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Manual
οΙ Glinical
ΡarΠtnff0ntΠΦ$
*B00κPuTE$'
A Dreat eift ldea!
Personalize your message!
Manual
οΙ Gliniοal
Pefi0dοntics
ffi^,:
DΕDιcArroNs
Τo the loves o...
TABLE OF CONTENTS
About the Authors
Preface. ..-.......4
Chapter 1:Problem-Based Periodontal Diagnosis and Disease Managem...
Chapter 7: Surgical Treatment: Principles .... 61
Basic Principles...... ....61
Categories of Surgery ...... ..... 61
When...
ABoUτ τHE AUτHoRs
ABOUT THE AUTHORS
FRANCIS G. SERIO, DMD, MS
Dr. Francis G. Serio is Professor and Chairman of the Depart...
PFEFACE
PREFACE
TheManuatofCtinicatPeriodonticsisu/rittenasaquickreferenceforgeneraldentists,dentalhygienists,dental
stude...
CHAPτEB 1 -
CHAPTER 1: PROBLEM-BASED PERIODONTAL
DIAGNOSIS AND DISEASE MANAGEMENT
The framework of effective periodontal t...
PRoBLEM-BASED PERloDoNτAL D|AGNoSΙs AND D|SEASE MANAGEMENτ
CΙassification is the art of categorizing individual clinical
c...
CHAPTER 1
over treatment needs for each case. For instance, a treat-
ment plan for a Τype lll moderate periodontitis case
...
PRoBLEM-BASED PERloDoNτAL DlAGNosls AND DlsEAsE MANAGEMENτ
What ls Meant by the Expressions "Evidence-
Based Thinking", "E...
CHAPτER 2
CHAPTER 2: ANATOMY, HISTOLOGY, AND PHYSIOLOGY OF THE
PERIODONTIUM
Α οlear understanding of the structure and fun...
ANAToMY, ΗtsτoLoGY, AND PHYsloLoGY oF τHE PERloDoNτlUM
. Rugae: The irregular ridges found on the anterior part of
the har...
CHAPτER 2
What Supporting Structures Lie Beneath the
Gingiva?
F|GURE 3A. τhe supporting structures Beneath the Tissue surf...
Ξ
ANAToMY. HlsτoLoGY. AND PHYsloLoGY oF τHE PERloDoNTlυM
F|GURE 5A. The Alveolar Bone. τhis section shows the relationship...
CΗAPTER 2
bone is supplied by branches of the anterior, middle, and
posterior superior arteries to the maxilla and branche...
Ξ
CHAPτER 3
CHAPTER 3: ETIOLOGY AND CLASSIFICATION OF THE
PERIODONTAL DISEASES
The etiology of the periodontal diseases is m...
I
I
ι
I
ET|oLoGY AND cLASslFlcATloN oF τΗE PERloDoΝτAL DlsEAsEs
Biofilms form on inert surfaces where bacteria to bacteria...
CHAPτER 3
microorganism as a pathogen is often expressed as percent
of total cultivabιe bacteria in a given culture. For e...
EτloLoGY AND clAsslFlcAτloN oF τHE PEBloDoNτAL DlsEAsEs
F|GURE 6. τhe exposure of subgingival' serumnal calculus aΙter a p...
CHAPτER 3
FlGURE 9. A palatogingival groove on a maxillary lateral incisor. τhe gfoove
couΙd have been partially responsib...
EτloLoGY AND clAsslFlcAτloN oF τHE PERloDoNτAL DlsEAsEs
4-
5.
iatrogeny offers the same threat to the periodontium
as food...
CHAPτER 3
Oral contraceptives mimic the hormonal levels seen
during pregnancy, and it is not uncommon to find
pregnancy-li...
EτloLoGY AND cLAsslF|cATloN oF TΗE PERIoDoNτAL DlsEAsEs
CLASSIFICATION OF PERIODONTAL DISEASES
Concepts about the etiology...
CHAPτER 3
During the ensuing decade, it Λ/as determined that this
disease classification system exοluded many of the disea...
EτloLoGY AΝD cLAsSlFlcATloN oF THE PER|oDoΝTAL DlSEASES
FIGURE 178. Drug-lnfluenced Gingivat Enlargements. Gingival enlarg...
CΗAPτER 3
'1
. Lichen planus (Figure 20)
F]GURΕ 20. Erosive Lichen Planus. Ιn its ulcerative form, this disease
can be qui...
EτloLoGY AND cLAsSIFlcAT|oN oF τHE PER|oDoNTAL DlsEAsEs
FIGURE 22C. Allergic Reactions Attributable to Food. An incisional...
CHAPτER 3
ll!. Aggressive Periodontitis*
A. Localized (Figure 24)
FιGURES 24A and B. Localized Αggressive Periodontitis. c...
EτloLoGY AΝD cLAsslFιcAτloN oF THE PΕRloDoNτAL D|SEASES
B. Necrotizing Ulcerative Periodontitis (NUP) (Figure
27)
FlGURE 2...
CHAPτER 3
D. occΙusal Trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma
"Cases of chronic and aggressive peri...
EτloLoGY AND clAsslFlcAτloΝ oF τHE PER|oDoNTAL DlsEASEs
Aggressive periodontitis. This category replaces what
used to be k...
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
Manual of clinical periodontics
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Manual of clinical periodontics

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Manual of clinical periodontics

  1. 1. Manual οΙ Glinical ΡarΠtnff0ntΠΦ$
  2. 2. *B00κPuTE$' A Dreat eift ldea! Personalize your message! Manual οΙ Gliniοal Pefi0dοntics ffi^,: DΕDιcArroNs Τo the loves of my life Cheryl, Andrew, and Grace. Τhanks for all of the wonderful things that you have brought to my life. -FGS To Jean for her encouragement, love, and dedication for so many years. Thank you. -Bud ACKNOI/VLEDGMENTS The Manual of CΙinical Periodontics exists in its present form as the result of the concerted efforts of the following individuals: Robert D. Kerscheη pub|isher and president of Lexi_Comp, lnc; Lynn D. Coppinger, managing editor; David C. Marcus, director of information systems; Brad Bolinski, product manager; and Tracey J. Reinecke, cover art design. NoτlcE This handbook is intended to serve the user as a handy, quick reference and not as a complete reference source on periodontics. While great care has been taken to ensure the accuracy of the information presented, the reader is advised that the authors, editors, reviewers, contributors, and publishers cannot be responsible for the continued currency of the information or for any errors, omissions, or the application of this information, or for any consequences arising therefrom. Therefore, the author(s) and/or the publisher shall have no liability to any person or entity with regard to claims, loss, or damage caused, or alleged to be caused, directly or indirectly, by the use of information contained herein. Because of the dynamic nature of clinical and drug information, readers are advised that decisions regarding treatment and/or drug therapy must be based on independent judgment of the clinician, changing information about a treatment or drug (ie, as reflected by the literature and drug manufacturer's most current product information), and changing dental practices. The editors are not responsible for any inaccuracy of quotation or for any false or misleading implication that may arise due to the text or formulas as used or due to the quotation of revisions no longer official. The editors, authors, and contributors have written this book in their private capacities. No official suppo( or endorsement by any federal agency, educational institution, or pharmaceutical company is intended or inferred. The publishers have made every effort to trace the copyright holders for borrowed material. lf they have inadvertently overlooked any, they will be pleased to make the necessary arrangements at the first opportunity. Copyright @ 2002by Lexi-Comp, lnc. All rights reserved. Printed in the United States of America. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior wriften permission of the publisher. , I Δ ' Lexi-Comp, lnc Ζ*E#ξ 11oo τerex Road llUf Hudson, ohio 44236 >'-' τoll free: 1-800-837-5394 Lεxl,CoιηB !πc www.lexi.comtsBN '1-930598-82-3
  3. 3. TABLE OF CONTENTS About the Authors Preface. ..-.......4 Chapter 1:Problem-Based Periodontal Diagnosis and Disease Management. ...........5 Ηealth and Disease ... ....... 5 Disease Categories ... ....... 5 Diagnosis and Classification ... ... ... 5 Evidence-Based Thinking ......... .. . I Equivalence Testing ...... 8 Superiority Testing ....... 8 Parameters of Care ... ....... I Chapter 2: Anatomy, Ηistology, and Physiology of the Periodontium. ............ 9 Functions of the Periodontium.. ......9 Surface Characteristics of the Periodontium. ......... 9 Histology of the Periodontium .. . 10 Clinically Healthy Gingiva .... . 10 Supporting Structures Beneath the Gingiva .... ..... 11 Blood Supply ........ 12 lnnervation ..........13 Biologicνη/idth.. .....13 AttachmentΑpparatus . . 13 Gingival Crevicular Fluid... ..........13 Chapter 3: Etiology and Classification of the Periodontal Diseases 15 Concepts of Etiology . . 15 Biofilms. .... . 15 Features of Periodontal Pathogens. ......... 16 Dental Calculus .... .. .......17 Risk Factors - Local and Systemic ...... .. . 18 Classification of Periodontal Diseases. ......22 1999 Classification System. .........23 Distinguishing Characteristics of Gingivitis, Periodontitis, and Other Periodontal Diseases and Conditions...... ......29 Chapter 4: Clinical Αssessment, Diagnosis, and τreatment Pιanning . . '.. 31 RiskΑssessment.... ........31 Components of the Clinical Periodontal Examination .. . . 31 lnstruments and Materials for Periodontal Assessment ..... 34 Radiographic Examination. ..........34 Periodontal Screening and RecordingτΜ Examination....... . ''.'' 34 Adjunctive DiagnosticTechniques ...........35 Periodontal Treatment Planning . .. . . 36 SamplePeriodontal ΤreatmentPlans. ..'...36 Periodontal Prognosis ....... 39 chapter5: Prevention of Disease and Maintenance of Ηealth ''''.''''' 41 Toothbrushing Methods ..... 41 lnterproximal Cleaning ...... 41 Antimicrobial Agents ........ 42 Dentifrices . . ..43 Therapeutic Endpoints . .. 43 Clinical Parameters of Success .43 Maintenance of Periodontal Health. ......... 44 Components of the Maintenance Visit. ..........45 Chapter 6: Nonsurgical Treatment: Scaling and Root Planing, occlusal Therapy, and Αntibiotic Therapy .......47 Scaling and Root Planing ......... .. 47 occlusal Τrauma ...'..' '.. ' ' 52 occlusal τherapy. . '''''52 Force Control ...... .... .. 55 Antibiotic τherapy ..... ...... 58 Suggested Systemic Αntibiotic Regimens ........... 59 Local AntibioticΤherapy. ............60
