Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9458
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dc.contributor.authorKim, Bom-Taecken
dc.contributor.authorMosekilde, Lisen
dc.contributor.authorDuan, Yunboen
dc.contributor.authorZhang, Xin-Zhouen
dc.contributor.authorTornvig, Liseen
dc.contributor.authorThomsen, Jesper Skovhusen
dc.contributor.authorSeeman, Egoen
dc.date.accessioned2015-05-15T22:33:41Z
dc.date.available2015-05-15T22:33:41Z
dc.date.issued2003-01-01en
dc.identifier.citationJournal of Bone and Mineral Research : the Official Journal of the American Society For Bone and Mineral Research; 18(1): 150-5en
dc.identifier.govdoc12510817en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9458en
dc.description.abstractTo 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.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherBiomechanical Phenomenaen
dc.subject.otherBone and Bones.anatomy & histology.physiologyen
dc.subject.otherFemaleen
dc.subject.otherGonadal Steroid Hormones.deficiency.physiologyen
dc.subject.otherGrowth Hormone.deficiency.physiologyen
dc.subject.otherHumansen
dc.subject.otherMaleen
dc.subject.otherOrchiectomyen
dc.subject.otherOsteogenesis.physiologyen
dc.subject.otherOsteoporosis.etiology.pathology.physiopathologyen
dc.subject.otherOvariectomyen
dc.subject.otherRatsen
dc.subject.otherRats, Inbred F344en
dc.subject.otherSex Characteristicsen
dc.subject.otherStress, Mechanicalen
dc.titleThe structural and hormonal basis of sex differences in peak appendicular bone strength in rats.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Bone and Mineral Researchen
dc.identifier.affiliationDepartment of Endocrinology, Austin and Repatriation Medical Center, University of Melbourne, Melbourne, Australiaen
dc.identifier.doi10.1359/jbmr.2003.18.1.150en
dc.description.pages150-5en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/12510817en
dc.type.austinJournal Articleen
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
crisitem.author.deptEndocrinology-
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