摘要
骨质疏松症是以骨量减低、骨组织微细结构破坏导致骨脆性增加、骨折风险升高的全身性骨病。正常的骨代谢依赖于成骨细胞介导的骨形成和破骨细胞调节的骨吸收作用平衡。当骨形成减低、骨吸收亢进时,骨代谢失衡引起骨量丢失。Wnt/β-catenin、RANKL/RANK/OPG等通路是参与骨代谢调节的重要通路,也是各类抗骨质疏松药物的作用靶点。目前骨质疏松的治疗药物通过作用于这些通路的关键靶点,调节成骨细胞和/或破骨细胞分化、成熟及其功能,发挥促进骨形成、抑制骨吸收的作用。抗骨质疏松药物的选择需综合考虑其对骨密度、骨转换、骨组织微细结构、药物不良反应及对机体代谢环境的影响等因素。本文旨在总结目前临床应用的抗骨质疏松药物的分子作用机制,通过对骨形成和骨吸收的不同影响,以及对其他组织的作用,探讨各类抗骨质疏松新药的作用特点,以期为骨质疏松症的临床应用治疗提供指导。
Osteoporosis is characterized by the decreasing of bone mineral density and bone strength, resulting in fragile bones and increased risk of bone fracture. The normal bone metabolism relies on the balance of remodeling by means of osteoblast induced bone formation and osteoclast stimulated bone resorption. When the bone formation decreases or bone resorption enhances, bone loss occurs leading to osteoporosis. Wnt/β-catenin signaling pathway, RANKL/RANK/OPG NF-κB pathways play important roles in regulating bone formation and bone resorption. Anti-osteoporosis agents act on the key molecular targets, regulating differentiation, maturation and function of osteoblasts and osteoclasts, and farther maitain the balancement of bone formation/bone resorption. The optimal choice of anti-osteoporosis agents depend on not only the bone mineral density, but also bone remodeling, micro-architecture, fracture risk, side effects, and even systemic metabolic environment. In this study, we summarized the current use of anti-osteoporosis medications, and discussed molecular mechanisms on bone fomation and bone resorption to provide therapeutic strategies.
作者
董冰子
孙晓方
DONG Bing-zi;SUN Xiao-fang(Department of Endocrinology and Metabolism,The Affiliated Hospital of Qingdao University,Qingdao 266003,Shangdong,China)
出处
《中华骨质疏松和骨矿盐疾病杂志》
CSCD
北大核心
2018年第6期620-627,共8页
Chinese Journal Of Osteoporosis And Bone Mineral Research
基金
国家自然科学基金青年基金(81600691)
山东省自然科学基金博士基金(ZR2016HB08)
关键词
骨质疏松症
骨吸收
骨形成
破骨细胞
钙敏感受体
osteoporosis
bone resorption
bone formation
osteoclast
calcium-sensing receptor
