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Essentials of

Clinical Periodontology

and

Periodontics

Shantipriya Reddy

BDS MDS (Periodontia)

Professor

Dr Syamala Reddy Dental College and Hospital

Bengaluru, Karnataka, India

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Essentials of Clinical Periodontology and Periodontics

© 2008, Shantipriya Reddy

All rights reserved. No part of this publication and DVD ROM should be reproduced, stored in a retrieval system, or transmitted in any
form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the
author and the publisher.

This book has been published in good faith that the materials provided by author is original. Every effort is made to ensure
accuracy of material, but the publisher, printer and author will not be held responsible for any inadvertent error(s). In case of any
dispute, all legal matters are to be settled under Delhi jurisdiction only.

First Edition: 2006
Second Edition: 

2008

ISBN 81-8448-148-9

Typeset at  JPBMP typesetting unit
Printed  at  Ajanta  Offset

Dedicated to

My late grandfather, who had believed in my abilities, it is because of

whom I chose this profession.

My grandmother, for her constant support.

My father and mother, for always being there.

My uncle for his continuous encouragement.

My husband for his unique mentorship.

My daughter and son for being so understanding

Any book requires the help and assistance of others in order to be completed successfully. In this regard, I would
like to extend special thanks to all those who had helped to accomplish this goal. First and foremost I would
like to thank my student Dr Deepti Sinha for drawing those excellent diagrams inserted in this book. Special
thanks must go to all my colleagues, postgraduate students, (Drs) Jeeth Rai, Keshav, Satish, Shabeer and Anil,
Mamatha and Sumaira, who have helped me to prepare the manuscript. I would like to extend my special thanks
to Dr Anil Kumar who helped me to collect the photographs used in this book. I am very grateful to Dr Prasad
MGS and Dr Sabna Kakarala for being so generous with their clinical photographs which helped to enhance
the overall excellence of this edition. Dr Divakaranand and Dr Rudrakshi’s helped in typing the manuscript of
this edition is greatly appreciated. My heartfelt thanks to Dr Srinivas for helping me in writing the chapter on
Oral Malodor. I would also like to thank Dr Ashwath (Smart desq navigators) for helping me with animation
photographs of various suturing techniques. The excellent co-operation of the publisher is also greatly acknowledged.

Acknowledgements

Preface to the Second Edition

I am extremely happy to present the second edition of Essentials of Clinical Periodontology and Periodontics.
Three new chapters including glossary of periodontal terminology has been included in this edition. Chapters
on Host Modulation and Oral Malodor are written with same clarity and simplicity, that has been religiously
followed in the previous edition. More photographs have been included to make the student understand the
subject better.

I thank all the fellow colleagues and students who have supported me with useful suggestions while revising

the first edition. I hope to receive the same support and suggestions for the second edition also.

Shantipriya Reddy

This basic text when conceived in the year 2003 has been written in an attempt to make our understanding
of periodontal disease accessible to the undergraduate students, general practitioners and dental hygienists. The
Essentials of Clinical Periodontology and Periodontics is a learning textbook intended to serve the needs of several
groups of dental care professionals and is written with credibility and readability maintained at every level.
Undergraduate students especially will find it useful in integrating the concepts they have been taught in a more
elaborate way. Clarity and simplicity in language has been my objective while writing this book. The organization
of the chapters and the key points with review questions at the end of every chapter serve as a programmed-
guide for the reader.

This text can be of help for the academicians to re-think the modes of presenting information and also as

a model to test whether the students have grasped the concepts they have been taught and are able to use
them in a practical manner.

All the efforts have been made to make the text as accurate as possible and the information provided in

this text was in accordance with the standards accepted at the time of publication. In order to attain these goals,
suggestions as well as critiques from many students and clinicians have been received and utilized.

Much of the style in this textbook is compact with adequate bibliographies. The reader is advised to use them

to gain greater depth of knowledge. The way of periodontist is hard and this book will reflect the difficulty of
that path. I hope that this textbook will fulfill all the requirements and expectations of the students and practitioners
as this is a special branch of our profession. The field of periodontics remains a work in progress.

Shantipriya Reddy

Preface to the First Edition

HISTORICAL BACKGROUND OF PERIODONTOLOGY

Various forms of gingival and periodontal diseases have affected the human race since the dawn of history. In
the earlier historical records almost all the writings have information regarding the diseases affecting oral cavity
and majority of it is about periodontal diseases.

Early Civilizations

Summerians of 3,000 BC first practiced oral hygiene. Babylonians and Assyrians, who also have suffered from
periodontal diseases, have treated themselves using gingival massage combined with various herbal medications.
Research on embalmed bodies of the ancient Egyptians pointed out that periodontal disease was the most common
of all the diseases. Medical writings of the time Ebers Papyrus had many references to gingival diseases and also
contain various prescriptions for strengthening the teeth and gums.

The medical works of ancient India, Susruta Samhita and Charaka Samhita describe severe periodontal disease

with loose teeth and purulent discharge from the gingiva and the treatment advised was to use a stick that is
bitter for cleaning teeth.

Periodontal disease was also discussed in Ancient Chinese books. The oldest book written in 2,500 BC describes

various conditions affecting oral cavity. Gingival inflammation, periodontal abscesses and gingival ulcerations are
described in detail. They were among the earliest people to use the toothbrush to clean the teeth.

Middle Ages

The systematic therapeutic approach was not developed until the middle ages. This was a period of golden age
of Arabic science and medicine. Avicenna and Albucasis made a refined, novel approach to surgical work. Albucasis
had a clear understanding of calculus as etiology of periodontal disease and described the technique of removing
it. He had also developed a set of scalers for removing calculus. He also wrote in detail on other treatment
procedures like extraction of teeth, splinting loose teeth with gold wire, etc.

18th Century

Modern dentistry was developed in 18th century. Pierre Fauchard in 1678 who is rightly considered as Father
of Modern Dentistry designed periodontal instruments and described the technique in detail. His book “The
Surgeon Dentist” published in 1728 presented all aspects of dental practice (i.e. restorative dentistry, prosthodontics,
oral surgery, periodontics and orthodontics). Fauchard wrote in that, confections and sweets destroy the teeth
by sticking to the surfaces producing an acid. John Hunter (1728-93) known as an anatomist, surgeon and
pathologist of 18th century wrote a book entitled “The Natural History of the Human Teeth” describing the
anatomy of the teeth and their supporting structures with clear illustrations.

Prolog

Thomas Berdmore (1740-85) known as “Dentist to His Majesty” published the Treatise in the disorders and

deformities of the teeth and gums. He not only offered detailed descriptions of instrumentation but also stressed
on prevention.

19th Century

A German born dentist, Leonard Korecker in his paper Philadelphia Journal of Medicine and Physical Sciences
mentioned the need for oral hygiene by the patient, to be performed in the morning and after every meal using
an astringent powder and a toothbrush.

Levi Spear Parmly was considered the Father of Oral Hygiene and the Inventor of Dental Floss. The name

“Pyorrhea Alveolaris” was used to describe periodontal disease. John W Riggs was the first individual to limit
his practice to periodontics and was considered the first specialist in this field. Periodontitis was known as “Riggs
disease.” Several major developments took place in the second half of the 19th century starting the era called
modern medicine.

The first was the discovery of anesthesia and second scientific breakthrough was made by Louis Pasteur who

established the Germ Theory of Disease. The third scientific finding was the discovery of radiographs by Wilhelm
Roentgen.

Also the late 19th century has witnessed a proper understanding of the pathogenesis of periodontal disease

based on histopathologic studies. GV Black in 1899 gave the term gelatinous microbic plaque and described
its relationship to caries. Xenophon recognized ANUG in 4th century BC Salomon Robicsek developed a surgical
technique called gingivectomy.

20th Century

Early 20th century witnessed major changes in the treatment of periodontal disease. Gottlieb published extensive
microscopic studies of periodontal diseases in humans. It was realized that, removal of calculus and other deposits
was not enough. In addition, removal of periodontal pockets was necessary to control the disease.

Leonard Widman and Newman described flap surgery for the removal of periodontal pockets. Removal of

bone was considered essential at that time.

After World War II, the focus was on periodontal research and this led to a better understanding to the pathological,

microbiological and immunological aspects of periodontal disease.

The first workshop in periodontology was conducted in 1951. It was realized at that time, scientific methods

should be introduced in the periodontal research. Subsequent workshops conducted in periodontics has witnessed
significant scientific contributions in the field of periodontics.

JOURNALS OF PERIODONTOLOGY

The various journals of periodontology available are:

• The Journal of Periodontology by Robert. J.Genco.

• Journal of Periodontal Research by Isao Ishikawa, Jorgen Slots, Maurizio Tonetti

• Journal of Clinical Periodontology by Jan Lindhe.

• Periodontology 2000 by Jorgen Slots.

• International Journal of Periodontics and Restorative Dentistry in India by Myron Nevins.
• Journal of Indian Society of Periodontology.

xiv

Essentials of Clinical Periodontology and Periodontics

Contents

Part I: The Normal Periodontium

Chapter 1: Anatomy and Development of the Structures
of Periodontium, 3

Introduction, 3
External Anatomic Features, 3
Development of Periodontium, 4

Early Development of Cementum, 4
Later Development of Cementum, 5
Development of Junctional Epithelium, 6

Chapter 2: Biology of Periodontal Tissues, 8

Introduction, 8
The Gingiva, 8
Macroscopic Features, 8

Marginal Gingiva, 8
Gingival Sulcus, 9
Attached Gingiva, 9
Interdental Gingiva, 9

Microscopic Features, 10

Morphologic Characteristics of the Different Areas of

Gingival Epithelium, 11

Cells of the Basal Layer, 11
Stratum Spinosum, 11
Stratum Granulosum, 12
Stratum Corneum, 12

Oral Sulcular Epithelium, 12
Junctional Epithelium, 12

Epithelium-Connective Tissue Interface, 13
Supra-alveolar Connective Tissue, 14

Cells, 14
Fibers, 14

Principal Fibers, 15
Secondary Fibers, 15

Blood Supply, Lymphatics and Nerves, 16
Periodontal Ligament, 16

Definition, 16

Structure, 16

Synthetic Cells, 17
Resorptive Cells, 17
Epithelial Cell Rests of Malassez, 17

Extracellular Components, 18

Fibers, 18

Principal Fibers, 18

Ground Substance, 19

Development of Principal Fibers, 19
Structure Present in the Connective Tissue, 20
Functions of Periodontal Ligament, 20
Clinical Considerations, 21

Alveolar Bone, 22

Definition, 22
Parts of Alveolar Bone, 22
Composition of Alveolar Bone, 22
Osseous Topography, 23
Fenestrations and Dehiscences, 23
Blood Supply to the Bone, 24
Clinical Considerations, 25

Cementum, 25

Definition, 25
Classification, 25
Functions, 26
Composition, 26
Cementoenamel Junction, 26
Cemental Resorption and Repair, 27

Chapter 3: Periodontal Structures in Aging Humans, 30

General Effects of Aging, 30

Skin, 30
Bone, 30

Age Changes in the Periodontium, 30

Oral Mucosa, 30
Periodontal Ligament, 31
Alveolar Bone and Cementum, 31
Bacterial Plaque and Immune Response, 31

Effects of Aging on the Progression of Periodontal Diseases, 31
Effects of Treatment on the Aging Individuals, 31

xvi

Essentials of Clinical Periodontology and Periodontics

Part II: Classification and Epidemiology of

Periodontal Diseases

Chapter 4: Classification Systems of Periodontal
Diseases, 35

Need for Classification, 35
Current Classification Systems of Periodontal Diseases,35

World Workshop in Clinical Periodontics (1988), 35
World Workshop in Clinical Periodontics (1989), 36
Genco (1990), 36
Ranney (1993), 36
European Workshop on Periodontology (1993), 36
AAP 1999 (International Workshop of Periodontal

Disease), 37

Synopsis of Types and Characteristics of Gingival

Diseases, 38

Synopsis of Types and Characteristics of Periodontal

Diseases, 39

Chapter 5: 

Epidemiology of Gingival and Periodontal

Diseases, 41

Definition, 41
Types of Epidemiologic Research, 41

Descriptive Study, 41
Analytical Study, 42
Experimental Epidemiology, 42

Index, 42

Definition, 42
Purposes and Uses of Index, 42
Characteristics of Index, 43

Various Indices Used to Assess Periodontal Problems, 43

To Assess Gingival Inflammation, 44

Papillary Marginal Attachment (PMA), 44
Gingivitis Component of Periodontal Disease, 44
Gingival Index by Loe H and Sillness J (1963), 44

Indices of Gingival Bleeding, 45

Sulcular Bleeding Index, 45
Papillary Bleeding Index, 45
Bleeding Points Index, 45
Interdental Bleeding Index, 45
Gingival Bleeding Index, 45

Indices Used to Measure Periodontal Destruction, 46

Russell’s Periodontal Index, 46
Periodontal Disease Index, 46
Extent and Severity Index, 47
Radiographic Approach, 47
The Periodontitis Severity Index, 47

Indices Used to Measure Plaque Accumulation, 47

Plaque Component of Periodontal Disease

Index, 47

Simplified Oral Hygiene Index, 48
Turesky-Gilmore-Glickman, 49
Plaque Index, 49
Modified Navy Plaque Index, 49

Plaque-free Score, 50
Papillary Bleeding on Probing, 50

Indices Used to Measure Calculus, 51

Calculus Component of Simplified Oral Hygiene

Index, 51

Probe Method of Calculus Assessment, 51
Calculus Surface Index, 51
Marginal Line Calculus Index, 51

Indices Used to Assess Treatment Needs, 51

Gingival Periodontal Index, 51
Community Periodontal Index of Treatment Needs,

52

Periodontal Treatment Need System, 52

Part III: Etiopathogenesis

Chapter 6: 

Periodontal Microbiology (Dental Plaque), 57

Definition, 57
Dental Plaque as a Biofilm, 57
Types of Dental Plaque, 57

Supragingival Plaque, 58
Subgingival Plaque, 58

Tooth-associated Subgingival Plaque, 58
Epithelium-associated Subgingival Plaque, 58
Connective Tissue-associated Plaque, 59

Composition of Dental Plaque, 59
Formation/Development of Dental Plaque, 59
Structural and Microscopic Properties of Plaque, 61
Clinical Significance of Plaque, 62
Microbial Specificity of Periodontal Diseases, 62

Non-specific Plaque Hypothesis, 62
Specific Plaque Hypothesis, 62

What Makes Plaque Pathogenic, 63
Microorganisms Associated with Periodontal Diseases, 63

Chapter 7: Calculus and Other Etiological Factors, 66

Calculus, 66

Definition, 66
Types, 66

Supragingival Calculus, 66
Subgingival Calculus, 66

Structure, 67
Composition, 67
Difference Between Supragingival and Subgingival

Calculus, 68

Formation of Calculus, 68
Pathogenic Potential of Calculus in Periodontal

Diseases, 69

Other Contributing Etiological Factors Including Food
Impaction, 69

Iatrogenic Factors, 69

Faulty Restorations, 69
Margins of Restorations, 69
Contour of Restorations, 69
Occlusion, 70

xvii

Contents

Material, 70
Design of Removable Partial Dentures, 70

Periodontal Problems Associated with Orthodontic

Therapy, 71

Food Impaction, 71
Unreplaced Missing Teeth, 71
Malocclusion, 72
Habits, 72

Chapter 8: Host Response: Basic Concepts, 76

Introduction, 76
Role of Saliva in the Host Defence, 76
Gingival Epithelium, 77
Gingival Crevicular Fluid, 77
Complement, 77
Inflammatory Cell Response, 78

Neutrophils, 78

Neutrophil Disorder Associated with Periodontal Disease,

80

Periodontal Diseases Associated with Neutrophil

Disorders, 80

Functions of Macrophages, 81
Immunological Mechanism, 82

Anaphylactic Reactions, 83
Cytotoxic Reactions, 84
Arthus Reactions, 84
Delayed Hypersensitivity, 84

Chapter 9: Trauma from Occlusion, 87

Physiologic Adaptive Capacity of the Periodontium to

Occlusal Forces, 87

Trauma from Occlusion, 87

Definition and Terminology, 87
Types, 88
Signs and Symptoms, 88
Histologic Changes, 89

Injury, 89
Repair, 89
Adaptive Remodeling, 89

Reversibility of Traumatic Lesion, 90
Effect of Increased Occlusal Forces on Pulp, 90

Role of the Trauma from Occlusion in the Progression of

Periodontal Disease, 90

Pathologic Tooth Migration, 92

Chapter 10: Role of Systemic Diseases in the Etiology
of Periodontal Diseases, 95

Introduction, 95
Dietary and Nutritional Aspects of Periodontal Disease,

95

Consistency of Diet, 95
Protein Deficiency, 96
Vitamin D Deficiency, 96

Effects of Hematological Disorders on Periodontium, 97

White Blood Cell Disorders, 97

Neutropenias, 97
Leukemia, 98
Thrombocytopenic Purpura, 99
Disorders of WBC Function, 99

Red Blood Cell Disorders, 99

Anemia, 99

Metabolic and Endocrine Disorders, 100

Diabetes mellitus, 100
Thyroid Gland, 101
Pituitary Gland, 101
Parathyroid Glands, 101
Gonads, 102

Cardiovascular Diseases, 103

Arteriosclerosis, 103

Antibody Deficiency Disorders, 103

AIDS, 103
HIV, 103

Other Systemic Diseases, 104

Bismuth Intoxication, 104
Lead Intoxication, 104
Mercury Intoxication, 104

Psychosomatic Disorders, 104

Chapter 11: Oral Malodor, 106

Introduction, 106
Classification of Halitosis, 106

Pseudo-halitosis, 106
Halitophobia, 107

Etiology, 107

Causes for Physiologic Halitosis, 107
Causes for Pathologic Halitosis, 107

Diagnosis of Halitosis, 107

Clinical Examination, 107
Measurement of Oral Malodor, 107

Organoleptic Method, 107
Gas Chromatography, 108
Halimeters, 108
BANA, 108
Chemiluminescence, 108

Treatment and Management of Oral Malodor, 108
Summary, 109

Chapter 12:  Pathogenesis of Periodontal Diseases, 110

Introduction, 110

Role of Bacterial Invasion, 110
Role of Exotoxins, 110
Role of Cell Constituents, 111
Role of Enzymes, 111
Evasion of Host Responses, 111

Host Derived Bone Resorbing Agents, 112

Cytokines, 113
Prostaglandins, 113

Chapter 13: Periodontal Medicine, 115

Introduction, 115
Era of Focal Infection, 115
Periodontal Disease and Coronary Heart Disease/

Atherosclerosis, 116

Effect of Periodontal Infection, 117

Ischemic Heart Disease, 117
Thrombogenesis, 117

Periodontal Infection and Stroke, 118
Periodontal Disease and Diabetes Mellitus,  118
Role of Periodontitis in Pregnancy Outcome, 119
Periodontal Disease and Chronic Obstructive Pulmonary

Disease, 119

Periodontal Disease and Acute Respiratory Infection, 120
Periodontal Medicine in Clinical Practice, 120

Chapter 14: Smoking and Periodontal Diseases, 122

Effect of Smoking on the Prevalence and Severity of

Periodontal Disease, 122

Effect of Smoking on the Etiology and Pathogenesis of

Periodontal Disease, 122

Microbiology, 122
Immunology, 122
Physiology, 123

Effect of Smoking on the Response to Periodontal

Therapy, 123

Effect of Smoking Cessation, 123

Chapter 15: Host Modulation in Periodontal Therapy,125

Introduction, 125
Regulation of Immune and Inflammatory Responses, 125
Excessive Production of MMP’s, 126

Role of MMP’s in Human Periodontal Diseases, 126

Production of Arachidonic Acid and Metabolites, 126
Regulation of Bone Metabolism, 127

Part IV: Periodontal Pathology

SECTION 1: GINGIVAL DISEASES

Chapter 16: Defence Mechanisms of the Gingiva, 131

Defence Mechanisms, 131

Non-specific Mechanisms, 131

Bacterial Balance, 131
Surface Integrity, 131
Surface Fluid and Enzyme, 131
Phagocytosis, 131
Inflammatory Reaction, 132

Specific Protective Mechanism, 132
Sulcular Fluid, 132

Anatomy of Gingival Crevice, 132
Significance of Gingival Sulcus and Fluid, 133
Significance of Gingival Vasculature and

Crevicular Fluid, 133

Permeability of Sulcular and Junctional Epithelia,

133

Methods of Collection, 134

Absorbing Paper Strips, 134
Micropipettes, 134
Gingival Washings, 135
Other Methods, 135

Composition of GCF, 135
Clinical Signficance, 138
Drugs in Gingival Fluid, 138
Influence in Mechanical Stimuli, 138
Periodontal Therapy and Gingival Fluid, 139

Chapter 17: Gingival Inflammation, 140

Introduction, 140
Initial Lesion, 140
Early Lesion, 141
Established Lesion, 141
Advanced Lesion, 142

Chapter 18: Clinical Features of Gingivitis, 143

Types of Gingivitis, 143

Depending on the Course and Duration, 143
Depending on the Distribution, 143

Clinical Findings, 143

Gingival Bleeding on Probing, 144
Color Change, 147
Change in Consistency, 147
Change in Size, 147
Surface Texture, 148
Position, 148

Recession, 148

Classification and Etiology, 148
Clinical Significance, 150

Chapter 19: Gingival Enlargements, 151

Introduction, 151
Classification, 151
Inflammatory Enlargement, 152

Acute Inflammatory Enlargement, 152
Chronic Inflammatory Enlargement, 153

Non-inflammatory Enlargement, 154

Phenytoin-induced Gingival Hyperplasia, 155
Idiopathic Gingival Fibromatosis, 157
Combined Enlargement, 157

Enlargement Associated with Systemic Disease or

Condition, 159

Conditioned Enlargement, 159
Enlargement in Pregnancy, 159
Enlargement in Puberty, 160
Vitamin C Deficiency, 160
Plasma Cell Gingivitis, 161
Granuloma Pyogenicum, 161
Systemic Disease Causing Gingival Enlargement, 161
Granulomatous Diseases, 163

xviii

Essentials of Clinical Periodontology and Periodontics

Neoplastic Enlargement, 165

Benign Tumors, 165
Malignant Tumors, 165

False Enlargement, 165

Underlying Osseous Lesions, 166
Underlying Dental Tissues, 166

Chapter 20: Acute Gingival Infections, 167

Classification of Various Acute Gingival Lesions, 167
Acute Necrotizing Ulcerative Gingivitis, 168

Terminology, 168
Clinical Features, 168
Intraoral/Extraoral Signs and Symptoms, 168
Clinical Course, 169
Etiology, 169
Histopathology, Diagnosis and Treatment, 170

Acute Herpectic Gingivostomatitis, 172

Clinical Features, 172
Etiology, 172
History, 173
Histopathology, 173
Diagnosis, 173
Differential Diagnosis, 173
Treatment, 174

Pericoronitis, 174

Definition, 174
Types, 174
Clinical Features, 174
Complications, 175
Treatment, 175

Chapter 21: Periodontal Diseases in Children and
Young Adolescents, 177

Introduction, 177
Anatomic Considerations in Children, 177

Gingiva, 177
Cementum, 177
Periodontal Ligament and Alveolar Bone, 178

Histopathology of Gingivitis in Children, 178
Microbiology of Periodontal Diseases in Children, 178
Classification of Periodontal Diseases in Children, 178
Gingival Lesions, 178

Acute Herpetic Gingivostomatitis, 178
Candidiasis, 180
Gingivitis Artefacta, 181
Localized Gingival Recession, 181

Types of Periodontitis, 181

Prepubertal Periodontitis, 181
Juvenile Periodontitis, 181

Periodontitis Associated with Syndromes, 183

Papillon-Lefévre Syndrome, 183
Ehler-Danlos Syndrome, 183
Down’s Syndrome, 183
Neutropenias, 183
Chédiak-Higashi Syndrome 183
Hypophosphatasia, 183

Chapter 22: Desquamative Gingivitis, 185

Introduction, 185
Diagnosis, 185
Clinical Features, 185

Mild Form, 185
Moderate Form, 186
Severe Form, 186

Histopathology, 186
Therapy, 186

Local Treatment, 186
Systemic Treatment, 188

Diseases Clinically Presenting as Desquamative

Gingivitis, 188

Lichen Planus, 188
Cicatricial Pemphigoid, 189
Bullous Pemphigoid, 189
Linear IgA Disease, 190
Dermatitis Herpetiformis, 190
Pemphigus Vulgaris, 190
Drug Reaction or Eruptions, 191

SECTION 2: PERIODONTAL DISEASES

Chapter 23: The Periodontal Pocket, 192

Introduction, 192
Definition, 192
Classification of Pockets, 192
Clinical Features, 193

Signs and Symptoms, 193

Pathogenesis, 194
Histopathology, 197

Changes in the Soft Tissue Wall, 197
Microtopography of the Gingival Wall of the Pocket, 197
Periodontal Pocket as Healing Lesions, 197
Pocket Contents, 198
Changes in Root Surface Wall, 198
Periodontal Disease Activity, 198

Relation of Loss of Attachment and Bone Loss to Pocket

Depth, 198

Periodontal Cyst, 198
Differences Between Suprabony and Infrabony Pocket,

200

Determination of Pocket Depth, 200
Treatment of Periodontal Pocket, 200

Chapter 24: Bone Loss and Patterns of Bone
Destruction, 202

Introduction, 202
Normal Anatomy of Alveolar Bone, 202
Mechanism of Bone Formation and Bone Destruction, 202

Local Factors, 203

Gingival Inflammation, 203
Trauma from Occlusion, 204

Systemic Factors, 204

Pharmacological Agents and Bone Resorption,

204

xix

Contents

Radius of Action, 204
Rate of Bone Loss, 204
Periods of Destruction, 204

Factors Determining Bone Morphology in Periodontal

Disease, 205

Bone Destruction Patterns in Periodontal Disease, 205

Angular Defects, 205
Osseous Craters, 206
Bulbous Bony Contours, 206
Reversed Architecture, 206
Ledges, 207
Furcation Involvements, 207

Prevalence and Distribution of Bone Defects, 207

Chapter 25: Chronic Periodontitis, 209

Introduction, 209
Definition, 209
Diagnostic Criteria, 209

Clinical Features, 209
Microbiological Features, 210
Radiographic Features, 210

Types Based on Disease Distribution and Severity, 210
Nature of Disease Progression, 211
Risk Factors for Disease, 211
General Concept for Etiology, 212

Chapter 26: Aggressive Periodontitis, 213

Introduction, 213
Localized Aggressive Periodontitis, 213

Historical Background, 213
Clinical Features, 214
Radiographic Findings, 215
Histopathologic Features, 215
Bacteriology, 215
Immunology, 216
Treatment, 216

Generalized Aggressive Periodontitis, 216

Clinical Characteristics, 216
Radiographic Findings, 217
Risk Factors, 217

Microbiologic Factors, 217
Immunologic Factors, 217
Genetic Factors, 217
Environmental Factors, 217

Chapter 27: Necrotizing Ulcerative Periodontitis,
Refractory Periodontitis and Periodontitis as a
Manifestation of Systemic Disease, 218

Necrotizing Ulcerative Periodontitis (NUP), 218

Non-AIDS type, 218
AIDS associated, 219

Refractory Periodontitis, 219

Etiology, 219

Clinical Features, 219
Treatment, 220

Periodontitis as a Manifestation of Systemic Disease, 220

Papillon-Lefévre Syndrome, 220
Chédiak-Higashi Syndrome, 221
Down Syndrome, 221
Hypophosphatasia, 221
Neutropenia, 221
Leukocyte Adhesion Deficiency, 221

Chapter 28: AIDS and the Periodontium, 223

HIV Opportunistic Infections, 223
Classification of Periodontal Diseases Associated with

HIV Infection, 223

Linear Gingivitis, 224
Necrotizing Ulcerative Gingivitis, 224
Necrotizing Ulcerative Periodontitis, 224
Necrotizing Stomatitis, 224
CDC Surveillance Care Classification, 224

Most Common Oral and Periodontal Manifestations of HIV

Infection, 225

Oral Hairy Leukoplakia, 225
Oral Candidiasis, 225
Kaposi’s Sarcoma, 225
Bacillary Angiomatosis, 225
Oral Hyperpigmentation, 225
Atypical Ulcers and Delayed Healing, 225

Management, 225

Part V: Treatment of Periodontal Diseases

SECTION 1: DIAGNOSIS, PROGNOSIS AND

TREATMENT PLAN

Chapter 29: Diagnosis of Periodontal Diseases, 229

Periodontal Diagnosis, 229
Principles of Diagnosis, 229
Clinical Diagnosis, 229

Stages of Diagnosis, 229
Diagnosis with Detailed Case History Recording, 230

Case History Proforma, 232

Chapter 30: Determination of Prognosis, 237

Definition of Prognosis, 237
Difference Between Prognosis and Risk, 237
Determination of Prognosis, 237
Factors for Determination of Prognosis, 238