  4. 4. Chapter 7: Surgical Treatment: Principles .... 61 Basic Principles...... ....61 Categories of Surgery ...... ..... 61 When ls Surgery Necessary? .. .... . 61 Flap Surgery ... .... . 63 Basic Approaches .... ...... .... . 63 Types of Flaps .. .... . 63 Anatomic Landmarks ... ..... 66 Wound Closure. ..... 68 Wound Healing . .70 Chapter8: Surgical τreatment: Repair, Resection, and Regeneration .... '.'''.73 Gingivectomy. .......7g Electrosurgery ...... .74 Apically-Positioned Flap . . .,. 75 Classification of Osseous Defects ...........77 Crown Lengthening . ........ 82 Periodontal Regeneration ........... 83 Meοhanisms for Bone Grovvth ....... 83 Materials for Regenerative Therapy . ........ 87 Techniques Used in Regenerative τherapy ..... .... 88 Chapter 9: Surgical Treatment: Periodontal Plastic Surgery ..... 91 Defects Treated by Periodontal Plastic Surgery Procedures ........ 91 Aesthetic Εvaluation. .....91 Gingival Recession .. ........ 92 Alveolar Ridge Defects ...... 93 Εxcessive Gingival Display- DiagnosisandTreatment...... '''.''.94 Procedures Used in Periodontal Plastic Surgery . .. .... 94 Chapter 10: Periodontal Emergencies . . .. 1ο5 Diagnosis of Periodontal Emergencies . .. 105 Signs, Symptoms, and Treatment of Periodontal Emergencies. ... 105 Periodontal Abscess ... 106 Pericoronitis .... 106 Αcute Herpetic Gingivostomatitis ... . .. 106 Necrotizing Ulcerative Gingivitis . ....... 1O7 Differential Diagnosis of an Endodonticand Periodontal Abscess. .......107 Chapter 11: Considerations in lmplant Dentistry . . . 109 Biomechanics of Modern lmplants . . 109 Signs of a Healthy and Αiling lmρlant ...... 109 Protocol for lmplant Maintenance .......... 110 APPENDIX Medical Considerations in the Periodontal Patient ......... 114 Calcium Channel Blockers and Gingival Ηyperplasia ....'. 115 Dental Drug lnteractions: Update on Drug Combinations Requiring Special Considerations........ 116 Occupationsl Exposure to Bloodborne Pathogens (Universal Precautions) ......... 121 Predominant Cultivable Microorganisms of the Oral Cavity . . . .. . . . 124 Reference Values for Adults .. . . . 125 Dentifrice Products . .. ...... 128 Oral Rinse Products. .......133 Prescription Writing ......134 Safe Writing Practices. .....'136 lnsurance Coding for the Periodontal Patient .. . . .. 137 Selected Readings - General .......141 Selected Readings - Specific .......142
  5. 5. ABoUτ τHE AUτHoRs ABOUT THE AUTHORS FRANCIS G. SERIO, DMD, MS Dr. Francis G. Serio is Professor and Chairman of the Department of Periodontics at the University of Mississippi School of Dentistry. He is a Diplomate of the Αmerican Board of PeriodontoΙogy. He received his B.A. from The Johns Ηopkins University, D.M.D. from the University of Pennsylvania, and M.S. and Certifiοate in Periodontics from the University of Maryland. Dr. Serio has been involved in education, research, and international volunteer activities since 1981 . He has published 30 articles, 3 books, several book chapters, and numerous abstracts. He has lectured throughout the United States and in six other countries on various aspects of Periodontics. Dr. Serio is the founder of the Dominican Dental Mission Project, a volunteer program that provides dental care to the rural poor in the Dominican Republic. ln 1991 , the project received the President's Volunteer Action Award from President George H.W. Bush, and was named one of the Points of Light in 2001 by President George W. Bush. ln addition to his academic responsibilities, Dr. Serio maintains a private practice limited to Periodontics and lmplant Dentistry. CHARLES E. HAνVLΕY, DDs, PhD Dr. Hawley was Professor in the Department of Periodontics, Dental School, University of Maryland from 1982- 2001. During that time period, Dr. Haw|ey directed, at one time or another, every eduοational program the department offered to predoctoral and postdoctoral students. He was Director of the Αdvanced Dental Education Program in Periodontics from 1996-2001. He is Professor Emeritus in the Department of Periodontiοs at Maryland and also Visiting Professor, Department of Periodontology, Tufts University. Dr. Hawley is a consultant in periodon- tics to the Commission on Dental Accreditation of the Αmerican Dental Association. He has published over 70 manuscripts, abstracts, and book chapters. From 1962-1982, Dr. Hawley νvas a career dental officer in the U.S. Army Dental Corps. Dr. Hawley Λ,as the first Director of the U.S. Army Residency Program in Periodontics at Ft. Gordon, GA. He retired from the Army at the rank of Colonel, and at that time, Dr. Hawley was awarded the Legion of Merit. Dr. Hawley received a Bachelors degree from The Johns Hopkins University, a DDS from the University of Pennsylvania, a Certificate in Periodontics and a Masters degree in Histology from the University of lllinois, and a PhD in Microbiology and lmmunology from the University of Maryland. He is a Diplomate of the American Board of Periodontology. During his professional life, Dr. Ηawley was elected to the lnternational College of Dentists, the American College of Dentists, and the Pierre Fauchard Αcademy.
  6. 6. PFEFACE PREFACE TheManuatofCtinicatPeriodonticsisu/rittenasaquickreferenceforgeneraldentists,dentalhygienists,dental students, and dental hygiene students. Both basic and clinical science topics.are arranged in a tabular form to allow for easy access to each chapιer. Each chapter is presented in a "Question & Answer'' format, providing a stepwise approach to thal particular area. This book has been written in a straighforward manner, making it a practical resource both in clinical practice and in an educational setting. Chapters are arranged by basic principles, disease entities, diagnosis, treatment planning, and then various treatment options. The authors intend that this book be a quick and easy reference to many of the clinical problems that challenge all practitioners and students of periodontics. :'.
  7. 7. CHAPτEB 1 - CHAPTER 1: PROBLEM-BASED PERIODONTAL DIAGNOSIS AND DISEASE MANAGEMENT The framework of effective periodontal therapy includes a working diagnosis and classifiοation of disease, the identifi- cation of pertinent etiologic factors, and a treatment plan that addresses eaοh of the etiologic agents in a logical sequence. Τo ignore pertinent etiologic factors in the treatment plan will translate to undertreatment and failure in therapy. Treaι ment of etiologic factors that either do not exist, or that have been incorrect|y identified, wiΙl produce overtreatment and unnecessary financial or physical hardships for the patient. Problem-based periodontal therapy begins wiih an under- standing ot health and knowing what it means to diagnose and classify a disease. What ls Health? Mhat ls a Normal Periodontium? What ls Meant by the Term "Disease"? Health is the absence of disease or abnormality. Periodontal health then is defined by the absence of marginal periodontal inflammation, the absence of inflammation in the periodontal ligament, or evidence of periodontal deformities. Success- fully treated and maintained gingivitis patients may be both free of disease and have a normal periodontium. Periodontitis patients who have received successful perio- dontal and maintenance therapy (ie, patients who are appar- ently free of periodontal inflammation with no ongoing injury in the periodontal ligament) may, by definition, be considered healthy as well. However, these patients may not have a normal periodontium. DiSeaSe is defined aS a ρrocess that is οharacterized by a series of morbid pathobiologic events that produce cliniοal signs and symptoms in the affected host. The process ocοurs in response to known or unknown etioΙogic factors. What Are the Fundamental Periodontal Disease Categories? Do These Periodontal Diseases Conform to the Definition of Disease? The basiο categories of periodontal diseases are: . Gingivitis. The gingival diseases are periodontal diseases in which the process is gingival inflammation, the primary etiologic factors may be microbiologic, systemic diseases, or physical injury, and the signs and symptoms are gingival bleeding, increases in probing depths, and pain. Loss of periodontal attachment, tooth mobility and/or fremitus of teeth, and tooth migration,are not ordinary features of gingivitis. As it is with all inflam- matory diseases, the pattern and severity of gingival inflammation in a given patient is affected qualitatively and quantitatively by local and/or systemic contributing factors. . Periodontitis. The types of periodontitis are periodontal diseases in which the process is periodontal inflamma- tion, the primary etiologic factor may be microbiologiο, systemic diseases, or physical injury, and the signs and symptoms are gingival bleeding, increases in periodontal probing depths, destruction of periodontal attachment, pain, and tooth loss. Mobility and/or fremitus and migra- tion of teeth are consequences of forces on teeth with reduced/lost periodontal attachment (see occlusal trau- matism below). The pattern and severity of periodontal inflammation in a given patient is affected qualitatively and quantitatively by local and systemic contributing faοtors. . Occlusal traumatism. Occlusal traumatism is a perio- dontal disease in which the process is inflammation ιΛ/ithin the periodontal Ιigament and the alveolar bone (the lesion of trauma from occlusion), the primary etio- logic factor is force acting on teeth, and the signs and symptoms are pain, tooth mobility and/or fremitus, and pathologic migration of teeth. The pattern and severity of the lesion of trauma from occlusion in a given patient is affected quantitativeΙy and qualitatively by local and systemic contributing factors. Each one of these categories conforms to the definition of disease. ln each disease, there is a process, there is a series of morbid pathobiologic events that are outcomes of the process, and there is a reΙated set of clinica| signs and symp- toms. What ls Meant by the Expressions "Diagnosis" and "Ctassification"? F|GURE 1. Photomicrograph of the ρrocess of inflammation in the marginal periodontium. τhe morbid outcome of the process is histologically repre- sented as evidence of resorbed alveolar bone and the level of attachment on cementum. Diagnosis is the aιt of identifying the disease process. lt is the product of a careful evaluation of the patient's history, the array of symptoms presented by the patient, and the clinical signs revealed during a clinical examination. For instance, the diagnosis of periodontitis is ordinarily achieved by detecting gingival bleeding with a periodontal probe, destruο- tion of periodontal attachment using radiographs and/or a probe, mobility and/or fremitus digitally, determining any pathologic migration and/or loss of teeth. Figure 1 represents histologically the process of marginal periodontal inflamma- tion and the morbid outcomes (ie, loss of both alveolar bone and periodontal attachment) of periodontitis.
