assessment of high-sensitivity c-reactive protein values in chronic periodontitis patients with and without cardiovascular disease: a cross-sectional study

Abstract

Background: Periodontal disease is characterized by inflammation and destruction of supporting tissues of the affected teeth. Pro-inflammatory cytokines originating at the site of local pathology activate hepatocytes to produce acute-phase proteins including C-reactive protein (CRP). Numerous cross-sectional studies have suggested that chronic periodontitis is a risk factor for cardiovascular disease (CVD) linked by inflammatory factors including CRP. Materials and Methods: A total of forty patients, twenty with chronic periodontitis only with no CVD (Group A) and twenty with CVD and chronic periodontitis (Group B), were selected for the study. Clinical parameters including gingival index (GI), plaque index, gingival bleeding index, Pocket probing depth (PD), and clinical attachment level (CAL) were recorded. In addition, high-sensitivity CRP (hsCRP) levels were measured from the peripheral blood using turbidimetric immunoassay technique. Results: As compared to the patients in Group A, those in Group B had more severe periodontitis with greater CAL (6.02 ± 0.53 mm vs. 6.63 ± 0.85 mm, P = 0.009), probing pocket depth (PPD) (5.20 ± 0.31 mm vs. 5.73 ± 0.52 mm, P < 0.001), and GI score (2.25 ± 0.51 vs. 2.65 ± 0.76, P = 0.06). Group B patients also had significantly higher hsCRP levels (12.3 ± 8.84 mg/L vs. 2.28 ± 0.38 mg/L; P < 0.001). The hsCRP levels had a significant positive correlation with PPD and GI. Multivariate regression analysis showed that the presence of CVD was independently associated with elevated hsCRP levels in the study population. Conclusion: The present study shows that CVD is associated with more severe periodontitis which is reflected in higher hsCRP levels. In addition, elevated hsCRP showed an independent association with CVD, incremental to various periodontitis measures. These findings suggest that periodontitis may add to the inflammation burden of the individual, which may potentially increase inflammatory activity in atherosclerotic lesions and thus the risk for cardiovascular events.