Evidence linking the association of periodontal viruses and pentraxins in periodontitis patients with coronary artery disease.

BACKGROUND AND OBJECTIVES: Though there are multiple literature evidences supporting a significant positive association between key periodontal pathogen and established inflammatory marker of periodontitis towards Coronary Artery Disease (CAD), their exact roles remain unclear. Especially, the role of viruses in the etiology and specific biomarkers have not been validated. Thus, the current study aims to evaluate the role of periodontal viruses such as Epstein barr virus (EBV), Cytomegalovirus (CMV) and Herpes simplex virus (HSV), the inflammatory marker pentraxin-3 and to analyse their association with CAD.

METHODOLOGY: The study consisted of two hundred and forty patients who were divided into 4 groups of 60 patients each, namely, non-periodontitis + non-cardiac (NP+NC) group, periodontitis + non-cardiac patients (P+NC) group, non-periodontitis + cardiac patients (NP+C) group, and periodontitis + cardiac (P+C) group. The C-S (cardiac surgery group) was a sub-group of NP+C and P+C. It consisted of 60 patients from the above mentioned two cardiac groups, where they are indicated for Coronary artery bypass graft (CABG). Demographic variables, cardiac parameters and periodontal parameters were recorded. The viruses (EBV, CMV, HSV) and the inflammatory marker pentraxin-3 were evaluated in the sub- gingival plaque samples of all the four groups and atheromatous plaque samples of sub-group C-S using RT-PCR (Reverse transcriptase Polymerase chain reaction) and qPCR (Real time quantitative Polymerase chain reaction) respectively and were compared between the groups. The results were obtained and statistically analysed.

RESULTS: The demographic variables did not differ significantly between the groups, except for age. Systolic blood pressure, diastolic blood pressure, low density lipoprotein, random blood sugar were significantly higher in NP+C and P+C whereas high density lipoprotein was significantly lower (p≤0.05) in the same. The plaque Index (PI), probing pocket depth (PPD) and clinical attachment loss (CAL) were significantly higher (p≤0.05) in P+NC and P+C. The pentraxins were significantly elevated in P+C among the four groups. On evaluating the subgingival plaque samples, EBV and CMV were significantly higher in the two periodontitis groups P+NC and P+C (p-value = 0.000). HSV was significantly higher in the two cardiac groups (NP+C and P+C) (p≤0.05). Cardiac EBV and CMV were significantly elevated in P+C group with the P-value of 0.004 and 0.033 respectively. Cardiac HSV was found in C+NP group with statistical insignificance (p value = 0.410) between the groups. On correlation, oral PTX were significantly associated with BI, PPD & CAL (p = 0.000). Similarly cardiac PTX also showed significant association with PI, BI (Bleeding index), PPD and CAL (p = 0.000). Oral and cardiac PTX also showed significant correlation with each other. Multiple logistic regression analysis revealed a significant association between CAL and oral EBV (p≤0.05). Similarly, cardiac EBV showed a significant association with CAL and oral EBV (p≤0.05). The multiple logistic regression analysis also revealed that both cardiac and oral PTX showed a significant association only with oral EBV, CMV and HSV.

CONCLUSION: The results of the current study suggests that the clinical severity of periodontitis (CAL), etiology of periodontitis (EBV & CMV) and inflammatory marker of periodontitis (Pentraxin-3) were found to be significantly elevated in CAD. These findings suggests that periodontal diseases may be a risk factor that could influence the progression of CAD. This article is protected by copyright. All rights reserved.