Clinical Periodontology and Implant Dentistry 4th edition_1 pdf

Kinane, Tord Berglundh and Jan Lindhe Initiation and progression of periodontal disease 150 Introduction 150 Initiation of periodontal disease 150 Initial, early, established and advance

Clinical Periodontology and Implant Dentistry

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Classification of Periodontal Diseases xix

Denis F Kinane and Jan Lindhe

Adult periodontitis — chronic periodontitis

Early-onset forms of periodontitis — aggressiveperiodontitis

Systemic disease forms of periodontitisNecrotizing forms of periodontitis — necrotizingforms of periodontal diseases

Contributors xxi

Basic Concepts

Chapter 1

Anatomy of the Periodontium 3

Jan Lindhe, Thorkild Karring and Mauricio Araujo

Blood supply of the periodontium 43

Lymphatic system of the periodontium 47

Nerves of the periodontium 48

Chapter 2

Epidemiology of Periodontal Diseases 50

Panos N Papapanou and Jan Lindhe

Periodontitis in children and adolescents 57

Periodontitis and tooth loss 61

Risk factors for periodontitis 61

Introduction and definitions 61

Studies of putative risk factors for periodontitis 63

Longitudinal studies and conclusions 68

Periodontal infections and risk for systemic disease

70

Atherosclerosis — cardiovascular/cerebrovascular

disease 70

Preterm birth 72 Diabetes mellitus 73

Concluding remarks 73

Chapter 3

Dental Plaque and Calculus 81

Niklaus P Lang, Andrea Mombelli and Rolf Attstrom

Microbial considerations 81General introduction to plaque formation 83Dental plaque as a biofilm 85 Structure ofdental plaque 85

Supragingival plaque 85 Subgingival plaque 90 Peri-implant plaque 98

Chapter 4

Microbiology of Periodontal Disease 106

Sigmund S Socransky and Anne D Haffajee

Mixed anaerobic infections 110

Return to specificity in microbial etiology of

Criteria for defining periodontal pathogens 112

Periodontal pathogens 114 Mixed infections

122

The nature of dental plaque —

the biofilm way of life 122

The nature of biofilms 122

The virulent periodontal pathogen 133

The local environment 133 Host

Denis F Kinane, Tord Berglundh and Jan Lindhe

Initiation and progression of periodontal disease

150

Introduction 150

Initiation of periodontal disease 150

Initial, early, established and advanced lesions 155

Host-parasite interactions 163

Introduction 163

Microbial virulence factors 164

Host defense processes 165

Overall summary 175

Chapter 6

Modifying Factors: Diabetes, Puberty, Pregnancy

and the Menopause and Tobacco Smoking 179

Richard Palmer and Mena Soory

Diabetes mellitus 179

Type 1 and Type 2 diabetes mellitus 180

Clinical symptoms 180

Oral and periodontal effects 180

Association of periodontal infection and diabetic

control 181

Modification of the host/bacteria relationship in

diabetes 182

Periodontal treatment 183

Puberty, pregnancy and the menopause 183

Puberty and menstruation 184

Pregnancy 184 Periodontal treatment during pregnancy 186 Menopause and osteoporosis 186

Hormonal contraceptives 187

Tobacco smoking 188

Periodontal disease in smokers 189 Modification of the host/bacteria relationship in smoking 190

Tooth abnormalities such as enamel pearls and cemental tears 200

Dental restorations 200 Root fractures 201 Cervical root resorption 201

Treatment of plaque induced gingivitis 201Gingival diseases modified by endocrine factors(see also Chapter 6) 201

Pregnancy associated gingivitis 201 Puberty associated gingivitis 202 Menstrual cycle associated gingivitis 202 Pyogenic granuloma of pregnancy 202

Gingival diseases modified by malnutrition 202Gingival diseases modified by systemic conditions203

Diabetes mellitus 203 Leukemias and other blood dysplasias 203

Gingival diseases modified by medications 203Necrotizing ulcerative gingivitis (see alsoChapter 10) 205

Microbiology, host response and predisposing factors 205

Host response in acute necrotizing ulcerative gingivitis 206

Treatment of NUG 207

Chapter 8

Chronic Periodontitis 209

Denis F Kinane and Jan Lindhe

Risk factors or susceptibility to chronic periodontitis211

Bacterial risk factors 211 Age 211

Smoking 211 Host response related 212

Scientific basis for periodontal therapy 213

Tooth loss 213 Subgingival instrumentation and maintenance 213

Effect of surgical treatment 214Comparisons of surgical and non-surgical therapy214

Bacterial damage to the periodontium 228 Host

response to bacterial pathogens 228 Genetic

aspects of host susceptibility 231 Environmental

aspects of host susceptibility 232 Current

Principles of therapeutic intervention 237

Elimination or suppression of the pathogenic flora 238

Chapter 10

Necrotizing Periodontal Disease 243

Palle Holmstrup and Jytte Westergaard

Involvement of alveolar mucosa 246

Swelling of lymph nodes 246

Fever and malaise 248

Oral hygiene 248

Acute and recurrent/chronic forms of necrotizing

gingivitis and periodontitis 249

Diagnosis 249

Differential diagnosis 249

Histopathology 250

Microbiology 251

Microorganisms isolated from necrotizing lesions 251

Pathogenic potential of microorganisms 252

Host response and predisposing factors 253

Systemic diseases 253

Poor oral hygiene, preexisting gingivitis and history of

previous NPD 254

Psychologic stress and inadequate sleep 254

Smoking and alcohol use 254

Caucasian background 255

Young age 255

Treatment 255

Acute phase treatment 255

Maintenance phase treatment 257

Chapter 11

The Periodontal Abscess 260

Mariano Sanz, David Herrera and Arie J van

Diagnosis 262

Differential diagnosis 264

Treatment 264Complications 266

Tooth loss 266 Dissemination of the infection 266

Chapter 12

Non-Plaque Induced Inflammatory Gingival Lesions 269

Palle Holmstrup and Daniel van Steenberghe

Gingival diseases of specific bacterial origin 269Gingival diseases of viral origin 269

Herpes virus infections 269

Gingival diseases of fungal origin 272

Candidosis 272 Linear gingival erythema 274 Histoplasmosis 275

Gingival lesions of genetic origin 275

Hereditary gingival fibromatosis 275

Gingival diseases of systemic origin 277

Mucocutaneous disorders 277 Allergic reactions 286 Other gingival manifestations of systemic conditions 287

Traumatic lesions 289

Chemical injury 289 Physical injury 289 Thermal injury 291 Foreign body reactions 291

Chapter 13

Differential Diagnoses: Periodontal Tumors and Cysts 298

Palle Holmstrup and Jesper Reibel

Reactive processes of periodontal soft tissues 298

Fibroma/focal fibrous hyperplasia 298 Calcifying fibroblastic granuloma 300 Pyogenic granuloma 301

Peripheral giant cell granuloma 301

Reactive processes of periodontal hard tissues 302

Periapical cemental dysplasia 302

Benign neoplasms of periodontal soft tissues 303

Hemangioma 303 Nevus 304 Papilloma 304 Verruca vulgaris 305 Peripheral odontogenic tumors 305

Benign neoplasms of periodontal hard tissues 306

Ameloblastoma 306 Squamous odontogenic tumor 307 Benign cementoblastoma 308

Malignant neoplasms of periodontal soft tissues 308

Squamous cell carcinoma 308 Metastasis to the gingiva 309 Kaposi's sarcoma 310

Malignant lymphoma 310

Malignant neoplasms of periodontal hard tissues

311

Osteosarcoma 311

Langerhans cell disease 311

Cysts of the periodontium 312

Gingival cyst 313

Lateral periodontal cyst 313

Inflammatory pm-Mental cyst 314

Odontogenic keratocyst 314

Radicular cyst 315

Chapter 14

Endodontics and Periodontics 318

Gunnar Bergenholtz and Gunnar Hasselgren

Influence of pathologic conditions in the pulp on

the periodontium 319

Impact of disease conditions in the vital pulp 319

Impact of pulpal necrosis 319

Manifestations of endodontic lesions in the marginal

periodontium from lateral canals 323

Manifestations of acute endodontic lesions in the

marginal periodontium 324

Impact of endodontic treatment measures on the

periodontium 326

Root perforations 328

Vertical root fracture 330

Influence of external root resorptions 333

Mechanisms of hard tissue resorption 333

Clinical manifestations of external root resorptions

334

Different forms of external root resorption 335

Influence of periodontal disease on the condition of

Endodontic considerations in root resection of

multirooted teeth in periodontal therapy 344

Differential diagnostic considerations 344

Treatment strategies for combined endodontic and

periodontal lesions 346

Chapter 15

Trauma from Occlusion 352

Ian Lindhe, Sture Nyman and Ingvar Ericsson

Definition and terminology 352

Trauma from occlusion and plaque-associated

Periodontitis as a Risk for Systemic Disease 366

Ray C Williams and David Paquette

Early beliefs 366The concept of risk 367Understanding the concept of risk 369Periodontitis as a risk for coronary heart disease 370

Consistency, strength and specificity of associations 372

Specificity of the associations between periodontitis and coronary heart disease 373

Correct time sequence 373 Degree of exposure 373 Biological plausibility 374 Experimental evidence 375

