1. CLASSIFICATION OF THE WORLD WORKSHOP, 1989A. GINGIVITISa. Dental plaque-induced gingival diseasb. Acute necrotizing ulcerative gingivitis (ANUG).c. Steroid hormone-induced gingivitis.d. Drug-induced gingival enlargements.e. Gingivitis associated with blood disorders, nutritional déficits, tumors, genetic factors, viral infections.f. Gingivitis descamativa.

B. PERIODONTITISa. Adult periodontitis.b. Early-onset periodontitis:i. Prepuberal periodontitis:1.1. Localized2.2. Generalizedii. Juvenile periodontitis1.1. Localized2.2. Generalizedc. Periodontitis associated with systemic diseasesd. Necrotising ulcerative periodontitise. Refractory periodontitis

2. LIMITATIONS OF THE WORLD WORKSHOP, 19891. There is an overlap between different categories, 2. Gingival disease is conspicuously absent, 3. Inappropriate emphasis is placed on the age of onset of the disease, as well on the rates of progression and 4. The presence of inadequate classification criteria.

3 CLASSIFICATION EUROPEAN WORKSHOP, 1993

A. PRIMARY DESCRIPTORSa. Adult periodontitib. Early-onset periodontitisc. Necrotising ulcerative periodontitis

B. SECONDARY DESCRIPTORSa. Tooth distribution.b. Rate of progression.c. Treatment response.d. Associated with systemic diseases.e. Microbiological characteristics.f. Ethnicity.g. Other factors.

4. LIMITATIONS OF EUROPEAN WORKSHOP, 1993Lacks details that are needed to properly identify the broad spectrum of periodontal illnesses encountered in clinical practice.

5. CLASSIFICATION OF PERIODONTAL DISEASES AND CONDITIONS OF THE INTERNATIONAL WORKSHOP (1999)

Advantages of this classification:

The development of a detailed classification of gingival diseases and lesions that are either dental plaque-induced or not primarily associated with dental plaque. An important feature of the section on dental plaque-induced diseases is acknowledgment that the clinical expression of gingivitis can be substantially modified by: 1) systemic factors such as perturbations in the endocrine system, 2) medications, and 3) malnutrition. The section on non-plaque induced gingival lesions includes a wide range of disorders that affect the gingiva. Many of these disorders are frequently encountered in clinical practice.

6. THE CRITERIA FOR THE CLASSIFICATION OF `CHRONIC PERIODONTITIS' Early-onset forms – now called aggressive periodontitis. The term early-onset periodontitis encompasses a group of diseases diagnosed in patients under the age of 35 years. The destruction of the periodontium is advanced for the age

of onset of the condition. Early-onset periodontitis has a tendency to aggregate in families. The characteristic clinical signs of chronic periodontitis include loss of clinical attachment, alveolar bone loss, periodontal pocket formation and inflammation of the gums. Gingival hypertrophy or recession, bleeding on probing, increased tooth mobility and suppuration may also be associated; symptoms may even lead to tooth loss. In chronic periodontitis, the infection progresses steadily or in bursts of activity

7. THE CRITERIA FOR THE CLASSIFICATION OF “AGGRESSIVE PERIODONTITIS”Adult periodontitis forms – now called chronic periodontitis. Adult periodontitis is probably initiated at or soon after puberty but does not manifest symptoms until the middle of the fourth decade . Adult periodontitis is a slowly progressing form of periodontitis. However, it may at any stage undergo an acute exacerbation with associated attachment loss. The common features of all forms of aggressive periodontitis are: patients who, except for the presence of the periodontal infection, are otherwise clinically healthy; rapid loss of clinical attachment and bone destruction, and a positive family history. Other features that generally present, albeit they are not universal to all patients, are: microbial deposits that are inconsistent with the severity of tissue destruction present, high proportions of Actino-bacillus actinomycetemcomitans or Porphyromonas gingivalis, phagocytic anomalies and an abnormal hyperresponsive macrophage phenotype with high levels of prostaglandin E2 and interleukin-1ß; the progression of bone loss and attachment may be dramatic

8. CLASSIFY THE DISTRIBUTION (LOCALIZED OR GENERALIZED) OF THE DISEASE BASED ON THE PUBLISHED CRITERIA

In chronic periodontitis, - Localized, if fewer than 30% of the sites are involved.- Generalized, if more than 30% of the sites are involved.

