Periodontology Chi-Cheng Tsai, D.D.S., Ph.D.

Periodontology Chi-Cheng Tsai, D.D.S., Ph.D.
Professor of Periodontology and Oral Pathology College of Dental Medicine Kaohsiung Medical University

Periodontal Pathogenesis
General Objective: To correlate the clinical characteristics of inflammatory periodontal disease with the underlying histopathological changes. Specific Objectives: 1. To acquire basic terminology dealing with periodontal pathology. 2. To list in a step-wise fashion the clinical and histopathological changes occuring during inflammatory periodontal disease. 3. Differentiate between a sulcus and a pocket. 4. Discuss the pathology of inflammatory responses.

Periodontal Pathogenesis (contd.)
5. To recognize those factors which can alter the pathogenesis of periodontal disease. a. To identify the local environmental factors which may enhance or inhibit the expression of bacterial pathogenicity. b. To list the central factors governing metabolism of host tissues which may condition the response to bacterial products.

Healthy Periodontium

Periodontium

Periodontal structure(ref.2, page 1)

Periodontal structureref.1-1
Facial interdental papilla Junctional epithelium Slucus Free gingiva Attached gingiva Mucogingival line Alveolar mucosa PDL Alveolar bone/Cribriform plate Lingual plate of bone Trabeculae (Cancellous bone)

Variability of gingival width(ref.2, page3)

Iodine test (Schiller 0r Lugol solution)
( oral mucosa: brown color (glycogen +), attached gingiva : unstained)

Top: Attachment loss (recession), toothbrush injury
Top: Attachment loss (recession), toothbrush injury. Bottom: Roll testref.1-120

Col(ref. 1, page 3)

Periodontiumref.4-227

Gingival and periodontal bundles, cementum, alveolar bone (ref
Gingival and periodontal bundles, cementum, alveolar bone (ref. 1, page 6)

Bony support apparatus(ref. 1, page 8)

Bony support apparatus
1. alveolar bone: cribriform plate, alveolar wall, lamina dura (radiograph). 2. trabecular bone. 3. compact bone.

Periodontal blood: from 1(periodontal ligament0, 2(alveolar process, 3(supraperiosteal & mucogingival tissues).(ref.1, page10)

Periodontal Probesref.1-118

Probes for diagnosis of furcations and root irregularitiesref.1-118
CH 3: fine and pointed, paired left and right, curved. For surfaces and narrow grooves. Nabers 2: Blunt, paired left and right, curved. For probing furcations. CP 12: Periodontal probe for horizontal measurement of furcation involvement (Hu-Friedy).

Healthy Crevice

Inflamed Gum with Normal PPD

Normal PPD and CAL

Periodontal Disease 1. Periodontal disease usually means the destructive inflammatory process affecting one or more of the four components of the periodontium. a). Alveolar bone b). Cementum c). Periodontal ligament proper d). Gingiva 2. Periodontal diseases are among the most common affections of mankind 3. Epidemiological surveys suggest that essentially all the world’s populations have experienced some forms of periodontal disease.

Pocket

Stage Four Periodontal Disease

Classification of pockets ref.1:77

Pocket Depth/Recession

PPD and CALref.1-117

PPD and CAL A. a 6-mm probing depth results from
3 mm of attachment loss and 3 mm of hyperplastic tissue. B. a 6-mm pocket results from 6 mm of attachment loss. C. a 6-mm pocket with 9 mm of

Pocket Depth:Recession

Pocket Depth and Recession

Infrabony Pocketsref.2-58
3-wall bony pockets: one tooth surface and three osseous surfaces. 2-wall bony pockets (interdental crater): two tooth surfaces and two osseous (one facial & one oral). 1-wall bony pockets: two tooth surfaces, one osseous surface (facial or lingual), a soft tissue border. Crater (Cup) defects: a combined form of pocket, defect surrounds the tooth.

Infrabony Pocketsref.1,page 78

Small 3-wall Pocketref.1-78 (3mm)

Deep 3-wall Bony Pocketref.1-78 (6 mm from the crest)

2-wall Bony Pocketref.1-79 (interdental crater, apical 3-wall defects)

1-wall Bony Defectref.1-79 (lingual plate remains)

Combined Pocketref.1-79 ( crater defect, a cup)

Buccal Furcation-bref.1-119

Mesial Furcation-mref.1-119

Distal Furcation-dref.1-119

Classification of furcation involvementref.2-60
F0: pocket, but without furcation involvement F1: furcation can be probed 3 mm in horizontal direction F2: furcation can be probed deeper than 3 mm F3: through-and through furcation

Classification of furcation ref. 1,80

F0: No Furcationref.1-80 (could have ca. 5 mm suprabony pocket)

F0: No Furcationref.1-80

F1 : Furcation 1ref.1-80 (< 3mm, performed from both lingual and buccal aspects)

F1: Furcation 1ref.1-80

F2: Furcation 2ref.1-81

F2: Furcation 2ref.1-81 (can probe more than 3 mm but not yet through-and through)

F3: Severe Furcationref.1-81

F3: Furcationref.1-81 (wide through-and-through, vertical bone loss >6mm)

Furcation Involvement

Degrees of Tooth Mobility
(500 g labio-lingual force) 0 = normal (physiologic mobility). 1 = detectably increased mobility. 2 = visible mobility up to 0.5 mm. 3 = severe mobility up to 1 mm. 4 = extreme mobility, vertical mobility, no longer functional.

Bacteria: Periodontal Diseases
Bacteria as primary etiologic agents in periodontal disease. experimental and epidemiologic studies: bacteria are required for initiation and perpetuation of inflammatory and destructive periodontal disease.

Bacteria: Dental Disease
Germ-free (gnotobiotic) animals do not have periodontitis or caries. Animals and man in whom the oral flora has been mechanically and chemotherapeutically removed or suppressed, show disease remission.

