Evaluation of CCL3/MIP-1alfa and CXCL2/MIP-2 in gingival tissue and gingival fibroblast from diabetic mice submitted to periodontal disease

Abstract

Periodontitis affects the supporting tissues of the teeth and is triggered by anaerobic gram-negative microorganisms in the periodontal biofilm. Antigens derived from these bacteria, for example the Lipopossacarídeos (LPS) in the patient periodontal site can initiate signaling through the gingival tissue cells, which activates the mechanism of inflammation. The gingival fibroblasts are the most abundant cells in the periodontal tissue, and can produce inflammatory mediators for help the elimination of pathogens. Chemokines are responsible for the recruitment of immune cells, however, with the presence of systemic diseases such as diabetes, exacerbation of chemokines production may occur, and thus worsening of periodontal disease. Furthermore, periodontal disease when present in diabetics can adversely modify the glycemic control. This inter-relationship between both disorders can affecting the quality of life of patients. Thus, this study aims to evaluate the mechanisms involved in the CCL3/MIP-1± and CXCL2/MIP-2 production in gingival tissue and gingival fibroblasts from diabetic or normal mice submitted to periodontal disease. Therefore being able to elucidate the role of chemokines CCL3 and CXCL2 in the development of periodontitis in the presence of diabetes.