Periodontitis as a risk for pregnancy complications376

Periodontitis as a risk for diabetic complications 378Periodontitis as a risk for respiratory infections 380Summary 381

Chapter 17

Genetics in Relation to Periodontitis 387

Bruno G Loos and Ubele Van der Velden

Introduction and definitions 387Evidence for the role of genetics in periodontitis 388

Heritability of aggressive periodontitis (early onset periodontitis) 388

Heritability of chronic periodontitis (adult periodontitis) 388

The twin model 388

Human genes and polymorphisms 390Genetics in relation to disease in general 391

A major disease gene associated with periodontitis392

Modifying disease genes in relation to periodontitis392

Cytokine gene polymorphisms 392

IL-1 gene polymorphisms 393

TNF-a gene polymorphisms 396 IL-10 gene polymorphisms 396

FcyR gene polymorphisms 396Conclusions and future developments 397

Clinical Concepts

Chapter 18

Examination of Patients with Periodontal Disease

403

Sture Nyman and Jan Lindhe

Symptoms of periodontal disease 403

The gingiva 404

The periodontal ligament – the root cementum 406

Assessment of pocket depth 406

Assessment of attachment level 406

Errors inherent in periodontal probing 407

Assessment of furcation involvement 409

Assessment of tooth mobility 409

The alveolar bone 409

Jan Lindhe, Sture Nyman and Niklaus R

Lang Screening for periodontal disease

415 Diagnosis 416

Treatment planning 416

Initial treatment plan 416 Single

tooth risk assessment 417 Case

Additional (corrective) therapy 422

Supportive periodontal therapy 422

Case reports 422

Patient K.A (female, 29 years old) 422

Patient B.H (female, 40 years old) 425

Patient P.O.S (male, 30 years old) 427

Chapter 20

Cause-Related Periodontal Therapy 432

Harald Rylander and Jan Lindhe

Objectives of initial, cause-related periodontal

therapy 432

Means of initial, cause-related periodontal therapy

432

Scaling and root planing 432

Removal of plaque-retention factors 441

Healing after initial, cause-related therapy 441

Importance of instruction and motivation in mechanical plaque control 459

Approaches to chemical supragingival plaque control 468

Vehicles for the delivery of chemical agents 469

Chemical plaque control agents 471Chlorhexidine 476

Toxicology, safety and side effects 476 Chlorhexidine staining 477

Mechanism of action 478 Chlorhexidine products 478

Clinical uses of chlorhexidine 479Evaluation of chemical agents and products 481

Studies in vitro 482 Experimental plaque studies 483 Experimental gingivitis studies 484 Home use studies 484

Clinical trial design considerations 485

Blindness 485 Randomization 485 Controls 486 Study groups 486

Chapter 23

The Use of Antibiotics in Periodontal Therapy 494 Andrea Mombelli

Principles for antibiotic therapy 494

The limitations of mechanical therapy 494 Specific characteristics of the periodontal infection 495 Infection concepts and treatment goals 496

Drug delivery routes 497

Evaluation of antimicrobial agents for periodontaltherapy 499

Systemic antimicrobial therapy in clinical trials 501

Local antimicrobial therapy in clinical trials 503

Comparison of treatment methods 506 Overall

Periodontal Surgery: Access Therapy 519

Jan L Wennstrom, Lars Heijl and Jan Lindhe

Techniques in periodontal pocket surgery 519

General guidelines for periodontal surgery 535

Objectives of surgical treatment 535

Indications for surgical treatment 535

Contraindications for periodontal surgery 537

Local anesthesia in periodontal surgery 538

Instruments used in periodontal surgery 540

Selection of surgical technique 543

Root surface instrumentation 545

Root surface conditioning/ biomodification 546

Suturing 546

Periodontal dressings 549

Postoperative pain control 550

Postsurgical care 550

Outcome of surgical periodontal therapy 550

Healing following surgical pocket therapy 550

Clinical outcome of surgical access therapy in

comparison to non-surgical therapy 552

The goals of periodontal infection control 561

Measurement of microbiological endpoints 562

Treatment of periodontal biofilms 562

The physical removal of microorganisms — mechanical

debridement 563

Antibiotics in the treatment of periodontal infections

565

Therapies that affect the microbial environment —

supragingival plaque removal 568

Combined antimicrobial therapies 571

Long-term effects of antimicrobial therapy 571

Concluding remarks 571Chapter 27

Mucogingival Therapy — Periodontal Plastic Surgery 576

Jan L Wennstrom and Giovan P Pini Prato

Root coverage 592

Root coverage procedures 594 Clinical outcome of root coverage procedures 610 Soft tissue healing against the covered root surface 613

Interdental papilla reconstruction 616Crown lengthening procedures 619

Excessive gingival display 619 Exposure of sound tooth structure 622 Ectopic tooth eruption 628

The deformed edentulous ridge 630

Prevention of soft tissue collapse following tooth extraction 630

Correction of ridge defects by the use of soft tissue grafts 631

Chapter 28

Regenerative Periodontal Therapy 650

Thorkild Karring, Jan Lindhe and Pierpaolo Cortellini

Introduction 650

Indications 650 Regenerative surgical procedures 651

Reliability of assessments of periodontalregeneration 652

Periodontal probing 652 Radiographic analysis and re-entry operations 652 Histologic methods 652

Periodontal wound healing 652

Regenerative capacity of bone cells 657 Regenerative capacity of gingival connective tissue cells 658

Regenerative capacity of periodontal ligament cells 659

Role of epithelium in periodontal wound healing 659 Root resorption 660

Regenerative procedures 661

Grafting procedures 662 Root surface biomodification 667 Growth regulatory factors for periodontal regeneration 668

Guided tissue regeneration (GTR) 669

Clinical application of GTR 669

Conclusions 694

Chapter 29

Treatment of Furcation-Involved Teeth 705

Gianfranco Carnevale, Roberto Pontoriero and Jan Lindhe

Furcation involvement degree 1 7 1 2

Furcation involvement degree II 712

Furcation involvement degree III 712

Scaling and root planing 712

Final prosthetic restoration 723

Regeneration of fureation defects 723

Extraction 726

Prognosis 726

Chapter 30

Occlusal Therapy 731

Jan Lindhe and Sture Nyman

Clinical symptoms of trauma from occlusion 731

Angular bony defect 731

Increased tooth mobility 731

Progressive (increasing) tooth mobility 731

Tooth mobility crown excursion/root displacement

731

Initial and secondary tooth mobility 731

Clinical assessment of tooth mobility (physiologic and

pathologic tooth mobility) 733

Treatment of increased tooth mobility 734

Orthodontic tooth movement in adults with

periodontal tissue breakdown 744

Orthodontic treatment considerations 748 Esthetic finishing of treatment results 751 Retention – problems and solutions; long-term follow-up 751

Possibilities and limitations; legal aspects 752

Specific factors associated with orthodontic toothmovement in adults 752

Tooth movement into infrabony pockets 752 Tooth movement into compromised bone areas 754 Tooth movement through cortical bone 756 Extrusion and intrusion of single teeth – effects on

periodontium, clinical crown length and esthetics 756 Regenerative procedures and orthodontic tooth movement 762

Traumatic occlusion (jiggling) and orthodontic treatment 763

Molar uprighting, furcation involvement 766 Tooth movement and implant esthetics 766

Gingival recession 768

Labial recession 768 Interdental recession 771

Minor surgery associated with orthodontic therapy772

Fiberotomy 772 Frenotomy 772 Removal of gingival invaginations (clefts) 774 Gingivectomy 776

Chapter 32

Supportive Periodontal Therapy (SPT) 781

Niklaus P Lang, Urs Bragger, Giovanni Salvi and Maurizio

S Tonetti

Definitions 781Basic paradigms for the prevention of periodontaldisease 782

Patients at risk for periodontitis without SPT 784SPT for patients with gingivitis 786

SPT for patients with periodontitis 786Continuous multilevel risk assessment 787

Subject risk assessment 787 Tooth risk assessment 792 Site risk assessment 794 Radiographic evaluation of periodontal disease progression 796

Clinical implementation 796

Objectives for SPT 797SPT in daily practice 797

Examination, Re-evaluation and Diagnosis (ERD) 798

Motivation, Reinstruction and Instrumentation ( MRI) 799

Treatment of Reinfected Sites (TRS) 799 Polishing, Fluorides, Determination of recall interval (PFD) 801

Implant Concepts

Chapter 33

Osseointegration: Historic Background and

Current Concepts 809

Tomas Albrektsson, Tord Berglundh and Jan Lindhe

Development of the osseointegrated implant 809

Early tissue response to osseointegrated implants

810

Osseointegration from a mechanical and biologic

viewpoint 813

Osseointegration in the clinical reality 817

Future of osseointegrated oral implants 818

Chapter 34

Surface Topography of Titanium Implants 821

Ann Wennerberg, Tomas Albrektsson and Jan

Lindhe Implant surface/ osseointegration 821

Measurement of surface topography 821

Instruments 821

Measuring and evaluating procedure 822

Implant surface roughness 823

Experimental studies investigating surface roughness

and osseointegration 823

Surface roughness of some commercially available

implants 825

Chapter 35

The Transmucosal Attachment 829

Jan Lindhe and Tord Berglundh

Normal peri-implant mucosa 829

Basic radiologic principles 838

Special requirements in the periodontally

compromised patient 838

Radiographic techniques for primary preoperative

evaluations 838

Intraoral and panoramic radiography 838

Radiographic techniques for secondary

preoperative evaluations 840

Requirements for cross-sectional tomography 842

Implants in the premolar and molar regions 843

Conventional versus computed tomography 845

The single implant case 845

Postoperative radiography 847

At abutment connection 847

Following crown-bridge installation 847

High demands on image quality 847

Analysis of postoperative radiographs 848

Subsequent follow-up examinations 849

Digital intraoral radiography 850

Principle comments on implant placement 857

Flap design 857 Bone drilling 858 Implant position 859 Implant direction 860 Cortical stabilization 861 Implant selection 862 Healing time 862 Abutment selection 863

