Textbook of Periodontology and Oral Implantology 2nd Edition

Textbook of
Periodontology and
Oral lmplantology
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Textbook of
Periodontology and
Oral lmplantology
SECOND EDITION
Edited by
DILIP G N AYAK MDS
Dean and Professor
Department of Periodontology
Manipal College of Dental Sciences
Mangalore, India
ASHITA UPPOOR MDS

Associate Dean and Professor
Mangalore, India
MAHESH CP MDS
Professor and Head
NIMS Dental College
Jaipur, India
ELSEVIER
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ELSEVIER
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Textbook of Periodontology and Oral Implantology: 2e, Nayak DG, Uppoor A, CP Mahesh
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Foreword
The spread of dental education worldwide has created The second edition Textbook of Periodontology and Oral
a scenario where dental knowledge can be sourced from Implantology brought out by Dr Dilip Nayak, Dr Ashita
unexplored quarters. Unlike before, when quality sources Uppoor, and Dr Mahesh CP is a step in this direction.
of dental information were exclusively textbooks from The authors are committed academicians and experi-
the West, we are now seeing a growing acceptance of enced teachers of the subject of periodontology. They
textbooks written by authors from developing countries, have various scientific publications and clinical trials to
especially from India. their credit.
The increase in the number of Indian textbooks is a A brief overview of the book reveals the amount of ef-
welcome sign. However, one should be selective in the fort put in by the authors and the contributors to update
choice of books to refer because this will have a bearing the latest advances in the field of periodontology. I wish
on our clinical decision making. Indian authors must them all the best in their endeavor to spread knowledge
focus on providing books of international standard with in periodontology and implantology. I wholeheartedly
quality content, illustrations, and references. recommend this book to all those who seek the same.
Dr V Surendra Shetty, MDS

Pro Vice Chancellor
Manipal University, Manipal
Karnataka, India
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List of Contributors
Abhay Kolte MOS Ashish Nichani MOS

Professor and Head Professor
Department of Periodontology AECS Maaruti Dental College and Research Centre
VSPM Dental College and Research Center Bangalore, Karnataka, India
Nagpur, Maharashtra, India
Ashwini Rao MOS
Ambalavanan N MOS Professor and Head
Professor and Head Department of Public Health Dentistry
Department of Periodontology Manipal College of Dental Sciences
Meenakshi Ammal Dental College Mangalore, Karnataka, India
Maduravoyal, Chennai, Tamil Nadu, India
Betsy Thomas MOS
Professor and Head
Ananthakrishna NC (Late) MD, FCCP
Department of Period ontology
Formerly Professor Emeritus
Faculty of Dentistry, MAHSA University
Department of Microbiology
Jalan Elmu, Off Jalan University
KS Hegde Medical Academy
Kuala Lumpur, Malaysia
Mangalore, Karnataka, India
Bhat KM MOS
Arvind Shetty MOS Professor
Professor and Head Department of Period ontology
DY Patil University School of Dentistry Manipal, Karnataka, India
Nerul Navi Mumbai, Maharashtra, India
Bhongade ML MOS
Ashita Uppoor MOS Professor and Head
Associate Dean and Professor Department of Period ontology
Department of Periodontology Sharad Pawar Dental College
Manipal College of Dental Sciences Wardha, Maharashtra, India
Biju Thomas MOS
Arun Kumar MS, MOS Professor and Head
Professor, Department of Periodontology Department of Period ontology
Yenepoya Dental College AB Shetty Memeorial Institute of Dental Sciences
Deralakatte, Mangalore, Karnataka, India Deralakatte, Mangalore, Karnataka, India
Aravind Shenoy MOS David Kadakampally MOS

Professor Associate Professor
Department of Conservative Dentistry Department of Period ontology
Bapuji Dental College Manipal College of Dental Sciences
Davangere, Karnataka, India Mangalore, Karnataka, India
Asavari Desai MOS Deepa G Karnath MOS

Assisitant Professor Professor and Head
Department of Orthodontics Department of Period ontology
Manipal College of Dental Sciences Manipal College of Dental Sciences
Mangalore, Karnataka, India Mangalore, Karnataka, India
vii
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viii LIST OF CONTRIBUTORS
Dilip G Nayak MOS Nancy Srivastava MOS

Dean and Professor Senior Lecturer
Department of Periodontology Department of Periodontology
Manipal College of Dental Sciences NIMS Dental College and Hospital
Mangalore, Karnataka, India Shobhanagar, Jaipur, Rajasthan, India
Dipen Shah MOS Nandini Manjunath MOS

Former Senior Lecturer Professor and Head
AMC Dental College, Khokra Department of Periodontology
Ahmedabad, Gujarat, India AJ Institute of Dental Sciences
Mangalore, Karnataka. India
Dwarakanath CD MOS
Professor and Head Neena Shenoy MOS
Vishnu Dental College Professor
Bhimavaram, Andhra Pradesh, India Department of Periodontology
AB Shetty Memorial Instiute of Dental Sciences
Faizuddin M MOS
Formerly Professor and Head
Department of Periodontology Neetha J Shetty MOS
MR Ambedkar Dental College Associate Professor
Bangalore, Karnataka, India Department of Periodontology
Mahesh CP MOS
Professor and Head
Department of Periodontology Neha Gupta MOS
NIMS Dental College Reader
Jaipur, Rajasthan, India Department of Periodontology
Shree Bankey Bihari Dental College
Ghaziabad, Uttar Pradesh, India
Mehta DS MOS
Vice Principal
Professor and Head Prathibha PK MOS
Department of Periodontology Professor and Head
Bapuji Dental College and Hospital Department of Periodontology
Davangere, Karnataka, India Manipal College of Dental Sciences
Manipal, Karnataka. India
Mohan Alexander MOS

Professor and Head Rajesh H MOS
Department of Oral and Maxillifacial Surgery Professor
Faculty of Dentistry Department of Periodontology
MAHSA University, Jalan Elmu, Off Jalan University Yenepoya Dental College, Deralakatte
Kuala Lumpur, Malaysia Mangalore, Karnataka, India
Nagarathna DV MOS Rajesh Kashyap MOS

Professor Professor
Department of Periodontology Department of Periodontology
AJ Institute of Dental Sciences Yenepoya Dental College
Mangalore, Karnataka, India Deralakatte, Mangalore, Karnataka, India
Nandakumar K MOS Rahul Nair MPH, MS

Professor and Head Assistant Professor
Department of Periodontology ARCPOH
Azeezia College of Dental Sciences & Research School of Dentistry
Kollam, Kerala, India University of Adelaide
SA, Australia-SOOS
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LIST OF CONTRIBUTORS ix
Ravikiran Ongole MOS Suresh RMOS

Professor Professor and Head
Department of Oral Medicine and Radiology Department of Periodontology
Manipal College of Dental Sciences Sri Ramachandra Dental College
Mangalore, Karnataka, India Chennai, Tamil Nadu, India
Ruchika Goel MOS Suruchi Jain MOS

Formerly Assistant Professor Formerly Assistant Professor
Department of Periodontology Department of Orthodontics
Manipal College of Dental Sciences Manipal College of Dental Sciences
Mangalore, Karnataka, India Mangalore, Karnataka, India
Swati MOS
Sachin Goyal MOS Reader
Reader Department of Periodontology
Bhojia Dental College and Hospital Mangalore, Karnataka, India
Bhud, Baddi, Himachal Pradesh, India
Vandana KL MOS
Sangeeta U Nayak MOS Senior Professor
Assistant Professor Department of Periodontology
Department of Periodontology College of Dental Sciences
Manipal College of Dental Sciences Davangere, Karnataka, India
Vidya Shenoy MOS
Professor
Siddarth Shetty MOS Department of Periodontology
Professor and Head AJ Institute of Dental Sciences
Department of Orthodontics Mangalore, Karnataka, India
Vijendra Singh Gangwar MOS
Former Senior Lecturer
Subraya Bhat MOS Department of Periodontology
Associate Professor Sardar Patel Postgraduate Institute of Dental and Medical
College of Dentistry Sciences
University of Dammam Raebareli Road
Dammam, Saudi Arabia Lucknow, Uttar Pradesh, India
Yeltiwar RK MOS
Sumita Singh MOS
Professor and Head
Senior Lecturer
Rungta College of Dental Sciences & Research
Sardar Patel Post Graduate Institute of Dental & Medical
Bhilai, Chhattisgarh, India
Sciences
Raibareli Road
Lucknow, Uttar Pradesh, India
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Preface
I believe life is constantly testing us for our level of com- also attempted to envisage upon the task of including
mitment, and life's greatest rewards are reserved for those topics such as, genetics, the biological, diagnostic, and
who demonstrate a never-ending commitment to act until they prosthodontic aspects of dental implants. Besides, the
achieve. This level of resolve can move mountains, but it must recent advances in periodontal surgery and the man-
be constant and consistent. As simplistic as this may sound, it agement of peri-implant diseases have been elaborated
is still the common denominator separating those who live their painstakingly by the authors.
dreams from those who live in regret. - Anthony Robbins In the course of writing the second edition of this text-
book, careful attention has been devoted to include the
procedures and concepts, as they were outlined originally,
The Textbook of Periodontology and Oral Implantology as well as recent concepts and developments in the field
was conceived with two primary goals in mind: to create of clinical periodontology. Any oversights in the previous
a book that would focus on the needs of undergraduates edition were unintentional and the editors have taken
during their training program in periodontology and to utmost care to set right the same if any in this edition as
facilitate the understanding of the complexities of the compared to the previous edition.
subject of periodontology, as it relates to dental practice, The editors would like to acknowledge the support
without omitting salient concepts and diluting the content and help provided by every individual who has been
of information provided. directly or indirectly associated with the making of this
The second edition, in keeping with the ethos of select- edition. We sincerely believe that we have succeeded in
ing contributors on the basis of their respectable stature encompassing the rapid and constant change related to
as leading researchers, clinicians, or teachers in periodon- the field of periodontology in a structured and simplified
tology, implant dentistry, and associated domains, has manner in this edition.
Dilip G Nayak
Ashita Uppoor
Mahesh CP
xi
Acknowledgments
The editors would like to express their deep gratitude Pathology; and Dr Evelyn Wagiyu, Dean, Faculty of Den-
to all the individuals who have extended their dedicated tal Sciences, University Dental Hospital, Nairobi, Kenya
and selfless efforts in the completion of this edition of the for providing us the photographs for various chapters.
Textbook of Periodontology and Oral Implantology. We would also like to acknowledge the able and
We sincerely acknowledge the encouragement and dedicated assistance provided in the compilation of spe-
guidance provided to us by Dr V. Surendra Shetty, Pro cific chapters by Dr Cham Shrestha, Dr Sunita Sharma,
Vice Chancellor, Manipal University, Karnataka, India. Dr Priti Shrestha, Dr Bhageshwar Dhami, Dr Pragyan
We are thankful for all the furtherance and support ren- Das, Dr Sridevi Shetty, Dr Clany D'souza, and Dr Sulagna
dered by him. Chakrabarty.
We offer our gratitude to all the contributors who have We would like to thank our publisher Elsevier (India)
shared their valuable knowledge and ideas for the com- for its constructive suggestions and unstinted support in
pilation of this book. publishing this book.
We appreciate the willing help and support offered We hope this book will be helpful to all students of
by our colleagues, especially Dr Karen Boaz, Profes- periodontology in understanding the contemporary sce-
sor and Head, Department of Oral Pathology; Dr Arati nario in the field of etiopathogenesis, diagnosis and thera-
Rao, Professor and head, Department of Pedodontology; peutic aspects of periodontal diseases, and the intricacies
Dr Nandita KP, Associate Professor, Department of Oral associated with the field of oral implantology.
Brief Contents
I TISSUES OF THE PERIODONTIUM

1. Gingiva 3
2. Periodontal Ligament 12
3. Cementum 17
4. Alveolar Bone 23
5. Age-related Changes in the Periodontium 29
II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES

6. Classification of Periodontal Diseases 35
7. Epidemiology of Periodontal Diseases 41
Ill ETIOLOGY OF PERIODONTAL DISEASES

8. Dental Plaque and Microorganisms Associated with Periodontal Health and Disease 55
9. Host Response - Basic Concepts 64
10. Host Microbial Interaction in Periodontal Disease 76
11. Dental Calculus 83
12. Smoking and the Periodontium 88
13. Trauma from Occlusion 93
14. Role oflatrogenic and Other Local Factors in Periodontal Disease 108
15. Systemic Diseases and Periodontium 120
16. Periodontal Medicine 131
17. Role of Genetics in Periodontal Therapy 140
IV PERIODONTAL PATHOLOGY
18. Defense Mechanisms of the Gingiva 153
19. Gingival Inflammation 161
20. Clinical Features of Gingivitis 166
21. Gingival Enlargement 172
22. Acute Gingival Infections 181
23. Desquamative Gingivitis 190
24. Periodontal Diseases in Childhood and Adolescents 198
25. Periodontal Pocket 204
26. Bone Loss in Periodontal Disease 211
27. Periodontitis: Chronic, Refractory, and Necrotizing Ulcerative 218
28. Aggressive Periodontitis 225
29. Periodontal Abscess 234
30. AIDS and Periodontium 238
31. Halitosis 24 7
xvi BRIEF CONTENTS
V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

32. Clinical Diagnosis 253
33. Role of Radiology in the Diagnosis of Periodontal Diseases 267
34. Advanced Diagnostic Methods 279
35. Determination of Prognosis 290
36. Periodontal Treatment Plan 297
3 7. Treatment of Periodontal Diseases in Medically Compromised Patients 300
38. Risk Assessment 313
VI PERIODONTAL THERAPY
39. Periodontal Instrumentation 321
40. Sonic and Ultrasonic Instrumentation 346
41. Plaque Control 353
4 2. Scaling and Root Planing 3 75
4 3. Chemotherapeutic Agents 3 79
44. Host Modulation 393
45. Periodontal Splints 397
46. General Principles of Periodontal Surgery 401
47. Gingival Surgical Procedures 412
48. Flap Surgery 419
49. Resective Osseous Surgery 4 31
50. Regenerative Osseous Surgery 440
51. Furcation Involvement and Its Management 450
52. Endodontic Periodontal Lesions and Their Management 458
53. Periodontal Plastic Surgery 468
54. Recent Advances in Periodontal Surgical Techniques 486
55. Periodontal Considerations in Restorative Dentistry 499
56. Ortho-Perio Interrelationships 505
57. Infection Control 514
58. Supportive Periodontal Treatment 523
59. Biological Aspects of Dental Implants 527
60. Diagnosis and Treatment Planning in Implantology 530
61. Prosthodontic Considerations in Implant Restorations 54 7
62. Advanced Surgical Procedures for Dental Implants 560
63. Peri-Implant Diseases and Management 571
64. Evidence-Based Periodontics 576
Index 585
Contents
Foreword V Composition of Alveolar Bone 25

List of Contributors vii Osseous Topography 26
Fenestration and Dehiscence 26
Preface xi Remodeling of Alveolar Bone 27
Acknowledgments xiii Questions 28
Brief Contents xv Suggested Readings 28
5. Age-related Changes in the Periodontium

I Dilip G Na yak
Vasculature 29
TISSUES OF THE Tooth-periodontium Relationship 29
PERIODONTIUM Gingival Epithelium 30
Gingival Connective Tissue 30
Periodontal Ligament 30
1. Gingiva Neha Gupta Cementum 30
Gingiva 3 Alveolar Bone 31
Gingival Connective Tissue 8 Bacterial Plaque 31
Questions 11 Immune Responses 31
Suggested Readings 11 Summary 31
Questions 32
Suggested Readings 32
2. Periodontal Ligament Neetha] Shetty
Origin and Development of the Periodontal
Ligament 12 II
Features of Periodontal Ligament 12
Functions of Periodontal Ligament 15 CLASSIFICATION AND
Clinical Considerations 16 EPIDEMIOLOGY OF
Questions 16
Suggested Readings 16 PERIODONTAL DISEASES
3. Cementum Ashita Uppoor 6. Classification of Periodontal Diseases

Ashita Uppoor
Physical Characteristics 17
Composition 17 Definition 35
Functions of Cementum 18 Requirement 35
Classification 18 Need for Classification 35
Cementoenamel Junction 19 Uses of Classification 35
Cementodentinal Junction 20 Hisrorical Development of the Classification
Developmental and Acquired Anomalies System 35
of Cementum 20 Changes Made in the Classification 39
Cementum Resorption and Repair 21 Future Challenges in Classifying Periodontal
Cementa! Tears 21 Diseases 39
Questions 22 Conclusion 39
Suggested Readings 22 Questions 40
4. Alveolar Bone Neetha] Shetty
7. Epidemiology of Periodontal Diseases Ashwini Rao
Parts of Alveolar Process 23
Hisrology of Alveolar Bone 23 Basic Considerations 41
lnterdental Septum 24 Classification of Indices 42
Bone Marrow 25 Public Health Significance of Periodontal Disease 42
xviii CONTENTS
Indices Used in Periodontics 42 11. Dental Calculus Ashita Uppoor

Questions 51
Suggested Readings 51 Definition 83
Classification 83
Composition 83
III Structure of Dental Calculus 84
Attachment of Calculus on Tooth Surface 84
Rate of Calculus Formation 85
ETIOLOGY OF Detection of Calculus 85
PERIODONTAL DISEASES Formation of Calculus 85
Theories Regarding Mineralization of Calculus 86
8. Dental Plaque and Microorganisms

Role of Microorganisms in Calculus Mineralization 87
Role of Calculus in Periodontal Disease
Associated with Periodontal Health (Clinical Implications) 87
and Disease Ambalavanan N Questions 87
Oral Flora 55
Dental Plaque 56
Specific Plaque Hypothesis 58 12. Smoking and the Periodontium
Virulence Mechanisms of Periodontal Pathogens 59 Vijendra Singh Gangwar
Microorganisms Associated with Periodontal Health and Disease 59
Description of Important Periodontal Pathogens 60 Effect of Smoking on Periodontal Disease 88
Questions 63 Clinical Features of Oral Tissues Associated with Smoking 89
Suggested Readings 63 Pathogenesis of Periodontal Disease in Smokers 89
Response to Periodontal Therapy in Smokers 91
Recurrent Periodontal Disease 91
9. Host Response - Basic Concepts
Tobacco Use Cessation 91
Ananthakrishna NC (Late) Questions 92
Cells of the Immune System 64 Suggested Readings 92
Role of Antibodies in Inflammatory Diseases 68
Immune Reactions 71 13. Trauma from Occlusion Vandana KL
Mediators of Immune Response and Inflammation 72
Influence of Host Response on Periodontal Disease 73 History 93
Periodontal Disease Activity 73 Definition and Terminology 93
Models of Periodontal Disease Activity (Socransky) 73 Physiologic Adaptive Capacity of Periodontium
Clinical Indications of Disease Activity 74 to Occlusal Forces 94
Prerequisites for Periodontal Disease Initiation and Progression 74 Types of Occlusal Forces 94
Conclusion 74 Occlusal Forces and Jaw Movement 94
Questions 74 Classification of Trauma from Occlusion 94
Suggested Readings 75 Etiology of Trauma from Occlusion 95
Trauma from Occlusion and Plaque Associated
10. Host Microbial Interaction Periodontal Disease 96
in Periodontal Disease Mahesh CP Glickman's Concept 96
Animal Studies 97
Identifying Putative Pathogens 76 Human Trials 98
Key Organisms 76 Tissue Response to Increased Occlusal Forces 98
Secondary Organisms 76 Clinical Epidemiologic Studies 99
Host Bacterial Interaction 76 Examination and Diagnosis of Trauma
Microbiologic Aspects of Microbial-host Interactions 77 from Occlusion 99
Microbial Mechanism of Host Tissue Damage 78 Signs ofTFO 100
Immunologic Aspects of Microbial-host Interaction 78 Symptoms ofTFO 101
Host Response of Gingiva and Periodontium Reversibility of Traumatic Lesion 102
in Different Stages of Gingivitis 79 TFO and Implants 102
Inflammatory Cells, Molecules, and Processes 79 Latest Advances in Evaluation of Occlusal Stresses
Adaptive Host Response 80 in the Periodontal Tissues 102
Humoral Immune Response 80 Treatment 102
Cell-mediated Immunity 80 Practical Clinical Conclusions and Guidelines 102
Microbiology and Immunology in Periodontal Diseases 80 Pathologic Migration 103
Conclusion 81 Conclusion 106
Questions 82 Questions 107
Suggested Readings 82 Suggested Readings 107
CO N T EN T S xix
14. Role of Iatrogenic and Other Orogranulocytes 157

Local Factors in Periodontal Disease Prathibha PK Saliva 158
Questions 160
Iatrogenic Factors 108 Suggested Readings 160
Local Contributing Factors 115
Conclusion 118 19. Gingival Inflammation Neha Gupta
Questions 118
Suggested Readings 118 Definition 161
Stages in the Pathogenesis of Gingivitis 161
15. Systemic Diseases and Periodontium Questions 165
Deepa G Karnath
Metabolic and Endocrine Disorders 120 20. Clinical Features of Gingivitis Neha Gupta
Hormonal Changes 123
Correlation of Clinical and Microscopic Features
Psychosomatic Disorders 126
in Health and Gingivitis 166
Hematological and Immune Disorders 127
Questions 171
Influence of Nutrition 128
Suggested Readings 1 71
Other Systemic Conditions 129
Questions 130
Suggested Readings 130 21. Gingival Enlargement Faizuddin M
Classification 1 72
16. Periodontal Medicine Suresh R Inflammatory Gingival Enlargement 173
Periodontitis as a Risk Factor for Systemic Disease 131 Fibrotic Gingival Enlargement 174
Periodontitis and Coronary Heart Disease 131 Combined Enlargement 176
Periodontitis as a Risk Factor for Preterm Pregnancy-associated Gingival Enlargement 1 77
Low-birth-weight Babies 133 Vitamin C Deficiency 1 77
Periodontal Disease and Diabetes Mellitus 135 Pyogenic Granuloma 177
Periodontal Disease and Chronic Obstructive Leukemia 178
Pulmonary Disease 137 Wegener Granulomatosis 178
Questions 139 Sarcoidosis 178
Suggested Readings 139 Benign Lesions of Gingiva 178
Malignant Lesions of Gingiva 1 79
False Gingival Enlargement 180
1 7. Role of Genetics in Periodontal
Questions 180
Therapy Mahesh CP and Nancy Srivastava Suggested Readings 180
Terminologies 140
Genetics 140 22. Acute Gingival Infections Deepa G Karnath
Types of Genetic Disorders 14 2
Mutation Versus Polymorphism 143 Necrotizing Ulcerative Gingivitis 181
Human Gene Polymorphism 143 Primary Herpetic Gingivostomatitis 186
Polymorphisms and Their Relationship to Periodontal Disease 143 Pericoronitis 188
Methods of Genetic Analysis 144 Questions 189
Role of Genetics in Aggressive Periodontitis 145 Suggested Readings 189
Association of Aggressive Periodontitis with Genetic
and Inherited Conditions 14 7 23. Desquamative Gingivitis Nagarathna DV
Role of Genetics in Chronic Periodontitis 14 7
Classification of Diseases that Clinically Present
Epigenetics 149
as Desquamative Gingivitis 190
Conclusion 149
Dermatologic Lesions 191
Questions 150
Allergic Reactions 195
Miscellaneous Conditions: Mimicking Desquamative
Gingivitis 196
IV Questions 197
PERIODONTAL
PATHOLOGY 24. Periodontal Diseases in Childhood
and Adolescents Deepa G Karnath
18. Defense Mechanisms of the Gingiva Mahesh CP Periodontium of Deciduous Dentition 198
Epithelial Barrier 153 Gingivitis 200
Gingival Crevicular Fluid 155 Types of Gingival Diseases in Childhood 200
xx CONTENTS
Types of Periodontal Diseases 202 Differential Diagnosis 236

Aggressive Periodontitis 202 Treatment 236
Questions 203 Periodontal Cyst 237
Suggested Readings 203 Questions 237
25. Periodontal Pocket Neha Gupta
30. AIDS and Periodontium Biju Thomas
Classification 204
Clinical Features 204 Definition of AIDS 238
Pathogenesis 206 Human Immunodeficiency Virus 238
Histopathology 206 Classification and Staging 240
Microtopography of the Gingival Wall of the Pocket 207 Oral and Periodontal Manifestations of AIDS 240
Morphology of the Tooth Wall 208 General Clinical Signs in AIDS Patient 240
Questions 210 Classification of Oral Lesions Associated
Suggested Readings 210 with HIV Infection 240
Investigations 243
Management of HIV/ AIDS Antiretroviral
26. Bone Loss in Periodontal Disease Sumita Singh
Treatment 244
Etiology of Bone Destruction 211 Infection Control Measures with a Focus
Histopathology 211 on the Dental Setting 244
Mechanism of Bone Destruction 212 Precautions for Dentists 245
Topography of the Alveolar Bone 213 Sterilization and Disinfection 245
Factors Determining Bone Morphology Questions 246
in Periodontal Disease 213 Suggested Readings 246
Bone Loss Patterns in Periodontal Disease 214
Diagnosis 215 31. Halitosis David Kadakampally
Questions 217
Incidence 24 7
Etiology 247
Intraoral Causes 24 7
2 7. Periodontitis: Chronic, Refractory, Extraoral Causes 248
and Necrotizing Ulcerative Deepa G Karnath Diagnosis 248
Treatment Aspects of Oral Malodor 249
Chronic Periodontitis 218
Questions 250
Refractory Periodontitis 221
Systemic Antibiotic Therapy in the Management
of Refractory Periodontitis 222
Necrotizing Ulcerative Periodontitis 222
Necrotizing Ulcerative Periodontitis V
in HIV/AIDS Patients 222
Questions 224 DIAGNOSIS, PROGNOSIS,
AND TREATMENT
28. Aggressive Periodontitis Mehta DS PLANNING
Classification 225
Historical Background 225 32. Clinical Diagnosis Subraya Bhat
Epidemiology 225 Importance of Diagnosing the Periodontal Condition 253
Prevalence 226 Components of Periodontal Examination 253
Localized Aggressive Periodontitis 226 Mucogingival Problems or Problems Related
Generalized Aggressive Periodontitis (GAP) 230 to Plastic Periodontal Surgery 262
Treatment 231 Teeth in Occlusion 264
29. Periodontal Abscess Sachin Goyal 33. Role of Radiology in the Diagnosis
of Periodontal Diseases Ravikiran Ongole
Classification 234
Etiology 234 Radiographic Application in the Diagnosis
Pathogenesis and Histopathologv 235 and Treatment Planning of Periodontal Disease 267
Diagnosis 235 Limitations of Radiographs 267
CO N T EN T S xxi
Radiographs Useful for Diagnosing Periodontal Disease 268 Clinical Risk Assessment in Periodontal
Imaging Considerations for Periodontal Disease 269 Disease 315
Characteristic Radiographic Features of Periodontal Diseases 274 Questions 316
Systemic Conditions Influencing Periodontitis 277 Suggested Readings 316
Systemic Conditions Mimicking Periodontitis
Radiographically 277
Questions 278
Suggested Readings 278 VI
34. Advanced Diagnostic Methods PERIODONTAL THERAPY
Rajesh Kashyap and Rajesh H
Uses 279 39. Periodontal Instrumentation Mahesh CP
Conventional Diagnosis 279
Classification of Periodontal Instruments 321
True Disease Status 280
Types of Strokes 339
AIDS in Clinical Diagnosis 281
Questions 345
AIDS in Radiographic Diagnosis 283
AIDS in Microbiological Diagnosis 284
AIDS Used in Immunological and Biochemical Diagnosis 284
Questions 288
40. Sonic and Ultrasonic Instrumentation
Suggested Readings 289 Neha Gupta
Sonic Scalers 346
35. Determination of Prognosis Dilip G Nayak Ultrasonic Scalers 346
Definition 290 Dental Contraindications 350
Overall Versus Individual Prognosis 290 Recommendations for Use 350
Determination of a Prognosis 290 Technique 350
Reevaluation of Prognosis After Phase 1 Therapy 295 Clinical Comparisons 351
36. Periodontal Treatment Plan Ashish Nichani 41. Plaque Control Mahesh CP
Rationale for Treatment Plan 297 Definition of Dental Plaque 353
Preferred Sequence of Treatment Phases 297 Fate of Dental Plaque 353
Questions 299 Time and Rate of Plaque Formation 353
Suggested Readings 299 Disclosing Agents 354
Plaque Control - Instruction Procedures 356
Toothbrushes 356
3 7. Treatment of Periodontal Diseases in
Classification of Gingival Embrasures 363
Medically Compromised Patients Nandini Manjunath Gingival Physiotherapy 366
Cardiovascular Diseases 300 Tongue Scraping 366
Endocrine Disorders 304 Chemical Plaque Control 366
Renal Diseases 306 Mouthrinses 366
Liver Diseases 307 Classification of Chemical Plaque Control Agents 367
Pulmonary Diseases 307 Anticalculus Agents 371
Immunosuppression and Chemotherapy 308 Dentifrices 372
Radiation Therapy 308 Questions 374
Pregnancy 308 Suggested Readings 374
Leukemia 309
Coagulation Disorders 309 42. Scaling and Root Planing Bhat KM
Infectious Diseases 311
Objective of Root Planing 375
Questions 312
Rationale for Root Planing 375
Indications of Root Planing as a Specific Periodontal
Treatment in Periodontitis 376
38. Risk Assessment Suresh R Instrumentation 376
So What Is "Risk?" 313 Procedure 376
Risk Factors for Periodontal Disease 314 Use of Lasers in Root Planing 377
Risk Indicators 315 Questions 378
Risk Markers/Predictors 315 Suggested Readings 378
xxii CONTENTS
43. Chemotherapeutic Agents Dipen Shah 48. Flap Surgery Neetha] Shetty
Rationale of Antibiotic Therapy 3 79 Definition 419
Importance of Combined Therapy 380 Objectives of Periodontal Flap Surgery 419
Treatment Goals 380 Classification of Flaps 419
Routes of Drug Administration 380 Incisions in Periodontal Flaps 420
Antimicrobial Agents in Periodontal Therapy 381 Healing after Flap Surgery 426
Ocher Antibiotics 383 Suturing 427
Guidelines for the Use of Antibiotic in Periodontal Questions 430
Disease 384 Suggested Readings 430
Local Delivery of Antibiotics in Periodontal
Disease 385
Local Delivery of Antiseptics in Periodontal 49. Resective Osseous Surgery Bhongade ML
Pocket 386 Historical Background 431
Local Versus Systemic Delivery of Antibiotics 387 Classification of Osseous Defects 431
Analgesics in Periodontal Therapy 387 Definitions 432
Questions 392 Surgical Procedure 433
Suggested Readings 392 Osteoplascy 437
Factors Affecting Outcome of Resective
44. Host Modulation Subraya Bhat Osseous Surgery 437
Anatomic Limitations and Considerations 437
Host Immunoinflammatory Response Related
Current Status of Osseous Resective Surgery 438
to Periodontal Destruction 393
Questions 438
Antioxidants 396
Questions 396
50. Regenerative Osseous Surgery N andakumar K
45. Periodontal Splints Ashita Uppoor
Principles of Osseous Regeneration 440
Definition 397 Periodontal Regeneration 442
Rationale of Splinting 397 Grafe Materials for Regeneration 442
Characteristics of an Ideal Splint 397 Types of Ceramic and Their Characteristic Tissue
Indications 397 Interaction Behavior 444
Contraindications 398 Regenerative Surgical Procedures 445
Basic Principles of Splinting 398 Future Bone Regeneration Approaches 448
Disadvantages of Splinting 398 Questions 449
Classification 398 Suggested Readings 449
Questions 400
51. Furcation Involvement and Its Management
46. General Principles of Periodontal Surgery Abhay Kolte and Yeltiwar RK
Mahesh CP Furcation 450
Furcation Involvement 450
Objectives of Surgical Treatment 401
Therapeutic Modalities in Furcation Involvement 454
Indications for Surgical Treatment 401
Questions 456
Contraindications for Periodontal Surgery 402
Outpatient Surgery 403
Questions 411
Suggested Readings 411 52. Endodontic Periodontal Lesions and Their
Management Aravind Shenoy and Neena Shenoy
4 7. Gingival Surgical Procedures Neetha J Shetty
Relationship of Pulpal and Periodontal Disease 458
Inadvertent Gingival Curettage 412 Pathways of Communication Between Pulp
Surgical Gingivectomy 414 and Periodontium 459
Gingivoplasty 414 Periodontal Disease 459
Healing after Surgical Gingivectomy 414 Pulpal Disease 459
Gingivectomy by Electrosurgery 414 Classification of Endodontic Periodontal
Laser Gingivectomy 417 Lesions 459
Chemical Gingivectomy 418 Diagnosis of Endodontic Periodontal Lesions 462
Questions 418 Tests 464
Suggested Readings 418 Treatment Protocol 465
CO N T EN T S xxiii
Conclusion 466 Orthodontic Stability Considerations in Periodontally

Questions 466 Compromised Patients 509
Suggested Readings 466 Periodontally Accelerated Osteogenic Orthodontics 511
Questions 512
53. Periodontal Plastic Surgery Dwarakanath CD
Common Mucogingival and Aesthetic Problems 468 5 7. Infection Control Sangeeta U Na yak
Significance of Attached Gingiva, Vestibular Depth,
Exposure Prevention Strategies 514
and Frenum 468
Protective Measures 515
General Factors Affecting the Outcome of PPS
Personal Protective Equipment or Barrier Precautions 516
Procedures 470
Transport and Processing of Contaminated Instruments 51 7
Augmentation of Attached Gingiva 471
Environmental Infection Control 521
Management of Aberrant Frenum 475
Vestibular Deepening Questions 522
478
Gingival Depigmentation Suggested Readings 522
480
Crown Lengthening 480
Reconstruction of Interdental Papilla 483 58. Supportive Periodontal Treatment
Ten Commandments of PPS 485 Deepa G Karnath
Acknowledgment 485
Questions 485 Rationale for Supportive Periodontal Treatment 523
Suggested Readings 485 Parts of Maintenance Phase 524
Recurrence of Periodontal Disease 524
Recall Intervals for Various Classes of Recall Patients 524
54. Recent Advances in Periodontal Referral of Patients to the Periodontist 524
Surgical Techniques Swati and Ruchika Goel Maintenance for Implant Patients 526
Conclusion 526
Laser in Periodontics 486
Questions 526
Components of a Laser Unit 486
Laser-tissue Interactions 488
Laser Application in Periodontal Therapy 490
Photodynamic Therapy 492 59. Biological Aspects of Dental Implants
Photodynamic Antimicrobial Therapy 492 Arvind Shetty
Clinical Cases Done Using 810 nm Diode Laser
(Picasso, AMO Lasers®) in Department Osseo integration 527
of Periodontology, MCODS, Mangalore, Bone Characteristics 527
Implant Soft Tissue Interface 528
Manipal University 494
Conclusion 529
Microsurgery 494
Questions 529
Conclusion 498
Questions 498
60. Diagnosis and Treatment Planning
55. Periodontal Considerations in lmplantology Betsy Thomas
in Restorative Dentistry Arun Kumar Indications 530
Restoration Margins 499 Contraindications 530
Restoration Contours 501 Patient Evaluation 531
Occlusal Considerations 502 Clinical Examination and Evaluation 532
Restorative Materials 502 Surgical Aspects of Implant Placement 537
Provisional Restorations 502 Implant Surgery 537
Pontic Design 502 Complications 539
Conclusion 503 Immediate Implant Treatment Modality 542
Questions 504 Surgical Protocol 543
Suggested Readings 504 Conclusion 545
Questions 546
56. Ortho-Perio Interrelationships Suggested Readings 546
Siddarth Shetty, Suruchi Jain and Asavari Desai
61. Prosthodontic Considerations
Orthodontic Treatment Considerations 505 in Implant Restorations Vidya Shenoy
Biomechanical Considerations 505
Timing and Sequence of Treatment 505 Impression Techniques 547
Adjunctive Orthodontics 506 Abutments in Implants 552
xxiv CONTENTS
Provisional Restorations 555 63. Peri-Implant Diseases and Management

Occlusal Considerations in Implant-Supported Prosthesis 555 Betsy Thomas
Cementation of the Implant Crowns 556
Types of Implant-Supported Restorations 557 Etiology 571
Conclusion 558 Risk Factors 571
Questions 559 Ailing, Failing, and Failed Implants 572
Suggested Reading 559 Diagnosis of Peri-Implant Tissue Breakdown 573
Peri- Implantitis: Treatment Options 573
62. Advanced Surgical Procedures Conclusion 575
Questions 575
for Dental Implants Mohan Alexander
Suggested Reading 575
Maxillary Sinus Lift Surgery 560
Bone Augmentation 564 64. Evidence-Based Periodontics RahulNair
Ridge Splitting 566
Guided Bone Regeneration 566 Basic Concepts 576
Distraction Osteogenesis 566 Clinical Practice and Evidence 578
Bone Grafts 566 Conclusion 582
Inferior Alveolar Nerve Repositioning 569 Questions 583
Conclusion 570 Suggested Readings 583
Questions 570
Suggested Readings 570 Index 585
SECTION I
TISSUES OF THE PERIODONTIUM

CHAPTER
1
Gingiva
Periodontium consists of the tissues that surround and tissues of periodontium are (i) gingiva, (ii) periodontal liga-
support the teeth. The word comes from the Greek terms ment, (iii) cementum, and (iv) alveolar process. Gingiva is
peri- meaning "around" and-odons meaning "tooth." Liter- considered as an investing tissue and periodontal ligament,
ally taken, it means that which is "around the tooth." The cementum, and alveolar process are the supporting tissues.
GINGIVA epithelial keratinization, and pigmentation. Gingiva is

demarcated clinically into:
The oral mucosa can be divided into three categories
1. Marginal gingiva (free or unattached)
on the basis of its function:
2. Attached gingiva
3. Interdental gingiva (papillary)
Marginal Gingiva (Free or Unattached)

Oral mucosa Marginal gingiva is the portion of the gingiva sur-
rounding the neck of the tooth that forms the soft tissue
wall of the gingival sulcus. After complete tooth erup-
Masticatory mucosa Specialized mucosa
tion, the free gingival margin is located on the enamel
(gingiva, hard palate) (dorsum of the tongue)
surface approximately 1.5-2 mm coronal to the cemen-
toenamel junction (CEJ). It is demarcated from the at-
Lining mucosa tached gingiva by a shallow depression called the free
(lips, cheeks, floor of the mouth, soft gingival groove.
palate, ventral aspect of the tongue)
A. FREE GINGIVAL GROOVE

The free gingival groove is delineated from the at-
tached gingival by the free gingival groove. It corresponds
Gingiva is defined as that part of the oral mucosa which
with the coronal margin of the junctional epithelium,
covers the alveolar process of the jaws and surrounds the
i.e., the bottom of the sulcus. It was observed that a free
necks of the teeth. The gingiva extends from the gingival
gingival groove is only present in about 30-50% of the
margin to the mucogingival junction except on the palatal
total population.
surfaces of maxillary molars where it merges with the
palatal mucosa. B. GINGIVAL SULCUS
The gingival sulcus is a shallow crevice between the
Macroscopic Features of the Gingiva marginal gingiva and the tooth. It is bordered by the sul-
The normal color of gingiva is "coral pink," and it is cular epithelium on one side, the tooth on the opposite
pigmented by melanin which makes the gingiva appear side, and the coronal end of junctional epithelium at its
darker. This melanin pigmentation varies in different most apical end. In germ-free animals or after intense
races. The color varies according to degree of vascularity, plaque control, the depth is 0 mm.
4 SECTION I TISSUES OF THE PERIODONTIUM
Functions of the attached gingiva are as follows:

• It braces the marginal gingiva and it lies in between
two epithelium that are movable, i.e., free gingiva and
alveolar mucosa.
• It allows for proper deflection of food.
• It provides room for proper placement of the
toothbrush.
• It has an esthetic value.
• It is critical for overall maintenance of gingival health.
• It prevents the apical spread of inflammation from
marginal gingiva to the deeper periodontium.
The mucogingival junction is the line between the al-
FIGURE 1.1 Normal clinical sulcus depth. veolar mucosa and the attached gingiva. The position of
this junction is fixed.
A probing depth of 1-3 mm is usually considered com- Interdental Gingiva (Papillary)

patible with gingival health (Fig. 1.1). The interdental gingiva occupies the gingival embra-
Attached Gingiva sures apical to the contact areas. The shape of the inter-
dental gingiva is determined by the distance between the
• It is continuous with marginal gingiva and extends contact point and the crest of alveolar bone, amount of
to the mucogingival junction on the facial and lingual embrasure space, root angulation, periodontal biotype,
aspects of the mandible and the facial aspect of the and the course of the CEJ. Since the interdental papilla has
maxilla. In the palate, there is no demarcation between a shape in conformity with the outline of the interdental
the attached gingiva and the masticatory mucosa. contact surfaces, a concavity - a col - is established in the
• It is firm, resilient, and tightly bound to periosteum of premolar and molar regions.
alveolar bone.
• In 40% of adults the surface texture of attached gingiva • It is a valley-like depression that connects the facial
shows stippling (orange peel appearance) (Fig. 1.2). and lingual papillae.
When present, it is more prominent on maxillary • It conforms to the shape of interproximal contact.
than mandibular arch; anterior maxilla than on the • The epithelium of the col is nonkeratinized due to
posterior and facial surfaces than on lingual surfaces. which it is prone to inflammation.
It is absent in infancy, appears at 5 years, increases until In the presence of diastema, the interdental papilla is
adulthood, and frequently disappears in old age. absent. It is pyramidal-shaped interdental papilla in the
Width of the attached gingiva: Usually, the facial at- incisor region. Due to the presence of interdental papillae,
tached gingiva is widest in the area of upper and lower the free gingival margin follows a more or less accentu-
incisors (3.5-4.5 mm in the maxilla and 3.3-3.9 mm in ated, scalloped course through the dentition (Fig. 1.3).
the mandible), and narrowest in the posterior segments
(1.9 mm in maxillary and 1.8 mm in mandibular first
Microscopic Features
premolars). On the lingual aspect of the mandible, it is
narrow in the incisor region and wide in the molar region. The gingival epithelium comprises the epithelial tissue
The width of attached gingiva increases with age and that covers the external surface of the gingiva called as
supraeruption of teeth. outer epithelium, epithelium lining, the gingival sulcus
Alveolar mucosa
MGJ
Attached gingiva
Marginal glngiva
~: . , ·• I> lnterdental papilla
FIGURE 1.2 Stippling seen in the core of the interdental papilla and
attached gingiva. FIGURE 1.3 Anatomical features of normal gingiva.
C H A PTER I G IN G IVA 5
The gingival epithelium is subdivided into three sec-
tions: (i) the oral epithelium; (ii) the sulcular epithelium;
and (iii) the junctional epithelium. The histologic char-
acteristics and functions of these types of epithelium are
different.
Oral Epithelium
Oral epithelium (OE) is a stratified, squamous keratin-
izing epithelium that lines the vestibular and oral surfaces
of the gingiva. It extends from the mucogingival junction
FIGURE 1.4 Generalized melanin pigmentation. to the crest of gingival margin. However, in the palatal
surface it blends with the palatal epithelium.
known as sulcular epithelium, and the junctional epi- Oral epithelium can be divided into the following cell
thelium that forms the base of the gingival sulcus. The layers:
principal cell type of the gingival epithelium is the ke-
ratinocyte. In addition to the keratin-producing cells, 1. Basal cell layer (stratum basale or stratum germinativum)
which comprise about 90% of the total cell population, 2. Prickle cell layer (stratum spinosum)
the epithelium contains the nonkeratinocytes, which are 3. Granular cell layer (stratum granulosum)
as follows: 4. Keratinized cell layer (stratum corneum)
1. Melanocytes 1. Basal cell layer (stratum basale). The basal cell layer
2. Langerhans cells represents the germinative layer. Basal layer cells
3. Merkel cells are mainly cylindrical or cuboidal in appearance
4. Inflammatory cells in contact with the basal lamina. Some cells of this
They are also called "clear cells" since in histologic sec- layer migrate through the entire epithelial thickness
tions, the zone around their nuclei appears lighter than and eventually keratinize; these are known as
that in the surrounding keratin-producing cells. keratinocytes. Cells in other layers cannot divide.
Hence, the basal cells are responsible for the important
Melanocytes function of protecting the underlying structure and
Melanocytes are specialized cells that synthesize mela- producing new epithelial cells. In addition, these
nin pigment. They are responsible for the melanin pig- cells synthesize and secrete the macromolecules that
mentation occasionally seen on the gingiva (Fig. 1.4). constitute the basal lamina.
Melanocytes are derived from neural crest cells that even- The basal lamina (basement membrane) under the
tually migrate into the basal and the spinous layer of the electron microscope reveals an electron-dense layer,
epithelium. In both light- and dark-pigmented individu- the lamina densa (LD) in contact with the connective
als, melanocytes are present in the epithelium. In dark- tissue compartment, and an electron-lucent layer,
skinned individuals, the gingiva may contain melanin the lamina lucida (LL) in contact with the epithelial
pigment to a greater extent than the adjacent alveolar cells. The cell membrane of the epithelial cells facing
mucosa. The melanin is produced in granules called as the lamina lucida harbors a number of electron-
the melanosomes, stored within the cytoplasm of the dense, thicker zones appearing at various intervals
melanocytes, and the adjacent keratinocytes. along the cell membrane. These structures are called
hemidesmosomes (HDs). The hemidesmosomes are
Langerhans Cells involved in the attachment of the epithelium to the
Langerhans cells are dendritic cells located among ke- underlying basement membrane. The lamina lucida
ratinocytes at suprabasal levels containing large granules is composed of laminin and other glycoproteins. The
called Birbeck granules. They are derived from the cellu- lamina densa is composed of an afibrillar type of
lar differentiation of monocytes. The Langerhans cells are collagen, type IV collagen. The so-called anchoring
believed to play a role in the defense mechanism of the fibers (AF) composed of type VII collagen extend from
oral mucosa. In the presence of an infection, Langerhans the undersurface of the lamina densa into the lamina
cells will take up and process microbial antigen to become propria where they appear to form loops around
fully functional antigen-presenting cells, thereby inhibit- collagen fibers.
ing or preventing further antigen penetration of the tissue. 2. Prickle cell layer (stratum spinosum). The cells
are polyhedral shaped characterized at the light
Merkel Cells microscopic level by apparent intercellular bridges.
Merkel cells have been suggested to have a sensory These cells possess decreased number of mitochondria
function. equipped with short cytoplasmic processes resembling
spines. The cytoplasmic processes occur at regular cell derives from a mitotic activity in the stratum ba-
intervals and give the cells a prickly appearance. sale and makes its way toward the intraoral epithelial
Together with intercellular protein-carbohydrate surface:
complexes, cohesion between the cells is provided by
II • There is no cell division.
numerous desmosomes" (pairs of hemidesmosomes)
• The cells are abundant in keratohyalin granules,
which are located between the cytoplasmic processes
keratin filaments, and macromolecules for the matrix-
of adjacent cells.
like fillagrin.
3. Granular cell layer (stratum granulosum). The layer
• The organelles required for protein synthesis and
between the stratum spinosum and the stratum comeum
energy production are lost.
consists of cells which are flatter and have granules called
• The cells are finally completely keratinized but still
as keratohyalin granules. They contain the keratolinin
interconnected by intercellular junctions.
and involucrin precursors of envelope which lies below
• The cells are finally sloughed away from the epithelial
the cell membrane and fillagrin. Epithelial cells become
surface and into the oral cavity as the cell-cell
flattened. Tonofibrils take up an increasing volume of
attachment (hemidesmosomes and gap junctions
the cytoplasmic contents. Keratohyalin granules contain
ultimately disintegrate).
Odland bodies. Odland bodies or keratinosomes, which
are modified lysosomes, are present in the uppermost Sulcular Epithelium
layers of the stratum spinosum and between the stratum
The sulcular epithelium is a stratified, squamous,
spinosum and stratum granulosum.
nonkeratinized epithelium. It lies between the junctional
4. Keratinized cell layer (stratum corneum). This is the
epithelium and the crest of the free marginal gingiva coro-
outermost layer of keratinized oral mucosa. It has cells
nally. It is epithelium that is continuous with the oral
that are flat and tightly packed. The epithelial cell here
epithelium and lines the lateral surface of the sulcus.
is the most differentiated and its matrix is formed of
Apically, it overlaps the coronal border of the junctional
fillagrin which has bundles of keratin tonofilaments.
epithelium, a structural design that minimizes ulceration
There is no nuclei present. This form of keratinization
of the epithelial lining in this region (Fig. 1.5). This epi-
is referred to as orthokeratinization, i.e., complete
thelium shares many of the characteristics of the oral
keratinization of the epithelial cells.
epithelium, including good resistance to mechanical
Schroder and Page have summarized the events forces and relative impermeability to fluid and cells. It
of continued differentiation that occurs as a new basal has the potential to keratinize if:
Lipid droplet
9• 1l Keratohyaline
~ Lamellated granules
, Golgi complex
~
½, • i'Ci= Mltochood,ia
lntercellular """"
A,~~ Granular endoplasmic

reticulum
-----------Desmosome
FIGURE 1.5 Stratified squamous epithelium: different layers.

• It is reflected and exposed to the oral cavity.
• Bacterial flora of the sulcus is totally eliminated.
• Conversely, the outer epithelium loses its keratinization
when it is placed in contact with the tooth. These
findings suggest that the local irritation of the
sulcus prevents sulcular keratinization. The overall
structure of the sulcular epithelium resembles that
of the oral epithelium, except for the surface layer
that is nonkeratinized than its counterpart in the oral
epithelium. The tightly sealed intercellular spaces
(ICS) contribute to the low permeability of sulcular
epithelium unlike the junctional epithelium, which is
heavily infiltrated by PMNs.
Junctional Epithelium
Junctional epithelium is a collar-like band of epithe-
lium that surrounds the tooth. It is a stratified squamous
nonkeratinizing epithelium. One aspect of this epithelium
faces the gingival connective tissue (i.e., the lamina pro-
pria of the gingiva) and the other aspect the tooth surface.
The junctional epithelium consists of 15-30 cell layers
coronally, and only 1-3 cell layers at its apical termina- 1-Normal gingival sulcus
tion giving it a wedge shape. The length of the junctional 2-lntemal basal lamina (epithelial attachment)
3-Apical extent of JE
epithelium ranges from 0.25 to 1.35 mm.
The suprabasal layer and the basal layer are the two
strata seen in the junctional epithelium. The basal layer FIGURE 1.6 Structure of junctional epithelium.
is the layer where mitotic division takes place rapidly.
New cells travel continuously coronally and are shed play a key role in attachment of junctional epithelium cells
in the gingival sulcus. Few cells of the suprabasal layer to the internal basal lamina.
help in the formation of epithelium attachment which The internal basal lamina and the hemidesmosomes
consists of internal basal lamina, hemidesmosomes, and form the epithelial attachment. This term is not synony-
suprabasal cells facing the tooth structure. Compared mous with junctional epithelium, which refers to the en-
with other epithelia, junctional epithelial cells are inter- tire epithelium. The junctional epithelium is divided into
connected by a few desmosomes only and occasionally three zones: coronal, middle, and apical.
by gap junctions. A variety of mononuclear leukocytes The junctional epithelium cells divide continuously
occupy these interstitial spaces. Antigen-presenting cells and this mitotic activity happens in all the cell layers. Af-
and Langerhans and other dendritic cells are present as ter the division the cells move coronally toward and along
well. The junctional epithelium, particularly its basal cell the tooth surface providing attachment and then desqua-
layers, is well innervated by sensory nerve fibers. mate at the base of the gingival sulcus. This mechanism
The junctional epithelium has two basal laminae, gives a self-renewing and a protective capacity to the JE.
the internal basal lamina and the external basal lamina The junctional epithelium is more permeable than the
(Fig. 1.6).They are continuous apically. The external base- oral or sulcular epithelium due to wide intercellular spac-
ment lamina of the junctional epithelium faces the lamina es. Bacterial substances can enter and gingival crevicular
propria and is similar to, in its structure and composition, fluid, host immune products, and inflammatory mediators
with other basement membranes that are present between can reach the gingival sulcus through it. While cell mitosis
an epithelium and a connective tissue. The internal basal occurs in basal layer and possibly also in some areas ad-
lamina is unique. It forms the epithelial attachment, i.e., jacent to it, the zone becomes infiltrated with chronic in-
the adhesion of gingiva to the tooth. The structure of this flammatory cells, primariy lymphocytes and plasma cells.
lamina lacks collagen types IV, VII, and laminin, which Since there are fewer intercellular junctions between
is present in the external basal lamina that faces the con- the junctional epithelium cells and wider spaces inter-
nective tissue. It comprises two zones: the electron-lucent cellularly the leukocytes can migrate from the vessels in
zone, the lamina lucida and the electron-dense zone, the the lamina propria into the gingival sulcus. In an healthy
lamina densa. The lamina densa is near the enamel and individual approximately 30,000 PMNs migrate per min-
the organic projections from the enamel extend into this ute through the junctional epithelia of all human teeth
zone. Hemidesmosomes attach to the lamina lucida which into the oral cavity. These PMNs together with the host
immune products play a vital role in defense mechanism A. GINGIVAL FIBERS (FIG. 1.7)
of gingiva. These are made of bundles of type I collage mainly.
There are few elastic and oxytalan fibers present in peri-
vascular areas in the lamina propria. These gingival fi-
bers are also called supragingival fiber apparatus. This
GINGIVAL CONNECTIVE TISSUE provides a resiliency to the attached gingiva and helps to
maintain the position of teeth within the dental arch. They
The gingival connective tissue is called as lamina consists of the microfibrillar component only, thereby
propria. It has two layers, i.e., papillary layer which are resembling very immature elastic fibers. Elastic fibers
present between the finger-like projections of epithelium are rather scarce in the lamina propria. They are a more
called as rete ridges and the reticular layer present below common constituent of the lining submucosa. The col-
the rete ridges. It is continuous with the periosteum of lagen fibers are irregularly or randomly distributed but
the alveolar bone. At its junction with the lining mucosa, most tend to be arranged in groups of bundles with a dis-
is the mucogingival junction. The lamina propria encloses tinct orientation. According to their insertion and course
the cells, fibers, and the neurovascular elements. in the tissue, they have been divided into the following
The gingival connective tissue is occupied by: (Table 1.1):
a. Principal fibers
• collagen fiber bundles 60-65%;
- Dentogingival
• cellular elements (fibroblasts 5%, various leukocytes,
- Alveologingival
mast cells, tissue macrophages, etc. 3%);
- Dentoperiosteal
• vascular elements (blood and lymph vessels), nerves,
- Circular
and ground substance about 35%.
- Transseptal
The ground substance occupies the space between b. Secondary fibers
cells, fibers, and neurovascular elements. It has high - Periosteogingival
water content, glycoproteins, e.g., fibronectin, and - Interpapillary
proteoglycans such as hyaluronic acid and chon- - Transgingival
droitin sulfate. The ground substance permits the - Intercircular
diffusion of biological substances between various - Intergingival
structural elements. - Semicircular
1. Dentogingival
- Coronal
- Horizontal
-Apical
2. Alveologingival
3. lnterpapillary
4. Transgingival
5. Circular
6. Dentoperiosteal
7. Transseptal
8. Periosteogingival
9. lntercircular
10. lntergingival
10 5 4 7 9 3
FIGURE 1. 7 Gingival fiber groups.

TABLE 1.1 Classification of Collagen Fibers
Name of fiber group Origin and orientation

PRINCIPAL GROUPS
Dentogingival group Originates from cementum and spreads laterally into the lamina propria
Alveologingival group Originates from the periosteum of the alveolar and spreads coronally into the lamina propria bone
Dentoperiosteal group Originates from cementum near the cementoenamel junction into the periosteum of the alveolar crest
Circular group Originates from within the free marginal and attached gingival coronal to the alveolar crest and encircles each tooth
Transseptal group Originates from interproximal cementum coronal to the alveolar crest and courses mesially and distally in the
interdental area into the cementum of adjacent teeth
SECONDARY GROUPS
Periosteogingival group Originates from the periosteum of the lateral aspect of the alveolar process and spreads into the attached gingiva
Interpapillary group Originates from within the interdental gingiva and follows an orofacial course
Transgingival group Originates within the attached gingiva intertwining along the dental arch between and around the teeth
Intercircular group Originates from cementum on the distal surface of a tooth spreading buccally and lingually around adjacent
tooth and inserting on the mesial cementum of the next tooth
Intergingival group Originates within attached gingiva immediately subjacent to epithelial basement membrane and courses mesio-
distally
Semicircular group Originates from cementum of the mesial surface of a tooth and courses distally and inserts on the cementum of
the distal surface of the same tooth
These collagen fiber groups provide support to gingiva,

attach gingiva to bone, anchor tooth to bone, protect peri-
odontal ligament, maintain contour and position of free
marginal gingiva, maintain relationships of adjacent teeth,
protect interproximal bone, secure alignment of the teeth
in the arch, and stabilize teeth in the arch.
1. Periodontal ligament
2. Alveolar process
B. CELLULAR ELEMENTS 3. Supraperiosteal
The major cellular elements in the gingival connective blood vessel
tissue include fibroblasts, macrophages, mast cells, poly-
morphonuclear leukocytes and plasma cells, and cells
that make up vascular channels and nerves. Adipose cells
and eosinophils, although scarce, are also present. Dur-
ing inflammation the fibrous component of gingiva is
replaced by the inflammatory cells such as neutrophils,
lymphocytes, and plasma cells. The predominant cell
of the gingival connective tissue is fibroblasts. They are
mesenchymal in origin and are responsible for the devel-
opment, remodeling, and repair of gingiva. These cells
synthesize collagen and elastic fibers and the ground
substance in which they are embedded. They phagocy-
tose collagen and also release the collagenase enzyme to
2
regulate collagen degradation.
3
C. VASCULAR ELEMENTS
a. Blood supply. The gingiva is supplied by blood vessels
in the periodontal ligament, the crest of the alveolar
process, and supraperiosteal blood vessels (Fig. 1.8). FIGURE 1.8 Blood supply of gingiva.
b. Lymphatics. The gingival tissues are supplied with propria found under it. Similarly, the loose connective tis-
lymphatic vessels that drain principally to submaxillary sue that supports the nonkeratinizing lining epithelium
lymph nodes. is largely responsible for the absence of keratinization in
c. Nerves. Branches of the trigeminal nerve provide this epithelium.
sensory and proprioceptive functions. In addition, If a connective tissue graft is taken from the mastica-
autonomic nerve endings are associated with the tory mucosa of the hard palate and is transplanted to
vasculature. a region which lacks an adequate covering of keratin-
izing mucosa, it will induce the overlying growing epi-
CONNECTIVE TISSUE-EPITHELIAL INTERACTIONS thelium to keratinize, even if the epithelium originates
The interaction of connective tissues and adjacent from an adjacent, nonkeratinized mucosal surface.
epithelia has a significant effect on epithelial tissue This interaction helps clinically in surgical procedures
differentiation. The stratified squamous epithelium of which are used to create a band of keratinized tissue
masticatory mucosa is maintained by the dense lamina where it is inadequate.
KEY POINTS
• The tissues that surround and support the teeth are as • Nonkeratinocytes include the following:
follows: 1. Melanocytes
1. Gingiva 2. Langerhans cells
2. Periodontal ligament 3. Merkel cells
3. Cementum 4. Inflammatory cells
4. Alveolar process • Melanocytes are pigment-synthesizing cells and are
• The color of gingiva is "coral pink"; normal racial pig- responsible for the melanin pigmentation occasionally
mentation makes the gingiva appear darker. seen on the gingiva.
• It varies according to the degree of vascularity, epithelial • Langerhans cells are dendritic cells located among kera-
keratinization, and pigmentation. tinocytes at suprabasal levels containing large granules
• Gingiva is demarcated clinically into the following: called Birbeck granules.
1. Marginal gingiva (free or unattached) • The gingival epithelium is subdivided into three sec-
2. Attached gingiva tions:
3. Interdental gingiva (papillary) 1. The oral epithelium (OE)
• The gingival groove is an indentation that parallels the 2. The sulcular epithelium (SE)
oral or vestibular surface of the gingival margin at a level 3. The junctional epithelium (JE)
corresponding to the level of the CEJ. • Oral epithelium is divided into the following layers:
• In 40% of adults, the surface texture of attached gingiva l. Basal cell layer (stratum basale or stratum germinati-
shows stippling (orange peel appearance). vum)
• Usually, the facial attached gingiva is widest in the area 2. Prickle cell layer (stratum spinosum)
of upper and lower incisors (3.5-4.5 mm in the maxilla 3. Granular cell layer (stratum granulosum)
and 3.3-3.9 mm in the mandible), and narrowest in the 4. Keratinized cell layer (stratum corneum)
posterior segments (1.9 mm in maxillary and 1.8 mm in • The basal cell layer represents the germinative layer.
mandibular first molars). On the lingual aspect of the • The basal lamina (basement membrane) under the elec-
mandible, it is narrow in the incisor region and wide in tron microscope reveals an electron-dense layer, the
the molar region. lamina densa (LD) (in contact with the connective tissue
• Functions of the attached gingiva are as follows: compartment), and an electron-lucent layer, the lamina
1. It braces the marginal gingiva. lucida (LL) (in contact with the epithelial cells).
2. It allows for proper deflection of food. • The sulcular epithelium is the stratified, squamous, non-
3. It provides room for proper placement of the tooth- keratinized epithelim which lines the gingival sulcus.
brush. • Junctional epithelium is a stratified squamous nonkera-
4. It has esthetic value. tinizing epithelium that surrounds the tooth like a collar
5. It is critical for overall maintenance of gingival health. with a cross-section resembling a thin wedge.
KEY POINTS (cont'd)
• The junctional epithelium tapers off in the apical direc- 1. Principal fibers
tion, and it consists of 15-30 cell layers coronally and - Dentogingival
only 1-3 cell layers at its apical termination. The length - Alveologingival
of the junctional epithelium ranges from 0.25 to 1.35 mm. - Dentoperiosteal
• The junctional epithelium has two basal laminas, one - Circular
that faces the tooth (internal basal lamina) and one that - Transseptal
faces the connective tissue (external basal lamina).
2. Secondary fibers
• The term "epithelial attachment" refers to the attachment
- Periosteogingival
apparatus, i.e., the internal basal lamina and hemides-
- Interpapillary
mosomes, that connects the junctional epithelium to the
- Transgingival
tooth surface.
- Intercircular
• The junctional epithelium is more permeable than the
- Intergingival
oral or sulcular epithelium due to wide intercellular
- Semicircular
spaces.
• In the absence of clinical signs of inflammation, • The gingival blood supply originates from blood vessels
approximately 30,000 PMNs migrate per minute through in the periodontal ligament, the marrow spaces of the
the junctional epithelia of all human teeth into the oral alveolar process, and supraperiosteal blood vessels.
cavity.
QUESTIONS Suggested readings

1. Hassel T. Tissues and cells of the periodontium. Periodontology 2000
1. Describe the ultrastructure of junctional epithelium. 1993;3:9-23.
2. Enumerate the blood supply of gingiva. 2. Lindhe J, Lang N, Karring T. Clinical Periodontology and Implant
3. Write a short note on gingival fibers. Dentistry. 5th ed. Copenhagen: Blackwell Munksgaard; 2008.
3. Newman MG, Takei H, Klokkevold PR, Carranza FA. Clinical
4. Describe the age-related changes in gingiva.
Periodontology. 10th ed. Philadelphia: Saunders; 2006.
5. Write a short note on "col." 4. Page RC, Schroder HE. Periodontal Diseases. 2nd ed. New York: Lea
6. Enumerate the functions of gingival fibers. & Febiger; 1990.
7. Enumerate the differences between attached gingiva 5. Schroder HE, Listgarten MA. The gingival tissues: the architecture
and alveolar mucosa. of periodontal protection. Periodontology 2000 1997;13:91-120.
8. Write a short note on the development of gingival
sulcus.
CHAPTER
2
Periodontal Ligament
The periodontal ligament occupies the space between maintains a constant soft tissue space between the mineral-
the cementum and the alveolar bone, thereby providing a ized fronts of the root cementum and the alveolar bone that
functional and dynamic link between the two structures. It is referred to as the periodontal ligament space.
ORIGIN AND DEVELOPMENT OF THE for physiologic movement of tooth is in the middle of
PERIODONTAL LIGAMENT the root. So, when the tooth moves during a function,
the space available for development of periodontal
Embryologically, periodontal ligament is derived from ligament space is less in the middle third, and so it is
the dental follicle. very thin. In multirooted teeth, the axis of rotation is
From the cervical loop of the dental organ the internal located in the bone between the roots. In compliance
and external enamel epithelia proliferate to form Her- with the mesial teeth migration, the periodontal
twig epithelial root sheath. As the growth changes take ligament is thinner on the mesial root surface than on
place, the root sheath stretches and fragments to form the the distal surface.
epithelial cell rests of Malassez. During eruption of teeth,
the cells and the fibers of the dental follicle, which will
form the future periodontal ligament, orient themselves
Formative Cells
initially, parallel to the long axis of the root. The various formative cells are given in Table 2.1.
• Fibroblasts
• Fibroblasts are the most abundant and active cells.
FEATURES OF PERIODONTAL LIGAMENT • They are stellate in shape with numerous cytoplasmic
projections. Cell-to-cell communication is through
1. Periodontal ligament occupies the periodontal space, gap junctions.
which is between the cementum and alveolar bone • Functions
proper. This extends coronally to the most apical part - Fibroblasts help in the production of collagen,
of connective tissue of gingiva. elastin, and ground substance.
2. Periodontal ligament space can be seen in the radiograph - They help in homeostasis and phagocytosis of old
as a radiolucent area or line between the lamina dura collagen fibers and degrade them.
and the root surface. - Myofibroblasts help in tooth eruption.
3. Width of periodontal ligament: Width varies in different • Cementoblasts
individuals, at different age in the same individual, and • Single layer along the cemental surface of
with different locations of the same tooth, location periodontal ligament
on the root, functions, and age. It ranges from 0.15 to • Separated from cementum by cementoid tissue
0.38 mm, the average being 0.21 mm. • Cuboidal in shape
4. Shape of periodontal ligament: Periodontal ligament • Usually closely packed, but due to gaps in certain
is hourglass in shape, being wider at both ends and areas, the principal fibers pass through them and get
narrower in the middle. Reason for this is that fulcrum embedded into the cementum as Sharpey fibers (Fig. 2.1)
C H A PT ER 2 PER IO D O N TA L LIG A M EN T 13
TABLE 2.1 Structural Components of Periodontal Ligament • Under light microscope, the surface of alveolar
Extracellular Connective tissue
bone shows resorption concavities called Howship
Cellular components components components lacunae in which lie the osteoclasts.
• Osteoclasts lying adjacent to the bone have a
Synthesizing cells Fibers Blood vessels
Fibroblasts Collagen Nerves
striated appearance called brush border or ruffled
Cementoblasts Principal group Lymphatics border.
Osteoblasts Secondary group • Underlying cytoplasm is devoid of organelles and
Resorptive cells Elastic is called clear zone or annular zone.
Fibroblasts Oxytalan • Cementoclasts
Cementoclasts Elaunin
Osteoclasts Ground substance
• Cementoclasts are cementum-resorbing cells.
Epithelial cells Protein • They undergo resorption only during pathology
Cell rests of Polysaccharides unlike bone and fibers.
Malassez Glycosaminoglycans • During resorption, these are multinucleated giant
Progenitor cells Proteoglycans cells.
Undifferentiated Glycoproteins,
mesenchymal cells especially fibronectin
Defense cells
Mast cells
Macrophages
Epithelial Cells
• These are found close to cementum throughout the
periodontal ligament mostly seen in the apical and
• Osteoblasts cervical regions. They diminish in number with age
• Present on the alveolar bone side of periodontal by degenerating and disappearing or by undergoing
ligament calcification to become cementicles.
• Help in formation of bone • As soon as root dentinogenesis begins, the Hertwig
• Cuboidal in shape epithelial root sheath loses its continuity and breaks
• Separated from mineralized bone by osteoid tissue into small islands or epithelial cell rests.
• Provide gap for principal fibers. • These islands persist in periodontal ligament and are
called epithelial cell rests of Malassez.
• Epithelial cells are cuboidal in shape and are arranged
Resorptive Cells in clusters called rests.
• Fibroblasts: Also act as resorptive cells, showing a dual • They do not have any function, but during inflammation,
role. undergo mitosis to give rise to cysts, especially
• Osteoclasts periapical cysts.
• Osteoclasts are bone-resorption cells.
• They are larger than osteoblasts with multiple
nuclei. Progenitor Cells
These are cellular entities of mesenchymal origin,
which are capable of differentiating into formative cells
(viz., cementoblasts, osteoblasts, and fibroblasts) and
resorptive cells (viz., osteoclasts).
The presence of these progenitor cells in the periodon-
tal ligament gives it the potential to provide cells dur-
ing the regenerative and reparative phases of healing
following periodontal disease. However, due to their
slower migratory potential, these cells take a longer time
to repopulate the root surfaces to form new cementum
and fibers.
Other Connective Tissue Cells

• Mast cells
• Mast cells are oval/round in shape.
FIGURE 2.1 Sharpey fibers. • They contain cytoplasmic granules.
• Granules contain Transseptal Fibers

- Mediators of inflammation such as histamine and These fibers are present between the cementum of
serotonin adjacent teeth just apical to the area where the gingiva
- Anticoagulants such as heparin attaches to the tooth.
• When stimulated, they degranulate, disseminating
their granular contents into the surrounding FUNCTIONS
connective tissue. They maintain the teeth in the arch.
• Macrophages
• Situated near blood vessels Alveolar Crest Fibers
• Phagocytic cells Alveolar crest fibers extend obliquely beneath the junc-
• Derived from blood monocytes tional epithelium from the cementum to the alveolar crest.
• Synthesize and release
- Interferon (antiviral) FUNCTIONS
- Prostaglandins (chemical mediator) They secure teeth in the socket. They resist lateral forc-
- Growth factors of fibroblasts es applied to the tooth.
• Functions
- Phagocytosis of dead cells in periodontal ligament Horizontal Fibers
and microbes Horizontal fibers extend from cementum to the alveo-
- Secretion of growth factor for fibroblasts. lar bone at right angles to the long axis of the tooth.
The periodontal ligament fibers are mainly composed
of collagen fibers. Collagen is secreted by fibroblasts, FUNCTIONS
chondroblasts, osteoblasts, and odontoblasts. The fibers They prevent lateral tooth movement.
are made up of collagen macromolecules called tropo-
collagen. Type I collagen is predominant and type III is Oblique Fibers
found to some extent. The collagen fibers are arranged Oblique fibers are the most numerous fibers in the peri-
as principal fiber bundle and secondary fibers. The other odontal ligament. They extend from cementum obliquely
fibers present are the elastic fibers. to the bone in a coronal direction.
As these fibers are found in abundance, they are be-
lieved to be responsible for absorbing the chewing forces.
Principal Fibers
FUNCTIONS
The periodontal ligament fibers are categorized accord-
They resist apically directed masticatory forces.
ing to their orientation to the tooth as transseptal fibers,
alveolar crest fibers, horizontal fibers, oblique fibers, api- Apical Fibers
cal fibers, and interradicular fibers (Fig. 2.2).
Apical fibers radiate from cementum in a rather ir-
regular manner to the bone at the apical region of the
socket.
FUNCTIONS
They prevent tooth tipping, resist forces of luxation,
and protect blood, lymph, and nerve supply.
Interradicular Fibers
Interradicular fibers fan out in the furcation areas of
multirooted teeth from the cementum.
Horizontal group / ~
lnterradicular
group
I I ~ " FUNCTIONS
They resist tipping of tooth, and forces of luxation and
Oblique group • r a ~~ rotation.
Elastic Fibers
Mature elastic fibers are not found in the periodontal
ligament. Two immature forms of this tissue, the oxytalan
FIGURE 2.2 Principal fibers of the periodontal ligament. and the elaunin fibers, are present. They form a meshwork
C H A PT ER 2 PER IO D O N TA L LIG A M EN T 15
extending from cementum to bone and sheathing the col- • Resistance to impact of occlusal forces (shock
lagen fiber bundles. absorption).
To explain shock absorption, three theories have been
Secondary Fibers put forward:
They are located between and among the principal 1. The tensional theory: This theory describes principal
fibers. These are nondirectional and randomly oriented fibers as the major factor responsible for supporting
collagen bundles of unknown function. They traverse the tooth and transmitting forces to the underlying bone.
periodontal ligament space coronoapically. When force is applied to the crown, the principal
fibers unfold and straighten and transmit force to the
underling bone. The bone undergoes elastic deformity
Ground Substance till the limit is reached and then the load is transmitted
The ground substance comprises glycoproteins such to the basal bone.
as fibronectin and laminin, and glycosaminoglycans 2. The viscoelastic theory: Tooth displacement is
such as hyaluronic acid. Both groups are composed of controlled by fluid movement and fibers play a
proteins and polysaccharides, but of different type and secondary role. When forces are applied on a tooth,
arrangement. The ground substance also contains high there is movement of the extracellular fluid from
water content. the periodontal ligament into the marrow spaces of
the bone through the cribriform plate. Once the tissue
fluids are depleted, the fiber bundles absorb the slack
Blood Supply and tighten leading to stenosis of the blood vessels.
Main blood supply is from superior and inferior alveo- There is ballooning of the vessels due to arterial back
lar arteries. The blood supply of periodontal ligament can pressure causing passage of blood ultrafiltrates into
be divided into three groups. tissues, replenishing them.
3. The thixotropic theory: This theory suggests that
• Apical group of arteries: from vessels supplying the
periodontal ligament has the rheologic behavior of a
pulp thixotropic gel (the property of becoming fluid when
• Alveolar group of arteries: also called perforating
shaken or stirred and then becoming semisolid again).
arteries
The shock absorption concept can also be explained by
• Gingival group of arteries: from gingival blood
this theory.
supply.
Transmission of Occlusal Forces to Bone
Nerve Supply Periodontal ligament transmits occlusal forces to the
bone differently for different types of forces. When axial
The superior and inferior alveolar nerves supply the force is applied to a tooth, the root has a tendency to dis-
periodontal ligament. place into the alveolus. When a horizontal force is applied,
tooth movement occurs in two phases: the first is within
Lymphatic Drainage the confines of the periodontal ligament and the second
produces a displacement of the facial and lingual bony
Networks of lymphatic vessels run parallel to the blood plates.
vessels providing lymph drainage and drain into the re- The apical portion of the tooth moves in a direction
gional lymph nodes, particularly the submaxillary group. opposite to the coronal portion. In sites of tension, the
principal fiber bundles become taut rather than wavy.
In sites of pressure, they become compressed, displacing
FUNCTIONS OF PERIODONTAL
the tooth, and, correspondingly, distorting the bone that
LIGAMENT
exists in the direction of root movement.
In single-rooted teeth, the axis of rotation is located
Physical Functions between the apical and middle third of the root. In mul-
• Protection of the underlying vessels and nerves from tirooted teeth, the axis of rotation is located in the bone
injury by mechanical forces by providing a soft tissue between the roots.
casing
• Transmission of occlusal forces to the bone
Formative and Remodeling
• Attachment of teeth to the bone
• Maintenance of gingival tissues in their proper Cells of the periodontal ligament take part in the
relationship to the teeth formation and resorption of cementum and bone.
The periodontal ligament cells constantly undergo re- CLINICAL CONSIDERATIONS

modeling. Fibroblasts form the collagen fibers and the
mesenchymal cells differentiate into osteoblasts and ce- Response of Periodontal Ligament to Trauma
mentoblasts.
Periodontal tissue responds in various stages: (i) injury,
(ii) repair, and (iii) adaptive remodeling.
In cases of acute trauma to the tooth, e.g., accidentally
Nutritive and Sensory biting hard substances or accidental blow, periodontal
The periodontal ligament supplies nutrients to the tissue injury occurs. Nature attempts to repair the injury
bone and gingiva by way of blood vessels. It is also sup- and restore the periodontium. This can occur if the trauma
plied with abundant nerve fibers capable of transmitting is removed or if the tooth drifts away from them.
tactile, pain, and pressure sensations. Nerve bundles pass In case of chronic trauma, the periodontal ligament is
into the periodontal ligament from the periapical area and remodeled. The ligament is widened at the expense of the
through channels from the alveolar bone. The bundles bone, angular bone defects occur without pockets, and
divide into single myelinated fibers and end in one of the tooth becomes loose.
four types of neural termination: Orthodontic tooth movement occurs when there is
resorption and formation of both alveolar bone and peri-
1. Free endings - carry pain sensation odontal ligament. When the orthodontic forces are ap-
2. Ruffini-like mechanoreceptors plied, the compression of the periodontal ligament on the
3. Coiled Meissner corpuscles - mechanoreceptors pressure side results in bone resorption and on the tension
4. Spindle-like endings - pressure and vibration. side bone formation occurs.
KEY POINTS
• The periodontal ligament is a specialized connective • The periodontal ligament fibers are mainly composed
tissue that attaches a tooth to the jawbone. of collagen fibers.
• It is defined as a soft, specialized connective tissue situ- • Type I collagen is predominant and type III is found to
ated between the cementum covering the root of the some extent.
teeth and the bone forming the socket wall. • Oblique fibers are the most numerous fibers in the peri-
• Thickness ranges from 0.15 to 0.38 mm, the average be- odontal ligament.
ing 0.21 mm. • Main blood supply is from superior and inferior alveolar
• Periodontal ligament is hourglass in shape, being wider arteries.
at both ends and narrower in the middle. • The periodontal ligament supplies nutrients to the bone
• Fibroblasts are the most abundant and active cells. and gingiva by way of blood vessels.
• Principal fibers get embedded into the cementum as
Sharpey fibers.
QUESTIONS 2. Bhaskar SN. Orban's Oral Histology and Embryology. 11th ed. St. Louis:
Mosby; 2005.
3. Lindhe J. Clinical Periodontology and Implant Dentistry. V ed. Oxford:
1. Enumerate various cells of the periodontal ligament. Blackwell Munksgaard Publications; 2008.
2. Enumerate periodontal ligament fibers. 4. Newman MG, Takei H, Carranza FA. Clinical Periodontology. 10th ed.
3. State the functions of periodontal ligament. Philadelphia: Saunders; 2006.
4. Write a note on oxytalan fibers. 5. Ten Cate AR. Oral Histology, Development, Structure and Function.
V ed. St. Louis: Mosby; 1998.
5. Enumerate blood supply of periodontal ligament.
Suggested readings
1. Beertsen W, Mcculloch Christopher AG, Sodek J. The periodontal
ligament: a unique, multifunctional connective tissue. Periodontal
20001997;13:20-40.
CHAPTER
3
Cementum
Cementum is a mineralized avascular noninnervated tal ligament. It is derived from Latin word "caementum"
dental tissue that covers the anatomic root of human teeth. which means "quarried stone."
It forms the interface between root dentine and periodon-
Cementum was first demonstrated in 1835 by two COMPOSITION

pupils of Purkinje.
It resembles bone structurally but differs in several Cementum comprises 45-50% inorganic salts which
important functional aspects. It has no innervation, no are present in the form of hydroxyapatite crystals; the re-
direct blood supply, and no lymph drainage. maining matrix is made of collagen fibers and noncollag-
enous matrix protein. Type I collagen is the predominant
form and constitutes 90% of its organic components. It is
known to promote cell attachment, and also is a critical
PHYSICAL CHARACTERISTICS molecule for maintaining the integrity of both soft and
hard connective tissues, during development as well as
• Hardness: Hardness of cementum is less than dentin in repair.
but greater than bone.
• Color: Cementum is light yellow in color, distinguished • The noncollagenous components of the interfibrillar
from enamel due to its darker hue and luster. ground substance are proteoglycans, glycoproteins,
• Cementum is relatively brittle. and phosphoproteins.
• Permeability: Cementum is softer and more permeable • The following are the two apparently unique cementum
than dentin. molecules:
• Cementum-derived attachment protein: An adhesion
Permeability decreases with age. molecule that mediates the attachment of connective
In cellular cementum, the canaliculi of cemento- tissue cells
cytes in lacunae are continuous with dentinal tubules • Cementum-derived growth factor: Insulin-like
in some areas. growth factor.
• Thickness: Cementum deposition is a continuous The inorganic content of cementum is less than that of
process that proceeds at varying rates throughout bone (65%), enamel (97%), and dentine (70%). Cementum
life. has the highest fluoride content.
• At CEJ, its thickness is 20-50 µm; it increases at apex
and inter-radicular area to about 150-200 µm. Cellular Elements of Cementum
Thickness of cementum is more on the distal side than Cementoblasts
on the mesial side; this contributes to the physiologic They are present along the forming cementa! surface.
mesial drift. The earlier cementoblasts originate from ectomesenchymal
cells of dental follicle and the later ones from undifferenti-

ated mesenchymal cells of periodontal ligament. They are
responsible for producing the network of collagen fibrils
and a proteoglycan ground substance, and also participate
in mineralization of cementum.
Cementocytes
When cellular cementum is being formed, the cemento-
blasts become trapped in lacunae within their matrix and
are known as cementocytes. Unlike cementoblasts their
metabolic activity is low.
They have numerous cytoplasmic processes coursing
into canaliculi; hence, they are referred to as spider-like
cementocytes.
Cementoclasts
They are multinucleated giant cells which are indis-
tinguishable from osteoclasts. They are responsible for
the extensive root resorption that leads to primary tooth
exfoliation and localized cemental resorption in adult
FIGURE 3.1 Acellular cementum showing incremental lines running
dentitions. parallel to the long axis of the tooth.
FUNCTIONS OF CEMENTUM
It furnishes a medium for attachment of collagen fibers,

which binds the tooth to the alveolar bone.
Its continuous deposition also helps in achieving the
crown length lost due to attrition; thus, it is crucial for
maintaining occlusal relationship.
It also serves as a major reparative tissue for root sur-
faces, thereby maintaining integrity of the root surface.
CLASSIFICATION
Cementum can be classified as follows:

1. Depending on location
I
__,.
a. Radicular cementum: It refers to cementum that
covers the root; in humans, radicular cementum
accounts for the bulk of cementum.
b. Coronal cementum: It refers to cementum found
FIGURE 3.2 Cellular cementum showing cementocytes lying within
on enamel; in humans, it is thin and poorly lacunae.
developed.
2. Depending on cellularity
Their differences are depicted in Table 3.1.
a. Acellular/primary cementum (Fig. 3.1)
3. Depending on the presence or absence of fibrils
b. Cellular/ secondary cementum (Fig. 3.2).
a. Fibrillar cementum: It is the most common form
Both acellular and cellular cementum consist of a
and contains well-defined, densely packed collagen
calcified interfibrillar matrix and collagen fibers. The
fibrils in its matrix.
two sources of collagen fibers are as follows:
b. Afibrillar cementum: It lacks the dense array of
- Sharpey ( extrinsic) fibers are formed by the
collagen fibrils in its organic matrix.
fibroblasts and are embedded in cementum.
- Intrinsic fibers are produced by cementoblasts and A separate classification of cementum has been sum-
belong to the cementum matrix. marized by Schroeder and Page:
C H A PT ER 3 C EM EN T U M 19
TABLE 3.1 Summary of Differences Between Acellular and extending from pre-CEJ to the apical third of the root.
Cellular Cementum It appears to contain cellular remnants of Hertwig
Acellular cementum Cellular cementum epithelial root sheath. The clinical significance of
No cellular elements Lacunae and canaliculi containing
the layer is that it contains enamel-like protein
cementocytes and their processes (amelogenin) which helps in attachment of cementum
to dentine.
Rate of development is Rate of development is relatively
relatively slow fast
Forms during root Forms after root formation and in CEMENTOENAMEL JUNCTION
formation response to functional demands
Collagen fibers are more Collagen fibers are irregularly The cementoenamel junction follows the overlapping-
organized organized meeting-gap rule (OMG) .
The clinical importance of cementoenamel junction lies
in root scaling procedures.
1. Acellular afibrillar cementum: This is found exclusively • The relation between cementum and enamel at
on the enamel near the cementoenamel junction (CEJ). cervical region of teeth is variable. There are three
It consists of a mineralized matrix but contains neither types of CEJ (Figs 3.3-3.5) as per Hopewell Smith
collagen fibrils nor cells. The lack of collagen fibrils (1918).
indicates that it has no function in tooth attachment. It
is formed when cementoblasts comes in contact with In about 60% of teeth, cementum overlaps cervical
enamel in the developmental phase. end of enamel for a short distance. This occurs when the
2. Acellular extrinsic fiber cementum: This is confined enamel epithelium degenerates at its cervical termination,
to the coronal half of the root. It is composed of permitting connective tissue to come in direct contact with
extrinsic fiber system consisting of Sharpey fibers but the enamel surface (Fig. 3.3).
does not harbor cementocytes within lacunae. The • In approximately 30% of all teeth, the cementum
formation commences shortly after crown formation and enamel meet as a butt joint forming a distinct
is completed. delineation at the cervical margin (Fig. 3.4) and 10%
The matrix consists of short type I collagen fibers have a gap between the cementum and enamel,
that are oriented perpendicular to the root surface. exposing root which can lead to sensitivity at the site.
The fibers remain short till the tooth is about to This occurs when enamel epithelium in the cervical
reach the occlusal plane, and then they elongate portion of the root is delayed in its separation from
and become continuous with periodontal fibers. dentine (Fig. 3.5). It has a clinical importance in
The cementoblasts produce loosely packed collagen gingival recession since it is associated with increased
fibrils that form a meshwork surrounding the sensitivity because of the exposed dentin.
principal fiber of the ligament in a plane parallel to
cemental surface. These "indifferent" cemental fibrils
as well as the principal fibers are surrounded by a
proteoglycan ground substance also synthesized by
cementoblasts.
3. Cellular intrinsic fiber cementum: This does not
encase any Sharpey fiber; instead, its organic matrix
consists of intrinsic fibers which are synthesized by
cementoblasts and not POL fibroblasts. This cementum
exhibits lacunae with cementocytes. Also, it grows at
a faster rate than any other type and hence can repair
a resorptive defect in reasonable time.
4. Cellular mixed stratified cementum: The intrinsic
fibers predominate over Sharpey fibers. Cellular
mixed stratified cementum appears primarily in the
apical third of the roots, the apices, and furcation areas.
It harbors both intrinsic and extrinsic fibers within
calcified matrix that also houses viable cementocytes.
It increases in thickness throughout life.
5. Intermediate cementum (or) the hyaline layer of
Hopewell Smith: It is an ill-defined zone (10 µm) FIGURE 3.3 Cementum overlapping the enamel.
• According to scanning electron microscopy, its width

is 2-3 µm.
• With age, it has no effect as its width remains stable.
• CDJ is relatively smooth in permanent teeth while
scalloped in deciduous teeth.
• In decalcified and stained histologic sections cementum
stains more intensely than dentin.
• Dentin can be separated from cementum by a zone
known as intermediate cementum, which does not
show features of either cementum or dentin.
• CDJ represents areas where cells of Hertwig epithelial
root sheath become trapped in rapidly deposited
cementum or dentin.
Sharpey Fibers
• Sharpey fibers are the portions of principal fibers of the
PDL which are embedded in the root cementum and
FIGURE 3.4 End-to-end relationship of enamel and cementum. in alveolar bone proper.
• These constitute extrinsic fiber system of cementum
and are produced by fibroblasts in the PDL.
• Sharpey fibers in the primary acellular cementum are
mineralized fully; however, those in cellular cementum
and bone are mineralized only partially at their
periphery.
DEVELOPMENTAL AND ACQUIRED

ANOMALIES OF CEMENTUM
The following anomalies in cementogenesis may have

an impact on the susceptibility of teeth to periodontal
disease and affect the treatment:
• Enamel projections: They are seen in localized
areas in the furcation of mandibular molars during
development. If amelogenesis does not stop before
the root formation, enamel projection may form over
portion of a root which is normally covered by Hertwig
epithelial root sheath.
• Enamel pearls: Globules of enamel on the root surface
in the cervical region are referred to as enamel pearls.
FIGURE 3.5 Space between enamel and cementum with dentine
exposed.
They appear as a result of localized failure of Hertwig
epithelial root sheath to separate from dentine surface,
thereby allowing cementogenesis to proceed. Large
pearls may contain pulpal extensions.
• Hypercementosis (cementa! hyperplasia) (Fig. 3.6):
CEMENTODENTINAL JUNCTION It indicates a prominent thickening of cementum.
It may be localized or generalized. It is not possible
Cementodentinal junction (CDJ) is defined as termi-
to distinguish between physiologic thickening of
nal apical area of cementum where it joins the internal root
cementum that occurs with age and hypercementosis.
canal dentin.
It occurs as a generalized thickening of root cementum
• It is important clinically as during root canal treatment with a nodular enlargement at the apical one-third or
obturating material should end at CDJ. as spike-like excrescences due to fusion of cementicles
C H A PT ER 3 C EM EN T U M 21
antagonists, embedded, replanted, and transplanted teeth,

and periapical or periodontal disease.
Systemic cases may be due to deficiency of calcium,
vitamin D, and vitamin A, hypothyroidism, fibrous os-
teodystrophy, and Paget disease.
Cementum resorption is not continuous and may al-
ternate with periods of repair and deposition of new
cementum. The newly formed cementum is demarcated
from the root by a deep-staining irregular line known as
reversal line. During repair there could be formation of
acellular or cellular cementum or alternate formation
of both. Cementum repair requires the presence of viable
connective tissue. If epithelium proliferates into an area
of resorption, repair will not take place. If during repair
FIGURE 3.6 Hypercementosis. the former outline of the root surface is reestablished,
it is called anatomic repair. If only thin layer of cementum
is deposited on the surface of deep resorption, it is called
functional repair.
to the roots or due to calcification of periodontal
ligament fibers which are inserted into cementum.
Their etiology is attributed to excessive orthodontic
CEMENTAL TEARS
or occlusal forces.
It could be defined as the detachment of a fragment of
Localized hypercementosis is seen in teeth without
cementum from root surface, owing to an acute injury or
antagonists to keep pace with active eruption or due
from intermittent episodes of sustained pressure.
to low-grade periapical irritation as a result of pulpal
disease. It is believed to be a compensatory mechanism • It follows one of the incremental lines.
to counteract the destruction of fibrous attachment of • Tears have been observed within unexposed cementum
the tooth. and exposed cementum within the pocket.
Generalized hypercementosis may be hereditary or • The cementa! tears can remain partially attached or
observed in patients with Paget disease. completely detached from the root surface.
• Cementicles: These are globular masses of cementum
arranged in concentric lamella that may be found either
lying free in PDL or adhering to the root surface. They
Ankylosis
may develop from Fusion of cementum and alveolar bone with oblit-
• Calcified epithelial cell rests of Malassez eration of periodontal ligament is known as ankylosis.
• Small spicules of cementum or alveolar bone that It occurs in teeth with cementa! resorption which may
are traumatically displaced into PDL represent a form of abnormal repair. Ankylosis may al-
• Calcified Sharpey fibers so develop following chronic periapical inflammation,
• Calcified thrombosed vessels in PDL. tooth replantation, and occlusal trauma around embed-
ded teeth.
CEMENTUM RESORPTION AND REPAIR Clinical Significance

• Ankylosed teeth are difficult to extract.
Cementum of erupted as well as of unerupted teeth • Ankylosed teeth lack physiologic mobility, which is a
is subject to resorption. It may be of microscopic pro- diagnostic sign of ankylotic resorption.
portion or extensive to be observed in a radiograph. • Ankylosed teeth show special metallic percussion
Cementum resorption appears microscopically as bay- sound.
like concavities in the root surface, which are lined by • Affected tooth is in infraocclusion.
multinucleated giant cells and large mononuclear mac- • Affected tooth exhibit loss of proprioception due to
rophages. Cementa! resorption may be due to local or deletion of receptors in PDL.
systemic causes. • Due to ankylosis, physiologic drifting and eruption
Among the local causes are trauma from occlusion, cannot take place.
active orthodontic movement, pressure from malaligned • Radiographically ankylosed teeth exhibit resorption
erupting teeth, cysts and tumors, teeth without functional lacunae filled with bone and PDL space missing.
KEY POINTS
• Cementum is a mineralized avascular dental tissue that 1. Acellular afibrillar cementum

covers the anatomic root of teeth. 2. Acellular extrinsic fiber cementum
• It comprises 45-50% inorganic salts which are present in 3. Cellular intrinsic fiber cementum
the form of hydroxyapatite crystals and the remaining 4. Cellular mixed stratified cementum.
matrix is made of collagen fibers and noncollagenous • In about 60% of teeth, cementum overlaps cervical end
matrix protein. of enamel for a short distance.
• Cementum has the highest fluoride content. • Fusion of cementum and alveolar bone with obliteration
• Sharpey (extrinsic) fibers are formed by the fibroblasts of periodontal ligament is known as ankylosis.
and are embedded in cementum. • Acellular cementum forms during root formation.
• A separate classification of cementum has been sum-
marized by Schroeder and Page:

1. Bhaskar SN. Orban's Oral Histology and Embryology. 11th ed. St. Louis:
1. Describe the structure of cementum and clinical Mosby;2005.
significance of cementoenamel junction (CEJ). 2. Bosshardt DD, Selvig KA. Dental cementum: the dynamic tissue
2. Enumerate the functions of cementum. covering of the root. Periodontal 2000 1997;13:41-75.
3. Hassel T. Tissues and cells of the periodontium. Periodontal 2000
3. Enumerate various types of cementoenamel junction
1993;3:9-23.
(CEJ). 4. Newman T, Carranza FA. Clinical Periodontology. 10th ed. Saunders:
4. Enumerate the causes of hypercementosis. St. Louis; 2006.
5. State the cemental changes during periodontal diseases. 5. Ten Cate AR. Oral Histologi;, Development, Structure and Function. 3rd
6. Classify cementum. ed. Mosby: St. Louis; 1989.
7. Define ankylosis.
CHAPTER
4
Alveolar Bone
The portion of the maxilla and the mandible that forms apparatus which helps in distributing the forces such as
and supports the tooth socket is called the alveolar process. masticatory forces (Fig. 4.1). It forms with the development
Alveolar bone in conjunction with the cementum and and eruption of the teeth and it gradually regresses once
periodontal ligament constitutes the tooth attachment the tooth is lost.
PARTS OF ALVEOLAR PROCESS • The spongy bone fills the space between the facial and
the lingual cortical plates and mesially and distally
The alveolar process, depending on the functional ad- between the alveolar bone proper. The facial and
aptation, consists of the parts mentioned in the following the lingual cortical plates meet at the alveolar crest
subsections. 1.5-2 mm apical to the cementoenamel junction.
Alveolar Bone Proper

Alveolar bone proper is a thin layer of bone lining the HISTOLOGY OF ALVEOLAR BONE
roots of the teeth and provides attachment to periodontal
ligament fibers. It is also referred to as the bundle bone Mature bones, whether compact (Fig. 4.3) or cancellous
because the bundles of the periodontal ligament fibers (Fig. 4.4), consist of layers or lamellae. Three different
continue into the bone as Sharpey fibers (Fig. 4.2). types of lamellae are present:
Radiographically, this bundle bone appears as a thin
radiopaque line surrounding the roots of teeth, called the 1. Circumferential lamellae: These form the outer casing
lamina dura. of the adult bone.
The alveolar bone is perforated with numerous open- 2. Concentric lamellae: These form the basic unit of bone,
ings by branches of intra-alveolar nerves and blood ves- the osteon, and also make up the bulk of the compact
sels and is therefore called the cribriform plate. It is also bone. The osteons are arranged parallel to the long
known as lamellated bone, as lamellae structure with axis of the bone with the haversian canal as its center.
haversian canal system is present. The most coronal as- Adjacent haversian canals are interconnected by the
pect of the alveolar bone is the alveolar crest which is horizontal Volkmann canals.
parallel to the cementoenamel junction (CEJ) and is situ- 3. Interstitial lamellae: These lamellae are present between
ated about 1-2 mm apical to it. two adjacent concentric lamellae.
Supporting Alveolar Bone

Periosteum
Supporting alveolar bone supports the alveolar bone
Surrounding each compact bone is the periosteum,
proper. It consists of two parts:
a connective tissue membrane. The periosteum con-
• The cortical plates form the outer and inner plates of sists of two layers: an inner layer and an outer layer.
the alveolar process, made up of compact bone. The inner layer, called the cambium, is next to the bone
Gingiva ,?;."j
Cementum ,
FIGURE 4.3 Histologic section showing compact bone.
FIGURE 4.1 Normal periodontium.
FIGURE 4.2 Sharpey fibers. FIGURE 4.4 Cancellous bone with marrow spaces.
INTERDENTAL SEPTUM
The interdental septum consists of cancellous bone bor-

surface and consists of bone cells, their precursors that dered by the socket wall made up of cribriform plate approx-
have the potential to differentiate into osteoblasts. The imating facial and lingual cortical plates (Fig. 4.5). In case
outer layer contains collagen fibers, fibroblasts, and rich of narrow interdental space, the septum consists of only
blood supply. cribriform plate. Radiographically, the position of
the interdental septum helps in determining the root
proximity. The mesiodistal angulation of the crest of
Endosteum the interdental septum (Fig. 4.6) usually parallels a line
The inner surface of both compact and cancellous bones drawn between the CEJ of the adjacent teeth. The dis-
is called the endosteum and is made up of single bone cell tance between the crest of the alveolar bone and the CEJ
layer that separates the bone surface from the bone mar- in young adults varies between 0.75 and 1.49 mm. This
row within. The inner layer is osteogenic and the outer distance increases with age to an average of 2.81 mm.
layer is fibrous in nature. The shape and dimensions of the interdental septum are
CH A PT ER 4 A LV EO LA R BO N E 25
FIGURE 4. 7 Histologic section showing marrow spaces.
inactive type of marrow. In adults, the yellow marrow is

found in the jaws, and the red marrow is found in the ribs,
FIGURE 4.5 Interradicular septum. sternum, vertebrae, skull, and humerus. Common sites of
yellow marrow in the jaws are the maxillary tuberosity,
maxillary and mandibular molar and premolar areas, the
mandibular symphysis, and the ramus area.
COMPOSITION OF ALVEOLAR BONE

Bone consists of 65% inorganic and 35% organic sub-
stances (Fig. 4.8).
Cells of the Alveolar Bone

Three types of cells are found in the alveolar bone. All
cell names start with "osteo" meaning "bone" in Greek.
The bone-forming cells are called the osteoblasts.

They are derived from the bone marrow and are
FIGURE 4.6 Alveolar crest.
governed by the size and convexity of the crowns of the ORGANIC

two approximating teeth, as well as by the position of INORGANIC
Type I collagen - 90%,
noncollagenous -
the teeth in the jaw and their degree of eruption. (hydroxy apatite) osteocalcin, osteonectin,
Calcium and phosphate bone morphogenetic
along with carboxyl, proteins, and
citrate, and traces of proteoglycans.
BONE MARROW sodium, magnesium, Osteopontin and bone
fluorine sialoprotein are cell
adhesion proteins
In embryos and newborns, all the bones are occupied
by red hematopoietic marrow (Fig. 4.7). It gradually un-
dergoes physiologic changes and is replaced by yellow FIGURE 4.8 Composition of alveolar bone.
mononucleated. They lay down a matrix called osteoid

that consists of bone collagen and other proteins. Their
function is to regulate calcium and mineral deposition.
They are present on the new bone surface.
Once the osteoblasts have completed filling the bone

cavity, they become flat and reach the bone surface and
are called the lining cells. Their function is then to regu-
late the passage of calcium in and out of the bone and to
stimulate the production of osteoclasts in the presence of
certain hormones.
FIGURE 4.9 Osteoclast in histologic section.
in lingual version, the margins are more coronally placed,

with the margins being blunt, rounded, and horizontal.
The cells within the bone matrix are called the osteo- FENESTRATION AND DEHISCENCE
cytes. These are derived from the osteoblasts.
As the osteoblasts are secreting bone matrix, a few of Isolated areas where the root is devoid of the overly-
them get entrapped in the matrix and become osteocytes. ing bone and is covered only by the soft tissue are called
The space in the matrix occupied by the osteocyte is called fenestration.
the osteocytic lacuna. Once the cells become osteocytes, Here, the marginal bone will be intact (Fig. 4.10).
they gradually lose their matrix-synthesizing property When the denuded area of the root involves the mar-
and get reduced in size. The radiating osteocytic processes ginal bone also, it is called dehiscence. Approximately
are housed by enclosed canaliculi of the lacunae, thus 20% of the teeth are seen to have these defects occurring
maintaining contact with adjacent osteocytes and the commonly bilaterally, on the facial aspect of anterior teeth.
osteoblasts or the lining cells. These defects occur on approximately 20% of the teeth;
they are more commonly seen on facial bone and anterior
teeth, and are frequently bilateral.
The causes of these defects are still not clear. The rea-
sons could be prominent root contours, tooth malposition,
and labial protrusion of the root combined with a thin
Osteoclasts (Fig. 4.9) are large cells that dissolve the bony plate.
bone. They originate from the bone marrow. They are
formed from two or more cells that fuse together, so the
osteoclasts usually have more than one nucleus. They are
found on the surface of the bone mineral next to the dis-
solving bone. They occupy shallow, hollowed-out depres-
sions on the bone surface created by themselves called the
Howship lacunae.
OSSEOUS TOPOGRAPHY
The bony contour conforms to the root prominence. On

teeth in labial version, the margins of the alveolar bone are
located apically when compared with teeth with normal
alignment. The bone margins are knife edged. On teeth FIGURE 4.10 Fenestration and dehiscence.
CH A PT ER 4 A LV EO LA R BO N E 27
REMODELING OF ALVEOLAR BONE + Blood calcium

~homeostasis
Remodeling of bone takes place due to continuous
bone formation and resorption that helps the bone to
l
adapt itself to mechanical loads. Homeostasis is brought
about by the balance in resorption and formation due to
which old bone is replaced by new bone. Because of this,
there is no change in the morphology of the bone and also
timulanon or~ i "'°"'''"
the mechanical integrity of the bone is maintained. This timulnnon of osteoblasts ~ of IL-6 -+ Stimulation of osteoclast
process is called remodeling.
The appearance of the osteoclasts on the quiescent bone
marks the beginning of the remodeling process.
Bone formation
FIGURE 4.11
-
Mechanism of bone resorption and formation.
• They attach to the bone tissue matrix and form a
ruffled border at the bone/ osteoclast interface that is
completely surrounded by a "sealing zone." Thus, the
osteoclast creates an isolated microenvironment.
bone. Bone remodeling is regulated by certain hormones
• Subsequently the osteoclast acidifies the microenviron-
and local factors.
ment and dissolves the organic and inorganic matrices
Bone contains 99% of body's calcium, forming the ma-
of the bone.
jor source of calcium when blood calcium levels decrease.
• Once the resorption stops, osteoblasts that are derived
Parathyroid hormone (PTH) is essentially the major hor-
from bone marrow, periosteum, and soft tissues appear
mone that mediates and regulates calcium homeostasis.
on the surface to deposit osteoid that undergoes
It brings about homeostasis by stimulating the release
mineralization to form new bone.
of calcium from the skeleton. The PTH stimulates bone
• Some of the osteoblasts are encapsulated in the osteoid
resorption by stimulating the ostoblastic cells to secrete
matrix and differentiate to osteocytes. Remaining
paracrine substances such as interleukin-1 which brings
osteoblasts continue to synthesize bone until they
about osteoclastogenesis.
eventually stop and transform to quiescent lining
Recently, it has been demonstrated that the cyto-
cells that completely cover the newly formed bone
kine interleukin-6 (IL-6), which potently induces os-
surface.
teoclastogenesis, is produced by osteoblastic cells in
A few osteoblasts get encapsulated in the bone matrix response to PTH. Thus, IL-6 may play a permissive
and differentiate to form osteocytes. A few others continue role in PTH-induced bone resorption and plays a role
synthesizing bone and, once their function is over, are in coupling PTH-induced bone resorption and forma-
transformed into lining cells that cover the newly formed tion (Fig. 4.11).
KEY POINTS
• The alveolar process is the thickened ridge of bone • The inner surface of both compact and cancellous bones
that contains the tooth sockets on bones that bear is covered by endosteum, a single layer of bone cells
teeth. that separates the bone surface from the bone marrow
• Alveolar bone proper is a thin layer of bone lining the within.
roots of the teeth and provides attachment to principal • The distance between the crest of the alveolar bone and
fibers of periodontal ligament. the cementoenamel junction in young adults varies be-
• Radiographically, this bundle bone appears as a thin tween 0.75 and 1.49 mm.
radiopaque line surrounding the roots of teeth, then • Bone consists of 65% inorganic and 35% organic sub-
called the lamina dura. stances.
• The alveolar bone is perforated with numerous openings • Osteoclasts occupy shallow, hollowed-out depressions
by branches of intra-alveolar nerves and blood vessels on the bone surface created by themselves called the
and is therefore called the cribriform plate. Howship lacunae.
• Mature bones, whether compact or cancellous, consist • Isolated areas in which the root is denuded of bone and
of layers or lamellae. Three different types of lamellae is covered only by the periosteum and overlying gingiva
are present. are called fenestration.
KEY POINTS (cont'd)
• When the denuded area includes the marginal bone, the of calcium homeostasis, producing several distinct and
defect is called dehiscence. independent effects on the bone-remodeling process,
• Parathyroid hormone (PTH) functions as a major me- resulting in both bone formation (anabolic activity) and
diator of bone remodeling and as an essential regulator bone resorption (catabolic activity).
QUESTIONS 2. Lindhe J. Clinical Periodontology and Implant Dentistry. V ed. Oxford:

Blackwell Munksgaard Publications; 2008.
3. Newman MG, Takei H, Carranza FA. Clinical Periodontology. 10th ed.
1. Describe the structure and composition of alveolar bone. Philadelphia: Saunders; 2006.
2. Define lamina dura. 4. Saffar JL, Lasfargues JJ, Cherruau M. Alveolar bone and the
3. Define fenestration and dehiscence. alveolar process: the socket that is never stable. Periodontal 2000
4. Define bundle bone. 1997;13:76-90.
5. Ten Cate AR. Oral Histology, Development, Structure and Function. 5th
5. Define remodeling of alveolar bone.
ed. St. Louis: Mosby; 1998.
6. Define periosteum and endosteum.
Suggested readings
1. Grant DA, Sternn IB, Listgarten MA. Periodontics. 6th ed. St. Louis:
Mosby; 1998.
CHAPTER
5
Age--related Changes in
the Periodontium
Aging is slowing of natural function, a disintegration changes may prepare the way for a pathologic state, this
of the balanced control and organization that characterize later hypothesis cannot be correlated with epidemiologic
the young adult. It is important to recognize age-related data and the evidence is equivocal. Age-related changes
changes in periodontium, since these may affect func- affect the periodontal tissues mentioned in the following
tion. While the option has been stated that age-related sections.
VASCULATURE capable of regeneration. The rate of collagen synthesis

decreases with age in rats as measured by in vitro label-
Arteriosclerosis is a frequent finding in aging humans, ing technique. Also, it has been shown that the cells of
and may be seen in large vessels with muscular elements the periodontal ligament of aged mice do not renew as
in the vessel wall, vessel in the alveolar bone, and ves- rapidly as those of young animals.
sels in the periodontal ligament. The relationship of this
vascular pathologic condition to other changes in the peri-
odontium is inconclusive. The relative ischemia that arte-
TOOTH-PERIODONTIUM
riosclerosis may produce in periodontal tissues because
RELATIONSHIP
of the reduction in blood flow has been hypothesized as
predisposing these tissues to disease or provoking other
• There is loss of tooth substance due to attrition.
changes such as fibrosis, loss of cellularity, and focal cal-
• There is reduction in cuspal height and inclination due
cification. It may also reduce bone metabolism and may
to wear.
be correlated with slower or altered wound healing.
• Bone loss results in an increase in crown/ root ratio.
The reduced arterial flow may be related to changes
• Tooth wear tends to modify increase in crown/root
that have been observed elsewhere in the body and in
ratio.
experimental animals. For instance, the loss of ground
• Wear on proximal surfaces results in physiologic mesial
substance may be a result of the reduced supply of oxygen
drifting.
associated with diminished arterial flow. Also, basement
membranes have been reported to be thicker in aged per- Attrition of tooth substance on occlusal and incisor
sons and markedly distinct from the surrounding ground surfaces and at the contact points is a well-recognized
substance. characteristic of aging. Vertical dimension and arch con-
Several other changes are noted in periodontal tissues. tinuity are usually maintained in old age, since wear is
There is a decrease in connective tissue cellularity and an compensated for bone apposition on distal surfaces and
increase in number and coarseness of collagenous fibers. at the fundus of the sockets. Continuous apposition of
The number of synthesizing cells is significantly great- the cementum at the apex also helps to compensate for
er in younger animals and a greater number of cells are such wear.
GINGIVAL EPITHELIUM interfibrillar areas are reduced in size. There is a decrease

in the ratio of ground substance to collagen. The periodon-
Thinning and decreased keratinization of the gingival tal ligament shows degenerative hyaline changes and also
epithelium have been reported with age. The significance chondroid degeneration. Both the hyalinization and chon-
of these findings could mean an increase in epithelial droid degeneration may be
permeability to bacterial antigens, a decreased resistance • Casually related to or an accompaniment of a reduced
to functional trauma, or both, which might influence long- vascular supply
term periodontal outcomes. Some reports show migration • A response to injury
of the junctional epithelium from its position in healthy • An undetermined effect of aging.
individuals (i.e., on enamel) to a more apical position on
the root surface with accompanying gingival recession. Calcified bodies are common in the periodontal liga-
With increasing age, there is an increase in the width ment of elderly humans.
of the attached gingiva, a change that is attributed to the Two types of rounded calcospheroid-like bodies
eruptive movement of the teeth rather than to the intrinsic are demonstrable: small rounded calcospherites and
aging phenomenon. The migration of the junctional epi- larger, irregularly shaped calcifications. The calcosphe-
thelium to the root surface could be caused by the tooth rites appear to be formed in relation to fiber bundles.
erupting through the gingiva in an attempt to maintain They coalesce to form the larger rounded or irregularly
occlusal contact with its opposing tooth (passive eruption) shaped bodies. Occasionally, they increase in number
as a result of tooth surface loss from attrition. and appear to calcify a complete fiber bundle, leading
Aging also brings an increased prevalence of gingival to ankylosis.
recession. This finding appears to be largely due to cumula- Epithelial rests in the periodontal ligament show al-
tive environmental effect of vigorous tooth brushing rather tered forms of aggregation. Rest aggregates tend to con-
than due to inflammatory periodontal disease or aging. tain more cells with both proliferative and degenerative
morphology. The aggregates are frequently encircled by
a thickened basement membrane. Rather than being situ-
GINGIVAL CONNECTIVE TISSUE ated near the root surface (as in young persons), these
epithelial rests are found irregularly located in the peri-
The fibroblasts that make up the gingival connective odontal ligament, near the tooth, midway between the
tissue are heterogeneous with respect to their biochemical tooth and bone, and near the bone. While some rests may
traits. It may be that with increasing age, selective pres- degenerate, others may become calcified.
sures favor predominance of fibroblast subpopulations Also, changes include decreased numbers of fibroblasts
with the phenotypic expression. Tissue culture studies and a more irregular structure, paralleling the changes in
of gingival fibroblasts obtained from older individuals the gingival connective tissues. Other findings include de-
have revealed a reduction in the rate of proliferation, a creased organic matrix production and epithelial cell rests
decrease in the quantity and quality of proteoglycans, and and increased amounts of elastic fiber. Conflicting results
diminished protein and collagen production. have been reported for changes in the width of periodon-
Increasing age results in coarser and more dense gin- tal ligament in human and animal models. Although true
gival connective tissues. Qualitative and quantitative variation might exist, this finding probably reflects the func-
changes to collagen have been reported. These include an tional status of the teeth in the studies because the width
increased rate of conversion of soluble to insoluble colla- of the space will decrease if the tooth is unopposed (hypo-
gen, increased mechanical strength, and increased denatur- function) or will increase with excessive occlusal loading.
ing temperature. These results indicate increased collagen
stabilization caused by changes in the macromolecular
conformation. Not surprisingly, a greater collagen content CEMENTUM
has been found in the gingiva of older animals despite a
lower rate of collagen synthesis decreasing with age. An increase in cemental width is a common finding;
this increase may be 5-10 times with increasing age.
The increase in width is greater apically and lingually.
PERIODONTAL LIGAMENT This may be attributable to occlusal wear and eruption
of teeth, although it has also been noted in impacted
The principal fibers of the periodontal ligament are teeth. This finding is not surprising because deposition
thicker in aging humans than in younger individuals. continues after tooth eruption. Although cementum
The well-organized bundles are broad and wavy. The has limited capacity for remodeling, an accumulation
CH A PT ER 5 A G E-R ELATED CH A N G ES IN TH E PERIO DO N T IU M 31
of resorption bays explains the finding of increasing For supragingival plaque, no real qualitative differ-
surface irregularity. ences have been shown for plaque composition.
Indications exist that cemental deposition slows in old For subgingival plaque, one study has shown sub-
age. In addition, the attachment of cementum to dentin gingival flora similar to a normal flora, whereas anoth-
may be weakened. The frequent cemental tears seen in er study reported increased numbers of enteric rods
specimens of aging humans may be related to age-related and pseudomonads in older adults. Mombelli suggests
changes in the ground substance of cementum, to re- caution in the interpretation of this finding because of
duced vascular supply, or to thickened and less extensible increased oral carriage of these species among older
ligament fibers embedded in the cementum. Spurring of adults. It has been speculated that a shift occurs in the
cementum is sometimes the result of the fusion of calco- importance of certain periodontal pathogens with age,
spheroid bodies near cementum or due to the calcification specifically including an increased role for Porphyromo-
of epithelial rest aggregates. nas gingivalis and a decreased role for Actinobacillus ac-
tinomycetemcomitans.
However, differentiating true age effects from the
ALVEOLAR BONE changes in ecological determinants for periodontal bac-
teria will be difficult.
Little evidence of continued bone apposition is present
in senescence. In view of this, physiologic tooth migration
may be slowed or even halted in old age.
Specific to the periodontium are findings of a more
IMMUNE RESPONSES
irregular periodontal surface of bone and less regular
Age has been recognized as having much less effect
insertion of collagen fibers. Although age is a risk factor
in altering the host response than previously thought.
for the bone mass reductions in osteoporosis, it is not
Differences between young and older individuals can be
causative and therefore should be distinguished from
demonstrated for T and B cells, cytokines, and natural
physiologic aging processes. The healing rate of bone in
killer cells but not for polymorphonuclear cells and mac-
extraction sockets appears to be unaffected by increas-
rophage activity.
ing age. The success of osseointegrated dental implants,
McArthur concludes, "Measurement of indicators of
which relies on intact bone healing responses, does not
immune and inflammatory competency suggested that,
appear to be age related. However, balancing this view is
within the parameters tested, there was no evidence for
the recent observation that bone graft preparations (decal-
age-related changes in host defenses correlating with
cified freeze-dried bone) from donors more than 50 years
periodontitis in an elderly (65 to 75 years) group of indi-
old possessed significantly less osteogenic potential than
viduals, with and without disease."
graft material from younger donors. The possible signifi-
cance of this phenomenon on normal healing responses
needs to be investigated.
Osteoporosis has been reported in aging, particularly SUMMARY
in alveolar bone of postmenopausal women, since the
decrease in the trabeculation of alveolar bone sometimes Periodontal disease increases in prevalence and se-
seen radiographically is more often related to the loss of verity with increasing age. The increase may be caused
function. by the cumulative effect of the number of bursts of peri-
odontal destruction, deterioration in plaque removal
efficiency, or an increase in the number of teeth retained
BACTERIAL PLAQUE in old age and therefore affected by plaque-induced
disease.
Dentogingival plaque accumulation has been suggested Attention should be directed toward the decline in
to increase with age. This might be explained by the in- immune function with age.
crease in hard tissue surface area as a result of gingival Clinical studies have led the investigators to conclude
recession and the surface characteristics of the exposed that chronological aging, per se, does not inevitably
root surface as a substrate for plaque formation compared lead to attachment loss or decrease in alveolar bone
with enamel. Other studies have shown no difference in support.
plaque quantity with age. This contradiction might reflect Although many contradictions exist, a survey of the
the different age ranges of experimental groups as variable literature demonstrates that some age-related changes are
degrees of gingival recession and root surface exposure. evident in the periodontium and host response.
KEY POINTS
• The relative ischemia that arteriosclerosis may produce in • Qualitative and quantitative changes to collagen include
periodontal tissues with age causing a reduction in blood an increased rate of conversion of soluble to insoluble
flow has been hypothesized as predisposing these tissues collagen, increased mechanical strength, and increased
to disease or provoking other changes such as fibrosis, loss denaturing temperature.
of cellularity, and focal calcification. • The periodontal ligament shows degenerative hyaline
• There is a decrease in connective tissue cellularity and changes and also chondroid degeneration.
an increase in number and coarseness of collagenous • An increase in cemental width is a common finding; this
fibers. increase may be 5-10 times with increasing age.
• Thinning and decreased keratinization of the gingival • Dentogingival plaque accumulation has been suggested
epithelium have been reported with age. to increase with age.
• With increasing age, there is an increase in the width of • It has been speculated that a shift occurs in certain peri-
the attached gingiva. odontal pathogens with age, specifically including an in-
• Tissue culture studies of gingival fibroblasts obtained creased role for Porphyromonas gingivalis and a decreased
from older individuals have revealed a reduction in the role for Actinobacillus actinomycetemcomitans.
rate of proliferation.

1. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Clinical
1. What is the effect of aging on the supporting tissues of Periodontology. 10th ed. Philadelphia: Saunders; 2006.
the periodontium? 2. Wilson Jr TG, Kornman KS. Fundamentals of Periodontics. New York:
2. What is the effect of aging on composition of bacterial Quintessence Publishers; 1996.
plaque?
3. What are the effects of aging on immune response?
SECTION II
CLASSIFICATION AND
EPIDEMIOLOGY OF PERIODONTAL
DISEASES
CHAPTER
6
Classification of Periodontal Diseases
CHAPTER OVERVIEW
Classification of diseases is required to scientifically all of them have shortcomings. To overcome them, in
study the etiology, pathogenesis, and treatment of a dis- 1999, the International Workshop for Classification of
ease. There have been numerous classification systems Periodontal Diseases of Conditions came up with a new
of periodontal diseases over the years. Unfortunately, classification.
DEFINITION USES OF CLASSIFICATION
Classification is the systematic collection of data or • Identification of the etiology and understanding of the
knowledge and its arrangement in sequential manner in pathology
order to facilitate its understanding or knowledge. • Diagnosis, prognosis, and treatment planning
Classification systems can be classified based on • Facilitation of communication among the clinicians,
researchers, educators, students, epidemiologists, and
1. Topography
public health workers.
2. Morphology
3. Etiology.
HISTORICAL DEVELOPMENT OF THE

REQUIREMENT CLASSIFICATION SYSTEM
1. Classification should not be rigid, should be adaptable, Development of classification systems was largely
and should respond to changing knowledge. influenced by paradigms that reflect the understand-
2. It should be consistent. ing of periodontal diseases during a given historical
period.
Classification systems are placed into three paradigms
NEED FOR CLASSIFICATION primarily based on the following:
• Clinical characteristic paradigm (1870-1920)
It allows for logical and systematic separation and • Classical pathology paradigm (1920-1970)
organization of knowledge about the disease so that one • Infection/host response paradigm (1970 to present).
may reason
• from the signs and symptoms seen in the patient to a
C.G. Davis Classification - 1879
presumed etiologic history;
• from the presumed etiologic history to identification 1. Gingival recession with minimal or no inflammation
of the condition; and 2. Periodontal destruction secondary to lime deposits
• from there to the prescribed course of treatment. 3. "Riggs disease" - loss of alveolus without loss of gums.
36 SECTION II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES
G.V. Black Classification - 1886 • Chronic irritation, drug action, idiopathic (gingivoma,
elephantiasis, fibromatosis)
1. Constitutional gingivitis: Mercurial gingivitis; scurvy • Traumatism
2. A painful form of gingivitis: Similar to necrotizing
• Periodontal traumatism - occlusal trauma.
ulcerative gingivitis (NUG)
3. Simple gingivitis: Associated with accumulation of de-
bris that eventually led to calcic inflammation of peri- Demerits
odontal membrane • Conclusion that some forms of periodontal diseases
4. Calcic inflammation of periodontal membrane: Associ- were caused by noninflammatory or degenerative
ated with salivary calculus process was primarily based on overinterpretation of
5. Phagedenic pericementitis. histopathologic studies.
• There is no scientific basis for retaining the concept that
there were noninflammatory or degenerative forms of
Orban Classification - 1942 destructive periodontal diseases.
He postulated, "Periodontal diseases followed the
same course as the diseases of the other organs. Minor American Academy of Periodontology - 1986
changes may be present but the basic pathologic changes
however are the same as those of other organs." Accord- 1. Gingival diseases and conditions
ing to the principles of general pathology, there are three a. Gingivitis
major tissue reactions: - Marginal gingivitis
- Acute necrotizing ulcerative gingivitis (ANUG)
• Inflammatory b. Gingivitis and other gingival changes with systemic
• Dystrophic involvement
• Neoplastic. - Gingival changes associated with sex hormones
- Gingival changes associated with diseases of the
Note: Neoplastic changes are not in the therapeutic skin and mucous membrane
realm of periodontics. Environmental factors, how- - Gingivitis in generalized systemic diseases
ever, dictate the inclusion of a third category in the - Infective gingivostomatitis
periodontology - "pathologic reaction produced by oc- - Drug-associated gingival changes
clusal trauma." o Systemic medications
o Compounds with local effects (caustic com-
• Inflammation:
pounds, heavy metals)
• Gingivitis
- Miscellaneous gingival conditions
- Local (calculus, food impaction irritating
o Gingival cysts, fistula, neoplasms, gingival
restoration, drug actions)
clefts, recession, aberrant frena, epulis, and
o Systemic (pregnancy, endocrine disorders, TB,
abscess
syphilis, nutritional disturbances, drug action,
2. Periodontal diseases and conditions
allergy, etc.)
a. Periodontitis in adults with no systemic involve-
• Periodontitis
ment
- Simplex (secondary to gingivitis) - bone loss,
b. Periodontitis in juveniles
pockets, abscess, calculus
- Localized/ generalized
- Complex (secondary to periodontosis) - etiologic
c. Periodontitis with systemic involvement
factors similar to periodontitis; have little, if any,
- Periodontitis in primary neutrophil disorders
calculus
- Periodontitis in systemic diseases with secondary
• Degenerative
or associated neutrophil impairments
• Periodontosis (attacks young girls and older men,
- Other systemic diseases associated with changes
often caries immunity)
in the structure of periodontal attachment
- Systemic (pregnancy, endocrine disorders, TB,
- Miscellaneous
syphilis, nutritional disturbances, drug action,
3. Periodontal changes associated with occlusal trauma
allergy, etc.)
a. Primary - bruxism, other parafunctional habits
• Atrophy
b. Secondary - periodontal diseases.
• Periodontal atrophy (recession, no inflammation, no
pockets, osteoporosis) due to local trauma, senile, This classification is intended to provide a current
disuse, following inflammation, idiopathic basis of terminology that is useful for communication
• Hypertrophy among practitioners, patients, and third parties involved
• Gingival hypertrophy in practice.
CHAPTER 6 CLASSIFICATION OF PERIODONTAL DISEASES 37
Merits • Periodontal diseases that progress from marginal
1. Clearly differentiates gingivitis, gingival enlargement, gingiva are infectious diseases caused by bacteria.
NUG, periodontitis, and so on • Inflammatory conditions restricted to the gingiva
2. Useful in teaching. itself fit into the defining term gingivitis, whereas
inflammation extending deeper to involve periodontal
Demerits ligament, cementum, and alveolar bone fits within the
term periodontitis.
1. Age-dependent criteria
• Although both gingivitis and periodontitis are of local
2. Rate of bone destruction.
origin, they can be influenced in their expression by
systemic conditions; same gingival abnormalities may
World Workshop in Clinical be caused primarily by systemic conditions as well.
No periodontitis has been documented to be of purely
Periodontology - 1989
systemic origin.
The workshop classified periodontal diseases into the
This classification accepts occlusal trauma as a physi-
following categories:
ologic adaptation rather than a disease.
1. Adult periodontitis
2. Early onset periodontitis 1. Gingivitis
a. Prepubertal periodontitis - localized/ generalized a. Gingivitis, plaque induced
b. Juvenile periodontitis - localized/ generalized - Nonaggravated
c. Rapidly progressing periodontitis - Aggravated by sex hormones, drugs, and sys-
3. Periodontitis associated with systemic diseases temic diseases
a. Down syndrome b.NUP
b. Diabetes, Papillon-Lefevre syndrome - Systemic determinants unknown
c. AIDS, etc. - Related to HIV
4. Necrotizing ulcerative periodontitis (NUP) c. Gingivitis, non plaque induced
5. Refractory periodontitis. - Associated with skin diseases
- Allergic infections
Classification depended on the following factors: 2. Periodontitis
1. Age criteria a. Adult periodontitis: nonaggravated/ systemically
2. Rate of progression aggravated
3. Host response of the affected patient b. Early onset periodontitis: localized/ generalized
4. Other forms not responding to conventional therapy, c. Related to systemic diseases
i.e., refractory periodontitis. 3. NUP: systemic determinants unknown - related
to HIV
Merits a. Related to nutrition
1. Ease with which patients could be placed into age- 4. Periodontal abscess.
based categories
Merits
Demerits
This system includes not only forms of gingivitis and
1. It did not include gingivitis or gingival disease
periodontitis other than those caused by plaque but also
category.
modifying factors, e.g., systemic aggravating factors, gen-
2. Periodontitis categories had nonvalidated age-
eral diseases status, and viral infections.
dependent criteria.
Compared with the World Workshop in Clinical Peri-
3. There was extreme crossover in rates of progression of
odontology, 1989, this classification system
the different categories of periodontitis.
4. There was extensive overlap in the clinical • Eliminated the "refractory periodontitis" catego-
characteristics of different categories of periodontitis. ry, since it was a heterogeneous group and it was
5. Refractory periodontitis and prepubertal periodontitis impossible to standardize the treatment that neces-
were heterogeneous categories. sarily would have to be given prior to making diag-
nosis
• Eliminated the "periodontitis associated with systemic
Ranney Classification - 1993
disease" category, since the expression of all forms of
Classification is based on principles including the fol- periodontitis can be modified by some systemic disease
lowing: or abnormality.
European Workshop on Periodontics - 1993 o Allergic reactions

,,, Dental restorative materials - mercury,
1. Adult periodontitis acrylic, etc.
a. Onset fourth decade ,,, Reactions attributed to toothpastes/
b. Slow rate of progression dentifrices, mouth rinses/washes, chewing
c. No host response defect gum additives, food, and additives
2. Early onset periodontitis ,,, Others
a. Onset prior to fourth decade
- Traumatic lesions - chemical, physical, thermal,
b. Rapid rate of progression factitious, iatrogenic, accidental
c. Defect in host response - Foreign body reactions
3. Necrotizing periodontitis
- Not otherwise specified
a. Tissue necrosis with attachment and bone loss.
2. Chronic periodontitis (based on clinical, radiographic,
Demerits historical, and laboratory characteristics)
a. Localized ( <30% of sites involved)
• Lacked adequate categorization of the broad spectrum
b. Generalized (>30% of sites involved)
of periodontal diseases encountered in clinical practice
Both groups can be categorized as - slight: 1-2 mm
• Gingival diseases not included.
CAL; moderate: 3-4 mm CAL; severe: ?.5 mm CAL.
It is prevalent in adults but can occur in children;
International Workshop for Classification of amount of destruction consistent with local factors;
Periodontal Diseases and Conditions - 1999 variable microbial pattern; subgingival calculus pres-
Goal ent; slow to moderate rate of progression; possibly
modified by systemic diseases, local factors, and envi-
"Course correction" or "fine-tuning" of 1989 classifica-
ronmental factors.
tion
3. Aggressive periodontitis (otherwise clinically
1. Gingival diseases healthy individuals, rapid attachment and bone loss,
a. Dental plaque induced not consistent with local deposits, familial aggre-
- Associated with dental plaque only with/ without gation)
other local contributing factors a. Localized (circumpubertal onset; first molar or in-
- Gingival diseases modified by systemic factors cisor has proximal attachment loss; robust serum
o Associated with the endocrine system: antibody response to infective agents)
puberty-associated gingivitis, menstrual cycle- b. Generalized (affects under 30 years of age; general-
associated gingivitis, pregnancy-associated ized proximal attachment loss; poor serum antibody
gingivitis, pyogenic granuloma, and diabetes response to infective agents; episodic nature of peri-
mellitus-associated gingivitis odontal disease)
o Associated with blood dyscrasias: leukemia- 4. Periodontitis as a manifestation of systemic diseases
associated gingivitis and others a. Associated with hematologic disorders
- Gingival diseases modified by medications - Acquired neutropenia, leukemia, and others
o Drug-induced gingival enlargements b. Associated with genetic disorders
o Drug-influenced gingivitis, for example, oral - LAD deficiency syndromes, and others
contraceptives 5. Necrotizing periodontal diseases - NUG, NUP
- Gingival diseases modified by malnutrition, for 6. Abscesses of the periodontium
example, vitamin C, and others a. Gingival, periodontal, pericoronal
b. Non plaque-induced gingival lesions 7. Periodontitis associated with endodontic lesions -
- Specific bacterial origin: Neisseria gonorrhoeae, combined periodontal-endodontic lesions
Treponema pallidum, Streptococcal species, and others 8. Developmental or acquired deformities and condi-
- Viral origin: herpes virus infections and others tions
- Fungal origin: Candida species infections, linear a. Localized tooth-related factors that modify or
gingival erythema, histoplasmosis, and others predispose to plaque-induced gingival diseases/
- Genetic origin: hereditary gingival fibromatosis, periodontitis
and others - Tooth anatomic factors
- Manifestations of systemic conditions - Dental restorations/ appliances
o Mucocutaneous disorders: lichen planus, - Root fractures
pemphigus, pemphigoid, etc. - Cervical root resorption and cemental tears
CHAPTER 6 CLASSIFICATION OF PERIODONTAL DISEASES 39
b. Mucogingival deformities and conditions around CHANGES MADE IN THE
teeth CLASSIFICATION
- Gingival/ soft tissues recession on facial/lingual/
interproximal/ papillary 1. Addition of a section on gingival diseases
- Lack of keratinized gingiva 2. Replacement of "adult periodontitis" with "chronic
- Decreased vestibular depth periodontitis"
- Aberrant frenum/ muscle position 3. Replacement of "early onset periodontitis" with
c. Gingival excess "aggressive periodontitis"
Pseudopockets, inconsistent gingival margin, 4. Elimination of separate disease category for refractory
excessive gingival display, gingival enlargement, periodontitis
abnormal color 5. Clarification of the designation "periodontitis as a
d. Mucogingival deformities and conditions on manifestation of systemic diseases"
edentulous ridges 6. Replacement of "necrotizing ulcerative periodontitis"
- Vertical and/ or horizontal ridges deficiency with "necrotizing periodontal diseases"
- Lack of gingival/keratinized tissue 7. Addition of a category on "periodontal abscess"
- Gingival/ soft tissue enlargement 8. Addition of a category on "periodontal-endodontic
- Aberrant frenum/ muscle position lesions"
- Decreased vestibular depth 9. Addition of a category on "developmental or acquired
- Abnormal color deformities and conditions."
- Occlusal trauma
o Primary occlusal trauma
o Secondary occlusal trauma FUTURE CHALLENGES IN CLASSIFYING
PERIODONTAL DISEASES
Classification of Periodontal Diseases and Conditions As we enter the postgenomic era with our increased
1. Gingival diseases understanding of the bacteria associated with periodon-
a. Plaque-induced gingival diseases tal infections and the genetic factors controlling host re-
b. Non plaque-induced gingival diseases sponses to these infections, it would seem that a more
2. Chronic periodontitis mechanistic or etiologic classification could be devised.
a. Localized One of the problems associated with any attempt at
b. Generalized subclassifying chronic periodontitis or other forms of peri-
3. Aggressive periodontitis od on ti tis is that these infections are polymicrobial and
a. Localized polygenic. The clinical expression of these diseases is al-
b. Generalized tered by important environmental and host-modifying
4. Periodontitis as a manifestation of systemic diseases conditions. It may eventually be possible to subclassify the
multiple forms of chronic periodontitis into discrete mi-
5. Necrotizing periodontal diseases
a. Necrotizing ulcerative gingivitis
croorganism/host genetic polymorphism groups such as
b. Necrotizing ulcerative periodontitis Group A - set no. 1 of microorganisms + set no. 1 of
6. Abscesses of the periodontium genetic polymorphisms
a. Gingival abscess Group B - set no. 2 of microorganisms + set no. 2 of
b. Periodontal abscess genetic polymorphisms
c. Pericoronal abscess
Group C - set no. 3 of microorganisms + set no. 3 of
7. Periodontitis associated with endodontic lesions genetic polymorphisms
a. Endodontic-periodontal lesion Group D - set no. 4 of microorganisms + set no. 4 of
b. Periodontal-endodontic lesion
c. Combined lesion
genetic polymorphisms.
8. Developmental or acquired deformities and conditions

a. Localized tooth-related factors that predispose to
plaque-induced gingival diseases or periodontitis CONCLUSION
b. Mucogingival deformities and conditions around teeth
c. Mucogingival deformities and conditions on edentulous All classification systems have inconsistencies or in-
ridges accuracies. The present effort is no exception. With our
d. Occlusal trauma.
increased understanding of the bacterial association with
periodontal infection and genetic factors controlling these that as we learn more about the etiology and pathogenesis
infections, it would seem that a new mechanistic or etio- of periodontal diseases, future revisions to the classifica-
logic classification could be devised. Thus, it is anticipated tion will be needed.
KEY POINTS
• Classification is the systematic collection of data educators, students, epidemiologists, and public
or knowledge and its arrangement in sequential health workers.
manner in order to facilitate its understanding or 2. Classification systems are placed into three para-
knowledge. digms:
1. Uses of classification are identification of the etiol- a. Clinical characteristic paradigm (1870-1920)
ogy and understanding of the pathology, diagnosis, b. Classical pathology paradigm (1920-1970)
prognosis, treatment planning, and facilitation of c. Infection/host response paradigm (1970 to
communication among the clinicians, researchers, present).
QUESTIONS 2. Armitage GC. Classifying periodontal diseases - a long standing

dilemma. Periodontal 2000 2002;30:9-23.
3. Genco RJ. Classification and clinical and radiographic features of
1. Classify periodontitis. Add a note on refractory periodontal disease. In: Contemporary Periodontics. St. Louis: Mosby;
periodontitis. 1990. p. 63-81.
2. Explain the 1999 classification of gingival diseases. 4. Grant DA, Sternn IB, Listgarten MA. Periodontics. VI ed. St. Louis:
Mosby; 1988.
5. Newman MG, Takei H, Klokkevold PR, Carranza FA. Clinical
Suggested readings Periodontology. 9th ed. Philadelphia: Saunders; 2006.
1. Armitage GC. Development of a classification system for periodontal

diseases and conditions. Ann Periodontol 1999;4 (1):1-6.
CHAPTER
7
Epidemiology of Periodontal Diseases
CHAPTER OVERVIEW
Dental index or indices are devices to find out the in- It helps to describe the status of the individual or group
cidence, prevalence, and severity of the disease, based on with respect to a condition being measured. An index score
which preventive programs can be adopted. An index is an can be more consistent and less subjective than a word
expression of the clinical observation as a numerical value. description of that condition.
BASIC CONSIDERATIONS • Point prevalence

• Period prevalence
Index Point prevalence of a disease is defined as the number
An index has been defined as a numerical value de- of all current cases (old and new) of a disease at one point
scribing the relative status of a population on a gradu- in time in relation to a defined population. It is calculated
ated scale with definite upper and lower limits, which is as follows:
designed to permit and facilitate comparison with other
populations classified by the same criteria and methods number of all current cases
(A.L. Russel). ( old and new) of a specified
Epidemiologic indices are attempts to quantitate clini- disease existing at a given
cal conditions on a graduated scale, thereby facilitating . point in time
Point prevalence=-----=--------- x 100
comparison among populations examined by the same estimated population at the
criteria and methods (Irving Glickman). same point in time
Period prevalence measures the frequency of all cur-

Incidence rent cases (old and new) existing during a defined period
Incidence rate is defined as "the number of new cases of time expressed in relation to a defined population. It is
occurring in a defined population during a specified pe- calculated as follows:
riod of time." It is calculated as follows:
number of all existing cases
number of new cases of specific ( old and new) of a specified
.d disease during a given time period disease existing at a given
InCI ence = --------='---=-----=----x 1 00 . d period of time interval
population at risk during that period P eno preva 1 ence = x 100
estimated midinterval
population at risk
Prevalence
Disease prevalence refers specifically to all current
Epidemiology
cases (old and new) existing at a given point in time, or
over a period of time, in a given population. Prevalence It is the study of the distribution and determinants of
is of two types: health-related states or events in specified populations
and the application of this study to the control of health The "D" (decayed) portion of DMFT index best
problems (John M. Last, 1988). exemplifies a disease index. The indices measuring
gingival/ sulcular bleeding are essentially symptom
indices. The "F" (filled) portion of DMFT index best
Epidemic
exemplifies treatment index.
It is the unusual occurrence in a community or region of 4. Dental indices can also be classified under special
a disease, specific health-related behavior, or other health- categories as simple or cumulative:
related events clearly in excess of expected occurrence. a. Simple index
It is the index that measures the presence or absence
of the condition, e.g., an index that would measure
Endemic the presence or absence of dental plaque.
It is the constant presence of a disease or infectious b. Cumulative index
agent within a given geographic area or population group, It is the index that measures all the evidences of
without importation from outside, e.g., common cold. a condition, past and present, e.g., DMF index for
dental caries.
Pandemic
It is an epidemic usually affecting a large proportion
PUBLIC HEALTH SIGNIFICANCE
of the population, occurring over a wide geographic area
OF PERIODONTAL DISEASE
such as section of a nation, the entire nation, a continent,
or the world.
Although many oral diseases are not always life-
threatening, they are important public health problems
because of their high prevalence, public demand, and
CLASSIFICATION OF INDICES their impact on individuals and society in terms of pain,
discomfort, social and functional limitations and handi-
1. Based on the direction in which their scores can
cap, and the effect on the quality of life. In addition, the
fluctuate, indices are classified as either reversible or
financial impact on the individual and community is
irreversible.
very high.
a. Reversible index
Periodontal disease affects people physically and psy-
It is the index that measures conditions that can be
chologically and influences how they enjoy life, look,
changed. Reversible index scores can increase or
speak, chew, taste food, and socialize as well as their feel-
decrease on subsequent examination, e.g., indices
ings of social well-being.
that measure plaque or gingivitis.
They experience pain, discomfort, disfigurement, acute
b. Irreversible index
and chronic infections, and eating and sleep disruption
It is the index that measures conditions that will not
as well as higher risk of hospitalization and high treat-
regress. Irreversible index scores, once established,
ment costs.
cannot decrease in value on subsequent examination,
The impact of oral diseases in pain, suffering, impaired
e.g., indices that measure dental caries.
function, and reduced quality of life is both extensive
2. Depending on the extent to which areas of oral cavity
and expensive. Treatment is estimated to account for a
are measured, indices are classified into full mouth or
considerable proportion of health costs in industrialized
simplified.
countries, and is beyond the resources of many develop-
a. Full mouth index
ing countries.
These indices measure the patient's entire
The fact that the cost of treating the disease is high
periodontium or dentition, e.g., Russell Periodontal
because of the organization of dental care qualifies it as a
Index.
dental public health problem.
b. Simplified index
These indices measure only a representative sample
of the dental apparatus, e.g., Oral Hygiene Index
Simplified. INDICES USED IN PERIODONTICS
3. Indices may be classified under certain general
categories according to the entity which they measure, Plaque Index (PU) (Silness and Loe, 1964)
such as
a. Disease index Purpose
b. Symptom index Its purpose is to assess the thickness of plaque only at
c. Treatment index the gingival surface of the tooth.
CHAPTER 7 EPIDEMIOLOGY OF PERIODONTAL DISEASES 43
TABLE 7.1 Scoring Criteria (Silness and Loe) Recording Format for Plaque Index
Score Criteria
0 No plaque in the gingival area D 1\-1
1 A film of plaque adhering to the free gingival

margin and adjacent area of tooth. The plaque may
be recognized only after application of disclosing
; 111 IIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIII
agent or by running a probe across the tooth 17 16 15 I4 IJ 12 11 21 22 2J 24 25 26 2
surface
2 Moderate accumulation of soft deposits within the 47 46 45 44 4J 42 41 JI 32 33 J4 35 J6 J

gingival pocket, on the gingival margin, and/ or on
adjacent tooth surface, which can be seen by the
naked eye : 1111 I I I I I I I• 1 I •1• I 1 • I 1 •• 1 I •1 I I 111 I I• 1 I I 1• I I
3 Abundance of soft matter within the gingival
pocket and/ or on the gingival margin and adjacent
tooth surface -r"
Exccllcnt/Good/Fair/l'oor
Instruments Turesky-Gilmore-Glickman Modification of the

Instruments used are mouth mirror, dental explorer, Quigley-Hein Plaque Index (G. Quigley and J.
and light source. Hein, 1962)
The Quigley-Hein Plaque Index was modified by S.
Selection of Teeth Turesky, N.D. Gilmore, and I. Glickman in 1970.
Teeth are selected on the following basis (Table 7.1):
Purpose
• Whole mouth basis - entire dentition
• Selected mouth basis - 16, 12, 24, 36, 32, 44 Quigley and Hein proposed a system for scoring
dental plaque. This was modified by Turesky et al.
to more explicitly describe mild to moderate plaque
Surfaces Examined
deposits.
• Only plaque at the cervical third of the tooth is
evaluated with no attention to plaque that has extended Instruments
to middle or incisal thirds.
Instruments used are mouth mirror and disclosing
• Four gingival areas of the tooth:
agent.
• Distofacial
• Facial Selection of Teeth
• Mesiofacial
• Lingual Plaque is assessed on the labial, buccal, and lingual
surfaces of all of the teeth using a disclosing agent.
Calculation
Procedure
Scoring by the Turesky modification (Table 7.2):
Plaque Index of each tooth = total score of each tooth
4 1. All teeth are assessed except third molars (maximum
number 28).
total of Plaque Index 2. A staining solution is used to show plaque deposits
of each tooth (Quigley and Turesky used basic fuchsin).
Plaque Index for individual= number of teeth examined 3. Both the facial and lingual surfaces are examined
(maximum number 56).
4. A score is assigned to each facial and lingual
Interpretation nonrestored surface.
Excellent: 0 The modification of the Quigley and Hein Plaque Index
Good: 0.1-0.9 redefined the scores of the gingival third area, emphasiz-
Fair: 1.0-1.9 ing the differences in plaque accumulation in the gingival
Poor: 2.0-3.0 third of the tooth.
TABLE 7 .2 Scoring Criteria (Turesky) The gingival measurement is made with the probe
Score Plaque scoring system for Quigley and Hein
held parallel to the long axis of the tooth and equidistant
from the mesial and distal surfaces. The probe should be
0 No plaque
simultaneously in contact with calculus and the incisal
1 Flecks of stain at the gingival margin edge of the tooth.
2 Definite line of plaque at the gingival margin The distal measurement is made by holding the probe
diagonally so that the tip is in contact with the distal as-
3 Gingival third of surface
pect of the tooth and the opposite end (the portion toward
4 Two-thirds of surface the shank of the probe) is bisecting the mesial incisal angle
5 Greater than two-thirds of surface of the tooth.
The mesial measurement is made by holding the probe
Modified plaque scoring system of Turesky et al.
diagonally so that the tip is in contact with the mesial
0 No plaque aspect of the tooth and the opposite end (the portion to-
1 Separate flecks of plaque at the cervical margin of ward the shank of the probe) is bisecting the distal incisal
the tooth angle of the tooth.
2 A thin continuous band of plaque (up to 1 mm) at the The smallest unit to score the presence of calculus is
cervical margin of the tooth 0.5mm.
3 A band of plaque wider than 1 mm covering less than
one-third of the crown of the tooth Calculation
4 Plaque covering at least one-third but less than The measurement may be calculated and expressed in
two-thirds of the crown of the tooth three different ways:
5 Plaque covering two-thirds or more of the crown of the • per measurement score;
tooth
• per tooth score;
• per subject score.
The "measurement score" is the total of all of the
Calculation scores divided by the number of measurements made.
The "tooth score" is the total of all of the scores divided
total score
Pl aque score=------------ by the number of teeth scored. The "subject score" is sim-
number of surfaces examined ply the total of all of the scores (subjects with fewer than
six teeth are excluded).
Interpretation
• A score of O or 1 is considered low.
• A score of 2 or more is considered high. Papillary Marginal Attachment Index
(Maury Massler and I. Schour, 1944)
Probe Method of Calculus Assessment (A.R. Purpose
Volpe, J .H. Manhold, and S.P. Hazen, 1965) It is used to quantitatively record the readily observ-
Purpose able inflammatory conditions of the gingivae.
It is used to assess the quantity of calculus, especially
in longitudinal studies. Instruments
Instruments used are mouth mirror and periodontal
Instruments probe.
Instruments used are mouth mirror and periodontal
probe. Selection of Scoring Surface
Areas Examined A gingival unit was divided into three component parts
(Table 7.3):
The lingual surfaces of the six mandibular anterior
teeth are examined for the presence of calculus. 1. Papillary gingivae (P) - the gingival portion between
the teeth
Procedure 2. Marginal gingivae (M)- the marginal collar surrounding
A mouth mirror is used to visualize and air is used the teeth
to dry the teeth prior to examination. Measurements are 3. Attached gingivae (A) - the gingival portion overlying
made in three planes: gingival, distal, and mesial. the bony alveolar process
TABLE 7 .3 Scoring Criteria Calculation
Score Plaque scoring system
PMA score= P+M+A
p
0 Normal, no inflammation Gingival Index (H. Loe and P. Silness, 1963)

1+ Mild papillary engorgement, slight increase in size
Purpose
2+ Obvious increase in size, hemorrhage on pressure It is used to assess the severity of gingivitis based on
3+ Excessive increase in size, spontaneous hemorrhage color, consistency, and bleeding on probing.
4+ Necrotic papilla
Instruments
5+ Atrophy and loss of papilla due to inflammation Instruments used are mouth mirror, blunt probe, and
M light source.
0 Normal, no inflammation
Selection of Teeth
1+ Engorgement, slight increase in size, no bleeding Teeth are selected on the following basis (Table 7.4):
2+ Obvious engorgement, hemorrhage on pressure
3+ Swollen collar, spontaneous hemorrhage, beginning • Selected mouth basis - 16, 12, 24, 36, 32, 44
infiltration into attached gingiva
4+ Necrotic gingivitis Surfaces Examined
5+ Recession of the free marginal gingiva below the CEJ • The tissues surrounding each tooth are divided into
A four gingival scoring areas of the tooth:
0 Normal, pale rose, stippled • Distofacial papilla
• Facial margin
1+ Slight engorgement with loss of stippling
• Mesiofacial papilla
2+ Obvious engorgement of attached gingiva with marked • Lingual margin
increase in redness and pocket formation
3+ Advanced periodontitis, deep pockets evident Calculation

total of Gingival Index
Procedure . . d f . d' .d of each tooth
G mg1va 1 1n ex or m 1v1 ua 1 =
The presence or absence of inflammation on each gin- number of teeth
gival unit is recorded. Usually only the facial surfaces of examined
incisors, canines, and premolars are examined.
where
Recording Format . . d f h h total score of each tooth
G mg1va 1 1 n ex o eac toot = ----------
15 14 13 12 11 21 22 23 24 25 4
p
Interpretation
Mild gingivitis: 0.1-1.0
M
Moderate gingivitis: 1.1-2.0
Severe gingivitis: 2.1-3.0
A
TABLE 7.4 Scoring Criteria (Loe and Silness)
Score Criteria
p 0 Absence of inflammation/normal gingiva
1 Mild inflammation - slight change in color, slight

edema; no bleeding on probing
M
2 Moderate inflammation - glazing, redness, edema, and
hypertrophy; bleeding on probing
A 3 Severe inflammation; marked redness and hypertrophy,
ulceration; tendency to spontaneous bleeding
45 44 43 42 41 31 32 33 34 35
Recording Format for Gingival Index Surfaces Examined

Each surface is examined grossly for color and swell-
D M
ing, and then a probe is gently placed in the sulcus to see
: 1111111111111111111111111111111111111111111 if bleeding occurs.
17 16 ll 1• 13 12 II 21 ll 23 l< 25 26 27
Calculation
•7 <6 <S 44 43 42 <I JI '2 JJ J4 Jl J6 J7
ii ii Ii I ii ii ii I I ii ii I
Scores for these units are added and divided by four.
Adding the scores of the undivided teeth and dividing
: 1111111111111111111111111111111111111111111
them by the number of teeth can determine the sulcus
bleeding index.
Seo•• D Interpretation
Mild gingivitis/Moderate gingivitis/Severe gingivitis
The total number of surfaces showing each of the scores
(0-5) is used to evaluate the distribution of changes as-
Sulcus Bleeding Index (SBI) (H.R. Muhlemann sociated with gingivitis.
and S. Son, 1971)
• Minimum sum of all SBI scores: 0
Purpose • Maximum sum of all SBI scores: 320
It is used for assessment of gingival bleeding (Table 7.5).
Instruments Gingival Bleeding Index (Harold G. Carter and
Instruments used are mouth mirror and blunt peri- George P. Barnes, 197 4)
odontal probe.
Purpose
Selection of Teeth
It is used to record the presence or absence of gingival
Sixteen (the anterior four in each quadrant, two on maxil- inflammation as determined by bleeding from interproxi-
la, and two on mandible) teeth in each quadrant are selected: mal gingival sulci.
1. Medial incisor
2. Lateral incisor Instruments
3. Cuspid Instruments used are mouth mirror and unwaxed den-
4. First premolar tal floss.
Four gingival units are scored systematically for each
Areas Examined
tooth: the labial and lingual marginal gingival (M units)
and the mesial and distal papillary gingival (P units). Each interproximal area has two sulci, which are scored
as one interdental unit or individually. Certain areas may
1. P mesial be excluded because of accessibility, tooth position, diaste-
2. P distal ma, or other factors and if exclusions are made, a consis-
Total number of readings: 64. tent procedure should be followed for an individual and
for a group. Third molars are excluded and 26 interdental
TABLE 7.5 Scoring Criteria for Sulcus Bleeding Index units are recorded.
(Muhlemann and Son)
Procedure
Score Criteria
• Pass the floss interproximally first on one side of the
0 Normal-appearing gingival, no bleeding
papilla and then on the other.
1 Apparently healthy with no change in color and no • Curve the floss around the adjacent tooth and bring
swelling but bleeding on probing the floss below the gingival margin.
2 Bleeding on probing. Change in color due to • Move the floss up and down for one stroke, with
inflammation; no swelling or macroscopic edema care not to lacerate the gingival. Adapt finger rests to
3 Bleeding on probing, change in color due to provide controlled, consistent pressure.
inflammation; mild inflammatory edema • Use a new length of clean floss for each area.
4 Bleeding on probing, color change, severe
• Retract for visibility of bleeding from both facial and
inflammatory edema lingual aspects.
• Allow 30 s for reinspection of an area that does not
5 Spontaneous bleeding; changes in color; marked
swelling with or without ulceration
show blood immediately either in the area or on the
floss.
Scoring Criteria TABLE 7.6 Scoring Criteria for Papillary Bleeding Index
Bleeding indicates the presence of disease. No attempt Score Criteria
is made to quantify the severity of bleeding because no 0 No bleeding
bleeding represents health.
1 A single discreet bleeding point appears
Recording Format 2 Several isolated bleeding points or a single fine
line of blood appears
I. Initial gingival bleeding score
Jntrrproxunal 2
j
j
4
4
.!
s
6
6
7
7
8
8
9
9
10
10
II
11 112
12 13
13
14 IS ...,.,, __
,. Toral scoreable
3 The interdental triangle fills with blood shortly
'"' after probing
Toni blttdini;
mas _ _
4 Profuse bleeding occurs after probing; blood flows
immediately into the marginal sulcus
.,.,.
lnttrprolQJlUI JO
JI
29
JO
28
29
27126
28 li
l.!
26
H
2.1
23
24
22
23
21 120
22 21
19
20
18
19
To,al nonbl«d1nc
um __
U. Subsequent gingiva.l blttding score

In,rrrroirnnul 2
= J 4
l 4
s 6 7
s 6 I 7
8
I 8
9
9
10
10
II
II
12
12
13
II
14
14
IS
I Procedure
.,.,.. __
·10:al l>IL,'UinK,
- I I A blunt periodontal probe is carefully inserted into

, ...
lntrrprcnamal JO
JI
29
JO
28
29
27
28
2612.1124
27 26 l.!
23
24
22
23
21
22
20
21
19
20
18
19
Tot-al nonbl«d,ng
mas _ _ the gingival sulcus at the base of the papilla on the
mesial aspect, and then moved coronally to the papilla
tip. This is repeated on the distal aspect of the same
Calculation papilla. The intensity of any bleeding thus provoked
The number of bleeding areas and scorable units are is recorded.
recorded.
Periodontal Index (A.L. Russell, 1956)
Papillary Bleeding Index (H.R. Muhlemann and Purpose
S. Son, 1977)
It is used to assess and score the periodontal disease
Purpose status of population and in epidemiologic studies.
It is used for assessment of gingival bleeding. It was
Instruments
introduced as a modification of the Sulcus Bleeding Index
of Muhlemann and Son (Table 7.6). Instruments used are mouth mirror and light source.
Instruments Selection of Teeth

Instruments used are mouth mirror and blunt peri- Teeth are selected on whole mouth basis - entire denti-
odontal probe. tion (Table 7.7).
TABLE 7. 7 Scoring Criteria for Periodontal Index
Score Criteria Additional radiographic features

0 Negative: there is neither overt inflammation in the investing tissues Radiographic features are normal
nor loss of function due to destruction of supporting tissue
1 Mild gingivitis: there is an overt area of inflammation in the free

gingivae, which does not circumscribe the tooth
2 Gingivitis: inflammation completely circumscribes the tooth but there

is no apparent break in the epithelial attachment
4 Used only when radiographs are available There is early notch-like resorption of the alveolar crest
6 Gingivitis with pocket formation: the epithelial attachment has been There is horizontal bone loss involving the entire
broken and there is a pocket. There is no interference with normal alveolar crest up to half of the length of the root
masticatory function; the tooth is firm in its socket and has not drifted
8 Advanced destruction with loss of masticatory function: the tooth Advanced bone loss involving more than half of the
may be loose; may have drifted; may sound dull on percussion with a tooth root or a definite infrabony pocket with widening
metallic instrument; may be depressible in its socket of periodontal ligament. There may be root resorption
or rarefaction at the apex
Recording Format for Periodontal Index TABLE 7.9 Scoring Criteria for Periodontal Disease Index
18 1716'1514 13 12 11 21 22 23 24 25 26 2728 Score Criteria

0 Absence of dental plaque
1 Dental plaque in the interproximal areas or at the
gingival margin covering less than one-third of
the gingival half of the facial or lingual surface
I 111111111111111 of the tooth
48 47 46 45 44 43 42 41 31 32 33 34 35 36 37 38 2 Dental plaque covering more than one-third but
less than two-thirds of the gingival half of the facial
Periodonral Index Score D 3

or lingual surface of the tooth
Dental plaque covering two-thirds or more of

linical Condition : _ the gingival half of the facial or lingual surface
of the tooth
"Russell's rule: When in doubt, assign the lesser score."

The original criteria of the plaque component were
Calculation modified by R.A. Shick and M.M. Ash in 1961.
It is given in Table 7.8. The formula is as follows:
Surfaces Examined
The scoring of plaque is restricted to the gingival half
Periodontal Index sum of individual scores of the facial and lingual surfaces of the index teeth.
score per person number of teeth present
Instruments
Instruments used are mouth mirror, dental explorer,
Periodontal Disease Index (POI) (Sigurd P. and light source.
Ramfjord, 1959)
Calculation
The POI is a clinician's modification of the Russell Peri-
odontal Index for epidemiologic surveys of periodontal
disease. Plaque score of an _ total score
individual number of teeth examined
Selection of Teeth
Teeth are selected on the following basis (Table 7.9):
Recording Format for Plaque Component of PDI
• Selected mouth basis - 16, 21, 24, 36, 41, 44
Components of the PDI

1. Plaque component 44 41 36
2. Calculus component
3. Gingival and periodontal component ffiffiffi
TABLE 7 .8 Interpretation Community Periodontal Index of Treatment
Needs (CPITN) (Ainamo et al., for the Joint
Individual Periodontal
Clinical condition Index score Working Committee of the World Health
Clinically normal supportive tissues 0-0.2 Organization and FDI, 1982)
Simple gingivitis 0.3-0.9 Purpose
Beginning destructive periodontal 1.0-1.9 It is used to survey and evaluate periodontal treatment
disease needs.
Established destructive periodontal 2.0-4.9
disease Instruments
Terminal disease 5.0-8.0
Instruments used are mouth mirror, CPITN probe, and
light source.
TABLE 7.10 Codes and Criteria for Community Periodontal TABLE 7.11 Treatment Needs
Index of Treatment Needs
TN Criteria
Code Criteria TN-0 A recording of code O or code X for all six
0 Healthy sextants indicates that there is no need for
treatment
1 Bleeding observed, directly or by using a mouth
mirror, after probing TN-1 A code of 1 or higher indicates a need for
improving the personal oral hygiene of the
2 Calculus detected during probing, but all of the
individual
black band on the probe visible
TN-2a A code of 2 or higher indicates need for
3 Pocket 4-5 mm (gingival margin within the black professional cleaning and removal of plaque
band on the probe)
retentive factors. In addition, the patient
4 Pocket 6 mm or more (black band on the probe not obviously requires oral hygiene instructions
visible) TN-2b A code of 3 indicates shallow to moderate
X Excluded sextant (less than two teeth present) pocketing. Oral prophylaxis and scaling will
usually reduce inflammation and bring 4 or
9 Not recorded 5-mm pockets to values of 3 mm or below.
Thus, sextants with these pockets are placed
in the same treatment category as scaling and
root planing
TN-3 A code of 4 indicates need for "complex

CPITN Probe or World Health treatment" such as deep scaling, root planing,
Organization Probe and more complex surgical procedures
It was described by the World Health Organization in
1978. It is designed for three purposes:
1. To measure the pocket depth

Recording Format for Community Periodontal
2. To detect the subgingival calculus
Index of Treatment Needs - CPITN
3. To manipulate the sensitive soft tissues around the Status:
teeth
17/16 11 26/27
• Probe is thin in the handle and is very lightweight
(5 g). It has a black band starting at 3.5 mm and
ending at 5.5 mm (CPITN-E).
• It has a ball tip of 0.5 mm diameter that allows easy
detection of subgingival calculus.
• The probe has two additional markings when used
in clinical work of 8.5 and 11.5 mm (CPITN-C).
47/46 31 36/37
Selection of Teeth (Tables 7.10 and 7.11)

• Index teeth (up to 19 years) -16, 11, 26, 36, 31, 46 Treatment need:
• Index teeth (aged 20 years or more) -17, 16, 11, 26, 27, 17/16 11 26/27
37,36,31,46,47
Advantages
1. Simplicity
2. Speed
3. International uniformity
47/46 31 36/37
Disadvantages
1. Recording is partial.
Community Periodontal Index ( CPI)
2. Some important signs of past periodontal breakdown
have been excluded, notably attachment loss. This index is a modification of the CPITN. The modi-
3. It is not a diagnostic tool and should not be used for fication is done by the inclusion of measurement of "loss
planning of specific clinical treatment of individual of attachment" and elimination of the "treatment needs"
patients. category.
TABLE 7.12 Codes and Criteria for Community Periodontal less than 4 mm (loss of attachment score = 0). The extent
Index of loss of attachment is recorded using the following
Code Criteria codes:
0 Healthy 0: Loss of attachment 0-3 mm (CEJ not visible and CPI
1 Bleeding observed, directly or by using a mouth score 0-3).
mirror, after probing
If the CEJ is not visible and the CPI score is 4, or if
2 Calculus detected during probing, but all of the the CEJ is visible:
black band on the probe visible
1: Loss of attachment 4-5 mm (CEJ within the black
3 Pocket 4-5 mm (gingival margin within the black
band on the probe)
band)
2: Loss of attachment 6-8 mm (CEJ between the upper
4 Pocket 6 mm or more (black band on the probe limit of the black band and the 8.5 mm ring)
not visible)
3: Loss of attachment 9-11 mm (CEJ between the 8.5
X Excluded sextant (less than two teeth present) and 11.5 mm rings)
9 Not recorded 4: Loss of attachment 12 mm or more (CEJ beyond the
11.5 mm ring)
X: Excluded sextant (less than two teeth present)
9: Not recorded (CEJ neither visible nor detectable)
Instruments
Recording Format for Community Periodontal
Instruments used are mouth mirror, CPI probe (earlier
Index- CPI
called CPITN-C probe), and light source.
17/16 11 26/27
Selection of Teeth (Table 7.12)
• Index teeth (up to 19 years) - 16, 11, 26, 36, 31, 46
• Index teeth (aged 20 years or more) -17, 16, 11, 26, 27,
37,36,31,46,47
Loss of Attachment
- 47/46 -~
31 36/37
-
Information on loss of attachment may be collected
from index teeth. The most reliable way of examining
for loss of attachment in each sextant is to record this Loss of attachment:
immediately after recording the CPI score for that par-
17/16 11 26/27
ticular sextant. The highest scores for CPI and loss of
attachment may not necessarily be found on the same
tooth in a sextant.
Loss of attachment should not be recorded for children
under the age of 15.
When the CEJ is not visible and the highest CPI score
for a sextant is less than 4 (probing depth less than 6 mm),
any loss of attachment for that sextant is estimated to be 47/46 31 36/37
KEY POINTS
• An index has been defined as a numerical value de- • Incidence rate is defined as "the number of new cases
scribing the relative status of a population on a gradu- occurring in a defined population during a specified
ated scale with definite upper and lower limits, which period of time."
is designed to permit and facilitate comparison with • Disease prevalence refers specifically to all current cases
other populations classified by the same criteria and (old and new) existing at a given point in time, or over
method. a period of time in a given population.
KEY POINTS (cont'd)
• Based on the direction in which their scores can fluctuate, • Indices may be classified under certain general cat-
indices are classified as either reversible or irreversible. egories according to the entity which they measure,
• Depending on the extent to which areas of oral cavity such as disease index, symptom index, and treatment
are measured, indices are classified into full mouth or index.
simplified.
QUESTIONS 3. Loe H, Silness P. Periodontal disease in pregnancy. Acta Odontol

Scand 1963;21:533.
4. Massler M. The P-M-A index for assessment of gingivitis.
1. Explain the CPITN. J Periodontol 1967;38:592.
2. What is Russell rule? 5. Muhlemann HR, Son S. Gingival sulcus bleeding - a leading
3. Define and classify indices. symptom in initial gingivitis. Helv Odontol Acta 1971;15:107.
4. Write in detail the public health significance of 6. Ramfjord SP. The periodontal disease index. J Periodontol 1967;38:602.
7. Soben P. Essentials of Public Health Dentistry. 5th ed. New Delhi: Arya
periodontal disease.
(Medi) Publishers; 2013.
5. Explain the Silness and Loe Plaque Index. 8. Turesky S, Gilmore ND, Glickman I. Reduced plaque formation
by the chloromethyl analogue of vitamin C. J Periodontal. 1970;
41(1):41-3.
Suggested readings 9. Volpe AR. Indices for measurement of hard deposits in clinical
1. Burt BA, Eklund SA. Dentistry. 6th ed. Dental Practice and the studies of oral hygiene and periodontal disease. J Periodontal Res
Community. Philadelphia: Elsevier; 2005. 1974;9(suppl 14):31.
2. Carter HG, Barnes GP. The gingival bleeding index. J Periodontal 10. World Health Organization. Oral Health Surveys; Basic Methods. 4th
1974;45:801. ed. Geneva: WHO; 1997.
SECTION III
ETIOLOGY OF PERIODONTAL
DISEASES
CHAPTER
8
Dental Plaque and Microorganisms
Associated with Periodontal
Health and Disease
Dental plaque, which exists in the form of biofilm, is cavity. The fact that certain microorganisms may be asso-
the primary etiological factor responsible for periodontal ciated with certain forms of periodontal diseases (e.g., the
disease. It is now well known that periodontal diseases association of Aggregatibacter actinomycetemcomitans with
are caused by polymicrobial infections. It was Antonie van aggressive forms of periodontal diseases) has given rise
Leeuwenhoek who first reported the presence of abundant to hopes of devising more effective treatment by way of
microorganisms in the mouth, which he termed as "ani- eradicating these pathogenic bacteria. However, the nature
malcules." Since that time there has been intense efforts to of such associations has remained obscure due to the sheer
quantify and qualify the microbial population of the oral magnitude and complexity of the oral flora.
ORAL FLORA the environment changes from aerobic to anaerobic. This

change in oxidation-reduction potential encourages the
The mouth of the fetus is sterile before birth. Coloniza- growth of anaerobic species such as Fusobacterium nuclea-
tion occurs during passage through the birth canal and tum. Anaerobic environment also exists in the depth of
subsequent exposure to atmosphere. Since then the oral periodontal pockets, leading to establishment of anaer-
flora grows and diversifies, reaching densities of 100 mil- obes such as Porphyromonas gingivalis. Bacteria acquire
lion bacteria per milligram plaque wet weight in the adult. their nutrient needs from diet, saliva, gingival crevicular
It is now estimated that over 500 species of microorgan- fluid, and other host products such as hemin (iron) and
isms may be residing in the oral cavity and considerable hormones. The bacteria themselves can provide nutrients
variations exist between different individuals and at dif- to each other. In fact, considerable microbial interaction
ferent times in the same individual. takes place within plaque and is an important factor in
Normal species are those that are always present in the growth of certain species. For example, protoheme, a
the oral cavity (e.g., Actinomyces), some of which enter metabolic by-product of Campylobacter rectus, is made use
into a stable relationship with the host and are present in of by P. gingivalis for its growth.
high numbers. Transient species are those that are pres-
1. Microbial population is also affected by host and
ent occasionally and may possess pathogenic potential.
bacterial inhibitory factors. Host inhibitory factors are
Oxidation-reduction potential in (the) different ecological
salivary IgA, lysozymes, lactoperoxidase, lactoferrin,
niches and availability of required nutrients determine the
etc., and bacterial inhibitory factors are organic
growth of a particular species. In general, saccharolytic
acids, H202, and certain enzymes. One important
microaerophilic organisms dominate in the supragingi-
factor that determines the colonization of organisms
val and soft tissue sites. During plaque maturation, the
onto oral surfaces is its ability to adhere as seen in
initial colonizers use the available oxygen and hence
56 SECTION Ill ETIOLOGY OF PERIODONTAL DISEASES
the formation of dental plaque. Plaque inhabits and with small amounts of magnesium, potassium, and
colonizes different surfaces of the oral cavity. Each of sodium.
these areas has distinct microbiological populations
and referred to as ecosystem. Some of the ecosystems
(niches) are Plaque as a Biofilm
a. supragingival areas and surfaces of teeth and Plaque is host-associated biofilm. Features of biofilm
restorations; are presence of microcolonies, primitive circulatory sys-
b. subgingival areas; tem with open fluid-filled channels, and the presence of
c. buccal, palatal epithelia, and floor of the mouth; an intercellular matrix. The channels help in acquiring
d. dorsum of the tongue; nutrients and removal of waste products. The matrix
e. tonsils; forms a protective barrier and aids in metabolic interac-
f. saliva, etc. tions between different bacteria.
DENTAL PLAQUE Formation of Dental Plaque

Dental plaque is formed in the sequence of three steps
Dental plaque is a biofilm consisting of bacterial aggrega- given in the following subsections.
tions that are attached to teeth and other hard surfaces such
as restorations. Taking the gingival margin as reference Formation of an Organic Pellicle
point it is classified into supragingival plaque (which Oral surfaces are covered by a lipoprotein pellicle. This
is coronal to gingival margin) and subgingival plaque involves the adsorption of positively charged salivary,
(which is apical to the gingival margin). Plaque, which crevicular fluid, and other environmental macromolecules
is in contact with the gingival margin, is referred to as to negatively charged hydroxyapatite surfaces of teeth
marginal plaque. through electrostatic, van der Waals, and hydrophobic
Materia alba is a term used to describe aggregations of forces. Although this pellicle is protective in nature, pro-
bacteria and other host-derived cells but lacking the or- viding lubrication and preventing tissue desiccation, its
ganized internal structure of plaque. In contrast to dental formation on the teeth and other hard surfaces forms the
plaque, materia alba can be easily displaced with a water substrate for colonization and subsequent proliferation
spray. of microorganisms.
Initial Bacterial Adherence

Formation of the organic pellicle aids in the adherence
Composition of Plaque
of certain bacteria to the tooth surface. These are the initial
Plaque is mainly composed of microorganisms. Each colonizers and are mainly gram-positive facultative mi-
milligram of wet weight of plaque consists of about croorganisms such as Streptococcus sanguis, Streptococcus
150-200 million bacteria. Other than bacteria organ- mitis, and Actinomyces spp. (Fig. 8.1). Bacterial adherence
isms such as yeasts, mycoplasma, protozoa, and viruses occurs through specific attachments such as extracellu-
are also present in small amounts along with host cells lar polymeric substances and specific molecules known
such as epithelial cells, macrophages, and leukocytes. as adhesins, which attach to the receptors in the dental
These proliferating microorganisms along with host pellicle. Evidence suggests that each oral bacterium pos-
cells exist on an adherent intercellular matrix. This in- sesses different cell surface binding sites for attachment
termicrobial matrix accounts approximately for 25% and multiplication. Bacteria such as Actinomyces viscosus
of plaque volume consisting of organic and inorganic get attached through adhesins present in their surface
materials derived from bacterial products, saliva, and appendages known as fimbriae.
gingival crevicular fluid. Organic matter mainly consists With the multiplication and growth of the primary
of polysaccharide protein complex produced by plaque colonizers, the extracellular matrix also increases through
microorganisms. Levans, glucans, galactose, and meth- accumulation of bacterial products such as extracellular
ylpentose are some of the carbohydrates produced by polymers.
microorganisms.
Small amount of lipids found in plaque are derived Plaque Maturation
from the disrupted cell walls of gram-negative bacte- The initial colonizers make use of the available oxy-
ria. Proteins such as albumin present in plaque are degen, leading to reduced oxygen levels and redox po-
rived from crevicular fluid. Calcium and phosphorus tential favoring the growth of gram-negative anaero-
are the main inorganic constituents of plaque along bic organisms such as F. nucleatum and Capnocytophaga
CH A PT ER 8 DEN TA L PLA Q U E A N D M IC RO O RG A N ISM S A SSO C IATED W IT H PERIO DO N TA L H EA LTH A N D DISEA SE 57
FIGURE 8.2 Aggregatibacter actinomycetemcomitans.

FIGURE 8.1 Fontana staining of a plaque sample showing cocci and
rods (Courtesy: Department of Microbiology, MADC). Recently, an analysis of 13,000 plaque samples showed
microorganisms to exist in complexes. The early coloniz-
ers were in the yellow (S. sanguis, S. mitis, S. oralis) and
species. These organisms have poor ability to get at- purple (A odontolyticus, Veillonella parvula) complexes. The
tached directly to the pellicle and hence adhere to cell secondary colonizers were in the green (Eikenella corrodens,
surface receptors of the initial colonizers. As the plaque Capnocytophaga, and A. actinomycetemcomitans) (Fig. 8.2),
matures there is considerable increase in the number of orange (Prevotella, Campylobacter, and F. nucleatum), and
gram-negative bacteria, and bacterial adherence to one red (P. gingivalis, Tannerella forsythia, and T. denticola) com-
another plays an important role in the process of second- plexes. The last described red complex organisms are
ary colonization. associated with bleeding on probing.
The term coaggregation is used to describe adherence
of one bacterium to another. In the early stages of plaque
formation, there is coaggregation between gram-negative
Description and Structure of Plaque
and gram-positive organisms such as F. nucleatum and Plaque is continuously formed on tooth and other hard
A. viscosus followed by coaggregation in the later stag- surfaces of the oral cavity. Small amounts of plaque are
es between gram-negative organisms as that which occurs detectable when scraped off the tooth surface with a probe
between F. nucleatum and P. gingivalis. or when stained with disclosing agents. After teeth are
For growth, the ever-multiplying bacteria within the cleaned, measurable amounts are formed within 1 h, and
plaque matrix require nutrients. The main source of nu- when left undisturbed, maximum accumulation occurs in
trient in supragingival plaque is saliva. In established 30 days. As it accumulates it is seen as a visible globular
plaque, substances produced by certain species become mass with a nodular surface having a whitish to yellowish
nutrients that are essential for the growth of other or- color. Rate of formation is affected by age, salivary flow
ganisms. Lactate and formate produced by Streptococci and consistency, diet, oral hygiene measures, tooth align-
and Actinomyces spp are used by Veillonella as an energy ment, and systemic factors. Hence, there is considerable
source. Hydrogen produced by Veillonella is made use of variation among individuals.
by other organisms such as Campylobacter. Some gram- Subgingival plaque (Fig. 8.3) is not clinically visible as
positive rods are able to produce vitamin K, which along it is formed within the gingival sulci or periodontal pock-
with hemin serves as growth factor for black-pigmented et. Its presence can be found only by probing below the
bacterial species. Microbial population in plaque is not gingival margin within the sulci. At a microscopic level
only one of interdependence but also one of competition subgingival plaque is differentiated into tooth-associated
where one species prevents the colonization of another plaque (which mainly consists of gram-positive, fila-
species. For example, Streptococci, while making use of mentous organisms) and epithelium-associated plaque
available oxygen, produce superoxide anions (02), hy- (which consists of gram-negative rods, cocci, and spi-
drogen peroxide (H2O2), and hydroxyl radicals, which rochetes) (Fig. 8.4). The epithelium-associated plaque
are bactericidal for many other oral bacteria such as Ag- is loosely adherent with one layer in contact with the
gregatibacter actinomycetemcomitans. epithelium and another loose layer within the sulcus or
, _ ..-=e · Epithelial-associated
plaque
!- ~ - } -' "'- Tooth-attached
plaque
FIGURE 8.3 Subgingival plaque and calculus.
FIGURE 8.5 Classification of subgingival plaque.

pocket lumen and is referred to as unattached plaque
(subgingival plaque picture) (Fig. 8.5). The apical border
of the subgingival plaque is separated from the junctional was well known that dental plaque plays an important
epithelium by a layer of leukocytes. role in the initiation and progression of periodontal dis-
eases. First it was thought that the severity was associated
Etiological Role of Plaque in Periodontal with the quantity of plaque formed. This is known as the
Diseases nonspecific plaque hypothesis. According to this hypothesis
when large amounts of plaque are allowed to accumulate,
Etiological role of plaque in periodontal diseases was the toxic and virulent factors produced by this increased
recognized even in the early 1950s. By the end of 1960s it mass of plaque lead to periodontal disease. It was Walter
Loesche in 1976 who delineated this from the specific
plaque hypothesis.
SPECIFIC PLAQUE HYPOTHESIS

According to this hypothesis, only certain microorgan-
isms in plaque are pathogenic. An increase in the number
of these specific bacteria will produce periodontal disease
due to the release of virulent factors by these bacteria.
In order to identify the periodontal pathogen respon-
sible for causing a particular form of periodontal disease,
Sigmund Socransky put forward the following criteria,
which were based on Koch postulates:
1. A potential pathogen associated with disease should
be increased in number at diseased sites.
FIGURE 8.4 Simple staining of a plaque sample showing spirochetes 2. After treatment it should be decreased in number at
(Courtesy: Department of Microbiology, MADC). sites that show clinical improvement.
3. It should produce some form of cellular or humoral because it is firmly bound to the cell surface and is
immune response in the host. released only when the cells are lysed. These substances
4. When experimentally inoculated into animal models, are heat stable, having molecular weights between 3000
it should be capable of causing the same disease. and 5000 (lipooligosaccharides) and several million
5. The pathogen should possess virulence factors capable (LPS). The presence of abundant gram-negative bac-
of causing periodontal tissue destruction. teria in periodontal pockets leads to release of endo-
toxins that interact with receptors on macrophages
Putative periodontal pathogens such as A. actinomy-
and monocytes, leading to release of cytokines such
cetemcomitans and P. gingivalis seem to fulfill Socransky
as interleukin-I and tumor necrosis factor. They also
criteria.
activate complements through alternative pathway.
They can cause intravascular coagulation and tissue
Ecologic Plaque Hypothesis necrosis and have cytotoxic effects on fibroblasts and
other cells. Endotoxins also have the ability to produce
Ecologic plaque hypothesis developed by Marsh and leukopenia and may play a pivotal role in the patho-
coworkers (1990) tries to unify the specific and nonspe- genesis of periodontal diseases.
cific plaque hypothesis. According to this the quantity of In vitro studies of diseased root fragments have shown
plaque, presence of specific pathogenic microorganisms, that endotoxins present in the cemental wall of periodon-
and changes in host response may all contribute to transi- tal pockets prevent the attachment of gingival fibroblasts
tion from health to disease. and also induce irreversible morphological changes in the
cells of the culture. Since the endotoxin is heat resistant,
these diseased root fragments produce inflammatory
VIRULENCE MECHANISMS OF response even after they were autoclaved.
PERIODONTAL PATHOGENS Peptidoglycan, which is a cell wall compound found in
many bacteria, is capable of stimulating bone resorption
Many periodontal pathogens are capable of colonizing and inducing macrophages to produce prostaglandin and
and invading the periodontal tissues. After invasion they collagenases. Tissue destruction is also brought about by
successfully evade host defenses, which allows them to capsular substances found on the outermost surface of
infect and damage the periodontal tissues. many bacterial cells and by toxic products such as volatile
Colonization is through adherence to host tissues sulfur compounds, butyric and propionic acid, indole, am-
and other microorganisms (coaggregation). Immuno- monia, etc.
globulins from saliva (IgA) and crevicular fluid (IgG)
try to inhibit and contain the colonization of bacteria but
are overwhelmed when there is an explosive increase MICROORGANISMS ASSOCIATED WITH
in the number of bacteria. In spite of the physical bar- PERIODONTAL HEALTH AND DISEASE
rier provided by the junctional epithelium, invasion of
pathogenic bacteria into periodontal tissues may occur In clinically healthy periodontium more than 65% of the
through ulcerations in the pocket epithelium or by di- microbial population within the gingival sulci is made up
rect penetration into epithelial or connective tissues, and of gram-positive cocci. Fusiform bacilli, motile rods, fila-
may serve as a reservoir leading to repopulation after ments, and spirochetes are also present. Gram-negative
debridement of the pocket. Having entered into the host organisms and motile rods are seen less frequently.
tissues, pathogens such as A. actinomycetemcomitans and In gingivitis associated with dental plaque only, there is a
P. gingivalis successfully suppress host defense cells. A. shift in the microbial flora from the gram-positive cocci
actinomycetemcomitans produces an exotoxin known as seen in healthy periodontium to one where there is an
leukotoxin, which inhibits PMN function and is also ca- increase in the numbers of gram-negative rods, filaments,
pable of killing mature Band T cells. IgA, IgG proteases, and spirochetes. Initially, Actinomyces species are more
fibrinolysin, catalase, and superoxide dismutase are some common, but in chronic gingivitis, gram-negative bac-
of the bacterial factors that are important in the eva- teria such as Fusobacterium and Veillonella make up 25%
sion of host defenses. of the flora.
Pathogenic bacteria also release a number of enzymes In pregnancy-associated gingivitis there is an increase
such as collagenases, hyaluronidase, gelatinase, aminopepti- in the number of anaerobic bacteria, especially Prevotella
dases, acid, and alkaline phosphatases, which lead to tissue intermedia. This is because P. intermedia can substitute
destruction and manifestation of periodontal disease. progesterone or estradiol for vitamin K as a growth fac-
The lipopolysaccharides (LPS) of gram-negative bac- tor. Increase in the levels of steroid hormones in gingival
terial cell walls consist of a complex lipid (lipid A) at- crevicular fluid during pregnancy favors the growth of
tached to a polysaccharide. This LPS is called endotoxin P. intermedia.
In diabetes mellitus-associated gingivitis the microbial are used, Streptococcus viridans is the most often isolated
flora approximately consists of Streptococci (36%), Actino- organism. Peptostreptococcus, S. intermedius, Bacteroides
myces (33%), V parvula (12%), and Fusobacterium (10%). and Veillonella spp., and E. corrodens are also sometimes
Diabetes mellitus-associated gingivitis is a consistent isolated.
feature found in children with poorly controlled IDDM.
In nonplaque-induced gingival lesions, nonplaque-related
pathogens overwhelm host resistance. These gingival le- DESCRIPTION OF IMPORTANT
sions occur due to infections with Neisseria gonorrhoeae, PERIODONTAL PATHOGENS
Treponema pallidum, Streptococci, and other organisms.
In chronic periodontitis the active sites show a striking • A. (Aggregatibacter) actinomycetemcomitans
increase in the number of gram-negative bacteria such • P. gingivalis
as P. gingivalis, P. intermedia, A. actinomycetemcomitans, • P. intermedia
Bacteroides spp., C. rectus, Eikenella spp., and spirochetes. • F. nucleatum
Viruses such as Epstein-Barr virus-1 and human cyto- • Capnocytophaga
megalovirus may also have a role in the pathogenesis of • C. rectus
chronic periodontitis. • E. corrodens
In localized aggressive periodontitis the most frequently • T. forsythia (B. Jorsythus)
detected microorganisms are A. actinomycetemcomitans, • Spirochetes.
Capnocytophaga spp., E. corrodens, P. intermedia, and C. rec-
tus. Of these A. actinomycetemcomitans has been regarded
as a key etiological agent due to the following findings:
Aggregatibacter actinomycetemcomitans
A. actinomycetemcomitans was first isolated by Klinger
1. In many clinical studies A. actinomycetemcomitans was
in Germany in 1912 from human cases of actinomycosis.
isolated from 90% of the lesions of localized aggressive
It is a gram-negative, nonmotile, capnophilic, non spore-
periodontitis.
forming, small, facultatively anaerobic rod.
2. Studies have shown elevated levels of the organism
A. actinomycetemcomitans cells are 1.0- 1.5 X 0.4-0.5 µm
in sites showing evidence of ongoing periodontal
in size and occur singly or in clumps. Primary colonies
destruction.
are translucent and glistening and exhibit a star-like in-
3. Investigations have reported significantly elevated
ner structure. They grow best on serum or blood agar in
levels of serum antibodies to A actinomycetemcomitans
an anaerobic atmosphere or in 10% CO2 at a temperature
in LAP patients.
of 37°C.
4. Clinical studies have shown a significant correlation
The organism is transmitted from one family member
between successful treatment and elimination of A.
to another in localized aggressive periodontitis, and
actinomycetemcomitans and vice versa.
may be in some forms of chronic periodontitis. Many
5. A. actinomycetemcomitans produces several virulence
periodontitis patients exhibit an elevated antibody
factors including a leukotoxin capable of inducing
response to this pathogen. A. actinomycetemcomitans
disease.
are capable of adhering to surfaces through fimbriae,
Generalized aggressive periodontitis is frequently associ- which are present on their cell surface enabling them
ated with P. gingivalis, Bacteroides Jorsythus, and A. actino- to colonize buccal mucosa as well as dental plaque. S.
mycetemcomitans. sanguis inhibits the growth of A. actinomycetemcomitans
In necrotizing ulcerative gingivitis a mixed flora of spi- by producing H2O2.
rochetes and fusobacteria along with P. intermedia is often A. actinomycetemcomitans is capable of invading the
found. Veillonella spp., and also Streptococci are sometimes host tissues and produces several virulence factors that
seen. individually or collectively could be involved in the
Necrotizing ulcerative periodontitis is associated with pathogenesis of aggressive forms of periodontal disease.
HIV-infected individuals. Microbiologic studies have They produce a heat-labile exotoxin known as leukotoxin,
indicated that these individuals harbor similar microor- which can kill human neutrophils. Monocytes, macro-
ganisms as non-HIV-infected individuals except for the phages, and T and B cells are also sensitive to leukotoxin.
increased prevalence of Candida albicans. Immunodefi- It may also possess an immunosuppressive factor that can
ciency leads to development of necrotic lesions. affect the lymphoid cells. The organism is also capable of
In periodontal abscess, microorganisms that colonize inhibiting fibroblasts, and endothelial and epithelial cell
periodontal abscesses are mostly gram-negative an- activities, and stimulates polyclonal antibody production.
aerobic rods. In most of the cases high frequencies of An important virulence factor of A. actinomycetem-
P. gingivalis, P. intermedia, F. nucleatum, C. rectus, and comitans is its cell wall LPS endotoxin, which is capable
Capnocytophaga spp. are seen. When aerobic techniques of inducing bone resorption, activating the alternative
complement pathway, and inducing lysosomal release The pigmented Prevotella-Porphyromonas group is the
fromPMNs. second most common group of anaerobic bacteria encoun-
The other most common infection associated with A. tered in human infections.
actinomycetemcomitans is subacute bacterial endocarditis.
F. nucleatum
P. gingivalis
F. nucleatum is one of the common isolates found in cul-
Originally classified under Bacteroides, these black- ture studies of subgingival plaque samples. It is a gram-
pigmented microorganisms were first isolated by Oliver negative, anaerobic, spindle-shaped rod. The cells are long,
and Wherry in 1921. P. gingivalis is a gram-negative, an- slender filaments with tapered ends and are 5-10 µm long.
aerobic, short rod. It is pleomorphic and thus may also On anaerobic blood agar, colonies are 1-2 mm in diam-
appear as cocci. Although it may be found in the ton- eter and slightly convex with irregular margins having a
sils, lateral border of the tongue, and buccal mucosa, it characteristic internal flecking. Production of butyric acid
is mostly found associated with subgingival plaque. It is is an important characteristic. Although F. nucleatum is
found in high numbers in subgingival sites associated with frequently isolated from active periodontal disease sites,
periodontitis and is capable of invading the host tissues. its role in the pathogenesis of periodontal disease is yet
It rarely occurs in the gingival sulci of normal healthy to be clearly understood.
periodontium. Of recent clinical interest is the ability of these organ-
P. gingivalis has a capsule that inhibits phagocytosis by isms to produce severe systemic infections following che-
host immune cells and the capsular polysaccharide may motherapy in hematologic patients with neutropenia and
also be important in cell adherence. It also has a fimbria, mucositis.
a filamentous surface structure that may aid the organ-
ism to adhere to tooth surface, sulcular epithelial cells,
or other bacteria. Capnocytophaga
P. gingivalis produces a number of virulence factors
such as collagenase, keratinases, phospholipase, hyal- Important species included under this genus are C.
uronidases, acid phosphatase, alkaline phosphatase, he- ochracea, C. sputigena, and C. gingivalis. These organisms
molysins, fibrinolysins, and a trypsin-like enzyme. The are called Capnocytophaga because they require CO2 for
trypsin-like enzyme is capable of degrading N-benzoyl- their growth. They are gram-negative, gliding, fusiform
DL-arginine-2-naphthylamide, which forms the basis for bacteria, which may appear straight or slightly curved.
a rapid diagnostic test for the presence of this group of They grow well on blood or chocolate agar in a CO2-
organisms in subgingival plaque samples. enriched environment. The colonies are yellowish or
In subjects with various forms of periodontitis there slightly pinkish with marginal finger-like projections.
is an elevated systemic and local immune response to P. Capnocytophaga may play an important role in the
gingivalis. pathogenesis of localized aggressive periodontitis along
with A. actinomycetemcomitans.
These organisms produce a number of virulence factors
P. intermedia that include large amounts of aminopeptidases, which
cause degradation of periodontal tissues. They also cause
These are another set of black-pigmented bacteria,
the release of bradykinins, which may increase vascular
which form black colonies, produce indole, and ferment
permeability, PMN accumulation, and pain. Capnocyto-
sucrose. The colonies of P. intermedia, when exposed
phaga produces substances that have a direct toxic effect
to ultraviolet light, give off a bright red fluorescence
on PMNs. They also disable the immune system by pro-
that is helpful in differentiating them from other black
ducing IgG and IgA proteases. The LPS of Capnocytophaga
colonies.
inhibits the response of T lymphocytes and resists bacte-
P. intermedia may release a number of toxic factors such
ricidal effects of human serum.
as endotoxin, epitheliotoxin, gelatinase, acid and alkaline
These organisms may gain entry into the bloodstream
phosphatase, trypsin-like enzyme, and also IgA and IgG
through oral ulcerations and bleeding gingiva, causing
proteases. They produce superoxide dismutase and resist
sepsis in patients with malignancy and granulocytopenia.
phagocytosis and intracellular killing by immunocompe-
tent cells. Of special interest is the fact that P. intermedia
commonly produces beta-lactamase and may be resistant C. rectus
to penicillin and other antibiotics.
P. intermedia is associated with pregnancy-associated C. rectus was originally named Wolinella recta. These
gingivitis, necrotizing ulcerative gingivitis, and chronic are gram-negative, motile, spiral-shaped bacilli, their
periodontitis. oxygen sensitivity ranging from microaerophilic to strictly
anaerobic. They usually have a single flagellum on one or name B. forsythus. The colonies often appear as satellites
both ends, which enables them to move with a character- of F. nucleatum. It is a gram-negative, strictly anaerobic,
istic corkscrew motion. These organisms are asacchrolytic pleomorphic rod.
and use hydrogen molecules or formate as their energy B. forsythus is the common species detected in the epi-
source. thelial cells recovered from periodontal pockets and is
C. rectus is found in high numbers in subgingival den- considered as an important risk factor for periodontitis.
tal plaque of patients suffering from chronic periodontitis. Its presence may lead to disease progression in adults.
Their numbers were found to decrease after successful
treatment of periodontal lesions. Similar to A. actinomy-
cetemcomitans, C. rectus also produces a leukotoxin, which
Spirochetes
augments its pathogenic potential. Spirochetes are ubiquitous to the subgingival plaque
and are part of the oral flora. They probably contribute to
gingival pathology when their numbers increase beyond
E. corrodens a certain threshold level. They can be readily discerned by
E. corrodens is a gram-negative, small rod that is asac- dark-field and phase contrast microscopic examination of
chrolytic and capnophilic. It is a part of the normal oral subgingival plaque. Spirochetes are corkscrew-like gram-
flora and upper respiratory tract. It is associated with negative anaerobic bacteria. They have internal flagella-
dental and periodontal infections, which include root like structures called axial filaments, which are located
canal infections and periapical abscesses. Because of its between the outer envelope and inner protoplasmic cyl-
pathogenicity, it can also cause head and neck infections inder. Based on their size they are classified as small (100-
and pleuropulmonary infections. In susceptible individu- 250 nm), intermediate (250-500 nm), and large (greater
als it may cause bacterial endocarditis. than 500 nm). Treponema vincentii, an intermediate-sized
These organisms are capable of adhering to human spirochete that was subsequently referred to as Borrelia
epithelial cells through a lectin-like protein present on vincentii, is implicated in necrotizing ulcerative gingivitis.
their surface. They also possess an outer membrane pro- Many studies have shown increased levels and propor-
tein, which may stimulate or depress macrophage activ- tions of spirochetes in chronic periodontitis and aggres-
ity. They impede phagocytosis through the synthesis of sive forms of periodontitis, their proportion ranging from
a slime layer. The outer membrane LPS has a number 21 % to 56% in plaque flora. Spirochetes contain endotoxin
of biological activities similar to other gram-negative that contributes to their pathogenicity. They are capable
bacteria. of immunosuppression. In vitro studies have shown that
E. corrodens is found in active periodontal disease sites they inhibit the functions of PMNs.
and in sites of patients who respond poorly to periodontal An uncultivable spirochete that reacts with monoclonal
therapy. It may also be associated with lesions of localized antibodies specific for T. pallidum has been demonstrated
aggressive periodontitis along with A. actinomycetem- in tissue specimens of NUG and periodontitis. This spiro-
comitans. chete, referred to as pathogen-related oral spirochete, is
the dominant species in some plaque samples and could
be important in the pathogenesis of periodontal diseases.
T. forsythia (B. forsythus) Studies have shown that a decrease in the levels of spi-
This is a black-pigmented bacteria that was isolated by rochetes such as T. denticola results in an improvement in
Dr. Anne Tanner of Forsyth Dental Center and hence the periodontal health.
KEY POINTS
• It is now estimated that over 500 species of microorgan- • The apical border of the subgingival plaque is separated
isms may be residing in the oral cavity, and considerable from the junctional epithelium by a layer of leukocytes.
variation exists between different individuals and at • According to the specific plaque hypothesis only certain
different times in the same individual. microorganisms in plaque are pathogenic. An increase
• Dental plaque is a biofilm consisting of bacterial aggre- in the number of these specific bacteria will produce
gations that are attached to teeth and other hard surfaces periodontal disease due to the release of virulent factors
such as restorations. by these bacteria.
• Materia alba is a term used to describe aggregations • According to ecologic plaque hypothesis the quantity
of bacteria and other host-derived cells but lacking the and quality of plaque along with host factors are impor-
organized internal structure of plaque. tant in the pathogenesis of periodontal disease.
KEY POINTS (cont'd)
• Pathogenic bacteria also release a number of enzymes progesterone or estradiol for vitamin Kasa growth fac-
such as collagenases, hyaluronidase, gelatinase, amino- tor.
peptidases, and acid and alkaline phosphatases, which • In localized aggressive periodontitis the most frequently
lead to tissue destruction and manifestation of periodon- detected microorganisms are A. actinomycetemcomitans,
tal disease. Capnocytophaga spp., Eikenella corrodens, P. intermedia, and
• In clinically healthy periodontium, more than 65% of the Campylobacter rectus.
microbial population within the gingival sulci is made • A. actinomycetemcomitans was first isolated by Klinger.
up of gram-positive cocci. • A. actinomycetemcomitans is capable of invading the host
• In pregnancy-associated gingivitis there is an increase tissues.
in the number of anaerobic bacteria, especially Prevotella • Porphyromonas gingivalis, originally classified under Bacte-
intermedia. This is because P. intermedia can substitute roides, was first isolated by Oliver and Wherry in 1921.
QUESTIONS 2. Darveau RP, Tanner A, Page RC. The microbial challenge in

periodontitis. Periodontal 2000 1997;14:12.
3. Lindhe L, Lang NP, Karring T. Clinical Periodontology and Implant
1. Define and classify dental plaque. Dentistry. 5th ed. Oxford: Blackwell Publishing Asia Pvt. Ltd.; 2008.
2. Describe the mechanism of plaque formation. 4. Marsh PD. Dental plaque: biological significance of a biofilm and
3. What is specific plaque hypothesis? community lifestyle. J Clin Periodontal 2005;32(suppl 6):7-15.
4. What is the difference between specific plaque 5. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Clinical
Periodontology. 10th ed. Philadelphia: Saunders; 2000.
hypothesis and ecologic plaque hypothesis?
6. Page RC, Schroeder HH. Structure and pathogenesis. In: Schluger S,
5. Define Socransky criteria for identification of Youdelis R, Page RC, editors. Periodontal Disease. Philadelphia: Lea
periodontal pathogens. and Febiger; 1977.
6. Describe virulence factors associated with A. 7. Slots J, Ting M. Actinobacillus actinomycetemcomitans and
actinomycetemcomitans. Porphyromonas gingivalis in human periodontal disease: occurrence
and treatment. Periodontal 20001999;20(1):82-121.
Suggested readings
1. Christersson LA, Albinin B, Zambon JJ. Dental bacterial plaques:
nature and role in periodontal disease. J Clin Periodontol l99l;l8:44l.
CHAPTER
9
Host Response - Basic Concepts
Microbial colonization by both pathogenic and com- The protected and moist environment of the oral cavity
mensal organisms invariably evokes a host response. The provides a haven for approximately 700 bacterial species,
balance between host and commensal flora represents a creating a formidable task in identifying specific organisms
relative harmonious coexistence that can be disturbed by that may play a role in periodontal diseases.
changes in the host defense and/ or bacterial composition
with the resultant expression of clinical disease.
Socransky modification of Koch postulates is widely CELLS OF THE IMMUNE SYSTEM

accepted and provides a valuable guide to identify patho-
gens in many infectious diseases: N eutrophils
1. An organism that is important in a disease process • They form the first line of defense.
should be commonly found in high numbers at sites • They are produced in the bone marrow.
of disease and absent or infrequently found at healthy • They comprise around 50% of the total circulating
sites. leukocytes.
2. Elimination/ suppression of the organism by treatment • They carry in granular form all the substances re-
should have a positive influence. quired for phagocytosis and killing of microor-
3. There should be an elevated immune response to the ganisms.
organism, which may be an elevated antibody/ cellular
Once these preformed granular contents are used up,
response.
cell death occurs.
4. Experimental implantation of the organism into
the gingival crevice of an animal should lead to
Neutrophil granules (Fig. 9.1)
development of at least some of the characteristics of
a naturally occurring disease. Specific granules Azurophilic granules
5. The putative pathogen should possess pathogenic/ Lysozymes M yeloperoxidase
virulent potential.
Collagenase Acid hydrolases
Some of the putative periodontal pathogens are Alkaline phosphatase Collagenase and elastase
• Porphyromonas gingivalis Lactoferrin Lysozyme
• Prevotella intermedia
• Actinobacillus actinomycetemcomitans
Mechanism of Action of Neutrophils
• Fusobacterium nucleatum
• Campylobacter rectus PROTECTIVE MECHANISMS
• Eikenella corrodens 1. Pavementing/ margination
• Peptostreptococcus micros. 2. Chemotaxis
CHAPTER 9 HOST RESPONSE - BASIC CONCEPTS 65
Erythrocytes DESTRUCTIVE MECHANISMS

Nuclear lobes
• PMNs carry potent substances such as acid hydrolases,
collagenase, and prostaglandins.
• They are responsible for destroying collagen and
other connective tissue substances and inducing bone
resorption.
• These substances are released during cell death.
Besides, enzymes escape from the cell to the interstitial
area due to incomplete closure of the phagocytic
vacuoles during phagocytosis.
• These substances activate complement components via
the alternate pathway.
FIGURE 9.1 Neutrophil granules. • They activate kinin-producing systems.
• They magnify inflammation.
3. Phagocytosis: engulfing and destroying noxious
substances such as immune complexes + damaged Neutrophil Defects
tissues, apart from various microorganisms and Defects in the PMN defense system are catastrophic to
antigenic substrates within phagolysosomes (Fig. 9.2). the periodontium.
Chernoraxi
Endogenous chemotactic agents Exogenous chemotacric agents
Complement activation product -Formyl peptide
Kinins
Prostaglandin
Cyrokincs
Fibrin
Collagen peptid
Tissue degradation product
Antimicrobial system
Oxidative mechanisms Nonoxidative mechanism
Microbial killing
• IgE-carrying mast cells + antigen

j,
• Sensitization
j,
• Degradation of cell
j,
• Release of heparin, histamine, SRS-A + proteases
j,
• Mediate inflammatory responses.
Macrophages
• They originate from peripheral blood monocytes.
These cells migrate from the blood vessels into the
interstitial spaces and differentiate into macrophages.
• The lymphocytes release certain potent agents, which
have an effect on the newly differentiated macrophages
and convert them into activated macrophages.
• The activated macrophages release a variety of
products that have both protective and destructive
functions.
Protective Functions
FIGURE 9.2 Phagocytosis.
• Phagocytosis + microbial killing
• Destroys damaged tissues
• Stimulates stem cell growth in the bone marrow
• Processes and presents antigen to lymphocytes
Neutrophil disorders associated with PDD are • Regulates fibroblast growth
• Synthesizes and secretes
• Diabetes mellitus • interferon;
• Papillon-Lefevre syndrome • complement components;
• Down syndrome • pyrogen; and
• Chediak-Higashi syndrome • PMN chemotactic factors.
• Drug-induced agranulocytosis
• Cyclic neutropenia. Destructive Functions
• Secretes prostaglandins + cyclic nucleotides
Periodontal Disease with Neutrophil Disorders • Cytotoxic factors: cytokines
• Acute ulcerative necrotizing gingivitis • Acid hydrolases
• Localized juvenile periodontitis • Neutral proteases including collagenase, elastase
• Prepubertal periodontitis plasminogen activators.
• Refractory periodontitis.
Lymphocytes
Mast Cells
Lymphocytes are cells that are synthesized in the thy-
• Widely distributed in the connective tissue mainly mus and bone marrow. They are associated with second-
around blood vessels ary immune response mechanisms. Lymphocytes are
• Present in the gingival connective tissue and junctional broadly categorized as T and B lymphocytes. Their role
epithelium in progression of periodontal disease constitutes mecha-
• Contain receptors for IgE antibodies which are found nisms that unfold various complex cellular interactions,
in the gingival environment as well as humoral mechanisms.
Lymphocyte
T lymphocytes
1
B lymphocytes atural killer cells
1
Thymu
1
Liver, spleen, bone marrow
1
Activated by Ag+ macrophage
1
ell-mediated immunity
1
Humoral immunity
T cells
Helper inducer T cells uppressor cytotoxic T cell

(Th cells, CD4+ve) (Ts cells, CD8+ve)
!
B cells
!
Differentiation to plasma cell
!
rirnulate cytotoxic+
microbicidal activity
of immune cell
!
Ab production Release of IL4 + IL5
Release of IL-2 + lfN-y Increase with decrease in gingival

inflammation
ubdivided into subset

(THl, THO, TH2)
!
Increase in adult periodonriri
B cells
!
Contain cell surface
immunoglobulin
(lgM + IgD)
!
erve as receptors for Ag
Jg
J
lgG
J
lgA
l
lgM
J
lg£
l
lgD
1 1 1 1 1
Heavy chains Heavy chains Heavy chains Heavy chains Heavy chain
1 1 1
ubclass Subclass Subcla
1
IgGl, IgG2
t t
IgG3, IgG4 IgA1,IgA2 IgM1,IgM2
Immunoglobulins ROLE OF ANTIBODIES IN

These are gamma globulins produced by plasma cells
INFLAMMATORY DISEASES
in response to antigens with which they can react in a
• Complement activation by Ag-Ab complexes ~
specific way either in vivo or in vitro.
protective
• lg molecules are composed of two light chains (K/X.) • Phagocytosis of Ag-Ab complex-» release of cytokines
and one of the five types of heavy chains (-y, a, µ, ~ protective and destructive
£, o). • Blocking of lymphocytes by free Ab/ Ag-Ab complex
• The heavy chain denotes the class of the lg molecules. J,
• Basic structure of the lg molecules resembles a "Y." • Suppression of cell-mediated immunity
• The tail of the Y contains the ends of the heavy chains • Neutralization of bacterial allergens/ reactions toxin/
~ "Fe fragment" ~ complement binding site. histolytic enzymes ~ protective
• The remaining area of the "Y" contains the light chains • Enhanced opsonization/bacteriolysis of plaque
and the remainder of the heavy chains ~ "Fab / bacteria ~ protective
antibody binding site."
• The number of binding sites is called the valence of the
molecule.
Complement System
• lgs are found in blood, tissues, and secretions and are • It is an amplifier of the immune system.
effectors of the humoral response. • It is made up of at least 22 proteins.
• On activation its components interact in a cascade
Functions of Immunoglobulins fashion, generating a variety of biologically active
Functions of immunoglobulins are explained in substances, and the process terminates in the lysis of
Table 9.1. antibody-tagged cells.
Complement system
I
Classical pathway Alternate pathway
TABLE 9.1 Irnrnunoglobulins: Functions
IgG IgA IgM IgE IgD

• Complement fixation • Serum IgA complement • Early antibody • Causes immediate • Unknown
• Delayed antibody fixation by alternate path- response hypersensitivity
response way • Complement fixation reactions (reaginic
• Opsonization • Secretory IgA protects antibody)
• Cross-placental barrier mucosa! surfaces
• Increased • Increased concentration in
concentration in GCF saliva
• Prevents adhesion of
bacteria to tissue surfaces,
especially in the early stages
of periodontal diseases
Classical Pathway
Activation lgM + lgM +Ag-Ab complex
Recognition + Initiation •
Clq
•
Clr
Cl
•
Cascade amplification
Cs Esterase
C4
Membrane attack pathway
I\
C4b C4a
ALTERNATE PATHWAY
\ C2
Aggregated Abs, IgG, IgA, lgE, endocoxins, fungi,

yeast, parasites, dextrans, plaque+ pure bacterial fac-
cors B, D + properdin
I\
C2a C2b
C4b C2b
l C3 Convertase J
•
Endotox.in
C3
C3
•
C36Bb
[C3 Converrase]
I\
C3a C3b
•
Further generates additional C3b
(+}
C3 Convertase
C4b2a3b
lC5 Convertase]
I
cs
5 Convercase I\
C5b C5a
\ C5b + C6 + C7
lC5b67J
MAC
Cell lysis
•
C5b6789 (MAC)
•
Lysis
The Lectin Pathway

The lectin pathway is a type of cascade reaction in
the complement system, similar in structure to the clas-
sical complement pathway. Following its activation, it
proceeds through the influence of C4 and C2 to produce
activated complement proteins. It is different from the
classical complement pathway in that it does not recog-
nize an antibody bound to its target. The lectin pathway
is initiated by mannose-binding lectin or ficolin binding
to certain sugars.
liver and can initiate the complement cascade by binding
to pathogen surfaces.
Biological Properties of Activated Complement

Factors
• Anaphylaxis ~ histamine release from mast cells +
permeability of capillaries ~ C3a + CSa
• Activation of B lymphocytes ~ C3b
• Chemotaxis ~ CSa, CSb, C6, C7
• Immune adherence ~ (adherence of Ag-Ab
complement complexes to leukocytes)+ opsonization
~C3b + CSb
• Lectin pathway
• Membrane damage (lysis of red blood cells, gram-
negative bacteria + leakiness of plasma membranes of
nucleated cellsj=-e CS+ C9
• Enhancement of blood clotting ~ C6
• Lysosomal enzyme release ~ CSa
• Promotion of phagocytosis ~ C3 + CS
[ Oegranulation J
• Inactivation of bacterial lipopolysaccharide ~ CS + C6.
IMMUNE REACTIONS
FIGURE 9.3 Type I anaphylaxis.
Immune reactions are basically characterized into four
types:
• Type I - anaphylactic reactions Since IgE-containing cells are not predominant in the
• Type II - cytotoxic reactions gingival tissues, the role of anaphylactic reactions in the
• Type III - immune complex reactions pathogenesis of gingival and periodontal disease has not
• Type IV - delayed hypersensitivity reactions. been shown.
The relationship of these immune reactions to the patho-

genesis of periodontal diseases is discussed herewith. Cytotoxic Reactions/Type II Hypersensitivity
Reactions
Immediate Hypersensitivity Reaction/ Mechanism
Anaphylaxis/Type I Hypersensitivity Reaction
(Fig. 9.3)
Ag/Haptens attached to tissue/cell membrane
Mediated by reaginic Ab-IgE l
Mechanism: IgG/lgM antibodies produced
IgE + masc cells
J,
(Sensitization)
Complement activated lysi
l
(+) Allergen
J, Phagocyrosi
Binds to Fab portion of IgE

l
Lysis by the effects of lymphoid cells
J,
rimularion of mast cell
J, There is no evidence for considering cytotoxic reactions
Release of mediators in the pathogenesis of periodontal disease.
J,
Histamine, SRS-A, bradykinin, platelet-activating Immune Complex Hypersensitivity/Type III
factor, prostaglandins, etc. Hypersensitivity (Fig. 9.4)
Cell-mediated hypersensitivity lesions are populated

predominantly by activated macrophages and a few lym-
phoid cells.
Inflammatory infiltrate in mild gingivitis contains both
Band T lymphocytes. As gingivitis becomes more se-
vere, B cells dominate, whereas in periodontitis, plasma
cells and B cells dominate ( <6% T lymphocytes). Due to
the reduced number of T cells in the tissues, this type of
reaction is not thought to be a major contributor to peri-
odontal disease.
MEDIATORS OF IMMUNE RESPONSE AND

INFLAMMATION (Table 9.2)
TABLE 9.2 Inflammatory Mediators Associated with Periodontal

Diseases
IL-lex, Macrophages Costimulation of antigen-

IL-113 presenting cells and T cells
Induction of acute phase
FIGURE 9.4 Immune complex reactions. protein synthesis
IL-2 Activated Proliferation of activated
Mechanism T cells Band T cells
IL-4 T cells Proliferation of Band
Immune basement the on deposited comple T cells
membrane of blood vessels Stimulation of mast cell
growth
Activation of complement
IL-6 Monocytes Growth and
J, differentiation of Band
eurrophil activation T cells
J, Macrophages, Induction of acute phase
T cells protein synthesis
Liberation of lysozyrnal enzyme
J, IL-8 Macrophages Neutrophil chemotaxis
Destruction of basement membrane IL-10 T cells, B cells Suppression of cytokine

production (anti-
inflammatory)
Bacterial antigens, antibodies to the bacteria, and com-
plement for activation are present in gingival tissues. It IFN-'Y Leukocytes Antiviral
Activation of
is observed that immune complexes commonly occur in
macrophages
gingival tissues derived from patients with periodontal
diseases. TNF-a Macrophages Proinflammatory
TGF-13 Macrophages Anti-inflammatory