Overall Clinical Factors, 238
Systemic/Environmental Factors, 239
Local Factors, 240
Prosthetic/restorative Factors, 241

Relationship Between Diagnosis and Prognosis, 241
Re-evaluation of Prognosis After Phase I Therapy, 243

Essentials of Clinical Periodontology and Periodontics

xx

Chapter 31: Related Risk Factors Associated with
Periodontal Diseases, 244

Definition, 244
Risk Factors, 244
Risk Determinants, 245
Risk Indicators, 245
Risk Markers/Predictors, 245
Clinical Risk Assessment, 246

Demographic Data, 246
Medical History, 246
Dental History, 246
Clinical Examination, 246

Chapter 32: Various Aids Including Advanced
Diagnostic Techniques, 247

Aids used in Clinical Diagnosis, 247

Periodontal Probes, 247
Conventional Probes, 247
PSR, 248

Aids used in Radiographic Diagnosis, 249

Orthopantomograph, 249
Xeroradiography, 249
Advanced Radiographic Techniques, 249

Iodine-125, 249
Photodensitometric Analysis, 250
Digital Radiography, 250
Subtraction Radiography, 250
CADIA, 250
Nuclear Medicine Bone Scan, 250

Aids in Microbiological Diagnosis, 250

Identification of Bacteria, 250
Speciation Techniques, 251

DNA Probes, 252

Aids in Immunological Diagnosis, 252

Immunofluorescence, 252
Latex Agglutination, 252
ELISA, 253
Flow Cytometry, 253

Biochemical Diagnosis, 253

Prostaglandins, 253
Collagenase, 253

Other Diagnostic Aids, 253

BANA Test, 253
FSEIA, 254
PCR, 254

Chapter 33: Treatment Plan, 256

Introduction, 256
Sequence of Therapeutic Procedures, 256

Emergency Phase, 256
Etiotropic Phase, 256
Surgical Phase, 256
Restorative Phase, 256

Preferred Sequence of Periodontal Therapy, 257

Chapter 34: Rationale for Periodontal Treatment, 258

Objectives of Periodontal Therapy, 258
Factors which Affect Healing, 259

Local Factors, 259
Systemic Factors, 259

Healing After Periodontal Therapy, 259

Regeneration, 259
Repair, 259
New Attachment, 259
Reattachment, 259

Chapter 35: Periodontal Instrumentarium, 262

Periodontal Instruments, 262
Classification of Periodontal Instruments, 262

Diagnostic Instruments, 262

Periodontal Probes, 263
Explorers, 264

Scaling and Root Planing, and Curettage Instruments,

262

Sickle Scalers, 264
Curettes, 265
Ultrasonic Instruments, 267
Dental Endoscope, 267

Cleansing and Polishing Instruments, 267
Surgical Instruments, 268

SECTION 2: PERIODONTAL THERAPY

(A) Non-Surgical Therapy

Chapter 36: Principles of Periodontal Instrumentation
including Scaling and Root Planing, 269

Introduction, 269
Accessibility, 269

Clinician Position, 269
Patient Position, 269

Visibility, Illumination and Retraction, 270
Condition of Instruments, 271
Maintaining a Clean Field, 271
Instrument Stabilization, 271

Instrument Grasp, 271
Finger Rest, 272

Instrument Activation, 273

Adaptation, 274
Angulation, 274
Lateral Pressure, 274
Strokes, 274
Stroke Direction, 275

Principles of Scaling and Root Planing, 275

Root Planing, 275
Supragingival Scaling Technique, 276
Subgingival Scaling, 276

Ultrasonic Instruments, 277

Aerosol Production, 278

xxi

Contents

Chapter 37: Plaque Control, 280

Definition, 280
Goals of Plaque Control Measures, 280
Rationale, 280
Basic Approaches for Plaque Control, 280
Mechanical Plaque Control, 280

Toothbrush, 281
Brushing Techniques, 282

Bass Method, 282
Modified Bass Method, 283
Stillman’s Method, 283
Modified Stillman’s Method, 283
Charter’s Method, 283
Roll Method/Fones Technique, 283

Powered Toothbrushes, 284
Dentifrices, 284
Interdental Cleaning Aids, 285
Other Aids, 286

Chemical Plaque Control, 286

Ideal Properties of a Mouthwash, 287
Classification of Antimicrobial Agents, 287

Bisbiguanides, 288

Disclosing Agents, 289

Section B: Surgical Therapy

Chapter 38: Principles of Periodontal Surgery, 291

Indications, 291
Contraindications, 291
General Principles of Surgery, 291

Patient Preparation, 292
Premedication, 292
Tissue Management, 292
Suturing Material, 292
Suturing Techniques, 293
Periodontal Dressing, 293
Instructions for the Patient After Surgery, 299

Complications During Surgery, 300

Syncope, 300
Hemorrhage, 300

Complications in the First Postoperative Week, 300
Hospital Periodontal Surgery, 301

Chapter 39: Gingival Curettage, 303

Definition, 303
Types, 303
Rationale, 303
Indications, 304
Procedure, 304

Basic Technique, 304
ENAP, 304
Ultrasonic Curettage, 305
Caustic Drugs, 305

Healing After Scaling and Curettage, 305
Clinical Appearance After Scaling and Curettage, 305

Chapter 40: Gingivectomy, 307

Introduction, 307
Definitions, 307
Pre-requisites, 307
Indications, 307
Contraindications, 308
Types of Gingivectomy, 308

Surgical Gingivectomy, 308
Procedure for Gingivoplasty, 310
Healing After Surgical Gingivectomy, 310
Electrosurgery, 310
Laser Gingivectomy, 312
Gingivectomy by Chemosurgery, 312

Chapter 41: Periodontal Flap, 314

Introduction, 314
Indications/Objectives of Flap Surgery, 314
Definition, 315
Classification, 315
Incisions, 316
Flap Techniques for Pocket Therapy, 320

Modified Widman Flap, 320
Undisplaced Flap, 325
Palatal Flap, 326
Apically-displaced Flap, 328
Distal Molar Surgery, 328

Healing After Flap Surgery, 329

Chapter 42: Osseous Surgery, 330

Definition, 330
Rationale, 330
Terminology, 330
Types of Osseous Surgery, 331
Resective Osseous Surgery, 331

Indications, 331
Contraindications, 331

Methods of Osseous Surgery, 332

Instruments Used, 332
Technique, 332

Vertical Grooving, 332
Radicular Blending, 332
Flattening of Interproximal Bone, 332
Gradualizing Marginal Bone, 332

Healing After Resective Osseous Surgery, 333
Reconstructive Osseous Surgery, 333

Evaluation of New Attachment, 333

Clinical Method, 333
Radiographic Methods, 333
Surgical Re-entry,  333
Histological Methods, 333

Nongraft-associated New Attachment, 334

Removal of Junctional and Pocket Epithelium, 334
Prevention of Epithelial Migration, 334

GTR, 334
Root Biomodification, 336

xxii

Essentials of Clinical Periodontology and Periodontics

Graft-associated New Attachment, 336

Terminology, 336
Ideal Requirements of a Bone Graft Material, 337
Autografts, 337
Allografts, 338
Xenografts, 338
Alloplasts, 338

Chapter 43: Mucogingival Surgery, 341

Definition, 341
Mucogingival Problems, 341
Objectives, Indications and Contraindications of

Mucogingival Surgery, 341

Techniques to Increase the Width of Attached Gingiva, 342

Free Soft Tissue Autograft, 342
Classic Technique, 342
Variant Techniques, 344

Accordian Technique, 346
Strip Technique, 346
Connective Tissue Technique, 346
Combination Techniques, 346

Healing of the Graft, 346
Apically-Displaced Flap, 346
Other Techniques, 348

Procedures for Root Coverage, 348

Indications, 348
Classification, 349
Conventional Procedures, 351

Laterally Displaced Flap, 352
Double Papilla Flap, 353
Coronally-Repositional Flap, 353
Semilunar Flap, 357

Subepithelial Connective Tissue Graft, 358

Modifications, 358

Envelope Technique, 358
Langer’s Technique, 360
Pouch and Tunnel Technique, 360

Guided Tissue Regeneration Technique for Root

Coverage, 360

Operations for Removal of Frena, 362

Frenectomy, 362
Frenotomy, 362
Technique, 362

Chapter 44: Furcation Involvement and Its
Management, 365

Definition, 365
Etiology, 365

Primary Etiologic Factor, 365
Anatomic Considerations, 365

Classification, 367
Clinical Features, 368
Prognosis, 368
Treatment, 369

Traditional Treatment, 369

Reconstructive/Regenerative Treatment, 369
Resective Treatment, 370

Definition, 370
Indications and Contraindications, 370

Chapter 45: Pulpoperiodontal Problems, 373

Introduction, 373
Pathways of Communication Between Pulp and

Periodontium, 373

Developmental Origin, 373
Pathological Origin, 373
Iatrogenic Origin, 373

Effects of Pulpal Disease on the Periodontium, 373
Effects of Periodontitis on the Pulp, 374
Classification of Endo-Perio Lesions, 375
Microbiological Findings of Endo-Perio Lesions, 375
Diagnosis and Treatment of Endo-Perio Lesions, 375

Chapter 46: Splints in Periodontal Therapy, 378

Definition, 378
Objectives of Splinting, 378
Classifications of Splints, 379
Various Commonly Used Splints, 379
Principles of Splinting, 379
Indications and Contraindications of Splinting, 379
Advantages and Disadvantages of Splinting, 380

Chapter 47: Dental Implants: Periodontal
Considerations, 381

Introduction, 381
Terminology, 381
Historical Background, 382
Biological Considerations of Implants, 382

Soft Tissue Implant Interface, 382
Bone Implant Interface, 383

Biomaterials Used for Implants, 383
Classification of Implants, 383
Classification of Implant Systems, 384
Treatment Planning, 384

Clinical Assessment, 384
Absolute Requirements, 384
Indications, 384
Absolute Contraindications, 385
Intraoral Contraindications, 385
Radiographs, 385
Other Radiographic Procedures, 385

Surgical Procedures, 385

One-stage: Endosseous Implant Surgery, 385
Two-stage: Endosseous Implant Surgery, 386
Healing Following Implant Surgery, 386
Early Phase, 386
Late Stage, 386

Peri-implant Complications, 387
Types of Peri-implant Disease, 387

xxiii

Contents

Clinical Features, 387
Diagnosis, 387
Management, 387
Maintenance, 388

Chapter 48: Maintenace Phase (Supportive Periodontal
Treatment), 390

Importance of Maintenance Phase, 390
Rationale for Supportive Periodontal Therapy, 390
Causes for Recurrence of Periodontal Disease, 390
Objectives of Maintenace Phase, 391
Parts of Maintenance Phase, 391

Part-I: Examination, 391
Part-II: Treatment, 391
Part-III: Schedule Next Procedure, 391

Determination of Maintenance Recall Intervals, 392

Management of Particular Type of Recall Patients, 392

Chapter 49: Occlusal Evaluation and Therapy in the
Management of Periodontal Disease, 394

Terminology, 394
Clinical Evaluation of Occlusion, 394

Temporomandibular Disorders, 394
Intraoral Evaluation, 395

Management of Trauma from Occlusion, 395
Occlusal Therapy, 395

Chapter 50: The Role of Orthodontics as an Adjunct
to Periodontal Therapy, 396

Introduction, 396
Rationale for Orthodontic Treatment in Periodontal

Therapy, 396

Reducing Plaque Retention, 396
Improving Gingival and Osseous Form, 396
Improving Esthetics, 397

Indications and Contraindications of Orthodontic Therapy,

397

Timing of Orthodontic Procedures in Periodontal

Treatment, 397

Iatrogenic Effects Associated with Orthodontic Treatment,

397

Response of Periodontal Ligament to Orthodontic Forces,

398

Chapter 51: Periodontal: Restorative Inter-relationship,
400

Margins of Restorations, 400
Restorative Margins Encroaching on the Biologic Width,

400

Crown Contour, 401
Hypersensitivity to Dental Materials, 401
Proximal Contact and Embrasure, 401
Pontic Design, 401

Chapter 52: Drugs Used in Periodontal Therapy, 403

Introduction, 403
Classification of Various Drugs Used in Periodontal

Therapy, 403

Depending on Antimicrobial Efficacy and

Substantivity, 403

Chemicals Used for Supragingival Plaque Control,

404

Phenols, 404
Quaternary Ammonium Compounds, 404

Antibiotics Used in Periodontal Therapy, 404

Systemic Administration of Antibiotics, 404
Local Administration of Antibiotics, 405

Tetracyclines, 405
Metronidazole, 406
Penicillins, 407
Non-steroidal Anti-inflammatory Drugs (NSAIDs), 407

Mechanism of Action of NSAID, 407

Local Administration of Antibiotics and Antimicrobial

Agents, 407

Classification of Controlled-Release, 408

Methods of Delivery of Chemotherapeutic Agents, 408

Keyes Technique, 408
Root Biomodification, 408
Home Irrigation Devices, 409

Conclusion, 409

53. Questionnaire for Clinical Case Discussion, 411

Glossary, 439

Index, 465

Essentials of Clinical Periodontology and Periodontics

xxiv

1

Anatomy and Development

of the Structures of

Periodontium

❒

❒

❒

❒

❒ EXTERNAL ANATOMIC FEATURES

❒

❒

❒

❒

❒ DEVELOPMENT OF PERIODONTIUM

• Early Development of Cementum

• Later Development of Cementum

• Development of Junctional Epithelium

INTRODUCTION

The term periodontium arises from the Greek word “Peri”
meaning around and “odont”  meaning tooth, thus it
can be simply defined as the “tissues investing and
supporting the teeth”. The periodontium is composed
of the following tissues namely alveolar bone, root
cementum, periodontal ligament (supporting tissues) and
gingiva (investing tissue).

The various diseases of the periodontium are

collectively termed as Periodontal diseases. Their
treatment is referred to as Periodontal therapy. The
clinical science that deals with the periodontium in health
and disease is called Periodontology.  The branch of
dentistry concerned with prevention and treatment of
periodontal disease is termed Periodontics or Periodontia.

EXTERNAL ANATOMIC FEATURES

The oral mucosa consists of three zones:

1. Masticatory mucosa: It includes the gingiva and the

covering of the hard palate.

2. Specialized mucosa: It covers the dorsum of the

tongue.

3. Lining mucosa: Is the oral mucous membrane that

lines the oral cavity. Among all the structures of the
periodontium, only the gingiva is visible clinically. The
gingiva is divided anatomically into free or marginal,
attached and interdental gingiva. The border or
groove between marginal and attached gingiva is
called as a free gingival groove, a shallow depression
on the faciogingival surface that roughly corresponds
to the base of the gingival sulcus. The junction
between the attached gingiva and alveolar mucosa
is called as mucogingival line or junction (Fig. 1.1).
The normal gingiva is pink in color (salmon coral

pink) and accumulation of melanin pigmentation is
normal. The surface of the gingiva exhibits an orange
peel-like appearance referred to as stippling. In health,
the gingiva completely fills the embrasure spaces between
the teeth and is known as the interdental gingiva. In the
posterior teeth, where the contact areas between the
teeth are usually broad, the interdental gingiva consists
of two papillae, facial and lingual which are connected
by the col. The significance of col is that, it is made up

4

Essentials of Clinical Periodontology and Periodontics

Fig. 1.1:

  Surface characteristics of the clinically-

normal gingiva

Fig. 1.2: 

Root sheath of Hertwig

Fig. 1.3:

  Proliferation of root sheath and further dentine

formation in an apical direction

of non-keratinized epithelium and hence represents the
most frequent site for initiation of disease process.

DEVELOPMENT OF PERIODONTIUM

To understand the development of periodontal tissues
one has to have a clear understanding of the root
formation. Development of cementum and roots of the
teeth starts once the formation of enamel is completed.
The outer and inner epithelia together form the epithelial
root sheath of Hertwig, which is responsible for deter-
mining the shape of the root.

Early Development of Cementum

The outer and inner epithelial layers become continuous
(without stratum intermedium or stellate reticulum) in
the area of the future cementoenamel junction and form
a two-layered sheath, which grows into the underlying
mesenchyme. The apical portion of the root sheath
remains constant whereas the coronal portion, which
is associated with dentin and cementum formation moves
in the direction of the oral cavity. The root sheath bends
horizontally at the level of future cementoenamel junction
forming the epithelial diaphragm, following which the
cervical opening becomes smaller (Figs 1.2 and 1.3).

Once the crown formation is complete the cells of

the inner enamel epithelium loose their ability to form
enamel and is called reduced enamel epithelium. They
retain the ability to induce perimesenchymal cells to
differentiate into odontoblasts and to proceed with the
formation of predentin and dentin.

After the dentin formation is completed, certain

changes occur in the root sheath. Recent studies have

5

Anatomy and Development of the Structures of Periodontium

Fig. 1.4:

  Fragmentation of root sheath

Fig. 1.5:

  Follicular cells and fibres contact dentine surface

Fig. 1.6:

  Early deposition of matrix

shown that, the epithelial cells of the root sheath produce
a layer on the root dentin, which is 10 /xm thick, has
a hyaline appearance and contains fine granules and
fibrils. This layer is called the hyaline layer of Hopewell
Smith or intermediate cementum. The epithelial cells of
the root sheath secrete enamel proteins such as
amehgenin or enameloids. The root sheath at this stage
becomes discontinuous and enables the surrounding
follicular mesenchyme to come in contact with the
amelogenin. These follicular cells then differentiate into

cementoblasts and deposit the organic matrix of
cementum on the root surface (Figs 1.4 and 1.5).

Later Development of Cementum

Cementoblasts are cuboidal cells that are arranged on
the outer surface of the hyaline layer. These cells are
responsible for the deposition of the organic matrix of
cementum, which consists of proteoglycan ground
substance, intrinsic collagen fibers and is followed by
subsequent mineralization of the organic matrix (Fig.
1.6).

Mineralization starts with the formation of a thin layer

called cementoid. Mineral salts are derived from the tissue
fluid containing calcium and phosphate ions and are
deposited as hydroxyapatite crystals.

The disintegrated Hertwigs root sheath slowly moves

away from the root surface and remain in the periodontal
ligament as epithelial cell rests of Malassez. The
periodontal ligament forms from the dental follicle soon
after root formation begins. Before a tooth erupts, fibers
from the follicle are incorporated in the cementum and
they lie parallel to the root surface. Once the tooth erupts,
the fibers are arranged in an oblique manner and are
regarded as the precursor of the periodontal ligament
fibers. As the cementum continues to increase in thickness,
more fibers become incorporated into the cementum
and eventually called as Sharpey’s fibers, when
periodontal ligament becomes established.

Alveolar bone forms around the periodontal ligament.

With continuous bone deposition the periodontal

6

Essentials of Clinical Periodontology and Periodontics

the surface of the enamel called primary enamel cuticle.
The inner enamel epithelium after laying down enamel
reduces to a few layers of flat cuboidal cells, which is
then called as reduced enamel epithelium. It covers the
entire enamel surface extending till the cemento-enamel
junction. During eruption, the tip of the tooth approaches
the oral mucosa leading to fusion of the reduced enamel
epithelium with the oral epithelium. As the crown
emerges into the oral cavity the former ameloblasts that
-are in contact with the enamel get transformed into
Junctional epithelium. Coronally the Junctional
epithelium is continuous with the oral epithelium. As the
tooth erupts, the reduced enamel epithelium grows
shorter gradually. A shallow groove, the gingival
sulcus may develop between the gingiva and the tooth
surface.

Hence, the ameloblasts pass through two phases, in

one they form enamel and in the other phase they help
in formation of primary epithelial attachment or
Junctional epithelium. When the Junctional epithelium
forms from the ameloblasts it is called primary epithelial
attachment. Junctional epithelium that forms after surgical
therapy takes its origin from the basal cells of oral

ligament space gradually becomes narrower. The alveolar
process develops during the eruption of the teeth and
cells responsible for bone formation are osteoblasts
(Fig. 1.7).

Development of Junctional Epithelium (Fig. 1.8)

When the enamel formation is complete the ameloblasts
become shorter, and they leave a thin membrane on

Fig. 1.7:

  Advanced formation of cementum

Fig. 1.8:

  Development of junctional epithelium

7

Anatomy and Development of the Structures of Periodontium

epithelium instead of ameloblasts. This is called secondary
epithelial attachment.

KEY POINTS TO NOTE

1. The periodontium is composed of alveolar bone, root

cementum, periodontal ligament (supporting tissue) and
gingiva (investing tissue).

2. The gingiva is the only structure of the periodontium that

is clinically visible and anatomically it can be divided into
marginal, attached and interdental gingiva.

3. The junction between the marginal and attached gingiva is

called free gingival groove, where as the junction between
the attached gingiva and alveolar mucosa is called as
mucogingival junction.

4. Once the dentin formation is completed, the root sheath

becomes discontinuous and allows the surrounding
mesenchyme to come in contact with the products of the
epithelial cells of the root sheath i.e. amelogenin. These
follicular cells then differentiate into cementoblasts,
fibroblasts and osteoblasts by which cementum, periodontal
ligament fibers and alveolar bone are deposited.

5. Fusion of the oral epithelium along with the reduced enamel

epithelium gives rise to the Junctional epithelium or epithelial
attachment.

REVIEW QUESTIONS

1. Define periodontology and periodontics.
2. What are the parts of periodontium?
3. Describe the development of structures of

periodontium.

BIBLIOGRAPHY

1. BG Jansen Van Rensburg. Oral Biology, Chapter 8.

Quintessence Publishing Co Ltd, 1995; 301-7.

2. BRR Varma, RP Nayak. Current Concepts in Periodontics,

Chapter 2. Arya Publishing, 2002; 4-8.

3. S.N.Bhasker. Orbans, Oral Histology and Embryology,

10th edition, CBSP Publishers and Distributers, New Delhi,

41-4.

4. Tencate. Oral Histology, Development, Structure and

Function, 3rd edition, Jaypee Bros. 228–43.

8

Essentials of Clinical Periodontology and Periodontics

INTRODUCTION

Periodontium is the functional unit of tissues supporting
the tooth including gingiva, the periodontal ligament,
the cementum and the alveolar process. The tooth and
periodontium are together called as the dentoperiodontal
unit. The main support of the tooth is provided by the
periodontal ligament, which connects the cementum of
the root to the alveolar bone or tooth socket, into which
the root fits. The main function of the gingiva is to protect
the surrounding tissues from the oral environment.

THE GINGIVA

Macroscopic Features

The gingiva is that part of the oral mucosa (masticatory
mucosa) that covers the alveolar process of the jaws and
surrounds the necks of the teeth. Anatomically the gingiva
is divided into—marginal, attached and interdental
gingiva (Fig. 2.1).

Marginal Gingiva or Free Gingiva or
Unattached Gingiva

It is defined as the terminal edge or border of the gingiva
surrounding the teeth in a collar-like fashion. In some
cases it is demarcated apically by a shallow linear
depression called the “free gingival groove”. Though the

❒

❒

❒

❒

❒ THE GINGIVA

• Macroscopic Features

• Microscopic Features

❒

❒

❒

❒

❒ TOOTH-SUPPORTING STRUCTURES

❒

❒

❒

❒

❒ PERIODONTAL LIGAMENT

• Definition

• Structure

• Cellular Composition

• Extracellular Components

• Development of Principal Fibers of

Periodontal Ligament

• Structures Present in the Connective

Tissue

• Functions of Periodontal Ligament

• Clinical Considerations

❒

❒

❒

❒

❒ ALVEOLAR BONE

• Definition

• Parts of Alveolar Bone

• Composition of Alveolar Bone

• Osseous Topography

• Blood Supply to the Bone

• Clinical Considerations

❒

❒

❒

❒

❒ CEMENTUM

• Definition

• Classification

• Functions

• Composition

• Thickness of Cementum

• Cementoenamel Junction

• Cemental Resorption and Repair

2

Biology of

Periodontal Tissues

9

Biology of Periodontal Tissues

Fig. 2.1: 

Normal gingiva in health

marginal gingiva is well-adapted to the tooth surface,
it is not attached to it (Fig. 2.2).

Gingival Sulcus

It is defined as the space or shallow crevice between the
tooth and the free gingiva, which extends apical to the
junctional epithelium. It is V-shaped and barely permits
the entrance of a periodontal probe. Under normal or
ideal conditions it is about 0 mm (seen only in germ
free animals). The so-called probing depth of a clinically-

Fig. 2.2: 

Anatomic land marks of gingiva

Fig. 2.3: 

Sulcus depth in healthy gingiva

normal gingival sulcus in humans is 2 to 3 mm
(Fig. 2.3).

Attached Gingiva

It is defined as that part of the gingiva that is firm, resilient
and tightly-bound to the underlying periosteum of the
alveolar bone. On the facial aspect it extends upto the
loose and movable alveolar mucosa, from which it is
demarcated by the mucogingival junction. The width of
attached gingiva is the distance between the mucogingival
junction and the projection on the external surface of
the bottom of the gingival sulcus or the periodontal
pocket.

It varies in different areas of the mouth, greater in

the maxilla than mandible, least width in the mandibular
first premolar area, greatest width in the maxillary incisor
region. The width of attached gingiva increases with age
and in supraerupted teeth.

Interdental Gingiva

Usually occupies the gingival embrasure. There are three
parts of interdental gingiva, facial papilla, lingual papilla
and col, which is a valley-like depression that connects
the facial and lingual papilla. The lateral borders and
tips of the interdental papilla are formed by continuation
of marginal gingiva and the intervening portion by the
attached gingiva. In the presence of diastema the
interdental papilla will be absent (Figs 2.4 and 2.5).

10

Essentials of Clinical Periodontology and Periodontics

Fig. 2.5: 

‘COL’ in various types of contacts

Fig. 2.6: 

Orthokeratinized epithelium

Fig. 2.7:

 Non-keratinized epithelium

Fig. 2.4: 

Absence of interdental papilla in

diastema cases

Microscopic Features

The gingiva consists of a central core of connective tissue
covered by stratified squamous epithelium. Three types
of epithelium exists in the gingiva.
1. The oral or outer epithelium (Keratinized epithelium)

(Fig. 2.6).

11

Biology of Periodontal Tissues

2. The sulcular epithelium
3. The junctional epithelium (non-keratinized epithe-

lium) (Fig. 2.7).
In the keratinized epithelium, the principal cell type

is the keratinocyte, which can synthesize keratin. The
process of keratinization involves a sequence of bioche-
mical and morphological events that occur in a cell as
it migrates from the basal layer towards the cell surface.

The non-keratinized epithelium contains clear cells,

which include Melanocytes, Langerhans cells, Merkel cells
and Lymphocytes.

The oral epithelium has the following cell layers:

1. Basal layer (Stratum basale or Stratum germinativum).
2. Spinous layer (Stratum spinosum).
3. Granular layer (Stratum granulosum).
4. Keratinized cell layer (Stratum corneum).

There are three distinct differences between the oral

sulcular epithelium, oral epithelium and the junctional
epithelium:
a. The size of the cells in the junctional epithelium is,

relative to the tissue volume, larger than in the oral
sulcular epithelium.

b. The intercellular space in the junctional epithelium

is, comparatively wider than in the oral epithelium.

c. Granular layer, which is seen in the oral epithelium,

is absent in sulcular and junctional epithelium.

Morphologic Characteristics of the Different
Areas of Gingival Epithelium

Oral or outer epithelium: It covers the crest and outer
surface of the marginal gingiva and the surface of the
attached gingiva. It is keratinized or parakeratinized or
combination of both. Keratinization varies in different
areas in the following order: palate (most keratinized),
gingiva, ventral aspect of the tongue and cheek (least
keratinized). The keratinized epithelium of the gingiva
consists of four layers, namely stratum basale, stratum
spinosum, stratum granulosum and stratum corneum.

The cells of the basal layer are either cylindrical

or cuboidal and are in contact with the basement

membrane. The basal cells possess the ability to divide,
it is in the basal layer that the epithelium is renewed
and therefore this is also called as stratum germinativum.
When two daughter cells have been formed by cell
division an adjacent “older” basal cell is pushed into the
spinous cell layer and starts as a keratinocyte, to traverse
the epithelium. It takes approximately one month
for a keratinocyte to reach the outer epithelial surface
where it becomes desquamated from the stratum
corneum.

The basal cells are separated from the connective

tissue by a basement membrane. In light microscopy
this membrane appears as a zone approximately 1 µm
wide and reacts positively to a PAS stain (periodic acid
Schiff stain), which indicates the presence of carbo-
hydrates (glycoproteins) in the basement membrane. In
electron micrograph, immediately beneath the basal cell,
an approximately 400 Å wide electrolucent zone can
be seen which is called lamina lucida. Beneath the lamina
lucida an electron dense zone – lamina densa is observed.
From the lamina densa so-called anchoring fibrils project
in fan-shaped fashion into the connective tissue. The
epithelial cells facing the lamina lucida contain a number
of electron dense, thicker zones called hemidesmosomes.
The hemidesmosomes are involved in the attachment
of the epithelium to the underlying basement
membrane.

