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. 2011 Dec;37(12):1624-9.
doi: 10.1016/j.joen.2011.09.006.

Association of endodontic infection with detection of an initial lesion to the cardiovascular system

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Association of endodontic infection with detection of an initial lesion to the cardiovascular system

Elisabetta Cotti et al. J Endod. 2011 Dec.

Abstract

Introduction: Dental infections might predispose toward the onset of cardiovascular disease (CVD). To date, only a few studies, yielding inconclusive findings, have investigated the potential correlation between apical periodontitis (AP) and CVD. The aim of this study (as the first part of a prospective study) was to evaluate, in the absence of CV risk factors, whether subjects with AP were more exposed to the pathogenetic indices of an atherosclerotic lesion.

Methods: Forty men between the ages of 20 and 40 years who were free from periodontal disease, CVD, and traditional CV risk factors were enrolled in the study; 20 subjects had AP, and 20 acted as controls. All subjects underwent dental examination and complete cardiac assessment: physical examination, electrocardiogram, conventional and tissue Doppler echocardiography, and measurement of endothelial flow reserve (EFR). The following laboratory parameters were tested: interleukins -1, -2, and -6 (IL-1, IL-2, IL-6), tumor necrosis factor alpha, and asymmetrical dimethylarginine (ADMA). Data were analyzed by using the 2-tailed Student's t test, Pearson t test (or Spearman t test for nonparametric variables), and multivariate linear regression analysis.

Results: Echocardiography revealed no abnormalities in any of the subjects studied. ADMA levels were inversely correlated with EFR (P < .05) and directly correlated with IL-2 (P < .001). Patients with AP presented with significantly greater blood concentrations of IL-1 (P < .05), IL-2 (P < .01), IL-6 (P < .05), and ADMA (P < .05) and a significant reduction of EFR (P < .05).

Conclusions: Increased ADMA levels and their relationship with poor EFR and increased IL-2 might suggest the existence of an early endothelial dysfunction in young adults with AP.

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