Based on severity, it is defined as:• Slight periodontitis: when clinical attachment loss is between 1 and 2 mm.• Moderate periodontitis: if attachment loss is between 3 and 4 mm.• Severe periodontitis: when clinical attachment loss is 5 mm or greater.

In aggressive periodontitis:Localized, Onset is around puberty with a high antibody response to infectious agents. Clinically it is characterized by interproximal attachment loss in the first molars and incisors or in at least two permanent teeth, one of which is a first molar and no more than two teeth other than first molars and incisors are involved. Generalized. Generalized aggressive periodontitis tends to manifest in patients over 30 years of age, although it can appear at older ages.Antibody response is poor. There are periods during which attachment is lost, involving three permanent teeth other than first molars and incisors.

9. LIST THE FUNCTIONS OF DIAGNOSTIC PROCEDURESArmitage proposed that diagnostic procedures serve five separate functions:

i) I) screening; ii) ii) diagnosis of specific periodontal diseases; iii) iii) identification of sites and subjects at risk of progression;iv) iv) treatment planning; and v) v) monitoring.

10. RECALL THAT A GOOD DIAGNOSIS CONTAINS: DISEASE,

SEVERITY AND DISTRIBUTION

11. RECORD THE AETIOLO GY OF THE DISEASE AND UNDERSTAND THE IMPORTANCE IN TREATMENT AND MANAGEMENTThe most important and most prevalent anaerobic gram-negative bacteria in the subgingival area are Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), and Tannerella forsythensis (Tf).These bacteria play an important role in the onset and subsequent development of periodontitis, participating in the formation of the periodontal pocket, connective tissue destruction, and alveolar bone resorption by means of an immunopathogenic mechanism. Once periodontitis has been established, an inflammatory infiltrate is formed consisting of different kinds of cells, such as macrophages and lymphocytes that will produce different cytokine subtypes, biological mediators responsible for the immunopathology of different illnesses

EPIDEMIOLOGY

1. EPIDEMIOLOGY The study of the distribution (& occurrence) of disease in human populations & factors influencing distribution

2. PREVALENCE: The proportion of persons in a population who have the disease at a given point or period of time. Prevalence is a measure of the amount of disease existing in a population, usually expressed as a percentage.

INCIDENCE: The average percentage of unaffected persons who will develop the disease during a given period of time.

Incidence is a measure of the occurrence of new disease.

SEVERITY: Amount or degree of involvement

EXTENT:Distribution of disease

3. INDICES USED TO RECORD DEBRIS

(1) Plaque Index (PI)

Developed by Silness and Loe The thickness of plaque at gingival margins is assessed The tooth surfaces examined are: facial, lingual (or palatal), mesial and distal A plaque disclosing agent may be used The total of all four surfaces is added up, and divided by the number of tooth surfaces examined. This gives

the PI score for each tooth. The total scores of all teeth are totaled and divided by the number of teeth examined. This gives the PI

score for the individual. The result may be calculated as follows:- 0 = excellent, 0.1 to 0.9 = good, 1.0 to 1.9 = fair and 2 to 3 = poor

(2) Oral Hygiene Index (OHI)

Oral hygiene index developed by Greene, Vermillion and and Waggenor, measures the overall oral hygiene. It divides the dentition into six parts, and the surface with the greater amount of plaque or calculus is taken into consideration. Thus twelve surfaces are calculated. It is further divided into: Debris Index (DI) and Calculus Index (CI)

Debris Index (DI): Debris is the soft, movable, foreign matter consisting of bacterial plaque and food debris.