Gnotobiotic Rat: Experimental Periodontitisref.7-378

Normal Histology

Histology: Experimental Periodontitis (Rat)

Experimental Gingivitis
Initial gingivitis Löe et al. (1965): Experimental gingivitis Bacterial etiology of gingivitis (a) Plaque free stage (b) Oral hygiene ceased stage Gram-positive cocci and rods filamentous organisms spirochetes—mild gingivitis (GI=1)

Experimental Gingivitis
Free from plaque remain periodontally healthy Established periodontal disease can be arrested by meticulous scaling and root planing, proper oral hygiene

Prophylaxis

Scalingref.4-135

Chronic Periodontitis

After Scaling and Root Planing

Scaling and Root Planing
Combined effect of subgingival scaling and controlled oral hygiene definitely reduced the incidence of gingivitis How gingivitis develops?: experimental gingivitis (Löe, 1965) Bacterial plaque—main aetiological factors

Microorganisms and Periodontal Disease
3) Microorganisms in various stages of periodontal disease 4) Microorganisms in various types of

Microbiota in different stages of periodontal disease
Healthy gingiva: Supragingival plaque: relatively few cells predominate by G(+) mainly streptococci and Actinomyces species Spirochetes and vibriolike are low number

Initial-early gingivitis: Decreased Streptococci Increased Actinomyces and rods

Established gingivitis: subgingival plaque G(+): Actinomyces G() increased: Rods and spirochetes

Destructive periodontitis: (gingivitis with loss of attachment) Microbiota are as in established stage (may be greater increase in G() bacteria) Microbial invasion of connective tissue including bone and periodontal ligament has been reported.

Normal Dental Plaqueref.8-170

Chronic Gingivitis from Dr. Listgarten,1976

Periodontitis: test tube brush, and of spirochetes (from Dr
Periodontitis: test tube brush, and of spirochetes (from Dr. Listgarten,1976; ref.5-97)

RPP: Test tube brush, sea of spirochetesref.8-154,ref.5-132

Prominent Cultivable Microorganisms Associated with Various Periodontal Conditions
Periodontal condition A B C D E F Healthy periodontium n.d Gingivitis Advanced periodontitis n.d Juvenile periodontitis Deep pockets Normal pockets A: Number of samples; B: % G(-) anaerobic flora; C:% G(-) facultative anaerobic flora; D:% G(+) anaerobic flora; E: % G(+) facultative anaerobic flora; F: % G(+) facultative anaerobic cocci.

Characterization of Subgingival Plaque
Clinical health: G(+), Streptococci G(-) facultative-anaerobic rods 40% in chronic gingivitis 65-75% in chronic periodontitis

Oral Microfloraref.1-19 Gram(+) Gram(-)
Facultative anaerobes Anaerobes Facultative anaerobes Anaerobes Streptococcus Peptostreptococcus Neisseria Veillonella S. mutans Peptococcus Branhamella V. alcalescens S. sanguis Streptococcus V.atypica S. salivarius V. paruvula S. milleri S. mitis Micrococcus Actinomyces Actimyces Actinobacillus Bacteroides A. naeslundii A. israelii A. actimycetem B. gingivitis A. viscosus A. odontolyticus comitans B. intermedius Bacterionema Arachinia Capnocytophaga B. forthythus Rothia Eubactrium C. gingivalis B. melanino.

Oral Microfloraref.1-19 Gram(+) Gram(-)
Facultative Anerobes Facultative anerobes Anerobes anaerobes Nocardia Propionibacterium C. ochracea B. loescheii Lactobacillus Bifidobacterium C. sputigena B. denticola L. acidophilus Eikenella B. corporis L. casei E. corrodens Fusobacterium L. fermentum Haemophilus Leptotrichia H. segnis Campylobacter Selenomonas Wolinella

Spirochetes and Other Microorganisms
Treponema T. vincentii T. denticola T. socranskii Mycoplsasma Candida C. albicans Entamoeba Trichomonas

Bacteria: Pathogenic Theory
Sufficient numbers of a pathogenic species Access to the target tissues Organisms are able to survive and multiply No or in low number of inhibiting organisms Susceptible host

Species Association Elimination Host Virulence Animal
Relative number of publications suggesting the role of additional species possible etiologic agents of destructive periodontitis Species Association Elimination Host Virulence Animal Response Factors Studies P. intermedia F. nucleatum B forsythus C. rectus E. corrodens P. microbs Selenomonas sp Eubacteriun sp Spirochetes ___________________________________________________________________ Modified from Socrasky and Haffajee (1990, 1991, 1992).

Microbial Composition of Subgingival Plaque in Healthy Gingiva
Sparse G(+) saccharolytic Gingival crevice has a low redox potential, a pH of around (or just below) neutrality Obligatory anaerobic species Recovered on occasions: spirochetes, some black-pigmented anaerobes Isolated infrequently and in relatively low numbers: A.a. and P.g.

Subgingival Plaque: Gingivitis
An increase in mass A shift from a Streptococcus-predominated microflora to one with higher proportions of Actinomyces Increased proportions of F. nucleatum and P. intermedia

Gingivitis: Subgingival Plaque
A. actinomycetemcomitans in low number, P. gingivalis rarely isolated. Gingivitis may favor the growth of species implicated in periodontitis.

