绝经后骨质疏松症发病机制研究进展

绝经后骨质疏松症(postmenopausal osteoporosis,PMOP)是指女性绝经后卵巢内分泌功能失调衰退,导致雌激素水平下降,从而导致破骨细胞的骨吸收大于成骨细胞的骨形成的一种代谢性疾病。骨质疏松症没有特异性的临床表现,直到轻微的创伤诱发骨折时才会引起重视,所以预防骨质疏松症是临床工作的重中之重。目前有很多研究报道了骨质疏松症发生发展的机制,在机体内雌激素的缺乏引起炎症因子与MicroRNA激活,从而引起RANKL-RANK-OPG轴的紊乱,引起骨质流失。同时雌激素充当抗氧化剂来保护骨,抵抗氧化应激。本文就绝经后骨质疏松症的发生机制做一综述。

Advances in research on the mechanism of postmenopausal osteoporosis

Postmenopausal osteoporosis (PMOP) is a metabolic disease that leads to the decrease of estrogen level in women, resulting in the osteoclastic bone resorption over osteoblastic bone formation. There are no specific clinical symptoms of osteoporosis, until a slight stress-induced fracture occurs when people may pay attention. Therefore, prevention of osteoporosis is the priority of the clinical work. Numerous studies have reported the mechanism of development of osteoporosis. The lack of estrogen in the body causes inflammation and microRNA activation, causing disorder of RANKL-RANK-OPG axis, then resulting in bone loss. Estrogen acts as an antioxidant to protect the bone loss and against oxidative stress. This article aims to summarize the mechanism of postmenopausal osteoporosis.