Calculus Index (CI): Calculus is the hard, stony, calcified deposit of inorganic material on the tooth surfaces.

The final score is calculated by adding the scores for each tooth divided by the number of sextants examined. The total scores of the DI and CI give the score of the OHI. The lowest possible score is 0, and the maximum score is 12.

(3) Quigley & Hein

Reduced crude measure of OHI Used for toothbrush studies

4. INDICES USED TO RECORD INFLAMMATION

(1) Papilla Marginal and Attached Gingival Index (PMA)It is a measure of the incidence and severity of gingivitis in a given population based on the examination

and rating of the degree of involvement of the interdental papilla and the marginal and attached portions of gingiva in each individual.

This dental index was developed by Schour and Massler. They gave a score of 0 to 5 depending upon the severity of disease in the gingiva. This index is no longer actively used.

(2) Gingival Index (GI):The three major parameters that the gingival index measures are the color, consistency and bleeding

on probing. This index was also developed by Loe and Silness. The gingiva is tested for all the three parameters with the help of a probe.

Each surface is given a score. The scores are added up, and divided by four. The new total is divided by 12, and this gives the GI for the individual. 0 = excellent health of gingiva, 0.1 to 1 = good, 1.1 to 2 = fair, 2.1 to 3.0 = poor health of gingiva.

5. INDICES USED TO RECORD LOSS OF PERIODONTAL SUPPORT

(1) Periodontal Index (PI)This index developed by Russel, is somewhat more comprehensive and thorough as compared to the gingival index. Not only does it consider the appearance of the oral tissues, it also stresses upon the functionality of the tooth.

• most widely used index up until 1980's batty• measures severity of PD not gingivitis; tooth site not recorded• records need for treatment (perio. status)• measures ir- & reversible aspects of disease; may decrease with tx• score of individual = teeth score/no of teeth• lesser score given when in doubt Each tooth is assigned a score, and the scores are added up. The total is then divided by the number of teeth examined.

Strength & weakness:• This index does not utilize periodontal probing, only a visual exam using a light source, mouth mirror and

explorer.• It uses a progressive scale from 1 to 8 that gives little weight to gingival inflammation and relatively great

weight to advanced periodontal disease.• It is easy to use but underestimates the prevalence of disease.

(2) Periodontal Disease Index (PDI) • The unique aspect of the PDI was the examination of six preselected teeth in the mouth, index teeth # 16,

21, 24, 36, 41, 44 (referred to as the Ramfjord teeth).• Another unique aspect the use of the CEJ as a fixed landmark for measuring attachment loss. • It consists of a gingivitis assessment, Pocket Depth, Calculus Attachment Loss on four sites per tooth

(M,D,F,L), attrition, mobility• score for individual = total teeth score/ no of teeth; average for pop • generally irreversible index; 0-3 healthy, 4-6 attachment loss

(3) Extent & Severity Index • bivariate index • expresses % of sites with disease (E-extent) • measures mean attachment loss (S-severity) • scores gingival bleeding, pocket depth, attachment loss on mid- & mesio- buccal aspects of all teeth in right or left 1/2 of maxilla & contralateral 1/2 of mandible • info, is retrospective & indicative of past disease (cumulative) • e.g. ESI (90, 2.5): generalized mild ESI (20,7.0): localized severe • descriptive epidemiology

7. CRITEROR FOR CPITN COMMUNITY PERIODONTAL INDEX OF TREATMENT NEED • developed through WHO initiate • developed for screening large population gps with respect to treatment needs

• Relatively recently, the CPITN has been renamed as the Community Periodontal Index (CPI) to denote its use as an epidemiological tool rather that as an aid to treatment planning.

• The CPITN is primarily a screening procedure which requires clinical assessment for the presence or absence of periodontal pockets, calculus and gingival bleeding.