  8. 8. PRoBLEM-BASED PERloDoNτAL D|AGNoSΙs AND D|SEASE MANAGEMENτ CΙassification is the art of categorizing individual clinical cases of disease according to treatment requirements. Clas- sification systems are frequently used by third pafty prov- iders to help understand treatment needs. For over 20 years, dentists have been using a classification system developed by the Αmerican Αcademy of Periodontology (AΑP) to facili- tate dialogue among dentists and between third party individ- uals concerning the severity of periodontal diseases, and by direct extension, treatment needs. This classification system consisted of: . Type l. Gingivitis where gingival inflammation νas present without radiographic evidence of intΘrproΧimaΙ bone loss. FIGURE 2. An artistic represenιation ot gingivitis" There is gingival erythema and edema. τhe clinical attachment levels are at the cementoenamel iunction. The alveolar bone height wilh respect to the cementoenamel iunction is normal. Restoraιion of a healthy periodontium without further loss of attachment may be predictably achieved with nonsurgical therapy. (Couftesy of Kala Addess, MS, RDH) . Type ll. Early periodontitis where gingival inflammation was superimposed over clinical evidence of mild bone loss without furοation invasions. FIGURE 3. An artistic representation of earιy periodon lfis. τherΘ is gingival erythema and edema. τhere is early loss of clinical attachment and reduclion of alveolar bone height. Furοation invasions wilι probably not be clinically or radiographically apparent. Periodontal health and func- tion may usually be restored by nonsurgical and/or surgicaΙ therapy. (cour1esy of Kala AddeSS' ΜS' RDH) . Type lll. Moderate periodontitis where gingival inflam- mation was superimposed over clinical evidence of moderate bone loss with early furcation invasions and possible tooth mobility. FiGURΕ 4. An artistic representation ot moderate periodontitis. τhere is gingival erythema and edema. τhere is moderate lοss of clinical atιach- ment and reduction of alveolar bone height. Furcation invasions are evident both cιinicaΙly and radiographically. Affected teeth may show degrees of mobility. Shaded area on the adiacent tooth indicates that regeneration ot Ιost periodontal tissues may be one outcome of successful periodontal theraρΥ. (courtesy of Karla AddeSS' Ms' RDH) . Type lV. Αdvanced periodontitis where gingival inflam- mation was superimposed over severe bone loss with extensive furcation invasions and tooth mobility. Cases of this type could display tooth loss due to periodontitis, pathologic migration of teeth, posterior bite collapse, and/or loss of occluding vertiοal dimension. FΙGUBE 5. An artistic representation oΙ advanced periodontitis. τhere is gingival erythema and edema. τhere is advanced loss of clinical attach- ment and alveolar bone height. Furcaliοn invasions are θxtensive. τooth mobilily and/or pathologic migration may be seen. τeeth with advanced periodontitis frequently have a poor prognosis, and decisions abοut therapy often include the placement of implants. (Couιlesy of Κarla Addess, MS, RDH) While the terms that defined each type were intentionally vague, the system did provide the framework for dialogue among therapists, allied personnel, and third party payers
  9. 9. CHAPTER 1 over treatment needs for each case. For instance, a treat- ment plan for a Τype lll moderate periodontitis case dispΙaying the osseous defects and furcation invasions shown in Figure 6 would be expected to include resective and/or regenerative surgical therapy. Τhe treatment plan for a Type ll early periodontitis οase, such as that shown in Figure 7, would probably not include resective or regenera- tive therapy. FIGURE 6. A dried human mandible showing periodontaΙ osseous defects and furcation invasions that are οonsistent with a type lll moderate periodon- titis case. FIGURE 7. A dried human mandible showing minor periodontal osseous deformities that are consistent with a type ll early periodontitis case. As the knowledge base about the patterns of periodontal diseases improved, this system of classification became inadequate. Models of periodontitis had emerged sug- gesting that not all cases of periodontitis behaved the same clinically, that small (<1 mm) changes in attachment level were difficult to detect clinically, and that there was evidence that all cases of periodontitis did not respond the same to therapy. An attempt to overcome many of these shortcomings occurred during the 1999 lnternational Workshop for a Clas- sification of Periodontal Diseases and Conditions. Here, scientists and clinicians agreed upon a reclassification system to improve the understanding of periodontal diseases among scientists, clinicians, and allied dental healthcare agencies. Each new or revised category of disease was based, in part, upon its etiology and the particular healthcare requirements to control etiology. The new System includes eight major οategories of perio- dontal diseases or conditions, and each of the categories is subdivided into specific etiology-based diseases or condi- tions. This new Classification System for Periodontal Diseases and Conditions was adopted by the AAP in 2000. Τo facilitate its use in every-day periodontiοs, the new system would be modified over time. How Are Scientifically-Based Decisions Made in Successful Periodontics? What ls Meant by the Expression "Art of Decision-Making in Periodontal Therapy"? Successful periodontal therapy is based upon scientifically- based decisions involving: the disease process, the identifi- cation of aΙl etiologic factors, a correct diagnosis, controlling the etiologic factors, and correcting deformities produced by disease. The arl of decision-making in periodontal therapy involves the synthesis of: 1. Clinical experience of the therapist 2. Τechnical ability of the therapist 3. lntuition 4. Experiences of others (type lll information) as reported and presented at professional forums 5. Evidence-based thinking F|GURE 8. οlinical decision_making in periodontics can be multifaceted. Evidence-based thinking b.ings the outcomes of sοientificalιy sound cΙinicaΙ trials into the process. While the traditional components of a deοision process remain impoftant ingredients (ie, a clinician will not ordinarily make a treatment decision that will involve a technique that is beyond the scope of his/her abilities), the fact remains that the knowledge base in a|l aspects of periodontiοs is rapidly expanding. lt is incumbent that clinicians keep current with new science and technology, evaluate reports in the litera- ture criticalΙy, and utilize new information in their practices when appropriate.
  10. 10. PRoBLEM-BASED PERloDoNτAL DlAGNosls AND DlsEAsE MANAGEMENτ What ls Meant by the Expressions "Evidence- Based Thinking", "Equivalence Testing", and "Superiority Testing"? Εvidence-based thinking occurs when the therapist logically and systematically utilizes scientifically-based clinical evidence in the process of making decisions about diag- nosis, prognosis, and treatment. Εquivalence testing in c|inical trials may show that a method is at least as effective as a commonly employed "gold stan- dard". Superiority testing may show that a given method will produce outcomes that will be more beneficial than another to a patient. lf there is evidence that a technique or concept of therapy is predictably equivalent or superior in a given clinical scenario, then, within the scope of experience and ability, it should be considered as a treatment option. ln doing so, the number of options available to the patient are increased, and the poten- tial for placebo effects, personal biases, or clinical experi- ences of the therapist that have no controls are kept to a minimum. The fallout of evidence-based thinking in clinical periodontics will inevitably be an increased number of treatment options, increased patient confidence, practice groλ/th, and improved therapeutic outcomes. What Are the Parameters of Care? The AAP took a leadership role in developing diagnostic and therapeutic guidelines for what might be considered the stan- dard of care for periodontal patients. The resulting Parame- ters of Care describe the scope of possible active treatment plans for the following clinical situations: ο Plaque-associated gingivitis o Chronic periodontitis with slight to moderate loss of peri- odontal support o Chronic periodontitis with advanced loss of periodontal support . Refractory periodontitis . Mucogingivalconditions ο Acute periodontal diseases . Αggressive periodontitis . Placement and management of the dental implant . Occlusal traumatism in patients with chronic periodontitis o Periodontitis associated with systemic conditions . Systemic conditions affected by periodontal diseases o Periodontal maintenance The emphasis of the current parameters is treatment and what therapeutic entities might be appropriate for given peri- odontal conditions. Each parameter is inclusive so as to give the reader (clinician, patient, third party healthcare provider, etc) an appreciation of the scope of acceptable care in each category. The parameters do not prescribe the care that every periodontal patient in a given category should receive. The final decision over what will constitute a treatment plan in a given case remains, as it should be, in the hands of the clinician and the patient. Definitions of terms and details of each of these parameters of care may be obtained at the web site of the American Αcademy of Periodontology, www.perio.org.
  11. 11. CHAPτER 2 CHAPTER 2: ANATOMY, HISTOLOGY, AND PHYSIOLOGY OF THE PERIODONTIUM Α οlear understanding of the structure and function of the periodontium is necessary in order to appreciate the disease process and treatment. The periodontium consists primarily of noncalcified and οalcified connective tissues covered by a protective layer of epithelium. lt is the destruction of the calοified conneοtive tissues due to the host response to the exogenous and endogenous periodontal pathogens that gives rise to a ιoss of periodontal Support and eventua| tooth loss. What Are the Functions of the Periodontium? . Attach the tooth to the alveolar bone proper . Resist and dissipate the forces generated by mastica- tion, speech, and deglutition . Αdjust to οhanges in functional demands through contin- uous remodeling, regeneration, and repair o Defend against the external pathogenic and environ- mental influences present in the oral cavity What Are the Surface Characteristics / Landmarks of the Periodontium? FlGURE 1Α. surface characteristics and Landmarks of the Periodontium. Free gingivat margin: This is the most coronal edge of the gingiva. Free gingival groove: A groove seen on the facial gingiva that approximates the location of the base of the sulcus. The free gingivaΙ groove is not always present (estimated in only 30% to 40"λ ot adults), nor is it an exact landmark for the base of the sulcus. Keratinized tissue: The surface of the tissue that comprises the free and attached gingiva. Τhe boundaries are from the free gingivaΙ margin to the mucogingival iunction on the facial and lingual surfaces. The keratinized tissue is continuous with the rest of the mastiοatory mucosa of the palate. The keratin is found in the stratum corneum of the epithelium and may be parakeratin (cell nucΙei remaining) or orthokeratin (thick layer of keratin without remaining cell nuclei). The epithelium covering is also referred to as the oral epithelium. Free gingiva: The gingiva from the free gingival margin to the base of the sulοus' This tissue is continuous with the attached gingiva but is not bound down to any underlying structure. Attached gingiva: Gingiva that is firmly bound down to underlying tooth structure, periosteum, and bone. Τhe boundaries of the attached gingiva are from the base of the sulcus to the mucogingival junction. The width of facial attached gingiva ranges from 1-9 mm and is greatest on the facial surface of the maxillary lateral incisor and narrowest on the facial surfaces of the mandibular canine and first premolar. On the lingual, attached gingiva was widest near the first and second molars and narrowest adjacent to the incisors and canines. The thickness of attached gingiva averages 1.25 mm + O.42 mm. Mucogingival junction: The demarcation between the attached gingiva and the alveolar mucosa apical to the attached gingiva. The mucogingival junction often appears as a distinct line between the two structures. lf the mucogingival junction is difficult to see, it may be identified as the fold area when the alveolar mucosa is gently pushed in a coronal direction. Alveolar mucosa: Part of the lining muοosa. The a|veolar muοosa is located apical to the attached gingiva on the facial and lingual surfaces. This tissue is loosely attached to the underlying bone, freely moveable, and relatively fragile compared to the gingiva. There are more elastic fibers in the alveolar mucosa. This tissue extends into the vestibule of the mouth and is continuous with the labial, buccal, and lingual mucosa. There is no alveolar muοosa on the hard palate' Masticatory mucosa: Keratinized tissue including the gingiva and the tissue covering the hard palate. Frenum (frenulum): The narrow band of tissue that attaches the labial and buccal mucosa to the alveolar mucosa. There is also a lingual frenum that attaches the anterior part of the tongue to the lingual aspect of the alveolar process and the floor of the mouth in the anterior region.FIGURE '1 B. Surface Characteristics and Landmarks of the Periodontium.
  12. 12. ANAToMY, ΗtsτoLoGY, AND PHYsloLoGY oF τHE PERloDoNτlUM . Rugae: The irregular ridges found on the anterior part of the hard palate adjacent to the incisors, canines, and first premolars. . Stippling: The irregular surface texture of the attached gingiva, similar to the surface of an orange peel, found in 40% ot adults. Stippling occurs at the intersection of epitheΙial ridges that causes the depression and the interspersing of connective tissue papillae between these intersections giving rise to the small bumps. . Sulcus: This is the space bounded by the free gingival margin, the tooth, and the most coronaΙ attachment of the junοtional epithelium. ln health, the sulcus usually measures from 1-3 mm deep. ln disease, this space is referred to as a pocket. . Col: This is the saddle-like depression in the interdental gingiva as seen from buccal to lingual apical to the contact of two adlacent posterior teeth. What Are the Layers of Cetls That Comprise the Oral Epithelium? What Are a Keratinocyte, Langerhans Cell, and a Melanocyte? The oral epithelium consists of four layers of cells: 1. Stratum basale: Basal layer of cuboidal cells along the basement membrane. This is where epithelial οell rep|i- cation occurs. Melanocytes are found in this layer. 2. Stratum spinosum: These cells appear to have cyto- plasmic spines when viewed by Ιight microscopy. Langerhans cells, involved in the processing of antigens, are found in this layer. Keratin synthesis begins in the stratum spinosum. 3. Stratum granulosum: Keratohyalin granules may be seen in this layer. Keratin synthesis is ongoing. Cells appear to be fΙattened. 4. Stratum corneum: This is the layer where para- or orthokeratinization are found. Keratinocyte: A cell of the epidermis and parts of the mouth that produce keratin. Because of their ability to produce keratins, epithelial cells are referred to as kerati- nocytes. Keratins are a family of approximately 30 proteins that form the intermediate filaments of the epithelial cell cytoskeleton. Keratins may be found eΧtra- celluΙarly in the stratum corneum and contribute to the protective function of epithelium. Langerhans cell: A dendritic cell in the epidermis.These cells are found in the suprabasal layers of the epithelium, Τhey do not have desmosomal attachments to adja- cent cells. Τhey move in and out of the epithelium, are derived from bone marro,v, and probablyhave an immu- nologic function for recognizing and processing antigens. . Melanocyte: Α celΙ of the basal layer that produces melanin pigment granules (melanosomes) that are trans- ferred to surrounding keratinoοytes for transpoι1' There are similar numbers of melanocytes in the epithelium re- gardless of the skin or gingival pigmentation present. What Does Clinically-Healthy Gingiva Look Like? FlGURE 2. characteristics of the Heaιthy Pefiodontium. τhe hea,thy periodon- tium is genefally coral pink, possibly with natural pigmentation. τhe gingival margins are scalloped to a fine edge. τhe tissue is firm, usually with a stippled surface. Color: The normal οolor of gingiva is often described as coral pink. Gingiva may also have slight to significant brown pigmentation from the melanoοytes located in the basal layer of the epithelium. Size: Gingival contours generally follow the cemento- enamel junctions of the teeth. Tissue thickness is in the 0.25-0.5 mm range. Α wider zone of gingiva is normally seen in the maxillary anterior region, with the narrowest zone of gingiva on the buccal surface of the mandibular first premolars. On the lingual, it is narrowest in the mandibular region and widest in the molar area. Contour: Gingiva has been described as being either thin and scalloped, or thick and flatter in contour. The contour of the gingiva depends on the οontour of the cementoenamel junction of the teeth, the amount of em- brasure space, and the nature of the contact between teeth. The gingiva appears prominent over the tooth root and may have a slightly concave appearance in the inter- proximal area. Consistency: Gingiva is generally firm to the touch and attached to the underlying bone and/or tooth. Surface texture: Gingiva may have either a smooth or stippled surface. Stippling is not an indicator of health nor is the absence of stippling an indiοator of disease. The reappearance of stippling during therapy may be an indi- cation of tissue returning to health.