Delayed, Type Hypersensitivity/Type IV Lymphocytes
Platelets
Hypersensitivity
Prostaglandins Monocytes Vascular permeability
Mechanism
PGE2 + PGD2 Macrophages Vascular dilatation
Antigen Metabolites of Neutrophils Neutrophil chemotaxis
J, Arachidonic Mast cells Stimulation of bone
-cell sensitization + activation acid resorption
J, Matrix metallo- Neutrophils Degradation of connective
Release of cytokines (24-48 h after exposure) proteinase (e.g., Macrophages tissue
collagenase)
C H A PT ER 9 H O ST RESPO N SE - BA SIC C O N C EPT S 73
Initiation + Progression of Periodontal Disease
Pathogenic plaque
Bacteria
Periodontitis with pocket

and bone destruction
Antibody response Neutrophil clearance
Inflammation and tissue destruction Compljonr activation ~
t
ytokines and inflammatory
mediator
Monocyte lymphocyte axi Penetration r bacterial product
atastrophic end result
INFLUENCE OF HOST RESPONSE ON TABLE 9.3 Periodontal Disease: Influence of Host Factors
PERIODONTAL DISEASE Disease
aspect Host factors
See Table 9.3. Bacterial Subgingivally, antibody complement in GCF
colonization inhibits adherence and coaggregation of bacteria
~ potentially reduces their number by lysis
PERIODONTAL DISEASE ACTIVITY Bacterial Antibody- and complement-mediated lysis

invasion ~ decreases bacterial counts
Neutrophils (chemotaxis, phagocytosis + lysis)
All cases of gingivitis do no progress to periodontitis. ~ decreases bacterial counts
The progress occurs with periods of active tissue de-
Tissue Antibody-mediated hypersensitivity
struction followed by period of quiescence.
destruction Cell-mediated immune response
The term periodontal disease activity refers specifically Activation of tissue factors ~ collagenase
to the stage of the disease, which is characterized by loss
Healing and Lymphocyte and macrophage produced chemo-
of attachment and alveolar bone.
fibrosis tactic factors for fibroblasts - fibroblast-activating
factors
MODELS OF PERIODONTAL DISEASE

ACTIVITY (SOCRANSKY)
Random Burst Theory
Continuous Paradigm
Progression of periodontal disease occurs as short peri-
Continuous paradigm implies slow, continuous, and ods of destruction followed by periods of nondestruction
progressive destruction of periodontal attachment until occurring randomly with respect to time and site within
tooth loss eventually results. an individual, for example, chronic periodontitis.
TABLE 9.4 Periodontal Disease Initiation and Progression: Prerequisites
Factors effecting virulence of periodontal pathogens (not all strains of a particular species are equally virulent)
Local environment Host susceptibility

• Beneficial species • Debilitating systemic disease: AIDS
• Reverse antagonism • Defects in PMN function
• Temperature • A poorly regulated immune response
• Osmotic pressure • Smoking, diet
• Concentration of iron, magnesium, calcium • Various systemic diseases: diabetes mellitus
• Pocket depth
Synchronous Multiple Burst Theory CONCLUSION

Tissue destruction occurs at a definite period of time
Depletion of the host defense mechanisms can have
in one's life and then passes on to a state of remission, for
catastrophic effects on the progression of periodontal
example, juvenile periodontitis.
disease. Various types of periodontal diseases have been
associated with a defective host defense mechanism, for
example, rapidly progressive periodontitis and juvenile
CLINICAL INDICATIONS OF DISEASE periodontitis. It is therefore necessary to have a substan-
ACTIVITY tially toned defense system to maintain general homeo-
stasis and well-being of an individual.
• Bleeding on probing
• Exudation
• Assessment of GCF for presence of products of tissue
destruction QUESTIONS
• Microbiological increase in gram-negative anaerobic
species 1. Describe the role of neutrophils in the host immune
• Increased sulcular temperature. mechanisms.
2. What is cell-mediated immunity?
3. Describe the alterations in leukocyte functions.
PREREQUISITES FOR PERIODONTAL 4. Describe the role of lymphocytes in the host immune
DISEASE INITIATION AND mechanisms.
PROGRESSION 5. Describe immunoglobulins.
6. What is the role of the complement system in
See Table 9.4. immune mechanisms?
KEY POINTS
• Cells involved in the immune mechanism. • Significance of immunoglobulin G in the host defense
• Neutrophils as the first line of defense. Protective and mechanism.
destructive mechanisms involved in neutrophil func- • Complement cascade: classical and alternate pathways.
tions. • Significance of various complement factors in immune
• Alterations in function of neutrophils. mechanisms.
• Macrophages and their role in the immune mechanism. • Association of immune reactions to pathogenesis of
• T and B lymphocytes. periodontal disease.
• Lymphocytic responses: role in immune mechanisms. • Role of inflammatory mediators in potentiating immune
• Role of immunoglobulins in the host defense mecha- responses.
nisms. • Periodontal disease activity.
7. Describe immune reactions and their association 2. Gemmel E, Seymour GJ. Cytokine profiles of cells extracted from
with periodontal diseases. humans with periodontal diseases. J Dent Res 1998;77:16-26.
3. Kinane OF. Regulators of tissue destruction and homeostasis as
8. What are cytokines? diagnostic aids in periodontology. Periodontology 2001;24:215-25.
9. State Socransky postulates. 4. Lindhe J. Clinical Periodontology and Implant Dentistry. 5th ed. Oxford:
10. Describe periodontal disease activity. Blackwell Munksgaard; 2008.
5. Newman MG, Takei H, Carranza FA. Clinical Periodontology. 10th ed.
Philadelphia: Saunders; 2006.
Suggested readings 6. Yamamato M, Fujihashi K, Hiroi T, McGhee JR, Van Dyke TE, Kiyono
H. Molecular and cellular mechanisms for peripodontal diseases: role
1. Aukhil I, Lopatin DE, Syed SA, Morrison EC, Kowalaski CJ. The of Thl and Th2 type cytokines in induction of mucosa! inflammation.
effects of periodontal therapy on serum antibody (IgG) levels to J Periodontal Res 1997;32:115-9.
plaque microorganisms. J Clin Periodontol 1988;15:544-50.
www.ajpdf.com
CH A P T E R
10
Host Microbial Interaction in
Periodontal Disease
• Host response in the periodontium is the defense susceptible host to a microbial biofilm containing gram-
mechanisms in periodontal tissues against bacterial negative bacterial pathogens.
infections. • In general, the host response functions in a protective
• Inflammation and destruction of periodontal tissues capacity, preventing the local infection from progressing
are largely considered to result from the response of a to a systemic, life-threatening infection.
IDENTIFYING PUTATIVE PATHOGENS • Fusobacterium nucleatum

• Campylobacter rectus
Socransky's modifications of Koch's postulates: • Eikenella corrodens
• Peptostreptococcus micros.
1. An organism that is important in a disease process
should be commonly found in high numbers at sites
of disease and absent or infrequently found at healthy
sites. HOST BACTERIAL INTERACTION
2. Elimination/ suppression of the organism by treatment
should have a positive influence. Virulence Factors
3. There should be an elevated immune response to the
Virulence is defined as the ability of a microbe to
organism. This may be an elevated antibody/ cellular
response. • enter a host;
4. Experimental implantation of the organism into the • find a unique ecologic niche;
gingival crevice of an animal should lead to develop- • circumvent or subvert the host's normal defenses;
ment of at least some of the characteristics of a natu- • replicate in the new environment; and
rally occurring disease. • express specialized pathogenic traits.
5. The putative pathogen should possess pathogenic/
virulent potential. Virulence Factors of A. actinomycetemcomitans
1. Factors that promote colonization and persistence in
KEY ORGANISMS the oral cavity:
a. Adhesins
• Porphyromonas gingivalis b. lnvasins
• Aggregatibacter actinomycetemcomitans. c. Bacteriocins
d. Antibiotic resistance
2. Factors that interfere with the host's defenses:
SECONDARY ORGANISMS a. Leukotoxin
b. Chemotactic inhibitors
• Prevotella intermedia c. Immunosuppressive proteins
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CH A PT ER 10 HO ST M IC RO BIA L IN T ERA CT IO N IN PERIO D O N TA L DISEA SE 77
3. Factors that destroy host tissues: • Bacteria that initially colonize the periodontal environ-
a. Cytotoxins ment most likely attach to the pellicle- or saliva-coated
b. Collagenase tooth surface. A relevant example is the adherence of
c. Bone resorption agents Actinomyces viscosus through fimbriae on the bacterial
d. Stimulators of inflammatory mediators surface to proline-rich proteins found on saliva-coated
4. Factors that inhibit repair of host tissues: tooth surfaces.
a. Inhibitors of fibroblast proliferation • Bacterial attachment to preexisting plaque is studied
b. Inhibitors of bone formation. by examining the adherence between different bacterial
strains (coaggregation).
Virulence Factors of P. gingivalis
1. Fimbriae Host Tissue Invasion
a. Adherence to host proteins Bacteria may enter host tissues through ulcerations
b. Intracellular signaling in the epithelium of the gingival sulcus or pocket and
c. Have specific receptors enhancing initial interac- have been observed in intercellular spaces of the gingival
tion - proline-rich proteins/ salivary glycoprotein/ tissues. Another means of tissue invasion may involve
statherins the direct penetration of bacteria into host epithelial or
2. Proteases connective tissue cells. Laboratory investigations have
a. Arg-gingipain: Disruption of fibrinogen-integrin demonstrated the ability of A. actinomycetemcomitans, P.
interactions in gingival fibroblasts gingivalis, F. nucleatum, and Treponema denticola to directly
b. Sustenins: Gingipain R degrades fibrinogen and invade host tissue cells.
activates prekallikrein directly in plasma. IL-
6 induction causes bone resorption/ osteoclast SIGNIFICANCE OF HOST TISSUE INVASION
formation
• Localization of bacteria to the tissues provides an
3. Hemagglutinins
ideal position from which the organism can effectively
4. Lipopolysaccharides.
deliver toxic molecules and enzymes to the host tissue
P. gingivalis produces an array of proteolytic enzymes cells.
with the potential to degrade collagen and other constitu- • Bacteria in the tissues may enable persistence of that
ents of the periodontal extracellular matrix. P. gingivalis species in periodontal pocket by providing a reservoir
proteases may participate in periodontal tissue destruc- for recolonization.
tion by the following mechanisms:
Bacterial Evasion of Host Defense Mechanisms
• direct action on periodontal collagen and ground
• To survive in the periodontal environment, bacte-
substances;
ria must neutralize or evade the host mechanisms
• inducing keratinocytes and fibroblasts to release matrix
involved in bacterial clearance and killing. Bacteria
metalloproteinases (MMPs);
produce substances that suppress the activity of poly-
• cleavage of host defense mediators such as immu-
morphonuclear leukocytes (PMNs) and lymphocytes.
noglobulins, plasma proteinases, and cytokines, and
• Bacterial adherence and invasion are representative
cleavage and activation of procollagenase.
strategies by which microorganisms accomplish this
task. The ability to adhere allows bacteria to avoid
displacement by host secretions, and eukaryotic cell
MICROBIOLOGIC ASPECTS OF invasion disrupts the natural barriers formed by host
MICROBIAL-HOST INTERACTIONS tissue cells.
• Periodontal bacteria neutralize or evade host defenses
Bacterial Colonization via numerous other mechanisms. For example,
immunoglobulins might function to facilitate
Bacterial Adherence and Mode of Attachment phagocytosis of bacteria by opsonization or block
• Gingival sulcus and periodontal pocket have adherence by binding to the bacterial cell surface and
continuous flow of gingival crevicular fluid (GCF). restricting access to bacterial adhesins. The production
Bacterial species that colonize that region must attach of immunoglobulin-degrading proteases by specific
to available surface to avoid displacement by fluid microorganisms may counteract these host defenses.
flow. Therefore, adherence represents a virulence factor Similarly, bacteria produce substances that suppress
for periodontal pathogens. the activity of or kill PMNs and lymphocytes normally
• Surfaces available for attachment are tooth/ root, involved in host defenses. An example of this is the
tissues, and preexisting plaque mass. production by A actinomycetemcomitans of two toxins
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TABLE 10.1 Bacterial Enzymes Capable of Degrading Host suggest that polyclonal activation of B cells induced by
Tissues bacteria in the resident flora may be an important patho-
Bacterial enzyme Species genic mechanism.
Collagenase P gingivalis The evidence that periodontitis-associated bacteria
A. actinomycetemcomitans contain potent polyclonal B-cell activation factors is very
strong. Clearly, antibodies directed against nonoral an-
Trypsin-like enzyme P. gingivalis
A. actinomycetemcomitans tigens are produced in the inflamed periodontal lesion,
T. denticola and polyclonal B-cell activation appears to contribute to
that production.
Arylsulfatase C. recius
Alterations in the regulation of B-cell responses to
N euraminidase P. gingivalis polyclonal B-cell activation factors are associated with
T. forsythia severe periodontal disease. However, evidence dem-
P. melaninogenica
onstrating that activated B cells and plasma cells are
Fibronectin-degrading P. gingivalis directly involved in the pathogenic mechanisms leading
enzyme P. intermedia to destruction of the periodontal support is still circum-
Phospholipase A P. intermedia stantial. Polyclonal B-cell activation and potential path-
P. melaninogenica ways by which polyclonal B-cell activation-stimulated
cells could be involved in periodontal destruction re-
main largely hypothetical. It appears that IL-1 is an
(a leukotoxin and cytolethal distending toxin) that may important osteoclast-activating agent, and that lipopoly-
be important in the virulence of this microorganism saccharide, which is a potent polyclonal B-cell activation
in aggressive periodontitis and possibly in chronic factor in many systems, can elicit IL-1 production by B
periodontitis. cells as well as by the monocyte/macrophage lineage.
It is also likely that polyclonal activation may lead to
production of autoantibody such as anti-type I and
MICROBIAL MECHANISM OF HOST anti-type III collagens, the destruction of self-tissues
TISSUE DAMAGE through immune complex formation, and complement
activation.
Bacterial products that lead to inhibition of growth or
alteration of metabolism of host tissue cells are mentioned
in Table 10.l. The host immune system involves a com- IMMUNOLOGIC ASPECTS OF
plex network of interactions among cells and regulatory MICROBIAL-HOST INTERACTION
molecules. Bacterial products may perturb the system,
resulting in tissue destruction. Well-characterized inter- Innate Host Response
actions involve the release of IL-1, tumor necrosis factor,
Innate immune mechanisms operate without any pre-
and prostaglandins from monocytes, macrophages, and
vious contact with the disease-causing microorganism.
PMNs exposed to bacterial endotoxin (lipopolysaccha-
These mechanisms include the physical barriers of the oral
ride). These host-derived mediators have the potential to
mucosal epithelial surfaces and vascular and cellular as-
stimulate bone resorption and activate or inhibit other host
pects of the inflammatory responses. The epithelial surface
immune cells.
is the first region of the periodontium which comes in
contact with and responds to bacteria attaching and colo-
Polyclonal B,Cell Activation nizing the dentogingival region. Prevention of attachment
and colonization is important for the host defenses, and
Periodontal diseases have inflammatory conditions
this is achieved through multiple innate mechanisms
which may include sufficient destruction of the periodon-
which include the washing effect of the saliva and GCF;
tium to result in loss of teeth. There are several potential
the constituents of these fluids such as antibodies and pro-
mechanisms whereby bacteria might directly initiate or
teases, complement, salivary antibacterial agents, lactofer-
perpetuate certain signs of disease, but host response fac-
rin, and other salivary proteins are detrimental to bacterial
tors, including immunologic responses, may be equally
growth and can be bactericidal. The oral mucosa itself is
important in determining the progression and severity
not simply a barrier but has a chemical composition which
of disease.
may be detrimental to bacteria.
The histopathology of established or advanced peri-
The cells of the epithelium can respond to the bacteria by
odontal lesions is dominated by B lymphocytes and plas-
ma cells, suggesting that the periodontal diseases may 1. producing and/ or releasing cytokines and other mol-
be primarily B-cell lesions. Also, a number of findings ecules that kill the microbes;
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2. releasing other molecules (e.g., IL-1) capable of b. Several fibroblasts within the lesion exhibit signs of
inducing or enhancing the inflammatory reaction. degeneration.
c. The basal cells of junctional and sulcular epithelium
The epithelium can also respond by increasing expres- start proliferating.
sion of surface molecules such as cell adhesion molecules 3. Established lesion
which can function with cytokines and chemoattractants a. Predominance of plasma cells and B lymphocytes
to bring leukocytes to the region. b. Increased collagenolytic activity
Molecules in saliva such as lactoferrin have several det- c. B cells found in the established lesion predominantly
rimental effects on bacteria, which include the binding of lg Gland G3 subclasses
and restriction of iron in the environment that prevents 4. Advanced lesion
microbial growth. In addition, lactoferrin is also highly a. Loss of CT attachment and alveolar bone
cidal for bacteria. Molecules present in the GCF include b. Extensive damage to collagen fibers
complement, which can kill bacteria directly or together c. Predominance of plasma cells.
with antibodies, and can bring PMNs to the region (via
chemotaxis). The presence of PMNs may be further det-
rimental to the bacteria.
INFLAMMATORY CELLS, MOLECULES,
AND PROCESSES
Toll-Like Receptors in Periodontal Tissues
• Proteinases and their inhibitors
• The periodontal tissue reveals the presence of very
• Matrix metalloproteinases
low numbers of immune cells such as macrophages,
• Polymorphonuclear leukocytes
Langerhans cells, tissue dendritic cells, and migratory
• Cytokines
neutrophils in GCF and the epithelial cell layer.
• Complements
• In addition to immune cells, cells of the periodontium
• Prostaglandins.
express Toll-like receptors.
Proteinases and their Inhibitors

Toll, Like Receptors Expressed on Gingival
Epithelium • Proteinases, or proteases, cleave proteins by hydrolyz-
ing peptide bonds.
These continually interact with components of oral • Release of proteases in the gingiva and the ere-
plaque bacteria that form biofilms attached to the tooth vicular area promotes inflammatory reactions and
surface. contributes to connective tissue damage via several
This toll-like receptor signaling results in innate im- pathways.
mune responses involving the release of antibacterial • Protease inhibitors serve as modulators of protease
peptides (f3-defensins, cathelicidin, and calprotectin) and function in the area and dampen the inflammatory
neutrophil-recruiting chemokine (IL-8). process.
Matrix Metalloproteinases
HOST RESPONSE OF GINGIVA AND
• They are a family of proteolytic enzymes found in
PERIODONTIUM IN DIFFERENT STAGES
neutrophils, macrophages, fibroblasts, epithelial cells,
OF GINGIVITIS
osteoblasts, and osteoclasts.
• They degrade extracellular matrix molecules such as
1. Initial lesion
collagen, gelatin, and elastin.
a. Increase in permeability of microvascular bed
• MMP-8 is released by infiltrating neutrophils, where-
b. Increase in GCF flow
as MMP-1 is expressed by resident cells including fi-
c. PMN cell migration facilitated by the presence
broblasts, monocytes/ macrophages, and epithelial
of various adhesion molecules, intercellular cell
cells.
adhesion molecule 1, ELAM-I in the dentogingival
vasculature
2. Early lesion
Polymorphonuclear Leukocytes
a. Leukocytes infiltrate the connective tissue in
the junctional epithelium, consisting mainly of • PMNs are the predominant leukocyte within the gin-
lymphocytes. gival crevice/pocket in both health and disease.
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• PMNs from the circulation are attracted to the area via PGE2, which are potent vasodilators and inducers of
chemotactic stimuli elicited from microorganisms in cytokine production by various cells.
the biofilm. • PGE2 acts on fibroblasts and osteoclasts, together
• The junctional epithelium expresses the chemotactic with cytokines, to induce MMP production, which
cytokine (chemokine) IL-8 and intercellular cell is relevant to tissue turnover and in the destructive
adhesion molecule 1. process in periodontitis.
• A gradient of the membrane-bound intercellular cell
adhesion molecule 1 and the soluble IL-8 molecules is
formed, with increased expression toward the outer
ADAPTIVE HOST RESPONSE
surface of the tissue.
Adaptive host response tends to be more effective be-
• This distribution is ideal for the migration of neutro-
cause here the host response is specifically "tailored"
phils into the gingival sulcus.
immunologic response to the offending pathogens.
• Neutrophils may use their adhesins to bind intercellular
cell adhesion molecule 1 on the epithelial cell in the
process of epithelial transmigration. HUMORAL IMMUNE RESPONSE
In humoral immune response antibodies are directed

Cytokines
against particular oral microorganisms, i.e., antibodies
Cytokines are soluble proteins, secreted by cells, which are effector of humoral response.
act as messenger molecules that transmit signals to other
cells.
CELL-MEDIATED IMMUNITY
Actions
• Cell-mediated immunity is initiated when antigen
• They initiate and maintain immune and inflammatory
from subgingival plaque penetrates into the connective
responses.
tissue through the junctional epithelium.
• They regulate growth and differentiation of cells.
• Antigen-presenting cells such as Langerhans cells
• Interleukins are involved in communication between
within the epithelium process the antigen.
leukocytes and other cells, such as epithelia, endothelia,
• They alter it to a form that is recognizable by the immune
and fibroblasts.
system (an antigenic peptide binds to class II MHC).
• IL-1, IL-6, and tumor necrosis factor appear to have a
• The T helper cells recognize this association of foreign
central role in periodontal tissue destruction.
antigen and MHC, become stimulated, proliferate, and
• IL-1 and tumor necrosis factor-a are produced by
release cytokines.
activated macrophages particularly in response to
• Cytokines then enter other lymphoid cells to produce
bacterial lipopolysaccharide.
tissue damage, inflammation, and bone resorption.
Complements
MICROBIOLOGY AND IMMUNOLOGY IN
• Complement comprises nine major proteins which PERIODONTAL DISEASES
circulate in inactive form and which are activated in a
cascade. Aggressive Periodontitis
• Once activated, a series of biologically active fragments
are formed by cleavage. Disease-associated bacteria are thought to cause de-
struction of the marginal periodontium via two related
• Some of the fragments, e.g., C3a and C5a, potentiate
inflammatory response and cause an increase in mechanisms:
vascular permeability. 1. The direct action of the microorganisms or their prod-
• C5a is a potent chemotactic factor for PMNs and ucts on the host tissues
monocytes, while C3b facilitates phagocytosis by 2. Their eliciting tissue-damaging inflammatory re-
opsonization. sponses:
• Human investigations have indicated that A acti-
Prostaglandins nomycetemcomitans is able to translocate across the
junctional epithelium and invade the underlying
• Prostaglandins are arachidonic acid derivatives, which connective tissue.
are important mediators of inflammation. • There is evidence of phagocyte abnormalities and
• Proinflammatory cytokines induce macrophages and hyperresponsive monocytes/macrophages, leading
other cells to produce prostaglandins, particularly to elevations in PGE2 and IL-1[1.
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• Specific antibodies against AgP-associated microor- • The rate of tissue destruction within the lesion will
ganisms and cleaved complement fragments have depend on the growth of bacteria inside the foci and
also been detected in crevicular fluid from AgP their virulence, as well as on the local pH.
lesions. • An acidic environment will favor the activity of lyso-
• Crevicular fluid titers of antibodies against AgP- somal enzymes and promote tissue destruction.
associated microorganisms are frequently higher
than in the serum of the same patient.
• High titers of A. actinomycetemcomitans-specific Necrotizing Periodontal Diseases
lg G2 have been demonstrated in LAP patients.
• Increased cortisol levels have been associated with a
depression of PMN function.
Chronic Periodontitis • There is altered lymphocyte function.
• Elevated steroid levels may provide essential nutrients
• Increases in serum and crevicular fluid antibody
for specific bacterial growth of P. intermedia.
specific to putative pathogens, including P. gingivalis,
• Various studies suggest the lack of protective anti-
A. actinomycetemcomitans, P. intermedia, E. corrodens, F.
bodies in the development of necrotizing ulcerative
nucleatum, and C. rectus, are evident in patients with
gingivitis.
periodontitis.
• Collagenase activity is associated with active periodon-
tal destruction.
• MMP-8 is elevated in chronic periodontitis, whereas Smoking
the levels of TIMP are not. • There is reduced serum lg G to A actinomycetemcomitans.
• Most of the collagenase activity associated with chronic • Higher levels of lg G2 against A actinomycetemcomitans
periodontitis is due to the neutrophil collagenase are thought to be protective.
MMP-8. • Some studies also demonstrate inhibition of prolifera-
tion and/ or function of Band T cells.
Abscesses • IL-4, a cell growth factor, was reduced in GCF of
smokers.
• Microorganisms that are prevalent in periodontal ab- • IL-1 and IL-6 are either reduced or constant. There are
scesses are P. intermedia, F. nucleatum, and P. gingivalis, increased tumor necrosis factor-a and IL-8 levels in
but other periodontal pathogens are also found, includ- GCF.
ing B. forsythus, P. micros, Prevotella melaninogenica, and
C. rectus.
• Histologic studies indicate the presence of neutrophils
and macrophages surrounding an internal region of CONCLUSION
dead leukocytes and tissue debris.
• In the absence of periodontitis, abscesses are typically • Depletion of the host defense mechanisms can have
associated with impaction of foreign objects. catastrophic effects on the progression of periodontal
• An inflammatory infiltrate is formed followed by disease.
destruction of the connective tissues, encapsulation of • Various types of periodontal diseases have been associ-
the bacterial mass, and pus formation. ated with a defective host defense mechanism.
• The lowered tissue resistance and the virulence as well • It is therefore necessary to have a substantially toned
as the number of bacteria present determine the course defense system to maintain general homeostasis and
of the infection. well-being of an individual.
KEY POINTS
• Virulence factors of A. actinomycetemcomitans • Role of cytokines, matrix metalloproteinases, comple-

• Virulence factors of P. gingivalis ments, and prostaglandins in periodontal tissue destruc-
• Polyclonal B-cell activation tion
• Toll-like receptors in periodontal tissue • Bacterial and immunologic factors in different types of
• Role of neutrophils in periodontal disease periodontitis.
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QUESTIONS 3. Lindhe J. Clinical Periodontology and Implant Dentistry. 5th ed. Oxford:
Blackwell Munksgaard; 2008.
4. Mahanonda R, Pichyangkul S. Toll like receptors and their role in
1. State the virulence factors of A periodontal health and disease. Periodontal 2000 2007;43:41-5.
actinomycetemcomitans. 5. Newman MG, Takei H, Klokkevold PR, Carranza FA. Clinical
2. State the virulence factors of P. gingivalis. Periodontology. 10th ed. Philadelphia: Saunders; 2006.
3. Describe the neutrophil defect in periodontal disease. 6. Roitt IM, Brostoff I, Male DK. Regulation of the Immune Response.
Immunology. London: Gower Medical Publication; 1985 10:10.
7. Roitt M, Jehner T. Immunology of Oral Disease. London: Blackwell
Suggested readings Scientific Publication; 1980.
8. Slots I. Actinobacillus actinomycetemcomitans and Porphyromonas
1. Gemmell E, Yamazaki K, Seymour I. The role of T cells in gingivalis in periodontal disease: introduction. Periodontal 2000
periodontal disease: homeostasis and autoimmunity. Periodontal 1999;20:7-13.
2000 2007;43:14-40.
2. Ishikawa I. Host response in periodontal disease: a preview.
Periodontal 2000 2007;43:9-13.
www.ajpdf.com
CHAPTER
11
Dental Calculus
Accumulation of dental plaque on teeth and restorative because it serves as a trap for increased plaque formation
surfaces has been considered as the prime etiological fac- and retention. Periodontal healing can take place in pres-
tor for periodontal disease. Over a period of time plaque ence of calculus if bacteria are controlled. Thus, calculus,
gets mineralized, ultimately leading to the formation of along with other plaque retentive factors, is referred to as a
dental calculus. Calculus is detrimental to gingival health secondary etiological factor of periodontal disease.
DEFINITION as the bone, dentin, and cementum. The principal inorganic

components are
Dental calculus is defined as an adherent calcified or
calcifying mass that forms on the surface of natural teeth 1. Calcium - 39%
and dental prosthesis. 2. Phosphorus -19%
3. Magnesium - 0.8%.
CLASSIFICATION Trace amounts of sodium, zinc, bromine, copper, sili-

con, iron, and fluorine.
Dental calculus is classified according to its relation At least two-thirds of the inorganic component is crys-
to the gingival margin as supragingival or subgingival talline in structure. The four main crystal forms with the
(Fig. 11.1), the differentiating factors of which are illus- approximate component percentage are as follows:
trated in Table 11.1.
1. Hydroxyapatite - 58%, appears as sand grain or rod-
like crystals
COMPOSITION 2. Magnesium whitlockite - 21 %, hexagonal (cuboidal,
rhomboidal) crystals
Dental calculus consists of 70-90% of inorganic salts 3. Octacalcium phosphate - 21 %, platelet-like crystals
and 10-30% of organic components. 4. Brushite - 9%.
These crystal forms do not occur with the same fre-

Inorganic Components quency in all calculus samples; generally two or more are
present in a sample. Their incidence varies with the age
Calcium phosphate - 75.9%
and location of the calculus sample. Hydroxyapatite and
Calcium carbonate - 3.1 %
octacalcium phosphate are the most common in 97-100%
Traces of magnesium phosphate and other metals.
of all supragingival calculus. Brushite is more common
The percentage of inorganic constituents in calculus is in the mandibular anterior region and magnesium whit-
similar to that in other calcified tissues of the body such lockite in the posterior areas.
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teins, e.g., galactose, glucose, rhamnose, mannose, and

Supragingival galactosamine.
calculus 3. Lipids - 0.2% of neutral fats, free fatty acids, cholesterol,
cholesterol esters, and phospholipids. These are prob-
ably derived from the cell walls of the bacteria that are
enveloped within the calculus during mineralization.
STRUCTURE OF DENTAL CALCULUS
Calculus is a very porous substance that contains nu-

merous spaces within the calcified matrix. These spaces
may represent uncalcified bacteria, or can be seen around
Subgingival individual calcified organisms themselves. The examina-
calculus
tion of ground section reveals that supragingival calcu-
lus is often a layered structure in which the degree of
calcification varies from layer to layer (heterogeneous
in nature), whereas subgingival calculus appears to be
more homogenous since it is built in layers with almost
FIGURE 11.1 Calculus: supragingival and subgingival. equal high density of minerals. A very significant feature
of calculus is that its surface is covered by a layer of un-
mineralized plaque.
Organic Components
Much of the organic content of calculus is a mixture
of protein polysaccharide complexes, minor fraction of ATTACHMENT OF CALCULUS ON
lipids, desquamated epithelial cells, leukocytes, and vari- TOOTH SURFACE
ous types of microorganisms.
The following four modes of attachment of calculus
1. Salivary protein - 5.9-8.2%. It includes most of the
have been described:
amino acids.
2. Polysaccharides -1.9-9.1 %. These are derived largely 1. Attachment by an organic pellicle or cuticle that seems
from proteoglycans of bacteria and salivary glycopro- to predominate on the enamel and is also observed
TABLE 11. 1 Distinguishing Features of Supragingival and Subgingival Calculus
Based on Supragingival calculus Subgingival calculus

Location Located coronal to the free gingival margin, predomi- Located below the crest of the free gingival margin
nately on the lingual aspect of mandibular anterior
and buccal aspect of maxillary first molars
Visibility Visible in the oral cavity Not visible on routine oral examination
May be found by tactile exploration
Consistency Hard and clay-like Flint-like
Color White or whitish yellow, which may be tobacco or Dark brown or greenish black due to blood and GCF prod-
food pigment stains ucts mixed with bacterial products
Ease of removal Easily detached from the tooth Firmly attached to the surface
Prevalence More commonly seen but uncommon below 9 years Uncommon in children
Composition Calcium:phosphate ratio is less than that in subgingi- Calcium:phosphate ratio is higher than that in supragingi-
val calculus val calculus
Sodium content increases with the depth of pocket
More of magnesium whitlockite and less of brushite and
octacalcium phosphate
Synonym Was referred to as salivary calculus based on the as- Referred to as serumal calculus on the assumption that it
sumption that it is derived from salivary components was derived from precipitation of constituents of serum in
the sulcus
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C H A PT ER 11 D EN TA L C A LC U LU S 85
TABLE 11.2 Factors Affecting Calculus Deposition
1. Oral hygiene habits
2. Access to professional care
3. Diet
4. Age
5. Ethnic origin
6. Time since last dental scaling
7. Systemic disease
8. Use of prescription medications
9. Calculus-inhibiting factors
when calculus forms on plastic strips. It occurs only

infrequently on the cementum.
2. Penetration of calculus bacteria into the cementum is FIGURE 11.2 Radiograph depicting subgingival calculus.
a mode not accepted by some investigators.
3. Mechanical interlocking into surface irregularities,
such as resorption lacunae and caries.
4. Close adaptation of calculus undersurface depressions Automated Calculus-Detection Technologies
to the gently sloping mounds of the unaltered cemen- Technologies used for calculus detection are
tum surface.
1. Fiber-optic endoscopy - delivered through a device
Calculocementum refers to calculus embedded deeply named Perioscopy
in cementum, which may appear morphologically similar 2. Spectro-optical technology - delivered through the
to cementum. device Detectar
3. Autofluorescence - delivered through the device O1-
AGNOdent
RATE OF CALCULUS FORMATION 4. Ultrasound - delivered through a device named
PerioScan
It is important to note that all plaques do not form into
calculus. Calcifying plaque may become mineralized by
50% in about 2 days or 90% in 12 days. The rate of calculus
formation varies from person to person, for different teeth FORMATION OF CALCULUS
and at different times in the same person. Thus, certain
people form calculus faster than others. Accordingly they Attached plaque
have been classified as heavy, moderate, mild, and non-
calculus formers. Factors affecting the rate of calculus
formation are summarized in Table 11.2. Between the 1st and 14th days of plaque formation
Precipitation of mineral salts (saliva/GCF)

DETECTION OF CALCULUS
Visibility and Tactile Sensation Early plaque of heavy calculus formers contains more
calcium, thrice more phosphorus, and less potassium
Appearance of Calculus on Radiographs (Fig. 11.2) (phosphorus may be more critical than calcium in plaque
Supragingival calculus is readily detectable on the mineralization)
radiographs as radiopaque entity, forming irregular con-
tours on the crown. Interproximal calculus, both suprag-
ingival and subgingival, is even more easily detectable as Crystal formation initially in the intercellular matrix, and on the
bacterial surfaces and then within the bacteria
irregularly shaped projections into the interdental space.
They do not indicate the depth of the pocket as the most
apical part of the calculus may not be calcified enough to Calcification begins along the inner surface of supragingival
be radiopaque. plaque and attached component of subgingival plaque
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3. Role of the enzymes in precipitation of calcium phos-

phate salts:
Separate foci of calcified masses coalesce and increase in size a. Phosphatases (liberated from plaque, desquamated
to form solid masses of calculus (filamentous bacteria increase
in number; focus of calcification converts from basophilic to
epithelial cells /bacteria)
eosinophilic) - Hydrolyze organic phosphates in saliva
- Increase concentration of free phosphate ions
- Initiate mineralization of plaque
Calculus formed in layers, separated by a thin cuticle which is b. Esterases (present in dental plaque, bacteria,
embedded in calculus as the calcification progresses leukocytes, macrophages, desquamated epithelial
cells)
Formation continues to maximum followed by a decline (because
- Esterases hydrolyze fatty esters into free fatty
of the vulnerability of calculus to mechanical wear from food, acids.
cheeks, lips, and tongue) - Fatty acids form soap with calcium and
magnesium.
- They convert to less-soluble calcium phosphate
The development, amount, and composition of calcu- salts.
lus vary in each person, at every site and over time.
The amount of calculus is influenced by numerous
variables, such as age, gender, ethnic background, diet, Epitactic Concept/Heterogeneous Nucleation
location in the oral cavity, oral hygiene, bacterial compo- Concept
sition, host response differences, access to professional According to this concept, calculus formation may
cleaning, mental or physical handicaps, systemic diseases, be initiated through epitaxis by organic complexes in
and prescribed medications. the matrix. Epitaxis implies crystal formation of a com-
pound through seeding. The formation of the initial
crystal or nucleus is called nucleation. The intercellular
THEORIES REGARDING matrix provides the architectural template for the initial
MINERALIZATION OF CALCULUS hydroxyapatite crystal. This focus of calcification en-
larges and coalesces to form a calcified mass. Seeding
Booster Mechanism or nucleating agents may be the intercellular matrix of
plaque, plaque bacteria, or lipid component of organic
The booster mechanism theory suggests that the pre-
matrix.
cipitation of calcium phosphate salts results from a local
rise in the degree of saturation of calcium and phosphate
ions because of the following ways: Carbohydrate-protein complexes
1. Increase in pH of saliva causes precipitation of calcium

and phosphate salts by lowering the precipitation con- Initiate calcification by eliminating calcium from saliva
stant. Increase in pH of saliva may be a result of (chelation)
a. loss of CO2,
b. ammonia formation by dental plaque bacteria, or
Bind with it to form nuclei
c. protein degradation during stagnation.
2. Colloidal proteins in saliva bind calcium and phos-
phate and maintain a supersaturated solution with Induce subsequent deposition of minerals
respect to calcium phosphate salts but
Stagnation of saliva Calculus Inhibition Theory

This concept considered calcification as occurring only
Settles down colloidal proteins at specific sites because of the existence of an inhibiting
mechanism at noncalcifying sites. When calcification oc-
curs, the inhibitors are apparently removed or altered.
Supersaturated state is no longer maintained Pyrophosphate is one possible inhibiting substance
thought to inhibit calcification by preventing the initial
nucleus from growing by "poisoning" the growth center
Precipitation of calcium and phosphate salts
of the crystal.
C H A PT ER 11 D EN TA L C A LC U LU S 87
ROLE OF MICROORGANISMS IN bacteria in calculus formation may be in ways given in

CALCULUS MINERALIZATION the next section.
The role of bacteria in calculus formation is apparently

complex. Although the formation of calculus in germ-free ROLE OF CALCULUS IN PERIODONTAL
animals indicates that bacteria are not essential, but when DISEASE (CLINICAL IMPLICATIONS)
present they obviously play an important role.
Strong associations between calculus deposits and
periodontitis have been demonstrated in experimental
Active Passive and epidemiological studies, but it has to be noted that
Forming phosphatases Bacteria are simply calcified along calculus is always covered by a viable bacterial plaque
with other plaque components
which is pathogenic. The role of calculus in periodontal
Increased plaque pH disease may be summarized as follows:
Induce mineralization 1. Brings plaque bacteria close to the supporting tissues
2. Provides a fixed nidus for continuous plaque accumu-
Mineralization occurs both extracellularly and in- lation
tracellularly around gram-positive and gram-negative 3. Interferes with local self-cleansing mechanisms
organisms. Filamentous organisms, diphtheroids, and 4. Acts as a reservoir for irritating substances such as
Bacterionema and Veillonella spp., have the ability to form endotoxins, antigenic material, and bone-resorbing
intercellular apatite crystals. Calculus formation spreads factors because of its permeability and porous nature
until the matrix and bacteria are calcified. The role of 5. Makes plaque removal more difficult for the patient.
KEY POINTS
• Dental calculus is defined as an adherent calcified or • Hydroxyapatite and octacalcium phosphate are the most
calcifying mass that forms on the surface of natural teeth common in 97-100% of all supragingival calculus.
and dental prosthesis. • Calculocementum refers to calculus embedded deeply in
• Dental calculus consists of 70-90% of inorganic salts and cementum which may appear morphologically similar
10-30% of organic components. to cementum.
• The four main crystal forms are • Calcifying plaque may become mineralized by 50% in
1. Hydroxyapatite - 58% appears as sand grain or rod- about 2 days or 90% in 12 days.
like crystals • Filamentous organisms, diphtheroids, and Bacierionema
2. Magnesium whitlockite - 21 % hexagonal (cuboidal, and Veillonella spp., have the ability to form intercellular
rhomboidal) crystals apatite crystals.
3. Octacalcium phosphate - 21 %
4. Brushite - 9%.
QUESTIONS 2. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant

Dentistry. 5th ed. Oxford: Blackwell Munksgaard; 2008.
3. Mandel I. Calculus formation: role of bacteria and muco-protein.
1. What is the etiological significance of calculus? Dent C/in North Am 1960;4:731.
2. Write in detail the composition of calculus. 4. Meissner G, Kocher T. Calculus-detection technologies and their
3. What are the theories of calculus formation? clinical application. Periodontal 2000 2011;55:189-204.
4. Enumerate the differences between supragingival and 5. Newman MG, Takei Henry H, Klokkevold PR, Carranza FA.
Carranza's Clinical Periodontology. 10th ed. Philadelphia: Saunders;
subgingival calculus.
2006.
5. Enumerate the anticalculus agents. 6. Selvig KA. Attachment of plaque and calculus to the tooth surfaces.
J Periodont Res 1970;5:8-18.
Suggested readings
1. Anerud A, Loe H, Boysen H. The natural history and clinical course
of calculus formation in man. J Clin Periodontol l99l;l8:l60.
CHAPTER
12
Smoking and the Periodontium
Thirty percent of the Indian population, 15 years or older characteristics. The World Health Organization predicts that
- 47% men and 14% of women - either smokes or chews to- tobacco deaths in India may exceed 1.5 million annually by
bacco. Tobacco consumption was significantly higher in poor 2020. The effect of smoking is direct and not simply a result
and less educated population. The prevalence of smoking of poor oral hygiene and increased dental plaque in smokers.
and chewing also varied widely between different states and Cigarette smoking is a major risk factor for periodontitis and
had a strong association with an individual's sociocultural also affects the prevalence, extent, and severity of disease.
EFFECT OF SMOKING National Health and Nutrition Examination Survey

ON PERIODONTAL DISEASE (NHANES III) in the United States assessed 12,000 in-
dividuals over the age of 18 years; this reported that, on
Gingivitis average, current smokers were four times as likely to
have periodontitis as nonsmokers when adjustment was
Smokers exhibit more supragingival calculus deposits,
done for age, race or ethnicity, income, and educational
and a trend toward decreased clinical signs of inflamma-
levels. The rate of periodontal disease progression and
tion. They have a decreased expression of clinical inflam-
tooth loss is greater in current smokers compared with
mation in the presence of plaque accumulation when
that in nonsmokers.
compared with nonsmokers. The appearance of gingiva is
The amount a person has smoked over a long period
often without redness and edema, and decreased bleeding
of time is measured by the number of pack years. It is cal-
on probing at younger age. The marginal gingiva tends
culated by multiplying the number of packs of cigarettes
to be fibrotic with a rolled margin.
smoked per day by the number of years the person has
smoked. For example, 1 pack year is equal to smoking
20 cigarettes (1 pack) per day for 1 year. Smokers dem-
Periodontitis
onstrate double the amount of bone loss over a period of
Frequency of smoking is positively related with in- 10 years compared with nonsmokers.
creasing level of periodontal disease observed among Local effect of smoking evident by the marked increase
smokers. Smokers are almost three times as likely to have in probing depth or attachment loss occurs in the maxil-
severe periodontitis as nonsmokers. Current smokers had lary palatal area and mandibular anterior teeth. Increased
higher probing depths, greater attachment loss, more severity of generalized aggressive periodontitis in young
bone loss, and fewer teeth compared with nonsmokers, adults is associated with smoking.
with similar plaque accumulation. Smokeless tobacco use has been associated with oral
Centers for Disease Control and Prevention (CDC) leukoplakia and carcinoma. However, no generalized
established the criteria to define current smokers as those effect on periodontal disease progression seems to occur,
who had smoked > 100 cigarettes over their lifetime and other than localized attachment loss and recession at the
smoked at the time of the interview, former smokers as site of tobacco product placement.
those who had smoked > 100 cigarettes in their lifetime Interestingly, risk of periodontitis is reduced in former
but were not currently smoking, and nonsmokers as those smokers compared with that in current smokers but is
who had not smoked > 100 cigarettes in their lifetime. more than that in nonsmokers, and this risk decreases
CH A PT ER 12 SM O KIN G A N D TH E PERIO D O N T IU M 89
with increasing number of years since the smoking was
quit. This suggests that
1. Effects of smoking on the host are reversible with
smoking cessation.
2. Smoking cessation programs should be an integral
component of periodontal education and therapy.
CLINICAL FEATURES OF ORAL TISSUES

ASSOCIATED WITH SMOKING
Smokers often present with relatively severe and wide-

spread disease, often without marginal gingival redness
and edema, and decreased bleeding on probing at young-
er age. The marginal gingiva tends to be fibrotic with a
rolled margin. There is often recession in maxillary and
mandibular anterior segments with resultant open em- FIGURE 12.1 Oral health status in smokers.
brasures (Fig. 12.1).
Smoking produces black or brown stains on the tooth
surfaces, and the tooth surfaces also exhibit more suprag-
ingival calculus deposits. Heavy smokers may have grayish
discoloration and hyperkeratosis of the gingiva. Smoking
has deleterious effect on gingival blood vessels. Nicotinic
stomatitis is frequently observed on the palatal mucosa of
heavy smokers (Fig. 12.2). A unique form of cancer called
"chutta" or palate cancer occurs due to reverse smoking.
PATHOGENESIS OF PERIODONTAL
DISEASE IN SMOKERS
Smokers demonstrate more aggressive periodontal

breakdown due to the alteration of host response to bac-
terial challenge. The pathogenesis of periodontal disease
in smokers involves the interaction in various factors and FIGURE 12.2 Nicotine stains.
smoking, that results in to the alteration in microflora,
immune downregulation, and alteration in physiology
(Table 12.1, Fig. 12.3).
Effect of Smoking on Periodontal Microflora

TABLE 12.1 Effect of Smoking on Periodontal Disease and its
Several studies have explored the changes that may oc- Pathogenesis
cur in subgingival plaque as a result of smoking with con- Periodontal
flicting and inconclusive results. In a study of 142 patients disease Effect of smoking
with chronic periodontitis, plaque samples from deep Gingivitis Decreased gingival inflammation and bleeding on
pockets (>6 mm) showed no differences in the counts of probing
Actinobacillus actinomycetemcomitans, Porphyromonas gingi- Periodontitis Increased pocket depth, attachment loss, and bone loss
valis, and Prevotella intermedia. Data from the Erie County
study demonstrate that A. actinomycetemcomitans-positive, Microbiology Increased colonization of periodontal pathogens in
shallow pockets and increased levels in deep pockets
P. gingivalis-positive, and Tannerella forsythia-positive sub-
jects were higher among smokers. Furthermore, smokers Immunology Altered neutrophil chemotaxis, phagocytosis, and
also reported the increased counts of exogenous flora oxidative burst
Increased TNF-a and PGE2
(Escherichia coli and Candida albicans). Increased neutrophil collagenase and elastase
Using checkerboard DNA-DNA hybridization tech-
nology to screen for 29 different subgingival species, it Physiology Decreased GCF flow and bleeding on probing
Decreased subgingival temperature
was found that members of the orange and red complexes
Poor general health,

Poor plaque control
attitude and behaviour
Aggressive periodontal destruction

Reduced inflammatory sign and symptoms
Increased periodontal
lmmunosuppression ,,.. I Smoking 1
pathogenic flora
Poor systemic health I •1 Impaired healing
Periodontal destruction
FIGURE 12.3 Interaction between smoking and other factors.
were significantly more prevalent in current smokers than also increase the release of tissue-destructive enzymes,
in nonsmokers and former smokers. Of interest was an contributing to the aggressive tissue destruction.
increased colonization of these periodontal pathogens in
shallow sites (pocket depth <4 mm) with no differences Effect of Smoking on Physiology
between smokers, former smokers, and nonsmokers in
Nicotine exerts local vasoconstriction, reducing blood
deeper pockets. In addition, these pathogenic bacteria were
flow, edema, and clinical signs of inflammation; thus,
more prevalent in the maxilla than in the mandible.
smokers present with reduced clinical inflammation and
These data suggest that the prevalence of colonization
gingival bleeding. In untreated deep periodontal sites,
of periodontal pathogens is higher in smokers than in non-
smoking creates a favorable subgingival environment
smokers or former smokers and that this leads to an in-
for colonization and growth of gram-negative anaerobic
creased prevalence of periodontal breakdown in smokers.
periodontal pathogens by decreasing the oxygen tension.
Smoking reduces the subgingival temperature. Local an-
Effect of Smoking on the Immune System esthetic-induced vasoconstriction takes a longer time to
Smoking downregulates the immune response to bacte- recover. Also, human gingival fibroblast can bind and
rial challenge. Numerous functions of oral or peripheral internalize nicotine, releasing it unmetabolized.
neutrophil are negatively affected by smoking or nicotine Smoking may also have a direct effect on connective
exposure, including chemotaxis, phagocytosis, superoxide tissue and bone. The detection of nicotine and its major
and hydrogen peroxide generation, integrin expression, and metabolite, cotinine, in the saliva, crevicular fluid, se-
protease inhibitor production. Alterations in gingival ere- rum, and urine demonstrates their systemic availability.
vicular fluid and peripheral blood mononuclear cell levels These substances also rapidly penetrate epithelium and
of various cytokines in smokers, tipping the balance in favor exert effects on fibroblasts. Toxic substances from tobacco
of tissue breakdown, have been noted. Smoking decreases can coat root surfaces of periodontally involved tooth in
salivary IgA and serum IgG, and specifically reduces IgG2 smokers and thereby interfere with postsurgical heal-
to A. actinomycetemcomitans. The ability of tobacco products ing. Nicotine can suppress osteoblast proliferation while
to decrease the proliferative capacity of T and B lympho- stimulating alkaline phosphatase activity.
cytes might contribute to this diminished production of
protective antibodies against periodontal pathogens.
Local Effects of Nicotine
In contrast, smokers demonstrate the elevated levels High nicotine concentration negatively affects the
of TNF-a, PGE2, neutrophil elastase, and matrix metal- exposed oral tissues in smokers. High concentrations
loproteinase-8 in the gingival crevicular fluid. In vitro (300 times) of nicotine are found in gingival crevicular
studies also have demonstrated that exposure to nicotine fluid compared with plasma concentrations in smokers
increases the secretion of PGE2 by monocytes in response (20 ng/mL). Impaired revascularization during wound
to lipopolysaccharide. healing of soft and hard tissues after periodontal therapy
These data suggest that smoking may impair the re- in smokers is evident due to local vasoconstriction effect
sponse of neutrophils to periodontal infection and may on gingival blood vessels. Nicotine alters the attachment
CH A PT ER 12 SM O KIN G A N D TH E PERIO D O N T IU M 91
of fibroblast and expression of integrin, by binding itself the defect and more episode of guided tissue regeneration
to root surface in smokers. It also increases the collagenase (GTR) membrane exposure.
and decreases collagen production. The periodontal liga- At recession sites when expanded polytetrafluoroeth-
ment (POL) fibroblast showed the reduced attachment to the ylene membranes (ePTFE) were utilized in GTR proce-
root surfaces of teeth extracted from the smokers. dures, smokers had significantly less root coverage (57%)
compared with nonsmokers (78%). There was no differ-
ence between smokers and nonsmokers in the treatment
RESPONSE TO PERIODONTAL
outcome of recession defects when defects were treated
THERAPY IN SMOKERS
with a coronally repositioned flap alone or with a bioab-
There is increasing evidence that there is less favor- sorbable membrane.
able response to periodontal therapy in smokers than in
Implant Therapy
nonsmokers.
The impact of smoking on implant success is unclear
Non surgical Therapy at present. Smokers demonstrate at least twice as many
failed implants as shown by the majority of studies. In
Current smokers demonstrate 50-75% clinical improve-
majority of cases implant failures occurred during the
ment compared with nonsmokers following nonsurgical
healing period before the delivery of prosthesis. No dif-
and surgical periodontal therapies. Gain in clinical at-
ference was found after the prosthesis was delivered in
tachment as a result of scaling and root planing is less
smokers and nonsmokers. The implants placed in the
pronounced in smokers. There is significantly greater
maxillary arch are more negatively affected than in the
average reduction in pocket depth and bleeding on prob-
mandible in smokers. For the long-term implant success,
ing in nonsmokers.
patients should be informed about the potential risk of
Antimicrobial Therapy smoking and implant failure and also advised of the ben-
Subgingival periodontopathogens are more difficult efits of smoking cessation.
to eliminate in smokers following mechanical therapy.
Thus, adjunctive use of antimicrobial therapy is recom- Maintenance Therapy
mended in smokers. When scaling and root planing is The effect of smoking on maintenance therapy was
used in combination with topical subgingivally placed seen to be detrimental and long lasting. It was found
local drugs, the smokers continue to show less pocket that when patients were evaluated each year, smokers
reduction than nonsmokers. consistently had deeper pockets and less gain in attach-
These enhanced results might be the result of antimi- ment than nonsmokers even with the similar plaque score.
crobial actions of adjunctive use of systemic amoxicil-
lin and metronidazole or locally delivered minocycline
microspheres, and anticollagenase activity in the case of
RECURRENT PERIODONTAL DISEASE
tetracycline derivatives following mechanical therapy in
Because of the hazardous effects of smoking on peri-
smokers.
odontitis, smokers become refractory to traditional peri-
Surgical Therapy odontal treatment and tend to show more periodontal
breakdown than nonsmokers. As a result, they continue
Open Flap Debridement to have progressive or recurrent periodontitis leading to
Open flap debridement surgery without regenerative tooth loss.
or grafting procedures is the most common surgical pro-
cedure used for accessing the root and osseous surfaces. TOBACCO USE CESSATION
Improvement in clinical attachment levels is less evident
in smokers following open flap debridement surgery with Impact of Smoking Cessation
initial probing depths "2.7 mm.
Smoking cessation reduces the rate of attachment loss
Soft and Hard Tissue Grafting and bone loss, and the severity of the diseases is intermedi-
The results of regenerative therapy in smokers are det- ate to nonsmokers and current smokers. Former smokers
rimental in interproximal and furcation defects, whether respond in a manner similar to nonsmokers for periodontal
treatment includes bone grafts alone, membranes alone, therapy. The changes in the probing depth and clinical at-
or combination of bone graft with membranes. Smokers tachment level were not related to the year since cessation
demonstrate significantly less improvement in probing when smoking quitted more than 1 year prior to the peri-
depth reduction and less attachment gain compared with odontal therapy. Similarly, success rates of implant placed
nonsmokers. Smokers show significantly less bone fill of in past smokers are similar to those for nonsmokers.
Role of Dental Health Professionals The brief intervention program is to offer information,
encouragement, and support to patients and to provide
Tobacco use intervention in the dental office involves information about resources that may help the patient
many possible approaches ranging from brief interven- become tobacco free.
tions to comprehensive cessation programs. These ser-
vices can include identifying patient tobacco use status,
supporting abstinence, and advising and preparing users Nicotine Replacement Therapy
to stop and to remain tobacco free for future, in addition
In the 1980s nicotine replacement therapies were in-
to offering cessation treatment.
troduced for tobacco cessation. The first-line therapies
The Agency for Health Care Research and Quality has
included the US Food and Drug Administration (FDA)-
recommended a brief intervention, five-step approach,
approved nicotine chewing gum, nicotine lozenges, nico-
known as the five A's for smoking cessation. This model
tine patches as over-the-counter products, and nicotine
includes the following:
nasal sprays and nicotine inhalers (require prescriptions)
1. Ask - systematically identifying the tobacco use status for use in patients who are attempting cessation. Sus-
of all patients tained-release bupropion, a non-nicotine medication, is
2. Advise - strongly advising to stop the use of tobacco also approved for tobacco cessation pharmacotherapy.
products In higher doses, bupropion is used as an antidepressant.
3. Assess - evaluating the patient's willingness to quit These medications have been proven safe and effective.
4. Assist - offering assistance in quitting The second-line pharmacotherapies include clonidine
5. Arrange - following up on the patient's cessation ef- and nortriptyline for cessation therapy. They have more side
forts, especially early in the process. effects and are not approved at this time by the US FDA.
KEY POINTS
• Smokers are almost three times as likely to have severe for periodontal plastic, regenerative, and implant
periodontitis as nonsmokers. procedures.
• Effect of smoking on the host is reversible with smoking • Gain in clinical attachment as a result of scaling and root
cessation. planing is less pronounced in smokers.
• Smoking impairs various aspects of the primary and • Tobacco use cessation does not reverse the past effects
secondary immune responses. of smoking, but there is abundant evidence that the rate
• Gingival blood flow is impaired due to the vasoconstric- of bone and attachment loss slows after patients quit
tive property of nicotine. smoking.
• Smoking affects the revascularization during soft
and hard tissue wound healing, which is critical
QUESTIONS 2. Kinane OF, Chestnutt IG. Smoking and periodontal disease. Crit Rev
Oral Biol Med 2000;11(3):356-65.
3. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant
1. Describe the effects of smoking on periodontal healing. Dentistry. 5th ed. Oxford: Blackwell Munksgaard; 2008. p. 316-322.
2. Describe the effects of smoking on pathogenesis 4. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds.
of periodontal disease. Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B.
3. Describe smoking as a risk factor in periodontics. Saunders Company; 2006.
5. Seymour RA, Heasman PA, Macgregor IDM. Drugs, Disease, and the
4. Describe nicotine replacement therapy.
Periodontium. New York: Oxford University Press; 1992.
Suggested readings
1. Johnson GK, Hil M. Cigarette smoking and the periodontal patient.
J Periodontol 2004;75:196-209.
CHAPTER
13
Trauma from Occlusion
Trauma from occlusion (TFO) has been linked with peri- is still not completely understood. In spite of these con-
odontal disease for many years. However, despite extensive troversies, thorough knowledge of the effect of traumatic
research over many decades, the role of occlusion in the occlusion on the periodontium is useful in the clinical man-
etiology and pathogenesis of inflammatory periodontitis agement of periodontal diseases.
HISTORY DEFINITION AND TERMINOLOGY
For decades there has been disagreement about the "Trauma from occlusion" is the term used to describe
role of abnormal occlusal forces in initiating periodontal pathologic alteration or adaptive changes that develop in
disease. It is generally accepted that occlusal traumatism the periodontium as a result of undue forces produced by
can be distinct pathologic entity associated with peri- masticatory muscles.
odontitis, and that related tissue changes are microscopic, Damage in the periodontium is caused by stress on
noninflammatory, and limited to attachment apparatus. the teeth produced directly or indirectly by teeth of the
When occlusal traumatism is associated with periodonti- opposing jaw (WHO, 1978).
tis, however, controversy arises. Can occlusal traumatism An injury to the attachment apparatus is a result of
initiate gingivitis or periodontitis? Does it modify the excessive occlusal force ( Glossary of Periodontic Terms, AAP,
response to local irritants that are primary etiologic fac- 1986). Trauma from occlusion is therefore the tissue injury,
tor, or is the joint occurrence of occlusal traumatism and not the occlusal force. An occlusion that produces such
periodontitis merely coincidental? Many attempts, some injury is called traumatic occlusion (Carranza, 2006).
excellent, have been made to resolve the controversy, yet
much of the argument supporting the various hypotheses Synonyms
is still based on empiricism. Further study must be carried
• Occlusal trauma (Muhleman 1961)
out to fill the serious gaps remaining in our knowledge
• Traumatogenic occlusion (Box 1930)
of this relationship.
• Periodontal traumatism
Occlusal traumatism is only one of the many terms
• Overload
used to denote injury to periodontium by forces of oc-
• Traumatizing occlusion.
clusion.
The term "traumatic occlusion" introduced by Stillman Occlusal forces affect the condition and structure of
denoted abnormal stress capable of producing injury to the periodontium. Periodontal health is not a static state.
dental or periodontal tissue. It depends on a balance between an internal systemic
Box advocated use of the term "traumatogenic occlu- control milieu that governs periodontal metabolism and
sion" for this stress and traumatic occlusion for the func- the external environment of the tooth of which occlusion
tional contact relationship of the occlusion that is the is an important component.
direct result of this trauma, e.g., a disturbed occlusion To remain structurally and metabolically sound,
resulting from tooth displacement in jaw fracture. the periodontal ligament and alveolar bone require
the mechanical stimulation of occlusal forces. An internal over short intervals have essentially the same resorbing
"margin of safety" common to all tissues permits some affect as constant pressure.
variation in occlusion without the periodontium being
adversely affected. However, when function is insuf-
ficient, the periodontium atrophies, and when occlusal
forces exceed the adaptive capacity of the tissues, they TYPES OF OCCLUSAL FORCES
are injured. The injury is called TFO.
• Physiologically normal occlusal forces: These are forces
that do not exceed SN and help to provide positive
PHYSIOLOGIC ADAPTIVE stimulus for periodontal ligament homeostasis.
CAPACITY OF PERIODONTIUM • Impact forces: These are forces high in magnitude but
TO OCCLUSAL FORCES last for shorter duration; however these forces exceed
the adaptive capacity of the periodontium resulting in
When there is an increased functional demand, the injury.
periodontium tries to adapt. The adaptive capacity var- • Continuous forces: These are very low forces; e.g.
ies in different persons as well as in the same person at orthodontic forces which are continuously applied
different times. The effect of occlusal forces upon the and cause selective remodeling of the bone.
periodontium is influenced by the magnitude of occlusal • Jiggling forces: These are most harmful forces to the
forces, direction frequency, and duration. periodontium and are intermittent multidirectional
When the magnitude of occlusal forces is increased, forces.
the periodontium responds by a thickening and increase
in the fibers in the periodontal ligament and an increase
in the density of alveolar bone. OCCLUSAL FORCES
Changing the direction of occlusal forces causes a re- AND JAW MOVEMENT
orientation of the stresses and strains within the peri-
odontium. • The forces exerted on the teeth during jaw movements
Principal fibers of the periodontal ligament are ar- such as chewing, swallowing and the performance
ranged so that they can best accommodate occlusal forces of parafunctional habits, including bruxism and
in long axis of tooth. When axial forces are increased, clenching, are well tolerated by the tooth supporting
there is viscoelastic distortion of periodontal ligament structures.
and ultimate compression of periodontal fibers and re- • The forces exerted on teeth during these contacts are
sorption of bone in the apical area. The fibers in relation of low magnitude, averaging 81 N lasting during small
to remainder of root are placed under the tension, and time period (20-50 ms).
new bone is formed. • At final closure in intercuspal position, the forces are
In designing dental restorations and prosthesis, every much higher, averaging 262 N for relatively longer
effort is made to direct occlusal forces axially to benefit duration of time (115 ms).
from the greater tolerance of the periodontium to forces • The occlusal forces during swallowing in intercuspal
in this direction. position are averaging around 296 N for duration of
Lateral or horizontal forces are ordinarily accommo- about 700 ms (Gibbs et al 1981).
dated by bone resorption in the areas of tension. The most
advantageous point of application of a lateral force is near So, when the occlusal forces exceed the adaptive capac-
the cervical line. As the point of application is moved ity of peridontium resultant injury occurs.
coronally, the distance from the center of rotation or lever
arms is lengthened, and force on the periodontal ligament
increases.
CLASSIFICATION OF TRAUMA
Torques or rotational forces cause both tension and
FROM OCCLUSION
pressure, which, under physiologic condition, result
in bone formation and bone resorption, respectively.
Acute and Chronic Trauma from Occlusion
Torques are the type of forces most likely to injure the
periodontium. Primary, secondary, and combined occlusal trauma
Duration and frequency affect the response of alveo- were originally described in the periodontal literature
lar bone to occlusal forces. Constant pressure on some in 1928 by Box.
causes resorption, whereas intermittent forces favor bone Trauma from occlusion may be acute or chronic.
formation. The time lapse between pressure applications Acute TFO results from an abrupt occlusal impact such
apparently influences the bone response. Recurrent forces as that produced by biting a hard object (e.g., stone,
C H A PT ER 13 T R A U M A FR O M O C C LU SIO N 95
olive pip). In addition, restorations or prosthetic appli- excessive occlusal forces can be superimposed are as
ances that interfere with or alter the direction of occlusal follows:
forces on the teeth may induce acute trauma. The results
1. Normal periodontium with normal height of bone
are tooth pain, sensitivity to percussion, and increased
2. Normal periodontium with reduced height of bone
tooth mobility. If the force is dissipated by shift in the
3. Marginal periodontitis with reduced height of bone.
position of the tooth or by wearing away or correction
of the restoration, the injury heals, and the symptoms The first is an example of primary occlusal trauma,
subside. Otherwise, periodontal injury may worsen whereas the last two represent secondary TFO.
and develop into necrosis, accompanied by periodontal
abscess formation, or persist as a symptom-free chronic
condition. Acute trauma can also produce cementum ETIOLOGY OF TRAUMA
tear. FROM OCCLUSION
Chronic TFO is more common than the acute form
and is of greater clinical significance. It most often de- Precipitating Factors
velops from gradual changes in occlusion produced by
Destructive occlusal force (primary etiologic agent)
tooth wear, drifting movement, and extrusion of teeth,
combined with a parafunctional habit such as brux- • Magnitude of occlusal forces: When the magnitude of
ism and clenching, rather than as a sequela of acute occlusal forces exceeds the normal range of forces for a
periodontal trauma. Chronic TFO can be primary or tooth, due to natural adaptive response, some changes
secondary. can be appreciated in the periodontal ligament. There is
widening of periodontal ligament (POL) space, increase
in the number of POL fibers, increase in the width of POL
Primary and Secondary Trauma from Occlusion fibers and increase in the density of alveolar bone.
Trauma from occlusion may be caused by alterations in • Direction of force application: Direction of occlusal
occlusal forces, reduced capacity of the periodontium to forces is changed; principal fibers are not able to
withstand occlusal forces, or both. When TFO is the result efficiently bear the forces hence injury results.
of alteration in occlusal forces, it is called primary TFO. • Duration offorce application: If the abnormal occlusal
In primary TFO, the primary etiologic factors are local forces are subjected to a tooth for a long duration of
alterations in the occlusion due to the following: time, they cause injury to periodontal tooth supporting
structures.
1. the insertion of a high filling; • Frequency of force application: Frequent application
2. the insertion of a prosthetic replacement that creates of abnormal occlusal forces results in more damage to
excessive forces on abutment and antagonist teeth; the periodontal tooth supporting structures than less
3. the drifting movement or extrusion of teeth into spaces frequent application.
created by unreplaced missing teeth; or
4. the orthodontic movement of teeth into functionally
unacceptable position. Changes produced by Predisposing Factor
primary trauma do not alter level of connective tissue Intrinsic Factor
attachment and do not initiate pocket formation
• Orientation of long axis of the teeth in relation to forces
because supracrestal gingival fibers are not affected
to which they are exposed.
and therefore prevent apical migration of the junctional
• Morphological characteristics of the roots. The size,
epithelium.
shape and the number of the roots determine how
Secondary TFO occurs when the adaptive capacity of occlusal forces are dissipated.
the tissues to withstand occlusal forces is impaired by • In general short, conical, slender or fused roots are
bone loss resulting from marginal inflammation. This more vulnerable to TFO.
reduces the periodontal attachment area and alters the • The morphology of the alveolar process, i.e. the quality
leverage on the remaining tissues. The periodontium and the quantity of the alveolar bone play an important
becomes more vulnerable to injury and previously well- role in absorbing the occlusal forces.
tolerated occlusal forces become traumatic.
Combined occlusal trauma refers to injury resulting Extrinsic Factor
from abnormal occlusal forces applied to a tooth or teeth • Local factors such as plaque which predisposes to the
with inadequate periodontal support. Trauma from oc- alveolar bone loss.
clusion may be caused by alterations in occlusal forces, • Long span bridges on few teeth.
reduced capacity of the periodontium to withstand oc- • Injudicious bone resection during surgical periodontal
clusal forces, or both. Three different situations by which therapy or oral surgical procedures.
• Parafunctional habits as a result of neurosis. tude are acting on teeth harboring subgingival plaque.
• Other factors include: food impaction, overhanging This would imply that the character of the progressive
fillings, poorly contoured crowns and bridges and ill- tissue destruction of the periodontium at a "traumatized
fitting partial dentures. tooth" will be different from that characterizing a "non-
traumatized" tooth. Instead of an even destruction of
the periodontium and alveolar bone (suprabone pockets
TRAUMA FROM OCCLUSION and horizontal bone loss), which according to Glickman
AND PLAQUE ASSOCIATED occurs at sites with uncomplicated plaque-associated le-
PERIODONTAL DISEASE sions, sites which are also exposed to abnormal occlusal
force will develop angular bony defects and infrabony
• Karolyi (1901) postulated that an interaction may pockets.
exist between "trauma from occlusion" and "alveolar Since the concept of Glickman regarding the effect of
pyorrhea." He implied a cause and effect relationship TFO on the spread of the plaque-associated lesion is often
between traumatic occlusion and periodontal disease cited, a more detailed presentation of this theory seems
progression. pertinent compared with "Waerhaug's concept" of what
• Box (1935) and Stone (1938) reported experiments autopsy studies have revealed regarding TFO and peri-
in sheep and monkey, the result of which seemed to odontal disease. The periodontal structure can be divided
indicate that "trauma from occlusion is an etiologic into two zones:
factor in production of the variety of periodontal
1. the zone of irritation and
disease in which there is vertical pocket formation
2. the zone of codestruction (Fig. 13.1).
associated with one or a varying number of teeth"
(Stones 1938).
Zone of Irritation
Brain Teaser
The zone of irritation includes the marginal and inter-
• Does occlusal trauma play an important role in etiology
dental gingiva. The soft tissue of this zone is bordered
of periodontal disease?
by hard tissue (the tooth) only on one side and is not
if so affected by forces of occlusion. This means that gingival
• Should occlusal therapy be considered for periodontally
inflammation cannot be induced by TFO but is the result
compromised dentition?
of irritation from microbial plaque. The plaque-associated
The answer to the key question does occlusal trauma lesion at a "nontraumatized" tooth propagates in apical
play an important role in etiology of periodontal disease, direction by first involving the alveolar bone and only
will determine the following: later the periodontal area. The progression of this lesion
results in an even (horizontal) bone destruction.
• Whether plaque-induced inflammation is influenced
by occlusal forces, and
• Whether destruction of the periodontium is enhanced
by occlusal forces.
Research studies designed to examine the effects of
occlusion fall into three categories:
• Human cadaver investigations -
0 C
0
Q).::;
• Animal studies -c
0 0 c.'!!
Q) .::; o·~
• Human clinical studies. c.!!! N .:
0 ·t:
N .=:
HUMAN CADAVER INVESTIGATIONS
• Studies published in the 1960s and 1970s were

C
inconclusive (Glickman 1962 and Waerhaug 1979). C:
0
,Q
n::, 0
::,
0~ 0~
Q) Q)
Q) Q) C -0
C -0 0 0
GLICKMAN'S CONCEPT 0 0
No No
Glickman and Smulow (1965, 1967) claimed that the A B

pathway of the spread of a plaque-associated gingival FIGURE 13.1 Zones of irritation and codestruction in periodontal
lesion can be changed if forces of an abnormal magni- disease: (A) facial or lingual surfaces; (B) interproximal area.
Zone of Codestruction according to Waerhaug, exclusively the result of inflam-

matory lesions associated with subgingival plaque.
The zone of codestruction includes the periodontal He concluded that angular bony defect and infrabony
ligament, the root cementum, and alveolar bone and is pockets occur when the subgingival plaque of one tooth
coronally demarcated by the transseptal (interdental) and has reached a more apical level than the microbiota on the
the dentoalveolar collagen. neighboring tooth, and when the volume of the alveolar
The tissue in this zone may become the seat of a lesion bone surrounding the roots is comparatively large.
caused by TFO. The fiber bundles that separate the zone
of codestruction from the zone of irritation can be affected
from two different directions: ANIMAL STUDIES
• from the inflammatory lesion maintained by plaque in Two popular animal studies have been described in
the zone of irritation and Table 13.1.
• from trauma-induced changes in the zone of
codestruction.
Inf ere nee from Animal Studies
Due to this exposure from two different directions the
It must be mentioned that animal studies did not reach
fiber bundles may become dissolved and/ or oriented into
some definitive conclusions, due to differences in experi-
a direction parallel to the root surface.
mental setup and different animal models. The results of
The spread of an inflammatory lesion from the zone
experimental animal studies cannot therefore be directly
of irritation directly down into the periodontal ligament
extrapolated to the human settings.
may hereby be facilitated. This alteration of the "normal"
pathway of spread of the plaque-associated inflammatory • Trauma from occlusion does not initiate gingivitis.
lesion results in the development of angular bony defects. • Trauma from occlusion does not initiate connective
Glickman (1967) stated that TFO is an etiologic factor, tissue attachment loss.
where angular bony defects combined with infrabony • Occlusion may play a secondary role in progression
pockets are found at one or several teeth. of periodontal disease.
• Inflammation should be removed initially and
potential occlusal factors subsequently reevaluated.
Waerhaug's Concept
• Healing following surgical treatment of periodontal
Waerhaug examined similar autopsy specimens as disease may be more advantageous in immobile than
Glickman, but measured in addition the distance between in mobile teeth.
the subgingival plaque and (i) the periphery of the associ-
ated inflammatory cell infiltrate in the gingiva and (ii) the Disadvantages of Animal Studies
surface of the adjacent alveolar bone.
Animal studies did not reach the same definitive con-
He concluded from his analysis that angular bony de-
clusions, due to:
fects and infrabony pockets occur equally often at peri-
odontal sites of teeth that are not affected by TFO as in • Differences in experimental setup and different
traumatized teeth. In other words, he refuted the hypoth- animal models.
esis that TFO played a role in the spread of gingival lesion • The results of experimental animal studies cannot
into the "zone of codestruction." The loss of connective therefore be directly extrapolated to the human
attachment and the resorption of bone around teeth are, situation.
TABLE 13.1 Comparison Between Two Popular Animal Studies
Variables Rochester group (Polson and coworkers 1976) Gothenburg group (Lindhe and coworkers 1974)
Animal Squirrel monkeys Beagle dogs
Follow-up period • 10 Weeks • 1 Year
Results • Occlusal trauma does not influence periodontal • Occlusal trauma could accelerate the progression of
disease progression periodontal disease
• No evidence of attachment loss in the presence of • They found evidence of attachment loss when plaque
plaque and occlusal forces and occlusal forces were both present
Conclusion • Adaptive changes in response to occlusal trauma can • In the presence of reduced healthy periodontium,
be largely reversible if inflammation is controlled occlusal trauma will not produce loss of attachment
• Occlusal trauma can cause bone loss • Ability of the periodontium to adapt to occlusal trauma
maybe inhibited in the presence of inflammation
HUMAN TRIALS
Given the complexity of the occlusal and periodontal

interaction and the multifactorial aspect of the pathology,
very few human studies have been published. Most stud-
ies have a limited number of subjects and the results are
analyzed on a subject basis rather than on a tooth basis.
Shefter et al 1984 and Pihlstrom, 1986: studied associa-
tion of occlusal trauma and periodontitis, teeth in patients
40
with occlusal disharmonies (centric relation-centric oc-
clusion, balancing; or protrusive contacts). But he did not I
demonstrate any greater severity of periodontitis when 20 I
compared to teeth without such contacts. I...,_
Bone resorption I
The studies have been recently summarized by Hall- lo--Bone formation I
mon (Hallmon 1999). A number of cross-sectional epide-
1 7 14 28 60 120
miologic studies found either no relationship between
the presence of premature contacts and increased probing
depth or bone loss, while others reported that mobil- FIGURE 13.2 Diagrammatic representation of various stages of tis-
sue response from occlusion (Source: Newman MG, Takei H, Carranza FA.
ity and radiographic evidence of a widened periodontal Clinical Periodontology. 10th ed. Philadelphia: Saunders; 2006).
ligament were associated with increased pocket depth,
attachment loss and bone loss (Jin & Cao 1992) (more
recent longitudinal studies). if the offending force is chronic, the periodontium is remod-
Harrel and Nunn (2001) found that teeth with prema- eled to cushion its impact. This ligament is widened at the
ture contacts at initial examination had a deeper probing expense of the bone, resulting in angular bone defects with-
pocket depth, an increased mobility, and a worse progno- out periodontal pockets, and tooth becomes loose.
sis. At the 1 year examination, teeth without premature Under the forces of occlusion, a tooth rotates around a
contacts originally, or teeth where premature contacts had fulcrum or axis of rotation, which in single-rooted teeth
been removed, showed a 66% reduced chance of a wors- is located in the junction between the middle and apical
ening periodontal situation. After a few months, teeth third of the clinical root. This creates areas of pressure and
with prematurities showed an increased probing depth tension on opposite sides of the fulcrum. Different lesions
compared with the teeth receiving occlusal adjustment. It are produced by different degrees of pressure and tension.
was concluded that premature contacts are a "catalyst" in If jiggling forces are exerted, these different lesions may
the progression of periodontal disease (Klineberg 2004). coexist in the same area.
Slightly excessive pressure stimulates resorption of al-
Conclusion from Human Trials veolar bone, with a resultant widening of the periodontal
ligament space. Slightly excessive tension causes elonga-
• Trauma from occlusion can have an effect on the tion of the periodontal ligament fibers and apposition of
supporting tissues of the teeth. alveolar bone. In areas of increased pressure, the blood
• There is NO consistent report at present that reveals vessels are numerous and reduced in size, while in areas
that traumatic occlusion is an etiological factor in of increased tension, they are enlarged.
human periodontitis. Greater pressure produces a gradation of changes in
the periodontal ligament, starting with compression of
fibers, which produces areas of hyalinization. Subsequent-
TISSUE RESPONSE TO INCREASED
ly, injury to the fibroblast and other connective tissue
OCCLUSAL FORCES (FIG. 13.2)
cells leads to necrosis of the areas of ligament. Vascular
changes are also produced: within 30 min, retardation
Stages of Tissue Response
and stasis of blood flow occur; at 2-3 h, blood vessels
Tissue response occurs in three stages: injury, repair, appear to be packed with erythrocytes that start to frag-
and adaptive remodeling of the periodontium. ment; and between 1 and 7 days there is disintegration of
blood vessel walls and release of contents to surrounding
Stage I: Injury tissue. In addition, increased resorption of alveolar bone
This stage involves tissue injury produced by excessive and resorption of tooth surface occurs.
occlusal forces. The body then attempts to repair the injury Severe tension causes widening of the periodontal liga-
and restore the periodontium. This can occur if the forces are ment, thrombosis, hemorrhage, tearing of the periodontal
diminished or if the tooth drifts away from them. However, ligament, and resorption of alveolar bone.
Pressure severe enough to force the root against bone The injury phase shows an increase in areas of re-
causes necrosis of the periodontal ligament and bone. The sorption and a decrease in bone formation, whereas the
bone is resorbed from viable periodontal ligament adja- repair phase demonstrates decreased resorption and
cent to necrotic areas and from marrow spaces, a process increased bone formation; after adaptive remodeling
called undermining resorption. of the periodontium, resorption and formation return
The area of the periodontium most susceptible to injury to normal.
from excessive occlusal forces is the furcations.
Injury to the periodontium produces a temporary de-
pression in mitotic activity and rate of proliferation and CLINICAL EPIDEMIOLOGIC STUDIES
differentiation of fibroblast, in collagen formation, and
in bone formation. These return to normal levels after Given the complexity of the occlusal and periodontal
dissipation of the forces. interaction and the multifactorial aspect of the pathol-
ogy, very few human studies have been published. Most
Stage II: Repair studies have a limited number of subjects and the results
Repair is constantly occurring in the normal periodon- are analyzed on a subject basis rather than on a tooth ba-
tium and TFO stimulates increased reparative activity. sis. The studies have been recently summarized by Hall-
The damaged tissues are removed, and new connective mon. A number of cross-sectional epidemiologic studies
tissue cells and fibers, bone, and cementum are formed found no relationship between the presence of prema-
in an attempt to restore the injured periodontium. Forces ture contacts and increased probing depth or bone loss,
remain traumatic only as long as the damage produced while others reported that mobility and radiographic
exceeds the reparative capacity of the tissues. evidence of a widened periodontal ligament were associ-
When bone is resorbed by excessive occlusal forces, ated with increased pocket depth, attachment loss, and
the body attempts to reinforce the thinned bony trabecula bone loss. More recent longitudinal studies found that
with new bone. This attempt to compensate for lost bone teeth with premature contacts at initial examination had
is called buttressing bone formation and is an important a deeper probing pocket depth, an increased mobility,
feature of the reparative process associated with TFO. It and a worse prognosis. At the 1-year examination, teeth
also occurs when bone is destroyed by inflammation or without premature contacts originally, or teeth where
osteolytic tumors. premature contacts had been removed, showed a 66%
Buttressing bone formation occurs within the jaws reduced chance of a worsening periodontal situation.
(central buttressing) and on the bone surface (peripheral After a few months, teeth with prematurities showed
buttressing). In central buttressing the endosteal cells an increased probing depth compared with the teeth
deposit new bone, which restores the bony trabecula receiving occlusal adjustment. It was concluded that
and reduces the size of the marrow spaces. Peripheral premature contacts are a "catalyst" in the progression
buttressing occurs on the facial and lingual surfaces of of periodontal disease (Klineberg 2004).
the alveolar plate. Depending on its severity, periph-
eral buttressing may produce a shelf-like thickening
of the alveolar margin, referred to as lipping or a pro- EXAMINATION AND DIAGNOSIS
nounced bulge in the contour of the facial and lingual OF TRAUMA FROM OCCLUSION
bone.
Diagnosis requires an understanding of the entire mas-
Stage III: Adaptive Remodeling tica tory system. A comprehensive patient history and
of the Periodontium examination is also needed. This includes
If the repair process cannot keep pace with the destruc-
• Review of detailed health questionnaire
tion caused by occlusion, the periodontium is remodeled
• An occlusal analysis evaluating the occlusal scheme,
in an effort to create a structural relationship in which the
tooth contact relationship, tooth mobility, fremitus,
forces are no longer injurious to the tissues.
percussion, attrition and the integrity of the arches,
This results in a thickened periodontal ligament, which
and restoration
is funnel shaped at the crest, and angular defects in the
• A radiographic analysis focusing on the integrity of the
bone, with no pocket formation. The involved teeth be-
lamina dura and the width of the periodontal ligament
come loose.
space
Increased vascularization has also been reported.
• An analysis of the temporomandibular joint (TMJ) and
The three stages in the evolution of traumatic lesions
masticatory musculature.
have been differentiated histometrically by means of the
relative amounts of periodontal bone surface undergoing Since TFO is a histologic lesion, clinical and radio-
resorption or formation. graphic indicators are necessary to assist in its diagnosis.
2. Widened periodontal ligament space (funneling or

saucerization) (Davies and Gray, 2001)
3. Bone loss (furcation, vertical circumferential)
4. Root resorption.
It should be understood that widening of periodon-
tal space and thickening of the lamina dura do not nec-
essarily indicate destructive changes. They may result
from thickening and strengthening of the periodontal
ligament and alveolar bone, which constitute a favor-
able response to increased occlusal forces (Carranza,
2006).
SIGNS OFTFO
Visual
Signs that can be seen in wear registration as transpar-
encies are points of contact, and not broad areas.
Excessively large areas of contact can also be detected
by using a variety of marketing materials such as carton
paper, tape, ribbon, or a dye.
Auditory
In centric relation, there is a distinct ringing sound
in maximum tooth contact with deflections present; the
FIGURE 13.3 Radiographic features of trauma from occlusion.
sound is dull or perceptible.
Tactile
Criteria for Early Diagnosis of Occlusal Trauma
In centric relation and in normal excessive movements,
Primary occlusal trauma can manifest itself clinically response to finger contact is smooth, with deflection pres-
in a subtle and inchoate manner, as a triad (Consolaro, ent; a roughness can be detected.
2012).
• Wear facets in areas of interference. Migration of Teeth
• Abfraction, especially in premolars.
• Mild V-shaped recession. Loss of interproximal contacts and migration of teeth
may be the sequela of traumatic occlusal relations. Un-
Clinical indicators of TFO may include one or more of usual habit pattern may cause tooth migration and TFO
the following (Fig. 13.3): beyond the function range of normal occlusal contacts.
1. Mobility
2. Fremitus
Mobility
3. Occlusion
4. Prematurities The most common clinical sign of trauma to peri-
5. Wear facets in presence of other clinical features odontium is increased tooth mobility. In injury stage
6. Tooth migration of TFO there is destruction of periodontal fibers, which
7. Fractured tooth/teeth will increase the mobility of the tooth. In the final stage
8. Thermal sensitivity. the accommodation of the periodontium to increased
forces entails a widening of the periodontal ligament,
Radiographic indicators of TFO may include one or
which also leads to increased tooth mobility. Although
more of the following (Fig. 13.3):
this tooth mobility is greater than the so-called normal
1. Discontinuity and thickening of lamina dura (Davies mobility, it cannot be considered pathologic because
and Gray, 2001) it is an adaptation and not a disease process. When it
progressively gets worse, it can be considered patho- contacts, as in the buccal surface of upper canines where
logic (Carranza, 2006). there is a steep lateral canine guidance. Those cervical
surfaces also show enamel abfraction. There is still con-
troversy regarding whether or not overload is an etiologic
Fremitus and Mobility factor in the recession, and consequently whether or not
the occlusion and the lateral guidance should be changed
The most arresting and obvious signs of trauma are
(Klineberg, 2004).
facets, fremitus, and mobility.
• Fremitus is an important tool.
Gingival Clefts
• Palpation and percussion are two methods used
routinely to check mobility. Gingival clefts are a combination of conditions caused
• Fremitus means palpable vibration or movements. A by toothbrush abrasion. This initially produces a linear
tooth with fremitus has excess contact, possibly related act injury that eventually develops into a gingival cleft.
to a premature contact. The test is used in conjunction Depending on the security of the conditions, clefts are
with occlusal analysis and adjustment. treated by curettage.
• Index finger is placed on each maxillary tooth at about
the cervical third, and patient is asked to click the
back teeth repeatedly. The degree recorded may be SYMPTOMS OF TFO
subjective but the following range has been suggested:
N: normal (without vibration or movement). Thermal Sensitivity
+: one-degree fremitus; only slight vibration can be
Trauma from occlusion produces pressure on venous
felt.
return leading to venous hyperemia, increased blood
++: two-degree fremitus; the tooth is clearly palpable
pressure in the pulp, and pain.
but movement is barely visible.
+++: three-degree fremitus; movement is clearly • The jaws are tired at the end of the day, more so on
observed visually. rising in the morning.
• A scratching or squeaky sound can be heard when the
teeth are pushed together.
Wear Patterns
Facets and abnormal wear patterns must be differenti- Habits
ated from attrition caused by a coarse diet.
Prematurities may initiate or perpetuate a habit pattern
• Shiny and irregular facets indicate tooth-to-tooth wear that is injurious to the periodontium.
that is associated with bruxism. Because of psychic tension, a patient continues to grind
• These worn and abraded teeth are invariably firm, with and clench his /her teeth.
no sign of mobility.
Muscle Hypertonicity
Gingival Recession Occlusal interferences are the main causes of muscle
At one time, gingival abnormalities, e.g., traumatic spasm and discomfort. The muscles of mastication, that is,
crescent that are cresent-shaped bluish-red zone of gin- the masseter and temporalis, but particularly pterygoids,
giva confined to about one-sixth of the circumference of should be inspected for hypertonicity and tenderness. This
the root recession, McCall festoons, and Stillman clefts, detects tooth-to-tooth or TMJ dysfunction or both. Sub-
were known as the cardinal signs of traumatic occlusion. luxation and crepitus in the TMJs associated with muscle
The mechanism of causing gingival recession was spasm are frequently caused by cuspal interferences.
never demonstrated.
Gingival recession may be provoked by direct con-
Loosening Teeth
tact of the teeth with the gingiva, as in severe overbite,
where the upper incisors damage the buccal gingiva of the In advanced conditions, the patient becomes aware of
lower incisors. This problem is not easy to solve and may the loosening teeth and may complain of soreness and
involve orthodontic treatment, orthognathic surgery, or tenderness in some areas.
extensive prosthetic rehabilitation requiring an increase in Pain in the jaw and TM regions are usually diagnostic
vertical dimension. It has been stated that gingival reces- of condyle displacement induced by occlusal interfer-
sion occurs with functional overload and/ or premature ences.
Effects of Excessive Occlusal Forces LATEST ADVANCES IN EVALUATION

on Dental Pulp OF OCCLUSAL STRESSES IN THE
PERIODONTAL TISSUES
Complete calcification of the pulpal canal may occur
in cases of long-standing severe trauma or may be seen • Photoelastic stress analysis, animal studies, math-
following a single serious traumatic accident to the tooth ematical models, laser holography and strain gauzes,
resulting in gross disturbances of the circulation. or Peizo electric transducers techniques are the ear-
lier methods of stress analysis. The recent intro-
Effects of Insufficient Occlusal Forces duction of finite element analysis (FEA) has made
(Hypofunction) possible the assignment of physical characteristics
to all tissues in complex dental-periodontal models.
Insufficient occlusal forces may also be injurious to the Stresses following the application of occlusal load
supporting periodontal tissue. can be calculated at multiple points throughout the
Insufficient stimulation causes thinning of the peri- structure.
odontal ligament, atrophy of the fibers, osteoporosis of the • Reddy and Vandana (2005) conducted a study to
alveolar bone, and reduction in bone height. Hypofunc- calculate the stress produced in the periodontium
tion can result from an open bite relationship, an absence at different bone levels under occlusal load and
of functional antagonists, or unilateral chewing habits that demonstrated maximum stress in the tooth was seen
neglect one side of the mouth. at the cervical region and to a greater extent at the apex
for all the models.
• In periodontal ligament, maximum stress was seen
REVERSIBILITY OF at the alveolar crest in models with normal alveolar
TRAUMATIC LESION bone height and with reducing alveolar bone height
maximum stress was at the apex.
TFO is reversible; in experimental animals the tissues • There was no significant stress distribution in alveolar
undergo repair when impact of artificially created forces bone, while no stress was seen on the pulp. The results
is relieved. of the study demonstrated a significant increase in
Although TFO is reversible under such conditions, it stress concentration at the apex with loss of alveolar
does not always correct itself, and it is not always tempo- bone height.
rary and of limited clinical significance.
The T-Scan® is a diagnostic device that measures rela-
• The injurious force must be relieved for repair to occur. tive biting forces, including occlusal force, timing, and
• The presence of inflammation in the periodontium location and is an ideal complementor to articulating
as a result of plaque accumulation may impair the paper. The technology was invented by Dr William Ma-
reversibility of traumatic lesions. ness in 1987 at Tufts University and MIT.
TFO AND IMPLANTS TREATMENT
Endosseous implants have no periodontal ligament as 1. Occlusal adjustment

an intimate implant-alveolar bone contact exists ("func- 2. Coronoplasty
tional ankylosis"). Implant failure can occur not only 3. Occlusal bite planes
4. Orthodontics
because of bacterial infection (peri-implantitis) but also
because of occlusal overload (biomechanical failure) in 5. Permanent or temporary splint.
combination with immunological host factors (Esposito The treatment for periodontal TFO depends on what
et al., 1998). Occlusal overload results in "osseodisintegra- the etiology is. Primary TFO is usually treated by one or
tion" over the complete implant surface without clinically more of the above procedures.
detectable pocket formation or signs of inflammation. Of-
ten the implant has no increased mobility in spite of pro-
nounced bone resorption along its entire surface. Clinical PRACTICAL CLINICAL CONCLUSIONS
measurement of implant mobility is not an accurate tool AND GUIDELINES
for evaluating osseointegration or disintegration of an
implant until late in the pathologic process. If increased • In healthy dentition with adequate tooth support, the
implant mobility occurs, osseointegration is by then usu- hypermobility caused by trauma from occlusion can be
ally destroyed (Klineberg, 2004). corrected by elimination of highpoints, overhangs, or
restorative procedures. These simple approaches will

reduce the hypermobility to physiologic levels.
• In healthy dentition with reduced tooth support,
occlusal adjustments are considered along with splinting
of mobile teeth to improve its functional support.
• Elimination of plaque induced inflammation is a must
before initiating any kind of treatment.
• Minor occlusal corrections should be included in the
etiotropic phase as a part of initial therapy as it results
in gain in attachment levels.
• Removal of premature contacts should be considered
only if it improves the periodontal health of the tooth.
• If the teeth do not respond to conventional periodontal
therapy, occlusal analysis should be considered along
with microbiological testing and revaluation.
• Overloading of implants leads to alveolar bone FIGURE 13.4 Aesthetic disfiguration from pathologic tooth
migration.
resorption and pocket formation, hence evaluation of
implants in the recall visits is a must.
Terminology
Trauma from Occlusion in Etiology Physiologic Tooth Migration
and Treatment of Periodontal Disease The eruptive force of the permanent molars causes a
• TFO neither causes gingivitis or periodontitis nor closing of any existing spaces between primary molar
accelerates the process from gingivitis to periodontitis. and primate space. It is also known as mesial drifting of
• The periodontal ligament dampens the excessive forces the tooth.
but in turn leads to hypermobility of teeth or alveolar
crest resorption. Drifting
• Occlusal trauma should be considered as a cofactor, It is the movement of the teeth into the spaces created
microbial plaque being the primary etiologic factor. by unreplaced missing teeth; drifting does not result from
• Occlusal therapy should be considered only if mobility destruction of periodontal tissues.
interferes with patients comfort and function.
• Elimination of plaque induced inflammation is a Extrusion!Supraeruption!Overeruption
prerequisite for occlusal therapy and there is no It is the eruption of the tooth well beyond the occlusal
substitute to it. table.
Etiology
PATHOLOGIC MIGRATION
The main factors which influence tooth position
Pathologic tooth migration (PTM) is a common com- directly or indirectly (Fig. 13.5) are
plication of moderate to severe periodontitis and is often • tissues of the periodontium;
the motivation for patients to seek periodontal therapy. • occlusal factors;
It can result in severe dental disfiguration (Fig. 13.4) and
devastate a patient's self-esteem. Tooth migration is often
the cause for the patients to seek periodontal therapy. Granulation-.....,- --
tissue
Definition
Gingivall----~
Pathologic tooth migration is defined as a change in enlargement
tooth position that occurs when there is disruption of

forces that maintain teeth in a normal relationship. -Upperllp
Prevalence
Lowerllp---
The prevalence of pathologic tooth migration in peri- Habits----"-/
odontitis patients was found to be 55.8% in recent reports. FIGURE 13.5 Factors influencing tooth position.
FIGURE 13.6 Diagram of transseptal fiber chain connecting teeth.
• soft tissue pressures of the cheek, tongue, and lips; and FIGURE 13. 7 Diagram of posterior bite collapse.
• a variety of oral habits.
Besides this periodontal inflammation and eruptive
forces also influence tooth position. 3. Class II malocclusion.
4. Occlusal interferences: Disruptions such as
Destruction of Periodontal Supporting Tissues supraerupted teeth have been described as one of the
The transseptal fibers may play an especially impor- etiologic factors for PTM.
tant role in PTM which is confirmed by various primate 5. Anterior component of force: It is believed that a
studies. These fibers form a chain (Fig. 13.6) from tooth portion of occlusal forces is projected anteriorly during
to tooth and are thought to help maintain contacts be- mastication or functional occlusion and has been
tween teeth throughout the arch. It has been suggested termed the anterior component of force. It is seen that
that the displacement of the teeth can occur because of in presence of periodontal disease the continuity of this
the disturbance in the balance of forces if the continuity of chain is broken or weakened; there is disruption in the
this chain is broken or weakened by periodontal disease. balance of forces and this may lead to displacement of
the teeth.
Occlusal Factors 6. Protrusive pattern of mastication.
There are various occlusal factors related to the etiol- 7. Bruxism: Abnormal forces exerted in bruxism are
ogy of PTM as follows: known to damage the dental attachment apparatus.
Also, it is known that these forces are frequent and
• posterior bite collapse from loss of posterior teeth; of long duration. Therefore, it is easy to understand
• class II malocclusion; how bruxism in some patients can act as an unfavor-
• occlusal interferences; able orthodontic force to cause PTM. Bruxism and
• the anterior component of force; parafunctional occlusal habits may act as a contribut-
• protrusive functional patterns of mastication; ing factor for PTM, but there does not appear to be
• bruxism; and scientific data to support this.
• shortened dental arches. 8. Shortened dental arches: These arches are where most
posterior teeth are missing, which results in loss of
1. Posterior bite collapse (PBC): PBC is often associated molar support and function. In patients with more than
with anterior flaring; in addition to this there are many 40 years of age there is increased spacing seen which is
other etiologic factors that can cause tooth migration probably related to the flaring of tooth in patients with
in the absence of PBC (Fig. 13.7). posterior bite collapse.
2. Arch integrity: It is closely related to posterior bite
collapse. Occlusal forces are transferred to teeth in the In summary, many factors associated with occlusion
arch through interproximal contacts. Any destruction are related to PTM. Failure to consider occlusal factors in
or disturbances in these contacts can lead to tooth the etiology of PTM may cause treatment failure. In the
migration. Besides tooth loss, other factors that can patients who had lost a significant amount of alveolar
destroy interproximal contacts include dental caries, bone, occlusal factors still worsen the scenario of PTM.
faulty restorations, and severe attrition. Recently,
tooth loss has been significantly correlated with Soft Tissue Pressure of the Tongue, Cheek, and Lips
PTM, supporting earlier observations that loss of arch After loss of periodontal support soft tissue forces
integrity is an important factor in PTM. of the tongue, cheek, and lips can move teeth, which is
already being confirmed by orthodontic studies. It is be- • Clinical examination: presence of spacing between
cause of not just these forces but also the long duration the teeth, presence or absence of gingival recession,
that these very light forces are thought to be more impor- pus and exudation, tooth mobility, and associated
tant than the relative short duration of occlusal contacts periodontal pockets.
during speech, swallowing, and mastication.
Periodontal and Periapical Inflammation Treatment

Hirschfeld in the year 1933 described pathologic mi-
Interdisciplinary approach is very effective in treat-
gration as drifting of the teeth resulting from pressure of
ment of severe PTM. In such cases orthodontic therapy
inflammatory tissue in the pockets, whereas Sutton pro-
that is preceded by nonsurgical and surgical periodontal
posed that the blood vessels and inflamed tissue account
therapy and prosthodontic treatment are done. Correc-
for abnormal tooth migration.
tion of pathologic tooth migration can be divided into
four categories:
Extrusive Forces
They are not directly linked to PTM. However, since 1. Extraction followed by replacement of migrated teeth
extrusion of incisors is a very common form of PTM, it in cases of severe pathologic migration.
is thought that eruptive forces may play major role as a 2. Early institution of periodontal therapy results in
contributing factor in PTM. spontaneous correction of migrated teeth.
3. Adjunctive orthodontic treatment.
Habits 4. Conventional orthodontic therapy.
Oral habits of patients may affect tooth position and Management of PTM requires multidisciplinary ap-
have been associated with pathologic tooth migration. proach. Patient must be cooperative, compliant, systemi-
Habits that have been associated with PTM include lip cally healthy, and well-motivated for the treatment proce-
and tongue habits, fingernail biting, thumb sucking, dures. Moderate to severe cases of PTM can be managed
pipe smoking, bruxism, and playing wind instruments. by extraction. Treatment is costly and time-consuming
To declare oral habits as a contributing etiologic factor patient education and motivation for treatment procedure
in PTM, it is important to see that duration of force is is must.
more important than force magnitude. Duration directly
determines the extent of tooth movement; the greater
the duration of the habit, the greater is the potential to Summary of PTM Treatment
move teeth.
1. Interdisciplinary approach is a must consisting of
a well-planned treatment plan formulated by a
Signs and Symptoms periodontist, prosthodontist, and orthodontist.
2. Patient factors dictate selection of treatment method
Symptoms
forPTM.
The symptoms include migration of teeth, increased 3. This correction has been reported after nonsurgical
spacing between the teeth, and unaesthetic appearance and surgical treatment. Early intervention using
because of the tooth migration. nonsurgical therapy helps in correction of PTM.
4. Elimination of plaque-induced inflammation is must
Signs before applying light orthodontic forces for correction
The signs include presence of spacing between the of extrusion.
teeth, history of increased spacing, presence of traumatic 5. Studies have shown that successful orthodontic
occlusion, bruxism, deleterious oral habits, presence of correction can only be achieved after elimination of
attrition/ware facets, tooth mobility, and gingival reces- plaque induced inflammation.
sion/periodontal pockets with associated tooth.
Preventing Pathologic Tooth Migration

Diagnosis
Tooth migration related to periodontal disease and
Diagnosis starts as follows:
other etiologies is preventable. The single most effective
• The case history; patients' chief complaints such as method to prevent PTM is control of periodontal disease.
movement of teeth in the space, space generation In addition, early detection of PTM also appears to be im-
between the teeth, or gradual increase in gap between portant in prevention. PTM is reversible with periodontal
the teeth treatment but only in early stages. In cases of severe PTM
there are significant psychological effects and treatment Few studies also suggest that tooth mobility may be clin-
is expensive and time consuming, so there is a need of ically associated with adverse effects on the periodontium
prevention and prompt early diagnosis. and affect long-term attachment response to therapy, but
is not necessarily always associated with occlusal trauma.
A good understanding of occlusal trauma and its effect
CONCLUSION on the periodontium can provide a sound rationale for
accurate diagnosis and predictable treatment planning
The effect of traumatogenic occlusion on the progres- for the periodontally compromised patient. In today's
sion of periodontitis has been an area of disagreement health care environment, patients seek and demand stable,
and may represent differences in study design, model long-term results and failure to understand the biological
selected for study, nature of applied "occlusal" forces, consequences of occlusal forces can cause the practitioner
and periodontal disease. to pursue an inadequate or unidentified course.
KEY POINTS
• Trauma from occlusion is the term used to describe of forces that maintain teeth in a normal relationship
pathologic alteration or adaptive changes that develop (Chasens A).
in the periodontium as a result of undue forces produced 1. Physiologic tooth migration: The eruptive force of
by masticatory muscles. the permanent molars cause a closing of any existing
• Jiggling forces are the most traumatic. They are inter- spaces between primary molar or primate space. It is
mittent forces in two different directions (premature also known as mesial drifting of the tooth.
contact on crowns, fillings) that result in widening of 2. Drifting: It is the movement of the teeth into the spac-
the alveolus and in increased mobility. es created by unreplaced missing teeth drifting does
• Acute trauma from occlusion results from an abrupt not result from destruction of periodontal tissues.
occlusal impact, such as that produced by biting a hard 3. Extrusion/supraeruption/overeruption: Eruption of
object. the tooth well beyond the occlusal table.
• Chronic trauma from occlusion most often develops The main factors which influence tooth position di-
from gradual changes in occlusion produced by tooth rectly or indirectly are tissues of the periodontium,
wear, drifting movement, and extrusion of teeth, com- occlusal factors, soft tissue pressures of the cheek,
bined with parafunctional habits such as bruxism and tongue, and lips; and, a variety of oral habits.
clenching, rather than as a sequela of acute periodontal 4. Symptoms: Migration of teeth, increased spacing
trauma. between the teeth, unesthetic appearance because of
• Glickman (1965, 1967) claimed that the pathway of the the tooth migration.
spread of a plaque associated with gingival lesion can be 5. Signs: Presence of spacing between the teeth, history
changed if forces of an abnormal magnitude are acting of increased spacing; presence of traumatic occlusion,
on teeth harboring subgingival plaque. bruxism, deleterious oral habits; presence of attri-
• The periodontal structure can be divided into two zones: tion/ware facets; tooth mobility, gingival recession/
1. the zone of irritation; and periodontal pockets with associated tooth.
2. the zone of codestruction. 6. Diagnosis: The case history, patients chief complaints
• Clinical indicators of occlusal trauma may include one like-movement of teeth in the space, space generation
or more of the following: between the teeth or gradual increase in gap between
1. Mobility the teeth.
2. Fremitus 7. Clinical examination: Presence of spacing between
3. Occlusion the teeth, presence or absence of gingival recession,
4. Prematurities pus and exudation, tooth mobility, associated peri-
5. Wear facets in presence of other clinical features odontal pockets.
6. Tooth migration 8. Treatment: Interdisciplinary approach is very ef-
7. Fractured tooth/teeth fective in treatment of severe PTM. In such cases,
8. Thermal sensitivity. orthodontic therapy that is preceded by nonsurgical
• Pathologic tooth migration (PTM) is defined as a change and surgical periodontal therapy and prosthodontic
in tooth position that occurs when there is disruption treatment are done.
QUESTIONS 9. Demetriou N, Tsami-Pandi A, Parashis A. Is it possible for periodon-

tal patients to recognize periodontal disease? Stomatologia (Athenai)
1991;47(5-6):284-95.
1. Describe the stages of tissue response to occlusal 10. Esposito M, Thomsen P, Moine J, Gretzer C, Ericson LE, Lekholm U.
forces. Immunohistochemistry of soft tissues surrounding late failures of
2. Differentiate primary trauma and secondary trauma Branemark implants. Clin Oral [mp/ants Res 1997;8:352-66.
from occlusion. 11. Gher ME. Changing concepts: the effects of occlusion on periodon-
titis. Dent Clin North Am 1998;42(2):285-99.
3. Briefly describe the clinical features of trauma from
12. Glaros AG, Rao SM. Effects of bruxism: a review of the literature.
occlusion. J Prosthet Dent 1977;38(2):149-57.
4. Describe fremitus test. 13. Glickman I, Smulow JB. Buttressing bone formation in the peri-
5. Describe the role of trauma from occlusion in odontium. J Periodontol 1965;36(5):365-70.
pathogenesis of periodontal disease. 14. Hallmon WW. Occlusal trauma: effect and impact on the periodon-
tium. Ann Periodontol 1999;4(1):102-8.
6. Describe radiographic features of trauma from
15. Harrel SKl, Nunn ME. The effect of occlusal discrepancies on peri-
occlusion. odontitis. II. Relationships of occlusal treatment to the progression
7. Define pathologic tooth migration. of periodontal disease. J Periodontol 2001;72(4):495-505.
8. What are the causes of pathologic tooth migration? 16. Hirschfeld L. The dynamic relationship between pathologically
9. What are the signs and symptoms of pathologic tooth migrating teeth and inflammatory tissue in periodontal pockets:
a clinical study. J Periodontol 1933;4:35-47.
migration?
17. Jin LJ, Cao CF. Clinical diagnosis of trauma from occlusion
10. Describe diagnosis of pathologic tooth migration. and its relation with severity of periodontitis. J Clin Periodontal
11. What is the treatment of pathologic tooth migration? 1992;19(2):92-7.
18. Jin L, Cao C. Trauma from occlusion index. J Clin Periodontal
1992;19:92-7.
Suggested readings 19. Klineberg I, Jagger RG. Occlusion and Clinical Practice. An
Evidence-Based Approach. Edinburgh, New York, Wright: Elsevier;
1. Box HK. Traumatic occlusion and traumatogenic occlusion. Oral 2004. pp. 84
Health 1930;20:642-6. 20. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant
2. Box HK. Experimental traumatogenic occlusion in sheep. Oral Health Dentistry. 5th ed. Blackwell Munksgaard; 2008.
1935;29:9-15. 21. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds. Carranza's
3. Brunsvold M, Zammit K, Dongari A. Spontaneous correction of Clinical Periodontology. 10th ed. Philadelphia: W.B. Saunders Com-
pathologic migration following periodontal therapy. Int J Periodontics pany; 2006.
Restorative Dent 1997;17:183-9. 22. Reddy MK, Vandana KL. Three dimensional finite element analysis
4. Brunsvold MA. Pathologic tooth migration. J Periodontal. 2005;76(6): of stress in the periodontium. J Int Acad Periodontol 2005;7(4):102-7.
859-66 Review. 23. Stern N, Brayer L. Collapse of the occlusion - aetiology, symptom-
5. Burgett FG. Trauma from occlusion: periodontal concerns. Dent Clin atology and treatment. J Oral Rehabil 1975;2(1):l-19.
North Am 1995;39:301. 24. Stillman PR. The management of pyorrhea. Dental Cosmos
6. Carranza Jr FA. Clinical Periodontology. 8th ed. Philadelphia, London, 1917;59:405-14.
Toronto, Montreal, Sydney, Tokyo: W.B. Saunders Company; 1995. 25. Stones JJ. An experimental investigation into the association of
7. Chasens AI. Periodontal disease, pathologic tooth migration and traumatic occlusion with periodontal disease. Proc Royal Soc Med
adult orthodontics.NY J Dent 1979;49(2):40-3. 1938;31:479-96.
8. Davies SJ, Gray RJ, Linden GJ, James JA. Occlusal considerations in 26. Waerhaug J. The infrabony pocket and its relationship to trauma from
periodontics. Br Dent J 2001;191(11):597-604. occlusion and subgingival plaque. J Periodontol 1979;50(7):355-65.
CHAPTER
14
Role of Iatrogenic and Other Local
Factors in Periodontal Disease
Periodontal diseases are predominantly microbial in are considered to modify and predispose to the develop-
origin and factors that enhance the accumulation of bacte- ment of chronic inflammatory periodontal disease. These
rial plaque, through promotion of its growth or inhibition include food impaction, malocclusion, enamel projections,
of its removal, contribute to the progression of this disease. crowding of teeth, position of teeth, and the problems aris-
In this regard, a number of anatomic and iatrogenic factors ing with faulty restorative and prosthetic dental treatment.
IATROGENIC FACTORS between the teeth brings about ischemia of interdental

gingiva or separates interdental gingiva from adjacent
Iatrogenic diseases are defined as "any untoward or ad- teeth. Forcing clamps subgingivally may cause stripping
verse consequence of preventive, diagnostic, or thera- of junctional epithelium and connective tissue attachment.
peutic regimen or procedure that causes impairment, Clamps left over tissues for a long time may induce tissue
handicap, disability, or death resulting from physician's sloughing and recession. Loose clamps may also cause
professional activity or professional activity of other similar damage. Dental floss used to tie up the rubber
health professions." dam strangulates and lacerates entrapped gingiva.
Faulty dental restorations and prostheses as well as Retraction of the gingiva is often necessary to gain access
inadequate dental procedures may injure the periodontal to the finish lines of tooth preparations. Transient trauma
tissues and instigate gingival inflammation and peri- to the gingival sulcus and junctional epithelium may be
odontal destruction or aggravate preexisting disease. produced in the process. Retraction cords forced api-
The understanding of the effects of restorative services cally past the gingival tissue cause laceration or contusion
on periodontal tissues is essential to regain optimal peri- of the gingiva. Cords impregnated with chemicals may
odontal health and function. cause lateral displacement of the gingiva, exposing the
margin of the preparation. Dry retraction strings can tear
away the epithelium adhering to the string. Therefore, the
Periodontal Considerations in Prosthetic and
string should be kept moist while in place.
Restorative Dentistry
Matrix bands not stabilized with wedges may slip apically
Most restorative procedures seem to affect the peri- lacerating the periodontal tissues. The gingival end of the
odontal tissues by retaining plaque, inducing physical matrix bands should not exceed the apical extent of the gin-
trauma, or evoking an allergic tissue response. These gival crevice. Proper contouring and stabilization of these
effects may be apparent throughout the various stages of matrix bands is therefore essential to prevent inadvertent
fabrication of the restoration. harm to the supporting tissues. Forcing the wedge interden-
The use of the rubber dam has become unavoidable in tally can inadvertently traumatize the interdental papilla.
the practice of dentistry today. Manipulation of the rubber Separation of teeth for access beyond the width of the
dam with no regard to the surrounding tissues leads to periodontal ligament space may compress or tear
inadvertent tissue damage. Too little rubber dam material the periodontal ligament. Slow separators are preferable
CHA PTER 14 ROLE OF IATROGENIC AND OTHER LOCA L FACTORS IN PERIO DONTAL DISEASE 109
to rapid tooth separation. At the same time, sliding of rub- action to render the area clean. At times, the interproximal
ber separators into the periodontium may cause abscess embrasure is obliterated by bulky solder joints or by the
formation. crown contours. The resultant pressure brings about a cra-
Mechanical trauma may also be caused by repeated in- tering of the interdental papilla, which allows entrapment
sertion and removal of impression compound. Improper of plaque. Encroachment of embrasures and interdental
use of copper bands tends to lacerate the gingival tissues. spaces will interfere with normal escape of food debris
Exothermic polymerizable impression materials generate and with oral hygiene measures.
considerable amount of heat which is potentially dam- Normally, tooth contact occurs around the junction of
aging to the periodontal tissues. Residues of impression the occlusal and middle third of the tooth toward the
materials left within the gingival sulcus may precipitate facial half. This arrangement provides space for the inter-
a severe periodontal reaction with loss of attachment. dental papilla and for the escape of food during mastica-
Rotary instruments and discs used beneath the gingival tion from the occlusal surface out the lingual spillway.
margin during tooth preparation traumatize the gingiva, Loose or open contacts have been suggested to
sulcular lining, epithelial attachment, and the underly- contribute to periodontal pocket formation by allowing
ing connective tissue. If the attachment apparatus is not food impaction. Hancock et al observed a significant rela-
breached, the trauma caused by the bur may be reversible. tionship between tooth contact type and food impaction.
Errors in recreating the facial and lingual contours Broad, flat contact points, as mentioned earlier, produce
may affect periodontal health. Overcontouring generally a soft crater-like depression of the interdental papilla in
occurs on the buccal or labial surfaces in the gingival between (Fig. 14.2).
third of crowns resulting in an area where oral hygiene Placement of restoration margins subgingivally has
procedures are difficult. At the same time, it prevents shown greater amounts of plaque accumulation, gingi-
the self-cleansing mechanism of the adjacent cheek, lips, vitis, and deeper pockets than supragingival margins
and tongue. The ensuing plaque accumulation produces (Fig. 14.3). Felton and coworkers observed significant
inflammatory and hyperplastic changes of the marginal periodontal tissue inflammation associated with subgin-
gingiva. Undercontour results in trauma to the marginal givally located crown margins due to marginal discrep-
gingiva and in food impaction (Fig. 14.1). ancies. Secondary carious lesions and gingival recession
Insufficient tooth reduction or too much bulk of re- were also more frequent around subgingival restorations.
storative material may produce an overcontouring of the Conventional hygiene aids and scaling instruments are
margins in the intrasulcular area. This mechanically holds unable to effectively remove plaque from within the sul-
the gingival margin, resulting in bulbous and irregular cus, and this may be an added limitation of subgingival
gingival contours. Undercontour in the intrasulcular area position of restorative margins. Supragingival restoration
occurs when the margin of the restoration falls short of the margins do not interfere with the periodontal condition.
prepared tooth margin. The gingival margin thus collapses In general, clinicians recommend using the biologic
into the space created, bringing about inflammatory changes width as a guide for placement of the restoration margin.
such as sulcular bleeding and increased probing depth. The biologic width is defined as the dimension of the soft
Establishment of good embrasure form will either pre- tissue, which is attached to the portion of the tooth coro-
vent debris retention or allow the lip, cheek, and tongue nal to the crest of the alveolar bone. A minimum of 3 mm
FIGURE 14.1 Marginal gingivitis along defective restorations. FIGURE 14.2 Restorations with broad contact areas and wide
occlusal tables.
FIGURE 14.3 Gingival proliferation in relation to subgingival FIGURE 14.5 Interproximal bone loss associated with overhang.
margin placement.
should exist from the restorative margin to the alveolar complicating plaque control. Displacement of the gingiva
bone, allowing for 2 mm of biologic width space and and violation of the biologic width may be another possi-
1 mm of sulcus depth. Nevins and Skurow suggested re- ble mechanism by which they damage the periodontium.
stricting the subgingival extent of the margin to 0.5-1 mm Overhanging restorations change the ecologic balance
as it is clinically difficult to detect the coronal limit of the of the gingival sulcus to one that favors the growth of
junctional epithelium. specific periodontal pathogens.
Consequently, intracrevicular placement of the restora- Traditionally, curettes, sonic/ultrasonic scalers, chisels,
tion margin at least 1 mm coronal to the junctional epi- diamond or finishing burs have been used to eliminate
thelial attachment avoids violation of the biologic width overhangs. The Cavitron® (Dentsply) and Profin® (Profin
and promotes gingival esthetics and periodontal health. Directional System, Dentatus USA) instrument systems
An overhanging dental restoration is defined as an exten- may also be used for the same purpose.
sion of the restoration material beyond the confines of It is essential to ensure that the restoration margin is
the cavity preparation. Significantly more inflammation, closely adapted to the tooth surface. Margins that were
deeper pockets, attachment, and bone loss have been open by more than 0.2 mm have been associated with
found adjacent to overhanging dental restorations (Eid alveolar bone loss. This is a consequence of plaque ac-
M, 1987), Figs 14.4 and 14.5). cumulation either due to roughness of the cement or the
Overhangs can impinge on the interproximal embra- dissolution and disintegration of the luting material.
sure space, making cleaning with floss difficult, thus The surfaces of various dental materials help to retain
plaque and may be a source of gingival inflammation
(Adamczyk E, Spiechowicz E; 1990). Stripes and scratches
on the surface of resin, gold, or porcelain restoration con-
tribute to surface roughness subgingivally. Self-polymer-
izing acrylic, amalgam, and tooth-colored materials retain
plaque on the surface by virtue of their porous nature.
After a period of time, composite resins show marked
surface roughness with erosive defects and marginal im-
perfections that retain food debris and result in gingival
inflammation (Fig. 14.6).
Ridge-lap designs prepared, from time to time, for
aesthetic reasons inevitably result in mucosal irrita-
tion, chronic inflammation, and ulceration of the area
(Fig. 14.7). Designing a sanitary pantie avoids contact
with the mucosal surface to provide space for cleaning
devices. Placement of panties into extraction sockets is
also a source of permanent irritation and may jeopardize
FIGURE 14.4 Overhanging restoration margin. the healing process of an extraction socket.
An increased ease of bleeding, redness, enlargement,

and pocketing was associated with gingival margins
covered by the denture base. This has been attributed to
gingival impingement caused by mechanical pressure,
especially during function (Zlataric DK, 2002), and to
bacterial colonization. Metallic removable partial denture
bases have been shown to elicit less gingival inflamma-
tory changes than the nonmetallic bases. Leaving the
gingival margin uncovered prevents the pinching and
strangulation of tissues and decreases the niches into
which food debris and bacteria may lodge. At times, how-
ever, inflammatory hyperplasia may occur in areas with
FIGURE 14.6 Gingivitis associated with rough restoration surfaces. intentional relief. This could be a result of the presence
of voids between the denture and the gingiva in which
tissue proliferates until it obliterates the space.
Maintenance of periodontal health requires proper
treatment, emphasis on good prosthesis hygiene, and high
level of patient cooperation. Adjunctive use of Chlorhexi-
dine mouthrinse may be considered as well (Sorensen JA
et al, 1991).
The location and design of the occlusal table of the pos-
terior teeth should allow transmission of forces in an axial
direction. Restoration of occlusal dimensions and cuspal
contours is thus crucial. A flat, wide occlusal table, as a
result of occlusal wear, provides little guidance for food to
be directed away from the interproximal area and makes
the involved tooth susceptible to increased occlusal load
(Fig. 14.2). Carving well-defined grooves, fossae, marginal
FIGURE 14. 7 Inflammatory changes with pocket around fixed ridges, and occlusal sluiceways can prevent food impac-
partial denture. tion interproximally. At the same time, occlusal load may
be directed axially by reducing the buccolingual width
of occlusal table to about 60% of the overall width of the
tooth.
Undiagnosed prematurities in centric relation give rise
to conditions such as overloading of individual posterior
teeth, traumatization of anterior teeth during protrusion
and laterotrusion, and temporomandibular joint (TMJ)
disorders. These occlusal imbalances may be averted by
prompt detection and elimination of high points. Hence,
it is essential that the restorations must have a balance of
form and function (Sachs RI, 1985).
Iatrogenic perforations are often a result of lack of at-
tention to the details of internal anatomy and a failure to
consider anatomic variations. Root perforations created by
boring, piercing, cutting, or resorption result in a commu-
nication between the pulp space and periodontal tissues.
This may result in secondary epithelial proliferation, bone
FIGURE 14.8 Ill-fitting denture with clasp impinging on gingival.
resorption, and necrosis which could worsen the prog-
nosis of the tooth. Perforations away from the gingival
Occlusal and retentive partial denture designs can exert sulcus and surrounded by healthy periodontium usually
excessive ocdusal stresses on abutment teeth and become have a fair prognosis.
traumatogenic to the attachment apparatus. Distal exten- Iatrogenic vertical root fractures occur in vital teeth hav-
sion dentures, in particular, may transmit jiggling forces. ing coronal restorations, pin restorations, full crowns,
Greater plaque accumulation is likely near ill-fitting or and inlays. Preparation of the canal for a post, selec-
inadequately polished dentures (Fig. 14.8). tion of an improper post, traumatic sealing of intracanal
restorations, and expansion of posts and pins as a result a variety of microorganisms compromising periodontal
of corrosion are additional causes of vertical root fracture. maintenance.
Root fractures are often associated with inflammation Cytotoxic corrosion products from bonding materials
of the gingiva because of the enhanced plaque accumula- and orthodontic appliances may also play a role in local-
tion in the fracture line. A pocket usually forms adjacent ized gingivitis. Among these, chemically cured materi-
to the site of the fracture, in contrast to the normal sulcus als were reported to be more cytotoxic than light cured
seen around other areas of the involved tooth. Osseous materials.
defects, periodontal abscess, fistulous tracts, and mobility Elastic bands, used in orthodontic appliances, may pre-
are therefore periodontal findings that manifest in verti- cipitate iatrogenic effects. Affected teeth exhibit red, hyper-
cal fractures. plastic gingivae with loss of bone, tenderness to percussion,
Restorative materials have been found, occasionally, and mobility. Apical sliding of elastics as a result of the
to be irritant to the periodontal tissues. Some restorative conical root design of incisors and premolars has even led
materials, such as resins or cast gold alloys containing to exfoliation of these teeth. Root resorption is a frequent
nickel, are known to precipitate allergic reactions. Solubil- complication on teeth with elastics because of the likeli-
ity, disintegration, and corrosion of restorative materials hood of jiggling forces (Brezniak N, Wasserstein A; 1993).
may alter the form of the restoration creating a rough In such cases, it is preferred to secure the elastic bands su-
surface with additional possibility of marginal leakage. pragingivally with either twisted steel wire or dental floss.
Electrical potentials and galvanism between restorations Gingival enlargement (associated with increased
of dissimilar metals may lead to gingival recession. probing depths and no loss of attachment) in presence of
Use of an ultrasonic endodontic instrument has been orthodontic bands is another common observation, seen
reported to induce severe damage to alveolar bone, gin- mostly in the interproximal gingiva and around posterior
giva, and nasal mucosa. The heat produced within the teeth. Difficulty in brushing posteriorly as well as ten-
root canal was conducted through the dentin, periodon- dency for food impaction may account for these changes.
tal ligament, and soft tissue. This emphasizes the need Strict oral hygiene measures may help improve the gin-
to maintain adequate cooling of ultrasonic instruments gival condition. Resolution of these gingival changes is
(Walters JD, Rawal SY; 2007). often seen following cessation of orthodontic treatment.
Tissue clefting is sometimes evident in the lower incisor
regions of orthodontically treated patients. The labial sur-
Orthodontic Therapy and Periodontal Health faces of the incisors are thin, and when the mandibular in-
Ideally, orthodontic treatment should be accomplished cisors are moved in a labial direction, the movement along
without traumatic lesions in the periodontium. However, with superimposed inflammatory changes compromises
orthodontic therapy may affect the periodontium by fa- the integrity of this area. Bunching of tissue is also apparent
voring plaque retention, by directly injuring the gingiva, in closed extraction sites as a result of excess gingiva being
or by creating excessive or unfavorable forces on the sup- compressed. These changes impair the patient's ability to
porting tooth structures. keep the area clean and exaggerate the resultant plaque-
The permanent interdental wire connections in fixed induced gingival inflammation (Fig. 14.9).
appliances create areas that are difficult to clean favoring
plaque retention and food impaction. Thus, tissue hyper-
plasia and deeper pocketing are frequently observed in
these areas. Hence, the use of simple appliances avoid-
ing hooks, elastomeric rings, and excess flash around the
bracket bases may promote improved maintenance of
oral hygiene.
Placement of bands may cause some degree of iatro-
genic damage since attachment from the tooth may be
stripped during placement. The arrival of direct bonding
techniques has considerably reduced the likelihood of
this type of injury.
At the same time, bands behave like overhanging res-
torations creating a subgingival ledge favoring growth of
pathogenic microflora such as Lactobacillus strains, spiro-
chetes, and fusiform bacteria. Furthermore, the margins of
bands can make periodontal maintenance more difficult.
Similarly, composites used as direct bonding adhe- FIGURE 14.9 Gingival cleft and marginal gingivitis associated with
sives have a polymeric matrix that can host and nurture orthodontic therapy.
Disturbance of occlusion during orthodontic treatment used in patients with a thin covering of gingiva since it
may produce jiggling type of forces, temporarily. In the tends to cause gingival recession. Cryotherapy is associated
presence of marginal inflammation, persistent occlu- with irreversible injury to epithelial cells. Lasers used in
sal trauma may result in periodontal breakdown. Light periodontal therapy have been associated with thermal
orthodontic forces should suffice in periodontally com- necrosis, sequestration of necrotic bone, and delayed
promised dentitions as the loss of alveolar bone results reepithelialization of laser wounds.
in the center of resistance of the involved teeth moving Occlusal adjustment on patients having clicking and in-
apically. The teeth are thus subjected to tipping rather termittent locking can cause an increase in TMJ symptoms.
than bodily type of movement. Rapid tipping of the teeth A complication of incomplete occlusal adjustment is that
may also shorten the alveolar crest. Intrusive forces can occlusal discrepancies can increase, thus subjecting the
be hazardous since the forces are concentrated at the root anterior teeth to trauma from occlusion. Similarly, splint-
apex leading to root resorption. ing in the presence of untreated periodontal disease will
When inclined planes of the opposing teeth interfere certainly fail. If one tooth in a periodontal splint is in a
with the movement of the teeth, there is a tearing and traumatic occlusal relationship, the periodontal tissues of
crushing of the periodontal ligament resulting in detach- the remaining teeth may also be injured. Hence, stabilizing
ment of important groups of periodontal ligament fibers the occlusion prior to splinting is of primary importance.
and loosening of the teeth. If mobility persists even after the best efforts to salvage
The use of auxiliary springs, intermaxillary elastics, or the tooth by periodontal therapy, splinting may not be
active removable appliances may produce jiggling of the advisable. Furthermore, the bonded areas in the splint
teeth, undermining bone resorption and numerous areas of can enhance plaque retention and formation of calculus.
root resorption. Maxillary incisors are the more commonly Crown lengthening involves reflection of full-thickness
involved teeth. Rapid palatal expansion has been associated mucoperiosteal flaps to expose the alveolar crest around
with root resorption of the first maxillary molars. the teeth. Bone removal must be done cautiously to pre-
Alveolar dehiscences on the facial surfaces of incisors vent reverse architecture, penetration into a furcation, or
moved facially by rapid bodily movement or during ex- destabilization of the tooth. Failure to consider specific
trusion are also possible. This is sometimes followed by indications or orthodontic alternatives prior to crown
gingival recession and loss of attachment. Pronounced lengthening can lead to poor crown to root ratio, loss of
recession of the gingival margin and extensive loss of the bone support, and poor cosmetic outcomes, particularly
connective tissue attachment are features of orthodontic in anterior teeth. Final restorations should be placed only
extrusion combined with supracrestal fiberotomy. after a healing period of 6-8 weeks.
Periodontal therapy usually precedes active orthodon- In the same way, extreme care has to be taken during
tic treatment as the presence of inflammation leads to gingivectomy to avoid exposure of the bone and maintain
rapid and irreversible breakdown of the periodontium. the width of the existing attached gingiva. Gingivectomy
However, pocket elimination surgery or correction of os- and modified Widman flap have occasionally resulted in
seous defects can be postponed as tooth movement may recession of localized areas.
modify gingival and osseous morphology. Incisions near the posterior regions of the mouth have
to abide by the natural landmarks to avoid injuring vital
structures or maceration with diamond burs or stones.
Periodontal Procedures
Gentle handling of flaps and soft tissue grafts in such a
Overzealous root planing may inadvertently lead to way that they do not tear or unduly compress soft tis-
hypersensitivity of the root surfaces. In addition, root sues is recommended. Traumatic surgical technique causing
planing in shallow pockets may lead to loss of attachment flap tear may precipitate recession and delayed healing.
if done without considering the critical probing depth. Poorly incorporated soft tissue grafts may be associated
Chemicals, such as 5% paraformaldehyde or potassium hy- with alterations in the color and thickness of the gingival
droxide, were formerly in use for gingivectomy. The depth of surface hindering aesthetics.
action of these chemicals could not be controlled. Epitheliali- Periodontal flaps should be extended only over the mini-
zation and reestablishment of the alveolar crest fiber system mum area needed for access to exposed root surfaces or
were slower in such chemically treated gingival wounds. bone that is to be removed during surgery. Prolonged
Use of electrosurgery (heat) and cryotherapy (freez- exposure and overexposure of the bone during flap sur-
ing) has also been associated with adverse effects. Deep gery must be avoided to ensure adequate hydration of
electrosurgical resections may exhibit slow healing, pain, the bone during osseous recontouring. Use of a chisel is
bone necrosis and sequestration, and loss of alveolar less traumatic during osseous surgery than crushing bone
height. Hyperemia of the pulp and burn marks once- with a rongeur.
mentum have been noted when the electrosurgery tip Treatment offurcations with tunneling has been associ-
contacts the root surface. Electrosurgery should not be ated with the development of root caries. Such teeth with
exposed furcations or resected roots should be contoured maxillary sinus, mental nerve, and inferior alveolar nerve.
so that the body of the tooth does not impede access for Numbness and tingling sensation are evidence of damage
control of plaque. Tight suturing may cause necrosis of the to nerves. An oroantral communication may develop if
margins and interdental papillae. the maxillary sinus is encroached. Placement of implants
close to the maxillary sinus provides a route for spread of
infection from the mouth, especially in patients with poor
Exodontic Procedures oral hygiene. Perforation of the maxillary sinus lining is
Faulty surgical techniques are known to adversely af- common during sinus lift procedures.
fect the periodontium. Thus, extreme care is indispensable Slippage of sharp instruments and burs has caused
while raising flaps, and luxating and elevating teeth, dur- injury to the floor of the mouth and even laceration of
ing debridement as well as during closure of the wound. the sublingual artery. Sublingual hemorrhage per se or
When flaps are pulled up on the crowns of the teeth with- airway obstruction due to hematoma formation has been
out regard to flap position during suturing, a pseudopocket reported to be fatal, at times. Swelling and ecchymosis
develops that has no attachment to enamel. This may have also been reported because of defective flap man-
lead to loss of attached gingiva and further periodontal agement, long duration of surgery, and improper healing
breakdown. of tissues.
Extraction of impacted third molars is usually com- During implant insertion, modifying the flap design
plicated by periodontal destruction around the adjacent by placing the soft tissue incision away from the osseous
tooth (Ash MM Jr et al, 1962). Consequently, soft tissue incision prevents epithelial encapsulation and encourages
debridement, correction of osseous defects, and careful rapid healing. Previously, all implants were designed with
soft tissue replacement are done to avoid persistence of an abrupt shoulder where the abutment post joins the
periodontal disease or development of new periodontal neck of the implant. This complicated oral hygiene pro-
disturbances. cedures and made subgingival periodontal maintenance
Careless use of forceps or elevators results in crushing impossible. Beveling the neck of the abutment allows for
of the alveolar bone. Elevators must be used with caution adequate maintenance.
to avoid loosening of the approximating teeth or crush- After surgical placement, the implant-bone fixture
ing radicular bone. It is imperative to avoid scratching must be maintained for a time period without occlusal
of the second molar during extraction. There is a risk of load. Primary stability may be destroyed if load applica-
hypersensitivity and loss of attachment in such an area. tion is done immediately.
Bone loss on the distal surface of the second molars Microbial and biomechanical factors are the prime
is considerable if the third molars are extracted after the cause for peri-implant crestal bone loss. Occlusal discrep-
roots are formed or in patients older than the early twen- ancies, therefore, if present, should be eliminated. Other
ties. This warrants extraction prior to completion of root etiologic factors such as traumatic surgical techniques
formation. However, such a decision may be deferred if and improper case selection, poor maintenance, traumatic
the third molars are completely covered. injuries, parafunctional habits, and faulty dentistry can act
as cofactors in the development of peri-implant disease.
Management of failing implants depends largely on the
Periodontal Considerations in Implant Dentistry cause.
Placement of dental implants for occlusal rehabilita- The objectives of periodontal preparation for implants
tion is becoming increasingly popular. However, this should not be limited to the elimination of periodontal
is extremely technique sensitive. Iatrogenic damage is pockets and restoration of gingival health. An adequate
a very likely possibility without adequate care during zone of attached gingiva and a buccal vestibule of suf-
placement compounded by insufficient knowledge and ficient depth have to be established allowing restorative
skill of the clinician. procedures and enhancing effective oral hygiene tech-
Iatrogenic complications may be precipitated by the niques. Free gingival grafts and apically positioned flaps
surgical procedure, improper case selection, negligence may be carried out for this purpose.
regarding asepsis, and inadequate care during follow-up.
Inadvertent drilling, excessive tapping, and threads be-
Chemical Irritation
ing destroyed have compromised the prognosis in many
cases. Overinstrumentation of the bone site has led to Acute inflammation with ulceration may be produced
inadequate mobilization of the implant. Excessive heat by the nonspecific injurious effect of chemicals on the
generation during implant placement has also affected gingival tissues. Topical application of aspirin to oral
the success of the surgical technique. mucosa for relief of toothache resulted in chemical burns.
Precise drilling position and angulation may prevent Epithelial sloughing with acidulated fluoride phosphate
perforation and damage to vital structures such as the gel has also been observed.
Radiation because of mechanical pressure on the gingiva. It may be

one of the reasons for increased destruction in localized
Radiotherapy has shown a gradient of responses in- areas. The food being impacted, in addition to helping in
cluding gingival hemorrhage, ulcerations, suppuration, plaque retention, can also have a mechanical effect and
recession, necrosis of bone, and loosening of teeth. In induce drifting of the teeth by virtue of the effect of the
addition, there is a change in the oral flora in individuals fibrous nature of the impacted food.
with xerostomia.
Malocclusion
LOCAL CONTRIBUTING FACTORS Tooth malalignment predisposes to plaque retention and
makes plaque removal difficult, thereby contributing to
A number of local factors, in the gingival environment, periodontal disease and caries. Increased prevalence and
predispose toward the accumulation of plaque deposits severity of periodontal disease has been observed in chil-
and prevent their removal. These are called plaque reten- dren with bimaxillary protrusions. Angle class II, division
tive factors. 2 cases are associated with retroclined anterior teeth. The
bony margin of such teeth is in the form of a ledge, which
Dental Calculus results in difficulty in plaque removal. Teeth in malposi-
tion have insufficient attached gingiva, which along with
Calculus is a calcified mass that forms on and adheres other predisposing and/ or precipitating factors may lead
to the surfaces of teeth and other solid objects in the to gingival recession. Furthermore, occlusal interferences
mouth, such as in restorations and dentures, which are not associated with malocclusion may precipitate trauma
exposed to friction. It has a secondary role in the etiology from occlusion.
of periodontal disease. Calculus promotes the retention of The incidence of gingival inflammation was found to
dental plaque and may increase the rate of plaque forma- be greater with an overjet of 6 mm or more. In deep bite,
tion. It helps in advancing plaque more apically. It also upper incisors may impinge on the lower labial gingiva
impairs oral hygiene measures. Its porosity can serve as or lower incisors on the palatal gingiva, causing inflam-
a reservoir for periodontal pathogens, thereby retaining mation and tissue destruction in the presence of plaque.
noxious bacterial components such as endotoxin. Open bite relationships lead to unfavorable periodontal
changes caused by the accumulation of plaque and an
absence of or diminution in function. Loss of contact with
Dental Caries
the opposing teeth leads to atrophy of the attachment
Dental caries contributes to periodontal disease by apparatus. Tongue thrust habits associated with this con-
destroying proximal contacts, retaining microbial plaque, dition result in forces subjected on these teeth from both
encouraging tooth drift, bite collapse, disturbing natural the tongue and the lips. Therefore, mobility and recession
chewing and cleansing habits, causing premature loss of are frequently associated with anterior teeth in open bite
teeth, and introducing iatrogenic factors that alter form cases. There is difficulty in maintaining oral hygiene since
and function. a considerable stretching of the lips and cheeks is needed
while performing oral hygiene measures to gain access to
the cervical areas of anterior teeth. Additionally, associ-
Food Impaction ated lip incompetence and mouth breathing habits are
Forceful wedging of food into the periodontium by oc- other factors provoking gingivitis.
clusal forces may occur interproximally or in relation to the In crossbite, there is reversal of the normal relationship
facial or lingual tooth surfaces because of open contacts, of the teeth, with the maxillary teeth being lingual to the
proximal caries, malpositioning of the teeth, wear, and im- mandibular teeth. Trauma from occlusion, food impac-
proper restorations. A "funneling" effect of adjacent tooth tion, spreading of the mandibular teeth, and associated
surfaces directs food into the interproximal areas. Oppos- gingival and periodontal alterations may be caused by
ing cusps that tend to forcibly wedge food are known as crossbite.
plunger cusps. In addition, lateral pressure from the lips,
cheeks, and tongue may force food into the gingival em-
Failure to Replace a Missing Tooth
brasures enlarged by recession.
Food impaction may initiate and aggravate the sever- Failure to replace extracted teeth initiates a series of
ity of preexistent disease. Gingival bleeding, foul taste, long-term changes producing varying degrees of peri-
gingival recession, periodontal abscess formation, al- odontal disease. Consequential tilting of the mandibular
veolar bone loss, and root caries are associated findings. molars and extrusion of the maxillary molars alters the
Ischemia, necrosis, and gingival stripping may also occur respective contact relationships of these teeth, thereby
favoring food impaction. Arch length deficiencies also

create abnormal relationships that may favor trauma
from occlusion. This creation of abnormal contacts with
the opposing jaw may trigger the development of para-
functional habits. Pocket formation and bone loss are
common in relation to these teeth. Tilting of the posterior
teeth also results in reduction in the vertical dimension,
accentuation of the anterior overbite with successive
labial migration, and diastema formation of the maxil-
lary anteriors.
Presence of enhanced plaque and calculus accumula-
tion is strikingly evident on the nonfunctional opposing
teeth.
Habits
FIGURE 14.11 Lack of lip seal associated with gingivitis.
Habits are often repeated static or functional exercises
or rituals. Examples of oral habits include nail biting, tables, supraeruption, altered interdental contacts and
cheek biting and biting foreign objects (pencils, pipes or marginal ridge relationships, tooth displacement and
hair pins). These oral habits may be detrimental to the mobility, muscle fatigue, muscle sensitivity to palpation,
supporting periodontium as they modify the magnitude, eccentric occlusion, mandibular deviation, and TMJ dys-
direction and frequency of forces exerted on teeth, result- function suggest bruxing activity.
ing in traumatic periodontal lesions (Fig. 14.10). Treatment for bruxism may include selective grinding
Bruxism, clenching, and doodling induce parafunc- of premature contacts and occlusal splints. The occlusal
tional forces on the periodontal tissues. Bruxism is the splint bite guard prevents cuspal contact and protects the
repetitive grinding/ gritting of teeth. It can occur as rhyth- periodontium from injury by lateral forces. The appliance
mic side-to-side movements or as a sustained clench. redistributes the forces applied throughout the arches,
Clenching is the fluctuating and repetitive force exerted thereby reducing the damaging effects on the periodon-
on teeth in opposing arches when the dentition is in a tium. Counseling and psychotherapeutic drugs may be
fixed position. Doodling is the repetitive toying, tapping, required for some patients.
or clenching on an isolated tooth or group of teeth when Mouth breathing is frequently associated with lack of
the mandible is in an eccentric position. lip seal. Hyperplastic gingivitis is common in the upper
Premature contacts and neuroses have been implicated incisor regions and is clearly demarcated by the lip line
in the development of this lesion. Clinically, evidence of (Fig. 14.11). Keeping the lips apart diminishes the normal
polished tooth facets, flat inclined planes, broad occlusal cleansing action of saliva in the anterior gingivae. The
subsequent dehydration of the tissues encourages plaque
accumulation.
Tongue thrusting entails persistent, forceful wedging of
the tongue against the teeth, particularly in the anterior
region. This tongue thrust causes tilting and lateral spread
of the anteriors leading to open bite in the anterior or
posterior regions. The altered inclination of the maxillary
anterior teeth results in change in the direction of func-
tional forces so that lateral pressure against the crowns
is increased. Thus, tongue thrusting may contribute to
pathologic tooth migration. At the same time, it interferes
with food excursion and favors the accumulation of food
debris at the gingival margin.
Treatment of tongue thrust can be performed with ap-
pliance therapy, myofunctional and speech therapy, or a
combination of these.
Tobacco smoking has an influence on prevalence and
severity of periodontal disease. Plaque deposits, stains,
calculus, pocket depths, and alveolar bone loss are greater
FIGURE 14.10 Habit contributing to gingival recession. in smokers than in nonsmokers. Moreover, smokers have
higher numbers of periodontal pathogens (Tannerella for- are found in 1.1-5.7% of molar teeth with high frequency
sythia and Treponema denticola) in their subgingival flora. of occurrence in the maxillary second molars. Enamel
Smoking apparently produces nicotine-related tran- projections extend into the furcations of maxillary and
sient initial increase in gingival fluid flow rate and then mandibular molars. These enamel surfaces may favor the
a prolonged vasoconstriction of the gingival vasculature. development of a pocket and interfere with regenerative
This tends to reduce the clinical signs of gingivitis associ- procedures.
ated with a decreased availability of leukocytes and anti- Cementa/ tears can be induced by sudden occlusal or
bodies in the gingival crevice. Smoking is associated with other forms of acute trauma seen as radiopaque fragments
the local production of greater quantities of proinflarn- in the periodontal ligament space. Surgical debridement
matory cytokines and acute phase proteins, which could may be necessary to resolve the associated periodontal
in turn lead to more severe destructive inflammation in defect.
the periodontal tissues. Placement of smokeless tobacco
in the buccal vestibules is associated with a significant in-
crease in localized gingival recession and attachment loss.
Soft Tissue Factors
Inadequate width of attached gingiva and vestibular
depth, frenular attachments, and retromolar and palate-
Tooth Abnormalities
gingival protuberances have also been implicated as pre-
Teeth with large, bulbous crowns and short, tapering disposing to periodontal disease. These anatomic defects
roots seem to be at an increased risk for trauma from support plaque accumulation that probably results from
occlusion. These teeth frequently show signs of fremitus compromised hygiene in the area.
and mobility during lateral excursive movements. At the
same time, a short, broad root offers less support than a
long, narrow root. Due consideration to these aspects is
Oral Hygiene Devices
essential prior to abutment selection. Chronic toothbrush trauma results in gingival reces-
Root concavities can vary from shallow flutings to deep sion in the absence of clinical inflammation. Abrasion
depressions present in the proximal surfaces. Cervical of cervical aspects of the tooth may be conspicuous. In
root resorption may also alter the root surface contour. Ex- addition, abrasive dentifrices, hard toothbrushes, inap-
posure of these areas by recession will complicate plaque propriate brushing technique, and excessive brushing
control procedures. corroborate with abrasion of tooth surfaces.
Grooves on the root surface or the cervical aspect of Toothbrush bristles may embed in the gingiva, caus-
the crown are plaque retentive areas, which result in lo- ing an acute gingival abscess. Furthermore, improper
calized gingivitis and pocket formation. They are most use of dental floss, toothpicks, or wooden interdental
commonly seen palatal to the upper incisors (Fig. 14.12). stimulators may result in gingival inflammation. Force-
Hence, odontoplasty may be needed to minimize plaque ful snapping of dental floss through the contact points
retention. may induce cuts/clefts in the gingiva (Fig. 14.13). Ag-
Enamel pearls are ectopic deposits of enamel usually gressive flossing motion may create grooves on the
associated with furcation areas on molars. Enamel pearls tooth surface.
FIGURE 14.12 Pocket associated with palatogingival groove. FIGURE 14.13 Improper use of a toothpick producing a gingival
cleft.
Thermal Factors increased understanding of the nature and progress of

Liquids and foods such as soup, coffee, and pizza It is now accepted that the preservation of health de-
commonly cause tissue burns, especially on the palatal pends largely on the ability to keep microbial plaque
mucosa. and factors that help retain it to a minimum. There is
Cold injury and necrosis (mucosal frostbite) have also no reliable means to completely remove the plaque that
been observed following prolonged continuous applica- constantly forms on the margins and surfaces of restora-
tion of ice cubes (7 h). The clinical appearance of a creamy tions that pass below the gingival crest. If convenient, all
white slough demarcated from adjacent areas by a thin restorations should be kept supragingivally. It is recom-
erythematous margin may be suggestive of such an injury mended that due consideration be given to the biologic
(Rawal SY; 2004). width during placement of the gingival margin.
The ability of the patient to remove plaque from res-
torations and teeth is another major factor influencing
Allergic Gingival Lesions periodontal health. If acceptable periodontal health is
Ingredients present in chewing gum, candies, denti- to be achieved and maintained, periodontal treatment
frices (Carranza FA, Jr; 1996), and periodontal dressings should be instituted before the restorative and prosthetic
have been reported to produce an allergic response. Gin- reconstruction is embarked on. At the same time, opti-
gival lesions may range from erythema to ulceration and mum patient cooperation in plaque control measures is
peeling of epithelium in susceptible individuals. Clinical indispensable.
signs may resolve completely after removal of the etio- The severity of involvement of the periodontal tissues
logic agent. will determine the management of traumatic injuries. It is
necessary in most cases to eliminate the offending agent
and provide symptomatic treatment. More disfiguring
defects may require surgical correction.
CONCLUSION In conclusion, adequate knowledge of local anatomy,
proper treatment planning, and careful and cautious ex-
Over the years, many concepts and clinical techniques ecution of treatment procedure with a multidisciplinary
have influenced the dynamics of the periodontal-restor- approach are often necessary to prevent unnecessary
ative interface. This makeover has been effective with the tissue trauma.
KEY POINTS
• A number of anatomic and iatrogenic factors are con- ning, and gentle handling of tissues during dental
sidered to modify and predispose to the development procedures.
of chronic periodontitis. • Existing pathologic/plaque retentive factors should
• Restorations that do not create a proper functioning be recognized and eliminated before any therapeutic
relationship of a tooth with that of its neighbor or an- procedure is undertaken.
tagonist may instigate periodontal disease, especially in • Surgical procedures should lay emphasis on minimal
situations where maintenance of oral hygiene is difficult. discomfort and optimal healing.
• Operator-induced damage can be prevented by • Special consideration should be given to achieve effec-
proper case selection, meticulous treatment plan- tive home care procedures.

1. Adamczyk E, Spiechowicz E. Plaque accumulation on crowns made
1. List various plaque retentive factors. of various materials. Int J Prosthodont 1990;3:285-91.
2. Describe the possible adverse effects of orthodontic 2. Brezniak N, Wasserstein A. Root resorption after orthodontic
treatment on periodontal health. treatment - part 1: literature review. Am J Orthod Dentofacial Orthop
1993;103:62-6.
3. What is the role of restoration in the etiology of
3. Eid M. Relationship between overhanging amalgam restorations and
periodontal disease? periodontal disease. Quintessence Int 1987;18:775-81.
4. Discuss the periodontal considerations in implant
therapy.
4. Felton DA, Kanoy BE, Bayne SC, Wirthman GP. Effect of in vivo 9. Rawal SY, Claman LJ, Kalmar JR, Tatakis DN. Traumatic lesions of
crown margin discrepancies on periodontal health. J Prosthet Dent the gingiva: a case series. J Periodontal 2004;75:762-9.
1991;65:357-64. 10. Sachs RI. Restorative dentistry and the periodontium. Dent Clin
5. Carranza FA, Jr. The role of iatrogenic and other local factors. In: Clinical North Am 1985;29(2):261-78.
Periodontology. 8 ed., W. B. Saunders Company; 1996: [chapter 12]: 11. Sorensen JA, Doherty FM, Newman MG, Flemming TF. Gingival
161-173. enhancement in fixed prosthodontics - part I: clinical findings.
6. Hancock EB, Mayo CV, Schwab RR, Wirthlin MR. Influence of J Prosthet Dent 1991;65:100-7.
interdental contacts on periodontal status. J Periodontol 1980;51:445-9. 12. Walters JD, Rawal SY. Severe periodontal damage by an endodontic
7. Nevins M, Skurow HM. The intracrevicular restorative margin, the device: a case report. Dent Traumata! 2007;23:123-7.
biologic width, and the maintenance of the gingival margin. Int 13. Zlataric DK, Celebic A, Valentic-Peruzovic M. The effect of
J Periodontics Restorative Dent 1984;3:31-49. removable partial dentures on periodontal health of abutment
8. Ash MM Jr, Costich ER, Hayward JR. A study of periodontal hazards and non-abutment teeth. J Periodontal 2002;73:137-44.
of third molars. J Periodontal. 1962; 33: 209.
CHAPTER
15
Systemic Diseases and Periodontium
A variety of systemic factors can alter the response of peri- The aim of this chapter is to discuss the effect of systemic
odontal tissue to bacterial plaque. Certain systemic disorders disease on the periodontal tissues and their response to
can have a direct effect on the periodontal tissues, and these bacterial plaque.
represent the periodontal manifestations of a systemic disease.
METABOLIC AND ENDOCRINE tissues to local factors, hastening bone loss and delaying
DISORDERS postsurgical healing of the periodontal tissues. Frequent
periodontal abscesses appear to be an important feature of
Endocrine disturbances and hormone fluctuations af- periodontal disease in diabetic patients. Gingival polyps
fect the periodontal tissues directly, modify the tissue and pyogenic granulomas are also seen in patients with
response to local factors, and produce anatomic changes diabetes (Figs 15.1-15.3).
in the gingiva that may favor plaque accumulation and There are two types of diabetes, type 1 and type 2, with
disease progression. Diabetes mellitus is the main endo- several less common secondary types.
crine disorder that affects the periodontium. Likewise, the Type 1 diabetes, formerly insulin-dependent diabetes
sex hormones can alter the response of the periodontal mellitus (IDDM), is caused by cell-mediated autoimmune
tissues to dental plaque. destruction of insulin-producing 13 cells of islet of Lang-
erhans in the pancreas which results in insulin deficiency.
Type 2 diabetes, formerly non insulin-dependent dia-
Diabetes Mellitus betes mellitus (NIDDM), is caused by peripheral resis-
Diabetes mellitus is a complex metabolic disorder tance to insulin action, impaired insulin secretion, and
characterized by chronic hyperglycemia (Table 15.1). Di- increased glucose production in the liver.
minished insulin production, impaired insulin action, or An additional category of diabetes is hyperglycemia
a combination of both results in inability of glucose to secondary to other diseases or conditions. A prime ex-
be transported from bloodstream into tissues which in ample of this type is gestational diabetes associated with
turn results in high blood glucose levels and excretion of pregnancy. Endocrine diseases such as acromegaly and
sugar in urine. Uncontrolled diabetes is associated with Cushing syndrome, tumors, pancreatectomy, and drugs
several long-term complications, including microvascular or chemicals that cause altered insulin levels are included
diseases (retinopathy, nephropathy, neuropathy), macro- in this group.
vascular diseases (cardiovascular, cerebrovascular), an
increased susceptibility to infections, and poor wound Oral Manifestations of Diabetes Mellitus
healing (Table 15.2). • Cheilosis
Uncontrolled or poorly controlled diabetes is associ- • Mucosal drying and cracking
ated with an increased susceptibility and severity of in- • Burning mouth and tongue
fections, including periodontitis. As with other systemic • Diminished salivary flow
conditions associated with periodontitis, diabetes mellitus • Alterations in the flora of the oral cavity with greater
does not cause gingivitis or periodontitis, but evidence predominance of Candida albicans and hemolytic
indicates that it alters the response of the periodontal streptococci and staphylococci.
CHAPTER 15 SYSTEMIC DISEASES AND PERIODONTIUM 121
TABLE 15.1 Characteristics of Type 1 and Type 2 Diabetes
Type 1 diabetes Type 2 diabetes

Age at onset Generally <30 years
Racial preference White Black, Hispanic, American Indian, Pacific Islanders
Presence of family history Common More common than type 1 diabetes

Most common morphotype Thin or normal stature Obese
Onset of clinical disease Abrupt Slow
Pathophysiology Autoimmune B-cell destruction Insulin resistance, impaired insulin secretion, increased liver
glucose production
Level of endogenous insulin production None Decreased, normal, or elevated (depends on stage of disease)
Susceptibility to ketoacidosis High Low
Common treatment regimens Insulin, diet, exercise Diet (weight loss), exercise, oral agents, insulin
TABLE 15.2 Classic Complications of Diabetes Mellitus
Retinopathy Blindness
Nephropathy Renal failure
Neuropathy Sensory
Macrovascular disease Autonomic
Peripheral vascular disease
Cardiovascular disease
( coronary artery disease)
Cerebrovascular disease
(stroke)
Altered wound healing
FIGURE 15.2 Pyogenic granuloma in a patient with diabetes mellitus.

TABLE 15.3 Interaction Between Diabetes and Periodontium Factors Contributing to the Development
of Periodontal Disease
Changes in subgingival Altered microbiota
environment Change in gingival crevicular fluid • Polymorphonuclear leukocyte (PMNL) function
composition • Altered collagen metabolism
• Advanced glycation end products
Altered tissue homeostasis Decreased collagen production
and wound healing Increased matrix metalloproteinase • Bacterial pathogens in diabetes mellitus.
activity
Accumulation of advanced Polymorphonuclear Leukocyte Function
glycation end product turnover In uncontrolled diabetes, reduced PMNL function re-
Changes in host immuno- Decreased polymorphonuclear sults in impaired chemotaxis, defective phagocytosis, or
inflammatory response leukocyte chemotaxis, adherence, impaired adherence. This can contribute to impaired host
phagocytosis defenses and progression of infection (Fig. 15.4). Crevicu-
Elevated proinflammatory
lar fluid collagenase activity, originating from PMNLs,
cytokine response from
monocytes/macrophages (IL-113,
was found to be increased in diabetic patients. The PMN
PGE2, TNF-a) enzymes 13-glucoronidase and elastase, in association with
Increased tissue oxidant stress diabetic angiopathy, have been detected at significantly
IL, interleukin; TNF, tumor necrosis factor. higher levels in poorly controlled diabetic patients. No
alteration of immunoglobulinA (IgA), G (IgG), or M (IgM)
has been found in diabetic patients.
Altered Collagen Metabolism

Diabetes and the Periodontium Chronic hyperglycemia is mainly associated with
Over the years, many possible interactions have been increased collagenase activity and decreased collagen
studied by which diabetes could affect the periodontium synthesis. It affects adversely the synthesis, maturation,
(Table 15.3). and maintenance of collagen and extracellular matrix. In
diabetic patients, both impaired production of the bone
DIABETES MELLITUS AND PERIODONTAL DISEASES matrix component by osteoblast and decreased collagen
• Attachment loss: It occurs more frequently and more synthesis by gingival and periodontal ligament (PDL)
extensively in moderate and poorly controlled diabetic fibroblast have been found.
patients.
• Probing depth: There are significantly more missing Advanced Glycation End Products
teeth and sextants with deep pockets found in diabetic In the hyperglycemic state, numerous proteins and
patients. matrix molecules undergo a nonenzymatic glycosylation,
• Gingivitis: It is more severe in children with diabetes resulting in advanced glycation end products (AGEs). The
than in those without the disease. formation of AGEs can occur at normal glucose levels, but
Impaired host defences
FIGURE 15.4 Fate of chronic hyperglycemia.

in hyperglycemic environments, AGE formation is exces- Hyperparathyroidism
sive. AGE formation cross-links collagen, making it less
soluble and less likely to be normally repaired or replaced. Hypersecretion of parathyroid gland produces gener-
As a result, collagen in the tissues of poorly controlled alized demineralization of the skeleton, increased oste-
diabetics is aged and more susceptible to breakdown. oclasis with proliferation of the connective tissue in the
enlarged marrow spaces, and formation of bone cysts and
Bacterial Pathogens in Diabetes Mellitus giant cell tumors.
Patients with type 1 diabetes suffering from periodon- Oral changes include malocclusion and tooth mobil-
titis have been reported to have a subgingival flora com- ity, radiographic evidence of alveolar osteoporosis with
posed mainly of Capnocytophaga, anaerobic vibrios, and closely meshed trabeculae, widening of the PDL space,
Actinomyces spp., Porphyromonas gingivalis, Prevotella in- absence of the lamina dura, and radiolucent cyst-like
termedia, and Actinobacillus actinomycetemcomitans, which spaces. Bone cysts become filled with fibrous tissue
are common in periodontal lesions of individuals without with abundant hemosiderin-laden macrophages and
diabetes, are present in low numbers in those with the giant cells. They have been called brown tumors, al-
disease. Other studies, however, found scarce Capnocyto- though they are not really tumors but reparative giant
phaga and abundant A. actinomycetemcomitans and black- cell granulomas.
pigmented Bacteroides, as well as P. intermedia, Prevotella
melaninogenica, and Campylobacter rectus. Black-pigmented
species, especially P. gingivalis, P. intermedia, and C. rectus,
are prominent in severe periodontal lesions of Pima Indians HORMONAL CHANGES
with type 2 diabetes.
Female Sex Hormones
Association of Periodontal Infection Gingival alterations such as pubertal gingivitis, preg-
and Diabetic Control nancy gingivitis, and menopausal gingivostomatitis are
Gram-negative bacteria can result in periodontal infec- associated with physiologic hormonal changes and are
tions, and poor metabolic control in diabetic patients can characterized by nonspecific inflammatory reactions with
predispose to periodontal disease progression (Fig. 15.5). a predominant vascular component, leading clinically to
Significant inflammatory lesions in severe periodon- a marked hemorrhagic tendency.
tal disease could contribute to exacerbation of diabetes During the reproductive years, the ovarian cycle is
(Fig. 15.6). Markers of inflammation common to diabe- controlled by the anterior pituitary gland. Gonadotro-
tes and periodontal disease are an indication of disease pins, follicle-stimulating hormone (FSH) and lutein-
control. izing hormone (LH), are produced from the anterior
pituitary gland. The secretion of gonadotropins is also
dependent on the hypothalamus. Ongoing changes
in the concentration of the gonadotropins and ovar-
Diabetic complications ian hormones occur during the monthly menstrual
cycle. Under the influence of FSH and LH, estrogen
and progesterone are steroid hormones produced by
the ovaries during the menstrual cycle. During the
reproductive cycle, the purpose of estrogen and pro-
Poor metabolic control of diabetes mellitus gesterone is to prepare the uterus for implantation of
the egg. The reproductive cycle has two phases. The
l initial phase is referred to as the follicular phase. Levels

of FSH are elevated, and estradiol (E2), the major form
of estrogen, is synthesized by the developing follicle
and peaks approximately 2 days before ovulation. The
Periodontal disease progression/infection effect of estrogen stimulates the egg to move down the
fallopian tubules (ovulation) and stimulates prolifera-
tion of the stroma cells, blood vessels, and glands of
the endometrium (Fig. 15.7). The second phase is the
luteal phase. The developing corpus luteum synthe-
sizes both estradiol and progesterone. Estrogen peaks
Pathogenic bacteria
at 0.2 ng/mL and progesterone at 10 ng/mL to com-
plete rebuilding the endometrium for implantation of
FIGURE 15.5 Diabetes control and periodontal disease progression. the fertilized egg.
Hyperglycemic
··-··-··t Poor. g.lycemic Diabetes mellitus I environnment
,l L__cootr_ol
I:
I I Degenerative vascular
chan9_es
Altered PMN
function numerous
extracellular matrix
• Host resistance
to infection Collagen turnover
t Collagenase
'I
Periodontal disease
i
'I !Lipopolysaccharides!
i -- - ----------~ Periodontal pathogens I

'I
Inhibition of tyrosine phosphorylation o
'! i nsu Ii n receptors
i
'I
'I
:.....·-··-··-··-··-··-··-··-·· Insulin resistance
FIGURE 15.6 Interrelationship between diabetes mellitus and periodontal disease. M0, hyperinflammatory monocyte.
Effects of Estrogen on the Periodontal Tissues • Increases the proliferation of the gingival fibroblasts
• Decreases keratinization which results in the diminu- • Increases the synthesis and maturation of gingival
tion in the effectiveness of the epithelial barrier connective tissues
• Increases cellular proliferation • Increases the amount of gingival inflammation with no
• Inhibits PMNL chemotaxis increase of plaque.
• Reduces proinflammatory cytokines released by hu-
man marrow cells Effects of Progesterone on the Periodontal Tissues
• Reduces T-cell-mediated inflammation • Improves vascular dilation, thus increasing permeability
Follicular Luteal
phase phase
-~0
:5
>
0
.•..•. ------
-·
0 4 8 12 16 20 24 28 4 days
FIGURE 15. 7 Female reproductive cycle (note the peak levels of estrogen and progesterone).
• Stimulates PMNL and prostaglandin E2 in the gingival
crevicular fluid
• Reduces glucocorticoid anti-inflammatory effect
• Inhibits collagen and noncollagen synthesis in PDL
fibroblast
• Alters rate and pattern of collagen production in
gingiva resulting in reduced repair and maintenance
potential.
Periodontal Changes Related to Female Sex Steroid

Hormones
PUBERTY
• Puberty is often accompanied by an exaggerated re- FIGURE 15.8 Pregnancy tumor.

sponse of gingiva to plaque. Pronounced inflamma-
tion, bluish red discoloration, edema, and gingival
enlargement resulting from local factors elicit a mild
present a raspberry appearance. The extreme redness
gingival response.
results from marked vascularity and there is increased
The severity of gingival reaction diminishes as adult- tendency to bleed. The gingival changes are usually pain-
hood approaches even when local factors persist. But less unless complicated by acute infection. In some cases
complete gingival health is restored only with removal the inflamed gingiva forms discrete tumor-like masses
of local factors. referred to as pregnancy tumor.
Microscopically gingival disease in pregnancy (Fig. 15.8)
MENSTRUATION appears as nonspecific vascularizing proliferative inflam-
Gingival changes associated with menstruation have mation. Marked inflammatory cellular infiltration occurs
been attributed to hormonal imbalances and in some with edema and degeneration of the gingival epithelium
patients may be accompanied by a history of ovarian and connective tissue. The epithelium is hyperplastic with
dysfunction. During the menstrual period, the prevalence accentuated rete pegs, reduced surface keratinization, and
of gingivitis increases. Some patients may complain of various degrees of intracellular and extracellular edema
bleeding gums or a bloated, tense feeling in the gums and infiltration by leukocytes. Newly formed engorged
in days preceding menstrual flow. The exudate from in- capillaries are present in abundance.
flamed gingiva is increased during menstruation and It has been reported that subgingival flora changes
as a result the existing gingivitis is aggravated by men- to a more anaerobic flora as pregnancy progresses. The
struation. The salivary bacterial count is increased during only microorganism that increases significantly during
menstruation and at ovulation for up to 14 days. pregnancy is P. intermedia. This increase appears to be
associated with elevations in systemic levels of estradiol
PREGNANCY and progesterone and to coincide with the peak in gin-
Pregnancy itself does not cause gingivitis. Gingivitis gival bleeding. It has also been suggested that during
in pregnancy is caused by bacterial plaque. Pregnancy pregnancy, a depression of the maternal T lymphocyte
accentuates the gingival response to plaque. Tooth mo- response may be a factor in the altered tissue response
bility, pocket depth, and gingival fluid are increased in to plaque.
pregnancy. The severity of gingivitis is increased during The aggravation of gingivitis in pregnancy has been
pregnancy beginning in the second or third month. It attributed principally to the increased levels of proges-
becomes more severe by the eighth month and decreases terone which produce dilation and tortuosity of gingi-
during the ninth month of pregnancy. Partial reduction in val microvasculature, circulatory stasis, and increased
the severity of gingivitis occurs by 2 months postpartum, susceptibility to mechanical irritation, all of which favor
and after 1 year condition of gingiva is stable. However, leakage of fluid into perivascular tissues.
gingiva does not return to normal as long as local factors It has also been suggested that the accentuation of gin-
are present. Tooth mobility, pocket depth, and gingival givitis in pregnancy occurs in two peaks: during the first
fluid are also reduced after pregnancy. trimester when there is overproduction of gonadotropins
Pronounced ease of bleeding is the most striking clini- and during the third trimester when estrogen and proges-
cal feature. The gingiva is inflamed and varies in color terone levels are the highest. Destruction of gingival mast
from a bright red to bluish red. The marginal and inter- cells by increased sex hormones and the resultant release
dental gingivae are edematous, pit on pressure, appear of histamine and proteolytic enzymes may also contribute
smooth and shiny, are soft and pliable, and sometimes to the exaggerated inflammatory response to local factors.
MENOPAUSE
Psychosocial stress
During menopause the usual rhythmic fluctuations of
the female cycle are ended as estradiol ceases to be the
major circulating estrogen. As a result females develop
Behavioral change
r
gingivostomatitis. This condition occurs during meno-
pause or in the postmenopausal period. It is not a very
common condition.
The gingiva and remaining oral mucosa are dry and Poor oral hygiene Overeating (high-
Poor compliance fat diet)
shiny, vary in color from abnormal paleness to redness,
and bleed easily. Microscopically the gingiva exhibits
atrophy of the germinal and prickle cell layers of the
epithelium and in some patients areas of ulceration. The I
l
Cortisol I
patient complains of a dry burning sensation through-
out the oral cavity associated with extreme sensitivity
to thermal changes; abnormal taste sensations described
as salty, peppery, or sour; and difficulty with removable
partial prosthesis. [
~·-··
Bacterial infectioi\""7
Corticosteroid Hormones l
Exogenous cortisone may have an adverse effect on
bone quality and physiology. The systemic administration FIGURE 15.9 Psychosocial stress and its effect on behavior as mani-
of cortisone in experimental animals results in osteoporo- fested by alterations in periodontal disease.
sis of alveolar bone; capillary dilation and engorgement,
with hemorrhage in the POL and gingival connective
tissue; degeneration and reduction in the number of col- 1. through the development of habits that are injurious
lagen fibers of the periodontal ligament; and increased to the periodontium;
destruction of the periodontal tissues associated with 2. by the direct effect of the autonomic nervous system
inflammation caused by local irritation. Stress increases on the physiologic tissue balance.
circulating cortisol levels through stimulation of adrenal
Psychological conditions, particularly psychological
gland. This increased exposure to endogenous cortisol
stress, have been implicated as risk indicators for peri-
may have adverse effects on the periodontium by dimin-
odontal disease.
ishing the immune response to periodontal bacteria.
Following are the periodontal manifestations associ-
ated with stress (Table 15.4):
PSYCHOSOMATIC DISORDERS 1. Osteoporosis of alveolar bone
2. Epithelial sloughing
Harmful effects that result from psychic influences on 3. Degeneration of periodontal ligament
the organic control of tissues are known as psychosomatic 4. Reduced osteoblastic activity
disorders (Fig. 15.9). The two ways in which psychoso- 5. Formation of periodontal pockets
matic disorders may be induced in the oral cavity are 6. Delayed wound healing of connective tissue and bone.
TABLE 15.4 Mechanisms by Which Stress May Affect Periodontal Wound Healing
Health-impairing behaviors Pathophysiologic effects

• Poor oral hygiene Higher glucocorticoid levels (cortisol) and higher catecholamine levels (epinephrine and norepinephrine),
• Increased consumption of which may lead to any or all of the following:
cigarettes • Hyperglycemia, which may impair neutrophil function and impair the initial phase of wound healing
• Forgetfulness and difficulty • Reduced levels of growth hormone, which may downregulate the tissue repair response
in concentrating • Altered cytokine profiles, which may affect recruitment of cells important to wound remodeling, such as
• Disturbed sleeping patterns macrophages and fibroblasts
• Poor nutritional intake • Reduced tissue matrix metalloproteinase levels, leading to impaired tissue turnover and reduced wound
remodeling
• Decreased natural killer cell levels, reducing the host ability to mount an appropriate immune response
to periodontal pathogens
• Altered Thl/Th2 ratio, leading to an increased susceptibility to periodontal disease
HEMATOLOGICAL AND IMMUNE patients with acute forms of leukemia, especially acute
DISORDERS monocytic leukemia. It is not found in edentulous
patients or in patients with chronic leukemia. Leukemic
Hematological disorders or disorders of blood and gingival enlargement consists of a basic infiltration of
blood-forming tissues can have major effect on the peri- gingival corium by leukemic cells that increases the
odontal tissues and their response to bacterial plaque. gingival thickness and creates gingival pockets where
Abnormal bleeding from the gingiva or other areas of bacterial plaque accumulates, initiating a secondary
the oral mucosa that is difficult to control is an important inflammatory lesion that contributes to enlargement of
clinical sign suggesting a hematological disorder. gingiva. Clinically gingiva appears initially bluish red
Deficiencies in the host immune response may lead to and cyanotic with rounding and tenseness of gingival
severely destructive periodontal lesions. These deficien- margin; then it increases in size, most often in the
cies may be primary or secondary, caused by immuno- interdental papilla and partially covering the crowns
suppressive drug therapy or pathologic destruction of of the teeth.
the lymphoid system. 2. Gingival bleeding: The gingival bleeding is secondary
to thrombocytopenia that accompanies the leukemia.
It is especially marked when the platelet count drops
Leukemia below 10,000/mL and is compounded by poor oral
The leukemias are malignant neoplasias of white blood hygiene. Bleeding gingiva is an early sign of leukemia.
cell (WBC) precursors characterized by It is caused by thrombocytopenia resulting from
replacement of bone marrow cells by leukemic cells
• Diffuse replacement of bone marrow with proliferating and from inhibition of normal stem cell function by
leukemic cells leukemic cells or their products.
• Abnormal numbers and forms of immature WBCs in 3. Periodontal infections: Infections of the periodontal tis-
the circulating blood sues secondary to leukemia can be of two types, either
• Widespread infiltrates in the liver, spleen, lymph an exacerbation of an existing periodontal disease or
nodes, and other body sites. through an increased susceptibility of the periodon-
According to lineage of WBCs involved, leukemias are tium to fungal, viral, or bacterial infections.
classified as lymphocytic or myelocytic; a subgroup of 4. Oral ulceration and infection: In leukemia the re-
myelocytic leukemia is monocytic leukemia. sponse to bacterial plaque and other local irritation
According to their evolution leukemias can be acute is altered; the cellular component of the inflamma-
which is rapidly fatal, subacute, or chronic. In acute leuke- tory exudates differs both quantitatively and quali-
mia the primitive blast cells are released into the peripheral tatively from that in nonleukemic individuals. There
circulation, whereas in chronic leukemia the abnormal is pronounced infiltration of immature leukemic
cells tend to be more mature with normal morphologic cells in addition to usual inflammatory cells. As a
characteristics and function when released into circulation. result, the normal inflammatory response may be di-
All leukemias tend to displace normal components minished. Granulocytopenia results from displace-
of bone marrow elements with leukemic cells resulting ment of normal bone marrow cells by leukemic cells
in reduced production of red blood cells (RBCs), WBCs, which increases the host susceptibility to opportu-
and platelets and leading to anemia, leukopenia, and nistic microorganisms and leads to ulceration and
thrombocytopenia. infection.
Anemia results in poor tissue oxygenation, making
tissue more friable and susceptible to breakdown. A re- Anemia
duction of normal WBCs in the circulation leads to an
increased susceptibility to infections. Thrombocytopenia Anemia is a deficiency in the quality or quantity of
leads to bleeding tendency which can occur in any tis- the blood, as manifested by a reduction in the number
sue, but in particular affects the oral cavity, especially the of erythrocytes and in the amount of hemoglobin.
gingival sulcus. Some patients may have normal blood Oral changes of sickle cell anemia include generalized
counts, while leukemic cells reside primarily in the bone osteoporosis of the jaws, with a peculiar stepladder align-
marrow. This type of disease is called aleukemic leukemia. ment of the trabeculae of interdental septa, along with
pallor, yellowish discoloration of the oral mucosa.
Periodontal Manifestations
1. Gingival enlargement: The enlargement is primarily
Thrombocytopenia
the result of a massive leukemic cell infiltration into
the gingival connective tissue. This is called leukemic It is the condition of reduced platelet count resulting
gingival enlargement. It has the highest incidence in from either lack of platelet production or increased loss
of platelets. Thrombocytopenic purpura is characterized food supply. Although some nutritional deficiencies can
by a low platelet count, a prolonged clot retraction and significantly exacerbate the response of the gingiva to
bleeding time, and normal or slightly prolonged clotting plaque bacteria, the precise role of nutrition in the initia-
time. The gingivae are swollen, soft, and friable. Bleed- tion or progression of periodontal diseases remains to be
ing occurs spontaneously or on the slightest provocation elucidated.
and is difficult to control. Gingival changes represent an
abnormal response to local irritation.
Fat-Soluble Vitamins
Leukocyte Disorders Vitamin A Deficiency

Vitamin A is an important factor for maintaining the
Disorders that affect production or function of leuko- health of epithelial cells of the skin and mucous mem-
cytes may result in severe periodontal destruction. The branes. Deficiency of vitamin A leads to degenerative
PMNLs, in particular, play a critical role in bacterial infec- changes in epithelial tissues, resulting in a keratinizing
tions because they are first line of defense. metaplasia. In experimental animals, vitamin A deficiency
Neutropenia results in hyperkeratosis and hyperplasia of the gingiva,
with a tendency for increased pocket formation.
It is a blood disorder that results in low levels of cir-
culating neutrophils. Cyclic neutropenia is characterized Vitamin D Deficiency
by a cyclical depression of PMNL count in peripheral
Vitamin D, or calciferol, is essential for the absorption
blood. Many case reports and reviews cite oral ulceration,
of calcium from the gastrointestinal tract, the maintenance
inflamed gingiva, and rapid periodontal breakdown. The
of the calcium-phosphorus balance, and the formation of
recurrent oral ulcerations often make mechanical plaque
teeth and bones.
control difficult and therefore exacerbate the periodontal
problem. Vitamin D deficiency with normal dietary calcium and
phosphorus in young dogs is characterized by osteoporo-
Lazy Leukocyte Syndrome sis of alveolar bone, osteoid forming at a normal rate but
remaining uncalcified, and failure of osteoid to resorb,
It is characterized by susceptibility to severe microbial
infections, neutropenia, defective chemotactic response leading to excessive accumulation.
by neutrophils, and an abnormal inflammatory response. Vitamin E Deficiency
Individuals diagnosed with lazy leukocyte syndrome are
Vitamin E serves as an antioxidant to limit free radical
susceptible to aggressive periodontitis with destruction
of bone and early tooth loss. reactions and protect cells from lipid peroxidation. No
relationship has been demonstrated between deficien-
Leukocyte Adhesion Deficiency cies in vitamin E and oral disease, but systemic vitamin
It is a very rare genetic disorder and results from the E appears to accelerate gingival wound healing in the rat.
inability to produce or failure to express normally an im-
portant cell surface integrin (CD18), which is necessary Water-Soluble Vitamins
for leukocytes to adhere to the vessel wall at the site of
infection. B-Complex Deficiency
The vitamin B complex includes thiamine, riboflavin,
Agranulocytosis niacin, pyridoxine (B6), biotin, folic acid, and cobalamin
It is characterized by a reduction in the number of cir- (B12). Oral disease is rarely the result of a deficiency in just
culating granulocytes and results in severe infections, in- one component of the B-complex group; the deficiency is
cluding ulcerative necrotizing lesions of the oral mucosa, generally multiple (Table 15.5).
skin, and gastrointestinal and genitourinary tracts. The Oral changes common to B-complex deficiencies are
gingival margin may not be involved. Gingival hemor- gingivitis, glossitis, glossodynia, angular cheilitis, and
rhage, necrosis, increased salivation, and fetid odor are inflammation of the entire oral mucosa. The gingivitis
the accompanying clinical features. in vitamin B deficiencies is nonspecific, as it is caused by
bacterial plaque rather than by the deficiency, but it is
subject to the modifying effect of the latter.
INFLUENCE OF NUTRITION
Vitamin C (Ascorbic Acid) Deficiency
Nutritional disorders not only are the result of in- Severe vitamin C deficiency in humans results in scur-
adequate dietary intake but also may be due to distur- vy, a disease characterized by hemorrhagic diathesis and
bances in absorption and utilization, from an adequate retardation of wound healing.
TABLE 15.5 Vitamin B-Complex Deficiency and Oral 1. Low levels of ascorbic acid influence the metabolism of
Manifestations collagen within the periodontium, thereby affecting the
Deficiency Oral manifestations ability of the tissue to regenerate and repair itself.
Thiamine • Hypersensitivity of oral mucosa 2. Ascorbic acid deficiency interferes with bone formation,
• Minute vesicles (simulating herpes) on the buc- leading to loss of periodontal bone.
cal mucosa, under the tongue, or on the palate 3. Ascorbic acid deficiency increases the permeability
• Erosion of the oral mucosa of the oral mucosa to tritiated endotoxin and tritiated
Riboflavin • Glossitis inulin and of normal human crevicular epithelium to
• Angular cheilitis tritiated dextran.
• Superficial vascularizing keratitis 4. Increasing levels of ascorbic acid enhance both the
• Patchy atrophy of lingual papillae
chemotactic and migratory action of leukocytes
• Engorged fungiform papillae
without influencing their phagocytic activity.
Niacin • Glossitis 5. An optimal level of ascorbic acid is apparently required
• Gingivitis
to maintain the integrity of the periodontal microvascula-
• Generalized stomatitis
ture, as well as the vascular response to bacterial irritation
Folic acid • Generalized stomatitis and wound healing.
• Ulcerated glossitis
6. Depletion of vitamin C may interfere with the ecologic
• Cheilitis
equilibrium of bacteria in plaque and thus increase its
pathogenicity.
Vitamin C deficiency (scurvy) results in defective
formation and maintenance of collagen, retardation or
cessation of osteoid formation, and impaired osteoblas- OTHER SYSTEMIC CONDITIONS
tic function. The classic clinical signs of scurvy describe
the gingiva as being bright red, swollen, ulcerated, and Hypophosphatasia
susceptible to hemorrhage. Vitamin C deficiency is also
characterized by increased capillary permeability, suscep- Patients with hypophosphatasia have a low level of
tibility to traumatic hemorrhages, hyporeactivity of the serum alkaline phosphatase and phosphoethanolamine in
contractile elements of the peripheral blood vessels, and serum and urine. Teeth are lost with no clinical evidence
sluggishness of blood flow. of gingival inflammation and show reduced cementum
Gingivitis seen as a result of vitamin C deficiency is formation. In adolescents, this disease resembles localized
also called as scorbutic gingivitis. aggressive periodontitis.
POSSIBLE ETIOLOGIC RELATIONSHIPS BETWEEN

ASCORBIC ACID AND PERIODONTAL DISEASE Metal Intoxication
It has been suggested that ascorbic acid may play a The ingestion of metals such as mercury, lead, and bis-
role in periodontal disease by one or more of the follow- muth may lead to oral manifestations caused by either in-
ing mechanisms: toxication or absorption without the evidence of toxicity.
KEY POINTS
• Hyperglycemia that results from defects in secretion of • Porphyromonas gingivalis and Prevotella intermedia are
the hormone insulin, impaired insulin action, or both is seen in increased numbers in pregnancy.
an important feature of diabetes mellitus. • Increased exposure to endogenous cortisol may have
• Reduced PMNL function and defective chemotaxis can adverse effects on the periodontium by diminishing the
contribute to impaired host defenses and progression of immune response to periodontal bacteria.
infection in uncontrolled diabetes mellitus. • The enlargement in leukemic patients is primarily a
• Increased collagenase activity and decreased collagen result of a massive leukemic cell infiltration into the
synthesis is seen in chronic hyperglycemia. gingival connective tissue. When present, it is usually a
• The circumpubertal period is often accompanied by feature of acute monocytic leukemia.
the exaggerated response of the gingiva to local ir- • Vitamin C deficiency (scurvy) results in defective forma-
ritation. tion and maintenance of collagen, retardation or ces-
• Pregnancy gingivitis is extremely common and affects sation of osteoid formation, and impaired osteoblastic
30-100% of all pregnant women. function.
QUESTIONS 2. Lindhe J. Clinical Periodontology and Implant Dentistry. 5th ed. Oxford:
3. Mealey BL, Moritz AJ. Hormonal influences: effects of diabetes
1. Describe diabetes as a risk factor in periodontal mellitus and endogenous female sex steroid hormones on the
disease. periodontium. Periodontal 2000 2003;32:59-81.
2. Define scorbutic gingivitis. 4. Newman MG, Takei HH, Klolkevold PR, Carranza F. Carranza's
3. Describe periodontal manifestation in leukemia. Clinical Periodontology. 10th ed. St. Louis: Mosby; 2007.
5. Seymour RA, Heasman PA. Drugs, Diseases and the Periodontium. New
4. Describe pregnancy tumor.
York: Oxford University Press; 1992.
6. Skully C. Medical Problems in Dentistry. 5th ed. Edinburgh: Churchill
Livingstone; 1997.
Suggested readings
1. Genco RJ, Goldman HM, Cohen OW. Contemporary Periodontics.
St. Louis: Mosby; 1990.
CHAPTER
16
Periodontal Medicine
Environmental and acquired risk factors are known to the interrelationship between periodontal disease and
to alter the onset, rate of progression, and clinical pre- systemic health.
sentation of periodontal disease as well as its response to It has already been mentioned that risk factors are
therapy. An increased risk relationship between systemic strongly associated with groups of individuals who have
disease and periodontitis has been suggested by the recent the disease in question in contrast to those who do not have.
findings; in addition to this, evidence is also emerging to Risk factors may be part of the causal chain or bring some-
support the idea that periodontitis has an adverse effect one in contact with the causal chain. Recently periodontitis
on systemic health. An increased risk of coronary heart has been proposed as a risk factor for various systemic dis-
disease, poor glycemic control, respiratory disease, and eases. This new branch of periodontology that is concerned
preterm low-birth-weight babies is associated with peri- with the effect of periodontal disease on a wide range of
odontal disease. A lot of importance is now being given organ systems is known as periodontal medicine.
PERIODONTITIS AS A RISK FACTOR which have strongly demonstrated periodontal disease

FOR SYSTEMIC DISEASE as the major risk factor for systemic diseases. At present,
periodontitis has been cited as risk factor for four major
The history of periodontal medicine dates back to early systemic diseases:
20th century (1900) when William Hunter and WD Miller
1. Coronary heart disease (CHD)
proposed the concept that oral infection is the likely cause
2. Preterm low birth weight (PTLBW)
of most systemic diseases. They proposed that prosthesis,
3. Type 2 diabetes mellitus (DM)
untreated periodontal disease, and dental caries were the
4. Chronic obstructive pulmonary disease (COPD).
source of microbes that acted as a focus of infection and
produced "subinfection" at distant sites. The next 40 years
that followed were referred to as the era of focal infection.
After four decades of widespread extraction, which failed PERIODONTITIS AND CORONARY
to eliminate systemic disorders and the fact that both HEART DISEASE
people with a healthy mouth and edentulous patients
also developed systemic disorders, dentists started to Coronary heart disease is a condition in which fibro-
realize that oral infections are not the sole cause for all fatty plaque accumulates on the walls of coronary arteries,
systemic conditions. supplying the heart muscle with oxygen-rich blood. The
After a period of lull, the end of the 20th century saw deposited plaque in turn narrows the arteries, thereby
resurgence in research regarding focal infection, with the reducing the blood flow to the heart muscle. Also, with
pioneering study done by who found a significant associa- this there is increased chance of forming blood clots in
tion between poor periodontal health and occurrence of the arteries which can partially or completely block blood
myocardial infarction. The provocative findings revealed flow leading to angina pectoris (temporary, constant,
by the above study led several other researchers to work short-acting chest pain usually brought on by exertion but
on similar lines. Research conducted from then on ranged sometimes occurring at rest not lasting more than 30 min)
from isolated case reports to interventional studies, all of or myocardial infarction (death of cardiac muscle due
to coronary insufficiency usually manifested by angina- the other side, different studies (case-control and cohort)
like pain lasting longer than 30 min and not necessarily have confirmed the strong association between periodon-
brought on by exertion). Over a period of time, coro- titis and coronary artery disease.
nary artery disease (CAD) can weaken heart and lead to When putative periodontal microbes forming the sub-
heart failure when the heart cannot pump enough blood gingival flora induce an inflammatory immune response
throughout the body. in the gingival tissues, resident cells and inflammatory
cells produce inflammatory cytokines and mediators. If
interventional treatment is not carried out, this gingivitis
Atherosclerosis (Fig. 16.1) progresses to periodontitis when there will be increased
Atherosclerosis comes from the Greek words athero cytokines, enzymes, and mediators. When there is pres-
(gruel or paste) and sclerosis (hardness) where deposits sure on the periodontium during brushing/mastication/
of fatty substances (low-density lipoproteins), cholesterol, tooth movement, the microbes, toxins, cytokines, and
cellular waste products, calcium, and other substances ac- mediators are pushed into the systemic blood circula-
cumulate in the blood vessel wall forming a plaque that tion. They travel to distant sites and initiate a pathology
elevates into the blood vessel blocking the blood flow. The specific to that organ/ system.
atherosclerotic plaque contains fat-laden macrophages Proposed mechanisms by which periodontal infections
called "foam cells," T cells, mast cells, and matrix metal- may affect the onset and progression of atherosclerosis
loproteinase (MMP). The plaque ruptures at the weakest and CHD / stroke (Fig. 16.2) are as follows:
part and travels to another site in the bloodstream as
an embolus. The ruptured plaque fragments can release 1. Certain microbes (Streptococcus sanguis and P. gingivalis)
certain procoagulant chemicals that may cause plate- express a protein called platelet aggregation-associated
let aggregation and in turn cause thrombus formation. protein (PAAP) and aggregate platelets leading to
The thrombi that are formed can also block major blood thromboembolic events.
vessels causing ischemia. If this happens in the cerebral 2. Periodontitis influences atherosclerosis in more than
vessels, a stroke results. There are many risk factors for one way:
atherosclerosis such as diabetes mellitus, smoking, intake a. Periodontal pathogen directly invades endothelial
of fatty diet, and hypertension. In addition, microbes and cells and induces cytokines, chemokines, and
viruses have also been implicated in producing inflam- adhesion molecules which may initiate/ accelerate
mation leading to atherosclerosis. Some of the bacteria atherosclerosis.
cited are Chlamydia pneumoniae and Helicobacter pylori b. Long-standing infections such as periodontitis may
along with viruses such as herpes simplex. Since microbes significantly upregulate inflammatory cascade that
have been implicated in the initiation of atherosclerosis, through systemic circulation reaches the vulnerable
researchers started to associate periodontal pathogens artery and shifts the status of endothelial cells from
with atheroma formation, especially Porphyromonas gin- antithrombotic to prothrombotic one. In addition,
givalis. Deshpande demonstrated periodontal pathogens periodontitis increases the production of coagulation
in atheromatous plaques and aortic endothelial cells. On factor VIII/von Willebrand factor (vWF) antigen,
increasing the risk of thrombus formation. Also,
periodontitis increases the fibrinogen level and
white blood cell (WBC) counts leading to increased
blood viscosity.
c. Phagocytic cells such as macrophages ingest peri-
odontal pathogens. Resistant to phagocytosis patho-
gens survive within the macrophages and travel to
distant sites. At certain areas these macrophages
with ingested live cells get attached to immunologi-
cally compromised endothelial cells and initiate the
atherosclerotic changes.
d. P. gingivalis has certain proteins such as heat
shock proteins (HSPs) that are similar to corre-
sponding human proteins. When these proteins
travel to sites, antibody directed toward these
FIGURE 16.1 Atherosclerosis. (1) Endothelial dysfunction; (2) fatty
streak formation; (3) advanced lesion with fibrous cap (FC); (4) unstable
bacterial HSPs, because of structural homology,
fibrous plaque (rupture of cap); (5) platelet aggregation. EC, endothelial reacts with human HSPs, inducing an autoim-
cells; F, foam cell; M, monocyte; Me, macrophage; P, platelets; SMC, mune reaction. This is called "molecular mim-
smooth muscle cell; T, T lymphocytes. icry."
CHA PTER 16 PERIO DONTAL M EDICINE 133
P. gingivalis
P. gingivalis strepto 2
O_ HSP 60
EC
Q
Inflammatory
mediators SMC
cytokines
Macrophage with microbe
FIGURE 16.2 Possible mechanisms of initiation and progression of atherosclerosis from periodontitis. EC, endothelial cell; HSP, heat shock
protein; PAAP, platelet aggregation-associated protein; SMC, smooth muscle cell.
A model of a pathway from dental plaque and peri- maternal periodontitis has been associated with adverse
odontal disease to infective endocarditis, atherosclerosis, pregnancy outcomes, such as preterm birth, preeclampsia
and coronary heart disease is given in Fig. 16.3. (pregnancy-induced hypertension), gestational diabetes,
delivery of a small-for-gestational-age infant, and fetal
loss. The strength of these associations suggests that there
PERIODONTITIS AS A RISK FACTOR FOR is an increased risk ranging from a twofold to sevenfold
PRETERM LOW,BIRTH,WEIGHT BABIES increase which is suggestive that periodontitis may be an
independent risk factor for adverse pregnancy outcomes.
A significant research in the area of maternal oral health Before we go further, it is necessary to know a little bit
and its effect on pregnancy outcomes has been initiated about reproductive anatomy. The amnion is a thin, tough
due to our increased understanding and recognition of the membranous sac that encloses the embryo or fetus of a
importance of good oral health. A total of 50-70% of all mammal, bird, or reptile. Chorion is another membrane
women develop gingivitis during their pregnancy mainly that exists during pregnancy between the developing
due to the result of varying hormone levels without any fetus and the mother (Fig. 16.4). The primary cause of
changes in the plaque level; this condition is commonly low-birth-weight deliveries is preterm labor or premature
referred to as pregnancy gingivitis. This type of gingivitis rupture of membranes (PROM). The World Health Orga-
is usually presented between the 2nd and the 8th month nization (WHO) defines preterm birth as any live birth at
of pregnancy and is mainly attributed to the increased less than 37 weeks of gestation. The other terminologies
levels of the hormones progesterone and estrogen which are very preterm with delivery at less than 32 weeks and
in turn have an effect on the small blood vessels of the gin- extremely preterm with delivery at less than 28 weeks.
giva, making it more permeable. As a result of increased Birth weight is strongly correlated with gestational age,
permeability of small vessels pathogenic bacteria can and studied independent of gestational age. Birth weights
proliferate and contribute to inflammation in the gingiva, are considered to be low if less than 2500 g, very low if
thereby increasing the mother's susceptibility to oral in- less than 1500 g, and extremely low if less than 1000 g. On
fections. Females often experience these changes during the health grounds, preterm babies suffer from respiratory
other periods of their life when hormones are fluctuat- distress syndrome (RDS), intraventricular/ periventricular
ing, such as puberty, menstruation, and pregnancy. New hemorrhage, cerebral palsy, and mental retardation, to
vistas of research have suggested that the presence of mention a few.
Dental Host periodontal tissue
Microbes I I Microbial toxins and products 11 Host cytokines and inflammatory I
Pcriodontitis
Tooth brushing/chewing
Bactercmia
ystemic
Microbes/microbial toxins and products/host cytokines and inflammatory
Travel to blood
~[
~ ~ ~ ij
nclothelial
I Blood flow
11
Macrophages I 1=Platclct
n n n n
t Chernokine 11 Sluggish I It IL-IP, TNF-o, lit Clumping/
aggregation
Atherosclerosis
FIGURE 16.3 A model of a pathway from dental plaque and periodontal disease to infective endocarditis, atherosclerosis, and coronary heart
disease. ICAM, intercellular adhesion molecule.
Many risk factors have been identified for PROM and periodontal infection and preterm birth; however, there
low birth weight (LBW) such as socioeconomic status, are a few studies that have failed to demonstrate such an
smoking, and alcohol, but all of these singularly or com- association. The role of maternal periodontal infection
bined account for only 75% of cases. So, in the remaining on other adverse pregnancy outcomes as reported in the
25% of cases, infection seems to be the possible cause. data of various studies is even less clear. According to the
Choriodecidual infections including chorioamnionitis available evidence inflammation and endothelial activa-
are significant predictors of preterm birth. This could tion have been suggested in the pathophysiology of pre-
be a direct one by the infection of chorioallantoic mem- eclampsia. Women who were diagnosed with periodontal
brane and an indirect one by hematogenous spread from infection at the time of delivery were found to carry a
a distant site (e.g., periodontitis). Offenbacher were the twofold increased risk for preeclampsia. Other reports
first to report a link between periodontitis and preterm also suggest of a possible association between maternal
birth. Evidence suggests a relationship between maternal periodontal infection and preeclampsia.
INFECTION
( Extragenital periodontitis ) ( Genital bacterial vaginosis)
l
dotoxin/microbial pro
l
Amnion
'-'---Chorion
Proinflammatory
cytokines/mediators
IL-1, TNF-a, MMPs,
PGE2
••
Preterm low birth weight
FIGURE 16.5 Proposed hypothetical model of the association

FIGURE 16.4 Developing fetus showing amnion and chorion. between periodontal disease and preterm low birth weight.
Possible Mechanism by Which Periodontitis

May Be a Risk Factor for Preterm • Type 1 insulin-dependent diabetes mellitus (IDDM)
Low-Birth-Weight Babies - Immune mediated
Prostaglandin E2 (PGE2) and prostaglandin F2a (PG- - Nonimmune mediated/idiopathic
F2a) are required for expulsion of fetus after the rupture • Type 2 noninsulin-dependent diabetes mellitus
of the amniochorionic membrane. (NIDDM)
When there is an infection, the microbes travel to pla- - Predominantly insulin resistant
centa and initiate inflammation. They stimulate the pro- - Predominantly secretory defect
duction of interleukin (IL)-1, IL-6, and tumor necrosis • Other specific types
factor (TNF)-a. The lipopolysaccharides of gram-negative - Genetic defects in insulin action
bacteria, either through TNF or directly, stimulate the pro- - Disease of the exocrine pancreas
duction of PGE2 and PGF, which in turn leads to rupture - Endocrinopathies
of membrane and expulsion of the fetus before delivery - Drug/chemical induced
time (Fig. 16.5). - Infections
• Other genetic problems
- Gestational diabetes
PERIODONTAL DISEASE • Complications of diabetes mellitus
AND DIABETES MELLITUS - Retinopathy
- Nephropathy
Diabetes is a syndrome characterized by clinically and - Neuropathy
genetically heterogeneous group of metabolic disorders - Macrovascular disease
which usually manifests itself by abnormally high lev- - Altered wound healing
els of glucose in the blood. It is now well accepted now - Periodontal disease (proposed sixth complication of
that this chronic hyperglycemia in turn causes long-term diabetes mellitus).
damage to different organs such as heart, eyes, kidneys,
nerves, and vascular system. New classification and diag-
nostic criteria for diabetes were proposed by the American Diabetes mellitus and periodontitis have a two-way
Diabetes Association in 1997. These criteria were later relationship. On one hand, diabetic patients are more
modified in 2003 to include the diagnosis of impaired prone to periodontitis by altered microbial flora, and in-
fasting glucose and impaired glucose tolerance: flammatory and immune processes, and on the other
hand, periodontitis has been proposed as a risk factor for serum inflammatory markers which results in increased
diabetes mellitus. insulin resistance and poor glycemic control.
Periodontal treatment not only reduces clinically evi-
dent inflammation but also has systemic effects that ex-
Periodontitis as a Risk Factor for Diabetes tend beyond the local periodontal environment such as
Mellitus decreased serum levels of IL-6 and CRP. The metabolic
An elevated systemic chronic inflammatory state in the state in diabetes is significantly affected, and also the
body is induced or perpetuated due to the periodontal risk of worsening of glycemic control over time can be
diseases. It has been shown that in people without dia- increased, due to the presence of periodontal disease. For
betes acute bacterial and viral infections increase insulin example, in a 2-year longitudinal trial, the risk of worsen-
resistance which often persists for weeks to months after ing of glycemic control over time was shown to increase
clinical recovery from the illness. Such illnesses and resul- sixfold in diabetic subjects with severe periodontitis when
tant increases in insulin resistance in people with diabetes measured at baseline compared with that in diabetic sub-
greatly aggravate glycemic control. jects without periodontitis.
Because of the increased prevalence of cardiovascular
Possible Mechanism by Which Periodontal diseases in a diabetic individual, a recent longitudinal
Infection May Be a Risk Factor for Diabetes trial examined the effect of periodontal disease on overall
Mellitus mortality and cardiovascular disease-related mortality in
Acute bacterial and viral infections are known to in- more than 600 subjects with type 2 diabetes. In subjects
crease insulin resistance. with severe periodontitis, the mortality rates due to isch-
emic heart disease (IHD) and diabetic nephropathy were
WHAT IS INSULIN RESISTANCE? 2.3 and 8.5 times, respectively. The overall mortality rate
All the cells in the body require glucose for their sur- from cardiorenal disease was 3.5 times higher in subjects
vival. The required glucose is transported into the cell with severe periodontitis. Interventional studies showed
with the help of insulin receptors. When cells require more that when type 1 diabetic patients with periodontitis were
energy, or if blood glucose level goes up, insulin receptors treated by scaling and root planing, localized gingivecto-
are exposed on the cell surface that help to increase the my, and selected tooth extraction combined with systemic
glucose transport into the cells from circulation. Glucose procaine penicillin G and streptomycin, their required
is stored in adipose tissue. Cells can become resistant to dose of insulin came down.
insulin; pancreas produces more insulin in an attempt to The hallmark of type 2 diabetes is an increase in insulin
force glucose into the cell. This is known as "insulin resis- resistance, which is also strongly linked to obesity and
tance." This compensatory insulin increase prolongs the body mass index (BMI); both act in two ways to produce
insulin level in blood leading to hyperinsulinemia. This this: (i) by increasing IL-6 and INF-a production that
increased insulin leads to increased fibrinogen and tri- stimulates liver cells to produce acute phase proteins and
glycerides and decreased high-density lipoprotein (HDL) (ii) by reducing the synthesis of adiponectin, a hormone
production. They increase lipid oxidation and deposit it produced by adipocytes (Fig. 16.6).
on coronary artery walls leading to atheromatous plaque A positive association between BMI and clinical at-
formation and hypercoagulability. In type 2 diabetes, tachment loss for a nondiabetic individual was revealed
there is an increased insulin resistance and infection (sys- recently by the Third National Health and Nutrition
temic/ periodontal) augments it. Periodontal therapy Examination Survey (NHANES III) data. Interestingly,
decreases the insulin resistance. Adipocytes, fat-storing overweight individuals (BMI: 27 kg/m2) with elevated
cells, produce molecules leptin and adiponectin and cyto- insulin resistance had a significant odds ratio of 1.48 for
kine INF-a. Obesity increases the INF-a production and severe periodontal disease compared with overweight
diabetes augments the production. individuals without insulin resistance. Elevated serum
Periodontal diseases may induce or perpetuate an el- levels of INF-a and soluble INF-a receptors were seen in
evated systemic chronic inflammatory state. Evidence subjects with highest quartile of body mass (BMI: 30.8 kg/ m2)
suggests that gram-negative organisms such as P. gingi- as compared with those in the lowest quartile of body
valis, T. forsythensis, and Prevotella intermedia colonizing mass, with a BMI <24.6 kg/m2• These data suggest that
the periodontitis patients have significantly higher serum increased BMI is associated with both systemic inflam-
markers of inflammation such as C-reactive protein (CRP), mation and periodontal disease.
INF-a, IL-6, and fibrinogen than those colonizing subjects Periodontal treatment consisting of mechanical de-
without periodontitis. These organisms or their products bridement and local delivery of minocycline delivered
when systemically disseminated may induce a bacteremia to type 2 diabetic subjects with periodontitis in a small
or endotoxemia, thereby producing an elevated inflam- study resulted in a significant reduction in serum INF-
matory state, and also this triggers an increased level of a levels that in turn results in a significant reduction in
Increased BMI
Obesity Decreased
adiponectin
Increased
adipocytcs
Increased IL-6 and TNF-o.
Increased acute phase

proteins in the liver
Increased insulin resistance
Type 2 diabetes rnellitus
FIGURE 16.6 Correlation of increased BMI and obesity with type 2 diabetes.
mean HbAlc levels from 8.0 to 7.1 %. As many as 143 re- occurs in which neutrophils and mononuclear inflamma-
ductions in HbAlc values were strongly correlated with tory cells accumulate within the lung tissue.
the reductions in serum INF-a levels across the patient This disease shares similar pathogenic mechanisms
population. Thus, periodontal treatment may have its with periodontal disease. In both diseases, a host inflam-
effect locally where it reduces inflammation and also matory response is mounted in response to chronic chal-
systemically where it has shown to decrease serum levels lenge: by bacteria in periodontal disease and by factors
of the inflammatory mediators which are known to cause such as cigarette smoke in COPD (tobacco smoking is the
insulin resistance, thereby positively affecting glycemic primary risk factor for COPD). The resulting neutrophil
control. influx leads to the release of oxidative and hydrolytic en-
zymes that cause tissue destruction directly. Recruitment
of monocytes and macrophages leads to further release
PERIODONTAL DISEASE AND CHRONIC of proinflammatory mediators. In a longitudinal study of
OBSTRUCTIVE PULMONARY DISEASE 1100 men, alveolar bone loss was found to be associated
Anatomy and Physiology

Air inhaled through the nose and mouth passes through
the throat into the trachea (Fig. 16.7). The trachea divides
into right and left bronchi and divides again, becom-
ing narrower and narrower (bronchioles) (Fig. 16.8). The
smallest airway ends in alveoli (like a bunch of grapes;
Fig. 16.9). Every alveolus is surrounded by tiny blood
vessels. Exchange of gas takes place between the alveolar
wall and the capillaries (Fig. 16.10).
In COPD, less air flows in and out of airway because:
(i) airway and air sacs lose elasticity, (ii) walls between air
sacs are destroyed, (iii) walls of the airway become thick
and inflamed, and (iv) there is more mucus secretion. In
pneumonia, the alveoli are filled with pus, mucus, and
other liquids, so oxygen exchange cannot take place. Most
common causes for pneumonia are bacteria, virus, and
inhalation of vomit or foreign substances.
COPD is a disease state characterized by airflow ob-
struction due to chronic bronchitis or emphysema. Bron-
chial mucous glands enlarge and an inflammatory process FIGURE 16. 7 Passage of air through the throat into the trachea.
FIGURE 16.8 Division of trachea into bronchi and bronchioles. FIGURE 16.10 Exchange of gas between the alveolar wall and the
capillaries. BV, blood vessel.
with the risk for COPD, and over a 25-year period, 23%
of subjects were diagnosed with COPD. Individuals with
had a significantly increased risk of subsequently devel-
poor oral hygiene were found to be at increased risk for
oping COPD compared with subjects with less bone loss.
chronic respiratory diseases such as bronchitis and em-
Scannapieco and Ho in a recent analysis which is based
physema. Even without other risk factors, subjects with
on a more recent and detailed survey found a significant
more severe bone loss at the baseline dental examination
association between COPD and periodontal attachment
loss.
The vast majority of pulmonary diseases is due to aero-
bic bacteria that are found in the oral flora but are not re-
lated to any oral diseases. In contrast, the list of anaerobes
(facultative or obligate) implicated in the destruction of
periodontal tissues and that of organisms isolated from in-
fected lungs are quite similar. For example, from infected
lungs both Aggregatibacter actinomycetemcomitans and Fu-
sobacterium nucleatum have been isolated and pulmonary
pathogen Pseudomonas aeruginosa has been isolated from
patients with "refractory" periodontitis. In an animal
model simulating aspiration the pulmonary pathogenicity
of Bacteroides gingivalis has been demonstrated.
However, Scannapieco and coworkers conducted a
study in a critical care ward; they were able to isolate
several known pulmonary pathogens (e.g., Klebsiella pneu-
moniae and Serratia marcescens) from dental plaque. The
protease activity (including degradation of fibronectin,
an adhesion protein) of periodontal pathogens is cor-
related with poor oral hygiene. Thus, fibronectinolytic
activity of the crevicular fluid promotes the adherence of
anaerobic gram-negative bacteria to the epithelium of the
upper airway, thus playing a role in the pathogenesis of
pneumonia. Pneumonia and poor oral health in elderly
FIGURE 16.9 Smallest airway ending in alveoli. people were reported in three retrospective studies and it
was found that the prevalence of respiratory tract infec- important risk factors for aspiration pneumonia after ad-
tion (RTI) was significantly greater among dentate than justment for established medical risk factors were dental
among edentulous subjects (40% vs. 27%) and was also decay, cariogenic bacteria, and periodontal pathogens as
greater among subjects with selected oral disorders than reported in a recent study.
among those without such conditions. The potentially
KEY POINTS
• There has been a resurgence in research regarding • Since microbes have been implicated in the initia-
focal infection, with the pioneering study done by who tion of atherosclerosis, researchers started to associ-
found a significant association between poor periodontal ate periodontal pathogens with atheroma formation,
health and occurrence of myocardial infarction. especially P. gingivalis obstructive pulmonary
• At present, periodontitis has been cited as a risk fac- disease.
tor for four major systemic diseases, i.e., coronary • Periodontitis is considered as the sixth complication of
heart disease, preterm low birth weight, type 2 dia- diabetes.
betes mellitus, and chronic obstructive pulmonary • The presence of periodontitis increases the risk of wors-
disease. ening of glycemic control over time.

