Estrogen, androgen, and the pathogenesis of bone fragility in women and men.
Estrogen, androgen, and the pathogenesis of bone fragility in women and men.
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DOI：
10.1007/s11914-004-0016-0
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发表时间：
2004-09-01
影响因子：
4.3
通讯作者：
Seeman, Ego
中科院分区：
文献类型：
--
作者：
Seeman, Ego
在生长过程中，女性雌激素缺乏可能会导致骨大小增加，这是由于去除了对骨膜附着的抑制，而失败的骨内膜附着会在较小的骨中产生薄的皮质和骨小梁。在男性中，雄激素缺乏导致骨膜和骨内膜附着减少，骨尺寸减小，皮质和骨小梁厚度减少。在纵向生长完成时，由于骨形成减少，年龄的增长与每个基本多细胞单位（BMU）中出现负骨平衡有关。骨丢失发生，但缓慢，因为重塑速度缓慢。在中年，在女性中，雌激素缺乏增加重塑速率，增加骨吸收的体积，并减少在其骨内膜（皮质内、小梁、皮质内）表面上重塑骨的众多BMU中的每一个中形成的骨体积，因此骨丢失加速。在男性中，重塑速率仍然缓慢，主要是由BMU中骨形成减少驱动的。20%至30%的老年男性性腺功能减退会导致骨质流失。在两种性别中，钙吸收不良和继发性甲状旁腺功能亢进可能部分是性激素依赖性的，并有助于皮质骨丢失。同时发生的骨膜附着部分抵消了骨内膜骨丢失，但女性的抵消程度低于男性。女性骨折多于男性，这是因为她们的骨骼较小，结构损伤较大，骨膜附着适应性较差。生长和衰老过程中的性激素缺乏是骨脆性发病机制的关键。
During growth, estrogen deficiency in females may produce increased bone size as a result of removal of inhibition of periosteal apposition, while failed endosteal apposition produces thin cortices and trabeculae in the smaller bone. In males, androgen deficiency produces reduced periosteal and endosteal apposition, reduced bone size, and cortical and trabecular thickness. At completion of longitudinal growth, advancing age is associated with emergence of a negative bone balance in each basic multicellular unit (BMU) because of reduced bone formation. Bone loss occurs, but slowly because the remodeling rate is slow. In midlife, in females, estrogen deficiency increases remodeling rate, increases the volume of bone resorbed, and decreases the volume of bone formed in each of the numerous BMUs remodeling bone on its endosteal (endocortical, trabecular, intracortical) surfaces so bone loss accelerates. In males, remodeling rate remains slow and is driven largely by reduced bone formation in the BMU. Hypogonadism in 20% to 30% of elderly men contributes to bone loss. In both sexes, calcium malabsorption and secondary hyperparathyroidism may partly be sex-hormone dependent and contributes to cortical bone loss. Concurrent periosteal apposition partly offsets endosteal bone loss, but less so in women than in men. More women than men fracture because their smaller skeleton incurs greater architectural damage and adapts less by periosteal apposition. Sex hormone deficiency during growth and aging is pivotal in the pathogenesis of bone fragility.