Estrogens and progestogens influence the bone. The major physiological effect of estrogen is the inhibition of bone resorption whereas progestogens exert activity through binding to specific progesterone receptors. New estrogen-free contraceptive and its possible implication on bone turnover are discussed in this review. Insufficient bone acquisition during development and/or accelerated bone loss after attainment of peak bone mass (PBM) are 2 processes that may predispose to fragility fractures in later life. The relative importance of bone acquisition during growth versus bone loss during adulthood for fracture risk has been explored by examining the variability of areal bone mineral density (BMD) (aBMD) values in relation to age. Bone mass acquired at the end of the growth period appears to be more important than bone loss occurring during adult life. The major physiological effect of estrogen is the inhibition of bone resorption. When estrogen transcription possesses binds to the receptors, various genes are activated, and a variety modified. Interleukin 6 (IL-6) stimulates bone resorption, and estrogen blocks osteoblast synthesis of IL-6. Estrogen may also antagonize the IL-6 receptors. Additionally, estrogen inhibits bone resorption by inducing small but cumulative changes in multiple estrogen-dependent regulatory factors including TNF-α and the OPG/RANKL/RANK system. Review on existing data including information about new estrogen-free contraceptives. All progestins exert activity through binding to specific progesterone receptors; hereby, three different groups of progestins exist: pregnanes, gonanes, and estranges. Progestins also comprise specific glucocorticoid, androgen, or mineralocorticoid receptor interactions. Anabolic action of a progestogen may be affected via androgenic, anti-androgenic, or synadrogenic activity. The C 19 nortestosterone class of progestogens is known to bind with more affinity to androgen receptors than the C21 progestins. This article reviews the effect of estrogens and progestogens on bone and presents new data of the currently approved drospirenone-only pill. The use of progestin-only contraceptives leading to an estradiol level between 30 and 50 pg/ml does not seem to lead to an accelerate bone loss.

中文翻译：

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无雌激素避孕中的骨骼健康。

雌激素和孕激素影响骨骼。雌激素的主要生理作用是抑制骨吸收，而孕激素通过与特定的孕激素受体结合发挥活性。本综述讨论了新的无雌激素避孕药及其对骨转换的可能影响。发育过程中骨获取不足和/或达到峰值骨量 (PBM) 后加速骨丢失是可能在以后的生活中易患脆性骨折的 2 个过程。通过检查面积骨矿物质密度 (BMD) (aBMD) 值与年龄相关的变异性，探讨了生长过程中骨获取与成年期骨丢失对骨折风险的相对重要性。在生长期结束时获得的骨量似乎比成年期发生的骨质流失更重要。雌激素的主要生理作用是抑制骨吸收。当雌激素转录与受体结合时，各种基因被激活，多种基因被修饰。白细胞介素 6 (IL-6) 刺激骨吸收，雌激素阻断 IL-6 的成骨细胞合成。雌激素也可以拮抗 IL-6 受体。此外，雌激素通过诱导多种雌激素依赖性调节因子（包括 TNF-α 和 OPG/RANKL/RANK 系统）发生微小但累积的变化来抑制骨吸收。审查现有数据，包括有关新的无雌激素避孕药的信息。所有孕激素都通过与特定的孕激素受体结合发挥活性；特此，存在三组不同的孕激素：孕酮、孕酮和异位孕酮。孕激素还包含特定的糖皮质激素、雄激素或盐皮质激素受体相互作用。孕激素的合成代谢作用可能会受到雄激素、抗雄激素或促肾上腺皮质激素活性的影响。与 C21 孕激素相比，已知 C 19 去甲睾酮类孕激素与雄激素受体结合的亲和力更强。本文回顾了雌激素和孕激素对骨骼的影响，并介绍了目前批准的仅屈螺酮丸的新数据。仅使用孕激素避孕药导致雌二醇水平在 30 至 50 pg/ml 之间似乎不会导致加速骨质流失。或盐皮质激素受体相互作用。孕激素的合成代谢作用可能会受到雄激素、抗雄激素或促肾上腺皮质激素活性的影响。与 C21 孕激素相比，已知 C 19 去甲睾酮类孕激素与雄激素受体结合的亲和力更强。本文回顾了雌激素和孕激素对骨骼的影响，并介绍了目前批准的仅屈螺酮丸的新数据。仅使用孕激素避孕药导致雌二醇水平在 30 至 50 pg/ml 之间似乎不会导致加速骨质流失。或盐皮质激素受体相互作用。孕激素的合成代谢作用可能会受到雄激素、抗雄激素或促肾上腺皮质激素活性的影响。与 C21 孕激素相比，已知 C 19 去甲睾酮类孕激素与雄激素受体结合的亲和力更强。本文回顾了雌激素和孕激素对骨骼的影响，并介绍了目前批准的仅屈螺酮丸的新数据。仅使用孕激素避孕药导致雌二醇水平在 30 至 50 pg/ml 之间似乎不会导致加速骨质流失。本文回顾了雌激素和孕激素对骨骼的影响，并介绍了目前批准的仅屈螺酮丸的新数据。仅使用孕激素避孕药导致雌二醇水平在 30 至 50 pg/ml 之间似乎不会导致加速骨质流失。本文回顾了雌激素和孕激素对骨骼的影响，并介绍了目前批准的仅屈螺酮丸的新数据。仅使用孕激素避孕药导致雌二醇水平在 30 至 50 pg/ml 之间似乎不会导致加速骨质流失。