  13. 13. CHAPτER 2 What Supporting Structures Lie Beneath the Gingiva? F|GURE 3A. τhe supporting structures Beneath the Tissue surface. side view, A. oral epithelium, B. suιcular epithelium, c. Junctional epithelium, D. Dentogingivaι fibers, E. circular fibers, F. Dentoalveolar fibers' G. Acellular cementum, H. Alveolar crestal fibers of the PDL, ι. cellular cementum, J. Horizontal fibers of the PDL, κ. Alveolar bone, L. oblique fibers of the PDL. FIGURE 38. lnterproximal view. A. Dentogingival fibers, B. Circular fibers, C" τransseptal fibers, D. Alveolar crestal fibers of the PDL, E. Horizontal fibers of the PDL, F. Oblique fibers of the PDL, G. Apical fibers of the PDL' Η. Alveolar bone, lnterradicular fibers not shown. . Sulcular epithelium: The epithelium that lines the sulοus. ln health, sulcular epithelium does not have epithelial ridge formation. o Junctional epithelium: The epithelium that attaches the gingiva to the surface of the tooth, or to compatible restorative materials' Τhe special part of the junctional epithelium that actually provides the attachment is called the epithelial attachment. τhis attachment consists of a lamina lucida, lamina densa, and hemidesmosomes. Connective tissue: The predominantly collagenous tissue found beneath the epitheΙium. The connective tissue contains collagen fibers (60%), fibroblasts (5%), and interfibrillar substanοe οomposed of noncollagenous proteins and mucopolysaccharides, small numbers of neutrophils and lymphocytes, blood vessels, lymphatics, and nerves (the remaining 35%). Τhe overlying epithe- lium must have intact connective tissue in order to survive. Most of the coΙlagen found in the periodontium is type I collagen. Gingival fibers: These are specially oriented fibers in the connective tissue. Also known as Ιhe supracrestal connective tissue fibers, these fibers are designated by their orientation: Dentogingival, dentoperiosteal, circular, and transseptal (connecting tνvo adjacent teeth) fibers. Some authors inοlude the transseptal fibers in the prin- cipaΙ fibers of the periodontal ligament, although they are actually tooth-to-tooth and not tooth-to-bone fibΘrs. Periodontal ligament (PDL): This is the collagenous tissue that surrounds the tooth root and attaches the tooth to the alveolar bone proper. The principal fibers of the periodontal ligament have been cΙassified as the alveolar crest, horizontal, oblique, apical, and interradic- ular (in the furcation area of multirooted teeth) fibers. Τhe oblique fibers are the most numerous. Fibroblasts, osteo- blasts, cementoblasts, osteoclasts, epithelium, and nerve celΙs are also found in the periodontal ligament space. The width of the PDL space is about 0.25 mm in normal function. Α tooth in hypofunction may have a narror/er PDL space and a tooth in hyperfunction may have a considerably wider PDL space. FlGURE 4. τhe Attachment Apparatus. From the left: Dentin, cementum, perio- dontal ligament fibers, alveolar bone. . AIveolar bone: Αlso known as Ιhe alveolar process, this is the portion of the maxilla and mandibΙe that form and support the tooth sockets. The alveolar process gives Support to the alveoΙi and consists of coιtical bone, cancellous trabeοulae, and the alveo|ar bone proper. A D c 11
  14. 14. Ξ ANAToMY. HlsτoLoGY. AND PHYsloLoGY oF τHE PERloDoNTlυM F|GURE 5A. The Alveolar Bone. τhis section shows the relationship of the roots of this molar to the alveolar bone proper and the rest of ιhe alveolar prοcess. FlGURE 58. τhe Alveolar Bone. ln cross section, corticaι bone can be seen on the surface of this mandible with trabecular bone within the confines of the iawbone. τhe density of the trabeculaιions can vary markedly from one area of the iaw to another and among individuaΙs. . Alveolar bone proper: That part of the alveolar bone that lines the tooth socket. lt is a perforated cribiform plate through which vessels and nerves pass between the PDL and marrow. . Basal bone: That part of the maxilla and mandible that supports the alveolar process. Basal bone is all that remains once all of the alveolar process is resorbed after the teeth are lost from the arch. . Cementum: The thin, calcif ied tissue of ectomesen- chymal origin covering the roots of teeth in which embedded collagen fibers attach the teeth to the alveo- lus. There are tivo types of cementum: Αcellular and cellular cementum. Acellular cementum does not con- tain cementocytes and is found on the οoronal half of the the tooth rooΙ. Cellular cΘmentum contains cementocytes and is found primarily on the apical third of the root. lt is continuously deposited throughout life. What ls the Blood Supply to the Periodontium? FlGURΕ 6Α. Local Blood supply to the Periodontium. supraperiosteal blood vessels and PDL vessels coalesce into the gingival plexus. F|GURΕ 68. Loοal Blood supply to the Periodontium. lnterseptal vessels supply the alveolar bone, PDL, and gingiva. The blood supply to the periodontium arises from the terminal branches of the internal maxillary aftery. Locally, the blood supply to the gingiva consists of supraperiosteal vessels. Vessels from the alveolar bone and periodontal liga- ment also contribute to the coalescence of vessels in the gingival papillae, known as Ιhe gingivaΙ plexus. The alveolar
  15. 15. CΗAPTER 2 bone is supplied by branches of the anterior, middle, and posterior superior arteries to the maxilla and branches of the inferior alveolar artery in the mandible. lntra-alveolar or inteμ dental vessels supply the interdental bone. Arterial blood generally flows in an apical-to-coronal direction. Large numbers of capillary loops that resemble renal glomeruli are found beneath the iunctional epithelium and sulcular epithe- lium near the surface of the gingiva. What ls the Innervation of the Periodontium? Nerve supply to the periodontium is derived from terminal branches of the maxillary and mandibular branches of the trigeminal nerve. The periodontium contains sensory recep- tors for pain, touch, and pressure as well as proprioceptors in the periodontal ligament but not in the gingiva. The sensory nerves have their center in the semilunar ganglion and the proprioceptive nerves are centered in the mesencephaliο nυcleus. What ls the BioIogic ι,vidth? duωcτιo*υ E SlλPιeAc'ιee'nL coilωep-I1ν€ Tι'Sιλ'E ΡιB,Ε!LS FtGURE 7. Biologic νlridth. Junctional epithelium and supracrestal connective tissue fibers (dentogingival, dentoalveolar, circular, transseptal) must be maintained in health. The biologic width is the apicocoronal distance that the junc- tional epithelium and supracrestal connective tissue (gingival) fibers are attached to the tooth. This distance is measured histologically from the most coronal part of the junctional epithelium (base of the sulcus) to the crest of the alveolar bone. The average measurement of the biologic width is 2.04 mm, approximately 1 mm for the junctional epithelium and 1 mm for the supracrestal connective tissue fibers. The sulcus depth is nof part of the biologic width. ΨVhy Is the BioIogic Vvidth lmportant? The body maintains the biologic width as a stable dimension. When the biologic width is encroached upon and iniured by extension of restorative preparations and materials into this area, uncontrolled inflammation may result as the body tries to reestablish this dimension. ln areas of thin gingiva, this may result in recession or bleeding upon gentle probing even when the patient has good plaque control and recession. What ls the Attachment Apparatus? The attachment apparatus is the alveolar bone proper, perio- dontal ligament fibers, and cementum that attach the root to the alveolar bone. Regeneration of the attachment apparatus is one of the surgical goals in periodontal therapy. Regenera- tion of the attachment apparatus is the only treatment proce- dure in dentistry where new tissue is histologically identical to that which has been lost due to the disease process. ΨVhat ls Gingival Crevicular Fluid? ln health, gingival crevicular fluid (GCF) is a transudate that emerges from the gingival sulcus. The gingival crevicular fluid may contain a variety of enzymes and cells, particularly desquamating epithelium and neutrophils, that are being shed through the sulcus. An increase in gingival crevicular fluid flow is the first detectable sign of inflammation. Once inflammation has ocοurred, the GCF is referred to aS an inflammatory exudate. This exudate contains higher levels of serum proteins and leukocytes. o', o. u cι d_.'o' gto η q: )t itζ Zι ζ
  16. 16. Ξ
  17. 17. CHAPτER 3 CHAPTER 3: ETIOLOGY AND CLASSIFICATION OF THE PERIODONTAL DISEASES The etiology of the periodontal diseases is multifactorial, but bacterial plaque is necessary for the initiation and progres- sion of infΙammatory periodontal disease. Αs indicated by the neνι Ctassification System for Periodontal Diseases and Conditions, etiologic faοtors have become the framework for periodontal diagnosis and classification What ls lnflammation? lnflammation is a soft tissue cellular and vascular response to local iniury of physical, thermal, chemical, or microbial origin. lnflammatory periodontal diseases are no exception to this paradigm as local periodontal etiologic factors may be phys- ical (factitial habits such as toothbrush abrasion or occlusal trauma), thermal, chemical (epithelial disorders associated With some mouthivashes, smokeless tobaοco, aspirin, and coοaine), and microbial (dental plaque induced gingival diseases). The most common inflammatory periodontal diseases are caused by a locaΙ accumulation of baοteria. What ls Meant by EtiologY? ΕtioΙogy is "the study or theory of the causation of any disease; the sum of knowledge regarding causes." Therefore, etiology is a noun that defines the science of disease causa- tion, but in common usage, etiology is a cluster of faοtors that contribute to disease (ie, the etiology of periodontal diseases). What Are the Microbiologiο Etiologic Factors in Periodontal Diseases? Τhe microbiologic etiologic factor in periodontal diseases is dental plaque with dental calculus as probably the most significant local contributing factor. Food debris and the bacteria it contains is probably a major etiologic factor in root caries. F|GURE 1. A photomicrograph showing severe marginaΙ inllammation and local etiologic factors of bacteriaι origin. There is littΙe dispute over the concept that bacteria are the primary etiologic factors in inflammatory periodontal diseases. ln 1965, Loe and co-workers published their classic work that demonstrated that gingival health could be reliably achieved with immaculate oral hygiene and that gingival inflammation could be caused by the aοcumulation of plaque on the teeth. Light microscopiο examination of tooth scrap- ings revealed that plaque ivas an adherent mat of bacteria, epithelial cells, and leukocytes encased in an amorphous protein and polysaccharide matrix, and that cocci, filamen- tous bacteria, spirochetes, and vibrios accumulated on teeth in an ordered sequence. The knowledge produced in this and later studies of plaque morphology and microbiology emphasied that plaque was a heterogeneous community of bacteria (see Figure 2). Generally speaking, bacteria assoοiated with periodontal health are characterized as Gram-positive, nonmotile faculta- tive anaerobes. Bacteria assoοiated with disease are gener- ally Gram-negative, motile, Strictly anaerobiο speοies. Τhe cell wall of Gram-negative bacteria consists of a lipopolysac- charide base, aΙso known as endotoxin, that has significant pathogenic potential. νγhile over 350 distinct speοies of bacteria have been isolated from the oral cavity, relatively few are associated with gingival or periodontal inflammation. The list of strongly associated pathogenic bacteria includes: ο Actinobacillus actinomycetemcomitans ο Bacteroidesforsythus . Fusobacteriumnucleatum . Peptostreptococcusmicros o Porphyromonasgingivalis o Prevotella intermedia/nigresens What ls Meant by the Term "Biofilm"? B FIGURE 2. A thin section eleclron photomicrograph of supragingival plaque (biofilm) showing a heterogeneous popu|ation of resident bacteriaΙ morphοtypes and bacterial debris. τhe interbacterial matrix permits the exchange of nutrients between microorganisms.
