasping action in which there is little or no
rotation in the canals. After insertion into the canal, it is pressed against the canal wall
and the instrument is then withdrawn while maintaining the pressure. The major effectiveness
of hard tissue removal by filing is in outstroke or withdrawal of the instrument by dragging
the flutes on the dentin wall.

Fig. 10.9: Basic design of file

K-FILE
First manufactured by “KERR MANUFACTURING COMPANY” in 1904, and so it is named
as K-files (Fig. 10.10).

Features
• K-file is square in cross-section. Tighter twisting of file spirals increases the number
of flutes in file (Fig. 10.11).
• 1 1/2 to 2 1/2 cutting blades per mm of their working end.
• The tip is cutting and pyramidal in shape.
• The angle of the flutes to long axis is about 25-40°.
• It is placed into canal at desired length, pressure is exerted against the wall and it
is withdrawn from canal without turning. It is used with rasping and pulling motion.
• This is the first instrument used to extirpate the pulp and shape the canal.

Cutting Flutes (Figs 10.12 and 10.13)

Files 1.5 to 2.5 per mm


Reamer 0.5 to 1 per mm

Modifications
K-flex file
Flex R-file
K-flexofile
Flexicut.
Endodontic Hand Instruments and Instrumentation 65

Essentials of Dentistry
Fig. 10.10: K-file

Fig. 10.11: K-file

Fig. 10.12: Reamer (microscopic view)


Essentials of Dentistry 66 Endodontic Hand Instruments and Instrumentation

A B
Figs 10.13A and B: (A) K-file (left), reamer (right) (B) Files of different sizes

K-FLEX FILE (D-TYPE FILE)


• K-flex file was introduced by Kerr manufacturing company in 1982. The main purpose
of developing this file is to increase the flexibility and cutting efficiency while maintaining
the shape of canals, especially curved canals.
• They are rhomboid or diamond shaped in cross-section. Angle at the tip is 25°-50°.
It is fabricated from V-4 steel and made from stainless steel by twisting / cross section.
• It has series of cutting flutes with alternate sharp (<60°) and obtuse noncutting edges.
The two acute angles which increase the sharpness and two obtuse angles give more
room for efficient removal of debris and also decrease the contact of instrument with
canal walls.
• It has greater cutting efficiency, increased flexibility and, because of increased space
between the working edges acting as a reservoir, it has increased ability to remove debris.

FLEXO FILE
• Flexo file was first manufactured by “MAILLEFER”. It is made up of stainless steel.
• It is same as K-File except that it has triangular cross section. This triangular cross
section gives sharper cutting blades and more room for debris than K-FILE.
• Its extremely flexibility helps in resisting fracture. It has noncutting tip (butt).

FLEX-R FILE
Flex-R file was developed in 1985 by Roane’s for use in the “BALANCED FORCE
TECHNIQUE”.
• The file is made by removing sharp cutting surface at the tip of cutting edge so the
tip rides along the canal rather than the gauge (stuck) into it. This design eliminates
the possibility of ledge (block) formation or canal transportation.
• Triangular in cross section. Flutes are sharper with less negative rake angle.
Endodontic Hand Instruments and Instrumentation 67

• Clockwise rotation with anticlockwise rotation and apical pressure create less canal
blockage and less extruded apical debris than step back technique.
• It is mainly advocated for curved canals.

Essentials of Dentistry
H-FILE (HEDSTROM FILE)
• Hedstrom file is manufactured from round wire that is machined to produce spiral flutes
resembling a series of intersecting cones. It resembles Wood screw or the Christmas
tree (Fig. 10.14).
• It is manufactured by cutting spiral grooves into round, tapered steel wire to produce
sharp cutting edges which cuts only on pulling strokes (retraction) (Fig. 10.15).
• It has elevated cutting edges which face towards the handle. They are larger from tip
towards handle and they cut on withdrawal stroke only.
• Highest cutting efficiency due to positive rake angle. Cutting edges are turned in the
same direction of applied force so they are very aggressive in cutting.
• The angle between the cutting edges and the long axis of the instrument is about 60-
65°. Thus, they are designed primarily for a linear filling motion (Figs 10.16 and 10.17).

Other Uses
• It is primarily used to clean and shape the coronal half of canal. It is quite effective
in irregular canals (immature teeth) and harbors debris.
• Hedstrom files are strong, aggressive cutters, and as they lack flexibility and are fragile
in nature. They are used to machine straight canals or coronal portion of curved canals.
• They are used to flare the canal orifices.
• They are used to remove broken instruments, gutta percha and silver points. The file
is placed alongside the material to be removed, then rotated, and pulled towards the
occlusal surface.

Drawbacks
• Weak due to smaller shaft diameter and prone to breakage on torquing motion.
Furthermore, it is almost impossible to remove the fractured file from the root once

Fig. 10.14: H-file

Fig. 10.15: H-file


Essentials of Dentistry 68 Endodontic Hand Instruments and Instrumentation

Fig. 10.16: H-file

Fig. 10.17: H-file

it is locked in the dentin. It can be withdrawn only by backing off until the flutes are
free.
• Screw like configuration further drives the instrument apically and cracks the weakened
or stressed root on clockwise rotation.

Modifications
Unifile/ Dynatrak
S-file
Safety H-file.
Endodontic Hand Instruments and Instrumentation 69

UNI FILE
Mc-spadden modified the traditional hedstrom file, which were marketed as Burns unifile.
• Unifiles are manufactured by cutting superficial grooves to produces a file in a double
helix design.

Essentials of Dentistry
• Blades present an S-shaped or double helix design rather than the single helix teardrop
shape of hedstrom file.
• Unifile has 2 continuous cutting edges.
• Uniform depth of flutes renders the tip more flexible. It is stiff in coronal and middle
thirds but bends at apical thirds to form noncutting tip.
• It can be used in both filling and reaming actions hence referred to as “universal file”.
• It is less effective in cutting but less subjected to fracture.

S-FILE
• S-file was developed in Sweden. It is machined from solid piece of wire to produce
a sharp, double, cutting edge forming double helix design. They are stiffer than H files.
• It is “S” shaped in cross section and has 90° cutting tip. It is available in size of 5
to 40.
• S-file has good cutting efficiency in both filing and reaming actions and thus it is also
classified as hybrid design.
• Angle of flute is constant and flute depth increases from tip to handle.
• Its noncutting sides with smoothened edges prevent ledging in curved canal.
• Millimeter scale is etched on the shaft of the file for length control.

SAFETY HEDSTROM FILE


• Kerr manufacturing co. introduced these files in 1998.
• It has a noncutting safety side along the length of blade which reduces the potential
for strip perforation.
• Noncutting side is oriented to the side of the canal where cutting is not desired. It
is indicated by a flattened side of handle (Fig. 10.18).

Fig. 10.18: Safety hedstrom file

• It is used with traditional vertical filling technique. When used in a linear filing motion,
it helps to prepare curved canals without ledging the outer wall.
CHAPTER Hand Instruments in
Conservative Dentistry and
11 Some Considerations for
Viva Voce

BASIC CLASSIFICATION OF DENTAL INSTRUMENTS


Dental instruments are classified in many ways, including by the number of working ends,
by function, by manufacturer’s name and number, and by Black’s number formula.

Number of Working Ends


According to the number of working ends, instruments can be divided into two categories;
single-ended and double-ended instruments. Single-ended instruments have only one
working end and long handles. Double-ended instruments have two working ends in the
following combinations.
• The two ends have similar functions, but one end is larger than the other (difference
in size).
• The two ends are paired right and left for preparing the right or the left side of the
cavity preparation (for example, gingival marginal trimmer).
• The two ends have a combination function in which the ends are used for the same
procedure but each end has a different use (for example, plastic filling instrument).

Instruments Classified by Function


Instruments are classified by function. Operative hand instruments are categorized as cutting
and noncutting. Other instruments are classified according to a specialty, use with a specific
material, or a procedure.

Manufacturer’s Number
The manufacturer’s number is written on the handle of the instrument. This number, used
for ordering the instrument, indicates the instrument’s placement in a set of instruments.
Some instruments are named or classified by the name of the individual who designed
the instrument.

Black’s Formula
GV Black developed the formula for standardizing the exact size and angulation of an
instrument. This formula minimizes discrepancies in the production of instruments from
one manufacturer to other and simplifies the ordering of these instruments.
Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce 71

DENTAL INSTRUMENTS CAN BE GROSSLY DIVIDED INTO FOLLOWING


TWO CATEGORIES
Cutting Instruments
Hand cutting instruments are used to assist in the design of the cavity preparation. They

Essentials of Dentistry
define and redefine the cavity walls and margins. There are six main hand cutting
instruments; chisels hatchets, hoes, gingival margin trimmers, angle formers and
excavators.
Hand Rotary
Hatchets Burs
Chisels Stones
Hoe Disks
Excavators Others
Others

Noncutting Instruments
Noncutting instruments include the basic examination instruments and the instruments
used to insert and finish amalgam and composite restorative materials. They can be
categorized as follow;
1. Condensing instruments:
Pluggers—Hand, Mechanical.
2. Plastic instruments:
• Spatulas
• Carvers
• Burnishers
• Packing instruments
3. Finishing and polishing instruments:
Hand Rotary
Hand held wooden stick Finishing burs
Polishing points Mounted stones
Finishing strips Rubber cups
Integrated disks
Wheels

4. Isolation instruments:
• Rubber dam kit
• Salivary ejectors
• Cotton roll holders
• Evacuating tips.
5. Miscellaneous instruments:
• Mouth mirror
• Explorers
• Probes
• Tweezers
• Pliers.
72 Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce

INSTRUMENT NOMENCLATURE
GV Black categorises the operative hand instruments as below:
1. Order: It indicates purpose of instrument (scaler, excavator)
2. Suborder: It indicates position or manner of use (push, pull)
Essentials of Dentistry

3. Class: It indicates form of working end (hatchet, chisel)


4. Subclass: It indicates shape of shank (monoangle, biangle)

INSTRUMENT FORMULA
GV Black gave the formula describing dimension and angulations of the hand instruments.
The formula consists of four units.

1st figure Width of blade in 10th of millimeter


2nd figure Angle between the cutting edge and the long axis of the handle (Primary cutting
edge angle). It is always greater than 50°
3rd figure Length of blade in millimeter
4th figure Angle which the blade forms with the axis of handle. It is expressed in 100th of
a circle or centigrade. It is always less than 50°

E.g. 10 – 80 – 10 – 12 indicates,
10 Blade width in 10th of 1 mm (10/10 = 1 mm)
80 Cutting edge angle in hundredths of circle
10 Length of blade in mm (8 mm)
12 Blade angle in centigrade

The basic formula was consisting of three units only. The second figure was added
later on. These three basic measurements are sufficient to indicate the majority of operative
instruments. However, the instruments with cutting edge and with angle other than the
angle of blade to long axis, requires a fourth unit. So it was added to the second place
on the basic formula.

EXPLORING INSTRUMENTS
Mouth Mirror
This instrument is used to reflect light onto the field of operation, to view the cavity indirectly,
and to retract the cheek or tongue, as necessary. It consists of stainless steel handle with
a round mirror which is angulated/straight to handle.

Types
A. Based on material:
• Stainless steel
• Plastic (Plastic mirrors are disposable).
B. Based on size:
• No. 3, No. 4, No. 5 (most commonly used are no. 4 and no. 5)
C. Based on reflecting surface of the mirror:
• Flat (plane, regular) surface mirrors
They have reflective surfaces (silver coating) on the back of the glass. This gives
the image- “a ghost image”; it reflects only once to give a clear view free of distortion.
Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce 73

• Concave
They magnify the image.
• Front surface mirrors
They have reflective coatings (rhodium) on top of the glass. This coating eliminates
the “ghost image”; it reflects only once to give a clear view free of distortion.

Essentials of Dentistry
D. One-sided, double-sided:
In double-sided mirror, one side is used to reflect the cheek or lips and the back
side provides illumination. Concave mirrors provide enlarged view of the sight but may
be misleading if the clinician is not well oriented with the amount of enlargement of view.

Uses
• For illumination
• For retraction and protection of soft tissue
• For percussion of tooth
• To check tooth mobility
• For indirect vision.

Explorer
Explorers are single-ended or double-ended instruments. The working end is a thin, sharp
point of flexible steel. This allows the operator to examine surface of the teeth to detect
any irregularities and hardness. It is used to identify where soft carious dentine is present.
There is a variety of angles of explorers, and often the ends are different so the operator
can access various areas of mouth. Several common shapes include the pig tail, the
shepherd’s hook, the right angle and the #17.
Care should be taken not to poke the explorer point into very small carious lesions.
This may destroy the tooth surface and the caries arrestment process. Also, do not probe
into deep cavities where you might damage or expose the pulp.

Parts
Handle, shank, tip.

Types

Straight Right angle Arch explorer Interproximal explorer


Shank is straight Shank is at right angle Shank is curved in a Shank has angle, and
except for a single to the tip. semi circular shape like the tip is pointed
curvature near the an arch, and the towards handle.
explorer tip. exploring tip, at right
angle to handle.
E.g. Shepherd’s hook
explorer

Uses
• For diagnosing carious lesion
• For detecting plaque and calculus
• For checking furcation involvement
• For percussion of tooth
• For checking overhanging restoration
• For checking smoothness of walls and floors.
74 Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce

Cotton Pliers (Tweezers)


Cotton pliers have got narrow and angulated working end. They may have serrations on
the inner aspect of the beaks for better holding of material. These instruments are used
for carrying cotton wool rolls, cotton wool pellets, wedges and articulation paper from
Essentials of Dentistry

the tray to the mouth and back. They are available in locking handles, and the tips may
be straight or angled.

Types
A. Locking and non-locking
B. Working ends can be:
– Straight/curved
– Serrated/smooth

Uses:
• To carry and hold the cotton rolls, thus aid in isolation.
• To remove any broken fragment of tooth or material from the mouth.
• To make cotton rolls.

INSTRUMENTS FOR TOOTH STRUCTURE REMOVAL


They are of three types:
1. Hand cutting and rotary instruments
2. Abrasive instruments
3. Ultrasonic instruments.

RESTORATIVE INSTRUMENTS
Mixing Instruments
Spatula
It is used for mixing of restorative materials. Some of these spatulas can cause discoloration
of the material being mixed. The selection of a mixing spatula is not critical except when
preparing a permanent anterior composite restoration. Some composite restoration material
discolors easily, so use the spatulas provided by the manufacturer when working with it.
They have flat, wide nibs with blunt edges and straight shank. They are available in
different sizes and stiffness. They are made up of stainless steel or plastic.

Plastic Filling Instruments


Plastic filling instruments are used to place and condense pliable restorative materials
and to place cement bases in the cavity preparation. It is also called as cement carrier.
They are made up of stainless steel, ivory or plastic, and are usually double ended.
They have flat sides with blunt corners. They may have Teflon coating to minimize adhesion
and facilitate easy cleaning.
Plugger end: This end is flat, round and nonserrated, and looks like smooth condenser.
Paddle end: It is flat and elongated.

Uses
Paddle end: To carry and handle materials after mixing while material is in plastic/
sticky stage.
Plugger end: To condense the material into prepared cavity.
Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce 75

Condensing Instruments
• They have hammer-like working end, which is large enough to compress the soft
amalgam without sinking into it. The working end of condenser is called “face”, and
the blade is called “nib”.

Essentials of Dentistry
• They are available in different shapes, shank angles and curvatures.
• They may be single-ended or double-ended. Double-ended instruments have one end
smaller and other larger.
• Amalgam condensers are often called “pluggers”.

Types
According to shape:
• Round
• Triangular
• Parallalogram.
According to basis of surface:
• Smooth surface for amalgam
• Serrated surface for gold.

Uses
• For condensing restorative materials
• For root canal obturation with hot gutta percha.

Burnishers
Burnishers are the instruments with smooth-faced nibs, and with different angulations and
curvature of shank.

Shapes
• Ball-shaped
• Egg-shaped
• Apple-shaped
• Beaver tail-shaped
• Conical
• Fish tail-shaped
• Bullet-shaped.

Uses
• For initial carving of amalgam.
• To burnish the amalgam before and after condensing so as to adapt amalgam to the
margins of restorations, reducing chances of leakage and deficient margins (Pre-carve
and postcarve burnishing).
• To contour the matrix band according to contour of tooth.

Carvers
Carvers are usually double-ended instruments and are available in different sizes.

Shapes
Working end is of different shapes.
• Flat (hollenback carver)
• Discoid (disc shape)
76 Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce

• Cleoid (pointed like claw of bird toe)


• Diamond.

Uses
Essentials of Dentistry

They are used for carving of amalgam restoration. The sharp end is used for carving the
occlusal anatomy like grooves and marginal ridge. Operator preference and shape of
restoration will dicate which carver is required.

HAND INSTRUMENTS
They are classified as:
A. Excavators
B. Chisels
C. Other cutting instruments.
Excavators

Excavators
Hatchet Hoe Angle former Spoon excavators

A dental hatchet resembles a Dental hoes look like a miniature It is a four numbered instrument The spoon excavator is modified
camper’s hatchet, except garden hoe. in which cutting edge is at an hatchet. It is a double-ended
much smaller. angle to the blade. It is instrument with a spoon, claw, or
combination of GMT and chisel disk-shaped blade. Spoon

General
because it encompasses the excavators are used primarily to
advantages of both. remove debris from tooth cavities.

– Hatchet blades are set at – Hoe blades are set at a 45- – It is a special type of – It has bin-angled or triple
45-90° angles from the to 90-degree angle from excavator with a bevel of angled shank for improved
shank. These instruments their handle. (Hoe is the 80° to the shaft which forms accessibility.
have different lengths and chisel with angle of blade an acute angle with the long – Their tips and sides are
widths of blades. greater than 12.5°) axis of the blade. designed for cutting action.
– The width of the blade of – It can be mesially beveled – Available as right and left The most common sizes
the instrument is (Edge is beveled towards sided instrument; single- or are the small and the large
approximately 1 mm. An the shaft) or distally beveled double-ended. spoon excavators.
example is the Ash 10-6-12. (Edge is beveled away from – Paired instrument with

Design
– The cutting edge and long the shaft) blade curved to right and
axis of the handle are in – Cutting edge is left.
the same plane. perpendicular to the long – Direction of curve of blade
– It may be single-ended or axis of tooth. makes it lateral cutting
double-ended. instrument.
– Circumferential bevel is
sharpened to thin edge.
– Cutting edge is ground to
semicircular shape.
Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce
77

Contd...

Essentials of Dentistry
Essentials of Dentistry

Contd...
They are of three sizes:
Small:
– The diameter of the spoon
is about 1 mm.
– An example is the Ash 153-
154. It is for use in small
cavities and for excavating
the caries. As the neck of the
instrument is rather fragile, it
can break if too much force
is applied whilst excavating.
Medium:
– The diameter of the spoon
is about 1.5 mm.
– An example is the Ash 131-
132. It is mainly used for

Sizes
removal of soft caries from
larger cavities. The rounded
surface of the spoon can
also be used to push mixed
restorative material into small
cavities.
Large:
– The diameter is about 2 mm.
– An example is the Ash 127-
128. This instrument can be
used in large cavities and for
removing of excess glass-
ionomer material from the
restoration.
78 Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce

– It has enlarged working


blade.
Contd...
Contd...

Discoid
– Circular disk-like shape.
– Circular blade placed at an
angle to shaft.
– Cutting edge extends all
around the periphery except

Shapes
where it joins to shank.
Cleoid
– Blades resemble claw of bird
– It is used with push – pull – They are used with a – It works in three motions: – Right/left lateral motion
motion. pulling motion to smooth Vertical, push, pull
– Right-sided instrument is and shape the floor and
moved from left to right

Motion
sides of cavity
and left sided instrument preparations.
is moved from right to left.
– Hatchets are used on the – Planning the prepared – To accentuate the internal – To remove caries
wall of the cavity preparation walls and forming line line and point angles of the – To carve amalgam and wax
to cleave enamel and to cut angles. pattern
cavity preparation
dentin to prepare a sharp
– Sharpening and defining (especially for cavity – To remove the temporary
cavity outline.
of the line angles. preparation for gold crowns
– This instrument is used
– Delicate cutting during the restoration) – To remove the temporary
for widening the entrance
to the cavity, for slicing gold restoration preparation – To create retention form in cements

Uses
away thin unsupported especially class III and V dentin
and carious enamel, left preparations.
after carious dentin has
been removed.
– It can be used to prepare
retentive undercuts in the
anterior teeth cavity
Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce

preparation.
79

Essentials of Dentistry
80 Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce

Chisels
Chisels are designed after ordinary carpenter’s tool and used to cut tooth structure. It
is beveled on one side and, usually, double-ended; one end with standard bevel on blade
and the other end with a reverse bevel.
Essentials of Dentistry

Uses
Chisels are used to cleave (split) tooth enamel, to smooth cavity walls, and to sharpen
cavity preparations.

Types
• Straight
• Mono angle
• Biangle—Cleave/split the undermined enamel
• Triple angle—To flatten the pulpal wall

Chisels
Straight Bi-angle Wedelstaedt

• Shank and blade are in • Shank has two • Unlike the straight chisel,
the same plane. angulations so called the blade is curved in
• Cutting edge is on one bin-angled chisel. relation to shank.
Design

side only with bevel of • Single bevel cutting • Usually it is available as


the blade at right angle edge: Mesial or distal a double-ended
to the shaft. • May be single- or double- instrument.
• Usually available as ended instrument • Cutting edge has single
single-ended instrument. bevel: Mesial or distal
It can be used in five • Mesially beveled instrument is used with push motion
Motion

different movements: • Distally beveled instrument is used with pull motion


Vertical, push, pull, right, left
• Used to cut enamel and • Used to clave and spit • To clave and plan
Use

dentin margins the undermined enamel enamel in the cavity


• To plan the walls of the • To cut and plane enamel preparation
cavity preparation in cavity preparation

Enamel Hatchet
Enamel hatchet is similar in design to the ordinary hatchet but the blades are larger and
heavier. It is a one-sided instrument. It is used to split undermined enamel in buccal and
lingual proximal walls and for placing grooves. Right-sided instrument is identified by ring
on shank.

Gingival Marginal Trimmers


• The gingival margin trimmers (GMTs) are modified hatchets that have working ends
with opposite curvatures and bevels.
• It is a four numbered instrument with the cutting edge at right angle to the blade and
the long axis of the handle. The blade has a curvature.
Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce 81

Uses
• It is primarily used with lateral cutting motion as the cutting edge is in a plane other
than that of shaft.
• GMTs are used to trim, to smoothen and to shape the gingival floor of a cavity preparation.

Essentials of Dentistry
• GMTs are available in double-ended styles and are used in pairs, such as the #26
and #27. This is because the working ends of the even-numbered instruments are
designed for use on the distal surfaces, and the odd numbered are used on the mesial
surfaces.
• It is also used for beveling and rounding of the axiopulpal line angle.

Number

90 to 100 To bevel distal margin


85 to 75 To bevel mesial margin
100, 75 For inlay/onlay
90, 85 For amalgam preparations

Other Cutting Instruments

Instruments
Others Feature Uses
Known as finishing knives or amalgam For trimming excess filling material
Knives or gold knives on gingival, facial and lingual
margins of a proximal restoration.
The teeth of the instruments are so To trim excess filling material,
Files positioned that it can be used in both particularly on gingival margin
push-pull motion
Discoid-cleoid The working ends of the instrument are – For carving occlusal anatomy
instruments larger than the discoid or cleoid excavators. – To burnish inlay-onlay margin

CONSIDERATIONS FOR OPERATIVE DENTISTRY AND ENDODONTIA


VIVA VOCE
• Mercury-free alloys: These are Gallium-indium alloys. They are made up of Ag-Sn
particles in Gallium-indium liquid. Ga-In substitutes for the Hg in dental amalgams.
Gallium melts at 28°C and can be used to produce liquid alloys at room temperature.
Disadvantages
– Surface roughness
– Marginal discoloration
– Tooth fracture due to expansion
– Difficult manipulation.
• If the adjacent proximal boxes are of different sizes, prepare the larger first so that
the preparation for the smaller can be kept more conservative, and conversely restore
the smaller first and the larger, last.
• Bevels
Single beveled instruments. It has bevel on only one side.
E.g. Enamel hatchet, GMT
82 Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce

Bibevelled instruments
It has beveling on both sides.
E.g. Ordinary hatchet, Osteotome
To determine whether the instrument has right or left bevel, the primary cutting edge is held down
Essentials of Dentistry

and pointing away, and if the bevel appears on right side then it is the right instrument of the pair.

Mesial bevel can be determined by observing the inside of the blade curvature.
If the primary bevel is visible, it is the mesial bevel. If primary bevel is not visible, it
is a distal bevel.
• Sharpness of the instrument can be tested by resting the cutting edge on a hard plastic
surface. If the cutting edge digs over the surface, the instrument is sharp. If it slides,
then the instrument is dull.
In other method, observe the primary cutting edge under the light. If the light reflects,
it indicates a blunt edge. Sharp edges don’t reflect the light.
• Number of blades:
1. Number of blades is always even.
2. Excavating burs have 6-10 blades.
3. Finishing and polishing burs have 12-40 blades.
4. Greater the number of blades, smoother will be the cutting at slow speed.
• Steel burs are mainly used for finishing procedures.
• Cross cuts are needed on fissure burs to obtain adequate cutting efficiency, even at
low speeds. They are not used at high speeds as they tend to produce an unduly
rough surface.
• Vibrations above 1300 rpm are imperceptible to the patients, so sensations are lost
at high speed range.
• Temperature during cavity preparation should not exceed 130°F or 60°C. When using
high speed, low pressure and water coolant should be used to prevent overheating.
• Pressure is directly proportional to heat generated. Whenever rpm is increased, pressure
has to be reduced. It should not exceed 4 ounces when using high speeds, and not
more than 12 ounces, when using low speeds.
• Noise level more than 75db causes hearing damage.
• Glass ionomer bonds best to enamel than dentin and cementum.

Classifications of GIC
According to use by manufacturer:

Type I Luting cement


Type II Restorative cement
Type III Liner and bases
Type IV Fissure sealant cement
Type V Orthodontic cement
Type VI Core build up cement
Type VII For geriatric and pediatric patients
Type VIII Esthetic restoration of anterior teeth
Type IX Posterior packable GIC
Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce 83

According to Application

Type I Luting cement


Type II Restorative cement
Type III Lining cement

Essentials of Dentistry
Type IV Fissure sealant
Type V Orthodontic cement

According to Wilson and McLean (1988)


Type I Luting cement
Type II Restorative cement
a. Restorative esthetic
b. Restorative reinforced

Latest Classification
Traditional glass ionomer Type I – Luting cement
Type II – Restorative cement
Type III – Liners and base
Metal modified glass a. Miracle mix
ionomer b. Cermet
Light cure glass ionomer Hydroxy Ethyl Methacrylate is added to liquid
Hybrid glass ionomer/ a. Composite resin in which filers substituted with glass ionomer
resin modified glass particles
ionomer b. Precured glasses blended into composites

CLINICAL CLASSIFICATION OF TRAUMATIC DENTAL INJURIES


INCLUDING CODES OF WHO INTERNATIONAL CLASSIFICATION
(a) Injuries to the hard dental tissues and the pulp
Code Injury Criteria
N 502.50 Enamel infarction An incomplete fracture (crack) of enamel without
loss of tooth substance
N 502.50 Enamel fracture A fracture with loss of tooth substance confined
(Uncomplicated crown fracture) to the enamel
(Fig. 11.1A)
N 502.51 Enamel-dentin fracture A fracture with loss of tooth substance confined to
(Uncomplicated crown fracture) enamel and dentin, but not involving the pulp
(Fig. 11.1B)
N 502.52 Complicated crown fracture A fracture involving enamel, dentin, and exposing
(Fig. 11.1C) pulp
N 502.54 Uncomplicated crown-root fracture A fracture involving enamel, dentin, and cementum
(Fig. 11.1D) but not exposing pulp
N 502.54 Complicated crown-root fracture A fracture involving enamel, dentin, and exposing
(Fig. 11.1E) pulp
N 502.53 Root fracture A fracture involving dentin, cementum and pulp.
(Fig. 11.1F) Root fractures can be further classified according
to displacement of the coronal fragments.
84 Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce

(b) Injuries to the periodontal tissues


Code Injury Criteria
N 503.20 Concussion An injury to the tooth-supporting structures
(Fig. 11.2A) without loosening or displacement of tooth, but
Essentials of Dentistry

with marker reaction to percussion


N 503.20 Subluxation (loosening) An injury to the tooth-supporting structures with
(Fig. 11.2B) abnormal loosening, but without displacement
of the tooth
N 503.20 Extrusive luxation (peripheral Partial displacement of the tooth out of its socket
dislocation, partial avulsion)
(Fig. 11.2C)
N 503.20 Lateral luxation Displacement of the tooth in a direction other than
(Fig. 11.2D) axially. This is accompanied by comminution or
fracture of the alveolar socket.
N 503.21 Intrusive luxation Displacement of the tooth into the alveolar bone.
(central dislocation) This injury is accompanied by comminution or
(Fig. 11.2E) fracture of the alveolar socket.
N 503.22 Avulsion (exarticulation) Complete displacement of the tooth out of its
(Fig. 11.2F) socket

(c) Injuries to the supporting bones


Code Injury Criteria
N 502.40 Comminution of the maxillary Crushing and compression of the alveolar
alveolar socket socket. This condition is found concomitantly
with intrusive and lateral luxation (Fig. 11.3A)
N 502.60 Comminution of the mandibular
alveolar socket
N 502.40 Fracture of the maxillary alveolar A fracture is confined to facial or oral socket wall
socket wall (Fig. 11.3B)
N 502.60 Fracture of the mandibular alveolar
socket wall
N 502.40 Fracture of the maxillary alveolar A fracture of the alveolar process which may or
process may not involve the alveolar socket
N 502.60 Fracture of the mandibular alveolar (Figs 11.3C and D)
process
N 502.42 Fracture of maxilla A fracture involving the base of maxilla or
mandible and often the alveolar process (jaw
N 502.61 Fracture of mandible fracture). The fracture may or may not involve
the alveolar socket (Fig. 11.3E and F)
Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce 85

(d) Injuries to gingiva or oral mucosa


Code Injury Criteria
S 01.50 Laceration of gingiva or oral A shallow or deep wound in mucosa resulting
mucosa from tear, and usually produced by a sharp object

Essentials of Dentistry
(Fig. 11.4A)
S 00.50 Contusion of gingiva or oral A bruise usually produced by impact with a blunt
mucosa object and not accompanied by a break in the
(Fig. 11.4B) mucosa, usually causing submucosal
hemorrhage
S 00.50 Abrasion of gingiva or oral A superficial wound produced by rubbing or
mucosa scraping of the mucosa leaving a raw, bleeding
(Fig. 11.4C) surface.

Figs 11.1A to F: Injuries to the hard dental tissues and pulp (A) Crown infarction and uncomplicated
fracture without involvement of dentin. (B) Uncomplicated fracture with involvement of dentin.
(C) Complicated crown fracture. (D) Uncomplicated crown-root fracture. (E) Complicated crown-root
fracture (F) Root fracture
Essentials of Dentistry 86 Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce

Figs 11.2A to F: Injuries to the periodontal tissues (A) Concussion. (B) Subluxation. (C) Extrusive
luxation. (D) Lateral luxation. (E) Intrusive luxation. (F) Exarticulation
Hand Instruments in Conservative Dentistry and Some Considerations for Viva Voce 87

Essentials of Dentistry
Figs 11.3A to F: Injuries to the supporting bone (A) Comminution of alveolar socket. (B) Fractures
of facial or lingual alveolar socket wall. (C and D) Fractures of alveolar socket with and without
involvement of tooth socket. (E and F) Fractures of mandible or maxilla with and without involvement
of the tooth socket

Figs 11.4A to C: Injuries to gingiva or oral mucosa (A) Laceration of gingiva.


(B) Contusion of gingiva. (C) Abrasion of gingiva
CHAPTER

12 Gingiva in Health and


Disease

Health Disease
C/F Clinically Histologically Clinically Histologically

Normal The size of gingiva Size increases in There are two types;
corresponds to sum case of gingival – Hypertrophy
of total bulk of cellular enlargement. Types Increase in size of
and intercellular of gingival cells.
elements and their enlargement are as – Hyperplasia
vascular supply. mentioned below; Increase in number
of cells. It can be
inflammatory or
noninflammatory.
I. Inflammatory
enlargement
A. Acute A. Purulent focus in
connective tissue
surrounded by
diffuse
inflammation.
Size

B. Chronic B. Exudative and


proliferative features
of chronic inflamm-
ation are seen.

II. Drug-induced Pronounced


enlargement hyperplasia of
connective tissue and
epithelium

III. Enlargement
associated with
systemic diseases
and conditions
A. Conditioned
enlargement

Contd....
Gingiva in Health and Disease 89

Contd....
Health Disease
C/F Clinically Histologically Clinically Histologically
1. Pregnancy 1. Increase in

Essentials of Dentistry
epithelial and
connective tissue
cells with newly
formed capillaries
along with chronic
inflammatory
infiltrate.
2. Puberty 2. Chronic
inflammatory
features.
3. Vitamin C 3. Chronic
deficiency inflammatory
features.
4. Plasma cell 4. Chronic
gingivitis inflammation with
dense plasma cell
infiltration.
B. Systemic diseases
causing gingival
Size

enlargement
1. Leukemia 1. Various degrees
of chronic
inflammation and
isolated surface
areas of acute
necrotizing
inflammation.
2. Granulomatous 2. Chronic
diseases inflammation with
scattered giant
cells and foci of
acute
inflammation with
microabscess.
IV. Neoplastic – Depends on type
enlargements of lesion.
(gingival tumors)
V. False enlargement – No abnormal
features.
Marginal and Due to gingival Color changes to – Due to vascular
attached gingiva vascular supply. 1. Red or bluish red in proliferation and
(Coral pink) Thickness and chronic gingivitis. reduction of
Alveolar mucosa degree of keratinized Changes start in keratinization due
(Red) epithelium. Presence interdental papillae to epithelium

Contd....
90 Gingiva in Health and Disease

Contd....

Health Disease
C/F Clinically Histologically Clinically Histologically
Essentials of Dentistry

Color is lighter in of pigment containing and gingival margin compression by


blond individuals cells. and spread to inflamed tissue.
compared to dark attached gingiva. – Bluish hue is due
haired individuals to venous stasis.
2. Pale gingiva Due to
E.g. Phenytoin –  Vascularization
induced gingival – Fibrosis
enlargement. –  Epithelial
keratinization
3. Intensely red in Due to
acute gingivitis. –  Vascularization
Changes may be – Gingival infiltration
Color

marginal (in – Red cell diapedesis


ANUG), diffuse (in – Tissue necrosis
Herpetic Gingiv-
ostomatitis) or
patch like (in
acute reaction to
chemicals).
4. Dull whitish gray – Tissue necrosis is
in severe acute demarcated from
necrotizing the adjacent
gingivitis. gingiva by a thin,
sharply defined
erythematous
zone.
Normal melanin Due to presence of Abnormal gingival – Occurs as a result
pigmentations are melanocytes in basal pigmentations of perivascular
present. and spinous layer of 1. Metallic precipitation of
Diffuse, deep, gingival epithelium. pigmentation, e.g. metallic sulfides in
purplish or irregularly- heavy metals like subepithelial
shaped brown and bismuth, arsenic, connective tissue.
light brown patches mercury, lead, Also due to
are seen. silver produce gingival
Pigmentation

Pigmentations are black or bluish inflammation,


predominant in line in gingiva,  permeability of
blacks and absent or which follows irritated blood
severely diminished contour of margin. vessels leads to
in albinos. May also appear seepage of metal
as an isolated ions into
black blotches surrounding
involving tissues.
interdental
marginal and
attached gingiva.

Contd....
Gingiva in Health and Disease 91

Contd....

Health Disease
C/F Clinically Histologically Clinically Histologically
2. In Addison’s

Essentials of Dentistry
disease isolated
patches of
discoloration
varying from
bluish black to
brown. – Due to increased
melanin
3. Peutz-Jeghers production.
syndrome and
Albright’s
syndrome
produce areas of
melanin
pigmentation.
Pigmentation

4. In jaundice, oral – Deposition of bile


mucosa becomes pigments in
yellowish. mucous
membrane.
5. In – Deposition of iron
hemochromatosis, pigments in
blue-gray pigme- mucous
ntation occurs in membrane.
oral mucosa.
6. Amalgam tattoo – Implantation of
produces amalgam particles
localized bluish- in mucosa.
black areas of
pigmentation.
Normal gingiva is firm, Due to Acute gingivitis
resilient and tightly – Collagenous 1. Diffuse puffiness 1. Acute
bound to underlying nature of lamina and softening inflammation
bone (except free propria (diffuse edema)
gingival margin) – Contiguity of 2. Sloughing with 2. Necrosis with
lamina propria grayish, flake like pseudomembrane
with particles adhering formation
Consistency

mucoperiosteum to the eroded (composed of


of alveolar bone surface. bacteria, PMNs,
– Gingival fibers degenerated
epithelial cells in
fibrinous network)
3. Vesicle formation 3. Intercellular and
intracellular
edema with
degeneration of
nucleus and
cytoplasm, rupture
of cell wall.

Contd....
92 Gingiva in Health and Disease

Contd....

Health Disease
C/F Clinically Histologically Clinically Histologically
Essentials of Dentistry

Chronic gingivitis
Both destructive
(edematous) and
reparative (fibrotic)
changes
coexist.
1. Soggy puffiness, 1. Due to marked
pitting on pressure infiltration by fluid
(in chronic and cells of
gingivitis) inflammatory
exudates.
2. Marked softness 2. Degeneration of
and friability, connective tissue
fragmentation on and epithelium
Consistency

exploration with associated with


probe, pin point inflammation,
surface areas of thinning of
redness and epithelium.
desquamation.
3. Firm and leathery 3. Fibrosis and
epithelial
proliferation.
Stippled gingival Stippling is produced In chronic inflam-
surface (numerous by alternate rounded mation, gingival
small depressions and protuberance and surface texture
elevations) similar to depression of gingival depends on whether
orange peel. epithelium into the process is
Stippling is restricted connective tissue. exudative or fibrotic.
to attached gingiva Papillary layer of Exudative
predominantly to the connective tissue 1. Smooth and shiny – Due to
subpapillary area with projects into with loss of surface inflammation
variable extension into elevations of stippling of gingiva leading to
interdental papilla. epithelium. occurs (in epithelial atrophy.
Prominence of atrophic gingivitis).
stippling is related to 2. Peeling of surface
Surface texture

degree of (in chronic


desquamative
keratinization.
gingivitis)
Fibrotic
Firm, nodular and – Leathery due to
leathery in consis- hyperkeratosis
tency (in drug and nodular due to
induced gingival gingival
overgrowth) overgrowth.
Marginal gingiva Contour of overlying Gingival contour is
envelops teeth in a gingiva follows the altered in disease.
collar like fashion and contour of alveolar – The marginal – Inflammatory
follows scalloped bone margin and gingiva becomes changes in
outline on facial and cementenamel rolled or rounded marginal gingiva.
lingual surface. junction. and interdental
Contd....
Gingiva in Health and Disease 93

Contd....

Health Disease
C/F Clinically Histologically Clinically Histologically
However, papilla becomes

Essentials of Dentistry
1. In teeth with blunt and flat (in
relatively flat chronic gingivitis).
surface, it forms
straight outline.
2. In teeth with pron- – Ballooning of – Inflammatory
ounced interdental changes in
mesiodistal papilla and marginal gingiva.
convexity, (e.g. gingival margin
Maxillary Canine) (in inflammatory
gingiva is located gingival
further apically. enlargement).
3. On teeth with – Flattened or – Acute necrotizing
lingual version, cratered inflammation of
gingiva is interdental papilla marginal gingiva.
horizontal or (in ANUG).
thickened.
The gingival appears – Irregularly-shaped – Inflammatory
prominent over the denuded changes in
tooth and slightly appearance (in marginal gingiva.
concave in the chronic
interproximal area. desquamative
gingivitis)
Contour

– Stillman’s clefts – Inflammatory


(Apostrophe- changes in
shaped marginal gingiva.
indentation of
gingival margin for
varying distance
on facial surface)
– McCall festoon
(Rolled, thickened
band of gingiva)
It is a life
preserver-shaped
enlargement of
margin.
– Exaggerated – Depends on the
scalloping (in cause of
gingival recession) recession.
Normally absent Normal histological 1. Chronic and – Dilation and
features of gingiva recurrent engorgement of
bleeding. capillaries due to
(In chronic gingival
gingivitis) inflammation.

Contd....
94 Gingiva in Health and Disease

Contd....

Health Disease
C/F Clinically Histologically Clinically Histologically
Essentials of Dentistry

– Capillaries lie
closer to the
surface.
– Thinning or
ulceration of
sulcular epithelium.
– Cell rich and
collagen poor
Bleeding on probing

tissue.
2. Acute episodes of – Engorged blood
bleeding. vessels in inflamed
(In injury/ connective tissue
spontaneously in are exposed by
ANUG) ulceration of
necrotic surface
epithelium.
3. Occurs – Failure of
spontaneously or hemostatic
after irritation. mechanism.
(Excessive and
difficult to control)
Normally, marginal Normal histological Gingival recession – Hyperemia of pulp.
gingiva envelops features of gingiva – Exposed root
Position

cervical margin of – Root caries


tooth crown in collar –  Hypersensitivity
like fashion at or near
CEJ.
CHAPTER

13 Dentogingival Junction

The dentogingival junction is an anatomical and functional interface between the gingiva
and the tooth structure. It provides attachment of the gingiva to the enamel surface via
hemidesmosomes. Biologic width is the term applied to the dimensions of the dentogingival
junction. It was first described by Sicher in 1959. Biologic width is the apicocoronal distance
in which the junctional epithelium and supracrestal connective tissue fibers are attached
to the tooth.
The body maintains the biologic width as a stable dimension. When the biologic width
is encroached upon and injured by extension of restorative preparations and materials into
this area, uncontrolled inflammation results as the body tries to reestablish this dimension.

DEFINITION
Gingival apparatus maintains the free gingiva and junctional epithelium in close
approximation to tooth. The attachment of the junctional epithelium to tooth is reinforced
by the gingival fibers, which brace the gingiva against the tooth surface. So that the gingival
fibers along with junctional epithelium is considered as functional unit referred to as
“Dentogingival unit” (Fig. 13.1).

COMPONENTS
1. Epithelial component is derived from reduced dental (enamel) epithelium and oral
epithelium. In some references, the epithelial part derived from the reduced dental
epithelium is referred as primary attached epithelium or initial junctional epithelium.
While in other references, a definitive epithelium replaces this initial one 3-4 years after
the tooth erupts.
2. Connective tissue component is derived from the lamina propria of the oral mucosa.
Gargiulo and colleagues studied the anatomy of the dentogingival junction and quantified
the average as a constant 2.04 mm (the epithelial attachment is 0.97 mm, and connective
is 1.07 mm). The distance is measured histologically from the most coronal part of
the junctional epithelium (base of the sulcus) to the crest of the alveolar bone.

DEVELOPMENT
Just before the reduced enamel epithelium comes in contact with the oral epithelium during
tooth eruption, the mitotic activity in the basal cells of the oral epithelium, at the cusp
tips of the erupting teeth, decreases.
The reduced enamel epithelium in the basal cell layer, close to the cusp tip, starts
displaying high mitotic activity.
After erupting, the cusp tip has become exposed in the oral cavity; it is surrounded
by a shallow sulcus ending in the still attached reduced enamel epithelium, and bordered
orally by the free gingival margin.
Essentials of Dentistry 96 Dentogingival Junction

Fig. 13.1: Dentogingival junction

As the tooth erupts, the reduced enamel epithelium is gradually replaced through
proliferation of its basal cells, and the new epithelium joining the tooth surface is called
“Junctional epithelium”. The attachment of this epithelium to the tooth surface is called
the “Epithelial attachment”.

MECHANISM OF ATTACHMENT OF THE DENTOGINGIVAL JUNCTION


• Electron microscopic findings revealed that the strong union between the soft gingival
tissues, namely junctional epithelium and the tooth surface, namely enamel and/or
cementum, are dependent on the presence of a basal lamina and hemidesmosomes.
• Junctional epithelium is associated with two basal laminae;
i. One is present between the junctional epithelium and the tooth surface which is
referred to as internal basal lamina.
ii. The other is present between the junctional epithelium and the underlying connective
tissue of the lamina propria, and it is called as external basal lamina.
Both basal laminae consist of a lamina lucida (clear layer) and lamina densa (dense
layer). Though both basal laminae are morphologically similar, their biochemical structure
is different. The basal lamina between the junctional epithelium and the tooth surface appears
Dentogingival Junction 97

to lack collagen types IV and VII. These collagen fibers are present at the basal laminae
at the epithelial/connective tissue interfaces.

AGE AND INFLAMMATION CHANGES

Essentials of Dentistry
• The level of the junctional epithelium relative to the tooth surface shifts apically with
increasing age, and it is believed that inflammation is an important factor that contributes
to this apical migration. This apical shift is gradual and if it is accelerated, this pathological
condition is referred to as gingival recession.
• The underlying connective tissue is believed to play a significant role in determining
the formation of the junctional epithelium. When connective tissue is destroyed during
the periodontal disease, junctional epithelium migrates apically until it reaches intact
connective tissue that provides the signal to stop its migration, forming long junctional
epithelium.

CLINICAL IMPLICATION
The concept of biological width is used as a decision-making guide to the amount of soft
tissue that should be removed during surgical procedure. The decision of surgical flap
therapy depends upon the biologic width.
CHAPTER

14 Cementum in Disease

The cementum is a specialized mineralized tissue covering the root surfaces and,
occasionally, small portions of the crown of the teeth. It has many features in common
with bone tissue. The cementum contains no blood or lymph vessels and has no
innervations. It does not undergo physiologic resorption or remodeling, but is characterized
by continuing deposition throughout life. Like other mineralized tissues, it contains collagen
fibers embedded in an organic matrix.
Exposed cementum is normally covered by a thin acquired pellicle of glycoproteins.
The pellicle is believed to play an active part in the selective adherence of bacteria to
the tooth surface.
Pathologic changes in exposed cementum are:
– Structural changes
– Cytotoxic changes
– Chemical changes
– Physical changes.

STRUCTURAL CHANGES
Presence of Pathologic Granules
Pathologic granules are 0.1 to 0.2 micrometer spaces between the external apical epithelial
cells and cemental surface. It represents the zone of collagen degradation/areas where
collagen fibrils have not been fully mineralized. It may represent the zone of bacteria/artifact.

Areas of Increased Mineralization


Exposure of cervical root surface to the oral cavity facilitates exchange of minerals at
cementum–saliva interface. Minerals that are increased in diseased root surfaces include
Ca, Mg, P, F. These areas of increased mineralization increase the tooth resistance to decay.

Areas of Demineralization
Areas of demineralization are often related to “root caries”. Exposure to oral fluid and bacterial
plaque results in proteolysis of embedded remnants of sharpey’s fibers.
Cementum may become soft and may undergo:
– Fragmentation
– Cavitation.
Root caries progress around the tooth rather than deep into the tooth.
Active carious lesion Yellowish or light brown areas covered by plaque. It has soft and leathery
consistency.
Inactive carious lesion Well-defined darker lesion with smooth surface and hard consistency on
probing.
Cementum in Disease 99

Dominant organisms are:


– Actinomyces viscosus
– Actinomyces naeslundii
– Streptococcus mutans
– Streptococcus salivarius

Essentials of Dentistry
– Streptococcus sanguis
– Bacillus cereus.
– Tooth may not be painful. Exploration of the surface reveals presence of a defect
and penetration of involved area with probe causes pain. Caries may lead to pulpitis,
sensitivity to sweet and thermal changes or severe pain.
– Necrotic cementum must be removed during scaling and root planing.
Clinically, softening of cementum surface is usually asymptomatic, but painful when
probe or explorer penetrates the area. They act as a reservoir for bacteria and reinfect
area after treatment. Necrotic areas should be removed by root planing until a smooth
hard surface reaches (Fig. 14.1).

CHEMICAL CHANGES
Mineral
• Chemical changes are in the form of increased mineral content of exposed cementum.
• Diseased cementum is characterized by either an absorption into or depletion of major
mineral components like calcium, magnesium and phosphorus from cementum. By
minerals absorption, cementum becomes highly calcified imparting increased resistant
to decay compared to normal cementum. Absorption of toxic mineral is harmful.
Prediseased Root Diseased Root
Ca + Mg 26% 27.5%
Phosphorus 12.3% 12.6%

CYTOTOXIC CHANGES
|
| |
Bacteria Endotoxins

Fig. 14.1: Pathogenesis


100 Cementum in Disease

I. Bacteria present are:


– Actinomyces viscosus – Streptococcus naeslundii
– Streptococcus mutans – Streptococcus salivarius
– Streptococcus sanguis.
Essentials of Dentistry

II. Bacterial products such as endotoxins are detected in the cementum wall of pocket.
Diseased cementum depresses the fibroblast proliferation and prevents the
attachment of fibroblasts. Cavitation and partial calcification as deep as 300 m,
without loss of contour, can harbor endotoxins. These endotoxins serve as a
substance for inflammatory exudates.
III. Exudates contain
– Histamine – Bradykinin
– IgG, IgA, IgM – Complement cementum
– Enzymes – Hyaluronidase
– Collagenase.
IV. Endotoxins act as an antigen and promote activation of host response leading to:
– Leukopenia
– Activate factor XII (Hageman factor) leading to intravascular coagulation
– Activate complement system
– Localized Schwartzman phenomenon with tissue necrosis occurs after two more
exposures
– Cytotoxic effects on cells like fibroblasts
– Bone resorption.

PHYSICAL CHANGES
Ankylosis
• Replacement resorption and ankylosis are often used as synonyms. Replacement
resorption describes the active process of resorption of tooth and replacement by bony
tissue while ankylosis is a Greek word for immobile.
• Ankylosis is a prerequisite for replacement resorption. It describes the fusion between tooth
and bone, which can be permanent or transient depending on size of resorption areas.

Resorption and Repair


• Resorption is not necessarily a continuous process. It may interchange with periods
of repair and forms a demarcating line called as “reversal lines”. However, cementum
repair requires viable connective tissues.
• Root exposed by pocket formation appears as isolated areas, and from these areas
bacteria penetrate into dentin. These areas undergo significant changes because they
may perpetuate the periodontal infection and may complicate periodontal treatment.
• Areas of cellular resorption of cementum and dentin are common in root unexposed
by periodontal disease. They are usually symptom-free and may undergo repair as
long as they are covered by periodontal ligament.

Hypercementosis
Hypercementosis is characterized by cementum formation beyond the physiologic limits
of the tooth. It may be localized to one tooth or affect the entire dentition. Excessive
proliferation of cementum may be seen in association with a wide range of neoplastic
and non-neoplastic conditions, including benign cementoblastoma, cementifying fibroma,
periapical cemental dysplasia, and florid cemento-osseous dysplasia.
CHAPTER

15 Tooth Mobility

INTRODUCTION
Tooth mobility is defined as a “degree of looseness of tooth” (Kenry AAP, 1986). Mobility
of tooth is one of the important signs as well as symptoms of periodontal disease. It helps
in the diagnosis of periodontal disease by determining the disease prognosis. Mobility
is a condition demanding immediate attention in order to save the tooth causing discomfort
to the patient, affecting speech, mastication and esthetics, and leading to psychological
trauma to the patient.
Mobility is most commonly noticed in the mandibular anterior region due to decreased
thickness of alveolar bone and comparative less support in this region.

