Cardiovascular implications of endodontic bone disease

Cardiovascular diseases (CVD) have a complex etiology determined by risk factors, which are in turn associated to a strong genetic component and to environmental factors. In the biological background for the development of CVD, low-grade chronic inflammation plays a role as a pathogenetic determinant of atherosclerosis. Dental infections have been associated with CVD. Periodontal disease is a chronic infection of the supporting tissues of the tooth that can lead to teeth loss. In recent years, a number of reports have demonstrated the possible relationship between periodontal disease and CVD. Apical periodontitis, on the other hand, is the late consequence of an endodontic infection, which is caused by the persistence of coronal caries and involves the root canal system of the tooth. Most of the time, it is a chronic infection. Some studies have found a correlation between a “composite status” of oral health (eg. caries, tooth loss, periodontal disease) and CVD, but only a few of them have addressed the association between apical periodontitis and CVD. The first part of our study consisted in a “state of the art” analysis concerning the relationship between chronic dental infections and CVD. The results of this analysis confirmed that to date, only a few studies, yielding inconclusive findings, have investigated the potential correlation between apical periodontitis (AP) and CVD. So, in the second part of our study (as the first part of a prospective study) the aim 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.