Stratum spinosum consists of large cells with short

cytoplasmic processes resembling spines. Since they are
arranged at regular intervals they give the cells a prickled
appearance. The cells are attached to one another by
numerous desmosomes (pairs of hemidesmosomes),
which are located between the cytoplasmic processes of
adjacent cells.

Composition of a desmosome: It consists of two adjoining
hemidesmosomes separated by a zone containing
electron dense granulated material (GM). In addition,
outer and inner leaflets of the cell (OL, IL)  and the
attachment plaque (AP), represent granular and fibrillar
material in the cytoplasm (GM) (Fig. 2.8).

12

Essentials of Clinical Periodontology and Periodontics

Stratum granulosum:  Electron dense keratohyalin
bodies begin to occur, these granules are believed to
be related to the synthesis of keratin. Here, there is
conversion of cells to  “acellular” structure bordered by
a cell membrane indicating keratinization of the cytoplasm
of the keratinocyte.

Stratum corneum: The cytoplasms of the cells in this
layer are filled with keratin and the entire nucleus is lost.
But in parakeratinized epithelia, the cells contain remnants
of nuclei.

Keratinization is considered as a process of diffe-

rentiation rather than degeneration. The keratinocytes
while traversing from the basal layer to the epithelial
surface undergoes certain changes.
a. From the basal layer to the granular layer both the

number of tonofilaments in the cytoplasm and the
number of desmosomes increase significantly.

b. In contrast, the number of organelles such as

mitochondria, lamellae of rough endoplasmic
reticulum and Golgi apparatus decrease.

Oral sulcular epithelium:  The soft tissue wall of the
gingival sulcus is lined coronally with sulcular epithelium,
extending from the gingival margin to the junctional

epithelium. It is made up of basal and prickle cell layer.
The sulcular epithelium resembles the oral/gingival
epithelium in all respects with the exception that it does
not become fully keratinized. Although it contains
keratinocytes they do not undergo keratinization.
However, the surface cells are flattened and exhibit a
tendency towards partial keratinization in response to
physical stimulation. Normally, there are no regular
retepegs in sulcular epithelium but they form during the
inflammation of the lateral wall.

Junctional epithelium:  Denotes the tissue that joins to
the tooth on one side and to the oral sulcular epithelium
and connective tissue on the other. It forms the base
of the sulcus. It has been examined in detail by several
investigators, many hypothesis have been put forward
to explain the mode of attachment of the epithelium
to the tooth surface.Prior to the Gottlieb concept, it was
believed generally, that the gingival soft tissues were closely
opposed, but not organically united to the surface of
the enamel. This concept was based on the clinical finding
that the gingiva could be easily deflected from the tooth
surface during instrumentation. However, experimental
and clinical observations have led Gottlieb to the concept
that the soft tissues of the gingiva are organically united
to the enamel surface. He termed it as “epithelial
attachment”. Although it was accepted generally, the
concept did not explain how exactly junctional epithelium
attaches to the root surface (Fig. 2.9).

Waerhaugh in 1952, based on his observations

presented the concept of the “epithelial cuff, he concluded
that the gingival tissues are closely apposed, but not
organically united to the tooth surface. In 1962 Stern
showed that the attachment to the tooth surface is
through hemidesmosomes. This was supported by
extensive studies conducted by Schroeder and
Listgarten, they revealed that there is a structural
continuity between the tooth surface and epithelium.
These studies by Schroeder and Listgarten states that
the epithelium-tooth interface was observed to be similar
to the epithelium-connective tissue interface and that is

Fig. 2.8: 

Composition of a desmosome

13

Biology of Periodontal Tissues

Fig. 2.9:

 Concepts of epithelial attachment

by hemidesmosome and basal lamina. A basal lamina
is always interposed between epithelial cells and crown
or root surface, and the epithelial cells are united to the
basal lamina by hemidesmosomes.

The junctional epithelium is attached to the tooth

surface by internal basal lamina and to the gingival
connective tissue by an external basal lamina. The internal
basal lamina consists of a lamina densa (adjacent to the
enamel) and a lamina lucida to which hemidesmosomes
are attached. Various studies have also shown that
junctional epithelial cells are involved in the production
of laminin and play a key role in the adhesion
mechanism. The attachment of the junctional epithelium
to the tooth surface is reinforced by the gingival fibers.
Hence  the junctional epithelium and gingival fibers are
considered as a functional unit, referred to as the
dentogingival unit.

General structural features of junctional epithelium: It
consists of a collar like band of stratified squamous non
keratinizing epithelium. Thickness varies from three or
four layers in early life and increases with age upto 15
to 20 layers at the base of the gingival sulcus, and only
1 or 2 cells at the most apical portion. The length of
the junctional epithelium ranges from 0.25 to 1.35 mm.
The cells are arranged into basal and suprabasal layers
and they do not have granular layer or cornified layers.
They exhibit unusual cytologic features and differ
significantly from other oral epithelia. Three zones in

junctional epithelium have been described, apical,
coronal and middle. Apical is for germination, middle
is for adhesion and coronal is permeable.

The basal cells are cuboidal or in some cases, flattened.

They contain slightly more rough endoplasmic reticulum
and lysosomal content. The content of mitochondria of
the cells as they migrate toward and along the tooth
surface decreases. Cells of the suprabasal layer especially
those adjacent to the tooth surface exhibit complex
microvillus formation and interdigitation. Junctional
epithelial cells, especially those near the base of the
gingival sulcus, appear to have phagocytic capacity.

The structural features of junctional epithelium

indicate that it is highly permeable. Leukocytes and
lymphocytes within junctional epithelium are seen even
in clinically healthy gingiva. The densities of desmosomes
that interconnect the cells are considerably less than that
of oral epithelia and represents wider intercellular
junctions.

Epithelium–Connective Tissue Interface

Histological sections have demonstrated that, the
retepegs of epithelial cells project deeply into the
connective tissue leading to the formation of a series of
inter- connecting epithelial ridges. Basement membrane
seems to form a continuous sheet that connects the
epithelium and connective tissue. Electron microscope
reveals a faintly fibrillar structure, called as the basal

14

Essentials of Clinical Periodontology and Periodontics

Fig. 2.11:

 The principal group of fibers

lamina, which is a part of the basement membrane. This
structure has lamina lucida adjacent to the basal epithelial
cells and  lamina densa towards connective tissue. Basal
lamina is produced by adjacent epithelial cells and is made
up of collagenous proteins and proteoglycans binded
together into a totally-insoluble complex. It also contains
laminin and fibronectin. Fibrils measuring 20 to 40 nm
in diameter seem to extend from the basal cells through
the basal lamina and into the lamina propria of the
connective tissue. These structures called as anchoring
fibrils are supposed to bind the basal cells, basal lamina
and connective tissue together (Fig. 2.10).

Supra-alveolar Connective Tissue

The connective tissue supporting the oral epithelium is
termed as the lamina propria and for descriptive purpose
it can be divided into two layers:
a. The superficial papillary layer—associated with the

epithelial ridges.

b. Deeper reticular layer—that lies between the papillary

layer and the underlying structures.

The term reticular here means net-like and refers to the
arrangement of collagen fibers. In the papillary layer,
the collagen fibers are thin and loosely-arranged and
many capillary loops are present. The reticular layer is
dominated by collagen arranged in thick bundles.

The lamina propria consists of cells, fibers, blood

vessels embedded in amorphous ground substances.
I. Cells:  Different types of cells present are:

a. Fibroblast
b. Mast cells
c. Macrophages
d. Inflammatory cells.

II. Fibers: The connective tissue fibers are produced by

fibroblasts and can be divided into:
a. Collagen fibers
b. Reticulin fibers
c. Oxytalan fibers
d. Elastin fibers.
Collagen type I form the bulk of the lamina propria

and provide the tensile strength to the gingival tissues.
Type II collagen is seen in the basement membrane.
The functions of gingival fibers are the following:
a. It braces the marginal gingiva firmly against the tooth.
b. It helps to withstand the forces exerted by mastication.
c. It unites the free gingiva to the root cementum and

the adjacent attached gingiva.
The arrangement of gingival fibers is described as

principal group of five bundles and secondary group
of minor fibers consisting of six sets (Fig. 2.11)

Fig. 2.10: 

Structure of the junction between epithelium

and connective tissue

15

Biology of Periodontal Tissues

The principal group fibers are:

1. Dentogingival fibers:  They project from the

cementum in a fan-like conformation towards the
crest and outer surface of the marginal gingiva. They
provide support to the gingiva by attaching it to the
tooth.

2. Alveolar gingival fibers:  They extend from the

periosteum of the alveolar crest coronally into the
lamina propria. Their function is to attach the gingiva
to the alveolar bone.

3. Dentoperiosteal fibers: They arise from the

cementum near the cementoenamel junction and
insert into the periosteum of the alveolar bone and
protect the periodontal ligament.

4. Circular fibers: They surround the tooth in a cuff or

ring like fashion and course through the connective
tissue of the marginal and attached gingiva.

5. Trans-septal fibers: They are located interproximally,

they extend from cementum of one tooth to the
cementum of the neighbouring tooth. Their function
is to protect the interproximal bone and maintain
tooth-to-tooth contact.

Fibers of the secondary group (Fig. 2.12) are:
1. Periosteogingival fibers: They extend from the

periosteum of the alveolar bone to the attached
gingiva. They help to attach the gingiva to the alveolar
bone.

2. Interpapillary fibers: They are seen in the interdental

gingiva extending in a faciolingual direction and
support the gingival papilla.

3. Transgingival fibers: These are seen in and around

the teeth with in the attached gingiva. They maintain
the alignment of teeth in the arch.

4. Intercircular fibers: They extend from the cementum

on distal surface of a tooth splaying buccally and
lingually around the next tooth and are inserted on
the mesial surface.

5. Intergingival fibers: They are seen within the attached

gingiva adjacent to the basement membrane

extending mesiodistally. They provide support and
contour for the attached gingiva.

6. Semicircular fibers: They extend from the mesial

surface of a tooth to the distal surface of same tooth
in a half circle.

7. Oxytalan fibers: They are present in all connective

tissue structures of the periodontium. The function
of these fibers is yet unknown.

8. Elastin fibers:  Elastin fibers are only present in

connective tissue of the gingiva and periodontal
ligament. They are also seen in the connective tissue
of alveolar mucosa in large numbers.

Extracellular matrix/ground substance: It is produced by
fibroblasts, followed by mast cells and other components
derived from the blood. The matrix is the medium in
which the connective tissue cells are embedded and is
essential for the maintenance of the normal function of
the connective tissue. Thus, the transportation of water,
electrolytes, nutrients, metabolites etc. to and from the
individual connective tissue cells occurs with in the matrix.

The main constituents of connective tissue matrix

are protein polysaccharide matrix. These complexes are
normally differentiated into proteoglycans and glyco-
proteins. The proteoglycans contains glycosaminogly-
cans, e.g. chondroitin sulfate, heparin sulfate, hyaluronic
acid etc. The proteoglycans act as a molecular filter and

Fig. 2.12: 

Secondary group of fibers

16

Essentials of Clinical Periodontology and Periodontics

in addition, play an important role in the regulation of
cell migration in the tissue. Due to their structure and
hydration, the macromolecules exert resistance and
hydration, towards deformation. Hence, when gingiva
is suppressed, the macromolecule become deformed,
when the pressure is eliminated the macromolecules
regain their original form. Thus, the macromolecules are
of importance for the resilience of the gingiva.

Blood Supply, Lymphatics and Nerves

Three major sources of blood supply to the gingiva (Fig.
2.13) has been described:
1. Supraperiosteal arterioles: Overlying the alveolar

bone along the facial and lingual surfaces, sends
branches to the surrounding tissue.

2. Vessels of the periodontal ligament: They extend into

the gingiva and anastamose with the capillaries in
the sulcus area.

3. Arterioles emerging from the crest of the interdental

septa.
Lymphatic drainage of the gingiva brings in the

lymphatics of the connective tissue papillae. It progresses
to the periosteum of the alveolar process and then to
regional lymph nodes (mainly submaxillary group).

Nerve supply to gingiva is derived from fibers arising

from nerves in the periodontal ligament and from the
labial, buccal and palatal nerves.

TOOTH-SUPPORTING STRUCTURES

PERIODONTAL LIGAMENT

Definition

Tooth-supporting structures include, the periodontal
ligament, cementum and alveolar bone. The periodontal
ligament is a connective tissue structure that surrounds
the root and connects it with the bone. In the past,
periodontal ligament has been described by many terms.
Among these are desmodont, gomphosis, pericemen-
tum, alveolodental ligament and periodontal membrane.
Since it is a soft connective tissue providing continuity
between two mineralized connective tissues, the term
periodontal ligament appears to be more appropriate.

In the coronal direction, the periodontal ligament is

continuous with the lamina propria of the gingiva and
communicates with the marrow spaces of the alveolar
bone through Volkmann’s canals.

Structure

The periodontal ligament space has the shape of an
hourglass and is narrowest at the mid-root level.
The width of periodontal ligament is approximately
0.25 mm ± 50 percent.

Cellular Composition

Cells of periodontal ligament are categorized as:
1. Synthetic cells

a. Osteoblasts
b. Fibroblasts
c. Cementoblasts

2. Resorptive cells

a. Osteoclasts
b. Cementoclasts
c. Fibroblasts

3. Progenitor cells
4. Other epithelial cells

a. Epithelial cell rests of Malassez

5. Connective tissue cells

a. Mast cells and macrophages.

Fig. 2.13: 

Blood supply to gingiva. Arterioles penetrating the

interdental bone (left), supra periosteal arterioles (right)

17

Biology of Periodontal Tissues

Characteristics of a Synthetic Cell

1. Should be actively-synthesizing ribosomes
2. Increase in the complement of rough endoplasmic

reticulum and Golgi apparatus

3. Large open faced or vesicular nucleus containing

prominent nucleoli.

Osteoblasts: Covers the periodontal surface of the
alveolar bone. Alveolar bone contains endosteum and
a periosteum. A periosteum contains at least two distinct
layers, cambium layer or cellular layer and a fibrous layer.
A cellular layer is present on the periodontal surface of
the alveolar bone.

Fibroblasts: It is the most prominent connective tissue
cell (65% of total cell population). Periodontal ligament
fibroblasts are phenotypically different from gingival
fibroblasts. They consist of subtypes with distinct
phenotypes and found to synthesize higher quantities
of chondroitin sulfates and lesser quantities of heparan
sulfate and hyaluranan sulfate. The main function of the
fibroblasts is the production of various types of fibers
and it is also instrumental in the synthesis of the
connective tissue matrix. The fibroblast is a stellate or
spindle-shaped cell which produce
• Collagen fibers
• Reticulin fibers
• Oxytalan fibers
• Elastin fibers

Various stages in the production of collagen fibers

are as follows:

The first molecule released by fibroblasts is tropo-

collagen which contains three polypeptide chains
interwined to form a helix. Tropocollagen molecules are
aggregated longitudinally to form protofibrils, which are
subsequently laterally-arranged in parallel to form colla-
gen fibrils. Collagen fibers are bundles of collagen fibrils.

Cementoblasts are seen lining the cementum.

Resorptive Cells

Osteoclasts: These are the cells that resorb the bone and
tend to be large and multinucleated. The precursor cells

of the osteoclasts are circulating monocytes. The
characteristic features of osteoclasts are the plasma
membrane of the cell lying adjacent to the bone that
has been actively undergoing resorption is raised in
characteristic folds and is termed as ruffled or striated
border.

Fibroblasts: It must be made clear that the fibroblasts
may be capable of both synthesis and resorption. The
fibroblasts responsible for resorption contain fragments
of collagen that appear to be undergoing digestion. The
presence of these cells indicates resorption of fibers
occurring during either disease or physiological turnover
or remodeling of periodontal ligament.

Cementoclasts: The main observation in this is that
cementum is not remodelled in the fashion of alveolar
bone and periodontal ligament, but that it undergoes
continual deposition during life. However resorption of
cementum occurs in certain circumstances and in these
instance cementoclasts are located in Howship’s lacunae.

Progenitor cells: Little is known about these cells. It is
believed that, generally, as and when the need arises,
the daughter cell after the division differentiates into the
functional type of connective tissue cells.

Epithelial cell rests of Malassez: They are found close
to cementum. These cells are first described by Malassez
in 1884 and are remnants of the epithelium of Hertwig’s
epithelial root sheath. The epithelial cell rests persists as
a network, strands, island or tubule like structures near
and parallel to the surface of the root.

Electron microscope observation shows that the

epithelial cell rests exhibits tonofilaments and they are
attached to one another by desmosomes. The physiologic
role of these cells is not known. When certain pathologic
conditions are present, cells of the epithelial rests can
undergo rapid proliferation and can produce a variety
of cysts and tumours of the jaws.

Mast cells: These are relatively small, round or oval cell
having a diameter of almost 12 to 15µm. The cells contain
numerous cytoplasmic granules with small or round

18

Essentials of Clinical Periodontology and Periodontics

Fig. 2.14: 

Principal fiber groups in periodontal ligament

nucleus. The granules have been shown to contain
heparin and histamine. The physiologic role of heparin
in mast cells does not appear to be clear. Where as mast
cell histamine plays a role in the inflammatory reaction
and they have been shown to degranulate in response
to antigen-antibody formation on their surface.

Macrophages may also be present in the ligament. They
are capable of phagocytosis.

Extracellular Components

1. Fibers:

• Collagen
• Oxytalin

2. Ground substance:

• Proteoglycans
• Glycoproteins

Periodontal fibers: The most important elements of the
periodontal ligament are the principal fibers. These fibers
are collagenous in nature and are arranged in bundles,
they follow a wavy course. The terminal portion of these
principal fibers that insert into the cementum and bone
are termed Sharpey’s fibers. Collagen is a specific, high
molecular weight protein to which a small number of
amino acids are attached, the most important of which
are glycine, proline and hydoxyproline. Collagen is
synthesised by fibroblasts, chondroblasts, osteoblasts,
odontoblasts and other cells. Several types of collagen
have been demonstrated. The principal fibers are
composed primarily of Type I collagen, where as reticular
fibers are made up of Type III collagen. Type IV collagen
is seen in the basal lamina.

The principal fibers of periodontal ligament (Fig. 2.14)

are arranged in six groups that develop sequentially in
the developing root. They are:
• Trans-septal group
• Alveolar crest, horizontal, oblique, apical and inter-

radicular fibers.

Trans-septal group: They may be considered to belong
to the gingiva because they do not have osseous
attachment.

Alveolocrestal group: They extend obliquely from the
cementum just beneath the junctional epithelium to the
alveolar crest. Their function is to retain tooth in socket,
resist lateral tooth movement and protect deeper
periodontal ligament structure.

Horizontal group: Extend from cementum to the alveolar
bone at right angles to the long axis of the tooth.

Oblique group: They are the largest group in the
periodontal ligament; extend coronally in an oblique
direction from the cementum to the bone. They resist
axially directed forces.

Apical group: They originate from cementum of root
apex, splaying apically and laterally into the bone of the
alveolar fundus. Their main function is it prevents tooth
tipping; resists luxation, protects blood, lymph and nerve
supply to the tooth.

Inter-radicular fibers: Extends from cementum of
bifurcation areas, splaying from apical into furcal bone.
It resists luxation and also tipping and torquing.

Secondary fibers of periodontal ligament: In addition
to the principal fiber groups, periodontal ligament
contains other well-formed fiber bundles, that inter-
digitate at right angles or splay around and between the
regular fiber bundles. These fibers are associated with

19

Biology of Periodontal Tissues

blood vessels and nerves of the periodontal ligament.
Although periodontal ligament does not contain mature
elastin, two immature forms have been described,
the so-called oxytalan fibers and eluanin. It was sug-
gested that, they provide elastic properties to periodontal
ligament. There are also reticulate fibers, which are fine,
immature collagen fibers with a lattice like arrangement.

In addition to the above fiber types, small collagen

fibers arranged in all directions, forming a plexus have
also been reported. They are closely-associated with
principal fibers and are termed as the indifferent fiber
plexus.

Ground substance: The space between cells, fibers, blood
vessels and nerves in the periodontal space is occupied
by ground substance. The ground substance is made
up of two major groups of substances. Glyco-
saminoglycans such as hyaluronic acid, proteoglycans
and glycoprotiens such as fibronectin and laminin. It also
has high water content (70%).

Development of principal fibers of periodontal ligament
(Fig. 2.15): The principal fibers develop in conjunction
with the eruption of the tooth. The fibroblasts surround-
ing the developing root produce collagen fibers. These
fibers are seen in the periodontal space without a specific
orientation. As and when the tooth erupts, the orientation
of the fibers alters.
1. First small, fine brush-like fibrils are seen arising from

the root cementum and projecting into the perio-
dontal ligament space.

2. Similar fibers are seen on the surface of the bone

but only in thin, small numbers.

3. Later on, the number and thickness of fibers

originating from the bone increase and elongate. They
radiate towards the loose connective tissue in the mid-
portion of the periodontal ligament.

4. The fibers originating from the cementum also

increase in length and thickness and fuses with the
fibers originating from the alveolar bone in the
periodontal ligament space.

5. They mature progressively towards the root apex as

the eruption progresses. When the tooth, following
eruption, reaches contact in occlusion and starts to
function, the principal fibers become organized in
bundles and run continuously from bone to cemen-
tum.
For long it was believed that this middle portion where

the splicing of fibers from cementum and bone takes
place,it forms the intermediate plexus. These plexus were
thought to play a significant role in orientation and
adjustment of fibers during eruption and functional
movement of teeth. But recent investigations have
revealed that, in humans these plexus disappears
once the fusion of cemental and osseous fibers are
completed.

Fig. 2.15: 

Development of periodontal ligament fibers

(principal)

20

Essentials of Clinical Periodontology and Periodontics

Structures Present in the Connective Tissue

1. Blood vessels
2. Lymphatics
3. Nerve innervation
4. Cementicles

Blood vessels: Periodontal ligament is supplied by
branches derived from three sources dental, inter-
radicular and interdental arteries (Fig. 2.16).
1. Dental artery before it enters apical foramen gives

off branches to the periodontal ligament which also
supplies the pulp.

2. The inter-radicular artery gives off branches in the

alveolar process that supplies the periodontal ligament
through the cribriform plate.

3. Interdental artery emerges from the crest of the

alveolar bone and supplies the coronal part of the
periodontal ligament.
Lymphatic vessels are seen to follow the path of blood

vessels in the periodontal ligament.

Nerve supply: In an un-erupted tooth, the developing
periodontal ligament is supplied by fine, unmyelinated
nerve fibers. Whether this persists after the tooth is
erupted is not known. Periodontal ligament is mainly
supplied by the dental branches of the alveolar nerve
through the apical perforations of the tooth socket or
from the cribriform plate. Many studies have proved

that periodontal ligament is richly supplied by
mechanoreceptors whose cell bodies are located in the
trigeminal ganglion. These receptors provide sense of
touch, pressure, pain, and proprioception during
mastication.

Cementicles are calcified masses adherent to or

detached from the root surface. They may be developed
from calcified epithelial rests, calcified Sharpey’s fibers,
and calcified thrombosed vessels within the periodontal
ligament.

Functions of Periodontal Ligament

The following functions of periodontal ligament have
been explained:
1. Physical
2. Formative and remodeling
3. Nutritional and sensory function

Physical Function

The physical functions of the periodontal ligament are:
a. Provides soft tissue “casing” in order to protect the

vessels and nerves from injury due to mechanical
forces.

b. Transmit the occlusal forces to the bone. Depending

on the type of force applied, axial force when applied
causes stretching of oblique fibers of periodontal
ligament. Transmission of this tensional force to the
alveolar bone encourages bone formation rather than
bone resorption. But when horizontal or tipping force
is applied the tooth rotates around the axis, at first
the tooth movement is within the confines of the
periodontal ligament. When a greater force is applied,
displacement of facial and lingual plates may occur.
The axis of rotation, in single rooted teeth is located
in the area between the apical and middle third of
the root. In multirooted teeth, the axis of rotation
is located at the furcation area.

c. Attaches the teeth to the bone
d. Maintains the gingival tissues in their proper

relationship to the teeth.

e. Shock absorption resists the impact of occlusal forces.

Fig. 2.16: 

Periodontal blood supply

21

Biology of Periodontal Tissues

Two theories have been explained for the mechanism

of tooth support.
A. Tensional theory
B. Viscoelastic theory
A. Tensional theory: According to it the principal fibers

of periodontal ligament plays a major role in
supporting the tooth and transmitting forces to the
bone. When forces are applied to the tooth, principal
fibers unfold and straighten and then transmit the
forces to the alveolar bone, causing elastic defor-
mation of the socket.

B. Viscoelastic theory is based on the fact that, the fluid

movement largely controls the displacement of the
tooth, with fibers playing a secondary role. When
the forces are transmitted to the tooth, the extra-
cellular fluid is pushed from the periodontal ligament
into the marrow spaces through the cribriform plate.
After the depletion of the tissue fluids, the bundle
fibers absorb the shock and tighten. This leads to
blood vessel stenosis → arterial back pressure →
ballooning of the vessels →Tissue replenishes with
fluids.

Formative and Remodeling Function

Cells of the periodontal ligament have the capacity to
control the synthesis and resorption of the cementum,
ligament and alveolar bone. Periodontal ligament
undergoes constant remodeling; old cells and fibers are
broken down and replaced by new ones.

Nutritional and Sensory Function

Since periodontal ligament has a rich vascular supply
it provides nutrition to the cementum, bone and gingiva.
Periodontal ligament is supplied by nerve fibers that can
transmit sensation of touch, pressure and pain to higher
centers. The nerve bundle follows the course of blood
vessel and enters the periodontal ligament from
periapical area through channels from the alveolar bone.
These bundles divide into single myelinated fibers, which
later on lose their myelin sheath and end in one of the
four types of neural termination.

• Free endings, carry pain sensations
• Ruffini like mechanoreceptors located in the apical

area

• Meissners corpuscles are also mechano receptors

located primarily in the mid-root region.

• Spindle like pressure and vibration endings, located

mainly in the apex.
Pain sensation is transmitted by small diameter nerves,

temperature by intermediate type; pressure by large
myelinated fibers.

Clinical Considerations

The primary role of periodontal ligament is to support
the tooth in the bony socket. Its thickness varies in
individuals and in different teeth in the same person.
Periodontal ligament is shaped like an hourglass and is
narrowest in the middle region of the root and thus seems
to be the fulcrum of physiological movement. In
connection with the physiological mesial migration of
the teeth, the periodontal ligament is thinner on the mesial
root surface than on the distal surface.

Due to acute trauma to the periodontal ligament or

in accidental blows, many pathological changes will be
produced, such as fracture or resorption of cementum
and alveolar bone. Hence there will be loss of alveolar
bone and widening of periodontal ligament, which results
in the tooth becoming loose. When the trauma is
removed repair usually will take place.

Orthodontic Tooth Movement

Depends on the resorption and formation of both bone
and periodontal ligament. These activities can be
stimulated by properly regulated pressure and tension.
If the movement of the tooth is within physiological limits,
the compression of the periodontal ligament on pressure
side results in bone resorption, where as on the tension
side bone apposition is seen. Application of the large
forces results in the necrosis of periodontal ligament and
alveolar bone.

If gingivitis is not controlled or treated it will invariably

extend to the periodontal ligament and bone and

22

Essentials of Clinical Periodontology and Periodontics

Fig. 2.17: 

Alveolar bone structure

produces the destruction of the same. Once they are
destroyed it is difficult for them to regenerate and
therefore the diseases of periodontal ligament are often
irreversible.

ALVEOLAR BONE

Definition

It is that portion of the maxilla and mandible that forms
and supports the tooth socket (alveoli). It is formed when
the tooth erupts, in order to provide osseous attachment
to the forming periodontal ligament and gradually
disappears after the tooth is lost.

Parts of Alveolar Bone (Fig. 2.17)

Alveolar bone consists of the following:
1. Inner and outer cortical plate.
2. The bone lining the socket.
3. An interior portion of cancellous bone.

The  cortical plates consist of compact bone, in

which the lamellae are often arranged circumferentially
around blood vessels forming Haversian systems, which
are the internal mechanisms that bring a vascular supply
to bones that are too thick to be supplied only by surface
vessels. The cortical plates and the bone lining the socket
meet at the alveolar crest, usually 2 mm below the
cementoenamel junction.

The bone lining the socket is also compact bone and

can be known as any of the following:
1. Bundle bone, since bundles of Sharpey’s fibers from

the periodontal ligament are embedded in it

2. The cribriform plate, because it is perforated by

numerous vascular channels

3. Alveolar bone proper, as it provides direct bony

support for the teeth

4. Lamina dura, which is radiographically seen as a

dense plate.