1. Deshpande RG, Khan MB, Genco CA. Invasion of aortic valve and
1. Describe periodontal care of patients on heart endothelial cells by Porphyromonas gingivalis. Infect lmmun
anticoagulant therapy. 1998;66:5337-43.
2. Describe periodontal management of patients with 2. Grossi SG, Genco RJ. Periodontal disease and diabetes mellitus - a
two-way relationship. Ann Periodontol 1998;3:51.
uncontrolled diabetes.
3. Grossi SG, Skrepcinski FB, DeCaro T, et al. Treatment of periodontal
3. Describe gingival changes in pregnancy. disease in diabetes reduces glycated hemoglobin. J Periodontal
4. Describe preterm low birth weight and periodontal 1997;68:713.
disease. 4. Mattila KJ, Nieminen MS, Valtonen VV, et al. Association between
5. Discuss antibiotic prophylaxis for infective disease dental health and acute myocardial infarction. Br Med J 1989;298:779.
5. Offenbacher S, Katz V, Fertik G, et al. Periodontal infection as
endocarditis.
a possible risk factor for preterm low birth weight. J Periodontal
6. Discuss role of periodontal disease in myocardial 1995;67(suppl):1103-13.
infarction. 6. Scannapieco FA, Stewart FM, Mylotte JM. Colonization of dental
7. State focal infection theory. plaque by respiratory pathogens in medical intensive care patients.
Crit Care Med 1992;20:740.
CH A PT ER
17
Role of Genetics in Periodontal Therapy
Periodontal disease is initiated by the accumulation of factors are believed to initiate the periodontal disease, the
microbial plaque in the gingival crevice inducing inflam- environmental modifiers (e.g., systemic disease, smoking)
mation of gingiva, called chronic gingivitis. This chronic have far-reaching effects on host and they modulate the
gingivitis may progress to chronic destructive inflam- disease process. Now, there is strong evidence supporting
matory condition called periodontitis. Not all individu- the role of an individual's susceptibility to disease which
als who develop gingivitis will progress to periodontitis. is governed by genetic makeup (Fig. 17.1). Thus, genes are
Periodontitis is believed to be a complex disease with mul- responsible for predisposition and progression of periodon-
tifactorial etiology; various biological pathways lead to the tal disease. This chapter gives a brief overview on genetics
development of this disease process. Although microbial and the role of genetics in periodontal disease.
TERMINOLOGIES Gene: It is a segment of a DNA molecule coded for

the synthesis of a single polypeptide; a unit of genetic
Allele: It refers to one of two or more different genes information.
that may occupy the same locus on a specific chromo- Genome: It is the complete chromosomal set derived
some. from one parent.
Autosome: It refers to chromosome other than sex Genotype: It is the genetic composition of an indi-
chromosome. vidual or defined population.
Autosomal dominant: It refers to the dominant effect Locus: It is the physical location of a gene within a
of one gene located on an autosome regardless of the chromosome or a portion of genomic DNA.
presence of the other, normal copy. Monozygotic twins: These are identical twins having
Autosomal recessive: Two copies of the gene must be identical sets of nuclear genes as a result of separation
present for the trait or disease to develop. of blastomeres.
Chromosome: It is one of the nuclear bodies that carry Mutations: These refer to alternation of the genomic
hereditary factors in cells. There are 46 chromosomes sequence compared with a reference state. Not all mu-
in humans. tations have harmful events (silent mutation).
Concordance: It is the probability that both individuals in a Phenotype: It is the physical expression of an indi-
pair will have a particular characteristic provided that one vidual's genotype.
of the individuals is having the characteristic. It is gener- Polymorphism: It refers to occurring in several forms
ally represented as a number ranging from Oto 1 or as a or having several morphological types.
percentage.
Dizygotic twins: These are fraternal twins as a result GENETICS
of fertilization of two separate eggs. They are no more
similar genetically than are siblings. The branch of biology that deals with hereditary and
DNA: It is a nucleic acid that constitutes the genetic variation of inherited trait among organisms is called
material of all cellular organisms. genetics. The basic unit of hereditary is gene and human
CHAPTER 17 ROLE OF GENETICS IN PERIODONTAL THERAPY 141
Environmental and acquired risk factors
I' 'I r r 'I

' Antigens I' 'I
LPS
Other Host immune

-
Cytokines
Prostanoids Connective Clinical signs

Microbial virulence tissue and of disease
inflammatory
challenge factors bone initiation and
response
metabolism progression
Antibodies
Matrix
PMNs metallo
__,, proteinases ,
' ~ .. ' ' ./
t t
Genetic risk factors
I I
FIGURE 17 .1 Overview of the pathogenesis of period on ti tis. Modified from Page RC, Kornman KS. The pathogenesis of human periodontitis: an
introduction. Periodontal 2000. 1997;14:9-ll.
genome contains about 25,000-35,000 genes. The chemi- DNA is contained in tightly coiled packets called chro-
cal substance of a gene is called DNA which is made up mosomes present in the nucleus of every cell. The chromo-
of two long chains twisted around one another to form some consists of DNA wrapped around with protein. The
a double-stranded helix (Fig. 17.2). The subunits of each human genome consists of 22 pairs of chromosomes called
strand are nucleotides, each of which contains any one autosomes and 2 sex chromosomes. Loci are the specific lo-
of four chemical constituents called bases. There are cations of genes on chromosomes and any variations in the
3 billion pairs of bases; they are adenine (A), thymine nucleotide sequence at a locus are referred to as alleles. In
(T), guanine (G), and cytosine (C) with adenine (A) a chromosome at a given locus individuals carrying identi-
complementing with thymine (T) and guanine (G) with cal alleles are homozygous, and if the alleles are different,
cytosine (C). they are termed heterozygous. A genetic marker can be
used to map the gene or nucleotide sequence to a specific
location or a region of chromosome which in turn can be
helpful for locating the diseased allele in a population.
Some alleles are associated with changes in the phenotypic
expressions while others are not. Thus, the interaction of
genotype and environment produces the phenotype of the
individual (Fig. 17.3). When both environment and genetic
factors lead to the development of a disease, it is called a
multifactorial disease. The disease might be caused by
a single gene (monogenic), several genes (oligogenic),
or many genes (polygenic). In monogenic diseases gene
alteration is mostly responsible for the disease expression
with environmental factor playing a minor role; here genes
are called causative genes. However, in a multifactorial dis-
ease genes are referred to as susceptibility genes/alleles, as
the presence of these susceptibility alleles predisposes the
individual to the development of disease but the disease
will be expressed only on exposure to the deleterious envi-
ronment. However, when exposed to similar environmen-
tal challenge, an individual responds differently which is
FIGURE 17 .2 Watson's double helix model of DNA. attributed to the individual's genetic profile.
Base pairs
+
DNA Complex diseases
+
Gene
+
Chromosome
FIGURE 1 7 .4 Types of genetic disorders.
+
Genome
+ J( Environment have very little influence over the disease phenotype,
also called major gene effect. The prevalence of such
Genotype
conditions is rare; example includes amelogenesis im-
+
Thus, determine phenotype
perfecta. If the gene causing the disease can be identi-
fied, it will be possible to diagnose the individual who
FIGURE 1 7 .3 Flow diagram showing basic sequence information carries the disease-causing mutation in the responsible
of genotype which under the influence of environment determines the gene and to predict the course of the clinical disease. The
phenotype of the individual. probability of its transmission through generations can
also be determined.
TYPES OF GENETIC DISORDERS

Complex Genetic Diseases
On a broader range two types of genetic disorders are Complex genetic diseases are much more prevalent in
known (Fig. 17.4). a population compared with simple Mendelian diseases.
The difference between these two groups is based on They are the result of interaction of multiple gene loci in
the method of transmission of the disease, thus giving a which environmental factors play a major role. Genetic
clue about the gene leading to the disease. polymorphisms are reported to be the genetic variants
responsible for this and they are reported to be less dis-
ruptive in altering the normal biological function. The
Simple Mendelian Diseases
presence of disease-associated alleles increases the risk of
Diseases that follow simple and predictable pattern disease; however, their mere presence is not deterministic.
of transmission and follow simple Mendelian laws of The diagnosis of such diseases is difficult as the presence
inheritance, i.e., autosomal dominant, autosomal reces- of polymorphism is difficult to interpret and must be
sive, or X-linked, are called simple Mendelian diseases. supported by other information. Table 17.1 shows the dif-
The etiology for such diseases is the alteration in a single ference between simple Mendelian diseases and complex
gene locus and the effect of environment and other genes diseases.
TABLE 17.1 Differences Between Simple Mendelian Diseases and Complex Diseases
Simple Mendelian diseases Complex diseases

Transmission Follow simple pattern of transmission Do not follow simple pattern of familiar distribution or
transmission
Etiology Alteration at single gene locus Interaction of multiple different gene loci
Environmental factors Less effect More effect
Type of genetic variation Mutation Gene polymorphism

Effect of gene variation Significant change in gene or protein product Variations in the gene are less disruptive and usually
leading to disruption of biological process work within normal range function
Potency for disease causation Sufficient Insufficient as they only increase the risk
Prevalence Rare occurrence with frequency of less than More prevalent with frequency of more than 1 % of the
0.1 % of the population population
Example Amelogenesis imperfecta Diabetes
Cleidocranial dysplasia Cardiovascular disease
Crouzon syndrome Periodontitis
TABLE 1 7 .2 Differences Between Mutations and Polymorphisms
Mutations Polymorphisms
A single gene locus causing mutation has a major physiological The genetic alteration that contributes to complex disease has
impact and considered to be deterministic to disease smaller effect
Seen less commonly in the population At least more than 1 % of the population is affected
Mutations have causally linked with Mendelian disease Mutation is not causally linked to disease, but alleles are seen more
frequently in diseased individuals
One-to-one correlation of a mutation and disease can be established No one-to-one correlation
MUTATION VERSUS POLYMORPHISM 3. the intron(s) or the gene intervening regions;

4. the 3' -untranslated region.
One major difference between simple Mendelian dis-
eases and complex diseases is the number of genes in- Types of Gene Polymorphism
volved and the contribution of each gene to the phenotype
of the disease process (Table 17.2). In simple Mendelian • Change in single base pair at genomic DNA [single
diseases alteration of a single gene locus can result in ma- nucleotide polymorphisms (SNRs)]
jor physiological changes and therefore is deterministic • Simple sequence of repeats of dinucleotide or trinucleo-
in disease process. Any compensation in the biological tide (variable number of tandem repeats or minisatel-
system will not overcome the effect of underlying genetic lites)
defect. However, environmental factors and alterations • Insertions and deletions of few bases, exons, or entire
at other allele modify the disease process leading to vari- gene
able clinical expression of the disease. The genetic variants With these polymorphisms they can affect the function
causing complex diseases are called polymorphism; they and expression of the entire gene and their products, re-
usually have smaller effect on the disease phenotype. The sulting in variation in phenotypic expression of a disease.
presence of this genetic alteration is not causally linked to Thus, knowledge of the gene polymorphisms is important
disease, but this diseased allele is found more in a diseased
to understand complex etiology of periodontal disease
individual. As it contributes to a small part of the disease
and to assess the potential influence of innate, inflamma-
process the disease phenotype requires the contributions tory, and immunological genetic variations from the view-
of multiple different genes with environmental factors be-
point of a genetic diagnostic approach to periodontitis.
ing critical to the etiology of most of the complex diseases.
HUMAN GENE POLYMORPHISM POLYMORPHISMS AND THEIR

RELATIONSHIP TO PERIODONTAL
Gene polymorphisms are locations within the genome
DISEASE
that vary in sequence among different individuals result-
Periodontitis is a multifactorial disease with complex
ing in subtle genetic changes that alter the function of
etiology and genetics is considered as a susceptibility fac-
gene product. Polymorphisms of human genes occur at
tor for this disease. Genotype polymorphism is the most
one or more of the following sites (Fig. 17.5):
common type of disease-modifying gene alteration which
1. the promoter or 5' -flanking region; is responsible for increased susceptibility of the individual
2. the exon(s) or the gene coding regions; to periodontal disease.
Start of (#2) Exons (coding region)

transcription
T /
5' 3'
(#1)
Promoter
•
Initiator
•
Termination
(#4)
Untranslated
(#3) lntrons (intervening
region codon region) codon region
FIGURE 17 .5 Diagram showing structure of human gene and sites where polymorphisms may occur. Regions where any possible polymorphic
DNA sequences locate are shown by #1-4. Courtesy: Shogo Takashiba & Koji Naruishi. Gene polymorphisms in periodontal health and disease. Periodontal
2000, Vol. 40, 2006, 94-106.
• Cytokine gene polymorphism • Calcitonin receptor gene polymorphism

• Interleukin (IL)-1 gene polymorphism • Antigen recognition-related gene polymorphism
• IL-10 gene polymorphism • HLA gene polymorphism
• Tumor necrosis factor (TNF)-cx gene polymorphism • Innate immunity receptor polymorphism
• Receptor and other gene polymorphism • TLR2 and TLR4 gene polymorphism
• Fc-yR gene polymorphism • CD14 gene polymorphism
• Cytokine and chemokine receptor polymorphism • CARD15 gene polymorphism
• Immune receptor gene polymorphism • Miscellaneous gene polymorphisms
• Metabolism-related gene polymorphism (Courtesy: Vijaylakshmi R, Gee/ha A, Rumakrishnan T, Emmadi P Genetic polymorp-
• Vitamin D receptor gene polymorphism hisms in periodontal diseases-An overview. Indian J Dent Res 2010; 21: 568-574)
Some of the important polymorphisms in relation to and macrophages; these are involved in the recogni-
periodontal disease are discussed as follows: tion of foreign antigen. HLA-DR4 and its subtypes,
HLA-DRBl.1501 and HLA-DRQl.0602 genotypes, are
IL-1 gene polymorphism: It was first reported by Ko-
associated with periodontal diseases.
rnman et al. in 1997; they reported that the combined
Immunoglobulin G2 variations: IgG molecules carry
carriage rate of the alleles for both IL-lex and IL-113 can
the genetically determined variation in the gamma
be designated as composite genotype. Therefore, the
chain called Gm allotype (G2m); it has been seen in
IL-1 composite genotype can be considered a putative
studies that refractory periodontitis patients who were
susceptibility factor for periodontitis in Caucasians.
positive for Gm allotype had higher antibody level
It was also reported by MacGurie and Nunn (1999)
against P. gingivalis.
that the IL-1 composite genotype increased the risk of
tooth loss by 2.7 times and when combined with heavy
smoking it increased to 7.7 times. METHODS OF GENETIC ANALYSIS
Fe-gamma receptor polymorphism: The Fe-gamma
receptor (FcyR) is the receptor present on phagocytes Ample clinical and scientific data support the idea
which binds immunoglobulin G (IgG) and plays an im- that genetic variants are the major determining factor
portant role in the phagocytosis of bacteria. The altera- for syndromic and nonsyndromic periodontitis. To crit-
tion in the binding of the receptor to immunoglobulin ically evaluate the strength of the evidence supporting
G due to polymorphism is responsible for increased such association a good knowledge about the genetic
susceptibility to periodontal disease. Kobayashi et al. analytical methods is a must. A variety of techniques
(2000) found that FcyRIIlb (NA2 allele) was linked can be used to study the genetic basis of disease; some
with AgP and possibly also an Fc-yRIIla allele. Meisel of these are general, whereas others help in the pre-
et al. (2001) assessed the association between FcyRIIIa cise identification of the genes involved in particular
(high-affinity receptor) and FcyRIIlb (low-affinity re- disease causation. Following are the methods used in
ceptor) and chronic periodontitis (CP) and reported genetic analysis:
that Fc-yRIIla was associated with CP.
Toll-like receptor polymorphism: Toll-like receptors 1. Familial aggregation
are signal molecules present on host cell which when 2. Twin studies
stimulated by bacterial components such as lipopoly- 3. Segregation analysis
saccharide (LPS) initiate the immune system to act 4. Linkage analysis
against the bacteria. Different functional polymor- 5. Association analysis
phisms of Toll-like receptors are associated with im- 1. Familial aggregation
paired LPS signal transduction. Schroeder et al. have
reported that polymorphism of Toll-like receptor-4 can The genetic basis of a disease can be studied by
act as a risk factor for development of chronic peri- overviewing the aggregation of the traits within the
odontitis. families as many diseases run in family.
Vitamin D receptor polymorphism: Vitamin D genes The technique employed is
have regulatory effects on bone turnover and it was
number of diseased cases in
Henning et al. who reported that TaqI VDR gene may
. the relatives of patients
act as risk factor for aggressive periodontitis. D egree o f c 1ustermg = -----------
Class II human leukocyte antigen: HLAs are present risk of disease in general
on the immune cells of the host such as T and B cells population
patterns of inheritance and the deviation is then

DZ Twins MZTwins measured.
4. Linkage analysis
It is a method of locating the allele for a particular trait
on a specific location on a chromosome. The fact that
genes are located in close proximity to one another on
a chromosome and are transferred from generation
to generation as a unit is exploited in this method of
genetic analysis. These genes are said to be "linked"
and they violate the Mendelian law of independent
assortment (Fig. 17.7). Geneticists follow a particular
trait as it segregates in the family and assess whether
the trait of interest segregates with a known genetic
polymorphism that has been localized to a particular
Different DNA Same DNA location on a chromosome. Since the precise location
of the genetic marker on the chromosome is known
whenever linkage is detected, the gene responsible
FIGURE 17.6 Effect of environment and gene on the phenotype of
for such trait can be traced around the genetic
dizygotic and monozygotic twins. DZ, dizygotic; MZ, monozygotic.
polymorphism. The disadvantage of this method is
that it cannot be used for complex diseases as complex
diseases are the result of multiple genes of minor
However, there are certain demerits of using this effect.
technique as the persons in the family will have 5. Association analysis
many genes in common and they also share the same In complex multifactorial diseases identifying a
environment (diet, nutrition, pollutants, smoking, and particular gene responsible for the causation of
socioeconomic influence). disease phenotype is difficult as genes present
2. Twin study in multiple loci interact with one another to
Twin study is useful for differentiating variations produce the susceptibility which interacts with the
due to environmental and genetic factors or a environmental factor to produce the actual disease.
combination of both (Fig. 17.6). Monozygotic twins To establish an association the frequency of allele at
have identical genetic makeup, so the difference in a given locus must be compared with the subjects
disease expression in the twins can be attributed with disease and healthy control derived from
to the environmental factor; in contrast, dizygotic the same population. This technique is helpful in
twins are like siblings, so they have about 50% of detecting the susceptibility genes. Two types of
the genes in common; hence, the difference could association analysis are commonly used in genetics
be due to both genetic and environmental factors. (Fig. 17.8).
Twin study can be used as a tool to measure the
concordance rates of twins with a particular trait or
disease of interest. ROLE OF GENETICS IN AGGRESSIVE
3. Segregation analysis PERIODONTITIS
It is the statistical analysis to determine the pattern
of transmission of trait or disease within a family. Aggressive periodontitis is a group of rapidly pro-
The mode of inheritance of any trait depends on the gressive form of periodontitis characterized by severe
following: and rapid destruction and early age of clinical manifesta-
a. The presence of diseased allele on the autosome or tion. Several studies have reported the high prevalence
sex chromosome of aggressive periodontitis among siblings and tendency
b. Whether it is dominant or recessive to aggregate in families, suggesting genetic factors to be
c. Whether it is fully or partially penetrant important for the susceptibility to this disease. Genetic
This technique is applied to assess whether the disease studies were conducted to assess the nature of trans-
is caused by a single gene with dominant or recessive mission and location of the diseased allele on specific
inheritance or by multiple genes or whether it is location on chromosome. Studies suggest Mendelian
caused because of the exposure to the environmental inheritance for the gene of major effect and presence
factors. Here, the pattern of transmission of a of such genes predisposes the individual to aggressive
disease in families is compared with the expected periodontitis.
Metaphase
Linkage
Linkage between
genes is detected
in crosses when
Anaphase
their alleles tend to
ij
BA , ab'-
segregate together
BA ab in meiosis.This
produces gametes
'- /
with chromosomes
that have the same
Gametes
/-\ allele combinations
as the parents.
i.e., ccntraryto Mendel's

second rule of
independent assortment
FIGURE 17. 7 Diagram showing linkage between the allele as they segregate together in meiosis. (Courtesy: http://bvetmedl.blogspot.in/2013/0l/
genes-and-genetics- l-lecture-98.html).
Evidence for the Role of Genetics in Aggressive and recessive mode of inheritance. Segregation analy-
Periodontitis sis was performed, but the results obtained varied;
Melnick et al. had proposed X-linked inheritance;
Segregation analysis: The pattern of transmission however, this theory was later refuted due to the
proposed for this disease includes both dominant number of bias in their study design. Autosomal re-
cessive mode of inheritance was noted in the Finnish
population, but the largest study conducted in the
United States has demonstrated autosomal domi-
nant pattern among African-American and Caucasian
Association analysis families.
Linkage analysis: Segregation analysis demonstrates
/ only the pattern of inheritance but does not reveal the
specific gene involved with the disease process, so for
Population based Family based
that linkage analysis was performed. With the help of
+
Case-control design (Marker allele frequencies are compared
linkage analysis the location of gene of major effect
between affected individual and unaffected individual selected on specific chromosome was determined (Table 17.3)
randomly from a population) and Boughman et al. reported it to be present on
vitamin O-binding locus on region q of chromosome
FIGURE 17 .8 Types of association analysis. in Brandywine population, but it was not confirmed
HLA-A9 and B15 increase the risk
HLA-A2 decreases the risk Periodontitis
FIGURE 1 7 .9 Diagram showing the various HLA antigens which decreases and increases the risk of aggressive periodontitis.
TABLE 17 .3 Results of Linkage Analysis Showing the Location of Apart from the HLA antigen, polymorphisms in genes
Gene of Major Effect on Specific Chromosome and the Gene Locus encoding for the following are present:
Chromosome Region Gene locus Immunoglobulin
Chromosome 4 q region Vitamin D-binding locus LPS-binding proteins
Chromosome 1 q25 region Cyclooxygenase 2 (COX-2) Prostaglandin
gene Cytokines
Chromosome 2 q 13-14 region IL-1 gene complex IL-1 polymorphism: Single-nucleotide base-pair sub-
stitution in IL-1[3 called IL-1[3+3954 is associated with in-
creased destruction.
Polymorphisms in IL-1 receptor antagonist gene,
vitamin D receptor, and N-formyl-1-methionyl-1-leucyl-
1-phenylalanine (FMLP) receptor gene are associated with
in further studies. Li et al. in 2004 have linked increased risk for aggressive periodontitis.
localized aggressive periodontitis with q25 region of
chromosome 1 in an area close to the cyclooxygenase 2
(COX-2) gene. Scapoli et al. in 2005 have shown linkage
on q13-14 region of chromosome 2 that contains the ASSOCIATION OF AGGRESSIVE
IL-1 gene complex. PERIODONTITIS WITH GENETIC AND
Association analysis: Rather than searching for specific INHERITED CONDITIONS
allele researchers have focused on the candidate genes
which means the region within or near gene that codes Aggressive periodontitis is seen in certain inherited or
for specific regulatory molecules or enzymes which cause genetic disorders, thereby providing us with a window
disease. The most commonly studied candidate gene is to know how gene mutation increases the risk for peri-
human leukocyte antigen (HLA), which is present on odontitis (Table 17.4).
chromosome 6 in humans. These antigens are associated
with many autoimmune diseases and since long they have
been considered as candidate gene marker for aggressive
periodontitis. These genes code for complement and
ROLE OF GENETICS IN CHRONIC
proinflammatory cytokine which is responsible for tissue
PERIODONTITIS
destruction in periodontitis. Two antigens consistently
Even with the very first reports titled Experimental Gin-
associated with aggressive periodontitis are HLA-A9 and
givitis in Man presented by Loe et al. in 1965 and Theilade
Bl5. In subjects with HLA-A9 and B15 the risk of disease
et al. in 1966, it was suggested that the onset and progres-
increases to about 1.5-3.5 times; however, presence of
sion of periodontitis varied among different individuals.
HLA-A2 appears to be protective in the expression of this
The explanation for this at that time was given that it
disease (Fig. 17.9).
could be due to differences in qualitative and quantitative
Class II DR4 antigen has been associated with diabetes- plaque. Recently, this "experimental gingivitis model"
related complication including periodontitis; it has been was studied in individuals having similar qualitative and
found that DR4 antigen has been associated with type 1 quantitative plaque and researchers found difference in
diabetes mellitus. the inflammatory response, which was attributed to the
TABLE 17 .4 Various Types of Genetic and Inherited Disorders Associated with Aggressive Periodontitis, the Tissue or Protein Defect,
and their Pattern of Inheritance
Disorder Protein or tissue defect Pattern of inheritance

Acatalasia Catalase
Cyclic neutropenia Neutrophil elastase Autosomal dominant
Hypophosphatasia Alkaline phosphatase

Chediak-Higashi syndrome Lysosomal trafficking regulator gene Autosomal recessive
Papillon-Lefevre syndrome CathepsinC Autosomal recessive
Haim-Munk syndrome CathepsinC Autosomal recessive
Prepubertal periodontitis (nonsyndromic) CathepsinC
Ehlers-Danlos syndrome type 4 Collagen Autosomal dominant

Ehlers-Danlos syndrome type 8 Collagen Autosomal dominant
Leukocyte adhesion deficiency type 1 Leukocyte chain adhesion molecule CD18 Autosomal recessive
Leukocyte adhesion deficiency type 2 Leukocyte chain adhesion molecule CD15 Autosomal recessive
Chronic familial neutropenia Defect unknown Autosomal dominant
Congenital disorder of glycosylation type Ile GDP-fructose transporter- I Autosomal recessive

Trisomy 21 Multiple
Kindler syndrome Actin-extracellular linkage
host-related factors possibly due to the genetic involve- periodontitis; the presence of this allele increases the risk
ment. There is convincing evidence from studies that to 6.8 times than in individuals without this allele. Ko-
there is genetic predisposition to periodontal disease and bayashi et al. have demonstrated association between
chronic periodontitis has an inherited component. neutrophil IgG receptor (FcyR) polymorphism and chron-
ic periodontitis; this gene is responsible for deterring the
efficiency of polymorphonuclear leukocytes (PMNs) to
Evidence for the Role of Genetics in Chronic phagocytose, with FcyRIIlb NA2 allele more prevalent
Periodontitis in individuals with recurrent form of disease (Fig. 17.10).
Twin Studies
Noack in 1940 recognized that identical twins present Commercially Available Genetic Susceptibility
with similar periodontal conditions. After that numer- Test for Severe Chronic Periodontitis
ous studies were conducted on identical twins and they
reported significant heritable component for chronic peri- A genetic test kit is being marketed currently for severe
odontitis. Minnesota group studied reared-together and chronic periodontitis and is called periodontal suscepti-
reared-apart adult twins; they attributed genetic altera- bility test (PST), which detects the presence of specific
tions in terms of gingivitis, probing depth, and clinical polymorphisms of the IL-lo'. and IL-1~ genes. Kornman
attachment loss to about 38-82% of the population. Twin et al. (1997) have reported that two of these IL-1 poly-
studies were also helpful in determining whether genes morphisms, when found together, are associated with a
affect the composition of oral microflora, and it was sug- significant increase in the risk for severe generalized peri-
gested that genes affect the initial microflora in the oral odontitis in nonsmokers. If this combination of polymor-
cavity, but the effect was not carried till adulthood. phisms (composite genotype) was present, the patients
were referred to as "genotype positive."
Association Studies
Many of the candidate genes are common between
aggressive periodontitis and chronic periodontitis such Common polymorphisms in chronic periodontitis:
as HLA antigen. HLA-B5 seems to be protective anti- IL-1 Composite-coding for IL-1 and TNF-a
gen against the disease. Kornman et al. have reported a FcyRlllb-NA2- responsible for PMN phagocytosis
"composite" IL-1 genotype to be associated with chronic FIGURE 17.10 Common polymorphisms in chronic periodontitis.
EPIGENETIC MECHANISMS
are affected by the following factors and processes: HEALTH END POINTS
• Development (in utero, childhood) __. - • Cancer
• Environmental chemicals • Autoimmune disease
• Drugs/Pharmaceuticals • Mental disorders
• Aging • Diabetes
• Diet
EPIGENETIC
FACTOR
CHROMOSOME J. METHYL GROUP
DNA methylation
Methyl group (an epigenetic factor found
in some dietary sources) can tag DNA
and activate repress genes.
DNA accessible, gene active
Histone modification
The binding of epigenetic factors to histone "tails"
Histones are proteins around which alters the extent to which DNA is wrapped around
DNA can wind for compaction and DNA inaccessible, gene inactive histones and the availability of genes in the DNA
gene regulation. to be activated.
FIGURE 17 .11 Diagram showing the mechanism of epigenetics and its effect on health endpoints. Source: http://nihroadmap.nih.gov/EPIGENOMICS/
images/epigeneticmechanisms.jpg.
EPIGENETICS leads to altered tissue response to the microorganism,

thus providing an insight into the complex etiology of
Epigenetics is aberrant genetic pattern; this is a rela- periodontal diseases.
tively new concept in periodontitis research that may be
able to explain the missing link between genetics, dis-
ease, and environment. Epigenetic variations are heritable CONCLUSION
changes in gene function that occur without a change
in the sequence of nuclear DNA. Epigenetic events act While periodontal research so far has focused on stud-
through chemical modifications of DNA and its associ- ies of microbiological pathogenesis and oral environ-
ated proteins by blocking the binding of transcription ments, it is now widely accepted that susceptibility to
factors through histone modifications (transient) or DNA inflammation is also determined by intrinsic factors
methylation (stable form). The three major methods of such as genetics. This is emphasized by the fact that
epigenetic regulation are methylation, histone modifica- some people are more disease susceptible or treatment
tion, and RNA interference (Fig. 17.11). resistant. Thus, development of periodontitis depends
Epigenetic mechanisms play an important role in the on the presence of a number of environmental factors in
pathogenesis of periodontitis as the cytokine genes have conjunction with genetic factors at a given point frame.
been suggested as targets of multiple epigenetic events Future strategy must be directed to develop genetic tests
including transcriptional activation via loss of DNA meth- that may prove useful for identifying patients who are
y lation and active histone modifications at regulatory likely to develop periodontal disease, suffer from recur-
elements. IL-1, IL-2, IL-6, IL-8, IL-10, IL-12, and TNF-a rent disease, or suffer tooth loss as a result of periodontal
are regulated by epigenetic modifications. This in turn disease.
KEY POINTS
• Now, there is strong evidence supporting the role of others help in the precise identification of the genes
an individual's susceptibility to disease which in turn involved in particular disease causation. These are
depends on the genetic makeup of the individual. Thus, familial aggregation, twin study, segregation analysis,
genes are responsible for predisposition and progression linkage analysis, and association study.
of periodontal disease. • Aggressive periodontitis is a group of rapidly progres-
• The branch of biology that deals with hereditary and sive form of periodontitis in which genetic basis of dis-
variation of inherited trait among organisms is called ge- ease has been reported in a large number of studies.
netics. The basic unit of hereditary is gene which is found Aggressive periodontitis is associated with inherited
on chromosome. Thus, the interaction of genotype and and genetic disorders.
environment produces the phenotype of the individual. • There is convincing evidence from studies that there
• Two types of genetic disorders are known: simple Men- is genetic predisposition to periodontal disease and
delian diseases and complex diseases. Diseases follow- chronic periodontitis has an inherited component.
ing simple and predictable pattern of transmission are • A genetic test kit is being marketed currently for se-
simple Mendelian diseases, whereas complex diseases vere chronic periodontitis and is called periodontal
are the result of interaction of multiple gene loci in susceptibility test (PST), which detects the presence
which environmental factors play a major role. of specific polymorphisms of the IL-la and IL-113
• Mutation is alteration in a single gene locus that has genes.
major physiological impact and is considered to be de- • Epigenetic variations are heritable changes in gene
terministic to disease, whereas gene polymorphisms function that occur without a change in the sequence of
are locations within the genome that vary in sequence nuclear DNA. Epigenetic events act through chemical
among different individuals resulting in subtle genetic modifications of DNA and its associated proteins by
changes that alter the function of gene product. blocking the binding of transcription factors through
• A variety of techniques can be used to study the genet- histone modifications (transient) or DNA methylation
ic basis of a disease; some of these are general, whereas (stable form).

1. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds.
1. Describe genetics as an etiology of periodontal dis- Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B. Saun-
eases. ders Company; 2006.
2. Describe the role of genetics in periodontal disease. 2. Lindhe J, Lang NP. Clinical and Implant Dentistry. 5th ed. Oxford:
3. What is the role of genetics in the etiopathogenesis of
3. Kinane OF, Hart TC. Genes and gene polymorphisms associated with
aggressive periodontitis? periodontal disease. Crit Rev Oral Biol Med 2003;14:430-49.
4. Describe the effect of IL-1 gene polymorphism in the 4. Vijaylakshmi R, Geetha A, Ramakrishnan T, Emmadi P. Genetic
progression of chronic periodontitis. polymorphisms in periodontal diseases - an overview. Indian J Dent
5. Describe the periodontal susceptibility test. Res 2010;21:568-74.
5. Takashiba S, Naruishi K. Gene polymorphisms in periodontal health
6. Describe the role of epigenetics in periodontal disease.
and disease. Periodontal 2000 2006;40:94-106.
SECTION IV
PERIODONTAL PATHOLOGY
CHAPTER
18
Defense Mechanisms of the Gingiva
CHAPTER OVERVIEW
The most common diseases of the tooth-supporting ap- sion can lead to the compromised tissue metabolism and
paratus are plaque-induced inflammatory alterations in the repair, thereby allowing for enhanced virulence of microbial
gingiva and periodontium. Gingivitis may persist for many factors and their increased pathogenicity.
years without progressing to periodontitis. Periodontitis, Local defense mechanisms play an important role in the
on the other hand, usually develops out of a more or less initial stages of gingival and periodontal diseases. These
pronounced gingivitis. The reasons why gingivitis pro- mechanisms, which are specific to the oral cavity, may ei-
gresses to periodontitis are still incompletely understood. ther induce or propagate an immune response that may be
As with all opportunistic infections, it appears that the initiated by interactions between the bacteria that colonize
proliferation of pathogenic microorganisms, their capacity the plaque biofilm.
to invade tissues, and the individual host response to such The various mechanisms that play an important role
infections, besides associated environmental factors, seem in the defense of the periodontal tissues against infection
to be the determining factors in the progression of gingivitis maybe
to periodontitis (Fig. 18.1). • Epithelial barrier
Alteration in the environment of gingival sulcus and • Gingival crevicular fluid (GCF)
periodontal pockets along with the changes in nutrient • Saliva
availability and the host response seen in disease progres- • Orogranulocytes.
EPITHELIAL BARRIER hemidesmosomes which mediate keratinocyte basement

membrane adhesion, and intercellular adherens junc-
Epithelial tissue is a protective covering forming a bar- tions connecting actin cytoskeleton to virtually all cell
rier between the body and the environment; these tissues types.
perform various functions in the body depending on their The cornified cell envelope of keratinized epithelia and ke-
location and, importantly, they protect the internal tis- ratinized epithelia itself function as a critical part of the
sues from environmental stresses, chemical damage, and protective barrier of this epithelial tissue.
bacterial infection. The stratified epithelia of the skin and In maintaining cell and tissue integrity and also in
oral mucosa are examples of the toughest and the most preventing desiccation both the cell adhesion junctions
protective epithelia. and the cornified envelope play an important role, which
In addition to the primary function of epithelial tissues is demonstrated in a large number of genetic and autoim-
of being a barrier, they perform additional specialized mune diseases showing altered expression or function of
functions based on their location. The most important these structures.
requirement for the stratified epithelia of the oral mucosa An increased permeability of the epithelial tight junc-
is to maintain tight cell adhesion in the living cells and tions is seen in case of acute, chronic, and neonatal stress
retaining the dead, keratinized squames so as to form a which affects the mucosal barrier. This increased para-
protective sheath. cellular permeability in turn depends on the release of
The basic component of epithelial cell adhesion requires interferons from CD4+ lymphocytes and also in the ac-
desmosomes for maintaining intercellular adhesion, tinomyosin ring contraction of epithelial cells due to the
154 SECTION IV PERIODONTAL PATHOLOGY
Disease
Bacteria Environmental Host response

factors
• Bacterial quantit • Positive host response
and quality • Inflammation
• Amount of plaque • Tissue fluid stasi • Intact integument
• Plaque composition • Increased GCF flow • Exudation
• Plaque retention • Hypoxia • Acute grunulocyte
emigration
• Elevated pH • Immune response
• Bleeding
• Depressed redox • Defective or
compromised host
potential response
• PMN defects
• Immune defect
• Systemic diseases
FIGURE 18.1 Determining factors in the progression of gingivitis to periodontitis.
mast cell activation. This altered permeability induces a Active antimicrobial substances produced by the junc-
local immune activation by favoring the permeability of tional epithelium, such as defensins, lysosomal enzymes,
antigens and toxins, and also the bacteria. chemokines [interleukin (IL)-8], and cytokines [IL-1, IL-6,
Junctional epithelium in antimicrobial defense: The first and tumor necrosis factor (TNF)-a] which are secreted as
line of defense against microbial invasion into the tissues a response to microbial challenge by the epithelial cells,
is formed by the junctional epithelium which consists of attract and activate professional defense cells such as
active populations of cells and has antimicrobial func- lymphocytes and polymorphonuclear leukocytes (PMNs).
tions. The internal and external basal laminas act as bar- These secreted products in turn cause further activation
riers against infective agents. of the junctional epithelial cells.
Constant and rapid cell turnover that occurs within the Osteopontin, a phosphorylated glycoprotein, has a
junctional epithelium is an important factor in the mi- pivotal role in the development of immune responses
crobial defense. One of the most important parts of the and subsequent repair process that occurs following tis-
antimicrobial defense mechanism at the dentogingival sue destruction in various inflammatory diseases. While
junction is the rapid shedding of epithelial cells as it fa- expression of osteopontin is increased in immune cells,
cilitates an effective removal of epithelial cells and also including neutrophils, lymphocytes, and macrophages,
the bacteria adhering to these cells. and in epithelial, endothelial, and fibroblastic cells of
C H A PTER 18 DEFEN SE M EC H A N ISM S O F TH E G IN G IV A 155
inflamed tissues, deciphering the specific functions of diseases) analysis of inflammatory markers in GCF may
osteopontin is difficult. prove to be a useful method. Methodological concerns
related to the collection and analysis of GCF are impor-
tant factors that need to be considered when studying
GINGIVAL CREVICULAR FLUID GCF.
The only site in the body in which the epithelial barrier Methods of Collection of GCF
is deliberately breached by the hard tissues (cementum
and enamel) is the oral epithelium; this must be sealed The fluid is collected by various means depending
by an external milieu. A fluid transudate flowing from the on the nature of the analyte under investigation. The
site of this seal is seen even in gingival health, presum- methods could be based on the placement of the filter
ably acting as a mechanical factor in minimizing bacterial paper strips within the gingival sulcus (intrasulcular) or
accumulation. This fluid being composed of a variety at its entrance (extrasulcular). The intrasulcular technique
of macromolecular components derives its origin from (Brill technique) carries the disadvantage of irritating the
serum and the interstitia of the gingiva. The size of the sulcular epithelium that can itself trigger the flow of GCF.
molecules is the deciding factor for the concentration of Filter paper strips are preferred for easy access and
these components, suggesting a passive filtering system transport and are used in enzyme assays, notably pro-
of the intact gingival tissues. Thus, the mechanical cleans- tease enzymes, which lend themselves to specific colo-
ing action of the fluid flow and these innate and acquired rimetric procedures. The disadvantage of this method
immune molecules may together be helpful in achieving of collection is the nonspecific attachment of the analyte
homeostasis. to the paper fibers, which reduces the quantity of the
With increasing inflammation of the gingiva there is detectable sample.
change in the nature of fluid from transudate to an inflam- Microcapillary tubes have been used by certain investi-
matory exudate which contains higher levels of serum- gators, which have the advantage over filter paper strips
derived molecules, vascular-derived cellular components in that they allow for complete collection and assessment
of inflammation, and locally derived molecules from the of the sample collected.
gingival tissues. Considering the fact that the oral cavity Crevicular washing methods may be of various types.
represents the entry portal for a vast array of antigenic One method uses an appliance consisting of an acrylic
challenges, the role of the GCF in maintaining health of plate, four collection tubes, and a peristaltic pump. A
the tissues is extremely important. modification of this method consists of an ejection and a
GCF is a fluid in the gingival crevice that occurs in collecting needle from which the sample is drained into
minute amounts. Regarding the nature of this fluid there a tube by continuous suction.
are two schools of thought: one believes it to be an inflam- Twisted threads inserted into the gingival sulcus have
matory exudate, whereas the other suggests it to be a fluid also been used in the collection of GCF.
involved in cleansing material from the crevice, contain- The GCF samples thus collected may be measured on
ing sticky plasma proteins that improve adhesions of the a "blotter" (Periopaper), employing an electronic trans-
epithelial attachment, have antimicrobial properties, and ducer (Periotron). The sample may also be analyzed by the
exert antibody activity. ninhydrin staining method planimetrically. Various other
The gingival crevice surrounding the teeth is the site methods such as the isotope dilution method have also been
from where GCF can be collected. GCF is a window employed to analyze the sample collected.
which provides an insight about the constituents of
serum, the cellular response in the periodontium, and
contributions from the gingival crevice. Research on
Composition of GCF
GCF has basically focused on defining the pathophysiol- The contents of GCF primarily consist of enzymes, cel-
ogy of periodontal disease and in the identification of a lular elements, electrolytes, organic compounds, and antibacte-
potential diagnostic test for active periodontitis. The po- rial factors. Enzymes in GCF may be host or bacterial in
tential candidates that have been identified from the ma- nature. As a result of many studies on lysosomal enzymes,
jority of markers for such test are measures of inflamma- PMNs have been shown to be the main source of a large
tion [i.e., prostaglandin E2 (PGE2), neutrophil elastase, majority of lytic enzymes in GCF. Studies on the devel-
and the lysosomal enzyme glucuronidase]. To define opment of periodontitis show a correlation between the
how certain systemic disorders (e.g., diabetes mellitus) active phases of tissue breakdown and PMN infiltration
can modify periodontal disease and how periodontal toward the sulcus area. Higher PMN activity in the sul-
disease/periodontal inflammation can influence certain cus area is observed during the breakdown phase of the
systemic disorders (i.e., cardiovascular/ cerebrovascular periodontal disease.
Host ceUs
,ucrobial plaque • Leukocytic enzyme Damaged host tissues

• Lactoferrin
• Lysozyme
• Endotoxins (LPS) • Myelopcroxidase • Collagcns
• Enzymes {acid • Proteoglycans
phosphatase, alkaline • Matrix proteins
phosphatase) (Ostconcctin)
• Metabolic end product
(Prostaglandin-l ike
product, Trypsin-like
enzyme)
Host factors
(immunne response)
• lmmunoglobulins
(lgG, lgA, lgM)
• Complement factors
• Eicosanoids
• Cyt.okincs(IL-1)
FIGURE 18.2 Constituents of GCF and their source. LPS, lipopolysaccharide.
It is generally recognized that the constituents of Electrolytes

GCF arise from a variety of sources, including microbial Electrolytes such as sodium, potassium, fluoride, cal-
plaque, host inflammatory cells, host tissues, and serum- cium, magnesium, and phosphates have been determined
derived factors (Fig. 18.2). in known amounts in the GCF.
A positive correlation exists between the sodium : po-
tassium ratio and inflammation because if the GCF passes
Cellular Elements in the GCF through intact tissues, the same proportions of sodium
Various cellular elements may be found in the GCF and potassium as plasma and extracellular fluid will
such as bacteria, desquamated epithelial cells, and leu- be found. If, however, the fluid traverses through dam-
kocytes (PMNs, lymphocytes, monocytes/macrophages). aged tissues, decreased sodium:potassium ratio would
These elements enter the GCF through the sulcular epi- be found because of the accumulation of intracellular
thelium. potassium from the disrupted cells.
The source of bacteria in the GCF is the adjacent plaque
mass. These bacteria play an important role in the ini- Organic Compounds
tiation and progression of periodontal disease. They are GCF contains carbohydrates, lipids, and proteins in
potent initiators of the immune response. varying amounts. Other organic compounds such as met-
Epithelial cells seen in the GCF basically originate abolic or bacterial products and antibacterial substances
from the oral sulcular and junctional epithelium. They may also be seen in reasonable amounts in the GCF.
represent the high turnover rate of the epithelium that Carbohydrates in the GCF are mainly in the form of
comprises the gingival sulcus. glucose, hexosamine, and hexuronic acid. These three
The leukocytes present in the GCF originate from the substances in the GCF have a dual origin. They reflect
gingival plexus of blood vessels. They are the primary ef- the altered metabolic activity of the adjacent tissues, but
fector cells of the immune response. PMNs play an impor- might also be influenced by the metabolic processes of
tant role in innate immunity. Monocytes/macrophages the local microflora.
and lymphocytes play important roles in cell-mediated No significant correlation has been found in the protein
immunity. content in the GCF and gingival inflammation, pocket
Erythrocytes are an incidental finding within the GCF. depth, and extent of bone loss. Histochemically, it has
They result from damage to the small blood vessels and been determined that the GCF contains proteins similar to
capillaries of the gingival connective tissue. that seen in the serum. Immunoglobulins G (IgG),A (IgA),
TABLE 18.1 Enzymes in the GCF Clinical Significance of GCF
• Acid phosphatase Circadian periodicity: There is a gradual increase
• Alkaline phosphatase in the flow of the GCF from 6 a.m. to 10 p.m. and a
• Pyrophosphatase decrease afterwards. However, the technique used
• ~-Glucuronidase in the collection of GCF also affects the flow of GCF.
• Lysozyme
Therefore, conflicting results have been reported
• Hyaluronidase
• Proteinases (mammalian/bacterial) concerning the possibility of a circadian pattern in the
• Cathepsin D flow ofGCF.
• Elastase Sex hormones: Clinical investigations have shown
• Cathepsin G exacerbation of gingivitis during pregnancy,
• Plasminogen activators
menstrual cycle, and at puberty. Increase in tooth
• Collagenase
• Lactic dehydrogenase mobility and pocket depth has also been reported to
occur during pregnancy. There is a relative increase
in the flow of GCF associated with these conditions.
Female sex hormones (estrogen and progesterone)
increase GCF flow by probably enhancing vascular
and M (IgM), besides various components of the comple-
permeability.
ment system, have also been detected in the GCF. Other
Mechanical stimulation: Toothbrushing, mastication,
proteins detected in the GCF include albumin, fibrinogen,
or any process that causes mechanical irritation of the
ceruplasmin, ~-lipoprotein, and transferrin.
sulcular epithelium may enhance the flow of GCF
GCF contains many classes of phospholipids as well
considerably.
as neutral lipids. Serum seems to be the most probable
Smoking: Smoking causes a transient increase in
source of lipids in the gingival fluid, although salivary,
the flow of GCF. This may be attributed to the initial
bacterial, and tissue sources cannot be ignored.
vasodilatation caused by smoking, besides the irritation
Metabolic and bacterial products detected in the GCF
caused by the cigarette smoke on the gingival sulcular
include lactic acid, hydroxyproline, prostaglandins, urea,
epithelium.
endotoxins, cytotoxic substances, antibacterial factors
Diabetes mellitus: In diabetic patients, there is a strong
(lysosomal enzymes, peroxidase-mediated antimicrobial
positive correlation between the concentrations of
system), and various enzymes and enzyme inhibitors (serum
glucose in the fluid and those in the serum, whereas
proteinase inhibitors; Table 18.1).
this is not the case in healthy individuals.
Periodontal therapy: There is a substantial increase in
Cellular and Humoral Activity in the GCF the flow of GCF during the healing period following
periodontal therapy. This increase may be due to the
GCF exhibits cellular and humoral immunity in both
inflammatory reaction from gingival trauma and the
healthy individuals and those with periodontal diseases.
loss of an epithelial barrier especially when the fluid
The cellular immune components present in the GCF in-
is collected by the intrasulcular technique. With the
clude PMNs (95-97%), monocytes (2-3%), T cells (29%),
restoration of gingival integrity, a gradual drop in
and B cells (71 %). The humoral immune components pres-
fluid flow may be noticed.
ent in the GCF include IgG (IgG1-IgG4), IgA, IgM, and
Drugs in the GCF: The process by which various
complement components. The presence of interferon-v in
drugs are excreted through the GCF may be an
the GCF as suggested by the preliminary evidence indi-
advantage in the management of periodontal diseases.
cates that due to its ability to inhibit the bone resorption
Drugs such as tetracyclines and metronidazole have
activity of IL-1~, it may have a protective role in peri-
been shown to be excreted in the GCF in considerable
odontal diseases.
amount so as to reduce periodontal disease
Numerous investigations have shown that IgG plasma
activity.
cells predominate in the GCF in advanced clinical stages
of periodontal diseases. This is reflected in the fact that
IgG is the primary immunoglobulin in the GCF. Local pro-
duction of immunoglobulins in the GCF cannot be ruled OROGRANULOCYTES
out. Positive correlations between IgG levels in the serum
and GCF have also been identified. This is consistent with In normal individuals, about 30,000 neutrophils/min
the finding that local antibody responses in the gingival enter the oral cavity via the gingival sulcus through the
tissues may manifest in the form of systemic antibodies, junctional epithelium surrounding the teeth. The pres-
a portion of which may be derived from local gingival ence of neutrophils is of utmost importance for peri-
responses to the infection. odontal health, and defects in neutrophil function and
chemotaxis are associated with early onset periodontal protection, cleansing, buffering, and maintenance of
disease in children. This flow of neutrophils may also be tooth integrity.
important for protection from caries. These viable neu- The various constituents of saliva serve as an effective
trophils present in the saliva are termed orogranulocytes system for lubricating and protecting the soft and hard
or salivary corpuscles. tissues. The presence of mucin and antiproteases in saliva
Functional PMNs migrate mainly through the oral mu- protects the soft tissues against desiccation, penetration,
cosa, particularly the gingival mucosa. These leukocytes ulceration, and effect of potential carcinogens. Soft tissue
can be readily collected in samples of saliva and they repair can be encouraged by saliva by reducing clotting
are believed to migrate into the mouth at a rate which is time and accelerating wound contraction. Saliva plays
characteristic of the extent of inflammation in the mouth - a pivotal role in protective function by maintaining the
the Oral Leukocyte Migratory Rate (OMR). ecological balance in the oral cavity via: (i) debridement/
The Oral Leukocyte Migratory Rate Index (OMRI) should lavage; (ii) aggregation and reduced adherence by both
allow an objective assessment of periodontal health and immunologic and nonimmunologic means; and (iii) direct
is suggested to be a reproducible index of the periodon- antibacterial activity. Other functions of saliva include its
tal health. The Orogranulocyte Migratory Rate (OMR) antifungal and antiviral properties and also saliva is effec-
has been shown to be a nonsubjective laboratory index tive in maintaining pH in the oral cavity, contributes to the
for inflammatory periodontal disease, not requiring in- regulation of plaque pH, and helps neutralize reflux acids
traoral manipulations and independent of investigator in the esophagus (Fig. 18.3). In saliva the most important
judgment. Statistically significant correlations have been salivary buffer is the bicarbonate-carbonic acid system.
found between the OMRI and (i) the Gingival Index
(GI) of Loe and Silness; (ii) the total pocket depth as
Functions of Saliva
measured on six aspects of each of the six teeth; (iii) the
Periodontal Disease Index (POI) of Ramfjord; and (iv) The composition of saliva is complex and varies accord-
the Simplified Oral Hygiene Index (OHI-S) of Green ing to the type of stimulus and the rate of flow. However,
and Vermillion. several important functions are carried out by different
components; the essential function is that saliva coats the
teeth and the mucosal lining of the oral cavity and as such
SALIVA provides protection as well as facilitates a number of physi-
ological activities. Humans who suffer from a decreased
Saliva forms an important aspect in the defense salivary secretion due to diseases affecting acini or as a
against microbial invasion due to its various inherent consequence of other systemic diseases or as a side effect
components and their associated functions. It provides of certain medications have difficulty in eating, swallow-
its antimicrobial defense mechanisms, besides catering ing, or speaking. These persons are susceptible to mucosal
to various other functions such as lubrication, physical infections and high incidence of dental caries.
Inorganic factors Organic factors
• Lysozyme
• Ions and gases • Lactoferrin
• Bicarbonates • Myeloperoxidasc
• Sodium • Lactoperoxidase
• Potassium
• Phosphates Agglutinins
• Calcium
• Fluorides • Glycoprolein
• Ammonium • Mucins
• Carbon dioxide • ~2 macroglobulins
• Fibronectins
• Antibodies
FIGURE 18.3 Constituents of saliva.

Specific Functions of Saliva Lysozyme, a hydrolytic enzyme, is effective against both
1. Protection: The fluid nature and the components of gram-negative and gram-positive organisms. It specifically
saliva protect the oral cavity in several ways. Saliva acts against the Actinobacillus and Veillonella spp.
provides a washing action that clears nonadherent, The Lactobacillus thiocyanate system is another effective
potentially harmful substances in the oral cavity. defense mechanism inherent in the saliva that has
Viscous components, for example, mucins, lubricate bactericidal properties to some strains of Lactobacillus
oral tissues and form a barrier against microbial and Streptococcus spp. It prevents the accumulation of
products. Bicarbonate, phosphate ions, as well as basic lysine and glutamic acid, both of which are essential
proteins in saliva maintain the near-neutral pH in the for growth of various bacterial species.
oral cavity, which prevents demineralization of enamel Lactoferrin is another antibacterial agent present in
that would otherwise occur due to acids produced by saliva that has a potent bactericidal action against the
sugar-metabolizing bacteria. Salivary proteins form Actinobacillus spp.
a thin coating on tooth surfaces, the salivary pellicle Myeloperoxidase, an enzyme released by leukocytes, has
that contributes to protecting these surfaces. Saliva is potent bactericidal activity against the Actinobacillus
supersaturated with calcium and phosphate ions and spp, besides preventing the attachment of certain
this state is maintained by certain calcium-binding initial colonizers, namely Actinomyces strains, to the
proteins, notably acidic praline-rich proteins and hydroxyapatite in the tooth surface.
statherin. This leads to posteruptive maturation of Tissue inhibitors of matrix metalloproteinases are
enamel surfaces, which increases their hardness and components in saliva with the ability to inhibit the
resistance to demineralization. Furthermore, such activity of collagen-degrading enzymes (collagenase),
environment favors remineralization of early carious which may be associated with bacterial activity or
lesions (white spots) provided that cavitation does not host-mediated cellular responses.
occur. Various blood coagulation factors have been identified
2. Digestion: Saliva contains two digestive enzymes, in the saliva. Coagulation factors predominantly seen
namely amylase that breaks down complex carbo- in the saliva include factors VIII, IX, and X, plasma
hydrates such as starch into glucose and maltose, thromboplastin antecedent (PTA), and Hageman factor.
and lipase (a product of lingual glands) that hy- The blood coagulation factors basically accelerate the
drolyzes triglycerides into monoglycerides and process of coagulation, thus protecting wounds against
diglycerides. bacterial invasion.
3. Antibacterial properties: Saliva plays a major bacterio- 4. Taste: The solubilization of ingested material by
static role in the oral cavity. It interferes with microbial saliva is essential for the functioning of taste buds
colonization, and mucins form a physical antimicrobial that act as chemoreceptors when they are in contact
barrier. with the dissolved material and initiate taste sensa-
Salivary IgA is an important factor in oral immune defense; tion.
together with salivary agglutinins (glycoproteins) Serum Little information is available about the relationship of
IgA causes clumping of certain microorganisms, thus salivary dysfunction with periodontal health. Saliva's
preventing them from adhering to oral and dental surfaces. mechanical cleansing and antimicrobial properties
Salivary antibodies appear to be synthesized locally, since are the reason for which it has been suggested to be
they react to strains of bacteria that are indigenous to the involved in gingival and periodontal health. Salivary
oral cavity. flow and composition influence calculus formation,
Other components, namely histatins, lysozyme, periodontal disease, and caries. Thus, saliva has a
lactoferrin, and myeloperoxidase, inhibit bacterial major role to play in the initiation and progression of
growth. periodontal diseases.
KEY POINTS
• The various mechanisms that play an important role • The basic component of epithelial cell adhesion requires
in the defense of the periodontal tissues against infec- desmosomes for maintaining intercellular adhesion,
tion are the epithelial barrier, the GCF, the saliva, and the hemidesmosomes which mediate keratinocyte basement
orogranulocytes. membrane adhesion, and intercellular adherens junc-
KEY POINTS (cont'd)
tions connecting actin cytoskeleton to virtually all cell • There is a gradual increase in the flow of the GCF from
types. 6 a.m. to 10 p.m. and a decrease afterwards.
• Active antimicrobial substances produced by the junc- • Tetracyclines and metronidazole have been shown to be
tional epithelium, such as defensins, lysosomal enzymes, excreted in the GCF in considerable amount.
chemokines (IL-8), and cytokines (IL-1, IL-6, and TNF-u) • These viable neutrophils present in the saliva are termed
which are secreted as a response to microbial challenge orogranulocytes or salivary corpuscles.
by the epithelial cells, attract and activate professional • Lactoferrin is another antibacterial agent present in
defense cells such as lymphocytes and PMNs. saliva that has a potent bactericidal action against the
• Methods of GCF collection could be based on the place- Actinobacillus spp.
ment of the filter paper strips within the gingival sulcus • Myeloperoxidase, an enzyme released by leukocytes,
(intrasulcular) or at its entrance (extrasulcular). has potent bactericidal activity against the Actinobacillus
• The cellular immune components present in the GCF in- spp, besides preventing the attachment of certain initial
clude PMNs (95-97%), monocytes (2-3%), T cells (29%), colonizers, namely Actinomyces strains, to the hydroxy-
and B cells (71 %). apatite in the tooth surface.
• The humoral immune components present in the GCF
include IgG (IgG1-IgG4), IgA, IgM, and complement
components.
QUESTIONS 2. Jukka UV. Gingival Crevicular Fluid. Periodontology 2000. Copenhagen:

Munksgaard; 2003 31.
3. Lindhe J, Lang NP. Clinical and fmplant Dentistn;. 5th ed. Copenhagen:
1. What is the role of saliva in oral defense mechanism? Oxford: Blackwell Munksgaard; 2008.
2. What are the functions of the GCF? 4. Nakamura M, Slots J. Salivary enzymes: origin and relation to
3. What are the antibacterial factors in saliva? periodontal disease. J Periodontal Res 1983;18:559.
4. What are the methods of GCF collection? 5. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Curranza's
Clinical Periodontology. 10th ed. St. Louis: Elsevier; 2006.
5. What drugs are secreted in the GCF?
6. Rose LF, Mealey BL, Genco R. Periodontal Medicine, Surgery and
Implants. 1st ed. St. Louis: Elsevier; 2004.
Suggested readings
1. Cimasoni G. The crevicular fluid. In: Myers H, editor. Monographs in
Oral Science, Vol 12. Basel: S. Karger; 1983.
CHAPTER
19
Gingival Inflammation
CHAPTER OVERVIEW
Gingivitis or the inflammation of gingiva is the most in gingivitis are associated with the presence of oral micro-
common form of gingival diseases. Pathological changes organisms in the gingival sulcus.
DEFINITION clinical and histopathological evidence. They divided the

progressing lesion into the following stages:
The American Academy of Periodontology defines
1. Stage I gingivitis or the initial lesion
gingivitis as an inflammation confined to the tissues of
2. Stage II gingivitis or the early lesion
the marginal gingiva.
3. Stage III gingivitis or the established lesion
4. Stage IV gingivitis or the advanced lesion.
STAGES IN THE PATHOGENESIS The advanced lesion was considered to reflect the pro-
OF GINGIVITIS gression of gingivitis to periodontitis or a state of transi-
tion of gingivitis to periodontitis.
Pathogenesis can be defined as the unfolding of a dis-
ease process, or the sequence of events in the develop- Stage I Gingivitis: The Initial Lesion
ment of a disease from its earliest beginnings. The natural It is generally believed that the features characterizing
history of inflammatory gingival and periodontal disease the initial lesion merely reflect the enhanced levels of ac-
is not understood completely, and important aspects of tivity of the mechanisms of host defense that normally are
its pathogenesis remain obscure. The sequence of events operative within the gingival tissues. This initial response
culminating in clinically apparent gingivitis has been of the gingiva is also called subclinical gingivitis. The initial
separated into the initial, early, and established stages, lesion is localized to the region of the gingival sulcus. The
and periodontitis has been designated as the advanced tissues affected include a portion of the junctional epithe-
stage. In spite of extensive research, we still cannot dis- lium, the oral sulcular epithelium, and the most coronal
tinguish definitively between the normal gingival tissue portion of the connective tissue.
and the initial stage of gingivitis. The factors comprising
this transition are not well understood. Clinical Features
Pristine gingiva (Fig. 19.1): Normal gingiva that is free Clinically, this initial response of the gingiva to bacte-
from "significant" accumulation of inflammatory cells rial plaque is not obvious or apparent.
histologically may be described as pristine gingiva or a
state of superhealth. Histologic Features
Healthy gingiva (Fig. 19.2): Clinically healthy gingiva • The initial lesion emerges within 2-4 days; when a
looks clinically similar to pristine gingiva but histologi- previously normal, infiltrate-free gingiva is subjected
cally features an inflammatory infiltrate with predomi- to the accumulation of microbial plaque, mild gingivitis
nantly neutrophils associated with junctional epithelium appears.
and lymphocytes in the subjacent connective tissue. • The initial lesion is a response to the generation of
Page and Schroeder in 1976 classified the progression chemotactic and antigenic substances in the region of
of gingival and periodontal inflammation on the basis of the gingival sulcus.
Increased neutrophil
Few neutrophils migrate into migration
coronal part of junctional
epithelium and gingival
sulcus Increased infiltrate
> J.: ·.;.-1 Dilated vessels, vascular

proliferation, increased
collagen loss, very few
plasma cells
FIGURE 19.1 Pristine gingiva.
• The most coronal portion of the junctional epithelium FIGURE 19.3 Early gingivitis.
is altered.
• Within 24 h, marked changes are evident in the gingival
microvasculature. epithelium, and in the connective tissue, the
• Classic vasculitis of vessels, subjacent to the junctional lymphocytes are almost exclusively T cells.
epithelium, occurs. • The gingival sulcus contains migrating leukocytes,
• The vessels of the gingival plexus become engorged sloughed epithelial cells, and bacteria.
and dilated, and many polymorphonuclear leukocytes
migrate into the junctional epithelium and the gingival
Stage II Gingivitis: The Early Lesion
sulcus.
• There is exudation of fluid from the gingival sulcus. The early lesion overlaps and evolves from the initial
• Serum proteins, especially extravascular fibrin, are lesion with no clear-cut dividing line (Fig. 19.3).
present.
• Loss of perivascular collagen occurs and the resultant Clinical Features
space is occupied by fluid, serum proteins, and • Signs of erythema may appear, mainly owing to the
inflammatory cells. proliferation of capillaries and increased formation of
• A few macrophages and blast-transforming capillary loops between rete pegs and ridges.
lymphocytes may appear within the junctional • Bleeding on probing may also be evident.
Histologic Features
• The early lesion appears at the site of initial lesion
Microbial colonization
within 4-7 days of plaque accumulation.
• There is accentuation of the features described for the
initial lesion.
• The lesion is the result of the formation and maintenance
of a dense lymphoid-cell infiltrate within the gingival
connective tissues.
0 • As mild gingivitis appears, a twofold to threefold
increase in the number of inflammatory cells occurs.
ooo The infiltrate continues to be composed predominantly
Monocytes,
lymphocytes, of lymphocytes and contains only a few plasma
and O cells.
neutrophils • Lymphoid cells accumulate immediately subjacent
in connective
tissue to the junctional epithelium at the site of acute
inflammation.
• Most of these lymphocytes are T cells; only about 6%
FIGURE 19.2 Healthy gingiva. are identifiable as B cells. They are diffusely arranged
CH A PT ER 19 G IN G IV A L IN FLA M M ATIO N 163
immediately under the epithelium at the zone of injury

(subjacent to the junctional epithelium) occupying the Greatly increased
papillae formed by the proliferated epithelium and also neutrophil emigration
the adjacent corium.
• The lymphocytic infiltration remains localized and
does not extend deeply into the tissues.
• The flow of gingival fluid and the number of
crevicular leukocytes reach their maximum and level Marked proliferation of
junctional epithelium
off between 6 and 12 days after the onset of clinical
gingivitis.
• Although the oral sulcular epithelium and the oral
epithelium generally do not become infiltrated, the
junctional epithelium contains a variably increased
number of transmigrating neutrophilic granulocytes Increased plasma
cells 10-30%
and infiltrating mononuclear cells, including
lymphocytes, macrophages, plasma cells, and mast
cells.
• Collagen-fiber content of the affected tissue is reduced
by about 70%. This alteration, which occurs at an early
stage of the disease, especially affects the dentogingival FIGURE 19.4 Established gingivitis.
and circular fiber groups that normally support the
junctional epithelium. The loss of collagen, therefore,
may be a major factor in continuing loss of tissue
integrity and normal gingival function as the disease Established lesions of two types apparently exist; some
progresses. remain stable and do not progress for months or years,
• The leukocytes infiltrate between the epithelial cells whereas others apparently become more active and con-
and may be present in sufficiently large numbers to vert to progressive destructive lesions.
disrupt the continuity of the epithelial barrier. The • The nature of this conversion has been studied but is
area of affected connective tissue can be distinguished not understood.
clearly from the surrounding normal tissue by the • The proportion of T cells decreases and that of B cells
presence of inflammatory cells and the decreased and plasma cells increases as gingivitis appears and
collagen content. becomes more severe.
• It has been suggested that a conversion from a
predominantly T-cell infiltrate to a B-cell infiltrate is
Stage III Gingivitis: The Established the major event in the conversion of stable established
Lesion (Fig. 19.4) lesions into aggressive destructive lesions.
Clinical Features • The destructive lesions are characterized by acute
inflammation with a great deal of exudation and by
• Features of the early lesion are presented in an the presence of many neutrophils.
accentuated form. • As destruction slows, the acute inflammation is
• This conversion is probably the result of subgingival resolved and the infiltrate becomes predominated by
plaque extension, which allows a shallow gingival lymphoid and other mononuclear cells.
pocket to form. • A likely cause of the conversion of a stable
• In these pockets, the tooth surface is covered by established lesion to an aggressive lesion is a change
bacterial plaque and the soft tissue wall is lined by a in the microbial flora or infection of the gingival
pocket epithelium. tissues.
• In some cases, the pocket epithelium may be thick
and resemble a long oral sulcular epithelium; more Histologic Features
frequently, however, the pocket epithelium becomes • The distinguishing feature of the established lesion
thin and ulcerated. is a predominance of plasma cells within the affected
• The blood vessels become engorged and congested, connective tissues at a stage prior to extensive bone
and therefore the venous return is impaired and loss.
the blood flow becomes sluggish. All this results in • Plasma cells appear along the blood vessels and
localized gingival anoxemia, which superimposes a between collagen-fiber bundles and deep within the
bluish hue on the reddened gingiva. connective tissue.
• Junctional epithelium shows widening of the

intercellular spaces filled with cell debris and
lysosomes derived from lymphocytes, monocytes, and
neutrophils.
• The junctional and oral sulcular epithelium may
proliferate and migrate into the infiltrated connective
tissue and along the root surface, with conversion to
pocket epithelium.
• The basal lamina may be destroyed in some areas.
• Continuing loss of collagen is apparent in the zone of
infiltration in other more distant regions; fibrosis and
scarring may begin to occur.
• Collagenase is present in the gingival tissues, which
can be produced by periopathogens and neutrophils.
FIGURE 19.6 Gingivitis.
• Chronically inflamed gingiva has elevated levels of acid
phosphatase, alkaline phosphatase, 13-glucuronidase,
13-glucosidase, esterases, aminopeptidase, and
cytochrome oxidase.
• Neutral mucopolysaccharide levels are decreased.
Stage IV Gingivitis: The Advanced Lesion

This stage is also known as the phase of periodontal
breakdown (Figs 19.5-19.7). Here, there is persistence of
features described for the established lesion but there is
extension of the lesion into the alveolar bone and peri-
odontal ligament.
Clinical Features
• Formation of periodontal pocket, suppuration, FIGURE 19. 7 Advanced lesion.
mobility, migration, and eventually tooth exfoliation
Histologic Features
• The advanced lesion represents frank and overt
periodontitis.
• Continued loss of collagen subjacent to the pocket
epithelium with fibrosis at more distant sites can be
seen.
• The junctional epithelium migrates apically from the
Colonization
cementoenamel junction.
by periodontal • The junctional epithelium is changed and is no longer
pathogens closely attached to the tooth surface. The pocket
Apical
epithelium that has now formed has a heavy leukocyte
migration
of JE infiltrate, predominantly of polymorphonuclear
leukocytes (PMNs), which eventually migrate across
Plasma the epithelium into the gingival pocket. The pocket
cells >50%
epithelium is more permeable to the passage of
substances into and out of the underlying connective
tissues and is temporarily ulcerated in many places.
• Alveolar bone loss occurs.
Bone loss
• There are widespread manifestations of inflammatory
and immunopathological tissue reactions.
• Plasma cells predominate in the lesion, although
FIGURE 19.5 Advanced gingivitis/periodontitis. lymphocytes and macrophages are also present.
CH A PT ER 19 G IN G IV A L IN FLA M M ATIO N 165
• The lesion is no longer localized; it may extend apically, • The highly organized fiber bundles of the marginal
as well as laterally, to form a variably broad band gingiva lose their characteristic orientation and
around the necks and roots of the teeth. architecture.
KEY POINTS
• Gingivitis or the inflammation of gingiva is the most • The initial response of the gingiva is also called subclini-
common form of gingival diseases. cal gingivitis.
• Pristine gingiva, normal gingiva that is free from "sig- • In Stage I, the lymphocytes are almost exclusively T cells.
nificant" accumulation of inflammatory cells, histologi- • Collagen-fiber content of the affected tissue is reduced
cally may be described as pristine gingiva or a state of by about 70% in Stage II. This alteration, which occurs
superhealth. at an early stage of the disease, especially affects the
• Page and Schroeder in 1976 classified the progression dentogingival and circular fiber groups that normally
of gingival and periodontal inflammation on the ba- support the junctional epithelium.
sis of clinical and histopathological evidence. They • Stage IV gingivitis, the advanced lesion, is also known
divided the progressing lesion into (i) Stage I gingivitis as the phase of periodontal breakdown. Here, there is
or the initial lesion, (ii) Stage II gingivitis or the early persistence of features described for the established le-
lesion, (iii) Stage III gingivitis or the established lesion, sion but there is extension of the lesion into the alveolar
and (iv) Stage IV gingivitis or the advanced lesion. bone and periodontal ligament.
QUESTIONS 2. Newman MG, Takei H, Carranza FA. Clinical Periodontology. 10th ed.
St. Louis: Saunders; 2006.
3. Page RC, Schroeder HE. Pathogenesis of chronic inflammatory
1. Enumerate the stages of gingivitis. periodontal disease - a summary of current work. Lab Invest
2. Discuss the established lesion in gingivitis. 1976;33:235-49.
3. Discuss the early lesion in gingivitis. 4. Page RC, Kenneth SK. Pathogenesis of human periodontitis - an
introduction. Periodontal 2000 1997;14:9-ll.
5. Rose LF, Mealey BL, Genco R. Periodontal Medicine, Surgery and
Suggested readings Implants. 1st ed. St. Louis: Elsevier; 2000.
1. Lindhe J, Lang NP. Clinical and Implant Dentistry. 5th ed. Copenhagen:
CH A P T E R
20
Clinical Features of Gingivitis
CHAPTER OVERVIEW
Inflammatory and immune reactions to microbial plaque the classic signs of inflammation - rubor (redness), tumor
are the predominant features of gingivitis and periodontitis. (swelling), calor (warmth), and dolor (pain). These signs
The inflammatory reaction is visible both microscopically may be readily apparent to the dentist, but the threshold for
and clinically in the affected periodontium and represents the discomfort is not commonly reached by patients with plaque-
host response to the plaque microbiota and its product. The associated gingivitis, in general, infected sites with one or
clinical signs of inflammation in the gingival tissue reflect more of the four common clinical signs of inflammation.
Gingivitis is often associated with the following: ever, are various hues of red. The best way to detect
inflammatory color change is to compare the color of
1. Presence of dental plaque
the gingival margin with the color of the adjacent al-
2. Signs and symptoms confined to the gingiva
veolar mucosa.
3. Clinical signs of inflammation - enlarged due to edema
Systemic causes for color changes can be endogenous
or fibrosis, color transition to red or bluish red, and
or exogenous (Table 20.2):
bleeding on probing
4. No loss of attachment 1. Localized pigmentation: Amalgam tattoo, graphite
5. Reversibility of the lesion by removing the etiology tattoo, or other tattoos, nevus, melanotic macules,
malignant melanoma, and Kaposi sarcoma
2. Multiple or generalized pigmentation (Fig. 20.2):
CORRELATION OF CLINICAL
a. Genetics: Idiopathic melanin pigmentation (racial
AND MICROSCOPIC FEATURES
or physiologic pigmentation) and Peutz-Jeghers
IN HEALTH AND GINGIVITIS
syndrome
b. Drugs: Smoking, betel, antimalarials, antimicro-
Color bials, minocycline, amiodarone, chlorpromazine,
The normal color of the gingiva (Fig. 20.1) is described adrenocorticotropic hormone (ACTH), zidovudine,
as coral pink or salmon pink. The factors determining the ketoconazole, methyldopa, busulfan, menthol, con-
color of gingiva are traceptive pills, and heavy metal exposure (gold,
bismuth, mercury, silver, lead, copper)
1. Vascular supply
c. Endocrine: Addison disease, Albright syndrome,
2. The thickness and degree of keratinization of the
pregnancy, and hyperthyroidism
epithelium d. Postinflammatory: Periodontal disease and
3. Melanin pigmentation postsurgical gingival repigmentation
Alveolar mucosa is thinner and nonkeratinized, has no e. Others: Hemochromatosis, generalized neuro-
rete pegs, and has a high vascularity that gives it a red, fibromatosis, incontinentia pigmenti, Whipple
smooth, and shiny appearance. It can be clearly distin- disease, Wilson disease, Gaucher disease, human
guished from the coral pink-colored gingiva. immunodeficiency virus (HIV) disease, thalas-
Inflamed gingival tissues can exhibit a wide range of semia, pigmented gingival cyst, and nutritional
color changes (Table 20.1). Most of the changes, how- deficiencies
C H A PT ER 20 C LIN IC A L FEATU R ES O F G IN G IV IT IS 167
FIGURE 20.1 Normal healthy gingiva. FIGURE 20.2 Generalized pigmentation.
TABLE 20.1 Color Changes in Inflamed Gingival Tissues
Acute Chronic (Fig. 20.2)

Is red because of increased vascularity in the inflamed site and due Bluish hue is seen in the gingiva, which is present due to venous
to decrease in the degree of keratinization. It can also change to pale stasis
pink due to decreased vascularity, increased fibrosis, and increased
keratinization. It can become dull gray due to tissue necrosis
TABLE 20.2 Endogenous and Exogenous Causes for Color Changes
Endogenous pigmentation Exogenous pigmentation

Iron, bilirubin, melanin, and bile pigments From atmospheric irritants, e.g., coal and metal dust, coloring
• Hemochromatosis: iron deposition; blue gray pigmentation agents added in foods, tobacco, and amalgam tattoo
• Jaundice: bile pigments; yellowish color
• Melanin: physiologic; in certain ethnic groups such as Africans
Pathological: Addison disease, Peutz-Jeghers syndrome, Albright Heavy metals such as bismuth, mercury, lead, and silver produce
syndrome (polyostotic fibrous dysplasia), von Recklinghausen disease a line in the marginal gingiva or are seen as patches in the at-
(neurofibromatosis) tached gingiva
Metallic pigmentation: only in areas of gingival inflammation;
systematically absorbed metal sulfides get precipitated in the peri-
vascular area in the subepithelial connective tissue. This happens
due to increased vessel permeability seen in inflammation
Melanin The gingivae are the most frequently pigmented intra-

Melanin, a nonhemoglobin-derived brown pigment, oral tissues. Microscopically, melanoblasts are normally
is the most common of the endogenous pigments and is present in the basal layers of the lamina propria. The most
produced by melanocytes present in the basal layer of common location is the attached gingiva (27.5%) followed
the epithelium. Melanin accumulates in the cytoplasm, in decreasing order by the papillary gingiva, the marginal
and the melanosome is transformed into a structureless gingiva, and the alveolar mucosa. The total number of
particle no longer capable of melanogenesis. melanophores in the attached gingiva is approximately 16
The number of melanocytes in the mucosa corre- times greater than that in the free gingiva. The prevalence
sponds numerically to that of skin; however, in the mu- of gingival pigmentation was higher on the labial part of
cosa their activity is reduced. Various stimuli can result the gingiva than on the buccal and palatal/lingual parts
in an increased production of melanin at the level of of the arches. The shade of pigment was classified as very
mucosa including trauma, hormones, radiation, and dark brown to black, brown, and light brown-yellow.
medications. Melanin pigmentation of the oral tissues usually does
• Idiopathic thrombocytopenic purpura and coagulation

disorders - hemophilia and Christmas disease
Clinical Significance
Objective signs offer the best diagnostic methods
of disease severity. In this case, bleeding on probing
is an objective method for examining gingival connec-
tive tissue inflammation. Ulceration of the periodontal
pocket wall epithelium causes bleeding, but bleeding
in and of itself is not diagnostic for a specific form of
disease.
Size
The sum total bulk of all cellular and extracellular com-
ponents comprises the size of gingiva.
FIGURE 20.3 Bleeding on probing. Gingival swelling or edema is a clinical feature of the
inflamed gingival tissues. Edematous gingival enlarge-
not present a medical problem, but patients complain of ment is caused by accumulation of fluids in the inflamed
black gums. connective tissue. The fluid is primarily serum that has
emerged from the blood vessels with increased perme-
ability because of local inflammation. Recognition of gin-
Bleeding on Probing gival edema is easy when it is marked. But in the early
The first clinical sign of gingivitis is bleeding subse- stages this edema is confined to the marginal gingiva and
quent to careful probing (Fig. 20.3). A blunt periodontal involves changes in the contour, shape, surface texture,
probe is inserted at the bottom of the gingival pocket and consistency.
and is moved gently along the lateral wall of gingiva. If
bleeding is provoked by this instrumentation, the site is Contour and Shape
considered inflamed.
The normal contour of gingiva is scalloped and knife
Causes edged (Table 20.3). Morphology of the teeth and embra-
• Gingivitis sures, arch position, alignment in the arch, and the loca-
Poor oral hygiene tion of the proximal contact determine the shape and
Inadequate plaque removal contour of the gingiva. This knife-edged margin is lost
Calculus accumulation in gingivitis.
• Periodontitis (advanced forms of gingivitis) McCall festoons and Stillman cleft were earlier con-
• Anticoagulants such as coumarin and heparin sidered to be due to trauma from occlusion but presently
• Self-inflicted oral trauma, such as toothbrush abrasion they are considered to represent the changes seen in in-
and improper flossing flammation of marginal gingiva.
• Infection, which can be either tooth- or gum-related
• Vitamin C deficiency
Consistency
• Vitamin K deficiency
• Hormonal changes during pregnancy Normal consistency of gingiva is firm and resilient
• Chemical irritants such as aspirin (Table 20.4). Collagen in the underlying lamina propria
• Leukemia and its continuation with the mucoperiosteum along with
• Placement of new dentures leading to denture sores/ the gingival group of fibers give gingiva its firmness and
irritations resiliency.
TABLE 20.3 Contour Changes During Gingival Inflammation
Gingivitis ANUG (Fig. 20.4) Stillman cleft McCall festoons
The margins become round, Reverse contour is seen when Is a narrow, triangular-shaped They are rolled, thickened mar-
rolled, and blunt, and the there is loss of the interdental gingival recession, which gins of gingiva seen near canine
adjacent tissues are somewhat papilla as in ANUG exposes cementum as the reces- when recession progresses till
enlarged and puffy sion progresses apically the mucogingival junction
FIGURE 20.4 Necrotizing ulcerative gingivitis.

FIGURE 20.5 Generalized recession in lower anterior teeth.
TABLE 20.4 Changes in Consistency During Gingival

Inflammation
Acute gingivitis Chronic gingivitis

It is seen as soft and edematous It is fibrotic because of fibrosis
(destructive), i.e., infiltration by and epithelial proliferation
inflammatory fluid and degen- associated with long-standing
eration of connective tissue inflammation
The consistency of gingiva is checked using the back

side of a periodontal probe and gently applying pressure
in the surface of gingiva.
Recession is the apical shift in the position of gingiva
exposing the root surface (Fig. 20.5).
• Actual position is the level of epithelial attachment.
• Apparent position is the level of crest of marginal FIGURE 20.6 Stippling seen on attached gingiva.
gingiva (Table 20.5).
Surface Texture cavity, the margin and sulcus are at the tip of the crown;
as eruption progresses, they are seen closer to the root.
Attached gingiva shows small depressions on the sur- Actual position of gingiva is more important than the
face. The depressions named stippling give the appear- apparent position as it shows the loss of attachment that
ance of orange peel (Fig. 20.6). has taken place. At certain times this denuded root surface
Surface texture is checked by drying the gingiva with is hidden by the inflamed pocket wall. This part of root
a piece of gauze. surface is known as hidden recession and the part that is
The changes in the surface texture during gingival visible clinically is called visible recession.
inflammation is described in Table 20.5.
Position of Gingiva Etiology of Gingival Recession

It refers to the level at which the gingival margin is at- • Faulty brushing technique: It includes scrub technique
tached to the tooth. When the tooth erupts into the oral of brushing or use of a hard -bristle toothbrush.
TABLE 20.5 Surface Texture Changes During Gingival Inflammation
Acute gingivitis Chronic desquamative gingivitis Drug-induced gingival enlargement

The surface texture becomes smooth and shiny due to Peeling of the epithelial surface If the reparative changes predominate, the
infiltration by inflammatory fluid. This appearance is occurs surface becomes firm and nodular
also seen in atrophic gingivitis
1 70 SECTION IV PERIODONTAL PATHOLOGY
TABLE 20.6 Classification of Gingivitis
Acute gingivitis Subacute gingivitis Recurrent gingivitis Chronic gingivitis

Acute gingivitis is of sudden A less severe phase of Recurrent gingivitis reappears after Chronic gingivitis is slow in onset
onset and short duration and the acute condition has having been eliminated by treatment and of long duration, and is pain-
can be painful been termed subacute or disappearing spontaneously less, unless complicated by acute or
subacute exacerbations
• Tooth malposition: Susceptibility to recession is

influenced by position of the tooth in the arch, the root
bone angle, and mesiodistal curvature of the tooth
surface. In rotated, tilted, and labially placed teeth, the
labial plate is thinned and reduced.
• Gingival ablation: It refers to pressure from soft tissues
such as the tongue and buccal mucosa.
• Gingival inflammation causes gingival recession.
• Iatrogenic causes: These include clasp of ill-fitting
denture, overhang restoration, and margins of FIGURE 20.7 Chronic generalized marginal gingivitis.
restoration violating the biologic width.
• Abnormal frenum attachment causes gingival
recession.
Clinical Significance
Gingival recession can lead to dentinal hypersensitiv-
ity, root caries, abrasion, or erosion of cementum and
aesthetics.
Gingival Exudate
Presence of gingival exudation signifies the presence
of disease activity or phase of active destruction taking
in the tissue. It does not indicate the depth of the pocket
or severity of the lesion. FIGURE 20.8 Chronic generalized diffuse gingivitis.
It is checked by placing the ball of the index finger
along the lateral aspect of marginal gingiva with a rolling
motion toward the crown. • Marginal gingivitis (Fig. 20.7) involves the gingival
margin and may include a portion of the contiguous
attached gingiva.
Classification (Table 20.6) • Papillary gingivitis involves the interdental papillae
Course, Duration, and Distribution and often extends into the adjacent portion of the
gingival margin.
• Localized gingivitis is confined to the gingiva of a • Diffuse gingivitis affects the gingival margin, the
single tooth or group of teeth. attached gingiva, and the interdental papillae
• Generalized gingivitis involves the entire mouth. (Fig. 20.8).
KEY POINTS
• The normal color of the gingiva is described as coral • Pathological endogenous pigmentation can be due to
pink or salmon pink. The factors determining the color Addison disease, Peutz-Jeghers syndrome, Albright
of gingiva are vascular supply, the thickness and degree syndrome (polyostotic fibrous dysplasia), and von Reck-
of keratinization of the epithelium, and melanin pigmen- linghausen disease (neurofibromatosis).
tation. • Drugs that cause gingival pigmentation are antimalarials,
• Bluish hue is seen in the chronic gingivitis, which is antimicrobials, minocycline, amiodarone, chlorpromazine,
present due to venous stasis. ACTH, zidovudine, ketoconazole, methyldopa, busulfan,
KEY POINTS (cont'd)

menthol, contraceptive pills, and heavy metal exposure they are considered to represent the changes seen in
(gold, bismuth, mercury, silver, lead, copper). inflammation of marginal gingiva.
• The first clinical sign of gingivitis is bleeding subsequent • Actual position of the gingiva is the level of epithelial
to careful probing. attachment.
• Reverse contour is seen when there is loss of the inter- • Apparent position of gingiva is the level of crest of mar-
dental papilla as in acute necrotizing ulcerative gingi- ginal gingiva.
vitis (ANUG). • Gingival recession can lead to dentinal hypersensitiv-
• McCall festoons and Stillman cleft were earlier consid- ity, root caries, abrasion, or erosion of cementum and
ered to be due to trauma from occlusion, but presently aesthetics.

1. Hassel MH. Periodontal tissue structure and function. Periodontology
1. Define gingival recession. Enumerate the causes. 2000;3:1993.
2. Describe the clinical and microscopic features of 2. Lindhe J. Clinical Periodontology and Implant Dentistry. 5th ed.
chronic gingivitis. Copenhagen: Blackwell Munksgaard; 2008.
3. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's
3. Define gingival bleeding. What are the causes?
Clinical Periodontology. 10th ed. St. Louis: Saunders; 2006.
4. What are McCall festoons and Stillman clefts? 4. Rose LF, Mealey BL, Genco R. Periodontal Medicine, Surgery and
[mp/ants. 1st ed. St. Louis: Elsevier; 2004.
CHAPTER
21
Gingival Enlargement
CHAPTER OVERVIEW
Alteration in the size of the gingiva is one of the clini- with regular oral hygiene procedures, and creates aesthetic
cal features of periodontal disease. Increase in the size of problems; in severe cases, it interferes with mastication and
gingiva, which is termed gingival enlargement or gingival phonation. In children, gingival enlargements may impede
overgrowth, is a common clinical sign of gingival disease the eruption of teeth.
and a matter of great clinical concern. Enlargement may involve one or more components of
Increase in the size alters the physiologic contour of the the gingiva. It may be confined to a limited area or may
gingiva, creates areas of plaque accumulation, interferes involve all the teeth.
CLASSIFICATION Increase in the size of the gingiva is a result of interac-

tion between host and a variety of other factors. Depend-
Depending on the involvement of components of gin- ing on etiology and pathogenesis, gingival enlargements
giva and its distribution, gingival enlargement is desig- are classified as follows:
nated as follows:
1. Inflammatory enlargement
• Localized: Limited to the gingiva adjacent to a single a. Chronic
tooth or group of teeth b. Acute
• Generalized: Involving the gingiva throughout the 2. Fibrotic enlargement
mouth a. Drug-induced enlargement
• Marginal: Confined to the marginal gingiva b. Hereditary or idiopathic gingival enlargement
• Papillary: Confined to the interdental papilla 3. Combined enlargement (inflammatory+ fibrotic)
• Diffuse: Involving the marginal and attached gingiva 4. Enlargements associated with systemic conditions
as well as papillae a. Conditioned enlargement
• Discrete: An isolated sessile or pedunculated tumor- - Pregnancy
like enlargement - Vitamin C deficiency
- Diabetes-induced gingival enlargement
The degree of gingival enlargement can be scored as
- Nonspecific conditioned enlargement
follows:
(granuloma pyogenicum)
• Grade 0: No signs of gingival enlargement b. Systemic diseases causing gingival enlargement
• Grade I: Enlargement confined to interdental - Leukemia
papilla - Granulomatous diseases (Wegener
• Grade II: Enlargement involving papilla and granulomatosis, sarcoidosis, and so on)
marginal gingiva 5. Neoplastic enlargement (gingival tumors)
• Grade III: Enlargement covering three quarters or a. Benign tumors
more of the crown b. Malignant tumors
6. False enlargements
C H A PT ER 21 G lN G IV A L EN LA R G EM EN T 173
INFLAMMATORY GINGIVAL Histologic Features

ENLARGEMENT Lesions that are soft and friable are smooth and shiny
on the surface. They have a preponderance of inflam-
Inflammatory gingival enlargement is the most com- matory cells and fluid with vascular engorgement, new
mon type of overgrowth, which manifests because of the capillary formation, and associated degenerative changes.
increase in volume of gingival tissue in response to local Lesions that are firm and resilient have a greater fibrotic
microbial irritation. Inflammatory enlargement may be component and abundance of fibroblasts and collagen
acute or chronic. fibers. The epithelium is thickened with acanthosis.
Treatment
Chronic Inflammatory Gingival Enlargement
Treatment consists of patient education, instructions
It results from long-standing local irritation of gingiva. in home care and meticulous plaque control regimen,
Overgrowth can be localized, generalized, or discrete. removal of dental deposits (plaque, calculus, stains), and
correction of plaque retention factors. If overgrowth per-
Clinical Features sists, surgical correction of gingival contour is necessary
Early signs of overgrowth are seen in the interdental by either gingivectomy or flap surgery.
area as the ballooning of papilla and thickening of gingi-
val margin, giving gingiva a characteristic lifesaver-like
form around the teeth (Fig. 21.1). It may be localized to Acute Inflammatory Gingival Enlargement
a few teeth or may be generalized. It is a painless and Gingival Abscess
slowly progressing lesion, which bleeds on provocation. A gingival abscess is a purulent infection localized to
Discrete lesions may be sessile or pedunculated and arise the marginal gingiva.
from interdental papilla, marginal gingiva, or attached
gingiva. Occasionally painful ulceration may occur in the CLINICAL FEATURES
fold between the growth and gingiva. An abscess is a suppurative inflammation associated
Etiology with pyogenic organisms. It is a localized, painful, rap-
idly expanding lesion that is usually of sudden onset and
Bacterial plaque is the prime cause of inflammatory lies confined to interdental papilla or marginal gingiva.
gingival enlargement. Factors that favor plaque accumu- Enlargement appears smooth and shiny (Fig. 21.2). Teeth
lation and retention, such as calculus, carious lesion and adjacent to it become sensitive to percussion. Abscess
overhanging margins of dental restorations, improperly usually is pointed and ruptures in 1 or 2 days to drain
designed prosthesis, malaligned teeth, and orthodontic on its own.
appliances, indirectly contribute to the pathogenesis of
chronic inflammatory overgrowth. Drying of gingiva ETIOLOGY
due to mouth breathing also is reported to cause chronic Acute gingival overgrowth results by traumatic inter-
inflammatory gingival overgrowth. ruption of the epithelial surface and implantation of bac-
teria in gingival tissue usually from toothbrush bristles,
FIGURE 21.1 Chronic inflammatory gingival overgrowth. FIGURE 21.2 Gingival enlargement associated with abscess in
relation to 15.
seeds, cornhusks, apple core, fish bone, dental procedures, TABLE 21. 1 Drugs Associated with Gingival Enlargement
and trauma from occlusion. Group of drug Agent
HISTOLOGIC FEATURES Anticonvulsants
Lesion shows purulent focus in the connective tissue Hydantoins Ethotoin

surrounded by diffuse infiltration of acute inflamma- Mephenytoin
Phenytoin
tory cells, edematous tissue, and vascular engorgement.
Surface epithelium shows intracellular and extracellular Succinimides Ethosuximide
edema, leukocytic infiltration, and ulceration. Methsuximide
Phensuximide
TREATMENT Valproic acid Valproic acid
Cause of the injury should be eliminated. Warm saline Immunosuppressant Cyclosporine
mouth rinses may be advised along with systemic anti- Tacrolimus
biotics, but if there is a periodontal pocket, it should be Calcium channel blockers
treated with curettage or gingivectomy.
Dihydropyridine derivatives Amlodipine
Felodipine
FIBROTIC GINGIVAL ENLARGEMENT Nicardipine
Nifedipine
Nimodipine
Noninflammatory fibrous gingival overgrowth is be- Nisoldipine
lieved to be the result of genetic predisposition or an ad- Nitrendipine
verse effect of a drug. A large number of drugs and genetic Benzothiazine derivatives Diltiazem
disorders are associated with occurrence of gingival over-
growth in susceptible individuals. They may be Phenylalkylamine derivatives Verapamil
1. Drug-induced gingival enlargements

2. Idiopathic gingival enlargements
acid, phenobarbitone, primidone, mephenytoin, and
ethosuximide. Valproic acid has a broad spectrum of
Drug-Induced Gingival Enlargement
antiepileptic activity compared with other anticonvul-
The drugs that are reported to be associated with sants. It is established that sodium valproate carries a
gingival overgrowth are anticonvulsants, immunosup- relatively low risk for developing gingival overgrowth
pressants, and calcium channel blockers (Table 21.1). and may be a reasonable treatment alternative to phe-
Despite their pharmacological diversity all these drugs nytoin. The clinical and microscopic features of valproic
have a similar mechanism of action at cellular level. acid-induced gingival overgrowth are comparable to
They are known to inhibit intracellular calcium ion in- phenytoin-induced overgrowth.
flux. Therefore, the action of these drugs on calcium and
sodium influx may prove to be the key to understand CLINICAL FEATURES
why these groups of dissimilar drugs have a common Phenytoin-induced gingival overgrowth is character-
side effect on a secondary target tissue such as gingiva ized by initial enlargement of the interdental papillae, and
in susceptible individuals.
The clinical features of gingival overgrowth induced
by these agents and even the histologic appearance are
reported to have common characteristics such as increase
in extracellular ground substance, number of fibroblasts,
and acanthosis of epithelium.
Anticonvulsants
Phenytoin has been used to control seizure disorders in
patients with epilepsy and in management of neuralgias.
Patients have been reported to develop gingival enlarge-
ment in the first 6 months of intake of the drug (Fig. 21.3).
Since then numerous investigations have been conducted
to study its effect on gingival tissue.
Anticonvulsant drugs that have been associated with
gingival overgrowth, other than phenytoin, are valproic FIGURE 21.3 Phenytoin-induced gingival overgrowth.
is less frequently accompanied by increased thickening
of the marginal tissue. Affected tissues typically present
a granular or pebbly surface, with the enlarged papilla
extending facially and/ or lingually covering the tooth
surfaces. Affected papillae may become enlarged such
that they contact resulting in the clinical appearance of
pseudoclefts. The facial gingiva of the anterior sextants
is more commonly affected.
Immunosuppressants
Cyclosporine is a widely used immunosuppressant
drug to prevent rejection of organ transplant and for
treating a variety of autoimmune diseases. Its exact
mechanism of action is not clearly understood, but it
appears to selectively and reversibly inhibit helper T
cells and NK cells, which play a role in cellular and FIGURE 21.4 Nifedipine-induced gingival overgrowth.
humoral immune responses. Inhibition of these cells is
believed to be based on the blocking of calcium chan-
nels of the cells. Other Drugs
Prevalence of cyclosporine-induced gingival over- The ability of sex hormones to induce hyperplastic gin-
growth varies from 25 to 70% according to various inves- givitis has been well established. Association of gingival
tigators and it seems to be dose dependent. Dosage more overgrowth with the use of contraceptives (estrogen/
than 50 mg/ day has been reported to induce gingival progesterone) has been reported. There is an interest-
overgrowth. Overgrowth is greater in patients who are ing case report implicating antibiotic erythromycin with
medicated with cyclosporine along with calcium chan- gingival overgrowth.
nel blockers.
Cyclosporine-associated overgrowth resembles phe- HISTOLOGIC FEATURES
nytoin-induced gingival overgrowth; however, it is re- Histologic features of all drug-induced gingival over-
ported to be more vascularized than phenytoin-induced growths are comparable. They consist of connective tissue
gingival overgrowth. with an overlying multilayered parakeratinized epithe-
Tacrolimus is another immunosuppressant drug that lium with varying thickness and long rete pegs. Lamina
is used because of its less severe side effects and is also propria is characterized by proliferation of fibroblasts
reported to cause gingival overgrowth. However, the and an increase in collagen formation accompanied by
enlargement is less when compared with cyclosporine. an increase in noncollagenous matrix proteins. Focal ac-
cumulation of infiltrative inflammatory cells within con-
Calcium Channel Blockers nective tissue has been demonstrated.
These are drugs used in the management of a variety
of cardiovascular conditions including hypertension, PATHOGENESIS
angina pectoris, coronary artery spasm, and cardiac ar- Pathogenesis of drug-induced gingival overgrowth
rhythmias. They act like phenytoin and cyclosporine by has not been clearly understood. It has been suggested
inhibiting calcium ion influx across the cell membrane that gingival overgrowth could possibly be due to inhi-
of the heart and smooth muscle cells, blocking its cel- bition of apoptosis. Calcium ion plays a significant role
lular mobilization of calcium. Calcium channel blockers in apoptosis. Despite their pharmacological diversity all
associated with gingival overgrowth are amlodipine, three types of drugs have a similar mechanism of action
felodipine, nicardipine, nifedipine, nimodipine, nisol- at cellular level, where they inhibit intracellular calcium
dipine, and nitrendipine. ion influx. Available evidence suggests the direct effect
Nifedipine is most commonly used and widely stud- of the involved drug on specific subpopulation of fibro-
ied drug. The incidence of overgrowth in patients on blasts in gingival connective tissue, intercellular calcium
nifedipine is about 20%. Nifedipine-induced gingival metabolism and exchange, molecular mechanisms [vari-
overgrowth is reported to be dose dependent, and dose ous cytokines such as epidermal growth factor (EGF),
reduction is shown to have reduced the volume of gingi- platelet-derived growth factor (PDGF)], inactivation of
val overgrowth (Fig. 21.4). collagenases, genetic predisposition, and inflammation
Clinical and histologic features of nifedipine-induced induced by plaque. These dynamic variables may act on
gingival overgrowth are comparable to those of phenyt- gingival milieu individually or collectively to alter the
oin-induced gingival overgrowth. hemostatic state resulting in gingival overgrowth.
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PREVENTION AND TREATMENT Gradual enlargement of entire gingiva is noticed dur-

Significant correlations between the occurrence and/ ing the eruption of permanent dentition, but occasionally
or severity of drug-induced gingival overgrowth and it may also be observed during eruption of deciduous
the presence of plaque and plaque retentive factors have dentition. Overgrowth may interfere with eruption of
been reported. Hence, patients should be encouraged to teeth. It has been observed on both facial and oral aspects
perform meticulous oral hygiene and frequent recall visits of maxilla and mandible. Involvement may be localized
for removal of local deposits and professional assistance. or generalized and limited to either of the jaws. In severe
Physician should be advised to refer the patient scheduled cases overgrowth covers the entire crown, disfigures the
to receive a drug associated with gingival overgrowth to a patient's face, and interferes with speech and mastication.
dentist for baseline evaluation and control of local causal The gingiva is of normal color, firm, and of leathery con-
factors. If gingival overgrowth occurs, the causative drug sistency. Surface of the gingiva demonstrates pronounced
may be substituted if possible with a suitable noninduc- stippling, giving it a characteristic pebbled appearance. It
tive drug in consultation with the patient's physician. is painless without bleeding unless secondarily infected.
Despite drug substitution if the growth persists, surgical The overgrowth regresses and disappears after extraction
intervention may be necessary. If small areas without of teeth. There is a case report of occurrence of overgrowth
attachment loss and adequate keratinized gingiva are in- in an edentulous jaw under a complete denture. Gingival
volved, gingivectomy is indicated. Whenever larger areas enlargements have been associated with various syn-
are involved with attachment and bone loss, flap surgery dromes. A genetic abnormality may be implicated with
may be performed. Placement of pressure appliances after this type of presentation (Table 21.2).
surgical correction of overgrowth to prevent or reduce
tendency for recurrence has been reported. Etiology
Management of drug-induced gingival overgrowth Etiology is not clearly understood. Some cases have
should be a team approach involving the physician, the a hereditary basis, but the genetic mechanisms involved
dentist, and the health care professionals, for prevention, are not completely understood. A study of several fami-
early diagnosis, and effective treatment. lies found the mode of inheritance to be autosomal re-
cessive and some autosomal dominant. In some cases
family history of inheritance cannot be established. The
Idiopathic Gingival Enlargement enlargement usually begins with eruption of primary or
It is a fibrotic gingival enlargement of rare occurrence secondary dentition and regresses after extraction of teeth,
and unknown etiology. It is called by synonyms such as suggesting the possibility of plaque being the initiating
hereditary gingival fibromatosis, hereditary gingival hy- factor. It may be accompanied by other systemic disorders
perplasia, elephantiasis gingivae, fibromatosis gingivae, and syndromes.
idiopathic fibromatosis, and diffuse fibroma.
Unlike drug-induced gingival overgrowth, idiopathic
Histologic Features
overgrowth is diffuse and involves marginal papillary Microscopic appearance of idiopathic gingival over-
and attached gingiva (Fig. 21.5). growth is comparable to drug-induced overgrowth. There
is acanthosis of epithelium with deep rete pegs. There is
an increase in the amount of connective tissue, which is
relatively avascular. Inflammatory changes are seen im-
mediately in crevicular lining.
Treatment
Surgical removal of enlarged tissue is necessary for
functional and aesthetic reasons. This could be accom-
plished by gingivectomy or flap operation. Recurrence
of the overgrowth, to a greater extent, depends on the
patient's oral hygiene status. With meticulous oral hy-
giene maintenance, recurrence can be rendered very slow.
COMBINED ENLARGEMENT
Fibrotic gingival enlargement produces conditions

favorable for plaque accumulation by interfering with
FIGURE 21.5 Idiopathic gingival enlargement. effective oral hygiene measures. This leads to secondary
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TABLE 21.2 Syndromes Associated with Fibrotic Gingival Enlargement
Name of syndrome Characteristic features

Rutherford syndrome Gingival fibromatosis with hypertrichosis, epilepsy, and mental retardation
Zimmermann-Laband syndrome Gingival fibromatosis with defects of ears, nose, bones, nails, and terminal phalanges
Tuberous sclerosis Gingival fibromatosis with triad of epilepsy, mental deficeincy and cutaneous angiofibromas
Murray-Puretic-Drescher syndrome Gingival fibromatosis with multiple fibromas of head trunk, and extremities
Cross syndrome Gingival and alveolar enlargement, microphthalmia, cloudy corneas, hypopigmentation,
and athetosis
Ramon syndrome Gingival fibromatosis, hypertrichosis, cherubism, mental retardation, and epilepsy:
characteristic perivascular fibrosis in gingival biopsy specimens
inflammatory changes in existing fibrotic enlargements. inflamed gingiva forms discrete tumor-like mass referred
This type of enlargement is known as combined enlarge- to as pregnancy tumors.
ment. In such enlargement, the removal of local factors
results in reduction in size by eliminating inflammatory
component. However, the fibrotic component persists and
Histologic Features
requires surgical correction. It is nonspecific, vascularizing, and proliferating inflam-
mation. There is marked inflammatory cell infiltration with
edema and degeneration of the epithelium and connective
tissue. The epithelium is hyperplastic with accentuated rete
PREGNANCY,ASSOCIATED GINGIVAL pegs, decreased keratinization, and extracellular edema.
ENLARGEMENT Connective tissues show engorged capillaries and infiltra-
tion of leukocytes.
Clinical Features
The prevalence of pregnancy gingivitis ranges from 35
to 100%. The gingiva shows increased levels of inflam- VITAMIN C DEFICIENCY
mation often characterized by edema, color and contour
change, and propensity to bleed on gentle stimulation. The oral effects of vitamin C deficiency in humans
The marginal and interdental gingivae are enlarged occur chiefly in the gingival and periodontal tissues. The
(Fig. 21.6). They pit on pressure, appear smooth and shiny, interdental and marginal gingiva appears bright red with
and are soft and pliable giving the gingiva raspberry-like a swollen, smooth, shiny surface. The gingiva becomes
appearance. The gingival changes are usually painless boggy, ulcerates, and bleeds. Sometimes, the enlarged
unless complicated by acute infection. In some cases the tissue may cover the clinical crowns of the teeth. In severe
chronic cases there is loss of bone and associated tooth
mobility.
PYOGENIC GRANULOMA
It is considered a nonspecific conditioned gingival

enlargement. It appears as a localized mass of highly
vascularized granulation tissue arising as an exagger-
ated response to plaque. It commonly arises from the
proximal gingival tissues and has pedunculated base
(Fig. 21.7). The surface of the lesion may show ulcer-
ation. Bleeding on mastication or even spontaneously
may be present. Treatment includes excision of the le-
sion accompanied by thorough debridement of the tooth
FIGURE 21.6 Pregnancy-associated gingival enlargement. surface.
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originate in the interdental papilla. The lesions are deep

red, nodular, and friable and have been referred to as
strawberry gingivitis because of their resemblance to
overripe strawberries.
Histologic Features
The tissue shows vasculitis with zone of necrosis and fi-
brinoid deposits in a background of granulomatous changes.
Eosinophils and multinucleated giant cells are also seen.
FIGURE 21.7 Pyogenic granuloma.

SARCOIDOSIS
LEUKEMIA It is a chronic disease affecting the skin, mucosal surfac-

es, salivary glands, lungs, and occasionally other organs.
Leukemia is a disorder of the leukocytes which demon- It consists of multiple noncaseating epithelioid granulo-
strates an abnormality in formation as well as functioning mas and fibrosis of adjacent tissue.
of the leukocytes. It manifests itself in the gingiva as an as-
sociated gingival enlargement in acute myeloid leukemia. Clinical Features
Oral lesions appear as diffuse submucosal enlarge-
Clinical Features ments or focal firm nodules. Lesions are usually symp-
tomless.
Oral lesions occur in both acute and chronic forms of
all types of leukemia: myeloid, lymphoid, and monocytic
types. In both acute and chronic leukemias, the gingival Histologic Features
overgrowth occurs in 10% of the patients. The gingival
Tissue contains multiple granulomas in a nodular pat-
hyperplasia, which may be one of the most constant fea-
tern, each consisting of an accumulation of epithelial cells,
tures of the disease expected in edentulous patients, is
macrophages, and multinucleated giant cells. The periph-
usually generalized and varies in severity. The gingiva is
ery of each granuloma is composed of cellular fibrous
boggy, edematous, and deep red. The gingival enlarge-
connective tissue.
ment is due to the leukemic cell infiltration in areas of
mild chronic irritation. In severe cases the teeth may be
completely hidden. BENIGN LESIONS OF GINGIVA
Histologic Features Focal Fibrous Hyperplasia (Irritation Fibroma)
Biopsy of enlarged gingivae will disclose the presence Focal fibrous hyperplasia is most often encountered
of leukemic infiltrate. It is differentiated from inflamma- in adults and is primarily located on the gingiva. It is a
tory gingival hyperplasia by the presence of mononuclear nodular lesion and usually has a dome-like growth with
blast cells that show cytologic atypia. a smooth surface of normal color. Surface hyperkeratosis
is sometimes encountered. It is a slowly progressing le-
sion and may remain of same size for many years. It is
WEGENER GRANULOMATOSIS sometimes referred to as peripheral fibroma.
Histologic Features
Wegener granulomatosis is an uncommon disease
The surface epithelium may be intact, exhibit hyperor-
consisting of an inflammatory granulomatous process
thokeratosis, or show foci of ulceration. This epithelium
characterized by severe vasculitis and necrosis involving
overlies an underlying mass of dense fibrous connective
the respiratory system and kidneys. The head and neck
tissue composed of significant amount of soft mature col-
are involved in 90% of cases and oral lesions are 2-5%.
lagen in a scar-like pattern.
Clinical Features Peripheral Ossifying Fibroma

The oral lesions are most commonly described as It is a gingival nodule consisting of a reactive hyper-
granulomatous hyperplastic gingivitis that appears to plasia of connective tissue containing focal areas of bone.
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The peripheral ossifying fibroma is a reactive fibrous and rarely results in a cluster of lesions. The lesion is of the
proliferation, probably of periosteal or periodontal liga- same color as the adjacent normal mucosa. It can occur in
ment origin. free or attached gingival or interdental papilla.
Clinical Features Histologic Features

It emanates from the interdental papillae, although Lesions are often small with the epithelial lining of
occasionally it is seen to arise from the facial/lingual at- two to five cells in thickness. They often exhibit neural
tached gingiva. The mass originates from within the peri- thickening. Sometimes clear cells may be seen.
odontal ligament. The overlying mucosa may be smooth
and of normal coloration, or there may be foci of surface
ulceration. MALIGNANT LESIONS OF GINGIVA
Histologic Features
Squamous Cell Carcinoma
Within the connective tissue are diffuse sheets of fi-
broblasts with plump monomorphic nuclei. The overall Squamous cell carcinoma is defined as a malignant
picture is one of hypercellularity with hyalinized col- neoplasm that is derived from squamous epithelium.
lagenous component. In focal areas, osteoid deposits can It is the most common malignant neoplasm of the oral
be identified. Rarely mature trabeculae of bone are seen. cavity representing 90% of the oral cancers. Lesions
of the gingival and alveolar ridges represent 4-6% of
the intraoral carcinoma. Mandible is affected more
Peripheral Giant Cell Granuloma than the maxilla and most of the lesions are present in
The peripheral giant cell granuloma is a hyperplastic posterior areas. Carcinoma of the gingiva is usually
reaction of the gingival connective tissue in which the manifested as an area of ulceration. The growth may
histiocytic and endothelial cellular components predomi- appear exophytic. It may or may not be painful. The
nate. attached gingiva is more commonly involved than the
free gingiva. Metastasis occurs in the submandibular
Clinical Features or cervical lymph nodes.
Peripheral giant cell granuloma is found in all age
groups with peak incidence in adults around 30 years of
Nodular Melanoma
age. It is common in females and equally distributed be-
tween maxilla and mandible. It is most commonly found It is a form of malignant melanoma occurring in the
anterior to the molars. Lesions begin as a reddish or pur- skin and occasionally the mucosa. It appears as a raised
plish dome-shaped swelling of the interdental papilla or mass with a limited radial growth phase and quickly
alveolar ridge. Larger lesions usually encircle one or more invades, and metastasized lesion consists of a combina-
teeth, often involving the periodontal ligament. These tion of pink, red, brown, and black nodules, which may
lesions produce loosening and movement of the teeth. be ulcerated.
Histologic Features Histologic Features

Microscopic appearance reveals a nodular arrangement Connective tissue is densely packed with tumor cells,
of giant cell tissue separated by fibrous septa. The giant which may be epithelioid, spindle-shaped, or lympho-
cell tissue consists of a mixture of mononuclear giant cells cyte-like. Melanin deposition is seen among the cells.
with background of red blood cells (RBCs). Capillary
vessels and sinusoidal spaces are usually present. Heavy
Kaposi Sarcoma
deposits of hemosiderin are common.
It comprises macular or nodular vascular lesions occur-
ring singularly or in multiples on the mucosa and skin of
Gingival Cyst
human immunodeficiency virus (HIV)-infected patients.
Gingival cyst develops in the gingival soft tissues out- The dominant locations within the oral cavity are the pal-
side bone and is derived from the cell rests of the dental ate and maxillary gingiva. The lesions are reddish to deep
lamina. purple and may be macular or nodular. Large gingival
lesions often interfere with mastication.
Clinical Features
Gingival cyst occurs as a firm, compressible, fluid-filled Histologic Features
swelling on the facial gingiva usually in the anterior or Lesions exhibit a proliferation of hyperchromatic
premolar region. It usually develops as a solitary lesion spindle-shaped or oval endothelial cells arranged in an
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irregular vascular pattern. Extravasated red blood cell a picture of gingival enlargement. Lesions of the bone-
and hemosiderin deposits are characteristically present. like central giant cell granuloma, Paget disease, and fi-
brous dysplasia cause expansion of the cortical plates of
the jaws, which may give a false appearance of gingival
FALSE GINGIVAL ENLARGEMENT enlargement. Unerupted teeth, usually in the children,
appear as localized enlargements.
Gingival contour may be altered by changes in the
underlying bone or the dental tissues. Lesions of the bone
or the underlying dental hard tissues may clinically give
KEY POINTS
• The increase in the size of gingiva is termed gingival • Anticonvulsant drugs that have been associated with
enlargement or overgrowth. gingival overgrowth are phenytoin, valproic acid, phe-
• Increase in the size alters the physiologic contour of the nobarbitone, primidone, mephenytoin, and ethosuxi-
gingiva, creates areas of plaque accumulation, interferes mide.
with regular oral hygiene procedures, and leads to aes- • Synonyms of idiopathic gingival enlargement are
thetic problems. hereditary gingival fibromatosis, hereditary gingi-
• An abscess is a suppurative inflammation associated val hyperplasia, elephantiasis gingivae, fibromato-
with pyogenic organisms. sis gingivae, idiopathic fibromatosis, and diffuse
• The drugs that are reported to be associated with gingi- fibroma.
val overgrowth are anticonvulsants, immunosuppres-
sants, and calcium channel blockers.

1. Alderer MJ, Bartold PM. Genetic disorders of gingivae and
1. Classify gingival enlargements. Describe the periodontium. Periodontal 2000 1998;18:7-20.
etiopathogenesis of drug-induced gingival 2. Carranza FA, Hogan EL. Gingival enlargement. In: Carranza's
enlargements. Clinical Periodontology. 10th ed. Philadelphia: Elsevier; 2000:
373-390.
2. Classify gingival enlargements. Add a note on
3. Carranza Jr FA. Gingival enlargement. Clinical Periodontology. 8th ed.
conditioned gingival enlargements. Prism Books Pvt. Ltd. Bangalore, India; 1996. p. 233-49.
3. Describe tuberous sclerosis. 4. Hallmon WW, Rossmann JA. The role of drugs in the pathogenesis
4. Describe false gingival enlargements. of gingival overgrowth - a collective review of current concepts.
5. Describe pyogenic granuloma. Periodontal 2000 1999;21:176-96.
6. Describe idiopathic gingival enlargements.
7. Describe gingival enlargements associated with
pregnancy.
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CHAPTER
22
Acute Gingival Infections
CHAPTER OVERVIEW
Acute gingival infections are those that can occur with this category are necrotizing ulcerative gingivitis, primary
sudden onset and are of short duration. They can be also herpetic gingivostomatitis, and pericoronitis.
very painful. The conditions that can be included under
NECROTIZING ULCERATIVE GINGIVITIS the marginal gingiva (Fig. 22.1). There is a rare
involvement of attached gingiva and oral mucosa.
Definition 2. Gray, pseudomembranous slough covers the gingival
craters. It is demarcated from the healthy gingiva by a
Necrotizing ulcerative gingivitis (NUG) is a microbial
pronounced linear erythema.
disease of the gingiva in the context of an impaired host
3. Lesion may be denuded of the pseudomembrane,
response, which is characterized by the death and slough-
exposing red, shiny, and hemorrhagic gingival surface
ing of gingival tissues and presents with characteristic
in some cases.
signs and symptoms.
4. The lesion will bleed on slight provocation.
Previously known as acute necrotizing ulcerative gin-
5. There is fetid odor and increased salivation.
givitis (ANUG), it was renamed as necrotizing ulcerative
gingivitis. It is also known as trench mouth because of
its prevalence in the soldiers working in trenches during Oral Symptoms
World War I. Vincent first described the bacteria associ-
ated with these infections; hence, the disease was also 1. Patient complains of a constant radiating, gnawing
known as Vincent angina. pain that is aggravated by eating spicy and hot foods
and on chewing.
2. There is metallic foul taste and a pasty saliva.
Clinical Features
It usually presents as an acute disease. Sometimes it
resolves on its own and has milder symptoms leading to Extraoral and Systemic Signs and Symptoms
a subacute stage. 1. Local lymphadenopathy and mild fever are the
History symptoms.
2. In severe cases, high fever, increased pulse rate,
Symptoms are sudden in onset.
leukocytosis, loss of appetite, and general lassitude
Patients may have an episode of debilitating disease
are the most common systemic signs.
or acute respiratory tract infection; also change in habits,
continuous work without rest, poor nutrition, tobacco use, These systemic signs and symptoms are more severe
and psychological stress are frequent features. in children.
Oral Signs
The following are the characteristic signs: Clinical Course
1. There are punched-out, crater-like depressions NUG may lead to necrotizing ulcerative periodontitis
at the crest of the interdental papillae; it may involve (NUP) if untreated.
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Stage 5 Necrosis involving the buccal and labial mucosa (6%)

Stage 6 Necrosis exposing alveolar bone (1 %)
Stage 7 Necrosis perforating skin of the cheek (0%)
(Fig. 22.2).
According to Homing and Cohen, stage 1 is NUG,

stage 2 may be either NUG or NUP because attachment
loss may have occurred, stages 3 and 4 would correspond
to NUP, stages 5 and 6 would correspond to necrotizing
stomatitis, and stage 7 would be noma.
Relation of Bacteria to the Characteristic

Lesion
FIGURE 22.1 Necrotizing ulcerative gingivitis - crater-like depres-
sions of the interdental papilla.
The characteristic lesion of NUG is studied under light
microscopy and electron microscopy to study the relation
of the bacteria in the lesion.
Listgarten described the following zones in the lesion,
When there is bone loss along with NUG, the condition which may overlap with one another; all zones may not
is termed NUP. be present at the same time:
Stages in progression of NUG are described by Pin-
Zone 1 (bacterial zone): The most superficial zone
dborg et al. The lesion starts as
composed of various types of bacteria and few
1. Erosion of the tip of the interdental papilla spirochetes of the small, medium, and large types
2. The lesion involving all of the papilla and also involving Zone 2 (neutrophil-rich zone): Contains numerous
the marginal gingiva leukocytes, predominantly leukocytes with bacteria,
3. The attached gingiva also involved including spirochetes of various types interspersed in
4. Exposure of the bone with complete loss of interdental between the leukocytes
papilla, marginal gingiva, and the attached gingiva Zone 3 (necrotic zone): Consists of disintegrated tissue
cells, fibrillar material, remnants of collagen fibers, and
Homing and Cohen extended the staging as follows:
numerous intermediate and large types of spirochetes,
Stage 1 Necrosis of the tip of the interdental papilla (93%) with few other bacteria
Stage 2 Necrosis of the entire papilla (19%) Zone 4 (zone of spirochetal infiltration): Consists of
Stage 3 Necrosis of the marginal gingiva (21 %) well-preserved tissue infiltrated with intermediate and
Stage 4 Necrosis extending to the attached gingiva (1 %) large spirochetes, without other organisms
FIGURE 22.2 Necrosis perforating skin of the cheek (noma). (Courtesy: Nairobi Dental College, Kenya, East Africa.)
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C H A PT ER 22 A C U T E G IN G IV A L IN FEC T IO N S 183
Psychological stress and anxiety
i
Increased corticosteroid production
Preexisting gingivitis
• .
I mmunosuppression
i Increased bacteria growth and invasion

lmmunosuppression
Viral infection
+
HIV infection
Necrotizing ulcerative gingivitis
i
eficient nutritioJ
l
+
Candida infection Noma ,. Viral infections
l
Linear gingival erythema---..........
~
rotozoal infections
Necrotizing ulcerative periodontitis
Necrotizing stomatitis
FIGURE 22.3 Necrotizing ulcerative gingivitis: possible etiologic mechanisms and sequelae.
Etiology (See Fig. 22.3) b. Systemic predisposing factors: Immunodeficient

patients are most commonly affected by NUG.
1. Bacteria: Plaut (1894) and Vincent (1869) introduced Immunodeficiency could be caused by nutritional
the concept that NUG is caused by specific bacteria: deficiencies (e.g., vitamin C, vitamin B2), fatigue caused
fusiform bacillus and spirochetal organism. Rosebury by chronic sleep deficiency, habits such as alcohol or
et al. described a fusospirochetal complex which drug abuse, and systemic diseases, e.g., diabetes.
consists of the following bacteria: Treponema Other debilitating diseases that may predispose
microdentium, intermediate spirochetes, vibrios, patients to NUG include chronic diseases such as
fusiform bacilli, and filamentous organisms, and syphilis and cancer, severe gastrointestinal disorder,
Borrelia sp. leukemia, anemia, and acquired immunodeficiency
Loesche et al. described a constant flora composed syndrome (AIDS).
of Prevotella intermedia, Fusobacterium, Treponema and c. Psychosomatic factors: The disease is often
Selenomonas spp., and Bacteroides melaninogenicus. associated with stressful situations, e.g., school
Borrelia, gram-positive cocci, ~-hemolytic streptococci, examination, induction into armed forces, patients
and Candida albicans have been isolated from the lesions with depression or other emotional disorders,
of human immunodefeciency virus (HIV)-associated and patients feeling inadequate at handling life
NUG. situations.
2. Predisposing factors: These can be divided into local
predisposing factors and systemic predisposing Psychiatric disturbances, e.g., trait anxiety, depres-
factors. sion, psychopathic deviance, and the impact of negative
a. Local predisposing factors: These include preex- life events, may lead to activation of the hypothalamic-
isting gingivitis, deep periodontal pockets, and pituitary-adrenal axis. This activation elevates the level
pericoronal flaps, which favor the proliferation of serum and urine cortisol levels and in turn causes
of anaerobic fusiform bacilli and spirochetes. depression of lymphocyte and polymorphonuclear leu-
There is localized area of gingival trauma usu- kocyte (PMN) function, which facilitates bacterial in-
ally due to trauma by an opposing tooth in mal- vasion and damage. Increased cortisol level may also
occlusion. reduce gingival microcirculation and salivary flow and
Frequency of NUG increases with smoking and enhance nutrition of P. intermedia, which is a constant
tobacco use. flora in NUG.
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Epidemiology and Prevalence Diagnosis

NUG occurs at all ages, with the highest incidence Diagnosis is primarily made based on the clinical find-
reported between ages 20 and 30 years, and ages 15 ings of gingival pain, ulceration, and bleeding.
and 20 years. It is not common in children in the United Microscopic examination of a bacterial smear or a bi-
States, Canada, and Europe, but it has been reported in opsy specimen does not give specific picture.
children from low socioeconomic groups in underde- The histologic picture greatly resembles marginal gin-
veloped countries. In India, 54 and 58% of the patients givitis, periodontal pockets, pericoronitis, or primary
in two studies were under age 10 years. In a random herpetic gingivostomatitis.
school population in Nigeria, NUG occurred in 11.3% However, bacterial smears can be useful in differen-
of children between the ages of 2 and 6 years, and in a tiating from specific infections of the oral cavity, such
Nigerian hospital population, it was present in 23% of as diphtheria, thrush, actinomycosis, and streptococcal
children under 10 years of age. It has been reported in stoma ti tis.
several members of the same family in low socioeco- Biopsy specimen can be used to differentiate NUG
nomic groups. NUG is more common in children with from specific infections such as tuberculosis or from neo-
Down syndrome than in other children with mental plastic disease.
deficiencies. NUG should be differentiated from other conditions
NUG is described as transmissible but not communi- such as herpetic gingivostomatitis, chronic periodontitis,
cable or contagious disease. and desquamative gingivitis (Tables 22.1 and 22.2).
Communicability refers to the capacity for the main-
tenance of infection by natural modes of spread, such as
direct contact through drinking water, food, and eating Treatment
utensils; the airborne route; or by means of arthropod Objectives of treatment of NUG include the following:
vectors.
1. Resolution of acute phase
The disease is transmissible if it has the capacity for the
2. Treatment of the chronic disease either underlying the
maintenance of an infectious agent in successive passage
through a susceptible animal host. acute involvement or elsewhere in the oral cavity
3. Alleviation of generalized symptoms such as fever and
A classical experiment by King: In an attempt to spread
NUG among humans, King traumatized an area in his malaise
4. Correction of the systemic etiologic factors, e.g.,
own gingiva and inoculated debris from a patient with
severe case of NUG. There was no response until he fell smoking and stress
ill shortly thereafter, and subsequent to his illness, he ob- NUG is managed in a systematic sequence of three
served the characteristic lesion of NUG. This experiment clinical visits.
demonstrated the role of predisposing factors along with Vincent angina is a fusospirochetal infection of the
the bacterial role. oropharynx and throat. In this condition patients have a
TABLE 22.1 Differentiation Among Necrotizing Ulcerative Gingivitis, Chronic Desquamative Gingivitis, and Chronic
Periodontal Disease
Necrotizing ulcerative gingivitis Desquamative gingivitis Chronic destructive periodontal disease

Bacterial smears show fusospirochetal Bacterial smears reveal numerous epithelial Bacterial smears are variable
complex cells, few bacterial forms
Marginal gingiva affected Diffuse involvement of marginal and Marginal gingiva affected
attached gingiva and other areas of oral
mucosa
Acute history Chronic history Chronic history

Painful May or may not be painful Painless if uncomplicated
Pseudomembrane Patchy desquamation of gingival epithelium Generally no desquamation, but purulent

material may appear from pockets
Papillary and marginal necrotic lesions Papillae do not undergo necrosis Papillae do not undergo noticeable necrosis
Affects adults of both genders, occasionally Affects adults, most often women Generally in adults, occasionally in children
children
Characteristic fetid odor None Some odor present, but not strikingly fetid
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TABLE 22.2 Differentiation Between Primary Herpetic Gingivostomatitis and Necrotizing Ulcerative Gingivitis
Primary herpetic gingivostomatitis Necrotizing ulcerative gingivitis

Etiology The main causative organism is a virus (HSV-1) The interaction between the host and bacteria
(fusospirochetal complex)
Clinical features Diffuse erythema and vesicular lesions, which rupture A necrotizing condition, with punched-out gingival
leaving slightly depressed area of ulcers margins covered by a pseudomembrane that peels off
Diffuse involvement of the gingiva Involvement of marginal gingiva only
Age Children and adolescents are more commonly affected Occurrence in children is a rare case
Course It has a course of 7-10 days No definite duration
Immunity and contagion Acute episodes lead to development of immunity and It does not develop an immunity and is not contagious
it is contagious
painful membranous ulceration of the throat with edema d. Patient is advised to get adequate rest and avoid
and hyperemic patches breaking down to form ulcers. strenuous exercise such as swimming and playing
games, which requires a greater physical activity.
First Visit e. An analgesic such as nonsteroidal anti-inflammatory
• Complete evaluation of the patient regarding medical drug can be prescribed for pain control.
history and history of recent illness is done.
• Dietary history, history of smoking, risk factors for HIV, Second Visit
and psychological factors are evaluated.
• It is usually 1 or 2 days after the first visit.
• General examination should be performed to examine
• Patient has to be examined for resolution of systemic
the vital signs and palpation of lymph nodes, especially
signs and symptoms.
submaxillary and submental nodes. Patient should also
• The area of the lesion will be erythematous but with
be examined for the skin lesions.
marked reduction of necrotic tissue. Scaling may be
• Treatment of the acute lesion is the primary goal. A
reperformed.
topical anesthetic is applied to the affected area. The
• Patient should follow the instructions as given during
area has to be swabbed with moist cotton pellet to
the first visit.
remove the pseudomembrane and nonattached surface
debris.
• Supragingival scaling with ultrasonic instruments can Third Visit
be performed. • After approximately 5 days of the second visit, patient
• Subgingival scaling and curettage is contraindicated is evaluated for the resolution of symptoms and
because it may lead to extension of infection into the complete protocol for the periodontal management is
deeper tissues and can cause bacteremia. planned.
• Periodontal surgery and extractions are postponed • A hydrogen peroxide rinse will be discontinued;
until the patient is symptom free. The time period chlorhexidine mouthwash can be continued for 2 or
usually required is 4 weeks for a patient to be symptom 3 weeks.
free. • A repeat scaling and root planing can be performed if
• Patient has to be placed on the following antibiotic required.
regimen: amoxicillin 500 mg orally every 6 h for • The patient should be reinstructed to follow the
10 days; if allergic to amoxicillin, erythromycin 500 mg appropriate plaque control measures.
every 6 h or metronidazole 500 mg twice daily for • The patient is further counseled on nutrition, smoking
7 days can be prescribed. cessation, and other habits associated with possible
recurrence.
INSTRUCTIONS TO THE PATIENT • Appointments should be scheduled for the treatment
a. Avoid tobacco, alcohol, and condiments. of chronic gingivitis, periodontal pockets, and
b. Patient is advised to rinse with 3% hydrogen peroxide pericoronal flaps, as well as for the elimination of all
mixed with equal amount of warm water every 2 h or local irritants including defective restorations.
twice daily with 0.2% chlorhexidine mouthwash. • Patient is reevaluated after 1 month for oral hygiene
c. Avoid overzealous toothbrushing and use of interdental maintenance, health habits, psychosocial factors,
cleaning devices. An ultrasoft toothbrush may be used and determination of the need for reconstructive or
to clean the surface debris. aesthetic surgery.
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Additional Treatment Considerations

CONTOURING OF GINGIVAL MARGIN
In cases of NUG when there is a severe loss of inter-
dental gingiva as well as bone, healing results in the for-
mation of shelf-like gingival margin, which is conducive
to plaque accumulation and is an aesthetic concern too.
This can be corrected by a periodontal plastic surgery or
by reshaping the gingiva surgically so that the normal
gingival architecture is restored.
NUTRITIONAL SUPPLEMENTS
Nutritional supplements may be indicated along with
local treatment in conditions where the patient is unable
to take food due to pain.
Patient may be given a standard multivitamin prepa- FIGURE 22.4 Primary herpetic gingivostomatitis - vesicle formation
ration along with therapeutic dose of vitamins B and C. and erythema seen on the gingiva.
PERSISTENT OR RECURRENT CASES sensory and autonomic nerves and persists as latent HSV
The following factors play a role in causing persistent in the neuronal ganglia that innervate the site. HSV-1 most
disease or recurrence: commonly resides in the trigeminal ganglion. Secondary
manifestation occurs as a result of various stimuli, such
1. Diseases that resemble NUG, e.g., desquamative as sunlight, trauma, fever, and stress.
diseases of the gingiva Secondary manifestations include herpes labialis, her-
2. Patients with underlying systemic diseases, e.g., HIV petic stomatitis, herpetic genitalis, ocular herpes, and
infection herpetic encephalitis. Secondary herpetic stomatitis can
3. Inadequate local therapy and patient compliance occur as a result of dental treatment. It presents as a char-
acteristic vesicle at a site away from the site of treatment.
PRIMARY HERPETIC
GINGIVOSTOMATITIS Oral Signs
Primary herpetic gingivostomatitis is an infection • It involves both the gingiva and the oral mucosa. In
of the oral cavity affecting mostly infants and children the initial stage, it is characterized by the presence of
younger than 6 years of age. The causative organism is discrete, spherical gray vesicles on the gingiva, labial
herpes simplex virus type 1 (HSV-1). Males and females and buccal mucosa, soft palate, pharynx, sublingual
are equally affected. mucosa, and the tongue.
• After approximately 24 h, the vesicles rupture and form
painful, small ulcers with a red, elevated, halo-like
Clinical Features
margin and a depressed, yellowish or grayish white
In most cases the primary infection is asymptomat- central portion. The ulcers may occur in clusters or can
ic. After primary infection, the virus ascends through be widely separated (Fig. 22.4).
Primary infecti_on by a virus
Virus ascends through sensory

and autonomic nerves unlight
Trauma
Fever
Remains latent at trigeminal ganglion tress
L Secondary manifestation
• Occasionally primary herpetic gingivitis may occur TABLE 22.4 Differentiation Between Primary Herpetic
without overt vesiculation. The clinical picture consists Gingivostomatitis and Desquamative Gingivitis
of diffuse erythematous, shiny discolouration and Primary herpetic
edematous enlargement of the gingiva with a tendency gingivostomatitis Desquamative gingivitis
towards bleeding. Etiology Viral Bacterial forms
• The lesion resolves on its own by 7-10 days. It heals
Sites Diffuse involvement of Diffuse involvement
without scarring. involved gingiva without peeling of gingiva and varying
Acute condition degrees of peeling are seen
Chronic condition
Oral Symptoms
• Patient complains of soreness of mouth with difficulty Other conditions resembling acute herpetic gingivo-
in eating and drinking. stomatitis are
• The lesions are painful and sensitive to touch, changes
in temperature, and food and beverages, especially • Erythema multiforme: It can be differentiated from
spicy foods and fruit juices and to the action of coarse primary herpetic gingivostomatitis as follows:
foods. It has extensive involvement of the tongue and skin
• Infants usually refuse to eat food due to pain. lesions with large vesicles.
Duration of erythema multiforme may be prolonged
These oral signs and symptoms are accompanied by more than a week.
by the following constitutional signs and symptoms: • Stevens-Johnson syndrome: It is a rare form of
cervical adenitis, high-grade fever, and generalized erythema multiforme with hemorrhagic vesicular
malaise. lesions in the oral cavity, skin, and eyes.
• Bullous lichen planus:
Prolonged indefinite course of a disease
Diagnosis Painful condition with large blisters on the tongue
The diagnosis in most cases can be established by his- and cheeks, and ruptures resulting in ulceration
tory and clinical examination. Oral lesions coexistent with skin lesions
Confirmatory tests include virus culture and immuno-
logic tests using monoclonal antibodies or DNA hybrid-
ization techniques. Treatment
Previously treatment of acute herpetic gingivostoma-
titis consisted of only supportive care. Recently an anti-
Differential Diagnosis viral therapy with 15 mg/kg of an acyclovir suspension
The lesion resembles the following conditions given five times daily for 7 days has been implicated to
(Tables 22.3 and 22.4): reduce the course of disease. This antiviral therapy re-
duces symptoms such as fever, difficulty in eating, and
• Necrotizing ulcerative gingivitis also the appearance of new extraoral lesions. It is found
• Desquamative gingivitis to be effective only if the lesions are diagnosed within
• Recurrent aphthous stomatitis (RAS) 3 days of onset.
• Erythema multiforme The patients reporting after 3 days of onset should be
• Stevens-Johnson syndrome given a palliative care that includes
• Bullous lichen planus
• Removal of plaque and food debris
TABLE 22.3 Differentiation Between Primary Herpetic • Administration of nonsteroidal anti-inflammatory
Gingivostomatitis and Recurrent Aphthous Stomatitis drug (NSAID) to reduce fever and pain
Primary herpetic • Nutritional supplements or topical anesthetic before
gingivostomatitis Recurrent aphthous stomatitis eating to aid in proper nutrition
Etiology Viral etiology Etiology is unknown; suspected • Periodontal therapy postponed until the acute
immunopathologic mechanism symptoms subside to prevent exacerbation
Sites Diffuse erythematous No diffuse involvement of gin- Herpetic gingivostomatitis is contagious at certain
involved involvement of the giva; isolated ulcers are seen
gingiva
stages such as when vesicles are present.
Herpetic infection called herpetic whitlow, infection on
Healing Lesion heals by Lesions less than 1 cm will heal the finger, can occur if a seronegative clinician becomes
scarring without scarring
infected with a patient's herpetic lesions.
PERICORONITIS
It refers to the inflammation of the gingiva or a peri-

coronal flap of an incompletely erupted tooth. The most
commonly involved tooth is the mandibular third mo-
lar. The major factor responsible for involvement of the
mandibular third molar is the space between the erupt-
ing tooth and the overlying flap. The involvement of
the mandibular third molar can be explained as given
in Fig. 22.5.
Clinical Features
• The pericoronal flap (Fig. 22.6) will be red and swollen
with presence of exudate.
• Patient complains of pain radiating to the ear, throat,
and floor of the mouth. FIGURE 22.6 Pericoronal flap in relation to third molar.
• Patient will be unable to open the jaws and will
complain of foul taste. • Cellulitis
• Lymphadenitis may be present. • Ludwig angina
• Systemic symptoms such as fever and malaise are also
present.
Treatment
Treatment largely depends on the following factors:
Complications
• Severity of inflammation
• Pericoronal abscess
• The systemic involvement
• Peritonsillar abscess
J
• The possibility of retaining the tooth
The acute pericoronitis is treated to relieve the acute
Space between crown and pericoronal flap
symptoms that consist of the following:
• Gentle irrigation of the area is performed with warm
saline to remove debris and exudates.
Site for accumulation of food debris
• Occlusion is evaluated to determine if an opposing
Area neglected by patients while brushing
tooth is occluding with the pericoronal flap. Occlusal
adjustment is necessary in case of opposing tooth
i traumatizing the flap.

• Antibiotics are administered in severe cases with
involvement of lymph nodes.
Area for bacterial colonization
• Drainage can be established if the swelling is fluctuant
by using a no. 15 blade.
i
Inflammation and ulceration of the flap
After resolution of the acute symptoms, the tooth
should be evaluated for possibility of erupting to a func-
tional position. If the tooth is to be retained, the pericoro-
i
Increased bulk of the flap due to inflammatory edema
nal flap should be surgically excised using the periodontal
knives. The surgical procedure to remove the operculum
is called operculectomy (Fig. 22.7). The operculum can also
be removed by electrosurgery.
i
Exacerbation of inflammation and ulceration
The removal of the flap should result in a site that can
be easily maintained by the patient. To ensure this the flap
covering the occlusal surface as well as the tissue distal
FIGURE 22.5 Pericoronitis: involvement of mandibular third molar. to the tooth has to be removed.
FIGURE 22. 7 Operculectomy.
KEY POINTS
• Necrotizing ulcerative gingivitis is a microbial disease • Pericoronitis is the inflammation of gingiva around an
of gingiva that can be attributed to various predisposing incompletely erupted tooth, which when untreated can
factors. lead to various complications.
• Primary herpetic gingivostomatitis is caused primarily
by HSV-1 and it is a communicable disease.
2. Ellen RP, Galimanas VB. Spirochetes at the forefront of periodontal

QUESTIONS infections. Periodontal 2000 2005;38:13-32.
1. Describe the clinical features of ANUG. Dentistry. 5th ed. Oxford: Blackwell Munksgaard; 2006.
2. What are the acute gingival infections? Describe any 4. Newman MG, Takei HH, Klokevold PR, Carranza FA. Carranza's
one in detail. Clinical Periodontology. 10th ed. St. Louis: Elsevier; 2006.
5. Rivera-Hidalgo F, Stanford TW. Oral mucosa! lesions caused by
3. Discuss the management of ANUG. infective microorganisms. Viruses and bacteria. Periodontal 2000.
4. What is pericoronitis? Discuss its management. 1999;21:106-24.
5. What are the clinical features of acute herpetic 6. Rowland RW. Necrotizing ulcerative gingivitis: abstract. Ann
gingivostomatitis? Periodontol 1999;4:65-73.
6. What are the complications of acute pericoronitis? 7. Seymour RA, Heasman PA, Macgregor IDM. Drugs, Diseases and the
Periodontium. Oxford: Oxford University Press; 1992.
Suggested readings
1. Carranza Jr FA, Newman MG. Carranza's Clinical Periodontology.
8th ed. Philadelphia: Saunders; 1996.
CHAPTER
23
Desquamative Gingivitis
CHAPTER OVERVIEW
Desquamative gingivitis is a clinical term to describe red, mucous membrane pemphigoid (MMP), lichen planus (LP),
painful, glazed, and friable gingiva, which may be a mani- and, to a lesser degree, pemphigus vulgaris (PV). However,
festation of some mucocutaneous conditions such as lichen chronic ulcerative stomatitis, bullous pemphigoid, linear IgA
planus or the vesiculobullous disorders. It is important to be disease, lupus erythematosus, and dermatitis herpetiformis
aware of this rare clinical entity so as to distinguish desquama- can also present as desquamative gingivitis.
tive gingivitis from plaque-induced gingivitis, which is an ex- McCarthy et al suggested that desquamative gingivitis
tremely common condition. Chronic desquamative gingivitis was not a specific disease entity but a gingival response
was first recognized and reported in 1894 by Prinz. The term associated with a variety of conditions.
chronic desquamative gingivitis was coined in 1932 to de- Difficulties are sometimes encountered in establishing
scribe a peculiar condition characterized by intense erythema, a definitive diagnosis of desquamative gingival diseases.
desquamation, and ulceration of the free and attached gingiva. An effective diagnostic protocol can be established that will
Generally, lesions appear erythematous or ulcerative, lead to correct identification of most oral diseases and disor-
but in some cases, hyperkeratotic. The condition was origi- ders. This protocol includes a thorough medical and dental
nally believed to represent a hormonally mediated disorder history, personal and family history of related diseases, a
most commonly found in women. Subsequently improved complete clinical oral examination, and, when indicated,
diagnostic techniques have demonstrated that chronic gin- the appropriate use of biopsies to perform histopathologic
gival desquamation may be associated with a wide variety and direct immunofluorescence examination.
of diseases and disorders including vesiculoulcerative dis- Therefore, to properly diagnose the condition respon-
orders and adverse reaction to medication. sible for desquamative gingivitis, clinical examination cou-
Approximately 75% of desquamative gingivitis (DG) cas- pled with a thorough medical history and routine histologic
es have a dermatologic origin and are mainly associated with and immunofluorescence studies is required.
CLASSIFICATION OF DISEASES
THAT CLINICALLY PRESENT AS
DESQUAMATIVE GINGIVITIS
• Derma tologic Dental restorative materials

Lichen planus Food (reaction to oral hygiene products, chewing
Mucous membrane pemphigoid gum, food)
Bullous pemphigoid Drug-induced mucocutaneous disorder
Pemphigus vulgaris • Traumatic lesions
Chronic ulcerative stomatitis Physical injury
Linear IgA disease Chemical injury
Lupus erythematosus Thermal injury
• Allergic reaction • Miscellaneous conditions
C H A PT ER 23 D ESQ U A M AT IV E G IN G IV IT IS 191
DERMATOLOGIC LESIONS
Lichen Planus
Lichen planus is the most common inflammatory mu-
cocutaneous disease involving mucosa (oral cavity, geni-
tal tract, and skin), also manifesting on the gingiva. It is
an immunologically mediated disorder in which host T
lymphocytes play a major role. The prevalence of oral
lichen planus in various populations has been found to be
0.1-4%. This disease may affect patients at any age, and
has a female predilection in the ratio of 2:1.
Clinical Features
Oral lichen planus (OLP) presents in different forms
FIGURE 23.1 Lichen planus.
of lesions: reticular, patch papular, atrophic, erosive, and
bullous. The disease runs a chronic course with periods 3. Dense "band-like" infiltrates, primarily of T lympho-
of quiescence and exacerbations. Any area of the oral mu- cytes, in the lamina propria are observed.
cosa may be affected by OLP, but the lesions often change 4. Colloid bodies (Civatte bodies) may be seen at
in clinical type and extension over years. These changes the epithelium-connective tissue interface. A
are clinically indistinguishable from oral leukoplakia. correlation between clinical, histopathologic, and
More than 50% show skin-associated lesions. The most immunofluorescence findings has to be made to arrive
common forms are reticular and erosive. at a diagnosis of lichen planus. Diagnosis of oral lichen
Reticular: The most characteristic clinical manifestation planus is direct in keratotic forms, and therefore biopsy
of the disease and the basis of clinical diagnosis are white should be obtained from these areas. But in ulcerative
papules and white striations that often form reticular forms of lichen planus histopathologic diagnosis is
patterns. They appear as striated, particularly reticular difficult to make.
form, linear papular lesions whose edges have fine Direct immunofluorescence shows linear deposits of
striae called the "Wickham striae." They form lace- fibrin in the basement membrane.
like interlacing, or annular forms, usually bilaterally Indirect immunofluorescence is negative.
symmetrical, that commonly involve the cheek and Immunohistochemical studies show higher T4/T8 ra-
tongue, but can occur anywhere. tio of lymphocytes in epithelium of lamina propria in
Erosive: These manifest as atrophic, erythematous, and lichenoid lesions.
ulcerated areas. Fine, white, radiating striations are
seen bordering these zones. These lesions are sensitive Differential Diagnosis
to hot, acidic, and spicy food. Atrophic and ulcerative • Lupus erythematosus
lesions are associated with moderate to severe pain, • Chronic ulcerative stomatitis
whereas papular, reticular lesions usually do not give • Cicatricial pemphigoid
rise to significant symptoms. • Pemphigus vulgaris
Gingival lichen planus comprises 7-10% of oral lichen • Linear IgA diseases
planus cases. Four patterns are seen: • Leukoplakia
• Electrogalvanic mucosal lesions
• Keratotic white lesions: Linear, papular, reticular, and • Linea alba buccalis
plaque-like • Leukoedema
• Erosive/ulcerative: Hemorrhagic areas that can be • Ectopic geographic tongue
focal or diffuse • Squamous cell carcinoma
• Vesicular /bullous: Fluid-filled lesions that rupture and • White sponge nevus
leave ulcerations on the gingiva
• Atrophic: Epithelial thinning that results in erythema Treatment
of gingiva (Fig. 23.1) Keratotic lesions of oral lichen planus are asymptom-
atic and do not require any treatment. Patients need to be
Histologic Features followed for any clinical change and erosive component
1. Microscopically, it shows hyperkeratosis, hydropic every 6-12 months.
degeneration of basal layer. The erosive, bullous, or ulcerative lesions of oral lichen
2. Rete ridges have "sawtooth configuration." planus can be treated with topical steroids such as 0.05%
fluocinonide ointment three times daily. A gingival tray

can also be used to deliver 0.05% clobetasol propionate
with 100,000 IU /mL of nystatin in Orabase. However, 3-5
minutes application of this mixture daily appears to be
effective in controlling erosive lichen planus.
Intralesional injections of triamcinolone acetonide,
10-20 mg, also prove to be helpful.
Short-term regimens of 40 mg of prednisone daily
for 5 days followed by 10-20 mg daily for an additional
2 weeks have been used in more severe cases. Because of
the potential side effects patients need to be monitored.
A promising therapeutic agent tacrolimus 0.1 % twice
daily is effective. Topical antifungal agents should be
included in the symptomatic oral lichen planus therapy.
Other modalities include retinoids, cyclosporine, hy- FIGURE 23.2 Cicatricial pemphigoid.
droxychloroquine, azathioprine, and cyclophosphamide.
Free gingival graft has also been used in a few cases. propria, leaving an intact basal layer. A mixed inflam-
matory infiltrate consisting of lymphocytes, plasma cells,
Mucous Membrane Pemphigoid neutrophils, and scarce eosinophils is observed in stroma.
Direct immunofluorescence reveals deposits of im-
Mucous membrane pemphigoid, also known as cica- munoglobulin G (IgG) and C3 restricted to the basement
tricial pemphigoid, is a group of putative autoimmune, membrane. Less than 25% of patients showed positive
chronic inflammatory, subepithelial blistering diseases indirect immunofluorescence finding.
predominantly affecting mucous membrane, with or
without clinically observable scarring. It predominantly Treatment
affects women in the fifth decade of life. Although rare, It can be controlled with topical corticosteroid appli-
it has been reported in young children. cation. If DG is present, custom-made trays can be used
Mucous membrane pemphigoid is characterized by for delivery of fluocinonide (0.05%) three times a day for
an immune reaction involving autoantibodies directed 6 months with clobetasol propionate. Oral hygiene must
against basement membrane zone, followed by comple- be improved, and regular professional cleaning should be
ment activation and subsequent leukocyte recruitment. emphasized. Irritation from dental prosthesis should
Proteolytic enzymes release and dissolve the basement be minimized. If ocular sites or skin is involved, then
membrane zone. Cicatricial pemphigoid involves the more potent medications such as systemic corticosteroids,
oral cavity conjunctiva and mucosa of the nose, vagina, azathioprine, sulfapyridine, or dapsone are used.
rectum, esophagus, and urethra. Some authors also advocated sulfonamides and tet-
The most common intraoral presentation is desquama- racyclines as the drug of choice for treatment of mucous
tive gingivitis. There might be areas of erythema, des- membrane pemphigoid. Connective tissue grafting can
quamation, ulceration, and vesiculation of the attached also be considered as treatment of choice to improve the
gingiva. Bullae have thick roof and rupture in 2-3 days to aesthetics and surface sensitivity.
leave ulcers that heal in up to 3 weeks. Other oral mucosal
sites involved are buccal mucosa, palate, alveolar ridge, Differential Diagnosis
and tongue. Rarely intact bulla is seen intraorally, the • Bullous pemphigoid
more common presentation being fibrin-covered super- • Linear IgA dermatosis
ficial erosions with irregular margins; oral lesions tend to • Bullous lichen planus
heal without scarring. • Erythema multiforme
The eyes can be affected in 25% of cases, with 15% • Dermatitis
developing permanent blindness as a result of subcon- • Epidermolysis bullosa acquisita
junctival scarring; symblepharon is also observed. Less • Herpetiformis.
commonly, strictures may form in the larynx, esophagus,
and genital mucosa with serious complications (Fig. 23.2).
Bullous Pemphigoid
Histology The term pemphigoid applies to a number of cutane-
Biopsy needs to be taken from areas with intact epithe- ous, immune-mediated, subepithelial bullous diseases
lium. Microscopically, there is subepithelial clefting with that are characterized by a separation of basement mem-
separation of the epithelium from the underlying lamina brane zone. Bullous pemphigoid is a chronic autoimmune
Treatment
Treatment is directed toward controlling signs and
symptoms. Localized lesions are treated with high-
efficacy topical steroids or tetracycline with or without
nicotinamide. Primary treatment is a moderate dose of
systemic prednisone.
Pemphigus Vulgaris
Pemphigus is one of the very few potentially fatal
mucocutaneous diseases characterized by intraepithe-
lial bullous formation. It is an uncommon condition and
usually affects females in their fourth to fifth decade of
FIGURE 23.3 Bullous pemphigoid (fluid-filled blisters and erosion). life. PV is the most important subtype to occur in the
mouth, and it can be the initial sign of presentation in
50% of cases. In pemphigus vulgaris, autoantibodies are
subepidermal bullous disease with tense bullae that rup- produced against pemphigus vulgaris antigens, which
ture and become flaccid. Developing bullae are subepithe- are glycoproteins of desmoglein family present on the
lial, unlike pemphis vulgaris where they are found to be keratinocytes. Damage to these cell-to-cell structures leads
intraepiteal. Bullous pemphigoid predominantly affects to epidermal and mucous membrane blisters.
the skin, but oral mucosa! involvement may occur.
Clinical Features
Clinical Features Oral pemphigus vulgaris presents as bullae that break
In 40% of cases desquamative or erosive oral lesions are down rapidly to leave persistent, irregular, ragged-edge,
seen. Any area of oral mucosa may be involved, but the painful erosions. Gingival involvement may manifest
main manifestation is desquamative lesion of the gingiva as desquamative gingivitis, though less commonly than
presenting intensely erythematous attached gingiva. The pemphigoid. Bullae on the gingiva rupture, leaving pain-
inflammatory changes, as always when not caused by ful eroded areas. Gentle pressure on the epithelium may
plaque, may extend over the entire gingival width and result in its separation; that is, Nikolsky sign is positive
even over the mucogingival junction. The rubbing of the and mastication becomes extremely painful for the pa-
gingiva may precipitate bullae formation. This denotes tient. Other sites that can be involved are esophagus,
positive Nikolsky sign and is caused by destroyed adhe- pharynx, larynx, and nasal and genital mucosa.
sion of epithelium to the connective tissue at the junction, Microscopically, PV lesions demonstrate a characteris-
resulting in exposed vessels inside the bullae. Usually, tic intraepithelial clefting above the basal cell layer giving
the eruption of bulla rapidly leaves fibrin-coated ulcers a characteristic tombstone appearance to the basal cell
(Fig. 23.3). also called suprabasilar split. Acantholysis is also seen.
Rounded acantholytic "Tzanck cell" is often visible in
Histologic Features the cleft.
The vesicles and bullae in this disease are subepider- Direct immunofluorescence demonstrates deposition
mal and nonspecific. of IgG and C3 intercellularly in a fishnet pattern. Circulat-
Direct immunofluorescence of normal and perilesional ing autoantibodies can usually be detected by immuno-
tissues reveals typical stratified epithelium-specific an- fluorescence, and such antibodies usually correspond to
tinuclear antibodies. It consists of deposits of IgG and disease activity and severity.
complement 3 with a speckled pattern mainly in the basal
epithelial cell layer. In addition, fibrin deposits are visual- Treatment
ized at the epithelium-connective tissue interface. PV is treated with systemic corticosteroids. Therapies
Indirect immunofluorescence also reveals the presence combine small doses of steroids and immunosuppres-
of circulating stratified epithelium-specific antinuclear sive agents such as azathioprine, cyclophosphamide,
antibodies in stratified epithelium. cyclosporine, dapsone, gold, and methotrexate. When
the patients respond well, the dose of systemic steroids
Differential Diagnosis can be reduced. Topical antifungal application may be
• Erosive lichen planus needed to eliminate iatrogenic candidiasis, which often
• Pemphigus vulgaris arises when topical steroids are used intraorally. Other
• Cicatricial pemphigoid treatment strategies include photoplasmapheresis and
• Linear IgA disease plasmapheresis. Rituximab is an anti-CD20 monoclonal
antibody aimed to remove desmoglein-reactive autoanti- Histopathology

bodies that is currently being evaluated as an adjunct to Lesions are similar to erosive lichen planus.
treat pemphigus vulgaris. Immunofiuorescence: Linear deposits of IgA are observed
Maintenance of oral hygiene is essential. In addition, at the epithelial-connective tissue interface.
fit and design of prosthesis should also be checked for
irritation that can lead to inflammation. Differential Diagnosis
• Erosive lichen planus
Chronic Ulcerative Stomatitis • Chronic ulcerative stomatitis
• Bullous pemphigoid
Chronic ulcerative stomatitis (CUS) clinically presents • Pemphigus vulgaris
with ulceration and has a predilection for women in the • Lupus erythematosus
fourth decade of life.
Treatment
Oral Lesions
Linear IgA disease can be treated with combination
The oral lesions consist of small blisters and erosions of sulfones and dapsone. Small doses of prednisone (10-
with surrounding erythema and pain mainly on the gin- 30 mg/ day) can be given. Tetracycline (2 g/ day) com-
giva and lateral border of the tongue. The hard palate may bined with nicotinamide (1.5 g/ day) has shown promis-
also present similar lesions. ing results. Recently, mycophenolate [1 g twice daily (bid)]
combined with prednisolone (30 mg daily) resulted in the
Histology
resolution of refractory ulcerations associated with LAD.
Microscopically, it resembles erosive lichen planus.
Direct immunofluorescent finding is typical stratified
epithelium with specific antinuclear antibodies. Lupus Erythematosus
Treatment Lupus erythematosus is a group of autoimmune con-
nective tissue disorders in which autoantibodies form
Mild cases of chronic ulcerative stomatitis are treated
to various cellular constituents including nucleus, cy-
with topical steroids (fluocinonide, clobetasol propio-
toplasm, and membrane. The etiology of lupus erythe-
nate); topical tetracycline may also be used. Recurrence
matosus is unknown, but deposits of antigen-antibody
is common. A dose of systemic corticosteroids may be
complexes appear to play a role in tissue damage. Lupus
used to achieve transient remission. Hydroxychloroquine
erythematosus includes two major clinical forms:
sulfate at a dosage of 200-400 mg/ day seems to be the
treatment of choice for long-lasting remission. The ini- • Systemic lupus erythematosus (SLE)
tial response to the chloroquine may end after several • Discoid lupus erythematosus (OLE)
months or years of treatment. In those cases a combined
therapeutic approach of corticosteroid and chloroquine Systemic Lupus Erythematosus
might be indicated. It occurs in third and fourth decades. It is characterized
by repeated remission and exacerbation, with common
sites being face, neck, upper arm, shoulders, and fingers.
Linear lgA Disease
The cutaneous lesions consist of erythematous patches
Linear IgA disease (LAD) is a rare subepithelial ve- on the face, which coalesce to form symmetrical pattern
siculobullous disease characterized by deposition of IgA over the cheek and across the bridge of the nose. Hence,
autoantibodies in a linear pattern along the basement this lesion has a butterfly distribution. This condition may
membrane zone. It clinically presents as a pruritic vesicu- involve a range of organ systems including kidney, heart,
lobullous rash usually during middle to late age, with and bone marrow.
more predilection in women. The face and perineum may The most common intraoral sites are buccal mucosa,
also be affected. Mucosal involvement including the oral lip, and palate. It begins as erythematous area, sometimes
mucosa ranges from 50 to 100% of the cases published. slightly elevated with hyperemia and edema. The lesions
have a greater tendency to bleed and form petechiae, sus-
Oral Lesions pected ulcerations surrounded by red halo. The intraoral
Oral lesions consist of vesicles, painful ulcerations or lesion is composed of central depressed, red atrophic
erosions, and erosive gingivitis/ cheilitis. The hard and areas surrounded by 2-4 mm elevated keratotic zone.
soft palates are more commonly affected. Tonsillar pillar,
buccal mucosa, tongue, and gingiva follow in frequency. Discoid Lupus Erythematosus
In addition, oral lesions of LAD and desquamative gin- It occurs in third and fourth decades. The most com-
givitis are also reported. mon sites are face, oral mucosa, chest, and extremities.
Cutaneous lesions are slightly elevated, red or purple Differential Diagnosis

macules that are often covered by gray or yellow ad- • Aphthous stomatitis
herent scales. The lesions increase in size by peripheral • Contact dermatitis or stomatitis
growth. Periphery of the lesion appears pink and red, • Acute necrotizing ulcerative gingivitis
while the center exhibits an atrophic scar. Butterfly dis- • Pemphigus
tribution on macular region and across the bridge of the • Dermatitis herpetiformis
nose is seen. • Bullous lichen planus
The most common intraoral sites are buccal mucosa, • Herpes zoster
tongue, palate, and vermillion border of the lip. It begins • Chicken pox
as erythematous area, slightly elevated but more often • Toxic epidermal necrolysis
depressed with induration and typically with white spots.
Occasionally, superficial painful ulceration may occur Treatment
with crusting or bleeding. There may be burning and Oral antihistamines are given to treat the lesions of
tenderness, which may be intermittent or disappears if erythema multiforme. Topical steroids, analgesics, lo-
the lesion becomes inactive. Central healing may result cal skin care, and soothing mouthwashes in the form of
in depression. chlorhexidine are also recommended.
Treatment
• Patients with SLE and OLE should be treated with ALLERGIC REACTIONS
antibiotic prophylaxis before dental treatment in or-
der to avoid bacteremia. Topical steroid application Several mechanisms may be involved in allergy, which
is needed for symptomatic lesions to be resolved. are exaggerated immune reactions. Oral mucosal reac-
For patients resistant to topical therapy, systemic tions are type I reactions, which are mediated by immuno-
antimalarial drugs may be used with good results. globulin E (IgE), or more often they are type IV mediated
• Cyclophosphamide and azathioprine are recommended by T cells.
for severe cases.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) are Dental Restorative Materials
advised for inflammatory conditions.
• Plasmapheresis alone, or with steroids, is also shown The oral mucosal reactions to restorative materials
to be useful. include reaction to mercury, nickel, gold, zinc, chromium,
• Recently, rituximab has been utilized and produced palladium, and acrylics.
dramatic long-term remissions.
Clinical Features
The lesions are reddish or whitish, sometimes ulcer-
Erythema Multiforme ated lesions. They clinically resemble oral lichen planus
or leukoplakia, but resolve after removal of the offending
Erythema multiforme is an acute self-limiting der- material.
matitis characterized by a distinctive clinical eruption In case of dental amalgam restoration, clinical mani-
manifested as the iris or target lesion. festation is confined to the area of contact with offending
The oral mucous membrane lesions are not usually a restorative material.
significant feature of the disease except for the pain and
discomfort. The hyperemic macules, papules, and vesicles Treatment
may become eroded or ulcerated and bleed profusely. The Elimination of the offending agent usually leads to
tongue, palate, buccal mucosa, and gingiva are commonly resolution of the lesion within a week.
affected sites.
Histopathology Reaction to Oral Hygiene Products, Chewing

Gum, and Food
Intracellular edema of the spinous layer of the epi-
thelium and edema of the superficial connective tissue Contact allergy rarely occurs after use of toothpaste
which may produce subepidermal vesicles are seen. Shk- and mouthwashes. The constituents responsible for al-
lar described a zone of severe liquefaction degeneration in lergic reactions are additives, preservatives, or flavoring
the upper layer of the epithelium, intraepithelial vesicle agents. Desquamative gingivitis has been documented
formation, and thinning with frequent absence of the due to calculus control agents such as pyrophosphates
basement membrane. and flavoring agents such as cinnamon compounds.
Clinical Features Drug Eruptions

Diffuse, fiery red, edematous gingivitis, sometimes Hypersensitivity to drugs sulfonamides, barbiturates,
with ulcerative lesions, may appear on labial, buccal, and and various antibiotics is seen. The drug acts as an allergen,
tongue mucosa. The lesions resolve after cessation of the sensitizes the tissues, and then causes allergic reactions.
use of the allergen containing the agent.
Stomatitis medicamentosa: Eruptions in the oral cavity
Allergic reaction attributable to food may manifest
due to sensitivity to drugs taken orally and parenterally
as both type I and type II reactions. The type I reaction
Stoma ti tis venenata/ contact stoma ti tis: Local reaction
occurs with severe swelling after intake of the food com-
due to medicament in the oral cavity, such as aspirin
ponent. Another food allergy results in gingivitis or gin-
and topical penicillin
givostomatitis. The lesions resolve after removal of the
allergen. Forms seen due to reactions to drugs are vesicular,
bullous, pigmented, and nonpigmented macular lesions.
Treatment
The treatment involves thorough clinical history and
removal of the causal agents. This leads to resolution of MISCELLANEOUS CONDITIONS:
the gingival lesions soon. MIMICKING DESQUAMATIVE
If removal of the offending medication is not possible, GINGIVITIS
topical corticosteroids and topical tacrolimus can be used
to treat the lesions. A group of heterogeneous conditions may masquerade
as desquamative gingivitis. Candidiasis, graft versus host
disease, Wegener granulomatosis, and foreign body gin-
Drug, Induced Mucocutaneous Disorder givitis can divert the attention of the clinician and result
A number of drugs show reverse effects in the oral in a diagnostic challenge.
mucosa. Common drugs that cause gingival hyperplasia Wegener granulomatosis is a disease of unknown eti-
are phenytoin, sodium valproate, cyclosporine, and dihy- ology which involves the vascular, renal, and respiratory
dropyridines. These lesions, to some extent, are plaque systems. Involvement of the oral cavity occurs with con-
dependent. Azathioprine is an antimetabolite used for siderable frequency in Wegener granulomatosis. In re-
immunosuppression in the treatment of autoimmune ported cases, involvement of the gingiva has been the most
and other types of diseases and to prevent rejection of common and characteristic manifestation and is termed
transplants. The mode of action is through inhibition "strawberry gingivitis." Brooke, in reviewing reported
of purine base synthesis, resulting in suppression of cases with oral lesions of this nature, has pointed out that
nucleic acid and protein synthesis. As a side effect this the gingival lesions may be ulcerations, friable granular
may cause oral ulcerations, which even include gingiva. lesions, or simply enlargements of the gingiva. The inflam-
Other drugs that cause oral stomatitis are antineoplastic matory process starts in the interdental papilla and spreads
drugs used in cancer therapy and methotrexate used in rapidly to the periodontal structure and leads to bone loss
leukemia. and tooth mobility. Israelson reported a case characterized
by hyperplastic gingivitis. Cyclophosphamide and pred-
Clinical Features nisone have provided a good prognosis for this condition.
Epithelial atrophy, superficial sloughing, intense ery- Rarely, candidiasis may be limited to the gingival tis-
thema, and ulceration are characteristic findings in the sue and may stimulate desquamative gingivitis. Foreign
oral mucosa of gingiva. The ulcerative lesions are fre- body gingivitis is clinically characterized by red or white
quently portals of entry for microorganisms via oral route, chronic lesions that may be painful and are reminiscent
which might lead to systemic complications. of desquamative gingivitis.
KEY POINTS
• Desquamative gingivitis is a clinical term to describe • The term chronic desquamative gingivitis was coined in
red, painful, glazed, and friable gingiva, which may 1932 to describe a peculiar condition characterized by
be a manifestation of some mucocutaneous conditions intense erythema, desquamation, and ulceration of the
such as lichen planus or the vesiculobullous disorders. free and attached gingiva (by Prinz).
KEY POINTS (cont'd)
• Approximately 75% of DG cases have a dermatologic • Cicatricial pemphigoid involves the oral cavity, conjunc-
origin and are mainly associated with MMP, LP, and, to tiva and mucosa of the nose, vagina, rectum, esophagus,
a lesser degree, PV. and urethra.
• To properly diagnose the condition responsible for des- • Lupus erythematosus includes two major clinical forms:
quamative gingivitis, clinical examination coupled with systemic lupus erythematosus and discoid lupus erythe-
a thorough medical history and routine histologic and matosus.
immunofluorescence studies is required. • Stomatitis medicamentosa refers to eruptions in the oral
• Gingival lichen planus comprises 10% of oral lichen cavity due to sensitivity to drugs taken orally and par-
planus cases. Four patterns are seen: keratotic, erosive/ enterally.
ulcerative, vesicular /bullous, and atrophic. • Stomatitis venenata/contact stomatitis refers to local reac-
• In lichen planus rete ridges have "sawtooth configuration caused due to medicament in the oral cavity, such
tion." as aspirin burn and topical penicillin.
QUESTIONS 2. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Clinical
Periodontology. 10th ed., 11th ed. Philadelphia: Saunders; 2006.
3. Nisengard RJ, Neiders M. Desquamative lesions of gingiva.
1. What is desquamative gingivitis? Enumerate the J Periodontol 1981;52:500-510.
lesions causing desquamative gingivitis. 4. Nisengard RJ. Periodontal implications: mucocutaneous disorders.
2. Discuss differential diagnosis of desquamative Ann Periodontol 1996;1:401-38.
gingivitis. 5. Rose LF, Mealey BL, Genco RJ, Cohen W. Periodontics: Medicine,
Surgery and Implants. 2nd ed. St. Louis: Mosby; 2004.
3. Classify desquamative gingivitis.
6. Scully C, Porter SR. The clinical spectrum of desquamative gingivitis.
4. Write a note on Nikolsky sign. Med Surg 1997;16:308.
5. Write a note on management of oral lichen planus. 7. Wary RD. A sign of mucocutaneous disorders - a review. Aust Dent
6. Explain "Tzanck test." J 2003;48:4.
8. Rajendran R, Shivapathasundaram B, Shafer W G, Shafer's Textbook
of Oral Pathology. 6th ed. New Delhi: Elsevier; 2009.
Suggested readings
Dentistry, 4th ed. Oxford: Munksgard 2003.
CHAPTER
24
Periodontal Diseases in Childhood
and Adolescents
CHAPTER OVERVIEW
Periodontal disease in adults is at least in part precipi- from primary to permanent, and the hormonal changes
tated by gingival inflammation in the formative years of associated with puberty bring about many changes in the
childhood and early adolescence. The exchange of dentition periodontium.
PERIODONTIUM OF DECIDUOUS • Eruptive stage

DENTITION • Posteruptive stage.
1. Shallower sulcus depth -2.1 mm. Preeruptive Stage

2. Interdental gingiva broad buccolingually and narrow Before eruption of the permanent tooth the gingiva re-
mesiodestally to confirm to morphology of deciduous veals a bulge that is firm and pink or blanched secondary
dentition. to the underlying permanent crown (Fig. 24.1).
3. Attached gingiva varies in width anteroposteriorly
being the widest in the incisor area, narrowing over Eruptive Stage
the cuspids and widening again over the posterior • This stage is associated with formation of gingival
molars. margin.
4. Free gingiva has fewer collagen bundles and is more • Marginal gingiva and sulcus develop as the crown
easily retracted away from deciduous tooth surface. penetrates the oral mucosa.
5. Radiographically, lamina dura is prominent with a • In the course of eruption, the gingival margin is usually
wider periodontal space. edematous, rounded, and slightly reddened.
6. Marrow spaces of bone are larger and crests of • During the period of mixed dentition, it is normal for
interdental bony septa are flat. marginal gingiva around the permanent teeth to be
7. Bony crests are within 1-2 mm of cementoenamel quite prominent, particularly in the maxillary anterior
junction. region. At this stage in tooth eruption, the gingiva is
still attached to the crown, and appears prominent
Physiologic Gingival Changes Associated with when superimposed on the bulk of the underlying
Tooth Eruption enamel (Fig. 24.2).
Gingival changes that occur during the eruption of Posteruptive Stage

tooth can be studied by dividing the eruption into three
The gingiva reduces in bulk and becomes thinner,
stages, as follows:
tighter, and more firmly attached around the cervical
• Preemptive stage portion of the tooth (Fig. 24.3).
CHA PTER 24 PERIO DONTAL DISEA SES IN CHILDHOO D AND ADOLESCENTS 199
Health
Plaque
Gingivitis
Drug therapy Stress, smoking, and
Hormones other factors
Puberty gingivitis Gingival overgrowth Necrotizing ulcerative

gingivitis and periodontitis
Plaque Host susceptibility
Periodontitis
Systemic Slow Rapid

diseases progression progression
Systemic disease Incipient (adult) Early onset

forms of periodontitis periodontitis periodontitis
t
Prepubertal Localized Generalized Incidental
early onset early onset early onset
periodontitis pe riodontitis periodontitis
Localized Generalized
prepubertal prepubertal
periodontitis periodontitis
FIGURE 24.1 Periodontal diseases that can occur in children.
FIGURE 24.2 Gingival changes seen in the preemptive stage. FIGURE 24.3 Gingival changes seen in the eruptive stage.
GINGIVITIS 4. Changes in surface texture of the gingiva

a. Loss of surface stippling is an early sign of gingivitis.
• It is the inflammatory involvement of gingival tissue. b. Chronic inflammation
• Microscopically, it is characterized by the presence of c. The surface is smooth, shiny, or firm, and nodular
inflammatory exudate and edema and destruction depending on whether changes are exudative or
of collagenous gingival fibers. fibrotic.
• Ulcerations of the epithelium are also seen.
Etiology of Gingival Diseases
Stages of Gingivitis 1. Local irritating factors
Stage I: Initial Lesion a. Bacterial plaque
1. Time period is 2-4 days.
b. Predisposing factors like materia alba, food debris,
2. Vascular dilatation and vasculitis is seen. malalignment of teeth, dental calculus, etc.
2. Local functioning factors
3. Junctional and sulcular epithelium are seen infiltrated
a. Malocclusion
by polymorphonuclear cells.
4. It is associated with mild change in color. b. Habits: Mouth breathing, tongue thrusting
c. Eruption of teeth
Stage II: Early Lesion 3. Systemic factors
a. Puberty
2. There is increased vascular proliferation. b. Vitamin or protein deficiency
c. Drugs and chemicals
3. Junctional and sulcular epithelium is seen infiltrated
by polymorphonuclear cells, rete peg formation, and d. Pregnancy
e. Hereditary
atrophic areas.
f. Metabolic disorders
4. Lymphocytes are predominant.
5. There is loss of collagen.
g. Hematologic disorder
h. Viral, bacterial, and fungal infections
6. Clinical findings include erythema and bleeding on
probing.
Stage III: Established Lesion TYPES OF GINGIVAL DISEASES

IN CHILDHOOD
2. There is increased vascular proliferation and blood
stasis. Eruption Gingivitis
3. Changes seen in the junctional and sulcular epithelium • It is seen during the eruption of teeth and subsides
are more severe compared with Stage II. soon after eruption.
4. Plasma cells are predominant. • Greatest incidence is 6-7 years when permanent teeth
5. There is severe loss of collagen. begin to erupt.
6. Clinical findings include changes in color, size, and • Reason for this is the lack of protection to the gingiva
texture. from the coronal contour of the tooth.
• It may be painful and may develop into pericoronitis
Stage IV: Advanced Lesion or pericoronal abscess.
1. The lesion extends into alveolar bone. • Management includes improving oral hygiene. Some
2. It is characterized by periodontal breakdown. severe cases may require antibiotic therapy.
Clinical Features of Gingivitis Gingivitis Associated with Poor Oral Hygiene

1. Gingival bleeding • Oral hygiene and gingivitis are directly related.
Two earliest symptoms of gingival inflammation are: • Adequate oral hygiene practice, leading to thorough
a. Increased gingival fluid production rate plaque removal, and eating raw fiber vegetables and
b. Bleeding from gingival sulcus on probing fruits have beneficial effect on reducing gingivitis.
2. Change in the color of gingiva • It can be grouped as early, moderate, and advanced
a. Normal color is coral pink. Inflamed tissue is red or gingivitis.
bluish red. • Early gingivitis is quickly reversible and treated with
3. Changes in consistency of gingiva good tooth brushing and flossing.
a. In chronic inflammation, both destructive (edematous) • Moderate and severe gingivitis requires more elaborate
and reparative (fibrotic) changes coexist. measures.
Gingivitis Associated with HSV I Infection interproximal necrosis and ulceration and the rapid
onset of gingival pain.
• It is caused by the herpes simplex virus (HSV). • Viral infections (including HIV), malnutrition,
• Herpetic stomatitis is a common oral disease, which emotional stress, lack of sleep, and a variety of systemic
develops in both children and young adults. diseases are the common predisposing factors
• It rarely occurs before the age of 6 months, apparently • Treatment involves mechanical debridement, oral
because of the presence of circulating antibodies in the hygiene instruction, and careful follow-up.
infant, derived from the mother. The disease occurring • If the patient is febrile, antibiotics may be an important
in children is usually the primary attack. adjunct to therapy. Metronidazole and penicillin have
• It is characterized by the development of fever, been suggested as drugs of choice.
irritability, headache, pain upon swallowing, and
regional lymphadenopathy.
• Within a few days, the mouth becomes painful and the Gingivitis Associated with Acute Bacterial
gingiva intensely inflamed. Infection
• The lips, tongue, buccal mucosa, palate, pharynx, and
• It is caused by streptococci group of bacteria.
tonsils may also be involved.
• The gingiva is painful and bleeds easily.
• Shortly yellowish, fluid-filled vesicles develop. These
• Papilla is enlarged with associated gingival abscess.
rupture and form shallow, ragged, extremely painful
Treatment includes broad-spectrum antibiotics,
ulcers covered by a gray membrane and surrounded
improvement of oral hygiene, and chlorhexidine
by an erythematous halo.
mouthwash.
• They heal spontaneously within 7-14 days and leave
no scar.
• Treatment is symptomatic such as application of topical Chronic N onspecifi.c Gingivitis
anesthetic agents on the ulcers, soft diet, and adequate
• It has no specific etiology. May be triggered by
fluids.
hormonal imbalance seen in the preteenage and
teenage children.
Gingivitis Associated with Aphthous Stomatitis • It may be localized to the anterior region or may be
more generalized.
• It can be triggered due to any stress, gastrointestinal • It is rarely painful, but persists for a longer period of time.
disturbance, nutritional deficiency, hormonal • Since the cause is nonspecific, the treatment is limited to
imbalance, infection, allergy, etc. maintaining the oral hygiene and regular professional
• Of the three types of apthous, minor aphthae are prophylaxis.
common.
• Prodromal phase of paresthesia at the site of ulceration
is observed. The ulcers appear in crops of two or three Puberty Gingivitis
and are less than 10 mm in diameter. They are painful • It occurs in the prepubertal and pubertal periods.
and discrete or confluent. • Gingival inflammation is confined to the anterior
• It persists for about 12 days and heals with no scar segment and may be limited to single arch only.
formation. • Gingiva on the lingual aspect is relatively uninvolved
• Treatment is symptomatic. Chlorhexidine, nystatin, or concerned with maintenance of adequate oral hygiene,
tetracycline can be prescribed if they are infected. removal of local irritants, and restoration of caries.
Acute N ecrotizing Ulcerative Gingivitis Hereditary Fibromatosis Gingival Enlargement

• Acute necrotizing ulcerative gingivitis (ANUG) is • It is characterized by slow, progressive, benign
caused by Borrelia vincentii and spirochetes. enlargement of the gingiva.
• Severe ulcerating gingivitis involving the interproximal • The surface is normal appearing.
papillae, covered by a psuedomembrane, is seen. • It appears as soon as the deciduous teeth erupt in the
• It is associated with fetid odor. oral cavity and cover the teeth completely.
• Recovery promptly occurs within 36 h after penicillin • They are fibrous tending to displace the teeth and are
therapy and application of hydrogen peroxide nonpainful.
• This can progress into necrotising periodontal disease • They regress only if the teeth are extracted.
(NPD) if left untreated • Surgical excision is the treatment of choice but may
• The two most significant findings used in the diagnosis recur to the original condition within a period of few
of necrotising periodontal diseases are the presence of years.
Drug- Induced Hyperplasia AGGRESSIVE PERIODONTITIS

• Phenytoin, an anticonvulsant drug, is the commonly
• Aggressive periodontitis may be more common in
seen to be the cause of hyperplasia of the gingiva.
children and adolescents, whereas chronic periodontitis
• Other drugs that induce hyperplasia are cyclosporine
is more common in adults.
and nifedipine.
• The important features of aggressive periodontitis
• It appears as early as 2-3 weeks after initiation of the
include a history of rapid attachment and bone loss
phenytoin therapy and peaks at 18-24 months.
with familial aggregation.
• They cause painless enlargement of the gingiva
• The other features include phagocyte abnormalities and
especially on the interproximal aspect.
a hyperresponsive macrophage phenotype. Aggressive
• Buccal and anterior segment are more often affected
periodontitis can be localized or generalized.
than the lingual and posterior segment.
• Localized aggressive periodontitis (LAgP): These
• Gingiva appears pink and firm unless infected.
patients have interproximal attachment loss on at
• They normally do not bleed readily.
least two permanent first molars and incisors, with
• There is formation of pseudopockets.
attachment loss on no more than two teeth other than
• There are associated problems during mastication,
first molars and incisors.
speech, etc.
• Generalized aggressive periodontitis (GAgP): These
• Management includes adequate oral hygiene
patients exhibit generalized interproximal attachment
maintenance, change of drug or dosage, and surgical
loss including at least three teeth that are not first
excision.
molars and incisors.
• In young individuals, the onset of these diseases is
often circumpubertal.
Scorbutic Gingivitis
• It is associated with vitamin C deficiency.
• Involvement is limited to marginal tissue and papillae. Localized Aggressive Periodontitis
• It is associated with severe pain and spontaneous • It is seen in otherwise healthy children.
hemorrhage. • It is characterized by rapid and severe loss of alveolar
• Management includes replacement of ascorbic acid and bone around more than one permanent tooth involving
oral hygiene maintenance. the first molars and incisors.
• It appears self-limiting.
• No tissue inflammation is seen, and little plaque or
calculus is present.
TYPES OF PERIODONTAL DISEASES
• Bone loss is three to four times faster than adult
periodontitis.
Prepubertal Periodontitis • It is caused by Actinobacillus actinomyceteomcomitans
• Normally it is generalized, but when it occurs in and bacteroid-like organisms.
deciduous dentition, it is localized. • Management includes early diagnosis, dental curettage,
• Loss of attachment and alveolar bone loss are seen in prophylaxis, removal of severely mobile teeth, and
deciduous dentition in the molar and incisor regions. broad-spectrum antibiotics.
• Plaque accumulation is minimum. Gingival
inflammation may be present.
Generalized Aggressive Periodontitis
• It is seen soon after the eruption of the primary teeth.
Premature loss of teeth is common and all teeth may 1. It is seen at around puberty.
be lost by 3 years of age. 2. It affects the entire dentition.
• Actinobacillus actinomyceteomcomitans, bacteroids, and 3. It is caused by nonmotile, facultative, anaerobic, gram-
Fusobacterium are found in the gingival pocket. negative rod Porphyromonas gingivalis.
• Management includes early diagnosis, dental curettage, 4. Management includes early diagnosis, dental curettage,
prophylaxis, removal of severely mobile teeth, and prophylaxis, removal of severely mobile teeth and
broad-spectrum antibiotics. broad-spectrum antibiotics.
KEY POINTS
• Various physiologic changes are associated with tooth phenytoin-induced gingival overgrowth, and scorbutic
eruption. gingivitis.
• The different types of gingival lesions seen in children • Periodontal lesions seen in children are prepubertal
are eruption gingivitis, gingivitis associated with poor periodontitis, chronic periodontitis, aggressive peri-
oral hygiene, acute gingival inflammation, chronic odontitis, and periodontitis as a manifestation of sys-
nonspecific gingivitis, puberty gingivitis, fibromatosis, temic diseases.
QUESTIONS 2. Loe H, Anerud A, Bousen H. The natural history of periodontal

disease in man: prevalence, severity and extent of gingival recession.
J Periodontol 1992;63:489.
1. Define eruption gingivitis. 3. Mattson L. Development of gingivitis in preschool children and
2. Enumerate various periodontal diseases in childhood. young adults: a comparative experimental study. J Clin Periodontal
3. Define localized aggressive periodontitis. 1978;5:24.
4. Molder T, Wondimu B. Periodontal disease in children and
adolescents. Dent Clin North Am 2000;44:633.
Suggested readings 5. Oh TJ, Eber R, Wang HL. Periodontal disease in the child and
adolescents. J Clin Periodontal 2002;29:400.
1. Albandar JM, Buischi AP, Mayer MP, Axellson P. Long term effect of
two preventive programs on the incidence of plaque and gingivitis
in children. J Periodontol 1994;65:605.
CHAPTER
25
Periodontal Pocket
CHAPTER OVERVIEW
A periodontal pocket is defined as a pathologically deepened gingival sulcus and is one of the important clinical
features of periodontal disease.
CLASSIFICATION 3. Complex: It is a spiral pocket that originates on one tooth

surface and twists around the tooth to involve one or
Pockets are classified according to morphology and more additional surfaces. Their only communication
their relationship to adjacent structures as follows: with the gingival margin is at the surface where the
pocket originates. It is more commonly observed in
1. Gingival pocket (relative/ false) (Fig. 25.1)
furcation areas (Fig. 25.3A-C).
It is formed by gingival enlargement without destruction
of the supporting tissues of the periodontium. There is
no apical proliferation of the epithelial attachment. CLINICAL FEATURES
2. Periodontal pocket (absolute/true)
Signs
It is formed by pathologic deepening of the gingival
sulcus due to destruction of the supporting tissues • Enlarged bluish-red marginal gingiva with rolled-out
of the periodontium and apical proliferation of the edge separated from the tooth surface
epithelial attachment. • Reddish-blue vertical zone from the gingival margin
to attached gingiva/ alveolar mucosa
True pockets are further subclassified into the follow-
• Break in faciolingual continuity of interdental gingiva
ing categories (Fig. 25.2A, B):
• Shiny discolored puffy gingiva
• Suprabony pocket (supracrestal/ supra-alveolar) • Gingival bleeding
• Infrabony pocket (intrabony, subcrestal) • Purulent exudate from the gingival margin in response
to digital pressure
The differences between suprabony and infrabony
• Looseness, extrusion, migration of teeth
pocket are depicted in Table 25.1.
• Development of diastema where none had previously
Periodontal pockets can also be classified according to
existed.
the number of surfaces involved as follows:
1. Simple: It involves only one tooth surface (Fig. 25.3).
Symptoms
2. Compound: Two or more tooth surfaces are involved.
The base of the pocket is in direct communication with • Localized pain or sensation of pressure after eating,
the gingival margin along each of the involved surfaces which gradually diminishes
(Fig. 25.3). • Foul taste in localized areas
CHA PTER 25 PERIO DONTAL PO CKET 205
(A) (B)
FIGURE 25.1 Gingival pocket.
FIGURE 25.2 (A) Suprabony pocket; (B) infrabony pocket.
TABLE 25.1 Differences Between Suprabony and lnfrabony Pockets
Suprabony pockets Infrabony pockets

1. Base of the pocket is coronal to the crest of the alveolar bone Base of the pocket is apical to the crest of the alveolar bone;
hence, bone is adjacent to the soft tissue wall
2. Bone destructive pattern is horizontal Vertical/ angular pattern of bone destruction
3. Interproximally, the transseptal fibers are restored horizontally Interproximally, the transseptal fibers are restored obliquely,
during progressive periodontal disease in the space between the from the cementum beneath the base of the pocket over the crest
base of the pocket and alveolar bone of the cementum of adjacent tooth
4. On the facial and lingual surfaces, the periodontal ligament On the facial and lingual surfaces the periodontal fibers beneath
fibers beneath the pocket follow their normal course between the the pocket follow the angular pattern of the adjacent bone
tooth and the bone
(A) (B) (C)
FIGURE 25.3 (A) Simple pocket; (B) compound pocket; (C) complex pocket.
• Tendency to suck material in the interdental areas epithelium as a result of rapidly proliferating bacteria,
• Radiating pain deep in the bone bacterial enzymes, and the relative volume of PMNs
• Gnawing feeling or itching in the gingiva and urge (60% or more of the junctional epithelium). Thus,
to dig a pointed instrument into the gums and relief the base of the gingival sulcus shifts apically and
obtained from resultant bleeding the sulcular epithelium is replaced by the pocket
• Food sticks in between the teeth or teeth feel loose epithelium.
• Sensitivity to heat and cold
The transformation of the gingival sulcus into a peri-
• Toothache in absence of caries.
odontal pocket creates an area where plaque removal
becomes impossible, and the following feedback mecha-
PATHOGENESIS nism is established.
Periodontal pockets are caused by microorganisms and

their products, which produce pathologic changes that Plaque
lead to deepening of the gingival sulcus. The deepening
Gingival inflammation
may occur by: More
• Movement of the gingival margin in the direction of
the crown (produces a gingival pocket)
plaque formation
j
• Migration of the junctional epithelium apically and its Pocket formation
separation from the tooth surface
• A combination of the aforementioned processes.
Changes involved in the transition from the normal Thus with continued inflammation, crest of the gin-
gingival sulcus to the pathologic pocket are associated gival margin extends coronally and the junctional epi-
with increased number of spirochetes and motile rods. thelium continues to migrate apically along the root and
separates from it.
• Inflammatory changes are observed in the connective
tissue wall of the sulcus. Several zones have been
described in the process of destruction of connective HISTOPATHOLOGY
tissue attachment.
• Apical to the junctional epithelium, an area of de- • The connective tissue is edematous and densely
stroyed collagen fibers develops and is occupied by infiltrated with plasma cells (approximately 80%) and
inflammatory cells and edema. Immediately apical to lymphocytes and a scattering of PMNs.
this is a zone of partial destruction and then an area of • Blood vessels are increased in number, dilated,
normal attachment. and engorged; single or multiple necrotic foci are
• Two hypotheses have been proposed in regards to the occasionally present.
mechanism of collagen loss: • Connective tissue also shows proliferation of the
Collagenases and other lysosomal enzymes from endothelial cells with newly formed capillaries,
PMNLs and macrophages become extracellular and fibroblasts, and collagen fibers.
destroy collagen. • The junctional epithelium at the base of the pocket
Fibroblasts phagocytize collagen fibers by extending is usually much shorter than that of a normal sulcus.
cytoplasmic process to the ligament interface and by The coronoapical length of the junctional epithelium
resorbing the inserted collagen fibrils and fibrils of is 50-100 µm.
the cementum matrix. • The most severe degenerative changes in the peri-
• As a consequence of the loss of collagen, the apical odontal pocket occur along the lateral wall. Epithelial
portion of the junctional epithelium proliferates along buds or interlacing cords of epithelial cells project from
the root, extending like projections 2-3 cells in thick- the lateral wall into the adjacent inflamed connective
ness. tissue and frequently extend farther apically than the
• Extension of junctional epithelium along the root junctional epithelium.
requires the presence of healthy epithelial cells. • Progressive degeneration and necrosis of the epithelium
Marked degeneration or necrosis of the junctional leads to ulceration of the lateral wall, exposure of the
epithelium retards rather than accelerates pocket underlying marked inflamed connective tissue, and
formation. suppuration.
• The coronal portion of the junctional epithelium • The severity of the degenerative changes is not
detaches from the root as the apical portion migrates. necessarily related to pocket depth. Ulceration of
This is due to loss of cohesiveness of the junctional the lateral wall may occur in shallow pockets, and
deep pockets are occasionally observed in which the 6. Area of ulceration: It is occasionally seen surrounded by
lateral epithelium is relatively intact and shows slight areas of hemorrhage. The bottom of the ulcer shows
degeneration. exposed collagen fibers and various connective tissue
• The epithelium at the gingival crest of a periodontal cells.
pocket is generally intact and thickened with prominent 7. Areas of hemorrhage: Numerous erythrocytes are present.
rete pegs.
• Filaments, rods, and coccoid organisms with predomi-
nant gram-negative cell walls have been found in
Periodontal Pockets as Healing Lesion
the intercellular space initially under exfoliating epi- The condition of the soft-tissue wall of the periodontal
thelial cells, but they are also found between deeper pocket results from the interplay of destructive and con-
epithelial cells and accumulating on the basement structive tissue changes. The destructive changes are char-
lamina. acterized by the associated degenerative changes initiated
• Some bacteria may traverse the basement lamina and by plaque bacteria. The reparative changes consist of the
invade the subepithelial connective tissue. formation of blood vessels in an effort to repair the tissue
damage caused by inflammation. Complete healing does
not occur because of persistence of local irritants, which
MICROTOPOGRAPHY OF THE GINGIVAL continue to stimulate fluid and cellular exudates, which in
WALL OF THE POCKET turn causes degeneration of the new tissue elements
formed in the continuous effort at repair. The balance
The following areas have been noted in a scanning elec- between destructive and reparative changes determines
tron microscope (SEM) study to analyze the salient fea- clinical features such as color, consistency, and surface
tures of the soft tissue wall in deep periodontal pockets: texture of the pocket wall (Table 25.2).
1. Area of relative quiescence: A relatively flat surface with
minor depressions and mounds and occasional shed-
Pocket Contents
ding of cells.
2. Areas of bacterial accumulation: Appear as depressions Periodontal pockets contain debris consisting princi-
on the epithelial surfaces, with abundant debris pally of microorganisms and their products (enzymes,
and bacterial clumps penetrating into the enlarged endotoxins, and other metabolic products), gingival fluid,
intercellular spaces. Cocci, rods, and filaments with food remnants, salivary mucin, desquamated epithelial
few spirochetes were the main bacteria and appeared cells, and leukocytes.
covered by a loose, intercellular, fibrillar substance.
3. Areas of emergence of leukocytes: Leukocytes appear in the
Significance of Pus Formation
pocket wall through holes located in the intercellular
spaces. Pus is a common feature of periodontal disease but it
4. Areas of leukocyte-bacterial interaction: Numerous leu- is only a secondary sign. The presence of pus or the ease
kocytes are present and covered with bacteria in an with which it can be expressed from the pocket merely re-
apparent process of phagocytosis. flects the nature of the inflammatory changes in the pocket
5. Area of intense epithelial desquamation: It shows wall. It is not an indication of the depth of the pocket or
semiattached and folded epithelial squames with one the severity of the destruction of the supporting tissues.
end usually attached to the pocket wall surface and the Extensive pus formation may occur in shallow pockets,
other end free toward the pocket space. whereas deep pockets may exhibit little or no pus.
TABLE 25.2 Correlations of Clinical Features and Histopathologic Features
Clinical features Histopathology features

1 Bluish-red color discoloration Circulatory stagnation
Flaccidity Destruction of the connective tissue fibers
Smooth shiny surface Edema and atrophy of the epithelium
Pitting on pressure Edema and degeneration of the connective tissue
2 Pink and firm gingival soft tissue wall Fibrotic changes predominate over exudation and degeneration
3 Bleeding elicited by gentle probing Increased vascularity, engorgement of blood vessels, and thinning and
ulceration of the sulcular epithelium
4 Inner aspect of the pocket wall is painful on probing Ulceration of the inner aspect of the pocket wall
5 Pus expressed on digital pressure Suppurative inflammation of the inner wall of the pocket
Root Surface Wall Changes

The root surface wall of the periodontal pocket often Calculus
undergoes changes that are significant because they may
perpetuate the periodontal infection, cause pain, and
complicate periodontal treatment. Structural, chemical,
and cytotoxic changes occur in the root cementum. Attached
plaque
Structural Changes
1. Presence of pathologic granules: They represent areas of
collagen degeneration or areas where collagen fibrils Unattached
plaque
have not been fully mineralized.
2. Increased mineralization: It is a result of an exchange,
on exposure to the oral cavity, of minerals and organic Junctional
components at the cementum-saliva interface. epithelium
3. Areas of demineralization: It is commonly related to root Partially lysed
CT fibers
caries.
Exposure of oral fluid and bacterial plaque results in
proteolysis of the embedded remnants of the Sharpey
fibers; the cementum may be softened and may undergo
Intact CT fibers
fragmentation and cavitation.
Active root caries appear as well-defined, yellowish or
light brown area, are frequently covered by plaque, and
FIGURE 25.4 Morphology of the tooth wall.
have a softened or leathery consistency on probing. Inac-
tive lesions are well-defined darker lesions with a smooth
surface and a harder consistency on probing. Involvement 5. Zone of semidestroyed connective tissue fibers apical to the
of the cementum is followed by bacterial penetration of JE: Zones 3, 4, and 5 compose the so-called plaque-free
the dentinal tubules resulting in destruction of dentin. zone seen in extracted teeth.
Chemical Changes
The mineral content of the exposed cementum is in- Relation of Loss of Attachment and Bone
creased, e.g., calcium, magnesium, phosphorus, and fluo- Loss to Pocket Depth
ride. Microhardness, however, remains unchanged.
Pocket formation causes loss of attachment and denu-
Cytotoxic Changes dation of the root surface. The severity of attachment loss
Bacterial endotoxins have been demonstrated in the is generally not always correlated to pocket depth.
cementum of untreated periodontally involved teeth. This is because the degree of attachment loss depends
Thus cementum may act to perpetuate the destructive on the location of the base of the pocket on the root sur-
effects of periodontal disease, by acting as a reservoir for face, whereas pocket depth is the distance from the base
potentially destructive products. of the pocket and the crest of the gingival margin.
Pockets of same depth may be associated with different
degrees of attachment loss (Fig. 25.5), and pockets of
MORPHOLOGY OF THE TOOTH WALL different depths may be associated with the same amount
of attachment loss as observed in Fig. 25.6. Severity of bone
The following zones can be seen at the bottom of a loss is generally correlated with pocket depth, but not al-
periodontal pocket (Fig. 25.4): ways extensive bone loss may be associated with shallow
1. Cementum covered by calculus: It exhibits all the afore- pockets and slight bone loss may occur in deep pockets.
mentioned root surface changes.
2. Attached plaque: It covers calculus and extends apically
Concept of Site Specificity
from it to a variable degree, probably 100-500 µm.
3. Zone of unattached plaque: It surrounds attached plaque The microflora, the anatomy, and the local immune
and extends apically. response at one site around one tooth may be totally
4. Zone of attachment of functional epithelium to the tooth: different from those at an adjacent site of the same tooth.
In normal sulci, its extension is more than 500 µm but This results in periodontitis at some sites next to sites with
is usually reduced in periodontal pockets to less than little or no periodontal destruction, which is referred to
100 µm. as the concept of site specificity of periodontal disease.
FIGURE 25.5 Variable attachment loss with similar levels of probing depth.
Effect of Periodotal Pocket on the Dental Pulp

Accessory /lateral canals and the apical foramen may
serve as a portal for the spread of infection from the
periodontal pocket to the dental pulp. These changes
may cause painful symptoms in the dental pulp. Al-
though inflammatory changes have been reported adja-
cent to accessory canals exposed to periodontal pockets,
periodontitis rarely produces significant changes in the
dental pulp. Severe breakdown of the pulp is usually
seen only when the periodontal pocket extends to the
FIGURE 25.6 Variable pocket depths with similar levels of tooth apex.
attachment loss.
KEY POINTS
• A periodontal pocket is defined as a pathologically deep- • Structural, chemical, and cytotoxic changes occur in the
ened gingival sulcus and is one of the important clinical root cementum exposed to pocket environment.
features of periodontal disease. • Accessory /lateral canals and the apical foramen may
• True pockets are further subclassified into suprabony serve as a portal for the spread of infection from the
pocket (supracrestal/ supra-alveolar) and infrabony pocket periodontal pocket to the dental pulp.
(intrabony, subcrestal). • Periodontal pockets contain debris consisting principally
Simple: It involves only one tooth surface. of microorganisms and their products (enzymes, endo-
Compound: Two or more tooth surfaces are involved. toxins, and other metabolic products), gingival fluid,
Complex: It is a spiral pocket that originates on one food remnants, salivary mucin, desquamated epithelial
tooth surface and twists around the tooth to involve cells, and leukocytes.
one or more additional surfaces.

1. Adriaens PA, De Boever JA. Ultra structural study of bacterial
1. Define and classify periodontal pocket. invasion in roots of periodontally diseased, caries free human teeth.
2. Describe in brief the pathogenesis of pocket formation. J Dent Res 1986;65:770.
3. Describe the microtopography of the soft tissue wall. 2. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant
4. Explain in detail the root surface wall changes in a Dentistry. 5th ed. Blackwell Munksgaard Publication; 2008.
3. Muller-Glauser W, Schroeder HE. The pocket epithelium: a light and
periodontal pocket. electron microscopic study. J Periodontol 1982;53:133.
5. Write a short note on periodontal disease activity. 4. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's
6. What are the differences between suprabony and Clinical Periodontology. 10th ed. Philadelphia: Saunders; 2006.
infrabony pockets? 5. Page RC, Schroeder HH. Structure and pathogenesis. In: Schluger
S, Youdelis R, Page R, editors. Periodontal Disease. Philadelphia: Lea
and Febiger; 1977.
6. Takada T, Donath K. The mechanism of pocket formation; a light
microscopic study of undecalcified human material. J Periodontal
1988;59:215.
CHAPTER
26
Bone Loss in Periodontal Disease
CHAPTER OVERVIEW
Untreated cases of chronic generalized periodontitis disease. The different architectures created due to the loss
leads to the loss of tooth due apical spread of infection. of osseous tissue result in the development of the ecologi-
This results when the alveolar bone support is lost and cal niches that are site-specific risk factors of periodontal
it is an important characteristic feature of destructive disease progression. The amount and severity of loss of
periodontal disease. Loss of alveolar bone support is alveolar bone is assessed by clinical and radiographic
one of the characteristic signs of destructive periodontal evaluation.
ETIOLOGY OF BONE DESTRUCTION The destructive periods result in loss of collagen and
alveolar bone with deepening of the periodontal pocket.
Pathologic microorganisms elicit a host response that Following changes are associated with periods of activ-
leads to periodontal hard tissue destruction, i.e., the alveo- ity or destruction:
lar bone and cementum. The immunoinflammatory host
1. Bursts of destructive activity are associated with
response along with the acquired and genetic risk factors
subgingival ulceration and an acute inflammatory
modifies the probable development as well as progression
reaction, resulting in rapid loss of alveolar bone.
of periodontal disease.
2. Bursts of destructive activity coincide with the
Bone destruction in periodontal disease is caused by
conversion of a predominately I-lymphocyte lesion
local and systemic factors.
to one with a predominance of B-lymphocyte-plasma
Local factors fall into the following groups:
cell infiltrated lesion.
• That cause gingival inflammation 3. Periods of exacerbation are associated with an increase
• That cause trauma from occlusion of the loose, unattached, motile, gram-negative,
anaerobic pocket flora, and periods of' remission
Reduction in the height of alveolar bone is caused
coincide with the formation of a dense, unattached,
by extension of gingival inflammation, whereas trauma
nonmotile gram-positive flora with a tendency to
from occlusion (TFO) causes bone loss lateral to the root
mineralize.
surface.
4. Tissue invasion by one or several bacterial species
is followed by an advanced local host defense that
Bone Destruction Caused by Extension controls the attack.
of Gingival Inflammation
• The uninhibited progression of inflammation from the
HISTOPATHOLOGY
gingival margin into the supporting tissues leads to
bone destruction.
• Gingival inflammation extends along the fiber bundles
• The transition from gingivitis to periodontitis is
and follows the course of the blood vessels.
associated with periods of destruction/ activity/
• Interproximally, inflammation spreads to the loose
Exacerbation
connective tissue around the blood vessels, through the
Periodontal destruction occurs in an episodic, inter- fibers, and then into the bone through vessel channels
mittent fashion, with periods of inactivity or quiescence. that perforate the crest, side, or at the angle of the
interdental septum entering the bone. Less frequently,

it spreads directly into periodontal ligament and then Periodontal
into interproximal bone. pathogens
(LPS)
• Facially and lingually, inflammation from the gingiva
spreads along the outer periosteal surface of the bone
and penetrates into marrow spaces by vessel channels
in the outer cortex.
• After inflammation reaches the bone by extension from
gingiva, it spreads into marrow spaces and replaces the
marrow with a leukocytic and fluid exudate.
• Multinuclear osteoclasts and mononuclear phagocytes
increase in number, bringing about bone destruction. lmcrlcukin-1 (IL-I) lmerleukm-l(IL-1) Interleukin- I (IL-I)
Tumor-necrosis Lymphotoxin (LT) Carhcpsins
Bone surface appears to be lined by Howship lacunae.
factor-alpha (NF-a)
l'Gt;2
Hydrolytic enzymes
Radius of Action
• Radius of action is the range of effectiveness within
which bacterial plaque can induce bone loss.
• It is postulated to be 1.5-2.5 mm. Beyond that there is
no effect.
Enhanced proinflammatory and catabolic acnvines
• Angular defects can appear only in spaces that are
wider than 2.5 mm as marrow spaces will be destroyed
completely.
In periodontitis, interproximal bone typically is
Periodontal tissue breakdown
resorbed faster than the dense facial or lingual/
palatal cortical plates.
Osseous plates measuring between 1.5 and 2 mm are
• Host mediated: prostaglandins, leukotrienes, heparin,
vulnerable to be completely destroyed by microbial
thrombin, bradykinin, cytokines, interleukin-1,6,
plaque causing horizontal bone resorption; in
tumor necrosis factor, transforming growth factor [3,
contrast, osseous plates thicker than 2 mm will
platelet-derived growth factor.
develop vertical bone defects.
Bone Formation in Periodontal Disease

MECHANISM OF BONE DESTRUCTION
Areas of bone formation are also found adjacent to the
sites of active bone resorption and along the trabecular
The cascade of events leading to the connective break-
surfaces at a distance from the inflammation in an effort
down is initiated by the interaction between the microbial
to reinforce the remaining bone (buttressing bone forma-
plaque activating the host defense cells which release a
tion). The response of alveolar bone to inflammation is not
wide array of mediators. The first step in the initiation
simply a destructive process but results from preponder-
of these events are the components of the dental plaque
ance of resorption over formation.
which have the inductive capacity for the infiltration and
recruitment of the host inflammatory cells such as PMNs,
lymphocytes, and macrophages. The lipopolysacchrides Bone Destruction Caused by Trauma
(LPS) from the bacterial cell wall stimulates the macro- from Occlusion
phages to synthesize and secrete a wide range of mol-
Bone destruction resulting from trauma from occlusion
ecules like interleukin-l(IL-1), tumor necrosis factor-a
may occur in the presence as well as absence of inflamma-
(TNF-a), PGE2, cytokines, and other hydrolytic enzymes.
tion. When there is no gingival inflammation the changes
The LPS of the bacterial cell wall activates the T-
caused by trauma from occlusion may vary from increased
lymphocytes that produce IL-1 and lymphotoxin (LT), a
compression and tension of the periodontal ligament and
molecule which possess similar properties as TNF-a. These
increased osteoclastic activity in the alveolar bone to ne-
cytokines have potent pro-inflammatory activity and cata-
crosis of the periodontal ligament and resorption of bone.
bolic nature, thus they ensue periodontal tissue destruction.
These changes are reversible if the offending forces are
• Bacteria mediated: lipopolysaccharides, lipoteichoic corrected. However, persistent trauma from occlusion
acids, peptidoglycan, capsular and surface-associated results in funnel-shaped widening of the crestal portion of
material, muramyl dipeptide, lipoprotein. the periodontal ligamentl with resorption of the adjacent
CHAPTER 26 BONE LOSS IN PERIODONTAL DISEASE 213
bone. These changes, which may cause the bony crest to FACTORS DETERMINING BONE
have an angular shape, represent adaptation of' the peri- MORPHOLOGY IN PERIODONTAL
odontal tissues aimed at "cushioning" increased occlusal DISEASE
forces, but the modified bone shape may weaken tooth
support and cause tooth mobility. • Normal variation in alveolar bone: The normal morphologic
The presence of gingival inflammation trauma from features of alveolar bone affect the bone-destructive
occlusion aggravates the bone destruction caused by the pattern in periodontal disease. The thickness of the
inflammation and results in the formation of bizarre bone compact cortical labial plates varies. In the incisor,
patterns. canine, and premolar regions, the buccal cortical plate
is thin and may be associated with fenestrations and
dehiscence of the cortical plates.
Bone Destruction Caused by Systemic Disorders
The shape of the interdental septa follows the
When a generalized tendency toward bone resorption alignment of adjacent CEJs. When the teeth are in
exists, bone loss initiated by local inflammatory processes close approximation, the interdental septum is narrow
may be magnified. This systemic influence on the re- or sometimes completely nonexistent; in such areas
sponse of alveolar bone has been termed the bone factor progression of periodontal disease is faster. In the
in periodontal disease. anterior region, there is a fusion of inner and outer
Periodontal bone loss may also occur in generalized cortical plates; trabecular bone here is often minimal.
skeletal disturbances (e.g., hyperparathyroidism, leuke- The interdental septum of posterior teeth is wide and
mia, or Langerhan cell histiocytosis) by mechanisms that contains relatively more trabecular bone. However,
may be totally unrelated to the usual periodontal way of the proximity of roots of "stacked" maxillary molars
destruction. allows for only a very thin plate of interproximal bone
Osteoporosis is a physiologic condition of postmeno- as shown in Fig. 26.1. The restricted access for cleaning
pausal women, resulting in loss of bone mineral content between stacked molars makes these sites susceptible
and structural bone changes. Periodontitis and osteopo- to plaque accumulation and the very thin interproximal
rosis share a number of risk factors (e.g., aging, smoking, alveolar bone is rapidly resorbed.
diseases, and medications that interfere with healing). Root, root trunk morphology, and the position of the
There are studies giving evidence of increased severity of root in alveolar process are the other factors affecting
bone loss if periodontitis is superimposed on osteoporosis. the pattern of resorption of alveolar bone.
• Exostoses: Bony projections of various shapes and sizes.
They can be in the form of nodules, sharp ridges, or
TOPOGRAPHY OF THE ALVEOLAR BONE spikes.
• Trauma from occlusion: A vertical bone loss of interdental
The tips of the interdental papillae are situated more coro- septum is seen. Buttressing bone formation is seen as
nally than the facial or lingual/ palatal height of the marginal a reparative process associated with TFO. This can
gingival. In health, the alveolar crest also follows a similar be seen as a pronounced bulge in the contour of the
wave-like pattern which is approximately 2 mm apical to the facial and lingual bone or as a shelf-like thickening of
cementoenamel junction (CEJ). This scalloped configuration alveolar margin referred to as "lipping."
is called "positive architecture." It is more pronounced in the • Aggressive periodontitis: Angular bone loss is seen
anterior regions of the jawbones than the posterior where it around the first molars and incisors. Bone defects
sometimes assumes an almost "flat architecture."
"Negative architecture" (a.k.a "reverse architecture")
exists, when either the gingiva or the bone is destroyed
in the interproximal regions resulting in interdental areas
being apical to the level of' the adjacent facial or lingual/
palatal gingiva or bone, respectively, for example, as seen
in necrotizing ulcerative perlodontitis (NUP) and in area
of chronic food impaction.
In health, the bone and gingiva. run in parallel waves
and probing depths are minimal (1-3 mm). In periodonti-
tis, interproximal bone typically is resorbed faster than the
dense facial or lingual/palatal cortical plates. Resorption
occurs at alveolar crest. Once it is destroyed, the underly-
ing bone marrow resorbs at a faster rate than the dense
buccal and lingual cortical plates FIGURE 26.1 Stacked molars - thin interproximal bone.
(A) (B)
FIGURE 26.2 (A) Generalized horizontal bone loss; (B) generalized vertical bone loss.
FIGURE 26.3 Surgical exposure demonstrating horizontal bone loss. FIGURE 26.4 Surgical exposure demonstrating vertical bone loss
with respect to mandibular left central incisor.
are wider than what are usually seen in chronic They are also called as infrabony or intrabony defects
periodontitis. (Fig. 26.4). The number of walls in the apical portion of
the defect may be greater than that in its occlusal portion,
in which case the term combined osseous defect is used. One-
BONE LOSS PATTERNS walled osseous defect is also called as the hemiseptum
IN PERIODONTAL DISEASE (Fig. 26.5).
As horizontal or vertical bone loss takes place, a variety
Bone loss can be in either a horizontal or a vertical of bony lesions or configurations result. They include:
manner. This loss may be generalized (most teeth in a
a. Interproximal Crater: It is the classic form of periodon-
quadrant are affected) or localized to one or two isolated
tal defect especially in the posterior regions. Between
tooth/teeth (Fig. 26.2).
Horizontal bone loss shall be characterized as horizontal
bone loss if it shows resorption pattern as being parallel
to the line joining the CEJs of the involved adjacent teeth.
Although the bone height is reduced, but the bone mar-
gins remain almost perpendicular to the tooth surface
(Fig. 26.3). It is also called the suprabony defect where
the base of the defect is located coronal to the alveolar crest.
Vertical bone loss is characterized by maintenance of ( ~
crestal bone height with loss of periodontal ligament and
supporting structure adjacent to the tooth root. They are
hollowed-out triangles in the bone alongside one or more
denuded root surfaces, enclosed by one, two, or three bone
walls called as one-, two-, or three-walled defect. The
base of the defect is apical to the residual alveolar bone. FIGURE 26.5 Hemiseptal defect as a result of vertical bone loss.
FIGURE 26.6 Interproximal crater.

FIGURE 26. 7 Furcation involvement of molar teeth in advanced
the dense buccal and lingual cortical plates lies a

cancellous core that is a vascular lattice-like struc- pocket. Osseous destructive pattern in furcation-in-
ture. Once the crestal cortical plate is destroyed by volved teeth varies and depends on the degree of in-
periodontitis, the central bone marrow resorbs more volvement. Pattern of bone loss around the individual
quickly than the buccal and lingual cortical plates and roots can be horizontal or vertical (Fig. 26.7).
an interproximal crater is formed. The boundaries of
the crater on the mesial and distal are the roots of the
adjacent teeth (Fig. 26.6). DIAGNOSIS
It is the most frequently noted osseous lesion
in periodontal disease, i.e., one-third of all osseous A thorough clinical examination with radiographs is
defects. They are more common in the posterior region. the key to diagnosis and treatment planning of osseous
Following reasons have been suggested for the high defects.
frequency of interdental craters:
1. Clinical examination and probing: This will determine
1. The interdental area between the posterior teeth the presence and the depth of the pocket on any
is somewhat difficult to clean as it requires a good surface of the tooth. Transgingival probing under
deal of manual dexterity, and cancellous bone is local anaesthesia can give general sense of the bony
more reactive and has a rapid turnover than cortical topography.
bone. 2. Radiographs: In periodontal disease, the alveolar bone
2. The shape of interdental bone in mandibular molars undergoes changes that affect the lamina dura, the
has a flat or concave architecture buccolingually crestal radiodensity, and the height and contour of
that may result in increased prevalence of osseous interdental bone. Radiographs do not reveal the extent
craters. of involvement on the facial and lingual surfaces or
3. Because of the presence of interdental col and the the presence of fenestration and dehiscence. It is
specific arrangement of capillaries in this region, obscured by the dense root structure. Dense cortical
inflammation results in midplane bone resorption, bones on the facial and lingual surfaces of interdental
with buccal and lingual plates being affected much septa obscure defects in the intervening cancellous
less as the buccolingual dimension is far greater than bone. Thus it is possible to have a deep interdental
the mesiodistal dimension. crater without having any radiographic evidence of
it. Also a minimum of 30% bone loss should occur
b. Ledges: Plateau-like bone margins caused by resorption
to be visible radiographically. Periodontal diseases
of thickened bony plates.
are more extensive than what they appear on the
c. Reverse architecture: Formed due to loss of interdental
radiograph.
bone including the facial and lingual bone without the
3. Surgical exposure: Direct observation during flap sur-
concomitant loss of radicular bone. It is found more
gery is the only definitive method for determining the
commonly in maxilla.
architecture of a bony deformity.
d. Furcation involvement: Invasion of the bifurcation and
trifurcation of multirooted teeth by periodontal dis- Normally, the crestal lamina dura extends to a point
ease. It is a phase in the apical extension of periodontal approximately 1-2 mm from the CEJ. The bone crest
FIGURE 26.8 Horizontal bone loss proximal to the posterior teeth. FIGURE 26.9 Intrabony - one walled.
FIGURE 26. 10 Surgical exposure demonstrating vertical bone loss with respect to maxillary second premolar and first molar.
running from the mesial of one tooth to the distal of the nary line drawn between the CEJs of adjacent teeth
adjacent tooth appears flat and parallel to the imaginary (Fig. 26.8).
line drawn from the CEJs of the same two teeth. Vertical (angular) bone loss mesial to the maxillary molar:
Horizontal bone loss proximal to the posterior teeth: Bone loss is considered vertical when the crest of the
Bone loss is considered horizontal when the crest proximal bone is not parallel to an imaginary line drawn
of the proximal bone remains parallel to an imagi- between the CEJs of adjacent teeth (Figs 26.9 and 26.10).
KEY POINTS
• Periodontal destruction occurs in an episodic, intermit- that perforate the crest, side, or at the angle of the inter-
tent fashion, with periods of inactivity or quiescence. dental septum entering the bone.
• Interproximally, inflammation spreads to the loose con- • Radius of action is the range of effectiveness within which
nective tissue around the blood vessels, through the bacterial plaque can induce bone loss. It is postulated to be
fibers, and then into the bone through vessel channels 1.5-2.5 mm. When combined with inflammation, trauma
KEY POINTS (cont'd)
from occlusion aggravates the bone destruction caused by • Ledges are plateau-like bone margins caused by
the inflammation and causes bizarre bone patterns. resorption of thickened bony plates.
• Topography of alveolar bone can be positive, negative, • Osseous defects can be diagnosed by transgingival prob-
or flat architecture. ing, radiographs, or surgical exposure.

