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雌激素替代治疗 (ERT)是绝经后骨质疏松症的首选治疗方案。ERT的作用机制尚不完全清楚 ,除通过钙调节激素间接起作用外 ,还可通过雌激素受体 (ER)直接调节成骨细胞 (OB)和破骨细胞 (OC)的增殖、分化或活性 ;也可通过抑制或促进细胞因子或生长因子的生成起作用 ;还可通过抑制OB和骨细胞的凋亡 ,促进OC的凋亡发挥作用。此外 ,新近提出雌激素可降低骨髓的信号强度阈值有利于在靠近骨髓的骨组织启动保存方式骨重建而保留骨组织。开展ERT的机制研究将为绝经后骨质疏松 (PMOP)的发病机制研究和预防、治疗开辟广阔的领域
Estrogen replacement therapy (ERT) is the treatment of choice for postmenopausal osteoporosis. The mechanism of action of ERT is not yet fully understood. In addition to the indirect role of calcium-regulated hormones, the proliferation, differentiation or activity of osteoblasts (OB) and osteoclasts (OC) can be directly regulated by the estrogen receptor (ER) ; Can also inhibit or promote the formation of cytokines or growth factors; also play a role in promoting the apoptosis of OC by inhibiting OB and osteoblast apoptosis. In addition, the newly proposed threshold signal intensity of estrogen can reduce the bone marrow helps bone tissue near the bone marrow to start preservation of bone remodeling and preservation of bone tissue. Research on the mechanism of ERT will open up a broad field of research on the pathogenesis of postmenopausal osteoporosis (PMOP) and its prevention and treatment