Cancellous bone: It consists of narrow irregular bony
trabeculae, which, by branching and uniting forms a
network of spaces between the trabeculae. There is a
considerable variation in the proportions of compact to
cancellous bone in different regions of the jaws and in
different tooth surfaces. For example: In relation to lower
anterior teeth i.e. lower incisors, there is a thin bone
that consists of an outer cortical plate and the bone lining
the socket with no intervening cancellous bone. In
contrast, the buccal and interdental bone of molars is
relatively thick and cancellous bone may predominate.

As the diameter of the tooth root gradually decreases

in an apical direction, there is a corresponding increase
in the thickness of alveolar bone with increase in
cancellous bone being present. These variations are
important to note because they influence the pattern
and progression of bone loss in destructive forms of
periodontal diseases.

Roentgenogram permits the classification of trabecular

patterns of the alveolar process into two main types:
• In type I, the interdental and inter-radicular

trabeculae are regular, horizontal and are arranged
in a ladder-like pattern. (Common in mandible)

• In type II, irregularly arranged numerous interdental

and inter-radicular trabeculae are seen most com-
monly in maxilla.

Composition of Alveolar Bone

It has two basic constituents:
a. The cells consist of osteoblasts, osteoclasts, and

osteocytes.

23

Biology of Periodontal Tissues

b. Extra-cellular matrix consists of 65 percent inorganic

and 35 percent organic matter.
The inorganic component is composed of minerals

such as calcium, phosphate along with hydroxyl,
carbonate, citrate and trace amounts of other ions, such
as sodium, magnesium and fluorine. The minerals are
in the form of hydroxyapatite crystals.

The organic matrix consists of 90 percent of type I

collagen, with small amounts of non-collagenous proteins
such as osteocalcin, osteonectin, bone morphogenetic
proteins, proteoglycans, and glycoproteins.

Cellular Components

a. Osteoblasts: They are cuboidal cells with well-

developed rough endoplasmic reticulum, a large
Golgi apparatus, and secretory vesicles. It synthesizes
bone matrix (osteoid), type I collagen and regulate
its mineralization. Each osteoblast carries out a cycle
of matrix synthesis after which it is either buried as
an osteocyte or remains on the surface as a resting
or inactive osteoblast. Osteoblasts are derived from
the progenitor cells at sites of bone formation. These
progenitor cells belong to the mesenchymal cell
family. In contrast, osteoclasts originate from blood
– borne monocytes.

b. Osteoclasts: They are large multinucleated giant cells.

They originate from hematopoietic tissue and are
formed by the fusion of mononuclear cells of
asynchronous populations. Generally they are found
in bay like depressions in the bone called Howship’s
lacunae. The part of the cell in contact with bone
shows a convoluted surface and a ruffled border
from which hydrolytic enzymes are believed to be
secreted. The ruffled border is surrounded by a clear
zone, which contains cytoplasm exclusively and is
believed to be associated with binding of cells to the
bone surface and isolation of areas of resorptive
activity.

c. Osteocytes: Alveolar bone is formed during foetal

growth by intra membranous ossification and consists
of a calcified matrix with osteocytes enclosed within

a space called lacunae. The osteocytes extend
processes into canaliculi that radiate from the lacunae.
The main function of these canaliculi is to bring
oxygen and nutrients to the osteocytes through the
blood and remove metabolic waste products.
The main cells responsible for bone resorption are

osteoclasts, on rare occasions bone resorption by
osteocytes has been reported which is called as “osteocytic
osteolysis”.

Osseous Topography

The anatomy of the alveolar bone varies from patient
to patient. Normally it conforms to the root prominence,
with intervening depressions that taper towards the
margin. The factors that affect the height and thickness
of the facial and lingual bony plates are alignment of
the teeth, angulation of the root to the bone and the
occlusal forces.

When the teeth are in a labial version, the margin

of the bone is located more apically and is thinned to
a knife-edge as compared to the teeth in proper
alignment. When teeth are in a lingual version, the facial
bony plate is thicker than normal and the margin is blunt,
rounded and horizontal rather than arcuate.

Fenestrations and Dehiscences (Fig. 2.18)

Fenestrations are isolated areas in which the root surface
is covered only by the periosteum and gingiva, but in
these situations, the marginal bone remains intact. When

Fig. 2.18: 

Fenestration and dehiscence

24

Essentials of Clinical Periodontology and Periodontics

the marginal bone is also denuded, the defect is called
dehiscence.

These defects are seen more often on the facial bone

than on the lingual, and are more common in anterior
teeth than on the posterior. The etiologies of these defects
are not clear; some of the predisposing factors are root
prominence, malposition, and teeth in labial version with
thin bony plates. The diagnosis of these defects is important
as it may affect the outcome of the surgical treatment.

Periosteum and Endosteum

The tissue covering the outer surface of bone is termed
as periosteum, where as the tissue lining the internal bone
cavities is called endosteum. The periosteum consists of
two layers, the inner layer, next to the bone surface,
consists of bone cells that have the potential to
differentiate into osteoblasts and an outer layer which
is more fibrous containing blood vessels and nerves.

The endosteum is composed of a single layer of

osteoprogenitor cells and a small amount of connective
tissue.

Remodeling and Resorption

During both embryonic bone development and the
entire pre adult period of human growth, bone is being
formed very rapidly, primarily on the periosteal surface.
Simultaneously, bone is being destroyed along the
endosteal surface and at focal points along the periosteal
surface (bone modeling).

Bone growth occurs by apposition of an organic

matrix that is deposited by osteoblasts. Although the
alveolar bone tissue is constantly changing in its internal
organization, it retains approximately the same form from
childhood through adult life. Haversian systems (osteons)
are the internal mechanisms that bring vascular supply
to bones too thick to be supplied only by surface vessels.
Bone deposition by osteoblasts is balanced by resorption
brought about by osteoclasts during tissue remodeling
and repair.

Osteoblasts, lay down non mineralised bone matrix

called osteoid, while new osteoid is being deposited, the

older osteoid becomes mineralized. Bone resorption is
a complex process and appears as eroded bone surfaces
namely Howship’s lacunae. It has been suggested that
bone resorption at any site is a chemotactic
phenomenon. This is, initiated by the release of some
chemotactic factors like interleukin-1 and 6, which
attract the monocytes to the target site. Osteoblasts release
Leukaemia inhibiting factor (LIF), which coalesce
monocytes to form multi-nucleated osteoclasts, which
then resorb bone.

During bone resorption three processes occur:

a. Decalcification
b. Degradation of matrix
c. Transport of soluble factors to the extra cellular fluid

Since calcified matrix is resistant to proteases of all

kinds, bone must first be decalcified. This is achieved
at the ruffled border of the osteoclasts by secretion of
some acids such as citric acid and lactic acid, which chelate
bone, the low pH leads to increase in solubility of
hydroxyapatite. The next step is degradation of matrix,
takes place by collagenase enzymes and other proteases
like cathepsin-B. Collagenolysis occurs outside the
osteoclast. Finally, the break down products of bone are
transported to the extracellular fluids and to the blood
vascular system.

Tencate described the following sequence of events

during bone resorption:
a. Attachment of osteoclasts to the mineralized bone

surface.

b. Creation of a sealed acidic environment, which

demineralises the bone and exposes the organic
matrix.

c. Degradation of exposed organic matrix by the action

of enzymes such as acid phosphatase and cathepsine.

d. Sequestering of mineral ions and amino acids within

the osteoclasts.

Blood Supply to the Bone

The vessels enter the interdental septa through nutrient
canals together with veins, nerves, and lymphatics. The
alveolar arteries sends off branches through periodontal

25

Biology of Periodontal Tissues

ligament and enter the marrow spaces through the
perforations in the cribriform plate.

Clinical Considerations

Bone although one of the hardest tissue of human body,
is biologically a highly plastic tissue. Bone is resorbed
on the side of pressure and apposed on the side of
tension. It has been shown that on the pressure side
there is an increase in the level of cyclic adenosine
monophosphate (cAMP) in cells, which may play a role
in bone resorption.

The most frequent and harmful change in the alveolar

process is that which is associated with periodontal
diseases. The bone resorption caused by periodontal
diseases is usually symmetrical, occurs in episodic manner,
and is both of the horizontal and vertical type. Once
lost, this bone is very difficult to regenerate. Regeneration
of just a few millimetres of bone that has been lost is
the greatest challenge to the periodontists across the
world.

CEMENTUM

Definition

Cementum is a calcified avascular mesenchymal tissue
that forms the outer covering of the anatomic root. It
provides anchorage mainly to the principal fibers of
periodontal ligament. Two sources of collagen fibers can
be found in the cementum:
1. Sharpey’s (extrinsic) fibers which are formed by the

fibroblasts.

2. Fibers belonging to the cementum matrix per se

(intrinsic) produced by cementoblasts.
Two types of cementum were described earlier:

a. Acellular cementum/primary cementum (Fig. 2.19)
b. Cellular cementum/secondary cementum.

The differences between the two are given in Table

2.1.

Classification

Depending on location, morphology and histological

Fig. 2.19: 

Acellular/cellular cementum

Table 2.1: Differences between acellular and

cellular cementum

Acellular cementum

Cellular cementum

a. Forms during root

Forms after the eruption

formation

of the tooth and in

response to functional

demands

b. Does not contain any cells

Contains cementocytes

c. Seen at the coronal

Seen at a more apical

portion of root

portion of root

d. Formation is slow

Deposition is more rapid

e. Arrangement of collagen

Collagen fibers are

fibers are more organized

irregularly arranged

appearance, Shroeder and Page have classified
cementum as:
a. Acellular afibrillar cementum (AAC): It contains only

the mineralized ground substance. It does not contain
collagen fibers nor does it exhibit entrapped
cementocytes. It is a product of cementoblasts and
is found almost exclusively on the enamel near the

26

Essentials of Clinical Periodontology and Periodontics

cementoenamel junction with a thickness of 1 to
15 µm.

b. Acellular extrinsic fiber cementum (AEFC): By

definition it is composed primarily of Sharpey’s fibers
of periodontal ligament but does not contain
cementocytes. Developmentally they come to occupy
the coronal one half of the root surface. Its thickness
is between 30 and 230 µm.

c. Cellular mixed stratified cementum (CMSC): It

harbours both intrinsic (cementoblasts derived) and
extrinsic (fibroblast derived) fibers and may contain
cells. In humans it is seen in the apical third of the
roots, apices and furcation areas. Its thickness varies
from 100 to 1000 µm.

d. Cellular intrinsic fiber cementum (CIFC): It contains

only intrinsic fibers secreted by cementoblasts and
not by the periodontal ligament fibroblasts. In
humans it fills the resorption lacunae.

e. Intermediate cementum (or) the hyaline layer of

Hope Well Smith: It is an ill-defined zone extending
from pre-cementoenamel junction to the apical
1/3rd of the root. It appears to contain cellular
remnants of Hertwigs Sheath embedded in calcified
ground substance. The significance of this layer is that,
it contains enamel like proteins, which helps in
attachment of cementum to dentin. It has been
observed by many that, when this layer is removed
during root planing procedure, the resultant
reparative cementum that is formed will not be
attached firmly on the dentin.

Functions

a. Primary function of cementum is to provide

anchorage to the tooth in its alveolus. This is achieved
through the collagen fiber bundles of the periodontal
ligament, whose ends are embedded in cementum.

b. Cementum also plays an important role in

maintaining occlusal relationships, whenever the
incisal and occlusal surfaces are abraded due to
attrition, the tooth supra erupts in order to
compensate for the loss and deposition of new
cementum occurs at the apical root area.

Composition

The cementum is composed of both inorganic (46%)
and organic matter. The organic matrix is chiefly
composed of 90 percent Type I collagen, 5 percent Type
III collagen and non-collagenous proteins like enamel
proteins, adhesion molecules like tenacin and fibronectin,
glycosaminoglycans like chondroitin sulfate, dermatan
sulfate and heparan sulfate which constitute the
remaining organic matrix.

Thickness of Cementum

Formation of cementum is a continuous process,
the formative rate of which varies throughout life.
It is most rapid at the apical regions. At the coronal half
the thickness varies from 16 to 60 µm (almost the
thickness of hair) and at the apical third it varies from
150 to 200 µm. It is thicker in the distal surfaces as
compared to the mesial surfaces and this can be
explained by functional stimulation following mesial
migration.

Hypercementosis or cemental hyperplasia is a

prominent thickening of the cementum. It can be
localized or generalized. It may appear as a generalized
thickening of the cementum, with nodular enlargement
at the apex or as spike like projections (cemental spikes).
The etiology of hypercementosis is not very well
understood. The spike like projections could be as a result
of excessive tension from orthodontic appliance or
occlusal forces. The generalized type may be associated
with a variety of situations like, teeth without antagonists,
in teeth with chronic pulpal and periapical infections.
Hypercementosis of the entire dentition may be seen
in patients with Paget’s disease.

Cementoenamel Junction (Fig. 2.20)

At the cementoenamel junction three types of
relationships may exist. In about 60 to 65 percent of
cases the cementum overlaps the enamel, in about 30
percent of cases end-to-end relationship of enamel and
cementum is seen and in 5 to 10 percent the cementum
and enamel fail to meet.

27

Biology of Periodontal Tissues

Cemental Resorption and Repair

Cemental resorption may be caused by local, systemic
or idiopathic factors. Local conditions that contribute to
cemental resorption are, trauma from occlusion,
orthodontic tooth movement, pressure from erupting
teeth, cysts and tumors, teeth without functional
antagonist, periapical disease and periodontal disease.
Systemic conditions that may predispose to cemental
resorption are calcium deficiency, hypothyroidism and
Paget’s disease.

The resorptive process may not necessarily be a

continuous process; it may alternate with periods of
repair and deposition, which can be demarcated by
formation of reversal line. Remodelling of cementum
requires the presence of viable connective tissue and
can occur even in non-vital teeth.

Cementum is not exposed to the oral environment

because it is covered by alveolar bone and gingiva. In
cases of gingival recession and as a consequence of loss
of attachment in pocket formation, cementum can
become exposed to the oral environment. Once
exposed, organic substances, inorganic ions and bacteria
penetrate the sufficiently permeable cementum. Caries
of the cementum may also develop.

KEY POINTS TO NOTE

The Gingiva

1. The gingiva is that part of the oral mucosa that covers the

alveolar process of the jaws and surrounds the necks of
the teeth.

2. Anatomically it is divided into marginal, attached and

interdental gingiva.

3. Microscopically, the gingival epithelium is divided into

keratinized i.e., oral epithelium and non-keratinized i.e.,
junctional and sulcular epithelium.

4. The keratinized epithelium of the gingiva consists of four

layers, namely stratum basale, stratum spinosum, stratum
granulosum and stratum corneum.

5. The granular layer, which is seen in the oral epithelium

is absent in sulcular and junctional epithelium.

6. Junctional epithelium is attached to the tooth surface by

hemidesmosomes and basal lamina.

7. Lamina propria/gingival connective tissue consists of cells,

fibers, and blood vessels, embedded in the extracellular
matrix.

Tooth-supporting Structures
Periodontal Ligament

8. Periodontal ligament is a connective tissue structure that

surrounds the root and connects it with the bone.

9. It consists of cells and extra-cellular substances.

10. Cellular components are categorized as synthetic cells,

resorptive cells, progenitor cells, epithelial cells and
connective tissue cells.

11. Extracellular matrix is composed of fibers like collagen,

oxytalin and ground substance with proteoglycans and
glycoproteins.

12. The principal fibers of periodontal ligament are arranged

in six groups i.e. transseptal group, alveolar crest group,
horizontal, oblique, apical and inter-radicular group.

13. In the connective tissue other structures like blood vessels,

nerves, and lymphatics are also present.

14. Functions of periodontal ligament are explained under,

physical function, formative and remodelling function,
nutritive and sensory function.

15. Finally any trauma to the periodontal ligament can result

in the loss of alveolar bone and widening of ligament but
once the trauma is removed repair usually takes place.

16. When the inflammation extends from the gingiva to the

periodontal ligament, destruction of periodontal structures
will result, which is difficult to regenerate, hence the disease
of periodontal ligament are often irreversible.

Fig. 2.20: 

Configuration of cementoenamel junction

28

Essentials of Clinical Periodontology and Periodontics

Alveolar bone

17. Alveolar bone is that portion of the maxilla and mandible

that forms and supports the tooth sockets.

18. It consists of inner and outer cortical plate, the bone lining

the socket and an interior portion of cancellous bone.

19. It has two basic constituents (a) cells like osteoblasts,

osteoclasts, and osteocytes, (b) extracellular matrix made
up of 65 percent inorganic and 35 percent organic.
Inorganic is composed of calcium, phosphate along with
some trace elements. Organic matrix consists of 90 percent
Type I collagen with small amounts of non-collagenous
proteins such as osteonectin, osteocalcin, bone
morphogenetic proteins etc.

20. Fenestrations are isolated areas in which the root surface

is covered only by periosteum and gingiva, but the
marginal bone remains intact. When marginal bone is also
involved, the defect is called dehiscence.

21. Bone resorption occurs by three processes—(a) decalcifi-

cation, (b) degradation of matrix and (c) transport of
soluble factors to the extracellular fluid.

Cementum

22. Cementum is a calcified avascular mesenchymal tissue that

forms the outer covering of the anatomic root.

23. Acellular cementum forms during root formation and is

seen at the coronal portion of the root, whereas cellular
cementum forms after eruption of the tooth and is seen
apically on the root.

24. The cementum consists of 46 percent inorganic matter and

the rest 90 percent organic being Type I collagen and the
remaining consists of non-collagenous proteins.

25. Three types of relationships of cementum may exist at the

cementoenamel junction. In 60 to 65 percent of cases
cementum overlaps the enamel, in 30 percent edge-to-
edge butt joint exists and in 5 to 10 percent the cementum
and enamel do not meet.

REVIEW QUESTIONS

The Gingiva

1. Describe the microscopic and macroscopic features

of gingiva.

2. Discuss the development, structure and mode of

attachment of junctional epithelium.

3. Describe the blood supply to the gingiva.
4. Describe various gingival fiber groups with

illustrations.

Tooth-Supporting Structures

Periodontal Ligament

5. Describe the development, structure and

composition of periodontal ligament.

6. Enumerate various principle fibers of periodontal

ligament with the help of illustrations.

7. Discuss in detail the functions of periodontal

ligament.

Alveolar Bone

8. Discuss the alveolar bone with reference to the

following:

I. Structure, composition and parts of alveolar bone

II. Fenestration and dehiscence

III. Resorption and remodeling.

Cementum

9. Discuss cementum with reference to the following:

I. Structure and composition of cementum

II. Cementoenamel junction

III. Hypercementosis

IV. Classification.

BIBLIOGRAPHY

The Gingiva

1. AR Tencate. Oral Histology, Development, Structure and

Function.  5th edition, Mosby Publication.

2. Jan Lindhe. Clinical Periodontology and Implant Dentistry.

4th edition 2003 Blackwell Munksgaard Publication.

3. Jansen Van Rensburg. Oral biology. Quintessence

Publishing Co, Inc 1995.

4. Newman, Takei, Fermin A Carranza. Clinical periodon-

tology, 9th edition 2002, W B Saunders Co.

5. Thomas M Hassell. Tissues and cells of the periodontium.

Periodontol 2000, 1993;3.

Tooth-Supporting Structures

Periodontal Ligament

6. Jan Lindhe. Clinical Periodontology and Implant

Dentistry, IV edition, Blackwell Munksgaard publication,

2003.

7. Newman, Takei, Fermin A Carranza. Clinical periodon-

tology, IX edition, WB Saunders Co, 2002.

8. Thomas M Hassell. Tissues and cells of the periodontium,

Periodontol 2000; vol 3, 1993.

29

Biology of Periodontal Tissues

Alveolar Bone

9. AR Tencate. Oral histology, Development, Structure and

Funtion, V edition, Mosby Publication.

10. Grant, Stern, Listgarten. Periodontics, VI edition, Mosby

Publication, 1998.

11. J.D Manson, B Meley. Outline of Periodontics III edition,

British Library Cataloguing in Publication Data, 1995.

12. Jan Lindhe. Clinical Periodontology and Implant Dentistry,

IV edition, Blackwell Munksgaard Publication, 2003.

13. Newman, Takei, Fermin A Carranza. Clinical Periodon-

tology, IX edition, WB Saunders Co, 2002.

Cementum

14. AR Tencate.  Oral Histology, Development, Structure and

Function, IIIrd edition, St. Louis: C.V. Mosby Company,

1989.

15. BG Jansen Van Rensburg. Oral Biology, Quintenssence

Books, Chicago, 1995.

16. Bhaskar S N. Orbans,  Oral Histology and Embryology, 11th

edition, St. Louis CV Mosby company.

17. Newman, Takei, Fermin A. Carranza. Clinical Periodon-

tology, IX edition, W.B.Saunders and Co, 2002.

18. Schroeder H F. Oral sructural Bology, Thieme Medical

Publishers, Inc. New York, 1991.

30

Essentials of Clinical Periodontology and Periodontics

GENERAL EFFECTS OF AGING

In the Skin

a. The dermis and epidermis are thinned
b. Keratinization is diminished
c. Blood supply is diminished
d. Degeneration of nerve endings occur
e. Capillaries appear to become more fragile which may

result in haemangiomas after minor traumas

f. Tissue elasticity is decreased.

Bone

a. Undergoes osteoporosis with aging

b. The bone is rarified, trabeculae are reduced in

number and cortical plates are thinned

c. Vascularity is reduced and lacunar resorption is more

prominent

d. Increased susceptibility to fracture
e. With age water content of bone is reduced, the

mineral crystals are increased in size and collagen
fibers are thickened.

AGE CHANGES IN THE PERIODONTIUM
(Fig. 3.1)

Gingiva and Other Areas of the Oral Mucosa

1. Decreased keratinization.

Fig. 3.1: 

Aging of the periodontium

❒ GENERAL EFFECTS OF AGING

❒ AGE CHANGES IN THE PERIODONTIUM

• Gingiva and Other Areas of the Oral

Mucosa

• Periodontal Ligament and Age Changes in

the Periodontium

• Changes in the Alveolar Bone and

Cementum

• Bacterial Plaque and Immune Response

❒ EFFECTS OF AGING ON THE PROGRES-

SION OF PERIODONTAL DISEASES

❒ EFFECTS OF TREATMENT ON THE AGING

INDIVIDUALS

3

Periodontal Structures in

Aging Humans

31

Periodontal Structures in Aging Humans

2. Reduced or unchanged amount of stippling.
3. Decreased connective tissue cellularity.
4. Decreased oxygen consumption—which may reflect

upon the metabolic activity.

5. Increased width of attached gingiva.
6. Greater amounts of intercellular substances.
7. Atrophy of the connective tissue with loss of elasticity.
8. Increase in the number of mast cells.

Periodontal Ligament and Age Changes

in the Periodontium

1. Decrease in vascularity.
2. Decrease in mitotic activity.
3. Decrease in fibroblasts.
4. Collagen fibers and mucopolysaccharides are

decreased.

5. Increase in elastic fibers and arteriosclerotic changes

are seen.

6. Both increase and decrease in the width of the

periodontal ligament is seen. The periodontal ligament
width is increased as a result of less number of teeth
supporting the entire functional load and decrease
in its width is associated with reduced strength of the
masticatory musculature and continuous deposition
of cementum and bone.

Changes in the Alveolar Bone and Cementum

1. Osteoporosis.
2. Decreased vascularity.
3. Reduction in metabolic rate and healing capacity.
4. Resorption activity is increased and the rate of bone

formation is decreased.

5. Continuous deposition of cementum occurs with age

and greater irregularity in the surface of both the
cementum and alveolar bone facing the periodontal
ligament is seen.

Bacterial Plaque and Immune Response

(Fig. 3.2)

1. Plaque accumulation has been suggested to increase

with age.

2. Some studies have shown a qualitative change in the

subgingival flora, it has been speculated that a shift
occurs in certain periodontal pathogens with age,
including increase in number of enteric rods,
Porphyromonas gingivalis and decreased role for
Actinobacillus actinomycetemcomitans. Some-age
related changes have been shown to affect the host
response, but there is no evidence to show that these
changes correlate with periodontitis in elderly
patients.

EFFECTS OF AGING ON THE
PROGRESSION OF PERIODONTAL
DISEASES

The conclusions drawn from the various studies are
strikingly-consistent and show that, age has either no
effect or provides a small and clinically insignificant
increased risk of loss of periodontal support. Therefore
age has been suggested to be not a true risk factor but
a background or an associated factor for periodontitis.

EFFECTS OF TREATMENT ON THE
AGING INDIVIDUALS

The few studies that have been done so far have clearly
demonstrated that inspite of certain changes in the
periodontium with aging, no differences in response to

Fig. 3.2: 

Periodontal changes associated

with aging

32

Essentials of Clinical Periodontology and Periodontics

nonsurgical or surgical treatment have been shown for
periodontitis.

REVIEW QUESTIONS

1. Describe the age changes in the periodontium.
2. Role of aging on the progression of periodontal

diseases.

BIBLIOGRAPHY

1. JD Manson, B Meley. Outline of Periodontics, Third

Edition 1995, British Library Cataloguing in Publication

Data.

2. Newman, Takei, Fermin A, Carranza. Clinical

Periodontology, Ninth edition, 2002 W.B. Saunders.

NEED FOR CLASSIFICATION

• For the purpose of diagnosis, prognosis and treatment

planning.

• To understand the etiology, pathology of the diseases

of the periodontium.

• For logical, systematic separation and organization of

knowledge about disease.

• Facts can be filed for future references.
• Helps to communicate among clinicians, researchers,

educators, students, epidemiologists and public health
workers.

CURRENT CLASSIFICATION SYSTEMS OF
PERIODONTAL DISEASES

World Workshop in Clinical Periodontics

(1988)

Gingivitis

• Childhood gingivitis
• Chronic (adult) gingivitis
• Acute necrotizing ulcerative gingivitis

Periodontitis

• Adult Periodontitis:

Possible sub-groups:
– High risk
– Normal risk
– Refractory periodontitis

• Early Onset Periodontitis:

– Localized juvenile periodontitis
– Rapidly progressive periodontitis
– Pre-pubertal periodontitis

* Localized
* Generalized

– Periodontitis associated with systemic

diseases

❒

❒

❒

❒

❒ NEED FOR CLASSIFICATION

❒

❒

❒

❒

❒ CURRENT CLASSIFICATION SYSTEMS

OF PERIODONTAL DISEASES

• Gingivitis

• Periodontitis

❒

❒

❒

❒

❒ SYNOPSIS OF TYPES AND

CHARACTERISTICS OF GINGIVAL

DISEASES

❒

❒

❒

❒

❒ SYNOPSIS OF TYPES AND

CHARACTERISTICS OF PERIODONTAL

DISEASES

4

Classification Systems of

Periodontal Diseases

36

Essentials of Clinical Periodontology and Periodontics

World Workshop in Clinical Periodontics (1989)

I. Adult periodontitis.

II. Early onset periodontitis.

• Prepubertal

– Generalized or localized

• Juvenile

– Generalized or localized

• Rapidly progressive periodontitis

III. Periodontitis associated with systemic diseases

• Down’s Syndrome
• Diabetes – Type I
• Papillon – Lefévre syndrome
• AIDS and other diseases

IV. Necrotizing ulcerative periodontitis

V. Refractory periodontitis

Genco (1990)

• Periodontitis in adults.
• Periodontitis in juveniles

– Localized form
– Generalized form

• Periodontitis with systemic involvement

– Primary neutrophil disorders
– Secondary or associated neutrophil impairment.
– Other systemic diseases

• Miscellaneous conditions

Ranney (1993)

Gingivitis

• Gingivitis, plaque bacterial
• Non-aggravated
• Systemically-aggravated by sex hormones, drugs,

systemic diseases

• Necrotizing ulcerative gingivitis
• Systemic determinants unknown
• Related to HIV
• Gingivitis, non-plaque
• Associated with skin diseases, allergic, infections.

Periodontitis

• Adult periodontitis

– Non-aggravated

– Systematically-aggravated (neutropenias, leuke-

mias, lazy leukocyte syndrome, AIDS, diabetes
mellitus, Crohn’s disease, Addison’s disease).