Bone healing – general aspects 867

Model of bone tissue formation 869 Bone grafting 876

Concept of guided tissue regeneration (GTR) 877

Animal studies 877 Human experimental studies 883

Clinical applications 885

Alveolar bone defect closure 885 Enlargement or augmentation of alveolar ridges 885 Alveolar bone dehiscences and fenestrations in association with oral implants 889

Immediate implant placement following tooth extraction 889

Perspectives in bone regeneration with GTR 892Chapter 39

Procedures Used to Augment the Deficient Alveolar Ridge 897

Massimo Simion

General considerations 897

Flap design 897 Initial preparation of the recipient site 897 Positioning of the barrier membrane 898 Preparation of the donor site 898 Surgical procedure in the region of the ramus 898 Surgical procedure in the region of the symphysis of the mandible 899

Positioning of the bone graft in the recipient site 900 Closure of the recipient site 900

Postoperative care 900

Case reports 901

Patient 1 – Alveolar ridge augmentation for single tooth restoration in the anterior maxilla 901

Patient 2 — Alveolar ridge augmentation for implant

restoration in the anterior maxilla 903

Patient 3 — Alveolar ridge augmentation for implant

restoration of multiple adjacent maxillary teeth 907

Patient 4 — Vertical ridge augmentation in the

anterior area of the mandible 909

Patient 5 — Vertical ridge augmentation to allow

implant placement in the posterior segments of the

mandible 911

Chapter 40

Implant Placement i n the Esthetic Zone 915

Urs Belser, Jean-Pierre Bernard and Daniel Buser

Basic concepts 915

General esthetic principles and related guidelines 916

Esthetic considerations related to maxillary anterior

implant restorations 917

Anterior single-tooth replacement 919

Sites without significant tissue deficiencies 922

Sites with localized horizontal deficiencies 925

Sites with extended horizontal deficiencies 928

Sites with major vertical tissue loss 928

Multiple-unit anterior fixed implant restorations 930

Sites without significant tissue deficiencies 934

Sites with extended horizontal deficiencies 934

Sites with major vertical tissue loss 934

Conclusions and perspectives 934

Scalloped implant design 936

Segmented fixed implant restorations in the

Indications for implant restorations in the load

carrying part of the dentition 947

Controversial issues 950

Restoration of the distally shortened arch with fixed

implant-supported prostheses 950

Number, size and distribution of implants 951

Implant restorations with cantilever units 952

Combination of implant and natural tooth support

954

Sites with extended horizontal bone volume

deficiencies and/or anterior sinus floor proximity 954

Multiple-unit tooth-bound posterior implant

restorations 958

Number, size and distribution of implants 958

Splinted versus single-unit restorations of multiple

adjacent posterior implants 960

Posterior single-tooth replacement 961

Premolar-size single-tooth restorations 962

Molar-size single-tooth restorations 962

Sites with limited vertical bone volume 964

Clinical applications 965

Screw-retained implant restorations 965

Abutment-level impression versus implant shoulder-level impression 968

Cemented multiple-unit posterior implant prostheses 968

Angulated abutments 970 High-strength all-ceramic implant restorations 970 Orthodontic and occlusal considerations related to posterior implant therapy 971

Concluding remarks and perspectives 975

Early and immediate fixed implant restorations 975

Initial examination 980 Treatment planning 980 Treatment 981

Concluding remarks 983

Patient 2Fixed restorations on implants and teeth 984

Initial examination 984 Treatment planning 985 Treatment 986

Concluding remarks 987

Patient 3Implants used to restore function in the maxilla987

Initial examination 987 Treatment planning 987 Treatment 989

Concluding remarks 990

Patient 4Implants used in a cross-arch bridge restoration991

Initial examination 991 Treatment planning 991 Treatment 992

Concluding remarks 994

Patient 5Implants used to solve restorative problemsoccurring during maintenance therapy 997

Treatment planning 997 Treatment (1) 999 Treatment (2) 1000 Treatment (3) 1000 Concluding remarks 1000

Patient 6Implants used to solve problems associated withaccidental root fractures of important abutmentteeth 1002

Initial examination 1002 Treatment planning and treatment 1002 Concluding remarks 1002

Chapter 43

Implants Used for Anchorage in Orthodontic

Therapy 1004

Heiner Wehrbein

Implants for orthodontic anchorage 1004

Orthodontic-prosthetic implant anchorage (OPIA)

1006

Potential peri-implant reactions/orthodontic load 1006

Indications for orthodontic-prosthetic implant anchorage

1007

Orthodontic implant anchorage (OIA) 1007

Insertion sites 1007

Implant designs and dimensions 1007

Aspects relating to the use of orthodontic implant

anchors 1007

Direct and indirect orthodontic implant anchorage

1009

Treatment schedule and anchorage facilities with

palatal orthodontic implant anchors 1009

Conclusions 1012

Chapter 44

Mucositis and Peri-implantitis 1014

Tord Berglundh, Jan Lindhe, Niklaus P Lang and

Lisa Mayfield

Excessive load 1014

Infection 1014

Peri-implant mucositis 1015Peri-implantitis 1016Treatment of peri-implant tissue inflammation 1019

Resolution of the inflammatory lesion 1019 Re-osseointegration 1020

Microbial aspects associated with implants inhumans 1020

Microbial colonization 1020

Conclusion 1021Chapter 45

Maintenance of the Implant Patient 1024 Niklaus P Lang and Jan Lindhe

Goals 1024The diagnostic process 1024

Bleeding on probing (BoP) 1025 Suppuration 1025

Probing depth 1025 Radiographic interpretation 1025 Mobility 1026

Cumulative Interceptive Supportive Therapy (CIST)1026

Preventive and therapeutic strategies 1026

Conclusions 1029

Index 1031

It often happens that a textbook is obsolete by the time

it is published Furthermore, a book written by several

authors is frequently lacking in both style and

meth-odology

This textbook, Clinical Periodontology and Implant

Dentistry, is therefore an unusual and stimulating

sur-prise to the reader The many chapters included are all

written by authors who apparently share an

epistemo-logical approach that guides the logic of research and

scientific discovery Each chapter tells the story of how

different problems related to etiology, pathogenesis,

treatment and prevention of different lesions in the

periodontal tissues led to the formulation of

hypothe-ses or theories that were subsequently subjected to

testing

We know that the formulation of a novel hypothesis

requires fantasy and creativity and that experiments

(testing) can be planned and meaningful observations

can be made after an intelligent hypothesis is

formu-lated The authors of this book seem convinced, for

logical reasons, that observations and experiments are

always best performed after the formulation of

hy-potheses, and that "science will never grow by merely

multiplying data and observations" Experiments are

performed to examine if the theories proposed were

correct, close to the truth or false

The history of periodontology — as of any scientificdomain — is also and above all the history of its errors.Indeed, the errors form the walls of our base of knowledge and allow us to appreciate the closeness to thetruth, once unraveled

The reading of Clinical Periodontology and Implant Dentistry invites student and specialist to take a fasci-nating intellectual journey that in the end allows her

or him to understand how knowledge in various fields

of this discipline of medicine was progressed and how

it should be used in the practice of dentistry Thosereading this book will not only learn what to do or not

to do in diagnosing, treating and preventing odontal pathologies, but they will never cease to un-dertake its activity of rational criticism and criticalcontrol, being continuously reminded of Einstein'swords that "all our knowledge remains fallible"

peri-Giorgio Vogel

ProfessorDepartment of Medicine, Surgery and Dentistry

University of Milan

Italy

Preparations for the 4th edition of Clinical

Periodontol-ogy and Implant Dentistry started in 2001 when all

senior authors of the various chapters of the current

text were identified and invited to join the team of

contributors The authors were selected because of

their reputations as leading researchers, clinicians or

teachers in Periodontology, Prosthetic Dentistry,

Im-plant Dentistry and associated domains Their task

was simple but demanding; within your field of

ex-pertise, find all relevant information, digest the

knowledge and present to the reader a "state of the

art" text that can be appreciated by (i) the student of

dentistry and dental hygiene, (ii) the graduate student

of Periodontology and related domains and (iii) the

practicing dentist; the general practitioner and the

specialist in Periodontology and/or Implant

Den-tistry

I am proud to present the outcome of this collectiveeffort as it appears in this 4th edition of Clinical Perio- dontology and Implant Dentistry.

