Evaluation of cell migration and chemokine expression in the progression of periodontal disease in obese and normal mice.

Abstract

Periodontal disease is characterized a group of lesions in the tissues that surround and support teeth in their sockets, which can result in tooth loss. The main etiologic agent of periodontal disease is bacterial plaque, but the host response that determines disease susceptibility. Although the host response has meant to be protective, it initiates a cascade of events that can lead to imbalance of substances released, which characterizes the appearance of pathological extracellular matrix degradation and bone resorption of periodontal tissues.Metabolic syndrome is associated with resistance to insulin action and describes a set of metabolic abnormalities, which are often present in obese individuals and are predictors of diabetes and cardiovascular disease. Whereas obese have a higher susceptibility to periodontal disease and this is more severe, with accelerating the resorption of alveolar bone, the objective of this project is to study the influence of obesity on fat intake mimicked by experimentally induced periodontal disease in rats by ligature of analyzing the expression qumiocinas CXCL1 (IL-8), CCL5 (RANTES), CCL3 (MIP1-±) and chemokine receptors CCR1, CCR5, CXCR1 and CXCR3, in addition to adhesion molecules ICAM, VCAM-1, ELAM-1 and PECAM-1 in normal and obese animals during the progression of periodontal disease.