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PAPAPANOU et al .
TABLE 4 Classification of periodontal abscesses based on the etiologic factors involved
Which are the main features that identify periodontitis? Loss of periodontal tissue support due to inflammation is the primary feature of periodontitis. A threshold of interproximal, CAL of ≥2 mm or ≥3 mm at ≥2 non‐adjacent teeth is commonly used. Clinicians typ - ically confirm presence of interproximal tissue loss through radio - graphic assessments of bone loss. Clinically meaningful descriptions of periodontitis should include the proportion of sites that bleed on probing, and the number and proportion of teeth with probing depth over certain thresholds (commonly ≥4 mm and ≥6 mm) and of teeth with CAL of ≥3 mm and ≥5 mm (Holtfreter et al. 7 ). Which criteria would need to be fulfilled to support the contention that chronic and aggressive periodontitis are indeed different diseases? (e.g., etiology, histology, pathophysiology, clinical presentation, other) Differences in etiology and pathophysiology are required to indicate presence of distinct periodontitis entities; variations in clinical pres - entation per se , i.e. extent and severity, do not support the concept of different diseases.
Does current evidence suggest that we should continue to differentiate between “aggressive” and “chronic” periodontitis as two different diseases? Current evidence does not support the distinction between chronic and aggressive periodontitis, as defined by the 1999 Classification Workshop, as two separate diseases; however, a substantial variation in clinical pres - entation exists with respect to extent and severity throughout the age spectrum, suggesting that there are population subsets with distinct disease trajectories due to differences in exposure and/or susceptibility. Is there evidence suggesting that early‐onset forms of periodontitis (currently classified under “aggressive periodontitis”) have a distinct pathophysiology (e.g., genetic background, microbiology, host‐response) compared to later‐onset forms? Although localized early onset periodontitis has a distinct, well‐rec - ognized clinical presentation (early onset, molar/incisor distribution, progression of attachment loss), the specific etiologic or pathological elements that account for this distinct presentation are insufficiently
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