• Use of a special CPITN periodontal probe (or its equivalent) is recommended.• For epidemiological purposes in adult populations, 10 specified index teeth are examined; for persons

under 20 years of age only six index teeth are specified. • In dental practice all teeth are examined and the highest score for each sextant noted. Only 6 scores are

recorded. • The main advantage of the index is that it is easy to use

Limitations of CPITN• The index is based on a hierarchical concept of the progression of periodontitis which implies that a tooth

with a score of 3 or 4 (a pocket present) should also have calculus present (score 2) and bleeding (score 1). The validity of this assumption has been challenged.

• Further limitations of CPITN are that it does not measure tooth mobility or attachment loss or furcation involvement.

• There are also doubts about the ability of any technique that examines the periodontium around just a few teeth to reflect the true state of periodontal health or disease in the mouth concerned.

• These limitations have led to the value of the CPITN being questioned as a reliable epidemiological tool

8. LIMITATIONS OF EPIDEMIOLGICAL FINDINGS• Full mouth examination and recording is very time consuming.• In epidemiologic studies, various partial mouth recording methods have been used due to

time/manpower/economic limitations.• The disadvantages of the various partial mouth recordings include an underestimation of disease prevalence

and the inability to compare results from survey to survey. • Methodologies of sampling, index criteria, statistics inconsistent.

In order to truly reflect disease activity, the combined use of CAL, PD and bleeding on probing should be considered instead of attachment loss

VALUE OF EPIDEMIOLGICAL FINDINGS• Dental professionals and researchers use indices to benefit their patients. • A dentist might use a PI to impress upon a patient the need for better oral hygiene. • A WHO researcher might use the same index to assess the home care practices of a population. • Indices will continue to be important and necessary tools for dental professionals.

9. PREVALENCE OF GINGIVITIS • Higher prevalence, extent, severity among developing vs developed countries • High prevalence of males vs females & blacks vs whites • 44% prevalence at less than 6% of sites examined, prevalence dec with age • (US & Denmark) prevalence 60% teenagers, 40-50% adults

10. PREVALENCE OF PERIODONTAL DISEASE IN CHILDREN • 'JP': blacks > whites; females > males for whites & opp for blacks or a • `JP' prevalence 0.02% Caucasians, 0.2% Asians, 0.8% Afro-Caribbeans (Saxby '87). Other studies generally Whites 1%, blacks > 1% • 10.2% mean prevalence rate of subjects (15 -17 year-old) with bone loss (Hansen et a/. '95); 8703 from 16 countries; great geographic variation • National health survey of oral health of US adolescents (n = 1,285) EOP prevalence 10% African Americans, 5% Hispanic, 1.3% white • Problem with classification, methodology, age groups, ethnic comp.

PREVALENCE OF ADULT PERIODONTITIS • US population (13 years) 90% LOA; 15% LOA 5mm males > females, blacks > hispanics > whites •National Health and Nutritional Examination Survey III : 11.9% LOA 6mm (5.1%

males, 2.5% females) • 1988 UK Survey - 10% of adults pockets > 6 mm, 5% disease free & 69% pockets 4 mm in depth • 8% rapidly progressing, 80% slowly progressing disease, 11% no periodontal breakdown (Loe et al., 1986) • Prevalence increases with age up to 50-60 years & due to tooth loss • AL > 3mm; 15% of 18-24 year-olds while 77% of 55-64

12. Risk Factor: Risk factor is an attribute or exposure that increases the probability of disease occurrence. Are confirmed in longitudinal studies

Lifestyle, environmental or inherited characteristic on basis of epidemiological evidence is associated with disease-related conditions. May cause increased probability of occurrence without causation. Example Medications, Smoking, Systemic disease

Causal Factor: Initiation factor; Must satisfy (a) strength of association (b) dose-response effect (c) temporal

consistency (d) consistency of findings (e) biologic plausibility (f) specificity of association. Example plaque causes gingivitis

Prognostic Factor: Disease predictor; characteristic related to the progression of pre-existing

disease. Example Baseline bone loss, abutment status, tooth location, and type were detected as prognostic factors for tooth loss

13. Odds Ratio: ratio of exposure among the cases over controls

Odds ratiosUsed to quantify increased risk for development of one disease relative to another condition– Example:• Incidence of oral cancer in a smoking population = 0.002• Incidence of oral cancer in a non‐smoking population = 0.0004• Odds ratio is 0.002/0.0004 = 5

• Odds Ratio Interpretation• Odds ratios >1 indicates positive association <1 indicates negative association=1 indicates no association

• How high must odds ratio be to indicate relational conclusion? ≥3????

