Herpesvirus in localized juvenile periodontitis.

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.