As was the case in the 3rd edition, this textbookconsists of three separate parts; Basic Concepts, Clinical Concepts and Implant Concepts; that together illustratemost, if not all, important aspects of contemporaryPeriodontology Several chapters from the 3rd edition

of this book have been thoroughly revised, some haverequired only modest amendment, while severalchapters in each separate part are entirely new Theamendments and additions illustrate that Periodon-tology is continuously undergoing change and thatthe authors of the textbook are at the forefront of thisconversion

Classification of Periodontal Diseases

DENIS F KINANE AND JAN LINDHE

In 1999 the American Academy of Periodontology

staged an International Workshop, the sole purpose of

which was to reach a consensus on the classification

of periodontal disease and conditions The most

nota-ble changes are in the terminology of the various

disease categories which reflect a better

under-standing of the disease presentations and their

differ-ences but also in the acceptance that adult and

early-onset forms of periodontitis can occur at any age Thus

we have: adult periodontitis becoming chronic

perio-dontitis; early-onset forms of periodontitis becoming

aggressive forms of periodontitis; systemic disease

forms of periodontitis; and necrotizing forms of

peri-odontitis

ADULT PERIODONTITIS

-CHRONIC PERIODONTITIS

The International Workshop recommended that the

term "adult periodontitis" be discarded since this

form of periodontal disease can occur over a wide

range of ages and can be found in both the primary

and secondary dentition (Consensus Report 1999)

The term "chronic periodontitis" was chosen as it was

considered less restrictive than the age-dependent

designation of "adult periodontitis" It was agreed

that chronic periodontitis could be designated as

lo-calized or generalized depending on whether less than

or more than 30% of sites within the mouth were

affected

EARLY-ONSET FORMS OF

PERIODONTITIS - AGGRESSIVE

PERIODONTITIS

The International Workshop recommended that the

term "early-onset periodontitis" be discarded since

this form of disease can occur at various ages and can

persist in older adults Thus aggressive periodontitis

can be considered either localized or generalized

Thus the term "localized aggressive periodontitis"

replaces the older term "localized juvenile

periodon-titis" or "localized early-onset periodonperiodon-titis" The new

term "generalized aggressive periodontitis" replaces "generalized juvenile periodontitis" or "generalizedearly-onset periodontitis" The classification term "prepubertal periodontitis" has been discarded andthese forms of periodontitis are described as localized

or generalized aggressive periodontitis occurring pubertally

pre-SYSTEMIC DISEASE FORMS OF PERIODONTITIS

The International Workshop agreed that certain temic conditions (such as smoking, diabetes, etc.) canmodify periodontitis (chronic or aggressive) and thatcertain systemic conditions can cause destruction ofthe periodontium (which may or may not be his-topathologically periodontitis), for example neu-tropenias or leukaemias

sys-NECROTIZING FORMS OF PERIODONTITIS — NECROTIZING FORMS OF PERIODONTAL

DISEASES

It was accepted by the International Workshop that "necrotizing ulcerative gingivitis" (NUG) and "ne-crotizing ulcerative periodontitis" (NUP) be collec-tively referred to as "necrotizing periodontal dis-eases" It was agreed that NUG and NUP were likely

to be different stages of the same infection and maynot be separate disease categories Both of these dis-eases are associated with diminished systemic resis-tance to bacterial infection of periodontal tissues Acrucial difference between NUG and NUP is whetherthe disease is limited to the gingiva or also involvesthe attachment apparatus

REFERENCE

Consensus Report on Chronic Periodontitis (1999) A n n a l s o f

Periodontology, 4, p 38.

MARTIN ADDY

Division of Restorative Dentistry

Department of Oral and Dental Science

Bristol Dental Hospital and School UK

Department of Prosthetic Dentistry

School of Dental Medicine

Department of Stomatology and Oral Surgery

School of Dental Medicine

University of Geneva

Switzerland

URS BRAGGERDepartment of Periodontology and FixedProsthodontics

School of Dental MedicineUniversity of BerneSwitzerlandDANIEL BUSERDepartment of Oral Surgery and StomatologySchool of Dental Medicine

University of BerneSwitzerlandGIANFRANCOCARNEVALE Via RidolfinoVenuti 38 Rome

ItalyNOEL CLAFFEYDublin Dental School and HospitalTrinity College

DublinRepublic of IrelandPIERPAOLOCORTELLINI Via C

Botta 16FlorenceItalyJOSE ECHEVERRIADepartment of PeriodonticsSchool of DentistryUniversity of BarcelonaSpain

INGVAR ERICSSONDepartment of Prosthetic DentistryFaculty of Odontology

Malmo UniversitySweden

HANS-GORAN GRONDAHLDepartment of Oral and Maxillofacial RadiologyFaculty of Odontology

The Sahlgrenska Academy at Goteborg UniversitySweden

Clinic for Fixed and Removable Prosthodontics

Centre for Dental and Oral Medicine and

Faculty of Health Sciences

School of Dentistry, Department of Periodontology

University of Copenhagen

Denmark

THORKILD KARRING

Department of Periodontology

Royal Dental College

Faculty of Health Sciences

The Sahlgrenska Academy at Goteborg UniversitySweden

JAN LINDHEDepartment of PeriodontologyFaculty of OdontologyThe Sahlgrenska Academy at Goteborg UniversitySweden

BRUNO G LoosDepartment of PeriodontologyACTA, Amsterdam

The NetherlandsLISA MAYFIELDDepartment of Periodontics and FixedProsthodontics

School of Dental MedicineUniversity of BerneSwitzerlandANDREA MOMBELLIDepartment of Periodontology and OralPathophysiology

University of GenevaSwitzerland

STURE NYMANDeceasedRICHARD PALMERDepartment of PeriodontologyGuy's, King's and St Thomas' Dental InstituteKing's College London

UKPANOS N PAPAPANOUDivision of PeriodonticsSchool of Dental and Oral SurgeryColumbia University

New York, NYUSA

DAVID W PAQUETTEDepartment of PeriodontologySchool of Dentistry University

of North CarolinaChapel HillNorth Carolina, NCUSA

ROBERTOPONTORIERO GalleriaPassarella 2 MilanItaly

GIOVAN PAULO PINI PRATO

Guy's, King's and St Thomas' Dental Institute

King's College London

UK

MAURIZIO S TONETTIDepartment of PeriodontologyEastman Dental InstituteUniversity College, University of LondonUK

UBELE VAN DER VELDENDepartment of PeriodontologyACTA, Amsterdam TheNetherlands

DANIEL VAN STEENBERGHESchool of Dentistry, Oral Pathology andMaxillofacial Surgery

Faculty of MedicineCatholic University of LeuvenBelgium

ARIE J VAN WINKELHOFFDepartment of Oral MicrobiologyACTA

AmsterdamThe NetherlandsGIORGIO VOGELDepartment of Medicine, Surgery and DentistryUniversity of Milan

ItalyHEINER WEHRBEINPoliklinik fur KieferorthopaedieAugustusplatz 2

MainzGermanyANN WENNERBERGDepartment of BiomaterialsDepartment of Prosthetic Dentistry/Dental MaterialScience

Faculty of MedicineThe Sahlgrenska Academy at Goteborg UniversitySweden

JAN L WENNSTROMDepartment of PeriodontologyFaculty of OdontologyThe Sahlgrenska Academy at Goteborg UniversitySweden

JYTTE WESTERGAARDPanum InstituttetSchool of DentistryUniversity of CopenhagenDenmark

RAY C WILLIAMS BJORN ZACHRISSON

Chapel Hill

North Carolina, NC

USA

BASIC CONCEPTS

Anatomy of the Periodontium

JAN LINDHE, THORKILD KARRING AND MAURICIO ARAITJO

Root cementum Alveolar bone Blood supply of the periodontium Lymphatic system of the periodontium Nerves of the periodontium

This chapter includes a brief description of the

char-acteristics of the normal periodontium It is assumed

that the reader has prior knowledge of oral

embryol-ogy and histolembryol-ogy The periodontium (pert = around,

odontos = tooth) comprises the following tissues (Fig

1-1): (1) the gingiva (G), (2) the periodontal ligament (PL),

(3) the root cementum (RC), and (4) the alveolar bone

(AP) The alveolar bone consists of two components,

the alveolar bone proper (ABP) and the alveolar process

The alveolar bone proper, also called "bundle bone"

is continuous with the alveolar process and forms the

thin bone plate that lines the alveolus of the tooth

The main function of the periodontium is to attach

the tooth to the bone tissue of the jaws and to maintain

the integrity of the surface of the masticatory mucosa

of the oral cavity The periodontium, also called "the

attachment apparatus" or "the supporting tissues of

the teeth", constitutes a developmental, biologic, and

functional unit which undergoes certain changes with

age and is, in addition, subjected to morphologic

changes related to functional alterations and

altera-tions in the oral environment

The development of the periodontal tissues occurs

during the development and formation of teeth This

process starts early in the embryonic phase when cells

from the neural crest (from the neural tube of the

embryo) migrate into the first branchial arch In this

position the neural crest cells form a band of

ectome-senchyme beneath the epithelium of the stomatodeum (

the primitive oral cavity) After the uncommitted

neural crest cells have reached their location in the jaw

space, the epithelium of the stomatodeum releases

Fig 1-1

factors which initiate epithelial-ectomesenchymal teractions Once these interactions have occurred, theectomesenchyme takes the dominating role in the fur-ther development Following the formation of the

in-dental lamina, a series of processes are initiated (budstage, cap stage, bell stage with root development)which result in the formation of a tooth and its sur-rounding periodontal tissues, including the alveolarbone proper During the cap stage, condensation ofectomesenchymal cells appears in relation to theden-

