Abstract

Introduction: The aim of this study was to assess whether apical lesions are associated with inflammatory serum markers of cardiovascular risk, especially high-sensitivity C-reactive protein (hsCRP), in young adults. Methods: In this cross-sectional study, otherwise healthy individuals with apical lesions of endodontic origin (ALEOs) and a clinical diagnosis of asymptomatic apical periodontitis and controls aged between 18 and 40 years were included. Patients' sociodemographic characteristics, medical history, and classic cardiovascular risk factors were recorded, and the pathobiological determinants of atherosclerosis in youth score was calculated. Oral clinical and radiographic examinations were performed. Blood samples were collected to determine the lipid profile, glycated hemoglobin, hsCRP, immunoglobulin G, interleukin (IL)-6, IL-10, IL-12p70, matrix metalloproteinase 8, soluble vascular cellular adhesion molecule-1, soluble intercellular adhesion molecule-1, and soluble E-selectin. Bivariate and multivariate analyses adjusting for oral and classic cardiovascular risk factors were performed. Results: hsCRP levels were significantly higher in ALEO patients versus controls (median = 2.54 vs 0.78), whereas the pathobiological determinants of atherosclerosis in youth score was comparable among the groups. Also, the levels of IL-6, matrix metalloproteinase 8, and soluble E-selectin were significantly higher in ALEO patients. hsCRP, IL-6, and IL-12 correlated with soluble adhesion molecules. Bivariate analysis based on hsCRP serum concentrations >= 1 mg/L showed an odds ratio (OR) = 6.8, and the risk increased 3.3 times for an additional ALEO. In multivariate analysis, ALEO was significantly associated with hsCRP levels mg/L (OR = 5.1-12.8) independently of the adjustment model. ALEO also associated with CRP levels >3 mg/L, which was significant after the adjustment for covariates (OR = 4.0). Conclusions: ALEO is associated with the systemic inflammatory burden and cardiovascular risk determined by hsCRP, supporting a mechanistic link for cardiovascular diseases in young adults.