Higher Prevalence of Epstein–Barr Virus DNA in Deeper Periodontal Pockets of Chronic Periodontitis in Japanese Patients

Abstract

Periodontitis, a complex chronic inflammatory disease caused by subgingival infection, is among the most prevalent microbial diseases in humans. Although traditional microbiological research on periodontitis has focused on putative bacteria such as Porphyromonas gingivalis, the herpes virus is proposed to be involved in the pathogenesis of periodontitis because bacterial etiology alone does not adequately explain various clinical aspects. In this study, we established for the first time, more Epstein–Barr virus (EBV) DNA is found deeper in periodontal pockets of chronic periodontitis in Japanese patients. Subgingival samples were collected from 85 patients with chronic periodontitis having two periodontal sites with probing depths (PD) of ≤3 mm (shallow) or ≥5 mm (deep) and were subjected to a nested polymerase chain reaction. EBV DNA was more frequently detected in patients with deeper PD sites (66%) than in those with shallow PD sites (48%) or healthy controls (45%). Coexistence of EBV DNA and P. gingivalis was significantly higher in patients with deeper PD sites (40%) than in those with shallow PD sites (14%) or healthy controls (13%). Although no difference in clinical index for periodontitis, the odds ratio of EBV DNA in patients with deeper PD sites was 2.36, which was 2.07-fold higher than that in those with shallow PD sites. Interestingly, the odds of acquiring chronic periodontitis (PD ≥5 mm) were higher in the presence of both EBV DNA and P. gingivalis compared with either EBV DNA or P. gingivalis only. In addition, we also observed that EBV-encoded small RNA (EBER) in positive cells of human gingival tissues. These results would suggest that EBV DNA may serve as a pathogenic factor leading to chronic periodontitis among Japanese patients.

Effects of initial periodontal therapy on interleukin-1β level in gingival crevicular fluid and clinical periodontal parameters

“…We previously reported that Epstein-Barr virus (EBV) DNA was detected more frequently in deeper (≥5 mm) PPD sites of CP patients than in shallow (≤3 mm) PPD sites or in healthy controls (4). In addition, coexistence of EBV and Porphyromonas gingivalis was significantly more frequent in deep PPD sites of patients as compared with shallow PPD sites and healthy controls.…”

“…Periodontopathic bacteria increase the risk of periodontitis, and immune responses against bacterial products and subsequent secretion of proinflammatory cytokines are crucial in periodontal tissue destruction (4,5). Interleukin-1β (IL-1β) is an important mediator of inflammatory response and is involved in cell proliferation, differentiation, and apoptosis, and in the pathophysiology of periodontitis (6).…”

Effects of miR-223 on expression of IL-1β and IL-6 in human gingival fibroblasts

“…It affects the periodontal tissues, and when advanced can result in tissue destruction, occasional pain, alveolar bone resorption, and eventual tooth loss (1)(2)(3). The response to periodontal pathogens is determined by the nature and control of both adaptive and innate immune responses (4).…”

MicroRNA expression in inflamed and noninflamed gingival tissues from Japanese patients

“…It is caused by specific bacteria and viruses and results in progressive destruction of the periodontal ligament and alveolar bone, with pocket formation (1,2). The rate of disease progression may be increased by local, systemic, and environmental factors that influence normal host-bacteria interaction.…”