1. Explain osseous craters. What are the procedures for Dentistry. 5th ed. Oxford: Blackwell Munksgaard; 2008.
eliminating osseous craters? 2. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's
2. What are the various osseous defects? Clinical Periodontology. 10th ed. St. Louis: Elsevier; 2006.
3. Write a short note on radius of action.
4. Write a note on reverse architecture
5. Classify osseous defects.
6. Describe infrabony defects.
CHAPTER
27
Periodontitis: Chronic, Refractory,
and Necrotizing Ulcerative
CHAPTER OVERVIEW
Chronic periodontitis is the most prevalent form of peri- factors such as diabtetes, smoking, or stress, disease progres-
odontitis. It is considered to start as plaque-induced gingivitis, sion may become aggressive. Chronic periodontitis lesions
if left untreated progresses into chronic periodontitis. It was include loss of attachment and bone, and are regarded as an ir-
formerly known as adult periodontitis or slowly progressing reversible condition. Although this disease is seen more com-
periodontitis. In the presence of systemic or environmental monly in adults, it can occur in children and adolescents also.
CHRONIC PERIODONTITIS • Exudation of crevicular fluid and suppuration from the

pocket.
Epidemiologic data and clinical experiences have sug- • Abscess formation in some cases when the pocket
gested that the adult form of periodontitis commonly occludes (Fig. 27.2).
seen in older individuals can also be seen in children and • Thickened fibrotic marginal tissues obscuring the
adolescents. Therefore, it was concluded that it would underlying inflammatory changes in cases of long-
be more accurate to adopt a nonspecific term such as standing, low-grade inflammation.
chronic periodontitis to characterize this constellation of • Supragingival and subgingival plaque accumulation
periodontal disease. (frequently associated with calculus formation).
Traditionally, this form of periodontitis has been char- • Presence of suprabony or infrabony pocket
acterized as a slowly progressive disease. However, there formation.
are also data indicating that in presence of factors like • Loss of clinical attachment.
diabetes, smoking, and stress, some patients may experi- • Tooth mobility in advanced cases.
ence short periods of rapid progression.
Chronic periodontitis has been defined as an infectious
disease resulting in inflammation within the supporting Radiographic Features
tissues of teeth, progressive attachment loss, and bone loss.
• Chronic periodontitis is diagnosed radiographically by
the evidence of bone loss.
Clinical Features • Pattern of bone loss observed may be vertical or
horizontal (Fig. 27.3).
The following are the most common clinical findings
• Vertical bone loss is when attachment and bone loss
associated with chronic periodontitis (Fig. 27.1):
on one tooth surface is greater than that on an adjacent
• Slightly to moderately swollen gingiva with alteration surface and is usually associated with angular bone
in color ranging from pale red to magenta. defects and intrabony pocket formation.
• Loss of gingival stippling with blunted or rolled • When attachment and bone loss occurs at a uniform
gingival margins and flattened or cratered papilla. rate on the majority of tooth surfaces, it is called
• Gingival bleeding either spontaneous or in response horizontal bone loss and is usually associated with
to probing. suprabony pockets.
CHA PTER 27 PERIO DONTITIS: CHRONIC, REFRACTORY, AND NECROTIZING ULCERATIVE 219
(A) (B)
FIGURE 2 7. 1 Clinical features of chronic periodontitis: (A) increased amount of calculus, redness, swelling, and edema of gingival margin;
(B) gingival recession with visible exudate and gingival stippling has been lost.
Fusobacterium nucleaium, Actinobacillus actinomyce-

temcomitans, Treponema, and Eubacterium species.
Symptoms
• Chronic periodontitis is usually painless unless
associated with caries due to exposed roots that are
sensitive to heat, cold, or both.
• Localized dull pain sometimes radiating deep into jaw;
areas of food impaction and gingival tenderness can
be found.
• Usually patient notices that their gums bleed while
brushing or eating; spaces appear between their teeth
or teeth start moving.
FIGURE 2 7 .2 Periodontal abscess.

Disease Distribution
According to area of disease distribution chronic peri-
odontitis may be classified as localized and generalized.
• Localized periodontitis: Periodontitis is considered
localized when less than 30% of sites assessed in the
mouth demonstrate attachment loss and bone loss.
• Generalized periodontitis: Periodontitis is considered
generalized when more than 30% of sites assessed
in the mouth demonstrate attachment loss and bone
loss.
Disease Severity
FIGURE 2 7 .3 Pattern of bone loss seen in chronic periodontitis. According to disease severity chronic periodontitis
may be classified as slight (mild), moderate, or severe.
Microbiologic Features
• Slight (mild) periodontitis: When no more than 1-2 mm
• Chronic periodontitis is associated with a variable of clinical attachment loss has occurred.
microbial pattern. • Moderate periodontitis: When 3-4 mm of clinical
• The microorganisms commonly found are attachment loss has occurred.
Porphyromonas gingivalis, Bacteroides Jorsythus, Prevotella • Severe periodontitis: When 5 mm or more of clinical
iniermedia, Campylobacter recius, Eikenella corrodens, attachment loss has occurred.
Disease Progression Plaque retentive factors are those that facilitate plaque ac-
cumulation or prevent the removal of plaque by routine oral
The rate of disease progression in chronic periodontitis hygiene procedures. They retain plaque microorganisms in
is slow but sometimes may be modified by systemic or proximity to the periodontal tissues, providing an ecologic
underlying factors. Several models have been proposed niche for plaque growth and maturation. Among the plaque
to describe the rate of disease progression retentive factors the most important is calculus because of
• Continuous paradigm its ability to retain and harbor plaque bacteria on its rough
• Random burst model surface. Other factors that are known to retain plaque or
• Asynchronous multiple burst model prevent its removal are subgingival carious lesions, furca-
tions exposed by loss of attachment and bone, crowded and
• Continuous model implies slow, continuous, and malaligned teeth, root grooves, and concavities.
progressive destruction of periodontium over time.
• Random burst model proposes that progression of disease Systemic Factors
occurs at short periods of active destruction, which are In plaque-induced chronic periodontitis, the rate of
followed by periods of remission that occurs randomly progression is considered to be slow. But when this type
with respect to site in an individual. of periodontitis occurs in a patient who also suffers from
• In asynchronous multiple burst model the majority of a systemic disease that influences host response, the rate
destructive disease takes place within a definite period of destruction is significantly increased. Diabetes type II
of the individual's life then followed by prolonged or noninsulin-dependent diabetes mellitus (NIDDM) is
periods of inactivity. considered as the most important systemic factor that can
lead to increased periodontal destruction. The synergistic
Differentiation Characteristics of Chronic effect of plaque accumulation and modulation of an effec-
Periodontitis tive host response through the effects of diabetes can lead
to severe and extensive periodontal destruction that may
• Prevalent in adults but can occur in children. be difficult to manage with standard clinical techniques
• Amount of destruction consistent with local factors. without controlling systemic condition
• Associated with variable microbial pattern.
• Subgingival calculus frequently found. Environmental and Behavioral Factors
• Slow to moderate rate of progression with possible Smoking is one such factor that has been found to in-
periods of rapid progression. crease the severity and extent of periodontal disease. It is
• Possibly modified or associated with the following: seen that smokers with chronic periodontitis have more
Systemic diseases such as diabetes mellitus and HIV attachment and bone loss, more furcation involvements,
infection. and deeper pockets compared with nonsmokers. The
Local factors predisposing to periodontitis. reasons behind this effect can be changes in subgingival
Environmental factors such as cigarette smoking microflora between smokers and nonsmokers in addition
and emotional stress. to effects of smoking on host response.
Emotional stress can also influence the extent and se-
verity of chronic periodontitis because of the effect of
Risk Factors for Chronic Periodontitis
stress on immune function.
Local Factors
Genetic Factors
Plaque accumulation is the primary initiating factor
in periodontal destruction. In addition to this, plaque Periodontal destruction frequently seen among family
retentive factors are also important in the development members and across different generations suggests the
and progression of chronic periodontitis. possibility that there is an underlying genetic factor that
Plaque that accumulates on the tooth and gingival plays a role in periodontal disease. Recent data indicate
surfaces at the dentogingival junction is considered to that a genetic variation or polymorphism in the genes
be the main etiologic factor in periodontal destruction. encoding interleukin-la (IL-la) and IL-113 is associated
Increase in the proportion of gram-negative organisms with an increased susceptibility to a more aggressive form
such as Poprphromonas gingivalis, Tanarella forsythia, and of chronic periodontitis.
Treponema denticola (known as red complex) are associated
with the ongoing attachment and bone loss in chronic Treatment Considerations in Chronic
periodontitis. It has been found that these bacteria may
Periodontitis
impart a local effect on the cells of the inflammatory re-
sponse and cells and tissues of the host resulting in a local, Clinical judgment is an integral part of the decision-
site-specific disease process. making process. Many factors affect the decisions for
appropriate therapy and expected therapeutic results, monitored, demonstrate additional attachment loss at
Patient-related factors include systemic health, age, com- one or more sites, despite well-executed therapeutic
pliance, therapeutic preferences, and patient's ability to measures and patient's efforts to stop the progression
control plaque, Other factors include the clinician's ability of disease.
to remove subgingival deposits, prosthetic demands, and The recent concept is that the refractory can be applied
the presence and treatment of teeth with more advanced to all forms of destructive periodontal disease that appear
chronic periodontitis. to be nonresponsive to treatment, e.g., refractory chronic
Treatment considerations can be divided into initial periodontitis and refractory aggressive periodontitis.
therapy, compromised therapy, and periodontal surgical Refractory periodontitis is completely different from
procedures as discussed in subsequent sections. recurrent periodontitis; as in the latter, a complete re-
mission occurs after therapy followed by recurrence of
Initial Therapy disease due to local factors.
1. Elimination, alteration, or control of risk factors like
diabetes, smoking, certain periodontal bacteria, genetic
predisposition, systemic diseases and conditions, stress, Etiology
nutrition, HIV infection, and medications that may
Refractory periodontitis occurs when conventional
contribute to chronic periodontitis should be attempted.
periodontal therapy has failed to eliminate microbial
Consultation with the patient's physician may be
reservoirs of infection or has resulted in the emergence
indicated in such cases
or superinfection of opportunistic pathogens.
2. Instruction, reinforcement and evaluation of the
It may also occur as a result of a complexity of un-
patient's plaque control should be performed.
known factors that may compromise the host's response
3. Supra- and subgingival scaling and root planing
to conventional periodontal therapy.
should be performed to remove microbial plaque and
The causative factors for refractory periodontitis can
calculus. be:
4. Antimicrobial agents or devices may be used as
adjuncts to the routine periodontal therapy. • Abnormal host response
5. Local factors contributing to chronic periodontitis • Resistant periodontopathic microorganisms
should be eliminated like removal of restorative • Failure to eliminate morphologic conditions such as
overhangs and overcontoured crowns, correction of furcation involvement and irregular root surface
ill-fitting prosthetic appliances, restoration of carious • Smoking and systemic diseases
lesions, and occlusal trauma should be corrected.
On the basis of causative factors, two types of refrac-
Compromised Therapy tory periodontitis have been considered.
In certain cases, because of severity and extent of dis- The first type comprises those with refractory sites,
ease and the age and health of the patient, initial therapy i.e., patients with adult periodontitis in whom anatomic
may become end point that should include timely peri- conditions favor the proliferation of periodontopathic
odontal maintenance. microorganisms.
The second type of refractory periodontitis is due to
Periodontal Surgical Procedures severe PMN defects or other immunologic problems, e.g.,
In patients with chronic periodontitis with advanced aggressive periodontitis associated with Papillon-Lefevre
loss of periodontal support, a variety of periodontal surgi- syndrome.
cal treatment modalities can be considered: The subgingival microbiota in refractory periodontitis
mainly consists of elevated levels of red complex species
1. Flap surgery and orange complex species. They include B. forsythus,
2. Gingivectomy P. gingivalis, Fusobacterium, Campylobacter, Prevotella, and
3. Periodontal plastic surgery Peptostreptococcus spp., and S. intermedius.
4. Regenerative therapy with bone grafts/ GTR membranes
5. Osseous resective surgery
6. Root resective therapy Clinical Features
The primary feature of refractory periodontitis is the
REFRACTORY PERIODONTITIS occurrence of additional attachment loss and bone loss
after repeated attempts to control the infection with con-
According to American Academy of Periodontology, ventional periodontal therapy.
the term refractory periodontitis refers to destructive peri- Refractory periodontitis should be diagnosed only
odontal diseases in patients who, when longitudinally after the conclusion of conventional active periodontal
therapy and in patients who follow a rigorous program of Clinical Features

periodontal maintenance and comply with recommended
oral hygiene procedures. Most of the clinical features are same as that seen in
necrotizing ulcerative gingivitis, i.e., necrosis and ulcer-
ation of tips of interdental papilla or gingival margin,
Treatment which gets covered by pseudomembrane. Ulcerated mar-
gins are surrounded by erythematous halo. The lesions
The goal of therapy for refractory periodontitis is to
are extremely painful and bleed on slight manipulation.
stop or slow the progression of the disease. Due to com-
The distinguishing feature of NUP is destructive progres-
plexity and many unknown factors a reasonable treatment
sion of the disease that includes periodontal attachment
objective is to slow the progression of the disease. Once
and bone loss. Deep interdental osseous craters typify
the diagnosis is made the following steps are indicated
periodontal lesions of NUP. The most striking feature of
in the treatment planning:
this lesion is absence of deep conventional pockets. This
1. Collection of subgingival microbial samples from is because ulcerative and necrotizing nature of this lesion
selected sites for analyses, possibly including antibiotic destroys the marginal epithelium resulting in gingival
sensitivity testing recession. Advanced lesions of NUP lead to severe bone
2. An appropriate antibiotic regimen should be selected loss, tooth mobility and ultimately tooth loss. In addi-
3. Along with administration of antimicrobial regimen, tion to these intraoral manifestations, NUP patients may
use of conventional periodontal therapies present with oral malodor, fever, malaise, or lymphade-
4. Periodontal maintenance program nopathy.
NECROTIZING ULCERATIVE
SYSTEMIC ANTIBIOTIC THERAPY IN PERIODONTITIS IN HIV/AIDS PATIENTS
THE MANAGEMENT OF REFRACTORY
PERIODONTITIS Necrotizing ulcerative periodontal lesions seen in HIV-
positive/ AIDS patients are much more destructive and
Systemic antibiotic therapy is administered to reinforce
result in complications that are rarely seen in non-HIV/
mechanical periodontal treatment and support the host
AIDS patients (Fig. 27.4).
defense system in overcoming the infection by killing
Periodontal attachment and bone loss associated with
subgingival pathogens that remain after conventional
these types of NUP are extremely rapid (10 mm of bone
mechanical periodontal therapy.
loss over a 62-month period). Many of these lesions have
The antibiotics that are commonly found effective are:
resulted in tooth loss.
• 250 mg of tetracycline hydrochloride four times daily The major complication seen is progression of lesions
for minimum of 1 week to involve large areas of soft tissue necrosis with exposure
• 250 mg of amoxicillin and 125 mg of clavulanate of bone and sequestration of bone fragments.
potassium three times daily for 14 days These lesions when extend to the vestibular area and
• 500 mg of metronidazole three times daily for 7 days palate are termed as necrotizing ulcerative stomatitis
• 150 mg of clindamycin hydrochloride four times daily (NUS).
for 7 days
• Combination of metronidazole-amoxicillin, Etiology
metronidazole-doxycycline, and metronidazole-
ciprofloxacin Bacterial pathogens, specifically a mixed fusiform-
spirochete bacterial flora, play a key role in the etiology
of NUP. Numerous predisposing factors have been attrib-
uted including poor oral hygiene, preexisting periodontal
NECROTIZING ULCERATIVE diseases, smoking, viral infections, immunocompromised
PERIODONTITIS status, psychosocial stress, and malnutrition.
When necrotizing ulcerative gingivitis (NUG) pro- Microbial Flora

gresses to the underlying periodontal structures, it results Microbiologic studies of NUP have demonstrated the
in attachment and bone loss. This condition is referred to presence of an anaerobic flora consisting of Treponema
as necrotizing ulcerative periodontitis (NUP). According and Selenomonas spp., Fusobacterium nucleatum, Prevotella
to the World Workshop of Periodontics, NUG and NUP intermedia, and Porphyromonas gingivalis.
can be collectively referred to as necrotizing periodontal It was also found that there was significantly greater
diseases. prevalence of opportunistic fungus Candida albicans and a
(A) (B)
FIGURE 2 7 .4 Necrotizing ulcerative period on ti tis (there is complete necrosis of interdental papilla).
higher prevalence of Actinobacillus actinomycetemcomitans, The possible explanation for this link can be the fact
P. intermedia, P. gingivalis, F. nucleatum, and Campylobacter that extreme malnutrition can diminish the host resistance
species in HIV-associ-ated NUP patients. to infection. It is seen that phagocytosis, cell-mediated
immunity and complement, antibody, and cytokine pro-
Immunosuppression duction and function is impaired which predisposes an
individual to oral infections
It has been seen that some form of immune dysfunc-
tion exists in NUP patients. The main reason for this
immunosuppression is likely reduced CD4+ cell counts, Treatment
<200 cells/mm. Also, there is a significant depression in
PMN phagocytosis and killing function. A thorough medical history and examination to rule
out any systemic diseases is mandatory. Periodontal treat-
Psychological Stress ment includes:
Although a direct link has not been demonstrated be- • Local anesthesia in area of involvement
tween stress and NUP, it has been found that NUG patient • Removal of all necrotic hard and soft tissues in areas
had more anxiety and higher depression scores. of involvement by scaling and root planing
It has been seen that any psychiatric disturbances can • Use of ultrasonic instrumentation with profuse
activate the hypothalamic-pituitary-adrenal axis, which irrigation preferably with 10% povidone iodine
can elevate serum and urine cortisol levels. This can result solution, which enhances debridement and flushing
in depression of lymphocyte and PMN function, which of deep lesions
can predispose to NUG. • Antimicrobial therapy to reduce gram-negative
anaerobes
Malnutrition • In some cases of fungal infection use of antifungal
An association has been made between malnutrition agents
and necrotizing periodontal diseases. Lesions resembling
NUG but with progression to become gangrenous sto- Home Care Procedures
matitis or noma have been described in children with • Brushing and interdental flossing
severe malnutrition in underdeveloped countries. In the • Chlorhexidine digluconate 0.12% rinses
advanced stages NUG lesions extending from gingiva to • Systematic follow-up visits with therapy until lesions
other areas of the oral cavity becomes gangrenous stoma- are resolved
titis and causing exposure, necrosis, and sequestration of • Frequent maintenance visits to prevent recurrence of
alveolar bone. old or developmental of new lesions
KEY POINTS
• The microorganisms commonly found are Por- • Generalized periodontitis: When more than 30% of sites
phyromonas gingivalis, Bacteroides forsythus, Pre- assessed in the mouth demonstrate attachment loss and
votella intermedia, Campylobacter recius, Eikenella bone loss.
corrodens, Fusobacterium nucleaium, Actinobacillus • Slight (mild) periodontitis: When no more than 1-2 mm of
actinomycetemcomitans, Treponema, and Eubacierium clinical attachment loss has occurred.
spp. • Moderate periodontitis: When 3-4 mm of clinical attach-
• Localized periodontitis: When less than 30% of sites as- ment loss has occurred.
sessed in the mouth demonstrate attachment loss and • Severe periodontitis: When 5 mm or more of clinical at-
bone loss. tachment loss has occurred.
QUESTIONS 2. Newman MG, Takei HH, Klolkevold PR, Carranza F. Car-ranza's

Clinical Periodontology. 10th ed. Philadelphia: Saunders; 2007.
3. Carranza FA, Newman MG. Carranza's Chinical Periodontology. 8th
1. Describe the clinical features of chronic periodontitis. ed. Philadelphia: Saunders; 1996.
2. Discuss the risk factors for chronic periodontitis. 4. Flemming TF. Periodontitis. Ann Periodontal 1999;4:32.
3. Describe the clinical features and management of 5. Novak MJ. Necrotising ulcerative periodontitis. Ann Periodontal
necrotizing ulcerative periodontitis. 1999;4:74.
6. Papapanou PN. Risk assessment in the diagnosis and treatment of
4. Write a short note on refractory periodontitis.
periodontal diseases. J Dent Educ 1998;62:822.
Suggested readings
1. Adams OF. Diagnosis and treatment of refractory periodontitis. Curr
Opin Dent 1992;2:33.
CHAPTER
28
Aggressive Periodontitis
CHAPTER OVERVIEW
All forms of periodontitis that progresses much faster than patients than does the chronic form. Unlike chronic peri-
chronic periodontitis, resulting in significant attachment loss, odontitis, the aggressive form of periodontitis mostly
irrespective of the age of the individual are termed aggressive affects the narrower range of young individuals. It may
periodontitis (AP). It is defined as the rare form of periodon- be universally distinguished from chronic periodontitis
titis occurring in an otherwise healthy young individual, by the age of onset, the rapid rate of disease progression,
and characterized by rapid loss of alveolar bone on more pattern of bone destruction, clinical signs of inflammation,
than one tooth of permanent dentition. The amount of bone and relative abundance of plaque and calculus. Indeed,
destruction is inconsistent with the amount of local factors. combinations of these clinical differences are the primary
Aggressive periodontitis is much less common than basis for placing affected individuals into one of the three
chronic periodontitis and generally affects younger major categories of periodontitis.
CLASSIFICATION of intense gingival inflammation. Initial stages of the

disease were not associated with local irritants such
Aggressive periodontitis occurs in two forms, i.e., lo- as dental plaque or calculus, and therefore the disease
calized and generalized forms on the basis of enough was subsequently referred to as diffuse atrophy of the
individually specific features. alveolar bone or periodontosis. According to this hy-
Localized and generalized chronic periodontitis are pothesis, the teeth drifted apart or migrated without
usually considered to be two clinical expressions of the the formation of periodontal pockets because of the
same disease. alveolar bone degeneration. It was in the late 1970s and
early 1980s, when it was shown that the condition was
an infection as it could be effectively treated by therapy
aiming at excellent plaque control. This concept prevails
Aggressive perlodontltl
today.
A variety of terminologies have been given so far to
Generalized
this form of periodontal disease, which is characterized
by deep periodontal pockets with advanced alveolar bone
loss in healthy young adolescents. It has been summa-
rized in Table 28.1.
HISTORICAL BACKGROUND EPIDEMIOLOGY
Aggressive periodontitis was not clearly described A major problem in the literature dealing with chronic
until late twentieth century. Initially it was considered and aggressive forms of periodontitis is the absence of uni-
as a noninflammatory or degenerative condition as it versally accepted case definitions. The prevalence varies
was found to be associated with defective deposition depending on many variables such as the geographic
of cementum (cementopathia) and because of absence location, race, ethnicity, oral hygiene, nutritional status,
TABLE 28.1 Timeline of Aggressive Periodontitis
S. No. Author Year Terminology

1. G.V. Black 1915 "Phagedenic pericementitis"
and "chronic suppurative
pericementitis"
2. Gottlieb 1923 Diffuse atrophy of

alveolar bone
3. Gottlieb 1928 Deep cementopathia/

cementopathiaprofunda
noninflammatory or
degenerative condition
4. Wannemacher 1938 Parodontitis marginalis

progressiva
5. Thoma and Goldman 1940 Periodontitis
6. Orban and Weinmann 1942 Periodontosis
7. World Workshop in 1966 The term "periodontosis"

FIGURE 28.1 Distolabial migration of maxillary central incisors
Periodontics was eliminated
noticed in LAP.
8. Chaput 1967 Juvenile periodontitis
9. Kaslick and Chasens 1968 Replaced periodontosis
with periodontitis Generalized Aggressive Periodontitis (GAP)
10. Buttler 1969 Juvenile periodontitis
• Blacks are at much higher risk than whites
11. Baer and Kaslick 1971 Retained the term • Male teenagers > female adolescents
"periodontosis"
Important Epidemiological Studies
12. Page and Schroeder 1982 Juvenile periodontitis
The important LAP-related epidemiological studies
13. World Workshop 1989 Juvenile periodontitis conducted in different parts of the world have been sum-
in Clinical (subset of "early onset marized in Table 28.2.
Periodontics periodontitis")
14. AAP International 1999 Aggressive periodontitis

Workshop for LOCALIZED AGGRESSIVE
Classification
of Periodontal
PERIODONTITIS
Diseases
Localized aggressive periodontitis is formerly called
localized juvenile periodontitis. Aggressive forms of
and socioeconomic factors. Further, 11 % of aggressive periodontal disease show some primary and secondary
periodontitis occurs among participants under 26 years features as follows (Lang, 1999):
of age.
TABLE 28.2 Prevalence of Localized Aggressive Periodontitis

PREVALENCE Geographic
location Investigators Prevalence (%)
Localized Aggressive Periodontitis (Fig. 28.1)
Africa Mac Gregor (1980) 0.80
• Low prevalence: 0.2% Brazil Gjermo et al (1984) 3.70
• Less than 11 % in the adolescent population
Chile Saxby (1987) 0.32
• Affects both males and females
• Females are affected more frequently in the period UK Saxby (1987) 0.10-0.80
between puberty and 20 years of age Japan Kowashi (1988) 0.47
• Blacks are at much higher risk for localized aggressive
USA Loe and Brown (1991) 0.14-2.05
periodontitis
• Black males are 2.9 times more likely to have the India
disease than black females • Chennai Miglani et al (1949) 0.10
• Mumbai Marshall Day and Shourie (1965) 17.60
• Black males > black females > white females > white
• Mumbai Rao and Tewani (1968) 6.80
males
C H A PT ER 28 A G G R ESSIV E PER IO D O N T IT IS 227
Primary Features
• Noncontributory medical history
• Rapid attachment loss and bone destruction
• Familial aggregation of cases
Secondary Features
• Amount of microbial deposits inconsistent with the
severity of periodontal tissue destruction
• Elevated proportions of Aggregatibacter actinomyce-
tomcomitans (Aa) and in some far east populations,
Prophyromonas gingivalis
• Phagocyte abnormalities
• Hyperresponsive phagocyte, including elevated
production of PGE2 and IL-113 in response to bacterial
endotoxins FIGURE 28.2 Clinical view showing deep periodontal pocket in
• Progression of attachment loss and bone loss may be relation to #12.
self-arresting
• Age of onset: Around puberty, but there are no fixed or
arbitrary upper age limits
• The patients are otherwise systemically healthy.
• The progression of disease: The loss of clinical attachment
in patients with aggressive periodontitis is about
three to four times faster. There are many factors that
influence how rapidly the periodontium is destroyed.
• Familial pattern: There is tendency of cases to aggregate
in families.
• Presence of local factors and periodontal destruction: There is
minimal amount of dental plaque (i.e., biofilm) present
on the affected teeth but the periodontal destruction
is extensive. Hence, the amount of plaque deposit is
inconsistent with the magnitude of bone destruction
which seems quality of plaque is a significant factor in
patients with LAP.
• Distribution: Localized to first molar/ incisor presen- FIGURE 28.3 Distolabial migration of maxillary incisors with dia-
tation with interproximal attachment loss on at least stema formation.
two permanent teeth, one of which is a first molar,
and involving no more than two teeth other than first
• Dental hypersensitivity: Patient may complain of
molars and incisors.
sensitivity of denuded root surfaces to thermal and
• Causative/specific microorganisms: The plaque contains tactile stimuli.
elevated levels of A actinomycetomcomitans, however,
• Burnout phenomenon: In many cases of LAP, the rate of
in Far East Asian country, the microorganism detected
disease progression slows down or stops entirely and
was P. gingivalis (Pg.).
disease appears to be self-limiting. The attachment
• Robust serum antibody response to the infecting
loss and bone destruction do not spread to other
microorganism (A actinomycetomcomitans).
teeth. This phenomenon of self-limitation of disease
• Gingival inflammation: There is low level of clinical activity with advancing age is called as "burn-out"
gingival inflammation despite the presence of deep
phenomenon. This can be explained by the possibility
periodontal pocket and advanced alveolar bone loss
that the periodontal disease merely goes into remission
(Fig. 28.2).
and can become active sometime in the future.
• Pathological migration: There is distolabial migration • Incidental attachment loss: There are isolated areas
of maxillary incisors resulting in diastema formation
of attachment loss in otherwise healthy dentitions
(Fig. 28.3).
including the recessions associated with:
• Tooth mobility: Increasing mobility of incisors and first
molars. Traumatic injuries
• Single or multiple periodontal abscess: Formation with Tooth position
lymph node enlargement. Impacted third molars
• Pain: Deep, dull, radiating pain during the mastication. Endodontic infection
The first molars and the incisors are the first perma-
nent teeth to erupt in the oral cavity, and get exposed to
microorganisms, deposits, and their toxins for a longer
period of time. Hence, these teeth are more susceptible
to periodontal tissue destruction.
After the initial invasion of the periodontal tissues
by the causative organism A. actinomycetomcomitans,
there is increased antibody formation to neutralize these
microorganisms. Hence, the spread of the disease to other
teeth may be arrested.
There may be possible colonization of some other mi-
FIGURE 28.4 Radiograph illustrating arc shaped bone loss in croorganisms considered to be antagonistic to the main
mandibular molar region.
causative organisms, thus localizing the A. actinomycetem-
comitans infection and tissue destruction.
Root fractures Due to the unknown etiology, the causative organ-
Subgingival caries ism, i.e., A. actinomycetemcomitans, may lose its ability to
Subgingival restoration. produce the virulence factors such as leukotoxins. This
phenomenon may arrest the existing disease activity and
The patient showing this clinical finding can be cat- prevents further colonization of microorganisms.
egorized under high risk for aggressive periodontitis or Some defects on the cemental surface (cemental hypo-
chronic periodontitis. plasia or aplastic cementum) may be responsible for the
It is necessary to understand that to assign a diagnosis localization of the lesion in LAP.
or classify the disease, not all the features/ characteristics
must be present. The diagnosis of disease may be based
Microbiology of LAP
on the clinical, radiological, historical data and labora-
tory testing. l. Aggregatibacter actinomycetemcomitans (Aa.) (about 90%)
2. P. gingivalis (Pg.)
3. Capnocytophaga spp.
Radiographic Features 4. Eikenella corrodens
The presence of vertical/ angular bone loss around 5. Campylobacter rectus
the first molars and incisor teeth (see Figs 28.4 and 28.5). 6. Fusobacterium nucleatum
"Arc shaped" alveolar bone loss around first molars 7. Bacteroides capillus
extending from the distal surface of second premolars to 8. Capnocytophaga spp.
the mesial surface of second molars. This bilateral "arc 9. Eubacterium brachy
shaped" bone loss is mirror image and characteristic of 10. Spirochetes
LAP (Figs 28.4 and 28.5). 11. Viruses: Human Cytomegalovirus, Epstein-Barr virus-I,
Herpes virus.
Area-Specific (First Molar/Incisor) Distribution A. Actinomycetemcomitans (Aa.)
in Localized Aggressive Periodontitis
This organism was first isolated in 1912 by Klinger (a
Although the exact etiology for the area-specific dis- German microbiologist) from the lesions of cervicofacial
tribution of LAP is not known, it can be explained as actinomycosis. Since the organism was isolated together
follows: with Actinomyces israelii, the species name stands actinomy-
cetemcomitans (together with Actinomyces). Furthermore, • Surface-associated material (SAM), which stimulates
in the genus name Actinobacillus, actino refers to star- bone resorption
shaped internal morphology of the colonies and bacillus • Lipopolysaccharide (LPS), which can also cause bone
refers to the cell shape. Recently, Niels Norskov-Lauritsen resorption
and Mogens Kilian (2006) renamed this bacterium as Ag- • Proteases that degrade immunoglobulins
gregatibacter (rod-shaped bacterium that aggregate with • Collagenase, which may degrade connective tissue
others) actinomycetemcomitans. collagen
A. actinomycetemcomitans is a fastidious, facultatively • The RANKL/OPG ratio is increased in the gingival
anaerobic, nonmotile, nonsporing, short cocco-bacilli, crevicular fluid
small gram-negative rod, 0.4-0.5 lm x 1.0-1.5 lm in size • Extracellular outer membrane vesicles
that has been strongly implicated in LAP (Zambon, 1983). • Factors affecting the immune response may inhibit IgG
Various studies have shown that A actinomycetemcomi- and IgM production
tans is the key microorganism found in more than 90% of • Factors damaging host cells including epithelial cells
patients diagnosed with LAP. and fibroblasts
A. actinomycetemcomitans is a human pathogen that can
cause severe extraoral infections including infective en-
docarditis, brain, facial and thyroid abscess, osteomylitis,
Immunologic Factors
meningitis, and urinary tract infection (UTI). The host immune response is crucial to neutralize effec-
In LAP, certain A actinomycetemcomitans serotypes and tively the periodontal pathogens and their by-products.
corresponding serotype antigens may be related to specific In aggressive periodontitis, the following immune defects
sites of infection. Six serotypes (a, b, c, d, e, and f) of A acti- have been implicated in its pathogenesis.
nomycetemcomitans have been identified. However, in LAP,
• Human leukocyte antigens (HLA), HLA-A9 and B15
serotype-b is significantly elevated in the subgingival plaque.
antigens are consistently associated with aggressive
periodontitis.
A. actinomycetemcomitans (Aa.) As a Key • HLA-A2 and HLA-B5 polymorphisms demonstrate
Etiologic Agent in LAP negative association to aggressive periodontitis.
• Functional defects of PMN s or monocytes or both
There are several lines of evidence that incriminate A
result into defective chemotaxis and phagocytosis.
actinomycetemcomitans a key etiologic agent in LAP. These • On exposure to microbial lipopolysaccharides, the
are summarized hereunder:
monocytes become hyperresponsive and produce
• This organism is found in high numbers in periodontal proinflammatory product prostaglandin E2 (PGE2)
lesions in LAP patients. However, it is either absent or ultimately responsible for the increased connective
present in low numbers in healthy sites in the same tissue and bone destruction.
patient. • Receptors for IgG2 antibodies monocyte Fc-yRII are
• Over 90% of patients with LAP patients have high titers immensely increased in patients with aggressive
of serum IgG antibodies to A actinomycetemcomitans. periodontitis.
• This organism possesses several potent virulence
In generalized aggressive periodontitis, autoimmu-
factors responsible for neutrophil dysfunction and
nity plays an important role. Host antibodies to collagen,
bone destruction in LAP.
DNA, and IgG may be observed in patients with aggres-
• Sites with evidence of disease progression often show
sive periodontitis.
elevated levels of A actinomycetemcomitans.
• Elimination of A actinomycetemcomitans from periodon-
tal lesions by therapeutic measures is associated with Genetic Factors
clinical improvement.
• Aggressive periodontitis tends to occur in families,
suggesting a genetic basis to the disease.
Virulence Factors Produced by • The precise nature of any immune defect or the specific
A. actinomycetemcomitans gene that is inherited in families is not apparent
presently.
A. actinomycetemcomitans produces a variety of factors • Familial clustering of neutrophil abnormalities has
that can damage the periodontal tissues in LAP: been observed in LAP.
• A leukotoxin that can destroy polymorphonuclear • The specific gene, which is inherited in families,
leukocytes (PMNs) and macrophages varies in different populations and ethnic groups.
• Cytolethal distending toxin causes apoptosis of cells • It is believed that the response of antibody to the
• Chemotactic inhibition factor causative organism (A actinomycetemcomitans) is under
• A bone resorption-inducing toxin genetic control and may be race dependent.
• The true heterogeneity in disease susceptibility may be Other Features of GAP

present.
• Various single nucleotide polymorphisms of a specific • Unlike LAP, there is marked plaque and calculus
gene (e.g. Pc-v receptor Illb/Ilbgenes) can also be accumulation and clinical signs of gingival
responsible for development of AgP. inflammation are evident.
• The segregational and linkage analyses have shown that • It is a heterogeneous condition, and as such it is difficult
a major gene plays a role in LAP and it is transmitted to determine its presence.
through the autosomal dominant mode of inheritance. • The familial nature of the GAP is unclear.
• At present, the existence of a gene of major effect is • The subgingival flora of GAP is much more complex
accepted, although it is considered unlikely that all than seen in LAP.
forms of aggressive periodontitis are due to same • The microbial flora in GAP unlike LAP is not diagnostic,
genetic variant. since these pathogens can be isolated from other forms
of periodontal disease.
• The loss of attachment and alveolar bone destruction
Environmental Factors are episodic in nature.
• Antibody level to the causative organism is elevated
Recent evidence has indicated that besides genetic
but not diagnostic, since this immune response is not
influences, environmental factors may affect the clinical
evident in all patients.
expression of aggressive periodontitis.
• Neutrophil dysfunction may play a key role in the
• Cigarette smoking is an important environmental pathogenesis of GAP. Reports have shown that the
risk factor for developing a more severe periodontal neutrophils from these patients may exhibit decreased
breakdown in patients with localized and generalized AP. chemotaxis.
• The frequency and duration of smoking are the • Because of the similarities between the LAP and GAP,
important variables that can influence the extent of it is presumed that the generalized form may be the
destruction in GAP. continuation of the localized disease process.
• Smokers with GAP have more affected teeth and
greater attachment loss than the nonsmoker GAP
Radiographic Feature of GAP
patients. Smokers also demonstrate poorer clinical
response to treatment compared with nonsmokers. Radiographic picture can range from severe bone loss
• The protective antibody (IgG2) response to A. associated with minimal number of teeth to advanced
actinomycetemcomitans in GAP patients with smoking bone loss affecting majority of the teeth in the dentition
habits is significantly depressed. (Fig. 28.6).
• Psychological stress and depression have also been
proposed to act as an environmental risk factor for AgP.
Microbiology of GAP
1. P. gingivalis
GENERALIZED AGGRESSIVE 2. Tannerella forsythia
PERIODONTITIS (GAP) 3. A. actinomycetemcomitans
4. Campyobacter rectus
It was formerly called generalized juvenile periodon- 5. Eubacterium spp.
titis or rapidly progressive periodontitis. 6. Treponema spp.
• Usually the individuals are younger than 30 years of
age, but older patients may also be affected
• Poor serum antibody response to infecting agents
• Pronounced episodic nature of the attachment loss and
alveolar bone destruction
• Generalized interproximal attachment loss affecting at
least three permanent teeth other than the first molars
and incisors.
Epidemiology of GAP
The prevalence of GAP has been estimated to be 0.13%
varying according to geographic location, ethnicity, and FIGURE 28.6 Severe bone loss seen in generalized aggressive
race. periodontitis.
7. Microbes from the Archaea domain 4. Subgingival application of 1 % chlorhexidine
8. Selenomonas spp. solution into the full depth of periodontal
9. Treponema lecithinolyticum pockets, three times in 10 min
5. Rinsing of mouth with 0.2% chlorhexidine
mouthwash for 2 min
Risk Factors
Antibiotic therapy
Although patients suffering from aggressive peri- 1. Elimination of A actinomycetemcomitans (main
odontitis show minimal amount of plaque accumula- causative organism) is the mainstay of treatment
tion, the specific organisms present in the plaque may of aggressive periodontitis.
be associated with extensive destruction of periodontal 2. The tissue invasive property by A actinomycetem-
tissues. comitans in LAP markedly affects the overall
A consortium of multiple microorganisms living in treatment planning.
biofilms participate in the events leading to periodontitis. 3. Systemic antibiotics such as tetracyclines
However, it is clear that localized and generalized aggres- are effective in the treatment of LAP, when
sive forms of periodontitis are not monoinfections. There administered as an adjunct to scaling and root
is compelling evidence that some subgingival microor- planing or surgical therapy.
ganisms are more important than others. 4. 250 mg ofTetracycline HCl QID for 14 days, (after
systemic administration), shows 2-10 times more
concentration in GCF than in serum.
TREATMENT 5. Semisynthetic preparation of tetracycline,
Doxycycline 100 mg/ day for 2 weeks, has also
Early diagnosis of this disease is crucial because the been successfully tried in conjunction with
successful treatment and prognosis of aggressive peri- periodontal surgery in the treatment of LAP.
odontitis is considered to be dependent on meticulous 6. Metronidazole 200 mg, three times daily for
debridement of microbial plaque, elimination of caus- 10 days, in combination with scaling and root
ative microorganisms, and providing an environment planing has proven its efficacy in the eradication
conducive to long-term maintenance. The treatment of of A. actinomycetemcomitans.
aggressive periodontitis must be pursued with a logical 7. The combination of metronidazole 500 mg three
and regimented approach. times daily plus amoxicillin 500 mg three times
daily is probably the most popular antibiotic
regimen in the current literature.
Nonsurgical Treatment
8. Deas and Mealy (2010) recommended that
Phase-L therapy: antibiotic therapy should be started 24 h before
1. Motivation and education of the patient scaling and root planing.
2. Oral hygiene instructions (OHi) 9. Microbiological monitoring of the subgingival
3. Counseling of the family members because of its flora for A actinomycetemcomitans is a critical aid
familial pattern in the successful therapy of LAP.
4. Scaling and root planing Local drug delivery system: This mode of drug
5. Correction of anatomical factors administration, especially in LAP, is a useful
6. Occlusal adjustment alternative for systemic antibiotic therapy. The
7. Recall appointments for the maintenance. therapeutic advantages of local drug delivery are
Full mouth disinfection: It has been observed as follows:
that A. actinomycetemcomitans has a tendency of 1. It enhances the exposure of the target organisms
translocation from person to person and from with higher concentrations of the drug.
site to site and may reinfect the treated sites by 2. Smaller total doses of topical agents can be
translocation from the infected sites in the oral delivered inside the pocket, thereby avoiding
cavity. Hence, to prevent it, Quirynen et al. proposed the side effects of systemic antibacterial agents.
the concept of "Full Mouth Disinfection" which is 3. It helps in achieving the higher therapeutic level
carried out as follows: of medication.
1. Full mouth scaling and root planing (two visits Host modulation: The current approach in the
within 24 h) treatment of aggressive periodontitis includes the
2. Brushing of dorsum of tongue by the patient for administration of agents that modulate the host
60 s with 1 % chlorhexidine gel response to the disease. The administration of
3. Spraying of peritonsillar regions twice daily with subantimicrobial-dose doxycycline (SOD) may help
chlorhexidine to prevent the periodontal tissue destruction
by controlling the activation of matrix metallo Extraction of the hopeless teeth.

proteinases (MMPs). Implant therapy is a very useful treatment modality
Photodynamic therapy (PDT): Recently, PDT in aggressive periodontitis patients.
has gained much popularity as one of the most
effective broad-spectrum antibacterial therapy for
aggressive periodontitis. This procedure involves
Dental Implants
the eradication of target cells, i.e., periodontal Initially, the use of dental implants was recommended
pathogens by reactive oxygen particles produced with much caution in patients with aggressive periodon-
by means of photosensitizing compounds (e.g., titis because of the fear of bone loss. Currently, it is sug-
toluidine blue) instilled in periodontal pocket that gested that use of dental implants must be considered
is activated by laser. in the overall treatment plan of patients with aggressive
period on ti tis.
Surgical (Regenerative and Resective) Therapy
Modified Widman flap surgery supplemented with Periodontal Maintenance Care
systemic tetracycline therapy shows good results. Frequent recall visits of the aggressive periodontitis
Osteoctomy and osteoplasty: These are of limited patients are very important factors in the control of the
value in LAP patients because of the severity of disease and to prevent its further progression or its re-
disease. currence. Each recall visit at every 3-4 months should
Regenerative procedure: include a thorough medical history review, a comprehen-
- Flap surgery+ bone graft+ antibiotic therapy+ sive periodontal and oral examination, thorough scaling
maintenance therapy. and root planing, and reenforcement of oral hygiene in-
- Flap surgery+ bone graft+ GTR membrane+ structions. Yearly radiographic examination of the teeth
antibiotics+ maintenance therapy. at risk should be taken.
Root resection/hemisection of the affected first
molar tooth, depending on the indication. • Localized recurrence: SRP + local drug delivery
Autotransplantation: Extraction of the affected • Generalized recurrence: Full mouth SRP + systemic
mandibular first molar and simultaneous auto- antibiotics + host modulation therapy
transplantation of incompletely (90%) erupted • Extraction of teeth with progressive disease to preserve
third molar in the extraction socket. alveolar bone
KEY POINTS
• Aggressive periodontitis is defined as the rare form of • The commonest microorganisms implicated in the GAP
periodontitis occurring in an otherwise healthy young are as follows:
individual, and characterized by rapid loss of alveolar 1.P. gingivalis
bone in about more than one tooth of permanent denti- 2.A. actinomycetemcomitans
tion. The amount of bone destruction is inconsistent with 3.Tannerella forsythia (formerly Bacteroides forsythus).
the amount of local factors. • Actinobacillus actinomycetomcomitans was first isolated in
• There is a robust serum antibody response to the infect- 1912 by Klinger.
ing microorganism (A. actinomycetemcomitans). • Five serotypes (a, b, c, d, and e) of A. actinomycetemcomi-
• There is presence of vertical/ angular bone loss around tans have been identified. However, in LAP, serotype-b
the first molars and incisor teeth. is significantly elevated in the subgingival plaque.
• The prevalence of localized aggressive periodontitis varies • Cigarette smoking is an important environmental risk
in different parts of the world ranging from Oto 17%. factor for GAP. Metronidazole 500 mg + amoxicillin 500
• Neutrophil dysfunction may play a key role in the patho- mg three times per day for 7 days+ surgical therapy has
genesis of GAP. Reports have shown that the neutrophils shown promising results in the treatment of GAP.
from these patients may exhibit decreased chemotaxis.
QUESTIONS 8. Zambon JJ, Christersson LA, Slots J, et al. Actinobacillus
actinomycetomcomitans in human periodontal disease: prevalence
in patient groups and distribution of bio-types and serotypes within
1. Describe the etiology and clinical features of aggressive families. J Periodontol 1983;54:707-11.
periodontitis. 9. Deas DE, Mealey BL. Response of chronic and aggressive
2. Write a note on diagnosis and management of periodontitis to treatment. Periodontal 2000 2010;53:154-66.
aggressive periodontitis. 10. Lang NP, Bartold PM, Cullinan M, Jeffcoat M, Mombelli A, et al.
Consensus report: aggressive periodontitis. Ann Periodontology
3. Describe the clinical and radiographic features of
1999;4:53.
aggressive periodontitis. 11. Loe H, Brown LJ. Early onset periodontitis in the United States of
4. Describe the microbiology of aggressive periodontitis. America. J Periodontal 1991;62:608-16.
5. Write a note on current concepts in the management 12. Gjermo P, Bellini HT, Santos VP, Martens JG, Ferracyoli JR.
of aggressive periodontitis. Prevalence of bone loss in a group of Brazilian teenagers assessed
in bitewing radiographs. J Clin Periodontol 1984;11:104-13.
13. Saxby MS. Juvenile periodontitis: an epidemiological study in
Suggested readings the west Midlands of the United Kingdom. J Clin Periodontal
1987;14:594-8.
1. Armitage GC. Development of a classification system of periodontal 14. Macgregor ID. Radiographic survey of periodontal disease in 264
diseases and conditions. Ann Periodontol 1999;4:l-6. adolescent schoolboys in Lagos, Nigeria. Community Dent Oral
2. Baer PN. The case for periodontitis as a clinical entity. J Periodontal Epidemiol 1980;8:56-60.
1971;42:l-6. 15. Kowashi Y. Prevalence of juvenile periodontitis among students at
3. Butler JH. Familial pattern of juvenile periodontitis (periodont). J Nagasaki University. Adv Dent Res 1988;2:395-6.
Periodontol 1969;40:115-8. 16. Miglani DC, Sharma OP. Incidence of acute necrotizing ulcerative
4. Gottlieb B. The formation of the pocket: diffuse atrophy of alveolar gingivitis and periodontosis among cases seen at the government
bone. J Am Dent Assoc 1928;15:462-76. hospital Madras, India. J All India Dent Assoc 1965;37:183-202.
5. Orban B, Weinmann JP. Diffuse atrophy of alveolar bone. J Periodontal 17. Marshall-Day CD, Shourie KL. A roentgenographic survey of
1942;13 :31. periodontal disease in India. J Am Dent Assoc 1949;39:572-88.
6. Quirynen M, Bollen CM, Vandekerckhove BN, et al. Full vs. partial- 18. Rao SS, Tewani SV. Prevalence of periodontosis among Indians.
mouth disinfection in the treatment of periodontal infections: J Periodontol 1968;39:27-34.
short term clinical and microbiological observations. J Dent Res 19. Lopez NJ, Rios V, Pareja MA, Fernandez 0. Prevalence of juvenile
1995;74:1459. periodontitis in Chile. J Clin Periodontol 1991;18:529-33.
7. Thoma KH, Goldman HM. Wandering and elongation of the teeth
and pocket formation in paradontosis. J Am Dent Assoc 1940;27:335.
CHAPTER
29
Periodontal Abscess
CHAPTER OVERVIEW
A periodontal abscess is a localized purulent infection most frequently encountered dental emergencies. It is also
of the periodontal tissues that may lead to destruction of referred to as a lateral or parietal abscess.
periodontal ligament and alveolar bone and is one of the
CLASSIFICATION Depending on Number

1. Single periodontal abscess: They are usually related to
According to Location
local factors that contribute to the closure of the peri-
1. Abscess in the supporting periodontal tissues along odontal pocket.
the lateral aspect of the root. 2. Multiple periodontal abscess: They have been reported in
2. Abscess in the soft-tissue wall of the deep periodontal diabetes mellitus and medically compromised patients.
pocket.
According to Onset or Course of Lesion ETIOLOGY

1. Acute periodontal abscess: It appears as a bright red
Periodontal abscesses have been associated either
ovoid elevation of the gingiva, which may be rela- directly to periodontitis (periodontitis-related abscess)
tively firm or pointed and soft. In most instances, or to sites without the prior existence of a periodontal
pus may be expressed from the gingival margin by pocket (nonperiodontitis-related abscess).
gentle digital pressure. It is accompanied by symp-
toms such as throbbing, radiating pain, sensitivity
to percussion, tooth mobility, and, in some cases, Periodontitis-Related Abscess
lymphadenopathy and systemic effects such as fever
1. The existence of tortuous pockets, with cul-de-sac that
and malaise.
eventually becomes isolated, may favor the formation
2. Chronic periodontal abscess (Fig. 29.1): It usually presents
of abscess.
a sinus that opens onto the gingival mucosa some-
2. The marginal closure of the periodontal pocket may
where along the root length. It is usually asymptom-
lead to an extension of infection into the surrounding
atic. However, the patient may complain of intermit-
periodontal tissues due to the pressure of suppuration
tent exudation, dull gnawing pain, slight elevation of
inside the closed pocket.
the tooth, and a desire to bite down on and grind the
3. The development of periodontal abscess in periodon-
tooth.
titis may occur at different stages during the course of
Acute lesions often subside but persist in the chronic the infection as an exacerbation of an untreated peri-
state, whereas chronic lesions may exist without being odontitis, during periodontal therapy, in refractory
acute. Chronic lesions frequently undergo acute exacer- periodontitis, or during periodontal maintenance. Also,
bation. fibrin secretions, leading to the local accumulation of
CHAPTER 29 PERIODONTAL ABSCESS 235
released by the bacteria, and the concomitant inflammatory
reaction leads to destruction of the connective tissues, the
encapsulation of the bacterial infection, and the produc-
tion of pus.
Histologically, intact neutrophils are found surround-
ing a central area of soft-tissue debris and destroyed leu-
kocytes. At a later stage, a pyogenic membrane composed
of macrophages and neutrophils is organized. An acute
inflammatory reaction surrounds the purulent area, and
the overlying epithelium exhibits intracellular and extra-
cellular edema and invasion of leukocytes. Gram-negative
bacteria may be seen invading the pocket epithelium and
the altered connective tissue.
DIAGNOSIS
FIGURE 29.1 Chronic periodontal abscess.
The diagnosis of the periodontal abscess requires cor-
pus, may favor the closure of gingival margin to the relation of the history, and clinical and radiographic find-
tooth surface. ings. The dental history can provide information about
4. Changes in composition of the microflora, bacterial previous periodontal treatments, endodontic therapy,
virulence, or host defenses could also make the pocket and previous abscesses.
lumen inefficient to drain the increased suppuration. The suspected area should be carefully probed
5. Treatment with systemic antibiotics without subgingi- (Fig. 29.2). Continuity of the lesion with the gingival
val debridement in patients with advanced periodon- margin serves as the clinical evidence that the abscess
titis may also cause abscess formation. is periodontal. Other findings are ovoid swelling of the
6. Abscess can form due to inadequate scaling which will gingiva, pain, tooth mobility, tooth elevation, suppura-
allow calculus to remain in the deepest pocket area, tion, either spontaneous or on digital pressure, and the
whereas the resolution of the inflammation at the coro- presence of deep periodontal pockets. Radiographically,
nal pocket area will occlude the normal drainage, and it appears as a discrete area of radiolucency along the lat-
entrapment of the subgingival flora in the deepest part eral aspect of the root. However, lesions in the soft-tissue
of the pocket. Also, calculus might get dislodged and wall of a periodontal pocket are less likely to produce
pushed into the soft tissue after procedures like scaling. radiographic changes than those deep in the supporting
tissues. Similarly abscesses on the facial or lingual sur-
faces are obscured by the radiopacity of the root.
N onperiodontitis- Related Abscess Also in the early stages, the acute periodontal abscess is
1. Impaction of foreign bodies, such as a toothbrush bristle, extremely painful but presents no radiographic changes.
a piece of dental floss, orthodontic elastic, a dislodged
cemental tear, food (such as fish bone) into the gingival
tissue, etc., can result in abscess formation. Periodontal
abscesses caused by foreign bodies, related with oral hy-
giene aids, have been named "oral hygiene abscesses".
2. Lateral perforation of the root during endodontic ther-
apy and trauma to the tooth.
3. Local factors affecting morphology of roots such as
cemental tears, external root resorption, invaginated
tooth, and cracked tooth may predispose to periodon-
tal abscess formation.
PATHOGENESIS AND HISTOPATHOLOGY
The entry of bacteria into the soft-tissue pocket wall

could be the first event to initiate the periodontal abscess.
Inflammatory cells are then attracted by chemotactic factors FIGURE 29.2 Diagnosis of periodontal abscess.
TABLE 29.1 Differentiation Between Gingival and Periodontal periodontal pockets, the location of abscess, and a careful
Abscess radiographic examination. It is differentiated from gingi-
Gingival abscess Periodontal abscess val abscess (Table 29.1) and periapical abscess (Table 29.2),
It is confined to the marginal It involves the supporting
which are the other abscesses found in the oral cavity that
gingiva periodontal structures have similar appearance and symptomatology, although
their etiologies are different.
It often occurs in former disease- It occurs in the course of chron-
free areas ic destructive periodontitis
It is an acute inflammatory The occlusion of the orifice of a

response that results when a preexisting periodontal pocket TREATMENT
foreign object (apple core, lobster prevents drainage of the puru-
fragment) is forcefully embedded lent material leading to abscess
into the gingiva formation Periodontal abscesses most often present as a painful
dental emergency. The patient should be treated immedi-
Treatment involves only drainage Treatment involves drainage,
and irrigation irrigation, and pocket elimina-
ately to relieve pain and resolve the infection, which may
tion procedure spread and lead to periodontal attachment loss.
Thus, the radiographic examination may reveal a

Treatment of Acute Periodontal Abscess
normal appearance or some degree of bone loss ranging
from a widening of the periodontal space to a dramatic It usually includes two stages:
radiographic bone loss especially with interproximal
1. The management of the acute lesion.
lesions.
2. The appropriate treatment of the residual lesion, once
the acute situation is under control.
DIFFERENTIAL DIAGNOSIS Establishing drainage of the lesion is one of the first
lines of treatment of the acute abscess. The affected area
The differential diagnosis of periodontal abscesses is anesthetized, and a flat instrument or probe is care-
should be made using different signs and symptoms, fully introduced into the pocket in an attempt to distend
such as pulp vitality, the presence of dental caries versus the pocket wall. A small curette can then be gently used
to penetrate the tissues and establish drainage. The root
TABLE 29.2 Differentiation Between Periapical and Periodontal surface is then thoroughly root planed to eliminate plaque
Abscess and calculus.
When drainage cannot be easily established via the
Periapical abscess Periodontal abscess
pocket or when the abscess can be seen pointing through
Pain may be sharp, intermittent, The pain is usually dull, steady, the gingiva, an external incision is indicated. With a No.
throbbing, severe, and diffuse and continuous
11 BP blade, a vertical incision is made at most fluctuant
Pain is not always localized, and The pain is localized, and the point. After the initial extravasation of blood and pus, the
the patient may not be able to patient usually can locate the area is irrigated with an antiseptic agent and the incision
locate the offending tooth offending tooth
is gently spread to facilitate drainage.
Vitality test does not show vital Vitality test shows vital pulp After therapy, the patient is instructed to rinse with
pulp warm saline and be examined for resolution of the abscess
The tooth is painful to percus- The tooth is usually not as after 24-48 h.
sion or with movement painful to percussion or with In the absence of systemic symptoms, antibiotic thera-
movement py is seldom recommended. Systemic antibiotics should
The abscess may be associated The abscess is associated with a be considered only if the patient has lymphadenopathy,
with deep restoration preexisting periodontal pocket, fever, and/ or malaise.
caries, or both The symptoms invariably disappear by 1 week and
Swelling usually present in api- Swelling usually includes the lesion is ready for the usual treatment of a chronic
cal area and sinus tract forma- gingival tissue and fistula tract periodontal abscess.
tion is common is uncommon
Clinically may have no peri- Unclinically there is presence of Treatment of Chronic Periodontal Abscess
odontal pocket, or if present, periodontal pocket; and radio-
probes as narrow defect graphically there is presence of The chronic periodontal abscess is usually asymptom-
vertical or argular bone loss or atic and the treatment is similar to the elimination of a
fuscation radiolucency
periodontal pocket by flap technique.
CHAPTER 29 PERIODONTAL ABSCESS 237
PERIODONTAL CYST followed by the anterior maxilla. It does not present dis-
tinct clinical symptoms except sometimes as a localized
The lateral periodontal cyst is an uncommon but well- tender swelling in the gingiva. The tooth is vital unless it
recognized type of developmental odontogenic cyst. The is secondarily infected; hence, the lesion is often reported
pathogenesis is still not very clear. It could be due to three mainly on routine radiographic examination. Radiographs
reasons: the dental lamina, the epithelial cell rests of Mal- depict a well-circumscribed, ovoid or round, radiolucent
assez, and the reduced enamel epithelium. The most com- zone surrounded by a sclerotic border, which cannot be
mon location of the cyst is the mandibular premolar area sometimes differentiated from the periodontal abscess.
KEY POINTS
• A periodontal abscess is a localized purulent infection of • Treatment of acute periodontal abscess usually includes
the periodontal tissues and is one of the most frequently two stages: the management of the acute lesion and
encountered dental emergencies. the appropriate treatment of the residual lesion once the
• In a periodontal abscess, the pain is usually dull, steady, acute situation is under control.
and continuous.
2. Dahlen G. Microbiology and treatment of dental abscess and peri-

QUESTIONS odontal-endodontic lesions. Periodontology 2000 2002;28:206.
3. Gillette WB, Van House RL. Ill effects of improper oral hygiene
1. Differentiate between periodontal and periapical procedures. J Am Dent Assoc 1980;101:476-81.
abscess. 4. Herrera D, Roldan S, Sanz M. The periodontal abcess: a review. J Clin
2. Write a short note on gingival abscess. Periodontal 2000;27:377.
5. Herrera D, Roldan S, Gonzalez I, Sanz M. The periodontal abscess.
3. Describe etiological factors considered in a Clinical and microbiologic findings. J Ciin Periodontal 2000;27:287.
periodontal abscess. 6. Herrera D, Silvia Rolda'N, Sanz M. The periodontal abscess - a
4. Write a short note on periodontal cyst. review. J Clin Periodontal 2000;27:377-86.
7. Lindhe J, Lang N, Karring T. Clinical Periodontology and Implant Den-
tistry. 5th ed. Blackwell Munksgaard; 2008.
Suggested readings 8. Meng HX. Periodontal abscess. Ann Periodontol 1999;4:79.
1. Corbet EF. Diagnosis of acute periodontal lesions. Periodontology 2000 Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B.
2004;34:204. Saunders Company; 2006.
CHAPTER
30
AIDS and Periodontium
CHAPTER OVERVIEW
In December 1981, there was a report about a group 1976 with lesions typical of AIDS. His wife had signs sug-
of 7 men who had severe infections with microorganisms gestive of HIV infection since 1967 and she died of AIDS in
that had previously infected only profoundly immuno- 1976. Their daughter, born in 1967, got symptoms in 1969
logically compromised individuals. Soon this disease and died in 1976. Frozen serum samples of all three were
came to be known as the acquired immunodeficiency syn- positive for HIV type 1 (HIV-1).
drome (AIDS). In May 1983, a new T-lymphotropic retrovirus was iso-
The first report on AIDS appeared in June 1981, in the lated by French investigators from a patient with lymph-
Morbidity and Mortality Weekly Report. However, cases of adenopathy. It was called lymphadenopathy-associated
AIDS before 1981 have been identified in retrospect. A virus (LAV). Some months later, American investigators
Danish woman who had evolved as a surgeon in Zaire isolated a virus from AIDS patients, which they named
since 1972 was flown home to Denmark in 1977 with an human T-cell lymphotropic virus type III (HTLV-III). Sub-
undetermined illness characterized by chronic diarrhea sequent studies have shown that LAV and HTLV-III are the
and lymphadenopathy, and after a few months, she died. same virus. In 1986, the AIDS retroviruses were officially
Her lung disease afterward proved to have been a Pneu- termed the human immunodeficiency virus, to be known
mocystis carinii infection, and it is suggested that she had in abbreviated form as HIV. The original form of HIV is
AIDS. There was also a report on a Norwegian sailor who now known as HIV-1, while the similar virus found pre-
had possible HIV-associated symptoms in 1966 and died in dominantly in West Africa is known as HIV type 2 (HIV-2).
DEFINITION OF AIDS animal populations. It is not likely that HIV caused dis-
ease in humans for many years before the onset of the
According to the World Health Organization (WHO)/ AIDS epidemic.
Centers for Disease Control and Prevention (CDC) case Some links have been drawn between AIDS and the
definition of AIDS, a case of AIDS is defined as a reliably African green monkey, which carries a virus closely related
diagnosed opportunistic disease in an adolescent or an to HIV that, however, does not cause disease in this spe-
adult at least moderately indicative of underlying cellular cies. As such the origin of HIV is not known, but a primate
immunodeficiency with no other known cause or any origin is suggested and appears likely, particularly for HIV-
other reduced resistance reported to be associated with 2. The origin of HIV-1 is more difficult to understand. The
an opportunistic disease, including secondary immuno- existence of animal lentiviruses with a predilection for the
deficiencies associated with immunosuppressive therapy, CD4+ T lymphocytes strongly suggests an animal origin
lymphoreticular malignancy, or starvation. for this virus also. However, it has been proposed that the
nonpathogenic precursor of HIV-1 has infected humans for
a long period, and that relatively recently it mutated to be-
HUMAN IMMUNODEFICIENCY VIRUS come the pathogenic virus that causes AIDS. HIV belongs
to the family of lentiviruses. As the name implies, infec-
The appearance of truly new organisms is extreme- tions caused by lentiviruses progress slowly with long
ly rare. New infectious agents do not arise in a vacu- incubation periods. After the initial recovery of viruses
um but evolve from preexisting ones, usually among from lymph nodes, HIV was isolated from peripheral
C H A PTER 30 A ID S A N D PERIO DO N T IU M 239
blood mononuclear cells (PBMCs) both in patients with of the disease as the immune system restricts the virus
clinical manifestations of AIDS and in patients without to the lymphoid tissues and hence the damaging
any clinical signs or symptoms. capacity of the virus is limited.
To distinguish between these two viruses, the initial 3. Intermediate immune deficiency (CD4 cell count 200-
HIV was named HIV-1, while the second virus was called 500 / mL): In this stage viral replication is very high
HIV-2. The course of the disease appears to be much lon- and CD4 cell turnover is rapid. Signs and symptoms
ger with HIV-2. indicating a compromise of the immune system begin
to appear.
4. Advanced immune deficiency (CD4 cell count
Life Cycle of HIV .:::;200/mL): The virus overcomes the immune system
HIV is transmitted by exchange of blood or body flu- and proliferates throughout the body. This results
ids. Once inside the host, the virus seeks or binds to the in the occurrence of opportunistic infections and
CD4 molecule of T-helper cells and other target cells. malignancies which require medical intervention.
These include bone marrow stem cells, macrophages,
endothelial cells, glial cells, lymph nodes, dendritic cells, Human Cells/Cell Lines and Tissues Susceptible
bowel enterochromaffin cells, cervical epithelium, and to HIV
possibly Langerhans cells. However, it is the effects of
HIV on T-helper cells that are the best known and that The extent of replication of HIV varies in different cells,
probably play a major role in the pathogenesis of HIV although it can multiply in all the cells.
disease, including AIDS. Binding of HIV to CD4+ target • Hematopoietic system: In the hematopoietic system the
cell involves interaction of the external envelope glyco- virus affects "T" and "B" lymphocytes, macrophages,
protein molecule gp120 with the CD4 molecule, although natural killer (NK) cells, megakaryocytes, dendritic
other cell receptors may be involved. This interaction can cells, promyelocytes, stem cells, thymic epithelium,
involve free viral particles, but direct cell-to-cell spread of and follicular dendritic cells.
HIV may also occur. The virus next enters the target cell, • Brain: In the brain the cells affected are the
or is internalized, through fusion of the viral envelope oligodendrocytes, choroid plexus, ganglia, neurons,
with the target cell membrane. and capillary endothelial cells.
Next, the viral RNA is subjected to reverse tran- • Skin: In the skin the fibroblasts and Langerhans cells
scription. This involves the production of a single- are affected and in the bowel the columnar and goblet
stranded DNA copy of the viral RNA and the destruc- as well as the colon carcinoma cells are affected.
tion of the viral RNA. A second strand of DNA is then • Others: The other cells which are affected include the
synthesized. cells of myocardium, prostate, testes, retina, synovial
The linear double-stranded DNA becomes circular membrane, cervix epithelium, and placental trophoblasts.
and then integrates into host chromosomal DNA. Here
the proviral DNA can remain latent for the lifetime of the Modes of Transmission of HIV
host cell. Alternatively, it can generate new viral RNA and
hence HIV virions. The transmission of HIV still remains the primary con-
Virions are assembled in the cytoplasm and eventually cern for dental providers who treat infected patients. The
bud from the cell surface. The processes of viral latency fear of contracting HIV is also a major concern in the com-
and replication are controlled in part by the HIV regula- munity at large, and providers need to be well informed
tory genes, acting directly or through the actions of host regarding known modes of transmission.
cell factors. There are three principal modes of HIV transmission:
through sexual contact, through exposure to infected
blood and blood products, and through perinatal contact
Stages of HIV Infection from infected mothers to their children. Other possible
routes of transmission of concern to dental health care
HIV infection can be described in four stages:
providers include saliva and cross-contamination with
1. Primary infection: In this stage there is a rapid spread of dental hand pieces.
the virus through the blood and lymph nodes. There is
a rapid decline of the CD4 cell count, which later comes Documented and Undocumented Modes of HIV
back to normal when the virus is controlled by the Transmission
immune system. This is referred to as seroconversion • Documented modes of transmission:
illness, and it usually resolves within weeks. Sexual transmission
2. Early immune deficiency (CD4 cell count >500/mL): In Exposure to blood and blood products
this stage the patients are without any active symptoms Vertical transmission from mother to fetus/ child
• Undocumented modes of transmission are probably the first ones to suspect this infection in the
Aerosol patients because many of the oral manifestations may
Dental rotary instrument herald or form a hallmark diagnostic sign of this disease.
Tears Dental surgeons during their clinical practice can come
Urine across not only patients with AIDS but also cases with the
Sweat AIDS-related complex (ARC) and those who are seroposi-
Hepatitis B vaccine tive for HIV but are without any syndromes currently.
Insect bites As known today the HIV affects the CD4 receptors of
Casual contact. the helper T lymphocytes, which form the major interlink
between cell-mediated and humoral immunity, thus result-
ing in serious deficiency of these immune responses of the
CLASSIFICATION AND STAGING body. The oral mucosa and periodontal structures, which
are under constant threat of infections, also get affected
In 1982 the CDC developed a surveillance case defi- because of this deficient immune status. This occurs due
nition for AIDS based on the presence of opportunistic to setting in of various opportunistic infections, and also
illnesses or malignancies secondary to defective cell-me- exacerbations of existing infections leading to an increased
diated immunity in HIV-positive individuals. This defini- pathological destruction of these otherwise healthy tissues.
tion was further expanded in 1985, 1987, and 1993. The
most significant change in the new CDC case definition
was the inclusion of severe immunodeficiency (CD4-T4 GENERAL CLINICAL SIGNS
lymphocyte count of less than 200/mm3 or a T4 lympho- IN AIDS PATIENT
cyte percentage of less than 14% of total lymphocytes) as
definitive for AIDS. This change was based on recogni- 1. Lymphadenopathy or swollen glands
tion that severe immunodeficiency results in increased 2. Unexpected and unexplained loss of appetite and
risk for opportunistic life-threatening conditions. bodyweight
3. Weakness in the legs and difficulty in climbing the
stairs
CDC Surveillance Case Classification ( 1993) 4. Unexpected fever of I-week duration or more
• Category A: It includes patients with acute symptoms 5. Night sweats
or asymptomatic diseases, along with individuals 6. Persistent and unexplained diarrhea
with persistent generalized lymphadenopathy, with 7. Persistent dry cough that cannot be explained by
or without malaise, fatigue, or low-grade fever. smoking or seasonal allergic manifestation
• Category B: Patients have symptomatic conditions 8. White patches in the mouth
such as oropharyngeal or vulvovaginal candidiasis; 9. Hairy leukoplakia
herpes zoster; oral hairy leukoplakia; idiopathic 10. Shingles
thrombocytopenia; or constitutional symptoms of 11. Lymphoma.
fever, diarrhea, and weight loss. The following are the most common opportunistic
• Category C: Patients are those with outright AIDS as infections:
manifested by life-threatening conditions identified
by CD4+ T4 lymphocyte levels of less than 206/mm3. 1. Cryptococcal meningitis
2. CNS toxoplasmosis
These staging categories reflect progressive immuno- 3. P. carinii pneumonia
logic dysfunction, but patients do not necessarily progress 4. Cryptosporidiosis
serially through the three stages, and the predictive value 5. Kaposi sarcoma
of these categories is not known. 6. Tuberculosis
7. Herpes simplex viruses
8. Mycobacterium avium-intracellulare.
ORAL AND PERIODONTAL
MANIFESTATIONS OF AIDS
CLASSIFICATION OF ORAL LESIONS
AIDS, as we are aware, is a multiple disease complex ASSOCIATED WITH HIV INFECTION
syndrome affecting almost every system of the body. The
oral cavity and periodontal structures have been found to The oral manifestations of HIV infection are classified
be affected more frequently with various opportunistic in- based on the clinical appearance of the lesion and also
fections that result from immunodeficiency caused by the on the basis of definitive criteria which is the result of
virus. It is not surprising that nowadays, dental surgeons investigations.
Group 1: Lesions Strongly Associated ERYTHEMATOUS CANDIDIASIS

with HIV Infection This form of candidiasis presents as red areas. It is
occasionally mixed with white spots. High rate of oc-
1. Candidiasis:
currence is seen on the palate and dorsum of the tongue
a. Erythematous
(Figs 30.1 and 30.2).
b. Pseudomembranous
2. Hairy leukoplakia PSEUDOMEMBRANOUS CANDIDIASIS
3. Kaposi sarcoma
• The condition is characterized by presence of white or
4. Periodontal disease
yellow spots or plaques.
a. Linear gingival erythema
• When removed, it leaves a red bleeding surface.
b. Ulcerative necrotizing gingivitis
• Definitive criteria include response to antifungal
c. Ulcerative necrotizing periodontitis
therapy.
5. Non-Hodgkin lymphoma.
• C. albicans is detected by smear culture.
Angular Cheilitis
Group 2: Lesions Less Commonly Associated • This is another form of oral candidiasis (Fig. 30.3).
with HIV Infection • It is seen as redness, cracking, or fissuring of
the commissural region. It may be unilateral or
1. Infections of bacterial origin
bilateral and can be seen associated with other oral
2. Hyperpigmentation of oral mucosa
manifestations.
3. Ulcerative necrotizing stomatitis
4. Oral conditions
a. Decreased salivary flow leading to dry mouth
b. Swelling of major salivary glands
5. Thrombocytopenic purpura
6. Nonspecific ulcerations
7. Infections of viral origin
a. Herpes simplex virus
b. Human papilloma virus
c. Varicella zoster virus
d. Herpes zoster virus
e. Varicella virus.
Group 3: Lesions which May Occur in HIV

Infection
1. Bacterial infections such as E.coli FIGURE 30.1 Candidiasis seen on the buccal mucosa in HIV patient.
2. Adverse drug reactions
3. Fungal infections of candidal origin
4. Neurologic disturbances
a. Facial palsy
b. Trigeminal neuralgia
5. Recurrent aphthous stomatitis
6. Infections of viral origin such as
a. Cytomegalovirus.
Candidiasis
• Oral candidiasis is a common early manifestation of
HIV infection caused predominantly due to Candida
albicans.
Commonest forms of Candida infections are as follows:
• Erythematous candidiasis
• Pseudomembranous candidiasis
• Angular cheilitis. FIGURE 30.2 Candidiasis seen on the gingiva in HIV patient.
FIGURE 30.3 Angular cheilitis. FIGURE 30.4 Necrotizing ulcerative gingivitis.
Periodontal Diseases NECROTIZING ULCERATIVE PERIODONTITIS

HIV-related periodontal disease includes three • NUP is characterized by generalized aggressive alveolar
conditions: bone loss and attachment apparatus destruction
(Fig. 30.5).
a. Linear gingival erythema • There is also deep-seated pain, spontaneous gingival
b. Necrotizing ulcerative gingivitis (NUG) bleeding, halitosis, and tooth mobility.
c. Necrotizing ulcerative periodontitis (NUP).
Viral Infections
NUG, NUP, and necrotizing stomatitis (NS) may be col-
lectively referred to as necrotizing gingivostomatitis (NG). HERPETIC GINGIVOSTOMATITIS
• Viral shedding into the oral environment is common
in immunosuppressed patients.
STAGING OF NECROTIZING GINGIVOSTOMATITIS
• The condition is characterized by gingival, palatal,
Staging of NG infections was proposed by Pindborg, dorsal tongue, and occasionally mucosal vesicles.
who described four stages: These rupture and leave painful, irregular one to two
1. Tip of the interdental papilla is affected. ulcers often in clusters.
2. Punched-out lesions of the interdental papilla are
confined to the marginal gingiva. VARICELLA ZOSTER INFECTIONS (HERPES ZOSTER
3. Lesions extend to the attached gingiva also. AND VARICELLA)
4. Underlying bone is exposed. • This disease manifests as a unilateral occurrence of
vesicles or ulcers in the area which is innervated by the
LINEAR GINGIVAL ERYTHEMA
• This is characterized by red to bluish red, edematous
gingival tissue.
• It usually appears with enlarged interdental papillae
and tendency to bleed easily.
• Significantly more bleeding sites and destruction of
interdental papillae are present in HIV-seropositive
patients.
NECROTIZING ULCERATIVE GINGIVITIS

• Necrotizing ulcerative gingivitis (NUG) in HIV patients
is seen as fiery red and enlarged gingiva with necrosis
and loss of interdental papilla (Fig. 30.4).
• The condition has extremely fast rate of progression
with destruction of the periodontal tissues and is
associated with severe pain. FIGURE 30.5 Necrotizing ulcerative periodontitis.
branch of the trigeminal nerve. The disease extends to
the bone leading to osteonecrosis, and is an extremely
painful condition.
MOLLUSCUM CONTAGIOSUM
• It is an infection of skin caused by a pox virus.
• Lesions are shiny, white, and hemispherical, and grow
up to 0.5 cm.
• Facial skin is commonly involved.
HAIRY LEUKOPLAKIA
• Hairy leukoplakia is seen in about one-fourth of HIV-
infected persons (Fig. 30.6).
• It is characterized by the presence of white to gray FIGURE 30. 7 Xerostomia in an AIDS patient.
lesions.
• It is seen on the lateral borders of the tongue usually
bilaterally and cannot be scraped off. • Kaposi sarcoma is usually seen as a red purple or bluish
• The lesions can extend to the ventral and dorsal patch, which later presents as nodules resembling
surfaces of the tongue, and may also involve the buccal hemangiomas or a peripheral giant cell granuloma.
mucosa. • It is initially seen in the subepithelial connective tissue.
• As the tumor progresses, pathological changes can
occur in the bone and other periodontal tissues.
XEROSTOMIA
• Some HIV-infected persons in an early stage of infection
experience xerostomia (Fig. 30.7). INVESTIGATIONS
• The xerostomia may be a complication of the prescribed
medications for the patients which may be xerostomic HIV Antibody Diagnosis
in nature.
• HIV salivary gland disease in HIV patients has been Testing for HIV antibodies invariably necessitates the
described as Sicca-type syndrome. It is associated with availability of at least two different assays:
diffuse infiltrative CDS lymphocytosis. • A screening test
Nonquantitative detection
KAPOSI SARCOMA Enzyme-linked immunosorbant assay (ELISA)
• It is a malignancy associated with HIV (Fig. 30.8). • A confirmatory test
• Oral Kaposi sarcoma typically presents as red-bluish Western blot assay
swellings with or without ulceration. DNA polymerase chain reaction (PCR)
• It is most common on the palate, gingiva, and dorsal Viral culturing
tongue. HIVDNAPCR
FIGURE 30.6 Hairy leukoplakia seen on the tongue. FIGURE 30.8 Kaposi sarcoma of palate.
• Rapid HIV antibody test Ritonavir

The single-use diagnostic system (SUDS) Indinavir
• Viral load Nelfinavir
Reverse transcriptase PCR (RT-PCR) • Integrase inhibitors:
Nucleic acid sequence-based amplification Agents that block the assembling of the virus and
(NASBA). their budding.
HAART
MANAGEMENT OF HIV/AIDS
ANTIRETROVIRAL TREATMENT Highly active antiretroviral therapy (HAART) is a type
of treatment procedure where a combination of three or
Antiretroviral drugs are agents that help to delay the more antiretroviral drugs are given in combination, over
progression of the disease from HIV to AIDS. This helps to a prolonged period of time in an effort to block the repli-
increase the life span of patients and provide a good quality cation of the HIV virus and improve the immune status
of life for them. Several advances have been made in the of the individual.
antiretroviral treatment protocols and their effectiveness NNRTI are used in combination with NRTI and PI.
has been well documented, during the last three decades. Although it was suggested initially that HAART should
not be administered until significant immune suppression
occurred, currently it is suggested that early treatment is
Antiretroviral Drugs more successful in HIV patients than delayed treatment.
The antiretroviral agents act at different stages of the HAART has been shown as a very successful treat-
life cycle of the HIV: ment protocol in reversing the immune suppression and
increasing the life expectancy in many individuals using
1. By blocking binding of HIV to the target cell
the therapy. However, HAART is seen to be not very
2. By blocking the viral RNA cleavage
effective in individuals with AIDS (before initiation of
3. By inhibiting the enzyme reverse transcriptase.
the therapy) and in those with a high viral load before
Qualities of an Ideal Antiretroviral Drug initiation of the therapy, noncompliance with the drug
regimen, injected drug abusers, patients with various
1. It should act on the specific organisms. bacterial, viral, or fungal infections, and various systemic
2. It should reduce viral production from infected cells. diseases.
3. It can be preferably administered orally.
4. It should penetrate the blood-brain barrier easily.
5. It should not develop resistance to the organism easily. INFECTION CONTROL MEASURES WITH
6. It should not be toxic to the tissues. A FOCUS ON THE DENTAL SETTING
However, none of the antiretroviral drugs available
today fulfill all these properties. Dental patients and dental health care personnel (DH-
CP) can be exposed to numerous pathogenic organisms,
Classification of Antiretroviral Drugs including the HIV.
• Inhibitors of viral attachment HIV can be transmitted in dental settings through
• Recombinant soluble CD4 (rsCD4) or immunoglobulins 1. Direct contact, e.g., blood, oral fluids, or patient
• Reverse transcriptase inhibitors: materials
Nucleoside analog RT inhibitors (NRTI) 2. Indirect contact, e.g., contaminated objects such as
- Dideoxythymidine (AZT) or zidovudine (ZDV) instruments and equipment
- Dideoxycytidine (ddl) or didanosine 3. Contact of mucosal surfaces, nasal, oral, or conjunctiva!
- Dideoxyinosine (ddC) or zalcitabine with droplets containing microorganisms from an
- Dideoxyadenosine (ddA) infected individual.
- Didehydrodeoxythymidine (D4T) or stavudine
- Deoxythiacytidine (3TC) or lamivudine Infection by any of the above mechanisms requires the
Non-nucleoside analog RT inhibitors (NNRTI) following conditions:
- Nevirapine 1. Adequate number of pathogenic organisms having
- Delavirdine sufficient virulence
- Thiobenzimidazoline derivatives 2. An area or medium that allows the pathogen to multiply
- Efavirenz (Sustiva) 3. A mechanism for transmission to the host
• Protease inhibitors (Pl): 4. A source of entry into the host for the pathogen
Saquinavir 5. A susceptible host.
If these events occur, it leads to infection. Infection appliances should be cleaned and disinfected each time
control strategies are designed to prevent disease trans- they are taken out from the patient's mouth and before
mission by interrupting one or more links in the chain, being handled in the dental laboratory. The disinfection
thus breaking the chain of infection and nullifying the procedures for each material should be carried out in
virulence of the organisms. accordance with the manufacturer's instructions.
4. Dental light handles, X-ray unit heads, and other
surfaces that are difficult to disinfect should be
PRECAUTIONS FOR DENTISTS completely wrapped in an aluminum foil or a clean
plastic wrap. After use with every single patient it
All oral fluids such as saliva, gingival crevicular fluid should be discarded and a new covering must be put
(GCF), and also blood from dental patients should be in its place.
considered infective. The following precautions should
be taken for preventing transmission of blood-borne
pathogens in dental practice:
STERILIZATION AND DISINFECTION
1. Surgical gloves, surgical masks, and protective eyewear
during all dental procedures where splashing of saliva The following are the methods to be used for steriliza-
and blood is likely. Rubber dams and high-speed tion:
evacuation, and also proper patient positioning, should
be used to minimize generation of droplets and spatter. 1. Sterilization
2. Handpieces should be flushed, cleaned with a chemical a. Boiling for 20-30 min
disinfectant, and then sterilized, after use with every b. Dry heat at 170°C for 1 h
patient. This is necessary as oral fluids such as saliva, c. Autoclaving at 121 °C, 15 lb pressure for 20 min
GCF, and blood can be aspirated into the handpiece. 2. Chemical disinfection is done by the following
Follow manufacturer's instructions for maintenance procedures:
of dental waterlines. The above precautions should be a. Ethanol: 70%
followed for ultrasonic scalers and air/ water syringes b. Formalin: 3-4%
also. c. Glutaraldehyde: 2% for 30 min
3. Oral fluids such as saliva and blood must be removed d. Povidone iodine
from the materials used in the mouth such as impression e. Calcium hypochlorite: 1.4 g/L
materials and also from intraoral devices such as £. Sodium hypochlorite: 5 g/L
acrylic appliances. These contaminated materials and g. Chloramine: 20 g/L.
KEY POINTS
• HIV is transmitted by exchange of blood or body flu- 2. NUG
ids. Once inside the host, the virus seeks or binds to 3. NUP
the CD4 molecule of T-helper cells and other target Testing for HIV antibodies invariably necessitates the
cells. availability of at least two different assays:
• Lesions strongly associated with HIV infection: 1. A screening test:
1. Candidiasis: a. Nonquantitative detection
a. Erythematous b. ELISA
b. Pseudomembranous
2. A confirmatory test:
2. Hairy leukoplakia a. Western blot assay
3. Kaposi sarcoma b. DNAPCR
4. Non-Hodgkin lymphoma c. Viral culturing
5. Periodontal diseases: d. HIV DNA PCR
a. Gingival erythema - linear
b. Ulcerative necrotizing gingivitis 3. Rapid HIV antibody test:
c. Ulcerative necrotizing periodontitis a. The SUDS
• HIV-related periodontal disease includes three 4. Viral load:

conditions: a. RT-PCR
1. Linear gingival erythema b. NASBA
QUESTIONS 3. Eley BM, Manson JD. Periodontics. 5th ed. Bristol: Wright; 2004.
4. Genco RJ, Goldman HM, Cohen DW. Contemporary Periodontics.
St. Louis: Mosby-Year Book; 2004.
1. Describe in detail the oral and periodontal 5. Laskaris G, Scully C. Periodontal Manifestations of Local and Systemic
manifestations in AIDS patients. Diseases: Colour Atlas and Text. New York: Springer; 1990.
2. Short essays: 6. Lindhe J, Karring T, Lang NP. Clinical Periodontologu and Implant
a. Kaposi sarcoma Dentistry. 4th ed. New York: Wiley-Blackwell; 2003.
7. Rateischak KH. Colour Atlas of Dental Medicine. Stuttgart: Thieme;
b. Elaborate on the precautions to be taken when
1989.
treating a patient with HIV infection. 8. Rose LF, Genco RJ, Mealey BL, Cohen DW. Periodontal Medicine.
Hamilton: BC Decker; 2000.
9. Rose LF, Mealey BL. Periodontics - Medicine, Surgery and Implants.
Suggested readings St. Louis: Mosby; 2004.
1. Axelsson P. Diagnosis and Risk Prediction of Periodontal Diseases, 10. Seymour RA, Heasman PA. Drugs, Diseases and the Periodoniium.
New York: Oxford University Press; 1992.
Vol 3. Chicago: Quintessence; 2002. p. 219-235.
2. Einstein E, Needleman HL, Karimbur N, Vandyke TE, editors. 11. Wilson TG, Kornman KS. Fundamentals of Periodontics. 2nd ed. New
Periodontal and Gingival Health and Diseases: Children Adolescents and York: Quintessence; 2003.
Young Adults. New York: Informa Healthcare; 2001.
CHAPTER
31
Halitosis
CHAPTER OVERVIEW
Breath ma/odor is an important social problem. Transient conditions can produce momentary malodor
Bad breath can be defined as the subjective perception (temporary/ transient oral malodor), and few examples are
after smelling one's breath. If unpleasant, the terms food intake, e.g., garlic, smoking, and morning breath experi-
breath ma/odor, halitosis, or bad breath can be applied. If enced on awakening. These do not reveal any health problems.
the odor has origin in the oral cavity, it is called oral Any persistent breath malodor may reflect some underlying
ma/odor. pathology, and diagnosis is important to treat the malodor.
INCIDENCE Volatile fatty acids such as fumarate and valerate are also
malodorous. These can be released through expired air or
Industrialized countries show an incidence of 50%. the GCF and can express themselves when they become
There is no gender predominance, and people between volatile.
age 18 and 64 years may be equally affected. The most Unpleasant breath can be due to intraoral or extraoral
prevalent causes of oral malodor are gingivitis, periodon- causes.
titis, and tongue coatings. Minority of patients showing
breath malodor reveal underlying systemic conditions
such as ear-nose-throat pathology, diabetes, hormonal INTRAORAL CAUSES
problems, metabolic problems, hepatic renal conditions,
bronchial carcinoma, or gastroenterologic pathology. Dental Causes
Imaginary breath or halitophobia are terms given to pa-
tients who imagine they have breath malodor (Table 31.1). Extraction wounds, carious cavities, and purulent dis-
charge all can contribute to oral malodor. Interproximal
food impaction and crowding of teeth cause accumulation
ETIOLOGY of food debris, which can result in halitosis.
Volatile sulfur compounds (VSCs) are the main cause

of breath malodor. These mainly include hydrogen sul-
Periodontal Pathology
fide, methyl mercaptan, and dimethyl sulfide. Various Aggregatibacter actinomycetemcomitans, Porphyromonas
other compounds have also been implicated in the etiol- gingivalis, Campylobacter rectus, and Tannerella forsythia are
ogy such as putrescine, indole, skatole, butyric acid, or responsible for pathogenesis of periodontitis and produc-
propionic acid. tion of VSCs. As the periodontal pocket depth increases,
The above-mentioned compounds are mostly formed it is seen that the concentration of the malodorous chemi-
by the degradation of compounds within the oral cavity cals increases. Deep pockets also cause the formation of
by various proteolytic microorganisms. putrescine and cadaverine.
Various peptides present in saliva, food debris, oral VSCs are themselves causative factors for aggravation
epithelium, gingival crevicular fluid (GCF), plaque, post- of periodontitis. They increase the epithelial and pocket
nasal drip, and blood are broken down to various chemi- permeability and contribute to the direct contact of peri-
cals mentioned above and contribute to oral malodor. odontal products to the tissues. Methyl mercaptan also
TABLE 31.1 Classification of Halitosis
Classification Treatment needs Description

I. Genuine halitosis Obvious malodor, intensity beyond socially acceptable level
A. Physiologic TN-1 1. Due to putrefactive process in the oral cavity. No specific disease nor pathologic condi-
halitosis tion is found
2. Origin is dorsoposterior region of the tongue
3. Temporary halitosis due to dietary factors should be excluded
B. Pathologic halitosis
(i) Oral TN-1 and TN-2 1. Caused by disease, pathologic condition, or malfunction of oral tissues
2. Halitosis derived from tongue coating, modified by pathologic condition
(e.g., periodontal disease, xerostomia)
(ii) Extraoral TN-1 and TN-3 1. Origin from nasal, and/or laryngeal regions
2. Origin from pulmonary tract or upper digestive tract
3. Disorders anywhere in the body, odor is blood-borne and emitted via the lungs (e.g.,
diabetes mellitus, hepatic cirrhosis)
II. Pseudo-halitosis TN-1 and TN-4 1. Malodor is not perceived by others, patient stubbornly complains of its existence
2. Counseling and simple oral hygiene measures provide relief
III. Halitophobia TN-1 and TN-5 1. After treatment for genuine halitosis or pseudo- halitosis, the patient still feels that he/
she has halitosis
2. Absence of physical or social evidence of halitosis
TN, treatment need.
(Source: Modified from Yaegaki K, Coil JM. Classification and treatment of halitosis - clinical perspective. J Can Dent Assoc 2000;66:257-61; Modified from Miyazaki H et al.
Tentative classification of halitosis and its treatment needs. Niigata Dent J. 1999;32: 7-11. Japanese).
can enhance the production of interstitial collagenases, Crypts of the tonsils can also cause accumulation of mi-
interleukin-I, and cathepsin B. These further aggravate croorganisms and putrefaction leading to oral malodor.
the periodontal breakdown. Malodorous compounds can
also alter fibroblasts and cell migration and proliferation.
Other conditions such as pericoronitis, acute necrotiz-
Lungs and Bronchus
ing ulcerative gingivitis (ANUG), and oral ulcers can also Chronic bronchitis, bronchiectasis, and bronchial car-
contribute to oral malodor. cinoma are also extraoral causes of oral malodor.
Xerostomia Gastrointestinal Tract

Dry mouth can cause the VSCs to escape, and absence Various conditions that contribute to oral malodor are
of saliva can cause an increase in the number of microor- Zenker diverticulum, hernia, gastric regurgitation, and
ganisms that produce VSCs. intestinal gas production.
Other extraoral causes that contribute to halitosis are
liver insufficiency, kidney insufficiency, type 1 diabetes
Contribution of Tongue
mellitus (OM), and hereditary disorders such as trimeth-
Dorsum of the tongue is irregular and can accommo- ylaminuria. Menstrual breath due to progesterone levels
date microorganisms and food debris. Desquamated calls in females and medications such as metronidazole also
and food remnants remain entrapped on the surface and cause oral malodor.
are consequently decomposed and contribute to oral mal-
odor. The dorsum of the tongue is considered to be the
primary etiologic factor for oral malodor. DIAGNOSIS
1. Self-evaluation: Involving the patient in the diagnosis

EXTRAORAL CAUSES can be important especially when there is an intraoral
cause. This helps to motivate the patient toward better
plaque control methods.
Ear-Nose-Throat
2. Organoleptic method: This is the gold standard for
Purulent sinusitis, pharyngitis, tonsillitis, and postna- assessing oral malodor. A trained judge sniffs the air
sal drip are among the extraoral causes of oral malodor. expired, assesses whether or not it is unpleasant, and
CHAPTER 31 HALITOSIS 249
gives a rating. The judge smells a series of different air Electronic Nose
samples as follows:
a. Oral cavity odor: The subject opens the oral cavity
A new device that is being developed and has the ca-
and refrains from breathing. Expression of VSCs pacities of the human nose is referred to as the electronic
by drying of the oral mucosa can relate to intraoral nose.
cause.
b. Breath odor: The judge smells the expired air of the
subject. The first part of the breath relates to intraoral
TREATMENT ASPECTS OF ORAL
causes while the latter part relates to factors from the
MALODOR (Table 31.2)
respiratory system.
c. Tongue coating: The judge takes a sample of tongue
Tongue Cleaning
coating and examines and presents it to patient or
relative to determine if the smell is similar to that Tongue cleaning has been recommended in patients
experienced. with thick coatings on their tongue. Going as far poste-
d. Nasal breath odor: When the patient expires through rior as possible is advised, as maximum load is seen in
the nose with the mouth closed and it is malodorous this area.
but the air expired from the mouth is not, a nasal
cause can be suspected.
Toothpastes
Cleaning the dentition and the tongue with a dentifrice
Gas Chromatography
has shown to reduce the levels of VSCs.
This is a device to test the saliva of the subject formal-
odorous substances. Recently, a portable machine Oral-
Chroma has been introduced for this purpose. Mouth Rinses
In addition to tongue cleaning, the use of different
mouth rinses has been advocated. Various mouth rinses
Portable Volatile Sulfide Monitor
containing cetylpyridinium chloride, triclosan, chlorhexi-
This machine helps to identify VSCs or methyl mer- dine, essential oils, chlorine dioxide, metal ions, etc., have
captan. The commercially available monitor is Halimeter been shown to be effective in controlling oral malodor.
(Fig. 31.1).
Chewing Gum
Saliva Incubation Test
Chewing gum containing metal salts such as fluorides
Incubating the saliva and testing for the various mal- or chlorhexidine helps in reducing the bacterial load and
odorous chemicals with the help of a Halimeter or gas reducing the levels of malodorous chemicals from the
chromatography also helps to identify various com- oral cavity. Long-term studies using these agents are
pounds that contribute to oral malodor. further needed.
TABLE 30.2 Description of Various Treatment Needs
Category* Description
TN-1 Explanation of halitosis and instructions for oral
hygiene ( reinforcement of a patient's own self-care
for improvement of oral hygiene)
TN-2 Oral prophylaxis, and treatment for oral diseases

TN-3 Referral to a physician
TN-4 Explanation of examination data, education, and

reassurance
TN-5 Referral to a clinical psychologist

TN, treatment need.
* TN-1 is applicable to all cases requiring TN-2 to TN-5.
(Source: Yaegaki K, Coil JM. Classification and treatment of halitosis - clinical
FIGURE 31. 1 Halimeter. perspective. J Can Dent Assoc 2000; 66: 257-61).
Masking the Malodor Since the oral cavity is the main origin of halitosis
or oral malodor, it is important for the dentist to be
Treatment modalities using rinses, mouth sprays, and familiar with the diagnosis and treatment plan of the
lozenges that contain pleasant volatile odors have only a condition.
short-term effect in controlling oral malodor.
Drinking water at frequent intervals and chewing of
gum can keep the VSCs in solution and prevent them
from producing oral malodor.
KEY POINTS
• Bad breath can be defined as the subjective percep- as putrescine, indole, skatole, butyric acid, or propionic
tion after smelling one's breath. If unpleasant, the acid.
terms breath ma/odor, halitosis, or bad breath can be • Organoleptic method: This is the gold standard for as-
applied. sessing oral malodor. A trained judge sniffs the air ex-
• Imaginary breath or halitophobia are terms given to pa- pired, assesses whether or not it is unpleasant, and gives
tients who imagine they have breath malodor. a rating.
• Volatile sulfur compounds are the main cause of breath • Gas chromatography is a device to test the air saliva of
malodor. These mainly include hydrogen sulfide, methyl the subject for malodorous substances. Recently, a por-
mercaptan, and dimethyl sulfide. Various other com- table machine OralChroma has been introduced for this
pounds have also been implicated in the etiology, such purpose.

1. Classify halitosis. Dentistry. 5th ed. Copenhagen: Blackwell Munksgaard; 2008.
2. Enumerate the etiologic factors in halitosis. 2. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds.
3. How do you go about the diagnosis of halitosis? Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B.
Saunders Company; 2006.
4. What is the role of halitosis in periodontal disease?
3. Yaegaki K, Coil JM. Classification and treatment of halitosis -clinical
perspective. J Can Dent Assoc 2000;66:257-61.
SECTION V
DIAGNOSIS, PROGNOSIS, AND

TREATMENT PLANNING
CHAPTER
32
Clinical Diagnosis
CHAPTER OVERVIEW
Periodontal diagnosis is an important part of the overall • Detect early stage disease in clinically asymptomatic
diagnosis of the oral cavity. It is an important label a clinician individuals (screening)
places on a patient's periodontal condition, but the diagnosis • Predict likely responders to specific treatments (treat-
should not be limited to giving name to the condition. It ment planning)
should find out the possible related etiological factors too. • Monitor treatment efficacy and detect disease recurrence
Diagnosis can be defined as the process of identifying a (monitoring).
disease by its signs, symptoms, and the results of various Naming the disease or assigning the name carries
biological assessments. with it the implication that the clinician has ruled out
Diagnostic procedures may be used to all other possible diseases it may resemble, with its signs
• Classify disease categories (classification) and symptoms, but with few differences, a differential
• Identify people at risk of developing disease (risk diagnosis.
assessment)
IMPORTANCE OF DIAGNOSING Information Gathering

THE PERIODONTAL CONDITION
Information gathering process begins with the collec-
tion of personal information, including name, age, sex,
• To find out the cause of the disease or condition
address, and phone number; most often this data collec-
• To find out what periodontal disease or condition the
tion can be done by a receptionist.
patient may have, if it is generalized or localized, and
It is important to know the proper name of the patient
how severe the problem is
because it helps in identification of the patient; also if you
• For easy communication between the clinicians
call the patient by his or her name during conversation,
• For the development of well-designed and appropriate
the patient feels more comfortable and happy to render
treatment plan
the details required for the diagnosis.
• For ascertaining the prognosis of the particular
condition. Knowledge of the exact age of the patient helps not
only in the diagnosis of the condition but also in assess-
A clinician arrives at a diagnosis of condition of the ing the prognosis.
patient by a systematic, methodical inclusion of the vari- Predilection of certain periodontal condition in par-
ous components of periodontal examination. ticular gender is the importance of recording the gender
of the patient properly.
Address and phone number are the two essential data
to be recorded for future communication with the patient;
COMPONENTS OF PERIODONTAL they also give a clue regarding certain endemic diseases
EXAMINATION of the patient.
• Information gathering Chief Complaints

• A thorough hands-on examination of extraoral and The chief complaint of the patient should be recorded
intraoral aspects, including periodontal examination. in his or her own words, as it gives an opportunity to
254 SECTION V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING
TABLE 32.1 Most Common Chief Complaints of the Patient A questionnaire used for this purpose is useful in
collecting all the data. It is also essential to review the
Bleeding from the gums or bleeding while brushing same at subsequent visits of the patients. It is essential
Bad breath that the patient fill the form with the help of receptionist
Mobile tooth
Increased spacing between the teeth
and sign it. This step is necessary prior to starting the
Food gets stuck between the teeth procedure, to avoid medicolegal complications which
Feel like sucking in between the teeth; get relief after that may arise.
Pain, which increases immediately after having food
Long appearance of the tooth
Gummy smile Dental History
Pain and inability to open the mouth, especially in 17- to 25-year- Recording dental history gives an opportunity to know
old patients
Sensitivity of the teeth
the following:
Dark gums (brown or black gums) • How much the patient is aware of the dental treatment;
future compliance of the patient can also be assessed
by this.
know the exact problem of the patient. A patient with • A patient who has gone to several dentists for the
periodontal disease often may not have any complaint at same complaint may not easily get satisfied with the
all; if told that he or she has a problem, the patient may treatment provided by you.
be suspicious of any suggestions that disease is present. • It also gives a clue regarding the possible iatrogenic
Nevertheless, the most common chief complaints of the causes of the periodontal disease; for example,
patients are listed in Table 32.1. patients complain of pain immediate next day of
the tooth restoration because of pulpal exposure or
Medical History high filling.
A thorough and detailed medical history is relevant • Previous eventful dental appointment may also
while diagnosing a periodontal condition. A definite for- give information regarding the hidden systemic
mat will be helpful in recording all possible information disease of the patient, for example, delayed healing
related to the patient, which is often neglected by a clini- of the socket and diabetes, uncontrolled bleeding
cian. Patients do not reveal all the information, thinking during dental surgical procedures, and bleeding/
that it is not necessary for a dentist to diagnose the oral clotting disorders.
conditions. Before taking a medical history its importance
in diagnosing the oral and periodontal changes and its Personal History
implications in treatment plan should be explained to the
It should include the brushing habits; use of tobacco
patient.
(smoking and nonsmoking); pan chewing, including gut-
IMPORTANCE ka; parafunctional habits such as bruxism, clenching, and
grinding; use of devices associated with the profession,
• Certain systemic diseases may require precautions to
for example, nail with the cobbler, needle with the tailor,
be taken before carrying out a treatment, for example,
wire opening with the electrician, and bobby pin opening
patients susceptible to infective endocarditis.
with the girls; and consumption of alcohol.
• Periodontal disease may be aggravated in the presence
of systemic condition/ diseases, for example, diabetes
mellitus/pregnancy. Brushing Habits
• Systemic diseases may be having oral manifestations Method of brushing, type of brush used, and frequency
as the only manifestation, for example, skin diseases of changing the toothbrush should be recorded. A note
such as lichen planus. of the type of dentifrice used, paste, or powder may also
• Systemic disease may be modified by periodontal be made. Uses of any type of interdental devices also
disease. A new branch of periodontology, periodontal should be noted. Tooth abrasion and gingival recession
medicine, is emerging. For example, insulin resistance may be related to the wrong brushing technique and hard
in periodontitis patients, preterm low birth weight, toothbrush.
stroke, and atherosclerosis is being related to the Patient's poor oral hygiene and gingival injuries may
periodontal disease. be related to a delay in changing the toothbrush after it is
• Patients may be taking medications that may have worn out. Patients may be asked to bring the toothbrush
unwanted effects on the periodontium, for example, along with them to assess the status of the brush. It is also
phenytoin and gingival overgrowth, and anticoagulants prudent to ask the patient to get the brush and tell him or
and bleeding from the gums. her to demonstrate the brushing in front of us so that it is
• Patients may be allergic to certain medications. easy to correct the technique of brushing.
C H A PT ER 32 C LIN IC A L D IA G N O SIS 255
Tobacco Use TM] Examination
Tobacco, with smoke or smokeless, is considered as Extra-auricular and/ or intra-auricular examination
a risk factor for periodontitis. Past smoking and current should be done to evaluate the changes in the TMJ, in
smoking activities should be recorded. Current smoking the form of clicking, popping, deviation, etc. Bruxism,
history should include number of cigarettes/beedies per failure to replace the missing teeth, and related vertical
day and number of years since smoking. Reverse smok- dimension changes may result in the alterations of TMJ
ing habits are associated with certain parts of the country. movement.
Palatal tissues are affected by this habit. Passive smoking
is becoming common due to the work environment and
other reasons. Recording the same may be necessary in lntraoral Examination
selected cases.
Mouth Odors or Halitosis
Pan Chewing Halitosis or fetor ex ore or bad breath is the most com-
Pan chewing habit is considered to be a risk factor mon chief complaint of the patient. Patient with this
for periodontal disease. Constant chewing increases the complaint should be assessed for the tongue coating,
masticatory load applied onto the tooth. Increased preva- food impaction areas, pericoronal areas, deep pockets,
lence of periodontitis is seen with the pan chewers, with and draining abscesses. History also should include the
or without tobacco (betel nut used alone). Frequency amount of water intake daily. Organoleptic measurement
of gingival recession is also found to be more with this is a sensory test scored on the basis of a subject's oral mal-
group of patients. Relation between pan chewing and oral odor. Other available methods are gas chromatography,
carcinomas is well-known. sulfide monitors such as Halimeter, and Tanita Breath
Alert to assess the hydrogen sulfide and methyl mercap-
Parafunctional Habit tan (see Chapter 31).
Patients with parafunctional habit may not know that
they have this habit. Proper history taking and associated Oral Hygiene Assessment
oral and extraoral changes help in diagnosing bruxism or Prior to conducting the detailed periodontal examina-
other habits. tion, plaque and calculus should be evaluated. Assess-
ment of plaque at the initial visit will help in understand-
Other Habits ing the oral hygiene status of the patient.
Periodontal disease may be worsened in case of habits Increase or decrease in the plaque scores at the subse-
such as keeping the needle between the teeth, opening of quent appointment is suggestive of poor or good main-
wire, bobby pin opening, etc. It also may be the cause of tenance of the patients, respectively. A simple index sys-
periodontal abscess. tem can be followed to assess the same (Simplified Oral
Hygiene Index). O'Leary Plaque Control Record, etc.,
Alcohol and Periodontal Disease can be used. Disclosing solution should be used once the
Periodontal changes may not be directly related to gingival examination is completed.
the consumption of alcohol. Chronic alcoholism, and
related changes in the liver, may be one of the factors for Soft Tissue Examination (Oral Mucosal
the gingival bleeding. Protein malnutrition occurs in this Examination)
type of patients and may affect the periodontal tissues. Lips, vestibule, buccal mucosa, tongue (dorsal surface),
After gathering the above-said information, hands-on palate (hard and soft), tongue (ventral surface), and floor
examination should be started. of the mouth are examined for the change in the color,
vesicle, bullae, ulcer, white and red lesions, etc.
Angular cheilitis and swelling of the lips should be
Extraoral Examination
noted. Possible etiology for this should be related. White
Examination of the symmetry of the face, lymph node, or red patches seen on the buccal mucosa may be sug-
and temporomandibular joint (TMJ) should be done sys- gestive of associated skin disease; there may be associ-
tema ti call y. ated gingival change (chronic desquamative gingivitis).
Asymmetry of the face because of any periodontal Changes in the tongue may be because of the underlying
conditions is not common. Rarely pericoronal abscess ap- nutritional deficiency.
pears as an extraoral swelling at the angle of the mandible. Smoker's palate is a common feature of the chronic
Lymph node examination: Most commonly submandibu- smokers. Ulcers not healed for a longer duration and with
lar lymph nodes are palpated. It should be seen if it is irregular borders may be suggestive of carcinoma. Refer-
tender and movable or fixed; if it is palpable and tender, ral to an oral and maxillofacial surgeon may be sought at
it is suggestive of systemic spread of infection. that time for further evaluation and treatment.
Overall assessment of periodontium - periodontal tissue looks like. Then only presence or absence of the
screening and recording (PSR) or basic periodontal ex- disease can be identified. The gingiva should be examined
amination (BPE) - a modification of CPITN (community for the color, size, contour, consistency, surface texture,
periodontal index of treatment needs) index system, is position, bleeding, and exudate. Gingival inflammation
depicted in Table 32.2. usually has two types of tissue response; most common
In many countries screening surveys have made use of is the edematous tissue response, which is characterized
a methodology largely derived from the CPITN. Periodon- by red, enlarged, soft, smooth, and glossy gingiva, which
tal screening and recording or basic periodontal examina- easily bleeds on probing. In another response, the gingiva
tion is designed to assess the periodontal status of an indi- is pink, enlarged, firm, and stippled, and may or may not
vidual, which gives a quick and general idea regarding the easily bleed.
periodontal status and its etiological factors to an extent. Color and size changes in the gingiva should be ex-
Periodontal screening and recording system is a ser- amined; the parts of the gingiva involved are papillary,
vice mark of the American Dental Association. Similarly, marginal, or diffuse. In chronic gingivitis, most often the
BPE found its way into use in the United Kingdom and involvement is seen with marginal and papillary gingiva
New Zealand, whereas the primary essential periodontal alone. In contrast, in chronic desquamative gingivitis,
examination (PEPE) was used in Australia. The use of diffuse involvement is observed.
WH0-621 probe (CPI probe, Maryland probe) is a com- Drug-induced gingival enlargement is confined to mar-
mon feature in all of these methodologies. ginal and papillary gingiva; in case of idiopathic gingival
enlargement, diffuse enlargement is noted.
Examination of the Gingiva The contour and shape of the gingiva change in the
Before conducting the gingival examination, it is nec- gingivitis. Scalloped border of the gingiva may remain
essary to have a good idea how a healthy periodontal the same, but it may be accentuated, or as seen in the
TABLE 32.2 Periodontal Screening and Recording (PSR)
Instrument used: CPI probe, which is a specially designed probe that has a 0.5 mm ball at the tip and is color coded from 3.5 to 5.5 mm; other
markings are at 8.5 and 11.5 mm
While recording the index, the patient's mouth is divided into six sextants:
Maxillary right (18-14) Maxillary anterior (13-23) Maxillary left (24-28)
Mandibular right (48-44) Mandibular anterior (43-33) Mandibular left (34-38)
Each tooth is probed with the clinician walking the probe around entire tooth to examine at least six points around each tooth: mesiofacial,
midfacial, distofacial, and the corresponding lingual/palatal areas. The deepest finding is recorded in each sextant, along with other find-
ings, according to the following codes:
Code 0- In the deepest sulcus of the sextant, the probe's colored band remains completely visible. Gingival tissue is healthy and does not
bleed on gentle probing. No calculus or defective margins are found. These patients require reinforcement of oral hygiene instructions
Code 1 -The colored band of the probe is completely visible in the deepest sulcus of the sextant. No calculus or defective margins are
found, but some bleeding after gentle probing is detected. These patients require supragingival and subgingival scaling and oral hygiene
instructions
Code 2 - The probe's colored band is still completely visible, but there is bleeding on probing and supragingival or subgingival calculus
and/ or defective margins are found. Treatment consists of supragingival and subgingival scaling, correction of plaque retentive areas such
as defective margins of restorations, followed by oral hygiene instructions
Code 3 - The colored band of the probe is partially submerged. This indicates the need for a comprehensive periodontal examination and
charting the affected sextant to determine the necessary treatment plan. If two or more sextants score code 3, a comprehensive full mouth
examination and charting are indicated
Code 4 - The colored band completely disappears in the pocket, indicating a depth greater than 5.5 mm. A comprehensive full mouth
examination and charting and treatment are needed
Code " - When any of the following abnormalities are seen, an asterisk(*) is entered: in addition to the code number furcation involve-
ment, tooth mobility, mucogingival problem, or gingival recession extending to the colored band of the probe, which is equal to or more than
3.5mm
The code finding of each sextant and the date are entered in the box and a record is maintained for the future
Sextant score
Month Day Year

FIGURE 32.1 Examining the consistency of the gingiva. FIGURE 32.3 Examining the bleeding on probing.
acute necrotizing ulcerative gingivitis (ANUG), it may be Position of the gingiva, coronal or apical to cemen-
flat or in reverse architecture. The shape of the gingiva toenamel junction (CEJ), should be recorded. Gingival
changes from knife edge border to rounded or blunt bor- recession, which is an apical shift in the position of the
der. Specific changes such as McCall festoon and Stillman gingiva, if present, should be classified according to
cleft should be noted, even though there is no special Miller classification. Coronal shift in the position oc-
significance to this. curs due to gingival enlargement, either inflammatory
Healthy gingiva is firm and resilient; the consistency of or drug induced; this becomes clinically important if
the gingiva is assessed by gently pressing the side of the it creates aesthetic problem, and it also makes plaque
probe against the gingival tissue for a few seconds and control difficult or interferes with the normal function.
then removing it (Fig. 32.1). If the tissue is edematous, Altered passive eruption is another situation that results
imprint of probe is seen. If the tissue is firm and fibrous, in short clinical crown and requires surgical correction
no imprint will be left. for aesthetic reasons.
Before examining for the surface texture, gingiva should Bleeding on probing is an important component of
be wiped with cotton and then examined (Fig. 32.2). The the gingival examination. It is an objective sign of gingi-
presence of the stippling is suggestive of the absence of val inflammation. Inflamed gingival tissue bleeds when
the disease; however, the absence of the stippling is not gently probed because of minute ulceration in the pocket
always suggestive of presence of the disease. epithelium and the fragility of the underlying vasculature.
A periodontal probe, which has a blunt tip, helps in
finding out the bleeding sites. Periodontal probe is passed
along the lateral wall of the gingival sulcus (it need not
be to the depth of the pocket), followed by a wait for 30 s
(Fig. 32.3).
Index system with just absence or presence of bleeding
or bleeding severity (grading 0, 1, 2, and 3) can be used
(Mombelli Bleeding Index; Table 32.3).
The percentage of sites that exhibit bleeding on prob-
ing prior to treatment is a clinically useful information to
compare it with the posttreatment bleeding sites and judge
the efficacy of the treatment rendered to the patient. It also
reassures the patient regarding the treatment provided.
Purulent exudate or suppuration is often seen at the
sites with chronic periodontitis, which is neutrophil-rich
exudate. Occasionally it is found at sites with gingivitis.
Pus formation does not occur in all periodontal pockets.
Presence of bleeding and exudate is suggestive of active
FIGURE 32.2 Examining the surface texture of the gingiva. disease site, a site that is inflamed and infected.
TABLE 32.3 Sulcus Bleeding Index is a tapered rod-like instrument having a blunt end, so
SCORING CRITERIA
that tissue is not perforated. Most commonly used peri-
odontal probe is University of Michigan "o" probe with
0 - No bleeding when periodontal probe is passed along the Williams markings and WHO probe.
gingival margin
Pocket depth recorded using a periodontal probe is
1 - Isolated gingival spots visible considered as clinical probing depth.
2 - Blood forms a confluent red line margin It is the distance between the base of the pocket and
gingival margin. It is not the true depth of the pocket.
3 - Heavy or profuse bleeding
Clinical studies carried out in the beagle dogs, regarding
the probe penetration in different clinical situations, re-
vealed that in healthy specimens, the probe penetrated the
The best way to detect the presence of pus is to gently epithelium to about two-thirds of its length; in gingivitis
apply digital pressure to overlying gingiva from muco- specimens, it stopped at 0.1 mm short of its apical end;
gingival junction toward the marginal gingiva. and in case of periodontitis, the probe tip went past the
In case of periodontal abscess, there is a localized en- most apical cells of the junctional epithelium. So clini-
largement of gingiva with collection of copious amounts cal probing depth may vary, but biological depth can be
of pus. It is often misunderstood that the presence of pus obtained in carefully prepared and adequately oriented
always means presence of an abscess. histological preparation, where distance between the
If there is no loss of attachment (gingival recession) or gingival margin and the base of the pocket (the coronal
periodontal pocket, the case can be diagnosed as gingivitis end of the junctional epithelium) is considered to be the
according to the parts of the gingiva involved, the number true depth of the periodontal pocket.
of teeth involved, and association with the plaque or not;
different diagnosis can be given (see the classification of METHOD OF PROBING - PROBING POCKET DEPTH
periodontal diseases). Both probing depth and clinical attachment level
should be recorded usually at six points around each
tooth (conventional method).
Assessment of Periodontal Status When measuring the pocket at a particular point, the
Periodontal examination includes examination of peri- probe is inserted with a firm gentle pressure to the bot-
odontal pocket, clinical attachment loss, furcation involve- tom of the pocket (Fig. 32.4); the shank should be aligned
ment, mobility, and pathological migration. parallel to the long axis of the tooth surface. Penetra-
tion should be stopped when soft tissue resistance is felt,
Periodontal Pocket which is nothing but base of the pocket. Pocket depth is
Pathological deepening of the gingival sulcus is one recorded at the level of the gingival margin.
of the signs of pathological changes in the periodontium. For the interproximal pocket and to detect the inter-
Therefore, examination of the existence of such a pocket dental crater, it is necessary to angulate the probe beneath
is considered to be an essential part of the periodontal the contact area, from both the facial and lingual areas.
examination.
Examination of periodontal pocket must include the
presence and distribution on each tooth surface, depth of
the pocket, and identification of suprabony or infrabony
type of pocket.
Visual examination of the gingiva should be carried
out to see the signs and symptoms of the pocket, before
using a periodontal probe to detect the pocket. Area of
the pocket may show the changes in clinical signs, such
as bluish red marginal gingiva, bluish red vertical zone
extending from the marginal gingiva to mucogingival
junction, separated buccal and lingual interdental papilla,
enlarged edematous gingiva, and rolled-out marginal gin-
giva, which can be easily separated from the tooth surface.
Measuring the pocket - clinical probing depth and histo-
logical or biological depth: A pocket measuring probe or
otherwise periodontal probe is an ad hoc instrument used
to measure the depth of the pocket. Several such conven-
tional periodontal probes are available. The typical probe FIGURE 32.4 Measuring the pocket.
If there is supragingival calculus observed during the tolerated. Before probing the sulcus, one can practice ap-
initial visit, periodontal pocket recording can be post- plying probing force by keeping the probe in the nail bed;
poned till the supragingival scaling has been carried out. amount of force to be applied may vary according to the
If there are subgingival deposits noted, delicate handling severity of inflammation.
of the probe must be employed.
Delineation between suprabony and infrabony pockets INFLAMMATORY STATUS OF THE TISSUE During gin-
can be made by simple clinical method or using some gival inflammation, connective tissue adjacent to pocket
other devices. Probe is inserted parallel to the long axis epithelium is filled with inflammatory fluid and cells.
of the tooth, and it is pulled toward the gingiva; if one Pocket epithelium is also infiltrated with inflammatory
feels bony resistance, pocket could be infrabony. Bony cells and ulcerated. This allows easy penetration of the
resistance felt is the bony wall of an infrabony pocket. periodontal probe even with the lightest probing force,
For the research purpose, gutta-percha point or silver and in some cases, probe penetrates as far as the bone mar-
points can be used with the radiograph, to assist in deter- gin, which results in overestimation of the pocket depth.
mining the different levels of attachment of periodontal Conversely, in treated cases, reduction in the pocket
pocket. depth is often misunderstood as gain in clinical attach-
ment. Results achieved after therapy should be consid-
OTHER ALTERNATE METHODS ered with caution.
Walking probing method (also called stepping): In this tech- The contour of the tooth and root surface is also found
nique, probe is inserted at the distal most surface of the to be affecting the probing pocket depth.
tooth, and walked or stepped toward the mesial surface of
the tooth, at 1 mm distance, without taking out the probe Clinical Attachment Loss and Relative
completely from the gingival sulcus. Attachment Loss
Measurement is recorded at each millimeter, and thus Clinical attachment loss (CAL) is the true measure of
deepest penetrated area is recorded. The advantage of this the periodontitis. It is the distance between the base of the
technique over the conventional method is that one will pocket and a fixed point on the crown such as CEJ. If the
not miss the deepest areas of involvement. However, the CEJ is missing because it has been destroyed by dental
process is time-consuming. caries or placement of a restoration or because of abra-
sion, another fixed reference point can be used to measure
TRANSGINGIVAL PROBING, TRANSSULCULAR the loss of attachment. Such landmarks might include
PROBING- SOUNDING apical margin of restoration or incisal edge of a tooth or
Easley, Tibbets, and Ochenbein and Ross (1969) de- composite point placed on the crown. When attachment
scribed a sounding technique for plotting the morpho- loss is taken other than from the CEJ, it is termed relative
logical outline of the alveolar bone. This procedure per- attachment loss (RAL). CAL or RAL is considered to be a
formed with local anesthesia utilized the periodontal better indication of the degree of periodontal destruction
probe pushed through the gingival tissue as a sounding than that of the pocket depth.
device till one feels the bony margin. This will deter-
mine the shape of the bony margin. This is also used to METHOD OF ASSESSING THE CLINICAL
determine the biological width. Even though not done ATTACHMENT LOSS
routinely, it is necessary to this procedure before planning As it is used in the pocket depth, probe is held par-
the surgical crown lengthening. allel to the long axis of the tooth. At first, the probe is
passed from the enamel (smoother surface) toward the
FACTORS AFFECTING ACCURACY OF THE PROBING cementoenamel junction (which is the first rough point).
THE SIZE OF THE PROBE Tip of the probe may vary Measurement is taken from the CEJ to the base of the
from 0.3 to 0.8 mm, for the different periodontal probes. probeable crevice (till soft tissue resistance is felt), at six
This variation will affect the measurement of the probing. points around each tooth. A case in which the CEJ is not
visible, at first measurement is taken from the crest of
ANGULATION OF THE PROBING Same angulation to the gingival margin to the base of the pocket (recorded
be used at each appointment is a difficult task. For the as A). After this, measurement is taken from the crest of
research purpose, acrylic stent can be used to measure the gingival margin to the CEJ (recorded as B). Then we
the pocket depth, at the same point each time. get A- B = CAL.
THE PROBING FORCE Penetration of the probe may RELATION BETWEEN POCKET DEPTH AND CLINICAL
vary depending on the force of introduction. Probing force ATTACHMENT LOSS
applied by different clinicians may vary from 30 to 130 g. Pocket depth and CAL are two different entities. The
Forces of 0.75 N have been found to be accurate and well relation between these two is explained as it is related to
the gingival margin. When the gingival margin is located

coronal to CEJ, pocket depth will be more than the clinical
attachment loss (CAL= distance from the gingival margin
to base of the pocket - distance from gingival margin
to CEJ). When the gingival margin is at the CEJ, pocket
depth and clinical attachment loss are same. When the
gingival margin is located apical to the CEJ, CAL is more
than the pocket depth.
DIAGNOSIS OF PERIODONTITIS In the presence of

CAL and/ or a true pocket, case can be diagnosed as peri-
odontitis. If the amount of plaque correlates with the
amount of periodontal destruction, the given case can
be diagnosed as chronic periodontitis. If there are less
than 30% sites involved, it is diagnosed as localized, and
if there are more than 30% sites, the case is diagnosed as
generalized. Furthermore, depending on the severity of
CAL, it can be further classified as mild (less than 2 mm
CAL), moderate (more than 2 mm, but less than 5 mm), FIGURE 32.5 Detecting the furcation involvement.
and severe (more than 5 mm). If there is less plaque and
severe destruction and rate of progression of disease is
faster than normal, the case can be diagnosed as an ag-
gressive periodontitis. If the involvement is confined to be passed through. For maxillary furcation detection,
first molars and incisors, it can be diagnosed as localized especially mesial and distal furcations, approach to the
aggressive periodontitis, and if it involves addition of two furcation differs from the usual. The Naber's lN probe
permanent teeth, other than the first molar and incisors, is specifically designed for mesial and distal furcations
the periodontitis is diagnosed as generalized aggressive on maxillary molars. Probing a maxillary molar furca-
periodontitis. tion may require an extraoral handrest in order to keep
the probe tip properly adapted. Approach any maxillary
Furcation Involvement molar mesial furcation from the lingual aspect because
Involvement of furcation of multirooted teeth is a sign this furcation is located two-thirds of the way across the
of periodontitis. There are several types of classification mesial surface from the buccal aspect, or one-third of the
available. Most commonly followed classification based way in from the lingual aspect. The distal furcation is
on horizontal involvement is the Glickman classification located on the distal surface, halfway between the buc-
and Hamp and coworkers' classification. To add to this, cal and lingual aspect. Approach it first from the buccal
to assess the vertical involvement of the furcation, Tarnow aspect and then from the lingual aspect.
and Fletcher classification is utilized. To assess the furca-
tion involvement, most commonly used instrument is the Mobility of the Tooth
Naber's probe. Mobility of teeth is one of the signs associated with
periodontitis. Even though teeth mobility may have sev-
HOW TO IDENTIFY THE FURCATION INVOLVEMENT? eral causes other than the periodontal infections, loss of
If the pocket depth is more than 5 mm, there are more alveolar bone from periodontitis is a major cause of ab-
chances of furcation involvement. Naber's lN probe, normal tooth mobility. It needs to be understood in detail
Naber's 2N probe, or a curette is commonly used. The because often this is the chief complaint of the patient.
curved shanks of the Naber's lN and 2N probes are ex- It is a visually perceptible movement of the tooth away
pressly designed for furcation detection. In case of non- from its normal position when a light force is applied. All
availability of the Naber's probe, periodontal probe can the teeth have some degree of mobility. This physiologi-
be used (Fig. 32.5). The probe is inserted parallel to the cal tooth mobility is the limited tooth mobility allowed
long axis of the tooth, at the midbuccal surface of the tooth by resilience of an intact periodontium on application of
and approximately 5 mm from the CEJ. It is angulated a normal force.
to find out the possible bone loss in the furcation area. Physiological (normal) tooth mobility basically oc-
If there is minimal bone loss, furcation can be felt like a curs in two stages: initial/intrasocket stage, which oc-
groove between the roots. If there is moderate bone loss, curs rapidly, in which tooth moves within the confines
probe can be easily entered in the furcation area, but can- of periodontal ligament space. This is associated with
not pass through. If there is severe bone loss, probe can the viscoelastic distortion of periodontal ligament, which
progresses until the complete elongation of the fibers is stages, funnel-shaped variation in the crest of the bone
achieved. The range of mobility is in the order of 0.05- results in increased tooth mobility.
0.10 mm, when forces of 100 lb are applied. Root resorption, which may occur especially when
In contrast, secondary stage occurs gradually, where excessive force is applied in case of orthodontic treatment,
elastic deformation of the alveolar bone takes place in also leads to increased tooth mobility.
response to forces of 500 lb. Mobility due to trauma from occlusion usually occurs
Range of tooth mobility varies from tooth to tooth in two stages: progressive hypermobility and permanent
(incisors, canines, premolars, molars). When forces are hypermobility. Sometimes, the term "adaptive tooth mo-
discontinued, teeth return to their original position in bility" is used when the changes in mobility are retained
two stages: immediate spring-like elastic recoil and slow for a long period of time.
recovery movement. Several factors affect tooth mobility:
number, shape, and length of the root; diurnal variation, OTHER CAUSES OF TOOTH MOBILITY
greater mobility in the morning, which progressively HORMONAL CHANGES Due to physicochemical
decreases thereafter; and females having more tooth mo- changes in the periodontal tissues, increased capillary
bility than males. Greater tooth mobility in the morning permeability, increased edema, and alteration in the col-
is due to slight extrusion of tooth from the socket, which lagen metabolism result in increased tooth mobility in
progressively decreases thereafter once masticatory forces case of pregnancy and oral contraceptive users. Similar
are applied on the tooth. Females usually will have more changes are observed during menstrual cycle also.
tooth mobility compared with males probably due to
hormonal variation. PATHOLOGICAL PROCESSES OF THE JAWS Cysts and
tumors involving the maxilla and mandible, and other
Pathological Tooth Mobility (Abnormal) infections of the bone such as osteomyelitis, result in in-
As the name designated, tooth mobility because of creased tooth mobility.
pathological processes within the periodontium is called
pathological or abnormal tooth mobility. Mobility occurs PERIODONTAL SURGERY A transient increase in
beyond the physiological range. tooth mobility is found immediately after the surgery
Principal causes for the pathological tooth mobility because normal arrangement of collagen fibers will form
are loss of alveolar bone, inflammatory changes in the only after 72 days.
periodontal ligament, and trauma from occlusion.
METHOD OF ASSESSING THE TOOTH MOBILITY
ALVEOLAR BONE LOSS (LOSS OF TOOTH SUPPORT) MANUAL METHOD Tooth is held firmly between
This is the most common cause of the tooth mobility. handles of two metallic instruments and force is applied
Here mobility of the tooth occurs because of an apical shift in the buccolingual direction (Fig. 32.6). Mobility is noted
in the fulcrum. The amount of tooth mobility depends on with the adjacent teeth.
the severity and distribution of bone loss on individual Common index used to measure the tooth mobility
tooth surface, length and shape of the root, and crown to was tooth mobility index by Mulhemann, which was later
root ratio. Same amount of bone loss at incisors and mo- modified by Grace and Smales (Table 32.4).
lars will have different severity of mobility. Even though
bone loss is severe on one side of the root surface, teeth
may not be having much mobility.
EXTENSION OF INFLAMMATION
Extension of inflammation from gingiva to the peri-
odontal ligament, or from the periapical region to the
periodontal region, may result in increased tooth mobility;
periodontal abscess and periapical abscess are the typical
examples for this.
TRAUMA FROM OCCLUSION

Trauma from occlusion results in increased tooth mo-
bility. During injury stage, loss of lamina dura results in
widening of periodontal ligament space.
In case of repair stage, attempt to strengthen the peri-
odontal structures also results in widening of periodontal
ligament space. Furthermore, in adaptive remodeling FIGURE 32.6 Detecting the mobility of tooth.
TABLE 32.4 Indices for Measuring the Tooth Mobility FACTORS INFLUENCING THE PATHOLOGICAL
MIGRATION The factors influencing pathological mi-
Mobility index - Miller gration include weakened periodontal support, pressure
Grade 0-Normal tooth mobility from the tongue, abnormal occlusal contact, tooth with
Grade 1 - Slightly more than the normal
abnormal proximal contact, absence of an antagonist,
Grade 2 - Moderately more than the normal
Grade 3 - Severe mobility faciolingually and mesiodistally com- pressure from food bolus during mastication, abnormal
bined with the vertical displacement lip sucking habit, etc.
Mobility index - Grace and Smales
Grade 1 - Mobility <1 mm buccolingually
Grade 2-Mobility 1-2 mm buccolingually MUCOGINGIVAL PROBLEMS OR
Grade 3-Mobility >2 mm buccolingually and/or vertical tooth PROBLEMS RELATED TO PLASTIC
mobility
PERIODONTAL SURGERY
Inadequate or Adequate Attached Gingiva
MECHANICAL/ELECTRONIC EVALUATION Mobilom-
eter, periodontometer, and Periotest measure the reaction When pocket or recession extends beyond the muco-
of the periodontium to a defined percussion force applied gingival junction, there is absence of an attached gingiva.
to the tooth via a tapping instrument. Even though controversy exists regarding the need for the
zone of attached gingiva, correction of such problems may
PATHOLOGICAL MIGRATION be required for aesthetic and functional reasons.
Tooth displacement results when the balance among
Steps in Measuring the Zone of Attached Gingiva
the factors that maintain physiological tooth position is
altered by periodontal disease (Fig. 32.7). The following are the steps to find out the mucogin-
This may be the presenting complaint of the patient, gival junction:
especially in the anterior region, and is the early sign 1. Clinical differentiation between the alveolar mucosa
of localized aggressive periodontitis, commonly called and attached gingiva: Color difference (red and pink,
wandering of the teeth. Pathological migration is usually respectively; Fig. 32.8).
accompanied by mobility and rotation; tooth may move in 2. Use of Schiller's potassium iodide solution to stain
any direction. Pathological migration in incisal/ occlusal the mucosa and attached gingiva: This solution stains
direction is called extrusion. the glycogen content of the tissue, and glycogen is
more in the alveolar mucosa than in the attached
CLINICAL DETECTION OF THE PATHOLOGICAL gingiva. Because glycogen is utilized for the process of
MIGRATION Clinically, one should look at the change keratinization in the attached gingiva, this stain gives
in the position of the tooth, and then observe for the pres- dark brown color to the alveolar mucosa and light
ence of pocket or loss of attachment. If it is present, then brown color to the attached gingiva. The differentiating
change in the position of the tooth in the arch is due to the line between these two colors is the mucogingival
loss of bone, and it should be considered as pathological junction.
migration.
FIGURE 32. 7 Pathological migration of right central incisor. FIGURE 32.8 Difference in the color between alveolar mucosa and
the attached gingiva.
FIGURE 32.9 Bunching of the tissue at the junction between alveolar

mucosa and the attached gingiva. FIGURE 32.10 Performing the tension test.
3. Passing the probe horizontally from alveolar mucosa Blanch test: Blanch test is performed to diagnose a
to the attached gingiva: Since the probe is moved from fleshy labial frenum. It is done by pulling the upper
the movable tissue to the firm tissue, bunching of the lip outward. Presence of a thick and fleshy frenum is
tissue occurs at the site of the mucogingival junction confirmed by the blanching of the tissue in the incisive
(Fig. 32.9). papilla region palatal to the two central incisors.
4. Anesthetizing the area, which blows out the loose
alveolar mucosa and leaves the firm attached gingiva Inadequate Depth of the Vestibule
and hence easily differentiates the mucogingival
junction. Normal depth of the vestibule helps in proper main-
5. Once the mucogingival junction is marked, measuring tenance of oral hygiene and also the movement of food
the distance between the crest of the gingival margin during mastication.
and the mucogingival junction using a periodontal In the absence of this, food accumulates on the mar-
probe (A); then pocket depth is measured (B). A - B ginal gingiva and gingival sulcular area, resulting in the
gives the width of attached gingiva. progression of the periodontal disease.
Identification of the Deficient Alveolar Ridge

Abnormal Frenal Attachment
Lack of sufficient bony and soft tissue may limit the
Placek and coworkers classified the frenal attachment
aesthetic value and oral hygiene habits of the patient
into four types: mucosal, gingival, papillary, and papil-
when prosthetic restorations are placed over the defec-
lary penetrating.
tive ridges.
In the presence of adequate attached gingiva, papillary
The prosthetic teeth that are placed frequently look like
and papillary penetrating types should be considered
as if they are resting on top of the flattened ridge. At pres-
as abnormal because they not only make it difficult for
ent ridge augmentation procedures are included under
an individual to keep the brush in that area, resulting
the periodontal plastic procedures. Siebert and Allen clas-
in plaque accumulation, but also cause gingiva to move
sification is used to classify the deficient alveolar ridge.
away from the tooth surface, making the area a plaque
retentive site.
Identification of the Black Triangle
Tension test: This test is performed to check the
or Loss of Interdental Papilla
abnormal frenal attachment and the adequate
attached gingiva. Here the lip is moved outward, Black triangle or black hole appearance between the
upward for the upper and downward for the teeth, especially in the anterior region, is of great aesthetic
lower, and also moved sideward. If the marginal concern. Patients often come with the complaint of un-
and/ or the interdental papilla moves away from aesthetic appearance of this area. Identification of such
the tooth surface, then the tension test is said to problems can be dealt with Nordland and Tarnow (1998)
be positive. If not, the test is said to be negative classification, which helps in planning out the treatment
(Fig. 32.10). plan and prognosis of such treatment.
Exposed Root Surface or Gingival Fremitus Test

Recession - Need for Root Coverage Fremitus is a measure of the vibratory patterns of the
Gingival recession is the apical shift in the position of teeth when the teeth are placed in contacting positions
the gingiva with the denudation of the root surface. It is and movements.
of aesthetic or functional concern. Classification of such To measure fremitus, a dampened index finger is
recession is necessary in order to develop the prognosis placed along the buccal and lingual surfaces of maxillary
after the root coverage procedure. teeth. The patient is asked to tap the teeth in the maximum
Miller classification of marginal tissue recession is help- intercuspal position and then grind systemically in the
ful in identifying the type of gingival recession. lateral and protrusive contacting movements and posi-
tions. The teeth that are displaced by the patient in these
Gingival Pigmentation jaw positions are then identified (Fig. 32.11).
This is one of the most common complaints of patients Generally this is limited to the maxillary teeth; howev-
nowadays. There are many depigmentation procedures er, in case of edge-to-edge occlusion or when there is little
available. However, before undertaking the procedure overlap of the teeth, mandibular teeth can be assessed.
pigmentation needs to be classified according to available The classification system used to differentiate different
classification [recent classification and gingival pigmen- degrees of fremitus is as follows:
tation index (GPI; Singh V, Bhat GS, Bhat KM, Kumar S,
• Class I fremitus - mild vibration or movement detected
2012)] and good-contrast photograph needs to be taken. • Class II fremitus - easily palpable vibration but no
visible movement
GP! Index
• Class III fremitus - movement visible with the naked
0 Absence of pigmentation, pink color of the gingiva eye
1 Spots of brown to black pigmentation Fremitus is a guide to the ability of the patient to dis-
2 Brown to black pigmentation, more than spots but not
place and traumatize the teeth. It differs from the mobility
diffuse (patches of pigmentation) in that fremitus refers to tooth displacement created by
the patient's own occlusal force.
3 Diffuse brown to black pigmentation involving papillary,
marginal, and attached gingiva
Assessment of Tooth Loss Substance
Hard Tissue Examination Attrition, abrasion, erosion, and abfraction should

be evaluated. For example, if there is erosion, history
Hard tissue examination includes finding out the num- related to esophageal reflux and food habits must be
ber of teeth present: missing teeth, carious teeth, and evaluated.
restored teeth. Especially proximal caries is considered Final diagnosis of the periodontal changes is done with
because this acts as a plaque retentive area. Restored teeth collective information available after the history, and
should be examined for the overhanging margins, which
may have encroached upon the biological width. Over-
hanging restorations can be evaluated with the dental
floss. Other plaque retentive areas such as palatal grooves,
cervical enamel projections, and enamel pearl may be
associated with localized deep pocket formation, which
needs correction during pocket elimination procedure.
TEETH IN OCCLUSION
Type of occlusion, deep bite or open bite, should be
evaluated.
Plunger cusp: It is a sharp cusp that forces the food into
the periodontium. Food impaction is the forceful wedging
of the food into the periodontium. Such a problem can be
revealed with the patient complaint and the local tissue
changes. The patient usually complains of the symptoms
of pocket formation. FIGURE 32.11 Performing the fremitus test.
gingival and periodontal examination. Once the diagno- However, for few gingival and periodontal changes such
sis is made, risk factors for the existing condition should as localized gingival enlargement, differential diagnosis
be evaluated. Differential diagnosis may not be always may be required. Furthermore, prognosis and treatment
sought for the commonly existing periodontal conditions. plan are planned.
KEY POINTS
• Periodontal probing is the important method for assess- • Presence of trauma from occlusion can be assessed clini-
ing the periodontal status. cally by fremitus test.
• Bleeding on probing is the important sign and • Width of attached gingiva is measured simply by tension
presence of bleeding is suggestive of periodontal test.
disease. • Medical history taking is very important to prevent the
• Assessment of furcation involvement is necessary in complications during the treatment.
periodontal diagnosis because maintenance and treat- • Walking probing is also called stepping, and transgingi-
ment of the furcation is essential in preserving the val probing or transsulcular probing (TSP) is also called
tooth. sounding.
QUESTIONS 12. Genco RJ, Goldman HM, Cohen DW. Periodontal diagnosis. In:
Contemporary of Periodontics. 2nd ed. St. Louis: Mosby, 1990.
13. Glickman I. Clinical Periodontology. Philadelphia: Saunders; 1953.
1. List any five common chief periodontal complaints. 14. Green C, Vermillion J. Simplified oral hygiene index. In: Peter S,
2. Discuss the method of probing at a given periodontal editor. Essentials of Preventive and Community Dentistru. 2nd ed. New
site. Delhi: Arya Publishing House; 2004. p. 126-240.
3. What are the factors affecting the accuracy of probing? 15. Grace AM, Smales FC, editors. Mobility Index. Periodontal Control: An
Effective System for the Diagnosis, Selection, and Treatment in General
4. List the etiology of the tooth mobility.
Practice. New York: Quintessence; 1989. p. 52.
5. Mention the steps in zone of attached gingiva. 16. Greenberg MS, Glick M. Burkett's Oral Medicine: L - Diagnosis
and Treatment. 10th ed. India: Elsevier; 2003.
Suggested readings 17. Hamp SE, Nyman S, Lindhe J. Periodontal treatment of multirooted
teeth results after 5 years. J Clin Periodontol 1975;2:126.
1. American Dental Association, American Academy of Periodontology. 18. Kalkwarf JJ, Kahldal WD, Patil KD. Comparison of manual and
Periodontal Screening and Recording Training Manual. 1992 pressure controlled periodontal probing. Periodontologu 1989;57:467.
[reprinted with permission from American Dental Association]. 19. Listgarten MA, Mao R, Robinson PJ. Periodontal probing and the
2. American Academy of Periodontology. Proceedings of the world relationship of the probe tip to periodontal tissues. J Periodontal
workshop in periodontics. In: Annals of Periodontology. Chicago: 1976;47:511.
American Academy of Periodontology, 1996. 20. Listgarten MA. Periodontal probing: what does it mean? J Clin
3. Armitage GC, Svanberg GK, Loe H. Microscopic evaluation of Periodontol 1980;7:165.
clinical measurement of connective tissue attachment levels. J Ciin 21. Loe H. Periodontal changes in pregnancy. J Periodontol 1965;36:209.
Periodontol 1977;1:173-5. 22. Lozda-Nur F, Miranda C. Oral lichen planus: epidemiology,
4. Bhlaji J. Orthodontics, Art and the Science. 1st ed. New Delhi: Arya clinical characteristics and associated disease. Semin Cutan Med
Publications:chap 35. Sur 1997;16:273.
5. British Society of Periodontology. Basic Periodontal Examination. 23. Miller Jr PD. A classification of marginal tissue recession. Int J
6. Butler RT, Kalkwarf KL, Kaldahl WB. Drug induced gingival Periodontics Restorative Dent 1985;5:9.
hyperplasia: phenytoin, cyclosporine and nifedipine. J Am Dent 24. Mombelli A, Van Oosten MAC, Schurch E Jr, Lang NP. Sulcus
Assoc 1987;114:56. bleeding index. In: Periodontal Control: An Effective System for the
7. Carranza AF, Takei HH. Clinical diagnosis. In: Carranza's Clinical Diagnosis, Selection, Control, and Treatment in General Practice.
Periodontology. 10th ed. Philadelphia: Elsevier; 2007. Vol 52. London: Quintessence; 1989.
8. Dajani AS, Talbert KA, Wilson W. Prevention of bacterial 25. Morita M, Wang HL. Association between oral malodour and adult
endocarditis: recommendations by the American Heart Association. periodontitis: a review. J Clin Periodontal 2001;2:257-63.
JAMA 1997;277:1794. 26. Mulhemann HQ. Periodontometry: a method of measuring tooth
9. Dussault G, Sheiham A. Medical theories and professional mobility. Oral Surg Oral Med Oral Pathol 1951;4:1220-32.
development: the theory of focal sepsis and dentistry in early 27. Murata T, Yamuga T, Lida T, Miyazaki K. Classification and
twentieth century. Br Soc Sci Med 1982;16:1405. examination of halitosis. Int Dent J 2002;52:181-6.
10. Easley J. Methods of determining the osseous form. J Periodontal 28. Nordland P, Tarnow S. Classification system for the papillary
1967;38:112. height. In: Lindhe J, ed. Textbook of Clinical.
11. Edwards JG. The diastema, the frenum and the frenectomy: a 30. Lindhe J, Karring T, Lang NP. Clinical Periodontology and Implant
clinical study. Am J Orthod 1997;3:489-508. Dentistry. 4th ed. Malden, MA: Blackwell Munskgaard; 2003:234-237.
31. Ochsenbein C, Ross F. A primer for the osseous surgery. Int J 39. Sumanth S, Bhat KM, Bhat GS. Periodontal health status in pan
Periodontics Restorative Dent 1986;6:9. chewers with or without use of tobacco. Oral Health Prev Dent
32. Parmar G, Sangwar P, Vashi P, Kulkarni P, Kumar S. Effect of 2008;6(37):223-9.
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and oral hygiene status. J Oral Sci 2008;50(1):57-62. cigarette smoking, bacterial pathogens and periodontal status.
33. Pattison GA. Self inflicted gingival injuries: literature review and Periodontology 1995;64:1225.
case report. J Periodontal 1983;54:299. 41. Tarnow D, Fletcher P. Classification of the vertical component of
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Quintessence. disease. J Am Dent Assoc 1969;78:549.
35. Rees TD, Mealey BL. Periodontal treatment of medically 43. Van der Vaiden V. Probing forces and the relationship of the probe
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CHAPTER
33
Role of Radiology in the Diagnosis
of Periodontal Diseases
CHAPTER OVERVIEW
Periodontal disease, an inflammatory condition affecting pus discharge from the gingival sulcus, tooth mobility,
the tooth and primarily its supporting structures (destruc- and pathologic migration. Apart from the classical clinical
tion of periodontal ligament and alveolar bone), is undoubt- signs, periodontal diseases are also evident in radiographs
edly still the only common cause for premature loss of teeth. in terms of alteration in periodontal ligament width and
In developing countries such as India the lack of awareness lamina dura, alveolar bone changes (interdental and alveo-
of the importance of high standards of oral health and its lar), furcation involvement, root resorption, etc.
effect on systemic health and inadequate health care facili- Although a thorough clinical examination will aid in
ties compounds the problem. making a good working diagnosis, it is universally accepted
Periodontal diseases are clinically characterized by gin- that radiographs supplement clinical examination and they
gival inflammation, gingival recession, periodontal pockets, help in formulating an ideal treatment plan.
RADIOGRAPHIC APPLICATION 3. Evaluation of root fractures and cementa/ tears

IN THE DIAGNOSIS AND TREATMENT 4. Assessment of local jaw pathology and systemic conditions
PLANNING OF PERIODONTAL DISEASE causing bone destruction
Local and systemic conditions that influence the 5. Assessment of bone quantity (especially important for
health of the periodontium can be assessed using intra- implant placement)
oral and extraoral radiographs. The following are the
6. Surgical planning and assessment of bone defects for
conditions that can be radiographically assessed to a
placement of bone grafts.
large extent:
Along with the inherent advantages of radiographs for
l. Assessment of local factors that predispose/aggravate
diagnosis of periodontal diseases they have their limita-
periodontal disease (Figs 33.1-33.4):
tions as listed in the next section.
a. Calculus (primarily subgingival calculus)
b. Overhanging restorations
c. Ill-fitting/poorly contoured crowns
d. Endo-perio lesions LIMITATIONS OF RADIOGRAPHS
2. Assessment of tooth morphology and supporting structures:
a. Crown-root ratio 1. Early bone changes may not be evident on the
b. Root morphology radiograph, as a minimum of 55-60% demineralization
c. Width of the periodontal ligament space should have occurred.
d. Integrity of lamina dura 2. Conventional imaging techniques such as the intraoral
e. Bone in the furcation area periapical, bitewing, and panoramic radiography
£. Interdental bone (condition of crestal bone and provide only a two-dimensional view of the three-
extent/pattern of bone loss) dimensional bone structure.
FIGURE 33.1 Intraoral periapical radiograph showing evidence

of subgingival calculus and minimal interdental bone loss (Courtesy
Department of Oral Medicine and Radiology, Manipal College of Dental
Sciences, Mangalore).
FIGURE 33.3 Poorly contoured crown associated with interdental

bone loss (Courtesy Department of Oral Medicine and Radiology, Manipal
College of Dental Sciences, Mangalore).
FIGURE 33.2 Overhanging restoration (Courtesy Department of Oral

Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).
3. Conventional imaging may result in superimposition

and overlapped images, thereby making the radiograph FIGURE 33.4 Endo-perio lesion associated with the maxillary canine
occasionally nondiagnostic. (Courtesy Department of Oral Medicine and Radiology, Manipal College of
4. Soft tissue changes are not evident on conventional Dental Sciences, Mangalore).
imaging techniques.
Conventional Radiography
RADIOGRAPHS USEFUL FOR 1. Intraoral periapical radiographs
DIAGNOSING PERIODONTAL DISEASE 2. Bitewing radiographs
3. Occlusal radiographs
Both traditional and newer imaging modalities can be 4. Orthopantomograms.
used for the diagnosis of periodontal disease. However,
the clinician needs to judge the inherent advantages and
Newer Imaging Techniques
limitations of each of the projections and employ them
as required. Cone beam computed tomography
CHAPTER 33 ROLE OF RADIOLOGY IN THE DIAGNOSIS OF PERIODONTAL DISEASES 269
IMAGING CONSIDERATIONS FOR shortened, or overlapped (Fig. 33.6). Paralleling technique

PERIODONTAL DISEASE along with the wire grid is the best technique to quantify
the amount of bone loss (Fig. 33.7). This technique pro-
Periodontal tissues encompass a wide range of struc- vides an image with the least amount of distortion.
tures with varying radiodensities from bone (cortical Bitewing radiographs (Fig. 33.8) are also useful alterna-
and cancellous) to cementum. In order to improve the tives for assessing early and initial destruction of inter-
diagnostic yield of the radiograph, an image with a wider dental bone, assessing crestal bone contour and height,
gray scale is desirable. and evaluating poorly contoured restorations and pros-
thetic crowns that initiate and aggravate periodontitis.
Traditionally horizontal bitewings are used for assessing
Patient Selection interdental bone loss. However, moderate to severe bone
It is always advisable that the clinician conducts a thor- destruction extending apically can be evaluated best with
ough clinical examination and takes into consideration vertical bitewings (Fig. 33.9).
patients' present symptoms and signs and their underly- A diagnostic-quality intraoral periapical radiograph
ing systemic condition before embarking on radiographic should be able to exhibit the full crown, full length of
investigations. It goes without saying that the periodontist the roots and at least 2 mm beyond the periapex and
should weigh the benefits of taking dental radiographs
against the risk of exposing the patient to radiation. Ra-
diographs should be advised only when the clinician feels
that the additional diagnostic information obtained from
radiographs will affect patient care.
Choice of Radiographic Projection

Both conventional and specialized imaging may be used
to image periodontal structures. Conventional imaging
techniques are still widely used as they are more univer-
sally available and inexpensive. Newer imaging techniques
such as Cone beam computed tomography (CBCT) are
now finding their use in implant planning and detailed
supporting bone assessment for periodontal surgery.
If an overall view of the status of supporting bone is
required, an extraoral radiograph such as the panoramic FIGURE 33.6 Intraoral periapical radiograph taken using bisecting
radiograph (Fig. 33.5) may be taken. However, if the clini- angle technique revealing overlapped and elongated image (Courtesy
cian requires minute details such as the condition of the Department of Oral Medicine and Radiology, Manipal College of Dental
lamina dura, width of the periodontal ligament space, and
height of the alveolar bone, area-specific intraoral periapi-
cal radiographs using either bisecting angle or paralleling
technique can be used. Intraoral periapical radiographs,
though widely taken using bisecting angle technique,
may frequently provide images that are elongated, fore-
FIGURE 33. 7 Radiograph taken using paralleling technique along

FIGURE 33.5 Panoramic radiograph taken as a screening radiograph with a wire grid to assess the amount of bone destruction (Courtesy
to assess periodontal bone destruction (Courtesy Department of Oral Department of Oral Medicine and Radiology, Manipal College of Dental
Medicine and Radiology, Manipal College of Dental Sciences, Mangalore). Sciences, Mangalore).
FIGURE 33. IO Diagnostic quality intraoral periapical radiograph

(Courtesy Department of Oral Medicine and Radiology, Manipal College of
Dental Sciences, Mangalore).
FIGURE 33.8 Bitewing radiograph showing early interdental bone
loss (Courtesy Department of Oral Medicine and Radiology, Manipal College
of Dental Sciences, Mangalore). The full mouth series consist of 17 periapical and 4 bite-
wing radiographs. These include maxillary centrals (1),
maxillary laterals (2), maxillary canines (2), maxillary
premolars (2), maxillary molars (2), mandibular central
and lateral incisors together (2), mandibular canines (2),
mandibular premolars (2), mandibular molars (2), and
bitewing radiographs (4) consisting of premolars (2) and
molars (2).
Panoramic radiograph provides a broad coverage and
view of the upper and lower teeth and the supporting
bone. However, owing to its low resolution, it does not
provide fine detail. Also, unequal magnification is an-
other important limitation in panoramic radiographs. A
study by Valchovic et al (1986) showed that the panoramic
radiograph in comparison to full mouth series of intra-
oral periapical radiographs exhibited low specificity in
detecting evidence of periodontal disease. However, the
sensitivity was high and comparable to intraoral periapi-
cal films ranging from 87 to 96%.
Cone Beam Computed Tomography in the

Detection of Periodontal Disease
Before the advent of cone beam computed tomog-
raphy (CBCT), periodontal bone destruction was pri-
marily assessed with conventional imaging and digital
imaging such as radiovisiography (RVG) which has the
FIGURE 33.9 Moderate amount of interdental bone loss evident on inherent limitation of two-dimensional imaging. Since
a vertical bitewing radiograph (Courtesy Department of Oral Medicine and the introduction of CBCT in diagnostic radiography,
Radiology, Manipal College of Dental Sciences, Mangalore). various studies were carried out to evaluate its role in
maxillofacial imaging including imaging of periodontal
proximal aspects of adjacent teeth (if present), and the in- structures.
terdental bone (Fig. 33.10). Likewise a diagnostic-quality CBCT is used to evaluate integrity of lamina dura,
bitewing should be able to display each proximal surface periodontal ligament space and periodontal bone de-
at least once. fects (furcation defects; osseous craters; pattern, extent,
A full mouth series of intraoral radiographs will help in and location of bone defects), and implant planning and
diagnosis and treatment planning for periodontal diseases. postimplant assessment (Figs 33.11-33.16).
FIGURE 33.11 Axial section reveals loss of cancellous bone and FIGURE 33.13 Sagittal section shows bone loss extending to the
labial cortical plate with respect to the edentulous region 13. Bone loss middle one third of the distal surface of the distobuccal root of the first
extends up to the mesial surface of the root of 14 labio-palatally (Courtesy molar. Bone loss extending to the apical one third of the roots of the
Department of Oral Medicine and Radiology, Manipal College of Dental second molar involving the furcation. Bone loss extending up to the
Sciences, Mangalore). apical one third of the third molar (Courtesy Department of Oral Medicine
and Radiology, Manipal College of Dental Sciences, Mangalore).
FIGURE 33.12 Coronal section revealing bone loss up to the apical

one third of the 31, 32, 33 and 41 (Courtesy Department of Oral Medicine FIGURE 33.14 Sagittal section reveals labial and lingual bone loss
and Radiologi]. Manipal College of Dental Sciences, Mangalore). extending up to the apical one third of the incisor.
There are still some conflicting reports with regards to a with conventional imaging is a possibility of overlap of
better imaging technique for visualizing periodontal liga- adjacent anatomical structures.
ment space. However, majority of the studies report that
conventional intraoral periapical radiographs are superior
to CBCT for assessing periodontal ligament space. How-
Choice of Image Receptor and Collimation
ever, in comparison to computed tomography (CT) scan, Imaging can be performed using digital image receptors
CBCT images provide more clarity. The only limitation such as charge-coupled device (CCD), photostimulable
phosphors (PSP), and complementary metal-oxide semi-

conductors (CMOS) or conventional analog films.
In various studies to compare speed of film with pa-
tient exposure, F (Insight) speed film was shown to reduce
patient exposure by about 20-50% when compared with
E (Ekta) speed films and the slower D speed film caused
30-40% more patient exposure when compared with E
speed films. Also digital receptors are known to cause
the least patient exposure, reducing the exposure almost
up to 60% when compared with conventional films. It is
also preferable to use a rectangular collimator and a long
cone technique (target to skin distance of 40 cm) to further
minimize radiation exposure.
Most of the dental X-ray machines in India have fixed
tube voltage (kVp) and tube current (mA) settings be-
tween 60 and 70 kVp and 8 and 10 mA, respectively. How-
ever, wherever possible a higher tube voltage and a lower
tube current produce a wide gray scale (low-contrast im-
age) showing even the minor changes in the supporting
alveolar bone and outlines of soft tissue, which is best
suited for diagnosis of periodontal disease.
FIGURE 33.15 Coronal section reveals bone loss up to the middle Normal Periodontal Radiographic Anatomy
third of the distobuccal root of the molar on the buccal aspect and
up to the apical third in relation to the palatal root. Mucosa! thick- Periodontal tissues include the gingiva, periodontal
ening is also evident at the floor of the maxillary sinus (Courtesy ligament, cementum, and alveolar bone. Of these, radio-
Department of Oral Medicine and Radiology, Manipal College of Dental graphically the periodontal ligament in terms of status
of lamina dura (presence or absence) and the width; ce-
mentum in terms of the root width; and alveolar bone in
terms of the morphology, location, pattern, and extent of
destruction are routinely assessed.
Cementum
The tooth root is covered with an extremely thin layer
of cementum which is poorly mineralized when com-
pared with dentine (just about 50% as that of dentine).
This low mineral content makes it invisible on radio-
graphs. In radiographic terms the contrast between den-
tine and the cementum is very minimal, thereby exhibit-
ing the same radiodensity as that of dentine. However,
excessive secondary cementum formation (Fig. 33.17) can
lead to either a generalized uniform bulbous enlargement
of the root (hypercementosis) or a localized mass of ra-
diodensity at the apex (nodular type of hypercementosis).
Lamina Dura and Periodontal Ligament Space

Lamina dura is a radiographic term used to describe
the dense bone that forms the tooth socket (Fig. 33.18).
Radiographically, on a two-dimensional image, it ap-
FIGURE 33.16 Reconstructed 3D view reveals bone loss involving pears as a uniform radiopaque line that is in continuation
the furcation and middle third of the mesial root of the first molar. Pres-
ence of a periapical bone defect at the mesial root of the tooth (Courtesy
with the alveolar crestal bone and surrounds the root of
Department of Oral Medicine and Radiology, Manipal College of Dental teeth. The integrity of the lamina dura, variation in the
Sciences, Mangalore). thickness, etc., are usually considered as associated with
average thickness ranged between 0.22 and 0.54 mm. Stud-
ies have shown that the lamina dura is generally dense and
relatively thicker for teeth under greater occlusal loading.
Periodontal ligament space is the radiolucent space
between the root of the tooth and the lamina dura. The
ligament space is generally widest in the region approxi-
mating the alveolar crest and the periapical region of the
tooth and relatively thinner at the middle third of the
tooth. Histologically, the width of the periodontal mem-
brane ranges from 0.15 to 0.38 mm.
Alveolar Bone ( Crestal, lnterdental,

and Periapical)
The alveolar crest is the term used to describe that part
of the alveolar bone that extends interdentally toward the
cervical margin of teeth and is continuous with the lamina
dura of adjacent teeth. The alveolar crest is bounded by
dense cortical bone. The presence of the dense cortical out-
FIGURE 33.17 IOPAR reveals bulbous roots of molar suggestive of line usually signifies healthy periodontium and absence
hypercementosis (Courtesy Department of Oral Medicine and Radiology, of active disease process. The morphology of the crestal
Manipal College of Dental Sciences, Mangalore). bone varies based on the location. In between the anterior
teeth, the alveolar crest is pointed (Fig. 33.19) and in the
region of the posterior teeth it is flat topped and located
1-1.5 mm below and parallel to an imaginary line joining
cementoenamel junctions of adjacent teeth. In healthy
individuals the junction between lamina dura and the
alveolar crest forms a sharp angle (Fig. 33.20).
Majority of the bone is cancellous /spongy/ trabecular
in nature which is enclosed within dense buccal, lingual,
and palatal cortical plates. The bone marrow trabeculae
vary in the morphology and density in both the maxilla
and mandible. Complete absence of the trabeculae or
destruction/ abnormal morphology/ density of the tra-
becular pattern when compared with the opposite side
may indicate a disease process.
Trabecular Pattern in the Maxilla

Trabecular pattern is relatively sparser in the mandible
when compared with the coarse, dense trabeculae in the
maxilla (Fig. 33.21A and B). However, individual trabecu-
lae are dense when compared with the maxilla.
In the anterior segment of the maxilla, the trabeculae
FIGURE 33.18 Photograph illustrating lamina dura surrounding are very slender and closely placed giving rise to numer-
the roots of teeth (Courtesy Department of Oral Medicine and Radiology, ous small marrow spaces. In the premolar-molar region
Manipal College of Dental Sciences, Mangalore).
the marrow spaces are slightly larger. However, the tra-
becular pattern remains the same.
pathologies. However, one should also be aware that the
appearance of lamina dura also depends on the projection Trabecular Pattern in the Mandible
geometry of the X-ray beam. When the X-ray beam is Compared with the maxilla the trabeculae are fewer
directed tangentially, it may not show lamina dura very and arranged in a set horizontal pattern with large mar-
distinctly in spite of absence of disease. row spaces (Fig. 33.22A and B). In the molar region the
In a study by Hubar (1993) to quantify the thickness trabeculae are literally absent.
of lamina dura it was found that the lamina dura varied It is believed that the stronger and tougher the cortical
in thickness between anterior and posterior teeth and the plates, more sparse is the trabeculae and vice versa.
FIGURE 33.19 Pointed alveolar crest in the maxillary anterior region

(Courtesy Department of Oral Medicine and Radiology, Manipal College of
CHARACTERISTIC RADIOGRAPHIC
FEATURES OF PERIODONTAL DISEASES
Chronic Periodontitis
Early Stage FIGURE 33.21 Sparse trabecular pattern of the anterior and
Radiographic changes are usually evident almost posterior parts of the maxilla (Courtesy Department of Oral Medicine and
8-10 months after the initial occurrence of periodontal Radiology, Manipal College of Dental Sciences, Man galore).
disease. The earliest changes include widening of the peri-

odontal ligament space at the lateral margin of the tooth
approximating the cementoenamel junction and rounded
appearance of the crestal margin. As the disease progress-
es, loss of the cortical margin of the crestal bone followed
by mild erosion of the crestal bone is evident (Fig. 33.23).
Intermediate Stage
As the disease progresses, bone defects become more
obvious with resorption of the buccal and/ or lingual
cortical plate or cancellous bone defects. The bone defects
are usually evident on conventional imaging techniques
as a horizontal pattern of bone destruction or angular/
vertical pattern of bone loss.
HORIZONTAL PATTERN OF BONE LOSS

FIGURE 33.20 Flat topped crestal margins of the posterior teeth
(Courtesy Department of Oral Medicine and Radiology, Manipal College of Horizontal pattern of bone loss is the most common
Dental Sciences, Mangalore). form of bone loss that occurs when the buccal, lingual,
FIGURE 33.23 Loss of the cortical margin and mild erosion of the
crestal bone (Courtesy Department of Oral Medicine and Radiology, Manipal
College of Dental Sciences, Mangalore).
The exact location and pattern of the osseous defect

is not possible to identify on a conventional two-dimen-
sional image.
There are four distinct patterns that are recognized
as angular bone defects, namely: interproximal craters,
interproximal hemiseptal defects, proximal intrabony
defects, and inconsistent bony margins. Other less com-
mon defects include ledges and reversed architecture.
INTERPROXIMAL CRATERS Like the name suggests

interproximal craters are seen on radiographs as shallow
saucer-shaped or crater-like defects located at the alveolar
crests between two teeth. The apical extent of the defect
is usually not clearly visualized. It is considered to be the
most common osseous defect that is seen in moderately
progressed form of periodontitis.
INTERPROXIMAL HEMISEPTAL DEFECTS lnterproxi-

FIGURE 33.22 Bony trabecular pattern in the anterior and posterior mal hemiseptal defect is radiographically evident as a
region of the mandible (Courtesy Department of Oral Medicine and Radiol-
ogy, Manipal College of Dental Sciences, Mangalore). V-shaped defect. It results when bone is resorbed from
either the mesial or distal aspect of the root. Many of
these defects usually progress to involve the bone on the
and cancellous bones interposed between have been uni- buccal aspect of teeth.
formly resorbed. The bone loss either is localized to a few
teeth or affects multiple teeth (Fig. 33.24). PROXIMAL INTRABONY DEFECTS Proximal intrabo-
ny defect is a three-walled defect extending in an apical
ANGULAR PATTERN OF BONE LOSS
direction from the alveolar crest along the root length. It
The bone level is angulated when compared with an is bounded by the interdental septal bone (hemisepta) and
imaginary horizontal line drawn across the cementoe- the two cortical plates (buccal and lingual). On a radio-
namel junction of adjacent teeth (Fig. 33.25). The base graph it appears as a well-demarcated V-shaped defect.
of the bone defect is typically located apical to the bone Use of a contrast agent such as a gutta-percha point may
adjacent to it. be used to track the full depth of the intrabony defect.
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FIGURE 33.26 Panoramic radiograph showing angular and hori-

zontal bone defects in the advanced stage of periodontitis (Courtesy
Department of Oral Medicine and Radiology, Manipal College of Dental
LEDGES When the thick cortical plates resorb, they

may occasionally produce margins of bone that resemble
FIGURE 33.24 Radiograph showing interdental horizontal bone plateaus, which are referred to as ledges.
loss (Courtesy Department of Oral Medicine and Radiology, Manipal College
of Dental Sciences, Mangalore).
REVERSED ARCHITECTURE These forms of osseous
defects are more frequently seen in the maxilla. In this
form of defect, the radicular bone remains intact. Howev-
er, the buccal, lingual, and interdental bones are resorbed,
causing a reversal of normal bony architecture.
Advanced Stage
In the advanced form of periodontitis there are both
angular and horizontal bone defects. The involvement is
more generalized and severe, resulting in tooth mobility,
and as the disease progresses, teeth are lost (Fig. 33.26).
Aggressive Periodontitis
Aggressive periodontitis was previously referred to as
juvenile periodontitis. Although it has been reported to
occur at any age, the term aggressive periodontitis is usu-
ally reserved for that form of periodontal disease which
affects individuals younger than 30 years of age with no
underlying systemic illness with a tendency to aggregate
within families and cause extensive periodontal tissue
destruction.
The extent of periodontal destruction does not correlate
with the amount of local irritants (calculus). There are two
FIGURE 33.25 Intraoral periapical radiograph showing angular forms that are recognized based on the extent of involve-
interdental bone loss extending up to the apical one third of the root ment: localized aggressive periodontitis and generalized
(Courtesy Department of Oral Medicine and Radiology, Manipal College of aggressive periodontitis.
The localized form of aggressive periodontitis is char-
acterized by clinically deep periodontal pockets and
radiographically extensive bone defects (Fig. 33.27)
affecting the incisors and molars. Bone destruction as-
INCONSISTENT BONY MARGINS When either the sociated with the bilateral molars is described as "arc-
lingual or buccal cortical plates are resorbed in an uneven shaped mirror image."
or irregular fashion, an inconsistent crestal bony margin According to the consensus report on aggressive peri-
is formed. Radiographically they are evident as irregular odontitis reported by Lang et al (1999), the term general-
coronal edges of the cortical plates superimposed over ized aggressive periodontitis is used when at least three
the root of the affected tooth. permanent teeth are affected other than the first molars
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and incisors. The radiographic features usually cover the
entire gamut of bone destruction from minimal crestal
destruction to extensive bone destruction exhibiting both
horizontal and angular defects.
Periodontal Abscess
A periodontal abscess is typically formed due to en-
trapment of a foreign substance or debris such as loose
fragment of calculus, etc., within a periodontal pocket
FIGURE 33.27 Panoramic radiograph showing extensive bone and subsequently getting infected. Another possible
loss associated with the incisors and molars in aggressive periodontitis etiology is closure of the marginal gingival over a local-
(Courtesy Department of Oral Medicine and Radiology, Manipal College of ized infection within the periodontal pocket resulting in
an area of increased pressure further causing a swelling
(Fig. 33.28A and B).
Based on the severity and duration radiographically
the findings may vary from a normal interdental bone
to widening of the periodontal ligament space, inter-
dental bone loss, or in severe cases of chronic nature
extensive bone loss extending up to and involving the
apex of the tooth, occasionally resulting in a floating
tooth appearance. As a thumb rule acute abscesses hardly
exhibit any radiographic changes.
SYSTEMIC CONDITIONS
INFLUENCING PERIODONTITIS
1 Papillon-Lel'evre syndrome Periodontitis with palmar

plantar keratosis
2 Chediak-Higashi syndrome Oral ulcers with severe

periodontal destruction
3 Down syndrome Generalized gingival recession

with periodontal pockets
4 Acquired immunodeficiency Necrotizing ulcerative gingivitis

syndrome and periodontitis
5 Diabetes mellitus Multiple periodontal abscesses,
rapid destruction of alveolar
bone
SYSTEMIC CONDITIONS MIMICKING

PERIODONTITIS RADIOGRAPHICALLY
1 Systemic sclerosis Widening of periodontal

ligament space
2 Hyperpituitarism Hypercementosis
(gigantism, acromegaly)
3 Hyperparathyroidism Complete or partial absence of

lamina dura
FIGURE 33.28 Photograph depicting palatal swelling in relation
4 Gaucher disease Widening of periodontal
to the right premolar and molar. Intraoral periapical radiograph shows
(lysosomal storage ligament space and loss of
evidence of interdental bone loss extending to the apex of the molar. A
disease) trabeculae
broken toothpick is also seen on the mesial aspect of the molar (Courtesy
Department of Oral Medicine and Radiology, Manipal College of Dental 5 Gingival squamous cell Destruction of interdental bone
Sciences, Mangalore). carcinoma
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KEY POINTS
1. A minimum of 55-60% demineralization of bone is 4. Interproximal craters, interproximal hemiseptal defects,
required to be evident radiographically. proximal intrabony defects, inconsistent bony margins,
2. Radiographically an image with a wider gray scale is ledges and reversed architecture are various patterns
desirable of detection of periodontal disease. of angular bone loss.
3. Intraoral periapical radiograph using paralleling 5. Bone destruction associated with bilateral molars
technique along with the wire grid is the best technique described as "arc-shaped mirror image" is characteristic
to quantify the amount of bone loss. of aggressive periodontitis.
QUESTIONS 4. Stafne EC, Gibilisco J. Stafne's Oral Radiographic Diagnosis. 5th

ed. Philadelphia: WB Saunders Company; 1985.
5. Corbet EF, Ho DKL, Lai SML. Radiographs in periodontal disease
1. What are the indications for radiographs in periodontal diagnosis and management. Aust Dent J 2009;54(1 suppl):S27-43.
diseases? 6. Jervoe-Storm PM, Hagner M, Neugebauer J, et al. Comparison of
2. What are the limitations of radiographs in the cone-beam computerized tomography and intraoral radiographs for
assessment of periodontal disease? determination of the periodontal ligament in a variable phantom. Oral
Surg Oral Med Oral Pathol Oral Radial Endod 2010;109(2):e95-e101.
3. Enumerate radiographic projections that can aid in
7. Lang N, Bartold PM, Cullinan M. Consensus report: aggressive
diagnosis of periodontal disease. periodontitis. Ann Peridontol 1999;4:53.
4. Discuss various radiographic features of periodontal 8. Tugnait A, Clerehugh V, Hirschmann PN. The usefulness of
diseases. radiographs in diagnosis and management of periodontal diseases:
5. Name some systemic conditions that can radiographically a review. J Dent 2000;28:219-26.
9. Akesson L, Hakansson J, Rohlin M. Comparison of panoramic and
mimic periodontal disease.
intraoral radiography and pocket probing for the measurement of
alveolar bone level. J Ciin Periodontol 1992;19:232-326.
10. Pepelassi EA, Tsiklakis K, Diamanti-Kipioti A. Radiographic
Suggested readings detection and assessment of the periodontal endosseous defects.
1. Valachovic RW, Douglass CW, Reiskin AB, Chauncey HH, McNeil BJ. J Clin Periodontol 2000;27:224-30.
The use of panoramic radiography in the evaluation of asymptomatic 11. Faculty of General Dental Practitioners (UK). Radiographs
adult dental patients. Oral Surg Oral Med Oral Pathol 1986;61(3):289-96. in periodontal assessment. In: Selection Criteria for Dental
2. White SC, Pharoah MJ. Oral Radiology. Principles and Interpretation. Radiography. London: Royal College of Surgeons; 1998:42-44.
1st South Asia ed New Delhi: Elsevier 2014. 12. Akesson L, Rohlin Hakansson J. Marginal bone in periodontal
3. Hubar JS. Quantification of the lamina dura. J Can Dent Assoc disease: an evaluation of image quality in panoramic and intraoral
1993;59(12):997-1000. radiography. Dentomaxillofac Radiol 1989;18:105-12.
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CHAPTER
34
Advanced Diagnostic Methods
CHAPTER OVERVIEW
Diagnosis is derived from the Greek word gnosis ("to defined as the process of identifying a disease by its signs,
know") and dia ("through"). Medical diagnosis has been symptoms, and results of various biological tests.
USES CONVENTIONAL DIAGNOSIS

• Clinical utility Periodontitis is an inflammatory process caused by
• Research utility host-parasite interactions, which lead to tissue destruc-
• Administrative utility. tion. This results in pocket formation, loss of connective
tissue attachment, bone loss, tooth mobility, and tooth
loss. Dentists have limited means to detect periodontal
Clinical Uses disease. Conventional diagnostic techniques have focused
Diagnostic procedures may be used to: on attachment loss and estimating alveolar bone loss on
radiographs, but these techniques have limitations as they
• Identify people at risk measure only the past disease.
• Screen for disease
• Classify disease The Basis
• Treatment planning
• Monitor treatment efficacy and detect disease recur- Classification helps in systematic study of diseases. It
rence. is the first step in the identification of disease. There are
two approaches to classification:
• Ontological approach
Research Uses • Physiological approach
• Classification of disease helps to identify patterns of Ontological approach deals with the general concept of
disease within populations and evaluate treatment. a disease. Physiological approach considers the particular
• Accurate diagnosis is essential for selection of samples case of illness in a specific patient. Both approaches are
from the population. essential in identifying and treating diseases. Diagno-
sis should have both clinical and biological plausibility.
Clinical utility means the diagnosis should dictate pos-
Administrative Uses sible treatment options and suggest the likely course of
• In developed nations, diagnosis is essential for claim- the disease. Biological plausibility means the diagnosis
ing dental insurance. should be able to distinguish between conditions that
• Diagnosis is essential for effective communication behave similar clinical presentations but different etiologies.
tween clinicians.
Evaluating Diagnostic Tests
The goal of periodontal diagnosis is to classify peri-
odontal disease, provide optimal therapy, and give a re- Some amount of uncertainty exists in the formulation
alistic prognosis. of diagnosis and the interpretation of all diagnostic tests.
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TABLE 34.1 Evaluation of Diagnostic Tests involved the use of sense of touch, sight, smell, and even
Results of test Presence of disease Absence of disease
taste and hearing. Systematic diagnosis evolved in the
sixteenth century.
Positive True-positive (1) False-positive (2)
Negative False-negative (3) True-negative (4)

Clinical Evaluation
Total 1+3 2+4
The periodontal probe was the first attempt to quantify
the data and record severity of disease.
A diagnostic test can give a positive or negative result. GV Black was the first to describe the systematic use
When the result is correct, it is true-positive, and if incor- of a noncalibrated probe. Simonton developed the cali-
rect, it is false-positive. Similarly, true-negative and false- brated University of California periodontometer and also
negative results may also exist (Table 34.1). the method of charting. Till date the use of visual signs
• The sensitivity of a test is the proportion of subjects and periodontal probe to quantify and record severity of
with the disease who test positive. periodontal disease has been the most popular tool.
• The specificity of a test is the proportion of subjects
with the disease who test negative.
Limitations of Probing
Probing depth does not necessarily correspond to
TRUE DISEASE STATUS pocket depth.
Factors that affect probing are as follows:
Sensitivity and specificity help in choosing an appro-
priate test. Once the result has come, the probability that 1. Nature of soft tissues
the test will be right is given by the predictive value. The 2. Probing force
probability that a person with a positive test has the dis- 3. Angulation of the probe
ease is called positive predictive value and vice versa. 4. Pocket configuration
5. Type and location of calculus
6. Degree of healing with long junctional epithelium after
Diagnostic Sequence treatment
Collection of Data 7. Morphology of the tooth.
Accurate data collection by a systematic approach is This resulted in a search for newer diagnostic aids to
necessary to arrive at a diagnosis. Organized and struc- overcome the limitations.
tured examination ensures that no aspect of the patient's Specific indices have been developed for the assess-
status is overlooked. The medium for recording exami- ment of other features such as gingival bleeding and tooth
nation findings may be just charting or computerized mobility.
medium. Miller proposed a graduated mobility scale to record
lateral movement when a tooth was displaced between
Primary Diagnosis two instrument handles.
Formulating a primary or presumptive diagnosis is Muhlemann developed a periodontometer for record-
essential. The goal is to limit uncertainty. This helps the ing horizontal mobility with greater precision.
clinician change the diagnosis later if required.
Histological Evaluation
Disease Activity
Janssens discovered the first microscope.
Disease activity is the loss of the clinical attachment GV Black described the principal fibers of periodon-
caused by periodontitis. There is no practical method tium and supported local inflammatory concept of peri-
available that can predict attachment loss. The clinician odontal disease.
has to rely on the record of attachment loss that has al- A group of Viennese researchers described in detail the
ready occurred. Recording disease activity is essential anatomy of periodontium.
because pretreatment disease severity plays an important Coolidge described the width of periodontium.
role in determining response to therapy. Waerhaug described the nature of attachment of gin-
gival epithelium and the role of plaque.
Early Approaches to Periodontal Diagnosis Disadvantage of Histological Evaluation
Diagnosis is mainly based on understanding patho- The disadvantage of histological evaluation is the
physiology of periodontitis. So the earliest instruments invasive nature of biopsy technique.
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C H A PT ER 34 A D VA N C ED D IA G N O ST IC M ET H O D S 281
Radiographic Diagnosis AIDS IN CLINICAL DIAGNOSIS

The first dental radiograph was taken by King.
• Gingival bleeding
Edmond Kells was the first to use X-rays for diagnosis.
• Gingival temperature
Thoma noted the use of radiograph in periodontics.
• Periodontal probing
Neumann used radiopaque markers to record pocket
• Tooth mobility.
topography.
Updegreaves developed the standardized film holders.
The use of conventional radiographic techniques has Gingival Bleeding
demonstrated certain limitations such as:
Color and texture changes are the visible signs of in-
1. Image distinction flammation. However, there may be underlying structural
2. Difficulty in reproducing the radiographs changes without visible clinical signs. Gingival bleeding is
3. Inability to identify initial signs of disease activity a good indicator of presence of inflammatory infiltrate in
4. Inability to identify etiologic factors. the connective tissue. It is more objective, while color and
Newer diagnostic methods have offered some promise. texture assessment is more subjective. Gingival bleeding
can be elicited by using a periodontal probe or wooden
interdental aids such as toothpicks, but its relationship to
Application of Microbiological Techniques disease progression is not clear. Bleeding on probing may
Antonie van Leeuwenhoek first described in 1683 five indicate periodontal stability except in smokers.
types of "animalculae" obtained from scrapings on hu-
man teeth.
WD Miller described that periodontal infection was
Gingival Temperature
nonspecific. According to Kung and coworkers, thermal probes are
Base and Johns made the first attempt to postulate that sensitive diagnostic devices used to measure early inflam-
a specific microorganism is responsible for periodontal matory changes in the gingival tissues. The Periotemp
disease. They demonstrated the use of smears of plaque probe (Abiomed, Danvers, MA) is a commercially avail-
collected from periodontal pockets, stained for amoeba able system. It helps clinician detect pocket temperature
as a diagnostic tool. difference to 0.1 °C from a referenced sublingual tempera-
Prinz used smears for Plaut-Vincent organisms. ture. Healthy sites have lower temperature than reference
Keyes used phase contrast microscopy to identify bac- sites. Temperature is increased in periodontal disease
terial morphotypes. sites. Individual temperature differences are compared
Culture studies have been used to identify specific with those expected for each tooth and the results are
microorganisms. shown by one of the three light-emitting diodes:
Newer techniques such as DNA probes have been used
• Green - inactive or low-risk site
to identify several bacterial species associated with dis-
• Yellow - intermediate-risk site
ease activity.
• Red - higher-risk site
Measurement of Host Response in Periodontal A natural temperature gradient exists in the dental
Disease arches. Posterior sites are warmer. Mandible is warmer.
The reason why temperature increases with probing
Metchnikoff was the first to describe the role of white depth is not known. It could be because of increased cel-
blood cells in inflammation. lular and molecular activities caused by increased peri-
Znamensky gave the observations that were similar to odontal inflammation. It is also found that subgingival
our current understanding of the pathogenesis of peri- temperature is elevated in areas showing attachment loss
odontitis. and periodontal pathogens. Variations in subgingival
Bass and Johns recommended microscopic examina- temperature have been observed in smokers as compared
tion of GCF contents. with nonsmokers.
Brill and coworkers described the contents and chemi-
cal composition of the gingival crevicular fluid (GCF).
Earlier, the diagnosis of periodontal disease was main- Periodontal Probing
ly based on symptoms. Improvement in understanding
Periodontal probing is a simple, yet an essential ele-
and development of technology in various disciplines has
ment of the intraoral examination. It is used to:
resulted in the development of newer diagnostic proce-
dures for early identification of the disease. This facilitates 1. Measure probing depth
effective and least invasive intervention. 2. Determine attachment levels
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3. Measure gingival recession and width of attached

gingiva
4. Assess nature of soft tissue
5. Detect bleeding on probing
6. Detect presence of plaque, calculus, and defective
margin of restorations.
The problems associated with the periodontal probes
are lack of sensitivity and reproducibility of measure-
ments. The disparity between measurements depends
on:
1. Probing technique
2. Probing force
3. Size of the probe
4. Angle of insertion of the probe
5. Precision of the probe calibration
6. Nature of the underlying soft tissues (whether inflamed
or fibrotic).
Different probe prototypes have been developed since
1980s to overcome these limitations.
The National Institute of Dental and Craniofacial Re-
search (NIDCR) proposed the following criteria for an FIGURE 34.1 Three types of Florida probe - cementoenamel junc-
ideal probe: tion (CEJ), stent, and disk. Courtesy: Sharad Pawar Dental College, Wardha.
1. A precision of 0.1 mm
2. A range of 10 mm continuous and three-dimensional topography of the
3. A constant and standardized probing force pocket being examined.
4. Noninvasive, lightweight, and easy to use • Fifth-generation probes: They aim to identify the attach-
5. Easy to access any location around all teeth ment level without penetrating it. These are noninva-
6. A guidance system to ensure proper angulation sive probes, e.g., ultrasound probe.
7. Complete sterilization of all portions entering the
mouth; cold sterilization not acceptable
8. No biohazard from material or electric shock Tooth Mobility Assessment
9. Direct electronic reading and digital output. Tooth mobility is one of the important clinical mani-
Periodontal probes may be divided into five generations: festations of an advanced periodontal disease. It may be
determined statically and dynamically. The static method
• First-generation probes: Conventional manual (hand- measures the deviation of tooth position when a prede-
held) probes. termined force is applied to the tooth at a defined point.
• Second-generation probes: Pressure-sensitive probes, e.g., The dynamic determination is used to gain information
true pressure-sensitive probes. Thirty grams of probing about the biophysical behavior of a tooth in its alveolus
pressure is sufficient to determine the probing pocket under the influence of changing forces.
depth. Fifty grams of probing pressure is required to Miller described the most commonly used clinical
detect alveolar bone defects. However, these probes method in which the tooth is held firmly between two
lack tactile sensitivity. instruments and moved back and forth. The mobility was
• Third-generation probes: Computerized probes, e.g., scored from 0 to 3 as follows (Table 34.2):
Florida probe (Fig. 34.1), Foster-Miller probe, and To-
ronto automated probes. 0: There is no detectable movement when force is
Limitations of automated probes: applied.
• Reduced tactile sensitivity 1: There is barely distinguishable tooth movement.
• Increased patient discomfort 2: The crown of the tooth moves up to 1 mm.
• Expensive. 3: The tooth can be depressed or rotated in its socket.
• Fourth-generation probes: These are under development. Percussion test is another method. It provides qualita-
In these devices an attempt to extend linear prob- tive information through the change in sound character-
ing in a serial manner is made to take account of the istics from "highly pitched" to "low pitched."
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TABLE 34.2 Miller's Evaluation of Tooth Mobility AIDS IN RADIOGRAPHIC DIAGNOSIS
Miller's original classification MI PTV
Dental radiographs are the conventional methods used
No movement distinguishable 0 -8 to +19
to assess the destruction of alveolar bone. They provide
First distinguishable sign of movement 1 +10 to +19 meaningful information on:
Crown deviates within 1 mm of its 2 +20 to +29
• Interproximal bone levels
normal position
• Crown-root ratio
Mobility is easily seen and tooth 3 +30 to +50 • Root length
moves 1 mm in any direction or can be
rotated in its socket
• Root proximity
• Integrity of lamina dura
Ml, Mobility index; PTV, Periotest value.
• Width of periodontal ligament space
• Presence of periapical lesions
• Height of remaining alveolar bone.
About 30% or more of alveolar bone should be lost
Manual method helps the assessment only after a pal-
before any detectable changes can be seen on the radio-
pable mobility exists and not during the early stages of
graph.
mobility.
The limitations of conventional radiographs are as
Periodontometer was introduced by Muhlemann to
follows:
measure tooth mobility. Laser techniques using helium-
neon gas laser were used by Ryden et al, but these meth- • Highly specific but lack sensitivity
ods were unsuitable for routine use. • Difficulty in reproducing radiographs due to the
In 1982, Schutle and coworkers developed a simple and variable projection geometry, contrast, and density
easy-to-manage, objective procedure called "Periotest" • Masking of bony changes by other anatomic structures
(Siemens AG, Germany; Fig. 34.2). • No information on buccal and lingual bony cortical
Periotest measures the reaction of the periodontium plates.
to a predetermined percussive force applied to the tooth.
The variations in projection geometry can be overcome
It measures the damping characteristics of the periodon-
by using paralleling technique. Variation in contrast and
tium. The instrument is similar in design and size to a
density can be overcome to some extent by standardizing
dental handpiece.
the film and other related radiologic accessories.
A metal rod is accelerated to a speed of 0.2 m/ s and
maintained at a constant speed. On impact, the tooth is
deflected and the rod deaccelerated. The contact time be- Digital Radiography
tween the tapping head and tooth varies between 0.3 and
0.2 ms and is shorter for stable than for mobile tooth. The Digital intraoral radiography can be used to overcome
Periotest value ranges from -8 to 50 (Table 34.2). the variations in image quality. It allows the use of com-
puterized images. These images can be stored, manipu-
lated, and corrected for underexposure or overexposure.
Digital intraoral radiography also reduces the radiation
dose by one-half to one-third.
Subtraction Radiography
Subtraction radiography relies on the conversion of
serial radiographs into digital images. These serial digi-
tal images are then superimposed and the composite is
viewed on a video screen. Changes in the bone density
and volume can be seen. Bone gain is seen as lighter ar-
eas and bone loss as darker areas. Computer-assisted
subtraction radiography helps in detecting changes from
the baseline images. This technique helps in detection of
minor changes in the bone by removing the unchanged
anatomic structures from the image. Thus, it increases
FIGURE 34.2 Periotest for implant mobility assessment. the sensitivity.
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The main disadvantage is the need to get an identical susceptibility testing can also be done. The disadvantages
alignment to obtain accurate sequential radiographs. of this method are as follows:
To overcome this disadvantage a new technique called
• Only live organisms can be grown. So strict sampling
diagnostic subtraction radiography (DSR) has been intro-
and transport conditions are required.
duced. This method combines a positioning device during
• Fastidious organisms are not easy to culture.
film exposure and specialized software. This software
• Sensitivity is low.
corrects any minor changes of alignment.
• Sophisticated equipment and experienced personnel
are required.
Computer-Assisted Densitometric Image • It is relatively time-consuming and expensive.
Analysis System
In computer-assisted densitometric image analysis Direct Microscopy
(CADIA) system a video camera measures the light trans-
Dark field or phase contrast microscopy can be used
mitted through a radiograph and the signals are con-
to assess the morphology and mobility of bacteria, but
verted into grayscale images. The camera is connected
most of the periodontal pathogens are nonmotile. So its
to an image processor and a computer. Here the images
utility is limited.
are stored and mathematical manipulation of the images
is done. This system has a higher sensitivity than other
systems. AIDS USED IN IMMUNOLOGICAL
AND BIOCHEMICAL DIAGNOSIS
Computerized Tomography
Immunodiagnostic Methods
Computerized tomography (CT) gives an exact picture
Immunological assays utilize antibodies that recognize
of the bone levels in all the three phases, namely coronal,
specific bacterial antigens to detect target microorgan-
axial, and sagittal planes in implant dentistry. A localized
isms. This principle is used in the following diagnostic
computerized tomography technique is also available.
procedures:
1. Direct immunofluorescent microscopy assays
Photodensitometric Image Analysis Technique
2. Indirect immunofluorescent assays
This technique is used to evaluate bone resorption in 3. Flow cytometry
furcation areas. Radiographic film absorbs a beam of light. 4. ELISA
Microdensitometer linked to a microcomputer enables the 5. Membrane assay
clinician to detect variations in bone density that cannot 6. Latex agglutination.
be detected by naked eye.
Direct Immunofluorescent Assays
They use both monoclonal and polyclonal antibodies.
AIDS IN MICROBIOLOGICAL DIAGNOSIS These antibodies are conjugated to a fluorescent marker
that binds with the bacterial antigen to form a fluorescent
Microbiological tests are used to identify putative immune complex detectable under a microscope (Fig. 34.3).
pathogens. These tests are used to: Indirect Immunofluorescent Assays
• Support the diagnosis This procedure employs a secondary fluorescein-
• Serve as indicators of disease initiation and progression conjugated antibody that reacts with the primary anti-
• Determine which periodontal sites are at high risk for gen-antibody complex. Both direct and indirect immune
active destruction fluorescent assays can detect the pathogen and measure
• Monitor the healing response. the quantity of the pathogen directly in a given plaque
smear (Fig. 34.3).
Bacterial Culturing Flow Cytometry
Culture methods have been used to characterize the - It helps in rapid identification of bacteria.
composition of supragingival plaque. They are still con- - Bacterial cells are labeled with species-specific antibody
sidered as the gold standard. Plaque samples are cultivat- and then with fluorescein-conjugated antibody.
ed under anaerobic conditions. Selective and nonselective - The suspension is then introduced into the flow
media are used. Several physical and biochemical tests are cytometer. This separates the bacterial cells into single
done to identify pathogenic microorganisms. Antibiotic cell suspension by means of laminar flow through
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Antibody
Fluorescent/
ctyemolewle
• T /Anbgon
.. .
Antibody~
" 4
4
.. 4
!
Cell surface Complement
added
e Antibody is e Antigen is adsorbed
1- 0
(Al
adsorbed to well to well
.. n
Anhbody~
.. • 4
..
-4
~
l
Anlibody to
f) f)
original antibody Patient sample is added; Patient antiserum is added;
complementary antigen binds complementary antibody binds
Fluoresce
~
1- toantibody lo antigen
. -·
dye
.. .. '· ~ • •
B C
FIGURE 34.3 Immunofluorescence assay.

e e
Enzyme-linked antibody specific Enzyme-linked anli-HISG is
for test antigen is added and binds added and binds to bound
a narrow tube. After incubation the cells are passed to antigen. forming sandwich antibody
through a focused beam of laser. The cells then scatter
the light at low and wide angles and the fluorescent +
emission can be measured by appropriate detectors. a
- However, it is very expensive.
0 0
Latex Agglutination Assay Enzyme's substrate (0) is added, Enzyme's substrate ( D) is
and reaction produces a visible added, and reaction produces
This assay is based on the binding of protein to latex. color change (•) a visible color change ( •)
Latex beads are coated with species-specific antibody.
(A) (B)
When it contacts antigen, cross-linking occurs. A visible
precipitate is seen in 2-5 min. There are two types: (i)
FIGURE 34.4 ELISA. (A) A positive direct ELISA to detect antigens;
indirect assay; (ii) inhibition assay. (B) a positive indirect ELISA to detect antigens.
Anti-HISG, Mouse monoclonal IgG2b antibody (commercially available
1. Indirect assay: Antibody is bound to latex. A suspension
antibody).
of plaque sample is mixed and gently agitated for
3-5 min; if the test is positive, agglutination occurs.
2. Inhibition assay: Here the expected agglutination
between known antigen and antibody is inhibited as 2. Require stringent sampling and transport methodology.
a result of competition.
EVALUSITE Enzymatic Methods

It is a membrane immunoassay. Here the immune com- P. gingivalis, T. forsythia, T. denticola, and Capnocyto-
plex is seen through a colorimetric reaction. It is designed phaga species release a trypsin-like enzyme. These en-
to detect Aggregatibacter actinomycetemcomitans, Porphy- zymes hydrolyze a colorless substrate called N-benzoyl-
romonas gingivalis, and Prevotella intermedia. DL-arginine-2-naphthylamide (BANA). They release a
chromophore ~-naphthylamide. This turns orange red
ELISA when a drop of fast garnet is added to the solution. The
Enzyme-linked immunosorbent assay (ELISA) is simi- commercially available diagnostic kit is called Perioscan.
lar to other radioassays. Microwells are coated with anti- Disadvantage: It only detects a limited species of
body. Then test samples are added and incubated. After pathogens.
washing, another antibody labeled with an enzyme is
added followed by a suitable substrate. The enzyme will Diagnostic Methods Based on Molecular Biology
break down the substrate to yield suitable color (Fig. 34.4).
Nucleic Acid Probes
Disadvantages of Immunological Assays A nucleic acid probe is a molecule of either DNA or
1. Cross-reactivity resulting in false-positive and false- RNA from a specific microorganism. It is artificially
negative results synthesized and labeled with an enzyme or radioisotope.
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POLYMERASE CHAIN REACTION (PCR)

I I
Target DNA
I I
(a) Melt DNA at 94°C
Add primers ( 0)
ATP, GTP, CTP TTP~
and heat-stable ~ ·
I I ,
· (b) Cool to 60°C
"Tl
jj
u,,
-fl
DNA polymerase 0
-<I
0:
ii
r
m
11
I
(c)
2 copies
II •
I (d)
Melt and cool
(e)
U>!
m,
0
o!
I·
z
! Jr !
0
()!
-<I
0:
FIGURE 34.5 DNA hybridization. r
m
These single-stranded nucleic acid hybridize (pair with

complementary DNA strands to produce double-stranded
nucleic acid) and thus detect the presence of target micro-
4 copies
I I II I 7 :i!
jj
0
organism (Fig. 34.5). DNA probes may target whole ge- s copies 111 111 U II U 111 U 111 Id
-<I
nomic DNA or individual genes (whole genomic probes O!
r
and oligonucleotide probes). Whole genomic probes have
FIGURE 34.6 Polymerase chain reaction.
been developed to detect A. actinomycetemcomitans, P.
ATP, adenosine triphosphate; GTP, guanosine triphosphate; CTP, cyti-
gingivalis, P. intermedia, and T. denticola. Examples of com- dine triphosphate; TTP, thymidine triphosphate.
mercially available probes are DMDx and Omnigene.
However, disadvantage is cross-reactivity. Oligonucle-
otide probes have been developed. These probes are as templates (Fig. 34.6). Then DNA or a portion of DNA is
complementary to variable regions of 16s and 50s RNA amplified using DNA polymerase enzyme. This enzyme
bacterial genes. requires a primer to act. To obtain large quantities of am-
plified fragments a second primer is used. This amplifica-
Checkerboard DNA-DNA Hybridization Technique tion is performed several times by a process called cycles.
It is used for detection and measuring levels of 40 bac- This technology helps in detection of many periodontal
terial species in the oral cavity. This assay uses whole pathogens. The limitation is that this test provides infor-
genomic, digoxigenin-labeled DNA probes. A single test mation only about prevalence of the tested bacteria. So it
can detect up to 40 species using hybridization technique. cannot be used for diagnostic and prognostic purposes.
Polymerase Chain Reaction Restriction Endonuclease Assay

Polymerase chain reaction (PCR) is most commonly Restriction endonuclease identifies and breaks double-
used for amplifying genes and their RNA transcripts. In stranded DNA at specific base pair sequences. The DNA
this procedure DNA is separated from fresh tissue speci- fragments are separated by electrophoresis, stained with
men. By heating DNA is split into single strands, which act ethidium bromide, and seen under ultraviolet light. Then
electrophoretic pattern of DNA fragments is analyzed. test does not discriminate between the sites with severe
Each pattern is like a fingerprint for each strain of bacteria. inflammation with or without attachment loss.
This technology has been used to identify different strains
of major periodontal pathogens. Alkaline Phosphatase
Alkaline phosphatase (ALP) is an enzyme found in ma-
ny cells of periodontium, such as osteoblasts, fibroblasts,
Advances in Characterizing the Host Response and neutrophils. It is found to be increased in periodontal
Assessment of host response is the study of mediators disease sites.
that are part of the individual response to the periodon-
tal infection. Potential sources of samples include saliva, {3-Glucuronidase
GCF, blood serum, blood cells, and urine. But saliva and It is a lysosomal enzyme found in azurophilic gran-
GCF components show a lot of promise. ules of neutrophils. It is found to be increased in active
Several techniques have been used for collection of disease sites.
GCF, from paper strips to micropipettes. The fluid vol-
ume can be measured in various ways. The most recent Elastase
technique is using Periotron 6000. It is a serine protease also found in azurophilic granules.
Saliva is another fluid that can be collected easily with It is found to be increased in sites with periodontitis. A
or without stimulation from major salivary glands. Di- rapid chairside kit called Periocheck has been developed.
agnostic markers found in saliva include proteins and
enzymes of host origin, host cells, hormones, bacteria and Cathepsins
bacterial products, volatile compounds, and ions. They are a group of acidic lysosomal enzymes found
to be elevated in periodontal disease and decreased after
therapy.
Inflammatory Mediators and Products
Cytokines are potent local mediators of inflammation Matrix Metalloproteinases
that are produced by a variety of cells. Cytokines used Matrix metalloproteinases (MMPs) are members of
as potential diagnostic markers include tumor necrosis a large subfamily of zinc-dependent and calcium-de-
factor (TNF-a), interleukin (IL)-la, IL-113, IL-6, and IL-8. pendent proteolytic enzymes. They are responsible for
These molecules appear to be good candidates as markers remodeling and degradation of extracellular matrix com-
of disease progression. ponents. Levels of MMPs are found to be increased d ming
periodontal disease. A decrease in MMP-8 levels is noted
after therapy. A chairside test stick has been developed
Host-Derived Enzymes for detection of MMP-8 levels in GCF.
Various enzymes are liberated from host cells during
the process of periodontal destruction. The enzymes that Tissue Breakdown Products
cause intracellular damage have the potential to be the
markers of active periodontal destruction. In periodontitis there is destruction of collagens and
extracellular matrices. The extracellular matrix contains
Aspartate Aminotransferase a variety of molecules such as glycoproteins (laminin,
fibronectin), proteoglycans (versican, decorin), and non-
Aspartate aminotransferase (AST) is an enzyme re-
collagenous proteins (elastin, osteocalcin, osteopontin).
leased from dead cells of a variety of tissues. A marked
All these matrix molecules can be theoretically detectable
elevation of AST levels has been noted during gingival
and potentially informative in terms of their clinical di-
inflammation and periodontal disease. A rapid chairside
agnostic utility. But further research is needed to confirm
test has been developed called Periogard. The test in-
their usefulness.
volves collection of GCF with a filter paper strip. Then it
is placed in tromethamine hydrochloride buffer.
A substrate reaction mixture containing L-aspartic and Other Diagnostic Aids
a-ketoglutaric acids is added and allowed to react for
10 min. AST catalyzes the conversion of aspartate and glu- Genetic Susceptibility Test
tarate to oxaloacetate and glutamate. The addition of dyes Genetic testing for the IL-1 genotypes in dentistry was
such as fast red results in colored product. The intensity begun in 1997 with the introduction of the periodontal
of this test is directly proportional to the AST activity in susceptibility test (PST®, Interleukin Genetics, Inc., San
the GCF sample. A correlation between presence of AST Antonio, TX). It provides only additional information
activity and periodontal pathogens is seen. However, this about a patient's susceptibility to chronic periodontitis.
It measures the absence or presence of specific markers of Strategies for Diagnostic Testing
the patient's inflammatory response to plaque. Clinician
should be aware of the risk/benefit ratio before conduct- Rationale for Testing
ing the test. This test is expensive and not every patient Tests should be done to promote optimal therapeutic
tested positive will necessarily develop periodontal dis- decisions. This diagnostic testing can be used to increase
ease because it is a multifactorial disease. diagnostic certainty, screen for hidden disease, obtain
prognostic data, reassure the patient and clinician, aid in
Chairside Test for Detection of Elastase the selection of antibiotics, monitor patients, and deter-
Chromatography paper discs impregnated with the mine therapeutic end points.
appropriate peptidyl derivative of 7-amino-trifluoro-
methylcoumarin (AFC) are placed in a multiwell plate Determinant for Using These Tests
and covered with the appropriate buffer. The GCF sample The decision to perform test should be based on clini-
is taken on a standard chromatography paper strip and cal findings and relevant dental and medical history.
eluted into the buffer in the appropriate well. If the en- The response to conventional therapy is the major de-
zyme is present, it reacts with the peptide substrate and terminant for further diagnostic testing in patients with
splits off the AFC fluorescent group. Fluorescence detec- periodontitis. However, in certain unresponsive cases of
tion system detects the intensity of the fluorescence under periodontitis, systemically ill individuals, and patients
ultraviolet (UV) light and is proportional to the amount taking long-term antibiotics, diagnostic testing may be
of enzyme in the sample. helpful before therapy is started.
A simple color detection system can be used by adding The clinician should be aware of the cost involved in
p-dimethylamine-cinnamaldehyde to the well. This mol- testing, malpractice concern, patient requests, and profes-
ecule binds to the AFC leaving group forming a colored sional peer pressure. Additional tests should be done only
Schiff reagent. where indicated.
KEY POINTS
• Accurate diagnosis is essential for assessment of prog- keep pace with the improved understanding of the dis-
nosis and effective therapeutic management. ease pathogenesis.
• Conventional diagnostic aids are still the basic yardstick • Clinician should be aware of the factors that dictate the
for the disease assessment. selection of the most appropriate diagnostic technique
• Advanced diagnostic methods have evolved to over- in different clinical situations.
come the limitations of conventional techniques and
QUESTIONS 4. Evalusite is used to detect

a. P. gingivalis
1. The most objective sign of gingival health is b. A. actinomycetemcomitans
a. Change in color c. P. intermedia
b. Absence of exudation d. All of the above
c. Absence of bleeding on probing Answer: d
d. None of the above 5. Periocheck is used to detect
Answer: c a. Serine protease
2. The source of sample for diagnostic purposes is b. Proteoglycans
a. Blood c. Glycoproteins
b. Saliva d. None of the above
c. Gingival crevicular fluid Answer: a
d. All of the above 6. DNA probe is
Answer: d a. Fourth-generation probe
3. Aspartate aminotransferase is an enzyme released by b. Used to detect microorganism
a. Living cells c. Used to assess genetic susceptibility
b. Dead cells d. All of the above
c. Both of the above Answer: b
d. None of the above
Answer: b
Suggested readings 7. Lindhe J, Nyman S. Occlusal therapy. In: Lindhe J, Karring T, Lang
NP, editors. Clinical Periodontology and Implant Dentistry. Oxford:
1. Armitage GC. Clinical periodontal examination. In: Rose FL, Genco Blackwell Munksgaard; 2003.
RJ, Mealey ML, Cohen DW, editors. Periodontics: Medicine, Surgery 8. Sanz M, Newman MG, Quirynen M. Advanced diagnostic tech-
and Implants. St Louis: Elsevier; 2004. niques. In: Newman MG, Takei HH, Klokkevold PR, Carranza FA,
2. Eley BM, Cox SW. Advances in periodontal diagnosis. Proteolytic and editors. Carranza's Clinical Periodontology. 10th ed. St Louis: Elsevier;
hydrolytic enzymes link with periodontitis. Br Dent J 1998;184:323-8. 2006.
3. Eley BM, Cox SW. Advances in periodontal diagnosis. Potential mark- 9. Sanz M, Lau L, Herrera D, Marilla JM, Silva A. Methods of detection
ers of cell death and tissue degradation. Br Dent J 1998;184(9):427-30. of Actinobacillus actinomycetemcomitans, P. gingivalis and T. forsythensis
4. Jeffcoat MK, Wang IC, Reddy MS. Radiographic diagnosis in peri- in periodontal microbiology, with special emphasis on advanced
odontics. Periodontal 2000 1995;7:54-68. molecular techniques: a review. J Clin Periodontal 2004;31:1034-47.
5. Kornman SK, Newman MG. Role of genetics in assessment, risk 10. Watts TLP. Periodontics in Practice: Science with Humanity. Illus-
and management of adult periodontitis. In: Rose FL, Genco RJ, trated ed. New York: Thieme; 2000.
Mealey ML, Cohen DW, editors. Periodontal Medicine. Hamilton,
St Louis: BC Decker; 2000.
6. Lamster IB. In-office diagnostic tests and their role in supportive
periodontal treatment. Periodontal 2000 1996;12:49-55.
CHAPTER
35
Determination of Prognosis
CHAPTER OVERVIEW
Prognosis is established after the diagnosis is made and • Risk factors are those characteristics of individuals that
before the treatment plan is established. It is based on spe- put them at an increased risk for getting a disease.
cific information about the disease and the manner in which
Prognosis is the prediction of the course or outcome of
it can be treated, but can also be influenced by clinician's
a disease.
experience with treatment outcomes.
Prognostic factors are characteristics that predict the
Prognosis is often confused with the term risk:
outcome of disease once the disease is present.
• Risk generally deals with the likelihood that an indi-
vidual will get the disease in a specified period.
DEFINITION DETERMINATION
OF A PROGNOSIS
Prognosis is a prediction of the probable course, dura-
tion, and outcome of a disease based on a general knowl- The factors given in the next subsections are considered
edge of the pathogenesis of the disease and the presence when determining prognosis.
of risk factors for the disease.
Overall Clinical Factors

OVERALL VERSUS INDIVIDUAL
PROGNOSIS • Patient age:
• For two patients with comparable remaining
Prognosis can be divided into the following: connective tissue attachment levels and alveo-
lar bone, the prognosis is better for the older of
• Overall prognosis: Concerned with the dentition as a the two. This is because even though the repara-
whole tive process in a younger individual is greater,
Factors affecting overall prognosis are as follows: the amount of bone lost in a span of few years is
more than the bone formed when compared with
• Clinical factors the older patient.
• Systemic/ environment factors • The younger patient may have an aggressive type
• Individual tooth prognosis: Determined after overall of periodontitis or disease progression may have
prognosis and is affected by it. increased because of systemic disease or smoking.
Factors affecting individual tooth prognosis are as • Although the younger patient would normally be
follows: expected to have a greater reparative capacity, the
occurrence of so much destruction in a relatively
• Local factors short period would exceed any naturally occurring
• Prosthetic and restorative factors. periodontal repair.
CHAPTER 35 DETERMINATION OF PROGNOSIS 291
(A) (B)
FIGURE 35.1 (A) A tooth with deep pocket and less attachment loss and (B) a tooth with shallow pocket and severe attachment loss.
• Disease severity: is not sufficient bone to support the tooth, prognosis is

• Patients with a history of previous periodontal poor (Fig. 35.3).
disease may be indicative of their susceptibility for
future periodontal breakdown. Type of Defect (Horizontal or Angular)
• Prognosis is affected by: In case of horizontal bone loss, the prognosis depends
- Level of attachment (base of the pocket) on the existing bone, as it is unlikely that a significant
- Endodontic-periodontic relationship amount of bone regeneration will be induced by therapy
- Height of remaining bone (Fig. 35.4).
- Type of defect (horizontal or angular). In case of angular or infrabony defects, if the contour
of the existing bone and the number of osseous walls
Level of Attachment (Base of the Pocket) are favorable, there are always chances of regenera-
Level of clinical attachment reveals the clinical extent tion of bone after therapy to approximately the level of
of root surface devoid of periodontal ligament. A tooth alveolar crest.
with deep pockets and little attachment and bone loss When there is greater bone loss on one tooth surface,
has better prognosis than one with shallow pockets and the bone height on the less involved surfaces should be
severe attachment and bone loss (Fig. 35.1). considered when determining prognosis. In such a situ-
If the base of the pocket/level of attachment is close to ation the center of rotation of the tooth will be nearer
the root apex, prognosis is adversely affected. Presence the crown which results in a more favorable distribution
of an apical disease because of endodontic involvement of forces to the periodontium and less tooth mobility
also worsens the prognosis (Fig. 35.2). (Fig. 35.5).
For a tooth with questionable prognosis, the chances
Height of Remaining Bone of successful treatment should be weighed against any
Prognosis is also related to the height of the remaining benefits that would accrue to the adjacent teeth if the
bone. In case of teeth with severe bone loss wherein there tooth under consideration was extracted. Never make
any heroic attempts to retain a hopeless tooth that may

jeopardize the adjacent teeth.
Plaque Control
Effective removal of plaque by the patient on a daily
basis is critical to the success and prognosis of periodontal
therapy.
Patient Compliance and Cooperation

The prognosis for patients with gingival and periodon-
tal involvement is critically dependent on the patient's
attitude, desire to retain the natural teeth, and willingness
and ability to maintain good oral hygiene.
If patients are unwilling to perform adequate plaque
control, or follow justifications and receive timely peri-
odic, maintenance checkups, then the dentist can:
• refuse to accept the patient for treatment; or
• extract teeth that have a poor prognosis and perform
scaling and root planing on remaining teeth.
Systemic and Environmental Factors

Genetics
• Periodontitis is a multifactorial disease of which ge-
netic factors are one of the causes.
FIGURE 35.2 Base of the pocket close to the apex. • Genetic factors influence:
• interleukin (IL-1) genes causing its polymor-
phism=-e increased production of IL-1[3 ~ increased
risk for severe generalized chronic periodontitis;
• serum immunoglobulin G2 (IgG2) antibody ti-
ters and expression of Fc--yII receptors on neutro-
phil ~ significant in aggressive periodontitis.
Detection of genetic factors can influence the prognosis
in several ways:
• It can help in early implementation of preventive and
treatment measures for these patients.
• During the course of treatment, it can influence treat-
ment recommendations.
• Identification of young individuals at risk can lead to
FIGURE 35.3 Radiographs showing severe and moderate bone loss. the development of interventional strategies.
Smoking
Studies have shown that smoking may be the most
important environmental risk factor impacting the devel-
opment and progression of periodontal disease.
Horizontal bone defect
• Systemic effects of smoking include inhibition of pe-
Angular bone defect ripheral blood and oral neutrophil function, reduced
antibody production, and alteration of peripheral im-
munoregulatory T cells.
• It is apparent that smoking tobacco reduces bleeding
FIGURE 35.4 Intraoral periapical (IOPA) radiograph showing hori- on probing in the gingiva, which means that inflam-
zontal and vertical bone loss. mation is underdiagnosed.
(A) (B)
FIGURE 35.5 The shift in the center of rotation depending on bone loss.
• The response of smokers to periodontal treatment is prognosis for most of the cases depends on the ability of
less as well. They do not respond to conventional as both the patient and the clinician to remove these local
well as surgical periodontal treatment as patients who factors.
have never smoked. Prognosis in patients who smoke
and have slight to moderate periodontitis is fair to
Subgingival Restorations
poor. In patients with severe periodontitis, the prog-
nosis may be poor to hopeless. Subgingival margins may contribute to increased
• However, it should be emphasized that cessation of plaque retention, leading to inflammation and bone
smoking can affect the treatment outcome and also the loss. Even overhanging margins can create a negative
prognosis. impact on the periodontium. In general, a tooth with
any discrepancy in its subgingival margin has a poor
Systemic Disease and Condition prognosis.
Patient's systemic background affects overall prognosis
in several ways, for example, diabetes mellitus. Anatomic Factors
The prognosis is questionable when surgical treat- • Short tapered roots with large crowns: Prognosis is
ment is required, but cannot be provided because of the poor as there is disproportionate crown-root ratio and
patient's health. Diseases affecting patients' motor func- reduced root surface is available for periodontal sup-
tions such as Parkinson disease limit their oral hygiene port.
performances, adversely affecting prognosis. • Cervical enamel projections (CEP): These are flat,
ectopic enamel projections extending beyond the nor-
Stress
mal contours of cementoenamel junction. These are
Physical and emotional stress may alter the pa- most commonly seen on the mandibular molars
tient's ability to respond to the periodontal treatment (28.6%) and least frequently on the maxillary pre-
performed. molars (17%). Enamel pearls are round, large enamel
deposits that are present in the furcation areas. They
Local Factors appear least on the permanent molars (1.1-5.5%)
with 75% of them appearing in maxillary third mo-
Plaque/Calculus lars. Seventy-three percent of the mandibular first
Microbial challenge by plaque is the most important molars show bifurcation ridge crossing from the me-
local factor in periodontal disease, and having a good sial to the distal root at the midpoint of the furcation.
Careful analysis of the above-mentioned factors allows

the clinician to establish one of the following prognoses
as given by McGurrie and Nunn:
• Excellent: No bone loss, excellent gingival condition,
good patient cooperation, and no systemic/ environ-
mental factors
• Good: One or more of the following:
• Adequate remaining bone support
• Possibilities to control etiologic factors and establish
a maintainable dentition
• Adequate patient cooperation and no systemic/
environmental factors
• Fair: One or more of the following:
• Less than adequate remaining bone support
• Some tooth mobility
• Grade I furcation involvement
• Adequate maintenance possible
• Acceptable patient cooperation
FIGURE 35.6 Palatogingival groove on the right maxillary central
incisor. • Presence of limited systemic/ environmental factors
• Poor: One or more of the following:
• Moderate to advanced bone loss
Presence of these projections on the root surfaces in-
• Tooth mobility
terferes with the attachment apparatus and prevents re-
• Grl and Gr2 furcation involvements
generative procedures from achieving their maximum
• Difficult-to-maintain areas or doubtful patient co-
potential.
operation
• Root concavities: These can create areas that are dif- • Presence of systemic/ environmental factors
ficult to maintain by both the dentist and the patient. • Hopeless: One or more of the following:
• Developmental grooves (palatogingival groove; • Advanced bone loss
Fig. 35.6): They start from the enamel and extend to • Nonmaintainable areas
some distance on the root surface, making it difficult • Extractions indicated
to maintain plaque retentive area. They are most com- • Presence of systemic or environmental factors
monly found on the maxillary lateral incisors (5.6%) • Questionable: One or more of the following:
and maxillary central incisors (3.4%). There is absence • Advanced bone loss
of attachment apparatus in this area creating a zone • Grade I and Grade II furcation involvements
of bacterial entry and also periodontal regenerative • Tooth mobility
procedures cannot be done on this area. • Inaccessible areas
• Presence of systemic/ environmental factors.
Tooth Mobility
Prognostication systems have been put forward by
Restoration of tooth stability is inversely proportional
various researchers either based on tooth mortality or on
to the extent of mobility caused by loss of supporting
the probability of obtaining stability of the periodontal
alveolar bone. Pockets on clinically mobile teeth do not
supporting apparatus.
respond well to periodontal treatment when compared
with pockets on nonmobile teeth. Splinting of mobile
teeth may have a beneficial impact on the overall and Prognosis for Patients with Gingival Disease
individual tooth prognosis. Dental plaque-induced gingival disease:
• Gingivitis associated with dental plaque only: This is
Prosthetic/Restorative Factors
a reversible disease that occurs due to accumulation
Sometimes, overall and individual tooth prognoses of bacterial plaque at the gingival margin; it can occur
overlap because the prognosis for key individual teeth may either on a periodontium that has no attachment loss
affect the overall prognosis for prosthetic rehabilitation. or on periodontium with nonprogressing attachment
loss. The prognosis for both is good as long as the local
Caries, Nonvital Teeth, and Root Resorption factors are removed.
Before undertaking periodontal treatment for grossly • Plaque-induced gingival disease modified by systemic
decayed teeth, adequate restorative and endodontic ther- factors: Sometimes even with a relatively small amount
apy should be considered. of bacterial plaque at the gingival margins, the signs of
inflammatory response are frank due to the presence of • Associated with hematological disorders such as
systemic factors such as endocrine-related changes as leukemia and neutropenia
in puberty, menstruation, pregnancy, and diabetes. The • Associated with genetic disorders such as Down
long-term prognosis of such patients depends on both syndrome and Papillon-Lefevre syndrome.
control of bacterial plaque and the systemic factors.
These disorders generally manifest early in life; hence,
• Plaque-induced gingival disease modified by medica-
their impact on the periodontium may be clinically similar
tions: These include gingival enlargement caused by
to that of generalized aggressive periodontitis with a fair
phenytoin, cyclosporine, nifedipine, and oral contra-
to poor prognosis.
ceptives. Reduction in dental plaque can reduce these-
verity of these lesions. But this alone does not prevent • Necrotizing periodontal diseases:
the development of the lesion as continued use of the • Necrotizing ulcerative gingivitis: Here, the primary
drug usually results in recurrence of the enlargement. predisposing factor is bacterial plaque, usually com-
Hence, the long-term prognosis depends on the intake plicated by the presence of predisposing factors such
of an alternate drug that does not cause gingival en- as smoking, poor nutrition, and acute psychological
largement. stress. With the control of both the bacterial plaque
• Plaque-induced gingival disease modified by malnutri- and the secondary predisposing factors, the prog-
tion: Prognosis of such patients depends on the severity nosis of necrotizing ulcerative gingivitis (NUG) is
and duration of the deficiency and on the likelihood of good.
reversing the deficiency. • Necrotizing ulcerative periodontitis: This is similar
to NUG, except that the necrosis extends from the
Non-plaque-induced gingival lesions:
gingiva to the periodontal ligament and alveolar
• Bacterial, fungal, or viral bone. In these patients, prognosis depends on al-
• Dermatoses such as lichen planus, pemphigoid, pem- leviating the plaque and secondary factors asso-
phigus vulgaris, erythema multiforme, and lupus ery- ciated with NUG. However, many patients with
thematoses necrotizing ulcerative periodontitis (NUP) are im-
• Allergic, toxic, or foreign body reaction munocompromised with systemic conditions such
as human immunodeficiency virus (HIV), wherein
Prognosis for these patients depends on the manage-
the prognosis also depends on dealing with the sys-
ment of the associated disorder.
temic problem.
Prognosis for Patients with Periodontitis

• Chronic periodontitis: It is a disease with slow progres-
sion, associated with local factors. It can present in a REEVALUATION OF PROGNOSIS
localized or a generalized form. Prognosis is good in AFTER PHASE 1 THERAPY
slight to moderate periodontitis case where the clinical
attachment loss and bone loss are minimal, provided Reduction in pocket depth and inflammation after
the local factors are removed. Prognosis is fair to poor phase 1 therapy indicates a better prognosis than previ-
in severe periodontitis where the condition is compli- ously assumed. Phase 1 therapy will at least temporarily
cated by furcation involvement and increasing clinical transform the prognosis of patients with an active ad-
mobility or in patients who are not compliant. vanced lesion, and the lesion should be reanalyzed after
• Aggressive periodontitis: It presents in localized or completion of phase 1 therapy. Thus, it may be advisable
generalized forms. Patients diagnosed with aggressive to establish a provisional prognosis until phase 1 therapy
periodontitis would have a poor prognosis. is completed and evaluated in cases with fair, poor, or
• Periodontitis as a manifestation of systemic diseases: questionable prognosis.
KEY POINTS
• Prognosis is defined as the prediction of the course, (CEJ). These are most commonly seen on the mandibular
duration, and outcome of a disease and its response to molars (28.6%) and least frequently on the maxillary
treatment. premolars (17%).
• CEP: These are ectopic enamel projections extending
beyond the normal contours of cementoenamel junction

1. Lindhe J, Lang N, Karring T. Clinical Periodontology and Implant
1. Define prognosis. Dentistry. 5th ed. Copenhagen: Blackwell Munksgaard; 2008.
2. What are the factors taken into consideration in deter- 2. Newman MG, Takei H, Klokkevold PR, Carranza FA. Clinical
mining prognosis of periodontally involved teeth? Periodontology. 10th ed. Philadelphia: Saunders; 2006.
3. Write a note on prognosis of teeth with furcation
involvement.
CHAPTER
36
Periodontal Treatment Plan
CHAPTER OVERVIEW
A treatment plan is a statement of the services to be based on the patient's oral, dental, and periodontal needs.
performed for the patient. The purpose of the treatment Except for emergencies no treatment should be started
plan is to organize an approach to comprehensive treatment before formulating a treatment plan.
RATIONALE FOR TREATMENT PLAN the patient should be placed on Phase IV therapy to pre-
serve the results obtained and prevent any further dete-
• Eliminate pain, gingival inflammation, and gingival rioration and recurrence of disease. In certain cases, this
bleeding. phase stops the progression of periodontal disease. The
• Reduce periodontal pockets and eliminate infection. phases of treatment are as follows:
• Arrest purulent exudate.
• Arrest the destruction of soft tissue and bone. • Preliminary phase: treatment of emergencies:
• Reduce abnormal tooth mobility. • Phase I: Etiotropic phase
• Establish optimal occlusal function. • Phase II: Surgical phase
• Restore tissue destroyed by disease in certain cases. • Phase II: Restorative phase
• Reestablish the physiological gingival contour. • Phase IV: Maintenance phase
• Prevent recurrence of disease. • Preliminary (emergency) phase:
• Reduce tooth loss. • Dental/periapical
• Periodontal
• Other
PREFERRED SEQUENCE • Extraction of hopeless teeth.
OF TREATMENT PHASES
Teeth that are considered "irrational to treat" may be
extracted in the preliminary or the initial phase of therapy.
Emergency phase The welfare of the dentition should not be jeopardized by
! a heroic attempt to retain questionable teeth such as the
Phase I following:
!
Reevaluation • Recurrent periodontal abscess during therapy
! • Periodontal endodontic lesion with poor prognosis
Phase IV (Maintenance/Supportive) • Mobile teeth that, when in function, are painful to the
i! i! patient
Phase II--_,. Phase lII • Attachment loss to the apex
(Surgery} (Restorative) • Endodontic complications
• Root fracture
• Grossly carious lesion, which extends into the root
Although the phases of treatment have been num- canal
bered, the recommended sequence does not follow the • Third molars without antagonists and with
numbers. Immediately after completion of Phase I therapy periodontitis/ caries.
It may be necessary to hold on the extraction until after c. Probing depth

treatment under the following circumstances: d. Attachment level
e. Caries and calculus.
• Strategic teeth from an aesthetic point of view
• Maintains posterior stops (extract once the prosthesis
is ready)
• Maintains posterior stops after implant placement, Phase II ( Surgical Phase)
which can be extracted once the implant is exposed • Various periodontal surgical procedures:
• Removal can be done during periodontal surgery of • Flap for debridement
adjacent areas • Resective osseous surgery
• Questionable restorability (extraction can be postponed • Regenerative osseous surgery
till the restorative phase). • Periodontal plastic surgery
• Implant placements
Phase I (Initial, Etiotropic, Nonsurgical, • Endodontic therapy
Cause- Related Phase of Therapy)
The objective of this phase of treatment is to eliminate Phase III (Restorative Phase)
as many of the local causes of periodontal disease as pos- • Final restorations
sible, including bacterial plaque and calculus, faulty den- • Fixed and/ or removable prosthesis
tal restorations, and any other contributory factors that
appear to be associated with periodontal inflammation Final restorative care should be delayed until all
or patient discomfort. active periodontal therapy is completed because tissue
contours may be altered during subsequent periodontal
• Scaling and root planing treatment.
• Patient education and oral hygiene instructions
• Nutrition and diet guidance
Reevaluation of Phase III
• Excavation of caries and restoration (temporary or
final) • Oral hygiene status
• Correction of prosthetic or restorative factors • Gingival inflammation and bleeding
• Occlusal correction • Probing depth
• Minor tooth movement • Attachment level
• Temporary splinting/prosthesis • Restoration status
• Antimicrobial therapy (local or systemic)
• Extraction of hopeless teeth.
Phase IV (Maintenance, Supportive Periodontal
Evaluation of Response to Phase I Treatment)
The objectives are to: Supportive periodontal therapy is an essential part of
any periodontal treatment plan. At the various recall visits
• Assess tissue response to therapy
the following procedures should be carried out:
• Assess patient's compliance with oral hygiene
• Overall systemic health
instructions
• Oral hygiene status
• Assess need/ advisability for further periodontal
• Gingival inflammation and bleeding
therapies
• Probing depth
Components of the reevaluation visit: • Attachment level
• Other parameters
1. It is performed 4-8 weeks following the completion of
• Performing required therapy (maintenance vs. active)
the initial phase of periodontal therapy.
• Scheduling the next recall visit.
2. All data collected in the initial visit should be
recollected at the reevaluation visit: Regardless of the type of treatment provided, peri-
a. Oral hygiene status odontal therapy will fail or will be less effective in the
b. Gingival inflammation and bleeding absence of adequate supportive periodontal therapy.
C H A PTER 36 PERIO DO N TA L TREATM EN T PLA N 299
KEY POINTS
• A treatment plan is a statement of the services to be per- • The phases of treatment are as follows: preliminary
formed for the patient. The purpose of the treatment plan phase - treatment of emergencies; Phase I - etiotropic
is to organize an approach to comprehensive treatment phase; Phase II - surgical phase; Phase III - restorative
based on the patient's oral, dental, and periodontal needs. phase; Phase IV - maintenance phase.
Except for emergencies no treatment should be started • Phase I is also called initial, etiotropic, nonsurgical,
before formulating a treatment plan. cause-related phase of therapy.