TYPES
The periodontal assessment includes an evaluation of tooth mobility. Tooth mobility should
be distinguished between physiologic and pathologic mobility.

Physiological
Physiologic mobility is the normal or expected mobility of a tooth. It is a function of the
height of the alveolar bone and the width of the periodontal ligament. It is limited tooth
movement or displacement permitted by resiliency of the alveolar bone and cushioning effect
of the periodontal ligament. All teeth have a slight degree of physiologic mobility due to
cushioning of periodontal ligament. Physiologic tooth movement occurs when moderate
forces are applied to the tooth during the oral examination and during the mastication.
Increased tooth mobility is physiologic in nature. It is due to the forces applied to the
teeth surrounded by horizontal or angular bone loss and/or increased width of periodontal
ligament but of normal composition. It depends on time, number and directions of the root.

Pathological or Abnormal
Tooth mobility beyond the physiologic range is termed as pathologic or abnormal. Only
progressively increasing tooth mobility, which may occur in conjunction with inflammatory
changes within the periodontal ligament, may be considered “Pathologic”. It is the
perceptible tooth movement in response to the force.

Other Terminologies
1. Altered tooth mobility
Transient or permanent changes in the periodontal apparatus supporting the tooth
leading to altered tooth movement are termed as altered tooth mobility.
102 Tooth Mobility

2. Functional mobility
Movement of tooth during functional and parafunctional forces is termed as functional
mobility.
Essentials of Dentistry

CAUSES
Mobility of tooth is caused by changes in periodontal structures (soft tissue changes, alveolar
bone changes, periodontal ligament changes).
1. Bone loss
• Loss of alveolar bone surrounding tooth is chiefly due to extension of the inflammation
from gingiva into the periodontal structures. Severity and distribution of bone loss
determines the degree of tooth mobility.
2. Inflammation
• Gingival inflammation extending into the periodontal ligament results in degenerative
changes that can increase tooth mobility, even in the absence of bone loss. These
inflammatory changes are responsible for the increased tooth mobility in case of
advanced gingivitis or early periodontal disease. The spread of inflammation from
acute periapical abscess produces a temporary increase in tooth mobility in the
absence of periodontal disease.
3. Trauma from occlusion
• Tooth mobility is the most common clinical sign of trauma to the periodontium.
It is seen in case of primary or secondary trauma from occlusion either in absence
or in association with inflammation.
• Tooth mobility during the injury stage is the increased tooth mobility.
• Primary trauma from occlusion occurs when teeth in normal periodontium are
subjected to excessive occlusal forces that cause pathologic mobility.
• Secondary trauma from occlusion occurs when teeth in a compromised periodontium
become mobile because they cannot withstand normal occlusal forces.
• Initially, mobility is seen as a result of resorption of cortical plate and subsequently,
reduced fiber support, and later on an adaptation phenomenon resulting in widened
periodontal space makes the tooth mobile.
4. Hypofunction
Hypofunction of tooth without antagonist widens the periodontal ligament space, and
bigger room for tooth displacement increases the tooth mobility.
5. Periodontal surgery
Tooth mobility increases immediately after the surgery but later on it diminishes below
the pretreatment level by 4th week.
6. Hormonal changes
Tooth mobility increases during pregnancy, menstruation or during use of hormonal
contraceptive. It is associated with pregnancy, particularly in the last weeks before
delivery, and it is probably due to increased hydration of connective tissue.
7. Habits and systemic diseases
Abnormal habits, such as grinding (bruxism) and clenching are common causes of
tooth mobility. Smokers exhibit increased tooth mobility. Other conditions that reduce
periodontal support may lead to mobility. For example, Down’s syndrome, Ehlers-Danlos
syndrome, cyclic neutropenia.
8. Blunt injury to tooth and crown/root fracture.

FACTORS AFFECTING TOOTH MOBILITY


• Severity and distribution of bone loss at individual root surfaces.
• Number, length and shape of the root.
Tooth Mobility 103

Single-rooted tooth exhibit more mobility than multirooted tooth. Likely, long-rooted
tooth manifests less mobility compared to short-rooted tooth (It is highest in the central
and lateral incisors).
• Frequency, duration, velocity and magnitude of occlusal forces. Periodontal ligament

Essentials of Dentistry
can tolerate tension much better than the compression.
• Root size compared to crown -
A tooth with short-tapered roots is more likely to loosen than one with normal size
or bulbous roots with same amount of bone loss (Ratio of crown-to-root length).
• Amount of inter-radicular bone.
• Number and distribution of remaining teeth in the arch.
• History of root amputation.
• Time.
In the morning, it is increased because of slight extrusion of tooth due to limited occlusal
contact during sleep and progressively decreases during the day time. During the waking
hours, mobility is reduced by effect of chewing and swallowing forces, which intrudes
the tooth into socket.

INCREASED VS INCREASING MOBILITY


Increased
It is an adaptation of periodontium to occlusal forces that may not necessarily be considered
pathological. Increased tooth mobility is observed in conjunction with trauma from occlusion.
However, it may also be the result of reduction of the height of alveolar bone with or without
accompanying angular bony defect.
Some of the factors producing increased tooth mobility are as follows:
• Loss of tooth support (bone loss)
• Trauma from occlusion
• Extension of inflammation from the gingiva or from the apex into periodontal ligament
• Periodontal surgery temporarily increases tooth mobility
• Pregnancy, menstrual cycle and hormonal contraceptives (Increases tooth mobility).
Mobile teeth with healthy connective tissue attachment can be maintained in the
absence of inflammation. A widened periodontal ligament space may be a manifestation
of adaptive changes to increased trauma. It may be accompanied by reduced height
of alveolar bone.
Treatment: Only occlusal equilibrium and perhaps splint therapy.
Removal of the excessive occlusal load by occlusal equilibrium and splint therapy can
decrease and even eliminate tooth mobility. Periodontal ligament regains its normal width
and bone apposition may occur.

Increasing
It is due to pressure or localized infection causing bone destruction, and always pathological.
Treatment: This condition must receive the periodontal therapy, an occlusal analysis
and equilibration, and if needed, followed by reevaluation for extraction or splinting of
the affected teeth.
Single-time measurements of mobility are of limited value. However, when they are
repeated at regular intervals and a change occurs, the alteration may be a significant finding
that pinpoints a localized change or indicates an alteration in parafunctional habits (e.g.
bruxism) that may affect the overall prognosis greatly.
104 Tooth Mobility

MILLER’S CLASSIFICATION (1950)

Class I Physiologic mobility


Class II Up to 1 mm transverse movement
Essentials of Dentistry

Class III More than 1mm in any direction, vertical or horizontal

GLICKMAN’S CLASSIFICATION (1972)

Grade I Slightly more than physiologic


Grade II Moderately more than physiologic
Grade III Severe mobility buccolingually and/or mesiodistally combined with vertical
displacement

LINDHE’S CLASSIFICATION

Degree I Movability of the crown of the tooth 0.2-1 mm in horizontal direction


Degree II Movability of the crown of the tooth exceeding 1 mm in horizontal direction
Degree III Movability of the crown of the tooth in vertical direction as well

STAGES OF TOOTH MOBILITY


Tooth mobility occurs in two stages.
1. Initial stage/intrasocket stage:
• It is the result of intraalveolar displacement of root and the movement occurs within
confines of periodontal ligament.
• Tooth moves within the confines of the periodontal ligament. It is associated with
viscoelastic distribution of ligament, and redistribution of periodontal fluids so varies
from person to person within the range of 0.05 to 0.10 mm (50-100 µm) with the
force of about 100 gm.
2. Secondary stage:
• There is gradual elastic deformation of alveolar bone in response to increased
horizontal forces. When a force of 500 gm is applied to the crown, the resulting
displacement is about 100 to 200 µm for incisors, 50 to 90 µm for canines, 8 to
10 µm for premolars, and 40 to 80 µm for molars.

MEASUREMENT OF TOOTH MOBILITY


Horizontal tooth mobility is the ability to move the tooth in a facial-lingual direction in its
socket. Horizontal tooth mobility is assessed by putting the handles of two dental instruments
on either side of the tooth and applying alternating moderate forces (Fig. 15.1).
• Tooth is held firmly between the handles of two metallic instruments. One on buccal/
labial side and the other, on the lingual side of the tooth. Alternatively, a metallic instrument
at one end and finger, as a substitute for other instrument, can also be used. But it
is not recommended, generally, because the soft tissue pads of fingers act as a cushion
and mask movement (Fig. 15.2).
• Now effort is made to move tooth in all directions (100 gm force is applied).
• Mobility is measured according to the ease and extent of tooth movement. A normal
tooth has minute amount of “give” to it (i.e. is not ankylosed). A tooth that moves more
than this minute amount but in total arc of less than 1 mm has class I mobility.
Tooth Mobility 105

Essentials of Dentistry
Fig. 15.1

Fig. 15.2
Figs 15.1 and 15.2: Assessment of tooth mobility

• Abnormal mobility, most often, occurs in faciolingual direction. It is graded according


to ease and extent of the tooth movement, using the above criteria. Mobility beyond
the physiologic range is termed as “pathologic”.
Vertical tooth mobility is the ability to get depressed the tooth in its socket, and is assessed
using the end of an instrument handle to exert pressure against the occlusal or incisal
surface of the tooth.
Instrument used to measure the tooth mobility is called as “Periodontometer”.
106 Tooth Mobility

Periotest
A new method for determining tooth mobility was presented by Schulte and coworkers
(Schulte 1987, Schulte et al, 1992) using “Periotest” (Siemens AG, Bensheim, Germany)
system. A tapping instrument delivers the controlled percussion force to the tooth and
Essentials of Dentistry

the reaction of the periodontium is recorded by the Periotest device. A metal rod is
accelerated to a speed of 0.2 m/s with the device, and maintained at a constant velocity.
The tooth is deflected, and the rod decelerated by impact with tooth. The contact time
between the tapping head and the tooth varies between 0.3 and 2 milliseconds, and is
shorter for stable than mobile teeth. Interpretation of Periotest is as mentioned below;
– 8 to +9 Clinically firm teeth
10 to 19 First distinguishable sign of movement
20 to 29 Crown deviates within 1 mm of its normal position
30 to 50 Mobility is readily observed

The Periotest values correlate well with:


1. Tooth mobility assessed with a metric system, and
2. Degree of periodontal disease and alveolar bone loss.

GENERALIZED TREATMENT OF MOBILITY


The primary thing in treatment of tooth mobility is removal of etiological factors. It is followed
by treatment of contributing etiologic factors.
CHAPTER

16 Food Impaction

Food impaction is one of the predisposing factors for localized gingival and periodontal
disease. It also aggravates the severity of preexistent pathologic changes. Failure to
recognize and eliminate food impaction may be responsible for the unsuccessful outcome
of thoroughly treated case of periodontal disease. It usually occurs in the interproximal
areas but can also be seen in relation to facial or lingual tooth surfaces. Food impaction
and subsequent retention may contribute to root caries in individuals who do not perform
proper oral hygiene interdentally.

DEFINITION
“Food impaction is forceful wedging of food into the periodontium by occlusal forces
(Hirschfeld 1930).”
However, in addition to vertical impaction due to chewing pressure, it also includes
horizontal impaction by the forcing food interproximally by tongue or cheek pressure (AAP
2001a).

TYPES
There are two ways of food impactions;

Vertical Food Impaction


It is due to open contacts, irregular marginal ridges and plunger cusps. Open contacts
between teeth may be anatomical in origin, iatrogenic in origin, or may be due to caries
and pathologic migration of periodontally involved tooth.

Horizontal Food Impaction


Horizontal food impaction occurs due to enlarged gingival embrasures. Lateral pressure
from cheeks and lips forces the food particles interdentally.

FACTORS AFFECTING FOOD IMPACTION (FIG. 16.1)


Normally forceful wedging of food is prevented by:
1. Integrity and location of the proximal contacts:
Absence of contact or presence of unsatisfactory proximal tooth relationship favors food
impaction and endangers the periodontal health (level of attachment) of adjacent teeth.
• Intact, firm proximal contact prevents food impaction interproximally.
• Coronally placed proximal contact reduces the funneling effect and forms smaller
occlusal embrasures, and thus prevents food impaction.
Essentials of Dentistry 108 Food Impaction

Fig. 16.1: Periodontal disease and food impaction

2. The contours of the marginal ridges and developmental grooves:


Occlusal surface loose the convexities and become oblique facets by attrition

Wedging effect of opposing cusp into the interproximal area is exaggerated

Food impaction
Contours of marginal ridges and related developmental grooves deflect the food
away from the interproximal surface.
3. Contour of facial and lingual surfaces.
4. Excessive anterior bite:
It is a common cause of food impaction on lingual surfaces of maxillary anterior teeth
and facial surfaces of opposing mandibular teeth. This can be prevented by restoration
of normal bite plane.

PLUNGER CUSP
Cusps that tend to forcefully wedge food interproximally are called plunger cusps. It occurs
due to occlusal wear or as a result of shift in tooth position after failure to replace missing
tooth (Fig. 16.2).

CLASSIFICATION OF FACTORS CAUSING FOOD IMPACTION


The classical analysis of the factors leading to food impaction was made by Hirschfeld
(1928) who recognized the following factors:
• Uneven occlusal wear
• Opening of contact point due to loss of proximal support or from excursion
• Congenital morphological abnormalities
• Improperly constructed restorations.

CLASS I Occlusal wear


CLASS II Loss of proximal contact
CLASS III Extrusion beyond the occlusal plane
CLASS IV Congenital morphological abnormality
CLASS V Improperly constructed restorations
Food Impaction 109

Essentials of Dentistry
Fig. 16.2: Plunger cusp

Fig. 16.3: Wedging effect due to occlusal wear

CLASS I: Occlusal Wear


Type A: Wedging action produced by plunger cusp into oblique facets (Fig. 16.3).
Type B: Remaining obliquely worn cusp of a maxillary tooth, overhanging the distal
surface of its functional antagonist (Fig. 16.4).
Type C: Obliquely worn mandible tooth, overhanging the distal surface of its functional
antagonist (Fig. 16.5).

CLASS II: Loss of Proximal Support


Type A: Loss of distal support through the removal of a distally adjacent tooth
(Fig. 16.6).
Type B: Loss of mesial support due to extraction
Type C: Oblique drifting due to nonreplacement of a missing tooth
Essentials of Dentistry 110 Food Impaction

Fig. 16.4: Obliquely worn cusp of maxillary tooth

Fig. 16.5: Obliquely worn cusp of mandibular tooth

Fig. 16.6: Loss of distal support leading to food lodgement


Food Impaction 111

Type D: Permanent occlusal openings to interdental spaces


i. Drifting after extraction
ii. Habits forcing teeth out of position
iii. Periodontal disease
iv. Caries

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CLASS III: Extrusion
CLASS IV: Congenital Abnormalities
Type A: Rotation of tooth
Type B: Emphasized embrasure between thick-neck teeth
Type C: Faciolingual tilting
Type D: Malposition (Facial or lingual).

CLASS V: Improperly Constructed Restoration


Type A: Loss of contact point
Type B: Improper location of contact point
Type C: Improper occlusal contour
Type D: Improperly constructed cantilever restorations
Type E: Scalloped cervical bevels on the tissue-born areas of prosthetic restorations.

SIGNS AND SYMPTOMS


1. Trouble
• Discomfort (feeling of pressure)
• Vague pain
• Root caries
• Halitosis.
2. Periodontal Changes
• Gingival inflammation (bleeding)
• Gingival recession
• Periodontitis
• Periodontal abscess formation
• Vertical alveolar bone loss
• Crater formation.

PREVENTION AND TREATMENT


1. Occlusal adjustment:
An occlusal adjustment to create adequate food escape grooves as well as to reduce
prominent opposing cusps and correct uneven marginal ridges may completely eliminate
food impaction (Fig. 16.7).
a. Plunger cusp: Rounding of the sharp cusp tips especially lingual cusp.
b. Level the occlusal height of the marginal ridges:
i. Restoration of marginal ridge depends on (Fig. 16.8);
1. Relation to opposing tooth structure to the overall plane of occlusion
2. Degree of discrepancy
3. Iatrogenic hazards.
ii. Consider the slope of the marginal ridge (external, internal)
iii. When a marginal ridge is being leveled, the proximal fossa is generally obliterated
which must be recarved.
Essentials of Dentistry 112 Food Impaction

Fig. 16.7: Occlusal adjustment

Fig. 16.8: Restoration of marginal ridge

c. Grooves and fossa (Fig. 16.9)


i. Recarve obliterated or missing fossa.
ii. Distinct but shallow, saucer-shaped fossa with slightly extended grooves mesially
and distally act as spillways or sluiceways to deflect food from interproximal
areas to buccal/lingual surface.
2. Periodontal treatment:
Scaling, flossing, curettage and surgical flap therapy, and elimination of bony defects
improve the periodontal condition.
Food Impaction 113

Essentials of Dentistry
Fig. 16.9: Grooves and fossa

3. Making ideal contact:


Intact, firm proximal contact relationships prevent forceful wedging of food interproximally
and protect interdental papilla.
Ideal contact should have ideal location, width, height and tightness. It can carefully
be checked with dental floss.
4. Permanent restoration and proper prosthesis:
Deficient areas require permanent restoration with proper
• Proximal contact
• Contour of occlusal surface
• Facial and lingual contour.
Faulty prosthesis should be replaced with proper proximal and occlusal relationship
with other teeth of the oral cavity.
CHAPTER

17 Halitosis

The word halitosis originates from the Latin word “halitus” meaning to breathe and the
Greek word—“osis” meaning abnormal or diseased. Halitosis itself is not a disease but
it is a symptom of a disease. It is also known as “fetor ex ore”, “fetor oris”, and “oral
malodor”. It was 1st described by “HOWE” in 1874.
Breath odor can be defined as the subjective perception after smelling someone’s breath.
It can be pleasant, unpleasant or even disturbing, if not repulsive. If unpleasant, the terms
breathe malodor, halitosis or bad breath can be applied.

DEFINITION
Halitosis is a foul or offensive odor emancipating from oral cavity and should be considered
as a symptom, not as a disease.

CLINICAL FEATURES
Halitosis varies with age, gender, hunger state, and also with the time of the day. Morning
is usually the worst. It also varies in intensity and quality.
Sex: More common in male
Age: More common above 40 years (85%).
It is experienced by the patient or by surrounding. It has impact on social environment,
business and persons with whom he lives. The distinct odor produced by different diseased
states has diagnostic importance. Oral malodor in healthy patients arises from the oral
cavity and generally originates on the dorsum of the tongue. Tongue is an excellent site
for growth of microorganisms and creates a unique ecological site.

TYPES
Transitory Halitosis
Transitory halitosis lasts between 24 and 72 hours, and is usually caused by foods such
as garlic, pepper, onion, or by smoking. Everyone has transitory halitosis. It often disappears
following eating, brushing teeth, flossing, and rinsing with specialized mouthwash. Breath
malodor should not be confused with these momentary disturbing odors.

Chronic Halitosis
The cause of chronic halitosis is usually oral in nature but 10 percent of cases are reported
to be caused by other factors such as a disease or ailment.
Halitosis 115

Physiological Pathological
Morning Breath Not time specific
Hunger Breath
Less intense More intense

Essentials of Dentistry
Transient Persistent
Nondistinct Distinct in quality
Generally responds to change in Requires treatment of the underlying cause and
habits improvement of oral hygiene

PRIMARY FACTORS AFFECTING HALITOSIS


• Saliva flow
• pH of saliva
• Gram-negative bacteria
• Presence of protein and food debris.

MICROBIOTA IN HALITOSIS
T. denticola
P. endodontalis
P. intermedia
P. metaninogenica
B. forsythus
R. denticariosca
Fusobacterium.

MECHANISMS
• As the mouth is exposed to less oxygen and is inactive during the night (decrease
in salivary secretion), the odor is usually worse upon awakening (“morning breath”).
• The most unpleasant odors are known to arise from proteins trapped in the mouth,
which are processed by oral bacteria, sheded epithelium and food debris.
• Halitosis is caused by liberation of volatile sulfur compound, specially hydrogen sulfide
and methylmercaptun, which results from bacterial putrification of proteins containing
sulfur, amino acids. These products could involve in transition from health to gingivitis
and then progressively to periodontitis.
• The gaseous substances consist primarily of hydrogen sulfide (H2S), dimethyl sulfide
([CH3]2S), methylmercaptan (CH3SH) and sulfur dioxide (SO2). The breakdown of
cysteine and methionine produce hydrogen sulfide and methyl mercaptan
respectively.
• Volatile fatty acids such as valerate, butyrate and proprionate are also malodorous.
• Tongue is the primary site for production of all these volatile substances. These locations
in descending prevalence order are: interdental and subgingival niches, faulty dental
work, food impaction areas in between the teeth, abscesses and unclean dentures.
Irregular surface topography of the tongue is an ideal niche for bacterial adhesion and
growth. Tongue coatings comprising accumulated food remnants, exfoliated cells and
bacteria cannot be easily removed.
116 Halitosis

Halitosis is experienced more in the morning because of the following physiological


changes during sleep like:
• Decreased salivary flow
• Decreased cleaning effect due to decreased movement of cheeks and tongue
Essentials of Dentistry

• Decreased BMR (Basal metabolic rate).

ETIOLOGY (FIG. 17.1)


There are more than 300 bacterial species associated with oral malodor. All odor
production is a result of gram-negative bacterial metabolism, the gram-positive contributes
very little.
The normal pH of the mouth is slightly acidic (6.5-6.9). A pH level of 7.2 or more in
the mouth increases the growth of gram-negative bacteria. A pH level of 6.5 or less in
the mouth increases the growth of gram-positive bacteria.
Etiologic factors can be categorized into two main categories: intraoral and extraoral.

Fig. 17.1: Pathogenesis of bacteria


Halitosis 117

Intraoral Causes
Nonpathological
1. Heavy smoking (Transient halitosis)
2. Vulcanite denture halitosis (Denture breath)

Essentials of Dentistry
3. Age-wise.
Children Sweet odor due to food entrapment at tonsillar crypt.
Old age Odor due to unclean dentures

Pathological
1. Poor oral hygiene due to any reason.
2. Food lodging areas in mouth resulting from;
• Malposed teeth
• Prosthetic, orthodontic or fractured appliance
• Deep carious lesion
• Loss of interdental papilla.
3. Periodontal pocket, pus and putrification of content materials.
Bacteria associated with gingivitis and periodontitis are almost gram-negative and
are known to produce VSCs (volatile sulfur containing substances). The low oxygen
tension in deep periodontal pockets also results in low pH and activation of the amino
acids to cadaverine and putrescine. These VSCs aggravate the periodontitis by
increasing the permeability of the pocket and mucosal epithelium, and thereby exposes
the underlying connective tissues of the periodontium to bacterial metabolites.
4. Other malodorous pathologies are:
• Pericoronitis
• Major recurrent oral ulcers
• Herpatic gingivitis
• Necrotizing ulcerative gingivitis.
5. Following surgery associated with oral bleeding and tissue necrosis resulting from
various causes like diabetic gangrene, leukemia, and malignant growth.
6. Dry socket
7. Coated tongue.
The dorsum of the tongue has very rough and uneven topography. The depressions
created by the filiform and fungiform papillae are ideal niches for adhesion and growth
of microorganisms. Food remnants intermingled with bacteria and exfoliated cells
are not easy to remove from the dorsum of the tongue, and it is the primary site
for oral malodor.
8. Dryness of mouth due to decreased salivary flow is associated with:
• Mouth breathing
• Heavy smoking
• Salivary gland aplasia
• Sjögren’s syndrome, Mikulicz’s disease
• Peritonsillar abscess
• Radiation therapy
• Diabetes, lung cancer
• Menopause in women
118 Halitosis

•Emotional distress (Vincent disease)


•Aging
•High fever
•Hormonal changes in the women.
Essentials of Dentistry

Large amount of deposits increasing the microbial load is frequently been observed
in the patients with xerostomia.
9. Postnasal drip at the posterior dorsum of the tongue
10. Cyst with fistula draining in the oral cavity.

Extraoral Causes
Nonpathological
1. Alcoholic breath:
Alcohol consumption causes dryness of mouth and alteration of microbial flora with
proliferation of odor fermenting organisms.
2. Hunger odor by putrefaction of pancreatic juice.
3. Stress:
It affects parasympathetic nervous system and decreases salivary secretion. Less
cleansing effect by decreased salivary flow along with decrease in amount of oxygen
present in oral cavity favors the growth of anaerobic organisms producing temporary
bad odor.
4. Smoking:
Liberation of certain chemicals from the smoke decreases salivary flow and also
decreases amount of oxygen within oral cavity.
5. Certain food partictes like:
Metabolites from certain ingested food excrete in the breathe air and impart odor to
breathe.
Onion, garlic impart odor to the breath by being absorbed in circulatory system
and then liberates volatile agents in air which is ventilated through lung (Garlic liberates
volatile sulfur).
Sugar containing diet is a good source of nutrition for anaerobic bacteria. Growth
of anaerobic bacteria is responsible for breath halitosis.
Dairy products like milk, cheese cause temporary halitosis. (They contain protein
lactase which is not digested by humans but broken by anaerobic group of
microorganisms).
Nonvegetarian food.

Pathological
Respiratory
Sinusitis Tonsillitis
Pharyngitis Tumors
Bronchitis Pulmonary tuberculosis
Pneumonia Lung abscess (Acid sweet odor)
Bronchiectasis (Foul putrefactive odor) Gangrene of lung
Halitosis 119

Liver (Sweetish odor), Kidney (Odor of ammonia, uremic odor)


Liver cirrhosis Gallbladder disease
Liver failure Uremia

Essentials of Dentistry
Gastrointestinal
Esophageal reflux Hiatus hernia
Pyloric stenosis Stomach cancer
Malabsorption Diabetes (Acetone odor, fruity)
Zenker’s diverticulum Regurgitation esophagitis

Other
Rheumatic fever (Fluctuant amine odor)
Scurvy
Blood dyscrasias

Drugs causing halitosis


Chloral hydrate Antiparkinsonians
Metronidazole Antidepressants
Amyl nitrate Anticholinergics
Narcotics Antihistaminics
Decongestants Antihypertensives
Antipsychotics Medication containing female hormones (estrogen, progesterone)

• Infections or lesions of respiratory tract.


Odor from aromatic substances in bloodstream such as excretory products of cell
metabolism is excreted in breathe air through the lung.
• Certain metabolic conditions involving enzymatic and transport anomalies like
Trimethylaminuria.
• Mucosa of oral cavity and upper respiratory tract is used to expel volatile compounds
from the body, including gases and metabolic end products of the diet (garlic, alcohol)
produced in oral cavities as well as extraoral sites.

DIAGNOSIS
1. Organoleptic methods:
– Breath consists of odor originating from both oral cavity and lungs.
– Ask the patient to close the nostrils and the smell indicates that of the oral cavity.
– Ask the patient to close the mouth and the smell indicates respiratory problems.
– Individuals are instructed to refrain from using any dental products, eating, or
using deodorants or fragrances 48 hours prior to visiting the dental clinic.
– Subject is instructed to close the mouth for 2 minutes and to refrain from swallowing
during this period. After 2 minutes, the subject breaths out gently at a distance
of 10 cm from the nose of their counterpart.
Organoleptic grading:
(Organoleptic rating—Rosenberg and McCulloch)
0 – No appreciable odor
1 – Barely noticeable odor
120 Halitosis

2 – Slight but clearly noticeable odor


3 – Moderate odor
4 – Strong odor
5 – Extremely foul odor.
Essentials of Dentistry

2. Tongue odor.
Odor emancipating from the tongue coating is definite indicator of halitosis. Scrape
the dorsum of patient’s tongue and immediately smell its odor. It is also known as
Spoon test.
3. Floss odor.
Smelling wax dental floss after passing interproximally between all posterior teeth
is also used for identifying halitosis.
4. Quantitative methods.
5. Dark field/phase contrast microscopy.
Periodontal diseases like gingivitis and periodontitis are associated with higher
incidences of motile organisms and spirochetes. Certain spirochetes have been
associated with a specific malodor which can be isolated by dark field/phase contrast
microscopy.
6. Gas chromatography.
Portable machines, such as the oral chroma, are currently being introduced. This
technology is specifically designed to digitally measure molecular levels of the three
major VSCs in a sample of mouth air (hydrogen sulfide, methyl mercaptan, and dimethyl
sulfide). It is accurate in measuring the sulfur components of the breath and produces
visual results in graphic form via computer interface. Breath odor changes in intensity
throughout the day depending on many factors, therefore, multiple testing may be
necessary.
7. Zinc oxide thin film semiconductor sensor.
8. Portable sulfide monitor (Helimeter).
It is a portable sulfide meter with an electrochemical voltmetric sensor which
generates signal when exposed to sulfide or mercaptan gases.
It measures the concentration of H2S in part per billion. However, it has drawbacks
in clinical applications. For example, other common sulfides (such as mercaptan)
are not recorded as easily and can be misrepresented in test results. Certain foods
such as garlic and onions produce sulfur in the breath for as long as 48 hours and
can result in false readings. The Helimeter is also very sensitive to alcohol, so one
should avoid drinking alcohol or using alcohol-containing mouthwashes for at least
12 hours prior to being tested. This analog machine loses sensitivity over time and
requires periodic recalibration to remain accurate.
9. BANA test:
This test is directed to find the salivary levels of an enzyme indicating the presence
of certain halitosis-related bacteria.
10. -galactosidase test:
Salivary levels of this enzyme were found to be correlated with oral malodor.
11. Electronic nose:
This device is based on sensor technology that can smell and produce unique profiles
for distinct odors.
12. Home tests are now available which use a chemical reaction to test for the presence
of polyamines and sulfur compounds on tongue swabs.
Halitosis 121

Specific characteristic of breath odor


Odor Indication
Rotten eggs smell Volatile sulfur compound

Essentials of Dentistry
Sweet (dead mice) Liver insufficiency
Rotten apples Insulin dependent-diabetes (accumulation of ketones)
Fish Kidney insufficiency
Foul odor Chest infections
Fruity malodor Oral thrush
Distinct metallic smell Ulcers

PREVENTION
1. Maintain oral health.
Gently cleaning the tongue surface twice daily is the most effective way to keep
bad breath in control as the tongue is the principle site of accumulation.
2. Eating a healthy breakfast with rough foods helps clean the very back of the tongue.
3. Chewing gum: As dry mouth can increase bacterial buildup and cause or worsen bad
breath, chewing sugarless gum can help in production of saliva and thereby help to
reduce bad breath.
4. Gargling right before bedtime with an effective mouthwash.
5. Maintain water levels in the body by drinking several glasses of water a day.

MANAGEMENT OF ORAL MALODOR


Accurate labelling and interpretation of different oral malodors contribute to the diagnosis
and treatment of the underlying disease. Improved oral hygiene is a key factor in the
successful clinical treatment of halitosis.
1. Local chemical/antimicrobial methods
• Mouth rinses have been used as a chemical approach but most of the commercially
available rinses merely mask odors and provide little antiseptic effect as the thick
layer of plaque and mucus protect the microbes. Most commercially available
products contain alcohol which can dry the oral tissue and again act as a risk factor.
• Zinc rinses available in chlorine, citrate or acetate form have been found to reduce
the oral malodor by preventing bisulfide group reduction to thiols.
• Chlorine dioxide rinses are also helpful in reducing oral malodor. Chlorine dioxide
is a strong oxidizing agent.
• Triclosan rinses are effective in most types of oral bacteria. However, combined
zinc and triclosan has cumulative effect.
• Hydrogen peroxide reduces the level of salivary thiol precursors.
• Topical Azulene ointment with a small dose of clindamycin and Breathnol—a propriety
mixture of edible flavors are also useful.
2. Oral hygiene maintenance
• Proper brushing and cleaning of tongue after each meal and use of flossing and
other interdental aids help in maintaining the oral hygiene. Scraping tongue reduces
oral malodor by approximately 75 percent.
• Elimination of local factors includes scaling and root planing, elimination of
periodontal pockets, restoration of carious lesions and correction of open contacts
122 Halitosis

between teeth, and extraction of unrestorable teeth. Correction of any defect to


minimize the accumulation of food debris and stagnation of saliva.
• Denture should be kept clean by brushing and putting in cleansing and disinfecting
solution.
Essentials of Dentistry

• Patient is asked to maintain the oral hygiene.


3. Salivary stimulation and/or substitutes
• Patient with xerostomia can use sodium carboxy ethylcellulose to moisturize oral
cavity.
4. Nasal mucus control methods
5. Avoidance of food, fluids and medications
– Sugar-free meal
– Use of fibrous food
– Use of plenty of liquid or water
– Less consumption of dairy products
– Bioadhesive tablets and lozenges
– Smoking should be discontinued.
6. Correction of anatomical abnormalities.
7. Medical management of systemic diseases.
8. If etiological factors other than local factors are suspected, laboratory tests like total
blood count, urine analysis should be preferred and consultation of physician is required.
9. Systemic antibacterial methods.
CHAPTER

18 Periodontal Probe

The clinical periodontal assessment is a fact-gathering process designed to provide a


complete picture of a patient’s periodontal health status. Much of the information collected
during the periodontal assessment involves the use of a periodontal probe. It is the most
widely-used diagnostic tool for assessment of connective tissue destruction in periodontitis.
The word probe is derived from the Latin word “Probo”, which means “to test”. Its
use was first described by FV Simonton of the University of California, San Francisco
(Simonton 1925), when he and others referred to it as periodontometer (Carranza and
Shklar 2003). Periodontal probes are used primarily to detect and to measure the periodontal
pockets and attachment loss. Orban described probe as “Eye of the examiner beneath
the gingival margin”.

DEFINITION
It is a slender, blunt-ended, tapering assessment instrument used to evaluate the health
status of the periodontal tissues.
The calibrated periodontal probe is a periodontal instrument that is marked in millimeter
increments.

DESIGN
Probes have blunt, rod-shaped working ends that may be circular or rectangular in shape.
There are many different types of periodontal probes, and each has its own manner of
indicating measurements on the tip of the instrument. The working end of the probe is marked
by indentations, grooves or color bands at certain millimeter intervals from the tip. There
may be some color bands in between two markings for easy identification of measurements.

FUNCTIONS
• It is used to measure the comprehensive findings of periodontal examination to determine
the health of the periodontal tissues.
• It is used to measure sulcus and pocket depths, to measure clinical attachment level,
to determine the width of attached gingiva, to assess bleeding on probing and
suppuration, and to measure the size of oral lesions.
• In addition, they are used to locate calculus, to measure gingival recession, and to
locate and measure the furcation involvement.
• Documenting measurements:
It is best to use anatomic references rather than “length” or “width” to document your
measurements on the chart (e.g. as the anterior-posterior measurement and the superior-
inferior measurement) (Fig. 18.1).
124 Periodontal Probe

• Determining the height of a raised lesion:


Place the probe tip on normal tissue alongside of the deviation. Imagine a line at the
highest part of the deviation, and record this measurement as the height (Fig. 18.2).
• Determining the depth of a sunken lesion:
Essentials of Dentistry

Carefully place the probe tip in the deepest part. Imagine a line running from edge-
to-edge of the deviation. The depth is the distance from this imaginary line to the base
of the deviation (Fig. 18.3).

CLASSIFICATION OF PROBES
In 1992, Pihlstorm et al classified probes into three generations for consistency of use
and academic purposes. In 2000, Watts extended his classification by adding fourth and
fifth generation probes.

Fig. 18.1: Dimensions of lesion

Fig. 18.2: Height of lesion


Periodontal Probe 125

Essentials of Dentistry
Fig. 18.3: Depth of lesion

1st Generation (Conventional) Probes


• They were invented in 1963 by periodontist Charles HM Williams. The Williams
periodontal probe is the prototype or benchmark for all first generation probes.
• Conventional (manual) probe do not control the probing pressure.
Williams probe, University
of Michigan O probe,
Routine clinical periodontal screening
Goldman Fox, Glickman,
Merritt A and B
Nabers probe Used to measure the horizontal component of furcation involvement
CPITN probe Used for screening and monitoring of the patients with CPITN index
UNC-15 Used in clinical research, if conventional probes are required

Advantages
• Easy availability and inexpensive
• Tactile sensitivity is preserved
• Tip is rounded to avoid tissue trauma
• Color-coded for easier and faster identification of readings
• Even in presence of subgingival calculus, probe can be inserted with little navigation
by the operator.

Disadvantages
• Heavy in weight
• Probing force is not controlled, so the tip of the probe may pass beyond the base
of the pocket
• In terms of reproducibility, it has limited value as precision varies from person to person
• An assistant is needed to transfer the readings to the chart
• Errors during visualizing the readings are possible.
126 Periodontal Probe

2nd Generation (Pressure Sensitive) Probes


• They were introduced by Hunter in 1994.
• They have disposable probe head and hemispheric probe tip with diameter of 0.5 mm.
• These probes have a visual guide and a sliding scale where two indicator lines meet
Essentials of Dentistry

at a specific pressure.
• These are pressure sensitive allowing improved standardization of probing pressure.
• It has shown that with force up to 20 gm, the probe remains within junctional epithelium.
• Force of 50 gm helps in diagnosis of osseous defect.
For example, True pressure sensitive probe, Yeaple probe

Advantages
• Standardization of probing forces
• Comfortable to patient
• Constant pressure.

Disadvantages
• Lacks tactile sensitivity
• Probe tip may pass beyond the junctional epithelium in inflamed tissues
• No computer storage of data
• Readings have to be performed manually, and an assistant is needed to record the
same on the patient chart
• It is used with a fixed amount of pressure regardless of the site, presence/absence
of inflammation, which may lead to inaccurate measurement and discomfort to
patient.

3rd Generation (Automated, Computerized) Probes


They were invented by Gibbs in 1988 in order to help minimize the errors of second
generation probes, such as reading errors, calculation errors.
• Probe is attached with the handpiece. It has got a digital read out, foot switch and
computer interface, and a computer.
• Probe tip is of 0.45 mm diameter. The probing force is automatically standardized at
15 gram.

Mechanism of Action
• The main mechanism of action is the detection of the cementoenamel junction.
• The ball tip moves over the root surface at a controlled speed and preset pressure.
Abrupt changes in the acceleration of the probe movement indicate the reach of
cementoenamel junction, and it stops at the base of the pocket.
• The position and acceleration time are analyzed to determine attachment level and
pocket depth.
• It reciprocates through sleeve, and measurements are made electronically and
transferred automatically to computer on pressing the foot switch.
• The software stores date of attachment loss, recession, pocket depth, furcation depth.
For example, Foster miller probe (detects distance from cementoenamel junction so
helps in assessing attachment loss) is the prototype of third-generation probes.
Florida probe, Toronto probe, InterProbe.
Periodontal Probe 127

Advantages
• Standardization of probing forces.
• High degree of accuracy and reproducibility of measurement as it detects the
cementoenamel junction, which is a better landmark than gingival margin because

Essentials of Dentistry
the latter may change depending on inflammation or recession.
• Errors in reading the probe and transferring the data are eliminated.
• Printout of the data from the computer can be used for patient education.

Disadvantages
• The main disadvantage is that it considers the root roughness or root surface irregularities
as the cementoenamel junction.
• Tactile sensitivity is decreased.
• Probe may pass beyond the junctional epithelium in inflamed sites, overestimating the
pocket depth.
• After the inflammation has resolved, probe may not penetrate beyond the long junctional
epithelium, leading to underestimation of the pocket depth.
• Use of fixed force setting throughout the mouth regardless of the site or inflammatory
status may generate inaccurate measurement or patient discomfort.

4th Generation Probes


They are still under investigation. These probes are aimed at recording sequential probe
positions along the gingival sulcus.

Advantages
• Three dimensional pocket configuration can be assessed
• Sequential probe positions are measured.

Disadvantages
• Invasive probe.

5th Generation Probes


• They were devised by Hinders and Companion at the NASA Langley Research Center.
• They are aimed to identify the attachment level without penetrating it.
• The probe has an ultrasonic beam projection. They are close enough in size to the
width of the periodontal ligament space to give the optimal coupling, and small enough
to inspect the area between the teeth, while still delivering sufficient signal strength
and depth of penetration to image the periodontal ligament space.
• They are suitable for universities and research institutes.
For example, Ultrasonographic (US) probe.

Advantages
• There is no possibility of imprecise readings due to the passing of the probe beyond
the junctional epithelium as it utilizes the ultrasonic waves to detect, image and map
the upper boundary of periodontal ligament.
• A noninvasive probe that provides painless probing to the patient.
• Provides information regarding the condition of gingival tissues.
• Computer storage of data and printout or visuals can be used for patient education.
128 Periodontal Probe

Disadvantages
• Expensive
• Operator needs training to interpret the image provided by the computer
• Requires learning curve.
Essentials of Dentistry

Fig. 18.4: Markings of Williams probe and Nabers probe

Periodontal probes Design

Marquis color-coded probe Calibrations are in 3 mm sections


University of North – Length of probe is 15 mm
Carolina (UNC-15) – Each mm from 1 to 15 is marked
color-coded probe – Black marking at 5 mm, 10 mm, 15 mm
Michigan “O” color-coded – Markings at 3 mm, 6 mm, 8 mm
probe – A modification of the probe with markings of Williams probe
is also available
– Probe shape is same as that of Williams probe but ends are
rounded
Nabers probe (Fig. 18.4) – Markings are at 3 mm, 6 mm, 9 mm
Williams probe (Fig. 18.4) – 13 mm in length, tip diameter is 1 mm
– Probe tips and handles are enclosed at 130°
– Markings at 1 mm, 2 mm, 3 mm, 5 mm, 7 mm, 8 mm, 9 mm,
10 mm (All from 1 to 10 except one number before and one after 5)
– 4 mm and 6 mm markings are absent to improve visibility and
avoid confusion in reading
WHO probe – 0.5 mm ball at tip and millimeter markings at 3.5 mm, 5.5 mm,
8.5 mm, 11.5 mm
(CPITN probe) – Color coding (black band) from 3.5 mm to 5.5 mm
Florida probe 0.45 mm tip diameter, 0.97 mm sleeve diameter
Goldman fox Markings are same as Williams probe
It is flat while Williams is round, tapered
CHAPTER

19 Probing

DEFINITION
“Probing is act of walking the tip of probe along the junctional epithelium within the sulcus
or pocket for the purpose of assessing the health status of periodontal tissue.”
Force Effect
0.75 N (25 gram) Well-tolerated by tissue and considered as an optimal force.
30 gram Required to penetrate up to junctional epithelium.
50 gram Required to detect bony defects.

It is the distance between gingival margin and the base of the pocket (coronal
Biological depth
end of junctional epithelium). It is a histological evaluation.
It is the distance between gingival margin and the apical end of the periodontal
Probing depth
probe penetration. It is a clinical evaluation.

In healthy gingiva, probe tip penetrates to most coronal intact junctional epithelium/
partly within the junctional epithelium/ sometimes up to coronal intact fibers of connective
tissue attached to the tooth surface.
In inflamed tissues, the probe passes through the junctional epithelium and to the
connective tissue. This means, true histologic depth of the pocket is not being measured.
Consequently, the term probing depth often replaces the more traditional term pocket depth
(Fig. 19.1). Pocket depth is the distance between the base of the pocket and the gingival
margin. It may change from time to time.

PROBING TECHNIQUE
• Insert the probe parallel to the vertical axis of the tooth surface (both mesiodistally
and labiolingually) and then walk circumferentially around each surface of each tooth
to detect area of deepest penetration (Fig. 19.2).
• Move the probe up and down in short bobbling strokes and go ahead in 1mm of
increments.
• The probe is not completely removed from the sulcus with each upward stroke as
repeated act of removal and insertion of probe can traumatize the marginal gingival.
• The probing forces varying from 20-25 gram have been suggested appropriate. Probe
should be activated with light pressure by gentle motion of wrist or finger. Several
investigators have found that 0.75 N of force is well-tolerated and accurate. This probing
force can be clinically determined by applying the probe tip to your fingernail bed,
where it will initiate blanching (Greenstein 1990, 2005).
Essentials of Dentistry 130 Probing

Fig. 19.1: Probing depth

Fig. 19.2: Probing technique

• Probe penetration can vary depending on the force of introduction, the shape and the
size of the probe tip, and the degree of tissue inflammation. Improper probing can
injure the junctional epithelium.
• The side of the probe tip (1-2 mm) should be kept in contact with the tooth surface.
Probe should be kept as parallel as possible to the tooth surface.
• Access the area beneath the contact area by tilting the probe to extend the tip beneath
the contact area, and gently press down to touch the junctional epithelium. Probe should
be placed from both facial and lingual surfaces to detect the deepest point beneath
the contact area (Fig. 19.3).
• Record the six measurements for each tooth and finally the deepest reading is recorded.
• In healthy gingiva, penetration of the probe gives more resistance while in presence
of inflammation, the probe tip may go beyond the junctional epithelium.
Probing 131

Essentials of Dentistry
Fig. 19.3: Probing below contact area

INTERPRETATION
The depth of a sulcus or the pocket is determined by measuring the distance from gingival
margin to the base of the gingival sulcus with a calibrated periodontal probe (Fig. 19.1).

Healthy gingiva 2/3 of the length of junctional epithelium


Gingivitis Probe stops 0.1 mm short of apical end of junctional epithelium
Periodontitis Probe tip consistently passes beyond the most apical cells of junctional epithelium.
Probe tip passes 0.3 mm in the connective tissue apical to the junctional
epithelium.

Normal Sulcus
In disease-free sulcus, junctional epithelium forms base of the sulcus by attaching to the
enamel of the crown near the cementoenamel junction. The probing depth of normal gingival
sulcus is 2-3 mm as measured with periodontal probe.

Periodontal Pocket
Periodontal pocket is pathologic deepening of the gingival sulcus due to apical migration
of the junctional epithelium. The junctional epithelium forming the base of the pocket is
somewhat more apical than normal position at cementoenamel junction. It is due to destruction
of periodontal ligament and alveolar bone. The normal sulcus deepens to 5-6 mm usually.
Actual pocket depth cannot be measured as the probe always penetrates the tissue
variably in periodontitis. Variables in measuring pocket depth are:
• Accurate probe gradations
• Diameter of probe, angle and force
• Degree of inflammation.
Essentials of Dentistry 132 Probing

Fig. 19.4: Probing of healthy sulcus and periodontal pocket

Probing depths are not reliable indicators of the extent of bone support because these
measurements are made from the gingival margin. The position of gingival margin changes
with tissue swelling, overgrowth and recession.

LIMITATIONS
Periodontal probing presents many problems in terms of sensitivity and reproducibility
of the measurements.
• Reading error may result from interference by the calculus from tooth and root surfaces,
presence of overhanging restorations or abnormal contour of crown.
• Operator’s error like incorrect angulations of the probe, misreading of the probe,
recording data imprecisely, and miscalculating the attachment loss.
• Clinical pocket depth readings normally do not coincide with the histologic pocket depth
because the probe normally penetrates the coronal level of the junctional epithelium,
if inserted properly, and the precise location of the probe tip varies depending on the
degree of inflammation of underlying connective tissues.

FACTORS AFFECTING PROBING


Various factors, such as probe tip size, probing technique, angle of insertion of probe,
probing pressure, precision of probe calibration, and degree of inflammation in underlying
periodontal tissues, affect the sensitivity and reproducibility of measurements (Fig. 19.4).
Inflamed tissues offer less resistance to probe penetration, whereas after the subgingival
instrumentation, healed gingiva offers increased resistance to probing. Likely, increased
fibrosis in smokers offers more resistance to probe tip penetration.

PROBING AT VARIOUS TIMES


1. Pretreatment probing in moderate or advanced cases may not be an accurate
representation of periodontal condition. Interference by abundant calculus and presence
Probing 133

of heavy inflammation hampers the accurate assessment. This pretreatment probing


with other clinical and radiographical findings aid to determine whether the tooth can
be saved or not.
2. After scaling and adequate plaque control by patient, the major inflammatory changes
disappear, and more accurate probing of the pockets reveals the level of attachment

Essentials of Dentistry
and degree of root and furcation involvement. The data from the second time probing
provides valuable information for treatment planning.
3. Later in periodontal treatment, probing is done to determine changes in pocket depth
and to ascertain healing progress after various procedure.
CHAPTER

20 Scalers and Curettes

Differences between scaler and curette


Scaler Curette
Use Supragingival scaling Subgingival scaling, root
(primary use) planing, curettage
Subgingival scaling (primary use)
(secondary use)
Blade Thicker Finer
Working tip Converge to pointed tip (Fig. 20.2) Round toe (Fig. 20.4)
Working edge 2 working edge (Fig. 20.1) Universal – 2
Area specific – 1 (Outer, convex)
(Fig. 20.3)
Design Heavy Fine, delicate, vital
Insertion Only 1 mm subgingivally More subgingivally
Adequate Good
Adaptation (Doesn’t adapt to root (Possible to adapt to
surface properly) deeper areas)
Triangular Semicircular or spoon
shaped
Cross
section

Stroke Scaling stroke – Root planning stroke –


Short, powerful, pull Moderate to light, pull
Curvature Curved in one plane Curved in two plane
Types U 15/30, Ball and Indiana Two basic types;
Jaquette sickle # 1,2 and 3 Universal
Curved 204 sickle – Barnhart
Nevi 2 posterior sickle scaler – Columbia
Area specific
– Gracey
– Langer
Scalers and Curettes 135

Essentials of Dentistry
Fig. 20.1: Features of scaler

Fig. 20.2: Design of scaler


Essentials of Dentistry 136 Scalers and Curettes

Fig. 20.3: Features of curette

Fig. 20.4: Design of curette


Scalers and Curettes 137

DIFFERENCES OF GRACEY CURETTE AND UNIVERSAL CURETTE


(FIG. 20.5A AND B)

Gracey curette (Fig. 20.5B) Universal curette

Essentials of Dentistry
Area of operation Area and surface specific Universal—Only one curette is used for all teeth
Different designs for by changing position of blade, fulcrum,
different areas adaptation and finger rest
Cutting edge One cutting edge is used, Both cutting edges are used, i.e. work with
i.e. work with outer edge either inner or outer cutting edges
only
Blade Curved in two planes. Curved in one plane.
Blade curves up and to Only upwards and not to the side
the sides
Blade angle Offset blade: face of blade Not offset blade: face of blade is beveled at
is beveled at 60° to 70° 90° to lower shank
from the lower shank
Working end The working end is The lower shank must be tilted slightly towards
automatically at the correct the tooth surface to establish correct angulation
angulation when the lower with tooth
shank is parallel to the
tooth surface

Gracey curettes
No. 1-2, 3-4 Anterior teeth
No. 5-6 Anterior and premolar teeth
No. 7-8, 9-10 Posterior teeth: facial and lingual
No. 11-12 Posterior teeth: mesial surface
No. 13-14 Posterior teeth: distal surface
No. 15-16 Blade of 11-12 and shank of 13-14
No. 17-18 Blade of 13-14 and shank extended by 3 mm

Figs 20.5A and B: (A) Universal curette, (B) Gracey cure tte
Essentials of Dentistry

COMPARISON OF SCALERS
Ultrasonic scaler
Hand scaler Sonic scaler
Magneto strictive Piezoelectric
Principle The conversation of 60 HZ, When electric energy is Compressed air over an
120 V current in an ultrasonic applied across the eccentric rod drives the rod
unit, which continually alters the piezoelectric substance, to vibrate.
– shape of a (magnetostrictive) measurable changes in form
bimetallic stack of nickel-cobalt of expansion and contraction
138 Scalers and Curettes

alloys, into an elliptical motion. of the crystal produces


linear motion of tip.
Tip
- Action Vertical Elliptical Linear (scraping) Orbital (rotary)
- Adaptibility Good Fair Fair Fair

- Application Removal of deposits is directly influenced by the angle of tip application onto the Removal of deposits is
tooth surface as only two tip surfaces are active at once. independent from tip
application the tooth
surface as all sides of tip are
active.