• Early onset periodontitis:

– Localized early onset periodontitis
– Neutrophil abnormality
– Generalized early onset periodontitis, neutrophil

abnormality, immunodeficient

• Early onset periodontitis related to systemic disease:

– Leukocyte adhesion deficiency, hypophospha-

tasia, Papillon- Lefevre syndrome, neutropenias,
leukemias, Chediak- Higashi syndrome, AIDS,
diabetes mellitus type-I, trisomy-21, histiocytosis
X, Ehlers Danlos syndrome (type VIII)

• Early onset periodontitis, systemic determinants

unknown

• Necrotizing ulcerative periodontitis

– Systemic determinants unknown
– Related to HIV
– Related to nutrition

• Periodontal abscess

European Workshop on Periodontology

(1993)

• Adult periodontitis
• Early onset periodontitis
• Necrotizing periodontitis

All the above-mentioned classification systems have

been widely used by clinicians and research scientists
throughout the world, unfortunately they have been many
shortcomings including:
1. Considerable overlap in disease categories.
2. Absence of a gingival disease component
3. Inappropriate emphasis on age of onset of disease

and rates of progression.

4. Inadequate or unclear classification criteria.

Hence, the need for a revised classification system

for periodontal diseases was emphasized and in 1999,
the international workshop had considered designing a
new classification system.

37

Classification Systems of Periodontal Diseases

Classification of Periodontal

Disease and Condition

By AAP 1999 (International Workshop for Classification
of Periodontal Disease).

Gingival Disease (Table 4.1)

A. Dental plaque–induced gingival diseases: These

diseases may occur on a periodontium with no
attachment loss or on one with attachment loss that
is stable and not progressing.
1. Gingivitis associated with dental plaque only:

a. Without local contributing factors.
b. With local contributing factors

2. Gingival diseases modified by systemic factors:

a. Associated with endocrine system:

i. Puberty-associated gingivitis

ii. Menstrual cycle—associated gingivitis

iii. Pregnancy-associated

– Gingivitis
– Pyogenic granuloma

iv. Diabetes mellitus – associated gingivitis

b. Associated with blood dyscrasias:

i. Leukemia-associated gingivitis

ii. Others

3. Gingival diseases modified by medications:

a. Drug-influenced gingival diseases

i. Drug-influenced gingival enlargements.

ii. Drug-influenced gingivitis

– Oral contraceptive- associated gingivitis
– Others

4. Gingival diseases modified by malnutrition:

a. Ascorbic acid deficiency gingivitis
b. Others

B. Nonplaque-induced gingival lesions:

1. Gingival diseases of specific bacterial origin.

a. Neisseria gonorrhoeae
b. Treponema pallidium
c. Streptococcal species
d. Others

2. Gingival diseases of viral origin

a. Herpes-virus infections

• Primary herpetic gingivostomatitis
• Recurrent oral herpes
• Varicella zoster

b. Others

3. Gingival diseases of fungal origin

a. Candida species infections; generalized gingival

candidiasis

b. Linear gingival erythema
c. Histoplasmosis
d. Others.

4. Gingival lesions of genetic origin

a. Hereditary gingival fibromatosis
b. Others

5. Gingival manifestations of systemic conditions

a. Mucocutaneous lesions:

i. Lichen planus

ii. Pemphigoid

iii. Pemphigus vulgaris

iv. Erythema multiforme

v. Lupus erythematosus

vi. Drug induced

vii. Others

b. Allergic reactions:

i. Dental restorative materials

– Mercury
– Nickel
– Acrylic
– Others

ii. Reactions attributable to:

– Toothpaste’s or dentifrices
– Mouth rinses or mouthwashes
– Chewing gum additives
– Foods and additives

iii. Others

6. Traumatic lesions (factitious, iatrogenic, or

accidental)
a. Chemical injury
b. Physical injury
c. Thermal injury

7. Foreign body reactions
8. Not otherwise specified (NOS).

38

Essentials of Clinical Periodontology and Periodontics

Table 4.1: Synopsis of types and characteristics of gingival diseases

Types of gingival disease Causes

Signs and symptoms

Treatment

Gingivitis

Bacterial plaque, local

Gingival redness and

Debridement, plaque control,

plaque—retention factors

swelling, bleeding, does

correct plaque retentive

not cause loss of clinical

factors, supportive

attachment

periodontal therapy

Acute necrotizing

Bacterial plaque, may be

Pain, gingival redness,

Debridement, plaque control,

gingivitis

associated with AIDS at any age

swelling, bleeding, necrosis

antimicrobial rinse, supportive

of interproximal papilla

periodontal therapy

Desquamative

Skin diseases, lichen planus,

Gingival redness, epithelial

Gentle plaque control,

gingival disease

pemphigus and cicatrical

denudation, pain with

palliative and symptomatic

pemphigoid

trauma  as on eating and

therapy, supportive

brushing

periodontal therapy

Gingivitis associated

Manifestation of systemic

Dependent on

Treatment of systemic disease,

with systemic

diseases in gingiva

systemic disease

atraumatic plaque control,

diseases

antimicrobial rinse, supportive
periodontal therapy

Gingivitis associated

Bacterial plaque, local

Gingival redness and

Debridement and plaque

with pregnancy

plaque, retentive factors,

swelling, bleeding,

control, supportive

hormonal influence

pyogenic granuloma

periodontal therapy, possile
excision of pyogenic granuloma

Drug-induced

Calcium channel blocking

Gingival enlargement

Debridement and plaque

gingival enlargement

drugs, phenytoin, cyclosporine

control, surgical excision, use of
alternative medications,
supportive periodontal therapy

Allergic reaction

Local allergens

Gingival redness and

Identification and elimination

swelling

of allergic agent

Herpetic

Herpes type I virus

Pain, vesicle formation,

Palliative and symptomatic

gingivostomatitis

ulceration

therapy, antiviral medication

Gingival disease of

Neiserria gonorrhoeae,

Varies according to

Identification and elimination

specific bacteria or

Treponema  pallidum,

infectious agent

or control of infectious

fungal origin

streptococcal species,

agent, appropriate

Candida, histoplasmosis

chemotherapy

Chronic Periodontitis (Table 4.2)

a. Localized

— Less than 30 percent of sites

involved or,

b. Generalized — More  than 30 percent of sites

involved.

c. Slight

— 1 to 2 mm clinical attachment

loss.

d. Moderate

— 3 to 4 mm clinical attachment loss

and,

e. Severe

— More than 5 mm clinical attachment

loss.

Aggressive Periodontitis

a. Localized–slight, moderate or severe
b. Generalized.

39

Classification Systems of Periodontal Diseases

Table 4.2: Synopsis of types and characteristics of periodontal diseases

Types of periodontal

Causes

Signs and symptoms

Treatment

disease
Chronic periodontitis

Bacterial plaque, smoking,

Overall slow progression

Plaque control, smoking

local plaque retentive factors

with generalized periodontal

cessation, scaling and

such as dental calculus and

pockets, bone and clinical

root planing, correction of

faulty restorations

attachment loss, may be

local plaque retentive factors

generalized or localized

antimicrobial chemotherapy,

periodontal surgery, supportive

periodontal  therapy

Aggressive

Bacterial plaque, superinfection

Severe and rapid periodontal Specific, antimicrobial therapy

periodontitis

with specific periodontal bacteria,

destruction possibly followed

based on microbial analysis,

possible impaired host response,

by periods of remission, may

smoking cessation,

smoking

be generalized or localized

debridement, possible

periodontal surgery,

supportive periodontal therapy

Refractory periodontitis

Bacterial plaque, superinfection,

Progression of disease

Specific, antimicrobial,

of any type

with specific, periodontal

despite good conventional

therapy based on microbial

bacteria, possible impaired host

therapy and supportive

analysis, smoking cessation

response, smoking

periodontal therapy

debridement, possible perio-

dontal surgery, supportive

periodontal therapy

Periodontitis as a

Associated with disorders of the

Generalized and localized

Treatment of systemic disease,

manifestation of

blood or blood forming organs

forms of severe destruction

atraumatic plaque control,

systemic diseases

such as neutropenia, leukemia

of bone and connective

anti-microbial rinse,

or genetic disorders

tissue tooth support

supportive periodontal therapy

Juvenile periodontitis:

Probably major autosomal

Localized juvenile,

Scaling and root planing,

localized and

gene effect and infection with

periodontitis: typically loss

specific antimicrobial therapy

generalized

Actinobacillus

of bone support of first

based on microbial analysis,

actinomycetemcomitans

molars and incisors.

possible regenerative surgery,

Generalized juvenile

supportive periodontal therapy

periodontitis: generalized

loss of support throughout

dentition

Periodontitis

May be of endodontic or

Periodontal pocket

If primarily of endodontic

associated with

periodontal origin

extending to area of

origin, endodontic therapy

endodontic lesions

endodontic lesion

alone, if primarily of

periodontal origin, endodontic

and periodontal therapy or

extraction may be necessary

Periodontal abscess

Subgingival bacteria

Painful, acute swelling of

Nonsurgical or surgical

periodontal tissues associated debridement, antibiotic

with deep periodontal pocket

therapy, regeneration of

lost periodontal support is often

a possibility

Acute necrotizing

Immunocompromised,

Pain, rapid loss of bone

Debridement, atraumatic

periodontitis

may be associated

and tooth support associated

plaque control, analgesic

with HIV

with gingival and

medication, antimicrobial rinse,

bony necrosis

supportive periodontal therapy

40

Essentials of Clinical Periodontology and Periodontics

Periodontitis as a Manifestation of
Systemic Diseases

a. Associated with hematological disorders:

i. Acquired neutropenia

ii. Leukemias

iii. Others

b. Associated with genetic disorders:

i. Familial and cyclic neutropenia

ii. Down’s syndrome

iii. Leukocyte adhesion deficiency syndrome

iv. Papillon-Lefévre syndrome

v. Chediak-Higashi syndrome

vi. Histiocytosis syndrome

vii. Glycogen storage disease

viii. Infantile genetic agranulocytosis

ix. Cohen syndrome

x. Ehlers-Danlos syndrome (Type IV and VIII)

xi. Hypophosphatasia

xii. Others

Necrotizing Periodontal Diseases

a. Necrotizing ulcerative gingivitis
b. Necrotizing ulcerative periodontitis.

Abscesses of the Periodontium

a. Gingival abscess
b. Periodontal abscess
c. Pericoronal abscess

Periodontitis Associated with Endodontic Lesions

a. Combined periodontic—endodontic lesions.

Developmental or Acquired Deformities
and Conditions

a. Localized tooth-related factors that modify or pre-

dispose to plaque induced gingival diseases/
periodontitis.

i. Tooth anatomic factors

ii. Dental restorations/appliances

iii. Root fractures

iv. Cervical root resorption and cemental tear

b. Mucogingival deformities and conditions around

teeth:

i. Gingival/soft tissue recession, facial or lingual

surfaces, interproximal (papillary)

ii. Lack of keratinized gingiva

iii. Decreased vestibular depth

iv. Aberrant frenum/muscle position

v. Gingival excess:.

– Pseudopocket
– Inconsistent gingival margin
– Excessive gingival display
– Gingival enlargement

vi. Abnormal color

c. Mucogingival deformities and conditions on eden-

tulous ridges:

i. Vertical and/or horizontal ridge deficiency.

ii. Lack of gingival/keratinized tissue

iii. Gingival/soft tissue enlargement

iv. Aberrant frenum/muscle position

v. Decreased vestibular depth

vi. Abnormal color

d. Occlusal trauma:

i. Primary occlusal trauma

ii. Secondary occlusal trauma

BIBLIOGRAPHY

1. Carranza Jr. Newman, Clinical Periodontology. W.B.

Saunders Company, Ninth Edition.

2. Gary C. Armitage, Development of a classification system

for periodontal diseases and conditions. Ann. Periodontol,

1999;4:1-6.

3. Ranney RR. Classification of periodontal diseases.

Periodontology 2000, 1993:2-13.

4. Robert J, Genco. Development of classification systems for

periodontal diseases and condition. Annals of

Periodontology December, 1999;4(1).

41

Epidemiology of Gingival and Periodontal Diseases

EPIDEMIOLOGY

Definition

Study of health and disease in populations and how the
states are influenced by heredity, biology, physical and
social environmental ways of living.

Types of Epidemiologic Research

a. Descriptive studies.
b. Analytical studies.
c. Experimental epidemiology.

Descriptive Studies

These are used to observe and document the occurrence,
progression and distribution of a disease or condition

in populations, in relation to host and environmental
factors (when, where and who).

Measurement of disease: Incidence can be obtained from
“Longitudinal studies” and prevalence from “cross-
sectional” studies.
a. Incidence rate: This is defined as the number of new

cases occurring in a defined population during a
specific period of time.

b. Prevalence rate: This refers to all current cases (new

and old) existing at a given point in time or over
a period of time in a given population.

Two types are described:
a. Point prevalence.
b. Period prevalence.

Longitudinal Studies

The observations are repeated in the same population
over a prolonged period of time by means of follow-
up examinations.

Uses

i. To study the natural history of disease and its future

outcome.

ii. For identifying the risk factors of disease.

iii. For  finding out the incidence rate or rate of

occurrence of new cases.

❒

❒

❒

❒

❒ DEFINITION, TYPES AND AIMS OF

EPIDEMIOLOGY

❒

❒

❒

❒

❒ DEFINITION, USES AND CHARACTERIS-

TICS OF AN INDEX

❒

❒

❒

❒

❒ VARIOUS INDICES USED TO STUDY

PERIODONTAL PROBLEMS

• To Assess Gingival Inflammation

• To Measure Periodontal Destruction

• To Measure Plaque Accumulation

• To Measure Calculus

• To Assess Treatment Needs

5

Epidemiology of Gingival

and Periodontal Diseases

42

Essentials of Clinical Periodontology and Periodontics

Disadvantages
They are difficult to organize and time consuming as
compared to cross-sectional studies

Cross-sectional Studies

It is the simplest form of an observation study. It is based
on a single examination of a cross-section of population
at one point of time. (It is also known as prevalence
study).

Uses

i. It is more useful for chronic (long-term diseases)

as compared to acute (short-term) diseases.

ii. It gives information about the distribution of a

disease in a population rather than its etiology.

Analytical Studies

Includes two distinct types:
a. Case control study
b. Cohort study

Case control or retrospective study: The study precedes
backwards from effect to cause.

Cohort study: It is a prospective study (incidence study
or longitudinal study), which is usually undertaken to
obtain, additional evidence to refute and support the
existence of an association between the suspected cause
and disease.

Experimental Epidemiology

It is used to test hypothesis further by introducing a
preventive or therapeutic agent and comparing the
outcome in the test subjects with concurrent observations
in control groups.

Aims of Epidemiology

Three main aims have been proposed:
a. To describe the distribution and size of disease

problems in human populations.

b. To identify the etiological factors in the pathogenesis

of disease.

c. To provide the data essential for the planning,

implementation and evaluation of services for the
prevention, control and treatment of disease.

INDEX

Definition

These are numerical values describing the relative
status of the population on a graduated scale with
definite upper and lower limits, which are designed
to permit and facilitate comparisons with other
populations and are classified by the same criteria and
methods.

Purposes and Uses of an Index

For Individual Patients

An index can,

i. Provide individual assessment to help a patient to

recognize an oral problem.

ii. Reveal the degree of effectiveness of present oral

hygiene practices.

iii. Motivate the person in preventive and professional

care for the elimination and control of oral
disease.

iv. Evaluate the success of an individual and

professional treatment over a period of time by
comparing index scores.

In Research

An index is used to,

i. Determine the baseline data before the

experimental factors are introduced.

ii. Measure the effectiveness of specific agents for

the prevention control and treatment of oral
conditions.

iii. Measures the effectiveness of mechanical devices

for personal care, such as, toothbrushes, interdental
cleaning devices or water irrigators.

43

Epidemiology of Gingival and Periodontal Diseases

In Community Health

An index

i. Can show the prevalence and trends of incidence,

of a particular condition occurring within a given
population.

ii. It provides a baseline data to show the existing

dental health practices.

iii. It assesses the needs of a community and compares

the effects of a community program and evaluates
the results.

Characteristics of an Index

1. It should be simple to use and accurate.
2. It should require minimal equipment and expenses.
3. It should have clear- cut criteria, which are readily

understandable.

4. It should be as free as possible from subjective

interpretation.

5. It should be reproducible by the same examiner or

different examiners.

6. Be amenable to statistical analysis, have validity and

reliability.

7. Not require an excessive amount of time to complete.
8. Not cause patient discomfort or be otherwise

unacceptable to a patient.

Indices used to Assess the following

Periodontal Problems

1. The degree of inflammation of the gingival tissues.
2. The degree of periodontal destruction.
3. The amount of plaque accumulated.
4. The amount of calculus present.
5. In addition, indices are developed to assess the

treatment needs.

Indices used to Assess Gingival Inflammation

a. PMA index by Schour and Massler.
b. Gingivitis component of the periodontal disease.
c. Gingival index by Loe and Sillness.
d. Indices of gingival bleeding.

i. Sulcus bleeding index (SBI) of Muhlemann and

Mazor.

ii. Papillary bleeding index by Muhlemann.

iii. Bleeding points index by Lennox and Kopczy K

iv. Interdental bleeding index by Caton and Polson.

v. Gingival bleeding index by Ainamo and Bay.

Indices used to Measure
Periodontal Destruction

a. Russell’s periodontal index.
b. Periodontal disease index by Ramfjord.
c. Extent and severity index by Carlos and co-workers.
d. Radiographic approaches to measure bone loss.

i. GBI—Gingival bone count index by Dunning and

Leach.

ii. PSI—Periodontal severity index by Adams and

Nystrom.

Indices used to Measure Plaque Accumulation

a. Plaque component of periodontal disease index by

Ramfjord.

b. Simplified oral hygiene index by Greene and

Vermillion.

c. Turskey-Gillmore-Glickman modification of the

Quigley-Hein plaque index.

d. Plaque index by Sillness and Loe.
e. Modified navy plaque index.
f. Patient hygiene performance index by Podshadley

and Haley.

g. Plaque weight.
h. Plaque free score by Grant, Stern and Everett.
i. Plaque control record by O’leary.

Indices used to Measure Calculus

a. Calculus component of simplified oral hygiene index

by Greene and Vermillion.

b. Calculus component of the periodontal disease index

by Ramfjord.

c. Probe method of calculus assessment by Volpe and

associates

44

Essentials of Clinical Periodontology and Periodontics

d. Calculus surface index by Ennever and co-workers
e. Marginal line calculus index by Muhlemann and

Villa

Indices used to Assess Treatment Needs

a. Gingival periodontal index.
b. Community periodontal index of treatment needs

by Ainamo and associates.

c. PTNS—Periodontal treatment need system by Belini

HT.

INDICES USED TO ASSESS
GINGIVAL INFLAMMATION

Papillary Marginal Attachment (PMA) Index by

Schour and Massler (1944)

The basic philosophy used in the development of the
PMA index was very similar to the DMF index, i.e. the
number of gingival units affected were counted rather
than the severity of the inflammation. A gingival unit
is divided into three component parts:

i. Papillary gingiva (P)

ii. Marginal gingiva (M)

iii. Attached gingiva (A)

The presence or absence of inflammation on each

gingival unit is recorded as 1 or 0 respectively. The P,
M, A numerical values for all the teeth are added
separately and then added together to express the PMA
index score per person. The developers of this index
eventually added a severity component for assessing
gingivitis, the papillary units (P) were scored on a scale
of 0 to 5, and the marginal (M) and attached gingiva
were scored on a scale of 0 to 3.

Gingivitis Component of the

Periodontal Disease

The periodontal disease index (PDI) is similar to PI, in
that; both are used to measure the presence and severity
of periodontal disease. The PDI does so by combining
the assessments of gingivitis and gingival sulcus depth

on six selected teeth (# 3, 9, 12, 19, 25 and 28). This
group of teeth frequently referred to as the Ramfjord
teeth, have been tested as reliable indicators for the
various regions of the oral cavity. Calculus and plaque
are also examined to assist in formulating a
comprehensive assessment of periodontal status.

A numerical score for the gingival status component

of the PDI is obtained by adding the values for all the
gingival units and dividing it by the number of teeth
present. This index has been used in epidemiological
surveys, longitudinal studies and clinical trials.

Gingival Index by Loe H and Sillness J (1963)

This index was solely developed for the purpose of
assessing the severity of gingivitis and its location in four
possible areas.

Method

The severity of gingivitis is scored on all surfaces of all
teeth, or selected teeth, or on selected surfaces of all
teeth, or, selected teeth. The tissues surrounding each
tooth are divided into four gingival scoring units:
• Distal facial papillae,
• Facial margin,
• Mesial facial papillae,
• Entire lingual gingival margin.

A blunt instrument is used for recording the scores

based on the following criteria:
0 — No inflammation
1 — Mild inflammation, no bleeding elicited on probing
2 — Moderate inflammation, bleeding on probing
3 — Severe inflammation

The scores around each tooth are added and divided

by four to arrive at the score for that particular tooth.
Total all the teeth scores and divide it by the number
of teeth. This provides the gingival index score per
person. The numerical values are correlated as follows:
0.1 to 1.0 — Mild gingivitis
1.1 to 2.0 — Moderate gingivitis
2.1 to 3.0 — Severe gingivitis

45

Epidemiology of Gingival and Periodontal Diseases

Indices of Gingival Bleeding

Sulcular bleeding Index by
Muhlemann and Son (1971)

The purpose of the index is to locate areas of the gingival
sulcus that bleed upon gentle probing and thus recognize
and record the presence of early inflammatory gingival
disease. Four gingival units are scored systemically for
each tooth: the labial and lingual marginal gingiva (M
units) and the mesial and distal papillary gingiva (P units).
The probe is held parallel with the long axis of the tooth
and 30 seconds after probing; scoring is done based on
the criteria, which ranges from 0 to 5. Each of the four
gingival units is scored 0 to 5. Scores for the four units
are added and divided by four. Adding the scores of
the undivided teeth and dividing them by the number
of teeth can determine the sulcus-bleeding index.

Scoring criteria:
0 — Normal appearing gingiva, no bleeding upon

probing

1 — No color or contour changes, but bleeding on

probing

2 — Bleeding on probing, color change (reddening),

no edema and contour changes

3 — Bleeding on probing, color change, mild

inflammatory edema

4 — Bleeding on probing, color change, severe

inflammatory edema.

5 — Spontaneous bleeding on probing, color change,

very severe inflammatory edema with or without
ulceration.

Papillary Bleeding Index by Muhlemann HR (1977)

It is based on bleeding elicited, following gentle probing
of the interdental papilla. A blunt periodontal probe is
carefully inserted into the gingival sulcus at the base of
the interdental papilla on the mesial aspects, and then
moved coronally to the papilla tip. This is repeated on
the distal aspect of the same papilla. The intensity of
any bleeding thus provoked will be recorded on a scale
of 0 to 4.

Scoring criteria:
0 — No bleeding
1 — A single discrete bleeding point appears
2 — Several isolated bleeding points or a single fine

line of blood appears

3 — The interdental triangle fills with blood shortly after

probing

4 — Profuse bleeding occurs after probing, blood flows

immediately into the marginal sulcus

Bleeding Points Index by Lennox and
Kopczy K

The index was developed to assess a patient’s oral hygiene
performance. It determines the presence or absence of
gingival bleeding interproximally and on the facial and
lingual surfaces of each tooth. A periodontal probe is
drawn horizontally through the gingival crevice of a
gradient, and the gingiva is examined for bleeding after
30 seconds.

Interdental Bleeding Index by
Caton and Polson

The index utilizes a triangle-shaped toothpick made of
soft, pliable wood to stimulate the interproximal
gingival tissue. The interproximal cleaner is inserted
horizontally between the teeth from the facial surface,
depressing the interproximal papillae by up to 2 mm.
The wooden cleaner is inserted and removed four times,
and the presence or absence of bleeding within 15 seconds
is noted. The score is determined by dividing the number
of bleeding sites by the number of sites evaluated.

Gingival Bleeding Index by Ainamo and Bay

The index was developed as an easy and suitable way
for the practitioner to assess a patient’s progress in plaque
control. The presence or absence of gingival bleeding
is determined by gentle probing of the gingival crevice
with a periodontal probe. The appearance of the bleeding
within 10 seconds indicates a positive score, which is
expressed as a percentage of the total number of gingival
margins examined.

46

Essentials of Clinical Periodontology and Periodontics

INDICES USED TO MEASURE
PERIODONTAL DESTRUCTION

Russell’s Periodontal Index by Russell AL (1956)

The index was intended to estimate deeper periodontal
disease by measuring the presence or absence of the
gingival inflammation and its severity, pocket formation
and masticatory function.

All the teeth present are examined. All of the gingival

tissues surrounding each tooth are assessed for gingival
inflammation and periodontal involvement. Russell
choses the scoring values (0, 1, 2, 6, 8) in order to relate
the stages of the disease in an epidemiological survey
to the clinical conditions observed.

Sum of individual scores

PI score per person = —————————————

Number of teeth present

Since only a mouth mirror and no calibrated probe

or radiographs is used while performing the PI
examination, the results tend to under estimate the true
level of periodontal disease. The number of periodontal
pockets without obvious supragingival calculus is also
underestimated in the periodontal index.

Scoring Criteria

Score Criteria and scoring

Additional X-ray criteria

for field studies

followed in the clinical test

0

Negative:  There is neither

Radiographic appearance

overt inflammation in the

is essentially normal

investing tissues nor loss
of function due to des-
truction of supporting
tissues.

1

Mild Gingivitis: There is
an overt area of inflam-
mation in the free gingiva,
but this area does not
circumscribe the tooth

2

Gingivitis:  Inflammation
completely circumscribing
the tooth, but there is no
apparent break in the
epithelial attachment.

4

Used when radiographs

There is early notch-like

are available

resorption of alveolar

crest

6

Gingivitis with pocket

There is horizontal bone

formation:  The epithelial

loss involving the entire

attachment has been

alveolar crest, up to half

broken and there is a

of the length of the tooth

pocket. There is no

root.

interference with normal
masticatory functions, the
tooth is firm and has not
drifted. There is hori-
zontal bone loss involving
the entire alveolar crest,
up to half of the length
of the tooth root.

8

Advanced destruction with

There is advanced bone

loss of masticatory func-

loss, involving more than

tion:  The tooth may be

one-half of the length of

loose, may have drifted,

tooth root, infrabony

may sound dull on per-

defects, widening of

cussion and may be

periodontal ligament,

depressible in socket.

root resorption.

Clinical Conditions and Periodontal Scores

Clinical conditions

Group PI scores

Stage of disease

Clinically-normal

0 to 0.2

supportive tissues
Simple gingivitis

0.3 to 0.9

Beginning of des-

0.7 to 1.9

Reversible

tructive–periodontal
disease
Established destructive

1.6 to 5.0

Irreversible

periodontal disease
Terminal disease

3.8 to 8.0

Irreversible

Uses

i. Epidemiological surveys.

ii. More data can be assembled using periodontal

index.

iii. Used in the National Health Survey (NHS).

Periodontal Disease Index by

Sigurd P Ramfjord (1959)

This index is a clinician’s modification of the Russell’s
periodontal index for epidemiological surveys of
periodontal disease. Emphasis is placed on the recording

Contd...

Contd...
Score Criteria and scoring

Additional X-ray criteria

for field studies

followed in the clinical test

47

Epidemiology of Gingival and Periodontal Diseases

of the attachment level of the periodontal disease relative
to the cementoenamel junction.

Only six selected teeth are scored for assessment of

the periodontal status of the oral cavity, which are 1,
6, 21, 24, 36, 41, 44. The first step is scoring of the
gingival status. The gingiva around the teeth is dried
superficially by gently dabbing it with absorbing cotton.
Changes in color, consistency, contour; evidence of
ulceration of gingiva is evaluated by a periodontal probe.
The next step is recording of the crevice depth related
to a cementoenamel junction. For this purpose a
University of Michigan 0 probe is used. The end of probe
should be placed against the enamel surface coronally
to the margin of the gingiva and minimal force is applied
in an apical direction maintaining tooth contact. The
crevicular measurements are recorded in the following
manner. Distance from free gingival margin to the
bottom of the gingival crevice or pocket on the buccal
and mesial aspect of the each tooth. The buccal measure-
ments should be made at the middle of the buccal
surfaces and the mesial measurement should be made
at the buccal aspect of the interproximal contact area.

The scoring criteria ranges from 0 to 6. The PDI score

for the individual can be obtained by adding the scores
for each tooth examined and then, dividing by the
number of teeth examined. The PDI score will range
from 0 to 6.

Scoring Criteria

0 — Absence of inflammation
1 — Mild to moderate inflammatory gingival changes

not extending all around the tooth

2 — Mild to moderately severe gingivitis extending all

around the tooth

3 — Severe gingivitis, characterized by marked

redness, tendency to bleed and ulceration

4 — Gingival crevice in any of the four measured areas

(mesial, distal, buccal, lingual), extending apically
to the CEJ, but not more than 3 mm

5 — Gingival crevice in any of the four measured areas

extending apically, 3-6 mm from the CEJ

6 — Gingival crevice in any of the four measured areas

extending apically more than 6 mm from the CEJ

Extent and Severity Index by

Carlos and Coworkers

In this newer model, periodontal disease is viewed as
a chronic process with intermittent periods of activity
and remission that affects individual teeth and sites around
the teeth at different rates within the same mouth. It
uses, a periodontal probe (NIDR probe) to determine
attachment levels. The ESI score is a bivariate statistic.
It expresses the percentage of sites that exhibit disease.
ESI is based on probe measurements (at the mesiobuccal,
interproximal and midbuccal locations on all teeth
excluding molars and at the mesiobuccal interproximal
and midbuccal of the mesial root of molars) at 14 sites
in half of the maxillary arch and at 14 sites in the
contralateral mandibular arch.Attachment level
measurements are made using the Ramfjord criteria.

