CHRONIC PERIODONTITIS
Periodontitis is inflammation of the supporting tissues of the teeth, which results in a progressively destructive change that leads to loss of bone and periodontal ligament. There is an extension of inflammation from gingiva into the adjacent bone and ligament. The primary clinical features include clinical attachment loss (CAL), alveolar bone loss, periodontal pocketing and gingival inflammation. In addition, enlargement or recession of the gingiva; bleeding of the gingiva following application of pressure and increased mobility, drifting, and/or tooth exfoliation may occur. With few exceptions, most forms of periodontitis are chronic inflammation that may progress continuously or by burst of activity.
In the United States, the estimate prevalence of moderate periodontitis was 44%, for ages 18 to 64 years old and 10-15% for advanced levels of periodontitis
CLINICAL SIGNS
- Presence of periodontal pathogens (subgingival plaque and calculus)
- Signs of inflammation
- bleeding upon probing
- red and/bluish-red hue
- enlarged gingival contours due to edema/fibrosis
- elevated sulcular temperature
- increased gingival exudate
- Signs of periodontal tissue damage
- increased probing depths
- radiographic bone loss
- increased tooth mobility
- presence of biochemical markers/tissue breakdown products
CLINICAL FEATURES
- most 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
- slow to moderate rate of progression but may have periods of rapid progression
- can be further classified on the basis of extent and severity
- can be associated with local predisposing factors eg. tooth-related or iatrogenic factors
- may be modified by and/or associated with systemic diseases eg. diabete mellitus and HIV infection
- can be modified by factors other than systemic disease such as cigarette smoking and emotional stress
DISEASE PROGRESSION
Patients appear to have the same susceptibility to plaque-induced chronic periodontitis throughout their lives. The rate of disease progression is usually slow, but may be modified by systemic and/or environmental and behavioural factors.
Onset of chronic periodontitis can occur at any time and the first signs may be detected during adolescence in the presence of chronic plaque and calculus accumulation. However, because of its slow rate of progression, chronic periodontitis usually becomes clinically significant in the mid-30s or later.
Chronic periodontitis does not progress at an equal rate in all affected sites throughout the mouth. Some involved areas may remain static for long periods of time whereas others may progress more rapidly. More rapidly progressive lesions occur most frequently in interproximal areas and are usually associated with areas of greater plaque accumulation and inaccessibility to plaque control measures eg. furcations areas, overhanging margins, sites of malposed teeth or areas of food impaction.
Progression is measured by determining the amount of attachment loss during a given time.
Disesase progression can be explained by two models: the gradual model or the random burst model (episodes of exacerbation and remission) (See figure below)
DISEASE PATHOGENESIS (slide presentation)
Chronic periodontiris has shown to be associated with the following pathogens:
- Porphyromonas gingivalis
- Actinobacillus actinomycetemcomtans
- Bacteroides forsythus