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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >The structural and hormonal basis of sex differences in peak appendicular bone strength in rats.
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The structural and hormonal basis of sex differences in peak appendicular bone strength in rats.

机译：大鼠峰值阑尾骨强度性别差异的结构和激素基础。

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摘要

To identify the structural and hormonal basis for the lower incidence of fractures in males than females, sex differences in femoral mid-shaft geometry and breaking strength were studied in growth hormone (GH)-replete and -deficient male and female rats. Sexual dimorphism appeared during growth. Cortical thickening occurred almost entirely by acquisition of bone on the outer (periosteal) surface in males and mainly on the inner (endocortical) surface in females. By 8 months of age, males had 22% greater bone width and 33% greater breaking strength than females. Gonadectomy (Gx) at 6 weeks reduced sex differences in bone width to 7% and strength to 21% by halving periosteal bone formation in males and doubling it in females. Gx had no net effect on the endocortical surface in males but abolished endocortical bone acquisition in females. GH deficiency halved periosteal bone formation and had no net effect on the endocortical surface in males, but abolished bone acquisition on both surfaces in females, leaving males with 17% greater bone width and 44% greater breaking strength than females. Sex hormone deficiency produces greater bone fragility in males than females by removing a stimulator of periosteal growth in males and removing an inhibitor of periosteal growth in females. GH deficiency produces less bone fragility in males than females because males retain androgen-dependent periosteal bone formation while bone acquisition on both surfaces is abolished in females. Thus, periosteal growth is independently and additively stimulated by androgens and GH in males, inhibited by estrogen, and stimulated by GH in females. The hormonal regulation of bone surfaces establishes the amount and spatial distribution of bone and so the sexual dimorphism in its strength.
机译：为确定雄性骨折的发生率低于雌性骨折的结构和激素基础，研究了在生长激素（GH）充足和不足的雄性和雌性大鼠中股骨中轴几何形状和断裂强度的性别差异。生长期间出现性二态性。皮质增厚几乎完全是通过雄性外骨骼（骨膜）表面上的骨骼采集而实现的，而雌性则主要在内（内膜）表面上采集骨骼。到8个月大时，男性的骨宽比女性大22％，断裂强度大33％。通过将男性的骨膜骨形成减半并将女性的骨膜形成倍增，在第6周进行性腺切除术（Gx）将性别差异减少到7％，将性别差异减少到21％。 Gx对雄性的皮质内膜表面没有净作用，但在雌性中取消了皮质内骨的获取。生长激素缺乏症使雄性骨膜的骨形成减少了一半，并且对皮质内膜表面没有净作用，但是雌性消除了两面的骨获取，使雄性的骨宽比雌性增加了17％，断裂强度也增加了44％。通过去除雄性骨膜生长的刺激物和去除雌性骨膜生长的抑制剂，性激素缺乏症比雄性产生更大的骨骼脆性。生长激素缺乏症在雄性中产生的脆性低于雌性，因为雄性保留了雄激素依赖性骨膜的骨形成，而雌性在两个表面上的骨吸收均被取消。因此，雄性激素和生长激素在男性中独立和累加地刺激了骨膜的生长，雌激素抑制了其生长，雌性生长激素的刺激了骨膜的生长。骨骼表面的激素调节建立了骨骼的数量和空间分布，因此建立了骨骼的性二态性。

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