Contd....
Ultrasonic scaler
Hand scaler Sonic scaler
Magnetostrictive Piezoelectric
Contd....

Oscillation 50-70 µm approximately 100-250 µm


Amplitude – Higher pressure damps down the oscillation approximately
Oscillations are
independent of contact
pressure
Frequency – 20,000 to 40,000 24,000 to 45,000 2,000 to 6,500
cycles/sec (Hz) cycles/sec (Hz) cycles/sec (Hz)
Force More (around 2N) Less force is required in comparison of hand scalers (It depends on tip frequency)
Efficiency Good, if proper Excellent (Sulcus lavage due to constant water irrigation have additional effect in
instrumentation technique is removing bio-film)
used
Time Time consuming Requires less time
Maintenance Medium Relatively high due to complex mechanism Medium
Cost Less High Medium
Aerosol formation No Aerosol formation is same for all
Health hazards Least High due to contagious aerosol formation
Noise Least Medium High
Heat No Metal stack in Quartz crystal is
magnetostrictive scaler piezoelectric scaler Lower than
generate less heat piezoelectric
compared to
magnetostrictive scalers
Resorption Less More (because of high frequency) Medium
Damage
Scalers and Curettes

Tissue abrasion There is no conclusive data.


It depends on various factors such as applied force, angle of tip placement, frequency of tip, etc.
139

Contd....
Essentials of Dentistry
Essentials of Dentistry

Ultrasonic scaler
Hand scater Sonic scaler
140 Scalers and Curettes

Magnetostrictive Piezoelectric
Comfort During removal of tenacious deposits, sonic and ultrasonic instruments produce less tissue trauma, if properly
manipulated and therefore less postoperative discomfort to the patient than hand instruments.
Asepsis Good Good but requires meticulous care to remove the debris from the hand piece and
to sterilize the core areas
Contraindication – – Patient with infectious and communicable diseases, as it may spread with aerosol
– Patient with respiratory and pulmonary diseases or those having difficulty in
breathing (e.g. Bronchitis, Asthma).
– Patients with metallic (older) cardiac pacemakers as ultrasonic waves may interfere
with its proper functioning. Sonic scalers do not produce the same effect.
– Patients with titanium implants can’t be treated with routine tips (Special titanium
tips,Teflon-coated or plastic tips can be used)
– Patients with compromised gag reflex
– Sometimes pediatric patients can be the relative contraindication as primary teeth
have large pulp chambers and the growing tissues are more susceptible to damage
by heat generated by instrument.
Scalers and Curettes 141

AREAS OF INSTRUMENTATION OF GRACEY CURETTES (FIGs 20.6 TO 20.8)

Essentials of Dentistry
Fig. 20.6: Areas of instrumentation of particular curette

Fig. 20.7: Gracey curettes

Extended shank curettes


The shank is extended by 3 mm than the standard gracey curette which allows the extension
into deeper periodontal pockets. They are available in all standard gracey numbers except
9-10.
For example, After five curettes
Miniblade curettes
These are modified after five curettes with the blade length half that of conventional
curettes. The shorter blade allows easier insertion and adaption in deep, narrow pockets
and furcation.
Essentials of Dentistry 142 Scalers and Curettes

Fig. 20.8: Operational areas of root surfaces for Gracey curettes

For example, Mini five curettes


Angulations in instrumentation
Angulation for blade insertion 0°
Angulation for scaling and root planing 45-90°
Angulation for curettage >90°

Angles in instrument
Blade angle of hoe 90°
Angle of blade with shank in universal curette 90°
Angle of blade with shank in gracey curette 60-70°
Angle between face and lateral surface of the blade 70-80°
Angle for sharpening 100-110°
CHAPTER

21 Gingival Curettage

DEFINITION
“Gingival curettage is the surgical procedure of scraping of gingival wall of periodontal
pocket to separate diseased soft tissue (Fig. 21.1).”
Gingival curettage is an older type of periodontal surgical procedure that involves an
attempt to scrape away the lining of the periodontal pocket. It is a surgical technique
designed to remove, by debridement, the inner aspect of the diseased gingival wall,
including the ulcerated and hyperplastic gingival epithelium and the contiguous zone of
damaged connective tissue downward and outward to the firm and intact aspect of the
gingival corium, thus converting diseased tissue to a surgical wound (Kon et al. 1969;
Pollack 1984). Removal of this tissue was assumed to enhance pocket reduction beyond
the results achieved by scaling and root planing alone, providing faster healing and the
formation of new connective tissue attachment to the root surface. This rationale has been
seriously questioned for many years and the procedure is no longer considered as standard
treatment.
Gingival curettage is a surgical procedure which consists of removal of inflamed soft
tissue lateral wall of pocket while subgingival curettage refers to a surgical procedure
performed apical to the epithelial attachment severing connective tissue attachment down
to osseous defects to remove the diseased tissues.

Fig. 21.1: Gingival curettage


144 Gingival Curettage

Closed crevicular curettage refers to performing soft tissue curettage rather than a flap
procedure in treating periodontal pockets. This approach has several advantages. It may
be used (1) for initial preparation to obtain predictable soft tissue shrinkage, (2) when
surgery is contraindicated for health or medical reasons, (3) when emotional patients cannot
Essentials of Dentistry

tolerate definitive surgery, (4) when esthetic concerns are a consideration (Pollack 1984).

RATIONALE
The goal of therapy is to remove chronically inflamed granulation tissue that forms the
lateral wall of periodontal pocket.
Along with granulation tissues, flakes of calculus and bacterial colonies are also removed
from root surface leading to shrinkage of soft tissue wall of pocket. By removal of epithelial
lining of the pocket and the underlying junctional epithelium by curettage gives chances
of new attachment. However, opinions differ regarding the extent of removal of pocket
lining and junctional epithelium.

INDICATIONS
1. It is done as nondefinitive surgery to reduce inflammation of lateral wall of pocket before
aggressive planned periodontal surgery.
2. It is indicated in patient who cannot be subjected to other surgical pocket elimination
procedure due to age or systemic condition as the goal of pocket elimination is
compromised and prognosis is marred.
3. It may be performed during recall visit as a part of maintenance therapy in cases treated
with pocket elimination surgery earlier.
4. Curettage eliminates suprabony pocket that are located in accessible areas and
have an inflammatory edematous pocket wall that shrinks to the sulcus depth after
treatment.
5. New attachment attempts in moderately deep infrabony pocket located in accessible
areas where a type of closed surgery is advisable.

CONTRAINDICATIONS
1. Furcation involvement.
2. Presence of bony craters, bony deformities.
3. The case of very deep infrabony pocket where instrumentation is not possible.
4. Pocket with fibrotic gingival wall.

LIMITATIONS
1. One should be careful while curetting thin friable gingiva as there is danger of perforating
or tearing such tissue.
2. Root planing mobilizes fragments of calculus and cementum that may be forced into
tissue during gingival curettage, if the procedures are done simultaneously.
3. Curettage does not eliminate cause of infection, for example, bacteria and plaque
deposits, so it should always be preceded by scaling and root planing.
4. Lack of predictability of removing the pocket epithelium, epithelial attachment and
subjacent altered connective tissue.
5. It is technically demanding and considered extremely difficult procedure to master.
6. It is often a “blind procedure” rather grossly inexact and depends solely on tactile
sensitivity.
Gingival Curettage 145

PROCEDURES
• It is usually done under local anesthesia after scaling and root planing with the help
of curettes.
• As curettage does not eliminate the causes of inflammation, it should always be preceded

Essentials of Dentistry
by scaling and root planning.
• Curettage can be done with help of curettes like Universal Columbia Curettes / a Specified
Gracey Curette.
• The instrument is inserted in such a way as to engage the inner lining of pocket wall
and the instrument is carried along with the soft tissue.
• Usually, the horizontal stroke is applied and at the same time the pocket wall may
be supported by a gentle finger pressure externally.
• The curette is placed under the cut edge of junctional epithelium to undermine it.
• In subgingival curettage, the tissues attached between bottom of pocket and alveolar
crest are also removed with a scooping movement of curette.
• The area is flushed to remove the flakes of calculus from root surface. By flushing
the pocket wall, debris and tags of tissue come out and periodontal dressing is applied.
• Suturing the papillae and application of periodontal pack may be indicated.

OTHER TECHNIQUES
ENAP (Excisional New Attachment Procedure)
Subgingival curettage is performed with knife (15/11 no. blade) is known as ENAP (Excisional
new attachment procedure). It is an approach to reestablish periodontal attachment and
reducing pocket depth. It is tempted by surgically removing sulcular and junctional
epithelium, the transseptal and gingival crest fibers, root calculus, through an internal
beveled incision without detachment of mucogingival complex. It was first presented and
evaluated experimentally and clinically in 1976 (Yuka et al 1976; Yuka 1976).
• After anesthetizing the area, an internal bevel incision is placed from free gingival margin
to a point below the bottom of the pocket on all the sides of tooth (facial, lingual and
interproximal).
• With preservation of as much interproximal tissues as possible, the inner portion of
soft tissue wall of the pocket is excised.
• Curette is used to remove the excised tissues and all exposed cementum is thoroughly
root planed. Connective tissue fibers are preserved on the root surface for better healing.
• Wound edges are approximated and wound is sutured. Bone contouring may be
performed, if required.

Ultrasonic Curettage
Ultrasonic devices deliver the vibrations that disrupt tissue continuity, separate collagen
bundles and lift off the epithelium. Morse scaler-shaped and rod-shaped ultrasonic
instruments are used for this purpose.
Some studies found ultrasonic devices equally effective as manual instruments and
at the same time resulted in less inflammation and less removal of underlying connective
tissue.

Chemical Curettage
Caustic drugs such as sodium hypochlorite, sodium sulfide and phenol have been used
for chemical curettage. However, the effect of these agents is not limited to the epithelium
and depth of penetration cannot be controlled. Thus, inability to control the extent of tissue
146 Gingival Curettage

destruction and increase in amount of tissues to be removed by enzymes and phagocytes


has proved it ineffective.

HEALING AFTER CURETTAGE


Essentials of Dentistry

• Immediately after curettage, blood clot fills the pocket area which is partly/totally devoid
of epithelial lining.
• Hemorrhage is present in tissue with dilated capillaries and abundant polymorphonuclear
leukocytes which is gradually followed by rapid proliferation of granulation tissue.
• Decrease in number of blood vessels is observed as healing progresses.
• Epithelialization of sulcus generally required 2-7 days.
• Restoration of junctional epithelium occurs within 5-7 days. Immature collagen fibers
reappear and establish within 3 weeks.
• Healing results in long, thin junctional epithelium and no new thin connective tissue
attachment.
• Tissue usually shrinks and takes its position apical to normal.
CHAPTER

22 Infrabony Pocket

Periodontal pocket is defined as “Pathological deepening of gingival sulcus due to apical


migration of junctional epithelium”.
Periodontitis starts as an inflammation of the gingiva in response to bacterial change.
The transformation of gingival sulcus into a periodontal pocket creates an area where
plaque removal becomes impossible. The pathogenesis of periodontal destruction involves
a complex interplay between bacterial pathogens and the host tissues. Inflammatory and
immune reactions extending deeper into the connective tissue beyond the base of the
pocket may also include alveolar bone loss in this destructive process. Periodontal pocket
shows following signs and symptoms.

SIGNS
• Change in morphology
Bluish red, thickened, rolled out marginal gingiva and blunted interdental papilla.
• Change in color
A bluish red, vertical zone extending from gingival margin to alveolar mucosa; change
in color of gingiva varies according to severity of inflammatory involvement.
• Smooth, shiny gingiva.
• Puffy, flaccid and edematous gingiva with loss of stippling and pitting on pressure.
• Discontinuity of interdental papilla, from both labial and lingual aspect.
• Bleeding by gently probing soft tissue wall of pocket.
• Suppuration may be present in many cases and pus may be expressed by applying
digital pressure.
• Loose, extruded tooth and tooth mobility may be present.
• Diastema formation.
• When explored with probe, inner aspect of pocket is generally painful.

SYMPTOMS
Periodontal pockets are generally painless but may give rise to following symptoms:
• Gnawing type of pain which may radiate to deeper periodontal structures. Severity
of pain varies according to severity of periodontal destruction.
• Bleeding from gingival tissue.
• Pus discharge even on digital pressure on attached gingiva.
• Food lodgment in localized region.
• Urge to dig with a pointed instrument and resultant bleeding gives relief.
• Feeling of itching in the gums.
• Foul taste in localized areas.
• Sensitivity with hot and cold, toothache in absence of caries.
148 Infrabony Pocket

CLASSIFICATIONS OF POCKETS
On the basis of position of epithelial attachment on tooth surface as well as position of
marginal gingiva, pockets can be classified as follows:
• Gingival pocket or pseudo pocket
Essentials of Dentistry

It occurs due to gingival enlargement without destruction of underlying periodontal


tissues. Coronal proliferation of marginal or papillary gingiva without any change in
epithelial attachment gives rise to deepening of gingival sulcus as a result of an increase
in size of gingiva, i.e. in case of chronic gingivitis.
• Periodontal pocket or true pocket
Periodontal pocket shows the change in position of epithelial attachment and
destruction of supporting periodontal tissues.

CLASSIFICATIONS OF PERIODONTAL POCKETS


Periodontal pockets are further classified as follows:

Depending on the Level of Bottom of Pocket


• Suprabony, supracrestal or supra-alveolar
The bottom of pocket and the junctional epithelium are coronal to underlying alveolar
bone. Deepening of gingival sulcus occurs with destruction of adjacent gingival fibers,
periodontal ligament fibers, and crestal alveolar bone and it is associated with apical
migration of the junctional epithelium. They are associated with horizontal bone loss.
• Intrabony, infrabony, subcrestal or intra alveolar
Deepening of gingival sulcus to a level at which the bottom of the pocket and the
junctional epithelium are apical to the crest of alveolar bone. They are associated with
the vertical bone loss.

Depending on Nature of Soft Tissue Wall


• Edematous pocket
• Fibrotic pocket

Depending on Disease Activity


• Active
• Passive

According to Number of Tooth Surfaces Involved


• Simple (involving one tooth surface)
• Compound (involving two or more surfaces)
• Complex or spiral pocket (periodontal pocket on one side may travel spirally, mesially
or distally involving one or more additional surfaces). They are most commonly seen
in furcation areas.

CLASSIFICATIONS OF INFRABONY DEFECTS


According to Number of Walls (Goldman and Cohen, 1958)
• One walled (Hemiseptum)
• Two walled
• Three walled (Infrabony)
• Combined osseous defect (The number of walls in the apical portion of the defect
are greater than that in its occlusal portion)
Infrabony Pocket 149

According to the Depth and Width of the Underlying Osseous Defect


Type I – shallow narrow
Type II – shallow wide
Type III – deep narrow

Essentials of Dentistry
Type IV – deep wide

Goldman and Cohen Classification of Intrabony Defects


According to by the number of walls around the lesion (JP, 58):
1. Three osseous walls
A three-walled intrabony defect is surrounded by three bone walls, with the root surface
as the fourth wall (Fig. 22.1). The walls may be at different level coronally. It occurs
most frequently in the interdental area. They may be called intrabony defect and they
are frequently associated with food impaction. They may also be seen on facial and
lingual surfaces having enough bone to support the formation of walls, e.g. defects
on facial and lingual of mandibular posterior teeth and palatal of maxillary teeth. These
3-walled defects are sometimes called wells.
a. Proximal, buccal, and lingual walls
b. Buccal, mesial, and distal
c. Lingual, mesial, and distal.
2. Two osseous walls
A two-walled intrabony defect (crater) is the most common osseous defect in the
interdental area (Fig. 22.1). Usually buccal and lingual walls are present and bone loss
occurs on the proximal surfaces of adjacent teeth. Two-walled defects with either facial
or lingual wall and a proximal wall are less common.
a. Buccal and lingual walls (crater)
b. Buccal and proximal walls
c. Lingual and proximal walls.
3. One osseous wall
One-walled intrabony defect usually exists in the interdental area. However, most
intrabony defects are of mixed types; e.g. the entrance has one wall or two walls but
the bottom has three walls (Fig. 22.1).
a. Proximal wall (hemiseptal)
b. Buccal wall
c. Lingual wall.
If the remaining bone wall is on the proximal surface, it is called a hemiseptal defect
and that on facial or lingual surface is called as a ramp. Shallow one-walled defects
may be managed by osseous surgery.
4. Combined osseous defect
In combined osseous defect, numbers of walls in the apical portion of the defect are
greater than those in its occlusal portion (Fig. 22.2). Such defects are more complex
apically than coronally. The depth, width, topography, number of remaining osseous
walls, and the configuration of the adjacent root surfaces are all important in determining
the therapeutic approach.
a. 3 walls + 2 walls
b. 3 walls + 2 walls + 1 wall
c. 3 walls + 1 wall
d. 2 walls + 1 wall
In the original classification by Cohen defects are also classified as follows:
Essentials of Dentistry 150 Infrabony Pocket

Fig. 22.2: 1-wall defect, 2-wall defect, 1-wall defect

Fig. 22.2: Combination defect

Zero-walled Defects
These are alveolar dehiscences and fenestrations found on facial and lingual surfaces
of teeth where the alveolar housing is typically thin or where tooth is abnormally inclined
or malpositioned. They are not seen on radiographs. Fenestrations in the presence of
Infrabony Pocket 151

marginal periodontitis may convert to dehiscence. Osseous surgery is not treatment of


choice for zero-walled dehiscence.

Four Osseous Walls (Circumferential)

Essentials of Dentistry
They are usually present with buccal, lingual, mesial and distal wall. Because they sometimes
encircle an entire tooth, four-walled defects have been called circumferential or moat defect.
Osseous surgery is not treatment of choice with four-walled defect.
But, later on they are removed from this classification.

ETIOLOGY OF INFRABONY POCKET AND INFRABONY DEFECT


Both suprabony and infrabony pockets are the result of plaque; however, there are some
differences of opinions for the factors that influence the formation of the infrabony pocket.
Most agree that vertical bone loss and subsequent infrabony pocket formation can occur
whenever there is direct extension of inflammation into the periodontal ligament, in the
presence of sufficient thickness of bone.
Bacterial plaque can induce bone loss within the radius of action of 1.5 to 2.5 mm
and there is no bone effect beyond 2.5 mm. Radius of action is principal factor for formation
of infrabony defect. Angular bony defects can appear only in the spaces wider than 2.5
mm because narrow spaces would be destroyed entirely. In addition to the important role
of local factors, that are plaque, calculus and material alba, trauma from occlusion plays
a major role.
1. Trauma from occlusion facilitates the spread of an inflammatory lesion from the zone
of irritation directly down into the periodontal ligament (i.e. not via the interdental bone).
This alteration of the “normal” pathway of spread of the plaque-associated inflammatory
lesion results in the development of angular bony defects. Trauma from occlusion
is found as an etiologic factor (codestructive factor) of importance in situations where
angular bony defects are combined with infrabony pockets. It may add to the effect
of infection by causing bone resorption lateral to periodontal ligament and leads to
creation of osseous defect. (Anatomic characteristics of area such as wide bone margin
may favor the production of angular lesion and infrabony defect).
2. It was stated that the forceful wedging of the food into the interproximal region may
result in unilateral destruction of the attachment apparatus and down growth of the
epithelial attachment. Food impaction and infrabony pocket often occurs together but
yet it is not established whether food impaction produces pockets or aggravates pockets
caused by other factors.

INCIDENCE
Vertical defects can appear on any surface of tooth. Angular defects increase with age. They
are found most often on the distal and mesial surfaces. Three-walled defects are more
frequently found on the mesial surfaces of second and third maxillary and mandibular molars.

DIAGNOSIS OF INFRABONY DEFECT


1. Radiograph
Vertical defects occurring interdentally can generally be seen on the radiograph, although
thick bony plates sometimes may obscure them. Defects appearing on facial and lingual
or palatal surfaces are not seen on radiographs.
X-rays can reveal existence of angular bone loss in interdental spaces but it will
not show the number of bony walls of defect. Radiographic marker (Hirschfeld points,
silver points, gutta-percha points) placed in the bony defects demonstrate the extent
Essentials of Dentistry 152 Infrabony Pocket

Fig. 22.3: Gutta-percha point in bony defect

of bone loss. Gutta-percha packed around the tooth can be helpful to identify the
configuration of defect (Fig. 22.3).
2. Clinical examination
Probing can determine the presence and depth of periodontal pockets around any
surfaces of any tooth. Both clinical and radiographic examination may suggest presence
of infrabony defect, if one or more of following are found.
i. Angular bone loss
ii. Irregular bone loss
iii. Pockets of irregular depth.
Under local anesthesia, osseous defect or morphology is detected by probing from
bottom of the pocket, both apically and laterally to alveolar bone. It is called as “Transgingival
probing or Sounding”. It is the process of walking the periodontal probe along the tissue-
tooth interface so as to examine, and predict the underlying osseous topography. Typical
finding of presence of interdental infrabony defect is sudden increase in the probing depth
compared to that of adjacent proximal surface.
However, the three-dimensional morphology of a defect cannot be determined until
the defect is visualized at the time of surgery. Surgical exposure and visual examination
provide the most definitive information regarding the bone architecture.

TREATMENT
Aims
1. Elimination of the periodontal pocket.
2. Reattachment of periodontal ligament to tooth surface and achievement of a tissue
shape which will allow the patient to carry out efficient plaque control.
3. Filling of osseous defect and improve tooth support.
Basic treatment consists of:
• Elimination of local irritants and inflammatory conditions.
• Correction of factors that are responsible for inflammation and that aggravate the effects
of trauma and food impaction leading to formation of infra bony pockets.
• To shape the bone in such a way that after healing and remodeling the resultant alveolar
architecture will allow effective oral hygiene measures to be carried out. This procedure,
osteoplasty, must be undertaken with great care.
Infrabony Pocket 153

• Make an attempt to obtain some fill-in of the bone defect. This may be achieved with
or without bone graft.
• To obtain new connective tissue regeneration.
Treatment plan is divided into:
1. Soft tissue phase

Essentials of Dentistry
2. Hard tissue phase
3. Functional phase
4. Maintenance phase.

Soft Tissue Phase


Management of soft tissue of pocket:
• The soft tissue wall of pocket consists of epithelial lining and granulation tissue. These
epithelial structures must be removed to make room for new connective tissue fibers
to attach to tooth surface.
Management of periodontal fibers adhering to bone surface:
• Periodontal fibers adhering to the bone must be removed to permit the flow of blood
and osteogenic cells into osseous defect.

Hard Tissue Phase


Initial periodontal therapy or basic treatment involving the removal of both sub and
supragingival plaque creates an environment conducive for periodontal regeneration.
Guided tissue regeneration (GTR) helps in acquiring new attachment on the root surface
covered by a membrane, and bone regeneration is expected in the osseous defect area.
However, in wide and deep osseous defects, osseous defects in which space making
is difficult, and osseous defects with furcation involvement, bone grafts may be used for
regeneration.
Management of root surface
Root surface is scaled and planed to remove all deposits, softened tooth structures, adherent
remnant and epithelium to make the root surface “hard” and “smooth”. It removes not
only soft and hard deposits from the root surface but also small amounts of tooth sub-
stance (thin layer of altered cementum) as tiny extensions of the subgingival calculus into
the root surface hamper the new attachment procedure.
Management of wall of osseous defect
Bony defect is curetted thoroughly to form a clean surface. The debridement of the exposed
root surfaces in the defect area is comprehensive. Since the location of the defect and width
of the bony defect entrance may limit the access of curettes for proper debridement. Surgical
flap therapy offers better visualization and eases the process of debridement. Granulation
tissues from the osseous defect are thoroughly removed to provide room for tissue attachment.
Furthermore, at the time of surgery, previously undiagnosed defects may be recognized
or some defects may have a more complex outline than initially anticipated. Exposed bone
surface of the defect is perforated with a 1/2 round bur after complete removal of granulation
tissue from the osseous defect. This facilitates the formation of blood coagulum on the
bone surface and accelerates the healing. This is known as “Regional acceleratory
phenomena”.
Three-walled infrabony defect often provides a better mould for bone repair than two-
walled or one-walled defects. Attachment gain can be achieved by flap curettage in a
three-walled defect area. New attachment can be achieved even in one-walled and two-
walled defects by using a barrier membrane. However, this approach is limited to deep
osseous defects due to requirements of space making. Important factors in determining
154 Infrabony Pocket

therapy for intrabony defects include depth of defect, width, position, number of remaining
bone walls, and adjacent root morphology.
1. One-walled angular defects usually require the bone to be reduced to the level of the
most apical portion of the defect.
Essentials of Dentistry

2. Three-walled defects, if narrow and deep, can be successfully treated by new attachment
and bone reconstruction therapy.
3. Two-walled defects can be treated with either of above method, depending on depth,
width and configuration of defect.
4. Ochsenbein proposed surgical therapy for combination defect that combined
regenerative and resective procedures. In combination defect, the wall coronal to a
three-walled combined-type intrabony defect has no hope for regeneration. The osseous
defect then is reshaped to three walls, and a barrier membrane is placed over the
osseous defect to facilitate regeneration.

Selection of Method
The method of achieving regeneration is selected after careful probing and clinical and
radiographic examination. The final decision is based on morphology of osseous defect
(depth and width), degree of furcation, and the anatomic condition of the root as observed
clinically after flap reflection (Fig. 22.4).

Fig. 22.4: Treatment planning


Infrabony Pocket 155

In shallow osseous defects, a resective procedure should be selected because bone


regeneration cannot be expected. However, morphology is not the only factor to consider
when selecting a method for treating the osseous defect.
The prognosis for successful resolution of infrabony defects is influenced by the:
1. Number of remaining osseous walls

Essentials of Dentistry
2. Size of the osseous defect (depth, width)
3. The proximity of the defect to important anatomical landmark
4. Number of root surfaces involved
5. Extent of bony destruction
6. Amount of bone that need to be removed to achieve positive bony architecture
7. Presence or absence of furcation involvement
8. Ability to effectively detoxify and debride the defect and tooth
9. The predictability of alternate form of therapy.
Segments of the periodontium with generalized horizontal patterns of bone loss and
multiple shallow interproximal osseous defects with less than three walls are traditional
indications for osseous surgery. As a general rule, defect with greater number of osseous
walls and also narrower in width, better the prognosis for regeneration. Defects that
conceivably will hold water offer excellent opportunities for bone graft containment and
periodontal regenerative procedures.
Regenerative procedures using a barrier membrane is another choice. However, it is
not applicable in the esthetic zone because remarkable postoperative gingival recession
occurs, if complete membrane coverage is not achieved.
Of the regenerative procedures, GTR is the method that requires preservation of the
interdental papilla and thick gingiva. Therefore, GTR cannot be used where there is thin
gingiva or gingival recession. Sufficient width of keratinized gingiva is necessary for flap
surgery without a barrier membrane. If there is insufficient keratinized gingiva in the surgical
area, increasing the keratinized gingiva with a free autogenous gingival graft is needed
as pretreatment (Fig. 22.5).

Fig. 22.5: Selection of method


156 Infrabony Pocket

Functional Phase
It includes following steps for correction of occlusal trauma to restore balanced occlusion,
• Selective reshaping of occlusal surfaces with the goal of establishing a stable,
nontraumatic occlusion is called as “Occlusal equilibrium or coronoplasty”. It eliminates
Essentials of Dentistry

premature contacts and reduces the loading of teeth that have lost bone due to
periodontal disease. As occlusal adjustment is an irreversible intervention, clinician
should be prudent to plan and to execute the cuspal reshaping.
• Removal of plunger cusp causing food impaction is an imperative procedure in treating
infrabony defect.
• Grinding of high point contact of restoration and marginal ridges alters contour of the
unfavorable, faulty restorations and helps in establishing stable functional relationships
favorable to the patient’s oral health.
• Occlusal rehabilitation by prosthesis in the form of crowns and bridges restores the
plane of occlusion and establishes the full mouth equilibration to the degree that
maximum intercuspation is coincident with centric relation. Building proper contacts
between adjacent teeth prevents food impaction.
The role of occlusal adjustment in the management of periodontal disease is more
complex because both periodontitis and trauma from occlusion can lead to tooth mobility.

Maintenance Phase
Patient should be advised to rinse with 0.12 percent chlorhexidine gluconate immediately
after surgical procedure and twice daily thereafter until normal plaque control technique
can be resumed. Plaque and food accumulation impair the healing so patient is advised
to keep the area as clean as possible by the gentle use of soft toothbrush. Vigorous brushing
is not feasible during the first few weeks after the surgical procedure. Proper brushing
technique is explained to the patient as the daily mechanical removal of plaque by the
patient is the only practical mean of maintaining oral health.

Suprabony pocket Infrabony pocket


Base of the pocket is coronal to alveolar Base of the pocket is apical to alveolar bone (i.e.
bone. pocket wall lies between bone and tooth).
Pattern of bone destruction is horizontal. Pattern of bone destruction is vertical.
The transseptal fibers are arranged The transseptal fibers are oblique rather than
horizontally in the space between base of horizontal. They extend from cementum beneath
pocket and alveolar bone. base of pocket along the alveolar bone and over
the crest to cementum of adjacent tooth.
On facial and lingual surfaces, periodontal On facial and lingual surfaces, periodontal ligament
ligament fibers beneath pocket follow their fibers follow angular pattern of adjacent bone.
normal course between tooth and bone.
CHAPTER

23 Bone Replacement Grafts

Numerous therapeutic grafting modalities for restoring periodontal osseous defects have
been investigated. Bone replacement grafts include autografts, allografts, xenografts, and
alloplasts. Bone replacement grafts are the most widely-used treatment options for the
correction of periodontal osseous defects. It has been proved that bone replacement grafts
provide clinical improvements in periodontal osseous defects compared with surgical
debridement alone. For the treatment of infrabony defects, bone grafts have been found
to increase bone level, reduce crestal bone loss, increase clinical attachment level, and
reduce probing pocket depths compared with open flap debridement procedures.
Periodontal defects as sites for transplantation differ from osseous cavities surrounded
by bony walls. Saliva and bacteria may easily penetrate along the root surface, and epithelial
cells may proliferate into the defect, resulting in contamination and possible exfoliation
of the grafts. Therefore, the principles established to govern transplantation of bone or
other materials into closed osseous cavities are not fully applicable to transplantation of
bone into periodontal defects.
Bone graft materials are generally evaluated based on their osteogenic, osteoinductive,
or osteoconductive potential. Osteogenesis refers to the formation or development of new
bone by cells contained in the graft. Osteoinduction is a chemical process by which molecules
contained in the graft (bone morphogenetic proteins) convert the neighboring cells into
osteoblast, which in turn form bone. Osteoconduction is a physical effect by which the matrix
of the graft forms a scaffold that favors outside cells to penetrate the graft and form new bone.
It would seem that graft materials which lack osteogenic potential act simply as a replacement
for the blood clot which usually breaks down, or as an inert scaffold on which some bone
formation takes place prior to the resorption of the graft. This is because cellular events of
periodontal regeneration involve the controlled integration of a number of cell signaling systems
for bone, cementum and periodontal ligament. Unless these are present in the graft material
and/or in the adjacent tissues in the right proportions, controlled regeneration cannot take
place. However, regeneration of new cementum, periodontal ligament and alveolar bone can
be achieved to some degree in intrabony defects with some grafting techniques.

EXTRA AND INTRAORAL DONOR SITES FOR AUTOGENOUS


BONE GRAFTS
If autogenous bone is considered the gold standard, its osteogenic potential is one feature
that differentiates it from the rest of the graft materials. The primary reason for its superiority
is its capacity to support osteogenesis in conjunction with its endogenous osteoinductive
and osteoconductive properties. Due to their osteogenic potential, autogenous bone grafts
of extra- and intraoral sources have been used in periodontal therapy.
The major drawback of the autogenous bone graft is that a donor site is required to
harvest the bone, which can lead to increased time, cost, and morbidity for patient. The
donor site and its individual variability limit the amount of bone that can be harvested.
158 Bone Replacement Grafts

Cancellous bone and marrow can be obtained from a number of sites in the mouth such
as the tuberosity, extraction sockets or the edentulous ridge, bone trephined from within the
jaw without damaging the roots. The maxillary tuberosity or a healing extraction site is typically
the donor choice for intraoral cancellous bone with marrow grafts (Cancellous bone marrow
Essentials of Dentistry

transplant). They are generally easy to manipulate, and revascularize rapidly. It is important
to remember that cancellous bone imparts no mechanical strength; when it is used to reconstruct
large continuity defects, additional rigid fixation is required. In the oral cavity, cancellous grafts
are used to fill bony defects, alveolar clefts, maxillary sinus, and other similar scenarios where
bone can be placed into an area and retained. The corticocancellous graft usually produces
the best results by combining the attributes of both cortical and cancellous forms. It allows
for mechanical stabilization while providing good revascularization.
Iliac grafts have been used fresh or frozen. One common complication is fresh marrow
tissue (Iliac autografts) often produces root resorption and ankylosis. Successful bone
fill has been demonstrated using iliac cancellous bone with marrow in furcations,
dehiscences, and intraosseous defects of various morphologies. But they have had only
limited use because of the difficulty in obtaining the graft material, morbidity, postoperative
infection, varying rates of healing, the possibility of root resorption and rapid recurrence
of the defect. In addition to these, it increases patient expense and is also found difficult
to procure the donor material so the technique is no longer in use.
Good clinical results have been achieved with the use of cancellous autogenous bone
grafts from an adjacent edentulous site. Other techniques report bone fill using cortical
bone chips and osseous coagulum or bone blend–type grafts. Studies report histologic
evidence of regeneration and new connective tissue attachment and the presence of a
long junctional epithelium following these procedures.

OSSEOUS COAGULUM
Osseous coagulum is a technique described by R. Earl Robinson using a mixture of bone
dust and blood. Small particles ground from cortical bone are used. The advantage of
the particle size is that it provides additional surface area for the interaction of cellular
and vascular elements. Graft materials can be taken from the lingual ridge on the mandible,
exostoses, edentulous ridges, the bone distal to a terminal tooth, bone removed by
osteoplasty or ostectomy, and the lingual surface of the mandible or maxilla.

BONE BLEND
Bone is removed from a predetermined site, triturated in the capsule to a workable, plastic-
like mass, and packed into bony defects.

BONE SWAGING
This technique requires an edentulous area adjacent to the defect, from which the bone
is pushed into contact with the root surface without fracturing the bone at its base.

ALLOGENIC BONE GRAFTS


Allogenic bone is nonvital, osseous tissue taken from one individual and transferred to
another of the same species. Iliac cancellous bone and marrow, freeze-dried bone allograft
(FDBA), and decalcified freeze-dried bone allograft (DFDBA) are the types of bone allografts
widely available from commercial tissue banks. Grafts are taken from cadaver bone, typically
freeze-dried and treated to prevent disease transmission. They are obtained from cortical
bone within 12 hours of the death of the donor, defatted, cut in pieces, washed in absolute
alcohol, and deep-frozen. The material may then be demineralized, and subsequently
Bone Replacement Grafts 159

ground and sieved to a particle size of 250 to 750 µm and freeze-dried. Finally, it is vacuum-
sealed in glass vials.
Numerous steps are also taken to eliminate viral infectivity. These include exclusion
of donors from known high risk groups and various tests on the cadaver tissues to exclude
individuals with any type of infection or malignant disease. The material is then treated

Essentials of Dentistry
with chemical agents or strong acids to inactivate the virus, if still present.

Freeze-dried Bone Allograft


FDBA works primarily through osteoconduction. The graft does not activate bone growth
but acts like a scaffold for natural bone to grow into. Eventually the graft is resorbed and
replaced by new bone. Freeze-drying the bone decreases the antigenicity of the allograft.
Radiographically, FDBA appears radiopaque because it is not demineralized. When using
FDBA to treat periodontal defects, trials indicate bone fill ranging from 1.3 to 2.6 mm.
A combination of FDBA with tetracycline has also shown promising results in the treatment
of defects resulting from juvenile periodontitis.

Demineralized (Decalcified) Freeze-dried Bone Allografts


Urist showed that DFDBA is osteoinductive. Demineralization in cold, diluted hydrochloric
acid exposes the components of bone matrix, which are closely associated with collagen
fibrils and have been termed bone morphogenetic proteins (BMPs). DFDBA is believed
to induce bone formation due to the influence of these bone-inductive proteins (BMPs)
exposed during the demineralization process. DFDBA is therefore thought to be
osteoinductive and osteoconductive.
DFDBA has demonstrated periodontal regeneration in controlled human histologic studies.
Superior gains in bone fill with DFDBA compared with openflap debridement have consistently
been reported. It has been observed in several reentry studies that grafting with DFDBA
is always superior to debridement alone when used for the correct indications. Laboratory
studies have found that DFDBA has a higher osteogenic potential than FDBA and is therefore
preferred. Studies have demonstrated that preparation of allograft material can differ from
one distributor to another and that the material may differ in its biologic activity. DFDBA
may also vary from batch to batch. Commercial bone banks do not verify the specific amount
of BMPs or the levels of inductive capacity in any graft material. The development of stricter
bone bank standards that evaluate the potency of their preparations, including (1) using
bones from individuals under a specific age, using bones from individuals free of bone
diseases, or using fresh bone, and (2) developing assays that can test the inductive capacity
of the material before sales, may lead to more consistent and reliable clinical results.
Comparison of freeze-dried bone allograft and demineralized freeze-dried bone allograft
FDBA DFDBA
Not demineralized Demineralized
Better space maintenance More bone morphogenetic protein
Slower resorption rate expression potential
compared with DFDBA Possible osteoinduction
Osteoconductive Osteoconductive
More radiopaque More radiolucent
Breakdown by way of foreign body Rapid resorption
reaction Primary indication: periodontal
Primary indication: bone augmentation disease associated with natural tooth
associated with implant treatment
(e.g. guided bone regeneration, sinus
grafting, ridge augmentation)
160 Bone Replacement Grafts

ALLOPLASTIC MATERIALS
Alloplastic materials are synthetic, inorganic, biocompatible, or bioactive bone graft
substitutes. Alloplastic materials are believed to promote bone healing through
osteoconduction. Currently, six types of alloplastic materials are commercially available:
Essentials of Dentistry

hydroxyapatite cement, nonporous hydroxyapatite, porous hydroxyapatite (replamineform),


beta tricalcium phosphate, polymethylmethacrylate/hydroxyethylmethacrylate (PMMA/
HEMA) calcium-layered polymer, and bioactive glasses and ceramics. Ideally, alloplast
bone substitutes should have the following properties: (1) biocompatibility, (2) minimal
fibrotic reaction, (3) the ability to undergo remodeling and support new bone formation,
(4) similar strength comparable to cortical/cancellous bone, and (5) similar modulus of
elasticity comparable to bone to prevent fatigue fracture under cyclic loading.
Calcium phosphate biomaterials have excellent tissue compatibility and do not elicit
any inflammation or foreign body response. These materials are osteoconductive, not
osteoinductive. Two types of calcium phosphate ceramics have been used, as follows:
1. Hydroxyapatite (HA) has a calcium-to-phosphate ratio of 1:67, similar to that found
in bone material. It is generally nonbioresorbable.
2. Tricalcium phosphate (TCP), with calcium-to -phosphate ratio of 1:5, is mineralogically
B-whitlockite. It is at least partially bioresorbable.
Bioactive glass is made from calcium salts, phosphate, sodium salts, and silicon. It
is used in the form of irregular particles measuring 90 to 170 pm (PerioGlas, Block Drug,
Jersey City, NJ) or 300 to 355 pm (BioGran, Ortho Vita, Malvern, Pa). When this material
comes into contact with tissue fluids, silicon forms a silica gel layer on the surface of these
particles which promotes formation of a hydroxycarbonate-apatite layer and incorporates
organic ground proteins such as chondroitin sulfate and glycosaminoglycans. On this layer
of hydroxycarbonate-apatite, osteoblasts are claimed to proliferate and form bone. These
materials have the ability to truly integrate or chemically bond with bone, because of its
capability to exchange ions or molecules with osseous tissue. Overall, histologic evaluation
of bioactive glass shows limited regenerative potential, with minimal bone regeneration
and no signs of new cementum or periodontal ligament. These bioactive glass materials
also appear to be encapsulated by collagen. Tricalcium phosphate and bioactive glass
are absorbable.
Porous and nonporous hydroxyapatite materials and PMMA/HEMA polymer are
nonabsorbable. Histologically, however, alloplast grafts tend to heal by encapsulation with
connective tissue with minimal or no bone formation. Some histologic evidence shows
that a very limited amount of regeneration may be possible following PMMA/HEMA polymer
grafts.
Coral-Derived Materials have been used in clinical periodontics. There are two different
coralline materials: natural coral and coral-derived porous hydroxyapatite. Both are
biocompatible, but whereas natural coral is resorbed slowly (several months), porous
hydroxyapatite is not resorbed or takes years for resorption.
Overall, the effect of alloplast material has been inconsistent. It appears that alloplastic
materials function as nonirritating fillers.

XENOGRAFTS
Xenograft (heterograft) is osseous tissue that is harvested from one species, processed,
and then transferred to a recipient site of a different species. They are bone from a different
species treated with ethylene diamine to remove the organic and antigenic fraction and
referred to as inorganic bone. These proprietary processes remove all cells and
Bone Replacement Grafts 161

proteinaceous material. It leaves behind inert, absorbable bone scaffolding. It is on this


scaffolding that revascularization, osteoblast migration, and woven bone formation
supposedly occur. Signs of periodontal regeneration have been reported with xenografts;
however, most data support a bone fill or repair of bone for guided bone regeneration
around implants, sinus lift procedures, and ridge augmentation.

Essentials of Dentistry
Calf bone treated by detergent extraction, sterilized, and freeze-dried, has been used
for the treatment of osseous defects. Kiel bone is calf or ox bone denatured with 20 percent
hydrogen peroxide, dried with acetone, and sterilized with ethylene oxide. These materials
have been tried and discarded for various reasons.
Currently, an inorganic, bovine-derived bone marketed under the brand name Bio-Oss
(OsteoHealth) has been successfully used both for periodontal defects and in implant
surgery. It is an osteoconductive, porous bone mineral matrix from bovine cancellous or
cortical bone. The organic components of the bone are removed, but the trabecular
architecture and porosity are retained.
CHAPTER

24 Hypersensitivity

Dental hypersensitivity is a major patient problem in dentistry and several explanations


for its mechanism have been given. It is a symptom complex rather than a disease.

DEFINITION
“It is a brief, sharp painful sensation in response to heat, cold, tactile and osmotic stimuli”.
A more specific definition was given by Holland and colleagues, who stated that dentin
hypersensitivity is a “short, sharp pain arising from exposed dentin in response to stimuli
typically thermal, evaporation, tactile, osmotic or chemical and which cannot be ascribed
to any other form of dental defect or pathology.”
It is the most common dental problem characterized by severe acute shooting pain.
Dental hypersensitivity is the particular problem in the patient after periodontal surgery.

BASIC CONCEPTS OF TOOTH SENSITIVITY


The most widely accepted explanation of dentin hypersensitivity is “Hydrodynamic theory”
by Brännstörm and Orchardson and Gillam.
According to this theory, various thermal, evaporation, tactile, osmotic stimuli causes
rapid outward flow of fluid in the dentinal tubules. Rapid flow causes a pressure changes
across the dentin, stimulating pulpal A- nerve fibers and resulting in perception of pain.
Cold is most common stimuli for dentin hypersensitivity.
Dentin hypersensitivity is more likely to occur when tubules are open and in
communication with the oral environment. Hypersensitive dentin contains larger and more
numerous tubules than normal nonsensitive dentin. Greater and larger tubules lead to
substantial increase in dentinal fluid flow and thereby amplify the severity of response
to external stimuli which may not be able to produce pain in normal dentin. The increase
in fluid flow with increasing tubule size is greater than might be expected because the
area of circle increases by square of radius.

PAIN MEDIATORS
• Nociceptors
• Sensory nerve terminals for pain
• A- nociceptors which mediates pain.

NEUROPHYSIOLOGY
The rich network of dental pulp is highly innervated by both myelinated and unmyelinated
nerve fibers (Fig. 24.1). Nerve fiber in pulp contains A and c fibers which are responsible
for conduction of stimuli.
Hypersensitivity 163

Essentials of Dentistry
Fig. 24.1: Dental neural structure

A and A fibers Are myelinated and conduct fast pain


C fibers Are unmyelinated and conduct slow pain. They are very sensitive to local anesthesia

Myelinated A and A fibers seem to be responsible for dentin sensitivity, whereas


C fibers are concerned with dull radiating pain sensation connected with pulpal inflammation.

OTHER THEORIES OF DENTIN HYPERSENSITIVITY


Odontoblastic Transduction Theory
This theory is based on the synaptic like relationship between the terminal nerve endings
and the odontoblastic processes. Such synaptic relation, if present, then it can be the
way for transmission of the stimuli from the tubules to the brain. It requires the acetylcholine
as a neurotransmitter.

Modulation Theory
Strong stimuli to the dentin may injure the odontoblasts which subsequently release variety
of neurotransmitting agents as well as vasoactive and pain producing amines and proteins.

Gate Control Theory


When dentin is irritated, all the pulpal nerves become activated from the stimuli-like vibration
and leads to hypersensitivity.

PREVALENCE
• 4-57 percent of adult population experience cervical dentin hypersensitivity in one or
164 Hypersensitivity

more teeth.
• It is commonly seen in 25–45 years of age group due to the general increase in exposed
root surfaces of the teeth from periodontal diseases, toothbrush abrasion or cyclic loading
fatigue of the thin enamel near cementoenamel junction (CEJ).
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• Generally, slightly higher incidence of hypersensitivity is reported in females than in males.


• It is substantially higher in periodontal patients (60-98 percent).

HIGHEST INCIDENT SITE


The most common locations for dentin hypersensitivity are cervical region of facial surfaces
of canines > premolars > incisors > molars and commonly on opposite side of the patient’s
dominant hand.
Regarding the side of mouth, in right-handed toothbrushers dentin hypersensitivity is
greater on the left-sided teeth.

PATHOPHYSIOLOGY
• Teeth sensitivity occurs more frequently in cervical area of the root where the cementum
is extremely thin. Scaling and root planing procedures may remove the thin layer of
cementum leading to hypersensitivity.
• Transmission of stimuli from surface of dentin to nerve endings located in dental pulp/
in pulpal region of dentin may occur through odontoblastic processes by displacement
of dentinal fluid.
• Sensitivity is encountered when physical, chemical, thermal, bacterial, and traumatic
stimuli are transmitted through tubule which initiates pain (Fig. 24.2).
• Dentin hypersensitivity is primarily dependent on remaining dentine thickness (effective
depth) and diameter of tubules.
• The tubules are shorter, more numerous and increase in diameter near the pulp. Deep
dentin is less effective pulpal barrier than superficial dentin near the dentinoenamel junction

Fig. 24.2: Pathophysiology


Hypersensitivity 165

or dentinocementum junction.

CAUSES
The primary etiological factor responsible for dentinal hypersensitivity is exposed dentinal

Essentials of Dentistry
tubules and tubules must be open. Exposed dentin is usually covered by a smear layer
made up of loosely bound organic and calcified debris that clogs the dentinal tubules
so that they are not open to the environment. When the smear layer is removed, the tubule
openings become exposed and are then susceptible to external stimuli, which can lead
to dentin hypersensitivity. The smear layer is easily removed by dietary acids, gastric acids,
and also detergents found in toothpaste and rinses.
Dentin may become exposed by two processes; either by loss of covering periodontal
structures (gingival recession) or by loss of enamel (tooth wear). The most common clinical
cause for exposed dentinal tubules is gingival recession.
Dental hypersensitivity is perhaps a symptom complex rather than a disease and results
from stimulus transmission across exposed dentin. A number of dental conditions are
associated with dentin exposure and therefore may produce the same symptoms.
Such conditions include:
– Gingival recession (Gingival recession doesn’t cause cervical hypersensitivity but rather
sets the stage for it by exposing root surfaces to the oral environment)
– Attrition, abrasion, erosion, abfraction
– Postperiodontal treatment (Scaling, root planing, periodontal surgery)
– Traumatic injury
– Chipped tooth
– Fractured restoration
– Restorative treatments
– Dental caries
– Cuspal grinding (during chewing)
– Crown preparation
– Aging.

CLINICAL IMPLICATIONS
Dental hypersensitivity manifests as short and sharp pain in response to certain stimuli.
Patient with hypersensitivity refrains from brushing because of pain and this leads to reduced
oral hygiene and vicious cycle of plaque accumulation. This aggravates the periodontal
problems and further leads to increase in hypersensitivity.

DIAGNOSTIC METHODS
According to a recent review, “Dentin hypersensitivity is usually diagnosed after other
possible conditions have been eliminated” and may be considered as a diagnosis of
exclusion.

Thermal Stimuli
Sensitivity to thermal stimuli, especially to cold appears to be the most prevalent feature.
Stimulus can be delivered to the tooth simply by gentle blow of the room temperature
air. Cold water testing method utilizes cold water (7°C) to provoke the sensitivity. Sometimes
heat can also act as stimulus.

Tactile Sensation
166 Hypersensitivity

This is a simplest method in which the tooth is gently touched with sharp explorer over
the suspected site (of attrition, abrasion) to grade the response on a severity scale.
Toothbrushing and flossing can also serve as stimuli.
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Osmotic Stimuli
Hyperosmotic salt solutions like sodium chloride, calcium chloride or sweet solutions like
glucose, sucrose are used to elicit the sensitivity.

Electric Stimuli
It can be delivered by using electric pulp tester. Its use is limited as it may act as harsh
stimuli and lead to severe hypersensitivity.

CONDITIONS TO RULE OUT HYPERSENSITIVITY


As many conditions are associated with dentinal hypersensitivity, a careful history together
with a thorough clinical and radiographic examination is necessary before arriving to
definitive diagnosis. Sometimes, there may be more than one condition coexist which makes
it difficult to approach a perfect diagnosis.
– Pulpal pathology
– Undisplaced palatal cusp
– Tooth with cracked cusp
– Fractured tooth with exposed dentin
– Fracture of restoration
– Areas of root involvement
– Areas of tooth in bruxism patient.

WAYS TO RULE OUT


– Careful history
– Clinical examination
– Radiographic examination.

OCCURRENCE OF PAIN
– Pain on brushing
– Pain on flossing
– Hot/warm beverages
– Eating of cold food especially ice cream
– Cold drinks
– Breathing of cold air
– Eating sour acidic food
– Eating sweet/sugary liquids.

PEOPLE AT RISK
– Over enthusiastic brushers (Hard bristle brushes)
– Periodontally treated patients
– Bulimics
– Patients with xerostomia
– Acidic food/drink consumers
– Older patients with gingival recession
Hypersensitivity 167

– Age-associated changes also produces sensitivity.