  18. 18. I I ι I ET|oLoGY AND cLASslFlcATloN oF τΗE PERloDoΝτAL DlsEAsEs Biofilms form on inert surfaces where bacteria to bacteria cohesive interactions or bacteria to surface adhesive interac- tions are allowed to occur. Biofilms are heterogeneous composites of bacterial communities within a nonbaοterial protein, polysaccharide, and glycoprotein matrix of bacterial and salivary origin. The matrix allows for a "circulation" of nutrients and baοterial metabolites betνveen communities and the environment outside the biofilm. τhere are extreme varia- tions in oxygen levels ranging from highly aerobic areas within fluid channels to almost completely anaerobic areas in microcolonies. What ls the "Nonspecific Plaque Hypothesis"? The basic tenets of the nonspecific plaque hypothesis state that inflammatory periodontal diseases (and possibly caries) are caused by composite effect of bacterial colonization and maturation on the surfaces of teeth, not by specific bacteria themselves. Gingival disease is the outcome from release of bacterial metabolites (such as butyrate or other short chain fatty acids) and immunogenic bacteriaΙ antigen components, such as lipopolysaοcharide (endotoxin) from Gram-negative cell walls during plaque growth. lnflammatory disease is the outcome of a microbial mass that is in excess of the local defense mechanisms of the host. What ls the "Specific PIaque Hypothesis"? The specific plaque hypothesis states that periodontitis is an infection caused by a limited number of periodontal microor- ganisms, and that these microorganisms characterize the plaque biofilms associated with periodontitis but not gingivitis or gingival health. lt appears that of the 300+ identifiable species found in the oral cavity, only a small proportion (10- 12 species) are actually found in active periodontitis sites. The bacteria believed to be pathogens in periodontitis do not conform to the classic dogma for microbial pathogenicity (ie, Koch's Postulates). The current understanding of mixed infections, bacterial invasion, virulence factors, conducive bacteria habitats, the role of so-called "beneficial species", and the susceptibility of the host have rendered Koch's Postulates obsolete when it comes to periodontitis. What ls Meant by "Putative Periodontal Pathogen"? The criteria for implicating oral microorganisms as perio- dontaΙ pathogens are: 1. The microorganism must be associated in high numbers in active periodontitis lesions and either absent (not culti- vable) or in low numbers in gingivitis or healthy sites. The numbers of the microorganism should have increased to a threshold level before the onset of disease. 2' Ιhe elimination of the microorganism, or its numerical reduction below threshold levels, should parallel remis- sion of active disease. 3. There should be a specific host immune response against the organism (ie, elevated serum, salivary, and crevicular fluid antibody titers). 4. The microorganism should evoke virulence factors that contribute to its pathogenicity or explain disease pathobi- ology. 5. The microorganism should produce periodontitis in animal model systems. What Features Do Most Periodontal Pathogens Have in Common? What Are the Exceptions to the Paradigm? This smalΙ group of putative periodontal pathogens possesses certain features in common. Most of them have a Gram- negative cell wall. The outer membrane of the Gram-negative cell wall contain lipopolysaccharide (LPS) Λ/hich has endo- toΧin activity (see Figure 3). Typically, LPS οontaining Gram- negative cell waΙl extracts are capable of promoting bone resorption, inhibiting osteogenesis, οhemotaxis of neutrophils, and other events associated with active periodontitis. Some pathogens release a LPS that suppresses the innate immune response. Many periodontal pathogens are strict or faculta- tive anaerobes and are asaccharolytic, permitting survival in the restricted ecosystem of the periodontal pocket. Among the strict anaerobes is the only presumptive periodontal path- ogen with a Gram-positive οell ν'ιall, Peptostreptococcus micros. F|GUHE 3- A terminaΙ outer membrane vesicle at the tip of Fusobacterium nucιeatum. High concentrations of lipopolysaccharide (endotoxin) are present in the outer membrane of Gram-negative cell walls, Actinobacill us actinomycetemcomitans and Porphyromonas gingivalis are the best studied and have been designated, along with Bacteroides forsythus, as true etiologic agents in periodontitis because of the host of virulence they produce and their ability to invade gingival tissues. Prevotella inter- media/nigrescens and Fusobacterium nucleatum have been widely studied as well, and appear to satisfy all criteria for periodontal pathogenicity. Because P. intermedia and strains ot F. nucΙeatum have also been found in areas of Severe gingival inflammation without evidence of attachment loss, controversy exists as to their true periodontal pathogenicity. Campylobacter rectus, Εikeneila corrodens, Εubacterium species, SeΙenomonas species, enteric rods/Pseudomonas speοies, and Treponema species satisfy some, but not all, criteria with any degree of confidence. Nonetheless, they remain among the list of periodontal pathogens, and microbi- ology testing serviοes commonly report their presence among cultivable flora. Relative risk values of periodontal pathogens in periodontal sites have emerged from archival reviews of data bases located in commercial testing facilities. The relative risk of a
  19. 19. CHAPτER 3 microorganism as a pathogen is often expressed as percent of total cultivabιe bacteria in a given culture. For example, the cultivability of A. actinomycetemcomitans at levels at or above 0.01% indicates a periodontal site at risk for active disease. The risk for P. gingivalis, C. rectus, P. intermedia, and P. micros in periodontal sites is 0.1%, 2%,2.5%, and 3"/", respectively. What ls Dental Calculus? Dental calculus is mineraΙized, mature plaque covered on its suface with nonmineralized plaque, material alba, desqua- mated epithelial cells, and formed blood elements. The bacterial components are largely branched and unbranched filamentous microorganisms that are usually nonvital or display minimal metabolic activity. These bacteria probably play a role in the mineralization of calculus as inorganic crys- tals are frequently found within and around microorganisms. Structurally, calculus retains much of the histologic morphology of its plaque precursor. Calculus may be classified as supragingival or subgingival based on location. lt may also be classified as salivary or serumal based on the source of inorganiο salts that comprise calculus. Root calculus is usually more strongly adherent to tooth surfaces than that found on enamel sudaces (see Figures 4 and 5). The inorganic components of calculus deposits are primarily organized into crystalline struοtures that vary according to the age of the deposit. For instance, in mature calculus (>6 months), the major crystalline structure is hydroxyapatite (Ca16[PO4]6(OH)r) with lesser amounts of octacalcium phos- phate (Cas[HPOa]a), whitlockite (Ca3[POo]r), and brushite (Ca[HPOo]2HrO). ln younger deposits (<3 months), brushite predominates, but with progressive aging, octacalcium phos- phate, whitlockite, and finally hydroxyapatite become more abundant. FlGURE 4. A heavy deposit of suρragingival, salivary calculus on the buccal and occlusal surfaces of nonfunctional maxillary premolar and molar teeth. Calculus deposits have also been desοribed as radiographi- cally apparent. The radiographiο detection of calculus is posi- tively influenced by the thickness of the deposit, the amount of surface area covered by the deposit, and the anatomy of the tooth. Only 40% to 50% of calculus deposits will be radio- graphicaΙly apparent. Therefore, radiographs should not solely be used to measure the presence or absence of calculus. How Does Calculus Attach to Teeth? Do the Attachment Mechanisms Have Any Clinical Significance? Calculus will attach to tooth suι'faces by several mechanisms. The most common mechanism of supragingival calculus attachment to smooth enamel surfaces is salivary pellicle, and it is usually easily removed using ultrasonic or hand instrumentation. The irregularities of unrestored caries and defective dental restorations complicate the removal of supragingival calculus. The attachment of subgingival calculus is further complicated by microscopic irregularities in cementum such as cementaι tears, cemental voids once occupied by Sharpey's fibers, resorption bays, and other surfaοe cemental defects. lt is for these reasons that clini- cians will further designate calculus deposits as either coronal or radicular to reflect the relative tenaciousness of radicular and coronal calculus, and in the οase of radicular calculus, the difficulty they may have in achieving total calοulus removal during root planing. FlGURE 5. serumnaι calculus deposits that have become supragingival due to gingival reοession caused by advanced periodontitis. Note the more generalized distribution of the deposits with no apparent relationship or proximity to ma,or salivary ducts. What ls the Pathogenic PotentiaΙ of Calculus? The current view is that calculus exerts its pathogenic poten- tial as a contributing factor that fosters plaque formation and promotes its retention on teeth. Also, there is little question that the microbiaΙ composition of calculus provides bacterial factors that, by themseΙves, produce an inflammatory reac- tion in tissue. Bacterial οomponents (outer membrane vesi- cles containing LPS, cell ivall material containing lipoteichoiο acids, periplasmic and cytopΙasmic enzymes, and bacterial metabolic factors) are all suspect pathogenic factors in dental calculus. The persistent inflammation in gingival tissue predictably seen adjacent to reasonably plaque free calculus is unequivocal evidence of the pathogenic effect of calculus. 17
  20. 20. EτloLoGY AND clAsslFlcAτloN oF τHE PEBloDoNτAL DlsEAsEs F|GURE 6. τhe exposure of subgingival' serumnal calculus aΙter a period of improved plaque control. Marginal inflammation has been reduced but erythema and edema persist. τhis is the same patient as seen in Figure 1' Aside from this, the rough surface of dental calculus is usually covered with a layer of plaque biofilm. Αs such, calculus tends to "present" plaque to periodontal soft tissues and interfere vvith efforts to improve plaque control. The phys- ical removal of dental calculus remains a critical component of mechanical periodontal inflammatory disease control. What Are the Risk Factors for Periodontal Diseases? What ls Meant by "Risk"? The expression risk in this context means that, in the pres- ence of a given factor, injury to or loss of periodontal tissue is a possibility. Risk factors may be local or systemic in nature. Local contributing factors to the etiology of periodontal diseases fall into two general categories: Anatomic or iatro- genic. They share in common their ability to either facilitate bacterial plaque, and therefore calculus, accumuΙation/reten- tion or their ability to interfere with plaque/calculus removal. Τhe loca| anatomic risk factors include: 1. Furcation anatomy. ln many instances, the entrance of bifurcations or trifurcations is restricted enough to limit access for mechanical root instrumentation. once access to the intrafurcaΙ space has been achieved, concavities in the furcal aspects of molar roots wiΙl limit instrumentation as well (see Figure 7). 2. lntermediate bifurcation ridges extending from the mesial furcation surfaοe of the distal root across the roof of the bifurcation to the distal sudace of the mesial root of mandibular molars. Τhese common anatomic deformities interfere with a patient's ability to effeοtively remove plaque biofilm. 3. Cervical enamel projections (CEP). CEPs are tooth developmental deformities of the CEJ found on molars. They are classified according to their involve- ment in tooth furcations. Α Grade l CEP presents with minimal projection of enamel tov/ard the entrance of the furcation. Α Grade ll οEP approximates the entrance of the furcation, and the tip of a Grade lll CEP is well within the furcation (see Figure 8). FlGURΕ 7. A maxiΙlary moΙar displaying a buccal to distal furcation invasion with a Nabers probe in place. The narrowness of the furcation entrances and the tortuousness of the furcation invasion mitigate against access for scaling and root planing. (Courtesy of Dr. Jeanne Salcetti) F|GURE 8. A human dried maxilla with a grade ll cervical enamel proiΘction (cEP) in the buccal furcation of the maxilΙary sΘcond molar. τhe cEP could have been partially responsible tor the furcation invasion and local- ized severe bone loss around the tooth. 4. Palato-gingival grooves (PGG). PGGs are tooth develοpmenta| deformities of maxilΙary central and lateral incisors. They begin in lingual piis and extend vertically onto root suιJaces. PGGs could, on rare occasions, extend to the root apex. PGGs are commonly associated with increased gingival inflam- mation, plaque aοcumulaiion, and probing depth (see Figure 9).