Bacteria: ANUG Fuso-spirochetal pattern of bacteria
A heterogeneous collection of cultivable organisms P. intermedia was isolated commonly F. nucleatum was only a minor component Organisms appear invade host tissue

Subgingival Plaque and Periodontal Disease

Bacteria: Destructive Periodontal Diseaseref.9-”371-376”
Dzink et al. 1985: active sites P. intermedia, B. forsythus, A.a., Wolinella recta F. nucleatum, P. gingivalis and E. corrodens Tanner et al. 1987: W. recta, B. gracilis and E. corrodens Proportions of all three species were less than 5% Viable count at sites (active/inactive) overlapped

Bacteria: LJP Microflora is sparse with relatively few species
A. actinomycetemcomitans (A.a.) (most produces a leukotoxin) Elevated antibody level to A.a. Some LJP sites had no A.a. been isolated

LJP: active pocket Mandell, 1984 E. corrodens and A.a. elevated
P. intermedia, F. nucleatum, Capnocytophaga decreased slightly, or not significantly increased

Adult (Chronic) Periodontitis
Microflora is difficult to define Diverse collections of microorganisms A progressive change in the composition of the microflora Burst of disease activity Microflora from “active” and “inactive” periodontitis sites

Haffajee et al. 1988 Predominant species in active lesions: F. nucleatum, Bacteroides spp., G(+) rods and Streptococci in other cases Many microbiologically distinct forms of periodontal disease

A.a.,P.g., P.i. Slots et al. 1986 A.a. P.g. P.i. as being of particular significance in the etiology One or more of the above species were isolated from 99% of progressive (active) sites, only about 40% of untreated non-progressive sites

Bacteria and Periodontitis
Wennström et al. 1987 Sites with one or more of the three (A.a. P.g. P.i.) species All three organisms were absent The absence of these three “indicator” bacteria appears to be a better predictor of no further loss of attachment than the presence of them is for disease progression.

Active vs. Inactive Lesion
Progression of periodontal breakdown A limited number of true “pathogens” Proposed organisms as being associated with “active” lesions

Bacteria associated with ”active” periodontal lesions in humans
Destructive periodontal disease W. recta B. fracilis E. corrodens Tanner et al. (1987) Recurrent periodontitis B. forsythus Lai et al. (1987) Localized and generalized destructive periodontal disease F. nucleatum (miscellaneous spp.) Haffajee et al. (1988c) The nomenclature is that of the original investigator(s).ref

Pathways of Tissue Alteration
Displacement of the JE from tooth surface: enzymatic activity Leukotoxins: hamper the functioning normal defense mechanisms Activation of acute inflammation and immunopathologic processes

Bacteria reported to be associated with various types of periodontitis
I. Frequently reported: Porphylomonas gingivalis Actinobacillus actinomycetemcomitans Spirochetes (Treponema spp.) II. Occasionally reported: Prevotella intemedia, P. denticola, P. oralis, P meloninogenica. Bactereroides forsythus, B, gracillis. Fusobacterium nucleatum, F. alocis, F. periodoticum. Eikenella corrodens, Wolinella recta, Selenomonas spp., Capno- cytophga spp., Treponema denticola, F. brachy, F. nodatium, F. tinidum

Complexes of Periodontal Pathogens
Yellow complex: S, mitis, S. oralis, S. sanguis; S. gordonii, S. intermedius. Purple complex: V. parvula, A. odontolyticus. Green complex: E. corrodens, Capnocytophaga spp.,A. actinomycetemcomitans. Orange complex: P. intermedia, P. nigrescens, P. micros, F. nucleatum; C. rectus, E. nodatum, C. showae. Red complex: P. gingivalis, B. forsythus, T. denticola.(more often in POB sites). (adapted from Carranza’s Clinical Periodontology, 9th ed., page104)

Periodontopathogens 牙周炎相關菌種(I)
非常強烈/強烈相關者(Very strongly/strongly associated) Actinobacillus actinomycetemcomitans Porphyromonas gingivalis Bacteroides forsythus (Tanerella forsythensis) Prevotella intermedia Campylobactor rectus Eubacterium nodatum Treponema species

Periodontopathogens 牙周炎相關菌種(II) 中等度相關者(Moderately associated)
Streptococcus intermedius Prevotella nigrescens Peptostreptococcus micros Fusobacterium nucleatum Eubacterium species Eikenella corrodens 2

Periodontopathogens 牙周炎相關菌種(III) Species are essential for initiation
Consequences of a sequential infection (multiple species) Consequences of overgrowth of commensal periodontal microflora or exogenous infections Microbial transmission among family members 3

Periodontopathogens 牙周炎相關菌種(IV)
Presence of a “pathogenic” flora and disease status Threshold for disease activity Combination or not with other strains Virulent or avirulent Environmental and ecology 4

Environmental Modification of the Virulence Potential of Subgingival Plaque
Microflora is a dynamic balance with the host The origin of the suspected periodontopathogens Plaque accumulates and causes an inflammatory response Enrichment of species (associated with periodontal disease) Numbers (infectious dose) of a pathogen(s) The pocket environment

Pathogenic Synergy in the Etiology of Periodontal Diseasesref.9-380
Bacteria capable of causing tissue damage directly (e.g. X,Y & Z) may be dependent on the presence of other cells (C or D) for essential nutrients or attachment, so that they can grow and resist the removal of GCF. Similarly, both groups of bacteria may be reliant for their survival on other organisms (Z,A or B) to modulate the host defenses. Individual bacteria may have more than one role (e.g.organism Z) in the etiology of disease, while different species could have similar role in different sites or subjects.

Pathogenic synergy in the etiology of periodontal diseasesref.9-380

Microbial Succession in Periodontal Diseaseref.9-382
Periodontal pathogens (closed symbols) in low number at healthy sites, but too low to cause disease; some pathogens may be acquired exogenously. Changes to the site ( altered nutrient availability; pH, reduced host resistance, etc.) may provide the opportunity for the outgrowth of some pathogens; this may further alter the environment and favor other organisms so that waves of microbial succession may occur. Depending on the original microflora of the pocket and on the sequence of environmental changes, then a range of microflora with disease potential could develop.

Microbial succession in periodontal diseaseref.9-382

Sites that lost attachment after therapy
Microflora of pockets before and after successful treatment, and of the refractory disease Sites that lost attachment after therapy A.a., B. forsythus, P. gingivalis, P. intermedia, P. melaninogenica, Peptostreptococcus micros, S. intermedius and W. recta Spirochetes and P. gingivalis showed a strong correlation with the continued loss of attachment Decreased proportion of P. gingivalis is positively correlated with the reduction of pocket depth

Mechanisms Bacterial products act directly on bone to cause resorption
Bacteria and endotoxins  cemental surface  inhibit reattachment potential  continuous pathologic tissue change

Bacterial Factors (I) Function Specific Factors
Adherence Adhesins (fimbriae, fibrils) Evasion of host defense Capsules, Slime layers, mechanisms Leukotoxin, Immunoglobulin proteases, Complement proteases, Supression of T-cells. Direct tissue damage Enzymes: trypsin-like protease, chymotrypsin, collagenase, hyaluronidase, chondroitin sulphatase, heparinase. Metabolic products(Cytotoxins): volatile fatty acid (butyric acid & propionic acid), indole, ammonia, amines, volatile sulphur compounds.