TREATMENT STRATEGIES
For long-term management, in addition to pain control, treatment strategies should include
the elimination or reduction of contributing factors. Hypersensitivity can resolve without

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the treatment or may require use of desensitizing agents for several weeks. Once diagnosed,
trace out the reason for the exposed dentinal tubules and any other etiological factor causing
hypersensitivity. Remove the etiological factors and educate the patient about the dietary
habits.
Treatment of hypersensitivity is challenging for both patient and clinician because:
1. The pain threshold differs from patient-to-patient.
2. It is difficult for patient to change the habit causing problem.
Single treatment modality may not be consistently effective in treating the hypersensitivity
therefore dentist must be familiar with alternative methods of treatment.
The principal treatment strategies are:
1. Desensitize the nerve, making it less responsive to stimuli.
2. Occlude tubules preventing the outward fluid flow.
This can be addressed by:
1. Home care with dentifrices
2. In office treatment modalities
3. Patient education.

MANAGEMENT OF HYPERSENSITIVITY
1. Home care with dentifrices
a. Potassium nitrate dentifrices (5%)
b. Strontium chloride dentifrices (10%)
c. Fluoride dentifrices (Sodium monofluorophosphate)
d. Bioactive glass (Calcium sodium phosphosilicate).
2. Professional/In office treatment modalities
a. Tubule sealants
– Dentin bonding agents
– Restorative resins.
b. Cavity varnishes
c. Treatments that partially blocks the tubules
– Iontophoresis
– Fluoride compounds: (Sodium fluoride, sodium silicofluoride, stannous fluoride)
– Tubule blocking agents (Potassium oxalate, Strontium chloride)
– Calcium compounds (Calcium hydroxide, Dibasic calcium phosphate)
– Silver nitrate
– Zinc chloride (Potassium ferrocyanide).
d. Antiinflammatory drugs
e. Miscellaneous
– Lasers
– Dental restorations.
3. Patient education
Patient education is of prime importance to control of etiological factors.
– Plaque control
– Proper toothbrushing technique with soft brushes
– Control of xerostomia
168 Hypersensitivity

– Diet counseling.
Hypersensitivity sometimes resolves without any kind of treatment. This can be attributed
to decreased dentin permeability because of natural mechanisms.
Natural mechanisms contributing to desensitization includes;
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1. Formation of reparative dentin by pulp


2. Obturation of dentinal tubules by mineral deposition.
Several factors can reduce dentin permeability and subsequently contribute to the
spontaneous remission of dentin hypersensitivity. For example, a dentin smear layer often
covers the exposed surface of dentin and may occlude the dentinal tubules, thereby reducing
dentin hypersensitivity. Adherence of salivary proteins to the outer dentinal surface and
adherence of plasma proteins to the inner dentin surface may also reduce hypersensitivity,
as can the formulation of less permeable reparative dentin by the pulp.

Home Care with Dentifrices


Medicated dentifrices are most widely advocated home care treatment modality for dentinal
hypersensitivity. It is the simple and inexpensive way to treat dentinal hypersensitivity.
However, the duration of relief is highly variable.
Advantages of using dentifrices
• Noninvasive
• Easy to use
• Inexpensive
• Treat multiple teeth simultaneously.

Disadvantages of using dentifrices


• Compliance
• Difficulty to deliver to specific sites
• Slow onset of action
• Requirement of continuous use.

Potassium Nitrate Dentifrices (5%)


The first approach to treat the dentinal hypersensitivity is to treat the tooth with a chemical
agent such as potassium nitrate or potassium chloride. The increased level of potassium
ions into the dentinal tubules reduces the sensitivity by inactivating voltage-gated sodium
channel, thereby blocking active potential generation. Therefore the tubules remain patent
and rapid fluid flow still occurs in response to stimuli, but the nerves are not activated.

Strontium Chloride Dentifrices (10%)


The second approach to treat the tooth with a chemical or physical agent such as strontium
chloride that creates a deposition layer and mechanically occludes dentin tubules, which reduces
sensitivity by prevention of pulpal fluid flow. Potassium nitrate is a diffusible-free radical of
nitric oxide that can reach the nerve endings easily. Hypersensitivity may reappear due to
toothbrush abrasion, the presence of acid challenges in the mouth or by degradation of coating.

Fluoride Dentifrices (Sodium Monofluorophosphate)


Fluoride helps in remineralization of dentin and works in three ways to reduce dentinal
hypersensitivity.
• It reduces the ability of bacteria to make acids.
• It reduces the acid dissolution of enamel.
Hypersensitivity 169

• It remineralizes the areas of tooth that have been attacked by acids from bacteria.

Bioactive Glass (Calcium Sodium Phosphosilicate)


Calcium sodium phosphosilicate is a highly biocompatible bioactive glass. In presence

Essentials of Dentistry
of body fluids, it deposits hydroxycarbonate apatite (HCA) on to the exposed dentinal
tubules and mechanically occludes the dentinal tubules.

Mechanism (Fig. 24.3)


Calcium sodium phosphosilicate exchanges sodium ions (Na+) with hydrogen
cations (H+ or H3O+) ions on exposure to aqueous environment

Rapid release of (Ca+) and phosphates (PO43-) which blocks the dentinal tubules by
forming Ca – P layer on the dentin surface

Multiple layers crystallize into biologically stable hydroxylapatite crystal

Professional/In Office Treatment Modalities


According to hydrodynamic theory, a rapid movement of fluid from dentinal tubules activates
the intradental sensory nerves and the hypersensitivity can be treated effectively by occluding
the dentinal tubules, reducing the diameter of the tubules or by covering the tubule orifice.
In office treatment modalities works mainly by obturating the dentinal tubules.

Tubule Sealants
Dentin bonding agent and restorative resins impregnate the dentinal tubule, form a polymeric
coating on the tooth surface and prevents the pain producing stimuli reaching the pulp.
Usually this is not employed for generalized root sensitivity but it can be an effective
alternative when other forms of therapy fail. Gluma desensitizer containing 30 percent HEMA
(Hydroxyethyl methacrylate) and 5 percent glutaraldehyde is an effective desensitizing
agent. Strong bonds of these agents to the dentin can provide relief from sensitivity when
other form of modality fails. They are relatively thin and susceptible to abrasion.

Fig. 24.3: Mechanism of action of bioactive glass


170 Hypersensitivity

Cavity Varnishes
Cavity varnishes when applied to the exposed dentinal surfaces, it forms a thin film and
blocks the stimuli reaching the pulp. It provides temporary relief however; varnishes
containing fluoride can be more effective due to sustain release of fluoride. They adhere
Essentials of Dentistry

to the dry or wet tooth surfaces and sets in contact with saliva. 5 percent sodium fluoride
contains 22600 ppm of fluoride and forms a protective layer of calcium fluoride that inhibits
fluid flow within tubules, which has been suggested to be effective treatment.

Treatments that Partially Blocks the Tubules


Iontophoresis
Iontophoresis works by forcing the fluoride ions deeply into the dentin which cannot be
achieved with topical fluoride application. It uses the electrical potential which transfers
the ions into the dentin. If the drug is negative, treatment electrode is also negative and
if drug is positive, treatment electrode is also positive. By completion of the circuit with
a second indifferent electrode, the drug is forced into the tissue to be treated.

Fluoride Compounds
Fluoride is well known desensitizing agent that works by precipitation of calcium and
phosphates in the dentinal tubules and reduces the lumen diameter.
NaF forms layer of CaF2 (Dominant reaction product) which occludes the tubules.
Acidulated sodium fluoride has acidic pH so it demineralizes the dentin and therefore
leads to deeper penetration of fluoride.
Sodium silicofluoride forms a gel by reacting with calcium of tooth and forms barrier
on the tooth surface. 0.6 percent sodium silicofluoride is highly potent desensitizing
agent.
Stannous fluoride releases tin and fluoride and forms highly insoluble tin-fluoride
phosphate complex on dentinal surface that is more resistant to dissolution by acid. 10
percent solution of stannous fluoride also blocks the tubules.

Strontium Chloride
Topical application of concentrated strontium chloride on the exposed dentin surface
penetrates up to the depth of 10–20 µm and plugs the tubules.

Oxalates
Oxalate ions react with the calcium ions in the dentinal tubules and form insoluble calcium
oxalate crystals that are deposited in the tubules. They are inexpensive, easy to apply
and well tolerated by patient. Potassium oxalate and ferric oxalate solutions are most
commonly used. It has been shown that potassium oxalate has both dentinal tubule
obturation properties and inhibitory effects caused by the potassium ions actions on nerve
activity. Oxalate ions react with calcium to form insoluble calcium oxalate crystals that
bind tightly to dentin and obturate the dentinal tubules.

Calcium Compounds (Calcium Hydroxide, Dibasic Calcium Phosphate)


These are very primitive and well known agents used for treatment of hypersensitivity.
The exact mechanism of action is unknown but they may work by:
• Blocking the dentinal tubules
Hypersensitivity 171

• Inducing peritubular dentin mineralization


• They may reduce the excitability of nerves at higher concentration.
The paste of calcium hydroxide is applied to root surface and allowed to remain there
for 3-5 minutes.

Essentials of Dentistry
Silver Nitrate
It blocks the tubules by precipitation of constituents of dentinal tubules.

Zinc Chloride (Potassium Ferrocyanide)


It forms a stable and highly crystalline precipitate which covers the exposed dentin.

Miscellaneous
Laser Treatment
There are a number of reports that suggest that laser treatment may be useful in the treatment
of dentin hypersensitivity, although definitive trials are lacking. Combination of dental laser
with other modes of treatment of dentinal hypersensitivity is an effective and lasting dentinal
tubule obturation procedure.

Patient Education
Plaque Control
The role of plaque as an etiological factor in dentin hypersensitivity is not resolved, although
it has been suggested that dental plaque promotes and sustains dentin hypersensitivity,
and that plaque control is important in preventing its development. However, it has been
noted that hypersensitive dentin is found in toothbrush abrasion areas that are almost
plaque-free.

Proper Toothbrushing Technique with Soft Brushes


Faulty brushing technique can lead to tooth wear resulting in hypersensitivity. Loss of dentin
can be prevented by use of proper brushing technique and selection of soft brush.

Control of Xerostomia
Reduced salivary secretion may lead to plaque accumulation and increase in intraoral
pH and subsequently hypersensitivity. Salivary substitutes can reduce the pH and prevent
the exposure of dentin.

Diet Counseling
Diet with high acidic content leads to erosion of tooth structure especially cementum of
exposed root surface leading to opening of dentinal tubules. Diet counseling should focus
on quantity and frequency of acid intake occurring in relation to the brushing time. Any
treatment may fail, if these factors are not controlled. The best way is to monitor diet chart
of the patients with dentinal hypersensitivity in order to advise those concerning eating habits.
Smear layer formed immediately after the scaling and root planing prevents the sensitivity
of teeth. However, fruit juices containing citric acid removes smear layer and leads to
hypersensitivity.
172 Hypersensitivity

Patient should be cautioned not to brush immediately after exposure of tooth surfaces
to dietary acid which greatly increased loss of dentin.

Reduce or Eliminate Parafunctional Habits


Essentials of Dentistry

Parafunctional habits such as clenching and grinding deliver eccentric occlusal forces to
the tooth and leads to tooth flexure resulting in an abfraction and hypersensitivity. The
patient should be encouraged to change any parafunctional oral habits that are contributing
to recession.

Anti-inflammatory Drugs
It has been suggested that corticosteroids reduce the pulpal inflammation which may be
responsible for hypersensitivity. However, more information is needed regarding the
relationship between these two conditions.

CONCLUSION
Dentin hypersensitivity is a significant and prevalent issue affecting dental profession. Two
conditions-gingival recession and erosive tooth wear—most commonly predispose a patient
to suffer the symptoms of dentin hypersensitivity. Differential diagnosis is critically important,
followed by a clinically appropriate management plan that also addresses any predisposing
conditions. The currently recommended management/treatment continuum for persistent
dentin hypersensitivity, depending on severity and extent of pain, should involve the least
invasive intervention. In some cases of long-term dentin hypersensitivity, gingival recession
and tooth surface loss involve more invasive periodontal and restorative treatments. In
all cases with an initial early diagnosis, minimally invasive options should be tried first.
CHAPTER
Definitions and
25 Questionnaire for
Periodontia Viva Voce

GINGIVA
It is the part of mucosa that covers the alveolar processes of jaws and surrounds the
necks of the teeth. A modern definition states that it is the fibrous investing tissue covered
by keratinized epithelium that immediately surrounds a tooth and is contiguous with its
periodontal ligament and the mucosal tissue of the mouth (AAP2001a).

Marginal Gingiva
Marginal gingiva or unattached gingiva is the terminal edge or border of the gingiva
surrounding teeth like a collar (Fig. 25.1).
It not directly attached to the tooth forming the soft tissue wall of the sulcus. It extends
1.0-1.5 mm on facial and lingual from gingival margin to free gingival groove. It has a
dull surface and firm consistency.

Free Gingival Groove


It is a fine groove running parallel to the gingival margin (at a distance of 0.5 to 1.5 mm)
dividing the free gingival from the attached gingiva, present in 30-40 percent teeth. It appears
as a shallow line or depression and often but does not necessarily corresponds to the
location of the bottom of the gingival sulcus. It is believed that it arise from functional
impacts on the movable free gingiva back on the attached and immovable gingiva (Orban
1948a).

Fig. 25.1: Marginal gingiva


174 Definitions and Questionnaire for Periodontia Viva Voce

Gingival Sulcus
It is the shallow crevice or space around tooth bounded on one side by surface of tooth
and on other side by epithelium lining-free gingiva margin. The depth of the gingival
crevice varies according to location, state of eruption, and presence and absence of
Essentials of Dentistry

disease. The average depth of the gingival crevice is usually less than 3 mm; however,
it should not be considered abnormal if greater than 2 or 3 mm (Ramfjord and Ash 1979c;
AAP2001a).

Attached Gingiva
It is the part of the gingiva that is continuous with marginal gingiva, which is firm, resilient
and tightly bound to the periosteum of underlying alveolar bone (Fig. 25.2).
It is frequently stippled, firm, and thick, lacking a submucous layer; and it has no glands.
It is located from free gingival groove to mucogingival junction. It is attached to tooth directly
in case of dehiscence. The width of facial attached gingival ranges from 0 to 10 mm. It
is greatest on the facial surface of the maxillary lateral incisor and narrowest over the facial
surface of the mandibular canine and premolars. The dimensions of marginal and attached
gingiva are intimately related to each other. In fact, it may be considered as a gingival
unit.

Functions
• It acts as an anchor between free gingival groove and alveolar mucosa.
• It dissipates forces from muscle fibers through alveolar mucosa.

Width of Attached Gingiva


It is the distance between the mucogingival junction to the projection on the external surface
of the bottom of the gingiva sulcus or periodontal pocket.
The width of attached gingiva is greater in adults than in children (Bowers, 1963). This
widening is not linear since the attached gingiva in newly erupted permanent tooth is
significantly narrower than that of its deciduous predecessor. It can be concluded that
the width of attached gingiva;
– changes concomitantly to changes in the sulcus and crevice depth during eruption
and shedding.

Fig. 25.2: Attached gingiva


Definitions and Questionnaire for Periodontia Viva Voce 175

– increases with age in the primary dentition.


– is significantly narrower in newly erupted permanent teeth than in their deciduous
predecessors.
– increases gradually with the eruption of the permanent teeth—however, in certain teeth
it may take many years.

Essentials of Dentistry
Interdental Gingiva
It is the part of the gingiva, which occupies the gingiva embrasures, e.g. The interproximal
space beneath the area of tooth contact.

Interdental Groove
Vertical groove parallel to long axis of adjacent teeth in interdental area of attached gingiva
is called as interdental groove.

Desmosomes
Keratinocytes are interconnected by structures on cell periphery called desmosomes.

Keratinosomes or Odland Bodies


Upper most cells of stratum spinosum contain numerous dense granules known as
keratinosomes.

Oral or Outer Epithelium


The epithelium, which covers the outer surface and crest of the marginal gingiva and the
outer surface of attached gingiva, is called as oral epithelium.

Alveolar Mucose
It has thin, nonkeratinized epithelium lacking retepegs. Its connective tissue is consisting
of thin lamina propria and vascular submucosa. It has predominantly elastic fibers, so
is loosely bound to underlying bone.

Sulcular Epithelium
Sulcular epithelium lines the gingival sulcus extending from upper limit of junctional
epithelium to the crest of gingiva margin.

Junctional Epithelium
It is a stratified squamous nonkeratinized epithelium that extends apically from bottom
of sulcus to form color like band around each tooth.
(It is approximately 1 mm in health. Proline/hydroxyproline secreted by epithelial cells
bind junctional epithelium to enamel or cementum).

Dentogingival Unit
Attachment of junctional epithelium to the tooth surface is reinforced by gingiva fibers,
which firmly braces marginal gingiva against tooth surface. Thus, gingiva fibers and
junctional epithelium works together as a functional unit called “DENTOGINGIVAL
UNIT”.
176 Definitions and Questionnaire for Periodontia Viva Voce

Cuticle
It is a thin, acellular structure which a homogenous matrix sometimes enclosed with in
a clearly demarcated linear borders.
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Coronal Cementum
It is a thin layer of homogenous organic material of variable thickness overlying the enamel
surface.

Gingiva Fluid or Sulcular Fluid


Fluid that seeps into gingiva sulcus from gingiva connective tissue through the thin sulcular
epithelium is called as sulcular fluid. As early as 1817, it was believed that this tissue fluid
was secreted by gingival glands, later called Serres glands (Serres 1817). The fluid was
soon found to be an inflammatory exudate (Bodecker 1933, 1945).

Gingiva Fibers
The connective tissue of marginal gingiva is densely collagenous, containing a prominent
system of collagen fibers bundles called gingiva fibers.
It stabilizes the attached gingiva to alveolar process and to the tooth and it is important
in postorthodontic relapse.

Stippling
The portion of gingival outer epithelium appears to be elevated and between them there
are shallow depressions corresponding to extensions of connective tissue papilla into
epithelium retepegs. This appearance is referred to as stippling. It appears as “matted”
in texture, just distance from the gingival margin; being associated with numerous regularly
distributed small depressions and giving the tissue “orange peel appearance” (Fig. 25.3)
(King 1945; Orban 1948a; Greene 1962; AAP2001a). The degree of stippling varies with
individuals and; it had been thought to be an expression of functional adaptation to
mechanical impacts. It has been described as “fine” or “coarse”, as variable between
individuals and ages, and as being finer in females than in males. (Wentz et al., 1952,
Rosenberg and Massler, 1967).

Fig. 25.3: Stippling (Orange peel appearance)


Definitions and Questionnaire for Periodontia Viva Voce 177

Melanin
Melanin is nonhemoglobin derived brown pigment, which is responsible for normal
pigmentation of the skin, gingiva and remainder of the oral mucous membrane.

Essentials of Dentistry
Anatomic Crown
The portion of tooth, which is covered by enamel is called anatomic root.

Clinical Crown
The part of tooth that has been denuded of its gingiva and projects into oral cavity is
known as clinical crown.

Anatomic Root
Anatomic root is the portion of the tooth, which is covered by cementum.

Clinical Root
Clinical root is the portion of tooth, which is covered by periodontal tissue.

Lamina Propria
The connective tissue beneath the gingiva that is made up of two layers: the papillary
layer immediately beneath the epithelium, which consists of papillary projections between
the retepegs; and the reticular layer which extends to the periosteum.
It is approximately 1 mm between CEJ and crest of bone. The primary cells of lamina
propria are the fibroblast.

Papillary Layer
It is the part of lamina propria subjacent to epithelium.

Reticular Layer
It is the part of lamina propria, which is continuous with periosteum of alveolar bone.

Active Eruption
The movement of teeth in the direction of occlusal plane is called active eruption.

Passive Eruption
The exposure of tooth by apical migration of gingiva is called passive eruption.

Gingival Recession
Gingival recession is exposure of tooth by apical migration of gingiva.

Physiologic Recession
Root exposure with increasing age is considered normal and referred to physiologic
recession.
178 Definitions and Questionnaire for Periodontia Viva Voce

Col
Col is a valley-like depression at the tip of the papilla that connects the facial and lingual
gingiva just beneath the contact point (AAP 2001a). This term is borrowed from
mountaineering, where it is used to describe a ridge-shaped depression adjoining two
Essentials of Dentistry

adjacent peaks (Fish 1961). This is considered as a site of least resistance (locus minoris
resistance) to invasion by microorganisms and/or their toxins. (Stahl 1963; Jablonski 1992)

THE TOOTH-SUPPORTING STRUCTURE


Periodontal Ligament
Periodontal ligament is a soft specialized connective tissue situated between the cementum
covering the root of tooth and bone forming the socket wall.
It has “hour glass” shape and it is narrowest at mid-root. Fibers run mainly in
“apicocoronal direction” from cementum to bone inserting as Sharpey’s fibers.

Sharpey’s Fibers
Terminal portions of the principle fibers of periodontal ligament that insert into cementum
and bone are termed as Sharpey’s fibers.

Collagen
Collagen is the protein composed of different amino acids, the most important of which
are glycine, proline, hydroxylysine and hydroxyproline.

Indifferent Fiber Plexus


In addition to principle fiber types, small collagen fibers also run in all directions forming
a plexus that is termed indifferent fiber plexus.

Cementicles
Small foci of calcified masses, which are adherent to or detached from root surface, are
called as cementicles.

Cementum
Cementum is a specialized, calcified avascular connective tissue that covers the anatomic
root of the tooth and gives attachment to the periodontal ligament.

Acellular Cementum
Acellular cementum is primary cementum and covers approximately the cervical third or
half of the root.

Cellular Cementum
Cellular cementum is secondary cementum formed after the tooth reaches the occlusal
plane and is more irregular containing cells in individual spaces.

Hypercementosis
It is a regressive change of teeth characterized by the deposition of excessive amounts
of secondary cementum on root surface.
Definitions and Questionnaire for Periodontia Viva Voce 179

Reversal Line
Newly formed cementum is demarcated from the root by a deeply staining irregular line
known as reversal line.

Essentials of Dentistry
Ankylosis
Fusion of cementum and alveolar bone with obliteration of the periodontal ligament is
known as ankylosis.

Alveolar Bone Proper


Inner wall of tooth socket is composed of thin compact bone, also known as lamina dura
or cribriform plate.

Osteoid
The bone matrix that is laid down by osteoblasts and which is not mineralized is known
as osteoid.

Bundle Bone
Bone adjacent to periodontal ligament that contains a great number of Sharpey’s fibers
is called as bundle bone.

Periosteum, Endosteum
The tissue covering the outer surface of bone is called as periosteum while endosteum
is the tissue lining the internal bone cavities.

Fenestrations
Isolated areas in which the root is denuded of bone and the root surface is covered only
by periosteum and overlying gingiva are called fenestrations. The term is derived from
Latin word fenestra, meaning “window”. In periodontology, it has been described as a
window-like aperture or opening in alveolar bone over the root of tooth with intact marginal
bone (AAP 2001a). Fenestration is more common in the maxilla.

Dehiscence
The absence of alveolar cortical plate sometimes exceeding more than half of the root
length and often results in a denuded root surface (Elliott and Bowers 1963; Larato 1970d).
When denuded areas extend through the marginal bone, the defect is called dehiscence.
Dehiscences are more common in the mandible (usually bilateral). Do not perform
scaling and root planing in the particular area with dehiscence. Sharpey’s fibers are not
removed and left in their intact position, if the area is healthy.

Pre-cementum or Cementoid
A meshwork of irregularly arranged collagen fibrils sparsely distributed in an irregularly
arranged ground substance or matrix is called precementum.

Intermediate Plexus
Individual fibers of periodontal ligament, rather than being continuous, consist of two
separate parts spliced together midway between cementum and bone in a zone called
intermediate plexus.
180 Definitions and Questionnaire for Periodontia Viva Voce

Physiologic Mesial Migration


Physiologic mesial migration is mesial movement of tooth due to flattening of proximal
areas with aging and wear.
Essentials of Dentistry

Trauma From Occlusion


Injury results when forces exceed adaptive capacity of periodontium are called trauma
form occlusion.

Dental Epidemiology
It is the study of the pattern and dynamics of dental diseases in human population.

Epidemiologic Indices
Indices is a numerical value describing relative status of population on a graduated scale
with definite upper and lower limit, which is designed to permit, and facilitate the comparison
between same group/other groups described by same criteria and method.

EPIDEMIOLOGY OF PERIODONTAL DISEASE AND GINGIVAL DISEASE


Dental Plaque
It is a soft deposit that forms the biofilm adhering to the tooth surface or other hard surfaces
in the oral cavity, including removable and fixed prosthesis.
It is the highly variable structural entity resulting from the colonization and growth and
sequential maturation of microorganisms on the surfaces of teeth, restorations, and oral
soft tissues and consisting of a number of microbial species and strains embedded in
an extracellular matrix.
It is defined by the AAP as an organized mass, consisting mainly of microorganisms,
that adheres to teeth, prosthesis, and oral surfaces and is found in the gingival crevice
and periodontal pockets. Other components include an organic polysaccharide protein
such as enzymes, food debris, desquamated epithelial cells, and inorganic components
such as calcium and phosphate (AAP 2001a).

Materia Alba
Materia alba is the yellowish or grayish-white, soft sticky deposits containing food debris,
desquamated tissue cells, bacteria, leukocytes and salivary proteins which lacks the
organized structure of plaque and can be easily displaced with a spray of water. It serves
as a medium of bacterial growth.

PERIODONTAL MICROBIOLOGY
Supragingival Plaque
Plaque found at or above the gingival margin is called as supragingival plaque.

Marginal Plaque
Supragingival plaque that is in direct contact with the gingival margin is called as marginal
plaque.
Definitions and Questionnaire for Periodontia Viva Voce 181

Subgingival Plaque
Plaque found below gingival margin between tooth and gingival sulcular tissues is called
as subgingival plaque.

Essentials of Dentistry
Co-aggregation
Ability of different species and genera of plaque microorganism to adhere to one another
by a process known as co-aggregation.

Chemotaxis
It is the direct movement of a cell along chemical gradient.

Opsonization
Opsonization refers to process of coating a particle with recolonization molecules to enable
phagocytic ingestion.

DENTAL CALCULUS
Calculocementum
Calculus embedded deeply in cementum may appear morphologically similar to cementum
termed as calculocementum.

Stains
Pigmented deposits on the tooth surface are called stains.

ROLE OF IATROGENIC AND OTHER LOCAL FACTORS


Food Impaction
Food impaction is the forceful wedging of food into the periodontium by occlusal force.

Plunger Cusps
Cusps that tend to forcibly wedge food interproximally are known as plunger cusps.

DENTAL OCCLUSION
Occlusion
Occlusion is the contact relationship of teeth in their functional state under the neuromuscular
control of the masticatory system (Musculature, TMJ, mandible, periodontium).

Physiologic Occlusion
It is an occlusion that exists in an individual who has no signs of occlusion-related pathosis.

Traumatic Occlusion
It is an occlusion associated with traumatic lesions or disturbances in supporting structures
of teeth, muscles and TMJ.
182 Definitions and Questionnaire for Periodontia Viva Voce

Therapeutic Occlusion
It is an occlusion used to counteract structural interrelationships-related to traumatic
occlusion.
Essentials of Dentistry

Border Movements
Border movements are the limits to which the mandible can move in any direction and
are not common during mandibular function.

Contact Movements
Contact movements are the movement of the mandible with one or more of the opposing
occlusal surfaces in contact.

Intraborder Movements
Any mandibular movement within the perimeter of border movement is called as intraborder
movements.

Excursions
Excursion is the movement of the mandible with the teeth in contact.

Bennett Movement
Lateral shift of condyle of mandible is called Bennett movement.

Physiologic Rest Position


When the teeth are not in contact in mastication, swallowing or speech, the lips are at
rest and jaws are apart. This is called physiologic rest position.

Free Way Space


The space between the mandible and maxillary teeth when the mandible is in the postural
position is called as free way space.

Masticatory or Chewing Cycle


The pathway of mandible in chewing is referred to masticatory cycle.

Supracontact
It is general term for any contact hindering the remaining occlusal surfaces from achieving
many pointed, stable contacts.
There are two types:
1. Intercuspal supracontacts
2. Retrusive supracontacts

Vertical Dimension of Occlusion


Vertical dimension is the distance between maxilla and mandible when teeth are in
intercuspal position.
Definitions and Questionnaire for Periodontia Viva Voce 183

Attrition
Attrition is the physiologic wearing of tooth surface as a result of tooth-to-tooth contact,
as in mastication. It primarily occurs on the incisal and occlusal edges of the teeth as
wear from tooth-to-tooth functional contact (e.g. buccal and lingual surfaces of anterior

Essentials of Dentistry
teeth in deep overbite relationship). Parafunctional attrition is often related to excessive
grinding motions. Reduced salivary flow may contribute to tooth wear as a result of increased
tooth-to-tooth friction.
It is characterized by:
– Matching wear of the occluding surfaces of teeth
– Shiny facets on amalgam contacts
– Enamel and dentin wear at the same rate
– Possible fracture of cusps of restorations.

Facets
Occlusal or incisal surfaces worn by attrition are called facets.

Erosion
Erosion is the loss of tooth structure by means of some chemical action that does not involve
known as bacterial action. It is an apparent chemical dissolution of enamel and dentin, unrelated
to caries, causing a cavity that has hard, smooth base. It is most commonly produced by
excessive and frequent intake of an acidic diet and less commonly by the reflux of hydrochloric
acid from the stomach. Acids demineralize and soften the enamel and dentin surfaces, making
them more susceptible to abrasion, particularly by toothbrushing. Dietary acids and gastric
acids are two most common causes of dental erosion. Dietary erosion is most commonly
observed as moderate, generalized erosion of the cervical and buccal surfaces of the maxillary
teeth and the occlusal and buccal surfaces of the mandibular teeth. Gastric erosion is more
severe than dietary erosion. It is commonly observed on the lingual aspects of anterior and
posterior maxillary teeth, buccal aspects of mandibular posterior teeth.
It is characterized by:
– Broad cavities within dull, smooth surface enamel
– Cupping of occlusal surfaces (incisal grooving) with dentin exposure
– Increased incisal translucency
– Wear on nonoccluding surfaces
– “Raised” occlusal restorations
– Clean, nontarnished appearance of amalgams
– Loss of surface characteristics of enamel in young children
– Preservation of enamel “cuff” in gingival crevice is common
– Dentin hypersensitivity
– Pulp exposure in deciduous teeth.

Frictional Ablation
It is the process caused by juxtaposition of natural and artificial dental surfaces and
hyperfunctional oral soft tissues.

Abrasion
Abrasion is the pathologic wearing of tooth surface by some mechanical forces such as
hard bristle toothbrush, coarse tooth powder, etc. Clinically, they are ‘V’ or wedge-shaped
defects and notches at or apical to the CEJ.
184 Definitions and Questionnaire for Periodontia Viva Voce

It is characterized by:
– Lesions that are more wide than deep
– Premolars and cuspids are commonly affected
– Usually located at cervical areas of teeth
Essentials of Dentistry

Some factors affecting the tooth abrasion are:


– Brushing technique
– Frequency of brushing
– Amount of time spent for brushing
– Force applied during the brushing
– Type of toothbrush
– Abrasiveness and amount of dentifrices used
– Personal habits, such as finger nail of thread biting and holding foreign objects with
the teeth (pipe smoking, seed shelling), may cause incisal or occlusal abrasion.

Abfraction
Abfraction is a noncarious cervical lesion hypothesized to be the result of microfractures
in enamel and dentin caused by eccentrically applied occlusal parafunctional forces. For
example, during bruxism, the changing back and forth direction of the occlusal forces
bends the tooth, causing side to side fatigue and microfracturing at the most flexed area
in the cervical region of the tooth.
It is characterized by:
– Deep, narrow, V-shaped notch
– Affects buccal and labial cervical areas of teeth
– Commonly affects single tooth with excursive interferences or eccentric occlusal loads.

Bruxism
Bruxism is the clenching or grinding of the teeth when the individual is not chewing or
swallowing.

INFLUENCE OF SYSTEMIC DISEASES ON PERIODONTIUM


Scurvy
It is the disease characterized by hemorrhagic diathesis and retardation of wound healing
caused by severe vitamin C deficiency.

Leukemia
It is a disease characterized by the progressive overproduction of WBC, which usually
appear in the circulatory blood in an immature form.

AIDS
It is the disease indicative of defect in cell-mediated immunity occurring in a person with
no known cause for immunodeficiency other than positive of HIV.

CLINICAL FEATURES OF GINGIVITIS


Acute Gingivitis
Acute gingivitis is a painful condition that comes on suddenly and is of short duration.
Subacute gingivitis is the less severe phase of acute condition.
Definitions and Questionnaire for Periodontia Viva Voce 185

Chronic Gingivitis
Chronic gingivitis is of long duration which is slowly progressing and is painless unless
complicated by acute or subacute exacerbations.

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Recurrent Gingivitis
Gingivitis which having been eliminated by treatment and then reappears again is called
as recurrent gingivitis.

Gingival Clefts
It is a narrow type of gingival deformity encountered on the marginal aspects of the gingiva
and extending regularly or irregularly from the gingival margin in an apical or lateral direction,
with margins that are usually thick and often rolled inward (Moskow and Bressman 1965).

Stillman’s Clefts
The gingival clefts have been defined as “small apostrophe-shaped fissures extending
apically from gingival margin for varying distances (usually 5 to 6 mm), usually on the
vestibular surface of teeth (Jablonski 1992). They were originally considered to be due
to regional circulatory disturbances within the gingiva initiated by traumatic occlusion
(Stillman 1921, Stillman and Mc Call 1937). However, researches have shown that there
is no evidence that such defects are brought about by occlusal disharmonies (Posselt
1959). They may be considered as epithelial down growths leading to splitting of the gingiva
(AAA2001a).

McCall’s Festoons
They are ‘life preserver’-shaped enlargements of the marginal gingival that occur primarily
on facial surfaces of anterior teeth and bicuspids. These semilunar enlargements were
named after John Oppie McCall, who along with Paul R Stillman, believed occlusal trauma
as an etiological factor (Stillman and McCall 1922). But later studies couldn’t substantiate
or show evidence that festoons was initiated by occlusal disharmonies (Posselt 1959).

GINGIVAL ENLARGEMENT
Gingival enlargement is increase in the size of gingiva so that soft tissue overfills the
interproximal spaces balloons out over the teeth and protrudes into the oral cavity.

Granuloma Pyogenicum
It is the tumor-like gingival enlargement that is considered as an exaggerated conditioned
response to minor trauma.

Epulis
It is a generic term used clinically to designate all discrete tumors or tumor-like masses
of the gingiva.

ACUTE GINGIVAL INFECTIONS


Acute Necrotizing Gingivitis (ANUG)
It is an inflammatory destructive disease of the gingiva that presents characteristic signs
and symptoms.
186 Definitions and Questionnaire for Periodontia Viva Voce

Vincent’s Angina
It is a fusospirochetal infection of the oropharynx and throat.

Pericoronitis
Essentials of Dentistry

It refers to inflammation of gingiva in relation to crown of an incompletely erupted tooth.


It is also known as operculitis.

DESQUAMATIVE GINGIVITIS AND ORAL MUCOUS MEMBRANE DISEASES


Desquamative Gingivitis
It is a unique condition of gingiva characterized by intense redness and desquamation
of the surface epithelium.

Lichen Planus
Lichen planus is an inflammatory disease of skin and mucous membranes characterized
by the eruption of papules.

Leukoplakia
Leukoplakia is a nonscrapable white lesion occurring in oral cavity, which cannot be classified
clinically or histopathologically under any other. It is usually more than 5 mm in size.

Pemphigus
Pemphigus is a serious chronic autoimmune disease involving skin and mucous membrane
characterized by the appearance of vesicle and bulla, small or large fluid filled blisters
that develop in cycles.

Erythema Multiforme
It is an acute inflammatory eruptive disease of unknown etiology involving the skin and
oral cavity.

Scleroderma
Scleroderma is the multisystem connective tissue disease that involves hardening of skin
and mucosa smooth muscle atrophy and fibrosis of internal organs.

PERIODONTAL POCKET
Eruption Gingivitis
It is gingivitis associated with tooth eruption.

Periodontal Pocket
Periodontal pocket is a pathological deepened gingival sulcus due to coronal growth of
gingiva or apical migration of junctional epithelium.

Gingival Pocket (False/ Pseudopsocket)


Gingival pocket is a pocket, which is formed by gingival enlargement without any destruction
of underlying periodontal tissue.
Definitions and Questionnaire for Periodontia Viva Voce 187

True Periodontal Pocket


It is a type of pocket occurs with destruction of the supporting periodontal tissue.

Suprabony Pocket

Essentials of Dentistry
Pocket with the bottom coronal to the underlying alveolar bone is also called supracrestal
or supraalveolar pocket.

Infrabony Pocket
If the bottom of the pocket is apical to the level of the adjacent alveolar bone, it is also
called subcrestal or intraalveolar pocket.

Spiral Pocket
Pocket which is originating on one tooth surface and twisted around the tooth to involve
one or more additional surfaces.

Periodontal Abscess
Periodontal abscess is a localized accumulation of pus in periodontal tissue. It is also
known as lateral or parietal abscess.

BONE LOSS AND PATTERN OF BONE LOSS


Exostoses
Exostoses are over growths of bone of varied size and shape.

Buttressing Bone Formation


Bone formation sometimes occurs in an attempt to buttress bone trabeculae weakened
by resorption.

Two Types
CENTRAL: when occurs within jaw.
PERIPHERAL: when occurs on external surface.
When it causes bulging of the bone contour, it is termed as “LIPPING”.

Osseous Craters
Osseous craters are concavities in the crest of the interdental bone confined to the facial
and lingual walls.

Bulbous Bone Contours


They are bony enlargement caused by exostoses, adaptation to function or buttressing
bone formation.

Reversed Architecture
A morphological relationship when the interdental gingival or bone is located apical to
midfacial and midlingual margins (AAP 2001a).
188 Definitions and Questionnaire for Periodontia Viva Voce

Ledges
They are plateau like bone margins caused by resorption of thickened bony plates.

Furcation Involvement
Essentials of Dentistry

Invasion of the bifurcation and trifurcation of multirooted teeth by periodontal diseases


is known as furcation involvement.

PERIODONTAL RESPONSE TO EXTERNAL FORCES


Pathologic Migration
Pathologic migration refers to the tooth displacement those results when the balance among
the factors that maintain physiologic tooth position is disturbed by periodontal disease.

Refractory Periodontitis
Cases that for unknown reasons therapy and/or recur soon after adequate treatment has
been referred to as refractory periodontitis.

PREPUBERTAL AND JUVENILE PERIODONTITIS


Juvenile Periodontitis
The term is used to describe disease of periodontium in the preadult years (11-19).

Papillon-Lefevre Syndrome
This syndrome is characterized by hyperkeratotic skin lesion; server destruction of the
periodontium and in some cases calcification of the dura.

Down’s Syndrome
Down’s syndrome is a congenital disease caused by chromosomal abnormality and
characterized by mental deficiency and growth retardation.

OTHER
Diagnosis
Diagnosis is determination of the nature of a case of a disease.

Lamina Dura
Radiopaque appearance of an alveolar bone proper on radiograph is called as lamina
dura.

Prognosis
It is a prediction of the duration course and termination of a disease and its response
to treatment.

Treatment Plan
It is the blue print for a case a management.
Definitions and Questionnaire for Periodontia Viva Voce 189

RATIONALE FOR PERIODONTAL TREATMENT


Regeneration
Regeneration is the growth and differentiation of new cells and intracellular substances
to form new tissues or parts by growth from the same type of tissue that has been destroyed

Essentials of Dentistry
(Jablonsky 1992). It is the biologic process by which the architecture and function of lost
tissue is completely restored.
It results in regrowth of precise tissue that were present before the damage or disease
occurred.

Reattachment
The modern definition for reattachment is “to attach again, the reunion of connective tissue
with a root surface on which viable periodontal tissue is present, the area of reattachment
is not affected by bacterial contamination” (Mellonig 1992; AAP 2001a). It is the reunion
of the connective tissue and root that have been separated by incision or injury but not
by disease. It is frequently necessary to move healthy tissue away from the tooth root
or bone temporarily during some types of periodontal surgery to allow access to damaged
parts of the periodontium on adjacent teeth. The expected healing in this type of incision
is by reattachment.

New Attachment
New attachment is the term used to describe the union of a pathologically exposed root
with connective tissue or epithelium.
New attachment occurs when the epithelial and connective tissues are newly attached
to a tooth root where periodontitis had previously destroyed the attachment. It differs from
the reattachment because new attachment must occur in an area formerly damaged by
disease, whereas reattachment occurs when tissues are separated in the absence of disease.

Repair
Repair is healing of wound by formation of tissue that does not truly restore the original
architecture or original function. It is healing by scar tissue formation. Certainly the healing
is complete following formation of scar during the healing of scar, but the tissue is not
precisely the same tissue in appearance or function that excised on the part before the
wound.

PRINCIPLE OF PERIODONTAL INSTRUMENTATION


Adaptation
Adaptation refers to the position of the first 1-2 mm of the lateral surface of instrument
in contact with the tooth.

Angulations
Angulations refer to the angle between the face of a bladed instrument and tooth surface.

Lateral Pressure
Lateral pressure refers to the pressure created when force is applied against the surface
of a tooth with the cutting edge of bladed instrument.
190 Definitions and Questionnaire for Periodontia Viva Voce

Scaling
Scaling is the process by which plaque and calculus are removed from both supragingival
and subgingival tooth surfaces.
Essentials of Dentistry

Root Planing
Root planing is a periodontal process by which residual embedded calculus and portion
of cementum contaminated with microorganisms and toxins are removed from the root
to produce a smooth hard clean surface.

Probe
Probe is a slender, blunt ended, tapering assessment instrument used to evaluate the
health status of the periodontal tissues.

Probing
Probing is the act of walking the tip of probe along the junctional epithelium within the
sulcus or pocket for the purpose of assessing the health status of the periodontal tissues.

Probing Depth
It is the measurement of the depth of a sulcus or periodontal pocket. It is determined
by measuring the distance from the gingival margin to the base of the sulcus or pocket
with a calibrated periodontal probe.

PLAQUE CONTROL
Plaque control is the removal of microbial plaque and the prevention of its accumulation
on the teeth and adjacent gingival surface.

Dentifrices
It is the therapeuticomechanical aid for cleaning and polishing tooth surfaces.

Disclosing Agent
These are the solution or wafers capable of staining bacterial deposits on the surface
of teeth, tongue and gingiva for instruction, evaluation and research.

Cavitation
Cavitation refers to formation of tiny bubbles in the water exiting form the electronically
powered instrument tip. When these tiny bubbles collapse, they produce shock waves
that destroy the bacteria by tearing the bacterial cell walls.

Periodontal Debridement
It refers to the removal or disruption of bacterial plaque, its products, and the plaque retentive
calculus deposits from coronal surfaces, root surfaces, and from within the pocket.
Periodontal debridement includes instrumentation of every square millimeter of root surface
for plaque and calculus removal, but does not include the deliberate, aggressive removal
of cementum.
Definitions and Questionnaire for Periodontia Viva Voce 191

QUESTIONNAIRE FOR PERIODONTIA VIVA VOCE


Q.1. What is the action of gingival massage?
Ans: Gingival massage increases the mitotic activity in the epithelium and connective tissue.
The increased keratinization occurs only on the oral gingiva not on the areas vulnerable

Essentials of Dentistry
to microbial attack like sulcular epithelium and interdental areas (gingival col). Epithelial
thickening, increased keratinization and increased blood circulation have not been shown
to be beneficial for restoring gingival health. Improvement in gingival health is more likely
due to plaque control rather than gingival massage.

Q.2. Can gingival massage with gum paint be performed in presence of local deposits?
Ans: No, gingival massage with gum paints can’t be carried out for longer duration or
regularly because in the presence of calculus or plaque massaging will cause friction
between the calculus and the gingiva underneath deposits causing the laceration.

Q.3. What does gum paint contain?


Ans: Contents of traditional gum paint are:
W/V
Potassium iodide 0.8%
Iodine 0.6%
Tannic acid 2.0%
Menthol 0.5%
Thymol 0.5%
Camphors 0.5%
Zinc phenol sulphonate 0.8%
Menthe oil 0.3%
Clove oil 0.3%
Phenol 0.2%
Glycerin Q.S

Q.4. At which stage you will say that gingivitis has progressed to periodontitis?
Ans: Theoretically, in the advance stage of gingivitis, the inflammatory changes cause
degeneration of connective tissue wall of the gingival sulcus. As consequences, collagen
fibers just apical to junctional epithelium are destroyed and apical cells of junctional
epithelium proliferate on the root. With migration of the apical portion of the junctional
epithelium, coronal portion detaches from the root. This stage of periodontal breakdown
marks the transition from normal gingival sulcus to pathogenic pocket.

Q.5. What is the interaction if bactericidal and bacteriostatic drugs are prescribed
together?
Ans: Depending on mechanism of antibiotic action, combinations of antibiotics may have
an additive, synergistic, antagonistic effect. Static antibiotics used in combinations generally
exhibit an additive effect, bactericidal antibiotics exhibit a synergistic effect, and combination
of bactericidal and bacteriostatic agents exhibits antagonistic effect.
Bactericidal drugs are effective only during the multiplication of the bacteria which is
inhibited by bacteriostatic drug. So when we are prescribing a bacteriostatic drug,
multiplication of bacteria will ultimately stop and it will make bactericidal drug less effective.
192 Definitions and Questionnaire for Periodontia Viva Voce

Q.6. How to find lesion is primary of endodontic or periodontal origin in endoperio-


lesion and what are the treatment strategies?
Ans: The differential diagnosis and treatment strategies of the endoperio lesion are
demanding.
Essentials of Dentistry

Differential diagnosis:
Factors to be considered are:
• Vitality of pulp
• Sequencing of clinical symptoms like pain and swelling and clinical signs like probing
depth.
• Location, form and extension of the radiolucency (Radiographic observation).
Pulp vitality test is of prime importance in differential diagnosis.
i. Presence of deep carious lesion, nonvital pulp and periapical radiolucency with
pocket not approximating the apex indicates the endodontic cause as a prime
factor.
ii. Deep periodontal pocket approximating the apex, vital pulp and no carious
involvement of tooth indicates the lesion is of primarily periodontal origin.
However, in many cases, the overlapping signs and symptoms may create dilemma
of accurately assessing the contribution of endodontic or periodontal cause.
Pulpal lesions Periodontal lesions
Vitality Nonvital Vital
Usual area of swelling Vestibule Attached gingiva
Pain Intermittent throbbing Dull, Continuous
Probing Narrow, isolated defect Non-isolated defect
Sinus tract location Mucosa Attached gingiva, Sulcus
Radiograph Localized bone loss Generalized bone loss of area
Local factors Variable Calculus
Etiology Deep caries or restoration Possibly non-restored

Treatment Strategies
It is clinically not possible to determine the extent to which endodontic or periodontal
lesion has affected the supporting tissues. Therefore, the treatment strategy for
combined endoperio lesion must be first focused on the pulpal infection. Thorough
endodontic treatment (phase-I) will resolve a part of lesion contributed by pulpal
infection. So the phase-I is followed by the period of observation (phase-II) to observe
the healing resulting from the endodontic treatment. Improvement in probing depth
can be observed within couple of weeks, while bone regeneration may require several
months. So, the periodontal treatment (phase-II) is postponed until the proper evaluation
of endodontic treatment.
If the periodontal disease is solely responsible for the combined endoperio lesion, the
endodontic treatment will not contribute to the periodontal healing as an endodontic lesion
being secondary involvement. In this case, the primary approach is periodontal therapy.
If primary lesion is of endodontic origin, the endodontic treatment should be delivered
first.
Whenever, there is a doubt regarding the source of origin (endodontic/periodontal)
of combined endoperio lesion, following guidelines should be followed.
Definitions and Questionnaire for Periodontia Viva Voce 193

Cause Condition of pulp Treatment


Endodontic Nonvital Endodontic
Periodontal Vital Periodontal

Essentials of Dentistry
Endodontic/periodontal Nonvital First – endodontic treatment
Second – phase of observation
Third – periodontal treatment, if necessary

Q.7. What are the different methods of diagnosis of infrabony defect?


Ans: There are three main methods.
• Transgingival probing
• Radiographs with radiopaque markers
• Surgical opening of flap is best to reveal the configuration of defect.
Q.8. Can the actual configuration of bony defect whether 3-walled or 2-walled be
diagnosed radiographically?
Ans: No. Sometimes radiographs can make it possible to predict the bony defect but
its accurate diagnosis by visual examination requires surgical exposure of flap.

Q.9. Difference between acanthosis and acantholysis?


Ans: Acanthosis—Thickening of spinous cell layer.
Acantholysis—Intraepithelial clefting by autoantibody to desmosomes, which connects
two cells. It is seen in pemphigus.

Q.10. What is the pathologic potential of calculus?


Ans: Calculus acts as a contributing factor for plaque formation and promotes its retention
on teeth. Also, the rough surface of calculus is usually covered by a layer of plaque. It
interferes with the efforts of improved plaque control and keeps plaque in the vicinity of
the periodontal tissues all the time. The persistent inflammation around the free calculus
itself is the unambiguous evidence of the pathologic effect of calculus.

Q.11. What does pus indicate?


Ans: There is tendency to overemphasize the importance of purulent exudates and to associate
it with severity of periodontal disease. Pus indicates ongoing suppurative process. It is the
evidence that no necrosis has taken place and cells are living which exudates pus. Pus
is a common feature of periodontal disease but it is only a secondary sign. Pus merely reflects
the nature of the inflammatory changes in the pocket wall. It is not an indication of the depth
of pocket or severity of destruction of the supporting tissues. Extensive pus may occur in
shallow pockets, whereas deep pockets may exhibit little or no pus. Pus formation indicates
the period of exacerbation while its absence reflects the period of quiescence.
Clinically, the presence of the pus can be determined by gently applying digital pressure
by ball of index finger along the lateral aspect of marginal gingiva in a rolling motion from
base of pocket towards the crown.
Visual examination without digital pressure may be insufficient as the purulent exudate
is formed from the lateral wall of pocket.

Q.12. How to determine mucogingival junction?


Ans: Various methods to determine the mucogingival junction are:
• Attached gingiva is tightly bound to underlying bone which extends to the relatively
loose and movable alveolar mucosa. The side of instrument (probe tip) is passed from
marginal gingiva apically, a feel of tag or stuck of instrument marks the mucogingival
junction (Fig. 25.4).
Essentials of Dentistry 194 Definitions and Questionnaire for Periodontia Viva Voce

Fig. 25.4: Mucogingival junction

• By using “Schiller’s solution” containing potassium iodide, keratin can be stained. Iodine
binds to protein of keratinized surface. As being keratinized, iodine stains the attached
gingiva and demarcates it from nonkeratinized alveolar mucosa.
• Another method to demarcate the mucogingival junction is pushing the lip (cheek)
coronally.

Q.13. What is red complex and what is its significance?


Ans: Red complex consists of B. forsythus, P. gingivalis, and T. pallidum [BPT]. This red
complex is most commonly related to bleeding on probing. (Remember other complexes
also).

Q.14. What is the reason for high prevalence of horizontal bone loss in anterior region
and vertical defects in posterior region?
Ans: Bacterial plaque can induce bone loss within the radius of 1.5-2.5 mm. There is no
effect beyond 2.5 mm (Radius of action). For that reason, interproximal angular defects
can appear only in spaces that are wider than 2.5 mm because narrow spaces would
be destroyed completely. Defects extending a distance of 2.5 mm from the tooth surface
may be due to presence of bacteria in tissue. In anterior region, interdental septum is
not as wide as that in posterior segment. This results in horizontal type of bone loss in
anterior segment and vertical defects in posterior segment.

