Epstein–Barr virus associated peri-implantitis: a split-mouth study
Objectives 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–bacteria...
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| Veröffentlicht in: | Clinical oral investigations Jg. 19; H. 2; S. 535 - 543 |
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| Hauptverfasser: | , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.03.2015
Springer Nature B.V |
| Schlagworte: | |
| ISSN: | 1432-6981, 1436-3771, 1436-3771 |
| Online-Zugang: | Volltext |
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| Zusammenfassung: | Objectives
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.
Methods
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).
Results
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).
Conclusions
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.
Clinical significance
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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| Bibliographie: | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
| ISSN: | 1432-6981 1436-3771 1436-3771 |
| DOI: | 10.1007/s00784-014-1250-1 |