  21. 21. CHAPτER 3 FlGURE 9. A palatogingival groove on a maxillary lateral incisor. τhe gfoove couΙd have been partially responsible for the sΘvere attachment loss around the tοoth. Note that because of its loss of support, the lateral incisοr has undergone pathologic migration. 5. Open contacts and food impaction. Open contacts between teeth may be anatomical in origin, iatrogenic in origin, or be due to caries and pathologic migration of periodontally involved teeth. Food impaction is defined as the forceful wedging of food between teeth. Any other accumulation of food or food debris around teeth should be categorized as food retention and is probably less threatening to the periodontium. Food impaction and subsequent retention may contribute to root caries in individuals who do not perform proper oral hygiene interdentalΙy. open contacts by themselves probably do not contribute to periodontal pathology, but, in the presence of food impaction, open contacts have been associated with periodontal destruction. This may be particularly noticeable in periodontitis cases where the progress of disease is in its early stages or particularly obvious where periodontitis is isolated to sites of open contacts/food impaction. F|GURE 10. surgical exposure of an anomalous maxillary first moΙar. The palatal root is bifurcated and the distopalatal root curues into the mesial furcation of the second molar. on the bucca| aspect, the mesiobuccaΙ root of the second molar is in close approximation to the distobuccal root of the first molar. Access for effective scaling and root planing is extremely limited. 6. Other anatomic risk factors of potential etiologic importance are: The width of the space between teeth and root proximity (so-called "kissing roots"). The iatrogenic risk factors are: 1. Overhanging dental restorations. Since dental restorations remain the mainstay of dental practice, it is not surprising that overhanging dental restorations are arguably the most common form of iatrogeny to affect marginaΙ periodontal health (see Figure 11). Overhanging and improperly placed dental restora- tions can be physicaΙly irritating' be pΙaque retentive, foster the growth of periodontal pathogens, alter the morphology of the interdental space, and violate the dentogingival junction (see 2 below). By virtue of their roughness and overall bulk, they may also interfere ivith interdentaι plaque control. FIGURE 11. A maxillary first molar with a mesial amalgam overhang that eπends into the furcation. lt is probable that the preparation Ιor this restoration impinged upon the biologic width. Note how the attachment level on the tooth parallels the extension of the overhang onto the cementum and into the furcation. Violation of the "biologic width". After overhanging restorations, iatrogenic invasion of the biologic width may be the next more serious insult to the periodon- tium a dentist can make. The impact of this insult is usually permanent as the margins of dental restora- tions are inevitably placed in the wake of the insult. The biologic width is one of nature's constant dimen- sions. lt is most constant within individuals and less constant betΛ/een individuals. lf it is injured, it will repair. lf however, restorative materials render the invasion of the biologic width permanent, periodontitis wilΙ produce apical migration of the .iunctional epithe- lium, resorption of crestal alveolar bone, loss of perio- dontal attachment, and possible vertical osseous defeοts (Figure 1 1). Α new bio|ogic width will repair a few mms apical to its original position on the tooth. This represents a net loss of attachment on the tooth. Open contacts and food impaction related to inadequate restorative dentistry. The impact of food impaction through open contacts created by 2. 3. Ξ
  22. 22. EτloLoGY AND clAsslFlcAτloN oF τHE PERloDoNτAL DlsEAsEs 4- 5. iatrogeny offers the same threat to the periodontium as food impaοtion associated with open contacts that have resulted from growth and development or occlusal Λrear. Occlusal traumatism associated with inadequate dentistry in 1, 2, and 3 above. Additional local iatrogenic risk factors for perio- dontal diseases include: Removable partial 2. dentures and overdentures, fixed bridges, removal of third molar teeth in older adults, placement of fixed orthodontic appliances, and orthodontic movement of periodontally involved teeth. Uncontrolled diabetics, poorly controlled diabetics, or diabetics whose control is unknown should only receive emergency periodontal therapy, and that treatment should be performed ,vith intraprocedural and/or postoperative antibiotic coverage. The patient's physician may also prescribe insulin or other antihyperglycemic agents to help limit post-operative infections or complications in wound healing. Ηlv/AlDs. Given the immunosuppressed state of these individuals (decreased CD4 lymphocytes), an expectation for severe periodontitis in patients with HIV/AIDS is reasonable. lndeed, these individuals suffer from other bacterial, viral, and fungal diseases more than those νvithout HIV infection. Many sucοumb to these infections. Early studies of the peri- odontal status in AIDS patients indicated that these individuals showed increased severity of periodontal diseases. H|V-gingivitis (linear erythema) and HIV- periodontitis (necrotizing ulcerative periodontitis) categories of periodontal diseases were quickly proposed to designate the unique cΙinical characteris- tics of periodontal diseases in this group. RecentΙy, the issue has been challenged by those who report no increases in the prevalence or extent of perio- dontal diseases among HlV-positive individuals. Smoking. Due to the vasoconstrictor effect of nico- tine and the paralysis by carbon monoxide on the ability of hemoglobin to transport oxygen, it is under- standable that smoking is a serious environmental risk factor for periodontal diseases. The length of time an individual has been smoking and the frequency of smoking play contributory roles in the severity of peri- odontal disease in smokers. Smokers also have a greater accumulation of plaque and οaΙcu|us than nonsmokers and may be more at risk to harbor perio- dontal pathogens. While probing depth reduction following conventional nonsurgical and surgical periodontal therapy has been reported in smokers, the amount of reduction has been reported as less than that achieved in nonsmokers. A growing body of evidence suggests strongly that the failure rate of implant therapy is higher in patients who smoke. lt is not uncommon for a therapist to recommend against the placement of dental implants in smokers. Patients must be coun- seled in this regard and supported in their attempts to overcome their addiction. Sex hormone imbalances. The most notable changes in the periodontium that are affected in part by hormonal changes occur in Λ/omen in their child- bearing years. ln the case of pregnancy, proges- terone and estrogen levels increase to levels that are several orders of magnitude greater than those seen during a normal menstrual cycle. Varying degrees of a reversible "pregnancy gingivitis" are common during pregnancy. The biologic impact of hormone changes range from the release of inflammatory mediators that increase vascular permeability (pros- taglandins), the alterations in immunoregulation and pro-inflammatory reguιators, the imbalances in the fibrinolytic system, and the abundant growth of the periodontal pathogen, P. intermedia. Because the duration of pregnancy is relatively short, hormonal changes associated with pregnancy have little effect on the more irreversible progress of periodontitis. What Are the Systemic Diseases and/or Conditions That Are Contributing Factors for Periodontal Diseases? Aside from the medications that affect the clinical presenta- tion of plaque-induced gingival diseases (nifedipine for control of hypertension, phenytoin for control of epileptic seizures, and cyclosporine to control organ transplant rejec- tion), most systemic diseases and conditions that may affeοt periodontal diseases generally alter host barrier and host defense mechanisms. The impact of diminished host suscep- tibility, along with the diverse virulence mechanisms invading microorganisms possess, help to explain the individual varia- tions in periodontal disease patterns Λ,e See in systemically ill periodontal patients. An assessment of systemic contribu- tions to periodontal diseases in our patients is critical to perio- dontal diagnosis and/or treatment planning. The systemic diseases and conditions that commonly affect periodontal diseases are: Uncontrolled type I and type ll diabetes mellitus, HIV/AIDS, hormone imbalances, genetic predisposition, medications, smoking, and malnutrition. 1. Diabeιes mellitus. Diabetes mellitus (DM) is atfecting a growing number of Americans. The inci- dence of the disease seems to vary according to ethnic origin, but it is estimated that 5% to 10% of individuals in the United States are affected with diabetes. DM is an aberration in carbohydrate, lipid, and protein metabolism. Most of the morbid compli- cations of DM stem from longterm impaired glucose metabolism. The characteristic hyperglycemia of uncontrolled DM is the basis for most of the vascular, cellular, and immune changes assoοiated with the disease. Epidemiologic data has made clear associations between increased severity of periodontal diseases and uncontrolled type I and type ll diabetes mellitus. Type I and type ll uncontrolled diabetics tend to present with more gingiva! inflammation, more loss of periodontal attachment, and radiographic evidence of more bone loss than controlled or nondiabetic individ- uals. There is agreement that periodontal patients whose DM is welΙ controlled may receive periodontal therapy without restriοtions' incΙuding periodontal surgery and implant placement. 3.
  23. 23. CHAPτER 3 Oral contraceptives mimic the hormonal levels seen during pregnancy, and it is not uncommon to find pregnancy-like changes in patients using birth οontrol pills (BCP). Because gingivaΙ sex hormone concen- trations tend to be lower during normal menstruation, it is not unexpected that women in their childbearing years may present with "cyclic" episodes of increased gingival inflammation. F|GURE'12. τhis lesion is a pyogenic granuloma in a 17-year-oιd femaΙe patient as a result in changes in sex hormone levels and plaque accumuιation. The most important οoncern of the dentist in managing patients who present with gingival disease related to hormone imbalances is to be certain that inflammatory disease control measures are effective (Figure 12). This is particularly important in women who are preg- nant because data exists to suggest a relationship betΛ/een periodontal infections (periodontitis) and preterm low birth weight babies. Antibiotiοs should be used only after a medical consultation in patients who are pregnant. Although οontroversial, there are reports of decreased effectiveness of oral οontracep- tives in individuals taking certain antibiotics. lndivid- uals who are taking BCPs should be advised that the use of prescribed antibiotics such as tetracyclines and some penicillins may interfere with the action of BCPs. To avoid unwanted pregnancy, these individ- ua|s should be so warned and use aΙternative methods of birth control ivhile taking antibiotics. 5. Genetic predisposition for periodontal diseases. There is general agreement that individual responses to plaque bacteria vary. lt has been suggested that disease pattern variations could be based, in part, on underlying genetically based differenοes in immune function. lndeed, the association of: a. Neutrophil receptor defects b' Αntibody responses (lgGr) to periodontal patho- gens c. οertain histoοompatibility antigens (HLΑ) d. Lymphocyte immune regulatory defeοts in patients with aggressive periodontitis adds credibility to this conοept. Studies in twins indicate that many of the clinical variations seen in chronic periodontitis can be attrib- uted to individual genetic differenοes. Recent reports of genetic pleomorphism in lL-1 genes and the elevated production of proinflammatory mediators, such as lL-1 , add another dimension to the impact genetic variations among individuals have on the patterns of chronic periodontitis.