Q.15. What is native bone level?


Ans: Native bone level is the alveolar crest level in the absence of any pathologic loss.
The constant distance between the lower edge of junctional epithelium and the alveolar
crest is 1.07 mm.

Q.16. What are the basic parameters for selection of antibiotics in periodontia?
Ans: Selection of antibiotic is customized for patient-to-patient and it depends on many
factors. But the empirical therapy for the patient with gingival and periodontal problems
is as below:
If gram-positive organisms are suspected, penicillin is preferred antibiotic group. If the
patient is allergic to penicillins, macrolides are second choice followed by fluoroquinolones.
If gram negative organisms are anticipated, imidazole derivatives (metronidazole/tinidazole)
are effective.
Definitions and Questionnaire for Periodontia Viva Voce 195

Q.17. What are Human leukocyte antigens (HLA)?


Ans: Human leukocyte antigens found on chromosome-6 and transmitted by heredity.
They regulate immune responses and have been associated with various autoimmune
diseases.

Essentials of Dentistry
Q.18. How the Fremitus test is performed?
Ans: Periodontal fremitus (vibrations or tremors) occurs in either of the alveolar bones
when an individual sustains trauma from occlusion. Fremitus test is the measurement of
the vibratory pattern of teeth when teeth are placed in occlusion and also during movements.
It is a result of teeth exhibiting slight mobility against the adjacent walls of their sockets.
An index finger (alternatively two fingers can also be placed vertically) is placed horizontally
along the labial vestibule against the alveolar bone to detect the fremitus. Fremitus may
be detected both in centric occlusion and in lateral excursive movements (lateral fremitus).
Patient is asked to close his or her mouth into maximum intercuspation and is asked to
grind his or her teeth slightly. The volume of vibrations is expanded by inflammatory
responses, bone resorption or both. If trauma from occlusion is present, it leads to abnormal
mobility; vibrations are felt at finger. Assessment of fremitus involves measurement of
vibratory patterns of teeth when teeth are placed in contacting position and movements.
It is easier to detect fremitus of maxillary teeth than the mandibular teeth. Fremitus is recorded
as +. There is no numerical fremitus scale.
Class I Mild vibration
Class II Easily palpable vibration but not visible movement

Class III Movement visible with naked eye

Q.19. Should any commercially available alcohol-based mouthwash be prescribed


in periodontitis?
Ans: Ethyl alcohol is commonly used both to stabilize certain active ingredients and to
improve the shelf-life of the product. In periodontitis, alcohol-based preparations causes
drying of mucosa and pocket content and aggravates the condition and halitosis.
(Mouthwashes containing more than 25 percent alcohol could increase the risk of oral
and pharyngeal (throat) cancer by 50 percent. Most, if not all, mouthwashes in the market
contain less than 15 percent alcohol.)

Q.20. Are stains harmful?


Ans: Yes. Stains are harmful as they produce rough surface and serve as a plaque retentive
factor.

Q.21. What do you mean by cleft and what’s its significant?


Ans: Cleft is break in continuity of gingival margin. Presence of cleft definitely indicates
recession.

Q.22. Why mobility increases immediately after surgery?


Ans: Body responds to an infection and trauma by developing inflammation. Immediately
after surgery, mo bility increases temporarily as a result of inflammation of the periodontal
ligament fibers in response to the surgical trauma. Raising flap detaches the connective
tissue fibers from tooth surface. Resolution of inflammatory changes and subsequent bone
condensation contribute to a significant extent. Also, regeneration and reformation of
connective tissue fibers during healing along with decrease in the inflammation diminishes
the tooth mobility below the pre-treatment level by fourth week.
196 Definitions and Questionnaire for Periodontia Viva Voce

Q.23. What is the change in the marginal gingiva in inflammation?


Ans: Normal knife-edge gingival margin becomes rolled out due to inflammatory changes
making oral hygiene practice more difficult to perform.
Essentials of Dentistry

Q.24. What is the cause of spontaneous or increased bleeding at morning in absence


of systemic diseases but in the presence of gingival inflammation?
Ans: Salivary flow carrying anticoagulant factors as well as antimicrobial agents is reduced
during the night. In addition, the absence of mechanical cleansing by tongue exacerbates
bacterial activity in presence of inflammation. All these together aggravate the existing
inflammation and undisturbed growth of bacteria produces vascular engorgement and
thinning of epithelium leading to bleeding.

Q.25. What is the observation in pre- and post-treatment radiograph in periodontal


therapy?
Ans: Periodontal reconstruction without use of bone graft shows little less bone level
compare to pretreatment radiograph. During surgery, raising the mucoperiosteal flap from
the bone, temporarily decreases blood supply and increases osteoclastic activity. As the
main blood supply for alveolar bone is the mucoperiosteum, cessation of blood supply
leads to decrease (little) in bone level. As healing progresses, it comes to normal level.
In order to determine whether the bone loss is progressing or not, standardized radiographs
are taken at regular interval and analyzed. Clinical evaluations by radiographs at 6 to 8
months help to decide the disease course.
While is case of periodontal flap surgery with bone grafting, the posttreatment change
in bone level depends on the amount of periodontal regeneration by graft material.

Q.26. What is the fate of regenerative bone graft procedure in case of horizontal and
vertical bone loss?
Ans: Bone grafting in horizontal bone loss have not responded well to bone fill regenerative
procedures. Lack of stability of the grafting material and the susceptibility to wash out
makes the procedure futile. These areas are best treated with pocket elimination flap
procedure with or without osseous resective surgery.
Vertical defects especially those with two or three walls, respond well to bone fill
regenerative procedure. When used in intrabony defects, easy adaptation of bone graft
material in angular defect provides more resistance to washing off effect of expensive material
by saliva and maximum benefit of grafting material is achieved.

Q.27. What are the limitations of radiographs as a diagnostic aid in periodontia?


Ans:
• Inorganic content of bone should be decreased by 30 percent to 60 percent to become
radiographically evident. So after initiation, any bone changes require around 6 to 8
months to be radiographically evident.
• Actual destruction is more than that appear on the radiograph so it may lead to
misinterpretation of actual condition.
• Radiographs are two-dimensional representation of a three-dimensional anatomy.
• Radiograph cannot determine the activity of disease.
Definitions and Questionnaire for Periodontia Viva Voce 197

Q.28. Effects of unilateral chewing habit.


Ans: Patients who are unilateral chewer, more function on one side and less function on another
side. The used side shows increased bone density (trabeculation), widened periodontal ligament
space and increased wearing of tooth whilst the unused side shows decreased in bone density,

Essentials of Dentistry
narrow ligament space and more plaque and calculus accumulation.

Q.29. Effect of cigarette smoking on periodontium.


Ans: Smoking is an important established environmental risk factor in periodontitis. It can
affect the vascular, inflammatory, immune and healing responses. Nicotine is main factor
responsible for the dependence-forming properties of tobacco smoking. Cotinine is a
metabolite of nicotine. The word ‘cotinine’ is an anagram of ‘nicotine’. The degree of
exposure to tobacco smoking can be measured in pack years or by measuring the serum
nicotine and cotinine levels.
Effects on vasculature: Smoking induced vasoconstriction could contribute to impaired
gingival flow and decrease the amount of oxygen and blood constituents that reach the
gingiva, whilst also reducing the capacity to remove tissue waste products, leading to damage
and / or compromised immune response. It alters the ability of hemoglobin to transport
the oxygen and creates the serious environmental risk factor for periodontal diseases. Smoking
suppresses the gingival inflammation and simultaneously the underlying periodontal disease
activity continues without manifestations of inflammation. Healing is also impaired because
of depleted nutrition and oxygen by diminished blood supply due to vasoconstriction.
Effects on immune system: Smoking has major effect on the protective elements of
the immune response, resulting in an increase in the extent and severity of periodontal
disease. Alteration in neutrophil number or function affects the critical functions such as
chemotaxis and phagocytosis. Impaired response of neutrophils to periodontal infection
and increased release of tissue-destructive enzymes reduces the protection against
periodontal infections.
It has been shown that the suppressed inflammatory response is reversible on smoking
cessation. In addition, reduction in smoking may have a beneficial effect on associated
periodontal disease. It is been observed that periodontal destruction is more in smokers
compared to non-smokers or former smokers. The extent of smoking exposure and the
dose may also increase the smoking associated risk of periodontal disease.

Q.30. Why necrosis starts with interdental papilla in case of ANUG?


Ans: Interdental papilla contains end arteries which are the terminal branches of artery
and there is no collateral circulation at the tip of papilla. So any interference in the blood
supply makes the area deprived of nutrition and makes it prone to necrosis.

Q.31. What are the indications of surgical pocket therapy?


Ans: In moderate and deep pockets this surgery is indicated for:
• To increase the accessibility to the root surface, making it possible to remove all irritants.
• Reduce or eliminate pocket depth, making it possible for the patient to maintain the
root surfaces free of plaque
• Reshape soft and hard tissues to attain a harmonious topography.
198 Definitions and Questionnaire for Periodontia Viva Voce

Q.32. How will you classify periodontal surgeries?


Ans: Periodontal surgeries are classified as follows:

Pocket reduction surgery


Essentials of Dentistry

Resective surgeries Gingivectomy, apically displaced flap and


undisplaced flap with or without osseous
resection
Regenerative surgeries Flaps with grafts and membranes, etc.

Correction of anatomical/Morphologic defects


Plastic surgery techniques to widen attached Free gingival grafts, and other techniques, etc.
gingiva
Esthetic surgery Root coverage, recreation of gingival papillae
Preprosthetic techniques Crown lengthening, ridge augmentation,
vestibular deepening
Placements of dental implants, including Guided bone regeneration, sinus grafts
techniques for site development for implants

Q.33. Probes
Ans: Following points should be mentioned to describe a probe;
WHO (CPITN) probe:
Parts Handle, shank, calibrated working end, ball tip
Markings 0.5 mm diameter of ball tip
Markings at 3.5, 5.5, 8.5,11.5 (in mm)
Color coding (black marking) from 3.5 to 5.5 mm
Interpretation If black band is visible, it indicates need for scaling and root planing.
If black band is submerged or not visible, it shows need for complex surgical
procedure.
Use Screening of large number of patients

Williams probe:
Parts Handle, shank, calibrated working end.
Markings 1, 2, 3, 5, 7, 8, 9, 10 (in mm)
Up to 3 mm – Normal, nonsurgical treatment.
Interpretation Up to 4 mm – Gingivitis
Up to 5-7 mm- Beginning of destructive periodontitis (Treatment depends on level
of attachment)
More than 7 mm – Advanced destruction, requires surgical treatment.

Nabers probe:
Parts Same as Williams probe but the end is curved.
Markings 3, 6, 9, 12 (in mm, at 3 mm interval)
Interpretation 3-6 mm: First black band (incipient furcation)
9-12 mm: Second black band
If bands submerged partially – grade II furcation involvement
If more (totally) – grade III/IV
Use To determine the horizontal component of furcation involvement
Definitions and Questionnaire for Periodontia Viva Voce 199

Severity of furcation involvement


Horizontal (Grade 0-3) Vertical (Subclass A-C)
F0 – Normal A – Up to 3 mm

Essentials of Dentistry
F1 – Up to 3 mm B – 4 - 6 mm
F2 – > 3 mm C - > 7 mm
F3 – Through and through between 2 roots

Working end selection: The correct working-end of the probe has been selected if the
lower (terminal) shank is positioned parallel to the tooth surface being examined. The
incorrect working-end has been selected if the lower shank is perpendicular to the long
axis of the tooth surface being examined.
Method to use furcation probe: Position the probe at the gingival line at a location
near where the furcation is suspected (Fig. 25.6). Direct the probe beneath the gingival
margin. At the base of the pocket, rotate the probe tip towards the tooth to fit the tip into
the entrance of the furcation (Fig. 25.5).

Q.34. How to diagnose a case of furcation involvement?


Ans: Furcation involvement can be diagnosed by two methods;
1. Clinical examination: A thorough clinical examination is the key to diagnosis and treatment
planning. Careful probing is performed by using Nabers probe. Transgingival probing
further helps to determine the anatomy of the furcation defect.
2. Radiographic examination: Radiographs can also be useful in diagnosing furcation
involvement.
Grade I Radiographic changes are not usually found
Grade II Radiographs may or may not depict the furcation involvement
Grade III Radiographs show a radiolucent area in the crotch of the tooth
Grade IV A clear radiolucent area is seen

Fig. 25.5: Furcation measurement


Essentials of Dentistry 200 Definitions and Questionnaire for Periodontia Viva Voce

Fig. 25.6: Furcation measurement

Q.35. Furcation classifications


Ans: Irving Glickman was the first one to classify furcation invasion based on the degree
of lateral periodontal destruction under the roof of the furcation in 1953.

Glickman’s furcation classification (1953)


Grade Description Symbol

I • The concavity—just above the furcation entrance—on


the root trunk can be felt with the probe tip; however,
the furcation probe cannot enter the furcation area.
^
• It is early-incipient stage of furcation involvement which
primarily affects the soft tissues only.
• Bone loss may have occurred but can’t be evident on
radiographic evaluation.
JE
• No horizontal component of furcation can be probed.
Bone
level

II • The probe is able to partially enter the furcation— 


extending approximately one-third of the width of the
tooth—but it is not able to pass completely through
the furcation. It is known as cul-de-sac effect. (Dead
end/ blind valley)
• Partial bone loss with definite horizontal component
• Radiographs may or may not show furcation
JE involvement.
• Both vertical and horizontal components are present.
Bone
level • One or more furcation of the same tooth can be
affected.

Contd....
Definitions and Questionnaire for Periodontia Viva Voce 201

Contd....

Glickman’s furcation classification


(Contd.)
(1953)
Grade Description Symbol

Essentials of Dentistry
III • The probe may pass completely through the furcation
between the mesial and distal roots. 
• Bone is not attached to the dome of the furcation but
the furcation may be filled with soft tissue and may
not be visible.
• On radiograph, there is a radiolucent defect is visible
at furcation area.
JE

Bone
level

• Same as a class III furcation involvement except that


IV
the entrance to the furcation is visible clinically owing 
to tissue recession.
• Destruction of interdental bone and recession of soft
tissue.
• Periodontal probe passes through and through.

JE

Bone
level

In 2000, Fedi et al. modified Glickman’s classification to include two degrees of a grade
II furcation defect:
Grade II degree I - exists when furcal bone loss possesses a vertical component of >1
but <3 mm.
Grade II degree II - exists when furcal bone loss possesses a vertical component of >3 mm,
but still does not communicate through-and-through.
Other classifications:
i. According to Goldman and Cohen (1968) –
1. Grade I – Incipient lesion
2. Grade II – Cul-de-sac lesion
3. Grade III – Through and through lesion
ii. According to Hamp et al (Hamp, Nyman and Lidhe, 1975).
The amount of furcation involvement in this classification is measured in millimeters.
He considered horizontal component of bone loss.
1. Degree I – Horizontal loss of periodontal tissue less than 3mm.
2. Degree II – Horizontal loss of periodontal tissue exceeding 3mm but not
encompassing the total width of furcation area.
3. Degree III – Horizontal through and through destruction of the periodontal tissue
in furcation.
iii. According to Tarnow and Fletcher (1984)
This system records vertical loss from the roof of the furcation apically to the level
of radicular bone in millimeter. It may be combined with any acceptable grade I, II,
III or other classifications.
202 Definitions and Questionnaire for Periodontia Viva Voce

1. Subclass A – vertical loss of 0-3 mm of interradicular height


2. Subclass B – vertical loss of 4-6 mm of interradicular height
3. Subclass C – vertical loss of interradicular height of 7 mm or greater.
Essentials of Dentistry

Q.36. What are the treatment guidelines for furcation involvement?


Ans:
Traditional procedures Regenerative procedures
Grade I Scaling, root planing, curettage, gingivoplasty, –
odontoplasty.
Grade II Scaling, root planing, curettage, gingivoplasty, Bone grafting, GTR, root conditioning,
odontoplasty, osteoplasty with limited coronally-displaced flap and
ostectomy, in shallow grade II invasion. In combination of procedures.
more severe furcation involvements root
resection/ hemisection is done.
Grade III Tunneling, root sectioning, hemisection, GTR and combination of procedures.
extraction.
Grade IV Maintenance –

Q.37. What is the reason for absence of pocket or gingivitis in association with trauma
from occlusion?
Ans: Trauma form occlusion mainly affects the supporting tissues and does not affect
the gingiva. The marginal gingiva is unaffected by trauma from occlusion because its blood
supply is not affected, even when the vessels the periodontal ligament are obliterated
by excessive occlusal forces. Thus, trauma from occlusion does not cause pocket or
gingivitis.

Q.38. What are the differences in compositions of calculus at different regions of


mouth?
Ans: Supragingival calculus most commonly contains hydroxyapatite and octacalcium
phosphate. Subgingival calculus contains same hydroxyapatite, more magnesium
whitelockite.
Hydroxyapatite is the major crystallite in both supra and subgingival calculus.
More common in mandibular anterior region as the principal source
Brusite of saliva for mandibular anterior region is submandibular and sublingual
glands though Warthin’s and Stensen’s duct respectively.
More common in posterior regions as the source of mineral is saliva
Magnesium whitelockite
from the parotid gland.

Q.39. Can mouthwash eliminate bad breath?


Ans: No, mouthwash alone cannot eliminate bad breath for long term. Mouthwash can
be used as a last step in the routine oral hygiene maintenance procedure as an added
regimen. Most of the mouthwashes with volatiles mask the bad breath for a few hours
only.
First, the food particles that can rot must be removed from in between the teeth
immediately after each meal. Brushing the teeth at least 2 times a day is essential. Apart
from these basic oral hygiene maintenance procedures, other etiological factors responsible
for halitosis should be treated accordingly. An effective way is to increase the secretion
of saliva or to lower the pH of saliva which increases the solubility of malodorous compounds.
Definitions and Questionnaire for Periodontia Viva Voce 203

Q.40. How far does a toothbrush penetrate below the free gingival margin?
Ans: It varies from person to person depending on anatomical variations, type of bristles
and method of brushing but the average value found is 0.9 mm.

Q.41. Few facts about plaque control.

Essentials of Dentistry
Ans:
• Flossing is 80 percent effective in removing interdental plaque in the presence of an
interdental papilla.
• In the absence of interdental papilla, brushing/flossing is 55 percent, Perio-Aid is 80
percent, and interdental brush is 95 percent effective.
• Mouth rinses penetrate 0.2-1.2 mm into the sulcus. Surface tension and outflow of
gingival crevicular fluid decrease ability to penetrate without force.

Q.42. Chlorhexidine as a chemical plaque control agent (Fig. 25.7).


Ans: Chlorhexidine is a cationic bisbiguanide and was first established as an antimicrobial
agent in 1954. It exists as acetate (diacetate), gluconate, and hydrochloride salts.
Chlorhexidine gluconate is commonly used. It is a broad spectrum antiseptic and widely
used as preventive and therapeutic agent. It is the dicationic nature of chlorhexidine, making
it extremely interactive with anions, which is relevant to its efficacy, safety, local side effects
and difficulties with formulation in products.

Fig. 25.7: Structure of chlorhexidine

Dose
The patient is informed to rinse twice a day for 30 seconds with 10 ml of 0.2 precent solution.
To maintain the almost optimum 20 mg doses derived from 10 ml of 0.2 precent rinses,
0.12 precent is recommended as a 15 ml rinse (18 mg dose). The studies revealed equal
efficacy for 0.2 precent and 0.12 precent rinses when used at appropriate similar doses
(Segreto et al. 1986). 0.12 precent concentration of chlorhexidine gluconate solution is
freely available in United States. In the unavailability of 0.12 precent solution, 1:1 dilution
of 0.2 precent solution gives 0.10 precent concentration which is nearer to 0.12 precent
concentration.

Clinical Efficacy

Reduction in salivary bacterial counts 80 to 90%


Reduction of plaque 45 to 60%
Reduction in severity of gingivitis 27 to 67%

Adverse Drug Reactions


• Brownish discoloration of teeth, restoration and dorsum of tongue. Most likely
mechanisms proposed for tooth staining are:
1. Degradation of chlorhexidine molecule release of parachloraniline.
2. Catalysis of Maillard reactions.
204 Definitions and Questionnaire for Periodontia Viva Voce

3. Protein denaturation with metal sulfide formation.


4. Precipitation of anionic dietary chromogens.
• Transient impairment of taste perception (disgeusia): Chlorhexidine affects primarily
salt/sweet tastes and intensities which return to normal after discontinuing the rinse.
Essentials of Dentistry

• Mucosal erosions (hypersensitivity) are rarely seen as an idiosyncratic reaction and


lesions are superficial.
• Unilateral/bilateral parotid swelling due to stenosis of parotid duct. It is very rare and
explanation is not available.
• Supragingival calculus promotion:
Chlorhexidine promotes supragingiva calculus formation by precipitation of salivary
protein to the tooth surface, thereby increasing pellicle thickness and/or precipitation of
inorganic salts on to the pellicle layer. It does not seem to decrease effectiveness and
is easily removed.

Mechanism of Action (Flow chart 25.1)


Chlorhexidine exhibits both antiplaque and antibacterial properties. The main target of
chlorhexidine is the bacterial cytoplasmic membrane. After chlorhexidine has caused
extensive damage to the cytoplasmic inner membrane, precipitation or coagulation of
proteins and nucleic acids occurs. Damage also occurs to the outer membrane in gram-
negative bacteria and the cell wall in gram-positive cells.
Chlorhexidine acts as bacteriostatic at low concentration and bactericidal at high
concentration. These concentrations vary between bacterial species.
At lower concentrations, chlorhexidine has a bacteriostatic effect against most gram-
positive bacteria (e.g. at 1 g/ml), many gram-negative bacteria (e.g. at 2 to 2.5 g/ml).
It strongly binds to the bacterial cell membranes leading to increased permeability of
cytoplasmic membrane and subsequently leakage of intracellular components including
potassium. At high concentration, it causes precipitation of bacterial cytoplasm and cell
death. At chlorhexidine concentrations of 20 g/ml or more, a bactericidal effect as well
as activity against yeasts can be expected.
The superior antiplaque activity of chlorhexidine is due to its property of sustained
availability—“Substantivity”. The antiseptic has a broad antimicrobial action, including a
wide range of gram-positive and gram-negative bacteria (Wade and Addy,1989). It is also
effective against some fungi and yeasts including candida, and some viruses including
HBV and HIV. Chlorhexidine inhibits the plaque by:
• Preventing pellicle formation by blocking acidic groups on salivary glycoproteins and
thereby reducing glycoprotein adsorption on to the tooth surface.
• Preventing adsorption of bacterial cell wall onto the tooth surface by binding to the
bacteria.
• Preventing binding of mature plaque by precipitating agglutination factors in the saliva
and displacing calcium from the plaque matrix.
Chlorhexidine has strong affinity for binding to skin and mucous membrane. It adsorbs
to the surfaces including pellicle coated teeth and slow release of the chlorhexidine from
these reservoir surfaces, resulting into “Bacteriostatic milieu” in the oral cavity. After a single
rinse with chlorhexidine, saliva itself exhibits antibacterial activity for about 5 hours and
suppresses salivary bacterial counts for over 12 hours (so the frequency of use is twice
a day). Following several rinses of chlorhexidine, the number of aerobic and anaerobic species
in saliva can be reduced by 80-90 percent. Chlorhexidine is potent antifungal agent.
This mechanism is similar to that associated with tooth staining. (This explains why the
anionic substances such as sodium lauryl sulfate of toothpaste and also the food containing
anionic dietary chromogens especially beverages like tea, coffee and red wine reduce the
Definitions and Questionnaire for Periodontia Viva Voce 205

effectiveness of chlorhexidine, if used shortly after the rinse). Patient should be instructed not
to take tea or coffee during the immediate period after rinse. Gargling at the night is recommended
as no beverages will be consumed at night and the sustained release throughout the night
gives protection when it is most sought because of decreased salivary secretion.

Essentials of Dentistry
Pin-cushion Effect
Flow chart 25.1: Mechanism of action of chlorhexidine
206 Definitions and Questionnaire for Periodontia Viva Voce

Safety
1. Chlorhexidine has very low systemic toxicity: Chlorhexidine is poorly absorbed in the
GI tract. Over 90 percent of swallowed chlorhexidine is excreted unchanged in the
feces.
Essentials of Dentistry

2. It has not produced any appreciable resistance of oral microorganisms.


3. It has not associated with teratogenic alterations.

Clinical Applications
1. Pretreatment rinse
2. Immunosuppressed patients
3. Postperiodontal surgery: Chlorhexidine used postoperatively reduces bacterial risk
factors associated with wound healing
4. Postextraction
5. Subgingival irrigation
6. Necrotizing ulcerative periodontitis
7. Aphthous stomatitis
8. Caries control
9. Oral malodor.

Q.43. Listerine as a chemical plaque control agent.


Ans:
• Listerine is an essential oil mouth rinse. It is available over-the-counter (nonprescription)
and is composed of a fixed combination of phenol-related essential oils: thymol (0.064%),
methyl salicylate (0.060%), eucalyptol (0.092%), and menthol (0.042%) in 26.9 percent
ethanol.
• At this concentration, the ethanol serves to dissolve the active ingredients. Contrary
to persistent myths, methanol (which is frequently confused with menthol) is not an
ingredient. Thymol is an antiseptic, methylsalicylate is a cleaning agent, and menthol
is a local anesthetic.
• Listerine has with the highest alcohol content. There has been concern that the use
of alcohol-containing mouthwash such as listerine may increase the risk of developing
oral pharyngeal cancer but there is now sufficient evidence to accept the proposition
that developing oral cancer is increased or contributed to by the use of alcohol-containing
mouthwashes. Whilst many of these products may have been shown to be effective
in penetrating oral microbial biofilms in vitro and reducing oral bacterial load, it would
be wise to restrict their use to short-term therapeutic situations if needed. Perhaps the
use of mouthwashes that do not contain alcohol may be equally effective. Further, mouth
rinses should be prescribed by dentists, like any other medication. There may well
be a reason for the use of alcohol-containing mouth rinses, but only for a particular
situation and for a limited and controlled period of time. It should be restricted to adults
for short durations and specific, clearly defined reasons.
• Chlorhexidine mouth rinse produces more extrinsic tooth staining and higher calculus
formation compared to essential oils containing mouth rinse. This may limit the patient
compliance for long-term use of chlorhexidine and as a long-term plaque-control adjunct
for moderate- to high-risk patients, essential oil mouth rinse is better.
• Listerine is mouth rinse of choice for the patient allergic to the chlorhexidine. It gives
25-35 percent reduction in gingivitis.
• It is very strong and may lead to burning sensation in the mouth. Also high content
of alcohol may exacerbate the xerostomia.
• The recommendation for use is twice a day for 30 seconds with 20 ml.
Definitions and Questionnaire for Periodontia Viva Voce 207

Q.44. Tetracycline-containing fibers (Actisite).


Ans:
• Actisite is a tetracycline fiber—a polymer fiber and ethyl/vinyl acetate 25 percent saturated
with tetracycline. It is placed without anesthesia using a blunt instrument like retraction
cord packer and leave in place 1-2 weeks. Adhesive (in kit) can also be used to hold

Essentials of Dentistry
in place.
• It is an ethylene/vinyl acetate copolymer fiber (diameter 0.5 mm) containing 12.7 mg
of drug per 9 inches and it maintains 1300 µm/ml of concentration of tetracycline in
GCF for 10 days.
• It is not used at initial and antiinfective phase of therapy but it is used only after traditional
methods have been employed.
• Predominantly used in refractory cases, ailing implants, or the periodontal abscess.
No tetracycline resistance has been found with fiber therapy.

Q.45. Subgingival doxycycline (Atridox).


Ans:
• Atridox is a 10 percent formulation of doxycycline in a bioabsorbable, “flowable” poly-
DL-lactide and N-methyl-2-pyrrolodone mixture delivery system that allows for controlled
release over 7 days.
• It is available in gel form and it is the only local drug delivery system accepted by ADA.

Q.46. Periochip.
Ans:
• It is an orange-brown, biodegradable, rectangular chip rounded at one end. It has an
active ingredient of chlorhexidine gluconate (2.5 mg) that is released into the pocket
over a period of 7 to 10 days.
• It is a resorbable delivery system consists of a small biodegradable hydrolyzed gelatin
chip (4.0 x 5.0 x 0.35 mm).

Q.47. Subgingival minocycline (Arestin).


Ans:
• Arestin is an ointment of 2 percent (wt/wt) minocycline hydrochloride. The 2 percent
minocycline is encapsulated into bioresorbable microspheres in a gel carrier.
• It is applied once every 2 weeks for four applications due to insufficient sustained-
release properties.

Q.48. What is the treatment guideline for ANUG?


Ans:
Treatment sessions for ANUG
• Removal of pseudomembrane and nonattached debris after the application
of topical anesthetics.
• Amoxicillin 500 mg orally every 6 hours for 10 days (For patients allergic
to amoxicillin, erythromycin 500 mg every 6 hours is good alternative) and
metronidazole 500 mg twice daily for seven days is given to patients with
First visit systemic manifestations.
• Deep scaling should be avoided at first visit. Supragingival scaling without
touching the marginal gingiva can be performed.
• Patient is advised to rinse with a glass full of equal dilution of 3 percent
H2O2 with warm water every 2 hours and/or twice daily with 0.12 percent
chlorhexidine solution.
Contd....
208 Definitions and Questionnaire for Periodontia Viva Voce

Contd....

Treatment sessions for ANUG


After 1-2 days of the 1st visit, scaling is performed and oral hygiene instructions
Second visit
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are given.
Approximately 5 days after 2nd visit, thorough scaling and root planing is
Third visit performed. The H2O2 rinses are substituted with chlorhexidine rinses which
are continued for 2-3 weeks.
Patients without other gingival diseases are dismissed for one week. Tooth
Subsequent visits extraction or periodontal surgery should be postponed for 4 weeks. Contouring
of the gingival margin can be done by gingivoplasty.

SCALING AND ROOT PLANING


Q.1. How much time does plaque takes to form on tooth surface after scaling and
polishing?
Ans: Plaque starts forming immediately within nanoseconds after scaling and polishing.

Q.2. In how many sittings scaling should be completed ideally and why?
Ans: Ideally, scaling should be completed in one sitting because after first sitting the
inflammatory infiltrate decreases in size and the pocket wall becomes fibrous. Dentogingival
tissue becomes more resistant to penetration of instrument making it difficult to access
the deeper calculus subsequently. Patients with small amount of calculus and relatively
healthy tissues can be treated in one appointment. However, in patients with heavy deposits
confined by deep edematous pockets, severe inflammatory changes limit the reach of
the instrument deep into the pocket at the first sitting. On subsequent sittings, gradual
reduction in inflammation and shrinkage of pocket wall make the unreachable areas
accessible. Most of the patients require several treatment sessions for the dentist to perform
a complete debridement of tooth surfaces. The selection of optimal therapy varies from
patient-to-patient depending on the oral condition.

Q.3. After what duration and why should patient be recalled for follow-up after scaling
and root planing?
Ans: Clinical evaluation of the soft tissue response to scaling and root planing, including
probing should not be conducted earlier than 4 weeks postoperatively. This permits sufficient
time for both epithelial and connective tissue healing and also allows the patient sufficient
practice with oral hygiene skills to achieve maximum improvement. Gingival inflammation
usually substantially reduced or eliminated within 3 to 4 weeks after removal of calculus
or local irritants.

Q.4. What is the difference between polishing by rubber cup and brush?
Ans: Polishing brush is more abrasive than the cup. Brush is advocated for cleaning pit
and fissures and stubborn stains. It should be avoided near cervical areas as it could
lacerate the gingiva and may abrade the cementum while rubber cup is safer to use near
the cervical region, root surface and less susceptible to cause abrasion.

Q.5. At what speed should the polishing tools be used?


Ans: Polishing tools should be rotated with lowest possible speed, only enough to keep
them rotating and high enough that removes the stains.
Definitions and Questionnaire for Periodontia Viva Voce 209

HISTORY
Q.1. What is history?
Ans: It is a systematic approach to patient for diagnosis and treatment.

Essentials of Dentistry
FEW POINTS ABOUT INTRAORAL EXAMINATION
General oral hygiene.
Oral hygiene can be evaluated from the accumulated deposits such as plaque, calculus,
food debris stains. Poor oral hygiene leads to periodontal diseases.
Oral (good, poor, fair) is related to the OHI score of particular patient.
(In examination of soft tissue, better to write is no pathological changes are found rather
than writing normal).

Stillman’s clefts.
It is a special type of recession consisting of narrow triangular-shaped gingival recession.
These are apostrophe-shaped indentations extending from and into gingival margin for
varying-distance. It varies in length from slight break in gingival margin to 5-6 mm of depth.

McCall’s festoon.
These are life preserver shaped enlargement of marginal gingiva that occurs most frequently
on the facial surfaces in canine and premolar areas.

Surface texture.
Gingival surface is textured with stippling. Stippling is present only on center of interdental
papilla and attached gingiva while it is absent on marginal gingiva. It is produced by alternate
elevations and depressions representing connective tissue retepegs projecting into
epithelium. It is the form of adaptive specialization or reinforcement for function. It is viewed
by drying the gingiva.
Changes occurring in disease: There is loss of stippling in inflammation due to epithelial
atrophy and edema of gingiva.
Surface: It is smooth and shiny when exudative process is predominant and it is firm
and nodular when fibrotic process is predominant. Leathery texture is seen in hyperkeratosis.
Peeling of surface occurs in chronic desquamative gingivitis. (It can be different in different
areas of oral cavity depending on changes in gingiva and is noted respectively in the
history form).

Width of attached gingiva (Fig. 25.8).


Width of attached gingiva can be measured by following ways:
i. Measurement approach
Width of attached gingiva = Distance between margins of gingiva to mucogingival
junction – Distance between margin of gingiva and free gingival groove (Sulcus/pocket
depth).
ii By using a solution called as “Schiller’s potassium iodide solution”.
Potassium iodide solution stains only the keratinized epithelium (marginal gingiva,
attached gingiva, interdental papilla). After staining the gingiva, width of attached gingiva
can be easily measured by measurement approach.
Width of attached gingiva = Stained gingiva – Pocket depth
iii. Tension test: It is a simple clinical determination of the quantity of attached gingival
surrounding tooth. Lip or cheek is stretched to demarcate the mucogingival junction
and to see any movement of free marginal gingiva. Any movement or blanching of
Essentials of Dentistry 210 Definitions and Questionnaire for Periodontia Viva Voce

Fig. 25.8: Width of attached gingiva

free marginal gingival during stretching of lips indicates inadequate width of attached
gingival (Kopczyk and Saxe 1974; Vincent et al. 1976).
Width of attached gingiva may increase with increasing the age due to coronal movement
of tooth (However, the gingiva must be healthy). The mucogingival junction remains stationary.
Increase in the width attached of gingiva occurs due to changes at the coronal level.

Position.
The position of gingiva refers to the level at which the gingival margin is attached to the
tooth.
a. Actual position of gingiva: It is the level of epithelium attachment on the tooth.
b. Apparent position: It is the level of the crest of the gingival margin.
Recession: “Gingival recession is the exposure of the root surface by an apical shift
of gingiva.”
Severity of recession is determined by the actual position of the gingiva, not by apparent
position. The prevalence, extent and severity of gingival recession increase with age and
more prevalent in male. Recession refers to the location of gingiva, not its condition. Receded
gingiva can be inflamed but may be normal. It can be localized or generalized.
Recession is the cumulative effect of minor pathologic involvement and repeated minor
direct trauma to the gingiva. Susceptibility of recession is also influenced by the position
of tooth in the arch, the root-bone angle, and the mesiodistal curvature of the tooth surface.
The rotated, tilted or facially displaced tooth may represent thinned or reduced buccal
bone plate. The effect of the angle of root in the bone on recession is often observed
in the maxillary molar area. Flaring of buccal and palatal roots thins the cervical bone
and repeated trauma results in recession.
Types:
i. Visible—Recession that is clinically observable.
ii. Hidden—Recession that is covered by gingiva can be measured only by inserting probe
into the level of epithelium attachment.
The total amount of recession is the sum of the two.
Definitions and Questionnaire for Periodontia Viva Voce 211

Causes:
Etiological factors include, but are not limited to (Figs 25.9 to 25.14):
• Gingival inflammation
• Tooth malposition, deep overbite

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Fig. 25.9: Appliance

Fig. 25.10: High frenum attachment

Fig. 25.11: Oral piercing


Essentials of Dentistry 212 Definitions and Questionnaire for Periodontia Viva Voce

Fig. 25.12: Orthodontic appliance

Fig. 25.13: Prominent roots

Fig. 25.14: Toothbrush trauma


Definitions and Questionnaire for Periodontia Viva Voce 213

• Toothbrushing injury (gingival abrasion)


• Friction from soft tissue (gingival ablation)
• Anatomical abnormalities (High frenum attachment, dehiscence, thin bony plates)
• Trauma from occlusion
• Iatrogenic causes (Damage by orthodontic band, faulty restorations, faulty prosthesis,

Essentials of Dentistry
oral piercing).
Significance:
• Exposed root surfaces are more susceptible to caries, abrasion, and erosion.
• Exposed accessory canals are vulnerable to infection.
• Wearing away of expose cementum causes dentinal sensitivity.
• Interproximal recession creates spaces, in which plaque accumulation aggravates
inflammation and also makes oral hygiene maintenance difficult.
Classifications:
i. Sullivan and Atkins classification (1968): Many authors have defined gingival recession
by its degree of severity and extent in order to help clinician to define treatment options
and prognosis. In 1968, Sullivan and Atkins defined gingival recession as exposure
of the root surface by an apical shift in the position of the marginal tissue. The classification
system describes the type of recession and expected amount of root coverage utilizing
the free gingival graft procedure. Deep-wide defects were thought not to be able to
be covered.
• Shallow-narrow
• Shallow-wide
• Deep-narrow
• Deep-wide.
ii. Guinard and Caffesse (1978):
• Visible recession: It is the amount of clinically observable root measured from the
cemento-enamel junction to the crest of the soft tissue margin.
• Hidden recession: It is the depth of the sulcus or pocket as measured from the
soft tissue margin to the epithelial attachment (junctional epithelium)
iii. Miller’s classification (1985):
PD Miller combined the four classes of Sullivan and Atkins into two (shallow and deep)
and then created two additional classes, all related to height if the interproximal bone
and the relation of the gingival recession to the mucogingival junction. This classification
helps clinicians to determine the degree of root coverage expected during periodontal
plastic surgery (Figs 25.15 to 25.18).
Marginal tissue recession does not extend to the mucogingival junction.
Class I There is no loss of bone or soft tissue in the interdental areas. This
type of recession can be narrow or wide.
Marginal tissue recession extends to or beyond the mucogingival To memorize
Class II junction. There is no loss of bone or soft tissue in the interdental
areas. This type of recession can be narrow or wide.
extends to or

Marginal tissue recession extends to or beyond the mucogingival


beyond
bone and soft

Class III junction. There is bone and soft tissue loss in the interdentally or
tissue loss

malpositioning of tooth.
Marginal tissue recession extends to or beyond the mucogingival
Class IV junction. There is severe bone and soft tissue loss interdentally or
severe tooth malposition.
214 Definitions and Questionnaire for Periodontia Viva Voce

Grade Treatment
Complete, 100 percent coverage of this type of recession can be achieved. For example,
Class I
by use of free connective tissue grafts
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Complete coverage of root surface can still be achieved. With such deep recession,
Class II guided tissue regeneration (GTR) with membrane can be employed instead of connective
tissue grafts.
Complete regeneration of such defects is not possible; the facial root surface can, at
Class III
best, be partially covered and rebuilding the papillae is hopeless.
Class IV Regeneration of lost tissue by surgical procedure is rarely possible.

Prognosis of class I and II is good to excellent. Only partial coverage can be expected
in Class III. Class IV has poor prognosis.
Level of the gingival margin: The level of the gingival margin can change over the time
period in response to trauma, medications, or disease. Three possible relationships exist
between the gingival margin and the cementoenamel junction (CEJ) of the tooth.
1. Gingival margin significantly covers the CEJ (Fig. 25.19).
a. In this instance, the gingiva covers a significant portion of the tooth crown.

Fig. 25.15: Class I Fig. 25.16: Class II

Fig. 25.17: Class III Fig. 25.18: Class IV


Definitions and Questionnaire for Periodontia Viva Voce 215

Essentials of Dentistry
Fig. 25.19: Gingival margin significantly covers the cementoenamel junction (CEJ)

b. The position of the gingival margin may be coronal to the CEJ owing to following
reasons;
• Swelling (edema)
• An overgrowth of the gingival tissues caused by certain medications taken by
patients as a part of treatment of medical condition
• An increase in the fibrous connective tissue of the gingiva caused by a long-
standing inflammation of the tissue
2. Gingival margin is at the CEJ (Fig. 25.20).
This is the natural position of the gingival margin.
3. Gingival margin is significantly apical to the CEJ (Fig. 25.21).
a. When the gingival margin is significantly apical to the CEJ, a portion of the root
surface is exposed in the mouth. This relationship is known as gingival recession.
b. Gingival recession is the movement of the gingival margin from its normal position—
usually with underlying loss of bone—resulting in the exposure of a portion of the
root surface. In recession, the gingival margin is apical to the CEJ and the papillae
may be rounded or blunted.
Technique to determine the gingival margin level:
When tissue swelling or recession is present, a periodontal probe is used to measure
the distance that the gingival margin is apical or coronal to the CEJ.
1. For gingival recession: If gingival recession is present, the distance between the CEJ
and the gingival margin is measured using a calibrated periodontal probe. This distance
is recorded as the gingival margin level (Figs 25.22 and 25.23).
2. When the gingival margin covers the CEJ: If the gingival margin covers the CEJ, the
distance between the margin and the CEJ is estimated using the following technique:
a. Position the tip of the probe at a 45-degree angle to the tooth.
b. Slowly move the probe beneath the gingival margin until the junction between the
enamel and cementum is detected.
c. Measure the distance between the gingival margin and the CEJ. This distance is
recorded as the gingival margin level.
Calculating clinical attachment level:
A competent clinician must understand the procedure for determining the Clinical
Attachment Level for the three possible relationships of the gingival margin to the CEJ.
1. The gingival margin may be apical to the CEJ, cover the CEJ, or be at the CEJ.
Essentials of Dentistry 216 Definitions and Questionnaire for Periodontia Viva Voce

Fig. 25.20: Gingival margin at the cementoenamel junction (CEJ)

Fig. 25.21: Gingival margin significantly apical to the cementoenamel junction: It is known as
recession, this relationship leads to exposure of the root surface

Fig. 25.22: Calculating the clinical attachment level


Definitions and Questionnaire for Periodontia Viva Voce 217

Essentials of Dentistry
Fig. 25.23: Loss of attachment

2. Two measurements are used to calculate the clinical attachment level:


a. The probing depth and
b. The level of the gingival margin (Distance from CEJ to gingival margin)
Note that both of these measurements are routinely taken and documented on a
periodontal chart.
Calculating clinical attachment level in the presence of gingival recession:
When recession is present, the CAL is calculated by adding the probing depth to the gingival
margin level (Fig. 25.24).
For example:
Probing depth measurement: 4 mm
Gingival margin level: 2 mm
Clinical attachment loss: 6 mm
Calculating clinical attachment level when the gingival margin covers the CEJ:
When the gingival margin is coronal to the CEJ, the clinical attachment level is calculated
by subtracting the gingival margin level from the probing depth (Fig. 25.25).
For example:
Probing depth measurement: 9 mm
Gingival margin level: 3 mm
Clinical attachment loss: 6 mm
Calculating clinical attachment level when the gingival margin is at the CEJ:
When the gingival margin is at the CEJ, no calculations are needed because the probing
depth and the clinical attachment level are equal (Fig. 25.26).
For example:
Probing depth measurement: 6 mm
Gingival margin level: 0 mm
Clinical attachment loss: 6 mm

BLEEDING ON PROBING (Fig. 25.27)


Gingival bleeding helps in clinical evaluation of degree of gingival inflammation. It is related
to persistent presence of plaque on the teeth. Bleeding on probing appears before other
signs of gingivitis requiring subjective estimation like color and texture changes and it
serves as an important objective sign of inflammation. Therefore, it is of value for the early
diagnosis and prevention of more advanced gingivitis. Gingival bleeding varies in severity,
duration, and ease of provocation. Severity of gingival bleeding increases with increase
Essentials of Dentistry 218 Definitions and Questionnaire for Periodontia Viva Voce

Fig. 25.24

Fig. 25.25 Fig. 25.26

Figs 25.24 to 25.26: Calculating clinical attachment level

in size of inflammatory infiltrate in the connective tissue at the base of sulcus. Bleeding
on gentle skimming examines the health of marginal gingiva and bleeding on probing
examines the health at the base of sulcus and pocket.
Definitions and Questionnaire for Periodontia Viva Voce 219

Essentials of Dentistry
Fig. 25.27: Bleeding on probing

Bleeding on gentle probing is a sign of inflammation. The insertion of a probe to the


bottom of the pocket elicits bleeding, if the gingiva is inflamed and the pocket epithelium
is atrophic or ulcerated. Bleeding on probing is an earlier sign of inflammation than gingival
change in color and other signs of inflammation. Depending on severity of inflammation,
bleeding can vary from a tenuous red line along the gingival sulcus to profuse bleeding.
In acute inflammation, it occurs as soon as probe is inserted into the sulcus while in chronic
inflammation; it occurs few seconds after the probe is removed. Therefore clinician should
recheck for bleeding 30 to 60 seconds after probing. The severity of bleeding (amount
of bleeding) and the ease of its provocation (the time between stimulation and appearance
of blood) depend on the intensity of the inflammation. The sulcus bleeding index by
Mühlemann provides an objective, easily reproducible assessment of the gingival status.
It is extremely useful for detecting early inflammatory changes and the presence of
inflammatory lesions located at the base of the periodontal pocket, an area inaccessible
to visual examination.
Bleeding on probing is an important diagnostic factor for clinicians to use in planning
periodontal therapy. The presence of bleeding is an indicator of active gingival inflammation,
and until it is controlled, the patient is at risk of continuing periodontal disease and tissue
destruction. Bleeding on probing is widely used by clinicians to measure outcomes of
treatment, and to motivate patients with their home care.
Limitations:
1. Longitudinal studies fail to demonstrate a significant relation between bleeding on
probing, other clinical signs and subsequent attachment loss.
2. Bleeding on probing from healthy site with intact periodontium further limits the use
of bleeding as an inflammatory parameter.
Conclusion:
Even after the limited predictive value of bleeding on probing for disease progression
(attachment loss), its absence indicates periodontal stability. It is an excellent negative predictor
of future attachment loss and therefore the absence of gingival bleeding on probing is desirable
and implies low risk for future clinical attachment loss. The documentation of bleeding points
during probing is important and should be included in the patient’s periodontal records.

SUPPURATION
The clinical assessment of suppuration, formation of pus within the periodontal pocket
is performed by gently pressing the ball of index finger along the lateral aspect of marginal
220 Definitions and Questionnaire for Periodontia Viva Voce

gingiva and rolling it towards the crown of tooth with pressure. Suppuration is formed
on inner pocket wall, but the external appearance of pocket wall is unchanged. Therefore,
the visual examination with digital pressure is required. Suppuration doesn’t occur in all
periodontal pockets. However, suppuration may be present, although not visibly detected,
Essentials of Dentistry

and therefore its clinical absence is not an indicator of periodontal stability. Clinically,
detectable suppuration should be documented in the patient’s periodontal records.

Q.1. What are the differences between gingival and periodontal abscess?
Ans:

Gingival Periodontal
Definition Abscesses localized in the gingiva, Periodontal abscess is localized
caused by injury to the outer surface of purulent inflammation in the periodontal
the gingiva, and not involving the tissues.
supporting structures are called gingival
abscess.
History It occurs in previously disease-free Generally, it occurs in the course of
gingiva. It is usually an acute chronic destructive periodontitis. It can
inflammatory response. be acute or chronic.
Etiology Gingival abscess if the localized, acute It results from extension of the infection
inflammatory lesion that may arise from into the still intact periodontal tissues
variety of sources, including microbial and lack of proper drainage. The
plaque infection, trauma, and foreign principal ways of abscess formation are;
body impaction. When a foreign a. Extension of infection from a
substance is forcefully embedded into periodontal pocket deeply into the
the gingiva, bacteria carried deep into supporting periodontal tissues.
the tissues produce acute inflammatory b. Lateral extension of inflammation
gingival enlargement. from the inner surface of the
periodontal pocket into the
connective tissue of the pocket wall.
c. Formation abscess in a pocket with
a tortuous course around the root.
d. Incomplete removal of calculus
during treatment followed by
shrinkage of gingival wall leading to
marginal closure of a deep
periodontal pocket.
e. Trauma to the root and accidental
root perforation during endodontic
therapy.
Location Gingival abscess generally remains According to location they are classified
limited to the marginal gingiva or as follows;
interdental papilla and does not involve a. Periodontal abscess involves the
the supporting periodontal tissue. supporting periodontal structures. It
is seen along the lateral aspect of the
root. It is not necessarily located on
the same surface of root from which
it is formed.
b. Abscess in the soft tissue wall of deep
periodontal pocket.

Contd....
Definitions and Questionnaire for Periodontia Viva Voce 221

Contd....

Gingival Periodontal
Clinical In the early stages, it appears as a red a. Acute: Appear as an ovoid elevation
course swelling with a smooth, shiny surface. of gingiva along the lateral aspect of

Essentials of Dentistry
Within 24 to 48 hours, the lesion usually the root. Pus may be expressed from
becomes fluctuant and pointed with a gingival margin on gentle digital
surface orifice from which a purulent pressure.
exudate may be expressed. b. Chronic: Usually it presents a sinus
that opens onto the gingival mucosa
somewhere along length of root.
Patient may present history of
intermittent exudation.
Signs The adjacent teeth are often sensitive to Acute – Throbbing, radiating pain,
and percussion. tenderness of gingiva on palpation, tooth
symptoms mobility, lymphadenitis, and systemic
effects like fever, fever, leukocytosis,
malaise.
Chronic – Usually it is asymptomatic but
there may be dull gnawing pain, slight
elevation of tooth, and a desire to bite
down on and grind the tooth. It presents
a sinus tract with difficult-to-detect
pinpoint opening on gingiva.
Diagnosis Based on history and clinical findings. Based on careful exploration of history,
clinical and radiographic findings.
Continuity of abscess with gingival
margin is the evidence of periodontal
abscess.
Treatment Treatment of gingival abscess is directed Acute – Treatment is aimed to alleviate
to reverse the acute phase and immediate symptoms, control the spread of
removal of the cause. Scaling and root infection, and establish drainage.
planing under local anesthesia ensures the Chronic – Scaling and root planing and
removal of microbial deposits. Fluctuant surgical therapy is recommended.
abscess is incised and purulent material is Antibiotic therapy may be indicated.
drained. Any foreign material, if present, is
removed. In case of large abscess, scaling
and root planing and surgical therapy
should be delayed until the major signs
have abated. In these patients, use of
adjunctive antibiotic therapy is
recommended. Gingivectomy is performed
and the fluctuant area is incised with scalpel
blade. The exudate may be expressed by
gentle digital pressure.