PATHOGENESIS

(1) RECALL THAT GINGIVITIS IS A REVERSIBLE PROCESS AND BE ABLE TO DESCRIBE ITS CLINICAL PRESENTATION

• Inflammation of the gingiva• characterized by edema, erythema, bleeding, and occasionally pain• Gingivitis is reversible with appropriate therapy

Gingivitis is an inflammatory condition of the soft tissues surrounding the teeth (the gingiva) and is a direct immune response to the dental microbial plaque building up on teeth. Gingivitis is modified by several factors such as smoking, certain drugs and hormonal changes that occur in puberty and pregnancy.

(2) RECALL THAT PERIODONTITIS IS A SEPARATE IRREVERSIBLE ENTITY WHICH IS NOT THE INEVITABLE CONSEQUENCE OF GINGIVITIS DUE TO DIFFERENT SUSCEPTIBILITIES OF PATIENTS

(3) CITE EVIDENCE FOR A PLAQUE AETIOLOGY FOR PERIODONTITISClinical trials have documented the importance of supragingival and subgingival microbial plaque in the treatment of gingivitis and periodontitis. In a classical long-term study on over 300 subjects, Axelsson et al. demonstrated that preventing plaque accumulation by a variety of professional and home-based techniques was extremely effective in preventing attachment loss over a period of 15 years. Clearly, gingivitis precedes periodontitis and this implies that prevention of gingivitis is also a primary preventive measure for periodontitis

(4) DISCUSS THE ROLE OF TREATMENT IN LIMITING THE PATHOGENESIS OF PERIODONTITIS VIA STABILIZATION OF DISEASE IN INITIAL PHASE THERAPY AND CORRECTION OF ANATOMICAL DEFECTS IN CORRECTIVE PHASE THERAPY

(5) EXPLAIN THE `BURST' AND `CONTINUUM' MODELS OF DISEASE ACTIVITY OF PERIODONTITISSocransky et al. suggested that periodontitis progresses in episodes of exacerbation and remission and termed this the “burst hypothesis”. More recent studies have suggested that progression may actually have a more continuous rather than episodic pattern. Periodontal disease progression can be considered a continuous process that undergoes periods of exacerbation. Therefore, both the continuous and episodic hypotheses of disease progression have merit. The progression of this disease is probably continuous with brief episodes of localized exacerbation and occasional remission.

(6) RECALL THAT DISEASE ACTIVITY VARIES WITH TIME, SITE AND PATIENT

(7) DESCRIBE THE HISTOPATHOGENESIS MODELS OF INITIAL, EARLY, ESTABLISHED AND ADVANCED LESIONS AS PROPOSED BY PAGE AND SCHROEDERThe initial lesion appears within 4 days of plaque accumulation. It is not clinically visible and is characterized by an acute inflammatory response to plaque accumulation. The initial lesion is localized to the region of the gingival sulcus, and the tissues affected include a portion of the junctional epithelium and the most coronal part of the connective tissue.

Features of the initial lesion: 1. Vasculitis of vessels below the junctional epithelium. 2. Exudation of fluid into tissues and the gingival sulcus. 3. Increased migration of leukocytes into the junctional epithelium and gingival sulcus. 4. Presence of serum proteins, especially fibrin, extravascularly. 5. Alteration of the most coronal portion of the junctional epithelium. 6. Loss of perivascular collagen

The early lesion: After approximately 7 days of plaque accumulation, an inflammatory infiltrate of mononuclear leukocytes develops at the site of the initial lesion as it progresses to the early lesion.

