Vanderschueren D, Bouillon R
Laboratorium voor experimentele geneeskunde en endocrinologie, Onderwijs en navorsing, Leuven, Belgium.
Calcif Tissue Int. 1995 May;56(5):341-6. doi: 10.1007/BF00301598.
Androgen receptors are present at low densities in osteoblasts. Androgens are also metabolized in bone. (Non)aromatizable androgens probably induce proliferation of osteoblasts and differentiation. A direct effect of androgens on osteoclasts has not been demonstrated. Androgens may however inhibit bone resorption indirectly, by an inhibition of the recruitment of osteoclast precursors from bone marrow, by decreased secretion of interleukin-6 and/or prostaglandin E2, and/or by an increased sensitivity of marrow cells or osteoblasts for bone resorption stimulating factors such as PTH. The recent demonstration of androgen receptors in bone marrow stromal and osteoclast-like cells opens new perspectives in this respect. During puberty, androgens stimulate bone growth both directly and indirectly. Observations in androgen-resistant animals clearly demonstrated that the sexual dimorphism of bone depends on the presence of a functional androgen receptor. Optimal peak bone mass seems related to an appropriately timed androgen secretion. In adults, androgens are also involved in maintenance of the male skeleton. Androgen replacement may prevent further bone loss in hypogonadal men, however, it seems difficult to fully correct bone mass in these men.
雄激素受体在成骨细胞中以低密度存在。雄激素也在骨骼中进行代谢。（非）芳香化雄激素可能诱导成骨细胞增殖和分化。雄激素对破骨细胞的直接作用尚未得到证实。然而，雄激素可能通过抑制骨髓中破骨细胞前体的募集、减少白细胞介素 -6 和 / 或前列腺素 E2 的分泌，和 / 或通过增加骨髓细胞或成骨细胞对诸如甲状旁腺激素等骨吸收刺激因子的敏感性来间接抑制骨吸收。最近在骨髓基质细胞和破骨细胞样细胞中发现雄激素受体，在这方面开辟了新的前景。在青春期，雄激素直接和间接地刺激骨骼生长。对雄激素抵抗动物的观察清楚地表明，骨骼的性别差异取决于功能性雄激素受体的存在。最佳峰值骨量似乎与适时的雄激素分泌有关。在成年人中，雄激素也参与维持男性骨骼。雄激素替代可能会预防性腺功能减退男性的进一步骨质流失，然而，似乎很难完全纠正这些男性的骨量。
