Abstract

Chronic periodontitis is a chronic inflammatory disease of infectious origin involving destruction of the supporting structures of the teeth including ligament, bone and may lead to tooth loss. The pathogenesis of periodontitis involves inflammatory and immunological processes that elicit the production of cytokines, prostaglandins and in some cases, acute phase reagents, such as C-reactive protein (CRP). CP has been associated with elevated levels of CRP in otherwise systemically health. Moreover, periodontal treatment has been associated with reduction of CRP levels. In dialysis patients, increased CRP levels have been associated with increased risk for cardiovascular diseases in both continuous ambulatory peritoneal dialysis (CAPD) and in hemodialysis patients. Dialysis-associated inflammation may explain why approximately 30% of patients on renal replacement therapy (RRT) display markers of chronic inflammation. However, it is unknown why in some CKD patients without an evident concurrent inflammatory process also present laboratory signs of inflammation. It is possible that periodontitis may be a source of inflammation in CKD individuals. The aim ofthis review is to present the relations between CKD, atherosclerosis and periodontitis, emphatizing a possible influence of periodontitis on the inflammatory process in CKD patients. In conclusion, both PD and CKD are chronic inflammatory diseases, and the inflammatory mechanisms and host responses may be responsible for their endpoints. Non traditional risk factors, such as periodontitis, may be associated to the high mortality observed in CKD. Periodontitis is highly prevalent in the population and is associated with high levels of CRP and endothelial dysfunction, early predictors of atherosclerosis. Periodontal treatment may reduce the inflammatory process, reducing the incidence of atherosclerotic complications in patient with CKD.

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