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Periodontitis lesions are a source of salivary cytomegalovirus and Epstein-Barr virus

Aim:  Several herpesvirus species can be detected in periodontal pockets and saliva. This study compared human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) DNA copy counts in periodontitis sites and in whole saliva, and evaluated the potential of periodontal therapy to reduce the salivary lev...

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Bibliographic Details
Published in:Journal of periodontal research 2005-04, Vol.40 (2), p.187-191
Main Authors: Saygun, Işıl, Kubar, Ayhan, Özdemir, Atilla, Slots, Jørgen
Format: Article
Language:English
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Summary:Aim:  Several herpesvirus species can be detected in periodontal pockets and saliva. This study compared human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) DNA copy counts in periodontitis sites and in whole saliva, and evaluated the potential of periodontal therapy to reduce the salivary level of the two viruses. Material and methods:  A total of 20 systemically healthy periodontitis patients, 21–56 years of age, participated in the study. All 20 patients were examined at baseline, and seven patients also at 3 months after periodontal therapy. Treatment included oral hygiene instruction, scaling and root planing, and surgery. Clinical parameters were evaluated using established methods. In each patient, virological samples were collected from one periodontal pocket of 6–10 mm probing depth, from the adjacent inflamed periodontal pocket wall, and from unstimulated whole saliva. Relationships between subgingival, gingival tissue and salivary herpesvirus counts were evaluated using Spearman's and Kendall's rank correlation coefficient tests. The 5′‐nuclease (TaqMan®) real‐time polymerase chain reaction (PCR) assay was employed to quantify genomic copies of periodontal HCMV and EBV. Results:  At baseline, the 20 periodontitis patients showed significant positive correlations between gingival tissue and salivary counts of HCMV DNA (p = 0.003) and EBV DNA (p = 0.045). Periodontal pocket depth was positively correlated with salivary EBV DNA counts (p = 0.002). Periodontal therapy reduced average full‐mouth periodontal pocket depth from 4.6 mm to 1.4 mm, plaque index from 2.1 to 0.9, and gingival index from 2.1 to 0.4. Following treatment, HCMV DNA counts decreased 37.5 fold in subgingival sites and 64.6 fold in saliva, and EBV DNA counts decreased 5.7 fold in subgingival sites and 12.9 fold in saliva. Conclusions:  The present study provides compelling evidence of a periodontitis source for salivary HCMV and EBV. The potential of periodontal therapy to decrease herpesvirus salivary counts may help diminish herpesvirus transmission from person to person and herpesvirus‐related diseases in exposed individuals. Further research is warranted to determine the relationship between periodontal herpesvirus counts and the risk of viral transmission to close acquaintances.
ISSN:0022-3484
1600-0765
DOI:10.1111/j.1600-0765.2005.00790.x