Q.2. Which clinical parameters may be used to judge the success of periodontal
treatment?
Ans: There are several clinical and radiographical parameters that may be used to judge
the success of periodontal therapy. The principle parameters are;
i. Reduction or absence of bleeding on probing:
Bleeding on gentle probing is still the best prognostic indicator of the potential for
future attachment loss. Absence of bleeding on probing is a 98 percent negative predictor
222 Definitions and Questionnaire for Periodontia Viva Voce

that the site will lose attachment in future. Since it is impossible to predict exactly which
site will lose attachment, the thrust of therapy is to control inflammation at all sites.
ii. Reduction of probing depth and gain in periodontal attachment:
Periodontal therapy is focused on removal of etiological agents and contributing factors
Essentials of Dentistry

and subsequent maintenance of health. One way to improve this possibility for both
the patient and practitioner is to reduce the probing depths. Persistence of periodontal
pathogens and progressive loss of attachment is associated with deeper pockets.
iii. Positive radiographic changes:
Positive radiographic changes related to the success of periodontal therapy include
the reappearance of a crestal lamina dura at the interproximal osseous crests, evidence
of bone fill in areas of regenerative therapy, narrowing of periodontal ligament space
in relation to teeth subjected to periodontal trauma and the absence of calculus on
coronal and root surfaces.
iv. Occlusal stability:
The main factors responsible for tooth mobility are presence of edema in gingival and
periodontal tissues, loss of attachment, and the effects of occlusal forces on the
attachment apparatus. After proper inflammatory control, teeth often exhibit decreased
mobility. Elimination of edema and reformation of supragingival connective tissue fibers
contribute to tooth stability, particularly in case of tooth with attachment loss. Judicial
occlusal adjustment by selective grinding also contributes to increased tooth stability.

Q.3. How will you manage a case of moderate to severe generalized periodontitis?
Describe the most preferred method for treating pockets in anterior segment?
Ans: Moderate to severe periodontitis constitutes symptoms and signs like:
– 4-5 mm or more attachment loss
– Moderate to through and through furcation involvement
– Moderate to excessive tooth mobility
Periodontitis is diagnosed based on disease activity and rate of attachment loss
Three models of periodontitis
1. Continuous paradigm (traditional concept)
It is a plaque-induced, slowly progressive disease.
• Continuous deepening of pockets
• Gradual loss of attachment.
2. Random burst (newer concept)
It is bacteria-induced disease.
• Destruction of attachment apparatus progresses by recurrent acute episodic
bursts of activity.
3. Asynchronous multiple burst
• Destruction occurred during a defined time
• Disease goes into remission for an indefinite time.
Health vs. disease:
There are 3 stages;
1. Periodontal health.
2. Periodontitis inactive: inflammation but no attachment loss.
3. Periodontitis active: inflammation with attachment loss.
On examination:
1. Considerations in diagnosis of periodontal disease are:
Active or inactive
Sulcus vs. pocket
Sulcus (healthy attachment, plaque < threshold)
Pocket (diseased attachment, plaque > threshold)
Definitions and Questionnaire for Periodontia Viva Voce 223

2. Assessment methods:
Clinical: Clinical methods of direct observations are:
– Subgingival plaque and calculus
– Gingival inflammation (color changes)
– Bleeding on probing

Essentials of Dentistry
– Suppuration
– Loss of form
– Pocket depth/probing depths (attachment level changes).
Histological:
It is difficult sometimes because of invasive nature of disease and it shows different
activities at multiple sites.
Microbiological:
Culture and sensitivity test
Organisms associated with different tissue conditions are;
Healthy sulcus Gram-positive organisms predominate
Gingivitis Shift from gram-positive organisms to gram-negative organisms
Adult periodontitis Gram-negative anaerobic rods, 30-50 percent motile rods and spirochetes

Immunological:
PMNs, lymphocytes, antibody titers, complement fractions, lymphokines.
Steps for treatment are:
1. Preliminary phase:
It includes treating emergency conditions like drainage of periodontal abscess, extraction
of hopeless teeth.
2. Removal of local irritants (phase I):
Local deposits like plaque and calculus can be removed by scaling and root planing.
Subgingival scaling is done along with root planing for final smoothening and planing
of the root surface.
Patient’s education
– Motivating patients to perform effective plaque control is one of the most critical and
difficult elements of long-term success in periodontal therapy.
– Proper brushing technique is explained and patient is instructed to maintain oral hygiene.
The brushing technique should emphasize access to the gingival margins of all
accessible tooth surfaces and extension as far onto the proximal surfaces as possible.
– Dental floss and other interdental aids like toothpicks, interdental brushes are advised,
if required.
– If dictated by the oral hygiene, patient is advised chemical plaque control agent for
aided benefits.
3. Evaluation of response to Phase I therapy.
Final decision on the need of periodontal surgery should be made only after thorough
evaluation of the effects of Phase I therapy. The assessment is usually made no less than
1-3 months and may extend up to 9 months after the completion of Phase I therapy. In
the reevaluation of Phase I, look for:
– Persistence of calculus
– Root caries
– Defective restorations
– Pocket depth
– All signs of persistent inflammation.
Evaluation of phase I therapy determines whether any surgical intervention is required
or not. Necessary surgical and restorative procedures are performed to retain the degree
224 Definitions and Questionnaire for Periodontia Viva Voce

of the health attained after Phase I. In moderate to severe periodontitis surgery is usually
needed because of one or more factors like:
– Presence of bone defects
– Deep pockets limiting the calculus removal
Essentials of Dentistry

– Persistent inflammation.
The transformation of the initial deep, active pocket into a shallower, inactive, maintainable
pocket requires some form of definitive pocket therapy and constant supervision thereafter.
4. Surgical phase.
Criteria for the selection of one of the different surgical techniques for pocket therapy
are based on clinical findings in the soft tissue pocket wall, tooth surface, underlying bone,
and attached gingiva. Clinician should determine morphological feature, thickness, and
topography of the soft tissue wall of pocket, presence of deposits, altered cementum,
accessibility of the root surface to instrumentation, morphology and architecture of
underlying bony defect, and presence or absence of an adequate width of attached gingiva
when selecting a pocket therapy.
Before planning for surgical phase, routine blood investigation and other tests, if
necessary, are carried out to evaluate patient’s systemic condition. Surgery for moderate
to severe periodontitis requires flap elevation. Flap surgery differs for anterior segment
and for posterior segment depending on variety of factors such as age of the patient,
esthetic requirement of patient, clinical findings etc.

For Anterior Segment


Selection of flap technique is crucial task and it depends on the deliberate examination and
prudent clinical judgment. If interdental space is wide enough, considering the esthetic requirement
of the patient, papillary preservation flap is preferred. It retains the entire papilla covering the
lesion. If interdental space is narrow making it impossible to perform a papilla preservation flap,
conventional flap with only crevicular incision is the better option. If some degree of gingival
enlargement is present and recession is permissible, modified Widman flap can be used. This
technique doesn’t remove the pocket wall, but it does eliminate the pocket lining.

For Posterior Segment


The two important landmarks to determine the amount of attached gingiva and subsequently
dictating surgical flap technique are pocket depth and location of mucogingival junction.
Undisplaced flap and modified Widman flap are commonly used depending upon situation.
The modified Widman flap eposes the root surface for meticulous instrumentation and
also removes the pocket lining. It is not intended to remove the pocket wall and the reduction
in pocket depth is merely due to healing by tissue shrinkage. Undisplaced flap is an
Excisional procedure and it is used only if the sufficient attached gingiva remains apical
to the incision. It removes the pocket wall, thereby reduces or eliminates the pocket.
If widening of the zone of attached gingiva is required along with the pocket eradication,
the apically displaced flap technique is used. It preserves and increases the width of attached
gingiva by transforming the previously unattached keratinized pocket wall into attached
gingiva. Attempts are directed towards maintaining the as much possible attached gingiva
along with pocket elimination.
For regenerative or reconstructive procedures like bone grafting, flap is elevated
accordingly. The conventional flap using only crevicular retain maximum amount of gingival
tissue, including the papilla. Unlike the resective surgeries, the flap is not thinned. The
thick flap is necessary to prevent exposure of the graft or the membrane.
5. Maintenance phase.
Patient must understand the importance of the maintenance program, and the dentist must
emphasize that preservation of teeth depends on the maintenance therapy. Regular follow
Definitions and Questionnaire for Periodontia Viva Voce 225

up is must to maintain the periodontal structures in healthy state. The interval between
the visits is set at 3 months but it may be varied according to the patient’s needs.
Recall visit during maintenance phase starts with examination and evaluation and
checking of the plaque control followed by treatment. At the recall examination changes
that have occurred since last evaluation are observed and noted. Radiographic examinations

Essentials of Dentistry
are carried out depending on the initial therapy to check the bone height and repair of
the osseous defects. Patient is asked to perform the plaque control immediately before
recall visit for review and correction of plaque control. Scaling and root planing are performed
as a prophylaxis, if required, after thorough review of medical and dental history, intraoral
and extraoral soft tissue examinations, a dental examination and a periodontal examination.
Some points to memorize
Diseases Principal immune response
ANUG Elevated antibody titers to intermediate sized spirochetes
and P. intermedia
Adult periodontitis Elevated antibody titers to P. gingivalis
Localized aggressive periodontitis Elevated antibody levels to A. atinomycetamcomitans
Generalized aggressive periodontitis Elevated antibody titers to P. gingivalis
Refractory periodontitis (RPP) Elevated antibody levels to P. gingivalis, T. forsythia,
F. nucleatum, P. micros, E. corrodens, Streptococcus
intermedius

Condition Brushing Technique


Gingival recession and root exposure Modified stillman
Healing wound after surgery Charters technique
Routine technique in patient with or without periodontal disease Bass or sulcular technique
Recommended technique in patient with periodontal disease Sulcular technique
Recommended for children Fones technique
Least effective Roll technique
Most commonly performed Scrub technique

Complexes
Yellow complex S. mitis
colonizers

S. sanguis
Initial

S. oralis
Purple complex V. parvula
A. odontolyticus
Red complex (BPT) P. gingivalis
T. denticola
B. forsythus
Secondary
colonizers

Orange complex P. intermedia


C. rectus
F. nucleatum
Green complex A. antinomycetamcomitans

Red complex is important as it is associated with bleeding on probing which is important


sign of periodontal destruction.
CHAPTER

26 Ameloblastoma

TUMORS
New growth of abnormal tissue of body is called tumor. It is defined as, “A mass of tissues
formed as a result of abnormal, excessive, uncoordinated, autonomous and purposeless
proliferation of cells.”
It can be malignant or benign.

Odontogenic Nonodontogenic

ODONTOGENIC TUMORS
Odontogenic structures are formed by inductive interactions between epithelium and
mesenchyme. It begins during 5th and 6th week of intrauterine life and because of that,
during this period, there is possibility for occurrence of odontogenic lesions resulting into
malformations, hamartomas and neoplasms.

CLASSIFICATION
Classification of epithelial odontogenic tumors is based on the principle of embryonal
inductive influence of epithelial cells on the connective tissue cells.

Epithelial Odontogenic Tumors


1. Tumors producing minimal inductive changes in connective tissue:
a. Ameloblastoma (adamantinoma)
b. CEOT (Calcifying epithelial odontogenic tumor/Pindborg tumor)
c. OAT (Adenoameloblastoma) odontogenic adenomatoid tumor.
2. Tumors producing extensive inductive changes in connective tissue:
a. Ameloblastic fibroma
b. Ameloblastic fibro-odontoma
c. Odontoameloblastoma
d. Odontoma
– Compound composite odontoma
– Complex composite odontoma.

Mesodermal Odontogenic Tumors


1. Central odontogenic fibroma
2. Odontogenic myxoma
Ameloblastoma 227

3. Cementoma
– Peripheral cemental dysplasia
– Cementifying fibroma
– Benign cementoblastoma
4. Dentinoma

Essentials of Dentistry
Tumors of Unknown Origin
Melanotic neuroectodermal tumor of infancy.

Malignant Odontogenic Tumors


1. Odontogenic carcinoma
– Primary intraosseous carcinoma
– Malignant ameloblastoma.
2. Odontogenic sarcoma
– Ameloblastic fibrosarcoma
– Ameloblastic odontosarcoma.

AMELOBLASTOMA
Ameloblastoma is the most common odontogenic tumor exhibiting minimal inductive
changes in connective tissue. It is a true neoplasm and most controversial lesion. Generally,
it is considered as a benign but it is a persistent and locally malignant in nature. There
are different names given to this tumor. It is also called as adamantinoma,
adamantinoblastoma, epithelial odontoma and multilocular cyst.

HISTORY
1827 Cuzack First recognized
1879 Falksson Follicular cystoids tumor
1885 Malassez Adamantinoma
1934 Ivy and Churchill Ameloblastoma

DEFINITION
Robinson defined as “Usually unicentric, nonfunctional, intermittent in growth, anatomically
benign and clinically persistent.”
WHO defined as “It is a true neoplasm of enamel organ type tissue which doesn’t
undergo differentiation to a point of enamel formation.”
It is a benign but locally invasive polymorphic neoplasm consisting of proliferating
odontogenic epithelium which is usually in a follicular or plexiform pattern, lying in fibrous
stroma.

ETIOLOGY
• Irritation: It might be considered as one of the etiological factors as it often occurs
in the posterior region of the mandible which is most susceptible to irritation.
• Infection: Robinson found that 1/3rd of the cases have history of oral infection, extraction
of teeth and injuries to teeth.
• Trauma: Trauma can be a causative factor for ameloblastoma.
228 Ameloblastoma

• Dietary deficiency: Dietary deficiency has been considered as a possible factor for,
e.g. pronounced defect in development of tooth germ as seen in rickets may lead to
irregularity in the ameloblastic layer.
• Virus: Infections from polyoma viruses have been shown to produce ameloblastoma
Essentials of Dentistry

like lesions in animals.

CLASSIFICATION
On pathological basis:
– Peripheral ameloblastoma
– Pituitary ameloblastoma
– Adamantinoma of long bones.
On histological basis:
– Follicular ameloblastoma
– Plexiform ameloblastoma
– Acanthomatous ameloblastoma
– Basal cell ameloblastoma
– Unicystic ameloblastoma
– Plexiform unicystic ameloblastoma
– Granular cell ameloblastoma
– Papilliferous ameloblastoma
– Hemangioameloblastoma
– Desmoplastic ameloblastoma
– Clear cell ameloblastoma
– Dentinoameloblastoma
– Melanoameloblastoma
– Keratoameloblastoma
Other classifications
1. Central/intraosseous
2. Peripheral/extraosseous.

PATHOGENESIS
According to Thomas and Wilms tumor arises from:
1. Developing enamel organ
2. Cell rests of enamel organ
– Remnants of dental lamina
– Remnants of Hertwig’s sheath/Epithelial rests of Malassez.
3. Basal cells of surface epithelium of jaws
4. Hetropic epithelium in other parts of body especially pituitary gland
5. Epithelium of odontogenic cysts particularly dentigerous cyst and odontomas.

INCIDENCE
1 percent of all oral tumors
18 percent of all odontogenic tumors.

AGE
It is common between 20–50 years.
It is mostly seen in individuals younger than 40 years old.
Average age is 32.7 years.
Unicystic ameloblastoma is more common in 2nd and 3rd decade of life and the
extraosseous form is more common in older age group.
Ameloblastoma 229

SEX
No sex predilection.

SITE

Essentials of Dentistry
It is more frequent in mandible than maxilla (2:1).
It develops in the molar-ramus area (approximately 3/4th of cases) in the mandible
and also occurs in maxilla in 3rd molar area, followed by maxillary sinus and floor of the
nose. The right side of the mandible is affected slightly more as compared to the left side.

SIZE
Size varies from 1 to 16 cm.

RACE
It is more common in Africans.

PRECEDING FACTORS
Neoplasm is frequently preceded by extraction of teeth, cystectomy or some other traumatic
episode.

ONSET
It begins as a central lesion of the bone which is slowly destructive but tends to expand
the bone rather than perforate it.

CLINICAL FEATURES
• It is generally asymptomatic in early stages but later on, it produces pain and swelling
that is slow growing, hard, nontender, and ovoid in shape.
• Other features includes:
Mobility of teeth
Exfoliation/Root resorption
Ill fitting dentures
Malocclusion
Ulceration.
Nerve involvement in later stage leads to sensory changes like lower lip paresthesia.
Tumor may produce expansion and thinning of cortex leading to “Egg shell crackling”
(this shell of bone cracks when palpated).
• In maxilla, it leads to nasal obstruction, bleeding, trismus and maxillary sinus involvement.
Maxillary lesions are more dangerous than mandibular lesions due to tendency of the
former lesion to spread more extensively in the porous maxillary bone and possibility
of the involvement of the cranial base.
• Central ameloblastoma has following features:
– Grows in all direction and thins the surrounding bone.
– Invasion of medullary space is the first feature.
– As being nonencapsulated, it enlarges and invades the neighboring tissues rather
than pushing them as seen in cysts.
– Destroys the bone by pressure and distention or by osteoclastic resorption.
– Locally invasive so compresses the vital structures, obstructs airway, and impairs
swallowing.
– May invade middle cranial fossa and causes gross facial deformity.
230 Ameloblastoma

• Peripheral ameloblastoma has following characteristics:


– It produces a small nodule with swelling entirely within the soft tissue.
– It grows slowly without massive growth potential of intraosseous lesion.

SPREAD
Essentials of Dentistry

Distant metastasis may occur in later stages.


Most common site is lung due to aspiration of tumor cells. Other sites are regional
lymph nodes, liver, kidney, long bones, skull, vertebra, etc.

RADIOGRAPHIC FEATURES
• Radiodensity:
In the early stages, there is area of bone destruction which is well-defined and is indicative
of slow growth with hyperostotic borders.
• Margins:
Outline is smooth, scalloped, well-defined and well-corticated. The walls of the cavity
are coarse. In some cases, the margins of the tumor are devoid of bony covering.
• Internal structure:
Usually it is multilocular but may be unilocular. Coarse or fine trabeculae may be present
within the tumor and it is common for the free margins of the tumor to be devoid of
bony covering.
• Appearance:
There is presence of the septa in the lesion. In some cases, number and arrangement
of the septa may give the area “Honey comb appearance” (numerous small
compartments) or a “Soap bubble appearance” (larger compartments). In advanced
stages, perforated cortical plate may contribute to a multilocular appearance.
• Progress:
In the early stage ameloblastoma presents a bubble-like appearance with fairly large, round
and distinct compartments. As the tumor grows and expands, the compartment may
coalesce and fuse. With further increase in size of lesion, cortex expands and is destroyed.
• Subclinical lesion:
A small subclinical lesion usually presents in radiographs as many small rounded cavities
in the bone having sharply defined and sometimes corticated borders.
• Effect on surrounding structures:
1. The jaws are likely to be enlarged, depending on overall size of the tumor.
2. Extensive root resorption may occur.
3. Thickening of membrane, cloudiness and destruction of walls are the findings when
the sinus is involved.
4. Expansion and thinning of cortical plate occurs leaving thin eggshell of bone.
5. Perforation of bone is the late feature.
• Radiographic appearance can be of four types:
1. Multiloculated multicystic (Figs 26.1 and 26.2)
2. Solid trabeculated
3. Unilocular
4. Separate.
• Desmoplastic ameloblastoma (a variant) is almost radiopaque due to dense connective
tissue content.
• Radiographic appearance is merely an adjunct to diagnosis. Occlusal view shows buccal
and lingual expansion of the tumor.
• New imaging techniques like computerized tomography and MRI can demonstrate
osseous and soft tissue pathology respectively.
• Definitive diagnosis is possible by microscopic examination.
Ameloblastoma 231

Essentials of Dentistry
Fig. 26.1: Multiloculated appearance

Fig. 26.2: Multiloculated appearance

DIAGNOSTIC AIDS
• History
• Age
• Signs and symptoms
• Bimanual palpation
• Radiographs (OPG, Lateral view, CT, MRI)
• Incisional biopsy including piece of normal bone tissue

HISTOLOGICAL FEATURES
• Follicular type is the most common. Central portion has loose network of polyhedral
or spindle-shaped cells surrounded by tall columnar cells with nuclei polarized (responsible
for high recurrence rate) and away from basement membrane (Figs 26.3A to C).
• Cystic degeneration of central portion leaves clear space lined by flat, stellate cells.
Essentials of Dentistry 232 Ameloblastoma

C
Figs 26.3A to C: Follicular type

• Plexiform pattern shows cords of columnar epithelial cells in double columns. Central
stellate cells are arranged in periphery of areas of cystic degeneration.
• Intraluminal ameloblastoma grows into the lumen without violating the wall of cyst.
• Mural ameloblastoma is one which grows into the wall of cyst and remains limited within
the wall.
• Invasive ameloblastoma extends beyond the wall of the cyst and into the adjacent bone
or soft tissues.
Ameloblastoma 233

MANAGEMENT
1. Treatment must be considered on the basis of behavior and potential of trauma.
– Growth characteristic, if various physical forms are present
– Anatomical site, if recurrence is evident

Essentials of Dentistry
– Clinical extent and size
– Histological assessment.
2. Surgical (age must be taken in consideration)
3. First operation should be definitive and offering best opportunity for cure and with least
psychological distress imposed on patient in future.
4. Curettage has highest recurrence rate.
Intraosseous multicystic – 55 to 100 percent
Intraosseous unicystic – 18 to 25 percent
5. Cancellous bone is easily invaded so there is more microscopic invasion into bone
than that seen in radiograph.
6. Dense cortices – buccal, lingual and inferior borders are temporary barriers and can
be easily destroyed by tumor.
7. Safe margin of normal bone of approximately 2 cm is resected.
8. Resorption of cortical plate permits growth into periosteum and once it is perforated
soft tissue spread occurs.
9. Periapical connective tissue stroma whether dense/loose may circumscribe the lesion
but does not encapsulate and tumor can grow through it.

SPECIFIC PRINCIPLES
Solid Multicystic Lesion
• Resection with or without continuity defect.
• Inferior alveolar nerve can be sacrificed, if within the lesion. Nerve grafting is planned
and it is best to graft at the time of resection.
• Resection is always performed away from the tumor. Thin inferior border should be
preserved, if possible. (It has high recurrence rate after previous operation due to reverse
polarity of the cells).
• Sharp resection instruments permit radiologic assessment of resection margins.
• Immediate reconstruction should be planned, if soft tissue involvement is not there
and if soft tissue involvement is present, then secondary reconstruction should be
planned.
• Adequate soft tissue coverage in the tissue bed should be available to cover the graft.
(If soft tissue invasion is present, second stage treatment is done otherwise bone graft
gets separated and there is also less soft tissue to cover the bone).
• Maxillary lesion should be resected aggressively because of ease with which tumor
spreads.

Intraosseous Unicystic Ameloblastoma


• It is diagnosed clinically and radiographically as cyst and often treated without biopsy.
• Careful X-ray examination may show solitary cyst.
• Complete enucleation is the key treatment and since it may impact deeply, adjunct
treatment of bone bed is done by chemical fixation with Carnoy’s solution.
• Curettage is discouraged.

Peripheral (Extraosseous)
• Excision biopsy is done with 1.5–2 cm of safety margin excision.
CHAPTER

27 Properties of X-rays

RADIATION
Radiation is mission and propagation of energy through a space or substance in the form
of wave or particles.

X-RADIATION
X-rays can be defined as the weightless bundles of photons (energy) that are without an
electrical charge and travel in waves with a specific frequency at the speed of light.

PROPERTIES OF X-RAYS
1. Appearance:
X-rays are electromagnetic radiation. They are invisible and cannot be detected
by any of the senses.
2. Mass and charge:
X-rays have no mass or weight and no charge.
3. Speed:
X-rays travel at the same speed of light in free space, i.e. 3×108 m/sec (1,86,000
miles/sec) and are not affected by magnetic field.
4. Dualistic behavior:
X-rays show dualistic behavior, i.e. wave and particle. They are electromagnetic waves.
According to quantum theory, X-rays are made up of discrete units of energy called
quantum of photon. Each wave pocket is equivalent to its energy and is called photon.
X-rays are made up of millions of photons of different energy.
5. Propagation:
No medium is required for propagation of X-rays. The electric and magnetic fields
are perpendicular to each other and perpendicular to the path of propagation.
6. Frequency:
Their frequency ranges from 2×1016 sec-1 to 3×1019 sec-1.
7. Wavelength:
X-rays travel in waves and have short wavelength with a high frequency. Wavelength
of X-ray used in diagnostic radiography is 0.1 to 0.5 Angstrom (Å). X-rays with shorter
wavelength have greater penetrating power and are called hard rays. X-rays having
relatively longer wavelength, possessing less energy and less penetrating power are
called Grenz rays.
8. Production:
X-rays belong to gamma rays group in the spectrum and are produced by interaction
of particulate radiation (cathode rays) with matter. So, X-rays are produced by the
conversion of electrical energy into radiation.
Properties of X-rays 235

Wavelength X-ray
1-2 Å Grenz or Super soft X-rays
1-0.5 Å Soft X-rays
0.5-0.1 Å Medium X-rays

Essentials of Dentistry
0.1 Å Hard X-rays
0.001 Å Gamma rays

9. Path of travel:
X-rays travel in straight lines in wave motion and can be deflected or scattered.
10. Diffraction and interference:
When a wave hits an object, the portion of wave that just missed the object spreads
in a circle or sphere, into the space behind the object. The edges of the object allow
the wave to ‘curl round’ behind the object (Figs 27.1A and B).
Close to the object is an area in shadow where no wave exists. Further away the
diffracted waves have spread until the waves from each edge begin to interfere with
each other. Waves are also diffracted by narrow slits (of width less than wavelength).
A wavelet is formed from the initial wave at the obstacle (Figs 27.2 and 27.3).
11. Focusing capability:
X-rays cannot be focused to a point and they always diverge from a point.

B
Fig. 27.1A and B: Diffraction
Essentials of Dentistry 236 Properties of X-rays

Fig. 27.2: Curling of wave

Fig. 27.3: Curling of multiple waves

12. Energy:
X-rays consist of wave pockets and its energy is equivalent to energy of electromagnetic
radiation that originated at the atomic level. The energy level varies from 25 to 125 keV.
Thus, energy of an X-ray depends on its wavelength. Shorter the wavelength, the
more is the energy and higher the penetration power.
13. Attenuation:
X-rays shows selective attenuation. When passing through the matter, the intensity
of radiation is reduced (attenuation) because the radiation energy is taken up by
the material (absorption) and some deflection from the original path, to travel in a
new direction (scattering).
Attenuation depends upon thickness of object, atomic number or density of object, etc.
14. Scattering:
When X-rays strike an object, some are scattered in all directions by atoms of the
object. This secondary radiation is called scattered radiation. X-rays produce different
types of scattered and secondary radiations. It is undesirable both for the operator
(decreases the image quality) and for the patient (increases the radiation dose).
Scattering depends upon the kilovoltage applied, the size and area to be examined,
and the size of X-rays beam.
An X-ray which reflects from the surface of a substance travels less distance than
an X-ray which reflects from a plane of atoms inside the crystal. The penetrating
X-ray travels down to the internal layer, reflects, and travels back over the same distance
before being back at the surface. The distance travelled depends on the separation
Properties of X-rays 237

Essentials of Dentistry
Fig. 27.4: Bragg’s law

of the layers and the angle at which the X-ray entered the material. This is expressed
by Bragg’s Law (Fig. 27.4).
15. Penetrating power (quality):
X-rays can penetrate a structure depending on its energy. More is the energy, more
is the penetrating power. Penetrability also depends on the composition of structure,
which determines whether X-ray beam will penetrate (pass through) or be absorbed.
The quality of X-ray beam is determined by the kilovoltage, milliampere, distance
between target and the object, time or length of exposure, filtration and target material.
X-rays can penetrate and pass through many solids that are opaque to light but cannot
penetrate through heavy metals and bones, and therefore cast a shadow of these
objects on film. This property forms foundation for diagnostic property.

1
I
D2
16. Intensity:
In free space, they obey the inverse square law, which states that for a point source
of radiation, the intensity (I) at any given place varies inversely as the square of the
distance (d) from the source to the place at which intensity are being considered.
17. Ability to produce fluorescence:
X-rays can cause certain substances to emit radiation or fluorescence (immediate
emission of visible light after exposure to radiation). For example, visible light is emitted,
when it is exposed on certain chemicals like phosphorus. Delayed emission of light
after exposure to radiation is called phosphorescence. This property is useful in
diagnostic radiography.
E.g. a) Intensifying screens
b) Fluoroscopy.
18. Effect on film:
They affect photographic film. For example X-rays can produce an image on
photographic film.
19. Ionization capability:
X-rays interacts with materials they penetrate and cause ionization. They are used
in photochemical for ionization of chemicals.
20. Biologic effect:
X-rays cause somatic or genetic changes in living tissue so it requires precautions
in radiography. It produces biological damage in the living tissues. The effect manifests
as either damage or death of cells.
CHAPTER

28 Considerations for Oral


Medicine Viva Voce

Congenital disease
The disease which is present at or before the birth, but it is not necessarily inherited (i.e.
transmitted through genes).
Hereditary conditions
Conditions that are apparent at birth but do not become evident for number of years after
the birth are called hereditary conditions.
Agnathia
Agnathia is a lethal anomaly, characterized by hypoplasiaor absence of the mandible, with
abnormally positioned ears having an autosomal recessive mode of inheritance.
Micrognathia
Micrognathia is an anomaly characterized by a small jaw, and either maxilla or mandible
is affected.
Macrognathia
Macrognathia is a condition of abnormally large jaws.
Hemihyperplasia
Hemihyperplasia is a rare developmental anomaly characterized by asymmetric overgrowth
of one or more body parts.
Fordyce’s disease/granules
Heteropic collections of the sebaceous glands at various sites in the oral cavity (especially
on the cheek mucosa opposite the molar region) are known as Fordyce’s granules.
Cheilitis glandularis
It is an uncommon poorly, understood inflammatory disorder of lip, characterized by
progressive enlargement and eversion of lower labial mucosa that results in obliteration
of mucovermilion interface.
Median rhomboid glossitis
It is the congenital abnormalities of the tongue due to failure of tuberculum impair to retract
before the fusion of the lateral halves of the tongue.
– It is seen as an ovoid, diamond, rhomboid-shaped smooth erythematous patch on
the dorsal surface of the tongue immediately anterior to the circumvallate papillae.
– It has a strong relationship with the localized chronic infection especially Candidiasis.
Benign migratory glossitis
(Geographic tongue, Wandering rash of the tongue, Glossitis areata exfoliativa, Erythematic
migrans).
Considerations for Oral Medicine Viva Voce 239

– Unknown etiology (Emotional stress).


– Multiple areas of the desquamation of the filiform papillae of the tongue in a circinate
pattern are seen.
Dentinogenesis imperfecta:

Essentials of Dentistry
Type Characteristic
Type I Dentinogenesis imperfecta without osteogenesis Obliteration of pulp chamber
imperfecta
Opalescent dentin
Shields type II
Capdepont teeth
Type II Bradywine type Large pulp space (Shell tooth)
Shields type III
Multiple pulp exposure in deciduous teeth

Dentin dysplasia (Rootless teeth)


It is a rare disturbance of dentin formation characterized by normal enamel but atypical
dentin formation with abnormal pulpal morphology.
Type Pulp characteristic
Type I – Radicular dysplasia (Dentin dysplasia) Deciduous – Completely obliterated
Permanent – Crescent-shaped remnant
Type II – Coronal dysplasia (Anomalous dysplasia Deciduous – Obliteration
of dentin)
Permanent – Large pulp chamber,
Thistle tube appearance

Papilloma
It is an exophytic growth made, up of numerous, small finger-like projections, which results
in a lesion with a roughened, verrucous or “cauliflower like” surface.
Nevus
It is a congenital, developmental tumor-like malformation of the skin or mucous membrane.
1. Congenital
2. Acquired
– Intradermal nevus (Common mole)
– Junctional nevus
– Compound nevus
– Spindle cell and/or epitheloid cell nevus
– Blue nevus.
Leukoplakia
It is a white patch/plaque which cannot be characterized clinically/pathologically as any
other condition.
Bowen’s disease
It is a special form of intraepithelial carcinoma occurring particularly in patients who had
an arsenical therapy.
Oral submucous fibrosis
It is an insidious chronic disease affecting any part of the oral cavity and sometimes the
pharynx. Although occasionally preceded by and/or associated with vesicle formation,
240 Considerations for Oral Medicine Viva Voce

it is always associated with a juxtaepithelial inflammatory reaction followed by a fibroelastic


change of the lamina propria, with epithelial atrophy leading to stiffness of the oral mucosa
and causing trismus and inability to eat.
Fibroma
Essentials of Dentistry

It is a benign soft tissue neoplasm of the oral cavity characterized by excessive proliferation
of fibroblast and synthesis of large amount of collagen.
Central giant cell fibroma of bone
It is a central neoplasm of the bone which is well demarcated, expansile, encapsulated
and composed of cellular fibrous tissue containing spherical calcifications and randomly
oriented bony structures.
Peripheral giant cell fibroma of bone
It is the common giant cell lesion which arises from tooth bearing areas of jaw and appears
as a purplish—red nodule.

TNM Classification and Staging


The TNM classification, applicable to squamous cell carcinoma of the oral cavity, is based
entirely on clinical findings and is developed by the American Joint Committee on Cancer
and the UICC in 1978.
T—Tumor size
N—Regional lymph nodes
M—Distance metastasis
Surface dimensions of the primary tumor are included as the most important parameter
for determining primary tumor staging in the oral cavity. The N staging system takes into
account the size and multiplicity as well as the unilateral or bilateral presence of metastatic
nodes as the parameters.
T—Primary tumor
TX Inability to meet the minimum requirements to assess the primary tumor
TO No evidence of primary tumor
Tis Carcinoma in situ (Preinvasive carcinoma)
T1 Tumor 2 cm or less in diameter (<2 cm)
T2 Tumor greater than 2 cm, not greater than 4 cm (>2 cm, <4 cm)
T3 Tumor greater than 4 cm in diameter (>4 cm )
T4 Tumor with extension to bone, muscle, skin, antrum neck, etc.
N—Regional lymph nodes
NX Inability to meet minimum requirements to assess the regional lymph nodes
N0 Clinically palpable lymph nodes, metastasis not suspected
N1 Clinically palpable homolateral cervical lymph nodes, not fixed, metastasis suspected
N2 Clinically palpable contralateral or bilateral lymph nodes, not fixed, metastasis suspected
N2a Metastasis in single ipsilateral lymph node, >3 cm but <6 cm in its greatest dimension.
N2b Metastasis in multiple ipsilateral lymph node, none >6 cm
N2c Metastasis in multiple bilateral or contralateral lymph nodes, none >6 cm in greatest
dimension
N3 Clinically palpable lymph nodes, Fixed, Metastasis suspected, >6 cm
M—Distant metastasis
M0 No distant metastasis
Mx Inability to meet the minimum requirements to assess the presence of distance metastasis.
M1 Clinical and/or radiographic evidence of metastasis other than to cervical lymph nodes.
Considerations for Oral Medicine Viva Voce 241

1. Pretreatment clinical classification (cTNM)


Based on clinical data before treatment
2. Postsurgical histopathological classification (pTNM)
Based on cTNM and surgical findings plus examination of the respected specimen.
The stage groupings for the TNM system classification for oral cancer are:

Essentials of Dentistry
Stage I T1 N 0 M 0
Stage II T2 N 0 M 0
Stage III T3N0M0, T1N1M0
T2N1M0
T3N1M0
Stage IVA T4N 0 M 0
T4N 1 M 0
Any T N2M0
Stage IVB Any T N3M0
Stage IVC Any T Any N M1

New Classification
A newer staging system that includes the exact site (S) in the oral cavity and histopathologic
grading (P). However, little is still known about the possible advantages of this S-TNM-
P classification over the internationally accepted TNM classification.

S-TNM-P Classification
S – Site
T – Tumor dimension
N – Lymph node involvement
M – Distance metastasis
P – Histopathology.

Histopathological Grading (G)

GX Grade of differentiation cannot be assessed


G1 Well-differentiated
G2 Moderately-differentiated
G3 Poorly-differentiated
G4 Undifferentiated

Presence/absence of Residual Tumor


RX Presence of residual tumor cannot be assessed
R0 No residual tumor
R1 Microscopic residual tumor
R2 Macroscopic residual tumor

Reference: Rapidis AD, Langdon JD, Patel MF, et al.Clinical classification and staging in oral cancer.
J Maxillofac Surg 1976,4:219-26.
242 Considerations for Oral Medicine Viva Voce

Rapidis AD, Langdon JD, Patel MF, et al. A new system for the clinicopathological
classification and identification of intraoral carcinomata. Cancer 1977,39:204-09).
Cyst
Cyst is a pathological cavity having fluid, semifluid, and gaseous contents which aren’t
Essentials of Dentistry

created by accumulation of pus frequently and may or may not be lined by epithelium
(Krumer 1974).
Dentigerous cyst
It can be defined as an odontogenic cyst that surrounds the crown of an impacted tooth;
caused by fluid accumulation between the reduced enamel epithelium and the enamel
surface, resulting in a cyst in which the crown is located within the lumen.
Epstein’s pearls
These are cystic, keratin filled nodules along the midpalatine raphe, probably derived from
entrapped epithelial remnants along the line of fusion.
Odontogenic keratocyst
A cyst derived from the remnants of the dental lamina, with a biologic behavior similar
to a benign neoplasm, with a distinctive lining of six to ten cells in thickness, and that
exhibits a basal cell layer of palisaded cells and a surface of corrugated parakeratin.
Dental lamina cyst of newborn
They are multiple, occasionally solitary, superficial raised nodules on edentulous alveolar
ridges of infants that resolve without treatment; derived from rests of the dental lamina
and consisting of keratin-producing epithelial lining.
Gingival cyst of adult
A small developmental odontogenic cyst of the gingival soft tissue derived from the rests
of the dental lamina, containing a lining of embryonic epithelium of cuboidal cells and
distinctive focal thickenings similar to the lateral periodontal cyst.
Lateral periodontal cyst
A slow growing, nonexpansile developmental odontogenic cyst derived from one or more
rests of the dental lamina, containing an embryonic lining of one to three cuboidal cells
and distinctive focal thickenings.
Eruption cyst
It is defined as an odontogenic cyst with the histologic features of a dentigerous cyst that
surrounds a tooth crown that has erupted through bone but not through soft tissue and
is clinically visible as a soft fluctuant mass on the alveolar ridges.
Bohn’s nodules
They are keratin filled cysts scattered over the palate, most numerous along the junction
of hard and soft palate and apparently derived from palatal salivary gland.
Ameloblastoma (Adamantinoma)
It is a true neoplasm of enamel organ type tissue which does not undergo differentiation
to the point of enamel formation.
Robinson defined it as
“Usually unicentric, nonfunctional, intermittent in growth, anatomically benign and clinically
persistent” (Key to memorize - UNIABC).
Considerations for Oral Medicine Viva Voce 243

Attrition
It is the physiologic wearing of tooth surface as a result of tooth-to-tooth contact, as in
mastication.
Abrasion

Essentials of Dentistry
It is the pathologic wearing of tooth surface by some mechanical forces such as hard
bristle toothbrush, coarse tooth powder, etc.
Erosion
Erosion is the loss of tooth structure by means of some chemical action that does not
involve bacterial action.
Papule
Papule is raised solid lesion smaller than 1 mm in diameter.
Plaque
Plaque is raised solid lesions greater than 1mm diameter.
Macule
Macule is well-circumscribed, flat lesions that are noticeable because of change from normal
skin.
Nodules
Nodules are the small tumor-like lesions present deep in dermis.
Vesicle
Vesicle is elevated blister-like lesions containing clear fluid that are less than 1 cm in diameter.
Bulla
Bulla is elevated blister-like lesions containing clear fluid that are over 1 cm in diameter.
Ulcer
Ulcer is a brick or discontinuity in the surface epithelium – skin or mucous membrane,
which appears as a well-circumscribed depressed lesion. Generally, they have fibrotic margin
and a bed of granulation tissue.
Carcinoma
Carcinoma is a malignant tumor of epithelial tissue origin.
Epidermoid carcinoma (Squamous cell carcinoma)
It is defined as, “a malignant epithelial, neoplasm exhibiting squamous differentiation as
characterized by the formation of keratin and/or the presence of intercellular bridges”
(Pindborg JJ, et al. 1977). It is flat, slowly growing, mildly malignant and rapidly infiltrated
tumor of skin.
Sarcoma
It is a rare cancerous tumor arising from connective tissues such as muscle/ bone.
Dysplasia
Abnormal development of tissue is called as dysplasia. It represents the earliest changes
of neoplastic transformation than can be detected at the microscopic level.
Anaplasia
Loss of differentiation and function is called anaplasia. Anaplastic lesions are composed
of cells, which resemble those of the tissue from which they arise.
244 Considerations for Oral Medicine Viva Voce

Parasitic Infections

Protozoa (Unicellular)
Plasmodroma Chilophora
Essentials of Dentistry

Helminths (Multicellular)
Nemathelminthes (roundworms)nematoda Platyhelminthes
Cestoda (tapeworms) Trematoda (flukes)

Dental caries
It is an irreversible, infectious microbial disease of the calcified tissues of the teeth
characterized by demineralization of the inorganic portion and destruction of the organic
substance of the tooth, which often leads to cavitation.
Zone of enamel caries:
Zone 1: Translucent zone lies at advancing front of enamel lesion
Zone 2: Dark zone lies adjacent and superficial to the translucent zone
Zone 3: Body of the lesion is greatest area of demineralization
Zone 4: Surface zone which is relatively unaffected because of greater degree of
mineralization
Zone of advanced dental caries:
Zone 1: Zone of fatty degeneration of tomes fibers.
Zone 2: Zone of dentinal sclerosis characterize by deposition of Ca++ in dentinal tubules
Zone 3: Zone of decalcification of dentin, a narrow zone preceding bacterial invasion
Zone 4: Zone of bacterial invasion in decalcified but intact dentin
Zone 5: Zone of decomposed dentin
Cellulitis
It is a diffuse inflammation of soft tissues which is not circumscribed or confined to one
area, but which, in contradistinction to the abscess, tends to spread through tissue spaces
and along fascial planes.
Ludwig’s angina
By Archer,
It is bilateral, acute, rapidly spreading, septic, inflammatory, indurated, wooden hard
cellulites of floor of mouth.
By thoma,
It is a gangrenous cellulitis of loose alveolar tissue which originates in the submandibular
space and spread rapidly towards the floor of mouth.
By Killey, Seward and Kay,
It is a clinical diagnosis and the name given to the massive brawny cellulitis occurring
bilaterally at the submandibular region which also involves sublingual space.
Bruxism
It is a habitual grinding of the teeth either during sleep or as an unconscious habit during
waking hours.
Biopsy
It is the removal of tissue from the living organism for the purpose of microscopic examination
and diagnosis.
Porphyria
It is inborn error of porphyrin metabolism characterized by over production of uroporphyrin
and related substances.
Considerations for Oral Medicine Viva Voce 245

Juxtaoral organ of Chievitz


Clusters of nests of squamous epithelial cells found microscopically in tissue taken from
approximate site used by dentist for injection of inferior alveolar nerve.

TYPES OF GEOGRAPHIC TONGUE

Essentials of Dentistry
Type I
“Normal” geographic tongue, in which the lesion on the tongue change from time to time,
without lesions of the mucosa elsewhere in the mouth.
Type II
Similar to type I but associated with similar lesions elsewhere in the mouth.
Type III
Lesions on the tongue not so typical as in type I and may or may not be associated with
lesions elsewhere in the oral cavity.
There are two subtypes:
a. Fied form—Only a few areas of the tongue are affected. The lesions come and
go, but always appear in the same place.
b. Abortive form—The lesions start as white-yellow spots, but disappear before taking
the classical appearance of geographic tongue.
Type IV
No lesion on the tongue—Lesions elsewhere in the oral mucosa resemble those of
geographic tongue.
(Reference: Hume WJ, Smith CJ, Franklin DC. Verruciform xanthoma. Br J Oral Surg 1980,
8:157-61).
Disease Etiology
Actinomycosis Actinomycosis israeli
Acute lymphonodular pharyngitis Coxsackie virus A10 group
Candidiasis Candida albicans
Coccidioidomycosis Coccidioides immitis
Diphtheria Cornybacterium diphtheria
Klebs-Loeffler bacillus
Gonorrhea Neisseria gonorrhoeae
Granuloma inguinale Donovania granulomatis
Herpangina Coxsackie virus A group Type 1, 6, 8, 10, 16, 22
Histoplasmosis Histoplasma capsulatum
Hand-foot-mouth disease Coxsackie virus A16 group, A5 and A6, occasionally B2,B5
Leprosy Mycobacterium leprae
Mumps Paramyxovirus
North American blastomycosis Blastomyces dermatitidis
Rhinoscleroma Klebsiella rhinoscleromatis
Scarlet fever -hemolytic streptococci
Syphilis Treponema pallidum
South American blastomycosis Blastomyces brasiliensis
Tularemia Pasteurella tularensis
Tetanus Clostridium tetani
Tuberculosis Acid-fast Mycobacterium tuberculosis
246 Considerations for Oral Medicine Viva Voce

Disease Synonyms
Acute necrotizing ulcerative gingivitis Vincent’s infection
Trench mouth
Essentials of Dentistry

Agranulocytosis Granulocytopenia
Amelogenesis imperfecta Hereditary enamel hypoplasia,
Hereditary opalescent teeth
Ameloblastoma Adamantinoma
Auriculotemporal syndrome Frey’s syndrome
Gustatory sweating
Recurrent aphthous minor Canker sore
Recurrent aphthous major Mikulicz’s aphthae,
Sutton’s disease
Basal cell carcinoma Rodent ulcer
Burkitt’s lymphoma African jaw lymphoma
Bifid rib-Jaw cyst-Basal cell nevus Gorlin-Goltz syndrome,
syndrome Basal cell nevus syndrome
Benign migratory glossitis Geographic tongue,
Wandering rash,
Aveata exfoliativa,
Erythema migrans
Chelitis granulomatosa Miescher’s syndrome
Candidiasis Thrush, Moniliasis
Cylindroma Adenocystic carcinoma
Calcifying odontogenic cyst Gorlin cyst,
Calcifying epithelial odontogenic cyst
Calcifying epithelial odontogenic tumor Pindborg’s tumor
Cementoma Periapical cemental dysplasia
Chronic focal sclerosing osteomyelitis Condensing osteitis
Chronic osteomyelitis with proliferative Chronic focal sclerosing osteomyelitis
periostitis
Cherubism Familial fibrous dysplasia of jaw
Cleidocranial dysplasia Marie and Sainton’s disease
Craniofacial dysostosis Crouzon disease
Cyclic neutropenia Periodic neutropenia
Dental lamina cyst of newborn Epstein’s pearls, Bohn’s nodules,
Gingival cyst of newborn
Developmental lingual salivary gland Stafne’s cyst,
depression Latent bone cyst,
Static bone cavity,
Static bone cyst
Dentinal dysplasia Rootless teeth
Dentinogenesis imperfecta Hereditary opalescent dentin
Dens in dente Dens invaginatus
Contd....
Considerations for Oral Medicine Viva Voce 247

Contd....

Disease Synonyms

Dens evaginatus Occlusal enamel pearl,


Leongs premolar

Essentials of Dentistry
Dentigerous cyst Follicular cyst
Developmental lingual mandibular Static bone cyst,
salivary gland depression Latent bone cyst,
Static bone
Down syndrome Trisomy 21
Encephalotrigeminal angiomatosis Sturge-Weber disease
Epidermoid carcinoma Squamous cell carcinoma
Erythroplakia Erythroplasia of Queyrat
Ewing’s sarcoma “Round cell” sarcoma
Facial hemiatrophy Parry Romberg syndrome
Fibromatosis gingivae Elephantiasis gingivae
Fissured tongue Scrotal tongue
Focal epithelial hyperplasia Heck’s disease
Focal dermal hyperplasia syndrome Goltz-Gorlin syndrome
Generalized cortical hyperostosis van Buchem disease
Herpes simplex Acute herpetic gingivostomatitis, Herpes labialis,
Fever blister, Cold sores
Herpangina Apthous pharyngitis
Hemophilia Bleeder’s disease,
Disease of Kings,
Disease of Haspburgs
Herpes zoster Shingles, Zona
Histoplasmosis Darling’s disease
Hereditary hemorrhagic telangiectasia Rendu-Osler-Weber syndrome
Hereditary intestinal polyposis syndrome Peutz-Jeghers syndrome
Horner’s syndrome Sympathetic ophthalmoplegia
Hypercementosis Cementum hyperplasia
Internal resorption Pink tooth of mummery
Odontoclastoma
Intraepithelial carcinoma Carcinoma in situ
Infantile cortical hyperostosis Caffey’s disease
Infectious mononucleosis Glandular fever
Jaw cyst-Basal cell nevus-Bifid rib Gorlin and Goltz syndrome
syndrome
Jaw-winking syndrome Marcus Gunn phenomenon
Juvenile periodontitis Periodontosis
Kaposi’s sarcoma Angioreticuloendothelioma
Contd....
248 Considerations for Oral Medicine Viva Voce

Contd....
Disease Synonyms
Keratoacanthoma Self-healing carcinoma
Essentials of Dentistry

Keratosis follicularis Darier’s disease


Leprosy Hansen’s disease
Massive osteolysis Vanishing bone disease
Mandibulofacial dysostosis Treacher Collins syndrome
Median anterior maxillary cyst Nasopalatine duct cyst, Incisive canal cyst
Median rhomboid glossitis Central papillary atrophy of tongue
Mumps Endemic perotitis
Measles Rubeola
Mucormycosis Phycomycosis
Multiple myeloma Plasma cell myeloma,
Plasmacytoma
Kahler’s disease
Mikulicz’s disease Benign lymphoepithelial lesion
Nasoalveolar cyst Klesdat’s cyst
Neurolemmoma Schwannoma,
Neurolemmoma
North American Blastomycosis Gilchrist’s disease
Noma Cancrum oris, Gangrenous stomatitis
Osteogenesis imperfecta Brittle bones, Osteopsathyrosis
Osteopetrosis Marble bone disease
Albers-Schonberg disease
Osteitis deformance Paget’s disease
Pernicious anemia Addison’s disease
Pits of lower lip and cleft of lip or palate vander Woude’s syndrome
Periapical granuloma Apical periodontitis
Palatal cyst of neonate Epstein pearls,
Bohn’s nodule
Peripheral cemental dysplasia Cementoma,
Perapical fibrous dysplasia
Peripheral ossifying fibroma Peripheral odontogenic fibroma,
Peripheral cementifying fibroma
Peripheral giant cell granuloma Giant cell epulis,
Reparative granuloma
Pleomorphic adenoma Mixed tumor
Rubella German measles
Recurrent aphthous stomatitis Canker sores
Regional odontodysplasia Ghost teeth,
Odontogenesis imperfecta,
Odontodysplasia
Contd....
Considerations for Oral Medicine Viva Voce 249

Contd....

