Correlation between Epstein-Barr virus and periodontopathogen in periimplantitis affected and healthy patient

Background: Synergism among herpesviruses and bacteria may play an important role in the onset and progression of periodontitis and periimplantitis. Herpesviruses are potent inducers of pro-inflammatory cytokines. An active herpesvirus infection can also impair antibacterial immune mechanisms and potentially cause an upgrowth of periodontopathic bacteria. Aim/Hypothesis: The aim of the present study is to compare the presence of periodontopathic bacteria and Epstein-Barr virus in periimplantitis affected and healthy periimplant sites in order to understand if a synergism in the infection is present. Material and methods: From January 2013 to August 2014, 45 consecutive subjects with implants affected by periimplantitis and 45 subjects with healthy implants, coming to routine check-up or spontaneous visits during the study period in three private clinics [Rome and Genova (Italy) and Belgrade (Serbia)] were enrolled in this clinical study. Quantitative real-time PCR was performed to detect the presence/absence and quantify the Epstein-Barr virus and 9 pathogens: Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Tannerella forsythensis (Tf), Treponema denticola (Td), Prevotella intermedia (Pi), Peptostreptococcus micros (Pm), Fusobacterium nucleatum (Fn), Campylobacter rectus (Cr), Eikenella corrodens (Ec). Implants internal connections and external surface were evaluated. Results were presented as frequencies and percentages. Chi – square test was conducted to assess statistical significance between categorical data. Results: 85 subjects (42 patients with healthy implants and 43 with periimplantitis affected implants) were included in the study. Seventy-seven dental implants affected by periimplantitis and 113 healthy implants were evaluated during the study (mean time of loading 6.25 1.6 years). Epstein-Barr virus was slightly more present in periimplantitis affected patients compared with healthy control (15.6% vs. 14.2%; P > 0.05). Epstein-Barr virus was detected in external samples at a significantly higher frequencies compared to internal samples (P < 0.01). No significant difference was shown in Aa, Pg, Tf, Pm, Cr, Ec bacteria frequency between periimplantitis samples and healthy samples (P > 0.05). Td,Pi and Fn were detected in periimplantitis samples at a significantly higher frequencies compared to healthy samples (P < 0.01). There was no statistically significant difference in the occurrence of Epstein-Barr virus and Aa, Pg, Tf, Td, Pi, Pm, Fn, Cr, Ec bacteria together among samples of periimplantitis patients and samples of healthy patients (P > 0.05). Conclusions and clinical implications: This study failed in finding a synergism between Epstein-Barr virus and bacteria in the periimplantitis etiopathogenesis.