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

Background: Although there is ample evidence in the literature supporting a significant positive association between key periodontal pathogens and established inflammatory markers of periodontitis and coronary artery disease (CAD), their exact role 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), as well as the inflammatory marker pentraxin-3 (PTX3), and to analyze their association with CAD.

Methods: The study included 240 patients divided into four groups of 60 patients each: nonperiodontitis + noncardiac (NP+NC) group, periodontitis + noncardiac patients (P+NC) group, nonperiodontitis + cardiac patients (NP+C) group, and periodontitis + cardiac (P+C) group. The cardiac surgery group (C-S) was a subgroup of NP+C and P+C. It consisted of 60 patients from the abovementioned two cardiac groups in whom coronary artery bypass graft (CABG) was indicated. Demographic variables, cardiac parameters, and periodontal parameters were recorded. The viruses (EBV, CMV, and HSV) and the inflammatory marker PTX3 were evaluated in the subgingival plaque samples of all the four groups and atheromatous plaque samples of the C-S using reverse transcriptase-polymerase chain reaction (RT-PCR) and quantitative polymerase chain reaction (qPCR), respectively, and were compared between the groups. The results were obtained and statistically analyzed.

Results: The demographic variables did not differ significantly between the groups, except for age. Systolic blood pressure, diastolic blood pressure, low-density lipoprotein, and 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. Plaque index (PI), probing pocket depth (PPD), and clinical attachment level (CAL) were significantly higher (p ≤ 0.05) in P+NC and P+C. PTX 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 = 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 the P+C group with a p value of 0.004 and 0.033, respectively. Cardiac HSV was found in the NP+C group with statistical insignificance (p = 0.410) between the groups. On correlation, oral PTX were significantly associated with bleeding index (BI), PPD, and CAL (p = 0.000). Similarly, cardiac PTX showed significant association with PI, BI, 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). 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 suggest that the clinical severity of periodontitis (CAL), etiology of periodontitis (EBV and CMV), and inflammatory marker of periodontitis (PTX3) 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.