1. What are the various phases of a periodontal treatment Dentistry. 5th ed. Oxford: Blackwell Munksgaard; 2006.
plan? 2. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's
2. Write briefly on Phase I therapy. Clinical Periodontology. 10th ed. Philadelphia: Elsevier; 2006.
CHAPTER
37
Treatment of Periodontal Diseases in
Medically Compromised Patients
CHAPTER OVERVIEW
In this chapter, we analyze new emerging evidence col- endocrine disorders, pulmonary diseases, renal diseases,
lected since the early 1990s, implicating periodontal infec- hemorrhagic disorders, etc. Therefore, the therapeutic re-
tion as a risk factor for several systemic conditions such as sponsibility of the clinician includes identification of the pa-
cardiovascular diseases, preterm low-birth-weight infants, tient's medical problems to formulate proper treatment plans.
CARDIOVASCULAR DISEASES Hypertension is not diagnosed on a single elevated

blood pressure (BP) recording. It is based on the average
Cardiovascular diseases are the most prevalent diseas- value of two or more BP readings taken at intervals. The
es in the world. Most cases of coronary heart disease and higher value of either the systolic or diastolic pressure
cerebrovascular disease (stroke) result from atherosclero- determines the patient's classification.
sis, an aberrant biologic process that causes narrowing of Hypertension is divided into primary (essential) and
arteries due to deposition of atheromatous plaque on the secondary types.
inner wall of the blood vessel walls. Atherosclerosis is a Primary hypertension occurs in approximately 95%
progressive disease process in which large- to medium- of all hypertensives, with no underlying pathology to
sized muscular and large elastic arteries become occluded explain the disease. Secondary hypertension occurs in
with fibrolipid lesions (atheromas). Health histories must 5% of hypertensives with underlying pathology, e.g., re-
be scrutinized for cardiovascular problems. These condi- nal disease, endocrinologic pathologies, and neurogenic
tions include hypertension, angina pectoris, myocardial changes.
infarction, previous history of cardiac bypass surgery, Periodontal procedures should not be performed un-
cardiovascular accident, presence of cardiac pacemakers/ til accurate BP measurements with appropriate medi-
automatic cardioverter defibrillators, congestive heart cal records of patients are considered. Dental treatment
failure, infective endocarditis, etc. for hypertensive patients on antihypertensive therapy
is generally safe. Physician consultation regarding pa-
tient's medical history must be considered especially
Hypertension when stressful or prolonged treatment is anticipated.
It is the most common cardiovascular disease affecting Morning dental appointments were suggested earlier for
more than 50 million American adults; many of them are hypertensive patients, but recent evidence indicates that
undiagnosed. The JNC-7 revised guidelines for evalua- BP increases around awakening and peaks at midmorn-
tion and management of hypertension have simplified ing. Lower BP occurs in the afternoon; hence, afternoon
classification of blood pressure (Table 37.1). JNC-7 guide- dental appointments are preferred.
lines emphasize the importance of systolic blood pressure No routine periodontal treatment should be given to
greater than 140 mm Hg, which is considered a greater patients with systolic BP greater than 180 mm Hg or dia-
risk factor for cardiovascular disease than elevated diastolic BP greater than 110 mm Hg. Treatment should be
stolic pressure. limited to emergency care until hypertension is controlled.
CHAPTER 37 TREATMENT OF PERIODONTAL DISEASES IN MEDICALLY COMPROMISED PATIENTS 301
TABLE 37.1 Classification of Adult Blood Pressure
Classification Systolic BP (mm Hg) Diastolic BP (mm Hg) Dental treatment

Normal <120 <80 No changes in dental treatment
Prehypertension 120-139 80-89 No changes in dental treatment
Stage 1 hypertension 140-159 90-99 No changes in dental treatment; inform patient and monitor BP;
medical consultation
Stage 2 hypertension > 160 > 100 Medical consultation, stress reduction; if systolic BP is <180 mm
Hg and diastolic BP is <110 mm Hg, perform selective dental
procedures
If the systolic BP is > 180 mm Hg and diastolic BP is > 100 mm
Hg, emergency dental care only
Use of local anesthetic containing an epinephrine concen- 3. Administer oxygen in reclined position.
tration greater than 1:100,000 should not be used. Howev- 4. If the signs and symptoms subside within 3 min, com-
er, small doses of epinephrine can be used with aspiration plete periodontal treatment at the earliest.
before injection for its profound benefits. If the patient is 5. If the signs and symptoms do not subside in 2-3 min,
anxious, conscious sedation may be given. administer another dose of nitroglycerin, call the pa-
The clinician should be aware of many side effects of tient's physician and monitor vital signs, and shift the
antihypertensive medications. Postural hypotension is patient to emergency department with an accompany-
common and can be minimized by slow positional changing person.
es on dental chair. Depression, nausea, sedation, oral dry- 6. A third dose of nitroglycerin can be administered 3 min
ness, lichenoid drug reaction, and gingival overgrowth after the second, and if the chest pain persists, then
are some of the other side effects. Drug interactions with it could be the sign of myocardial infarction. Patient
local anesthetic may cause severe hypertension and bra- should be immediately shifted to medical emergency
dycardia, resulting in a decrease in vascular perfusion and department.
possible death. Therefore, epinephrine-containing local
Myocardial infarction is a type of ischemic heart dis-
anesthetics should be used cautiously and only in small
ease. Dental treatment is avoided for 6 months post-MI
amounts with careful monitoring of vital signs.
because peak mortality occurs during this time. MI pa-
tients are treated like stable angina patients.
Ischemic Heart Diseases Angioplasty, cardiac bypass, femoral artery bypass,
and many procedures are conducted on patients with
Ischemic heart diseases include disorders such as an-
ischemic heart disease. Elective dental procedures must be
gina pectoris and myocardial infarction (Ml).
carried out with the consultation of physician regarding
Angina pectoris occurs when myocardial oxygen de-
the myocardial damage, stability of patient's condition,
mand exceeds supply, resulting in temporary myocardial
infective endocarditis, and graft stability. However, pro-
ischemia. Patients with unstable angina should be treated
phylactic antibiotics are not usually necessary for cardiac
only for emergencies with physician consultation. Patients
bypass patients unless recommended by cardiologist.
with stable angina can undergo elective dental treatment.
Profound anesthesia and conscious sedation may be re-
quired to reduce the stress, which can trigger angina at- Congestive Cardiac Failure
tack. Oxygen supplementation should be available on
Congestive heart failure (CHF) is a condition in which
the chair side. Patients should be instructed to bring their
the pumping function of the heart is unable to supply
medications to dental appointments. Nitroglycerin should
sufficient amount of oxygenated blood to the body. It
be kept in the medical emergency kit. Care should be taken
begins with left ventricular failure caused by dispropor-
while administering local anesthetics containing epineph-
tion between hemodynamic load and the capacity to
rine, as adverse reactions are same as hypertension.
handle that load. CHF could be due to chronic diseases
If the patient becomes uncomfortable or complains of
such as hypertension, valvular diseases, direct damage
chest pain and increased heart rate, treatment should be
to myocardium (MI, rheumatic fever), or an increase
discontinued and following precautions should be taken:
in the body's oxygen requirement (anemia, pregnancy,
1. Discontinue the periodontal treatment. thyrotoxicosis).
2. Reassure the patient with administration of sublingual Poorly controlled or untreated CHF patients are not
nitroglycerin (0.3-0.6 mg) and loosen the restrictive candidates for elective dental procedures, as they are at
garments. risk of sudden death following ventricular arrhythmias.
Treated CHF patients require physician consultation TABLE 37.2 Cardiac Conditions Associated with Endocarditis
regarding the severity of CHF and medications. In some ENDOCARDITIS PROPHYLAXIS RECOMMENDED
CHF patients, there may be orthopnea (difficulty in
breathing unless in upright position); dental chair should High-risk category
be adjusted to a comfortable position. Short appointments • Prosthetic cardiac valves, including bioprosthetic and homo-
with local anesthesia and, if required, conscious sedation graft valves
to reduce stress and oxygen supplementation should be • Previous bacterial endocarditis
• Complex cyanotic congenital heart disease (e.g., single ventricle
ensured in case of emergency.
states, transposition of the great arteries of Fallot)
• Surgically constructed systemic pulmonary shunts or conduits.
Cardiac Pacemakers/Implantable Cardioverter Moderate-risk category

Defibrillators • Most other congenital cardiac malformations (other than above
and below)
Some of the cardiac arrhythmias are treated with im- • Acquired valvular dysfunction (e.g., rheumatic heart diseases)
plantable pacemakers or automatic cardioverter defibril- • Hypertrophic cardiomyopathy
lators. Pacemakers are implanted in the chest wall and • Mitra! valve prolapse with valvular regurgitation and/or thick-
enter the heart intravenously. Automated cardiodefibril- ened leaflets.
lators are often implanted subcutaneously or directly Negligible-risk category (no greater risk than the general
attached to the epicardium. Physician consultation is population)
necessary for the cardiac status. Older pacemakers were • Isolated secundum atrial septa! defect
unipolar and could be disrupted by dental equipment • Surgical repair of atrial septa! defect, ventricular septa! defect,
that generated electromagnetic fields such as ultrasonic or patent ductus arteriosus (without residual defect beyond
and electrocautery units. Newer units are bipolar and are 6 months)
• Previous coronary artery bypass graft surgery
generally not affected by dental equipment. Cardioverter
• Mitra! valve prolapse without valvular regurgitation
defibrillators activate without warning when arrhythmias • Physiological, functional, or innocent heart murmurs
occur. Stabilization of patient and the operating field dur- • Previous Kawasaki disease without valvular dysfunction
ing periodontal treatment is suggested with bite blocks to • Previous rheumatic fever without valvular dysfunction
prevent unexpected trauma. • Cardiac pacemakers (intravascular and epicardial) and im-
planted defibrillators.
Antibiotic Prophylaxis for Susceptible Patients

Undergoing Periodontal Treatment
TABLE 37.3 Dental Procedures and Endocarditis Prophylaxis
1. Patients with a susceptible heart condition.
2. Microorganisms may settle on the endocardium, dam- ENDOCARDITIS PROPHYLAXIS RECOMMENDED
aged or rendered defective by acquired or congenital • Dental extractions
heart disease, and cause infective endocarditis. It has • Periodontal procedures including surgery, scaling and root
therefore been suggested that antibiotic prophylaxis planing, probing, and recall maintenance
should be administered whenever susceptible patients • Dental implant placement and reimplantation of avulsed teeth
are exposed to bacteremia. Bacteremia may arise from • Endodontic (root canal) instrumentation or surgery only beyond
the apex
certain dental procedures. Although bacteremia may • Subgingival placement of antibiotic fibers or strips
follow these procedures, the likelihood of infective en- • Initial placement of orthodontic bands but not brackets
docarditis seems to vary considerably, and with many • Intraligamentary local anesthetic injections
procedures, the risk is insignificant. • Prophylactic cleaning of teeth or implants where bleeding is
anticipated
• Restorative dentistry (operative and prosthodontic) with or
without retraction cord
Susceptible Patients • Local anesthetic injections (non-intraligamentary)
• Intracanal endodontic treatment; postplacement and buildup
Possible susceptible patients may be in the following
• Placement of rubber dams
three categories: • Postoperative suture removal
• Placement of removable prosthodontic or orthodontic appli-
1. Patients with prosthetic joint replacements.
ances
2. Immunosuppressed patients. • Taking of oral impressions
3. Patients with a susceptible heart condition. Patients • Fluoride treatments
with a susceptible heart condition are divided into • Taking of oral radiographs
three categories of high, moderate, and negligible risk • Orthodontic appliance adjustment
• Shedding of primary teeth
(Tables 37.2-37.4).
TABLE 3 7 .4 Prophylactic Regimens for Dental, Oral, Respiratory Tract, or Esophageal Procedures
Situation Agent Regimen

Standard general prophylaxis Amoxicillin Adults: 2.0 g
Children: 50 mg/kg orally 1 h before procedure
Unable to take oral medications Ampicillin Adults: 2.0 g intramuscularly (IM) or intravenously (IV)
Children: 50 mg/kg IM or IV within 30 min before procedure
Allergic to penicillin Clindamycin Adults: 600 mg

Cephalexin or cefadroxil Adults: 2.0 g
Azithromycin or clarithromycin Adults: 500 mg
Allergic to penicillin and unable to take Clindamycin Adults: 600 mg
oral medications Children: 20 mg/kg IV within 30 min before procedure
Cefazolin Adults: 1.0 g
Children: 25 mg/kg IM or IV within 30 min before procedure
High Risk Dental Causes of Transient Bacteremia

Patients in this category have a higher risk for con- Bacteremia can arise from oral and dental sepsis fol-
tracting infective endocarditis with or without exposure lowing tooth extraction. Transient bacteremia can occur
to a treatment-induced bacteremia, and a high level of with poor oral hygiene, periodontal disease, or periapi-
mortality. The conditions in this category are as follows: cal infection, and is stimulated by normal functions such
as eating, chewing, and toothbrushing. The incidence
• Prosthetic heart valves including both bioprosthetic
is related to the severity of infection. Individuals at risk
and homograft valves
should maintain best oral health in order to reduce the
• Previous history of infective endocarditis
continuous source of potential bacteremias.
• Complex cyanotic congenital heart disease (e.g., single
ventricle states, transposition of great arteries, and
Tetralogy of Fallot) Infective Endocarditis
• Surgically constructed systemic-pulmonary shunts or
conduits. Infective endocarditis (IE) is the disease in which mi-
croorganisms colonize the damaged endocardium or heart
Moderate Risk valves. The term infective endocarditis is preferred to the
Patients in this category have a lesser risk of contracting previous term bacterial endocarditis because the disease
infective endocarditis than the first group. They comprise: can also be caused by fungi and viruses. It is a serious
disease with poor prognosis despite modern therapy. The
• Acquired valvular dysfunction, e.g., rheumatic heart
most common causative organisms are alpha-hemolytic
disease
streptococci (e.g., Streptococcus viridans); however, non-
• Hypertrophic cardiomyopathy
streptococcal organisms often found in the periodontal
• Mitral valve prolapsed with valvular regurgitation
pocket have been implicated, which include Eikenella
and/ or thickened leaflets
corrodens, Actinobacillus actinomycetemcomitans, Capnocy-
• Congenital cardiac diseases.
tophaga, and Lactobacillus species. Infective endocarditis
Negligible Risk has been divided into:
• Individuals with physiological, functional, or innocent • Acute form: Involves virulent organisms, generally
murmurs nonhemolytic streptococci and strains of staphylococci
• Mitral valve prolapsed without valvular regurgitation that invade normal cardiac tissue, produce septic em-
• Previous Kawasaki disease without valvular dysfunction boli, and cause infections rapidly with fatal course.
• Previous rheumatic fever without valvular dysfunction • Subacute form: Results from colony formation on dam-
• Cardiac pacemakers (intravascular and epicardial) and aged endocardium or heart valves by low-grade patho-
implanted defibrillators genic organisms, e.g., rheumatic carditis consequent to
• Isolated secundum arterial septal defect rheumatic fever.
• Surgical repair of atrial septal defect, ventricular septal The treatment of periodontal diseases is related to IE.
defect, or patent ductus arteriosus (beyond 6 months Dental procedures involve bleeding with transient bacte-
without any residue). remia. American Heart Association (AHA) recommends
CONDITIONS AND PROCEDURES CAUSING TRANSIENT BACTEREMIA
• Chewing, toothbrushing, and flossing in the presence of • Periodontal surgery

inflammation spread from local areas of infections • Restorative procedures involving gingival margin or
• Oral surgical procedures including tooth extraction crevice
• Reimplantation of avulsed tooth • Endodontic surgery
• Dental implant placement • Initial placement of orthodontic bands without brackets
• Periodontal probing • Intraligamental local anesthesia
• Supragingival and subgingival scaling and root planing • Polishing of teeth and implants with gingival bleeding
• Subgingival placement of local drug delivery system
(antimicrobial fibers or strips)
antibiotic prophylaxis before procedures associated with dicated. The classic signs of diabetes include polydipsia
significant bleeding from hard and soft tissues, periodon- (excessive thirst), polyuria (excessive urination), and poly-
tal surgery, scaling, and root planing. phagia (excessive hunger, often with unexplained concur-
Preventive measures to reduce the risk of IE are as rent weight loss). If the patient has any of these signs or
follows: symptoms, or if the clinician's index of suspicion is high,
further investigation with laboratory studies and physi-
1. Define the susceptible patient with proper medical
cian consultation is indicated.
history.
If a patient is suspected of having undiagnosed diabe-
2. Provide oral hygiene instructions, which include gentle
tes, the following procedures should be performed:
toothbrushing and oral rinses to reduce the microbial
load. 1. Consult the patient's physician.
3. During periodontal treatment, antibiotic prophylaxis 2. Analyze laboratory tests: fasting blood glucose and
should be given to all susceptible patients. random/ casual glucose.
4. Periodontal treatment should be designed for suscep- 3. Rule out acute orofacial infection or severe dental infec-
tible patients, since periodontal disease is an infection tion; if present, provide emergency care immediately.
with potentially wide range of systemic effects. All 4. Establish best possible oral health through nonsurgi-
periodontal treatment procedures including probing cal debridement of plaque and calculus; institute oral
require antibiotic regimen. Pretreatment chlorhexidine hygiene instruction. Limit more advanced care until
rinses are recommended before all procedures. Reduce diagnosis has been established and good glycemic
the number of visits to minimize bacterial resistance to control obtained.
antibiotics. A gap of 7-14 days between the appoint-
ments is recommended. Laboratory Evaluation of Diabetes Control: Glycosylated
Hemoglobin Assay (HbA1J
Regular recall appointments to emphasize good oral
hygiene and maintenance of periodontal health are very 4-6% Normal
important in IE patients. <7 % Good diabetes control
7-8% Moderate diabetes control
ENDOCRINE DISORDERS >8% Action suggested to improve diabetes control
Diabetes Mellitus
Periodontal infection may worsen glycemic control and
The two major types of diabetes are type 1 (formerly should be managed aggressively. Diabetic patients with
known as "insulin-dependent diabetes") and type 2 (for- periodontitis should receive oral hygiene instructions,
merly called "non-insulin-dependent diabetes"). Over mechanical debridement to remove local factors, and reg-
the past decade, the medical management of diabetes has ular maintenance. When possible, an HbA1c of less than
changed significantly in an effort to minimize the debili- 10% should be established before surgical treatment is
tating complications associated with this disease. Patients performed. Systemic antibiotics are not needed routinely,
are more tightly managing their blood glucose levels although recent evidence indicates that tetracycline anti-
(glycemia) through diet, oral agents, and insulin therapy. biotics in combination with scaling and root planing may
If the clinician detects intraoral signs of undiagnosed positively influence glycemic control. If the patient has
or poorly controlled diabetes, a thorough history is in- poor glycemic control and surgery is absolutely needed,
DIAGNOSTIC CRITERIA FOR DIABETES MELLITUS
Diabetes mellitus may be diagnosed by any one of the 2. Fasting plasma glucose ::?.126 mg/dL. "Fasting" is defined as
three different laboratory methods. Whichever method is no caloric intake for at least 8 h. (Normal fasting glucose
used, it must be confirmed on a subsequent day by using is 70-100 mg/dL.)
any one of the following three methods: 3. Two-hour postprandial glucose ::?.200 mg/dL during an oral
glucose tolerance test. The test should be performed us-
1. Symptoms of diabetes plus casual (nonfasting) plasma glucose
ing a glucose load containing the equivalent of 75 g of
::?.200 mg/dL. Casual glucose may be drawn at any time
anhydrous glucose dissolved in water. (Normal 2-h post-
of day without regard to time since the last meal. Classic
prandial glucose is <140 mg/dL.)
symptoms of diabetes include polyuria, polydipsia, and
unexplained weight loss.
prophylactic antibiotics may be given; penicillins are most 4. After the procedure, the blood glucose can be checked
often used for this purpose. Frequent reevaluation after again to assess fluctuations over time.
active therapy is needed to assess treatment response and 5. Any time the patient feels symptoms of hypoglycemia,
prevent recurrence of periodontitis. blood glucose should be checked immediately. This
Almost all diabetic patients use glucometers for im- may prevent onset of severe hypoglycemia, a medical
mediate blood glucose self-monitoring. These devices use emergency.
capillary blood from a simple finger stick to provide blood
glucose readings in seconds. Diabetic patients should be
asked whether they have glucometers and how often they Signs and Symptoms of Hypoglycemia
use them. Because these devices provide instantaneous
Shakiness or tremors
assessment of blood glucose, they are highly beneficial
in the dental office environment. Confusion
The following guidelines should be observed: Agitation and anxiety
1. Patients should be asked to bring their glucometer to Sweating
the dental office at each appointment.
Tachycardia
2. Patients should check their blood glucose before any
long procedure to obtain a baseline level. Patients with Dizziness
blood glucose levels at or below the lower end of nor- Feeling of "impending doom"
mal before the procedure may become hypoglycemic
Unconsciousness
intraoperatively. It is advisable to have such a patient
consume some carbohydrate before starting treatment. Seizures
For example, if a 2-h procedure is planned and the
pretreatment glucose level is 70 mg/ dL (lower end of
Thyroid and Parathyroid Disorders
normal range), providing 4 oz of juice preoperatively
may help prevent hypoglycemia during treatment. Periodontal therapy requires minimal alterations in
If pretreatment glucose levels are excessively high, the patient with adequately managed thyroid disease.
the clinician should determine whether or not the pa- Patients with thyrotoxicosis and those with inadequate
tient's glycemic control has been poor recently. This medical management should not receive periodontal ther-
can be done by thorough patient questioning and by apy until their condition is stabilized. Patients with a his-
determining the most recent HbA1c values. If glycemic tory of hyperthyroidism should be carefully evaluated to
control has been poor over the preceding few months, determine the level of medical management, and treated
the procedure may need to be postponed until better in a way that limits stress and infection. Hyperthyroidism
glycemic control is established. If glycemic control has may cause tachycardia and other arrhythmias, increased
been good, and the currently high glucometer reading cardiac output, and myocardial ischemia. Medications
is a fairly isolated event, the surgical procedure may such as epinephrine and other vasopressor amines should
proceed. be given with caution in patients with treated hyperthy-
3. If the procedure lasts several hours, it is often benefi- roidism, although the small amounts used in dental anes-
cial to check the glucose level during the procedure to thetics rarely cause problems. These drugs should not be
ensure that the patient does not become hypoglycemic. given to patients with thyrotoxicosis or poorly controlled
thyroid disorders. Patients with hypothyroidism require ranted. Again, in an emergency situation, increasing
careful administration of sedatives and narcotics because the steroid dose before the procedure may decrease the
of the potential for excessive sedation. chances of acute adrenal crisis. If emergency treatment is
Routine periodontal therapy may be provided to pa- not needed, consultation with the physician before treat-
tients with parathyroid disease once that disorder has ment is best.
been identified and the proper medical treatment given. Management of the patient in an acute adrenal insuf-
However, patients who have not received medical care ficiency crisis is as follows:
may have significant renal disease, uremia, and hyperten-
1. Terminate periodontal treatment.
sion. Also, if hypercalcemia or hypocalcemia is present,
2. Summon medical assistance.
the patient may be more prone to cardiac arrhythmias.
3. Give oxygen.
4. Monitor vital signs.
Adrenal Insufficiency 5. Place the patient in a supine position.
6. Administer 100 mg of hydrocortisone sodium succinate
Acute adrenal insufficiency is associated with signifi- (Solu-Cortef) intravenously for over 30 s or intramus-
cant morbidity and mortality as a result of peripheral
cularly.
vascular collapse and cardiac arrest. Therefore, the perio-
dontist should be aware of the clinical manifestations and Equivalent doses of corticosteroids:
ways of preventing acute adrenal insufficiency in patients
with histories of primary adrenal insufficiency (Addison
Corticosteroid Equivalent dose (mg)
disease) or secondary adrenal insufficiency (most often
caused by the use of exogenous glucocorticosteroids). Cortisone 25
Manifestations of acute adrenal insufficiency (adrenal Hydrocortisone 20
crisis): Prednisone 5
1. Mental confusion, fatigue, and weakness Prednisolone 5

2. Nausea and vomiting
Methylprednisone 5
3. Hypertension
4. Syncope Methylprednisolone 4
5. Intense abdominal pain, lower back pain, and leg pain Triamcinolone 4
6. Loss of consciousness
Dexamethasone 0.75
7. Coma.
Betamethasone 0.6
The use of systemic corticosteroids is common in
patients with allergic, endocrine, respiratory, joint, in-
testinal, neurologic, renal, liver, skin, and connective
tissue disorders. Significant complications associated
RENAL DISEASES
with corticosteroid use include alterations in glucose
The most common causes of renal failure are glo-
metabolism (steroid-induced diabetes), increased risk
merulonephritis, pyelonephritis, kidney cystic disease,
of infection, altered wound healing, osteoporosis, skin
renovascular disease, drug nephropathy, obstructive
disorders, cataracts, glaucoma, and suppression of the
uropathy, and hypertension. Renal failure may result
hypothalamic-pituitary-adrenal (HPA) axis. In a normal
in severe electrolyte imbalances, cardiac arrhythmias,
healthy patient, stress activates the HPA axis, stimulating
pulmonary congestion, CHF, and prolonged bleeding.
increased endogenous cortisol production by the adrenal
Because the dental management of patients with renal
glands. Exogenous steroids may suppress the HPA axis
disease may need to be drastically altered, physician
and impair the patient's ability to respond to stress with
consultation is necessary to determine the stage of renal
increased endogenous cortisol production, leading to the
disease, regimen for medical management, and alterations
potential for acute adrenal crisis. The degree of adrenal
in periodontal therapy. It is preferable to treat the patient
suppression depends on the drugs used, dose, duration
before, rather than after, transplant or dialysis. The fol-
of administration, time elapsed since steroid therapy was
lowing treatment modifications should be used:
terminated, and route of administration.
For patients taking large doses of greater than 20 mg 1. Consult the patient's physician.
cortisol equivalent per day and requiring stressful peri- 2. Monitor blood pressure (patients in end-stage renal
odontal procedures, doubling or tripling the normal ste- failure are usually hypertensive).
roid dose 1 h before the procedure is often recommended. 3. Check laboratory values: partial thromboplastin time
For those patients receiving low doses for short periods (PTT), prothrombin time (PT), bleeding time, and plate-
(i.e., <1 month), no supplementation is generally war- let count; hematocrit; blood urea nitrogen (do not treat
if <60 mg/ dL); and serum creatinine (do not treat if Transplant patients take immunosuppressive drugs
<1.5 mg/dL). that greatly reduce resistance to infection. Excessive
4. Eliminate areas of oral infection to prevent systemic bleeding may occur during or after periodontal treatment
infection. because of drug-induced thrombocytopenia, anticoagula-
• Good oral hygiene should be established. tion, or both. A periodontal abscess is a potentially life-
• Periodontal treatment should aim at eliminating threatening situation; therefore, a dental team approach
inflammation or infection and providing easy main- should be used before transplantation to determine which
tenance. Questionable teeth should be extracted if teeth can be easily maintained. Teeth with severe bone
medical parameters permit. and attachment loss, furcation invasion, periodontal ab-
• Frequent recall appointments should be scheduled. scesses, or extensive surgical requirements should be
5. Drugs that are nephrotoxic or metabolized by the kid- extracted. The following should be considered for the
ney should not be given (e.g., phenacetin, tetracycline, renal transplant patient:
aminoglycoside antibiotics).
1. Hepatitis B and C screening.
Acetaminophen may be used for analgesia and diaz- 2. Determination of level of immune system compromise
epam for sedation. Local anesthetics such as lidocaine are resulting from antirejection drug therapy.
generally safe. 3. Prophylactic antibiotics (using AHA recommenda-
The patient who is receiving dialysis requires modifications). Not all transplant patients require antibiotic
tions in treatment planning. Only hemodialysis patients coverage, and physician consultation is warranted
require special precautions. These patients have a high before prescribing.
incidence of viral hepatitis, anemia, and prolonged hem-
orrhage. The risk for hemorrhage is related to anticoagu-
lation during dialysis, platelet trauma from dialysis, and
LIVER DISEASES
the uremia that develops with renal failure. In addition
Liver diseases may range from mild conditions to com-
to guidelines for patients with chronic renal disease, the
plete liver failure. Major causes of liver disease include
following recommendations are made for those receiving
drug toxicity, cirrhosis, viral infections (e.g., hepatitis
hemodialysis:
B and C), neoplasms, and biliary tract disorders. Many
1. Screen for hepatitis B and hepatitis C antigens and drugs are metabolized in the liver; thus, liver disease
antibodies before any treatment. alters normal drug metabolism. Treatment recommenda-
2. Provide antibiotic prophylaxis to prevent endarte- tions for patients with liver disease include the following:
ritis of the arteriovenous fistula or shunt. [Intermit-
1. Consultation with the physician concerning current
tent peritoneal dialysis (IPD) and chronic ambulatory
stage of disease, risk for bleeding, potential drugs to be
peritoneal dialysis (CAPD) patients do not generally
prescribed during treatment, and required alterations
require prophylactic antibiotics.]
to periodontal therapy
3. Patients receive heparin anticoagulation on the day
2. Screening for hepatitis B and C
of hemodialysis. Therefore, provide periodontal treat-
3. Checking laboratory values for PT and PTT.
ment on the day after dialysis, when the effects of hepa-
rinization have subsided. Hemodialysis treatments are
generally performed three or four times a week. (IPD PULMONARY DISEASES
and CAPD patients are not systemically heparinized;
therefore, they usually do not have the potential bleed- The periodontal treatment of a patient with pulmonary
ing problems associated with hemodialysis.) disease may require alteration depending on the nature
4. Be careful to protect the hemodialysis shunt or fistula and the severity of the respiratory problem. Pulmonary
when the patient is in the dental chair. If the shunt or diseases range from obstructive lung diseases (e.g., asth-
fistula is placed in the arm, do not cramp the limb; ma, emphysema, bronchitis, acute obstruction) to restric-
blood pressure readings should be taken from the other tive ventilatory disorders caused by muscle weakness,
arm. Do not use the limb for the injection of medica- scarring, obesity, or any condition that could interfere
tion. Patients with leg shunts should avoid sitting with with effective lung ventilation.
the leg dependent for longer than 1 h. If appointments Acute respiratory distress may be caused by slight
last longer, allow the patient to walk about for a few airway obstruction or depression of respiratory func-
minutes and then resume therapy. tion. Because of their limited vital lung capacity, these
5. Refer the patient to the physician if uremic problems patients also have decreased cough effectiveness. They
develop, such as uremic stomatitis. To prevent systemic must continually deal with the mental anxiety caused by
dissemination, refer to the physician if oral infections air hunger and alter their position in attempts to improve
do not resolve promptly. their ventilatory efficiency.
The following guidelines should be used during peri- is preferable to evaluate the patient before initiation of
odontal therapy: chemotherapy. Teeth having a poor prognosis should be
extracted, with thorough debridement of remaining teeth
1. Identify and refer patients with signs and symptoms
to minimize the microbial load. The clinician must teach
of pulmonary disease to their physician.
and emphasize the importance of good oral hygiene. Anti-
2. In patients with known pulmonary disease, consult
microbial rinses such as chlorhexidine are recommended,
with their physician regarding medications (antibiotics,
especially for patients with chemotherapy-induced mu-
steroids, chemotherapeutic agents) and the degree and
cositis, to prevent secondary infection.
severity of pulmonary disease.
Chemotherapy is usually performed in cycles, with
3. Avoid elicitation of respiratory depression or distress:
each cycle lasting several days, followed by intervening
• Minimize the stress of a periodontal appointment.
periods of myelosuppression and recovery. If periodontal
The patient with emphysema should be treated in
therapy is needed during chemotherapy, it is best done
the afternoon, several hours after sleep, to allow for
the day before chemotherapy is given, when white blood
airway clearance.
cell counts are relatively high. Coordination with the on-
• Avoid medications that could cause respiratory de-
cologist is critical. Dental treatment should be done when
pression (e.g., narcotics, sedatives, general anesthet-
white cell counts are above 2000/mm3, with an absolute
ics).
granulocyte count of 1000-1500/mm3•
• Avoid bilateral mandibular block anesthesia, which
could cause increased airway obstruction.
• Position the patient to allow maximal ventilatory RADIATION THERAPY
efficiency; be careful to prevent physical airway ob-
struction; keep the patient's throat clear; and avoid The use of radiotherapy, alone or in conjunction with
excess periodontal packing. surgical section, is common in the treatment of head and
4. In a patient with a history of asthma, especially if neck tumors. The side effects of ionizing radiation include
asthma attacks are frequent, make sure the patient's dramatic perioral changes of significant concern to dental
medication (inhaler) is available. The inhaler should health personnel. The extent and severity of mucositis,
be readily accessible on the countertop in the dental dermatitis, xerostomia, dysphagia, gustatory alteration,
treatment room. radiation caries, vascular changes, trismus, temperoman-
5. Patients with active fungal or bacterial respiratory dibular joint degeneration, and periodontal change de-
diseases should not be treated unless the periodontal pend on the type of radiation used, fields of irradiation,
procedure is an emergency. number of ports, types of tissues in the fields, and dosage.
High-dose radiation therapy results in hypovascularity
of irradiated tissues with a reduction in wound-healing
IMMUNOSUPPRESSION AND capacity. Most severe among the resulting oral compli-
CHEMOTHERAPY cations is osteoradionecrosis (ORN). Decreased vascular-
ity renders the bone less capable of resolving trauma or
Immunosuppressed patients have impaired host infection. Such events may cause severe destruction of
defenses as a result of an underlying immunodeficien- bone. The risk of ORN continues for the remainder of the
cy or drug administration (primarily related to organ patient's life and does not decrease with time.
transplantation or chemotherapy). Because chemotherapy
is often cytotoxic to bone marrow, destruction of plate-
lets and red and white blood cells results in thrombocy- PREGNANCY
topenia, anemia, and leukopenia. Immunosuppressed
individuals are at greatly increased risk for infection, The aim of periodontal therapy for a pregnant patient
and even minor periodontal infections can become life- is to minimize the potential exaggerated inflammatory
threatening if immunosuppression is severe. Intraorally, response related to pregnancy-associated hormonal al-
viral, bacterial, and fungal infections may manifest. Pa- terations. Meticulous plaque control, scaling, root plan-
tients receiving bone marrow transplantation require ing, and polishing should be the only nonemergency
special attention because these patients receive extremely periodontal procedures performed.
high-dose chemotherapy and are particularly susceptible The second trimester is the safest time to perform
to dissemination of oral infections. treatment. However, long, stressful appointments and
Treatment in these patients should be directed toward periodontal surgical procedures should be delayed until
the prevention of oral complications that could be life- postpartum period. As the uterus increases in size dur-
threatening. The greatest potential for infection occurs ing the second and third trimesters, obstruction of the
during periods of extreme immunosuppression; there- vena cava and aorta may occur if the patient is placed in
fore, treatment should be conservative and palliative. It a supine position. The reduction in return cardiac blood
supply may cause supine hypotensive syndrome, with systemic dissemination. Antibiotic therapy, combined
decreased placental perfusion. Decreasing blood pressure, with nonsurgical or surgical, is indicated.
syncope, and loss of consciousness may occur. This may 4. Oral ulcerations and mucositis are treated pallia-
be prevented by placing the patient on her left side (left tively with agents such as viscous lidocaine. Systemic
lateral position) or by elevating the right hip 5-6 in. during antibiotics may be indicated to prevent secondary
treatment. Appointments should be short, and the patient infection.
should be allowed to change the positions frequently. 5. Oral candidiasis is common in the leukemic patient and
Other precautions during pregnancy relate to the po- can be treated with nystatin suspensions (100,000 U / mL
tential toxicity or teratogenic effects of therapy on the four times a day or clotrimazole vaginal suppositories
fetus. Ideally, no medications should be prescribed. How- 910 mg four or five times daily).
ever, analgesics, antibiotics, local anesthetics, and other 6. For patients with chronic leukemia and those in re-
drugs may be required, depending on the patient's needs. mission, scaling and root planing can be performed
Before being prescribed, all drugs should be reviewed for without complications, but periodontal surgery should
potential adverse effects on the patients. be avoided if possible.
7. Platelet count and bleeding time should be measured
on the day of the procedure. If either is low, postpone
LEUKEMIA the appointment and refer the patient to the physician.
1. Refer the patient for medical evaluation and treatment.

2. Before chemotherapy, a complete periodontal treatment COAGULATION DISORDERS
plan should be developed with a physician.
a. Monitor hematologic laboratory values daily: bleed- The main inherited coagulation disorders include he-
ing time, coagulation time, PT, and plasma count. mophilia A and Band von Willebrand disease (Table 37.5).
b. Administer antibiotic coverage before any peri- Hemophilia A results in a deficiency of coagulation fac-
odontal treatment because infection is a major tor VIII, and the clinical severity of the disorder depends
concern. on the level of factor VIII remaining. Patients with severe
c. Extract all hopeless, nonmaintainable, or potentially hemophilia who have less than 1 % of normal factor VIII
infectious teeth at least 10 days before the initiation levels may have severe bleeding on the slightest provo-
of chemotherapy, if systemic conditions allow. cation, whereas those with more moderate hemophilia
d. Periodontal debridement should be performed and (1-5% factor VIII) have less frequent spontaneous hemor-
thorough oral hygiene instructions given if the pa- rhage but still bleed with minimal trauma.
tient's condition allows. Twice-daily rinsing with Patients with mild hemophilia (6-30% factor VIII) rare-
0.12% chlorhexidine gluconate is recommended ly bleed spontaneously but may still have hemorrhage
after oral hygiene procedures. Recognize the poten- after severe trauma or during surgical procedures. The
tial for bleeding caused by thrombocytopenia. Use clinician should consult the patient's physician before
pressure and hemostatic agents as indicated. dental treatment to determine the risk for bleeding and
3. During acute phases of leukemia the patient should treatment modifications required.
receive only emergency periodontal care. Any source Hemophilia B, or Christmas disease, results in a defi-
of potential infection must be eliminated to prevent ciency of factor IX. The severity of the disorder depends
TABLE 37.5 Inherited Coagulation Disorders
Type Prolonged Normal Treatment

Hemophilia A Partial thromboplastin time 1. Prothrombin time 1. DDAVP (desmopressin)
2. Bleeding time 2. Factor VIII concentrate or cryoprecipitate
3. Fresh-frozen plasma
4. Fresh whole blood
5. e-aminocaproic acid (EACA)
6. Tranexamic acid
Hemophilia B Partial thromboplastin time 1. Prothrombin time 1. Purified prothrombin complex concentrates
2. Bleeding time 2. Factor IX concentrates
3. Fresh-frozen plasma
von Willebrand disease 1. Bleeding time 1. Prothrombin time 1. DDAVP (desmopressin)

2. Partial thromboplastin time 2. Platelet count 2. Factor VIII concentrate or cryoprecipitate
3. Variable factor VIII deficiency
on the relative amount of existing factor IX. Surgical simple extractions usually require an INR less than
therapy requires a factor IX level of 30-50% and is usu- 2.0-2.5. Complex surgery or multiple extractions may
ally achieved by administration of purified prothrombin require an INR less than 1.5-2.0.
complex concentrates or factor IX concentrates. 3. The physician should be consulted about discontinu-
von Willebrand disease results from a deficiency of von ing or reducing anticoagulant dosage until the desired
Willebrand factor, which mediates adhesion of platelets INR is achieved. The dentist must inform the phy-
to the injured vessel wall and is required for primary he- sician what degree of intraoperative and postopera-
mostasis. von Willebrand factor also carries the coagulant tive bleeding is usually expected with the procedures
portion of factor VIII in the plasma. The disorder has three planned. Discontinuing anticoagulant therapy before
major subtypes with a wide range of clinical severity. In dental surgery was common in the past. However,
fact, many cases of von Willebrand disease go undiag- most clinicians no longer recommend discontinuing
nosed, and bleeding during dental treatment may be the anticoagulation for many procedures because this has
first sign of the underlying disease. significant potential risks to patient health. If the INR
Periodontal treatment may be performed in patients is higher than the level at which significant bleeding is
with these coagulation disorders, provided that sufficient likely to accompany a particular procedure, the physi-
precautions are taken. Probing, scaling, and prophylaxis cian may elect to change anticoagulant therapy. Often,
can usually be done without medical modification. More the anticoagulant is discontinued for 2-3 days before
invasive treatment, such as local block anesthesia, root periodontal treatment ( clearance half-life of warfarin is
planing, or surgery, dictates prior physician consultation. 36-42 h), and the INR is checked on the day of therapy.
Complete wound closure and application of pressure will If the INR is within the acceptable target range, the
reduce hemorrhage. Antihemostatic agents such as oxi- procedure is done and the anticoagulant resumed im-
dized cellulose or purified bovine collagen may be placed mediately after treatment.
over surgical sites or into extraction sockets. The antifi- 4. Careful technique and complete wound closure are
brinolytic agent epsilon-aminocaproic acid (EACA), given paramount. For all procedures, application of pres-
orally or intravenously, is a potent inhibitor of initial clot sure can minimize hemorrhage. Use of oxidized cel-
dissolution. lulose, microfibrillar collagen, topical thrombin, and
Tranexamic acid is a more potent antifibrinolytic agent tranexamic acid should be considered for persistent
than EACA and has been shown to prevent excessive oral bleeding.
hemorrhage after periodontal surgery and tooth extrac-
Aspirin interferes with normal platelet aggregation and
tion. All coagulation disorders are hereditary. Coagula-
can result in prolonged bleeding. Because it binds irrevers-
tion may be impaired by vitamin K deficiency, long-term
ibly to platelets, the effects of aspirin last at least 4-7 days.
alcohol abusers, or chronic hepatitis.
Aspirin is generally used in small doses of 325 mg or less
Dental treatment planning for patients with liver dis-
per day, which usually does not alter bleeding time. In gen-
ease should include the following:
eral, patients taking low doses of aspirin daily do not need
1. Physician consultation to discontinue aspirin therapy before periodontal proce-
2. Laboratory evaluations: PT, bleeding time, platelet dures. However, higher doses may increase bleeding time
count, and PTT (in patients in later stages of liver dis- and predispose the patient to postoperative bleeding. For
ease) patients taking more than 325 mg of aspirin per day, aspi-
3. Conservative, nonsurgical periodontal therapy, when- rin may need to be discontinued 7-10 days before surgical
ever possible therapy.
4. If surgery is required (may require hospitalization): Heparin is generally used for short-term anticoagula-
a. International normalized ratio (INR; PT) should tion and is given intravenously (usually in a hospital en-
generally be less than 2.0. For simple surgical pro- vironment). It is a powerful anticoagulant with a duration
cedures, INR less than 2.5 is generally safe. of action of 4-8 h. Periodontal treatment is rarely required
b. Platelet count should be less than 80,000/mm3• while a patient is taking heparin.
Periodontal treatment should be altered as follows:
1. Consult the patient's physician to determine the nature
Thrombocytopenic Purpura
of the underlying medical problem and the degree of Thrombocytopenic purpura is defined as a platelet count
required anticoagulation. of less than 100,000/mm3• Bleeding caused by throm-
2. The procedure to be done determines the acceptable bocytopenia may be seen with idiopathic thrombocy-
INR. Infiltration anesthesia, scaling, and root planing topenic purpura, radiation therapy, myelosuppressive
may be done safely in patients with an INR less than drug therapy (e.g., chemotherapy), leukemia, or infec-
3.0. Block anesthesia, minor periodontal surgery, and tions. Purpuras are hemorrhagic diseases characterized
TABLE 37.6 Hemostatic Tests
Vascular Platelet Coagulation Lytic

1. Tourniquet test 1. Platelet count 1. Prothrombin time (PT, measures extrinsic and com- 1. Euglobulin clot
N: 10 petechiae N: 150,000-300,000/mm3 mon pathways: factors I, II, V, VII, and X) lysis time
Abn: > 10 petechiae Abn: Thrombocytopenia N: 11-14 s (depending on laboratory) measured N: <90min
<100,000/mm3; clinical against control Abn: >90min
bleeding occurs at <80,000/ PT is reported as international normalized ratio
mm3; spontaneous bleeding (INR): N: INR = 1.0
occurs at <20,000/mm3 Abn: INR>l.5
2. Bleeding time 2. Bleeding time 2. Partial thromboplastin time (PT-F, measures intrinsic
N: 1-6min 3. Clot retraction and common pathways: factors III, IX, and XI, and
Abn: >6 min 4. Complete blood cell count low levels of factors I, II, V, X, and XII)
N: 25-40 s (depending on laboratory) measured
against control
Abn: > 1.5 times normal
3. Clotting (coagulation) time
N: 30-40min
Abn: >l h
Clinical disease association
Vascular (capillary wall Thrombocytopenia All three tests Increase in

defect) Rule out: 1. fibrinolytic
Rule out: a. Vascular wall defect a. Liver disease activity
a. Thrombocytopenia b. Acute/chronic leukemia b. Warfarin therapy
purpuras c. Aplastic anemia c. Aspirin or NSAID therapy
b. Telangiectasia d. Liver disease d. Malabsorption syndrome or long-term antibiotic
c. Aspirin or NSAID e. Renal dialysis therapy (lack of vitamin K utilization)
therapy 2. Prothrombin time: factor VII deficiency
d. Leukemia 3. Partial thromboplastin time: hemophilia
e. Renal dialysis Renal dialysis
Abn, abnormal; N, normal; NSATD, nonsteroidal anti-inflammatory drug.
by extravasation of blood into the tissues under the skin Thrombasthenia occurs in uremia, Glanzmann disease,
or mucosa, producing spontaneous petechiae (small red aspirin ingestion, and von Willebrand disease.
patches) or ecchymoses (bruises). Both types of nonthrombocytopenic purpura may re-
Periodontal therapy for patients with thrombocyto- sult in immediate bleeding after gingival injury. Treatment
penia should be directed toward reducing inflammation consists primarily of direct pressure applied for at least
by removing local irritants to avoid the need for more 15 min. This initial pressure should control the bleeding
aggressive therapy. Oral hygiene instructions and fre- unless coagulation times are abnormal or reinjury occurs.
quent maintenance visits are of paramount importance. Surgical therapy should be avoided until the qualitative
Physician referral is indicated for a definitive diagnosis and quantitative platelet problems are resolved.
and to determine any alterations in planned therapy.
Scaling and root planing are generally safe unless platelet
Laboratory Tests for Bleeding Disorders
counts are less than 60,000/mm3• No surgical procedures
should be performed unless the platelet count is greater Laboratory tests for bleeding disorders are described
than 80,000/mm3• Platelet transfusion may be required in Table 37.6.
before surgery. Surgical technique should be as atrau-
matic as possible, and local hemostatic measures should
be applied. INFECTIOUS DISEASES
N onthrombocytopenic Purpuras Hepatitis

Nonthrombocytopenic purpuras result from either Six distinct types of hepatitis have been identified:
vascular wall fragility or thrombasthenia (impaired plate- hepatitis A, B, C, D, E, and G. Majority of hepatitis infec-
let aggregation). Vascular wall fragility may result from tions are undiagnosed. The clinician must be aware of
hypersensitivity reactions, scurvy, infections, chemicals high-risk groups such as health care workers, dialysis
(phenacetin, aspirin), dysproteinemia, and other causes. patients, immunosuppressed patients, patients requiring
blood transfusions, drug users, homosexuals, and insti- The hepatitis B virus (HBV) vaccine should also be ad-
tutionalized patients. ministered if the individual has not previously received it.
The following procedures need to be followed while
treating hepatitis patients:
1. Do not provide periodontal therapy unless there is an HIV and AIDS
emergency. The periodontal treatment is influenced by the patient's
2. For treated/recovered hepatitis, perform routine peri- overall systemic health and coincident oral infections or
odontal care with consultation with physician regard- diseases. Extensive periodontal treatment plans must be
ing the type of hepatitis, mode of transmission, and considered in regard to patient's systemic health, prog-
length and course of disease. nosis, and survival time.
3. For patients with active hepatitis with positive hepatitis
B surface antigen (HBsAg) or positive hepatitis C virus
(HCV) carrier requiring emergency treatment. Tuberculosis
With physician's consultation, treat the patient using Any patient who gives a history of poor medical follow-
all disposable items which after use should be placed in up or shows signs and symptoms indicating tuberculosis
one lined wastebasket, labeled and disposed off. If bleed- should be referred to physician for evaluation. Adequate
ing is likely to occur during treatment, measure PT and treatment for tuberculosis requires minimum 18 months,
bleeding time. and thorough posttreatment follow-up should include
Aseptic technique should be followed all the time; chest radiograph and sputum cultures. Review patient's
minimize aerosol. Do not use ultrasonic instruments, symptoms every 12 months. When medical clearance
high-speed handpieces, air syringes, etc. Prerinse with is given and sputum culture results are negative, these
chlorhexidine gluconate for 30 s is recommended. patients can be treated normally.
KEY POINTS
• Afternoon appointments are preferred in hypertensive • The primary test used to assess glycemic control in
patients, as the blood pressure is more in the morning. a known diabetic patient is the glycated hemoglobin
• In prehypertension, the systolic blood pressure is assay.
120-139 mm Hg and diastolic blood pressure is • Exogenous steroids may suppress the HPA axis and
80-89 mm Hg. impair the patient's ability to respond to stress with
increased endogenous cortisol production.
• A patient having an angina attack on the dental chair
should receive immediately a tablet of nitroglycerin
0.3-0.6 mg sublingually.
QUESTIONS 2. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial en-
docarditis. Recommendations of the American Heart Association.
JAMA 1997;277:1794-801.
1. Describe antibiotic prophylactic regimen for patients 3. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial en-
susceptible to infective endocarditis. docarditis. Recommendations by the American Heart Association.
2. Describe periodontal management of patients with Circulation 1997;96:358-66.
thrombocytopenic purpura. 4. Mealy BL. Periodontal implications: medically compromised pa-
tients. Ann Periodontol 1995;1:256.
3. Describe periodontal management of patients with
5. Newman MG, Takei H, Klokkevold PR, Carranza FA. Clinical Peri-
respiratory disease. odontology. 10th ed. Philadelphia: Saunders; 2006.
4. How would you manage a patient with a history of 6. Pallasch TJ, Slots J. Antibiotic prophylaxis and the medically com-
myocardial infarction for periodontal treatment? promised patient. Periodontal 2000 1996;10:107.
7. Chilo V, Borea G, Strong M. Life Threatening Emergencies in Den-
Suggested readings tistry. Padova: Piccin Nuova; 1988.
1. Barco CT. Prevention of infective endocarditis: a review of medical

and dental literature. J Periodontol 1991;62:510.
CHAPTER
38
Risk Assessment
CHAPTER OVERVIEW
Periodontitis is a multifactorial disease, the microbial study, subjects with mere presence of plaque deposits
plaque being the primary initiating factor. Several other did not develop periodontitis, raising the question as to
factors contribute to its progression and the outcome. what other factors could influence the occurrence of the
This fact is highlighted by the classic study by Loe et al disease. Attempts to explain variations of disease occur-
(1965), who concluded that mere presence of plaque is rence between individuals led to the establishment of
not sufficient for the occurrence of periodontitis. In their "the concept of risk."
SO WHAT IS "RISK?" increase in the exposure to risk factors results in a directly

proportional increase in disease occurrence, for example,
Risk refers to the exposure of an individual to certain smoking and diabetes (Table 38.1).
factors/ characteristics with the result that he/ she has a
greater likelihood of acquiring/ developing the disease of
Risk Determinants
interest within a given time frame.
This alteration in the health condition of an individual Some of the risk factors may be alterable and some may
can occur due to endogenous/exogenous factors occur- be nonalterable. The nonalterable ones are called "risk
ring alone or in tandem. determinants" or "background characteristics." They are
Hence, risk can be defined as the probability that an predictive of the possibility of disease occurrence but
individual develops a specific disease in a given period of are usually not a part of the causal chain, for example,
time. The factors that increase the probability of disease age, genetics, gender, and socioeconomic status.
occurrence are called "risk elements."
Risk elements include risk factors, risk determinants,
Risk Indicators
risk indicators, and risk markers.
Some of the risk factors have been identified to be asso-
ciated with the disease only in cross-sectional studies and
Risk Factors the association has not been confirmed in the longitudinal
Risk factors are individual/ group of factors the expo- studies. These probable/putative risk factors are called
sure to which increases the possibility of occurrence of "risk indicators," for example, osteoporosis, human im-
the disease, as demonstrated by long-term studies (lon- munodeficiency virus (HIV), and infrequent dental visits.
gitudinal studies).
The risk factors can be environmental, biological, and
Risk Markers/Predictors
behavioral in nature. They may be an etiological factor
or expose the host to etiological factors resulting in dis- Some factors when present are highly predictive of risk
ease occurrence. They can occur at a single point of time for occurrence of a disease in an individual. They can be
(genetic), over multiple separate points of time (plaque), modified through intervention but are not the part of the
or continuously. causal chain. These are called risk predictors/markers,
Risk factors must occur in advance of the disease and for example, bleeding on probing and previous history
may also demonstrate dose/response effect; that is, an of periodontal disease.
TABLE 38.1 Study Designs That Are Used to Determine the Red Complex Pathogens
Lines of Evidence with Weightage Ratings
Pathogens consisting of Porphyromonas gingivalis, Trepo-
Meta-analysis and systematic reviews ***** Very high nema denticola, and Tannerella forsythensis are implicated in
Randomized control trials - prospective, **** High progression of periodontitis, along with a few organisms
longitudinal studies such as Fusobacterium nucleatum and Campylobacter rectus.
Cohort studies, case-control studies, *** Moderate
cross-sectional studies Predisposing Factors
Case series, case reports ** Low
Anatomic factors such as developmental grooves, fur-
Anecdotes and clinical observations * Very low cation areas, and prosthetic restorations favor accumula-
tion of plaque and thereby act as a risk factor.
Diabetes
This cause-effect relationship conferred by risk factors
is supported by "lines of human evidence." These lines Diabetes is one of the most prevalent chronic diseases
of human evidence are determined by certain study de- in the world. Landmark study by Genco et al has dem-
signs that have different weightage ratings, which enable onstrated a high prevalence of periodontitis in the Pima
to differentiate a characteristic/ attribute as a risk factor, Indian community (that has highest prevalence of diabe-
indicator, or marker (Paquette, 1999). tes in the world). Of late, a two-way relationship has been
The lines of evidence include: demonstrated with the proinflammatory cytokine tumor
necrosis factor (TNF)-a implicated in the pathogenesis
1. Consistency of association: Most studies dealing with
of periodontitis and insulin resistance in type 2 diabetes.
the relationship produce similar results.
Risk determinants include:
2. Strength of association: Study should be free of error
for a stronger association. Age
3. Appropriate time sequence: The potential factor Gender
must precede the occurrence of the disease. Genetic factors
4. Specificity of association: A specific association may
be causal in nature.
Genetics as a Risk for Periodontitis
5. Degree of exposure/ dose-response effect: Higher
level of exposure to the characteristic will result in a The primary etiological factor in chronic periodontitis
higher risk for the disease occurrence. is dental plaque, but not all individuals with dental plaque
6. Biological plausibility: The association between the develop periodontitis lesions. In addition, early onset or
risk factor and the disease should be associated by aggressive periodontitis patients have been shown to
plausible biological mechanisms. have very little plaque. Moreover, these periodontitis
7. Support from experimental evidence: Experimental forms have been shown to have a familial distribution.
reproduction of disease should occur frequently in Genetic alterations as a risk factor have been reported
animals (humans when possible) when exposed to by various studies. Early onset periodontitis has been
the risk factor. found to have a familial aggregation. The second line of
evidence has come from twin studies, which have dem-
onstrated a 50% heritability component for chronic peri-
RISK FACTORS FOR odontitis.
PERIODONTAL DISEASE The third important evidence is the existence of gene
polymorphisms in a population. Some of the well-studied
They include factors identified to be associated with gene polymorphisms in periodontal diseases are on im-
the disease through longitudinal studies. munoglobulin receptors, TNF-a, interleukin (IL)-1[3, etc.
Individuals with polymorphisms in the genes coding for
these mediators/ cytokines / receptors have a great risk of
Smoking
suffering from severe forms of periodontitis.
Smoking is one of the well-established risk factors
for several of the periodontal diseases. It affects the pro-
Age
gression through effects on microbiological profile (in-
crease in anaerobic organisms), physiology (decrease in Early evidence demonstrates that both prevalence and
pocket temperature), and immune system (decreased severity increase with older age. Van der Velden sug-
chemotaxis). gested that age may be a marker for periodontal tissue
CHAPTER 38 RISK ASSESSMENT 315
support loss. However, the age effect most likely rep- RISK MARKERS/PREDICTORS
resents the cumulative effect of prolonged exposure to
true risk factors. Effects of age on periodontal disease These factors predict the probability of disease occur-
progression could be considered negligible when good rence. They include:
oral hygiene is maintained.
1. Bleeding on probing
2. Previous history of periodontal disease.
Gender
Multiple studies have demonstrated poor periodontal
health in men as compared with that in women. Bleeding on Probing
Gender association with periodontitis is related to pre- Lay et al have reported that repeated bleeding on prob-
ventive practices rather than any genetic factors. ing at a given site on two consecutive visits is associated
with 30% probability of attachment loss at the same site
and lack of bleeding on probing is an excellent indicator
RISK INDICATORS of gingival health.
These are factors that have been assessed for associa-

tion with disease by cross-sectional study design. They Previous History of Periodontal Disease
include stress, HIV /acquired immune deficiency syn-
drome (AIDS), and osteoporosis. Presence of previous periodontal disease has been
found to be associated with a higher risk of developing
periodontal disease in future.
Stress
Various studies have shown that individuals under
psychological stress are more likely to develop periodon- CLINICAL RISK ASSESSMENT
tal diseases such as acute necrotizing ulcerative gingivitis IN PERIODONTAL DISEASE
(ANUG) and periodontitis. A significant association be-
tween elevated scores of social strain and periodontitis 1. Demographic data
has been described by various studies. a. Age
The following factors may play a role in the mechanism - Time of exposure
underlying the association between psychological factors - Duration of exposure
and periodontitis: - Age-related changes
1. There is increased production of IL-6 in response to b. Sex
increased psychological stress; c. Socioeconomic status
2. Host response to P. gingivalis infection may d. Dental awareness
be compromised in psychologically stressed - Frequency of dental visits.
individuals; and 2. Medical history
3. Individuals under stress are less likely to perform a. Diabetes
regular good oral hygiene and prophylaxis. b. Tobacco smoking
c. HIV /AIDS
d. Osteoporosis
HIV/AIDS e. Stress.
Conflicting data due to variation in the study and pa- 3. Dental history
rameter design have resulted in lack of strong associa- a. Family history of early tooth loss
tion between HIV/ AIDS and periodontitis. Necrotizing b. Previous history of periodontal disease
ulcerative periodontitis has been shown to be associated c. Frequency of dental care.
with severity of disease in patients suffering with AIDS. 4. Clinical examination
a. Plaque accumulation
b. Bleeding on probing
Osteoporosis
c. Extent of loss of attachment
There are conflicting reports by van Wovern et al, who d. Aggressive form of disease
found that there is increased attachment loss in subjects e. Tooth examination
with osteoporosis as compared with controls, and Krebbs £. Plaque retentive areas
et al, who observed no difference in periodontal param- g. Anatomic factors
eters between osteoporotic women and control groups. h. Restorative factors.
Medical history
Dental history
Periodontal
Risk
factor/Determinant identification <:===~
Elimination
of risk elements
Periodontal therapy ]
I positive response I I negative response I

n
Maintenance
n
Reassess risk
factors/Determinants
FIGURE 38.1 Steps in clinical risk assessment.
A comprehensive assessment of the above-mentioned Risk assessment is done before the initiation of therapy
factors and intervention constitutes clinical risk assess- and a reassessment should be done after a negative re-
ment (Fig. 38.1). sponse to therapy.
The major risk factor has to be identified for the diag-
nosis and successful management of periodontal disease.
KEY POINTS
• Attempts to explain variations of disease occurrence • Risk elements include risk factors, risk markers, risk
between individuals led to the establishment of "the determinants, and risk indicators.
concept of risk." • The risk factors can be environmental, biological, and
• Risk can be defined as the probability that an indi- behavioral in nature.
vidual develops a specific disease in a given period of • Nonmodifiable risk factors are genetics, age, gender, and
time. stress.
QUESTIONS 2. Kobayashi T, Sugita N, Van der Pol WL, et al. The Fey receptor
genotype as a risk factor for generalized early onset periodontitis in
Japanese patients. J Periodontal 2000;71:1425-32.
1. Define risk factor. 3. Kornman KS, Crane A, Wang HY, et al. The interleukin-I genotype
2. What are risk determinants? as a severity factor in adult periodontal disease. J Clin Periodontal
3. Enumerate the risk indicators. 1997;72:1324-31.
4. Define risk markers with examples. 4. Kribbs PJ. Comparison of mandibular bone in normal and osteopo-
rotic women. J Prosthet Dent 1990;63:218.
5. Lang NP, Schatzle MA, Loe H. Gingivitis as a risk factor in periodon-
Suggested readings tal disease. J Clin Periodontal 2009;36(10):3-8.
6. Lindhe J, Lang N, Karring T. Clinical Periodontology and Implant Den-
1. Craandijk J, Van Kugten MV, Verweji CL, et al. Tumour necrosis tistry. 5th ed. Oxford: Blackwell Munksgaard; 2008.
factor a gene polymorphisms in relation to periodontitis. J C/in 7. Loe H, Thelaide E, Jensen SB. Experimental gingivitis in man. J Peri-
Periodontol 2001;28:1137-44. odontol 1965;36:177.
CHAPTER 38 RISK ASSESSMENT 317
8. Marazita ML, Burnerster IA, Gunsolley JC, et al. Evidence for auto- 15. Shangase L, Feller L, Blingnaut E. Necrotising ulcerative gingivitis/
somal dominant inheritance and race specific heterogeneity in early period on ti tis as indicators of HIV infection. S Afr Dent J 2004;59:105.
onset periodontitis. J Periodontol 1994;41:156-63. 16. Susin C, Dalla Vecchia CF, Oppermann RV, et al. Periodontal attach-
9. Michalowicez BS, Diehl SR, Gunsolly JC, et al. Evidence of a sub- ment loss in an urban population of Brazilian adults: effect of demo-
stantial genetic bases for risk for adult periodontitis. J Periodontal graphic, behavioral, and environmental risk indicators. J Periodontal
1991;62:293-9. 2004;75(7):1033-41.
10. Moss ME, Beck JD, Kaplan BH, et al. Exploratory case-control anal- 17. Swango PA, Kleinnman DV, Konzdman JL. HIV and periodontal
ysis of psychosocial factors and adult periodontitis. J Periodontal health: a study of military personnel with HIV. J Am Dent Assoc
1996;67(10):1060-9. 1991;122:49.
11. Nelson RG, Shlossman M, Budding LM, et al. Periodontal dis- 18. Rees TD. Global risk factors for periodontal disease. Periodontology
ease and NIDDM in Pima Indians. Diabetes Care 1990;13(8):836-40. 2000;29:200.
12. Nishimura F, Murayama Y. Periodontal inflammation and insulin re- 19. Starford TW. Periodontal risk factors and indicators. Periodontology
sistance lessons from obesity. J Dent Res 2001;80(8):1690-964. 2000;32:2003.
13. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds. 20. Van der Velden U. Effect of age on the periodontium. J Clin Periodontal
Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B. 1984;11(5):281-94.
Saunders Company; 2006. 21. Van Dyke TE, Sheilesh D. Risk factors for periodontitis. J Int Acad
14. Paquette DW, Madianos P, Offenbacher S, et al. The concept of "risk" Periodontal 2005;7(1):3-7.
and the emerging discipline of periodontal medicine. J Con temp Dent 22. Van Wouvern J, Klausen B, Kollorup G. Osteoporosis - a risk in
Pract 1999;1(1):l-8. periodontal disease. J Periodontol 1994;65:134.
SECTION VI
PERIODONTAL THERAPY
CHAPTER
39
Periodontal Instrumentation
CHAPTER OVERVIEW
Removal of plaque and calculus is the prime motive in odontal instrumentation is a vital requisite for the atrau-
the management of periodontal disease. Periodontal in- matic and successful management of periodontal disease.
strumentation, whether surgical or nonsurgical is a crucial Besides this, a complete knowledge of various periodontal
factor in the armamentarium possessed by a periodontist in instruments as well as specific indications for their utility
his/her quest for elimination of local factors and diseased forms an important aspect of surgical as well as nonsurgical
tissues. Thorough knowledge of the fundamentals of peri- periodontal therapy.
CLASSIFICATION OF PERIODONTAL SIMPLE SHANK DESIGN

INSTRUMENTS The shank of a periodontal instrument usually bends
in one or more places. A shank that is bent in one plane
Periodontal instruments can be classified as: has a simple shank design. Instruments with simple
1. Dental mirrors shanks are used on anterior teeth. The crowns of an-
2. Periodontal probes terior teeth are wedge shaped. An instrument with a
3. Explorers simple shank will reach along an anterior crown and
4. Scaling and curettage instruments on to the root surface.
5. Cleansing and polishing instruments.
COMPLEX SHANK DESIGN
A shank that is bent in two planes has a complex
shank design. The crowns of posterior teeth are round-
Instrument Parts (Fig. 39.1)
ed and overhang their roots. An instrument with a com-
l. Handle: For holding the instrument. plex shank is needed to reach around the crown and
2. Working end: Does the work of the instrument. on to the root surface. Complex shank designs were
There are many types of working ends. The instru- developed to allow subgingival instrumentation of
ments may have either one or two working ends. posterior teeth.
a. The working end might be a small mirror.
b. Another type is shaped and beveled to have sharp FUNCTIONAL AND LOWER SHANK (FIG. 39.2)
edges. The functional shank is the portion of the shank from
c. A working end can be thin and wirelike. the working end to the last bend next to the instrument
3. Shank: The rod-shaped length of metal between the handle. The lower shank is the section of the shank nearest
handle and the working end. to the working end. This part of the shank is also called the
terminal shank. The lower shank begins below the work-
ing end and extends to the first shank bend (Table 39.1).
Design Features of Instrument Shank
The instrument shank is an extension device that in- Working End
creases the length of the instrument so that working end The working end of the instrument is that por-
can be placed on the tooth surface. tion of the instrument that comes in contact with the
322 SECTION VI PERIODONTAL THERAPY
O'l ,;:::~
Mirror end !
I
I
I
I
I
Shank
I
I
I
I
I
! Handle
I
I Shank
Shank Handle
I
"Tl
~ 'ffl'Tll'ffn'YY'fYlm---------------ii
~
Shank i
Working Handle
end
FIGURE 39.1 Parts of a periodontal instrument.
tooth and performs the intended task. The working

end of the manual instrument can be wirelike, rod
shaped, or a blade. Instrument can have one working
end, termed single-ended instruments, or two work-
ing ends, termed double-ended instruments. Double-
ended instruments can be paired or unpaired.
The actual parts of the working end vary with each in-
strument. Some working ends are wirelike or rod shaped
with a sharp or blunt point, whereas others have a blade,
Functional shank
face, lateral sides, back, and toe.
Terminal shank Explorers and probes are wirelike or rod shaped, form-
ing a sharp or blunt point at the end. The working ends
of scaling instruments are slightly integral. The face and
lateral sides join to form a blade or cutting edge.
Dental Mirrors
FIGURE 39.2 Parts of the instrument shank. The dental mirror is used to enhance access to instru-
mentation (Fig. 39.3).
TABLE 39.1 Shank Flexibility
Shank type Intended use

• Flexible shanks yield as the working end encounters rough sur- Detection of subgingival calculus deposits; removal of light calculus
faces or deposits deposits and endotoxins, e.g., explorer, area-specific curette
• This type provides the most tactile information to the clinician's
finger
• Moderately flexible shanks yield slightly as the working end Removal of medium-sized or small calculus deposits, e.g., universal
encounters rough surfaces or deposits curette
• This type provides some tactile information to the clinician's
finger
• Rigid shanks will withstand strong forces applied during calculus Removal of large-size calculus deposits, e.g., sickle scaler, periodon-
removal tal file
• This type provides very limited tactile information to the clini-
cian's finger
CH A PT ER 39 PERIO DO N TA L IN ST RU M EN TATIO N 323
FIGURE 39.3 Dental mirror.
FIGURE 39.5 Periodontal probes.

FIGURE 39.4 Transillumination.
1. Indirect vision TABLE 39.2 Types ofTransillumination

2. Retraction
Types Characteristics
3. Indirect illumination
Plane (flat) surface • Reflecting surface is applied to the back
4. Transillumination (Fig. 39.4). surface of the mirror lens
The primary purpose of the mirror is to see oral struc- • Image reflected in the mirror may be
double (ghosted)
tures that cannot be seen directly without compromising
operator positioning. This technique is known as indirect Concave surface • Produces a magnified image
vision and the reflected image is reversed in the mirror. • Image reflected in the mirror may be
distorted
Indirect vision is essential for instrumentation in maxil-
lary right palatal aspect and the palatal aspects of anterior Front surface • Reflecting surface is applied to the front
teeth. The mirror is also used to retract tissue to enhance surface of the mirror lens
• Mirror surface is easily scratched
visibility with direct vision. The cheek and tongue can • Image reflected in mirror is clear;
be gently moved by the face of the mirror to enhance vis- eliminates double images
ibility. Illumination allows the clinician to use the mirror
as a spotlight to reflect light from the dental light onto a
specific area of the mouth. Periodontal Probes
Transillumination seemingly makes the tooth trans-
parent. This technique is useful in the anterior sextants The periodontal probe is an instrument of evaluation
and consists of placing the mirror behind the teeth and used in assessing the periodontal health of the tissue.
directing the dental light perpendicular to the long axis There are two basic types of periodontal probes: calibrated
of the teeth (Table 39.2). and furcation probes (Fig. 39.5).
FIGURE 39.6 Explore.
Periodontal probes are used to locate, measure, Scaling and Curettage Instruments
and mark pockets, as well as determine their course
on individual tooth surfaces. Probe is a tapered, rod- Sickle Scaler (Supragingival Scaler)
like instrument calibrated in millimeters with a blunt The sickle scalers are used to remove supragingival
rounded tip. calculus deposits from enamel surfaces and are used with
When measuring a pocket, the probe is inserted with a pull stroke. Sickle scalers have a flat surface and two cut-
a firm and gentle pressure to the bottom of the pocket. ting edges that converge in sharply pointed tips (Figs 39.7
The shank should be aligned with the long axis of the and 39.8).
tooth surface to be probed. It is also used to measure Posterior sickle scalers have two paired working ends
the level of attachment along the surface of the tooth; (Fig. 39.9). The paired working ends are mirror images
e.g., the World Health Organization (WHO) probe has of one another. Both of these working ends are needed
millimeter markings and a small round ball at the tip. to debride all the tooth surfaces of a posterior sextant.
These probes are thin and the shank is angled to allow The paired working end of a posterior scaler may be
easy insertion into the pocket. found on two single-ended instruments or may be com-
Furcation involvement can be best evaluated with bined on one double-ended instrument; e.g., UlS/30,
curved and blunt Nabers probe. Ball and Indiana University sickles are large; Jaquette
The calibrated periodontal probe is used to: sickles number 1, 2, and 3 have medium-sized blades
(Table 39.3).
1. Determine the consistency of the gingival tissue Nevi 2 posterior sickle scaler is a new design to be
2. Survey sulcus and pocket depths inserted several millimeters subgingivally for removal of
3. Measure clinical attachment levels moderated ledges of calculus.
4. Measure the width of the attached gingival Sickles with straight shanks are designed for use on
5. Evaluate the presence of bleeding and/ or purulent anterior teeth and premolars and contra-angled shanks
exudate. adapt to posterior teeth.
Explorer
The explorer is an instrument of evaluation and is
specifically designed to provide excellent tactile infor-
mation to the clinician's fingers. Explorers are used to
(Fig. 39.6):
1. Locate subgingival deposits
2. Locate carious areas
3. Check the smoothness of the root surfaces after root
planing.
Explorers are designed with different shapes and an-
gles for a variety of uses.
Explorer Design Feature

The explorer has a fine, wirelike working end. It is
made of flexible metal and circular in cross-section. The
working end of an explorer is 1-2 mm long and is referred
to as its tip. FIGURE 39.7 Supragingival scalers.
TABLE 39.3 Design Features of Sickle Scalers
Lateral surfaces Straight; meet in a pointed tip
Relationship of face to shank Face at a 90° to lower shank
Number of cutting edges Two cutting edges per working

end
Sickle scaler
Working end in cross- Triangular
section
Functional shank Short, rigid
Application to sextants and Anterior designs limited to use on

surfaces anterior teeth; posterior designs
limited to use in posterior teeth
Universal curette Use of crown and root Limited to use on enamel tooth
surfaces surfaces
lateral border of the convex base forms cutting edges

on both sides of the blade (Fig. 39.9). Both single- and
double-end curettes may be obtained, depending on the
Area-specific curette preference of the operator.
There are two basic types of curettes:
FIGURE 39.8 Instrument design of a curette.
1. Universal
2. Area specific.
UNIVERSAL CURETTE (FIG. 39.10)

Universal curettes have cutting edges that may be
inserted in most areas of the dentition by altering and
adapting the finger rest, fulcrum, and hand position of the
operator. Universal curettes are used to remove light or
medium supragingival and subgingival calculus deposits
Universal curette
from enamel and cemental tooth surfaces. Like posterior
sickle scalers, universal curettes have two paired, mirror-
image working ends. The face of the blade is perpendicu-
lar (90° angle) to the lower shank when seen from the
cross-section of the tip. The blade of the universal curette
is curved in one direction from the head of the blade to
the toe, e.g., Barnhart curettes number 1-2 and 5-6, and
Columbia curettes number 13-14 (Table 39.4).
AREA-SPECIFIC CURETTES
Curette Scaler GRACEY CUREITES The Gracey curettes are a special

set of instruments designed to permit greater accessibil-
ity and adaptability when the clinician is scaling and
FIGURE 39.9 Working end of a curette and scaler. root-planing areas of the mouth that are periodontally
Curettes
A curette is a periodontal instrument with sharp cut-
ting edges that meet at a rounded toe, used primarily
for subgingival scaling and root planing (Fig. 39.8). The
curette is the instrument of choice for removing deep sub-
gingival calculus, root planing altered cementum, and the
soft-tissue lining the periodontal pocket. In cross-section,
the blade appears semicircular with a convex base. The FIGURE 39.10 Universal curette.
TABLE 39.4 Design Characteristics of Universal Curettes TABLE 39.5 Gracey Curette Series
Gracey curette
Working end Curves upward
number Specific area of use
Cutting edges Straight; parallel to one another 1/2 Anterior teeth
Relationship of face to shank Face at 90° angle to lower shank 3/4 Anterior teeth
Number of cutting edges Two cutting edges per working 5/6 Anterior teeth and premolar
end
7/8 Posterior teeth: facial and lingual surfaces
Working end in cross-section Semicircular
9/10 Posterior teeth: facial and lingual surfaces
Functional shank Design vary from short to long
and rigid to flexible 11/12 Posterior teeth: mesial surfaces
Application to sextants and A single universal curette may 13/14 Posterior teeth: distal surfaces
surfaces be used on all anterior and
posterior surfaces
Use of crown and root surfaces Enamel and cementum surfaces TABLE 39.6 Differences between Gracey Curette and Universal
Curette
Gracey curette Universal curette

Area of use Set of many curettes One curette for all areas
designed for specific and surfaces
areas and surfaces
CUITING EDGE
Use One cutting edge used; Both cutting edges

work with outer edge used; work with either
only outer or inner edge
Curvature Curved in two planes; Curved in one plane:

blade curved up, to the blade curved up, not to
side the side
Blade Offset blade: face of Not offset: face of blade

angle blade beveled at 60° to beveled at 90° to shank
shank
FIGURE 39.11 Gracey curettes (area-specific curettes). acutely angled no. 13-14 shank. The new shank angula-
tion of the Gracey no. 15-16 allows the better adaptation
to posterior mesial surfaces from a front position with
involved. The Gracey curettes were designed in the late intraoral rest. The Gracey no. 17-18 is a modification of
1930s by Dr Clayton H Gracey (Fig. 39.11). no. 13-14. It has a terminal shank elongated by 3 mm and
These curettes and their modifications are probably the a more accentuated angulation of the shank to provide
best instruments for subgingival scaling and root planing complete occlusal clearance and better access to all pos-
because they provide the best adaptation to complex root terior distal surfaces.
anatomy (Table 39.5).
Single-ended Gracey curette can also be obtained that EXTENDED SHANK CURETTES Extended shank cu-
consists of a set of 14 instruments. The Gracey curettes rettes such as the Hu-Friedy After Five curettes are modi-
differ from the universal curettes in that the blade is not fications of the standard Gracey curette design. The termi-
at 90° angle to the lower shank. The term offset blade is nal shank is 3 mm longer, allowing extension into deeper
used to describe the Gracey curettes because they are periodontal pockets of 5 mm or more. Other features
angled approximately 60-70° from the lower shank. This include a thinned blade for smoother subgingival inser-
unique angulation allows the blade to be inserted in the tion and reduced tissue distention and a large-diameter,
precise position necessary for subgingival scaling and root tapered shank. All standard Gracey numbers except for
planing (Table 39.6). no. 9-10 are available in the After Five series.
Recent addition: Number 15-16 and 17-18. The Gracey The After Five curettes are available in finishing
no. 15-16 is the modification of the standard no. 11-12 and or rigid designs. For heavy or tenacious calculus remov-
is designed for the mesial surfaces of the posterior teeth. al, rigid After Fives should be used. For light scaling or
It consists of a Gracey no. 11-12 combined with more deplaquing in a periodontal maintenance patient, the
thinner, finishing After Fives will insert subgingivally
more easily.
MINI-BLADED CURETTES Mini-bladed curettes such

as the Hu-Friedy Mini Five curettes are modifications
of the After Five curettes. They feature blades that are half
the length of the After Five or standard Gracey curettes. FIGURE 39.12 Hoe scalers.
The shorter blade allows easier insertion and adapta-
tion in deep, narrow pockets; furcations; developmental
grooves; line angles; and deep, tight, facial, lingual, or Hoe scalers are used for scaling of ledges or rings of cal-
palatal pockets. culus. The blade is bent at a 99° angle; the cutting edge is
The Mini Five curettes are available in both the finish- formed by the junction of the flattened terminal surface
ing and the rigid designs. Rigid Mini Fives are recom- with the inner aspect of the blade (Fig. 39.12).
mended for calculus removal. The more flexible shanked, The cutting edge is beveled at 45°. The blade is slight-
finishing Mini Fives are appropriate for light scaling and ly bowed so that it can maintain contact at two points
deplaquing in periodontal maintenance patients with on a convex surface. The back of the blade is rounded,
tight pockets. As with the After Fives, the Mini Fives and the blade has been reduced to minimal thickness
are available in all standard Gracey numbers except for to permit access to the roots without interference from
no. 9-10. the adjacent tissues.
This stabilizes the instrument and prevents nicking
THE GRACEY CURETTES The Gracey curettes are an- of the root, and the instrument is activated with a firm
other set of four mini-bladed curettes: pull stroke toward the crown, with every effort being
made to preserve the two-point contact with the tooth;
• Sub-O and no. 1-2 are used for anteriors and premolars
e.g., McCall's Hoe scalers no. 3, 4, 5, 6, 7, and 8 are a set
• No. 11-12 is used for posterior mesial surfaces
of six Hoe scalers designed to provide access to all tooth
• No. 13-14 is used for posterior distal surfaces.
surfaces. Each instrument has a different angle between
The blade length of these instruments is 50% shorter the shank and the handle.
than that of the conventional Gracey curette, and the
blade has been curved slightly upward. This curvature Files
allows the Gracey curettes to adapt more closely to Files have a series of very narrow hoes. Their primary
the tooth surface than any other curettes, especially on the function is to fracture or crush tenacious calculus. Files
anterior teeth and online angles. can easily gouge and roughen root surfaces when used
improperly. Therefore, they are not suitable for fine scal-
LANGER AND MINI-LANGER CURETTES This is a set ing and root planing. Mini-bladed curettes are currently
of three curettes that combines the shank design of the preferred for areas where files were once commonly used.
standard Gracey no. 5-6, 11-12, and 13-14 curettes with Files are sometimes used for removing overhanging mar-
a universal blade honed at 90° rather than the offset blade gins of dental restorations.
of the Gracey curette.
The Langer no. 5-6 curette adapts to the mesials and
Chisel Scalers
distals of anterior teeth; the Langer no. 1-2 curette (Gracey
no. 11-12 shank) adapts to the mesial and distal surfaces It is a double-ended instrument with a curved shank
of mandibular posterior teeth; and the Langer no. 3-4 at one end and a straight shank at the other. The blades
curette (Gracey no. 13-14 shank) adapts to the mesial and are slightly curved and have a straight cutting edge bev-
distal surfaces of maxillary posterior teeth. eled at 45°. It is usually used in the anterior part of the
These instruments can be adapted to both the mesial mouth. The chisel is inserted from the facial surface. The
and the distal tooth surfaces without changing instru- slight curve of the blade makes it possible to stabilize it
ments. The standard Langer curette shanks are heavier against the proximal surface, whereas the cutting edge
than a finishing Gracey but less rigid than the rigid Grac- engages the calculus without nicking the tooth. The in-
ey. They are also available with either rigid or finishing strument is activated with a push motion while the side
shanks and can be obtained in the extended shank (After of the blade is held firmly against the root.
Five) and mini-bladed (Mini Five) versions.
Ultrasonic and Sonic Instruments
Hoe Scalers Ultrasonic and sonic scalers are power-driven instru-
Periodontal hoe have broad use and, depending on the ments used during periodontal treatment. These in-
size, can negotiate the full depth of periodontal depth. struments use vibratory action to fracture and dislodge
Instrument working end can be classified into one of

the four design types: (i) wrench-shaped; (ii) crescent-
shaped; (iii) hoe-like; and (iv) working end that is similar
to conventional metal periodontal instrument (probe,
sickle scaler, and curette). It is recommended that an
instrument kit contains all four of these working end
design types.
Branemark System, Nobelpharma Implant

Instruments
The Nobelpharma universal instrument is used for
FIGURE 39.13 Ultrasonic tips. cleaning the apical portion of the prosthetic framework.
Strokes should be in a facial-to-lingual direction. The
Nobelpharma facial instrument is used to clean the facial
surface of the abutment using vertical strokes.
deposit from the tooth surface. A water lavage is continu-
ously supplied to cool the tip of the instrument and flush Hu-Friedy Implacare Implant Instruments
away debris (Fig. 39.13).
Ultrasonic instruments may be used for removing Hu-Friedy Implacare system is comprised of a reus-
plaque, scaling, curetting, and removing stain. The two able, sterile metal handle into which paired, disposable
types of ultrasonic units are magnetostrictive and piezo- plastic instrument tips are secured. The conventional
electric. In both types, alternating electrical current gener- working end design of the Implacare tips is easily adapt-
ates oscillations in materials in the handpiece that cause ed for use around abutment posts and single implant
the scaler tip to vibrate. crowns. Implacare tips are made of a high-grade resin
Depending on the manufacturer, these ultrasonic vibra- that provides rigidity for calculus removal but does not
tions at the tip of the instruments of both types range from damage titanium abutments or leave plastic residue on
20,000 to 45,000 cycles per second (also referred to as hertz the abutment.
[Hz]). In magnetostrictive unit, the pattern of vibration
ImplaMed Wiz-Stik Implant Instrument
of the tip is elliptical, which means that all sides of the
tip are active and will work when adapted to the tooth. It is double-ended - One end is wrench-shaped and
In piezoelectric units, the pattern of vibration of the tip the other is crescent-shaped.
is linear, or back and forth, meaning that the two sides of
the tip are the most active. Implant-Prophy+Plastic Instrument
Sonic units consist of a handpiece that attaches to a Implant-Prophy+Plastic instruments are made up
compressed airline and uses a variety of specially de- of a hard, high-performance polymer plastic. Implant-
signed tips. Vibrations at the sonic tip range from 2000 Prophy+ Plastic instruments duplicate the working ends
to 6500 cycles per second, which provides less power for and shanks of traditional steel instruments. Instruments
calculus removal than ultrasonic units. may be reused, have good durability, and have working
Ultrasonic and sonic tips with different shapes are ends that can be sharpened.
available for scaling, curetting, root planing, and debrid- Implant-Prophy+Plastic instruments are available in
ing during periodontal surgery. Columbia 13/14U and Gracey 5/6, 11/12, and 13/14
Advantages of Ultrasonic and Sonic Scaling designs. A small raised dome on the shanks of the Gracey
• Decrease in time spent in plaque and calculus removal instruments provides the clinician with a visual and tac-
• Debris, blood, and necrotic tissue flushed away by tile reference for locating the cutting edge on each work-
water lavage ing end.
• Antimicrobial effect
• Decreased clinician fatigue
• Delivery of antimicrobial agents Cleansing and Polishing Instruments
• Increased patient comfort. Rubber Cups
Rubber cups consist of a rubber shell with or without
Plastic Instruments for Implants webbed configurations in the hollow interior. They are
Plastic instruments are used on titanium and other used in the handpiece with a special prophylaxis angle.
implant abutment materials. It is imperative that plastic The handpiece, prophylaxis angle, and rubber cup must
rather than metal instruments be used to avoid scarring be sterilized after each patient use, or a disposable plastic
and permanent damage to the implants. prophylaxis angle and rubber cup may be used and then
FIGURE 39.14 Polishing cups. FIGURE 39.15 Kirkland gingivectomy knife.
discarded. A good cleansing and polishing paste that con- 3. Periosteal elevators
tains fluoride should be used and kept moist to minimize 4. Surgical chisels
frictional heat as the cup revolves (Fig. 39.14). 5. Surgical files
6. Scissors
Bristle Brushes 7. Hemostats and tissue forceps.
Bristle brushes are available in wheel and cup shapes.
The brush is used in the handpiece with a polishing paste.
Because the bristles are stiff, use of the brush should be Excisional and lncisional Instruments
confined to the crown to avoid injuring the cementum Periodontal Knives (Gingivectomy Knives)
and the gingiva. The Kirkland knife is representative of knives com-
Dental Tape monly used for gingivectomy. These knives can be ob-
tained as either double- or single-ended instruments.
Dental tape with polishing paste is used for polishing The entire periphery of these kidney-shaped knives is the
proximal surfaces that are inaccessible to other polish- cutting edge (Fig. 39.15).
ing instruments. The tape is passed interproximally while
being kept at a right angle to the long axis of the tooth and Interdental Knives
is activated with a firm labiolingual motion. Particular care These spear-shaped knives have cutting edges on both
is taken to avoid injury to the gingiva. The area should be sides of the blade and are designed with either double-or
cleansed with warm water to remove all remnants of paste.
single-ended blades, e.g., the Orban's knife no. 1-2 and
Air-Powder Polishing the Merrifield knives no. 1, 2, 3, and 4 (Fig. 39.16).
In the early 1980s, a specially designed handpiece was
introduced that delivers an air-powered slurry of warm
water and sodium bicarbonate; this instrument is called
the Prophy-jet. This system is effective for the removal
of extrinsic stains and soft deposits. The slurry removes
stains rapidly and efficiently by mechanical abrasion and
provides warm water for rinsing and lavage. The flow rate
of abrasive cleansing power can be adjusted to increase
the amount of powder for heavier stain removal.
Surgical Instruments
They include:
1. Excisional and incisional instruments
2. Surgical curettes and sickles FIGURE 39.16 Orban knife.
FIGURE 39.19 Surgical chisel.
Surgical Chisels and Hoes

Chisels and hoes are used during periodontal surgery
FIGURE 39.17 Surgical blades.
for removing and reshaping bone. The hoe has a curved
shank and blade, whereas the Wiedelstadt and Todd-
Gilmore chisels are straight shanked. The surgical hoe has
Surgical Blades a flattened, fishtail-shaped blade with a pronounced con-
vexity in its terminal portion. The cutting edge is beveled
Scalpel blades of different shapes and sizes are used
with rounded edges and projects beyond the long axis of
in periodontal surgery. The most commonly used blades
the handle to preserve the effectiveness of the instrument
are no. 120, 15, and 15C. The no. 120 blade is a beak-
when the blade is reduced by sharpening. The surgical
shaped blade with cutting edges on both sides, allowing
hoe is generally used for detaching pocket walls after the
the operator to engage narrow, restricted areas with both
gingivectomy incision, but it is also useful for smoothing
pushing and pulling cutting motions. The no. 15 blade
root and bone surfaces made accessible by any surgical
is used for thinning flaps and for all-around use. The
procedure (Fig. 39.19).
no. 15C blade, a narrower version of the no. 15 blade,
The Ochsenbein no. 1-2 is a useful chisel with a semi-
is useful for making the initial, scalloping type incision.
circular indentation on both sides of the shank that allows
The slim design of this blade allows for incising into the
the instrument to engage around the tooth and into the
narrow interdental portion of the flap. All of these blades
interdental area. Surgical hoes are usually used with a pull
are discarded after one use (Fig. 39.17).
stroke, whereas chisels are engaged with a push stroke.
Periosteal Elevators Surgical Files

These instruments are necessary to reflect and move Periodontal surgical files are used primarily to smooth
the flap after the incision has been made for flap sur- rough, bony ledges and to remove all areas of bone; e.g.,
gery. The no. 24G and the Goldman-Fox no. 14 are well- the Schluger and Sugarman files are similar in design and
designed periosteal elevators (Fig. 39.18). can be used with a push-and-pull stroke, primarily in the
interdental areas (Fig. 39.20).
Scissors and Nippers

Scissors and nippers are used in periodontal surgery
for such purposes as removing tabs of tissue during gin-
givectomy, trimming the margins of flaps, enlarging in-
cisions in periodontal abscesses, and removing muscle
attachments in mucogingival surgery. There are many
types, and the choice is a matter of individual preference,
e.g., the Goldman-Fox no. 16 scissors with a curved bev-
eled blade with serrations and the nippers (Fig. 39.21).
Needleholders
Needleholders are used to suture the flap at the de-
FIGURE 39.18 Periosteal elevator. sired position after the surgical procedure has been
FIGURE 39.22 Needle holder.
2. Improvement in instrument control. A dull cutting

edge must be pressed with greater force against the
tooth.
FIGURE 39.20 Surgical files. 3. Reduction of clinician fatigue and stress to the finger,
hand, and wrist.
4. Reduction in the possibility of burnishing calculus.
Dull instruments tend to nick the deposit instead of
removing it entirely.
5. Improvement in the tactile sensitivity during instru-
mentation.
6. Reduction in the possibility of grooving or scratching
the root surface.
Testing Sharpness
Sharpness can be determined by visual and tactile tests.
• A sharp cutting edge appears as a line having no shape
or width. A dull cutting edge has a wide, rounded
shape. When light is directed on a dull cutting edge, it
reflects the light and appears shiny.
• The tactile test for sharpness uses an acrylic test stick.
The instrument is held in the dominant hand with a
FIGURE 39.21 Surgical scissors. modified pen grasp whereas the test rod is held in
the nondominant hand. Following the principles of
instrumentation for activation, the clinician should
completed. The regular type of needleholder is illustrated press the cutting edge of the instrument into the stick.
in Fig. 39.22, whereas the Castroviejo needleholder is used If the instrument catches or cuts making a pinging
for delicate, precise techniques requiring quick and easy sound into the acrylic, the instrument is sharp. When
release and grasp of the suture. the instrument glides over the stick, the instrument is
considered dull.
Sharpening of Periodontal Instruments Sharpening Technique
The cutting edges of hand-activated instruments must The sharpening technique uses the grinding of a coarse
be sharp for efficient and effective periodontal debride- stone against the instrument to create a sharp edge.
ment with minimal tissue trauma. The following three different hand-sharpening meth-
A sharp cutting edge on the working end of a hand- ods result in sharp instruments:
activated instrument allows:
1. Reducing the face of the blade
1. Reduction of the operating time required for the pro- 2. Reducing the lateral surface to create a sharp edge
cedure. Decrease the number of strokes required to through movement of a sharpening stone against a
remove the deposit. stationary cutting edge
These may be used in two ways:

• The instrument may be stabilized and held stationary
while the stone is drawn across it.
• The stone may be stabilized and held stationary while
the instrument is drawn across it.
Principles of Sharpening
1. Choose a stone suitable for the instrument to be sharp-
ened. It should be one that is of an appropriate shape
and abrasiveness.
2. Use a sterilized sharpening stone if the instrument to
be sharpened will not be resterilized before it is used
on a patient.
3. Establish the proper angle between the sharpening
stone and the surface of the instrument on the basis of
an understanding of its design.
4. Maintain a stable, firm grasp on both the instru-
ment and the sharpening stone. This ensures that
FIGURE 39.23 Arkansas sharpening stone. the proper angulation is maintained throughout
the controlled sharpening stroke. In this manner,
the entire surface of the instrument can be reduced
3. Moving the instrument against a stationary evenly, and the cutting edge is not improperly beveled.
sharpening stone. 5. Avoid excessive pressure. Heavy pressure causes the
stone to grind the surface of the instrument more
quickly and may shorten the instrument's life unnec-
Sharpening Stones essarily.
Sharpening stones may be quarried from natural 6. Avoid the formation of a "wire edge," characterized by
mineral deposits or produced artificially. In either case, minute filamentous projections of metal extending as
the surface of the stone is made up of abrasive crystals a roughened ledge from the sharpened cutting edge.
that are harder than the metal of the instrument to be When the instrument is used on root surfaces, these
sharpened. projections produce a grooved surface rather than a
Coarse stones have larger particles and cut more rapid- smooth surface. A wire edge is produced when the
ly; they are used on instruments that are dull. Finer stones direction of the sharpening stroke is away from, rather
with smaller crystals cut more slowly and are reserved for than into or toward, the cutting edge.
final sharpening to produce a finer edge and for sharpen-
When back-and-forth or up-and-down sharpen-
ing instruments that are only slightly dull.
ing strokes are used, formation of a wire edge can be
Types:
avoided by finishing with a downstroke toward the
1. Natural abrasive stones like India and Arkansas oilstones cutting edge.
(Fig. 39.23)
1. Lubricate the stone during sharpening. This minimizes
2. Synthetically produced stones like carborundum, ruby,
clogging of the abrasive surface of the sharpening
and ceramic stones.
stone with metal particles removed from the instru-
Sharpening stones can also be categorized by their ment. It also reduces heat produced by friction. Oil
method of use: should be used for natural stones and water for syn-
thetic stones.
1. Mounted rotary stones: These stones are mounted on a
2. Sharpen instruments at the first sign of dullness. A gross-
metal mandrel and used in a motor-driven handpiece.
ly dull instrument is inefficient and requires more pres-
They may be cylindrical, conical, or disk shaped. These
sure when used, which hinders control.
stones are generally not recommended for routine use.
2. Unmounted stones: They are available in a variety Furthermore, sharpening such an instrument requires
of sizes and shapes. Some are rectangular with flat the removal of a great deal of metal to produce a sharp
or grooved surfaces, whereas others are cylindric cutting edge. This shortens the effective life of the instru-
or cone shaped. ment (Fig. 39.24).
4. Angle the stone away from the cutting edge to obtain
a 110° angle to the face of the blade.
5. Use light pressure, beginning at the heel of the instru-
ment, and activate the stone in a downstroke 0.5-1 in.
in length.
6. Rotate the stone along its vertical axis as the stone is
moved from heel to toe.
7. Follow the curvature of the blade with the sharpening
stroke, while using slight overlapping strokes.
8. Complete sharpening action on a downstroke when
the stone contacts the line of the toe.
9. Round the toe from the cutting edge every fourth or
fifth sharpening.
10. Clear wire edges with conical stone and remove
sludge with gauze.
11. Check instrument sharpness.
FIGURE 39.24 Method of sharpening.
TECHNIQUE USED TO SHARPEN UNIVERSAL
CURETTES
Sharpening Individual Instruments 1. Position the instrument in the nondominant hand.
TECHNIQUE USED TO SHARPEN SICKLE SCALERS 2. Place the instrument handle against the counter-
top with the face of the blade parallel to the floor.
1. Position the instrument in the nondominant hand.
3. Place the stone in the dominant hand and position
2. Place the instrument handle against the countertop
it against the entire length of the cutting edge of the
with the face of the blade parallel to the floor.
instrument at a 90° angle to the face of the blade.
3. Place the sharpening stone in the dominant hand and
4. Move the stone away from the cutting edge to obtain
position it against the heel of the surface.
4. Angle the stone at 90° to the face of the blade.
5. Using light pressure, along the entire length of the cut-
5. Move the stone away from the cutting edge to obtain
ting edge, activate the stone in a downstroke 0.5-1 in.
in length.
6. Activate the stone in a downward stroke that is
6. Continue with downstrokes and upstrokes without
0.5-1 in. in length.
moving the stone forward.
7. Follow the curvature of the blade with the sharpening
7. Complete sharpening action on a downstroke.
stroke while using slight overlapping strokes.
8. Sharpen the opposite cutting edge in the similar
8. Complete sharpening action on a downward stroke
manner.
when the toe portion is flat against the stone.
9. Round the toe from the cutting edge once every fourth
9. Sharpen the opposite cutting edge in the similar
or fifth sharpening event.
manner.
sludge with gauze.
sludge with gauze.
General Principles of Instrumentation

TECHNIQUE USED TO SHARPEN AREA-SPECIFIC
Principles of Positioning (Accessibility)
CURETTES
These include proper position of the: (1) clinicians
1. Position the instrument in the nondominant hand.
(Figs 39.25-39.27), (2) patients, (3) dental units and patient
2. Place the instrument's handle against the counter-top
relative to clinician, (4) clinician relative to the treatment
with the face of the blade parallel to the floor. (The
area, and (5) patient's head relative to the treatment area
handle of the instrument must be angled to the right
(Tables 39.7-39.10).
or left.)
3. Place the stone in the dominant hand and position it
against the heel of the blade at a 90° angle to the face Dental Light Position
of the blade: the anterior portion of the stone will For mandibular treatment areas, position the den-
not be in contact with the instrument. tal light directly above the patient's head, so that the
FIGURE 39.25 Clinician seated to the back of the patient and directly behind the patient.
FIGURE 39.26 Clinician seated to the side of the patient. FIGURE 39.2 7 Clinician seated to the front of the patient.
light beams shine directly into the patient's mouth TABLE 39. 7 Clinician Position
(Fig. 39.28).
Seat height Adjust the chair seat so that:
For maxillary treatment areas, position the dental • With your back against the seat back, you can
light above the patient's chest area. Tilt the dental light move your knees and lower legs freely
so that the light beams shine into the patient's mouth • Your thighs are parallel to the floor and the
at an angle. knees slightly higher than the thighs
• Your feet are flat on the floor
Seat back Adjust the chair back so that:

Visibility, Illumination, and Retraction • It supports the lumbar region of your back
• The angle between the seat and the chair back
Visibility and illumination may be direct and indirect. should be between 85° and 100°
Direct vision with direct illumination from the dental
light is most desirable. If this is not possible, indirect vi- Body position Your head and neck are in the same vertical
plane
sion may be obtained by using the mouth mirror, and
TABLE 39.8 Patient's Position: The Supine Position TABLE 39.10 Position of the Dental Unit Relative to the
Clinician
Body position • Position the patient in a supine position. The
Guidelines for positioning the patient and equipment relative
chair back should be nearly parallel to the
to the clinician
floor
• The patient's heel should be slightly higher Clinician Legs and the stool base should form a tripod,
than the tip of his or her nose. This position somewhat like the legs of a three-legged stool.
maintains good blood flow to the head This tripod formation creates a very stable
position. Keep knees apart, with your legs in a
Head position The top of the patient's head should be even V formation
with the edge of the headrest. If necessary, ask
the patient to slide up in the chair to assume this Height of Recline the patient chair in supine position
position the patient and adjust the height so that the tip of the
chair patient's nose is at or below the level of clinician
Head rest If the headrest is adjustable, raise or lower it so waist. Clinician should not raise his or her arms
that the patient's neck and head are aligned with above waist level when working in the patient's
the torso
mouth
Clinician's Maintain your upper arms in a vertical position,
body with elbows held slightly away from your sides, at
TABLE39.9 Patient's Head Position position waist level. Your lower arms are in a horizontal po-
sition and raised slightly so that the angle formed
Patient's head To be able to see and reach the patient's between your lower and upper arms is slightly
position on the mouth comfortably, the top of the patient's less than 90°. In this position, your muscles are
headrest head must be even with the end of the head- well positioned to make and control fine wrist and
rest. This principle is true for all treatment finger movement
areas and clinician positioning zones
Bracket Position it slightly above patient's body. The lower
Patient's head for Ask patient to open the mouth and tilt the table the tray, the easier for you to see the periodontal
mandibular areas head downward. The term for this patient instruments resting on it
head position is the chin-down position
Dental Position the light at a comfortable arm's length
Patient's head for Ask patient to open the mouth and position light away from your head. Position the light as far
maxillary areas the head in the neutral position. The term away from the patient's face as possible while still
for this patient's head position is the chin- keeping it within easy reach. Positioning the light
up position closer is less effective in illuminating the intraoral
treatment areas
Possible patient's Ask the patient to position his or her head
head positions in an appropriate manner for each treat-
ment area in order to assist you in instru-
mentation. Possible head position includes:
looking straight ahead, turning toward the
clinician, or turning away from the clinician
indirect illumination may be obtained by using the mirror

to reflect light to where it is needed. Indirect vision and
indirect illumination are often used simultaneously.
Retraction provides visibility, accessibility, and illumi-
nation. Depending on the location of the area of operation,
the fingers and/ or the mirror are used for retraction. The
mirror may be used for retraction of the cheeks or the
tongue; the index finger is used for retraction of the lips
or cheeks.
The following methods are effective for retraction:
1. Use of the mirror to deflect the cheek while the fingers
of the nonoperating hand retract the lips
2. Use of the mirror alone to retract the lips and cheek
3. Use of the fingers of the nonoperating hand to retract
the lips
4. Use of the mirror to retract the tongue
5. Combinations of the preceding methods. FIGURE 39.28 Dental light position.
Condition of Instruments (Sharpness)

Before any instrumentation, all instruments should be
inspected to make sure that they are clean, sterile, and in
good condition. The working ends of pointed or bladed
instruments must be sharp to be effective. Sharp instru-
ments enhance tactile sensitivity and allow the clinician
to work more precisely and efficiently. Dull instruments
may lead to incomplete calculus removal and unneces-
sary trauma because of the excess force usually applied
to compensate for their ineffectiveness.
Maintaining a Clean Field

The pooling of saliva interferes with visibility during
instrumentation and impedes control because a firm fin-
ger rest cannot be established on wet, slippery tooth sur- FIGURE 39.29 Modified pen grasp.
faces. Adequate suction is essential and can be achieved
with a saliva ejector or with an aspirator.
Gingival bleeding is an unavoidable consequence of
subgingival instrumentation. In areas of inflammation,
this is not necessarily an indication of trauma from in-
correct technique; instead, it indicates ulceration of the
pocket epithelium. Blood and debris can be removed
from the operative field with suction and by wiping or
blotting with gauze squares. The operative field should
also be flushed occasionally with water.
Compressed air and gauze squares can be used to
facilitate visual inspection of tooth surfaces just below
the gingival margin during instrumentation. A jet of air
directed into the pocket deflects a retractable gingival
margin. Retractable tissue can also be deflected away from
the tooth by gently packing the edge of a gauze square
into the pocket with the back of a curette. Immediately
after the gauze is removed, the subgingival area should
FIGURE 39.30 Palm and thumb grasp.
be clean, dry, and clearly visible for a brief interval.
Instrument Grasp
Instrument grasp describes how the clinician holds
the instruments. Two types of grasp used during dental
procedure are:
1. The modified pen grasp (Fig. 39.29)
2. The palm grasp (Fig. 39.30).
The palm grasp has limited uses, i.e., to hold and use
the air /water syringe or tuck the mirror away when not
in use. With the palm grasp, the syringe or instrument is
held in the palm of the dominant hand, and the fingers are
wrapped around the handle. The thumb is free to activate
the air and water buttons or to provide leverage on the
shank of an instrument.
The modified pen grasp is a variation of the pen grasp
(Fig. 39.31). Pen grasp varies from person to person; the
modified pen grasp requires that all clinicians hold
the instrument in a similar manner. FIGURE 39.31 Standard pen grasp.
The modified pen grasp offers the following three ad-
vantages:
• Control of the instrument
• Prevention of finger fatigue
• Increase in tactile sensitivity.
The instrument is held in the dominant hand with the
pads of the index finger and thumb opposite each other
on the handle closest to the working end. The thumb
and index finger do not touch, thereby creating a tripod
effect with the middle finger placed along the shank of
the instrument. This tripod effect balances the instrument
in the clinician's hand to provide stability and control.
Keeping the index finger and thumb separated allows the
clinician to roll the instrument between these digits with
ease and control. The thumb is either straight or slightly
bent in C shape, whereas the index finger is bent at the FIGURE 39.32 Conventional finger rest.
second joint. The index finger bends at the second joint,
and the instrument handle rests somewhere between the
second and the third joints.
The side pad near the fingernail of the middle finger is
against the shank and serves to guide the instrument. The
middle and ring fingers always should remain in contact
somewhere along the length of either finger. This con-
tact ensures proper wrist motion and limits the amount
of finger motion to activate the instrument.
Fulcrum or Finger Rest

The pad, especially the tip of the ring finger of the
dominant hand, serves as the fulcrum finger. When ac-
tivating the instrument, the clinician exerts downward
pressure on the fulcrum finger and slightly squeezes the
instrument with the index finger and thumb to increase
the stability and control during scaling while not caus- FIGURE 39.33 Cross-arch finger rest.
ing patient discomfort. General guidelines for an ap-
propriate fulcrum include the placement of ring finger
on the solid tooth surface, in the same arch and close to
the work area. 2. Cross-arch: Requires a finger placement on the solid
The fulcrum finger serves as the pivot point for in- tooth structure (Fig. 39.33). Although the placement
strument adaptation and activation. This action of the is in the same arch, it is in the opposite quadrant of
fulcrum finger and wrist is what is needed to activate instrumentation.
the instrument. 3. Opposite arch: The finger rest is established on tooth
Finger rests may be generally classified as intraoral surfaces on the opposite arch (e.g., mandibular arch
finger rests or extraoral fulcrums. Intraoral finger rests on finger rest for instrumentation on the maxillary arch)
tooth surfaces ideally are established close to the work- (Fig. 39.34).
ing area. Variations of intraoral finger rests and extraoral 4. Finger-on-finger: The finger rest is established on the
fulcrums are used whenever good angulation and a suf- index finger or thumb of the nonoperating hand
ficient arc of movement cannot be achieved by a finger (Fig. 39.35); it works best in the maxillary right quad-
rest close to the working area. rant (left quadrant for the left-handed clinician) dur-
ing instrumentation of the buccal surfaces and in the
Intraoral Finger Rest mandibular anterior facial sextant.
l. Conventional: The finger rest is established on tooth 5. Reinforced: Allows the clinician to exert more pres-
surfaces immediately adjacent to the working area sure on scaling. Requires caution to prevent the instru-
(Fig. 39.32). ment from breaking or injury to the patient. Pressure is
FIGURE 39.34 Opposite-arch finger rest.
FIGURE 39.36 Palm-down fulcrum.
FIGURE 39.35 Finger-on-finger rest.
gently exerted by the index finger or thumb to increase

lateral pressure on the instrument to remove the de-
posit.
This technique is ideal in the maxillary left palatal
quadrant.
Extraoral fulcrums are essential for effective instru-
mentation of some aspects of the maxillary posterior teeth
where instrument angulation may be challenging. FIGURE 39.37 Palm-up fulcrum.
The two most commonly used extraoral fulcrums are
as follows:
1. Palm-up (Fig. 39.36): The palm-up fulcrum is estab- 2. Palm-down (Fig. 39.37): The palm-down fulcrum is es-
lished by resting the backs of the middle and fourth tablished by resting the front surfaces of the middle and
fingers on the skin overlying the lateral aspect of the fourth fingers on the skin overlying the lateral aspect
mandible on the right side of the face. of the mandible on the left side of the face.
tilts the instrument handle as close to the tooth surface as
possible, permitting easy insertion with the toe one-third
of the working end beneath the gingival margin and pre-
venting injury to hard and soft tissues.
Once the insertion angle is accomplished, various
angles are established, depending on the type of stroke
applied. If the clinician is beginning an exploratory or ex-
amination stroke, then the angle should be approximately
5° so that the cutting edge of the scaling instruments is
not engaged against the tooth surface.
If the working stroke is a scaling stroke for calculus
removal, then the angulation will be closer to but less
than 90°. This angulation affords the clinician the greatest
opportunity to engage the hard deposit.
If the working stroke is for root planing, then the
angulation will lessen to 60-80°. A smaller angulation
FIGURE 39.38 Adaptation. smoothes the root surface and does not cut or gauge the
root, which is the goal of root planing. As a general rule,
proper angulation is established when the terminal shank
Both intraoral finger rests and extraoral fulcrums may of the instrument is parallel to the long axis of the tooth.
be reinforced by applying the index finger or thumb of This position is accomplished by tilting of the instru-
the nonoperating hand to the handle or shank of the ment handle slightly from the tooth after the instrument
instrument for added control and pressure against the is inserted.
tooth. The tip of the powered instrument is inserted gently
beneath the gingiva, adapted to the tooth surface and
activated. The tip never remains for more than a second
Adaptation
in any given location because energy from the number of
Proper adaptation of the instrument to the tooth sur- vibrations or cycles per second generated by the tip may
face means placement of the lower one-third to two-thirds cause heat and result in tooth damage and sensitivity.
of the instrument working end, especially the lower one- The exact blade angulation depends on:
third of the cutting edge of the scaling instruments or
1. The amount and nature of the calculus
the side tip of the explorer and probe against the tooth
2. The procedure being performed
(Fig. 39.38).
3. The condition of the tissue.
The goal is to keep the side tip or lower one-third of the
cutting edge or working end against the tooth surface at
all times, while the terminal shank is maintained parallel Activation
to the long axis of the tooth.
Instrument activation can be defined as a single un-
Clinicians can adapt the instrument by rolling the han-
broken movement made by an instrument. Activation
dle between the index finger and the thumb and pivot-
is divided into exploratory strokes and working strokes.
ing on the fulcrum finger. Another aspect of appropriate
adaptation is the initial placement of the lower one-third
of the instrument on a specific area of the tooth. The tooth
surface location varies from instrument to instrument. TYPES OF STROKES
Three basic types of strokes are used during instru-
Advantages mentation:
• Avoid trauma to the soft tissues and root surfaces. 1. The exploratory stroke
• Ensure maximum effectiveness of instrumentation. 2. The scaling stroke
3. The root-planing stroke.
Angulation
1. Exploratory strokes are used to detect calculus and root
Initial angulation to insert an instrument to the base irregularities. These strokes are used intermittently
of the sulcus should be as close to 0° as possible. This with scaling instruments or continually with explor-
angulation requires the face of the blade to be against ers and probes. Exploratory strokes are light and long,
the tooth surface. To achieve this position, the clinician covering the entire root surface. Work-scaling strokes
for calculus removal are firm, short, and controlled;

whereas root-planing strokes are not firm and are
longer.
2. Scaling strokes are used on the enamel and root surface
for the removal of plaque biofilm and calculus, and
root-planing strokes are used only on the root surface
for debridement of residual calculus deposits and re-
moval of plaque biofilm and endotoxins.
3. Root-planing strokes are designed to smooth the root
surface and follow scaling strokes. The instrument
grasp is light for exploratory strokes, a bit firmer for
root-planing strokes, and very firm for scaling strokes.
The root-planing stroke is a moderate to light pull
stroke that is used for final smoothing and planing of
the root surface. Although hoes, files, and ultrasonic
instruments have been used for root planing, curettes
are widely acknowledged to be the most effective and
versatile instruments for this procedure. The design of
the curette, which allows it to be more easily adapted to
subgingival tooth contours, makes curettes particularly
suitable for root planing in periodontal patients. With a
moderately firm grasp, the curette is kept adapted to the
tooth with even, lateral pressure. A continuous series of
long, overlapping shaving strokes is activated. As the
surface becomes smoother and resistance diminishes,
lateral pressure is progressively reduced.
Proper pressure is necessary to ensure that calculus is
efficiently removed without removing an excess amount
of cementum and dentin.
Lateral Pressure
The pressure the clinician exerts on the instrument
with the thumb and index finger while pushing with the
fulcrum finger determines the firmness of the instrument
FIGURE 39.39 Strokes in a vertical and oblique direction.
grasp, known as lateral pressure, which varies with the
type of stroke used. Lateral pressure may be firm, moder-
ate, or light. When removing calculus, lateral pressure is
applied firmly or moderately initially and is progressively The direction, length, pressure, and number of strokes
diminished until light lateral pressure is applied for the necessary for either scaling or root planing are determined
final root-planing strokes. by four major factors:
Calculus should not be removed in layers because it
1. Gingival position and tone
burnishes the deposit into the root surface. Burnished
2. Pocket depth and shape
calculus is difficult to remove and can prevent complete
3. Tooth contour
tissue healing.
4. Amount and nature of the calculus or roughness.
Any of basic strokes may be activated by a pull or a
push motion in a vertical, oblique, or horizontal direction. Certain circumstances require a horizontal or circum-
Vertical and oblique strokes are used most frequently. ferential stroke direction. Some mandibular anterior teeth
Vertical and oblique strokes are predominantly used are extremely narrow, prohibiting proper adaptation of the
on the proximal surfaces of the tooth or root, and oblique instrument working end. These strokes are also used on line
strokes are predominantly used mainly on facial and angles of posterior teeth because of lack of proper adapt-
lingual surfaces of the tooth or root (Fig. 39.39). The toe ability. Circumferential strokes must be used with care to
one-third of the instrument is adapted to the tooth surface, prevent damage to the epithelial attachment. To accomplish
and the instrument is pulled by the action of the lateral this stroke, the toe is inserted into the sulcus at a 90° angle
action of the wrist and forearm. to the epithelium. Short and controlled strokes are used
needed and the instrument is never held in one place for
more than 1 s - usually less than a full second.
Principle of Use of Sickle Scaler, Universal

Curettes, and Area-specific Curettes
Use of Sickle Scaler on Anterior Tooth Surfaces
MANDIBULAR ANTERIORS, FACIAL ASPECTS
Cutting edges: An anterior sickle scaler has two cutting
edges, Cl and C2, per working end.
The step-by-step approach to using a sickle scaler
on anterior teeth is shown for the facial aspect of the
mandibular left anteriors, mesial surfaces, and the
mandibular right anteriors, distal surfaces. Debridement
of the remaining surfaces of the mandibular anteri-
ors and the maxillary anteriors is done in the similar
manner.
1. Adapt the leading one-third of the cutting edge at the
midline of the facial surface of the left canine. Notice
that it is not possible to adapt the entire possible length
of the cutting edge of the tooth.
2. Establish a 70-80° instrument phase to tooth surface
angulation. Apply pressure with your thumb on the
shank to engage the working end against the tooth.
3. Push down with your fulcrum finger and activate a
working stroke.
4. Relax your grasp and reposition the leading one-third
of the cutting edge in preparation for the next stroke.
Adapt the working end and establish correct angula-
tion. Activate a stroke.
5. Roll the instrument handle to obtain proper adaptation
to the mesiofacial line angle of the tooth. Establish cor-
rect angulation and activate a stroke.
6. Roll the instrument handle to adapt the leading edge
to the mesial surface. Establish correct angulation and
activate a stroke.
FIGURE 39.40 Strokes in a horizontal direction. 7. The working end should extend beneath the contact
area so that the strokes cover at least half of the mesial
surface from the facial aspect. (The other half of the
mesial surface will be instrumented from the lingual
in a horizontal direction (Fig. 39.40). This stroke direction
aspect.)
requires more finger motion than wrist and forearm motion.
8. Instrument the left lateral incisors in the simi-
Various types of strokes are used with different in-
lar manner, beginning at the midline of the tooth.
struments. A pull stroke is the common stroke used for
Continue working across the facial aspect of
scaling instruments to remove calculus, although some
the sextant, ending with the distal surface of the man-
instruments require the push stroke for calculus removal.
dibular right canine.
A combined push-pull stroke that is equally light in pres-
sure is used with the explorer in an exploratory stroke
around the tooth. The walking stroke is used with the Use of Sickle Scaler on Posterior Tooth Surface
periodontal probe to walk the instrument along the junc- MANDIBULAR RIGHT POSTERIOR, FACIAL ASPECT
tional epithelium.
Selecting the correct cutting edge:
Stroke or instrument movement with a powered in-
strument consists of short, rapid instrument movement 1. Grasp the instrument in a modified pen grasp and
against the surface being debrided. Lateral pressure is not establish a fulcrum.
2. Place either working end on a proximal surface apical 7. At the mesiofacial line angle roll the handle to readapt
to the contact area. the leading one-third of the cutting edge as you work
3. Establish an appropriate finger rest. Position the handle on the mesial surface.
so that it is as parallel as possible to the long axis of the 8. Continuing making strokes across the mesial surface.
tooth. Continue strokes until at least one-half of the mesial
4. Look closely at the shank nearest to the working end. surface has been instrumented from the facial aspect.
The other half of the mesial surface will be accessed
If the lower shank is parallel with the proximal surface,
from the lingual aspect.
this is the correct cutting edge for this tooth surface.
9. Extend strokes past the center of the proximal surface.
Rule: For posterior tooth, the lower shank should be
10. Move onto the next tooth in the sextant. Begin at the
parallel to the proximal surface.
distofacial line angle and work onto the distal surface.
Cutting edges: A posterior sickle scaler has two paired
working ends. Each working end has two cutting edges, Use of Universal Curette on Anterior Tooth
Cl and C2 or C3 and C4. Surfaces
• The two cutting edges Cl and C2 are used on the facial Cutting edges: A universal curette has two paired work-
aspect of a sextant. ing ends. Each working end has two cutting edges, Cl
• Cutting edge Cl is used from distofacial line angle to and C2 or C3 and C4.
midline of the distal surface. Steps for selecting the correct edge of universal curette
• Then, cutting edge C2 is used from distofacial line on the anterior tooth surface:
angle to midline of the mesial surface.
1. Grasp the instrument in a modified pen grasp and
• The two cutting edges C3 and C4 are used in lingual
establish a fulcrum.
aspect of a sextant.
2. Place either working end on the tooth surface on which
• Cutting edge C3 is used from distolingual line angle
you wish to work.
to midline of the distal surface.
3. Hold the instrument so that the handle is parallel to
• Cutting edge C4 is used from distolingual line angle
the long axis of the tooth surface.
to midline of the mesial surface.
4. Look closely at the working end that is adapted against
1. Application of posterior sickle scaler to posterior tooth the tooth surface.
surfaces: First select the correct working end of the
If the instrument face tilts away from the tooth surface,
posterior sickle scaler.
this the incorrect cutting edge for this tooth surface. Both
2. The tooth surfaces of the facial aspect should be com-
cutting edges on this working end are incorrect edge for
pleted initially.
use on this tooth surface.
3. Begin with the last molar in the sextant.
If the instrument face tilts toward the tooth, this is the
Adapt the leading one-third of the cutting edge of
correct cutting edge for this tooth surface.
the distofacial line angle. The tip of the working end
Rule: For anterior teeth, the face of the working end
should point toward the back of the mouth because
should tilt toward the tooth.
this is the direction in which you are working.
Complete a work stroke by: MANDIBULAR ANTERIORS, FACIAL ASPECT
a. Establishing a 60-80° angulation
The step-by-step approach to using a universal curette
b. Using the ring finger as a supporting beam pushing
on anterior teeth is shown for the facial aspect of the man-
down on the fulcrum point
dibular left anteriors, mesial surfaces, and the mandibular
c. Using the thumb to press the cutting edge against
right anteriors, distal surface. Debridement of the remain-
the tooth
ing surface of the mandibular anterior and the maxillary
d. Activating a stroke with the hand and arm.
anteriors is done in the similar manner.
4. After each stroke, relax your hand and reposition the
working end for the next stroke. Roll the handle to 1. Select the correct cutting edge for use on the facial
maintain adaptation of the leading one-third of the aspect of mandibular left canine, working from the
cutting edge after each stroke. midline of the facial and onto the mesial surface.
5. While maintaining your fulcrum point, lift the work- 2. Establish a 70-80° instrument face to the tooth surface
ing end away from the tooth and turn the working end angulation and engage the working against the tooth.
so that the tip points forward toward the front of the 3. Push down with your fulcrum finger and activate a
mouth. Reposition the cutting edge at the distofacial working stroke.
line angle. Activate an oblique working stroke. 4. Relax your grasp. Roll the instrument handle to adapt
6. Work across the facial surface, using a series of oblique the working end to the next area. Establish correct an-
strokes. gulation and activate a stroke.
5. Roll the instrument handle to obtain proper adaptation 6. If furcation involvement is present, use the leading
to the mesiofacial line angle. Establish correct angula- one-third of the cutting edge against the mesial sur-
tion and activate a stroke. face of the distal root.
6. Relax your grasp and roll the instrument handle to 7. Continue making a series of oblique strokes across the
adapt to the mesial surface. Angulate, engage the cut- facial surface.
ting edge, and activate a stroke. 8. Roll the instrument handle slightly to readapt the
7. Continue strokes until the facial half of the mesial leading one-third of the cutting edge to the curved
proximal surface has been covered. root surface.
9. At the mesiofacial line angle, roll the handle to re-
Use of Universal Curette on Posterior Tooth adapt the leading one-third of the cutting edge as you
Surfaces work on the mesial surface.
10. Continue making strokes across the mesial surface.
Cutting edges: A posterior universal curette has two
11. Continue strokes until at least one-half of the mesial
paired working ends. Each working end has two cutting
surface has been instrumented from the facial aspect.
edges, Cl and C2 or C3 and C4.
The other half of the mesial surface will be accessed
Application of universal curette to posterior tooth
from the lingual aspect.
surfaces:
• The two cutting edges Cl and C2 are used on the facial
aspect of a sextant. Use of Area-Specific Curette on Anterior Tooth
• Cutting edge Cl is used from distofacial line angle to Surfaces
midline of the distal surface. Identifying the cutting edge for tooth surface
• Then, cutting edge C2 is used from distofacial line debridement:
angle to midline of the mesial surface. 1. Only one cutting edge per working end of an area-
• The two cutting edges C3 and C4 are used on lingual specific curette is used to debride the coronal and root
aspect of a sextant. surfaces of the teeth.
• Cutting edge C3 is used from distolingual line angle 2. To identify the cutting edge, hold an area-specific cu-
to midline of the distal surface. rette so that you are looking at the toe of the working
• Cutting edge C4 is used from distolingual line angle end.
to midline of the mesial surface. 3. Raise or lower the instrument handle until the
shank nearest the working end is perpendicular to the
MANDIBULAR RIGHT POSTERIORS, FACIAL ASPECT floor.
1. First select the correct working end of the universal 4. With the working end in this position, one cutting edge
curette. is tilted toward the terminal shank and the other tilts
2. The tooth surfaces of the facial aspect should be com- away from the terminal shank.
pleted in the order shown in the figure below.
The cutting edge that tilts away from the terminal
3. Begin with the last molar in the sextant.
shank is the one designed for tooth surface debridement.
Adapt the leading one-third of the cutting edge of
Other ways of describing this cutting edge are the lower
the distofacial line angle. The tip of the working end
cutting edge, the outside cutting edge, and the longer cut-
should point toward the back of the mouth because
ting edge.
this is the direction in which you are working.
The step-by-step approach to using an area-specific
Complete a work stroke by:
curette on anterior teeth is shown for the facial as-
a. Establishing a 60-80° angulation
pect of the mandibular left anteriors, mesial surfaces,
b. Using the ring finger as a supporting beam pushing
and the mandibular right anteriors, distal surfaces.
down on the fulcrum point
Debridement of the remaining surfaces of the mandibu-
c. Using the thumb to press the cutting edge against
lar anteriors and the maxillary anteriors is done in the
the tooth
similar manner.
d. Activating a stroke with the hand and arm.
4. Make a series of strokes across the distal surface ending 1. Select the correct cutting edge for use on the facial
beneath the contact area. aspect of mandibular left canine, working from the
5. While maintaining your fulcrum point, lift the work- midline of the facial and on to the mesial surface.
ing end away from the tooth and turn the working end 2. Establish a 70-80° instrument face to the tooth surface
so that the toe points forward toward the front of the angulation and engage the working against the tooth.
mouth. Reposition the cutting edge at the distofacial 3. Push down with your fulcrum finger and activate a
line angle. Activate an oblique working stroke. working stroke.
4. Relax your grasp. Roll the instrument handle to adapt 2. Place either working end on a surface.
the working end to the next area. Establish correct an- 3. Look closely at the shank nearest to working end of the
gulation and activate a stroke. instrument.
5. Roll the instrument handle to obtain proper adaptation
If the lower shank is parallel to the proximal surface,
to the mesiofacial line angle. Establish correct angula-
then this is the correct cutting edge for this tooth surface.
tion and activate a stroke.
Rule: The lower shank should be parallel to the proxi-
6. Relax your grasp and roll the instrument handle to
mal surface.
adapt to the mesial surface. Angulate, engage the cut-
ting edge, and activate a stroke. Root Surface Debridement: Multidirectional Work
7. Continue strokes until the facial half of the mesial Strokes
proximal surface has been covered.
Light, multidirectional work strokes are used to de-
Use of Area-Specific Curettes on Posterior Tooth bride the tooth surface of residual calculus granules
Surfaces and bacterial endotoxins. Multidirectional strokes are
achieved by employing all three stroke directions, one
Cutting edges: Only one cutting edge on each working
by one, in succession.
end of an area-specific curette is used for tooth surface
It is important to have a defined knowledge of root
debridement. To complete a posterior sextant, facial and
morphology in order to debride the root surfaces effec-
lingual aspects, requires four area-specific curettes, e.g.,
tively. The majority of instrumentation is done on root
Gracey 11, 12, 13, and 14. These curettes may be combined
surfaces that are hidden from view within a pathologi-
on two double-ended instruments.
cally deepened sulcus. A clear mental picture of root anat-
Application of area-specific curette to posterior tooth
omy and a keen tactile sense are necessary for periodontal
surfaces:
instrumentation to be successful.
• Cutting edges Cl and C2 are used on the facial aspect
of a sextant. GUIDELINES FOR DEBRIDEMENT OF IMPLANTS
• Cutting edge Cl is used from distofacial line angle to • The titanium surface of the abutment is easily re-
midline of the distal surface. moved. Great care must be taken not to scratch the
• Then, cutting edge C2 is used from distofacial line titanium abutment or disrupt the biological seal.
angle to midline of the mesial surface. • Plastic instruments are recommended. Metal instru-
• Cutting edges C3 and C4 are used on lingual aspect of ments and ultrasonic or sonic devices with metal tips
a sextant: are contraindicated.
• Cutting edge C3 is used from distolingual line angle • Instrumentation should be restricted to supragingival
to midline of the distal surface. deposit removal.
• Cutting edge C4 is used from distolingual line angle • Strokes should be short, controlled, and activated with
to midline of the mesial surface. light pressure. Calculus does not adhere to titanium as
tenaciously as on the natural teeth.
Steps for selecting the correct edge of a posterior area-
• Use the basic skills of operator and patient's position,
specific curette:
grasp, and fulcrum.
1. Randomly select one of the posterior area-specific cu- • Direction of strokes is in an oblique, vertical, or hori-
rettes for use on the distal surface; e.g., use either a zontal direction away from the peri-implant tissues.
Gracey 13 or 14. Grasp the instrument in a modified
pen grasp and establish a fulcrum.
KEY POINTS
• Explorers are used to locate subgingival deposits, cari- • Hoe scalers are used for scaling of ledges or rings of
ous areas, and check the smoothness of the root surfaces calculus. The blade is bent at a 99° angle.
after root planing. • The blade length of Gracey curvettes is 50% shorter than
• There are two basic types of curettes: universal and area- that of the conventional Gracey curette, and the blade
specific. has been curved slightly upward.
• The term offset blade is used to describe the Gracey • Langer and Mini-Langer curettes is a set of three curettes
curettes because they are angled approximately 60-70° that combines the shank design of the standard Gracey
from the lower shank. no. 5-6, 11-12, and 13-14 curettes with a universal blade
KEY POINTS (cont'd)
honed at 90° rather than the offset blade of the Gracey • Interdental knives are spear-shaped knives, have cutting
curette. edges on both sides of the blade, and are designed with
• Depending on the manufacturer, these ultrasonic vibra- either double- or single-ended blades, e.g., the Orban knife
tions at the tip of the instruments of both types range no. 1-2 and the Merrifield knives no. 1, 2, 3, and 4.
from 20,000 to 45,000 cycles per second. • General principles of instrumentation are principles of
• Sonic units consist of a handpiece that attaches to a positioning (accessibility), visibility, illumination, and
compressed airline and uses a variety of especially de- retraction, condition of instruments (sharpness), main-
signed tips. Vibrations at the sonic tip range from 2000 taining a clean field, instrument grasp, fulcrum or finger
to 6500 cycles per second, which provides less power rest, adaptation, angulation, and activation.
for calculus removal than ultrasonic units.
• The Kirkland knife is representative of knives commonly
used for gingivectomy.

1. Lindhe J, Lang NP, Karring T. Clinical Periodontologv and Implant Den-
1. Classify periodontal probes. Add a note on its use. tistry. 5th ed. Copenhagen: Blackwell Munksgaard; 2008.
2. Write a note on Gracey curettes. 2. Newman MG, Takei HH, Klokkevold PR, Carranza FA.
3. What are area-specific curettes? Carranza's Clinical Periodontology. 10th ed. Philadelphia: Elsevier;
2007.
4. What are the differences between scalers and curettes?
3. Patisson AM. The use of hand instruments in supportive periodontal
5. What are the differences between universal and Gracey treatment. Periodontologv 2000 1996;12:71.
curettes?
6. What are the principles of periodontal instrumentation?
7. Write a note of instrument grasp.
CHAPTER
40
Sonic and Ultrasonic Instrumentation
CHAPTER OVERVIEW
The term ultrasonics applied to sound refers to anything then. Earlier devices were large, heavy units with single,
above the frequency of audible sound and is above 20,000 Hz. bulky universal tip. Now they are replaced by a variety
In 1950, ultrasonics was first introduced for periodon- of slimmer tips.
tal procedures and has undergone many changes since Basically, there are two types of power-driven scalers.
SONIC SCALERS Magnetostrictive Ultrasonic Scaler

The magnetostrictive ultrasonic (Fig. 40.1) insert con-
Sonic instruments are small power-scaling devices
sists of a scaler tip that is attached to a transducer that is
that produce mechanical vibrations from air pressure
made up of metal stacks or rods. This apparatus is insert-
instead of electricity. The unit has a compressed airline
ed into the hand piece of the unit system where electrical
which is connected to handpiece. Air causes the move-
energy is applied to the coil in the special handpiece when
ment of rotor system in the handpiece which vibrates
the foot pedal is depressed. When alternating current
the different specially designed tips at a frequency of
(AC) passes through the metal stack, an electromagnetic
3000-6000 cycles per second (cps). Hard, heavy, tena-
cious calculus is difficult to remove with sonic scalers. field is produced that changes the dimension of the metal
stack and produces and elliptical movement of the tip at
The sonic scaler operates at a much lower perceptible
a frequency of about 25,000-30,000 cps. Electrical current
range than the ultrasonic devices. Its effectiveness is
enables the transducer to produce ultrasonic vibrations
influenced by the type of tip used, air-pressure input,
that are dissipated as heat. When the tip is parallel to
and the application load.
the tooth surface, it causes the removal of hard and soft
There is no electrical unit, and this gives the sonic
deposits.
scaler the advantage of easy mobility in the dental setting.
The entire unit is movable and compact and attaches
Heat is not generated during operation of the sonic
to electrical and water outlets. It has manual power and
scaler, but water passes through the handpiece to the tip
water controls, and the on/ off switch is located in the foot
to reduce the frictional heat that may be produced and to
pedal. Significant generation of heat necessitates water for
act as a lavage. Example of this type of scaler is the Star
cooling. An example of this type is the Cavitron.
Titan sonic scaler.
Piezoelectric Ultrasonic Scaler

ULTRASONIC SCALERS
In 1880, Pierre and Jacques Curie found that crystals
Ultrasonic scaling instruments are electronically pow- of various materials placed under mechanical stresses
ered devices that produce vibratory motions to fracture develop electrical charges on their surfaces. This conver-
deposits from tooth surfaces. The ultrasonic unit consists sion of mechanical energy into electrical energy is called
of an electric generator, a handpiece assembly, a set of the piezoelectric effect. When electrical energy is applied
interchangeable debridement inserts, and a foot control. across piezoelectric substances, small and rapid changes
They are divided into two types. in shape occur in these materials. These vibrations have
C H A PT ER 40 SO N IC A N D U LT R A SO N IC IN ST R U M EN TAT IO N 347
FIGURE 40.3 Magnetostrictive insert.
The tip movement is generally linear and allows two sides

of the tip to be active. No magnetic field is produced,
so less heat is generated. Water is for lavage only. The
piezoelectric tip has cutting edges that help remove tooth
deposits. These cutting edges are located along the side
of the working tip.
The magnetostrictive or piezoelectric unit has its own
advantages and disadvantages.
1. Since in magnetostrictive tips (Fig. 40.3), elliptical
movement of the tip causes the scaler to leave the
tooth surface during activation that causes it to bang
against the tooth surface. This leads to cavitation effect
all around the tip and therefore more effective removal
FIGURE 40.1 Magnetostrictive unit.
of the pathogen. All the sides of the tip are used.
2. Piezoelectric tips (Fig. 40.4) have advantage of having
a specific frequency and amplitude. Piezoelectric instru- two working sides which cause a linear and do not
ments (Fig. 40.2) use this principle. allow the tip to leave the tooth when it is activated.
Alternating current of high frequency is applied to Proper adaptation causes less surface roughness. Piezo-
a piezoelectric crystal housed in the handpiece, which electric tips are small and can be separated from the
causes corresponding lengthening and shortening of the handpiece, which reduces the cost and can be easily
crystal over tiny distances, resulting in physical vibrations. stored.
Piezoelectric units operate between 25,000-50,000 cps.
The difference in tip vibration between piezoelectric
and magnetostrictive designs is very subtle and probably
without the significant clinical importance.
FIGURE 40.2 Piezoelectric unit. FIGURE 40.4 Piezoelectric insert.

Mechanism of Action • High-power setting generates pronounced aerosol and

splatter formation and may reduce the volume of cool-
High-frequency sound waves are the principal action ing agent that is delivered in the pocket.
of the ultrasonic scaling instrument. These waves vibrate • Power setting should be reduced to a low or medium
at a rate of 24,000-50,000 cps. Ultrasonic scaling units level.
convert high-frequency electrical current into mechani-
cal vibrations. These conversions are attained by either
magnetostrictive or piezoelectric transducers. Sonic in- Water Flow
struments are driven by air turbine.
• It is controlled by the water knob present on the unit.
• Water contributes to three physiologic effects that en-
Frequency hance the efficacy of power scalers:
• The no. of cycles per unit time. It is the no. of cycles 1. Acoustic streaming
completed by scaler tip in linear, orbital, or elliptical 2. Acoustic turbulence
strokes. 3. Cavitation.
• It determines the area of insert tip that is active (that
Acoustic Streaming
can remove deposits).
• Higher frequency results in lesser active area of the tip It is the unidirectional fluid flow caused by ultrasonic
(30,000: 4.2 mm; 25,000: 4.3 mm). waves produced by the rapid movement of the ultrasonic
scaler.
Stroke Acoustic Turbulence
It is the maximum distance the insert tip travels during It is created when the movement of the tip causes the
one cycle or stroke path. coolant or the water to accelerate, producing an intensi-
fied swirling effect. This continues until cavitation occurs.
Amplitude Cavitation
• It is equal to one-half the distance of the stroke. A unique characteristic of the ultrasonic scalers is the
• Power knob/ setting on the unit controls the stroke cavitation effect. Cavitational activity is the term encom-
length of the insert during one cycle. passing all of the linear and nonlinear oscillatory motions
• There is higher power setting-longer stroke pattern of gas- and/ or vapor-filled bubbles in an acoustic field
and vice versa while the frequency remains constant. (Khambay BS, 1999) (Fig. 40.5).
Bubble attains
maximum size
Cavitation bubble growth

in negative pressure
New bubble
growth-
cycle repeats Bubble collapse and
compression
FIGURE 40.5 Cavitation and implosion. 0

When the water during ultrasonic instrumentation • Gentler to the soft tissue than hand scaling
comes under the influence of the rapidly alternating • More comfortable for the patient
tensile and compressive forces, it causes marked local- • Significantly less stressful for the dentist or hygienist
ized reduction in pressure. This leads to creation of small • Decreased chair time
bubbles that are formed at the end of the ultrasonic tip, • Simultaneous water lavage and scaling
where the maximum vibration occurs. These bubbles are • Some systems allow working with an antiseptic
filled with water vapor/ gas and vibrate along with their irrigating solution
source. These bubbles grow and become so large that • Less technically demanding, and the tips do not require
they cannot vibrate, which causes them to implode and sharpening.
form a mass of microbubbles which leads to shock waves.
This phenomenon is called cavitation and it depends on
Disadvantages of Ultrasonics
the frequency, and not the amplitude, of the ultrasonic
vibration. • The production of contaminated aerosols
The lavage affect associated with using ultrasonics • Interference with pacemakers
has many advantages. They continuously wash away • Reduced tactile sensitivity
the debris from areas of treatment. Bubbles formed from • Less control in difficult-access areas
cavitation contact the tooth surface collapse and release • The potential to gouge root surfaces if not used
energy, which disrupts the bacterial cell walls. It can also properly
destroy a spirochete cell membrane. • Amount of water coolant necessary for magnetostrictive
Acoustic streaming, produced by ultrasound in the systems to bring down the heat produced is more and
presence of a fluid environment, is also effective in remov- hence difficult to suction
ing plaque biofilm. • Expensive
Heat generated automatically from magnetostrictive • Damage to the ear due to increase in sound production.
units also assists in detoxification. Areas of the tooth
where the tip does not touch may inadvertently be de-
Advantages of Hand Instrumentation
toxified as well. For example, if the tip of an insert does
not fit into a furcation area, getting it as close as possible • Higher tactile sensitivity
may be enough to detoxify the area being treated. • Superior adaptation, various designs
Ultrasonic devices can also be used to deliver antimi- • No aerosol
crobial agents as they allow their addition through the • No heat production
waterline, instead of water. This helps to enhance pocket • Excellent access, different designs
depth reduction and gain in clinical attachment more than • Better visibility.
it can be achieved by hand instrumentation or ultrasonic
debridement alone.
Disadvantages of Hand Instrumentation
Role of Coolant • Requires proper blade angulation
• Requires heavy lateral pressure
• The high-frequency oscillation of sonic and ultrasonic
• Tiring for clinician
scaler tips generates heat, which necessitates the
• More potential for carpel tunnel syndrome
application of a cooling irrigation fluid to keep the
• Requires sharpening of blade.
tissues surrounding the scaler tip within a physiologic
temperature range.
• A flow rate of at least 14 mL/ min to 23 mL/ min cooling Contraindications for Use
agent appears to be sufficient to prevent thermal
1. The degree of aerosolization from the spray of water at
damages in periodontal pockets, as the penetration of
the tip is the main reason that patients with a known
the coolant used correlates well with the depth of the
communicable disease should not be subjected to the
pocket treated.
ultrasonic or sonic scaler. It has been shown that patho-
• The water also helps in the lavage effect in the
gens from the oral cavity of one person may be passed
periodontal pocket.
to that of another in the dental environment, and it is
advisable to reduce that risk by using hand instruments
Advantages of Using Automated Scalers
instead of powered devices. It has been suggested that
• Highly effective in eliminating plaque and toxins, the an antimicrobial rinse, such as chlorhexidine or povi-
causes of periodontal disease done iodine, used just before treatment may reduce the
• Faster and at least as effective as hand scaling in number of airborne bacteria. However, the herpes or
removing deep calculus hepatitis viruses are unaffected by these medicaments.
2. In the case of a patient with a known respiratory risk, 3. Keep the tip constantly in motion and use quick, light,
such as chronic pulmonary disease, there is a concern back-and-forth brush strokes.
that septic material and microorganisms from bacterial 4. Remove any roughness present on the instrument tips
plaque associated with diseased periodontal pockets to prevent scratching of the tooth surface.
may be aspirated into the lungs. As with any form of 5. Wear protective glasses and a face mask when per-
instrumentation, the use of power scaling devices in the forming these procedures.
treatment of immunosuppressed patients may warrant 6. Frequently check the tooth surfaces with the un-
antibiotic premedication due to the susceptibility powered instrument tip or a dental explorer for the
of these patients to infection. Some examples of remaining adherent deposits.
immunosuppressive conditions include leukemia, HIV, 7. Finish scaling and plaque removal with hand instru-
uncontrolled diabetes, and organ transplants. Aerosol ments to obtain a smooth tooth surface that is free of
contaminants created by particle size discrepancy subgingival deposits.
(PSD) may remain airborne for a period of time. These 8. Do not apply pressure with the instrument tip against
contaminants have the potential to be passed to other the tooth. It will not increase the effectiveness of calcu-
patients in close proximity. lus removal and can damage tooth and root surfaces,
3. The substantial amount of water that can fill the mouth and restorations.
may be uncomfortable for patients presenting with 9. Do not use an ultrasonic scaler if the patient or cli-
swallowing or gagging problems. Mouth breathers or nician has a pacemaker or another electronic life-
people who cannot breathe through their nose for any support device.
reason will find this procedure intolerable. Patients 10. Water lines of the handpiece should be left on for
who are predisposed to infection (such as after an sometime at the beginning of each day so that the
organ transplant), or have a known communicable stagnant water is cleared and biofilms are reduced
disease transmitted by aerosols (such as tuberculosis), from the tubing.
respiratory diseases (such as severe asthma), or an
unshielded pacemaker should not be treated with an
ultrasonic.
TECHNIQUE
DENTAL CONTRAINDICATIONS 1. A light pen grasp and fulcrum (either intraoral or ex-
traoral) are used, since a light touch is required even
1. Primary and newly erupted permanent teeth with large for heavy calculus removal.
pulp chambers vibrations and heat from the ultrasonic 2. Medium-power settings are recommended for mod-
can cause damage. Children may also exhibit fear of erate-to-heavy debris removal, and lower-power set-
sound and sensitivity to the vibrating tip. tings are recommended for light debris removal and
2. Precautions should be exercised when using ultrasonics deplaquing procedures.
on restorative materials including composites, 3. Water should be adjusted until a fine mist or a mist
amalgams, porcelain, and gold. with water droplets is observed. Minimizing the mist
3. Ultrasonics should be avoided in titanium implants from the ultrasonic tip minimizes aerosols outside the
without a plastic- or Teflon-coated tip. mouth.
4. The long-term effect of noise and vibration on the 4. Patient can be asked to rinse with an approved anti-
operator has yet to be fully determined. Prior to microbial prior to treatment, and using high-speed
performing any treatment, a thorough medical history evacuation also helps to minimize these aerosols.
should always be conducted. Increasing the power increases aerosol formation,
which results in reduced water cooling and cavita-
tional effect, and can increase patient sensitivity.
5. In the case of magnetostrictive ultrasonics, power is
RECOMMENDATIONS FOR USE
dispersed through several areas on the tip (Fig. 40.6).
The point of the insert tip is the most powerful sur-
In 1985, the ADA Council on Dental Materials, Instru-
face. The concave surface (inner surface) is the second
ments, and Equipment provided a list of the following
most powerful area, followed by the convex (back)
recommendations for the use of ultrasonic scalers:
surface. The least amount of energy is generated on
1. Use the lowest power setting possible, yet one that is the sides of the insert. By adapting the various sur-
still effective for removing calculus, cement, etc. faces of the insert (concave, convex, and lateral) to the
2. Use an adequate supply of water to avoid heat build- tooth, the clinician can regulate energy dispersion and
up at the tip of the instrument and tooth surfaces. control patient sensitivity.
FIGURE 40. 7 Strokes associated with ultrasonic scalers.
CLINICAL COMPARISONS
FIGURE 40.6 Power dispersion of a magnetostrictive insert tip:
(i) Point of tip, (ii) lateral surface, (iii) concave side, and (iv) convex
1. It has been concluded that improvements in clinical
back side. parameters like probing depth, bleeding on probing are
nearly equal for all types of mechanical instruments as
long as sufficient time is spent to thoroughly debride
the roots. However, powered scalers have some advan-
6. To avoid root damage, clinicians should use inserts tages over hand instrumentation.
on low power with light lateral pressure and tip an- 2. Effect of instrumentation on the integrity of the
gulation close to zero degrees. The point of the insert root surface - the curette produced the smoothest
should never be applied to the tooth at a 90° angle, roots, followed by the piezoelectric instruments,
which can result in gouging and root-surface damage. and the least smooth was with the magnetostrictive
7. Two basic motions are used when using an ultrasonic instrument.
device. First is a" gentle tapping" or" chipping" motion 3. Ultrasonics are beneficial when removing cement, over-
against deposits to break them up. The second motion hangs, heavy deposits, and stain, as well as debriding
is a "sweeping" motion to remove bacteria and de- areas.
toxify the areas being treated. This is accomplished by
continuous, back-and-forth, multidirectional overlap-
ping strokes (Fig. 40.7) covering every millimeter of the Plaque Removal
tooth. Debridement can then be performed by moving
Plaque removal is achieved by power-driven or hand
the insert in short, overlapping, horizontal, and vertical
instruments. The added advantage of the lavage effect
strokes along the root surface. Releasing the foot pedal
provides a constant flushing of the periodontal pocket
periodically allows for aspiration of water and debris.
during instrumentation, and gives an improved thera-
8. To ensure patient's comfort, keep the tip moving at
peutic effect. Cavitation and acoustic microstreaming
all times when in contact with the tooth.
improves the dislodgement of plaque slightly beyond the
9. Operator seating positions are typically the same as
reach of the instrument tip.
for hand instrumentation.
10. Direct vision is preferred when using an ultrasonic,
since indirect vision is compromised due to the mist
of the irrigant interfering with the mouth mirror.
Endotoxin and Cementum Removal
11. Ultrasonic tips do not last forever and should periodi- Present concept says that endotoxin is a superficial-
cally be evaluated for wear. As the tip of the insert ly associated surface substance that is easily removed.
wears, scaling efficiency decreases. A good rule of Complete cementum removal is not the goal of periodon-
thumb to follow is that one millimeter of tip wear tal therapy. Therefore, extensive root planing to remove
results in approximately 25% loss of efficiency. altered cementum of the past is not necessary to achieve
periodontal healing. Ultrasonics easily remove this endo- provides more surface area at the end of the tip, which
toxin without harming the root. makes it especially suited for cleaning furcations and
concavities.
Access to Furcations
Efficiency
Hand instruments are inadequate to remove at-
tached plaque and calculus from furcations. Ultrasonic 1. Time of instrumentation is less with ultrasonics.
instrumentation is superior in accessing deep, narrow 2. Hand fatigue is significantly reduced, because ultra-
defects and Class II and III furcations. Class II and sonic scalers are used with a light touch.
III furcations are narrower than the working end of a 3. Ultrasonic and sonic scalers have similar results as
curette, even minicurets. The advanced, thinner peri- hand instruments for removing plaque, calculus, and
odontal ultrasonic inserts are best suited to penetrate endotoxin.
deep pockets. Ultrasonics are clinically superior in the 4. Ultrasonics used at medium power produce less sur-
treatment of Class II and Class III furcations. New tip face damage than hand or sonic scalers.
designs that are 0.55 mm in diameter have become the 5. Due to instrument width, ultrasonic scaler tips are
choice instruments for these areas. This small sphere more effective in furcations.
KEY POINTS
• The term ultrasonics applied to sound refers to lengthening and shortening of the crystal over tiny dis-
anything above the frequency of audible sound and tances, resulting in physical vibrations.
is above 20,000 Hz. • Water contributes to three physiologic effects that en-
• It was first introduced for periodontal procedures in the hance the efficacy of power scalers:
1950s. 1. Acoustic streaming
• Sonics work at a frequency of about 3000-6000 cycles 2. Acoustic turbulence
per second (cps). 3. Cavitation
• Ultrasonics work at a frequency of 24,000-50,000 cps. • Antimicrobial rinse, such as chlorhexidine or povidone io-
• The magnetostrictive ultrasonic insert consists of a scaler dine, are used just before ultrasonic treatment to reduce
tip that is attached to a transducer that is made up of the number of airborne bacteria.
metal stacks or rods. • A light pen grasp and fulcrum ( either intra oral or extra-
• Piezoelectric scaler - Alternating current of high oral) are used even if there is heavy calculus removal.
frequency is applied to a piezoelectric crystal housed • All three types of ultrasonic scalers show similar results
in the handpiece, which causes corresponding clinically.
QUESTIONS 2. Khambay BS, Walmsley AD. Acoustic microstreaming; detection

and measurement around ultra sonic scalers. J Clin Periodontal
1999;70:626.
1. What are the differences between magnetostrictive and 3. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant
piezoelectric scalers? Dentistry. 5th ed. Copenhagen: Blackwell Munksgaard; 2008.
2. Describe the mechanism of action of ultrasonic scalers. 4. Newman MG, Takei H, Klokkevold PR, Carranza FA. Clinical Peri-
3. What are the advantages and disadvantages of ultra- odontology. 10th ed. Philadelphia: Saunders; 2006.
5. Rose LF, Mealey BL, Genco R. Periodontics: Medicine, Surgery and
sonic scaling?
Implants. 1st ed. Mosby; 2004.
4. What are the contraindications of ultrasonic scaling? 6. Trenter SC, Walmsley AD. Ultrasonic dental scaler associated haz-
ards. J Clin Periodontal 2003;30:90.
Suggested readings
1. Drisko C. American Academy of Periodontology report. Sonic and
ultrasonic scalers in periodontics. J Periodontal 2000;71:1792.
CHAPTER
41
Plaque Control
CHAPTER OVERVIEW
Plaque is the major etiology of periodontal diseases. for periodontal patients. This mainly consists of various
Plaque control is the regular removal of dental plaque and mechanical and chemical plaque control methods. Good
preventing its accumulation on teeth and adjacent gingival plaque control facilitates the return to health for patients
surfaces. Plaque control practices are particularly important with gingival and periodontal disease.
Dental disease is today the most common human FATE OF DENTAL PLAQUE
disease worldwide. Dental caries and periodontal
diseases are the two most common chronic diseases Once formed, dental plaque remains viable unless it is
of the oral cavity. The constant buildup of plaque on mechanically removed from the tooth surface. The plaque
and between teeth serves as a constant irritation to the remains viable due to the multiplication and growth of
gingiva. Experimental and epidemiological studies bacteria while dead bacteria form a loose, easily remov-
have demonstrated that dental caries and periodontal able whitish film on the surface of the plaque which is
diseases are dependent on the microorganisms present known as materia alba, this contains mostly dead bacteria
in plaque. and desquamated epithelial cells.
Dental caries are virtually ubiquitous; they begin Calcification of dental plaque due to deposition of cal-
soon after the teeth erupt and increase in prevalence cium salts leading to the hardening of plaque is known
with age. as dental calculus. On dental calculus plaque is again
Furthermore, periodontal diseases are the most prev- formed which may undergo calcification forming further
alent chronic diseases affecting children, adolescents, calculus. Thus calculus formation usually occurs in layers
adults, and the elderly. Approximately half of the adults and remains covered by dental plaque.
in the United States have gingivitis, the first stage of peri-
odontal disease, and 80% have some degree of gingival
inflammation that has led to the destruction of the bone TIME AND RATE OF PLAQUE
that supports the teeth (periodontitis), which if progresses FORMATION
can lead to tooth loss. In addition, recent research indi-
cates a high correlation between periodontal disease and Immediately after a tooth surface is cleaned, plaque
cardiovascular disease, heart attack, stroke, and low- formation begins and it takes about 4-9 days (average
birthweight babies. 7 days) for full maturation of plaque (Table 41.1).
Diet, age, salivary flow, oral hygiene, tooth alignment,
systemic disease, and host factors are the factors affecting
DEFINITION OF DENTAL PLAQUE the rate of plaque formation.
It is often difficult for the patient to ensure that
Dental plaque is defined as a highly specific, variable, plaque removal is complete because the patient cannot
structural entity formed by sequential colonization of easily determine (either visually or otherwise) whether
microorganisms on the tooth surface, epithelium, and all the plaque has been removed. Plaque is translucent
restorations. or tooth-colored and therefore not visible. This problem
TABLE 41.1 Differences Between Early (24 h) and Mature

Plaque (4-10 days)
Characteristic Early plaque Mature plaque

Gram reaction Positive Positive with some
negative
Morphotypes Cocci, Cocci, branching rods,

branching rods filaments, spirochetes
Energy metabolism Facultative Facultative, anaerobic
Tolerated by host Generally well Can cause caries and

gingivitis
Disclosing agent Stains pink Stains blue

(stains the glycoprotein
layer of plaque)
can be surmounted through the use of plaque disclosing FIGURE 41. 1 Disclosing agent.
agents.
Therefore such a procedure can demonstrate the pres-

DISCLOSING AGENTS ence of deposits and the areas that need special attention
during personal oral care.
Disclosing agents (Fig. 41.1) are applied to the teeth
and help in the detection of dental plaque, and it can be
Utility of Disclosing Agent
shown easily as they color the dental plaque. This method
is very useful as the location of areas of dental plaque can 1. Personalized patient instruction and motivation
be detected and it can then be removed from teeth by a 2. Self-evaluation by the patient
dentist or an individual at home (Table 41.2). 3. Evaluation of the effectiveness of oral hygiene
A disclosing agent is prepared in liquid, tablet, or loz- maintenance
enge form, which contains a dye or other coloring agent. 4. Preparation of plaque indices
A disclosing agent is used for the identification of bacte- 5. Research studies with regard to effectiveness of plaque
rial plaque, which might otherwise be invisible to the control devices like toothbrushes and dentifrices.
naked eye.
When applied to the teeth, the agent imparts its color
Properties of an Acceptable Disclosing Agent
to soft deposits but can be rinsed easily from clean
tooth surfaces. After staining the deposits that can be l. Intensity of color: A distinct staining of deposits should
distinctly seen provide a valuable visual aid in patient be evident. The color should contrast with normal col-
instruction. ors of the oral cavity.
TABLE 41.2 Clinical and Microscopic Features of Mature and Immature Plaque Stained by Disclosing Agents
Immature/early plaque Mature/older plaque

Disclosing agent stains it pink Disclosing agent stains it blue
Extreme thinness, to the extent that sometimes it is hard to obtain Considerably greater thickness than pink plaque
sufficient material for examination
No evidence of any orderly architecture High degree of architectural organization. Cocci, rods, and/or
filaments arranged in parallel rows forming fan-shaped patterns
Low density of organisms Filaments intertwined forming a meshwork
No motility Motility present in some blue plaques

No filaments, spiral organisms, or vibrios; on some teeth treated with Spiral organisms and vibrios
the dye an intermediate zone could be distinguished between the red
and blue areas with definite purple color. This intermediate area
appears to look more like blue plaque than red plaque but the thickness
of this plaque was less than that of blue plaque
CH A PTER 41 PLA Q U E CO N T RO L 355
2. Duration of intensity: The color should not rinse off
with ordinary rinsing methods, or be removable by
the saliva for the period of time required to complete
the instruction or clinical service. It is desirable for the
color to be removed from the gingival tissue and lips
by the completion of the appointment, as the patient
might react to the color retained for a long period of
time.
3. Taste: An unpleasant taste often discourages the use of
the disclosing agent. An unflavored or highly flavored
substance is often not accepted by the patient. The
main reason for using the disclosant is to motivate the
patient. Therefore, the agent should be pleasant and
encourage the patient to use it on a regular basis.
4. Irritation to the mucous membrane: The patient should
be questioned concerning the possibility of an idio-
syncrasy to an ingredient. When this information is FIGURE 41.2 Application of disclosing agent.
obtained, it should be entered on the patient's per-
manent history record. Because of the possibility of
allergy, more than one type of disclosing agent should
be available for use. b. FD&CredNo.3
5. Diffusibility: A solution should be thin enough so that It mainly stains mature plaque blue and immature
it can be applied readily to the exposed surface of the plaque red/pink.
teeth, yet thick enough to impart an intensive color to 9. Basic fuchsin
bacterial plaque.
6. Astringent and antiseptic properties: These properties
may be highly desirable in that the disclosing agent Application of Disclosing Agents
may contribute to other factors. It is frequently rec- The disclosing solution is directly applied onto the
ommended that an antiseptic be applied prior to scal- tooth surface using cotton pellets or may be rinsed after
ing, and if an antiseptic disclosing agent is used, one proper dilution (Fig. 41.2). In addition to painting on the
solution serves a dual purpose. A disclosant may teeth, the novel dye can be formulated as a chewable
inhibit the growth of microorganisms. In quantitative tablet, wafer, powder, lozenges, aerosol, liquid concen-
plaque research studies, therefore, it would be nec- trate, etc. The tablets and wafers may be chewed, swished
essary to use disclosing agents lacking antibacterial around the mouth for 30-60 s, and rinsed. Disclosing
properties. agents form an important aspect of plaque control by
staining plaque and aiding the patient in developing an
efficient system of plaque removal.
Agents Used for Disclosing Plaque
1. Iodine preparations
a. Skinner iodine solution
Recent Advancement
b. Diluted tincture of iodine. 1. A toothbrush dispensing plaque disclosing agent con-
2. Mercurochrome preparations sists of:
a. Mercurochrome solution 5% a. A handle designed with a head portion and a grasp-
b. Flavored mercurochrome disclosing solutions. ing portion, an upper surface and a lower surface,
3. Bismarck brown (Easlick disclosing solution) and a hollow interior comprising a reservoir that is
4. Merbromin being designed and constructed to contain dental
5. Erythrosine plaque disclosing agent.
a. FD & C No. 3/No. 28 b. A number of bristles placed on and attached to the
6. Fast green upper surface of head portion of the handle.
a. FD & C green No. 3 c. A conduit in communication with reservoir that ex-
7. Fluorescein tends into head portion. This conduit is connected to
a. FD & C yellow No. 8 (used with special ultraviolet and terminates in an outlet aperture in head portion.
source to make the agent visible) (Plak-Lite) d. A dispensing mechanism operationally connected
8. Two tone solutions to conduit and adapted to control flow through
a. FD & C green No. 3 conduit.
e. A quantity of a dental plaque disclosing agent Objectives of Plaque Control

in a nondentifrice solution contained within
1. The objective of oral hygiene is to reduce the num-
reservoir.
2. The toothbrush contains dental plaque disclosing agent ber of microorganisms on the teeth. All accessible den-
comprising a dye-containing erythrosine or a mixture tal plaque and debris should be removed from the
of sulphan blue and tartrazine yellow. gingival margins, proximal tooth surfaces, and possible
3. The handle is partially transparent. gingival sulci. This reduces factors of inflammation and
4. Dispensing mechanism is a peristaltic pump. irritation.
2. One of the causes of halitosis may be removed.
5. The outlet aperture is located on the lower surface of
3. Gingival stimulation (massage) may play a role in in-
head portion of the handle.
6. The toothbrush with dental plaque disclosing agent is creasing gingival tone, surface keratinization, gingival
in a concentration such that effective plaque disclosure vascularity, and gingival circulation.
is achieved by delivery of approximately one drop of
said solution. Plaque Control
7. The toothbrush where a concentration of solution and
a quantity of solution contained within reservoir are Plaque control is defined as the removal of dental plaque
chosen such that solution includes at least about 100 and prevention of its accumulation on the teeth and adjacent
times a quantity of dental plaque disclosing agent re- gingival tissues. This can be achieved by:
quired for effective plaque disclosure. 1. Mechanical plaque control
2. Chemical plaque control.
PLAQUE CONTROL - INSTRUCTION

PROCEDURES
TOOTHBRUSHES
Plaque control refers to procedures that are intended to
remove bacterial plaque from the teeth (Table 41.3). This
may be accomplished via professional plaque removal,
Introduction
patient-performed oral hygiene, or chemical plaque con- Toothbrush is described as "the most classic and prin-
trol. Plaque control is the most effective means of prevent- cipal method employed in oral hygiene."
ing accumulation of microbial dental deposits, thereby According to ADA's Council on Dental Therapeutics
interfering with the initiation, development, or progres- "It is designed primarily to promote cleanliness of teeth
sion of periodontal disease (Lisgarten). and oral cavity."
TABLE 41.3 Mechanical Plaque Control Aids
Aids for gingival Aids for edentulous or partially

Toothbrushes Interdental aids stimulation Others edentulous patients
Manual toothbrush Dental floss Rubber tip stimulator Gauze strips Denture and partially clasp brushes
Electrical toothbrush Triangular toothpicks Balsa wood edge Pipe cleansers Cleansing solutions
Handheld triangular Water irrigation device
toothpicks
Proxapic
Interdental brushes
Proxa brush
Bottle brushes
Single tufted
brushes(flat/ tapered)
Yarn
Superfloss
Perio-aid
Dentifrice dispensing toothbrush with replaceable cartridge: The present invention rests on the fact that a toothbrush pumps dentifrice
material from a replaceable cartridge to the brush head. Also, this invention provides means that increases the pumping efficiency and
have a cover having plug with sliding mechanism for sealing the opening in the brush head and pumping means during periods of
nonuse. One type of brush dispenses the dentifrice material at the base of the brush head where the bristles are attached. Another type
dispenses dentifrice material directly onto the top of the brush surface. Most brushes store dentifrice material directly in a reservoir in
the brush handle.
History TABLE 41.4 Types of Bristles
Since ancient times, people have made devices for Natural bristles Synthetic bristles
cleaning their teeth. Chewing sticks were most likely Obtained from hair of hog or wild Bristles are made from
the first toothbrushes made by Babylonians as early as boar nylon
3500 BC. These chew sticks, also called siwaks, were Bristles are tubular in form Bristles are uniform in size
small twigs that were frayed by chewing on the ends
More susceptible to fraying, Do not easily lose their
and rubbing the frayed ends against the teeth. Bristle breaking, and loss of elasticity elasticity
toothbrushes (made from coarse, stiff hog's hair at-
Prone to fracture Resistant to fracture
tached to handles made of bone or bamboo) appeared
in China around 1498. These toothbrushes were exported More susceptible to contamination Do not get contaminated
to Europe, where people found the boar bristles to be too with microbial debris
stiff (causing their gums to bleed); they substituted horse
hair for the boar's hair.
The first mass production of toothbrushes appeared in Toothbrush bristles (Table 41.4)
England around 1780, which were made by William Ad-
dis of Clerkenwald, England. The first American to patent 1. Hard and soft
a toothbrush was HN Wadworth in 1857; mass production 2. Natural and synthetic
of toothbrushes in the United States began after the Civil 3. Multitufted and space tufted.
War, around 1885. Wallace H Carothere invented nylon in
1937; in 1938 nylon bristle toothbrushes were produced
Factors Affecting Stiffness of Bristles
and marketed.
Toothbrush remains the most effective and widely used • Diameter of bristles: Bristles wider in diameter are stiffer
device to remove dental plaque biofilm. as compared to bristles with a lesser diameter. They can
vary in size from 0.0035 to 0.0190 in.
• Length of the bristles: Stiffness of the bristle is inversely
Types of Toothbrushes proportional to its length. Shorter bristles are stiffer as
compared to longer bristles.
1. Manual toothbrushes
• Number offilaments in a tuft: Each filament gives support
2. Powered toothbrushes
to adjacent filaments and each tuft gives support to
3. Sonic and ultrasonic toothbrushes
adjacent tufts.
4. Ionic toothbrushes.
• Curvature of the filament: Curved filament may be more
flexible and less stiff than straight filaments of equal
length and diameter.
Ideal Characteristics for a Toothbrush
Multitufted brushes show better cleaning ability.
1. It should fulfill individual patient requirement in
Rounded ends produce fewer lacerations.
size, shape, and texture.
Nylon filaments are superior in terms of:
2. It should be easily and effectively manipulated.
3. It should be readily cleaned and aerated, impervious • Homogeneity
to moisture. • Uniformity of bristle size
4. It should be durable and inexpensive. • Elasticity; resistance to fracture
5. It should be designed for utility, efficiency, and • Repulsion of water and debris.
cleanliness.
ADA Specification of a Toothbrush
Manual Toothbrushes
PARTS OF A TOOTHBRUSH Brushing surface:
1. Handle: The part grasped in the hand during tooth 1. 1-1.25 in. in length
brushing. 2. 5/16-3/8 in. in width
2. Head: The working end of a toothbrush that holds the 3. 2-4 rows of bristles
bristles or filaments. 4. 5-12 tufts/row.
3. Tufts: Clusters of bristles or filaments secured into a
head.
Toothbrush Modifications
4. Brushing plane: The surface formed by the free ends of
the bristles or filaments. 1. Long and contoured handles: better grip
5. Shank: The section that connects head and handle. 2. Double angulation of the handle and neck.
of bristles rotates 1.5 revolutions in one direction and

reverses 1.5 revolutions in the opposite direction at a
rate of 4200 rpm.
Rotary Toothbrushes
A rotary toothbrush resembles a dental professional
rotary instrument and is uniquely different from tradi-
tional powered toothbrush. Additional instructions may
be required for the patient to become adept at using this
device effectively. This powered brush has three inter-
FIGURE 41.3 Powered toothbrushes. changeable tips that include a single tuft of bristles, a
hollow-cup brush, and an elongated brush tip that rotates.
Sonic and Ultrasonic Toothbrushes

Toothbrush Head Modification
The mechanism of action of these types of toothbrushes
1. Concave surface is that it produces high-frequency vibrations (1.6 Hz),
2. Deep grooved design which in turn leads to the phenomenon of cavitation and
3. Conventional flat multitufted acoustic microstreaming. This phenomenon is an effective
4. Special indicator bands. way for the disruption of the bacterial cell wall (bacteri-
cidal) and also aids in stain removal.
Powered Toothbrushes
They were introduced in the 1960s.They are also Ionic Toothbrushes
known as automatic, mechanical, or electric toothbrush-
es. The heads of these toothbrushes show two types of Ionic toothbrushes assist in plaque removal by chang-
motion, either it oscillates in a side-to-side motion or ing the surface charge of a tooth by an influx of posi-
it has a rotary motion. In an ordinary powered tooth- tively charged ions as a result of which the plaque with
brush the frequency of oscillations may be around 40 Hz a similar charge is repelled from the tooth surface and
(Fig. 41.3). will be attracted by the negatively charged bristles of the
toothbrush.
INDICATIONS However, further studies have to be carried out to
prove the efficacy of these type of toothbrushes.
• Young children
• Handicapped patients
• Individuals lacking manual dexterity
Objectives of Toothbrushing
• Patients with prosthodontic or endosseous implants
• Orthodontic patients • To clean teeth surfaces and interdental spaces of food
• Institutionalized patients including the elderly who are remnants, debris, stain, etc.
dependent on care providers • To prevent formation of plaque.
• Patients on supportive periodontal therapy. • To disrupt and remove plaque.
• To stimulate and massage gingival tissue.
ADVANTAGES • To clean the tongue.
1. By increased patient motivation a better patient
compliance can be achieved. Toothbrushing Techniques
2. Increased accessibility to the interproximal and lingual
tooth surfaces. Depending on the individual cases, the techniques
3. No specific technique of brushing is required. of toothbrushing may have to be altered to achieve the
4. Less brushing force than manual toothbrushes. maximum beneficial effect (Tables 41.5-41.11).
5. By incorporating brushing timer, it has helped the Classification of toothbrushing techniques according
patient in brushing for the required duration. to Greene (1966):
• Roll technique: modified Stillman/ rolling stroke
COUNTER ROTATIONAL POWERED TOOTHBRUSHES
• Vibratory technique: Stillman, Charter, and Bass method
The head of the counter rotational toothbrush is • Circular technique: Pone method
similar in shape to a manual toothbrush with 10 tufts • Vertical technique: Leonard method
of rotating bristles that are 0.0005 diameter. Each tuft • Physiological technique: Smith method (Figs 41.4-41.10)
TABLE 41.5 Bass Method or Sulcus Cleaning Method (1948)
Indications Advantages Disadvantages

1. For all patients for dental plaque removal 1. Effective method for removing plaque 1. Overzealous brushing may convert the very
adjacent to and directly beneath the adjacent to and directly beneath the short strokes into a scrub brush technique
gingival margins gingival margin, cervical areas, and sulcus and cause injury to the gingival margin
2. Adaptable for open interproximal areas, 2. Provides good gingival stimulation 2. Time consuming
cervical areas beneath the height of contour
of the enamel, and exposed root surfaces
3. Recommended for routine patients with 3. Easy to learn 3. Dexterity requirement is too high in
or without periodontal involvement certain patients
4. Recommended for routine patient with or

without periodontal involvement
Technique: The bristles are placed at an angle to the gingiva and moved in small circular motions. With three teeth at a time, strokes are
repeated around 20 times. On the lingual side of anterior teeth the brush is inserted vertically and the heel of the brush is used to reach the
gingival sulci and proximal surfaces at a 45° angle. The bristles are then activated. By pressing the bristles firmly against the pits and
fissures and then activating the bristles, occlusal surfaces are cleaned.
TABLE 41.6 Modified Bass Technique
Indications Advantages Disadvantages

1. As a routine oral hygiene measure 1. Excellent sulcus cleaning 1. Moderate dexterity of wrist is required
2. Intrasulcular cleansing 2. Good interproximal and gingival cleaning

3. Good gingival stimulation
Technique: This technique is a combination of the vibratory and circular movements of the Bass technique and the sweeping motion of the roll
technique. The toothbrush bristles are at 45° to the gingiva and the bristles are then gently vibrated by moving the brush handle in back and
forth motion. With a single motion the bristles are swept over the sides of teeth toward their occlusal surfaces (Figs 41.4-41.7).
Charter Method (1928) Physiological Method - Smith Method (1940)

This was described by Smith and advocated later by
Vertical Method - Leonard Method (1939)
Bell.
Leonard advocated a vertical stroke in which max- Principle: Toothbrush should follow the physiological
illary and mandibular teeth are brushed separately pathway that food does when it traverse over the tissues
(Table 41.12). in a natural masticatory act (Table 41.13).
FIGURE 41.4 Modified Bass method - Palatal aspect of upper FIGURE 41.5 Modified Bass method - occlusal surface.
anteriors.
TABLE 41.7 Modified Stillman Technique (1932) TABLE 41.10 Roll Technique
Indications Disadvantages Indications Disadvantages

1. Removal of dental plaque from 1. Time consuming 1. Children and adult patients with 1. Brushing too high during
cervical areas below the height of limited dexterity initial placement can
2. Improper brushing
contour of the enamel and from lacerate the alveolar
can damage 2. Patients requiring gingival
exposed proximal surfaces mucosa
the epithelial massage and stimulation
2. For cleaning tooth surfaces and attachment 2. Tendency to use quick,
3. Cleaning gingiva and removal of
massaging the gingiva sweeping strokes
plaque, materia alba, and food
resulting in no brushing
3. For cleaning areas demonstrating debris from the teeth without
for the cervical third of
progressing gingival recession emphasis on gingival sulcus
the tooth, since the brush
and root exposure so as to prevent
4. For general cleaning in tips pass over rather than
abrasive tissue destruction
conjunction with the use of into the area and likewise
Technique: The bristles are positioned partly on the cervical aspects vibratory technique (Charter, for the interproximal
of teeth and partly on the adjacent gingiva with bristles pointing Stillman, or Bass)
3. Replacing the brush with
apically with an oblique angle to the long axis of the tooth. By short filament tips directed
5. Useful for preparatory
back and forth motions the bristles are activated and simultaneously
instruction for modified Stillman into the gingiva may
moved in a coronal direction following 20 strokes; on adjacent teeth
technique, since the initial brush produce punctuate
the same procedure is repeated systematically with a soft toothbrush lesions
placement is the same
(Figs. 41.8 and 41.9).
Technique: This method of brushing is also known as the rolling
stroke method or ADA method or the sweep method. It works
fairly well for patients with anatomically normal gingival
tissues.
In this method, the bristles are placed at a 45° angle and lightly
TABLE 41.8 Charter Method rolled across the tooth surface toward the occlusal surfaces. This
technique requires some flexibility around the wrist.
Indications Disadvantages
1. Individuals having open 1. Brush ends do not engage
interdental spaces with missing the gingival sulcus to
papilla and exposed root remove subgingival
surfaces bacterial accumulations
TABLE41.11 Fones Method or Circular Scrub Method (1934)
2. Those wearing FPO or 2. The correct placement of
orthodontic appliances brush becomes limited Indications Advantages Disadvantages
or impossible in some
3. For patients who have had peri- Young 1. As compared to Bass 1. Trauma to
areas of mouth where
odontal surgery children who technique, this tech- gingiva is
modifications become
do not have nique has equal or better possible
4. Patients with moderate degree necessary, this in turn
the muscle potential in terms of
of gingival recession particularly adds to the complexity of 2. Interdental
development plaque removal and
in interproximal areas the procedure areas are
for such prevention of gingivitis
not cleaned
5. Massage and stimulation 3. Requirements in digital techniques
2. Technically simple so it properly
for marginal and interdental dexterity are high but insists on
is easy to learn
gingiva brushing 3. For adults
on their 3. Takes less time especially
Technique: For this technique a soft/medium multitufted own, which who have
toothbrush is indicated and the bristles are placed at an angle of requires more 4. Simpler technique for
the tendency
45° to the gingiva with the bristles directed coronally. With the coordinations physically/ emotionally
of brushing
bristle ends laying interproximally, these bristles are activated by handicapped individuals
vigorously, this
mild vibratory strokes (Fig. 41.10). technique can
5. Patients lacking dexterity
for a more technical be detrimental.
brushing method
6. Improves gingival health
if provided with good
TABLE 41.9 Scrub Brush Method stimulation
Advantage Disadvantages Technique: The child is asked to stretch his/her arms such that
they are parallel to the floor and is then asked to make big
It is the virtual free- 1. Ineffective at plaque removal circles using the whole arm to draw circles in the air. The circles
style of brushing, and are reduced in diameter until very small circles are made in
2. Tooth abrasion and gingival recession
it requires vigorous front of the mouth. With this now, the child is ready to make
horizontal, vertical, 3. Detrimental to general oral health circles on the teeth with the toothbrush, making sure that the
and circular motions. teeth and gums are covered.
FIGURE 41.6 Modified Bass method. FIGURE 41.9 Modified Stillman method.
FIGURE 41. 7 Modified Bass method - vibratory strokes. FIGURE 41. 10 Charter method.
TABLE 41.12 Leonard Method
Advantages Disadvantages
• Most convenient and effec- • Interdental spaces of the per-
tive for small children with manent teeth of the adults
deciduous teeth are not properly cleaned
Technique: With the clenched anterior and posterior teeth the

bristles of the toothbrush are placed at 90° angle to the facial sur-
face. When the teeth are in edge to edge relation, place the brush
with the filaments against the teeth at right angles to the long axis
of the teeth. Brush vigorously, without great pressure with a stroke
that is mostly up and down on the tooth surfaces with just a slight
rotation or circular movement after striking the gingival margin
with force. Enough pressure is used. It is not intended that the up-
per and lower teeth shall be brushed in the same series of strokes.
FIGURE 41.8 Placement of toothbrush in modified Stillman's tech- Teeth are placed edge to edge to keep the brush from slipping over
nique. the incisal and occlusal surfaces.
TABLE 41.13 Smith Method

4. Use of long brisk strokes with excessive pressure over a long
Advantages Disadvantages period of time
1. Natural self-cleansing 1. Interdental spaces and 5. Habitual prolonged brushing in one area
mechanism sulcus areas of teeth are
not properly cleaned 6. Excessive pressure applied with worn-out nonresilient brush
2. Supragingival cleaning is good
Suggested corrective measures
Technique: A soft brush with small tufts of fine bristles arranged
in four parallel rows and trimmed to an even length was used in 1. Use of softer toothbrush
a brushing stroke. Bristles are pointed incisally or occlusally and 2. Demonstration of proper brushing technique
then along and over the tooth surfaces and gingiva. The motion
is gentle sweeping from incisal or occlusal surfaces over to facial
surfaces and progressing toward and over the gingiva. It is almost
Abrasion of the teeth
an attempt to duplicate nature's self-cleansing and gingival
stimulation mechanism during mastication of food. It is the loss of tooth substance produced by mechanical wear
other than by mastication or
Defined as the pathologic wearing away of tooth substance
Effects of Improper Toothbrushing through some abnormal mechanical process
Toothbrush trauma: Gingival alterations. Contributing factors

Acute alterations (lacerations) Precipitating factors 1. Hard toothbrush
Scuffled epithelial surface Horizontal or vertical scrubbing 2. Horizontal brushing
with denuded underlying toothbrushing method with 3. Excessive pressure during brushing
connective tissue pressure (either manual/ 4. Abrasive agent in the dentifrice
powered) 5. Prominence of the tooth surface labially or buccally
Punctuate lesions that appear Overvigorous placement and

as red pinpoint spots application of toothbrush
Location of abraded areas
Diffuse redness and denuded Penetration of gingiva by
attached gingiva filament ends 1. Facial surface of canines, premolars, and sometimes first molars
or any tooth in bucco- or labia-version, those most available to
Use of toothbrush with frayed, pressure of the toothbrush (canines are most susceptible because
broken bristles or filaments of their prominence on the curvature of the dental arches)
2. Most abraded areas are on the cervical areas of exposed root
Application of filaments beyond
surfaces, but occasionally may occur on enamel
attached gingiva
Appearance
Saucer-shaped or wedge-shaped indentations with smooth shiny
Chronic alterations surfaces
1. Usually appear on the facial gingiva because of the vigor with
which the toothbrush is used Corrective measures
1. Explain the problem to the patient to assure full cooperation
2. Areas most commonly involved are around canines or teeth in
2. Advise a specific brush with soft textured bristles or filaments
labio-/bucco-version
3. Change the toothbrushing technique
3. It is inversely proportional to the right- or left-handedness of 4. Recommend a less abrasive dentifrice
the patient 5. Use a smaller amount of dentifrice
Recession Changes in gingival contour

1. Appearance: Margin of Rolled, bulbous, hard, firm
the gingiva has receded marginal gingiva in piled-up or Toothbrush Replacement and Care
toward the apex and the festoon shape
cementum is exposed For a toothbrush to remain effective, it must be re-
placed periodically.
2. Predisposing anatomic Gingival cleft
factors
Toothbrushes have an average life span of 3-6 months.
a. Malposition of teeth However, they should be replaced as soon as there is any
b. Narrow band of evidence of fraying, as frayed toothbrushes do not clean
attached gingiva cannot teeth efficiently and may cause wearing of teeth or gin-
withstand pressures of
gival recession. Other reasons include illness, continuous
brushing
exposure to water or other foreign substances, and dam-
Precipitating factors age to the handle.
3. Repeated use of vigorous rotary, vertical, or horizontal Most investigators have observed that the toothbrush
toothbrushing techniques over a long period of time may act as a vehicle in breeding and transmitting various
organisms in the oral cavity. Experts thus advise cleaning CLASSIFICATION OF GINGIVAL
the toothbrush daily in antiseptic mouthwashes such as EMBRASURES
phenolic derivatives.
Storing toothbrush in a dry area is a necessity, as moist CLASS I (Fig. 41.11) No gingival recession with interdental
surfaces may allow bacterial proliferation. papilla filling the space
Toothbrushes should be kept in open air with the head
CLASS II (Fig. 41.12) Moderate papillary recession
in an upright position.
Toothbrushes should not be kept in contact with other CLASS III (Fig. 41.13) Complete loss of the interdental papilla
toothbrushes because proximity is a rich source of bacterial
cross-contamination.
Interdental aids for embrasure types
Interdental cleaning aids Class I Class II Class III

Interdental aid embrasure embrasure embrasure
lnterdental brushes are appropriate for Class II and Class III
embrasures and furcation, for tooth surfaces adjacent to missing Dental floss v
teeth and for orthodontic appliances. In conjunction with
toothbrushing, interdental brushes have been found to be more
Dental tape v
effective in the removal of plaque biofilm from proximal tooth Power flosser v
surfaces.
Textured floss
Toothbrush is an excellent device for plaque removal on surfaces
that are accessible. However, it is not adequate for interproximal Floss holder v
cleaning. Interdental aids are adjunctive devices, which are
used to remove plaque from the interproximal tooth surfaces.
Floss threader v
lnterdental brushes are also a vehicle for chemotherapeutic Interdental brush v v
delivery interproximally.
End-tufted brush v
Instructions for use Toothpicks v v
• After loading the appropriate-size brush in the reusable handle, Wood or plastic v v
insert the tip of the brush gently into the interproximal space sticks
similar to the placement of a toothpick.
• With a gentle motion, slightly wiggle or ease the brush into the
interproximal embrasure space as far as possible. If the brush is
bending, then most likely too much pressure is being applied.
Lighten up on the grasp, decrease the pushing force, and gently
wiggle the brush into the interproximal space for maximal
efficiency.
• Gently remove the brush from the embrasure space and move to
the next contact area.
• The brush also needs to be reinserted from the opposing facial
and lingual surfaces for most effective interdental cleaning.
Using the interdental brush between anterior teeth with intact
interdental papilla is not recommended.
Some reports describe the papilla being flattened by repeated use,

causing some esthetic concern in this area.
Recommendations for self-care interdental cleaning aids should

be based on the following:
1. Type of gingival embrasure
2. Alignment of teeth Insertion of a dental floss into type I gingival embrasure
3. Fixed prosthesis/ orthodontic appliances

4. Open furcation areas
5. Contact areas
6. Desired clinical outcomes

Type I gingival embrasure
7. Dexterity of the patient
8. Patient preference
FIGURE 41.11 Class I gingival embrasure.
lnterdental brush indicated for type II gingival embrasure
FIGURE 41.14 Dental floss.
The development of dental floss is attributed to Levi

Spear Parmly, a New Orleans dentist (Fig. 41.14). He rec-
Type II gingival embrasure
ommended that the waxed silken thread be passed be-
tween the teeth "to dislodge that irritating matter which
no brush can remove and which is the real source of dis-
FIGURE 41.12 Class II gingival embrasure. tress." Later, Dr Charles Bass, a physician, developed
nylon floss as a replacement for silk.
Today in addition to nylon, floss may be made out of
Goretex type of material called polytetrafluoroethylene
(PTFE).
Interdental cleaning aids to remove plaque from in-
terproximal surfaces in Type I gingival embrasures. Floss
may be waxed/unwaxed and flavoring often is added
to improve patient compliance. Floss may be enhanced
with fluoride in addition to other therapeutic or cosmetic
agents. However, the efficacy of additives has not been
evaluated in clinical trials.
Dental tape: A flattened and wider form of dental floss is
recommended for cleaning Class I and Class II embrasures.
Power Jlossers: The introduction of power flossers has
provided an alternative to manual floss. Evidence indi-
cates that these devices can remove biofilm and reduce
gingivitis and bleeding similar to manual floss. Tip or
Unitufted brush indicated for Type Ill gingival embrasure
filament shape, speed, and mechanism of action vary
between brands and can affect clinical outcomes.
Texturedfloss: Tufted or textured floss is a type of floss that
offers additional features (compared with traditional floss
varieties) for cleaning proximal surfaces and subgingival
areas. Some manufacturers have added a spongy or textured
surface to floss to assist in proximal cleaning for Class II and
Class III embrasures, around fixed orthodontic appliances,
under panties, and around abutments of crown and implants.
Textured dental floss is usually dispensed as a single strand
Type Ill gingival embrasure and may have additional features such as a stiff nylon end
for threading and regular floss for Class I embrasures.
Floss holder: It is designed to assist in traditional man-
FIGURE 41.13 Class III gingival embrasure. ual flossing methods. They range from small plastic
disposable units with floss attached to handles that have Unwaxed dental floss is better than Bonded and nonbonded
spools of floss contained in the handle. Other floss hold- waxed because of the following dental floss:
reasons:
ers are sold as a handle without floss; floss can be pulled
into place for the proximal surface with the floss holder. 1. It is small in diameter and Bonding prevents the
Floss threader: It is a device that allows floss to be pulled passes more easily through tight fibers from spreading
interproximal contacts. apart when used on a
through the interdental space (buccal or lingual) under
tooth surface.
the contact point for Class I embrasure. Floss threaders re- 2. Under tension it flattens out
semble a sewing needle with a loop for the floss and have on the tooth surface with each The fibers may or may not
component thread adding have a waxed coating.
sufficient flexibility and strength to be easily threaded
separately as a cutting edge to
under the contact point. The dental floss is then used to dislodge debris.
Waxed dental floss is often
clean each proximal surface. used for flossing between
3. Unwaxed floss makes a squeaking teeth with tight contacts
noise when used on a clean tooth or rough margins of
surface, and this noise can be restorations.
Available in various forms
used to monitor performance.
1. Multifilament-twisted/nontwisted
2.Bonded/nonbonded
Methods of using dental floss
3. Thick/ thin Spool method Circle/loop method
4. Waxed/nonwaxed Used by adults and teenagers Indicated for physically and
with mental maturity mentally challenged patients
Disadvantages
About 45 cm/18 in.-long floss From about 45 cm/18 in.-long
1. Time consuming
is taken and from each of the piece, a loop or circle of the
2. Difficult from technical aspect ends about 10 cm/ 4 in. is wound floss is made and both ends
around the middle finger of the are tied securely with three
3. Risk of tissue damage each hand. knots.
4. Furcation The last three fingers of both the The floss is held by both the
hands are folded and closed and hands having about 2.5 cm/1
both the hands are moved apart. in. floss between fingers of
both the hands and all the
Functions of dental floss With this about 5 cm/2 in.-long
fingers except the thumbs
floss is held between the index
1. Removal of adherent plaque and food debris from the inter- of both the hands are placed
fingers of both the hands.
proximal embrasure and under the pantie of FPO within the loop.
2. Polishing of the tooth surface during removal of the plaque and

debris
Wooden tips
3. Stimulating and massaging the interdental papillae
• Toothpicks have been used for centuries and were a part of early
4. Helping in locating the following: toiletry kits dating back to 3000 BC.
• Subgingival calculus deposits • They are an ideal substitute for the dental floss in Type II
• Overhanging margins of the restorations gingival embrasures.
• Proximal carious lesions • These are manufactured from orange wood and are triangular
in cross-section.
5. Improves oral hygiene • They are inserted into the gingival embrasures with the base of
6. Reduces gingival bleeding the triangle oriented toward the gingiva.
• The wooden tip then may be repeatedly moved in and out of
7. Vehicle for application of polishing or therapeutic agents to the embrasures, thereby removing soft deposits from the teeth
interproximal and subgingival area and also mechanically stimulating the gingiva.
For this purpose tapes are better than floss. Before the advent of • Their use is, however, restricted to the facial aspects of the ante-
nylon, dental tapes and floss were made of silk rior teeth.
• However, specific handles have been designed, attached to
which the wooden tips may be used throughout the oral cavity.
Specialized flosses: They have thin stiff sections and soft, puff
lnterproximal or interdental brushes
sections all within 1 % length.
• Proven to be the best choice for plaque removal from interproxi-
Thin flosses are preferred by those who have tight contacting teeth
mal tooth surfaces in case of Type II gingival embrasures.
without sharp edges from poor fillings.
• Design: Similar to a bottle brush.
Wider ribbonlike flosses provide greater surface contact with the • They can be mounted onto specifically designed handles, to make
enamel surface to help remove plaque. The waxed flosses are its use in the posterior areas of the mouth more comfortable.
generally easier to hold and slide readily between tight contacts • They may also be used to clean furcation areas and root
even when they appear to be of heavier weight. concavities.
Powered interdental brushes

• Efficient as any other interdental aid in achieving plaque re-
moval and reducing inflammation.
• It requires less dexterity and makes access to gingival areas
easier.
Unitufted/single tufted brushes

• These types of interdental aids are used in Type III gingival
embrasures. FIGURE 41.15 Interdental brush.
• They may also be used to carry antimicrobial agents (chlorhexi-
dine) into the interproximal areas.
Technique
Irrigation devices (Water Pik): Irrigation devices have Brushing: Place the side of the brush on the dorsum
been proven to be a valuable supplement for mechanical of the tongue with the tip directed toward the throat.
plaque control measures. It is mainly beneficial in the re- Apply light pressure and move the brush forward and
moval of unattached plaque and debris. Irrigation devices out; repeat to cover the entire surface.
are mainly composed of a built-in pump and a reservoir. A dentifrice may be used to improve cleansing if it does
These devices may also be used to deliver antimicrobial not prove unpleasant to the patient.
agents, e.g., chlorhexidine (CHX), subgingivally. When Tongue cleaning devices: Plastic tongue scrapers are also
used as an adjunct to toothbrushing, these devices have available. They are available in various designs. They may
beneficial effect on periodontal health by retarding plaque be flexible or rigid. Device is placed toward the back of
and calculus formation. However, transient bacteremia the tongue on the dorsal surface, and then pulled forward
has been reported following the use of subgingival irriga- with a light pressure.
tion devices, especially in the presence of inflammation They can be recommended for patients when they have
(Fig. 41.15). elongated papillae, deep fissures, or surface coating.
GINGIVAL PHYSIOTHERAPY CHEMICAL PLAQUE CONTROL
Rationale: Mechanical stimulation of gingiva either by Ideal requisites of an antiplaque agent:

toothbrushing or interdental cleansing with various aids 1. Should significantly reduce plaque and gingivitis.
or simple finger massage. This leads to: 2. Should prevent growth of pathogenic bacteria.
1. Increased keratinization 3. Should prevent development of resistant bacteria.
2. Increased blood flow 4. Should be compatible with the oral tissues.
3. Increased flow of GCF within the gingival sulcus. 5. Should not stain teeth/ alter taste.
6. Should exhibit good retentive properties
This resulted in an overall improvement in the gin- (substantivity).
gival health due to modulation of gingival-host defense 7. Should be inexpensive and easy to use.
mechanism.
MOUTHRINSES
TONGUE SCRAPING
Of the various oral hygiene products available, mouth-
Tongue scraping is defined as the process by which rinses are very popular in many individuals who also
debris from the surface of the tongue is removed with the appreciate the mouth-freshening properties of many of
help of some form of scraper designed for this purpose. these mouthrinses.
It is relatively a new phenomenon. To date, mouthrinses containing chlorhexidine remain
Recent studies have shown a correlation between the so-called gold standard of antiplaque agents.
tongue scraping and a reduction in halitosis, gingival On the other hand, it is also recognized that oral hy-
disease and tooth decay. Most tongue scrapers are made giene products also have the potential of causing harm
of flexible plastic. However, a soft toothbrush may also in the mouth, some of which may be more serious and
be used for this purpose. long-lasting than others.
The harm produced may range from production of a 3. For example, 3. For example, 3. For example,
cosmetic nuisance to more permanent damage to the den- antibiotics, phenols, bis-biguanides delmopinol
tal hard tissues. The cosmetic derangement such as stain- quaternary
ing occurs as a result of the use of cationic antiseptics like ammonium
chlorhexidine and cetylpyridinium chloride (fast acting). compounds, and
sanguinarine
However, the damage to hard tissues is due to the possible
erosive and abrasive effects of low-pH mouthrinses and
toothpastes, respectively.
Of serious concern is the ability to produce carcinogen- Bis, Biguanides
ic changes to the oral mucosa through the use of alcoholic
Chlorhexidine Gluconate (0.2%)
mouthrinses (tissue irritation), which is still a controversy.
Alcohol was used in mouthrinses for the following It is a cationic bis-biguanide which is effective against
reasons: an array of organisms including gram-positive and gram-
negative organisms including fungi, yeasts, and viruses.
• To solubilize antimicrobial compounds in order to Chlorhexidine exhibits both antiplaque and antibacterial
make them bioavailable. properties (Fig. 41.16)
• To solubilize flavor masking agents. This is particularly
relevant for hiding the flavr and taste of chlorhexidine. MECHANISM OF ACTION
• To improve the shelf-life of the mouthrinse and, to
some extent, improve the pleasurable characteristics ANTIPLAQUE ACTION OF CHLORHEXIDINE
of mouthrinsing. The superior antiplaque activity of chlorhexidine is
due to substantivity, a property of sustained availability,
In the article by Addy, with reference to present-day
which means there is a reservoir of chlorhexidine which
evidence, the potential harm of oral hygiene products to
slowly dissolves from all oral surfaces, resulting in the
oral and systemic health is fully reviewed.
bacteriostatic milieu in the oral cavity.
The problem of halitosis certainly is a major stigma for
Chlorhexidine desorbed from the oral mucosa has
many individuals, although it is considered as a cosmetic
three mechanisms of plaque inhibition:
nuisance. In most individuals, the microbial degradation
of organic substrates in the mouth resulting in the produc- 1. Prevents pellicle formation by blocking acidic
tion of volatile sulphur compounds such as hydrogen sul- groups on salivary glycoprotein, thereby reducing
fide and methyl mercaptan results in halitosis. Treatment glycoprotein adsorption onto the tooth surface.
for which consists of not only the mechanical removal of 2. Prevents adsorption of bacterial cell wall onto the tooth
microorganisms and substrates by using instruments such surface by binding to the bacteria.
as tongue scrapers, which helps to remove debris and 3. Prevents binding of mature plaque precipitating ag-
bacteria from the dorsum of the tongue, but also the use of glutination factors in saliva and displacing calcium
mouthrinses and toothpastes containing various chemicals from the plaque matrix.
are of great help. Some of these chemicals mask the oral
malodor only, whereas others produce antibacterial effects
or they neutralize the volatile sulfur compounds.
CLASSIFICATION OF CHEMICAL
PLAQUE CONTROL AGENTS
First-generation Second-generation Third-generation

antiplaque agents antiplaque agents antiplaque agents
1. Reduce plaque 1. Overall plaque 1. They block
scores by about Reduction by binding of
20-50%. about 70-90%. microorganisms
to the tooth or
to each other.
2. They exhibit poor 2. Better retained by 2. They do not
retention within the oral tissues exhibit good
the mouth. and exhibits slow retentive
release properties properties as
compared to
chlorhexidine. FIGURE 41.16 Chlorhexidine mouthwash.
At the tooth surface chlorhexidine has been shown to Adverse Effects of Chlorhexidine
exert its activity, where it binds and inhibits the subsequent 1. Brownish staining of teeth on restorations, which
plaque formation. Because of this binding, chlorhexidine is may be associated with precipitation of melanoidins
effective in inhibiting plaque formation on a clean surface, from the saliva. This precipitation may be enhanced
but has little effect on preexisting plaque. by a high-lipid/ carbohydrate diet and may vary on
individual basis. The staining, however, is reversible.
ANTIBACTERIAL ACTION OF CHLORHEXIDINE 2. Loss of taste sensation: Studies have demonstrated
Chlorhexidine is a dicationic bisguanide with broad that chlorhexidine severely impairs perception of ap-
antibacterial activity. It exhibits a wide spectrum of activ- preciation of salty and bitter taste sensations. This dam-
ity, encompassing gram-positive and gram-negative bac- age reflects the effects of chlorhexidine on salty taste
teria, yeasts, dermatophytes, and some lipophilic viruses. mainly, it seemingly blocks all saltiness, and selectively
Chlorhexidine has strong affinity for binding to skin and blocks taste of a subset of bitter stimuli. The mecha-
mucous membrane. nism of inhibition of salty taste remains unclear, but
Chlorhexidine shows different effects at different con- it is believed that chlorhexidine may block ion chan-
centrations, that is: nels in taste receptor cell membranes or interfere with
paracellular ion movements. Molecular, physiological,
• Bacteriostatic at low concentration
and psychophysical evidence consistent with multiple
• Bactericidal at high concentration (Fig. 41.17).
bitter receptors could account for its bitter stimulus
These concentrations vary between bacterial species. selectivity, as chlorhexidine binds to the same subset
After a single rinse with chlorhexidine, saliva itself ex- of bitter receptors that is used by quinine. In fact, the
hibits antibacterial activity for about 5 h and suppresses effect of chlorhexidine on bitterness can be, to a large
salivary bacterial counts for over 12 h. Following several extent, replicated by a 3-min exposure to quinine.
rinses of CHX, the number of aerobic and anaerobic spe- 3. Rarely hypersensitivity to chlorhexidine has been re-
cies in the saliva can be reduced by 80-90%. Chlorhexi- ported.
dine has also been found to be a potent antifungal agent 4. Stenosis of the parotid duct has also been reported
in the oral cavity. (extremely rare).
5. Supragingival calculus formation:
OPTIMIZING USE OF CHLORHEXIDINE a. The dead bacteria due to the use of chlorhexidine
Chlorhexidine fails to distinguish between bacterial may act as an initiator for supragingival calculus
and other proteins found within the mature plaque. So, formation, which is based on the seeding mecha-
extraneous proteins must be first removed professionally nism of calculus formation.
in order to optimize the effect of chlorhexidine. b. Due to the precipitation of salivary proteins onto the
Chlorhexidine prevents plaque formation. Its mode tooth surface, which increases the pellicle thickness
of action does not allow it to remove plaque efficiently. and/ or precipitation of inorganic salts onto or into
It is recommended not to use chlorhexidine before/ the pellicle layer.
immediately after using toothpaste as the interaction 6. Oral mucosal erosion: This appears to be an idiosyn-
with anionic surfactants found within the formulations cratic reaction and is concentration dependent.
reduces effective delivery of chlorhexidine as an ac-
tive form. Toothpaste should be used prior to using Indications for Chlorhexidine Use
chlorhexidine and excess toothpaste rinsed away with
1. In the oral hygiene phase of periodontal treatment
water.
it could be used as an adjunct to mechanical oral
Local precipitation reaction occurring between tooth-
hygiene, especially in case of moderate to severe
bound chlorhexidine and elveo-mogens found within
inflammation.
food stuff and beverages explains the chlorhexidine-
2. Secondary prevention following oral surgical
associated teeth staining. With the reduced intake of
procedures, including periodontal therapy.
tea and coffee immediately after morning rinse with
3. To improve oral hygiene and reduce the bacterial
chlorhexidine, this effect may be minimized. Therefore,
load in saliva of patients with intermaxillary
use of mouthwash is recommended as the last thing in
fixation.
the night and no beverages should be consumed before
4. For plaque control in physically and mentally
retiring for the day. Chlorhexidine should be targeted
challenged individuals (institutionalized
at the patient group for whom clinical benefit is most
patients).
desirable:
5. In medically compromised patients who are
1. Patient with compromised oral hygiene predisposed to oral infections like oral candidiasis
2. Patients with physical/mental/social handicap. and denture stomatitis, chlorhexidine is effective as
Pin cushion effect
nc charged end of the CHX molecule binds ro rhe roorh surface

Other remains available ro As rhc microorganism
l l
initiate the interaction with approaches the tooth
the bacterial membrane surface
Tooth I CHX molecule I Bacteria
Rapidly attracted
Bacterial cell wall to the negatively
{negatively charged) hargcd bacterial cell
wall
l
04 + P04 (Sulfates and phosphates) Dicarionic positively charged
With specific and strong adsorption co phosphate-containing compounds
hlorhexidine is attracted toward the inner cell membrane
Bacterial cell membrane inrcgriry ,s altered

HX + PMOSPHOLJPID hlorhexidine binds to rhe phospholipids in the inner membrane
l
Increases the perrneabiliry of the mncr membrane
l
Leakage of low-molecular-weight compound
E.g., Potassium compounds
Viral cell elements leak our

Harmful substances gain entry into the cell
This is the bacreriostatic (sublerhall stage where the effect of chlorhexidine is reversible
Bactericidal action
Increased concentration of chlorhexidine
Bacterial cell membrane
''
Greater damage ro membrane
Large molecular weight compounds are lost from the cell
~ /
Coagulation and precipitation of cytoplasm,
hy [orrnntion of phosphnrcd compounds such as ATP and nucleic acids
'
Free chlorhcxidinc molecules enter into the cell and causes coagulation of cytoplasmic protein
'
Vital cell activity ceases
'
Cell death
irreversible]
FIGURE 41.1 7 (Cont)
an anticandidal antiseptic and has been shown to be • It has a broad spectrum of activity against gram-
useful in combination with antifungal agents. positive and gram-negative bacteria. Its spectrum of
6. Chlorhexidine appears to offer synergistic effects to activity also includes Mycobacterium spores and Candida
fluoride in caries prevention in case of patients with species.
high-risk caries.
7. In patients suffering from minor recurrent aphthous Mechanism of Action
ulceration. Triclosan acts on the microbial cytoplasmic membrane.
8. In patients undergoing removable and fixed It induces leakage of cellular constituents and causes
orthodontic treatment. bacteriolysis.
9. In implant dentistry there is only limited information It has recently been introduced in toothpaste and
on the use of chlorhexidine. mouthrinses in order to reduce plaque formation, along
10. In long-stay hospital patients, elderly patients, and with zinc citrate or gantrez (methoxyethylene and malic
terminally ill patients. acid) to enhance it retention in the oral cavity.
11. To limit bacteria and operatory contamination by oral Triclosan can delay plaque maturation and also inhibits
bacteria. formation of prostaglandins and leukotrienes, which are
key mediators of inflammation, via inhibition of both the
Triclosan cyclooxygenase and lipoxygenase pathways.
• It is a phenol derivative.
• Recently it has been included in mouthrinses and
Metallic Ions
toothpaste. Some metal ions have a plaque inhibitory capacity.
• It is synthetic, nonionic, and is used as a topical Salts of zinc and copper are the one most commonly
antimicrobial agent. used.
Mechanism of action Povidone Iodine
Metallic salts reduce the glycolytic activity in microor- This particular agent does not appear to have a sig-
ganisms and inhibit bacterial and crystal growth. In com- nificant plaque inhibitory activity when used as a 1 %
mercially available mouthwashes or dentifrices the use of mouthwash. Besides, a significant amount of iodine is
copper salts has been restricted because of their unpleasant absorbed through the oral mucosa, making this com-
taste, potential to cause stain, and potential toxicity. pound unsatisfactory for prolonged use in the oral cav-
Metal ions are also capable of stimulating volatile sul- ity. However, certain studies have shown that povidone
fur-containing compounds, which are produced by gram- iodine solution can reduce inflammation and progression
negative bacteria in gingival pockets. These substances of periodontal diseases.
have been associated with halitosis.
Delmopinol
Quaternary Ammonium Compounds
Delmopinol is a low-molecular-weight amino alco-
They are cationic antiseptics and surface active agents, hol. It is a morpholinoethanol derivative. It has been
and tend to be more active against gram-positive than shown to inhibit plaque growth and reduce gingivitis.
gram-negative organisms. They are therefore effective However, it exhibits limited substantivity compared to
against developing plaque, which consists of predomi- chlorhexidine.
nantly gram-positive organisms.
Mechanism of Action
Mechanism of Action
Dextran in the extracellular matrix is targeted by del-
The positively charged molecule with negatively charged
mopinol which occurs by blocking synthesis, reducing the
cell membrane phosphates disrupts the cell wall structure
viscosity, and also selectively inhibiting dextran-producing
of microorganisms, for example, benzethonium chloride,
streptococci. In terms of minimum inhibitory concentra-
benzalkonium chloride, and cetylpyridinium chloride.
tion, its antimicrobial is relatively weak; however, its rate
of kill approaches that of chlorhexidine against selected
Sanguinarine streptococci.
It interferes with plaque matrix formation and also
It is a benzophenanthridine alkaloid, which is derived reduces bacterial adherence. It causes weak binding of
from the plant Sanguinaria canadensis. They are effective the plaque to tooth surface, thus aiding in easy removal
against a wide variety of gram-negative organisms. San- of plaque by mechanical procedures.
guinarine exhibits good retentive properties with dental Indication: As a prebrushing mouthrinse.
plaque when used as a mouthrinse. Sanguinarine can be Delmopinol has been reputed to be effective in both
disclosed under long-wave ultraviolet light because of its rapid and slow plaque formers. It also dissolves formed
fluorescent properties. plaque in the absence of mechanical plaque control.
Antibiotics Adverse Effects

1. Transient staining of tongue and teeth
Antibiotics such as vancomycin, erythromycin, ni- 2. Taste disturbance
damycin, and kanamycin have been used as agents for 3. Sometimes mucosa! soreness and erosion.
plaque control.
Use of these agents has been reduced considerably due
to potential problems of bacterial resistance and hyper-
sensitivity reactions. ANTICALCULUS AGENTS
Dentifrices containing either soluble pyrophosphatase

Enzymes and zinc compounds have demonstrated 10-50% reduc-
Enzymes have been used as active agents in antiplaque, tion in calculus.
as they are able to break down already formed matrix of
plaque calculus. Certain proteolytic enzymes are bacteri-
Mechanism of Action
cidal to microorganisms and would therefore be effective
when applied topically in the mouth. The anticalculus effects of pyrophosphatase and zinc
For example, mucinase, dehydrated pancreas, mu- compounds are thought to be produced by their absorp-
tanase, dextranase, lactoperoxidase, and thiocyanate tion onto small hydroxyapatite crystals, thus inhibiting
synthase. growth of larger and more organized crystals.
Anticalculus agents are mostly designed to inhibit individuals at some point in their lives, affecting about
the mineralization of the so-called petrified plaque, e.g., 15% of the population worldwide. The etiology of den-
pyrophosphates, zinc citrate, zinc chloride, gantrez (a tine hypersensitivity is multifactorial and can occur due
copolymer of methyl vinyl ether and malice anhydride). to both tooth wear (erosion/ abrasion), and periodontal
disease and its treatment, which exposes either coronal
or radicular dentin, or indeed both. For dentine hyper-
DENTIFRICES sensitivity to occur, the tubules must be about 1 µm in
diameter and patent to the pulp. Without recourse to den-
For years toothpastes have been known for their clean- tist/hygienist-applied treatments, the use of chemicals,
ing potential by way of detergents and toothpaste abra- primarily in toothpaste, is the major method of controlling
sives incorporated in them (possibly even producing or eliminating symptoms. Among the wide range of prod-
detrimental effects such as abrasion), but they are now ucts available these days, majority of them are thought to
also believed to be an appropriate vehicle for the incor- be effective through occlusion of the dentine tubules or
poration of chemicals that may have a preventive and/ or nerve stabilization with potassium ions.
therapeutic role in oral disease (Table 41.14). According to the American Dental Association Council
A number of studies have reported that use of triclosan on Dental Therapeutics "A dentifrice is a substance used
with the copolymer gantrez in toothpaste helps in the with a toothbrush for the purpose of cleaning accessible
reductions of plaque and gingivitis. It has also been sug- surfaces of the teeth."
gested that the specific chemicals present in them may be Webster described the term dentifrice as derived from
beneficial in reducing periodontitis. dens (tooth) and fricare (to rub).
Dentine hypersensitivity causing oral discomfort Dorland described it as a preparation for cleaning and
and pain are reported to be major problems for many polishing the tooth surfaces.
TABLE 41.14 Composition of Dentifrices
Ingredients Percentage Functions Commonly used chemicals

Polishing/ 15-45% 1. Mechanically clean the teeth • Calcium carbonate
abrasive agents 2. Mild abrasive action that aids in eliminating plaque • Dicalcium phosphate dehydrate
from tooth surface • Alumina
3. They remove stained pellicle from the tooth surface, • Silica
restore natural luster, and also enhance enamel whiteness
Binding/ thicken- Up to2% 1. Binds the solid to form homogeneous paste Water-soluble agents
ing agents 2. Controls stability and consistency of a toothpaste • Alginates
3. Effects ease of dispersion of the paste in the mouth • Carrageenans
• Sodium carboxymethylcellulose
Water-insoluble agents
• Magnesium aluminum silicate
• Colloidal silica
• Sodium magnesium silicate
Detergents or 1-5% 1. Produces the foam, which aids in the removal of food Sodium lauryl sulfate
surfactants debris and also dispersion of the product within the Sodium dodecyl sulfate - new
mouth detergent
2. Antimicrobial property Less chemically displaced and
foaming is more
Humectants 25-40% 1. To maintain the consistency of the paste Sorbitol glycerin polyethylene glycol
2. Aids in reducing the loss of moisture from the toothpaste
Flavoring agents Up to 1% 1. They render the product pleasant to use Peppermint oil
2. Leave a fresh taste in the mouth after use Spearmint oil
Oil of Wintergreen
Sweeteners and Up to2% Saccharin

coloring agents
Water 20-30% As vehicle and solvent medium Double distilled water
Preservatives Up to 0.5% To prevent microbial growth Benzoic acid

Therapeutic agents Up to 2% To provide specific therapeutic action to the paste Tetrasodium pyrophosphatase zinc chloride
TABLE 41.15 Active Ingredients Application of Dentifrices
Antibacterial Prevent bacterial growth • Triclosan The amount of toothpaste/ gel needed for effective
agents • Delmopinol cleaning is a pea-sized dab on the top half of the tooth-
• Metallic ions brush. The dentifrice should preferably be dispersed in
• Zinc citrate trihydrate
between the bristles rather than on the tips. Children un-
Anticaries Active agents: fluoride • Sodium der 6 years of age should only be given half the amount
agent • Inhibit demineralization monofluorophosphate of dentifrice as compared to that of the adult. For some
• Enhance • Sodium fluoride
individuals, oral soreness produced by numerous oral
remineraliza tion • Stannous fluoride
• Inhibit the enzyme pathological conditions can render their lives miserable.
activity in bacteria by Direct application of medicaments via home-use products
acidifying the cells can be of immense value for some individuals as it helps
Anticalculus • Inhibit the • Pyrophosphates in reducing the pain and duration of their symptoms.
agents mineralization of • Zinc citrate Some of these drugs, such as topical analgesic gels and
plaque - also known as • Zinc chloride antiseptic mouthwashes, can be used. Others, such as
crystal growth inhibitors • Gantrez acid corticosteroids, anticandidal gels and antiviral creams,
(copolymer of
tend to be available primarily via pharmacies.
methylvinyl ether
and maleic The problem of oral xerostomia is also of equal dis-
anhydride) comfort to some patients; they have been associated
with numerous causes and equally numerous forms of
Desensitizing Decreases the sensitivity • Sodium fluoride
agents • Potassium nitrate treatment. Apart from being a source of discomfort, xe-
• Strontium chloride rostomia may result in other oral problems, such as an
increased propensity for dental caries and candidiasis in
denture wearers. Simple procedures, such as increasing
salivary flow through chewing, or the use of salivary
It may contain the following (Table 41.15): substitutes, may help these patients immensely. The use
of nonsteroidal anti-inflammatory drugs has been shown
1. The therapeutic agent such as fluoride, etc., to inhibit to reduce the rate of alveolar bone loss, but it is suggested
dental caries. that the benefit remains only while the individual takes
2. Antimicrobial agents such as chlorhexidine, cetrimides, the drug, and, indeed, discontinuation of the drugs may
etc., to reduce microorganisms. result in a return or accelerated rate of bone loss known
3. An anticalculus agent such as zinc chloride, etc., to as the rebound effect.
dissolve calculus. Moreover, appropriate control of subgingival and
supragingival plaque is of utmost importance in main-
taining periodontal (gingival) health and still there is a
Functions of Toothpaste in Conjuction
general reluctance for the use of nonsteroidal anti-inflam-
with Toothbrushing
matory drugs as a result of their inherent side effects, in
1. Minimizing buildup of plaque particularly as they have the tendency to produce gastro-
2. Anticaries action intestinal irritation (ulceration) and impaired hemostasis.
3. Removal of stains More recently, the use of host modulation therapy with
4. Removal of food debris subinhibitory doses of doxycycline has been introduced.
5. Mouth freshener. In the review article by Preshaw, periodontal pathogen-
esis, and conventional and host modulation treatments,
are looked at and the potential value of the latter in the
Recent Development in Dentifrices
management of periodontal disease is explored.
• Toothpaste for children The use of probiotics in the management of various
• Natural/herbal toothpastes oral diseases such as candidiasis, oral malodor, dental
• Whitening toothpastes: They contain highly abrasive caries and periodontal disease is one exciting area of re-
silica particles, and hence are not recommended for search.
regular use. In the article by Teughels et al, the use of probiotics in
• Sodium bicarbonate toothpastes (some products both oral and extraoral health conditions and infections
contain peroxide, which may irritate the gingival and is discussed. The only major trend seen in the oral hy-
oral tissues) giene market over the past few years is the introduction
• Breath-freshening toothpastes of tooth whitening products, which remove extrinsic
• Liquid dentifrice containing triclosan. stain primarily by way of toothpaste abrasives or by the
employment of professionally delivered or home-use persuade patients to quit smoking is the prescribed
bleaching kits. drugs (such as bupropion and varenicline) from the
As the dental team, comprising the dentist, the hy- pharmacy and nicotine substitutes from these and oth-
gienist, and the dental nurse, could be very effective at er general outlets also. As can be seen from this intro-
communicating with patients, their advice can be of duction, the home-use preventive and therapeutic prod-
immense value in helping patients to quit their habit. ucts also have great potential in promoting oral health
One of the recognized and useful tools in the fight to for the individual.
KEY POINTS
Utility of disclosing agent: Personalized patient in- • Classification of toothbrushing techniques according to
struction and motivation, self-evaluation by the patient, to Greene (1996): the roll technique; modified Stillman/
evaluate the effectiveness of oral hygiene maintenance, rolling stroke; the vibratory technique: Stillman, Char-
preparation of plaque indices, in research studies with re- ters, and Bass method; the circular technique: Fone
gard to effectiveness of plaque control devices like tooth- method; the vertical technique: Leonard method; the
brushes and dentifrices, etc. physiological technique: Smith's method.
• Classification of gingival embrasures: Class I, no gingival
• Parts of a toothbrush are handle, head, tufts, brushing
recession with interdental papilla filling the space; Class
plane, and shank.
II, moderate papillary recession; Class III, complete loss
• Toothbrush bristles are classified as hard and
of the interdental papilla.
soft, natural and synthetic, multitufted and space tufted.
• Dentifrices containing either soluble pyrophosphatase
• Nylon filaments are superior in terms of
and zinc compounds have demonstrated 10-50% reduc-
homogeneity, uniformity of bristle size, elasticity,
tion in calculus.
resistance to fracture, and repulsion of water and debris.
• ADA specification of a toothbrush: 1-1.25 in. in
length, 5/16-3/8 in. in width, 2-4 rows of bristles, and
5-12 tufts/row.

