Loss of estrogens or androgens increases the rate of bone remodeling by removing restraining effects on osteoblastogenesis and osteoclastogenesis, and also causes a focal imbalance between resorption and formation by prolonging the lifespan of osteoclasts and shortening the lifespan of osteoblasts. Conversely, androgens, as well as estrogens, maintain cancellous bone mass and integrity, regardless of age or sex. Although androgens, via the androgen receptor (AR), and estrogens, via the estrogen receptors (ERs), can exert these effects, their relative contribution remains uncertain. Recent studies suggest that androgen action on cancellous bone depends on (local) aromatization of androgens into estrogens. However, at least in rodents, androgen action on cancellous bone can be directly mediated via AR activation, even in the absence of ERs. Androgens also increase cortical bone size via stimulation of both longitudinal and radial growth. First, androgens, like estrogens, have a biphasic effect on endochondral bone formation: at the start of puberty, sex steroids stimulate endochondral bone formation, whereas they induce epiphyseal closure at the end of puberty. Androgen action on the growth plate is, however, clearly mediated via aromatization in estrogens and interaction with ERalpha. Androgens increase radial growth, whereas estrogens decrease periosteal bone formation. This effect of androgens may be important because bone strength in males seems to be determined by relatively higher periosteal bone formation and, therefore, greater bone dimensions, relative to muscle mass at older age. Experiments in mice again suggest that both the AR and ERalpha pathways are involved in androgen action on radial bone growth. ERbeta 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. Such androgen action on bone is mediated by the AR and ERalpha.

中文翻译：

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雄激素和骨头。

雌激素或雄激素的丧失通过消除对成骨细胞和成骨细胞生成的抑制作用而增加了骨重塑的速率，并且还通过延长破骨细胞的寿命并缩短了成骨细胞的寿命而导致了吸收和形成之间的局部失衡。相反，无论年龄或性别，雄激素以及雌激素均保持松质骨质量和完整性。尽管雄激素通过雄激素受体（AR）和雌激素通过雌激素受体（ER）可以发挥这些作用，但它们的相对作用仍然不确定。最近的研究表明，雄激素对松质骨的作用取决于雄激素（局部）芳香化为雌激素。但是，至少在啮齿动物中，即使没有ERs，雄激素对松质骨的作用也可以通过AR激活直接介导。雄激素还通过刺激纵向和径向生长来增加皮质骨的大小。首先，雄激素与雌激素一样，对软骨内骨形成具有双相作用：在青春期开始时，性类固醇刺激软骨内骨形成，而在青春期结束时它们诱导骨epi闭合。然而，雄激素在生长板上的作用显然是通过雌激素的芳香化作用以及与ERalpha的相互作用来介导的。雄激素增加径向生长，而雌激素减少骨膜骨形成。雄激素的这种作用可能很重要，因为男性的骨强度似乎是由相对较高的骨膜相对于较高年龄的骨质所决定的，因此，骨膜的骨尺寸相对较高。小鼠实验再次表明，AR和ERalpha途径均参与雄激素对in骨生长的作用。ERbeta可能介导雌激素对女性的生长限制作用，但似乎不参与男性的骨大小调节。总之，雄激素可以通过维持松质骨质量和扩张皮质骨来保护男性免受骨质疏松症的侵害。这种雄激素对骨骼的作用是由AR和ERalpha介导的。