The results indicate that subgingival EBV-1, HCMV, and viral coinfections are associated with the subgingival presence of some periodontal pathogens and periodontitis. Herpesviruses may exert periodontopathic potential by decreasing the host resistance against subgingival colonization and multiplication of periodontal pathogens.

Herpesvirus genomic sequences can be detected in gingival crevicular fluid of adult periodontitis lesions. Herpesviruses are immunosuppressive and may facilitate establishment of subgingival pathogens. Electron microscopic studies have identified nuclear and cytoplasmic virus-like inclusions in gingival inflammatory cells from localized juvenile periodontitis (LJP). The present study aimed to determine if herpesviruses occur in LJP lesions and if human cytomegalovirus (HCMV) activation is associated with elevated levels of subgingival Actinobacillus actinomycetemcomitans, the putative bacterial pathogen of LJP. Eleven systemically healthy patients exhibiting LJP (10-23 yr) were studied. In each patient, subgingival samples were pooled from 3 periodontitis lesions around first molar and incisor teeth (5-11 mm periodontal pocket depth) and from 3 gingivitis/healthy sites around canines (2-3 mm periodontal pocket depth). Polymerase chain reaction (PCR) was used to detect herpesvirus DNA and HCMV cDNA of major capsid protein transcripts, indicative of viral activation. Selective culture and 16S rRNA PCR were used to identify A. actinomycetemcomitans. Of 11 deep periodontal samples, 8 showed HCMV, 7 showed Epstein-Barr virus type 1 (EBV-1), 1 showed EBV type 2, 6 showed herpes simplex virus (HSV) and 8 showed viral co-infection. Of 11 shallow periodontal samples, 2 showed HCMV, 2 showed EBV-1, 1 showed HSV and 2 showed viral co-infection. The difference in occurrence of HCMV and viral co-infection between deep and shallow periodontal sites was statistically significant (p =0.031). HCMV activation was detected in deep pockets of all 5 virally positive patients with early LJP (aged 10-14 years) but only in 1 of 3 virally positive LJP patients older than 14 years, and not in any shallow pocket tested. HCMV activation appeared related to absence of radiographic crestal alveolar lamina dura, a possible indication of periodontal disease progression. A. actinomycetemcomitans tended to be more prevalent in samples showing active than latent HCMV infection. The present findings are consistent with the notion that periodontal herpesvirus infection and possibly HCMV activation constitute important features of the etiopathogenesis of LJP.

Recent studies have identified various herpesviruses in human periodontal disease. Epstein-Barr virus type 1 (EBV-1) infects periodontal B-lymphocytes and human cytomegalovirus (HCMV) infects periodontal monocytes/ macrophages and T-lymphocytes. EBV-1, HCMV and other herpesviruses are present more frequently in periodontitis lesions and acute necrotizing ulcerative gingivitis-lesions than in gingivitis or periodontally healthy sites. Reactivation of HCMV in periodontitis lesions tends to be associated with progressing periodontal disease. Herpesvirus-associated periodontitis lesions harbor elevated levels of periodontopathic bacteria, including Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Bacteriodes forsythus, Prevotella intermedia, Prevotella nigrescens and Treponema denticola. It may be that active periodontal herpesvirus infection impairs periodontal defenses, thereby permitting subgingival overgrowth of periodontopathic bacteria. Alteration between latent and active herpesvirus infection in the periodontium might lead to transient local immunosuppression and explain in part the episodic progressive nature of human periodontitis. Tissue tropism of herpesvirus infections might help explain the localized pattern of tissue destruction in periodontitis. Absence of herpesvirus infection or viral reactivation might explain why some individuals carry periodontopathic bacteria while still maintaining periodontal health. Further studies are warranted to delineate whether the proposed herpesvirus-periodontopathic bacteria model might account for some of the pathogenic features of human periodontal disease.