老年骨质疏松机制及股骨转子间骨折治疗的研究进展.docx

老年骨质疏松机制及股骨转子间骨折治 疗的研究进展 才林艾光禹孙强 新疆维吾尔自治区独山子石化医院外二科 摘要: 骨质疏松症是一种以脆性骨折为显著表现的全身性、代谢性骨骼系统疾病。其发 病原因包括多种因素，根据目前的流行病学研究，骨质疏松及相关性骨折的发 病率会继续增加。本文主要关注老年骨质疏松的机制、涉及相关基因、信号传递 方面的基础研究及其继发股骨粗隆间骨折的临床治疗的进展。成骨细胞通过Wnt 信号通路，促进成骨细胞活化。骨细胞通过产生前列腺素E2,促进细胞核因子 kB受体激活蛋白(RANK)与细胞核因子kB受体激活蛋白配体(RANKL)结合, 促进破骨细胞分化及其对骨的吸收。而成骨细胞则阻碍上述过程。丝裂原活化蛋 白激酶信号通路中的ERK1/2通路、JNK通路、P38通路与骨质疏松的治疗有关。 牛长激素和胰岛素样牛长因子通过JAKSTAT信号通路，保持成骨细胞和破骨细 胞稳定维持骨量，若两者之间的关系破坏，则会出现骨质疏松。基于上述基础研 究，临床上出现了更多的抗骨质疏松药物。在手术治疗方面，传统动力覩螺钉、 解剖型钢板、Gamma钉、股骨近端髓内钉的地位继续下降，股骨近端防旋髓内钉 (PFNA)及其改型PENA-II的发明和使用，坚持了科学的髓内固定，增加了对于 股骨颈骨质的充填、提高了把持力、抗旋力和纵行加压，成为目前老年骨质疏松 性粗隆间骨折临床治疗的首选。对于部分患者，髓关节置换也成为首次治疗或者 补救性治疗的方法，虽然有较多缺点，但可提高手术疗效，早期下地。 关键词： 骨质疏松;覩骨折;信号传导;治疗; 作者简介：才林，Email :agy001@163. com 收稿日期：2016-08-26 Research progress of the mechanism of senile osteoporosis and the teatment of intertrochanteric fracture Cai Lin Ai Guangyu Sun Qiang Department of Second Surgery, Dushanzi Petrochemical Hospital, Xinjiang Uygur Autonomous Region; Abstract： Osteoporosis is a kind of bri ttle fracture as a significant manifestation of systemic，metabolic bone diseases. As a multifactorial diseases, the incidence of osteoporosis and related fractures will continuc to increase, based on current epidemiological studies. This review focuses on progress of osteoporosis-related genes, signal transfer aspects of basic research and clinical treatment of secondary intertrochanteric fracture. Osteoblasts promote activation of osteoblast with Wnt pathway. By pros taglandin E2 (PGE2) bone cells promote the combina tion of receptor activator of NF~k B and receptor activator of nuclear factor k B ligand (RANK/RANKL) , promoting osteoclast differentiation and bone absorption. Osteoblasts to the opposite. In the mitogen-activated protein kinase signaling pathway, ERK pathway, JNK pathway, P38 pathway and treatment of osteoporosis arc closely linked Through the JAK-STAT pathway, growth hormone and insulin-like growth factor-1 maintain the ratio osteoblasts and osteoclasts and then bone mass. Ratio