Disease Synonyms
Radicular cyst Apical periodontal cyst,
Periapical cyst,

Essentials of Dentistry
Dental root end cyst
Sjögren’s syndrome Sicca syndrome
Small pox Variola
Chicken pox Varicella
South American Blastomycosis Lutz’s disease
Syphilis Lues
Sphenopalatine neuralgia Lower-half headache, Horton’s syndrome,
Cluster headache, Periodic migrainous neuralgia,
Atypical facial neuralgia, Vidian nerve neuralgia
Stomatitis nicotina Pipe smoker’s palate
Squamous cell carcinoma Epidermoid carcinoma
Systemic sclerosis Scleroderma
Thalassemia Cooley’s anemia
Mediterranean disease
Tetanus Lock jaw
Traumatic neuroma Amputation neuroma
Traumatic cyst Solitary bone cyst, Hemorrhagic cyst,
Unicameral bone cyst, Simple bone cyst,
Idiopathic bone cavity
Trigeminal neuralgia Tic douloureux, Trifacial neuralgia,
Fothergill’s disease, Six inch syndrome
Uveoperotid fever Heerfordt’s syndrome
von Willebrand’s disease Pseudohemophilia
van Buchem syndrome Generalized cortical hyperostosis
Warthin’s tumor Papillary cyst adenoma lymphomatosum
White sponge nevus Canon’s disease

Cells Histology Seen in

Arbiskov cells Modified monocytes Myeloblastoma


Asteroid bodies – Spirotrichosis
Anitschkow cells Modified epithelial cells with Aphthous ulcer
elongated nuclei containing linear Sickle cell disease
bar of chromatin with radiating Iron deficiency anemia
processes of chromatin extending
towards the nuclear membrane
Angulate body cells – Granular cell myeloblastoma
Corp, ronds, grains – Benign dyskeratotic cells
Civatte/cytoid/hyaline – Lichen planus
/colloid bodies
Contd....
250 Considerations for Oral Medicine Viva Voce

Contd....

Cells Histology Seen in


Döhle bodies – Chédiak-Higashi syndrome
Essentials of Dentistry

Downey cells – Infectious mononucleosis


Foam cells Lipid laden cells Periapical granuloma
Gaucher’s cells Pale cells containing eccentric Gaucher’s disease
nucleus and a wrinkled or
“crumpled silk” cytoplasm
Ghost cells Eosinophilic swollen epithelial cells Compound odontoma
without nucleus Ameloblastic fibroodontoma
Craniopharyngioma
Gorlin cyst
Hyaline cells Modified myoepithelial cells Pleomorphic adenoma
Howell Jolly bodies – Pernicious anemia
Cabot’s ring
Handerson Peterson Eosinophilic intracytoplasmic Molluscum contagiosum
bodies
Molluscum bodies inclusion bodies
Hurler cell/Clear/ Fibroblasts Hurler’s syndrome
Gorgyle cells Mucopolysaccharidoses
Lipschutz bodies Eosinophilic, ovoid, homogenous Primary herpetic stomatitis
material which displace nuclear
chromatin peripherally
Lacunar cells B-lymphocyte (Histologic variant Nodular sclerosis type of Hodgkin’s
of Reed-Sternberg cells) disease
LE cells Rosette of neutrophils surrounding Systemic lupus erythematosus
pale nuclear mass derived from
lymphocyte
Lepra cells Vacuolated macrophages or Lepromatous leprosy
histiocytes
Niemann-Pick cells Lipid laden cells distributed Niemann-Pick disease
throughout reticuloendothelial
system
Negri bodies – Rabies
Pale- dark cells – Odontogenic myxoma
Reed-Sternberg cell Multinucleated cells, derived from Malignant cells of Hodgkin’s Disease
B-lymphocyte or monocyte
machrophage
Racquet cells Modified spindle cells Rhabdomyosarcoma
Ribbon cells
Reily bodies Metachromatic granules in Hurler’s syndrome
lymphocyte
Russel bodies Immature plasma cells unable to Seen in chronic inflammatory
produce antibody disease like periapical granuloma,
multiple myeloma
Contd....
Considerations for Oral Medicine Viva Voce 251

Contd....
Cells Histology Seen in
Rushton bodies – In lining epithelium of odontogenic
cyst

Essentials of Dentistry
Tzanck cells Multinucleated giant cell. Herpes simplex, Varicella (Chicken
Characterized by degenerative pox), Pemphigus vulgaris,
changes which include swelling of Granular cell myoblastoma
nuclei and hyperchromatic
staining.
Clumps of epithelial cells
Target cells, Safety RBC Thalassemia
pin cells
Verocay bodies – Neurilemmoma/Schwannoma

Characteristic Signs Disease


Auspitz’s sign- Dry papule covered by silver scales which Psoriasis
on removal leaves tiny bleeding points
Blue sclera Osteogenesis imperfect
Marfan’s syndrome
Ehlers-Danlos syndrome
Osteopetrosis
Bence Jones protein-Unusual protein which coagulates Multiple myeloma
when urine is heated to 40°C to 60°C and disappear
when urine is boiled.
C-shaped/ Chinese character trabeculae Monostotic fibrous dysplasia
Carpet tack extension of lesion Discoid lupus erythematosus
Café-au-lait spots (Brownish melanin pigmentation) Polyostotic fibrous dysplasia
Neurofibroma,
Peutz-Jegher’s syndrome
Hypothyroidism
Crowe’s sign (Axillary freckling) von Recklinghausen’s
neurofibromatosis
Centrifugal growth pattern of bone (tumor grows by Central ossifying fibroma
expansion equally in all directions resulting in a round Central cementifying fibroma
tumor mass) Central cement-ossifying fibroma
Cotton wool appearance Paget’s disease
Egg cell crackling Ameloblastoma, Osteosarcoma
Hypermobility of joints Ehlers-Danlos syndrome
Marfan’s syndrome
Osteogenesis imperfect
Down syndrome
Herald spot Ptyriasis rosea
Koplik’s spots Measles
Liesegang rings Pindborg tumor

Contd....
252 Considerations for Oral Medicine Viva Voce

Contd....

Characteristic signs Disease


Mouse eaten furrowed ulcer Oral tuberculosis
Essentials of Dentistry

Mosaic pattern of bone Paget’s disease


Jig saw puzzle appearance of bone
Monro’s abscess Psoriasis, Benign migratory glossitis
Nikolsky’s sign-Epithelium readily strips off from Pemphigus,
connective tissue on nonulcerated area on pressure Desquamative gingivitis,
leaving raw sensitive surface which readily bleeds. Haily-haily disease
Epidermolysis bullosa
Palmar plantar keratosis Gorlin-Goltz syndrome
Papillon-Lefèvre syndrome
Follicular keratosis
Pseudoepitheliomatous hyperplasia Granular cell myoblastoma
Pink tooth Internal resorption
Punched out lesion-Crest of interdental papillae ANUG
destroyed forming hallow out area
Target lesion, Iris, Bull’s eye Erythema multiforme

Appearance Disease

Angelic look/Eyes towards heaven Cherubism


Bird-like face Mandibulofacial dysostosis,
Pierre Robin’s syndrome
Bilateral TMJ ankylosis
Buffalo hump, Moon’s face Cushing’s syndrome
Butterfly distribution of lesion Discoid or systemic lupus erythematosus
Bumpy lips Type III MEN syndrome
Cart wheel/Checker board appearance Multiple myeloma
Claw hand Scleroderma, Hurler’s syndrome
Coup-de-sabre appearance Scleroderma
Cobblestone appearance Keratosis follicularis, Pyostomatitis vegetance
Fish face appearance Treacher Collins syndrome
Herculean appearance Congenital myotonia
Hebra nose Rhinoscleroma
Honey comb appearance, Cylindroma
Swiss cheese pattern
Mask-like face Scleroderma, Bell’s palsy
Parrot’s beak Craniofacial dysostosis, Syphilis
Petrified man Generalized myositis ossification
Rubber man Ehlers-Danlos syndrome
Risus sardonicus, Opisthotonus Tetanus
Starry sky appearance Burkitt’s lymphoma
Contd....
Considerations for Oral Medicine Viva Voce 253

Contd....

Appearance Disease
Saw tooth appearance Lichen planus

Essentials of Dentistry
Sarrowful appearance Myasthenia gravis
Sailor’s skin/Farmer’s skin Solar elastosis
Spidery fingers Marfan’s syndrome
Swan neck Dystrophic myotonia

Skin disease Characteristic features


Ectodermal dysplasia - Congenital dysplasia of one or more ectodermal structures
- Hypohydrosis, hypotrichosis, hypodontia
Lichen planus - Whickham’s stria, bilateral symmetrical distribution of lesion
with female predilection
- Saw tooth retepegs, liquefaction degeneration of basal layer
- Colloid/ civatte bodies
- Grinspan’s syndrome
Psoriasis - Auspitz’s sign, painless nonpruritic papules
- No involvement of oral mucosa and Monro’s abscess
Pityriasis rosea - Herald spot
Erythema multiforme - Target iris/Bull’s eye lesion
- Recent history of herpes simplex infection
- Stevens-Johnson syndrome, Toxic epidermal necrolysis
Keratosis follicularis - Corps, ronds and grains
(Darier disease) - Leafing out pattern of parabasal cells
- Cobblestone appearance
- Characteristic nail changes
- Typical suprabasal cleavage
White sponge nevus - Hyperparakeratosis, acanthosis
- Thickened and folded mucosa with soft, spongy texture,
peculiar white opalescent hue
Pemphigus - Nikolsky’s sign, Tzank cells, Suprabasilar spilt
Cicatrial pemphigoid/ - Separation of basement membrane with epithelium from the
Benign mucous underlying connective tissue
membrane pemphigoid - Lesion of skin are rare except on genitalia
Familial benign chronic - Nikolsky’s sign is positive
pemphigus - Dilapidated brick wall defect
(Hailey-hailey disease)
Lupus erythematosus - Butterfly distribution of lesion
- Carpet tack extensions
- LE phenomenon, lupus band test
Systemic sclerosis - Mask-like appearance of the face and claw-like appearance
of hands - CREST syndrome
- Extreme widening of periodontal ligament
Ehlers-Danlos syndrome - Hyperelasticity of skin (rubber man), hyperextensibility of joints,
defective healing
- Cutaneous fragility
254 Considerations for Oral Medicine Viva Voce

Contd....
Bone disease Characteristic features
Osteogenesis imperfecta - Extreme fragility and fractures of bones, blue sclera, brownish or
yellowish discoloration of teeth
Essentials of Dentistry

- Abnormality of phosphorylase enzyme


Infantile cortical hyperostosis - Hyperostosis, tender, deeply placed soft tissue swellings
- Seen mainly in infants
- Mandible and clavicle are more frequently affected
Cleidocranial dysplasia - Brachycephalic skull, abnormalities of clavicle
- Presence of wormian bones, open fontanels
- Sagittal sutures remains sunken
- Hypermobility of shoulder joint due to absence of clavicle
- Multiple unerupted supernumerary teeth
- Absence of cellular cementum
Craniofacial dysostosis Cranial
Early synostosis of sutures, small maxilla, triangular frontal defect
Facial
Hypoplasia of maxilla (Class III malocclusion)
Parrot beak appearance, Hypertelorism
Mandibulofacial dysostosis - Antimongoloid palpebral fissure, Hypoplasia of malar bones and
mandible, facial clefts, malformation of ears
- Fish/bird like face, deficiency of eyelashes
Pierre Robin syndrome - Cleft palate, micrognathia, glossoptosis, bird face
Marfan syndrome - Defective organization of collagen
- Excessive length of tubular bones, long and narrow skull and face
- Cardiovascular complications
- Multiple odontogenic cyst
Down syndrome - Trisomy of 21
- Mongoloid faces, subnormal mentality, large mandible,
macroglossia
- Low caries incidence than in normal people and high incidence
of periodontal disease
Osteopetrosis - Endosteal bone formation along with lack of normal bone
resorption
- Pathologic fracture of bones
- Elevated level of acid phosphatase
- Medullary cavities replaced by bone, thickened cortex
predisposing to osteomyelitis
Achondroplasia - Dwarfism, disturbance of endochondral bone formation
- Brachycephalic skull, bowed legs, limited joint motion
- Premature fusion of bones
- Mandibular prognathism (CL III)
Paget’s disease - Enlargement of skull and jaw bones, predilection for maxilla
- Compression of nerves in their foramina
- Headache, deafness, blindness, bone pain, facial paralysis
- Both osteolytic and osteoblastic lesion
- “Mosaic and jigsaw puzzle” appearance of bone on histological
examination, reversal lines are seen
- “Cotton wool appearance” on radiograph
Contd....
Considerations for Oral Medicine Viva Voce 255

Bone disease Characteristic features


- Isolated lesions are called as “osteoporosis circumscripta”
- Hypercementosis, loss of lamina dura
- Elevated alkaline phosphatase level

Essentials of Dentistry
- Increased susceptibility to development of osteosarcoma
Massive osteolysis - Also called vanishing disease of bone
- Resorption of bone with ultimate total disappearance of bone
Fibrous dysplasia of bone Polyostotic (Jaffe’s type/ Albright syndrome)
- Lesion involving more than one bone
- Albright type is associated with endocranial disturbances,
Café-au-lait spots
Monostotic
- Lesion involving one bone
- Chinese letter shaped trabeculae
- Mottled, ground glass or peau d’orange appearance
Cherubism - Chubby face, angelic look of eyes towards of heaven
appearance
- Premature exfoliation of deciduous teeth in 3 years of age
- Teeth appear as “floating in cystic spaces” on radiograph
- Presence of giant cells in histologic examination

Radiographic appearance Disease


Crew cut Thalassemia, Sickle cell anemia
Hair on end appearance
Crescent-shaped pulp remnants Dentinal dysplasia
Thistle tube pulp chamber
Cherry blossom Sjögren’s syndrome
Driven snow appearance Pindborg tumor
Floating teeth Cherubism
Ghost teeth Regional odontogenic dysplasia
Ground glass appearance Monostotic fibrous dysplasia
Hyperparathyroidism
Heart-shaped radiolucency Median anterior maxillary cyst
Honey comb appearance Ameloblastoma
Pindborg tumor
Odontogenic keratosis
Aneurysmal bone cyst
Central giant cell granuloma
Hypercementosis Paget’s disease
Hyperpituitarism
Match band Incipient caries
Mirror image-shaped vertical bone loss Localized juvenile periodontitis
Moth eaten appearance Chronic osteomyelitis
Orange peel appearance Monostotic fibrous dysplasia
Onion skin appearance Ewing’s sarcoma
Garre’s osteomyelitis
Caffey’s disease
Contd....
256 Considerations for Oral Medicine Viva Voce

Contd....

Radiographic appearance Disease


Periapical radiolucency
Irregular Periapical abscess
Essentials of Dentistry

Regular Periapical granuloma/Periapical cyst


Pear-shaped radiolucency between lateral Globulomaxillary cyst
incisor and canine
Punched out radiolucent area in bone, Multiple myeloma
regular
Punched out radiolucent area in bone, Eosinophilic granuloma
irregular
Soap bubble appearance - Ameloblastoma
- Aneurysmal bone cyst
- Central giant cell granuloma
- Hemangioma
- Odontogenic myxoma
- Odontogenic keratocyst
Sunray appearance Osteosarcoma
Central hemangioma
Ewing’s sarcoma
Shell tooth Dentinogenesis imperfecta
Type III (radicular)
Tennis racket appearance Odontogenic myxoma
Thistle tube appearance of tooth Dentinogenesis imperfecta
Type II (coronal)
Widening of periodontal ligament Osteosarcoma
Scleroderma
Juvenile periodontitis
Obliteration of periodontal ligament space Paget’s disease
Hypercementosis
Ankylosis
Hypofunction of tooth
Onion peel appearance Ewing’s sarcoma
Orange peel appearance Monostotic fibrous dysplasia

SYNDROMES WITH CHARACTERISTIC FEATURES


Albright syndrome:
Polyostotic fibrous dysplasia
Café-au-lait pigmentation
Precocious puberty.
Aldrich’s syndrome:
Thrombocytopenic purpura, eczema, increased susceptibility to infection (immune
deficiency), bloody diarrhea (secondary to thrombocytopenia).
(It is also sometimes called as eczema-thrombocytopenia-immunodeficiency syndrome
in keeping with Aldrich’s original description in 1954).
Considerations for Oral Medicine Viva Voce 257

Ascher’s syndrome (ABN)


A—Acquired double lip
B—Blepharochalasis
(Drooping of the eyelid between eyebrow and the edge of the upper eyelid caused
by relaxation of the supratarsal fold a result of the atrophy and thinning of the skin)

Essentials of Dentistry
N—Nontoxic thyroid enlargement
Apert’s syndrome
Crouzan’s disease with syndactyly
Behçet’s syndrome
Recurrent oral ulcers, recurrent genital ulcers, ocular inflammation.
[Behçet disease (Behçet’s syndrome, Morbus Behçet, Silk Road disease) is a form of
vasculitis that can lead to ulceration and other lesions. It can be interpreted as a chronic
disturbance in the body’s immune system. This system, which normally protects the body
against infections through controlled inflammation, becomes overactive and produces
unpredictable outbreaks of exaggerated inflammation. This extra inflammation affects blood
vessels, usually the small ones. As a result, symptoms occur wherever there is a patch
of inflammation, and can be anywhere where there is a blood supply].
Beckwith’s hypoglycemic syndrome
Macroglossia
Neonatal hypoglycemia
Mild microcephaly
Umbilical hernia
Fetal visceromegaly
Postnatal somatic gigantism.
B-K mole syndrome
Large pigmented nevi and high risk of development of melanoma.
Bowen’s disease
Special form of intraepithelial carcinoma occurring on skin particularly in patients who
have had arsenic therapy.
(It is also known as “Familial atypical multiple mole–melanoma (FAMMM) syndrome”,
“Familial melanoma syndrome,” and “ Dysplastic nevus syndrome”. It is a cutaneous
condition described in certain families, and characterized by unusual nevi and multiple
inherited melanomas).
Chédiak-Higashi Syndrome
Malignant lymphoma, albinism, nystagmus, recurrent infections, gingivitis, glossitis.
Costen’s syndrome
Tinnitus, otalgia, headache, dizziness, burning tongue and throat.
Cowden syndrome (Multiple hamartoma and neoplasia syndrome)
Facial trichilemmoms associated with GI tract, thyroid, CNS and musculoskeletal
abnormalities, oral papillomatous lesion.
(It is a disease with impaired bacteriolysis due to failure of phagolysosome formation.
As a result of disordered intracellular trafficking there is impaired lysosome degranulation
with phagosomes, so phagocytosed bacteria are not destroyed by the lysosome’s enzymes.
In addition, secretion of lytic secretory granules by cytotoxic T cells is also affected. The
258 Considerations for Oral Medicine Viva Voce

disease is characterized by large lysosome vesicles in phagocytes (neutrophils), which


thus have poor bactericidal function, leading to susceptibility to infections, abnormalities
in nuclear structure of leukocytes, anemia, and hepatomegaly).
CREST syndrome
Essentials of Dentistry

Calcinosis cutis
Raynaud’s phenomenon
Esophageal dysfunction
Sclerodactyly
Telangiectasia.
(The limited cutaneous form of systemic sclerosis scleroderma is often referred to as
CREST syndrome).
Crouzon’s syndrome (craniofacial dysostosis—early fusion of cranial sutures):
Prognathic mandible, hypoplastic maxilla, high-arched palate, parrot beak appearance,
hypertelorism.
(Crouzon syndrome is a genetic disorder known as a branchial arch syndrome.
Specifically, this syndrome affects the first branchial (or pharyngeal) arch, which is the
precursor of the maxilla and mandible. Since the branchial arches are important
developmental features in a growing embryo, disturbances in their development create
lasting and widespread effects).
Down’s syndrome (Trisomy 21, Mongolism, Trisomy G)
Hypermobility, macroglossia, flat face, large anterior fontanelle, sexual underdevelopment,
cardiac abnormalities.
Eagle’s syndrome
Elongation of styloid process (more than 30mm) or ossification of stylohyoid ligament
leading to sore throat, otalgia and glossodynia.
[Two forms of eagle syndrome exist: The classic form and the vascular one.
Patients with the classic “Eagle syndrome” can present with unilateral sore throat,
dysphagia, tinnitus, unilateral facial and neck pain, and otalgia.
In patients with the vascular form of “Eagle syndrome”, the elongated styloid process
is in contact with the extracranial internal carotid artery. This can cause a compression
(while turning the head) or a dissection of the carotid artery causing a transient ischemic
accident or a stroke].
Ehlers-Danlos syndrome (Rubber man)
Hyperelasticity of skin (rubber man), hyperextensibility of joints, defective healing, cutaneous
fragility.
[The syndrome is named after two doctors, Edvard Ehlers of Denmark, and Henri-
Alexandre Danlos of France, who identified it at the turn of the 20th century. It is a group
of inherited connective tissue disorders, caused by a defect in the synthesis of collagen
(a protein in connective tissue). The collagen in connective tissue helps tissues to resist
deformation (decreases its elasticity). In the skin, muscles, ligaments, blood vessels, and
visceral organs collagen plays a very significant role and with increased elasticity, secondary
to abnormal collagen, pathology results].
Fanconi syndrome
Aplastic anemia, microcephaly, hypogenitalism, olive brown pigmentation.
Frey’s syndrome (Auriculotemporal syndrome)
Gustatory sweating.
Considerations for Oral Medicine Viva Voce 259

Floppy infant syndrome


Generalized weakness due to hypotonia, inability to sit, stand, and walk.
(The term “floppy infant syndrome” is used to describe abnormal limpness when an
infant is prone. Floppy babies are hypotonic infants who are unable to maintain flexed
ligaments, and are able to extend them beyond normal lengths).

Essentials of Dentistry
Grinspan’s syndrome
Lichen planus
Hypertension
Diabetes mellitus
(Lichen planus with two most common diseases).
Gardener’s syndrome
Multiple unerupted supernumerary teeth
Multiple polyposis of large intestine
Osteomas of the bones
Multiple epidermoid or sebaceous cysts
Desmoid tumors.
Goltz-Gorlin syndrome (Focal dermal hypoplasia)
Multiple papillomas, atrophy of skin, polydactyly, sunken eye, sparse hair.
Hutchinson’s triad
Interstitial keratitis, 8th nerve deafness, mulberry molars
Horner’s syndrome
Ptosis, anhydrosis, myosis, enophthalmos, loss of ciliospinal reflex (Mnemonic to memorise
is PAMELa).
Horton’s syndrome (Sphenopalatine Neuralgia)
It is characterized by unilateral paroxysms of intense pain in the region of the eyes, the
maxilla, the ear, and the mastoid, base of the nose, and beneath the zygoma.
Jaw cyst—Basal cell nevus—Bifid rib syndrome (Basal cell nevus syndrome, Gorlin
and Goltz syndrome)
Cutaneous anomalies Basal cell carcinoma, other benign dermal cysts and tumors, palmar
pitting, palmar and plantar keratosis, dermal calcinosis
Dental and osseous Odontogenic keratocysts, mild mandibular prognathism, rib anomalies
anomalies (bifid), vertebral anomalies, brachymetacarpalism
Ophthalmologic Hypertelorism with wide nasal bridge, dystopia canthorum, congenital
anomalies blindness, internal strabismus
Neurological anomalies Mental retardation, dural calcification, agenesis of corpus callosum,
congenital hydrocephalus, medulloblastoma
Sexual abnormalities Hypogonadism in males, ovarian tumors

Jaw-Winking syndrome
Ptosis, rapid elevation of ptotic eyelid on movement of mandible to contralateral side.
Marfan syndrome
Long thin extremities, hyperextensibility of joints, spidery fingers, arachnodactyly, bifid uvula,
CVS complication.
Myofacial pain dysfunction syndrome (MPDS)
Masticatory muscle tenderness, pain, limitation of motion, clicking noise.
260 Considerations for Oral Medicine Viva Voce

Multiple endocrine neoplasm syndrome


MEN I (PPPACU) MEN II (PAMT) Sipple’s syndrome MEN III (NAMTO)
• Hyperplasia of pituitary, • Also called Sipple’s syndrome • Mucocutaneous
Essentials of Dentistry

parathyroid, pancreatic • Parathyroid hyperplasia neuromas,


islets and adrenal cortex Pheochromocytoma of adrenal Pheochromocytomas of
medulla adrenal medulla
• Peptic ulcer and gastric • Medullary carcinoma of the thyroid • Medullary carcinoma of
hypersecretion (Placed black strike through to the thyroid
differentiate from MEN I) Marfanoid habitus

Median cleft-face syndrome


Median cleft of premaxilla and palate (Cleft)
Hypertelorism, Cranium bifidum occultum (Face)
Melkerson-Rosenthal syndrome
Cheilitis granulomatosa
Scrotal tongue
Facial paralysis
(Mnemonic to memorise is CSF).
Möbius syndrome
Partial or complete facial paralysis, drooling of saliva, congenital facial diplegia, difficulty
in mastication.
[Möbius syndrome (also spelled Moebius) is an extremely rare congenital neurological, disorder
which is characterized by facial paralysis and the inability to move the eyes from side-to-side.
Most people with Möbius syndrome are born with complete facial paralysis and cannot close
their eyes or form facial expressions. Limb and chest wall abnormalities sometimes occur with
the syndrome. Most people with Möbius syndrome have normal intelligence, although their lack
of facial expression is sometimes incorrectly taken to be due to dullness or unfriendliness. It
is named for Paul Julius Möbius, a neurologist who first described the syndrome in 1888].
Orofacial digital syndrome
Cleft of tongue and mandibular alveolar process.
Papillon-Lefèvre syndrome
Juvenile periodontitis, palmar plantar keratosis, calcification of Falx cerebri.
Pierre Robin syndrome
Cleft palate, micrognathia, glossoptosis.
[At some time during the stage of the formation of the bones of the fetus, the tip of the
jaw (mandible) becomes ‘stuck’ in the point where each of the collar bones (clavicle) meet
(the sternum), effectively preventing the jaw bones from growing. When the fetus begins to
move, the movement of the head causes the jaw to “pop out’ of the collar bones. From this
time on, the jaw of the fetus grows as it would normally, with the result that, when born, the
jaw of the baby is much smaller (micrognathia) than it would have been with normal development,
although it does continue to grow at a normal rate until the child reaches maturity].
Peutz-Jeghers syndrome
Familial generalized intestinal polyposis (hamartomatous).
Pigmented spots on the face, oral cavity, hand and feet (mucocutaneous melanotic macules)
Plummer-Vinson syndrome
Triad of Iron deficiency anemia, carcinoma of hypopharynx (post cricoids carcinoma),
koilonychia.
Considerations for Oral Medicine Viva Voce 261

Ramsay Hunt Syndrome


Herpes zoster infection of the geniculate ganglion.
[Ramsay Hunt syndrome type 2 also known as herpes zoster oticus is a disorder that
is caused by the reactivation of pre existing herpes zoster virus in a nerve cell bundle in the
head (the geniculate ganglion). The neurons in this ganglion are responsible for the movements

Essentials of Dentistry
of facial muscles, the touch sensation of a part of ear and ear canal, the taste function of
the frontal two-thirds of the tongue, and the moisturization of the eyes and the mouth. The
syndrome specifically refers to the combination of this entity with weakness of the muscles
activated by the facial nerve. In isolation, the latter entity would be called Bell’s palsy].
Reiter’s Syndrome
Urethritis, arthritis, conjunctivitis, mucocutaneous lesion.
Reader’s Syndrome (Paratrigeminal syndrome)
Severe headache, sign of ocular sympathetic paralysis.
Rubinstein-Taybi syndrome
Talon cusp, developmental retardation, broad thumbs and great toes, delayed/incomplete
descend of testis in males, stature, head circumference and bone age below 50th percent.
[The CREBBP gene makes a protein that helps control the activity of many other genes.
The protein, called CREB binding protein, plays an important role in regulating cell growth
and division and is essential for normal fetal development. If one copy of the CREBBP
gene is deleted or mutated, cells make only half of the normal amount of CREB binding
protein. A reduction in the amount of this protein disrupts normal development before
and after birth, leading to the signs and symptoms of Rubinstein-Taybi syndrome. It is
also known as Broad Thumb-Hallux syndrome].
Stevens-Johnson syndrome
Severe bullous form of erythema multiforme involving skin, eyes, oral cavity, genitalia.
[Stevens-Johnson syndrome (SJS) is a form of erythema multiforme which is a life-
threatening condition affecting the skin in which cell death causes the epidermis to separate
from the dermis. The syndrome is thought to be a hypersensitivity complex affecting the
skin and the mucous membranes. Although the majority of cases are idiopathic, the main
class of known causes is medications, followed by infections and (rarely) cancers].
Sjögren’s syndrome
Rheumatoid arthritis, Keratoconjunctivitis sicca, Xerostomia.
(The hallmark symptoms of the disorder are dry mouth and dry eyes)
Treacher Collins syndrome (Mandibulofacial dysostosis)
Hypoplasia of mandible and malar bone, macrostomia, malformation of external ear, high
arched palate, bird/fish like face and antimongoloid slant with coloboma of lower eyelids.
Trotter’s syndrome
Tumors of nasopharynx producing pain similar to trigeminal neuralgia.
Wallenberg’s syndrome
Sensational loss on opposite side of the body due to vascular occlusion of posterior
cerebellar artery affecting V, IX and X cranial nerves.
Waterhouse-Friderichsen syndrome
Bilateral adrenal hemorrhage, purpura, death due to septicemia caused by meningostrepto-
pneumococci.
[Waterhouse-Friderichsen syndrome (WFS) or hemorrhagic adrenalitis is a disease of
the adrenal glands most commonly caused by the bacterium Neisseria meningitidis. The
Essentials of Dentistry

Film
Projection Head position Projection of central ray Exposure Important features
placement
PA view of Vertical Centered in front of the Posterior to anterior 70 kVp • Used to examine skull for
skull cassette with the canthomeatal direction perpendicular to 30-50 mAs disease, trauma and sinus·
line parallel to the floor. the plane of film • PA view with 10° tilt is called
Canthomeatal line is 10° “Caldwell projection”·
above the horizontal • Good for visualization of facial
plane and Frankfort plane is structures
perpendicular to the same • Best for viewing coronoid
process
Lateral skull or Vertical The left side of the face Is directed towards the 70 kVp • Cephalometric view shows soft
cephalometric should be positioned near the external auditory meatus 15-25 mAs tissue profile.
262 Considerations for Oral Medicine Viva Voce

view cassette and the midsagittal perpendicularly to the plane • Used to assess facial structures
plane should be parallel with the film and mid sagittal and skull for disease and
rapidly developing adrenocortical insufficiency].

the plane of the film plane trauma and facial growth.


• Right-sided structures are
more clearly visible.
Water’s Vertical The sagittal plane of head Central rays passes through 70 kVp • Best for viewing zygoma
projection should be perpendicular to the maxillary sinus 100 mAs fractures, paranasal sinus
(Occipito- the plane of film. Chin is (esp. maxillary) and nasal
mental raised such that canthomeatal cavity·
projection) line is 37° above horizontal • It’s variation of PA view.
plane
Reverse- Vertical Canthomeatal line is 25-30° Central rays is directed 70 kVp • Best for diagnosing condylar
Towne’s downwards towards the occipital bone 100 mAs neck fractures (esp. medially
projection displaced)
• Reveals Posterolateral wall of
the maxillary antrum.
characterized by overwhelming bacterial infection meningococcemia, low blood pressure
and shock, disseminated intravascular coagulation (DIC) with widespread purpura, and
infection leads to massive hemorrhage into one or (usually) both adrenal glands. It is

Contd....
Contd....

Film
Projection Head position Projection of central ray Exposure Important features
placement

Submento- Vertical Patient’s head and neck Central rays is directed from 70 kVp • Contraindicated in patient of
vertex should be extended below the mandible towards 100 mAs cervical spondilities
backwards such that the the vertex of skull • Best for viewing fracture of
vertex of the skull is on the base of skull and zygomatic
center of the cassette arch
• Frankfort plane is vertically
oriented and parallel to
film.
• For viewing zygomatic
arch exposure time is
reduced to 1/3 rd than that
used for visualization of
skull.

Projection Film placement Head position Projection of central ray Exposure Important features
Lateral oblique Placed against patient’s Directed towards 1st molar 65 kVp • Best for viewing inferior
mandibular cheek over the 1st molar. region, 2 cm below the 10 mAs border of mandible·
body Parallel to lower border angle of mandible
projection of mandible. • Shows premolar and molar
2cm below the lower Tilted towards the region.
border of mandible. side being
examined
Lateral oblique Placed over the ramus far . Directed posteriorly 65 kVp • Used often for examining 3rd
Mandible is
mandibular posteriorly to include protruded. towards the ramus, 2cm 10 mAs molar region of maxilla and
ramus condyle. Parallel to lower below the inferior border mandible.
projection border of mandible. 2cm • Gives view of the ramus
Considerations for Oral Medicine Viva Voce

below the lower border of from the angle to condyle.


mandible.
263

Essentials of Dentistry
264 Considerations for Oral Medicine Viva Voce

Radiographic projection Synonyms


Occipitomental projection Water’s view
Submentovertex projection Base view, Full axial view, Jug handle view
Essentials of Dentistry

Transpharyngeal projection PARMA view, Infracranial projection, Mcqueen projection


Transorbital projection Transmaxillary view, Zimmer projection

Structure Best radiographic projection


Fracture of zygomatic arch Submentovertex (Jug handle view, 1/3rd exposure)
Base of skull Submentovertex
Maxillary sinus Water’s view
Nasal septum
Fractures of zygoma
Condylar neck fracture Reverse-Towne’s view
Medially displaced condylar fracture PA view
Coronoid process of mandible PA view of skull
Midmandibular ramus to condylar apex Transpharyngeal view
Bony ankylosis of TMJ CT scan
Fibrous ankylosis of TMJ MRI
Internal derangement of disk
Disk perforation Arthrography
CHAPTER

29 Orbital Blow Out Fracture

Orbital fractures are often associated with ocular injuries and midfacial fractures. Fractures
involving solely the floor of orbit are termed as blow out fractures and represent the third
most common isolated midfacial fracture. In 1957, Smith and Regan coined the term “blow
out fracture”.

DEFINITION
“It is a depressed fracture of orbital floor with herniation and incarceration of periorbital
soft tissues in maxillary sinus”.

ETIOLOGY
1. The most widely accepted theory concerning the cause of blow out fracture is that
the globe is struck by an object of greater transverse diameter than itself. The kinetic
energy with which the object strikes the globe is suddenly converted into hydraulic
energy by fluid-filled globe. This is then transmitted uniformly to the orbital walls.
Direct trauma to the orbit with a larger object like fist/cricket ball.

Increased hydraulic pressure within the orbit

Compression of orbital content and
Fracture of orbital floor due to its upwards inclination and thinness (Fig. 29.1)
2. Many times a direct blow to the inferior orbital rim leads to buckling of the floor.

TYPES (FLOW CHART 29.1)


In 1960 Converse and Smith introduced the concept of “pure” (isolated floor) “impure”
(floor and rim) blow out fractures.
Pure fractures are thought to be caused by a sudden instantaneous increase in
intraorbital pressures from direct blunt trauma to the globe itself. Impure fractures are caused
by direct trauma and compression of the bony rim and collapse of the surrounding facial
bones, and result in the disruption of internal orbital walls (Fig. 29.2).

SITES
Blow out fracture involving the floor of orbit most commonly occurs in the posterior area
of the floor medial to the infraorbital fissure, the thinnest portion of the orbit.
Note: Along with floor the weak medial wall also fractures (20 to 50% cases).
Essentials of Dentistry 266 Orbital Blow Out Fracture

Fig. 29.1: Fracture of orbital floor

Flow chart 29.1: Types of orbital floor fracture

Fig. 29.2: Facial features and fracture line


Orbital Blow Out Fracture 267

CLINICAL SIGNS
• Signs and symptoms are masked by edema and ecchymosis during the immediate
posttraumatic phase.
• They become clinically evident after increase in orbital volume of 1.5-2.0 ml or when

Essentials of Dentistry
diplopia occurs.
1. Circumorbital and subconjunctival ecchymosis: It may be associated with surgical
emphysema due to leakage of air from the paranasal air sinuses.
2. Limitation of eye movement in upward gaze due to tethering of inferior muscles.
3. Enophthalmos: It occurs because of the enlargement of the orbital volume leading
to herniation of orbital contents (fat) through floor of orbit.
4. Pseudoptosis and deepening of the supratarsal fold accompany the enophthalmos.
If the eyelid covers the pupil, the patient will attempt to elevate both eyelids, and
lid retraction will be seen on the opposite side.
5. Double vision (Diplopia): It may be due to restricted ocular motility from proplapse
of the periorbital contents into the underlying maxillary sinus. Such diplopia may
also be due to entrapment or direct impingement on the fine suspensory ligamentous
system of the orbit or, less frequently, of the extraocular muscles. It is commonly
due to interference in acting of inferior oblique and inferior rectus muscles.
It usually takes 7 to 10 days for the initial edema or bleeding, or both, to disappear
and resorb. It is therefore difficult to ascertain during that period whether the diplopia
noted is of a transitory nature.
6. Infraorbital paresthesia due to damage to infraorbital nerve.

DIAGNOSIS
It is difficult to make a clinical diagnosis of an isolated blowout fracture. On occasion,
these fractures are not recognized until the diplopia is noted. Early on, visual inspection
is often of limited value because edema may mask any enophthalmos and also makes
palpation difficult.
Diagnosis is mainly by:
a. Force duction test
b. Radiographic examination.
a. Force-duction test:
The eye should be anesthetized topically and the test is performed.
Grasp the tendon of inferior rectus muscle with a small
tissue holding forcep (Adson’s forcep)

Patient is asked for the entire range of movement

Inability to rotate the globe superiorly
signifies entrapment of muscles in floor.
b. Radiographic examination:
• Waters view
It allows visualization of the orbital roof and floor so it is particularly useful for evaluation
of the orbital floor blowout fractures (Fig. 29.3). With this view, the petrous portion
of the temporal bones is projected below the maxillary sinuses and indirect signs
of fracture can be noted such as “teardrop formation” or air-fluid levels. It shows
“hanging drop sign” due to proposal of orbital fat into maxillary sinus (Fig. 29.4).
Essentials of Dentistry 268 Orbital Blow Out Fracture

Fig. 29.3: Blow out fracture on left side

Fig. 29.4: Fracture of orbital floor

• Caldwell-Luc view
• CT scan
Sagittal CT scans are the most accurate diagnostic aid. It shows “Trapdoor
deformity” with mechanical impingement of orbital structures indicating blow
out fracture.

MANAGEMENT
Surgical exploration and reconstruction of orbital floor.

Indications for Surgery


The goals of acute or primary reconstruction of primary orbital fractures are to alleviate
any functional deficit and to restore the facial esthetics by restoring the configuration of
the orbital walls, return prolapsed orbital contents to the orbit proper, and eliminate any
impingement or entrapment of orbital soft tissues.
Orbital Blow Out Fracture 269

Essentials of Dentistry
Fig. 29.5: Surgical repair

Indication Aim of treatment


Diplopia not resolving during first 10 days Restoration of ocular motility
after injury
Herniation of soft tissue into antrum Repair of floor and correction of enophthalmos
Incarceration of tissue which causes retraction Reconstruction, prevention of fibrosis
of globe in upward direction
Enophthalmos > 3 mm Restoration of the orbital volume

Decision of surgery is taken only after 7-10 days while edema subsides. Volume changes
account for abnormal globe positioning. The goal of reconstruction (Fig. 29.6) is to restore
the anatomic position of the bony rim and associated facial bones and to reapproximate
the normal bony volume with reconstructive materials (Fig. 29.7).
270 Orbital Blow Out Fracture

Incisions (Flow chart 29.2)


There are three basic incisions used for accessing the orbital floor (Fig. 29.5):
1. Transconjunctival with/without lateral canthotomy
2. Subciliary
Essentials of Dentistry

3. Infraorbital.
Subciliary and transconjunctival incisions are the most popular due to superior esthetics
and generous access.

Fig. 29.6: Surgical reconstruction


Orbital Blow Out Fracture 271

Flow Shart 29.2: Steps of incisions and grafting

Essentials of Dentistry
Fig. 29.7: Before and after treatment

Materials
Numerous materials have been described for the reconstruction, such as porous
polyethylene, bioresorbable polydioxanone, nylon, marlex mesh, gelatin film, titanium mesh,
and autogenous bone grafts (Fig. 29.8). Each has its own pros and cons related to strength,
application, reactivity, infection rate, biointegration, and complication rate.
Many surgeons prefer autogenous graft as allograft has risk of extrusion and becoming
encapsulated in cyst like swelling. However, porous polyethylene sheet is extremely
biocompatible and nonresorptive with sufficient tensile strength and flexibility.
Autogenous grafts are perhaps most favored for significant floor defects. They are highly
biocompatible but require second surgical procedure. The donor sites that are usually
harvested have been the inner aspect of anterior and posterior iliac crest or unicortical
or bicortical calvarial bone.
Essentials of Dentistry 272 Orbital Blow Out Fracture

Fig. 29.8: Reconstruction of orbital floor

Titanium mesh or orbital floor plates with screw fixation and autogenous graft are quite
useful in severe or comminuted injuries. Graft can be stabilized by simple wiring/by using
microplates if required.
(Note: Lesser wing of sphenoid surrounds the optic foramen and protects optic nerve
from injury so there is no blindness in maxillofacial trauma).
CHAPTER

30 Considerations for Oral


Surgery Viva Voce

LEUKOPLAKIA (WHO—1975)
Leukoplakia is any white patch or plaque that cannot be characterized clinically or
pathologically as any other disease.

ORAL SUBMUCOUS FIBROSIS (OSMF)


It is an insidious chronic disease affecting any part of oral; cavity and sometimes pharynx
although occasionally preceded by and/or associated with vesicle formation, it is always
associated with juxtaepithelium inflammatory reaction followed by fibroelastic change of
lamina propria/with epithelial atrophy leading to stiffness of oral mucosa and causing trismus
and inability to eat.

SIALOSIS
Sialosis is noninflammatory, nonneoplastic enlargement of salivary gland.

SIALADENITIS AND SIALODOCHITIS


Inflammation of salivary gland arising from various infectious and noninfectious causes
is called sialadenitis and inflammation of salivary duct is called as sialodochitis.

SIALADENOSIS
Sialadenosis is an unusual noninflammatory, nonneoplastic disorder characterized by
salivary gland enlargement, particularly involving parotid gland.

XEROSTOMIA
Xerostomia refers to a subjective sensation of a dry mouth; it is frequently, but not always,
associated with salivary gland hypofunction.

SIALOLITHIASIS
Calculi or stone within ductal system of major and minor salivary gland is known as
sialolithiasis.

SIALECTASIS
Sialectasis is atrophy of part or total salivary gland.

SIALORRHEA/PTYLISM
Sialorrhea is excessive secretion of saliva greater than 4 ml/min.
274 Considerations for Oral Surgery Viva Voce

TRIGEMINAL NEURALGIA
It is a sensory disturbance of 5th cranial nerve characterized by sudden, spontaneous,
sharp, shooting, lancinating, paroxysmal, intense pain that is usually confined to the specific
branches of trigeminal nerve.
Essentials of Dentistry

PAIN
Pain is an unpleasant emotional experience usually initiated by noxious stimuli and
transmitted over a specialized neural network to the central nervous system where it is
interpreted as such.

LOCAL ANESTHESIA
Loss of sensation in circumscribed area of body caused by depletion of excitation in nerve
ending or by inhibition of conduction process in peripheral nerve without inducing loss
of consciousness is known as local anesthesia.

LUDWIG’S ANGINA
Given by Archer,
It is bilateral, acute, rapidly spreading, septic, inflammatory, indurate, wooden hard
cellulites of floor of mouth.
By Thoma,
It is a gangrenous cellulites of loose alveolar tissue which originates in the submandibular
space and spread rapidly towards the floor of mouth.
By Killey, Seward and Kay,
It is a clinical diagnosis and the name given to the massive brawny cellulites occurring
bilaterally at the submandibular region which also involves sublingual space.

BELL’S PALSY
It is an idiopathic lower motor neuron facial paralysis of sudden onset and unrelated to
disease elsewhere in the body.

OSTEOMYELITIS
Osteomyelitis is inflammation of medullary portion of bone marrow/cancellous bone.
It is defined as an inflammatory condition of bone that begins as an infectian of medullary
cavity and haversian system of the cortex and extends to involve the periosteum of the
affected area.

CYST
Cyst is a pathological cavity having fluid, semifluid, and gaseous contents which are not
created by accumulation of pus frequently and may or may not be lined by epithelium
(Krumer 1974).

MARSUPIALIZATION
It refers to the procedure of creating a surgical window in the wall of the cyst and evacuation
of the cystic content. This process decrease the intracystic pressure promotes the shrinkage
of the cyst and bone fill.
Considerations for Oral Surgery Viva Voce 275

NEURALGIA
It is an intense paroxysmal pain that is confined to the specific branches of the nerves
of the head and neck.

Essentials of Dentistry
TUMORS/NEOPLASM
New growth of abnormal tissues of the body is known as tumors.

SOME CONSIDERATIONS FOR VIVA VOCE


• Spellings of all ester type of local anesthetics have only one “i”, e.g. tetracaine, cocaine,
while that of all amide type of local anesthetics have two “i”, e.g. lidocaine, bupivacaine.
• Heart rate is 72 and respiratory rate is 16 per minute, so ratio of chest compression
and mouth breathing is 4:1 in CPR.
• Antibiotics should be given preoperatively as the incised wound is most susceptible
to infection during first six hours. It takes six hours to activate immunity after placing
incision, so preoperative antibiotics protects wound during this period and prevent
bacteremia.
• Odontotomy – Tooth division or tooth splitting
Odontectomy – Transalveolar extraction.

Principle Mechanical advantage


Wheel and axle 4.6
Wedge principle 2.5
Lever principle 3

Some Numerical about Local Anesthesia


1. Two percent lignocaine means – 2 gm (2000 mg) in 100 ml, i.e. 1 ml contains 20 mg
of lignocaine. Same way, 3 percent means, 1 ml contains 30 mg of lignocaine.
2. Increasing concentration of local anesthetic solution from 2 to 5 percent causes rapid
onset of action due to availability of more amount of nonionic local anesthetic molecules
(RN). But the duration of binding to receptor is not dependent on concentration. So
duration is not affected.
3. 1:2,00,000 adrenalin means – 1 g (1000 mg) of adrenalin in 2, 00,000 ml of local anesthetic
solution. So 1 ml of local anesthetic solution contains 0.005 mg of adrenalin. For example,
1:1000 adrenalin means 1 ml solution contains 0.005 mg of adrenalin.
4. How many cartridge of 2 percent xylocaine without adrenalin can be given safely to
the patient? Safe dose of local anesthetic without adrenalin – 300 mg
In 2 percent xylocaine, 1 ml solution contains 20 mg of lignocaine. So 300/20 = 15
ml or 7 cartridge. (1 cartridge contains 2 ml approximately).
5. How many cartridges of local anesthetic with 1:2,00,000 adrenalin can be given to a
normal healthy patient?
1:2,00,000 means 1 ml contains 0.005 mg of adrenalin.
Safe dose of adrenalin in healthy patients is 0.2 mg so 0.2/0.005= 40 ml or 20 cartridges
(Approximately)
6. How many cartridges of local anesthetic with 1:1,00,000 adrenalin can be given for
a cardiac patient?
1:1,00,000 means 1 ml solution contains 0.001 mg of adrenalin.
Safe dose of adrenalin on cardiac patient = 0.004 mg. So 0.04/0.01 = 4 ml or 2 cartridges.
276 Considerations for Oral Surgery Viva Voce

A fibers Myelinated and conduct fast


pain

C fibers Unmyelinated and conduct


slow pain. They are very
Essentials of Dentistry

sensitive to local anesthesia.


Natural local anesthetic agent Cocaine
Local anesthetic with intrinsic vasoconstriction property Cocaine
Local anesthetic with most potent vasodilating property Procaine
Local anesthetic with least vasodilating propertyLocal anesthetic
for patients in whom vasoconstrictors are not recommended Mepivacaine
Safest local anesthetic for children (Due to short duration and
less toxicity), Local anesthetic with shortest duration of action 2-chloroprocaine
Most toxic of all local anesthetics Propoxycaine
Local anesthetic which causes methemoglobinemia Prilocaine, Articaine
EMLA (Eutectic mixture of local anesthesia) Lidocaine + Prilocaine
Local anesthetic with high pKa value Procaine

• The receptors for pain are free nerve endings. The loss of sensation after the
administration of local anesthetic is in the order of pain, temperature, touch and
proprioception. The return of sensation is in the reverse of preceding order.
• Mepivacaine has least vasodilating effect. 3 percent mepivacaine without vasoconstrictor
is ideal when vasoconstrictor is contraindicated as in hyperthyroidism.
• Mepivacaine is the most commonly used local anesthetics in pediatric dentistry.
• Methylparaben is most commonly used preservative in local anesthetic solution. It has
bacteriostatic, fungistatic and antioxidant properties.
• Sodium bisulfate is the most commonly used antioxidant in local anesthetic solution.
It prolongs the self-life of solution by rendering it more acidic and thus prevents
deterioration of epinephrine.
• RN (lipophilic) – nerve penetration
RNH+ (hydrophilic) – connective tissue penetration.

Low pH (more H+)  diffusion,  penetration


+
High pH (less H ) (In case of infection)  diffusion,  penetration
Low pKa (Benzocaine)  penetration,  diffusion
High pKa  penetration,  diffusion

• The gauge of needle used in dental syringes refers to internal diameter of the lumen.
Larger the gauge, smaller the diameter.
• Main barrier for diffusion of local anesthetic is the perineurium. Endoneurium is the
actual site of action and rate of diffusion depends on lipid solubility of drug.
• The maxillary tooth that is difficult to anesthetize by infiltration is first molar due to the
presence of thick zygomatic buttress.
• After the removal, tissue should be immediately placed in 10 percent formalin (4%
glutaraldehyde). Volume should be at least 20 times the volume of specimen.
• One unit of platelet rich plasma raises the platelet count approximately by 7000–10000
per µl.
• One unit fresh blood raises the hemoglobin concentration by 1 gm percent.
Considerations for Oral Surgery Viva Voce 277

• 1 unit (150 ml) of fresh frozen plasma contains 200 µ factors VIII, 200 µ factor XI and
400 mg fibrinogen. It is stored at 30°C.
• Cryoprecipitate contains factor VIII (100 µ), factor XIII, von Willebrand factor and
fibrinogen (250 mg).
• Hypovolemic shock develops after loss of 40 percent of blood. Initial resuscitation should

Essentials of Dentistry
be done with crystalloids such as Normal saline or Ringer lactate.
• Fluids to replace the 1 liter of blood are:
1:3 = Blood: Colloidal fluid
1:1 = Blood: Crystalloid fluid
• Antidote for narcotic analgesics is naloxone.
• The drug of choice in treating the anaphylaxis is 0.2–0.5 ml of 1:1000 solution of adrenalin
by IM or SC route.
• Mental foramen opening is directed backward and lateral direction.
• Phentolamine, an alpha-adrenergic blocking agent is used to reverse the effect of local
anesthesia.
However, it does not reverse anesthetics themselves. Instead, it competes with
epinephrine for receptors. Epinephrine or neocobefrin are included in most dental anesthetic
formulations as vasoconstrictors to keep the anesthetic in the targeting area. Dilation of
blood vessels washes the anesthetic agent away. By blocking the vasoconstrictors,
phentolamine accelerates this clearance. It accelerates the recovery of normal sensations.
Phentolamine has been used since the 1950s as an antihypertensive in a 5- to 10-mg
dose, and can cause fainting and other side effects in these doses. A 1.7-ml cartridge
of OraVerse contains only 0.4 mg of phentolamine. Dentists can inject OraVerse as a cartridge
in the same manner and at the same site of injection of anesthetics.
The drug could be used with any minor procedure, such as a restoration, in which
long-term anesthesia is not needed.

