DeCherney A
Department of Obstetrics and Gynecology, Tufts University School of Medicine, Boston, Massachusetts.
J Reprod Med. 1993 Dec;38(12 Suppl):1007-14.
Estrogen deficiency has a primary role in the pathogenesis of osteoporosis, a major cause of morbidity and mortality in postmenopausal women. Estrogen therapy is associated with increased peak bone mass premenopausally and prevention of bone loss postmenopausally. The mechanisms by which estrogen exerts its effects on bone are not completely understood. Nonetheless, estrogen does affect calcium balance, and evidence suggests a direct mechanism via estrogen receptors on bone. The role of progestins in preventing bone loss is less well understood than that of estrogen. Studies in postmenopausal women and studies of add-back therapy in younger women have shown that norethindrone, but not medroxyprogesterone, treatment has a bone-sparing effect on cortical bone but not on trabecular bone. In addition, norethindrone, 5 or 10 mg daily, has effects on biochemical markers of bone turnover similar to those of estrogen, providing further evidence of a bone-sparing effect. The mechanisms for the effects of norethindrone on bone are unknown, although translocation of the estrogen receptor in an animal model and conversion in vivo to ethinyl estradiol have been postulated.
雌激素缺乏在骨质疏松症的发病机制中起主要作用，骨质疏松症是绝经后女性发病和死亡的主要原因。雌激素治疗与绝经前骨峰值增加以及绝经后骨质流失的预防有关。雌激素对骨骼发挥作用的机制尚未完全了解。尽管如此，雌激素确实会影响钙平衡，并且有证据表明存在一种通过骨骼上的雌激素受体的直接机制。与雌激素相比，孕激素在预防骨质流失方面的作用了解较少。对绝经后女性的研究以及对年轻女性的补充治疗研究表明，炔诺酮治疗对皮质骨有保骨作用，但对小梁骨没有，而甲羟孕酮则没有这种作用。此外，每天5或10毫克的炔诺酮对骨转换生化标志物的影响与雌激素相似，这进一步证明了其保骨作用。炔诺酮对骨骼产生作用的机制尚不清楚，尽管在动物模型中已推测雌激素受体会发生易位，并且在体内会转化为炔雌醇。
