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Characterization of the inflammatory and immune mechanisms involved in periodontal disease in rats obese

Grant number: 11/19375-9
Support type:Regular Research Grants
Duration: March 01, 2012 - February 28, 2014
Field of knowledge:Biological Sciences - Immunology
Principal Investigator:Dagmar Ruth Stach - Machado
Grantee:Dagmar Ruth Stach - Machado
Home Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

Periodontal disease is characterized as 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 immune response determines disease susceptibility. Although the host response means to be protective, it initiates a cascade of events that can lead to imbalance of released substances , which characterizes the appearance of pathological extracellular matrix degradation and bone resorption of periodontal tissues. While the degradation of extracellular matrix is mediated by proteases such as matrix metalloproteinases (MMPs), whose regulation is essential for tissue homeostasis, bone resorption is a direct effect of increased osteoclastogenesis, mediated primarily by the balance between the factor binding nuclear kappa B (RANKL) and its soluble inhibitor, the osteoprotegerin (OPG).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 diseases. Whereas obese have a higher susceptibility to periodontal disease and this is more severe, 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. Will be analyzed the following parameters in the gingiva of normal and obese rats during the progression of periodontal disease:*Pattern of gene expression of the metalloproteinases and their inhibitors and the mediators of bone resorption.*Pattern of gene expression and protein level of pro-inflammatory and anti-inflammatory cytokines*Pattern of gene expression of chemokines and its receptors.*Pattern of the immune and inflammatory cells. (AU)