Radiographic Approaches to

Measure Bone Loss

Gingival Bone Count Index by Dunning and Leach

This index records the gingival condition on a scale of
0 to 3 and the level of the crest of the alveolar bone.

The Periodontitis Severity Index
by Adams and Nystrom

The index assesses the presence or absence of
periodontitis as the product of clinical inflammation and
interproximal bone loss determined radiographically using
a modified schei rule.

INDICES USED TO MEASURE
PLAQUE ACCUMULATION

Plaque Component of Periodontal

Disease Index by Ramfjord

The index is used on the six teeth selected by Ramfjord
(teeth number 3, 9, 12, 19, 25 and 28) after staining
with Bismarck brown solution. The criteria is to measure

48

Essentials of Clinical Periodontology and Periodontics

the presence and extent of plaque on a scale of 0 to
3, looking specifically at all interproximal facial and lingual
surfaces of the index teeth. The scoring criteria is as
follows:
0 — No plaque present.
1 — Plaque present on some but not all interproximal,

buccal and lingual surfaces of the tooth.

2 — Plaque present on all interproximal buccal and

lingual surfaces, but covering less than one half
of the surfaces.

3 — Plaque extending over all interproximal, buccal

and lingual surfaces, and covering more than one
half of these surfaces.

Only fully-erupted teeth are scored and missing teeth

should not be substituted.

Total score

Plaque score of an individual = —————————

Number of teeth

examined

Uses

Suitable for:
a. Longitudinal studies of periodontal disease.
b. Epidemiological surveys.
c. Clinical trials of preventive or therapeutic agents.

Simplified Oral Hygiene Index by

Greene and Vermillion (1964)

The OHI-S measures the surface area of the tooth that
is covered by debris and calculus. It consists of two
components:
a. Debris index-simplified (DI-S).
b. Calculus index-simplified (CI-S).

Scoring Criteria for D1-S

0 — No debris or stain present.
1 — Soft debris covering not more than one-third of

the tooth surface or the presence of extrinsic stains
without other debris, regardless of surface area
covered.

2 — Soft debris, covering more than one-third but not

more than two- thirds of the exposed tooth
surface.

3 — Soft debris, covering more than two-thirds of the

exposed tooth surface.

Scoring Criteria for CI-S

0 — No calculus present.
1 — Supragingival calculus covering not more than

one-third of the exposed tooth surface.

2 — Supragingival calculus covering more than one-

third, but not more than two-thirds of the exposed
tooth surface or the presence of the individual
flecks of subgingival calculus around the cervical
portion of the tooth or both.

3 — Supragingival calculus covering more than two-

thirds of the exposed tooth surface or a continuous
heavy band of subgingival calculus around the
cervical portion of the tooth, or both.

Method

Each component is assessed on a scale of 0 to 3. Only
a mouth mirror and a Shepherd’s Crook or sickle-type
dental explorer, and no disclosing agent are used for
examination. The six tooth surfaces examined are No
3, 8, 14, 24 (Facial surface) and No 19, 30 (Lingual
surfaces). Each tooth surface is divided horizontally into
gingival, middle and incisal thirds. For the DI-S, a dental
explorer is placed on the incisal third and moved towards
the gingival third and scores are awarded according to
the criteria. The DI-S score per person is obtained by
totaling the debris score per the tooth surface and dividing
it by the number of surfaces examined. The CI-S
assessment is performed by gently placing a dental
explorer into the distal gingival crevice and drawing it
subgingivally from the distal contact area to the mesial
contact area. Scoring is done according to the criteria.
The CI-S score per person is obtained by totaling the
calculus scores per tooth surface and dividing it by the
number of surfaces examined. The OHI-S score per

49

Epidemiology of Gingival and Periodontal Diseases

person is the total of DI-S and CI-S scores per person.
The clinical levels of oral cleanliness for debris that can
be associated with groups (DI-S, CI-S) scores are as
follows:

Good — 0.0 to 0.6
Fair

— 0.7 to 1.8

Poor — 1.9 to 3.0
The clinical levels of oral hygiene that can be

associated with group OH1-S scores are as follows:

Good — 0.0 to 1.2
Fair

— 1.3 to 3.0

Poor — 3.1 to 6.0

Turesky-Gilmore-Glickman Modification of the

Quigley Hein Plaque Index (1970)

Plaque is assessed on the facial and lingual surfaces of
all of the teeth after using a disclosing agent. A plaque
score per person is obtained by totaling all the plaque
scores and dividing it by the number of surfaces
examined. This system of scoring plaque is relatively easy
to use because of the objective definitions of each
numerical score. The strength of this plaque index is its
application to longitudinal studies and clinical trials of
prevention and therapeutic agents.

Scoring Criteria

0 — No plaque
1 — Separate flecks of plaque at the cervical margin

of the tooth

2 — A thin, continuous band of plaque (upto 1 mm)

at the cervical margin

3 — A band of plaque wider than 1 mm but covering

less than one-third of the crown

4 — Plaque covering atleast one-third but less than

two-thirds of the crown

5 — Plaque covering two-thirds or more of the

crown.

Plaque Index by Sillness and Loe (1964)

It is unique among the indices used for assessment of
plaque because it ignores the coronal extent of plaque

on the tooth surface area and assesses only the thickness
of plaque at the gingival area of the tooth.

Method

The evaluation or scoring is done on the entire dentition
or on selected teeth. The surfaces examined are the four
gingival areas of the tooth i.e. the distofacial, facial,
mesiofacial and lingual surfaces. A mouth mirror, light
source, a dental explorer and air-drying of the teeth and
gingiva are used in the scoring of this index. Only plaque
of the cervical third of the tooth is evaluated with no
attention to plaque that has extended to the middle or
incisal thirds.

Scoring Criteria

0 — No plaque in the gingival area
1 — A film of plaque adhering to the free gingival

margin and adjacent area of the tooth. The plaque
may be recognized only by running a probe across
the tooth surface

2 — Moderate accumulation of soft deposits within the

gingival pocket and on the gingival margin and/
or adjacent tooth surface that can be seen by
naked eye

3 — Abundance of soft matter within the gingival

pocket and/or on the gingival margin and adjacent
tooth surface.

The score for the area is obtained by totaling the

four scores per tooth and dividing it by four. The plaque
index score for the person is obtained by adding the
plaque index scores per tooth and dividing by the
number of teeth examined.

Modified Navy Plaque Index

Advantage

It is of value in assessing health education programs and
the ability of the individuals to perform oral hygiene
practices. A variation of the modified navy plaque index
is the DMPI (Distal mesial plaque index), which places
more emphasis on the gingival, interproximal areas of
a tooth.

50

Essentials of Clinical Periodontology and Periodontics

Procedure

Each tooth surface is divided into gingival, middle and
incisal third. Gingival 3rd is divided into two halves
(horizontally) both the gingival halves are again divided
longitudinally into distal, middle and mesial thirds. The
middle 3rd is divided into distal and mesial halves. The
incisal 3rd is not subdivided, thereby emphasizing more
of gingival two-thirds of the tooth.

Total scores per

tooth surface

Modified navy plaque index = ——————————

 Number of

surfaces examined

Patient Hygiene Performance Index (PHP)

by Podshadley and Hadley

Advantages

i. It was the first index developed for the sole purpose

of assessing an individual’s performance in
removing debris after tooth brushing instruction.

ii. It is easy to use and can be performed.

iii. For  individual patient education.

Selection of Teeth and Surfaces

Six surfaces of the six teeth (3, 8, 18, 19, 24 and 30)
are selected.

It records presence or absence of debris as 1 or 0

respectively.

Total debris score

PHP =

No of teeth scored

Suggested Nominal Scale

Rating
Excellent — score
Good

— 0.1 to 1.7

Fair

— 1.8 to 3.4

Poor

— 3.5 to 5.0

Plaque Weight

1. Sand-blasted standardized mylar foils attached to the

lingual surface of lower anterior teeth are weighed
on removal after a set time.

2. Removal of plaque directly from the tooth and

subsequent weighing is less precise but simpler than
the foil techniques.

Plaque-free Score by Grant, Stern and Everett

Purpose

To determine the location, number and percentage of
plaque-free surfaces for individual motivation and
instruction.

Selection of Teeth and Surfaces

All erupted teeth are included; four surfaces are recorded
for each tooth (facial, lingual, mesial and distal).

Procedure

Apply disclosing agent and examine each tooth surface
for evidence of plaque and record the surfaces in red
color.

Papillary Bleeding on Probing

Total the number of small circles marked for bleeding.
For a person with 32 teeth there are 30 interdental areas.
The mesial or distal of tooth adjacent to an edentulous
area is probed and counted.

Calculations

Plaque-free score = Total the number of teeth present
and total the number of surfaces with plaque

Number of

 plaque-free scores

Plaque-free score =

 × 100

Number of

available surfaces

Plaque Control Record by O’Leary

Similar to plaque-free score by Grant, Stern and
Everett.

Interpretations

Although 0 percent is ideal, less than 10 percent has
been suggested as a guideline in periodontal therapy.
After initial therapy, when a patient reached 10 percent

51

Epidemiology of Gingival and Periodontal Diseases

level of plaque control necessary periodontal and
restorative procedures are initiated. In comparison, a
similar evaluation using a plaque-free score record would
mean a goal of over 90 percent or better plaque-free
score before the surgical phase of treatment should be
undertaken.

INDICES USED TO MEASURE CALCULUS

Calculus Component of the Simplified Oral

Hygiene Index by Greene and Vermillion—

Discussed in Plaque Index

Calculus Component of the Periodontal Disease

Index by Ramjford

Advantages

1. It has a high degree of examiner reproducibility.
2. It can be performed quickly and has the best

application in epidemiological surveys and
longitudinal studies.

Procedure

Six teeth are examined (3, 9, 12, 19, 25 and 28).
Four surfaces are recorded (facial, lingual, mesial, distal)
with the help of an explorer and score ranges from
0 to 3.
1. Supragingival plaque extending not more than 1mm
2. Moderate amount of supragingival and subgingival

calculus

3. Abundance of supragingival and subgingival calculus

Total number

of scores

Calculus index for an individual =

Number of teeth

Probe Method of Calculus Assessment by

Volpe and Associates

Advantages and Disadvantages

It has been shown to possess a high degree of
interexaminer and intra–examiner reproducibility.
However, excessive training under a experienced
investigator is required to master it.

Purpose

It is used for longitudinal studies.

Method

The lingual surfaces of six mandibular teeth are measured
in millimeter divisions with the help of graduated
periodontal probe.

Calculus Surface Index by

Ennever and Coworkers

Objective

It is to determine rapidly whether a specific agent has
any effect on reducing or preventing supragingival or
subgingival calculus.

Four mandibular incisors are examined for the

presence or absence by visual and tactile exami-
nation.

Scoring Criteria

1. Calculus not exceeding 0.5 mm in width or thickness
2. Calculus not exceeding 1 mm
3. Calculus exceeding more than I mm in width and

thickness

Marginal Line Calculus Index

by Muhlemann and Villa

Purpose

To assess the supragingival calculus along the margins
of the gingiva. It only scores the supragingival calculus
formed in the cervical area along the marginal gingiva
on the lingual side of the four mandibular incisors.

INDICES USED TO ASSESS
TREATMENT NEEDS

Gingival Periodontal Index

It assesses three components of periodontal disease:
gingival status, periodontal status, and collectively materia
alba, calculus and overhanging restorations. The maxillary
and mandibular arches are each divided into three

52

Essentials of Clinical Periodontology and Periodontics

segments: the six anterior teeth, the left posterior teeth,
and the right posterior teeth. The primary objective in
using this index is to determine the tooth or surrounding
tissues with the severest condition within each of the six
segments. Each segment is assessed for each of the three
components of periodontal disease described previously.

The specific criteria for the gingival status components

of the GPI are as follows:
0 — Tissue tightly adapted to the teeth, firm consistency

with physiologic architecture.

1 — Slight to moderate inflammation, as indicated by

changes in color and consistency, involving one
or more teeth in the same segment but not
completely surrounding any one tooth.

2 — The above changes occur either singly or

combined completely encircling one or more teeth
in a segment.

3 — Marked inflammation, as indicated by loss of

surface continuity (ulceration), spontaneous
hemorrhage, loss of faciolingual continuity or any
interdental papilla, marked deviation from normal
contour, recession and clefts.

The area with the highest score determines the gingival

score for the entire segment, and the gingival status for
the oral cavity is obtained by dividing the sum of the
gingival scores by the number of segments.

Community Periodontal Index of Treatment

Needs by Ainamo and Associates

Procedure

The periodontal treatment needs are recorded for
sextants. Third molars are not included except when they
are functioning in place of second molars. The treatment
need in a sextant is recorded only when 2 or more teeth
are present and are not indicated for extraction. If only
one functioning tooth is remaining in the maxilla, the
jaw would be recorded as one sextant. Missing sextants
are indicated with a diagonal line through the appropriate
box. The index teeth to be examined are:

WHO Numbering

American Equivalent

17,16

11

26,27

2,3

8

14,15

47,46

31

36,37

31,30

25

18,19

The worst findings from these teeth surfaces are

recorded. WHO probe is used.

Criteria

Periodontal status:
a. Healthy periodontium
b. Bleeding observed directly or by using mouth mirror.
c. Calculus felt during probing, but entire blunt area

of the probe is visible.

d. Pocket 4 or 5 mm
e. Pocket more than 6 mm

Treatment needs:
0 No treatment neede
1 Oral hygiene needs improvement
2 Oral hygiene improvement and professional scaling
3 Oral hygiene improvement, professional scaling and

complex treatment.

Advantages

The value of CPITN is that it permits rapid examination
of a population to determine periodontal treatment
needs.

Disadvantages

1. A great deal of useful information is lost when only

the worst score per sextant is recorded.

2. CPITN underestimates the pockets greater than 6 mm

in older age groups and overestimates the need for
scaling in younger age groups.

Periodontal Treatment Need System by Bellini HT

It attempts to place individuals into one of the four classes
based on treatment procedures relative to time
requirements. It considers the presence or absence of

53

Epidemiology of Gingival and Periodontal Diseases

Table 5.1: Criteria for periodontal treatment

need system

PTNS

Unit

Plaque Calculus Inflam- Pocket

classification

and/or mation

depth

overhangs

Class-0

Mouth

No

No

No

No

Class-A

Mouth

Yes

No

Yes

<5 mm

Class-B

Quadrant

Yes

Yes

Yes

<5 mm

Class-C

Quadrant

Yes

Yes

Yes

>5 mm

gingivitis and plaque, and the presence of pockets 5 mm
or deeper in each quadrant of mouth.

Criteria for periodontal treatment need system is

described in Table 5.1.

BIBLIOGRAPHY

1. Esther M Wilkins. Clinical Practice of the Dental Hygienist, 8th

Edition. Wolters Kluwer Company.

2. Newman, Takei, Fermin A. Carranza: Clinical Periodontology,

Ninth Edition (2002), W.B. Saunders.

3. Soben Peter: Essentials of Preventive and Community

dentistry, First Edition, Arya (MEDI), Publishing House.

‘

DEFINITION

Dental Plaque

Dental Plaque is an adherent intercellular matrix
consisting primarily of proliferating microorganisms, along
with a scattering of epithelial cells, leukocytes and
macrophages.

Plaque

Plaque can also be defined as the soft deposits that form
the biofilm adhering to the tooth surface or other hard

surfaces in the oral cavity, including removable and fixed
restorations. Dental Plaque is a host-associated biofilm.

Biofilms

Biofilms are defined as “Matrix—enclosed bacterial
populations adherent to each other and or/to surface
or interfaces (by Costerton). According to the recent data
(Widerer and Charaklis 1989) Biofilm is defined as the
relatively undefinable microbial community associated
with a tooth surface or any other hard, non-shedding
material.

DENTAL PLAQUE AS A BIOFILM

Structurally dental plaque is now considered to be a
biofilm of complex and dynamic microbial community.
It contains areas of high and low bacterial biomass
interlaced with aqueous channels of different size, which
are the nutrient channels for bacterial colonization. The
intercellular matrix forms a hydrated gel in which bacteria
can survive and proliferate. Hence, biofilm adheres firmly
to the tooth surface and is resistant to mechanical
removal, as well as antibiotics.

TYPES OF DENTAL PLAQUE

Based on its relationship to the gingival margin, plaque

❒

❒

❒

❒

❒ DEFINITION

❒

❒

❒

❒

❒ DENTAL PLAQUE AS A BIOFILM

❒

❒

❒

❒

❒ TYPES OF DENTAL PLAQUE

❒

❒

❒

❒

❒ COMPOSITION OF DENTAL PLAQUE

❒

❒

❒

❒

❒ FORMATION/DEVELOPMENT OF DENTAL

PLAQUE

❒

❒

❒

❒

❒ STRUCTURAL AND MICROSCOPIC

PROPERTIES OF PLAQUE

❒

❒

❒

❒

❒ CLINICAL SIGNIFICANCE OF A PLAQUE

❒

❒

❒

❒

❒ MICROBIAL SPECIFICITY OF

PERIODONTAL DISEASES

❒

❒

❒

❒

❒ WHAT MAKES PLAQUE PATHOGENIC

❒

❒

❒

❒

❒ MICROORGANISMS ASSOCIATED WITH

PERIODONTAL DISEASES

❒

❒

❒

❒

❒ BACTERIA ASSOCIATED WITH

PERIODONTAL HEALTH AND DISEASE

6

Periodontal Microbiology

(Dental Plaque)

58

Essentials of Clinical Periodontology and Periodontics

Table 6.1: Differences between supragingival and subgingival plaque

Supragingival plaque

Subgingival plaque

1.  Matrix

50% Matrix

Little or no matrix

2.  Flora

Mostly Gram-positive

Mostly Gram-negative

3.  Motile bacteria

Few

Common

4.  Anaerobic/ Aerobic

Aerobic unless thick

Highly anaerobic areas present

5.  Metabolism

Predominantly carbohydrates

Predominantly proteins

Fig. 6.1: 

Supragingival plaque

is differentiated into two categories, supragingival and
subgingival plaque (Table 6.1).

Supragingival plaque is further differentiated into:
Coronal plaque, which is in contact with only the

tooth surface, and Marginal plaque, which is associated
with the tooth surface at the gingival margin.
Subgingival plaque can be further differentiated into:
• Attached plaque
• Unattached subgingival plaque
• Attached plaque can be tooth, epithelium and/or

connective tissue associated.

Supragingival Plaque (Fig. 6.1)

It can be detected clinically only after it has reached a
certain thickness. Small amounts of plaque can be

visualized by using disclosing agents. The color varies
from grey to yellowish-grey to yellow. The rate of
formation and location of plaque vary among individuals
and is influenced by diet, age, salivary factors, oral
hygiene, tooth alignment, systemic diseases and host
factors.

Subgingival Plaque (Figs 6.2 and 6.3)

It is usually thin, contained within the gingival sulci or
periodontal pocket and thus cannot be detected by direct
observation. Its presence can be identified only by
running the end of a probe around gingival margin (Table
6.2).

Tooth-associated Subgingival Plaque

The structure is similar to the supragingival plaque. The
flora is dominated by Gram-positive cocci, rods,
filamentous bacteria and some/few Gram-negative cocci
and rods. This flora is associated with calculus formation,
root caries and root resorption.

Epithelium-associated Subgingival Plaque

This type of plaque is loosely adherent because it lacks
the interbacterial matrix and is in direct association with
the gingival epithelium, extending from the gingival margin
to the junctional epithelium. This plaque predominantly
contains Gram-negative rods and cocci, as well as a large
number of flagellated bacteria and Spirochetes.

Table 6.2: Characteristics of subgingival plaque

Sl.  No.

Tooth-associated subgingival plaque

Epithelium-associated plaque

1.

Gram-positive bacteria predominates

Gram- positive and Gram-negative bacteria

2.

Does not extend to junctional epithelium

Extends to junctional epithelium

3.

May penetrate cementum

May penetrate epithelium and connective tissue

4.

Associated with calculus formation and root caries

Associated with gingivitis and periodontitis

59

Periodontal Microbiology

Fig. 6.2: 

Subgingival plaque bacteria associated with

tooth surface and periodontal tissues

Fig. 6.3: 

Subgingival plaque and calculus

Connective Tissue-associated Plaque

It is usually demonstrated in ANUG and localized juvenile
periodontitis patients. The clinical significance is unclear.
The unattached plaque can be seen anywhere. Thus,
the tooth-associated subgingival plaque is most important
in calculus formation, root caries and slowly progressive
periodontal destruction, whereas unattached bacterial
component is associated with rapid periodontal
destruction.

COMPOSITION OF DENTAL PLAQUE

Bacteria + Intercellular matrix = Dental plaque

Bacteria make up approximately 70 to 80 percent

of total material.One mg of dental plaque is estimated
to contain 250 million bacteria. Other than bacteria,
mycoplasma, fungi, protozoa and viruses may be present.
The material among the bacteria in dental plaque is termed
as inter microbial/cellular matrix. It contains organic and
inorganic portions. The organic matrix is composed of
protein—polysaccharide complex produced by micro-
organisms.Carbohydrates in the form of levans (fructans)
provides mainly energy while glucans (dextran) provide
not only energy, but also act as the organic skeleton of
plaque. Other carbohydrates are galactose and rhamnose.
Glycoproteins provide the protein component and small
amounts of lipids are also present. Inorganic components
include, primarily calcium, phosphorus with small amounts
of magnesium, potassium and sodium.

FORMATION/DEVELOPMENT OF
DENTAL PLAQUE

Pellicle is the initial organic structure that forms on the
surfaces of the teeth and artificial prosthesis. The first
stage in pellicle formation involves adsorption of salivary
proteins to apatite surfaces. This results from the
electrostatic ionic interaction between hydroxyapatite
surface which has negatively-charged phosphate groups
that interacts with opposite charged groups in the salivary
macromolecules. The mean pellicle thickness varies from
100 nm at 2 hours to 500 to 1,000 nm.

The transition from pellicle to dental plaque is

extremely rapid. The first components include mainly
cocci with small number of epithelial cells and PMNL’s,
they form a monolayer within a few hours, and the
attached bacteria proliferate and form small colonies of
cocci. With time other types of microorganisms proliferate
and form different microcolonies.

Hence, in dental plaque development, two adhesion

processes are required. First, bacteria must adhere to

60

Essentials of Clinical Periodontology and Periodontics

the pellicle surface and become sufficiently attached to
withstand oral cleansing forces. Second, they must grow
and adhere to each other to allow plaque accumulation.

Bacterial Adherence

During initial adherence, interactions occur mainly
between specific bacteria and the pellicle. They are:

Bacterial Attachment via Electrostatic Interactions

Oral bacteria bear an overall net negative charge,
negatively-charged components of the bacterial surface
and negatively-charged components of pellicle become
linked by cations such as calcium (Fig. 6.4).

Bacterial Attachment via Hydrophobic Interactions

These interactions are based on the close structural fit
between molecules on the pellicle and bacterial surfaces.
The nature of the hydrophobicity of the cell is not clearly
known. The contributing factor might be (LTA)
lipoteichoic acid, which may provide a long hydrophobic
area (Fig. 6.5).

Bacterial Attachment via Specific Lectin-like
Substances (Fig. 6.6)

Lectins in the bacterial surfaces recognize specific
carbohydrate structure in the pellicle and become linked.

Adhesion and attachment (Fig. 6.7) occurs between:

• Bacteria and clean tooth surface
• Bacteria and pellicle
• Bacteria and same species
• Bacteria and different species
• Bacteria and matrix

Next step in plaque formation is:

Growth and Accumulation of Bacteria

Once the bacteria is adhered to the pellicle, subsequent
growth leads to bacterial accumulation and increased
plaque mass. Dental plaque growth (Fig. 6.8) depends on:
a. Growth via adhesion of new bacteria
b. Growth via multiplication of attached bacteria

Fig. 6.4: 

Bacterial attachment via electrostatic

interactions

Fig. 6.5: 

Bacterial attachment via

hydrophobic interactions

Fig. 6.6: 

Bacterial attachment via specific lectin-like

interactions

61

Periodontal Microbiology

Fig. 6.7: 

Role of saliva in the development and

maturation of dental plaque

Fig. 6.8: 

Growth of dental plaque

Fig. 6.9: 

Bacterial succession in dental plaque

The initial bacteria that colonize the pellicle surface

are mostly Gram-positive facultative microorganisms such
as Actinomyces viscosus and Streptococcus sanguis, as
the plaque matures, secondary colonization of Prevotella
intermedia, Capnocytophaga, Porphyromonas gingivalis
takes place. This ability of bacteria to adhere to different
species and genera of micro-organisms is known as co-
aggregation (Fig. 6.9).

STRUCTURAL AND MICROSCOPIC
PROPERTIES OF PLAQUE

Supragingival Plaque

It is usually adherent to the tooth surface. It contains
gram-positive cocci and gram-negative rods and
filaments. The morphologic arrangement of the flora in
supragingival plaque described as “corncob” formations,
characterized by central core consisting of rod-shaped
bacterial cells, e.g. Fusobacterium nucleatum and coccal
cells, e.g. streptococci which attaches along the surface
of the rod-shaped cell.

The subgingival plaque differs from supragingival

plaque, in that it contains many large filaments with
flagella and is rich in Spirochetes. Tooth-associated plaque
is similar to supragingival plaque; whereas tissue-
associated plaque is covered with flagellated bacteria
without a well-defined extracellular matrix and numerous
bristle—brush formations. This arrangement is also called
as “test tube-brush” formation characterized by large

62

Essentials of Clinical Periodontology and Periodontics

filaments that forms the long axis; and short filaments
or Gram-negative rods embedded in a amorphous
matrix (Fig. 6.10).

CLINICAL SIGNIFICANCE OF PLAQUE

The microbial aggregations on the tooth surface if
prevented from maturing may become compatible with
gingival health. Supragingival plaque if allowed to grow
and mature, may induce gingivitis and can lead to the
formation of a microenvironment that permits the deve-
lopment of subgingival plaque. Therefore, supragingival
plaque strongly influences the growth, accumulation and
pathologic potential of sub gingival plaque, especially
in the early stages of gingivitis and periodontitis.

Subgingival Plaque

In association with the presence of supragingival plaque,
there are inflammatory changes that modify the
anatomic relationships of the gingival margin and tooth
surface. This result in enlarged gingiva, which increases
the space for bacterial colonization and also protects
bacteria from normal cleansing mechanisms. They derive
nutrients from gingival crevicular fluid. Many of these
microorganisms lack the adherence ability and utilizes
supragingival plaque bacteria as a means of colonization
of the subgingival area.

Electron microscopic studies have demonstrated the

existence of an organic material called cuticle between
the root surface and subgingival plaque. It is covered
by a dense layer of microorganisms and is believed to
be a remnant or secretory product of the junctional
epithelial cells.

MICROBIAL SPECIFICITY OF
PERIODONTAL DISEASES

Walter Loesche proposed the non-specific and specific
plaque hypothesis in 1976. The non-specific plaque
hypothesis states that it is the total bulk of plaque, which
determines the pathogenicity rather than the individual
species within it. In other words all plaque is equally
pathogenic. According to this, when only small amounts
of plaque are present, the products released by this gets
neutralized by the host. Similarly, large amounts of plaque
would produce large amounts of noxious products, which
would overwhelm the host’s defenses. However, several
authors have contradicted this concept. First, many
patients have considerable amounts of plaque and
calculus as well as gingivitis, but only a minority suffer
from destructive periodontal disease even then in only
few sites. This paradox might be explained by specific
plaque hypothesis, which states that destructive
periodontal disease is a result of specific microbial
pathogens in plaque. Thus although the amount of
plaque present correlates well with disease severity it
correlates poorly in individual patients.

But it is the non-specific plaque hypothesis, which

forms the basis for virtually all the current modalities for
treatment, and prevention, which relies on the principle
of reducing plaque scores to a minimum. Thus, although
the non-specific plaque hypothesis has been discarded
in favor of the specific plaque hypothesis, much clinical
treatment is still based on the non-specific plaque
hypothesis.

Specific Plaque Hypothesis

It states that, not all plaque is pathogenic and its
pathogenicity depends on the presence of certain specific

Fig. 6.10: 

Mature plaque diagram

63

Periodontal Microbiology

microbial pathogens in plaque. This is based on the fact
that, the specific microorganisms responsible for
periodontal diseases release certain damaging factors that
mediates the destruction of the host tissue. This concept
was accepted easily due to the recognition of
Actinobacillus actinomycetemcomitans as a possible
pathogen responsible for localized juvenile periodontitis.