1. Addy M, Moran JM. Toothpaste, mouthrinses and other topical
1. Write a short note on antiplaque and anticalculus remedies in periodontics. Periodontology 2000;1997;15:40-51.
agents. 2. Drisko CH. Non-surgical periodontal therapy pharmaco-
2. What is the mechanism of action of chlorhexidine? therapeutics. Ann Periodontol 1996;1:491.
3. Write a short note on dental floss. 3. Greene JC. Oral health care for prevention and control of periodontal
disease. World Workshop in Periodontics. Ann Arbor: University of
4. Write a short note on disclosing agents. Michigan Press. 1996.
5. What are the interdental cleaning aids? 4. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant
6. What are the adverse effects of long-term chlorhexidine Dentistry. 5th ed. Copenhagen: Black-well Munksgaard; 2008.
use? 5. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds.
7. Classify chemical plaque control agents. Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B.
8. What is the ADA specification of toothbrush? 6. Rose LF, Mealey BL, Genco R. Periodontics, Medicine, Surgery and
Implants. 1st ed. St. Louis: Elsevier; 2004.
CHAPTER
42
Scaling and Root Planing
CHAPTER OVERVIEW
The aims and objectives of periodontal therapy are arrest margin, within the sulcus. Subgingival scaling is carried
of disease, regeneration of lost tissues, and maintenance of out with subgingival hoe scalers and curettes (Fig. 42.1).
state of health of the periodontium. In this regard, scaling Root planing is a process of meticulous instrumentation
and root planing are the basic treatment procedures car- by which residual embedded calculus and portions of ce-
ried out during periodontal management. These are the mentum are removed from the root surface to render it bio-
two primary modes of treatment aimed at elimination of logically clean and clinically smooth and hard. Thus, it helps
bacteria from the tooth surface by means of professional to remove the softened, necrosed cementum. A healthy root
instrumentation. surface is a critical element in establishing periodontal health
Scaling is a process of removal of all the surface ac- and achieving regeneration by eliminating inflammation
cretions, i.e., plaque, calculus, stains, and "materia alba" and arresting disease progression. In subgingival scaling,
from the teeth by means of instrumentation. It can be su- there is no intentional removal of cementum, whereas in root
pragingival or subgingival. Removal of deposits present planing, there is a deliberate attempt to remove the altered
coronal to the gingival margin is termed as supragingival (disease/necrosed) cementum. Root planing has two faces.
scaling; whereas removal of deposits present apical to 1. It is carried out as part of nonsurgical treatment when it
the gingival margin is termed subgingival scaling. In helps to restore the soft-tissue health by reducing inflam-
practice, however, while doing supragingival scaling, mation. The smoothness of root surface also facilitates
the instruments have to be engaged subgingivally to better plaque control and maintenance.
dislodge the calculus and remove it "en bloc," since the 2. Root planing performed as a part of surgical treatment, e.g.,
base of the calculus invariably lies apical to the gingival during flap surgery, helps in achieving new attachment.
OBJECTIVE OF ROOT PLANING cemental surface must be removed to eliminate these

deposits.
• To restore health by removing elements that provoke • Smoothness of the root surface: When the root surface is ex-
gingival inflammation posed to plaque in the pocket environment, its surface
• To remove pathogenic periodontal microflora. is contaminated by toxic substances of plaque bacteria,
notably endotoxins. The diseased layer of cementum is
soft. Hence, the only way to be reasonably certain that
cementum surface is free of irritants is by achieving a
RATIONALE FOR ROOT PLANING
hard and smooth surface following root planing; i.e.,
root smoothness is a clinical determinant of root health.
• Removal of calculus: Plaque and calculus on exposed
root surfaces pose different problems unlike when Recent evidence suggests that these toxic substances
they are present on the enamel surface. Deposits of are only superficially attached (adsorbed) and do not
calculus on root surfaces are frequently embedded permeate deeply into the root surface (about 100 µm).
in cemental irregularities. Therefore, scaling alone Since they are weakly adherent, the extent of cementum
is insufficient to remove them and a portion of the removal during root planing is questionable.
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FIGURE 42.1 Curette and hoe.
FIGURE 42.2 The blade design of hoe is preferred for removal of

heavy ledges of calculus.
INDICATIONS OF ROOT PLANING
AS A SPECIFIC PERIODONTAL
TREATMENT IN PERIODONTITIS
Root planing may be considered as a definitive thera-

peutic procedure in the following situations:
• Very aged individuals who cannot sustain trauma of
surgery
• Medically compromised patients who are not fit for
periodontal microsurgery
• Psychologically unprepared patients
• Esthetic considerations: Where severe gingival recession is
expected following surgical treatment especially in the
anterior segment, surgery would be unacceptable.
• Extremely advanced cases wherein pocket eradication
by surgery is not practical or would be impossible,
and where extraction of many teeth and multiple
replacements are unacceptable to the patient.
FIGURE 42.3 Subgingival instrumentation with a hoe.
INSTRUMENTATION hand instruments for root planing (Fig. 42.4). Modifications

of Gracey area-specific curettes like After-Five, Mini-Five,
Hoe subgingival scalers are specially used for removal and curettes are selected in specific situations. Sonic and
of heavier deposits of calculus from the root surface, since ultrasonic instruments may also be used. Slim-line insert
greater force needs to be applied in this case (Figs 42.2 ultrasonic tips are recent additions for root instrumentation.
and 42.3). A set of six hoe scalers are required to have ac- Rotary devices such as fine diamonds and tapering tips
cess to all the surfaces of the teeth for planing of the whole mounted on a handpiece can also be used for root planing.
dentition. Subsequent to removal of calculus, a curette
should be considered for final and finer smoothening of
the root surface. Sometimes during "forceful" stroking PROCEDURE
of the root surface for calculus removal, one is likely to
break a fine instrument like a curette. In such instances, Supragingival calculus being attached to enamel sur-
heavy-duty /rigid shank curettes may be employed for face by means of pellicle can be dislodged relatively eas-
initial subgingival calculus removal. ily. During scaling, short, overlapping, powerful pull
During surgery, once the root surface is exposed by flap strokes are applied. The blade of the scaler should make
reflection, the identification and removal of root surface dean angulation of 45-90° with the tooth surface. If the
posits becomes much easier with direct visibility of the root angulation becomes less or more than this, the calculus
surfaces. Curettes, either universal or area specific, are ideal will get burnished rather than being dislodged.
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C H A PT ER 42 SC A LIN G A N D RO O T PLA N IN G 377
Once the residual embedded calculus is removed, the
tooth surface will be smoothened with the use of curettes,
either universal or area specific. The area planned for root
planing may be anesthetized. The strokes must be long,
firm, and overlapping to achieve a smooth and clean
surface on the root. The smoothness should be confirmed
with a fine explorer. The area may be irrigated with saline.
Presently, full-mouth root planing is suggested to be
carried out in one or two appointments instead of being
carried out quadrant-wise in more number of appoint-
ments, to minimize the possibility of the treated area get-
ting reinfected from untreated sites during the healing
period. This ensures full-mouth disinfection.
USE OF LASERS IN ROOT PLANING
With the advent of light amplification by stimulated

FIGURE 42.4 Instrumentation with a curette. emission of radiation (LASER) device, clinician has an
additional option for periodontal treatment. Application
Subgingival scaling and root planing, being closed of lasers in soft tissue treatment is well documented; hard
(blind) procedures, require the additional clinical skill of tissue applications are emerging. Laser has been applied
tactile feeling to locate as well as remove subclinical cal- to root surface treatment using Neodymium: yttrium-
culus deposits. The clinician should recollect the anatomy aluminum-garnet (Nd:YAG wavelength 1064 nm) and
of each root surface for accessing the concavities, irregu- Erbium: yttrium-aluminum-garnet (Er: YAG - 2740 nm).
larities, and furcation areas. The instruments have to be Lasers effectively ablate all tissues that contain water
adapted to the root surface accordingly. molecules and are applicable for both soft and hard tis-
The subgingival calculus is difficult to remove as com- sues. Photoablation by laser causes the detoxification and
pared to supragingival calculus. This is due to the following root conditioning effect of the contaminated root surface.
reasons: In addition, laser has bactericidal ability. Laser therapy is
capable of removing plaque and calculus with extremely
1. The calculus is thin and flint like. Hence engaging the
low mechanical stress and without formation of a smear
instrument is difficult.
layer on the root surface. Laser may also provide better
2. The calculus is firmly attached to the natural irregu-
access to sites that conventional mechanical instruments
larities of the cemental surface with mechanical inter-
cannot reach.
locking.
Root planing with lasers has shown potentially delete-
3. The calculus is not visible, since the subgingival area
rious side effects like thermal injury to root surface, gin-
is covered by gingiva.
gival tissue, pulp, and bone tissue. Use of laser has a dis-
4. Bleeding during instrumentation hampers the visibility.
advantage of need of elaborate precautionary measures
During dislodgement/removal, if the instrument is not to be employed. Even with noncontact mode lasers can
engaged properly or if the blade is not sharp, the calculus will affect surrounding tissues including patient's eyes by
only get burnished or scraped but not removed completely. causing inadvertent radiation due to the scattered rays.
KEY POINTS
• The aims and objectives of periodontal therapy are arrest cementum are removed from the root surface to render
of disease, regeneration of lost tissues, and maintenance the root surface biologically clean and clinically smooth
of state of health of the periodontium. and hard.
• Scaling is a process of removal of all the surface accre- • Curettes, either universal or area specific, are ideal hand
tions, i.e., plaque, calculus, stains, and "materia alba" instruments for root planing.
from the teeth by means of instrumentation. • The blade of the scalar makes an angulation of 45-90°
• Root planing is a process of meticulous instrumentation with the tooth surface.
by which residual embedded calculus and portions of
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QUESTIONS disease with scanning electron microscope immunohistochemistry.

J Periodontal Res 1988;23:100.
5. Hughes FJ, Smales FC. Immunohistochemical investigation
1. Define scaling and root planing. of the presence and distribution of cementum associated
2. What are the indications of root planing? lipopolysaccharides in periodontal disease with scanning electron
3. What is the rationale for root planing? microscope immunohistochemistry. J Periodontal Res 1986;21:660.
6. Mongardini C, Van Steenberghe D, Dekeyser C, et al. One stage
full versus partial mouth disinfection in the treatment of chronic
Suggested readings adult or generalized early onset peri-odontal disease: I - long term
clinical observations. J Periodontol 1999;70(6):632.
1. Aleo J, De Renzis F, Farber P, et al. The presence and biological 7. Mosques T, Listgarten MA, Phillips RW. Effect of scaling and root
activity of cementum bound endotoxin. J Periodontal 1974;45:672. planing on the composition of human subgingival microflora. J
2. Greenstein G. Non surgical periodontal therapy in 2000: a Periodontal Res 1980;7:199.
literature review. J Am Dent Assoc 2000;131(111):1580. 8. Nakib NM, Bissada NF, Simmelink JW, et al. Endotoxin
3. Hatfield CG, Baumhammers A. Cytotoxic effects of peri-odontally penetration into root cementum of periodontally healthy and
involved surfaces of human teeth. Arch Oral Biol 1971;16:465. diseased human teeth. J Periodontal 1982;53:368.
4. Hughes FJ, Auger DW, Smales FC. Investigation of the distribution 9. Selvig KA. Attachment of plaque and calculus to tooth surfaces. J
of cementum-associated lipopolysaccha-rides in periodontal Periodontal Res 1970;5:8.
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CHAPTER
43
Chemotherapeutic Agents
CHAPTER OVERVIEW
Periodontal diseases, especially periodontitis, occur as burden. However, certain forms of period on ti tis still require
a consequence of the inflammatory and immunologic reac- the adjunctive use of antibiotics to effectively eliminate the
tions of the host to bacterial plaque. Control and elimination tissue-invading bacteria that escape the mechanical therapy.
of bacterial challenge thus become the primary objective of Similarly, some anti-inflammatory agents can reduce host's
the treatment, followed by modification of excessive in- self-destructive immunologic response to bacterial patho-
flammatory response of the host. The best way to control gens and thus help in control of the disease. This chapter
the bacterial challenge is natural mechanical therapy that covers the uses of various antibiotic and anti-inflammatory
breaks the biofilm and eliminates the majority of this bio- agents in the treatment of periodontal disease.
RATIONALE OF ANTIBIOTIC THERAPY antibiotic agents and increasing resistance to these

formerly potent agents.
Every case of periodontitis does not respond to the 2. Change of intestinal flora: The use of antibiotics may
mechanical therapy alone due to the following reasons: disturb the delicate ecological balance of the intestinal
flora and permit the proliferation of resistant organ-
1. Tissue invasion: The ability of the microorganism to in-
isms that may initiate new infections that are worse
vade the periodontal tissue or escape into the dentinal
than the original offenders.
tubules so mechanical therapy cannot achieve their
3. Toxicity: All antimicrobial agents, being extraneous
elimination
chemicals, carry with them an inherent risk of toxicity.
2. Inaccessible sites: Inaccessible sites like furcations
and root concavities provide shelter from instrumen- Hence the use of antibiotics is a responsible decision
tation. and the decision should be based on the following sound
3. Bacterial translocation: Bacterial translocation to the sites principles.
previously treated. Sites like dorsum of the tongue and
D Data: Data from authentic studies should substanti-
tonsils provide that nidus of bacteria for translocation.
ate the use of antibiotics in clinical situation.
Thus, the combination approach of antibiotics with A Advantage over conventional treatment: Documenta-
mechanical therapy can provide the enhanced effect on tion is needed to justify the use of the drugs over the
bacterial elimination. conventional therapy.
N No major side effects: Use of antibiotics should be
Principle of Antibiotic Use weighed against its potential side effects.
C Concentration of drugs: It should be adequate at
It is worthy to note that, however, in the developing
the diseased sites to inhibit or kill the target patho-
world, overuse of antibiotic has caused lot series of dif-
gens; concentration should be maintained over a long
ferent problems which are stated as follows:
time.
1. Bacterial resistance: Over the years, bacteria have devel- E Efficiency of drugs: Drugs should show enough in
oped a remarkable array of mechanisms to withstand vitro activity to eliminate the target pathogens.
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IMPORTANCE OF COMBINED THERAPY
Unassisted use of antimicrobial agents, however, can-

not provide long-term solution and should always be
preceded by mechanical therapy. Following reasons show Endogenous
I r ompromised ~pportunist~
host infection
-
ic
organism
why antibiotic, when used alone may fail.
1. Antibiotics cannot eliminate the calculus or food debris, _1 Superinfection
which provide surface for further bacterial attachment.
2. Bacteria may reside in biofilm that has complex archi-
tecture and hence may prove obstacle for antimicrobial
actions by the following mechanisms:
a. Bacterial extracellular polymers that are present in
Exogenous
organisms -l True infection
biofilm matrix may prevent penetration and activity

of antibiotics.
b. Bacteria gain increased antimicrobial resistance in FIGURE 43.1 Different types of periodontal infection.
biofilm due to diffusion barriers and selective de-
composition of microbial agents.
a healthy crevice. So if the goal of therapy is their elimi-
3. Moreover, certain commensal microorganisms can also
nation, it is unlikely to be achieved. Hence more practi-
degrade the microbial agents before they reach their
cal goal would be to suppress the population of these
target bacterial population.
microorganisms up to a level that cannot cause clinical
This implies that treatment of periodontal diseases by infection.
antimicrobials alone will probably not suffice and should Targeted antimicrobial therapy: It is an irony that even
be combined with mechanical instrumentation to disrupt a healthy human gingival crevice may show up to 500
the biofilm and remove the bulk of bacterial deposits. different microbial species. Here many organisms show
synergism and antagonism. Hence targeting only harm-
ful microorganism and inducing the growth of their an-
TREATMENT GOALS tagonistic bacteria appears to be useful. Narrow spectrum
antibiotic that degrades only target bacteria should be
It is essential to understand the type of infections to selected on the basis of antibiotic sensitivity and microbial
determine the goals of periodontal therapy. culture test.
Endogenous infection: In this situation, the innocuous Use of antagonist bacteria: As mentioned previously,
commensal bacteria switches to a parasitic existence due promoting the growth of bacteria that are antagonistic
to various opportunities offered either by the host or by to target bacteria may prove to be useful. These healthy,
the environment, thus causing disease. This infection can antagonist bacteria are generally referred as probiotic.
be called as endogenous infection if local environment is Local areas seeded with these healthy commensals may
altered or opportunistic infection of host is compromised. help eradicate the pathogens and should be the area to
Exogenous infections: Here pathogens are transmitted explore in future.
to healthy subjects via vectors, which may be diseased
humans, animals, or healthy carriers that show no signs
of infection and can cause true infection. ROUTES OF DRUG ADMINISTRATION
Superinfection: It is a new infection that complicates
treatment of an existing infectious process. Superinfection Drugs can be administered into the periodontal pocket
is also used to describe a multiple outburst of an infec- by following routes:
tion caused by the same pathogen. It can be a synonym
1. Systemic
for a secondary infection by a microorganism on top of a
2. Local
pre-existing infection by another microorganism. Both/
either endogenous or exogenous bacteria can cause su- Systemic route: It is generally most commonly used
perinfection (Fig. 43.1). route. In the situations where bacteria have widely colo-
Goals of treatment are as following: nized the oral cavity, this route is preferred, since local
Suppression rather than elimination of pathogens: Since A placement of antibiotic cannot cover the wider area
actinomycetemcomitans and P. gingivalis are considered as and has a risk of bacterial translocation. However, side
primary periodontal pathogens, their elimination logi- effects and adverse drug reactions are more observed
cally seems to be the goal of therapy. On the contrary, A than local antimicrobial placement. When using sys-
actinomycetemcomitans and P. gingivalis are present even in temic antibiotics, careful dosing according to clinical
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CH A PT ER 43 C H EM O T H ERA PEU T IC A G EN T S 381
TABLE 43.1 Routes of Drug Administration
Parameters Systemic Local

Drug distribution Wider area of coverage Only localized area is covered
Drug concentration Higher dosage may be required to reach therapeutic Very high drug concentration at localized sites can be
drug concentration at the site of infection reached without affecting other areas.
Clinical use When periodontal infection is generalized In localized periodontitis
Disadvantages Side effects and adverse drug reactions are high Bacterial translocation from untreated sites
Clinical limitations Requires good patient compliance Effective only when infection is limited to the treated site
Diagnostic problems Identification of pathogens, selection of agents Distribution pattern of lesions and pathogens, identifica-
tion of sites to be treated
severity and body mass is needed prior to prescription. Bacteriostatic antibiotics inhibit the growth and multi-
Clinicians also have to rely on patient compliance for plication of microorganisms, whereas bactericidal antibi-
the success of this route. otics kill microorganisms. While bacteriostatic antibiotics
Local route: It can provide an excellent option for the alter the metabolic pathways or synthesis of cellular com-
delivery of antiseptic agents that are too toxic to be de- ponents in microorganisms, bactericidal drugs interfere
livered systemically. If the periodontal infection has with the synthesis or function of the cell wall, cell mem-
spread locally, e.g., localized periodontitis, then local brane, or both. When two bactericidal antibiotics are given
placement of drugs into pocket may prove to be more together, they may exert a greater effect than when each is
advantageous. Very high concentration of drugs can be given alone. This is called "antibiotic synergism." Some-
reached by this route. However, maintenance of this con- times, however, when a bacteriostatic and a bactericidal
centration is an issue with local delivery. Mouthwash or antibiotic are given together, their effectiveness is negated
subgingival irrigation with antiseptics cannot reach the or reduced. This is called "antibiotic antagonism."
deep areas of pocket. Also, they are almost immediately
washed out by gingival crevicular fluid. Hence, for the Single or Combination of Antibiotics
successful local drug delivery, biodegradable reservoir is
needed, which provides control release of antimicrobial Due to the complex nature of the subgingival microbial
agents and at the same time maintain the integrity in niche containing several putative periodontopathogens
subgingival environment without premature dislodge- with varying antimicrobial susceptibility, combination
ment (Table 43.1). drug therapy has been advocated.
Advantages:
1. Wider spectrum of activity
ANTIMICROBIAL AGENTS IN 2. Reduced emergence of bacterial resistance
PERIODONTAL THERAPY 3. Synergistic action between each drug potentiates action
of each other and allow administration of lower doses
Properties of an ideal antibiotic: 4. Adverse effects due to high doses of drugs can be re-
1. It should be selective and effective against microorgan- duced.
isms without injuring the host. Amoxicillin and metronidazole is the most preferred
2. It should destroy microorganisms (bactericidal action) combination for periodontal therapy and both drugs
rather than retard their growth (bacteriostatic action). show marked synergism especially against A. actinomy-
3. It should not become ineffective as a result of bacterial cetemcomitans. However, some drugs show antagonistic
resistance. effect and reduce each other's therapeutic effect when
4. It should not be inactivated by enzymes, plasma pro- used together, e.g., tetracycline and metronidazole.
teins, or body fluids. There are certain adverse reactions reported with
5. It should quickly reach bactericidal levels throughout the use of these drugs. Table 43.2 describes some of the
the body and be maintained for long periods. common side effects of the most commonly used drugs
6. It should have minimal adverse effects. (Fig. 43.2).
Antibiotics can be classified in the following ways ac- Tetracyclines
cording to type of action:
The Tetracyclines consist of group of closely related
1. Bacteriostatic antibiotics those are bacteriostatic and provide a "broad
2. Bactericidal spectrum" of activity. Tetracycline usage became more
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TABLE 43.2 Side Effects of Most Commonly Used Drugs
Antimicrobial agent Frequent effects Infrequent effects

Penicillins Hypersensitivity (mainly rashes), nausea, diarrhea Hematological toxicity, encephalopathy, pseudomembranous
colitis (ampicillin)
Tetracyclines Gastrointestinal intolerance, candidiasis, dental Photosensitivity, nephrotoxicity, intracranial hypertension

staining and hypoplasia in childhood, nausea,
diarrhea, interaction with oral contraceptives
Metronidazole Gastrointestinal intolerance, nausea, antabuse Peripheral neuropathy, furred tongue

effect, diarrhea, unpleasant metallic taste
Clindamycin Rashes, nausea, diarrhea Pseudomembranous colitis, hepatitis
Gaycopeptide• Earlier reports mentioned that concentration of tetra-

Teitop~nn
Vancomy~ cyclines in gingival crevicular fluid (GCF) can reach up
to 10 times than its plasma concentration after systemic
.. administration. However, in recent studies approximately
Carbapenema 50% samples of GCF did not achieve the tetracycline con-
lmpenem
lv"cropcncm centration of 1 µg/mL, well short of its plasma concen-
Fluoroquinolon••
tration, possibly explaining much of the variability in
Ouzolkllnones
C1prot!cx.Jan
Lcvonoxacin
L,nemld clinical response to systemic tetracyclines observed in
Nahchic Acid clinical practice.
MacrolidH
Ery1tvomyan
Mlacellan.ou,
~ftboni~z°'8
The oral dose for tetracycline is 250 mg four times daily
Clanttvomycm
Az,!hrcmyoln
Tetracychnes for 2 weeks adjunct to both nonsurgical and surgical treat-
ment. The oral dose for the doxycycline and minocycline
FIGURE 43.2 Various antibiotics and their groups. is 100-200 mg once a day, for 3 weeks.
Penicillins
widespread in 1970. Tetracycline has following properties Penicillins are the drugs of choice for the treatment
that are beneficial in periodontal infection: of many serious infections in humans and are the most
widely used antibiotics. Penicillins are natural and semi-
1. Wider coverage of microorganism. However, it is more
synthetic derivatives of broth cultures of the Penicillium
suitable against gram-positive organisms.
mold. They inhibit bacterial cell wall production and
2. Considerable activity against A. actinomycetemcomitans.
therefore are bactericidal.
Since A. actinomycetemcomitans invades the tissue, it is
The first group of antibiotics that were tested for peri-
difficult to eradicate by mechanical therapy alone and
odontal therapy was that of penicillins. Although many
hence Tetracycline is a choice of drug in aggressive
penicillins are available, amoxicillin is the most wide-
periodontitis.
ly used penicillin due to its wider coverage. However,
3. Anticollagenase activity, which prevents the inflamma-
due the emergence of penicillinase-resistant microor-
tory breakdown of tissues and prevent bone resorption
ganism, the combination of amoxicillin with clavulonic
4. Binding to the tooth surface and periodontal tissues
acid (Augmentin) has shown increased usage in recent
and slow release over a long period.
times. Penicillins other than amoxicillin and amoxicillin-
Tetracyclines can be used by oral route or by local clavulanate potassium have not been evaluated, and their
placement in periodontal therapy. All tetracycline are use in periodontal therapy does not appear to be justified.
absorbed by gut and their efficiency is considerably re- Penicillins may induce allergic reactions and bacterial
duced when taken with milk or milk products. Especially, resistance; up to 10% of patients may be allergic to penicil-
doxycycline has the side effect of esophagitis if drug re- lin. Amoxicillin may be useful in the management of pa-
mains in esophagus for long time. The patient is advised tients with aggressive periodontitis, both in the localized
to swallow it with full glass of water. Tetracycline gets and generalized forms. Augmentin, the combination of
deposited in bone and oral tissues and hence it is not amoxicillin with clavulanate potassium, makes it resistant
used for children in whom dental tissues are developing. to penicillinase enzymes produced by some bacteria. Aug-
Tetracycline is better avoided in patients with renal dys- mentin may be useful in the management of patients with
function, where it should be substituted with doxycycline refractory or localized aggressive periodontitis. Bueno
or minocycline that are excreted through faeces. and coworkers reported that Augmentin arrested alveolar
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bone loss in patients with periodontal disease that was that are being utilized in the field of periodontics like it
refractory to treatment with other antibiotics including is known to penetrate both healthy and diseased peri-
tetracycline, metronidazole, and clindamycin. odontal tissues and also it maintains chemotherapeutic
Recommended dosage for amoxicillin is 500 mg three levels in excess of the maximum inhibitory concentration
times daily for 8 days. Augmentin is administered as (MICs) of the majority of periodontopathogens. It also
625 mg dose (500 mg amoxicillin+ 125 mg clavulonate penetrates fibroblasts and phagocytes and achieves
potassium) two times daily for 8 days. concentrations 100-200 times greater than that of the
extracellular compartment. The azithromycin is actively
transported to sites of inflammation by phagocytes and
Metronidazole then released directly into the sites of inflammation as
Metronidazole belongs to nitroimidazole group and the phagocytes rupture during phagocytosis.
has a high activity against protozoa and anaerobic bacte- Convenient dosing is a major advantage of azithro-
ria. Due to its anaerobic spectrum, it is used commonly in mycin. It is usually prescribed as a 500 mg initial loading
periodontal infection. It is generally taken by oral route dose followed by 250 mg/ day once daily for 4 days. Alter-
that shows good absorption. Metronidazole shows very natively, it can also be administered as 500 mg once daily
high crevicular fluid concentration after 5 days of oral for 3 consecutive days. This schedule provides therapeutic
therapy. It is also excreted in saliva. Susceptible organisms concentrations for 10 days.
have not shown to develop resistance against metronida-
zole and hence justifies its use in periodontics Clindamycin
Combination therapy of metronidazole and amoxicil-
Clindamycin is a lincomycin derivative effective
lin, as shown by various studies, is very effective and
against gram-positive cocci and gram-negative an-
used in many forms of periodontitis. This therapy when
aerobic rods. However it has limited activity against
used in aggressive periodontitis, it achieves almost com-
A.actimycetamcomitans. It has nearly 100% absorption af-
plete eradication of A. actimycetomcomitans and results are
ter oral administration and peak blood levels are reached
sustained for almost 11 months. Apart from A. actimyce-
after 1 h. Clindamycin gets concentrated in polymor-
tomcomitans, when used together amoxicillin and met-
phonuclear leukocytes (PMNs) and in bone. Clindamy-
ronidazole, eliminates almost all the major periodontal
cin can cause potential adverse side effects especially
pathogens and used in chronic periodontitis and necrotiz-
pseudomembranous colitis by Clostridium difficile. Since
ing ulcerative gingivitis.
side effects outweigh its benefits, its use in periodontal
The metronidazole is administered as 400 mg tablets
diseases is limited.
three times daily for 8 days. Combination therapy with
However, various studies have shown that clindamy-
amoxicillin requires the dosage of each drug to be 250 mg
cin may be useful in advanced periodontal infection and
three times daily for 8 days.
refractory cases. The oral dose for clindamycin is 300 mg
three times daily for 8 days adjunct to both nonsurgical
Macro lid es and surgical treatment.
Macrolide inhibits protein synthesis by binding to the
50 S ribosomal subunits of sensitive microorganisms. OTHER ANTIBIOTICS
They can be bacteriostatic or bactericidal, depending on
the concentration of the drug and the nature of the mi- Fluoroquinolones like ciprofloxacin and ofloxacin are
croorganism. In the past, erythromycin and spiramycin bactericidal due to its mode of action on bacterial DNA
were used for the treatment of periodontal diseases with replication. They have excellent activity against a wide
little success. range of gram-negative aerobic and facultative bacteria
Azithromycin, a member of the azalide class of macro- but little activity against obligate gram-negative anaer-
lides, offers potential advantages like it provides excellent obes. Ciprofloxacin is excreted in human breast milk and
and prolonged drug concentrations in tissue and serum. may cross the placenta barrier. Thus, it is contraindicated
This drug has certain differences from erythromycin; un- during lactation and pregnancy. Streptococcus group of
like erythromycin, it is broad-spectrum antibiotic acting species that is believed to be associated with periodontal
against a number of bacteria including gram-negative health is least affected by ciprofloxacin. Thereby, cipro-
anaerobes and in vitro it has shown good activity against floxacin therapy may facilitate the establishment of a
all serotypes of A. actinomycetemcomitans and P. gingivalis. microflora associated with periodontal health. At pres-
The drug presents with few adverse effects and is ent, ciprofloxacin is the only antibiotic in periodontal
believed to be nontoxic. Due to the excretion of this therapy to which all strains of A. actinomycetemcomitans
drug in breast milk, azithromycin is contraindicated in are susceptible and has been used in combination with
nursing mothers. However, it has certain advantages metronidazole.
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Clinical diagnosis
Health
Chronic
periodontitis l l Aggressive, refractory, or
medically related periodontitis
Periodontal therapy including:

• Scaling and root planing
• Oral hygiene maintenance
• Surgical peridontal therapy in Microbial
generalized cases and for regeneration analysis
• Local antibiotic placement in localized
cases
1
microbial analysis
Effective J Ineffective ]----

Maintenance care
J
FIGURE 43.3 Guideline for the use of antimicrobial therapy.
Cephalosporins are frequently used in medicine and odontal abscess and pericoronitis. Another is when the
are resistant to a number of ~-lactamas normally active patient requires pretreatment prophylaxis due to systemic
against penicillin. However, they are generally not used condition such as infective endocarditis (Fig. 43.3).
to treat dental-related infections. The penicillins are su- Antimicrobial Sensitivity Testing
perior to cephalosporins in their rane of action against It is a common practice to prescribe antibiotics em-
periodontopathic bacteria. pirically based on the data of previous studies since the
microbial profile of most periodontal infection is mostly
predictable. However, emergence of resistant microor-
GUIDELINES FOR THE USE OF ganism has been observed against amoxicillin and even
ANTIBIOTIC IN PERIODONTAL DISEASE metronidazole. Hence, when further course of antibiotic
is considered in such refractory cases, it should be based
Adjunctive Use of Mechanical Therapy on antibiotic sensitivity testing. Bacterial cultures for sen-
The antibiotics should always be used as an adjunct sitivity testing should be obtained from each quadrant
to mechanical therapy. When antibiotic is used prior to and that is from deepest area of the pocket. Suppurating
mechanical instrumentation, the effects are minimal since site is not favorable for sampling due to technical issues.
antibiotic penetration into the biofilm is minimal. Hence, These tests are carefully selected, which should be sensi-
even if clinical situation demonstrates minimal or no de- tive and comprehensive.
posits, all the pockets and teeth surface are instrumented
to break the biofilm.
Combination Therapy
In routine clinical scenarios, response of mechanical
therapy is evaluated first before prescribing antibiotics. Currently, an ideal antibiotic (silver bullet) for the
Persistent periodontal pockets, bleeding on probing, sup- treatment of periodontal diseases does not exist. Al-
puration after mechanical therapy in patients who have though oral bacteria are susceptible to many antibiotics,
reasonably good oral hygiene generally requires prescrip- no single antibiotic at concentrations achieved in body
tion of antibiotics along with mechanical therapy. Usually fluids inhibits all putative periodontal pathogens. In-
antibiotic is initiated on the evening after scaling and deed, a combination therapy (e.g., metronidazole plus
root planing or surgical treatment. However, there are amoxicillin) appears more appropriate to predictably
exceptions present to this rule. The first is presence of eliminate periodontal pathogens such as A. actinomy-
signs of acute infection like fever and malaise in peri- cetemcomitans compared with monotherapy. Sufficient
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studies are available to validate the use of antibiotic decreased bleeding tendency and reduce recurrence com-
combination therapy in cases of P. gingivalis- and/ or A. pared to control sites (Figs 43.4 and 43.5).
actinomycetemcomitans-associated aggressive forms of
periodontitis as well as in generalized refractory peri- Minocycline (Arestin)
odontitis patients with evidence of periodontal infection Minocycline is used in two forms in local drug delivery.
despite optimal mechanical therapy. In different studies, 2% minocycline ointment (dento-
Finally, carefully tailored maintenance program for the mycin) has been investigated. Ointment application at
individual patient is of great importance after resolution 1 week or 2 weeks interval has shown improved clinical
of ongoing periodontal infection to sustain the effects of results that sustained for a period of 15 months. However,
the therapy. better results were obtained with 10% minocycline micro-
spheres (arestin). These bioresorbable spheres when ap-
plied subgingivally resulted in significant probing depth
LOCAL DELIVERY OF ANTIBIOTICS IN reduction if used as an adjunct to scaling and root planing.
PERIODONTAL DISEASE
Doxycycline (Atridox)
The concern over the possibility of some individuals Doxycycline is available as two syringe mixing system
experiencing an adverse reaction to systemic agents and the for local drug delivery. One syringe contains the bioresorb-
easy access of the dentogingival surfaces have encouraged able vehicle, poly (DL-lactide), whereas other syringe con-
the development of vehicles to release antimicrobial agents tains doxycycline hyclate. Upon mixing, 10% doxycycline
directly into the periodontal pocket called as local drug de- hyclate gel is produced that is introduced into the pocket.
livery. Many drugs have been tested in clinical trials for local Various clinical trials have shown improved clinical out-
drug delivery. Although many of these drugs have shown come comparing doxycycline hyclate plus scaling and root
beneficial effects, the value of the drug over mechanical planing to scaling and root planing alone.
therapy is shown in most studies. The most significant area
of application for local drug delivery is recurrent lesions that
is addressed by very few studies. The most commonly used
local drug delivery systems are described further.
Tetracyclines
All the drugs of tetracycline group, including tetra-
cycline, doxycycline, and minocycline, have been tested
for local drug delivery. Since tetracycline has property of
adsorption on cemental and tissue surface, better thera-
peutic results can be expected.
Tetracycline hydrochloride (actisite)

Chronic periodontitis cases have been investigated
for local tetracycline use. Mainly tetracycline fibers con- FIGURE 43.4 Tetracycline fibers.
taining 25% tetracycline hydrochloride powder, known
as Actisite, has been used in clinical trials. These fibers
are made up of biologically inert, plastic copolymer that
shows controlled release of tetracycline over a period of
2 weeks. Figures 43.4 and 43.5 show the tetracycline fibers
and its placement in periodontal pocket respectively.
Placement protocol: The site is scaled and root planed
properly. The tetracycline fibers are placed in the pocket
and cyanoacrylate adhesive is applied to secure the fibers.
These fibers are generally left in place for 1-2 weeks and
then removed. The local concentration of tetracycline can
reach up to 1000 mg/mL. However, serum concentration
remains below detection level.
Various studies have demonstrated positive effects of
tetracycline therapy like reduction in pocket depth and
increase in attachment level. The treated sites have shown FIGURE 43.5 Placement of tetracycline fibers in pocket.
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Metronidazole fluid. It was seen that in the sites receiving mechanical

treatment only the average pocket depth reduction was
Selective antimicrobial action against the obligate an-
less than in the treated sites with the chip. Another study
aerobes is one of the main reasons for investigators to use
reported similar results in which chlorhexidine chip was
metronidazole as a potential agent for local antimicrobial
used as an adjunct to scaling and root planing in compari-
therapy. For delivery of metronidazole, various devices son to mechanical treatment alone.
like dialysis tubing, acrylic strips, and poly-OH butyric
acid strips have been tested in the past. However, semi-
solid suspension of 25% metronidazole benzoate in a Povidone- Iodine
mixture of glyceryl mono-oleate and sesame oil (Elyzol
The wide use of povidone-iodine is because of its prop-
Dental Gel, Dumex, Copenhagen, Denmark) is the most
erty of being water soluble and it does not irritate healthy
extensively tested and used device for metronidazole
or diseased oral mucosa with no adverse side effects. The
application. The mode of application for this drug is the
contraindications for its use are the patients with iodine
insertion of a syringe into the pocket, whereby the gel
hypersensitivity and thyroid pathosis, as well as pregnant
increases in viscosity after placement. Evidence suggests
and nursing women in order to protect the infant. For
that 40% of the applied gel remains in place, while 60%
subgingival irrigation, an effective concentration is 10%
was immediately lost into the oral environment. Met-
povidone-iodine applied repeatedly by an endodontic
ronidazole benzoate then gradually disintegrates into
syringe to obtain a contact time of at least 5 min. Usu-
metronidazole thereby delivering high concentrations
ally this is performed upon completion of each session
of the drug to the periodontal pocket for approximately
of scaling and root planing, but in order to reduce the
24 h after placement. It is normally recommended as two
risk of bacteremia this can be done prior to mechanical
applications of the dental gel to be administered 1 week
debridement to particularly in medically compromised
apart. Various clinical trials evaluating the efficacy of lo-
individuals and in patients with severe gingival inflam-
cally applied metronidazole have shown mixed results.
mation. For use in ultrasonic scalers, 10% povidone-iodine
Various studies have also compared the efficacy of
is diluted by mixing 1 part solution with 9 parts or less of
different local drug delivery system. However, clear supe-
water, dependent upon patient acceptance.
riority of one system over other has not been established.
In vitro findings have suggested that short durations of
Moreover, local drug delivery system itself has failed to
povidone-iodine when comes in contact with various peri-
establish the compelling evidence for its use over me-
odontopathic bacteria leads to their killing. Also marked
chanical therapy alone.
anticytomegalovirus activity, a herpes virus implicated in
the pathogenesis of periodontitis, is seen with their use. To
LOCAL DELIVERY OF ANTISEPTICS IN date, emergence of resistant microorganism against povi-
PERIODONTAL POCKET done-iodine has not been reported. In a study by Rosling
et al. it was found that 0.1 % povidone-iodine used as an
An antiseptic is an agent that, applied to living tis- irrigant with ultrasonic debridement resulted in significant
sues, is able to prevent or arrest the growth or action of decrease in probing pocket depth and more gain in probing
microorganisms. Antiseptics have a considerably broader attachment level during the first 12 months posttreatment
spectrum of activity than antibiotics and in contrast to and significant loss of attachment over the entire 13-year
antibiotics, often have multiple intracellular targets that study period than ultrasonic scaling using water irrigation.
reduce the likelihood of resistance development. With the
exception of chlorhexidine, most of the antiseptic agents
have been employed by oral irrigation as an alternative
Sodium Hypochlorite
delivery system for accessing the periodontal pocket. Sodium hypochlorite has broad antimicrobial activ-
ity, rapid bactericidal action and relative nontoxicity at
use concentrations thereby these properties resembles
Chlorhexidine
many of the properties of an ideal antimicrobial agent.
The wide popularity of chlorhexidine gluconate in oral Hypochlorite is lethal to most bacteria, fungi and viruses.
hygiene maintenance makes this antiseptic a valuable Although 0.5% is used in the past, the recommended
candidate for being used into delivery devices. A 2.5 mg concentration of sodium hypochlorite for subgingival
chlorhexidine (PerioChip, Perio Products, Jerusalem, Is- irrigation is 0.1 %. If the solution is not stored in closed
rael) containing biodegradable gelatin chip has been the brown opaque containers, hypochlorite will gradually
most extensively tested delivery device in this category. lose its strength, so that fresh solutions should be pre-
The gelatin chip is placed directly into the periodontal pared every time. Irritation of mucous membranes when
pocket releasing chlorhexidine over a period of 7-10 days. used in high concentrations, bleaching of colored fab-
Chlorhexidine levels, within the pocket, reach an average rics, and corroding effect on some metals are some of the
concentration equivalent to 125 µg/ mL of gingival crevice disadvantages with the use of this solution. However, no
contraindications exist. Kalkwarf et al. recommended the Finally, due to the emergence of resistant flora that is
use of subgingival sodium hypochlorite irrigation in the now a worldwide problem drawing enormous concern,
maintenance phase of periodontal therapy. Perova et al. administration of systemic antibiotics should be a care-
found markedly better regeneration of connective tissue fully weighed decision.
at the gingival base of sites that had received an applica-
tion of 0.1 % hypochlorite for 10 min during periodontal
surgery than in control sites. ANALGESICS IN PERIODONTAL
THERAPY
Other Antiseptic Agents
Pain arising as a result of different diseases or condi-
Stannous fluoride was used in the past. However, com-
tions of the dental, oral, facial, or nearby structures is the
pared with scaling and root planing alone, no supplemen-
main cause for the patient to seek dental advice or treat-
tary microbial benefits have been reported after additional
ment and sometimes after dental treatment also pain may
single or multiple pocket irrigation. Similarly in case of
occur. Hence, it is of utmost importance for the dentists to
hydrogen peroxide, neither repeated professional nor self-
diagnose the source and nature of the pain and be familiar
performed subgingival application can induce additional
with strategies for the management of dental, oral, facial,
microbial shifts compared with saline irrigation, at least
and postoperative pain.
when applied in combination with thorough subgingival
Inflammation of the oral, dental, or associated tissues is
debridement.
the cause for majority of painful dental problems requir-
ing analgesics. This inflammation could be attributed to
LOCAL VERSUS SYSTEMIC DELIVERY various factors such as infection, trauma, and following an
OF ANTIBIOTICS operative procedure. If infection is the cause for pain, local
dental treatment with or without antibiotics is required.
Clear indications for the selection of local or systemic an- If the problem is purely inflammatory in origin, an anti-
tibiotic therapy have still not been established. Various stud- inflammatory drug would be indicated. In some cases,
ies that compare the local versus systemic approach have analgesics may be more appropriate, either alone or in con-
failed to provide direct evidence for favoring one approach junction with other medications. It is important to realize
over other. The view of using local drug delivery for few the fact that analgesics should only be used as adjuncts to
diseased sites is challenged. In one study, combination ap- other treatment as they do not have any therapeutic effect
proach of tetracycline fibers at few diseased sites along with on the underlying disease and they essentially act by block-
full-mouth scaling and root planing versus employment ing the pain sensation being experienced by the patient.
of tetracycline fibers alone at few diseased sites showed For acute pain management, basically two major groups
clear advantage of combination approach. This suggests of drugs are used: the nonnarcotic analgesics (e.g., nonste-
that even when only few sites are having increased pocket roidal anti-inflammatory drugs (NSAIDs) and paracetamol)
depth, full-mouth scaling and root planing is warranted. and the opioids (or narcotics). Aspirin, ibuprofen, and
paracetamol are the most commonly used nonnarcotic an-
Conclusions algesics in dentistry and are available as over-the-counter
Mechanical periodontal therapy is the mainstay for medications. The NSAIDs are very popular and widely
the most clinical situations. However, local or systemic used as they provide good to excellent pain relief. This
antibiotics can enhance its effects in certain scenarios. could be attributed largely due to their combined anti-
Acute periodontal infections and aggressive forms of inflammatory and analgesic action. Paracetamol is not clas-
periodontitis, certainly are benefitted by adjunctive use sified as an NSAID as it has effective analgesic action but
of antimicrobials. Also some patients with compromised has very little anti-inflammatory action. Because opioids
immune function may require use of antibiotics along are powerful analgesics with significant side effect, they are
with mechanical therapy. reserved for severe pain only. Corticosteroids are another
The indications for locally delivered antibiotics include group of drugs that can be used for managing inflamma-
localized recurrent disease or nonresponding sites of fo- tion (and hence pain) but their use in dentistry is limited
cal infection. The success of the treatment largely rests to just a few very specific situations.
on the mechanical debridement prior to antimicrobial
therapy and institution of mechanical plaque control after
therapy. Subgingival irrigation with povidone-iodine or N onsteroidal Anti-inflammatory Drugs
0.1 % sodium hypochlorite along with oral rinsing with
0.12-0.2% chlorhexidine constitute effective, essentially
Mechanisms
safe, and inexpensive antimicrobial therapies that can Arachidonic acid is fundamentally found in the cell
readily be incorporated into the current armamentarium membrane, where it is bound to phospholipids. Physical,
for periodontal treatment. chemical, or mechanical stimuli (tissue damage, hypoxia,
immune processes, etc.) induce arachidonic acid release COX-1, whereas others inhibit COX-1 and COX-2 with
and its metabolization. The metabolites produced (prosta- roughly equal potency. More recently developed drugs
glandins and thromboxanes) are known to exert effects on selectively inhibit COX-2 and therefore do not elicit the
practically all body organs and tissues. Cyclooxygenase GI and antiplatelet side effects common to drugs that
(COX) is the enzyme responsible for the transformation of inhibit COX-1.
arachidonic acid into prostaglandins and thromboxanes Apart from the inhibition of prostaglandin synthesis,
that are generically referred to as eicosanoids because adverse effects that are not unequivocally related to this
their precursors contain 20 carbon atoms; nonsteroidal mechanism include hepatic effects (hepatitis, hepatic ne-
anti-inflammatory drugs are known for inhibition of these crosis, cholestatic jaundice, increased serum aminotrans-
enzymes. The prostaglandins have been known for their ferases), dermal effects (photosensitivities, Stevens-John-
vasodilating action in relation to inflammation thereby son syndrome, toxic epidermal necrolysis, onycholysis),
leading to increased vascular permeability leading to the central nervous system (CNS) effects (headaches, dizzi-
extravasation of fluids and white blood cells - all these ness, tinnitus, deafness, drowsiness, confusion, nervous-
phenomena contributing to inflammation. Therefore, by ness, increased sweating, aseptic meningitis), ocular ef-
inhibiting cyclooxygenase synthesis, an anti-inflammato- fects (toxic amblyopia, retinal disturbances), and certain
ry effect could be achieved. renal effects (acute interstitial nephritis, acute papillary
In anti-inflammatory therapy, basically two different necrosis).
forms (isoenzymes) of cyclooxygenase can be identi-
fied: cyclooxygenase-1 (COX-1) and cyclooxy genase-2 Contraindications and Drug Interactions
(COX-2). Previous history of ulcer disease, advanced age, poor
COX-1 (constitutive isoenzyme) has a role in main- health status, treatment with certain drugs (discussed lat-
taining the general homeostasis and is found in most er), long duration of NSAID therapy, smoking, and heavy
organs and tissues. In contrast, COX-2 is not detected in alcohol use are some of the comorbid factors that increases
tissues and only appears in response to certain stimuli the risk of NSAID-induced GI bleeding. For patients who
(inducible isoenzyme). Considering the hypothesis that have had a hypersensitivity reaction to salicylates or any
selective inhibition of COX-2 would induce the desired other NSAID, the use of NSAIDs is contraindicated. A
anti-inflammatory effects without the undesirable side ef- caution must always be taken while prescribing NSAIDs
fects (particularly at gastric level) associated with COX-1 in patients with renal impairment, heart failure, hyperten-
inhibition, drugs known as "coxibs" or selective COX-2 sion, and edema as they have effect on renal system. Asth-
inhibitors have been developed. ma tics are at particular risk for these reactions. During
pregnancy, NSAIDs should be used only if the potential
Adverse Effects benefit outweighs the risk to the fetus.
Inhibition of prostaglandin synthesis by the NSAIDs A significant number of drug interactions are common
is responsible for a number of toxicities caused by them. to most of the NSAIDs. The use of corticosteroids (long
NSAIDs are known to increase gastric acid secretion and term), other NSAIDs, bisphosphonates, or anticoagu-
also inhibit blood clotting which in turn can lead to GI tox- lants concomitantly along with the NSAIDs increases
icity. Mild reactions, such as heartburn and indigestion, the likelihood of NSAID-induced GI toxicity. Certain
may be decreased by adjusting the dosage, using antacids, drugs like warfarin when coprescribed by NSAIDs in-
or administering the drugs after meals. Sometimes occult crease the risk of GI bleeding by competing for protein
loss of blood from the gastrointestinal (GI) tract and iron binding sites. Agents that cause thrombocytopenia (e.g.,
deficiency anemia are also possible. Prolonged NSAID myelosuppressive antineoplastic drugs) can also in-
therapy can result in more serious toxicity like peptic crease the likelihood that NSAIDs will cause bleeding.
ulceration and, rarely, GI hemorrhage. NSAIDs by decreasing the clearance of methotrexate
Impairment of renal function, causing fluid retention can result in severe hematological and GI toxicity, which
and hypersensitivity reactions, including bronchospasm, does not appear to be a significant problem with low-
aggravation of asthma, urticaria, nasal polyps, and, rarely, dose methotrexate used in the treatment of rheumatoid
anaphylactoid reactions, can also be seen with the use of arthritis; however, higher methotrexate doses used in
NSAIDs. These reactions may occur even in those who the treatment of psoriasis or cancer may produce this
have previously used NSAIDs without any ill effects. toxicity. NSAIDs, when used in conjunction with im-
NSAIDs inhibit uterine contraction and can cause prema- munosuppressive agents, can mask fever and other signs
ture closure of the fetal ductus arteriosus. of infection.
The inhibition of specific COX isoforms amounts NSAIDs by decreasing prostaglandin synthesis in the
to the spectrum of toxicity produced by each NSAID. kidney increases the risk of the nephrotoxicity of agents
The earliest of the NSAIDs inhibits both isoforms such as aminoglycosides, amphotericin B, cidofovir, cis-
of COX. Certain of these drugs are more specific for platin, cyclosporine, foscarnet, ganciclovir, pentamidine,
Tissue injury
C Arachidonic acid
I
x- Nonselective cox
inhibitors ,-----xl
Cox-2
Cox-1 (inducible)
(constitutional)
Selective cox-z
(inhibitors) ~---x
i
Cytoprotective Inflammatory
prostaglandins prostaglandins
FIGURE 43.6
r: Protection of gastric
mucosa
Platelet aggregation
Pathway of inflammation and NSAIDS mechanism.

• lnflammat:J
• Pain
• Fever
1on
and vancomycin. NSAIDs can decrease the renal excretion rhinitis, urticaria, angioedema, asthma, or shock. Those
of drugs such as lithium and also decreases the effec- who already suffer from recurrent urticaria, nasal pol-
tiveness of antihypertensive drugs such as blockers and yps, or asthma are more susceptible.
diuretics. The elderly and those with decreased renal • Reye syndrome: Epidemiological evidence relates aspi-
function are at particular risk for this interaction. Elevated rin use to the development of the rare Reye syndrome
hepatic enzymes and hepatic toxicity can occur with some (encephalopathy, liver injury) in children recovering
drugs (Fig. 43.6). from febrile viral infections (respiratory, varicella).
Acknowledging this, aspirin should not be given to
Salicylates children under 12 years unless specifically indicated,
They are the salts of salicylic acid. Among the salicy- e.g., for juvenile arthritis, and should be avoided in
lates, aspirin and sodium salicylate are by far the most those up to and including 15 years (paracetamol is
commonly used. preferred).
Mode of action: Acetylsalicylic acid is unique among
Doses: 75 -150 mg/day is used to prevent thrombotic
NSAIDs in that it also irreversibly inhibits COX by ac-
vascular occlusion; 300 mg as immediate treatment for
ylating the active site of the enzyme, so preventing the
myocardial infarction; 300-900 mg every 4-6 h for anal-
formation of products including thromboxane, pros-
gesia.
tacyclin, and other prostaglandins, until more COX is
synthesized. Paracetamol (Acetaminophen)
Adverse effects: Gastrointestinal effects are those of
This popular domestic analgesic and antipyretic for
NSAIDs in general. Effects particularly associated with
adults and children can be bought over the counter. Its
aspirin are
analgesic efficacy is equal to that of aspirin, but in thera-
• Salicylism (the symptoms of too high dose) is expressed peutic doses, it has only weak anti-inflammatory effects.
as tinnitus and hearing difficulty, dizziness, headache, Paracetamol inhibits prostaglandin synthesis in the brain,
and confusion. but hardly at all in the periphery; it does not affect platelet
• Allergy: Aspirin is a common cause of allergic or pseu- function. Paracetamol is effective in mild-to-moderate
doallergic symptoms and signs. Patients exhibit severe pain such as headache or dysmenorrhea.
Dose: The oral dose is 0.5-1 g every 4-6 h; maximum Oxicams

daily dose 4 g. The oxicams are as effective as indomethacin, and
Adverse effects: Paracetamol is usually well tolerated by their long half-life allows for once-daily dosing. Piroxi-
the stomach because inhibition of prostaglandin synthesis cam is a nonspecific COX inhibitor with much higher
in the periphery is weak; allergic reactions and skin rash affinity for COX-1 than for COX-2. Due to the selective
sometimes occur. Heavy, long-term daily use may predis- inhibition of COX-1, a large proportion (over 30%) of
pose to chronic renal disease. patients receiving long-term therapy have reported side
effects with this drug. Adverse GI reactions have been
Diclofenac the most frequently reported side effect, but edema,
Rheumatoid arthritis, osteoarthritis, ankylosing spon- dizziness, headache, rash, and changes in hematologi-
dylitis, and dysmenorrhea are some of the conditions cal parameters have also occurred in 1-6% of patients.
where the use of diclofenac is indicated and topically If the recommended dosage is exceeded or if aspirin is
it is used for the treatment of ocular inflammation and concurrently prescribed with this drug, it can cause seri-
actinic keratosis. Equal selectivity for COX-1 and COX-2 ous GI bleeding, ulceration, and perforation, particularly
has been shown by diclofenac with their most common in the elderly.
adverse reactions to be GI disturbances and headache. In Dose: Single dose of 20-40 mg/ day.
15% of patients a reversible elevation of serum transami-
nases occurs. Recently introduced drug in this category, meloxicam,
Dose: 75-100 mg orally, daily in two to three divided is used for the treatment of osteoarthritis, rheumatoid
doses after food and 75 mg by deep IM injection once or arthritis, and certain acute conditions. Although reported
twice daily. to be a selective COX-2 inhibitor, meloxicam is sometimes
considerably less selective than celecoxib or rofecoxib.
Its adverse effect resembles to those of piroxicam and
Ibuprofen other NSAIDs; however, the frequency of GI side effects
Ibuprofen is used as an analgesic and antipyretic as is lower for meloxicam than for piroxicam and several
well as a treatment for rheumatoid arthritis and degen- other NSAIDs.
erative joint disease. Mechanism of action of ibuprofen
includes inhibition of COX-1 and COX-2 equally. The ad-
verse effects include GI side effects, the incidence of which Selective COX-2 Inhibitors
is lower than that with indomethacin, visual changes, Highly selective COX-2 inhibitors are Celecoxib,
and cross-sensitivity to aspirin. Like aspirin, it decreases Rofecoxib, and Etoricoxib. Because of their selectivity,
platelet aggregation, but the duration is shorter and the less erosion of the gastro-intestinal mucosa and less
effect is quantitatively lower. Ibuprofen prolongs bleeding inhibition of platelet aggregation is caused by them
times toward high normal value and should be used with in comparison to non-selective COX inhibitors. Short-
caution in patients who have coagulation deficits or are term (6 months to a year) clinical trials have shown
receiving anticoagulant therapy. that they produce less GI toxicity than nonselective
Presentations NSAIDs. However, serious GI bleeding and ulceration
A 200,400, and 600 mg tablet. have occurred in patients taking these drugs, and long-
As a suspension (Ibuprofen 100 mg/5 mL). term prospective studies of their safety have yet to be
Effervescent granules (Ibuprofen 600 mg). completed. Like the nonselective NSAIDs, the selective
COX-2 inhibitors can produce renal side effects such as
Dose: Analgesia for adults, Ibuprofen 1.2-1.8 g daily in hypertension and edema.
divided doses. For children, 20-40 mg/kg. Dose
Contraindications: A history of allergy to aspirin or
any other NSAID is a contraindication for the use of Celecoxib: 200 mg/12-24 h
ibuprofen. The drug should not be prescribed to asth- Rofecoxib: 25-50 mg/24 h
matics (can precipitate bronchoconstriction) or patients Etoricoxib: 30-60 mg/ day
with a history of angioedema and urticaria. Patients with
active peptic ulceration (ibuprofen is ulcerogenic) or
patients with hemorrhagic disorders, as it affects plate- Decision Making in Pain Management
let aggregation are also contraindications for the use The primary factor governing the choice of a non-
of this drug. Repeated use of the ibuprofen should be steroidal anti-inflammatory drug should be based on
limited in patients who exhibit renal, cardiac, or hepatic its efficacy and adverse effect. One should always start
impairment, since the drug can result in a deterioration the therapy with most efficacious and least toxic agent.
in renal function. If pain is suspected to be persistent over a long period
of time, it may be logical to choose an agent with a long drug are gastrointestinal, respiratory, and skin aller-
half-life and prolonged clinical effect. Hence, ibuprofen gic reactions which appear to be precipitated by the
should be used as a first-line agent for dental pain of inhibition of cyclooxygenase-1. Of particular interest
short duration. is that cyclooxygenase-2 inhibitors have been reported
For those at high risk of developing adverse gastro- to be well tolerated by patients who are intolerant of
intestinal effects, mucosa-protective agents like protein traditional nonsteroidal anti-inflammatory drugs. Some
pump inhibitors (PPI) should be added as there are chanc- authors have suggested that cyclooxygenase-2 inhibitors
es of adverse events even in short-term use. may safely be used by patients with traditional nonste-
Opioids along with paracetamol can be used to roidal anti-inflammatory drug.
increase the efficacy whenever nonsteroidal anti- An algorithm for decision making for dental pain is
inflammatory drugs are not appropriate. Opioids, how- proposed in Fig. 43.7. As the inflammatory process sub-
ever, should not be used as a sole agent in view of the sides, postoperative pain following dental procedures
high frequency of adverse events and also due to their should also decrease over the course of 3-5 days. If the
lack of efficacy in dental pain (only indicated when both pain persists even after continuous analgesic therapy it
nonsteroidal anti-inflammatory drugs and acetamino- should be evaluated thoroughly to determine the exact
phen are contraindicated). Most of the traditional ad- cause of the pain, e.g., infection or misdiagnosis, and
verse effects induced by nonsteroidal anti-inflammatory treated on the basis of the diagnosis (Fig. 43.7).
Mild to moderate dental pain
Paracetamol upto
4g/day
Persistent pain
r r
Risk of No risk of
NSAIDs not
gastrointestinal gastrointestinal
suitable
bleeding bleeding
r
Ibuprofen
1.2 g/day plus PPI
cotherapy
Ibuprofen
2.4 g/day
l Cardiac, renal,
Persistent pain Allergic to NSAIDs hepatic
__j impairment
Persistent pain
Diclofenac,
ketorolac, or
I Unable to
tolerate PPI \....__
oxicams
Persistent pain Opioids with or COX-2 inhibitors Opioids, other

Diclofenac, COX-2 inhibitors without after allergy combinations
ketorolac, or in patients with COX-2 inhibitors paracetamol testing analgesics
oxicams with PPI no cardiovascular in patients with
cotherapy risk factors no cardiovascular
risk factors
Persistent pain
Persistent pain
NSAIDs + Paracetamol + PPI COX-2 inhibitors + Paracetamol
FIGURE 43. 7 Decision-making algorithm for selection of analgesics.

KEY POINTS
• Bacteriostatic antibiotics inhibit the growth and multipli- • Combinations of metronidazole with amoxicillin, aug-
cation of microorganisms, whereas bactericidal antibiot- mentin, or ciprofloxacin have been used successfully
ics kill microorganisms. While bacteriostatic antibiotics in the treatment of advanced A. actinomycetemcomitans-
alter the metabolic pathways or synthesis of cellular associated periodontitis.
components in microorganisms, bactericidal drugs in- • Combination therapy (e.g., metronidazole plus amoxicil-
terfere with the synthesis or function of the cell wall, cell lin) appears more appropriate to predictably eliminate
membrane, or both. periodontal pathogens such as A. actinomycetemcomitans
• When two bactericidal antibiotics are given together, compared with monotherapy.
they may exert a greater effect than when each is given • Actisite periodontal fiber is a monolithic thread of a
alone. Advantages of this combination drug therapy biologically inert, nonresorbable plastic copolymer (eth-
are, wider spectrum of activity, reduced emergence of ylene and vinyl acetate) containing 25% tetracycline
bacterial resistance, administration of drugs at a lower hydrochloride powder.
concentration, due to the synergistic activity of two • A degradable gelatin chip containing 2.5 mg chlorhexi-
complementary agents, reduction in the toxicity, and dine is available as PerioChip.
side effects of high-level dosing.
QUESTIONS 3. Mombelli A. Chemotherapy of periodontal diseases. In: Lindhe

J, Karring T, Lang NP, editors. Clinical Periodontology and Implant
Dentistry. Copenhagen: Munksgaard; 2002.
1. Write short notes on metronidazole. 4. Rooney J, et al. Adjunctive effect to non surgical therapy of systemic
2. Write a note on the use of tetracyclines in periodontitis. metronidazole and amoxicillin alone or combined-a placebo con-
3. What are the advantages of local drug delivery? trolled study. J Clin Periodontal 2002;29:242-50.
4. What are the indications of antibiotic prophylaxis? 5. Samaranayake LP, Johnson N. Guidelines for the use of antimicro-
bial agents to minimize the development of resistance. Int Dent J
1999;49:189-95.
Suggested readings 6. Samaranayake LP. Essential Microbiology for Dentistry. 2nd ed. Edin-
burgh: Churchill Livingstone; 2002.
1. Dahlene G, Wikstorm M, Renvert S. Treatment of periodontal disease 7. Van Winkelhoff AJ, Rams TE, Slots J. Systemic antibiotic therapy in
based on periodontal diagnosis. A 5 year follow up on individual periodontics. Periodontology 2000.1996;10:45-78.
patterns. J Periodontol 1996;67:879-87. 8. Slots J. Selection of antimicrobial agents in periodontal therapy.
2. Hererra D, et al. A systemic review on the effect of system- J Periodontal Res 2002;37:389-98.
ic antimicrobials as an adjunct to scaling and root planing
in periodontitis patients. J Clin Periodontal 2002;29(Suppl 3):
136-59.
CHAPTER
44
Host Modulation
CHAPTER OVERVIEW
Pathogenesis of periodontal disease is complex and un- Modifying the host response will help in evading several
folding with involvement of several processes. A complex other risk factors like environmental and genetic, which
microbial plaque biofilm initiates the inflammatory process, modify the periodontal disease.
which triggers an immunoinflammatory response, and ulti- Host response begins with the acute inflammatory re-
mately results in destruction of connective tissue and the bone. sponse and ends up with the regulation and resolution
Initiator of this inflammatory response, plaque biofilm, phase. Host itself has several in-built mechanisms to combat
can be easily controlled. Various mechanical and chemical the immunoinflammatory destruction of the connective tis-
plaque control approaches have been established since long sue and the bone, but these often may not be sufficient in
and routinely followed in the treatment of periodontal disease. the presence of bacterial load and/ or other host defective
However, the periodontal destruction related immunoinflam- mechanism. In such situation, externally given or modu-
matory process is not easy to control. Altering or modifying lated response by therapeutic agents may help in com-
the immunoinflammatory response is the right step in pre- bating the immunoinflammatory response to prevent the
venting the destruction of the connective tissue and the bone. periodontal destruction.
HOST IMMUNOINFLAMMATORY and stimulation of apoptosis of matrix-producing cells.

RESPONSE RELATED TO PERIODONTAL The activity of IL-1 and TNF are further aggravated by
DESTRUCTION lL-6, lL-17, lL-18, and MCP-1.
Polymorphonuclear leukocytes (PMNs) and macro-

phage, which are recruited to the site of inflammation,
Prostaglandins
produce several inflammatory mediators and related Major source of prostaglandins are activated macro-
products. They are proinflammatory cytokines and oth- phages, fibroblasts, and platelets. Arachidonic acid ac-
er mediators. Proinflammatory cytokines are IL-1, IL-6, tivation, through the cyclo-oxygenase pathway (COX-1
IL-12, TNF-a, and TNF-~. Among the other major and COX-2), results in the production of thromboxane,
mediators of bone destruction are prostaglandins and prostaglandins, and prostacyclins. Lipooxygenase path-
leukotrienes. way results in the production of leukotrienes. There is
also the production of lipoxins (A4 and B4) and 15-epi-
lipoxins. All these comprise primary pathway of alveolar
IL,1 and TNF bone destruction, to begin with vasodilation, increasing
IL-1 (a and B) and TNF (a and B) are mainly released capillary permeability, and bone destruction.
and produced by monocytes/macrophages, PMNs, fibro-
blasts, epithelial cells, endothelial cells, and osteoblasts.
Matrix Metalloproteinases
They induce several immunoinflammatory reactions;
stimulate adhesion molecules, chemokine expression, and Matrix metalloproteinases (MMPs) are a family of pro-
production of PGE2; enhance osteoclast formation and its teolytic enzymes involved in the physiological degra-
activity; and induce matrix metalloproteinase expression dation of extracellular matrix and basement membrane
(MMP-1 to MMP-17). Among the important MMPs are piroxicam, and ketoprofen. Cox-2 inhibitors also have
MMP-1, MMP-8, MMP-9, and MMP-13. They form a key been tried with successful results. Long-term evaluation
role in the degradation of collagen, elastin, proteoglycans, for 18 months demonstrated significantly lower bone
and laminin. loss rate.
Other stimulators of bone resorption are parathyroid NSAIDs act by inhibiting the prostaglandins and other
hormone (PTH), macrophage colony stimulating factor inflammatory mediators and thus help in arresting peri-
(M-CSF), receptor activator of NFKb (RANK), RANK odontal bone destruction.
ligand, and 1-25 dihydroxyvitamin 03. There are several
inhibitors too, to combat the stimulators of bone resorp-
tion; they are interferon gamma (IFN--y), osteoprotegerin, Why NSAIDs Are Commonly Not Used?
estrogens, androgens, calcitonin, and IL-1 ra (receptor
antagonist). • Systemic administration of these drugs has been shown
Modulation of these host responses is possible and to cause gastric irritation and bleeding tendency.
beneficial. Initial studies, which were done on the rheu- • Periodontal disease progression returned upon with-
matoid arthritis patients who were on long-term NSAIDs, drawal of this agent, and the drug did not provide any
showed a decrease in pocket depth and a gain in attach- residual effect. However, recent short-term studies of
ment level. adjunctive use of flurbiprofen 100 mg for 10 days, in
The concept of host modulation was first introduced by smokers and nonsmokers, showed an adjunctive ben-
William (1990) and Golub et al (1992). William introduced efit of this agent with the smokers.
the concept of NSAIDs, and host modulation with tetra- To overcome the systemic unwanted effects, topical
cycline and chemically modified analogs was introduced administration of these medications was tried. Few of
by Golub et al. these NSAIDs were lipophilic and well observed into
"Modulation" refers to the alteration of function or the gingival tissues. Several NSAIDs like acetylsalicylic
status of something in response to a stimulus or an altered acid rinse (0.3%), ketorolac-trimethamine rinse (0.1 %),
physical or chemical environment. ketoprofen dentifrice, flurbiprofen 1 % (w /w) tooth paste,
"Host modulation" concept in periodontics is the treat- 0.3% gel, and 0.3% local drug delivery resulted in early
ment concept that aims to reduce tissue destruction and resolution of gingival inflammation. However, long-term
even regeneration of the periodontium by modifying studies are warranted. All these are future common modali-
or downregulating the destructive aspects of the host ties of host modulation.
response and upregulating protective or regenerative
process.
Normal defensive immunoinflammatory reaction is Chemically Modified Tetracyclines (CMTs)
essential to fight against the pathogenic bacteria, but ame-
liorating the excessively elevated inflammatory process The advantage of the chemical/molecular structure
to enhance the opportunities for the wound healing is the of tetracycline is that antimicrobial and anticollagenase
host modulation therapy. properties can be separated and only anticollagenous
Even though a better understanding of the molecular part can be utilized in the treatment of host modulation,
aspects of pathogenesis of periodontal destruction helps to reduce the effect of collagenase, without antimicrobial
us in designing the new strategies in host modulation, side effects.
basically there are three potential approaches to the host Tetracycline can be modified by removing the di-
modulation: ethyl amino group to retain anticollagenase. Golub et al
synthesized ten different analogs of CMTs (CMT-1 to
• Blocking prostaglandins and proinflammatory cyto- CMT-10); among these CMT-1 and CMT-3 are commonly
kines with anti-inflammatory drugs used.
• Inhibiting MMPs with antiproteinases CMTs are found to be useful in controlling host col-
• Inhibiting activation of osteoclast with sparing agents.
lagenase, especially in diabetic-induced rats, at the dose
• Other host modifiers.
of 10 mg per day for 4 weeks. There was significantly less
periodontal destruction.
NSAIDs Mechanism of Action of Chemically Modified

Inhibition of periodontal disease progression utilizing Tetracyclines (CMTs)
NSAID was first demonstrated with indomethacin in a • Inhibition of production of epithelial-derived MMPs
ligature-induced canine periodontitis model. There are by inhibiting cellular expression and synthesis.
a series of experiments done with different NSAIDs like • Inhibits or chelates the calcium ions that MMPs re-
flurbiprofen, ibuprofen, naproxen, meclofenamic acid, quires for their action - carbonyl oxygen and hydroxyl
C H A PT ER 44 H O ST M O D U LAT IO N 395
group at carbon 11 and carbon 12, respectively, bind to nate molecule that is chemically stable and resists
Ca and Zn on collagenase, which deactivates it. It also hydrolysis via pyrophosphate and alkaline phosphatase.
shows inhibiting effect on the gelatinase. Bisphosphonates bind to HA crystals and prevent their
• Inhibit already active MMPs. dissolution. They also increase osteoblast differentiation.
• Scavenges reactive oxygen species. Decreased adhesion and recruitment of osteoclasts with
• Modulates the osteoclast functions. increased osteoclast apoptosis result in decreased depth
of bone resorption sites. These cellular-level changes de-
CMTs are still not available for human use. Further,
crease number of new bone multicellular units and bone
the development of recombinant tissue inhibitor of
turnover due to decrease bone resorption and net positive
matrix metalloproteinase (TIMP) and synthetic MMP
bone balance. Thus this bone-sparing agents are exten-
inhibitors offers promising therapeutic approaches for
sively used in the management of osteoporosis and other
the treatment of conditions characterized by excessive
resorptive conditions
MMP activity.
Three generations of bisphosphonates are available,
including etidronate, alendronate, and risedronate.
Subantimicrobial Dose Doxycycline ( SDD) Bisphosphonates used in controlled clinical trials dem-
onstrated a significant decrease in the alveolar bone loss
Subantimicrobial dose doxycycline is approved by and improvement in alveolar bone height. However, more
the US Food and Drug Administration, the UK Medicine long-term evaluation studies are awaited to apply these
and Healthcare Products Regulatory Agency, and similar agents in regular use.
agencies throughout the world. It is available under the Caution about bisphosphonate use: Avascular necrosis of
trade name PERIOSTAT (Collagenax Pharmaceuticals In., the jaw, particularly the mandible, with increased risk
Newtown, PA). of bone necrosis following dental extraction has been
PERIOSTAT is a 20 mg dose doxycycline hyclate. At reported. This has been termed as "bisphosphonate as-
this subantimicrobial dose it acts as host response modu- sociated osteoradionecrosis."
lator. It inhibits the activity of MMPs by a variety of syn-
ergistic mechanisms independent of any antimicrobial
properties. Combination Therapy
Mechanism of action involves direct inhibition of ac- PERIOSTAT (20 mg twice daily), flurbiprofen 50 mg
tive MMPs by cation chelation dependent on Ca and Zn four times daily, or combination of these drugs for
binding properties. It is more effective in inhibiting the 3 weeks has shown reduction in the collagenase and ge-
neutrophil collagenase than the fibroblast collagenase. It latinase activity.
inhibits oxidative activation of latent collagenase; it also CMT-8 combination with bisphosphonates in the ex-
downregulates expression of key inflammatory cytokines perimental periodontitis model in rats has shown success-
(IL-1, IL-6, and TNF-a) and PGE2; it scavenges and inhib- ful reduction in MMP-8 and MMP-9.
its production of reactive oxygen species produced by Subantimicrobial dose of doxycycline(SDD) com-
the neutrophils. It indirectly protects the al-proteinase bined with the local drug delivery doxycycline gel (10%
inhibitor, stimulates fibroblast collagen production, re- Atridox) placed in a pocket more than 5 mm with root
duces osteoclast activity and bone resorption, and also surface instrumentation resulted in significant clinical
inhibits osteoclast MMPs. improvement.
Doxycycline hyclate, 20 mg taken twice daily for
3-9 months, acts as an adjunct to root surface debridement
in the treatment of periodontitis. In a larger clinical trial Future Host Modulation Therapy
for 9 months, attachment gain and probing depth reduc- Several molecular agents, mediators of inflammation,
tions were statistically significantly greater in patients and end products have been involved in the pathogen-
treated with PERIOSTAT than with placebo. esis of periodontal disease. Adjunctive use of agents
to block these molecules will be helpful in resolving
inflammation.
Bone Sparing Agents - Bisphosphonates
Bisphosphonates represent a class of chemical com- Lipoxins, Resolvins, and Protectins as Novel
pounds structurally related to pyrophosphates, which
Proresolving Lipid Mediators
regulate mineralization by binding to hydroxyapatite
crystals. They are extensively used in the management of Resolution of inflammation is equally important as
osteoporosis and other resorption conditions. preventing the active inflammation. If resolution takes
The replacement of the oxygen atom with a car- longer time than the normal, it will cause increased peri-
bon atom results in the formation of a bisphospho- odontal destruction.
Lipoxins and other related agents mentioned here are ANTIOXIDANTS

derived from the omega-3 fatty acids, which stimulate the
resolution of inflammation through several mechanisms, Oxygen is utilized by all mammalian cells to produce
including preventing neutrophil penetration, phagocytizing energy. Metabolic products of utilization of oxygen is
apoptotic neutrophils to clear the lesions, and enhancing reactive oxygen species (ROS). They are essential for the
clearance of inflammation within the lesion to promote re- normal function and metabolism of the cells. However,
generation. Lipoxins are arachidonic acid-derived bioactive during its process, it is also capable of initiating lipid
lipids that are formed by interaction between lipoxygenase peroxidation and damaging cell membrane and DNA.
pathways and appear to play an important role in down- To combat the untoward actions of this ROS, there are
regulating neutrophil response to inflammation. many antioxidants that are released. Normally, there is a
continuous balance between ROS activity and antioxidant
defense capacity. However, when there is a reduction in
Pluronic Polyols the antioxidant defense or increase in ROS production or
These surface active agents have been found to be ef- activity, oxidative stress results, leading to potential dam-
fective in tissue repair and wound healing. They have age of the tissue that it surrounds. Excessive production
positive effect on fibroblast growth in culture and also of ROS has been associated with pathogenesis of many
enhance the burn wound healing. inflammatory diseases, including periodontitis.
Antioxidants can be classified as:
• Endogenous antioxidants: These are synthesized by the
Probiotics
body, including catalase, superoxide dismutase, and
Emerging therapeutic models where utilization of live glutathione peroxidase.
microorganisms (lactobacilli and bifidobacteria) in ad- • Exogenous antioxidants: These are obtained through the
equate amounts confers health benefits in the host are diet, such as carotenoids, ascorbic acid, and tocopher-
the best example. ols. Utilization of these exogenous antioxidants may
Host response is a double-edged sword. Immuno- be useful for the management of periodontitis. Many
inflammatory reaction is essential for wound healing; clinical intervention studies are in progress.
however, excess inflammatory reaction results in host- • Other future agents: Anti-integrins, inhibition of iNOS
mediated periodontal destruction. Modulation of these (nitric oxide) with mercaptor alkyl guanidines, receptor
host responses at an appropriate step may help in arrest- antagonists are the other agents may be utilized in
ing the periodontal disease. future.
KEY POINTS
• Host response is a double-edged sword. Modulation of gistic mechanisms independent of any antimicrobial
these host responses at an appropriate step may help in properties.
arresting periodontal disease. • NSAIDs act by inhibiting the prostaglandins and other
• Bisphosphonates used in controlled clinical trials inflammatory mediators of periodotal bone destruction,
demonstrated a significant decrease in the alveolar bone thus help in arresting the bone destruction.
loss and improvement in alveolar bone height. • Antioxidants are required to balance the unwanted
• PETIOSTAT is a 20 mg dose doxycycline hyclate. It effects of ROS.
inhibits the activity of MMPs by a variety of syner-

1. Genco JR. Clinical innovations in managing periodontal diseases.
1. What are chemically modified tetracyclines? J Periodontal 2008;79(8 Suppl):1609-11.
2. State the role of NSAIDs in the treatment of periodontal 2. Giannobellie WV. Host response therapeutics for periodontal disease.
disease. J Periodontal 2008;79:1592-600.
3. Salvi GE, Lang NP. Host response modulation in the management
3. Describe bisphosphonates and their use in the treat-
of periodontal disease. J Clin Peridontal 2005;32:108-29.
ment of periodontitis. 4. Van dyke TE. The management of inflammation in periodontal
disease. J Periodontol 2008;79:1601-8.
CHAPTER
45
Periodontal Splints
CHAPTER OVERVIEW
When teeth are loosened by acute trauma or periodontal prevent or cure periodontal disease. The prime objective of
disturbances, stabilization by splinting can become a valuable temporary or long-term splinting is to provide rest to the
adjunct before, during, and after corrective therapy. A splint affected structures by redistributing functional and parafunc-
is a device to immobilize teeth. Splinting, however, does not tional forces, reducing mainly the horizontal forces.
DEFINITION 6. Psychologic well-being: Stabilization by splinting and

restoration not only improves function, but can also
A splint is an appliance for the immobilization or sta- restore a sense of solid-feeling dentition as well as of
bilization of injured or diseased parts. comfort and good looks.
A periodontal splint is an appliance used for maintain-
ing or stabilizing mobile teeth in their functional position.
CHARACTERISTICS
OF AN IDEAL SPLINT
RATIONALE OF SPLINTING
1. Easy and economically prepared
1. Rest: Immobilization permits undisturbed healing. 2. Rigid, durable, and stable
Thus occlusal rest provided by splint therapy helps 3. Easily removed and replaced
to eliminate or at least neutralize some of the adverse 4. Self-cleansing in design and easily maintainable by
occlusal factors that compound the effects of an already usual home care procedure
existing periodontitis. 5. Esthetically acceptable and well adapted in fit
2. Redirection offorces: Axial forces are least traumatic to 6. Nonirritating to adjacent dental or gingival tissues.
the periodontium, thus splinting leads to redirection
of forces in an axial direction over all teeth included in
the splint. INDICATIONS
3. Redistribution of forces: This is done to distribute the
forces over a number of teeth and thereby prevent ex- 1. Stabilize moderate to advanced tooth mobility that
cessive forces on the mobile teeth. Thus jiggling move- cannot be treated by any other means.
ments, which can contribute to further bone loss in an 2. Stabilize teeth in secondary occlusal trauma.
existing periodontitis, can be prevented. 3. Stabilize teeth when increased tooth mobility interferes
4. Restoration offunctional stability: Sometimes when the with normal masticatory function and comfort of the
missing teeth are replaced in a splint, it not only re- patient.
stores a functional occlusion but stabilizes the remain- 4. Prevent tipping or drifting of teeth.
ing mobile abutment teeth. 5. Stabilize teeth following orthodontic movement.
5. Maintenance of arch integrity: The proximal contacts are 6. Create adequate stability when replacing missing teeth.
restored by a splint that may prevent food impaction 7. Stabilize teeth following acute trauma.
and further breakdown of periodontal tissues. 8. Prevent extrusion of unopposed tooth.
CONTRAINDICATIONS 6. Lack of physiological tooth movement of splinted

teeth, thus loss of functional adaptability of the peri-
1. There is moderate to severe tooth mobility in presence odontium.
of periodontal inflammation.
2. Prior occlusal adjustment has not been done on teeth
with occlusal interference and prior occlusal trauma.
CLASSIFICATION
3. There is insufficient number of nonmobile teeth to
adequately stabilize the mobile teeth.
Periodontal splints can be classified on the basis of the
4. Inadequate oral hygiene is present.
duration as:
1. Temporary splints: Utilized on a short-term basis to sta-
BASIC PRINCIPLES OF SPLINTING bilize teeth during periodontal treatment.
2. Provisional splints: Utilized for several months to sev-
1. Splinting should be considered only after completion eral years for diagnostic purpose.
of elimination of local factors contributing to inflam- 3. Permanent splints: Utilized indefinitely and can be ei-
mation. ther fixed or removable.
2. Occlusal adjustment should be done prior to splinting.
They can also be classified based on the method of
The exception to this is when the remaining teeth are
splinting:
so mobile that they have to be stabilized to facilitate
occlusal correction. 1. Extracoronal splints: If the coronal portions of the teeth
3. A sufficient number of nonmobile teeth should be in- are in relatively good condition, extracoronal splinting
cluded in a splint. The support of posterior teeth is is used, e.g., interdental ligature, acrylic splints, fiber
often necessary when anterior segments are mobile. mesh reinforced composite splint (Fig. 45.1).
4. If, in case of occlusal trauma associated with severe 2. Intracoronal splinting: If, however, the teeth require
bone loss, all the teeth demonstrate hypermobility, extensive restorative therapy, intracoronal splinting is
cross-arch splinting is beneficial as the pattern of mo- preferred, e.g., wire and resin splint (Fig. 45.2), chrome
bility of some teeth is in a buccolingual direction and cobalt bars with resin.
others in a mesiodistal direction. With splinting, a
Teeth can be splinted in Phase I therapy before peri-
group of single-rooted teeth in effect becomes a multi-
odontal surgery, utilizing temporary or provisional
rooted teeth.
splints. Permanent splints utilizing cast restorations may
5. Splinting should not impede normal functions like
be placed as part of the restorative phase of therapy.
phonetics, mastication, or oral hygiene maintenance
of the patient.
Temporary Splint
6. It should not irritate the gingival tissues.
7. It should be esthetically acceptable. Temporary splinting of mobile teeth is often of value
as a means of stabilization before, during, and after peri-
odontal therapy. It aids in determining whether teeth with
DISADVANTAGES OF SPLINTING a borderline prognosis will respond to therapy. It may
or may not lead to other types of splinting. Temporary
1. Quality control cannot be compromised on any part splints are used in the following cases:
of the splint, as a weak portion of a splint makes the
1. Mobility due to orthodontic repositioning or accidental
whole splint weak. It is similar to a weak link that can
trauma of a reversible kind.
weaken a whole chain.
2. Following periodontal therapy in order to achieve
2. Due to the rigidity of the splint, it can act as a lever;
uneventful healing and regeneration.
hence, forces applied to some teeth in the splint can be
3. To determine the prognosis of questionable tooth.
greater than before the splinting procedure.
4. When extensive restorative methods cannot be under-
3. If one tooth in a splint is in a traumatic occlusal rela-
taken due to economic reasons, poor general health,
tionship, the periodontal tissues of the remaining teeth
poor prognosis of all remaining teeth, or if the patient
may also be affected.
cannot emotionally accept lengthy procedures of per-
4. Incidence of caries formation is increased.
manent fixation.
5. Self-performed plaque-control methods may be diffi-
cult, which may enhance gingival inflammation lead- Temporary splints may be used for a period of
ing to further periodontal breakdown. Thus splints 2-6 months or more but on a short-term basis until the
demand an extra measure of motivation and diligence mobility has reduced; the teeth can function without the
for patients. splint or until it requires a permanent stabilization.
CHA PTER 45 PERIO DONTAL SPLINTS 399
(8)
FIGURE 45.1 Fiber mesh reinforced composite splint. (A) Isolation and acid etching. (B) Bonding agent applied on fiber mesh: light curing.
(C) Outer layer of composite is cured.
Provisional Splints 4. It also affords the opportunity to determine the correct

esthetic, phonetic, and functional occlusal qualities
It serves as a transitional fixed appliance until the per- necessary for each individual patient.
manent splint is inserted. It plays a key role in the manage-
ment of borderline cases where the result of periodontal
and occlusal therapy is unpredictable. It also plays a role Permanent Splints
in patients requiring periodontal and restorative therapy. It
Permanent splints are indicated in dentitions that
allows the observation of the response of treatment before
cannot maintain final stability after periodontal and
designing a more permanent form of stabilization. These
restorative treatment. In certain cases retention of mo-
splints are used for a period of 6-12 months or more.
bile teeth may be important from both anesthetic and
Objectives:
a functional point of view. A permanent splint may be
1. It protects the prepared tooth until final restorations given in such cases wherein the pretreatment dilem-
are inserted. mas of questionable teeth would have been solved and
2. It reduces pathological mobility. a more predictable treatment plan can be formulated.
3. It protects the dental pulp from irritation following For example, cast metal resin-bonded FPO, swing-lock
tooth preparation. denture, endodontic splints.
(A)
(B)
FIGURE 45.2 Wire reinforced composite splint. (A) Preparation of tooth surface (lingual groove): stainless steel-wire measured. (B) Composite
applied and cured over the wire.
KEY POINTS
• A splint is an appliance for the immobilization or stabi- • On the basis of method of splinting, they are classified
lization of injured or diseased parts. into extracoronal and intracoronal.
• Periodontal splints can be classified on the basis of the
duration as: temporary splints, provisional splints, per-
manent splints.

1. Grant DA, Stern IB, Listgarten MA. Periodontics. 6th ed. St. Louis:
1. Define and classify periodontal splints. Mosby; 1988 p 1056.
2. What are the indications and contraindications of 2. Goldman HM, Cohen DW. Periodontal Therapy. St. Louis: Mosby;
splints? 1980 p 535.
3. What is the rationale of splinting?
CHAPTER
46
General Principles of Periodontal Surgery
CHAPTER OVERVIEW
Surgical procedures are usually performed in dental of- and practically for the surgery. This chapter covers the
fice. In some cases hospital periodontal surgery is preferred. general considerations that are common to all periodontal
The patient should be prepared medically, psychologically, surgical procedures.
OBJECTIVES OF SURGICAL Finally, the fact that proper plaque control, maintained by
TREATMENT the patient, is a decisive factor for a good prognosis must
be considered prior to the initiation of surgery.
Traditionally, pocket elimination has been the main ob- The main objective of periodontal surgery is to con-
jective of periodontal therapy. The removal of the pocket tribute to the long-term preservation of the periodontium
by surgical means has served two purposes: by facilitating plaque removal and plaque control, and
periodontal surgery can serve this purpose by:
1. The pocket, which established an environment con-
ducive to progression of periodontal disease, was • creating accessibility for proper professional scaling
eliminated. and root planing;
2. The root surface was made accessible for scaling and, • establishing a gingival morphology that facilitates the
after healing, for self-performed tooth cleaning. patient's self-performed plaque control;
• regeneration of periodontal attachment lost due to
During recent years, our understanding of the patho-
destructive disease.
genesis of periodontal disease, biology, and the healing
capacity of the periodontium has markedly increased.
This new information has thus formed the basis for a
more differentiated understanding of the role played by
INDICATIONS FOR SURGICAL
periodontal surgery in the preservation of teeth.
TREATMENT
In the past, increased pocket depth was the main indi-
cation for periodontal surgery. However, pocket depth is
Impaired Access for Scaling and Root Planing
no longer as unequivocal a concept as it used to be. The
probable depth, i.e., the distance from the gingival margin There are a number of difficulties such as:
to the point where further periodontal probe penetration
1. Increasing depth of the periodontal pockets
is stopped by tissue resistance may only rarely correspond
2. Increasing width of the tooth surfaces
to the "true" depth of the pocket. Furthermore, regard-
3. The presence of root fissures, root concavities, furca-
less of the accuracy with which pockets can be measured,
tions, and defective margins of dental restorations in
there is no established correlation between probable pock-
the subgingival area.
et depth and the presence or absence of active disease.
This means that symptoms other than increased prob- With correct technique and suitable instruments, it is
ing depth should be present to justify surgical therapy. usually possible to properly debride pockets up to 5 mm
These include clinical signs of inflammation, especially deep. However, this limit cannot be used as a universal
exudation and bleeding on probing (to the bottom of the rule of thumb. Reduced accessibility and the presence of
pockets), as well as aberrations of gingival morphology. one or several of the aforementioned impeding conditions
may prevent proper debridement of shallow pockets, CONTRAINDICATIONS FOR

whereas at sites with good accessibility and favorable root PERIODONTAL SURGERY
morphology, proper debridement can be accomplished
even in deeper pockets. Patient Cooperation
Following scaling, the root surface should be smooth
- roughness will often indicate the presence of remaining A typical recall schedule for periodontal patients in-
subgingival calculus. It is also important to monitor care- volves professional consultations for supportive peri-
fully the gingival reaction to subgingival debridement. If odontal therapy once every 3-6 months. Patients who
inflammation persists and if bleeding is elicited by gentle cannot maintain satisfactory oral hygiene over such a
probing in the subgingival area, the presence of subgingi- period should normally be considered unsuited for peri-
val deposits should be suspected. If such symptoms are odontal surgery.
not resolved by repeated subgingival instrumentation,
surgical treatment should be performed to expose the root
Cardiovascular Disease
surfaces for proper cleaning.
• Arterial hypertension
• Angina pectoris
Impaired Access for Self -performed • Myocardial infarction: Patients should not be subjected
Plaque Control to periodontal surgery within 6 months following hos-
pitalization
The level of plaque control is determined not only by • Anticoagulant treatment: Implies increased propensity
patient's interest and dexterity but also, to some extent, for bleeding
by the morphology of the dentogingival area. • Rheumatic endocarditis, congenital heart lesions, and
The patient's responsibility includes the cleansing of heart/vascular implants
the supragingival tooth surfaces and the marginal part of • Organ transplantation: Prophylactic antibiotics are rec-
the gingival sulcus. This means that the tooth area coronal ommended in transplant patients taking immuno-
to the gingival margin and at the entrance to the gingival suppressive drugs
sulcus should be the target for the patient's home-care • Blood disorders: Acute leukemia, agranulocytosis, and
efforts. lymphogranulomatosis must not be subjected to peri-
Pronounced gingival hyperplasia and gingival cra- odontal surgery.
ters, the presence of restorations with defective margin-
al fit or adverse contour, and surface characteristics at
the gingival margin may seriously compromise plaque Hormonal Disorders
removal.
By the professional treatment of periodontal disease, • Diabetes mellitus: Entails lowered resistance to infection,
the dentist prepares the dentition in such a way that propensity for delayed wound healing, and predisposi-
home care can be effectively managed. At the completion for arteriosclerosis.
tion of treatment, the following objectives should have • Adrenal function: May be impeded in patients receiving
been met: large doses of corticosteroids over an extended period.
These conditions involve reduced resistance to physical
• No sub- or supragingival dental deposits and mental stress, and the doses of corticosteroid may
• No pathological pockets (no bleeding on probing to have to be altered during the period of periodontal
the bottom of the pockets) surgery.
• No plaque-retaining aberrations of gingival morphology
• No plaque-retaining parts of restorations in relation to
the gingival margin. N eurologic Disorders
These requirements lead to the following indications Multiple sclerosis, Parkinson's disease, paresis,
for periodontal surgery: impaired muscular function, tremor, and uncontrol-
lable reflexes may necessitate treatment under general
• Accessibility for proper scaling and root planing
anesthesia.
• Establishment of a morphology of the dentogingival
area conducive to plaque control
• Pocket depth reduction
Smoking
• Correction of gross gingival aberrations
• Shift of the gingival margin to a position apical to Although smoking negatively affects wound healing,
plaque-retaining restorations it may not be considered a contraindication for surgical
• Facilitation of proper restorative therapy. periodontal treatment.
CHAPTER 46 GENERAL PRINCIPLES OF PERIODONTAL SURGERY 403
OUTPATIENT SURGERY cons of each approach. At the time of surgery, the patient
should again be informed, verbally and in writing, of the
Patient Preparation procedure to be performed, and he or she should indicate
agreement by signing the consent form.
Re-Evaluation After Phase I Therapy
Almost every patient undergoes initial or preparatory
phase of therapy, which basically consists of thorough Emergency Equipment
scaling and root planing and removing all irritants re- The operator, all assistants, and office personnel should
sponsible for the periodontal inflammation. These probe trained to handle all the possible emergencies that may
cedures are: arise. Drugs and equipment for emergency use should be
1. Eliminating some lesions entirely readily available at all times.
2. Rendering the tissues more firm and consistent, thus The most common emergency is syncope or a tran-
permitting a more accurate and delicate surgery sient loss of consciousness due to a reduction in cerebral
3. Acquainting the patient with the office and the op- blood flow. The most common cause is fear and anxiety.
erator and assistants, thereby reducing the patient's Syncope is usually preceded by a feeling of weakness,
apprehension and fear. and then the patient develops pallor, sweating, coldness
of the extremities, dizziness, and slowing of the pulse.
The re-evaluation phase consists of reprobing and re- The patient should be placed in a supine position with
examining all the pertinent findings that previously in- the legs elevated; tight clothes should be loosened, and a
dicated the need for the surgical procedure. Persistence wide open airway ensured. Administration of oxygen is
of these findings confirms the indication for surgery. The also useful. Unconsciousness persists for a few minutes.
number of surgical procedures, expected outcome, and A history of previous syncopal attacks during dental ap-
postoperative care necessary are all decided beforehand. pointments should be explored before treatment is begun,
These are discussed with the patient and a final decision and, if these are reported, extra efforts to relieve the pa-
is made, incorporating any necessary adjustments to the tient's fear and anxiety should be made.
original plan.
Infection Control
Premedication Universal precautions, including protective attire and
Some studies have reported reduced postoperative barrier techniques, are strongly recommended and often
complications including reduced pain and swelling when required by law. They include the use of disposable sterile
antibiotics are given before periodontal surgery and con- gloves, surgical masks, and protective eyewear.
tinuing for 4-7 days after surgery. The value of admin- All surfaces possibly contaminated with blood or saliva
istering antibiotics routinely for periodontal surgery has that cannot be sterilized (such as light handles and unit
not been clearly demonstrated in the patients who are not syringes) must be covered with aluminum foil or plastic
medically compromised. wrap. Aerosol-producing devices, such as the Cavitron,
The prophylactic use of antibiotics in patients who are should not be used on patients with suspected infections,
otherwise healthy has been advocated for bone grafting and their use should be kept to a minimum in all other
procedures and claimed to enhance the chances of new patients. Special care should be taken when using and dis-
attachment. posing of sharp items such as needles and scalpel blades.
Smoking
Smoking has deleterious effect on healing of periodon- Sedation and Anesthesia
tal wounds. Periodontal surgery should be performed painlessly.
Advise patients to quit or stop smoking for a minimum The most reliable means of providing painless surgery is
of 3-4 weeks after the procedure. the effective administration of local anesthesia. The area to
Patients who are unwilling to follow this advice, an al- be treated should be thoroughly anesthetized by means of
ternate treatment plan, not including highly sophisticated regional block and local infiltration injections. Injections
techniques such as regenerative procedures and muco- directly into the interdental papillae may also be helpful.
gingival and esthetic techniques, should be considered. Apprehensive and neurotic patients require special
management with antianxiety or sedative hypnotic agent.
Perhaps the simplest, least invasive method to alleviate
Informed Consent
anxiety in the dental office is nitrous oxide and oxygen
The patient should be informed at the time of the initial inhalation sedation.
visit about the diagnosis, prognosis, the different possible For individuals with mild to moderate anxiety, oral
treatments with their expected results, and all pros and administration of a benzodiazepine can be effective in
decreasing anxiety and producing a level of relaxation. ensuring that flaps remain moist during entire operation
Commonly used benzodiazepine agents are alprazolam, and by carefully limiting the amount of time the flap is
diazepam, and lorazepam. reflected.
Intravenous (IV) administration of a benzodiazepine,
alone or in combination with other agents, can be used
Hemorrhage Control
to achieve a greater level of sedation in individuals with
moderate to severe levels of anxiety. The amount of bleeding should be carefully monitored
and controlled during operation. Hemorrhage frequent-
ly follows the removal of diseased soft tissues; infected
lntraoperative Considerations granulomatous tissue is typically highly vascular. Addi-
tional sources of bleeding can be small tears or partially
Tissue Management
cut vessels that continue to ooze rather than functionally
1. Operate gently and carefully. Tissue manipulation collapse.
should be precise, deliberate, and gentle. Thorough-
ness is essential, but roughness must be avoided
because it produces excessive tissue injury, causes Avoiding Dead Space
postoperative discomfort, and delays healing. When preparing for flap closure, the surgeon should
2. Observe the patient at all times. It is essential to pay seek hemostasis as completely as possible, since a large
careful attention to the patient's reactions. Facial ex- blood clot is an excellent medium for bacterial growth
pressions, pallor, and perspiration are some distinct and hinders effective healing. A large blood clot causes
signs that may indicate the patient is experiencing pain, a dead space to form, resulting in ischemia and infection
anxiety, or fear. The doctor's responsiveness to these of flap margin.
signs can be the difference between success and failure.
3. Be certain the instruments are sharp. Successful treat- Wound Closure
ment is not possible without sharp instruments; instru- Selecting the proper suture material and even greater
ments must be sharp to be effective. Dull instruments requirement is the proper suturing technique.
inflict unnecessary trauma due to poor cutting and
excessive force applied to compensate for their inef- GOALS OF WOUND CLOSURE
fectiveness. • Firm closure with good approximation
• Full coverage to alveolar bone; close adaptation to the
Scaling and Root Planing tooth
All exposed root surfaces should be carefully ex- • Thin fibrin clot
plored and planed as needed as part of the surgical
This serves the following purposes:
procedure. In particular, areas of difficult access such
as furcations or deep pockets often have rough areas • Avoids flap ischemia caused by excessively tight and
or even calculus that was undetected during the pre- improperly placed sutures
paratory sessions. The assistant who is retracting the • Reduces marginal bone loss
tissues and using the aspirator should also check for the • Provides an environment that enhances the chances
presence of calculus and the smoothness of each surface for periodontal regeneration in depths of infrabony
from a different angle. pockets.
Vascular Supply and Hydration Periodontal Dressings (Periodontal Packs)

During the surgery, operator must ensure maintenance In most cases, after the surgical periodontal proce-
of sufficient blood flow in the flaps and proper hydration dures, the area is covered with a surgical pack. In general,
of both the flaps and surgical sites. The base of the flap dressings have no curative properties; they assist healing
should be of ample width and of sufficient thickness to by protecting the tissue rather than providing "healing
provide adequate blood flow to the edge of the flap. factors."
Very thin flaps, especially split flaps, with very styl-
ized scalloped architecture, providing attractive marginal ADVANTAGES OF PERIODONTAL DRESSING
adaptation, often slough as a result of inadequate blood • Minimizes the postoperative infection and hemorrhage
supply. This results in postoperative pain and exces- • Facilitates healing by preventing surface trauma during
sive loss of attachment and marginal alveolar bone. If mastication
dehydration occurred during the operation, it can cause • Protects against pain induced by contact of the wound
necrosis of the flap. Dehydration should be avoided by with food or the tongue during mastication.
Zinc oxide-eugenol packs
Packs based onthe reaction of zinc oxide and eugenol
include the Wondr-Pak developed by Ward in 1923.
The addition of zinc acetate (accelerators) provides
better working time.
Zinc oxide-eugenol dressings are supplied as a liquid
and a powder that are mixed prior to use.
DISADVANTAGES OF EUGENOL PACKS

• Eugenol may act as tissue irritant.
• It may induce an allergic reaction that produces
reddening of the area and burning pain in some
patients.
• Asbestos in pack may cause not only chronic destruc-
tive lung disease but also carcinoma of the lung and
mesothelioma.
• Tannie acid in pack may cause liver damage. Antibacte- FIGURE 46.2 Two tubes of Coe-Pak.
rial substances in the pack may cause variations in the
complex oral microflora and lead to fungal ingrowth.
ADVANTAGES
• This dressing does not contain asbestos or eugenol,
Non-Eugenol Packs thereby avoiding the problems associated with these
COE-PAK substances.
The reaction between a metallic oxide and fatty acids is • It has better fracture strength than eugenol packs.
the basis for Coe-Pak (Fig. 46.1), which is the most widely Other Non-Eugenol Packs
used dressing in the United States. This is supplied in two
tubes, the contents of which are mixed immediately before • Barricaid: A light curing dressing, e.g., Barricaid™
use until a uniform color is obtained. (Dentsply International Inc., Milford, DE, USA),
One tube contains zinc oxide, an oil (for plasticity), is useful in the anterior tooth region, and particu-
gum (for cohesiveness), and lorothidol (a fungicide). larly following mucogingival surgery, because it
The other tube contains liquid coconut fatty acids has a favorable esthetic appearance and it can be
thickened with colophony resin (or rosin) and chloro- applied without dislocation the soft tissue. However,
thymol (a bacteriostatic agent) (Fig. 46.2). the light curing dressing is not the choice of dressing
to be used in situations where the flap has to be api-
cally retained, due to its soft state before curing.
• Cyanoacrylates: Cyanoacrylates have also been used
as periodontal dressings with varying success. Dress-
ings of the cyanoacrylate type are applied in a liquid
directly onto the wound or sprayed over the wound
surface. Cyanoacrylate tissue adhesives are set by po-
lymerization in the presence of anions, such as OH.
Cyanoacrylates are apparently biodegradable and
are gradually depolymerized and phagocytosed. The
production of hemostasis, flap immobilization, and
possibly quicker healing are described as the princi-
pal advantages of the technique. Disadvantage of the
dressing may be some bone resorption due to heat
of polymerization, difficulty in application in certain
areas, and the impossibility of adjusting the dressing
after application. Although the application of this kind
of dressing is simple, its properties often do not meet
clinical demands, which is why its use is rather limited
FIGURE 46.1 Non-eugenol packs. at present.
RETENTION OF PACKS PREPARATION AND APPLICATION

The pack can be retained mechanically by interlocking OF THE PERIODONTAL DRESSING
in interdental spaces and joining its lingual and facial Zinc oxide packs are mixed with eugenol or non-
portions. eugenol liquids on a wax paper pad with a wooden
Retention of the pack may be difficult in isolated teeth tongue depressor (Fig. 46.3). The powder is gradually
or when several teeth in an arch are missing. Numerous incorporated with the liquid until a thick paste is formed.
reinforcements and splints and stents for this purpose Coe-Pak is prepared by mixing equal lengths of paste
have been described. Placement of dental floss tied loosely from tubes containing the accelerator and the base until
around the teeth enhances retention of the pack. the resulting paste is of uniform color. A capsule of tet-
racycline powder can be added at this time. The pack is
ANTIBACTERIAL PROPERTIES OF PACKS then placed in a cup of water at room temperature. In
Improved healing and patient comfort with less odor 2-3 min, the paste loses its tackiness and can be handled
and taste have been obtained by incorporating antibiotics and molded; it remains workable for 15-20 min. Working
in the pack. Bacitracin, 5 oxytetracycline (Terramycin), neo- time can be shortened by adding a small amount of zinc
mycin, and nitrofurazone have been tried, but all may pro- oxide to the accelerator (pink paste) before spatulating.
duce hypersensitivity reactions. The emergence of resistant The pack is then rolled into two strips approximately the
organisms and opportunistic infection has been reported. length of the treated area. First strip is brought forward
Incorporation of tetracycline powder in Coe-Pak is along the facial surface to the midline and gently pressed
generally recommended, particularly when long and into place along the gingival margin and interproximally.
traumatic surgeries are performed. The second strip is applied from the lingual surface. It is
FIGURE 46.3 Preparation and application of periodontal pack.

joined to the pack at the distal surface of the last tooth, • During the first day, apply ice intermittently on the face
and then brought forward along the gingival margin to over the operated area; this will keep tissue cool and
the midline. The strips are joined interproximally by ap- reduce inflammation and swelling.
plying gentle pressure on the facial and lingual surfaces • Follow your daily activities but avoid exertion.
of the pack. For isolated teeth separated by edentulous
spaces, the pack should be made continuous from tooth First Postoperative Week
to tooth, covering the edentulous areas.
Patients should be told to rinse with 0.12% chlorhexi-
When split flaps have been performed, the area should
dine gluconate immediately after periodontal surgery
be covered with tin foil to protect the sutures before plac-
and twice daily thereafter until normal plaque control
ing the pack. The pack should cover the gingiva, but over-
technique can be resumed.
extensions onto uninvolved mucosa should be avoided.
Following complications may arise in the first postop-
Excess pack irritates the mucobuccal fold and floor of the
erative week:
mouth and interferes with the tongue. Overextension also
jeopardizes the remainder of the pack because the excess l. Persistent bleeding after surgery: Bleeding should be
tends to break off, taking pack from the operated area stopped with pressure, electrocautery, and repacking
with it. Pack that interferes with the occlusion should of the area.
be trimmed away before the patient is dismissed. The 2. Sensitivity to percussion: Sensitivity may be caused by
operator should ask the patient to move the tongue forc- the extension of inflammation into the periodontal
ibly out and to each side, and the cheek and lips should ligament.
be displaced in all directions to mold the pack while it is
still soft. After the pack has set, it should be trimmed to Treatment of Sensitive Roots
eliminate all excess.
As a general rule, the pack is kept on for 1 week after Root hypersensitivity is a relatively common problem
surgery. It is not a rigid requirement; the period may be in periodontal practice. It may occur spontaneously when
extended, or the area may be repacked for an additional the root is exposed as a result of gingival recession or
week. Fragments of the surface of the pack may come off pocket formation, or it may appear after scaling and root
during the week, but this presents no problem. If a portion planing and surgical procedures. It is manifested as pain
of the pack is lost from the operated area and the patient induced by cold or hot temperature, more commonly cold
is uncomfortable, it is usually best to repack the area. The by citrus fruits or sweets; or by contact with a toothbrush
clinician should remove the remaining pack, wash the or a dental instrument.
area with warm water, and apply a topical anesthetic be- Root sensitivity occurs more frequently in the cervical
area of the root, where the cementum is extremely thin.
fore replacing the pack, which is then retained for 1 week.
Again, patients may develop pain from an overextended Scaling and root planing procedures remove this thin ce-
margin that irritates the vestibule, floor of the mouth, or mentum, inducing hypersensitivity. An important factor
tongue. The excess pack should be trimmed away, making for reducing or eliminating hypersensitivity is adequate
sure that the new margin is not rough, before the patient plaque control. However, hypersensitivity may prevent
is dismissed. plaque control, and therefore a vicious circle of escalating
The light curing dressing (Barricaid™) is preferably hypersensitivity and plaque accumulation may be created.
applied with the supplied syringe, adjusted, and then
cured by light. It is important to carefully dry teeth and Possible Mechanisms of Hypersensitivity
soft tissue before the application for optimal adherence. • Direct neural stimulation: The dentinal tubules are
Excess of dressing material can easily be removed fol- innervated by nerves, which extend upto 100 µm
lowing the curing with a knife or finishing burs in a low- along tubules. Whenever there is injury to these
speed handpiece. dentinal tubules, the stimuli reach the nerve ending
in the inner dentine. The stimulated nerve causes
Instructions for the Patient After Surgery hypersensitivity.
• Transduction theory: Membranes of the odontoblast
After the pack is placed, printed instructions are given
process are excited by the stimulus and release
to the patient to be read before he or she leaves the chair.
neurotransmitters, and thus impulse is conducted to
• The pack should remain in place until it is removed in the nerve endings in the inner dentine.
the office at the next appointment. • Hydrodynamic theory: Dentinal fluid movement
• For the first 3 h after the operation, avoid hot foods to may disturb the movement of odontoblast and this
permit the pack to harden. movement may cause the sensation of pain via
• Do not smoke. intimately associated mechanoreceptor (AS) like nerve
• Do not brush over the pack. endings.
The patient should be informed about the possibility of 4. Formalin

root hypersensitivity before treatment is undertaken. The a. Fluoride compounds
following information on how to cope with the problem - Sodium fluoride
should also be given to the patient: - Stannous fluoride
b. Calcium compounds
1. Hypersensitivity appears as a result of the expo-
- Calcium hydroxide
sure of dentine, which is inevitable if calculus and
- Dibasic calcium phosphate
plaque and their products, buried in the root, are to
c. Iontophoresis
be removed.
d. Strontium chloride
2. Hypersensitivity slowly disappears over a few weeks.
e. Potassium oxalate
3. Plaque control is important for the reduction of hyper-
f. Restorative resin
sensitivity.
g. Dentine bonding agents.
4. Desensitizing agents do not produce immediate relief.
They have to be used for several days or even weeks In addition to these, recently lasers have been used for
to produce results. the treatment of dentinal hypersensitivity. Lasers have the
potential to cause pulp damage.
According to Trowbridge and Silver, reduction in den-
tinal tubule diameter can be attained by:
1. Formation of a smear layer produced by burnishing Healing of Periodontal Wounds
the exposed surface HEALING OF EXCISION AL SURGERY
2. Topical application of agents that form insoluble pre- The initial response after excision of gingival tissue is
cipitates within the tubules an acute inflammatory reaction. This is followed by a de-
3. Impregnation of tubules with plastic resins crease in inflammation and commencement of epitheliali-
4. Sealing of the tubules with plastic resins. zation. Connective tissue repair with vascular proliferation
and redistribution occurs, along with possible resorption
AGENTS USED BY THE PATIENT and remodeling of subjacent alveolar bone. A new lamina
propria is formed along with a new epithelial sheath that
The most common agents used by the patient for oral
encloses a pyramidal zone of connective tissue.
hygiene are dentifrices. Although many dentifrice prod-
ucts contain fluoride, additional active ingredients for
desensitization are strontium chloride, potassium nitrate, INITIAL HEALING (0-5 H) Hemorrhage leads to a sero-
and sodium citrate. The following dentifrices have been fibrinous exudate and blood clot that covers the wound.
approved by the American Dental Association for desen- The outer surface of the clot approximates the form of
sitizing purposes: the excised tissue and acts to contain fluid within the
dermis, important for early epithelialization. In the con-
• Sensodyne and Thermodent, which contain strontium nective tissue, acute inflammation is progressing, with
chloride marked migration of PMNs into the clot and to the wound
• Crest Sensitivity Protection, Denquel and Promise, surface. By 5 h, a band of PMNs (polyband) has formed
which contain potassium nitrate; and under the clot.
• Protect, which contains sodium citrate
• Fluoride rinsing solutions and gels can also be used 5 H TO 1 DAY Epithelium: A distinct movement of epi-
after the usual plaque control procedures. thelial cells that originate at the wound margin begins to
Desensitizing agents act via the precipitation of crys- cross the surface of the wound. This migration is from the
talline salts on the dentine surface, which block dentinal spinous layer and occurs by cells wedging themselves
tubules. Patients must be aware that their use will not between the surface coagulum and the underlying viable
prove to be effective unless used continuously for a period connective tissue of the wound. Epithelial proliferation
of at least 2 weeks. has also begun at the wound edge.
The clot and polyband serve a protective function un-
AGENTS USED IN THE DENTAL OFFICE til the epithelium forms a continuous sheath over the
wound. The clot and PMNs disappear later when the
Cavity varnishes epithelial sheath is formed.
Anti-inflammatory agents
Treatments that partially obturate dentinal tubules
2-3 DAYS Epithelial cells are covering the wound at
1. Burnishing of dentine a rate of 0.5 mm/ day. The smoother the surface of the
2. Silver nitrate connective tissue after the surgical procedure, the faster
3. Zinc chloride the rate of epithelialization. Both basal cells of the wound
margin and cells that have migrated onto the wound apical migration of the attachment (apical migration may
surface are proliferating. There is a decrease in inflamma- occur if excess connective tissue is destroyed during the
tory cells (PMNs) below the migrating epithelial cells. The scaling step of the EBG). Clinically, the teeth should be
connective tissue is beginning to organize. polished immediately after removal of the dressing and
plaque control should be resumed.
4-10 DAYS Connective tissue proliferation has begun If a piece of calculus is accidentally left behind after
away from the wound margin. As soon as the epithelium surgery, then excessive local granulation tissue sometimes
covers the wound (in 4-7 days on the average there is forms, which slows healing. Any remaining calculus or
histologic evidence, depending on the size of the exci- resultant granulation tissue should be removed with a
sion), cells under the basement membrane assume further sharp curette at the first post-op visit.
production of connective tissue. This activity produces
HEALING OF INCISION AL SURGERY
a vascular granulation tissue, which is the progenitor
of the new lamina propria. Connective tissue adjacent INITIAL HEALING (0-4 DAYS) After the flap is po-
to the tooth begins to proliferate in an occlusal direc- sitioned in its desired position, a blood clot is formed
tion, creating the gingival sulcus and gingival margin. between the flap and the underlying bone. The clot con-
Although inflammatory cells are decreasing elsewhere tributes somewhat to maintaining the flap in position
on the wound, there is an increase of inflammatory cells once it is sutured to place. A thinner clot is more desir-
in the connective tissue adjacent to the forming gingival able than a thick one because: (i) a smaller amount of
sulcus. This may be a reason for the slower healing rate interposed reparative tissue is necessary for attachment,
seen in the area of the future epithelial attachment, even and (ii) there is less clot to be resorbed before reattach-
though the epithelium has already covered the wound. ment can occur.
This probable explanation has great clinical significance, Irreversible bone resorption is greatest in areas where
because the gingiva will appear normal at this stage, alveolar bone is thin and comprises two plates of compact
while the epithelial attachment has several weeks to go bone fused together (e.g., over prominent roots and the
before healing is completed. labial areas of mandibular incisors). Less irreversible de-
struction of bone occurs where cancellous or supporting
10-28 DAYS As granulation tissue is transformed into bone exists between the outer cortical plate and alveolar
the new lamina propria, there is decrease in vascularity bone proper because the marrow spaces and vascular sites
and further organization of tissue elements. Collagen is act as a reservoir for healing.
formed gradually over a 3- to 4-week period. At 21 days,
the epithelium appears clinically normal over the wound 4-10 DAYS After the first 3-4 days, the fibrin clot starts
and is now similar in configuration and keratinization to undergoing resorption and is usually completely replaced
presurgical epithelium. Epithelial progression into the 6-7 days postoperatively by young connective tissue pro-
shallow crevice, present between the tooth and soft tis- liferation from the underside of the flap and the POL. The
sue margin, is forming the epithelial attachment. Here a POL is the prime source of early connective tissue reat-
few inflammatory cells still persist. By the 28th day the tachment to tooth and marginal bone, tenuously joining
epithelial attachment has "sealed" to the tooth and the the corium (dermis) of the flap to tooth and bone. Revas-
sulcular epithelium has healed. cularization tends to follow the pattern of new connective
tissue formation, which moves coronally as the clot is
resorbed. By 1 week epithelial cells have approximated
CLINICAL IMPLICATIONS OF EXCISION AL
the root surface by migration and initiated the epithe-
SURGERY HEALING
lial attachment and sulcular lining. Bone resorption has
If a long bevel is made (exposing a greater wound peaked at about 8-10 days postoperation. At this time the
surface), then the healing will take longer because the flap is bluish red in color from an inflammatory response,
epithelial cells have further to migrate. The more accurate showing loss of stippling and a shiny appearance with an
the bevel is to 45°, the less the height in the regenerated exudate and oozing present. The tooth may have some
gingival margin (especially when a thick gingival ledge mobility and may be tender to palpation or percussion
is seen). because of edema and ellular activity in the POL.
If the excision of tissue provides a smooth wound
bed (no tissue tags or irregularities), then rapid epithe- 10-21 DAYS Healing at 10-21 days shows an inflam-
lialization results and lamina propria development is matory response, less marked than before, and a changing
enhanced. pattern with respect to bone. Crestal resorption can be
In the presence of inflammation, healing is delayed. seen to a minor degree, but repair in the form of osteoid
Therefore, meticulous oral hygiene is indicated. The form- tissue being laid down has begun. The periosteal bone
ing sulcus is inflamed from the start, which may cause undergoes peak resorption from days 14-17 with buildup
on the periodontal surface and resorption on the perios- flap surgery the curetted root surface may be repopulated
teal. The soft tissues show signs of healing and matura- by four different types of cells:
tion with collagen fiber bundles replacing the finer fibrils
1. Epithelial cells
previously present. Cementum, which showed initial re-
2. Cells derived from the gingival connective tissue
sorption where the root was curetted, is re-forming. As the
3. Cells derived from the bone
POL and supracrestal fibers form, they are incorporated
4. Cells derived from the periodontal ligament.
into this calcified tissue. Some investigators think this
cementum formation is what stops the apical epithelial Regeneration is the reproduction or reconstitution of a
migration during healing. lost or injured part. As applied to periodontics, it means
the formation of new bone, cementum, and periodontal
ligament on a previously diseased root surface.
21 DAYS AND BEYOND Cementum anchors periodon- New attachment means the reunion of connective tissue
tal fibers to the tooth. Maturation and repair of all tissues with a root surface that has been deprived of its peri-
involved is occurring. Bone formation repairs most of the odontal ligament. This reunion occurs by the formation
lost bone. The end results are a slight decrease in crestal of new cementum with inserting collagen fibers. The
height and a slight thinning of the alveolar septum, the formation of new bone is not necessarily a condition of
extent depending on the quality and thickness of bone. new attachment. In addition, new attachment to a root
By 1 month the flap is firmly attached via dense, orga- surface may be mediated through epithelial adhesion
nized connective tissue and cementum. Epithelium of (junctional epithelium) or connective tissue adhesion.
attached gingiva shows rete peg formation. The sulcular Reattachment means to attach again, the reunion of
epithelium is thin and free from rete pegs. Gentle sulcular connective tissue with a root surface on which viable
probing can be done at this time but usually is delayed periodontal tissue is present. The area of reattachment is
until 3 months. not affected by bacterial contamination.
Attachment apparatus refers to the cementum, the alveo-
2-3 MONTHS The correct positioning of the flap dur- lar bone, and the periodontal ligament.
ing the first few weeks is critical to proper healing. The Repair is the healing of a wound by tissue that does
flap should be positioned just coronal to the bony margin. not fully restore the architecture or function of the part.
Loose sutures or muscular activity may create spaces filled
ROLE OF EPITHELIUM IN PERIODONTAL
with a large clot that would be temporarily detrimental to
healing. For good flap adaptation, gentle, but firm, pres- WOUND HEALING
sure with a wet gauze for several minutes immediately Downgrowth of epithelium into the periodontal lesion
after surgery is recommended. This will create a thin has most likely occurred to a varying extent during heal-
fibrin clot between the flap and bone. Proper oral hygiene ing following most flap and grafting procedures applied
creates an environment for optimal epithelialization of in regenerative periodontal therapy. The apical migration
crestal soft tissues, promotes the formation of a new epi- of epithelium reduces the coronal gain of attachment,
thelial attachment and sulcular epithelium, and reduces evidently by preventing periodontal ligament cells from
inflammation. Hygiene measures (i.e., light brushing and repopulating the root surface.
flossing) can be initiated almost immediately. This view is supported by the results of the study by
A prophylaxis should be performed the first and third Caton et al (1980). These investigators examined healing
weeks postoperatively. If the epithelial attachment is not in ligature-induced periodontal lesions following treat-
removed via an IBG, it can act as a focus of epithelial pro- ment with four different modalities of regenerative sur-
liferation and migration and cause a more apical position gical procedures: root planing and soft tissue curettage,
of the epithelial attachment than would normally be seen Widman flap surgery without bone grafting, Widman
postoperatively. flap surgery with the placement of frozen autogenous
red bone marrow and cancellous bone, or beta-tricalcium
phosphate in intrabony defects. Healing following all
PERIODONTAL REGENERATION treatment modalities resulted in the formation of a long
Regeneration of the periodontium must include the junctional epithelium extending to or close to the same
formation of new cementum with inserting collagen fibers level as before treatment.
on the previously periodontitis-involved root surfaces
and the regrowth of the alveolar bone. In 1976, Melcher, ROLE OF BONE GRAFTS IN WOUND HEALING
in a review paper, suggested that the type of cell that The use of bone grafts in regenerative periodontal
repopulates the root surface after periodontal surgery de- therapy is based on the assumption that the promotion
termines the nature of the attachment that will form. After of bone regrowth may also induce cells in the bone to
produce a new cementum layer with inserting collagen Bone fill is the presence of hard tissue in a periodontal
fibers on previously periodontitis-involved root surfaces. osseous defect, as determined by clinical re-entry of the
However, histologic studies in both humans and animals original defect site. This term does not indicate the nature
have demonstrated that grafting procedures often result of the histologic attachment to the tooth. The amount
in healing with a long junctional epithelium rather than of bone fill is usually determined by surgical re-entry
a new connective tissue attachment. procedures.
KEY POINTS
• Types of periodontal dressings • Healing of periodontal wounds
• Desensitizing agents
QUESTIONS 3. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds.
Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B.
1. Write a short note on periodontal dressings. 4. Trowbridge HO, Silver DR. A review of current approaches in of-
2. Describe in-office treatment for dentinal hypersen- fice management of tooth hypersensitivity. Dent Clin North Am
sitivity. 1990;34:538.
3. What is the difference between new attachment and 5. Sachs HA, Fanroush A, Cheechi L, et al. Current status of periodontal
dressings. J Periodontol 1984;55:689.
reattachment?
6. Caton J, Nyman S, Zander H. Histometric evaluation of periodontal
surgery. II. Connective tissue attachment levels after four regenera-
Suggested readings tive procedures. J Clin Periodontol 1980;7(3):224-31.
7. Melcher AH. On the repair potential of periodontal tissues. J Peri-
1. Curro FA. Tooth hypersensitivity. Dent Clin North Am 1990;34:403.
odontol 1976;47(5):256-60.
2. Lang NP, Karring T, Lindhe J. Clinical Periodontology and Implant
8. Ward AW. Inharmonius cusp relation as a factor in periodontoclasia.
J Am Dent Assoc 1923;10:471.
CHAPTER
47
Gingival Surgical Procedures
CHAPTER OVERVIEW
Surgical procedures that are limited to the gingival referred to as gingival surgical procedures. These include
soft tissue and do not involve any osseous structures are gingival curettage, gingivoplasty, and gingivectomy.
In periodontics, the word "curettage" means scraping Gingival curettage aids in the removal of this chroni-
the gingival wall of a periodontal pocket to remove in- cally inflamed granulation tissue, thus reducing bacte-
flamed soft tissue. rial load and eliminating infected tissue. Root planing in
Curettage is of two types: association with gingival curettage establishes a healthy
root surface further reducing the antigenic load, thus
1. Gingival curettage: Removal of soft tissue lateral to the
allowing the host immune cells to scavenge the residual
pocket wall (Fig. 47.1).
granulation tissue and neutralizing the effect of bacterial
2. Subgingival curettage: Performed apical to the epithelial
contamination.
attachment, severing the connective tissue attachment
down to the osseous crest (Fig. 47.2).
Indications
1. Moderately deep intrabony pockets located in acces-
INADVERTENT GINGIVAL CURETTAGE sible areas
2. When more aggressive surgical techniques are con-
Some degree of curettage that occurs unintentionally traindicated in patients because of their age, sys-
when scaling and root planing is performed is termed as temic problems, psychological problems, or other
inadvertent curettage. factors
3. As a method of maintenance treatment for areas of
Rationale recurrent inflammation and pocket depth.
1. To reduce pocket depth.

2. To maintain esthetics. Procedures
3. To provide therapy in systemically compromised Basic Procedure
patients.
Gingival curettage always requires some type of local
4. To improve probing attachment levels.
anesthesia. Once the area is anesthetized, the selected
The lateral wall of the periodontal pocket is often com- curette is inserted, so as to engage the inner lining of the
posed of chronically inflamed granulation tissue due pocket wall, and is carried along the soft tissue, usually in
to angioplastic proliferation and fibroblastic coloniza- a horizontal stroke. The pocket wall should be supported
tion. Besides, this tissue is also composed of calculus and externally by gentle finger pressure. Then, the curette is
microbial colonies. The presence of microbial colonies placed under the cut edge of the junctional epithelium to
further accentuates the pathological processes and alters undermine it.
healing. The granulation tissue thus formed is lined by In case of subgingival curettage, the tissues attached
epithelium that prevents the attachment of new fibers by between the bottom of the pocket and the alveolar crest
acting as a biologic barrier in this zone. are removed with a curette by a scooping motion to the
C H A PT ER 47 G IN G IVA L SU R G IC A L PRO C ED U R ES 413
(A) (B)
FIGURE 4 7 .3 Excisional new attachment procedure. (A) Internal

bevel incision to point below bottom of pocket. (B) After excision of
tissue, scaling and root planing are performed.
Technique
1. Adequately anesthetize the area.
2. An internal bevel incision is given from the margin of
the free gingiva apically to a point below the bottom of
FIGURE 4 7 .1 Gingival curettage performed with a horizontal stroke the pocket. The incision is continued interproximally
of the curette. on both the facial and lingual sides, retaining as much
interproximal tissue as possible.
3. A sulcular incision is performed to the level of the first
tooth surface. The area is irrigated and the tissue adapted incision.
to the tooth surface with gentle finger pressure. 4. Remove the excised tissue with a curette and plane the
root surface to achieve a smooth, hard consistency. Pre-
Excisional New Attachment Procedure
serve all connective tissue fibers that remain attached
This procedure has been developed and used by the US to the root surface.
Naval Dental Corps. It is a definitive subgingival curettage 5. The wound edges are approximated; if they do not
procedure performed using a surgical knife (Fig. 47.3). meet passively, recontour the bone until good adapta-
tion is achieved.
6. Sutures are placed and a periodontal dressing is given.
Ultrasonic Curettage
Gingival curettage can also be done using ultrasonic
devices. Ultrasonic vibrations disrupt tissue continuity,
lift off epithelium, dismember collagen fibers, and alter
the morphologic features of fibroblast nuclei when ap-
plied to experimental animals. Ultrasonic devices debride
the epithelial lining of periodontal pockets resulting in
a narrow band of necrotic tissue (microcauterization),
which strips off the inner lining of the pocket.
Caustic Drugs
Drugs such as antiformin, sodium sulfide, and phe-
nol have been proposed for gingival curettage and then
discarded after studies showed their ineffectiveness. The
other drawbacks with these agents were that the extent
of tissue destruction could not be controlled and they
increased the amount of tissue destruction to be removed
FIGURE 4 7 .2 Subgingival curettage. by enzymes and phagocytes rather than reducing them.
SURGICAL GINGIVECTOMY GINGIVOPLASTY
Gingivectomy means excision of the gingiva or surgical Gingivoplasty is the reshaping of gingiva to create physi-
removal of gingival tissue. ologic gingival contours in the absence of pockets (Fig. 47.5).
Rationale Indications
• Gingival clefts and craters.
1. To improve visibility and accessibility for complete
• Shelf-like interdental papilla caused by acute necrotiz-
calculus removal and thorough smoothening of roots.
ing ulcerative gingivitis.
2. To create a favorable environment for gingival healing.
• Gingival enlargements.
3. To restore a physiological gingival contour.
Indications Steps of Gingivoplasty

• Tapering the gingival margin.
1. Elimination of supragingival pockets in fibrotic pockets
• Creating a scalloped marginal outline.
irrespective of the pocket depth.
• Thinning the attached gingiva.
2. Elimination of gingival enlargements.
• Creating vertical interdental grooves and shaping in-
3. Elimination of suprabony periodontal abscesses.
terdental papilla.
Contraindications
HEALING AFTER SURGICAL
1. When bone surgery is indicated. GINGIVECTOMY
2. Where the bottom of the pocket is apical to mucogin-
gival junction. 1. Immediately after gingivectomy, there is formation
3. When esthetics, especially in the anterior maxilla, is of a protective surface clot, which is then replaced by
the primary concern. granulation tissue.
2. Within 24 h, there is an increase in the number of new
connective tissue cells, especially angioblasts, just be-
Techniques for Surgical Gingivectomy low the inflamed surface layer.
1. External bevel gingivectomy: When the face of the blade is 3. After 24 h, there is migration of epithelial cells from
directed coronally (Fig. 47.4) (external bevel incision). the margins of the wound over the granulation tissue,
2. Internal bevel gingivectomy: When the face of the blade separating it from the surface clot.
is directed apically (internal bevel incision). 4. In 36 h, the new epithelial cells arising from the basal
and spinous layers of the wound edge epithelium mi-
Procedure grate over the wound and later are resorbed and re-
1. The pockets are recorded and marked with a Crane- placed by connective tissue bed.
Kaplan pocket marker to create bleeding points. 5. Within 14 days, surface epithelialization is completed.
2. With a Kirkland periodontal knife B. P. blade (No. 15), 6. Complete epithelial repair takes about 1 month.
start the incision such that it is beveled at approxi- 7. Complete connective tissue repair takes place in
mately 45° to the tooth surface about 1 mm apical to ?weeks.
the bleeding points both on the facial and on the lingual 8. Although postgingivectomy healing is same in all in-
surfaces. dividuals, the time required for complete healing may
3. In case of external bevel gingivectomy, the incision is vary depending on the area of the cut surface and in-
directed coronally to a point between the base of the terference from local irritants and infection.
pocket and the crest of the bone, as close as possible to
the bone without exposing it, to remove the soft tissue
coronal to the bone. GINGIVECTOMY BY ELECTROSURGERY
4. In case of internal bevel gingivectomy, the incision is
directed apically to the level of alveolar crest to incor- Electrosurgery is a technique in which electric current
porate the pocket lining. is used for incisions (Fig. 47.6).
5. The incisions can be discontinuous or continuous.
6. Excised pocket wall is removed, and the area cleaned. Technique
7. The granulation tissue is curetted, and any remaining
calculus and necrotic cementum are removed. 1. For gingivoplasty and gingivectomy, needle electrodes
8. Area is covered with a periodontal pack. supplemented by ovoid loop or diamond-shaped
FIGURE 4 7 .4 External bevel gingivectomy. (A) Preoperation. (Band C) Pockets marked with a pocket marker. (D) External bevel incision given.
(E) Interdental incision given. (F) Tissue removed. (G) Periodontal pack placed. (H) Healing after 10 days.
FIGURE 4 7 .5 Gingivoplasty by electrosurgery.
Before surgery Needle electrode being used
Immediate post-op
FIGURE 4 7 .6 Gingivectomy by electrosurgery.
electrodes are used. A fully rectified cutting and co- Disadvantages

agulation current is used. The electrode is activated
and moved in a shaving motion. 1. It cannot be used in patients with noncompatible and
2. For acute periodontal abscesses, incision for drainage
poorly shielded cardiac pacemakers.
2. It causes an unpleasant odor.
is made using a needle electrode.
3. If the electrode point touches the bone, irrepairable
3. For hemostasis, the ball electrode is used.
bone damage occurs.
4. Heat generated by injudicious use can cause tissue
Healing after Electrosurgery damage and bone loss.
5. If electrode touches the bone, cementum burns are
1. Some researchers have not found significant difference
produced.
in gingival healing after resection with electrosurgery
compared to resection with periodontal knives.
2. Others have found delayed healing, greater reduction LASER GINGIVECTOMY
in gingival height, and more bone injury.
Commonly used lasers in dentistry are the carbon di-
oxide and the neodymium:yttrium-aluminum-garnet
Advantages of Electrosurgery
lasers. For gingival growth excisions, mostly the carbon
1. Adequate contouring of the tissue dioxide laser is used. Precautions are to be taken during
2. Control of hemorrhage. use of lasers for oral surgical procedures to avoid beam
reflection on instrument surfaces resulting in injury of
neighboring tissues and operator's eyes (Fig. 47.7).
Pre-op showing enlargement in relation to 31, 32 Gingivectomy performed using laser
Immediate post-op
FIGURE 4 7. 7 Gingivectomy using laser.
CHEMICAL GINGIVECTOMY 2. Gingival remodeling could not be accomplished ef-

fectively.
Previously, chemicals such as 5% formaldehyde or 3. Compared to scalpel surgeries, epithelialization and
potassium hydroxide were used to remove gingiva, but reformation of the junctional epithelium and the rees-
they are now obsolete. The disadvantages with chemical tablishment of alveolar crest-fiber system are slower.
gingivectomy were:
1. Depth of action could not be controlled, causing dam-
age to the healthy attached gingiva underlying the
pocket.
KEY POINTS
• Curettage is of two types: gingival curettage, removal gival enlargements; and elimination of suprabony
of soft tissue lateral to the pocket wall; subgingival cu- periodontal abscesses.
rettage, performed apical to the epithelial attachment, • Gingivoplasty is the reshaping of gingiva to create physi-
severing the connective tissue attachment down to the ological gingival contours in the absence of pockets.
osseous crest. • After gingivectomy, complete epithelial repair takes
• Indications of gingivectomy are: elimination of about 1 month; complete connective tissue repair takes
supragingival pockets, in fibrotic pockets irre- place in 7 weeks.
spective of the pocket depth; elimination of gin-

1. How do you manage a case of soft, edematous, 4 mm Dentistry. 5th ed. Oxford: Blackwell Munksgaard; 2008.
deep pocket? 2. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds.
2. Define curettage and write about the indications and Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B.
contraindications of the procedure. Saunders Company; 2006.
3. Rose LF, Mealey BL, Genco R. Periodontics: Medicine, Surgery, Implants.
3. Write a note on ENAP. 1st ed. St Louis: Elsevier; 2004.
4. Describe the healing after gingivectomy.
CHAPTER
48
Flap Surgery
CHAPTER OVERVIEW
When accessibility and visibility of the root surface be- surgery. There are various techniques of performing flap
comes difficult or impossible with nonsurgical procedures, surgery that are discussed in this chapter.
accessibility is gained by performing a periodontal flap
DEFINITION • On the basis of placement of flap at the end of a surgical

procedure:
A periodontal flap is a part of the gingiva and/ or al- • Repositioned (positioned, displaced) flap
veolar mucosa surgically elevated from the underlying - Lateral displaced flap
tissues to provide visibility and access to the bone and - Coronally displaced flap
root surface. - Apical displaced flap
• Unrepositioned (undisplaced) flap
• On the basis of design of the flap
• Conventional flap
OBJECTIVES OF PERIODONTAL - Modifed Widman flap
FLAP SURGERY - Nondisplaced flap
- Apically displaced flap
1. To gain surgical access to deep or tortuous pockets • Papilla preservation flap.
for adequate debridement and smoothening of root
surfaces.
2. To facilitate plaque control by reduction or elimination Full, Thickness Flap
of potential plaque retention areas, e.g., periodontal It includes all the tissues covering the bone, includ-
pockets and bony ledges. ing the periosteum. Thus tooth and bone are bared by
3. To provide an adequate restorative and prosthetic en- the reflection of this type of flap. Generally the full-
vironment, e.g., crown lengthening, alveolar ridge al- thickness flap is used whenever the tissue is thin, i.e.,
teration, and correction of mucogingival defects. 2 mm or less, or when osseous surgery is implicated.
4. For periodontal regenerative therapy. It is elevated by blunt dissection (e.g., periosteal
5. To improve esthetics, e.g., gummy smile. elevator).
Partial, Thickness Flap

CLASSIFICATION OF FLAPS
It splits the gingival tissue. This flap is indicated
• On the basis of exposure of the bone after flap eleva- when the gingiva is thick and fibrotic, or in cases where
tion: bone exposure is to be avoided, e.g., in dehiscence and
Full-thickness (mucoperiosteal) flap fenestrations. It is elevated by sharp dissection (e.g.,
• Partial-thickness (mucosal/ split) flap BP blade).
Flaps for Reconstructive Surgery
LJQOLJ
In recent years, bone grafts, membranes, or combina-
tion of both have been used for better results in recon-
structive surgery. Therefore, flap designs should be set up
in such a way that the maximum amount of gingival tis-
Sulcular incisions on the facial side
sue and papilla are retained to cover the materials placed
in the pocket.
Flap designs available for reconstructive surgery are:
1. Conventional flap with only crevicular incision
2. Papilla preservation flap (most preferable).
Semilunar incision on palatal aspect
Conventional Flap
In this type of flap the interdental papilla is split below
the contact point of the two approximating teeth, which
allows reflection of buccal and lingual flap. It is used
when there are no interdental spaces and the flap has to
be displaced. Papillae are reflected with the facial flap
Papilla Preservation Flap

Here the entire papilla is included into the facial flap.
The lingual or the palatal incisions in the interdental area
consist of a semilunar incision starting on the mesiopala-
tal line angle of one tooth to the distopalatal line angle of
the adjacent tooth so that the incision is 5 mm below the
crest of the papilla. In case of osseous defects, this can be
treated with reconstructive procedures, papilla preserva- Reflected flap with exposed osseous defects
tion flap becomes the flap of choice because it protects the
interproximal areas where the defects are usually present.
It can only be done in presence of wide interdental spaces
(Figs. 48.1-48.4).
Sutures placed
INCISIONS IN PERIODONTAL FLAPS
FIGURE 48.1 Papilla preservation flap.
• Horizontal incisions are given along the margins of

gingiva in mesial and distal directions.
1. Internal bevel incision (reverse bevel/ first incision)
2. Crevicular incision (sulcular / second incision)
3. Interdental (third incision).
Internal Bevel Incision

It is also called as the first incision or the reverse-bevel
incision. By this the flap is reflected to expose the underly-
ing bone defects. It is given with the no. 11 or 15 surgical
scalpel.
Indications
1. Primary incision of flap surgery
2. To correct bone morphology FIGURE 48.2 Papillae reflected with the facial flap with exposed
3. Thick gingiva osseous defect.
CHAPTER 48 FLAP SURGERY 421
FIGURE 48.3 Placement of sutures. FIGURE 48.5 Vertical incision.
4. Deep periodontal pockets lnterdental Incision

5. Crown lengthening. It is also called the third incision. It separates the
Note: Thickness of flap should be greater than 1.5 mm. collar of gingiva that is left after the first two incisions
are given. Orban interdental knife is used to give this
ADVATAGES incision.
1. Provides knife edge margins
• Vertical incisions (releasing/relaxing incision) (Fig. 48.5)
2. Removes pocket lining
3. The uninvolved outer surface of gingiva becomes the The vertical incision has the following advantages:
attached gingiva when it is positioned apically.
1. It allows for adequate access without increased flap
reflection especially in the presence of isolated deep
Sulcular Incision
pockets. It can be done on one or both ends of the hori-
It is also called the second incision or the crevicular zontal incision.
incision. It is given from the base of the pocket to the 2. It provides flap flexibility, which helps in repositioning
crest of the bone. No. 12 surgical blade is used to give a flap. Repositioned flaps need vertical incisions at both
this incision. ends of the horizontal incisions.
Indications of Sulcular Incision The use of a vertical incision during routine flap
1. Narrow band of attached gingiva reflection is a function of the clinician's preference and
2. Thin gingival margin judgement. If vertical incisions are used, the following
3. Shallow periodontal pocket rules should be followed:
4. As a secondary incision of flap surgery
1. The incision should always be made at a line angle,
5. For regenerative procedures
never directly in the center of an interdental papilla or
6. To reduce postoperative gingival recession.
over the radicular surface.
2. Vertical incisions on the lingual or palatal areas should
be preferably avoided.
3. Short flaps with long apically directed horizontal in-
cisions must be avoided as they compromise on the
blood supply.
4. Vertical incisions must extend beyond the mucogingi-
val junction for the release of the flap.
Envelope flaps are the flaps where only horizontal

incisions are given. No vertical incisions are utilized.
(Fig. 48.6).
Papilla preservation flap - This flap offers the advan-
tage of better postsurgical aesthetics and more protection
for the interdental bone, which is especially important
FIGURE 48.4 Placement of sutures on lingual aspect. when bone-regeneration techniques are attempted.
Internal bevel incision Sulcular incision
FIGURE 48.8 Reflection of flap.
lnterdental incision Flap elevated
FIGURE 48.6 Schematic diagram showing steps for envelop flap

reflection.
Flap Technique for Treatment of Pockets

(Modified Widman Flap)
The original Widman flap was described in 1918 by
Leonard Widman, and was a procedure that was aimed FIGURE 48.9 Sulcular incision.
at removal of the pocket epithelium and pocket elimina-
tion by apical displacement. It resulted in exposure of the
root surfaces and, in some cases, alveolar bone exposure.
Ramfjord and Nissle modified this procedure in 1974 as
a technique for open curettage aimed at reattachment
rather than pocket elimination. The procedure is much
more conservative than pocket-elimination procedures,
as it involves replacing the flap in its original position to
avoid root exposure (Figs. 48.7-48.11).
FIGURE 48.10 Curettage and debridement.
FIGURE 48. 7 Internal bevel incision. FIGURE 48.11 Suture placement.

INDICATIONS OF MODIFIED WIDMAN FLAP

1. Pockets where the bases are located coronal to the mu-
cogingival junction
2. Little or no thickening of the marginal bone
3. Shallow to moderately deep pockets
4. Esthetics important especially in the anterior region of
patients with a high smile line.
ADVANTAGES
1. It exposes the root surface for effective debridement
and root planing.
2. It also allows complete removal of pocket epithelium.
3. The flaps can be replaced at the original location to
encourage healing by primary intention.
PROCEDURE
FIGURE 48.12 Preoperative.
l. Internal bevel Incision: An internal bevel incision is
made 1 mm from the gingival margin on both the
facial and lingual sides of either the upper or lower
arches. The aim of this incision, as with other flap
techniques, is to separate the pocket epithelium and
inflamed connective tissue from the flap. No vertical
relieving incisions are made unless necessary for re-
flection purposes.
2. Reflection of the flap: Full-thickness mucoperiosteal
flap is reflected with a periosteal elevator, in order to
expose the roots of the teeth and the bone margin.
3. Sulcular incision: The second incision is made after the
reflection from the base of the sulcus to the crest of the
bone.
4. Interdental incision: The third incision is made with
sharpened Orban interdental knives following the con-
tour of the crest and the interproximal septum to excise
the loosened collar of tissue.
5. Curettage, degranulation, and debridement: The collar of
FIGURE 48.13 Internal bevel incision given.
tissue is removed with curettes and the root surfaces
are debrided. Diseased granulation tissue is cleared
from the surface of infrabony lesions to create the best
conditions for bone regeneration.
6. Suturing: The flaps are then coapted in their original
position and secured with interrupted sutures. Every
effort is made to ensure total interdental coverage and
avoid any root exposure. In some cases, flaps may have
to be thinned and some bone removed from the outer
aspects of the alveolar process to ensure coaptation of
the flaps.
APICALLY DISPLACED FLAP

An apically displaced flap is a full-thickness or a
partial-thickness flap made with an internal bevel inci-
sion or sulcular incision that is displaced apically from
the original position at or slightly coronal to the alveolar
crest (Figs. 48.12-48.16). FIGURE 48.14 Tissue excised.
THE UNDISPLACED FLAP

The undisplaced flap differs from the modified Wid-
man flap in that the soft-tissue pocket wall is removed
with the initial incision; thus, it is also referred as an in-
ternal bevel gingivectomy. This procedure is performed
only in those cases where there is an adequate amount
of attached gingiva even after elimination of the pocket
wall, e.g., fibrotic gingival enlargement and palatal flap.
The advantage of this procedure is that it minimizes the
exposed postsurgical wound surface.
TECHNIQUE
1. After the pockets are measured with a periodontal
probe, bleeding points are created on the outer surface
of these pockets with a crone kaplan pocket marker.
2. Following the bleeding points, an internal bevel inci-
sion is given apical to the alveolar crest.
The flap should be thinned with the initial incision.
3. Using a periosteal elevator, a mucoperiosteal flap is
reflected.
FIGURE 48.15 Sutures placed. 4. A second incision, the crevicular incision is given from
the base of the pocket to the alveolar crest detaching
the connective tissue from the bone.
5. An interdental incision is made separating the connec-
tive tissue from the underlying bone.
6. A triangular wedge of tissue is removed and the area
is debrided.
7. After the necessary scaling and root planing procedure,
the flap edge should rest on the root-bone junction.
8. A continuous sling suture is placed and a periodontal
pack given.
DISTAL WEDGE PROCEDURES

The treatment of periodontal pockets on the distal sur-
face of the terminal tooth in the arch is complicated due
to the following reasons:
1. Presence of bulbous tissues over the tuberosity
2. A prominent retromolar pad in the mandible
3. Inadequately attached gingiva
4. Abruptly ascending tuberosity
FIGURE 48.16 Postoperative. 5. A close ascending ramus of the mandible.
The gingivectomy procedure is the first approach in
INDICATIONS treating distal pockets that have no osseous lesions and
1. Moderate to deep pockets, especially those where the adequate amount of attached gingiva.
base is apical to the mucogingival junction However, when only limited amounts or no keratin-
2. Increase in the width of keratinized gingiva ized tissue is present or an angular osseous deformity is
3. Crown lengthening procedures present, distal-wedge procedure is advocated.
4. Treatment of furcation involvement, especially Grade The following considerations determine the location
III types of the incision for distal molar surgery:
CONTRAINDICATIONS 1. Accessibility
1. Esthetic reasons (compromised esthetics). 2. Amount of attached gingiva
2. In patients at risk for root caries, as the flap leads to 3. Pocket depth
exposure of the root surface. 4. Available distance from the distal aspect of the tooth
3. Dentinal hypersensitivity. to the end of tuberosity or retromolar pad.
Technique (Figs. 48.17 and 48.18) 2. The facial and lingual incisions should be extended in
a mesial direction along the buccal and lingual surfaces
1. Buccal and lingual incisions are made in a vertical
of the molar to facilitate flap elevation.
direction through the tuberosity or retromolar pad
3. The facial and lingual walls of the tuberosity or ret-
to form a triangular wedge. The outline of the inci-
romolar pad are reflected and the incised wedge of
sions may be rectangular or triangular. Rectangular
tissue is dissected and separated from the bone.
incisions may be utilized in the maxillary tuberosity
4. The flaps are then reduced in thickness by undermining
areas where the attached gingiva is adequate. Inci-
incisions. Loose tissue tags are removed, and the root
sions may be close to either the buccal or lingual,
surfaces are scaled and root planed.
which is determined by the amount and position of
5. The flaps are replaced over the exposed alveolar bone
the attached gingiva.
and the edges trimmed to avoid overlapping wound
margins. Sutures are then placed (Figs. 48.18-48.21).
Incision is given in areas of attached gingiva
Undermining incisions given to reduce

the thickness of the flap
FIGURE 48.1 7 Digital wedge. FIGURE 48.19 Periodontal pocket distal to third molar.
FIGURE 48.18 Preoperative. FIGURE 48.20 Distal wedge surgery performed.

After thorough debridement and osseous surgery, if

required, flaps are then adapted at the root bone junction
and sutured.
INTERDENTAL DENUDATION PROCEDURE It is the

excision of all interproximal soft tissue in the reflection of
a flap to bare the interproximal bone. The root surfaces are
planed and the flap is sutured below the alveolar crest. A
periodontal dressing is placed over the bared bone. Heal-
ing is by secondary intention.
HEALING AFTER FLAP SURGERY

Initial Healing ( 0 to Within 24 H)
After the flap is positioned in its desired position, a
FIGURE 48.21 Sutures placed. blood clot is formed between the flap and the underly-
ing bone. It consists of a fibrin reticulum with polymer-
phonuclear neutrophils (PMNs), red blood cells (RBCs),
debris from injured cells, and capillaries at the edge of
the wound. There are also bacteria and an exudate or
THE PALATAL FLAP transudate as a result of tissue injury. A thinner clot is
Since the masticatory mucosa has no elastic or desirable than a thick one because: (i) a smaller amount of
loose connective tissue fibers, the palatal flap cannot interposed reparative tissue is necessary for attachment;
be positioned apically nor can a partial thickness flap (ii) there is less clot to be resorbed before reattachment
be deflected. Thus the initial incision for the palatal can occur.
flap should be such that when the flap is sutured, it
is precisely adapted at the root-bone junction. Hence 1-3 Days
the location of the initial incision is important for final
placement of the flap. The epithelial cells migrate over the border of the flap.
A minimal inflammatory response is observed when the
ESTIMATING THE POSITION OF THE INITIAL INCI- flap is closely adapted to the alveolar bone.
SION The position of the initial incision depends on the
pocket depth, thickness of tissue, and the position of the os- 4-10 Days
seous crest on the palatal root following osseous recontour-
ing. The initial incision varies with the anatomic situation: After the first 3-4 days the fibrin clot starts undergoing
resorption and is usually completely replaced 6-7 days
1. The initial incision may be the usual internal bevel postoperatively by young connective-tissue prolifera-
incision followed by the crevicular and interdental tion from the underside of the flap and the periodontal
incisions. ligament. The periodontal ligament is the prime source
2. If the tissue is thick, a horizontal gingivectomy incision of early connective tissue reattachment to the tooth and
may be made followed by an internal bevel incision marginal bone. Revascularization tends to follow the
that starts at the edge of this incision and ends on the pattern of new connective tissue formation, which moves
lateral surface of the underlying bone. coronally as the clot is resorbed.
3. The thicker the tissue, the more apical the incision By 1 week, epithelial cells have approximated the root
should be placed. surface by migration and initiated the epithelial attach-
Flaps should be thinned to adapt to underlying osseous ment and sulcular lining. Bone resorption has peaked at
tissue and provide a thin knife-edge margin. Scalloping of about 8-10 days postoperatively. At this time, the flap
the gingival margin should be reproduced. The triangular is bluish red in color from an inflammatory response
papilla portion should be thin enough to fit snugly against showing loss of stippling and a shiny appearance with
the bone and into the interdental area. the presence of an exudate. The tooth may have some
mobility and may be tender to palpation or percussion The needle should be entered at right angles to the
because of edema and cellular activity in the periodontal tissue when penetrating through tissues.
ligament. Sutures should be placed no closer than 2-3 mm from
the flap edges to prevent tearing through the flap during
postoperative swelling.
10-21 Days The flaps should be approximated without blanch-
Healing at 10-21 days shows an inflammatory re- ing when sutured as to prevent restriction to the blood
sponse that is less marked than before and a changing supply
pattern with respect to bone. Cresta! resorption can be
seen to a minor degree, but repair in the form of osteoid Suture Types
tissue being laid down starts. The periosteal bone under- • Nonabsorbable
goes peak resorption from days 14-17 with buildup on • Silk sutures
the periodontal surface and resorption on the periosteal • Polyester sutures
surface. - Nonfilament (i.e., Ethibond)
The soft tissues show signs of healing and maturation - PTFE (poly tetrafluoroethylene)
with collagen fiber bundles replacing the finer fibrils pre- • Absorbables
viously present. • Surgical gut
- Plain (resorption rate 3-5 days)
- Chromic (resorption rate 7-10 days)
21 Days and beyond
• Coated vicryl
Cementum anchors periodontal fibers to the tooth. - Polyglactin 910 suture (resorption rate
Maturation and repair of all tissues involved is occurring. 21-28 days).
Bone formation repairs most of the lost bone. The end
results are a slight decrease in crestal height and a slight
thinning of the alveolar septum, the extent depending on Techniques
the quality and thickness of bone. The suturing techniques
By 1 month, the flap is firmly attached via dense The independent, interrupted suturing techniques
organized connective tissue and cementum. A fully consist of the simple-loop technique and the figure-8
epithelialized gingival crevice with a well-defined epi- technique.
thelial attachment is present. Supracrestal fibers begin Simple loop suturing technique is used to coapt
to adapt a functional arrangement. Gentle sulcular prob- tension-free surgical flaps as in edentulous ridges,
ing can be done at this time but is usually delayed until modified Widman flap, and periodontal regenerative
2-3 months. procedures.
In this technique, the needle passes through the facial
and the lingual or the palatal tissue.
SUTURING The interrupted suture encompasses two suturing
techniques:
The main objective of suturing is to secure and po-
sition the periodontal flaps to promote healing by pri- • The simple loop
mary intention. When sutured properly, the sutures • The figure 8.
should hold the flap in position until the wound has Simple loop: Most commonly and routinely used sutur-
healed sufficiently enough to withstand functional ing technique in flap surgery. It is commonly used in the
stresses. suturing of vertical releasing incisions, periosteal sutur-
ing, and modified Widman flap. Here, the needle passes
Principles of Suturing through the facial and the lingual tissues.
During suturing, the sutures should first be inserted The figure-8 technique (Fig. 48.22): This suture is simi-
through the mobile tissue flap first. lar to the simple loop, only difference being that, on the
Suturing is usually started from the distal most tooth, lingual or palatal aspect, the needle penetrates through
in each interproximal space, and continued in a mesial the outer surface and not the inner surface of the lingual
direction. or palatal flap.
Only needle holders should grasp suture needles, and The suture is placed similarly to the simple loop on
the latter should be inserted and pulled through the tissue the buccal aspect; however, on the lingual aspect, the
in line with the circle. needle penetrates through the outer, not inner, surface of
FIGURE 48.22 Figure-8 technique.

FIGURE 48.23 Horizontal mattress suture.
the lingual flap. This results in suture thread being inter- Types of Sutures
posed between the surgical flaps. Both of the interrupted Mattress sutures: In areas where tension-free flap clo-
suture techniques achieve similar results when used for sure cannot be achieved, mattress sutures are used.
wound closure with tension-free flaps. Figure-8 technique The various mattress sutures are vertical, apical or
is useful when suturing on the lingual aspect of the lower coronally repositioned, vertical sling, and horizontal
molars, especially in a patient with an active gag reflex or mattress.
a large, cumbersome tongue.
FIGURE 48.24 Sling suture.
When performing a mattress suture, the needle pen- is independently repositioned to its original position or
etration through the surgical flap should be about 8 mm coronally repositioned. In the author's opinion, the sling
away from the flap edge, or just coronal to the mucogin- suture technique is especially useful when performing
gival junction, and always in keratinized tissue. coronally repositioned sliding flaps.
Horizontal mattress suture (Fig. 48.23): It is given by Continuous sutures: They can be used to attach two
penetrating the needle at the mesiobuccal gingiva, apical surgical flap edges or secure multiple interproximal papil-
to the mucogingival junction and exited at the mesiolin- lae of one flap independently of the other flap. Although
gual position. The suture then penetrates the diatolin- there is a distinct advantage of the continuous suture in
gual position and exits the flap through the distobuccal that there are fewer individual suture ties, the disadvan-
position and the suture ends are tied at the mesiobuccal tages of using any continuous suture far outweigh the
position. advantages of its use. This is most likely because there is
Sling suture (Fig. 48.24): The interrupted suspensory a tremendous likelihood that one knot or loop will break,
suture, commonly referred to as the sling suture, is used resulting in a compromise in the integrity of the entire
when only one side, or one or more papillae of a flap, surgical site.
KEY POINTS
• A periodontal flap is a section of the gingiva and/ or • Indications of modified Widman flap are: (i) pockets
alveolar mucosa surgically elevated from the underlying where the bases are located coronal to the mucogin-
tissues to provide visibility and access to the bone and gival junction, (ii) there is little or no thickening of
root surface. the marginal bone, (iii) shallow to moderately deep
• Repositioned (positioned, displaced) flaps include: pockets, and (iv) esthetics is important especially in
(i) laterally displaced flap, (ii) coronally displaced flap, the anterior region of patients with a high smile line.
and (iii) apical displaced flap. • Indications for apically positioned flap include:
• Incisions in periodontal flap are: (i) internal bevel inci- (i) moderate-to-deep pockets, especially those whose
sion (reverse bevel/ first incision), (ii) crevicular incision base is apical to the mucogingival junction, (ii) in-
(sulcular / second incision), and (iii) interdental (third crease in the width of keratinized gingiva, (iii) crown
incision). lengthening procedures, and (iv) treatment of furca-
• The original Widman flap was described in 1918 by tion involvement, especially Grade III types.
Leonard Widman and was a procedure that was aimed
at removal of the pocket epithelium and pocket elimina-
tion by apical displacement.

1. Klaus H, Rateitschak ME, Wolf HF, Hassel Thoma M. Colour Atlas of
1. Define a periodontal flap. State the indications and Periodontology. Vol. 60. 1989; p. 599-603.
contraindications of flap surgery. 2. Lindhe J. Clinical Periodontology and Implant Dentistry. 5th ed. Oxford:
2. Enumerate the different methods of pocket elimination. Blackwell Munksgaard; 2008.
3. Describe the modified Widman procedure.
4. Classify flaps. Saunders Company; 2006.
4. Ramfjord SP. Present status of modified widman flap procedure.
J Periodontal 1977;48:558.
5. Rose LF, Mealey BL, Genco R. Periodontics: Medicine, Surgery and
Implants. 1st ed. St Louis: Elsevier; 2004.
CHAPTER
49
Resective Osseous Surgery
CHAPTER OVERVIEW
Bacterial plaque has been implicated as the major etio- and connective tissue. The other method for eliminating
logic agent in the initiation and progression of inflamma- an intrabony defect is to remove the walls of the defect.
tory periodontal disease. Resorption of the osseous margin As a result the gingival tissues can be placed more apical.
with an apical shift of the connective tissue and junctional Reversals in bony topography seen in periodontal disease
epithelium attachment occurs with periodontitis, hence have to be corrected to achieve ideal topography. The re-
forming an uneven osseous topography. To eliminate in- moval of both the supporting bone referred to as ostec-
trabony or hemiseptal defects the ideal method is to re- tomy and nonsupporting bone known as osteoplasty along
generate periodontal ligament, lost bone, and cementum, with an apically positioned flap is an objective of osseous
which results in a new position of the junctional epithelium resective surgery.
HISTORICAL BACKGROUND of normal contours and anatomic aberrations present in

the patient's osseous form (Clarke, 1971).
For the treatment of periodontal disease removal of in-
• Nonpathological osseous defects:
terproximal bone and superficial radicular bone has been
• Fenestrations
utilized for a long period. Pierre Fauchard in 1776 stated
• Dehiscence
that: "If however the bone is carious then it must be uncov-
• Exostosis
ered to its whole extent and the cure carried out." Previous-
• Tori
ly it was thought that bone was necrotic and infected and
• Prominent mylohyoid ridge.
had to be removed. Many earlier therapists advocated the
• Pathological osseous defects:
use of gingivectomy along with radicular and interproxi-
• Horizontal bone defect
mal denudation. Widman however reshaped the alveolus
• Angular or vertical bone defects:
to facilitate flap placement, and Neumann (1982) also tried to
- One-wall infrabony defect (hemiseptum)
recontour bone to mimic more normal anatomy. Kronfeld in
- Two-wall infrabony defect
his classic work stated that bone in periodontal disease was
- Three-wall infrabony defect (intrabony defect)
neither necrotic nor infected and it need not be removed.
- Combined defect - combination with
Schluger in 1949 stated the principles of osseous surgery for
different number of walls at various levels of de-
bone recontouring so that the elimination of the periodontal
fects
pocket was more predictable and less likely to return over
• Osseous crater
time. The technique for osseous surgery in the treatment
• Bulbous bone contour
of periodontitis was popularized by Schluger and his col-
• Buttressing bone formation
leagues JP Richard, N Friedman, and C Ochsenbein.
• Inconsistent bony margin/ reverse architecture
• Ledges
CLASSIFICATION OF OSSEOUS DEFECTS • Osseous defects associated with furcation involve-
ment:
In osseous surgery, the existing bony topography is - Class I
changed to eliminate periodontal pockets. When a thera- - Class II
pist performs osseous resection, there must be awareness - Class III
DEFINITIONS over the facial and lingual prominences of the roots.

A flat osseous architecture may be created in order to
Osseous Surgery preserve bone and to avoid opening furcations.
2. An alveolar crest parallel to the adjacent cementoenam-
• Periodontal surgery involving modification of the bony el junction: The interdental bone margins in the bicus-
support of the teeth (AAP, 1992). pid and anterior regions are curved to conform to the
• The procedure by which changes in the alveolar bone contour of the cementoenamel junctions. In contrast,
can be accomplished to rid it of deformities induced interdental septum in the molar region is relatively flat
by the periodontal disease process or other related fac- or straight.
tors, such as exostosis and tooth supraeruption. When 3. A thin alveolar margin: The bony margin on the facial
further osseous reshaping would not improve the over- and lingual aspects of the teeth should be 0.5-1 mm
all result, it is termed definitive osseous surgery, and wide. The alveolar bone becomes thicker as it pro-
when the bone pattern cannot be improved without gresses apically.
significant osseous removal that would be detrimental 4. The bone is festooned in buccolingual contour. Some
to the overall result, it is termed compromised osseous grooves are made on the facial and some on lingual
reshaping. surfaces apical to interdental areas and furcations.
Additive Osseous Surgery These grooves improve gingival form and provide
access for plaque control.
It includes procedures directed at restoring the alveolar
5. The contour in the level and shape of the bone is made
bone to its original level.
harmonious gradually. Precipitous changes in the bo-
Subtractive!Resective Osseous Surgery ny contours are not usually followed by the gingiva.
It is designed to restore the form of preexisting alveolar Gradual changes in the height and contour of the bone
bone to the level existing at the time of surgery or slightly allow the gingival tissues to duplicate the form of the
more apical to this level. underlying bone.
6. Since thick fibrotic gingiva prevents compatibility be-
1. Osteoplasty: Reshaping of the alveolar process to tween gingiva and bone, dense connective tissue in the
achieve a more physiologic form without removal of tuberosity and palatal regions is thinned.
supporting bone
2. Ostectomy: The actual removal of the alveolus, which INDICATIONS OF RESECTIVE OSSEOUS SURGERY
directly supports the root (the bony portion or attach- 1. To eliminate osseous defects that are not suitable for
ment portion of attachment apparatus). attempts at treatment to gain a new attachment ap-
OBJECTIVES AND RATIONALE OF RESECTIVE paratus. Such infrabony pockets (defects) usually
OSSEOUS SURGERY have a shallow or wide aspect to their topography.
The volume of missing or destroyed periodontium
Osseous resective surgery is the most predictable is greater in proportion to the remaining bony walls
pocket reduction technique. However, more than any of the defect or the remaining walls are composed of
other surgical technique, osseous resective surgery is thin cortical plates of bone. These factors can be
performed at the expense of bony tissue and attachment grouped as the "quantity and quality" factor of the
level (Carranza, 1956). Thus, its value as a surgical ap- remaining osseous tissue.
proach is limited by the presence, quantity, and shape of 2. To eliminate shallow to moderately deep osseous de-
the bony tissues, and by the amount of attachment loss fects around stable teeth with long, large, well-formed
that is acceptable. roots. Such teeth have a favorable crown-root-bone
The major rationale for osseous resective surgery is relationship and can withstand the loss of moderate
centered on the discrepancies in the levels and shapes amounts of support without untoward clinical effects.
of the bone and gingival margin that predispose to the 3. To eliminate ledging, inconsistent bony margins, lip-
recurrence of pocket postsurgically (Ochsenbein, 1977). ping of the crestal bone, exostoses, tori, and so on,
The goal of osseous resection is to keep the alveolar which may interfere with the management of the soft
bone free of bony discrepancies that predispose to recur- tissue portion of the lesion. Bony aberrations that
rence of pocket depth. In osseous surgery, alveolar bone interfere with placement and stabilization of the over-
is resulted to establish an ideal osseous architecture with lying tissue flap must be reshaped if desired contours
the following characteristics: are to be produced in the healed soft tissue portion
1. A positive osseous architecture (scalloping): This oc- of the treated lesion so that the host is able to cleanse
curs when the alveolar bone is more coronal inter- the teeth without interference because of unfavorable
dentally and in the facial and lingual fractions than soft tissue-osseous tissue topography.
CHAPTER 49 RESECTIVE OSSEOUS SURGERY 433
4. To alter soft tissue-osseous tissue topography adjacent 6. Anatomic factors such as the close proximity of the
to incipient or moderate furcation involvement areas maxillary antrum or the ramus.
to facilitate cleansing of the area and lessening of the
tendency for plaque accumulation. Advantages
5. To alter osseous contours adjacent to: 1. Dependability: The procedure is dependable, for
a. Root resection areas one has visual assurance that the pockets have been
b. Hemisections eliminated and the desired contours produced.
c. Fractured crowns or roots and other such problems Nothing is left to change in the hope that the de-
associated with periodontal-endodontic lesions fects will fill with bone and new attachment to the
d. Traumatic fractures roots will take place. This obviates the possibility that
e. Deep-seated caries. future second-stage reentry procedures may become
a necessity to eliminate residual portions of osseous
CONTRAINDICATIONS OF RESECTIVE defects that did not completely "fill" where new at-
OSSEOUS SURGERY tachment procedures were done.
1. Osseous defects whose overall topography would fa- 2. Promptness: Promptness becomes important when
cilitate attempts at treatment to gain a new attachment a succession of procedures must be completed, each
apparatus. Such pockets associated with these defects in its turn, to treat a complicated case. Many patients
have narrow, deeper conformations and a more favor- cannot afford to make themselves available for the
able ratio between the volume of the periodontium treatment or remain in one location for long periods
to be regenerated and the surface area present in the of time.
surrounding bony walls. Also, the osseous walls of 3. Simplicity: The skill level and training required to raise
the pocket have ample cancellous bone and marrow a surgical flap and contour osseous tissues to the de-
spaces lateral to them that are capable of furnishing sired degree fall well within the treatment capabilities
the progenitor cells necessary to effect regeneration of of the general practitioner who is interested in treating
bone, collagen fibers, and cementum. periodontal disease. The skill required to accomplish
2. Osseous defects of large volume and dimension, the mechanics of the procedures can be mastered with-
which if treated by osseous recontouring to produce out undue difficulty.
physiologic contours at more apical levels, would
Disadvantage
necessitate the removal of excessive amounts of bone
and irreparably weaken the support of the teeth in the Sacrifice of attachment apparatus: In some instanc-
area. es, nonsupporting bone is removed, but in most
3. Infrabony pockets and associated osseous defects of instances, attachment apparatus is intentionally
shallow depth or dimension around mobile teeth with sacrificed. In the latter instances, the bony portion
short, cone-shaped roots. Such teeth have an unfavor- of the alveolus into which the principal fibers of the
able crown-root-bone relationship and cannot with- periodontal ligament insert is removed, and
stand the loss of minimal to moderate support without the amount of root structure embedded into the sup-
untoward clinical effects. porting socket is lessened, which compromises the
4. Osseous defects, which if considered as a separate en- attachment apparatus.
tity, could be treated by osseous resection, but whose
adjacent soft tissues do not permit successful treatment
to be accomplished. This is frequently experienced in SURGICAL PROCEDURE
infrabony defects distal to second and third molars in
which the contiguous soft tissue is loose, elastic alveo-
Initial Preparation
lar mucosa, the contents of the hamular notch area,
and so on. Since both the osseous lesion and soft tissue Meticulous attention is devoted to the prerequisites of:
lesion must be treated, it is not infrequent that the at- (i) documentation, (ii) scaling, (iii) root planing, (iv) oc-
tendant mucogingival problem dictates the course of clusal adjustment, and (v) control of habits and traumatic
therapy to be followed, if any, and assumes a position occlusion. One can approach the surgical procedure fully
of greater importance in therapy than the underlying informed of the problems to be surmounted.
osseous portion of the pocket.
5. Where the underlying osseous structures have pro-
duced lipping, exostoses, and so on, and a resulting
Diagnosis or Evaluation of Osseous Defects
flat or shelf-like gingival topography, but where no Procedures that maximize the potential for repair of the
pockets exist. attachment at more coronal levels on the roots of the teeth
are preferred over the ones that eliminate the osseous 5. Rongeurs: Friedman and 90° Blumenthal
defects by resection procedures. Depending on the mor- 6. Diamond burs.
phology of the defect, the quantity and quality (marrow-
cortical ratio) of the bone composing the walls of the os-
seous defects, and the orthodontic-occlusal relationships Flap Design and Management
that exist, osseous defects may be treated by single-stage Of paramount importance is the location of the mu-
or multistage procedures. cogingival junction and width or the zone of attached
Osseous resection has been the procedure of choice gingiva that surrounds the infrabony pocket. The design
of most periodontists to eliminate osseous defects that of the flap, how it is raised from the bone, how much it is
are not suitable to be treated by new attachment pro- reflected, how it is handled during the retraction phase of
cedures. Osseous resection is limited to defects whose surgery, and how and where it is placed for stabilization
base is located 3-5 mm from cementoenamel junction. during initial stages of wound repair all reflect on how
The removal of supporting bone in defects greater than well the soft tissue component of the infrabony pocket
7 mm becomes self-defeating because of the excessive will be resolved.
loss of attachment apparatus that is incurred in eliminat- The flap can be thinned in the marginal area and made
ing the defects. to follow the contours carved into the bone. It covers the
It is important for the clinician to have knowledge of bone in a veneer-like fashion, and the margin of the flap is
the underlying bone tissue prior to flap reflection. The preferably placed at the <lento-osseous margin. Since the
clinician must gain as much indirect knowledge as pos- thinned flap has a minimum amount of connective tissue,
sible from soft tissue palpation, radiographic assessment, its minimal biologic thickness will place the oral surface of
and transgingival probing (sounding). the flap approximately 1-1.5 mm above the bony margin
Radiographic examination can reveal the existence of next to the planed root of the tooth. If the flap is placed
angular bone losses in the interdental spaces; these usu- too far coronally, especially in the interdental areas, it
ally coincide with infrabony pockets. The radiograph will is likely that the flap-tooth interface will be covered by
not show the number of bony walls of the defect, nor epithelium, resulting in a healed sulcus of greater depth
will it determine with accuracy the presence of angular than desired. It is better to place the flap slightly coronal
bone defects on facial or lingual surfaces. to the <lento-osseous margin. The granulation tissue from
Clinical examination and probing will determine the the periodontal ligament (POL) will quickly fill the void,
presence and depth of periodontal pockets on any surface and the chances of attaining a shallow sulcus postopera-
of the tooth and can also give a general sense of the bone tively are improved.
topography, but infrabony pockets can go undetected by The bone that is removed via ostectomy exposes root
probing. Both clinical and radiographic examinations can structure (cementum) that has not been exposed in the
indicate the presence of infrabony pockets when: (i) angu- pocket. This cementum is vital, and the POL fibers are tom
lar bone losses, (ii) irregular bone losses, or (iii) pockets as this bone is removed. It is important that this area of the
of irregular depth in adjacent areas of the same tooth or root not be planed with curette, for to do so would destroy
adjacent teeth are found. the severed collagen fibers embedded in the cementum.
Transgingival probing is extremely useful just prior If the cut edge of the connective tissue of the flap is ap-
to flap reflection. It is necessary to anesthetize the tissue proximated against these fibers remaining in the root, it
locally prior to inserting the probe. The probe should be is possible to have the flap reattach to the teeth.
"walked" along the tissue-tooth interface so that the op- If the projected final position of the alveolar crest, in
erator can feel the bony topography. The probe may also the mandibular buccal and lingual and maxillary buccal
be passed horizontally through the tissue to provide more areas, is apical to the mucogingival junction, the gingival
three-dimensional information regarding bony contours flap is dissected in a way that allows its movement in an
(i.e., thickness, height, shape). apical direction (Friadman, 1962). A precise anchorage
of the flap in the desired position can be enhanced by
initially performing a split-thickness or a thinned full-
thickness or split-thickness flap that is then secured with
Armamentarium
periosteal sutures. To mobilize the flap vertical incisions
1. High-speed handpiece with fiber optics and surgical may be given mesially or distally. Apical positioning of
burs, which come with longer shanks (no. 8, 6, 4 car- the flap palatally is not possible. The palatal flap can be
bide); flame-shaped and spear-shaped (carbides) scalloped to follow the crest of the bone. Palatally vertical
2. Bone files: Schluger, Buck, and/ or Sugarman incisions may be necessary to achieve good access to the
3. Chisels: Wedelstaedt, back action, Rhodes and bone beneath.
Ochsenbein The primary incision of the apically positioned flap
4. Ultrasonic scalar can be at varying distances from the gingival margin or
it can be intrasulcular. The apicocoronal dimension of
the keratinized tissue and the probing depth dictate the
design and the position of this incision. If there is "ad-
equate" dimension of gingiva, the distance of the primary
incision from the gingival margin is proportional to the
differences in probing depths of the adjacent teeth. The
gingival margin coincides with the crest by the apical
positioning of the flap. If there is "inadequate" keratin-
ized tissue, the primary incision should be intrasulcu-
lar and the flap apically positioned at the osseous crest.
The final tissue position can be facilitated by vertical
incisions. In the palate, the position of the primary scal-
loped incision and thinning of the flap are dictated by the
anatomy of the palatal vault and the probing depth of the
teeth. In the case of a shallow palatal vault the primary FIGURE 49.1 Thick alveolar housing on buccal aspect.
incision is closer to the gingival margin. In the case of a
deep vault the distance of the primary incision from the
gingival margin is approximately coincidental with the
probing depths.
In areas of aesthetic importance it is important to limit
the soft tissue recession both in the buccal radicular and in
interproximal aspects. The papilla preservation technique
in association with a thinned palatal flap can be used.
If osseous defects are confined only to palatal aspects,
a palatal approach without the use of a buccal flap can
be utilized.
Technique
In order to handle the multitude of clinical situations,
the following sequential steps are suggested:
1. Vertical grooving
2. Radicular blending
3. Flattening interproximal bone FIGURE 49.2 Vertical grooving reducing the thickness of alveolar
4. Gradualizing marginal bone housing.
All the steps are not necessary in all the cases, but the
sequence of steps in the order given is necessary to expe-
dite the reshaping procedure, as well as to minimize the
removal of bone. It is classically applied to shallow craters
with thick faciolingual ledges.
Vertical Grooving
It is designed to reduce the thickness of the alveolar
housing and to provide relative prominence to the ra-
dicular aspects of the teeth (Figs 49.1-49.3). It also pro-
vides continuity from the interproximal surface onto
the radicular surface. It is the first step of the resective
process because it can define the general thickness and
subsequent form of the alveolar housing. It is generally
performed with rotary instruments such as round carbide
burs or diamonds.
The advantages of vertical grooving are most appar- L /
ent with thick, bony margins; shallow crater formations ._ _
(Fig. 49.4); or other areas that require maximal osteoplasty FIGURE 49.3 Vertical grooving.
Flattening of Interproximal Bone

It requires the removal of very small amounts of sup-
porting bone (Fig. 49.5). It is indicated when interproxi-
mal bone levels vary horizontally: one-wall interproximal
defects (hemiseptal defects). The omission of this step in
such cases results in increased pocket depth on the most
apical side of the bone loss. This step is not necessary in
classic crater formations or in flat interproximal defects.
It is best utilized in defects that have a coronally placed
one-wall edge over a three-wall angular defect, and it can
be helpful in obtaining good closure and, subsequently,
improved healing in three-wall defects.
It is limited in the treatment of advanced lesions.
Large hemiseptal defects would require removal of inor-
FIGURE 49.4 Shallow interdental craters. dinate amount of bone to provide a flattened architecture,
and the operation would be too costly in terms of bony
support. Compromise osseous architecture is the only
logical solution.
and minimal ostectomy. Vertical grooving is contraindicated

in areas with close root proximity or thin alveolar housing. Gradualizing Marginal Bone
It is also an ostectomy process (Figs 49.6, 49.7). Bone
removal is minimal but necessary to provide a sound,
Radicular Blending regular base for the gingival tissue to follow. Failure
It is an extension of vertical grooving (Fig. 49.5). It is an to remove small bony discrepancies on the gingival
attempt to gradualize the bone over the entire radicular line angles (widow's peaks) allows the tissue to rise to
surface to provide the best result from vertical grooving. a higher level than the base of the bone loss in the in-
This provides a smooth, blended surface for good flap terdental area. This may make the process of selective
adaptation. It is not necessary if vertical grooving is very recession and subsequent pocket reduction incomplete.
minor or if the radicular bone is thin or fenestrated. Both This step also requires gradualization and blending of
of the above steps are purely osteoplastic techniques that radicular surfaces.
do not remove supporting bone. They compose the bulk These two steps of ostectomy should be performed
of osseous resective surgery. Shallow craters, thick osse- with great care so as not to produce niches or grooves
ous ledges on radicular surface, and class I and early class on the roots. For this reason, various hand instruments
II furcation involvements are treated almost totally with are preferable over rotary instruments for gradualizing
these two steps. marginal bone.
FIGURE 49.5 Radicular blending and flattening of interproximal bone. FIGURE 49.6 Gradualizing marginal bone.
3. Depth and width of osseous defects

4. Number of osseous walls surrounding the osseous
defects
5. Type of bone (cortical plate or cancellous)
6. Tooth mobility
7. Tooth vitality
8. Root anatomy and dimension of root trunk of multi-
rooted teeth
9. Axial inclination of a tooth
10. Prominence of tooth position and alveolar housing
11. Root proximity
12. Bone loss in furcation areas
13. Dimensions of interdental septum in mesiodistal and
buccolingual directions
FIGURE 49. 7 Ideal bone architecture achieved by radicular blending 14. Width of interradicular septum of multirooted teeth
and gradualizing marginal bone. 15. Anatomic structures (external oblique ridge, tori,
maxillary sinus, mental foramen, etc.).
Flap Placement and Closure

ANATOMIC LIMITATIONS AND
Flap is repositioned apically and suturing is done. Mar- CONSIDERATIONS
gin of the flaps is preferably placed at the dento-osseous
margin. Suturing is done with minimal tension on the In the maxillary arch, the dimension and extension of
flaps, to prevent their separation, and also to maintain the maxillary sinus must be kept in mind as the bone is re-
the position of the flaps. Area is covered by periodontal duced. This anatomic area may force one to compromise
dressing for 8-10 days. the resective therapy as there is danger to perforate into the
sinus in an attempt to completely remove the osseous
defects. The divergence of the roots of maxillary molars
Postoperative Instructions
and proximity of the location of furcation areas usually
• Application of ice-pack for 3-4 hours postsurgery. requires a palatal approach for the resection of craters in
• Sutures removal after 8-10 days. the maxillary posterior area. The root trunk for maxillary
• No brushing at the site of surgery. molars extends 3-6 mm apical to the cementoenamel
• Chlorhexidine mouth rinse 0.2 % twice daily. junction. The buccal furcation is usually located 3-4 mm
apical to the cementoenamel junction, and the proximal
furcations are located slightly more apically at 4-6 mm
OSTEOPLASTY from the cementoenamel junction. If one were to remove
the buccal wall of a crater by using a buccal approach for the
Definition: Reshaping of the alveolar process to osseous resection, the buccal furcation could needlessly
achieve a more physiological form without removal of be exposed with loss of the thin bone supporting the
supporting bone. buccal roots. As bone is removed on the buccal surfaces,
the distance between the converging roots ( distobuccal
first molar-mesiobuccal second molar) narrows, thereby
Indications of Osteoplasty reducing the width of the interdental area and creating
1. Lingual or buccal ledges or tori a less favorable environment for the interdental papilla.
2. Buccal or lingual intrabony defects that are shallow Removal of the lingual wall of the crater has less of a
3. Interproximal areas that are thick tendency to involve the proximal furcations and turns
4. Incipient furcation involvements where supporting the topography of the palatal root into a premolar one.
bone need not be removed. The palatal approach increases the distance (mesiodis-
tally) between the palatal roots of adjacent teeth, and
permits greater access to the defect, space for an inter-
FACTORS AFFECTING OUTCOME OF dental papilla, and more convenient access for plaque
RESECTIVE OSSEOUS SURGERY control.
In the mandibular arch the mylohyoid ridge frequently
1. Crown-root-bone relationships presents as a shelf of bone extending lingually in a hori-
2. Relationship of mucogingival tissues zontal direction. As one extends the flap further apically,
the contour drops off precipitously into an undercut been proven to be one of the main periodontal treatment
as the contour cuts back upon itself. A long bevel must modalities.
be produced in the bone in this area so that the contours Although osseous surgical techniques cannot be ap-
may be blended and the flap readapted to the bone in a plied to every single bony abnormality or topographic
smooth tapering profile from the floor of the mouth to the modification, it has been clearly demonstrated that osse-
<lento-osseous margin. ous resective surgery can eliminate and modify defects,
as well as gradualize excessive bony ledges, irregular al-
veolar bone, early furcation involvement, excessive bony
exostosis, hemiseptal defects, and tori. When properly
CURRENT STATUS OF OSSEOUS performed, osseous resective surgery achieves a physi-
RESECTIVE SURGERY ologic architecture of marginal alveolar bone conducive to
gingival flap adaptation. The advantages of this surgical
Osseous resective surgery necessitates the proper con- modality include a predictable amount of pocket reduc-
touring of the bone and the proper placement of the gin- tion that can enhance oral hygiene and periodic mainte-
gival tissues. The use of resective osseous surgery is lim- nance. It also preserves the width of attached gingiva,
ited in treating cases with deep intrabony or hemiseptal while removing granulomatous tissue and providing
defects. These should be treated using different surgical access for debridement of radicular surfaces. All factors
approaches. Osseous surgery provides the best method lead to the conclusion that osseous resective surgery can
for reducing pockets with a hemiseptal or intrabony com- be an important technique to provide a maintainable
ponent of 3 mm or less. Osseous resective surgery has periodontium for periodontal patients.
KEY POINTS
• Resective osseous surgery is the procedure by • A positive osseous architecture (scalloping) is when
which changes in the alveolar bone can be accomplished the alveolar bone is more coronal interdentally and
to rid it of deformities induced by the periodontal disin the facial and lingual fractions than over the facial and
ease process or other related factors, such as exostosis lingual prominences of the roots.
and tooth supraeruption. • The following sequential steps are suggested for resec-
• Osteoplasty is reshaping of the alveolar process to tive osseous surgery:
achieve a more physiologic form without removal of 1. Vertical grooving
supporting bone. 2. Radicular blending
• Ostectomy is the actual removal of the alveolus that di- 3. Flattening interproximal bone
rectly supports the root (the bony portion of attachment 4. Gradualizing marginal bone.
apparatus).
• Osseous resective surgery is the most predictable pocket
reduction technique.