Bacterial Factors (II)
Induction of bone resorption Lipoteichoic acid Lipopoysaccharide Capsules Indirect tissue damage Antigenic stimulation leading to immune responses and inflammation Interleukin productin and proteinase synthesis in response to plaque antigens Activation of alternative complement pathway

Bone Resorptionref.1-30

Clinical and Histopathological Features of Periodontal Disease

Developmental Stages of Periodontal Disease
Clinically healthy gingival tissue: Very small areas of less dense collagen tissue adjacent to JE Light infiltration with lymphocytes and monocytes Less than 10% are PMNs and plasma cells

Healthy Gingivaref.1-22

Stages of Periodontal Disease
Initial lesions: 2-4 days after plaque accumulation Swelling of vascular plexus with leakage of PMNs into tissues Dilated intercellular spaces are observed Collagen destruction begins perivascularly Page and Schroeder

Early lesion (occurs 4-7 days after plaque accumulation) Connective tissue adjacent to JE becomes infiltrated by lymphocytes (primarily) Loss of collagen fibers occurs in infiltrated areas JE becomes disrupted due to underlying infiltration and begins to desquamate more rapidly into sulcus Page and Schroeder

Initial / Early Gingivitisref.1-22

Established Stage(I week after plaque accumulation) Extension of infiltrated collagen-poor connective tissue Cellular component of infiltrate: decrease in lymphocytes (B>T) increase in plasma cells and immunologically differentiating blast cells Ulceration and extensive rete peg proliferations, thinning of sulcular epithelium Can persist for years without progressing Page and Schroeder

Established Gingivitisref.1-23

Advanced stage: periodontitisref.2-19
Adherent gram +, non-adherent gram – (pocket) bacteria Apical proliferation of pocket epithelium, true pocket formation; ulceration of pocket epithelium Acute inflammatory responses as in gingivitis; predominance of plasma cells; exudate often suppurative; expansion of inflammatory and immunopathologic reactions Further collagen loss in the infiltrated tissues, Loss of alveolar bone (attachment loss) Periods of quiescence and exacerbation Progression: chronic (slow), aggressive (rapid, RPP,JP)

Advanced Stage: Periodontitisref.1-23

Advanced Stage: Periodontitisref
Advanced Stage: Periodontitisref.1-24 (blue arrows: exudate, PMNs; red: sloughing JE cells)

Periodontitisref.1-24 Proliferation and apical expansion of bacterial plaque Formation of a true periodontal pocket A change in the direction of flow of the exudate from the infiltrate perpendicularly toward the plaque-covered tooth surface

Periodontitis Proliferation and apical expansion of bacterial plaque: periodontal pocket Change in the direction of flow of exudate: from the infiltrate perpendicularly toward the plaque-covered tooth surface (blue arrows: exudate,PMNs; red arrows: sloughing JE cells). Epithelial attachment has been forced apically.

Cyclic Nature of Periodontitis
Acute episodes of tissue destruction G(-) anaerobic motile bacteria Direct invasion of microorganisms Tissue response: formation of mininecrosis or abscesses Loss of attachment Periods of relative dormancy : host response can eliminate bacterial insult and lead to stagnation of the acute exacerbation. A certain degree of regeneration may occur.

Initial gingivitis ref.2, page 10

Cyclic Nature Increased in pathogenic bacteria in subgingival plaque: tissue evasion: acute inflammation within the periodontium(red arrows): attachment loss and bone resorption. An enhanced host response can eliminate the bacterial insult: stagnation of the acute exacerbation: tissue regeneration may occur.

Gingivitis The most prevalent and mildest manifestation of periodontal disease Associated with bacterial plaque Limited to inflammation of the marginal gingiva, no loss of attachment of the periodontal tissues Gingival enlargement-increased sulcus depth, reversible if properly treated Can remain stable for many years

Dental Plaque: Gingivitis

Stained Plaque: Gingivitisref.1-47

Subgingival Calculusref. 1-14 (lt. formerly subg. calculus is now supg
Subgingival Calculusref.1-14 (lt. formerly subg. calculus is now supg., reflecting the gingiva reveals the subg. Calculus)

Necrotizing Gingivitis
Manifest initially as necrosis of gingiva (apex of the pyramidal interdental papilla) Ulcerated craters, overlying necrotic tissues Tender, low-grade fever, general malaise, halitosis Spirochetes superimposed by other microorganisms

ANUG Thought of as “fuso-spirochetal” in origin
High levels of Treponema (32%) and Selenomonas (6%) Viable count: significant levels of Bacteroides (Prevotella) intermedia (24%) and Fusobacterium spp. (3%)

Four Zones of ANUG Zone 1: bacterial zone, the most superficial
Zone 2: neutrophil-rich zone Zone 3: nccrotic zone, disintegrated tissue cells Zone 4: zone of spirichetal infiltration, intermediate-sized and large types of spirochetes

Severe ANUGref.1-53

ANUGref.1-51

Herpetic Gingivostomatitis
Children and young adults Fever, painful swelling of lymph nodes Acute, painful gingivitis with blister-like aphthae Predisposing factors Spontaneous healing within 1-2 weeks

Herpetic Gingivostomatitisref.1-69

Severe Herpetic Gingivostomatitis

Chronic Gingivitis A balance is established between the organisms in the gingival sulcus and local inflammatory defense systems Upset of equilibrium: Allow disease to advance in an apical direction

