Herpesviruses in localized juvenile periodontitis

Abstract

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.

Prevalence of Herpesvirus and Correlation with Clinical Parameters in Indian Subjects with Chronic Periodontitis

“…It is seen that an individual with herpesvirus infection may not reveal herpesvirus in all periodontal sites or if inactive state. 26 The other possibility being the samples could be from sites which are inactive or the virus being in the latent state, or the plaque collected may not be from the sites which were virus-rich in periodontium.…”

Viruses in Endodontic Infections

“…11 CMV infection during the development causes defective peridontium and cemental hypoplasia. During puberty, hormonal changes can cause reactivation of cytomegalovirus (HCMV), suppresion of immune defenses against bacteria and this in turn causes overgrowth of A actinomycetemcomitans, which inhibits epithelial cell proliferation by means of cytolethal toxins.…”

High prevalence of human cytomegalovirus in a population of periodontally healthy subjects

“…In aggressive localized periodontitis HCMV appears to increase the odds of having the disease, especially when P. gingivalis is also present (7). Moreover, active sites do show a consistent presence of virus as compared to shallow or stable sites (8). Furthermore, HCMV has been associated with acute necrotizing ulcerative gingivitis and periodontitis in HIV-positive subjects (9).…”