A paradigm shift several decades ago elucidated that aggressive periodontitis (AgP) was not a degenerative disorder but a rapid progressive form of plaque-induced inflammatory periodontal disease. Ensuing years of research have led to linkage analysis identification of specific genetic defects responsible for AgP in some families and to the finding that subgingival detection of A. actinomycet-emcomitans JP2 clone is a predictive factor for disease onset and progression. However, rather disappointingly, these 'proven' risk factors are only detected in a small subset of AgP cases. Recent advances are leading to a new paradigm shift, with the realization that genetically-driven dysbiotic changes in the subgingival microbiota may predispose to a cascade of events leading to the rapid periodontal tissue destruction seen in AgP. This review tries to dissect the existing literature on the host response-microbial axis of AgP and to propose possible pathogenic pathways in line with current theories.
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