Fig 1-2.

tal epithelium (the dental organ (DO)), forming the

dental papilla (DP) that gives rise to the dentin and the

pulp, and the dental follicle (DF) that gives rise to the

periodontal supporting tissues (Fig 1-2) The decisive

role played by the ectomesenchyme in this process is

further established by the fact that the tissue of the

dental papilla apparently also determines the shape

and form of the tooth

If a tooth germ in the bell stage of development is

dissected and transplanted to an ectopic site (e.g the

connective tissue or the anterior chamber of the eye),

the tooth formation process continues The crown and

the root are formed, and the supporting structures, i.e

cementum, periodontal ligament and a thin lamina of

alveolar bone proper, also develop Such experiments

document that all information necessary for the

for-mation of a tooth and its attachment apparatus is

obviously residing within the tissues of the dental

organ and the surrounding ectomesenchyme The

dental organ is the formative organ of enamel, the

dental papilla is the formative organ of the

dentin-pulp complex, and the dental follicle is the formative

organ of the attachment apparatus (the cementum, the

periodontal ligament and the alveolar bone proper)

The development of the root and the periodontal

supporting tissues follows that of the crown

Epi-thelial cells of the external and internal dental epithe

lium (the dental organ) proliferate in apical

direction forming a double layer of cells named

Hertwig's epithelial root sheath (RS) The odontoblasts (

OB) forming the dentin of the root differentiate from

ectomesenchy-Fig 1-3

mal cells in the dental papilla under inductive ence of the inner epithelial cells (Fig 1-3) The dentin(D) continues to form in apical direction producing theframework of the root During formation of the root,the periodontal supporting tissues including acellularcementum develop Some of the events in the cemen-togenesis are still unclear, but the following concept isgradually emerging

influ-At the start of dentin formation, the inner cells ofHertwig's epithelial root sheath synthesize and se-crete enamel-related proteins, probably belonging tothe amelogenin family At the end of this period, theepithelial root sheath becomes fenestrated andthrough these fenestrations ectomesenchymal cellsfrom the dental follicle penetrate and contact the rootsurface The ectomesenchymal cells in contact withthe enamel-related proteins differentiate into cemen-toblasts and start to form cementoid This cementoid

Fig 1-4.

Fig 1-5

represents the organic matrix of the cementum and

consists of a ground substance and collagen fibers,

which intermingle with collagen fibers in the not yet

fully mineralized outer layer of the dentin It is

as-sumed that the cementum becomes firmly attached to

the dentin through these fiber interactions The

forma-tion of the cellular cementum, which covers the apical

third of the dental roots, differs from that of acellular

cementum in that some of the cementoblasts become

embedded in the cementum

The remaining parts of the periodontium are

formed by ectomesenchymal cells from the dental

follicle lateral to the cementum Some of them

differ-entiate into periodontal fibroblasts and form the fibers

of the periodontal ligament while others become

osteoblasts producing the alveolar bone proper in

which the periodontal fibers are anchored In other

words, the primary alveolar wall is also an

ectome-senchymal product It is likely, but still not

conclu-sively documented, that ectomesenchymal cells

re-main in the mature periodontium and take part in the

turnover of this tissue

GINGIVA

Macroscopic anatomy

The oral mucosa (mucous membrane) is continuouswith the skin of the lips and the mucosa of the softpalate and pharynx The oral mucosa consists of (1)the masticatory mucosa, which includes the gingiva andthe covering of the hard palate, (2) the specialized mu- cosa, which covers the dorsum of the tongue, and (3)the remaining part, called the lining mucosa.

Fig 1-4 The gingiva is that part of the masticatorymucosa which covers the alveolar process and sur-rounds the cervical portion of the teeth It consists of

an epithelial layer and an underlying connective sue layer called the lamina propria The gingiva obtainsits final shape and texture in conjunction with erup-tion of the teeth

tis-In the coronal direction the coral pink gingiva minates in the free gingival margin, which has a scal-loped outline In the apical direction the gingiva iscontinuous with the loose, darker red alveolar mucosa (lining mucosa) from which the gingiva is separated

ter-by a, usually, easily recognizable borderline called

Fig 1-5 There is no mucogingival line present in the

palate since the hard palate and the maxillary alveolar

process are covered by the same type of masticatory

mucosa

Fig 1-6 Two parts of the gingiva can be differentiated:

1 the free gingiva (FG)

2 the attached gingiva (AG)

The free gingiva is coral pink, has a dull surface and

firm consistency It comprises the gingival tissue at the

vestibular and lingual/palatal aspects of the teeth, and

the interdental gingiva or the interdental papillae On the

vestibular and lingual side of the teeth, the free

gingiva extends from the gingival margin in apical

direction to the free gingival groove which is positioned

at a level corresponding to the level of the

cemento-enamel junction (CEJ) The attached gingiva is in apical

direction demarcated by the mucogingival junction (

MGJ)

Fig 1-7 The free gingival margin is often rounded insuch a way that a small invagination or sulcus isformed between the tooth and the gingiva (Fig 1-7a).When a periodontal probe is inserted into this in-vagination and, further apically, towards the cemento-enamel junction, the gingival tissue is separated from

the tooth, and a "gingival pocket" or "gingival crevice" isartificially opened Thus, in normal or clinicallyhealthy gingiva there is in fact no "gingival pocket"

or "gingival crevice" present but the gingiva is in closecontact with the enamel surface In the illustration tothe right (Fig 1-7b), a periodontal probe has beeninserted in the tooth/gingiva interface and a "gingivalcrevice" artificially opened approximately to the level

of the cemento-enamel junction

After completed tooth eruption, the free gingivalmargin is located on the enamel surface approxi-mately 1.5 to 2 mm coronal to the cemento-enameljunction

Fig 1-8 The shape of the interdental gingiva (theinterdental papilla) is determined by the contact rela-tionships between the teeth, the width of the approxi-mal tooth surfaces, and the course of the cemento-

Fig 1-9 Fig 1-9c.

Vestibular gingiva

5 3

Fig 1-10

enamel junction In anterior regions of the dentition,

the interdental papilla is of pyramidal form (Fig 1-8b)

while in the molar regions, the papillae are more

flattened in buccolingual direction (Fig 1-8a) Due to

the presence of interdental papillae, the free gingival

margin follows a more or less accentuated, scalloped

course through the dentition

Fig 1-9 In the premolar/molar regions of the

denti-tion, the teeth have approximal contact surfaces (Fig

1-9a) rather than contact points Since the interdental

papilla has a shape in conformity with the outline of

the interdental contact surfaces, a concavity —a col — is

established in the premolar and molar regions, as

demonstrated in Fig 1-9b, where the distal tooth has

been removed Thus, the interdental papillae in these

areas often have one vestibular (VP) and one

lin-gual/palatal portion (LP) separated by the col region

The col region, as demonstrated in the histological

section (Fig 1-9c), is covered by a thin non-keratinized

epithelium (arrows) This epithelium has many

fea-tures in common with the junctional epithelium (see

Fig 1-34)

Fig 1-10 The attached gingiva is, in coronal direction,

demarcated by the free gingival groove (GG) or, when

such a groove is not present, by a horizontal plane

placed at the level of the cemento-enamel junction In

clinical examinations it was observed that a free

gin-gival groove is only present in about 30-40% of

The attached gingiva extends in the apical direction

to the mucogingival junction (arrows), where it comes continuous with the alveolar (lining) mucosa (AM) It is of firm texture, coral pink in color, andoften shows small depressions on the surface Thedepressions, named "stippling", give the appearance

Fig 1-11

2

5 3

3 5 7

9Fig 1-12

of orange peel It is firmly attached to the underlying

alveolar bone and cementum by connective tissue

fibers, and is, therefore, comparatively immobile in

relation to the underlying tissue The darker red alveo

lar mucosa (AM) located apical to the mucogingival

junction, on the other hand, is loosely bound to the

underlying bone Therefore, in contrast to the attached

gingiva, the alveolar mucosa is mobile in relation to

the underlying tissue

Fig 1-11 describes how the width of the gingiva varies

in different parts of the mouth In the maxilla (Fig

1-11a) the vestibular gingiva is generally widest in the

area of the incisors and most narrow adjacent to the

premolars In the mandible (Fig 1-11b) the gingiva on

the lingual aspect is particularly narrow in the area of

the incisors and wide in the molar region The range

of variation is 1-9 mm

Fig 1-12 illustrates an area in the mandibular

premo-lar region where the gingiva is extremely narrow The

arrows indicate the location of the mucogingival

junc-tion The mucosa has been stained with an iodine

solution in order to distinguish more accurately

be-tween the gingiva and the alveolar mucosa

Fig 1-13 depicts the result of a study in which the

width of the attached gingiva was assessed and

re-lated to the age of the patients examined It was found

that the gingiva in 40 to 50-year-olds was significantly

wider than that in 20 to 30-year-olds This observation

indicates that the width of the gingiva tends to

in-crease with age Since the mucogingival junction

re-mains stable throughout life in relation to the lower

border of the mandible, the increasing width of the

gingiva may suggest that the teeth, as a result of

occlusal wear, slowly erupt throughout life

Microscopic a n a t o m y

Oral epithelium

Fig 1-14a presents a schematic drawing of a histologic

section (see Fig 1-14b) describing the composition

of

mm

mmFig 1-13

the gingiva and the contact area between the gingivaand the enamel (E)

Fig 1-14b The free gingiva comprises all epithelial andconnective tissue structures (CT) located coronal to ahorizontal line placed at the level of the cemento-enamel junction (CEJ) The epithelium covering thefree gingiva may be differentiated as follows:

• oral epithelium (OE), which faces the oral cavity

• oral sulcular epithelium (OSE), which faces the toothwithout being in contact with the tooth surface

• junctional epithelium (JE), which provides thecontact between the gingiva and the tooth

Fig 1-14a

Oral sulcular epithelium

Junctional epithelium

Connective tissue -

Bone

Oral epithelium

Fig 1-14b Fig 1-14c.

