Abstract
The purpose of the present investigation was to compare the presence of Epstein-Barr virus type 1 (EBV-1) and of Human Cytomegalovirus (HCMV) in crevicular fluid samples from deep and shallow periodontal pocket sites of Brazilian patients with aggressive periodontitis. A total of 30 systemically healthy patients with aggressive periodontitis participated in the study. Paper points were inserted into 2 gingivitis sites (<3 mm) and into 2 periodontitis sites (>5 mm) in each patient. PCR assay was used to identify genomic copies of HCMV and EBV-1. Twenty-three patients (77%) were positive for EBV-1, while only 2 patients (6%) were positive for HCMV. The McNemar test revealed a positive association between EBV-1 and periodontal lesions (p=0.043). Thirty-four (57%) out of 60 periodontitis sites were positive for EBV-1, whereas 18 (30%) gingivitis sites were positive (p=0.01). Only two sites (6.7%) were positive for HCMV. No positive association was found between HCMV and periodontitis or gingivitis (p=0.479). The elevated occurrence of EBV-1 DNA in periodontal pockets of patients with aggressive periodontitis supports a possible periodontopathic role of this virus.
Highlights
Many studies have suggested that the coexistence of periodontal herpesviruses, periodontopathic bacteria and the local host immune response are involved in periodontal disease evolution.[3,6,10,12,19,20]
The involvement of herpesviruses in the etiology of periodontal disease was suggested by its presence in gingival tissue, gingival crevicular fluid and subgingival plaque affected by periodontal disease.[6]
Twenty-three out of 30 (77%) patients demonstrated the presence of Epstein-Barr virus type 1 (EBV-1) DNA
Summary
Little is known about the conversion of gingivitis sites into periodontitis sites[21] or why periodontal tissue breakdown progresses in a localized and bilaterally symmetrical pattern.[4,15] Many studies have suggested that the coexistence of periodontal herpesviruses, periodontopathic bacteria and the local host immune response are involved in periodontal disease evolution.[3,6,10,12,19,20]The association of herpesviruses with oral disease is not a novel issue. Genomes of two types of herpesviruses, HCMV and EBV, occur at high frequency in progressive periodontitis in adults,[12,27] localized[24] and generalized aggressive periodontitis,[12,20,24] HIV-periodontitis,[4,24] acute necrotizing gingivitis,[3] periodontal abscesses,[20] Pappilon Lefrève periodontitis[26] and 21 trisomic periodontitis.[9] Rones et al.[18] (1983) demonstrated a significant positivity of both epithelial and fibroblast cells from the gingival sulcus area for the herpes simplex virus in vitro, suggesting that those cells could be a reservoir for the latent virus. The role of HCMV and EBV-1 in periodontal disease pathogenesis remains to be elucidated
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