WHAT MAKES PLAQUE PATHOGENIC?

The following are the possible pathogenic mechanisms
by which the plaque microorganisms can cause
periodontal disease.
a. Physical nature of plaque
b. Invasion of tissues by bacteria
c. Release of toxic and inflammatory substances
d. Role of bacterial specificity

MICROORGANISMS ASSOCIATED WITH
PERIODONTAL DISEASES

It is well accepted that a plaque bacteria is the primary
etiologic agent in periodontal disease. Bacteria are seen
in the oral cavity from birth to death. It is estimated that
about 400 different species are capable of colonizing in
the mouth. Counts in subgingival sites range from about
10

3

 in healthy sulci to greater than 10

8

 in deep periodontal

pockets. It has not been possible to identify and study
all the organisms present in the bacterial plaque, of nearly
400 species; only 30 of them are considered to be
periodontopathic. Koch’s postulates, generally used to
identify the periodontopathogenecity of a micro-
organism, are not applicable in periodontal disease, as
more than one organism is involved in periodontal
diseases. Hence, Socransky (1977) had proposed the
following criteria for identifying the possible causative
organisms in periodontal diseases:
1. The number of etiologic organisms in the diseased

site must be increased and conversely the number
of organisms must be reduced or absent in healthy
sites.

2. If the etiologic organism is eliminated or suppressed

the disease should stop.

3. Presence of specific antibodies to those micro-

organisms.

4. Presence of virulence factors associated with certain

microorganisms, e.g. toxins, enzymes, etc.).

5. In vitro or animal experiments should be able to

demonstrate the human disease process.
There are many speculations regarding the pathogens

responsible for periodontitis whether they could be
exogenous or components of indigenous flora. To explain
this controversy, two theories have been proposed.

According to the first theory, periodontopathic

organisms are a part of indigenous flora and they tend
to overgrow during the disease progression. The second
proposal is that, they are not components of indegenous
oral flora, but are of exogenous pathogens derived from
outside sources. This concept hints that, the quantity of
plaque is not necessary for disease onset. Instead, the
site should be contaminated with specific periodonto-
pathogens.

Recent reports have demonstrated a possibility of viral

etiology in periodontitis and implicated viruses are Epstein
Barr virus, human cytomegalovirus and mixed herpes
viral infections. Viral infection can contribute to
periodontitis by altering the functions of neutrophils,
macrophages and lymphocytes which inturn promotes
the overgrowth of periodontopathic organisms in the
subgingival flora. The other possibility is that, the viral
infection can destroy the oral epithelial cells thus
disrupting the barrier function of the periodontium.

Bacteria Associated with Periodontal

Health and Disease

See Table 6.3.

Health

• Actinomyces  (viscosus and naeslundii)
• Streptococcus  (S. mitis and S. sangius)
• Veillonella parvula, small amounts of Gram-negative

species are also found.

64

Essentials of Clinical Periodontology and Periodontics

Chronic Gingivitis

Gram-positive (56%), Gram-negative (44%) organisms
are found. Predominant Gram-positive species include,
S. sangius, S. mitis, S. oralis, A. viscosus, A. naeslundii,
Peptostreptococcus micros.

Gram-negative organisms are:
• Fusobacterium nulceatum
• Prevotella intermedia
• Veillonella parvula as well as Haemophilus,

Capnocytophaga  and  Campylobacter  species

Pregnancy-associated gingivitis
• Prevotella intermedia

Acute necrotizing ulcerative gingivitis
• Spirochetes
• Prevotella intermedia

Adult periodontitis
• Porphyromonas gingivalis
• Bacteroides forsythus
• Prevotella intermedia
• Campylobacter rectus
• Eikenella corrodens
• Fusobacterium nucleatum
• Actinobacillus actinomycetemcomitans
• Peptostreptococcus micros
• Treponema, and
• Eubacterium  species.

Viruses such as:
• EBV-1 (Ebstein-Barr virus)
• HCMV (Human cytomegalovirus)

Table 6.3: Reclassification of periodontal bacteria

Previous status

Current status

Wolinella recta

Campylobacter rectus (C. rectus)

Bacteroides gingivalis

Porphyromonas gingivalis (P. gingivalis)

Bacteroides intermedius

Prevotella intermedia (P. intermedia)

Bacteroides melaninogenicus

Prevotella melaninogenica (P. melaninogenica)

Localized juvenile periodontitis
• Actinobacillus actinomycetemcomitans
• Porphyromonas gingivalis
• Eikenella corrodens
• Campylobacter rectus
• Fusobacterium nucleatum
• Bacteroides capillus
• Eubacterium brachy
• Capnocytophaga
• Herpes  virus.

Generalized juvenile periodontitis
• Actinobacillus actinomycetemcomitans
• Porphyromonas gingivalis
• Prevotella intermedia
• Capnocytophaga
• Eikenella corrodens
• Neisseria

Refractory periodontitis
• Actinobacillus actinomycetemcomitans
• Bacteroides forsythus
• Porphyromonas gingivalis
• Prevotella  intermedia
• Wolinella recta

Abscesses of the periodontium

•

Fusobacterium nucleatum

•

Prevotella intermedia

•

Peptostreptococcus micros

•

Bacteroides forsythus

•

Porphyromonas gingivalis

65

Periodontal Microbiology

KEY POINTS TO NOTE

1. Dental plaque is defined as an adherent intercellular matrix,

composed primarily of proliferating microorganisms, along
with a scattering of epithelial cells, leukocytes and
macrophages.

2. Structurally dental plaque is now considered to be a biofilm

of complex and dynamic microbial community.

3. Based on its relationship to the gingival margin, plaque is

differentiated into two categories, supragingival and
subgingival plaque.

4. Subgingival plaque can be, tooth-associated, epithelium-

associated, connective tissue-associated and unattached
plaque.

5. Dental plaque is mainly composed of bacteria and

intercellular matrix.

6. In the formation of dental plaque first step is pellicle

formation followed by bacterial adherence and growth and
accumulation of bacteria.

REVIEW QUESTIONS

1. Define plaque and describe the steps in formation

of plaque.

2. What are the types and composition of dental plaque?
3. What is specific and non-specific plaque hypothesis?
4. Describe the role of plaque in periodontal disease.
5. What is the clinical significance of plaque?
6. What are differences between supra and subgingival

plaque?

BIBLIOGRAPHY

1. Jan Lindhe. Clinical Periodontology and Implant Dentistry.

Fourth Edition 2003, Blackwell Munksgaard Publication.

2. Jorgen slots and Martin A Taubman. Contemporary oral

microbiology and immunology.

3. Newman, Nissengaard. Oral microbiology and immunology,

II edition, WB Saunders and company.

4. Max A, Listgarten. The structure of dental plaque. Periodontol

2000;5:1994.

5. Sigmund S, Socransky, Anne D. Haffajee. Dental biofilms:

difficult therapeutic targets. Periodentol 2000;28:2002.

6. Sigmund, Socransky, Anne D. Haffajee. Evidence of bacterial

etiology, a historical perspective. Periodontol 2000;5:1994.

7. WEC Moore, Lillian VH Moore. The bacteria of periodontal

diseases. Periodontol 2000;5:1994.

66

Essentials of Clinical Periodontology and Periodontics

CALCULUS

Definition

Dental calculus is an adherent, calcified or calcifying mass
that forms on the surfaces of teeth and dental appliances.
It is covered on its external surface by vital, tightly
adherent, nonmineralized plaque.

Types

Depending upon the position of calculus in relation to
the marginal gingiva it is classified as:
1. Supragingival calculus.
2. Subgingival calculus.

Supragingival Calculus

It is the tightly adherent calcified deposit that forms on
the clinical crowns of the teeth above the free gingival

margin. Hence it is clinically-visible. It is also called as
salivary calculus because it forms from the saliva.

Subgingival Calculus

As the name implies, it is that calcified deposits that is
formed on the root surfaces below the free marginal
gingiva. It is believed to be formed from the gingival

Fig. 7.1: 

Radiograph illustrating subgingival deposits in

lower anterior and posterior teeth

❒

❒

❒

❒

❒ CALCULUS

• Definition

• Types

• Structure

• Composition

• Differences between Supra and

Subgingival Calculus

❒

❒

❒

❒

❒ OTHER CONTRIBUTING ETIOLOGICAL

FACTORS INCLUDING FOOD IMPACTION

7

Calculus and other

Etiological Factors

67

Calculus and other Etiological Factors

exudate and hence called serumal calculus (Figs 7.1 and
7.2).

Structure

The deposits of supragingival calculus are usually whitish-
yellow in color and can get stained by tobacco or food
pigments, consistency is hard and clay-like. Since they
derive the mineral salts from salivary secretions, they
are most abundant on the lingual surfaces of lower
anterior teeth, opposite Wharton’s duct and Bartholin’s
duct and buccal aspects of maxillary molars opposite
the Stenson’s duct (Fig. 7.3).

Subgingival calculus is usually dark-brown or

greenish-black in color and the deposits are firmly

attached to the tooth surface. Since they are hard and
firm, it cannot be removed easily. Unlike supragingival
calculus, subgingival calculus can be found on any root
surface with a periodontal pocket. Morphologically, it
can appear in different forms, most commonly ring-like
or ledge-like formations and crusty, spiny or nodular
deposits. Less frequently it can be seen as finger-like and
fern-like formations (Fig. 7.4).

Composition

It consists of inorganic and organic components (Tables
7.1 and 7.2).

Trace amounts of zinc, strontium, bromine, copper,

manganese, gold and aluminium are also seen. Atleast,

Fig. 7.2: 

Subgingival deposits on the root surface of

extracted lower anterior tooth

Fig. 7.3: 

Supragingival calculus on the lingual surfaces of

lower anteriors

Fig. 7.4: 

Radiograph illustrating subgingival calculus in

the interproximal areas

Table 7.1: Inorganic components

Component

Dry weight (in percent)

Inorganic

70-90

Calcium

27-29

Phosphorus

16-18

Carbonate

2-3

Sodium

1.5-2.5

Magnesium

0.6-0.8

Fluoride

0.003-0.04

Crystal forms
Hydroxyapatite

58

Magnesium whitlockite

21

Octacalcium phosphate

12

Brushite

9

68

Essentials of Clinical Periodontology and Periodontics

two-thirds of inorganic component is crystalline in
structure. The main crystal forms are: Hydroxyapatite,
Magnesium whitlockite, Octacalcium phosphate and
Brushite.

Differences between Supragingival and

Subgingival Calculus

See Table 7.3.

Attachment to the Tooth Surface

Four types of attachment of calculus to tooth surface
have been reported.
1. Attachment by means of an organic pellicle.
2. Mechanical interlocking into surface irregularities such

as resorption lacunae and caries.

3. Penetration of calculus bacteria into cementum.
4. Close adaptation of calculus under surface depre-

ssions to the gently sloping mounds of the unaltered
cementum surface.

Calculus when embedded deeply in cementum may

appear similar in morphology and thus has been termed
as calculocementum.

Formation of Calculus

Calculus is nothing but, dental plaque that has undergone
mineralization. Calculus is formed by the precipitation
of mineral salts, which can start between 1st and 14th
day of plaque formation. In two days plaque can be
50 percent mineralized and 60 to 90 percent gets
mineralized in 12 days. Calcification starts in separate
foci on the inner surface of the plaque. These foci of
mineralization gradually increase in size and coalesce to
form a solid mass of calculus.

Calculus formation continues until it reaches

maximum levels in about 10 weeks and 6 months, after
which there is a decline in its formation, due to
mechanical wear from food and from the lips, cheeks
and tongue. This decline is referred to as reversal
phenomenon.

Theories of Calculus Formation

It can be explained mainly under two categories:
1. Precipitation of minerals can occur from a local rise

in the degree of saturation of calcium and phosphate
ions, this is explained in,
a. Booster mechanism: According to this theory,

precipitation of calcium phosphate salts results
from a local rise in the pH of the saliva. Factors
such as loss of carbon dioxide and production
of ammonia could lead to rise in pH.

Other ways by which the precipitation of

calcium phosphate salts can occur are:

b. Colloidal proteins in saliva bind to calcium and

phosphate ions thus producing a super-saturated
solution. When saliva stagnates in the oral cavity,
colloids settle and result in the precipitation of
calcium and phosphorous salts.

c. Phosphatase liberated from dental plaque,

desquamated epithelial cells, or bacteria

Table 7.2: Organic components

Component

Dry weight (in percent)

Mixture of protein, polysaccharide

1.9-9.1

complexes, desquamated epithelial
cells, leukocytes and various
micro-organisms. Carbohydrate
(consists of glucose, galactose,
rhamnose, mannose)
Proteins

5.9-8.2

Lipids

0.2

Table 7.3: Differences between supra and

subgingival calculus

Supragingival

Subgingival

Location—above the gingival

Deposits present below the

margin

margins of the gingiva

Color—white, yellow in color

Brown or greenish-black

Source—derived from

Formed from gingival

salivary secretions

exudate

Composition—more brushite

Conversely less brushite and

and octacalcium phosphate

octacalcium phosphate and

less magnesium whitlockite

more magnesium whitlockite

Salivary proteins are present

They are absent

Sodium content is lesser

Sodium content increases

with the depth of the pocket

69

Calculus and other Etiological Factors

precipitate calcium phosphate by hydrolyzing
organic phosphates in saliva, thus increasing the
concentration of free phosphate ions.

2. Another concept that has been most widely held is

“Epitactic Concept”. (heterogenous nucleation).
According to this, seeding agents induce small foci
of calcification. These foci enlarge and coalesce to
form calculus. Hence more appropriately called as
heterogenous nucleation. The seeding agents in
calculus is not clearly known, but suspected agents
could be, intercellular matrix of plaque, carbohydrate
protein complexes and plaque bacteria.

3. Inhibition theory: This theory considers the possibility

of calcification occurring only at specific sites because,
there exists an inhibiting mechanism at non-calcifying
sites. Where ever calcification occurs, the inhibitor
is either altered or removed. One such inhibiting
agents could be pyrophosphate which prevents the
initial nucleus from growing, by possibly ‘poisoning’
the growth centers of the crystal.

Pathogenic Potential of Calculus in

Periodontal Diseases

Before 1960s the belief was that calculus was the principle
etiologic factor in periodontal diseases. However, the
current view is that the initial damage to the gingival
margin in the periodontal disease is due to the pathogenic
effects of microorganisms in plaque. However, the effect
could get more pronounced by calculus accumulation
because it further provides retention of more plaque
microorganisms.

Hence, there is no doubt that, the mineralized

deposits can—
a. Bring the bacterial deposits more closely to the

supporting structures.

b. Interfere with the local self cleansing defense

mechanisms.

c. And also enable the patients to perform proper oral

hygiene methods.

OTHER CONTRIBUTING ETIOLOGICAL
FACTORS INCLUDING FOOD IMPACTION

Iatrogenic Factors

Faults in the dental restorations and prosthesis referred
to as iatrogenic factors are common causes of gingival
inflammation and periodontal destruction.

Faulty Restorations

Six characteristics of restorations are important from
periodontal point of view.
a. Margins of restorations
b. Contours and overhanging dental restorations
c. Occlusion
d. Materials
e. Design of removable partial dentures
f. Restorative procedures themselves

Biologic width is defined as the dimension of the soft

tissue, which is attached to the portion of the tooth
coronal to the crest of the alveolar bone. The biologic
width is commonly stated to be 2.04 mm, which
represents the sum of epithelial and connective tissue
measurements. Hence encroachment of the biologic
width frequently leads to gingival inflammation, clinical
loss of attachment and bone loss.
a. Margins of restorations: Subgingival restorations can

contribute to periodontal diseases by,

i. Providing ideal locations for the accumulation

of plaque.

ii. Changing the ecological balance of the gingiva

to one that favors the growth of the disease
associated organisms, at the expense of the
health-associated organisms.

iii. It  was also demonstrated by Waerhaug et al

(1978) that subgingival restorations are plaque
retentive areas that are inaccessible to scaling
instruments, hence greater chance of severe
gingivitis and deeper pockets (Fig. 7.5).

b. Contour of restorations/artificial crowns: Over-

contoured or improperly-contoured restorations tend

70

Essentials of Clinical Periodontology and Periodontics

to accumulate plaque and possibly prevent the self-
cleansing mechanisms of the adjacent cheek, lips and
tongue. Proper contours of the artificial crown are
necessary for maintaining gingival health. In a review
of periodontal prosthetic interactions, Becker and
Kaldahl (1981) opined that buccal and lingual crown
contours should be ‘flat’, not fat, usually <0.5 mm
wider than the CEJ and that the furcation areas,
should be “fluted or barrelled  out” to accommodate
oral hygiene in these areas.

Overhanging dental restorations has been

considered to be a contributing factor to gingivitis
and possible periodontal attachment loss. Many
authors have demonstrated radiographic bone loss
adjacent to posterior teeth with overhanging
restorations. The placement of the subgingival
overhangs result in the changes in the associated
microflora to that of one resembling the flora seen
in  chronic periodontitis. Hence overhangs not only
increase plaque mass but also increase the specific
periodontal pathogens in the plaque (Fig. 7.6).

c. Occlusion: Poorly-constructed restoration will cause

occlusal disharmonies that may be injurious to the
supporting normal periodontal tissues. This type of
tissue injury is called “primary trauma from the
occlusion”. Some of the examples are:

i. Insertion of a “high filling”.

ii. Insertion of a prosthesis, replacement that

creates excessive forces on abutment or
antagonistic teeth.

iii. The drifting movement or extrusion of the teeth

into spaces created by unreplaced missing teeth
or,

iv. The orthodontic movement of teeth into

functionally unacceptable positions.

d. Materials: In general, restorative materials are not by

themselves injurious to the periodontal tissues. It is
the rough, unpolished surfaces that favor plaque
accumulation and contributes to periodontal diseases.
Compared to all restorative materials that are
available to the clinician, glass ionomer restorations
and porcelain seems to retain less plaque and thus
are more acceptable from periodontal point of view.
Fluoride constantly leaking from the glass ionomer
cement prevents the attachment of the bacteria to
the pellicle and it also interferes with the metabolism
and growth of bacteria, where as highly-polished
surfaces of porcelain inhibits plaque formation and
permits its rapid removal too.

e. Design of removable partial dentures: Several studies

have shown that after the insertion of partial dentures,
there is an increase in the mobility of the abutment
teeth within gingival inflammation and periodontal
pocket formation. This is due to the increased plaque
accumulation. The presence of removable partial
dentures not only induces quantitative changes in

Fig. 7.6: 

Radiographic illustration of overhanging

amalgam restoration

Fig. 7.5: 

Margins of restoration in relation to lower

anterior teeth

71

Calculus and other Etiological Factors

plaque, but also qualitative changes by promoting
the development of most pathogenic bacteria. Hence
from periodontal point of view fixed prosthesis is
more acceptable than the removable one.

f. Restorative procedures themselves can also cause

destruction of periodontium. The use of the rubber
dam clamps, copper bands, matrix bands and discs
in such a manner as to lacerate the gingiva, results
in the varying degrees of inflammation.

Periodontal Problems Associated with
Orthodontic Therapy

Orthodontic therapy may affect the periodontium by:
a. Favoring plaque retention and also modifying the

gingival ecosystem.

b. Directly injuring the gingiva as a result of over

extended bands which may also lead to forceful
detachment of gingiva from tooth causing gingival
recession.

c. Creating excessive and/or unfavorable forces on the

supporting tooth structures causes necrosis of the
periodontal ligament and adjacent alveolar bone,
excessive forces also increase the risk of apical root
resorption (Fig. 7.7).

Food Impaction

It is the forceful wedging of the food into the
periodontium by occlusal forces. Cusps that tend to

forcibly wedge food interproximally are known as
“Plunger cusps”.

According to Hirschfeld food impaction can occur

in the following conditions:
a. Uneven occlusal wear: It can lead to food impaction

because deflection of food away from the proximal
areas does not occur.

b. Loss of proximal contact: This is one of the most

common cause for food impaction. It may be due
to, periodontal disease, non-replaced missing teeth,
proximal caries and abnormal biting habits.

c. Congenital morphologic abnormalities of teeth.
d. Improperly-constructed restorations.
e. Lateral food impaction: In addition to food impaction

caused by occlusal forces, lateral pressure from the
lips, cheeks, tongue may force food interproximally.
This usually occurs when the gingival embrasure is
enlarged by periodontitis or by recession.
The following signs and symptoms may occur in the

association with food impaction:

i. Feeling of pressure and urge to dig the material

from between the teeth.

ii. Vague pain that radiates deep in the jaws.

iii. Gingival inflammation with bleeding and a foul

taste in the involved area.

iv. Gingival recession.

v. Periodontal abscess formation.

vi. Varying degrees of inflammatory involvement of

periodontal ligament, sensitivity to percussion.

vii. Destruction of the alveolar bone.

viii. Root caries.

Unreplaced Missing Teeth

Failure to replace extracted teeth initiates a series of
changes that produce various degrees of periodontal
diseases. The pattern of changes that may follow, failure
to replace missing first molars is characteristic (Fig. 7.8).
In extreme cases it consists of the following:
a. The second and third molars tilt, resulting in a decrease

in the vertical dimension.

b. The pre-molars move distally and the mandibular

incisors tilt or drift lingually.

Fig. 7.7:

 Periodontal changes associated with orthodontic

therapy

72

Essentials of Clinical Periodontology and Periodontics

c. The anterior overbite is increased. The mandibular

incisors strike the maxillary incisors near the gingiva
or traumatize the gingiva.

d. The maxillary incisors are pushed labially and laterally.
e. The anterior teeth extrude because the incisal

opposition has largely-disappeared.

f. Diastema is created by the separation of the anterior

teeth.

Loss of proximal contact relationships lead to,

Food impaction

↓

Gingival inflammation

↓

Pocket formation

↓

Followed by bone loss and tooth mobility.

Extraction of impacted third molars: Numerous clinical
studies have reported that the extraction of third molars
often results in the creation of vertical defects distal to
the second molars and appears to occur more often in
individuals older than 25 years than in those younger
than 25.

Malocclusion

Depending on its nature, malocclusion exerts varied
effect on the etiology of gingivitis and periodontal diseases
(Fig. 7.9).
a. Irregular alignment of teeth: Makes plaque control

difficult.

b. Spacing between teeth: Same sequelae following loss

of proximal contact can occur.

c. Facially-displaced teeth: Can lead to gingival

recession.

d. Occlusal disharmony: Results in injury to periodontium.
e. Deep bite: Inflammation of palatal mucosa.
f. Open bite: Leads to accumulation of plaque and

periodontal atrophy.

Habits

Sorren has classified habits of significance in the etiology
of periodontal diseases as follows:
a. Neurosis: Such as lip biting and cheek biting which

would lead to extra functional positioning of the
mandible, others include tongue thrusting, fingernail
biting and occlusal neurosis.

Figs 7.8A and B: 

Sequelae of unreplaced

missing first molar

Fig. 7.9: 

Gingival changes associated with malocclusion

A

B

73

Calculus and other Etiological Factors

Fig. 7.10: 

Gingival changes associated with mouth

breathing

b. Occupational habits: Such as holding of nails in the

mouth, e.g. carpenters, cobblers, etc.

c. Miscellaneous habits: Such as pipe or cigarette

smoking, tobacco chewing, incorrect methods of tooth
brushing, mouth breathing and thumb sucking.

I. Mouth breathing: Gingivitis is often associated with

mouth breathing. The gingival changes include
erythema, edema, enlargement and a diffuse shiny
appearance on the exposed areas (Fig. 7.10).

II. Tongue thrusting: It is the persistent, forceful wedging

of the tongue against the teeth. Instead of the dorsum
of the tongue being placed against the palate with
the tip behind the maxillary teeth during swallowing,
the tongue is thrust forward against the anterior teeth.

Tongue thrusting causes excessive lateral pressure,

which may be traumatic to the periodontium. It also
causes spreading and tilting of the anterior teeth,
which tilt and also spread laterally.

↓

Numerous secondary sequelae may develop from

tongue thrusting. They include, change in the
direction of the functional forces so that lateral
pressure against the crowns is increased.

↓

Also interferes with food excursion and favors the
accumulation of the food debris at the gingival
margin.

Fig. 7.11: 

Anterior overbite, pathologic migration

associated with tongue thrusting

Tongue thrusting is an important contributing factor
in the pathologic tooth migration (Fig. 7.11).

III. Use of tobacco: The following oral changes may occur

in the smokers:

1. Brownish, tar-like deposits and discoloration of tooth

structure. (Due to the nicotine and its major
metabolite, cotinine are deposited on the root
surfaces).

2. Diffuse greyish discoloration and leukoplakia of the

gingiva may occur.

3. “Smokers palate” (nicotinic stomatitis), characterized

by prominent mucous glands with inflammation of
the orifices and a diffuse erythema or by a wrinkled,
“cobble stone” surface, may occur.

4. Predisposition to acute necrotizing ulcerative gingivitis
5. Delayed post-surgical healing.
6. Marked increase in gingival crevicular fluid flow.
7. More severe gingivitis and periodontitis have been

reported in smokers.

Special type of gingivitis, termed “gingivitis toxica”

characterized by destruction of the gingiva and
alveolar bone has been attributed to the chewing of
tobacco (Fig. 7.12).

8. Oral polymorphonuclear cells from smokers show

reduced ability to phagocytose particles.

74

Essentials of Clinical Periodontology and Periodontics

IV. Toothbrush trauma: Acute or chronic gingival changes.
Acute changes are:
1. Sloughing of the epithelial surface occurs along with

denudation of the underlying connective tissue to
form a painful gingival bruise.

2. Punctate lesions are produced by the penetration of

the gingiva by the toothbrush bristles.

3. Painful vesicle formation in the traumatized areas is

also seen.

4. Diffuse erythema and denudation of the attached

gingiva throughout the mouth may be the striking
sequelae of the overzealous brushing.

The acute gingival changes noted can commonly

occur when the patient uses a new brush.

5. Tooth bristles forcibly embedded and retained in the

gingiva are a common cause of the acute gingival
abscess.

Chronic toothbrush trauma results in:
1. Gingival recession with denudation of root surface
2. Often the gingival margin is enlarged and appears

to be “piled up”, as if it were molded in conformity
with the strokes of the toothbrush.

Chemical irritation: Acute gingival inflammation may be
caused by chemical irritation. The gingival changes range
from simple erythema to painful vesicle formation and
ulceration. The substances include, strong mouthwashes,
dentifrices or denture materials, application of aspirin

tablet to alleviate toothache and injudicious use of
escharotic drugs.

Radiation:  Patients with cancer of the oral cavity and
adjacent regions who are treated with radiations initially
develop erythema and desquamation of the oral mucosa
including gingiva, which leads to   ulcerations, infections
and suppuration. The bone also undergoes degeneration.
Radiation also includes atrophy of the salivary glands
leading to xerostomia and changes in the oral flora
predisposing to dental caries.

Occlusal neurosis or parafunctional habits: They are
bruxism and clenching.

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

Clenching: It is the closure of the jaws under vertical
pressure.

Bruxism may lead to fracture of the teeth or dental

restorations, tooth wear or uncosmetic muscle
hypertrophy.

Two types of bruxism have been reported Nocturnal

Bruxism/Nonstress bruxists and diurnal bruxism/stress
bruxists.
Clinical features of bruxism: Clinically you can diagnose
bruxism by the presence of facet patterns.  Sleep studies
have shown that bruxism occurring during REM (rapid
eye movement) sleep may be the most damaging. No
association has been shown between bruxism and
periodontitis or gingival inflammation.
Treatment of bruxism: Occlusal adjustment is contra-
indicated.
Maxillary stabilization appliance is advised, which is the
most effective means of treating Bruxism. The main aim
of this appliance is to protect the tooth surface and to
dissipate forces built up in the musculoskeletal system
through the bruxism. This is more ideal to treat nocturnal
bruxism than for correcting daytime clenching habits.
It results in an immediate reduction in the masseter and
temporalis muscle activity levels. The appliance should

Fig. 7.12: 

Tobacco stains on the lingual surface of the

lower anterior teeth

75

Calculus and other Etiological Factors

be readjusted in 2 to 4 weeks and thereafter over longer
intervals bruxofacets should be observed in the follow
up visits and the surface should be burnished with a
smooth, pumice impregnated rubber wheel.

KEY POINTS TO NOTE

Calculus

1. Dental calculus is an adherent, calcified or calcifying mass

that forms on the surface of the teeth and dental
appliances.

2. Two types of calculus, supragingival and subgingival

calculus is seen.

3. It is made up of organic and inorganic constituents.
4. Four types of attachments of calculus to the tooth surface

has been reported.

5. Calculus formation takes place by the precipitation of

mineral salts.

