Efeito de diferentes doses de alendronato no reparo ósseo de fraturas simples em fêmur de ratos

• Autor(a) principal: Tiboni, Fernanda
• Data de Publicação: 2018
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório do Centro Universitário Braz Cubas
• Texto Completo: https://repositorio.cruzeirodosul.edu.br/handle/123456789/2080
• topic: Odontologia; Alendronato; Fraturas ósseas; Fatores de crescimento transformadores beta; CNPQ::CIENCIAS DA SAUDE::ODONTOLOGIA

Introduction: Sodium alendronate (ALN) is a potent inhibitor of osteoclastic absorption in bone disease treatments. Its activity by regulating the action of osteoblasts and osteoclasts is attributed, in part, to the release of osteogenic growth factors derived from the matrix, including TGFβ-1, whose function is to promote polymorphonuclear cell chemotaxis, fibroblast proliferation and synthesis of collagen I, aiding in bone repair. Objective: The objective of this study is to evaluate the effect of ALN, in different doses, on rats submitted to femoral fracture. Materials and methods: We used 45 Wistar rats, approximately 500 mg, divided into 3 groups: A1 (ALN 1mg / kg), A2 (ALN 3mg / kg) and C (saline solution). The rats were submitted to transverse femoral fracture surgically reduced with titanium plates and screws. In the immediate postoperative period the medication /placebo was initiated by intraperitoneal injection, 3 times a week, during 45 days. After euthanasia, the animals had histological evaluation of the kidneys and liver, and the femur was submitted to histomorphometric and immunohistochemical evaluation with TGF β-1 marker. The differences between samples were analyzed in groups by Kruskal-Wallis. Results: Analysis of the A1 group showed hyaline degeneration and tubular ectasia. Statistical evaluation was performed using the Statistical Packger for Social Science program with a 95% confidence interval. Results: Analysis of the A1 group showed hyaline degeneration and tubular ectasia. In the A2 group, the cells presented hyaline degeneration, tubular ectasia and amyloid degeneration, with ballooned cells. In the livers of the A1 and A2 groups the presence of liver cells with clear cytoplasm and microguticular aspect characteristic of hepatic steatosis was observed. Regarding the femur, in the histomorphometric analysis, there was no difference in the amount of internally and externally to the callus bone trabeculate measured (p ≥ 0.05). The immunohistochemical evaluation showed positivity of the TGF β-1 in the control group, being the marking predominantly in the spinal area. It also presented positive marking in small chondrocytes but negative in hypertrophic ones. In the A1 group it was possible to observe an intense area of cartilaginous expansion, with a predominance of intensely positive hypertrophic cartilage TGF β-1, even in areas with bone matrix. There was a small positivity in the medullar area in contrast to the control. Group A2 presented an intense amount of chondroid matrix in the medium of hypertrophic cartilage and moderate number of TGFβ-1 cells with little area of positivity in the medullary area. Conclusions: The dosage of 1mg / kg sodium alendronate promotes a greater cellular differentiation activity in the region of the bone callus with mild systemic involvement of the kidney and liver. Alendronate 3mg / kg dose became toxic, causing significant impairment of the kidneys and liver, without positive alterations in cell differentiation.