Purpose of review: Periodontitis is an infectious disease, but the specific mechanisms by which tooth-supportive tissues are lost remain obscure. This article proposes an infectious disease model for periodontitis in which herpesviral–bacterial interactions assume a major etiopathogenic role.
Recent findings: Epstein–Barr virus type 1, cytomegalovirus and other herpesviruses occur at a high frequency in aggressive periodontitis lesions. Also, herpesvirus-infected periodontitis lesions tend to harbor elevated levels of classic periodontopathic bacteria, including Porphyromonas gingivalis, Dialister pneumosintes, Prevotella intermedia, Prevotella nigrescens, Campylobacter rectus, Treponema denticola and Actinobacillus (Aggregatibacter) actinomycetemcomitans.
Summary: Conceivably, a herpesvirus active infection in the periodontium impairs local defenses, thereby permitting overgrowth and increased aggressiveness of periodontopathic bacteria. In turn, periodontal pathogenic bacteria may augment the virulence of periodontal herpesviruses. It is suggested that interactions among herpesviruses and specific bacterial species constitute an important pathogenetic feature of periodontitis and maybe also of various non-oral infections.