Fig 1-16

Fig 1-14c The boundary between the oral epithelium (OE) and the underlying connective tissue (CT) has awavy course The connective tissue portions whichproject into the epithelium are called connective tissue papillae (CTP) and are separated from each other byFig 1-15

Fig 1-17.

epithelial ridges — so-called rete pegs (ER) In normal,

non-inflamed gingiva, rete pegs and connective tissue

papillae are lacking at the boundary between the

junc-tional epithelium and its underlying connective tissue

(Fig 1-14b) Thus, a characteristic morphologic

fea-ture of the oral epithelium and the oral sulcular

epi-thelium is the presence of rete pegs, while these

struc-tures are lacking in the junctional epithelium

Fig 1-15 presents a model, constructed on the basis of

magnified serial histologic sections, showing the

sub-surface of the oral epithelium of the gingiva after the

connective tissue has been removed The subsurface

of the oral epithelium (i.e the surface of the epithelium

facing the connective tissue) exhibits several

depres-sions corresponding to the connective tissue papillae (

in Fig 1-16) which project into the epithelium It can

be seen that the epithelial projections, which in

his-tologic sections separate the connective tissue

papil-lae, constitute a continuous system of epithelialridges

Fig 1-16 presents a model of the connective tissue,corresponding to the model of the epithelium shown

in Fig 1-15 The epithelium has been removed,thereby making the vestibular aspect of the gingivalconnective tissue visible Notice the connective tissuepapillae which project into the space that was occu-pied by the oral epithelium (OE) in Fig 1-15 and bythe oral sulcular epithelium (OSE) on the back of themodel

Fig 1-17a In 40% of adults the attached gingiva shows

a stippling on the surface The photograph shows acase where this stippling is conspicuous (see also Fig.1-10)

Fig 1-17b presents a magnified model of the outer

Fig 1-18.

surface of the oral epithelium of the attached gingiva

The surface exhibits the minute depressions (1-3)

which, when present, give the gingiva its

charac-teristic stippled appearance

Fig 1-17c shows a photograph of the subsurface (i.e

the surface of the epithelium facing the connective

tissue) of the same model as that shown in Fig 1-17b

The subsurface of the epithelium is characterized by

the presence of epithelial ridges which merge at

vari-ous locations (1-3) The depressions (1-3) seen on the

outer surface of the epithelium (shown in Fig 1-17b)

correspond with the fusion sites (1-3) between

epi-thelial ridges Thus, the depressions on the surface of

the gingiva occur in the areas of fusion between

vari-ous epithelial ridges

Fig 1-18a A portion of the oral epithelium covering

the free gingiva is illustrated in this photomicrograph

The oral epithelium is a keratinized, stratified, squamous

epithelium which, on the basis of the degree to which

the keratin-producing cells are differentiated, can be

divided into the following cell layers:

1 basal layer (stratum basale or stratum

germinati-vum)

2 prickle cell layer (stratum spinosum)

3 granular cell layer (stratum granulosum)

4 keratinized cell layer (stratum corneum)

It should be observed that in this section, cell nuclei

are lacking in the outer cell layers Such an epithelium

is denoted orthokeratinized Often, however, the cells of

the stratum corneum of the epithelium of human

gingiva contain remnants of the nuclei (arrows) as

seen in Fig 1-18b In such a case, the epithelium is

denoted parakeratinized.

Fig 1-19 In addition to the keratin-producing cells

which comprise about 90% of the total cell population,

the oral epithelium contains the following types of

cytoplas-in the surroundcytoplas-ing keratcytoplas-in-produccytoplas-ing cells

The photomicrograph shows "clear cells" (arrows)located in or near the stratum basale of the oral epi-thelium Except the Merkel's cells, these "clear cells",which are not producing keratin, lack desmosomalattachment to adjacent cells The melanocytes are pig-ment-synthesizing cells and are responsible for themelanin pigmentation occasionally seen on thegingiva However, both lightly and darkly pigmentedindividuals present melanocytes in the epithelium

Fig 1-21.

The Langerhans cells are believed to play a role in the

defense mechanism of the oral mucosa It has been

suggested that the Langerhans cells react with

anti-gens which are in the process of penetrating the

epi-thelium An early immunologic response is thereby

initiated, inhibiting or preventing further antigen

penetration of the tissue The Merkel's cells have been

suggested to have a sensory function

Fig 1-20 The cells in the basal layer are either cylindric

or cuboid, and are in contact with the basement

mem-brane that separates the epithelium and the connective

tissue The basal cells possess the ability to divide, i.e

undergo mitotic cell division The cells marked with

arrows in the photomicrograph are in the process of

dividing It is in the basal layer that the epithelium isrenewed Therefore, this layer is also termed stratum germinativum, and can be considered the progenitor cell compartment of the epithelium

Fig 1-21 When two daughter cells (D) have beenformed by cell division, an adjacent "older" basal cell (OB) is pushed into the spinous cell layer and starts, as

a keratinocyte, to traverse the epithelium It takesapproximately 1 month for a keratinocyte to reach theouter epithelial surface, where it becomes shed fromthe stratum corneum Within a given time, the number

of cells which divide in the basal layer equals thenumber of cells which become shed from the surface.Thus, under normal conditions there is complete equi-librium between cell renewal and cell loss so that theepithelium maintains a constant thickness As the ba-sal cell migrates through the epithelium, it becomesflattened with its long axis parallel to the epithelialsurface

Fig 1-22 The basal cells are found immediately cent to the connective tissue and are separated fromthis tissue by the basement membrane, probably pro-duced by the basal cells Under the light microscopethis membrane appears as a structureless zone ap-proximately 1 to 2 µm wide (arrows) which reactspositively to a PAS stain (periodic acid-Schiff stain).This positive reaction demonstrates that the basementmembrane contains carbohydrate (glycoproteins) Theepithelial cells are surrounded by an extracellularsubstance which also contains protein-polysaccharidecomplexes At the ultrastructural level, the basementmembrane has a complex composition

adja-Fig 1-23 is an electronmicrograph (magnification x 70000) of an area including part of a basal cell, thebasement membrane and part of the adjacent connec-tive tissue The basal cell (BC) occupies the upperportion of the picture Immediately beneath the basalcell an approximately 400 A wide electron lucent zonecan be seen which is called lamina lucida (LL) Beneaththe lamina lucida an electron dense zone of approxi-mately the same thickness can be observed This zone

is called lamina densa (LD) From the lamina densa called anchoring fibers (AF) project in a fan-shapedfashion into the connective tissue The anchoring fi-bers are approximately 1µm in length and terminatefreely in the connective tissue The basement mem-brane, which appeared as an entity under the lightmicroscope, thus, in the electronmicrograph, appears

so-to comprise one lamina lucida and one lamina densawith adjacent connective tissue fibers (anchoring fi-bers) The cell membrane of the epithelial cells facingthe lamina lucida harbors a number of electron-dense,thicker zones appearing at various intervals along thecell membrane These structures are called hemides- mosomes (HD) The cytoplasmic tonofilaments (CT) in

Fig 1-24 Fig 1-25.

Fig 1-22.

the cell converge towards such hemidesmosomes The

hemidesmosomes are involved in the attachment of

the epithelium to the underlying basement

mem-brane

Fig 1-24 illustrates an area of stratum spinosum in the

gingival oral epithelium Stratum spinosum consists

of 10-20 layers of relatively large, polyhedral cells,

equipped with short cytoplasmic processes

resem-bling spines The cytoplasmic processes (arrows)

oc-cur at regular intervals and give the cells a prickly

appearance Together with intercellular

protein-car-bohydrate complexes, cohesion between the cells is

provided by numerous "desmosomes" (pairs of

hemidesmosomes) which are located between the

cy-toplasmic processes of adjacent cells

Fig 1-23.

