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TAKE‐HOME POINTS
A. Molar/incisor pattern periodontitis was designated as a separate disease – localized aggressive periodontitis – in the 1999 AAP classification because of the location of lesions and its aggressive nature, characterized by early onset and familial aggregation; affected individuals are otherwise systemically healthy [4,5].
Molar/incisor pattern is defined as interproximal loss of attachment localized to at least two permanent first molars/incisors, one of which is a first molar, and involving no more than two teeth other than first molars and incisors. When the interproximal loss of attachment extends to at least three permanent teeth other than first incisors and molars, then the condition is classified as generalized periodontitis. If left untreated, 35% of originally classified molar/incisor pattern periodontitis may progress to generalized periodontitis [6].
B. Molar/incisor pattern periodontitis was formerly called “periodontosis” [7,8] and later called “early‐onset periodontitis” and “localized prepubertal/juvenile periodontitis” in the 1989 AAP classification because the disease generally affects young patients. Molar/incisor pattern periodontitis was later called “localized aggressive periodontitis” in the 1999 AAP classification, based on clinical, radiographic, historical and/or laboratory findings, rather than the age of the patient.
The current classification grouped “chronic” and “aggressive” under a single category “periodontitis” because the specific etiologic or pathologic elements that account for early onset and molar/incisor pattern clinical presentation are insufficiently defined. Current evident does not support the distinction between chronic and aggressive periodontitis as two separate diseases.
C. The following are primary features [9].
Rapid attachment loss accompanied with severe bone destruction. The progression rate of molar/incisor pattern periodontitis is about three to four times faster than that of periodontitis with grade A or B. The rapidly progressive vertical bone loss is often half‐moon shaped and symmetric to the contralateral tooth [10].
Patients will usually be medically healthy children or adolescents.
Strong familial aggregation.
Secondary features that are frequently but not always present include the following.
Inconsistency in the relationship between the amount of microbial deposits (i.e. supragingival plaque) and the severity of periodontal destruction.
Elevated levels of Aggregatibacter actinomycetemcomitans and/or Porphyromonas gingivalis.
Patients usually exhibit hyperactive polymorphonuclear neutrophils (PMNs) in chemotaxis and superoxide (O2 –) production with hyperresponsive macrophages [11,12].
Elevated levels of inflammatory cytokines (e.g. PGE2, IL‐1α, IL‐1β) from primed macrophages.
Progression of attachment loss and bone loss may be self‐arresting and remain stationary for years.
D.
Table 1.5.1 Features