Instrument Use
Ash forceps To extract lower incisor
Rowe’s disimpaction forceps To reduce the tooth bearing portion of upper jaw
Walsham or Asche’s forceps To reduce nasal complex fracture
Bristow’s elevator To elevate fractured zygomatic bone
Osteotome (bibeveled) To split tooth
Chisel (monobeveled ) To remove bone
Bone rongeur To trim bone
Bone gauge To make window in maxillary antrum
Gigli saw (Surgical saw) To cut bone
No. 16 cowhorn forceps To extract mandibular molars

Glasgow Coma Scale


Motor response Best verbal response Eye opening
5 Obeys commands Well-oriented -
4 Localized pain Confused conversation Spontaneous
3 Flexion response to pain Inappropriate speech On request
2 Extension response to pain Incomprehensible As response to pain
1 None None None
278 Considerations for Oral Surgery Viva Voce

SOME COMMONLY USED COMPOSITIONS


White head varnish Iodoform – 10 mg
Benzoin – 10 gm
Prepared storax – 7.5 ml
Essentials of Dentistry

Balsam of tolu – 5 gm
Solvent ether – 100 ml
It consists of a number of aromatic resins which slowly
broken down to produce benzoic acid, a potent
antiseptic.
Carnoy solution (Used for fixing the Absolute alcohol – 6 ml
tissues in the tumor bed) Chloroform – 3 ml
Glacial acetic acid – 1 ml
Bone wax (To reduce bleeding) 7 parts yellow wax
2 parts olive oil
1 part phenol
Tabot’s solution Iodine
(Used as astringent in pericoronitis) Zinc iodine
Glycerin water
McInns solution (Bleaching of 1 part anesthetic ether
vital tooth) 5 part HCL (36%)
5 parts of H2O2 (30%)
Monsel’s solution It contains ferric sulphate.
It acts by precipitating proteins.
It is effective in arresting the capillary bleeding and
post-extraction bleeding in medullary bone.

Important Signs
Colman’s sign Hematoma in floor of mouth due to rupture of dorsal lingual vein in
symphyseal/body fracture.
Guardsman’s/Parade Symphysis fracture associated with bilateral subcondylar fracture.
ground fracture Commonly seen in epileptics and soldiers.
Battle’s sign Hematoma below and behind the mastoid process associated with
fracture of base of skull.
Commonly seen in mandibular condylar fracture.
Guerin’s sign Hematoma at greater palatine foramen.
Commonly seen in Le Fort I fracture
Bucket handle fracture Downward and backward displacement of the anterior part of the
mandible leading to respiratory distress.

CLASSIFICATIONS
Dentoalveolar Fracture
Andreasen and Andreasen, 1994
1. Dental hard tissue injury
a. Crown infraction (crack of enamel or incomplete fracture)
b. Crown fracture—enamel only
c. Crown fracture—enamel + dentin
Considerations for Oral Surgery Viva Voce 279

d. Crown fracture—enamel + dentin + pulp


e. Crown—root fracture (vertical fracture)
f. Crown—root fracture (oblique fracture)
g. Root fracture.
2. Periodontal injury

Essentials of Dentistry
a. Concussion (no displacement of tooth but tender to percussion)
b. Subluxation (loosening of tooth without displacement)
c. Intrusion
d. Extrusion
e. Lateral luxation (loosening of tooth with displacement)
f. Avulsion.
3. Alveolar bone injury
a. Intrusion of tooth with comminution of socket
b. Fracture of single wall of socket or alveolus
c. Fracture of both walls of socket or alveolus
d. Fracture of mandible or maxilla involving the alveolus and/or tooth socket.
4. Gingival injury:
a. Contusion
b. Abrasion
c. Laceration.
5. Combination of above

Mandibular Fracture
I. Dingman and Natvig
a. Symphyseal
b. Parasymphyseal
c. Body
d. Angle
e. Ramus
f. Condylar process
g. Coronoid process
h. Alveolar process.

II. Kazanjian and Converse


Depending upon presence or absence of serviceable teeth in relation to line of fracture:

Class I Teeth present on both sides of fracture line


Class II Teeth on one side of fractured line
Class III Edentulous patient

III. Rowe and Killey


Those involving basal bone Those not involving basal bone
Single unilateral fracture Alveolar process
Double unilateral
Bilateral
Multiple
280 Considerations for Oral Surgery Viva Voce

IV. Kruger
– Simple
– Compound
– Comminuted.
Essentials of Dentistry

V. Kruger and Schilli


a. Relation to external environment
– Simple
– Compound.
b. Types of fracture
– Incomplete
– Complete
– Greenstick
– Comminuted.
c. Dentition of jaw within reference to use of splints
– Sufficiently dentulous jaw
– Edentulous or insufficiently dentulous jaw
– Primary and mixed dentition.
d. Localization
– Fracture of symphysis region between canines
– Fracture of canine region
– Fracture of body of mandible between canine and angle
– Fracture of angle in third molar region
– Fracture of mandibular ramus between angle and sigmoid notch
– Fracture of coronoid process
– Fracture of condylar process.

VI. Mandibular Angle Fracture


(Depending upon direction of fracture line and effect of muscle action on fracture fragment)
i. Vertically favorable or unfavorable (Seen on occlusal view)
ii. Horizontally favorable or unfavorable (Seen on OPG).

VII. Other Classification

A. Types of fracture
a. Simple fracture
These are linear fractures which are not in communication with exterior. Usually,
they are found in the region of condyle, coronoid process, ascending ramus,
edentulous mandible, in the angle posterior to 3rd molar tooth. Green stick fracture
seen in children is a variant of simple fracture.
b. Compound fracture
Fracture of the tooth bearing portion of the mandible, with extraoral or intraoral wound
involving fracture line is present. Such fracture communicates to the site with potential
of infection through mouth via periodontal ligament or through skin.
c. Comminuted fracture
Comminuted fractures are characterized by two or more fragments of bone at the
fracture site. The main etiological factor for comminuted fracture is direct violence
Considerations for Oral Surgery Viva Voce 281

to mandible from penetrating sharp objects or missiles delivering high degree of


kinetic energy upon limited area. They are usually compound by nature and
complicated to manage due to bone, soft tissue loss.
d. Pathological fracture
These are spontaneous fractures of the bone as a result of a normal degree of

Essentials of Dentistry
muscular contraction, or following minimal trauma. They result from minimum trauma
to mandible which is already weakened by pathological condition such as
osteomyelitis, neoplasm or generalized skeletal disease.
e. Complicated fracture
Complicated fractures can be defined as those fractures that either directly or
indirectly involve surrounding major vessels nerves, or joints. As mandible itself
contains the inferior alveolar neurovascular bundle, most mandibular fractures can
be thought of as complicated fractures.
f. Impacted fracture
Impacted fractures are those in which the fractured fragments interdigitate to such
an extent that there is little or no movement at the fracture site. They are very rare
in mandible but are commonly seen with midfacial fractures.
g. Greenstick fracture
In children, elasticity of bone allows it to bend instead of fracturing full thickness
of bone. Only the one sided cortex fractures while that on another side remains
intact in position.
B. Site of fracture
• Dentoalveolar
• Condyle
• Coronoid
• Ramus
• Angle
• Body
• Parasymphysis
• Symphysis.
C. Cause of fracture
• Direct violence
• Indirect violence
• Excessive muscular contraction.
(Coronoid fracture because of sudden reflex contraction of temporalis).

Condylar Fracture
I. Comprehensive Classification (Lindahl 1977)
a. Depending upon level of fracture
1. Condylar head or intracapsular
It is difficult radiographically to differentiate the exact anatomical confines of the
head. By definition, a condylar head fracture is within the capsule and is therefore
termed ‘intracapsular’. It may be further divided into vertical, compression and
comminuted.
2. Condylar neck
The radiographic constriction representing the condylar neck corresponds
anatomically to the region of the inferior attachment of the joint capsule.
3. Subcondylar
This is the region below the neck extending down to the most inferior point on
the sigmoid notch anteriorly, while its posterior limit is situated more inferiorly
282 Considerations for Oral Surgery Viva Voce

corresponding with the point of maximum curvature of the natural concavity of the
posterior border of the mandible in that region.
b. Relation of condylar fragment to mandible
1. Undisplaced
Essentials of Dentistry

2. Deviated
This is a simple angulation of the condylar process in relation to the main mandibular
fragment without overlap.
3. Displaced with medial overlap of condylar segment.
4. Displaced with lateral overlap.
5. Anterior posterior overlap (infrequently seen).
6. No contact between the fragments.
c. Relation of condylar head to fossa
1. Not displaced (the joint space appear normal).
2. Displaced (the joint space is increased but the condyle is still related to the glenoid
fossa).
3. Dislocation (the condylar fragment is completely out of the fossa).

II. Clinical Classification (MacLennan 1952)


a. No displacement
b. Fracture deviation: There is simple angulation of the condylar process to the major
fragment. This is the green-stick fracture of childhood.
c. Fracture displacement: There is overlap of the condylar process and major mandibular
fragments.
d. Fracture dislocation: The head of the condylar process has been completely disrupted
from the articular fossa.

III. Classification of Condylar Neck Fractures (Spiessl and Schroll)


Type I Condylar neck fracture without serious dislocation
Type II Deep seated condylar neck fracture with dislocation
Type III High condylar neck fracture with dislocation
Type IV Deep-seated condylar neck fracture with luxation
Type V High condylar neck fracture with luxation
Type VI Head or intracapsular fracture

IV. Other
Temporomandibular joint fractures are also classified according to the height of the
fracture.
a. Intracapsular fractures: These fractures run irregularly, usually diagonally through the
head. Because of anatomic variations in the capsular attachment, they can lie within
the capsule and outside it.
b. High temporomandibular joint fractures: These fractures are below the capsule and
muscle attachment but above the sigmoid notch.
c. Low temporomandibular joint fractures: These fractures run from the sigmoid notch
to the back edge of the mandibular ramus.
Considerations for Oral Surgery Viva Voce 283

Fracture of Zygomatic Complex and Arch

I. Knight and North (1961)


Based on Water’s Radiograph,

Essentials of Dentistry
Group 1:
Undisplaced fracture
Group 2:
Isolated displaced arch fracture
Group 3:
Displaced body fracture might rotate
Group 4:
a. Medially rotated but at malar buttress
b. Inward at frontozygomatic suture
Group 5: a. Lateral rotation: up at infraorbital margin
b. Out at frontozygomatic suture
Group 6: Additional fracture line (Comminuted)

II. Rowe and Williams


1. Fracture stable after elevation
a. Arch only (medially displaced)
b. Rotation around vertical axis.
– Medially
– Laterally.
2. Fracture unstable after elevation
a. Arch only (inferior displacement)
b. Rotation around horizontal axis
– Medially
– Laterally.
c. Dislocation en-bloc
– Inferiorly
– Medially
– Posterior laterally.
d. Comminuted fractures.

Fracture of Middle-third of Face

I. Rowe and Williams (1985)


A. Fracture not involving occlusion
1. Central region
a. Fracture of nasal bone and/or nasal septum
i. Lateral nasal injury
ii. Anterior nasal injury.
b. Fracture of frontal process of maxilla
c. Fracture of types (a) and (b) which extend into the ethmoid bone (nasoethmoidal
injury)
d. Fracture of types (a), (b) and (c) which extends into the frontal bone (fronto-orbital-
nasal dislocation)
2. Lateral region:
Fracture involving zygomatic bone, arch and maxilla (zygomatic complex) excluding
dentoalveolar component.
284 Considerations for Oral Surgery Viva Voce

B. Fracture involving occlusion


1. Dentoalveolar fractures
2. Subzygomatic fracture
– Le Fort I (low-level or Guerin)
Essentials of Dentistry

– Le Fort II (pyramidal).
3 Suprazygomatic
– Le Fort III (high level or craniofacial dysjunction).

Nasoethmoidal Orbital (Noe) Fracture


1. Isolated nasoethmoid injury without other fractures of the midface
a. Bilateral
b. Unilateral.
2. Combined nasoethmoid injury with other fractures of the midface
a. Bilateral
b. Unilateral.

Frontal Sinus Fracture


I. First Classification
A. Anterior wall fracture
1. Frontonasal drainage intact.
2. Frontonasal drainage compromised.
B. Combined anterior and posterior wall fracture
C. Posterior wall fracture (B), (C) almost always involve frontonasal duct.

II. Second Classification


A. Anterior table fracture
1. Linear (Undisplaced)
2. Displaced.
B. Posterior table fracture
C. Outflow duct injury

TOOTH IMPACTION
A tooth is entitled as impacted only if the root formation is complete and yet it has not
erupted fully up to the final position.

Pell and Gregary Classification


1. Relation of tooth to ramus of the mandible and 2nd molar
Class I Sufficient space to accommodate the mesiodistal diameter of crown of the 3rd molar.
Class II The space between distal surface of 2nd molar and ramus is less than mesiodistal
diameter of the crown of the 3rd molar.
Class III The 3rd molar is located within the ramus

2. Based on relative depth of 3rd molar


Position A The highest portion of tooth at the level of occlusal plane or above it.
Position B The highest portion of tooth is below the occlusal plane but above the cervical line
of 2nd molar.
Position C The highest portion of the tooth is below the cervical line of the 2nd molar.
Considerations for Oral Surgery Viva Voce 285

Essentials of Dentistry
Fig. 30.1: Winter’s lines

3. Based on position of long axis of 3rd molar in relation to the long axis of 2nd molar
(Winter’s classification)
Vertical, horizontal, inverted, mesioangular, distoangular, linguoversion, unusual
positions.
The exact position and depth of the tooth can be ascertained by three imaginary lines
called as Winter’s Lines (Fig. 30.1).
1. White line: Line drawn touching the occlusal surfaces of 1st and 2nd molars is extended
posteriorly over the 3rd molar region. It indicates the difference in occlusal level of
2nd and 3rd molars.
2. Amber line: Runs at the level of the crest of interdental septum between the molars
and represents the bone level covering the impacted tooth.
3. Red line: It is drawn perpendicular from the amber line to an imaginary point of application
of elevator. It indicates the depth of the tooth in the bone and the difficulty encountered
in removing the tooth.
Condition Position of the patient
During recovery form syncope Semireclined and Trendelenburg
positions
During CPR Supine position
A patient with suspected cervical fracture Body and neck extended
Preferable patient position in recovery room Lateral
after ambulatory general anesthesia
Pregnant patient in syncope Left lateral position
Patients affected with orthostatic hypertension Upright position or with her trunk
slightly to one side
Congestive heart failure patient Upright position,
(Supine position should be avoided)
CHAPTER
Morphological Differences
31 between Primary and
Permanent Teeth

Primary Teeth Permanent Teeth

General
Develops directly from dental lamina. Develops as a lingual or distal extension of
dental lamina.
Usually they are not covered with bony crypts. They are completely covered with bony crypts.
All the primary teeth erupt into oral cavity at All the permanent teeth except 3rd molar erupt
the age of 21/2–3 years. For root completion, into oral cavity at the age of 12–13 years. For
it takes 1-11/2 years after eruption. root completion, it takes 2-3 years after eruption.
i.e. Root formation of primary teeth is completed i.e. Root formation of primary teeth is completed
by 3-4 years of age. by 14-16 years of age.
All primary teeth develop and erupt almost in Permanent teeth develop in different planes.
the horizontal plane and occupy a more vertical
position in the jaws.
Duration of deciduous dentition ranges from Average duration of permanent teeth is about
12-14 years (Fig. 31.1). 60 years of life time (Fig. 31.2).
Deciduous teeth are smaller in all dimensions Larger in all dimensions than that of
(about 1/2) than that of corresponding corresponding primary teeth.
permanent teeth except deciduous 2nd molar
(Figs 31.3 to 31.6).
Relation between upper and lower teeth is Relation between upper and lower teeth is
tooth-to-tooth relation. (Edge-to-edge contact) intercuspal relation.
Number of teeth: 20 Number of teeth: 32
Premolars are absent. Premolars are present.
5 in each quadrant. 8 in each quadrant.
2 incisors, 1 canine, 2 molars. 2 incisors, 1 canine, 2 premolars, 3 molars.

Key to memorize:
Development (4 points), Duration, Dimensions, Relation, Number.
Morphological Differences between Primary and Permanent Teeth 287

Essentials of Dentistry
Fig. 31.1: Deciduous dentition

Fig. 31.2: Permanent dentition


288 Morphological Differences between Primary and Permanent Teeth

The crown

Lighter in color—bluish white also called as milk Darker in color—grayish or yellowish white.
teeth as its refractive index is same as milk (1)
Essentials of Dentistry

The contact areas between molars are The contact areas between molars are situateds
broader, flatter and situated gingivally. occlusally.
Cervical ridges are more pronounced Cervical ridges are more flat.
especially on the buccal aspect of the first molar.
Cuspids are slender and tend to be more conical. Cuspids are less conical.
Crowns are wider in mesiodistal dimensions in Crowns of anterior teeth are larger in
relation to the cervicoocclusal height. This gives cervico-occlusal dimensions than the
a cup shaped appearance to anterior teeth and mesiodistal. This gives a longer appearance
squat shape to molars. to anterior teeth.
The enamel is thinner and has a more The enamel is thicker and has a thickness of
consistent depth of about 1 mm thickness about 2-3 mm.
throughout the entire crown.
The enamel road at the cervical slopes The rods are oriented gingivally.
occlusally from the DEJ.
Supplemental grooves are more. Supplemental grooves are less.
Mammelons are absent. Mammelons are present at the incisal edges
of newly erupted teeth.
Occlusal plane is relatively flat. Occlusal plane has curved contour.
Buccal and lingual surfaces of molars converge There is less convergence of buccal and lingual
towards occlusal surface so that they have surfaces of molars towards occlusal surface.
narrow occlusal table in a buccolingual plane.
1st molars are more bulbous and are sharply They have less constriction of neck.
constricted (bell shaped) cervically.
They are smaller in dimension than 2nd molar. They are larger in dimension than 2nd molar.
Key to memorize:
C – Color, Contact area, Cervical ridge, Cuspids
D – Dimensions
E – Enamel, Enamel rods, Supplemental grooves, Mammelons.
Occlusal plane, Occlusal table, 1st molar.

Fig. 31.3
Morphological Differences between Primary and Permanent Teeth 289

Essentials of Dentistry
Fig. 31.4

Fig. 31.5

Fig. 31.6
Figs 31.3 to 31.6: Differences between deciduous and permanent teeth
290 Morphological Differences between Primary and Permanent Teeth

Root
1. The roots are larger and more slender in 1. The roots are shorter and bulbous in
comparison to crown size. comparison to crown size.
Essentials of Dentistry

2. Roots of the primary molars are more 2. Roots are less divergent and do not
divergent and flare outwards as they have flare to a great degree.
to accommodate the permanent tooth bud.
3. Furcation is more towards cervical area so 3. Placement of furcation is apical thus the
that root trunk is smaller. root trunk is larger.
4. Undergo physiologic resorption during 4. Physiologic resorption is absent so
shedding of primary teeth so position of position of apical foramen and length of
apical foramen varies with age. root canal is fixed.
3
Key to memorize:
2

4
1

Pulp
Pulp volume is large compared to tooth volume. Pulp volume is less compared to tooth volume.
High degree of cellularity and vascularity of Comparatively less degree of cellularity and
tissue at least in stages prior to advanced vascularity in tissue.
physiologic resorption of roots.
High potential for repair. Comparatively less potential for repair.
Pulp outline follows DEJ more closely and pulp Pulp outline doesn’t follow DEJ exactly and
horns are closer to outer surface. pulp horns are away from the outer surface.
No marked cervical constriction between Marked cervical constriction between coronal
coronal pulp and root canal. pulp and root canal.
Comparatively less tooth structure around pulp. More tooth structure surrounding pulp offers
more protection and increases potential for
repair.
Greater thickness of dentin over the pulpal wall Lesser thickness of dentine over the pulpal wall
at the occlusal fossa of molars. at the occlusal fossa of molars.
Ratio of thickness of dentin in primary in permanent teeth is 1:2.
Numbers of dentinal tubules are less. Number of dentinal tubules are more about
50,000–90,000 per mm2.
Root canals are more ribbon-like. Radicular Root canals are well-defined and less
pulp is thin and tortuous. branching.

Floor of pulp is porous and accessory canals Floor of pulp chamber usually doesn't have any
from the floor of pulp chamber leads directly accessory canals.
to inter-radicular furcation.
Nerves terminate at pulpodental junction and Nerves terminals transverse the whole length
their branches enter the dentinal tubules but of dentinal tubules and end in the
end away from the dentinoenamel junction. dentinoenamel junction.
Morphological Differences between Primary and Permanent Teeth 291

Histological differences
Roots have wider apical foramina, and resultant Foramina are restricted, and reduced blood
abundant blood supply demonstrates a more supply favors calcific response.
typical inflammatory response.

Essentials of Dentistry
Incidence of reparative dentin formation Reparative dentin formation is less.
beneath carious lesion is more extensive and
more irregular.
Localization of infection and inflammation is Infection and inflammation is usually local.
poorer in pulp.
Pulp nerve fibers pass to the odontoblastic Pulp nerve fibers terminate mainly among
area, where they terminate as free nerve odontoblasts and even beyond the predentin.
endings.
Density of innervations is less so primary teeth Density of innervations is more, making tooth
are less sensitive to operative procedure. more sensitive to operative procedures.
Neural tissue degenerated first during root
resorption.
Dentinoenamel junction is relatively flat. Dentinoenamel junction is scalloped.
Key to memorize:
3 for foramina
2 for innervations
1 for DEJ
4, 5
1, 2, 3

Mineral content
Enamel and dentin are less mineralized, so acid More mineralized so acid etching time is less.
etching time is more for primary teeth.
Organic content is more. Organic content is less.
Neonatal lines are present. Neonatal lines are present only in 1st
permanent molar.
Enamel:
Stria of Retzius are less common which may Stria of Retzius are more common.
be responsible for bluish white color of enamel.
Dentin: Dentin:
Tubules are less regular. Tubules are more regular.
Thickness is half than that of permanent teeth. Thickness is double than that of deciduous
teeth.
Dentin forming cells are active functionally for Dentin forming cells are functionally active by
360 days. 700 days.
Interglobular dentin is absent. Interglobular dentin is present.
Dentin is less dense. This can be observed Dentin is more dense and difficult to cut.
clinically by resistance offered by it to bur while
cutting. Dentin is cut more easily and abrades
rapidly.
292 Morphological Differences between Primary and Permanent Teeth

Periodontal ligament
Area of periodontal ligament is less. Area of periodontal ligament is more.
Lamina dura is relatively thick. Lamina dura is relatively thin.
Essentials of Dentistry

Other
Cementum is very thin and of the Secondary cementum is present.
primary type.
Alveolar atrophy is rare. Alveolar atrophy occurs.
CHAPTER

32 Definitions in Pedodontia

PEDODONTICS

By American Academy of Pediatric Dentistry


Pediatric dentistry is an age-defined specialty that provides both primary and comprehensive
preventive and therapeutic oral healthcare for infants and children through adolescence,
including those with special healthcare needs.

PSYCHOLOGY
Psychology is the science dealing with human nature, function and phenomenon of his
own soul in the main.

CHILD PSYCHOLOGY
Child psychology is the science that deals with the mental power or an interaction between
the conscious and subconscious element in a child.

CHILD MANAGEMENT
Child management is defined as the means by which a course of treatment for a young
patient can be completed in the shortest possible period, while at the same time ensuring
that he will return for the next course willingly (PJ Holloway, JN Swallow)

EMOTION
It is an effective state of consciousness in which joy, sorrow, fear, hate or the likes are
expressed. Emotion is a state of mental excitement characterized by physiological,
behavioral changes and alteration of feelings.

BEHAVIOR
Behavior is any change observed in the functioning of the organism.

FEAR
Fear is a reaction to a known danger (augmenting the flight or fright response). It may
be defined as unpleasant emotion or effect consisting of psychological changes in response
to realistic threat or danger to one’s own experience.

ANXIETY
Anxiety is an emotion similar to fear but arising without any objective sources of danger.
294 Definitions in Pedodontia

PHOBIA
Phobia is an irrational fear resulting in the conscious avoidance of a specific feared object,
activity or situation.
Essentials of Dentistry

BEHAVIORAL SCIENCE
Behavior science is the science which deals with the observation of behavioral habits of
man and lower animals in various physical and social environments including behavior
pedodontics, psychology, sociology and social anthropology.

BEHAVIOR MANAGEMENT
Behavior management is the means by which dental health team effectively and efficiently
performs treatment for a child and at the same time instills positive dental attitude. (Wright
1975)

BEHAVIOR SHAPING
Behavior shaping is the procedure which slowly develops behavior by reinforcing a
successive approximation of the desired behavior until the desired behavior comes into
being.

BEHAVIOR MODIFICATION
Behavior modification is defined as the attempt to alter human behavior emotion in a
beneficial way and in accordance with the laws of learning (Mathewson).

NURSING CARIES
It is a unique pattern of dental decay in young children due to prolong nursing habit.

RAMPANT CARIES
It is suddenly appearing, widespread, rapidly spreading, burrowing type of caries resulting
in early involvement of pulp and affecting those teeth, which are usually regarded as immune
to decay (Massler, 1945).

PLUNGER CUSP
Cusp that tends to forcefully wedge food interproximally are called plunger cusp. It occurs
due to wear, as a result of shift in tooth position after failure to replace missing tooth.

PIT AND FISSURE SEALANTS


It is “A material that is introduced into the pits and fissures of caries susceptible teeth,
thus forming a micromechanically bonded, protective layer cutting access of caries
producing bacteria from their source of nutrients” (Simonsen).

INDIRECT PULP CAPPING


It is defined as procedure where in small amount of carious dentin is retained in deep
areas of cavity to avoid exposure of pulp. Followed by placement of a suitable
medicaments and restorative material that seals off the carious dentin and encourages
pulp recovery.
Definitions in Pedodontia 295

DIRECT PULP CAPPING


It is defined as the placement of a medicament or nonmedicated material on a pulp that
has been exposed in course of excavating the last portions of deep dentinal caries or
as a result of trauma (Kopel, 1992).

Essentials of Dentistry
PULPOTOMY
It can be defined as complete removal of the coronal portion of the dental pulp, followed
by placement of a suitable dressing or medicament that will promote healing and preserve
vitality of the tooth (Finn, 1995).

PULPECTOMY
It is defined as complete removal of the necrotic pulp from the root canals of primary
teeth and filling them with an inert resorbable material so as to maintain the teeth in the
dental arch (Mathewson, 1995).
Pulpectomy is removal of all pulpal tissues from the coronal and radicular portions of the
tooth (Finn).

APEXOGENESIS
It is defined as the treatment of a vital pulp by capping or pulpotomy in order to permit
continued growth of the root and closure of the open apex.

APEXIFICATION
It is the method of inducing the development of root apex in an immature pulp less tooth
by formation of osteocementum or other bone like tissue (Cohen).

PREVENTIVE ORTHODONTICS
Preventive orthodontics is defined as the actions taken to preserve the integrity of what
appears to be normal occlusion at a specific time (Grabber, 1966).

INTERCEPTIVE ORTHODONTICS
It is that phase of science and art of orthodontics employed to recognize and eliminate
the potential irregularities and malpositions in the developing dentofacial complex (American
association of Orthodontists, 1969).

SPACE CONTROL
It is defined as careful supervision of the developing dentition; it reflects an understanding
of the dynamic nature of occlusal development (Gainsforth, 1955).

SPACE MAINTENANCE
It is defined as the process of maintaining a space in a given arch previously occupied
by a tooth or a group of teeth.

SPACE MAINTAINER
It is a fixed or removable appliance designed to preserve the space created by the premature
loss of a primary tooth or a group of teeth (Boucher).
296 Definitions in Pedodontia

HABIT
It can be defined as a fixed or constant practice established by frequent repetition.
It is defined as a tendency towards an act or an act that has become a repeated performance,
relatively fixed, consistent, easy to perform and almost automatic (Boucher OC).
Essentials of Dentistry

THUMB SUCKING
Thumb sucking is defined as placement of the thumb in varying depths into mouth.

TONGUE THRUSTING
Tongue thrusting is a forward placement of the tongue between the anterior teeth and
against the lower lip during swallowing.

MOUTH BREATHING
Mouth breathing is defined as habitual respiration through the mouth instead of nose
(Sassouni, 1971).

BRUXISM
Bruxism is defined as the habitual grinding of teeth when an individual is not chewing
or swallowing. (Ramfjord, 1966).

SELF-INJURIOUS HABIT
Self-injurious habit is repetitive act that results in physical damage to the individual. These
habits are seen with increased incidence in the mentally retarded population.

HANDICAPPED PERSON
WHO has defined a handicapped person as “ One who over an appreciable period is
prevented by physical or mental conditions from full participation in the normal activities
of their age group including those of a social, recreational, educational and vocational
nature.”

MENTAL RETARDATION
It is a general term is applied to persons whose intellectual development is significantly
lower than that of normal persons and whose ability to adapt to their environment is
consequently limited.
It is defined as subaverage general intellectual functioning which originates during the
developmental period and is associated with impairment in adaptive behavior (American
Association of Mental Deficiency).

CEREBRAL PALSY
It is defined as a nonprogressive lesion which occurs in the developing brain before, during,
after birth, leaving the child with a variety of neurological problems.
Instructions to the Reader
Reader

Some important things to be kept in mind before appearing for the final year examination
are mentioned below. Most of the students tend to forget the same during hectic exam
schedule.
• Final year exam for dental undergraduate students is very tiring. It exhausts all the
energy by the last paper. Most of the time it lasts for almost a month. One should
not stretch himself/herself more for the initial papers otherwise; he/she will be completely
exhausted by last papers.
• Keep yourself relaxed and tension free. Take enough sleep and have healthy food.
Do remember that you can do better only if you are physically and mentally fit. Peace
of mind is absolutely mandatory while writing papers.
• Avoid junk food and irregularities in sleep and take daily meal regularly at least two
months before the exam. Falling ill during this time can spoil your year's hard work.
• Do not forget to keep your exam identity card/no and other armamentarium like pen,
pencil, scale, rubber, sharpener and colors ready with you; it will reduce wastage of
time during precious exam hours.
• It is always advisable to keep all instruments for practical exams ready in sets well
in advance. This will avoid missing of instruments during exam rush time.
• Keep your journals and work records ready in certified form.
• Be in touch with your patients whom you have planned for practical exams.
• Be through with all definitions as each viva starts with definition. Viva may not move
further if first question is wrongly answered.
• Answer only that you know well. Answers to initial questions draw your viva. It depends
on the candidate to direct viva in a desired direction. Do not speak anything you are
not confident about or you do not know correctly. Speak only what is necessary.
• Do not try to impress examiner by throwing excessive information. Be precise and to
the point.
• Decent attire, body language and facial expression are very important. Professional
dress up reflects your sincerity. Aprons should be tidy and clean, do remember that
everybody likes pleasant personality. First impression has major impact on your viva,
so make your efforts accordingly.
With the hope that this information would be useful to all the doctors who are going
to face the most challenging task of their life—the final exam.
I wish all the best to them.
Index

A Areas of
demineralization 98
Abfraction 184
increased mineralization 98
Ability to produce fluorescence 237
instrumentation of
Abrasion 183, 243
Gracey curettes 141
of gingiva 87f
particular curette 141f
Acellular cementum 178
Armamentarium 1f
Acidulated sodium fluoride 170
Arrested caries 27
Active
Ascher’s syndrome 257
carious lesion 98
Assessment of tooth mobility 105f
eruption 177
Attached gingiva 174, 174f
Acute
Attrition 183, 243
gingival infections 185
gingivitis 184
B
necrotizing gingivitis 185
Adamantinoma 242 Backward caries 28
Adhesion 38 Bana test 120
Adhesive joint 38 Barbed broach 61, 62f
Adult periodontitis 223 Basal
Advantages of bleaching 55 cell nevus syndrome 259
Adverse drug reactions 203 classification of dental instruments 70
Agnathia 238 concepts of tooth sensitivity 162
Ainsworth rubber dam punch 8f design of file 64f
Albright syndrome 256 Battle’s sign 278
Alcoholic breath 118 Beckwith’s hypoglycemic syndrome 257
Aldrich’s syndrome 256 Behçet’s syndrome 257
Allogenic bone grafts 158 Bell’s palsy 274
Alloplastic materials 160 Bending of file 23f
Alveolar Bennett movement 182
bone injury 279 Bevels 81
bone proper 179 B-galactosidase test 120
mucose 175 Bioactive glass 169
Always cut wet 24f Biopsy 244
Amalgam cavity preparation 31f B-K mole syndrome 257
Ameloblastoma 226, 227, 242 Black’s formula 70
Anaplasia 243 Bleaching 48
Anatomic techniques 51
crown 177 Blow out fracture on left side 268f
root 177 Bohn’s nodules 242
Angulations in instrumentation 142 Bonding systems 38
Ankylosis 179 Bone
Anti-inflammatory drugs 172 blend 158
Anxiety 293 loss 102, 187
Apert’s syndrome 257 replacement grafts 157
Apexification 295 swaging 158
Apexogenesis 295 Border movements 182
300 Essentials of Dentistry

Bowen’s disease 239, 257 Coated tongue 117


Bragg’s law 237, 237f Cocoa butter 9
Bruxism 184, 244, 296 Collagen 178
Bulbous bone contours 187 Colman’s sign 278
Bulla 243 Color coding 60f
Bundle bone 179 Combination defect 150f
Burnishers 75 Combined osseous defect 149
Buttressing bone formation 187 Comminuted fracture 280
Comminution of alveolar socket 87f
C Comparison of scalers 138
Complicated
Calcium
crown
compounds 170
fracture 85f
hydroxide 170
root fracture 85f
sodium phosphosilicate 169
fracture 281
Calculocementum 181
Compound fracture 280
Caldwell-Luc view 268
Condensing instruments 75
Cancellous bone marrow transplant 158
Carbamide peroxide 51 Conditions to rule out
Carbon steel 59t hypersensitivity 166
Carcinoma 243 Condylar fracture 281
Carvers 75 Congenital
Cast restorations 32f abnormalities 111
Cause of fracture 281 disease 238
Cavitation 27, 190 Connective tissue component 95
Cavity Considerations for oral
preparation 29f medicine 238
for cast restorations 32f surgery viva voce 273
varnishes 170 Contact movements 182
Cellular cementum 178 Contour of facial and lingual
Cellulitis 244 surfaces 108
Cementicles 178 Control of xerostomia 171
Cementoenamel junction 216 Contusion of gingiva 87f
Cementum 178 Coronal cementum 176
in disease 98 Costen’s syndrome 257
Central giant cell fibroma of bone 240 Cotton pliers 74
Cerebral palsy 296 Cowden syndrome 257
Chédiak-Higashi syndrome 257 Cross-section of
Cheilitis glandularis 238 instruments 61f
Chemical curettage 145 reamer 63f
Chemotaxis 181 Crouzon’s syndrome 258
Child Crown infarction and uncomplicated
management 293 fracture 85f
psychology 293 Curling of
Chisels 80 multiple waves 236f
Chronic wave 236f
gingivitis 185 Curvature of canal 23f
halitosis 114 Cuticle 176
Circumorbital and subconjunctival Cutting
ecchymosis 267 flutes 64
Classification of instruments 71
bleaching agents 48 Cyst 242, 274
factors causing food impaction 108
probes 124
D
endodontic instruments 56
infrabony defects 148 Deciduous
periodontal pockets 148 and permanent teeth 289
pockets 148 dentition 287f
Clinical features of gingivitis 184 Degree of looseness of tooth 101
Index 301

Dental Endosteum 179


adhesion 38 Endotoxins 100
adhesive systems 40, 41f Enophthalmos 267
calculus 181 Epidemiologic indices 180
caries 244 Epidemiology of periodontal
classifications 26f disease 180
epidemiology 180 Epidermoid carcinoma 243
hard tissue injury 278 Epstein’s pearls 242
lamina cyst of newborn 242 Epulis 185
neural structure 163f Erosion 183, 243
occlusion 181 Eruption
plaque 180 cyst 242
wedge 16f gingivitis 186
Dentigerous cyst 242 Eryma multiforme 186
Dentin Excavators 77
bonding systems 39 Excessive anterior bite 108
dysplasia 239 Excursions 182
treatment 14 Exostoses 187
Dentoalveolar fracture 278 Explorer 73
Dentogingival Exploring instruments 72
junction 95, 96f
Extended shank curettes 141
unit 95, 175
External basal lamina 96
Depth of lesion 125f
Extrusion 111
Design of
cavity preparation 19
curette 136f
F
scaler 135f Facets 183
Desmosomes 175 Facial features and fracture line 266f
Desquamative gingivitis 186 Factors affecting
Determining bleaching 53
depth of sunken lesion 124 food impaction 107
height of raised lesion 124 probing 132
Diagnosis of infrabony defect 151 tooth mobility 102
Dibasic calcium phosphate 170 Fanconi syndrome 258
Diet counseling 171 FDI rubber dam template 10f
Different wedging methods 19 Features of
Dimensions of lesion 124f
curette 136f
Diplopia 267
endodontic instruments cutting
Direct pulp capping 295
blade 60
Disadvantages of bleaching 54
Gates Glidden drill 23f
Double vision 267
scaler 135f
Down’s syndrome 102, 188, 258
Fenestrations 179
Drugs causing halitosis 119
Fibroma 240
Dysplasia 243
Fifth generation probes 127
Files of different sizes 66f
E Final tooth preparation stage 12
Eagle’s syndrome 258 Finishing and polishing instruments 71
Ehlers-Danlos syndrome 102, 258 First generation probes 125
Electric Flexo file 66
pulp tester 34f Flexogates 25
stimuli 166 Flex-R file 66
Electrolyte 33 Floor and rim 265
Electronic nose 120 Floppy infant syndrome 259
Emotion 293 Fluctuant amine odor 119
Enamel Fluoride
hatchet 80 compounds 170
wall etching 14 dentifrices 168
Endodontic hand instruments and Focal dermal hypoplasia 259
instrumentation 56 Follicular type 231, 232f
302 Essentials of Dentistry

Food impaction 107, 181 H


Force-duction test 267
Habits and systemic diseases 102
Fordyce’s disease/granules 238
Halitosis 114
Formation of hybrid layer 42f
Hand instruments 76
Forward caries 28
in conservative dentistry 70
Four osseous walls 151
Fourth generation probes 127 Hanging frame holder 3, 5f
Fracture Hard tissue phase 153
involving occlusion 284 Harm prevention 2
of middle-third of face 283 Harty’s classification 56
of orbital floor 266f, 268 Hedstrom file 67
of zygomatic complex and arch 283 Healing after curettage 146
Free Healthy
gingival groove 173 gingiva 131
way space 182 sulcus 223
Freeze-dried bone allograft 159 Height of lesion 124f
Frey’s syndrome 258 Helminths 244
Frictional ablation 183 Hemihyperplasia 238
Frontal sinus fracture 284 Herald spot 251
Furcation Herpes zoster oticus 261
involvement 188 H-file 67, 68f
measurement 199f, 200 High frenum attachment 211f
Honey comb appearance 230
G Horizontal
food impaction 107
Gardener’s syndrome 259 tooth mobility 104
Garlic liberates volatile sulfur 118 Horner’s syndrome 259
Gates glidden drill 21f Horton’s syndrome 259
Gingiva 173 Hutchinson’s triad 259
fibers 176 Hydrogen peroxide 49
fluid 176 bleaching 50f
in health and disease 88 concentration 53
Gingival Hydroxyapatite 160
clefts 185 Hypercementosis 100, 178
curettage 143f
cyst of adult 242 I
enlargement 185
injury 279 Iliac autografts 158
margin significantly covers Immune system 197
cementoenamel junction 215 Impacted fracture 281
marginal trimmers 80 Improperly constructed restoration 111
pocket 186 In office bleaching 51
recession 177 Inactive carious lesion 98
sulcus 174 Incipient caries 27
Gingivitis 131, 223 Indifferent fiber plexus 178
Glasgow coma scale 277 Indirect pulp capping 294
Glickman’s classification 104 Influence of systemic diseases
Goldman and Cohen classification on periodontium 184
of intrabony defect 149 Infrabony pocket 147, 156, 187
Goltz-Gorlin syndrome 259 and infrabony defect 151
Gorlin and Goltz syndrome 259 Initial tooth preparation stage 12
Gracey curette and universal curette 137 Injuries to
Granuloma pyogenicum 185 gingiva or oral mucosa 85, 87f
Greenstick fracture 281 hard dental tissues and pulp 85f
Grinspan’s syndrome 259 periodontal tissues 84, 86f
Guerin’s sign 278 supporting bone 84, 87
Gutta-percha point in bony defect 152f Inlay 30f
Index 303

Insertion of wedge 17f, 18 Lichen planus 186


Instrument Lindhe’s classification 104
classified by function 70 Location of retainer 19
debriding 56 Loss of
exploring 56 distal support leading to food
for tooth structure removal 74 lodgement 110f
formula 72 proximal support 109
nomenclature 72 Lubricant 9
obturating 56 Ludwig’s angina 244, 274
shaping 56
standardization 58f M
tips 61
used for cavity preparation 29f Macrognathia 238
Integrity and location of proximal Macule 243
contacts 107 Malignant odontogenic tumors 227
Interceptive orthodontics 295 Management of
Interdental hypersensitivity 167
gingiva 175 oral malodor 121
groove 175 periodontal fibers adhering 153
Intermediate plexus 179 root surface 153
Internal basal lamina 96 soft tissue of pocket 153
Intraborder movements 182 wall of osseous defect 153
Intraluminal ameloblastoma 232 Mandibular
Intraosseous unicystic angle fracture 280
ameloblastoma 233 fracture 279
Invasive ameloblastoma 232 Mandibulofacial dysostosis 261
Iontophoresis 170 Manufacturer’s number 70
ISO and FDI classification 57 Manufacturing of endodontic
Isolated floor 265 instruments 59
Isolation instruments 71 Marfan syndrome 259
Marginal
J gingiva 173, 173f
plaque 180
Jaw-winking syndrome 259 Markings of Williams probe and
Junctional epithelium 175 Nabers probe 128f
Juvenile periodontitis 188 Marsupialization 274
Juxtaoral organ of Chievitz 245 Masticatory or chewing cycle 182
Materia alba 180
K Materials used for manufacturing
Keratinosomes or Odland bodies 175 instruments 59
K-file 64, 65f McCall’s festoon 185, 209
K-flex file 66 Measurement of tooth mobility 104
Koplik’s spots 251 Mechanism of
action 41
bioactive glass 169f
L
attachment of dentogingival
Laceration of gingiva 87f junction 96
Lamina Median
dura 188 cleft-face syndrome 260
propria 177 rhomboid glossitis 238
Lateral Melanin 177
periodontal cyst 242 Melkerson-Rosenthal syndrome 260
pressure 189 Mental retardation 296
rotation around hemispherical Mercury-free alloys 81
floor 13 Mesodermal odontogenic tumors 226
Liesegang rings 251 Methods of insertion 17
Leukemia 184 Michigan “O” color-coded 128
Leukoplakia 186, 239, 273 Microbiota in halitosis 115
Level of gingival margin 215 Micrognathia 238
304 Essentials of Dentistry

Micromechanical bonding 38 Odor of ammonia 119


Mikulicz’s disease 117 One osseous wall 149
Miller’s classification 104 Onlay preparation 31f
Miniblade curettes 141 Operational areas of root surfaces for
Minimal fibrotic reaction 160 Gracey cure 142
Miscellaneous instruments 71 Opsonization 181
Mixing instruments 74 Oral
Möbius syndrome 260 or outer epithelium 175
Modeling compound 9 piercing 211f
Monro’s abscess 252 submucous fibrosis 239, 273
Mouth Orange peel appearance 176f
breathing 296 Orbital blow out fracture 265
mirror 72 Orofacial digital syndrome 260
Mucogingival junction 194f Orthodontic appliance 212f
Multiloculated appearance 231f Osmotic stimuli 166
Multiple Osseous
endocrine neoplasm syndrome 260 coagulum 158
hamartoma and neoplasia craters 187
syndrome 257 Osteoid 179
Mural ameloblastoma 232 Osteomyelitis 274
Myofacial pain dysfunction Out office bleaching 52
syndrome 259
P
N
Paddle end 74
Nabers probe 128 Pain 274
Napkin 7, 8f mediators 162
Nasoethmoidal orbital fracture 284 Papillary layer 177
Neuralgia 275 Papilloma 239
Nevus 239 Papillon-Lefevre syndrome 188, 260
Newer adhesive developments 45 Papule 243
Nikolsky’s sign 252 Parasitic infections 244
Nodules 243 Paratrigeminal syndrome 261
Noncutting Parts of wedges 15
end 20f Passive eruption 177
instruments 71 Pathogenesis of bacteria 116f
Nonvital bleaching 51, 52 Pathologic migration 188
Normal sulcus 131 Pathological fracture 281
Number of Pattern of bone loss 187
blades 82 Pedodontia 293
tooth surfaces involved 148 Pedodontics 293
working ends 70 Peeso reamer 21f
Nursing caries 294 Pemphigus 186
Penetrating power 237
O Pericoronitis 186
Periodontal
Obliquely worn cusp of abscess 187
mandibular tooth 110f assessment 123
maxillary tooth 110f debridement 190
Occlusal disease and food impaction 108f
adjustment 111, 112f injury 279
displacement 14f ligament 178, 292
pit and fissure caries 26 microbiology 180
wear 109 pocket 131, 186
Occult caries 27 probe 123
Occurrence of pain 166 response to external forces 188
Odontogenic surgery 102
keratocyst 242 treatment 112
tumors 226 Periodontitis 131
Index 305

Periodontometer 105 Proximal displacement of


Periosteum 179 entire restoration 13
Periotest 106 proximal portion 13
Peripheral giant cell fibroma of bone 240 Pulp tester with lip clips 36f
Permanent Pulpectomy 295
dentition 287f Pulpotomy 295
teeth 286
Petroleum jelly 9 Q
Peutz-Jeghers syndrome 260
Questionnaire for periodontia
Phobia 294
viva voce 191
Physiologic
mesial migration 180
occlusion 181 R
recession 177 Radiation 234
rest position 182 Rake angle 61
Pierre Robin syndrome 260 Rampant caries 294
Pin-cushion effect 205 Ramsay Hunt syndrome 261
Pit and fissure sealants 294 Ratio of crown-to-root length 103
Placement of Rationale
electrode 35f for periodontal treatment 189
etchant 14 of adhesive systems 43
rubber dam 10 Reader’s syndrome 261
Plaque 243 Reamer 63f
control 171, 190 Reconstruction of orbital floor 272f
Plastic Recurrent gingivitis 185
filling instruments 74 Reduce or eliminate parafunctional
instruments 71 habits 172
rubber dam holder 5f Reduction of canal curvature 24f
Plexiform pattern 232 Refractory periodontitis 188
Plugger end 74 Regional acceleratory phenomena 153
Plummer-Vinson syndrome 260 Regurgitation esophagitis 119
Plunger cusp 108, 109f, 181, 294 Reiter’s syndrome 261
Pocket Removal of rubber dam 11
depth 129 Requirements for adhesion 38
reduction surgery 198 Residual caries 28
Porphyria 244 Restoration of marginal ridge 112f
Potassium Restorative instruments 74
ferrocyanide 171 Retainer forcep 7
nitrate dentifrices 168 Retention
Preparation for cast restoration 30f form for amalgam 12
Prepubertal and juvenile grooves and occlusal dovetail 13f
periodontitis 188 Reticular layer 177
Presence of pathologic granules 98 Retraction and access 1, 2f
Preventive orthodontics 295 Reversal line 179
Primary Reversed architecture 187
factors affecting halitosis 115 Rheumatic fever 119
retention form 12 Role of iatrogenic and or local
teeth 286 factors 181
Primer and adhesive 41 Root
Principle of periodontal caries 98
instrumentation 189 fracture 85f
Probing 129 planing 190
below contact area 131f Rootless teeth 239
depth 130f, 190 Rubber dam
of healthy sulcus and periodontal clamp 6f, 7f
pocket 132f isolation 1
technique 129, 130f sheets 4f
Proper toothbrushing technique with template 10
soft brushes 171 Rubinstein-Taybi syndrome 261
306 Essentials of Dentistry

S Stillman’s clefts 185, 209


Straightening canal 23
Safety hedstrom file 69, 69f
Strontium chloride 170
Sarcoma 243
dentifrices 168
Scaler and curette 134, 134t
Structure of chlorhexidine 203f
Scaling and root planing 208
Subgingival plaque 181
Scleroderma 186
Sulcular
Scurvy 184
epithelium 175
Sealants 9
fluid 176
Sealed environment 54
Suprabony pocket 156, 187
Second generation probes 126
Secondary Supragingival plaque 180
caries 27 Sweetish odor 119
retention form 14
Selection of method 154, 155f T
Self-injurious habit 296
Tactile sensation 165
Senile caries 26
Taper 61
S-file 69
Third generation probes 126
Sharpey’s fibers 178
Thomas and Wilms tumor 228
Sialadenitis 273
Three osseous walls 149
Sialadenosis 273
Thumb sucking 296
Sialectasis 273
TNM classification and staging 240
Sialodochitis 273
Tongue thrusting 296
Sialolithiasis 273
Tooth
Sialorrhea 273
impaction 284
Sialosis 273
mobility 101
Silver nitrate 171
preparation 12
Simple fracture 280
Site Toothbrush trauma 212f
for placement of electrode 34f Tooth-supporting structure 178
of fracture 281 Total etch system 46
Sizes of Transgingival probing or sounding 152
Gates Glidden drill 20 Transitory halitosis 114
Peeso reamer 21 Trauma from occlusion 102, 180
Sjögren’s syndrome 117, 261 Traumatic occlusion 181
Smooth surface caries 26 Treacher Collins syndrome 261
Soap bubble appearance 230 Tricalcium phosphate 160
Sodium Trigeminal neuralgia 274
monofluorophosphate 168 Trotter’s syndrome 261
silicofluoride 170 True periodontal pocket 187
Soft tissue phase 153 Tubule sealants 169
Solid multicystic lesion 233 Two osseous walls 149
Space Types of
maintainer 295 fracture 280
maintenance 295 geographic tongue 245
Spatula 74 pulp testers 33
Specific characteristic of breath wedges 15
odor 121
Sphenopalatine neuralgia 259 U
Spiral pocket 187
Spoon test 120 Ulcer 243
Squamous cell carcinoma 243 Ultrasonic curettage 145
Stages Uncomplicated
and steps for tooth preparation 12 crown-root fracture 85f
of tooth mobility 104 fracture with involvement of
Stainless steel 59t dentin 85
Stannous fluoride 170 Universal rubber dam template 10f
Steps for placement of rubber dam 10 Uremic odor 119
Stevens-Johnson syndrome 261 Usefulness in preparing root canals 22
Index 307

V Wedging effect due to occlusal


wear 109f
Vertical Width of attached gingiva 174, 210f
dimension of occlusion 182 Williams probe 128
food impaction 107 Winter’s lines 285f
tooth mobility 105
Vincent’s angina 186 X
Vital bleaching 51
Xenografts 160
Xerostomia 273
W X-radiation 234
Walking bleach 54f
Wallenberg’s syndrome 261 Z
Waterhouse-Friderichsen syndrome 261 Zenker’s diverticulum 119
Waters view 267 Zero-walled defects 150
Waxed dental floss 9f Zinc chloride 171
Wedge Zone of
design 18f advanced dental caries 244
insertion 17f enamel caries 244

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