Fig 1-25 shows an area of stratum spinosum in anelectronmicrograph The dark-stained structures be-tween the individual epithelial cells represent the des- mosomes (arrows) A desmosome may be considered

to be two hemidesmosomes facing one another Thepresence of a large number of desmosomes indicatesthat the cohesion between the epithelial cells is solid.The light cell (LC) in the center of the illustrationharbors no hemidesmosomes and is, therefore, not akeratinocyte but rather a "clear cell" (see also Fig 1-19)

Fig 1-26 is a schematic drawing describing the position of a desmosome A desmosome can be con-

com-sidered to consist of two adjoining hemidesmosomes

separated by a zone containing electron-dense

granu-lated material (GM) Thus, a desmosome comprises

the following structural components: (1) the outer

leaf-lets (OL) of the cell membrane of two adjoining cells, (

2) the thick inner leaflets (IL) of the cell membranes

and (3) the attachment plaques (AP), which represent

granular and fibrillar material in the cytoplasm

Fig 1-27 As mentioned previously, the oral

epithe-lium also contains melanocytes, which are responsible

for the production of the pigment melanin

Melano-cytes are present in individuals with marked

pigmen-tation of the oral mucosa (Indians and Negroes) as

well as in individuals where no clinical signs of

pig-mentation can be seen In this electronmicrograph a

melanocyte (MC) is present in the lower portion of the

stratum spinosum In contrast to the keratinocytes,

this cell contains melanin granules (MG) and has no

tonofilaments or hemidesmosomes Note the large

amount of tonofilaments in the cytoplasm of the

adja-cent keratinocytes

Fig 1-28 When traversing the epithelium from the

basal layer to the epithelial surface, the keratinocytes

undergo continuous differentiation and

specializa-tion The many changes which occur during this

proc-ess are indicated in this diagram of a keratinized

stratified squamous epithelium From the basal layer

(stratum basale) to the granular layer (stratum

granu-losum) both the number of tonofilaments (F) in the

cytoplasm and the number of desmosomes (D)

in-crease In contrast, the number of organelles such as

mitochondria (M), lamellae of rough endoplasmic

reticulum (E) and Golgi complexes (G) decrease in the

keratinocytes on their way from the basal layer

to-wards the surface In the stratum granulosum,

elec-tron dense keratohyalin bodies (K) and clusters of

gly-cogen containing granules start to occur Such

gran-Str granulosum

Str spinosumF

Fig 1-26.

ules are believed to be related to the synthesis of

keratin

Fig 1-29 is a photomicrograph of the stratum

granu-losum and stratum corneum Keratohyalin granules

(arrows) are seen in the stratum granulosum There is

an abrupt transition of the cells from the stratum

granulosum to the stratum corneum This is indicative

of a very sudden keratinization of the cytoplasm of the

keratinocyte and its conversion into a horny squame

The cytoplasm of the cells in the stratum corneum (SC)

is filled with keratin and the entire apparatus for

protein synthesis and energy production, i.e the

nu-cleus, the mitochondria, the endoplasmic reticulum

and the Golgi complex, is lost In a parakeratinized

epithelium, however, the cells of the stratum corneum

contain remnants of nuclei Keratinization is

consid-ered a process of differentiation rather than degenera

tion It is a process of protein synthesis which

requires energy and is dependent on functional cells,

i.e cells containing a nucleus and a normal set of

organelles

Summary

The keratinocyte undergoes continuous

differentia-tion on its way from the basal layer to the surface of

the epithelium Thus, once the keratinocyte has left the

basement membrane it can no longer divide but main

tains a capacity for production of protein

(tonofila-ments and keratohyalin granules) In the granular

layer, the keratinocyte is deprived of its energy- and

protein-producing apparatus (probably by enzymatic

breakdown) and is abruptly converted into a

keratin-filled cell which via the stratum corneum is shed from

the epithelial surface

Fig 1-30 illustrates a portion of the epithelium of the

alveolar (lining) mucosa In contrast to the epithelium

of the gingiva, the lining mucosa has no stratum

cor-neum Notice that cells containing nuclei can be iden

tified in all layers, from the basal layer to the

surface of the epithelium

Fig 1-29

Fig 1-30

RE

b

dc

Fig 1-31

Dento-gingival epithelium

The tissue components of the dento-gingival region

achieve their final structural characteristics in

con-junction with the eruption of the teeth This is

illus-trated in Fig 1-31a-d

Fig 1-31a When the enamel of the tooth is fully

devel-oped, the enamel-producing cells (ameloblasts)

be-come reduced in height, produce a basal lamina and

form, together with cells from the outer enamel

epi-thelium, the so-called reduced dental epithelium (RE)

The basal lamina (epithelial attachment lamina: EAL)

lies in direct contact with the enamel The contact

between this lamina and the epithelial cells is

main-tained by hemidesmosomes The reduced enamel

epi-thelium surrounds the crown of the tooth from the

moment the enamel is properly mineralized until the

tooth starts to erupt

Fig 1-31b As the erupting tooth approaches the oral

epithelium, the cells of the outer layer of the reduceddental epithelium (RE), as well as the cells of the basallayer of the oral epithelium (OE), show increasedmitotic activity (arrows) and start to migrate into theunderlying connective tissue The migrating epithe-lium produces an epithelial mass between the oralepithelium and the reduced dental epithelium so thatthe tooth can erupt without bleeding The formerameloblasts do not divide

Fig 1-31c When the tooth has penetrated into the oralcavity, large portions immediately apical to the incisalarea of the enamel are covered by a junctional epithe-lium (JE) containing only a few layers of cells Thecervical region of the enamel, however, is still covered

by ameloblasts (AB) and outer cells of the reduceddental epithelium

Fig 1-31d During the later phases of tooth eruption,all cells of the reduced enamel epithelium are replaced

by a junctional epithelium This epithelium is continu

ous with the oral epithelium and provides the

attachment between the tooth and the gingiva If the

free gingiva is excised after the tooth has fully

erupted, a new junctional epithelium,

indistinguishable from that found following tooth

eruption, will develop during healing The fact that

this new junctional epithelium has developed from

the oral epithelium indicates that the cells of the oral

epithelium possess the ability to differentiate into

cells of junctional epithelium

Fig 1-32 is a histologic section cut through the border

area between the tooth and the gingiva, i.e the

dento-gingival region The enamel (E) is to the left Towards

the right follow the junctional epithelium (JE), the oral

sulcular epithelium (OSE) and the oral epithelium (OE).

The oral sulcular epithelium covers the shallow

groove, the gingival sulcus located between the

enamel and the top of the free gingiva The junctional

epithelium differs morphologically from the oral

sul-cular epithelium and oral epithelium, while the two

latter are structurally very similar Although ual variation may occur, the junctional epithelium isusually widest in its coronal portion (about 15-20 celllayers), but becomes thinner (3-4 cells) towards thecemento-enamel junction (CEJ) The borderline be-tween the junctional epithelium and the underlyingconnective tissue does not present epithelial rete pegsexcept when inflamed

individ-Fig 1-33 The junctional epithelium has a free surface

at the bottom of the gingival sulcus (GS) Like the oralsulcular epithelium and the oral epithelium, the junc-tional epithelium is continuously renewed throughcell division in the basal layer The cells migrate to thebase of the gingival sulcus from where they are shed.The border between the junctional epithelium (JE) andthe oral sulcular epithelium (OSE) is indicated byarrows The cells of the oral sulcular epithelium arecuboidal and the surface of this epithelium is kerati-nized

Fig 1-33

Fig 1-3:

Fig 1-34.

Fig 1-34 illustrates different characteristics of the junc

tional epithelium As can be seen in Fig 1-34a, the

cells of the junctional epithelium (JE) are arranged

into one basal layer (BL) and several suprabasal

layers (SBL) Fig 1-34b demonstrates that the basal

cells as well as the suprabasal cells are flattened with

their long axis parallel to the tooth surface (CT =

connective tissue, E = enamel space.)

There are distinct differences between the oral

sul-cular epithelium, the oral epithelium and the

junc-tional epithelium:

1 The size of the cells in the junctional epithelium

is, relative to the tissue volume, larger than in the

oral epithelium

2 The intercellular space in the junctional

epithelium is, relative to the tissue volume,

comparatively wider than in the oral epithelium

3 The number of desmosomes is smaller in the

junc-tional epithelium than in the oral epithelium

Note the comparatively wide intercellular spaces

be-tween the oblong cells of the junctional epithelium,

and the presence of two neutrophilic granulocytes (

PMN) which are traversing the epithelium

The framed area (A) is shown in a higher

magnifi-cation in Fig 1-34c, from which it can be seen that the

basal cells of the junctional epithelium are not in direct

contact with the enamel (E) Between the enamel and

the epithelium (JE) one electron-dense zone (1) and

one electron-lucent zone (2) can be seen The electron

-lucent zone is in contact with the cells of the

junctional

epithelium (JE) These two zones have a structure verysimilar to that of the lamina densa (LD) and laminalucida (LL) in the basement membrane area (i.e theepithelium (JE)-connective tissue (CT) interface) de-scribed in Fig 1-23 Furthermore, as seen in Fig 1-34d,the cell membrane of the junctional epithelial cellsharbors hemidesmosomes (HD) towards the enamel

as it does towards the connective tissue Thus, theinterface between the enamel and the junctional epi-thelium is similar to the interface between the epithe-lium and the connective tissue

Fig 1-35 is a schematic drawing of the most apicallypositioned cell in the junctional epithelium Theenamel (E) is depicted to the left in the drawing Itcan be seen that the electron-dense zone (1) betweenthe junctional epithelium and the enamel can beconsidered a continuation of the lamina densa (LD)

in the basement membrane of the connective tissueside Similarly, the electron-lucent zone (2) can beconsidered a continuation of the lamina lucida (LL) Itshould be noted, however, that at variance with theepithelium-connective tissue interface, there are noanchoring fibers (AF) attached to the lamina densa-like structure (1) adjacent to the enamel On the otherhand, like the basal cells adjacent to the basementmembrane (at the connective tissue interface), thecells of the junctional epithelium facing the laminalucida-like structure (2) harbor hemidesmosomes.Thus, the interface between the junctional epitheliumand the enamel is structurally very similar to theepithelium-connective tissue interface, which meansthat the junctional epi-

Fig 1-36.

