Periodontal inflammation is associated with many systemic diseases, being called periodontal medicine, among them, cardiovascular diseases, diabetes (DM) and osteoporosis. Periodontitis (PD) is an inflammatory and infectious process of the ligament and alveolar bone that support the teeth where the release of inflammatory mediators occurs. Periodontitis involves local involvement of the renin-angiotensin system (RAS), since angiotensin acts on inflammation. Spontaneously hypertensive rats (SHR) have been used as genetic model of hypertension (DC). These animals are characterized by high blood pressure, significant changes in bone metabolism and a high activation of the sympathetic nervous system. Mast cells (MCs) play a fundamental role since they act in the tissue repair and in the defense of the organism. MCs have been observed in both the normal and inflamed periodontium, thus, it is assumed that MCs may participate in a possible inflammatory response, which may result in destruction and /or tissue and bone protection. Many studies have proposed that specific proteases (tryptase and chymase) and inflammatory mediators released by MCs are involved in the tissue destruction present in PD, but the mechanisms involved in this process are still unknown. MicroRNAs (miRNAs) play an important role in the regulation of bone metabolism and the immune-inflammatory response; however, the role of miRNAs in periodontal inflammation and bone metabolism in hypertensive animals has not yet been fully elucidated. The purpose of the present study is to investigate the role of MCs and RAS on bone metabolism in SHR submitted to experimental periodontitis. The methodology includes evaluating the role of MCs, miRNAs and RAS involved in osteoblastic and osteoclastic activity in cell culture assays. The prediction is to gain new insights into the response of miRNAs and RAS related to systemic and local mechanisms in periodontal disease and hypertension in relation to changes in bone metabolism. These data will contribute to the development of new drug therapy targets for these diseases.
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