Herpesviruses in periapical pathosis: an etiopathogenic relationship?

Much remains to be learned about the etiopathogenesis of periapical pathosis, especially about the molecular events preceding and causing disease onset. Human cytomegalovirus and Epstein-Barr virus, 2 herpesviruses, are discussed in this review as they relate to apical periodontitis in humans.

Cytomegalovirus or Epstein-Barr virus active infections are detected in more than 90% of granulomas of symptomatic and large periapical lesions. Dual infection with cytomegalovirus and Epstein-Barr virus is closely associated with symptomatic lesions. Herpes simplex virus active infection has no apparent relationship to periapical disease.

The available evidence suggests the involvement of active cytomegalovirus and Epstein-Barr infections in the etiopathogenesis of apical periodontitis. In periapical pathosis, herpesviruses may cause the release of tissue-destructive cytokines, the overgrowth of pathogenic bacteria, and the initiation of cytotoxic or immunopathologic events. Immune impairment resulting from herpesvirus infection may aid bacteria at several stages of the pathogenesis of periapical lesions, including growth in the periapical environment, possible invasion of tissue, and direct damage to tissue. Unraveling the etiology and pathogenesis of periapical pathosis may require a broadening of our experimental approaches to include studies on interactions among herpesviruses, bacteria, and host immune reactions. Understanding the significance of herpesviruses in the development of periapical lesions may aid in the diagnosis, prevention, and treatment of the diseases.