  24. 24. EτloLoGY AND cLAsslF|cATloN oF TΗE PERIoDoNτAL DlsEAsEs CLASSIFICATION OF PERIODONTAL DISEASES Concepts about the etiology, pathogenesis, and treatment of the periodontal diseases have changed significantly over the years. NeΛ/ levels of understanding are reflected in the clas- sification systems for these diseases and conditions. The tΛ/o most recent widely accepted classification Systems of the periodontal diseases and conditions were developed in 1989 and 1999. The current system, more comprehensive than any of its predecessors, is admittedly still a work in progress. Ηoνv Has the Understanding of Periodontal Diseases Changed Over the Years? For many years, the periodontal diseases were thought of as degenerative diseases. Early confirmation of the role of bacterial plaque in the initiation and progression of gingivitis was only presented in the 1960s. Since that time, many of the earlier tenets have fallen by the wayside. Currently, it is clear that both gingivitis and periodontitis in their varied forms are caused by the accumulation of a bacterial plaque biofilms on the teeth and in the subgingival area, the host response to that aοcumulation, and the various systemic and local factors that may affect the host response. lt is also clear that only a relatively few bacteria are associated with inflam- matory periodontal disease. The exact role of these bacteria, their relationship with each other and their interaction with the immune system in the initiation and progression of disease is still not clearly understood. There also appears to be a genetic component to the initiation and progression of disease in some patients. At this iuncture, controlling the acοumulation of plaque is the first line of defense in preventing disease, no matter what other factors may be present. What ls the Difference BetιΛreen Gingivitis and Periodontitis? FlGURE '|3. Gingivitis in a 12-year-old female. τhe severe gingivitis was due to the interaction of increased levels of progesterone and plaque. Gingivitis is inflammation of the gingival tissues in the absence of οlinical attachment loss (Figure 13). lt may be οharacterized by edema, erythema, increased gingival temperature, and oοcasionally pain. As the inflammation and loss of connective tissue is confined to the soft tissues, teeth are not in jeopardy of being lost. Gingivitis is ordinarily reversible with appropriate therapy. Periodontitis is infΙam- mation that affects and destroys the attachment apparatus (Figure l4). The histology is marked by apical migration of the junctional epithelium from the οementoenamel junction, Ιoss of connective tissue attachement, loss of periodontal Ιigament, and destruction of bone. lncreased probing depths may occur or the gingiva may recede as attachment is lost. Continuation of this loss of attachment will eventually lead to the loss of the tooth. The progress of periodontitis may be arrested Λ/ith proper therapy. ln certain Situations, lost attachment apparatus may be surgicaΙly regenerated. FIGURE 14. Periodontitis in a 37-year-old male. Note the significant calculus and plaque accumulations, severe gingival inflammatiοn, and recession associated with the mandibular anterior teeth. What ls the "Traditional" Classification of the Periodontal Diseases? The 1989 World Workshop in Clinical Periodontics recom- mended the following categories of periodontitis. This system iS the one most familiar to a majority of cliniοians' l. Αdult periodontitis ll. Early-onset periodontitis A. Prepubertal periodontitis 1. Generalized 2. Localized B' JuveniΙe periodontitis 1. Generalized 2. Localized C. Rapidly progressive periodontitis lll. Periodontitis associated with systemic disease lV. Necrotizing ulcerative periodontitis V. Refractory periodontitis One of the generally accepted classifications for gingivitis vι/as: l. Plaque-associated gingivitis ll. Αcute necrotizing ulcerative gingivitis (ANUG) lll. Hormonal gingivitis lV. Drug-induced gingival overgrowth V. Desquamative gingivitis (associated with vesiculo- bullous diseases)
  25. 25. CHAPτER 3 During the ensuing decade, it Λ/as determined that this disease classification system exοluded many of the diseases and conditions of the periodontium that clinicians and researοhers confront on a dai|y basis. Further work was necessary to develop a neνv, more inclusive system. VVhat Is the 1999 Classification of Periodontal Diseases? The American Academy of Periodontology convened the 1999 lnternational Workshop for a Classification of Perio- dontal Diseases and Conditions to reassess the disease classification system that ivas developed by the 19B9 νvorld Workshop in Clinical Periodontics. Based on current knoννΙ- edge and philosophies, a more comprehensive classification system of diseases and conditions that affect the periodon- tium Λ/as proposed. Major οhanges include the addition of a section on gingivaΙ diseases, changing the names of adult periodontitis to chronic periodontitis, early onset periodontitis to aggressive periodontitis, and the elimination of refractory periodontitis as a distinct disease class. Periodontitis as a manilestation of systemic disease has been further clarified, new categories added on periodontal absοesses, perio- dontic-endodontiο lesions, and the developmental or acquired deformities and conditions, and the replacement of necrotizing ulcerative periodontitis with necrotizing perio- dontal diseases. l. Gingival Diseases A. Dental Plaque-lnduced Gingival Diseases .l . Gingivitis associated with dental plaque only a. Without Ιocal contributing factors (Figure 15) FIGURE 15. Gingivitis associated with dental plaque only. Note that the gingival inflammation is worse on the maxillary left side than the right side. τhis may be relatθd to the hand with which the patient biushes his teeth. As the patient turns his hand to maneuver the brush, the lateral incisor and canine are ofιen missed. b. V/ith local contributing factors 2. GingivaΙ diseases modified by systemic factors a. Αssociated with the endocrine System 1. Puberty-associated gingivitis (Figure 16) FIGURE 16. Puberty-Associated Gingivitis. τhis is related to the patient in FigurΘ 13. 2. Menstrual cycle-associated gingivitis 3. Pregnancy-associated - Gingivitis - Pyogenic granuloma (see Figure 12) 4. Diabetes mellitus-associated gingivitis b. Associated with blood dyscrasias 1. Leukemia-associated gingivitis 2. Other 3. Gingival diseases modified by medications a. Drug-influenced gingival diseases 1. Drug-influenced gingival enlargements (Figure 17) FlGURE'17Α. Drug-lnfluenced Gingival Enlargements. Gingival enlarge- ment due to phenytoin the,aPy. 23
  26. 26. EτloLoGY AΝD cLAsSlFlcATloN oF THE PER|oDoΝTAL DlSEASES FIGURE 178. Drug-lnfluenced Gingivat Enlargements. Gingival enlarge- ment due to nifedipine therapy superimposed on chronic periodon- titis. 2. Drug-influenced gingivitis - Oral contraceptive-associated gingivitis - Other 4. Gingival diseases modified by maιnutrition a. Αscorbiο acid-deficiency gingivitis b. Other B. Nonplaque-lnduced Gingival Lesions 1. Gingival diseases of specific baοterial origin a. Νeisseria gonorrhea-associated lesions b. Treponema pallidum-associaied lesions c. Streptococcal species-associated lesions d. Other 2. Gingival disease of viral origin a. Herpesvirus infections 1. Primary herpetic gingivostomatitis 2' Reοurrent oraΙ herpes (Figure 1B) FIGURE 18A. Recurrent Oral Herpes. General herpetic outbreak on the gingival tissues. F|GURE 188. Recurrent oraι Herpes. Herpes outbreak localized to one side of the hard palate several days after periodontal surgery on the same side ot the maxilla. - VaricelΙa-zoster infectionS b. Other 3. Gingival diseases of fungal origin a. Candida-sρecies infections - Generalized gingival candidiasis b. Linear gingival erythema (Figure 19) FIGURE '19. Linear Gingival Erythema. Seen in some HIV+ patients. ο. Ηistoplasmosis d. Other Gingival lesions of genetic origins a. Ηereditary gingival fibromatosis b. Other Gingival manifestations of systemic conditions a. Mucocutaneousdisorders 5.
  27. 27. CΗAPτER 3 '1 . Lichen planus (Figure 20) F]GURΕ 20. Erosive Lichen Planus. Ιn its ulcerative form, this disease can be quite painful for the patient. 2. Pemphigoid (Figure 21) fe #j FlGURΕ 21Α. Benign Mucous Membrane (cicatricial) Pemphigoid. A posi- tive Νikolsky sign is seen over the maxillary right lateral incisor. τhis indicates that a vesiculobullous disease is present. FlGURE 21B' Benign Mucous Membrane (cicaιricial) Pemphigoid. lmmu- notluorescence contirms the diagnosis ot pemphigoid. 3. Pemphigus vulgaris 4. Erythema multiforme 5. Lupus erythematosus 6. Drug induced 7 " Other b. Αllergic reactions 1. Dental restorative materials - Mercury - Nickel - Acrylic - Other 2. Reactions attributable to - Toothpastes/dentifriοes - Mouthrinses/mouthwashes - Chewing gum additives - Foods and additives (Figure 22) 3. Other FlGURΕ 22Α. Allergic Reactions Attributable to Food. This patient presented With severe gingival infΙammation associated with perio- dontal disease. The patient had no history or cΙinical findings suggesιive of sysιemic disease. 9q FΙGURΕ 22B' AΙlergic Reactions Atlributable to Food' After contrοl of local factors, there was still a signiricant amount of inflammation.
  28. 28. EτloLoGY AND cLAsSIFlcAT|oN oF τHE PER|oDoNTAL DlsEAsEs FIGURE 22C. Allergic Reactions Attributable to Food. An incisional biopsy revealed a diagnosis of plasma ceΙl gingivitis (allergic reac- tion)- FIGURE 22D. Allergic Reactions Attributable to Food. After eliminating curry peppers from her diet, this patient's gingiva returned to health. 6. Traumatic lesions (factitious, iatrogenic, acci- dental) - Chemiοal injury - Physical injury - Thermal injury 7. Foreign body reaction 8. Noi otherffise specified (NOS) ll. Chronic Periodontitis (Figure 23)- FlGURΕ 23Α. Generalized chronic Periodontitis. A' ln spite of significant plaque and calculus accumulations in the mandibular arch, ιhis palient had minimal gingival intlammation. FiGURE 23B. Generaιized chronic Periodontitis. τhe right buccal segment showed minimal soft tissue infΙammation buι probe depths ranged from 7-10 mm. FlGURE 23c. Generalized chronic Periodontitis. τhe radiographs showed significant bone loss in this area. F|GUΗΕ 23D. Generalized chronic Periodontitis. once a full thickness mucoperiosteal flap was reflected, the extent of bone loss was apparent. Α. Localized B. Generalized 26
  29. 29. CHAPτER 3 ll!. Aggressive Periodontitis* A. Localized (Figure 24) FιGURES 24A and B. Localized Αggressive Periodontitis. clinical and radiographic evidence of localized severe periodontal destruction. FlGURΕ 24ο. Localized Aggressive Periodontitis. Note the severe bone loss on the mesial of the tirst molar and no bone loss on the adia- cent distal of the second premolar. B. Generalized (Figure 25) FΙGURE 25. Generalized Aggressive Periodontitis. τhis 1g-year-old patient has already lost several teeth due to periοdontal disease. τhe entire dentition has been affected by disease. Periodontitis as a Manifestation of Systemic Diseases Α. Αssociated With Ηematologic Disorders 1. Acquired neutropenias 2. Leukemias 3. Other B. Αssociated With Genetic Disorders 1. Familial and οyοιic neutropenia 2. Down syndrome 3. Leukocyte adhesion deficiency syndromes 4. Papillon-Lefevre syndrome 5. Chediak-Higashisyndrome 6. Histiocytosis syndromes 7. Glyοogen siorage disease 8. lnfantile genetic agranulocytosis 9. Cohen syndrome 10. EhΙers-Danlos syndrome (Types lV and VlΙl) 1 1. Hypophosphatasia 12. Other Necrotizing Periodontal Diseases Α. Necrotizing Ulcerative Gingivitis (NUG) (Figure 26) FlGURΕ 26. Νecrotizing Ulceraιive Gingivitis. These lesions are quite painful and exude a distinctive unpleasant odor. tv. v.