LL Fig 1-35.

thelium is not only in contact with the enamel but is

actually physically attached to the tooth via

hemides-mosomes

Lamina propria

The predominant tissue component of the gingiva is

the connective tissue (lamina propria) The major

components of the connective tissue are collagen fibers

(around 60% of connective tissue volume), fibroblasts (

around 5%), vessels and nerves (around 35%) which are

embedded in an amorphous ground substance

(ma-trix)

Fig 1-36 The drawing illustrates a fibroblast (F)

resid-ing in a network of connective tissue fibers (CF) The

intervening space is filled with matrix (M) which

constitutes the "environment" for the cell

Cells

The different types of cell present in the connective

tissue are: (1) fibroblasts, (2) mast cells, (3) macrophages

and (4) inflammatory cells.

Fig 1-37 The fibroblast is the most predominant

con-nective tissue cell (65% of the total cell population)

The fibroblast is engaged in the production of various

types of fibers found in the connective tissue, but is

also instrumental in the synthesis of the connective

tissue matrix The fibroblast is a spindle-shaped or

stellate cell with an oval-shaped nucleus containing

one or more nucleoli A part of a fibroblast is shown

in electron microscopic magnification The cytoplasm

contains a well-developed granular endoplasmicreticulum (E) with ribosomes The Golgi complex (G)

is usually of considerable size and the mitochondria (M) are large and numerous Furthermore, the cyto-plasm contains many fine tonofilaments (F) Adjacent

to the cell membrane, all along the periphery of thecell, a large number of vesicles (V) can be found

Fig 1-38 The mast cell is responsible for the production

of certain components of the matrix This cell alsoproduces vasoactive substances, which can affect thefunction of the microvascular system and control theflow of blood through the tissue A mast cell is pre-sented in electron microscopic magnification The cy-toplasm is characterized by the presence of a largenumber of vesicles (V) of varying size These vesiclescontain biologically active substances such as pro-teolytic enzymes, histamine and heparin The Golgi

Fig 1-37.

Fig 1-38 Fig 1-39.

Fig 1-40.

complex (G) is well developed, while granular

en-doplasmic reticulum structures are scarce A large

number of small cytoplasmic projections, i.e

mi-crovilli (MV), can be seen along the periphery of the

cell

Fig 1-39 The macrophage has a number of different

phagocytic and synthetic functions in the tissue A

macrophage is shown in electron microscopic

magni-fication The nucleus is characterized by numerous

invaginations of varying size A zone of

electron-dense chromatin condensations can be seen along the

periphery of the nucleus The Golgi complex (G) is

well developed and numerous vesicles (V) of varyingsize are present in the cytoplasm Granular endoplas-mic reticulum (E) is scarce, but a certain number of freeribosomes (R) are evenly distributed in the cytoplasm.Remnants of phagocytosed material are often found

in lysosomal vesicles: phagosomes (PH) In the riphery of the cell, a large number of microvilli ofvarying size can be seen Macrophages are particu-larly numerous in inflamed tissue They are derivedfrom circulating blood monocytes which migrate intothe tissue

pe-Fig 1-40 Besides fibroblasts, mast cells and

macro-Fig 1-41.

CF

Fig 1-42

phages, the connective tissue also harbors

inflamma-tory cells of various types, for example neutrophilic

granulocytes, lymphocytes and plasma cells

The neutrophilic granulocytes, also called

polymor-phonuclear leukocytes, have a characteristic appearance

(Fig 1-40a) The nucleus is lobulate and numerous

lysosomes (L), containing lysosomal enzymes, are

found in the cytoplasm

The lymphocytes (Fig 1-40b) are characterized by an

oval to spherical nucleus containing localized areas of

electron-dense chromatin The narrow border of

cyto-plasm surrounding the nucleus contains numerous

free ribosomes, a few mitochondria (M) and, in

local-ized areas, endoplasmic reticulum with fixed

ribo-somes Lysosomes are also present in the cytoplasm

The plasma cells (Fig 1-40c) contain an eccentrically

located spherical nucleus with radially deployed

elec-tron-dense chromatin Endoplasmic reticulum (E)

with numerous ribosomes is found randomly

distrib-uted in the cytoplasm In addition, the cytoplasm

contains numerous mitochondria (M) and a

well-de-veloped Golgi complex

Fibers

The connective tissue fibers are produced by the

fi-broblasts and can be divided into: (1) collagen fibers, (2)

reticulin fibers, (3) oxytalan fibers and (4) elastic fibers.

Fig 1-41 The collagen fibers predominate in the

gingi-val connective tissue and constitute the most essential

components of the periodontium The

electronmi-crograph shows cross- and longitudinal sections of

collagen fibers The collagen fibers have a

charac-teristic cross-banding with a periodicity of 700 A

be-tween the individual dark bands

Fig 1-42 illustrates some important features of thesynthesis and the composition of collagen fibers pro-duced by fibroblasts (F) The smallest unit, the colla-gen molecule, is often referred to as tropocollagen A

tropocollagen molecule (TC) which is seen in the per portion of the drawing is approximately 3000 Along and has a diameter of 15 A It consists of threepolypeptide chains intertwined to form a helix Eachchain contains about 1000 amino acids One third ofthese are glycine and about 20% proline and hy-droxyproline, the latter being found practically only

up-in collagen Tropocollagen synthesis takes place up-insidethe fibroblast from which the tropocollagen molecule

is secreted into the extracellular space Thus, the lymerization of tropocollagen molecules to collagenfibers takes place in the extracellular compartment.First, tropocollagen molecules are aggregated longitu-dinally to protofibrils (PF), which are subsequentlylaterally aggregated parallel to collagen fibrils (CFR),with an overlapping of the tropocollagen molecules

po-by about 25% of their length Due to the fact thatspecial refraction conditions develop after staining atthe sites where the tropocollagen molecules adjoin, across-banding with a periodicity of approximately 700

A occurs under light microscopy The collagen fibers (CF) are bundles of collagen fibrils, aligned in such away that the fibers also exhibit a cross-banding with aperiodicity of 700 A In the tissue, the fibers areusually arranged in bundles As the collagen fibersmature, covalent crosslinks are formed between thetropocollagen molecules, resulting in an age-relatedreduction in collagen solubility

Cementoblasts and osteoblasts are cells which alsopossess the ability to produce collagen

Fig 1-43.

Fig 1-44

Fig 1-43 Reticulin fibers — as seen in this

photomicro-graph — exhibit argyrophilic staining properties and

are numerous in the tissue adjacent to the basement

membrane (arrows) However, reticulin fibers also

occur in large numbers in the loose connective tissue

surrounding the blood vessels Thus, reticulin fibers

are present at the epithelium-connective tissue and the

endothelium-connective tissue interfaces

Fig 1-44 Oxytalan fibers are scarce in the gingiva butnumerous in the periodontal ligament They are com-posed of long thin fibrils with a diameter of approxi-mately 150 A These connective tissue fibers can bedemonstrated light microscopically only after pre-vious oxidation with peracetic acid The photomicro-graph illustrates oxytalan fibers (arrows) in the peri-odontal ligament, where they have a course mainlyparallel to the long axis of the tooth The function ofthese fibers is as yet unknown The cementum is seen

to the left and the alveolar bone to the right

Fig 1-45 Elastic fibers in the connective tissue of thegingiva and periodontal ligament are only present inassociation with blood vessels However, as seen inthis photomicrograph, the lamina propria and submu-cosa of the alveolar (lining) mucosa contain numerouselastic fibers (arrows) The gingiva (G) seen coronal tothe mucogingival junction (MGJ) contains no elasticfibers except in association with the blood vessels

Fig 1-46 Although many of the collagen fibers in thegingiva and the periodontal ligament are irregularly

or randomly distributed, most tend to be arranged ingroups of bundles with a distinct orientation Accord-ing to their insertion and course in the tissue, theoriented bundles in the gingiva can be divided into thefollowing groups:

1 Circular fibers (CF) are fiber bundles which run theircourse in the free gingiva and encircle the tooth in acuff- or ring-like fashion

2 Dentogingival fibers (DGF) are embedded in the mentum of the supra-alveolar portion of the rootand project from the cementum in a fan-like con-figuration out into the free gingival tissue of thefacial, lingual and interproximal surfaces

ce-3 Dentoperiosteal fibers (DPF) are embedded in thesame portion of the cementum as the dentogingivalfibers, but run their course apically over the ves-tibular and lingual bone crest and terminate in thetissue of the attached gingiva In the border areabetween the free and attached gingiva, the epithe-lium often lacks support by underlying orientedcollagen fiber bundles In this area the free gingivalgroove (GG) is often present

4 Transseptal fibers (TF), seen on the drawing to theright, extend between the supra-alveolar cemen-tum of approximating teeth The transseptal fibersrun straight across the interdental septum and areembedded in the cementum of adjacent teeth

Fig 1-47 illustrates in a histologic section the tion of the transseptal fiber bundles (arrows) in thesupra-alveolar portion of the interdental area Itshould be observed that, besides connecting the ce-mentum (C) of adjacent teeth, the transseptal fibers