Dept of prosthodontics, Sri hasanamba dental college, Hassan.
Online published on 25 June, 2012.
Periodontal disease and cardiovascular disease (CVD) share characteristics with respect to a number of risk factors. Some individuals frequently possesses a hyper-inflammatory monocytes phenotype, where peripheral blood monocytes secrete high levels of PGE2 IL-1α and TNFα mediators, thus placing them at greater risk for both periodontitis and CHD. The concept of focal infection has recently reappeared and may be applicable to the role of periodontitis in systemic disease. Circulating lipopolysaccharide (LPS), released from Gram-negative bacteria, can predispose to thromboembolic events in the vascular tree, and LPS released from putative periodontal pathogen may contribute to tissue damage in this manner. Oral bacteria, including Streptococcus sanguis and the putative periodontal pathogen Porphyromonas gingivalis, have been shown to have effects on the cardiovascular system by increasing platelet aggregation. Periodontal pathogens have been identified in atheromatous plaque. Oral infection increases the systemic inflammatory challenge to the vascular tree, with potentially damaging consequences. As an example, adult periodontal patients have been shown to have a high serum level of C-reactive protein (CRP), and levels of this particular inflammatory marker also correlate with measures of cardiovascular pathology. An increase in neutrophil numbers or their state of activation as a result of periodontal disease, or even gingivitis, may similarly have adverse effects on the cardiovascular system. Particular emphasis has been placed on links between periodontal disease and cardiovascular disease.
thromboembolism, Atherosclerosis, Monocytes, Lipopolysaccharide