1. Caffesse RG. Resective procedures. In: Proceedings of the World
1. Define osteoplasty and ostectomy. Workshop in Clinical Periodontics. Vol IV. Chicago: American Acad-
2. Describe the steps of resective osseous surgery. emy of Periodontology; 1989:1-8.
3. Describe diagnosis of osseous defects. 2. Fauchard P. The Surgeon Dentist or Treatise on the Teeth. London:
Butterworth; 1946:86. [Translated from 2nd ed., 1776, by Lilian
4. What is the rationale of resective osseous surgery?
Lindsay.]
3. American Academy of Period ontology. Glossary of Periodontal Terms. 8. Schluger S. Osseous resection - a basic principle in periodontal sur-
3rd ed. Chicago: American Academy of Periodontology; 1992 34-35. gery. Oral Surg Oral Med Oral Pathol Oral Radial Endod 1949;2:3-12.
4. Gold SI. Robert Neumann: a pioneer in periodontal flap surgery. J 9. Clarke MA, Bueltmann KW. Anatomical considerations in periodon-
Periodontol 1982;53:456-9. tal surgery. J Periodontal. 1971 oct;42(10):610-25.
5. Kronfeld R. The condition of the alveolar bone underlying periodon- 10. Carranza FA, Carranza Jr FA. The management of the alveolar bone
tal pockets. J Periodontol 1935;6:22-9. in the treatment of the periodontal pocket. J Periodontol 1956;27:29-35.
6. Carranza FA, Newman MG. Clinical Periodontology. -8th ed. Phila- 11. Ochsenbein C. Current status of osseous surgery. J Periodontal.
delphia: WB Saunders; 2002:615-621. 1977;48:577-86.
7. Prichard JF. Advanced Periodontal Disease. 2nd ed. Philadelphia: Saun- 12. Friedman N. Mucogingival surgery: the apically repositioned flap.
ders; 1972 558-565. J Periodontal. 1962;33:328-40.
CHAPTER
50
Regenerative Osseous Surgery
CHAPTER OVERVIEW
The ultimate goal of periodontal therapy is the com- part of current mode of periodontal treatment approach.
plete restoration of the structure and function of diseased However, in order to make possible a truly biologic and
periodontal tissues. Although many conventional peri- functionally complete regeneration, additional important
odontal treatment strategies have been employed to attain prerequisites must be fulfilled in the region of the peri-
this goal, results have not been satisfactory. Despite the odontal defect: a biocompatible root surface, presence of
fact that some regeneration may occur following minimal precursor cells, exclusion of the epithelium and gingival
periodontal invasive procedures, complete regeneration connective tissue from the root surface, and stabilization
seems to be an unrealistic goal. Conventional periodon- of the wound area (protection of the coagulum and its
tal therapy aims at only treating periodontal pathology, adhesion to the biomodified root surface). Use of bone
not focusing on regeneration of the lost tissues. Regen- substitute grafts, especially in angular bone defects, re-
eration of periodontium is considered to be an essential sulted in bone regeneration.
PRINCIPLES OF OSSEOUS • Basic fibroblast growth factor (bFGF)

REGENERATION • Bone morphogenetic protein (BMP)
• Transforming growth factor (TGF).
Therapeutic bone regeneration approaches use the
principles of osteogenesis, osteoconduction, and osteo- Osseous regeneration has been tried by means of:
induction in an attempt to maximize the clinical bone • Closed or open root planing
regeneration. • Bone substitute grafts
1. Osteogenesis has been described as the direct transfer • Guided tissue regeneration (GTR)
of vital cells to the area that will regenerate new bone. • Guided bone regeneration
2. Osteoconduction embraces the principle of providing • Matrix proteins and growth factors/ differentiating
the space and a substratum for the cellular and bio- factors
chemical events progressing to bone formation. • Combinations of above-listed methods.
3. Osteoinduction embodies the principle of convert- Platelet-rich plasma (PRP) is yet another example of
ing pluripotent, mesenchymal-derived cells along tissue engineering that has potential clinical applications
the osteoblast pathway with subsequent formation in bone grafting. It contains:
of bone.
• A high-level mixture of platelets
Current research is exploring the use of the various • A concentration of growth factors.
growth factors to stimulate regeneration of lost bone, peri-
odontal ligament, and cementum, restoring the complete
periodontal attachment apparatus such as: Alveolar Bone Defects in Periodontal Disease
• Platelet-derived growth factor (PDGF) • Alveolar bone is the least stable of the periodontal tis-
• Insulin-like growth factor (IGF) sues because its structure is in a state of flux.
C H A PT ER 50 REG EN ERATIV E O SSEO U S SU R G ERY 441
FIGURE 50.1 (A) Deep three-wall vertical osseous defect in relation to left central incisor. (B) After mucoperiosteal flap elevation and debride-
ment, a bioresorbable collagen membrane placed over the defect. (C) Reentry after 1 year showing bone regeneration and complete bone fill of
the defect.
(A) (B)
FIGURE 50.2 (A) Intraoral radiograph showing vertical bone defects mesial to maxillary first premolar. (B) Postoperative radiograph showing
bone fill after periodontal regenerative therapy with alloplastic graft material.
• Moreover, during periodontal disease bone remodeling Goldman and Cohen Classification According to the Number of
by means of resorption and formation causes various Bony Defects
types of osseous deformities.
One-wall bony When bordered by two tooth surfaces, one
• Periodontal disease alters the morphological fea- defects osseous surface (facial or oral), and soft
tures of the bone in addition to reducing bone height tissue
(Fig. 50.1).
Two-wall bony When boarded by two tooth surfaces and
• Different patterns of bone destruction such as hori- defects two osseous surfaces (one facial and one oral)
zontal and vertical defects can be produced by peri-
odontal disease. Their presence may be evident on Three-wall bony When boarded by one tooth surface and
defects three osseous surfaces
radiographs (Fig. 50.2), but careful probing and
surgical exposure of the areas are required to deter- Four-wall bony When boarded by all the tooth surfaces and
mine their configuration and dimensions. Transgin- defects surrounding osseous surfaces
gival probing is a more accurate method of evaluat- Combined osseous When the number of walls is different in
ing the true nature and architecture of the existing defect the apical area of the pocket from that in
bone. the occlusal area
• An infrabony pocket is a periodontal lesion situ-
ated in an osseous defect with its base apical to
Periodontal Osseous Defects
the crestal margin of the alveolar bone. Once such
a pocket is present there is a net loss of the attach- Periodontal disease can result in various types of bony
ment apparatus - bone, periodontal ligament, and deformities, which can be treated by various bone regen-
cementum. erative procedures (Fig. 50.3).
FIGURE 50.3 Periodontal osseous defects.
In addition to this, various osseous deformities are production of other required tissues will subsequent-
present: ly occur.
• Osseous craters The types of graft materials used in various regenera-

• Hemisepta tive procedures can be broadly divided into:
• Inconsistent margins
• Ledges and exostosis Natural Synthetic
• Bulbous contours Autografts All op las tic grafts
• Dehiscence and fenestration.
Isografts
Allografts
Xenografts
PERIODONTAL REGENERATION
• Periodontal therapy is directed toward arresting the

periodontal tissue destruction with the goal of stabiliz-
ing the long-term prognosis of the periodontium. GRAFT MATERIALS FOR REGENERATION
• Regeneration involves the replacement of tissues with
new, identical tissues that function the same as original Regenerative therapy comprises various procedures
tissues. that are designed to restore those parts of the tooth-
• Periodontal tissues are limited in their regenerative supporting apparatus that have been lost due to peri-
capacity, and considerable research is being devoted odontal diseases. Regeneration of bone defects associated
to developing techniques and materials to augment with periodontal disease by using numerous therapeutic
host processes that facilitate regeneration. grafting modalities has been investigated.
• Regenerative therapies have generally been directed Boyne stated that an ideal graft material should:
at the production of one tissue type of the periodon-
tium. For example, as bone is required for successful • Exist in an unlimited supply
regeneration, a variety of therapies, both biologic • Exist without the need for violation of distant donor site
and membrane types, have been directed at its re- • Provide immediate osteogenesis for rapid consolidation
generation with the assumption that the appropriate • Exist with no adverse host responses.
TABLE 50.1 Characteristics of Some Common Alloplastic and Allogenic Materials
Graft material Physical characteristics Advantages

Deproteinized sterilized bovine bone Natural bone mineral with trabecular architecture Osteoconductive bone substitute
Hydroxyapatite (bovine; coral; nonceramic) Porous Osteoinductive
Demineralized freeze-dried bone Blocks, granules Osteoinductive, essentially no

disease transmission
13-Tricalcium phosphate 10-65 µm porous granules Bone regeneration
Calcium sulfate Porous crystals, pellets, powder Osteogenic

Bioactive glass 90-710 µm resorbable spheres composed of silicon, Osteogenic
calcium, sodium, and phosphorus
Polymethylmethacrylate Highly porous copolymethacrylate and Radiopaque, osteopromotive,
polyhydroxymethylmethacrylate with barium sulfate hypoallergenic, hydrophilic
and calcium hydroxide or calcium carbonate coating
• Facilitate revascularization, which assists early healing • Generally cancellous bone is preferred as graft material,
and resistance to infection but chips or shavings of cortical bone mixed with blood
• Stimulate osteoinduction of recipient site cells and pulverized into a coagulum have also been used
• Be adaptable to a variety of physical requirements with success in periodontal defects.
• Cause no impediment to growth or orthodontic tooth • Extraoral sites, such as the iliac crest, provide adequate
movement quantity of graft material with excellent osteogenic,
• Provide support and stability where discontinuity or osteoinductive, and osteoconductive properties, and
mobility exists have proved successful in the management of bony
• Provide a framework for osteoconduction and be com- defects.
pletely replaced by host bone of the same or superior • Regeneration occurred more frequently with the use
quality and quantity as quickly as possible of grafts, but iliac crest marrow frequently resulted in
• Be capable of inducing or enhancing cementogenesis ankylosis and root resorption.
Different types of materials are available from differ- Allogenic grafts were utilized in attempts to stimulate
ent sources. They can be either bone graft materials or bone formation in intrabony defects in order to avoid
non-bone graft materials. the additional surgical insult associated with the use of
Bone graft materials can be obtained: autogenous grafts. Allografts are grafts transferred be-
tween members of the same species, which are genetically
• From the same individual (autografts)
dissimilar.
• From a different individual of same species (allografts)
Two types of bone allografts are used clinically:
• From a different species (xenografts)
• From non-bone graft materials, which include sclera, • Viable cancellous bone and marrow mineralized freeze-
dura, cartilage, ceramics, and coral-derived materials dried bone allografts (FDBA)
• Demineralized freeze-dried bone allografts (DFDBA)
Bone Graft Materials
Non-Bone Graft Materials
Many osseous grafting materials have been used to-
ward the goal of obtaining periodontal regeneration, of Bioceramic Materials
which autograft harvested from intraoral or extraoral Bioceramic materials are explained in Table 50.2.
sites is the most predictable osteogenic organic graft for
osseous tissue regeneration (Table 50.1). Autogenous
grafts retain some cell viability and are considered to TABLE 50.2 Classes of Synthetic Biomaterials
promote bone healing mainly through osteogenesis and/ Metals Requirements
or osteoconduction. Polymers No toxicity
Intraoral autografts are obtained from:
Ceramics Mechanically stable
• Edentulous areas of the jaws Do not corrode
• Healing extraction sites No stimulation of undesirable growths or
• Maxillary tuberosities or the mandibular retromolar chemical reaction in body fluids or tissues
Resorbabili ty
area
• Bioceramics are defined as "specially designed ceram- • Histological evidence suggests that porous hydroxy-
ics for the repair, reconstruction, and replacement of apatite supports bone formation, but since no evidence
diseased or damaged part of the body." of a new connective tissue attachment or cementum
• Bioceramic implants consist of inorganic chemical com- was noted, it should be considered a biocompatible
pounds/minerals, processed thermally or through filling material.
other means to obtain useful forms/microstructures
for specific application.
• The basic compounds are oxides, nitrides, or carbides Tricalcium Phosphate
of metals, phosphate minerals, silicates, and/ or their • Tricalcium phosphate is a porous form of calcium phos-
combinations. phate, the most commonly used form of which is beta-
• Major classes of bioceramics are crystalline ceramics, tricalcium phosphate.
glassy materials (bioactive glasses and glass ceramics), • It has excellent tissue compatibility and does not elicit
coating cements, and composites. any inflammation or foreign body response.
• Bioceramic alloplasts consist primarily of calcium • Conversion of the graft is pivotal to periodontal regen-
phosphate, with the proportion of calcium and phos- eration, first serving as a scaffold for bone formation,
phate similar to bone. and then permitting replacement with bone.
• The two most widely used forms are hydroxyapatite • It serves as biologic filler, which is partially resorbable
and tricalcium phosphate. and allows bone replacement.
• The tricalcium phosphate particles generally become
encapsulated by fibrous connective tissue and do not
stimulate bone growth.
TYPES OF CERAMIC AND THEIR
CHARACTERISTIC TISSUE
INTERACTION BEHAVIOR Calcium Phosphate Bone Cement
• The advent of self-setting bone cements based on cal-
Hydroxyapatite (Table 50.3) cium phosphates is considered as a breakthrough in
• This is calcium phosphate mineral with chemical for- skeletal repair.
mula Ca10(PO4)6(OHh. It is the basic inorganic content • They combine osteoconductivity and biocompatibility
of vertebrate bone. of hydroxyapatite implants, and moldability of acrylic
• The material is well-known for its biocompatibility bone cements.
and ability to integrate with hard tissue. Generally, • These are hydraulic (water-based) cements, which
hydroxyapatite is not osteoinductive, but osteocon- undergo acid-base reactions to form biocompatible
ductive. calcium phosphate mass.
• It was one of the first biomaterials used as a scaffold, • Most of the studies indicated minimal tissue reaction
seeded with osteoprogenitor cells from periosteum or and warranted the regeneration of bone at the defect
bone marrow, for bone and cartilage engineering. sites with the use of calcium phosphate bone cement
• The hydroxyapatite (HA) products used in periodon- (CPC). Bone and cementum formation was consistently
tology are of two forms: nonresorbable ceramic form observed in the sites.
and resorbable ceramic form. • New cementum and periodontal ligament-like tis-
sue were observed between the cemental and the root
surface. Also, new connective tissue attachment and
adhesion were significantly enhanced in the bone sub-
TABLE 50.3 Different Classes of Implants with their stitute graft sites compared with those in the nonbone
Characteristics, and Examples substitute graft sites.
Class of
implant Characteristics Example
Bioinert No direct bone-material Alumina, Bioactive Glasses
interaction. Thin fibrous zirconia, TiO2 ,
tissue forms at their interface SiN • These mainly contain CaO, SiO2, and P2O5•
• Silica chains in the material act as a container for
Bioactive Direct bone bonding through Hydroxyapatite other ions such as Na, Ca, and P, and provide Si-OH
HCA at the interface bioacti ve glasses
groups for surface reactions when implanted in bony
Bioresorbable Material remineralized to [3-Tricalcium sites.
biologic apatite phosphate, • The dissolution of ions produces local supersatura-
calcium salts
tion, leading to the formation of carbonate apatite
(hydroxyapatite with substituted carbonates) layer • All grafting techniques require initial therapy and expo-
and, subsequently, to a strong implant-tissue interface. sure of the defect by mucoperiosteal flap surgery. The
They can also bond with soft tissue. flap technique best suited for grafting purposes is the
papilla preservation flap, since it provides complete cov-
erage of the interdental area after suturing.
Biologic Modifiers
• Biologic modifiers are materials or proteins and factors
Root Surface Biomodification
that have the potential to alter the host tissue so as to
stimulate or regulate the wound healing process. In periodontal disease, root surfaces are contaminated
• Biologic modifiers may have the potential to promote by bacterial products, especially endotoxins in the nee-
regeneration of periodontal tissues through a variety rotized cementa! surfaces (Fig. 50.4). In vitro study dem-
of cell-tissue interactions, including promoting cell onstrated that diseased root surfaces do not favor the at-
migration, attachment and subsequent spreading of tachment or growth of fibroblasts, but promote epithelial
cells at the local site, cell proliferation, cell differentia- migration along the root surface.
tion, and matrix synthesis. The root surface biomodification has the following
• A significant regeneration potential of these factors was effects:
demonstrated in animal models as well as in various
• It induces osteoblastic cells to secrete factors that en-
clinical studies.
hance differentiation and alter their responses to os-
teogenic factors.
• It decreases osteoclast formation and activity.
• Root planing and removal of diseased cementum aim
REGENERATIVE SURGICAL
at the desirable goal of attaining a biologically accept-
PROCEDURES
able root surface. This can be accomplished by vari-
ous hand instruments such as curettes, hoes, files, and
Regenerative therapy comprises various procedures
ultrasonics.
that are designed to restore those parts of the tooth-
• Chemical demineralization and detoxification on the
supporting apparatus that are lost due to periodontal
root surfaces by using various chemicals - citric acid,
diseases. Diagnosis, treatment planning, and careful ex-
tetracycline, fibronectin, ethylenediaminetetraacetic
ecution of the regenerative surgical technique are all im-
acid (EDTA), sodium deoxycholate, complement (C3,
portant factors in achieving success. The clinician must
C6, C7), and human plasma fraction - have added ef-
carefully evaluate the various regenerative and reparative
fect of removing smear layer and exposing the collagen
approaches, and then decide which technique may result
matrix, which enhances regeneration.
in the best clinical outcome.
• By root conditioning the root surface areas are instant-
• Periodontal regeneration has been reported following ly exposed to a medium containing blood and oth-
a variety of surgical approaches - root planing with er biomolecules, which enhances the regenerative
biomodification and soft tissue curettage. action.
FIGURE 50.4 (A) Mucoperiosteal flap reflected in the maxillary region showing the bony defects and subgingival deposits on the root surface.
(B) Biomodification with chemical agents on the root surface to obtain a biocompatible surface.
• Enamel matrix proteins, mainly amelogenin, in- Bone Graft-Associated Regeneration

duce acellular cementum formation during tooth
formation stage. These proteins are believed to enhance Schallhorn defined the criteria for selection of a mate-
periodontal regeneration by promoting bone cell atrial (Figs 50.5 and 50.6):
tachment and cell spreading and enhance the prolifera- • Biologic acceptability
tion of more immature bone cells while stimulating the • Predictability
differentiation of more mature bone cells.
(A)
(8)
(C)
FIGURE 50.5 (A) Mucoperiosteal flap reflected showing bony defect mesial to maxillary right central incisor and the defect is filled with autog-
enous bone graft. (B) Mucoperiosteal flap reflected showing bony defect distal to maxillary left canine, and the defect is filled with allogenous bone
graft. (C) Mucoperiosteal flap reflected showing bony defect distal to mandibular right first premolar, and the defect is filled with xenograft material.
FIGURE 50.6 (A) Intraoral periapical (IOP) radiograph showing extensive bone loss in relation to maxillary right lateral incisor. (B) Postopera-
tive radiograph showing tooth is restored with endodontic and periodontic regenerative procedure. Note the bone fill obtained after the therapy.
FIGURE 50. 7 (A) Periodontal pocket of 6 mm on buccal aspect of maxillary right central incisor. (B) Mucoperiosteal flap, debridement, and
biomodification expose the buccal as well as proximal osseous defects. (C) Proximal defect is filled with alloplast graft. (D) Platelet concentrate
was placed over the graft before suturing the flap.
FIGURE 50.8 (A) Vertical intraosseous bone defect in relation to maxillary first premolar. (B) Platelet concentrate filled in the defect. (C) Reen-
try after 6 months showing bone fill in the defect. (D and E) Preoperative and postoperative radiographs showing evidence of bone fill. Note the
reappearance of intact lamina dura in the site.
• Clinical feasibility
• Minimal postoperative sequelae and patient acceptance.
Grafting with autogenous bone grafts and bone sub-
stitutes is the most common form of regenerative thera-
py for restoring all types of periodontal osseous defects
(Figs 50.7 and 50.8).
Osseous grafts could be described as "tissues placed
in osseous defects to stimulate bone formation or
periodontal regeneration." A graft is a viable tissue
that, after removal from the donor site, is implanted
within a host tissue that is then restored, repaired, or
regenerated.
Materials to be grafted can be obtained from the same
individual (autogenous grafts), from a different indi-
FIGURE 50.9 In guided tissue regeneration (GTR) procedure, re-
vidual of the same species (allogenous grafts), or from sorbable collagen membrane is used to cover the bone graft in specific
different species (xenografts). areas - interdental and furcation areas.
Platelet, Rich Plasma in Regeneration factors is initiated by the clotting process of blood and
Platelet-rich plasma is an autologous concentrate of begins within 10 min after clotting.
platelets. It is also a concentration of the seven funda-
mental protein growth factors, which are actively secret-
Barrier Materials in Regeneration
ed by platelets to initiate wound healing. These growth
factors include the three isomers of PDGF (PDGF-AA, The concept of GTR led to the development of a series
PDGF-AB, PDGF-BB), two of the numerous TGF (TGF-bl, of barrier materials, which could be incorporated in the
TGF-b2), vascular endothelial growth factor, and epi- surgical wound so as to physically separate and exclude
thelial growth factor. PRP works via degranulation and tissues from some part of the defects (Figs 50.9 and 50.10).
granules in platelets, which contain the synthesized and Barrier materials should be biologically compatible and
packed growth factors. Active secretion of these growth nontoxic, inhibit apical migration of epithelial tissue, be
FIGURE 50.10 (A) Periodontal osseous crater defect between maxillary left lateral and canine. (Band C) Mucoperiosteal flap was elevated and
debrided, the root prepared, and dumbbell-shaped bioresorbable membrane placed extending both buccally and palatally to cover entire osseous
defect. (D) Periosteal flap sutured back covering the membrane.
occlusive to the gingival connective tissue, provide sta- and reduction in mobility - will give an indication
bilization to the clot in the wound, and be easy to handle of regeneration of periodontal tissues after periodontal
and suture. therapy, the exact nature of regenerated periodontal
tissues is still controversial.
• The first barrier material to be used in periodontal
healing sites was a Millipore filter. Of these techniques, surgical reentry provides a good
• Expanded polytetrafluoroethylene (ePTFE) membranes view of the state of the bone that can be compared with
were subsequently successfully used by several inves- the view taken during the initial surgical procedure. Ra-
tigators. Results of periodontal regeneration achieved diographic evaluation of periodontal regeneration allows
with ePTFE membranes are now regarded as the "gold assessment of the bone tissue adjacent to the tooth. His-
standard" against which later techniques are compared. tological analysis can determine the type of attachment
• To overcome some of the limitations of nonresorbable obtained in the healed site. But this procedure is not prac-
membranes, such as the need for a second surgical pro- tical due to ethical reasons. However, many cases that
cedure for their removal with the added risk of loss of the clinically are considered successful, including cases with
regenerated periodontium further to flap reflection, they significant regrowth of alveolar bone, may histologically
were largely replaced with bioabsorbable membrane. show an epithelial lining along the treated root surface
• In GTR technique, the use of matrix proteins and instead of deposition of new cementum.
growth factors is extremely promising. The regenera-
tive treatment techniques are indicated primarily in
cases of vertical osseous defects, in furcation involve- FUTURE BONE REGENERATION
ment, and for covering areas of gingival recession. APPROACHES
The paradigms of periodontal disease therapy have

Tissue Engineering in Regeneration changed markedly over the past decades, due to the peri-
• Tissue engineering as a possible technique for regen- odontal regenerative approaches directed toward molecu-
erating lost tissue was proposed by Langer in 1993. lar, cellular, and genetic tissue engineering technologies.
• This approach reconstructs natural target tissue by Studies to date have demonstrated varying degrees of
combining three elements: a scaffold or matrix, signal- success in the promotion of periodontal wound healing
ing molecules (e.g., growth and differentiation factors by growth differentiation factor (GDF) application.
and genes), and cells. • The molecular approach using BMPs has received the
• Tissue engineering for periodontal regeneration can most attention because of the bone-inducing capacity.
be achieved by protein-based, cell-based, and gene • Another growth factor, platelet-rich plasma, showed
delivery-based approaches. rapid and dense bone formation when used along with
• Much of the current tissue engineering research is di- grafting materials.
rected toward the areas of cell manipulation (isolation, • The use of mesenchymal stem cells for the or
expansion, and differentiation) and scaffold design development of an immortalized osteoblast line shows
(biomaterials, design, and fabrication; Fig. 50.10). promise for bone regeneration.
However, in order to make possible a truly biologic
Evaluation of Regeneration and functionally complete regeneration, it is appropriate
• Successful regeneration is assessed by periodontal to use an evidence-based approach when a treatment plan
probing, radiographic analysis, direct measurement is made in treating a periodontal disease case with an
of new bone, and histology. intention of regenerating lost tissues. It can be predicted
• Even though the clinical parameters - reduction in in future that there will be a growing recognition of re-
probing pocket depth, gain in clinical attachment, generative approaches in periodontal therapy.
KEY POINTS
• Osteogenesis has been described as the direct transfer various chemicals - citric acid, tetracycline, fibronectin,
of vital cells to the area that will regenerate new bone. EDTA, sodium deoxycholate, complement (C3, C6, C7),
• Osteoconduction embraces the principle of providing and human plasma fraction.
the space and a substratum for the cellular and bio- • Enamel matrix proteins, mainly amelogenin, induce acel-
chemical events progressing to bone formation. lular cementum formation during tooth formation stage.
• Osteoinduction embodies the principle of converting • Platelet-rich plasma is an autologous concentrate of
pluripotent, mesenchymal-derived cells along the os- platelets. It is also a concentration of the seven funda-
teoblast pathway with subsequent formation of bone. mental protein growth factors. These growth factors in-
• When the number of walls is different in the apical area clude the three isomers of PDGF (PDGF-AA, PDGF-AB,
of the pocket from that in the occlusal area, this can be PDGF-BB), two of the numerous TGF (TGFb-1, TGFb-2),
described as a combined osseous defect. vascular endothelial growth factor, and epithelial growth
• Transgingival probing is a more accurate method of factor.
evaluating the true nature and architecture of the exist- • Tissue engineering for periodontal regenera-
ing bone. tion can be achieved by protein-based approaches,
• The types of graft materials used in various regenerative cell-based approaches, and gene delivery-based
procedures can be broadly divided into natural (auto- approaches.
grafts, isografts, allografts, xenografts) and synthetic • The structural and intercellular complexity of periodon-
(alloplastic) grafts. tal tissues is probably one of the reasons why it is so
• Intraoral autografts are obtained from edentulous areas difficult to regenerate the periodontium.
of the jaws, healing extraction sites, maxillary tuberosi- • Current evidence is that regenerative periodontal ther-
ties, or the mandibular retromolar area. apies to date restore only a fraction of original tissue
• Bioactive glass consists of 90-710 µm resorbable spheres volume.
composed of silicon, calcium, sodium, and phosphorous.
• Biomodification on the root surfaces is done by using

1. Caton JG, Defuria EL, Polson AM, et al. Periodontal regeneration via
1. What are the various methods to evaluate new attach- selective cell regeneration. J Periodontol 1987;58:546.
ment procedures? 2. Cochran DL, Wozney JM. Biological mediators for periodontal re-
2. Classify bone grafts. generation. Periodontal 2000 1999;19:40.
3. Ellegaard B. Bone grafts in periodontal attachment procedures. J Clin
3. Classify GTR membranes. What is its principle?
Periodontol 1976;3:5.
4. Define osteoinduction and osteoconduction. 4. Mellonig JT. Freeze-dried bone allografts in periodontal reconstruc-
5. Write short notes on osseous coagulum and bone blend. tive surgery. Dent Clin North Am 1991;35:505.
6. Describe alloplasts in bone regeneration. 5. Proceedings of the 1996 World Workshop in Periodontology, con-
7. Write a short note on growth factors in periodontal sensus report: periodontal regeneration around natural teeth. Ann
Periodontal. 1996;7:667.
regeneration.
CHAPTER
51
Furcation Involvement
and Its Management
CHAPTER OVERVIEW
Microbial plaque is the primary causative factor in de- impactions, inadequate or overextended gingival restora-
structive periodontal disease. The invasion of the bifurca- tions, and other iatrogenic factors localized in the furcation
tion and/ or trifurcation of multirooted teeth is the most provide the ideal ecologic niche for fostering the microflora,
serious complication of marginal periodontitis. Furcation perpetuating marginal inflammatory process, and initiat-
involvement makes the performance of effective plaque ing caries on root surfaces. If left untreated and allowed
control more difficult. Plaque retention, calculus, food to progress, the furcation invasion can result in tooth loss.
FURCATION both horizontal and vertical, and creates a definite

space with an arched roof created by the £urea and
Furcation is the anatomic part of a multirooted tooth bordered by roots and bone. The lesions may appear on
where the roots divide from the common root trunk in any aspect of the tooth, but do not extend sufficiently
bifurcation or trifurcation. into the £urea to communicate with any invasion on
the opposite side of the tooth (Figs 51.2 and 51.3). The
radiograph reveals a small area of radiolucency in the
FURCATION INVOLVEMENT furcation.
Grade III: In this type of furcation involvement the inter-
Invasion of the bifurcation and/ or trifurcation of mul- radicular alveolar bone has been completely destroyed
tirooted teeth due to periodontal disease process is called to permit the passage of a probe buccolingually on the
furcation involvement. mandibular molars and mesiodistally and buccolin-
Glickman classified furcation invasions based on gually on the maxillary molars. However, the facial
the degree of lateral penetration of the periodontal de- and/ or lingual orifices of the furcation are occluded by
struction under the roof of the furcation. Accordingly the gingival tissue. Radiograph reveals a distinct trian-
furcation involvements were divided into following gular area of radiolucency in the furcation (Fig. 51.4).
four grades: Grade IV: In this type of furcation involvement the in-
terradicular alveolar bone and soft tissue have been
Grade I: This type of furcation involvement is the in-
destroyed to such a degree that the furcation is open
cipient or early lesion. It develops by moderate and
and clinically visible. It is similar to Grade III furcation
uniform horizontal bone loss with a soft tissue lesion
but there is gross amount of gingival recession, which
or periodontal extending into the flute of the £urea
exposes the furcation area (Fig. 51.5).
with no intrabony lesion and no horizontal component
(Fig. 51.1). This involvement of the periodontium is Hamp provided a classification that described the hori-
without any radiographic evidence of bone loss. zontal extent of the furcal invasions:
Grade II: This type of furcation involvement is a cul-
de-sac lesion. It presents significant pocket depth and Class I: Horizontal loss of periodontal tissue support that
varying amounts of interradicular bone resorption, is less than 3.00 mm
CH A PTER 51 FU RC ATIO N IN V O LV EM EN T A N D ITS M A N A G EM EN T 451
FIGURE 51.1 Clinical picture of Grade I furcation involvement. FIGURE 51 .4 Intraoral periapical (IOPA) radiograph of Grade III
furcation involvement.
FIGURE 51.2 Clinical picture of Grade II furcation involvement.
FIGURE 51.5 Clinical picture of Grade IV furcation involvement.
So far, classification of teeth with furcation involve-

ment has been based on the horizontal components of
bone loss. Later, (classified it in millimeters) and (clas-
sified vertical loss in thirds of interradicular loss) pre-
sented a classification based on vertical involvement
of the furcation lesions. The subclasses proposed were
as follows:
Subclass A: Vertical destruction up to one-third of the

total interradicular height (1-3 mm)
Subclass B: Vertical destruction reaching two-thirds of
FIGURE 51.3 Grade II furcation involvement on surgical exposure. the interradicular height (4-6 mm)
Subclass C: Interradicular osseous destruction into or
beyond the apical third (;:::7 mm).
Class II: Horizontal loss of periodontal tissue support
which exceeds 3.00 mm but does not encompass the Furcations would thus be classified as Class IA, Class
total width of the furcation area IB, Class IC, Class IIA, Class IIB, Class IIC, Class IIIA,
Class III: Horizontal loss of the periodontal tissue with Class IIIB, and Class IIIC.
through and through destruction of the periodontal Anatomic features affecting the onset offurcation involve-
tissue in the furcation area. ment and the outcome of therapy: Several general conditions
prevailing and morphologic characteristics of the tooth to the palatal surface, while that of the distal furcation
may influence the onset of furcation involvement. These is located midway between the buccal and palatal sur-
include: faces. The distal maxillary furcation is the most frequently
involved.
• Primary factor: Bacterial plaque
• Predisposing factors: FURCATION ENTRANCE DIAMETER
• Furcation morphology
The furcation entrance diameter of first permanent
• Facial/lingual radicular bone
molar teeth was extensively studied by. In a sample of
• Enamel projections
114 maxillary and mandibular teeth, he noted that overall
• Enamel pearls
furcation entrance diameter was smaller than the blade
• Root anatomy
face width of commonly used periodontal curettes in 58%
• Complicating factors
of the furcations examined. With this background, it is
• Occlusal traumatism
inevitable to state that due to this size disparity, curettes
• Accessory pulp canals
when used alone may not efficiently clean the furcation
• Iatrogenic factors.
entrance area in a clinical situation.
Bower also noted that the buccal furcation entrance
Primary Factor: Bacterial Plaque diameter of maxillary first molar teeth examined was
smaller than either the mesiopalatal or distopalatal. Simi-
Bacterial plaque is the most common cause of furcation
larly, the buccal entrance diameter in the mandibular first
involvement in marginal periodontitis, which progres-
molar teeth examined was smaller than the lingual. Bower
sively invades one or more furcation areas to varying
also found that the mesiodistal widths at the CEJ of both
degrees, resulting in irreversible bone loss in the inter-
maxillary and mandibular first molar teeth were found
radicular area. Any iatrogenic factor that may enhance
to have very low correlation with this furcation entrance
plaque overgrowth and prevent oral hygiene of the area
diameter. Therefore, large teeth do not necessarily have
gives rise to chronic local inflammation, which in turn
large furcation entrance diameters.
increases the degree of furcation involvement.
ROOT CONCAVITIES
Predisposing Factors The internal furcation root surface morphology was
extensively studied by Bower, and the most significant
Furcation Morphology
findings were as follows:
LOCATIONS OF FURCATION RELATIVE TO CEJ
• On mandibular first molar teeth:
The closer the position of the furcation relative to ce-
• Mesial and maximum of distal roots presented with
mentoenamel junction (CEJ), the greater is the chance of
concavity of the furcal aspect.
furcation involvement. If the furcation becomes diseased
• Deeper concavity was found on the mesial root than
in a tooth with a long trunk and short root anatomy, the
on the distal root.
remaining roots will have little surface area embedded
• Wider root separation is associated with larger fur-
in surrounding osseous structure and, as a result, the
cation entrance diameter.
prognosis will be often poor. Conversely, the tooth hav-
• On maxillary first molar teeth:
ing short trunk is more likely to develop early furcation
• The furcal aspect of root was concave in maximum
involvement but often has longer remaining roots, giving
of mesiobuccal roots, intermediate of distobuccal
the tooth greater potential for corrective therapy.
roots, and minimum of palatal roots.
FURCATION SHAPE • The deepest concavity was in the furcal aspect of
mesiobuccal root.
The furcal shape varies widely with the relative spread
• Maximum furcal aspects of the buccal roots diverge
of the roots forming it. Usually the more vertical the roots,
toward the palate with a mean divergence of 22°.
the more constricted is the furcal zone and the more acute
is their angle of junction. The smaller the degree of root Bower also noted that the furcation concavities are
divergence, the smaller the spatial dimension of the furca- caused by more cementum than the adjacent convexities.
tion chamber would be. This may have clinical significance due to cementum's
ability to absorb and/ or adsorb toxic bacterial products
LOCATION OF FURCATION ENTRANCE such as endotoxins when altered by the inflammatory
The mandibular furcation entrance is usually located process. Incomplete removal of this diseased thicker ce-
midway between the mesial and distal surfaces of the mentum would thus discourage ultimate union of healthy
tooth. On the maxillary molars, the mesial furcation en- fibroblasts and epithelial cells after treatment, resulting
trance is located two-thirds the distance from the buccal in persistence of periodontal pockets.
Facial and Lingual Radicular Bone Root Anatomy
The buccolingual dimension of the alveolar process The following factors may also predispose the furca-
and the depth of the overlying gingival tissues influence tion involvement:
the nature of the defect and its extent into the £urea. The
1. Morphology (divergence, convergence, fused)
presence of thick buccal and lingual ledges of bone, and
2. Clinical length (short, long)
also of tori, does not permit soft tissue recession. The
3. Proximal shape (flat, concave)
result is the formation of deep pockets and intrabony
4. Topography (alignment on the arch).
lesions surrounding the furcal regions. Conversely, nar-
row buccolingual alveolar processes are usually ac- Bifurcation Ridges
companied by individual root prominences and loss
Everett (1958) described a ridge on mandibular mo-
of crestal bone height is commonly accompanied by
lar that originated from the mesial surface of the distal
gingival recession. Exposure of the furcal area is less
root, ran across the bifurcation, and ended high up on
of a problem.
the mesial root, where it blended into the commonly
Enamel Projections occurring concavity of the distal surface of the mesial
A cervical enamel projection is an apical extension of root. Histologic examination revealed that the ridge is
enamel into the furcation area of a multirooted tooth, usu- formed mostly of cementum. The presence of such a
ally a lower molar. This anatomic anomaly is covered by ridge may demand special consideration in determining
a junctional epithelial attachment instead of a connective the method of treatment of a periodontal lesion within the
tissue attachment. A junctional epithelial attachment is bifurcation areas of the mandibular molars, as this ana-
less resistant to periodontal disease, which usually re- tomic structure creates niche where plaque can accumu-
sults in the development of isolated periodontal defect late undisturbed when the furcation is exposed to the
in furcation area. oral environment.
Masters and Hoskins classified the cervical enamel
projections as: Complicating Factors
Grade I: Short enamel projection from CEJ Occlusal Traumatism
Grade II: Longer enamel projection approaching the
As the periodontal ligament between the crest of the
furcal area
interradicular bone and dome of the £urea is lying in a
Grade III: Enamel projection extending directly into the
horizontal plane, even slightly increased forces in cen-
£urea.
tric occlusion would have the same effect as increased
Some investigators speculate that enamel projec- lateral forces on periodontal ligament arranged in a verti-
tions might provide direct access for bacteria into the cal plane.
furcal area, since no organic attachment of connec- Osseous destruction within the furcation can also be at-
tive tissue is possible into the enamel surface of these tributed to occlusal disease. It has been demonstrated that
projections. jiggling trauma results in the loss of crestal bone height
as well as a reduction in the quantity of alveolar bone.
Enamel Pearls The magnitude, duration, frequency, or direction of the
According to the American Academy of Periodon- occlusal forces can readily exceed the reparative capac-
tology's Glossary of Periodontal Terms (1986), "an enamel ity of the attachment apparatus because the quantity of
pearl is a small focal mass of enamel formed apical to bone within the most coronal aspect of the furcation is
the cementoenamel junction." In other words, enamel limited. The degree of susceptibility to occlusal trauma of
pearls differ from enamel projections in that they are iso- the interradicular bone is influenced by the degree
lated islands of ectopic enamel rather than extensions of of root divergence, the presence of bifurcation ridge,
coronal enamel, and also differ from enamelomas in that and root concavities. Occlusal traumatism superimposed
enamelomas are not found attached to the root but are in on an existing inflammatory lesion has been shown to ac-
the periodontal ligament. celerate bone loss and the apical migration of the gingival
Enamel pearls can be found on lateral surface of the attachment.
root. It has been reported that in molars with enamel
pearls the only situation in which enamel pearls may Accessory Pulp Canals
become contributors or predispose to periodontal break- Histologic studies in animals and on extracted human
down occurs when inflammatory process contacts their molars have demonstrated accessory canals, especially
coronal aspect. Therefore, the closer the enamel pearl to in the region of furcations. Bender and Seltzer found that
the CEJ, the greater is its chance of becoming a contribu- accessory canals and foramina were in greater numbers in
tory factor. the furcation regions of premolar and molar teeth.
The high incidence of accessory canal foramina open- The normal gingival architecture is regained postscal-
ing at the furcation region suggests that pulpal disease ing, which facilitates the oral health maintenance.
could be a cofactor in the pathogenesis of furcation in- • Grade II to Grade IV:
volvement. Lateral or accessory canals may extend into • Regenerative procedures
the furcal area and provide access to this area for the • Hemisection/bicuspidization
products of pulpal necrosis, resulting in resorption of • Tunnel preparation
the interradicular bone and periodontal lesions. • Root resection
Pulp necrosis resulting in periapical periodontitis may • Regenerative Procedure: The present therapeutic
also progress to establish a communication with the oral regenerative modalities include bone augmentation,
cavity by extending coronally along the periodontal liga- guided tissue regeneration, application of growth fac-
ment and open out through the gingival sulcus or through tors, and/ or combination of any of the procedures.
a deepening pocket coincident to periodontitis. In this
Bone Augmentation: These procedures have been
way furca of multirooted teeth with pulpal pathosis, free
widely used in the recent past with the aim of complete
of acute symptoms, is vulnerable to the destruction of
defect fill in cases of periodontal osseous defects. Various
periodontium in the furcal region. Several cases of furcal
materials used include autografts and allografts with
invasion have been reported, which were attributable to
quite encouraging results. The augmentation material
pulpal pathosis and were resolved with regeneration of
may act by the principles of osteoconductivity or osteo-
attachment by endodontic therapy.
inductivity.
• Guided Tissue Regeneration: As envisioned by
Iatrogenic Factors and dealt with extensively by Gottlow et al, this
Supragingival margins and undercontours are gener- procedure offers the possibility of producing new
ally more compatible with gingival health than subgin- attachment in teeth with advanced periodon-
gival margins and overcontours. Restorations with open tal destruction (Fig. 51.6). This technique involves
or overhanging margins contribute to the progressive the placement of barrier membrane that bridges the
destruction of the periodontium and to the inflammatory space between alveolar crest and cervical portion of
lesion in the region of a furca. the tooth, thus preventing apical migration of epithelial
cells from the surgical flap into the defect space and
facilitating repopulation by the cells of periodontal
ligament. Evaluation of various clinical trials under-
THERAPEUTIC MODALITIES IN taken to treat Grade II furcation defects has yielded
FURCATION INVOLVEMENT good results as far as attachment gain is considered.
Furcation-involved teeth are treated either surgically With the premise of possible synergism of combin-
or nonsurgically keeping in view the following objectives: ing osseous grafting and guided tissue regeneration the
therapeutic modality seems to be the treatment of choice
1. The treatment rendered should control the periodontal especially for Grade II and, in some cases, Grade III furca-
disease process and prevent further loss of attachment. tion defects. Carranza (1991), in a combination of guided
2. The site treated should simulate the normal gingival tissue regeneration and bone augmentation procedures
and periodontal architecture so that it is more ame- in mandibular molars, obtained very good results as far
nable for postoperative maintenance. as periodontal regeneration was concerned. This was bet-
3. The treatment should either reduce or obliterate the ter than that achieved with either of the treatment alone.
furcation defects.
The treatment regimen to be selected for an individ- Platelet, Rich Plasma in Furcation Defects
ual case should take into consideration all the details of
Platelet-rich plasma (PRP) and platelet-rich fibrin can
furcation defects, anatomic variations, configuration
serve as regenerative modalities in the treatment of furca-
of bone destruction, and presence or absence of traumatic
tion defects. PRP, which is an autologous volume of plasma
occlusion.
with a fourfold to fivefold increased platelet concentration,
Broadly depending on the grade of furcation involve-
is a proven source of growth factors. The use of PRP is based
ment, the following therapeutic modalities indicated can
on the potential of the plasma to release multiple wound-
be utilized.
healing growth factors and cytokines which are responsible
• Grade I: Scaling and root planing - the furcation for increasing collagen production, recruiting other cells
involvement being an incipient lesion, removal of to the site of injury, increasing cell mitosis, inducing cell
the local deposits by scaling and root planing is usually differentiation, and initiating vascular ingrowth. Some of
the only treatment procedure required for resolution. the clinical trials have found the use of PRP alone or in
FIGURE 51. 7 (A and B) Presurgical and postsurgical intraoral peri-

apical (IOPA) radiographs of furcation treated with bone augmentation.
of mandibular molars that do not have a third root that

obscures the cleaning process. The teeth to be tunneled
must have sufficient root divergence to accommodate
cleaning devices, but the procedure may jeopardize
the tooth by removing too much supporting bone. It
may also increase the risk of developing root surface
caries within and adjacent to such tunnels, especially in
patients who are not able to maintain good standards
of oral hygiene.
• Tooth Sectioning: Tooth sectioning procedures such as
FIGURE 51.6 (A and B) Intrasurgical pictures of guided tissue re- root resection, root separation, and hemisection have
generation; (C) reentry picture at 6 months postsurgically . often been used for the treatment of severely involved
Grade II and Grade III furcation (Figs 51.7 and 51.8).
According to the American Academy of Periodontol-
combination with bone graft material to be useful in the
ogy' s Glossary of Periodontal Terms, these procedures
treatment of Grade II and Grade III furcation defects.
have been defined as mentioned. Root resection is the
• Tunnel Preparation: Tunnel preparation empties the removal of a root apical to the furcation without remov-
surgical exposure of the entire furcation area to provide al of the crown in a multirooted tooth. Root separation
access for cleaning the area with special brushes or or bicuspidization is a procedure involving section-
curettes. This procedure can be adopted only in cases ing of the multirooted tooth so as to convert it into
FIGURE 51.8 Intraoral periapical (IOPA) of Grade III furcation FIGURE 51.9 Intraoral periapical (IOPA) radiograph showing Grade
involvement. III furcation involvement treated by bicuspidization.
separate single-rooted teeth (Fig. 51.9). Hemisection is extent of furcation involvement, the amount and topog-
the surgical procedure in which a root or roots may be raphy of supporting bone, the root canal anatomy, and
surgically removed along with the associated portion periapical health of the remaining roots. However, with
of the crown. the advent of the widely popular and practiced regenera-
tive therapies, the utility of tooth sectioning procedures
Before attempting any tooth sectioning procedures, a has grossly been reduced. Nevertheless, some situations
proper endodontic restoration is a prerequisite. Basically warrant their use according to proper indications with
determining which roots to be resected is based on the profound success.
KEY POINTS
• Invasion of the bifurcation and/ or trifurcation of multi- • Osseous destruction within the furcation can also be
rooted teeth due to periodontal disease process is called attributed to occlusal disease. It has been demonstrated
furcation involvement. that jiggling trauma results in the loss of crestal bone
• Glickman classified furcation invasions based on the de- height as well as a reduction in the quantity of alveolar
gree of lateral penetration of the periodontal destruction bone.
under the roof of the furcation. • The treatment regimen to be selected for an individual
• Hamp described a classification that described the hori- case should take into consideration all the details of
zontal extent of the furcal invasions. furcation defects, anatomic variations, configuration of
• Tarnow and Fletcher (classified it in millimeters) and bone destruction, and presence or absence of traumatic
(classified vertical loss in thirds of interradicular loss) occlusion.
presented a classification based on vertical involvement
of the furcation lesions.

1. Bender IB, Seltzer S. The effect of periodontal disease on the pulp.
• Define and classify furcation involvement. Oral Surg Oral Med Oral Pathol Oral Radial Endod 1972;33:435.
• Describe the anatomic features affecting the onset of 2. Bower RC. Furcation morphology relative to periodontal treatrnent-
furcation involvement and the outcome of therapy. furcation entrance architecture. J Periodontol 1979;50:23.
3. Bower RC. Furcation morphology relative to periodontal treatrnent-
• Describe root resection and bicuspidization.
furcation root surface anatomy. J Periodontol 1979;50:366.
• Define treatment of Grade II furcation involvement.
4. Carranza Jr FA, Jolkovsky DL. Current status of periodontal therapy 8. Gottlow J, Nyman S, Lindhe J, Karring T, Wennstrom J. New
for furcation involvement. Dent Clin North Am 1991;35:555. attachment formation in the human periodontium by guided tis-
5. Eskow RN, Kapin SH. Furcation invasions: correlating a classifi- sue regeneration - case reports. J Clin Periodontol 1986;13:604.
cation system with therapeutic considerations. Part I. Examina- 9. Hamp SE, Nyman S, Lindhe J. Periodontal treatment of multirooted
tion, diagnosis and classification. Compend Cantin Educ Dent 1984; teeth - results after 5 years. J Clin Periodontol 1975;2:126.
5:527. 10. Masters DH, Hoskins SW. Projection of cervical enamel into molar
6. Everett FG, Jump EB, Holder TD, Williams GG. The intermediate furcations. J Periodontol 1964;35:49.
bifurcational ridge - a study of the morphology of the bifurcation 11. Melcher A. On the repair potentials of periodontal tissues. J Periodontal
of the lower first molar. J Dent Res 1958;34:162. 1976;47:256.
7. Glickman I. Clinical Periodontology. 1st ed. Philadelphia: Saunders; 12. Tarnow D, Fletcher P. Classification of the vertical component of
1953. furcation involvement. J Periodontol 1984;55:283.
CHAPTER
52
Endodontic Periodontal Lesions
and Their Management
CHAPTER OVERVIEW
The interrelationship between periodontal and end- tooth, termed combined lesions, where the treatment de-
odontic disease has often aroused confusion due to the pends on the degree of involvement of the tissues. Both
intimate interrelationsip between these tissues through a endodontic and periodontal diseases are caused by a mixed
variety of portals of communication. anaerobic infection. It is often difficult to differentiate be-
The relationship between the pulp and the periodontium tween pain of pulpal and periodontal origin. It is essential
has been extensively studied; however, queries regarding to know the nature of pain to determine the etiology. Clini-
the diagnosis, prognosis, and treatment continue to be vexa- cal and radiographic evaluations are essential to help clarify
tious. Pulpal infection can drain through the periodontal the issue. Both pulpal and periodontal infections are ca-
ligament space and give an appearance of periodontal de- pable of cross-infecting each other. It is therefore important
struction, termed retrograde periodontitis. Similarly, both to analyze and evaluate the different disease processes that
pulpal and periodontal infections can coexist in the same make up this complex web of endo-perio interrelationship.
RELATIONSHIP OF PULPAL AND smear layer formation, but unfortunately, this smear
PERIODONTAL DISEASE layer has been shown to dissolve as early as 1 week
after surgery, resulting in a return of dentin hyper-
While the deleterious effects of pulpal disease on the sensitivity. Although this pulpitis is usually revers-
periodontium are well documented, there is uncertainty ible, palliative endodontic therapy may be necessary
about converse effect of periodontal disease on the pulp. in some cases.
Some authors have reported a strong correlation be- As previously stated, the pulp generally will not
tween periodontal disease and inflammatory and de- succumb to periodontal lesions that do not involve the
generative changes in the pulp, while others have found apical foramen. However, it must be remembered that
no such correlation. Langeland, Zehnder, and others the effects of a lifetime of caries, operative procedures,
found that the pulp succumbed only when periodontal periodontal disease, and treatment are cumulative,
lesions involved the apical foramen; otherwise, only with the pulp losing some of its recuperative power
minor changes occurred in the pulp. The clinical symp- with each added insult. Periodontal disease, therefore,
toms of pulpitis commonly seen in periodontal patients can contribute to pulpal inflammation even when the
are related more closely to the treatment than to the apical foramen is not involved. In any case, these ef-
disease. fects are certainly less dramatic than the effects com-
Vigorous root planing may remove cementum and monly seen in the periodontium of endodontic lesions
expose numerous dentinal tubules through which - an interesting situation, as the pathways involved
etiologic agents may enter and inflame the pulp. Fur- are reciprocal.
thermore, these exposed tubules are subject to hydro- A closer examination of the two disease processes is
dynamic stimuli. This to some extent is mitigated by necessary to explain this apparent discrepancy.
C H A PT ER 52 EN D O DO N T IC PERIO DO N TA L LESIO N S A N D TH EIR M A N A G EM EN T 459
PATHWAYS OF COMMUNICATION in intrapulpal pressure. Areas of infarction and coagulation

BETWEEN PULP AND PERIODONTIUM necrosis result as the pulp succumbs incrementally.
As the disease progresses, toxic agents may be expressed
• Pathways of developmental origin: through patent channels, including the apical foramen and
• Apical foramen lateral and accessory canals. Corresponding lesions in the
• Accessory canals and lateral canals adjacent periodontium may eventually coalesce.
• Congenital absence of cementum exposing the den- While any endodontic lesion may drain along the peri-
tinal tubules at the cervical region of teeth odontal ligament and form fistulas that penetrate the gingival
• Permeability of cementum sulcus, lesions in close proximity to the gingival margin, such
• Developmental grooves as those associated with lateral canals in the coronal half
• Enamel projections and enamel pearls at the cervical of the root and accessory canals in the floor of multirooted
area teeth, are the most likely to do so, forming pseudopockets
• Pathways of pathological origin: that simulate periodontal disease. Termed as a retrograde
• Empty spaces on the root created by destruction of periodontitis, this type of lesion progresses in the opposite
Sharpey fibers direction of a marginal periodontitis without any of the ba-
• Vertical tooth fracture sic characteristics of periodontal disease and very possibly
• Idiopathic resorption - internal and external without permanently damaging the cementum and its fibers.
• Loss of cementum due to external irritants The loss of attachment produced by these lesions may
• Pathways of iatrogenic origin: be completely reversible with endodontic therapy alone;
• Exposure of dentinal tubules following root planing however, if not treated early, secondary periodontal in-
• Accidental lateral perforation during endodontic volvement may progressively undermine the prognosis.
procedure Simultaneous existence of pulpal and periodontal lesions
• Root fracture due to endodontic procedure. may complicate diagnosis and treatment planning.
CLASSIFICATION OF ENDODONTIC
PERIODONTAL DISEASE PERIODONTAL LESIONS
Periodontal disease has a progressive nature. It be- Pulpo-periodontal lesions have been classified based
gins in the sulcus and migrates to the apex as deposits of on different criteria. Some have given importance to etiol-
plaque and calculus produce inflammation, which slowly ogy and sequence involvement while others have classi-
destroys the attachment apparatus. As a constant pathway fied on the basis of treatment.
for drainage usually remains via the gingival sulcus, acute Classification suggested by Simon et al (1972) is the
episodes are uncommon. These lesions may infiltrate lat- one that is widely employed.
eral canals, accessory canals, or exposed dentinal tubules,
but the path of least resistance is generally sulcular.
Furthermore, healthy pulp tissue is a highly vascular tis- Simon's Classification
sue that is quite resistant to infection. As long as the vascular
Simon et al, based on etiology, diagnosis, prognosis,
supply is maintained through the apical foramen, the pulp
and treatment, classified endodontic periodontal lesions
usually resists attack via these other pathways, although
into five groups:
calcifications or minor degenerative changes may be seen
histologically. If the periodontal lesion, or its treatment, ulti- 1. Primary endodontic lesion (Fig. 52.1)
mately compromises the vascular supply through the apical 2. Primary endodontic with secondary periodontal in-
foramen, pulpal necrosis will occur and further exacerbate volvement (Fig. 52.2)
the periodontal breakdown. While the prognosis for such 3. Primary periodontal involvement (Fig. 52.3)
a tooth basically depends on the nature of the periodontal 4. Primary periodontal with secondary endodontic in-
lesion, endodontic therapy must be performed first because volvement (Fig. 52.4)
pulpal irritants otherwise would preclude repair. 5. True combined lesions (Fig. 52.5).
Classification as Recommended by World Workshop

PULPAL DISEASE for Classification of Periodontal Diseases ( 1999)
Unlike periodontal disease, pulpal disease commonly ex- Periodontitis Associated with Endodontic Disease
hibits both chronic and acute phases. When chronic, pulpal 1. Endodontic-periodontal lesion
degeneration may occur rather slowly. Pulpal inflammation, 2. Periodontal-endodontic lesion
in a low-compliance system, is accompanied by an increase 3. Combined lesion
FIGURE 52.4 Primary periodontal with secondary pulpal involve-

FIGURE 52.1 Primary endodontic lesion. ment.
..•••......,
..
•••
,
t'lfl,.,,
••
f\ "'"
• fl
..
f\ C\ • fl •
FIGURE 52.2 Primary endodontic with secondary periodontal lesion . FIGURE 52.5 True combined lesions.
From the point of view of treating these cases effica-

ciously, a better clinical classification was provided by
Torabinejad and Trope in 1996.
Based on the Origin of the Periodontal Pocket

• Endodontic origin
... . .. • Periodontal origin

• Combined endo-perio lesions:
,.......
"•., • Separate endodontic and periodontal lesions:
...... ·
, Lesions with communication
.. .
Lesions with no communication
FIGURE 52.3 Primary periodontal lesion.

FIGURE 52.6 Narrow sinus-tract probing pattern in primary end-

odontic lesion.
sulcus, thus mimicking periodontal disease. In actual

fact there is a sinus tract which leads from the source
FIGURE 52. 7 Probing pattern in typical periodontal lesions.
of infection and traces itself along a path of least re-
sistance to finally drain through the periodontal tis-
sue apparatus. It is critical for the clinician to find PRIMARY PERIODONTAL LESION
the true source of the infection by tracing this sinus These lesions are generally initiated by periodontal
using a gutta-percha cone and a radiograph. Probing pathogens. Chronic periodontal disease tends to migrate
of such lesions usually reveals a pocket which is nar- apically along the root surface in the presence of local fac-
row and lacks width (Fig. 52.6). Primary endodontic tors such as plaque and microorganisms. The pulp tends
diseases usually heal following root canal treatment. to be healthy in most cases, and response to vitality tests
Patients with the primary endodontic lesion present is normal. Probing in such cases usually reveals wider
only diagnostic and treatment decisions related to the pockets with a periodontal probing pattern (Fig. 52.7).
endodontic lesions. The prognosis depends on the stage of periodontal dis-
ease and the efficacy of periodontal therapy. Presence of
a deep pocket, extending to the apical foramen or to the
PRIMARY ENDODONTIC WITH SECONDARY opening of an accessory canal, is indicative of this type of
PERIODONTAL INVOLVEMENT lesion. Radiographic evidence of bone loss is a common
Pulp inflammation or necrosis may lead to an inflam- finding. In some cases spread of infection from the peri-
matory response in the periodontal ligament at the apical odontal aspect to the pulp may occur, leading to fibrosis
foramen or foramina or at the site of a lateral or accessory and calcifications within the pulp.
canal. The resulting inflammatory lesion can range in
extent from a minimal inflammatory process confined
to the periodontal ligament to extensive destruction of PRIMARY PERIODONTAL WITH SECONDARY PULPAL
the periodontal ligament, tooth socket, and surrounding INVOLVEMENT
bone. Such a lesion may result in a localized or diffuse In severe cases of periodontal disease the chronic infec-
swelling that occasionally may involve the gingival at- tion migrates apically along the length of the tooth and
tachment. Lesions secondary to pulpal necrosis can some- can sometimes lead all the way to the apex of the tooth. In
times drain through a sinus tract in the alveolar mucosa such cases the pulp may lose its vitality due to exposure of
or the attached gingiva. In some cases it can even drain lateral canals, accessory canals, or the apical foramen. The
through the gingival sulcus of the affected tooth or the prognosis in single-rooted tooth is poor, but multirooted
adjacent tooth. By and large thorough debridement of the teeth may respond more favorably.
root canal system during endodontic therapy will lead The pulp response to cementum and dentin removal
to complete resolution of the lesion. Progression of the and exposure of patent dentinal tubules by periodontal
primary endodontic lesion into the deeper aspects of the root planing will vary with the remaining dentin thick-
periodontium leads to pocket formation and bone loss, ness. Unless dentin removal is excessive, pulp response
which may be evident radiographically. Pulp vitality tests will be negligible. Although the pulp is exposed to a
may be negative. bacterial challenge through patent dentinal tubules, it is
quite capable of repair and healing. Production of repara- MANAGEMENT

tive dentin and reduced canal diameter may result, but • Endodontic therapy
pulp tissue remains relatively unaffected. Unless peri- • Periodontal therapy.
odontal disease has progressed to involve the tooth apex,
the effect of periodontal disease on the pulp appears to
be negligible. Prognosis for a tooth involved with peri- DIAGNOSIS OF ENDODONTIC
odontal disease is determined by the outcome expected PERIODONTAL LESIONS
from periodontal therapy. An existing periodontal lesion (Tables 52.1, 52.2)
may extend apically to the apical foramen, resulting in a
secondary pulpal infection. This is referred to as "retro- Pulpal and periodontal infections can manifest with
grade pulpitis." Such cases usually present with severe different signs and symptoms. Symptoms usually include
periodontitis with subsequent clinical manifestations of pain, swelling, and tooth mobility. Differential diagnosis
pulpitis. is usually based on clinical examination and tests, includ-
ing periodontal probing, vitality tests, palpation, percus-
TRUE COMBINED LESIONS sion, and radiographs, among others.
A true combined lesion results from the development
and extension of an endodontic lesion into an existing
Pain
periodontal lesion. It basically presents with characteris-
tics of both the diseases. Most often a developing periapi- In lesions of primary endodontic origin the onset of
cal lesion extends coronally to connect with a preexisting, pain is acute and intensity severe. It is often spontane-
chronic, wide-based periodontal pocket. The two lesions ous, poorly localized, and commonly referred to other
can either merge or exist separately. Teeth with vertical sites. Localization is usually seen once the infection
fractures also belong to this category. Pain from the loss of spreads to the periodontium and often the intensity
pulpal vitality is the most common presenting complaint can increase in such cases. Often, potent analgesics
of patients with the combined lesions. Pulp vitality tests are not adequate to control endodontic pain, which
may be related to the status of pulpal involvement, and can at times awaken the person from sleep. Endodon-
radiographic evidence of bone loss may be observed. tic pain can often be eliminated only by root canal
True combined endodontic-periodontal disease oc- treatment.
curs less frequently than other endodontic-periodontal As opposed to the previous scenario, pain of peri-
problems. Since these lesions have two sources of infec- odontal origin is usually mild to moderate and respon-
tion they tend to be large and the prognosis is guarded. sive to analgesics. It is only in cases of acute exacer-
In molars with only a single root badly affected resection bations that the pain is severe. This severe pain often
of the affected root can help salvage the situation in many regresses following drainage. It does not awaken a pa-
cases. In single-rooted teeth, however the prognosis can tient from sleep.
often be hopeless. The endodontic component generally Combined lesions can present with minimal pain, usu-
tends to heal following successful endodontic therapy. ally because significant periodontal destruction permits
Tissue loss secondary to periodontal disease may not the drainage of exudate through the gingival sulcus or
respond as favorably. through a sinus or fistula.
TABLE 52.1 Lesion Characteristics
Lesion Pain Swelling Periodontal pocketing Radiographic Vitality

Primary endodontic Moderate to Possible None unless sinus tract Possible periapical Nonvital
severe radiolucency
Primary endodontic-secondary Moderate to Likely Evident or sinus tract Radiolucency from apex Nonvital
periodontal severe to sulcus, decreased
crestal bone height
Primary periodontal None to moderate Possible Moderate Decreased crestal bone Vital
height
Primary periodontal-secondary None unless acute Possible Severe Bone loss approaching Vital
endodontic endo apex
Combined pulpal-periodontal Moderate to Likely Severe, connects with Bone loss extending to Nonvital
severe periapex apex
TABLE 52.2 Current Concepts Regarding the Interrelationship Between, and Clinical Management of, Endodontic Periodontal Lesions
Diagnosis Considerations Therapeutic sequence Prognosis

Endodontic lesion May be a risk factor for Endodontic therapy only Excellent
further attachment loss in the
periodontitis-prone patient;
inflammation may spread
through cervical tubules as well
as through larger canals
Periodontal lesion With advanced disease consider Periodontal therapy only Depends on the state of tissue
the reliability of vitality testing, loss. Guarded
especially in multirooted teeth
Endodontic lesion with Diagnosis is supported when Endodontic therapy first; Excellent
secondary periodontal pulp vitality is clearly lacking: periodontal therapy follows
involvement avoid overzealous root once sufficient time has elapsed
instrumentation that might to ensure resolution of active
denude connective tissue from endodontic disease (generally
healthy root surfaces half a month)
Periodontal lesion with second- Traditionally, a more difficult Endodontic therapy first; Excellent for the endodontic
ary endodontic involvement clinical diagnosis to support periodontal therapy to follow component. Prognosis for
than the endodontic lesion periodontal component is
with secondary periodontal guarded
involvement
True combined lesion A classic presentation is a frac- Concurrent endodontic and Endodontic and periodontal
tured or perforated root periodontal therapy will be surgery is frequently required;
necessary and are occasionally grafting, guided tissue
carried out simultaneously regeneration, compatible
cements, and tissue-compatible
resins should all be considered.
Prognosis poor
Swelling edge of the swelling, probing is once again within normal

limits (Fig. 52.8). The width of the detached gingival can
Swelling secondary to endodontic infections can often be as broad as the entire buccal or lingual surface of the
be localized to the mucobuccal fold and could spread into tooth. This swelling can be characterized as having "blown
facial spaces leading to facial swellings. out" the entire attachment on that side. Endodontic
Swelling secondary to periodontal disease usually
tends to be well localized in the attached gingiva and is
usually short of the mucogingival line. Facial swelling
is rare.
Periodontal Probing
ACUTE OR "BLOW-OUT" LESIONS
When a patient presents with a localized swelling that
involves the gingival sulcus, it may be difficult to deter-
mine if the swelling is due to a periodontal abscess or an
abscess of endodontic origin. The tooth must be pulpless.
The swelling is usually on the labial or buccal side of the
tooth but may be on the lingual side. As the sulcus is
probed there is usually normal sulcus depth all the way
around the tooth until the area of the swelling is probed.
At the edge of the swelling the probe drops precipitously
to a level near the apex of the tooth, and the probing depth
remains the full width of the swelling. At the opposite FIGURE 52.8 Wide probing pattern.
treatment only is indicated. As a result of endodontic TESTS

management of the swelling, complete periodontal reat-
tachment occurs within 1 week in most cases. Percussion
Tenderness to percussion is an indicator of periradicu-
TYPICAL PERIODONTAL LESIONS In periodontal dis- lar inflammation and does not disclose the condition of
ease bone loss always begins at crestal bone level and progresses the pulp. Abnormal reactions to percussion are indicative
apically. The typical lesion is conical in contour. The prob- of inflammation of the periodontal ligament, which in
ing may start from a sulcus depth that is within normal turn may be secondary to pulpal infection. The presence
limits, then gradually step down a slope to the apical of proprioceptive fibers in an inflamed periodontal liga-
extent of the lesion, and then step up again on the other ment is helpful in localizing the tooth in question.
side to a sulcus depth within normal limits. Occasionally Light digital pressure on the teeth should be followed
the clinical presentation of a periodontal lesion will have by gentle tapping with the handle of an instrument to
the sloping contour of a conical lesion on one side but a elicit a response. Care should be taken to not inflict pain
more precipitous, sharp drop-off on the other. Such prob- on the patient and when mild digital pressure elicits a
ing should be considered to be of the "periodontal type" painful response, it is usually unnecessary to continue
of probing (Fig. 52.7). A periodontal lesion will not resolve with further testing.
in response to root canal treatment even if the associated
tooth is pulpless.
Palpation
LESIONSWITHNARROWSINUSTRACT-TYPEPROBING Digital palpation of the mucosa! tissue around the roots
A periodontal lesion may or may not be detectable ra- and apices of the teeth is helpful in detecting periradicular
diographically. In many clinical situations a lesion may abnormalities. Isolated "hot zones" that produce a pain-
be probed for some distance down the root surface of the ful response, crepitus, and localized swellings can all be
involved tooth, but the defect is in fact a sinus tract. Usu- detected through palpation.
ally, probing will show sulcus depth within normal limits
with the exception of one very narrow area that can be Pulp Testing
probed along the root surface of the tooth to a consider-
able distance and in many cases all the way to the apex of The most commonly used pulp vitality tests are cold
the tooth (Fig. 52.6). Usually the break in the attachment is test, electric test, heat test, and cavity test. The pres-
only about 1 mm wide, and probing on either side of the ence or absence of vital tissue in a tooth with a single
lesion will be normal. This lesion is a sinus tract, and canal can be determined with confidence with current
the probing represents a typical sinus tract type of prob- pulp testing procedures. The same degree of confidence
ing. The tooth is nonvital and conventional root canal cannot be ascribed to positive pulp test responses in
treatment is indicated. The lesion does not need curettage multirooted teeth.
or surgical intervention. It is strictly a sinus tract similar
to a sinus tract exiting in the alveolar mucosa or attached Cold
gingiva. Usually the orifice into such a sinus tract will
close within 1 week after cleaning and shaping the root The cold test is one of the easiest tests available to eval-
canal system. uate tooth sensibility. In normal cases application of a cold
stimulus elicits a painful response which is transient and
disappears when the stimulus is removed. In cases where
Mobility the pulp is acutely and irreversibly inflamed the test will
elicit a sharp early response, which could linger even
Mobility around an isolated tooth could indicate either after the stimulus is removed. In cases of pulp necrosis
pulpal or periodontal pathology. In acute cases, however or chronic inflammation the response is either delayed or
it is more likely to be endodontic in origin. Generalized absent. The test cannot be repeated immediately since the
mobility on the other hand is almost always periodon- pulp needs time to recover from the stimulus and usually
tal or occlusal in origin. Tooth mobility depends on the dichlorodifluoromethane (Frigi-Dent) is used to provide
integrity of the attachment apparatus or on the degree the stimulus.
of inflammation in the periodontal ligament. Hypermo-
bility is quite common in cases of primary endodontic
Electric
involvement and should not be confused with true mobil-
ity caused by periodontal destruction. In cases of primary This test involves the use of localized electrical stimuli
endodontic pathology the mobility resolves within a week of to elicit a response. Patients usually provide a yes or no re-
initiating endodontic therapy. sponse. However, one should not rely on any one pulp test.
Heat
The normal response of a healthy pulp is pain that
increases in intensity until the stimulus is removed. Once
the heat is removed the pain disappears immediately.
Lingering pain indicates an irreversibly inflamed pulp.
When pain persists after removal of the heat stimulus
from periodontally involved teeth, pulpitis should be
suspected. Hot gutta-percha should be applied to the
tooth coated with petroleum jelly to prevent the material
from sticking to the tooth surface. If a crown is present,
a rotating rubber prophylaxis cup can be run on a dried
tooth to create heat.
Test Cavity
This test is rarely used and that too if tooth sensibility FIGURE 52.9 Sinus tract located on the attached gingiva.
cannot be established by other tests. The test is carried
out without administering local anesthesia. A small test
cavity is prepared in the tooth and the patient response
is gauged as the cavity progresses pulpally. This test does
not give information as to the status of the pulp other than
whether or not it is vital.
Radiographs
Interpretation of periapical or lateral lesions and peri-
odontal lesions is of clinical importance in suggesting the
cause of the lesion. Often, the initial phases of periapical
bone resorption of endodontic origin are confined only to
cancellous bone and cannot be detected unless the cortical
bone is also affected. When there is radiographic evidence
that bone loss extends from the level of crestal bone to or
near the apex of the tooth, the radiograph is of little value
in determining the cause. Periodontal and endodontic
FIGURE 52.10 Tracking the sinus tract with a gutta-percha point.
problems can radiographically mimic each other. If bone
loss exists around one tooth in an otherwise periodontally
healthy patient and pulp tests are negative, then this loss
of bone may be of endodontic origin. The prognosis is
excellent for the regeneration of these structures. Peri- cone is inserted through the sinus opening and gently
odontally susceptible patient may exhibit lesions that manipulated along the sinus tract till resistance is met.
appear to be of pulpal origin but are not. When bone loss A radiograph is taken to trace the course of the sinus
exists in these situations and pulp test results are normal, tract to the origin of the inflammatory process (Figs 52.10
the lesion is of periodontal origin. and 52.11).
Fistula Tracing
Endodontic and periodontal lesions can develop a TREATMENT PROTOCOL
fistulous sinus tract. Inflammatory exudate is prone to
travel along the path of least resistance and drain through In general, the focus should be on treating the primary
a sinus intraorally in the oral mucosa or extraorally on disease, either pulpal or periodontal as the case may be.
the facial skin. These fistulas can usually be spotted dur- By and large endodontic therapy precedes periodontal
ing clinical examination of the attached gingiva or the therapy. However, in some cases the secondary disease is
mucosa in the vestibule. Gutta-percha cones are usually also established and in such cases it is essential to initiate
used to trace these fistulas (Fig. 52.9). The gutta-percha treatment for both the primary and the secondary disease.
several months before it can be radiographically detected.

Thus, periodontal therapy including deep scaling with
and without periodontal surgery should be postponed
until the result of the endodontic treatment can be prop-
erly evaluated.
CONCLUSION
In general, the treatment for pulpal or periodontal

disease is the same as it would be were they to occur
independently of each other. It is pertinent to note that
tissue loss subsequent to endodontic disease is gener-
ally reversed very rapidly after endodontic treatment.
The same cannot be said about tissue loss subsequent
to periodontal disease. The part of the lesion caused by
FIGURE 52.11 Radiograph with gutta-percha in the sinus tract, the plaque infection may also heal following periodontal
pointing to source of the lesion. therapy, although little or no regeneration of the attach-
ment apparatus can be expected. This suggests that the
Periodontal therapy may or may not be required depend- larger the part of the lesion caused by the root canal infec-
ing on disease status. The complete healing of destroyed tion, the more favorable the prognosis is for regeneration
periodontal support can be expected following the treat- of the attachment.
ment of pulpal pathology. The resolution of extensive Researchers have shown that the presence of endodon-
destruction following the treatment of chronic periodontic pathosis may be a risk factor for loss of periodontal
titis is less predictable. It is important to realize that it is attachment, at least in periodontitis-prone patients who
clinically not possible to determine the extent to which have undergone extensive root planing. In addition, ex-
one or the other of the two disorders (endodontic or peri- isting microbiological data now support the hypothesis
odontal) has affected the supporting tissues. Therefore, that advanced periodontal lesions may adversely affect
the treatment strategy must be first to focus on the pulpal endodontic health.
infection and to perform debridement and disinfection of When approaching endodontic periodontal lesions,
the root canal system. The second phase includes a period clinicians should sequence the clinical therapy to opti-
of observation whereby the extent of periodontal heal- mize the histologic outcome. Furthermore, advances in
ing resulting from the endodontic treatment is followed. regenerative therapy and materials science may offer
Reduced probing depth can usually be expected within promising new techniques for salvaging previously con-
a couple of weeks while bone regeneration may require demned teeth.
KEY POINTS
• Pathways of communication between pulp and peri- pulp vitality tests, radiographic analysis, and advanced
odontium are of developmental origin, pathological diagnostic techniques.
origin, and iatrogenic origin. • Treatment of endodontic periodontal lesion depends on
• Diagnosis of endodontic periodontal lesions is done the type of lesion.
by routine periodontal and endodontic examinations,

1. Armitage GC. Development of a classification system for periodontal
1. Classify endodontic periodontal lesions. diseases and conditions. Ann Periodontol 1999;4(1):l-6.
2. Describe diagnosis of endodontic periodontal lesions. 2. Genco RJ, Goldman HM, Cohen DW. Contemporary Periodontics.
3. Describe retrograde periodontitis. St Louis: Mosby; 1990.
4. Describe true combined lesions. 3. Harrington G, Stiener D, Ammons Jr W. The periodontal-cndodontic
controversy. Periodontal 2000 2002;30:123-30.
4. Ingle IJ, Bakland LK, Baumgastner JC. Ing/e's Endodontics. 6th ed. 8. Shenoy A, Shenoy N. Endo-perio lesions: diagnosis and clinical
Hamilton: BC Decker; 2008. considerations. Indian J Dent Res 2010;21(4):579-85.
5. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds. 9. Simon JHS, Glick DH, Frank AL. The relationship of endodontic
Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B. periodontic lesions. J Periodontol 1972;43:202-8.
Saunders Company; 2006. 10. Solomon C, Chalfin H, Kellert M, Weseley P. The endodontic peri-
6. Paul BF, Hutter JW. The endodontic periodontal continuum revisited- odontal lesion - a rational approach to treatment. J Am Dent Assoc
new insights into etiology, diagnosis and treatment. J Am Dent Assoc 1995;126:473-9.
1997;128:1541-8. 11. Walton RE, Torabinejad M. Principles and Practice of Endodontics.
7. Rotstein I, Simon JH. Diagnosis, prognosis and decision-making in 3rd ed. Philadelphia, PA: WB Saunders Company; 2002:466-484.
the treatment of combined periodontal endodontic lesions. Periodon- 12. Zehnder M, Gold SI, Hasselgren G. Pathologic interactions in pulpal
tal 2000 2004;34:165-203. and periodontal tissues. J Clin Periodontol 2002;29:663-71.
CHAPTER
53
Periodontal Plastic Surgery
CHAPTER OVERVIEW
The World Workshop in Periodontics in its proceed- Periodontal plastic surgery is defined as the surgical
ings in 1996 accepted the term periodontal plastic surgery procedures performed to correct or eliminate anatomic,
(PPS), as originally proposed by Miller, to be included in developmental, or traumatic deformities of the gingiva or
the periodontal nomenclature. This replaced the older alveolar mucosa.
term mucogingival surgery, which was in vogue for well The scope and ramifications of these procedures are
over three decades. The change of nomenclature was huge, ranging from the management of an aberrant frenum
necessitated due to the phenomenal advancement in peri- to complex procedures such as ridge augmentations. Fur-
odontal surgical techniques as a result of total paradigm thermore, the increased aesthetic and cosmetic concerns of
shift from resective techniques to regeneration and aes- the dental patients seen today require all dental practitioners
thetic considerations. to be well conversant with the various solutions available.
COMMON MUCOGINGIVAL AND SIGNIFICANCE OF ATTACHED GINGIVA,

AESTHETIC PROBLEMS VESTIBULAR DEPTH, AND FRENUM
Irrespective of whether it is a natural tooth, prosthesis, Controversies and different schools of thought regard-
or an implant, the dental practitioner can come across the ing the minimum width of attached gingiva necessary to
following problems related to either soft tissue abnormali- maintain gingival health have existed in periodontics for
ties or aesthetic concerns: a long time. Indeed, the original rationale for mucogin-
gival procedures was predicted on the assumption that
1. Inadequate attached gingiva (Fig. 53.1)
a narrow zone of attached gingiva is detrimental to the
2. Lack of sufficient vestibular depth (Fig. 53.2)
overall periodontal health, and hence an array of surgi-
3. Aberrant frenum (Fig. 53.3)
cal procedures were advocated to increase the zone of
4. Gingival recession (Fig. 53.4)
attached gingiva with variable results.
5. Open interproximal spaces (Fig. 53.5)
However, several studies have questioned the view
6. Excessive physiological gingival pigmentation
that a good zone of attached gingiva is more resistant
(Fig. 53.6)
against bacterial challenge than a narrow zone. Subjects
7. Inadequate crown length for restorative procedures
with meticulous oral hygiene may maintain areas without
(Fig. 53.7)
significant zone of attached gingiva in a healthy state.
8. Excessive gingival display and gingival asymmetry
Hence, at present, no specific amount of attached gingiva
(Fig. 53.8)
has been determined as adequate. Decisions regarding the
9. Alveolar ridge defects (Fig. 53.9)
need to perform a graft where narrow bands of attached
10. Impacted/unerupted teeth requiring orthodontic
gingiva exist depend on clinical judgment. However, in
management.
situations where subgingival restorations are planned,
Fortunately, with improved knowledge and advance- teeth serving as abutments, around dental implants
ment in various surgical techniques, solutions are avail- and before orthodontic treatment, augmenting attached
able for all the above-mentioned problems. gingiva may be necessary.
C H A PT ER 53 PER IO D O N TA L PLA ST IC SU R G ER Y 469
FIGURE 53.1 Inadequate attached gingiva. FIGURE 53.4 Gingival recession.
FIGURE 53.2 Lack of sufficient vestibular depth. FIGURE 53.5 Open interproximal spaces.
FIGURE 53.3 Aberrant frenum. FIGURE 53.6 Excessive physiological gingival pigmentation.
of little clinical significance, as it occurs secondary to the

problems of lack of attached gingiva or malpositioning of
lower incisors. As it is not a frenal problem per se, mandib-
ular frenectomy as a separate procedure is not indicated.
However, if the lingual frenum is involved resulting in
speech problems and movement of tongue, it calls for
surgical correction.
GENERAL FACTORS AFFECTING THE

OUTCOME OF PPS PROCEDURES
Periodontal plastic surgical procedures, apart from

FIGURE 53. 7 Inadequate crown length for restorative procedures. being technique sensitive and requiring a lot of experi-
ence and practice to master, are influenced by various
factors. Before attempting to perform these procedures,
the clinician should take into consideration all the criteria
given subsequently.
The success of the procedure depends on the following:
• Oral hygiene: Meticulous maintenance of oral hygiene
is important. Patients who cannot maintain plaque-
and inflammation-free dentition are unsuitable for
these procedures. So, it is needless to emphasize that
before attempting PPS procedures, all the basic peri-
odontal procedures should be completed.
• Correct brushing technique: While good oral hygiene is
fundamental to the success of any form of periodontal
therapy, it is also equally vital to ensure that the pa-
FIGURE 53.8 Excessive gingival display. tient does not suffer from faulty toothbrushing. Many
mucogingival problems such as gingival recession, loss
of attached gingiva, and traumatic injuries are a result
of vigorous brushing. The clinician must supervise
the patient's brushing technique and correct it, if it is
found to be injurious to the tissues.
• Periodontal status: It is absolutely essential that all other
forms of periodontal diseases are treated before at-
tempting PPS procedure and the patient has a stable
periodontal status.
• Systemic health: Like for any other periodontal surgery,
PPS procedure is contraindicated in medically compro-
mised patients and those with unstable systemic status.
• Smoking: While it is not an absolute contraindication,
the success of periodontal plastic surgeries is much
less in heavy smokers than in nonsmokers.
FIGURE 53.9 Alveolar ridge defects. • Arch form, tooth alignment, and occlusion: Narrow arches,
malaligned teeth, particularly those labially placed,
teeth with increased root prominence, and malocclu-
It is the belief of many clinicians that a minimum ves- sions impede successful outcome of PPS procedure.
tibular depth is required for proper oral hygiene main- Often, orthodontic treatment procedures offer better
tenance. Again, this concept has been challenged. Except and long-lasting solutions in such cases.
for prosthetic reasons involving retention of dentures, • Patient motivation: It is very important to have discern-
vestibular deepening procedures just to facilitate oral ing and well-motivated but pragmatic patient suitable
hygiene maintenance have been out of vogue. for PPS procedure. Patients must be clearly explained
Frenal aberrations requiring corrections are mostly all the aspects of the procedures and given a realistic
related to the maxillary frenum. Mandibular frenum is view of what to expect from such surgeries.
AUGMENTATION OF ATTACHED 2. Discomfort experienced by the patient during tooth-

GINGIVA brushing and/ or chewing due to an interfering lining
mucosa
The attached gingiva may be augmented as a separate 3. When orthodontic tooth movement is planned and the
procedure or may be combined with other objectives such final positioning of the tooth can be expected to result
as vestibular deepening, root coverage, and frenal relief. in an alveolar bone dehiscence
Some of the techniques for the procedure include: 4. When subgingival restorations are placed in areas with
a thin marginal tissue.
1. Free gingival grafts
2. Laterally positioned flap Contraindications:
3. Subepithelial connective tissue graft 1. Aesthetic zone
4. Apically positioned flap. 2. Limited availability of donor tissue for extensive
procedures
Among the above-mentioned procedures, the free gin- 3. Mobile teeth
gival graft is the most predictable and practical one - and 4. Trauma from occlusion.
shall be discussed in detail.
Free Gingival Grafts (Fig. 53.10) Technique

Recipient site preparation (Fig. 53.lOB): A firm connective
Synonyms: Free mucosal autograft and free
tissue bed devoid of tissue tags needs to be prepared to
epithelialized soft tissue graft.
receive the graft. For this, a horizontal incision at the exist-
Main objective: To increase zone of attached gingiva.
ing mucogingival junction is made with a no. 15 blade to
Secondary objectives: Root coverage and vestibular
the desired depth. This is joined by two vertical incisions
deepening.
outlining the recipient site into the alveolar mucosa. A
Indications: partial-thickness flap is separated by the same blade and
1. Areas of minimal or no attached gingiva where the extended to the depth of the vertical incisions. Some clini-
movable alveolar mucosal margins interfere with cians recommend suturing this flap at the apical portion,
plaque control but this is not mandatory. All the tissue tags are swiped off
FIGURE 53.10 Free gingival graft. (A) Preoperative; (B) recipient site; (C) graft stabilized; (D) postoperative.
with surgical scissors and the area is irrigated and hemo- Initially, the graft survives by diffusion of nutrients.
stasis obtained by firm pressure with stent or wet gauze. This is followed by new blood vessels proliferating from
Template preparation: An accurate template of the re- the surrounding areas and establishing a plexus with
cipient site is prepared using a sterile tin foil to facilitate the vessels already present in the graft. This is followed
obtaining the graft of exact dimension. Once the template by maturation and functional integration, which, in the
is obtained, the recipient area is covered by a moist gauze. normal course of events, takes place by 3 weeks. This
Securing the graft from the donor site: The usual sites for includes complete renewal of the epithelium. However,
obtaining the graft are mucous membrane of the hard the graft is clearly discernible from the surrounding areas
palate, edentulous ridges, and retromolar areas, but the for many months.
most common donor site is the hard palate. Here also, the
exact area for obtaining the graft is important. Anterior to
Root Coverage
first premolar presents rugae, which is not suitable, and
going beyond distal of second molar involves the risk Gingival recession, besides being aesthetically un-
of damaging greater palatine vessels with the resultant pleasant, may result in root caries, pulpal hyperemia, and
hemorrhage. Hence, the ideal area is between distal of hypersensitivity. Root coverage, therefore, is a tangible
first premolar and the mesial of second molar. benefit a patient appreciates and is the most commonly
A simple Hawley appliance may be previously fabri- performed of all the PPS procedures. Before attempting
cated so as to enable placement of a periodontal dressing root coverage, it is important to understand the type of
postoperatively, thereby protecting the donor site. recession and its prognosis. PD Miller classification of
The template is placed over the donor site and a shallow gingival recession is mainly designed to predict the treat-
incision is made around the same with a no. 15 blade. The ment outcome.
blade is inserted into the desired thickness (between 1 and
1.5 mm), so that a graft consisting of epithelium and a layer PD Miller Classification
of connective tissue is slowly separated. It is recommended Class I: Marginal tissue recession that does not extend
that a suture be passed through the graft margin and this to the mucogingival junction (MGJ). There is no loss
be used to gently retract the graft as the blade continues of interdental bone or soft tissue. Complete root cover-
to separate the same, rather than holding the graft with age can be anticipated. This type of recession can be
tissue forceps. Special mucotomies are available to harvest narrow or wide.
the graft, but many clinicians find them difficult to use. Class II: Marginal tissue recession that extends to
Graft stabilization (Fig. 53.lOC): The harvested graft is or beyond the MGJ. There is no loss of interdental
immediately transferred to a Petri glass containing saline, bone or soft tissue. This type can be subclassified
and any tissue tags and fatty submucosa are removed. into wide and narrow. Complete root coverage can
The gauze covering the recipient area is removed and be anticipated.
any hemorrhage is controlled. The thick blood clot is also Class III: Marginal tissue recession that extends to
removed. The graft is placed accurately over the recipient or beyond the MGJ. There is loss of bone or soft tis-
site and secured to the margins with 4-0 silk sutures. It sue, apical to the cementa-enamel junction (CEJ) but
is also secured to the base with sutures. The graft is then coronal to the level of the recession defect, or mal-
gently pressed with wet gauze so as to eliminate dead positioning of the tooth. Partial root coverage can be
space, which would otherwise interfere with healing. The anticipated.
area is covered with a tin foil and a periodontal dressing Class IV: Marginal tissue recession that extends be-
is placed over it. yond the MGJ. There is loss of interdental bone or
The donor area is protected by a periodontal dress- soft tissue apical to the level of recession and/ or se-
ing and, as described earlier, a previously fabricated vere malposition of the tooth. No root coverage can
Hawley appliance fitted so as to protect the donor site. be anticipated.
Usual postoperative instructions and medications are
Besides the above-mentioned factors, it is also neces-
prescribed. The periodontal dressing on the recipient site
sary to examine the arch form, alignment of teeth, root
is changed at the end of 1 week. The dressing may have
protuberance, root caries, and cervical restoration, which
to remain in place for up to 2-3 weeks.
could have an effect not only on the surgical result but
also on the long-term maintainability.
Healing of Free Gingival Grafts
The healing of free gingival grafts occurs in three stages: Techniques for Root Coverage
1. Stage of plasmatic circulation The various techniques for root coverage can be con-
2. Stage of vascularization veniently classified as given in the table by Bouchard et al
3. Stage of maturation (Table 53.1).
TABLE 53.1 Classification of Root Coverage Techniques extent. Sharp tooth margins around cervical abra-
sions, if present, should be smoothened.
1. Pedicle soft tissue grafts Flap preparation: A vertical incision is made from the
a. Rotational flaps
- Laterally positioned flap
gingival margin of one or two teeth adjacent to the
- Double papilla flap and oblique rotated flap recipient area. Like in other situations, the incision
b. Advanced flaps should never be placed in the midradicular or mid pa-
- Coronally advanced flap (CAF) pilla area. The incision should include the periosteum
- Semilunar flap and be extended to the alveolar mucosa up to the base
2. Free soft tissue grafts
a. Nonsubmerged graft
of the defect. It should be slightly tilted so as to ensure
- One stage (free gingival graft) that the base of the flap is wider than the apex, thereby
- Two stage (free gingival graft + coronally positioned flap) ensuring good blood supply (Fig. 53.11B).
b. Submerged grafts
- Connective tissue graft + laterally positioned flap A horizontal incision made along the gingival margin
- Connective tissue graft + double papilla flap and interdental papilla helps in raising a flap consisting
- Connective tissue graft+ coronally positioned flap
- Envelope techniques, pouch techniques, and so on
of epithelium and layer of connective tissue.
3. Additive treatments The portion of flap actually covering the denuded root
a. Root surface modification agents should be of full thickness, whereas the remaining portion
- Enamel matrix proteins covering the donor area should be of partial thickness.
- Guided tissue regeneration (CTR) - nonresorbable barrier This ensures that the alveolar bone margin on the donor
membranes
b. Resorbable barrier membranes
area does not undergo resorption.
Coronally Advanced Flap and Semilunar

Lateral Positioned Flap Coronally Advanced Flap
Synonyms: Pedicle graft, sliding flap, laterally Indications:
displaced flap, and horizontally positioned flap 1. Aesthetic coverage of exposed roots
(Fig. 53.llA-F). 2. For tooth sensitivity owing to gingival recession.
This is a comparatively simple surgical procedure
used in treating solitary, isolated gingival recessions. The Contraindications:
important prerequisites are that the adjacent area where 1. Shallow vestibule
the donor tissue is taken should be free of any periodontal 2. Insufficient width of attached gingiva.
disease or bone defects such as dehiscences or fenestra-
tions and, importantly, should have a good zone of kera- This is comparatively a less technique-sensitive proce-
tinized gingiva. dure and the results are highly predictable. The prereq-
uisite is to have a zone of at least 3 mm wide keratinized
gingiva apical to the recession. This procedure can also be
Indications: used to treat multiple adjacent recession defects.
1. When the interproximal papillae adjacent to the mu- Technique: After obtaining anesthesia, two vertical in-
cogingival problem are sufficiently wide cisions are given bordering the recession extending well
2. Isolated gingival recessions and teeth with narrow beyond the mucogingival junction. Next, an internal bevel
mesiodistal dimensions incision is given from the gingival margin to the base of
3. Absence of periodontal pockets. the sulcus and a partial-thickness flap is elevated up to the
Contraindications: extent of vertical incisions (Fig. 53.12B). After planing the
1. Presence of deep interproximal pockets roots and debridement, a nick is given to the periosteum
2. Excessive root prominences at the base of the raised flap, taking care not to perforate
3. Deep or extensive root abrasion or erosion it. This enables the flap to be moved easily. The flap is
advanced coronally to cover the entire recession and sta-
4. Significant loss of interproximal bone height.
bilized with 5-0 sutures (Fig. 53.12C and D).
The procedure is as follows:
Recipient site preparation: The gingival margin of CAF with Subepithelial Connective
about 0.5-1 mm is incised and resected around the Tissue Graft
exposed root. The tissues are removed and the roots The coronally advanced flap (CAF) may be com-
are planed to get a smooth, hard surface. If the root bined with guided tissue regeneration using a
prominence is excessive, it can be reduced to some resorbable barrier subepithelial connective tissue
(B)
FIGURE 53.11 Lateral positioned flap. (A) Preoperative; (B) graft laterally positioned and sutured; (C) 15 days postoperative; (D) 1 month
postoperative; (E) 9 months postoperative; (F) 15 months postoperative.
graft (SCTG; Figs 53.13 and 53.14) or with membrane released, it collapses coronally, covering the denuded
(Fig. 53.15A-E). root (Fig. 53.16C). Usually, no sutures are required,
but a suspensory sling suture may be given to pre-
CAF with Guided Tissue Regeneration vent shrinkage during healing. The donor site heals
A variant of this technique has been proposed by uneventfully.
Tarnow (Fig. 53.16A-D). Here, a semilunar incision
is made following the curvature of the receded gingi-
Management of Multiple Recessions
val margin, which ends about 3 mm short of interden-
tal papilla. Following this, an intrasulcular incision Root coverage of multiple gingival recessions pos-
is made from the base of the pocket and joined with es a challenge to the periodontists. Many techniques
the previous incision (Fig. 53.16B). Once the tissue is have been proposed but the predictability of outcome
FIGURE 53.12 Coronally advanced flap. (A) Preoperative; (B) flap raised; (C) flap coronally advanced; (D) advanced flap sutured; (E) postop-
erative appearance after 12 months showing complete root coverage.
remains doubtful. Coronally advanced flap in a group MANAGEMENT OF ABERRANT FRENUM

of teeth with or without subepithelial connective tissue
grafts could be tried but the problem is to harvest large Problems with the frenum have often been overem-
amount of graft tissue. To address this problem, off late phasized. This is particularly true with the mandibular
an acellular dermal matrix membrane obtained from frenum, which apparently seems to be aberrant when
tissue banks is being used with considerable success actually it is a problem of lack of keratinized gingiva
(Fig. 53.17 A-F). with or without gingival recession. However, maxillary
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(0)
FIGURE 53.13 CAF with subepithelial connective tissue graft. (A) Preoperative; (B) incisions in the donor site to obtain SCTG; (C) SCTG being
removed; (D) SCTG obtained; (E) SCTG placed over defect and flap coronally advanced and sutured; (F) postoperative.
labial frenum may present problems due to aesthetics or 3. Papillary - when the fibers are extending into the in-
interference in orthodontic treatment. It is common to find terdental papilla
thick fibrous frenum associated with midline diastema. 4. Papilla penetrating - when the frenal fibers cross
The labial frenal attachments have been classified as the alveolar process and extend up to the palatine
mucosal, gingival, papillary, and papilla penetrating. papilla.
1. Mucosal-when the frenal fibers are attached up to the If an abnormal frenulum is left in place, it can re-
mucogingival junction sult in gingival recession, diastema formation, accu-
2. Gingival - when the fibers are inserted within the at- mulation of debris by reflection, and opening of the
tached gingiva sulcus.
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FIGURE 53.14 CAF with subepithelial connective tissue graft. (A) Preoperative site; (B) incisions placed in recipient site; (C) partial-thickness
flap elevated in the recipient site; (D) graft obtained from donor site; (E) SCTG placed over the defect and flap coronally advanced and sutured;
(F) postoperative.
Frenectomy 3. location of attachment in edentulous ridge interfering

retention and stability of prostheses; and
Relocation of frenum with a frenotomy or complete 4. attachment obstructing mechanical tooth cleaning.
removal with a frenectomy becomes necessary. It is im-
portant to note here that frenectomy should be performed
after the orthodontic treatment. If done prior, then it is Classic Technique
mandatory that the orthodontic treatment is started at This technique is an excision-type frenectomy which
the earliest. includes the interdental tissues and the palatine papilla
along with the frenulum. The frenum is engaged with a
Indications: hemostat which is inserted into the depth of the vestibule
1. restrictive problems associated with lip or tongue and incisions are placed on the upper and the undersurface
movement; of the hemostat until the hemostat is free. The triangular
2. closure of a midline diastema by orthodontic treatment; resected portion of the frenum with the hemostat is re-
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FIGURE 53.15 CAF with guided tissue regeneration. (A) Preoperative; (B) flap reflected; (C) resorbable membrane placed; (D) flap coronally
positioned and sutured; (E) postoperative.
moved. A blunt dissection is done on the bone to relieve normally it should not be difficult for a motivated pa-
the fibrous attachment. The edges of the diamond-shaped tient to maintain plaque control in that area. However,
wound are sutured (Fig. 53.18A and B). shallow vestibule may pose difficulties in placement
of removable partial prosthesis. Furthermore, shallow
vestibule is usually associated with inadequate zone
VESTIBULAR DEEPENING of keratinized gingiva and gingival recession. In such
cases, gingival augmentation with a free gingival graft
The present opinion is that a shallow vestibule also results in increasing vestibular depth.
does not necessarily jeopardize periodontal health. Mere vestibular deepening with procedures such as
This problem is usually seen in mandibular anterior fenestration, as was done in the past, without gingival
region, which is the most visible part in the mouth, and grafts has been found to be unsuccessful.
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FIGURE 53.16 A variant of CAF. (A) Preoperative; (B) semilunar incision placed; (C) flap coronally advanced; (D) postoperative.
FIGURE 53.17 Management of multiple recessions using acellular dermal matrix (AlloDerm [TM]). (A) Preoperative view; (B) horizontal inci-
sions given; (C) flap raised; (D) AlloDerm placed; (E) flap coronally advanced and sutured; (F) postoperative view.
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GINGIVAL DEPIGMENTATION
Gingival pigmentation is affected by various factors

including racial differences. Often, patients complain of
excessive pigmentation, which is unaesthetic. Such hyper-
pigmented gingiva can be managed by mucosal excision
(Fig. 53.19A-D), laser surgery (Fig. 53.20A-D), or cryo-
surgery (Fig. 53.20E-H). It should be clearly understood
here that such procedures could be attempted only on
otherwise normal gingiva. Pathologic lesions resulting in
altered color of the gingiva should not be managed with
these procedures.
The results of depigmentation are maintained for a
period ranging from 6 to 18 months after which pig-
mentation returns. Results obtained following cryo-
surgery last longer as compared with surgical mucosal
excision.
CROWN LENGTHENING
Indications:
1. To provide adequate tooth structure in cases of subgin-
gival tooth fracture, subgingival caries, root resorption,
and uneven gingival levels;
2. Unaesthetic short crowns due to tooth wear;
3. Inadequate axial height for retention of restorations;
FIGURE 53.18 Frenectomy. (A) Preoperative; (B) postoperative. 4. Altered passive eruption of a single or multiple teeth;
FIGURE 53.19 Surgical depigmentation. (A) Preoperative; (B) depigmentation using scalpel; (C) immediate postoperative; (D) postoperative.
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FIGURE 53.20 Laser depigmentation. (A) Preoperative; (B) depigmentation using diode laser; (C) immediate postoperative; (D) postoperative.
Cryosurgical de-pigmentation: (E) Pre-operative; (F) application of cryoprobe; (G) intra operative view showing formation of ice crystals;
(H) postoperative view after one month.
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FIGURE 53.21 (A) Gingival asymmetry and excessive display; (B) internal bevel incisions with recontouring; (C) redundant tissues removed;
(D) appearance before suturing; (E) postoperative appearance showing symmetrical gingiva with a pleasant smile.
5. In cases of a gingival smile - called a "gummy smile" - strengthen the anchoring of the restored teeth, by sur-
with short natural crowns (Fig. 53.21). gically moving the alveolar crest bone to a more apical
position, thereby providing adequate tooth structure to
safely prepare the restoration. It also helps to reestablish
Contraindications:
the new physiological biological width.
1. Deep caries or fracture requiring excessive bone
Biological width is the term applied to the dimensional
removal
width of the dentogingival junction (epithelial attach-
2. Postsurgery creating unaesthetic outcomes
ment and underlying connective tissue). Gargiulo and
3. Tooth with inadequate crown-root ratio (ideally 2:1
colleagues studied the anatomy of the dentogingival junc-
ratio is preferred)
tion and quantified the average as a constant 2.04 mm (the
4. Nonrestorable teeth
epithelial attachment is 0.97 mm, and connective tissue
5. Tooth with increased risk of furcation involvement.
is 1.07 mm) with a sulcus depth of 0.69 mm. Placing re-
6. Unreasonable compromise of aesthetics
storative margins within the biological width frequently
7. Unreasonable compromise on adjacent alveolar bone
leads to gingival inflammation, clinical attachment loss,
support.
and bone loss. This is thought to be due to the destruc-
The objective of crown lengthening in restorative tive inflammatory response to microbial plaque located
cases is to increase the axial length of the crown, and to at deeply placed restorative margins. Clinically, these
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FIGURE 53.22 Crown lengthening. (A) Preoperative frontal view; (B) preoperative palatal view; (C and D) internal bevel gingivectomy; (E)
flap elevation and osseous recontouring; (F) suturing done; (G and H) final prosthesis placed.
changes are manifested as deepened periodontal pockets RECONSTRUCTION OF INTERDENTAL

in case of thick gingival biotype or gingival recession in PAPILLA
case of thin biotype.
Merely excising the marginal gingiva to increase the Open interproximal spaces often referred to as black tri-
crown length is inadequate. There will be a rebound of the angles are highly unaesthetic, besides being areas of food
gingival margin, which compromises biological width. lodgment (Fig. 53.24A-D). Whereas orthodontic treat-
Hence, the ideal crown lengthening procedure should ment, modification of crowns, providing aesthetic resto-
consist of ostectomy along with apically repositioned flap rations, and so on, can solve the problem to some extent,
(Figs 53.22 and 53.23). Again, highest priority should be the real challenge for a periodontist is the reconstruction
given to aesthetics. of lost or missing papilla. Many techniques have been
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FIGURE 53.23 Surgical crown lengthening. (A) Preoperative; (B) postoperative.
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employed, some of them requiring microsurgery, but none 4. Success reproducibility, lack of morbidity, and
have been found to be predictable. economy should be the guiding principles.
5. Practice makes you better and better.
TEN COMMANDMENTS OF PPS 6. Keep records. Follow up each case.
7. Use good instruments.
1. Assess the prevailing factors thoroughly. 8. Microsurgery yields good results (never mind if you
2. Be realistic. Do not attempt heroic techniques. get habituated to it).
3. Manual dexterity is absolutely vital. 9. Do it on a deserving, discerning, and diligent patient.
10. Be cautious of patients with high aesthetic demand.
KEY POINTS
• The term periodontal plastic surgery was originally • PD Miller classified gingival recession into Class I, Class
proposed by Miller. II, Class III, and Class IV.
• Periodontal plastic surgery is defined as the surgical • Root coverage is usually obtained by subepithelial con-
procedures performed to correct or eliminate anatomic, nective tissue graft, and coronally advanced flap.
developmental, or traumatic deformities of the gingiva • Crown lengthening is an established procedure to
or alveolar mucosa. assist restorative dentistry and also to improve
• Good zone of attached gingiva is not necessarily more aesthetics.
resistant against bacterial challenge than a narrow zone. • Hyperpigmented gingiva can be managed by mucosal
• However, attached gingiva is deemed essential around excision, cryosurgery, or laser surgery.
artificial crowns, abutments, and implants. • Papilla reconstruction is one of the most difficult tasks
• Attached gingiva may be augmented with procedures in periodontal plastic surgery.
such as free gingival grafts, laterally positioned flap, and
apically positioned flap.
ACKNOWLEDGMENT Suggested readings

1. Allen EP. Aesthetics and plastic surgery in periodontics. Periodontal
The author gratefully acknowledges the assistance 2000. 1996;11:7-11.
of Dr Sruthima G, Reader, Department of Periodontics, 2. Bouchard P, Malet J, Borghetti A. Decision-making in aesthetics: root
Vishnu Dental College, Andhra Pradesh, India, in the coverage revisited. Periodontal 2000. 2001;27:97-120.
3. Ito T, Johnson JD. Colour Atlas of Periodontal Surgery. St Louis: Mosby;
preparation of this chapter.
1994; 175-253.
4. Lindhe J, Lang NP, Karring T. 5th ed. Clinical Periodontology and Im-
plant Dentistrv, 2. London: Blackwell Munksgaard; 2008; 955-1028.
1. Define periodontal plastic surgery
6. Nowzari H. Aesthetic periodontal therapy. Periodontal 2000.
2. What are the indications for periodontal plastic 2001;27:45-58.
surgery? 7. Rose LF, Mealey BL, Genco R. Periodontics, Medicine, Surgery, Implants.
3. Write the current thinking on the significance of 1st ed. Mosby; 2004; 405-487.
attached gingiva. 8. Sato N. Periodontal Surgery: A Clinical Atlas. New York: Quintessence;
2000; 335-447.
4. Describe the free gingival procedure.
5. Name the various techniques of root coverage.
6. Describe the sub epithelial connective tissue grafting
procedure.
7. Describe the various gingival depigmentation proce-
dures.
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CHAPTER
54
Recent Advances in Periodontal
Surgical Techniques
HISTORICAL LANDMARK
• Albert Einstein postulated the theory of stimulated • TH Maiman produced the first ruby laser in 1960.
emission in 1916. • Introduction of first true dental laser was in 1989.
LASER IN PERIODONTICS Wavelength of Dental Lasers

The dental laser devices have emission wavelength
Laser is an acronym for light amplification by stimu-
lated emission of radiation. Lasers can concentrate light ranging approximately from 500 to 10,600 nm (Tables 54.2
and 54.3). Most of the lasers used in dentistry emit an
energy and exert a strong effect on the target tissue at an
invisible infrared light wavelength and fall in the nonion-
energy level much lower than natural light. Amplification
izing portion of electromagnetic spectrum called thermal
of light energy, resulting in production of laser, occurs by
radiation. Argon lasers fall under the visible wavelength
stimulated emission. When a photon is absorbed by an
excited atom, it results in release of two identical pho- portion of electromagnetic spectrum. The wavelengths of
a laser are important as they determine the characteristics
tons. These photons excite more photons, which further
and uses of respective lasers (Fig. 54.3).
produce more identical atoms and a chain reaction sets
in leading to production of laser (Fig. 54.1). Delivery Systems
Characteristics of a laser light are as follows:
The laser energy should be delivered to the surgical
1. It is monochromatic: has a single wavelength. site by a system which allows minimum loss of energy.
2. It is collimated: beam is nondivergent. Commonly used delivery systems are:
3. It is coherent: all the waves are in same phase.
4. It has concentrated energy. • Flexible fiber-optic system with bare glass fiber (quartz
fiber):
• Diode laser, neodymium-doped yttrium aluminum
garnet (Nd:YAG) laser
COMPONENTS OF A LASER UNIT (Fig. 54.2)
• Articulated arms:
• Active medium (Table 54.1):
• Erbium lasers, CO2 laser
Gas, solid, or liquid suspended in an optical cavity
• Semiflexible hollow waveguide:
• Power supply:
• Erbium lasers, CO2 laser.
• External energy source that acts as a pumping
The delivery system of erbium lasers has components
mechanism to continue stimulated emission
for water and air supply. The lasers also have rigid quartz
• Optical resonator or sapphire tips added in the end to interact with the tar-
• Mirrors for amplification get tissue. The lasers are also equipped with aiming beam
• Delivery system. delivered coaxially with fiber or waveguides.
CHA PTER 54 RECENT ADVANCES IN PERIO DONTAL SURGICA L TECHNIQ UES 487
TABLE 54.1 Types of Lasers Used in Dentistry Based on Active
Excited atom Medium
Photon
~
--~
--~
Photon
Photon
Laser type
Argon laser
Diode laser
Active medium
Argon gas
Solid semiconductor medium

• Aluminum gallium (AlGa)
• Gallium arsenide (GaAs)
• Aluminum gallium arsenide (AlGaAs)
FIGURE 54.1 Stimulated emission.
• Indium gallium arsenide (InGaAs)
Nd:YAG laser Solid medium

• Neodynium-doped yttrium aluminum garnet
Modes of Use of Dental Lasers Er:YAG laser Solid medium

• Erbium-doped yttrium aluminum garnet
• Contact mode: The laser tip works in light contact with
Er, Cr:YSGG Solid medium
the target tissue. laser • Erbium- and chromium-doped yttrium scan-
• Noncontact mode: The laser tip is a few millimeters dium gallium garnet
away from the target tissue.
CO2 laser Carbon dioxide gas
Er, Cr:YSGG, erbium- and chromium-doped yttrium scandium gallium garnet.
Modes of Emission of Laser Energy
• Continuous wave mode: The laser energy is emitted
continuously and produces constant tissue interaction.
• Gated pulsed mode: A mechanical shutter with time TABLE 54.2 Specific Wavelengths of Commonly Used Dental
circuit or digital mechanism is used to produce laser Lasers
energy in intervals, i.e., in pulsed mode. The pulse Dental lasers Wavelengths (nm)
durations and intervals can be in milliseconds, e.g., Argon lasers 488, 514 (visible)
20 ms, 30 ms, etc.
• Free-running pulsed mode: The laser energy is Diode lasers 810,910,940,980
emitted with very short bursts due to flashlamp Nd:YAG lasers 1064
pumping mechanisms. The pulse duration is in
Er, Cr:YSGG laser 2790
microseconds, e.g., 100 µs. There are relatively long
pulse intervals. CO2 laser 10,600
Er, Cr:YSGG, erbium- and chromium-doped yttrium scandium gallium garnet.
External Energy Source

flashlamp, electricity.
Active
~
Partially
mirror transmissive mirror
-Optical resonator-J - Delivery system -
FIGURE 54.2 Components of laser.

TABLE 54.3 Wavelengths of Certain Lasers Not So Commonly LASER-TISSUE INTERACTIONS

Used in Dentistry
A laser can have four types of interaction once it comes
Alexandrite laser 377nm
in contact with the tissue, depending on the optical prop-
HeNe laser 632nm erties of the tissue (Fig. 54.6):
Ho:YAG laser 2120 nm • Reflection
Ho:YAG, holmium-doped yttrium aluminum garnet. • Transmission
• Scattering
• Absorption.
Important Parameters and Terminologies (Figs 54.4
and 54.5) • Reflection: The laser beam is simply redirected without
having any effect on the tissue. This reflection can
• Joule: Standard unit for laser energy. be dangerous as the beam could be directed to an
• Watt: Standard unit for power of laser unit. unintentional target, such as eyes, and is a major safety
• Hertz: Standard unit for frequency of pulses. concern during the use of lasers.
• Power density: Measured in W / cm 2. It depends on the • Transmission: The laser beam passes through the
fiber size. tissue without having any effect on the target tissue.
• Energy density: Measured in J / cm 2. It is the amount of This effect is dependent on the wavelength of laser
energy delivered to the tissue surface area. light.
Invisible Ionizing Radiation Visible Invisible Thermal Radiation

400 nm 750 nm
Ultraviolet Near Infrared Mid-Infrared Far Infrared
FIGURE 54.3 Wavelengths of dental lasers on electromagnetic spectrum.
~1 --------·-···········-·--·-··········
Power= 3W
Pulse length = 0.5 s
Average power = 1.5 W
- -- --
0 0.5 1.0 1.5 2.0 s
FIGURE 54.4 Average power - power over a sustained basis, e.g., in gated pulsed mode.
Average power = 2 W
Pulse length = 100 µs
Peak power= 1000 W
FIGURE 54.5 Peak power - power level during a pulse, e.g., in free-running pulsed mode.
CHAPTER 54 RECENT ADVANCES IN PERIODONTAL SURGICAL TECHNIQUES 489
tissue lasers." The carbon dioxide laser wavelengths are
Laser irradiation Reflection
absorbed both by hydroxyapatite and then by water. But
still they are not the lasers of choice for hard tissues be-
cause they are more readily absorbed by hydroxyapatite
than by water (unlike erbium lasers). They may in fact
damage the hydroxyapatite crystals. Thus, their use is
restricted to soft tissues based on their absorption by
Tissue
. water also.
; T Based on the absorption characteristics and uses, lasers
can be broadly classified as:
• Soft tissue lasers - argon, diode, Nd:YAG, and carbon
dioxide
Transmission • All tissue lasers - erbium lasers.
FIGURE 54.6 Interaction of human tissue and laser irradiation. Ideal laser-tissue interaction requires the operator to:
• Identify target tissue
• Scattering: The laser beam is deflected in different
• Assess correct wavelength for maximum interaction
directions. It causes the transfer of laser energy to the • Use minimum power values to achieve desired tissue
tissue adjacent to the surgical site. It could be useful
interaction
when the laser is used in noncontact mode.
• Expose tissue to laser light for minimum time to
• Absorption: The laser energy is absorbed by the tar- achieve interaction
get tissue depending on the contents of the tissue. It • Achieve maximum thermal relaxation to prevent
is the usual desirable effect and forms the basis for
collateral thermal damage.
use of laser for various purposes. The water mol-
ecules, proteins, pigments, and other macromole- Photobiological effect of laser:
cules present in biological tissues are responsible for • Photothermal effect
absorption. • Photochemical effect
Different laser wavelengths have different absorption • Photoacoustic effect
coefficients for primary dental tissue components, i.e., • Fluorescence
water, melanin pigments, hemoglobin, and hydroxyapa- • Biostimulation.
tite (Table 54.4). Those primary components are called
• Photothermal effect: It is the principal laser-tissue
chromophores. These chromophores are absorbers of interaction. The laser energy is transformed into heat.
specific wavelengths and determine the various applica- This leads to warming and further vaporization and
tions of lasers.
ultimately ablation of the tissue. This effect is made use
Diode and Nd:YAG laser wavelengths are by pigments of in surgical cutting and coagulation. If the tissues are
such as melanin and hemoglobin present in soft tissues heated to a higher temperature, it leads to carboniza-
(gingiva, oral mucosa). They are not absorbed much by tion of the tissues (Table 54.5).
water and hydroxyapatite. Thus, they are considered • Photochemical effect: Laser energy can stimulate
"soft tissue" lasers. Erbium laser wavelengths are readily
chemical reactions. This effect is used in curing of com-
absorbed by water present in soft tissues. They are also posites. Photosensitive compounds when exposed to
readily absorbed by water and then by hydroxyapatite laser energy can produce singlet oxygen radical which
present in hard tissues, so they are considered as "all tis-
can be used for disinfection of periodontal pockets.
sue lasers." They are also sometimes referred to as "hard
This principal is used in photodynamic therapy.
TABLE 54.4 Absorption Characteristics of Lasers in Dentistry
Tissue components responsible for

Dental lasers absorption (maximum to minimum) TABLE 54.5 Effect of Tissue Temperature on Tissues
Argon lasers Hemoglobin > melanin Tissue temperature (°C) Observed effect
Diode laser Melanin > water 37-50 Warming, bacterial decontamination
Nd:YAG laser Melanin > water > hydroxyapatite >60 Coagulation, protein denaturation
Erbium laser Water > hydroxyapatite 100-150 Vaporization, ablation
CO, laser Hydroxyapatite > water >200 Carbonization

• Photoacoustic effect: Laser energy when absorbed by Precautions to be taken while using lasers:
water present in hard tissue (hydroxyapatite) leads to
• Use glasses provided by the manufactures (specific for
vaporization of water. This increases pressure within
wavelengths) for eye protection (patient, operator, and
the tissues leading to explosion. This photoacoustic
assistants).
effect forms the basis for hard tissue cutting by erbium
• Prevent inadvertent irradiation.
lasers.
• Avoid reflection from shiny metal surfaces.
• Fluorescence: When laser light is absorbed by certain
• The surgical environment should have a warning sign
biological pigments, it leads to fluorescence. This is
and limited access.
helpful in detection of caries within teeth.
• Ensure adequate high-speed evacuation to capture the
• Biostimulation: When used in noncontact and lower-
laser plume.
power settings, lasers elicit beneficial cellular and bio-
logical responses. It is helpful in rapid tissue healing,
pain relief, and increased collagen growth and has LASER APPLICATION IN PERIODONTAL
anti-inflammatory effect. This is also referred to as THERAPY
low-level laser therapy.
Advantages of using lasers for periodontal therapy: Soft Tissue Surgical Application
• Precise surgical cutting Soft tissue lasers are being widely used as a tool for gin-
• Less need for anesthesia gival soft tissue procedures, i.e., gingivoplasty, gingivec-
• Better visualization of cutting (hemostasis and tomy, frenectomy, gingival depigmentation, second-stage
coagulation) exposure of implant, and soft tissue crown lengthening
• Detoxification of a wound (Table 54.6). Nd:YAG, CO2, and diode lasers are used for soft
• Minimal wound contraction and scarring tissue procedures. Nd:YAG laser was one of the first to be
• Minimal swelling approved by the Food and Drug Administration (FDA). It
• Minimal suturing required has the disadvantage of deeper depth of penetration leading
• Patient acceptance. to damage to underlying tissue. Its use with peri-implant
tissue is contraindicated as it may damage the implants.
Disadvantages:
The diode laser has been introduced over the past few
• Cost is high. years for dental use, obtaining FDA safety clearance. The
• Use of lasers requires training and complete knowledge diode laser has been shown to have similar tissue effects as
to attain all the benefits of lasers without collateral the Nd:YAG laser in comparable studies, with less thermal
damage. effects on the deeper tissues. The CO2 laser was also intro-
• Modification of clinical technique may be required. duced long back for soft tissue application. It has the ad-
• No single wavelength optimally treats all dental vantage of lesser depth of penetration, but more of charred
diseases. tissues are formed which might delay wound healing.
TABLE 54.6 Specific Uses of Dental Lasers Based on the Various Tissue Interactions
Laser medium Wavelength (nm) Dental uses

Argon 488-514 Tooth bleaching and advanced curing lights
Carbon dioxide (CO2 ) 10,600 Gingivectomy / gingivoplasty, second-stage implant exposure, periodontal curettage
(advocated but not evidence based)
Diode 655-980 Gingivectomy / gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies,
dentinal desensitizing), second-stage implant exposure, periodontal curettage (advo-
cated but not evidence based)
Neodymium:yttrium- 1064 Gingivectomy / gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies,
aluminum-garnet dentinal desensitizing), second-stage implant exposure, periodontal curettage (advo-
(Nd:YAG) cated but not evidence based)
Erbium:YAG (Er:YAG) 2940 Gingivectomy / gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies,
dentinal desensitizing), second-stage implant exposure, periodontal curettage (advo-
cated but not evidence based), hard tissue cutting (dentin and osseous)
Erbium, chromium:yttrium 2780 Gingivectomy / gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies,
(Er, Cr:YSGG) dentinal desensitizing), second-stage implant exposure, periodontal curettage (advo-
cated but not evidence based), hard tissue cutting (dentin and osseous)
YSGG, yttrium scandium gallium garnet.
Erbium lasers can also be used for soft tissue surgery. They based on clinical attachment gain are needed to determine
are absorbed only in superficial layer and are therefore if laser-assisted SRP has a beneficial effect.
advantageous. Their cost factor may be a limitation.
Surgical Pocket Therapy
Nonsurgical Treatment of Periodontal Disease
Degranulation During Flap Surgery
Laser-Mediated Sulcular/Pocket Debridement Lasers can be useful in debridement of areas with lim-
Diode and Nd:YAG lasers have been used for pocket ited accessibility such as deep defects and furcation ar-
debridement. Recent studies have shown that instrumen- eas. Nd:YAG and diode lasers are generally not used for
tation of the periodontal pocket wall tissues with a diode degranulation. CO2 lasers can be used for degranulation
laser leads to complete epithelial removal while instru- but cause carbonization of bone. Erbium lasers are most
mentation with conventional curettes may leave epithelial appropriate to be used for degranulation of bony defects
remnants. But based on clinical parameter of reduction as they do not have any harmful effect on bone. Further
of pocket depth or gain in clinical attachment level laser studies are required to establish additional benefits of
curettage has little to no benefit beyond scaling and root laser application in flap surgery.
planing (SRP) as either monotherapy or adjunctive to SRP. Low-level laser therapy application during and after
periodontal surgical and regenerative therapy has been
Reduction of Subgingival Bacterial Levels shown to enhance the gingival fibroblast and periodontal
The bactericidal and detoxifying effect of laser treatment ligament cell proliferation and release of growth factors
is advantageous in periodontal therapy. Diode laser and in vitro. Studies have also suggested that low-level laser
Nd:YAG laser are a good choice for pigmented bacteria. therapy (LLLT) can enhance new bone formation by pro-
Diode lasers are found to be effective in suppression of A. moting osteoblast proliferation.
actinomycetemcomitans in cases of aggressive periodontitis.
But still lasers as a group have been found to be unpredict- Osseous Surgery
able and inconsistent in their ability to reduce subgingival Erbium lasers can easily be used for osseous contour-
microbial loads beyond that achieved by SRP alone. ing during flap surgery and in crown lengthening cases.
Photodynamic therapy has been used to reduce micro- Some studies have refuted their use as they may have
bial load by free radicals produced during the therapy. lower cutting efficiency as compared with conventional
The evidence for benefit of use of diode laser in photo- instruments and lack of depth control may be a limitation.
dynamic therapy in reduction of microbial load as mono- There has been limited evidence to support the use
therapy or adjunct to SRP is conflicting. Only a few stud- of lasers over conventional therapy in treatment of peri-
ies have shown photodynamic therapy to be effective in odontal disease. Much of this uncertainty arises from not
reducing subgingival microbial load. making proper comparisons in terms of the type of lasers
utilized and the way that studies are designed.
Scaling and Root Planing
Nd:YAG lasers have deeper depth of penetration and Surgical Procedures in Implant Placement
carry the risk of intrapulpal temperature elevations during
laser irradiation on the root surface. They also cause sur- Erbium lasers can be used for implant site prepara-
face pitting, crater formation, and melting of root surface. tion, causing less damage than conventional bur drill-
The carbonization caused by CO2 laser inhibits the soft ing. Preparation time has also been found to be accept-
tissue attachment post-root planing. Thus, use of Nd:YAG able. Whether faster and superior osseointegration can
and CO2 lasers is not advisable for calculus removal. Diode be achieved using erbium lasers is yet to be established.
lasers are ineffective in removal of calculus. Lack of depth control might be a limitation which can
Nevertheless, erbium lasers have shown great poten- easily be overcome using advanced methods of imaging
tial for effective root debridement. In vitro studies have during implant procedures.
shown positive results in removal of calculus, reduction Diode and erbium lasers can undoubtedly be used
of endotoxin, and enhancement of fibroblast attachment. for second-stage implant exposure without causing any
But during in vivo removal of calculus by erbium laser, damage to underlying tissue and implant.
there is potential for root damage as the healthy hard tis-
sue may get lased along with calculus. With introduction
Treatment of Peri-Implantitis
of a new laser system combining diode laser-induced
fluorescence with erbium-doped YAG (Er:YAG), calculus Nd:YAG laser is contraindicated in treatment of peri-
removal might be possible without risk of damaging root implantitis as it may damage the titanium implant sur-
surface as the feedback system ensures the Er:YAG laser is face. CO2 lasers are also not used as they may carbon-
inactivated once the calculus is removed. Further studies ize the adjacent bone. Diode lasers can be used. Erbium
lasers are preferred for degranulation and implant surface • gallium-aluminum-arsenide diode lasers (630-690,
decontamination as they can be used for both hard and 830, or 906 nm); and
soft tissue ablation. • argon lasers (488-514 nm).
High-level-energy laser irradiation is not used to ac-
Treatment of Dentinal Hypersensitivity tivate the photoactive dye because relatively low-level
Nd:YAG, CO2, erbium, and diode lasers have been tried exposure produces a high bactericidal effect.
in treatment of dentinal hypersensitivity. All the lasers
are used at low-power settings. Nd:YAG laser irradiation Photosensitizer
causes melting and fusion of dentine and therefore the
closure of exposed dentinal tubules. CO2 lasers are used An ideal photosensitizer:
for treatment of dentinal hypersensitivity by sealing or 1. Should be nontoxic and should be activated on
narrowing of dentinal tubules. Erbium lasers also reduce illumination
dentinal hypersensitivity by sealing of dentinal tubules, 2. Should bind with bacteria and plaque without staining
at lower settings; they seem to reduce fluid movement in the gingiva and other soft tissues
dentin by evaporating the superficial layers of dentinal 3. Should be acceptable to patients
fluid. The diode laser relies on depressed nerve transmis- 4. Should have an access to pathogens present in deeper
sion changes within the dental pulp, rather than altera- periodontal pockets.
tions in the exposed dentine surface. The diode laser may
also stimulate the normal physiological cellular functions. The various photosensitizers used are as follows:
At subsequent appointments, it stimulates the production 1. Dyes:
of sclerotic dentin, thus promoting the internal oblitera- a. Tricyclic dyes with different meso-atoms - methylene
tion of dentinal tubules. Lasers when used along with blue, toluidine blue 0, and acridine orange
fluoride gel and varnishes may show better results. b. Phthalocyanines - aluminum disulfonated phthalo-
cyanine
Wound Healing c. Cationic Zn(II) - phthalocyanine
2. Chlorines: chlorine e6, stannous(IV) chlorine e6,
Decreased swelling, scarring, pain, and faster healing
chlorine e6-2.5 N-methyl-o-glucamine (BLC1010),
response have been suggested with use of lasers. But the
polylysine, and polyethyleneimine conjugates of
evidence regarding faster healing of wounds is conflict-
chlorine e6
ing. It is important to use the lasers with appropriate
3. Porphyrins: hematoporphyrin HCl, photofrin and
power settings to achieve better wound healing after sur-
5-aminolevulinic acid (ALA), benzoporphyrin deriva-
gical therapy. Low-level laser therapy using diode lasers
tive (BPD)
with wavelengths 635-810 nm at low-power, noncontact
4. Xanthenes: erythrosine
mode can be used to promote wound healing, suppress
5. Monoterpene: azulene.
inflammation, and stimulate cellular ATP.
PHOTODYNAMIC THERAPY
PHOTODYNAMIC ANTIMICROBIAL
Photodynamic therapy (PDT) is defined as the eradi- THERAPY
cation of target cells by reactive oxygen species that are
produced by means of a photosensitizing compound, and It is based on the principle that a photosensitizer binds
light of an appropriate wavelength. to the target cells and can get activated by light of a suit-
Photodynamic therapy basically involves three non- able wavelength. Following this, singlet oxygen and other
toxic ingredients: very reactive agents are produced which are extremely
toxic to certain cells and bacteria.
• Visible harmless light Two pathways explain the mechanism of action of an-
• A nontoxic photosensitizer timicrobial photodynamic therapy. After irradiation with
• Oxygen. light of a specific wavelength (lasers), the photosensitizer
at ground state is activated to a highly energized triplet
Light state (Fig. 54.7). This triplet state has a longer lifetime
and this enables the photosensitizer to interact with the
Light sources of a specific wavelength are used and
surrounding molecules and generate cytotoxic species.
are mostly:
The triplet-state photosensitizer follows two different
• helium-neon lasers (633 nm); pathways (types I and II) to react with biomolecules.
Ground state sensitizer
Light
l
I Moleo,lac 0><ygeo V
Highly energized triplet-state photosensitizer
I Organic substrate I
Pathway II Pathway I
Reactive oxygen Radical ions (free radicals)
(singlet oxygen)
l I Molecular oxygen
Reactive oxygen species
FIGURE 54. 7 Mechanism of action of photodynamic therapy.
Type I reactions involve hydrogen-atom abstraction ing an intensive light by a special tip applied in the pocket
or electron-transfer reactions between the excited state of (Fig. 54.9). Because of technical simplicity of the method
the photosensitizer and an organic substrate molecule of and the high effectiveness of bacterial killing, the ap-
the cells, which produces free radicals and radical ions. plication of antimicrobial photodynamic therapy in the
These free radical species are generally highly reactive treatment of periodontal and peri-implant diseases has
and interact with endogenous molecular oxygen to pro- been often advocated.
duce highly reactive oxygen species such as superoxide,
hydroxyl radicals, and hydrogen peroxide, which are
harmful to cell membrane integrity, causing irreparable
Advantages
biological damage. 1. Noninvasive
In the type II reaction, the triplet-state photosensitizer 2. Thorough elimination of pathogens in inaccessible
reacts with oxygen to produce an electronically excited areas in short span of time
and highly reactive state of oxygen, known as singlet 3. No anesthesia required
oxygen, which can interact with a large number of bio- 4. Avoids risk of bacteremia.
logical substrates as a result of its high chemical reactivity,
inducing oxidative damage and ultimately lethal effects
on the bacterial cell by damaging the cell membrane and
cell wall.
Singlet oxygen has a short lifetime in biological systems
( <0.04 µs) and a very short radius of action (0.02 µm);
hence, the reaction takes place within a limited space,
leading to a localized response. The process of antimi-
crobial photodynamic therapy is generally mediated by
a type II reaction, which is accepted as the major pathway
in microbial cell damage.
Applications
1. In nonsurgical treatment of aggressive periodontitis
2. As an adjunct to nonsurgical periodontal treatment
3. In destruction of periodontopathogenic bacteria.
The photosensitizer is applied at the diseased site using
a syringe (Fig. 54.8). Photosensitization is performed us- FIGURE 54.8 Application of the dye using a syringe.
Depigmentation (Fig. 54.lSA-C)

Crown lengthening (Fig. 54.16A and B).
MICROSURGERY
Microsurgery is defined as surgery performed under a

microscope using a magnification of lOx or more.
First reports on microsurgery go back to the nineteenth
century when a microscope was developed for use in oph-
thalmology. Carl Nylen, who is considered the father of
microsurgery, first used the binocular microscope for ear
surgery. However, its use gained acceptance in medicine
in the 1960s. Apotheker and Jako in 1978 introduced the
microscope to dentistry. Shanelec and Tibbetts in 1993
FIGURE 54.9 Photosensitization with laser light. presented a continuing education course on periodon-
tal microsurgery at the annual meeting of the American
Academy of Periodontology.
Adverse Effects
Concepts in Microsurgery
1. Phototoxic, photoallergic side effects
2. Overgrowth of single resistant species Three elements, i.e., magnification, illumination, and
3. Pain or burning sensation. instruments, are called the microsurgical triad, the im-
provement of which is a prerequisite for improved accu-
racy in surgical interventions. Without any one of these,
CLINICAL CASES DONE USING 810 NM microsurgery is not possible.
DIODE LASER (PICASSO, AMD LASERS®)
IN DEPARTMENT OF PERIODONTOLOGY,
MCODS, MANGALORE, MANIPAL Magnification
UNIVERSITY Vision is a complex process that involves the coopera-
tion of multiple links between the eye, the retina, the optic
Frenectomy (Fig. 54.lOA and B) nerve, and the brain. An important element to assess in
Lingual frenectomy (Fig. 54.llA and B) human eyesight is visual acuity. It is the ability to perceive
Gingivoplasty (Fig. 54.12A and B) two objects separately. It is influenced by anatomic and
Operculectomy (Fig. 54.13A and B) physiological factors. Lighting is another important factor
Gingival polyp excision (Fig. 54.14A and B) influencing visual acuity.
FIGURE 54.10 (A) Preoperative; (B) immediate postoperative.


(B)
FIGURE 54.15 (A) Preoperative; (B) immediate postoperative; (C) 1 week postoperative.
Visualization of fine details is enhanced by increasing optical axis. With coaxial lighting, no shadows are pro-
the image size of the object. It is done in two ways: by duced. The surgeon can view perfectly the deepest reach-
getting closer to the object and by using magnification. es of the oral cavity, including into subgingival pockets
and angular bony defects. Definitive visualization of
Optical Principles of Loupes root surface deposits and irregularities is possible only
In dentistry two basic types of magnification systems at magnification and resolution provided by a surgical
are used: the surgical microscope and loupes. The latter microscope. Using the microscope, surgeons can view
can be classified as single-lens magnifiers and multilens periodontal anatomy that previously could not be seen.
telescopic loupes. Clinical decisions can be made based on certain knowl-
Single-lens magnifiers produce the required diopter edge of pathologic anatomy rather than decisions based
magnification that simply adjusts the working distance on blind, educated guesses.
to a set length. As diopter increases, the working distance
decreases. With a set working distance, there is no range
and no opportunity for movement; this can create diffi- Microsurgical Instruments
culty in maintaining focus and, therefore, may cause neck Proper instrumentation is fundamental for microsurgi-
and back strain from poor posture. Single-lens magnifiers cal intervention.
also give a poor image quality, which restricts the quality The instruments should be approximately 18 cm long;
of work. These types of glasses cannot be considered to they should be slightly top-heavy to facilitate accurate
be a true means of magnification. handling. In order to avoid an unfavorable metallic glare
Telescopic loupes (compound/prism) offer improved under the light of the microscope, the instruments often
ergonomic posture as well as significant advancements in have a colored coating surface. The weight of each instru-
optical performance. Instead of increasing the thickness of ment should not exceed 15-20 g (0.15-0.20 N).
a single lens to increase magnification, compound loupes Appropriate sets of steel or titanium instruments for
use multiple lenses with intervening air spaces. These periodontal surgery are available from different manu-
allow an adjustment of magnification, working distance, facturers.
and depth of field without an excessive increase in size/ Periodontal procedures, be they resective, regenerative,
weight. or periodontal plastic procedures and implants, all de-
Prism loupes are the most optically advanced type mand intricate surgical skills. The use of magnification in
of loupe magnification available. They are actually low- periodontology leads to a less invasive surgical approach.
power telescopes. They contain Feehan or Schmidt prisms
that lengthen the light path through a series of mirror
reflections within the loupes. Prism loupes produce bet- Application of Microsurgery for Periodontal
ter magnification, larger fields of view, wider depths of Procedures
field, and longer working distances than the other loupes.
• Root preparation: Magnification has shown to improve
Optical Principles and Components of a Surgical the visual access to root surface, thereby increasing the
Microscope ability to obtain a clean and smooth root surface.
The surgical microscope is a complicated system of • Regenerative therapy: Use of magnification in regen-
lenses that allows stereoscopic vision at a magnification of erative periodontal procedures helps to obtain and
4-40x with an excellent illumination of the working area. maintain primary closure of the tissues over the barrier
In contrast to loupes, the light beam falls parallel onto membrane.
the retinas of the observer so that no eye convergence is • Periodontal plastic surgery: Microsurgical closure of
necessary and the demand on the lateral rectus muscles the palatal donor site allows healing by primary in-
is minimal. tention without painful period of open granulation,
thereby reducing postoperative pain.
Illumination
Illumination of the microsurgical field is an important
Advantages of Microsurgery
consideration. Periodontists are accustomed to lateral • Enhanced surgical decision making
illumination from side-mounted dental lights. Clinicians • Enhanced motor skills as the instruments are designed
who work with loupes often require a headlamp to com- for precision grip of hand
pensate for the decreased illumination of dental loupes. • Decreased need for vertical incisions
Fiber-optic coaxial illumination is a major advantage of • Reduced incision size
the operating microscope over surgical loupes. Coaxial • Decreased postoperative pain
lighting focuses the light parallel to the microscope's • Rapid healing.
CONCLUSION important adjunct in treatment of periodontal disease and

will soon become an integral part of periodontal therapy
Lasers are widely and successfully being used for soft in times to come.
tissue surgical procedures. But valid evidences through Periodontal microsurgery is still in its infancy. It is a
standardized randomized controlled trials are still re- skill that requires practice for proficiency. It is technique
quired to establish the use of lasers in periodontal ther- sensitive and is beneficial in various periodontal proce-
apy over traditional methods. At present, lasers are an dures.
KEY POINTS
• Laser light is monochromatic, collimated, and coherent • Soft tissue lasers are being widely used as a tool for
and has concentrated energy. gingival soft tissue procedures, i.e., gingivoplasty, gin-
• The laser energy is absorbed by the target tissue depend- givectomy, frenectomy, gingival depigmentation, sec-
ing on the contents of the tissue. It is the usual desirable ond-stage exposure of implant, and soft tissue crown
effect and forms the basis for use of lasers for various lengthening.
purposes. • Microsurgery is defined as surgery performed under a
• Argon, diode, Nd:YAG, and carbon dioxide are soft tis- microscope using a magnification of lOX or more.
sue lasers and erbium lasers are all tissue lasers. • Microsurgical triad includes magnification, illumination,
• Advantages of using lasers for periodontal therapy are and instruments.
precise surgical cutting, less need for anesthesia, better • Improved healing, decreased postoperative pain,
visualization of cutting due to hemostasis and coagula- and decreased vertical incisions are advantages of
tion, and detoxification of a wound. microsurgery.
QUESTIONS 2. Academy of Laser Dentistry. An Overview of Lasers in Dentistry. Coral

Springs, FL: Academy of Laser Dentistry; 2008.
3. Goldstep F. Diode lasers for periodontal treatment: the story so far.
1. Describe use of lasers for periodontal procedures. Oral Health. 2009; 44-46.
2. Describe photodynamic therapy for treatment of 4. American Academy of Periodontology statement on the efficacy of
periodontal disease. lasers in the non-surgical treatment of inflammatory periodontal
3. Describe use of microsurgery for periodontal disease. J Periodontal. 2011;82: 513-514.
procedures.
Suggested readings
1. Convissar RA. Principles and Practice of Laser Dentistry. Mosby:
Elsevier; 2010.
CHAPTER
55
Periodontal Considerations
in Restorative Dentistry
CHAPTER OVERVIEW
Prior to any restorative procedure the dental surgeon ensures that the restorative managements are easier and
should carry out a routine periodontal treatment in- long lasting. A good periodontal maintenance program
cluding professional plaque control and instructions on always improves the prognosis and the life span of
home care by the patient. A healthy periodontal status restorations.
RESTORATION MARGINS complex and thus help the patients in maintaining the
oral hygiene.
Biologic Width
Crown Lengthening and Biologic Width
The concept was first put forward by Ingber et al, who Crown lengthening or exposing the coronal tooth
defined it as "the minimal width at the gingival sulcus structure is a valuable adjunctive procedure in restor-
required to maintain a normal gingival attachment" ative dentistry that may be indicated for a number of
(Fig. 55.1). reasons. Encroachment on the biologic width by the
The dimensional relationship between the crest of the tooth preparation, caries, tooth fracture, restorative ma-
alveolar bone, the length of the epithelium attachment, terials, or orthodontic devices can lead to bacterial ac-
and the sulcus depth is consistent. The dimension of the cumulation and inflammation, increased probing depths,
healthy sulcus depth averaged 0.69 mm, the epithelium gingival recession, or a combination of all these. To avoid
attachment 0.97 mm, and the connective tissue 1.07 mm encroachment on the biologic width, the restorative den-
(Fig. 55.2). tist should measure the probing pocket depth before
Any attempts to place restorations with subgingival preparing teeth.
margins that impinge and encroach on connective tissue In healthy sulci, normally margins can be placed
and epithelial attachment will result in gingival inflam- 0.5 mm into the sulcus. In areas of insufficient tooth struc-
mation and periodontal reactions. ture, to allow adequate soft tissue attachment, crown
• Periodontium will react by crestal bone resorption and lengthening may be necessary. The crown lengthening
apical migration of dentogingival complex to reestab- can be accomplished by surgery or by orthodontic ex-
lish the inherent biologic width. trusion.
• Violating the biologic width by placing subgingival Another indication for crown lengthening is in situa-
margin causes physical trauma; subgingivally placed tions of short clinical crowns. Additional tooth structure
restorations act as plaque traps. has to be removed to provide adequate retention for fixed
• Subgingivally placed and poorly contoured restora- restorations.
tions impinge on the sulcular space, causing hyper- If there is less than 2 mm of sound tooth structure be-
plasia of the gingiva surrounding it. yond post and core, crown lengthening is indicated.
Crown lengthening may also be done for aesthetic
Keeping the margins of the restorations up to 0.5 mm reasons in cases of so-called gummy smile or excessive
into the sulcus will keep it away from attachment display of gingival tissue. Where excessive suprabony
FIGURE 55.1 Inflammation of the periodontal tissues resulting from

a restoration that impinges on the biologic width.
FIGURE 55.3 (A) Violation of the biologic width; restoration margins

on tooth number 11 was placed subgingivally in close proximity to the
alveolar bone. Notice the inflammatory changes on the marginal gingiva
in respect to 11. (B) In a patient with thin periodontium, it is often wise
to select supragingival margin placement.
restorations near the crest of the gingiva interfered with

FIGURE 55.2 Line drawing of the biologic width. JE is the junctional
epithelium and CT the connective tissue attachment to the root surface. gingival health; subgingivally placed margins had the
The combined width of these is approximately 2 mm. Sis the gingival most harmful effects on the gingiva (Fig. 55.3A).
sulcus and B is the alveolar bone. Increased gingival inflammation can be attributed to
one or more of the following factors:
• Roughness at the tooth/margin interface
gingival tissue is present (more than 3 mm), gingivoplasty
• Surface finish of the restorative materials
of up to 1.5 mm can be performed.
• Contour of the cervical crown.
As attachment is progressively lost and gingiva starts

Location and Preparation of Restorative
receding, a large percentage of subgingival margins be-
Margins
come supragingival after 5 years (Fig. 55.3B). The closer
The restoration margins can be located supragingivally, the subgingival margin is to the base of the sulcus, the
at the crest of the gingiva, or subgingivally. When margins more severe is the inflammation.
are placed subgingivally, difficulties in impression mak- If a subgingival margin is unavoidable (situations such
ing and finishing the restorations often result in marginal as subgingival caries, tooth fracture, presence of old fill-
discrepancies and the presence of cement margins. This ings, and aesthetics), it should be placed not more than
is a source of bacterial infection and gingival irritation 0.5 mm into the sulcus.
(Fig. 55.1). When even this is not possible, the crown should be
Silness found that restorations with supragingival lengthened without compromising the tooth support and
margins gave the most favorable gingival response; exposing furcation.
CHAPTER 55 PERIODONTAL CONSIDERATIONS IN RESTORATIVE DENTISTRY 501
Marginal Fit Fit and Quality of Restorations

It has been proved that the gingival inflammation is Fit and quality of the margins of restorations of both
directly related to the level of marginal opening. Margins provisional and final are important determinants of peri-
that are significantly open (several tenths of a millimeter) odontal health. Several clinical studies have confirmed
are capable of causing bacterial accumulation and inflam- that defective margins are directly related to severity of
matory response. periodontal diseases.
Gingival Retraction and Impression Making Insertion and Cementation of Restorations

Physical retraction: This procedure uses untreated cords. When cementing restorations, excess cement at the
Placement and removal of dry cords will damage the margins should be completely removed, especially when
gingival sulcular epithelium. it is subgingivally placed. If the margins are placed su-
Chemically treated cords: It is the most acceptable method pragingivally, it is easy to eliminate the excess cement at
to achieve effective gingival retraction without induc- the margin.
ing irreversible damage to gingival tissues (Fig. 55.4).
These include 100% alum, 0.03% aluminum chloride,
and 8% racemic adrenaline. However, care should be RESTORATION CONTOURS
taken, as adrenaline has possible cardiovascular side
effects. Theories of Crown Contouring
Surgical: The "gingitage technique" involves simultane- The crown contours help in establishing a favorable
ously preparing the tooth and cutting the inner lining periodontal environment. Three prominent theories of
of gingival sulcus using a specialized rotary diamond crown contour have evolved:
instrument.
Electrosurgery: This method uses high-frequency elec- 1. Gingival protection theory (proposed by Wheeler):
trical energy to expose the preparation margins and Contours of cast restorations are designed to protect
obtain a bloodless gingival cuff to obtain good impres- marginal gingiva from mechanical injury. It protects
sion. and stimulates the gingiva and produces self-cleansing
contours.
Advantages: 2. Muscle action theory: It states that crown contour
• Easy retraction of multiple abutments must facilitate cleansing actions by the tongue,
• Clear vision of finishing line cheek, and lips. Overcontoured restorations
• Increased bulk of impression material at margins prevent normal cleansing actions of the musculature.
• Reduced operative time for patient and dentists 3. Theory of access for oral hygiene: This is based on
• Good hemostasis the concept that plaque is primary etiological factor
• Predictable tissue healing. for periodontal disease and crown contours should
facilitate plaque removal and not its accumulation.
Disadvantages:
• Unpleasant odor and taste
Buccal and Lingual Contours
• Risk of serious tissue damage
• High cost of equipment Ideally the final restoration should exhibit a straight
• Low tactile sense by inexperienced hands. or concave emergence profile, which is tooth profile
FIGURE 55.4 The periodontium is readily displaced vertically by a gingival retraction cord in relation to 11, 21.
to checking eccentric relations. Occlusal relations in inter-

cuspal and functional positions should be checked when
the teeth are prepared to ensure sufficient thickness of
restorative material.
Occlusion and Periodontal Disease

It is now generally agreed that occlusal trauma alone
will not cause or initiate periodontal disease. Loss of
periodontal support from plaque-associated periodon-
tal disease, traumatic occlusion, or combination of both
may result in tooth mobility. Osseous mineralization was
found to be slightly greater when both traumatic forces
and inflammation were resolved.
FIGURE 55.5 Provisional prosthesis should be fabricated with
the proper contour and emergence profile, both interproximally and RESTORATIVE MATERIALS
labiopalatally, to allow the patient access to all areas to maintain peri-
odontal health.
Accumulation of plaque on different materials used in
the restorative dentistry varies according to the surface
roughness. All materials used in proximity to gingival
emerging from gingival sulcus. If this profile is incor- margin should therefore be as smooth as possible.
rectly reproduced, all other contours will be incorrect Glazed porcelain, polished gold, and well-polished
(Fig. 55.5). heat-cured acrylic make better materials when compared
with composite and amalgam as restorative materials.
Contact Area and Embrasure Space
Both occlusal/ gingival and facial/lingual contact ar-
PROVISIONAL RESTORATIONS
eas should be large enough to allow for normal gingival
While providing the provisional restorations the mar-
papilla and should not impinge on col.
ginal fit, contour, and surface finish of these restorations
Ramfjord recommends placement of contact areas as
must be checked to maintain the health and position of
far occlusally as possible to facilitate access for intraproxi-
the gingiva till the time the final restorations are made
mal plaque control.
(Fig. 55.5). Poor provisional restorations with unfavorable
Since a minimal thickness of material is required for
contours, margins, and surface can cause inflammation,
aesthetics and structural durability, sufficient tooth tissue
enlargement, or recession of gingiva. These changes in
should be removed during crown preparation to allow
the tissue architecture can even compromise the success
proper crown buildup.
of the final restoration.
Furcation Involvement
PONTIC DESIGN
Restorations on tooth with furcation exposed by peri-
odontal disease should be fluted to eliminate plaque traps Different types of pantie designs are used while re-
and also favor plaque control. placing the missing teeth with the help of fixed partial
dentures. They can be:
• Sanitary type
OCCLUSAL CONSIDERATIONS • Bullet shaped
• Ridge lap
Occlusal Surface • Modified ridge lap
In an ideal situation, contact on occlusal surface should Sanitary type offers maximum space between the un-
produce a force along the long axis of the tooth. There dersurface of the pantie and edentulous ridge, whereas
should be minimal horizontal component of resultant the ridge lap type is the closest to the soft tissue.
force. Vertical forces are always damaging the tooth. Res- Nearly all authors agree that inflammation of the eden-
torations should be constructed with satisfactory centric tulous mucosa adjacent to panties is probably a response
jaw movements in function or parafunction in addition to plaque accumulation on the surface of panties.
CHAPTER 55 PERIODONTAL CONSIDERATIONS IN RESTORATIVE DENTISTRY 503
Many authors felt that glazed porcelain is the material
of choice for contact against the edentulous ridge, but
some others felt that there is no such change between the
glazed or unglazed porcelain, cast gold, and acrylic. Thus,
they concluded that it is the design of the pontic rather
than the material used in the pontic which is important
in preventing the inflammatory reactions.
Stein's classic article on pontic design changed the phi-
losophy from "sanitary" design to "modified ridge lap,"
which is commonly used nowadays (Figs 55.6-55.8). The
ridge lap design in the anterior and modified ridge lap
in the posterior offer minimal tissue contact, acceptable
cosmetic value, proper tissue support, and acceptability
for oral hygiene.
In addition to the undersurface of pontic, it is impera- FIGURE 55. 7 Saddle or ridge lap pontic.
tive to open the embrasure spaces adjacent to the abut-
ments to allow room for interproximal tissue and access
for oral hygiene procedures.
The occlusal surface should not be narrowed, as it fa-
vors food impaction and/ or plaque retention, like in a
malpositioned tooth.
The embrasure space between two panties is usually
closed to provide added strength, reduce food and plaque
retention, and facilitate oral hygiene procedures under
the pontic.
FIGURE 55.8 Modified ridge lap pontic.
CONCLUSION
Failure to recognize the importance of relationship

between restorative dentistry and periodontal health,
which is often neglected by dental practitioners, can
lead to poor long-term prognosis of final restorations,
clinical problems, and tooth loss. Meticulous plaque
control is a very essential part in continuing good health
of the teeth and periodontium following restorative
FIGURE 55.6 Sanitary or hygienic pontic. procedures.
KEY POINTS
• If there is less than 2 mm of sound tooth structure be- • Surface finish of the restorative materials
yond post or core, crown lengthening is indicated. • Contour of the cervical crown.
• Glazed porcelain, polished gold, and well-polished heat- • If a subgingival margin is unavoidable, it should be
cured acrylic make better materials when compared with placed not more than 0.5 mm into the sulcus.
composite and amalgam as restorative materials. • The" gingitage" technique involves simultaneously prepar-
• Increased gingival inflammation can be attributed to one ing the tooth and cutting the inner lining of gingival sulcus
or more of the following factors: using a specialized rotary diamond instrument.
Roughness at the tooth/margin interface
QUESTIONS 7. Morris M. Artificial crown contours and gingival health. J Prosthet

Dent 1962;12:1146-56.
8. Newcomb GM. The relationship between the location of the sub-
1. What is the importance of biologic width in restora- gingival crown margins and gingival inflammation. J Periodontal
tions? 1974;45:151-4.
2. Describe location and preparation of gingival margins. 9. Ramfjord SP. Periodontal aspects of restorative dentistry. J Oral
Rehabil 1974;1:1007-126.
10. Schluger S, Youdelis RA, Page RC. Periodontal Disease. Philadelphia:
Suggested readings Lea and Febiger; 1977 586-617.
11. Silness J. Periodontal conditions in patients treated with dental
1. Behrend DA. The mandibular fixed partial denture. J Prosthet Dent bridges III: the relationship between the location of crown margins
1977;37:622. and the periodontal conditions. J Peridontal Res 1970;5:225-9.
2. Block PL. Restorative margins and periodontal health: a new look 12. Stein RS. Pontic-residual ridge interrelationship: a research report.
at old perspective. J Prosthet Dent 1987;57:683-9. J Prosthet Dent 1966;16:251.
3. Ericsson I, Lindhe J. The effect of long standing jiggling on experi- 13. Tupac RG, Neacy K. A comparison of cord gingival displacement
mental marginal periodontitis in the beagle dog. J Clin Periodontal with the gingitage technique. J Prosthet Dent 1981;46:509-15.
1982;9:497-503. 14. Tylman SD. Theory and Practice of Crown and Bridge Prosthodontics.
4. Goldberg PV, Higginbottom FL, Wilson Jr TG. Periodontal con- 5th ed. St. Louis: Mosby; 1965 822-865.
siderations in restorative and implant therapy. Periodontal 2000. 15. Wheeler RC. Complete crown form and the periodontium. J Prosthet
2001;25:100-9. Dent 1961;11:722-34.
5. Jenkins WMM. Periodontal aspects of restorative dentistry. Part 1. 16. Yap UJ, Ong G. Periodontal considerations in restorative dentistry.
Dent Update 1981;8:489-94. 1: operative considerations. Dent Update 1994;12:413-8.
6. Lang NP, Robert A, Kiel RA, Anderhalden K. Clinical and micro- 17. Yuodelis RA, Faucher R. Provisional restorations: an integrated
biological effects of subgingival restorations with overhanging or approach to periodontics and restorative dentistry. Dent Clin North
clinically perfect margins. J Clin Periodontol 1983;10:563-78. Am 1980;24:285.
CHAPTER
56
Ortho- Perio Interrelationships
CHAPTER OVERVIEW
In recent years there has been a dramatic increase in do not exist with the younger patients. These problems
the number of adults seeking orthodontic treatment. Treat- are related to periodontal breakdown and mucogingival
ment of adults brings with it a set of problems that simply problems.
ORTHODONTIC TREATMENT of a normally supported one. The absolute magnitude

CONSIDERATIONS of the force used to move teeth must be reduced when
periodontal ligament support has been lost, to prevent
The key element in the orthodontic management of damage to the PDL, bone, cementum, and root. In ad-
adult patients with periodontal problems is to eliminate dition, the greater the loss of attachment, the smaller
or reduce plaque accumulation and gingival inflamma- the area of supported root and the further apical the
tion. This implies much emphasis on oral hygiene in- center of resistance will become. Tooth movement is
structions, appliance construction, and periodic checkups quite possible despite bone loss, but lighter forces and
throughout treatment. The orthodontic appliance design relatively larger counterbalancing moments are required
must be simple, without causing tissue irritation, and (Fig. 56.1).
must be aesthetically acceptable. To counteract the ten-
dency of orthodontic appliances to increase the accumu-
lation of plaque on the teeth, attempts should be made
TIMING AND SEQUENCE
to keep the appliances simple. Orthodontic attachments
OF TREATMENT
such as hooks, elastomeric rings, and excess bonding
resin outside the bracket bases should be avoided. The
Periodontal disease must be brought under control
use of steel ligatures is recommended on all brackets,
before any orthodontic treatment is initiated because
since elastomeric rings have been shown to be signifi-
orthodontic tooth movement superimposed on poorly
cantly more plaque attractive than steel ligatures. Bonded
controlled periodontal health can lead to rapid and irre-
teeth are preferable to bands as they show less plaque
versible breakdown of the periodontal support apparatus.
accumulation.
• A period of 6 months is required to allow healing and
resolution of inflammation before tooth movement
BIOMECHANICAL CONSIDERATIONS begins.
• Scaling, curettage, and gingival grafts should be un-
Since patients who need adjunctive orthodontic treat- dertaken as appropriate before any tooth movement
ment often have periodontal problems, the amount of is done.
bone support of each tooth should be an important • Surgical pocket elimination and osseous surgery
consideration. When bone has been lost, the periodon- should be delayed until completion of orthodon-
tal ligament (PDL) area decreases and the same force tic phase of treatment because a significant amount
against the crown produces greater pressure in the PDL of soft tissue and bone recontouring occurs during
of a periodontally compromised tooth than in the PDL treatment.
orthodontic tooth movement must be avoided at all costs

in patients with active periodontal disease and must be
done only after the disease is eliminated.
Tooth Movement into Sites of Deficient Bone

Movement of teeth into areas of reduced bone has been
suggested to result in the healing and regeneration of the
infrabony pocket. However, studies show that if teeth are
moved into an infrabony pocket, then no new attachment
is created; instead a long junctional epithelium is created.
Also loss of attachment might result when tooth is moved
into an area with a bony defect (Fig. 56.2).
FIGURE 56.1 The center of resistance of a tooth shifts apically due Orthodontic Intrusion
to bone loss.
Orthodontic intrusion can be done to improve the
crown-root ratio of a tooth. The intrusion however might
ADJUNCTIVE ORTHODONTICS also result in transfer of supragingival pathogens sub-
gingivally resulting in periodontitis. Intrusion in healthy
Adjunctive orthodontic treatment is tooth movement periodontium might also result in increase in attachment
carried out to facilitate other dental procedures necessary after flap operations to eliminate pocket epithelium.
to control disease and restore function. It involves only a The leveling of occlusal plane to treat deep overbite
part of the dentition, and the main goal usually is to make might result in deepening of infrabony pockets. Intrusion
it easier or more effective to replace missing or damaged has been reported to alter cementoenamel junction and
teeth. Typically appliances are required in only a portion angular crest relationships and result in only epithelial
of the dental arch and for only a short time. Adjunctive attachment. Therefore, a periodontally susceptible patient
treatment implies limited orthodontic goals, improving is at risk of future breakdown (Fig. 56.3).
a particular aspect of the occlusion rather than compre-
hensively altering it.
Management of Traumatic Occlusion
Occlusal trauma plays a role in enhancing bone loss
Tooth Movement in Patients with Active
especially in case of deep overbite and also might delay
Periodontitis
healing following periodontal surgery. The anterior teeth
Orthodontics can be a useful adjunct for enhancing are traumatized in all excursive movements. Bite planes
periodontal health. However, when teeth are moved in have been used to correct traumatic occlusion by depres-
the presence of periodontitis, the resorption of bone is sion of anterior teeth and posterior supraeruption.
enhanced and bone formation is inhibited. This is because The clinical diagnosis of occlusal trauma is by the pres-
preosteoclasts are attracted to the site by cytokine me- ence of tooth mobility and the radiographic appearance of
diators; osteoblast histogenesis is suppressed. Therefore, widened periodontal ligament spaces and a loss of lamina
FIGURE 56.2 Movement of a tooth into a bony defect.

CHAPTER 56 ORTHO-PERIO INTERRELATIONSHIPS 507
FIGURE 56.3 Incisor intrusion in a periodontally compromised

patient.
dura. Occlusal adjustment by selective grinding may also

help in cases with occlusal trauma (Fig. 56.4).
Forced Eruption
This term applies to procedures which involve orth-
odontic movement with gentle forces. The purpose of
the forced eruption procedure is the coronal shift of the
bone at the base of infrabony defects, thus reducing the
depth of the defect. The elongated tooth thereafter can
be reduced in height by grinding and elimination of the
infrabony defect.
Forced eruption can also be done to manage teeth
which have fractured to make possible the restoration of
the tooth which would otherwise be difficult to restore FIGURE 56.5 Various methods of forced eruption.
when the fracture margin extends subgingivally. The
extension of the crown margin too subgingivally would
result in the invasion of the biologic width. The eruption of the tooth would result in more tooth material available
for crown preparation and thus sufficient biologic width
is available for crown preparation.
The root must be long enough so that a one-to-one
crown-root ratio will be preserved after the root has been
erupted. If the crown-root ratio is less than this amount,
there may be too little root remaining in the bone for sta-
bility. In the latter situation, it may be prudent to extract
the root and place a bridge or implant.
To erupt the tooth either the adjacent teeth must be
bracketed and a wire must be placed or a wire must be
bonded directly to the adjacent teeth and an elastic trac-
tion must be applied from the wire to the tooth. If a root
is being erupted for restoration, then there must be a post
in the root canal for attachment of the elastic traction
(Figs 56.5 and 56.6).
Molar Uprighting and Furcation Involvement

FIGURE 56.4 An anterior bite plane to relieve the occlusion of Molars which have tipped into adjacent extraction
interferences. space cause periodontal problems as they form areas
C:
u :I: u
( ) M ·e
E §
.s 0j C:
0)
~ ti §
:I: wj -
~ (0
0 C:
:I:
~ ~§
(.)
~
:E
<3
\r
0
0 e
0
e 0
·.esu e WI
V e ·eu
13
·c .s (1)
C:
(1)
~C: u <(
C:
<( u
Preoperative C/R = 10/6 Postoperative C/R = 6/6
FIGURE 56.6 The shallowing of a bony defect by forced eruption
followed by crown reduction to get a good crown-root ratio.
which are difficult to maintain since pseudopockets result

from the distortion of interproximal gingiva. The mesial
tipping of the teeth also results in them being unsuitable
for later use as abutments for restorations.
The uprighting of the teeth can be done by two meth-
ods: distal crown movement of the crown or mesial move-
ment of the root. Both present with unique advantages and
disadvantages. The distal crown movement will result in
the opening of space where a pontic has to be placed which FIGURE 56. 7 The uprighting of a mesially tipped molar using a
will not be seen in the case of mesial root movement. Dis- Tloop.
tal crown movement will usually be accompanied by the
eruption of the crown due to reactive forces. It is usually
desirable if there is an infrabony defect present on the me- tally into adjacent old extraction sites and implants can
sial aspect of the crown since it will result in the occlusal be placed into the bone in the space they have vacated.
migration of the base of the bony pocket resulting in the Also if the space for the implant has been reduced by
shallowing of the defect. Mesial root movement has the migration of the adjacent teeth, space can be regained by
advantage of closing the edentulous space and eliminates orthodontic means.
the need for a prosthetic replacement. But mesial root
movement is possible only if there is sufficient bone to al- Reduction of Gingival Recession by Orthodontic
low root movement; in the absence of adequate ridge there Tooth Movement
might be dehiscence when the root is moved mesially.
Following uprighting the teeth an intracoronal retainer Labial tooth movement in cases where the labial bone
must be cemented to maintain the space gained (Fig. 56.7). cortex is thin and is accompanied by a thin gingiva might
When molar uprighting is done, one must try and result in gingival recession. Gingival recession accompa-
avoid inadvertent extrusion of the tooth if there is furca- nied by thin labial cortex and bony dehiscences can be im-
tion involvement. This will further exacerbate the furcation proved by lingual movement of the teeth. The thickness of
involvement. If the tooth to be uprighted has a furcation the bone as well as the gingival covering will be improved
involvement, then periodontal therapy is essential. as the tooth is moved into the alveolar bone (Fig. 56.8).
Adjunctive Orthodontics for Implant Placement Elimination of Dark Triangles in the lnterdental
Regions
Orthodontic treatment prior to placement of an im-
plant can result in better prognosis for the implant. The The unsightly dark triangles between two teeth might
orthodontic procedures that are done include the vertical be due to a variety of reasons. They could be due to de-
eruption of hopeless tooth to improve the bone level for struction of the interdental septum due to pathology
implant placement. Also teeth can be moved horizon- or might be the result of tooth morphology where the
FIGURE 56.8 Labial movement of incisors when the labial gingiva is thin might result in gingival recession.
contacts are unusually coronally placed. They could be or teeth may be another important factor in the aesthetic
due to excessive divergence of roots of the two teeth. appearance of the crowns. When adult patients have
The solutions are dictated by the etiology. If periodon- gingival margin discrepancies between adjacent teeth,
tal destruction has resulted in papilla loss, then regenera- the orthodontist must determine the proper solution
tive therapy can be done to improve the papilla position for the problem: orthodontic movement to reposition
or more commonly interproximal reduction of enamel can the gingival margin or surgical correction (gingivec-
be done and the teeth can be moved close together and tomy) to increase the crown length of single or several
the dark triangle reduced. If the tooth morphology is to teeth.
blame, then the tooth morphology must be altered with
composite buildup and the dark triangles eliminated. If
the root divergence is more, then the roots must be ap- ORTHODONTIC STABILITY
proximated to eliminate the triangles. CONSIDERATIONS IN PERIODONTALLY
COMPROMISED PATIENTS
Management of Teeth with Significant Abrasion
According to Proffit, two major primary factors are
Excessive grinding of teeth will result in wear of the involved in the equilibrium which determines the final
crowns. Restorations of the crowns are difficult due to position of teeth. These are the resting pressures of lip
insufficient crown structure for preparation. One option or cheek and tongue, and forces produced by metabolic
is extensive crown lengthening by elevating a flap, reactivity within the periodontal membrane. With an intact
moving sufficient bone, and apically positioning the flap periodontium, unbalanced tongue-lip forces are normally
to expose adequate tooth length for crown preparation. counteracted by forces from the periodontal membrane.
However, this type of procedure is contraindicated in However, when the periodontium breaks down, its sta-
the patient with short, tapered roots because it could ad- bilizing function no longer exists and the teeth begin to
versely affect the final root-to-crown ratio and potentially move.
open gingival embrasures between the anterior teeth. Hence, due to these biologic differences in tissue reac-
Orthodontic intrusion of the anterior teeth is the other tions between adults and children, adults undergoing
option to create restorative space for crown buildup. extensive orthodontic treatment will generally need at
least a longer period of retention than would an adoles-
cent patient. For patients with minimum to moderate loss
Finishing a Case with Uniform Height of
of periodontal tissue, longer retention periods may be
Gingival Margins sufficient. The optimal long-term retainer for adults with
In patients with high or normal smile lines, the rela- reduced periodontium is the flexible spiral wire (FSW)
tionship of the gingival margins of the maxillary anteri- retainer bonded lingually on each tooth in a segment. At
Fiberotomy
The problem of relapse of orthodontically treated
teeth in general, and rotated teeth in particular due to the
supracrestal gingival tissues, has been well recognized
for years. The technique of circumferential supracrestal
fiberotomy (CSF) which consists of inserting a scalpel into
the gingival sulcus and severing the epithelial attachment
surrounding the involved teeth can effectively reduce
rotational relapse (Fig. 56.9).
Frenectomy and Frenotomy

The contribution of the maxillary labial frenum to the
etiology of a persisting midline diastema, and to reopening
of diastemas after orthodontic closure, has been a subject
FIGURE 56.9 Circumferential supracrestal fiberotomy done to sever
gingival fibers and prevent the relapse of rotations.
of much controversy. In the past, the most common surgi-
cal procedure was frenectomy, an excision-type operation,
which was often carried over to the palatal aspects. How-
ever, a frequently observed complication may be an unde-
the same time as the FSW retainer works as a reliable, sirable loss of the interdental papilla between the maxillary
invisible orthodontic retainer, it concomitantly acts as central incisors. On the other hand, the frenotomy, which is a
a periodontal splint, which allows the individual teeth more gentle operation, produces aesthetically preferable results.
within the splint to exert physiological mobility. With frenotomy, the attachment of the frenum to gingiva
Several forms of minor periodontal surgeries may be and periosteum is severed, and the insertion of the frenum
used to improve or stabilize the results achieved by orth- is relocated several millimeters up onto the alveolar bone
odontic treatment of malocclusions. and may be combined with fiberotomy (Fig. 56.10).
FIGURE 56.10 Frenectomy done after diastema closure to improve the stability of correction.
PERIODONTALLY requiring expansion or extractions, and mild Class III

ACCELERATED OSTEOGENIC malocclusions.
ORTHODONTICS
Clinical Considerations
A number of attempts have been made to accelerate
tooth movement and one of the recent methods is peri- The clinical procedure consists of flap reflection, selec-
odontally accelerated osteogenic orthodontics (PAOO) or tive alveolar corticotomy, particulate bone grafting, and
Wilckodontics described by Wilcko in 2001. It is based on the application of orthodontic forces. The placement of
the bone healing pattern known as the regional accelera- orthodontic brackets and activation of the arch wires are
tory phenomenon (RAP). typically done the week before the surgical aspect of PAOO
is performed. However, they can be done up to 1 week after
the surgery and initiation of orthodontic force should not
be delayed any further. The orthodontist has between 4 and
Case Selection
6 months to accomplish accelerated tooth movement, after
PAOO can be used in most cases in which traditional which tooth movements occur at the normal rate. With this
fixed orthodontic therapy is used. It has been shown to technique, teeth can be moved two to three times further in
be efficacious in the treatment of Class I malocclusions one-third to one-quarter of the time required by traditional
with moderate-to-severe crowding, Class II malocclusions orthodontic therapy (Figs 56.llA-C and 56.12A and B).
FIGURE 56.11 Steps in PAOO (A) Flap reflection; (B) selective decortication; (C) particulate bone grafting.
FIGURE 56.12 Molar protraction assisted by PAOO (A) Before molar protraction; (B) 1 month after initiating tooth movement.
The advantages of PAOO are that it decreases treat- bone thickness, and enhances posttreatment stability. Its
ment duration, reduces incidence of root resorption when disadvantages are the increased cost and the surgery with
compared with conventional treatment, increases alveolar its attendant risks, however minor they might be.
KEY POINTS
1. Tooth movement is quite possible despite bone loss, healing following periodontal surgery, thus must be
but lighter forces and relatively larger counterbalancing relieved orthodontically.
moments are required. 7. When molar uprighting is done, one must try and avoid
2. Orthodontic tooth movement superimposed on poorly inadvertent extrusion of the tooth if there is furcation
controlled periodontal health can lead to rapid and involvement.
irreversible breakdown of the periodontal support ap- 8. Labial tooth movement in cases where the labial bone
paratus. cortex is thin and is accompanied by a thin gingiva
3. Adjunctive treatment implies limited orthodontic goals, might result in gingival recession.
improving a particular aspect of the occlusion rather 9. When adult patients have gingival margin discrepan-
than comprehensively altering it. cies between adjacent teeth, the proper solution for the
4. When teeth are moved in the presence of periodontitis, problem is orthodontic movement to reposition the
the resorption of bone is enhanced and bone formation gingival margin.
is inhibited. 10. The problem of relapse of orthodontically treated teeth
5. The purpose of the forced eruption procedure is the in general and rotated teeth in particular might be due
coronal shift of the bone at the base of infrabony defects, to the stretched supracrestal gingival tissues.
thus reducing the depth of the defect. 11. PAOO /Wilckodontics can be used to achieve rapid tooth
6. Occlusal trauma plays a role in enhancing bone loss movement with increased alveolar bone volume and
especially in case of deep overbite and also might delay better stability.
QUESTIONS 3. What are the periodontal considerations as far

as stability in orthodontic treatment results is
1. What are the orthodontic considerations in periodon- concerned?
tally compromised patients? 4. Write the implications of gingival recession on orth-
2. Enumerate the various adjunctive orthodontic proce- odontic tooth movement.
dures and talk in detail about forced eruption.
Suggested readings 6. Graber TM, Vanarsdall RL. Orthodontics - Current Principles and
Techniques. 3rd ed. St. Louis: Mosby; 1994.
1. Proffit WR. Contemporary Orthodontics. 3rd ed. St. Louis: Mosby; 1986. 7. Wilcko TM, Wilcko WM, Bissada NF. An evidence based analysis of
2. Proffit WR. Conicmporanj Orthodontics. 4th ed. St. Louis: Mosby; 2006. periodontally accelerated orthodontic and osteogenic techniques: a
3. Lindhe J. Clinical Periodontology and Implant Dentistry. 4th ed. Oxford: synthesis of scientific perspectives. Semin Orthod 2008;14:305-16.
Blackwell Munksgaard; 2003. 8. Murphy KG, Wilcko TM, Wilcko WM, Ferguson DJ. Periodontal
4. Carranza FA. Clinical Periodontology. 9th ed. Philadelphia: WB Saun- accelerated osteogenic orthodontics: a description of the surgical
ders (an imprint of Elsevier Science); 2003. technique. J Oral Maxillofac Surg 2009;67:2160-6.
5. Marks MH, Corn H. Atlas of Adult Orthodontics: Functional and
Esthetic Advancement. Philadelphia, London: Lea and Febiger;
1989.
CHAPTER
57
Infection Control
CHAPTER OVERVIEW
Control of transmission of infections among patients exposure" to a given pathogen, while disease transfer from
and therapists in dental offices has reached a high level of one patient to another in the dental clinics is considered
effectiveness in this century. Well-publicized concern over "cross-infection."
the acquired immunodeficiency syndrome (AIDS) epidemic Infection control should always be a prime consider-
has further focused attention on infection control in general ation in the dental office. Most dentists are aware, at least
and on dental field in specific. to some degree, of the potential risks posed by the trans-
Apart from human immunodeficiency virus (HIV) and mission of infectious diseases. Several infectious diseases,
AIDS there is a plethora of blood-borne and other common notably hepatitis, are of great concern in the dental office.
diseases encountered in the dental clinic that may pose a To prevent the transmission of these diseases, each office
risk. Based on the evidence, information, and rules, local to must establish an infection control system that can deal
either the country or region, high standards of Dental Infec- with both the known risks, as in the cases of diagnosed
tion Control & Occupational Safety must be followed by the AIDS patients, and with unknown cases of transmissible
dental team for the safety of the patients and dental health disease. Hence, infection control measures should be es-
care workers. Disease transfer to the dentist and dental tablished on the belief that any patient can be a source of
staff during dental care is considered an "occupational infection (Table 57.1).
Dentists and dental auxiliary personnel are exposed • In a study conducted among health care personnel who
to various infectious microorganisms, including bacte- had percutaneous exposure to HIV-infected blood, an
ria, such as Streptococcus and Mycobacterium tuberculosis, increased risk for HIV infection was related with ex-
fungi, and viruses, such as the HIV, hepatitis, cytomegalo- posure to a relatively large amount of blood because
virus, and herpes simplex virus. Each of these agents may of deep injury, presence of blood on the device, or a
be transmitted directly from patients to dental auxiliary procedure including needle placement in an artery or
or from the dentist to patient. Transmission can occur by vein.
direct contact, by droplet infection, or by the formation of • The risk was also higher if the exposure was from pa-
infectious aerosols generated by high-speed hand pieces. tient's blood with terminal disease, because higher titer
Indirect spread of infection can occur via contaminated of HIV in the late-stage AIDS was found.
instruments or dental charts and via water sprays used
for rinsing or cooling. When the microorganisms make
contact with water from the handpiece, air-water sy- EXPOSURE PREVENTION STRATEGIES
ringe, or ultrasonic scaler, this water is sucked back into
the waterlines when the instrument is turned off; this is Primary methods used to prevent occupational exposures
known as water retraction. So, the running of the instru- to blood in health care settings include standard precautions,
ment for several minutes prior to use will minimize the engineering controls, work practice controls, and adminis-
contamination. trative controls. Engineering controls that eliminate/isolate
Several factors affect the risk of HIV spread after an the hazard are the primary strategies for protecting dental
occupational exposure. health care personnel (DHCP) and patients.
C H A PT ER 57 IN FEC T IO N C O N T R O L 515
TABLE 57.1 CDC Recommendations on Infection Control for Dentistry
Universal precautions Standard precautions Transmission-based precautions

• These are termed blood and body fluid precau- • In 1996 • Are necessary for interrupting the
tions • The CDC combined the key components spread of certain pathogens such
• In 1980 and in early 1990s of universal (body fluids and blood) and as TB, influenza, and chicken pox
• According to this every patient should be treated body substances separation precautions that are transmitted by air drop-
as potentially infectious. This is due to the fact that (planned to decline the risk of trans- lets, and direct or indirect contact
many patients with blood-borne infections may be mission of pathogens from moist body with contaminated sources
in the asymptomatic state or unaware about their substances) • Along with standard precautions
infection • This helps in protection of dental health they also include the following:
• Preventive measures used to lower the blood care personnel (DHCP) and patients by • Patient placement (isolation)
exposures include the following: the pathogens which can be spread by: • Ventilation and specific respira-
• All the sharp/pointed instruments should be • Blood tory precautions should be
handled carefully • Any other body fluid secretion and followed by the DHCP
• A proper hand washing/ scrubbing should be excretion (except sweat) irrespective of • Nonemergent dental proce-
followed every time whether they contain blood or not dures will be rescheduled
• Use of rubber dams to minimize blood spatter- • Cut or injured skin and mucous mem-
ing should be incorporated in daily practice branes
• Use of protective barriers (gloves, masks, gown, • Saliva
and protective eyewear) should be practiced • Elements of standard precautions
Work practice controls that result in safer behavior and to minimize the risk of cross-infection in the dental care
personal protective equipment (PPE) and can prevent settings:
exposure in case of failure or inappropriate engineering
1. Education and protection of DHCP
controls should be employed.
2. Prevention of transmission of blood-borne pathogens
Exposure risk to certain diseases such as tuberculosis
3. Usage of glove for hand hygiene
(TB) can be reduced by following administrative controls.
4. PPE (face mask, face shields, and protective eyewear)
In spite of following so many precautionary measures,
5. Contact dermatitis and latex hypersensitivity
blood exposure incidences are continuing to occur. Postex-
6. Sterilization and disinfection of patient care items
posure management is essential. Elements of an effective
7. Environmental infection control protocol
postexposure management program include:
8. Dental unit waterlines, biofilms, and water quality
1. The protocol that clearly states postexposure 9. Special devotions for dental handpiece, and other de-
management vices, radiology, parenteral medications, oral surgical
2. Training of DHCP in prevention strategies (including procedures, handling of tissue specimens, and dental
evaluation of safety devices), protocol for postexposure laboratories
management, the importance of early reporting, and 10. Disposal of materials (blood, other contaminated flu-
PPE effectiveness and toxicity ids, and disposal of solid waste).
3. Resources for quick access to clinical care, postexpo-
According to CDC guidelines hands should be cleaned
sure prophylaxis, as well as testing of both source and
if they are noticeably dirty or if contaminated objects have
injured health care personnel (preferably with a rapid
been touched with bare hands, prior to and after patient
HIV test).
management, that is, prior to glove placement and im-
The major fundamentals of postexposure management mediately after removal of the glove (Fig. 57.1).
comprise wound management and exposure reporting. Hand hygiene is a common word that applies to use of
The evaluating health care professional should assess hand washing, antiseptic hand wash, alcohol-based hand
the risk of infection by examining the type and severity rub, or surgical hand hygiene/ antisepsis.
of exposure, the blood-borne status of the source person, Washing of hands using plain soap and water is termed
and the susceptibility (immune status) of the exposed hand wash.
person. A detailed follow-up is needed for assessing the
• Washing hands using water and soap or detergents
risk of infection considering all these factors.
containing an antiseptic agent, such as triclosan or
chlorhexidine, is termed antiseptic hand wash.
PROTECTIVE MEASURES • Using an agent containing 60-95% ethanol or isopro-
panol-containing preparation is named as an alcohol-
In 2003, the Centers for Disease Control and Preven- based hand rub (antiseptic hand rub). These are new
tion (CDC) published its guidelines for infection con- agents which have been added to the dental guidelines
trol in dental health care settings, which are intended and have become more frequently used in the United
FIGURE 5 7 .2 Personal protective equipment (PPE): protective

eyewear, disposable face mask, gloves, and head cap.
FIGURE 57.1 Hand wash preoperatively and postoperatively.
States to improve compliance with hand washing in face protection with soap and water between patients; if
hospitals in dental practices. visibly soiled, clean, and disinfect.
• Hand scrub performed preoperatively by surgical per- Long-sleeved disposable/reusable gowns, lab coats, or
sonnel to eliminate microorganisms on hands using uniforms that cover skin and personal clothing likely to
an antiseptic hand wash or alcohol-based hand rub is become soiled with blood, saliva, or infectious material
termed surgical antisepsis. Antiseptic preparations for should be worn by the DHCP. They should be changed if
surgical hand hygiene should have persistent (long- they become visibly soiled or as soon as possible if pen-
lasting) antimicrobial activity. The hands should first be etrated by blood or other potentially infectious fluids.
washed with soap and water prior to an alcohol-based Before leaving patient care or laboratory areas all the
hand rub use. protective clothing should be removed (Fig. 57.3).
PERSONAL PROTECTIVE EQUIPMENT Gloves

OR BARRIER PRECAUTIONS By using gloves health care personnel can
• Minimize the risk of acquiring infections from infected
PPE is an important component of standard precau-
individuals
tions. Usage of rotary dental and surgical instruments
• Prevent transmission of pathogenic organisms from
(e.g., handpieces, ultrasonic scalers) and air-water sy-
health care personnel to patient
ringes produces a visible spray that comprises mainly
• Reduce contamination of health care personnel's hands
large-particle droplets of water, saliva, blood, microor-
by organisms that can be transmitted from one patient
ganisms, and other debris. This spatter can travel only
to another
a short distance and settles out quickly, landing on the
floor, operatory surfaces, DHCP, or the patient (Fig. 57.2). Immediately prior to putting on and after removal
The skin and the mucous membranes of DHCP are of gloves proper hand hygiene must be followed because
protected mainly by PPE from exposed infectious or po- gloves might have small holes or tears that are not no-
tentially infectious materials. PPE should be worn when- ticeable, or hands can become contaminated as gloves
ever there is potential for contact with spray or spatter are removed. Such situations elevate the risk of wound
and should be removed when leaving treatment areas. contamination and exposure of the DHCP's hands to
Protection of mucous membranes from spatter gener- microorganisms from patient.
ated during dental procedures is done by the use of a For the safety of DHCP and patients, gloves should
standard surgical mask which covers the nose and mouth. always be worn in situations whenever contact with
Eye protection with solid side shields or a face shield blood, saliva, and mucous membrane is possible. After
eyewear will provide protection for the eyes. the patient care gloves should be removed and it should
A mask should be replaced between patients or if it be followed by hand wash. Hand wash is must prior to
becomes wet during patient treatment. Clean reusable putting on gloves (Fig. 57.4).
Several agents can be used to kill surface vegetative
pathogenic organisms, but not necessarily spore forms
or viruses.
The first step is cleaning. This must be done prior to
disinfection or sterilization.
TRANSPORT AND PROCESSING OF

CONTAMINATED INSTRUMENTS
Prevention of injury or exposure to infection can be

done by careful handling of the contaminated instru-
ments. Instruments should be kept in a proper container
while in use to prevent injuries or during the transporta-
tion time to the instrument processing.
• Instrument processing area: Central processing area
is divided into receiving, cleaning, and decontam-
ination of reusable instruments and supplies. All
the instruments should be processed in this area by
the DHCP. Equipment should be received, stored,
cleaned, and decontaminated in one section of the
processing area.
It should include elimination of debris as well as
organic and inorganic contamination. This is done by
scrubbing with a surfactant detergent and water or an
automated process (ultrasonic cleaner or washer disin-
fector). After cleaning, the chemical or detergent residue
from the instruments should be removed by rinsing
them with water.
• Automated cleaning equipment such as ultrasonic clean-
FIGURE 5 7 .3 Protective clothing (gowns and jackets)/ operation
er and washer disinfector do not need presoaking or
protection. scrubbing of instruments and can increase the pro-
ductivity, improve cleaning effectiveness, and reduce
worker's exposure to blood and body fluids.
If gloves get torn, cut, or punctured, they should be • Washer disinfector: It uses high-temperature cycle rath-
changed as soon as possible. Surgical or examination gloves er than a chemical bath for the cleaning and thermal
should not be washed prior to use. They should not be disinfection of the instrument. It is an automatic unit
washed, disinfected, or sterilized for the purpose of reuse. (Figs 57.6 and 57.7).
Washing of gloves can lead to a condition called "wicking." • Manual cleaning is not performed immediately. Instru-
It can also allow the penetration of liquids through unde- ments /items will be placed in a puncture-resistant
tected holes in the gloves. These incidents may elevate the container as a safety measure. All the instruments
risk of wound contamination and exposure of the DHCP's should be soaked in chemicals or detergents. Sharp
hands to microorganisms from patients. Disinfecting agents, instruments should be scrubbed using long-handled
oils, certain oil-based lotions, and heat treatments such as brushes to avoid hand injury. Hands should be pro-
autoclaving may result in deterioration of gloves. tected by using puncture-resistant heavy utility
Dental offices, such as hospital operating room, can- gloves. A mask, protective eyewear, and gown should
not be sterilized (i.e., cannot be made free of all microbial be worn as splashing possibilities exist.
forms). Sterilization is possible with instruments, hand-
pieces, and other materials that come in direct contact
Preparation and Packaging
with the patients. CDC has categorized the instruments
as critical, semicritical, and noncritical depending on the All cleaned instruments and other dental supplies
potential risk for infection associated with their intended should be inspected, assembled into sets or trays, and
use (Fig. 57.5; Table 57.2). wrapped, packed, and placed into container systems
(A) (C)
FIGURE 57 .4 (A) Gloving; (B) punctured glove (glove injury); (C) glove washing.
for sterilization in the other section of the processing and placed in a container. Penetration of the steriliza-
area. Hinged instruments should be processed open tion agent to maintain sterility of the processed item
and unlocked. Every package should have an internal after sterilization will be allowed by packing materi-
chemical indicator. An external chemical indicator (in- als. During transport and storage wrapped perforated
dicator tape) should be used in case of invisibility of instrument cassettes, peel pouches of plastic or paper,
internal indicator from outside. Critical and semicriti- and sterilization wraps (woven and non woven) will be
cal instruments that will be stored should be wrapped used.
TABLE 5 7 .2 Infection Control Types of Patient Care Instruments
Critical items Semicritical items Noncritical dental items

• Soft tissue penetration or bone • These items come in contact with mucous mem- • These contact intact skin
handling is done using these instru- branes or nonintact skin • Chances of transmitting infection are
ments • These will not penetrate the soft tissue, contact least among these items
• These instruments enter into or bone, and enter into and contact the bloodstream • In majority of cases, cleaning is done
come in contact with bloodstream or or other sterile tissues only when they are visibly soiled;
normally sterile tissue • Transmission of infection is minimal with these cleaning should be followed by disin-
• Threat of transmitting infection is items fection with Environmental Protection
highest among these instruments • These are heat tolerable and sterilized by heat Agency (EPA)-registered disinfectant
• Heat sterilization should be followed • If a semicritical item is heat sensitive, it should be • Use of disposable barrier protection
• Surgical instruments, periodontal processed with high-level disinfection can be used as an alternative
scalers, scalpel blades, and surgical • Dental mouth mirror, amalgam condenser, reus- • Radiograph head/ cone, blood pres-
dental burs able dental impression tray, and dental handpieces sure cuff, facebow, and pulse oximeter
(A)
(8)
(C)
FIGURE 5 7 .5 (A) Critical item; (B) semicritical item; (C) noncritical items.
Sterilization sterilization of all the instruments/ items. Removing

and handling of instrument packs is done only after
The use of a physical or chemical procedure to destroy they are dried inside the sterilizer chamber. Hot packs
all microorganisms including substantial numbers of re- should not be touched since they act as wicks, absorb-
sistant bacterial spores is termed sterilization. ing moisture and bacteria from hands which leads
The processing area should have ample space for load- to contamination of the instruments. Steam steriliza-
ing, unloading, and cooldown. Incubators for analyzing tion (121 °C, 15 psi pressure for 15-30 min) is the most
spore tests and enclosed storage for sterile and disposable dependable, economical, commonly used device. All
items also should be incorporated in this area. wrapped and unwrapped critical and semicritical items
which are not sensitive to heat and moisture can be
Sterilization Procedure sterilized using this. In this each item gets exposed to
The Food and Drug Administration (FDA)-approved direct steam for the specific amount of time to kill mi-
medical sterilization equipment should be used for the croorganisms (Table 57.3).
will not be fully sterilized. To remove all air prevacuum

pumps should be used. Efficiency of the prevacuum steril-
izers should be checked periodically.
Dry Heat Sterilization

Instruments which can be damaged by moist heat can
be sterilized using dry heat, for example, burs and certain
orthodontic instruments. Dry heat sterilization is cost-
effective and noncorrosive, but prolonged procedure and
high temperature are required. Dry heat sterilizers used
in dentistry are the static air type commonly called oven-
type sterilizers. Heating coils in the bottom or sides of the
units cause hot air in the chamber. Forced air-type/rapid
heat transfer sterilizers circulate heated air throughout the
chamber at a high velocity, permitting more rapid transfer
FIGURE 5 7 .6 Ultrasonic cleaner. of energy from air to item (Table 57.4).
Unsaturated Chemical Vapor Sterilization

It contains heating a chemical solution of primarily
alcohol with 0.23% formaldehyde in a closed pressur-
ized chamber. Unsaturated chemical vapor sterilization
of carbon steel instruments causes less corrosion than
steam sterilization because of the low level of water pres-
ent during the cycle. Sterilization of all the items should
be done only when the items are totally dry. Hazardous
waste disposal should be taken care of.
Flash Sterilization
Sterilization of unwrapped items can be done by flash
sterilization. Patient care items for immediate use can
be sterilized by this method. Critical instruments ster-
ilized unwrapped should be transferred immediately
by using aseptic methods from sterilization area to real
working place. Critical instruments should not be stored
FIGURE 57.7 Autoclave.
unwrapped. Semicritical instruments should be used in
a short time.
Gravity Displacement Additional Sterilization Methods

Different types are available in the market. This type is Liquid chemical germicide registered by the FDA as a
commonly used in dental practice (glass bead sterilizer). sterilant can be used for the sterilization of heat-sensitive
In this, steam is admitted through steam lines, a steam critical and semicritical items and devices. Toxic residue
generator, or self-generation of steam within the chamber from the item should be removed by rinsing them with
wall. Inaccurate packaging or overloading of the steril- water and then transferred to working area in an aseptic
izing chamber will result in cool air pockets and items manner. For efficiency, a minimum of 12-h liquid chemical
TABLE 57.3 Parameters of Sterilization for Autoclaves

TABLE 57.4 Parameters of Sterilization for Dry Heat Sterilizers
Parameters Standard cycle Fast cycle
Parameter Slow cycle Fast cycle Rapid heat
Sterilization time 15-20 min 3-5min
Temperature 160°C (320°F) 170°C (340°F) 190°C (375°F)
Temperature 121 °C (250°F) 134°C (273°F)
Sterilization 120 min 60min 6-12 min
Pressure 15 psi 30 psi time
immersion is required. Shorter immersion time - 12- TABLE 57.5 Waste Collection and Disposal Chart
90 min - with high-level disinfection can be used. Eth-
ylene oxide gas is generally used in health care settings Waste collection and disposable chart
All the wastes should be strictly disposed in the below-mentioned
for low-temperature sterilization. Handpieces cannot be colored bags
effectively sterilized because ethylene oxide (ETO) gas
l. Human anatomic waste: human tissue
fails to pass through narrow lumen.
ENVIRONMENTAL INFECTION
0 2. Microbiology and biotechnology wastes: laboratory cell,
cultures, infectious agents, dishes, and devices used
for transfer of cultures
3. Soiled wastes: materials contaminated with blood and
CONTROL body fluids such as cotton, dressing, linens, etc.
Waste disposal: incineration
•
Surfaces/ equipment that do not contact patient direct- l. Solid disinfected wastes: waste generated from dispos-
ly can become contaminated during patient care (light al other than waste sharps, such as cotton, dressing,
handle, unit switches, and drawer knobs) and are in- linens, etc.
Waste disposal: chemical disinfection and then sent for
cluded in environmental infection control. There are shredding
two kinds of environmental surfaces - clinical contact
surfaces (potential for direct contamination from spray 1. Waste sharps (disinfected): needles, syringes,
scalpels, blades, glass, etc. (include both used and
or spatter or by contact with DHCP's gloved hand) and unused sharps)
housekeeping surfaces which do not come into contact Waste disposal: needles to be burnt in the needle burner
with patients/ devices and have less chances of disease Used and disinfected syringes to be sent for shredding
•
transmission. 1. Discarded medicines: outdated, contaminated, and
discarded medicines
2. Chemical wastes (solids): chemicals used in disinfec-
Waste Disposal tion such as solid sodium hypochlorite solution
There is no evidence that traditional medical waste Waste disposal: disposal at corporation landfill
management has contributed to increased levels of dis-
ease in the community or among health care personnel.
The large amount of waste generated in a medical or medical waste can be handled in a leak-resistant biohaz-
dental office (-98-99%) is not considered infectious and ard bag. Scalpel blades, needles, syringes, and unused
can be disposed of in the regular trash. Examples include sterile sharps can be handled using puncture-resistant
used gloves, masks, and lightly bloodied gauze. containers with a biohazard label.
Certain wastes, such as used needles, extracted teeth, Storage and disposal of medical waste (both nonregu-
and gauze soaked in blood, may pose a potential risk of lated and regulated) should be done as per the federal,
infection. Special precautions should be taken during state, and local Environmental Protection Agency (EPA)
handling and disposal (Table 57.5) of these items. Federal, regulations.
state, and local regulations for proper treatment and dis- Regulated waste such as on-site or off-site should be
posal should be followed. handled by autoclaving and incineration. Dental amal-
Regulated medical waste needs cautious containment gam and extracted teeth should not be mixed with regu-
for treatment or disposal. All the nonsharp, regulated lated waste when disposed by one of these methods.
KEY POINTS
• Steam sterilization (121 °C, 15 psi pressure for 15-30 min) is • Agent with 60-95% ethanol- or isopropanol-containing
the most dependable, economical, commonly used meth- preparation is called an alcohol-based hand rub
od for wrapped and unwrapped critical and semicritical (antiseptic hand rub).
items that are not sensitive to heat and moisture. • Heating a chemical solution of chiefly alcohol with 0.23%
• Sterilization of unwrapped items can be done by flash formaldehyde in a closed pressurized chamber is done
sterilization. in unsaturated chemical vapor sterilization.
• Antiseptic hand wash states use of washing hands with
water and soap/other detergents with an antiseptic
agent.

