Lindberg M K, Vandenput L, Movèrare Skrtic S, Vanderschueren D, Boonen S, Bouillon R, Ohlsson C
Division of Endocrinology, Department of Internal Medicine, Sahlgrenska University Hospital, Göteborg, Sweden.
Minerva Endocrinol. 2005 Mar;30(1):15-25.
Loss of estrogens or androgens causes bone loss by increasing the rate of bone remodeling, and also causes an imbalance between resorption and formation by prolonging the lifespan of osteoclasts and shortening the lifespan of osteoblasts. Conversely, treatment with androgens, as well as estrogens, maintains cancellous bone mass and integrity, regardless of age or sex. Both androgens, via the androgen receptor (AR), and estrogens, via the estrogen receptors (ERs) can exert these effects, but the relative contribution of these 2 pathways remains uncertain. Androgens, like estrogens, stimulate endochondral bone formation at the start of puberty, whereas they induce epiphyseal closure at the end of puberty, thus, they have a biphasic effect. Androgen action on the growth plate is, however, clearly mediated via aromatization into estrogens and interaction with ER alpha. Androgens increase, while estrogens decrease radial growth. This differential effect of the sex steroids may be important because bone strength in males seems to be determined by higher periosteal bone formation and, therefore, greater bone dimensions. Experiments in mice suggest that both the AR and ER alpha pathways are involved in androgen action on radial bone growth. ER beta may mediate growth-limiting effects of estrogens in the female but does not seem to be involved in the regulation of bone size in males. In conclusion, androgens may protect men against osteoporosis via maintenance of cancellous bone mass and expansion of cortical bone. This androgen action on bone is mediated by the AR and ER alpha.
雌激素或雄激素的缺失会通过提高骨重塑速率导致骨质流失，还会通过延长破骨细胞寿命和缩短成骨细胞寿命，造成吸收与形成之间的失衡。相反，雄激素以及雌激素治疗可维持松质骨量和完整性，无论年龄或性别。雄激素通过雄激素受体（AR）以及雌激素通过雌激素受体（ER）均可发挥这些作用，但这两条途径的相对贡献仍不确定。与雌激素一样，雄激素在青春期开始时刺激软骨内成骨，而在青春期结束时诱导骨骺闭合，因此，它们具有双相作用。然而，雄激素对生长板的作用显然是通过芳香化转化为雌激素并与ERα相互作用介导的。雄激素促进，而雌激素抑制径向生长。性类固醇的这种差异作用可能很重要，因为男性的骨强度似乎取决于较高的骨膜骨形成，因此骨尺寸更大。小鼠实验表明，AR和ERα途径均参与雄激素对径向骨生长的作用。ERβ可能介导雌激素对女性生长的限制作用，但似乎不参与男性骨大小的调节。总之，雄激素可能通过维持松质骨量和扩大皮质骨来保护男性免受骨质疏松症的影响。雄激素对骨的这种作用由AR和ERα介导。
