Estudo do ranelato de estrôncio no reparo ósseo de defeitos críticos em calvária de ratos : participação da via RANK/RANKL/OPG

• Ano de defesa: 2013
• Autor(a) principal: Fiallos, Ana Cristina de Mello
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Regeneração Óssea; Citocinas; Estrôncio
• Link de acesso: http://www.repositorio.ufc.br/handle/riufc/6873

The bone repair is a multifunctional process involving various mediators. Among the many drugs that interfere with this process, we highlight the Strontium Ranelate (SrR), which has a dual mechanism of action, stimulating neoformation at the same time, which inhibits bone resorption. To evaluate the osteoinductive capacity, models of study that investigate the potential for bone repair site have been used, such as induction of critical size defects (CSD) in rat calvaria. The aim of this study was to evaluate bone healing induced by SrR in critical defects of 8 mm in diameter in rat calvaria. For this purpose, immediately after surgery, the CSD received a single application of SrR (2.1 and 6.3 mg) or no treatment (Control). Groups of animals were sacrificed at 0 h and at 15, 45, 90 and 120 days after induction of CSD and calvarial samples were removed and processed for analysis by macroscopic type Cone Beam Computed Tomography (CBCT), histological (HE) and immunohistochemical for RANKL and OPG. In CBCT analysis, it was found that induction of CSD group SrR 6.3 mg caused a significant reduction of the areas of CSD at 90 days (67.79 ± 2.32 mm²) and at 120 days (62.28 ± 4.17 mm²) compared to calvariae newly induced (0 h) (78.61 mm² ± 0.96) (p<0.05) but not compared to Control groups at 90 days (74.2 ± 2.73 mm²) and at 120 days (72.04 ±1.74 mm²) (p>0.05). We observed in the histological analysis of calvariae of Control groups significant changes related to bone repair when compared to normal group (p<0.05). The animals that received SrR (2.1 mg) showed no significant histological changes, compared to the Control groups in all experimental periods (p>0.05), while animals of SrR 6.3 mg group showed significantly histological features consistent with bone repair at 90 days and at 120 days as neoformation in edge and center of the CSD when compared to Control or SrR 2.1 mg groups (p<0.05). To complement these results, the calvariae of animals after 120 days of topical application of SrR (6.3 mg) showed intense immunostaining for OPG and RANKL negative, whereas the calvariae of Control groups showed moderate immunoreactivity only for RANKL. Thus, it can be concluded that the local treatment with SrR (6.3 mg) revealed its role favoring osteoinductive bone repair by modulating the CSD RANK/RANKL/OPG.