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The structural and hormonal basis of sex differences in peak appendicular bone strength in rats.

Authors
Kim, BT; Mosekilde, L; Duan, Y; Zhang, XZ; Tornvig, L; Thomsen, JS; Seeman, E
Citation
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 18(1):150-155, 2003
Journal Title
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
ISSN
0884-04311523-4681
Abstract
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.
MeSH terms
AnimalsBiomechanicsBone and Bones/anatomy & histology*Bone and Bones/physiology*FemaleGonadal Steroid Hormones/deficiencyGonadal Steroid Hormones/physiology*Growth Hormone/deficiencyGrowth Hormone/physiology*HumansMaleOrchiectomyOsteogenesis/physiologyOsteoporosis/etiologyOsteoporosis/pathologyOsteoporosis/physiopathologyOvariectomyRatsRats, Inbred F344Sex CharacteristicsStress, Mechanical
DOI
10.1359/jbmr.2003.18.1.150
PMID
12510817
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Family Practice & Community Health
AJOU Authors
김, 범택
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