1. CDC. Guidelines for Infection Control in Dental Health Care Settings.
1. Write briefly about infection control dentistry. Atlanta, GA: CDC; 2003.
2. Write about universal and standard precaution. 2. Genco RJ, Goldman HM, Cohen DW. Contemporary Periodontics.
3. Write briefly about waste disposal management. St. Louis: Elsevier; 1990.
3. Wood PR. Cross-Infection Control in Dentistry -A Practical Illustrated
Guide. St. Louis: Mosby Year Book, Wolfe Publishing; 1992.
CHAPTER
58
Supportive Periodontal Treatment
CHAPTER OVERVIEW
Supportive periodontal treatment (SPT) is an integrated other names such as recall, maintenance phase, or super-
part of the overall periodontal therapy. This is initiated after vised recall program. The term "supportive periodontal
the completion of active periodontal therapy and contin- treatment" was recommended at the World Workshop in
ued at periodic intervals for life of the dentition or implant Clinical Periodontics in 1989. Essentially, the rationale for
replacement. Transfer of patients from the active treatment supportive periodontal therapy is prevention. The mainte-
status to SPT is a definitive step in total patient care that nance phase starts immediately after completion of phase
requires time and effort on the part of the dentist and the I therapy (Fig. 58.1).
staff. Supportive periodontal treatment is also known by
RATIONALE FOR SUPPORTIVE appear to be successfully treated can become reinfected

PERIODONTAL TREATMENT with potential pathogens.
4. Microscopic nature of dentogingival unit healing after
The rationale for maintenance phase/SPT is to pre- periodontal treatment: Histologic studies have shown
vent/minimize the recurrence of periodontal disease by that after periodontal procedures, tissues usually
controlling factors known to contribute to the disease do not heal by formation of new connective tissue
process. attachment to root surfaces but result in long junc-
The causes for recurrence of periodontal diseases are tional epithelium. It has been seen that this type of
likely to be the following: dentogingival unit is weaker, and inflammation may
rapidly separate the long junctional epithelium from
l. Incomplete subgingival plaque removal: If subgingival the tooth. Thus, treated periodontal patient can pre-
plaque is left behind during scaling, it will regrow dispose to recurrent pocket formation if maintenance
within the pocket. The regrowth of subgingival plaque case is not optimal.
is a slow process compared with that of supragingival 5. Subgingival scaling alters the microflora of periodon-
plaque. During this period, the subgingival plaque tal pockets: It has been seen that a single session of
may not induce inflammatory reactions that can be subgingival scaling resulted in significant changes
discerned at the gingival margin. So, there will be con- in subgingival microflora. Reported alterations in-
tinuous loss of attachment even without the presence clude a decrease in the proportion of motile rods for
of clinical gingival inflammation. 1 week, a marked elevation in the proportion of cocci
2. Presence of bacteria in the gingival tissue in adult and ag- for 21 days, and a marked reduction in the propor-
gressive periodontitis cases: Eradication of intragingival tion of spirochetes for 7 weeks. Subsequent reports
microorganisms may be necessary for a stable peri- concluded that arbitrary assignment of treated peri-
odontal result. odontitis patient to 3-month maintenance intervals
3. Transmission of bacteria associated with periodontitis be- appears to be effective in preventing recurrence of
tween spouses and other family members: Patients who periodontitis.
RECURRENCE OF PERIODONTAL
II/correct .~eq11e11ce of'pcriodontai treatment phases DISEASE
Phase I
.( l Occasionally, lesions may recur. This can often be traced
Reevaluation to inadequate plaque control on the part of the patient or
failure to comply with recommended SPT schedules.
.( l
Other causes of recurrence are the following:
Phase II (Periodontal surgery)
.( l 1. Inadequate/insufficient treatment that has failed
to remove all the potential factors favoring plaque
Phase Ill (Restorative)
accumulation
.( l
2. Incomplete calculus removal in areas of difficult access,
Phase IV (Maintenance) which is a common problem
3. Inadequate restorations placed after the periodontal
Correct sequence ofperiodontal treatment treatment was completed
Phase I 4. Failure of patient to return for periodic checkups
.( l 5. Presence of some systemic disease that may affect host
resistance to previously acceptable levels of plaque
Reevaluation
.( l A failing case can be recognized by the following:
Phase IV (Maintenance) 1. Recurring inflammation revealed by gingival changes
and bleeding of the sulcus on probing
2. Increasing depth of sulci leading to recurrence of
Phase 11 Phase ITl
pocket formation
3. Gradual increase in bone loss as determined by
(Periodontal surgery) (Restorative)
radiographs
FIGURE 58.1 Sequence of maintenance visits.
4. Gradual increase in tooth mobility as ascertained by
clinical examination.
PARTS OF MAINTENANCE PHASE

RECALL INTERVALS FOR VARIOUS
Part I: Examination (Approximate Time - 1 7 min) CLASSES OF RECALL PATIENTS
• Medical history changes The first year after periodontal therapy is important
• Oral pathologic examination in terms of indoctrinating patients in a recall pattern and
• Oral hygiene status reinforcing oral hygiene techniques. In addition, it may
• Gingival changes take several months to evaluate accurately the results
• Pocket depth changes of some periodontal surgical procedures. Consequently,
• Mobility changes some areas have to be re-treated because the results may
• Occlusal changes not be optimal. Furthermore, the first-year patient often
• Dental caries has etiologic factors that may have been overlooked and
• Restorative and prosthetic status may be more amenable to treatment at this early stage.
• Radiographic examination according to individual For these reasons the recall intervals for first-year patients
needs. should not be longer than 3 months.
Table 58.1 lists several categories of maintenance pa-
Part II: Treatment (Approximate Time - 35 min) tients and suggested recall intervals for each.
• Oral hygiene reinforcement

• Scaling and polishing REFERRAL OF PATIENTS TO THE
• Chemical irrigation. PERIODONTIST
Part Ill: Schedule Next Procedure (Approximate The question of where to draw the line between the
Time - 1 min) cases to be treated in the general dental office and those
to be referred to a specialist varies for different practi-
• Schedule next recall visit. tioners and patients. The diagnosis indicates the type of
• Schedule further periodontal treatment. periodontal treatment required. If periodontal destruc-
• Schedule or refer for restorative or prosthetic treatment. tion necessitates surgery on the distal surfaces of second
CHAPTER 58 SUPPORTIVE PERIODONTAL TREATMENT 525
TABLE 58.1 Recall Intervals for Various Classes of Recall Patients
Merin classification Characteristics Recall interval

First year First-year patient: routine therapy and uneventful healing 3 months
First-year patient: difficult case with complicated prosthesis, furcation 1-2 months
involvement, poor crown-root ratios, questionable patient cooperation
Class A Excellent result well maintained for 1 year or more 6 months to 1 year
Patient displays good oral hygiene, minimal calculus, no occlusal problems,
no complicated prosthesis, no remaining pockets, and no teeth with less than
50% alveolar bone remaining
Class B Generally good results maintained for 1 year or more but patient displays 3-4 months (decide on recall in-
some of the following factors: tervals based on the number and
Inconsistent/poor oral hygiene severity of negative factors)
Heavy calculus formation
Systemic disease that predisposes to periodontal breakdown
Occlusal problems
Complicated prosthesis
Ongoing orthodontic therapy
Recurrent dental caries
Some teeth with less than 50% of alveolar bone support
Smoking
Positive family history or genetic test
Bleeding of more than 20% of pockets on probing
Class C Generally poor results following periodontal therapy and/ or several negative 1-3 months (decide on recall in-
factors from the following: terval based on the number and
Inconsistent/poor oral hygiene severity of negative factors)
Heavy calculus formation
Systemic disease that predisposes to periodontal breakdown
Many remaining pockets
Occlusal problems
Complicated prosthesis
Recurrent dental caries
Periodontal surgery indicated but not considered for medical, psychological,
or financial reasons
Many teeth with less than 50% of alveolar bone support
Condition too far advanced to be improved by periodontal surgery
Smoking
Positive family history or genetic test
Bleeding of more than 20% of pockets on probing
molars, extensive osseous surgery, or complex regen- junction may have a prognosis of rapid decline. Teeth
erative procedures, the patient is usually best treated with furcation lesions may be at risk even when more than
by a specialist. On the other hand, patients who require 50% of bone support remains. Therefore, cases in which
localized gingivectomy or flap curettage, usually, can be strategically important teeth fall into these categories are
treated by the general dentist. usually best treated by specialists.
The decision to have the general practitioner treat a Whether the maintenance therapy should be per-
patient's periodontal problem should be guided by a con- formed by the general practitioner or the specialist is
sideration of the degree of risk that the patient will lose a determined by the amount of periodontal deterioration
tooth or teeth for periodontally related reasons. The most present.
important factors in the decision are the extent and loca- Class A recall patients should be maintained by the
tion of the periodontal deterioration. Teeth with pockets general dentist, whereas Class C patients should be main-
of 5 mm or more as measured from the cementoenamel tained by the specialist. Class B patients can alternate
recall visits between the general practitioner and the 4. Bacterial monitoring is performed more frequently be-
specialist. cause the presence of bacteria may play a contributory
role in the loss of fixtures.
5. Patients with implants must use ultrasoft brushes,
MAINTENANCE FOR IMPLANT chemotherapeutic rinses, tartar control pastes,
PATIENTS irrigation devices, and yarn-like materials to keep the
implants clean.
Patients with implants are susceptible to a form of
bone loss called peri-implantitis, and it has been seen
that such patients may be more prone to plaque-induced
inflammation than those with natural teeth. Because
CONCLUSION
peri-implantitis is difficult to treat, it is extremely im-
A successful long-term maintenance program is based
portant to provide good supportive therapy for implant
on good communication. This involves the following:
patients.
In general, procedures for the maintenance of patients 1. Informing patients of their current periodontal status
with implants are similar to those with natural teeth, but and any alteration in treatment if indicated
there some differences: 2. Consultation with other care providers who will be
providing additional dental care
1. Plaque control is performed during postsurgical
3. Future planning.
healing periods.
2. No metal instrumentation is used for calculus removal For patients with a history of active periodontitis, visits at
for implants. Only plastic instrument or specially 3-month intervals are recommended. However, the sched-
designed gold instruments should be used because uling of future SPT visits should be based on evaluations
implant surfaces can be easily scratched. of clinical findings and assessments of the disease status.
3. Acidic fluoride prophylactic agents are avoided because In short, the success of any SPT is based on periodic
they cause surface damage to titanium abutments. evaluation and appropriate retreatment if indicated.
KEY POINTS
• Supportive periodontal treatment is also known by other • The rationale for maintenance phase/SPT is to prevent/
names such as recall, maintenance phase, or supervised minimize the recurrence of periodontal disease by con-
recall program. trolling factors known to contribute to the disease process.
1. What is supportive periodontal therapy? 3. Rose LF, Mealey BL, Genco R. Periodontics, Medicine, Surgery, Implants.
2. What is Merin classification? 1st ed. St. Louis: Mosby; 2004.
Suggested readings
CHAPTER
59
Biological Aspects of Dental Implants
CHAPTER OVERVIEW
Although osseointegration forms the main basis of suc- A key determinant for clinical success is the diagnosis
cessful implantology, maintenance of a healthy soft tissue bar- of bone density around an implant. The strength of bone
rier is equally important for long term success of an implant is directly related to bone density. Factors such as the
supported prosthesis. It is a highly complex process which is amount of bone contact, the modulus of elasticity, and
influenced by the soft and hard tissue quality, implant surface axial stress contours around an implant are all affected
tomography, and maintenance around implants. Increase by the density of bone. As a consequence, the treatment
in the surface roughness of the titanium implants improves plan, which includes implant number and size, should be
bone integration with respect to the amount of bone formed modified as stress factors increase and/ or bone density
at the interface, and leads to better osseointegration. increases.
OSSEO INTEGRATION bone is the mechanically efficient distribution of compact

and cancellous bone. Factors governing the ability of
The association of endosseous implant and the sur- bone to support an implant are host's metabolic status,
rounding bone can be either osseointegration or fibro-osseous manipulation of the bone during implant surgery along
integration. Osseointegration is defined as direct functional with its healing response to this mechanical stimulus, and
and structural connection between living bone and the surface of the functional load at a later stage.
the load-carrying implant. This concept was first proposed by
Branernark et al and called functional ankylosis by Schroeder
et al. Osseointegration refers to the direct contact of the Bone Healing
bone with the implant at light microscopic level. The osseointegration process observed after implant
Osseointegration or functional ankylosis can be insertion can be compared with bone fracture healing. Im-
achieved only if the implant exhibits proper initial fixa- plant site osteotomy preparation (bone wounding) initiates
tion (stability) when installed in the recipient site. This a sequence of events which are an inflammatory reaction,
initial stability is the result of the contact relationship bone resorption, release of growth factors, and attraction
(friction) that is established between the mineralized by chemotaxis of osteoprogenitor cells to the site. These
bone at the recipient site and the implant. Factors de- osteoprogenitor cells then differentiate into osteoblasts
termining the predictability of osseointegration are the which form the bone at the implant-bone interface. Histo-
biocompatibility and sterility of the implant used, atrau- logically bone is composed of four tissue types which are
matic surgical placement of the implant under strict woven, lamellar, bundle, and composite bone. Woven bone is a
aseptic conditions, initial implant stability, and undis- highly cellular osseous tissue which forms in response to
turbed adequate healing period prior to implant loading growth or injury and serves an important role in the stabili-
(2-4 months for mandible and 4-6 months for maxilla). zation of initial healing of an endosseous implant. Lamellar
bone serves as a principal load-bearing tissue and is highly
BONE CHARACTERISTICS mineralized. Bundle bone is found at the ligament/tendon
and at bone interfaces. Composite bone is a combination of
Bone is a highly ordered composite of organic matrix lamellar and woven bone and its formation is an important
and inorganic minerals. The fundamental architecture of landmark in achieving stabilization of an implant.
Immobility of the implant relative to the bone must The implant surface can be modified by either additive or
be maintained for bone formation at the surface. When subtractive process. Additive process is the process of coat-
micromovements at the implant-bone interface exceed ing the implant surface with active materials, for example,
150 µm, it impairs the differentiation of osteoblasts and hydroxyapatite, whereas in subtractive process the implant
favors fibrous scar tissue formation at this interface. surface is treated with acid etching or blasting procedures.
Therefore, it is important to avoid excessive forces, such
as occlusal loading, during the early healing period.
IMPLANT SOFT TISSUE INTERFACE
Primary and Secondary Bone Contact Soft tissue surrounding the dental implant is termed
The intimate bone to implant contact essential for sta- peri-implant mucosa. The peri-implant mucosa forms the
bility of implants can be derived by the adequate bone soft tissue attachment of the bone-implant interface and
quantity and quality or by the rigid connections at the it serves as the seal. This seal serves as an effective bar-
coronal aspects intraorally. Immediately after the implant rier to isolate the peri-implant environment from that of
placement, some areas of primary bone contact are seen the oral cavity. The interface between the epithelial cells
which forms the instantaneous osseointegeration. During and the titanium surface is characterized by presence of
the healing process formation of new bone takes place hemidesmosomes and a basal lamina. A dense connective
on the titanium surface and the cut bone trabeculae as well tissue is present between this epithelial attachment and
as remodeling of bone takes place leading to the formation the marginal bone. The total height of the biological width
of secondary bone contact. Both the primary and secondary surrounding the implant is 3-4 mm.
bone contacts play a vital role in the implant success. The most important difference in the soft tissue sur-
rounding the implant and that surrounding the natural
tooth is the absence of the periodontal ligament around the
Implant Surface Characteristics (Microdesign) implant, thus reducing the vascularity of the peri-implant
Implant surface characteristics (microtopography) have mucosa and making any movement of the implant impos-
been shown to positively influence the healing process. sible (Fig. 59.1). The absence of this resilient periodontal
,.-----------Sulcular C+----------Sulcular
(crevicular) epithelium
epithelium
---------Junctional .;---------Junctional
epithelium epithelium
~~,f---
§i-j\ ~onnective
tissue
\·_ Connective
tissue
(A) (B)
FIGURE 59.1 Comparison of hard and soft tissue around a tooth (A) and an implant (B). (Source: Newman MG, Takei HH, Klokkevold PR, Carranza FA.
Clinical Periodontology. 12th ed. Philadelphia: Saunders; 2015).
CHA PTER 59 BIO LOGICA L ASPECTS OF DENTAL IM PLA NTS 529
ligament leads to direct impact of the occlusal distur- Similar attachment characteristics occur between the
bances on the bone-implant interface, jeopardizing the mucosa and the titanium surface in one-stage and two-
success of the implant placed. Absence of the periodontal stage implant systems.
ligament reduces the tactile sensitivity and reflex function
of the implant placed.
CONCLUSION
Influence of Implant Design on Soft Tissue Multiple factors interfere with the predictable estab-
Barrier Formation lishment of osseointegeration. The bone-implant interface
Abrahamsson et al demonstrated that the material used and the associated rigidity are critical in achieving the
in the abutment portion of the implant was of decisive biomechanical success of the implant and the soft tissue
importance for the location and the quality of the attach- interface is crucial in the long-term maintenance of stable
ment that occurred between the mucosa and the implant. marginal bone levels around the implant. Clinicians
The peri-implant mucosa around the abutments made up should also know about the underlying molecular and
of titanium or ceramic was similar to the healthy mucosa, cellular events occurring at these interfaces.
whereas that around the gold alloy abutments showed
improper wound healing and seal.
KEY POINTS
• Fibro-osseous integration • Osseointegration
• Additive and subtractive processes • Biological width
• Peri-implant mucosa
QUESTIONS 3. Schroeder A, van der Zypen E, Stich H, Sutter F. The reactions of

bone, connective tissue, and epithelium to endosteal implants with
titanium-sprayed surfaces. J Maxillofac Surg 1981;9:15-25.
1. What are primary and secondary bone contacts? 4. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds.
2. What is the main difference in the soft tissue around Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B.
implant and that around a natural tooth? Saunders Company; 2006.
3. What is the biological width around dental implant? 5. Misch CE. Contemporary Implant Dentistry. 2nd ed. St. Louis: Mosby;
1999 225-236.
4. What influence does the surface topography have on
6. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's
osseointegration? Clinical Periodontology. 11th ed. Philadelphia: W.B. Saunders
5. How does quality of bone affect the primary stability Company; 2012.
of an implant? 7. Lindhe J, Lang NP, Karring T. Clinical Periodontology and fmplant
8. Abrahamsson I, Berglundh T, Lindhe J. The mucosa! barrier following
Suggested readings abutment dis/reconnection. An experimental study in dogs. J Clin
Periodontol 1997;24:568-72.
1. Albrektsson T, Br anern ark P-I, Hansson H-A, Lindstrom J. 9. Buser D, Weber HP, Donath K, Fiorelljni JP, Paquette DW, Williams
Osseointegrated titanium implants. Requirements for ensuring RC. Soft tissue reactions to non-submerged unloaded titanium
a long-lasting, direct bone anchorage in man. Acta Orthop Scand implants in beagle dogs. J Periodontol 1992;63:226-36.
1981;52:155-70.
2. Branemark PI, Adell R, Breine U, Hansson BO, Lindstrom J, Ohlsson
A. Intra-osseous anchorage of dental prostheses. I. Experimental
studies. Scand J Plast Reconst Surg 1969;3:81-100.
CHAPTER
60
Diagnosis and Treatment Planning
in lmplantology
CHAPTER OVERVIEW
Diagnosis and treatment planning is the key to any implant position, angulation, size, soft tissue health, contour,
successful treatment. A good treatment planning allows and color must be ideal to obtain the result. Hence, after
for an organized documentation of patient's pretreatment clinical, radiographic, and model analysis the dentist should
condition and allows proper case selection before embark- discuss the treatment options such as number of implants,
ing on with implant treatment modality. position, steps of treatment, time required, expenditure, and
Selection of a case for implant placement depends on a de- the limitations of treatment planned.
tailed history taking, clinical examination, radiographic ex- The success of the implants can be jeopardized by
amination, and study cast evaluation. History taking should the various medical conditions, behavioral factors, and
evaluate general condition of patients and their financial general factors of the patient which can affect bone
situation, and should identify the specific oral problems, and healing. Those medical conditions of the patient that
and the aesthetic and functional demands of patients before can interfere with healing both directly and indirectly
committing to implant therapy. When the patient's expecta- should be evaluated in order to identify absolute and rela-
tions are high, all conditions such as bone volume, location, tive contraindications.
INDICATIONS Medical
• Autoimmune diseases
The treatment indications for dental implants are ex-
tensive and include patients with • Uncontrolled diabetes mellitus
• Patients undergoing radiation therapy
• Edentulous mandible • Patients on steroid therapy
• Edentulous maxilla • Psychological problems
• Edentulous frontal regions • Smoking and stress.
• Kennedy class 2 and class 3
• Single tooth loss.
Dental
CONTRAINDICATIONS • Local pathology
• Poor oral hygiene
These are described under general, medical, and dental • Close proximity to the vital structures
conditions. • Inadequate bone.
All the above contraindications do not necessarily
General
mean that implants should not be placed in such patients
• Cost factor at all. They indicate a less than optimal success rate for
• Nonmotivated patient. the implants.
CH A PT ER 60 DIA G N O SIS A N D TREATM EN T PLA N N IN G IN IM PLA N T O LO G Y 531
Absolute contraindications for implant therapy may be sum- challenging in them because the disease frequently
marized as follows: interferes with patients' manual dexterity. In addition,
these patients are usually on multiple medications
1. Recent myocardial infarction
including steroids which may interfere with healing
2. Uncontrolled and treatment-resistant diabetes
and also result in secondary osteoporosis.
3. Valvular prosthesis
3. Metabolic bone diseases
4. Severe renal disease
These include Paget disease, hyperparathyroidism,
5. Advanced and untreated osteoporosis
osteomalacia, and osteoporosis. These diseases alter
6. Severe and uncontrolled endocrine gland disease
calcium, phosphorous, and vitamin D homeostasis
7. Acquired immuno deficiency syndrome (AIDS)
which in turn impairs the mineralization needed for
8. Chemotherapy in progress
osseointegration.
9. Radiotherapy in progress
4. Neurologic diseases
Although neurologic diseases themselves may not
preclude successful implant treatment, problems such
PATIENT EVALUATION as cerebral palsy, muscular atrophies, and Parkinson
disease may compromise the patient's ability to main-
Treatment planning should be done for every case ir- tain oral hygiene.
respective of simplicity or complexity of the case in a 5. Renal disease
sequential manner. History of a patient should be empha- Patients with impaired renal function are at high risk
sized on general, medical, and behavioral factors. for skeletal surgical procedures. Chronic renal fail-
ures can result in secondary hyperparathyroidism and
impaired vitamin D metabolism. Renal osteodystro-
General Evaluation phy results in poor bone quality and excessive min-
Age eralized osteoid formation which in turn can interfere
with osseointegration. Hence, such patients should be
The minimum age of the patient is often a concern
avoided.
for maxillary anterior tooth replacement. Most often age
6. Corticosteroid therapy
guidelines are related to the patient's biological age more
This may pose an increased risk of implant failure as
than chronological age. As a general rule implant inser-
it can cause suppression of the inflammatory response
tion in the anterior maxilla is delayed for females until
and modify wound healing.
at least 15-16 years of age and in males until 17-18 years
7. Radiation therapy
of age.
This can affect cell population as well as blood vessels
and can damage DNA. Acute changes seen in such
Medical Evaluation patients include mucositis and xerostomia and late
changes include cell death, impaired susceptibility
The most commonly encountered medical problems to infection, impaired and delayed bone healing, and
that need special attention are as follows: osteoradionecrosis. Thus, the end result may be hypo-
l. Diabetes mellitus vascular, hypocellular, and hypoxic tissue that does
This is a metabolic disease that affects various organs not tolerate traumatic and surgical insult. Based on
throughout the body and is common in the elderly. animal trials certain authors have recommended wait-
Microvascular abnormalities seen in these patients re- ing 1 year after radiation to ensure that patient is free
sult in thickening of the capillary basement membrane of disease and to improve the healing capacity of the
and can impede circulation to the implant bed, and bone before preimplant placement.
thus healing may be impaired. Diminished neutrophil
chemotaxis and decreased phagocytic activity make Behavioral Factors
these patients more susceptible to infection and these
findings were similar for both insulin-dependent and Smoking
non-insulin-dependent patients. Hence, the decision Nicotine, the most determinantal component of tobac-
to place implants in such patients must be carefully co, causes discharge of norepinephrine and epinephrine
made. resulting in vasoconstriction. It also affects the adhesive-
2. Rheumatologic disease ness of platelets resulting in an increased risk of throm-
Owing to the widespread systemic effects that are found botic microvascular occlusion and ischemia. Smoke is
in these patients, higher incidence of complications found to interfere with the blood's oxygen-carrying
and failures is associated with them. Adequate post- capacity resulting in cellular hypoxia and impaired
operative oral hygiene and home care may be more wound healing. Although placement of implants in
smokers is controversial, it is advisable to ask the pa- there is large amount of facial bone resorption resulting
tient to refrain from smoking for 1 week before surgery in facial concavities along the bony ridge. Inadequate
and 2 months after surgery to promote the early stages care while osteotomy preparation can result in facial
of osseointegration. cortical perforation.
3. Arch form
Alcoholism The arch form plays an important role in the treatment
Chronic alcoholism can result in liver dysfunction, planning for multiple or full-arch implant placement,
impaired coagulation, abnormal white blood cell counts, as it can influence the number and positions of the
anemia, cardiac disorders, and neurologic disorders. This implants required for implant prosthesis. A square arch
can influence the surgical outcome and is considered as a requires only two implants in the canine positions to
relative contraindication for implant placement. restore the anterior maxilla and mandibular region.
But an ovoid arch requires three implants - one at the
Parafunctional habits central incisor region and one implant on either side in
Habits such as bruxism are considered as a potential the canine positions to restore the anterior maxilla and
risk factor for implant failure and are generally considered mandibular region - and a tapered arch form requires
as a contraindication for dental implants. five implants anterior to canine region (Fig. 60.1).
4. Adjacent tooth mobility
When tooth adjacent to the edentulous area is peri-
CLINICAL EXAMINATION
odontally involved, mobility of the tooth is a frequent
AND EVALUATION
finding. During excursions the teeth may move out of
occlusion and the load of several teeth may be exerted
This step includes inspection and palpation along with
solely on the implant crown. Hence, single-tooth im-
radiographic evaluation. Here a thorough examination
plants surrounded by anterior mobile teeth are not
of oral tissues is done with emphasis on the following:
indicated unless the occlusion is relieved to distribute
1. Oral hygiene and detection of any soft tissue pathology forces to the natural teeth.
Implant procedure should be initiated only if the level 5. Interarch and interdental space
of maintenance of oral hygiene is satisfactory as poor Judgment of interarch and interdental space is es-
oral hygiene is an established risk factor for implant sential for the accessibility of instruments as well as
failure. Advanced periodontitis should be treated prosthesis construction (Fig. 60.2A and B). Interarch
before implant therapy and any pathology detected distance is measured from the occlusal plane to the
should be treated before implant placement. bone level. A minimum of 8 mm of crown height space
2. Ridge morphology is required for a single-unit cement-retained restora-
Anterior mandible is the area where the bony ridge tion. If the crown height space is less than 8 mm, it
changes its axial direction at different stages of resorp- can cause problems such as compromised retention of
tion. Careful evaluation should be done at this site to cement-retained prosthesis and inadequate space for
avoid any dehiscence through the facial and lingual occlusal ceramic layer buildup. Due to lack of vertical
cortical plate during osteotomy preparation. In the pos- dimension, if an ideal implant position is not possible,
terior mandible, care should be taken to avoid the pen- angulated abutments could be another option in some
etration of the submandibular fossa which is located situations.
below the mylohyoid line posterior to first molar. In Interdental space refers to the mesiodistal dimensions
the maxilla in patients with longer edentulous state of the edentulous area. Diameter of the implant should
FIGURE 60.1 Arch forms. (A) Tapered arch; (B) ovoid arch; (C) square arch.
FIGURE 60.2 Spaces (A) Adequate interarch space; (B) adequate interdental space.
FIGURE 60.3 Interdental space (A) Distance of 1.5-2 mm between the implant and tooth; (B) distance of 3 mm between two adjacent implants.
be selected in such a way that there is adequate bone diameter and position of the implants as greater forces
between two adjacent implants, and between the Im- are expected when an opposing natural dentition is
plants and adjacent teeth. A distance of a minimum present when compared with a full denture.
of 1.5-2 mm between the implant and the tooth and a 7. Aesthetic considerations
minimum of 3 mm between two adjacent implants is For an aesthetic implant the ideal requirement would
preferred as it enables spontaneous papilla regrowth be a proper bone volume and a healthy gingiva. The
at the crest and helps to maintain the vitality of inter- various factors to consider when planning implants
septal bone (Fig. 60.3A and B). in the aesthetic region are gingival smile line, thick-
6. Status of opposing dentition and occlusal plane ness and health of the overlying soft tissues, presence
Edentulous state for a longer duration may result in of adjacent restorations, size and shape of interdental
supraeruption of the opposing teeth or mesial drifting papilla, dimensions of edentulous space, and height
of the adjacent teeth. And this may interfere during the and thickness of the ridge. A medium lip line and a
implant placement and restoration. Hence, any occlusal high lip line expose the clinical crown, as well as the
discrepancy should ideally be corrected before implant interdental papilla, making aesthetic implant therapy
placement. in such patients a great challenge. Hard and soft tissue
The type of dentition opposite to an edentulous arch manipulation often becomes mandatory to achieve ide-
should also be considered when deciding on the al aesthetics. Implant diameter that is selected should
closely match the restoration diameter for a smoother

emergence profile and to minimize the potential of
overhangs. An ideal implant position in the aesthetic
region should be in such a way that the implant is in-
clined faciolingually toward the incisal edge, the me-
siodistal angulation is parallel to the adjacent teeth,
and apicocoronally it is 3-5 mm above the adjacent
r-------
cementoenamel junction (CEJ).
H
8. Soft tissue/gingiva
L
a. Thick keratinized gingiva and gingival biotype
The soft tissues around an implant prosthesis play
an important role in the success of an implant resto-
ration. Presence of an adequate zone of nonmobile,
keratinized soft tissue around an implant restoration
has shown to resist marginal tissue recession and
pen-implant infection.
--r-------·
L-
Moreover, thickness of the gingiva is also an impor-
tant factor in predicting the aesthetic outcome of the
restored implant. A thin scalloped periodontium
_____________l _
has a tendency to develop soft tissue recession in
response to trauma and periodontal infection which FIGURE 60.4 Width (W), height (H), and length of the implant (L).
can create an empty space called black triangle. So
soft tissue grafting is advocated when there is a b. Available bone length
deficiency of thick keratinized gingiva around an The mesiodistal width of available bone is limited
implant. by adjacent teeth or implants. A minimum of 1.5 mm
b. Position and architecture of the interdental papilla of bone should be there between an implant and the
When a tooth is lost, the thin interseptal bone disap- tooth. This enables spontaneous papilla regrowth at
pears and the bone remodels in a sloping fashion the crest and maintains the vitality of the interseptal
from palatal to the more apical facial bony plate. As bone. If multiple single implants are placed, then
a result the interdental papilla is depressed com- the gap space has to be divided accordingly. If two
pared with its level between healthy adjacent teeth. implants are placed, then there should be a 3.0 mm
The papilla height is also affected as a result of the of bone between two implants. It is very much es-
lack of interproximal contact with the missing tooth. sential for an implantologist to keep in mind a mini-
Hence, soft tissue manipulation to restore the proper mum and a maximum diameter for the implant to
contour of the papilla is often required around the replace a particular tooth to avoid postrestorative
implant. complication.
9. Availability of bone in the edentulous region of the jaw c. Available bone height
This is an important factor in selection of the The length of an implant is selected based on the
implant diameter, position, and number. The implant available height. The height of available bone is
dimensions are expressed in terms of width and length. measured from the crest of the edentulous ridge to
The implant length corresponds to the height of avail- the landmarks such as maxillary sinus or the man-
able bone. And the diameter of the implant is related dibular canal. This means when working above
to the width and mesiodistal length of bone (Fig. 60.4). the inferior alveolar nerve, a minimum height of
a. Available bone width 9-10 mm is needed for the safety placement of a
This is measured between the facial and lingual 7-mm-long implant. Whenever possible the im-
plates at the crest of potential implant site. The plant fixture length should be 10 mm or longer
minimum buccolingual width of bone needed for for a standard 3.75-mm-wide implant. Shorter
an implant of 3.75 mm diameter is 4 mm, so that implant should not be used in areas of potentially
implant in final position is covered by at least high stress. If the length is increased by 10-15 mm,
1 mm bone on all sides for predictable results. then the maximum cervical load is reduced by 10%
There are different methods of measuring this buc- and if the diameter is increased from 3.8 to 6.5 mm,
colingual dimension. The most commonly used the maximum cervical load is reduced by 60%.
method is the use of a bone caliper. A diagnostic 10. Root inclinations
cast also helps in determining the width of the The main areas of concern are the maxillary and man-
ridge. dibular canine regions. Maxillary canine shows distal
FIGURE 60.5 X-ray showing implant close to the adjacent teeth. FIGURE 60.6 Implants placed in tripod position.
inclination of its root, while mandibular canine shows design, surgical approach, healing time, and progres-
the mesial inclination of its root. Hence, while replac- sive bone loading.
ing maxillary first premolar, implant apex should be Classification and clinical significance
angled distally to remain parallel to the maxillary Lekholm and Zarb have given four groups to describe
canine root. Improper planning and placement of the the quality of bone tissue based on its density as 01,
implants can encroach upon the periodontal ligament 02, 03, and 04. The bone quality that is found primar-
of the adjacent teeth, making them symptomatic, and ily in the anterior mandible or symphysis is 01, i.e.,
may require root canal therapy (Fig. 60.5). dense compact bone. This bone can support great force;
11. Bone and implant angulation thus, shorter and fewer implants can be placed in this
The angulation of implants is an important factor in region. But 01 bone is difficult to prepare and requires
predicting the success/failure rates of implants. Ide- more irrigation to prevent overheating during prepa-
ally an implant is aligned with the forces of occlusion ration. Another drawback of this bone is that there is
and is parallel to the long axis of the prosthetic restora- less blood supply to this bone compared with that to
tion. Minor discrepancies are not clinically significant other types. And since the blood supply is mainly from
but if loads are at an angle of 20° or more to the long periostium only minimal reflection of the periostium
axis of implant, load magnification can result lead- should be done during the surgery. 02 bone is found
ing to progressive irreversible bone loss. Most of the in edentulous areas, posterior mandible, and anterior
time in the anterior region due to labial undercuts maxilla. It consists of a thick layer of compact bone sur-
and resorption after tooth loss, implants are placed rounded by a core of dense trabecular bone. Compact
at an angle. Similarly in the posterior mandible due bone offers a much greater surface area for mineralized
to submandibular fossa the first premolar is placed tissue to implant contact than cancellous bone. Clinical
at 10° to horizontal plane. First molar is placed at 15° studies have shown that areas of the jaw exhibiting thin
and second molar at 20-25°. layer of cortical bone and large cancellous space such as
Another factor to be taken into consideration posterior maxilla have significantly lower success rates
when deciding the implant position during multiple than areas of dense bone structures. 03 bone consists
implant placement is that they should be placed in a of a thin layer of cortical bone which is surrounded by
tripod position (edentulous areas) in order to mini- a low-density trabecular bone. This is mainly found
mize the transmission of bending forces on each im - in the anterior maxilla. 04 bone is most commonly
plant (Fig. 60.6). seen in long-term edentulous posterior maxilla and
12. Bone quality consists of fine trabecular bone. With large marrow
The shape and bone quality must be regarded as the spaces a smaller direct implant to bone contact area
most influential factors affecting implant survival. results, which means that forces are distributed over
Bone quality depends on good vascularity and densi- a smaller given area. Implant failures are more in 04
ty, whereas quantity refers to the volume of remaining bone. Hence, this type of bone requires longer, wider,
bone. The density of bone can influence the implant and numerous implants replacing each tooth.
TABLE 60.1 Implant Placement and Anatomical Consideration
Structure Minimum required distance

Maxillary sinus 1 mm
Nasal cavity 1 mm
Inferior alveolar 2 mm from the superior aspect of the

canal bony canal
Mental nerve 5 mm from anterior or bony foramen
Inferior border 1 mm
13. Anatomical considerations

Implant surgeons should be fully conversant with all
anatomical structures that they are likely to encoun-
ter or that will affect implant placement, and these
include: FIGURE 60. 7 Sectioned maxillary cast for ridge mapping to gauge
a. In the maxilla the dimensions of the underlying bone.
Air sinuses, nasopalatine canal, floor of nose, nasal
spine, and palatine and pterygoid vessels
b. In the mandible
Sublingual vessels, mental nerve, inferior dental angulations, thickness, and vertical bone height at the
nerve, incisive branch of inferior dental nerve, and center of the jaw.
genial tubercles Panoramic radiography: Although the resolution and
c. Teeth sharpness of panoramic radiographs are less than
Position, length, and angulations of roots adjacent those of intraoral radiographs, this is an excellent tool
to implant sites. for the overview of maxillofacial area. Angular mea-
The recommended safety margin in relation to the surements on this view tend to be accurate, but linear
anatomical structures is given in Table 60.1. measurements are not. Since an accurate estimate of
the distance between the marginal bone crest and the
Diagnostic Casts critical anatomical structures is necessary in order to
select implants of appropriate lengths for placement,
These help to determine the height and width of the magnification in orthopantomogram (OPG) can be
edentulous ridge and the amount of ridge resorption. determined by placing ball bearings at the site during
This is done by ridge mapping where the width of the exposure. The diameter of the spheres on the X-ray
overlying mucosa is probed and measured from differ- film must be compared with their actual 5-mm sizes.
ent directions to gauge the actual width of the underly- This can help in determining the amount of available
ing bone (Fig. 60.7). The minimum buccolingual width bone in that region (Fig. 60.8).
of bone needed for an implant of 3.75 mm is 4 mm. Computerized tomography: This was earlier indicated
in difficult cases such as placement of implant close to
Radiographic Examination and Imaging nerve, extreme atrophy, or unusual anatomy and when
Techniques considering augmentation. With advancement in the
diagnostic technologies today, majority of the implan-
The objectives of preoperative implant imaging in- tologists prefer dental computerized tomography (CT)
clude all necessary surgical and prosthetic information scans as they give an accurate three-dimensional mea-
to determine the quantity, quality, and angulations of surement of the available bone. Computerized implant
bone, to select the potential implant site, and to verify planning on a 30 computerized tomographic data and
absence of pathology. The radiographic techniques navigated surgery have shown to improve the accuracy
commonly used for implant treatment planning are as of prosthodontic-driven implant positioning and mini-
follows: mize the risk of damaging vital anatomical structures.
Periapical: This view gives higher resolution and The disadvantages of navigated surgery are the initial
greater accuracy. It is indicated for single-tooth im- cost of the system and training time. Moreover, the
plant placement but is of limited value for extensive accuracy depends on the various components of the
edentulous sites. system. However, at present there is no ideal imaging
Lateral cephalograms are used for completely edentu- techniques in the field of oral implantology that would
lous patients especially in mandible because they show be acceptable for all patients.
One-Stage Versus Two-Stage Implant Surgeries

Endosseous implants can be placed as either one-stage
implant, meaning the coronal portion stays exposed
through gingiva during the healing period, or two-stage
implant, meaning the top of the implant is completely
submerged under gingiva. In two-stage procedure, the
head of the implant needs to be surgically exposed with
a second surgery. In the mandible, the implants are left
undisturbed for 2-3 months after placement, whereas
in the maxilla, they remain covered for approximately
4-6 months because of slower healing due to less dense
bone. Even in one-stage implant surgical approach the
implants can be left unloaded and undisturbed for a pe-
FIGURE 60.8 X-ray with ball bearings.
riod similar to the implants placed in the two-stage ap-
proach when the situation is not aesthetically demanding
or when the primary stability is less than 35 N m.
The advantage of one-stage surgical approach is that
SURGICAL ASPECTS OF IMPLANT the mucogingival management around the implant is
PLACEMENT easier, and patient comfort increases because of fewer
surgeries. But when there is an extensive bone loss around
Informed Consent the implants and in a situation where augmentation is
necessary, a two-stage surgical approach is recommended.
Oral implantology is never a lifesaving necessity.
Hence, one can do without dental implants even if this Second Stage Surgical Technique
means that the quality of life is less and function is more Second stage surgery is done after 3-4 months in case
difficult. Lord Templeman in Sidaway v Board of Governors
of mandible and 5-6 months in case of maxilla as this bone
of the Bethlem Royal Hospital and the Maudsley Hospital is normally more cancellous. When soft bone is present,
said that the only way a medical practitioner can law- healing time should be extended by 1 or 2 months so that
fully carry out nonemergency treatment on a patient quality of bone is improved.
is with the patient's consent. Hence, a signed written
Exposure of the implant at stage 2 can be achieved with
informed consent stating his/her wish to undergo im- minimal flap reflection or sometimes making a very small
plantology treatment is a must before the initiation of incision over the implant just to allow removal of the
the treatment. If consent has been obtained, then if the
cover screw and attachment of a gingiva former /healing
treatment is competently carried out but nevertheless abutment. This helps to create good mucosal adaptation
results in damage by virtue of one of the risks which and healing before selection of the abutment for the final
had been explained, no action will lie in negligence. The restoration (Fig. 60.9).
patient can consent to the proposed implant treatment
only if the issues such as treatment alternatives, risk of
implant surgery, long-term prognosis, and cost have
been discussed.
IMPLANT SURGERY
It goes without saying that all implant surgeries should
be performed in a sterile environment to avoid contami-
nation of the implant fixture and to enhance the long-
term stability. Generally implant surgery is done under
local anesthesia. But oral or intravenous sedation can
also be used if necessary. The patient should rinse with
chlorhexidine gluconate for 30 s immediately before the
procedure. Every effort should be made to minimize
the risk of contamination of the implant surfaces from
gloves, instruments, suction tubing, or saliva. FIGURE 60.9 Implants with gingival former.
FIGURE 60.10 Flap design (A) Cresta! incision; (B) mucoperiosteal flap reflection.
In some cases bone grows over the cover screw and this additional length when drilling near vital anatomi-
this necessitates greater soft tissue reflection to allow bone cal structures.
removal with hand instruments or burs. Orientation of the osteotomy site can be checked with a
direction indicator. When placing more than one implant,
Two Stage Surgical Technique place a direction indicator into the completed 2-mm pilot
hole and proceed to the next implant site. Align the 2-mm
Flap Design and Incision drill parallel to the direction indicator and drill the next
The two different flap designs used are vestibular in- osteotomy.
cision and crestal incision. The initial rationale of using Next the osteotomy site is enlarged at the alveolar crest
vestibular incision was to keep the incision site away from with a round bur. This prevents subsequent burs from
the implant. At present there is no evidence to show that locking on jagged alveolar crest. The osteotomy site is
one technique is more advantageous than the other. So then gradually enlarged to the size of implant diameter
the decision to use crestal or vestibular incision is based by sequential drilling (first 2 mm, then 3.5 mm, and finally
on the surgeon's preference. The crestal incision is usually 4.3 mm; Figs 60.11 and 60.12).
preferred due to the ease in handling the tissue. This is
followed by vertical releasing incisions in order to allow Dense Bone Protocol
better exposure of the surgical site and to allow proper If dense bone is present, 4.3 mm drill is followed by a
repositioning of the surgical flap without tension. A muco- dense bone drill that matches the size and length of the
periosteal flap is reflected on the buccal and lingual sides. final tapered drill used. This is done at 800 rpm.
Thus, it is possible to inspect any concavities or protru-
sions of the jaws, nerve entrances, and structures that Screw Tap Protocol
may influence the positioning of the implants (Fig. 60.lOA Using internal irrigation, place the end of the screw
and B). Alveolar crest is visualized and bone is leveled in tap into the prepared implant site with firm pressure and
the presence of any sharp bone edges. The crest should
be 2 mm wider than the implant being used.
Drilling Sequences
Once the implant length and diameter are finalized, the
pilot drill of 2 mm is used to initiate the osteotomy. Care
should be taken not to expose the bone to a temperature
more than 43°C as it can lead to bone necrosis leading to
the formation of fibrous tissue around the implant instead
of bone. This can be avoided with the help of external
and internal irrigation, and the drilling must be done at
a speed of 1200-2500 rpm. The pilot drill has horizontal
markings corresponding to the length of the implant to
be placed. The drills are approximately 1 mm longer than FIGURE 60.11 Sequence of drills used for placement of Noble Replace
the implant being placed. Hence, one should allow for 4.3 mm diameter implant.
FIGURE 60.12 Steps in implant procedure. (A) Pilot drill for initial preparation of osteotomy site; (B) 3.5 mm narrow platform till the desired
depth; (C) 4.3 mm regular platform to the desired depth; (D) dense bone drill of 4.3 mm diameter to the desired depth; (E) screw tap of 4.3 mm
diameter; (F) implant insertion; (G) Cover screw in place.
begin rotating the screw tap slowly at 50 rpm. When the overcompress the surrounding bone, compromising os-
threads engage, switch the handpiece to the reverse mode seointegration. A surgical manual torque wrench with a
and back the screw tap out. Do not pull on screw tap. surgical adapter can be attached to the implant driver
to place the implant to its final depth. Implant in final
Implant Placement position should be firm and immobile following which
Once the implant osteotomy is completed, the sterile a cover screw is placed. The flaps are then approximated
implant is removed from the sterile vial. Set the drill- without tension (Fig. 60.13).
ing unit on low-speed drilling (25 rpm) and choose the
torque depending on bone quality (20-45 N cm). The
implant driver is then connected to the contra-angle
handpiece and the implant is picked up and carried to COMPLICATIONS
the osteotomy site. Implant is placed into the osteotomy
site until it is fully seated into the prepared site. Do Complications during implant placement surgery can
not exceed 45 N cm of torque as overtightening may be classified as intraoperative complications or postopera-
compromise the integrity of the internal connection and tive complications. For a better understanding this can be
FIGURE 60. 13 Implant procedure (A) Implants in place with cover screw; (B) flap approximated.
categorized as treatment plan related, procedure related nerve injury is not taking care of the anterior loop of the
(Fig. 60.14A-G). inferior alveolar nerve.
The complications could manifest as a paresthesia when
1. Treatment plan related
the lesion is due to nerve compression, or a minor
This includes improper patient selection, improper selec-
stiffening of nerve fibers, without sectioning any of
tion of the implant diameter /length, improper selection
them (neuropraxia). Dysesthesia may occur in cases
of the type of prosthesis, and improper decision regard-
of nerve compression, traction, partial crushing, or
ing the position of the implants.
stretching (axonotmesis) of nerve fibers with differ-
2. Procedure related
ent intensities. Hypoesthesia or hyperesthesia may
This includes nerve injury, bleeding, sinus perfora-
be caused by extreme stretching and direct trauma
tion, cortical plate perforation, and devitalization of
on nerve fibers (neurotmesis).
adjacent teeth.
This includes excess widening of the osteotomy site,
Sinus Perforation and Implant Displacement
tearing of flap, lack of primary stability, off-axis im-
plant placement, wrong angulation, implants placed Invasion of maxillary sinus by an implant can occur
too close to each other, necrosis of bone due to excess during surgery as a result of displacement of implant
torque/heat during drilling, and gaping of the wound into the sinus. If this occurs, it needs to be removed im-
due to loose sutures. mediately. While performing sinus lift surgery if the per-
Infection, excess inflammation, and early exposure of foration is small, it may heal without much problem. But
the cover screw. when the perforations are large, it is better not to proceed
with implant placement.
Neurosensory Impairment
Neurosensory impairment may occur at any time dur- Wrong Placement
ing implant surgery including anesthesia administration, A wrong planning that involves a malposition or an
incision, raising a flap, during osteotomy preparation, overangulation would create an obstacle for carrying out
bone augmentation, implant placement, or due to soft tis- the prosthetic restoration and can also deteriorate long-
sue swelling after surgery. Most of the time radiographs term implant viability throughout the implant treatment.
taken are not of adequate quality and hence tracing of
nerve and canal becomes a problem, especially in poste- Bleeding
rior region. As a result implant placement is done with- This is a common complication that can happen in
out proper planning and this can result in nerve injury. some surgeries as a consequence of local anatomical
Calculations without considering the magnification and systemic causes and to a certain extent this can be
factor can also result in selection and placement of longer avoided with the help of CT in evaluating variations in
implant which result in nerve injury. Another cause of the anatomy.
FIGURE 60.14 Complications. (A) Perforation of buccal cortical plate; (B) improper positioning of the implant; (C) cover screw exposure;
(D) infection at the site of implant placement; (E) dehiscence at the implant site; (F) the site treated with bone graft; (G) abutment screw fracture.
Soft Tissue Lesions Lack of Primary Stability

A series of lesions can occur in soft tissues such as burn Lack of control over the instruments and not maintain-
lesions on the labial mucosa resulting from overheating of ing the drilling protocol can result in an enlarged osteotomy
the handpiece or flap tear due to excessive traction or by site which can affect the primary stability of the implant.
incorrect use of instruments. Hence, soft tissue handling Improper selection of implant in case of immediate implant
should be done with utmost care. placement can also result in lack of primary stability.
Dehiscence and Fenestration thus lead to loss of osseointegration around the neck of
Perforation of the buccal cortical plate is another factor the implant. An occlusal overload is found to occur in
which can affect the long-term survival of the implant. clinical situations such as implants placed in poor quality
Hence, if it occurs, the area needs to be augmented with of bone, heavy occlusal function associated with para-
bone grafts in conjunction with the guided bone regenera- function, and when prosthetic superstructure does not fit
tive (GBR) membrane. the implants precisely. Unfavorable forces may also lead
to mechanical complications such as screw loosening,
Swelling/Edema screw fracture, or fixture fracture.
Swelling can appear after surgery and can lead to tris- The three main causes attributed to implant fractures
mus and discomfort to the patient. Such swellings nor- are fatigue of design and materials, nonpassive fit of the
mally decrease with time. Wide flaps, bone regenerating prosthetic framework, and physiologic or biomechanical
techniques, and longer surgery time are the factors that overload. Abutment screw fracture is another frequent
trigger the occurrence of edemas. However, careful man- problem which is of major concern. If the fractured abut-
agement of the tissues can reduce this to a large extent. ment is buried within the internal threads of the implant,
it may be impossible to retrieve the screw. Such an im-
MUCOSAL DEHISCENCE plant may then be left buried beneath the mucosa. In
Mucosal dehiscences are associated with patients of some cases screw retrieval sets can be used successfully
poor-quality mucosa (thin biotype). Another factor lead- to salvage implants with deep broken fragments.
ing to surgical wound dehiscence is flap closure under
tension. Biological Complications
Infection These are bacterial in origin and characterized by bone
loss combined with a soft tissue inflammatory response
All sterilization and disinfection measures should be
that demonstrates suppuration with probing depth great-
carried out during implant surgery in order to avoid post-
er than 6 mm. This will be described in detail in the sec-
implant infection. If the infection is limited to soft tissue,
tion "Peri-implant Diseases and Management."
it will appear as a boil over the implant site. This can be
treated by establishing proper drainage. But if there is a
continuous purulent discharge, then there is a need for Postoperative Care
intervention as the infection may have reached the bone- After implant surgery, patients should be warned to
implant interface. If the implant is mobile at this stage, expect some swelling and some discomfort which can
then immediate removal of the implant is advocated. usually be controlled with oral analgesics. At times some
The vast majority of complications in implant surgery transitory disturbance in sensation is felt if surgery has
can be prevented by correctly selecting patients and been close to a nerve.
treating difficult cases in the most adequate way, while Patients should be advised:
knowing the risks, trying to avoid them with the neces-
sary information, and having carefully devised a specific • In most circumstances, not to wear dentures over the
plan for every patient. surgical area to avoid loading of the implants during
the healing period and due to the possibility of disrupt-
IMPLANT FAILURES ing the sutures.
The term implant failure is given when the implant • To use analgesics and ice packs to reduce swelling and
is not in a functional state. And this occurs in osseointe- pain.
grated implants and is often the result of excessive load • To keep the areas clean by using chlorhexidine mouth-
(mechanical) or infection (biological). wash 0.2% for 1 min twice daily.
• Not to smoke. This compromises healing of soft tissue
and bone and may increase the risk of implant failure.
Mechanical Complications Ideally patients should stop smoking for some weeks
Mechanical complications may arise as a result of oc- before surgery and for as long as possible thereafter.
clusal overloading. Forces resulting from functional or
parafunctional occlusal contacts of the natural teeth result
in physiologic adaptation of the tissues of the attachment IMMEDIATE IMPLANT TREATMENT
apparatus. If it exceeds beyond the adaptive capacity, then MODALITY
it results in occlusal traumatism. Since osseointegrated
implants have no periodontal ligament the adverse forces Immediate implant therapy has now become a most
generated by occlusal activity may lead to high stress and widely opted method in implant treatments as it reduc-
microfractures in the coronal bone to implant contact and es the treatment time compared with the conventional
techniques. There are various recommendations regarding Contraindications
timing of implant placement following tooth extraction.
• Presence of active infection with suppuration
• Presence of fenestration or fracture of buccal cortical
Immediate Placement
plate
Timing: At the same time as extraction. • Periapical lesion more than 5 mm
Advantages: • Insufficient healthy bone beyond the socket
• Thin tissue biotypes as it can cause recession resulting
• It leads to reduced waiting time, number of visits, and
in aesthetic disaster.
surgical procedures.
• It optimizes visualization of extraction socket. As is known, one surgeon's contraindication is
• Flap elevation is unnecessary. another's case report success, so there is no absolute con-
• It helps in preservation of bone at the implant site. traindication that has been suggested. In order to achieve
• Nonfunctional restorations may restore immediate greater success rate, it is advisable to follow certain guide-
aesthetics. lines. They are as follows:
Disadvantages: 1. Immediate extraction and implant placement should be
attempted only in single-rooted teeth and immediate
• Site morphology may complicate placement of
nonfunctional restoration can be a choice in the aesthetic
implants.
region provided a primary stability more than 35 N cm
• There is lack of soft tissue closure.
is achieved. A closed healing protocol is preferred in the
• Less initial bone to implant contact percentage can
anterior region when the primary stability is less than
affect the stability of the implant.
25 N cm in order to avoid any micromovement of the
implant during the initial healing period.
Early Placement 2. Maxillary canines have very long roots and the facial
Timing: 2-6 weeks after extraction. bone around them is very thin. This increases the chances
Advantages: of damage of the facial bone during extraction. Hence,
attempting immediate extraction and implant placement
• There is sufficient time for resolution of infection. in such a case can be a heroic attempt.
• It allows soft tissue healing to cover socket. 3. Selection of widest and longest possible implant
• It allows early healing of bone. is preferred to achieve maximum area of contact
Disadvantages: between the bone and the implant surface and to
achieve primary stability. A minimum of 3-5 mm of
Additional surgical procedure is required. bone height apical to the extraction socket should
There may be insufficient bone to achieve primary be available to adequately engage the implant apex
stability of the implant. and in case of submerged implants it would be ideal
to place the implants 1-2 mm apical to the bone crest
Delayed Placement to avoid micromovement.
Timing: 3-6 months after extraction.
Advantages:
• Allows more fill of socket with woven bone to provide
SURGICAL PROTOCOL
initial implant stability in large socket
1. Perform extraction of the nonsalvageable tooth without
• High predictability.
damaging the bony walls.
Disadvantages: 2. Debride the socket to remove any infected granulation
tissue and create healthy bleeding from the socket.
It results in thin labial plate due to resorptive process.
Check for any dehiscence and fenestrations at the
The success of an immediate implant placement into an
surgical site.
extraction socket is based on various clinical parameters
3. Measure the mesiodistal width of the extracted root
and the skilled approach of the implantologist.
and select the implant diameter so as to match the
mesiodistal dimension of the root at the CEJ.
Indication for Immediate Implant Placement 4. Measure the length of the root and select a length that
• Tooth loss due to trauma with minimum bone loss would allow the placement at the apex by at least
• Nonrestorable carious teeth 3-5 mm longer than the measured root length.
• Endodontic failures 5. A 2-mm pilot drill is inserted impacting the palatal bone
• Vertical and horizontal fractures of the roots. in the maxilla and the lingual bone in the mandible.
FIGURE 60.15 Immediate implant placement: Case 1. (A) Preoperative X-ray showing the root without the crown; (B) extraction of the root;
(C) final drill in place; (D) osteotomy site; (E) implant being placed at the osteotomy site; (F) implant fully seated;
FIGURE 60.15 (cont.) (G) implant with gingival former; (H) postoperative X-ray showing implant in place; (I) 3 months after removal of the
gingival former; (J) implant-supported restoration.
The drill should be inserted at least 2-3 mm beyond CONCLUSION

the socket apex.
6. Osteotomy is sequentially carried out depending on The goal of implant therapy is to obtain optimal aes-
the system specification without damaging the buccal thetics and function which requires a team approach of
cortical plate. specialists who can develop a mutidisciplinary treatment
7. Implant is placed and primary stability is checked with plan. Effective communication between the team and the
a torque rench. patient is key to its successful outcome.
8. The buccal gap is inspected and if more than 2 mm, a
bone substitute should be placed before suturing. This
distance is called jumping distance (Fig. 60.15).
KEY POINTS
• To ensure a proper case selection systematic data have • The selection of an implant diameter depends on me-
to be collected starting from patients' dental history siodistal space and buccolingual width of the alveolar
and medical history to clinical and radiographic bone available.
evaluation. • Select the implant length so that its apices are at least
at 2 mm distance from vital structures.
QUESTIONS 5. Buser D, Schenk RK, Steinemann S, Fiorellini JP, Fox CH, Stich H.
Influence of surface characteristics on bone integration of titanium
implants. A histomorphometric study in miniature pigs. J Biomed
1. Enumerate the absolute and relative contraindications. Mater Res 1991;25:889-902.
2. Enumerate the drilling sequence for implant placement. 6. Jovanovic SA. The management of peri-implant break down
around functioning osseointegrated dental implants. J Periodontal
1993;64:1176-83 [review].
Suggested readings 7. Mefefert RM, Lanager B, Fritz ME. Dental implants - a review. J
Periodontol 1992;63(11):859-70.
1. Adell R, Eriksson B, Lekholm U, et al. Long term follow up study
8. Meffert RM. Maintenance and treatment of the ailing and failing
of osseointegrated implants in the treatment of totally edentulous
implant. J Indian Dent Assoc 1994;73(3):22-5.
jaws. Int J Oral Maxillofac Implants 1990;5(4):347-59.
9. Meffert RM. Treatment of the ailing failing implant. J Calif Dent
2. Albreksston T, Br a n ern ar k PI, Hansson HA, Lindstrom J.
Assoc 1992;20(6):42-5.
Osseointegrated titanium implants; requirements for ensuring a
10. Worthington P. Medicolegal aspects of oral implant surgery aspect
long lasting, direct bone to implant anchorage in man. Acta Orthop
of oral implant surgery. Aust Prosthod J 1995;9(suppl):13-7.
Scand 1981;52:155.
11. Zablotysy MH. A retrospective analysis of the management of ailing
3. Albrektsson T, Zarb G, Worthington P, Eriksson ARA. Long term
and failing endosseous dental implants. Implant Dent 1998;73:185-91.
efficacy of currently used dental implants - a review and proposed
criteria of success. Int J Oral Maxillofac Implants 1986;1:ll-25.
4. Becker W, Becker BE, Newman MG, et al. Clinical and microbiological
findings that may contribute to dental implant failure. Int J Oral
Maxillofac Implants 1990;5(1):31-8.
CHAPTER
61
Prosthodontic Considerations
in Implant Restorations
CHAPTER OVERVIEW
The restorative phase of implant treatment starts even provisional restorations, planning occlusion, and cementing
before the implants are placed. Basic procedures involved the restoration. This chapter briefly outlines the various
in the restorative phase of implant treatment includes treat- prosthodontic procedures involved in delivering a success-
ment planning based on restorative-driven implant place- ful implant restoration.
ment, accurate impression registration, abutment selection,
IMPRESSION TECHNIQUES 3. Pickup-type impression coping: It is incorporated in the

impression and is removed from the mouth together
The objective of impression making in implant den- with the set impression. It is used with an open tray
tistry is to accurately capture the position of the implant impression technique (Fig. 61.2C).
platform and to accurately represent the soft tissue. There-
fore, the impression technique should be precise, utiliz-
ing a material which has a high resistance to permanent Laboratory Analogs
deformation, thereby ensuring master cast accuracy. They are replicas of implant restorative platforms and
abutments. Analogs need to be manufactured with accu-
racy as the fit of the final restoration depends on accuracy
Classification of the Impression Techniques
of the analogs.
Implant impression techniques are classified as follows
(Fig. 61.1): l. Abutment implant analog
l. Abutment level impression technique The abutment analogs are exact replicas of implant
2. Implant level impression technique
abutments and have to be manufactured to high degree
of accuracy. They are used with abutment level impres-
sion technique (Fig. 61.3A).
Impression Copings 2. Implant analog
Implant analogs screw into the apical portions of im-
There are three types of impression copings:
plant impression copings via the impression coping
l. Abutment impression coping: Abutment impression cop- screws. They are used with implant level impression
ings are placed directly onto standard abutments that technique (Fig. 61.3B).
have been placed onto implants. They identify the
location of abutments after they have been placed into
Abutment Level Impression Technique
the implants (Fig. 61.2A).
2. Transfer-type impression coping: It is retained in the Some standard abutments come with individual plastic
mouth when the set impression is removed. It is used push-on impression coping (e.g., Easy Abutment, Snappy
with a closed tray impression technique (Fig. 61.2B). Abutment of Nobel Biocare; Fig. 61.4).
I Impression
I techniques
Abutment level Implant level

technique technique
'
FIGURE 61.1 Classification of impression technique.
FIGURE 61.3 (A) Abutment analog; (B) implant analog.
Advantages
With this technique, laboratory technicians do not have
to arbitrarily grind or remove material from the master
cast to make properly contoured restorations.
Implant Level Impression Technique

It is the recommended technique with all abutment
types. An impression of the implant platform is recorded
to produce a working model.
Two commonly employed methods are as follows
(Table 61.1):
FIGURE 61.2 (A) Abutment impression coping; (B) transfer impres-
sion coping; (C) pickup impression coping. 1. Closed tray technique
2. Open tray technique
1. The selected abutment is placed into position on the Closed Tray Impression Technique (Indirect
implant platform (Fig. 61.4A). Transfer Impression Technique)
2. Plastic push-on impression copings are seated onto the In this technique implant head orientation is trans-
abutment and they should snap into place (Fig. 61.4B). ferred using the closed tray transfer impression coping.
3. An appropriate size of stock impression tray is selected.
4. The impression material (polyether or vinyl polysi- STEP-BY-STEP PROCEDURE
loxane) is injected around the coping and the loaded 1. With a hex driver the healing abutment is removed and
impression tray is seated (Fig. 61.4C). the implant platform is exposed (Figs 61.5 and 61.6).
5. Once impression material is set, the tray is removed. The implant platform should be free of soft and hard
6. The impression coping should firmly adhere within tissues (Fig. 61.6A).
the impression material (Fig. 61.40). 2. Seat the transfer impression coping and secure the
7. The abutment implant analog is now positioned into coping screw (Figs 61.5A and 61.6B). Impression cap
the coping. A working model is prepared. is placed over the coping (Fig. 61.5B).
8. The abutment can be left in position in the mouth and 3. Syringe and completely cover the coping assembly
provisional restoration is delivered or can be stored in with low-viscosity, light-body impression material and
the lab and the gingival former is replaced. load the stock tray or closed custom tray with heavy
body impression material to make a full-arch impres-
Indications sion (Figs 61.SC and 61.6C).
This technique is used only when the selected abut- 4. Remove the impression tray leaving the transfer impres-
ment does not require any modification. sion coping attached to the implants (Fig. 61.50).
C H A PTER 61 PRO STH O DO N T IC CO N SID ERATIO N S IN IM PLA N T RESTO RATIO N S 549
FIGURE 61.4 (A-D) Abutment level impression technique.
TABLE 61.1 Difference Between Open Tray and Closed Tray Technique
Open tray technique Closed tray technique

Pickup-type impression copings are used Transfer-type impression copings are used
Copings are removed from the mouth together with the set impression Copings remain in the mouth on removal of the set impression
A window has to be cut in the impression tray to allow access to the An impression tray without any window is used
retaining screw to allow release of the screw prior to removal of the
impression coping - impression assembly
The impression coping will be embedded in the impression material. After removal of the tray the impression coping is removed from
The implant analog is attached later the mouth and implant analog is attached. This assembly is re-
placed in the indentation left on the set impression
5. Unscrew the transfer impression coping from the implant tant that the coping relocates positively (Figs 61.SF and
and replace the gingival former on the implant. 61.6E).
6. Assemble the implant analog manually to the transfer 8. Apply lubricant where soft tissue replica material is to
impression coping using coping screw (Figs 61.SE and be applied. Syringe soft tissue replica material around
61.6D). the analog (Figs 61.SG and 61.6F).
7. Insert the implant analog-coping assembly into the 9. Working cast is prepared for further laboratory proce-
corresponding location in the impression. It is impor- dures. The resulting master cast should be an accurate
FIGURE 61.5 (A-G) Closed tray impression technique.
representation of both the soft tissue anatomy and not be sufficient space for access to the screws with the
fixture location (Fig. 61.6G). impressions in place.
2. It is indicated in patients with exaggerated gag reflex
ADVANTAGES where the impression needs to be removed quickly.
The technique is simple and quick.
DISADVANTAGE Open Tray Impression Technique

Reseating the transfer impression copings manually (Direct Pickup Technique)
into the impression may introduce potential inaccuracies. In this technique, implant platform orientation is
transferred using the open tray pickup-type impres-
INDICATIONS FOR CLOSED TRAY IMPRESSION sion coping. The pickup-type impression coping is the
TECHNIQUE more accurate type of impression coping as errors oc-
1. When there is limited mouth opening, closed tray cur on removal and replacement of the transfer-type
impression is indicated as the retaining screws of the impression copings, especially in the occlusogingival
pickup impression copings are longer and there may direction.
Remove healing cap Place the transfer coping Place the impression cap Make full arch impression
Index coping into impression Create soft tissue model Fabricate working cast
(E)
Assemble coping and implant analog
FIGURE 61.6 Closed tray impression technique. (A) Remove healing cap; (B, C) place the transfer coping and impression coping; (D) make full-arch
impression; (E) assemble coping and implant analog; (F) index coping into impression; (G) create soft tissue model; (H) fabricate working cast.
STEP-BY-STEP PROCEDURE 3. A stock tray may be modified or the custom tray may
1. With a hex driver the healing abutment is removed be fabricated. A window is cut out of the tray to allow
(Fig. 61.7). The implant platform should be free of soft clearance for the long coping screw and to allow for
and hard tissues (Fig. 61.7 A). the coping screw to be removed, as the body of the
2. Seat pickup impression coping and secure the coping transfer post will remain within the impression. Try in
screw (Fig. 61.7B). of the custom tray is done to verify that the long coping
Remove healing cap Place the transfer coping Block out hex hole Make full arch impression
l(E) • I
Assemble coping and implant analog Index coping into impression Create soft tissue model Fabricate working cast
FIGURE 61. 7 Open tray impression technique. (A) Remove healing cap; (B, C) place the transfer coping and block out hex hole; (D, E) make full-arch
impression and assemble coping and implant analog; (F) index coping into impression; (G) create soft tissue model; (H) fabricate working cast.
screw protrudes through it without interference. The 2. Height of implant level impression coping is
window is sealed with wax. significantly below the occlusal plane.
4. Syringe impression material around the coping to
completely cover the coping assembly and load the CONTRAINDICATION
tray with impression material to make a full-arch The method is contraindicated when there is insufficient
impression. The tips of the impression coping should be intraoral access as the coping screw is long and unscrew-
felt through the wax covering the window (Fig. 61.7C). ing the impression coping becomes difficult.
5. After the impression material has set, the copings are
unscrewed through the window on the tray and the PRECAUTIONS TO BE TAKEN WHEN MAKING
impression is removed from the mouth along with THE IMPRESSION
impression coping. On visual inspection, coping 1. Radiograph is made to ensure complete seating of the
margin should be clear and free from excess impression impression coping into the implant.
material. Impression material should be completely 2. Vinyl gloves should be used when a vinyl polysiloxane
adapted around the pickup impression copings. impression material is used to prevent inhibition of
6. Place the gingival former back in position on the setting reaction from the interaction of latex gloves
implant. with the material.
7. Assemble the implant analog to the impression coping
using coping screw (Fig. 61.70). ABUTMENTS IN IMPLANTS
8. Apply lubricant where soft tissue replica material is to
be applied. Syringe soft tissue replica material around Abutment is a component of the implant that supports
the analog (Fig. 61.7E). and/ or retains a prosthesis or implant superstructure. It
9. Working cast is prepared for further laboratory prevents rotation between components. The abutment
procedures (Fig. 61.7F). needs to resist conventional compressive, tensile, and
rotational forces.
ADVANTAGES
The transfer coping remains in the impression and the Types
inaccuracies of transferring are avoided.
Different types of abutments are available (Fig. 61.8)
DISADVANTAGE and can be categorized as follows:
There are more parts to manipulate. 1. Depending on the method offabrication
a. Prefabricated abutments (ready-made)
INDICATIONS
- Standard abutments
1. When multiple nonparallel implants(> 25°) are present, - Angled abutments
open tray technique is ideal as the impression is easily - Conical abutments
removed and inaccuracies in coping placement can be - Abutments for implant-supported complete
avoided. dentures.
Depending on the
axial relationship of Number of abutment
Method of fabrication Material Type of restoration Duration of use
the implant and the parts
abutment
.- Prefabricated . Gold - Cement

retained
.. Provisional - Straight .. Single piece
-- Custom made •.. Titanium

Screw •.. Permanent - Angulated •.. Two piece
retained
•.. For
Ceramic
attachments
FIGURE 61.8 Classification of abutments.

b. Custom-made abutments Prefabricated Abutments
- Castable abutments (UCLA abutments) • Standard abutments: They are implant restorative
- CAD/CAM abutments. components that attach directly to implants with
2. According to the number of abutment parts abutment screws that are made with titanium or
a. Single-piece abutments gold alloy. They are generally manufactured from
b. Two-piece abutments. commercially pure titanium as well as zirconium.
3. Depending on the material used They are symmetrical with a flat fixed gingival margin
a. Gold abutments for the restoration and available in various heights.
b. Titanium abutments They have a flat surface on the retentive element to
c. Ceramic abutments. prevent rotation. They can be screwed directly or press
4. Depending on the type of restoration fitted with some systems directly to implant head.
a. Abutments for cement-retained restorations They are used only for cement-retained restorations
b. Abutments for screw-retained restorations (Fig. 61.9A).
c. Abutments for attachments.
5. Depending on the axial relationship of the implant and the Several designs of standard abutments are available:
abutment
a. Straight abutment • Aesthetic abutments: Aesthetic abutments have
b. Angulated abutment. variable collar height which is lower on the facial
6. Depending on the duration of use and higher on the lingual side. These abutments are
a. Provisional abutments generally preferred for both anteriors and bicuspids
b. Permanent abutments. (Fig. 61.9B).
(A) (B)
FIGURE 61.9 (A) Standard abutment; (B) esthetic abutment; (C) angulated abutment.
• Angulated abutments: They are standard abutments with DISADVANTAGE

an angle of 15° to implant long axis (Fig. 61.9C). They are more expensive than standard abutments.
• Tapered abutments: They are standard abutments with
a conical shape. Two-Piece Abutments
The two-piece abutments have one component to en-
ADVANTAGES OF PREFABRICATED ABUTMENTS gage the antirotational element of the implant and the
1. Cost-effective other piece is the screw which is used to fix the abutment
2. Simple to use and implant body.
3. Limited chairside and laboratory time ADVANTAGE
4. Predictable retention for crown.
1. Antirotational under shear forces.
DISADVANTAGES
1. Margin of the crown does not follow the gingival DISADVANTAGES
contour because of the flat collar. 1. Screw loosening
2. It cannot be adjusted if the inclination of the implant 2. Torque and countertorque devices needed for preload
is not ideal. 3. Proper seating with radiograph required to be ensured.
3. It cannot be used in situations where multiple implants
with divergent angulations or adjacent tilted teeth are One-Piece Abutment
present. The one-piece abutment does not engage the antiro-
4. It cannot be used when reduced crown height is tational element of the implant but fits with the implant
present. platform.
INDICATION ADVANTAGES
1. Their use is limited to ideal situations where esthetics 1. No torque wrench needed
is not very critical. 2. Stronger
3. No screw loosening
4. Easy complete seating
CONTRAINDICATIONS
5. Less expensive
1. There is insufficient interocclusal space where the 6. Thicker walls to allow great freedom of preparation.
abutment would not have sufficient height to retain a
crown. DISADVANTAGES
2. Implant requires an angle correction of greater 1. Only to multiple abutments
than 15°. 2. Not indicated in single tooth restoration
3. Need for splinting multiple implants with divergent 3. Not for angled abutments.
angles exists.
4. If the collar height (the distance between the implant
platform and the gingival margin) is more than 1 mm Factors Affecting Abutment Selection (Table 61.2)
greater than the largest collar height offered by the 1. Depth of soft tissue: The depth of the soft tissue is the
manufacturer. vertical height from implant platform to the gingival
margin measured at the shallowest point on the labial
Custom-Made Abutments surface. This can be measured intraorally with a
They are individualized for each clinical situation. periodontal probe. It runs from the superior surface
The abutment is contoured to anatomic form. They can of the implant to marginal gingiva. To hide the metal
be semiprepared, fully customized (either cast or CAD/ collar of the abutment the chosen abutment should
CAM), or prepable abutments. They are available in a have the labial margin at least 1 mm subgingival. If the
variety of metals and ceramics. depth is more than 3 mm, restorations are difficult to
seat and removal of excess cement becomes difficult.
ADVANTAGES In these situations a customized abutment is indicated
1. They are more versatile. They can be used in situations as it allows the margin to be placed in relation to the
where multiple implants with divergent angulations, gingival contour.
extremes of crown height space, or labially inclined 2. Emergence profile: It is easier to achieve a good emergence
implants are present. profile if there is at least 3 mm of vertical space from
2. They help to achieve optimum emergence profile for the implant platform to gingival margin. This allows
the crown and thereby improve the aesthetics. a transition from an implant head which is often at
TABLE 61.2 Factors Affecting Selection of the Implant adequate required torque is reached, the screw should
Abutment be left for 2-5 min before retightening to the same
prescribed torque. This allows for the embedment
• Depth of the peri-implant soft tissues
relaxation of the screw and will allow the screw to
• Emergence profile
• Orientation of the implant perform optimally.
• Interocclusal space
• Retrievability
• Special aesthetic requirements
• Final restoration PROVISIONAL RESTORATIONS
The provisional crown should provide excellent emer-
gence profile and must be contoured well. Provisional
least 2-3 mm narrower than the cervical margin of the restorations are cemented using conventional eugenol- or
proposed restoration. If it is necessary to flare from noneugenol-based temporary cements.
the implant head to a wide-necked restoration in a
short vertical space, it is most readily achieved using
a customized abutment.
Temporization Prior to Second-Stage Surgery
3. Orientation of the implant: Small degrees of labial Totally Edentulous Patient
angulation can be accommodated by the standard 1. The existing denture is relieved over the implant sites
abutments. If standard abutments are used in and relined with a soft material.
situations with more labial angulation, they may result 2. Transitional implants may be placed in between
in overcontoured restorations or a labial surface that the permanent implants. A provisional restoration can
is too thin to mask the color of the metal. Angulation be fabricated or the existing denture may be modified
correction of more than 15° can be done only with to be supported by the transitional implants.
customized abutments. However, some amount of
abutment height around the abutment screw hole
Partially Edentulous Patient
must be present to provide adequate retention for the
crown. 1. A removable appliance can be made which is relieved
4. Interocclusal space: The distance from implant platform to protect the implant from function.
to the opposing tooth needs to be assessed. The 2. A "resin-bonded bridge" can be fabricated.
standard abutments require a minimum vertical space
of 6-7 mm. If less space exists, a fully customized Temporization After Second-Stage Surgery
abutment may be indicated. If the crown height space
is excessive, customized abutments are preferred Cement-Retained Restoration
where the height of the abutment can be optimized to 1. A provisional crown or bridge restoration can be
produce the best result. fabricated on a titanium or plastic temporary abutment.
5. Retrievability: A screw-retained restoration will be Techniques used for traditional temporaries on natural
easier to remove at a later stage if it is envisaged that teeth are used.
this will be required. A cemented crown will be difficult
to remove. Specific abutments for single tooth are Screw-Retained Restoration
available for the screw-retained restorations.
1. Screw-retained provisional restorations can be
6. Special aesthetic requirements: If the implant platform is
close to the labial cortical plate surface or if the labial fabricated using plastic or titanium temporary
gingival tissue is thin, the metal abutment shows abutments.
through the gingiva causing graying and a poor
appearance. A ceramic abutment is indicated in these
situations.
OCCLUSAL CONSIDERATIONS IN
7. Abutment tightening: Abutment is tightened with a
IMPLANT,SUPPORTED PROSTHESIS
hand torque wrench, to achieve a prescribed amount
of torque. The amount of torque will vary with
Importance of Occlusion
different implant systems and should be checked to
ensure optimal tightening of the abutment. Excessive The development of proper occlusion plays a crucial
forces could fracture the screw, while insufficient role in the success of the implant prosthesis. The implant-
force will leave the patient with a potential weak supported restorations function in a different manner
screw joint prone to screw loosening. Once the compared with the natural teeth. The fundamental
difference lies in the absence of periodontal ligament but not the implant. The occlusal contact at this stage
between the implant and the bone. should show similar intensity of contacts over both the
A healthy tooth will intrude by 28 microns supported implant crown and adjacent teeth, thereby sharing the
by the periodontal ligament. In the natural dentition, the load equally.
periodontal ligament acts as a shock absorber. The tooth The implant crown should not be placed without oc-
also receives protective feedback from the periodontal clusal contacts as this could result in movement of the
mechanoreceptors. Therefore, presence of overload will opposing teeth.
elicit a reflex from the patient in the form of sensitiv- The occlusal contacts are first checked in the intercus-
ity, pain, and mobility depending on the amount of pal position. Next the crown is checked for protrusive and
overload. lateral contacts. In protrusive movement, if the crown is
The fundamental nature of osseointegration (no peri- to be in contact, it should be shared with other teeth and
odontal ligament) means that proprioceptive and adap- not be the sole point of contact. In the lateral movement
tive potential is less than with natural teeth. the crown should confirm to the existing occlusal scheme,
either a group contact or canine guided. It is not desir-
• Implant is rigidly attached and therefore will move or
able for the implant restoration to act as the only guiding
intrude to a lesser degree.
surface for lateral movement. The contacts should be on
• The presence of overload will not elicit a reflex from
the center of the restoration so as to direct the forces along
the patient due to lack of proprioception.
the long axis of the implant.
• The implant does not have the adaptability to alter its
position much as tooth does.
Factors to Consider in Implant Occlusion

Occlusal Goal for Implant-Supported Factors to consider in implant occlusion are described
Restorations in Fig. 61.10.
1. Bilateral simultaneous contact
2. No prematurities in retruded contact position
3. Smooth, even, lateral, excursive movement with no CEMENTATION OF THE IMPLANT
working interferences CROWNS
4. Equal distribution of occlusal forces
5. Freedom from deflective contacts in intercuspal Prior to final cementation of the crown, the abut-
position ment screw should be checked for tightness and the
6. Anterior guidance whenever possible. abutment screw hole should be filled with cotton wool,
soft wax, gutta-percha, or similar soft material. This
will prevent the interference of the screws with the
Occlusal Adjustment in Implant Restorations cement which could prevent access in the future and
the head remains undamaged if the crown ever needs
The implant restoration should be adjusted with a thin
to be removed.
articulating paper (less than 25 microns) while the pa-
In considering implant-supported crowns, the ideal ce-
tient lightly taps the teeth together in centric occlusion
ment should be strong enough to retain the crown indefi-
(Table 61.3). Implant restoration should exhibit barely any
nitely, yet weak enough to allow the clinician to retrieve it
contact and the natural teeth in the arch should exhibit
if necessary. Traditional cements such as zinc phosphate
greater initial contact.
and glass ionomers are often recommended, but care has
Once the equilibration with light force is completed,
to be taken to ensure that the viscosity of the cement is low
the same foil should be held by the patient when heavy
enough for the crown to be fully seated. Temporary ce-
bite forces are applied. This depresses the natural teeth
ments are also recommended because of ease of removal
of the crown at a later date.
TABLE 61.3 Ideal Occlusion for Single Tooth Implant It is essential that exactly the right amount of cement
should be used as excessive cement extruding into the
No contact under light forces
gingival sulcus may be difficult to detect and remove. The
Light contact under heavy forces implant cement residue around the implant head can lead
Smooth, even, lateral, excursive movement with no working/ to peri-implant inflammation.
nonworking interferences Following cementation an intraoral periapical radio-
graph is taken to verify the seating and to detect the pres-
Occlusal forces directed down the long axis of the implant
ence of residual cement.
Bone quality
Extended healing time Occlusal contacts
Progressive loading Occlusal morphology Position
Flat central fossa Distribution and type of
Reduce cuspal inclination prosthesis
Bone quantity Reduce occlusal lable Decreased cantilever length
Implant number Along implant axis Cross-bite
lmDlant diameter redconta, Splinting Implant
Position
FIGURE 61.10 Factors to consider in implant occlusion.
Screw, Retained Restorations

TYPES OF IMPLANT,SUPPORTED
RESTORATIONS (Table 61.4). They are indicated when interarch space is limited
and/ or a screw-retained restoration is planned. The res-
l. Screw-retained restorations toration is retained by a screw that enters through the
2. Cement-retained restoration. occlusal surface of the prosthesis and threads into the
TABLE 61.4 Difference between Screw- and Cement-Retained Restorations
Screw-retained restorations Cement-retained restorations

Aesthetics Screw access hole in the labial region can affect aesthetics Aesthetics is not a problem
Retrievability Allows retrieval of the crown in the future due to easy Retrieval of the crown is difficult due to difficult access
access to the abutment screw to the abutment screw
Interocclusal Restorations can be secured to implants with a minimum Minimum of 5 mm abutment height is required to obtain
space 4 mm interocclusal space optimum retention for the restoration; hence, more interoc-
clusal space is required
Implant Implant angulation is critical to place the screw access hole Implant angulation is not so critical
angulation in the nonaesthetic area
Passivity Difficult to obtain passive fit for the restoration The restoration is more passive because of the cement space
Occlusion Screw access hole is closed with composite resin. This More stable occlusion can be achieved
can affect the occlusal table design and more chances of
ceramic fracture
Excess cement Removal of excess cement is not an issue Excess cement removal is an issue
implant. In anterior screw-retained crowns, the implant Advantages

is placed lingually to allow screw emergence through the 1. Simplicity of the procedure
cingulum area. In posterior screw-retained restorations, 2. Reduced cost
the access hole will exit through the central fossa of the 3. Hermetic sealing of the abutment-crown interface
prosthetic tooth. 4. Favorable aesthetics and crown contour
5. A single interface between abutment and implant
6. Elimination of unaesthetic screw access holes and
Advantages
greater resistance to porcelain fracture.
1. Easy retrievability of the crown at a later stage when
indicated Disadvantages
2. No margin of cement 1. Cement-retained restoration requires more vertical space
3. Takes less space than cement-retained restorations to accommodate the abutment, cement, and crown.
4. Easy access to the abutment screw if tightening 2. It is difficult to retrieve at a later date.
required 3. There is potential of an abutment screw becoming loose,
5. Predictable retention. while the cement-retained crown remains cemented to
the abutment.
Disadvantages 4. When the peri-implant tissue depth is more, there is
limited access to excess cement removal.
1. Screw hole must exit in suitable position for aesthetics.
2. Screw hole may sacrifice occlusal morphology as Indications
composite resin is used to seal the access hole.
1. Single- or multiple-unit implant restorations
2. Totally edentulous or partially edentulous arch
Indications 3. When long axis of the implant would create a screw
1. In situations where there is limited interarch space to access opening in the facial or buccal surface or a
accommodate cement-retained abutment screw-retained implant restoration
2. When there is a need to remove restorations or join
implants to further implants in the future
3. If the implant margin extends greater than 3 mm into
CONCLUSION
the subgingival environment.
Attention to detail during the prosthetic phase of
implant treatment can produce highly functional and
Cement, Retained Restorations aesthetic restoration. The treatment planning phase is
essential to make sure that the prosthodontic treatment
An implant abutment is screwed onto the implant. The is kept as simple and straightforward as possible and any
crown or restoration is cemented to the prepared abut- deviation from the fundamental principles can result in
ment, much like a prepared tooth. failed restorations.
KEY POINTS
• Implant treatment plan should be prosthetically driven; • The implant-supported restorations function in
therefore, restorative phase of implant treatment starts a different manner compared with the natural
even before the implants are placed. teeth.
• The impression technique should be precise, utilizing • Implant is rigidly attached and therefore will move or
a material which has a high resistance to permanent intrude to a lesser degree.
deformation, thereby ensuring master cast accuracy. • The presence of overload will not elicit a reflex from the
• The abutment needs to resist conventional compressive, patient due to lack of proprioception.
tensile, and rotational forces and must be carefully se- • The implant does not have the adaptability to alter its
lected. position much as tooth does.
QUESTIONS 9. Differentiate between screw-retained and cement-

retained implant restorations.
1. Classify impression techniques in implant dentistry.
2. Explain abutment level impression technique.
Suggested Reading
3. Explain closed tray impression technique.
4. Explain open tray impression technique. 1. Misch Carl E. Contemporary Implant Dentistry. 3rd ed. St Louis: Mosby
Elsevier; 2008.
5. Write indications for open tray and closed tray impres-
2. Carl Drago, Richard J Lazzara. Guidelines for Implant Abutment
sion techniques. Selection for Partially Edentulous Patients The Compendium of
6. Classify implant abutments. Continuing Education in Dentistry. January 2010 issue.
7. What are the various factors affecting abutment selection? 3. W Chee, S Jivra. Impression techniques for implant dentistry. British
8. Write a note on occlusal considerations in single tooth Dental Journal 2006; 201: 429-432.
implant restorations.
CHAPTER
62
Advanced Surgical Procedures
for Dental Implants
CHAPTER OVERVIEW
Dental implant therapy has brought about a paradigm bone in these sites and thus may require advanced pro-
shift in the concept of prosthetic rehabilitation of partially cedures to make them eligible to receive implants. These
as well as completely edentulous patients. A large per- problems may be overcome by various methods such as
centage of these patients have enough bone available in bone grafting, guided bone regeneration (GBR), sinus lift
the edentulous sites for routine implant placement. But procedures, distraction osteogenesis, bone expansion, and
up to 35% of them may have moderate to severe loss of bone augmentation.
MAXILLARY SINUS LIFT SURGERY tear of the lining membrane. The Schneiderian membrane
(the lining mucosa! membrane) of the maxillary antrum
This procedure may safely be done in most patients has rich blood supply as does the antrum itself, with the
requiring augmentation of the posterior maxilla, except posterior, middle, and anterior alveolar branches of the
in case of involvement of the maxillary sinus with chronic maxillary artery doing the honors. Since the lining and
or acute inflammation, pathology, infection, etc. Systemic the bony walls of the antrum have their own rich blood
factors that would preclude this procedure are the same supply, there is a high chance of bone graft survival in this
as those that contraindicate routine dental implant place- procedure, even if a tear of the membrane occurs.
ment, such as uncontrolled diabetes mellitus and drug or The material for augmentation may be autogenous
alcohol abuse. bone, xenografts, bone substitutes such as hydroxyapa-
tite, freeze-dried demineralized bone, etc. The sinus floor
augmentation can be mainly done by either the osteotome
Anatomy technique or the lateral window technique.
The maxillary sinus is pyramidal in shape, with its
apex toward the zygomatic bone and the base being the Osteotome Technique
lateral wall of the nasal cavity. The floor of the sinus forms For the classic osteotome technique (aka crestal ap-
part of the alveolar process of the posterior maxilla with proach, Summer technique, internal sinus lift) to be car-
close relationship to the roots of the maxillary molars and ried out, a bone height of 8-10 mm in the area is required,
premolars. When these teeth are lost, the alveolus loses its although with the more recent techniques, even 6-8 mm
function and undergoes atrophy. This, together with pos- bone height is sufficient for implant placement.
sible expansion of the sinus with advancing age, makes In this, a full-thickness flap is raised from the alveolar
the alveolar bone in this region very thin for placement crest and a pilot drill (2 mm diameter) is used to prepare
of implants. This is when the sinus lift procedure, which the osteotomy site up to 2 mm short of the sinus floor.
is a ridge augmentation technique, is mainly indicated. Then osteotomes of varying dimensions or widening
The maxillary sinus may be subdivided by septa/ septae drills are used sequentially to the same level. If the bone
in up to 30% of patients. This can make it more difficult for is of poor density, using osteotomes results in condens-
the sinus lift procedure to be carried out without causing a ing the bone laterally, thus enhancing peri-implant bone
CHA PTER 62 ADVANCED SURGICA L PROCEDURES FOR DENTAL IM PLANTS 561
density. The final osteotome diameter should be a little and the largest osteotome is tapped till sufficient amount
less than that of the intended implant, and this is tapped of sinus membrane elevation is achieved. This is followed
to fracture the sinus floor. Then the graft material is added by insertion of the implant (Case 1).
CASE 1 Osteotome technique. (A) Edentulous site with vertical bone height of 7 mm; (B) crestal incision; (C) mucoperiosteal flap reflected
and initial site marked with bur; (D) pilot drill used for preparation of the osteotomy site; (E) sequential drilling to widen the osteotomy site;
(F) final drill being used at the osteotomy site; (Continued)
CASE 1 (cont.) (G) osteotome insertion into the osteotomy site; (H) Osteotome being tapped to the desired depth; (I) implant placement;
(J) post-op radiograph after implant placement. Courtesy: Betsy S Thomas.
This technique has the advantages of being less inva- osteotomy can be done using a diamond/ carbide bur in
sive, no barrier membrane being required, less amount a rotary instrument. An oval-shaped window is prefer-
of grafting material used, etc. But it also has the disad- able since it would not have sharp edges which might
vantages of limited amount of sinus elevation, chances of tear the membrane. The bone may be left on the mem-
misalignment of osteotome long axis, mental trauma to brane in which case it would form the superior wall of
patient due to tapping, etc. the space created after the membrane is elevated or the
In the hydraulic sinus lift, the membrane is lifted using bony window may be eliminated using a bur to thin it
controlled water pressure. down completely (Fig. 62.lA and B). Utmost care should
Another method of hydraulic sinus lift is the intralift be taken while elevating the membrane with hand instru-
technique using the Piezotome intralift kit (Satelec). ments to prevent tearing/perforation. These instruments
are gradually inserted all around the prepared window
until the membrane is separated from the bone to the
Lateral Window Technique desired height. This space can be grafted with the chosen
In this, the Schneiderian membrane is exposed by cre- material and simultaneous/delayed implant placement
ating a window in the lateral wall of the sinus, the mem- may be carried out. The antrostomy may or may not be
brane elevated, and graft is placed above the alveolar bone. covered with a resorbable barrier membrane before the
For this, a trapezoidal mucoperiosteal flap is elevated closure. Delayed implant placement is done 4-6 months
to expose the lateral wall of the maxillary antrum. The after the sinus lift procedure (Case 2).
CASE 2 Sinus lift using lateral window technique. (A) Cresta! incision given for mucoperiosteal elevation; (B) lateral window preparation;
(C) separating the membrane from the bony wall; (D) pushing the lateral window inside; (E) sinus membrane lifted; (F) sinus cavity being filled
with bone graft; (G) lateral wall covered with PRF membrane; (H) flap approximated and sutured. Courtesy: Betsy 5 Thomas.
BONE AUGMENTATION
Resorption of the alveolar ridge in one or more dimen-
\J
~
Posterior
osteotomy
sions due to loss of teeth poses a challenge to the clinician,
when it comes to placement of dental implants. This loss oc-
curs at a rapid rate during the first year after extraction and
· parallel to continues for many years. The maxillary labial bone may be
maxillary
buttress
lingual to its original location within 3 years of extraction,
with almost 25% decrease in width of crestal bone occurring
Anterior osteotomy parallels lateral Sinus floor
nasal wall during the first year and up to 40% loss occurring by 3 years.
The mandibular posterior region resorbs around four
(B)
Sinus membrane times faster than the anterior region resulting in narrow
ridges. These changes make preservation and recontour-
ing of the labial surface of the alveolus one of the main
factors in ideal implant aesthetics.
Widening of the alveolar ridge may be achieved by
various methods such as osteoplasty, augmentation, bone
expansion, distraction osteogenesis, and ridge splitting.
If there is sufficient bone length, osteoplasty may be
done. But the loss of cortical bone during this process
---Bone flap tends to leave the implant in the less dense trabecular
bone resulting in less bone to implant contact. This in turn
may lead to less primary stability of the implant.
Bone augmentation is a very commonly done pro-
cedure. The problems associated with this are second
surgical site in case of autogenous graft, increased cost
and morbidity, etc.
The viscoelastic properties of bone are made use of by
two techniques, viz., bone expansion (Case 3) and ridge
splitting. Since soft tissue is left attached to the trans-
ported segment, expansion of the soft tissue also occurs,
thus improving the contour of both types of tissues. Ridge
expansion may be done in areas where the width is not
less than 4 mm so that osteotomes may be inserted. But
FIGURE 62.1 (A) Lateral diagram showing the desired locations if there is dense cortical bone with nil or very less cancel-
for the osteotomy cuts. (B) The location of the incision and osteotomies
lous bone in between the cortical plates, or if there are
when there is a wide band of attached gingiva in the posterior edentu-
lous maxilla. Courtesy: S Umesh Acharya. severe undercuts, then it might be wise to avoid ridge
expansion procedures. This technique is used in types III
and IV maxillary bone by relocating the alveolar bone.
Complications
The main uses of this technique would be for expanding
One of the main complications of the sinus grafting is buccal/labial bone for aesthetic reasons, for changing the
the perforation/tearing of the membrane. This is more emergence angulation, and for reducing the maxillary
likely in septated antra. If it happens, the procedure can undercuts.
be stopped and tried again after a few weeks when re- Some of the advantages of this technique are as follows:
generation would have taken place. Or the membrane
elevation can be continued all around the perforation 1. It retains total bone mass, whereas the drill removes
and a collagen barrier membrane may be placed over the the bone.
perforated area and grafting continued. 2. At the time of the expansion itself, implant placement
Piezoelectric bone surgery has been advocated by ma- may be carried out.
ny authors as well as clinicians for sinus lift procedure. 3. Heat generation is avoided and there is greater tactile
Since this does not cut soft tissue, the incidence of perfo- sensitivity.
ration of the lining membrane has come down to around 4. This technique is cost-effective and minimally invasive.
3% from 11-55% with the traditional methods. It has the 5. Initial stability of the implant is good as bone is com-
added advantages of precision, favorable bone healing pressed with this technique resulting in better bone to
due to narrow kerf, etc. implant contact.
CASE 3 Ridge expansion using osteotome technique. (A) Narrow ridge in 12 region; (B) osteotomes; (C) pilot drill for initial osteotomy
preparation; (D) insertion of osteotome to the desired length; (E) implant with cover screw; (F) post-op radiograph showing implant in 12 region;
(G) implant supported restoration in 12 region. Courtesy: Betsy S Thomas.
The disadvantages are as follows: and avoid the risk of fracturing. Implant placement may
be done in the second stage after around 6 weeks. This
1. It requires the use of serial osteotomes and a mallet to
approach is mainly indicated in the mandible.
widen the ridge, which might not be well tolerated by
some patients.
2. This is mainly for use in the upper jaw and because of
mouth-opening restrictions it might be difficult to use GUIDED BONE REGENERATION
in the posterior region.
3. If controlled force is not used, osteotomy site may Periodontologists have, for quite a long time now, been
fracture. using the principles of guided tissue regeneration (GTR)
to develop new techniques in periodontal therapy. The
concept was that specific tissues are formed from specific
Technique cells and that different cellular components in the tissue
After raising a mucoperiosteal flap through a crestal have varying rates of migration into a wound area during
incision, initial drilling is done through the cortical bone healing, provided a mechanical hindrance could exclude
to the desired depth using a 1.5-mm drill. Bone is en- the invasion of inhibiting substances such as fibroblasts.
tered 1 mm labial to the palatal bone, the latter serving This mechanical hindrance may be provided by mem-
as the reference point for proper angulation. The tip of branes which are resorbable or nonresorbable. The basic
the smallest osteotome is inserted into the pilot hole and characteristics of these are biocompatibility, cell occlu-
is used in a rotatory motion. A mallet may be necessary siveness, space making, tissue integration, and clinical
to tap the osteotome to the desired depth, if the bone is manageability. Examples of resorbable membranes may
dense. It is advised that the osteotome be left in place for be natural ones such as collagen, chitosan, or chitosan-
a minute to allow for flexure of the bone. The osteotomy collagen hybrid, or synthetic membranes such as polyrt-
site is enlarged by inserting larger-sized osteotomes se- lactide) (PLLA) and poly(L-lactide-co-glycolide) (PLGA).
quentially. Implant placement may be done during the Nonresorbable membranes such as expanded polytetra-
same appointment. flouroethylene (e-PTFE) and titanium-reinforced e-PTFE
may also be used.
One of the main factors for success of the barrier mem-
branes would be mechanical stability. Membrane fixing
RIDGE SPLITTING pins, screws, etc., may be used for the same.
When the alveolar bone is of insufficient width to per-

mit the use of round osteotomes, the ridge might be split
to accommodate the implants.
DISTRACTION OSTEOGENESIS
This is mainly done when vertical ridge enlargement
Alveolar distraction osteogenesis is a predictable meth-
is not needed and in the anterior maxilla with adequate
od of increasing the bone availability, but it might cause
cortical thickness (with some amount of cancellous bone
considerable discomfort to some patients. There are very
present). But if the ridge width is less than 2 mm or the
few contraindications for this procedure. The advantages
bone height is less than 10 mm, then it is preferable to
of this technique are that there is no donor site morbidity
avoid this technique.
as there is no graft being taken, it regenerates soft tissue
The ridge split technique may be done as a single-stage
also, and the result is more predictable. The disadvantages
or a two-stage procedure. A simple corticotomy at the
are that patient compliance may be difficult since it is a
crest of the buccal aspect of the edentulous area is carried
long-term treatment and this technique might be difficult
out after reflecting a mucoperiosteal flap. The entire bony
in extremely atrophied mandible.
segment is opened like an "envelope," maintaining the
vitality of bone. Only if primary stability is assured are
implants inserted in the initial stage itself. In this case, af-
ter the desired width is achieved, pilot drills are used and BONE GRAFTS
then the implant placement procedure is continued. Bone
grafting of the peri-implant areas has been advocated by Bone can completely regenerate itself if certain cri-
many authors to prevent soft tissue from growing into teria are met. One of these is that the area of bone loss
the depths. should be a confined space, without ingrowth of adjacent
In the two-stage procedure, buccal segment lateraliza- soft tissues, etc. As early as 1957, Murray and Rosch-
tion and periosteum suturing are done in the first stage. Ian have shown that if a bony cavity with good blood
Vertical releasing incisions may be given in 02-03 bone supply and source of osteoblasts is not protected from
in order to direct the bone lamellae toward the vestibule adjacent tissues, it would fill with fibrous connective
tissue, whereas if it was protected, it would fill with bone. freeze-dried bone allograft (DFDBA) is believed to have
Some of the other criteria for bone regeneration are that osteoinductive properties also, as it retains some of the
an adequate blood supply should be established, there original BMPs.
should be rigid fixation of the area, the space should be
maintained, etc. Most of the criteria may be met by bone
grafts. The biological principles that help these grafts in Surgical Technique for a Chin Graft
bone regeneration are osteoconduction, osteoinduction, The recipient site should be prepared first by reflect-
and osteogenesis. ing a mucoperiosteal flap, creating small perforations in
In osteoconduction, the graft material acts as a scaf- the cortex using a small round or straight fissure bur to
fold for new bone growth, wherein osteoblasts from the enhance blood supply to the graft.
periphery of the defect spread on to it and generate new For harvesting bone from the mandibular symphysis
bone. Osteoconduction is the minimum property that (chin graft), an initial myomucosal incision is placed in
every graft material should have. the lower anterior vestibule, tissues dissected, and the
Stimulation of blood cells or osteoprogenitor cells from periosteal incision placed separately. The periosteum is
the defect to differentiate into osteoblasts and form new reflected upward and also downward taking care to stop
bone is known as osteoinduction. This is brought about by 5 mm short of the lower border of the mandible. Later-
mediators such as bone morphogenetic proteins (BMPs). ally, care should be taken so as to not damage the mental
Theoretically a graft with both osteoconductive and os- nerves by stopping the reflection again 5 mm short of the
teoinductive properties would result in faster integration premolars. While harvesting the grafts, the midline of
of the graft. the symphysis should be avoided, with graft being taken
When living osteoblasts from the bone graft contribute from either side of the mental protuberance, superior limit
to new bone growth (along with the above two mecha- being 5 mm short of the incisor apices.
nisms), it is known as osteogenesis. The graft having the desired shape is outlined using
Even though autografts remain the gold standard for burs under constant irrigation with saline and the graft
grafting, other grafts can also be used depending on indi- is teased out by gentle tapping with a curved osteotome.
cations, such as allografts, xenografts, or alloplastic grafts. The depth of the harvesting should not be more than 6 mm
The advantages of an autograft are as follows: and the lingual plate should not be involved. Bone grafts
1. It is cost-effective. of 2 cm width and 3 cm length may be obtained from the
2. It has osteoconductive, osteoinductive, and osteogenic symphysis. The wound is closed in layers after copious
properties. irrigation, making sure that the mentalis muscle is sutured
3. The chances of rejection are less as they are taken from properly. The harvested graft may be placed in the already
the same patient's body. prepared recipient site, adapted properly and at least two
holes are drilled through the graft into the host site to de-
Some of the disadvantages of autografts are as follows: sired depth and the block is immobilized at the recipient
1. Chances of morbidity are more as there is a second site using two fixation screws. If there are gaps around
surgical site. the graft, particulate bone from the chin (with or without
2. Resorption rate is faster. hydroxyapatite) may be used to fill these spaces. A barrier
3. The surgeon's surgical skill should be of a higher order. membrane may be used to cover the whole grafted site,
especially if a large amount of particulate graft has been
New bone formation from an autograft occurs in two used. The flap should be sutured without tension over the
phases. In the first phase, the viable osteoblasts and site to achieve primary closure (Case 4).
osteoprogenitor cells from the graft initiate new bone Although implant placement may be carried out at the
formation at the recipient site (phase I osteogenesis). same time, it might be better to wait 4-6 months before
Later, competent cells from the recipient site bring about implant insertion. It is advised that any functional load-
remodeling and replacement of the graft by osteoconduc- ing, including soft tissue-supported dentures, be avoided
tion and osteoinduction (phase II osteogenesis). during this period.
The autograft may be obtained from extraoral or intra- Overenthusiastic retraction of the tissues during
oral sites. The intraoral bone harvesting has the advan- the procedure can cause damage to the mental nerve,
tages of the procedure being done under local anesthe- resulting in paresthesia/hypoesthesia of the chin re-
sia, which results in less cost and no hospitalization, less gion. If the extent of the surgical site mentioned earlier
morbidity, donor site being close to the recipient site, etc. is followed, damage to the root apices, mental nerve,
Intraorally, the graft may be obtained from the mandibu- etc., can be avoided. A "witch's chin" may result if soft
lar symphysis region or the ramus. tissue detachment is carried out till the lower border
Allografts have the advantage of no donor site morbid- of the mandible or if the mentalis is not sutured back
ity, acting as a natural biological scaffold, etc. Decalcified properly.
CASE 4 Bone augmentation using chin graft. (A) Deficient labial wall; (B) osteotomy cuts being made for harvesting the chin graft; (C) harvest-
ing the chin graft; (D) donor site after harvesting the graft; (E) donor site being sutured; (F) fixing the graft on the recipient site; (G) hydroxyapatite
is used to fill the gap between the autogenous bone and the recipient site. Courtesy: Betsy S Thomas.
For the bone graft to succeed, certain conditions must PRF can be mixed with bone graft to enhance bone
be met, as follows: regeneration potential, can be used in internal sinus lift
as well as lateral window procedures to facilitate further
1. The surgical sites should be free of infection.
sinus membrane elevation without membrane tear and
2. The space of the grafted site should be maintained long
also to cover small sinus membrane tears, etc.
enough for bone to fill the area.
3. Primary soft tissue closure without tension should be
achieved.
4. The graft should be fixed firmly without any movement.
5. The graft should have good blood supply.
INFERIOR ALVEOLAR NERVE
REPOSITIONING
The role of growth factors in the healing of wounds
has gained a lot of attention in recent years. Growth factor When the bone in the mandibular posterior region
preparations such as platelet-rich plasma (PRP), plasma undergoes resorption to a great extent, or because of bone
rich in growth factors (PRGF), and platelet-rich fibrin (PRF) loss in the region due to infection, trauma, pathology,
deserve special mention. At present PRF seems to be the etc., the inferior alveolar nerve may be close to the crest
preferred preparation with advantages such as ease of of the alveolar ridge. Placement of implants under these
preparation, less expense, no need of anticoagulant, long circumstances may cause injury to the nerve. The solution
period of storage after preparation, and ease of application. for this may lie in relocating the nerve (Fig. 62.2A-D).
(B)
FIGURE 62.2 (A) Preparation ofbuccal window for the nerve repositioning procedure; (B) removal of cortical plate using fine chisel; (C) retrac-
tion of nerve to facilitate insertion of implant; (D) implant insertion completed keeping the nerve retracted. Courtesy: 5 Umesh Acharya.
For this, a crestal incision is started from the molar reused as an interpositional material between the implant
gion and proceeded anteriorly. In the region of premolars, and the nerve to protect the latter from direct contact.
care is taken to make the incision only through the super- Complications are not common, but if dysesthesia or
ficial mucosa. In the canine region, a vertical releasing paresthesia persists for more than 1 or 2 months, it might
incision may be given, the mucoperiosteal flap elevated be better to consult a specialist.
carefully, the mental nerve and its branches identified,
and periosteal dissection carried out around the nerve to
free it from the surrounding soft tissue. The canal, which
is usually located 2-3 mm below the foramen, may be CONCLUSION
outlined on the bone with a marker such as methylene
blue. Lateral cortex in the area is cut to the depth of the The advanced surgical procedures discussed above al-
buccal cortex in a rectangular shape and this is removed low clinicians to offer dental implant therapy for almost
gently with the help of fine osteotomes or chisels. Once the all patients. Careful patient selection, proper diagnosis
nerve is exposed, it is isolated and retracted using a vessel and treatment planning, adherence to biological prin-
loop or a nerve retractor out of the way of the implant. ciples, etc., ensure predictable success of advanced surgi-
Placement of implant should be done under direct vision. cal procedures for dental implant therapy, in competent
Various materials such as autografts and gel foam may be hands.
KEY POINTS
• Patients with moderate-to-severe bone loss can be can- • Techniques as well as materials for ridge augmentation
didates for dental implant placement. should be chosen in a deliberate, scientific manner to
• Bone can regenerate if certain criteria are met. ensure consistent results.
QUESTIONS 2. Simian M, Jovanovic SA, Tinti C, et al. Long-term evaluation of

osseointegrated implants inserted at the time or after vertical ridge
augmentation. Clin Oral Implant Res 2001;12:35.
1. Compare and contrast the different types of maxillary 3. Toffler M. Osteotome-mediated sinus floor elevation: a clinical report.
sinus lift procedures. Int J Oral Maxillofac Implants 2004;19:266.
2. Describe the ideal properties of a bone graft. 4. Nevins M, Mellong JT. The advantages of localized ridge augmen-
3. Discuss bone augmentation. tation prior to implant placement. A staged event. Int J Periodontics
Restorative Dent 1994;14:96.
Suggested readings
1. Bruschi GB, Scipion A, Calesini G, et al. Localized management of
sinus with simultaneous implant placement: a clinical report. Int J
Oral Maxillofac Implants 1998;13:219.
CH A PT ER
63
Peri- Implant Diseases and Management
CHAPTER OVERVIEW
Peri-implant diseases are of two forms: peri-implant peri-implantitis is characterized by an inflammatory pro-
mucositis and peri-implantitis. Peri-implant mucositis has cess around an implant which included soft tissue inflam-
been described as a disease in which presence of inflammation and progressive loss of supporting bone beyond
mation is confined to the soft tissues surrounding a den- biological bone remodeling.
tal implant with no signs of loss of supporting bone. And
ETIOLOGY 1. Previous periodontal disease

Systematic reviews have indicated that although
As soon as an implant is exposed to the oral cavity gly- the implant survival rate may not be affected
coproteins from saliva adhere to exposed titanium surfaces by the periodontal history, peri-implantitis was a
with concomitant microbiological colonization. The forma- more frequent finding in patients with a history of
tion of a biofilm plays a significant role in the initiation and periodontitis.
progression to peri-implant disease and is essential for the 2. Poor plaque control/inability to clean
development of infections around dental implants. More- Implant prosthesis design can obviate the patient's
over, peri-implant diseases have been associated with gram- ability to mechanically clean the site with brushes,
negative anaerobic bacteria similar to those found around interdental brush, and floss. Hence, it is incumbent
natural teeth in patients with severe chronic periodontitis. on dental providers to educate the patient in proper
Features of experimentally created peri-implantitis and plaque control and to ensure establishment of regular
periodontitis by Lindhe have shown that clinical and radio- periodontal maintenance. This will help to assess the
graphic signs of tissue destruction were more pronounced adequacy of plaque removal and to intervene as early
in peri-implantitis. The increased susceptibility for bone loss as possible if problems are detected.
around the implants may be related to the absence of insert- 3. Residual cement
ing collagen fibers into the implant. Studies have shown It is quite possible for cement to be left behind because of
that all implants appear to be susceptible to peri-implantitis. implant positioning and the subsequent suprastructure
Hence, primary objective for treating peri-implantitis is design, which may hamper mechanical nonsurgical
similar to that for treating peri-implant mucositis which therapy to access the subgingival space. Dental cement
is the elimination of the biofilm from the implant surface. causes inflammation and the disease may be related to
When peri-implantitis is diagnosed very late, complete loss its roughness which itself may cause inflammation and
of osseointegration occurs, and this will be followed by the provide a positive environment for bacterial attachment
removal of the implant. (Fig. 63.1).
4. Smoking
Systematic reviews have concluded that there is an
RISK FACTORS increased risk for peri-implantitis in smokers with
odds ratios ranging from 3.6 to 4.6.
A number of risk factors have been identified which 5. Genetic factors
may lead to the establishment and progression of peri- Genetic variations have been cited as a risk factor for
implantitis. They are as follows: peri-implantitis. However, the association between
FIGURE 63. 1 X-ray showing residual cement after crown FIGURE 63.2 Case of peri-implant mucositis.
cementation.
Interleukin (IL)-1 gene polymorphism and peri- the therapy. The signs and symptoms of a failing implant
implantitis remains to be determined. are pocketing, bleeding on probing, presence of purulent
6. Diabetes exudate, and progressive bone loss despite periodontal
Evidence regarding the association between diabetes therapy. Therefore, an implant that exhibits progressive
and peri-implantitis is limited because of the small bone loss but is clinically stable can be defined as a failing
number of studies. Current evidence from systematic implant (Fig. 63.3). Similar microorganisms have been
reviews does not allow a definitive conclusion that observed in failing implants and chronic periodontitis.
diabetic patients have a higher incidence of peri- Clinically a failed implant demonstrates clinical mo-
implantitis, but it points out that diabetic control is an bility, peri-implant radiolucency, and a dull sound when
important factor when assessing the relationship. percussed. The failed implant must be removed because
7. Occlusal overload
it is nonfunctional and will only lead to further deteriora-
Differences in magnitude, duration, direction, and tion of the implant site.
frequency of the applied occlusal load and the tolerance The signs and symptoms that have been used to clas-
threshold of the host are the underlying reasons for sify the ailing and failing implants are tissue tone, pocket
the conflicting reports regarding occlusal overload.
Implants are considered less tolerable to nonaxial
occlusal load compared with teeth because of lack of a
periodontal ligament. Studies have shown that occlusal
load is concentrated at the implant marginal bone.
Excessive stress can cause microfracture within bone
and eventual bone loss. However, poor oral hygiene
is still the key causative factor.
AILING, FAILING, AND FAILED

IMPLANTS
Clinically unhealthy implants are classified as "ail-

ing" or "failing." An implant exhibiting peri-implant
mucositis is an ailing implant as it involves only inflam-
matory changes confined to the soft tissue surround-
ing an implant (Fig. 63.2). The organism associated with
mucositis is similar to gingivitis. In some cases the ailing
implant may exhibit early bone loss along with soft tissue
changes. But the bone loss does not progress further with FIGURE 63.3 Failing implant.
C H A PT ER 63 PERI-IM PLA N T DISEA SES A N D M A N A G EM EN T 573
depth, attachment levels, bleeding on probing, suppura- color changes have also been documented as signs of
tion, mobility, microbiological characterization of subgin- peri-implant diseases.
gival flora, and vertical destruction of the crestal bone.
The defect is usually saucer shaped, with osseointegration
only at the apical part of the fixture. Pain is an unusual
Radiographic Assessment
factor but when present is associated with acute infection. Conventional radiographs have been widely used
Peri-implantitis if left untreated can progress deep into to evaluate the peri-implant bone status as well as the
supporting bone and can lead to implant mobility which marginal bone level. However, minor changes in the
is a characteristic feature of a failed implant. Hence, the bone morphology may not be noticed until they reach
tissues around the implants should be monitored at regu- a significant size. And it is always advised to compare
lar intervals in order to diagnose any arising complication the periapical intraoral radiographs with the baseline
and arrest the disease. radiographs.
DIAGNOSIS OF PERI-IMPLANT PERI-IMPLANTITIS: TREATMENT

TISSUE BREAKDOWN OPTIONS
Various clinical parameters are used to assess peri- Treatment options for ailing and failing implants are
implant conditions. These include evaluation of oral hy- varied. The overall goal of therapy is to establish a resto-
giene, peri-implant tissues, and bone-implant interface. ration which is functionally and aesthetically acceptable.
Peri-implant tissues are evaluated on the basis of mobility, Therefore, any therapy should be focused on arresting the
bleeding on probing, gingival index, probing depth, and disease process and establishing a healthy peri-implant
radiographic evaluation. mucosal seal.
Mobility Nonsurgical Therapy

Implant mobility indicates lack of osseointegration. But This mode of conservative therapy includes mechani-
at times implant may appear clinically stable even in case cal debridement, occlusal therapy, and pharmacologi-
of peri-implantitis due to osseointegration in the apical cal therapy. Mechanical debridement is the first line of
portion. Mobility therefore represents a highly specific treatment for an ailing or failing implant. Instruments
parameter for monitoring clinical stability but is not a made of plastic, graphite, or nylon, or those with a Teflon
sensitive parameter. coating are recommended in order to avoid any damage
to the titanium surfaces. Treatment of implant surface
can be achieved with a supersaturated solution of cit-
Bleeding on Probing and Probing Depth
ric acid for 30-60 s in order to remove the endotoxins
Although bleeding on probing (BOP) indicates inflam- from the implant surfaces. Irradiation with soft laser for
mation in the pocket or sulcus, it is not a reliable indicator elimination of bacteria associated with peri-implantitis
for progression of disease. But absence of BOP can be has also shown promising results in the destruction of
considered as a predictor for stability. bacterial cell.
The soft tissue cuff around an implant is said to be In order to improve the response to mechanical de-
about 3-3.5 mm regardless of the system and the connec- bridement antimicrobials have been advocated. Chlorhex-
tive tissue attachment of 1-1.5 mm. Probing of dental im- idine is widely used as a mouthwash and as an irrigant
plant is often debated due to possibility of disrupting the because of its antimicrobial effect and substantivity at the
perimucosal seal between the soft tissue and implant, but affected site in patients presenting with an ailing implant.
there has been no scientific evidence for this concern. A Antibiotics such as amoxicillin, combination of amoxicil-
rigid plastic probe is preferred as it avoids damaging the lin and metronidazole, combination of amoxicillin and
implant surface. Another factor to be kept in mind is that clavulanate have also been found to be effective against
probing depths differ around dental implants depend- the bacteria of a failing implant.
ing on the length of the abutment used. So when placing Occlusal interferences may also contribute to ailing and
implants one should ideally try not to create deep pockets failing implants. Hence, occlusal adjustment is necessary
as those over 5 mm would be ideal niches for periodontal when premature contacts or interferences are present.
pathogens. A deeper probing depth indicates periodontal A third nonsurgical therapy recommended for treat-
pathology when there is bleeding on probing. Presence ing the ailing or failing implant is mechanical debride-
of exudates, increased probing depth over a time as com- ment. Local debridement of tissues surrounding an im-
pared with baseline data, calculus buildup, swelling, and plant using either plastic hand instruments or ultrasonic
instruments with a plastic tip has been suggested. Plastic treatment, radiographs of the implant should be taken at
instruments are necessary to debride plaque from tita- each 3-month recall visit. Later radiographs need to be
nium dental implants without damaging the soft titanium taken only annually. Studies have reported that marginal
surface. Preparation of implant surface can be achieved bone loss around implant is over 0.9-1.6 mm during the
with a supersaturated solution of citric acid for 30-60 sin first year and in the follow-up period bone loss decreased
order to remove the endotoxins from the implant surfaces. to 0.05-0.13 mm. Removal of the deposits on the implant
Irradiation with soft laser for elimination of bacteria as- should be accomplished with instruments that do not
sociated with peri-implantitis has also shown promising scratch the implant surface. Plastic, resin, graphite, and
results in the destruction of bacterial cell. gold-tipped scalers are acceptable for implant debride-
ment. Instruments such as stainless steel curettes and
standard ultrasonic and sonic instruments are not rec-
Surgical Techniques ommended to be used on implants. A rubber cup can be
Surgical techniques are indicated when nonsurgical used to polish the implant surface with a nonabrasive
therapies are ineffective. These include resective tech- toothpaste, fine polishing paste, or tin oxide.
nique and regenerative technique. Resective therapy is
used to reduce pockets, correct negative osseous archi-
Home Care Methods
tecture, and smoothen the implant surfaces. Regenerative
therapy is used to reduce pockets but with the ultimate Adequate oral hygiene is required both for natural
goal of regeneration of lost bone tissue (Fig. 63.4). teeth and around implants in order to maintain health.
A soft sulcular toothbrush is the primary plaque con-
trol device around an implant restoration. Powered and
Maintenance Therapy sonic toothbrushes are also safe to use around titanium
After successful implant therapy the patient should be implants. Interproximal brushes, superfloss, and wood-
recalled at regular intervals in order to provide optimal en tips are some of the auxiliary devices that can assist
preventive services and to facilitate treatment of disease plaque removal from embrasure spaces and beneath the
processes. It is advised to record baseline data such as prob- restorations.
ing, pocket depth, soft tissue margins, and radiographic Chemical antiplaque agents can be delivered with in-
bone levels before the initiation of the treatment. In the terdental aids to enhance their effectiveness. A prosthesis
recall visits a detailed examination of the implant should be that is fixed to the implant and not removed by the client
done prior to instrumentation. This includes evaluation of requires a more detailed home care regimen. Powered
soft tissue around the implant, implant mobility, prosthesis, toothbrushes, floss with threaders, and interdental aids
radiographs, and plaque and calculus scores. are recommended for use in fixed implant prosthesis. In
The evaluation is done initially after 1 day, 1, 3, and patients who are able to remove their prosthesis, the bar
6 months, and then at yearly intervals. In the first year of attachments and ball attachments can be cleaned with
soft bristle brush, end tuft brush, or the interproximal
brushes. Every patient with dental implants requires a
lifetime careful evaluation and maintenance to ensure
implant health and longevity.
Antibiotics and Implant Treatment

Although the benefits of prophylactic antibiotics are
well recognized, their routine use in placement of den-
tal implants remains controversial. Systematic review
published in Cochrane database by M Esposito et al has
concluded that there is no appropriate scientific evidence
to recommend or discourage the use of prophylactic sys-
temic antibiotics to prevent complications and failures
of dental implants. But they have recommended the use of
antibiotics for patients with high and moderate risk for
endocarditis or metabolic diseases, or when an extensive
or prolonged surgery is anticipated.
A treatment plan for peri-implantitis maintenance and
treatment can be suggested based on the various clinical
FIGURE 63.4 Regenerative technique around a failing implant. presentations as follows:
C H A PT ER 63 PERI-IM PLA N T DISEA SES A N D M A N A G EM EN T 575
Clinical presentation Treatment plan CONCLUSION

Case 1 Probing depth <3 mm Oral Hygiene Instructions
Bleeding on probing (OHI) Fortunately unhealthy implants are uncommon be-
Presence of plaque Local debridement cause of the high success rate of implant therapy. How-
Case 2 Probing depth 4-5 mm OHI ever, as with any procedure failure can occur; hence,
Bleeding on probing Mechanical debridement a clinician should recognize unhealthy implants and
No bone loss Chemical plaque control determine whether they are ailing, failing, and failed
Open flap debridement implants prior to beginning any salvage effects. The
Case 3 Probing depth 4-5 mm OHI best step to avoid encountering failing implants include
Bleeding on probing Mechanical debridement proper case selection, excellent surgical technique, ad-
Bone loss > 2 mm Chemical plaque control equate restoration, and frequent maintenance recall
Systemic/local antibiotic therapy
visits.
Resective or regenerative therapy
Case 4 Probing depth >5 mm Explanation

Bleeding on probing
Bone loss >50% of
implant length
Mobility of implant
KEY POINTS
1. Peri-implantitis involves progressive loss of peri-implant 3. Four treatment modalities of cumulative interceptive
bone as well as soft tissue inflammatory changes. supportive therapy include mechanical debridement,
2. Warning signs of implant failure include gingival chemical plaque control, systemic antibiotics, and
bleeding, purulent exudate from pockets, pain, angular surgical therapy.
bone loss, and long-standing infection.
QUESTIONS Suggested reading

1. Berglundh T, Lindhe J, Lang NP, et al. Mucositis and periimplantitis.
1. Enumerate the risk factors of peri-implantitis. In: Lindhe J, Karring T, Lang NP. Clinical Periodontology and
2. Discuss the clinical features of an ailing implant. Implant Dentistry. 4th ed. Copenhagen: Blackwell Munksgaard; 2003.
www.ajpdf.com
CHAPTER
64
Evidence--Based Periodontics
CHAPTER OVERVIEW
Over time clinical practice for dental professionals has From these research-focused branches, evidence-based
transformed, where the amount of changes in the tech- medicine was developed to cater to the specific needs of
niques and technologies requires practitioners to enter a health practitioners to help determine the quality of evi-
cycle of continuous skill and knowledge upgrades. These dence in a systematic and easy manner. It is widely adopted
are usually done via continuing education courses and by health care organizations including dental organizations
reading scientific articles. Most of these avenues for up- around the world and is widely adopted for scientific prac-
grading skills and knowledge are meant for a reader who tice by health care professionals.
understands how to evaluate the information for further This chapter will use "evidence-based dentistry" (EBD)
determining its usability and specific applications in her/ as the approach to scientific literature that aims to combine
his clinical practice. clinical expertise with the best clinical evidence available,
Epidemiology being the branch of science dealing with and adapting it to the specific clinical situation, while includ-
the determinants, distribution, and effects of diseases and ing the specific patient's expectation and values in consider-
health states; along with statistics, that deals with the analy- ation. This chapter will provide a brief outline of the process
sis and interpretation of these data forms the essential back- involved in assimilating the best evidence into clinical prac-
bone of this clinical information. tice of periodontology.
BASIC CONCEPTS example that there are those with and without exposure
(smokers and nonsmokers) and also those with disease and
There are a few basic concepts that you must know without periodontal disease (with outcome and without
while you are looking to understand the process and the outcomes). Clinicians recognize from experience that not all
results of the evidence-based approach. Following list is smokers will get periodontal disease, and not all nonsmok-
from the perspective of epidemiology: ers will avoid the disease. With this information, examine
the following:
• Understand some of the terms that are used in relation
to study methodology.
• Understand the features that differentiate study Time
designs.
• Be able to distinguish the various study designs. Outcome/
• Understand the hierarchy of evidence and the extent Exposure/ Periodontal
Smoking disease
of its usefulness.
Most study designs of interest to clinicians would have
at a minimum comparison of exposures and their effects No exposure/ No Outcome/
No smoking
on outcomes, for example, smoking and its link to peri- No
Periodontal
odontal disease. The answer that clinicians require for disease
their communication and treatment decisions is linked
to how smokers are different from nonsmokers in their
chances for getting periodontal diseases. We can see in this
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CHAPTER 64 EVIDENCE-BASED PERIODONTICS 577
In this basic illustration there are two groups with dif- participants or groups of participants get the exposure,
ferent exposures, in this case smokers and nonsmokers, and which ones do not get that specific exposure, it
and there are different possible outcomes of interest, pres- is an experimental design. On the other hand, if the
ence or absence of periodontal diseases. Quite often, a researcher does not assign the exposure, then it is
well-focused study would concentrate on an exposure of an observational design. Please note that the setting of
interest and an outcome that may be linked to the expo- both the observational design and the experimental
sure. As noted earlier, there are some nonsmokers who design could be in a community or clinic. Similarly
have periodontal disease, and some smokers who avoid it. both types of studies could involve an exposure that
It usually takes combined knowledge from several stud- could include a surgery, a medication, or a session of
ies to make up the science for a disease condition such as health education.
There are several ways that a relationship between c. Observational studies
smoking and periodontal disease can be investigated. Let us take the example of smoking with cancer
Based on the choices that are made, the study can be clas- and compare that with the earlier example which
sified into one of the designs that are listed as follows is smoking and periodontal disease. Of the two
(Table 64.1): outcomes (periodontal disease and cancer) cancer is a
rare occurrence and periodontal disease is a common
a. Descriptive studies
occurrence. Practicality of carrying out studies would
At early stages of research, for generating hypothesis,
limit the options for the rare occurrence. So the easiest
clinicians and researchers may carry out studies
option for studying link of cancer would be to carry out
using a single patient where there is a link between
a study by recruiting those with cancer and a similar
the exposure and outcome of interest, where it will be
group without cancer and then looking at the past
an attempt to describe the patient and the conditions
exposure with smoking in both the groups. This design
related to the patient in detail and give some possible
is looking backward in time, where the outcome has
hypothesis for the occurrence. This report of a single
already occurred. This design where the participants
patient or participant is called a case study or a case
are recruited based on their disease status is known as
report. It is useful for reporting rare or new occurrences a case-control study. Here the cases are the ones with
that are newsworthy. Some surgical reports and new disease and controls are those without. It could also be
pathologies form a large part of this. There could also different levels of a parameter, such as attachment loss,
be a number of these cases that are combined to form a
where we categorize it based on those with a certain
single report called a case series. Both a case study and
degree of attachment loss versus those with a lesser
a case series are useful to generate hypothesis, but not
degree of attachment loss.
for inferring the relationship between an exposure and
If the study is based on some rare exposure that is
an outcome. of interest, then there are two ways to do this. While
There could also be relationships between variables
comparing "smoking and periodontal disease" and
that are tested in one time, where a larger number of "orthodontic treatment and periodontal disease," it is
people are asked about smoking and checking their
evident (in many parts of the developing world) that
periodontal disease status at the same point in time
the proportion of smokers in the whole population
in a community or clinical setting. These studies are
would be much higher than the proportion of people
cross-sectional studies, and they can quantify data better who have had orthodontic treatment. Then instead of
than a case study or a case series. They do not start
recruiting those with periodontitis and then looking
with a clear hypothesis, and do not have selection of for those who had orthodontic treatment, where
participants based on the needs of a hypothesis testing.
you would need a large number of participants with
But they are also good for generating hypothesis and
periodontitis and without, to get a fair number of those
less so for showing clearly the causal link between two with orthodontic treatment, it would be easier to look
variables.
at past records of those with orthodontic treatment
b. Analytical studies and those without, from clinical registers, and then
Analytical studies are studies that are planned with contacting those for current status of periodontitis. This
a clear hypothesis that is planned to be tested and could be done prospectively or retrospectively. So if the
is usually designed around it. Among the study participants are recruited and initial measurements are
designs that are analytical, there are studies that are made before they have the outcome of interest, here
observational and experimental. The difference between periodontitis, then it is a prospective cohort study. If the
the observational studies and the experimental study starts after the outcome of interest has taken
studies (also called clinical trials) is the assignment place, then it is a retrospective cohort study. The common
of exposure. That is, if the investigator decides which feature of cohort studies is the recruitment and analysis
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TABLE 64.1 Questions That Can Lead You to the Common c. Prospective cohort studies
Study Designs That Have a Hypothesis d. Case-control studies, retrospective cohort studies
e. Cross-sectional studies
1. There is random assignment of exposure: randomized controlled f. Narrative reviews, expert opinion
trial (RCT). Always prospective, as the outcome cannot happen
without the intervention. Note the absence of laboratory-based studies and other
2. There is assignment of exposure without random sequence: studies that are modeling the usual disease activity. The
quasi-RCT. Always prospective like an RCT.
3. No assignment of treatment+ prospective: prospective cohort.
exclusion is because this book is for clinicians, and trans-
This study will be planed around an exposure of interest by lating these designs is not appropriate for clinical practice.
recruiting those with exposure of interest and those without But those are good for doing studies in humans using
the exposure of interest. They are then followed to check the one of the epidemiologic designs for generating pertinent
outcome of interest as it develops in the future. evidence.
4. No assignment of treatment+ retrospective: retrospective cohort
or a case-control study. If the recruitment and the analysis are
It is also important to remember that not all RCTs
based on outcome of interest (such as a disease), then it is a would have better information than the studies lower
case-control study. If the recruitment and analysis are based on on the list. Here the hierarchy indicates the ability of the
two levels of exposure of a group identified in the past, it is a study to avoid the erroneous results.
retrospective cohort study.
5. All data collected in one point in time+ usually no clear hypoth-
esis driving the design of the study: cross-sectional study.
Some other concepts worth noting include bias, error, confounding, relative
risk, odds ratio, p-value, sensitivity, specificity, and validity. For more
CLINICAL PRACTICE AND EVIDENCE
information on study designs, please refer to Dawson and Trap.
The traditional education approach for clinical sciences
involved acquiring knowledge from points of authority.
These could be teachers, speakers, and/ or books that
based on groups based on a well-defined exposure imparted the information. This was an easy method of
(with and without, or with different extents). learning that needed less initiative from the learner. It is
d. Experimental studies (clinical trials) based on the assumption that the point of authority has
As the researcher decides the assignment of the correct, updated knowledge and is unbiased. This is not
exposure, it can be done using a random sequence that usually true and the general concepts may not be the most
does not bias the two or more groups of participants updated expertise that is required by individual patients.
based on exposure. When a random sequence is used, This is also reflected in the hierarchy of evidence.
it is called a randomized controlled trial (RCT). If the The overall methodology used in this chapter is similar
sequence of assignment is not a random sequence, then to that widely accepted and published.
it is a quasi-randomized controlled trial. It is to be noted Steps involved in the evidence-based approach:
again that although the experimental designs are also 1. Frame the clinical question.
called clinical trials, it is the assignment of exposure 2. Search for the relevant articles.
and not the location of the experiment (in a clinic) that 3. Assess the quality of articles.
defines them. 4. Ascertain the applicability of the articles to the clinical
Exposures that can cause harm, such as smoking, situation.
should not be carried out by using experimental 5. Discuss with the patient and help patient decide on the
designs, as it would be unethical to expose someone procedures.
to an exposure that is well known to be harmful. Such
exposures are usually studied using observational
designs. Framing the Question
There are several threats to how correct the results of There are four parts to an answerable question. These
the study are with respect to the study population. An are as follows: population, intervention, comparison, and
important criterion that can decide the ability of a study outcome (Table 64.2).
design to control these is the study design. Based on this Here the intervention and comparison can be replaced
criterion, there is an ordering of the common study de- with the presence of exposure and its absence, based on
signs. This ordering is also known as the hierarchy of whether the study is experimental or not. For clinical
evidence. practice, most of the information may come from RCTs,
so the abbreviation will still work well. In the format of
Hierarchy of evidence: null hypothesis, this would still be the population, in-
a. Systematic reviews dependent variable (intervention, comparison), and the
b. Randomized controlled trials dependent variable (outcome).
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TABLE 64.2 Parts of a Question These questions seem adequate at first glance, but
need more details, while making them more specific
P Population that the question applies to the population and yet answerable questions. For the first question, the
that the answer should apply to. (e.g., Middle aged adults
with type II periodontitis)
clinician should be aware of the types of therapies that
may be available for the outcome of interest, i.e., reduce
Intervention or exposure whose affects you are attachment loss. Here the question is related to therapy,
investigating (e.g., root planing)
if we are interested in the comparison between the ef-
C Comparison is what is this intervention compared (e.g., fectiveness of surgical therapy and that of nonsurgical
surgical intervention vs. root planing) therapy.
0 Outcome would refer to a health state, possibly disease, The question could be written up to include the de-
that the intervention and comparison are linked to (e.g.. mographic information that is important in the popula-
pocket depth in millimeter) tion. If there is no reason to include age in the question,
as the results seem consistent across age, then you can
leave that alone. If there is a difference based on gender
that you are expecting based on prior research, then
In the treatment and prevention of periodontal diseases include it in the question. Thus, formulate the "popu-
among those with it or at risk for it, clinicians are often lation" part of the question, based on prior knowledge
faced with questions related to: and the clinical situation that you are facing. Here be
1. Therapy sure to add the medical history, such as diabetes, when
2. Prognosis it is an important part of the question that is being
3. Diagnosis answered.
4. Etiology /harm The details of the procedure should be refined to the
point where there is no ambiguity about the treatment
Mnemonic for the above is ThePro DiEt. and the comparison of interest. What could be includ-
There are four types of questions that can commonly ed in the comparisons? For example, the nonsurgical
arise from clinical practice. These questions open all parts therapy could be scaling and root planing alone, scaling
of clinical practice to questions on the availability of evi- and root planing followed by regular flossing, regular
dence and the practice of best available evidence. The flossing alone, etc. Thus, pick the parts of the question
components of questions (PICO) would be used to write that make sense from the point of view of your practice.
all the four types of questions that are given here. Similarly the outcome can be defined according to the
expectation of the patient and the possibilities based on
Answerable Question prior science. Making an answerable question is one of
Since the first step in this process is curiosity and a the skills that improves with practice. If it is too specific,
question from clinical scenarios, making a question that is it may be tough to get an adequate number of articles
answerable becomes a first step in the process. This step to make an informed answer. If it is too broad, then ap-
is important for carrying out a successful enquiry and plying it back to the specific situation becomes tougher.
there are some easy guidelines for accomplishing this. But once you figure out a situation, updating yourself
Mnemonic used is PICO. becomes much easier.
Once the parts of a question are understood, keep the
level of detail of each part as specific as needed. Let us
take an example where a clinician has a 53-year-old fe-
Search Strategy
male patient from a (hypothetical) BigCity, who has pock- Searching on the internet is now a common practice,
et depth of 8 mm on the mesial aspect of 16 (maxillary first up to the point that searching and Googling have become
molar - right side) with Class 1 furcal involvement on the synonymous. There are many strategies for searching
same tooth. The patient has a history of diabetes mellitus for articles using various search engines. Two of the free
(type 2) for 5 years and is taking metformin 1000 mg BID. search engines are PubMed and Google Scholar.
Current HbAlc is 6.1. The patient is regular with her visits PubMed is a very pertinent choice of searching health
to the dentist and is able to control her diet for diabetes. care-related publications. Constant upgrades to the search
There are several questions that may arise to the mind and the built-in functions make it a very valuable tool. The
of a clinician. For instance, what therapy can I use for easiest way to learn the search strategy is to search for
this patient? What will be the effect of diabetes on the PubMed tutorials and look for quick tours to watch the
periodontal condition? What will be the effect of diabetes short videos given there. MeSH search and Advanced
on the therapy? Does this medication have any effect on Search Builder are invaluable resources that can get you
the therapy? Will a radiograph improve the diagnostic the most relevant results. Remember that it is pointless
accuracy (validity)? if you cannot find the most relevant evidence that might
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be out there, so search strategy is often a limitation if the beginning of the study, to reduce the chances of errone-
searcher does not have the necessary skills for it. ous results.)
Assess the Quality of Articles Systematic Reviews

The criteria listed as follows are optimized for Cochrane
Scientific articles, like any information, come with a
reviews (therapy), but are applicable to other systematic
chance of being false. The two large categories of these
reviews as well:
are the type 1 and type 2 errors. Type one error, where
we erroneously conclude that the treatment (exposure) 1. Clear explanation of the study methodology: The
works and type 2 error where we erroneously conclude study methodology should be clear to the point where
that the treatment does not work. The altered chance a reader who is trained with the terms could repeat
could reflect the difference in the choices made in clinics. the study. The materials and methods that are part of
If you think that a therapy would work 50% of the time the study should be able to give information about the
and another 40% when all else is equal, a change in those study methodology.
chances could tilt the choice quite easily. While under- a. Inclusion criteria: These contain important informa-
standing causes of diseases (etiology /harm), the same tion regarding the types of studies, and the PICO
holds true where the risk of a disease (outcome) becomes of the review. The types of studies included would
much higher, as the chances of the outcome happening give a clue of the study designs that are included.
as a result of the cause (exposure) increases. So a 1 in 10 Quite often they are RCTs (especially in the case of
chance of cancer becomes much more drastic than 1 in Cochrane reviews). The higher the studies are in the
5000 or 1 in 10,000. So besides the possibility of an outright hierarchy of evidence, the higher the confidence we
wrong answer, the skewing of chances can also have a can have in the results. The PICO again would be
considerable impact on the clinical practice. The chances useful to determine the appropriateness of the study
of these three scenarios are lower as we go higher in the for the clinical question that the clinician starts with.
hierarchy of evidence. But within each type of study, there b. Search criteria: Extensive search strategy that should
is the range of how free it is from erroneous results. As be able to give all the relevant articles using several
the hierarchy indicates which designs can do better, how databases is considered the norm for systematic
well each was conducted also decides how free of errors reviews. If the systematic review includes clinical
the results can be. trials, the search strategy should also include clini-
For therapies used in clinical practice, there should be cal trial registries that are relevant for these trials
an expectation of evidence from well-conducted RCTs or and would have invaluable information about the
systematic reviews, where possible. This would ensure exposure and outcome of interest. Searching among
higher confidence in the reproducibility of the evidence other sources such as databases for dissertations is
in your clinical practice. also commonly undertaken to get information that
We can use three checklists to help with appraisal of the may not have been published in the peer-reviewed
articles. The checklists are aimed at appraisal of: scientific journals. Hand searching is another com-
mon strategy aimed at including studies that may
1. Systematic reviews
not show up in the electronic search results.
2. Analytical designs (RCT, cohort, case-control)
c. Methodology for selecting the relevant articles: The
3. Diagnostic instruments.
criteria for the initial screening of the voluminous
Clear question or hypothesis: All the studies should have results and selecting the articles that are relevant
a clear hypothesis or a question that they are trying to should be explained. After this, a method for imple-
address through the study design and the analysis. The menting the selection criteria with multiple review-
information that you need here should be present in the ers going through the same articles (usually two
abstract or the last few sentences of the introduction/ reviewers) and, in case of disagreement, a methodol-
literature review in the article. Now the PICO of the ogy for settling disputes (possibly a third reviewer)
article can be elicited and you can compare the PICO of should be explained.
the article with the PICO in your clinical question (the d. Quality assessment: This includes selecting the cri-
one you started with). If these two match to satisfaction, teria that are required for inclusion, not restricted
then you can go ahead with the rest of the evaluation to blinding, random assignment, similarity of the
of the articles. groups at baseline, control using placebo or other
(Note: If there is no clear hypothesis or question, then treatments (or the group without exposure of inter-
it may be a cross-sectional design or an exploratory study est), analyzing all the participants (even those who
trying to look for new hypothesis. It would be good to left) of the study groups in the same groups that
find another study that has a clear hypothesis at the they started with, reports of adverse effects, etc.
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2. Results: The results section could have the results lead to skewing of the results. The opposite could also
of the individual studies listed separately or may be true of an examiner knowing the smoking status
contain analysis that combines the results of the and checking the periodontal status more thoroughly.
individual studies to give a combined result. When In these cases, having prior knowledge of the exposure
the combined result is given, the systematic review is or outcome while measuring the other leads to skewing
also called a meta-analysis. of the results. Studies where the patients are recruited
a. Similarity of results between studies: Consistency based on the exposure have higher chances of bias
of results gives higher confidence in the results. If while recording the outcome, as there is a chance that
there are large differences between results of the the examiner knows the exposure status. Similarly in
individual studies, then this should be discussed studies that are recruited and planned based on the
adequately, and this discussion could give insights disease status (outcome) such as in the case of case-
into the studies and the reasons for variations. The control studies, there could be skewing of the results
variations between studies would also determine if the researcher measuring the exposure may know
the feasibility of combining results of various the disease status of the participant. Blinding the re-
studies. searcher who is taking the measurements of exposure
b. Overall results of the meta-analysis: When available, and outcome can overcome some of the reasons for the
the combined results would provide a better skewing of the results. Presence of standardized pro-
estimate of the relationship between the exposure tocol for measurement of exposure and outcome, ap-
and outcome. plied similarly to both groups, is also a good sign that
c. Appropriateness of using the results in the clinical the results may have less skewing in one direction or
setting that inspired the question and the evidence- the other.
based approach to the clinical question at hand: 3. Intention to treat and loss to follow-up: Intention to
This would involve understanding the changes in treat is a concept that is especially important in clini-
the parameters of the study including PICO, and cal trials. For example, if there is a treatment that has
other factors that are important determinants of how severe adverse effects, such as in the case of chemo-
the exposure and the outcome would be linked. If therapy among cancer patients, there may be a lot of
there are genetic, social, or health conditions that patients who may stop the medication due to these
may be different between the study populations and adverse effects. If these patients are combined with
the population that is served by the clinical setting those who do not take the drug, then the drug will
served by the clinician, the results should be taken seem to work better than it will in clinics prescribing it.
with caution, and more appropriate evidence should This is because we need the results that would reflect
be collected. what would happen if the drug is given to a group of
patients and in the case of the chemotherapy, some
will stop taking it and these are the clinical experience
Analytical Studies and the results that the doctor will get with the drug. A
1. Similarity of participants in the two exposure groups related issue is the rate of follow-up. This is especially
(for RCT and cohort studies) or the outcome groups (in true of all the prospective designs, as participants may
case-control studies): Of all the designs, RCT has the not be easy to track over time. If there is low follow-up,
most similarity between the groups at baseline. For then we must consider if there is a discussion of the
cohort and case-control studies, efforts should be nature of those who were lost and if those are different
made to ensure the similarity between the groups from the ones who are left in the study. If there is some
by using inclusion and exclusion criteria to enroll difference between those who are left in the study, then
similar individuals (age range, gender distribution, it is important to recognize what effect that would have
comorbidities, etc.). Similar groups at baseline as- on the results of the study.
sure that the results are not influenced by dissimilar 4. Temporal relationship: It is important to be able to
groups, and the outcome is due to the exposure of ascertain if the exposure occurred before the outcome.
interest. In the case of RCT, random assignment of Proper measurement of the exposure and outcome
exposure and the experimenter being blinded to the at baseline followed by analysis using changes to the
assignment of exposure (leading to less bias) ensure outcome can ensure that the changes occurred after the
similarity of groups. exposure.
2. Assessment of exposure and outcome: In the earlier 5. Results: The results of the study will indicate the statis-
example of smoking and periodontal disease, if the in- tical significance of the results (denoted by a p-value).
vestigator who is asking about the smoking knows the The p-value works like a cutoff where usually a value
periodontal status, then she or he may ask more or less less than 0.05 is taken as statistically significant. But a
about smoking based on the disease status. This could lower value can also indicate that there is lower chance
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of type 1 error, provided the assumptions of the test involve understanding the changes in the parameters
are complied with. There is usually a 95% confidence of the study including PICO, and other factors that are
interval that is also given for the important results such important determinants of how the exposure and the
as odds ratio or relative risk. The narrower confidence outcome would be linked. If there are genetic, social,
interval indicates higher precision of the results. More or health conditions that may be different between the
precise results are more desirable. For results with study populations and the population that is served by
relative risk and odds ratio, a higher number indicates the clinical setting served by the clinician, the results
a stronger association between the exposure and out- should be taken with caution, and more appropriate
come that were used to calculate it. evidence should be collected.
6. Discussion: The results of other studies and how the
present study is similar or differs from the results
found elsewhere would give a good measure of con-
sistency of results with other studies. Consistency is CONCLUSION
important, especially if the PICO of the previous stud-
ies and their methodology is similar. No single article An accelerating number of publications, a lack of sci-
can prove or disprove any hypothesis, so in science entific evidence that is directly applicable to many clinical
consistency among the results is important for drawing scenarios, and increasing presence of commercial interests
conclusions. In the absence of adequate consistency, the necessitate clinicians who are capable to decipher good
clinician can wait for better evidence that can figure the evidence from less applicable one. With an understanding
reason for the lack of consistency. of the basic concepts related to study methodology, clini-
7. Appropriateness of using the results in the clinical set- cians can easily aspire to amass relevant evidence, assess
ting that inspired the question and the evidence-based those using checklists, and apply the relevant evidence
approach to the clinical question at hand: This would to specific clinical scenarios.
KEY POINTS
Basics: • The hierarchy of evidence sorts studies based on how
correct the results might be. This hierarchy can be
• An exposure is a factor that may, over time, lead to the
changed when a specific study design is not operation-
outcome that it is related to.
alized properly.
• A harmful exposure can increase the chance for a disease
or make it worse, whereas a beneficial exposure may
reduce the chance for a disease or increase the chance Evidence-based approach:
for a cure. • Answerable questions are created for diagnosis, therapy,
• A descriptive study does not set out to test a hypothesis. prognosis, or etiology /harm. This forms the first step in
It merely tries to describe a situation. making a clinically relevant inquiry for evidence.
• Case-control studies start with groups with and without • After a thorough search for literature and finding the
outcome/ disease. Instead of with and without, they could relevant articles, these articles must be assessed for es-
also have various levels of outcome/ disease. timating how accurate their results can be.
• Cohort studies always start with exposure groups, that • While applying the results, the PICO of the study and
is, those with and without exposure or groups with vari- that of your clinical situation must match for the ele-
ous levels of exposure, and then compare the chance of ments that are liable to change the results in your patient
outcomes among those groups. population.
• Analytical studies that have assignment of exposure are • The final and critical step is to explain the evidence to
called experimental studies. your patients, so that they can help choose the interven-
• If the assignment of exposure follows a random se- tions that would help them the most.
quence, those studies are called randomized controlled
trials.
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1. Evidence-Based Dentistry. American Dental Association. http:// ebd.
1. How are descriptive studies different from the ada.org/en/
experimental studies? 2. The CONSORT (Consolidated Standards of Reporting Trials)
2. Distinguish between a case study and a case-control statement and flow chart.
3. PRISMA: check list for systematic reviews, with an easy flow chart.
study.
4. Dawson B, Trapp RG. Basic & clinical biostatistics. 4th ed. New York:
3. Distinguish between analytical studies and descriptive Lange Medical Books/McGraw-Hill, Medical Pub. Division. x; 2004
studies. 438p.
4. List the various observational study designs and 5. Moher D, et al. CONSORT 2010 explanation and elaboration:
distinguish them. updated guidelines for reporting parallel group randomised trials.
BM] 2010;340:c869.
5. What is the key characteristic of a study that makes it
6. Moher D, et al. Preferred reporting items for systematic reviews and
an experimental study? meta-analyses: the PRISMA statement. PLoS Med 2009;6(7):e1000097.
6. List the hierarchy of evidence.
7. Describe the process of assessing a systematic review.
8. Describe the process of assessing an analytical study.
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Index
A generalized, 226 Angular bone defects, 275

Aa. See Aggregatibacter actinomycetomcomitans localized, 226 inconsistent bony margins, 276
(Aa) treatment of, 231 interproximal craters, 275
Aberrant frenum, management of, 475 nonsurgical, 231 interproximal hemiseptal
Abfraction, 97, 264 AHA. See American Heart Association (AHA) defects, 275
Abnormal frenal attachment, 263 AIDS. See Acquired immunodeficiency ledges, 276
Abrasion, 97, 254, 509 syndrome (AIDS) proximal intrabony defects, 275
Abutment level impression technique, 547, 549 Ailing implant, 573 reversed architecture, 276
advantages, 548 Albright's syndrome, 166 Ankylosis, 21
indications, 548 Allergic reactions, 195 Annular zone, 13
Abutment selection, factors responsible, 554 dental restorative materials, 195 Antibiotic, 371
AC. See Alternating current (AC) clinical features, 195 antagonism, 381
Accessibility, 46, 335 treatment, 195 principles of, 379
Accessory pulp canals, 453 drug-induced mucocutaneous disorder, 196 bacterial resistance, 379
Acellular afibrillar cementum, 19 clinical features, 196 intestinal flora, change of, 379
Acidic fluoride prophylactic agents, 526 drug eruptions, 196 toxicity, 379
Acoustic Altered collagen metabolism, 122 synergism, 381
microstreaming, 351 Alternating current, 346 therapy, 231, 379
streaming, 348 Alveolar bone, 23, 31 bacterial translocation, 379
turbulence, 348 bone, thin layer of, 23 inaccessible sites, 379
Acquired immunodeficiency syndrome bundle bone, 23 tissue invasion, 379
(AIDS), 183, 238, 277, 514 cells of, 25 Anticalculus agents, 371
clinical signs, 240 osteoblasts, 26 Antimicrobial therapy, 91
periodontal manifestation of, 240 osteoclasts, 26 Antioxidants, 396
Acrylic test stick, 331 osteocytes, 26 Antiretroviral drugs, 244
ACTH. See Adrenocorticotropic hormone composition of, 25 Antrostomy, 562
(ACTH) definition of, 27 ANUG. See Acute necrotizing ulcerative
Actinobacillus actinomycetemcomitans, 31, 64, histology of, 23 gingivitis (ANUG)
89,303 circumferential lamellae, 23 Arc-shaped mirror image, 276
Actinomyces, 55 concentric lamellae, 23 Arg-gingipain, 77
Actinomyces uiscosus, 56, 77 interstitial lamellae, 23 Arteriosclerosis, 29
Actisite, 385 intra-alveolar nerves, branches of, 23 Aspartate aminotransferase (AST), 287
Activated complement factors, biological osteoporosis, 31 AST. See Aspartate aminotransferase (AST)
properties of, 71 aging, 31 Asynchronous multiple burst model, 77
Acute gingival infections, 181 remodeling of, 27 Atherosclerosis, 132
Acute leukemia, 309 topography of, 213 Attached gingiva, 4
Acute necrotizing ulcerative gingivitis trabeculation of, 31 functions of, 4
(ANUG), 36, 181, 256, 315 Alveolar crest, 25,273,274 Attached gingiva, augmentation of, 471
Acute periodontal abscess, 277 Alveolar distraction osteogenesis, 566 coronally advanced flap, 473
Adaptive host response, 80 Alveolar process, 23 indications, 473
Adaptive remodeling, 16, 98 alveolar bone proper, 23 technique, 473
Addison's disease, 306 supporting alveolar bone, 23 free gingival grafts, 471
Adhesins, 56, 77 Alveolar wall and capillaries, blood vessel, contraindications, 471
Adrenocorticotropic hormone (ACTH), 166 exchange of gas, 138 healing of, 472
Advanced glycation end products (AGE), 122 Alveoli, 138 indications, 471
Afibrillar cementum, 18 Amelogenin, 19, 446 PD Miller classification, 472
AGEs. See Advanced glycation end products American Academy of Periodontology, 36 rootcoverage,472,473
(AGE) American Heart Association (AHA), 303 synonyms, 471
Aggregatibacter actinomycetomcomitans (Aa), 57, Amnion, 133, 135 technique applied, 471
76,138,227,247,285 Amoxicillin, 91, 222, 381 lateral positioned flap, 473
Aggressive periodontitis, 202, 213, 225 Amylase, 159 contraindications, 473
classification of, 225 Anaphylaxis, 71 flap preparation, 473
epidemiology, 225 Anchoring fibers, 5 indications, 473
historical background, 225 Anesthesia recipient site preparation, 473
prevalence, 226 local, 223 synonyms, 473
www.ajpdf.com
586 INDEX
Attrition, 18, 29 extension of gingival inflammation, caused CAPO. See Chronic ambulatory peritoneal
Autoclaving, 245, 518 by, 211 dialysis (CAPO)
Autograft mechanism of, 212 Capnocytophaga, 303
advantages of, 567 periodontal disease, bone formation Carcinoma, 88
disadvantages of, 567 in, 212 Cardiac arrhythmias, 175, 306
Automated calculus-detection systemic disorders, bone destruction Cardiovascular diseases, 300
technologies, 85 caused by, 212 cardiac pacemakers, 302
autofluorescence, 85 trauma from occlusion, bone destruction congestive heart failure, 301
fiber-optic endoscopy, 85 caused by, 212 hypertension, 300
spectro-optical technology, 85 Bone expansion, 564 ischemic heart diseases, 301
ultrasound, 85 Bone fill, 411 Cardioverter defibrillators, 300
Autotransplantation, 232 Bone grafts, 566 Case-control study, 577
Axial filaments, 62 Bone marrow, 25 Case study, 494
Bone morphogenetic protein (BMP), 440, 567 crown lengthening, 494
B Bone morphology in periodontal disease, depigmentation, 494
Bacteremia, 303 factors determining, 213 frenectomy, 494
Bacterial colonization, 59 Bone regeneration approaches, 448 gingival polyp excision, 494
Bacterial endocarditis, 61, 303 Bone sparing agents, 395 gingivoplasty, 494
Bacterial plaque, 31 Booster mechanism, 86 lingual frenectomy, 494
dentogingival, 31 BOP. See Bleeding on probing (BOP) operculectomy, 494
subgingival, 31 BP. See Blood pressure (BP) Cause-related phase of therapy, 298
supragingival, 31 BPE. See Basic periodontal Cavitational activity, 348
Bacterial zone, 182 examination (BPE) CBCT. See Cone beam computed tomography
Bacteriocins, 76 Breath malodor, 247 (CBCT)
Bacteroides gingivalis, 138 Brill' s technique, 155 CCD. See Charge-coupled device (CCD)
Bacteroides melaninogenicus, 183 Brown tumors, 123 CDC. See Centers for Disease Control and
Bad breath, 247 Brushing plane, 357 Prevention (CDC)
Basic fibroblast growth factor (bFGF), 440 Brushite, 83 CD4 molecule, 239
Basic fuchsin, 355 Bruxism, 95, 116 CEJ. See Cementoenamel junction (CEJ)
Basic periodontal examination (BPE), 256 Bullous lichen planus, 187 Cell-mediated immunity, 80
B-cell lesions, 78 Bupropion, 92, 374 Cellular cementum, 19
B-complex deficiency, 128, 129 Burn-out phenomenon, 227 Cellular elements in GCF, 155
Benign lesions of gingiva, 178 Buttressing bone formation, 99, 212 Cellular intrinsic fiber cementum, 19
focal fibrous hyperplasia, 178 Cellular mixed stratified cementum, 19
histological features, 178 C Cementa! hyperplasia, 20
Benzethonium chloride, 371 Cadaverine, 247 Cementa! resorption, 18
N-Benzoyl-DL-arginine-2-naphthylamide CADIA. See Computer-assisted densitometric Cementa! tears, 21
(BANA),285 image analysis (CADIA) clinical significance, 21
Betel nut, 255 CAF. See Coronally advanced flap (CAF) definition of, 21
bFGF. See Basic fibroblast growth factor CAL. See Clinical attachment loss (CAL) Cementicles, 13, 20
(bFGF) Calcospherites, 30 Cementoblasts, 17
Birbeck granules, 5 Calculocementum, 85 Cementoclasts, 18
Birth weight, 133 Calculus assessment, 44 Cementocytes, 18
Bite guard, 116 probe method of, 44 Cementodentinal junction (CDJ), 20
Bitewing radiographs, 269,270 Calculus deposition, factors affecting, 85 Cementoenamel junction, 19
Black colonies, 61 access to professional care, 85 clinical importance of, 19
Black hole, 263 age,85 overlapping- meeting-gap rule, 19
Bleeding on probing (BOP), 540, 573 calculus-inhibiting factors, 85 Cementoenamel junction (CEJ), 3, 213, 452
Blood pressure (BP), 300 diet, 85 Cementum, 12, 17, 30
Blood supply, 15 ethnic origin, 85 classification of
Bluish hue, 163 last dental scaling, time since, 85 based on cellularity, 18
BMP. See Bone morphogenetic oral hygiene habits, 85 acellular / primary, 18
protein (BMP) prescription medications, use of, 85 cellular/ secondary, 18
Bone augmentation systemic disease, 85 based on location, 18
advantages of, 564 Calculus inhibition theory, 86 coronal, 18
disadvantages of, 566 Calculus mineralization, 87 radicular, 18
technique used, 566 role of microorganisms in, 87 based on presence or absence of
Bone, characteristics of, 527 Cambium,23 fibrils, 18
bone healing, 527 Campylobacter rectus, 55, 64, 76,230,247,314 a fib rillar, 18
Bone, composition of, 527 Cancellous bone, 24 fibrillar, 18
bundle, 527 marrow spaces, 24 composition, 17
composite, 527 Candida, 38 cementoblasts, 17
larnellar, 527 Candida albicans, 70, 89, 120, 183, 222 cementoclasts, 18
wooven, 527 Candidiasis, 241 cementocytes, 18
Bone destruction, 211 erythematous, 241 developmental and acquired anomalies
etiology of, 211 pseudomembranous, 241 of, 20
INDEX 587
functions of, 18 symptoms of, 219 COPD. See Chronic obstructive pulmonary
collagen fibers, attachment of, 18 treatment by, 220 disease (COPD)
occlusal relationship, 18 compromised therapy, 221 Corkscrew motion, 61
root surface integrity, 18 initial therapy, 221 Coronal cementum, 18
overlapping of, 19 periodontal surgical procedures, 221 Coronally advanced flap (CAF), 473
physical characteristics, 17 Circumferential supracrestal fiberotomy with guided tissue regeneration, 474,479
resorption and repair, 21 (CSF), 510 multiple recessions, management of, 474
Centers for Disease Control and Prevention Cleansing instruments, 328, 329 with subepithelial connective tissue
(CDC), 88, 515 air-powder polishing, 329 graft, 473, 476
Central buttressing, 99 bristle brushes, 329 Coronary heart disease (CHD), 131
Central nervous system (CNS), 388 dental tape, 329 Corticosteroids, 306
CEP. See Cervical enamel projections (CEP) rubber cups, 328 Cortisone, 126
Ceramic-tissue interaction behavior, 444 Clinical attachment loss (CAL), 259 Counter rotational powered
bioactive glasses, 444 Clinical considerations, 16 toothbrushes, 358
biologic modifiers, 445 periodontal ligament to trauma, response COX-1, 388
calcium phosphate bone cement, 444 of, 16 COX-2, 388
hydroxyapatite, 444 Clinical diagnosis, aids in, 281 Coxibs, 388
tricalcium phosphate, 444 gingival bleeding, 281 CPITN. See Community periodontal index of
Cervical enamel projections (CEP), 293 gingival temperature, 281 treatment needs (CPITN)
Cetylpyridinium, 249 periodontal probing, 281 C-reactive protein (CRP), 136
C G Davis classification, 35 tooth mobility assessment, 282 Cribriform plate, 15, 24
Charge-coupled device (CCD), 271 Clinical epidemiologic studies, 99 Critical instruments, 518
Charter's method, 359 Clinical features and histopathologic features, Cross-arch finger rest, 337
CHD. See Coronary heart disease (CHD) correlations of, 207 Crossbite, 115
Checkerboard DNA-DNA hybridization Clinician position, 333,334 Cross syndrome, 177
technique, 286 Clonidine, 92 Crown lengthening, 480,483
Chediak-Higashi syndrome, 66, 277 CMOS. See Complementary metal-oxide contraindications, 482
Cheilitis, angular, 241 semiconductors (CMOS) indications, 480
Chemical gingivectomy, 418 CNS. See Central nervous system (CNS) Crown-root ratio, 267
Chemical irritation, 114 Coaggregation, 57, 77 CRP. See C-reactive protein (CRP)
Chemically modified tetracyclines (CMT), 394 Coagulation disorders, 309 Cryptococcus neoformans, 70
Chemical plaque control, 356 hemophilia A, 309 CSF. See Circumferential supracrestal
Chemotaxis, 79, 90 hemophilia B, 309 fiberotomy (CSF)
Chemotherapy, 308 Combination therapy, 395 CT. See Computerized tomography (CT)
CHF. See Congestive heart failure (CHF) Combined enlargement, 176 Curettes, 325, 412
Chief complaints, 105, 253 Combined osseous defect, 214 area specific, 325
Chin-down position, 335 Combined therapy extended shank, 326
Chin graft, surgical techniques for, 567 importance of, 380 Gracey curvettes, 325, 326, 327
Chisel scalers, 327 treatment goals, 380 !anger, 327
Chlorhexidine gluconate, 367 endogenous infection, 380 mini-bladed, 327
adverse effects of, 368 exogenous infection, 380 mini !anger, 327
antibacterial action of, 368, 369 superinfection, 380 gingival, 412, 413
antiplaque action of, 367 Community periodontal index (CPI), 49, 50 subgingival, 412, 413
indications for use, 368 Community periodontal index of treatment universal, 325,326
Chorioamnionitis, 134 needs (CPITN), 48, 49 Current smokers, 88, 91
Christmas disease, 309 Compact bone, histologic section of, 24 Cyclosporine, 175
Chronic ambulatory peritoneal dialysis Complementary metal oxide semiconductors Cytokine interleukin-6 (IL-6), 27
(CAPD),307 (CMOS),271 Cytolethal distending toxin, 77, 229
Chronic gingivitis, 59, 256 Complement system, 68 Cytomegalovirus, 60
Chronic obstructive pulmonary disease alternate pathway, 68 Cytotoxic reactions, 71
(COPD), 131, 137 classical pathway, 68
anatomy, 137 lectin pathway, 70 D
physiology, 137 Complex pocket, 205 Decalcified freeze-dried bone allograft
Chronic periodontitis, 60, 218 Compound pocket, 205 (DFDBA), 567
clinical features, 218 Computer-assisted densitometric image Deciduous dentition, periodontium
differentiation characteristics of, 220 analysis (CADIA), 284 of, 198
disease distribution, 219 Computed tomography (CT), 271 physiologic gingival changes, 198
disease progression, 220 Cone beam computed tomography eruptive stage, 198
disease severity, 219 (CBCT), 270 posteruptive stage, 198
microbiologic features, 219 Congenital cardiac diseases, 49 preemptive stage, 198
radiographic features, 218 Congestive heart failure (CHF), 301 Dehiscence, 26, 542
risk factors for, 220 Connective tissue cells, 13 Delayed-type hypersensitivity, 72
environmental factors, 220 macrophages, 14 Delmopinol, 371
genetic factors, 220 mast cells, 13 Demineralized freeze-dried bone grafts
localfactors,220 Continuous sutures, 429 (DFDBA), 443
systemic factors, 220 Conventional finger rest, 337 Denquel, 408
586 INDEX
Dental calculus, 83 Dental pulp, 102 advantages of, 552

classification of, 83 excessive occlusal forces, 102 contraindications, 552
composition of, 83 insufficient occlusal forces, 102 disadvantage of, 552
inorganic components, 83 Dentifrices, 372 indications of, 552
organic components, 84 application of, 373 procedure of, 551
definition of, 83 composition of, 372 Disclosing agents, 354
detection of, 85 recent development in, 373 application of, 355
rate of formation, 85 Dentinal hypersensitivity, treatment of, 492 examples of, 355
structure of, 84 Dentin hypersensitivity, 458 properties of, 354
Dental caries, 353 Dentistry, 108 utility of, 354
Dental contraindications, 350 gingiva, retraction of, 108 Disease prevalence, 41
Dental disease, 353 rubber dam, use of, 108 Disease status, 280
Dental floss, 364 Dentists, precautions for, 245 clinical evaluation, 280
dental tape, 364 Dentomycin, 385 diagnostic sequence, 280
floss holder, 364 Dermatologic lesions, 191 data, collection of, 280
floss threader, 365 bullous pemphigoid, 192 primary diagnosis, 280
functions of, 365 clinical features, 193 disease activity, 280
power flossers, 364 differential diagnosis, 193 histological evaluation, 280
textured floss, 364 histologic features, 193 microbiological techniques, application
Dental follicle, 12 treatment, 193 of, 281
Dental health care personnel (DHCP), 514 chronic ulcerative stomatitis. 194 periodontal diagnosis, early approaches
Dental health professionals, role of, 92 histology, 194 to, 280
Dental implants, 232 oral lesions, 194 probing, limitations of, 280
surgical aspects of, 537 treatment of, 194 radiographic diagnosis, 281
biological complications, 542 lichen planus, 191 Distal wedge procedures, 424, 425
two stage surgical technique, 538 clinical features, 191 OM. See Type 2 diabetes mellitus (OM)
complications, 539 differential diagnosis, 191 Down syndrome, 277
dense bone protocol, 538 histologic features, 191 Drug administration, routes of, 380, 381
drilling sequences, 538 treatment of, 191 local route, 381
flap design, 538 mucous membrane pemphigoid, 192 systemic route, 380
implant placement, 539 differential diagnosis, 192
screw tap protocol, 538 histology, 192 E
mechanical complications, 542 treatment, 192 EACA. See Epsilonaminocaproic acid (EACA)
one-stage versus two-stage implant pemphigus vulgaris Early gingivitis, 162
surgeries, 537 clinical features, 193 Easlick disclosing solution, 355
second stage surgical technique, 537 treatment of, 193 EBO. See Evidence-based dentistry (EBO)
therapy, 560 Desquamative gingivitis (DG), 187, 190 Ecologic plaque hypothesis, 59
treatment planning, 530 Dexterity, 215 Eikenella corrodens, 64, 76, 303
contraindications, 530 Dextranase, 371 ELAM-1, 79
dental, 530 DFDBA. See Decalcified freeze-dried Electronic nose, 249
general, 530 bone allograft (DFDBA); See also Electrosurgery, 414, 416
medical, 530 Demineralized freeze-dried bone advantages of, 417
indications, 530 grafts (DFDBA) disadvantages of, 417
Dental lasers DG. See Desquamative gingivitis (DG) healing process, 417
delivery systems, 486 DHCP. See Dental health care personnel technique used, 414
laser energy, emission modes, 487 (DHCP) Elephantiasis gingivae, 176
continuous wave mode, 487 Diabetes mellitus, 120, 122, 135, 277 ELISA. See Enzyme-linked immunosorbant
free running pulsed mode, 487 bacterial pathogens in, 123 assay (ELISA)
gated pulsed mode, 487 complications of, 121 Elyzol, 385
wavelength of, 486-488 oral manifestations of, 120 Embolus, 132
Dental mirrors, 322, 323 burning mouth and tongue, 120 Enamel epithelia, 12
Dental office, agents used in, 408 cheilosis, 120 Endocrine disorders, 120
Dental plaque, 56, 353, 354 diminished salivary flow, 120 diabetes mellitus, 304
bacterial aggregations, 56 mucosa! drying and cracking, 120 insulin-dependent diabetes, 304
biofilm, 56 and periodontal disease, interrelationship laboratory evaluation of, 304
calcification of, 353 between, 124 non insulin-dependent diabetes, 304
composition of, 56 Diagnostic casts, 536 polydipsia, 304
definition of, 56, 353 radiographic examination, 536 polyphagia, 304
description of, 57 Diagnostic testing, strategies for, 288 polyuria, 304
fate of, 353 determinant, use of, 288 Endodontic lesions, primary, 460, 462
formation of, 56 rationale for testing, 288 Endodontic periodontal lesions
bacterial adherence, 56 Dicationic bisguanide, 368 classification of, 459
organic pellicle, 56 Dichlorodifluoromethane, 465 by Simon, 459, 460
plaque maturation, 56 Diffuse gingivitis, 170 by world workshop for classification of
rate of formation, 353 Digital wedge, 425 periodontal diseases, 459
structure of, 57 Direct pickup technique, 550 on origin of periodontal pocket, 460
INDEX 587
periodontitis associated with Exostoses, 213 Full mouth disinfection, 4
endodontic disease, 459 Expanded polytetrafluoroethylene, 91, 448 Full-thickness flap, 419
diagnosis of, 462, 463 Explorer instruments, 324 Functional ankylosis, 527
pain, 462 Extracoronal splinting, 398, 399 Functionalshank,321
periodontal probing, 463 Extraoral fulcrums, 338 Funneling, 100
swelling, 463 palm-down, 338 Furcation, 450
tests of, 464 palm-up, 338 Furcation involvement, 215, 260, 450
cold, 465 bacterial plaque, 452
electric, 465 F bifurcation ridges, 453
fistula tracing, 465 Failing implant, 572 enamel earls, 453
heat, 465 Tetralogy of Fallot, 303 enamel projection, 453
palpation, 464 False gingival enlargement, 180 furcation defects, platelet-rich plasma
percussion, 464 Fat-soluble vitamins, 128 in, 454
pulp testing, 464 vitamin A, 128 tooth sectioning, 455,456
radiographs, 465 vitamin D, 128 tunnel preparation, 455
test cavity, 465 vitamin E, 128 furcation morphology, 452
Endosteum, 24 FDA. See US Food and Drug Administration entrance diameter, 452
Endotoxin, 62 (FDA) entrance location, 452
Environmental infection control, 521 FDBA. See Freeze-dried bone allografts location of, 452
Environmental Protection Agency (FDBA) root concavities, 452
(EPA),521 FEA. See Finite element analysis (FEA) grade I, 450
Enzyme-linked immunosorbant assay Female reproductive cycle, 124 grade II, 450
(ELISA), 243, 285 Female sex steroid hormones, periodontal grade III, 450
Enzymes, 371 changes grade IV, 450
EPA. See Environmental Protection Agency corticosteroid hormones, 126 lingual radicular bone, 453
(EPA) menopause, 126 root anatomy, 453
Epidemiologic indices, 41 menstruation, 125 therapeutic modalities in, 454
Epidemiology, 41, 576 pregnancy, 125 Fusobacterium nucleaium, 55, 64, 76, 138,
analytical studies, 577 puberty, 125 222,314
clinical practice, 578 Fenestration, 26
question framing, 578, 579 Fiberotomy, 510 G
search strategy, 579 Fibrillar cementum, 18 Gantrez, 372
descriptive studies, 577 Fibrotic gingival enlargement, 174 GAP. See Generalized aggressive
determinants, study of, 41 drug-induced gingival enlargement, 174 periodontitis (GAP)
distribution, study of, 41 anticonvulsants, 174 Gap junctions, 6
experimental studies, 578 calcium channel blockers, 175 Gaucher disease, 277
observational studies, 577 clinical features, 174 GCF. See Gingival crevicular fluid (GCF)
Epigenetics, 149 histological features, 175 Generalized aggressive periodontitis (GAP),
definition of, 149 immunosuppressants, 175 202,230
mechanism of, 149 pathogenesis, 175 microbiology of, 230
pathogenesis of periodontitis, 149 prevention and treatment, 176 radiographic feature of, 230
Epitactic concept, 86 Fibrotic gingival enlargement, syndromes risk factors, 231
Epithelial cells, 13 associated with, 177 Genetic analysis, methods of, 144
Epithelial tissue, 153 File hoes, 327 association analysis, 144
Epithelium-associated plaque, 57 Fimbriae, 77 familial aggregation, 144
Epsilonaminocaproic acid (EACA), 310 Finger-on-finger rest, 338 linkage analysis, 144
Epstein-Barr virus, 60 Finger rests, 337 segregation analysis, 144
ePTFE. See Polytetrafluoroethylene First-generation antiplaque agents, 367 twin studies, 144
membranes (ePTFE) Flat contact, 109 Genetic disorders, types of, 142
Erythema multiforme, 187, 195 Flexible spiral wire (FSW), 509 complex genetic diseases, 142
differential diagnosis, 195 Foam cells, 132 simple mendelian diseases, 142
histopathology, 195 Folic acid, 128, 129 Genetics, 140
treatment, 195 Formative cells, 12 definition of, 140
Erythematous candidiasis, 241 cementoblasts, 12 nucleotides, 141
Erythromycin, 175 fibroblasts, 12 adenine, 141
Erythrosine, 355 osteoblasts, 13 cytosine, 141
Escherichia coli, 89 Foster-Miller probe, 282 guanine, 141
European Workshop on Periodontics, 38 Free gingival groove, 3 thymine, 141
Evidence-based dentistry (EBO), 576 Freeze-dried bone allografts (FDBA), 443 terminology, 140
Excisional instruments, 329 Frenectomy, 477, 510 allele, 140
Excisional new attachment procedure, 413 Frenotomy, 510 autosomal dominant, 140
caustic drugs, 413 FSW. See Flexible spiral wire (FSW) autosomal recessive, 140
technique, 413 Fulcrum autosome, 140
ultrasonic curettage, 413 palm-down, 338 chromosome, 140
Exodontic procedures, 113 palm-up, 338 concordance, 140
Exogenous infections, 380 Fulcrum finger, 337 dizygotic twins, 140
586 INDEX
Genetics (cont.) hereditary fibromatosis gingival techniques used for, 414

gene, 140 enlargement, 201 Gingivectomy knives, 329
genome, 140 with HSV I infection, 201 Gingivitis, 37, 88, 166, 200
genotype, 140 with poor oral hygiene, 200 classification of, 170
locus, 140 puberty gingivitis, 201 acute, 170
monozygotic twins, 140 scorbutic gingivitis, 202 chronic, 170
mutations, 140 Gingival embrassures, 363 recurrent, 170
phenotype, 140 classification of, 363 subacute, 170
polymorphism, 140 class 1,363 clinical features of, 166, 200
Gestational diabetes, 133 class 2,364 bleeding on probing, 168
GI. See Gingival index (GI) class 3,364 consistency, 168
Gingipain R, 77 Gingival enlargement, 172 contour and shape, 168
Gingitage technique, 501 classification of, 172 gingiva, color of, 166
Gingiva, 12 degree of, 172 epithelium, keratinization of, 166
anatomical features, 4 distribution of, 172 melanin pigmentation, 166
attached, 4 pregnancy-associated, 177 vascular supply, 166
connective tissue of, 12 clinical features, 177 gingival recession, etiology of, 169
definition of, 3 histological features, 177 faulty brushing technique, 169
interdental gingiva, 4 Gingival epithelium, 30 gingival ablation, 170
macroscopic features, 3 keratinization of, 30 gingival inflammation, 170
Langerhans cells, 5 significance of, 30 tooth malposition, 170
melanocytes, 5 Gingival exudate, 170 melanin, 167
Merkel cells, 5 classification, 170 position of gingiva, 169
oral epithelium (OE), 5 distribution of, 170 size, 168
marginal gingiva, 3 Gingival index (GI), 45, 158 surface texture, 169
free gingival groove, 3 Gingival inflammation, 161, 211 diabetes mellitus-associated, 60
gingival sulcus, 3 definition of, 161 host response of, 79
microscopic features, 4 factors of, 500 to periodontitis, progression of, 154
and periodontal abscess, differentiation marginal fit, 501 determining factors, 154
between, 236 retraction, 501 pregnancy-associated, 59
Gingival anoxemia, 163 chemically treated cords, 501 stages of, 200
Gingival bleeding index, 46 electrosurgery, 501 advanced lesion, 200
Gingival connective tissue, 30 physical retraction, 501 early lesion, 200
Gingival crevicular fluid (GCF), 77, 155, surgical, 501 established lesion, 200
281,382 Gingival margin initial lesion, 200
cellular and humoral activity, 157 contouring of, 186 Gingivoplasty, 414
clinical significance of, 157 nutritional supplements, 186 indications, 414
circadian periodicity, 157 persistent or recurrent cases, 186 steps of, 414
diabetes mellitus, 157 discrepancies, 509 Glossitis, 128
mechanical stimulation, 157 Gingival physiotherapy, 366 Grace and Smales, mobility index, 262
periodontal therapy, 157 Gingival pigmentation, 480 CTR. See Guided tissue regeneration (GTR)
sex hormones, 157 Gingival pocket, 163 Guided bone regeneration, 566
smoking, 157 Gingival polyp, 121 Guided tissue regeneration (GTR), 91,
composition of, 155 Gingival protection theory, 501 440,566
antibacterial factors, 155 Gingival squamous cell carcinoma, 277 Gutka, 254
cellular elements, 155 Gingival sulcus, 3, 4, 161 G V Black classification, 36
electrolytes, 155 Gingival swelling, 168
enzymes, 155 Gingival wall of pocket, microtopography H
organic compounds, 155 of, 207 HAART. See Highly active antiretroviral
methods of collection, 155 periodontal pockets as healing lesion, 207 therapy (HAART)
crevicular washing methods, 155 pocket contents, 207 Halimeter, 249
filter paper strips, 155 pus formation, significance of, 207 Halitophobia, 247, 248
microcapillary tubes, 155 root surface wall changes, 208 Halitosis, 247
twisted threads, 155 chemical changes, 208 diagnosis of, 248
Gingival curettage, 412 cytotoxic changes, 208 breath odor, 249
Gingival cyst, 179 structural changes, 208 electronic use, 249
Gingival depigmentation, 480 Gingiva, malignant lesions of, 179 gas chromatography, 249
Gingival diseases, 200 Kaposi sarcoma, 179 nasal breath odor, 249
in childhood, types of, 200 nodular melanoma, 179 oral cavity odor, 249
with acute bacterial infection, 201 squamous cell carcinoma, 179 organoleptic method, 248
acute necrotizing ulcerative Gingivectomy, 414,415 portable volatile sulfide monitor, 249
gingivitis, 201 contraindications, 414 saliva incubation test, 249
with aphthous stornatitis, 201 by electrosurgery, 414 self-evaluation, 248
chronic nonspecific gingivitis, 201 healing process, 414 tongue coating, 249
drug-induced hyperplasia, 202 indications, 414 extraoral causes, 248
eruption gingivitis, 200 rationale, 414 ear-nose-throat,248
INDEX 587
gastrointestinal tract, 248 Host modulation therapy, 395 early placement, 543
lungs, 248 Host tissue damage, microbial mechanism immediate placement, 543, 544
intraoral causes, 247 of, 78 contraindications, 543
dental causes, 247 Howship lacunae, 13 indications for, 543
periodontal pathology, 247 HPA. See Hypothalamic-pituitary-adrenal Immune complex hypersensitivity, 71
tongue, contribution of, 248 (HPA) axis Immune reactions, 71
xerostomia, 248 Hu-Friedy implacare system, 328 anaphylactic reactions, 71
oral malodor, treatment aspects for, 249 Human gene polymorphism, 143 complex reactions, 71
gum chewing, 249 types of, 143 cytotoxic reactions, 71
masking of, 250 Human immunodeficiency virus (HIV), 238, delayed hypersensitivity reactions, 71
mouth rinses, 249 295,514 Immune response, mediators of, 72
tongue cleaning, 249 antibody diagnosis, 243 Immune system
toothpastes, 249 antiretroviral treatment, 244 cells of, 64
HCV. See Hepatitis C virus (HCV) CDC surveillance case classification, 240 immunoglobulins, 68
HDL. See High-density lipoprotein (HDL) life cycle of, 239 lymphocytes, 66
Heat shock proteins, 132 oral lesion classification, 240 macrophages, 66
Helicobacter pylori, 132 less commonly associated, 241 mast cells, 66
Hematological disorders, 127 strongly associated, 241 neutrophils, 64
anemia, 127 stages of, 239 effect of smoking on, 90
leukemia, 127 advanced immune deficiency, 239 Immunoglobulins, 68
periodontal manifestations, 127 early immune deficiency, 239 functions of, 68
thrombocytopenia, 127 intermediate immune deficiency, 239 gamma globulins, 68
Hemidesmosomes, 5 primary infection, 239 IgA, 68
Hemiseptum, 214 tissues susceptible to, 239 IgD, 68
Hemochromatosis, 166 transmission modes, 239 IgE, 68
Hemoglobin, 127 viral infections, 242 IgG, 68
Heparin, 310 hairy leukoplakia, 243 IgM, 68
Hepatitis B virus (HBV), 312 herpetic gingivostomatitis, 242 Immunological diagnosis, aids in, 284
Hepatitis C virus (HCV), 312 Kaposi sarcoma, 243 enzyme-linked immunosorbent assay, 285
Hereditary gingival fibromatosis, 38 molluscum contagiosum, 243 evalusite, 285
Herpes simplex virus, 186 varicella zoster infections, 242 immunodiagnostic methods, 284
Herpetic gingivostomatitis, 186 xerostomia, 243 direct immunofluorescent assays, 284
Herpetic whitlow, 187 Human leukocyte antigen (HLA), 147,229 flow cytometry, 284
Hertwig epithelial root sheath, 12 Humoral immune response, 80 indirect immunofluorescent assays, 284
Heterogeneous nucleation concept, 86 Hydraulic sinus lift, 562 latex agglutination assay, 285
High-density lipoprotein (HDL), 136 Hydrogen peroxide, 57 Immunosuppression, 308
Highly active antiretroviral therapy Hydroxyl radicals, 57 Implamed Wiz-Stik instrument, 328
(HAART), 244 Hypercalcemia, 48 Implant-bone interface, 527
HIV. See Human immunodeficiency virus Hypercementosis, 272 Implant crowns, cementation of, 556
(HIV) Hyperkeratosis, 89 Implant dentistry, periodontal considerations
HLA. See Human leukocyte antigen (HLA) Hypermobility, 261 in, 114
Hoe scalers, 327 Hyperparathyroidism, 123, 277 microbial and biomechanical factors, 114
Horizontal mattress suture, 429 Hyperpituitarism, 277 objectives of, 114
Hormonal changes, 123 Hyperthyroidism, 166 Implant displacement, 540
female sex hormones, 123 Hypertrichosis, 177 Implant level impression technique, 548
gonadotropins, follicle-stimulating Hypocalcemia, 306 closed tray, 548
hormone (FSH), 123 Hypoglycemia, 305 open tray, 548
luteinizing hormone (LH), 123 Hypophosphatasia, 129 Implant occlusion factors, 556, 557
Host bacterial interaction, 76 Hypothalamic-pituitary-adrenal (HPA) axis, 306 Implant patients, maintenance for, 526
immunologic aspects of, 78 Implant placement, surgical aspects of, 537
innate host response, 78 I informed consent, 537
microbiologic aspects of, 77 Iatrogenic diseases, 108 Implant placement, surgical procedures
bacterial adherence, 77 Iatrogenic factors, 108 in, 491
bacterial evasion of, 77 IDDM. See Insulin-dependent diabetes Implant-prophy+plastic instruments, 328
host tissue invasion, significance of, 77 mellitus (IDDM) Implant restoration, 547
virulence factors of, 76 Idiopathic gingival enlargement, 176 Implants, abutments in, 552
Aggregatibacter actinomycetemcomitans, 76 etiology, 176 custom-made abutments, 554
Porphyromonas gingivalis, 77 histological features, 176 advantages, 554
Host immunoinflammatory response, 393 treatment, 176 disadvantages, 554
bisphosphonates, 395 IE. See Infective endocarditis (IE) one-piece abutment, 554
chemically modified tetracyclines, 394 IGF. See Insulin-like growth factor (IGF) advantages, 554
inflammatory mediators, 393 IHD. See Ischemic heart disease (IHD) disadvantages, 554
matrix metalloproteinases, 393 IL-6. See Cytokine interleukin-6 (IL-6) prefabricated abutments, 553
proinflammatory cytokines, 393 Immediate hypersensitivity reaction, 71 advantages of, 554
prostaglandins, 393 Immediate implant treatment modality, 542 contraindications, 554
subantimicrobial dose doxycycline, 395 delayed placement, 543 disadvantages of, 554
586 INDEX
Implants, abutments in (cont.) Inferior alveolar nerve repositioning, 569 Interproximal crater, 215
indications, 554 Inflammatory cells, 79 Interradicular septum, 25
standard, 553 complements, 79 Intracoronal splinting, 398, 400
two-piece abutments, 554 cytokines, 79 Intraoral finger rest, 337
advantages, 554 metalloproteinases, 79 conventional, 337
disadvantages, 554 polymorphonuclear leukocytes, 79 cross arch, 337
types, 552 prostaglandins, 79 finger-on-finger, 337, 338
Implant-soft tissue interface, 528 proteinases, 79 opposite arch, 337, 338
Implant-supported Inflammatory diseases, role of antibodies in, 68 reinforced, 337
prosthesis, occlusal considerations in, 555 ag-ab complex, phagocytosis of, 68 Ionic toothbrushes, 357
importance of, 555 bacterial allergens, neutralization of, 68 IPD. See Intermittent peritoneal dialysis
occlusal adjustment, 556 cell-mediated immunity, suppression of, 68 (IPD)
occlusal goal, 556 complement system activation, 68 Irrigation devices, 366
restorations, types of, 557 lymphocytes, blocking of, 68 Irritation fibroma, 178
cement-retained, 558 plaque bacteria, opsonization/bacteriolysis Ischemia, 29
advantages, 558 of, 68 Ischemic heart disease (IHD), 136
disadvantages, 558 Inflammatory gingival enlargement, 173
indications, 558 chronic inflammatory, 173 J
screw-retained, 557 clinical features, 173 Jiggling, 113
advantages, 558 etiology, 173 Junctional epithelium, 154
disadvantages, 558 histologic features, 173
indications, 558 treatment, 173 K
Impression copings, 547, 548 acute inflammatory, 173 Kanamycin, 371
abutment, 547 clinical features, 173 Kawasaki disease, 303
pick-up type, 547 etiology, 173 Keratinocyte, 5
transfer type, 547 gingival abscess, 173 Keratin-producing cells, 4
Impression technique, 547 histological features, 174 Kirkland knife, 329
abutment level, 547 treatment of, 174 Klebsiella pneumoniae, 138
implant level, 547 Inflammatory process, 79 Knife-edged margin, 168
Inadvertent gingival curettage, 412 Infrabony pockets, 205
indications, 412 Innate host response, 78 L
procedures, 412 gingival epithelium, toll-like receptors Labial frenal attachments, 476
rationale, 412 expressed on, 79 gingival, 476
Incidental attachment loss, 227 periodontal tissues, toll-like receptors in, 79 muscosal, 476
Index, 41 Instrument activation, 339 papilla penetrating, 476
classification of, 42 Instrument adaptation, 339 papillary, 476
cumulative, 42 Instrument angulation, 339 Laboratory analogs, 547, 548
disease, 42 Instrumentation, principles of, 333 abutment implant, 547
full mouth, 42 dental light position, 334, 335 implant, 547
irreversible, 42 positioning, 333 Lactobacillus thiocyanate system, 159
reversible, 42 Instrument grasp, 336 Lactoferrin, 55
simple,42 modified pen, 336 Lactoperoxidase, 55
simplified, 42 palm,336 Lamina densa, 5
symptom,42 Instrument shank Lamina lucida, 5
treatment, 42 design features of, 321 Lamina propria, 5
definition of, 41 complex, 321 Langer curettes, 327
Indirect transfer impression technique, 548 functional and lower, 321, 322 Langerhans cells, 5
advantages of, 550 simple, 321 LAP. See Localized aggressive periodontitis
disadvantages of, 550 working end of, 321 (LAP)
indications for, 550 Insulin-dependent diabetes mellitus LAP, Aa as etiologic agent, 229
procedure of, 548 (IDDM), 120 environmental factors, 230
Individual tooth prognosis, 290 Insulin-like growth factor (IGF), 440 genetic factors, 229
Infections, transmission control of, 514 Insulin resistance, 136 immunologic factors, 229
contaminated instruments, transport Intercellular adherens, 153 virulence factors, 229
of, 517 Interdental LASER. See Light amplification by stimulated
automated cleaning equipment, 521 brushes, 356 emission of radiation (LASER)
instrument processing area, 517 cleaning aids, 364 Laser gingivectomy, 417
manual cleaning, 518 gingiva, 4 Lasers
exposure prevention strategies, 514 knives, 329 biostimulation of, 490
personal protective equipment, 516 papilla, reconstruction of, 483 fluorescence of, 490
protective measures, 515 septum, 24 photoacoustic effect of, 490
Infectious diseases, 311 Interferons, 153 photochemical effect of, 489
hepatitis, 311 Intermediate cementum, 19 photothermal effect of, 489
HIV, 312 Intermittent peritoneal dialysis (IPD), 307 Laser-tissue interactions, 488
tuberculosis, 312 Internal bevel gingivectomy, 414 absorption, 488
Infective endocarditis (IE), 303 International normalized ratio, 310 reflection, 488
INDEX 587
scattering, 488 Manual toothbrushes, 357 Molecular biology, diagnostic methods based
transmission, 488 Marginal plaque, 56 on,285
Lateral periodontal cyst, 237 Marrow cells, 124 checkerboard DNA-DNA hybridization
LBW. See Low birth weight (LBW) Marrow spaces, histologic section, 25 technique, 286
Leonard method, 359,361 Mast cells, 66 detection of elastase, chairside test
Leukemia, 178 connective tissue, 66 for, 288
clinical features, 178 gingival connective tissue, 66 genetic susceptibility test, 287
histological features, 178 Materia alba, 56 host-derived enzymes, 287
Leukocyte disorders, 128 Matrix metalloproteinases (MMP), 77, Aalkaline phosphatase, 287
agranulocytosis, 128 231,287 aspartate aminotransferase alkaline, 287
lazy leukocyte syndrome, 128 Mattress sutures, 429 cathepsin, 287
leukocyte adhesion deficiency, 128 Maxillary sinus lift surgery, 560 elastase, 287
neutropenia, 128 anatomy, 560 ~-Glucuronidase,287
Leukopenia, 59 complications, 564 matrix metalloproteinases, 287
Leukotoxin, 59 lateral window technique, 562 host response characterization, 287
Lichen planus (LP), 190 osteotome technique, 560 inflammatory mediators, 287
Light amplification by stimulated emission of MBL. See Mannan-binding lectin nucleic acid probes, 285
radiation (LASER), 377 (MBL) polymerase chain reaction, 286
Linear gingival erythema, 242 McCall festoons, 101 restriction endonuclease assay, 286
Linear IgA disease (LAD), 194 Mechanical plaque control, 128 Mombelli bleeding, 257
differential diagnosis, 194 Medical diagnosis, 279 Morpholinoethanol, 371
histopathology, 194 administrative uses, 279 Mucogingival junction, 3
oral lesions, 194 clinal uses, 279 Mucogingival problems, 468
treatment, 194 research uses,279 Mucous membrane pemphigoid
Lines of human evidence, 314 Melanin pigmentation, 5 (MMP), 190
Lipopolysaccharides, 59 Melanocytes, 5 Murray-Puretic-Drescher syndrome, 177
Lipoxins, 395 derived from neural crest cells, 5 Muscle action theory, 501
Liquid dentifrice, 373 Mendelian diseases, 142 Mutations and polymorphisms, difference
Liver diseases, 307 Menopausal gingivostomatitis, 123 between, 143
causes of, 307 Merbromin, 355 Mycobacterium avium iniracellulare, 240
LLLT. See Low-level laser therapy (LLLT) Mercurochrome preparations, 355 Mycobacterium tuberculosis, 514
Local drug delivery system, 231 Merkel cells, 5 Myocardial infarction (MI), 301
Localized aggressive periodontitis (LAP), 60, Metabolic disorders, 120
202,228 Metal intoxication, 129 N
microbiology of, 228 Metallic ions, 370 National Health and Nutrition Examination
Localized periodontitis, 219 MI. See Myocardial infarction (MI) Survey (NHANES III), 88
Low birth weight (LBW), 134 Microbial colonization, 64 National Institute of Dental and Craniofacial
Low-level laser therapy (LLLT), 491 commensal, 64 Research (NIDCR), 282
LP. See Lichen planus (LP) pathogenic, 64 Nd:YAG laser wavelengths, 489
Lupus erythematosus, 194 Microbiological diagnosis, aids in, 284 Necrotizing gingivostomatitis, 242
discoid lupus erythematosus (DLE), 194 bacterial culturing, 284 Necrotizing ulcerative gingivitis (NUG), 36,
systemic lupus erythematosus (SLE), 194 direct microscopy, 284 181,222,242,295
Lymphatic drainage, 15 Microphthalmia, 177 bacteria to characteristic lesion, relation
Lymphocytes, 66, 156 Microsurgery, 494 of, 182
B lymphocytes, 66 advantages of, 497 clinical features, 181
secondary immune response, 66 illumination, 494, 497 definition of, 181
synthesis of, 66 instruments, 494, 497 diagnosis, 184
T lymphocytes, 66 magnification, 494 epidemiology and prevalence, 184
Lymphotoxin, 212 for periodontal application, 497 etiology, 183
Lysozyme,55 periodontal plastic surgery, 497 extraoral and systemic signs and
regenerative therapy, 497 symptoms, 181
M root preparation, 497 oral symptoms, 181
Macrophages, 66 Microtopography, 528 treatment of, 184
destructive functions, 66 additive, 528 Necrotizing ulcerative periodontitis (NUP),
peripheral blood monocytes, 66 subtractive, 528 37,222,242,295
protective functions, 66 Mimicking desquamative gingivitis, 196 etiology, 222
Magnesium whitlockite, 83 Mineralization of calculus, theories in HIVpositive/ AIDS patients, 222
Magnetostrictive ultrasonic scaler, 346 regarding, 86 immunosuppression, 223
Magnetostrictive unit, 328 booster mechanism, 86 malnutrition, 223
Magnification systems, 497 calculus inhibition theory, 86 microbial flora, 222
prism loupes, 497 epitactic concept, 86 psychological stress, 223
surgical microscope, 497 heterogeneous nucleation concept, 86 treatment, 223
telescopic loupes, 497 Mini-Langer curettes, 327 Necrotizing ulcerative stomatitis (NUS), 222
Malocclusion, 115 MMP. See Matrix metalloproteinases Neisseria gonorrhoeae, 38
tooth malalignment, 115 (MMP); See also Mucous membrane Neodymium:yttrium-aluminum-garnet
Mannan-binding lectin (MBL), 70 pemphigoid (MMP) (Nd: YAG), 490
586 INDEX
Nerve supply, 15 occlusal surface, 502 regeneration, 440

Neurofibromatosis, 166 periodontal disease, 502 surgery, 431, 432
Neurosensory impairment, 540 Occlusal forces, types of, 94 additive, 432
Neutrophil-rich zone, 182 Occlusal stresses in periodontal tissues subtractive, 432
Neutrophils, 64 treatment of, 102 ostectomy, 432
defects, 65 coronoplasty, 102 osteoplasty, 432
disorders, periodontal disease with, 66 occlusal adjustment, 102 topography, 26
mechanism of, 64 occlusal bite planes, 102 Osteoplasty, indications of, 437
NHANES III. See National Health and orthodontics, 102 Osteopontin, 154
Nutrition Examination Survey permanent or temporary splint, 102 Osteoprogenitor cells, 527
(NHANES III); See also Third Occlusal traumatism, 93, 453 Osteoradionecrosis (ORN), 308
national health and nutrition Occlusion, primary trauma from, 95 Outpatient surgery, 403
examination survey (NHANES III) Octacalcium phosphate, 83 intraoperative considerations, 404
Nicotine Odland bodies, 6 dead space avoiding, 404
effects of, 90 OHL See Oral hygiene instructions (OHI) hemorrhage control, 404
replacement therapy, 92 OMR. See Oral leukocyte migratory rate scaling, 404
Nicotinic stomatitis, 89 (OMR) tissue management, 404
Nidamycin, 371 OMRI. See Oral leukocyte migratory rate vascular supply, 404
NIDCR. See National Institute of Dental and index (OMRI) wound closure, 404
Craniofacial Research (NIDCR) Open flap debridement, 91 patient preparation, 403
NIDDM. See Non-insulin-dependent diabetes Operculectomy, 188 emergency equipment, 403
mellitus (NIDDM) Opportunistic infections, 239 infection control, 403
Nifedipine, 175 Opposite-arch finger rest, 338 informed consent, 403
Nikolsky sign, 193 Oral premedication, 403
Ninhvdrin staining method, 155 diseases, 42 sedation, 403
Nobelpharma universal instrument, 328 dental care, 42 smoking, 403
Non-eugenol packs, 405 impact of, 42 Oxidation-reduction potential, 55
antibacterial properties of, 406 epithelium (OE), 5
barricaid, 405 basal cell layer, 5 p
Coe-Pak, 405 granular cell layer, 6 Pacemakers, 302
cyanoacrylates, 405 keratinized cell layer, 6 Pain management, decision making in, 390
retention of, 406 prickle cell layer, 5 Palatal flap, 426
Non-insulin-dependent diabetes mellitus flora, 55 initial incision, position determination
(NIDDM), 120 hygiene instructions (OHI), 231 of, 426
Nonperiodontitis-related abscess, 235 leukocyte migratory rate (OMR), 158 interdental denudation procedure, 426
Nonplaque-induced gingival lesions, 60 leukocyte migratory rate index Pan,255
Nonspecific plaque hypothesis, 58 (OMRI), 158 Panoramic radiograph, 269
Nonsteroidal anti-inflammatory drug leukoplakia, 88 PAOO. See Periodontally accelerated
(NSAID), 187, 387 mucosa, schematic representation, 3 osteogenic orthodontics (PAOO)
adverse effects, 388 tissues, clinical features of, 89 Papilla
diclofenac, 390 Orban classification, 36 interdental, 4
drug interactions, 388 Orogranulocytes, 157 preservation flap, 420
ibuprofen, 390 Orthodontics, 102 Papillary bleeding index, 47
mechanism of action, 387, 389 intrusion, 321 Papillary gingivitis, 170
oxicarns, 390 stability considerations, 509 Papillary marginal attachment index, 44
paracetamol, 389 therapy, 112 Papillon-Lefevre syndrome, 37, 277
salicylates, 389 treatment, 505 Paracetamol, 390
selective COX-2 inhibitors, 390 adjunctive orthodontics for implant, 506, Parathyroid hormone (PTH), 27
Nonsurgical therapy, 91 508 Parietal abscess, 234
antimicrobial therapy, 91 biomechanical considerations for, 505 Partial denture, 110
Normal periodontium, 24 considerations for, 505 Partial-thickness flap, 419
Nortriptyline, 92 dark triangles, elimination of, 508 Partial thromboplastin time (PTT), 306
NSAID. See Nonsteroidal anti-inflammatory forced eruption, 507 Particle size discrepancy (PSD), 350
drug (NSAID) gingival recession reduction, 508 Pathogenesis of
Nucleic acid sequence-based amplification intrusion, 506 gingivitis, stages in, 161
(NASBA), 244 molar uprighting, 507 stage I gingivitis or the initial
NUG. See Necrotizing ulcerative gingivitis teeth management with abrasion, 509 lesion, 161
(NUG) timing of, 505 clinical features, 161
NUP. See Necrotizing ulcerative periodontitis traumatic occlusion, management of, 506 histological features, 161
(NUP) Orthokeratinization, 6 stage II gingivitis: the early lesion
Nutrition, influence of, 128 Osseodisintegration, 102 clinical features, 162
Osseointegration, 527 histologic features, 162
0 Osseous stage III gingivitis: the established
Observational design, 577 defects, classification of, 431 lesion, 163
Obstructive lung diseases, 307 nonpathological, 431 clinical features, 163
Occlusal considerations, 502 pathological, 431 histological features, 163
INDEX 587
stage IV gingivitis: the advanced PCR. See Polymerase chain reaction (PCR) intraoral examination, 255
lesion, 164 PDGF. See Platelet-derived growth factor of gingiva, 256
clinical features, 164 (PDGF) halitosis, 255
histological features, 164 PDL. See Periodontal ligament (PDL) oral hygiene assessment, 255
periodontitis, overview of, 141 PD Miller's classification, 472 soft tissue examination, 255
Pathogenic bacteria, 59 PDT. See Photodynamic therapy (PDT) Periodontal diseases, 37, 42, 58, 80, 88, 122,
Pathogen-related oral spirochete Pemphigus vulgaris (PV), 190 135,137,198,267,459
(PROS), 62 PEPE. See Primary essential periodontal activity, clinical indications of, 73, 74
Pathological tooth mobility, 261 examination (PEPE) continuous paradigm, 73
Pathologic migration, 103, 227 Peptidoglycan, 59 random burst theory, 73
definition of, 103 Peptostreptococcus micros, 64, 76 synchronous multiple burst theory, 74
diagnosis, 105 Periapical abscess, 236, 261 in adolescents, 198
etiology, 103 Pericoronitis, 188 alveolar bone defects in, 440
extrusive forces, 102 clinical features, 188 antibiotics usage, guidelines for, 385
occlusal factors, 104 complications, 188 antimicrobial sensitivity testing, 384
periodontal and periapical mucosa, 528 combination therapy, 384
inflammation, 105 mucositis, 572 mechanical therapy, 384
periodontal supporting tissues, tissue breakdown, diagnosis of, 573 bone loss patterns in, 214
destruction of, 104 bleeding on probing, 573 horizontal bone loss, 214
prevalence of, 103 mobility, 573 vertical bone loss, 214
signs and symptoms, 105 radiographic assessment, 573 calculus, role of, 87
terminologies, 103 Peri-implantitis, 571 in childhood, 198
drifting, 103 etiology, 571 classification of, 35
extrusion, 103 risk factors, 571 changes made in, 39
physiologic tooth migration, 103 diabetes, 572 data, systematic collection of, 35
treatment, 105 genetic factors, 571 definition of, 35
Pathologic tooth migration (PTM), 103, 105 occlusal overload, 572 etiology, 35
Patients poor plaque control, 571 future challenges, 39
with gingival disease, prognosis for, 294 previous periodontal disease, 571 historical development of, 35
dental plaque-induced, 294 residual cement, 571 morphology, 35
non plaque-induced, 295 smoking, 571 need for, 35
instructions after surgery, 407 treatment, 573 paradigms, 35
hypersensitivity, mechanisms of, 407 antibiotics, 574 classical pathology, 35
direct neural stimulation, 407 home care methods, 574 clinical characteristics, 35
hydrodynamic theory, 407 maintenance therapy, 574 infection/host response, 35
transduction theory, 407 nonsurgical therapy, 573 requirement, 35
postoperative week, 407 surgical techniques, 574 topography, 35
sensitive roots, treatment of, 407 PerioChip, 386 uses of, 35
with periodontitis, prognosis for, 295 Periodontal abscess, 234 clinical risk assessment of, 315, 316
position, 333, 335 acute, 234 factors contributing, 122
behavioral factors, 531 chronic, 234 advanced glycation end products, 122
alcoholism, 532 classification of, 234 altered collagen metabolism, 122
parafunctional habits, 532 diagnosis of, 235 bacterial pathogens in diabetes
smoking, 531 differential diagnosis, 236 mellitus, 122
clinical examination, 532 etiology of, 234 polymorphonuclear leukocyte (PMNL)
adjacent tooth mobility, 532 histopathology, 235 function, 122
arch form, 532 multiple, 234 host response in, 281
bone quality, 535 pathogenesis, 235 imaging considerations for, 269
gingiva, 534 single, 234 cone beam computed tomography, use
implant angulation, 535 treatment of, 236 of, 270,271
interdental space, 532 Periodontal cyst, 237 image receptor and collimation, choice
jaw, edentulous region of, 534 Periodontal diagnosis, 253 of, 271
opposing dentition, 533 examination, components of, 253 patient selection, 269
oral hygiene, 532 brushing habits, 254 radiographic projection, choice of, 269
ridge morphology, 532 chief complaint, 253, 254 inflammatory mediators, 72
root inclinations, 534 dental history, 254 influence of host response on, 73
general, 531 information gathering, 253 local drug delivery, 385
medical medical history, 254 chlorhexidine, 386
corticosteroid therapy, 531 pan chewing, 255 metronidazole, 385
diabetes mellitus, 531 parafunctional habit, 255 povidone-iodine, 386
metabolic bone diseases, 531 personal history, 254 sodium hypochlorite, 386
neurologic diseases, 531 tobacco use, 255 stannous fluoride, 387
radiation therapy, 531 extraoral examination, 255 tetracyclines, 385
renal diseases, 531 lymph node, 255 microbiology and immunology in, 80
rheumatologic disease, 531 temporomandibular joint, 255 abscesses, 81
Pavementing, 64 importance of, 253 aggressive periodontitis, 80
586 INDEX
Periodontal diseases (cont.) bunching of tissue, 112 Periodontal pocket, 204, 234, 258
chronic periodontitis, 81 cytotoxic corrosion products, 112 classification of, 204
necrotizing periodontal diseases, 81 and disease microorganisms, association clinical features, 204
smoking, 81 of, 59 signs, 204
nonsurgical treatment of, 491 elastic bands, 112 symptoms, 204
laser-mediated sulcular, 491 gingival enlargement, 112 definition of, 204
root planing, 491 orthodontic forces, 112 histopathology, 206
subgingival bacterial levels, reduction placement of bands, 112 pathogenesis, 206
of, 491 plaque retention, 112 Periodontal probes, 282, 323
pathogenesis of, 89 tissue clefting, 112 calibrated, 323
plaque, etiological role of, 58 Periodontal index, 47 computerized, 282
prerequisites for, 74 Periodontal infection and diabetic control, conventional manual, 282
public health significance of, 42 association of, 123 furcation, 323
radiographic application in, 267, 268 Periodontal inflammation, 161 noninvasive, 282
radiographic features, 274 Periodontal instruments pressure sensitive, 282
aggressive periodontitis, 276 classification of, 321 three-dimensional topography, 282
bone loss curettage instruments, 321 Periodontal procedures, 113
angular pattern, 275, 276 dental mirrors, 321 crown lengthening, 113
horizontal pattern, 274, 276 explorers, 321 cryotherapy, 113
chronic periodontitis, 274 periodontal probes, 321 electrosurgery, 113
radiographs polishing instruments, 321 furcations, treatment of, 113
as diagnostic tools, 268 parts of, 321, 322 gingivectomy, 113
conventional radiography, 268 sharpening of, 331 modified Widman flap, 113
newer imaging techniques, 268 area specific curettes, 333 occlusal adjustment, 113
limitations of, 267 sharpening stones, 332 periodontal flaps, 113
recurrence of, 524 mounted rotary, 332 root planing, 113
risk factors for, 314 natural abrasive, 332 splinting, 113
age,314 principles of, 332 suturing, 113
diabetes, 314 synthetically produced, 332 traumatic surgical technique, 113
gender, 315 unmounted, 332 Periodontal radiographic anatomy, 272
genetics, 314 sharpening technique, 331 alveolar bone, 273
predisposing factors, 314 sickle scalers, 333 cementum,272,273
red complex pathogens, 314 test for, 331 lamina dura, 272, 273
smoking, 314 universal curettes, 333 periodontal ligament space, 272
risk indicators for, 315 Periodontal knives, 329 trabecular pattern in
HIV, 315 Periodontal ligament, 12, 30 mandible, 273, 275
osteoporosis, 315 dental follicle, derived from, 12 maxilla, 273, 274
stress, 315 development of, 12 Periodontal regeneration, 410, 442
risk markers for, 315 features of, 12 Periodontal screening and recording
bleeding on probing, 315 functions of (PSR), 256
previous history of, 315 formative and remodeling, 15 Periodontal splints, 397
smoking, effect of, 88, 89 nutritive and sensory, 15 basic principles of, 398
gingivitis, 88 occlusal forces to bone, transmission characteristics of, 397
periodontitis, 88 of, 15 classification of, 398
treatment protocol, 465 physical functions, 15 extracoronal, 398
types of, 202 origin of, 12 intracoronal, 398
prepubertal periodontitis, 202 Periodontal ligament (PDL), 434, 505 permanent, 398
Periodontal dressing, 404 Periodontally accelerated osteogenic provisional, 398
advantages of, 404 orthodontics (PAOO), 511 temporary, 398
preparation of, 406 Periodontal maintenance care, 232 contraindications of, 398
Periodontal flap, 419 Periodontal microflora, effect of smoking definition of, 397
classification of, 419 on, 89 indications of, 397
full-thickness, 419 Periodontal osseous defects, 441, 442 rationale of, 397
partial-thickness, 419 Periodontal packs, 404 forces, redirection of, 397
designs of, 420 Periodontal pathogens, virulence forces, redistribution of, 397
conventional, 420 mechanisms of, 59 functional stabily, restoration of, 397
papilla preservation flap, 420 Periodontal plastic surgical procedures psychologic well-being, 397
incisions in commandments of, 485 rest, 397
flap technique, use of, 422 factors affecting, 470 Periodontal status, assessment of, 258
interdental, 421 brushing technique, 470 Periodontal structure, zone of, 96
internal bevel, 420, 422 oral hygiene, 470 codestruction, 96
sulcular, 421, 422 patient motivation, 470 irritation, 96
for reconstructive surgery, 420 periodontal status, 470 Periodontal surgery, contraindications
Periodontal flap surgery, 419 smoking, 470 for, 402
healing process after, 426 systemic health, 470 cardiovascular disease, 402
Periodontal health, 112 tooth alignment, 470 angina pectoris, 402
INDEX 587
anticoagulant treatment, 402 risk factor for Plaque removal, 351
arterial hypertension, 402 preterm low-birth-weight babies, 133 Plaque retentive factors, 115
blood disorders, 402 risk factor for systemic diseases, 131 allergic gingival lesions, 118
myocardial infarction, 402 chronic obstructive pulmonary disease dental calculus, 115
organ transplantation, 402 (COPD), 131 dental caries, 115
hormonal disorders, 402 coronary heart disease (CHD), 131 food impaction, 115
adrenal function, 402 preterm low-birth-weight (PTLBW), 131 habits, 116
diabetes mellitus, 402 type 2 diabetes mellitus (DM), 131 malocclusion, 115
neurologic disorders, 402 role of genetics in, 146 oral hygiene devices, 117
patient cooperation, 402 association analysis, 147 soft tissue factors, 117
smoking, 402 linkage analysis, 146 thermal factors, 118
Periodontal susceptibility test (PST), 148 segregation analysis, 146 tooth abnormalities, 117
Periodontal therapy, 305 root planing for, 376 Plasma cells, 68
analgesics in, 387 instrumentation, 376 Plasma rich in growth factors (PRGF), 569
antimicrobial agents in, 381 lasers, use in, 377 Plastic instruments, 328
antibiotics procedure, 376 Plastic periodontal surgery, problems related
classification of, 381 Periodontometer, 283 to, 262
combination of, 381 Periodotal pocket on the dental pulp, effect abnormal frenal attachment, 263
properties of, 381 of, 209 adequate attached gingiva, 262
azithromycin, 383 Periopaper, 155 alveolar ridge, identification of, 263
ciprofloxacin, 383 Periostat, 395 black triangle, identification of, 263
clindamycin, 383 Periosteal elevators, 330 frenal attachment, abnormal, 263
metronidazole, 383 Periosteum, 23 blanch test, 263
ofloxacin, 383 Periotemp probe, 281 tension test, 263
penicillins, 382 Periotest, 283 gingival pigmentation, 264
tetracyclin, 381 Periotron, 155 gingival recession, 264
laser application in, 490 Peripheral hard tissue examination, 264
soft tissue surgical application, 490 buttressing, 99 vestibule, inadequate depth of, 263
pregnant patient, 308 fibroma, 178 Pia tel et aggregation associated
Periodontal tissues giant cell granuloma, 179 protein, 132
estrogen effects, 124 ossifying fibroma, 178 Platelet-derived growth factor (PDGF), 440
progesterone effects, 124 Permanent splints, 399 Platelet-rich fibrin (PRF), 569
Periodontal treatment Personal protective equipment (PPE), 515 Platelet-rich plasma (PRP), 440, 569
patients, antibiotic prophylaxis for, 302 Petrified plaque, 371 Pluronic polyols, 396
high risk, 303 Peutz-Jeghers syndrome, 166 PMN. See Polymorphonuclear leukocyte
moderate risk, 303 Phagocytosis, 12 (PMN)
negligible risk, 303 Phase 1 therapy, re-evaluation of, 295 Pneumocystis carinii, 238
plan, 297 Phenotypic expressions, 141 Pneumonia, pathogenesis of, 138
preferred treatment sequence Phenytoin, 174 Pocket depth, 247
phases, 297 Photodensitometric image analysis Polishing instruments, 328, 329
etiotropic phase, 298 technique, 284 Polyclonal b-cell activation, 78
maintenance phase, 298 Photodynamic antimicrobial therapy, 492, 493 Polymerase chain reaction (PCR), 286
restorative phase, 298 advantages of, 493 Polymorphism, 143
surgical phase, 298 adverse effects of, 494 periodontal disease, relationship
rationale for, 297 applications of, 493 with, 143
Periodontal wound healing, 408 type II reactions, 493 Fe-gamma receptor polymorphism, 144
excisional surgery, 408 type I reactions, 493 IL-1 gene polymorphism, 144
incisional surgery, 409 Photodynamic therapy (PDT), 232, 491, 492 toll-like receptor polymorphism, 144
role of bone grafts in, 410 light, 492 vitamin D receptor polymorphism, 144
role of epithelium in, 410 photosensitizer, 492 Polymorphonuclear leukocyte (PMN), 77,
Periodontics, 486 Photostimulable phosphors (PSP), 271 122,154,183
indices used in, 42 Physiology, effect of smoking on, 90 Polytetrafluoroethylene membranes
lasers Piezoelectric (ePTFE), 91
characteristics of, 486 bone surgery, 564 Pontic design, 502
components of, 486, 487 ultrasonic scaler, 346 Porphyromonas gingivalis, 31, 55, 64, 76, 89,
use of, 486 units, 347 222,247,285,314
Periodontist, referral of patients to, 524 PII. See Plaque index (PII) Povidone iodine, 371
Periodontitis, 88, 131, 143, 279 Plaque control, 3, 356 PPE. See Personal protective equipment
adult, 38 chemical, 366 (PPE)
advanced stage of, 276 classification of, 367 PPL See Protein pump inhibitors (PPI)
aggressive stage of, 276, 277 mouthrinses, 366 Predictors, 315
classification of, 279 definition of, 356 Pregnancy gingivitis, 123
ontological approach, 279 mechanical, 356 Pregnancy tumor, 177
physiological approach, 279 objectives of, 356 Premature rupture of membranes
conventional diagnosis, 279 Plaque index (PII), 42 (PROM), 133
diagnostic tests, evaluation of, 279,280 recording format for, 43 Preterm low-birth-weight (PTLBW), 131
586 INDEX
Prevotella intermedia, 64, 76, 89,183,222,285 tooth preparation, 109 Ramon syndrome, 177
PRF. See Platelet-rich fibrin (PRF) vertical root fractures, 111 Random burst model, 220
PRGF. See Plasma rich in growth factors Protectins, 395 Randomized controlled trial (RCT), 578
(PRGF) Protein pump inhibitors (PPI), 391 Ranney classification, 37
Primary bone contact, 528 Provisional restorations, 502, 555 RAP. See Regional acceleratory phenomenon
Primary essential periodontal examination second-stage surgery, temporization (RAP)
(PEPE), 256 after, 555 RAS. See Recurrent aphthous stomatitis
Primary herpetic gingivostomatitis, 186 cement-retained restoration, 555 (RAS)
clinical features, 186 screw-retained restoration, 555 RCT. See Randomized controlled trial (RCT)
diagnosis, 187 second-stage surgery, temporization prior RDS. See Respiratory distress syndrome
oral signs, 186, 187 to, 555 (RDS)
treatment, 187 partially edentulous patient, 555 Reactive oxygen species (ROS), 396
Principal fibers, 14 totally edentulous patient, 555 Recall intervals, 524, 525
alveolar crest fibers, 14 Provisional splints, 399 Recurrent aphthous stomatitis (RAS), 187
apical fibers, 14 PRP. See Platelet-rich plasma (PRP) Recurrent gingivitis, 170
horizontal fibers, 14 PSD. See Particle size discrepancy (PSD) Recurrent periodontal disease, 91
interradicular fibers, 14 Pseudomembranous candidiasis, 241 Refractory periodontitis, 221
oblique fibers, 14 Pseudomonas aeruginosa, 138 clinical features, 221
transseptal fibers, 14 PSP. See Photostimulable phosphors (PSP) etiology, 221
Pristine gingiva, 162 PSR. See Periodontal screening and recording systemic antibiotic therapy, 222
Probing depth, 88 (PSR) Regenerative surgical procedures, 445
Probiotics, 396 Psychosomatic disorders, 126 bone graft-associated regeneration, 446
Progenitor cells, 13 PTH. See Parathyroid hormone (PTH) regeneration, barrier materials in, 447
Prognosis PTH-induced bone resorption, 27 regeneration, platelet-rich plasma in, 447
definition of, 290 PTLBW. See Preterm low-birth-weight root surface biomodification, 445
determination of, 290 (PTLBW) Regenerative therapy, 442
anatomic factors, 293 PTT. See Partial thromboplastin time (PTT) bone graft materials, 443
attachment, level of, 291 Puberty, 125 non-bone graft materials, 443
bone, height of, 291 Pulmonary diseases, 307 Regional acceleratory phenomenon
clinical factors, 290 periodontal therapy guidelines, 308 (RAP),511
disease severity, 291 Pulpal disease, 459 case study, 511
patient age, 290 Pulp and periodontal disease, 458 clinical considerations, 511
defect, type of, 291 communication pathways, 459 Relative attachment loss (RAL), 259
local factors, 293 for developmental origin, 459 Renal diseases, 306
plaque, 293 for iatrogenic origin, 459 drug nephropathy, 306
subgingival restorations, 293 for pathological origin, 459 glomerulonephritis, 306
patient compliance and cooperation, 292 Putative pathogens, identification of, 76 hypertension, 306
plaque control, 292 Putative periodontal pathogens, 64 kidney cystic disease, 306
prosthetic factors, 294 Putrescine, 247 obstructive uropathy, 306
restorative factors, 294 PV. See Pemphigus vulgaris (PV) pyelonephritis, 306
systemic factors, 292 Pyogenic granuloma, 121, 177 renovascular disease, 306
genetics, 292 Resective osseous surgery, 432
smoking, 292 Q advantages, 433
tooth mobility, 294 Quasi-randomized controlled trial, 578 anatomic limitations, 437
PROM. See Premature rupture of membranes Quaternary ammonium compounds, 371 contraindications of, 433
(PROM) Quigley-Hein plaque index, 43 current status of, 438
Prophyromonas gingioalis, 227 disadvantages, 433
Proresolving lipid mediators, 395 R factors affecting outcome of, 437
lipoxins, 395 Radiation therapy, 114,308 indications of, 432
protectins, 395 Radiographic diagnosis, aids in, 228, 283 objectives of, 432
resolvins, 395 computer-assisted densitometric image Resolvins, 395
Prospective cohort study, 577 analysis system, 284 Resorptive cells, 13
Prosthetic and restorative dentistry, computerized tomography, 284 Respiratory distress syndrome (RDS), 133
periodontal considerations, 108 digital radiography, 283 Respiratory syncytial virus, 70
allergic reactions, 112 localized aggressive periodontitis, area- Respiratory tract infection (RTI), 138
embrasure form, 109 specific distribution in, 228 Restoration contours, 501
impression materials, 109 photodensitometric image analysis crown contouring, theories of, 501
lingual contours, 109 technique, 284 furcation involvement, 502
matrix bands, 108 subtraction radiography, 283 Restoration margins, 499
occlusal table, 111 Radiographs, 215 biologic width, 499,500
overhanging dental restoration, 110 limitations of, 267 crown lengthening, 499
partial denture, 110 conventional imaging techniques, use preparation of, 500
restoration margins, 109 of, 267 Restorative dentistry materials, 502
root perforations, 111 soft tissue changes, 268 Retraction, 335
separation of teeth, 109 Radiovisiography (RVG), 270 Retrograde periodontitis, 458
tooth contact, 109 RAL. See Relative attachment loss (RAL) Retrograde pulpitis, 462
INDEX 587
Retrospective cohort study, 577 Soft tissue lesions, 541 Surgical procedure, 433
Reye syndrome, 389 Sonic scalers, 346 armamentarium, 434
Ridge splitting, 566 Specific plaque hypothesis, 58 flap design, 434
Risk, 313 Spiral pocket, 204 initial preparation, 433
definition of, 313 Spirochetes, 112 osseous defets, evaluation of, 433
determinants, 313 Spool method, 365 technique involved, 435
factors, 313 SPT. See Supportive periodontal treatment interproximal bone, flattening of, 436
indicators, 313 (SPT) marginal bone, gradualizing, 436
markers, 313 Sterilization, 519 radicular blending, 436
Root hypersensitivity, 407 chemical vapor, unsaturated, 520 vertical grooving, 435
Root planing dry heat, 520 Surgical protocol, 543
objective of, 375 flash,520 Surgical therapy, 91
rationale for, 375 gravity displacement, 520 implant therapy, 91
calculus, removal of, 375 Stevens-Johnson syndrome, 187 maintenance therapy, 91
root surface, smoothness of, 375 Stillman cleft, 101 open flap debridement, 91
ROS. See Reactive oxygen species (ROS) Stippling, 4 soft and hard tissue grafting, 91
Rotary toothbrushes, 358 Stratum Surgical treatment, 401
RTL See Respiratory tract infection (RTI) corneurn, 6 impared access for, 401
Russell's rule, 48 granulosum, 6 scaling, 401
Rutherford syndrome, 177 spinosum, 5 self-performed plaque control, 402
RVG. See Radiovisiography (RVG) Strawberry gingivitis, 178 Sustained-release bupropion. 92
Streptococcus, 514 Sustenins, 77
s Streptococcus mitis, 56 Suture, types of, 429
Salicylism, 389 Streptococcus sanguis, 56 continuous, 429
Saliva, 158 Streptococcus viridans, 60, 303 horizontal mattress, 428, 429
composition of, 158 Strokes, 339 mattress, 429
functions of, 158 exploratory, 339 sling, 429
antibacterial properties, 159 lateral pressure, 340 Suturing, 427
digestion, 159 root planing, 339 principles of, 427
protection, 159 scaling, 339 types of, 427
taste, 159 types of, 341 Suturing techniques, 427
microbial invasion, defense against, 158 Subantimicrobial-dose doxycycline (SOD), figure-8 technique, 428
Sanguinaria canadensis, 371 231,395 simple loop, 428
Sanguinarine, 371 Subclinical gingivitis, 161 Syncope,308
Sarcoidosis, 178 Subgingival calculus, 84, 377 Systemic antibiotic therapy, 222
clinical features, 178 Subgingival plaque, 57, 58 Systemic conditions, 129
histological features, 178 Subluxation, 97 Systemic sclerosis, 277
Scaling instruments, 324, 325 Sulcular epithelium, 4, 6
Scanning electron microscope (SEM), 207 Sulcus bleeding index (SBI), 46, 258 T
Scrub brush method, 360 Sulcus cleaning method, 359 Tachycardia, 305
SOD. See Subantimicrobial-dose doxycycline Sulcus depth, 4 Tacrolimus, 175, 196
(SOD) Supporting alveolar bone, 23 Tactile sensation, 85
Secondary bone contact, 528 cortical plates, 23 Tannerella forsythensis, 314
Secondary fibers, 15 spongy bone, 23 Tannerella forsythia, 89, 230, 247
Secondary herpetic stomatitis, 186 Supportive periodontal therapy, 298 Teeth in occlusion, 264
Secondary organisms, 76 Supportive periodontal treatment (SPT), 523 fremitus test, 264
Campylobacter rectus, 76 dentogingival, microscopic nature of, 523 plunger cusp, 264
Eikenella corrodens, 76 gingival tissue, presence of bacteria in, 523 tooth loss substance, assessment of, 264
Fusobacterium nucleaium, 76 maintenance phase, parts of, 524 Temporary splints, 398
Peptostreptococcus micros, 76 examination, 524 TFO. See Trauma from occlusion (TFO)
Prevotella intermedia, 76 schedule next procedure, 524 TGF. See Transforming growth factor (TGF)
Secondary trauma from occlusion, 95 treatment, 524 Third-generation antiplaque agents, 367
Second-generation antiplaque agents, 367 subgingival plaque removal, 523 Third national health and nutrition
SEM. See Scanning electron microscope (SEM) subgingival scaling, 523 examination survey
Semilunar coronally advanced flap, 473 transmission of bacteria in (NHANES III), 136
Sensodyne, 408 periodontitis, 523 Thrombasthenia, 311
Serratia marcescens, 138 Suprabony defect, 214 Thrombocytopenic purpura, 310
Severe periodontitis, 88 Suprabony pockets, 204, 205 Thyroid disorders, 305
Sharpey fibers, 24 Supragingival calculus, 84 adrenal insufficiency, 306
Shingles, 240 Surgical blades, 330 Thyrotoxicosis, 305
Simple pocket, 205 Surgical chisel, 330 TIMP. See Tissue inhibitor of matrix
Sinus grafting, 564 Surgical files, 330, 331 metalloproteinase (TIMP)
Sling suture, 424 Surgical instruments, 329 Tissue engineering, 448
Smith method, 359 Surgical pocket therapy, 491 Tissue inhibitor of matrix metalloproteinase
Smoking cessation, impact of, 91 flap surgery, degranulation during, 491 (TIMP),395
Soft and hard tissue grafting, 91 osseous surgery, 491 TNF. See Tumor necrosis factor (TNF)
586 INDEX
Tobacco use cessation, 91 diagnosis of, 99 Vancomycin, 371

Tongue scraping, 366 examination of, 99 Varenicline, 374
Tooth abnormalities, 117 Trauma from occlusion (TFO), 93, 211 Vasculature, 29
cementa! tears, 117 acute, 94 collagenous fibers, 29
enamel pearls, 117 definition of, 93 coarseness of, 29
enamel projections, 117 history of, 93 collagen synthesis, 29
grooves, 117 signs of, 100 rate of, 29
root concavities, 117 auditory, 100 synthesizing cells, 29
Toothbrush bristles, 357 fremitus, 97 Vasoconstriction effect, 90
ADA specification of, 357 gingival clefts, 98 Vestibular deepening, 478
stiffness affecting factors, 357 gingival recession, 97 Vibratory technique, 358
Toothbrushes,356 migration of teeth, 100 Visibility sensation, 85
characteristics of, 357 mobility, 100 Vitamin B-Complex, 129
definition of, 356 tactile, 100 deficiency, 129
ionic, 358 visual, 100 oral manifestations, 129
modifications of, 357 wear patterns, 97 Vitamin C deficiency, 177
objectives of, 358 symptoms of, 98 Volatile sulfur compounds (VSC), 247
parts of, 357 habits, 101 Von Willebrand disease, 309
powered, 358 loosening teeth, 101 VSC. See Volatile sulfur compounds (VSC)
replacement, 362 muscle hypertonicity, 100
rotary, 358 thermal sensitivity, 101 w
types of, 357 terminology of, 93 Walking probing method, 259
ultrasonic, 358 Traumatic lesion, reversibility of, 102 Water-soluble vitamins, 128
Toothbrushing, improper, 362 Treponema denticola, 314 vitamin B complex, 128
Toothbrushing techniques, 358 Treponema microdentium, 183 vitamin C, 128
Bass method, 358, 359 Treponema paliidum, 38 Wegener granulomatosis, 178
Pone method, 358 Triclosan, 370 clinical features, 178
Leonard method, 358 Tuberous sclerosis, 177 histological features, 178
rolling stroke method, 358, 360 Tumor necrosis factor (TNF), 154 Western blot assay, 243
Smith method, 358 Type 2 diabetes mellitus (DM), 131 WHO. See World Health Organization
Tooth mobility assessment, 282, 283 Tzank cell, 193 (WHO)
Tooth, mobility of, 260 Wickham striae, 191
alveolar bone loss, 261 u Widman flap, 423
hormonal changes, 261 Ultrasonic instruments, 327 advantages of, 423
inflammation extension, 261 advantages of, 328 apically displaced, 423
occlusion trauma, 261 use of, 328 contraindications of, 424
periodontal surgery, 261 Ultrasonic scalers, 346 procedures, 423
Tooth-periodontium amplitude, 348 curettage, 423
relationship of, 29 automated scalers, advantages of, 349 flap, reflection of, 423
crown/root ratio, increase in, 29 coolant, role of, 349 interdental incision, 423
cuspal height, reduction in, 29 disadvantages of, 349 internal bevel incision, 423
physiologic mesial drifting, 29 frequency, 348 sulcular incision, 423
tooth substance, loss of, 29 hand instrumentation suturing, 423
Tooth surface, attachment of calculus on, 84 advantages of, 349 undisplaced flap, 424
Tooth wall, morphology of, 208 disadvantages of, 349 World Health Organization (WHO), 133, 324
Tranexamic acid, 310 magnetostrictive, 346, 347 World workshop in clinical
Transforming growth factor (TGF), 440 mechanism of action, 348 periodontology, 37
Transgingival probing, 259 piezoelectric, 346, 347 Wrong placement, 540
accuracy affecting factors, 259 stroke, 348
angulation of, 259 water flow, 348 X
force, 259 acoustic streaming, 348 Xenografts, 443, 447, 560
probe size, 259 acoustic turbulence, 348 Xerostomia, 114, 243
Transient bacteremia, dental cause of, 303 cavitation, 348
Transillumination. 323 Undercontour, 109 z
Trauma US Food and Drug Administration (FDA), 92 Zenker diverticulum, 248
classification of, 94 Zimmermann-Laband syndrome, 177
from occlusion, 94 V Zinc compounds, 371
from occlusion Valproic acid, 174 Zinc oxide-eugenol packs, 405

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Textbook of

ASHITA UPPOOR MDS

Copyright© 2015, by Reed Elsevier India Pvt. Ltd.

Sr Project Manager-Education Solutions: Shabina Nasim

Laser typeset by Thomson Digital

Dr V Surendra Shetty, MDS

Abhay Kolte MOS Ashish Nichani MOS

Aravind Shenoy MOS David Kadakampally MOS

Asavari Desai MOS Deepa G Karnath MOS

Dilip G Nayak MOS Nancy Srivastava MOS

Dipen Shah MOS Nandini Manjunath MOS

Mohan Alexander MOS

Nagarathna DV MOS Rajesh Kashyap MOS

Nandakumar K MOS Rahul Nair MPH, MS

Ravikiran Ongole MOS Suresh RMOS

Ruchika Goel MOS Suruchi Jain MOS

I TISSUES OF THE PERIODONTIUM

II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES

Ill ETIOLOGY OF PERIODONTAL DISEASES

V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

Foreword V Composition of Alveolar Bone 25

5. Age-related Changes in the Periodontium

3. Cementum Ashita Uppoor 6. Classification of Periodontal Diseases

Indices Used in Periodontics 42 11. Dental Calculus Ashita Uppoor

8. Dental Plaque and Microorganisms

14. Role of Iatrogenic and Other Orogranulocytes 157

Types of Periodontal Diseases 202 Differential Diagnosis 236

Conclusion 466 Orthodontic Stability Considerations in Periodontally

Provisional Restorations 555 63. Peri-Implant Diseases and Management

TISSUES OF THE PERIODONTIUM

GINGIVA epithelial keratinization, and pigmentation. Gingiva is

Marginal Gingiva (Free or Unattached)

A. FREE GINGIVAL GROOVE

Functions of the attached gingiva are as follows:

A probing depth of 1-3 mm is usually considered com- Interdental Gingiva (Papillary)

A,~~ Granular endoplasmic

FIGURE 1.5 Stratified squamous epithelium: different layers.

FIGURE 1. 7 Gingival fiber groups.

TABLE 1.1 Classification of Collagen Fibers

Name of fiber group Origin and orientation

These collagen fiber groups provide support to gingiva,

KEY POINTS (cont'd)

QUESTIONS Suggested readings

Other Connective Tissue Cells

• Granules contain Transseptal Fibers

The periodontal ligament cells constantly undergo re- CLINICAL CONSIDERATIONS

Cementum was first demonstrated in 1835 by two COMPOSITION

cells of dental follicle and the later ones from undifferenti-

It furnishes a medium for attachment of collagen fibers,

Cementum can be classified as follows:

• According to scanning electron microscopy, its width

DEVELOPMENTAL AND ACQUIRED

The following anomalies in cementogenesis may have

antagonists, embedded, replanted, and transplanted teeth,

CEMENTUM RESORPTION AND REPAIR Clinical Significance

• Cementum is a mineralized avascular dental tissue that 1. Acellular afibrillar cementum

QUESTIONS Suggested readings

Alveolar Bone Proper

Supporting Alveolar Bone

FIGURE 4.3 Histologic section showing compact bone.

FIGURE 4.1 Normal periodontium.

The interdental septum consists of cancellous bone bor-

FIGURE 4. 7 Histologic section showing marrow spaces.

inactive type of marrow. In adults, the yellow marrow is