Analise da influencia do diabetes tipo I induzido na progressão da doença periodontal experimental em ratos / Analysis of the influence of diabetes type I induced in the progression of experimental periodontal disease in rats

AUTOR(ES)
DATA DE PUBLICAÇÃO

2006

RESUMO

The periodontal disease is characterized as a group of lesions that affect the tissues which surround and support the teeth in their correct places. The bacterial plaque is the major ethiological agent, and most evidences suggest the periodontal disease is not simply associated with oral cavity colonization by pathogenic microorganisms, but to host susceptibility or resistance to the disease, once that, the destruction of periodontal tissue can occur depending on the immune response activated by these microorganisms. In health periodontal tissues there is a slightly equilibrium between bacterial plaque microorganisms and host response. Although the immune response is essentially protective, ir s influenced by some factors which can develop an exacerbated immune response, and in this way, contributing to appearance of worse lesions and a periodontal disease more severe. The Diabetes Mellitus is one of many risk factors and is characterized by inefficient production of insulin or its inadequate utilization by the individual, affecting the protein, carbohydrate and lipids metabolisms, resulting in severe metabolic disorders. The aim of this project was to study the development of experimental periodontal disease in rats under influence of diabetes induced by streptozotocin (STZ), characterizing the morphological changes found in epithelial and connective tissues, considering that patients affected by this disease shows a delay in the healing capacities. Our results confirmed that the diabetic animaIs presented a chronic inflammatory response with an increase of inflammatory cells in the periodontal tissues, and higher and faster collagen fibers degradation occurred, causing their accumulation. Moreover, the amount of fibroblasts raised, the reticulin fibers that support the basal membrane were more destroyed, and finally there was an involution in dermic papillas and a comium layer thicker. In the diabetic animaIs, the fibrosis was more emphasized with the inflammation progression, affecting the structural organization of epithelial and connective tissues, probably due to the increase in extracellular matrix degradation. In this way, we evaluated the MMP 2 and 9, called gelatinases, which has a proteolytic activity in the extracellular matrix. The MMPs enzymatic activity quantification by zymography showed that, the MMP2 isoform expressions was significantly lower in diabetic animaIs when compared to controls, during alI the experimental time. However, the MMP9 enzymatic activity was higher in diabetic animaIs. These data were confirmed by immunoflorescence, because MMP2 in controls was expressed in more than one cellular type such as basal epithelial cells, endothelium cells, Cl»)J)ecÚve tjssues and some regions between musc1e fibers. Otherwise, in diabetic animaIs, its expression was limited to epithelial cells and connective tissue. The MMP2 expression in quantitative PCR showed no significant differences between diabetic and control animaIs, while MMP9 presented a genic expression inversely proportional. In controls, the MMP9 expression was minimal in lack of inflammatory stimulation and showed an increase during the experimental time. Otherwise, in the diabetic animaIs the MMP9 expression was higher, and during the inflammatory response, its expression decreased. These data suggest that MMP2 and MMP9 can be involved in dynamics of periodontal tissue response, acting in the extracellular matrix and resulting in different pattems of fibrosis in control and diabetic animaIs

ASSUNTO(S)

fibrose gelatinase b diabetes mellittus doença periodontal periodontal disease fibrosis gelatinase a diabetes mellittus

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