Features of the early lesion: 1. Accentuation of the features described for the initial lesion. 2. Accumulation of lymphoid cells immediately below the junctional epithelium. 3. Cytopathic alterations in resident fibroblasts. 4. Further loss of the collagen fiber network of the marginal gingiva. 5. Early proliferation of the basal cells of the junctional epithelium.

The established lesion: After 2 to 3 weeks of plaque accumulation, the early lesion evolves into the established lesion. Clinically this lesion will exhibit more edematous swelling and could be regarded as “established” gingivitis.

Features of the established lesion: 1. Persistence of inflammatory features. 2. Increased proportion of plasma cells but without bone loss. 3. Presence of immunoglobulins in the connective tissues, junctional epithelium and gingival crevice. 4. Continuing loss of collagen fibers and fibrous connective tissue matrix. 5. Proliferation, apical migration, and lateral extension of the junctional epithelium. 6. Early pocket formation may appear due to gingival swelling (false pocket).

The advanced lesion is characterized by the same features present in the established gingival lesion, but is accompanied by destruction of the connective tissue attachment to the root surface and the apical migration of the epithelial attachment. The progression of gingivitis to periodontitis is marked by the change in T-cell to B-cell predominance

Features of the advanced lesion: 1. Persistence of the established lesion features. 2. Extension of the lesion into alveolar bone and periodontal ligament with significant bone loss. 3. Continued loss of collagen fibers and matrix below the pocket epithelium and in the periodontal ligament space. 4. Formation of periodontal pocketing and apical migration of junctional epithelium.

(8) DISCUSS THE IMPACT OF INITIATING OR CAUSAL FACTORS, RISK

FACTORS (ENVIRONMENTAL AND GENETIC) AND PROGNOSTICFACTORS ON THE PROGRESSION OF DISEASEPeriodontal disease is considered to have multiple risk factors. Risk factors are part of the causal chain for a particular disease or can lead to the exposure of the host to a disease . The presence of a risk factor implies a direct increase in the probability of a disease occurring. Although specific microorganisms have been considered as potential periodontal pathogens, it has become apparent that pathogens are necessary but not sufficient for disease activity to occur . Destructive periodontal disease is a consequence of the interaction of genetic, environmental, host and microbial factors (86. The presence of microorganisms is a crucial factor in inflammatory periodontal disease, but the progression of the disease is related to host based risk factors. Other risk factors include genetics, age, sex, smoking, socioeconomic factors and certain systemic diseases.

AgePeriodontal disease prevalence is seen to increase with age . However, it is not clear if becoming older is related to an increased susceptibility to periodontal disease or if the cumulative effects of disease over a lifetime explain the increased prevalence of disease in older people. Horning et al. stated that age is a risk factor for periodontitis, although loss of attachment and alveolar bone with age is dependent upon the presence of plaque and calculus.

Socioeconomic status and raceIn a more recent study, when periodontal status was adjusted for oral hygiene and smoking, the association between lower socioeconomic status and more severe periodontal disease was not seen. Data from the third National Health and Nutrition Examination Survey (1988–1994) in the United States (NHANES III) indicated that destructive periodontitis was consistently more prevalent in males than females and more prevalent in blacks and Mexican Americans than in whites.

SmokingRisk for periodontitis is considerable if an individual uses tobacco products, with estimated ratios being of the order of 2.5 to 7.0 or even greater for smokers as compared with nonsmokers . Even when the level of plaque accumulations and gingival inflammation were not significantly different between smokers and nonsmokers, the smokers exhibited an increase prevalence as well as severity of destructive disease .Smoking impairs the outcome of both surgical and nonsurgical periodontal therapy , and it has been suggested that since the healing and microbial response to treatment is comparable between former smokers and nonsmokers, that smoking cessation may restore normal periodontal healing. The mechanisms by which smoking leads to loss of attachment are not well understood . It has been noted that the occurrence, relative frequency, or combinations of microorganisms associated with periodontal destruction did not differ between groups of smokers and nonsmokers . However, others have reported that smokers harbored significantly higher levels and were at significantly greater risk for infection with B. forsythus than nonsmokers . Smokers with periodontal disease have less clinical inflammation and gingival bleeding compared with nonsmokers. This may be explained by the fact that one of the numerous tobacco smoke by-products, nicotine, exerts local vasoconstriction reducing blood flow, edema and clinical signs of inflammation.