6. Theories that are explained in calculus formation are:

a. Booster mechanism.
b. Epitactic or heterogenous nucleation
c. Inhibition theory

7. Finally, although a positive correlation exists between

calculus and periodontal disease, it is plaque that shows
a greater correlation with periodontal disease.

Other Contributing Etiological Factors including
Food Impaction

8. Faults in the dental restorations and prosthesis are referred

to as iatrogenic factors.

9. From the periodontal point of view, 6 characteristics of

restorations are important:
a. Margins of restorations.
b. Contours and overhanging dental restorations.
c. Occlusion.
d. Materials.
e. Design of removable partial dentures.
f. Restorative procedures themselves.

10. Orthodontic therapy may affect the periodontium by,

directly injuring the gingiva due to over extension of
bands, favoring the plaque retention and changing
gingival ecosystem and creating unfavorable forces on the
supporting tooth structures.

11. Food impaction is defined as the forceful wedging of the

food into the periodontium.

12. Bruxism is the clenching or grinding of the teeth when

the individual is not chewing or swallowing. Clenching
is the closure of the jaws under vertical pressure.

REVIEW QUESTIONS

Calculus

1. Define dental calculus. Describe the types and theories

of formation of dental calculus.

2. What is the composition of dental calculus?
3. Differences between supragingival and subgingival

calculus.

Other Contributing Etiological Factors

including Food Impaction

4. What are the effects of overhanging restorations on

periodontium?

5. What are the causes for the food impaction?
6. What is the sequelae following unreplaced missing

teeth?

7. What are the effects of smoking on periodontium?
8. What are para functional habits?

BIBLIOGRAPHY

1. Genco. Contemporary Periodontics. CV Mosby Company

Publication 1990.

2. Grant, Stern, Listgarten. Periodontics. Mosby Publications,

6th edn 1988.

3. JD Manson, Bmeley. Outline of Periodontics. 3rd edn. British

Library Cataloguing in Publication Data 1995.

4. Kenneth S, Kornman, Harold Loe. The role of local factors

in the etiology and periodontal diseases. Periodontol

2000;2:1993.

5. Kourkenta, Walsh, Pavis. The effect of porcelain laminate

veneers on gingival health and bacterial plaque characteristics,

Journal of Clinical Periodontol 1994;21:638-40.

6. Newman, Takei, Fermin A. Carranza. Clinical Periodontology.

WB Saunders Co, Ninth Edition 2002.

7. Robert G Keim. Esthetics in clinical orthodontic periodontic

interaction. Periodontology 2000;27:2001.

8. Robert I Sachs: Restorative dentistry and periodontium.

Dental Clinics of North America 1985;29:266-78.

9. Robert J Genco. Contemporary Periodontics. CV Mosby

Company Publications 1990.

76

Essentials of Clinical Periodontology and Periodontics

INTRODUCTION

Health is not a static condition. It is a dynamic state in
which the living and functioning organism or tissue
remains in balance with a constantly changing
environment. This constant process of readjustment to
maintain a functional integrity is known as “Homeostasis”.
It is a well known fact that bacteria constitute an important
part of environment and all the external surfaces in
nature including living tissues are covered by bacteria,
the skin, the gut and oral mucosa are of no exceptions.
When different forms of life exist together there is
competition for existence, hence various mechanisms
have evolved to help one form to protect it from another
called “Host defence mechanisms”.

The tissues of the periodontium are exposed to various

environmental factors in the oral cavity. Over 300 species

of bacteria have been isolated in the oral cavity. The
periodontal tissues remain in a state of partnership
(symbiosis) with most of the bacteria and only under
certain circumstances do we suffer from their attack
because, host defence system strikes a balance between
the two.

The host responds to the attack of bacteria and its

toxins at various levels.

ROLE OF SALIVA IN THE HOST DEFENCE

1. A vehicle for swallowing bacteria.
2. Inhibition of attachment of bacteria.
3. Bactericidal action by the peroxidase system.
4. Bactericidal action by lysozyme, lactoferrin and other

factors.

Salivary Peroxidase System

SCN

–

 

+

H

2

O

2

→

HOSCN

(Thiocyanate (Generated

(Peroxidase

Hypothio-

from salivary by salivary

enzyme)

cyanous

glands)

glands, bacteria,

acid, kills the

neutrophils, etc.)

bacteria)

Peroxidase  is synthesized by salivary gland acini and
secreted into the saliva, where it becomes bound to
bacteria and thiocyanate is secreted into saliva by the

❒

❒

❒

❒

❒ ROLE OF SALIVA IN THE HOST

DEFENCE

❒

❒

❒

❒

❒ GINGIVAL EPITHELIUM

❒

❒

❒

❒

❒ GINGIVAL CREVICULAR FLUID

❒

❒

❒

❒

❒ COMPLEMENT

❒

❒

❒

❒

❒ INFLAMMATORY CELL RESPONSE

❒

❒

❒

❒

❒ IMMUNOLOGICAL MECHANISMS

❒

❒

❒

❒

❒ IMMUNOLOGY OF PERIODONTAL

DISEASE

8

Host Response:

Basic Concepts

77

Host Response: Basic Concepts

ductal cells. Hydrogen peroxide is constantly secreted
in low concentration by bacteria, neutrophils and other
host cells and is used by peroxidase to oxidize the
thiocyanate to hypothiocyanous acid, which kills bacteria.

Lactoferrin: It is secreted by serous salivary gland, which
binds iron, an important growth factor or requirement
for many micro-organisms. This action is bacteriostatic
rather than bactericidal.

Lysozyme: It is an antimicrobial enzyme in the saliva
secreted mainly by mucous salivary glands and it degrades
mucopeptides in the cell wall of gram-positive bacteria,
weakening the wall and causing lysis.

GINGIVAL EPITHELIUM

Gingival epithelium has three functions:
1. Epithelial cells are tightly attached to each other.
2. Keratinization to resist trauma.
3. Presence of permeability barriers.

GINGIVAL CREVICULAR FLUID

Gingival crevicular fluid functions are:
1. Washing non-adherent bacteria and their products

out of the crevice.

2. Reducing the diffusion of plaque products into the

tissues.

3. It also carries a steady supply of inflammatory

mediators, protease inhibitors and host defence
agents such as complement and antibody, into the
crevice.

COMPLEMENT (Fig. 8.1)

The functions of complement are:
a. Chemotaxis cellular activation: Complement products

released in this reaction attracts phagocytes to the
site of infection, e.g. C

3a

 and C

5a

.

b. Opsonization:  Once they arrive at the site of infection

the complement components coat the bacterial
surface and allow the phagocytes to recognize the
bacteria and there by facilitating the bacterial
phagocytosis, e.g. C

3b

.

c. Cytolysis: Damage to the plasma membranes of the

cells can lead to lysis of the cell, e.g. C

1

-C

9

.

The complement system comprises of nine major

complement proteins which circulate in an inactive form
and which, like the clotting system, are activated in an
enzyme cascade.

C

1

-C

9

 causes cytolytic and cytotoxic damage to the cell.

Fig. 8.1: 

Complement activation

78

Essentials of Clinical Periodontology and Periodontics

Classical Pathway

The sequence is C

1

, C

4

, C

2

, C

3

, C

5

, C

6

, C

7

, C

8

, C

9

.

Alternate Pathway

It is activated by antibodies of immunoglobulins and also
endotoxins .They can intiate the third component of the
complement without starting from the beginning of the
cascade.

The sequence is C

3

, C

5

, C

6

, C

7

, C

8

, C

9

.

THE INFLAMMATORY CELL RESPONSE

It involves emigration of neutrophils, macrophages and
lymphocytes from the blood vessels into the tissues.
Neutrophils and macrophages perform inflammatory
functions whereas macrophages and lymphocytes
perform immunological functions.

Neutrophils

They are the initial leukocytes seen in the gingiva. They
exit the circulation and migrate into the junctional
epithelium and gingival crevice, where they provide the
first cellular host mechanism to control periodontopathic
bacteria.

Functions of Neutrophils

Emigration and chemotaxis:
Leukocytes normally travel along the center of the lumen
of the blood vessel, but in inflamed tissues the blood
flow is slowed by fluid exudation and they adhere more
readily to endothelial cells, the mechanism is  called
“rolling” and “margination”. When the neutrophils
migrate across the endothelium it is called “diapedesis”
and “interendothelial transmigration”.

Hence there are two phases of leukocyte endothelium

adherence.
a. The selectin-dependent phase (primarily in rolling and

margination).

b. The integrin-dependent phase (primarily in diape-

desis).

The selectin-dependent phase: The various selectins

are:
1. L-selectin—Expressed on the surface of the leukocyte.
2. P-selectin—Stored in the granules of endothelial cells

(Weibel-Palade bodies).

3. E-selectin—Expressed by endothelial cells.

P-selectin and E-selectin: They both strengthen the
binding between the leukocyte and the endothelial cell
and increase the number of leukocyte “rolling”.

The integrin-dependent phase: (Leukocyte B

2

-integrins):

The three leukocyte integrins are sequestered in the
specific granules of leukocytes,
• LFA-1—leukocyte function-associated antigen-1
• CD

11a

/ CD

18

(or)
Mac-1 / CD

11b

  / CD

18

• CD

11c

/

 

CD

18

These leukocyte B

2

-integrins act as the molecular

mediators of binding to the endothelial cells and their
binding affinity can be increased or decreased as the
leukocyte traverses the postcapillary venule.

Chemotaxis: It is the directed movement of a cell along
a chemical gradient. The neutrophils are attracted by
chemical signals from multiple sources, e.g. chemotaxins
which include compounds such as complement fragments
(C

5a

) (Fig. 8.2).

LTB

4

: It is secreted by mast cells, neutrophils macro-

phages, and also bacterial products including LPS and
factors released by damaged tissues.

Chemotaxis requires phagocyte, which possess

specific chemotaxin receptors, and the most well-studied
chemotaxin receptor is the receptor for formylmethionyl
peptides, known as the FPR (Formylmethionyl Peptide
Receptor).

Stages in neutrophil chemotaxis (Fig. 8.3)

Stage I: Soluble products diffuse forming a concentration
gradient.

79

Host Response: Basic Concepts

Fig. 8.2: 

Chemotaxis and migration

Fig. 8.3: 

Stages in neutrophil chemotaxis

Fig. 8.4: 

Phagocytosis

Stage IV: Neutrophils crawl upto the concentration
gradient.

Stage V: When concentration is constant, directional
migration ceases.

II Phagocytosis (Fig. 8.4)
Once they arrive at the site of inflammation, the
phagocytes have to recognize the infectious agent. This
can be enhanced if the organism has been coated by
C

3b

. They may then attach to micro-organism via their

non-specific cell surface receptors. After attachment the
phagocytes proceed to engulf the micro-organism by
extending pseudopodia around it. Once inside,
lysozymes fuse with the phagosome /phagocytic vacuole
to form a phagolysozyme and the infectious agent is
killed by a battery of microbiocidal mechanisms.

The main stages of bacterial killing by phagocytes:
For efficient phagocytosis, the particle should be coated

with one or more host serum proteins. This process is
called “opsonization” (meaning “to prepare for eating).
The two principal types of serum proteins referred to
as opsonins are IgG and C

3b

. There are receptors of these

two proteins on the phagocytes. Hence the opsonization
could be either complement-dependent, antibody-

Stage II: Resting neutrophils detect chemotaxins using
surface receptors.
Stage III: Receptors move to front of neutrophils, which
becomes polarized.

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Essentials of Clinical Periodontology and Periodontics

Fig. 8.5:

 Neutrophil: Oxidative and non-oxidative mechanisms for controlling microbes

dependent and the combination of both. Once the
organism has been internalised, lysozymes fuse with the
phagosome to form a phagolysozyme. Various killing
mechanisms are activated, they are (Fig. 8.5):
A. Non-oxygen-dependent killing mechanisms.
B. Oxygen-dependent killing mechanisms.

Oxidative mechanism: Stimulation of phagocytic cells
leads to an increase in cellular consumption of molecular
oxygen, a process termed as the “respiratory burst”. This
is associated with the generation of various oxygen
metabolites, which are injurious to many species of micro-
organisms. The majority of the oxygen consumed by
the phagocyte is converted directly to superoxide anion
(O

2

¯) through the action of a membrane—bound NADPH

oxidase. Superoxide radicals inturn may undergo
conversion to hydrogen peroxide (H

2

O

2

) either

spontaneously or via superoxide dismutase and
contribute significantly to microbicidal activity of the
phagocytic cells. Additional oxidants, e.g. hypochlorous
acid and toxic aldehydes are generated as a consequence
of the interaction between hydrogen peroxide and
azurophil enzyme (MPO). Hence the oxygen-dependent
bactericidal activity is further divided into:
• Myeloperoxidase—dependent
• Myeloperoxidase—independent.

Non-oxidative mechanisms: It appears to be based

on the various components of the cell. Neutrophils
contain three types of granules:
1. Primary granules/azurophilic granules: Myeloperoxi-

dase, lysozyme, acid phosphatase, and acid
hydrolases.

2. Secondary/specific granules: Lactoferrin, lysozyme,

azurocidin.

3. Tertiary granules: Alkaline phosphatase, collagenase,

and gelatinase.

Neutrophil Disorders Associated with
Periodontal Diseases

1. Diabetes mellitus.
2. Papillon Lefevre syndrome.
3. Down’s-syndrome.
4. Chediak-Higashi syndrome.
5. Drug-induced agranulocytosis.
6. Cyclic neutropenia.

Periodontal Diseases Associated with
Neutrophil Disorders

• Acute necrotizing ulcerative gingivitis (ANUG).
• Localized juvenile periodontitis (LJP).
• Prepubertal periodontitis (PPP).

81

Host Response: Basic Concepts

• Rapidly progressive periodontitis (RPP).
• Refractory periodontitis (RP).

Functions of Macrophages in the Gingiva,

Crevice, and Pocket

Macrophages develop from blood monocytes, which
emigrate into the tissues from the blood and are triggered
to develop into mature macrophages by cytokines, other
inflammatory mediators, bacterial products such as
endotoxins.

Functions of macrophages (Fig. 8.6) includes:

1. Phagocytose and kill bacteria.
2. Remove damaged host tissue during inflammation
3. And also trap and present antigens to lymphocytes

for induction of immune responses.
Because these functions unite inflammation and

immunity the macrophages play an important role in
all bacterial infections.

Most of the above mentioned functions are carried

out through the secretion of inflammatory mediators,
including cytokines, prostaglandins, leukotrienes and
complement components. Particularly important is the
secretion of the cytokines and although other cells such
as fibroblasts, endothelial cells and keratinocytes also

secrete cytokines, macrophages secrete the greatest
quantities. The most significant cytokine in inflammation
is interlenkin-1 (IL-1), which is a key mediator both in
inflammation and immunity-induced by bacteria. Tumor
necrosis factor (TNF) is also produced by macrophages.
Both TNF and IL-1 have similar functions.

They increase inflammation by, releasing histamine

from mast cells, attracting neutrophils and more
macrophages into the tissues and by causing many other
cells to release prostaglandins.

In summary, macrophages, like neutrophils are

required for the effective host response, but can mediate
a small amount of bystander damage. The damage could
be caused by direct effect that is by secreting enzymes
and toxins (similar to neutrophils) and indirectly by
secretion of cytokines. In excess amounts IL-1 and TNF
can have several damaging effects such as stimulation
of bone resorption and tissue fibrosis.

Other cells such as mast cells, fibroblasts, endothelial

cells, plasma cells and epithelial cells are also seen in
gingival connective tissue during inflammatory response.

Lymphocytes (Fig. 8.7): Three types of cells are included,
1. T-lymphocytes or T-cells: Derived from the thymus

and play a role in cell-mediated immunity.

2. B-lymphocytes or B-cells: Derived from liver, spleen

and bone marrow. They are precursors for plasma
cells and play a role in humoral immunity.

3. Natural killer (NK) cells.

Fig. 8.6: 

Functions of macrophage in periodontal tissues

Fig. 8.7:

 Derivation and response of B and T lymphocytes

82

Essentials of Clinical Periodontology and Periodontics

Antigens, which pass into the tissues, are carried to the
local lymph nodes, probably by macrophages, where
they are presented to lymphocytes, which circulate
continually through the nodes and tissues. The
lymphocytes, which recognize each individual antigen,
are activated, undergo clonal expansion and differentiate
into plasma cells, which secrete antibody under the
control of helper and suppressor T-lymphocytes. Most
of the lymphocytes and plasma cells remain in the lymph
nodes and secrete antibodies into the blood stream. The
antibody predominantly is IgG, which can opsonize and
activate the complement. Small amounts of IgM is also
seen which is more of an activator of the complement
and less of an effective opsonin. These antibodies pass
into the gingival inflammatory exudates and then out
into the gingival crevice in the crevicular fluid.

Possible mechanisms of action of antibodies in
periodontitis:
I. Binding to bacteria, Thus:

a. Opsonizing for phagocytosis
b. Activating neutrophil enzyme secretion
c. Coating bacteria and inhibiting attachment
d. Activating complement and thus enhancing

opsonization

e. Directly inhibiting bacterial metabolism.

II. Binding to soluble factors; Thus:

a. Neutralizing toxins.
b. Inhibiting enzymes.

The cell-mediated response in periodontal diseases: It
is so called because it involves contact between cytotoxic
T-cells and the target to be destroyed. These reactions
are effective against persistent antigens, which are
resistant to degradation, and the cells infected with viruses
and tumor cells (Fig. 8.9).

IMMUNOLOGICAL MECHANISMS (FIG. 8.10)

They are stimulus – specific and differentiate between
individual pathogenic species and sometimes-individual
strains. Micro-organisms and their products are
recognized as being different from the host because they

Fig. 8.8: 

Systemic humoral immune response

Different types of T-cells include:

Helper inducer T-cells (TH-cells) or CD

4

: They aid in the

cellular response of the B-cells to differentiate into plasma
cells and produce antibodies.

Suppressor-cytotoxic T-cells (TS-cells) or CD

8

: Stimulates

cytotoxic and microbicidal activity of the immune cells.
Subdivided into TH

1

 TH

2

 TH

0

.

• TH cells release IL-2 and IFN (interferons)
• TS cells release interleukin: IL-4 and IL-5
• In adult periodontitis TH cells increase and TS cells

decrease with increased gingival inflammation.

The humoral response to plaque (Fig. 8.8): Plaque
bacteria and their soluble products such as enzymes and
toxins carry out activation of the humoral response.

83

Host Response: Basic Concepts

Fig. 8.9:

 Local cellular immune response

Fig. 8.10: 

Antibody production by salivary and humoral

immune systems and by polyclonal B cell activation

contain structures, which are not found in the human
body. These so called antigens (antibody –generating)
are first recognized by the lymphocytes and each
lymphocyte is capable of recognizing only one foreign
antigen and when it comes in contact with that antigen
it is triggered to divide several times and therefore with
in few days there are many more cells with the same
specificity. This amplification process is known as clonal
expansion. This will result in the production of larger
pool of cells, which are differentiated to protect the host
either by humoral or cell-mediated mechanisms.

Humoral responses are carried out by lymphocytes,

which differentiate into plasma cells and secrete antibody
directed against the original antigen. Cell mediated
responses, in contrast, do not require antibody, but
depend on the clonal expansion to provide large number
of lymphocytes, which destroy targets directly. This direct
effect of an immune reaction against a foreign antigen
results in significant tissue damage is referred to as
hypersensitivity reaction.

Type I or Anaphylactic Reactions

Two variations in the anaphylactic hypersensitivity may
occur, depending on the route of the administration of
antigen. If injected locally into the skin, the reaction is
called cutaneous anaphylaxis.

If the antigen is injected intravenously it is called

systemic or generalized anaphylaxis. The basic
mechanisms of both types are similar (Fig. 8.11).

Mechanisms of Anaphylactic Hypersensitivity

 Anaphylaxis occurs when two Ig E antibodies that are
fixed to a mast cell or basophil react with the antigen
through the Fab portion of the antibodies. This antibody-
antigen reaction causes the release of the pharma-
cologically-active substances from the sensitized-cells.

These mediators released by the human mast cells

include:
a. Histamine—Increased capillary permeability.
b. Alpha 2-macroglobulins—Collagenase activation.
c. SRS-A—Smooth muscle contraction.

84

Essentials of Clinical Periodontology and Periodontics

To date evidence suggests an important role for the
cytotoxic reactions in the gingivitis and periodontitis.

Type III: Immune Complex or Arthus Reactions

When high levels of antigen are present and persist
without being eliminated antigen-antibody (IgG or IgM)
complexes precipitate in and around small blood vessels
and with subsequent complement activation cause tissue
damage at the site of the local reaction. Inflammation,
haemorrhage and necrosis may occur. Tissue damage
appears to be due to the release of lysozymal enzymes
from various cells such as neutrophils, mast cells, etc.
This reaction is referred to as immune complex or Arthus
reaction.

Type IV: Cell-Mediated or Delayed

Hypersensitivity

Cellular immunity does not include circulating antibodies
but is based on the interaction of the antigens with the
surface of T-Lymphocytes.

IMMUNOLOGY OF PERIODONTAL DISEASE
(Fig. 8.12)

Immune responses may be both beneficial and
detrimental. Several components of the immune system
are active in periodontal disease. These host variables
may influence bacterial colonization, bacterial invasion,
tissue destruction, healing and fibrosis (Tables 8.1 and
8.2).

Fig. 8.11:

 Immunologic mechanism of tissue damage

d. Bradykinin—Increased permeability same as SRS-A.

(Slow release substance of anaphylaxis).

Type II: Cytotoxic Reactions

 In cytotoxic type, antibodies react directly with antigens
tightly bound to cells. A cytotoxic reaction involving these
cells will result in hemolysis. Cytotoxic antibodies are of
IgG or IgM class. In addition to inducing cell lysis, cytotoxic
antibodies may cause tissue damage by increasing the
synthesis and release of lysozymal enzymes by cells
(PMNs). The tissue in the vicinity of these enzymes will
then be damaged.

Cytotoxic reactions are seen in the autoimmune

diseases where antibodies react with body’s own tissue
components. For example, this occurs in pemphigus where
antibodies react with cell membranes and pemphigoid
antibodies react with the epithelial basement membrane.

Table 8.1: Influence of host responses on

periodontal diseases

• Bacterial colonization: Subgingivally, antibody, complement

in crevicular fluid inhibits adherence and co-aggregation of

bacteria and potentially reduces their numbers by lysis.

• Bacterial invasion: Antibody-complement-mediated lysis

reduces bacterial counts. Neutrophil-mediated lysis also

reduces bacterial counts.

• Tissue destruction: Antibody-mediated hypersensitivity, cell-

mediated immune responses, activation of tissue factors such

as collagenase.

• Healing and fibrosis: Lymphocytes and macrophage

produced chemotactic factor for fibroblasts, fibroblast-

activating factors.

85

Host Response: Basic Concepts

Fig. 8.12: 

Host defence against local and systemic infections of periodontal origin

86

Essentials of Clinical Periodontology and Periodontics

Table 8.2: Significant immune findings in periodontal diseases

Disease

Immune response

ANUG

• PMN chemotactic defects
• Elevated antibody titres to Prevotella intermedia and intermediate-sized spirochetes

Pregnancy gingivitis

• No significant findings reported

Adult periodontitis

• Elevated antibody titres to the Porphyromonas gingivalis and other pathogens
• Presence of immune complexes in tissues
• Cell-mediated immunity to gingival bacteria

Juvenile Periodontitis:
LJP

• Polymorphonuclear leukocytes chemotactic defect and depressed phagocytosis
• Elevated antibody levels to Actinobacillus actinomycetemcomitans
• Defect in GP

110

 receptors

GJP

• PMN chemotactic defect and depressed phagocytosis
• Elevated antibody levels to P. gingivalis

Prepubertal periodontitis

• PMN and monocyte chemotactic defects

Rapidly-progressing periodontitis

• Suppressed or enhanced PMN, monocyte chemotaxis
• Elevated antibody levels to several Gram-negative bacteria

Refractory periodontitis

• Reduced PMN chemotaxis

KEY POINTS TO NOTE

1. Host defence is established at different levels.
2. Saliva acts as a vehicle for swallowing bacteria, inhibits the

attachment of bacteria, and kills the bacteria by the
peroxidase system, lysozyme and lactoferrin.

3. Functions of gingival epithelium are structural arrangement

of epithelial cells, prevents bacterial entry, keratinization,
resists trauma and also has a permeability barrier.

4. Complement functions are cellular activation, opsonization

by C

3b

 and cytolysis (C

1

-C

9

).

5. The complement activation can be classical pathway with

the sequence of C

1

, C

4

, C

2

, C

3

, C

5

, C

6

, C

7

, C

8

, C

9

, alternative

pathway C

3

, C

5

, C

6

, C

7

, C

8

, C

9

.

6. Various killing mechanisms of neutrophils are, non-oxygen-

dependent mechanisms and oxidative mechanisms.

7. Macrophages phagocytose and kill bacteria, removes

damaged host tissue during inflammation and also traps and
presents the antigens to lymphocytes for induction of
immune responses.

8. There are three types of lymphocytes, T-lymphocytes, B-

lymphocytes and natural killer (NK) cells.

REVIEW QUESTIONS

1. What are the function of saliva and gingival crevicular

fluids ?

2. Role of neutrophils in periodontal disease.
3. Describe the complement activation and functions

of antibodies.

BIBLIOGRAPHY

1. Erica Gemmell, Gregory J Seymour, Modulation of immune

response to periodontol bacteria. Current Opinion in
Periodontol 1994:18–34.

2. Genco. Contemporary Periodontics. CV Mosby Company

Publication, 1990.

3. JD Manson, B Meley. Outline of Periodontics, British library

Cataloguing in Publication data, Third edition (1995).

4. Jeffrey L, Ebersole, Martin A Taubman. The Protective nature

of host responses in periodontal disease. Periodontol 2000;
5:1994.

5. Newman, Takei, Fermin. A. Carranza, Clinical Periodontology,

9th edn, WB Sounders Co., 2002.

6. Robert J Genco, Host response in periodontal disease: Current

concepts. Jr of Periodontol 1992;63(4).

7. Sigmund S. Socransky, Anne D Haffajee, Bacterial etiology

of destructive periodontal disease: current concepts Jr. of
periodontal April 1992 (Supply Copy), Vol 63 No.4.

8. Thomas E Van Dyke, Jaywanth Vaikuntan. Neutrophil

function and dysfunction in periodontal disease. Current
Opinion in periodontol 1994:19–28.

9. Williams, Francis J Hughey. Pathology of Periodontal Disease

1992 Oxford Medical Publications.

87

Trauma from Occlusion

PHYSIOLOGIC ADAPTIVE CAPACITY OF THE
PERIODONTIUM TO OCCLUSAL FORCES

 One must appreciate the dynamics of the periodontium
to accomodate the forces exerted on the crown, which
is called as adaptive capacity. This varies in different
persons and in the same person at different times. This
is mainly explained by four factors which mainly influences
the effect of occlusal forces on the periodontium.
a. Magnitude (the amount): When it is increased the

periodontium responds (a) with a thickening of the

periodontal ligament, (b) an increase in the number
and width of periodontal ligament fibers and an (c)
increase in the density of the alveolar bone.

b. Direction: Changes in the direction causes a

reorientation of the stresses and strains within the
periodontium (lateral or horizontal forces, torque or
rotational forces are more likely to injure the
periodontium).

c. Duration: Constant pressure on the bone is more

injurious than intermittent forces.

d. Frequency: The more frequent the application of an

intermittent force, the more injurious to the
periodontium.

TRAUMA FROM OCCLUSION (TFO)

Definition and Terminology

According to Orban and Glickman et al (1968): Trauma
from occlusion is defined as, when occlusal forces exceed
the adaptive capacity of the periodontal tissues, the tissue
injury results. This resultant injury is termed as trauma
from occlusion.

WHO in 1978 defined trauma from occlusion as

“damage in the periodontium caused by, stress on the
teeth produced directly or indirectly by the teeth of the
opposing jaw”.

❒

❒

❒

❒

❒ PHYSIOLOGICAL ADAPTIVE CAPACITY

OF THE PERIODONTIUM TO OCCLUSAL

FORCES

❒

❒

❒

❒

❒ TRAUMA FROM OCCLUSION

• Definition and Terminology

• Types

• Signs and Symptoms

• Histologic Changes

• Other Properties

* Effect of Insufficient Occlusal Force

* Reversibility of Traumatic Lesion

* Effect of Increased Forces on Pulp

❒

❒

❒

❒

❒ ROLE OF THE TRAUMA FROM

OCCLUSION IN THE PROGRESSION OF

PERIODONTAL DISEASE

❒

❒

❒

❒

❒ PATHOLOGIC TOOTH MIGRATION

❒

❒

❒

❒

❒ OTHER CAUSES

9

Trauma from Occlusion