Consequences of the presence of ligature-induced periodontitis on rat blood pressure and in vitro vasomotor response

Abstract

Inflammation is an adaptive response triggered by noxious stimuli such as infections and tissue damage that aims to restore homeostasis. Chronic destruction of periodontal attachment apparatus due to an intense inflammatory response to bacteria leads to a clinical condition known as periodontal disease. Periodontal inflammation usually causes superficial ulcers in the gingival sulcus, where blood capillaries are exposed to bacteria. Periodontal pathogens can then translocate to the gingival sulcus and reach the bloodstream, and thus have peripheral effects. The periodontal pocket is also an important reservoir of inflammatory mediators, which can reach the bloodstream. In this way, periodontitis may have effects on organs and regions distant from the site of infection. In fact, the relationship between periodontal disease and bacterial myocarditis in humans was the first evidence in this sense, and then, additional studies have also documented the relationship between periodontal disease and endothelial dysfunction, which was reversible by dental treatment. However, the mechanisms and the pharmacological mediators that support the correlation between periodontitis and vascular alterations are not fully defined; on this point, the use of animal models of the disease is the best way to focus this question. In our laboratory we are currently studying the vasomotor response in vitro of aortic rings prepared from tissue isolated from rats with ligature-induced periodontitis, and the preliminary results show that the presence of periodontitis causes significant increase in the contractile response of the rings to norepinephrine, when compared with the response of vessels obtained from control animals (Sham). Considering the importance of the effects of periodontal disease in remote organs, particularly the cardiovascular mentioned above, this project aims to evaluate the influence of ligature-induced periodontitis in rats on blood pressure and the in vitro vascular reactivity of both conductance (aorta) and resistance (mesenteric artery) vessels. Also, attempts will be made towards the characterization of the mediators involved, with special emphasis on the products of the different isoforms of the enzymes cyclooxygenase (COX) and nitric oxide synthase (NOS), in view of the results obtained in previous works that evidenced the beneficial effects of inhibiting COX (with NSAIDs) or NOS (in particular, iNOS) on alveolar bone loss secondary to periodontitis. However, the participation of other pharmacological mediators should also be addressed, depending on the results to be obtained from the in vitro vascular reactivity experiments. (AU)