Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/9458
Title: The structural and hormonal basis of sex differences in peak appendicular bone strength in rats.
Authors: Kim, Bom-Taeck;Mosekilde, Lis;Duan, Yunbo;Zhang, Xin-Zhou;Tornvig, Lise;Thomsen, Jesper Skovhus;Seeman, Ego
Affiliation: Department of Endocrinology, Austin and Repatriation Medical Center, University of Melbourne, Melbourne, Australia.
Issue Date: 1-Jan-2003
Citation: Journal of Bone and Mineral Research : the Official Journal of the American Society For Bone and Mineral Research; 18(1): 150-5
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.
Internal ID Number: 12510817
URI: http://ahro.austin.org.au/austinjspui/handle/1/9458
DOI: 10.1359/jbmr.2003.18.1.150
URL: http://www.ncbi.nlm.nih.gov/pubmed/12510817
Type: Journal Article
Subjects: Animals
Biomechanical Phenomena
Bone and Bones.anatomy & histology.physiology
Female
Gonadal Steroid Hormones.deficiency.physiology
Growth Hormone.deficiency.physiology
Humans
Male
Orchiectomy
Osteogenesis.physiology
Osteoporosis.etiology.pathology.physiopathology
Ovariectomy
Rats
Rats, Inbred F344
Sex Characteristics
Stress, Mechanical
Appears in Collections:Journal articles

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