  30. 30. EτloLoGY AΝD cLAsslFιcAτloN oF THE PΕRloDoNτAL D|SEASES B. Necrotizing Ulcerative Periodontitis (NUP) (Figure 27) FlGURE 27. Necrotizing Ulcerative Periodontitis' τhis lesion is often seen in an Hlv+ patient or a patient with fully developed ΑlDs. Vl. Abscesses of the Periodontium A. Gingival Abscess B. Periodontal Αbscess (Figure 28) FiGURE 28. Periodontal Abscess. τhis lesion is associated with some popcorn that was trapped in the subgingival area. C. Pericoronal Abscess Vll. Periodontitis Associated With Endodontic Lesions Α' Combined Periodontic-Endodontic Lesions Vlll. Developmental or Acquired Deformities and Conditions A. Localized Tooth-Related Factors That Modify or Predispose to Plaque-lnduοed Gingival Diseases/ Periodontitis 1. Tooth anatomic factors 2. Dental resiorations/appliances 3. Root fraοtures 4' Cervical root resorption and οemental tears B' Muοogingival Deformities and Conditions Around Teeth 1. GingivaΙ/soft tissue recession (Figure 29) F|GURE 29. Gingival/soft Tissue Recession. τhe recession is related to a lack οf attached gingiva and the buccaι frenum altachment. a. Facial or lingual surfacΘs b. lnterproximal (papillary) 2. Lack of keratinized gingiva 3. Decreased vestibular depth 4. Αberrant frenum/muscle position 5. Gingival excess a- Pseudopocket b. lnconsistent gingival margin c. Excessive gingival display d. Gingivalenlargement 6. Abnormal color C. Mucogingival Deformities and Conditions on EdentuΙous Ridges 1. Vertical and/or horizontal ridge deficiency 2. Lack of gingival/keratinized tissue 3. Gingival/soft tissue enlargement 4. Aberrant frenum/muscle position 5. Decreased vestibular depth 6. Abnormal color (Figure 30) FTGURE 30. Abnormal Color. This abnormal gingival color is due to retro- grade endodontic surgery and a resultant amalgam tattoo.
  31. 31. CHAPτER 3 D. occΙusal Trauma 1. Primary occlusal trauma 2. Secondary occlusal trauma "Cases of chronic and aggressive periodontitis may be generally described by the extent and severity of the disease. Localized disease would be <30o/o of sites involved and generalized disease as >30% of sites involved. Slight disease would have 1-2 mm of clinical attachment loss (CAL), moderate disease 3-4 mm CAL, and severe disease >5 mm CAL. What Are Some of the Distinguishing Characteristics of the New Classifications of Gingivitis? Gingivitis associated νιrith dental plaque only. As the name implies, bacterial plaque must be present to initiate the gingival infΙammation. This inflammation may be character- ized by changes in gingival color, contour, and possibly consistenοy; slight elevation of intrasulcular temperature; bleeding on gentle probing; an increase in gingival crevicular fΙuid flow (now as an exudate); and the inflammation is confined to the soft tissues. Local factors may include resto- ration overhangs, open contacts, and other plaque traps and impediments to good oral hygiene. Gingival diseases modified by systemic factors: Pubefiy-associated gingivitis, menstrua! cycle-associ- ated gingivitis, and pregnancy-associated gingivitis. These conditions are all associated with changes in steroid hormone levels, primariΙy progesterone and estrogen. Τhey have been associated with increased levels of Prevotella intermedia in the infΙamed sites. ln puberty-associated gingi- vitis, the inflammation may be exaggerated even with appar- ently minimal amounts of plaque. Menstrual cycle-associated gingivitis may appear in a very mild form. lncreased gingival crevicular fluid flow has been seen in a majority of subjects during ovulation. Pregnancy-associated gingivitis has perhaps the most radical changes, rvith the possible appear- ance of a pyogenic granuloma. lt is an extreme response to gingival inflammation, characterized as a painless protuber- ance of the gingiva that bΙeeds readily at slight provocation. Gingival diseases modified by medications. There are three major drugs that can induce an overgroΛ/th of gingival tissues. Phenytoin is used as an antiseizure medication, nifedipine and several of the other calcium channel blockers are antihypertensive/antiarrhythmic drugs, and cyclosporine Α is an immunosuppressant. overgrowth appears to be related to the level of plaque accumulation. Approximately 50% of phenytoin patients are susceptible to this overgro,νth. lt has been estimated Ιhat 2o"/" of patients on calcium_ channel blockers, and 2O/" to 30% of patients on cyclo- sporine A are susceptible to drug-induced gingival over- growth. Nonplaque-induced gingival lesions. Many of these lesions are relativeΙy rare with the exception of the herpes- virus and Candida infections. Herpesvirus infections must be cautiously treated due to their contagious nature Λ/hile the lesions are shedding virus. Treatment must be deferred νvhen the patient presents with a weeping lesion. Candida infections may be problematic if there is no apparent cause (reοent antibiotic use' illness) for the infeοtion. Candidaintec- tions have a high association r/ith human immunodeficiency virus (HlV) infection, so a thorough patient work-up may be necessary in the face of an unexplainable Candida infection. Gingival manifestations of systemic conditions. Muco- cutaneous disorders: These disorders include the dermato- logic/autoimmune diseases of lichen planus, pemphigoid, pemphigus vulgaris, erythema multiforme, lupus erythema- tosus, and drug-induced disorders. These disorders at one time were classified as desquamative gingivitis, a descriptive term signifying desquamation or falling away of the surface epithelium of the gingiva. These disorders are actually auto- immune in nature with no clear etiology. lt is critical that a definitive diagnosis be obtained, for while they all may have a similar appearanοe, pemphigus has a higher morbidity, while the mucocutaneous disorders are difficult to manage for patient comfort. Gingival manifestations of systemic conditions: Linear gingival erythema. This lesion is characterized by a bright erythematous margin of the free gingiva. lt is associated with immunosuppression, particularly ΗlV infection. The erythema does not resolve with the removal of plaque. Gingival manifestations of systemic οonditions: Aller- gies' Αllergic reactions may take on a Variety of forms from mild erythema and edema to severe inflammation to an apparent lichenoid appearance. The challenge is to be sure that the inflammation is not plaque related. A diagnosis of plasma cell gingivitis may be made by biopsy. The allergen must then be identified and, if possible, eliminated from the oral cavity. Allergens incΙude amalgam, base metals used in fixed prosthodontics, flavoring agents in dentifrices and cheνving gum' chili peppers, and other foodstuffs. lt may be difficult to identify the offending agent. Changes must be made one at a time, often a time-consuming process, in order to identify the allergen. What Are Some of the Distinguishing Characteristics of the New Classifications of Periodontitis? The new classifiοation system for periodontitis is more descriptive and not temporal as νvas the previous system. The terms adult, juvenile, early onset, and prepubertal have been replaced with various forms of chronic and aggressive disease. ln addition, many periodontal conditions that νvere not addressed in any previous classification system have been described. The term refractory periodontitis has been removed as a distinct disease entity, as the current thinking is that any type of periodontitis may be refractory. Chronic periodontitis. As the name implies, this type of periodontitis has a relatively long-standing history in a patient. This disease is characterized by relatively slow progress, loss of attachment and underlying bone with increased pocket depth. lt may have periods of rapid attach- ment Ιoss foΙlowed by prolonged periods of inactivity. Ιt is related to the presence of plaque and calculus, ι/ith a variety of associated bacteria involved. There may be modifying local factors, such as restorative overhangs, food impaction, or open contaοts, and systemic factors, such aS uncontrolΙed diabetes mellitus or cigarette smoking. Most often, chronic periodontitis is responsive to mechanical therapy. lt is no longer referred to as adult periodontitis as this disease may, albeit rarely, be seen in οhildren.
  32. 32. EτloLoGY AND clAsslFlcAτloΝ oF τHE PER|oDoNTAL DlsEASEs Aggressive periodontitis. This category replaces what used to be known as the early-onset periodontal diseases. Localized aggressive periodontitis replaces the older term, juvenile periodontitis, that is manifest by rapid and severe attachment loss in the incisor and permanent first molar regions. Actinobacillus actinomycetemcomitans is assoοi- ated with a majority of cases. Τhese patients have shown abnormalities in neutrophil function that may be related to a hyperimmune effect of their macrophages. This type of aggressive periodontitis has a fairly clear inheritance pattern. Τhe loοalized ρattern affects 14 or fewer teeth, mostly confined to the incisors and first molars. The generalized form of aggressive periodontitis, formerly known as rapidly progressive periodontitis, affects 15 or more teeth with possible immunologic changes as well. lt is characterized by episodic, rapid, and severe attachment loss. At times, this disease may be difficult to control. Periodontitis as a manifestation of systemic diseases. Λ/ith the exception of Down syndrome, most of the listed genetic disorders are relatively rare. τhe Down syndrome patient is a challenge because of the difficulty in maintaining good oral hygiene. The prevalence and severity of periodon- titis is high compared to unaffected siblings, and attaοhment loss may appear in the deciduous dentition. As the roots of teeth are often short, these patients may lose teeth earlier due to the early onset of disease and the root anatomy. What Are Some of the Distinguishing Characteristics of Some of the Other Periodontal Diseases and Conditions? Necrotizing periodontal diseases. Τhis οategory includes both necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP). NUG and NUP have been classified together as they may be different stages of the same disease. NUG is characterized by necrosis of the tips of the interdental papilla with a pseudomembrane appear- ance, pain, foul odor, spontaneous bleeding, and possible fever and lymphadenopathy. There is no attachment loss associated with NUG. Fusiforms and spirochetes, as well as Prevotella intermedia,haνe been implicated in the etiology of NUG. Significant contributing factors include stress, fatigue, poor oral hygiene, smoking, and poor nutrition, basically factors associated with immunosuppression. NUG and NUP are also associated with HIV infection. NUP shares many of the clinical characteristics of NUG along Λ/ith attachment loss. Abscesses of the periodontium. Periodontal abscesses are local infections of the gingival or periodontal tissues. The etiology may be a foreign object such as a popcorn hull or loose piece of calculus. This type of abscess is marked by localized swelling and tenderness or pain. As the marginal gingiva begins to heal ιΛ,ith treatment, the orifice to deeper drainage of infection may be closed off. lt may be drained either externally or through the wall of the periodontal pocket. Periodontitis associated with endodontic lesions. Endo- dontic and periodontal Iesions may coexist separately asso- ciated with the same tooth or may communicate with each other. Two separate lesions may coalesce or there may be a root fracture or root perforation. Occasionally, an isolated endodontic lesion may masquerade as a periodontal lesion, such as in an isolated furcation defect on a mandibular first molar. ln this case, proper endodontic therapy will heal the furοation lesion as weΙl. ln a true combined lesion, the endo- dontic therapy must be performed first in order for the even- tual periodontal therapy to succeed as well. Developmental or acquired deformities and conditions. Most of the deformities and conditions classified here are self-explanatory by name. Specific conditions such as mucogingival deformities, edentulous ridge deficiencies, and ocοlusal trauma are described elsewhere in Ιhis Manual. How ls a Periodontal Case Type Formulated Using the American Academy of Periodontology Case Type System? The case type refers to the level of disease sΘverity, not the specific diagnosis. Case type may be applied to each type of gingivitis and periodontitis (also see Chapter l). Case Type 1: Gingivitis. lnflammation confined to the soft gingival tissues only. All gingivitis, irrespeοtive of the level of inflammation, is considered to be in this category. Case Type 2: Mild Periodontitis. This category signifies the beginning of attachment loss, up to approxi- maΙely 2o"/" of the attachment apparatus on the root. τhere may be some pocketing and initial mobility. Furcation involvement, when present, is confined to a Class I involvement. Case Type 3: Moderate Periodontitis. This category signifies further loss of the attachment apparatus, up to approximately 40% Ιo 45"/o. There is increased bone loss, pocket depth, mobility, and furcation involvement. Furcas may have Class ll involvement. Case Type 4: Severe Periodontitis. There is severe attachment loss, deep pocketing, mobility, pathologic migration of teeth, and Class ll and possibly Class lll f urcation involvement. 30

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