Systemic diseaseSystemic diseases can adversely effect host defense systems and therefore act as risk factors for both gingivitis and periodontitis. Depressed neutrophil number and function (as in neutropenia and Chédiak-Higashi syndrome, Down’s syndrome and Papillon-Lefèvre syndrome) have been reported in association with severe periodontitis. There is positive evidence linking diabetes mellitus to increased risk for the inflammatory periodontal diseases . All diabetic patients may be at a higher risk for periodontal disease than the population in general. However, certain subgroups including those with those with poor oral hygiene and/or poor diabetic control and diabetic complications appear to be at particularly high risk .Other possible risk factors for periodontal diseasesPreliminary studies suggest that stress, distress, and coping behavior are associated with increased severity of destructive periodontal disease. The first links made between stress and periodontal conditions were concerned with acute necrotizing ulcerative gingivitis, also called “trench mouth” after its diagnosis among soldiers on the front lines during the First World War . Clearly, acute necrotizing ulcerative gingivitis may have a stress-related causation, but there is insufficient data to substantiate the hypothesis that psychosocial factors are of causative importance in the more common inflammatory periodontal diseases.

GeneticsConvincing evidence from twin studies has shown that genetic factors predispose people to periodontal disease and in the rarer and more severe types of periodontitis affecting younger age groups (early-onset periodontitis), family studies provide good evidence for a prominent genetic role . Researchers are currently trying to identify the genes that may be involved in the various types of periodontitis. Indeed, a gene mutation for prepubertal periodontitis was recently identified that overlaps the region of chromosome 11q14 that contains the cathepsin C gene responsible for Papillon-Lefèvre and Haim-Monk syndromes . However, it is likely that the search for genes that are responsible for other forms of periodontitis may be hampered by the lack of efficient methods to accurately diagnose and classify the periodontal diseases and by the strong probability that multiple genes are involved. Recently much attention has been focused on genetic polymorphisms associated with the genes involved in cytokine production that have been linked to an increased risk of adult peridontitis. Recently, a genetic test has become available to test patients for periodontal disease risk. This test determines if people possess a combination of alleles in two interleukin-1 genes. This particular combination has been associated with severe disease in nonsmoking Caucasians. Others reported an increased frequency of a different interleukin-1 genotype in people with advanced adult periodontitis compared to those with early or moderate disease. There is also retrospective evidence that genetic testing for the specific interleukin-1 genotype may give an indication of increased susceptibility to tooth loss in periodontal maintenance patients

Local risk factors in periodontal diseaseAlthough general risk factors are currently gaining much attention it is important to consider that any plaque retentive factor such as restoration overhangs or deficiencies may contribute to the local risk of periodontal disease.

(9) DISCUSS THE ROLE HOST DEFENCE AND MICROBIAL CHALLENGE IN THE PATHOGENESIS OF PERIODONTAL DISEASEThe pathogenic processes of the periodontal diseases are largely the result of the host response to microbially induced tissue destruction. These destructive processes are initiated by bacteria but are propagated by host cells. Thus, it is the host response that results in tissue destruction. The host produces enzymes that break down tissue. This is a necessary process that is initiated and controlled by the host in order to allow the tissues to retreat from the destructive lesions initiated by bacteria.

