Correlation Between Subgingival Infections Of Human Cytomegalovirus And Inflammator Cytokines In Periodontitis Lesions

ObjectivePeriodontitis is an infectious disease attributable to complex interactions between periodontal pathogens and host defense systems. Although the role of bacteria in the pathogensis of periodontitis is well established, it has recently been suggested that herpesviruses appear to assume a major etiopathogenic role in various severe types of periodontal disease. Among several herpesviruses, human cytomegalovirus (HCMV) appears to be significantly associated with initiation and progression of periodontitis. Human cytomegalovirus is a ubiquitous herpesvirus that infects humans early in life. They are present latently in a great variety of cells, and may be reactivated under various conditions. Although several stuides have demonstrated a significant association of HCMV with periodontal disease, the mechanisms by which HCMV may actually cause periodontal destruction remain hypothetical. Ongoing research on HCMV infections of the periodontium may produce significant progress in the prevention and treatment of periodontitis.The purpose of this study was to quantify HCMV DNA loads in subgingival specimens from the patients with aggressive and chronic periodontitis, and to determine whether HCMV proliferation is associated with elevated levels of inflammatory cytokines in periodontitis lesions.Methods42 subjects with periodontitis (18 with aggressive periodontitis and 24 with chronic periodontitis) were included in the study. A group of 15 periodontally healthy individuals served as controls. Subgingival plaque and GCF samples were obtained from two sites in each subject. Standard quantification was performed with recombinant plasmid containing a conserved fragment of HCMV. The S YBR Green I fluorescent quantitative real-time polymerase chain reaction assay was established based on positive plasmid. HCMV in subgingival plaque samples were detected by real-time polymerase chain reaction. IL-1βand TNF-a levels in GCF were evaluated by enzyme-linked immunosorbent assays. Statistical analysis was performed using chi-square test, Wilcoxon-Mann-Whitney test, Kruskall-Wallis test and Spearman correlation test, p<0.05 was considered statistically significant.Results1. HCMV were detected in 58.3% of aggressive periodontitis sites and 41.7% of chronic periodontitis sites, however, only 6.7% of periodontally-healthy sites were HCMV positive. The frequency of HCMV was significantly higher in periodontitis lesions than in periodontally-healthy sites (p<0.01). High copy-counts of HCMV (>104 copies/ml) was more frequently dectected in aggressive priodontitis lesions (33.3%) than in chronic periodontitis lesions (10.4%)(p<0.05).2. Both in aggressive periodontitis and chronic periodontitis lesions, the levels of IL-1βand TNF-a in GCF showed no significant differences between the mediate copy-counts group of HCMV (102-104 copies/ml) and the low copy-counts group (<102 copies/ml), whereas a significant increase was observed in the levels of IL-1βand TNF-a in the high copy-counts group (>104 copies/ml) when compared with the low copy-counts group. The HCMV DNA loads in subgingival specimens showed positive correlations with levels of both IL-1βand TNF-αin GCF.Conclusion1. Although the prevalence of HCMV was similar between aggressive periodontitis and chronic periodontitis, the quantity of virus load was different in the two diseases. Active HCMV infection may be more relative to the rapid tissue destruction of aggressive periodontitis.2. HCMV proliferation is associated with elevated levels of inflammatory cytokines in periodontitis lesions. Reactivation of HCMV in periodontal sites may constitute a particularly important pathogenic event in the development of periodontitis.