Prior J C
Division of Endocrinology and Metabolism, University of British Columbia, Vancouver, Canada.
Endocr Rev. 1990 May;11(2):386-98. doi: 10.1210/edrv-11-2-386.
Experimental, epidemiological, and clinical data indicate that progesterone is active in bone metabolism. Progesterone appears to act directly on bone by engaging an osteoblast receptor or indirectly through competition for a glucocorticoid osteoblast receptor. Progesterone seems to promote bone formation and/or increase bone turnover. It is possible, through estrogen-stimulated increased progesterone binding to the osteoblast receptor, that progesterone plays a role in the coupling of bone resorption with bone formation. A model of the interdependent actions of progesterone and estrogen on appropriately-"ready" cells in each bone multicellular unit can be tied into the integrated secretions of these hormones within the ovulatory cycle. Figure 5 is an illustration of this concept. It shows the phases of the bone remodeling cycle in parallel with temporal changes in gonadal steroids across a stylized ovulatory cycle. Increasing estrogen production before ovulation may reverse the resorption occurring in a "sensitive" bone multicellular unit while gonadal steroid levels are low at the time of menstrual flow. The bone remodeling unit would then be ready to begin a phase of formation as progesterone levels peaked in the midluteal phase. From this perspective, the normal ovulatory cycle looks like a natural bone-activating, coherence cycle. Critical analysis of the reviewed data indicate that progesterone meets the necessary criteria to play a causal role in mineral metabolism. This review provides the preliminary basis for further molecular, genetic, experimental, and clinical investigation of the role(s) of progesterone in bone remodeling. Much further data are needed about the interrelationships between gonadal steroids and the "life cycle" of bone. Feldman et al., however, may have been prophetic when he commented; "If this anti-glucocorticoid effect of progesterone also holds true in bone, then postmenopausal osteoporosis may be, in part, a progesterone deficiency disease."
实验、流行病学和临床数据表明，孕酮在骨代谢中具有活性。孕酮似乎通过与成骨细胞受体结合直接作用于骨骼，或通过竞争糖皮质激素成骨细胞受体间接作用于骨骼。孕酮似乎能促进骨形成和/或增加骨转换。通过雌激素刺激增加孕酮与成骨细胞受体的结合，孕酮有可能在骨吸收与骨形成的偶联中发挥作用。孕酮和雌激素在每个骨多细胞单元中对适当“就绪”细胞的相互依存作用模型，可以与排卵周期内这些激素的综合分泌联系起来。图5说明了这一概念。它展示了骨重塑周期的各个阶段，与一个程式化排卵周期中性腺类固醇的时间变化并行。排卵前雌激素分泌增加可能会逆转在性腺类固醇水平在月经期间较低时，一个“敏感”骨多细胞单元中发生的吸收过程。然后，随着孕酮水平在黄体中期达到峰值，骨重塑单元将准备开始形成阶段。从这个角度来看，正常的排卵周期就像是一个自然的骨激活、连贯周期。对所审查数据的批判性分析表明，孕酮符合在矿物质代谢中起因果作用的必要标准。本综述为进一步进行孕酮在骨重塑中作用的分子、遗传、实验和临床研究提供了初步基础。关于性腺类固醇与骨“生命周期”之间的相互关系，还需要更多的数据。然而，费尔德曼等人评论时可能具有先见之明：“如果孕酮的这种抗糖皮质激素作用在骨骼中也成立，那么绝经后骨质疏松症可能部分是一种孕酮缺乏症。”