Periodontitis Apical down growth of plaque
Expansion of the zone of collagen loss of periodontal fiber attachment Deepening of the gingival sulcus periodontal pocket Proliferation of the dentogingival epithelium Pocket epithelium

Periodontitis (contd.)
Continuous traffic of PMNs Continuous outpouring of plasma proteins Extension of inflammatory cell infiltrate Activation of osteoclasts

Symptoms of Periodontitis
Further symptoms of periodontitis Gingival swelling Pocket activity: bleeding, exudate and pus Pocket abscess; furcation abscess Fistula Gingival shrinkage (recession) Tooth migration, tipping, extrusion Tooth mobility Tooth loss

Chronic Periodontitisref.4-112

Rapidly Progressive Periodontitis (RPP)
20-30 years of age, females more often All teeth may be involved Some authors called postjuvenile periodontitis Mainly vertical bone loss in advanced cases Acute stages with specific anaerobes (invasion): A.a., P.g. PMN and monocyte defects

X-ray Films: RPP

Juvenile Periodontitis
Begins around age of puberty Bilaterally symmetric semilunar bone loss LJP: permanent incisors and first molars GJP: disseminated LJP? Tooth mobility, pathologic migration

JP: Calculus, Plaque, Severe Gingivitisref.1-96

JP: 9mm Probing Depthref.2-68

Radiographs: JP

LJP: Maxillary Molarsref.1-96

Classification Classification of Periodontal Diseases and Conditions

Classification System:1989ref.3-1
Shortcomings Considerable overlap in disease categories Absence of a gingival diseases component Inappropriate emphasis on age of onset of disease and rates of progression Inadequate or unclear classification criteria

Changes in the Classification System for Periodontal Diseasesref.3-1
Addition of a Section on “Gingival Diseases”. Replacement of “Adult Periodontitis” with “Chronic Periodontitis”. Replacement of “Early-Onset Periodontitis” with “Aggressive Periodontitis”. (Contd.)

Changes in the Classification System for Periodontal Disease ref.3-4
*Clarification of the designation periodontitis as a menifestation of systemic disease. *Replacement of necrotizing ulcerative periodontitis with necrotizing periodontal diseases. *Addition of a category on periodontal abscess. *Addition of a category on developmental or acquired deformities and conditions.

Classification System for Periodontal Diseases and Conditionsref.3-2
I. Gingival Diseases A. Dental plaque-induced gingival diseases 1. Gingivitis associated with dental plaque only. a. without other local contributing factors. b. with local contributing factors

Classification (II)ref.3-2
2. Gingival diseases modified by systemic factors a. associated with the endocrine system 1) puberty-associated gingivitis 2) menstrual cycle-associated gingivitis 3) pregnancy-associated gingivitis a) gingivitis b) pyogenic granuloma 4) diabetes mellitus-associated gingivitis b. associated with blood dyscrasias 1) Leukemia-associated gingivitis 2) Other

Classification (III)ref.3-2
3. Gingival diseases modified by medications a. drug-influenced gingival diseases 1) drug-influenced gingival enlargements 2) drug-influenced gingivitis a) oral contraceptive-associated gingivitis b) other 4. Gingival diseases modified by malnutrition a. ascorbic acid-deficiency gingivitis b. other

Classification (IV)ref.3-2
B. Non-plaque-induced gingival lesions 1. Gingival diseases of specific bacterial origin a. Nesseria gonorrhea-associated lesions b. Treponema pallidum-associated lesions c. streptococcal species-associated lesions d. other

Classification (V)ref.3-2
2. Gingival diseases of viral origin a. herpesvirus infections 1) primary herpetic gingivostomatitis 2) recurrent oral herpes 3) varicella-zoster infections b. other

Classification (VI)ref.3-2
3. Gingival diseases of fungal origin a. Candida-species infections 1) generalized gingival candidosis b. linear gingival erythema c. histoplasmosis d. other 4. Gingival lesions of genetic origin a. hereditary gingival fibromatosis b. other

Classification (VII)ref.3-2
5. Gingival manifestations of systemic conditions a. mucocutaneous disorders 1) lichen planus 2) pemphigoid 3) pemphigus vulgaris 4) erythema multiforme 5) lupus erythematosus 6) drug-induced 7) other

Classification (VIII)ref.3-2
b. allergic reactions 1) dental restorative materials a) mercury b) nickel c) acrylic d) other

Classification (IX)ref.3-2
2) reactions attributable to a) toothpastes/dentifrices b) mouthrinses/mouthwashes c) chewing gum additives d) food and additives 3) other

Classification (X)ref.3-2
6. Traumatic lesions (factitious, iatrogenic, accidental) a. chemical injury b. physical injury c. thermal injury 7. Foreign body reactions 8. Not otherwise specified (NOS)

Classification (XI)ref.3-3
II. Chronic Periodontitis A. Localized B. Generalized III. Aggressive Periodontitis A. Localize IV. Periodontitis as a Manifestation of Systemic Diseases

Periodontitis as a Manifestation of Systemic Diseases (1)ref.3-3
A. Associated with hematological disorders 1. Acquired neutropenia 2. Leukemia 3. Other B. Associated with genetic disorders 1. Familial and cyclic neutropenia 2. Down syndrome 3. Leukocyte adhesion deficiency syndrome 4. Papillon-Lefèvre syndrome 5. Chediak-Higashi syndrome

Periodontitis: Systemic Diseases (2)ref.3-3
6. Histiocytosis syndrome 7. Glycogen storage disease 8. Infantile genetic agranulocytosis 9. Cohen syndrome 10. Ehlers-Danlos syndrome (Types IV & VIII) 11. Hypophosphatasia 12. Others C. Not otherwise specified (NOS)

Classification (XI)ref.3-3
V. Necrotizing Periodontal Diseases A. Necrotizing ulcerative gingivitis (NUG) B. Necrotizing ulcerative periodontitis (NUP) VI. Abscess of the Periodontium A. Gingival abscess B. Periodontal abscess C. Pericoronal abscess

