Herpesviral-bacterial synergy in the pathogenesis of apical periodontitis: New insights and future perspectives
Apical periodontitis (AP) represents a persistent inflammatory reaction within periapical tissues of teeth devoid of vital pulp. Although it is considered as a multifactorial disease, in most of the cases it develops from the exposure of the vital pulp to different oral microbiota as a result of dental caries, accidental trauma or iatrogenic causes. Healthy dental pulp is a sterile environment, and, hypothetically, any microbe from the oral cavity may cause endodontic infection with subsequent destruction of tooth supporting tissues in the periapical region. The presence of herpesviral DNA in samples of periapical lesions was identified for the first time in 2003, suggesting its potential implication in the pathogenesis of AP. Namely, Slots and co-workers proposed a herpesviral-bacterial hypothesis by which herpesviruses may cause the destruction of periapical tissues as a result of direct cytopathogenic effects of different cell types in periapical region. They also claimed that herpesviruses may impair the local host defense and enhance aggressiveness of resident bacterial pathogens by several indirect mechanisms including inhibition of the major histocompatibility complex class I and II expression on the surface of macrophages, induction of pro-