4.5 Article

Epstein-Barr virus associated peri-implantitis: a split-mouth study

Journal

CLINICAL ORAL INVESTIGATIONS
Volume 19, Issue 2, Pages 535-543

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s00784-014-1250-1

Keywords

Peri-implantitis; Human herpesvirus 4; Epstein-Barrvirus infections; Treponema denticola; Polymerase chain reaction; Microbiology; Saliva

Funding

  1. Andalusian Regional Government, Granada, Spain [CTS-167]

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Herpesviral-bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on specific microbial challenge and host susceptibility. This cross-sectional split-mouth study aimed to substantiate herpesviral-bacterial co-infection in PI patients and assess associations with periodontopathogen salivary contamination. PCR-based identification was performed on 23 patients presenting PI and contralateral healthy implants, and compared to unstimulated whole saliva. Clinical evaluation included probing depths, bleeding on probing, and suppuration. Radiographs were assessed for the presence of lamina dura and bone loss. Three sample sites per patient were tested: PI lesions, healthy implant sulci, and saliva. Quantitative PCR evaluated Epstein-Barr virus (EBV) and cytomegalovirus (CMV) copy counts. Significance of group comparisons for binary-dependent variables, within-subjects designs, was determined by McNemar's chi-square test. Risk analysis was evaluated through odds ratios (OR). PI lesions were 14.2 (P = 0.001; 95 % confidence interval [CI], 1.6-124.1) and 3 times (P = 0.03; 95 % CI, 0.7-11.9) more likely to harbor EBV than healthy implants and saliva, respectively. EBV positive predictive value was 90 %. PI was associated with absence of lamina dura and higher periodontopathogen proportions. Saliva sampling showed high agreement with PI bacterial detection (89-100 % rate) but not with EBV (44.4 %). The OR of PI lesions harboring Treponema denticola or Tannerella forsythia was 6.79 (P = 0.007; 95 % CI, 1.8-25.0) and 3.3 (P < 0.0001; 95 % CI, 0.3-34.3) times higher than healthy implants, respectively. Saliva of patients with PI was 5.6 times more likely to be contaminated with Prevotella nigrescens than healthy peri-implant sulci (P = 0.002). PI lesions were 1.92 times more likely to harbor Prevotella nigrescens than healthy implants (P = 0.04). EBV is a potential candidate in peri-implantitis etiopathogenesis. Saliva PCR analysis is useful in predicting peri-implantitis-specific bacterial infection but not EBV or CMV. Herpesviral-bacterial synergism may favor ongoing microbial challenge in peri-implant disease and exacerbate its progression. EBV infection may explain non-responsive to treatment PI. Peri-implantitis individuals may benefit from antiviral therapy.

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