(10) LIST THE COMMONLY IMPLICATED PUTATIVE PATHOGENS OF PERIODONTITIS

The microbes involved in periodontal disease are largely gram negative anaerobic bacilli with some anaerobic cocci and a large quantity of anaerobic spirochetes. The main organisms linked with deep destructive periodontal lesions are Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus, Actinobacillus actinomycetemcomitans and Treponema denticola. P. gingivalis is more frequently detected in severe adult periodontitis, in destructive forms of disease and in active lesions than in health or gingivitis or edentulous subjects. They are reduced in numbers in successfully treated sites but are seen in sites with recurrence of disease after therapy

(11) NON-SPECIFIC', SPECIFIC, AND `ECOLOGICAL' PLAQUE HYPOTHESES

The specific plaque hypothesis proposed that only a few organisms out of the diverse collection in the plaque flora were actively involved in the disease. Preventive measures targeting specific bacteria (e.g. immunization) would be a logical consequence of this hypothesis. (Treatment of periodontitis by debridement (nonsurgical or surgical) and oral hygiene measures focuses on the removal of plaque and its products and is founded in the nonspecific plaque hypothesis. Thus although the nonspecific plaque hypothesis has been discarded in favor of the specific plaque hypothesis, much clinical treatment is still based on the nonspecific plaque hypothesis.)

• The non-specific plaque hypothesis considered the carious process to be caused by the overall activity of the total plaque microflora. A consequence of this approach is that all plaque should be disturbed by mechanical plaque control (toothbrushing).

• The ecological plaque hypothesis proposes that the organisms associated with disease may be present at sound sites. Demineralization will result from a shift in the balance of these resident microflora driven by a change in the local environment. Frequent sugar intake (or decreased sugar clearance if salivary secretion is low) encourages the growth of acidogenic and aciduric species, thus predisposing a site to caries. The consequence of this hypothesis is that both mechanical cleaning and some restriction of sugar intake are important in controlling caries progression.

(12) EXPLAIN THE BACTERIAL VIRULENT MECHANISMS WHICH AID IN COLONIZATION AND EVASION OF THE HOST DEFENCES

(13) EXPLAIN THE DIRECT AND INDIRECT EFFECTS OF TISSUE DAMAGE DUE TO HOST DEFENCEPeriodontal pathogens and other anaerobes produce a variety of enzymes and toxins that can damage the tissues and initiate inflammation . They also produce noxious waste products that further irritate the tissue. Their enzymes break down extracellular substances such as collagen and even host cell membranes in order to produce nutrients for their growth. Many of the microbial surface protein molecules are actually capable of inciting an immune response in the host and are also capable of creating local tissue inflammation. Therefore, the microbes can damage the host tissues and instigate inflammatory and immune responses, but their main objective is to multiply, grow and survive within the periodontal pocket. Once the immune and inflammatory processes are initiated, various inflammatory molecules such as proteases, cytokines, prostaglandins and host enzymes are released from leukocytes and fibroblasts or structural cells of the tissues. Proteases tend to break up the collagen structure of the tissues and thus, create spaces for further leukocyte infiltration to occur. The breakdown of tissue proceeds largely under control of the host. The periodontal tissues become loosely adapted to the tooth and the tissues become swollen and inflamed. In periodontitis, as the connective tissue attachment to the tooth is destroyed, the epithelial cells proliferate apically along the root surface and the pocket becomes deeper. As the periodontal pocket deepens, so too does the extent of the tissue inflammatory infiltrate. Moreover, osteocytes begin the destruction of bone. The accumulation of subgingival plaque increases and, therefore, there is a greater microbial density to further propagate this destructive periodontal lesion. As the pocket deepens, the flora becomes more anaerobic and the host response becomes more destructive and chronic. Eventually, the periodontitis lesion progresses to such an extent that the tooth is lost.

(14) RECALL THE COMMON CYTOKINES AND INFLAMMATORY MEDIATORS WHICH CAUSE TISSUE DAMAGE (E.G. IL-1, IL-6, IL-8,TNF-A AND PG-E2) AND DISCUSS THEIR ROLE IN PATHOGENESIS OF PERIODONTAL DISEASE