Classification (XII)ref.3-3
VII. Periodontitis Assoc. with Endodontic Lesions A. Combined periodontic-endodontic lesions VIII. Developmental or Acquired Deformities and Conditions A. Localized tooth-related factors that modify or predispose to plaque-induced gingival diseases/periodontitis

Classification (XIII)ref.3-3
A. Localized tooth-related factors that modify or predispose to plaque-induced gingival diseases/periodontitis 1. Tooth anatomic factors 2. Dental restoration/appliances 3. Root fractures 4. Cervical root resorption and cemental tears B. Mucogingival deformities and conditions around teeth 1. Gingival/soft tissue recession a. facial or lingual surfaces b. interproximal (papillary)

Mucogingival Deformities and Conditions (contd.)ref.3-3
2. Lack of keratinized gingiva 3. Decreased vestibular depth 4. Aberrant frenum/muscle position 5. Gingival excess a. pseudopocket b. inconsistent gingival margin c. excessive gingival display d. gingival enlargement (I.A.3. I.B.4.) 6. Abnormal color

Mucogingival Deformities and Conditions/Occlusal Traumaref.3-3
C. Mucogingival deformities and conditions on edentulous 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 D. Occlusal trauma 1. Primary occlusal trauma 2. Secondary occlusal trauma

Characteristics Common to All Gingival Diseasesref.3-8
Signs and symptoms that are confined to the gingiva Dental plaque: initiates and/or exacerbates the severity Clinical signs of inflammation With no loss of attachment or on a stable but reduced periodontium Reversibility of the disease by removing the etiology(ies) Possible role as a precursor to attachment loss around teeth

Characteristics of Plaque-induced Gingivitisref.3-9
Plaque present at gingival margin Disease begins at the gingival margin Change in gingival color Change in gingival contour Sulcular temperature change Increased gingival exudate Bleeding upon provocation Absence of attachment loss Absence of bone loss Histological changes Reversible with plaque removal

Plaque-induced Gingivitis on a Reduced Periodontiumref.3-9
Plaque present at gingival margin Disease begins at the gingival margin Change in gingival color Change in gingival contour Sulcular temperature change Increased gingival exudate Bleeding upon provocation Histological changes Reversible with plaque removal

Plaque disclosureref.2-72

Stained plaqueref.2-40

Histology: Gingivitis

Gingival Disease Modified by Systemic Factorsref.3-2
A. association with the endocrine system Puberty-associated gingivitis Menstrual cycle-associated gingivitis Pregnancy-associated gingivitis Pyogenic granuloma Diabetes mellitus-associated gingivitis

Systemic Factorsref.3-2 B. Associated with blood dyscrasia
1) leukemia-associated gingivitis 2) other

Characteristics of Drug-influenced Gingival Enlargementref.3-11
Variation in interpatient and intrapatient pattern predilection for anterior gingiva Higher prevalence in children Onset within 3 months Enlargements first observed at the interdental papilla Reduction in dental plaque can limit the severity of lesion Must be using phenytoin, cyclosporine A, or certain calcium channel blockers

Gingival Diseases: Medicationref.3-11
A. Drug-influenced gingival enlargements Anticonvulsant Immunosuppressant Calcium channel blocker B. Drug-influenced gingivitis Oral contraceptive gingivitis

Pill Gingivitisref.3-12 Long term, regular use
Hemorrhage (bleeding upon provocation) Mild erythema and edema (change in gingival color) Increased gingival exudate Duration of drug therapy Reversible following discontinuation of pills

Characteristics of Oral Contraceptive-associated Gingivitisref.3-12
Plaque present at gingival margin Reversible following discontinuation of oral contraceptives

Pregnancy Gingivitisref.3-10
Plaque present at gingival margin Onset is in pregnant women(2nd or 3rd trimester) Reversible at parturition

Pregnancy Gingivitis Frequency: 30-100% 2nd month (begin)
8th month (maximum) Increased progesterone altering tissue metabolism Pregnancy tumor (epulis)

Mild Pregnancy Gingivitis

Severe Pregnancy Gingivitis
Histologic section of gingiva: normal epithelium, a relatively mild inflammatory infiltrate and widely dilated vessels. Radiograph of Gravid epulis: some horizontal loss of the crestal compact bone of the interdental septa.

Severe Pregnancy Gingivitisref.1-56

Gravid epulis: Severe Pregnancy Gingivitisref.1-56

Gravid epulisref.1-56

Gingivitis: (3 months after gingivoplasty;2 months Post-partum)ref

Characteristics of Pregnancy-associated Pyogenic granuloma
Plaque present at gingival margin Can occur anytime during pregnancy More common in maxilla More common interproximally Sessile or pedunculated protuberant mass Regresses following parturition (ref.3-11)

Pregnancy-induced Pyogenic granuloma(epulis)ref.6-350

Pyogenic granuloma

Characteristics of Leukemia-associated Gingivitisref.3-13
Gingival lesions are primarily found in acute leukemias Enlargement first observed at the interdental papilla Reductions in dental plaque can limit the severity of lesion

Acute Myelocytic Leukemia

Gingival Over-growth Elicited by Drugs
Phenytoin seizure disorders Nifedipine hypertension, post-myocardial syndrome Cyclosporine-A: immunosuppressive drugs solid organ and bone marrow transplants Others: Sodium valproate (antiepileptic) Bleomycin (anticarcinogen)

Gingival Hyperplasia

Drug-induced Gingival Enlargementref.6-347 (dilantin : epilepsy)

Cyclosporine-induced Gingival Enlargementref.6-348(immunosuppresant)

Mild Phenytoin-induced Gingival Enlargementref.1-58

Severe Phenytoin-induced Gingival Overgrowthref.1-58

Mild to Moderate Nifedipine-induced Gingival Overgrowthref.1-59

Severe Cyclosporine-A-induced Overgrowthref.1-60

Nutritional Deficiency
Severe scorbutics, severe protein/caloric deficiency Necrotizing periodontitis and stomatitis A weak association Ascorbic deficiency and periodontal conditions

