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  • Title: Physiologic and pharmacologic effects of estrogen and progestins on bone.
    Author: DeCherney A.
    Journal: J Reprod Med; 1993 Dec; 38(12 Suppl):1007-14. PubMed ID: 8120857.
    Abstract:
    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. A lack of estrogen plays a key role in the development of osteoporosis which is common in postmenopausal women. Estrogen therapy (e.g., oral contraceptives) reduces menopause-related bone loss and the risk of bone fracture. It increases bone mass premenopausally. Medical researchers do not yet clearly know the mechanisms by which estrogen affects bone. Possible mechanisms include direct, receptor-mediated actions and indirect actions on systemic hormones. Regulation of cytokine production in the local bone microenvironment may mediate estrogen's antiresorptive effect. Estrogen may modify the hormones that regulate calcium balance, e.g., calcitonin. Researchers are even less sure of the role of progestins in preventing bone loss. Research in postmenopausal women and of add-back therapy suggests that norethindrone protects cortical bone but not trabecular bone. Medroxyprogesterone does not have this effect, however. A daily dose of 5 or 10 mg of norethindrone has the same effects on biochemical markers of bone turnover as does estrogen. Possible mechanisms by which progestins affect bone are stimulation of translocation of the estrogen receptor in the rat liver and part of norethindrone is converted in vivo to ethinyl estradiol. Even though more research is needed to clarify the effects of estrogens and progestins on bone, the existing findings suggest that these hormones do not adversely affect bone and may even increase bone mass.
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