雌激素衰退可诱发骨重建活跃及骨质疏松性骨关节炎（Osteoarthritis, OA）。OA是中老年人群主要致残原因之一，目前尚无有效药物阻断其病理进程。关节软骨与软骨下骨间生物信息交流已成为OA防治研究的新靶点。课题组前期研究发现，骨吸收抑制剂降钙素（calcitonin，CT）对机械损伤造成的OA模型具有一定的保护作用，但对骨质疏松OA干预效果及机制尚不明确。本项目拟以去势诱发的大鼠骨质疏松性OA模型为干预对象，以Wnt信号通路对软骨代谢和骨重建的双重调控作用为切入点，通过体内外研究，探讨CT能否通过干预Wnt信号通路对关节软骨和软骨下骨的双靶向调控阻止骨质疏松性OA的病理进程，为将CT开发为新型治疗OA的药物提供重要的实验证据，并为其他通过对软骨和软骨下骨的双靶向调控干预OA进程的的药物研发提供参考。

Estrogen deficiency leads to abnormal subchondral bone remodeling and thereby overlying cartilage degeneration, which is defined as osteoporotic osteoarthritis(OA). OA is one of the most common cause of disability in the elderly popoulation. Currently there is no structure modifying treatments approved for OA.Biological crosstalk between cartilage and subchondral bone has become a therapeutic target in OA. Our previous study indicated that a bone resorption inhibitor, calcitonin (CT) had some certain protective role in a secondary OA model induced by mechanical instability yet is unclear on the intervention effect and mechanism of osteoporotic OA.This project aims to, in view of the dual role of Wnt signaling pathway in modulating cartilage metablism and subchondral bone remodeling, investigate whether CT can inhibit the cartilage degeneration in osteoporotic OA in ovariectomized rat by modulating the cartilage and subchondral bone remodeling through Wnt signaling pathway by in vivo and in vitro study, therefore provide some major theoretical and experimental fundamentals for developing CT as structure modifying treatment for OA, at the same time, it can produce some valuable references for the other studies aiming to develop new treatment for OA through the targeted-regulation of both cartilage and subchondral bone.