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Correlation of cytomegalovirus and human herpesvirus 7 with CD3 + and CD3 + CD4 + cells in chronic periodontitis patients
Author(s) -
Thomasini R. L.,
Bo S. H.,
Durante P.,
Costa S. C. B.
Publication year - 2012
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.2011.01413.x
Subject(s) - human cytomegalovirus , cd3 , periodontitis , cd8 , chronic periodontitis , pathogenesis , immune system , pathology , immunology , medicine , cd19 , biology , virus
Thomasini RL, Bonon SH, Durante P, Costa SCB. Correlation of cytomegalovirus and human herpesvirus 7 with CD3+and CD3+CD4+cells in chronic periodontitis patients. J Periodont Res 2012; 47: 114–120. © 2011 John Wiley & Sons A/S Background and Objective: Human chronic periodontitis is an inflammatory process characterized by dense accumulation of immune cells in the periodontal tissue. The periodontitis can lead to loss of teeth in the patient and the pathogenesis of this disease is not completely known. This study tested the hypothesis that chronic periodontitis‐affected sites can harbor betaherpesviruses and that viruses are linked to a profile of the inflammatory infiltrate. Material and Methods: Biopsies of periodontal tissue were taken from periodontitis‐affected patients and from healthy subjects. Immunohistochemistry was performed to count CD19 + B cells, CD3 + total T cells, T‐CD4 + and T‐CD8 + cell subsets, and PCR was performed to detect cytomegalovirus and human herpesvirus 6 and 7 in the samples. One slide of each sample was stained with Giemsa for histopathological examination and to evaluate the quality of the cellular infiltrate. Results: As expected, tissues collected from healthy subjects presented no significant level of inflammatory infiltration and were therefore excluded from immunostaining procedures. Results showed that CD19 + B cells were in higher number than CD3 + T cells in the periodontitis‐affected tissue, but this was not statistically significant. The T‐CD4 + lymphocyte subset was significantly higher than the T‐CD8 + lymphocyte subset ( p = 0.004) in the samples. Cytomegalovirus and human herpesvirus 7 were found at periodontitis‐affected sites, but not in tissue collected from healthy subjects ( p = 0.04 and p = 0.04, respectively). Human herpesvirus 6 was rarely detected. We found a correlation between cytomegalovirus and lower CD19 + /CD3 + ratios (ratio < 0.9, p = 0.003) and between human herpesvirus 7 and lower CD19 + /CD3 + ratios (ratio < 0.9, p = 0.003) and higher CD4 + /CD8 + ratios (ratio > 1.1, p = 0.002). Conclusion: This study shows that cytomegalovirus and human herpesvirus 7 can be present at periodontitis‐affected sites but are uncommon at healthy periodontal sites. Moreover, our data suggest that cytomegalovirus can be related to an inflammatory infiltrate with predominance of CD3 + T cells, whereas human herpesvirus 7 can be associated with an infiltrate with predominance of T‐CD4 + cells. However, further studies are necessary to support this hypothesis. Herpesviruses could play a role in human chronic periodontitis by modulation of the T cell response.