Non-plaque-induced Gingival Lesionsref.3-2
1. Infectious gingivitis . Viral infections Herpes simplex virus types 1 and 2 Varicella-zoster virus . Fungal infections Candidosis; histoplasmosis Bacterial infection Neisseria gonorrhea

Herpetic Gingivostomatitisref.2-54

Candida

Candidiasis

Gingival lesion of genetic originref.3-2
Hereditary gingival fibromatosis Other

Hereditary Gingival Hyperplasia

Idiopathic Gingival and Bone Thickening

Hypertrichosis: Gingival Fibromatosis

Hypertrichosis (10 years old boy)

Non-plaque-induced Gingival Lesionsref.3-2
Gingival manifestations of systemic conditions a. Mucocutaneous Disorders Pemphigoid Pemphigus vulgaris Erythema multiforme Lupus erythematosus Lichen planus

Lichen Planusref.1-67

Reticular Lichen Planus: Wickham’s Striaeref.1-67

Pemphigoid Women beyond middle age
Oral mucosa, gingiva, conjunctiva, pharynx, skin Subepithelial blister IgG and C3 deposits on basement membrane

Pemphigoidref.1-66

Pemphigus Vulgaris Elderly females more often
Mucosal surfaces through the body, skin, oral mucosa and gingiva Intraepithelial vesicles  Rupture  Painful erosions  Epithelial desquamation Therapy: immunosuppresants and systemic corticosteroids

Bullous Pemphigus Lesion

Erythma multiforme: Crustsref
Erythma multiforme: Crustsref (ulceration and crusts of the vermilion part of the lip)

Primary herpes: palatal gingiva with confluency of the punctiform lesions of a childref.6-336

Erythema multiformeref.6-345

Erythema multiforme Precipitating factors: herpes simplex infection (the most common) and other infections, drugs. In young adults, males Sloughing of the mucosa, diffuse redness From small red macules-bullae-rupture-sloughing mucosal surface Stevens-Johnson: severe EM (mucosa, conjunctiva, and skin are involved)

Non-plaque-induced Gingival Lesions
Gingival manifestation of systemic conditions b. Allergic reactions (ref.3-2) - Dental restorative materials - Toothpaste and mouthwashes

Characteristics of Chronic Periodontitisref.3-38
May be prevalent in adults, but can occur in children and adolescents Amount of destruction is consistent with the presence of local factors Subgingival calculus is a frequent finding Associated with a variable microbial pattern

Characteristics of Chronic Periodontitisref.3-38
Slow to moderate rate of progression, but may have periods of rapid progression Can be further classified on the basis of extent and severity: a. slight or early periodontitis (CAL of 1-2 mm, PPD of 3-4mm), b. moderate periodontitis (CAL up to 4 mm, PPD of 5-7 mm, tooth mobility, moderate bone loss,< than class I furcation involvement), c. severe or advanced periodontitis (CAL>5 mm, usually >/= 7 mm); a. localized (<30% of sites involved), b. generalized (>30% of sites involved). Possibly modified by or associated with: systemic diseases (diabetes mellitus, HIV infection), local factors predisposing to periodontitis, environmental factors (cigarette smoking, emotional stress)

Characteristics of Aggressive Periodontitis
Prior to age 35 Rapid attachment loss and bone destruction Familial aggregation? Subgingival flora:elevated proportions of Actinobacillus actinomycetemcomitans Host defense defect (Phagocyte abnormalities) Hyper-responsive macrophage phenotype, including elevated levels of PGE2 and IL-1 Subclassifications: prepubertal (localized: usually not associated with a systemic disease; generalized: usually accompanied by alteration of PMN functioning), juvenile (LJP, GJP)

Periodontitis as a Manifestation of Systemic Diseasesref.3-64
Associated with genetic disorders Familial and cyclic neutropenia Down syndrome Leukocyte adhesion deficiency syndrome Papillon-Lefèvre syndrome Chediak-Higashi syndrome Histocytosis syndrome Glycogen storage disease Cohen syndrome Hypophosphatasis Other

Cyclic Neutropenia

Periodontitis as a Manifestation of Systemic Diseasesref.3-64
Associated with hematological disorders Acquired neutropenia Leukemias other

Blood Dyscrasias Acute/chronic myeloid leukemia
Acute/chronic lymphatic leukemia Sub- or aleukemic leukemia Aplastic anemia

Hypoplastic Anemia

Acute Lymphatic Leukemia (AIDS)ref.1-64

Lymphatic Leukemia

Down Syndrome Poor oral hygiene Plaque flora
Multiple immune dysfunction anatomical/structural dysplasia Tissues: Exaggerated immuno-inflammatory response with high T4/T8 ratio

Down Syndromeref.1-104

Down Syndrome: Post-treatment of Periodontitisref.1-104

Trisomy 21:Karyotyperef.1-105

Mongoloid Symptom: Scrotal Tongueref.1-105

Papillon-Lefèvre syndrome (Hyperkeratosis palmo-plantaris)
Structural abnormalities PMN dysfunctions Plaque flora: A.a., Cap. spp. Accurate diagnosis Children with periodontitis

PLSref.1-106

Hyperkeratosis: PLSref.1-107

Hyperkeratosis: Elbowsref.1-107

Hyperkeratosis: PLS: Sole Border of Footref.1-107

Ehlers-Danlos Syndrome
Type VIII Type III collagen defect more severe periodontal destruction Type I Severe hard tissue dysplasia

Hypophosphatasia Inherited (autosomal recessive trait) deficiency
Alkaline phosphatase Defective structure Bone, cementum, PDL, dentin?/enamel Early exfoliation: deciduous teeth P. gingivalis Serological evidence

Necrotizing Ulcerative Gingivitis
Fusiform-spirochete bacteria flora Four zones of NUG: bacterial zone, neutrophil rich zone, necrotic zone, spirochetal infiltration zone Constant cultivable flora: P. intermedia, Fusobacterium sp., Treponema, Selenomonas sp.

NUG Predisposing Factors * psychological stress * immunosuppression
(HIV-G, HIV-P) * malnutrition (protein intake/secondary viral infection: measles) * other predisposing factors: smoking, pre-existing gingivitis, trauma

Acute Necrotizing Gingivitis: Homo. With ARC.

Tooth-Related Issues Tooth anatomic factors Tooth position
cervical enamel projections and enamel pearls furcation anatomy and location Tooth position Root proximity Open contact

Tooth-Related Factors
Root abnormalities grooves Tooth restorations restorative marginal discrepancies effects of restorative materials Endodontic considerations Tooth fractures External root resorption

Palatogingival Groove

Enamel Projection: Furcation Involvement

Enamel Projection

Enamel Projection: FI3

Position of Teeth Teeth in malocclusion does predispose patients to disease. Malocclusion + teeth protrude buccally Occlusal trauma Dehiscence Gingival recession

Crowding: Plaque Retentionref.2-134

Iatrogenic Factors Favoring Plaque Accumulation (Restorative Dentistry)
Clinically acceptable proximal restoration Amalgam restoration with overhang Crown margin overhang and open margins

Overhanging Amalgamref.2-126

Sanitary Pontic

Crown Contour Respect to periodontitis Under contour, over contour
Over bulky crowns Plaque stagnation Periodontal lesions Improper crown contours

Crown Margins Four factors: fit, location, smoothness and material
Place crown margins subgingivally Periodontal lesions Crown placed supragingivally Tissue health Rough margins: hard to keep clean Zinc phosphate cement Irritation and plaque accumulation

Overhanging Crown Marginsref.2-128

Over-hanging Restoration

Poor Restoration

Pontics, Materials Placed under the tissue Leave a slight clearance
Great area of plaque irritation Leave a slight clearance Patient can get under it to clean Materials Glazed porcelain: best tissue response More important how the prosthesis is constructed rather than what material it is made of

Improper Bridge Pontic Form

Convex Sanitary Pontic Design

Removable Partial Dentures
No increased periodontal problems Causes abutment teeth to loosen The rocking motion of the RPD

Partial Dentures

Frenulae, Vestibular Depth and Inadequate Gingiva
The minimal width of keratinized gingival tissue and gingival health Narrow zone of keratinized tissue and frenum pull and/or shallow vestibular depth

Pocket: High Frenum

Trauma from occlusion Glickman’s concept:
1. zone of irritation: marginal and interdental gingiva– not affected by force of occlusion [transseptal (interdental) and the dentoalveolar collagen bundles] 2. zone of codestruction: PDL, root cementum, alveolar bone

Periodontal Inflammation with OTref
Periodontal Inflammation with OTref (inflammatory infiltrate spreads directly into the PDL)

Occlusal Trauma (OT)

Normal periodontal tissues and OTref.5-225
1. normal periodontal tissues exposed to jiggling forces: signs acute inflammation including resorptions of collagen, bone and cementum – PDL space gradually increases 2. after compensation, PDL shows no sign of inflammation 3. the supraalveolar connective tissue is not affected by the jiggling forces and no apical down growth of dentogingival epithelium

Healthy periodontium with reduced height + OT( jiggling forces)ref
Alterations occurs in the PDL tissues: 1. a widened PDL space 2. an increases tooth mobility but do not lead to further loss of connective attachmant

Inflammation + jiggling forcsref.5-230
1. pathological and adaptive alterations occur within the PDL space 2. tissue alterations including: collagen, bone, and cementum resorptions, widened PDL space and increased tooth mobility but no further loss of connective tissue attachment

Inflammation with infrabony pocket+ jiggling forcesref.5-232
1. pathological alterations occur within a zone of the periodontium which is also occupied by inflammatory cell infiltrate 2. increasing tooth mobility may also associated with an enhanced loss of connective tissue attachment and further downgrowth of dentogingival epithelium

Pathways of inflammation in periodontitis
A. interproximally: 1. from gingiva into the bone 2. from the bone into the PDL 3. from the gingiva into the PDL B. Facially and lingually 1. from the gingiva along the outer periosteum 2. from the periosteum into the bone

Pathway: Inflammation without OT( inflammatory lesion propagates into the alveolar bone)

Pathway: Inflammation without OTref.5-222

Professor Chi-Cheng Tsai, D.D.S., Ph.D.
Periodontology (2006) Kaohsiung Medical University College of Dental Medicine Professor Chi-Cheng Tsai, D.D.S., Ph.D.

Reference Ref. 1: Color Atlas of Dental Medicine 1, Periodontology, K.H. Rateitschak ed., Thieme, 1987. Ref. 2: Color Atlas of Periodontology, Rateitschak/Wolf/Hassell eds., Thieme,1985. Ref.3: Annals of Periodontology, volume 4, No. 1, Dec. 1999; 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. Ref.4: Advances in Periodontics, Wilson/Kornman/Newman eds., Quintessence Publishing Co. Inc., 1992. Ref. 5: Textbook of Clinical Periodontology, Jan Lindhe ed., Munksgaard,1983. Ref.6: Textbook of Clinical Periodontology, Jan Lindhe ed., Munksgaard,1997. Ref.7: Glickman’s Clinical Periodontology, 6th edition, 1984. Ref. 8: Grant/Stern/Listgarten, Periodontics, 6th edition, Mosby, 1988. Ref.9: Risk markers for oral diseases, vol. 3, Periodontal diseases, markers of disease susceptibility and activity, N.W. Johnson ed., Cambridge Univ. Press, 1991.

Periodontology Chi-Cheng Tsai, D.D.S., Ph.D.

Similar presentations

Presentation on theme: "Periodontology Chi-Cheng Tsai, D.D.S., Ph.D."— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Periodontology Chi-Cheng Tsai, D.D.S., Ph.D.

Similar presentations

Presentation on theme: "Periodontology Chi-Cheng Tsai, D.D.S., Ph.D."— Presentation transcript:

Similar presentations

About project

Feedback